MD is a practicing psychiatrist in Queens, NY. She completed a fellowship in autism research and is the author of authored “Don’t Medicate–Educate! One Family, Three Cases of Autism, Safe Treatment for Dangerous Behavior.”

My 18-year-old daughter has severe autism. She was doing relatively well at an 

 day school with home support, but as she grew older and hit puberty, with all the challenges that brings, things changed.

One evening, my daughter was sitting on the couch. Suddenly, she got up, forcefully hit herself in the head with her hands, ran upstairs into my room and thrust herself over my bed, banging her head into the mattress. Then she started chasing and trying to attack me. In fear, I locked myself in the bathroom. After what I perceived to be 5 minutes, I came out—only to find her drinking hand sanitizer. I removed it. She calmed down and went to the basement to play on her swing, laughing and giggling as if nothing ever happened. Her nose and mouth were bleeding, but she showed no signs of distress. That night, she fell asleep early and slept through the night, again as if nothing ever happened.

The next day, the dentist told me that my daughter had broken her frenulum. Had her hand been positioned slightly differently, she would have fractured her teeth. That is when I started to ask myself if I should be keeping her at home. Had a patient’s parent reported to me a similar experience with their child, I would have recommended 

 for the child’s safety, along with an applied behavior analysis program. After all, I am a psychiatrist, with advanced fellowship training in autism. I realized that I could not—and should not—treat myself and my child any differently.

I am no stranger to autism, its impact on the family as well as on the individual. My identical twin brothers also have autism. My brother banged his head so hard that he needed surgery, intravenous antibiotics, and 5 months of medical hospitalization. We were so relieved when a residential school accepted him. That was not a hard decision, given its antecedents. He has been doing well since, off medications for over 30 years, working and going on trips.

Typically, it upset me when parents rejected my recommendations for residential educational placement with applied behavior analysis. Some parents would not let go despite the dangers at home. While I always tried to be empathetic, sometimes I saw them as selfish because they did not put their child’s needs first. Yet with my daughter, it was different. I often second-guessed myself, wondering if I was doing it for myself or for my daughter, maybe choosing this because subconsciously I wanted a life of my own and had tired of watching every dime while paying for autism school tuition and home therapies.

“Was I exaggerating her behaviors?” I asked myself, wondering if I was inventing excuses to send her away. I worried that she would not understand that I planned to visit often. Maybe she would wonder if we would ever see one another again. I had nightmares about sending her away. Still, I knew I could not keep her safe at home.

One morning, my daughter bit the bus driver. Yes, the same daughter with the beautiful smile and giggles. Still unable to decide, I called a friend who works in mental health, requesting reassurance.

I kept resisting what I knew was the right decision, even after a board-certified behavior analyst evaluated her and assured me that this was the best decision available for bad circumstances. My self-doubt persisted. Was my concern about potential traumatic brain injury exaggerated, even unfounded? How could I, a parent, be objective with my own child? Yet when I showed a video to my daughter’s developmental pediatrician, she, too, agreed. How much more reassurance did I need?

While all this was transpiring, my black and blue marks from my daughter’s aggression remained. There were still more stories to tell. Once, when she was applying her deodorant, she started to squeeze me hard. I backed away—and she ate her deodorant. Her pica had been constant in the past. It had improved with applied behavior analysis, and now occurred only every few months. Yet even one-off behavior can be life-threatening, and I was helpless to stop her.

When the pandemic began, schools closed. Life became a nightmare. My husband had heart surgery. My daughter’s community habilitation worker quit. With no one to care for my daughter, I postponed my own doctors’ appointments. Without school, she regressed, staying up at night, giving herself bloody noses, attacking me and my husband, and running out of the house.

With my daughter’s school closed, I found myself providing most of the therapy, but I was alone, without the full crisis team available at school. When she once again attacked me while I was following the school directed curriculum, I was forced to lock myself in the bathroom out of fear. I did not want to activate 

 when New York (as well as other states) was in crisis mode, with limited resources and police who are not usually trained to handle this population.

During the pandemic, I could practice psychiatry only a few hours a week. One time, while evaluating a patient, my daughter bit me. While her teeth were in me, I cursed, for the first time ever on the job. I was very embarrassed. In a role reversal, the patient asked me if I were okay.

At the end of a session, a patient was annoyed with the background noise. I apologized and told her that my daughter has autism. Afterwards, I started my sessions with, “If you hear loud noises, I apologize in advance. My daughter has autism.”

