Article

Hidradenitis suppurativa (HS) has an unpredictable disease course and poses substantial therapeutic challenges. It carries an increased risk for adverse cardiovascular outcomes and all-cause mortality. It also is associated with comorbidities including mood disorders, tobacco smoking, obesity, diabetes mellitus, sleep disorders, sexual dysfunction, and autoimmune diseases, which can complicate its management and considerably affect patients’ quality of life (QOL).¹ Hidradenitis suppurativa also disproportionately affects minority groups and has far-reaching inequities; for example, the condition has a notable economic impact on patients, including higher unemployment and disability rates, lower-paying jobs, less paid time off, and other indirect costs.^2,3 Race can impact how pain itself is treated. In one study (N = 217), Black patients with extremity fractures presenting to anemergency department were significantly less likely to receive analgesia compared to White patients despite reporting similar pain (57% vs 74%, respectively; P = .01).⁴ In another study, Hispanic patients were 7-times less likely to be treated with opioids compared to non-Hispanic patients with long-bone fractures.⁵ Herein, we highlight pain management disparities in HS patients.

Treating HS Comorbidities Helps Improve Pain

Pain is reported by almost all HS patients and is the symptom most associated with QOL impairment.^6,7 Pain in HS is multifactorial, with other symptoms and comorbidities affecting its severity. Treatment of acute flares often is painful and procedural, including intralesional steroid injections or incision and drainage.⁸ Algorithms for addressing pain through the treatment of comorbidities also have been developed.⁶ Although there are few studies on the medications that treat related comorbidities in HS, there is evidence of their benefits in similar diseases; for example, treating depression in patients with irritable bowel disease (IBD) improved pain perception, cognitive function, and sexual dysfunction.⁹

Depression exacerbates pain, and higher levels of depression have been observed in severe HS.^10,11 Additionally, more than 80% of individuals with HS report tobacco smoking.¹ Nicotine not only increases pain sensitivity and decreases pain tolerance but also worsens neuropathic, nociceptive, and psychosocial pain, as well as mood disorders and sleep disturbances.¹² Given the higher prevalence of depression and smoking in HS patients and the impact on pain, addressing these comorbidities is crucial. Additionally, poor sleep amplifies pain sensitivity and affects neurologic pain modulation.¹³ Chronic pain also is associated with obesity and sleep dysfunction.¹⁴

Treatments Targeting Pain and Comorbidities

Treatments that target comorbidities and other symptoms of HS also may improve pain. Bupropion is a well-studied antidepressant and first-line option to aid in smoking cessation. It provides acute and chronic pain relief associated with IBD and may perform similarly in patients with HS.^15-18 Bupropion also demonstrated dose-dependent weight reduction in obese and overweight individuals.^19,20 Additionally, varenicline is a first-line option to aid in smoking cessation and can be combined with bupropion to increase long-term efficacy.^21,22

Other antidepressants may alleviate HS pain. The selective norepinephrine reuptake inhibitors duloxetine and venlafaxine are recommended for chronic pain in HS.⁶ Selective serotonin reuptake inhibitors such as citalopram, escitalopram, and paroxetine are inexpensive and widely available antidepressants. Citalopram is as efficacious as duloxetine for chronic pain with fewer side effects.²³ Paroxetine has been shown to improve pain and pruritus, QOL, and depression in patients with IBD.²⁴ Benefits such as improved weight and sexual dysfunction also have been reported.²⁵

Metformin is well studied in Black patients, and greater glycemic response supports its efficacy for diabetes as well as HS, which disproportionately affects individuals with skin of color.²⁶ Metformin also targets other comorbidities of HS, such as improving insulin resistance, polycystic ovary syndrome, acne vulgaris, weight loss, hyperlipidemia, cardiovascular risk, and neuropsychologic conditions.²⁷ Growing evidence supports the use of metformin as a new agent in chronic pain management, specifically for patients with HS.^28,29

Final Thoughts

Hidradenitis suppurativa is a complex medical condition seen disproportionately in minority groups. Understanding common comorbidities as well as the biases associated with pain management will allow providers to treat HS patients more effectively. Dermatologists who see many HS patients should become more familiar with treating these associated comorbidities to provide patient care that is more holistic and effective.

Hidradenitis suppurativa (HS) has an unpredictable disease course and poses substantial therapeutic challenges. It carries an increased risk for adverse cardiovascular outcomes and all-cause mortality. It also is associated with comorbidities including mood disorders, tobacco smoking, obesity, diabetes mellitus, sleep disorders, sexual dysfunction, and autoimmune diseases, which can complicate its management and considerably affect patients’ quality of life (QOL).¹ Hidradenitis suppurativa also disproportionately affects minority groups and has far-reaching inequities; for example, the condition has a notable economic impact on patients, including higher unemployment and disability rates, lower-paying jobs, less paid time off, and other indirect costs.^2,3 Race can impact how pain itself is treated. In one study (N = 217), Black patients with extremity fractures presenting to anemergency department were significantly less likely to receive analgesia compared to White patients despite reporting similar pain (57% vs 74%, respectively; P = .01).⁴ In another study, Hispanic patients were 7-times less likely to be treated with opioids compared to non-Hispanic patients with long-bone fractures.⁵ Herein, we highlight pain management disparities in HS patients.

Treating HS Comorbidities Helps Improve Pain

Pain is reported by almost all HS patients and is the symptom most associated with QOL impairment.^6,7 Pain in HS is multifactorial, with other symptoms and comorbidities affecting its severity. Treatment of acute flares often is painful and procedural, including intralesional steroid injections or incision and drainage.⁸ Algorithms for addressing pain through the treatment of comorbidities also have been developed.⁶ Although there are few studies on the medications that treat related comorbidities in HS, there is evidence of their benefits in similar diseases; for example, treating depression in patients with irritable bowel disease (IBD) improved pain perception, cognitive function, and sexual dysfunction.⁹

Depression exacerbates pain, and higher levels of depression have been observed in severe HS.^10,11 Additionally, more than 80% of individuals with HS report tobacco smoking.¹ Nicotine not only increases pain sensitivity and decreases pain tolerance but also worsens neuropathic, nociceptive, and psychosocial pain, as well as mood disorders and sleep disturbances.¹² Given the higher prevalence of depression and smoking in HS patients and the impact on pain, addressing these comorbidities is crucial. Additionally, poor sleep amplifies pain sensitivity and affects neurologic pain modulation.¹³ Chronic pain also is associated with obesity and sleep dysfunction.¹⁴

Treatments Targeting Pain and Comorbidities

Treatments that target comorbidities and other symptoms of HS also may improve pain. Bupropion is a well-studied antidepressant and first-line option to aid in smoking cessation. It provides acute and chronic pain relief associated with IBD and may perform similarly in patients with HS.^15-18 Bupropion also demonstrated dose-dependent weight reduction in obese and overweight individuals.^19,20 Additionally, varenicline is a first-line option to aid in smoking cessation and can be combined with bupropion to increase long-term efficacy.^21,22

Other antidepressants may alleviate HS pain. The selective norepinephrine reuptake inhibitors duloxetine and venlafaxine are recommended for chronic pain in HS.⁶ Selective serotonin reuptake inhibitors such as citalopram, escitalopram, and paroxetine are inexpensive and widely available antidepressants. Citalopram is as efficacious as duloxetine for chronic pain with fewer side effects.²³ Paroxetine has been shown to improve pain and pruritus, QOL, and depression in patients with IBD.²⁴ Benefits such as improved weight and sexual dysfunction also have been reported.²⁵

Metformin is well studied in Black patients, and greater glycemic response supports its efficacy for diabetes as well as HS, which disproportionately affects individuals with skin of color.²⁶ Metformin also targets other comorbidities of HS, such as improving insulin resistance, polycystic ovary syndrome, acne vulgaris, weight loss, hyperlipidemia, cardiovascular risk, and neuropsychologic conditions.²⁷ Growing evidence supports the use of metformin as a new agent in chronic pain management, specifically for patients with HS.^28,29

Final Thoughts

Hidradenitis suppurativa is a complex medical condition seen disproportionately in minority groups. Understanding common comorbidities as well as the biases associated with pain management will allow providers to treat HS patients more effectively. Dermatologists who see many HS patients should become more familiar with treating these associated comorbidities to provide patient care that is more holistic and effective.

Hidradenitis suppurativa (HS) has an unpredictable disease course and poses substantial therapeutic challenges. It carries an increased risk for adverse cardiovascular outcomes and all-cause mortality. It also is associated with comorbidities including mood disorders, tobacco smoking, obesity, diabetes mellitus, sleep disorders, sexual dysfunction, and autoimmune diseases, which can complicate its management and considerably affect patients’ quality of life (QOL).¹ Hidradenitis suppurativa also disproportionately affects minority groups and has far-reaching inequities; for example, the condition has a notable economic impact on patients, including higher unemployment and disability rates, lower-paying jobs, less paid time off, and other indirect costs.^2,3 Race can impact how pain itself is treated. In one study (N = 217), Black patients with extremity fractures presenting to anemergency department were significantly less likely to receive analgesia compared to White patients despite reporting similar pain (57% vs 74%, respectively; P = .01).⁴ In another study, Hispanic patients were 7-times less likely to be treated with opioids compared to non-Hispanic patients with long-bone fractures.⁵ Herein, we highlight pain management disparities in HS patients.

Treating HS Comorbidities Helps Improve Pain

Pain is reported by almost all HS patients and is the symptom most associated with QOL impairment.^6,7 Pain in HS is multifactorial, with other symptoms and comorbidities affecting its severity. Treatment of acute flares often is painful and procedural, including intralesional steroid injections or incision and drainage.⁸ Algorithms for addressing pain through the treatment of comorbidities also have been developed.⁶ Although there are few studies on the medications that treat related comorbidities in HS, there is evidence of their benefits in similar diseases; for example, treating depression in patients with irritable bowel disease (IBD) improved pain perception, cognitive function, and sexual dysfunction.⁹

Depression exacerbates pain, and higher levels of depression have been observed in severe HS.^10,11 Additionally, more than 80% of individuals with HS report tobacco smoking.¹ Nicotine not only increases pain sensitivity and decreases pain tolerance but also worsens neuropathic, nociceptive, and psychosocial pain, as well as mood disorders and sleep disturbances.¹² Given the higher prevalence of depression and smoking in HS patients and the impact on pain, addressing these comorbidities is crucial. Additionally, poor sleep amplifies pain sensitivity and affects neurologic pain modulation.¹³ Chronic pain also is associated with obesity and sleep dysfunction.¹⁴

Treatments Targeting Pain and Comorbidities

Treatments that target comorbidities and other symptoms of HS also may improve pain. Bupropion is a well-studied antidepressant and first-line option to aid in smoking cessation. It provides acute and chronic pain relief associated with IBD and may perform similarly in patients with HS.^15-18 Bupropion also demonstrated dose-dependent weight reduction in obese and overweight individuals.^19,20 Additionally, varenicline is a first-line option to aid in smoking cessation and can be combined with bupropion to increase long-term efficacy.^21,22

Other antidepressants may alleviate HS pain. The selective norepinephrine reuptake inhibitors duloxetine and venlafaxine are recommended for chronic pain in HS.⁶ Selective serotonin reuptake inhibitors such as citalopram, escitalopram, and paroxetine are inexpensive and widely available antidepressants. Citalopram is as efficacious as duloxetine for chronic pain with fewer side effects.²³ Paroxetine has been shown to improve pain and pruritus, QOL, and depression in patients with IBD.²⁴ Benefits such as improved weight and sexual dysfunction also have been reported.²⁵

Metformin is well studied in Black patients, and greater glycemic response supports its efficacy for diabetes as well as HS, which disproportionately affects individuals with skin of color.²⁶ Metformin also targets other comorbidities of HS, such as improving insulin resistance, polycystic ovary syndrome, acne vulgaris, weight loss, hyperlipidemia, cardiovascular risk, and neuropsychologic conditions.²⁷ Growing evidence supports the use of metformin as a new agent in chronic pain management, specifically for patients with HS.^28,29

Final Thoughts

Hidradenitis suppurativa is a complex medical condition seen disproportionately in minority groups. Understanding common comorbidities as well as the biases associated with pain management will allow providers to treat HS patients more effectively. Dermatologists who see many HS patients should become more familiar with treating these associated comorbidities to provide patient care that is more holistic and effective.

Practice Gap

Scalp defects that extend to or below the periosteum often pose a reconstructive conundrum. Secondary-intention healing is challenging without an intact periosteum, and complex rotational flaps are required in these scenarios.¹ For a tumor that is at high risk for recurrence or when adjuvant therapy is necessary, tissue distortion of flaps can make monitoring for recurrence difficult. Similarly, for patients in poor health or who are elderly and have substantial skin atrophy, extensive closure may be undesirable or more technically challenging with a higher risk for adverse events. In these scenarios, additional strategies are necessary to optimize wound healing and cosmesis. A cadaveric split-thickness skin graft (STSG) consisting of biologically active tissue can be used to expedite granulation.²

Technique

Following tumor clearance on the scalp (Figure 1), wide undermining is performed and 3-0 polyglactin 910 epidermal pulley sutures are placed to partially close the defect. A cadaveric STSG is placed over the remaining exposed periosteum and secured under the pulley sutures (Figure 2). The cadaveric STSG is replaced at 1-week intervals. At 4 weeks, sutures typically are removed. The cadaveric STSG is used until the exposed periosteum is fully granulated and the surgeon decides that granulation arrest is unlikely. The wound then heals by unassisted granulation. This approach provides an excellent final cosmetic outcome while avoiding extensive reconstruction (Figure 3).

Practice Implications

Scalp defects requiring closure are common for dermatologic surgeons. Several techniques to promote tissue granulation in defects that involve exposed periosteum have been reported, including (1) creation of small holes with a scalpel or chisel to access cortical circulation and (2) using laser modalities to stimulate granulation (eg, an erbium:YAG or CO₂ laser).^3,4 Although direct comparative studies are needed, the cadaveric STSG provides an approach that increases tissue granulation but does not require more invasive techniques or equipment.

Autologous STSGs need a wound bed and can fail with an exposed periosteum. Furthermore, an autologous STSG that survives may leave an unsightly, hypopigmented, depressed defect. When a defect involves the periosteum and a primary closure or flap is not ideal, a skin substitute may be an option.

Skin substitutes, including cadaveric STSG, generally are classified as bioengineered skin equivalents, amniotic tissue, or cadaveric bioproducts (Table). Unlike autologous grafts, these skin substitutes can provide rapid coverage of the defect and do not require a highly vascularized wound bed.⁶ They also minimize the inflammatory response and potentially improve the final cosmetic outcome by improving granulation rather than immediate STSG closure creating a step-off in deep wounds.⁶

Cadaveric STSGs also have been used in nonhealing ulcerations; diabetic foot ulcers; and ulcerations in which muscle, tendon, or bone are exposed, demonstrating induction of wound healing with superior scar quality and skin function.^2,7,8 The utility of the cadaveric STSG is further highlighted by its potential to reduce costs⁹ compared to bioengineered skin substitutes, though considerable variability exists in pricing (Table).

Consider using a cadaveric STSG with a guiding closure in cases in which there is concern for delayed or absent tissue granulation or when monitoring for recurrence is essential.

Practice Gap

Scalp defects that extend to or below the periosteum often pose a reconstructive conundrum. Secondary-intention healing is challenging without an intact periosteum, and complex rotational flaps are required in these scenarios.¹ For a tumor that is at high risk for recurrence or when adjuvant therapy is necessary, tissue distortion of flaps can make monitoring for recurrence difficult. Similarly, for patients in poor health or who are elderly and have substantial skin atrophy, extensive closure may be undesirable or more technically challenging with a higher risk for adverse events. In these scenarios, additional strategies are necessary to optimize wound healing and cosmesis. A cadaveric split-thickness skin graft (STSG) consisting of biologically active tissue can be used to expedite granulation.²

Technique

Following tumor clearance on the scalp (Figure 1), wide undermining is performed and 3-0 polyglactin 910 epidermal pulley sutures are placed to partially close the defect. A cadaveric STSG is placed over the remaining exposed periosteum and secured under the pulley sutures (Figure 2). The cadaveric STSG is replaced at 1-week intervals. At 4 weeks, sutures typically are removed. The cadaveric STSG is used until the exposed periosteum is fully granulated and the surgeon decides that granulation arrest is unlikely. The wound then heals by unassisted granulation. This approach provides an excellent final cosmetic outcome while avoiding extensive reconstruction (Figure 3).

Practice Implications

Scalp defects requiring closure are common for dermatologic surgeons. Several techniques to promote tissue granulation in defects that involve exposed periosteum have been reported, including (1) creation of small holes with a scalpel or chisel to access cortical circulation and (2) using laser modalities to stimulate granulation (eg, an erbium:YAG or CO₂ laser).^3,4 Although direct comparative studies are needed, the cadaveric STSG provides an approach that increases tissue granulation but does not require more invasive techniques or equipment.

Autologous STSGs need a wound bed and can fail with an exposed periosteum. Furthermore, an autologous STSG that survives may leave an unsightly, hypopigmented, depressed defect. When a defect involves the periosteum and a primary closure or flap is not ideal, a skin substitute may be an option.

Skin substitutes, including cadaveric STSG, generally are classified as bioengineered skin equivalents, amniotic tissue, or cadaveric bioproducts (Table). Unlike autologous grafts, these skin substitutes can provide rapid coverage of the defect and do not require a highly vascularized wound bed.⁶ They also minimize the inflammatory response and potentially improve the final cosmetic outcome by improving granulation rather than immediate STSG closure creating a step-off in deep wounds.⁶

Cadaveric STSGs also have been used in nonhealing ulcerations; diabetic foot ulcers; and ulcerations in which muscle, tendon, or bone are exposed, demonstrating induction of wound healing with superior scar quality and skin function.^2,7,8 The utility of the cadaveric STSG is further highlighted by its potential to reduce costs⁹ compared to bioengineered skin substitutes, though considerable variability exists in pricing (Table).

Consider using a cadaveric STSG with a guiding closure in cases in which there is concern for delayed or absent tissue granulation or when monitoring for recurrence is essential.

Practice Gap

Scalp defects that extend to or below the periosteum often pose a reconstructive conundrum. Secondary-intention healing is challenging without an intact periosteum, and complex rotational flaps are required in these scenarios.¹ For a tumor that is at high risk for recurrence or when adjuvant therapy is necessary, tissue distortion of flaps can make monitoring for recurrence difficult. Similarly, for patients in poor health or who are elderly and have substantial skin atrophy, extensive closure may be undesirable or more technically challenging with a higher risk for adverse events. In these scenarios, additional strategies are necessary to optimize wound healing and cosmesis. A cadaveric split-thickness skin graft (STSG) consisting of biologically active tissue can be used to expedite granulation.²

Technique

Following tumor clearance on the scalp (Figure 1), wide undermining is performed and 3-0 polyglactin 910 epidermal pulley sutures are placed to partially close the defect. A cadaveric STSG is placed over the remaining exposed periosteum and secured under the pulley sutures (Figure 2). The cadaveric STSG is replaced at 1-week intervals. At 4 weeks, sutures typically are removed. The cadaveric STSG is used until the exposed periosteum is fully granulated and the surgeon decides that granulation arrest is unlikely. The wound then heals by unassisted granulation. This approach provides an excellent final cosmetic outcome while avoiding extensive reconstruction (Figure 3).

Practice Implications

Scalp defects requiring closure are common for dermatologic surgeons. Several techniques to promote tissue granulation in defects that involve exposed periosteum have been reported, including (1) creation of small holes with a scalpel or chisel to access cortical circulation and (2) using laser modalities to stimulate granulation (eg, an erbium:YAG or CO₂ laser).^3,4 Although direct comparative studies are needed, the cadaveric STSG provides an approach that increases tissue granulation but does not require more invasive techniques or equipment.

Autologous STSGs need a wound bed and can fail with an exposed periosteum. Furthermore, an autologous STSG that survives may leave an unsightly, hypopigmented, depressed defect. When a defect involves the periosteum and a primary closure or flap is not ideal, a skin substitute may be an option.

Skin substitutes, including cadaveric STSG, generally are classified as bioengineered skin equivalents, amniotic tissue, or cadaveric bioproducts (Table). Unlike autologous grafts, these skin substitutes can provide rapid coverage of the defect and do not require a highly vascularized wound bed.⁶ They also minimize the inflammatory response and potentially improve the final cosmetic outcome by improving granulation rather than immediate STSG closure creating a step-off in deep wounds.⁶

Cadaveric STSGs also have been used in nonhealing ulcerations; diabetic foot ulcers; and ulcerations in which muscle, tendon, or bone are exposed, demonstrating induction of wound healing with superior scar quality and skin function.^2,7,8 The utility of the cadaveric STSG is further highlighted by its potential to reduce costs⁹ compared to bioengineered skin substitutes, though considerable variability exists in pricing (Table).

Consider using a cadaveric STSG with a guiding closure in cases in which there is concern for delayed or absent tissue granulation or when monitoring for recurrence is essential.

The practice of body piercing has been present in cultures around the world for centuries. Piercings may be performed for religious or spiritual reasons or as a form of self-expression. In recent years, body piercings have become increasingly popular in all genders, with the most common sites being the ears, mouth, nose, eyebrows, nipples, navel, and genitals.¹ The prevalence of body piercing in the general population is estimated to be as high as 50%.² With the rising popularity of piercings, there also has been an increase in their associated complications, with one study noting that up to 35% of individuals with pierced ears and 30% of all pierced sites developed a complication.³ Common problems following piercing include infections, keloid formation, allergic contact dermatitis, site deformation, and tooth fractures.⁴ It is of utmost importance that health care professionals are aware of the potential complications associated with such a common practice. A comprehensive review of complications associated with cutaneous and mucosal piercings is lacking. We conducted a systematic review to summarize the clinical characteristics, complication types and frequency, and treatments reported for cutaneous and mucosal piercings.

METHODS

We conducted a systematic review of the literature adhering to PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-analyses) reporting guidelines.⁵

Search Strategy, Study Eligibility Criteria, and Study Selection

A literature search of the Embase, MEDLINE, and PubMed databases was performed on June 20, 2022, using search terms related to body piercing and possible piercing-induced complications (Supplemental Information online). All studies reporting complications following body piercing were included. In vitro and animal studies were excluded. Title and abstract screening were completed by 6 independent researchers (S.C., K.K., M.M-B., K.A., T.S., I.M.M.) using Covidence online systematic review software (www.covidence.org). Six reviewers (S.C., K.K., M.M-B., K.A., T.S., I.M.M.) independently evaluated titles, abstracts, and full texts to identify relevant studies. Conflicts were resolved by the senior reviewer (I.M.M.).

Data Extraction and Synthesis

Five reviewers (S.C., K.K., M.M-B., K.A., T.S.) independently extracted data from eligible studies using a standardized extraction form that included title; authors; year of publication; sample size; and key findings, including mean age, sex, piercing location, complication type, and treatment received.

Treatment type was placed into the following categories: surgical treatments, antimicrobials, medical treatments, direct-target therapy, oral procedures, avoidance, miscellaneous therapies, and no treatment. (Data regarding treatments can be found in the Supplemental Information online.)

RESULTS

The combined search yielded 2679 studies, 617 of which underwent full-text review; 319 studies were included (Figure). Studies were published from 1950 to June 2022 and included both adult and pediatric populations.

Patient Characteristics

In total, our pooled analysis included data on 30,090 complications across 36,803 pierced sites in 30,231 patients (Table 1). Demographic data are available for 55% (n=30,231) of patients. Overall, 74% (22,247/30,231) of the individuals included in our analysis were female. The mean age was 27.8 years (range, 0–76 years).

Overall, 36,803 pierced sites had a reported complication. The oral cavity, location not otherwise specified, was the most common site associated with a complication, accounting for 67% (n=24,478) of complications (Table 1). Other reported sites included (in decreasing frequency) the ears (21%, n=7551), tongue (5%, n=1669), lip (3%, n=998), navel (2%, n=605), nose (1%, n=540), nipple (1%, n=344), face/body (1%, n=269), genitals/groin (0%, n=183), eyebrow (0%, n=161), hand (0%, n=4), and eyelid (0%, n=1). Piercing complications were more commonly reported among females across all piercing locations except for the eyebrow, which was equal in both sexes.

Complications

Local Infections—Local infections accounted for 36% of reported complication types (n=10,872/30,090): perichondritis (1%, n=85); abscesses (0%, n=25); bacterial colonization (1%, n=106); and local infections, not otherwise specified (98%, n=10,648)(Table 2). The majority of local infections were found to be secondary to piercings of the ear and oral cavity. The nipple was found to be a common site for abscesses (40%, n=10), whereas the tongue was found to be the most common site for bacterial colonization (69%, n=73).

Immune-Mediated Issues—Immune-mediated issues encompassed 5% of the total reported complications (n=1561/30,090). The most commonly reported immune-mediated complications included allergies (31%, n=482), edema and swelling (21%, n=331), dermatitis (18%, n=282), and inflammatory lesions (17%, n=270). The majority were found to occur secondary to ear piercings, with the exception of edema, which mainly occurred secondary to tongue piercings (45%, n=150), and allergy, which primarily was associated with oral piercings (51%, n=245)(Table 2).

Tissue Damage—Tissue damage accounted for 43% of all complications (n=13,036/30,090). The most common forms of tissue damage were trauma (55%, n=7182), dysesthesia (22%, n=2883), bleeding and bruising (18%, n=2376), and pain (3%, n=370)(Table 2). Trauma was mainly found to be a complication in the context of oral piercings (99%, n=7121). Similarly, 94% (n=2242) of bleeding and bruising occurred secondary to oral piercings. Embedded piercings (92%, n=127), deformity (91%, n=29), and necrosis (75%, n=3) mostly occurred following ear piercings. Lip piercings were found to be the most common cause of damage to surrounding structures (98%, n=50).

Oral—Overall, 3193 intraoral complications were reported, constituting 11% of the total complications (Table 2). Oral complications included dental damage (86%, n=2732), gum recession (14%, n=459), and gingivitis (0%, n=2). Dental damage was mostly reported following oral piercings (90%, n=2453), whereas gum recession was mostly reported following lip piercings (59%, n=272).

Proliferations—Proliferations accounted for 795 (3%) of reported piercing complications. The majority (97%, n=772) were keloids, 2% (n=16) were other benign growths, and 1% (n=7) were malignancies. These complications mostly occurred secondary to ear piercings, which resulted in 741 (96%) keloids, 6 (38%) benign growths, and 4 (57%) malignancies.

Systemic—Overall, 2% (n=633) of the total complications were classified as systemic issues, including functional impairment (45%, n=282), secondary organ involvement (24%, n=150), cardiac issues (3%, n=21), and aspiration/inhalation (1%, n=8). Nonlocalized infections such as hepatitis or an increased risk thereof (17%, n=107), tetanus (8%, n=52), chlamydia (1%, n=9), HIV (0%, n=1), herpes simplex virus (0%, n=1), gonorrhea (0%, n=1), and bacterial vaginosis (0%, n=1) also were included in this category. The tongue, ear, and genitals were the locations most involved in these complications (Table 2). Secondary organ involvement mostly occurred after ear (36%, n=54) and genital piercings (27%, n=41). A total of 8 cases of piercing aspiration and/or inhalation were reported in association with piercings of the head and neck (Table 2).

COMMENT

Piercing Complications

Overall, the ear, tongue, and oral cavity were found to be the sites with the most associated complications recorded in the literature, and local infection and tissue damage were found to be the most prevalent types of complications. A plethora of treatments were used to manage piercing-induced complications, including surgical or medical treatments and avoidance (Supplemental Information). Reports by Metts⁶ and Escudero-Castaño et al⁷ provide detailed protocols and photographs of piercings.

