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Familiarizing yourself with Alcoholics Anonymous dictums
From “90 minutes in 90 days,” to “people, places, and things,” to “cucumbers and pickles,” Alcoholics Anonymous (AA) slogans have been influencing the public’s understanding of the addictive process for almost a century. Regrettably, these terms have, inadvertently, alienated the scientific community. The translation and subsequent use of AA slogans has been a valuable tool in engaging science experts with mutual-help fellowships such as AA.
Recent advances in the neurobiology and neurochemistry of addiction have validated several of the memorable sayings of AA.1 As a result, physicians and scientists are now more willing to explore AA’s mottos.
Here are five well-known AA slogans that we have translated into medical terms and then briefly assessed in terms of their validity and relevance in today’s treatment of alcohol addiction:
1. “90 meetings in 90 days”
TRUE! Clinically, the first three months of sobriety constitute the most severe part of prolonged withdrawal syndrome and pose the most dangerous opportunities for a relapse.
2. “Keep it simple”
NOT TRUE! Clinical research and everyday practice of addiction treatment show that combination approaches—with medications, group psychotherapy, individual psychotherapy, involvement in mutual-help groups, family therapy, primary care, and treatment of psychiatric comorbidities—typically result in better outcomes than singular approaches.2
3. “Denial is not just a river in Egypt”
NOT TRUE! Since motivational inter-viewing was introduced in the treatment of addiction, we have learned how to effectively work with patients who are in complete denial and have absolutely no interest in changing anything about their life.3
4. “Beware of people, places, and things”
TRUE! Otherwise known as “cues” in psychology literature, triggers of relapse have been implicated in both the basic understanding of the addictive process and its treatment. “Classical conditioning” and “operant conditioning” models of behavior incorporate triggers. Additionally, cognitive behavior therapy helps extensively with maintaining sobriety. Even the DSM-5 gives a nod to “people, places, and things” by introducing “cravings” as a bona fide criterion of a substance use disorder.
5. “A cucumber that has become a pickle cannot become a cucumber again”
EQUIVOCAL. It is not clear, and highly debatable, whether an alcoholic who has been sober for more than 20 years still has a heightened vulnerability to reverting to alcoholism after consumption of alcohol. What is evident is that, even if the neuroadaptations responsible for hijacking the pleasure-reward pathways of the brain one day return to a normal, pre-addiction state, this healing process takes a long time—probably measured in decades, not years.
Click here for another Pearl on alternatives to 12-step groups.
Disclosure
The authors report no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Volkow ND, Baler RD. Addiction science: Uncovering neurobiological complexity. Neuropharmacology. 2013; (13)217-7.
2. Nunes EV, Selzer J, Levounis P, et al. Substance dependence and co-occurring psychiatric disorders: Best practices for diagnosis and clinical treatment. New York, NY: Civic Research Institute, 2010.
3. Levounis, P, Arnaout B. Handbook of motivation and change: A practical guide for clinicians. Arlington, VA: American Psychiatric Publishing, Inc.; 2010.
From “90 minutes in 90 days,” to “people, places, and things,” to “cucumbers and pickles,” Alcoholics Anonymous (AA) slogans have been influencing the public’s understanding of the addictive process for almost a century. Regrettably, these terms have, inadvertently, alienated the scientific community. The translation and subsequent use of AA slogans has been a valuable tool in engaging science experts with mutual-help fellowships such as AA.
Recent advances in the neurobiology and neurochemistry of addiction have validated several of the memorable sayings of AA.1 As a result, physicians and scientists are now more willing to explore AA’s mottos.
Here are five well-known AA slogans that we have translated into medical terms and then briefly assessed in terms of their validity and relevance in today’s treatment of alcohol addiction:
1. “90 meetings in 90 days”
TRUE! Clinically, the first three months of sobriety constitute the most severe part of prolonged withdrawal syndrome and pose the most dangerous opportunities for a relapse.
2. “Keep it simple”
NOT TRUE! Clinical research and everyday practice of addiction treatment show that combination approaches—with medications, group psychotherapy, individual psychotherapy, involvement in mutual-help groups, family therapy, primary care, and treatment of psychiatric comorbidities—typically result in better outcomes than singular approaches.2
3. “Denial is not just a river in Egypt”
NOT TRUE! Since motivational inter-viewing was introduced in the treatment of addiction, we have learned how to effectively work with patients who are in complete denial and have absolutely no interest in changing anything about their life.3
4. “Beware of people, places, and things”
TRUE! Otherwise known as “cues” in psychology literature, triggers of relapse have been implicated in both the basic understanding of the addictive process and its treatment. “Classical conditioning” and “operant conditioning” models of behavior incorporate triggers. Additionally, cognitive behavior therapy helps extensively with maintaining sobriety. Even the DSM-5 gives a nod to “people, places, and things” by introducing “cravings” as a bona fide criterion of a substance use disorder.
5. “A cucumber that has become a pickle cannot become a cucumber again”
EQUIVOCAL. It is not clear, and highly debatable, whether an alcoholic who has been sober for more than 20 years still has a heightened vulnerability to reverting to alcoholism after consumption of alcohol. What is evident is that, even if the neuroadaptations responsible for hijacking the pleasure-reward pathways of the brain one day return to a normal, pre-addiction state, this healing process takes a long time—probably measured in decades, not years.
Click here for another Pearl on alternatives to 12-step groups.
Disclosure
The authors report no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products.
From “90 minutes in 90 days,” to “people, places, and things,” to “cucumbers and pickles,” Alcoholics Anonymous (AA) slogans have been influencing the public’s understanding of the addictive process for almost a century. Regrettably, these terms have, inadvertently, alienated the scientific community. The translation and subsequent use of AA slogans has been a valuable tool in engaging science experts with mutual-help fellowships such as AA.
Recent advances in the neurobiology and neurochemistry of addiction have validated several of the memorable sayings of AA.1 As a result, physicians and scientists are now more willing to explore AA’s mottos.
Here are five well-known AA slogans that we have translated into medical terms and then briefly assessed in terms of their validity and relevance in today’s treatment of alcohol addiction:
1. “90 meetings in 90 days”
TRUE! Clinically, the first three months of sobriety constitute the most severe part of prolonged withdrawal syndrome and pose the most dangerous opportunities for a relapse.
2. “Keep it simple”
NOT TRUE! Clinical research and everyday practice of addiction treatment show that combination approaches—with medications, group psychotherapy, individual psychotherapy, involvement in mutual-help groups, family therapy, primary care, and treatment of psychiatric comorbidities—typically result in better outcomes than singular approaches.2
3. “Denial is not just a river in Egypt”
NOT TRUE! Since motivational inter-viewing was introduced in the treatment of addiction, we have learned how to effectively work with patients who are in complete denial and have absolutely no interest in changing anything about their life.3
4. “Beware of people, places, and things”
TRUE! Otherwise known as “cues” in psychology literature, triggers of relapse have been implicated in both the basic understanding of the addictive process and its treatment. “Classical conditioning” and “operant conditioning” models of behavior incorporate triggers. Additionally, cognitive behavior therapy helps extensively with maintaining sobriety. Even the DSM-5 gives a nod to “people, places, and things” by introducing “cravings” as a bona fide criterion of a substance use disorder.
5. “A cucumber that has become a pickle cannot become a cucumber again”
EQUIVOCAL. It is not clear, and highly debatable, whether an alcoholic who has been sober for more than 20 years still has a heightened vulnerability to reverting to alcoholism after consumption of alcohol. What is evident is that, even if the neuroadaptations responsible for hijacking the pleasure-reward pathways of the brain one day return to a normal, pre-addiction state, this healing process takes a long time—probably measured in decades, not years.
Click here for another Pearl on alternatives to 12-step groups.
Disclosure
The authors report no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Volkow ND, Baler RD. Addiction science: Uncovering neurobiological complexity. Neuropharmacology. 2013; (13)217-7.
2. Nunes EV, Selzer J, Levounis P, et al. Substance dependence and co-occurring psychiatric disorders: Best practices for diagnosis and clinical treatment. New York, NY: Civic Research Institute, 2010.
3. Levounis, P, Arnaout B. Handbook of motivation and change: A practical guide for clinicians. Arlington, VA: American Psychiatric Publishing, Inc.; 2010.
1. Volkow ND, Baler RD. Addiction science: Uncovering neurobiological complexity. Neuropharmacology. 2013; (13)217-7.
2. Nunes EV, Selzer J, Levounis P, et al. Substance dependence and co-occurring psychiatric disorders: Best practices for diagnosis and clinical treatment. New York, NY: Civic Research Institute, 2010.
3. Levounis, P, Arnaout B. Handbook of motivation and change: A practical guide for clinicians. Arlington, VA: American Psychiatric Publishing, Inc.; 2010.
Alternatives to 12-step groups
Persons addicted to drugs often are among the most marginalized psychiatric patients, but are in need of the most support.1 Many of these patients have comorbid medical and psychiatric problems, including difficult-to-treat pathologies that may have developed because of a traumatic experience or an attachment disorder that dominates their emotional lives.2 These patients value clinicians who engage them in an open, nonjudgmental, and empathetic way.
Eliciting a patient’s reasons for change and introducing him (her) to a variety of peer-led recovery group options that complement and support psychotherapy and pharmacotherapy can be valuable. Although most clinicians are aware of the traditional 12-step group model that embraces spirituality, many might know less about other groups that can play an instrumental role in engaging patients and placing them on the path to recovery.
SMART (Self-Management and Recovery Training) Recovery5 is a nonprofit organization that does not employ the 12-step model; instead, it uses evidence-based, non-confrontational, motivational, behavioral, and cognitive approaches to achieve abstinence.
Women for Sobriety6 helps women achieve abstinence.
LifeRing Secular Recovery7 works on empowering the “sober self” through groups that de-emphasize drug and alcohol use in personal histories.
Rational Recovery8 uses the Addictive Voice Recognition Technique to empower people overcoming addictions. This technique trains individuals to recognize the “addictive voice.” It does not support the theory of continuous recovery, or even recovery groups, but enables the user to achieve sobriety independently. This program greatly limits interaction between people overcoming addiction and physicians and counselors—save for periods of serious withdrawal.
The Community Reinforcement Approach (CRA)9 is an evidence-based program that focuses primarily on environmental and social factors influencing sobriety. This behavioral approach emphasizes the role of contingencies that can encourage or discourage sobriety. CRA has been studied in outpatients—predominantly homeless persons—and inpatients, and in a range of abused substances.
Click here for another Pearl on familiarizing yourself with Alcoholics Anonymous dictums.
Disclosure
The authors report no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Kreek MJ. Extreme marginalization: addiction and other mental health disorders, stigma, and imprisonment. Ann N Y Acad Sci. 2011;1231:65-72.
2. Wu NS, Schairer LC, Dellor E, et al. Childhood trauma and health outcomes in adults with comorbid substance abuse and mental health disorders. Addict Behav. 2010;35(1):68-71.
3. Moderation Management. http://www.moderation.org. Accessed April 12, 2013.
4. Moderation Management. What is moderation management? http://www.moderation.org/whatisMM.shtml. Accessed August 6, 2013.
5. SMART (Self Management and Recovery Training) Recovery. http://www.smartrecovery.org. Accessed April 12, 2013.
6. Women for Sobriety. http://www.womenforsobriety.org. Accessed April 12, 2013.
7. LifeRing. http://lifering.org. Accessed April 12, 2013.
8. Rational Recovery. http://www.rational.org. Published October 25, 1995. Accessed April 12, 2013.
9. Miller WR, Meyers RJ, Hiller-Sturmhofel S. The community-reinforcement approach. http://pubs.niaaa.nih.gov/publications/arh23-2/116-121.pdf. Accessed August 6, 2013.
Persons addicted to drugs often are among the most marginalized psychiatric patients, but are in need of the most support.1 Many of these patients have comorbid medical and psychiatric problems, including difficult-to-treat pathologies that may have developed because of a traumatic experience or an attachment disorder that dominates their emotional lives.2 These patients value clinicians who engage them in an open, nonjudgmental, and empathetic way.
