Ellen Mausner, MD, PhD

Like hotshot detectives from Scotland Yard, psychiatrists are often asked to make sense of mysterious situations. In the case described here, a young man was admitted to the hospital with perplexing psychiatric and neurologic symptoms. (The identifying details of the patient have been changed to protect the patient’s identity.) Since symptoms of medical disorders can mimic neuropsychiatric disorders, it would take careful interviewing and some detective work to arrive at the right diagnosis.

“Roger,” a Hispanic male, aged 34 years, residing alone, presented to the emergency department with severe depression, marked by difficulty getting up in the morning for work, crying spells, chronic insomnia, and passive suicidal ideation—all worsening over the past 6 weeks. He complained of auditory and visual hallucinations, reporting that he “often heard voices muttering in the background,” although he could not decipher what they were saying. He also “sometimes saw shadows in the corner of the room.” He further noted that he was concerned about “missing a lot of work and forgetting things.”

According to Roger, he had been well until approximately 3 years ago when he began experiencing depression. He already had 2 prior psychiatric admissions at another hospital, about 2 months apart, with each hospitalization lasting 2 weeks. After the second discharge, about 6 weeks prior, he was referred back to his therapist in their outpatient clinic.

Roger was prescribed fluoxetine 20 mg by mouth (po) every morning (qAM), risperidone 1 mg po twice daily (BID), and benztropine 0.5 mg po BID. He admitted he was not as careful as he should be with medication adherence, noting that he takes the medications “some of the time. Sometimes I forget.” He complained that the fluoxetine had sexual adverse effects, reducing frequency of erections, and it “also interrupted my sleep.” He complained of ongoing fatigue and memory lapses.

He reported that he did not like the outpatient clinician, saying, “I never really felt comfortable with her.” He admitted missing a number of follow-up appointments at the mental health clinic. When the symptoms persisted, the patient “decided to try another hospital” and was admitted to our psychiatry unit.

The patient presented with severe depression with insomnia, decreased appetite, anhedonia, and increasing social withdrawal. Roger denied any suicidal plans, but he admitted to having passive thoughts of “not living anymore.” He firmly denied any history of suicide attempts and had no intention of harming himself. Roger also denied any history of violence.

Roger was particularly troubled by his decreased appetite, but he denied dieting or having any kind of eating disorder. He noted that he “didn’t enjoy cooking,” and his diet consisted mainly of take-out and fast food. Roger acknowledged that he should eat better and said he was not taking any vitamins or supplements.

Roger also complained of worsening memory loss and confusion: “A year or so ago, I started misplacing things: my phone, my house keys…I have trouble concentrating. I even forgot my mother’s birthday. That’s never happened before. I forgot the rent was due and had to pay a late fee.” He also noted that he was having trouble walking, which worsened over the past year or so. He denied any physical trauma. He noted that his legs “felt weaker” and his balance was “off.” He had fallen at home a few times. The patient also presented with vertical nystagmus, which was present for the past year.

Roger was pleasant upon approach. He said he was glad he had sought admission and was “less lonely now.” He had a fresh-faced look, with good hygiene, and he maintained good eye contact. He said his mood was depressed: “a 7 or 8 on a scale of 1 to 10.” The mental status exam was normal except for some difficulty with short-term memory. He scored 22 of 30 on the mini-mental state examination, which is consistent with mild cognitive impairment. On the Montreal Cognitive Assessment Test for Dementia, Roger scored 18 of 30, which is consistent with mild dementia. The score can be influenced by factors like fatigue or sedating medications. His long-term memory was adequate.

In ascertaining his substance use history, Roger said he was a social drinker but “had managed to stop entirely over the past year.” He also noted that, up until a year ago, he drank to help with his sleeping problem, saying he “would take a couple of shots of tequila or vodka to knock me out.” He felt this strategy was “necessary to cope.” He stopped alcohol use when he had memory issues and fell at home a few times.

Insomnia, however, was still an issue. He noted that he had tried over-the-counter sleep aids, which “did nothing for me.” He volunteered that he had experimented with mushrooms while in college, which he had enjoyed, but he denied using them since then. He denied using cannabis or any other street drugs. His urine toxicology on admission was negative.

