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Obesity is a prevalent global problem that affects patients with major mental illness disproportionately.

 It is associated with cardiovascular risk factors, including hypertension, dyslipidemia, and impaired glucose tolerance. Not surprisingly, the prevalence of these conditions is also high in patients with major mental illness. In fact, patients with major mental illness have a lifespan 

 than the general population, with cardiovascular mortality largely accounts for this difference.

Several biological, psychological, behavioral, and social factors predispose patients with major mental illness to obesity. One well-established risk factor is the weight gain-inducing side effect of antipsychotic drugs.

 Two features of this risk factor make it stand out: It is modifiable, and it is under the control of the prescriber.

Weight Gain-Inducing Risk of Antipsychotic Drugs

Most early antipsychotic drugs caused acute and chronic motor side effects. Clozapine was different because it was not haloperidol-like or a high-potency dopamine-2 full antagonist, but its routine use was prevented by the risk of agranulocytosis. Several safer atypical antipsychotic drugs have become available, and they are now standard treatment for schizophrenia and other approved indications. Despite this progress, an important side effect of clozapine—weight gain—has remained an issue with later-generation antipsychotics.

Researchers use 2 measures to determine the weight gain-inducing side effects of psychotropic drugs

: how many patients exposed to a given drug gain weight and how much weight is gained by patients. The latter can be measured as a crude number, or it can be standardized as a proportion of weight gain from baseline. Generally, weight gain greater than 7% from baseline is considered significant.

We now have extensive research on the weight gain-inducing and metabolic risks of antipsychotic drugs, including meta-analyses of the data.

 If we leave subtle differences and academic discussions aside, the common antipsychotic drugs can be grouped into 3 categories of weight gain-inducing potential (

There are a few important things to remember when contending with weight gain-inducing risk. First, weight gain is an individual-specific phenomenon; therefore, each patient must be monitored individually. Second, young patients who were not previously exposed to an antipsychotic drug (ie, drug-naive patients) are at a much higher risk of weight gain than older individuals who are not drug-naïve.

 Third, there is some evidence that metabolic complications (dyslipidemia and/or glucose intolerance) may result from these drugs independent of significant weight gain.

 Lastly, antipsychotic drug use is associated with weight gain irrespective of the diagnosis.

Limiting and Managing Drug-Induced Weight Gain

A preventive approach. Losing excess weight is tough for anyone and even tougher for individuals with major mental illness.

 Obesity might not receive much clinical attention because it is not acutely distressing or life-threatening. In the long term, however, it contributes to morbidity and mortality. In addition, young, nonobese, drug-naive patients can gain significant weight within a matter of months when exposed to antipsychotic drugs with a high risk of weight gain.

 Once they have gained that weight, many of them will never be able to lose it.

Differences in the efficacy of commonly used antipsychotics are marginal, but differences in their weight gain-inducing potential are huge.

 There is little justification for prescribing an antipsychotic drug that has a high potential to induce weight gain when there are safer alternatives. A more reasonable approach would be to start with a low-risk medication and switch to another medication in case of inefficacy or intolerance.

Despite limited evidence, second-generation antipsychotics are used for several off-label conditions.

 Psychiatric conditions generally have a high placebo response, which may be what off-label antipsychotic use offers, but at a much higher side-effect burden than placebo. It is quite concerning that off-label antipsychotic use is prevalent in children and adolescents, who are particularly prone to these weight gain-inducing and metabolic side effects. The Choosing Wisely 

Baseline assessment and ongoing monitoring. In 2004, the APA along with other associations issued a consensus statement on baseline assessment and monitoring of patients who are prescribed an antipsychotic drug for any indication (

 Measurement of waist circumference may not be practical in some cases, but tracking body mass index should not be a problem. Inquiring about family history of antipsychotic drug use, including response and side effects, could also provide useful information.

According to the guidelines, several factors contribute to nonadherence. These include clinicians’ lack of knowledge, psychiatrists’ limited training in monitoring patients’ physical health, limited resources, time constraints, diffusion of roles, and patient nonadherence.

 If an abnormality is detected that warrants further assessment or treatment, it should be communicated to the patient’s general physician with clarity about role designation for further assessment and management. Poor physical health care of patients with major mental illness is a systemic problem. Psychiatrists should use their social influence to shift health care culture, clinical prompts, and monitoring tools to 

 an integrated or coordinated health care approach.

