Image Quizzes

The correct diagnosis is adolescent posttraumatic stress disorder (PTSD), as the patient's symptoms — recurrent nightmares, flashbacks, hypervigilance, and avoidance behaviors — are closely linked to her recent traumatic experience, fitting the clinical profile of PTSD. The MRI finding, although abnormal, does not correlate with a neurologic cause for her symptoms and may be incidental.

Temporal lobe epilepsy can cause behavioral changes but does not explain the specific PTSD symptoms like flashbacks and nightmares. 

Chronic migraine could explain the headaches but not the full spectrum of PTSD symptoms. 

Major depressive disorder could account for some of the emotional and social symptoms but lacks the characteristic re-experiencing and avoidance behaviors typical of PTSD.

Adolescent PTSD is a significant public health concern, causing significant distress to a small portion of the youth population. By late adolescence, approximately two thirds of youths have been exposed to trauma, and 8% of these individuals meet the criteria for PTSD by age 18. The incidence is exceptionally high in cases of sexual abuse and assault, with rates reaching up to 40%. PTSD in adolescents is associated with severe psychological distress, reduced academic performance, and a high rate of comorbidities, including anxiety and depression. There are specific populations (including children who are evacuated from home, asylum seekers, etc.) that show higher rates of PTSD. 

PTSD can lead to chronic impairments, comorbid psychiatric disorders, and an increased risk for suicide, with cases documented in toddlers as young as 1 year old. Thus, it is important to consider the individual's background and social history, as older children with PTSD may present with symptoms from early childhood trauma, often distant from the time of clinical evaluation.

Intrusion symptoms are a hallmark of PTSD, characterized by persistent and uncontrollable thoughts, dreams, and emotional reactions related to the traumatic event. These symptoms distinguish PTSD from other anxiety and mood disorders. Children with PTSD often experience involuntary, distressing thoughts and memories triggered by trauma cues, such as sights, sounds, or smells associated with the traumatic event. In younger children, these intrusive thoughts may manifest through repetitive play that re-enacts aspects of the trauma.

Nightmares are also common, although in children the content may not always directly relate to the traumatic event. Chronic nightmares contribute to sleep disturbances, exacerbating PTSD symptoms. Trauma reminders, which can be both internal (thoughts, memories) and external (places, sensory experiences), can provoke severe distress and physiologic reactions.

Avoidance symptoms often develop as a coping mechanism in response to distressing re-experiencing symptoms. Children may avoid thoughts, feelings, and memories of the traumatic event or people, places, and activities associated with the trauma. In young children, avoidance may manifest as restricted play or reduced exploration of their environment.

The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR) outlines specific criteria for diagnosing PTSD in individuals over 6 years old, which includes exposure to actual or threatened death, serious injury, or sexual violence, and the presence of symptoms such as intrusion, avoidance, negative mood alterations, and heightened arousal. The DSM-5-TR provides tailored diagnostic criteria for developmental differences in symptom expression for children under 6.

Managing PTSD in children requires a patient-specific approach, with an emphasis on obtaining consent from both the patient and guardian. The American Academy of Child and Adolescent Psychiatry (AACAP) recommends psychotherapy as the first-line treatment for pediatric PTSD. However, patients with severe symptoms or comorbidities may initially be unable to engage in meaningful therapy and may require medication to stabilize symptoms before starting psychotherapy.

Trauma-focused psychotherapy, including cognitive-behavioral therapy (CBT), exposure-based therapy, and eye movement desensitization and reprocessing (EMDR) therapy, is the preferred treatment for PTSD. Clinical studies have shown that patients receiving trauma-focused psychotherapy experience more remarkable symptom improvement than those who do not receive treatment and, in children, psychotherapy generally yields better outcomes than pharmacotherapy.

While selective serotonin reuptake inhibitors like sertraline and paroxetine are FDA-approved for PTSD treatment in adults, their efficacy in children often produces outcomes similar to those of placebo. Medications are typically reserved for severe symptoms and are used as an off-label treatment in pediatric cases. Pharmacologic management may be necessary when the severity of symptoms prevents the use of trauma-focused psychotherapy or requires immediate stabilization.

Heidi Moawad, MD, Clinical Assistant Professor, Department of Medical Education, Case Western Reserve University School of Medicine, Cleveland, Ohio.

Heidi Moawad, MD, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

The correct diagnosis is adolescent posttraumatic stress disorder (PTSD), as the patient's symptoms — recurrent nightmares, flashbacks, hypervigilance, and avoidance behaviors — are closely linked to her recent traumatic experience, fitting the clinical profile of PTSD. The MRI finding, although abnormal, does not correlate with a neurologic cause for her symptoms and may be incidental.

Temporal lobe epilepsy can cause behavioral changes but does not explain the specific PTSD symptoms like flashbacks and nightmares. 

Chronic migraine could explain the headaches but not the full spectrum of PTSD symptoms. 

Major depressive disorder could account for some of the emotional and social symptoms but lacks the characteristic re-experiencing and avoidance behaviors typical of PTSD.

Adolescent PTSD is a significant public health concern, causing significant distress to a small portion of the youth population. By late adolescence, approximately two thirds of youths have been exposed to trauma, and 8% of these individuals meet the criteria for PTSD by age 18. The incidence is exceptionally high in cases of sexual abuse and assault, with rates reaching up to 40%. PTSD in adolescents is associated with severe psychological distress, reduced academic performance, and a high rate of comorbidities, including anxiety and depression. There are specific populations (including children who are evacuated from home, asylum seekers, etc.) that show higher rates of PTSD. 

PTSD can lead to chronic impairments, comorbid psychiatric disorders, and an increased risk for suicide, with cases documented in toddlers as young as 1 year old. Thus, it is important to consider the individual's background and social history, as older children with PTSD may present with symptoms from early childhood trauma, often distant from the time of clinical evaluation.

Intrusion symptoms are a hallmark of PTSD, characterized by persistent and uncontrollable thoughts, dreams, and emotional reactions related to the traumatic event. These symptoms distinguish PTSD from other anxiety and mood disorders. Children with PTSD often experience involuntary, distressing thoughts and memories triggered by trauma cues, such as sights, sounds, or smells associated with the traumatic event. In younger children, these intrusive thoughts may manifest through repetitive play that re-enacts aspects of the trauma.

Nightmares are also common, although in children the content may not always directly relate to the traumatic event. Chronic nightmares contribute to sleep disturbances, exacerbating PTSD symptoms. Trauma reminders, which can be both internal (thoughts, memories) and external (places, sensory experiences), can provoke severe distress and physiologic reactions.

Avoidance symptoms often develop as a coping mechanism in response to distressing re-experiencing symptoms. Children may avoid thoughts, feelings, and memories of the traumatic event or people, places, and activities associated with the trauma. In young children, avoidance may manifest as restricted play or reduced exploration of their environment.

The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR) outlines specific criteria for diagnosing PTSD in individuals over 6 years old, which includes exposure to actual or threatened death, serious injury, or sexual violence, and the presence of symptoms such as intrusion, avoidance, negative mood alterations, and heightened arousal. The DSM-5-TR provides tailored diagnostic criteria for developmental differences in symptom expression for children under 6.

Managing PTSD in children requires a patient-specific approach, with an emphasis on obtaining consent from both the patient and guardian. The American Academy of Child and Adolescent Psychiatry (AACAP) recommends psychotherapy as the first-line treatment for pediatric PTSD. However, patients with severe symptoms or comorbidities may initially be unable to engage in meaningful therapy and may require medication to stabilize symptoms before starting psychotherapy.

Trauma-focused psychotherapy, including cognitive-behavioral therapy (CBT), exposure-based therapy, and eye movement desensitization and reprocessing (EMDR) therapy, is the preferred treatment for PTSD. Clinical studies have shown that patients receiving trauma-focused psychotherapy experience more remarkable symptom improvement than those who do not receive treatment and, in children, psychotherapy generally yields better outcomes than pharmacotherapy.

While selective serotonin reuptake inhibitors like sertraline and paroxetine are FDA-approved for PTSD treatment in adults, their efficacy in children often produces outcomes similar to those of placebo. Medications are typically reserved for severe symptoms and are used as an off-label treatment in pediatric cases. Pharmacologic management may be necessary when the severity of symptoms prevents the use of trauma-focused psychotherapy or requires immediate stabilization.

Heidi Moawad, MD, Clinical Assistant Professor, Department of Medical Education, Case Western Reserve University School of Medicine, Cleveland, Ohio.

Heidi Moawad, MD, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

The correct diagnosis is adolescent posttraumatic stress disorder (PTSD), as the patient's symptoms — recurrent nightmares, flashbacks, hypervigilance, and avoidance behaviors — are closely linked to her recent traumatic experience, fitting the clinical profile of PTSD. The MRI finding, although abnormal, does not correlate with a neurologic cause for her symptoms and may be incidental.

Temporal lobe epilepsy can cause behavioral changes but does not explain the specific PTSD symptoms like flashbacks and nightmares. 

Chronic migraine could explain the headaches but not the full spectrum of PTSD symptoms. 

Major depressive disorder could account for some of the emotional and social symptoms but lacks the characteristic re-experiencing and avoidance behaviors typical of PTSD.

Adolescent PTSD is a significant public health concern, causing significant distress to a small portion of the youth population. By late adolescence, approximately two thirds of youths have been exposed to trauma, and 8% of these individuals meet the criteria for PTSD by age 18. The incidence is exceptionally high in cases of sexual abuse and assault, with rates reaching up to 40%. PTSD in adolescents is associated with severe psychological distress, reduced academic performance, and a high rate of comorbidities, including anxiety and depression. There are specific populations (including children who are evacuated from home, asylum seekers, etc.) that show higher rates of PTSD. 

PTSD can lead to chronic impairments, comorbid psychiatric disorders, and an increased risk for suicide, with cases documented in toddlers as young as 1 year old. Thus, it is important to consider the individual's background and social history, as older children with PTSD may present with symptoms from early childhood trauma, often distant from the time of clinical evaluation.

Intrusion symptoms are a hallmark of PTSD, characterized by persistent and uncontrollable thoughts, dreams, and emotional reactions related to the traumatic event. These symptoms distinguish PTSD from other anxiety and mood disorders. Children with PTSD often experience involuntary, distressing thoughts and memories triggered by trauma cues, such as sights, sounds, or smells associated with the traumatic event. In younger children, these intrusive thoughts may manifest through repetitive play that re-enacts aspects of the trauma.

Nightmares are also common, although in children the content may not always directly relate to the traumatic event. Chronic nightmares contribute to sleep disturbances, exacerbating PTSD symptoms. Trauma reminders, which can be both internal (thoughts, memories) and external (places, sensory experiences), can provoke severe distress and physiologic reactions.

Avoidance symptoms often develop as a coping mechanism in response to distressing re-experiencing symptoms. Children may avoid thoughts, feelings, and memories of the traumatic event or people, places, and activities associated with the trauma. In young children, avoidance may manifest as restricted play or reduced exploration of their environment.

The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR) outlines specific criteria for diagnosing PTSD in individuals over 6 years old, which includes exposure to actual or threatened death, serious injury, or sexual violence, and the presence of symptoms such as intrusion, avoidance, negative mood alterations, and heightened arousal. The DSM-5-TR provides tailored diagnostic criteria for developmental differences in symptom expression for children under 6.

Managing PTSD in children requires a patient-specific approach, with an emphasis on obtaining consent from both the patient and guardian. The American Academy of Child and Adolescent Psychiatry (AACAP) recommends psychotherapy as the first-line treatment for pediatric PTSD. However, patients with severe symptoms or comorbidities may initially be unable to engage in meaningful therapy and may require medication to stabilize symptoms before starting psychotherapy.

Trauma-focused psychotherapy, including cognitive-behavioral therapy (CBT), exposure-based therapy, and eye movement desensitization and reprocessing (EMDR) therapy, is the preferred treatment for PTSD. Clinical studies have shown that patients receiving trauma-focused psychotherapy experience more remarkable symptom improvement than those who do not receive treatment and, in children, psychotherapy generally yields better outcomes than pharmacotherapy.

While selective serotonin reuptake inhibitors like sertraline and paroxetine are FDA-approved for PTSD treatment in adults, their efficacy in children often produces outcomes similar to those of placebo. Medications are typically reserved for severe symptoms and are used as an off-label treatment in pediatric cases. Pharmacologic management may be necessary when the severity of symptoms prevents the use of trauma-focused psychotherapy or requires immediate stabilization.

Heidi Moawad, MD, Clinical Assistant Professor, Department of Medical Education, Case Western Reserve University School of Medicine, Cleveland, Ohio.

Heidi Moawad, MD, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

Obesity is a chronic disease affecting more than 20% of adults in the United States. In 2022, prevalence was 20.5% among those aged 18 to 24 and 39.9% among those aged 45 to 54 years. This patient meets criteria for obesity (BMI ≥ 30), and it is likely that her obesity contributed to development of T2D, hypertension, osteoarthritis, and joint edema (as shown in the image). 