Infections

Our review found that local infections were commonly reported complications associated with body piercings, which is consistent with other studies.¹ The initial trauma inherent in the piercing process followed by the presence of an ongoing foreign body lends itself to an increased risk for developing these complications. Wound healing after piercing also varies based on the piercing location.

The rate and severity of the infection are influenced by the anatomic location of the piercing, hygiene, method of piercing, types of materials used, and aftercare.⁸ Piercing cartilage sites, such as the helix, concha, or nose, increases susceptibility to infections and permanent deformities. Cartilage is particularly at risk because of its avascular nature.⁹ Other studies have reported similar incidences of superficial localized infections; infectious complications were seen in 10% to 30% of body piercings in one study,³ while 45% of American and Australian college students reported infection at a piercing site in a second study.¹⁰

Systemic Issues

Systemic issues are potentially the most dangerous piercing-induced complications, though they were rarer in our analysis. Some serious complications included septic emboli, fatal staphylococcal toxic shock syndrome, and death. Although some systemic issues, such as staphylococcal toxic shock syndrome and septic sacroiliitis, required extensive hospital stays and complex treatment, others had lifelong repercussions, such as hepatitis and HIV. One report showed an increased incidence of endocarditis associated with body piercing, including staphylococcal endocarditis following nasal piercings, Neisseria endocarditis following tongue piercings, and Staphylococcus epidermidis endocarditis following nipple piercings.¹¹ Moreover, Mariano et al¹²—who noted a case of endocarditis and meningitis associated with a nape piercing in a young female in 2015—reinforced the notion that information pertaining to the risks associated with body piercing must be better disseminated, given the potential for morbid or fatal outcomes. Finally, nonsterile piercing techniques and poor hygiene were found to contribute substantially to the increased risk for infection, so it is of utmost importance to reinforce proper practices in piercing salons.⁴

Immune-Mediated Issues

Because piercings are foreign bodies, they are susceptible to both acute and chronic immune responses. Our study found that allergies and dermatitis made up almost half of the immune-mediated piercing complications. It is especially important to emphasize that costume jewelry exposes our skin to a variety of contact allergens, most prominently nickel, heightening the risk for developing allergic contact dermatitis.¹³ Moreover, a study conducted by Brandão et al¹⁴ found that patients with pierced ears were significantly more likely to react to nickel than those without pierced ears (P=.031). Although other studies have found that allergy to metals ranges from 8.3% to 20% in the general population,¹⁵ we were not able to quantify the incidence in our study due to a lack of reporting of common benign complications, such as contact dermatitis.

Tissue Damage and Local Problems

Our review found that tissue and oral damage also were commonly reported piercing complications, with the most common pathologies being trauma, dysesthesia, bleeding/bruising, and dental damage. Laumann and Derick¹⁶ reported that bleeding, tissue trauma, and local problems were common physical health problems associated with body piercing. Severe complications, such as abscesses, toxic shock syndrome, and endocarditis, also have been reported in association with intraoral piercings.¹⁷ Moreover, other studies have shown that oral piercings are associated with several adverse oral and systemic conditions. A meta-analysis of individuals with oral piercings found a similar prevalence of dental fracture, gingival recession, and tooth wear (34%), as well as unspecified dental damage (27%) and tooth chipping (22%). Additionally, this meta-analysis reported a 3-fold increased risk for dental fracture and 7-fold increased risk for gingival recession with oral piercings.¹⁸ Another meta-analysis of oral piercing complications found a similar prevalence of dental fracture (34%), tooth wear (34%), gingival recession (33%), unspecified dental damage (27%), and tooth chipping (22%).¹⁹ Considering the extensive amount of cumulative damage, wearers of oral jewelry require periodic periodontal evaluations to monitor for dental damage and gingival recession.²⁰ There are limited data on treatments for complications of oral piercings, and further research in this area is warranted.

Proliferations and Scars

Although proliferations and scarring were among the least common complications reported in the literature, they are some of the most cosmetically disfiguring for patients. Keloids, the most common type of growth associated with piercings, do not naturally regress and thus require some form of intervention. Given the multimodal approach used to treat keloids, as described by the evidence-based algorithm by Ogawa,²¹ it is not surprising that keloids also represented the complication most treated with medical therapies, such as steroids, and also with direct-target therapy, such as liquid nitrogen therapy (Supplemental Information).

Other proliferations reported in the literature include benign pyogenic granulomas²² and much less commonly malignant neoplasms such as basal cell carcinoma²³ and squamous cell carcinoma.²⁴ Although rare, treatment of piercing-associated malignancies include surgical removal, chemotherapy, and radiation therapy (Supplemental Information).

Limitations

There are several limitations to our systematic review. First, heterogeneity in study designs, patient populations, treatment interventions, and outcome measures of included studies may have affected the quality and generalizability of our results. Moreover, because the studies included in this systematic review focused on specific complications, we could not compare our results to the literature that analyzes incidence rates of piercing complications. Furthermore, not all studies included the data that we hoped to extract, and thus only available data were reported in these instances. Finally, the articles we reviewed may have included publication bias, with positive findings being more frequently published, potentially inflating certain types and sites of complications and treatment choices. Despite these limitations, our review provides essential information that must be interpreted in a clinical context.

CONCLUSION

Given that cutaneous and mucosal piercing has become more prevalent in recent years, along with an increase in the variety of piercing-induced complications, it is of utmost importance that piercing salons have proper hygiene practices in place and that patients are aware of the multitude of potential complications that can arise—whether common and benign or rare but life-threatening.

The practice of body piercing has been present in cultures around the world for centuries. Piercings may be performed for religious or spiritual reasons or as a form of self-expression. In recent years, body piercings have become increasingly popular in all genders, with the most common sites being the ears, mouth, nose, eyebrows, nipples, navel, and genitals.¹ The prevalence of body piercing in the general population is estimated to be as high as 50%.² With the rising popularity of piercings, there also has been an increase in their associated complications, with one study noting that up to 35% of individuals with pierced ears and 30% of all pierced sites developed a complication.³ Common problems following piercing include infections, keloid formation, allergic contact dermatitis, site deformation, and tooth fractures.⁴ It is of utmost importance that health care professionals are aware of the potential complications associated with such a common practice. A comprehensive review of complications associated with cutaneous and mucosal piercings is lacking. We conducted a systematic review to summarize the clinical characteristics, complication types and frequency, and treatments reported for cutaneous and mucosal piercings.

METHODS

We conducted a systematic review of the literature adhering to PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-analyses) reporting guidelines.⁵

Search Strategy, Study Eligibility Criteria, and Study Selection

A literature search of the Embase, MEDLINE, and PubMed databases was performed on June 20, 2022, using search terms related to body piercing and possible piercing-induced complications (Supplemental Information online). All studies reporting complications following body piercing were included. In vitro and animal studies were excluded. Title and abstract screening were completed by 6 independent researchers (S.C., K.K., M.M-B., K.A., T.S., I.M.M.) using Covidence online systematic review software (www.covidence.org). Six reviewers (S.C., K.K., M.M-B., K.A., T.S., I.M.M.) independently evaluated titles, abstracts, and full texts to identify relevant studies. Conflicts were resolved by the senior reviewer (I.M.M.).

Data Extraction and Synthesis

Five reviewers (S.C., K.K., M.M-B., K.A., T.S.) independently extracted data from eligible studies using a standardized extraction form that included title; authors; year of publication; sample size; and key findings, including mean age, sex, piercing location, complication type, and treatment received.

Treatment type was placed into the following categories: surgical treatments, antimicrobials, medical treatments, direct-target therapy, oral procedures, avoidance, miscellaneous therapies, and no treatment. (Data regarding treatments can be found in the Supplemental Information online.)

RESULTS

The combined search yielded 2679 studies, 617 of which underwent full-text review; 319 studies were included (Figure). Studies were published from 1950 to June 2022 and included both adult and pediatric populations.

Patient Characteristics

In total, our pooled analysis included data on 30,090 complications across 36,803 pierced sites in 30,231 patients (Table 1). Demographic data are available for 55% (n=30,231) of patients. Overall, 74% (22,247/30,231) of the individuals included in our analysis were female. The mean age was 27.8 years (range, 0–76 years).

Overall, 36,803 pierced sites had a reported complication. The oral cavity, location not otherwise specified, was the most common site associated with a complication, accounting for 67% (n=24,478) of complications (Table 1). Other reported sites included (in decreasing frequency) the ears (21%, n=7551), tongue (5%, n=1669), lip (3%, n=998), navel (2%, n=605), nose (1%, n=540), nipple (1%, n=344), face/body (1%, n=269), genitals/groin (0%, n=183), eyebrow (0%, n=161), hand (0%, n=4), and eyelid (0%, n=1). Piercing complications were more commonly reported among females across all piercing locations except for the eyebrow, which was equal in both sexes.

Complications

Local Infections—Local infections accounted for 36% of reported complication types (n=10,872/30,090): perichondritis (1%, n=85); abscesses (0%, n=25); bacterial colonization (1%, n=106); and local infections, not otherwise specified (98%, n=10,648)(Table 2). The majority of local infections were found to be secondary to piercings of the ear and oral cavity. The nipple was found to be a common site for abscesses (40%, n=10), whereas the tongue was found to be the most common site for bacterial colonization (69%, n=73).

Immune-Mediated Issues—Immune-mediated issues encompassed 5% of the total reported complications (n=1561/30,090). The most commonly reported immune-mediated complications included allergies (31%, n=482), edema and swelling (21%, n=331), dermatitis (18%, n=282), and inflammatory lesions (17%, n=270). The majority were found to occur secondary to ear piercings, with the exception of edema, which mainly occurred secondary to tongue piercings (45%, n=150), and allergy, which primarily was associated with oral piercings (51%, n=245)(Table 2).

Tissue Damage—Tissue damage accounted for 43% of all complications (n=13,036/30,090). The most common forms of tissue damage were trauma (55%, n=7182), dysesthesia (22%, n=2883), bleeding and bruising (18%, n=2376), and pain (3%, n=370)(Table 2). Trauma was mainly found to be a complication in the context of oral piercings (99%, n=7121). Similarly, 94% (n=2242) of bleeding and bruising occurred secondary to oral piercings. Embedded piercings (92%, n=127), deformity (91%, n=29), and necrosis (75%, n=3) mostly occurred following ear piercings. Lip piercings were found to be the most common cause of damage to surrounding structures (98%, n=50).

Oral—Overall, 3193 intraoral complications were reported, constituting 11% of the total complications (Table 2). Oral complications included dental damage (86%, n=2732), gum recession (14%, n=459), and gingivitis (0%, n=2). Dental damage was mostly reported following oral piercings (90%, n=2453), whereas gum recession was mostly reported following lip piercings (59%, n=272).

Proliferations—Proliferations accounted for 795 (3%) of reported piercing complications. The majority (97%, n=772) were keloids, 2% (n=16) were other benign growths, and 1% (n=7) were malignancies. These complications mostly occurred secondary to ear piercings, which resulted in 741 (96%) keloids, 6 (38%) benign growths, and 4 (57%) malignancies.

Systemic—Overall, 2% (n=633) of the total complications were classified as systemic issues, including functional impairment (45%, n=282), secondary organ involvement (24%, n=150), cardiac issues (3%, n=21), and aspiration/inhalation (1%, n=8). Nonlocalized infections such as hepatitis or an increased risk thereof (17%, n=107), tetanus (8%, n=52), chlamydia (1%, n=9), HIV (0%, n=1), herpes simplex virus (0%, n=1), gonorrhea (0%, n=1), and bacterial vaginosis (0%, n=1) also were included in this category. The tongue, ear, and genitals were the locations most involved in these complications (Table 2). Secondary organ involvement mostly occurred after ear (36%, n=54) and genital piercings (27%, n=41). A total of 8 cases of piercing aspiration and/or inhalation were reported in association with piercings of the head and neck (Table 2).

COMMENT

Piercing Complications

Overall, the ear, tongue, and oral cavity were found to be the sites with the most associated complications recorded in the literature, and local infection and tissue damage were found to be the most prevalent types of complications. A plethora of treatments were used to manage piercing-induced complications, including surgical or medical treatments and avoidance (Supplemental Information). Reports by Metts⁶ and Escudero-Castaño et al⁷ provide detailed protocols and photographs of piercings.

Infections

Our review found that local infections were commonly reported complications associated with body piercings, which is consistent with other studies.¹ The initial trauma inherent in the piercing process followed by the presence of an ongoing foreign body lends itself to an increased risk for developing these complications. Wound healing after piercing also varies based on the piercing location.

The rate and severity of the infection are influenced by the anatomic location of the piercing, hygiene, method of piercing, types of materials used, and aftercare.⁸ Piercing cartilage sites, such as the helix, concha, or nose, increases susceptibility to infections and permanent deformities. Cartilage is particularly at risk because of its avascular nature.⁹ Other studies have reported similar incidences of superficial localized infections; infectious complications were seen in 10% to 30% of body piercings in one study,³ while 45% of American and Australian college students reported infection at a piercing site in a second study.¹⁰

Systemic Issues

Systemic issues are potentially the most dangerous piercing-induced complications, though they were rarer in our analysis. Some serious complications included septic emboli, fatal staphylococcal toxic shock syndrome, and death. Although some systemic issues, such as staphylococcal toxic shock syndrome and septic sacroiliitis, required extensive hospital stays and complex treatment, others had lifelong repercussions, such as hepatitis and HIV. One report showed an increased incidence of endocarditis associated with body piercing, including staphylococcal endocarditis following nasal piercings, Neisseria endocarditis following tongue piercings, and Staphylococcus epidermidis endocarditis following nipple piercings.¹¹ Moreover, Mariano et al¹²—who noted a case of endocarditis and meningitis associated with a nape piercing in a young female in 2015—reinforced the notion that information pertaining to the risks associated with body piercing must be better disseminated, given the potential for morbid or fatal outcomes. Finally, nonsterile piercing techniques and poor hygiene were found to contribute substantially to the increased risk for infection, so it is of utmost importance to reinforce proper practices in piercing salons.⁴

Immune-Mediated Issues

Because piercings are foreign bodies, they are susceptible to both acute and chronic immune responses. Our study found that allergies and dermatitis made up almost half of the immune-mediated piercing complications. It is especially important to emphasize that costume jewelry exposes our skin to a variety of contact allergens, most prominently nickel, heightening the risk for developing allergic contact dermatitis.¹³ Moreover, a study conducted by Brandão et al¹⁴ found that patients with pierced ears were significantly more likely to react to nickel than those without pierced ears (P=.031). Although other studies have found that allergy to metals ranges from 8.3% to 20% in the general population,¹⁵ we were not able to quantify the incidence in our study due to a lack of reporting of common benign complications, such as contact dermatitis.

Tissue Damage and Local Problems

Our review found that tissue and oral damage also were commonly reported piercing complications, with the most common pathologies being trauma, dysesthesia, bleeding/bruising, and dental damage. Laumann and Derick¹⁶ reported that bleeding, tissue trauma, and local problems were common physical health problems associated with body piercing. Severe complications, such as abscesses, toxic shock syndrome, and endocarditis, also have been reported in association with intraoral piercings.¹⁷ Moreover, other studies have shown that oral piercings are associated with several adverse oral and systemic conditions. A meta-analysis of individuals with oral piercings found a similar prevalence of dental fracture, gingival recession, and tooth wear (34%), as well as unspecified dental damage (27%) and tooth chipping (22%). Additionally, this meta-analysis reported a 3-fold increased risk for dental fracture and 7-fold increased risk for gingival recession with oral piercings.¹⁸ Another meta-analysis of oral piercing complications found a similar prevalence of dental fracture (34%), tooth wear (34%), gingival recession (33%), unspecified dental damage (27%), and tooth chipping (22%).¹⁹ Considering the extensive amount of cumulative damage, wearers of oral jewelry require periodic periodontal evaluations to monitor for dental damage and gingival recession.²⁰ There are limited data on treatments for complications of oral piercings, and further research in this area is warranted.

Proliferations and Scars

Although proliferations and scarring were among the least common complications reported in the literature, they are some of the most cosmetically disfiguring for patients. Keloids, the most common type of growth associated with piercings, do not naturally regress and thus require some form of intervention. Given the multimodal approach used to treat keloids, as described by the evidence-based algorithm by Ogawa,²¹ it is not surprising that keloids also represented the complication most treated with medical therapies, such as steroids, and also with direct-target therapy, such as liquid nitrogen therapy (Supplemental Information).

Other proliferations reported in the literature include benign pyogenic granulomas²² and much less commonly malignant neoplasms such as basal cell carcinoma²³ and squamous cell carcinoma.²⁴ Although rare, treatment of piercing-associated malignancies include surgical removal, chemotherapy, and radiation therapy (Supplemental Information).

Limitations

There are several limitations to our systematic review. First, heterogeneity in study designs, patient populations, treatment interventions, and outcome measures of included studies may have affected the quality and generalizability of our results. Moreover, because the studies included in this systematic review focused on specific complications, we could not compare our results to the literature that analyzes incidence rates of piercing complications. Furthermore, not all studies included the data that we hoped to extract, and thus only available data were reported in these instances. Finally, the articles we reviewed may have included publication bias, with positive findings being more frequently published, potentially inflating certain types and sites of complications and treatment choices. Despite these limitations, our review provides essential information that must be interpreted in a clinical context.

CONCLUSION

Given that cutaneous and mucosal piercing has become more prevalent in recent years, along with an increase in the variety of piercing-induced complications, it is of utmost importance that piercing salons have proper hygiene practices in place and that patients are aware of the multitude of potential complications that can arise—whether common and benign or rare but life-threatening.

The practice of body piercing has been present in cultures around the world for centuries. Piercings may be performed for religious or spiritual reasons or as a form of self-expression. In recent years, body piercings have become increasingly popular in all genders, with the most common sites being the ears, mouth, nose, eyebrows, nipples, navel, and genitals.¹ The prevalence of body piercing in the general population is estimated to be as high as 50%.² With the rising popularity of piercings, there also has been an increase in their associated complications, with one study noting that up to 35% of individuals with pierced ears and 30% of all pierced sites developed a complication.³ Common problems following piercing include infections, keloid formation, allergic contact dermatitis, site deformation, and tooth fractures.⁴ It is of utmost importance that health care professionals are aware of the potential complications associated with such a common practice. A comprehensive review of complications associated with cutaneous and mucosal piercings is lacking. We conducted a systematic review to summarize the clinical characteristics, complication types and frequency, and treatments reported for cutaneous and mucosal piercings.

METHODS

We conducted a systematic review of the literature adhering to PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-analyses) reporting guidelines.⁵

Search Strategy, Study Eligibility Criteria, and Study Selection

A literature search of the Embase, MEDLINE, and PubMed databases was performed on June 20, 2022, using search terms related to body piercing and possible piercing-induced complications (Supplemental Information online). All studies reporting complications following body piercing were included. In vitro and animal studies were excluded. Title and abstract screening were completed by 6 independent researchers (S.C., K.K., M.M-B., K.A., T.S., I.M.M.) using Covidence online systematic review software (www.covidence.org). Six reviewers (S.C., K.K., M.M-B., K.A., T.S., I.M.M.) independently evaluated titles, abstracts, and full texts to identify relevant studies. Conflicts were resolved by the senior reviewer (I.M.M.).

Data Extraction and Synthesis

Five reviewers (S.C., K.K., M.M-B., K.A., T.S.) independently extracted data from eligible studies using a standardized extraction form that included title; authors; year of publication; sample size; and key findings, including mean age, sex, piercing location, complication type, and treatment received.

Treatment type was placed into the following categories: surgical treatments, antimicrobials, medical treatments, direct-target therapy, oral procedures, avoidance, miscellaneous therapies, and no treatment. (Data regarding treatments can be found in the Supplemental Information online.)

RESULTS

The combined search yielded 2679 studies, 617 of which underwent full-text review; 319 studies were included (Figure). Studies were published from 1950 to June 2022 and included both adult and pediatric populations.

Patient Characteristics

In total, our pooled analysis included data on 30,090 complications across 36,803 pierced sites in 30,231 patients (Table 1). Demographic data are available for 55% (n=30,231) of patients. Overall, 74% (22,247/30,231) of the individuals included in our analysis were female. The mean age was 27.8 years (range, 0–76 years).

Overall, 36,803 pierced sites had a reported complication. The oral cavity, location not otherwise specified, was the most common site associated with a complication, accounting for 67% (n=24,478) of complications (Table 1). Other reported sites included (in decreasing frequency) the ears (21%, n=7551), tongue (5%, n=1669), lip (3%, n=998), navel (2%, n=605), nose (1%, n=540), nipple (1%, n=344), face/body (1%, n=269), genitals/groin (0%, n=183), eyebrow (0%, n=161), hand (0%, n=4), and eyelid (0%, n=1). Piercing complications were more commonly reported among females across all piercing locations except for the eyebrow, which was equal in both sexes.

Complications

Local Infections—Local infections accounted for 36% of reported complication types (n=10,872/30,090): perichondritis (1%, n=85); abscesses (0%, n=25); bacterial colonization (1%, n=106); and local infections, not otherwise specified (98%, n=10,648)(Table 2). The majority of local infections were found to be secondary to piercings of the ear and oral cavity. The nipple was found to be a common site for abscesses (40%, n=10), whereas the tongue was found to be the most common site for bacterial colonization (69%, n=73).

Immune-Mediated Issues—Immune-mediated issues encompassed 5% of the total reported complications (n=1561/30,090). The most commonly reported immune-mediated complications included allergies (31%, n=482), edema and swelling (21%, n=331), dermatitis (18%, n=282), and inflammatory lesions (17%, n=270). The majority were found to occur secondary to ear piercings, with the exception of edema, which mainly occurred secondary to tongue piercings (45%, n=150), and allergy, which primarily was associated with oral piercings (51%, n=245)(Table 2).

Tissue Damage—Tissue damage accounted for 43% of all complications (n=13,036/30,090). The most common forms of tissue damage were trauma (55%, n=7182), dysesthesia (22%, n=2883), bleeding and bruising (18%, n=2376), and pain (3%, n=370)(Table 2). Trauma was mainly found to be a complication in the context of oral piercings (99%, n=7121). Similarly, 94% (n=2242) of bleeding and bruising occurred secondary to oral piercings. Embedded piercings (92%, n=127), deformity (91%, n=29), and necrosis (75%, n=3) mostly occurred following ear piercings. Lip piercings were found to be the most common cause of damage to surrounding structures (98%, n=50).

Oral—Overall, 3193 intraoral complications were reported, constituting 11% of the total complications (Table 2). Oral complications included dental damage (86%, n=2732), gum recession (14%, n=459), and gingivitis (0%, n=2). Dental damage was mostly reported following oral piercings (90%, n=2453), whereas gum recession was mostly reported following lip piercings (59%, n=272).

Proliferations—Proliferations accounted for 795 (3%) of reported piercing complications. The majority (97%, n=772) were keloids, 2% (n=16) were other benign growths, and 1% (n=7) were malignancies. These complications mostly occurred secondary to ear piercings, which resulted in 741 (96%) keloids, 6 (38%) benign growths, and 4 (57%) malignancies.

Systemic—Overall, 2% (n=633) of the total complications were classified as systemic issues, including functional impairment (45%, n=282), secondary organ involvement (24%, n=150), cardiac issues (3%, n=21), and aspiration/inhalation (1%, n=8). Nonlocalized infections such as hepatitis or an increased risk thereof (17%, n=107), tetanus (8%, n=52), chlamydia (1%, n=9), HIV (0%, n=1), herpes simplex virus (0%, n=1), gonorrhea (0%, n=1), and bacterial vaginosis (0%, n=1) also were included in this category. The tongue, ear, and genitals were the locations most involved in these complications (Table 2). Secondary organ involvement mostly occurred after ear (36%, n=54) and genital piercings (27%, n=41). A total of 8 cases of piercing aspiration and/or inhalation were reported in association with piercings of the head and neck (Table 2).

COMMENT

Piercing Complications

Overall, the ear, tongue, and oral cavity were found to be the sites with the most associated complications recorded in the literature, and local infection and tissue damage were found to be the most prevalent types of complications. A plethora of treatments were used to manage piercing-induced complications, including surgical or medical treatments and avoidance (Supplemental Information). Reports by Metts⁶ and Escudero-Castaño et al⁷ provide detailed protocols and photographs of piercings.

Infections

Our review found that local infections were commonly reported complications associated with body piercings, which is consistent with other studies.¹ The initial trauma inherent in the piercing process followed by the presence of an ongoing foreign body lends itself to an increased risk for developing these complications. Wound healing after piercing also varies based on the piercing location.

The rate and severity of the infection are influenced by the anatomic location of the piercing, hygiene, method of piercing, types of materials used, and aftercare.⁸ Piercing cartilage sites, such as the helix, concha, or nose, increases susceptibility to infections and permanent deformities. Cartilage is particularly at risk because of its avascular nature.⁹ Other studies have reported similar incidences of superficial localized infections; infectious complications were seen in 10% to 30% of body piercings in one study,³ while 45% of American and Australian college students reported infection at a piercing site in a second study.¹⁰

Systemic Issues

Systemic issues are potentially the most dangerous piercing-induced complications, though they were rarer in our analysis. Some serious complications included septic emboli, fatal staphylococcal toxic shock syndrome, and death. Although some systemic issues, such as staphylococcal toxic shock syndrome and septic sacroiliitis, required extensive hospital stays and complex treatment, others had lifelong repercussions, such as hepatitis and HIV. One report showed an increased incidence of endocarditis associated with body piercing, including staphylococcal endocarditis following nasal piercings, Neisseria endocarditis following tongue piercings, and Staphylococcus epidermidis endocarditis following nipple piercings.¹¹ Moreover, Mariano et al¹²—who noted a case of endocarditis and meningitis associated with a nape piercing in a young female in 2015—reinforced the notion that information pertaining to the risks associated with body piercing must be better disseminated, given the potential for morbid or fatal outcomes. Finally, nonsterile piercing techniques and poor hygiene were found to contribute substantially to the increased risk for infection, so it is of utmost importance to reinforce proper practices in piercing salons.⁴

Immune-Mediated Issues

Because piercings are foreign bodies, they are susceptible to both acute and chronic immune responses. Our study found that allergies and dermatitis made up almost half of the immune-mediated piercing complications. It is especially important to emphasize that costume jewelry exposes our skin to a variety of contact allergens, most prominently nickel, heightening the risk for developing allergic contact dermatitis.¹³ Moreover, a study conducted by Brandão et al¹⁴ found that patients with pierced ears were significantly more likely to react to nickel than those without pierced ears (P=.031). Although other studies have found that allergy to metals ranges from 8.3% to 20% in the general population,¹⁵ we were not able to quantify the incidence in our study due to a lack of reporting of common benign complications, such as contact dermatitis.

Tissue Damage and Local Problems

Our review found that tissue and oral damage also were commonly reported piercing complications, with the most common pathologies being trauma, dysesthesia, bleeding/bruising, and dental damage. Laumann and Derick¹⁶ reported that bleeding, tissue trauma, and local problems were common physical health problems associated with body piercing. Severe complications, such as abscesses, toxic shock syndrome, and endocarditis, also have been reported in association with intraoral piercings.¹⁷ Moreover, other studies have shown that oral piercings are associated with several adverse oral and systemic conditions. A meta-analysis of individuals with oral piercings found a similar prevalence of dental fracture, gingival recession, and tooth wear (34%), as well as unspecified dental damage (27%) and tooth chipping (22%). Additionally, this meta-analysis reported a 3-fold increased risk for dental fracture and 7-fold increased risk for gingival recession with oral piercings.¹⁸ Another meta-analysis of oral piercing complications found a similar prevalence of dental fracture (34%), tooth wear (34%), gingival recession (33%), unspecified dental damage (27%), and tooth chipping (22%).¹⁹ Considering the extensive amount of cumulative damage, wearers of oral jewelry require periodic periodontal evaluations to monitor for dental damage and gingival recession.²⁰ There are limited data on treatments for complications of oral piercings, and further research in this area is warranted.

