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worked with experts from multiple areas in psychiatry to bring you discussions of important topics, such as identifying and treating victims of human trafficking; diagnosing and managing fibromyalgia; and ethically evaluating dangerousness in individuals with personality disorders. Here are some highlights from our selection of this year’s Continuing Medication Education (CME) articles:

Psilocybin Revisited: The Science Behind the Drug and Its Surprising Therapeutic Potential

Psilocybin and psilocin are the main psychedelic agents of the psychoactive mushroom genus Psilocybe.

 Historical and cultural use of these psychoactive mushrooms dates back 3000 years in Mexico and the Southwestern regional areas of the present-day United States. Scientifically, psilocybin was isolated and identified in 1958, synthesized in 1959, and used in various experimental research studies in the early 1960s. During that time, psilocybin and other psychedelic agents such as lysergic acid diethylamide (LSD) generated considerable controversy. Outside of recreational use, could they be used safely as therapeutic interventions? 

Fibromyalgia: What It Is and How to Treat It

Fibromyalgia (FM) is one of the most controversial diagnoses in the field of pain management. Some experts believe that it does not exist and actually represents an accidental or purposeful misdiagnosis of other conditions, while others believe that it is badly underdiagnosed.

 The truth likely falls somewhere between these 2 extremes. FM is a real syndrome, but it is also perhaps overdiagnosed, both because many physicians are unaware of the actual diagnostic criteria, and because there may be a desire to avoid diagnosing patients with other conditions that could explain the symptoms of FM—most notably mental disorders. 

Psychiatric Evaluation of the Peripartum Patient

The peripartum period is not necessarily a time of emotional well-being,

 highlighted by the fact that about 1 in 13 women develop new-onset major depressive disorder (MDD) while pregnant.

 (The term “peripartum” in this article refers to pregnant women and women who are up to 1 year postpartum.) In the postpartum period, 1 in 7 women will develop MDD and are at high risk for psychiatric hospitalization.

 Thus, comprehensive psychiatric evaluation of the peripartum patient is an essential skill. The mainstay of assessment remains the clinical interview; as such, careful and systematic psychiatric evaluation during these periods is crucial for diagnosis, risk assessment, and treatment. The general psychiatric evaluation, however, must be expanded and tailored to the needs of the peripartum patient. 

Psychiatrists’ Response to Human Trafficking

Human trafficking is a public health issue that involves exploiting individuals for forced sex or labor. Traffickers perpetuate the cycle of exploitation by utilizing methods such as emotional, economic, or physical abuse; isolation; and threats. Physical, mental, legal, and social sequelae of human trafficking can persist for years after individuals survive their trafficking situations. Individuals with a preexisting history of psychiatric illnesses, including substance use disorders, are especially vulnerable to being trafficked. 

Here is a full list of our CMEs from 2021:

Microglial Involvement With Psychiatric Diseases

Neuropsychiatric Symptoms of Multiple Sclerosis

Opportunities in Managing Treatment-Resistant Depression and Tardive Dyskinesia

Psychological and Cognitive Insight: How to Tell Them Apart and Assess for Each

Different Strokes: How to Spot and Treat Poststroke Depression

Transgenerational Transmission of Resilience After Catastrophic Trauma

Prognostic Considerations in Anti-NMDA Receptor Encephalopathy With Psychiatric Manifestations

Cognitive/Neuropsychological Functioning and Suicidal Behavior: A Review of Research and Implications for Clinical Practice

Be sure to stay up-to-date by subscribing to the 

Do you have a comment on any of these or other articles? Have a good idea for an article and want to write? Interested in sharing your perspectives? Write to us at 

Psychiatric Times featured a wide variety of psychiatric issues in this year’s CMEs.

CMEs 2021: A Year in Review

 have focused on lithium’s advantages. The well-known downsides, including renal impairment, have also been discussed. However, a recent consultation reminded me that there is an infrequent, but important, toxic effect of lithium that deserves increased awareness: the Syndrome of Irreversible Lithium-Effectuated Neurotoxicity, or SILENT.