I hired a sitter but sometimes even the sitter needed help in managing my daughter’s behaviors. Once she ran up the basement stairs, ahead of the sitter. I interrupted my session with a depressed patient to redirect her out of the kitchen, where she might eat soap or a banana peel. The patient started laughing. When I commented about her laughter, the patient seemed embarrassed and explained that she was not laughing at my daughter, but at what I said, “It’s good you can laugh,” I replied, “A lot of people with depression can’t.”

After I abruptly interrupted sessions due to self-injury or aggression on the part of my daughter, some patients empathized with me, saying, “It must be hard,” or “You have a lot of problems.” At the beginning of sessions, some patients would ask, “How is your daughter?” I would give some nonspecific yet truthful answer like, “She’s hanging in there, one day at a time,” and redirect to how the patient was doing. I found it very hard to focus on the job. For the first time I could remember, it took great effort to remain professional and patient with my patients. I had urges to say rude things. It was exceedingly difficult to serve my patients after my daughter had just attacked me, and after I had a night of disrupted sleep.

During my daughter’s 3 and a half months out of school, I lost 5 pounds and was extremely sleep deprived. There were times I was so unfocused, I put napkins in the refrigerator and even a metal pot in the microwave. Fortunately, I noticed the sparks before anything happened.

Yet there was a silver lining to COVID-19. Unlike her teachers, on some programs, I had felt frustrated with her slow progress, but then I discovered that she knew all the letters by sound and recognized a few words by sight. I taught her to request her favorite foods by handing me the word. I learned how to turn every activity of the day into a learning experience.

When I finally decided to place my daughter in residential care, I felt guilty for not spending more time with her before she left. Now, after COVID-19, I will never feel that way again. We have some great memories from our time at home, and she is happy in her new environment. In fact, she has adjusted better than I did. I now know that we, as psychiatrists, must not only recommend residential placement for safety, but we must also reassure guilt-ridden and self-doubting parents that they are acting in their child’s interests.

MD is a practicing psychiatrist in Queens, NY. She completed a fellowship in autism research and is the author of authored “Don’t Medicate–Educate! One Family, Three Cases of Autism, Safe Treatment for Dangerous Behavior.” More information can be found on her website 

Articles

What happens when a clinician has to give herself news she does not want to hear?

A Doctor, Her Daughter, and a Difficult Dilemma

When working with older individuals with psychiatric symptoms, most clinicians are familiar with the adage “start low and go slow” to guide their prescribing. This refrain has often been augmented with the phrase “but do go” to emphasize the importance of not stopping too early in the titration process. What are the roots of this approach? And, how should it unfold when applied to 3 common psychiatric disorders seen in later life: neurocognitive disorders, depression, and anxiety?

The first principle of prescribing any medication in later life is to appreciate important changes in drug metabolism due to aging organ systems. In terms of pharmacokinetics (ie, what the body does to the drug), absorption time is generally stable since decreases in intestinal absorption are offset by increased transit time; distribution varies by type of drug since increased body fat and decreased body water lead to increased volume of distribution for lipophilic drugs and decreased for hydrophilic drugs; bioavailability is increased for many drugs since there is upwards of a 30% reduction in initial hepatic metabolism; and half-lives are often lengthened since renal excretion is slowed by up to 50%.1 In terms of pharmacodynamics (ie, what the drug does to the body), drug response is less predictable due to alterations in receptor sensitivity, neuronal loss, and changes in key cholinergic and serotonergic pathways. In addition, older individuals tend to be more sensitiveto drug effects and may require lower doses, especially with opioids, anesthetics, and benzodiazepines. Some of the most concerning side effects are due to anticholinergic, antihistaminic, extrapyramidal, and sedating properties of medications.

One major guideline for safe prescribing in later life is The Beers Criteria for Potentially Inappropriate Medication Use in Older Adults, also called the Beers List, which was first developed in 1991 by geriatrician Mark Beers, MD. The list highlights medications that pose undue risk for negative outcomes, including falls, injuries, and even death.2 Since 2011, the American Geriatric Society have been revising and updating the list based on both consensus and evidence-based approaches. With these considerations in mind, we can explore several psychiatric conditions frequently seen in older individuals who have multiple comorbid conditions and polypharmacy.

There are no cures nor disease-modifying treatments for Alzheimer disease, aside from several experimental agents. Instead, there are 2 categories of medications that are US Food and Drug Administration-approved to improve its symptoms. These include 3 acetylcholinesterase inhibitors (AChEIs) that are indicated for mild-to-severe Alzheimer such as donepezil, rivastigmine, and galantamine; and 1 NMDA (glutamate) receptor antagonist called memantine for moderate-to-severe Alzheimer. There is also evidence that these agents can improve symptoms in Lewy body dementia and vascular dementia.