The Inpatient Unit: The Triad Comes to Light

Basic admission bloodwork results were normal. Thyroid function tests were normal. Chest X-ray was negative.

Roger was initially placed on risperidone 1 mg po BID, benztropine 0.5 mg po BID, and bupropion 75 mg po daily. He was started on desyrel 50 mg po (qHS), as needed, for the insomnia, which he said helped him sleep. He participated in many activities and groups on the unit. He was observed chatting with peers in a friendly way.

To further explore the diagnostic differential, a neurology consult was completed. The neurologist found no physical explanation for the nystagmus and ataxic gait. He concluded that both symptoms were psychogenic.

Since Roger believed he had a computed tomography (CT) scan during a prior hospitalization without any reports of abnormalities, one was not immediately completed on admission. The team requested records for the 2 prior psychiatric hospitalizations and, to be thorough, ordered a CT scan.

Similarly, an ophthalmology consult was ordered. It revealed normal healthy eyes except for the vertical nystagmus.

This triad—the combination of an eye disorder (in this case, vertical nystagmus, but it could be another ocular disturbance); a broad-based, ataxic gait; and a context of memory decrease along with mood and psychotic symptoms—was suggestive of Wernicke encephalopathy (WE) or Korsakoff psychosis.

 Interestingly, this syndrome usually occurs in the context of heavy alcohol consumption, and Roger noted upon admission that he was merely a social drinker. Upon physical examination, he had no signs of chronic or advanced alcohol use, eg, broken facial capillaries (“gin blossoms”), palmar erythema, or jaundice. The liver function tests on his admission chemistry labs were elevated, but they were still within normal limits. While on the unit, he showed no signs of alcohol withdrawal.

To further explore the possibility of WE, the team chatted again with Roger about his alcohol use to ascertain more details. For instance, Roger now noted that for his long history of sleep issues, he had drunk “several glasses”—not shots—“of vodka or tequila nightly since about the age of 22 or 23.” He was now 34. Clarification of the term “several” was also pursued. Roger explained that meant “4 or 5 regular glasses; it takes that much to calm me down so I can finally sleep. I drink a lot of coffee during the day.”

Roger also admitted that this was his nightly routine, not just an occasional thing. He denied ever having any blackouts or withdrawal tremors. He explained, “I’ve always had a high tolerance for booze. It runs in my family.” He did not share these insights regarding alcohol intake at the initial interview.

He further noted, again, that he decided to stop drinking about a year ago: “I was forgetting too much stuff, oversleeping sometimes, falling at home. I didn’t want to get fired.” Roger said he “had stopped on his own,” without going to an inpatient detoxification or rehabilitation facility, and he denied any withdrawal seizures. He said he attended a few Alcoholics Anonymous meetings but did not like the vibe and stopped.

The head CT with contrast showed changes in the thalamus consistent with WE. There were abnormalities noted in the cerebellum consistent with ataxia. Perhaps the head CTs at the prior hospital had not been interpreted properly.

 We ordered a serum thiamine (vitamin B1) level, which showed that he was severely deficient in thiamine. Based on these new findings, the criteria for WE diagnosis were met.

His loss of appetite and eating habits suggested the possibility of other vitamin deficiencies. We tested for serum vitamin B12 and vitamin D; he was severely deficient in both. This may well have contributed to his depressed mood.

To correct these vitamin deficiencies, the patient was transferred to a medicine inpatient unit. He received an intravenous (IV) bolus infusion of thiamine 500 mg 3 times daily for 2 days, then 250 mg IV daily for 5 days.

 In addition, Roger was started on vitamin B12 injections and high-dose vitamin D tablets. Within about 2 weeks, all of his vitamin levels were restored to the normal range.

His vertical nystagmus stopped completely. His ataxic gait resolved. The depression lessened considerably, and his hallucinations ended.

Roger was discharged on the same psychotropic medications that he received as an inpatient: bupropion, 75 mg po qAM; risperidone, 1 mg po BID; benztropine, 0.5 mg po BID; and desyrel, 50 mg po qHS as needed for insomnia. He was also prescribed vitamin supplements of thiamine, vitamin B12, and vitamin D, as well as a therapeutic multivitamin. Finally, he received a consult with a nutritionist to address his eating habits and was referred for supportive psychotherapy to help address his depression and family issues.