 First named in the 1980s, SILENT was diagnosed in 90 case reports in peer-reviewed publications as of 2005, starting in 1949 when lithium chloride was being used as a substitute for table salt.

The clinical profile of SILENT varies, but persistent cerebellar dysfunction is the most common finding, with extrapyramidal symptoms also typically present. Many of these cases involve insidious progression in patients on normal or low therapeutic levels of 

. The first sign may be decreased alertness or slight apathy, followed by muscular rigidity or fasciculations and mild ataxia. These symptoms increase and become severe, and then impaired consciousness with a stupor-like presentation can develop.

When lithium is stopped, some or all of these symptoms may persist beyond 2 months, with some reports describing continued symptoms for 5 years. Most cases have residual impairments such as ataxia and dysarthria that continue for 1 year. Sometimes there is persisting cognitive dysfunction with memory loss and other symptoms of dementia. In other cases, additional atypical symptoms accompany the core features, including nystagmus, papilledema, and choreoathetoid movements suggestive of tardive dyskinesia.

SILENT’s cause is unknown. Demyelination has been found on biopsy of peripheral nerves and may occur in the cerebellum and elsewhere.

 This may account for the persistence of the neurological sequelae.

Precipitating or predictive factors may include diagnosis of schizoaffective disorder, marked psychosis, abnormal EEG prior to treatment, preexisting neurological illnesses including Alzheimer disease, and fever—especially high fever.

 Readers may recall the famous 1970s cases of neurotoxicity arising from the use of lithium plus haloperidol.

 All patients in those cases had very high fevers and high lithium levels, and they are now thought to have had cases of SILENT. Some other possible contributing factors could be hypertension, heart failure, rapid lowering from high lithium levels, and epilepsy.

To prevent SILENT, it may be helpful to avoid high lithium levels through regular and frequent monitoring (eg, every 4-6 months). If symptoms develop, 

. Treat persisting symptoms with appropriate physical rehabilitation and cognitive training as you would for dementia.

The other side of the coin on lithium neurotoxicity, as discussed in a previous column,

 is the positive neurotrophic effects of lithium that benefit many patients. In a recent pilot study, for example, 12 patients recovering from stroke were prescribed open-label lithium for 60 days (target levels, 0.4-0.6 mEq/L). Gray matter volume as measured by MRI increased numerically (but not significantly; P = .07), and there was a significant correlation between higher lithium dose and gray matter volume increase (P = .004) and improved verbal memory (P = .05).

In conclusion, lithium’s benefits to brain health are substantial, but there are rare cases of serious toxicity that should be detected as early as possible.

is an associate professor of psychiatry at Harvard Medical School and codirector of the US Department of Veterans Affairs’ National Bipolar Disorder Telehealth Program, in Brockton, Massachusetts. The author reports no conflicts of interest concerning the subject matter of this article.

The syndrome of irreversible lithium-effectuated neurotoxicity. 

2. Hanlon LW, Romaine M III, Gilroy FJ, Deitrick JE. 

Lithium chloride as a substitute for sodium chloride in the diet; observations on its toxicity.

Lithium carbonate, haloperidol, and irreversible brain damage.

5. Sun YR, Herrmann N, Scott CJM, et al. 

Lithium carbonate in a poststroke population: exploratory analyses of neuroanatomical and cognitive outcomes.

This infrequent, but important, toxic effect of lithium deserves increased awareness.

Lithium Neurotoxicity: The SILENT Syndrome

From seasonal affective disorder to 24/7 contact with visiting family to finding the perfect gifts, the holidays can be a minefield of stressful situations for patients! The following are 10 tips to share with patients so they not only survive the holidays, but remember to thrive during this hectic time.

For patients to get the most out of their interactions with family this year, encourage them to share specific stories from their lives. For instance, advise them that instead of saying, “life is good,” patients should tell family and friends about how a walk in the snow reminded them of peace and beauty, or how they felt relief after finding a meaningful gift for their partner after weeks of searching. Encourage them to use emotional words to help them tune into what is going on in their world and to build connections.