Eliciting a patient’s reasons for change and introducing him (her) to a variety of peer-led recovery group options that complement and support psychotherapy and pharmacotherapy can be valuable. Although most clinicians are aware of the traditional 12-step group model that embraces spirituality, many might know less about other groups that can play an instrumental role in engaging patients and placing them on the path to recovery.
SMART (Self-Management and Recovery Training) Recovery5 is a nonprofit organization that does not employ the 12-step model; instead, it uses evidence-based, non-confrontational, motivational, behavioral, and cognitive approaches to achieve abstinence.
Women for Sobriety6 helps women achieve abstinence.
LifeRing Secular Recovery7 works on empowering the “sober self” through groups that de-emphasize drug and alcohol use in personal histories.
Rational Recovery8 uses the Addictive Voice Recognition Technique to empower people overcoming addictions. This technique trains individuals to recognize the “addictive voice.” It does not support the theory of continuous recovery, or even recovery groups, but enables the user to achieve sobriety independently. This program greatly limits interaction between people overcoming addiction and physicians and counselors—save for periods of serious withdrawal.
The Community Reinforcement Approach (CRA)9 is an evidence-based program that focuses primarily on environmental and social factors influencing sobriety. This behavioral approach emphasizes the role of contingencies that can encourage or discourage sobriety. CRA has been studied in outpatients—predominantly homeless persons—and inpatients, and in a range of abused substances.
Click here for another Pearl on familiarizing yourself with Alcoholics Anonymous dictums.
Disclosure
The authors report no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products.
Persons addicted to drugs often are among the most marginalized psychiatric patients, but are in need of the most support.1 Many of these patients have comorbid medical and psychiatric problems, including difficult-to-treat pathologies that may have developed because of a traumatic experience or an attachment disorder that dominates their emotional lives.2 These patients value clinicians who engage them in an open, nonjudgmental, and empathetic way.
Eliciting a patient’s reasons for change and introducing him (her) to a variety of peer-led recovery group options that complement and support psychotherapy and pharmacotherapy can be valuable. Although most clinicians are aware of the traditional 12-step group model that embraces spirituality, many might know less about other groups that can play an instrumental role in engaging patients and placing them on the path to recovery.
SMART (Self-Management and Recovery Training) Recovery5 is a nonprofit organization that does not employ the 12-step model; instead, it uses evidence-based, non-confrontational, motivational, behavioral, and cognitive approaches to achieve abstinence.
Women for Sobriety6 helps women achieve abstinence.
LifeRing Secular Recovery7 works on empowering the “sober self” through groups that de-emphasize drug and alcohol use in personal histories.
Rational Recovery8 uses the Addictive Voice Recognition Technique to empower people overcoming addictions. This technique trains individuals to recognize the “addictive voice.” It does not support the theory of continuous recovery, or even recovery groups, but enables the user to achieve sobriety independently. This program greatly limits interaction between people overcoming addiction and physicians and counselors—save for periods of serious withdrawal.
The Community Reinforcement Approach (CRA)9 is an evidence-based program that focuses primarily on environmental and social factors influencing sobriety. This behavioral approach emphasizes the role of contingencies that can encourage or discourage sobriety. CRA has been studied in outpatients—predominantly homeless persons—and inpatients, and in a range of abused substances.
Click here for another Pearl on familiarizing yourself with Alcoholics Anonymous dictums.
Disclosure
The authors report no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Kreek MJ. Extreme marginalization: addiction and other mental health disorders, stigma, and imprisonment. Ann N Y Acad Sci. 2011;1231:65-72.
2. Wu NS, Schairer LC, Dellor E, et al. Childhood trauma and health outcomes in adults with comorbid substance abuse and mental health disorders. Addict Behav. 2010;35(1):68-71.
3. Moderation Management. http://www.moderation.org. Accessed April 12, 2013.
4. Moderation Management. What is moderation management? http://www.moderation.org/whatisMM.shtml. Accessed August 6, 2013.
5. SMART (Self Management and Recovery Training) Recovery. http://www.smartrecovery.org. Accessed April 12, 2013.
6. Women for Sobriety. http://www.womenforsobriety.org. Accessed April 12, 2013.
7. LifeRing. http://lifering.org. Accessed April 12, 2013.
8. Rational Recovery. http://www.rational.org. Published October 25, 1995. Accessed April 12, 2013.
9. Miller WR, Meyers RJ, Hiller-Sturmhofel S. The community-reinforcement approach. http://pubs.niaaa.nih.gov/publications/arh23-2/116-121.pdf. Accessed August 6, 2013.
1. Kreek MJ. Extreme marginalization: addiction and other mental health disorders, stigma, and imprisonment. Ann N Y Acad Sci. 2011;1231:65-72.
2. Wu NS, Schairer LC, Dellor E, et al. Childhood trauma and health outcomes in adults with comorbid substance abuse and mental health disorders. Addict Behav. 2010;35(1):68-71.
3. Moderation Management. http://www.moderation.org. Accessed April 12, 2013.
4. Moderation Management. What is moderation management? http://www.moderation.org/whatisMM.shtml. Accessed August 6, 2013.
5. SMART (Self Management and Recovery Training) Recovery. http://www.smartrecovery.org. Accessed April 12, 2013.
6. Women for Sobriety. http://www.womenforsobriety.org. Accessed April 12, 2013.
7. LifeRing. http://lifering.org. Accessed April 12, 2013.
8. Rational Recovery. http://www.rational.org. Published October 25, 1995. Accessed April 12, 2013.
9. Miller WR, Meyers RJ, Hiller-Sturmhofel S. The community-reinforcement approach. http://pubs.niaaa.nih.gov/publications/arh23-2/116-121.pdf. Accessed August 6, 2013.
Do glucocorticoids hold promise as a treatment for PTSD?
As symptoms of posttraumatic stress disorder (PTSD) progress, the involved person’s physical and mental health deteriorates.1 This sparks lifestyle changes that allow them to avoid re-exposure to triggering stimuli; however, it also increases their risk of social isolation. Early clinical investigation has found that patients who experience hyperarousal symptoms of overt PTSD—difficulty sleeping, emotional dyscontrol, hypervigilance, and an enhanced startle response—could benefit from the stress-reducing capacity of glucocorticoids.
Decreased glucocorticoids
After a distressing situation, norepinephrine levels rise acutely.2,3 This contributes to a protective retention of potentially threatening memories, which is how people learn to avoid danger.
Glucocorticoid secretion enhances a patient’s coping mechanisms by helping them process information in a way that diminishes retrieval of fear-evoking memories.2,3 Glucocorticoid, also called cortisol, is referred to as a “stress hormone.” Cortisol promotes emotional adaptability following a traumatic event; this action diminishes future, inappropriate retrieval of frightening memories as a physiologic mechanism to help people cope with upsetting situations.3
PTSD pathogenesis involves altered hypothalamic-pituitary-adrenal axis function; sustained stress results in decreased levels of circulating glucocorticoid. This is a consequence of enhanced negative feedback and increased glucocorticoid receptor sensitivity, which is evidenced by results of abnormal dexamethasone suppression tests.1 Downregulation of corticotropin-releasing hormone (CRH) receptors in the pituitary glands and increased CRH levels have been documented in PTSD patients.1,4 An association between high CRH levels and an increase in startle response explains the exaggerated startle response observed in patients with PTSD. Higher circulating glucocorticoid has the opposite effect4; there is an inverse relationship between the daily level of glucocorticoid and startle amplitude. A low level of circulating glucocorticoid promotes recall of frightening events that results in persistent re-experiencing of traumatic memories.2,3
Glucocorticoids in PTSD
Glucocorticoid administration reduces psychological and physiological responses to stress.3 Exogenous glucocorticoid administration affects cognition by interacting with serotonin, dopamine, and ã-aminobutyric acid by actions on the amygdala, medial prefrontal cortex, and hippocampus.2,3 Research among veterans with and without PTSD recorded a decrease in startle response after administration of a single dose of 20 mg of hydrocortisone.4 Results of a large study documented that one dose of hydrocortisone administered at >35 mg can inhibit threatening memories and improve social function.3 Hydrocortisone is linked to anxiolytic effects in healthy persons and patients with social phobia or panic disorder.3,4 Because treatment of PTSD with antidepressants and benzodiazepines often is ineffective,5 glucocorticoids may offer a new pharmacotherapy option. Glucocorticoids have been prescribed as prophylactic agents shortly after an acutely stressful event to prevent development of PTSD.4 Hydrocortisone is not FDA-approved to treat PTSD; informed consent, physician discretion, and close monitoring are emphasized.
Glucocorticoid use in mitigating PTSD symptom emergence is under investigation. Research suggests that just one acute dose of hydrocortisone might benefit patients prone to PTSD.3,4 Further study is needed to establish whether prescribing hydrocortisone is efficacious.
Disclosure
The authors report no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Jones T, Moller MD. Implications of hypothalamic-pituitary-adrenal axis functioning in posttraumatic stress disorder. J Am Psychiatr Nurses Assoc. 2011;17(6):393-403.
2. Blundell J, Blaiss CA, Lagace DC, et al. Block of glucocorticoid synthesis during re-activation inhibits extinction of an established fear memory. Neurobiol Learn Mem. 2011;95(4):453-460.
3. Putman P, Roelofs K. Effects of single cortisol administrations on human affect reviewed: coping with stress through adaptive regulation of automatic cognitive processing. Psychoneuroendocrinology. 2011;36(4):439-448.
4. Miller MW, McKinney AE, Kanter FS, et al. Hydrocortisone suppression of the fear-potentiated startle response and posttraumatic stress disorder. Psychoneuroendocrinology. 2011;36(7):970-980.
5. Nin MS, Martinez LA, Pibiri F, et al. Neurosteroids reduce social isolation-induced behavioral deficits: a proposed link with neurosteroid-mediated upregulation of BDNF expression. Front Endocrinol (Lausanne). 2011;2(73):1-12.
As symptoms of posttraumatic stress disorder (PTSD) progress, the involved person’s physical and mental health deteriorates.1 This sparks lifestyle changes that allow them to avoid re-exposure to triggering stimuli; however, it also increases their risk of social isolation. Early clinical investigation has found that patients who experience hyperarousal symptoms of overt PTSD—difficulty sleeping, emotional dyscontrol, hypervigilance, and an enhanced startle response—could benefit from the stress-reducing capacity of glucocorticoids.
Decreased glucocorticoids
After a distressing situation, norepinephrine levels rise acutely.2,3 This contributes to a protective retention of potentially threatening memories, which is how people learn to avoid danger.
Glucocorticoid secretion enhances a patient’s coping mechanisms by helping them process information in a way that diminishes retrieval of fear-evoking memories.2,3 Glucocorticoid, also called cortisol, is referred to as a “stress hormone.” Cortisol promotes emotional adaptability following a traumatic event; this action diminishes future, inappropriate retrieval of frightening memories as a physiologic mechanism to help people cope with upsetting situations.3
PTSD pathogenesis involves altered hypothalamic-pituitary-adrenal axis function; sustained stress results in decreased levels of circulating glucocorticoid. This is a consequence of enhanced negative feedback and increased glucocorticoid receptor sensitivity, which is evidenced by results of abnormal dexamethasone suppression tests.1 Downregulation of corticotropin-releasing hormone (CRH) receptors in the pituitary glands and increased CRH levels have been documented in PTSD patients.1,4 An association between high CRH levels and an increase in startle response explains the exaggerated startle response observed in patients with PTSD. Higher circulating glucocorticoid has the opposite effect4; there is an inverse relationship between the daily level of glucocorticoid and startle amplitude. A low level of circulating glucocorticoid promotes recall of frightening events that results in persistent re-experiencing of traumatic memories.2,3
Glucocorticoids in PTSD
Glucocorticoid administration reduces psychological and physiological responses to stress.3 Exogenous glucocorticoid administration affects cognition by interacting with serotonin, dopamine, and ã-aminobutyric acid by actions on the amygdala, medial prefrontal cortex, and hippocampus.2,3 Research among veterans with and without PTSD recorded a decrease in startle response after administration of a single dose of 20 mg of hydrocortisone.4 Results of a large study documented that one dose of hydrocortisone administered at >35 mg can inhibit threatening memories and improve social function.3 Hydrocortisone is linked to anxiolytic effects in healthy persons and patients with social phobia or panic disorder.3,4 Because treatment of PTSD with antidepressants and benzodiazepines often is ineffective,5 glucocorticoids may offer a new pharmacotherapy option. Glucocorticoids have been prescribed as prophylactic agents shortly after an acutely stressful event to prevent development of PTSD.4 Hydrocortisone is not FDA-approved to treat PTSD; informed consent, physician discretion, and close monitoring are emphasized.