Here are several key do’s and don’ts to keep in mind when prescribing these medications:

keep expectations modest; the goal is symptomatic improvement and not curing the disease.

promise disease slowing, but educate patients and caregivers about realistic expectations and side effects.

start with the lowest dose and titrate slowly, per guidelines.

combine multiple acetylcholinesterase inhibitors.

combine acetylcholinesterase inhibitors with memantine as the disease progresses into moderate and advanced stages.

monitor closely for important side effects of AChEIs such as nausea, vomiting, diarrhea, nightmares, or slowed heart rate; and sedation, dizziness or confusion with memantine use.

start early. The later in the disease course you initiate use of cognitive enhancers, the less benefit you may see. Remember that studies have shown significant symptomatic benefit even in moderate-to-severe disease states.

Treating older individuals with depression poses unique challenges and considerations. Various forms of late-life depression affect 9% to 18% of individuals older than 55, and these rates increase significantly after the age of 85, especially for individuals in nursing homes and hospitals. On the other hand, the more serious and specific diagnosis of major depressive disorder is less prevalent than in younger individuals, with rates of 2% versus 6% to 7%.

Depression can have significant impacts on our bodies by accelerating brain aging and increasing the risk for medical conditions such as diabetes mellitus, cancer, neurocognitive disorders, and both cardiovascular and cerebrovascular disease and events. Risk factors associated with late-life depression include female gender, chronic medical illness, neurocognitive impairment, functional impairment, social isolation, and major life stresses. In many older individuals, depression may present with less mood-related symptoms and more physical or functional complaints and social issues, including fatigue, weight loss, pain, social isolation, resistance, agitation, self-neglect, and substance use. Up to 30% of older individuals with depression may have impairment in executive dysfunction, often due to vascular damage to frontolimbic white matter tracts. This “depression executive dysfunction syndrome,”as described by George S. Alexopoulos, MD, is notable for a poorer response to antidepressants and cognitive-behavioral therapy, earlier relapse, and a greater risk for recurrence.

In terms of selecting an antidepressant for older individuals, there is no favored agent based on multiple studies and meta-analyses, but they all work better than placebo.

 In general, individuals older than 55 years have slightly lower response rates and higher relapse rates compared to younger individuals.

Augmentation strategies that have shown efficacy for late-life depression include the use of antipsychotics, lithium, and methylphenidate. The addition of acetylcholinesterase inhibitors may help improve cognitive deficits, but they have not been shown to be helpful for depressive symptoms. Although antidepressants can improve depression and quality of life associated with medical illnesses, they do not clearly improve the medical conditions themselves. The exception of this is post-myocardial infarct depression, for which they may reduce the risk of recurrent cardiac events, procedures, and overall mortality.

Anxiety disorders are very common conditions in late life, affecting 1.2% to 28% of older patients depending on the subtype of disorder; generalized anxiety disorder and phobias are the most common. Higher rates are seen in chronic obstructive pulmonary disease, diabetes, depression, Alzheimer disease, and Parkinson disease. Antidepressants are first-line treatments, with both selective serotonin reuptake inhibitors and serotonin and norepinephrine reuptake inhibitors most commonly used.

Benzodiazepine use in older patients is often necessary but must be managed carefully. On the one hand, they work quickly and effectively, and at low doses there is little risk of dose escalation or addiction. In general, there is a low risk of drug-drug interactions except with alcohol or other sedative-hypnotics. The purported risk of dementia associated with benzodiazepine use has limited evidence; even if true, it is less of a priority when working with older adults suffering from acute anxiety, especially when they may already have neurocognitive impairment.

 There is good reason for caution, however, given their concerning risk-to-benefit ratio, especially when prescribed by non-specialists. In older patients, benzodiazepine use is associated with an increased risk of falls with fractures, excess sedation, cognitive deficits, and motor vehicle accidents, and an overall elevated mortality rate.

Here are several important suggestions for safer benzodiazepine use:

use in individuals who have a history of unsteady gait, falls, or who are already on multiple medications affecting the central nervous system.

combine with other benzodiazepines or sedative-hypnotics.

 use when there is active alcohol or other substance abuse.

long-term use, escalate doses unnecessarily, or abruptly withdraw the medication.

use antidepressants as the pharmacologic base for anxiety disorders, with benzodiazepines as short-term options for severe symptoms.

use cognitive behavioral therapy, sleep hygiene, and other forms of psychotherapy.

remember that lorazepam and temazepam have no active metabolites since they are metabolized by conjugation only.

