Pearls

Certain clinical features of posttraumatic stress disorder (PTSD) appear in other psychiatric diagnoses and therefore can confound accurate diagnosis and treatment. PTSD is frequently comorbid with other classes of psychiatric disorders, including mood, personality, substance use, and psychotic disorders, which can further complicate diagnostic clarity. Comorbidity in PTSD is important to recognize because it has been associated with worse treatment outcomes.¹

In DSM-5, the updated criteria for PTSD included Criterion D: “Negative alterations in cognitions and mood associated with the traumatic event(s) ….”² In addition to inability to remember an important aspect of the traumatic event, this criterion may be met by developing persistent and exaggerated negative beliefs or expectations about oneself, blaming oneself or others for the event, and developing a persistent negative emotional state and decreased interest.² These characteristics overlap with DSM-5 criteria for major depressive disorder (MDD), including low self-worth, guilt, depression, and anhedonia. It is easy to imagine how one could diagnose MDD based on these features if a full history has not been obtained. Similarly, many of the elements in Criterion D overlap with the criteria for anxiety disorders, including irritable behavior, problems with concentration, and sleep disturbance. Re-experiencing symptoms can exist on a continuum with primary psychotic symptoms, and comorbid substance use disorders can add additional diagnostic complexity.

We created the mnemonic FIGHT to help remember the updated DSM-5 criteria for PTSD when considering the differential diagnosis.

Flight. Avoidant symptoms, including efforts to avoid distressing memories, thoughts, or feelings about the traumatic event, as well as avoidance of external reminders.

Intrusive symptoms, such as distressing dreams, intrusive memories, and physiological distress when exposed to cues.

Gloomy cognitions. Negative cognitions and mood associated with the traumatic event.

Hypervigilance. Alterations in arousal, such as irritability, angry outbursts, reckless behavior, and exaggerated startle response.

Trauma. Exposure to actual or threatened death, serious injury, or sexual violence.

A diagnosis of PTSD requires ≥1 month of symptoms that cause significant distress or impairment and are not attributable to the physiological effects of a substance or medical condition. Specifiers in DSM-5 include with depersonalization or derealization, as well as delayed expression.²

Vigilance in the assessment and treatment of PTSD will aid the clinician and patient in producing better care outcomes.

Certain clinical features of posttraumatic stress disorder (PTSD) appear in other psychiatric diagnoses and therefore can confound accurate diagnosis and treatment. PTSD is frequently comorbid with other classes of psychiatric disorders, including mood, personality, substance use, and psychotic disorders, which can further complicate diagnostic clarity. Comorbidity in PTSD is important to recognize because it has been associated with worse treatment outcomes.¹

In DSM-5, the updated criteria for PTSD included Criterion D: “Negative alterations in cognitions and mood associated with the traumatic event(s) ….”² In addition to inability to remember an important aspect of the traumatic event, this criterion may be met by developing persistent and exaggerated negative beliefs or expectations about oneself, blaming oneself or others for the event, and developing a persistent negative emotional state and decreased interest.² These characteristics overlap with DSM-5 criteria for major depressive disorder (MDD), including low self-worth, guilt, depression, and anhedonia. It is easy to imagine how one could diagnose MDD based on these features if a full history has not been obtained. Similarly, many of the elements in Criterion D overlap with the criteria for anxiety disorders, including irritable behavior, problems with concentration, and sleep disturbance. Re-experiencing symptoms can exist on a continuum with primary psychotic symptoms, and comorbid substance use disorders can add additional diagnostic complexity.

We created the mnemonic FIGHT to help remember the updated DSM-5 criteria for PTSD when considering the differential diagnosis.

Flight. Avoidant symptoms, including efforts to avoid distressing memories, thoughts, or feelings about the traumatic event, as well as avoidance of external reminders.

Intrusive symptoms, such as distressing dreams, intrusive memories, and physiological distress when exposed to cues.

Gloomy cognitions. Negative cognitions and mood associated with the traumatic event.

Hypervigilance. Alterations in arousal, such as irritability, angry outbursts, reckless behavior, and exaggerated startle response.

Trauma. Exposure to actual or threatened death, serious injury, or sexual violence.

A diagnosis of PTSD requires ≥1 month of symptoms that cause significant distress or impairment and are not attributable to the physiological effects of a substance or medical condition. Specifiers in DSM-5 include with depersonalization or derealization, as well as delayed expression.²

Vigilance in the assessment and treatment of PTSD will aid the clinician and patient in producing better care outcomes.

Certain clinical features of posttraumatic stress disorder (PTSD) appear in other psychiatric diagnoses and therefore can confound accurate diagnosis and treatment. PTSD is frequently comorbid with other classes of psychiatric disorders, including mood, personality, substance use, and psychotic disorders, which can further complicate diagnostic clarity. Comorbidity in PTSD is important to recognize because it has been associated with worse treatment outcomes.¹

In DSM-5, the updated criteria for PTSD included Criterion D: “Negative alterations in cognitions and mood associated with the traumatic event(s) ….”² In addition to inability to remember an important aspect of the traumatic event, this criterion may be met by developing persistent and exaggerated negative beliefs or expectations about oneself, blaming oneself or others for the event, and developing a persistent negative emotional state and decreased interest.² These characteristics overlap with DSM-5 criteria for major depressive disorder (MDD), including low self-worth, guilt, depression, and anhedonia. It is easy to imagine how one could diagnose MDD based on these features if a full history has not been obtained. Similarly, many of the elements in Criterion D overlap with the criteria for anxiety disorders, including irritable behavior, problems with concentration, and sleep disturbance. Re-experiencing symptoms can exist on a continuum with primary psychotic symptoms, and comorbid substance use disorders can add additional diagnostic complexity.

We created the mnemonic FIGHT to help remember the updated DSM-5 criteria for PTSD when considering the differential diagnosis.

Flight. Avoidant symptoms, including efforts to avoid distressing memories, thoughts, or feelings about the traumatic event, as well as avoidance of external reminders.

Intrusive symptoms, such as distressing dreams, intrusive memories, and physiological distress when exposed to cues.

Gloomy cognitions. Negative cognitions and mood associated with the traumatic event.

Hypervigilance. Alterations in arousal, such as irritability, angry outbursts, reckless behavior, and exaggerated startle response.

Trauma. Exposure to actual or threatened death, serious injury, or sexual violence.

A diagnosis of PTSD requires ≥1 month of symptoms that cause significant distress or impairment and are not attributable to the physiological effects of a substance or medical condition. Specifiers in DSM-5 include with depersonalization or derealization, as well as delayed expression.²

Vigilance in the assessment and treatment of PTSD will aid the clinician and patient in producing better care outcomes.

As psychiatrists, we all come across patients who press our buttons and engender negative feelings, such as anger, frustration, and inadequacy.¹ These patients have been referred to as “hateful” or “difficult” because they disrupt the treatment alliance.^1,2 We are quick to point our fingers at such patients for making our jobs harder, being noncompliant, resisting the therapeutic alliance, and in general, being “problem patients.”³ However, the physician–patient relationship is a 2-way street. Although our patients knowingly or unknowingly play a role in this dynamic, we could be overlooking our role in adversely affecting this relationship. The following factors influence the physician–patient bond.^1,2

Countertransference. We may have negative feelings toward a patient based on our personalities and/or if the patient reminds us of someone we may not like, which could lead us to overprescribe or under­prescribe medications, conduct unnecessary medical workups, distance ourselves from the patient, etc. Accepting our disdain for certain patients and understanding why we have these emotions will allow us to better understand them, ensure that we are not impeding the delivery of appropriate clinical care, and improve rapport.

Listening. It may seem obvious that not listening to our patients negatively impacts rapport. However, in today’s technological world, we may not be really listening to our patients even when we think we are. Answering a text message or reading the patient’s electronic medical record while they are talking to us may increase productivity, but doing so also can interfere with our ability to form a therapeutic alliance. Although we may hear what our patients are saying, such distractions can create a hurdle in listening to what they are telling us.