Proliferations and Scars

Although proliferations and scarring were among the least common complications reported in the literature, they are some of the most cosmetically disfiguring for patients. Keloids, the most common type of growth associated with piercings, do not naturally regress and thus require some form of intervention. Given the multimodal approach used to treat keloids, as described by the evidence-based algorithm by Ogawa,²¹ it is not surprising that keloids also represented the complication most treated with medical therapies, such as steroids, and also with direct-target therapy, such as liquid nitrogen therapy (Supplemental Information).

Other proliferations reported in the literature include benign pyogenic granulomas²² and much less commonly malignant neoplasms such as basal cell carcinoma²³ and squamous cell carcinoma.²⁴ Although rare, treatment of piercing-associated malignancies include surgical removal, chemotherapy, and radiation therapy (Supplemental Information).

Limitations

There are several limitations to our systematic review. First, heterogeneity in study designs, patient populations, treatment interventions, and outcome measures of included studies may have affected the quality and generalizability of our results. Moreover, because the studies included in this systematic review focused on specific complications, we could not compare our results to the literature that analyzes incidence rates of piercing complications. Furthermore, not all studies included the data that we hoped to extract, and thus only available data were reported in these instances. Finally, the articles we reviewed may have included publication bias, with positive findings being more frequently published, potentially inflating certain types and sites of complications and treatment choices. Despite these limitations, our review provides essential information that must be interpreted in a clinical context.

CONCLUSION

Given that cutaneous and mucosal piercing has become more prevalent in recent years, along with an increase in the variety of piercing-induced complications, it is of utmost importance that piercing salons have proper hygiene practices in place and that patients are aware of the multitude of potential complications that can arise—whether common and benign or rare but life-threatening.

The Diagnosis: Congenital Cutaneous Langerhans Cell Histiocytosis

Although the infectious workup was positive for herpes simplex virus type 1 and cytomegalovirus antibodies, serologies for the rest of the TORCH (toxoplasmosis, other agents [syphilis, hepatitis B virus], rubella, cytomegalovirus) group of infections, as well as other bacterial, fungal, and viral infections, were negative. A skin biopsy from the right fifth toe showed a dense infiltrate of CD1a+ histiocytic cells with folded or kidney-shaped nuclei mixed with eosinophils, which was consistent with Langerhans cell histiocytosis (LCH) (Figure 1). Skin lesions were treated with hydrocortisone cream 2.5% and progressively faded over a few weeks.

Langerhans cell histiocytosis is a rare disorder with a variable clinical presentation depending on the sites affected and the extent of involvement. It can involve multiple organ systems, most commonly the skeletal system and the skin. Organ involvement is characterized by histiocyte infiltration. Acute disseminated multisystem disease most commonly is seen in children younger than 3 years.¹

Congenital cutaneous LCH presents with variable skin lesions ranging from papules to vesicles, pustules, and ulcers, with onset at birth or in the neonatal period. Various morphologic traits of skin lesions have been described; the most common presentation is multiple red to yellow-brown, crusted papules with accompanying hemorrhage or erosion.¹ Other cases have described an eczematous, seborrheic, diffuse eruption or erosive intertrigo. One case of a child with a solitary necrotic nodule on the scalp has been reported.²

Our patient presented with disseminated, nonblanching, purple to dark red papules and nodules of the skin and oral mucosa, as well as nail dystrophy (Figure 2). However, LCH in a neonate can mimic other causes of congenital papulonodular eruptions. Red-brown papules and nodules with or without crusting in a newborn can be mistaken for erythema toxicum neonatorum, transient neonatal pustular melanosis, congenital leukemia cutis, neonatal erythropoiesis, disseminated neonatal hemangiomatosis, infantile acropustulosis, or congenital TORCH infections such as rubella or syphilis. When LCH presents as vesicles or eroded papules or nodules in a newborn, the differential diagnosis includes incontinentia pigmenti and hereditary epidermolysis bullosa.

Langerhans cell histiocytosis may even present with a classic blueberry muffin rash that can lead clinicians to consider cutaneous metastasis from various hematologic malignancies or the more common TORCH infections. Several diagnostic tests can be performed to clarify the diagnosis, including bacterial and viral cultures and stains, serology, immunohistochemistry, flow cytometry, bone marrow aspiration, or skin biopsy.³ Langerhans cell histiocytosis is diagnosed with a combination of histology, immunohistochemistry, and clinical presentation; however, a skin biopsy is crucial. Tissue should be taken from the most easily accessible yet representative lesion. The characteristic appearance of LCH lesions is described as a dense infiltrate of histiocytic cells mixed with numerous eosinophils in the dermis.¹ Histiocytes usually have folded nuclei and eosinophilic cytoplasm or kidney-shaped nuclei with prominent nucleoli. Positive CD1a and/or CD207 (Langerin) staining of the cells is required for definitive diagnosis.⁴ After diagnosis, it is important to obtain baseline laboratory and radiographic studies to determine the extent of systemic involvement.

Treatment of congenital LCH is tailored to the extent of organ involvement. The dermatologic manifestations resolve without medications in many cases. However, true self-resolving LCH can only be diagnosed retrospectively after a full evaluation for other sites of disease. Disseminated disease can be life-threatening and requires more active management. In cases of skin-limited disease, therapies include topical steroids, nitrogen mustard, or imiquimod; surgical resection of isolated lesions; phototherapy; or systemic therapies such as methotrexate, 6-mercaptopurine, vinblastine/vincristine, cladribine, and/or cytarabine. Symptomatic patients initially are treated with methotrexate and 6-mercaptopurine.⁵ Asymptomatic infants with skin-limited involvement can be managed with topical treatments.

Our patient had skin-limited disease. Abdominal ultrasonography, skeletal survey, and magnetic resonance imaging of the brain revealed no abnormalities. The patient’s family was advised to monitor him for reoccurrence of the skin lesions and to continue close follow-up with hematology and dermatology. Although congenital LCH often is self-resolving, extensive skin involvement increases the risk for internal organ involvement for several years.⁶ These patients require long-term follow-up for potential musculoskeletal, ophthalmologic, endocrine, hepatic, and/or pulmonary disease.

The Diagnosis: Congenital Cutaneous Langerhans Cell Histiocytosis

Although the infectious workup was positive for herpes simplex virus type 1 and cytomegalovirus antibodies, serologies for the rest of the TORCH (toxoplasmosis, other agents [syphilis, hepatitis B virus], rubella, cytomegalovirus) group of infections, as well as other bacterial, fungal, and viral infections, were negative. A skin biopsy from the right fifth toe showed a dense infiltrate of CD1a+ histiocytic cells with folded or kidney-shaped nuclei mixed with eosinophils, which was consistent with Langerhans cell histiocytosis (LCH) (Figure 1). Skin lesions were treated with hydrocortisone cream 2.5% and progressively faded over a few weeks.

Langerhans cell histiocytosis is a rare disorder with a variable clinical presentation depending on the sites affected and the extent of involvement. It can involve multiple organ systems, most commonly the skeletal system and the skin. Organ involvement is characterized by histiocyte infiltration. Acute disseminated multisystem disease most commonly is seen in children younger than 3 years.¹

Congenital cutaneous LCH presents with variable skin lesions ranging from papules to vesicles, pustules, and ulcers, with onset at birth or in the neonatal period. Various morphologic traits of skin lesions have been described; the most common presentation is multiple red to yellow-brown, crusted papules with accompanying hemorrhage or erosion.¹ Other cases have described an eczematous, seborrheic, diffuse eruption or erosive intertrigo. One case of a child with a solitary necrotic nodule on the scalp has been reported.²

Our patient presented with disseminated, nonblanching, purple to dark red papules and nodules of the skin and oral mucosa, as well as nail dystrophy (Figure 2). However, LCH in a neonate can mimic other causes of congenital papulonodular eruptions. Red-brown papules and nodules with or without crusting in a newborn can be mistaken for erythema toxicum neonatorum, transient neonatal pustular melanosis, congenital leukemia cutis, neonatal erythropoiesis, disseminated neonatal hemangiomatosis, infantile acropustulosis, or congenital TORCH infections such as rubella or syphilis. When LCH presents as vesicles or eroded papules or nodules in a newborn, the differential diagnosis includes incontinentia pigmenti and hereditary epidermolysis bullosa.

Langerhans cell histiocytosis may even present with a classic blueberry muffin rash that can lead clinicians to consider cutaneous metastasis from various hematologic malignancies or the more common TORCH infections. Several diagnostic tests can be performed to clarify the diagnosis, including bacterial and viral cultures and stains, serology, immunohistochemistry, flow cytometry, bone marrow aspiration, or skin biopsy.³ Langerhans cell histiocytosis is diagnosed with a combination of histology, immunohistochemistry, and clinical presentation; however, a skin biopsy is crucial. Tissue should be taken from the most easily accessible yet representative lesion. The characteristic appearance of LCH lesions is described as a dense infiltrate of histiocytic cells mixed with numerous eosinophils in the dermis.¹ Histiocytes usually have folded nuclei and eosinophilic cytoplasm or kidney-shaped nuclei with prominent nucleoli. Positive CD1a and/or CD207 (Langerin) staining of the cells is required for definitive diagnosis.⁴ After diagnosis, it is important to obtain baseline laboratory and radiographic studies to determine the extent of systemic involvement.

Treatment of congenital LCH is tailored to the extent of organ involvement. The dermatologic manifestations resolve without medications in many cases. However, true self-resolving LCH can only be diagnosed retrospectively after a full evaluation for other sites of disease. Disseminated disease can be life-threatening and requires more active management. In cases of skin-limited disease, therapies include topical steroids, nitrogen mustard, or imiquimod; surgical resection of isolated lesions; phototherapy; or systemic therapies such as methotrexate, 6-mercaptopurine, vinblastine/vincristine, cladribine, and/or cytarabine. Symptomatic patients initially are treated with methotrexate and 6-mercaptopurine.⁵ Asymptomatic infants with skin-limited involvement can be managed with topical treatments.

Our patient had skin-limited disease. Abdominal ultrasonography, skeletal survey, and magnetic resonance imaging of the brain revealed no abnormalities. The patient’s family was advised to monitor him for reoccurrence of the skin lesions and to continue close follow-up with hematology and dermatology. Although congenital LCH often is self-resolving, extensive skin involvement increases the risk for internal organ involvement for several years.⁶ These patients require long-term follow-up for potential musculoskeletal, ophthalmologic, endocrine, hepatic, and/or pulmonary disease.

The Diagnosis: Congenital Cutaneous Langerhans Cell Histiocytosis

Although the infectious workup was positive for herpes simplex virus type 1 and cytomegalovirus antibodies, serologies for the rest of the TORCH (toxoplasmosis, other agents [syphilis, hepatitis B virus], rubella, cytomegalovirus) group of infections, as well as other bacterial, fungal, and viral infections, were negative. A skin biopsy from the right fifth toe showed a dense infiltrate of CD1a+ histiocytic cells with folded or kidney-shaped nuclei mixed with eosinophils, which was consistent with Langerhans cell histiocytosis (LCH) (Figure 1). Skin lesions were treated with hydrocortisone cream 2.5% and progressively faded over a few weeks.

Langerhans cell histiocytosis is a rare disorder with a variable clinical presentation depending on the sites affected and the extent of involvement. It can involve multiple organ systems, most commonly the skeletal system and the skin. Organ involvement is characterized by histiocyte infiltration. Acute disseminated multisystem disease most commonly is seen in children younger than 3 years.¹

Congenital cutaneous LCH presents with variable skin lesions ranging from papules to vesicles, pustules, and ulcers, with onset at birth or in the neonatal period. Various morphologic traits of skin lesions have been described; the most common presentation is multiple red to yellow-brown, crusted papules with accompanying hemorrhage or erosion.¹ Other cases have described an eczematous, seborrheic, diffuse eruption or erosive intertrigo. One case of a child with a solitary necrotic nodule on the scalp has been reported.²

Our patient presented with disseminated, nonblanching, purple to dark red papules and nodules of the skin and oral mucosa, as well as nail dystrophy (Figure 2). However, LCH in a neonate can mimic other causes of congenital papulonodular eruptions. Red-brown papules and nodules with or without crusting in a newborn can be mistaken for erythema toxicum neonatorum, transient neonatal pustular melanosis, congenital leukemia cutis, neonatal erythropoiesis, disseminated neonatal hemangiomatosis, infantile acropustulosis, or congenital TORCH infections such as rubella or syphilis. When LCH presents as vesicles or eroded papules or nodules in a newborn, the differential diagnosis includes incontinentia pigmenti and hereditary epidermolysis bullosa.

Langerhans cell histiocytosis may even present with a classic blueberry muffin rash that can lead clinicians to consider cutaneous metastasis from various hematologic malignancies or the more common TORCH infections. Several diagnostic tests can be performed to clarify the diagnosis, including bacterial and viral cultures and stains, serology, immunohistochemistry, flow cytometry, bone marrow aspiration, or skin biopsy.³ Langerhans cell histiocytosis is diagnosed with a combination of histology, immunohistochemistry, and clinical presentation; however, a skin biopsy is crucial. Tissue should be taken from the most easily accessible yet representative lesion. The characteristic appearance of LCH lesions is described as a dense infiltrate of histiocytic cells mixed with numerous eosinophils in the dermis.¹ Histiocytes usually have folded nuclei and eosinophilic cytoplasm or kidney-shaped nuclei with prominent nucleoli. Positive CD1a and/or CD207 (Langerin) staining of the cells is required for definitive diagnosis.⁴ After diagnosis, it is important to obtain baseline laboratory and radiographic studies to determine the extent of systemic involvement.

Treatment of congenital LCH is tailored to the extent of organ involvement. The dermatologic manifestations resolve without medications in many cases. However, true self-resolving LCH can only be diagnosed retrospectively after a full evaluation for other sites of disease. Disseminated disease can be life-threatening and requires more active management. In cases of skin-limited disease, therapies include topical steroids, nitrogen mustard, or imiquimod; surgical resection of isolated lesions; phototherapy; or systemic therapies such as methotrexate, 6-mercaptopurine, vinblastine/vincristine, cladribine, and/or cytarabine. Symptomatic patients initially are treated with methotrexate and 6-mercaptopurine.⁵ Asymptomatic infants with skin-limited involvement can be managed with topical treatments.

Our patient had skin-limited disease. Abdominal ultrasonography, skeletal survey, and magnetic resonance imaging of the brain revealed no abnormalities. The patient’s family was advised to monitor him for reoccurrence of the skin lesions and to continue close follow-up with hematology and dermatology. Although congenital LCH often is self-resolving, extensive skin involvement increases the risk for internal organ involvement for several years.⁶ These patients require long-term follow-up for potential musculoskeletal, ophthalmologic, endocrine, hepatic, and/or pulmonary disease.

Adults with asthma who were newly prescribed mepolizumab showed significant improvement in symptoms after 1 year regardless of comorbidities, based on data from 822 individuals.

Comorbidities including chronic rhinosinusitis with polyps (CRSwNP), gastroesophageal reflux disease GERD), anxiety and depression, and chronic obstructive pulmonary disorder (COPD) are common in patients with severe asthma and add to the disease burden, wrote Mark C. Liu, MD, of Johns Hopkins University, Baltimore, and colleagues.

“Some comorbidities, such as CRSwNP, share pathophysiological mechanisms with severe asthma, with interleukin-5 (IL-5),” and treatments targeting IL-5 could improve outcomes, they said.

In the real-world REALITI-A study, mepolizumab, a humanized monoclonal antibody that targets IL-5, significantly reduced asthma exacerbation and oral corticosteroid use in severe asthma patients, they said.

To assess the impact of mepolizumab on patients with comorbidities, the researchers conducted a post hoc analysis of 822 adults with severe asthma, including 321 with CRSwNP, 309 with GERD, 203 with depression/anxiety, and 81 with COPD. The findings were published in the Journal of Allergy and Clinical Immunology: In Practice.

The main outcomes were the rate of clinically significant asthma exacerbations (CSEs) between the 12 months before and after mepolizumab initiation, and the changes from baseline in the daily maintenance use of oral corticosteroids (OCS).

Across all comorbidities, the rate of CSEs decreased significantly from the pretreatment period to the follow-up period, from 4.28 events per year to 1.23 events per year.

“A numerically greater reduction in the rate of CSEs was reported for patients with versus without CRSwNP, whereas the reverse was reported for patients with versus without COPD and depression/anxiety, although the confidence intervals were large for the with COPD subgroup,” the researchers wrote.

The median maintenance dose of oral corticosteroids decreased by at least 50% across all comorbidities after mepolizumab treatment; patients with CRSwNP had the greatest reduction (83%).

In addition, scores on the Asthma Control Questionnaire–5 decreased by at least 0.63 points, and least squared (LS) mean changes in forced expiratory volume per second (FEV₁) increased from baseline across all comorbidities after mepolizumab treatment by at least 74 mL.

Although patients with versus without CRSwNP had greater improvements, patients without GERD, depression/anxiety, and COPD had greater improvements than did those without the respective conditions with the exception of greater FEV₁ improvement in patients with vs. without COPD.

“Patients with severe asthma and comorbid CRSwNP are recognized as having a high disease burden, as demonstrated by more frequent exacerbations,” the researchers wrote in their discussion. “Mepolizumab may serve to reduce the disease burden of this high-risk group by targeting the common pathophysiological pathway of IL-5 and eosinophilic-driven inflammation because it has proven clinical benefits in treating asthma and CRSwNP separately and together,” and the current study findings support the use of mepolizumab for this population in particular, they said.

The findings were limited by several factors including the incomplete data for voluntary assessments, the post hoc design and relatively small numbers of patients in various subgroups, notably COPD, and the potential inaccurate diagnosis of COPD, the researchers noted.

“Nevertheless, because the amount of improvement in each outcome following mepolizumab treatment differed depending on the comorbidity in question, our findings highlight the impact that comorbidities and their prevalence and severity have on outcomes,” and the overall success of mepolizumab across clinical characteristics and comorbidities supports the generalizability of the findings to the larger population of adults with severe asthma, they concluded.

The study was supported by GlaxoSmithKline. Dr. Liu disclosed research funding from GSK, Boehringer Ingelheim, and Gossamer Bio, and participation on advisory boards for AstraZeneca, GSK, and Gossamer Bio.

Adults with asthma who were newly prescribed mepolizumab showed significant improvement in symptoms after 1 year regardless of comorbidities, based on data from 822 individuals.

Comorbidities including chronic rhinosinusitis with polyps (CRSwNP), gastroesophageal reflux disease GERD), anxiety and depression, and chronic obstructive pulmonary disorder (COPD) are common in patients with severe asthma and add to the disease burden, wrote Mark C. Liu, MD, of Johns Hopkins University, Baltimore, and colleagues.

“Some comorbidities, such as CRSwNP, share pathophysiological mechanisms with severe asthma, with interleukin-5 (IL-5),” and treatments targeting IL-5 could improve outcomes, they said.

In the real-world REALITI-A study, mepolizumab, a humanized monoclonal antibody that targets IL-5, significantly reduced asthma exacerbation and oral corticosteroid use in severe asthma patients, they said.

To assess the impact of mepolizumab on patients with comorbidities, the researchers conducted a post hoc analysis of 822 adults with severe asthma, including 321 with CRSwNP, 309 with GERD, 203 with depression/anxiety, and 81 with COPD. The findings were published in the Journal of Allergy and Clinical Immunology: In Practice.

The main outcomes were the rate of clinically significant asthma exacerbations (CSEs) between the 12 months before and after mepolizumab initiation, and the changes from baseline in the daily maintenance use of oral corticosteroids (OCS).

Across all comorbidities, the rate of CSEs decreased significantly from the pretreatment period to the follow-up period, from 4.28 events per year to 1.23 events per year.

“A numerically greater reduction in the rate of CSEs was reported for patients with versus without CRSwNP, whereas the reverse was reported for patients with versus without COPD and depression/anxiety, although the confidence intervals were large for the with COPD subgroup,” the researchers wrote.

The median maintenance dose of oral corticosteroids decreased by at least 50% across all comorbidities after mepolizumab treatment; patients with CRSwNP had the greatest reduction (83%).

In addition, scores on the Asthma Control Questionnaire–5 decreased by at least 0.63 points, and least squared (LS) mean changes in forced expiratory volume per second (FEV₁) increased from baseline across all comorbidities after mepolizumab treatment by at least 74 mL.

Although patients with versus without CRSwNP had greater improvements, patients without GERD, depression/anxiety, and COPD had greater improvements than did those without the respective conditions with the exception of greater FEV₁ improvement in patients with vs. without COPD.

“Patients with severe asthma and comorbid CRSwNP are recognized as having a high disease burden, as demonstrated by more frequent exacerbations,” the researchers wrote in their discussion. “Mepolizumab may serve to reduce the disease burden of this high-risk group by targeting the common pathophysiological pathway of IL-5 and eosinophilic-driven inflammation because it has proven clinical benefits in treating asthma and CRSwNP separately and together,” and the current study findings support the use of mepolizumab for this population in particular, they said.

The findings were limited by several factors including the incomplete data for voluntary assessments, the post hoc design and relatively small numbers of patients in various subgroups, notably COPD, and the potential inaccurate diagnosis of COPD, the researchers noted.

“Nevertheless, because the amount of improvement in each outcome following mepolizumab treatment differed depending on the comorbidity in question, our findings highlight the impact that comorbidities and their prevalence and severity have on outcomes,” and the overall success of mepolizumab across clinical characteristics and comorbidities supports the generalizability of the findings to the larger population of adults with severe asthma, they concluded.

The study was supported by GlaxoSmithKline. Dr. Liu disclosed research funding from GSK, Boehringer Ingelheim, and Gossamer Bio, and participation on advisory boards for AstraZeneca, GSK, and Gossamer Bio.

Adults with asthma who were newly prescribed mepolizumab showed significant improvement in symptoms after 1 year regardless of comorbidities, based on data from 822 individuals.

Comorbidities including chronic rhinosinusitis with polyps (CRSwNP), gastroesophageal reflux disease GERD), anxiety and depression, and chronic obstructive pulmonary disorder (COPD) are common in patients with severe asthma and add to the disease burden, wrote Mark C. Liu, MD, of Johns Hopkins University, Baltimore, and colleagues.

“Some comorbidities, such as CRSwNP, share pathophysiological mechanisms with severe asthma, with interleukin-5 (IL-5),” and treatments targeting IL-5 could improve outcomes, they said.

In the real-world REALITI-A study, mepolizumab, a humanized monoclonal antibody that targets IL-5, significantly reduced asthma exacerbation and oral corticosteroid use in severe asthma patients, they said.

To assess the impact of mepolizumab on patients with comorbidities, the researchers conducted a post hoc analysis of 822 adults with severe asthma, including 321 with CRSwNP, 309 with GERD, 203 with depression/anxiety, and 81 with COPD. The findings were published in the Journal of Allergy and Clinical Immunology: In Practice.

The main outcomes were the rate of clinically significant asthma exacerbations (CSEs) between the 12 months before and after mepolizumab initiation, and the changes from baseline in the daily maintenance use of oral corticosteroids (OCS).

Across all comorbidities, the rate of CSEs decreased significantly from the pretreatment period to the follow-up period, from 4.28 events per year to 1.23 events per year.

“A numerically greater reduction in the rate of CSEs was reported for patients with versus without CRSwNP, whereas the reverse was reported for patients with versus without COPD and depression/anxiety, although the confidence intervals were large for the with COPD subgroup,” the researchers wrote.

The median maintenance dose of oral corticosteroids decreased by at least 50% across all comorbidities after mepolizumab treatment; patients with CRSwNP had the greatest reduction (83%).

In addition, scores on the Asthma Control Questionnaire–5 decreased by at least 0.63 points, and least squared (LS) mean changes in forced expiratory volume per second (FEV₁) increased from baseline across all comorbidities after mepolizumab treatment by at least 74 mL.

Although patients with versus without CRSwNP had greater improvements, patients without GERD, depression/anxiety, and COPD had greater improvements than did those without the respective conditions with the exception of greater FEV₁ improvement in patients with vs. without COPD.

“Patients with severe asthma and comorbid CRSwNP are recognized as having a high disease burden, as demonstrated by more frequent exacerbations,” the researchers wrote in their discussion. “Mepolizumab may serve to reduce the disease burden of this high-risk group by targeting the common pathophysiological pathway of IL-5 and eosinophilic-driven inflammation because it has proven clinical benefits in treating asthma and CRSwNP separately and together,” and the current study findings support the use of mepolizumab for this population in particular, they said.

The findings were limited by several factors including the incomplete data for voluntary assessments, the post hoc design and relatively small numbers of patients in various subgroups, notably COPD, and the potential inaccurate diagnosis of COPD, the researchers noted.

“Nevertheless, because the amount of improvement in each outcome following mepolizumab treatment differed depending on the comorbidity in question, our findings highlight the impact that comorbidities and their prevalence and severity have on outcomes,” and the overall success of mepolizumab across clinical characteristics and comorbidities supports the generalizability of the findings to the larger population of adults with severe asthma, they concluded.

The study was supported by GlaxoSmithKline. Dr. Liu disclosed research funding from GSK, Boehringer Ingelheim, and Gossamer Bio, and participation on advisory boards for AstraZeneca, GSK, and Gossamer Bio.

For many years, attention-deficit/hyperactivity disorder (ADHD) was thought of as a disorder of childhood; however, it is now increasingly being recognized as a chronic, lifelong disorder that persists into adulthood in approximately two-thirds of patients.¹ While our knowledge about ADHD in adults has increased, most research in this population focused on young or middle-aged adults; less is known about ADHD in older adults. Older adults with ADHD may be newly diagnosed at any point in their lives, or not at all.² Because ADHD may present differently in older adults than in children or young adults, and because it may impair domains of life in different ways, a closer look at late-life ADHD is needed. This article summarizes the literature on the prevalence, impairment, diagnosis, and treatment of ADHD in adults age >60.

Challenges in determining the prevalence

Few studies have examined the age-specific prevalence of ADHD among older adults.³ Compared with childhood ADHD, adult ADHD is relatively neglected in epidemiological studies, largely due to the absence of well-established, validated diagnostic criteria.^1,4 Some experts have noted that DSM-5’s ADHD criteria were designed for diagnosing children, and the children-focused symptom threshold may not be useful for adults because ADHD symptoms decline substantially with age.² One study evaluating DSM-5 ADHD criteria in young adults (N = 4,000, age 18 to 19) found ADHD was better diagnosed when the required number of clinically relevant inattention and hyperactivity symptoms was reduced from 6 to 5 for each category.⁵ They also found the DSM-5 age-at-onset criterion of symptoms present before age 12 had a significant effect on ADHD prevalence, reducing the rate from 23.7% (95% CI, 22.38 to 25.02) to 5.4% (95% CI, 13.99 to 16.21).⁵ This suggests that strict usage of DSM-5 criteria may underestimate the prevalence of ADHD in adults, because ADHD symptoms may not be detected in childhood, or self-reporting of childhood ADHD symptoms in older adults may be unreliable due to aging processes that compromise memory and recall. These findings also indicate that fewer ADHD symptoms are needed to impair functioning in older age.