Prioritizing discussions of weight gain, its complications, and healthy lifestyle. Clinical encounters are often too brief to tackle all important matters. In the hierarchy of priorities, discussion of weight and healthy lifestyle are often at the bottom of the list. However, patients with major mental illness are prone to obesity even without an iatrogenic contribution. Furthermore, personal and socioeconomic factors often make it more difficult for individuals with mental illness to adopt healthy lifestyles.

 Obesity is associated with stigma and poor self-esteem; presenting weight issues as a medical problem can help destigmatize it. Discussions about obesity and its complications would automatically become a focus of clinical attention if the aforementioned APA guidance (

 were incorporated into clinical practice.

Involvement of other experts for healthy lifestyle interventions.

 Healthy lifestyle interventions are most effective in helping obese patients lose weight and offer the best long-term outcome.

 They should be offered to all suitable patients irrespective of other offered interventions.

For a healthy lifestyle intervention to be effective, it should include individualized counseling on diet and exercise, cognitive and behavioral interventions, setting well-defined, attainable goals, objective monitoring of progress, and expertise to plan and implement the interventions.

 Most psychiatrists do not have the time or expertise to take on these tasks, so involving relevant professionals (eg, dieticians, psychologists, occupational therapists, and case managers for obese patients) is a good idea. Patients who are already obese or who are gaining unhealthy amounts of weight should be referred to these professionals after appropriate counseling. In addition to monitoring measures of obesity, the 

 can be used to monitor general physical fitness.

 Adopting a healthy lifestyle is very difficult for patients with major mental illness due to several factors, many of which are not in their control.

 High failure rates in the form of nonadherence and drop-outs are normal and should not be taken as a disappointment in the intervention or the patient.

Nonacademic medical centers may not have access to healthy lifestyle intervention professionals who have experience working with patients with major mental illness. In such situations, psychiatrists who are knowledgeable about the interventions can guide their colleagues on matters specific to this patient population.

Another efficient approach is to offer them in a group setting. A group setting validates the widespread nature of the problem, and patients can draw encouragement from each other. However, only psychiatrically stable patients would be suitable candidates for a group intervention and, in some cases, patient advocacy, staff capacity building, leadership engagement, and change in organizational policy may be needed.

Switching out a higher-risk antipsychotic drug for one that has a lower risk of inducing weight gain can help some patients. The 

summarizes the main elements of drug switching.

Switching antipsychotic medications must take into account various factors, including therapeutic response to the current medication, the patient’s comfort with the switch, and pharmacokinetic and pharmacodynamic properties of both drugs. Furthermore, sufficient time must be allowed to clinically document the process of the switch and its effects. The aim should be to completely replace one drug with another, but in rare cases, combination therapy may be justified based on clinical outcome.

 as adjunctive treatment to counter antipsychotic medication-induced weight gain.

 and topiramate have the best evidence of efficacy and safety.

The metformin studies in patients with major mental illness are heterogeneous in terms of the patient population, duration of current exposure to an antipsychotic drug, and history of chronic exposure to antipsychotic drugs. Review of individual studies shows that metformin is 

 as an add-on treatment for antipsychotic drug-induced weight gain when it is introduced early in the course of treatment of patients who are young, have not been exposed to antipsychotic drugs chronically, and who have gained significant amounts of weight over a short period of time.

 Metformin may also help diminish insulin resistance associated with obesity. The beneficial effect of metformin is likely to diminish over the long term compared with healthy lifestyle interventions.

Topiramate add-on treatment to prevent or reverse antipsychotic drug-induced weight gain has been studied in several trials as well.

 Overall, topiramate was shown to be superior to placebo, with modest weight loss comparable to that observed in the trials with metformin (a mean weight loss of approximately 3 kilograms versus placebo over the course of 16 to 24 weeks).

 As with metformin, the greatest benefit is likely to happen in young, previously drug-naive individuals who gained significant weight over a short period of time. An added benefit of topiramate therapy is that it might address some of the mental illness symptoms as well.

 Long-term benefits of topiramate add-on therapy are less well known than those of metformin.

Weight gain associated with the use of atypical antipsychotic drugs is akin to tardive dyskinesia resulting from high-potency, typical antipsychotics. It evolves over time, leads to chronic complications, and is very difficult to reverse. Pharmacologic interventions used to tackle weight gain, namely switching from a higher-risk antipsychotic to one with a lower risk and adding an adjunct medication to counter weight gain, are modestly effective and worth considering in suitable cases. Healthy lifestyle interventions offer the best long-term outcomes, but their availability is limited by a host of factors.