Patients with obesity are at high risk of developing cardiometabolic disease and osteoarthritis. Obesity is a key driver of T2D and cardiovascular disease development through its influence on insulin and lipid metabolism and proinflammatory changes. Factors associated with obesity that foster arthritis development include the erosive effects of adiponectin and leptin on cartilage and direct inflammation in joint tissues. 

It is important for patients with obesity and comorbid T2D and hypertension to receive multidisciplinary care designed to address all aspects of their health and minimize their risk for progression. The primary goal for this patient should be to promote weight loss safely while also improving her glycemic control and blood pressure. For patients with obesity and comorbid T2D, the American Diabetes Association recommends glucagon-like peptide-1 receptor agonists (GLP-1 RAs; semaglutide or liraglutide) or the dual gastric inhibitory polypeptide (GIP)/GLP-1 RA tirzepatide. The GLP-1 RA drugs reduce the risk for major cardiovascular events for patients with T2D while also providing substantial reductions in glucose levels without increasing hypoglycemia risk. They are available in higher doses (semaglutide 2.4 mg weekly, liraglutide 3.0 mg daily) for patients with obesity. These drugs also have salubrious effects on cardiorenal health and reduce progression of kidney disease. Tirzepatide produced greater reductions in A1c vs semaglutide in patients with T2D in the SURPASS-2 trial. It also has been shown to reduce atherosclerotic cardiovascular events in patients with overweight or obesity (without diabetes) in a post hoc analysis of the SURMOUNT-1 trial. Its effect on a broad set of cardiac, renal, and metabolic outcomes is being studied in the ongoing SURMOUNT-MMO trial. The American Gastroenterological Association and other organizations recommend treatment with antiobesity medications along with lifestyle modifications for patients with obesity (BMI ≥ 30) and weight-related complications (BMI > 27). 

Pharmacologic interventions for osteoarthritis include nonsteroidal anti-inflammatory drugs, including ibuprofen, naproxen, meloxicam, diclofenac, or celecoxib. These may be used with regular follow-up to assess cardiovascular and gastrointestinal health. Topical nonsteroidal anti-inflammatory drugs also may be useful. For more intractable joint pain, options include injecting corticosteroid or sodium hyaluronate into the affected joints or joint replacement.

In addition, comprehensive care includes lifestyle modifications designed to promote weight loss, reduce sodium, and increase exercise and intake of healthy foods. While maintaining intensive lifestyle modifications can be challenging, achieving weight loss of ≥ 5% can improve cardiometabolic risk factors in patients with obesity and T2D. Greater benefit is seen with greater reductions in body weight. Other interventions include behavioral modification and encouragement of increased physical activity to the extent of the patient's ability. Achieving substantial weight loss also could help relieve stress on the patient's joints, improve physical function, and mitigate osteoarthritis-related pain. The patient also may benefit from nonpharmacologic approaches to joint pain, including hot or cold compresses, physical therapy, and strength and resistance training to improve the strength of muscles supporting the joints. 

Carolyn Newberry, MD, Assistant Professor of Medicine, Director of GI Nutrition, Innovative Center for Health and Nutrition in Gastroenterology (ICHANGE), Division of Gastroenterology, Weill Cornell Medical Center, New York, NY.

Disclosure: Carolyn Newberry, MD, has disclosed the following relevant financial relationships:

Serve(d) as a speaker or a member of a speakers bureau for: Baster International; InBody.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

Obesity is a chronic disease affecting more than 20% of adults in the United States. In 2022, prevalence was 20.5% among those aged 18 to 24 and 39.9% among those aged 45 to 54 years. This patient meets criteria for obesity (BMI ≥ 30), and it is likely that her obesity contributed to development of T2D, hypertension, osteoarthritis, and joint edema (as shown in the image). 

Patients with obesity are at high risk of developing cardiometabolic disease and osteoarthritis. Obesity is a key driver of T2D and cardiovascular disease development through its influence on insulin and lipid metabolism and proinflammatory changes. Factors associated with obesity that foster arthritis development include the erosive effects of adiponectin and leptin on cartilage and direct inflammation in joint tissues. 

It is important for patients with obesity and comorbid T2D and hypertension to receive multidisciplinary care designed to address all aspects of their health and minimize their risk for progression. The primary goal for this patient should be to promote weight loss safely while also improving her glycemic control and blood pressure. For patients with obesity and comorbid T2D, the American Diabetes Association recommends glucagon-like peptide-1 receptor agonists (GLP-1 RAs; semaglutide or liraglutide) or the dual gastric inhibitory polypeptide (GIP)/GLP-1 RA tirzepatide. The GLP-1 RA drugs reduce the risk for major cardiovascular events for patients with T2D while also providing substantial reductions in glucose levels without increasing hypoglycemia risk. They are available in higher doses (semaglutide 2.4 mg weekly, liraglutide 3.0 mg daily) for patients with obesity. These drugs also have salubrious effects on cardiorenal health and reduce progression of kidney disease. Tirzepatide produced greater reductions in A1c vs semaglutide in patients with T2D in the SURPASS-2 trial. It also has been shown to reduce atherosclerotic cardiovascular events in patients with overweight or obesity (without diabetes) in a post hoc analysis of the SURMOUNT-1 trial. Its effect on a broad set of cardiac, renal, and metabolic outcomes is being studied in the ongoing SURMOUNT-MMO trial. The American Gastroenterological Association and other organizations recommend treatment with antiobesity medications along with lifestyle modifications for patients with obesity (BMI ≥ 30) and weight-related complications (BMI > 27). 

Pharmacologic interventions for osteoarthritis include nonsteroidal anti-inflammatory drugs, including ibuprofen, naproxen, meloxicam, diclofenac, or celecoxib. These may be used with regular follow-up to assess cardiovascular and gastrointestinal health. Topical nonsteroidal anti-inflammatory drugs also may be useful. For more intractable joint pain, options include injecting corticosteroid or sodium hyaluronate into the affected joints or joint replacement.

In addition, comprehensive care includes lifestyle modifications designed to promote weight loss, reduce sodium, and increase exercise and intake of healthy foods. While maintaining intensive lifestyle modifications can be challenging, achieving weight loss of ≥ 5% can improve cardiometabolic risk factors in patients with obesity and T2D. Greater benefit is seen with greater reductions in body weight. Other interventions include behavioral modification and encouragement of increased physical activity to the extent of the patient's ability. Achieving substantial weight loss also could help relieve stress on the patient's joints, improve physical function, and mitigate osteoarthritis-related pain. The patient also may benefit from nonpharmacologic approaches to joint pain, including hot or cold compresses, physical therapy, and strength and resistance training to improve the strength of muscles supporting the joints. 

Carolyn Newberry, MD, Assistant Professor of Medicine, Director of GI Nutrition, Innovative Center for Health and Nutrition in Gastroenterology (ICHANGE), Division of Gastroenterology, Weill Cornell Medical Center, New York, NY.

Disclosure: Carolyn Newberry, MD, has disclosed the following relevant financial relationships:

Serve(d) as a speaker or a member of a speakers bureau for: Baster International; InBody.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

Obesity is a chronic disease affecting more than 20% of adults in the United States. In 2022, prevalence was 20.5% among those aged 18 to 24 and 39.9% among those aged 45 to 54 years. This patient meets criteria for obesity (BMI ≥ 30), and it is likely that her obesity contributed to development of T2D, hypertension, osteoarthritis, and joint edema (as shown in the image). 

Patients with obesity are at high risk of developing cardiometabolic disease and osteoarthritis. Obesity is a key driver of T2D and cardiovascular disease development through its influence on insulin and lipid metabolism and proinflammatory changes. Factors associated with obesity that foster arthritis development include the erosive effects of adiponectin and leptin on cartilage and direct inflammation in joint tissues. 

It is important for patients with obesity and comorbid T2D and hypertension to receive multidisciplinary care designed to address all aspects of their health and minimize their risk for progression. The primary goal for this patient should be to promote weight loss safely while also improving her glycemic control and blood pressure. For patients with obesity and comorbid T2D, the American Diabetes Association recommends glucagon-like peptide-1 receptor agonists (GLP-1 RAs; semaglutide or liraglutide) or the dual gastric inhibitory polypeptide (GIP)/GLP-1 RA tirzepatide. The GLP-1 RA drugs reduce the risk for major cardiovascular events for patients with T2D while also providing substantial reductions in glucose levels without increasing hypoglycemia risk. They are available in higher doses (semaglutide 2.4 mg weekly, liraglutide 3.0 mg daily) for patients with obesity. These drugs also have salubrious effects on cardiorenal health and reduce progression of kidney disease. Tirzepatide produced greater reductions in A1c vs semaglutide in patients with T2D in the SURPASS-2 trial. It also has been shown to reduce atherosclerotic cardiovascular events in patients with overweight or obesity (without diabetes) in a post hoc analysis of the SURMOUNT-1 trial. Its effect on a broad set of cardiac, renal, and metabolic outcomes is being studied in the ongoing SURMOUNT-MMO trial. The American Gastroenterological Association and other organizations recommend treatment with antiobesity medications along with lifestyle modifications for patients with obesity (BMI ≥ 30) and weight-related complications (BMI > 27). 

Pharmacologic interventions for osteoarthritis include nonsteroidal anti-inflammatory drugs, including ibuprofen, naproxen, meloxicam, diclofenac, or celecoxib. These may be used with regular follow-up to assess cardiovascular and gastrointestinal health. Topical nonsteroidal anti-inflammatory drugs also may be useful. For more intractable joint pain, options include injecting corticosteroid or sodium hyaluronate into the affected joints or joint replacement.

In addition, comprehensive care includes lifestyle modifications designed to promote weight loss, reduce sodium, and increase exercise and intake of healthy foods. While maintaining intensive lifestyle modifications can be challenging, achieving weight loss of ≥ 5% can improve cardiometabolic risk factors in patients with obesity and T2D. Greater benefit is seen with greater reductions in body weight. Other interventions include behavioral modification and encouragement of increased physical activity to the extent of the patient's ability. Achieving substantial weight loss also could help relieve stress on the patient's joints, improve physical function, and mitigate osteoarthritis-related pain. The patient also may benefit from nonpharmacologic approaches to joint pain, including hot or cold compresses, physical therapy, and strength and resistance training to improve the strength of muscles supporting the joints. 

Carolyn Newberry, MD, Assistant Professor of Medicine, Director of GI Nutrition, Innovative Center for Health and Nutrition in Gastroenterology (ICHANGE), Division of Gastroenterology, Weill Cornell Medical Center, New York, NY.

Disclosure: Carolyn Newberry, MD, has disclosed the following relevant financial relationships:

Serve(d) as a speaker or a member of a speakers bureau for: Baster International; InBody.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

The correct diagnosis is posttraumatic stress disorder (PTSD). The patient's anxiety, irritability, sleep difficulties, and other symptoms are directly related to the recent traumatic event (car crash), and he has no significant physical injuries or neurologic abnormalities. 

Generalized anxiety disorder is incorrect because it involves chronic worry about various life aspects for at least 6 months, unrelated to a specific trauma. 

Postconcussion syndrome is not applicable because of the lack of concussion evidence and other symptoms, such as headaches or dizziness. 

Acute stress disorder is similar to PTSD but is diagnosed when symptoms occur within 3 days to 1 month after a trauma. Because this patient's symptoms have persisted beyond 1 month, PTSD is the most likely diagnosis.

Patients with PTSD exhibit pronounced cognitive, affective, or behavioral responses to trauma reminders; these responses may include severe anxiety, dissociative episodes, flashbacks, and hyperreactive behaviors. The intensity of these symptoms and the resulting psychosocial impairment are more severe in individuals with PTSD compared with people who experience trauma without developing the disorder. To manage such heightened arousal, individuals with PTSD often engage in avoidance behaviors, leading to emotional numbing; reduced interest in daily activities; and, in severe cases, detachment from others. 

The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR) outlines specific criteria for diagnosing PTSD in individuals older than 6 years. These criteria include: (A) exposure to actual or threatened death, serious injury, or sexual violence; (B) the presence of one or more intrusion symptoms related to the traumatic event; (C) persistent avoidance of stimuli associated with the trauma; (D) negative alterations in cognitions and mood related to the trauma; and (E) marked alterations in arousal and reactivity, evidenced by two or more specific symptoms.

Early intervention is key in the treatment of PTSD to prevent the condition from becoming chronic. Although more empirical data are needed, especially regarding pharmacotherapy, early supportive interventions such as psychoeducation and case management have shown promise in acutely traumatized individuals. 