Determining the prevalence of ADHD among older adults is further complicated by individuals who report symptoms consistent with an ADHD diagnosis despite having never received this diagnosis during childhood.^6-8 This may be due to the considerable number of children who meet ADHD criteria but do not get a diagnosis due to limited access to health care.⁹ Thus, many studies separately analyze the syndromatic (with a childhood onset) and symptomatic (regardless of childhood onset) persistence of ADHD. One epidemiological meta-analysis found the 2020 prevalence of syndromatic ADHD in adults age >60 was 0.77% and the prevalence of symptomatic ADHD was 4.51%, which translates to 7.91 million and 46.36 million affected older adults, respectively.⁸ Other research has reported higher rates among older adults.^6,7,10 The variations among this research may be attributed to the use of different diagnostic tools/criteria, study populations, sampling methods, or DSM versions. Heterogeneity among this research also further supports the idea that the prevalence of ADHD is heavily dependent on how one defines and diagnoses the disorder.

Reasons for late-life ADHD diagnosis

There are many reasons a patient may not be diagnosed with ADHD until they are an older adult.¹¹ In addition to socioeconomic barriers to health care access, members of different ethnic groups exhibit differences in help-seeking behaviors; children may belong to a culture that does not traditionally seek health care even when symptoms are evident.^6,9 Therefore, individuals may not receive a diagnosis until adulthood. Some experts have discussed the similarity of ADHD to other neurodevelopmental disorders, such as autism spectrum disorder or social communication disorder, where ADHD symptoms may not manifest until stressors at critical points in life exceed an individual’s capacity to compensate.²

The life transition model contextualizes ADHD as being associated with demand/resource imbalances that come and go throughout life, resulting in variability in the degree of functional impairment ADHD symptoms cause in older adults.^2,12 Hypothetically, events in late life—such as the death of a spouse or retirement—can remove essential support structures in the lives of high-functioning individuals with ADHD. As a result, such events surpass these individuals’ ability to cope, resulting in a late-life manifestation of ADHD.

The plausibility of late-onset ADHD

In recent years, many studies identifying ADHD in adults have been published,^2,10,12-15 including some that discuss adult ADHD that spontaneously appears without childhood symptoms (ie, late-onset ADHD).^2,4,12 Research of late-onset ADHD attracts attention because the data it presents challenge the current rationale that ADHD symptoms should be present before age 12, as defined by DSM-5 criteria. While most reports of late-onset ADHD pertain to younger adults, little evidence exists to reinforce the concept; to date just 1 study has reported cases of late-onset ADHD in older adults (n = 7, age 51 to 59).¹¹ In this study, Sasaki et al¹¹ acknowledged the strong possibility their cases may be late manifestations of long-standing ADHD. Late-onset ADHD is further challenged by findings that 95% of individuals initially diagnosed with late-onset ADHD can be excluded from the diagnosis with further detailed assessment that accounts for co-occurring mental disorders and substance use.¹⁶ This suggests false positive cases of late-onset ADHD may be a symptom of narrow clinical assessment that fails to encompass other aspects of a patient’s psychiatric profile, rather than an atypical ADHD presentation.

Comorbidity and psychosocial functioning

ADHD symptoms and diagnosis in older adults are associated with clinically relevant levels of depression and anxiety. The Dutch Longitudinal Aging Study Amsterdam (LASA) examined 1,494 older adults (age 55 to 85) using the Diagnostic Interview for ADHD in Adults version 2.0.¹⁰ The 231 individuals identified as having symptoms of ADHD reported clinically relevant levels of depressive and anxiety symptoms. ADHD was significantly associated with these comorbid symptoms.

Continue to: Little is known regarding...

Little is known regarding the manifestation of symptoms of ADHD in older age and the difficulties these older adults face. Older adults with ADHD are more often divorced and report more loneliness than older adults without this disorder, which suggests loneliness in older age may be more pressing for the older ADHD population.¹⁷ ADHD in older adults has also been associated with poor quality-of-life measures, including moderate to severe problems in mobility, self-care, usual activity, pain/discomfort, and anxiety/depression (Table 1^14,17).

Qualitative research has described a domino effect of a lifetime of living with ADHD. In one American study, older adults with ADHD (N = 24, age 60 to 74) reported experiencing a tangible, accumulated impact from ADHD on their finances and long-term relationships with family, friends, and coworkers.¹³ Another study utilizing the Dutch LASA data examined how ADHD may impact patient’s lives among participants who were unaware of their diagnosis.¹⁸ One-half of patients reported low self-esteem, overstepping boundaries, and feeling different from others. When compared to younger adults with ADHD, older adults report significantly greater impairments in productivity and a worse life outlook.¹⁹

Differential diagnosis

When assessing whether an older adult has ADHD, it is important to consider other potential causes of their symptoms (Table 2^11,15,20-23). The differential diagnosis includes impaired vision and hearing as well as medical illness (vitamin B12 deficiency, hyperthyroidism, hypothyroidism, hyperparathyroidism, and infectious diseases such as herpes simplex virus or syphilis).^11,15,20-23 Neurological causes include brain tumors, traumatic brain injuries, postconcussive syndrome, stroke, and neurocognitive disorders.^11,15,20-23 Other potential causes include obstructive sleep apnea, mood disorders, substance use disorders, and medication adverse effects (especially with polypharmacy).^11,15,20-23 In this population, other causes are often responsible for “late-manifestation ADHD symptoms.”^1,15 Neurocognitive disorders and other psychiatric conditions are especially difficult to differentiate from ADHD.

In older adults, ADHD symptoms include frontal-executive impairments, inattentiveness, difficulty with organization or multitasking, forgetfulness, and challenges involving activities of daily living or socialization that can appear to be a mild or major neurocognitive disorder (Table 3^11,24,25). This includes major neuro­cognitive disorder due to Alzheimer’s disease, Lewy body disease, and vascular disease.^2,26 However, frontotemporal lobar degeneration is reported to have more symptom overlap with ADHD.^21,22,26,27 A way to differentiate between neurocognitive disorders and ADHD in older adults is to consider that patients with neurocognitive disorders often progress to visual hallucinations and more extreme personality changes than would be expected in ADHD.¹¹ Each disease also has its own identifiable characteristics. Extreme changes in memory are often Alzheimer’s disease, personality changes suggest fronto­temporal lobar degeneration, stepwise decline is classic for vascular disease, and parkinsonian features may indicate dementia with Lewy bodies.²¹ In addition, the onset of ADHD usually occurs in childhood and can be traced throughout the lifespan,² whereas neurocognitive diseases usually appear for the first time in later life.^2,28 There are nuances in the nature of forgetfulness that can distinguish ADHD from neurocognitive disorders. For instance, the forgetfulness in early-onset Alzheimer’s disease involves “the lack of episodic memories,” while in contrast ADHD is thought to be “forgetfulness due to inadvertence.”¹¹ Furthermore, patients with neurocognitive disorders are reported to have more severe symptoms and an inability to explain why, whereas those with ADHD have a steady level of symptoms and can provide a more comprehensive story.²⁴ Two recent studies have shown that weak performance on language tests is more indicative of a neuro­degenerative process than of ADHD.^29,30 Research has suggested that if an older adult shows a sudden, acute onset of ADHD-like symptoms, this is most likely reflective of cognitive decline or a mood disorder such as depression.^2,15,24

Several other psychiatric conditions share many symptoms with ADHD. Overlapping symptomology between ADHD and mood and anxiety disorders presents challenges.²⁷ Emotional dysregulation is a feature of adult ADHD, and this often causes a mood disorder to be diagnosed without considering other possible explanations.^{21,22,27,31-34} Features of mania can overlap with ADHD symptoms, including psychomotor agitation, talkativeness, and distractibility.²⁷ Several other disorders also include distractibility, such as depression, anxiety, and substance use disorders.³⁵ Depression and anxiety can be an outcome of untreated ADHD, or can co-occur with ADHD.^21-23,27 ADHD can also co-occur with bipolar disorder (BD), substance use disorders, and personality disorders (borderline and antisocial personality disorder) (Figure 1^21-23,27,35). One suggested method of establishing an appropriate diagnosis is to study the efficacy of the treatment retrospectively. For example, if a patient is presumed to have depression and they do not respond to several selective serotonin reuptake inhibitors, this may be undetected ADHD.²⁷ In addition, the argument about the chronicity of the symptoms should also be considered. ADHD symptoms are pervasive whereas BD symptoms are episodic.³⁵ Depression can be chronic; however, there are often discrete major depressive episodes. It is important to have a clear timeline of the patient’s symptoms. Ask about age of onset, because in theory, ADHD is supposed to start in childhood.²² It is sometimes difficult to ascertain this information because many older adults grew up during a time where ADHD was not a recognized diagnosis.²¹

Continue to: Diagnosis and workup

Diagnosis and workup

The key aspects of diagnosing ADHD are the interview based on DSM-5 criteria, exclusion of other diagnoses, and collateral information. Research has shown that clinical interviews and longitudinal family histories provide critical information that can differentiate ADHD from other psychiatric conditions.³⁵ DSM-5 criteria are adjusted for adults: 5 out of 9 criteria for inattention and/or hyperactivity-impulsivity must be fulfilled, as opposed to 6 out of 9 in children age <17.^21,31,36 However, no criteria are specific for older adults.³⁷ Since the differential diagnosis involves multiple entities, it is important to follow DSM-5 criteria for ADHD, which include eliminating other conditions that can explain these symptoms.¹⁵ Additionally, in DSM-5, the age-of-onset threshold for ADHD diagnosis was increased from 7 and younger to 12 and younger, addressing criticism that the previous cutoff was too restrictive.^24,31 The age of onset of childhood symptoms can be challenging to verify in older adults. Older patients can have unreliable memories and their childhood records are not always available.^2,20 In this population, childhood symptoms are mainly underreported but sometimes overreported.^10,38 However, to establish a diagnosis, the patient should have experienced some symptoms of the disorder within their first 50 years of life, including having impaired functionality in multiple settings.^15,26 The goal is to establish the chronicity of this condition to distinguish it from other psychiatric conditions.²² Overall, using DSM-5 criteria without any modifications may lead to underdiagnosis of ADHD in adults.²³ At this time, however, DSM-5 remains the main criteria used to make a diagnosis.

While tools to assist in screening and diagnosing ADHD have been validated in adults, none have been validated specifically for older adults.²² Structured diagnostic interviews to diagnose ADHD include³⁹:

• Adult ADHD Clinical Diagnostic Scale version 1.2
• ADHD Lifespan Functioning interview
• Conners’ Adult ADHD Diagnostic interview for DSM-IV
• Diagnostic Interview for ADHD in Adults version 2.0
• Structured Clinical Interview for DSM-5.

ADHD symptom measures that can be used for screening and to look at treatment response include³⁹:

• ADHD Rating Scale 5
• Adult ADHD Self-Report Scale Symptom Checklist
• Barkley Adult ADHD Rating Scale IV
• Barkley Quick-Check for Adult ADHD Diagnosis
• Young ADHD Questionnaire
• RATE Scales.

Adult ADHD inventories consider problems that adults with ADHD face. These include³⁹:

• Brown Attention Deficit Disorders Scales—Adult version
• Conners’ Adult ADHD Rating Scales
• Wender-Reimherr Adult Attention Deficit Disorder Scale.

Since these scales were not designed for older adults, they may miss nuances in this population.⁴⁰

Continue to: It can be particularly...

It can be particularly perplexing to diagnose ADHD in older adults because the other possible causes of the symptoms are vast. During the interview, it is important to ask questions that may rule out other psychiatric, neurologic, and medical conditions.²¹ Screen for other diagnoses, and include questions about a patient’s sleep history to rule out obstructive sleep apnea.²¹ To screen for other psychiatric conditions, the Mini International Neuropsychiatric Interview 5.0.0 may be used.²² Other tools include the Saint Louis University AMSAD screen for depression, the Geriatric Depression Scale, and the Beck Anxiety Inventory.^28,41 To screen for cognitive functioning, the Saint Louis University Mental Status Exam, Montreal Cognitive Assessment, or Mini-Mental State Examination can be used.^22,28,42,43 Once screening is performed, a physical and neurologic examination is the best next step.²⁶ Additionally, laboratory data and imaging can rule out other conditions; however, these are not routinely performed to diagnose ADHD.

Laboratory tests should include a comprehensive metabolic panel, complete blood count, thyroid-stimulating hormone level, B12/folate level, and possibly a vitamin D level.^11,36 These tests cover several conditions that may mimic ADHD. Brain MRI is not routinely recommended for diagnosing ADHD, though it may be useful because some research has found brain structural differences in individuals with ADHD.^28,44,45 Neurocognitive disorders have notable MRI findings that distinguish them from ADHD and each other.²⁴ If there is significant concern for neurocognitive disorders, more specific tests can be employed, such as CSF studies, to look for phosphorylated tau and beta amyloid markers.¹¹

Ask about family history (first-degree relative with ADHD) and obtain collateral information to make sure no other diagnoses are overlooked. Family history can help diagnose this disorder in older adults because there is evidence that ADHD runs in families.^2,25 This evidence would ideally come from someone who has known the patient their entire life, such as a sibling or parent.²⁴ The collateral information will be especially helpful to discern the chronicity of the patient’s symptoms, which would point toward a diagnosis of ADHD. To summarize (Figure 2):

• obtain a thorough interview that may be supported by a screening tool
• rule out other conditions
• conduct a physical examination
• obtain laboratory results
• collect collateral information
• obtain neuroimaging if necessary.

Treatment

ADHD symptoms can be treated with medications and psychotherapy. Research has shown the efficacy of ADHD medications in older adults, demonstrating that treatment leads to better functioning in multiple settings and decreases the risk for developing comorbid psychiatric conditions (mood disorder, substance use disorders).^25,27 Symptoms that improve with medication include attention, concentration, self-efficacy, functioning, self-esteem, psychomotor agitation, mood, energy, and procrastination.^21,31,46 If a patient with ADHD also has other psychiatric diagnoses, treat the most impairing disorder first.²² This often means mood disorders and substance use disorders must be remedied before ADHD is treated.²¹

Medication options include stimulants and nonstimulants. First-line treatments are stimulant medications, including methylphenidate, amphetamines, and mixed amphetamine salts.^{12,22,27,31,35} Stimulants have shown significant efficacy in older adults, although the American Geriatrics Society’s Beers Criteria list stimulants as potentially inappropriate for older adults.³³ Adults show significant improvement with methylphenidate.^21,23,47 In an observational study, Michielsen et al⁴⁶ found stimulants were safe and efficacious in older adults if patients are carefully monitored for adverse effects, especially cardiovascular changes. Second-line treatments include the nonstimulant atomoxetine.^12,22,27,31 Clonidine and guanfacine are FDA-approved for treating ADHD in children, but not approved for adults.²⁶ There is little evidence for other treatments, such as bupropion.^12,22,27 All of these medications have adverse effects, which are especially important to consider in older adults, who experience age-related physiological changes.

Continue to: Medications for ADHD symptoms...

Medications for ADHD symptoms are thought to act via catecholaminergic mechanisms.²¹ As a result, adverse effects of stimulants can include headache, appetite suppression, nausea, difficulty sleeping, tremor, blurred vision, agitation, psychosis, increased heart rate, arrhythmia, and hypertension.^22,27,32-34 Especially in older adults, adverse effects such as reduced appetite, disrupted sleep, or increased blood pressure or heart rate may be harmful.^21,23 Using caffeine or pseudoephedrine can exacerbate these adverse effects.²¹ Atomoxetine’s adverse effects include appetite suppression, insomnia, dizziness, anxiety, agitation, fatigue, dry mouth, constipation, nausea, vomiting, dyspepsia, and increased heart rate or blood pressure.^27,32,35 Genitourinary adverse effects have also been reported, including priapism (rare), decreased libido, and urinary hesitancy and retention.^26,32 Before any medication is initiated, it is important to conduct a physical and neurologic examination and a detailed clinical interview.

Before starting medication, as with any medical treatment, conduct a risk vs benefit analysis. Record baseline values for the patient’s heart rate, blood pressure, and weight.^23,26,27,31 During the interview, screen for family and personal cardiovascular conditions,^27,33 and obtain an electrocardiogram for any patient with cardiovascular risks.^23,26,27,31 Once the patient is deemed to be an appropriate candidate for pharmacologic treatment, begin with low doses and titrate the medication slowly until reaching a therapeutic level.^23,48

Medications should be combined with psychotherapy (eg, cognitive-behavioral therapy or dialectical behavioral therapy) and other lifestyle changes (exercise, mindfulness, support groups).^{18,22,23,27,31,49} Psychotherapy can help patients come to terms with receiving an ADHD diagnosis later in life and help with organization and socialization.^12,50 Pharmacologic treatments are thought to be helpful with attention challenges and emotional instability.⁵⁰ Taken together, medications and behavioral interventions can help individuals experience an improved quality of life.

Future directions

Given the relatively recent interest in ADHD in older adults, there are several areas that need further research. For future editions of DSM, it may be prudent to consider establishing ADHD criteria specific to older adults. Research has also shown the need for clear diagnostic and validated tools for older adults.⁸ Few analyses have been undertaken regarding pharmacotherapy for this population. Randomized controlled clinical trials are needed.^23,37,48 More research about the relative utility of psychotherapy and behavioral interventions would also be useful, given their potential to improve the quality of life for older adults with ADHD.

Bottom Line

Although generally thought of as a disorder of childhood, attention-deficit/ hyperactivity disorder (ADHD) has substantial effects in older adults. When the condition is appropriately diagnosed, pharmacologic treatment and psychotherapy are associated with improved quality of life for older patients with ADHD.

Related Resources

• Children and Adults with Attention-Deficit/Hyperactivity Disorder. Living with ADHD: A lifespan disorder. https://chadd.org/for-adults/living-with-adhd-a-lifespan-disorder/
• Attention Deficit Disorder Association. Support groups for adults. https://add.org/adhd-support-groups/

Drug Brand Names

Amphetamine/dextroamphetamine • Adderall
Atomoxetine • Straterra
Bupropion • Wellbutrin
Clonidine • Catapres
Guanfacine • Intuniv
Methylphenidate • Ritalin

For many years, attention-deficit/hyperactivity disorder (ADHD) was thought of as a disorder of childhood; however, it is now increasingly being recognized as a chronic, lifelong disorder that persists into adulthood in approximately two-thirds of patients.¹ While our knowledge about ADHD in adults has increased, most research in this population focused on young or middle-aged adults; less is known about ADHD in older adults. Older adults with ADHD may be newly diagnosed at any point in their lives, or not at all.² Because ADHD may present differently in older adults than in children or young adults, and because it may impair domains of life in different ways, a closer look at late-life ADHD is needed. This article summarizes the literature on the prevalence, impairment, diagnosis, and treatment of ADHD in adults age >60.

Challenges in determining the prevalence

Few studies have examined the age-specific prevalence of ADHD among older adults.³ Compared with childhood ADHD, adult ADHD is relatively neglected in epidemiological studies, largely due to the absence of well-established, validated diagnostic criteria.^1,4 Some experts have noted that DSM-5’s ADHD criteria were designed for diagnosing children, and the children-focused symptom threshold may not be useful for adults because ADHD symptoms decline substantially with age.² One study evaluating DSM-5 ADHD criteria in young adults (N = 4,000, age 18 to 19) found ADHD was better diagnosed when the required number of clinically relevant inattention and hyperactivity symptoms was reduced from 6 to 5 for each category.⁵ They also found the DSM-5 age-at-onset criterion of symptoms present before age 12 had a significant effect on ADHD prevalence, reducing the rate from 23.7% (95% CI, 22.38 to 25.02) to 5.4% (95% CI, 13.99 to 16.21).⁵ This suggests that strict usage of DSM-5 criteria may underestimate the prevalence of ADHD in adults, because ADHD symptoms may not be detected in childhood, or self-reporting of childhood ADHD symptoms in older adults may be unreliable due to aging processes that compromise memory and recall. These findings also indicate that fewer ADHD symptoms are needed to impair functioning in older age.

Determining the prevalence of ADHD among older adults is further complicated by individuals who report symptoms consistent with an ADHD diagnosis despite having never received this diagnosis during childhood.^6-8 This may be due to the considerable number of children who meet ADHD criteria but do not get a diagnosis due to limited access to health care.⁹ Thus, many studies separately analyze the syndromatic (with a childhood onset) and symptomatic (regardless of childhood onset) persistence of ADHD. One epidemiological meta-analysis found the 2020 prevalence of syndromatic ADHD in adults age >60 was 0.77% and the prevalence of symptomatic ADHD was 4.51%, which translates to 7.91 million and 46.36 million affected older adults, respectively.⁸ Other research has reported higher rates among older adults.^6,7,10 The variations among this research may be attributed to the use of different diagnostic tools/criteria, study populations, sampling methods, or DSM versions. Heterogeneity among this research also further supports the idea that the prevalence of ADHD is heavily dependent on how one defines and diagnoses the disorder.

Reasons for late-life ADHD diagnosis

There are many reasons a patient may not be diagnosed with ADHD until they are an older adult.¹¹ In addition to socioeconomic barriers to health care access, members of different ethnic groups exhibit differences in help-seeking behaviors; children may belong to a culture that does not traditionally seek health care even when symptoms are evident.^6,9 Therefore, individuals may not receive a diagnosis until adulthood. Some experts have discussed the similarity of ADHD to other neurodevelopmental disorders, such as autism spectrum disorder or social communication disorder, where ADHD symptoms may not manifest until stressors at critical points in life exceed an individual’s capacity to compensate.²

The life transition model contextualizes ADHD as being associated with demand/resource imbalances that come and go throughout life, resulting in variability in the degree of functional impairment ADHD symptoms cause in older adults.^2,12 Hypothetically, events in late life—such as the death of a spouse or retirement—can remove essential support structures in the lives of high-functioning individuals with ADHD. As a result, such events surpass these individuals’ ability to cope, resulting in a late-life manifestation of ADHD.

The plausibility of late-onset ADHD

In recent years, many studies identifying ADHD in adults have been published,^2,10,12-15 including some that discuss adult ADHD that spontaneously appears without childhood symptoms (ie, late-onset ADHD).^2,4,12 Research of late-onset ADHD attracts attention because the data it presents challenge the current rationale that ADHD symptoms should be present before age 12, as defined by DSM-5 criteria. While most reports of late-onset ADHD pertain to younger adults, little evidence exists to reinforce the concept; to date just 1 study has reported cases of late-onset ADHD in older adults (n = 7, age 51 to 59).¹¹ In this study, Sasaki et al¹¹ acknowledged the strong possibility their cases may be late manifestations of long-standing ADHD. Late-onset ADHD is further challenged by findings that 95% of individuals initially diagnosed with late-onset ADHD can be excluded from the diagnosis with further detailed assessment that accounts for co-occurring mental disorders and substance use.¹⁶ This suggests false positive cases of late-onset ADHD may be a symptom of narrow clinical assessment that fails to encompass other aspects of a patient’s psychiatric profile, rather than an atypical ADHD presentation.

Comorbidity and psychosocial functioning

ADHD symptoms and diagnosis in older adults are associated with clinically relevant levels of depression and anxiety. The Dutch Longitudinal Aging Study Amsterdam (LASA) examined 1,494 older adults (age 55 to 85) using the Diagnostic Interview for ADHD in Adults version 2.0.¹⁰ The 231 individuals identified as having symptoms of ADHD reported clinically relevant levels of depressive and anxiety symptoms. ADHD was significantly associated with these comorbid symptoms.

Continue to: Little is known regarding...

Little is known regarding the manifestation of symptoms of ADHD in older age and the difficulties these older adults face. Older adults with ADHD are more often divorced and report more loneliness than older adults without this disorder, which suggests loneliness in older age may be more pressing for the older ADHD population.¹⁷ ADHD in older adults has also been associated with poor quality-of-life measures, including moderate to severe problems in mobility, self-care, usual activity, pain/discomfort, and anxiety/depression (Table 1^14,17).

Qualitative research has described a domino effect of a lifetime of living with ADHD. In one American study, older adults with ADHD (N = 24, age 60 to 74) reported experiencing a tangible, accumulated impact from ADHD on their finances and long-term relationships with family, friends, and coworkers.¹³ Another study utilizing the Dutch LASA data examined how ADHD may impact patient’s lives among participants who were unaware of their diagnosis.¹⁸ One-half of patients reported low self-esteem, overstepping boundaries, and feeling different from others. When compared to younger adults with ADHD, older adults report significantly greater impairments in productivity and a worse life outlook.¹⁹

Differential diagnosis

When assessing whether an older adult has ADHD, it is important to consider other potential causes of their symptoms (Table 2^11,15,20-23). The differential diagnosis includes impaired vision and hearing as well as medical illness (vitamin B12 deficiency, hyperthyroidism, hypothyroidism, hyperparathyroidism, and infectious diseases such as herpes simplex virus or syphilis).^11,15,20-23 Neurological causes include brain tumors, traumatic brain injuries, postconcussive syndrome, stroke, and neurocognitive disorders.^11,15,20-23 Other potential causes include obstructive sleep apnea, mood disorders, substance use disorders, and medication adverse effects (especially with polypharmacy).^11,15,20-23 In this population, other causes are often responsible for “late-manifestation ADHD symptoms.”^1,15 Neurocognitive disorders and other psychiatric conditions are especially difficult to differentiate from ADHD.