There are 2 important things that need to be done. First, the iatrogenic burden of obesity should be minimized by using low-risk antipsychotics preferentially over those with higher risk for weight gain whenever possible. Second, patients should be monitored for obesity and its complications, and counseled to improve awareness about obesity and the importance of a healthy lifestyle. Efforts to develop antipsychotic drugs with a neutral affect on weight are ongoing. A few have already become available, but a shift in clinical practice for their preferential use will take its due time.

recently retired as an associate professor of psychiatry at Memorial University of Newfoundland, Canada. He was the head of the divisions of Geriatric and Consultation & Liaison Psychiatry at Eastern Health St. John’s, Newfoundland and Labrador. Currently he is a freelance health care activist focusing on public health education and health care reform.

1. Hasnain M, Vieweg WVR. Do we truly appreciate how difficult it is for patients with schizophrenia to adapt a healthy lifestyle? 

2. de Mooij LD, Kikkert M, Theunissen J. 

Dying too soon: excess mortality in severe mental illness

3. Hasnain M, Vieweg WVR, Hollett B. Weight gain and glucose dysregulation with second-generation antipsychotics and antidepressants: a review for primary care physicians. 

4. Musil R, Obermeier M, Russ P, Hamerle M. Weight gain and antipsychotics: a drug safety review. 

5. Pillinger T, McCutcheon RA, Vano L, et al. 

Comparative effects of 18 antipsychotics on metabolic function in patients with schizophrenia, predictors of metabolic dysregulation, and association with psychopathology: a systematic review and network meta-analysis

6. Bak M, Fransen A, Janssen J, et al. Almost all antipsychotics result in weight gain: a meta-analysis. 

7. Huhn M, Nikolakopoulou A, Schneider-Thoma J, et al. Comparative efficacy and tolerability of 32 oral antipsychotics for the acute treatment of adults with multi-episode schizophrenia: a systematic review and network meta-analysis. 

8. Tek C, Kucukgoncu S, Guloksuz S, et al. Antipsychotic-induced weight gain in first-episode psychosis patients: a meta-analysis of differential effects of antipsychotic medications. 

9. Maayan L, Correll CU. Weight gain and metabolic risks associated with antipsychotic medications in children and adolescents. 

10. Maglione M, Maher AR, Hu J, et al. Off-Label Use of Atypical Antipsychotics: An Update. Comparative Effectiveness Review No. 43. Agency for Healthcare Research and Quality; 2011. AHRQ publication 11-EHC087-EF.

11. American Board of Internal Medicine, American Psychiatric Association. Choosing wisely: five things physicians and patients should question. Accessed February 23, 2021. 

https://www.choosingwisely.org/wp-content/uploads/2015/01/Choosing-Wisely-Recommendations.pdf

12. American Diabetes Association, American Psychiatric Association, American Association of Clinical Endocrinologists, North American Association for the Study of Obesity. Consensus development conference on antipsychotic drugs and obesity and diabetes. 

13. Ali RA, Jalal Z, Paudyal V. Barriers to monitoring and management of cardiovascular and metabolic health of patients prescribed antipsychotic drugs: a systematic review. 

14. Melamed OC, Wong EN, LaChance LR, et al. 

Interventions to improve metabolic risk screening among adult patients taking antipsychotic medication: a systematic review

15. American Diabetes Association. 2. Classification and diagnosis of diabetes: standards of medical care in diabetes—2020. 

16. McGinty EE, Gudzune KA, Dalcin A, et al. Bringing an effective behavioral weight loss intervention for people with serious mental illness to scale. 

17. Naslund JA, Aschbrenner KA, Scherer EA, et al. Lifestyle intervention for people with severe obesity and serious mental illness. 

18. Bernard P, Romain AJ, Vancampfort D, Baillot A, Esseul E, Ninot G. Six minutes walk test for individuals with schizophrenia. 

19. Hasnain M, Vieweg WVR. Weight considerations in psychotropic drug prescribing and switching. 

20. Dayabandara M, Hanwella R, Ratnatunga S, et al. 

Antipsychotic-associated weight gain: management strategies and impact on treatment adherence

21. Goh KK, Chen CH, Lu ML. Topiramate mitigates weight gain in antipsychotic-treated patients with schizophrenia: meta-analysis of randomised controlled trials. 

Metformin for weight gain associated with second-generation antipsychotics in children and adolescents: a systematic review and meta-analysis

23. Hasnain M, Vieweg WVR, Fredrickson SK. 

Metformin for atypical antipsychotic-induced weight gain and glucose metabolism dysregulation: review of the literature and clinical suggestions

24. Correll CU, Maayan L, Kane J, et al. Efficacy for psychopathology and body weight and safety of topiramate-antipsychotic cotreatment in patients with schizophrenia spectrum disorders: results from a meta-analysis of randomized controlled trials. 