Trauma-focused psychotherapy is recommended as the first-line treatment for most adults with PTSD. This approach, which includes exposure-based therapies, is generally preferred over other therapies or pharmacologic treatments, such as selective serotonin reuptake inhibitors (SSRIs) or serotonin-norepinephrine reuptake inhibitors. However, in patients with comorbid conditions (eg, depression, psychosis) that impair their ability to engage in trauma-focused therapy, initial pharmacologic management is advised until symptoms stabilize, after which psychotherapy can be introduced.

Clinical trials and meta-analyses have demonstrated the efficacy of various trauma-focused therapies, including trauma-focused cognitive-behavioral therapy, prolonged exposure therapy, and eye movement desensitization and reprocessing. The treatment choice should be collaborative, based on patient presentation, preference, and therapist expertise.

For individuals with PTSD experiencing significant sleep disturbances, particularly nightmares, prazosin is suggested. Clinical studies demonstrate that prazosin effectively reduces overall PTSD symptoms, nightmares, and sleep disturbances in approximately half of the patients treated.

Medication regimens effective for PTSD should be continued for at least 6 months to 1 year to prevent relapse or recurrence. Multiple clinical trials in patients with PTSD who completed acute treatment with SSRIs have demonstrated that those who continued with SSRIs were less likely to have relapse compared with those receiving placebo.

Jasvinder Chawla, MD, Professor of Neurology, Loyola University Medical Center, Maywood; Director, Clinical Neurophysiology Lab, Department of Neurology, Hines VA Hospital, Hines, IL.
Jasvinder Chawla, MD, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

The correct diagnosis is posttraumatic stress disorder (PTSD). The patient's anxiety, irritability, sleep difficulties, and other symptoms are directly related to the recent traumatic event (car crash), and he has no significant physical injuries or neurologic abnormalities. 

Generalized anxiety disorder is incorrect because it involves chronic worry about various life aspects for at least 6 months, unrelated to a specific trauma. 

Postconcussion syndrome is not applicable because of the lack of concussion evidence and other symptoms, such as headaches or dizziness. 

Acute stress disorder is similar to PTSD but is diagnosed when symptoms occur within 3 days to 1 month after a trauma. Because this patient's symptoms have persisted beyond 1 month, PTSD is the most likely diagnosis.

Patients with PTSD exhibit pronounced cognitive, affective, or behavioral responses to trauma reminders; these responses may include severe anxiety, dissociative episodes, flashbacks, and hyperreactive behaviors. The intensity of these symptoms and the resulting psychosocial impairment are more severe in individuals with PTSD compared with people who experience trauma without developing the disorder. To manage such heightened arousal, individuals with PTSD often engage in avoidance behaviors, leading to emotional numbing; reduced interest in daily activities; and, in severe cases, detachment from others. 

The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR) outlines specific criteria for diagnosing PTSD in individuals older than 6 years. These criteria include: (A) exposure to actual or threatened death, serious injury, or sexual violence; (B) the presence of one or more intrusion symptoms related to the traumatic event; (C) persistent avoidance of stimuli associated with the trauma; (D) negative alterations in cognitions and mood related to the trauma; and (E) marked alterations in arousal and reactivity, evidenced by two or more specific symptoms.

Early intervention is key in the treatment of PTSD to prevent the condition from becoming chronic. Although more empirical data are needed, especially regarding pharmacotherapy, early supportive interventions such as psychoeducation and case management have shown promise in acutely traumatized individuals. 

Trauma-focused psychotherapy is recommended as the first-line treatment for most adults with PTSD. This approach, which includes exposure-based therapies, is generally preferred over other therapies or pharmacologic treatments, such as selective serotonin reuptake inhibitors (SSRIs) or serotonin-norepinephrine reuptake inhibitors. However, in patients with comorbid conditions (eg, depression, psychosis) that impair their ability to engage in trauma-focused therapy, initial pharmacologic management is advised until symptoms stabilize, after which psychotherapy can be introduced.

Clinical trials and meta-analyses have demonstrated the efficacy of various trauma-focused therapies, including trauma-focused cognitive-behavioral therapy, prolonged exposure therapy, and eye movement desensitization and reprocessing. The treatment choice should be collaborative, based on patient presentation, preference, and therapist expertise.

For individuals with PTSD experiencing significant sleep disturbances, particularly nightmares, prazosin is suggested. Clinical studies demonstrate that prazosin effectively reduces overall PTSD symptoms, nightmares, and sleep disturbances in approximately half of the patients treated.

Medication regimens effective for PTSD should be continued for at least 6 months to 1 year to prevent relapse or recurrence. Multiple clinical trials in patients with PTSD who completed acute treatment with SSRIs have demonstrated that those who continued with SSRIs were less likely to have relapse compared with those receiving placebo.

Jasvinder Chawla, MD, Professor of Neurology, Loyola University Medical Center, Maywood; Director, Clinical Neurophysiology Lab, Department of Neurology, Hines VA Hospital, Hines, IL.
Jasvinder Chawla, MD, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

The correct diagnosis is posttraumatic stress disorder (PTSD). The patient's anxiety, irritability, sleep difficulties, and other symptoms are directly related to the recent traumatic event (car crash), and he has no significant physical injuries or neurologic abnormalities. 

Generalized anxiety disorder is incorrect because it involves chronic worry about various life aspects for at least 6 months, unrelated to a specific trauma. 

Postconcussion syndrome is not applicable because of the lack of concussion evidence and other symptoms, such as headaches or dizziness. 

Acute stress disorder is similar to PTSD but is diagnosed when symptoms occur within 3 days to 1 month after a trauma. Because this patient's symptoms have persisted beyond 1 month, PTSD is the most likely diagnosis.

Patients with PTSD exhibit pronounced cognitive, affective, or behavioral responses to trauma reminders; these responses may include severe anxiety, dissociative episodes, flashbacks, and hyperreactive behaviors. The intensity of these symptoms and the resulting psychosocial impairment are more severe in individuals with PTSD compared with people who experience trauma without developing the disorder. To manage such heightened arousal, individuals with PTSD often engage in avoidance behaviors, leading to emotional numbing; reduced interest in daily activities; and, in severe cases, detachment from others. 

The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR) outlines specific criteria for diagnosing PTSD in individuals older than 6 years. These criteria include: (A) exposure to actual or threatened death, serious injury, or sexual violence; (B) the presence of one or more intrusion symptoms related to the traumatic event; (C) persistent avoidance of stimuli associated with the trauma; (D) negative alterations in cognitions and mood related to the trauma; and (E) marked alterations in arousal and reactivity, evidenced by two or more specific symptoms.

Early intervention is key in the treatment of PTSD to prevent the condition from becoming chronic. Although more empirical data are needed, especially regarding pharmacotherapy, early supportive interventions such as psychoeducation and case management have shown promise in acutely traumatized individuals. 

Trauma-focused psychotherapy is recommended as the first-line treatment for most adults with PTSD. This approach, which includes exposure-based therapies, is generally preferred over other therapies or pharmacologic treatments, such as selective serotonin reuptake inhibitors (SSRIs) or serotonin-norepinephrine reuptake inhibitors. However, in patients with comorbid conditions (eg, depression, psychosis) that impair their ability to engage in trauma-focused therapy, initial pharmacologic management is advised until symptoms stabilize, after which psychotherapy can be introduced.

Clinical trials and meta-analyses have demonstrated the efficacy of various trauma-focused therapies, including trauma-focused cognitive-behavioral therapy, prolonged exposure therapy, and eye movement desensitization and reprocessing. The treatment choice should be collaborative, based on patient presentation, preference, and therapist expertise.

For individuals with PTSD experiencing significant sleep disturbances, particularly nightmares, prazosin is suggested. Clinical studies demonstrate that prazosin effectively reduces overall PTSD symptoms, nightmares, and sleep disturbances in approximately half of the patients treated.

Medication regimens effective for PTSD should be continued for at least 6 months to 1 year to prevent relapse or recurrence. Multiple clinical trials in patients with PTSD who completed acute treatment with SSRIs have demonstrated that those who continued with SSRIs were less likely to have relapse compared with those receiving placebo.

Jasvinder Chawla, MD, Professor of Neurology, Loyola University Medical Center, Maywood; Director, Clinical Neurophysiology Lab, Department of Neurology, Hines VA Hospital, Hines, IL.
Jasvinder Chawla, MD, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

The most likely diagnosis for this patient is veteran posttraumatic stress disorder (PTSD), given his history of combat exposure and symptoms, such as severe headaches, difficulty concentrating, mood swings, nightmares, flashbacks, increased startle response, and hypervigilance. MRI findings showing significant changes in the limbic system and hippocampal regions support this diagnosis. Other potential diagnoses, like traumatic brain injury, chronic migraine, and major depressive disorder, are less likely because of their inability to account for the full range of his symptoms and specific MRI abnormalities.

PTSD, experienced by a subset of individuals after exposure to life-threatening events, has a lifetime prevalence of 4%-7% and a current prevalence of 1%-3%, with higher rates in older women, those with more trauma, and combat veterans. Nearly half of US veterans are aged 65 or older, many being Vietnam-era veterans at elevated risk for PTSD. Prevalence rates in older veterans range between 1% and 22%.

PTSD is characterized by intrusive thoughts, flashbacks, nightmares, avoidance of reminders, hypervigilance, and sleep difficulties, significantly disrupting interpersonal and occupational functioning. Screening tools like the primary care (PC) PTSD-5 and PCL-5, used in primary care settings, are effective for early detection, provisional diagnosis, and monitoring of symptom changes. The clinician-administered PTSD scale for Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition DSM-5 (CAPS-5) is the gold standard for diagnosis, particularly among veterans, with multimethod assessments combining self-report measures and semi-structured interviews recommended for accuracy. The DSM-5 criteria for PTSD diagnosis describe exposure to traumatic events, intrusion symptoms, avoidance behaviors, negative mood, and altered arousal, with symptoms persisting for over a month and causing significant distress or functional impairment. 

Research has identified consistent anatomical and functional changes in PTSD patients, such as smaller hippocampi, decreased corpus callosum and prefrontal cortex, increased amygdala reactivity, and decreased prefrontal cortex activity. PTSD, linked to alterations in brain regions involved in fear learning and memory, shows diminished structural integrity in executive function areas, reduced cortical volumes in the cingulate brain cortex and frontal regions, and reduced white matter integrity in key brain pathways. Neuroimaging findings, however, are primarily used for research currently and have yet to be widely implemented in clinical guidelines.

International PTSD treatment guidelines consistently recognize trauma-focused cognitive-behavioral therapies (CBTs), such as cognitive processing therapy (CPT), prolonged exposure (PE), and eye movement desensitization and reprocessing (EMDR) as the gold standard. Recent guidelines have expanded the list of recommended treatments: The 2023 Department of Veterans Affairs and Department of Defense guidelines in the United States also endorse therapies like written narrative exposure and brief eclectic therapy. Internationally, guidelines do not perfectly coincide, as the 2018 update from the United Kingdom's National Institute for Health and Care Excellence (NICE) gives the highest recommendations to PE and CPT but rates EMDR slightly lower for military veterans because of limited evidence. Overall, guidelines consistently advocate for trauma-focused psychological interventions as the primary treatment for PTSD.

Guidelines from NICE and the World Health Organization do not recommend medications as the primary treatment; the American Psychiatric Association and the US Department of Veterans Affairs support selective serotonin reuptake inhibitors and prazosin but advise against benzodiazepines. Inpatient care may be necessary for individuals who pose a danger to themselves or others, or for those with severe PTSD from childhood abuse, to aid in emotional regulation and treatment.

Jasvinder Chawla, MD, Professor of Neurology, Loyola University Medical Center, Maywood; Director, Clinical Neurophysiology Lab, Department of Neurology, Hines VA Hospital, Hines, IL.
Jasvinder Chawla, MD, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

The most likely diagnosis for this patient is veteran posttraumatic stress disorder (PTSD), given his history of combat exposure and symptoms, such as severe headaches, difficulty concentrating, mood swings, nightmares, flashbacks, increased startle response, and hypervigilance. MRI findings showing significant changes in the limbic system and hippocampal regions support this diagnosis. Other potential diagnoses, like traumatic brain injury, chronic migraine, and major depressive disorder, are less likely because of their inability to account for the full range of his symptoms and specific MRI abnormalities.

PTSD, experienced by a subset of individuals after exposure to life-threatening events, has a lifetime prevalence of 4%-7% and a current prevalence of 1%-3%, with higher rates in older women, those with more trauma, and combat veterans. Nearly half of US veterans are aged 65 or older, many being Vietnam-era veterans at elevated risk for PTSD. Prevalence rates in older veterans range between 1% and 22%.

PTSD is characterized by intrusive thoughts, flashbacks, nightmares, avoidance of reminders, hypervigilance, and sleep difficulties, significantly disrupting interpersonal and occupational functioning. Screening tools like the primary care (PC) PTSD-5 and PCL-5, used in primary care settings, are effective for early detection, provisional diagnosis, and monitoring of symptom changes. The clinician-administered PTSD scale for Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition DSM-5 (CAPS-5) is the gold standard for diagnosis, particularly among veterans, with multimethod assessments combining self-report measures and semi-structured interviews recommended for accuracy. The DSM-5 criteria for PTSD diagnosis describe exposure to traumatic events, intrusion symptoms, avoidance behaviors, negative mood, and altered arousal, with symptoms persisting for over a month and causing significant distress or functional impairment. 