Benzodiazepines can be helpful in the short run for acute anxiety and panic while waiting for the more enduring antidepressant to take effect. Thereafter, they are best used only on an as-needed basis and always with close supervision. Individuals with Alzheimer disease and other neurocognitive disorders will be especially vulnerable to side effects of confusion and sedation. In some circumstances, low dose antipsychotics and trazodone can substitute for benzodiazepines, but only under the careful management of a geriatric psychiatrist or other specialist.

is a geriatric psychiatrist and senior vice president for Behavioral Health and the chief medical officer for MIND Institute at Miami Jewish Health. His discussed these issues during his “The Top Dos and Don’ts in the Psychopharmacologic Treatment of Geriatric Patients: Focus on Dementia and Late-Life Depression and Anxiety” presentation at Virtual Psych Congress 2020.

1. Shi S, Klotz U. Age-related changes in pharmacokinetics. 

2. American Geriatrics Society Beers Criteria Update Expert Panel. American Geriatrics Society 2019 Updated AGS Beers Criteria for Potentially Inappropriate Medication Use in Older Adults. 

3. Kok RM, Reynolds CF. Management of depression in older adults: a review. 

4. Alexopoulos GS. Mechanisms and treatment of late-life depression. 

5. Cipriani A, Furukawa TA, Salantiet G, et al. Comparative efficacy and acceptability of 21 antidepressant drugs for the acute treatment of adults with major depressive disorder: a systematic review and network meta-analysis. 

6. Tedeschini E, Levkovitz Y, Lovieno N, et al. Efficacy of antidepressants for late-life depression: a meta-analysis and meta-regression of placebo-controlled randomized trials. 

7. Kim JM, Stewart R, Yong-Seong L, et al. Effect of escitalopram vs placebo treatment for depression on long-term cardiac outcomes in patients with acute coronary syndrome: a randomized clinical trial. 

8. Crocco EA, Jaramillo S, Cruz-Ortiz C, Camfield K. Pharmacological management of anxiety disorders in the elderly. 

9. Salzman C, Shader RI. Benzodiazepine use and risk for Alzheimer disease.

10. Markota M, Rummans TA, Bostwick JM, Lapid MI. Benzodiazepine use in older adults: dangers, management, and alternative therapies. 

When working with older individuals with psychiatric symptoms, most clinicians are familiar with the adage “start low and go slow.” But what other tips should you consider when prescribing psychopharmacology? 

Do’s and Don’ts of Psychopharmacology in Late Life: Key Challenges and Opportunities

“Dude,” the medical student said with an informal millennial drawl, “do you even like psychiatry?”

He stared at the books that line my office shelves. Mixed among the Freuds (both Sigmund and Anna), the Jaspers, and the textbooks are any number of works by Foucault, Laing, and Szasz. Between my 

. I have a number of books on philosophy, history, and scientology. This particular student finally picked up the nearly extinct first American edition of 

I, Pierre Rivière, having slaughtered my mother, my sister, and my brother…

“Dude, why?” he asked semi-innocently.

“OK,” I said to him. “I’ll let you in on the dirty, little, ill-kept secret of psychiatry.”

He leaned in and I, looking shiftily left then right, confessed in a stage whisper, “Psychiatrists have an inferiority complex.”

Psychiatry–and do not let its more blustery practitioners kid you–is a pseudo-science. A fact that makes some neuroscientists, historians, sociologists, and generations of Freud-haters dance almost gleefully. A fact that makes some practitioners in the field tomato-faced and defensive. I never quite understood why. Frankly, this uncertainty–and the impossibility of certainty–is the reason I went into the field. In fact, I would counter that most of medicine today at best remains pseudo-scientific, relying on an ‘evidence-base’ that changes on a near-daily basis

, and is easily manipulated by any number of industries. At worst, it is dogmatic–think Al Capone, “It’s right because I say it’s right”–and this makes for far more potential danger.

But more to the point, I would wager that more than half of the patients in any given general hospital at any given time are there for vague somatic symptoms with no known medical illness. Or, if there is a medical issue, it is not one that would typically require acute stabilization. Instead, the issues are either directly related to, or exacerbated by, underlying psychiatric issues.

The bottom line is that pseudo-scientific psychiatric treatments are no less effective than any scientific treatments in medicine.

But–especially in these end of days–there are many psychiatrists who do so desperately wish to be neuroscientists. They do so want to be “real” doctors. They call themselves 

 establish departments of neuropsychiatry, and even hide behind journals titled 

. They want to point to an MRI with confidence and say, “See. There. We have isolated the source of your self-loathing to the right frontal cortex. A simple excision, and you’ll be fine.”

Witness the current bandwagon of interventional and neuromodulatory psychiatry.