In general, WE is reversible with thiamine infusions. However, failure to diagnose WE can lead to a serious amnestic syndrome (Korsakoff syndrome). Korsakoff psychosis is generally irreversible. Therefore, it is extremely important that patients are diagnosed and treated as promptly as possible.

When a patient admits to social drinking, it is helpful to pinpoint the exact extent of alcohol use in terms of type of alcohol, quantity, and frequency.

 An assessment of a patient’s eating habits and nutritional intake (or lack thereof) can also contribute to the diagnosis and treatment of common psychiatric disorders.

A variety of evidence-based cognitive rating scales exist for WE.

 Heirene et al compared the neuropsychological tests used to assess alcohol-related cognitive impairment with tests that screen for alcohol-related dementia and Korsakoff syndrome (

 They concluded that there is a heterogeneity in presentation and suggested using the more broad and inclusive diagnostic conceptualizations of alcohol-related cognitive impairment instead of the discrete diagnoses of Korsakoff syndrome and alcohol-related dementia.

Meanwhile, Sgouros et al have pursued the development of a Thiamine Deficiency Questionnaire (TDQ) to assess thiamine deficiency in patients with severe alcohol dependence.

 Unfortunately, they concluded that further refinement and evaluation were needed before endorsing TDQ’s validity.

Alcohol use (as well as the use of other nonprescribed drugs) is often underreported by patients.

 According to Livingston and Callinan, “population surveys typically produce underestimates of alcohol consumption of approximately 40% to 50%.”

 Thus, it is essential in the initial patient interview to receive answers that are as specific as possible regarding what kind of alcohol is being consumed, how much is consumed in a drinking session, and how often the sessions occur. If the patient admits to “a couple of beers,” ask if those are 12-ounce, 16-ounce, or 24-ounce drinks. Ask about the drinking pattern: Do they drink more on weekends than on weeknights when they have to get to work the next day? Listen for words like 

lonely, isolated, homesick, bored, trouble sleeping, frustration

, as these can be common triggers for high levels of alcohol consumption.

Possible Causes of Wernicke Encephalopathy

Alcohol use disorder is not the only cause of WE; the culprit can be any condition that compromises the body’s access to vitamin B1 (thiamine) (

 But those are cases for another day. This one is closed.

is a board-certified psychiatrist. She is on the staff of Manhattan Psychiatric Center and works in its mental health outpatient clinic. Her new book

1. Chandrakumar A, Bhardwaj A, ’t Jong GW. 

Review of thiamine deficiency disorders: Wernicke encephalopathy and Korsakoff psychosis

2. Wijnia JW, Oudman E, Bresser EL, et al. 

Need for early diagnosis of mental and mobility changes in Wernicke encephalopathy

3. Isenberg-Grzeda E, Kutner HE, Nicolson SE. 

Wernicke-Korsakoff-syndrome: under-recognized and under-treated

Underreporting in alcohol surveys: whose drinking is underestimated?

How is alcohol consumption affected if we account for under-reporting? a hypothetical scenario.

Drinking pattern is more strongly associated with under-reporting of alcohol consumption than socio-demographic factors: evidence from a mixed-methods study

7. Heirene R, John B, Roderique-Davies G. 

Identification and evaluation of neuropsychological tools used in the assessment of alcohol-related cognitive impairment: a systematic review

8. Sgouros X, Baines M, Bloor RN, et al. 

Evaluation of a clinical screening instrument to identify states of thiamine deficiency in inpatients with severe alcohol dependence syndrome

9. Choi EY, Gomes WA, Haigentz M Jr, Graber JJ. 

Association between malignancy and non-alcoholic Wernicke’s encephalopathy: a case report and literature review

Malnutrition-induced Wernicke’s encephalopathy following a water-only fasting diet

11. Shible AA, Ramadurai D, Gergen D, Reynolds PM. 

Dry beriberi due to thiamine deficiency associated with peripheral neuropathy and Wernicke’s encephalopathy mimicking Guillain-Barré syndrome: a case report and review of the literature

12. Togay-Işikay C, Yiğit A, Mutluer N. 

Wernicke’s encephalopathy due to hyperemesis gravidarum: an under-recognised condition

Articles

Alcohol use is often underreported by patients. This case demonstrates the importance of obtaining the most accurate information possible in the initial patient interview.