Research has identified consistent anatomical and functional changes in PTSD patients, such as smaller hippocampi, decreased corpus callosum and prefrontal cortex, increased amygdala reactivity, and decreased prefrontal cortex activity. PTSD, linked to alterations in brain regions involved in fear learning and memory, shows diminished structural integrity in executive function areas, reduced cortical volumes in the cingulate brain cortex and frontal regions, and reduced white matter integrity in key brain pathways. Neuroimaging findings, however, are primarily used for research currently and have yet to be widely implemented in clinical guidelines.

International PTSD treatment guidelines consistently recognize trauma-focused cognitive-behavioral therapies (CBTs), such as cognitive processing therapy (CPT), prolonged exposure (PE), and eye movement desensitization and reprocessing (EMDR) as the gold standard. Recent guidelines have expanded the list of recommended treatments: The 2023 Department of Veterans Affairs and Department of Defense guidelines in the United States also endorse therapies like written narrative exposure and brief eclectic therapy. Internationally, guidelines do not perfectly coincide, as the 2018 update from the United Kingdom's National Institute for Health and Care Excellence (NICE) gives the highest recommendations to PE and CPT but rates EMDR slightly lower for military veterans because of limited evidence. Overall, guidelines consistently advocate for trauma-focused psychological interventions as the primary treatment for PTSD.

Guidelines from NICE and the World Health Organization do not recommend medications as the primary treatment; the American Psychiatric Association and the US Department of Veterans Affairs support selective serotonin reuptake inhibitors and prazosin but advise against benzodiazepines. Inpatient care may be necessary for individuals who pose a danger to themselves or others, or for those with severe PTSD from childhood abuse, to aid in emotional regulation and treatment.

Jasvinder Chawla, MD, Professor of Neurology, Loyola University Medical Center, Maywood; Director, Clinical Neurophysiology Lab, Department of Neurology, Hines VA Hospital, Hines, IL.
Jasvinder Chawla, MD, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

The most likely diagnosis for this patient is veteran posttraumatic stress disorder (PTSD), given his history of combat exposure and symptoms, such as severe headaches, difficulty concentrating, mood swings, nightmares, flashbacks, increased startle response, and hypervigilance. MRI findings showing significant changes in the limbic system and hippocampal regions support this diagnosis. Other potential diagnoses, like traumatic brain injury, chronic migraine, and major depressive disorder, are less likely because of their inability to account for the full range of his symptoms and specific MRI abnormalities.

PTSD, experienced by a subset of individuals after exposure to life-threatening events, has a lifetime prevalence of 4%-7% and a current prevalence of 1%-3%, with higher rates in older women, those with more trauma, and combat veterans. Nearly half of US veterans are aged 65 or older, many being Vietnam-era veterans at elevated risk for PTSD. Prevalence rates in older veterans range between 1% and 22%.

PTSD is characterized by intrusive thoughts, flashbacks, nightmares, avoidance of reminders, hypervigilance, and sleep difficulties, significantly disrupting interpersonal and occupational functioning. Screening tools like the primary care (PC) PTSD-5 and PCL-5, used in primary care settings, are effective for early detection, provisional diagnosis, and monitoring of symptom changes. The clinician-administered PTSD scale for Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition DSM-5 (CAPS-5) is the gold standard for diagnosis, particularly among veterans, with multimethod assessments combining self-report measures and semi-structured interviews recommended for accuracy. The DSM-5 criteria for PTSD diagnosis describe exposure to traumatic events, intrusion symptoms, avoidance behaviors, negative mood, and altered arousal, with symptoms persisting for over a month and causing significant distress or functional impairment. 

Research has identified consistent anatomical and functional changes in PTSD patients, such as smaller hippocampi, decreased corpus callosum and prefrontal cortex, increased amygdala reactivity, and decreased prefrontal cortex activity. PTSD, linked to alterations in brain regions involved in fear learning and memory, shows diminished structural integrity in executive function areas, reduced cortical volumes in the cingulate brain cortex and frontal regions, and reduced white matter integrity in key brain pathways. Neuroimaging findings, however, are primarily used for research currently and have yet to be widely implemented in clinical guidelines.

International PTSD treatment guidelines consistently recognize trauma-focused cognitive-behavioral therapies (CBTs), such as cognitive processing therapy (CPT), prolonged exposure (PE), and eye movement desensitization and reprocessing (EMDR) as the gold standard. Recent guidelines have expanded the list of recommended treatments: The 2023 Department of Veterans Affairs and Department of Defense guidelines in the United States also endorse therapies like written narrative exposure and brief eclectic therapy. Internationally, guidelines do not perfectly coincide, as the 2018 update from the United Kingdom's National Institute for Health and Care Excellence (NICE) gives the highest recommendations to PE and CPT but rates EMDR slightly lower for military veterans because of limited evidence. Overall, guidelines consistently advocate for trauma-focused psychological interventions as the primary treatment for PTSD.

Guidelines from NICE and the World Health Organization do not recommend medications as the primary treatment; the American Psychiatric Association and the US Department of Veterans Affairs support selective serotonin reuptake inhibitors and prazosin but advise against benzodiazepines. Inpatient care may be necessary for individuals who pose a danger to themselves or others, or for those with severe PTSD from childhood abuse, to aid in emotional regulation and treatment.

Jasvinder Chawla, MD, Professor of Neurology, Loyola University Medical Center, Maywood; Director, Clinical Neurophysiology Lab, Department of Neurology, Hines VA Hospital, Hines, IL.
Jasvinder Chawla, MD, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

Binge-eating disorder is more prevalent in women than men and has one of the strongest associations with obesity; among patients with obesity, lifetime prevalence of binge eating is approximately 5.5%. Large population studies suggest that binge-eating disorder may be present in 2%-4% of adolescents, with a mean age of onset of 12-13 years. This patient probably had milder binge-eating disorder as an adolescent and young adult, which was exacerbated by the pandemic. 

Both new diagnoses and reports of clinical worsening in patients with preexisting diagnoses of binge-eating disorder during the pandemic have been documented. Food insecurity has been associated with binge eating, consistent with this patient's anxiety over food and grocery availability during the pandemic. The definition of binge-eating disorder includes recurrent specific episodes of overeating that are not consistent with the patient's usual behavior, eating to the point of being uncomfortably full, eating more quickly or when not hungry, and having feelings of loss of control during episodes and of guilt or disgust afterward. 

Obesity and eating disorders share some common risk factors and approaches to management. Binge eating has been associated with type 2 diabetes, hypertension, asthma, sleep disorders, and menstrual disorders, all of which are also affected by obesity. The presence of both conditions increases the adverse outcomes associated with each, including negative impacts on cardiometabolic and psychological health. Workup of patients presenting with binge eating and obesity should always include complete blood/metabolic panels and cardiovascular and renal health, as well as assessments of nutrition status, electrolyte imbalances, gastrointestinal reflux disease, and chronic pain.

In general, where binge-eating disorder and obesity are concurrent, cognitive-behavioral therapy (CBT) for binge-eating disorder should be the first priority, with obesity management (medication or surgery) to follow. CBT has the strongest evidence of benefit for patients with binge-eating disorder and is the recommended treatment approach. Other psychotherapeutic interventions that may be of benefit include dialectical behavioral therapy (to reduce binge-eating frequency), technology-based options, and family-based therapy when symptoms are recognized in children or adolescents. Structured behavioral weight management strategies for management of obesity and overweight do not increase symptoms of eating disorders and may instead relieve some symptoms. An emerging approach to binge eating in patients with obesity is CBT that integrates therapeutic approaches to both issues. 

Medications to treat binge-eating disorder are limited and should not be used without concurrent psychotherapy; lisdexamfetamine has demonstrated benefit, is recommended by the American Psychiatric Association, and is approved by the US Food and Drug Administration specifically to treat adults with binge-eating disorder. 

The success of psychological interventions and lifestyle modifications for obesity is heavily dependent on the individual's ability and motivation to comply with recommended interventions. The American Gastroenterological Association and other organizations recommend treatment with antiobesity medications along with lifestyle modifications for patients with obesity (BMI ≥ 30) and weight-related complications (BMI > 27). Recommended medications include phentermine-topiramate and bupropion-naltrexone (which may benefit those with binge-eating disorder), as well as injectable glucagon-like peptide receptor agonists (GLP-1 RAs) at the approved dosage for obesity management (semaglutide 2.4 mg weekly or liraglutide 3.0 mg daily). Orlistat is not recommended. Ongoing research on the potential benefit of GLP-1 RAs in management of binge eating offers additional support for a role in patients, like this one, with binge-eating disorder and obesity. 

Carolyn Newberry, MD, Assistant Professor of Medicine, Director of GI Nutrition, Innovative Center for Health and Nutrition in Gastroenterology (ICHANGE), Division of Gastroenterology, Weill Cornell Medical Center, New York, NY.

Disclosure: Carolyn Newberry, MD, has disclosed the following relevant financial relationships:

Serve(d) as a speaker or a member of a speakers bureau for: Baster International; InBody.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.
 

Binge-eating disorder is more prevalent in women than men and has one of the strongest associations with obesity; among patients with obesity, lifetime prevalence of binge eating is approximately 5.5%. Large population studies suggest that binge-eating disorder may be present in 2%-4% of adolescents, with a mean age of onset of 12-13 years. This patient probably had milder binge-eating disorder as an adolescent and young adult, which was exacerbated by the pandemic. 

Both new diagnoses and reports of clinical worsening in patients with preexisting diagnoses of binge-eating disorder during the pandemic have been documented. Food insecurity has been associated with binge eating, consistent with this patient's anxiety over food and grocery availability during the pandemic. The definition of binge-eating disorder includes recurrent specific episodes of overeating that are not consistent with the patient's usual behavior, eating to the point of being uncomfortably full, eating more quickly or when not hungry, and having feelings of loss of control during episodes and of guilt or disgust afterward. 

Obesity and eating disorders share some common risk factors and approaches to management. Binge eating has been associated with type 2 diabetes, hypertension, asthma, sleep disorders, and menstrual disorders, all of which are also affected by obesity. The presence of both conditions increases the adverse outcomes associated with each, including negative impacts on cardiometabolic and psychological health. Workup of patients presenting with binge eating and obesity should always include complete blood/metabolic panels and cardiovascular and renal health, as well as assessments of nutrition status, electrolyte imbalances, gastrointestinal reflux disease, and chronic pain.

In general, where binge-eating disorder and obesity are concurrent, cognitive-behavioral therapy (CBT) for binge-eating disorder should be the first priority, with obesity management (medication or surgery) to follow. CBT has the strongest evidence of benefit for patients with binge-eating disorder and is the recommended treatment approach. Other psychotherapeutic interventions that may be of benefit include dialectical behavioral therapy (to reduce binge-eating frequency), technology-based options, and family-based therapy when symptoms are recognized in children or adolescents. Structured behavioral weight management strategies for management of obesity and overweight do not increase symptoms of eating disorders and may instead relieve some symptoms. An emerging approach to binge eating in patients with obesity is CBT that integrates therapeutic approaches to both issues. 

Medications to treat binge-eating disorder are limited and should not be used without concurrent psychotherapy; lisdexamfetamine has demonstrated benefit, is recommended by the American Psychiatric Association, and is approved by the US Food and Drug Administration specifically to treat adults with binge-eating disorder. 

The success of psychological interventions and lifestyle modifications for obesity is heavily dependent on the individual's ability and motivation to comply with recommended interventions. The American Gastroenterological Association and other organizations recommend treatment with antiobesity medications along with lifestyle modifications for patients with obesity (BMI ≥ 30) and weight-related complications (BMI > 27). Recommended medications include phentermine-topiramate and bupropion-naltrexone (which may benefit those with binge-eating disorder), as well as injectable glucagon-like peptide receptor agonists (GLP-1 RAs) at the approved dosage for obesity management (semaglutide 2.4 mg weekly or liraglutide 3.0 mg daily). Orlistat is not recommended. Ongoing research on the potential benefit of GLP-1 RAs in management of binge eating offers additional support for a role in patients, like this one, with binge-eating disorder and obesity. 

Carolyn Newberry, MD, Assistant Professor of Medicine, Director of GI Nutrition, Innovative Center for Health and Nutrition in Gastroenterology (ICHANGE), Division of Gastroenterology, Weill Cornell Medical Center, New York, NY.

Disclosure: Carolyn Newberry, MD, has disclosed the following relevant financial relationships:

Serve(d) as a speaker or a member of a speakers bureau for: Baster International; InBody.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.
 