Post-pandemic interactions can be difficult and maybe even awkward, especially for patients with social anxiety disorder. Have your patient think of someone with whom they want to connect, and then reach out to that person to ask for advice: perhaps about cooking, ideas for gifts, outfits for certain occasions, etc. The next step for your patient is for them to bring their advisor along on the journey with follow-up conversations. Have your patient tell their advisors how the cooking experiment went, what the gift recipients thought, how the outfit looked, etc.

Help patients truly connect with others by giving their full attention and engaging. Have them ask specific questions. For instance, encourage patients to use open-ended questions such as “how do you decide what to buy people for gifts?” Or even something silly like “what do you think about the new Starbucks Christmas cup patterns? Which is your favorite?” Show them how asking specific open-ended questions is better than asking “how’s it going?” A quick internet search for “open-ended conversation starters” might be helpful for them.

If patients need a break from family, yet have nowhere to take such a break, encourage them to engage in “parallel play.” Parallel play is commonly employed when children engage in activities near each other, but not in direct contact or with each other, and this strategy can also be used by adults. An example might be reading a book in the kitchen while their family member is cooking. Advise patients that spending time with family can be a balance of direct interaction and parallel play to help patients limit social burnout. Read more about different types of play 

Do some of your patients tend to get into difficult situations more when they have had some drinks? Are tired? Have not exercised? Are hungry? Ask patients to think about these vulnerability factors and how they can do their best to mitigate them. By considering these factors, patients will be set up for success and be able to handle situations more peacefully and with ease. Read more about vulnerability factors 

After patients have taken time to mitigate vulnerability factors, ask them what they can do to add strengthening factors to their holiday plans. Have patients think about what they can realistically take care of themselves when their regular schedule is not in effect, and then choose to do a meditation challenge, go for a walk a few times per week, or something similar. Advise them to pick something easy that they know they can achieve.

Sometimes it is difficult, or impossible, for individuals to understand a perspective or feeling that differs from their own, and patients may be especially reminded of this during the holidays. If patients are interacting with people who are not able or willing to listen to, understand, or validate their feelings, advise them to plan to satiate those needs elsewhere by talking to you, a friend, or a family member who will validate. Remind patients that writing in a journal may be useful.

8) Give yourself credit for the small things

When life is stressful, even the little things can be difficult, particularly for patients with anxiety and stress disorders. Encourage patients to take time to personally acknowledge themselves for all the things they have accomplished, no matter how big or small. Tell them that this is a self-gratitude practice, and it can change their outlook immensely and help them build self-esteem.

9)Plan some real vacation time in the future

The December holiday season might present with time off work, but is it really rest for a lot of patients? Encourage patients to plan a vacation for January or February: a short weekend getaway, or a staycation in bed with some good TV shows. Knowing there is time to actually relax right around the corner can help patients get through the hustle and bustle of December.

Remind patients that they cannot control if their flight home is delayed, or if their family members hound them about their love life. When patients feel like so many things in life are up in the air, advise them to focus on what they can control: their reaction and their attitude. A good example of this is Viktor Frankl, MD, PhD, whose discussion on how he believes his attitude helped him survive concentration camps during World War II appears in 

 is an author, counsellor, and teacher. Her book, 

The Conversation Guide: How to Communicate, Set Boundaries, and Be Understood

Are your patients feeling stressed out? Here are 10 tips to share with them for a less stressful holiday season.

Helping Patients Thrive This Holiday Season

Negative symptoms of schizophrenia are challenging to treat and often persistent. The recommended duration for clinical trials for negative symptoms is 6 months.

 However, negative symptoms improve during acute-phase antipsychotic trials. A previous meta-analysis investigated the dose-response relationship between antipsychotics and total symptoms in acute-phase schizophrenia.

 However, data on the dose-response relationship between antipsychotics and negative (versus positive) symptoms are lacking. Identification of near-maximum effective doses would help guide clinical decision-making.