In older adults, ADHD symptoms include frontal-executive impairments, inattentiveness, difficulty with organization or multitasking, forgetfulness, and challenges involving activities of daily living or socialization that can appear to be a mild or major neurocognitive disorder (Table 3^11,24,25). This includes major neuro­cognitive disorder due to Alzheimer’s disease, Lewy body disease, and vascular disease.^2,26 However, frontotemporal lobar degeneration is reported to have more symptom overlap with ADHD.^21,22,26,27 A way to differentiate between neurocognitive disorders and ADHD in older adults is to consider that patients with neurocognitive disorders often progress to visual hallucinations and more extreme personality changes than would be expected in ADHD.¹¹ Each disease also has its own identifiable characteristics. Extreme changes in memory are often Alzheimer’s disease, personality changes suggest fronto­temporal lobar degeneration, stepwise decline is classic for vascular disease, and parkinsonian features may indicate dementia with Lewy bodies.²¹ In addition, the onset of ADHD usually occurs in childhood and can be traced throughout the lifespan,² whereas neurocognitive diseases usually appear for the first time in later life.^2,28 There are nuances in the nature of forgetfulness that can distinguish ADHD from neurocognitive disorders. For instance, the forgetfulness in early-onset Alzheimer’s disease involves “the lack of episodic memories,” while in contrast ADHD is thought to be “forgetfulness due to inadvertence.”¹¹ Furthermore, patients with neurocognitive disorders are reported to have more severe symptoms and an inability to explain why, whereas those with ADHD have a steady level of symptoms and can provide a more comprehensive story.²⁴ Two recent studies have shown that weak performance on language tests is more indicative of a neuro­degenerative process than of ADHD.^29,30 Research has suggested that if an older adult shows a sudden, acute onset of ADHD-like symptoms, this is most likely reflective of cognitive decline or a mood disorder such as depression.^2,15,24

Several other psychiatric conditions share many symptoms with ADHD. Overlapping symptomology between ADHD and mood and anxiety disorders presents challenges.²⁷ Emotional dysregulation is a feature of adult ADHD, and this often causes a mood disorder to be diagnosed without considering other possible explanations.^{21,22,27,31-34} Features of mania can overlap with ADHD symptoms, including psychomotor agitation, talkativeness, and distractibility.²⁷ Several other disorders also include distractibility, such as depression, anxiety, and substance use disorders.³⁵ Depression and anxiety can be an outcome of untreated ADHD, or can co-occur with ADHD.^21-23,27 ADHD can also co-occur with bipolar disorder (BD), substance use disorders, and personality disorders (borderline and antisocial personality disorder) (Figure 1^21-23,27,35). One suggested method of establishing an appropriate diagnosis is to study the efficacy of the treatment retrospectively. For example, if a patient is presumed to have depression and they do not respond to several selective serotonin reuptake inhibitors, this may be undetected ADHD.²⁷ In addition, the argument about the chronicity of the symptoms should also be considered. ADHD symptoms are pervasive whereas BD symptoms are episodic.³⁵ Depression can be chronic; however, there are often discrete major depressive episodes. It is important to have a clear timeline of the patient’s symptoms. Ask about age of onset, because in theory, ADHD is supposed to start in childhood.²² It is sometimes difficult to ascertain this information because many older adults grew up during a time where ADHD was not a recognized diagnosis.²¹

Continue to: Diagnosis and workup

Diagnosis and workup

The key aspects of diagnosing ADHD are the interview based on DSM-5 criteria, exclusion of other diagnoses, and collateral information. Research has shown that clinical interviews and longitudinal family histories provide critical information that can differentiate ADHD from other psychiatric conditions.³⁵ DSM-5 criteria are adjusted for adults: 5 out of 9 criteria for inattention and/or hyperactivity-impulsivity must be fulfilled, as opposed to 6 out of 9 in children age <17.^21,31,36 However, no criteria are specific for older adults.³⁷ Since the differential diagnosis involves multiple entities, it is important to follow DSM-5 criteria for ADHD, which include eliminating other conditions that can explain these symptoms.¹⁵ Additionally, in DSM-5, the age-of-onset threshold for ADHD diagnosis was increased from 7 and younger to 12 and younger, addressing criticism that the previous cutoff was too restrictive.^24,31 The age of onset of childhood symptoms can be challenging to verify in older adults. Older patients can have unreliable memories and their childhood records are not always available.^2,20 In this population, childhood symptoms are mainly underreported but sometimes overreported.^10,38 However, to establish a diagnosis, the patient should have experienced some symptoms of the disorder within their first 50 years of life, including having impaired functionality in multiple settings.^15,26 The goal is to establish the chronicity of this condition to distinguish it from other psychiatric conditions.²² Overall, using DSM-5 criteria without any modifications may lead to underdiagnosis of ADHD in adults.²³ At this time, however, DSM-5 remains the main criteria used to make a diagnosis.

While tools to assist in screening and diagnosing ADHD have been validated in adults, none have been validated specifically for older adults.²² Structured diagnostic interviews to diagnose ADHD include³⁹:

• Adult ADHD Clinical Diagnostic Scale version 1.2
• ADHD Lifespan Functioning interview
• Conners’ Adult ADHD Diagnostic interview for DSM-IV
• Diagnostic Interview for ADHD in Adults version 2.0
• Structured Clinical Interview for DSM-5.

ADHD symptom measures that can be used for screening and to look at treatment response include³⁹:

• ADHD Rating Scale 5
• Adult ADHD Self-Report Scale Symptom Checklist
• Barkley Adult ADHD Rating Scale IV
• Barkley Quick-Check for Adult ADHD Diagnosis
• Young ADHD Questionnaire
• RATE Scales.

Adult ADHD inventories consider problems that adults with ADHD face. These include³⁹:

• Brown Attention Deficit Disorders Scales—Adult version
• Conners’ Adult ADHD Rating Scales
• Wender-Reimherr Adult Attention Deficit Disorder Scale.

Since these scales were not designed for older adults, they may miss nuances in this population.⁴⁰

Continue to: It can be particularly...

It can be particularly perplexing to diagnose ADHD in older adults because the other possible causes of the symptoms are vast. During the interview, it is important to ask questions that may rule out other psychiatric, neurologic, and medical conditions.²¹ Screen for other diagnoses, and include questions about a patient’s sleep history to rule out obstructive sleep apnea.²¹ To screen for other psychiatric conditions, the Mini International Neuropsychiatric Interview 5.0.0 may be used.²² Other tools include the Saint Louis University AMSAD screen for depression, the Geriatric Depression Scale, and the Beck Anxiety Inventory.^28,41 To screen for cognitive functioning, the Saint Louis University Mental Status Exam, Montreal Cognitive Assessment, or Mini-Mental State Examination can be used.^22,28,42,43 Once screening is performed, a physical and neurologic examination is the best next step.²⁶ Additionally, laboratory data and imaging can rule out other conditions; however, these are not routinely performed to diagnose ADHD.

Laboratory tests should include a comprehensive metabolic panel, complete blood count, thyroid-stimulating hormone level, B12/folate level, and possibly a vitamin D level.^11,36 These tests cover several conditions that may mimic ADHD. Brain MRI is not routinely recommended for diagnosing ADHD, though it may be useful because some research has found brain structural differences in individuals with ADHD.^28,44,45 Neurocognitive disorders have notable MRI findings that distinguish them from ADHD and each other.²⁴ If there is significant concern for neurocognitive disorders, more specific tests can be employed, such as CSF studies, to look for phosphorylated tau and beta amyloid markers.¹¹

Ask about family history (first-degree relative with ADHD) and obtain collateral information to make sure no other diagnoses are overlooked. Family history can help diagnose this disorder in older adults because there is evidence that ADHD runs in families.^2,25 This evidence would ideally come from someone who has known the patient their entire life, such as a sibling or parent.²⁴ The collateral information will be especially helpful to discern the chronicity of the patient’s symptoms, which would point toward a diagnosis of ADHD. To summarize (Figure 2):

• obtain a thorough interview that may be supported by a screening tool
• rule out other conditions
• conduct a physical examination
• obtain laboratory results
• collect collateral information
• obtain neuroimaging if necessary.

Treatment

ADHD symptoms can be treated with medications and psychotherapy. Research has shown the efficacy of ADHD medications in older adults, demonstrating that treatment leads to better functioning in multiple settings and decreases the risk for developing comorbid psychiatric conditions (mood disorder, substance use disorders).^25,27 Symptoms that improve with medication include attention, concentration, self-efficacy, functioning, self-esteem, psychomotor agitation, mood, energy, and procrastination.^21,31,46 If a patient with ADHD also has other psychiatric diagnoses, treat the most impairing disorder first.²² This often means mood disorders and substance use disorders must be remedied before ADHD is treated.²¹

Medication options include stimulants and nonstimulants. First-line treatments are stimulant medications, including methylphenidate, amphetamines, and mixed amphetamine salts.^{12,22,27,31,35} Stimulants have shown significant efficacy in older adults, although the American Geriatrics Society’s Beers Criteria list stimulants as potentially inappropriate for older adults.³³ Adults show significant improvement with methylphenidate.^21,23,47 In an observational study, Michielsen et al⁴⁶ found stimulants were safe and efficacious in older adults if patients are carefully monitored for adverse effects, especially cardiovascular changes. Second-line treatments include the nonstimulant atomoxetine.^12,22,27,31 Clonidine and guanfacine are FDA-approved for treating ADHD in children, but not approved for adults.²⁶ There is little evidence for other treatments, such as bupropion.^12,22,27 All of these medications have adverse effects, which are especially important to consider in older adults, who experience age-related physiological changes.

Continue to: Medications for ADHD symptoms...

Medications for ADHD symptoms are thought to act via catecholaminergic mechanisms.²¹ As a result, adverse effects of stimulants can include headache, appetite suppression, nausea, difficulty sleeping, tremor, blurred vision, agitation, psychosis, increased heart rate, arrhythmia, and hypertension.^22,27,32-34 Especially in older adults, adverse effects such as reduced appetite, disrupted sleep, or increased blood pressure or heart rate may be harmful.^21,23 Using caffeine or pseudoephedrine can exacerbate these adverse effects.²¹ Atomoxetine’s adverse effects include appetite suppression, insomnia, dizziness, anxiety, agitation, fatigue, dry mouth, constipation, nausea, vomiting, dyspepsia, and increased heart rate or blood pressure.^27,32,35 Genitourinary adverse effects have also been reported, including priapism (rare), decreased libido, and urinary hesitancy and retention.^26,32 Before any medication is initiated, it is important to conduct a physical and neurologic examination and a detailed clinical interview.

Before starting medication, as with any medical treatment, conduct a risk vs benefit analysis. Record baseline values for the patient’s heart rate, blood pressure, and weight.^23,26,27,31 During the interview, screen for family and personal cardiovascular conditions,^27,33 and obtain an electrocardiogram for any patient with cardiovascular risks.^23,26,27,31 Once the patient is deemed to be an appropriate candidate for pharmacologic treatment, begin with low doses and titrate the medication slowly until reaching a therapeutic level.^23,48

Medications should be combined with psychotherapy (eg, cognitive-behavioral therapy or dialectical behavioral therapy) and other lifestyle changes (exercise, mindfulness, support groups).^{18,22,23,27,31,49} Psychotherapy can help patients come to terms with receiving an ADHD diagnosis later in life and help with organization and socialization.^12,50 Pharmacologic treatments are thought to be helpful with attention challenges and emotional instability.⁵⁰ Taken together, medications and behavioral interventions can help individuals experience an improved quality of life.

Future directions

Given the relatively recent interest in ADHD in older adults, there are several areas that need further research. For future editions of DSM, it may be prudent to consider establishing ADHD criteria specific to older adults. Research has also shown the need for clear diagnostic and validated tools for older adults.⁸ Few analyses have been undertaken regarding pharmacotherapy for this population. Randomized controlled clinical trials are needed.^23,37,48 More research about the relative utility of psychotherapy and behavioral interventions would also be useful, given their potential to improve the quality of life for older adults with ADHD.

Bottom Line

Although generally thought of as a disorder of childhood, attention-deficit/ hyperactivity disorder (ADHD) has substantial effects in older adults. When the condition is appropriately diagnosed, pharmacologic treatment and psychotherapy are associated with improved quality of life for older patients with ADHD.

Related Resources

• Children and Adults with Attention-Deficit/Hyperactivity Disorder. Living with ADHD: A lifespan disorder. https://chadd.org/for-adults/living-with-adhd-a-lifespan-disorder/
• Attention Deficit Disorder Association. Support groups for adults. https://add.org/adhd-support-groups/

Drug Brand Names

Amphetamine/dextroamphetamine • Adderall
Atomoxetine • Straterra
Bupropion • Wellbutrin
Clonidine • Catapres
Guanfacine • Intuniv
Methylphenidate • Ritalin

For many years, attention-deficit/hyperactivity disorder (ADHD) was thought of as a disorder of childhood; however, it is now increasingly being recognized as a chronic, lifelong disorder that persists into adulthood in approximately two-thirds of patients.¹ While our knowledge about ADHD in adults has increased, most research in this population focused on young or middle-aged adults; less is known about ADHD in older adults. Older adults with ADHD may be newly diagnosed at any point in their lives, or not at all.² Because ADHD may present differently in older adults than in children or young adults, and because it may impair domains of life in different ways, a closer look at late-life ADHD is needed. This article summarizes the literature on the prevalence, impairment, diagnosis, and treatment of ADHD in adults age >60.

Challenges in determining the prevalence

Few studies have examined the age-specific prevalence of ADHD among older adults.³ Compared with childhood ADHD, adult ADHD is relatively neglected in epidemiological studies, largely due to the absence of well-established, validated diagnostic criteria.^1,4 Some experts have noted that DSM-5’s ADHD criteria were designed for diagnosing children, and the children-focused symptom threshold may not be useful for adults because ADHD symptoms decline substantially with age.² One study evaluating DSM-5 ADHD criteria in young adults (N = 4,000, age 18 to 19) found ADHD was better diagnosed when the required number of clinically relevant inattention and hyperactivity symptoms was reduced from 6 to 5 for each category.⁵ They also found the DSM-5 age-at-onset criterion of symptoms present before age 12 had a significant effect on ADHD prevalence, reducing the rate from 23.7% (95% CI, 22.38 to 25.02) to 5.4% (95% CI, 13.99 to 16.21).⁵ This suggests that strict usage of DSM-5 criteria may underestimate the prevalence of ADHD in adults, because ADHD symptoms may not be detected in childhood, or self-reporting of childhood ADHD symptoms in older adults may be unreliable due to aging processes that compromise memory and recall. These findings also indicate that fewer ADHD symptoms are needed to impair functioning in older age.

Determining the prevalence of ADHD among older adults is further complicated by individuals who report symptoms consistent with an ADHD diagnosis despite having never received this diagnosis during childhood.^6-8 This may be due to the considerable number of children who meet ADHD criteria but do not get a diagnosis due to limited access to health care.⁹ Thus, many studies separately analyze the syndromatic (with a childhood onset) and symptomatic (regardless of childhood onset) persistence of ADHD. One epidemiological meta-analysis found the 2020 prevalence of syndromatic ADHD in adults age >60 was 0.77% and the prevalence of symptomatic ADHD was 4.51%, which translates to 7.91 million and 46.36 million affected older adults, respectively.⁸ Other research has reported higher rates among older adults.^6,7,10 The variations among this research may be attributed to the use of different diagnostic tools/criteria, study populations, sampling methods, or DSM versions. Heterogeneity among this research also further supports the idea that the prevalence of ADHD is heavily dependent on how one defines and diagnoses the disorder.

Reasons for late-life ADHD diagnosis

There are many reasons a patient may not be diagnosed with ADHD until they are an older adult.¹¹ In addition to socioeconomic barriers to health care access, members of different ethnic groups exhibit differences in help-seeking behaviors; children may belong to a culture that does not traditionally seek health care even when symptoms are evident.^6,9 Therefore, individuals may not receive a diagnosis until adulthood. Some experts have discussed the similarity of ADHD to other neurodevelopmental disorders, such as autism spectrum disorder or social communication disorder, where ADHD symptoms may not manifest until stressors at critical points in life exceed an individual’s capacity to compensate.²

The life transition model contextualizes ADHD as being associated with demand/resource imbalances that come and go throughout life, resulting in variability in the degree of functional impairment ADHD symptoms cause in older adults.^2,12 Hypothetically, events in late life—such as the death of a spouse or retirement—can remove essential support structures in the lives of high-functioning individuals with ADHD. As a result, such events surpass these individuals’ ability to cope, resulting in a late-life manifestation of ADHD.

The plausibility of late-onset ADHD

In recent years, many studies identifying ADHD in adults have been published,^2,10,12-15 including some that discuss adult ADHD that spontaneously appears without childhood symptoms (ie, late-onset ADHD).^2,4,12 Research of late-onset ADHD attracts attention because the data it presents challenge the current rationale that ADHD symptoms should be present before age 12, as defined by DSM-5 criteria. While most reports of late-onset ADHD pertain to younger adults, little evidence exists to reinforce the concept; to date just 1 study has reported cases of late-onset ADHD in older adults (n = 7, age 51 to 59).¹¹ In this study, Sasaki et al¹¹ acknowledged the strong possibility their cases may be late manifestations of long-standing ADHD. Late-onset ADHD is further challenged by findings that 95% of individuals initially diagnosed with late-onset ADHD can be excluded from the diagnosis with further detailed assessment that accounts for co-occurring mental disorders and substance use.¹⁶ This suggests false positive cases of late-onset ADHD may be a symptom of narrow clinical assessment that fails to encompass other aspects of a patient’s psychiatric profile, rather than an atypical ADHD presentation.

Comorbidity and psychosocial functioning

ADHD symptoms and diagnosis in older adults are associated with clinically relevant levels of depression and anxiety. The Dutch Longitudinal Aging Study Amsterdam (LASA) examined 1,494 older adults (age 55 to 85) using the Diagnostic Interview for ADHD in Adults version 2.0.¹⁰ The 231 individuals identified as having symptoms of ADHD reported clinically relevant levels of depressive and anxiety symptoms. ADHD was significantly associated with these comorbid symptoms.

Continue to: Little is known regarding...

Little is known regarding the manifestation of symptoms of ADHD in older age and the difficulties these older adults face. Older adults with ADHD are more often divorced and report more loneliness than older adults without this disorder, which suggests loneliness in older age may be more pressing for the older ADHD population.¹⁷ ADHD in older adults has also been associated with poor quality-of-life measures, including moderate to severe problems in mobility, self-care, usual activity, pain/discomfort, and anxiety/depression (Table 1^14,17).

Qualitative research has described a domino effect of a lifetime of living with ADHD. In one American study, older adults with ADHD (N = 24, age 60 to 74) reported experiencing a tangible, accumulated impact from ADHD on their finances and long-term relationships with family, friends, and coworkers.¹³ Another study utilizing the Dutch LASA data examined how ADHD may impact patient’s lives among participants who were unaware of their diagnosis.¹⁸ One-half of patients reported low self-esteem, overstepping boundaries, and feeling different from others. When compared to younger adults with ADHD, older adults report significantly greater impairments in productivity and a worse life outlook.¹⁹

Differential diagnosis

When assessing whether an older adult has ADHD, it is important to consider other potential causes of their symptoms (Table 2^11,15,20-23). The differential diagnosis includes impaired vision and hearing as well as medical illness (vitamin B12 deficiency, hyperthyroidism, hypothyroidism, hyperparathyroidism, and infectious diseases such as herpes simplex virus or syphilis).^11,15,20-23 Neurological causes include brain tumors, traumatic brain injuries, postconcussive syndrome, stroke, and neurocognitive disorders.^11,15,20-23 Other potential causes include obstructive sleep apnea, mood disorders, substance use disorders, and medication adverse effects (especially with polypharmacy).^11,15,20-23 In this population, other causes are often responsible for “late-manifestation ADHD symptoms.”^1,15 Neurocognitive disorders and other psychiatric conditions are especially difficult to differentiate from ADHD.

In older adults, ADHD symptoms include frontal-executive impairments, inattentiveness, difficulty with organization or multitasking, forgetfulness, and challenges involving activities of daily living or socialization that can appear to be a mild or major neurocognitive disorder (Table 3^11,24,25). This includes major neuro­cognitive disorder due to Alzheimer’s disease, Lewy body disease, and vascular disease.^2,26 However, frontotemporal lobar degeneration is reported to have more symptom overlap with ADHD.^21,22,26,27 A way to differentiate between neurocognitive disorders and ADHD in older adults is to consider that patients with neurocognitive disorders often progress to visual hallucinations and more extreme personality changes than would be expected in ADHD.¹¹ Each disease also has its own identifiable characteristics. Extreme changes in memory are often Alzheimer’s disease, personality changes suggest fronto­temporal lobar degeneration, stepwise decline is classic for vascular disease, and parkinsonian features may indicate dementia with Lewy bodies.²¹ In addition, the onset of ADHD usually occurs in childhood and can be traced throughout the lifespan,² whereas neurocognitive diseases usually appear for the first time in later life.^2,28 There are nuances in the nature of forgetfulness that can distinguish ADHD from neurocognitive disorders. For instance, the forgetfulness in early-onset Alzheimer’s disease involves “the lack of episodic memories,” while in contrast ADHD is thought to be “forgetfulness due to inadvertence.”¹¹ Furthermore, patients with neurocognitive disorders are reported to have more severe symptoms and an inability to explain why, whereas those with ADHD have a steady level of symptoms and can provide a more comprehensive story.²⁴ Two recent studies have shown that weak performance on language tests is more indicative of a neuro­degenerative process than of ADHD.^29,30 Research has suggested that if an older adult shows a sudden, acute onset of ADHD-like symptoms, this is most likely reflective of cognitive decline or a mood disorder such as depression.^2,15,24

Several other psychiatric conditions share many symptoms with ADHD. Overlapping symptomology between ADHD and mood and anxiety disorders presents challenges.²⁷ Emotional dysregulation is a feature of adult ADHD, and this often causes a mood disorder to be diagnosed without considering other possible explanations.^{21,22,27,31-34} Features of mania can overlap with ADHD symptoms, including psychomotor agitation, talkativeness, and distractibility.²⁷ Several other disorders also include distractibility, such as depression, anxiety, and substance use disorders.³⁵ Depression and anxiety can be an outcome of untreated ADHD, or can co-occur with ADHD.^21-23,27 ADHD can also co-occur with bipolar disorder (BD), substance use disorders, and personality disorders (borderline and antisocial personality disorder) (Figure 1^21-23,27,35). One suggested method of establishing an appropriate diagnosis is to study the efficacy of the treatment retrospectively. For example, if a patient is presumed to have depression and they do not respond to several selective serotonin reuptake inhibitors, this may be undetected ADHD.²⁷ In addition, the argument about the chronicity of the symptoms should also be considered. ADHD symptoms are pervasive whereas BD symptoms are episodic.³⁵ Depression can be chronic; however, there are often discrete major depressive episodes. It is important to have a clear timeline of the patient’s symptoms. Ask about age of onset, because in theory, ADHD is supposed to start in childhood.²² It is sometimes difficult to ascertain this information because many older adults grew up during a time where ADHD was not a recognized diagnosis.²¹

Continue to: Diagnosis and workup

Diagnosis and workup

The key aspects of diagnosing ADHD are the interview based on DSM-5 criteria, exclusion of other diagnoses, and collateral information. Research has shown that clinical interviews and longitudinal family histories provide critical information that can differentiate ADHD from other psychiatric conditions.³⁵ DSM-5 criteria are adjusted for adults: 5 out of 9 criteria for inattention and/or hyperactivity-impulsivity must be fulfilled, as opposed to 6 out of 9 in children age <17.^21,31,36 However, no criteria are specific for older adults.³⁷ Since the differential diagnosis involves multiple entities, it is important to follow DSM-5 criteria for ADHD, which include eliminating other conditions that can explain these symptoms.¹⁵ Additionally, in DSM-5, the age-of-onset threshold for ADHD diagnosis was increased from 7 and younger to 12 and younger, addressing criticism that the previous cutoff was too restrictive.^24,31 The age of onset of childhood symptoms can be challenging to verify in older adults. Older patients can have unreliable memories and their childhood records are not always available.^2,20 In this population, childhood symptoms are mainly underreported but sometimes overreported.^10,38 However, to establish a diagnosis, the patient should have experienced some symptoms of the disorder within their first 50 years of life, including having impaired functionality in multiple settings.^15,26 The goal is to establish the chronicity of this condition to distinguish it from other psychiatric conditions.²² Overall, using DSM-5 criteria without any modifications may lead to underdiagnosis of ADHD in adults.²³ At this time, however, DSM-5 remains the main criteria used to make a diagnosis.

While tools to assist in screening and diagnosing ADHD have been validated in adults, none have been validated specifically for older adults.²² Structured diagnostic interviews to diagnose ADHD include³⁹:

• Adult ADHD Clinical Diagnostic Scale version 1.2
• ADHD Lifespan Functioning interview
• Conners’ Adult ADHD Diagnostic interview for DSM-IV
• Diagnostic Interview for ADHD in Adults version 2.0
• Structured Clinical Interview for DSM-5.

ADHD symptom measures that can be used for screening and to look at treatment response include³⁹:

• ADHD Rating Scale 5
• Adult ADHD Self-Report Scale Symptom Checklist
• Barkley Adult ADHD Rating Scale IV
• Barkley Quick-Check for Adult ADHD Diagnosis
• Young ADHD Questionnaire
• RATE Scales.

Adult ADHD inventories consider problems that adults with ADHD face. These include³⁹:

• Brown Attention Deficit Disorders Scales—Adult version
• Conners’ Adult ADHD Rating Scales
• Wender-Reimherr Adult Attention Deficit Disorder Scale.

Since these scales were not designed for older adults, they may miss nuances in this population.⁴⁰

Continue to: It can be particularly...

It can be particularly perplexing to diagnose ADHD in older adults because the other possible causes of the symptoms are vast. During the interview, it is important to ask questions that may rule out other psychiatric, neurologic, and medical conditions.²¹ Screen for other diagnoses, and include questions about a patient’s sleep history to rule out obstructive sleep apnea.²¹ To screen for other psychiatric conditions, the Mini International Neuropsychiatric Interview 5.0.0 may be used.²² Other tools include the Saint Louis University AMSAD screen for depression, the Geriatric Depression Scale, and the Beck Anxiety Inventory.^28,41 To screen for cognitive functioning, the Saint Louis University Mental Status Exam, Montreal Cognitive Assessment, or Mini-Mental State Examination can be used.^22,28,42,43 Once screening is performed, a physical and neurologic examination is the best next step.²⁶ Additionally, laboratory data and imaging can rule out other conditions; however, these are not routinely performed to diagnose ADHD.

Laboratory tests should include a comprehensive metabolic panel, complete blood count, thyroid-stimulating hormone level, B12/folate level, and possibly a vitamin D level.^11,36 These tests cover several conditions that may mimic ADHD. Brain MRI is not routinely recommended for diagnosing ADHD, though it may be useful because some research has found brain structural differences in individuals with ADHD.^28,44,45 Neurocognitive disorders have notable MRI findings that distinguish them from ADHD and each other.²⁴ If there is significant concern for neurocognitive disorders, more specific tests can be employed, such as CSF studies, to look for phosphorylated tau and beta amyloid markers.¹¹

Ask about family history (first-degree relative with ADHD) and obtain collateral information to make sure no other diagnoses are overlooked. Family history can help diagnose this disorder in older adults because there is evidence that ADHD runs in families.^2,25 This evidence would ideally come from someone who has known the patient their entire life, such as a sibling or parent.²⁴ The collateral information will be especially helpful to discern the chronicity of the patient’s symptoms, which would point toward a diagnosis of ADHD. To summarize (Figure 2):

• obtain a thorough interview that may be supported by a screening tool
• rule out other conditions
• conduct a physical examination
• obtain laboratory results
• collect collateral information
• obtain neuroimaging if necessary.

Treatment

ADHD symptoms can be treated with medications and psychotherapy. Research has shown the efficacy of ADHD medications in older adults, demonstrating that treatment leads to better functioning in multiple settings and decreases the risk for developing comorbid psychiatric conditions (mood disorder, substance use disorders).^25,27 Symptoms that improve with medication include attention, concentration, self-efficacy, functioning, self-esteem, psychomotor agitation, mood, energy, and procrastination.^21,31,46 If a patient with ADHD also has other psychiatric diagnoses, treat the most impairing disorder first.²² This often means mood disorders and substance use disorders must be remedied before ADHD is treated.²¹

Medication options include stimulants and nonstimulants. First-line treatments are stimulant medications, including methylphenidate, amphetamines, and mixed amphetamine salts.^{12,22,27,31,35} Stimulants have shown significant efficacy in older adults, although the American Geriatrics Society’s Beers Criteria list stimulants as potentially inappropriate for older adults.³³ Adults show significant improvement with methylphenidate.^21,23,47 In an observational study, Michielsen et al⁴⁶ found stimulants were safe and efficacious in older adults if patients are carefully monitored for adverse effects, especially cardiovascular changes. Second-line treatments include the nonstimulant atomoxetine.^12,22,27,31 Clonidine and guanfacine are FDA-approved for treating ADHD in children, but not approved for adults.²⁶ There is little evidence for other treatments, such as bupropion.^12,22,27 All of these medications have adverse effects, which are especially important to consider in older adults, who experience age-related physiological changes.

Continue to: Medications for ADHD symptoms...

Medications for ADHD symptoms are thought to act via catecholaminergic mechanisms.²¹ As a result, adverse effects of stimulants can include headache, appetite suppression, nausea, difficulty sleeping, tremor, blurred vision, agitation, psychosis, increased heart rate, arrhythmia, and hypertension.^22,27,32-34 Especially in older adults, adverse effects such as reduced appetite, disrupted sleep, or increased blood pressure or heart rate may be harmful.^21,23 Using caffeine or pseudoephedrine can exacerbate these adverse effects.²¹ Atomoxetine’s adverse effects include appetite suppression, insomnia, dizziness, anxiety, agitation, fatigue, dry mouth, constipation, nausea, vomiting, dyspepsia, and increased heart rate or blood pressure.^27,32,35 Genitourinary adverse effects have also been reported, including priapism (rare), decreased libido, and urinary hesitancy and retention.^26,32 Before any medication is initiated, it is important to conduct a physical and neurologic examination and a detailed clinical interview.