Empathy often is confused for sympathy. Sympathy entails expressing concern and compassion for one’s distress, whereas empathy includes recognizing and sharing the patient’s emotions. Identifying with and understanding our patients’ situations, drives, and feelings allows us to understand what they are experiencing, see why they are reacting in a negative manner, and protect them from unnecessary emotional distress. Empathy can lead us to know what needs to be said and what should be said. It also can demystify a patient’s suffering. Not providing empathy or substituting sympathy can disrupt the therapeutic alliance.

Projective identification. Patients can project intolerable and negative feelings onto us and coerce us into identifying with what has been projected, allowing them to indirectly take control of our emotions. Our subsequent reactions can unsettle the physician–patient relationship. We need to be attuned to this process and recognize what the patient is provoking within us. Once we understand the process, we can realize that this is how they deal with others under similarly stressful conditions, and then react in a more supportive and healthy manner, rather than reviling our patients and negatively impacting the therapeutic relationship.

As psychiatrists, we all come across patients who press our buttons and engender negative feelings, such as anger, frustration, and inadequacy.¹ These patients have been referred to as “hateful” or “difficult” because they disrupt the treatment alliance.^1,2 We are quick to point our fingers at such patients for making our jobs harder, being noncompliant, resisting the therapeutic alliance, and in general, being “problem patients.”³ However, the physician–patient relationship is a 2-way street. Although our patients knowingly or unknowingly play a role in this dynamic, we could be overlooking our role in adversely affecting this relationship. The following factors influence the physician–patient bond.^1,2

Countertransference. We may have negative feelings toward a patient based on our personalities and/or if the patient reminds us of someone we may not like, which could lead us to overprescribe or under­prescribe medications, conduct unnecessary medical workups, distance ourselves from the patient, etc. Accepting our disdain for certain patients and understanding why we have these emotions will allow us to better understand them, ensure that we are not impeding the delivery of appropriate clinical care, and improve rapport.

Listening. It may seem obvious that not listening to our patients negatively impacts rapport. However, in today’s technological world, we may not be really listening to our patients even when we think we are. Answering a text message or reading the patient’s electronic medical record while they are talking to us may increase productivity, but doing so also can interfere with our ability to form a therapeutic alliance. Although we may hear what our patients are saying, such distractions can create a hurdle in listening to what they are telling us.

Empathy often is confused for sympathy. Sympathy entails expressing concern and compassion for one’s distress, whereas empathy includes recognizing and sharing the patient’s emotions. Identifying with and understanding our patients’ situations, drives, and feelings allows us to understand what they are experiencing, see why they are reacting in a negative manner, and protect them from unnecessary emotional distress. Empathy can lead us to know what needs to be said and what should be said. It also can demystify a patient’s suffering. Not providing empathy or substituting sympathy can disrupt the therapeutic alliance.

Projective identification. Patients can project intolerable and negative feelings onto us and coerce us into identifying with what has been projected, allowing them to indirectly take control of our emotions. Our subsequent reactions can unsettle the physician–patient relationship. We need to be attuned to this process and recognize what the patient is provoking within us. Once we understand the process, we can realize that this is how they deal with others under similarly stressful conditions, and then react in a more supportive and healthy manner, rather than reviling our patients and negatively impacting the therapeutic relationship.

As psychiatrists, we all come across patients who press our buttons and engender negative feelings, such as anger, frustration, and inadequacy.¹ These patients have been referred to as “hateful” or “difficult” because they disrupt the treatment alliance.^1,2 We are quick to point our fingers at such patients for making our jobs harder, being noncompliant, resisting the therapeutic alliance, and in general, being “problem patients.”³ However, the physician–patient relationship is a 2-way street. Although our patients knowingly or unknowingly play a role in this dynamic, we could be overlooking our role in adversely affecting this relationship. The following factors influence the physician–patient bond.^1,2

Countertransference. We may have negative feelings toward a patient based on our personalities and/or if the patient reminds us of someone we may not like, which could lead us to overprescribe or under­prescribe medications, conduct unnecessary medical workups, distance ourselves from the patient, etc. Accepting our disdain for certain patients and understanding why we have these emotions will allow us to better understand them, ensure that we are not impeding the delivery of appropriate clinical care, and improve rapport.

Listening. It may seem obvious that not listening to our patients negatively impacts rapport. However, in today’s technological world, we may not be really listening to our patients even when we think we are. Answering a text message or reading the patient’s electronic medical record while they are talking to us may increase productivity, but doing so also can interfere with our ability to form a therapeutic alliance. Although we may hear what our patients are saying, such distractions can create a hurdle in listening to what they are telling us.

Empathy often is confused for sympathy. Sympathy entails expressing concern and compassion for one’s distress, whereas empathy includes recognizing and sharing the patient’s emotions. Identifying with and understanding our patients’ situations, drives, and feelings allows us to understand what they are experiencing, see why they are reacting in a negative manner, and protect them from unnecessary emotional distress. Empathy can lead us to know what needs to be said and what should be said. It also can demystify a patient’s suffering. Not providing empathy or substituting sympathy can disrupt the therapeutic alliance.

Projective identification. Patients can project intolerable and negative feelings onto us and coerce us into identifying with what has been projected, allowing them to indirectly take control of our emotions. Our subsequent reactions can unsettle the physician–patient relationship. We need to be attuned to this process and recognize what the patient is provoking within us. Once we understand the process, we can realize that this is how they deal with others under similarly stressful conditions, and then react in a more supportive and healthy manner, rather than reviling our patients and negatively impacting the therapeutic relationship.

Eating disorders are thought to affect only the young. Although the mean age of presentation is 17 years for anorexia nervosa and 18 to 25 years for bulimia nervosa, many women >65 years suffer from these disorders.¹ Often, geriatric patients with a history of eating disorders during their youth that partially remitted have the same disorders re-emerge during their golden years. Because many practitioners think of eating disorders as a younger person’s illness, we could miss an opportunity to help these individuals when screening our geriatric patients.

DSM-5² categorizes feeding and eating disorders as:

• binge eating disorder
• anorexia nervosa
• bulimia nervosa
• other specified feeding and eating disorders
• pica
• avoidant/restrictive food intake disorder.

Binge eating disorder’s main feature is recurrent binge eating, which is the sense that one has lost control when consuming a larger amount of food within a discrete time period than what most people might eat in the same time period. Binge eating may include eating rapidly, feeling uncomfortably full, feeling embarrassment from the amount of food consumed, eating alone and/or feeling self-disgust. Because these patients lack compensatory behaviors, such as purging, they could be at risk of obesity.

Anorexia nervosa is defined as the restriction of energy intake relative to necessary energy requirements, leading to significantly low body weight in the context of age, sex, developmental trajectory, and physical health, as well as an intense fear of gaining weight or persistent behaviors interfering with weight gain.

Bulimia nervosa is repetitive loss of control when eating large amounts of food (more than most would eat in a period), with compensatory behaviors to prevent weight gain. It is possible that the value attached to youthful slenderness leads to dissatisfaction among older women as their bodies change; binging might provide a sense of control during a time of uncertainty.

Body mass index typically is highest at middle age and slowly declines. In part, this decline is caused by a reduction in energy intake because of modifications in eating habits and lowered appetite often seen during aging. Older women eat 30% fewer calories than younger women.^3,4 Social isolation, chronic disease, and depression also contribute to diminished food intake. It is important to remember that distorted body image can occur in older individuals as well. Anorexia nervosa has the highest fatality rate among psychiatric conditions,⁵ and geriatric patients could be at particularly high risk.

Assessment

Assess for eating disorders in a geriatric patient by exploring the patient’s perception of body image and ruling out underlying causes of weight loss and medical comorbidities. Take a detailed history, including:

• body image and disordered thinking about food
• abnormal behaviors or rituals surrounding food
• history of eating disorders, psychiatric illness, or hospitalization
• medical history
• current and past medications
• illicit drug use or addiction to prescription medications.

Collateral informants, such as partners and adult children of the patient, may yield important information. Because geriatric patients often take several medications, contacting the primary care physician is important in the integrated care of the patient.