Glucocorticoid use in mitigating PTSD symptom emergence is under investigation. Research suggests that just one acute dose of hydrocortisone might benefit patients prone to PTSD.3,4 Further study is needed to establish whether prescribing hydrocortisone is efficacious.
Disclosure
The authors report no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products.
As symptoms of posttraumatic stress disorder (PTSD) progress, the involved person’s physical and mental health deteriorates.1 This sparks lifestyle changes that allow them to avoid re-exposure to triggering stimuli; however, it also increases their risk of social isolation. Early clinical investigation has found that patients who experience hyperarousal symptoms of overt PTSD—difficulty sleeping, emotional dyscontrol, hypervigilance, and an enhanced startle response—could benefit from the stress-reducing capacity of glucocorticoids.
Decreased glucocorticoids
After a distressing situation, norepinephrine levels rise acutely.2,3 This contributes to a protective retention of potentially threatening memories, which is how people learn to avoid danger.
Glucocorticoid secretion enhances a patient’s coping mechanisms by helping them process information in a way that diminishes retrieval of fear-evoking memories.2,3 Glucocorticoid, also called cortisol, is referred to as a “stress hormone.” Cortisol promotes emotional adaptability following a traumatic event; this action diminishes future, inappropriate retrieval of frightening memories as a physiologic mechanism to help people cope with upsetting situations.3
PTSD pathogenesis involves altered hypothalamic-pituitary-adrenal axis function; sustained stress results in decreased levels of circulating glucocorticoid. This is a consequence of enhanced negative feedback and increased glucocorticoid receptor sensitivity, which is evidenced by results of abnormal dexamethasone suppression tests.1 Downregulation of corticotropin-releasing hormone (CRH) receptors in the pituitary glands and increased CRH levels have been documented in PTSD patients.1,4 An association between high CRH levels and an increase in startle response explains the exaggerated startle response observed in patients with PTSD. Higher circulating glucocorticoid has the opposite effect4; there is an inverse relationship between the daily level of glucocorticoid and startle amplitude. A low level of circulating glucocorticoid promotes recall of frightening events that results in persistent re-experiencing of traumatic memories.2,3
Glucocorticoids in PTSD
Glucocorticoid administration reduces psychological and physiological responses to stress.3 Exogenous glucocorticoid administration affects cognition by interacting with serotonin, dopamine, and ã-aminobutyric acid by actions on the amygdala, medial prefrontal cortex, and hippocampus.2,3 Research among veterans with and without PTSD recorded a decrease in startle response after administration of a single dose of 20 mg of hydrocortisone.4 Results of a large study documented that one dose of hydrocortisone administered at >35 mg can inhibit threatening memories and improve social function.3 Hydrocortisone is linked to anxiolytic effects in healthy persons and patients with social phobia or panic disorder.3,4 Because treatment of PTSD with antidepressants and benzodiazepines often is ineffective,5 glucocorticoids may offer a new pharmacotherapy option. Glucocorticoids have been prescribed as prophylactic agents shortly after an acutely stressful event to prevent development of PTSD.4 Hydrocortisone is not FDA-approved to treat PTSD; informed consent, physician discretion, and close monitoring are emphasized.
Glucocorticoid use in mitigating PTSD symptom emergence is under investigation. Research suggests that just one acute dose of hydrocortisone might benefit patients prone to PTSD.3,4 Further study is needed to establish whether prescribing hydrocortisone is efficacious.
Disclosure
The authors report no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Jones T, Moller MD. Implications of hypothalamic-pituitary-adrenal axis functioning in posttraumatic stress disorder. J Am Psychiatr Nurses Assoc. 2011;17(6):393-403.
2. Blundell J, Blaiss CA, Lagace DC, et al. Block of glucocorticoid synthesis during re-activation inhibits extinction of an established fear memory. Neurobiol Learn Mem. 2011;95(4):453-460.
3. Putman P, Roelofs K. Effects of single cortisol administrations on human affect reviewed: coping with stress through adaptive regulation of automatic cognitive processing. Psychoneuroendocrinology. 2011;36(4):439-448.
4. Miller MW, McKinney AE, Kanter FS, et al. Hydrocortisone suppression of the fear-potentiated startle response and posttraumatic stress disorder. Psychoneuroendocrinology. 2011;36(7):970-980.
5. Nin MS, Martinez LA, Pibiri F, et al. Neurosteroids reduce social isolation-induced behavioral deficits: a proposed link with neurosteroid-mediated upregulation of BDNF expression. Front Endocrinol (Lausanne). 2011;2(73):1-12.
1. Jones T, Moller MD. Implications of hypothalamic-pituitary-adrenal axis functioning in posttraumatic stress disorder. J Am Psychiatr Nurses Assoc. 2011;17(6):393-403.
2. Blundell J, Blaiss CA, Lagace DC, et al. Block of glucocorticoid synthesis during re-activation inhibits extinction of an established fear memory. Neurobiol Learn Mem. 2011;95(4):453-460.
3. Putman P, Roelofs K. Effects of single cortisol administrations on human affect reviewed: coping with stress through adaptive regulation of automatic cognitive processing. Psychoneuroendocrinology. 2011;36(4):439-448.
4. Miller MW, McKinney AE, Kanter FS, et al. Hydrocortisone suppression of the fear-potentiated startle response and posttraumatic stress disorder. Psychoneuroendocrinology. 2011;36(7):970-980.
5. Nin MS, Martinez LA, Pibiri F, et al. Neurosteroids reduce social isolation-induced behavioral deficits: a proposed link with neurosteroid-mediated upregulation of BDNF expression. Front Endocrinol (Lausanne). 2011;2(73):1-12.
Dihydropyridine calcium channel blockers in dementia and hypertension
Dementia affects 34 million people globally, with the most common cause of dementia, Alzheimer’s disease (AD), affecting 5.5 million Americans.1,2 The connection between cerebrovascular disorders and AD means that antihypertensive agents may play a role in dementia prophylaxis and management.1,2
Hypertension increases the risk of intellectual dysfunction by increasing susceptibility to heart disease, ischemic brain injury, and cerebrovascular pathology.1 In addition to senile plaques, ischemic brain lesions are observed in autopsies of AD patients,1 and brain infarctions are more common among AD patients than among controls.2 Brain pathology suggestive of AD was found in 30% to 50% of postmortem examinations of patients with vascular dementia.1
It is useful to note that dihydropyridines, a subgroup of calcium channel blockers, may inhibit amyloidogenesis.3
Hypertension and cognition
Hypertension-induced hyperdense lesions in cerebral white matter reflect pathology in small vessels, inflammatory change, and disruption of the blood-brain barrier, which may precede cognitive decline.1 Even subclinical ischemic changes may increase the probability of developing dementia.2 Hypertension also reduces cerebral perfusion, especially in the hippocampus, which may promote degeneration of memory function.1 Prolonged cerebral hypoxia increases amyloid precursor protein production and β-secretase activity.1,2 Patients who died of brain ischemia show prominent β-amyloid protein and apolipoprotein E in histopathologic analysis of the hippocampus.1 Compression of vessels by â-amyloid protein further augments this degenerative process.1
Inhibition of amyloidogenesis
Long-term administration of antihypertensive medications in patients age <75 decreases the probability of dementia by 8% each year.1 Calcium channel blockers protect neurons by lowering blood pressure and reversing cellular-level calcium channel dysfunction that occurs with age, cerebral infarction, and AD.
Select dihydropyridines may inhibit amyloidogenesis in apolipoprotein E carriers:
• amlodipine and nilvadipine reduce β-secretase activity and amyloid precursor protein-β production3
• nilvadipine and nitrendipine limit β-amyloid protein synthesis in the brain and promote their clearance through the blood-brain barrier3
• nilvadipine-treated apolipoprotein E carriers experience cognitive stabilization compared with cognitive decreases seen in non-treated subjects.
Dihydropyridines can produce therapeutic effects for both AD and cerebrovascular dementia patients, indicating the potential that certain agents in this class have for treating both conditions.
Disclosure
The authors report no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Valenzuela M, Esler M, Ritchie K, et al. Antihypertensives for combating dementia? A perspective on candidate molecular mechanisms and population-based prevention. Transl Psychiatry. 2012;2:e107.
2. Pimentel-Coelho PM, Rivest S. The early contribution of cerebrovascular factors to the pathogenesis of Alzheimer’s disease. Eur J Neurosci. 2012;35(12):1917-1937.
3. Paris D, Bachmeier C, Patel N, et al. Selective antihypertensive dihydropyridines lower Aβ accumulation by targeting both the production and the clearance of Aβ across the blood-brain barrier. Mol Med. 2011;17(3-4):149-162.
Dementia affects 34 million people globally, with the most common cause of dementia, Alzheimer’s disease (AD), affecting 5.5 million Americans.1,2 The connection between cerebrovascular disorders and AD means that antihypertensive agents may play a role in dementia prophylaxis and management.1,2
Hypertension increases the risk of intellectual dysfunction by increasing susceptibility to heart disease, ischemic brain injury, and cerebrovascular pathology.1 In addition to senile plaques, ischemic brain lesions are observed in autopsies of AD patients,1 and brain infarctions are more common among AD patients than among controls.2 Brain pathology suggestive of AD was found in 30% to 50% of postmortem examinations of patients with vascular dementia.1
It is useful to note that dihydropyridines, a subgroup of calcium channel blockers, may inhibit amyloidogenesis.3
Hypertension and cognition
Hypertension-induced hyperdense lesions in cerebral white matter reflect pathology in small vessels, inflammatory change, and disruption of the blood-brain barrier, which may precede cognitive decline.1 Even subclinical ischemic changes may increase the probability of developing dementia.2 Hypertension also reduces cerebral perfusion, especially in the hippocampus, which may promote degeneration of memory function.1 Prolonged cerebral hypoxia increases amyloid precursor protein production and β-secretase activity.1,2 Patients who died of brain ischemia show prominent β-amyloid protein and apolipoprotein E in histopathologic analysis of the hippocampus.1 Compression of vessels by â-amyloid protein further augments this degenerative process.1
Inhibition of amyloidogenesis
Long-term administration of antihypertensive medications in patients age <75 decreases the probability of dementia by 8% each year.1 Calcium channel blockers protect neurons by lowering blood pressure and reversing cellular-level calcium channel dysfunction that occurs with age, cerebral infarction, and AD.
Select dihydropyridines may inhibit amyloidogenesis in apolipoprotein E carriers:
• amlodipine and nilvadipine reduce β-secretase activity and amyloid precursor protein-β production3
• nilvadipine and nitrendipine limit β-amyloid protein synthesis in the brain and promote their clearance through the blood-brain barrier3
• nilvadipine-treated apolipoprotein E carriers experience cognitive stabilization compared with cognitive decreases seen in non-treated subjects.
Dihydropyridines can produce therapeutic effects for both AD and cerebrovascular dementia patients, indicating the potential that certain agents in this class have for treating both conditions.
Disclosure
The authors report no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products.