Before starting medication, as with any medical treatment, conduct a risk vs benefit analysis. Record baseline values for the patient’s heart rate, blood pressure, and weight.^23,26,27,31 During the interview, screen for family and personal cardiovascular conditions,^27,33 and obtain an electrocardiogram for any patient with cardiovascular risks.^23,26,27,31 Once the patient is deemed to be an appropriate candidate for pharmacologic treatment, begin with low doses and titrate the medication slowly until reaching a therapeutic level.^23,48

Medications should be combined with psychotherapy (eg, cognitive-behavioral therapy or dialectical behavioral therapy) and other lifestyle changes (exercise, mindfulness, support groups).^{18,22,23,27,31,49} Psychotherapy can help patients come to terms with receiving an ADHD diagnosis later in life and help with organization and socialization.^12,50 Pharmacologic treatments are thought to be helpful with attention challenges and emotional instability.⁵⁰ Taken together, medications and behavioral interventions can help individuals experience an improved quality of life.

Future directions

Given the relatively recent interest in ADHD in older adults, there are several areas that need further research. For future editions of DSM, it may be prudent to consider establishing ADHD criteria specific to older adults. Research has also shown the need for clear diagnostic and validated tools for older adults.⁸ Few analyses have been undertaken regarding pharmacotherapy for this population. Randomized controlled clinical trials are needed.^23,37,48 More research about the relative utility of psychotherapy and behavioral interventions would also be useful, given their potential to improve the quality of life for older adults with ADHD.

Bottom Line

Although generally thought of as a disorder of childhood, attention-deficit/ hyperactivity disorder (ADHD) has substantial effects in older adults. When the condition is appropriately diagnosed, pharmacologic treatment and psychotherapy are associated with improved quality of life for older patients with ADHD.

Related Resources

• Children and Adults with Attention-Deficit/Hyperactivity Disorder. Living with ADHD: A lifespan disorder. https://chadd.org/for-adults/living-with-adhd-a-lifespan-disorder/
• Attention Deficit Disorder Association. Support groups for adults. https://add.org/adhd-support-groups/

Drug Brand Names

Amphetamine/dextroamphetamine • Adderall
Atomoxetine • Straterra
Bupropion • Wellbutrin
Clonidine • Catapres
Guanfacine • Intuniv
Methylphenidate • Ritalin

“ Hope is engagement with the act of mapping our destinies.” ¹

—Valerie Braithwaite

Why should psychiatrists care about climate change and try to mitigate its effects? First, we are tasked by society with managing the psychological and neuropsychiatric sequelae from disasters, which include climate change. The American Psychiatric Association’s position statement on climate change includes it as a legitimate focus for our specialty.² Second, as physicians, we are morally obligated to do no harm. Since the health care sector contributes significantly to climate change (8.5% of national carbon emissions stem from health care) and causes demonstrable health impacts,³ managing these impacts and decarbonizing the health care industry is morally imperative.⁴ And third, psychiatric clinicians have transferrable skills that can address fears of climate change, challenge climate change denialism,⁵ motivate people to adopt more pro-environmental behaviors, and help communities not only endure the emotional impact of climate change but become more psychologically resilient.⁶

Most psychiatrists, however, did not receive formal training on climate change and the related field of disaster preparedness. For example, Harvard Medical School did not include a course on climate change in their medical student curriculum until 2023.⁷ In this article, we provide a basic framework of climate change and its impact on mental health, with particular focus on patients with serious mental illness (SMI). We offer concrete steps clinicians can take to prevent or mitigate harm from climate change for their patients, prepare for disasters at the level of individual patient encounters, and strengthen their clinics and communities. We also encourage clinicians to take active leadership roles in their professional organizations to be part of climate solutions, building on the trust patients continue to have in their physicians.⁸ Even if clinicians do not view climate change concerns under their conceived clinical care mandate, having a working knowledge about it is important because patients, paraprofessional staff, or medical trainees are likely to bring it up.⁹

Climate change and mental health

Climate change is harmful to human health, including mental health.¹⁰ It can impact mental health directly via its impact on brain function and neuropsychiatric sequelae, and indirectly via climate-related disasters leading to acute or chronic stress, losses, and displacement with psychiatric and psychological sequelae (Table 1^11-29).

Direct impact

The effects of air pollution, heat, infections, and starvation are examples of how climate change directly impacts mental health. Air pollution and brain health are a concern for psychiatry, given the well-described effects of air deterioration on the developing brain.¹¹ In animal models, airborne pollutants lead to widespread neuroinflam­mation and cell loss via a multitude of mechanisms.¹² This is consistent with worse cognitive and behavioral functions across a wide range of cognitive domains seen in children exposed to pollution compared to those who grew up in environments with healthy air.¹³ Even low-level exposure to air pollution increases the risk for later onset of depression, suicide, and anxiety.¹⁴ Hippocampal atrophy observed in patients with first-episode psychosis may also be partially attributable to air pollution.¹⁵ An association between heat and suicide (and to a lesser extent, aggression) has also been reported.¹⁶

Worse physical health (eg, strokes) due to excessive heat can further compound mental health via elevated rates of depression. Data from the United States and Mexico show that for each degree Celsius increase in ambient temperature, suicide rates may increase by approximately 1%.¹⁷ A meta-analysis by Frangione et al¹⁸ similarly concluded that each degree Celsius increase results in an overall risk ratio of 1.016 (95% CI, 1.012 to 1.019) for deaths by suicide and suicide attempts. Additionally, global warming is shifting the endemic areas for many infectious agents, particularly vector-borne diseases,¹⁹ to regions in which they had hitherto been unknown, increasing the risk for future outbreaks and even pandemics.²⁰ These infectious illnesses often carry neuropsychiatric morbidity, with seizures, encephalopathy with incomplete recovery, and psychiatric syndromes occurring in many cases. Crop failure can lead to starvation during pregnancy and childhood, which has wide-ranging consequences for brain development and later physical and psychological health in adults.^21,22 Mothers affected by starvation also experience negative impacts on childbearing and childrearing.²³

Indirect impact

Climate change’s indirect impact on mental health can stem from the stress of living through a disaster such as an extreme weather event; from losses, including the death of friends and family members; and from becoming temporarily displaced.²⁴ Some climate change–driven disasters can be viewed as slow-moving, such as drought and the rising of sea levels, where displacement becomes permanent. Managing mass migration from internally or externally displaced people who must abandon their communities because of climate change will have significant repercussions for all societies.²⁵ The term “climate refugee” is not (yet) included in the United Nations’ official definition of refugees; it defines refugees as individuals who have fled their countries because of war, violence, or persecution.²⁶ These and other bureaucratic issues can come up when clinicians are trying to help migrants with immigration-related paperwork.

Continue to: As the inevitability of climate change...

As the inevitability of climate change sinks in, its long-term ramifications have introduced a new lexicon of psychological suffering related to the crisis.²⁷ Common terms for such distress include ecoanxiety (fear of what is happening and will happen with climate change), ecogrief (sadness about the destruction of species and natural habitats), solastalgia²⁸ (the nostalgia an individual feels for emotionally treasured landscapes that have changed), and terrafuria or ecorage (the reaction to betrayal and inaction by governments and leaders).²⁹ Climate-related emotions can lead to pessimism about the future and a nihilistic outlook on an individual’s ability to effect change and have agency over their life’s outcomes.

The categories of direct and indirect impacts are not mutually exclusive. A child may be starving due to weather-related crop failure as the family is forced to move to another country, then have to contend with prejudice and bullying as an immigrant, and later become anxiously preoccupied with climate change and its ability to cause further distress.

Effect on individuals with serious mental illness

Patients with SMI are particularly vulnerable to the impact of climate change. They are less resilient to climate change–related events, such as heat waves or temporary displacement from flooding, both at the personal level due to illness factors (eg, negative symptoms or cognitive impairment) and at the community level due to social factors (eg, weaker social support or poverty).

Recognizing the increased vulnerability to heat waves and preparing for them is particularly important for patients with SMI because they are at an increased risk for heat-related illnesses.³⁰ For example, patients may not appreciate the danger from heat and live in conditions that put them at risk (ie, not having air conditioning in their home or living alone). Their illness alone impairs heat regulation³¹; patients with depression and anxiety also dissipate heat less effectively.^32,33 Additionally, many psychiatric medications, particularly antipsychotics, impair key mechanisms of heat dissipation.^34,35 Antipsychotics render organisms more poikilothermic (susceptible to environmental temperature, like cold-blooded animals) and can be anticholinergic, which impedes sweating. A recent analysis of heat-related deaths during a period of extreme and prolonged heat in British Columbia in 2021 affirmed these concerns, reporting that patients with schizophrenia had the highest odds of death during this heat-related event.³⁶

COVID-19 has shown that flexible models of care are needed to prevent disengagement from medical and psychiatric care³⁷ and assure continued treatment with essential medications such as clozapine³⁸ and long-acting injectable antipsychotics³⁹ during periods of social change, as with climate change. While telehealth was critical during the COVID-19 pandemic⁴⁰ and is here to stay, it alone may be insufficient given the digital divide (patients with SMI may be less likely to have access to or be proficient in the use of digital technologies). The pandemic has shown the importance of public health efforts, including benefits from targeted outreach, with regards to vaccinations for this patient group.^41,42Table 2 summarizes things clinicians should consider when preparing patients with SMI for the effects of climate change.

Continue to: The psychiatrist's role

There are many ways a psychiatrist can professionally get involved in addressing climate change. Table 3^43-53 outlines the 3 Ps of climate action (taking actions to mitigate the effects of climate change): personal, patient (and clinic), and political (advocacy).

Personal

Even if clinicians believe climate change is important for their clinical work, they may still feel overwhelmed and unsure what to do in the context of competing responsibilities. A necessary first step is overcoming paralysis from the enormity of the problem, including the need to shift away from an expanding consumption model to environmental sustainability in a short period of time.

A good starting point is to get educated on the facts of climate change and how to discuss it in an office setting as well as in your personal life. A basic principle of climate change communication is that constructive hope (progress achieved despite everything) coupled with constructive doubt (the reality of the threat) can mobilize people towards action, whereas false hope or fatalistic doubt impedes action.⁴³ The importance of optimal public health messaging cannot be overstated; well-meaning campaigns to change behavior can fail if they emphasize the wrong message. For example, in a study examining COVID-19 messaging in >80 countries, Dorison et al⁴⁴ found that negatively framed messages mostly increased anxiety but had no benefit with regard to shifting people toward desired behaviors. The best public health messages are brief, repeated, and delivered by a trusted person.⁴⁵ Good messages are targeted to a concrete concern and where action would pay off now and not in some distant future.

In addition, clinicians can learn how to confront climate disavowal and difficult emotions in themselves and even plan to shift to carbon neutrality, such as purchasing carbon offsets or green sources of energy and transportation. They may not be familiar with principles of disaster preparedness or crisis communication.⁴⁶ Acquiring those professional skills may suggest next steps for action. Being familiar with the challenges and resources for immigrants, including individuals displaced due to climate change, may be necessary.⁴⁷ Finally, to reduce the risk of burnout, it is important to practice self-care, including strategies to reduce feelings of being overwhelmed.

Patient

In clinical encounters, clinicians can be proactive in helping patients understand their climate-related anxieties around an uncertain future, including identifying barriers to climate action.⁴⁸Emphasizing that climate action has health benefits for them and their communities now (eg, less polluted air leading to fewer health problems related to pollution) may engage patients unsure about their role in the fight against climate change. This simple message overcomes the human preference for immediate and concrete benefits over investment in long-term gains. Some patients may respond to the suggestion that adopting a plant-based diet is beneficial for their own health as well as for planetary health, given the substantial contribution of animal farming to global warming.⁴⁹

Continue to: Clinics must prepare for disasters...

Clinics must prepare for disasters in their communities to prevent disruption of psychiatric care by having an action plan, including the provision of medications. Such action plans should be prioritized for the most likely scenarios in an individual’s setting (eg, heat waves, wildfires, hurricanes, or flooding).

It is important to educate clinic staff and include them in planning for emergencies, because an all-hands approach and buy-in from all team members is critical. Clinicians should review how patients would continue to receive services, particularly medications, in the event of a disaster. In some cases, providing a 90-day medication supply will suffice, while in others (eg, patients receiving long-acting antipsychotics or clozapine) more preparation is necessary. Some events are predictable and can be organized annually, such as clinicians becoming vaccine ambassadors and organizing vaccine campaigns every fall⁵⁰; winter-related disaster preparation every fall; and heat wave education every spring (leaflets for patients, staff, and family members; review of safety of medications during heat waves). Plan for, monitor, and coordinate medical care and services for climate refugees and other populations that may otherwise delay medical care and impede illness prevention. Finally, support climate refugees, including connecting them to services or providing trauma-informed care.

Political

Some clinicians may feel compelled to become politically active to advocate for changes within the health care system. Two initiatives related to decarbonizing the health care sector are My Green Doctor⁵¹ and Health Care Without Harm,⁵² which offer help in shifting your office, clinic, or hospital towards carbon neutrality.

Climate change unevenly affects people and will continue to exacerbate inequalities in society, including individuals with mental illness.⁵³ To work toward climate justice on behalf of their patients, clinicians could join (or form) climate committees of special interest groups in their professional organizations or setting. Joining like-minded groups working on climate change at the local or national level prevents an omission of a psychiatric voice and counteracts burnout. It is important to stay focused on the root causes of the problem during activism: doing something to reduce fossil fuel use is ultimately most important.⁵⁴ The concrete goal of reaching the Paris 1.5-degree Celsius climate goal is a critical benchmark against which any other action can be measured.⁵⁴

Planning for the future

Over the course of history, societies have always faced difficult periods in which they needed to rebuild after natural disasters or self-inflicted catastrophes such as terrorist attacks or wars. Since the advent of the nuclear age, people have lived under the existential threat of nuclear war. The Anthropocene is a proposed geological term that reflects the enormous and possibly disastrous impact human activity has had on our planet.⁵⁵ While not yet formally adopted, this term has heuristic value, directing attention and reflection to our role and its now undisputed consequences. In the future, historians will debate if the scale of our current climate crisis has been different. It is, however, not controversial that humanity will be faced with the effects of climate change for the foreseeable future.¹⁰ Already, even “normal” weather events are fueled by energy in overcharged and altered weather systems due to global warming, leading to weather events ranging from droughts to floods and storms that are more severe, more frequent, and have longer-lasting effects on communities.⁵⁶

Continue to: As physicians, we are tasked...

As physicians, we are tasked by society to create and maintain a health care system that addresses the needs of our patients and the communities in which they live. Increasingly, we are forced to contend with an addition to the traditional 5 phases of acute disaster management (prevention, mitigation, preparedness, response, and recovery) to manage prolonged or even parallel disasters, where a series of disasters occurs before the community has recovered and healed. We must grapple with a sense of an “extended period of insecurity and instability” (permacrisis) and must better prepare for and prevent the polycrisis (many simultaneous crises) or the metacrisis of our “age of turmoil”⁵⁷ in which we must limit global warming, mitigate its damage, and increase community resilience to adapt.

Leading by personal example and providing hope may be what some patients need, as the reality of climate change contributes to the general uneasiness about the future and doomsday scenarios to which many fall victim. At the level of professional societies, many are calling for leadership, including from mental health organizations, to bolster the “social climate,” to help us strengthen our emotional resilience and social bonds to better withstand climate change together.⁵⁸ It is becoming harder to justify standing on the sidelines,⁵⁹ and it may be better for both our world and a clinician’s own sanity to be engaged in professional and private hopeful action¹ to address climate change. Without ecological or planetary health, there can be no mental health.

Bottom Line

Clinicians can prepare their patients for climate-related disruptions and manage the impact climate change has on their mental health. Addressing climate change at clinical and political levels is consistent with the leadership roles and professional ethics clinicians face in daily practice.

Related Resources

• Lim C, MacLaurin S, Freudenreich O. Preparing patients with serious mental illness for extreme HEAT. Current Psychiatry. 2022;21(9):27-28. doi:10.12788/cp.0287
• My Green Doctor. https://mygreendoctor.org/
• The Climate Resilience for Frontline Clinics Toolkit from Americares. https://www.americares.org/what-we-do/community-health/climate-resilient-health-clinics
• Climate Psychiatry Alliance. https://www.climatepsychiatry.org/

Drug Brand Names

Clozapine • Clozaril

“ Hope is engagement with the act of mapping our destinies.” ¹

—Valerie Braithwaite

Why should psychiatrists care about climate change and try to mitigate its effects? First, we are tasked by society with managing the psychological and neuropsychiatric sequelae from disasters, which include climate change. The American Psychiatric Association’s position statement on climate change includes it as a legitimate focus for our specialty.² Second, as physicians, we are morally obligated to do no harm. Since the health care sector contributes significantly to climate change (8.5% of national carbon emissions stem from health care) and causes demonstrable health impacts,³ managing these impacts and decarbonizing the health care industry is morally imperative.⁴ And third, psychiatric clinicians have transferrable skills that can address fears of climate change, challenge climate change denialism,⁵ motivate people to adopt more pro-environmental behaviors, and help communities not only endure the emotional impact of climate change but become more psychologically resilient.⁶

Most psychiatrists, however, did not receive formal training on climate change and the related field of disaster preparedness. For example, Harvard Medical School did not include a course on climate change in their medical student curriculum until 2023.⁷ In this article, we provide a basic framework of climate change and its impact on mental health, with particular focus on patients with serious mental illness (SMI). We offer concrete steps clinicians can take to prevent or mitigate harm from climate change for their patients, prepare for disasters at the level of individual patient encounters, and strengthen their clinics and communities. We also encourage clinicians to take active leadership roles in their professional organizations to be part of climate solutions, building on the trust patients continue to have in their physicians.⁸ Even if clinicians do not view climate change concerns under their conceived clinical care mandate, having a working knowledge about it is important because patients, paraprofessional staff, or medical trainees are likely to bring it up.⁹

Climate change and mental health

Climate change is harmful to human health, including mental health.¹⁰ It can impact mental health directly via its impact on brain function and neuropsychiatric sequelae, and indirectly via climate-related disasters leading to acute or chronic stress, losses, and displacement with psychiatric and psychological sequelae (Table 1^11-29).

Direct impact

The effects of air pollution, heat, infections, and starvation are examples of how climate change directly impacts mental health. Air pollution and brain health are a concern for psychiatry, given the well-described effects of air deterioration on the developing brain.¹¹ In animal models, airborne pollutants lead to widespread neuroinflam­mation and cell loss via a multitude of mechanisms.¹² This is consistent with worse cognitive and behavioral functions across a wide range of cognitive domains seen in children exposed to pollution compared to those who grew up in environments with healthy air.¹³ Even low-level exposure to air pollution increases the risk for later onset of depression, suicide, and anxiety.¹⁴ Hippocampal atrophy observed in patients with first-episode psychosis may also be partially attributable to air pollution.¹⁵ An association between heat and suicide (and to a lesser extent, aggression) has also been reported.¹⁶

Worse physical health (eg, strokes) due to excessive heat can further compound mental health via elevated rates of depression. Data from the United States and Mexico show that for each degree Celsius increase in ambient temperature, suicide rates may increase by approximately 1%.¹⁷ A meta-analysis by Frangione et al¹⁸ similarly concluded that each degree Celsius increase results in an overall risk ratio of 1.016 (95% CI, 1.012 to 1.019) for deaths by suicide and suicide attempts. Additionally, global warming is shifting the endemic areas for many infectious agents, particularly vector-borne diseases,¹⁹ to regions in which they had hitherto been unknown, increasing the risk for future outbreaks and even pandemics.²⁰ These infectious illnesses often carry neuropsychiatric morbidity, with seizures, encephalopathy with incomplete recovery, and psychiatric syndromes occurring in many cases. Crop failure can lead to starvation during pregnancy and childhood, which has wide-ranging consequences for brain development and later physical and psychological health in adults.^21,22 Mothers affected by starvation also experience negative impacts on childbearing and childrearing.²³

Indirect impact

Climate change’s indirect impact on mental health can stem from the stress of living through a disaster such as an extreme weather event; from losses, including the death of friends and family members; and from becoming temporarily displaced.²⁴ Some climate change–driven disasters can be viewed as slow-moving, such as drought and the rising of sea levels, where displacement becomes permanent. Managing mass migration from internally or externally displaced people who must abandon their communities because of climate change will have significant repercussions for all societies.²⁵ The term “climate refugee” is not (yet) included in the United Nations’ official definition of refugees; it defines refugees as individuals who have fled their countries because of war, violence, or persecution.²⁶ These and other bureaucratic issues can come up when clinicians are trying to help migrants with immigration-related paperwork.

Continue to: As the inevitability of climate change...

As the inevitability of climate change sinks in, its long-term ramifications have introduced a new lexicon of psychological suffering related to the crisis.²⁷ Common terms for such distress include ecoanxiety (fear of what is happening and will happen with climate change), ecogrief (sadness about the destruction of species and natural habitats), solastalgia²⁸ (the nostalgia an individual feels for emotionally treasured landscapes that have changed), and terrafuria or ecorage (the reaction to betrayal and inaction by governments and leaders).²⁹ Climate-related emotions can lead to pessimism about the future and a nihilistic outlook on an individual’s ability to effect change and have agency over their life’s outcomes.

The categories of direct and indirect impacts are not mutually exclusive. A child may be starving due to weather-related crop failure as the family is forced to move to another country, then have to contend with prejudice and bullying as an immigrant, and later become anxiously preoccupied with climate change and its ability to cause further distress.

Effect on individuals with serious mental illness

Patients with SMI are particularly vulnerable to the impact of climate change. They are less resilient to climate change–related events, such as heat waves or temporary displacement from flooding, both at the personal level due to illness factors (eg, negative symptoms or cognitive impairment) and at the community level due to social factors (eg, weaker social support or poverty).

Recognizing the increased vulnerability to heat waves and preparing for them is particularly important for patients with SMI because they are at an increased risk for heat-related illnesses.³⁰ For example, patients may not appreciate the danger from heat and live in conditions that put them at risk (ie, not having air conditioning in their home or living alone). Their illness alone impairs heat regulation³¹; patients with depression and anxiety also dissipate heat less effectively.^32,33 Additionally, many psychiatric medications, particularly antipsychotics, impair key mechanisms of heat dissipation.^34,35 Antipsychotics render organisms more poikilothermic (susceptible to environmental temperature, like cold-blooded animals) and can be anticholinergic, which impedes sweating. A recent analysis of heat-related deaths during a period of extreme and prolonged heat in British Columbia in 2021 affirmed these concerns, reporting that patients with schizophrenia had the highest odds of death during this heat-related event.³⁶

COVID-19 has shown that flexible models of care are needed to prevent disengagement from medical and psychiatric care³⁷ and assure continued treatment with essential medications such as clozapine³⁸ and long-acting injectable antipsychotics³⁹ during periods of social change, as with climate change. While telehealth was critical during the COVID-19 pandemic⁴⁰ and is here to stay, it alone may be insufficient given the digital divide (patients with SMI may be less likely to have access to or be proficient in the use of digital technologies). The pandemic has shown the importance of public health efforts, including benefits from targeted outreach, with regards to vaccinations for this patient group.^41,42Table 2 summarizes things clinicians should consider when preparing patients with SMI for the effects of climate change.

Continue to: The psychiatrist's role

There are many ways a psychiatrist can professionally get involved in addressing climate change. Table 3^43-53 outlines the 3 Ps of climate action (taking actions to mitigate the effects of climate change): personal, patient (and clinic), and political (advocacy).

Personal

Even if clinicians believe climate change is important for their clinical work, they may still feel overwhelmed and unsure what to do in the context of competing responsibilities. A necessary first step is overcoming paralysis from the enormity of the problem, including the need to shift away from an expanding consumption model to environmental sustainability in a short period of time.

A good starting point is to get educated on the facts of climate change and how to discuss it in an office setting as well as in your personal life. A basic principle of climate change communication is that constructive hope (progress achieved despite everything) coupled with constructive doubt (the reality of the threat) can mobilize people towards action, whereas false hope or fatalistic doubt impedes action.⁴³ The importance of optimal public health messaging cannot be overstated; well-meaning campaigns to change behavior can fail if they emphasize the wrong message. For example, in a study examining COVID-19 messaging in >80 countries, Dorison et al⁴⁴ found that negatively framed messages mostly increased anxiety but had no benefit with regard to shifting people toward desired behaviors. The best public health messages are brief, repeated, and delivered by a trusted person.⁴⁵ Good messages are targeted to a concrete concern and where action would pay off now and not in some distant future.

In addition, clinicians can learn how to confront climate disavowal and difficult emotions in themselves and even plan to shift to carbon neutrality, such as purchasing carbon offsets or green sources of energy and transportation. They may not be familiar with principles of disaster preparedness or crisis communication.⁴⁶ Acquiring those professional skills may suggest next steps for action. Being familiar with the challenges and resources for immigrants, including individuals displaced due to climate change, may be necessary.⁴⁷ Finally, to reduce the risk of burnout, it is important to practice self-care, including strategies to reduce feelings of being overwhelmed.

Patient

In clinical encounters, clinicians can be proactive in helping patients understand their climate-related anxieties around an uncertain future, including identifying barriers to climate action.⁴⁸Emphasizing that climate action has health benefits for them and their communities now (eg, less polluted air leading to fewer health problems related to pollution) may engage patients unsure about their role in the fight against climate change. This simple message overcomes the human preference for immediate and concrete benefits over investment in long-term gains. Some patients may respond to the suggestion that adopting a plant-based diet is beneficial for their own health as well as for planetary health, given the substantial contribution of animal farming to global warming.⁴⁹

Continue to: Clinics must prepare for disasters...

Clinics must prepare for disasters in their communities to prevent disruption of psychiatric care by having an action plan, including the provision of medications. Such action plans should be prioritized for the most likely scenarios in an individual’s setting (eg, heat waves, wildfires, hurricanes, or flooding).

It is important to educate clinic staff and include them in planning for emergencies, because an all-hands approach and buy-in from all team members is critical. Clinicians should review how patients would continue to receive services, particularly medications, in the event of a disaster. In some cases, providing a 90-day medication supply will suffice, while in others (eg, patients receiving long-acting antipsychotics or clozapine) more preparation is necessary. Some events are predictable and can be organized annually, such as clinicians becoming vaccine ambassadors and organizing vaccine campaigns every fall⁵⁰; winter-related disaster preparation every fall; and heat wave education every spring (leaflets for patients, staff, and family members; review of safety of medications during heat waves). Plan for, monitor, and coordinate medical care and services for climate refugees and other populations that may otherwise delay medical care and impede illness prevention. Finally, support climate refugees, including connecting them to services or providing trauma-informed care.

Political

Some clinicians may feel compelled to become politically active to advocate for changes within the health care system. Two initiatives related to decarbonizing the health care sector are My Green Doctor⁵¹ and Health Care Without Harm,⁵² which offer help in shifting your office, clinic, or hospital towards carbon neutrality.