Solving the Case of the Perplexing Symptoms

Many professions are associated with occupational hazards. Dancers and athletes risk injury. Coalminers risk lung-disease. Psychiatry is no exception. Over the course of my career, I have noticed quite a few psychiatry-specific occupational hazards. I am sure that many psychiatrists will have met with some of these dangers themselves—and could probably add a few of their own.

Working with mentally ill individuals is risky. Whether one’s clients are severely and chronically mentally ill or the worried well, psychiatrists always face the risk of losing a patient to suicide. This can occur despite one’s best efforts. One feels great guilt and despair, even if on review the act was not preventable.

There is also the risk of violence. Psychiatrists could be assaulted or even killed by a patient with a grudge, or one responding to voices telling them to do harm.

There is the risk of being stalked by a patient. With the internet, psychiatrists’ home addresses can be found. Even if they are not literally stalked, some doctors face patients who hold grudges for committing them involuntarily or, in the patients’ words, “forcing them to take meds” that they perceived as poison. It can be hard to live a normal life when you know that someone out there wishes you ill.

Here is an extreme example of this hostility. There is a museum in Los Angeles called “Psychiatry: Industry of Death.” It accuses the field of psychiatry of inflicting torture on its patients, be it through medications, confining them to locked wards, prescribing electroshock therapy or other treatments. It is operated by the Citizens Commission on Human Rights (CCHR), an antipsychiatry organization founded by the Church of Scientology and psychiatrist Thomas Szasz, MD.

There is the frustration that comes with trying hard to help patients but encountering resistance. This can be resistance to keeping appointments or taking medications, or even filling prescriptions. It can make one feel helpless and ineffective. We see patients get hospitalized over and over again. Some clients relapse frequently due to noncompliance with medication and appointments. Naturally, substance abuse disorders make these patients even more difficult to stabilize.

Those of us who work in emergency rooms know all too well the “frequent flyer” that returns week after week with the same complaints or self-inflicted wounds. One can easily become exhausted, cynical, and burnt-out. Human effort and thousands of dollars are spent on the same work-ups, with no real progress over time.

I think the general public does not realize how hard it is to do what we do. It takes a strong stomach to handle others’ crises. It can be heart-breaking and depressing to hear patients’ stories of abuse, sexual assault, and tragedy. On several occasions, I have had the experience of having a patient confide in me that I was the very first person on earth to whom she or he has ever disclosed being raped. It takes effort and dedication to remain present and supportive no matter what.

We want to help our patients. However, it is not natural or particularly healthy to spend one’s work week listening to folks who are anxious, depressed, disturbed, or psychotic. It can leave one reeling with mental exhaustion and world-weariness. One comes to expect suffering as the norm.

During my residency, one of the senior attendings said that psychiatrists are “grandiose masochists.” I assume he meant grandiose in the sense that we like to feel empowered to heal patients with our extensive knowledge and training, and masochists because along the way we ourselves suffer as we sit with those who are suffering. 

After a busy work week, have you ever walked down the street and seen a happy individual and wondered, “What are they so happy about?” When happiness starts to look odd, it is time for a break.

It is crucial for self-preservation that we not bring our work home. But how do we leave it all behind? We counsel our patients about good self-care: relaxation, meditation, the importance of exploring hobbies, and, of course, taking vacation. We need to do the same for ourselves.

I have observed other occupational hazards. Socially, when you tell someone you are a psychiatrist, they often express fear: “Are you gonna analyze me? I’d better watch what I say!” Or outright hostility: “You’re a shrink? Every shrink I’ve ever met is nuts!” Or how about: “Didn’t you ever want to be a 

Then there is the opposite reaction: the casual acquaintance who wants free advice or an instant consultation. Some folks have no qualms about disclosing their mental health histories on the spot and asking your opinion of their meds or other treatments. How about those who even think it is appropriate to ask for a prescription or refill? I have learned to set boundaries and refer them to their own practitioners. Also, I would like them to respect my free time outside of the office.

This goes for co-workers, friends, and family members as well I refer them to their own therapists and prescribers. Keeping the boundaries helps preserve all your relationships.