 The parade includes the tried and true ECT along with the shinier, newer transcranial magnetic stimulation, side by side with the rebranding of the old deep brain stimulation, psychosurgical ablations, vagal nerve stimulation, IVIG, and ketamine infusions. All of which are potentially well and good, if not nearly as miraculous as once hoped or advertised, except that these techniques mislead both patient and psychiatrist away from the heart of the patients’ problems. That is, they lead once again toward neurology and away from psychiatry, ignoring the inconvenient fact that what ties psychiatry and neurology together is that neither field can offer lasting cures.

Perhaps better put, like every other American specialty, what psychiatry wants more than anything is corporate respectability. Case in point: The National Institute for Mental Health has inaugurated a multi-billion dollar enterprise called the “

 There is a complicated website, well-disguised in untranslatable jargon, in an effort to subsume psychiatry under neurology.

No real definition of the project is provided anywhere on the website. As of this writing, the best I can find is a description of their framework. In their words, at least as of this writing, it is a matrix, or matrices, I suppose, that “represent specified functional constructs… characterized in aggregate by the genes, molecules, circuits, etc (sic) used to measure it. Constructs are in turn grouped into higher-level domains of functioning.” These domains are as follows: negative valence systems, positive valence systems, cognitive systems, systems for social processes, and arousal/regulatory systems.

This model was proposed just before the founder of this enterprise abruptly up and took off for the artificially greener pastures of Silicon Valley. Initially accepting a job offer from Google Life Science (now Verily), he has since hightailed it yet again, to a start-up ominously called Mindstrong. There he designs mental health apps

, an endeavor now boosted by the ethically questionable volunteering of his time as mental health czar of California.

The founder’s personal peregrinating issues aside, billions of dollars have now been devoted in these recent years to exploring what amounts to various euphemisms: molecular psychiatry, genetic psychiatry, translational psychiatry, all subheadings of the grander movement toward so-called biologic psychiatry.

What is the grander motive? (Or, perhaps more appropriately, what was the motive, as the guru has since jumped ship.) Whatever the tense, the answer remains: potential procedural dollars on par with other specialties. Never mind that for all the investment not a single meaningful new treatment has emerged, and never mind that few have suggested at least some of that money be diverted toward social or educational or vocational programs for the severely and chronically mentally ill, programs that have a proven track record of efficacy; the bureaucratic foundation has been laid. Another inquisitorial framework is in place, and Lord help the poor shrink who points out the obvious: that psychopathology, at bottom, remains a social disease.

“Embrace it!” I cry from my lonesome perch here in the wilds of suburban Boston.

The fact that psychiatry is so openly out there as a pseudoscience is the beauty of psychiatry.

Psychiatry, at this moment anyway, remains blood-test and imaging-free. It offers the last frontier of semi-free thought to the thinking person who wishes to enter medicine, to try to understand people, to try to understand really what makes people sick, to understand their need or desire to be sick. Hence my eclectic collection of books, and my ongoing admonition to my students–those who actually wish to understand their patients better–to continue to read as widely and broadly as they can.

Psychiatry is also, it should be noted, the only specialty with a political and social movement specifically directed against it. The so-called anti-psychiatry movement

 was initiated and has been maintained over the years, for the most part, by none other than psychiatrists themselves, with healthy assists, of course, from the legal trade, Hollywood intellectual heavyweights, and the ludicrously well-funded scientologists. How cool is that?

And, well, that at least makes me feel, however ineffectually, somewhat like a resistance fighter.

For one thing, where would all the hopeless cases go? Because believe me, there is no clamor from the other side to subsume psychiatry.

Director of Medical Psychiatry at the Newton-Wellesley Hospital in Newton, MA, and a Clinical Assistant Professor of Psychiatry at Tufts University School of Medicine in Boston.

1. Little M. Book Reviews: Miriam Solomon, Making Medical Knowledge, Oxford University Press, 2015. 

https://kiej.georgetown.edu/miriam-solomon-making-medical-knowledge-oxford-university-press-2015/

2. Ioaniddis JPA. How Many Contemporary Medical Practices Are Worse Than Doing Nothing or Doing Less? 

https://www.mayoclinicproceedings.org/article/S0025-6196(13)00403-5/fulltext

3. Dubovsky S. How Well Do Psychiatric Treatments Work? 

https://www.jwatch.org/na34660/2014/05/21/how-well-do-psychiatric-treatments-work

4. Mass General Neuroscience. Massachusetts General Hospital. Accessed September 17, 2020.

5. Williams NR, Taylor JJ, Kerns S, Short EB, et al. Interventional Psychiatry: Why Now? 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4221242/