Binge-eating disorder is more prevalent in women than men and has one of the strongest associations with obesity; among patients with obesity, lifetime prevalence of binge eating is approximately 5.5%. Large population studies suggest that binge-eating disorder may be present in 2%-4% of adolescents, with a mean age of onset of 12-13 years. This patient probably had milder binge-eating disorder as an adolescent and young adult, which was exacerbated by the pandemic. 

Both new diagnoses and reports of clinical worsening in patients with preexisting diagnoses of binge-eating disorder during the pandemic have been documented. Food insecurity has been associated with binge eating, consistent with this patient's anxiety over food and grocery availability during the pandemic. The definition of binge-eating disorder includes recurrent specific episodes of overeating that are not consistent with the patient's usual behavior, eating to the point of being uncomfortably full, eating more quickly or when not hungry, and having feelings of loss of control during episodes and of guilt or disgust afterward. 

Obesity and eating disorders share some common risk factors and approaches to management. Binge eating has been associated with type 2 diabetes, hypertension, asthma, sleep disorders, and menstrual disorders, all of which are also affected by obesity. The presence of both conditions increases the adverse outcomes associated with each, including negative impacts on cardiometabolic and psychological health. Workup of patients presenting with binge eating and obesity should always include complete blood/metabolic panels and cardiovascular and renal health, as well as assessments of nutrition status, electrolyte imbalances, gastrointestinal reflux disease, and chronic pain.

In general, where binge-eating disorder and obesity are concurrent, cognitive-behavioral therapy (CBT) for binge-eating disorder should be the first priority, with obesity management (medication or surgery) to follow. CBT has the strongest evidence of benefit for patients with binge-eating disorder and is the recommended treatment approach. Other psychotherapeutic interventions that may be of benefit include dialectical behavioral therapy (to reduce binge-eating frequency), technology-based options, and family-based therapy when symptoms are recognized in children or adolescents. Structured behavioral weight management strategies for management of obesity and overweight do not increase symptoms of eating disorders and may instead relieve some symptoms. An emerging approach to binge eating in patients with obesity is CBT that integrates therapeutic approaches to both issues. 

Medications to treat binge-eating disorder are limited and should not be used without concurrent psychotherapy; lisdexamfetamine has demonstrated benefit, is recommended by the American Psychiatric Association, and is approved by the US Food and Drug Administration specifically to treat adults with binge-eating disorder. 

The success of psychological interventions and lifestyle modifications for obesity is heavily dependent on the individual's ability and motivation to comply with recommended interventions. The American Gastroenterological Association and other organizations recommend treatment with antiobesity medications along with lifestyle modifications for patients with obesity (BMI ≥ 30) and weight-related complications (BMI > 27). Recommended medications include phentermine-topiramate and bupropion-naltrexone (which may benefit those with binge-eating disorder), as well as injectable glucagon-like peptide receptor agonists (GLP-1 RAs) at the approved dosage for obesity management (semaglutide 2.4 mg weekly or liraglutide 3.0 mg daily). Orlistat is not recommended. Ongoing research on the potential benefit of GLP-1 RAs in management of binge eating offers additional support for a role in patients, like this one, with binge-eating disorder and obesity. 

Carolyn Newberry, MD, Assistant Professor of Medicine, Director of GI Nutrition, Innovative Center for Health and Nutrition in Gastroenterology (ICHANGE), Division of Gastroenterology, Weill Cornell Medical Center, New York, NY.

Disclosure: Carolyn Newberry, MD, has disclosed the following relevant financial relationships:

Serve(d) as a speaker or a member of a speakers bureau for: Baster International; InBody.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.
 

FHM is a rare phenotype of migraine with aura with a characteristic presentation of motor aura. Motor aura presents as unilateral muscle weakness that tends to be felt first in the hands or arm and may spread to the face. To date, three distinct types have been identified by mutations in one of three genes. Type 1 is the most common and is associated with mutations in the gene CACNA1A. Mutations in ATP1A2 underlie type 2 FHM, and mutations in SCN1A underlie type 3 FHM.

FHM is distinguished from other hemiplegic migraine by family history of one or more affected first- or second-degree relatives. Genetic studies have shown FHM to have autosomal dominant inheritance. From half to three quarters of patients with FHM will have one of the more than 30 identified mutations on CACNA1A that diagnose type 1 FHM. These mutations affect transmission of glutamate in the neurons and neuronal reactions, increasing the susceptibility to cortical spreading depression associated with migraine. Mutations in ATP1A2 are found in about 20% of patients with FHM (type 2). More than 80 individual mutations have been identified, which alter sodium-potassium metabolism in neurons. About 5% of patients have type 3 FHM, associated with mutations in SCN1A that create gain of function or loss of function in neuronal voltage-gated sodium channels. Studies of other possible genes and mutations in relation to FHM, including PRRT2, are ongoing, but to date the associations are not clearly established. 

Patients with FHM may also report sensory symptoms, visual disturbances, or aphasia. FHM generally affects people in their teens and twenties (women more than men) and has an estimated prevalence of 0.003% of the population. On average, patients report having two to three attacks per year, and some patients go for extended periods without a recurrent attack. Motor aura may occur on the same or opposite side of the body as headache and may alternate affected sides with each attack. Differential diagnoses that should be ruled out include transient ischemic attacks, infections (eg, meningitis, encephalitis), tumors, seizures, other inherited disorders, and metabolic issues.

Like other forms of migraine with aura, FHM is treated with abortive and/or preventive medications. Given the rarity of FHM, there are few studies specifically in families with this phenotype. Patients should be counseled on trigger avoidance to limit exposure. Acute treatment includes nonsteroidal anti-inflammatory drugs, acetaminophen, and other nonopioid pain relievers. The class of calcitonin gene-related peptide (CGRP) antagonists (rimegepant, ubrogepant, zavegepant) may be considered. However, with FHM, medications associated with ischemia must be avoided. As such, triptans and ergotamines are generally contraindicated, as are beta-blockers. Patients with FHM and more frequent or severe attacks may be considered for preventive treatment to improve function and quality of life and avoid reliance on acute therapies. Options include CGRP monoclonal antibodies (mAbs), administered subcutaneously or by intravenous infusion, and onabotulinumtoxinA injection. Current CGRP mAbs include eptinezumab, erenumab, fremanezumab, and galcanezumab. Combined CGRP mAb therapy with onabotulinumtoxinA may be an effective alternative for patients with resistant FHM. 

Heidi Moawad, MD, Clinical Assistant Professor, Department of Medical Education, Case Western Reserve University School of Medicine, Cleveland, Ohio.

Heidi Moawad, MD, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

FHM is a rare phenotype of migraine with aura with a characteristic presentation of motor aura. Motor aura presents as unilateral muscle weakness that tends to be felt first in the hands or arm and may spread to the face. To date, three distinct types have been identified by mutations in one of three genes. Type 1 is the most common and is associated with mutations in the gene CACNA1A. Mutations in ATP1A2 underlie type 2 FHM, and mutations in SCN1A underlie type 3 FHM.

FHM is distinguished from other hemiplegic migraine by family history of one or more affected first- or second-degree relatives. Genetic studies have shown FHM to have autosomal dominant inheritance. From half to three quarters of patients with FHM will have one of the more than 30 identified mutations on CACNA1A that diagnose type 1 FHM. These mutations affect transmission of glutamate in the neurons and neuronal reactions, increasing the susceptibility to cortical spreading depression associated with migraine. Mutations in ATP1A2 are found in about 20% of patients with FHM (type 2). More than 80 individual mutations have been identified, which alter sodium-potassium metabolism in neurons. About 5% of patients have type 3 FHM, associated with mutations in SCN1A that create gain of function or loss of function in neuronal voltage-gated sodium channels. Studies of other possible genes and mutations in relation to FHM, including PRRT2, are ongoing, but to date the associations are not clearly established. 

Patients with FHM may also report sensory symptoms, visual disturbances, or aphasia. FHM generally affects people in their teens and twenties (women more than men) and has an estimated prevalence of 0.003% of the population. On average, patients report having two to three attacks per year, and some patients go for extended periods without a recurrent attack. Motor aura may occur on the same or opposite side of the body as headache and may alternate affected sides with each attack. Differential diagnoses that should be ruled out include transient ischemic attacks, infections (eg, meningitis, encephalitis), tumors, seizures, other inherited disorders, and metabolic issues.

Like other forms of migraine with aura, FHM is treated with abortive and/or preventive medications. Given the rarity of FHM, there are few studies specifically in families with this phenotype. Patients should be counseled on trigger avoidance to limit exposure. Acute treatment includes nonsteroidal anti-inflammatory drugs, acetaminophen, and other nonopioid pain relievers. The class of calcitonin gene-related peptide (CGRP) antagonists (rimegepant, ubrogepant, zavegepant) may be considered. However, with FHM, medications associated with ischemia must be avoided. As such, triptans and ergotamines are generally contraindicated, as are beta-blockers. Patients with FHM and more frequent or severe attacks may be considered for preventive treatment to improve function and quality of life and avoid reliance on acute therapies. Options include CGRP monoclonal antibodies (mAbs), administered subcutaneously or by intravenous infusion, and onabotulinumtoxinA injection. Current CGRP mAbs include eptinezumab, erenumab, fremanezumab, and galcanezumab. Combined CGRP mAb therapy with onabotulinumtoxinA may be an effective alternative for patients with resistant FHM. 

Heidi Moawad, MD, Clinical Assistant Professor, Department of Medical Education, Case Western Reserve University School of Medicine, Cleveland, Ohio.

Heidi Moawad, MD, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

FHM is a rare phenotype of migraine with aura with a characteristic presentation of motor aura. Motor aura presents as unilateral muscle weakness that tends to be felt first in the hands or arm and may spread to the face. To date, three distinct types have been identified by mutations in one of three genes. Type 1 is the most common and is associated with mutations in the gene CACNA1A. Mutations in ATP1A2 underlie type 2 FHM, and mutations in SCN1A underlie type 3 FHM.

FHM is distinguished from other hemiplegic migraine by family history of one or more affected first- or second-degree relatives. Genetic studies have shown FHM to have autosomal dominant inheritance. From half to three quarters of patients with FHM will have one of the more than 30 identified mutations on CACNA1A that diagnose type 1 FHM. These mutations affect transmission of glutamate in the neurons and neuronal reactions, increasing the susceptibility to cortical spreading depression associated with migraine. Mutations in ATP1A2 are found in about 20% of patients with FHM (type 2). More than 80 individual mutations have been identified, which alter sodium-potassium metabolism in neurons. About 5% of patients have type 3 FHM, associated with mutations in SCN1A that create gain of function or loss of function in neuronal voltage-gated sodium channels. Studies of other possible genes and mutations in relation to FHM, including PRRT2, are ongoing, but to date the associations are not clearly established. 

Patients with FHM may also report sensory symptoms, visual disturbances, or aphasia. FHM generally affects people in their teens and twenties (women more than men) and has an estimated prevalence of 0.003% of the population. On average, patients report having two to three attacks per year, and some patients go for extended periods without a recurrent attack. Motor aura may occur on the same or opposite side of the body as headache and may alternate affected sides with each attack. Differential diagnoses that should be ruled out include transient ischemic attacks, infections (eg, meningitis, encephalitis), tumors, seizures, other inherited disorders, and metabolic issues.

Like other forms of migraine with aura, FHM is treated with abortive and/or preventive medications. Given the rarity of FHM, there are few studies specifically in families with this phenotype. Patients should be counseled on trigger avoidance to limit exposure. Acute treatment includes nonsteroidal anti-inflammatory drugs, acetaminophen, and other nonopioid pain relievers. The class of calcitonin gene-related peptide (CGRP) antagonists (rimegepant, ubrogepant, zavegepant) may be considered. However, with FHM, medications associated with ischemia must be avoided. As such, triptans and ergotamines are generally contraindicated, as are beta-blockers. Patients with FHM and more frequent or severe attacks may be considered for preventive treatment to improve function and quality of life and avoid reliance on acute therapies. Options include CGRP monoclonal antibodies (mAbs), administered subcutaneously or by intravenous infusion, and onabotulinumtoxinA injection. Current CGRP mAbs include eptinezumab, erenumab, fremanezumab, and galcanezumab. Combined CGRP mAb therapy with onabotulinumtoxinA may be an effective alternative for patients with resistant FHM. 

Heidi Moawad, MD, Clinical Assistant Professor, Department of Medical Education, Case Western Reserve University School of Medicine, Cleveland, Ohio.

Heidi Moawad, MD, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

Overall, persons with schizophrenia are more likely than the general population to be overweight and have cardiovascular risk factors before starting treatment with antipsychotics, and such treatment generally worsens these measures. Weight gain and associated morbidity and mortality are common side effects of antipsychotic medications. Olanzapine is associated with significant weight gain of 7% or more, higher than other second-generation antipsychotics. Olanzapine treatment is the major contributor to this patient's additional weight gain over the past 2 years. This added weight has translated to excess wear and tear on her joints, leading to evidence of osteoarthritis. Treatment with olanzapine is also independently associated with detrimental changes in cardiometabolic parameters.