A thorough physical and mental status examination will provide information about the patient’s physical appearance. For example, if the patient appears emaciated or weak, the content and process of thoughts related to food will help rule out other etiologies, such as psychosis, depressive disorders, or anxiety. Vital signs and a full physical examination are needed when caring for patients with an eating disorder, regardless of age, but particularly in medically fragile geriatric patients. Because osteoporosis and osteopenia are concerns for many older patients, it’s important to collaborate with the primary care physician early to help minimize bone loss.

Treatment

While ensuring medical stability of the patient, psychotherapy is the treatment of choice for eating disorders in geriatric patients. Moderate to severe binge eating disorder can be treated with lisdexamfetamine. For bulimia nervosa, consider a combination of SSRI and psychotherapy. There is no FDA-approved medication for treating anorexia nervosa; therefore identifying and treating underlying medical causes and/or psychiatric comorbidities can help improve prognosis. Despite this, 1 study showed 20% of geriatric patients with an eating disorder die of complications from eating disorders.⁶

Eating disorders are thought to affect only the young. Although the mean age of presentation is 17 years for anorexia nervosa and 18 to 25 years for bulimia nervosa, many women >65 years suffer from these disorders.¹ Often, geriatric patients with a history of eating disorders during their youth that partially remitted have the same disorders re-emerge during their golden years. Because many practitioners think of eating disorders as a younger person’s illness, we could miss an opportunity to help these individuals when screening our geriatric patients.

DSM-5² categorizes feeding and eating disorders as:

• binge eating disorder
• anorexia nervosa
• bulimia nervosa
• other specified feeding and eating disorders
• pica
• avoidant/restrictive food intake disorder.

Binge eating disorder’s main feature is recurrent binge eating, which is the sense that one has lost control when consuming a larger amount of food within a discrete time period than what most people might eat in the same time period. Binge eating may include eating rapidly, feeling uncomfortably full, feeling embarrassment from the amount of food consumed, eating alone and/or feeling self-disgust. Because these patients lack compensatory behaviors, such as purging, they could be at risk of obesity.

Anorexia nervosa is defined as the restriction of energy intake relative to necessary energy requirements, leading to significantly low body weight in the context of age, sex, developmental trajectory, and physical health, as well as an intense fear of gaining weight or persistent behaviors interfering with weight gain.

Bulimia nervosa is repetitive loss of control when eating large amounts of food (more than most would eat in a period), with compensatory behaviors to prevent weight gain. It is possible that the value attached to youthful slenderness leads to dissatisfaction among older women as their bodies change; binging might provide a sense of control during a time of uncertainty.

Body mass index typically is highest at middle age and slowly declines. In part, this decline is caused by a reduction in energy intake because of modifications in eating habits and lowered appetite often seen during aging. Older women eat 30% fewer calories than younger women.^3,4 Social isolation, chronic disease, and depression also contribute to diminished food intake. It is important to remember that distorted body image can occur in older individuals as well. Anorexia nervosa has the highest fatality rate among psychiatric conditions,⁵ and geriatric patients could be at particularly high risk.

Assessment

Assess for eating disorders in a geriatric patient by exploring the patient’s perception of body image and ruling out underlying causes of weight loss and medical comorbidities. Take a detailed history, including:

• body image and disordered thinking about food
• abnormal behaviors or rituals surrounding food
• history of eating disorders, psychiatric illness, or hospitalization
• medical history
• current and past medications
• illicit drug use or addiction to prescription medications.

Collateral informants, such as partners and adult children of the patient, may yield important information. Because geriatric patients often take several medications, contacting the primary care physician is important in the integrated care of the patient.

A thorough physical and mental status examination will provide information about the patient’s physical appearance. For example, if the patient appears emaciated or weak, the content and process of thoughts related to food will help rule out other etiologies, such as psychosis, depressive disorders, or anxiety. Vital signs and a full physical examination are needed when caring for patients with an eating disorder, regardless of age, but particularly in medically fragile geriatric patients. Because osteoporosis and osteopenia are concerns for many older patients, it’s important to collaborate with the primary care physician early to help minimize bone loss.

Treatment

While ensuring medical stability of the patient, psychotherapy is the treatment of choice for eating disorders in geriatric patients. Moderate to severe binge eating disorder can be treated with lisdexamfetamine. For bulimia nervosa, consider a combination of SSRI and psychotherapy. There is no FDA-approved medication for treating anorexia nervosa; therefore identifying and treating underlying medical causes and/or psychiatric comorbidities can help improve prognosis. Despite this, 1 study showed 20% of geriatric patients with an eating disorder die of complications from eating disorders.⁶

Eating disorders are thought to affect only the young. Although the mean age of presentation is 17 years for anorexia nervosa and 18 to 25 years for bulimia nervosa, many women >65 years suffer from these disorders.¹ Often, geriatric patients with a history of eating disorders during their youth that partially remitted have the same disorders re-emerge during their golden years. Because many practitioners think of eating disorders as a younger person’s illness, we could miss an opportunity to help these individuals when screening our geriatric patients.

DSM-5² categorizes feeding and eating disorders as:

• binge eating disorder
• anorexia nervosa
• bulimia nervosa
• other specified feeding and eating disorders
• pica
• avoidant/restrictive food intake disorder.

Binge eating disorder’s main feature is recurrent binge eating, which is the sense that one has lost control when consuming a larger amount of food within a discrete time period than what most people might eat in the same time period. Binge eating may include eating rapidly, feeling uncomfortably full, feeling embarrassment from the amount of food consumed, eating alone and/or feeling self-disgust. Because these patients lack compensatory behaviors, such as purging, they could be at risk of obesity.

Anorexia nervosa is defined as the restriction of energy intake relative to necessary energy requirements, leading to significantly low body weight in the context of age, sex, developmental trajectory, and physical health, as well as an intense fear of gaining weight or persistent behaviors interfering with weight gain.

Bulimia nervosa is repetitive loss of control when eating large amounts of food (more than most would eat in a period), with compensatory behaviors to prevent weight gain. It is possible that the value attached to youthful slenderness leads to dissatisfaction among older women as their bodies change; binging might provide a sense of control during a time of uncertainty.

Body mass index typically is highest at middle age and slowly declines. In part, this decline is caused by a reduction in energy intake because of modifications in eating habits and lowered appetite often seen during aging. Older women eat 30% fewer calories than younger women.^3,4 Social isolation, chronic disease, and depression also contribute to diminished food intake. It is important to remember that distorted body image can occur in older individuals as well. Anorexia nervosa has the highest fatality rate among psychiatric conditions,⁵ and geriatric patients could be at particularly high risk.

Assessment

Assess for eating disorders in a geriatric patient by exploring the patient’s perception of body image and ruling out underlying causes of weight loss and medical comorbidities. Take a detailed history, including:

• body image and disordered thinking about food
• abnormal behaviors or rituals surrounding food
• history of eating disorders, psychiatric illness, or hospitalization
• medical history
• current and past medications
• illicit drug use or addiction to prescription medications.

Collateral informants, such as partners and adult children of the patient, may yield important information. Because geriatric patients often take several medications, contacting the primary care physician is important in the integrated care of the patient.

A thorough physical and mental status examination will provide information about the patient’s physical appearance. For example, if the patient appears emaciated or weak, the content and process of thoughts related to food will help rule out other etiologies, such as psychosis, depressive disorders, or anxiety. Vital signs and a full physical examination are needed when caring for patients with an eating disorder, regardless of age, but particularly in medically fragile geriatric patients. Because osteoporosis and osteopenia are concerns for many older patients, it’s important to collaborate with the primary care physician early to help minimize bone loss.

Treatment

While ensuring medical stability of the patient, psychotherapy is the treatment of choice for eating disorders in geriatric patients. Moderate to severe binge eating disorder can be treated with lisdexamfetamine. For bulimia nervosa, consider a combination of SSRI and psychotherapy. There is no FDA-approved medication for treating anorexia nervosa; therefore identifying and treating underlying medical causes and/or psychiatric comorbidities can help improve prognosis. Despite this, 1 study showed 20% of geriatric patients with an eating disorder die of complications from eating disorders.⁶

Somatization is the experience of psychological distress in the form of bodily symptoms. Somatic symptom and related disorders frequently prompt psychiatric consultation. Patients with suspected somatization disorders might resist psychiatric intervention, therefore modified approaches to the initial interview are helpful. Here I present an approach to such resistance.