6. Research Domain Criteria (RDoC). National Institute of Mental Health. Accessed September 17, 2020. 

https://www.nimh.nih.gov/research/research-funded-by-nimh/rdoc/index.shtml

7. Rogers A. Star Neuroscientist Tom Insel Leaves the Google-Spawned Verily… For a Startup? 

https://www.wired.com/2017/05/star-neuroscientist-tom-insel-leaves-google-spawned-verily-startup/

8. Sheridan K. California names former Google scientist as the state’s ‘mental health czar.’ 

https://www.statnews.com/2019/05/22/tom-insel-california-mental-health-czar/

9. Horwitz A. Social Constructions of Mental Illness. In: Harold Kincaid, ed. 

The Oxford Handbook of Philosophy of Social Science

. Oxford, Oxford University Press; 2012. 

https://www.oxfordhandbooks.com/view/10.1093/oxfordhb/9780195392753.001.0001/oxfordhb-9780195392753-e-23

10. Desai N. Antipsychiatry: Meeting the Challenge. 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2921130/

Dr Martin shares psychiatry's "dirty, little, ill-kept secret..." 

Is It Time to Do Away With Psychiatry?

, talks about National Depression Education and Awareness Month and National Depression Screening Day, October 8.

He briefly explains the epidemiology and impact of depression both worldwide and in the United States and describes how he screens for and treat depression. Also discussed are common screening tools such as the PHQ-9 and Beck Depression Inventory.

Dr Lagoy speaks to the prevalence and probability of treatment-resistant depression and the different options for treatment. He describes the process of switching a medication versus his rationale for adding an adjunctive medication. Lastly, he briefly mentions other alternative non-medication treatments for depression if medications fail.

Videos

Prepare for National Depression Education and Awareness Month with a discussion on initiatives and treatments. 

Shining a Light on Depression Awareness

Slideshows

With most chronic pain conditions, the exact pathology is uncertain. In such cases, psychiatrists may be called to assess for illness beyond medical diagnosis.

10 Factors Leading to  Pain Complaints  in the Absence of a Medical Diagnosis

Over 30 million Americans live with diagnosable chronic insomnia. It can impair their everyday functions when awake and affect their mood. Chronic insomnia is also a risk factor for other chronic illnesses and psychiatric disorders (up to 40% also have depressive symptoms).

Existing pharmacological treatments are designed for short-term use, which may not be enough to combat a long-term illness. In this Mental Health Minute, Yuri Maricich, MD introduces Somryst, the first FDA-authorized prescription digital therapeutic (PDT) for treating chronic insomnia. It is a 9-week program that is accessible through mobile devices, including smartphones and tablets. He discusses two studies on the effectiveness of this new PDT.

(Note: in the video, Dr Maricich says that the FDA authorized Somryst in 2023. The FDA authorized it in 2020.)

A new treatment has been found effective for treating a common sleep disorder.

Introducing the First FDA-authorized Prescription Digital Therapeutic for Chronic Insomnia

Dr Pies is Professor Emeritus of Psychiatry and Lecturer on Bioethics and Humanities, SUNY Upstate Medical University; Clinical Professor of Psychiatry, Tufts University School of Medicine; and Editor in Chief Emeritus of 

 (2007-2010). Dr Pies is the author of several books. A collection of his works can be found on

Anyone who thinks all psychiatric disease categories are merely “socially constructed labels” cooked up by modern-day, “institutional psychiatry” should read Avicenna’s writings on melancholia—and then think again.

Avicenna (980 CE-1037 CE) is the Latinized name of 

, the Persian philosopher, thinker, and physician who is often considered “the most famous and influential of the philosopher-scientists of the medieval Islamic world.”

 By one account, Avicenna had read and memorized the entire Qurʾān by age 10! Among philosophers of the medieval period, Avicenna is probably best remembered for his distinction between 

—an esoteric matter we need not pursue here.

 But among historians of medicine, ibn Sina is probably best known as the author of 

), which served as the preeminent European medical text as recently as the 17th century.

Why should psychiatrists today care about a thousand-year-old manuscript?

As a specialist in mood disorders, my interest in 

 lies in Avicenna’s remarkable description of 

He saw it, first of all, as affecting both the 

, and he divided melancholia into early phase and chronic phase. Symptoms of early phase melancholia included suspicions of evil, fear without cause, quick anger, involuntary muscle movements, dizziness, and tinnitus. Chronic melancholia symptoms included moaning, suspicion, sadness, restlessness, [and] “abnormal fear, such as . . . that the sky may fall on one’s head . . . [or] being swallowed by the earth.”

 These fears certainly sound like delusions, thus suggesting psychotic features in chronic melancholia. Avicenna also noted some features of chronic melancholia that are consistent with—or similar to—what we would now call a “mixed state” or perhaps a switch into mania: increased libido, involuntary laughter and imagining “that [one] is king.”