There are also hazards that can occur in one’s personal relationships. I have observed that some psychiatrists are drawn to partners who have untreated mental health issues or are quite troubled. In my opinion, this is a pitfall to be aware of and guard against. The psychiatrist in us is tempted to treat and win the love of the partner. Who doesn’t want to be a hero? It would feel great.

In the long run, I have found, this mostly does not work. It is better to be drawn to another’s mental health and strength, rather than to their symptomatology (no matter how fascinating). Ultimately, that partner may resent and reject the help, whether consciously or unconsciously. She or he may become hostile and turn it against you, saying, “Stop trying to change me or fix me. You knew who I was when we met.” Try to be mindful of this dynamic and avoid it.

Instead, try to find a romantic partner who is already reasonably psychologically healthy. Two healthy individuals have a better chance. If emotional issues arise, make sure your significant other gets her or his own therapist or psychiatrist. Do not take it all upon your shoulders. Refer them for help. Do not prescribe for loved ones, even if tempted. That is not your role. Just be the loving partner. Keeping such boundaries is very important; you will protect and preserve your relationship.

Also try to avoid someone who is not at all psychologically minded or even ridicules our field or the use of medications. They say opposites attract, but do not mistake the repression of feelings or closed-mindedness for serenity. If you enjoy discussing human behavior but your partner thinks you’re just over-analyzing everything, you may end up frustrated and lonely.

There are a few other occupational hazards that are minor but still a bit galling. Many individuals do not realize that a psychiatrist is a physician. Many do not know the difference between a psychiatrist, a psychologist, and a therapist. We who have toiled for one of the longest training periods known to mankind (college/med school/4 years of residency), we do enjoy getting that MD recognition.

Sitting all day is another occupational hazard, one that we share with all sedentary office workers and airline pilots. Weight gain and hemorrhoids are no fun. As standing desks grow in popularity, perhaps one day we will find a way to stand during sessions.

I hope this list will make you smile and, more importantly, appreciate how hard this work can be. Just as we need to have compassion for our patients, we need to have compassion for ourselves. Let’s treat ourselves very well in our time off.

is a board-certified psychiatrist. She is on the staff of Manhattan Psychiatric Center and works in their mental health outpatient clinic. Her new book 

What special dangers do psychiatrists face in their professional, social, and home lives? 

Occupational Hazards of Psychiatry

Psychiatrists are often called when there is a complicated case without an obvious answer. Since symptoms of medical disorders can mimic neuropsychiatric disorders, it takes a careful history and some detective work to ascertain the correct diagnosis. In this case, a relatively young man was admitted to the hospital with perplexing psychiatric and neurologic symptoms. (The identifying details of the patient have been changed to protect the patient’s identity.)

“Roger,” a 34-year-old single Hispanic male, presented to the emergency department with severe depression, difficulty getting up in the morning for work, crying spells, chronic insomnia, and passive suicidal ideation—all worsening over the past 6 weeks. He also complained of auditory and visual hallucinations. He reported he “often heard voices muttering in the background,” although he could not decipher what they were saying. He also “sometimes saw shadows in the corner of the room.” He was concerned about “missing a lot of work and forgetting things.”

Roger explained he had been well until approximately 3 years ago when he began experiencing depression. He had already had 2 prior psychiatric admissions at another hospital (each hospitalization lasted 2 weeks apiece and were about 2 months apart). After the second discharge, he was referred back to his therapist in their outpatient clinic.

Roger had been discharged from his second hospitalization 6 weeks prior to this presentation. He was on fluoxetine 20 mg po qAM, risperidone 1 mg po twice a day, and benztropine 0.5 mg po BID. He admitted he was not as careful with medication adherence, noting he takes the medications “some of the time. Sometimes I forget.” He complained that the fluoxetine had sexual adverse effects of reducing frequency of erections, and “also interrupted my sleep.” He complained of ongoing fatigue and memory lapses.

He reported not liking the outpatient clinician, and said, “I never really felt comfortable with her.” He admitted missing a number of follow-up appointments at the mental health clinic. When the symptoms persisted, the patient “decided to try another hospital” and was admitted to our psychiatry unit.