Antipsychotic-induced weight gain evolves over time, leads to chronic complications, and is very difficult to reverse. Pharmacologic interventions used to tackle weight gain are modestly effective and worth considering in certain cases.

Addressing Obesity in Patients Taking Antipsychotics

 and there is evidence that activation of the maternal immune system during pregnancy—whether by infection, chronic inflammation, or autoimmune disease—is associated with increased risk of neurodevelopmental disorders in the 

 In the case of the latter, maternal autoantibodies may cross the placenta and alter fetal development through epigenetic changes, brain microglial cell activation, and modulation of 

 Previous studies have focused on the association between maternal autoimmune disease and autism spectrum disorders, whereas attention-deficit/hyperactivity disorder (ADHD) has been less studied. Only 1 previous study examined the association between any maternal autoimmune disease and ADHD risk in 

Nielsen and colleagues aimed to investigate the association between any (and specific) maternal autoimmune disease and ADHD in children, and to incorporate those results into 

a systematic review and meta-analysis on this topic

 Using the New South Wales (NSW) Perinatal Data Collection, they identified all women with full-term, singleton live births from July 2000 to December 2010. Birth data were linked to all hospital admissions for both mother and child, and pharmaceutical data from the child for treatment of ADHD through registers. A child was considered to have ADHD if they had a stimulant prescription for ADHD and/or a hospital diagnosis of ADHD. Children linked to a first ADHD event before age 3 were excluded. Children were followed to death or at the end of follow-up in December 2014.

Maternal autoimmune disease was determined based on the mother’s hospitalization records. Children whose mother had at least 1 hospitalization for autoimmune disease were considered exposed. Exposed and nonexposed mothers were propensity matched based on age, country of birth, socioeconomic status, place of residency, parity, smoking during pregnancy, and mental health diagnosis. Cox proportional hazard models were used to examine the association of maternal autoimmune disease and ADHD, adjusting for child sex. Analyses were performed for any maternal autoimmune disease and individual conditions with at least 15 cases of ADHD among exposed children.

The authors also performed a systematic search of MEDLINE, Embase, and Web of Science to identify studies on the association between maternal autoimmune disease and ADHD. Included studies were assessed for study quality using the Newcastle-Ottawa Quality Assessment Scale. Meta-analyses of any (and specific) maternal autoimmune disease with ADHD in the offspring were performed by calculating random-effects pooled hazard ratios (HRs) and inverse-variance weighting.

In the NSW Perinatal Data Collection, 831,718 mothers and children were including and 12,767 (1.5%) exposed to maternal autoimmune disease. Propensity score matching including a cohort of 12,610 exposed children and 50,440 controls. During follow-up, 1094 male (3.4%) and 332 female (1.1%) children were diagnosed with ADHD. After adjustment, any maternal autoimmune disease (HR = 1.30), type 1 diabetes mellitus (HR = 2.23), psoriasis (HR = 1.66), and rheumatic fever or carditis (HR = 1.75) were associated with increased risk of ADHD, and this association was not moderate by child sex. When considering mothers diagnosed before or within 180 days of birth (N = 9700), any maternal autoimmune disease (HR = 1.28) and type 1 diabetes mellitus (HR = 1.95) remained significantly associated with ADHD.

Five studies, including the present cohort, were included in the meta-analysis. Two studies estimated the association with any maternal autoimmune disease, and 11 specific conditions were investigated in 2 or more individual studies. In the meta-analyses, any maternal autoimmune disease (HR = 1.20), type 1 diabetes mellitus (HR = 1.53), hyperthyroidism (HR = 1.15), and psoriasis (HR = 1.31), were all associated with increased risk of ADHD.

The authors found an association between any maternal autoimmune disease, type 1 diabetes mellitus, and psoriasis in both the present study and meta-analysis, and an association with hyperthyroidism in the meta-analysis. They noted significant heterogeneity in findings across individual studies, and that non-immune factors such as glycemic control (in type 1 diabetes) and endocrine aspects of hyperthyroidism may also contribute to associations with ADHD.

Strengths of the present study include the hybrid design, including a large population-based cohort and meta-analysis. Limitations include the lack of outpatient/primary care records for identifying maternal autoimmune disease, absence of data on the clinical status of the mother’s autoimmune disease and associated medications, and absence of data on nonstimulant ADHD medications and severity of ADHD.