Climate change unevenly affects people and will continue to exacerbate inequalities in society, including individuals with mental illness.⁵³ To work toward climate justice on behalf of their patients, clinicians could join (or form) climate committees of special interest groups in their professional organizations or setting. Joining like-minded groups working on climate change at the local or national level prevents an omission of a psychiatric voice and counteracts burnout. It is important to stay focused on the root causes of the problem during activism: doing something to reduce fossil fuel use is ultimately most important.⁵⁴ The concrete goal of reaching the Paris 1.5-degree Celsius climate goal is a critical benchmark against which any other action can be measured.⁵⁴

Planning for the future

Over the course of history, societies have always faced difficult periods in which they needed to rebuild after natural disasters or self-inflicted catastrophes such as terrorist attacks or wars. Since the advent of the nuclear age, people have lived under the existential threat of nuclear war. The Anthropocene is a proposed geological term that reflects the enormous and possibly disastrous impact human activity has had on our planet.⁵⁵ While not yet formally adopted, this term has heuristic value, directing attention and reflection to our role and its now undisputed consequences. In the future, historians will debate if the scale of our current climate crisis has been different. It is, however, not controversial that humanity will be faced with the effects of climate change for the foreseeable future.¹⁰ Already, even “normal” weather events are fueled by energy in overcharged and altered weather systems due to global warming, leading to weather events ranging from droughts to floods and storms that are more severe, more frequent, and have longer-lasting effects on communities.⁵⁶

Continue to: As physicians, we are tasked...

As physicians, we are tasked by society to create and maintain a health care system that addresses the needs of our patients and the communities in which they live. Increasingly, we are forced to contend with an addition to the traditional 5 phases of acute disaster management (prevention, mitigation, preparedness, response, and recovery) to manage prolonged or even parallel disasters, where a series of disasters occurs before the community has recovered and healed. We must grapple with a sense of an “extended period of insecurity and instability” (permacrisis) and must better prepare for and prevent the polycrisis (many simultaneous crises) or the metacrisis of our “age of turmoil”⁵⁷ in which we must limit global warming, mitigate its damage, and increase community resilience to adapt.

Leading by personal example and providing hope may be what some patients need, as the reality of climate change contributes to the general uneasiness about the future and doomsday scenarios to which many fall victim. At the level of professional societies, many are calling for leadership, including from mental health organizations, to bolster the “social climate,” to help us strengthen our emotional resilience and social bonds to better withstand climate change together.⁵⁸ It is becoming harder to justify standing on the sidelines,⁵⁹ and it may be better for both our world and a clinician’s own sanity to be engaged in professional and private hopeful action¹ to address climate change. Without ecological or planetary health, there can be no mental health.

Bottom Line

Clinicians can prepare their patients for climate-related disruptions and manage the impact climate change has on their mental health. Addressing climate change at clinical and political levels is consistent with the leadership roles and professional ethics clinicians face in daily practice.

Related Resources

• Lim C, MacLaurin S, Freudenreich O. Preparing patients with serious mental illness for extreme HEAT. Current Psychiatry. 2022;21(9):27-28. doi:10.12788/cp.0287
• My Green Doctor. https://mygreendoctor.org/
• The Climate Resilience for Frontline Clinics Toolkit from Americares. https://www.americares.org/what-we-do/community-health/climate-resilient-health-clinics
• Climate Psychiatry Alliance. https://www.climatepsychiatry.org/

Drug Brand Names

Clozapine • Clozaril

“ Hope is engagement with the act of mapping our destinies.” ¹

—Valerie Braithwaite

Why should psychiatrists care about climate change and try to mitigate its effects? First, we are tasked by society with managing the psychological and neuropsychiatric sequelae from disasters, which include climate change. The American Psychiatric Association’s position statement on climate change includes it as a legitimate focus for our specialty.² Second, as physicians, we are morally obligated to do no harm. Since the health care sector contributes significantly to climate change (8.5% of national carbon emissions stem from health care) and causes demonstrable health impacts,³ managing these impacts and decarbonizing the health care industry is morally imperative.⁴ And third, psychiatric clinicians have transferrable skills that can address fears of climate change, challenge climate change denialism,⁵ motivate people to adopt more pro-environmental behaviors, and help communities not only endure the emotional impact of climate change but become more psychologically resilient.⁶

Most psychiatrists, however, did not receive formal training on climate change and the related field of disaster preparedness. For example, Harvard Medical School did not include a course on climate change in their medical student curriculum until 2023.⁷ In this article, we provide a basic framework of climate change and its impact on mental health, with particular focus on patients with serious mental illness (SMI). We offer concrete steps clinicians can take to prevent or mitigate harm from climate change for their patients, prepare for disasters at the level of individual patient encounters, and strengthen their clinics and communities. We also encourage clinicians to take active leadership roles in their professional organizations to be part of climate solutions, building on the trust patients continue to have in their physicians.⁸ Even if clinicians do not view climate change concerns under their conceived clinical care mandate, having a working knowledge about it is important because patients, paraprofessional staff, or medical trainees are likely to bring it up.⁹

Climate change and mental health

Climate change is harmful to human health, including mental health.¹⁰ It can impact mental health directly via its impact on brain function and neuropsychiatric sequelae, and indirectly via climate-related disasters leading to acute or chronic stress, losses, and displacement with psychiatric and psychological sequelae (Table 1^11-29).

Direct impact

The effects of air pollution, heat, infections, and starvation are examples of how climate change directly impacts mental health. Air pollution and brain health are a concern for psychiatry, given the well-described effects of air deterioration on the developing brain.¹¹ In animal models, airborne pollutants lead to widespread neuroinflam­mation and cell loss via a multitude of mechanisms.¹² This is consistent with worse cognitive and behavioral functions across a wide range of cognitive domains seen in children exposed to pollution compared to those who grew up in environments with healthy air.¹³ Even low-level exposure to air pollution increases the risk for later onset of depression, suicide, and anxiety.¹⁴ Hippocampal atrophy observed in patients with first-episode psychosis may also be partially attributable to air pollution.¹⁵ An association between heat and suicide (and to a lesser extent, aggression) has also been reported.¹⁶

Worse physical health (eg, strokes) due to excessive heat can further compound mental health via elevated rates of depression. Data from the United States and Mexico show that for each degree Celsius increase in ambient temperature, suicide rates may increase by approximately 1%.¹⁷ A meta-analysis by Frangione et al¹⁸ similarly concluded that each degree Celsius increase results in an overall risk ratio of 1.016 (95% CI, 1.012 to 1.019) for deaths by suicide and suicide attempts. Additionally, global warming is shifting the endemic areas for many infectious agents, particularly vector-borne diseases,¹⁹ to regions in which they had hitherto been unknown, increasing the risk for future outbreaks and even pandemics.²⁰ These infectious illnesses often carry neuropsychiatric morbidity, with seizures, encephalopathy with incomplete recovery, and psychiatric syndromes occurring in many cases. Crop failure can lead to starvation during pregnancy and childhood, which has wide-ranging consequences for brain development and later physical and psychological health in adults.^21,22 Mothers affected by starvation also experience negative impacts on childbearing and childrearing.²³

Indirect impact

Climate change’s indirect impact on mental health can stem from the stress of living through a disaster such as an extreme weather event; from losses, including the death of friends and family members; and from becoming temporarily displaced.²⁴ Some climate change–driven disasters can be viewed as slow-moving, such as drought and the rising of sea levels, where displacement becomes permanent. Managing mass migration from internally or externally displaced people who must abandon their communities because of climate change will have significant repercussions for all societies.²⁵ The term “climate refugee” is not (yet) included in the United Nations’ official definition of refugees; it defines refugees as individuals who have fled their countries because of war, violence, or persecution.²⁶ These and other bureaucratic issues can come up when clinicians are trying to help migrants with immigration-related paperwork.

Continue to: As the inevitability of climate change...

As the inevitability of climate change sinks in, its long-term ramifications have introduced a new lexicon of psychological suffering related to the crisis.²⁷ Common terms for such distress include ecoanxiety (fear of what is happening and will happen with climate change), ecogrief (sadness about the destruction of species and natural habitats), solastalgia²⁸ (the nostalgia an individual feels for emotionally treasured landscapes that have changed), and terrafuria or ecorage (the reaction to betrayal and inaction by governments and leaders).²⁹ Climate-related emotions can lead to pessimism about the future and a nihilistic outlook on an individual’s ability to effect change and have agency over their life’s outcomes.

The categories of direct and indirect impacts are not mutually exclusive. A child may be starving due to weather-related crop failure as the family is forced to move to another country, then have to contend with prejudice and bullying as an immigrant, and later become anxiously preoccupied with climate change and its ability to cause further distress.

Effect on individuals with serious mental illness

Patients with SMI are particularly vulnerable to the impact of climate change. They are less resilient to climate change–related events, such as heat waves or temporary displacement from flooding, both at the personal level due to illness factors (eg, negative symptoms or cognitive impairment) and at the community level due to social factors (eg, weaker social support or poverty).

Recognizing the increased vulnerability to heat waves and preparing for them is particularly important for patients with SMI because they are at an increased risk for heat-related illnesses.³⁰ For example, patients may not appreciate the danger from heat and live in conditions that put them at risk (ie, not having air conditioning in their home or living alone). Their illness alone impairs heat regulation³¹; patients with depression and anxiety also dissipate heat less effectively.^32,33 Additionally, many psychiatric medications, particularly antipsychotics, impair key mechanisms of heat dissipation.^34,35 Antipsychotics render organisms more poikilothermic (susceptible to environmental temperature, like cold-blooded animals) and can be anticholinergic, which impedes sweating. A recent analysis of heat-related deaths during a period of extreme and prolonged heat in British Columbia in 2021 affirmed these concerns, reporting that patients with schizophrenia had the highest odds of death during this heat-related event.³⁶

COVID-19 has shown that flexible models of care are needed to prevent disengagement from medical and psychiatric care³⁷ and assure continued treatment with essential medications such as clozapine³⁸ and long-acting injectable antipsychotics³⁹ during periods of social change, as with climate change. While telehealth was critical during the COVID-19 pandemic⁴⁰ and is here to stay, it alone may be insufficient given the digital divide (patients with SMI may be less likely to have access to or be proficient in the use of digital technologies). The pandemic has shown the importance of public health efforts, including benefits from targeted outreach, with regards to vaccinations for this patient group.^41,42Table 2 summarizes things clinicians should consider when preparing patients with SMI for the effects of climate change.

Continue to: The psychiatrist's role

There are many ways a psychiatrist can professionally get involved in addressing climate change. Table 3^43-53 outlines the 3 Ps of climate action (taking actions to mitigate the effects of climate change): personal, patient (and clinic), and political (advocacy).

Personal

Even if clinicians believe climate change is important for their clinical work, they may still feel overwhelmed and unsure what to do in the context of competing responsibilities. A necessary first step is overcoming paralysis from the enormity of the problem, including the need to shift away from an expanding consumption model to environmental sustainability in a short period of time.

A good starting point is to get educated on the facts of climate change and how to discuss it in an office setting as well as in your personal life. A basic principle of climate change communication is that constructive hope (progress achieved despite everything) coupled with constructive doubt (the reality of the threat) can mobilize people towards action, whereas false hope or fatalistic doubt impedes action.⁴³ The importance of optimal public health messaging cannot be overstated; well-meaning campaigns to change behavior can fail if they emphasize the wrong message. For example, in a study examining COVID-19 messaging in >80 countries, Dorison et al⁴⁴ found that negatively framed messages mostly increased anxiety but had no benefit with regard to shifting people toward desired behaviors. The best public health messages are brief, repeated, and delivered by a trusted person.⁴⁵ Good messages are targeted to a concrete concern and where action would pay off now and not in some distant future.

In addition, clinicians can learn how to confront climate disavowal and difficult emotions in themselves and even plan to shift to carbon neutrality, such as purchasing carbon offsets or green sources of energy and transportation. They may not be familiar with principles of disaster preparedness or crisis communication.⁴⁶ Acquiring those professional skills may suggest next steps for action. Being familiar with the challenges and resources for immigrants, including individuals displaced due to climate change, may be necessary.⁴⁷ Finally, to reduce the risk of burnout, it is important to practice self-care, including strategies to reduce feelings of being overwhelmed.

Patient

In clinical encounters, clinicians can be proactive in helping patients understand their climate-related anxieties around an uncertain future, including identifying barriers to climate action.⁴⁸Emphasizing that climate action has health benefits for them and their communities now (eg, less polluted air leading to fewer health problems related to pollution) may engage patients unsure about their role in the fight against climate change. This simple message overcomes the human preference for immediate and concrete benefits over investment in long-term gains. Some patients may respond to the suggestion that adopting a plant-based diet is beneficial for their own health as well as for planetary health, given the substantial contribution of animal farming to global warming.⁴⁹

Continue to: Clinics must prepare for disasters...

Clinics must prepare for disasters in their communities to prevent disruption of psychiatric care by having an action plan, including the provision of medications. Such action plans should be prioritized for the most likely scenarios in an individual’s setting (eg, heat waves, wildfires, hurricanes, or flooding).

It is important to educate clinic staff and include them in planning for emergencies, because an all-hands approach and buy-in from all team members is critical. Clinicians should review how patients would continue to receive services, particularly medications, in the event of a disaster. In some cases, providing a 90-day medication supply will suffice, while in others (eg, patients receiving long-acting antipsychotics or clozapine) more preparation is necessary. Some events are predictable and can be organized annually, such as clinicians becoming vaccine ambassadors and organizing vaccine campaigns every fall⁵⁰; winter-related disaster preparation every fall; and heat wave education every spring (leaflets for patients, staff, and family members; review of safety of medications during heat waves). Plan for, monitor, and coordinate medical care and services for climate refugees and other populations that may otherwise delay medical care and impede illness prevention. Finally, support climate refugees, including connecting them to services or providing trauma-informed care.

Political

Some clinicians may feel compelled to become politically active to advocate for changes within the health care system. Two initiatives related to decarbonizing the health care sector are My Green Doctor⁵¹ and Health Care Without Harm,⁵² which offer help in shifting your office, clinic, or hospital towards carbon neutrality.

Climate change unevenly affects people and will continue to exacerbate inequalities in society, including individuals with mental illness.⁵³ To work toward climate justice on behalf of their patients, clinicians could join (or form) climate committees of special interest groups in their professional organizations or setting. Joining like-minded groups working on climate change at the local or national level prevents an omission of a psychiatric voice and counteracts burnout. It is important to stay focused on the root causes of the problem during activism: doing something to reduce fossil fuel use is ultimately most important.⁵⁴ The concrete goal of reaching the Paris 1.5-degree Celsius climate goal is a critical benchmark against which any other action can be measured.⁵⁴

Planning for the future

Over the course of history, societies have always faced difficult periods in which they needed to rebuild after natural disasters or self-inflicted catastrophes such as terrorist attacks or wars. Since the advent of the nuclear age, people have lived under the existential threat of nuclear war. The Anthropocene is a proposed geological term that reflects the enormous and possibly disastrous impact human activity has had on our planet.⁵⁵ While not yet formally adopted, this term has heuristic value, directing attention and reflection to our role and its now undisputed consequences. In the future, historians will debate if the scale of our current climate crisis has been different. It is, however, not controversial that humanity will be faced with the effects of climate change for the foreseeable future.¹⁰ Already, even “normal” weather events are fueled by energy in overcharged and altered weather systems due to global warming, leading to weather events ranging from droughts to floods and storms that are more severe, more frequent, and have longer-lasting effects on communities.⁵⁶

Continue to: As physicians, we are tasked...

As physicians, we are tasked by society to create and maintain a health care system that addresses the needs of our patients and the communities in which they live. Increasingly, we are forced to contend with an addition to the traditional 5 phases of acute disaster management (prevention, mitigation, preparedness, response, and recovery) to manage prolonged or even parallel disasters, where a series of disasters occurs before the community has recovered and healed. We must grapple with a sense of an “extended period of insecurity and instability” (permacrisis) and must better prepare for and prevent the polycrisis (many simultaneous crises) or the metacrisis of our “age of turmoil”⁵⁷ in which we must limit global warming, mitigate its damage, and increase community resilience to adapt.

Leading by personal example and providing hope may be what some patients need, as the reality of climate change contributes to the general uneasiness about the future and doomsday scenarios to which many fall victim. At the level of professional societies, many are calling for leadership, including from mental health organizations, to bolster the “social climate,” to help us strengthen our emotional resilience and social bonds to better withstand climate change together.⁵⁸ It is becoming harder to justify standing on the sidelines,⁵⁹ and it may be better for both our world and a clinician’s own sanity to be engaged in professional and private hopeful action¹ to address climate change. Without ecological or planetary health, there can be no mental health.

Bottom Line

Clinicians can prepare their patients for climate-related disruptions and manage the impact climate change has on their mental health. Addressing climate change at clinical and political levels is consistent with the leadership roles and professional ethics clinicians face in daily practice.

Related Resources

• Lim C, MacLaurin S, Freudenreich O. Preparing patients with serious mental illness for extreme HEAT. Current Psychiatry. 2022;21(9):27-28. doi:10.12788/cp.0287
• My Green Doctor. https://mygreendoctor.org/
• The Climate Resilience for Frontline Clinics Toolkit from Americares. https://www.americares.org/what-we-do/community-health/climate-resilient-health-clinics
• Climate Psychiatry Alliance. https://www.climatepsychiatry.org/

Drug Brand Names

Clozapine • Clozaril

As psychiatrists know, many of our severely traumatized adult patients were victims of abuse during childhood. We routinely ask every new patient about physical, emotional, or sexual abuse when they were growing up because of the well-established, serious neurobiological and mental repercussions.^1,2

Perhaps one of the worst experiences for a child is to witness bitterly adversarial parents (their vital role models) who argue viciously, despise each other, and hurl insults (and even punches) at each other. Such a chronically and emotionally traumatic upbringing can haunt kids well into adulthood, disrupting their hypothalamic-pituitary-adrenal axis and triggering anxiety, depression, and even psychosis due to epigenetic changes that ultimately lead to abnormal brain development.³

It often feels that the governance of our country, or the national “political family,” is seriously fractured like a hopelessly dysfunctional family. Could that be negatively impacting the mental health of the citizenry? Having 2 antagonistic political parties expressing visceral hatred and undisguised contempt for each other 24/7 (thanks to the enabling era of cable TV, the internet, and social media) has transformed each party’s fanatic followers from fellow citizens to ideological combatants. In this poisonous societal zeitgeist of bidirectional acrimony and mutual detestation, the opposing parties and their “intellectual militias” label each other as “extremists” or “radicals.” They become completely blind to any redeeming social value in the ideas or principles of their political opponents. They spend enormous time and energy on undermining each other instead of attending to the myriad vital issues involved in the governance of a massive and complex country.

Winston Churchill said, “Democracy is the worst form of government, except for all the others that have been tried.”⁴ The current toxic cloud of intense “hyperpartisanship” is emblematic of the dark Machiavellian side of democracy. But those who lament the current distorted version of democracy should contemplate living in a dictatorship or totalitarian regime, where a despot would execute any dissenter or invade and destroy an adjacent country at a whim.

Churchill made that statement in 1947. The internet, social media, and smartphones were science fiction back then. Those technological advances have added fuel to the political process and significantly stoked the flames of hyperpartisanship. It’s now democracy on steroids, where freedom of expression goes to extremes, highlighting the warts and pitfalls of the democratic system. Political rivals can now communicate their ferocious disagreements to millions of their disciples instantaneously, triggering immediate rebuttals and counterattacks by their adversaries. This “virtual guerilla warfare” is mentally and emotionally exhausting to all involved, especially to the subset of neutral bystanders who are unaffiliated with either political party, which, due to the “religification” of politics, have become like secular religions.⁵ Chronic, unremitting, inescapable stress is a sure pathway for anxiety, depression, posttraumatic stress disorder, and even brain atrophy.

Optimists may point out that the United States has weathered and emerged stronger from many serious traumas, including the Civil War (with its lethal divisiveness), World War I, the deadly 1918 influenza pandemic, the Great Depression, Pearl Harbor, World War II, the Cold War, the Vietnam War, the Watergate political scandal, the 9/11 terrorist attacks, the banking collapse and recession, and most recently the COVID-19 pandemic, which brought society to a standstill and induced so much anxiety and uncertainty.

On the other hand, pessimists would insist those sequential crises left indelible scars that cumulatively altered the mindset of political rivals, predisposing them to extreme views of each other. Alienation inevitably leads to fanaticism. It’s perplexing but fascinating how the fierce bidirectional missives of weaponized ideas can be as virulent and destructive as a traditional physical war. Perhaps in this era, the pen is mightier than the sword after all.

Continue to: From a psychiatric perspective...

From a psychiatric perspective, the intransigent groupthink of political partisanship eerily resembles folie en masse, a psychiatric syndrome for which there is no established treatment. It has become a serious threat to our modern democracy. So I decided to ask the “know-it-all” artificial intelligence ChatGPT, whom I previously had “invited” to write a “guest editorial” about myths surrounding psychiatry,⁶ to answer 3 burning questions:

1. Is there toxic hyperpartisanship in the USA today? (Box 1)

Box 1

2. How can severe hyperpartisanship be corrected? (Supplemental Box 1)

Supplemental Box 1

3. What can cause the collapse of a democracy? (Supplemental Box 2).

Supplemental Box 2

Judge for yourself, but I believe the ChatGPT responses were spot-on.

As psychiatrists know, many of our severely traumatized adult patients were victims of abuse during childhood. We routinely ask every new patient about physical, emotional, or sexual abuse when they were growing up because of the well-established, serious neurobiological and mental repercussions.^1,2

Perhaps one of the worst experiences for a child is to witness bitterly adversarial parents (their vital role models) who argue viciously, despise each other, and hurl insults (and even punches) at each other. Such a chronically and emotionally traumatic upbringing can haunt kids well into adulthood, disrupting their hypothalamic-pituitary-adrenal axis and triggering anxiety, depression, and even psychosis due to epigenetic changes that ultimately lead to abnormal brain development.³

It often feels that the governance of our country, or the national “political family,” is seriously fractured like a hopelessly dysfunctional family. Could that be negatively impacting the mental health of the citizenry? Having 2 antagonistic political parties expressing visceral hatred and undisguised contempt for each other 24/7 (thanks to the enabling era of cable TV, the internet, and social media) has transformed each party’s fanatic followers from fellow citizens to ideological combatants. In this poisonous societal zeitgeist of bidirectional acrimony and mutual detestation, the opposing parties and their “intellectual militias” label each other as “extremists” or “radicals.” They become completely blind to any redeeming social value in the ideas or principles of their political opponents. They spend enormous time and energy on undermining each other instead of attending to the myriad vital issues involved in the governance of a massive and complex country.

Winston Churchill said, “Democracy is the worst form of government, except for all the others that have been tried.”⁴ The current toxic cloud of intense “hyperpartisanship” is emblematic of the dark Machiavellian side of democracy. But those who lament the current distorted version of democracy should contemplate living in a dictatorship or totalitarian regime, where a despot would execute any dissenter or invade and destroy an adjacent country at a whim.

Churchill made that statement in 1947. The internet, social media, and smartphones were science fiction back then. Those technological advances have added fuel to the political process and significantly stoked the flames of hyperpartisanship. It’s now democracy on steroids, where freedom of expression goes to extremes, highlighting the warts and pitfalls of the democratic system. Political rivals can now communicate their ferocious disagreements to millions of their disciples instantaneously, triggering immediate rebuttals and counterattacks by their adversaries. This “virtual guerilla warfare” is mentally and emotionally exhausting to all involved, especially to the subset of neutral bystanders who are unaffiliated with either political party, which, due to the “religification” of politics, have become like secular religions.⁵ Chronic, unremitting, inescapable stress is a sure pathway for anxiety, depression, posttraumatic stress disorder, and even brain atrophy.

Optimists may point out that the United States has weathered and emerged stronger from many serious traumas, including the Civil War (with its lethal divisiveness), World War I, the deadly 1918 influenza pandemic, the Great Depression, Pearl Harbor, World War II, the Cold War, the Vietnam War, the Watergate political scandal, the 9/11 terrorist attacks, the banking collapse and recession, and most recently the COVID-19 pandemic, which brought society to a standstill and induced so much anxiety and uncertainty.

On the other hand, pessimists would insist those sequential crises left indelible scars that cumulatively altered the mindset of political rivals, predisposing them to extreme views of each other. Alienation inevitably leads to fanaticism. It’s perplexing but fascinating how the fierce bidirectional missives of weaponized ideas can be as virulent and destructive as a traditional physical war. Perhaps in this era, the pen is mightier than the sword after all.

Continue to: From a psychiatric perspective...

From a psychiatric perspective, the intransigent groupthink of political partisanship eerily resembles folie en masse, a psychiatric syndrome for which there is no established treatment. It has become a serious threat to our modern democracy. So I decided to ask the “know-it-all” artificial intelligence ChatGPT, whom I previously had “invited” to write a “guest editorial” about myths surrounding psychiatry,⁶ to answer 3 burning questions:

1. Is there toxic hyperpartisanship in the USA today? (Box 1)

Box 1

2. How can severe hyperpartisanship be corrected? (Supplemental Box 1)

Supplemental Box 1

3. What can cause the collapse of a democracy? (Supplemental Box 2).

Supplemental Box 2

Judge for yourself, but I believe the ChatGPT responses were spot-on.

As psychiatrists know, many of our severely traumatized adult patients were victims of abuse during childhood. We routinely ask every new patient about physical, emotional, or sexual abuse when they were growing up because of the well-established, serious neurobiological and mental repercussions.^1,2

Perhaps one of the worst experiences for a child is to witness bitterly adversarial parents (their vital role models) who argue viciously, despise each other, and hurl insults (and even punches) at each other. Such a chronically and emotionally traumatic upbringing can haunt kids well into adulthood, disrupting their hypothalamic-pituitary-adrenal axis and triggering anxiety, depression, and even psychosis due to epigenetic changes that ultimately lead to abnormal brain development.³

It often feels that the governance of our country, or the national “political family,” is seriously fractured like a hopelessly dysfunctional family. Could that be negatively impacting the mental health of the citizenry? Having 2 antagonistic political parties expressing visceral hatred and undisguised contempt for each other 24/7 (thanks to the enabling era of cable TV, the internet, and social media) has transformed each party’s fanatic followers from fellow citizens to ideological combatants. In this poisonous societal zeitgeist of bidirectional acrimony and mutual detestation, the opposing parties and their “intellectual militias” label each other as “extremists” or “radicals.” They become completely blind to any redeeming social value in the ideas or principles of their political opponents. They spend enormous time and energy on undermining each other instead of attending to the myriad vital issues involved in the governance of a massive and complex country.

Winston Churchill said, “Democracy is the worst form of government, except for all the others that have been tried.”⁴ The current toxic cloud of intense “hyperpartisanship” is emblematic of the dark Machiavellian side of democracy. But those who lament the current distorted version of democracy should contemplate living in a dictatorship or totalitarian regime, where a despot would execute any dissenter or invade and destroy an adjacent country at a whim.

Churchill made that statement in 1947. The internet, social media, and smartphones were science fiction back then. Those technological advances have added fuel to the political process and significantly stoked the flames of hyperpartisanship. It’s now democracy on steroids, where freedom of expression goes to extremes, highlighting the warts and pitfalls of the democratic system. Political rivals can now communicate their ferocious disagreements to millions of their disciples instantaneously, triggering immediate rebuttals and counterattacks by their adversaries. This “virtual guerilla warfare” is mentally and emotionally exhausting to all involved, especially to the subset of neutral bystanders who are unaffiliated with either political party, which, due to the “religification” of politics, have become like secular religions.⁵ Chronic, unremitting, inescapable stress is a sure pathway for anxiety, depression, posttraumatic stress disorder, and even brain atrophy.