The patient presented with severe depression with insomnia, decreased appetite, anhedonia, and increasing social withdrawal. Roger denied any suicidal plans, but he admitted to having passive thoughts of “not living anymore.” He firmly denied any history of suicide attempts and had no intention of harming himself. He denied any history of violence. He also had the aforementioned auditory and visual hallucinations

Roger He was particularly troubled by his decreased appetite, but he denied dieting or having any kind of eating disorder. He noted that he “didn’t enjoy cooking,” and his diet consisted mainly of take-out and fast-food. He added, “I should really eat better.” He denied taking any vitamins or other supplements.

Roger also complained of worsening memory loss and confusion: “A year or so ago, I started misplacing things: my phone, my house keys…I have trouble concentrating. I even forgot my mother’s birthday. That’s never happened before. I forgot the rent was due and had to pay a late fee.” He also noted that he was having trouble walking, which worsened over the past year or so. He denied any physical trauma. He noted that his legs “felt weaker” and his balance was “off.” He had fallen at home a few times. The patient also presented with vertical nystagmus, which was present for the past year. 

Roger was pleasant upon approach. He said he was glad he had sought admission and was “less lonely now.” He had a fresh-faced look, with good hygiene, and he maintained good eye contact. He said his mood was depressed “a 7 or 8 on a scale of 1 to 10.” The mental status exam was normal except for some difficulty with short-term memory. He scored 22 out of 30 on the Mini-mental state examination, which is consistent with mild cognitive impairment. On the Montreal Cognitive Assessment Test for Dementia (MoCa), Roger scored 18 out of 30, which is consistent with mild dementia. The score can be influenced by factors like fatigue or sedating medications. His long-term memory was adequate.

Regarding substance use history, Roger said he was a social drinker but “had managed to stop entirely over the past year.” He noted he had trouble sleeping most nights and up until a year ago he “would take a couple of shots of tequila or vodka to knock me out.” In the past he felt this was “necessary to cope.” He stopped alcohol use the prior year when he had memory issues and fell at home a few times.

Insomnia, however, was still an issue. He noted he had tried over-the-counter sleep aids, which “did nothing for me.” He volunteered that he had “experimented with mushrooms while in college, which he had enjoyed, but he denied using them since then.” He denied using cannabis or any other street drugs. His urine toxicology on admission was negative.

Roger grew up in Dallas, Texas, but both parents were from Mexico. He had a younger sister and brother, with whom he was close. The family still lived in Dallas. He “was the only one on the East Coast,” where he had moved for his job as an administrative assistant at an art museum. He mentioned that he was “homesick and missed them very much.” He had had some friction with his father that started a decade earlier after the patient came out as gay. He stated his father was macho, and “had real trouble accepting it. Everyone else is fine with it.” It pained him that sometimes his father would not come to the phone when the patient called home. He felt rejected and had not gone home for the past year.

On the inpatient unit, Roger was initially placed on risperidone 1 mg po BID, benztropine 0.5 mg po BID, and bupropion 75 mg one tab orally a day. He was started on desyrel 50 mg po qHS, as needed, for the insomnia, which he said helped him sleep. He participated in many activities and groups on the unit. He was observed chatting with peers in a friendly way.

Since Roger believed he had a computed tomography (CT) scan during a prior hospitalization without any reports of abnormalities, one had not been immediately completed on admission. The team requested records for the 2 prior psychiatric hospitalizations and ordered a CT scan to be thorough.

This triad—the combination of an eye disorder (in this case, vertical nystagmus, but it could be another ocular disturbance), and a broad-based, ataxic gait in the context of memory decrease and mood and psychotic symptoms was suggestive of 

Wernicke’s encephalopathy or Korsakoff psychosis (WE)

 Although this syndrome usually occurs in the context of heavy alcohol consumption, Roger noted upon admission that he was merely a social drinker. Upon physical examination, he had no signs of chronic or advanced alcohol use, eg, broken facial capillaries (“gin blossoms”), palmar erythema, or jaundice. The liver function tests on his admission chemistry labs were elevated but still within normal limits. There were no signs of alcohol withdrawal on the unit.