Maternal autoimmune disease is associated with increased risk of ADHD in offspring, adding evidence that adverse maternal immune function during pregnancy may alter fetal neurodevelopment. Children of affected mothers may benefit from additional follow-up and support for developmental issues.

is professor in the Department of Psychiatry and Health Behavior, Augusta University, Augusta, Georgia. He is on the Editorial Board and serves as the schizophrenia section chief for 

. The author reports that he receives research support from Augusta University, the National Institute of Mental Health, the Brain and Behavior Research Foundation, and the Stanley Medical Research Institute.

1. Kipnis J. Multifaceted interactions between adaptive immunity and the central nervous system. 

2. Knuesel I, Chicha L, Britschgi M, et al. Maternal immune activation and abnormal brain development across CNS disorders. 

3. Estes ML, McAllister AK. Maternal immune activation: Implications for neuropsychiatric disorders. 

4. Gumusoglu SB, Stevens HE. Maternal inflammation and neurodevelopmental programming: a review of preclinical outcomes and implications for translational psychiatry. 

5. Nielsen PR, Benros ME, Dalsgaard S. Associations between autoimmune diseases and attention-deficit/hyperactivity disorder: a nationwide study. 

6. Nielsen TC, Nassar N, Shand AW, et al. Association of maternal autoimmune disease with attention-deficit/hyperactivity disorder in children. 

Activation of the maternal immune system during pregnancy is associated with increased risk of neurodevelopmental disorders in children. A recent review and meta-analysis examine the link in ADHD.

Maternal Autoimmune Disease and ADHD Risk in Children

MDD is a highly prevalent mental health condition. There is evidence that, in China, co-occurring somatic symptoms, including headache and stomachache might contribute to misdiagnosis of depression and delayed 

 Previous studies of somatic symptoms in MDD have yielded conflicting or inconclusive results, although there is some evidence for increased gastrointestinal 

 Given growing evidence for the microbiota-gut-brain axis in depressive disorders, GI symptoms might be a marker for 

Huang and colleagues estimated the frequency and clinical correlates of GI symptoms during depressive episodes in a large, nationwide sample of patients with 

 They hypothesized that the presence of GI symptoms would be associated with comorbidity in MDD, including insomnia, hopelessness, anxiety, and suicidal ideation. Study participants were from the National Survey on Symptomatology of Depression (NSSD) in China, which included inpatient and outpatient participants 18 years or older with a current DSM-IV episode of MDD.

Exclusion criteria were a lifetime diagnosis of bipolar or psychotic disorder, imminent risk of suicide or homicide, received electroconvulsive therapy within the past month, current pregnancy or breastfeeding, and substance use disorder over the past year. Patients were interviewed by trained psychiatrists on a broad range of symptoms, including depression and somatic symptoms, over the previous 2 weeks. Sociodemographic and clinical characteristics between patients with different severity of GI symptoms were performed with 1-way analysis of variance. Multiple linear regression analysis was used to analyze associations between GI symptoms and psychopathology, adjusting for potential confounding factors.

A total of 3256 patients (mean age 41, 40% male) were included in the analyses. Of those, 1750 patients (71%) had GI symptoms, with a frequency of several days/week for 38%, more than half of days for 23%, and almost daily for 10%. Patients with more GI symptoms had a significantly increased prevalence of anxiety; insomnia; poor concentration; limb and body pain; hopelessness; anger and irritability; and feelings of failure. In linear regression, suicidal ideation, anxiety, insomnia, anger, feelings of failure, and body pain were independently and significantly associated with GI symptoms in patients with MDD (

The authors concluded that more than 70% of patients with MDD reported GI symptoms during depressive episodes. Strengths of the study include the large, nationwide sample. Limitations include the cross-sectional nature of the study design, unmeasured and residual confounding factors, as well as the absence of data on specific GI symptoms. These findings are germane to investigations of the microbiota-gut-brain axis in depressive disorders.

“Mr S” is a 26-year-old Caucasian male with a history of recurrent major depressive disorder (MDD) and anxiety disorder. The onset of his depressive illness began when he was 19 years old. For the past 2 to 3 months during an exacerbation of his depression, he reports significant nausea and vomiting on a daily basis, particularly in the morning, which was not attributable to increased anxiety. Mr S reports that his gastrointestinal (GI) symptoms did not respond to treatment with either H-2 blockers or a proton-pump inhibitor. Subsequently, his antidepressant was changed to a different selective serotonin reuptake inhibitor, and a low-dose long-acting benzodiazepine was also added for anxiety. Over the next month, he reported significant improvement in not only mood and anxiety, but also nausea and vomiting, such that he was able to return to full-time employment.