Sabe and colleagues conducted a systematic review and dose-response meta-analysis of double-blind randomized controlled trials (RCTs) of fixed antipsychotic doses for negative and positive symptoms in acute exacerbations of (chronic) schizophrenia or schizoaffective disorder.

 They included all fixed-dose double blind, parallel group RCTs of antipsychotic versus placebo with a duration of at least 3 weeks. The primary outcome was the intent-to-treat score change from baseline for negative symptoms assessed with either the Positive and Negative Syndrome Scale (PANSS) negative subscale or the Scale for Assessment of Negative Symptoms (SANS). The secondary outcome was the intent-to-treat score change from baseline for positive symptoms assessed with either the PANSS positive subscale or the Scale for Assessment of Positive Symptoms (SAPS). The authors estimated flexible dose-response models from sets of correlated mean differences, which were combined into pooled dose-response curves. From these curves, they estimated 50% (ED50) and 95% (ED95) effective doses for each antipsychotic. The ED50 is the mean dose that produces half of the maximum reduction of symptoms, and the ED95 is the near-maximal effective dose.

Among 4398 articles, the authors identified 612 articles for full-text review, of which 40 met the inclusion/exclusion criteria. These 40 trials included 15,689 patients (mean illness duration 14 years) and investigated 13 different oral and 3 different long-acting injectable antipsychotics. The median study duration was 6 weeks (range 4-13). The 

provides resulting data on the ED50 and ED95 for negative and positive symptoms for various antipsychotics.

The resulting dose-response curve types could be trichotomized into: 1) plateau after an initial increase, 2) still increasing at the maximum dose, and 3) bell-shaped. Most of the dose-response curves suggested that the ED95 may be in the low to medium range of approved doses. For most antipsychotics with a plateau-shaped dose response curve (the most common pattern), the ED95 was lower for negative than positive symptoms, except for aripiprazole and asenapine. For olanzapine and quetiapine ER (for negative symptoms) and ziprasidone (for positive symptoms), the dose-response curves were still increasing at the upper end of the investigated dose range, raising the possibility that higher doses could be more efficacious.

The authors noted that the primary limitations of their analyses were the small number of RCTs and limited dose range investigated for some antipsychotics. Another limitation was the absence of RCTs of clozapine. Furthermore, findings do not permit inferences on effects of longer durations of treatment beyond the acute phase of illness.

Findings can help clinicians optimize antipsychotic dosing during acute illness exacerbations. Antipsychotic doses above the ED95 may not confer additional efficacy for most agents.

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, and the Stanley Medical Research Institute.

1. Marder SR, Davidson M, Zaragoza S, et al. 

Issues and perspectives in designing clinical trials for negative symptoms in schizophrenia: consensus statements

Dose-response meta-analysis of antipsychotic drugs for acute schizophrenia

Antipsychotics for negative and positive symptoms of schizophrenia: dose-response meta-analysis of randomized controlled acute phase trials

Should we go up? Researchers performed a dose-response meta-analysis of randomized controlled trials in acute phase schizophrenia.

Antipsychotic Dose-Response in Acute Phase Schizophrenia

Developed in 1985 and approved by the US Food and Drug Administration in 2008, transcranial magnetic stimulation (TMS) technology has been gaining clinical interest as an effective treatment option for patients with treatment-resistant depression. Two-thirds of TMS patients experienced either full remission of their depression symptoms or noticeable improvements.

 TMS is a noninvasive outpatient procedure without serious adverse effects, making it an attractive option for patients who have not found relief from other treatments, including psychopharmacology and psychotherapy.

TMS uses an alternating current passed through a metal coil placed against the scalp to generate rapidly alternating magnetic fields. These pass through the skull nearly unimpeded and induce electric currents that depolarize neurons in a focal area of the surface cortex.

The magnetic field generated by TMS is comparable to that of a standard magnetic resonance imaging device (MRI), measured at approximately 1.5 to 3 Teslas. However, the TMS field is focal (beneath the coil), whereas the MRI field is large and fills the room housing the MRI device.