Dementia affects 34 million people globally, with the most common cause of dementia, Alzheimer’s disease (AD), affecting 5.5 million Americans.1,2 The connection between cerebrovascular disorders and AD means that antihypertensive agents may play a role in dementia prophylaxis and management.1,2
Hypertension increases the risk of intellectual dysfunction by increasing susceptibility to heart disease, ischemic brain injury, and cerebrovascular pathology.1 In addition to senile plaques, ischemic brain lesions are observed in autopsies of AD patients,1 and brain infarctions are more common among AD patients than among controls.2 Brain pathology suggestive of AD was found in 30% to 50% of postmortem examinations of patients with vascular dementia.1
It is useful to note that dihydropyridines, a subgroup of calcium channel blockers, may inhibit amyloidogenesis.3
Hypertension and cognition
Hypertension-induced hyperdense lesions in cerebral white matter reflect pathology in small vessels, inflammatory change, and disruption of the blood-brain barrier, which may precede cognitive decline.1 Even subclinical ischemic changes may increase the probability of developing dementia.2 Hypertension also reduces cerebral perfusion, especially in the hippocampus, which may promote degeneration of memory function.1 Prolonged cerebral hypoxia increases amyloid precursor protein production and β-secretase activity.1,2 Patients who died of brain ischemia show prominent β-amyloid protein and apolipoprotein E in histopathologic analysis of the hippocampus.1 Compression of vessels by â-amyloid protein further augments this degenerative process.1
Inhibition of amyloidogenesis
Long-term administration of antihypertensive medications in patients age <75 decreases the probability of dementia by 8% each year.1 Calcium channel blockers protect neurons by lowering blood pressure and reversing cellular-level calcium channel dysfunction that occurs with age, cerebral infarction, and AD.
Select dihydropyridines may inhibit amyloidogenesis in apolipoprotein E carriers:
• amlodipine and nilvadipine reduce β-secretase activity and amyloid precursor protein-β production3
• nilvadipine and nitrendipine limit β-amyloid protein synthesis in the brain and promote their clearance through the blood-brain barrier3
• nilvadipine-treated apolipoprotein E carriers experience cognitive stabilization compared with cognitive decreases seen in non-treated subjects.
Dihydropyridines can produce therapeutic effects for both AD and cerebrovascular dementia patients, indicating the potential that certain agents in this class have for treating both conditions.
Disclosure
The authors report no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Valenzuela M, Esler M, Ritchie K, et al. Antihypertensives for combating dementia? A perspective on candidate molecular mechanisms and population-based prevention. Transl Psychiatry. 2012;2:e107.
2. Pimentel-Coelho PM, Rivest S. The early contribution of cerebrovascular factors to the pathogenesis of Alzheimer’s disease. Eur J Neurosci. 2012;35(12):1917-1937.
3. Paris D, Bachmeier C, Patel N, et al. Selective antihypertensive dihydropyridines lower Aβ accumulation by targeting both the production and the clearance of Aβ across the blood-brain barrier. Mol Med. 2011;17(3-4):149-162.
1. Valenzuela M, Esler M, Ritchie K, et al. Antihypertensives for combating dementia? A perspective on candidate molecular mechanisms and population-based prevention. Transl Psychiatry. 2012;2:e107.
2. Pimentel-Coelho PM, Rivest S. The early contribution of cerebrovascular factors to the pathogenesis of Alzheimer’s disease. Eur J Neurosci. 2012;35(12):1917-1937.
3. Paris D, Bachmeier C, Patel N, et al. Selective antihypertensive dihydropyridines lower Aβ accumulation by targeting both the production and the clearance of Aβ across the blood-brain barrier. Mol Med. 2011;17(3-4):149-162.
New ‘legal’ highs: Kratom and methoxetamine
The demand for “legal highs”—intoxicating natural or synthetic substances that are not prohibited by law—continues to increase. Young adults may use these substances, which are widely available on the internet, at “head shops,” and at gas stations. Such substances frequently cause adverse medical and psychiatric effects, exemplified by recent reports concerning the dangers of using synthetic cannabinoids (eg, “Spice,” “K2”) and synthetic cathinones (“bath salts”). Although these 2 substances now are illegal in many jurisdictions, other novel substances of misuse remain legal and widely available, including Kratom and methoxetamine.
Because these substances usually are not detectable on standard urine toxicology screens, clinicians need to be aware of them to be able to take an accurate substance use history, consider possible dangerous interactions with prescribed psychotropics, and address medical and psychiatric complications.
Kratom is an herbal product derived from Mitragyna speciosa, a plant native to Southeast Asia. Traditionally used as a medicinal herb, it increasingly is being used for recreational purposes and remains legal and widely available in the United States. Kratom’s leaves contain multiple alkaloids, including mitragynine and 7-hydroxymitragynine, which are believed to act as agonists at the μ-opioid receptor. Mitragynine also may have agonist activity at post-synaptic
α2-adrenergic receptors, as well as antagonist activity at 5-HT2A receptors.1 Mitragynine is 13 times more potent than morphine, and 7-hydroxymitragynine is 4 times more potent than mitragynine.2
Kratom is available as leaves, powdered leaves, or gum. It can be smoked, brewed into tea, or mixed with liquid and ingested. Effects are dose-dependent; lower doses tend to produce a stimulant effect and higher doses produce an opioid effect. A typical dose is 1 to 8 g.3 Users may take Kratom to experience euphoria or analgesia, or to self-treat opioid withdrawal symptoms.3 Kratom withdrawal syndrome shares many features of classic opioid withdrawal—diarrhea, rhinorrhea, cravings, anxiety, tremor, myalgia, sweating, and irritability—but has been reported to be less severe and shorter-lasting.1 Kratom withdrawal, like opioid withdrawal, may respond to supportive care in combination with opioid-replacement therapy. Airway management and naloxone treatment may be needed on an emergent basis if a user develops respiratory depression.2 There have been case reports of seizures occurring following Kratom use.2
Methoxetamine is a ketamine analog originally developed as an alternative to ketamine. It isn’t classified as a controlled substance in the United States and is available on the internet.2 Methoxetamine is a white powder typically snorted or taken sublingually, although it can be injected intramuscularly. Because methoxetamine’s structure is similar to ketamine, its mechanism of action is assumed to involve glutamate N-methyl-d-aspartate receptor antagonism and dopamine reuptake inhibition. Doses range from 20 to 100 mg orally and 10 to 50 mg when injected. Effects may not be apparent for 30 to 90 minutes after the drug is snorted, which may cause users to take another dose or ingest a different substance, possibly leading to synergistic adverse effects. Effects may emerge within 5 minutes when injected. The duration of effect generally is 5 to 7 hours—notably longer than ketamine—but as little as 1 hour when injected.
No clinical human or animal studies have been conducted on methoxetamine, which makes it difficult to ascertain the drug’s true clinical and toxic effects; instead, these effects must be surmised from user reports and case studies. Desired effects described by users are similar to those of ketamine: dissociation, short-term mood elevation, visual hallucinations, and alteration of sensory experiences. Reported adverse effects include catatonia, confusion, agitation, and depression.4 In addition, methoxetamine may induce sympathomimetic toxicity as evidenced by tachycardia and hypertension. Researchers have suggested that patients who experience methoxetamine toxicity and require emergency treatment be managed with supportive care and benzodiazepines.5
Staying current is key
New and potentially dangerous substances are being produced so quickly distributors are able to stay ahead of regulatory efforts. When one substance is declared illegal, another related substance quickly is available to take its place. To provide the best care for our patients, it is essential for psychiatrists to stay up-to-date about these novel substances.
Disclosure
Dr. Troy reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
1. McWhirter L, Morris S. A case report of inpatient detoxification after kratom (Mitragyna speciosa) dependence. Eur Addict Res. 2010;16(4):229-231.
2. Rosenbaum CD, Carreiro SP, Babu KM. Here today, gone tomorrow…and back again? A review of herbal marijuana alternatives (K2, Spice), synthetic cathinones (bath salts), Kratom, Salvia divinorum, methoxetamine, and piperazines. J Med Toxicol. 2012;8(1):15-32.
3. Boyer EW, Babu KM, Macalino GE. Self-treatment of opioid withdrawal with a dietary supplement, Kratom. Am J Addict. 2007;16(5):352-356.
4. Corazza O, Schifano F, Simonato P, et al. Phenomenon of new drugs on the Internet: the case of ketamine derivative methoxetamine. Hum Psychopharmacol. 2012;27(2):
145-149.
5. Wood DM, Davies S, Puchnarewicz M, et al. Acute toxicity associated with the recreational use of the ketamine derivative methoxetamine. Eur J Clin Pharmacol. 2012; 68(5):853-856.
The demand for “legal highs”—intoxicating natural or synthetic substances that are not prohibited by law—continues to increase. Young adults may use these substances, which are widely available on the internet, at “head shops,” and at gas stations. Such substances frequently cause adverse medical and psychiatric effects, exemplified by recent reports concerning the dangers of using synthetic cannabinoids (eg, “Spice,” “K2”) and synthetic cathinones (“bath salts”). Although these 2 substances now are illegal in many jurisdictions, other novel substances of misuse remain legal and widely available, including Kratom and methoxetamine.
Because these substances usually are not detectable on standard urine toxicology screens, clinicians need to be aware of them to be able to take an accurate substance use history, consider possible dangerous interactions with prescribed psychotropics, and address medical and psychiatric complications.
Kratom is an herbal product derived from Mitragyna speciosa, a plant native to Southeast Asia. Traditionally used as a medicinal herb, it increasingly is being used for recreational purposes and remains legal and widely available in the United States. Kratom’s leaves contain multiple alkaloids, including mitragynine and 7-hydroxymitragynine, which are believed to act as agonists at the μ-opioid receptor. Mitragynine also may have agonist activity at post-synaptic
α2-adrenergic receptors, as well as antagonist activity at 5-HT2A receptors.1 Mitragynine is 13 times more potent than morphine, and 7-hydroxymitragynine is 4 times more potent than mitragynine.2
Kratom is available as leaves, powdered leaves, or gum. It can be smoked, brewed into tea, or mixed with liquid and ingested. Effects are dose-dependent; lower doses tend to produce a stimulant effect and higher doses produce an opioid effect. A typical dose is 1 to 8 g.3 Users may take Kratom to experience euphoria or analgesia, or to self-treat opioid withdrawal symptoms.3 Kratom withdrawal syndrome shares many features of classic opioid withdrawal—diarrhea, rhinorrhea, cravings, anxiety, tremor, myalgia, sweating, and irritability—but has been reported to be less severe and shorter-lasting.1 Kratom withdrawal, like opioid withdrawal, may respond to supportive care in combination with opioid-replacement therapy. Airway management and naloxone treatment may be needed on an emergent basis if a user develops respiratory depression.2 There have been case reports of seizures occurring following Kratom use.2
Methoxetamine is a ketamine analog originally developed as an alternative to ketamine. It isn’t classified as a controlled substance in the United States and is available on the internet.2 Methoxetamine is a white powder typically snorted or taken sublingually, although it can be injected intramuscularly. Because methoxetamine’s structure is similar to ketamine, its mechanism of action is assumed to involve glutamate N-methyl-d-aspartate receptor antagonism and dopamine reuptake inhibition. Doses range from 20 to 100 mg orally and 10 to 50 mg when injected. Effects may not be apparent for 30 to 90 minutes after the drug is snorted, which may cause users to take another dose or ingest a different substance, possibly leading to synergistic adverse effects. Effects may emerge within 5 minutes when injected. The duration of effect generally is 5 to 7 hours—notably longer than ketamine—but as little as 1 hour when injected.
No clinical human or animal studies have been conducted on methoxetamine, which makes it difficult to ascertain the drug’s true clinical and toxic effects; instead, these effects must be surmised from user reports and case studies. Desired effects described by users are similar to those of ketamine: dissociation, short-term mood elevation, visual hallucinations, and alteration of sensory experiences. Reported adverse effects include catatonia, confusion, agitation, and depression.4 In addition, methoxetamine may induce sympathomimetic toxicity as evidenced by tachycardia and hypertension. Researchers have suggested that patients who experience methoxetamine toxicity and require emergency treatment be managed with supportive care and benzodiazepines.5
Staying current is key
New and potentially dangerous substances are being produced so quickly distributors are able to stay ahead of regulatory efforts. When one substance is declared illegal, another related substance quickly is available to take its place. To provide the best care for our patients, it is essential for psychiatrists to stay up-to-date about these novel substances.
Disclosure
Dr. Troy reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
The demand for “legal highs”—intoxicating natural or synthetic substances that are not prohibited by law—continues to increase. Young adults may use these substances, which are widely available on the internet, at “head shops,” and at gas stations. Such substances frequently cause adverse medical and psychiatric effects, exemplified by recent reports concerning the dangers of using synthetic cannabinoids (eg, “Spice,” “K2”) and synthetic cathinones (“bath salts”). Although these 2 substances now are illegal in many jurisdictions, other novel substances of misuse remain legal and widely available, including Kratom and methoxetamine.