Gastrointestinal symptoms are common in the clinical presentation of MDD. GI symptoms may be associated with the onset and clinical severity of depression, which could be a potential ancillary indicator in the management of MDD.

 is professor in the Department of Psychiatry and Health Behavior, Augusta University, Augusta, Georgia. He is on the Editorial Board and serves as the schizophrenia section chief for 

1. Smith K. Mental health: a world of depression. 

2. Harshaw C. Interoceptive dysfunction: toward an integrated framework for understanding somatic and affective disturbance in depression. 

3. Bruce-Keller AJ, Salbaum JM, Berthoud HR. Harnessing gut microbes for mental health: getting from here to there. 

4. Guo F, Cai J, Jia Y, et al. Symptom continuum reported by affective disorder patients through a structure-validated questionnaire. 

A study estimates the frequency and clinical correlates of GI symptoms during depressive episodes in a large, nationwide sample of patients with MDD in China.

Gastrointestinal Symptoms During Depressive Episodes

General medical illness can contribute to affective disorders in elderly patients. Treating the medical illness is an integral part in treating depression in these patients.


5 Medical Comorbidities Linked to Depression in Older Patients

Between mid-February and mid-March 2020, the number of sleep prescriptions in the United States rose by 14.8%. The increase may be due to the pandemic, says Manoj Malhotra, MD. Based on his experience, he says “the current environment, with myriads of shifts in our day-to-day lives, is a perfect storm for sleep challenges.”

In this Mental Health Minute, Malhotra explains how to distinguish between a general lack of sleep and chronic insomnia, and how to treat the latter.

 is vice president, United States medical affairs for the neurology business group at Eisai.

Have you seen more patients with sleep problems during the pandemic? 

Share comments with your colleagues by emailing 

. Comments may be shared online pending review and editing for style.

Key considerations for healthcare providers seeking to manage their patients’ insomnia.  

The COVID-19 Pandemic Is a Perfect Storm for Sleep Challenges

In approximately half of patients with Huntington disease, symptoms of depression, irritability/aggression, executive dysfunction, psychosis, cognitive decline, and dementia present long before progressive motor symptoms. 

8 Neuropsychiatric Symptoms and Treatments of Huntington Disease

Body dysmorphic disorder (BDD) is a mental health disorder in which you cannot stop thinking about perceived defects or flaws in your appearance, flaws that are often minor or even invisible to others. This condition currently affects around 2-3% of the general population.

, we speak to Katharine Phillips, MD, about her pioneering research on BDD, her books on the topic, and options for treatment.

is currently professor of psychiatry, DeWitt Wallace Senior Scholar, and Residency Research Director for the Department of Psychiatry at Weill Cornell Medicine. She is also an attending psychiatrist at New York-Presbyterian Hospital and adjunct professor of Psychiatry and Human Behavior at the Alpert Medical School of Brown University.

Millions of Americans have a skewed view of their own bodies, leading to serious depression and suicidality.  

Body Dysmorphic Disorder: Widespread and Potentially Deadly

Maybe I have heightened interest in blindness as a conversion symptom because I can sympathize with it. Sudden blindness happened to me during a diagnostic attempt to figure out the precise location of my brain bleed, and it left me with permanent right hemianopsia. I know that terrible moment: everything seems to be working fine—and then it is not.

Here is what being treated for sudden blindness was like for me, an experience that many patients with conversion symptoms might share. For 24 hours little flashlights appear as if by magic. Whoever is shining them seems to think that perhaps this time the result will be different than when the last individual shined a light in your eye. Everyone from the nursing aid to the senior neurologist sternly directs you to tell them how many fingers they are holding up. This continues long past the point when you are more than convinced that you cannot see fingers at all. Eventually they give up on finger counting and leave you to settle into the world that you can no longer see.

By the next day your newly discovered blindness is condensed down in their minds to an incidental mention in the morning report. Should you recover from the stroke, as I did, and be assertive enough to get a full copy of your hospital record, you may find that on the morning of the fateful event, the clinical statement is “patient complaining that he cannot see on the right side.” 

 is such a convenient word for the clinician, whose procedure has just rendered the patient with half a field of vision for the rest of his life. 

 suggests that it is really a small thing that the annoying patient is making into some big deal.