At first glance,Avicenna’s composite description—probably based on many patients he had observed—may seem like a hodgepodge of unrelated signs and symptoms. But upon closer examination, I believe Avicenna’s description sorts out into 5 main clusters: encompassing anxious/depressive, manic, psychotic, cognitive and somatic features (

). I have noted, in brackets, what might be our modern-day analogues of some of Avicenna’s terms.

Avicenna’s concept of melancholia overlaps with, but is not identical to, some modern formulations of melancholia5—which also differ from the DSM-5’s specifier, “with melancholic features” (

A cautionary note: my analysis is based on a 12th century translation from Avicenna’s original Arabic into Latin and then into English which almost guarantees problems of interpretation.

 Nevertheless, I believe we can still draw meaningful conclusions from Avicenna’s rich description of melancholia. Indeed, I believe Avicenna was identifying a clinical entity that is consistent with what today we would call a 

. This has been succinctly described by S. Nassir Ghaemi, MD, MPH, and Sivan Mauer, MD, as follows

It is . . . important to acknowledge that the phenomenology of mood conditions involves the frequent, if not usual, admixture of manic and depressive symptoms at the same time—called mixed states. In this scenario, a full-blown clinical depression may be present, but some manic symptoms may also be present such as rapid thoughts, increased sexual drive, and marked anger and mood lability. Thus, one can think of mood episodes on a spectrum from pure depression to pure mania, with many mixed states in between.

Ghaemi and Mauer draw a remarkable conclusion from the prevalence of such mixed states

If this phenomenology is correct, then it has important implications for the classification of diagnoses. The current [DSM] diagnostic system is based completely on the distinction of depression and mania. If manic vs depressive states cannot be distinguished in most cases, then the current diagnostic system would be very difficult to implement validly. Put otherwise, the frequent presence of mixed states would invalidate the diagnostic system built on a mania vs depression dichotomy.

There are a few things that should be considered as part of this discussion.

There remains some controversy regarding the nosological status of melancholia.

 For instance, there is some debate as to whether it constitutes a stand-alone category, or whether—invoking a dimensional model—melancholia represents simply a more severe type of depression.

of these issues is provided by Gordon Parker, MD, PhD, DSc, in 

, January 20, 2017. With respect to melancholia as a distinct category or illness, Max Fink, MD, and Michael Alan Taylor, MD, have propounded a very specific description of a discrete disease entity, characterized by “specific behaviors, vegetative signs, and validated by neuroendocrine abnormalities (cortisolemia).”

In the discussion, I am alluding to the title of Julian Jaynes’s controversial book, 

The Origin of Consciousness in the Breakdown of the Bicameral Mind. 

In their seminal paper, Ghaemi and Dalley lay out the case for breaking down the dichotomous classification of mood disorders and for returning to a more Kraeplinian understanding of manic and depressive states. Ghaemi and Dalley first explain the difference between the Kraeplinian concept of manic-depressive illness (MDI) and our present DSM model of unipolar versus bipolar disorder. In essence

For bipolar disorder, the condition is defined by polarity: presence or absence of a manic episode…For MDI, the condition is defined by episodicity: recurrent mood episodes define the illness, irrespective of polarity…MDI means recurrent manic 

depressive episodes. Bipolar disorder means recurrent manic 

depressive epi­sodes. These are quite different concepts.

The authors also punch some holes in the DSM category of major depressive disorder (MDD), which they argue is of “questionable” validity. My own view of MDD, as I have quipped to Dr Ghaemi, is that it is broad and vague enough to apply to a week-old ham sandwich! 


1. Fink M, Taylor MA. Resurrecting melancholia. 

2. Ghaemi SN, Dalley S. The bipolar spectrum: conceptions and misconceptions. 

On this last point, Ghaemi has much more to say regarding what I would call—with a nod to Julian Jaynes—“the breakdown of the bicameral model” (

). Indeed, allowing for the difficulties of translation, I believe Avicenna would be in agreement with this non-dichotomous—or perhaps we should say unified—view of mood disorders. Moreover, Avicenna’s observation of apparent psychotic features in melancholia should not be surprising, since delusions or hallucinations occur in about one-half of manic states and in about 10% of depressive states.8 Indeed, recent work by van Bergen et al9 found that a lifetime history of psychotic symptoms was present in 73.8% of patients with bipolar type I and included delusions in 68.9% of patients and hallucinations in 42.6%.