Interventions to prevent or mitigate weight gain with antipsychotics are limited. In general, the American Psychiatric Association does not recommend switching antipsychotics for patients whose schizophrenia is well managed. However, there is increasing evidence that metformin may have a role in mitigating weight gain as well as beneficially modifying cardiometabolic factors in patients with schizophrenia being treated with olanzapine. A systematic review of emerging evidence with metformin in patients with schizophrenia suggests that metformin may also improve some cognitive symptoms of the illness, although further research is needed. The randomized, double-blind MELIA trial of metformin plus lifestyle intervention in antipsychotic-induced weight gain is ongoing. Starting metformin as a preventive measure at the same time as antipsychotic therapy may help to limit excess weight gain. 

Research continues on the potential benefit of adding weight loss medications, including glucagon-like peptide-1 (GLP-1) receptor agonists, to antipsychotics. Daily liraglutide is most widely studied, but a published case series with weekly semaglutide also demonstrated weight loss in this setting. Liraglutide also has shown beneficial cardiometabolic effects in patients using antipsychotic medications. More studies of these drugs and of GLP-1/glucose-dependent insulinotropic polypeptide agonists are needed to elucidate the optimal use of these therapies for patients with schizophrenia.

There are few other effective ways to mitigate weight gain with olanzapine. Patients should be counseled on nutrition and lifestyle modifications. Evidence supports improvement with structured lifestyle modifications across a range of patients with less severe mental health issues, and structured programs combined with motivational interviewing were associated with reductions in antipsychotic-induced weight gain in patients with severe mental illness. As with any patient with obesity, however, the success of lifestyle modifications is heavily dependent on the individual's ability and motivation to comply with recommended interventions. 

Nonpharmacologic interventions to address joint pain include heat or cold compresses, physical therapy, and strength and resistance training to improve the strength of muscles supporting the joints. If these measures are ineffective, nonsteroidal anti-inflammatory drugs (NSAIDs), including ibuprofen, naproxen, meloxicam, diclofenac, or celecoxib may be used with regular follow-up to assess cardiovascular and gastrointestinal health. Topical NSAIDs also may be useful. For more intractable joint pain, options include injecting a corticosteroid or sodium hyaluronate into the affected joints or joint replacement. 

Carolyn Newberry, MD, Assistant Professor of Medicine, Director of GI Nutrition, Innovative Center for Health and Nutrition in Gastroenterology (ICHANGE), Division of Gastroenterology, Weill Cornell Medical Center, New York, NY.

Disclosure: Carolyn Newberry, MD, has disclosed the following relevant financial relationships:

Serve(d) as a speaker or a member of a speakers bureau for: Baster International; InBody.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

Overall, persons with schizophrenia are more likely than the general population to be overweight and have cardiovascular risk factors before starting treatment with antipsychotics, and such treatment generally worsens these measures. Weight gain and associated morbidity and mortality are common side effects of antipsychotic medications. Olanzapine is associated with significant weight gain of 7% or more, higher than other second-generation antipsychotics. Olanzapine treatment is the major contributor to this patient's additional weight gain over the past 2 years. This added weight has translated to excess wear and tear on her joints, leading to evidence of osteoarthritis. Treatment with olanzapine is also independently associated with detrimental changes in cardiometabolic parameters.

Interventions to prevent or mitigate weight gain with antipsychotics are limited. In general, the American Psychiatric Association does not recommend switching antipsychotics for patients whose schizophrenia is well managed. However, there is increasing evidence that metformin may have a role in mitigating weight gain as well as beneficially modifying cardiometabolic factors in patients with schizophrenia being treated with olanzapine. A systematic review of emerging evidence with metformin in patients with schizophrenia suggests that metformin may also improve some cognitive symptoms of the illness, although further research is needed. The randomized, double-blind MELIA trial of metformin plus lifestyle intervention in antipsychotic-induced weight gain is ongoing. Starting metformin as a preventive measure at the same time as antipsychotic therapy may help to limit excess weight gain. 

Research continues on the potential benefit of adding weight loss medications, including glucagon-like peptide-1 (GLP-1) receptor agonists, to antipsychotics. Daily liraglutide is most widely studied, but a published case series with weekly semaglutide also demonstrated weight loss in this setting. Liraglutide also has shown beneficial cardiometabolic effects in patients using antipsychotic medications. More studies of these drugs and of GLP-1/glucose-dependent insulinotropic polypeptide agonists are needed to elucidate the optimal use of these therapies for patients with schizophrenia.

There are few other effective ways to mitigate weight gain with olanzapine. Patients should be counseled on nutrition and lifestyle modifications. Evidence supports improvement with structured lifestyle modifications across a range of patients with less severe mental health issues, and structured programs combined with motivational interviewing were associated with reductions in antipsychotic-induced weight gain in patients with severe mental illness. As with any patient with obesity, however, the success of lifestyle modifications is heavily dependent on the individual's ability and motivation to comply with recommended interventions. 

Nonpharmacologic interventions to address joint pain include heat or cold compresses, physical therapy, and strength and resistance training to improve the strength of muscles supporting the joints. If these measures are ineffective, nonsteroidal anti-inflammatory drugs (NSAIDs), including ibuprofen, naproxen, meloxicam, diclofenac, or celecoxib may be used with regular follow-up to assess cardiovascular and gastrointestinal health. Topical NSAIDs also may be useful. For more intractable joint pain, options include injecting a corticosteroid or sodium hyaluronate into the affected joints or joint replacement. 

Carolyn Newberry, MD, Assistant Professor of Medicine, Director of GI Nutrition, Innovative Center for Health and Nutrition in Gastroenterology (ICHANGE), Division of Gastroenterology, Weill Cornell Medical Center, New York, NY.

Disclosure: Carolyn Newberry, MD, has disclosed the following relevant financial relationships:

Serve(d) as a speaker or a member of a speakers bureau for: Baster International; InBody.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

Overall, persons with schizophrenia are more likely than the general population to be overweight and have cardiovascular risk factors before starting treatment with antipsychotics, and such treatment generally worsens these measures. Weight gain and associated morbidity and mortality are common side effects of antipsychotic medications. Olanzapine is associated with significant weight gain of 7% or more, higher than other second-generation antipsychotics. Olanzapine treatment is the major contributor to this patient's additional weight gain over the past 2 years. This added weight has translated to excess wear and tear on her joints, leading to evidence of osteoarthritis. Treatment with olanzapine is also independently associated with detrimental changes in cardiometabolic parameters.

Interventions to prevent or mitigate weight gain with antipsychotics are limited. In general, the American Psychiatric Association does not recommend switching antipsychotics for patients whose schizophrenia is well managed. However, there is increasing evidence that metformin may have a role in mitigating weight gain as well as beneficially modifying cardiometabolic factors in patients with schizophrenia being treated with olanzapine. A systematic review of emerging evidence with metformin in patients with schizophrenia suggests that metformin may also improve some cognitive symptoms of the illness, although further research is needed. The randomized, double-blind MELIA trial of metformin plus lifestyle intervention in antipsychotic-induced weight gain is ongoing. Starting metformin as a preventive measure at the same time as antipsychotic therapy may help to limit excess weight gain. 

Research continues on the potential benefit of adding weight loss medications, including glucagon-like peptide-1 (GLP-1) receptor agonists, to antipsychotics. Daily liraglutide is most widely studied, but a published case series with weekly semaglutide also demonstrated weight loss in this setting. Liraglutide also has shown beneficial cardiometabolic effects in patients using antipsychotic medications. More studies of these drugs and of GLP-1/glucose-dependent insulinotropic polypeptide agonists are needed to elucidate the optimal use of these therapies for patients with schizophrenia.

There are few other effective ways to mitigate weight gain with olanzapine. Patients should be counseled on nutrition and lifestyle modifications. Evidence supports improvement with structured lifestyle modifications across a range of patients with less severe mental health issues, and structured programs combined with motivational interviewing were associated with reductions in antipsychotic-induced weight gain in patients with severe mental illness. As with any patient with obesity, however, the success of lifestyle modifications is heavily dependent on the individual's ability and motivation to comply with recommended interventions. 

Nonpharmacologic interventions to address joint pain include heat or cold compresses, physical therapy, and strength and resistance training to improve the strength of muscles supporting the joints. If these measures are ineffective, nonsteroidal anti-inflammatory drugs (NSAIDs), including ibuprofen, naproxen, meloxicam, diclofenac, or celecoxib may be used with regular follow-up to assess cardiovascular and gastrointestinal health. Topical NSAIDs also may be useful. For more intractable joint pain, options include injecting a corticosteroid or sodium hyaluronate into the affected joints or joint replacement. 

Carolyn Newberry, MD, Assistant Professor of Medicine, Director of GI Nutrition, Innovative Center for Health and Nutrition in Gastroenterology (ICHANGE), Division of Gastroenterology, Weill Cornell Medical Center, New York, NY.

Disclosure: Carolyn Newberry, MD, has disclosed the following relevant financial relationships:

Serve(d) as a speaker or a member of a speakers bureau for: Baster International; InBody.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

Migraine is a form of recurrent headache that can present as migraine with aura or migraine without aura, with the latter being the most common form. As in this patient, migraine without aura is a chronic form of headache of moderate to severe intensity that usually lasts for several hours but rarely may persist for up to 3 days. Headache pain is unilateral and often aggravated by triggers such as routine physical activity. The American Headache Society diagnostic criteria for migraine without aura include having symptoms of nausea and/or hypersensitivity to light or sound. This patient also described symptoms typical of the prodromal phase of migraine, which include yawning, temperature control, excessive thirst, and mood swings.

Patients who have migraine with aura also have unilateral headache pain of several hours' duration but experience visual (eg, dots or flashes) or sensory (prickly sensation on skin) symptoms, or may have brief difficulty with speech or motor function. These aura symptoms generally last 5 to 60 minutes before abating. 

The worldwide impact of migraine potentially reaches a billion individuals. Its prevalence is second only to tension-type headaches. Migraine occurs in patients of all ages and affects women at a rate two to three times higher than in men. Prevalence appears to peak in the third and fourth decades of life and tends to be lower among older adults. Migraine also has a negative effect on patients' work, school, or social lives, and is associated with increased rates of depression and anxiety in adults. For patients who are prone to migraines, potential triggers include some foods and beverages (including those that contain caffeine and alcohol), menstrual cycles in women, exposure to strobing or bright lights or loud sounds, stressful situations, extra physical activity, and too much or too little sleep. 

Migraine is a clinical diagnosis based on number of headaches (five or more episodes) plus two or more of the characteristic signs (unilateral, throbbing pain, pain intensity of ≥ 5 on a 10-point scale, and pain aggravated by routine physical motion, such as climbing stairs or bending over) plus nausea and/or photosensitivity or phonosensitivity. Prodrome symptoms are reported by about 70% of adult patients. Diagnosis rarely requires neuroimaging; however, before prescribing medication, a complete lab and metabolic workup should be done.

Management of migraine without aura includes acute and preventive interventions. Acute interventions cited by the American Headache Society include nonsteroidal anti-inflammatory drugs and acetaminophen for mild pain, and migraine-specific therapies such as the triptans, ergotamine derivatives, gepants (rimegepant, ubrogepant), and lasmiditan. Because response to any of these therapies will differ among patients with migraine, shared decision-making with patients about benefits and potential side effects is necessary and should include flexibility to change therapy if needed. 

Preventive therapy should be offered to patients experiencing six or more migraines a month (regardless of impairment) and those, like this patient, with three or more migraines a month that significantly impair daily activities. Preventive therapy can be considered for those with fewer monthly episodes, depending on the degree of impairment. Oral preventive therapies with established efficacy include candesartan, certain beta-blockers, topiramate, and valproate. Parenteral monoclonal antibodies that inhibit calcitonin gene-related peptide activity (eptinezumab, erenumab, fremanezumab, and galcanezumab) and onabotulinumtoxinA may be considered if oral therapies provide inadequate prevention. 

Tension-type headache is the most common form of primary headache. These headaches are bilateral and characterized by a pressing or dull sensation that is often mild in intensity. They are different from migraine in that they occur infrequently, lack sensory symptoms, and generally are of shorter duration (30 minutes to 24 hours). Fasting-related headache is characterized by diffuse, nonpulsating pain and is relieved with food. 

Heidi Moawad, MD, Clinical Assistant Professor, Department of Medical Education, Case Western Reserve University School of Medicine, Cleveland, Ohio.

Heidi Moawad, MD, has disclosed no relevant financial relationships.
 

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.
 