So I know the routine of the probing flashlights, and the insistent fingers, and the report that you are complaining. It makes me feel connected with the folks brought to the emergency department (ED) with sudden-onset blindness. Of course, possibilities such as stroke, or tumor, or multiple sclerosis must be ruled out, and flashlights have their role in the diagnostic. But when all those mechanical reasons for malfunction have been ruled out, we sometimes hear that there is no cause found, so it must be conversion disorder.

Conversion disorder is a diagnosis of elimination: when nothing can be identified by scan or blood work, the ED physician concludes that this is a rare case of conversion disorder. The DSM-5 named these experiences 

, which was meant to be less pejorative (not to mention less sexist) than the previous term 

 is from the Greek word for uterus). The word “conversion” is used to convey the sense that forbidden emotional conflicts are being converted to physical symptoms. This comes directly from Freudian explanations about how things work in the mind, and to my knowledge it is the only scrap of Freudian orthodoxy that remains in current psychiatric nomenclature. To me, the fact that DSM-5 is still using language derived from Freud suggests that there is little new thinking about how the brain produces the experience of blindness or, in other cases, paralysis, anesthesia, or seizures.

In a remarkable German study, researchers reported on a unique clinical situation, in which conversion disorder produced blindness in only 2 quarters of the visual field. The researchers were able to detect differences in the electrophysiological indices of visual processing, meaning that there were amplitude differences between the area of visual cortex where vision was occurring and the area of visual cortex where vision was not occurring. Psychodynamic therapy for this patient continued for a year and a half, augmented by a technique in which “a facilitator uses descriptive language intended to psychologically benefit mental imagery, often involving several or all senses, in the mind of the listener.”

The report specified that a great deal of effort went into helping the woman develop her own language to express feelings in a biographical framework. All of this therapy proceeded on the Freudian assumption that physical symptoms were expressions of emotion, but rather than experiencing forbidden emotions, the woman may simply have lacked the words to articulate and identify her own feelings. The woman regained her full field of vision, but the transition from being blind to experiencing full vision involved a period when she could see swirls, and then later periods when she could see clearly for brief periods of time. 

 reported that having achieved full visual field, a re-measurement of the electrophysiological indices found them to be equivalent in all 4 quadrants.

The article contains a graphic of the physiologic measurements of the evoked potential of the cortex response to the non-seeing eye area compared, to the same measurement normal vision area of the eye. There is a clear difference between the 2 traces, with the seeing portion of the eye producing a potential that is about double that which is measured from the non-seeing area. The publisher has not given permission to reproduce this remarkable figure, but 

it may be found online here (see figure 2).

This Schoenfield paper is amazing in several dimensions. Being able to measure electrophysiological activation deep in the visual cortex with such precision is a remarkable technological feat. Identifying a study participant who had blindness in just 2 of her 4 visual field quadrants was a statistical improbability. Even more remarkable (to this American practitioner) was the availability and funding of such high-quality multimodal therapy for a full year and a half.

Current medical education on conversion disorders suggests that the symptoms develop instantly and then resolve quickly, as soon as it is revealed to the patient that there is no medical justification for their symptom. The German article suggests otherwise, as this woman’s vision deteriorated in spite of good ophthalmologic care over a period of 4 years, and it recovered in gradual steps over a period of 18 months.

This study carries forward our understanding of the process and electrophysiological correlates of conversion blindness, but it does not offer any answers to questions such as: What is the body-mind alliance that institutes these changes? Why in this case was the symptom blindness and not muscle weakness or gastro-intestinal disturbance or migraines? Why opposite quadrants and not whole field vision? Even without giving answers to those questions, we are brought to consider that if the body-mind alliance is strong enough to cause this undesired change to happen, why would it not be strong enough in other circumstances to cause desired changes to happen?

Our training in allopathic skills does not carry us to any clear view, and so we tend to ignore the evidence. The body-mind alliance is there, in plain sight, waiting for us to recognize it and for us to use it as a healing tool.

is a community psychiatrist contracting telepsychiatry services to small community mental health centers in the rural area of his state. The author reports no conflicts of interest concerning the subject matter of this article.

1. Schoenfeld MA, Hassa T, Hopf J-M, et al. Neural correlates of hysterical blindness. 

A case in Germany overturns old ideas about conversion disorders. 

Hidden in Plain Sight

While psychotropic medications for schizophrenia, bipolar disorder, and other psychiatric disorders can cause weight gain, patients can take small steps to improve their health.

15 Steps to Helping Psychiatric Patients Achieve and Maintain a Healthy Weight

 for significant procognitive effects for antipsychotics and other pharmacologic approaches.