To further explore this possibility, there was a further discussion with Roger about his alcohol use, this time looking for more details. For instance, Roger had noted that a long history of sleep issues for which he drank “several glasses (not shots) of vodka or tequila nightly since about the age of 22 or 23.” He was now 34. Clarification of the term “several” was also pursued. Roger explained that meant “4 or 5 regular glasses; it takes that much to calm me down so I can finally sleep. I drink a lot of coffee during the day.”

Roger also added that this was his nightly routine, not just an occasional thing. He denied ever having any blackouts or withdrawal tremors. He explained, “I’ve always had a high tolerance for booze. It runs in my family.” He did not share this degree of 

 He further noted he decided to stop drinking about a year ago: “I was forgetting too much stuff, over-sleeping sometimes, falling at home. I didn’t want to get fired.” Roger said he “had stopped on his own” without going to an inpatient detoxification or rehabilitation facility. He denied having any withdrawal seizures. He said he “had gone to a couple of Alcohol Anonymous meetings but stopped” because “I didn’t like the people there. It had a ‘homeless’ vibe.”

An Answer to the Mystery—and a Treatment Plan

The head CT with contrast showed changes in the thalamus consistent with WE. There were abnormalities noted in the cerebellum consistent with ataxia. Perhaps the head CTs at the prior hospital had not been interpreted properly.2 We ordered a serum thiamine (vitamin B1) level, which showed that he was severely deficient in thiamine. He now met the criteria for WE.

To correct these vitamin deficiencies, the patient was transferred to a medicine inpatient unit. He received an IV bolus infusion of thiamine 500 mg TID for 2 days, then 250 mg IV daily for 

In addition, Roger was started on vitamin B12 injections and high-dose vitamin D tablets. Within about 2 weeks, all of his vitamin levels were restored to the normal range.

Roger was discharged on the same psych meds: bupropion, 75 mg po qAM, risperidone, 1 mg po BID, benztropine, 05 mg po BID, and desyrel, 50 mg po qHS prn insomnia. He was also prescribed vitamin supplements of thiamine, vitamin B12, and vitamin D, as well as a therapeutic multivitamin. A nutrition consult was done for him to learn how to improve his eating habits. He was referred for supportive psychotherapy to an outpatient mental health clinic that specializes in treatment of the LGBQT+ community.

Wernicke’s Encephalopathy-Korsakoff’s Psychosis Considered

In general, WE is reversible with thiamine infusions. However, failure to diagnose WE can lead to a serious amnestic syndrome (Korsakoff syndrome). Korsakoff psychosis is generally irreversible. Therefore, it is extremely important that such patients are diagnosed and treated as 

When a patient admits to social drinking, it is helpful to pinpoint the exact extent of alcohol use in terms of type of alcohol, quantity, and 

There are a variety of evidence-based cognitive 

 Heirene et al compared the neuropsychological tests used to assess alcohol-related cognitive impairment and compared it with tests that screen for alcohol-related dementia and Korsakoff syndrome.

Meanwhile, Sgouros et al has pursued the development of a Thiamine Deficiency Questionnaire (TDQ) to assess thiamine deficiency in patients with 

 Unfortunately, they concluded that further refinement and evaluation was needed before endorsing TDQ’s validity.

Alcohol use (as well as the use of other street drugs) is 

 According to Livingston and Callinan, “population surveys typically produce underestimates of alcohol consumption of approximately 40%-50%.”

 Thus, it is critical to be as specific as possible regarding what kind of alcohol is being consumed, how much at a drinking session, and how often in the initial patient interview. If the patient admits to “a couple of beers,” ask if those are 12-ounce, 16-ounce, or 24-ounce drinks. Ask for the pattern: are they drinking more on weekends than on weeknights when they have to get to work the next day? Listen for words like 

 as these can be common triggers for high levels of alcohol consumption.

Alcohol use disorder is not the only cause of WE. Any condition that compromises the body’s access to vitamin B1 (thiamine) can 

1. Chandrakumar A, Bhardwaj A, 't Jong GW. Review of thiamine deficiency disorders: Wernicke encephalopathy and Korsakoff psychosis. 

2. Wijnia JW, Oudman E, Bresser EL, et al. Need for early diagnosis of mental and mobility changes in Wernicke encephalopathy. 