Migraine is a form of recurrent headache that can present as migraine with aura or migraine without aura, with the latter being the most common form. As in this patient, migraine without aura is a chronic form of headache of moderate to severe intensity that usually lasts for several hours but rarely may persist for up to 3 days. Headache pain is unilateral and often aggravated by triggers such as routine physical activity. The American Headache Society diagnostic criteria for migraine without aura include having symptoms of nausea and/or hypersensitivity to light or sound. This patient also described symptoms typical of the prodromal phase of migraine, which include yawning, temperature control, excessive thirst, and mood swings.

Patients who have migraine with aura also have unilateral headache pain of several hours' duration but experience visual (eg, dots or flashes) or sensory (prickly sensation on skin) symptoms, or may have brief difficulty with speech or motor function. These aura symptoms generally last 5 to 60 minutes before abating. 

The worldwide impact of migraine potentially reaches a billion individuals. Its prevalence is second only to tension-type headaches. Migraine occurs in patients of all ages and affects women at a rate two to three times higher than in men. Prevalence appears to peak in the third and fourth decades of life and tends to be lower among older adults. Migraine also has a negative effect on patients' work, school, or social lives, and is associated with increased rates of depression and anxiety in adults. For patients who are prone to migraines, potential triggers include some foods and beverages (including those that contain caffeine and alcohol), menstrual cycles in women, exposure to strobing or bright lights or loud sounds, stressful situations, extra physical activity, and too much or too little sleep. 

Migraine is a clinical diagnosis based on number of headaches (five or more episodes) plus two or more of the characteristic signs (unilateral, throbbing pain, pain intensity of ≥ 5 on a 10-point scale, and pain aggravated by routine physical motion, such as climbing stairs or bending over) plus nausea and/or photosensitivity or phonosensitivity. Prodrome symptoms are reported by about 70% of adult patients. Diagnosis rarely requires neuroimaging; however, before prescribing medication, a complete lab and metabolic workup should be done.

Management of migraine without aura includes acute and preventive interventions. Acute interventions cited by the American Headache Society include nonsteroidal anti-inflammatory drugs and acetaminophen for mild pain, and migraine-specific therapies such as the triptans, ergotamine derivatives, gepants (rimegepant, ubrogepant), and lasmiditan. Because response to any of these therapies will differ among patients with migraine, shared decision-making with patients about benefits and potential side effects is necessary and should include flexibility to change therapy if needed. 

Preventive therapy should be offered to patients experiencing six or more migraines a month (regardless of impairment) and those, like this patient, with three or more migraines a month that significantly impair daily activities. Preventive therapy can be considered for those with fewer monthly episodes, depending on the degree of impairment. Oral preventive therapies with established efficacy include candesartan, certain beta-blockers, topiramate, and valproate. Parenteral monoclonal antibodies that inhibit calcitonin gene-related peptide activity (eptinezumab, erenumab, fremanezumab, and galcanezumab) and onabotulinumtoxinA may be considered if oral therapies provide inadequate prevention. 

Tension-type headache is the most common form of primary headache. These headaches are bilateral and characterized by a pressing or dull sensation that is often mild in intensity. They are different from migraine in that they occur infrequently, lack sensory symptoms, and generally are of shorter duration (30 minutes to 24 hours). Fasting-related headache is characterized by diffuse, nonpulsating pain and is relieved with food. 

Heidi Moawad, MD, Clinical Assistant Professor, Department of Medical Education, Case Western Reserve University School of Medicine, Cleveland, Ohio.

Heidi Moawad, MD, has disclosed no relevant financial relationships.
 

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.
 

Migraine is a form of recurrent headache that can present as migraine with aura or migraine without aura, with the latter being the most common form. As in this patient, migraine without aura is a chronic form of headache of moderate to severe intensity that usually lasts for several hours but rarely may persist for up to 3 days. Headache pain is unilateral and often aggravated by triggers such as routine physical activity. The American Headache Society diagnostic criteria for migraine without aura include having symptoms of nausea and/or hypersensitivity to light or sound. This patient also described symptoms typical of the prodromal phase of migraine, which include yawning, temperature control, excessive thirst, and mood swings.

Patients who have migraine with aura also have unilateral headache pain of several hours' duration but experience visual (eg, dots or flashes) or sensory (prickly sensation on skin) symptoms, or may have brief difficulty with speech or motor function. These aura symptoms generally last 5 to 60 minutes before abating. 

The worldwide impact of migraine potentially reaches a billion individuals. Its prevalence is second only to tension-type headaches. Migraine occurs in patients of all ages and affects women at a rate two to three times higher than in men. Prevalence appears to peak in the third and fourth decades of life and tends to be lower among older adults. Migraine also has a negative effect on patients' work, school, or social lives, and is associated with increased rates of depression and anxiety in adults. For patients who are prone to migraines, potential triggers include some foods and beverages (including those that contain caffeine and alcohol), menstrual cycles in women, exposure to strobing or bright lights or loud sounds, stressful situations, extra physical activity, and too much or too little sleep. 

Migraine is a clinical diagnosis based on number of headaches (five or more episodes) plus two or more of the characteristic signs (unilateral, throbbing pain, pain intensity of ≥ 5 on a 10-point scale, and pain aggravated by routine physical motion, such as climbing stairs or bending over) plus nausea and/or photosensitivity or phonosensitivity. Prodrome symptoms are reported by about 70% of adult patients. Diagnosis rarely requires neuroimaging; however, before prescribing medication, a complete lab and metabolic workup should be done.

Management of migraine without aura includes acute and preventive interventions. Acute interventions cited by the American Headache Society include nonsteroidal anti-inflammatory drugs and acetaminophen for mild pain, and migraine-specific therapies such as the triptans, ergotamine derivatives, gepants (rimegepant, ubrogepant), and lasmiditan. Because response to any of these therapies will differ among patients with migraine, shared decision-making with patients about benefits and potential side effects is necessary and should include flexibility to change therapy if needed. 

Preventive therapy should be offered to patients experiencing six or more migraines a month (regardless of impairment) and those, like this patient, with three or more migraines a month that significantly impair daily activities. Preventive therapy can be considered for those with fewer monthly episodes, depending on the degree of impairment. Oral preventive therapies with established efficacy include candesartan, certain beta-blockers, topiramate, and valproate. Parenteral monoclonal antibodies that inhibit calcitonin gene-related peptide activity (eptinezumab, erenumab, fremanezumab, and galcanezumab) and onabotulinumtoxinA may be considered if oral therapies provide inadequate prevention. 

Tension-type headache is the most common form of primary headache. These headaches are bilateral and characterized by a pressing or dull sensation that is often mild in intensity. They are different from migraine in that they occur infrequently, lack sensory symptoms, and generally are of shorter duration (30 minutes to 24 hours). Fasting-related headache is characterized by diffuse, nonpulsating pain and is relieved with food. 

Heidi Moawad, MD, Clinical Assistant Professor, Department of Medical Education, Case Western Reserve University School of Medicine, Cleveland, Ohio.

Heidi Moawad, MD, has disclosed no relevant financial relationships.
 

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.
 

As seen in red on the radiogram, the patient's heart is grossly enlarged, indicating cardiomegaly. Cardiomegaly often is first diagnosed on chest imaging, with diagnosis based on a cardiothoracic ratio of < 0.5. It is not a disease but rather a manifestation of an underlying cause. Patients may have few or no cardiomegaly-related symptoms or have symptoms typical of cardiac dysfunction, like this patient's dyspnea and edema. Conditions that impair normal circulation and that are associated with cardiomegaly development include hypertension, obesity, heart valve disorders, thyroid dysfunction, and anemia. In this patient, cardiomegaly probably has been triggered by uncontrolled hypertension and ongoing obesity. This patient's bloodwork also indicates prediabetes and incipient type 2 diabetes (T2D) (the diagnostic criteria for which are A1c ≥ 6.5% and fasting plasma glucose ≥ 126 mg/dL).

As many as 42% of adults in the United States meet criteria for obesity and are at risk for obesity-related conditions, including cardiomegaly. Guidelines for management of patients with obesity have been published by The Obesity Society and the American Association of Clinical Endocrinologists, and management of obesity is a necessary part of comprehensive care of patients with T2D  as well. For most patients, a BMI ≥ 30 diagnoses obesity; this patient has class 1 obesity, based on a BMI of 30 to 34.9. The patient also has complications of obesity, including stage 2 hypertension and prediabetes. As such, lifestyle management plus medical therapy is the recommended approach to weight loss, with a goal of losing 5% to 10% or more of baseline body weight.

The Obesity Society states that all patients with obesity should be offered effective, evidence-based interventions. Medical management of obesity includes use of pharmacologic interventions with proven benefit in weight loss, such as glucagon-like peptide-1 receptor agonists (GLP-1 RAs; eg, semaglutide) or dual gastric inhibitory polypeptide (GIP)/GLP-1 RAs (eg, tirzepatide). Semaglutide and tirzepatide are likely to have cardiovascular benefits for patients with obesity as well. Other medications approved for management of obesity include liraglutide, orlistat, phentermine HCl (with or without topiramate), and naltrexone plus bupropion. The American Diabetes Association (ADA) recommendations for management of obesity in patients with T2D give preference to semaglutide 2.4 mg/wk and tirzepatide at weekly doses of 5, 10, or 15 mg, depending on patient factors. 

As important for this patient is to get control of hypertension. Studies have shown that lowering blood pressure improves left ventricular hypertrophy, a common source of cardiomegaly. Hypertension guidelines from the American College of Cardiology/American Heart Association recommend a blood pressure goal < 130/80 mm Hg for most adults, which is consistent with the current recommendation from the ADA. Management of hypertension should first incorporate a low-sodium, healthy diet (such as the Dietary Approaches to Stop Hypertension [DASH] diet), physical activity, and weight loss; however, many patients (especially with stage 2 hypertension) require pharmacologic therapy as well. Single-pill combination therapies of drugs from different classes (eg, angiotensin-converting enzyme inhibitor plus calcium channel blocker) are preferred for patients with stage 2 hypertension to improve efficacy and enhance adherence.

Romesh K. Khardori, MD, PhD, Professor, Department of Internal Medicine, Division of Diabetes, Endocrine, and Metabolic Disorders, Eastern Virginia Medical School; EVMS Medical Group, Norfolk, Virginia.

Romesh K. Khardori, MD, PhD, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

As seen in red on the radiogram, the patient's heart is grossly enlarged, indicating cardiomegaly. Cardiomegaly often is first diagnosed on chest imaging, with diagnosis based on a cardiothoracic ratio of < 0.5. It is not a disease but rather a manifestation of an underlying cause. Patients may have few or no cardiomegaly-related symptoms or have symptoms typical of cardiac dysfunction, like this patient's dyspnea and edema. Conditions that impair normal circulation and that are associated with cardiomegaly development include hypertension, obesity, heart valve disorders, thyroid dysfunction, and anemia. In this patient, cardiomegaly probably has been triggered by uncontrolled hypertension and ongoing obesity. This patient's bloodwork also indicates prediabetes and incipient type 2 diabetes (T2D) (the diagnostic criteria for which are A1c ≥ 6.5% and fasting plasma glucose ≥ 126 mg/dL).

As many as 42% of adults in the United States meet criteria for obesity and are at risk for obesity-related conditions, including cardiomegaly. Guidelines for management of patients with obesity have been published by The Obesity Society and the American Association of Clinical Endocrinologists, and management of obesity is a necessary part of comprehensive care of patients with T2D  as well. For most patients, a BMI ≥ 30 diagnoses obesity; this patient has class 1 obesity, based on a BMI of 30 to 34.9. The patient also has complications of obesity, including stage 2 hypertension and prediabetes. As such, lifestyle management plus medical therapy is the recommended approach to weight loss, with a goal of losing 5% to 10% or more of baseline body weight.

The Obesity Society states that all patients with obesity should be offered effective, evidence-based interventions. Medical management of obesity includes use of pharmacologic interventions with proven benefit in weight loss, such as glucagon-like peptide-1 receptor agonists (GLP-1 RAs; eg, semaglutide) or dual gastric inhibitory polypeptide (GIP)/GLP-1 RAs (eg, tirzepatide). Semaglutide and tirzepatide are likely to have cardiovascular benefits for patients with obesity as well. Other medications approved for management of obesity include liraglutide, orlistat, phentermine HCl (with or without topiramate), and naltrexone plus bupropion. The American Diabetes Association (ADA) recommendations for management of obesity in patients with T2D give preference to semaglutide 2.4 mg/wk and tirzepatide at weekly doses of 5, 10, or 15 mg, depending on patient factors. 

As important for this patient is to get control of hypertension. Studies have shown that lowering blood pressure improves left ventricular hypertrophy, a common source of cardiomegaly. Hypertension guidelines from the American College of Cardiology/American Heart Association recommend a blood pressure goal < 130/80 mm Hg for most adults, which is consistent with the current recommendation from the ADA. Management of hypertension should first incorporate a low-sodium, healthy diet (such as the Dietary Approaches to Stop Hypertension [DASH] diet), physical activity, and weight loss; however, many patients (especially with stage 2 hypertension) require pharmacologic therapy as well. Single-pill combination therapies of drugs from different classes (eg, angiotensin-converting enzyme inhibitor plus calcium channel blocker) are preferred for patients with stage 2 hypertension to improve efficacy and enhance adherence.