Because these substances usually are not detectable on standard urine toxicology screens, clinicians need to be aware of them to be able to take an accurate substance use history, consider possible dangerous interactions with prescribed psychotropics, and address medical and psychiatric complications.
Kratom is an herbal product derived from Mitragyna speciosa, a plant native to Southeast Asia. Traditionally used as a medicinal herb, it increasingly is being used for recreational purposes and remains legal and widely available in the United States. Kratom’s leaves contain multiple alkaloids, including mitragynine and 7-hydroxymitragynine, which are believed to act as agonists at the μ-opioid receptor. Mitragynine also may have agonist activity at post-synaptic
α2-adrenergic receptors, as well as antagonist activity at 5-HT2A receptors.1 Mitragynine is 13 times more potent than morphine, and 7-hydroxymitragynine is 4 times more potent than mitragynine.2
Kratom is available as leaves, powdered leaves, or gum. It can be smoked, brewed into tea, or mixed with liquid and ingested. Effects are dose-dependent; lower doses tend to produce a stimulant effect and higher doses produce an opioid effect. A typical dose is 1 to 8 g.3 Users may take Kratom to experience euphoria or analgesia, or to self-treat opioid withdrawal symptoms.3 Kratom withdrawal syndrome shares many features of classic opioid withdrawal—diarrhea, rhinorrhea, cravings, anxiety, tremor, myalgia, sweating, and irritability—but has been reported to be less severe and shorter-lasting.1 Kratom withdrawal, like opioid withdrawal, may respond to supportive care in combination with opioid-replacement therapy. Airway management and naloxone treatment may be needed on an emergent basis if a user develops respiratory depression.2 There have been case reports of seizures occurring following Kratom use.2
Methoxetamine is a ketamine analog originally developed as an alternative to ketamine. It isn’t classified as a controlled substance in the United States and is available on the internet.2 Methoxetamine is a white powder typically snorted or taken sublingually, although it can be injected intramuscularly. Because methoxetamine’s structure is similar to ketamine, its mechanism of action is assumed to involve glutamate N-methyl-d-aspartate receptor antagonism and dopamine reuptake inhibition. Doses range from 20 to 100 mg orally and 10 to 50 mg when injected. Effects may not be apparent for 30 to 90 minutes after the drug is snorted, which may cause users to take another dose or ingest a different substance, possibly leading to synergistic adverse effects. Effects may emerge within 5 minutes when injected. The duration of effect generally is 5 to 7 hours—notably longer than ketamine—but as little as 1 hour when injected.
No clinical human or animal studies have been conducted on methoxetamine, which makes it difficult to ascertain the drug’s true clinical and toxic effects; instead, these effects must be surmised from user reports and case studies. Desired effects described by users are similar to those of ketamine: dissociation, short-term mood elevation, visual hallucinations, and alteration of sensory experiences. Reported adverse effects include catatonia, confusion, agitation, and depression.4 In addition, methoxetamine may induce sympathomimetic toxicity as evidenced by tachycardia and hypertension. Researchers have suggested that patients who experience methoxetamine toxicity and require emergency treatment be managed with supportive care and benzodiazepines.5
Staying current is key
New and potentially dangerous substances are being produced so quickly distributors are able to stay ahead of regulatory efforts. When one substance is declared illegal, another related substance quickly is available to take its place. To provide the best care for our patients, it is essential for psychiatrists to stay up-to-date about these novel substances.
Disclosure
Dr. Troy reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
1. McWhirter L, Morris S. A case report of inpatient detoxification after kratom (Mitragyna speciosa) dependence. Eur Addict Res. 2010;16(4):229-231.
2. Rosenbaum CD, Carreiro SP, Babu KM. Here today, gone tomorrow…and back again? A review of herbal marijuana alternatives (K2, Spice), synthetic cathinones (bath salts), Kratom, Salvia divinorum, methoxetamine, and piperazines. J Med Toxicol. 2012;8(1):15-32.
3. Boyer EW, Babu KM, Macalino GE. Self-treatment of opioid withdrawal with a dietary supplement, Kratom. Am J Addict. 2007;16(5):352-356.
4. Corazza O, Schifano F, Simonato P, et al. Phenomenon of new drugs on the Internet: the case of ketamine derivative methoxetamine. Hum Psychopharmacol. 2012;27(2):
145-149.
5. Wood DM, Davies S, Puchnarewicz M, et al. Acute toxicity associated with the recreational use of the ketamine derivative methoxetamine. Eur J Clin Pharmacol. 2012; 68(5):853-856.
1. McWhirter L, Morris S. A case report of inpatient detoxification after kratom (Mitragyna speciosa) dependence. Eur Addict Res. 2010;16(4):229-231.
2. Rosenbaum CD, Carreiro SP, Babu KM. Here today, gone tomorrow…and back again? A review of herbal marijuana alternatives (K2, Spice), synthetic cathinones (bath salts), Kratom, Salvia divinorum, methoxetamine, and piperazines. J Med Toxicol. 2012;8(1):15-32.
3. Boyer EW, Babu KM, Macalino GE. Self-treatment of opioid withdrawal with a dietary supplement, Kratom. Am J Addict. 2007;16(5):352-356.
4. Corazza O, Schifano F, Simonato P, et al. Phenomenon of new drugs on the Internet: the case of ketamine derivative methoxetamine. Hum Psychopharmacol. 2012;27(2):
145-149.
5. Wood DM, Davies S, Puchnarewicz M, et al. Acute toxicity associated with the recreational use of the ketamine derivative methoxetamine. Eur J Clin Pharmacol. 2012; 68(5):853-856.
Tips for discussing sexual dysfunction with oncology patients
Cancer therapy presents unique challenges to health care providers because of the evolving nature of managing a patient’s diagnosis, treatment, and recovery. Be conscientious about a patient’s mental health and physical health when considering treatment and support.
Sexual health is important
Sexual dysfunction is one of many variables a patient considers when deciding on a cancer treatment plan—particularly those who have a gynecological, gastrointestinal, or reproductive-tract cancer. Additionally, sexual dysfunction remains one of the major health complaints after many cancer therapies, which may be overlooked because of patients’ hesitancy to initiate discussion.
Many oncologic treatment options—surgery, chemotherapy, radiotherapy, and hormone therapy—are associated with sexual side effects, including radiation sequelae, erectile dysfunction, decreased lubrication, and vaginal atrophy.1 Because sexual dysfunction often is multifactorial, an approach that involves psychological assessment and treatment usually is optimal. A mental health provider can explore the interactions of such factors as decreased self-esteem, negative body image, altered interpersonal relationships, and change or loss of libido when assessing reported sexual dysfunction.2
The mnemonic SEMEN can help you address sexual health topics with oncology patients:
Take a Sexual history at diagnosis and before treatment begins.
Provide Educational materials to warn of potential adverse sexual side effects of various treatments.
Maintain an open dialogue during cancer therapy. Discuss any adverse sexual side effects the patient may be experiencing.
Educate and treat your patient. Offer information on medications, devices, and techniques that target sexual dysfunction.
For men with erectile dysfunction, recommend a phosphodiesterase type 5 (PDE5) inhibitor (sildenafil citrate, tadalafil, vardenafil), a vacuum pump, or intracavernosal penile injection, such as synthetic prostaglandin E1.
For men experiencing premature ejaculation, consider providing instruction on the “squeeze-pause” technique or prescribing a topical anesthetic cream such as lidocaine/prilocaine (available under the brand name EMLA), which is applied to the head of the penis and wiped off before intercourse. Some selective serotonin reuptake inhibitors, including fluoxetine, paroxetine, and sertraline, have been used off-label to treat premature ejaculation.
Women experiencing vaginal dryness or vaginal atrophy might benefit from vaginal estrogen (such as conjugated or estradiol estrogen tablets), an estradiol cream, or the estradiol vaginal ring. Other options include a vaginal moisturizing agent or lubricant.
Additional sexual education topics include:
• adjusting sexual positions
• enhancing foreplay
• seeking help from support organizations
• engaging a sexual therapist (recommend one who specializes in treating oncology patients).
Make Normality the goal after treatment or recovery. Encourage your patient to maintain a healthy sexual lifestyle by continuing discussions about sexual health, supporting healthy self-perception, and addressing possible future sexual dysfunction.
Being given a diagnosis of cancer, undergoing treatment, and surviving the experience are life-altering. Healthcare providers should be open to discussing patients’ past and current sexual practices; along with treating physical illness, you should attempt to maintain a sense of normality, which includes maintaining healthy sexuality.
1. Levenson JL. Textbook of psychosomatic medicine. Washington, DC: American Psychiatric Publishing; 2005.
2. National Institutes of Health. National Cancer Institute. Treatment of sexual problems in people with cancer. http://www.cancer.gov/cancertopics/pdq/supportivecare/sexuality/HealthProfessional/page5. Accessed March 26, 2013.
Cancer therapy presents unique challenges to health care providers because of the evolving nature of managing a patient’s diagnosis, treatment, and recovery. Be conscientious about a patient’s mental health and physical health when considering treatment and support.
Sexual health is important
Sexual dysfunction is one of many variables a patient considers when deciding on a cancer treatment plan—particularly those who have a gynecological, gastrointestinal, or reproductive-tract cancer. Additionally, sexual dysfunction remains one of the major health complaints after many cancer therapies, which may be overlooked because of patients’ hesitancy to initiate discussion.
Many oncologic treatment options—surgery, chemotherapy, radiotherapy, and hormone therapy—are associated with sexual side effects, including radiation sequelae, erectile dysfunction, decreased lubrication, and vaginal atrophy.1 Because sexual dysfunction often is multifactorial, an approach that involves psychological assessment and treatment usually is optimal. A mental health provider can explore the interactions of such factors as decreased self-esteem, negative body image, altered interpersonal relationships, and change or loss of libido when assessing reported sexual dysfunction.2
The mnemonic SEMEN can help you address sexual health topics with oncology patients:
Take a Sexual history at diagnosis and before treatment begins.
Provide Educational materials to warn of potential adverse sexual side effects of various treatments.
Maintain an open dialogue during cancer therapy. Discuss any adverse sexual side effects the patient may be experiencing.
Educate and treat your patient. Offer information on medications, devices, and techniques that target sexual dysfunction.
For men with erectile dysfunction, recommend a phosphodiesterase type 5 (PDE5) inhibitor (sildenafil citrate, tadalafil, vardenafil), a vacuum pump, or intracavernosal penile injection, such as synthetic prostaglandin E1.
For men experiencing premature ejaculation, consider providing instruction on the “squeeze-pause” technique or prescribing a topical anesthetic cream such as lidocaine/prilocaine (available under the brand name EMLA), which is applied to the head of the penis and wiped off before intercourse. Some selective serotonin reuptake inhibitors, including fluoxetine, paroxetine, and sertraline, have been used off-label to treat premature ejaculation.
Women experiencing vaginal dryness or vaginal atrophy might benefit from vaginal estrogen (such as conjugated or estradiol estrogen tablets), an estradiol cream, or the estradiol vaginal ring. Other options include a vaginal moisturizing agent or lubricant.
Additional sexual education topics include:
• adjusting sexual positions
• enhancing foreplay
• seeking help from support organizations
• engaging a sexual therapist (recommend one who specializes in treating oncology patients).
Make Normality the goal after treatment or recovery. Encourage your patient to maintain a healthy sexual lifestyle by continuing discussions about sexual health, supporting healthy self-perception, and addressing possible future sexual dysfunction.
Being given a diagnosis of cancer, undergoing treatment, and surviving the experience are life-altering. Healthcare providers should be open to discussing patients’ past and current sexual practices; along with treating physical illness, you should attempt to maintain a sense of normality, which includes maintaining healthy sexuality.
Cancer therapy presents unique challenges to health care providers because of the evolving nature of managing a patient’s diagnosis, treatment, and recovery. Be conscientious about a patient’s mental health and physical health when considering treatment and support.