Collecting a detailed history of physical symptoms can help the patient feel that you are listening to him (her) and that the chief concern is important. A detailed review of psychiatric symptoms (eg, hallucinations, paranoia, suicidality, etc.) should be deferred until later in the examination. Asking questions relating to psychiatric symptoms early could lead to further resistance by reinforcing negative preconceptions that the patient might have regarding mental illness.

Explicitly express empathy regarding physical symptoms throughout the interview to acknowledge any real suffering the patient is experiencing and to contradict any notion that psychiatric evaluation implies that the suffering could be imaginary.

Ask, “How has this illness affected your life?” This question helps make the connection between the patient’s physical state and social milieu. If somatization is confirmed, then the provider should assist the patient in reversing the arrow of causation. Although the ultimate goal is for the patient to understand how his (her) life has affected the symptoms, simply understanding that there are connections between the two is a start toward this goal.¹

Explore the response to the previous question. Expand upon it to elicit a detailed social history, listening for any social stressors.

Obtain family and personal histories of allergies, substance abuse, and medical or psychiatric illness.

Review psychiatric symptoms. Make questions less jarring² by adapting them to the patient’s situation, such as “Has your illness become so painful that at times you don’t even want to live?”

Perform cognitive and physical examinations. Conducting a physical examination could further reassure the patient that you are not ignoring physical complaints.

Educate the patient that the mind and body are connected and emotions affect how one feels physically. Use examples, such as “When I feel anxious, my heart beats faster” or “A headache might hurt more at work than at the beach.”

Elicit feedback and questions from the patient.

Discuss your treatment plan with the patient. Resistant patients with confirmed somatization disorders might accept psychiatric care as a means of dealing with the stress or pain of their physical symptoms.

Consider asking:

• What would you be doing if you weren’t in the hospital right now?
• Aside from your health, what’s the biggest challenge in your life?
• Everything has a good side and a bad side. Is there anything positive about dealing with your illness? Providing the patient with an example of negative aspects of a good thing (such as the calories in ice cream, the high cost of gold, etc.) can help make this point.
• What would your life look like if you didn’t have these symptoms?

Somatization is the experience of psychological distress in the form of bodily symptoms. Somatic symptom and related disorders frequently prompt psychiatric consultation. Patients with suspected somatization disorders might resist psychiatric intervention, therefore modified approaches to the initial interview are helpful. Here I present an approach to such resistance.

Collecting a detailed history of physical symptoms can help the patient feel that you are listening to him (her) and that the chief concern is important. A detailed review of psychiatric symptoms (eg, hallucinations, paranoia, suicidality, etc.) should be deferred until later in the examination. Asking questions relating to psychiatric symptoms early could lead to further resistance by reinforcing negative preconceptions that the patient might have regarding mental illness.

Explicitly express empathy regarding physical symptoms throughout the interview to acknowledge any real suffering the patient is experiencing and to contradict any notion that psychiatric evaluation implies that the suffering could be imaginary.

Ask, “How has this illness affected your life?” This question helps make the connection between the patient’s physical state and social milieu. If somatization is confirmed, then the provider should assist the patient in reversing the arrow of causation. Although the ultimate goal is for the patient to understand how his (her) life has affected the symptoms, simply understanding that there are connections between the two is a start toward this goal.¹

Explore the response to the previous question. Expand upon it to elicit a detailed social history, listening for any social stressors.

Obtain family and personal histories of allergies, substance abuse, and medical or psychiatric illness.

Review psychiatric symptoms. Make questions less jarring² by adapting them to the patient’s situation, such as “Has your illness become so painful that at times you don’t even want to live?”

Perform cognitive and physical examinations. Conducting a physical examination could further reassure the patient that you are not ignoring physical complaints.

Educate the patient that the mind and body are connected and emotions affect how one feels physically. Use examples, such as “When I feel anxious, my heart beats faster” or “A headache might hurt more at work than at the beach.”

Elicit feedback and questions from the patient.

Discuss your treatment plan with the patient. Resistant patients with confirmed somatization disorders might accept psychiatric care as a means of dealing with the stress or pain of their physical symptoms.

Consider asking:

• What would you be doing if you weren’t in the hospital right now?
• Aside from your health, what’s the biggest challenge in your life?
• Everything has a good side and a bad side. Is there anything positive about dealing with your illness? Providing the patient with an example of negative aspects of a good thing (such as the calories in ice cream, the high cost of gold, etc.) can help make this point.
• What would your life look like if you didn’t have these symptoms?

Somatization is the experience of psychological distress in the form of bodily symptoms. Somatic symptom and related disorders frequently prompt psychiatric consultation. Patients with suspected somatization disorders might resist psychiatric intervention, therefore modified approaches to the initial interview are helpful. Here I present an approach to such resistance.

Collecting a detailed history of physical symptoms can help the patient feel that you are listening to him (her) and that the chief concern is important. A detailed review of psychiatric symptoms (eg, hallucinations, paranoia, suicidality, etc.) should be deferred until later in the examination. Asking questions relating to psychiatric symptoms early could lead to further resistance by reinforcing negative preconceptions that the patient might have regarding mental illness.

Explicitly express empathy regarding physical symptoms throughout the interview to acknowledge any real suffering the patient is experiencing and to contradict any notion that psychiatric evaluation implies that the suffering could be imaginary.

Ask, “How has this illness affected your life?” This question helps make the connection between the patient’s physical state and social milieu. If somatization is confirmed, then the provider should assist the patient in reversing the arrow of causation. Although the ultimate goal is for the patient to understand how his (her) life has affected the symptoms, simply understanding that there are connections between the two is a start toward this goal.¹

Explore the response to the previous question. Expand upon it to elicit a detailed social history, listening for any social stressors.

Obtain family and personal histories of allergies, substance abuse, and medical or psychiatric illness.

Review psychiatric symptoms. Make questions less jarring² by adapting them to the patient’s situation, such as “Has your illness become so painful that at times you don’t even want to live?”

Perform cognitive and physical examinations. Conducting a physical examination could further reassure the patient that you are not ignoring physical complaints.

Educate the patient that the mind and body are connected and emotions affect how one feels physically. Use examples, such as “When I feel anxious, my heart beats faster” or “A headache might hurt more at work than at the beach.”

Elicit feedback and questions from the patient.

Discuss your treatment plan with the patient. Resistant patients with confirmed somatization disorders might accept psychiatric care as a means of dealing with the stress or pain of their physical symptoms.

Consider asking:

• What would you be doing if you weren’t in the hospital right now?
• Aside from your health, what’s the biggest challenge in your life?
• Everything has a good side and a bad side. Is there anything positive about dealing with your illness? Providing the patient with an example of negative aspects of a good thing (such as the calories in ice cream, the high cost of gold, etc.) can help make this point.
• What would your life look like if you didn’t have these symptoms?

Acupuncture is an ancient therapeutic tool known to be the core of traditional Chinese medicine. Two theories suggest positive outcomes in patients treated with acupuncture:

• The oxidative stress reduction theory states that a “large body of evidences demonstrated that acupuncture has [an] antioxidative effect in various diseases, but the exact mechanism remains unclear.”¹
• The neurophysiological theory states that “acupuncture stimulation can facilitate the release of certain neuropeptides in the CNS, eliciting profound physiological effects and even activating self-healing mechanisms.”²

For decades, acupuncture has been used for addiction management. Here we provide information on its utility for patients with substance use disorders.

Opioid use disorder. Multiple studies have looked at withdrawal, comorbid mood disorders, and its management with acupuncture alone or in combination with psychotherapy and/or opioid agonists. Studies from Asia reported good treatment outcomes but had low-method quality.³ Western studies had superior method quality but found that acupuncture was no better than placebo as monotherapy. When acupuncture is combined with psychotherapy and an opioid agonist, treatment results are promising, showing faster taper of medications (methadone and buprenorphine/naloxone) with fewer adverse effects.