We should note that not all the signs and symptoms observed by Avicenna map neatly onto modern-day descriptions of mixed states. For example, Avicenna describes “laziness” and “inertia” in melancholia, whereas recent work by Koukopoulos et al

 suggests that most mixed states are characterized primarily by psychomotor excitation—eg, rapid thoughts, marked rage/irritability, agitation, and impulsivity—added to depressive features. This discrepancy should not be surprising. Avicenna’s global description probably reflected his experience with many different patients with varying presentations of melancholia, which, for Avicenna, encompassed the entire range of both depressive and manic symptoms.

Finally, we should note that the DSM-5’s mixed features modifier—defined as the presence of non-overlapping mood symptoms from the opposite mood state—differs in several important respects from mixed states as described by Ghaemi and Mauer,7 who are critical of the DSM-5’s formulation.

Avicenna’s forbears: Aristotle and ibn Imran

To be sure, Avicenna was not the first or the last ancient or classical writer to describe melancholia. Aristotle (384 BCE–322 BCE) described not only melancholia, but—very likely—manic-depressive illness.

 Indeed, as with Avicenna, Aristotle’s concept of melancholia probably “included what today would be called mania.”

And, about a century before Avicenna, the Iraqi-Arab physician ibn Imran (died c 906 CE) wrote a treatise describing melancholia and manic-depressive illness in strikingly modern terms.13 Notably, Avicenna may have been among the first physicians to document that anger is often a transitional state from melancholic depression to mania—implicitly recognizing the switch phenomenon.

The term “melancholia” is derived from 2 Greek words: 

, meaning “black” and “bile,” respectively. Black bile is one component of the theory of the 4 humors, which dominated medical theory and practice from the time of Hippocrates (ca 460–c. 370 BCE) until the middle of the 19th century.

 Avicenna’s concept of melancholia owed much to this theory, and attributed melancholia to “an excess of black bile in the brain.”

 We can set aside this long-outdated humoral theory without diminishing the importance of Avicenna’s clinical description of melancholia and its relevance to our modern construct of mixed states. Furthermore, we should take careful note of Avicenna’s view of melancholia as a multi-system disease, particularly one involving the heart

[I]n most cases, some heart diseases initiate a process which ultimately leads to depression; and [even] if the cause of depression in some cases originates from the brain, [the] heart will be involved and make the problem worse.

It is really only within the last century or so that Avicenna’s intuition has been partially validated, although the specific mechanisms he posited differ considerably from those of modern medicine. Recent studies show that, indeed, there are important connections between clinical depression and cardiac disease. For example, approximately 20% of patients with ischemic heart disease (IHD) suffer from comorbid depression, and depression is an independent predictor of IHD in otherwise healthy individuals, even after controlling for risk factors such as smoking.

Serious psychiatric diseases have plagued mankind for at least the period of recorded human history, and probably much earlier. Although I have cited sources going back to classical Greece, narratives from the Hebrew Bible suggest that melancholia and various mixed affective states were recognized even in Biblical times, eg, in the condition 

 The medieval physician and philosopher Avicenna appears to have described a type of mixed affective state—embodying manic, depressive, and psychotic features—a millennium before institutional psychiatry existed. To be sure, the humoral mechanisms he posited are no longer credited, but his clinical observations of melancholic patients are largely consistent with those of modern-day clinicians. In short, the notion that melancholic depression, mixed states and manic-depressive illness are inventions of modern-day psychiatry is, historically speaking, flatly wrong. Finally, Avicenna’s description of melancholia presenting as a mixed state has important implications for our modern-day nosology and our treatment of mood disorders.

: I wish to express my appreciation to my friend and colleague, Dr Nassir Ghaemi, for his valuable comments, suggestions, and perspectives on an earlier draft of this article.

 is professor emeritus of psychiatry and lecturer on bioethics and humanities, SUNY Upstate Medical University; clinical professor of psychiatry, Tufts University School of Medicine; and editor in chief emeritus of 

1. Flannery M. Avicenna, Persian philosopher and scientist. Britannica.com. Accessed September 16, 2020. 

https://www.britannica.com/biography/Avicenna

2. Rizvi SH. Avicenna (Ibn Sina) (c. 980-1037). 

3. Araj-Khodaei M, Noorbala AA, Parsian Z, et al. Avicenna (980-1032CE): The Pioneer in Treatment of Depression. 

The Nature of Melancholy: From Aristotle to Kristeva. 

5. Fink M, Taylor MA. Resurrecting melancholia. 

January 20, 2017. Accessed September 16, 2020. 

https://www.psychiatrictimes.com/view/update-melancholia

Avicenna may have been among the first physicians to document that anger is often a transitional state from melancholic depression to mania—implicitly recognizing the “switch” phenomenon.

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