Optimists may point out that the United States has weathered and emerged stronger from many serious traumas, including the Civil War (with its lethal divisiveness), World War I, the deadly 1918 influenza pandemic, the Great Depression, Pearl Harbor, World War II, the Cold War, the Vietnam War, the Watergate political scandal, the 9/11 terrorist attacks, the banking collapse and recession, and most recently the COVID-19 pandemic, which brought society to a standstill and induced so much anxiety and uncertainty.

On the other hand, pessimists would insist those sequential crises left indelible scars that cumulatively altered the mindset of political rivals, predisposing them to extreme views of each other. Alienation inevitably leads to fanaticism. It’s perplexing but fascinating how the fierce bidirectional missives of weaponized ideas can be as virulent and destructive as a traditional physical war. Perhaps in this era, the pen is mightier than the sword after all.

Continue to: From a psychiatric perspective...

From a psychiatric perspective, the intransigent groupthink of political partisanship eerily resembles folie en masse, a psychiatric syndrome for which there is no established treatment. It has become a serious threat to our modern democracy. So I decided to ask the “know-it-all” artificial intelligence ChatGPT, whom I previously had “invited” to write a “guest editorial” about myths surrounding psychiatry,⁶ to answer 3 burning questions:

1. Is there toxic hyperpartisanship in the USA today? (Box 1)

Box 1

2. How can severe hyperpartisanship be corrected? (Supplemental Box 1)

Supplemental Box 1

3. What can cause the collapse of a democracy? (Supplemental Box 2).

Supplemental Box 2

Judge for yourself, but I believe the ChatGPT responses were spot-on.

Mr. S, age 77, is admitted to a long-term care facility due to progressive cognitive impairment and sexually inappropriate behavior. He has a history of sexual assault of medical staff. His medical history includes significant frontotemporal dementia (FTD) with behavioral disturbances, abnormal sexual behaviors, subclinical hypothyroidism, schizoid personality disorder, Parkinson disease, posttraumatic stress disorder, and hyperammonemia.

Upon admission, Mr. S’s vital signs are within normal limits except for an elevated thyroid-stimulating hormone (4.54 mIU/L; reference range 0.40 to 4.50 mIU/L). Prior cognitive testing results and updated ammonia levels are unavailable. Mr. S’s current medications include acetaminophen 650 mg every 4 hours as needed for pain, calcium carbonate/vitamin D twice daily for bone health, carbidopa/levodopa 25/100 mg twice daily for Parkinson disease, melatonin 3 mg/d at bedtime for insomnia, quetiapine 25 mg twice daily for psychosis with disturbance of behavior and 12.5 mg every 4 hours as needed for agitation, and trazodone 50 mg/d at bedtime for insomnia. Before Mr. S was admitted, previous therapy with selective serotonin reuptake inhibitors (SSRIs) had been tapered and discontinued. Mr. S had also started antipsychotic therapy at another facility due to worsening behaviors.

In patients with dementia, the brain is experiencing neurodegeneration. Progressively, neurons may stop functioning, lose connections with other neurons, and ultimately face cell death. The specific dementia diagnosis and its clinical features depend on the type of neurons and region of the brain affected.^1,2

FTD occurs in response to damage to the frontal and temporal lobes. The frontal lobe correlates to executive functioning, while the temporal lobe plays a role in speech and comprehension. Damage to these areas may result in loss of movement, trouble speaking, difficulty solving complex problems, and problems with social behavior. Specifically, damage to the orbital frontal cortex may cause disinhibition and abnormal behaviors, including emotional lability, vulgarity, and indifference to social nuances.¹ Within an FTD diagnosis, there are 3 disorders: behavioral-variant FTD (bvFTD), semantic dementia, and progressive nonfluent aphasia.¹ Specifically, bvFTD can result in abnormal sexual behaviors such as making sexually inappropriate statements, masturbating in public, undressing in public, inappropriately or aggressively touching others, or confusing another individual as an intimate partner. In addition to cognitive impairment, these neurobehavioral symptoms can significantly impact an individual’s quality of life while increasing caregiver burden.²

Occurring at a similar frequency to Alzheimer’s disease in patients age <65, FTD is one of the more common causes of early-onset dementia. The mean age of onset is 58 and onset after age 75 is particularly unusual. Memory may not be affected early in the course of the disease, but social changes are likely. As FTD progresses, symptoms will resemble those of Alzheimer’s disease and patients will require assistance with activities of daily living. In later stages of FTD, patients will exhibit language and behavior symptoms. Due to its unique progression, FTD can be commonly misdiagnosed as other mental illnesses or neurocognitive disorders.¹

Approaches to treatment: What to consider

Both nonpharmacologic and pharmacologic interventions are appropriate for addressing FTD. Because nonpharmacologic options improve patient safety and overall physical health, they should be used whenever practical. These interventions include safe driving measures, exercise, speech therapy, redirection, offering simple choices when making decisions, and managing environmental cues for behaviors that should be encouraged or discouraged.³

There are no FDA-approved medications to cure or slow the progression of FTD. Therefore, treatment is focused on alleviating neurobehavioral symptoms. The symptoms depend on the type of FTD the patient has; they include cognitive impairment, anxiety, insomnia or sleep disturbances, compulsive behaviors, speech and language problems, and agitation. While many medications have been commonly used for symptomatic relief, evidence for the efficacy of these treatments in FTD is limited.²

Continue to: A review of the literature...

A review of the literature on potential treatments for cognitive impairment and behavioral symptoms of FTD identified 2 trials and 1 case series (Table 1^4-6) in addition to a 2014 review article⁷ of current pharmacologic treatments. These trials evaluated cognitive improvement with rivastigmine, memantine, galantamine, and donepezil. None of the trials found a significant benefit from any of these medications for cognitive improvement in FTD. Data were conflicting on whether these medications improved or worsened behavioral symptoms. For example, the case series of 3 patients by Swanberg⁶ suggested improvement in behavior with memantine, while an open-label study analyzed in a 2014 review article⁷ found that donepezil may have worsened behaviors. Use of cholinesterase inhibitors or memantine in FTD is not recommended unless it is not certain if the patient has FTD or Alzheimer’s disease.⁷

Addressing sexual behaviors. Creating a treatment regimen for FTD behavioral symptoms—specifically for abnormal sexual behaviors—can be challenging. Before starting pharmacotherapy directed at behavioral symptoms secondary to FTD, other causes of symptoms such as delirium, pain, or discomfort should be excluded. Nonpharmacologic approaches should be aimed at the type of sexual behavior and likely underlying environmental cause. For example, patients may inappropriately disrobe themselves. To address this behavior, hospital staff or caregivers should first eliminate environmental causes by ensuring the room is at a comfortable temperature, dressing the patient in light, breathable clothing, or checking if the patient needs to use the bathroom. If no environmental causes are found, a one-piece jumpsuit with closures on the back of the garment could be utilized to increase the difficulty of undressing.

Other nonpharmacologic methods include providing private areas for patients who are behaving inappropriately or removing potentially stimulating television or media from the environment. Another option is to increase the use of positive, pleasant stimuli. One approach that has shown benefit is music therapy, utilizing popular music genres from the patient’s youth.³

Evidence for pharmacotherapy is limited and largely from case reports and case series. A 2020 meta-analysis by Trieu et al⁸ reviewed 23 studies to expand on current clinical guidance for patients with bvFTD. These studies showed improvements in behavioral symptoms and reductions in caregiver fatigue with citalopram, trazodone, paroxetine, and fluvoxamine. Six of the trials included in this meta-analysis that evaluated these 4 medications are summarized in Table 2.^9-14 

Due to the lower risk of adverse effects and favorable safety profiles, SSRIs and trazodone are considered first-line treatment options. Benefit from these medications is theorized to be a result of their serotonergic effects, because serotonin abnormalities and dysfunction have been linked to FTD symptoms. For example, in a patient experiencing hypersexuality, the common adverse effect of low libido associated with SSRIs can be particularly beneficial.⁸

Continue to: Other medication classes studied in patients...

Other medication classes studied in patients with FTD include antipsychotics, stimulants, anticonvulsants, benzo­diazepines, and hormonal therapies. In addition to a black box warning for increased mortality in older patients with dementia-related psychosis, antipsychotics are associated with other serious adverse effects and should be used with caution.⁷

FTD is a debilitating disease that has a major impact on quality of life, particularly when behavioral symptoms accompany cognitive decline. Though some therapies may possibly improve behavioral symptoms, their routine use remains controversial due to a lack of clear evidence of benefit. In caring for patients with FTD and behavioral symptoms, a multimodal, team-based approach is vital.¹

CASE CONTINUED

The treatment team starts Mr. S on several of the modalities discussed in this article over the span of 2 years, with limited efficacy. Nonpharmacologic methods do not provide much benefit because Mr. S is extremely difficult to redirect. Given Mr. S’s past trials of SSRIs prior to admission, sertraline was retrialed and titrated over 2 years. The highest dose utilized during his admission was 200 mg/d. The team starts estrogen therapy but tapers and discontinues it due to ineffectiveness. Mr. S’s use of carbidopa/levodopa is thought to be contributing to his behavioral abnormalities, so the team tapers it to discontinuation; however, Mr. S’s sexually inappropriate behaviors and agitation continue. The team initiates a plan to reduce the dose of quetiapine and switch to gabapentin, but Mr. S fails gradual dose reduction due to his worsening behaviors. He starts gabapentin. The team gradually increases the dose of gabapentin to decrease libido and agitation, respectively. The increase in sertraline dose and use of nonpharmacologic modalities causes Mr. S’s use of as-needed antipsychotics to decrease.

Related Resources

• Ellison JM. What are the stages of frontotemporal dementia? BrightFocus Foundation. July 5, 2021. Accessed July 7, 2023. https://www.brightfocus.org/alzheimers/article/what-are-stages-frontotemporal-dementia
• Dementia and sexually inappropriate behavior. ReaDementia. January 31, 2022. Accessed July 7, 2023. https://readementia.com/dementia-and-sexually-inappropriate-behavior/

Drug Brand Names

Carbidopa/levodopa • Sinemet
Citalopram • Celexa
Donepezil • Aricept
Fluvoxamine • Luvox
Gabapentin • Neurontin
Galantamine • Razadyne
Memantine • Namenda
Paroxetine • Paxil
Quetiapine • Seroquel
Rivastigmine • Exelon
Sertraline • Zoloft
Trazodone • Desyrel

Mr. S, age 77, is admitted to a long-term care facility due to progressive cognitive impairment and sexually inappropriate behavior. He has a history of sexual assault of medical staff. His medical history includes significant frontotemporal dementia (FTD) with behavioral disturbances, abnormal sexual behaviors, subclinical hypothyroidism, schizoid personality disorder, Parkinson disease, posttraumatic stress disorder, and hyperammonemia.

Upon admission, Mr. S’s vital signs are within normal limits except for an elevated thyroid-stimulating hormone (4.54 mIU/L; reference range 0.40 to 4.50 mIU/L). Prior cognitive testing results and updated ammonia levels are unavailable. Mr. S’s current medications include acetaminophen 650 mg every 4 hours as needed for pain, calcium carbonate/vitamin D twice daily for bone health, carbidopa/levodopa 25/100 mg twice daily for Parkinson disease, melatonin 3 mg/d at bedtime for insomnia, quetiapine 25 mg twice daily for psychosis with disturbance of behavior and 12.5 mg every 4 hours as needed for agitation, and trazodone 50 mg/d at bedtime for insomnia. Before Mr. S was admitted, previous therapy with selective serotonin reuptake inhibitors (SSRIs) had been tapered and discontinued. Mr. S had also started antipsychotic therapy at another facility due to worsening behaviors.

In patients with dementia, the brain is experiencing neurodegeneration. Progressively, neurons may stop functioning, lose connections with other neurons, and ultimately face cell death. The specific dementia diagnosis and its clinical features depend on the type of neurons and region of the brain affected.^1,2

FTD occurs in response to damage to the frontal and temporal lobes. The frontal lobe correlates to executive functioning, while the temporal lobe plays a role in speech and comprehension. Damage to these areas may result in loss of movement, trouble speaking, difficulty solving complex problems, and problems with social behavior. Specifically, damage to the orbital frontal cortex may cause disinhibition and abnormal behaviors, including emotional lability, vulgarity, and indifference to social nuances.¹ Within an FTD diagnosis, there are 3 disorders: behavioral-variant FTD (bvFTD), semantic dementia, and progressive nonfluent aphasia.¹ Specifically, bvFTD can result in abnormal sexual behaviors such as making sexually inappropriate statements, masturbating in public, undressing in public, inappropriately or aggressively touching others, or confusing another individual as an intimate partner. In addition to cognitive impairment, these neurobehavioral symptoms can significantly impact an individual’s quality of life while increasing caregiver burden.²

Occurring at a similar frequency to Alzheimer’s disease in patients age <65, FTD is one of the more common causes of early-onset dementia. The mean age of onset is 58 and onset after age 75 is particularly unusual. Memory may not be affected early in the course of the disease, but social changes are likely. As FTD progresses, symptoms will resemble those of Alzheimer’s disease and patients will require assistance with activities of daily living. In later stages of FTD, patients will exhibit language and behavior symptoms. Due to its unique progression, FTD can be commonly misdiagnosed as other mental illnesses or neurocognitive disorders.¹

Approaches to treatment: What to consider

Both nonpharmacologic and pharmacologic interventions are appropriate for addressing FTD. Because nonpharmacologic options improve patient safety and overall physical health, they should be used whenever practical. These interventions include safe driving measures, exercise, speech therapy, redirection, offering simple choices when making decisions, and managing environmental cues for behaviors that should be encouraged or discouraged.³

There are no FDA-approved medications to cure or slow the progression of FTD. Therefore, treatment is focused on alleviating neurobehavioral symptoms. The symptoms depend on the type of FTD the patient has; they include cognitive impairment, anxiety, insomnia or sleep disturbances, compulsive behaviors, speech and language problems, and agitation. While many medications have been commonly used for symptomatic relief, evidence for the efficacy of these treatments in FTD is limited.²

Continue to: A review of the literature...

A review of the literature on potential treatments for cognitive impairment and behavioral symptoms of FTD identified 2 trials and 1 case series (Table 1^4-6) in addition to a 2014 review article⁷ of current pharmacologic treatments. These trials evaluated cognitive improvement with rivastigmine, memantine, galantamine, and donepezil. None of the trials found a significant benefit from any of these medications for cognitive improvement in FTD. Data were conflicting on whether these medications improved or worsened behavioral symptoms. For example, the case series of 3 patients by Swanberg⁶ suggested improvement in behavior with memantine, while an open-label study analyzed in a 2014 review article⁷ found that donepezil may have worsened behaviors. Use of cholinesterase inhibitors or memantine in FTD is not recommended unless it is not certain if the patient has FTD or Alzheimer’s disease.⁷

Addressing sexual behaviors. Creating a treatment regimen for FTD behavioral symptoms—specifically for abnormal sexual behaviors—can be challenging. Before starting pharmacotherapy directed at behavioral symptoms secondary to FTD, other causes of symptoms such as delirium, pain, or discomfort should be excluded. Nonpharmacologic approaches should be aimed at the type of sexual behavior and likely underlying environmental cause. For example, patients may inappropriately disrobe themselves. To address this behavior, hospital staff or caregivers should first eliminate environmental causes by ensuring the room is at a comfortable temperature, dressing the patient in light, breathable clothing, or checking if the patient needs to use the bathroom. If no environmental causes are found, a one-piece jumpsuit with closures on the back of the garment could be utilized to increase the difficulty of undressing.

Other nonpharmacologic methods include providing private areas for patients who are behaving inappropriately or removing potentially stimulating television or media from the environment. Another option is to increase the use of positive, pleasant stimuli. One approach that has shown benefit is music therapy, utilizing popular music genres from the patient’s youth.³

Evidence for pharmacotherapy is limited and largely from case reports and case series. A 2020 meta-analysis by Trieu et al⁸ reviewed 23 studies to expand on current clinical guidance for patients with bvFTD. These studies showed improvements in behavioral symptoms and reductions in caregiver fatigue with citalopram, trazodone, paroxetine, and fluvoxamine. Six of the trials included in this meta-analysis that evaluated these 4 medications are summarized in Table 2.^9-14 

Due to the lower risk of adverse effects and favorable safety profiles, SSRIs and trazodone are considered first-line treatment options. Benefit from these medications is theorized to be a result of their serotonergic effects, because serotonin abnormalities and dysfunction have been linked to FTD symptoms. For example, in a patient experiencing hypersexuality, the common adverse effect of low libido associated with SSRIs can be particularly beneficial.⁸

Continue to: Other medication classes studied in patients...

Other medication classes studied in patients with FTD include antipsychotics, stimulants, anticonvulsants, benzo­diazepines, and hormonal therapies. In addition to a black box warning for increased mortality in older patients with dementia-related psychosis, antipsychotics are associated with other serious adverse effects and should be used with caution.⁷

FTD is a debilitating disease that has a major impact on quality of life, particularly when behavioral symptoms accompany cognitive decline. Though some therapies may possibly improve behavioral symptoms, their routine use remains controversial due to a lack of clear evidence of benefit. In caring for patients with FTD and behavioral symptoms, a multimodal, team-based approach is vital.¹

CASE CONTINUED

The treatment team starts Mr. S on several of the modalities discussed in this article over the span of 2 years, with limited efficacy. Nonpharmacologic methods do not provide much benefit because Mr. S is extremely difficult to redirect. Given Mr. S’s past trials of SSRIs prior to admission, sertraline was retrialed and titrated over 2 years. The highest dose utilized during his admission was 200 mg/d. The team starts estrogen therapy but tapers and discontinues it due to ineffectiveness. Mr. S’s use of carbidopa/levodopa is thought to be contributing to his behavioral abnormalities, so the team tapers it to discontinuation; however, Mr. S’s sexually inappropriate behaviors and agitation continue. The team initiates a plan to reduce the dose of quetiapine and switch to gabapentin, but Mr. S fails gradual dose reduction due to his worsening behaviors. He starts gabapentin. The team gradually increases the dose of gabapentin to decrease libido and agitation, respectively. The increase in sertraline dose and use of nonpharmacologic modalities causes Mr. S’s use of as-needed antipsychotics to decrease.

Related Resources

• Ellison JM. What are the stages of frontotemporal dementia? BrightFocus Foundation. July 5, 2021. Accessed July 7, 2023. https://www.brightfocus.org/alzheimers/article/what-are-stages-frontotemporal-dementia
• Dementia and sexually inappropriate behavior. ReaDementia. January 31, 2022. Accessed July 7, 2023. https://readementia.com/dementia-and-sexually-inappropriate-behavior/

Drug Brand Names

Carbidopa/levodopa • Sinemet
Citalopram • Celexa
Donepezil • Aricept
Fluvoxamine • Luvox
Gabapentin • Neurontin
Galantamine • Razadyne
Memantine • Namenda
Paroxetine • Paxil
Quetiapine • Seroquel
Rivastigmine • Exelon
Sertraline • Zoloft
Trazodone • Desyrel

Mr. S, age 77, is admitted to a long-term care facility due to progressive cognitive impairment and sexually inappropriate behavior. He has a history of sexual assault of medical staff. His medical history includes significant frontotemporal dementia (FTD) with behavioral disturbances, abnormal sexual behaviors, subclinical hypothyroidism, schizoid personality disorder, Parkinson disease, posttraumatic stress disorder, and hyperammonemia.

Upon admission, Mr. S’s vital signs are within normal limits except for an elevated thyroid-stimulating hormone (4.54 mIU/L; reference range 0.40 to 4.50 mIU/L). Prior cognitive testing results and updated ammonia levels are unavailable. Mr. S’s current medications include acetaminophen 650 mg every 4 hours as needed for pain, calcium carbonate/vitamin D twice daily for bone health, carbidopa/levodopa 25/100 mg twice daily for Parkinson disease, melatonin 3 mg/d at bedtime for insomnia, quetiapine 25 mg twice daily for psychosis with disturbance of behavior and 12.5 mg every 4 hours as needed for agitation, and trazodone 50 mg/d at bedtime for insomnia. Before Mr. S was admitted, previous therapy with selective serotonin reuptake inhibitors (SSRIs) had been tapered and discontinued. Mr. S had also started antipsychotic therapy at another facility due to worsening behaviors.

In patients with dementia, the brain is experiencing neurodegeneration. Progressively, neurons may stop functioning, lose connections with other neurons, and ultimately face cell death. The specific dementia diagnosis and its clinical features depend on the type of neurons and region of the brain affected.^1,2

FTD occurs in response to damage to the frontal and temporal lobes. The frontal lobe correlates to executive functioning, while the temporal lobe plays a role in speech and comprehension. Damage to these areas may result in loss of movement, trouble speaking, difficulty solving complex problems, and problems with social behavior. Specifically, damage to the orbital frontal cortex may cause disinhibition and abnormal behaviors, including emotional lability, vulgarity, and indifference to social nuances.¹ Within an FTD diagnosis, there are 3 disorders: behavioral-variant FTD (bvFTD), semantic dementia, and progressive nonfluent aphasia.¹ Specifically, bvFTD can result in abnormal sexual behaviors such as making sexually inappropriate statements, masturbating in public, undressing in public, inappropriately or aggressively touching others, or confusing another individual as an intimate partner. In addition to cognitive impairment, these neurobehavioral symptoms can significantly impact an individual’s quality of life while increasing caregiver burden.²

Occurring at a similar frequency to Alzheimer’s disease in patients age <65, FTD is one of the more common causes of early-onset dementia. The mean age of onset is 58 and onset after age 75 is particularly unusual. Memory may not be affected early in the course of the disease, but social changes are likely. As FTD progresses, symptoms will resemble those of Alzheimer’s disease and patients will require assistance with activities of daily living. In later stages of FTD, patients will exhibit language and behavior symptoms. Due to its unique progression, FTD can be commonly misdiagnosed as other mental illnesses or neurocognitive disorders.¹

Approaches to treatment: What to consider

Both nonpharmacologic and pharmacologic interventions are appropriate for addressing FTD. Because nonpharmacologic options improve patient safety and overall physical health, they should be used whenever practical. These interventions include safe driving measures, exercise, speech therapy, redirection, offering simple choices when making decisions, and managing environmental cues for behaviors that should be encouraged or discouraged.³

There are no FDA-approved medications to cure or slow the progression of FTD. Therefore, treatment is focused on alleviating neurobehavioral symptoms. The symptoms depend on the type of FTD the patient has; they include cognitive impairment, anxiety, insomnia or sleep disturbances, compulsive behaviors, speech and language problems, and agitation. While many medications have been commonly used for symptomatic relief, evidence for the efficacy of these treatments in FTD is limited.²

Continue to: A review of the literature...

A review of the literature on potential treatments for cognitive impairment and behavioral symptoms of FTD identified 2 trials and 1 case series (Table 1^4-6) in addition to a 2014 review article⁷ of current pharmacologic treatments. These trials evaluated cognitive improvement with rivastigmine, memantine, galantamine, and donepezil. None of the trials found a significant benefit from any of these medications for cognitive improvement in FTD. Data were conflicting on whether these medications improved or worsened behavioral symptoms. For example, the case series of 3 patients by Swanberg⁶ suggested improvement in behavior with memantine, while an open-label study analyzed in a 2014 review article⁷ found that donepezil may have worsened behaviors. Use of cholinesterase inhibitors or memantine in FTD is not recommended unless it is not certain if the patient has FTD or Alzheimer’s disease.⁷

Addressing sexual behaviors. Creating a treatment regimen for FTD behavioral symptoms—specifically for abnormal sexual behaviors—can be challenging. Before starting pharmacotherapy directed at behavioral symptoms secondary to FTD, other causes of symptoms such as delirium, pain, or discomfort should be excluded. Nonpharmacologic approaches should be aimed at the type of sexual behavior and likely underlying environmental cause. For example, patients may inappropriately disrobe themselves. To address this behavior, hospital staff or caregivers should first eliminate environmental causes by ensuring the room is at a comfortable temperature, dressing the patient in light, breathable clothing, or checking if the patient needs to use the bathroom. If no environmental causes are found, a one-piece jumpsuit with closures on the back of the garment could be utilized to increase the difficulty of undressing.

Other nonpharmacologic methods include providing private areas for patients who are behaving inappropriately or removing potentially stimulating television or media from the environment. Another option is to increase the use of positive, pleasant stimuli. One approach that has shown benefit is music therapy, utilizing popular music genres from the patient’s youth.³

Evidence for pharmacotherapy is limited and largely from case reports and case series. A 2020 meta-analysis by Trieu et al⁸ reviewed 23 studies to expand on current clinical guidance for patients with bvFTD. These studies showed improvements in behavioral symptoms and reductions in caregiver fatigue with citalopram, trazodone, paroxetine, and fluvoxamine. Six of the trials included in this meta-analysis that evaluated these 4 medications are summarized in Table 2.^9-14 

Due to the lower risk of adverse effects and favorable safety profiles, SSRIs and trazodone are considered first-line treatment options. Benefit from these medications is theorized to be a result of their serotonergic effects, because serotonin abnormalities and dysfunction have been linked to FTD symptoms. For example, in a patient experiencing hypersexuality, the common adverse effect of low libido associated with SSRIs can be particularly beneficial.⁸

Continue to: Other medication classes studied in patients...

Other medication classes studied in patients with FTD include antipsychotics, stimulants, anticonvulsants, benzo­diazepines, and hormonal therapies. In addition to a black box warning for increased mortality in older patients with dementia-related psychosis, antipsychotics are associated with other serious adverse effects and should be used with caution.⁷

FTD is a debilitating disease that has a major impact on quality of life, particularly when behavioral symptoms accompany cognitive decline. Though some therapies may possibly improve behavioral symptoms, their routine use remains controversial due to a lack of clear evidence of benefit. In caring for patients with FTD and behavioral symptoms, a multimodal, team-based approach is vital.¹

CASE CONTINUED

The treatment team starts Mr. S on several of the modalities discussed in this article over the span of 2 years, with limited efficacy. Nonpharmacologic methods do not provide much benefit because Mr. S is extremely difficult to redirect. Given Mr. S’s past trials of SSRIs prior to admission, sertraline was retrialed and titrated over 2 years. The highest dose utilized during his admission was 200 mg/d. The team starts estrogen therapy but tapers and discontinues it due to ineffectiveness. Mr. S’s use of carbidopa/levodopa is thought to be contributing to his behavioral abnormalities, so the team tapers it to discontinuation; however, Mr. S’s sexually inappropriate behaviors and agitation continue. The team initiates a plan to reduce the dose of quetiapine and switch to gabapentin, but Mr. S fails gradual dose reduction due to his worsening behaviors. He starts gabapentin. The team gradually increases the dose of gabapentin to decrease libido and agitation, respectively. The increase in sertraline dose and use of nonpharmacologic modalities causes Mr. S’s use of as-needed antipsychotics to decrease.

Related Resources

• Ellison JM. What are the stages of frontotemporal dementia? BrightFocus Foundation. July 5, 2021. Accessed July 7, 2023. https://www.brightfocus.org/alzheimers/article/what-are-stages-frontotemporal-dementia
• Dementia and sexually inappropriate behavior. ReaDementia. January 31, 2022. Accessed July 7, 2023. https://readementia.com/dementia-and-sexually-inappropriate-behavior/

Drug Brand Names

Carbidopa/levodopa • Sinemet
Citalopram • Celexa
Donepezil • Aricept
Fluvoxamine • Luvox
Gabapentin • Neurontin
Galantamine • Razadyne
Memantine • Namenda
Paroxetine • Paxil
Quetiapine • Seroquel
Rivastigmine • Exelon
Sertraline • Zoloft
Trazodone • Desyrel