One hypothesis on how TMS works is that the stimulation of discrete cortical regions alters pathologic activity within a network of gray matter brain regions, specifically those involved in mood regulation and connected to the targeted cortical sites.

 Functional imaging studies support this hypothesis by showing TMS can change activity in brain regions remote from the site of stimulation.

TMS has many molecular effects comparable to electroconvulsive therapy (ECT), including increased monoamine turnover and normalization of the hypothalamic pituitary axis.

 However, unlike ECT, TMS does not require general anesthesia and is not associated with impaired cognition. Additionally, in one neuroimaging study of depressed patients, a prefrontal serotonin deficiency at baseline normalized after treatment with TMS.

High-frequency stimulation is thought to excite the targeted neurons and is typically used to activate the left prefrontal cortex. Low-frequency stimulation appears to inhibit cortical activity and is usually directed at the right prefrontal cortex.

Consistent with this hypothesis, a review examined 66 studies in patients with depression who were treated with TMS targeting the dorsolateral prefrontal cortex. It found that high-frequency TMS generally increased regional cerebral blood flow, whereas low-frequency TMS generally decreased regional cerebral blood flow, which is reduced in a depressed brain.

TMS is indicated for patients with unipolar major depression who have failed at least 1 antidepressant medication. In addition, TMS is indicated for patients who responded to a prior course of TMS.

 Its use for these patients is consistent with treatment guidelines from the American Psychiatric Association, Canadian Network for Mood and Anxiety Treatments, and the Royal Australian and New Zealand College of Psychiatrists.

The patient evaluation should confirm the primary diagnosis of treatment-resistant depression and determine whether the TMS intervention can be used safely. The assessment includes examinations of psychiatric history, general medical history, physical health, and mental status with emphasis upon depressive symptoms. This should emphasize risk factors for seizures and preexisting neurologic disease, such as epilepsy, intracranial masses, and vascular abnormalities.

TMS is contraindicated in patients with: increased risks for seizures, implanted metallic hardware (aneurysm clips, bullet fragments, etc), cochlear implants, implanted electrical devices (pacemakers, intracardiac lines, medication pumps, etc), and unstable general medical disorders. The 

 shares a 12-item questionnaire to determine if a patient is a good TMS candidate.

Multiple reviews have found consistent evidence that TMS provides a clinically relevant benefit to patients with treatment-resistant depression. In patients with acute major depression who have not responded to at least 1 antidepressant medication, numerous meta-analyses of randomized trials have found TMS superior to placebo treatment.

 It is not known if maintenance treatment with TMS for unipolar major depression is beneficial.

A meta-analysis of 34 randomized trials compared TMS with placebo treatment in 1383 patients with treatment-resistant major depression. It found that improvement was greater with active treatment.

 Add-on treatment with TMS was efficacious in patients who had not responded to an adequate antidepressant therapy. Response (for example, the reduction of baseline symptoms ≥ 50%) occurred in more patients who received active (47%) versus placebo (22%) TMS.

There have been no consistent predictors of response according to a meta-analysis. A 1-year, prospective observational study of 120 patients who responded or remitted with acute TMS found that the durability of response to TMS was not associated with age, sex, severity of depressive symptoms prior to TMS, nor the number of failed antidepressant trials prior to TMS.

For treatment of major depression, TMS is less efficacious than ECT. Follow-up studies of patients with major depression who were treated acutely with TMS in randomized trials indicate that the short-term benefits of TMS are stable.

 With regard to longer-term benefits of TMS, prospective, observational studies lasting at least 6 months suggest that in patients with major depression who improve with acute TMS, relapse occurs in about 35%.

For patients with unipolar major depression who improve with a course of TMS and subsequently deteriorate or relapse, reintroduction of TMS using the same stimulation parameters may be helpful.