Cocaine use disorder. Most studies had poor treatment outcomes of acupuncture over placebo and were of low quality. A number of small studies were promising and found that patients treated with acupuncture were most likely to have a negative urine drug screen.³ Although acupuncture is widely used in the United States to treat cocaine dependence, evidence does not confirm its efficacy.

Tobacco use disorder. A small group of studies favored acupuncture for smoking cessation.³ Other studies reported no benefit compared with placebo or neutral results. Some studies agreed that any intervention (acupuncture or sham acupuncture) with good results is better than no intervention at all.

Alcohol use disorder. Almost no advantage over placebo was found. Studies with significant findings were in small populations.³

Amphetamine, Cannabis, and other hallucinogen use disorders. Available data on stimulants were too limited to be relevant. No studies were found on Cannabis and hallucinogens.

Further studies are needed

There is a lack of conclusive, good quality studies supporting acupuncture’s benefits in treating substance abuse. Acupuncture has been known to lack adverse effects other than those related to needle manipulation, which is dependent on the methods (depth of needle insertion, accurate anatomical location, angle, etc.). Because this treatment option is virtually side-effect free, inexpensive, with positive synergistic results, more high-method quality studies are needed to consider it for our patients.

Acupuncture is an ancient therapeutic tool known to be the core of traditional Chinese medicine. Two theories suggest positive outcomes in patients treated with acupuncture:

• The oxidative stress reduction theory states that a “large body of evidences demonstrated that acupuncture has [an] antioxidative effect in various diseases, but the exact mechanism remains unclear.”¹
• The neurophysiological theory states that “acupuncture stimulation can facilitate the release of certain neuropeptides in the CNS, eliciting profound physiological effects and even activating self-healing mechanisms.”²

For decades, acupuncture has been used for addiction management. Here we provide information on its utility for patients with substance use disorders.

Opioid use disorder. Multiple studies have looked at withdrawal, comorbid mood disorders, and its management with acupuncture alone or in combination with psychotherapy and/or opioid agonists. Studies from Asia reported good treatment outcomes but had low-method quality.³ Western studies had superior method quality but found that acupuncture was no better than placebo as monotherapy. When acupuncture is combined with psychotherapy and an opioid agonist, treatment results are promising, showing faster taper of medications (methadone and buprenorphine/naloxone) with fewer adverse effects.

Cocaine use disorder. Most studies had poor treatment outcomes of acupuncture over placebo and were of low quality. A number of small studies were promising and found that patients treated with acupuncture were most likely to have a negative urine drug screen.³ Although acupuncture is widely used in the United States to treat cocaine dependence, evidence does not confirm its efficacy.

Tobacco use disorder. A small group of studies favored acupuncture for smoking cessation.³ Other studies reported no benefit compared with placebo or neutral results. Some studies agreed that any intervention (acupuncture or sham acupuncture) with good results is better than no intervention at all.

Alcohol use disorder. Almost no advantage over placebo was found. Studies with significant findings were in small populations.³

Amphetamine, Cannabis, and other hallucinogen use disorders. Available data on stimulants were too limited to be relevant. No studies were found on Cannabis and hallucinogens.

Further studies are needed

There is a lack of conclusive, good quality studies supporting acupuncture’s benefits in treating substance abuse. Acupuncture has been known to lack adverse effects other than those related to needle manipulation, which is dependent on the methods (depth of needle insertion, accurate anatomical location, angle, etc.). Because this treatment option is virtually side-effect free, inexpensive, with positive synergistic results, more high-method quality studies are needed to consider it for our patients.

Acupuncture is an ancient therapeutic tool known to be the core of traditional Chinese medicine. Two theories suggest positive outcomes in patients treated with acupuncture:

• The oxidative stress reduction theory states that a “large body of evidences demonstrated that acupuncture has [an] antioxidative effect in various diseases, but the exact mechanism remains unclear.”¹
• The neurophysiological theory states that “acupuncture stimulation can facilitate the release of certain neuropeptides in the CNS, eliciting profound physiological effects and even activating self-healing mechanisms.”²

For decades, acupuncture has been used for addiction management. Here we provide information on its utility for patients with substance use disorders.

Opioid use disorder. Multiple studies have looked at withdrawal, comorbid mood disorders, and its management with acupuncture alone or in combination with psychotherapy and/or opioid agonists. Studies from Asia reported good treatment outcomes but had low-method quality.³ Western studies had superior method quality but found that acupuncture was no better than placebo as monotherapy. When acupuncture is combined with psychotherapy and an opioid agonist, treatment results are promising, showing faster taper of medications (methadone and buprenorphine/naloxone) with fewer adverse effects.

Cocaine use disorder. Most studies had poor treatment outcomes of acupuncture over placebo and were of low quality. A number of small studies were promising and found that patients treated with acupuncture were most likely to have a negative urine drug screen.³ Although acupuncture is widely used in the United States to treat cocaine dependence, evidence does not confirm its efficacy.

Tobacco use disorder. A small group of studies favored acupuncture for smoking cessation.³ Other studies reported no benefit compared with placebo or neutral results. Some studies agreed that any intervention (acupuncture or sham acupuncture) with good results is better than no intervention at all.

Alcohol use disorder. Almost no advantage over placebo was found. Studies with significant findings were in small populations.³

Amphetamine, Cannabis, and other hallucinogen use disorders. Available data on stimulants were too limited to be relevant. No studies were found on Cannabis and hallucinogens.

Further studies are needed

There is a lack of conclusive, good quality studies supporting acupuncture’s benefits in treating substance abuse. Acupuncture has been known to lack adverse effects other than those related to needle manipulation, which is dependent on the methods (depth of needle insertion, accurate anatomical location, angle, etc.). Because this treatment option is virtually side-effect free, inexpensive, with positive synergistic results, more high-method quality studies are needed to consider it for our patients.

Asthma medications comprise several drug classes, including leukotriene antagonists and steroid-based inhalers. These drugs have been implicated in behavioral changes, such as increased hyperactivity, similar to symptoms of attention-deficit/hyperactivity disorder (ADHD) and oppositional defiant disorder (ODD)¹; this scenario is more of a concern in children than adults. This raises the question of whether these medications are physiologically linked to behavioral symptoms because of a suggested association with serotonin.^2,3 If this is the case, it is necessary to identify and evaluate possible psychiatric effects of these asthma agents.

How asthma medications work

Some asthma agents, such as montelukast, act as either leukotriene-related enzyme inhibitors (arachidonate 5-lipoxygenase) or leukotriene receptor antagonists. These drugs block production of inflammatory leukotrienes, which cause bronchoconstriction. Leukotrienes also can trigger cytokine synthesis, which can modulate leukotriene receptor function. Therefore, leukotriene antagonists could interfere with cytokine function.^3,4

Corticosteroid inhalers suppress inflammatory genes by reversing histone acetylation of inflammatory genes involved in asthma. These inhalers have been shown to reduce cytokine levels in patients with chronic lung disease and those with moderate to severe asthma.^5,6 Corticosteroids also have been associated with a decrease in serotonin levels, which could contribute to depression.⁷

Possible link between asthma and serotonin

Serotonin plays an integral role in observable, dysfunctional behaviors seen in disorders such as ADHD and ODD. In previous studies, serotonin modulated the cytokine network, and patients with asthma had elevated levels of plasma serotonin.^2,3 These findings imply that asthma medications could be involved in altering levels of both cytokines and serotonin. Pretorius² emphasized the importance of monitoring serotonin levels in children who exhibit behavioral dysfunction based on these observations:

• Persons with asthma presenting with medical symptoms have elevated serotonin levels.
• Decreased serotonin levels have been associated with ADHD and ODD; medications for ADHD have been shown to increase serotonin levels.
• Asthma medications have been shown to decrease serotonin levels.^2,3

Asthma medications might be partially responsible for behavioral disturbances, and therapeutic management should integrate the role of serotonin with asthma therapy.^2,3

Clinical considerations

Therapeutic management of asthma should consider psychiatric conditions and treatments. Future research should investigate the overall predisposition for behavioral dysfunction in persons with respiratory syncytial virus, a precursor for asthma. Once an asthma patient’s risk of a psychiatric disorder has been identified, the clinician can determine the most effective medications for treating the condition. If potential medications or genetic or environmental factors are identified, we might expect a move toward personalized care in the not too distant future.