Romesh K. Khardori, MD, PhD, Professor, Department of Internal Medicine, Division of Diabetes, Endocrine, and Metabolic Disorders, Eastern Virginia Medical School; EVMS Medical Group, Norfolk, Virginia.

Romesh K. Khardori, MD, PhD, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

As seen in red on the radiogram, the patient's heart is grossly enlarged, indicating cardiomegaly. Cardiomegaly often is first diagnosed on chest imaging, with diagnosis based on a cardiothoracic ratio of < 0.5. It is not a disease but rather a manifestation of an underlying cause. Patients may have few or no cardiomegaly-related symptoms or have symptoms typical of cardiac dysfunction, like this patient's dyspnea and edema. Conditions that impair normal circulation and that are associated with cardiomegaly development include hypertension, obesity, heart valve disorders, thyroid dysfunction, and anemia. In this patient, cardiomegaly probably has been triggered by uncontrolled hypertension and ongoing obesity. This patient's bloodwork also indicates prediabetes and incipient type 2 diabetes (T2D) (the diagnostic criteria for which are A1c ≥ 6.5% and fasting plasma glucose ≥ 126 mg/dL).

As many as 42% of adults in the United States meet criteria for obesity and are at risk for obesity-related conditions, including cardiomegaly. Guidelines for management of patients with obesity have been published by The Obesity Society and the American Association of Clinical Endocrinologists, and management of obesity is a necessary part of comprehensive care of patients with T2D  as well. For most patients, a BMI ≥ 30 diagnoses obesity; this patient has class 1 obesity, based on a BMI of 30 to 34.9. The patient also has complications of obesity, including stage 2 hypertension and prediabetes. As such, lifestyle management plus medical therapy is the recommended approach to weight loss, with a goal of losing 5% to 10% or more of baseline body weight.

The Obesity Society states that all patients with obesity should be offered effective, evidence-based interventions. Medical management of obesity includes use of pharmacologic interventions with proven benefit in weight loss, such as glucagon-like peptide-1 receptor agonists (GLP-1 RAs; eg, semaglutide) or dual gastric inhibitory polypeptide (GIP)/GLP-1 RAs (eg, tirzepatide). Semaglutide and tirzepatide are likely to have cardiovascular benefits for patients with obesity as well. Other medications approved for management of obesity include liraglutide, orlistat, phentermine HCl (with or without topiramate), and naltrexone plus bupropion. The American Diabetes Association (ADA) recommendations for management of obesity in patients with T2D give preference to semaglutide 2.4 mg/wk and tirzepatide at weekly doses of 5, 10, or 15 mg, depending on patient factors. 

As important for this patient is to get control of hypertension. Studies have shown that lowering blood pressure improves left ventricular hypertrophy, a common source of cardiomegaly. Hypertension guidelines from the American College of Cardiology/American Heart Association recommend a blood pressure goal < 130/80 mm Hg for most adults, which is consistent with the current recommendation from the ADA. Management of hypertension should first incorporate a low-sodium, healthy diet (such as the Dietary Approaches to Stop Hypertension [DASH] diet), physical activity, and weight loss; however, many patients (especially with stage 2 hypertension) require pharmacologic therapy as well. Single-pill combination therapies of drugs from different classes (eg, angiotensin-converting enzyme inhibitor plus calcium channel blocker) are preferred for patients with stage 2 hypertension to improve efficacy and enhance adherence.

Romesh K. Khardori, MD, PhD, Professor, Department of Internal Medicine, Division of Diabetes, Endocrine, and Metabolic Disorders, Eastern Virginia Medical School; EVMS Medical Group, Norfolk, Virginia.

Romesh K. Khardori, MD, PhD, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

Migraines are episodic or chronic headaches, typically occurring on one side of the head, that have distinct characteristics and definitions from the International Classification of Headache Disorders, 3rd edition (ICHD 3). Migraine can occur at any age and is thought to affect about 5% of children before puberty, increases in prevalence after puberty, and reaches about 30% prevalence at age 25-30 years. Patients with migraine with aura have recurrent, fully reversible symptoms that can include diplopia, motor or sensory disturbances, and/or trouble with language that generally precede headache development. In some cases, aura may develop and resolve without headache. Migraine with aura can present at any age from early childhood onward and is present in about 30% of children and adolescents with migraine. In general, migraine with aura is more prevalent in female than in male individuals, especially adolescents. 

Migraine with brainstem aura, as is the case here, is a specific subtype of migraine with aura, in which the aura specifically reflects an origin within the brainstem. Brainstem symptoms include diplopia, vertigo, difficulty controlling speech muscles, tinnitus, hearing loss, loss of coordination, and possibly impaired consciousness. For the diagnosis of migraine with brainstem aura, patients must not have motor or retinal symptoms. Aura development often is preceded by premonitory symptoms, such as fatigue, hunger or food cravings, and mood elevations.

Migraine without aura, in contrast, is characterized by recurrent moderate to severe pulsating headache lasting from a few hours to up to 3 days. Migraine without aura often causes nausea and sensitivity to light and/or sound.

Chronic migraine is defined as headache (with or without aura) occurring 15 or more days per month for at least the past 3 months. This patient's history does not fit the definition of chronic migraine.

Tension-type headaches generally are bilateral, with durations ranging from minutes to days. They tend to be mild to moderate in intensity and symptoms are not worsened by physical activity. In addition to their bilateral nature, these headaches differ from migraine in lacking associated visual, cortical, or other symptoms. 

Any diagnosis of migraine requires assessment over time, using diagnostic criteria established by the International Headache Society in ICHD 3. It is not necessary to perform neuroimaging studies or CT in patients with migraine symptoms and an otherwise normal neurologic exam.

When a diagnosis of migraine with brainstem aura is established, pediatric or adolescent patients and their families should first be counseled on nonpharmacologic interventions. These interventions, which have demonstrated benefits in reducing headache frequency, include lifestyle modifications, regular sleep and meal schedules, adequate fluid intake, cognitive-behavioral therapy, stress management techniques, massage, and biofeedback techniques. Recommended for acute treatment of migraine are nonsteroidal anti-inflammatory drugs, acetaminophen, and triptans. There is limited evidence in pediatric or adolescent patients with use of preventive medications, such as topiramate, amitriptyline, or onabotulinumtoxinA. In clinical trials, patients receiving placebo saw improvements, and active treatments were only marginally, if at all, more effective. Current guidelines recommend a frank discussion with parents about the limitations of preventive therapies before making decisions to use them. 

Heidi Moawad, MD, Clinical Assistant Professor, Department of Medical Education, Case Western Reserve University School of Medicine, Cleveland, Ohio.

Heidi Moawad, MD, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

Migraines are episodic or chronic headaches, typically occurring on one side of the head, that have distinct characteristics and definitions from the International Classification of Headache Disorders, 3rd edition (ICHD 3). Migraine can occur at any age and is thought to affect about 5% of children before puberty, increases in prevalence after puberty, and reaches about 30% prevalence at age 25-30 years. Patients with migraine with aura have recurrent, fully reversible symptoms that can include diplopia, motor or sensory disturbances, and/or trouble with language that generally precede headache development. In some cases, aura may develop and resolve without headache. Migraine with aura can present at any age from early childhood onward and is present in about 30% of children and adolescents with migraine. In general, migraine with aura is more prevalent in female than in male individuals, especially adolescents. 

Migraine with brainstem aura, as is the case here, is a specific subtype of migraine with aura, in which the aura specifically reflects an origin within the brainstem. Brainstem symptoms include diplopia, vertigo, difficulty controlling speech muscles, tinnitus, hearing loss, loss of coordination, and possibly impaired consciousness. For the diagnosis of migraine with brainstem aura, patients must not have motor or retinal symptoms. Aura development often is preceded by premonitory symptoms, such as fatigue, hunger or food cravings, and mood elevations.

Migraine without aura, in contrast, is characterized by recurrent moderate to severe pulsating headache lasting from a few hours to up to 3 days. Migraine without aura often causes nausea and sensitivity to light and/or sound.

Chronic migraine is defined as headache (with or without aura) occurring 15 or more days per month for at least the past 3 months. This patient's history does not fit the definition of chronic migraine.

Tension-type headaches generally are bilateral, with durations ranging from minutes to days. They tend to be mild to moderate in intensity and symptoms are not worsened by physical activity. In addition to their bilateral nature, these headaches differ from migraine in lacking associated visual, cortical, or other symptoms. 

Any diagnosis of migraine requires assessment over time, using diagnostic criteria established by the International Headache Society in ICHD 3. It is not necessary to perform neuroimaging studies or CT in patients with migraine symptoms and an otherwise normal neurologic exam.

When a diagnosis of migraine with brainstem aura is established, pediatric or adolescent patients and their families should first be counseled on nonpharmacologic interventions. These interventions, which have demonstrated benefits in reducing headache frequency, include lifestyle modifications, regular sleep and meal schedules, adequate fluid intake, cognitive-behavioral therapy, stress management techniques, massage, and biofeedback techniques. Recommended for acute treatment of migraine are nonsteroidal anti-inflammatory drugs, acetaminophen, and triptans. There is limited evidence in pediatric or adolescent patients with use of preventive medications, such as topiramate, amitriptyline, or onabotulinumtoxinA. In clinical trials, patients receiving placebo saw improvements, and active treatments were only marginally, if at all, more effective. Current guidelines recommend a frank discussion with parents about the limitations of preventive therapies before making decisions to use them. 

Heidi Moawad, MD, Clinical Assistant Professor, Department of Medical Education, Case Western Reserve University School of Medicine, Cleveland, Ohio.

Heidi Moawad, MD, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.

Migraines are episodic or chronic headaches, typically occurring on one side of the head, that have distinct characteristics and definitions from the International Classification of Headache Disorders, 3rd edition (ICHD 3). Migraine can occur at any age and is thought to affect about 5% of children before puberty, increases in prevalence after puberty, and reaches about 30% prevalence at age 25-30 years. Patients with migraine with aura have recurrent, fully reversible symptoms that can include diplopia, motor or sensory disturbances, and/or trouble with language that generally precede headache development. In some cases, aura may develop and resolve without headache. Migraine with aura can present at any age from early childhood onward and is present in about 30% of children and adolescents with migraine. In general, migraine with aura is more prevalent in female than in male individuals, especially adolescents. 

Migraine with brainstem aura, as is the case here, is a specific subtype of migraine with aura, in which the aura specifically reflects an origin within the brainstem. Brainstem symptoms include diplopia, vertigo, difficulty controlling speech muscles, tinnitus, hearing loss, loss of coordination, and possibly impaired consciousness. For the diagnosis of migraine with brainstem aura, patients must not have motor or retinal symptoms. Aura development often is preceded by premonitory symptoms, such as fatigue, hunger or food cravings, and mood elevations.

Migraine without aura, in contrast, is characterized by recurrent moderate to severe pulsating headache lasting from a few hours to up to 3 days. Migraine without aura often causes nausea and sensitivity to light and/or sound.

Chronic migraine is defined as headache (with or without aura) occurring 15 or more days per month for at least the past 3 months. This patient's history does not fit the definition of chronic migraine.

Tension-type headaches generally are bilateral, with durations ranging from minutes to days. They tend to be mild to moderate in intensity and symptoms are not worsened by physical activity. In addition to their bilateral nature, these headaches differ from migraine in lacking associated visual, cortical, or other symptoms. 

Any diagnosis of migraine requires assessment over time, using diagnostic criteria established by the International Headache Society in ICHD 3. It is not necessary to perform neuroimaging studies or CT in patients with migraine symptoms and an otherwise normal neurologic exam.

When a diagnosis of migraine with brainstem aura is established, pediatric or adolescent patients and their families should first be counseled on nonpharmacologic interventions. These interventions, which have demonstrated benefits in reducing headache frequency, include lifestyle modifications, regular sleep and meal schedules, adequate fluid intake, cognitive-behavioral therapy, stress management techniques, massage, and biofeedback techniques. Recommended for acute treatment of migraine are nonsteroidal anti-inflammatory drugs, acetaminophen, and triptans. There is limited evidence in pediatric or adolescent patients with use of preventive medications, such as topiramate, amitriptyline, or onabotulinumtoxinA. In clinical trials, patients receiving placebo saw improvements, and active treatments were only marginally, if at all, more effective. Current guidelines recommend a frank discussion with parents about the limitations of preventive therapies before making decisions to use them. 

Heidi Moawad, MD, Clinical Assistant Professor, Department of Medical Education, Case Western Reserve University School of Medicine, Cleveland, Ohio.

Heidi Moawad, MD, has disclosed no relevant financial relationships.

Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.