 It is not known if maintenance treatment with TMS for unipolar major depression is beneficial, as few randomized trials using standard protocols have been conducted. However, in several small, observational studies of patients, the results suggest that maintenance TMS may, perhaps, be beneficial.

TMS is generally safe and well-tolerated. For example, in a randomized trial of 301 patients, investigators found that study discontinuation due to adverse effects was comparable for active and placebo TMS (5% and 3%, respectively).

The most serious adverse effect of TMS is a generalized tonic-clonic seizure. However, the risk of seizure appears to be comparable to that for anti-depressant medications. Seizures probably occur in less than 0.1 to 0.5% of patients when safety guidelines are followed regarding patient selection and stimulation parameters. Seizures that have occurred were self-limited, required no medications, and did not recur.

 Factors that increase the risk of seizures can be found in the 

Other effects include hypomania and mania, described in randomized trials

 and reports of patients with major depression (both unipolar and bipolar) who were treated with TMS.

However, the clinical significance is not known, because patients with bipolar major depression can switch to mood-elevated states in the absence of an antidepressant treatment. Treatment of unipolar major depression with TMS does not appear to increase suicidal ideation or behavior.

 A review of randomized trials in patients with major depression found that the incidence of headache with active treatment and placebo treatment was 28% and 16%, respectively. The incidence of scalp pain with active and placebo treatment was 39% and 15%, respectively. No migraine headaches have been reported. Headache and scalp pain may be more pronounced when higher stimulation frequencies and intensities are used. Topical lidocaine may reduce scalp pain. Reducing stimulation intensity can decrease scalp discomfort, but this can also reduce efficacy of treatment. For sensitive patients, the dose of TMS can be titrated up during the first week. Headache and scalp pain generally resolve over the first 2 weeks, although some patients may require an analgesic, such as acetaminophen or ibuprofen.

Transient (< 4 hours) increase in auditory threshold.

 This is caused by repeated clicks that are produced as current passes through the stimulating magnetic coil and mechanically deforms the coil. Hearing loss is prevented with foam earplugs or noise protection ear coverings.

 Management generally consists of reassurance.

For older patients with major depression, TMS can be beneficial if the stimulation intensity is sufficient.

 Prefrontal atrophy in older patients can increase the distance between the coil and cortex to the point that lower-intensity stimulation, which typically penetrates to a depth of 2 to 3 cm, does not affect cortical activity. Increasing the intensity above the motor threshold can overcome the added distance.

Depression frequently occurs after stroke, and TMS may help these patients.

 For these patients with major depression, observational studies suggest that TMS may possibly be safe and effective. It appears unlikely that the fetus is directly affected by TMS because magnetic fields rapidly attenuate with distance.

TMS is an exciting and promising therapy that can provide real and lasting relief for patients with treatment-resistant depression. Conducted in an outpatient setting, TMS is a noninvasive procedure that is generally safe and well-tolerated. This provides patients with the flexibility to seek treatment in a way that does not disrupt their daily lives. TMS has an equally promising future, with studies exploring its expanded applications, as well as its use as an ongoing maintenance treatment.

is a psychiatrist and regional medical director at

1. Carpenter LL, Janicak PG, Aaronson ST, et al. 

Transcranial magnetic stimulation (TMS) for major depression: a multisite, naturalistic, observational study of acute treatment outcomes in clinical practice

Neurobiological mechanisms of repetitive transcranial magnetic stimulation on the underlying neurocircuitry in unipolar depression

Regional cerebral blood flow changes after low-frequency transcranial magnetic stimulation of the right dorsolateral prefrontal cortex in treatment-resistant depression

4. Fitzgerald PB, Sritharan A, Daskalakis ZJ, et al. 

A functional magnetic resonance imaging study of the effects of low frequency right prefrontal transcranial magnetic stimulation in depression

Daily left prefrontal repetitive transcranial magnetic stimulation for acute treatment of medication-resistant depression

6. Noda Y, Silverstein WK, Barr MS, et al. 

Neurobiological mechanisms of repetitive transcranial magnetic stimulation of the dorsolateral prefrontal cortex in depression: a systematic review