Asthma medications comprise several drug classes, including leukotriene antagonists and steroid-based inhalers. These drugs have been implicated in behavioral changes, such as increased hyperactivity, similar to symptoms of attention-deficit/hyperactivity disorder (ADHD) and oppositional defiant disorder (ODD)¹; this scenario is more of a concern in children than adults. This raises the question of whether these medications are physiologically linked to behavioral symptoms because of a suggested association with serotonin.^2,3 If this is the case, it is necessary to identify and evaluate possible psychiatric effects of these asthma agents.

How asthma medications work

Some asthma agents, such as montelukast, act as either leukotriene-related enzyme inhibitors (arachidonate 5-lipoxygenase) or leukotriene receptor antagonists. These drugs block production of inflammatory leukotrienes, which cause bronchoconstriction. Leukotrienes also can trigger cytokine synthesis, which can modulate leukotriene receptor function. Therefore, leukotriene antagonists could interfere with cytokine function.^3,4

Corticosteroid inhalers suppress inflammatory genes by reversing histone acetylation of inflammatory genes involved in asthma. These inhalers have been shown to reduce cytokine levels in patients with chronic lung disease and those with moderate to severe asthma.^5,6 Corticosteroids also have been associated with a decrease in serotonin levels, which could contribute to depression.⁷

Possible link between asthma and serotonin

Serotonin plays an integral role in observable, dysfunctional behaviors seen in disorders such as ADHD and ODD. In previous studies, serotonin modulated the cytokine network, and patients with asthma had elevated levels of plasma serotonin.^2,3 These findings imply that asthma medications could be involved in altering levels of both cytokines and serotonin. Pretorius² emphasized the importance of monitoring serotonin levels in children who exhibit behavioral dysfunction based on these observations:

• Persons with asthma presenting with medical symptoms have elevated serotonin levels.
• Decreased serotonin levels have been associated with ADHD and ODD; medications for ADHD have been shown to increase serotonin levels.
• Asthma medications have been shown to decrease serotonin levels.^2,3

Asthma medications might be partially responsible for behavioral disturbances, and therapeutic management should integrate the role of serotonin with asthma therapy.^2,3

Clinical considerations

Therapeutic management of asthma should consider psychiatric conditions and treatments. Future research should investigate the overall predisposition for behavioral dysfunction in persons with respiratory syncytial virus, a precursor for asthma. Once an asthma patient’s risk of a psychiatric disorder has been identified, the clinician can determine the most effective medications for treating the condition. If potential medications or genetic or environmental factors are identified, we might expect a move toward personalized care in the not too distant future.

Asthma medications comprise several drug classes, including leukotriene antagonists and steroid-based inhalers. These drugs have been implicated in behavioral changes, such as increased hyperactivity, similar to symptoms of attention-deficit/hyperactivity disorder (ADHD) and oppositional defiant disorder (ODD)¹; this scenario is more of a concern in children than adults. This raises the question of whether these medications are physiologically linked to behavioral symptoms because of a suggested association with serotonin.^2,3 If this is the case, it is necessary to identify and evaluate possible psychiatric effects of these asthma agents.

How asthma medications work

Some asthma agents, such as montelukast, act as either leukotriene-related enzyme inhibitors (arachidonate 5-lipoxygenase) or leukotriene receptor antagonists. These drugs block production of inflammatory leukotrienes, which cause bronchoconstriction. Leukotrienes also can trigger cytokine synthesis, which can modulate leukotriene receptor function. Therefore, leukotriene antagonists could interfere with cytokine function.^3,4

Corticosteroid inhalers suppress inflammatory genes by reversing histone acetylation of inflammatory genes involved in asthma. These inhalers have been shown to reduce cytokine levels in patients with chronic lung disease and those with moderate to severe asthma.^5,6 Corticosteroids also have been associated with a decrease in serotonin levels, which could contribute to depression.⁷

Possible link between asthma and serotonin

Serotonin plays an integral role in observable, dysfunctional behaviors seen in disorders such as ADHD and ODD. In previous studies, serotonin modulated the cytokine network, and patients with asthma had elevated levels of plasma serotonin.^2,3 These findings imply that asthma medications could be involved in altering levels of both cytokines and serotonin. Pretorius² emphasized the importance of monitoring serotonin levels in children who exhibit behavioral dysfunction based on these observations:

• Persons with asthma presenting with medical symptoms have elevated serotonin levels.
• Decreased serotonin levels have been associated with ADHD and ODD; medications for ADHD have been shown to increase serotonin levels.
• Asthma medications have been shown to decrease serotonin levels.^2,3

Asthma medications might be partially responsible for behavioral disturbances, and therapeutic management should integrate the role of serotonin with asthma therapy.^2,3

Clinical considerations

Therapeutic management of asthma should consider psychiatric conditions and treatments. Future research should investigate the overall predisposition for behavioral dysfunction in persons with respiratory syncytial virus, a precursor for asthma. Once an asthma patient’s risk of a psychiatric disorder has been identified, the clinician can determine the most effective medications for treating the condition. If potential medications or genetic or environmental factors are identified, we might expect a move toward personalized care in the not too distant future.

Taking over the care of a patient with a complex medication regimen consisting of multiple psycho­tropics is a common experience for many practicing psychiatrists. Increasing attention has been paid to the risks of polypharmacy and the importance of “deprescribing”—reducing or stopping medication—when the risks of a drug outweigh the benefits.^1,2 However, successfully reducing medication burden can be a challenge, particularly when there is fear of decompensation or if the patient is psycho­logically attached to the complex medication regimen.

We describe a pragmatic approach to deprescribing, outlining 6 steps that we have used successfully in several treatment settings, which can assist prescribers facing similar challenges in their own practices.

1. Obtain a detailed history. First compile a comprehensive list of the patient’s medications, including psychotropics, other drugs, and supplements. If necessary, coordinate with your patient’s primary care provider. Then reassess the patient’s history of illness and efficacy of pharmacologic and non-pharmacologic treatments and how the current regimen has evolved. Understand the patient’s course of illness, coping styles, strengths, and vulnerabilities with an eye toward deprescribing.

2. Investigate underlying meaning. Even the most biologically oriented prescribers can benefit from exploring the underlying meaning the patient ascribes to the medication regimen. Common themes include:

• hesitation to relinquish a complex medication regimen because the patient fears decompensation (which could be either realistic or unrealistic)
• attachment to the “sick role”
• interpreting the complex regimen as evidence of the provider’s care and concern.

A series of sensitive conversations exploring these factors and addressing their underlying meaning can help increase a patient’s trust in the process of deprescribing.

3. Assess risk vs benefit. Weigh and educate the patient on the potential risks and benefits of each medication, as well as drug interactions and additive side effects.

4. Start with:
The most risky. Medications with significant risk for serious adverse effects (eg, high doses of a QTc-prolonging medication in a patient with elevated QTc) should be targeted early.

The least likely to be missed. If there are no high-risk medications that need to take priority, discontinuation of a “redundant” medication, such as a low-dose anti­histamine prescribed with multiple other sedating medications, can be an achievable first step. By starting with a medication that the patient is unlikely to miss, the provider can make efficient initial progress while building patient confidence in the deprescribing process.

Medication the patient is most motivated to discontinue. This strategy can enhance the therapeutic alliance and increase the likelihood of successful patient engagement for patients hesitant to decrease medications, so long as there are no significant contraindications to discontinuing the medication.

5. Go slowly. As long as there are no medications that put the patient at risk and require rapid discontinuation, going slowly increases the likelihood of long-term success by:

• permitting careful monitoring for any worsening symptoms
• allowing more time for physiologic readjustment
• enabling the patient and provider to build confidence in the process over time.