Sexual health is important
Sexual dysfunction is one of many variables a patient considers when deciding on a cancer treatment plan—particularly those who have a gynecological, gastrointestinal, or reproductive-tract cancer. Additionally, sexual dysfunction remains one of the major health complaints after many cancer therapies, which may be overlooked because of patients’ hesitancy to initiate discussion.
Many oncologic treatment options—surgery, chemotherapy, radiotherapy, and hormone therapy—are associated with sexual side effects, including radiation sequelae, erectile dysfunction, decreased lubrication, and vaginal atrophy.1 Because sexual dysfunction often is multifactorial, an approach that involves psychological assessment and treatment usually is optimal. A mental health provider can explore the interactions of such factors as decreased self-esteem, negative body image, altered interpersonal relationships, and change or loss of libido when assessing reported sexual dysfunction.2
The mnemonic SEMEN can help you address sexual health topics with oncology patients:
Take a Sexual history at diagnosis and before treatment begins.
Provide Educational materials to warn of potential adverse sexual side effects of various treatments.
Maintain an open dialogue during cancer therapy. Discuss any adverse sexual side effects the patient may be experiencing.
Educate and treat your patient. Offer information on medications, devices, and techniques that target sexual dysfunction.
For men with erectile dysfunction, recommend a phosphodiesterase type 5 (PDE5) inhibitor (sildenafil citrate, tadalafil, vardenafil), a vacuum pump, or intracavernosal penile injection, such as synthetic prostaglandin E1.
For men experiencing premature ejaculation, consider providing instruction on the “squeeze-pause” technique or prescribing a topical anesthetic cream such as lidocaine/prilocaine (available under the brand name EMLA), which is applied to the head of the penis and wiped off before intercourse. Some selective serotonin reuptake inhibitors, including fluoxetine, paroxetine, and sertraline, have been used off-label to treat premature ejaculation.
Women experiencing vaginal dryness or vaginal atrophy might benefit from vaginal estrogen (such as conjugated or estradiol estrogen tablets), an estradiol cream, or the estradiol vaginal ring. Other options include a vaginal moisturizing agent or lubricant.
Additional sexual education topics include:
• adjusting sexual positions
• enhancing foreplay
• seeking help from support organizations
• engaging a sexual therapist (recommend one who specializes in treating oncology patients).
Make Normality the goal after treatment or recovery. Encourage your patient to maintain a healthy sexual lifestyle by continuing discussions about sexual health, supporting healthy self-perception, and addressing possible future sexual dysfunction.
Being given a diagnosis of cancer, undergoing treatment, and surviving the experience are life-altering. Healthcare providers should be open to discussing patients’ past and current sexual practices; along with treating physical illness, you should attempt to maintain a sense of normality, which includes maintaining healthy sexuality.
1. Levenson JL. Textbook of psychosomatic medicine. Washington, DC: American Psychiatric Publishing; 2005.
2. National Institutes of Health. National Cancer Institute. Treatment of sexual problems in people with cancer. http://www.cancer.gov/cancertopics/pdq/supportivecare/sexuality/HealthProfessional/page5. Accessed March 26, 2013.
1. Levenson JL. Textbook of psychosomatic medicine. Washington, DC: American Psychiatric Publishing; 2005.
2. National Institutes of Health. National Cancer Institute. Treatment of sexual problems in people with cancer. http://www.cancer.gov/cancertopics/pdq/supportivecare/sexuality/HealthProfessional/page5. Accessed March 26, 2013.
Tips for making the transition from inpatient to outpatient practice
Years of outpatient practice and supervising residents as they move from inpatient to outpatient rotations prompted me to examine the advice I give to clinicians transitioning to outpatient care.
1. Slow down! Keep in mind that your full assessment may take more than
1 session. Take advantage of follow-up appointments to add details or round out your sense of what is going on with your patient.
2. You don’t always have to ‘do something.’ We often feel that we need to “do something.” Perhaps it’s the difficulty of sitting with someone who’s suffering, or our own feelings of helplessness. Recognize this urge and evaluate whether your findings are something you must act on or if it’s your anxiety that is driving you.
3. Know the particulars of outpatient prescribing. Keep in mind that you should treat the whole person, not just her (his) symptoms. Sometimes it’s appropriate to treat individual symptoms but the justification for this and any other medical decisions needs to be documented.
- Be methodical. Often, this means making one medication change at a time. Although the urgency of inpatient hospitalization sometimes necessitates starting several medications simultaneously, outpatient psychiatry rarely requires that step. Most illnesses in outpatients are chronic;clinicians need to balance the need for treatment with the understanding that the patient may require psychiatric medication indefinitely. Starting several medications at once often leaves the patient and psychiatrist wondering which medications are helping and which may be causing adverse effects.
- Practice educated polypharmacy. Be careful and deliberate; maximize dosages before adding adjunctive therapy. Consider interactions with other medications (such as warfarin or omeprazole), their side effects, and alternative psychosocial treatments.
- Know the cost of medication. Consider generic drugs or medications on the $4 list available at some pharmacies. Be cognizant of less expensive dosing options and combinations. For example, one month of duloxetine, 90 mg/d, costs $587 if prescribed as 30-mg pills; the same dosage costs $390 when prescribed as 30-mg pills and 60-mg pills.1 Advise patients to shop around when purchasing prescriptions because cost can vary significantly among pharmacies.
- Often, patients should be weaned off medications.2 Most selective serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors can cause a discontinuation syndrome. Fluoxetine can be tapered faster; paroxetine and venlafaxine are notorious for causing issues. Abrupt discontinuation of mood stabilizers—especially lithium3—can cause rebound mania, and should be tapered cautiously.
Disclosure
Dr. Pheister reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
References
1. DRX. Drug compare. https://drugcompare.destinationrx.com/Home.aspx. Accessed October 17, 2012.
2. Baldessarini RJ, Viguera AC, Tondo L. Discontinuing psychotropic agents. J Psychopharmacol. 1999;13(3):292-293; discussion 299.
3. Faedda GL, Tondo L, Baldessarini RJ, et al. Outcome after rapid vs gradual discontinuation of lithium treatment in bipolar disorders. Arch Gen Psychiatry. 1993;50(6):448-455.
Years of outpatient practice and supervising residents as they move from inpatient to outpatient rotations prompted me to examine the advice I give to clinicians transitioning to outpatient care.
1. Slow down! Keep in mind that your full assessment may take more than
1 session. Take advantage of follow-up appointments to add details or round out your sense of what is going on with your patient.
2. You don’t always have to ‘do something.’ We often feel that we need to “do something.” Perhaps it’s the difficulty of sitting with someone who’s suffering, or our own feelings of helplessness. Recognize this urge and evaluate whether your findings are something you must act on or if it’s your anxiety that is driving you.
3. Know the particulars of outpatient prescribing. Keep in mind that you should treat the whole person, not just her (his) symptoms. Sometimes it’s appropriate to treat individual symptoms but the justification for this and any other medical decisions needs to be documented.
- Be methodical. Often, this means making one medication change at a time. Although the urgency of inpatient hospitalization sometimes necessitates starting several medications simultaneously, outpatient psychiatry rarely requires that step. Most illnesses in outpatients are chronic;clinicians need to balance the need for treatment with the understanding that the patient may require psychiatric medication indefinitely. Starting several medications at once often leaves the patient and psychiatrist wondering which medications are helping and which may be causing adverse effects.
- Practice educated polypharmacy. Be careful and deliberate; maximize dosages before adding adjunctive therapy. Consider interactions with other medications (such as warfarin or omeprazole), their side effects, and alternative psychosocial treatments.
- Know the cost of medication. Consider generic drugs or medications on the $4 list available at some pharmacies. Be cognizant of less expensive dosing options and combinations. For example, one month of duloxetine, 90 mg/d, costs $587 if prescribed as 30-mg pills; the same dosage costs $390 when prescribed as 30-mg pills and 60-mg pills.1 Advise patients to shop around when purchasing prescriptions because cost can vary significantly among pharmacies.
- Often, patients should be weaned off medications.2 Most selective serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors can cause a discontinuation syndrome. Fluoxetine can be tapered faster; paroxetine and venlafaxine are notorious for causing issues. Abrupt discontinuation of mood stabilizers—especially lithium3—can cause rebound mania, and should be tapered cautiously.
Disclosure
Dr. Pheister reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
References
1. DRX. Drug compare. https://drugcompare.destinationrx.com/Home.aspx. Accessed October 17, 2012.
2. Baldessarini RJ, Viguera AC, Tondo L. Discontinuing psychotropic agents. J Psychopharmacol. 1999;13(3):292-293; discussion 299.
3. Faedda GL, Tondo L, Baldessarini RJ, et al. Outcome after rapid vs gradual discontinuation of lithium treatment in bipolar disorders. Arch Gen Psychiatry. 1993;50(6):448-455.
Years of outpatient practice and supervising residents as they move from inpatient to outpatient rotations prompted me to examine the advice I give to clinicians transitioning to outpatient care.
1. Slow down! Keep in mind that your full assessment may take more than
1 session. Take advantage of follow-up appointments to add details or round out your sense of what is going on with your patient.
2. You don’t always have to ‘do something.’ We often feel that we need to “do something.” Perhaps it’s the difficulty of sitting with someone who’s suffering, or our own feelings of helplessness. Recognize this urge and evaluate whether your findings are something you must act on or if it’s your anxiety that is driving you.
3. Know the particulars of outpatient prescribing. Keep in mind that you should treat the whole person, not just her (his) symptoms. Sometimes it’s appropriate to treat individual symptoms but the justification for this and any other medical decisions needs to be documented.
- Be methodical. Often, this means making one medication change at a time. Although the urgency of inpatient hospitalization sometimes necessitates starting several medications simultaneously, outpatient psychiatry rarely requires that step. Most illnesses in outpatients are chronic;clinicians need to balance the need for treatment with the understanding that the patient may require psychiatric medication indefinitely. Starting several medications at once often leaves the patient and psychiatrist wondering which medications are helping and which may be causing adverse effects.
- Practice educated polypharmacy. Be careful and deliberate; maximize dosages before adding adjunctive therapy. Consider interactions with other medications (such as warfarin or omeprazole), their side effects, and alternative psychosocial treatments.
- Know the cost of medication. Consider generic drugs or medications on the $4 list available at some pharmacies. Be cognizant of less expensive dosing options and combinations. For example, one month of duloxetine, 90 mg/d, costs $587 if prescribed as 30-mg pills; the same dosage costs $390 when prescribed as 30-mg pills and 60-mg pills.1 Advise patients to shop around when purchasing prescriptions because cost can vary significantly among pharmacies.
- Often, patients should be weaned off medications.2 Most selective serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors can cause a discontinuation syndrome. Fluoxetine can be tapered faster; paroxetine and venlafaxine are notorious for causing issues. Abrupt discontinuation of mood stabilizers—especially lithium3—can cause rebound mania, and should be tapered cautiously.
Disclosure
Dr. Pheister reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
References
1. DRX. Drug compare. https://drugcompare.destinationrx.com/Home.aspx. Accessed October 17, 2012.
2. Baldessarini RJ, Viguera AC, Tondo L. Discontinuing psychotropic agents. J Psychopharmacol. 1999;13(3):292-293; discussion 299.
3. Faedda GL, Tondo L, Baldessarini RJ, et al. Outcome after rapid vs gradual discontinuation of lithium treatment in bipolar disorders. Arch Gen Psychiatry. 1993;50(6):448-455.
Neuropsychiatric impairment in a septic shock survivor
The effect of sepsis survivorship on cognition is a substantially under-recognized public health problem.1 Sepsis survivorship has implications for patients’ families and the health care system.2 Research has demonstrated that older patients may develop impaired cognition and functional capacity after severe sepsis3; limited evidence shows neurocognitive decline in non-geriatric patients.3 There are no reports of exacerbation of psychiatric illness after severe sepsis or septic shock, and existing literature indicates that the causative factors, epidemiology, and predisposition that may worsen psychiatric illness after septic shock are poorly defined.
Case: Sepsis-induced cognitive decline?