7. Perera T, George MS, Grammer G, et al.

 The Clinical TMS Society consensus review and treatment recommendations for TMS therapy for major depressive disorder

Quantitative review of the efficacy of slow-frequency magnetic brain stimulation in major depressive disorder

9. Berlim MT, Van den Eynde F, Jeff Daskalakis Z. 

Clinically meaningful efficacy and acceptability of low-frequency repetitive transcranial magnetic stimulation (rTMS) for treating primary major depression: a meta-analysis of randomized, double-blind and sham-controlled trials

10. Berlim MT, Van den Eynde F, Daskalakis ZJ. 

A systematic review and meta-analysis on the efficacy and acceptability of bilateral repetitive transcranial magnetic stimulation (rTMS) for treating major depression

Transcranial magnetic stimulation in the management of mood disorders

Transcranial magnetic stimulation for the treatment of major depression

Antidepressant efficacy of high-frequency transcranial magnetic stimulation over the left dorsolateral prefrontal cortex in double-blind sham-controlled designs: a meta-analysis

14. Kedzior KK, Reitz SK, Azorina V, Loo C. 

Durability of the antidepressant effect of the high-frequency repetitive transcranial magnetic stimulation (rTMS) in the absence of maintenance treatment in major depression: a systematic review and meta-analysis of 16 double-blind, randomized, sham-controlled trials

15. Avery DH, Holtzheimer PE, Fawaz W, et al. 

A controlled study of repetitive transcranial magnetic stimulation in medication-resistant major depression

Repetitive transcranial magnetic stimulation as an augmentative strategy for treatment-resistant depression, a meta-analysis of randomized, double-blind and sham-controlled study

Treatment-emergent mania in unipolar and bipolar depression: focus on repetitive transcranial magnetic stimulation

18. Stultz DJ, Osburn S, Burns T, et al. 

Transcranial Magnetic Stimulation (TMS) safety with respect to seizures: a literature review

19. Dolberg OT, Schreiber S, Grunhaus L. 

Transcranial magnetic stimulation-induced switch into mania: a report of two cases

Acute manic symptomatology during repetitive transcranial magnetic stimulation in a patient with bipolar depression

21. Abdelnaim MA, Langguth B, Deppe M, et al. 

Anti-suicidal efficacy of repetitive transcranial magnetic stimulation in depressive patients: a retrospective analysis of a large sample

22. O’Reardon JP, Solvason HB, Janicak PG, et al. 

Efficacy and safety of transcranial magnetic stimulation in the acute treatment of major depression: a multisite randomized controlled trial

23. Rossi S, Hallett M, Rossini PM, et al. 

Safety, ethical considerations, and application guidelines for the use of transcranial magnetic stimulation in clinical practice and research

Pascual-Leone A. Screening questionnaire TMS: an update

How can transcranial magnetic stimulation help patients with treatment-resistant depression?

TMS: A Useful Clinical Tool for Treatment-Resistant Depression

 is not a disease, but rather a variation of normal human experience. This view arguably originated with the writings of the 1960s antipsychiatrist R.D. Laing and is now echoed by some within the existential, sociological, and psychological communities. For instance, a recent report published by the British Psychological Society

 suggests that schizophrenia is not an illness. This view has obvious implications for psychiatric patients and for the discipline of psychiatry itself. I wish here to provide a brief refutation of this notion and an examination of schizophrenia as a pathology that differs in kind from normal human experience.

It has been known for more than a century that psychotic symptoms are widely distributed among the general population.

 One European study showed that roughly 25% of people experience hypnopompic hallucinations (those occurring at sleep onset), and about 7% experience hypnagogic hallucinations (those occurring upon waking), with about half of these psychotic symptoms being associated with specific pathologies.

 Similarly, transient paranoid experiences may result under extreme stress and are also commonly found in nonpsychotic psychiatric disorders, such as the borderline personality. Those writing from a trauma-informed perspective have noted that individuals who have endured abuse and other traumas are more prone to psychotic disturbance.