With slow discontinuation, normal emotions, such as transient, situationally appropriate anxiety about a life stressor, are less likely to be misinterpreted by the patient or provider as an inability to tolerate medication reduction because there is more opportunity to observe overall trends in symptoms.

6. Replace medications with alternatives. Offering non-pharmacological treatment when possible can greatly facilitate reducing the number of medications. Examples include:

• teaching a patient breathing exercises or mindfulness while preparing to decrease an as needed anxiolytic
• engaging the patient in cognitive-behavioral therapy for insomnia before reducing sleep medications
• working together to identify opportunities for behavioral activation and exercises that are the most achievable for the patient.

This replacement strategy can work in a physiologic sense and address a patient’s fear that medications are “taken away” without alternatives in place.

Although these strategies might not work for every patient and are not recommended for reducing medications that are medically necessary, using this approach will increase the likelihood of long-term success and maintain the patient–provider alliance when reducing unnecessary and potentially risky polypharmacy. An article by Gupta and Cahill¹ describes some similar approaches with additional discussion and considerations.

Taking over the care of a patient with a complex medication regimen consisting of multiple psycho­tropics is a common experience for many practicing psychiatrists. Increasing attention has been paid to the risks of polypharmacy and the importance of “deprescribing”—reducing or stopping medication—when the risks of a drug outweigh the benefits.^1,2 However, successfully reducing medication burden can be a challenge, particularly when there is fear of decompensation or if the patient is psycho­logically attached to the complex medication regimen.

We describe a pragmatic approach to deprescribing, outlining 6 steps that we have used successfully in several treatment settings, which can assist prescribers facing similar challenges in their own practices.

1. Obtain a detailed history. First compile a comprehensive list of the patient’s medications, including psychotropics, other drugs, and supplements. If necessary, coordinate with your patient’s primary care provider. Then reassess the patient’s history of illness and efficacy of pharmacologic and non-pharmacologic treatments and how the current regimen has evolved. Understand the patient’s course of illness, coping styles, strengths, and vulnerabilities with an eye toward deprescribing.

2. Investigate underlying meaning. Even the most biologically oriented prescribers can benefit from exploring the underlying meaning the patient ascribes to the medication regimen. Common themes include:

• hesitation to relinquish a complex medication regimen because the patient fears decompensation (which could be either realistic or unrealistic)
• attachment to the “sick role”
• interpreting the complex regimen as evidence of the provider’s care and concern.

A series of sensitive conversations exploring these factors and addressing their underlying meaning can help increase a patient’s trust in the process of deprescribing.

3. Assess risk vs benefit. Weigh and educate the patient on the potential risks and benefits of each medication, as well as drug interactions and additive side effects.

4. Start with:
The most risky. Medications with significant risk for serious adverse effects (eg, high doses of a QTc-prolonging medication in a patient with elevated QTc) should be targeted early.

The least likely to be missed. If there are no high-risk medications that need to take priority, discontinuation of a “redundant” medication, such as a low-dose anti­histamine prescribed with multiple other sedating medications, can be an achievable first step. By starting with a medication that the patient is unlikely to miss, the provider can make efficient initial progress while building patient confidence in the deprescribing process.

Medication the patient is most motivated to discontinue. This strategy can enhance the therapeutic alliance and increase the likelihood of successful patient engagement for patients hesitant to decrease medications, so long as there are no significant contraindications to discontinuing the medication.

5. Go slowly. As long as there are no medications that put the patient at risk and require rapid discontinuation, going slowly increases the likelihood of long-term success by:

• permitting careful monitoring for any worsening symptoms
• allowing more time for physiologic readjustment
• enabling the patient and provider to build confidence in the process over time.

With slow discontinuation, normal emotions, such as transient, situationally appropriate anxiety about a life stressor, are less likely to be misinterpreted by the patient or provider as an inability to tolerate medication reduction because there is more opportunity to observe overall trends in symptoms.

6. Replace medications with alternatives. Offering non-pharmacological treatment when possible can greatly facilitate reducing the number of medications. Examples include:

• teaching a patient breathing exercises or mindfulness while preparing to decrease an as needed anxiolytic
• engaging the patient in cognitive-behavioral therapy for insomnia before reducing sleep medications
• working together to identify opportunities for behavioral activation and exercises that are the most achievable for the patient.

This replacement strategy can work in a physiologic sense and address a patient’s fear that medications are “taken away” without alternatives in place.

Although these strategies might not work for every patient and are not recommended for reducing medications that are medically necessary, using this approach will increase the likelihood of long-term success and maintain the patient–provider alliance when reducing unnecessary and potentially risky polypharmacy. An article by Gupta and Cahill¹ describes some similar approaches with additional discussion and considerations.

Taking over the care of a patient with a complex medication regimen consisting of multiple psycho­tropics is a common experience for many practicing psychiatrists. Increasing attention has been paid to the risks of polypharmacy and the importance of “deprescribing”—reducing or stopping medication—when the risks of a drug outweigh the benefits.^1,2 However, successfully reducing medication burden can be a challenge, particularly when there is fear of decompensation or if the patient is psycho­logically attached to the complex medication regimen.

We describe a pragmatic approach to deprescribing, outlining 6 steps that we have used successfully in several treatment settings, which can assist prescribers facing similar challenges in their own practices.

1. Obtain a detailed history. First compile a comprehensive list of the patient’s medications, including psychotropics, other drugs, and supplements. If necessary, coordinate with your patient’s primary care provider. Then reassess the patient’s history of illness and efficacy of pharmacologic and non-pharmacologic treatments and how the current regimen has evolved. Understand the patient’s course of illness, coping styles, strengths, and vulnerabilities with an eye toward deprescribing.

2. Investigate underlying meaning. Even the most biologically oriented prescribers can benefit from exploring the underlying meaning the patient ascribes to the medication regimen. Common themes include:

• hesitation to relinquish a complex medication regimen because the patient fears decompensation (which could be either realistic or unrealistic)
• attachment to the “sick role”
• interpreting the complex regimen as evidence of the provider’s care and concern.

A series of sensitive conversations exploring these factors and addressing their underlying meaning can help increase a patient’s trust in the process of deprescribing.

3. Assess risk vs benefit. Weigh and educate the patient on the potential risks and benefits of each medication, as well as drug interactions and additive side effects.

4. Start with:
The most risky. Medications with significant risk for serious adverse effects (eg, high doses of a QTc-prolonging medication in a patient with elevated QTc) should be targeted early.

The least likely to be missed. If there are no high-risk medications that need to take priority, discontinuation of a “redundant” medication, such as a low-dose anti­histamine prescribed with multiple other sedating medications, can be an achievable first step. By starting with a medication that the patient is unlikely to miss, the provider can make efficient initial progress while building patient confidence in the deprescribing process.

Medication the patient is most motivated to discontinue. This strategy can enhance the therapeutic alliance and increase the likelihood of successful patient engagement for patients hesitant to decrease medications, so long as there are no significant contraindications to discontinuing the medication.

5. Go slowly. As long as there are no medications that put the patient at risk and require rapid discontinuation, going slowly increases the likelihood of long-term success by:

• permitting careful monitoring for any worsening symptoms
• allowing more time for physiologic readjustment
• enabling the patient and provider to build confidence in the process over time.

With slow discontinuation, normal emotions, such as transient, situationally appropriate anxiety about a life stressor, are less likely to be misinterpreted by the patient or provider as an inability to tolerate medication reduction because there is more opportunity to observe overall trends in symptoms.

6. Replace medications with alternatives. Offering non-pharmacological treatment when possible can greatly facilitate reducing the number of medications. Examples include:

• teaching a patient breathing exercises or mindfulness while preparing to decrease an as needed anxiolytic
• engaging the patient in cognitive-behavioral therapy for insomnia before reducing sleep medications
• working together to identify opportunities for behavioral activation and exercises that are the most achievable for the patient.

This replacement strategy can work in a physiologic sense and address a patient’s fear that medications are “taken away” without alternatives in place.