 Therefore, treatment of cognitive impairment in schizophrenia represents a tremendous area of unmet need.

 on the effects of exercise on brain structure and functional performance.

 found that aerobic exercise exerted a positive effect on global cognition and some, but not all, cognitive domains in patients with schizophrenia. Unfortunately, findings are limited by small samples, as well as variable types and intensity of exercise and study designs.

“Mrs Morris” is a 48-year-old Black woman with a history of chronic schizophrenia. During hospitalization for an episode of illness exacerbation, her antipsychotic medication was modified. Over the next 4 months, she gained approximately 50 lb. Mrs Morris declined to lower the dose of her antipsychotic or change medications because of her clinical improvement. She worried about risk of another illness relapse. However, she was receptive to the recommendation for increased physical activity for weight loss.

Mrs Morris started walking with a neighbor for about 30 minutes at a moderate pace at least 3 times per week. Over the next year, she lost 36 lb. Although there were no clinically appreciable changes in her cognitive function, she reported feeling better as a result of her exercise regimen.

 performed a 12-week randomized controlled trial of the effects of aerobic walking on cognitive function in patients with schizophrenia.

 The goal was to determine if the intensity of aerobic walking is associated with changes in cognition. Patients were randomized 1:1 based on age and sex to usual treatment with antipsychotics with or without aerobic walking. Inclusion criteria were 20 to 60 years, DSM-5 diagnosis of schizophrenia, stable antipsychotic dose for at least 1 month, Positive and Negative Syndrome Scale (PANSS) total score < 95, no history of major physical illness, and no physical disability that caused difficulty walking.

The program comprised 150 minutes/week of outdoor walking, typically divided over 3 to 5 sessions and each with a 5-minute warm-up, followed by a 5-minute cool-down. Transportation was provided to the exercise sessions as needed. Participants wore a Fitbit to monitor heart rate and exercise intensity and were supervised by research staff who provided guidance based on heart rate. The patients could rest if needed. Participants were stratified into high- and low-intensity groups based on the average in-session heart rate reserve. Cognition was evaluated with the Brief Assessment of Cognition in Schizophrenia (BACS).

Data were analyzed using intention-to-treat and per-protocol analyses. Multivariate general linear model repeated measures were used to investigate the effects of time, group, and the time x group interaction on cognition, controlling for illness duration. The authors randomized 67 patients to treatment as usual (TAU, n = 34) or aerobic walking (n = 33) who completed the baseline assessment. Thirty-three patients in the TAU and 31 in the aerobic walking group completed the 12-week trial (

). At baseline, participants in the aerobic walking group scored approximately 0.5 standard deviations lower on 

 than the TAU group. The mean duration of aerobic walking was 129 minutes/week. Eleven patients achieved high-intensity walking and 22 maintained low-intensity. In the entire intent-to-treat sample, the authors found a trend for a group effect for greater improvement in verbal fluency in the aerobic walking group. They also found a significant group effect on attention and processing speed in high- versus low-intensity aerobic walking.

This was the first trial of the effects of aerobic walking and exercise intensity on 

in schizophrenia, according to the study authors. Most (> 90%) patients completed the trial with a mean of 3 days of exercise per week. The findings suggest that this intervention is feasible and acceptable to patients, and that supervision and transportation are associated with retention. Study limitations included the modest sample size (especially in the high-intensity group) and a relatively short study duration, as well as the inability for blinding to the intervention.

A supervised aerobic walking program involving moderate-intensity exercise is feasible and acceptable in patients with schizophrenia. Higher intensity aerobic exercise may have modest procognitive effects in these patients. Considering the other health benefits of aerobic walking, these programs can be useful for patients with schizophrenia.

is a professor in the Department of Psychiatry and Health Behavior, Augusta University, Augusta, Georgia. He is on the Editorial Board and serves as the schizophrenia section chief for 

. The author reports that he receives research support from Augusta University, the National Institute of Mental Health, the Brain & Behavior Research Foundation, and the Stanley Medical Research Institute.

Pharmacological cognitive enhancement in schizophrenia

The magic of movement; the potential of exercise to improve cognition

Rosenbaum S, et al. Aerobic exercise improves cognitive functioning in people with schizophrenia: a systematic review and meta-analysis

Effects of aerobic walking on cognitive function in patients with schizophrenia: a randomized controlled trial

An earlier version of this article was published online as 

Exercise and Cognition in Schizophrenia: Is There a Link?

 This article appeared in the March 2021 print issue of 

Aerobic exercise has been found to exert a positive effect on global cognition and some, but not all, cognitive domains in patients with schizophrenia.

Psychosomatics