Following an intensive care admission for septic shock, Mr. J, age 49, presents to the outpatient behavioral medicine department with worsening mood, lethargy, agitation, suicidal ideations, hallucinations, and poor work performance for 10 months. He was diagnosed with major depressive disorder 13 years prior, but has no history of hospitalization for psychiatric illness. His depressive symptoms respond well to paroxetine, 60 mg/d. Subsequently, Mr. J becomes delusional, has intense command hallucinations, and attempts suicide, resulting in hospitalization. Neuropsychological testing reveals dementia and significant psychiatric distress, including elevated levels of depression and suicidal ideation. He is stabilized with duloxetine, 90 mg/d, and quetiapine, 50 mg/d. Two years later, Mr. J still exhibits cognitive and psychiatric disturbances.
Long-term results
The underlying mechanism of septic shock on the brain may be similar to the mechanisms that exacerbate psychiatric illnesses. This case validates the use of neuropsychological testing in septic shock survivors and encourages recognition of the effect septic shock has on neuropsychiatric illness.
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers
of competing products.
References
1. Iwashyna TJ, Ely EW, Smith DM, et al. Long-term cognitive impairment and functional disability among survivors of severe sepsis. JAMA. 2010;304(16):1787-1794.
2. Safdieh J. Cognition after sepsis. Neurology Alert. 2010; 29(4):30-31.
3. Williams GS. Older severe sepsis survivors are at risk for cognitive and developmental disability. Pulmonary Reviews. 2010;15(12):17-18.
The effect of sepsis survivorship on cognition is a substantially under-recognized public health problem.1 Sepsis survivorship has implications for patients’ families and the health care system.2 Research has demonstrated that older patients may develop impaired cognition and functional capacity after severe sepsis3; limited evidence shows neurocognitive decline in non-geriatric patients.3 There are no reports of exacerbation of psychiatric illness after severe sepsis or septic shock, and existing literature indicates that the causative factors, epidemiology, and predisposition that may worsen psychiatric illness after septic shock are poorly defined.
Case: Sepsis-induced cognitive decline?
Following an intensive care admission for septic shock, Mr. J, age 49, presents to the outpatient behavioral medicine department with worsening mood, lethargy, agitation, suicidal ideations, hallucinations, and poor work performance for 10 months. He was diagnosed with major depressive disorder 13 years prior, but has no history of hospitalization for psychiatric illness. His depressive symptoms respond well to paroxetine, 60 mg/d. Subsequently, Mr. J becomes delusional, has intense command hallucinations, and attempts suicide, resulting in hospitalization. Neuropsychological testing reveals dementia and significant psychiatric distress, including elevated levels of depression and suicidal ideation. He is stabilized with duloxetine, 90 mg/d, and quetiapine, 50 mg/d. Two years later, Mr. J still exhibits cognitive and psychiatric disturbances.
Long-term results
The underlying mechanism of septic shock on the brain may be similar to the mechanisms that exacerbate psychiatric illnesses. This case validates the use of neuropsychological testing in septic shock survivors and encourages recognition of the effect septic shock has on neuropsychiatric illness.
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers
of competing products.
References
1. Iwashyna TJ, Ely EW, Smith DM, et al. Long-term cognitive impairment and functional disability among survivors of severe sepsis. JAMA. 2010;304(16):1787-1794.
2. Safdieh J. Cognition after sepsis. Neurology Alert. 2010; 29(4):30-31.
3. Williams GS. Older severe sepsis survivors are at risk for cognitive and developmental disability. Pulmonary Reviews. 2010;15(12):17-18.
The effect of sepsis survivorship on cognition is a substantially under-recognized public health problem.1 Sepsis survivorship has implications for patients’ families and the health care system.2 Research has demonstrated that older patients may develop impaired cognition and functional capacity after severe sepsis3; limited evidence shows neurocognitive decline in non-geriatric patients.3 There are no reports of exacerbation of psychiatric illness after severe sepsis or septic shock, and existing literature indicates that the causative factors, epidemiology, and predisposition that may worsen psychiatric illness after septic shock are poorly defined.
Case: Sepsis-induced cognitive decline?
Following an intensive care admission for septic shock, Mr. J, age 49, presents to the outpatient behavioral medicine department with worsening mood, lethargy, agitation, suicidal ideations, hallucinations, and poor work performance for 10 months. He was diagnosed with major depressive disorder 13 years prior, but has no history of hospitalization for psychiatric illness. His depressive symptoms respond well to paroxetine, 60 mg/d. Subsequently, Mr. J becomes delusional, has intense command hallucinations, and attempts suicide, resulting in hospitalization. Neuropsychological testing reveals dementia and significant psychiatric distress, including elevated levels of depression and suicidal ideation. He is stabilized with duloxetine, 90 mg/d, and quetiapine, 50 mg/d. Two years later, Mr. J still exhibits cognitive and psychiatric disturbances.
Long-term results
The underlying mechanism of septic shock on the brain may be similar to the mechanisms that exacerbate psychiatric illnesses. This case validates the use of neuropsychological testing in septic shock survivors and encourages recognition of the effect septic shock has on neuropsychiatric illness.
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers
of competing products.
References
1. Iwashyna TJ, Ely EW, Smith DM, et al. Long-term cognitive impairment and functional disability among survivors of severe sepsis. JAMA. 2010;304(16):1787-1794.
2. Safdieh J. Cognition after sepsis. Neurology Alert. 2010; 29(4):30-31.
3. Williams GS. Older severe sepsis survivors are at risk for cognitive and developmental disability. Pulmonary Reviews. 2010;15(12):17-18.
Take CAUTION in emergency and inpatient psychiatric settings
Mental health care professionals are at increased risk of being assaulted by patients, especially in emergency and inpatient settings. Less experienced clinicians are at an even higher risk: Studies estimate that up to 56% percent of psychiatric residents have been physically assaulted by a patient.1 Some researchers have examined systematic approaches to improving violence risk assessment2; however, the assessment and interview process itself poses a risk to residents and medical students. We recommend using the mnemonic CAUTION to remind clinicians about safety considerations when working in psychiatric settings.
Communication. Talking about safety should be a priority during daily rounds. Routinely ask staff and other personnel about safety concerns. In inpatient settings, post a safety board where hospital staff can record aggressive behaviors and other safety issues displayed by patients. Notify staff whenever you plan to interact with patients at risk for aggression or when a patient seems agitated.
Attire. Follow proper dress codes to ensure personal safety and improve your ability to quickly assist others in need. Avoid wearing necklaces, ties, and high heels in inpatient psychiatric units. Valuable accessories (eg, expensive wrist watches) should not be worn because they may be broken during a “take down.”
Untreated symptoms. Be aware of patients with untreated or undertreated symptoms, including psychosis or substance intoxication. Emergency room patients or newly admitted inpatients often present the greatest risk because of their untreated symptoms (eg, patients with paranoid delusions).
Threats. Patients who express threats are at significantly increased risk of assaulting someone.3 Patients who have recently voiced threats should not be engaged alone or without adequate staff support. Inform all residents and students about specific patients who have voiced threats. Agitated and threatening patients can pose a risk to everyone in the unit, regardless of whether they have worked directly with the clinician.
Impulsivity. Approach impulsive and aggressive patients with particular caution. Until the aggression is controlled, these patients are at risk for sudden assaults when they feel provoked. Warning signs include punching a wall or breaking objects on the unit, facial muscle tightening, clenching of fists, and pacing. If a patient does not respond to redirection from staff, he or she may require seclusion, emergency medications, or both.
Options. Whenever possible, provide patients with choices, especially when a patient requests discharge or demands a particular medication. Avoid taking an authoritarian stance by clarifying reasons why the patient’s requests are being denied and by providing alternatives and options. For instance, if discharge is not indicated, direct a patient to contact the patients’ rights advocate. You also can give some agitated patients the option of taking a voluntary “timeout” or going to an isolated area to calm down.
Navigate safely. Identify potential exits from the room before the encounter. Residents and medical students should have a clear understanding of where to escape from a potential assault. Also, it is important to point out to patients where the door is should they feel threatened. Do not block the door when interviewing paranoid patients.
We suggest that less experienced clinicians refer to this mnemonic before starting work in emergency and inpatient psychiatric settings. Safety is an important consideration. By considering these basic concepts, we believe that safety can be improved.
1. Antonius D, Fuchs L, Herbert F, et al. Psychiatric assessment of aggressive patients: a violent attack on a resident. Am J Psychiatry. 2010;167(3):253-259.
2.Teo AR, Holley SR, Leary M, et al. The relationship between level of training and accuracy of violence risk assessment. Psychiatr Serv. 2012;63(11):1089-1094.
3. Maier GJ. Managing threatening behavior: the role of talk down and talk up. J Psychosoc Nurs Ment Health Serv. 1996;34(6):25-30.
Mental health care professionals are at increased risk of being assaulted by patients, especially in emergency and inpatient settings. Less experienced clinicians are at an even higher risk: Studies estimate that up to 56% percent of psychiatric residents have been physically assaulted by a patient.1 Some researchers have examined systematic approaches to improving violence risk assessment2; however, the assessment and interview process itself poses a risk to residents and medical students. We recommend using the mnemonic CAUTION to remind clinicians about safety considerations when working in psychiatric settings.
Communication. Talking about safety should be a priority during daily rounds. Routinely ask staff and other personnel about safety concerns. In inpatient settings, post a safety board where hospital staff can record aggressive behaviors and other safety issues displayed by patients. Notify staff whenever you plan to interact with patients at risk for aggression or when a patient seems agitated.
Attire. Follow proper dress codes to ensure personal safety and improve your ability to quickly assist others in need. Avoid wearing necklaces, ties, and high heels in inpatient psychiatric units. Valuable accessories (eg, expensive wrist watches) should not be worn because they may be broken during a “take down.”
Untreated symptoms. Be aware of patients with untreated or undertreated symptoms, including psychosis or substance intoxication. Emergency room patients or newly admitted inpatients often present the greatest risk because of their untreated symptoms (eg, patients with paranoid delusions).
Threats. Patients who express threats are at significantly increased risk of assaulting someone.3 Patients who have recently voiced threats should not be engaged alone or without adequate staff support. Inform all residents and students about specific patients who have voiced threats. Agitated and threatening patients can pose a risk to everyone in the unit, regardless of whether they have worked directly with the clinician.
Impulsivity. Approach impulsive and aggressive patients with particular caution. Until the aggression is controlled, these patients are at risk for sudden assaults when they feel provoked. Warning signs include punching a wall or breaking objects on the unit, facial muscle tightening, clenching of fists, and pacing. If a patient does not respond to redirection from staff, he or she may require seclusion, emergency medications, or both.
Options. Whenever possible, provide patients with choices, especially when a patient requests discharge or demands a particular medication. Avoid taking an authoritarian stance by clarifying reasons why the patient’s requests are being denied and by providing alternatives and options. For instance, if discharge is not indicated, direct a patient to contact the patients’ rights advocate. You also can give some agitated patients the option of taking a voluntary “timeout” or going to an isolated area to calm down.
Navigate safely. Identify potential exits from the room before the encounter. Residents and medical students should have a clear understanding of where to escape from a potential assault. Also, it is important to point out to patients where the door is should they feel threatened. Do not block the door when interviewing paranoid patients.
We suggest that less experienced clinicians refer to this mnemonic before starting work in emergency and inpatient psychiatric settings. Safety is an important consideration. By considering these basic concepts, we believe that safety can be improved.
Mental health care professionals are at increased risk of being assaulted by patients, especially in emergency and inpatient settings. Less experienced clinicians are at an even higher risk: Studies estimate that up to 56% percent of psychiatric residents have been physically assaulted by a patient.1 Some researchers have examined systematic approaches to improving violence risk assessment2; however, the assessment and interview process itself poses a risk to residents and medical students. We recommend using the mnemonic CAUTION to remind clinicians about safety considerations when working in psychiatric settings.
Communication. Talking about safety should be a priority during daily rounds. Routinely ask staff and other personnel about safety concerns. In inpatient settings, post a safety board where hospital staff can record aggressive behaviors and other safety issues displayed by patients. Notify staff whenever you plan to interact with patients at risk for aggression or when a patient seems agitated.
Attire. Follow proper dress codes to ensure personal safety and improve your ability to quickly assist others in need. Avoid wearing necklaces, ties, and high heels in inpatient psychiatric units. Valuable accessories (eg, expensive wrist watches) should not be worn because they may be broken during a “take down.”