3. Isenberg-Grzeda E, Kutner HE, Nicolson SE. Wernicke-Korsakoff-syndrome: under-recognized and under-treated. 

4. Livingston M, Callinan S. Underreporting in alcohol surveys: whose drinking is underestimated? 

5. Boniface S, Shelton N. How is alcohol consumption affected if we account for under-reporting? A hypothetical scenario. 

6. Boniface S, Kneale J, Shelton N. Drinking pattern is more strongly associated with under-reporting of alcohol consumption than socio-demographic factors: evidence from a mixed-methods study. 

7. Heirene R, John B, Roderique-Davies G. Identification and evaluation of neuropsychological tools used in the assessment of alcohol-related cognitive impairment: a systematic review. 

8. Sgouros X, Baines M, Bloor RN, et al. Evaluation of a clinical screening instrument to identify states of thiamine deficiency in inpatients with severe alcohol dependence syndrome. 

9. Choi EY, Gomes WA, Haigentz M Jr, Graber JJ. Association between malignancy and non-alcoholic Wernicke’s encephalopathy: a case report and literature review. 

10. Hutcheon DA. Malnutrition-induced Wernicke’s encephalopathy following a water-only fasting diet. 

11. Shible AA, Ramadurai D, Gergen D, Reynolds PM. Dry beriberi due to thiamine deficiency associated with peripheral neuropathy and Wernicke's Encephalopathy mimicking Guillain-Barré syndrome: a case report and review of the literature. 

12. Togay-Işikay C, Yiğit A, Mutluer N. Wernicke's encephalopathy due to hyperemesis gravidarum: an under-recognised condition. 

Psychiatrists face diagnostic puzzles almost every day. Find out how one clinician cracked a tough case.  

A Young Man Presents With Perplexing Symptoms: What Is Going on Here? 

An article in the December 2020 issue, “

The Intertwining Effect of Mood Disorders and Infertility

,” made many important points. I would like to raise to a few additional issues that seem to be often overlooked.

Women taking serotonin uptake inhibitors (SSRIs) to help them cope with infertility are actually increasing their serum prolactin to an unhealthy level. This hyperprolactinemia, in turn, 

 Unknowingly, they are hindering their changes of conception. This is the biology underlying the common folk wisdom that one cannot usually become pregnant while lactating/breastfeeding. This is when prolactin levels are very high.

I urge all women with fertility issues, especially those on SSRIs, to get a simple blood test measuring their serum prolactin level. An elevated serum prolactin level can be corrected with oral dopamine agonists (dopamine-stimulating) medications.

Certain antipsychotic meds, whether typical or atypical, can also elevate serum prolactin levels. Risperidone in particular can cause hyperprolactinemia in female and males, which causes lactation (galactorrhea) from their breasts. A third, less common cause of hyperprolactinemia is a tumor of the anterior pituitary gland, known as an anterior pituitary adenoma. This can be detected by an MRI of the brain.

Once identified, hyperprolactinemia can be readily corrected by dopamine agonists such as 

 Once the prolactin level has come back down to the normal rage, ovulation can occur. The patient can then discuss with her psychiatrist whether or not to continue the psychotropic medications at the current doses or lower, depending on the severity of her particular symptoms and stressors.

In conclusion, women struggling to conceive who are on SSRIs and/or antipsychotic medication should request that their serum prolactin levels be checked. This cause of infertility can be readily corrected. Therefore, it should be checked, especially before moving on to more invasive and uncomfortable fertility tests, such as a hysterosalpingogram, and certainly before beginning the injections to prepare for IVF.

is a psychiatrist at the Manhattan Psychiatric Center, in the Outpatient Department on 125th St., NYC. She is the author of 

, forthcoming from Amazon, and played Dr Zalutsky on “The Sopranos.”

1. Torre DL, Falorni A. Pharmacological causes of hyperprolactinemia. 

2. Matsuzaki T, Azuma K, Irahara M, et al. Mechanism of anovulation in hyperprolactinemic amenorrhea determined by pulsatile gonadotropin-releasing hormone injection combined with human chorionic gonadotropin. 

3. Schlechte JA. Long-term management of prolactinomas. 

In addressing mood disorders associated with infertility, sometimes the cure may be worse than the disease. 

Ellen Mausner, MD, PhD

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