Although these strategies might not work for every patient and are not recommended for reducing medications that are medically necessary, using this approach will increase the likelihood of long-term success and maintain the patient–provider alliance when reducing unnecessary and potentially risky polypharmacy. An article by Gupta and Cahill¹ describes some similar approaches with additional discussion and considerations.

Many individuals read about the health benefits of certain foods, such as coffee, grapefruit, and red wine, but psychiatrists might neglect to inform their patients that these common foods could interact with drugs, thereby preventing certain psychotropics from achieving maximum benefit or causing toxicity. Educate your patients about food–drug interactions and to refrain from alcohol and specific foods when taking psychotropics. Although far from comprehensive, we present a discussion of the most frequently encountered and preventable food/nutrient–drug interactions.

Grapefruit juice may alter bioavailability of many psychotropics by inhibiting cytochrome P450 (CYP) 3A4 and 1A2 isoforms, interfering with prehepatic metabolism, and enteric absorption. Common medications affected by this interaction include alprazolam, buspirone, sertraline, carbamazepine, and methadone.¹ Patients should be advised about eating grapefruit or drinking grapefruit juice as it could require dose adjustment to avoid drug toxicity.

Table salt. Lithium is a salt, and less table salt intake could cause lithium levels to rise and vice versa. Lithium and other salts compete for absorption and secretion in the renal tubules, which are responsible for this interaction. Therefore, it is advisable to keep a stable salt intake throughout treatment. Patients should be cautioned about eating salty foods during the summer because excessive sweating could lead to lithium intoxication.

Caffeine is a widely used stimulant; however, it can decrease blood lithium levels and block clozapine clearance via inhibition of the CYP1A2 enzyme. Excessive caffeine intake can lead to clozapine toxicity.²

Beef liver, aged sausage and cheese, and wine contain tyramine. Tyramine is broken down by monoamine oxidase (MAO) enzymes in the body, which are inhibited by MAO inhibitors (MAOI) such as phenelzine and selegiline. A patient taking a MAOI cannot catabolize tyramine and other amines. These exogenous amines could cause a life-threatening hyperadrenergic crisis. Physicians should educate their patients about the MAOI diet and monitor adherence to the food avoidance list.

St. John’s wort is a herb commonly used for treating mild depression. It is a strong inducer of the CYP3A4 enzyme and reduces plasma concentrations and could decrease clinical effectiveness of aripiprazole, quetia­pine, alprazolam, and oxycodone.³ It could interact with serotonin reuptake inhibitors causing serotonin syndrome.

Full vs empty stomach. Food is known to affect bioavailability and enteral absorption of different psychotropics. Some medications are best taken on a full stomach and some on an empty one. For example, the antipsychotic ziprasidone should be taken with meals of at least 500 calories for optimal and consistent bioavailability. Benzodiazepines are rapidly absorbed when taken on an empty stomach.

Discuss dietary habits with patients to encourage a healthy lifestyle and provide valuable direction about potential food/nutrient–drug interactions.

Many individuals read about the health benefits of certain foods, such as coffee, grapefruit, and red wine, but psychiatrists might neglect to inform their patients that these common foods could interact with drugs, thereby preventing certain psychotropics from achieving maximum benefit or causing toxicity. Educate your patients about food–drug interactions and to refrain from alcohol and specific foods when taking psychotropics. Although far from comprehensive, we present a discussion of the most frequently encountered and preventable food/nutrient–drug interactions.

Grapefruit juice may alter bioavailability of many psychotropics by inhibiting cytochrome P450 (CYP) 3A4 and 1A2 isoforms, interfering with prehepatic metabolism, and enteric absorption. Common medications affected by this interaction include alprazolam, buspirone, sertraline, carbamazepine, and methadone.¹ Patients should be advised about eating grapefruit or drinking grapefruit juice as it could require dose adjustment to avoid drug toxicity.

Table salt. Lithium is a salt, and less table salt intake could cause lithium levels to rise and vice versa. Lithium and other salts compete for absorption and secretion in the renal tubules, which are responsible for this interaction. Therefore, it is advisable to keep a stable salt intake throughout treatment. Patients should be cautioned about eating salty foods during the summer because excessive sweating could lead to lithium intoxication.

Caffeine is a widely used stimulant; however, it can decrease blood lithium levels and block clozapine clearance via inhibition of the CYP1A2 enzyme. Excessive caffeine intake can lead to clozapine toxicity.²

Beef liver, aged sausage and cheese, and wine contain tyramine. Tyramine is broken down by monoamine oxidase (MAO) enzymes in the body, which are inhibited by MAO inhibitors (MAOI) such as phenelzine and selegiline. A patient taking a MAOI cannot catabolize tyramine and other amines. These exogenous amines could cause a life-threatening hyperadrenergic crisis. Physicians should educate their patients about the MAOI diet and monitor adherence to the food avoidance list.

St. John’s wort is a herb commonly used for treating mild depression. It is a strong inducer of the CYP3A4 enzyme and reduces plasma concentrations and could decrease clinical effectiveness of aripiprazole, quetia­pine, alprazolam, and oxycodone.³ It could interact with serotonin reuptake inhibitors causing serotonin syndrome.

Full vs empty stomach. Food is known to affect bioavailability and enteral absorption of different psychotropics. Some medications are best taken on a full stomach and some on an empty one. For example, the antipsychotic ziprasidone should be taken with meals of at least 500 calories for optimal and consistent bioavailability. Benzodiazepines are rapidly absorbed when taken on an empty stomach.

Discuss dietary habits with patients to encourage a healthy lifestyle and provide valuable direction about potential food/nutrient–drug interactions.

Many individuals read about the health benefits of certain foods, such as coffee, grapefruit, and red wine, but psychiatrists might neglect to inform their patients that these common foods could interact with drugs, thereby preventing certain psychotropics from achieving maximum benefit or causing toxicity. Educate your patients about food–drug interactions and to refrain from alcohol and specific foods when taking psychotropics. Although far from comprehensive, we present a discussion of the most frequently encountered and preventable food/nutrient–drug interactions.

Grapefruit juice may alter bioavailability of many psychotropics by inhibiting cytochrome P450 (CYP) 3A4 and 1A2 isoforms, interfering with prehepatic metabolism, and enteric absorption. Common medications affected by this interaction include alprazolam, buspirone, sertraline, carbamazepine, and methadone.¹ Patients should be advised about eating grapefruit or drinking grapefruit juice as it could require dose adjustment to avoid drug toxicity.

Table salt. Lithium is a salt, and less table salt intake could cause lithium levels to rise and vice versa. Lithium and other salts compete for absorption and secretion in the renal tubules, which are responsible for this interaction. Therefore, it is advisable to keep a stable salt intake throughout treatment. Patients should be cautioned about eating salty foods during the summer because excessive sweating could lead to lithium intoxication.

Caffeine is a widely used stimulant; however, it can decrease blood lithium levels and block clozapine clearance via inhibition of the CYP1A2 enzyme. Excessive caffeine intake can lead to clozapine toxicity.²

Beef liver, aged sausage and cheese, and wine contain tyramine. Tyramine is broken down by monoamine oxidase (MAO) enzymes in the body, which are inhibited by MAO inhibitors (MAOI) such as phenelzine and selegiline. A patient taking a MAOI cannot catabolize tyramine and other amines. These exogenous amines could cause a life-threatening hyperadrenergic crisis. Physicians should educate their patients about the MAOI diet and monitor adherence to the food avoidance list.

St. John’s wort is a herb commonly used for treating mild depression. It is a strong inducer of the CYP3A4 enzyme and reduces plasma concentrations and could decrease clinical effectiveness of aripiprazole, quetia­pine, alprazolam, and oxycodone.³ It could interact with serotonin reuptake inhibitors causing serotonin syndrome.

Full vs empty stomach. Food is known to affect bioavailability and enteral absorption of different psychotropics. Some medications are best taken on a full stomach and some on an empty one. For example, the antipsychotic ziprasidone should be taken with meals of at least 500 calories for optimal and consistent bioavailability. Benzodiazepines are rapidly absorbed when taken on an empty stomach.

Discuss dietary habits with patients to encourage a healthy lifestyle and provide valuable direction about potential food/nutrient–drug interactions.