Untreated symptoms. Be aware of patients with untreated or undertreated symptoms, including psychosis or substance intoxication. Emergency room patients or newly admitted inpatients often present the greatest risk because of their untreated symptoms (eg, patients with paranoid delusions).
Threats. Patients who express threats are at significantly increased risk of assaulting someone.3 Patients who have recently voiced threats should not be engaged alone or without adequate staff support. Inform all residents and students about specific patients who have voiced threats. Agitated and threatening patients can pose a risk to everyone in the unit, regardless of whether they have worked directly with the clinician.
Impulsivity. Approach impulsive and aggressive patients with particular caution. Until the aggression is controlled, these patients are at risk for sudden assaults when they feel provoked. Warning signs include punching a wall or breaking objects on the unit, facial muscle tightening, clenching of fists, and pacing. If a patient does not respond to redirection from staff, he or she may require seclusion, emergency medications, or both.
Options. Whenever possible, provide patients with choices, especially when a patient requests discharge or demands a particular medication. Avoid taking an authoritarian stance by clarifying reasons why the patient’s requests are being denied and by providing alternatives and options. For instance, if discharge is not indicated, direct a patient to contact the patients’ rights advocate. You also can give some agitated patients the option of taking a voluntary “timeout” or going to an isolated area to calm down.
Navigate safely. Identify potential exits from the room before the encounter. Residents and medical students should have a clear understanding of where to escape from a potential assault. Also, it is important to point out to patients where the door is should they feel threatened. Do not block the door when interviewing paranoid patients.
We suggest that less experienced clinicians refer to this mnemonic before starting work in emergency and inpatient psychiatric settings. Safety is an important consideration. By considering these basic concepts, we believe that safety can be improved.
1. Antonius D, Fuchs L, Herbert F, et al. Psychiatric assessment of aggressive patients: a violent attack on a resident. Am J Psychiatry. 2010;167(3):253-259.
2.Teo AR, Holley SR, Leary M, et al. The relationship between level of training and accuracy of violence risk assessment. Psychiatr Serv. 2012;63(11):1089-1094.
3. Maier GJ. Managing threatening behavior: the role of talk down and talk up. J Psychosoc Nurs Ment Health Serv. 1996;34(6):25-30.
1. Antonius D, Fuchs L, Herbert F, et al. Psychiatric assessment of aggressive patients: a violent attack on a resident. Am J Psychiatry. 2010;167(3):253-259.
2.Teo AR, Holley SR, Leary M, et al. The relationship between level of training and accuracy of violence risk assessment. Psychiatr Serv. 2012;63(11):1089-1094.
3. Maier GJ. Managing threatening behavior: the role of talk down and talk up. J Psychosoc Nurs Ment Health Serv. 1996;34(6):25-30.
Adoption by mentally ill individuals: What to recommend
Ms. T, age 28, wishes to adopt a child. She has a history of bipolar disorder, but has been stable for several years. She asks her psychiatrist if her diagnosis will disqualify her as a potential parent. She also wants to know how the psychiatrist can help with the adoption process because he has been treating her long-term and is familiar with her psychiatric history.
Many adults with a history of psychiatric illness prefer to adopt rather than have biological children. Their preference may be fueled by concerns regarding psychiatric destabilization during pregnancy or fear of psychotropic-induced fetal teratogenicity. Child adoption laws vary from state to state. Although some licensed adoption agencies sympathize with potential adoptive parents with a history of mental illness, the law usually considers the following factors:
• the potential adopter’s emotional ties to the child
• their parenting skills
• emotional needs of the child
• the potential adopter’s desire to maintain continuity of the child’s care
• permanence of the family unit of the proposed home
• the physical, moral, and mental fitness of the potential parent.
The psychiatrist’s role
So long as the adoptee’s well-being is the reason for adoption, and the adoption is in the “best interest of the child,”1 a history of mental illness does not necessarily exclude an individual from adopting a child. The psychiatrist needs to consider the potential adopter’s motives, intellectual capacity, and judgment with regards to caregiving. The psychiatrist needs to assess the degree to which the patient’s mental disorder may or may not interfere with their parenting. The clinician also needs to consider potential changes that may occur in the adopter’s personal life, work hours, recreational and social activities, and sleep patterns.
It also is important to estimate the changes that an adoption may cause in the potential adopter’s living arrangements, daily schedule, and life events such as family vacations. Based on knowledge of the patient’s psychiatric history, a clinician may need to consider whether adoption-related stress could destabilize or exacerbate the potential parent’s psychiatric condition.2 Other psychosocial factors of importance are the reliability of the adopter’s support system, their history of previous child-rearing success, care-taking arrangements, etc.1
What to consider
The potential adoptee’s unique needs also should be considered. Is the child physically handicapped or mentally challenged, and is your patient capable of handling these issues? Would there be a good temperament fit between the potential adoptive parent and child?
Because child adoption laws vary from state to state, there are no established criteria for determining the eligibility of an individual with a history of mental illness. The success of a child adoption by an individual with a history of mental illness will depend on state laws and the policy of the adoption agency. Some U.S. states and territories (Alaska, Arizona, California, Kentucky, North Dakota, and Puerto Rico) regard parental mental illness as “aggravated circumstances.”1
Although psychiatrists are not expected to be able to accurately predict the future, courts and adoption agencies may request a psychiatrist’s professional opinion on a specific adoption. See the Table for a list of suggested information to share when approached by an adoption agency or court.
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Bacani-Oropilla T, Lippmann SB, Turns DM. Should the mentally ill adopt children? How physicians can influence the decision. Postgrad Med. 1988;84(6):201-205.
2. Linn L. Clinical manifestations of psychiatric disorder: the Homes-Rahe scale of stress of adjusting to change. In: Fredman A, Kaplan H, Sadock B, eds. Modern synopsis of comprehensive textbook of psychiatry, II. 2nd ed. Baltimore, MD: Williams & Wilkins; 1976:785.
Ms. T, age 28, wishes to adopt a child. She has a history of bipolar disorder, but has been stable for several years. She asks her psychiatrist if her diagnosis will disqualify her as a potential parent. She also wants to know how the psychiatrist can help with the adoption process because he has been treating her long-term and is familiar with her psychiatric history.
Many adults with a history of psychiatric illness prefer to adopt rather than have biological children. Their preference may be fueled by concerns regarding psychiatric destabilization during pregnancy or fear of psychotropic-induced fetal teratogenicity. Child adoption laws vary from state to state. Although some licensed adoption agencies sympathize with potential adoptive parents with a history of mental illness, the law usually considers the following factors:
• the potential adopter’s emotional ties to the child
• their parenting skills
• emotional needs of the child
• the potential adopter’s desire to maintain continuity of the child’s care
• permanence of the family unit of the proposed home
• the physical, moral, and mental fitness of the potential parent.
The psychiatrist’s role
So long as the adoptee’s well-being is the reason for adoption, and the adoption is in the “best interest of the child,”1 a history of mental illness does not necessarily exclude an individual from adopting a child. The psychiatrist needs to consider the potential adopter’s motives, intellectual capacity, and judgment with regards to caregiving. The psychiatrist needs to assess the degree to which the patient’s mental disorder may or may not interfere with their parenting. The clinician also needs to consider potential changes that may occur in the adopter’s personal life, work hours, recreational and social activities, and sleep patterns.
It also is important to estimate the changes that an adoption may cause in the potential adopter’s living arrangements, daily schedule, and life events such as family vacations. Based on knowledge of the patient’s psychiatric history, a clinician may need to consider whether adoption-related stress could destabilize or exacerbate the potential parent’s psychiatric condition.2 Other psychosocial factors of importance are the reliability of the adopter’s support system, their history of previous child-rearing success, care-taking arrangements, etc.1
What to consider
The potential adoptee’s unique needs also should be considered. Is the child physically handicapped or mentally challenged, and is your patient capable of handling these issues? Would there be a good temperament fit between the potential adoptive parent and child?
Because child adoption laws vary from state to state, there are no established criteria for determining the eligibility of an individual with a history of mental illness. The success of a child adoption by an individual with a history of mental illness will depend on state laws and the policy of the adoption agency. Some U.S. states and territories (Alaska, Arizona, California, Kentucky, North Dakota, and Puerto Rico) regard parental mental illness as “aggravated circumstances.”1
Although psychiatrists are not expected to be able to accurately predict the future, courts and adoption agencies may request a psychiatrist’s professional opinion on a specific adoption. See the Table for a list of suggested information to share when approached by an adoption agency or court.
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Ms. T, age 28, wishes to adopt a child. She has a history of bipolar disorder, but has been stable for several years. She asks her psychiatrist if her diagnosis will disqualify her as a potential parent. She also wants to know how the psychiatrist can help with the adoption process because he has been treating her long-term and is familiar with her psychiatric history.
Many adults with a history of psychiatric illness prefer to adopt rather than have biological children. Their preference may be fueled by concerns regarding psychiatric destabilization during pregnancy or fear of psychotropic-induced fetal teratogenicity. Child adoption laws vary from state to state. Although some licensed adoption agencies sympathize with potential adoptive parents with a history of mental illness, the law usually considers the following factors:
• the potential adopter’s emotional ties to the child
• their parenting skills
• emotional needs of the child
• the potential adopter’s desire to maintain continuity of the child’s care
• permanence of the family unit of the proposed home
• the physical, moral, and mental fitness of the potential parent.
The psychiatrist’s role
So long as the adoptee’s well-being is the reason for adoption, and the adoption is in the “best interest of the child,”1 a history of mental illness does not necessarily exclude an individual from adopting a child. The psychiatrist needs to consider the potential adopter’s motives, intellectual capacity, and judgment with regards to caregiving. The psychiatrist needs to assess the degree to which the patient’s mental disorder may or may not interfere with their parenting. The clinician also needs to consider potential changes that may occur in the adopter’s personal life, work hours, recreational and social activities, and sleep patterns.
It also is important to estimate the changes that an adoption may cause in the potential adopter’s living arrangements, daily schedule, and life events such as family vacations. Based on knowledge of the patient’s psychiatric history, a clinician may need to consider whether adoption-related stress could destabilize or exacerbate the potential parent’s psychiatric condition.2 Other psychosocial factors of importance are the reliability of the adopter’s support system, their history of previous child-rearing success, care-taking arrangements, etc.1
What to consider
The potential adoptee’s unique needs also should be considered. Is the child physically handicapped or mentally challenged, and is your patient capable of handling these issues? Would there be a good temperament fit between the potential adoptive parent and child?
Because child adoption laws vary from state to state, there are no established criteria for determining the eligibility of an individual with a history of mental illness. The success of a child adoption by an individual with a history of mental illness will depend on state laws and the policy of the adoption agency. Some U.S. states and territories (Alaska, Arizona, California, Kentucky, North Dakota, and Puerto Rico) regard parental mental illness as “aggravated circumstances.”1
Although psychiatrists are not expected to be able to accurately predict the future, courts and adoption agencies may request a psychiatrist’s professional opinion on a specific adoption. See the Table for a list of suggested information to share when approached by an adoption agency or court.
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Bacani-Oropilla T, Lippmann SB, Turns DM. Should the mentally ill adopt children? How physicians can influence the decision. Postgrad Med. 1988;84(6):201-205.
2. Linn L. Clinical manifestations of psychiatric disorder: the Homes-Rahe scale of stress of adjusting to change. In: Fredman A, Kaplan H, Sadock B, eds. Modern synopsis of comprehensive textbook of psychiatry, II. 2nd ed. Baltimore, MD: Williams & Wilkins; 1976:785.
1. Bacani-Oropilla T, Lippmann SB, Turns DM. Should the mentally ill adopt children? How physicians can influence the decision. Postgrad Med. 1988;84(6):201-205.
2. Linn L. Clinical manifestations of psychiatric disorder: the Homes-Rahe scale of stress of adjusting to change. In: Fredman A, Kaplan H, Sadock B, eds. Modern synopsis of comprehensive textbook of psychiatry, II. 2nd ed. Baltimore, MD: Williams & Wilkins; 1976:785.