For these and other reasons, it has been alleged that schizophrenia exists on the same continuum as these nonpathological or nonschizophrenic experiences and represents a difference only of degree, not of kind. From this perspective, schizophrenia is viewed not as a disease, but as an extreme variation of normality. Those associated with the anti- or critical psychiatry movement go on to assert that antipsychotic treatment and even psychotherapies aimed at treating schizophrenia are misguided at best, and abuses at worst; to these authors, there can be no treatment for a disease that “does not exist.”

It must be clarified at this point that schizophrenia as a single, unitary disease has been disputed since the age of Bleuler,

[emphasis added].” It is now generally accepted that what we call schizophrenia is likely a grouping of many different disease processes, perhaps upwards of 200. But this heterogeneity does not repudiate the pathological nature of the human conditions we now refer to as “schizophrenia.”

Quantity of Symptoms and Qualitatively Different Nature

All differences that occur in nature are essentially quantitative ones, but it is the difference in quantity that produces the qualitative or categorical difference. A normal person may experience hypnagogic or hypnopompic hallucinations; an anxious individual may believe that their boss is talking behind their back, or a jealous spouse may have a fit of paranoid rage. But as long as these experiences are quantitatively so minimal that the individual can keep them in check (ie, the experiences do not produce any impairment), then we do not consider them schizophrenia.

 of the symptoms reaches a certain level—when the symptoms gain the upper hand, creating dysfunction and impairment in the individual’s life, and when, as the late psychiatrist Silvano Arieti, MD, so aptly put it, “the way of living of the patient expresses itself not in contrast to, but in accordance with, the symptoms”

Thus, at different quantitative levels, we have such dramatic changes in the experience of the symptoms, their persistence, and the degree of impairment caused by them that the total picture (schizophrenia) acquires a truly qualitatively different nature and is ruled by different mechanisms. Hypertension remains pathological despite the fact that all living persons have a blood pressure; likewise, schizophrenia remains pathological despite the fact that all persons have a mind that, at times, may be prone to transient psychotic aberrations.

This basic misunderstanding of the relationship between quantitative and qualitative differences—ie, that the quantity or degree of symptoms can transform the entire picture from a normal to a pathological one—forms the basis of much of the confusion regarding the nature of schizophrenia and psychiatric disorder in general. The same faulty argument has been made against the conceptualization of depression as a pathology: Because all human beings experience periods of sadness, it is alleged that depression is not a disorder.

Yet, anyone who has ever treated, or even interacted at length with, a person with schizophrenia or severe depression knows that these conditions differ in significant ways from ordinary human experience. The patient with schizophrenia cannot be convinced of the irrationality of his or her delusional beliefs, and the melancholic cannot be willed into a state of happiness or joy. The degree of impairment caused by these symptoms has produced a state that is governed by a different set of rules; the condition takes on a life of its own,so that it is so qualitatively different from normal mental functioning as to be unrecognizable to those who have not observed the situation in others before. This is the very essence of pathological states.

This point also underscores the fact that disease is most accurately defined as a state that characteristically produces some combination of suffering and dysfunction, regardless of whether it is associated with any known or putative biological abnormality. That is to say that schizophrenia exists as a disease entity despite the fact that there remain no biological tests for it, because the quantity of its symptoms produces a state that differs qualitatively from normal. Indeed, schizophrenia will remain indefinitely classified as a disease even if no biological cause or causes are ever discovered for it.

 note, “The lack of a universally clear boundary between the normal and abnormal does not mean that the concept of discrete illness becomes invalid.”

Despite the obfuscations of those who deny the pathological nature of schizophrenia, many of whom are driven by antipsychiatry motives, schizophrenia can rightly be considered a disease in so far as it represents a state that differs in kind from normal human mental life.

 is Instructor of Psychiatry at the University of Central Florida College of Medicine in Orlando, FL, and Adjunct Instructor of Psychiatry at Tufts University School of Medicine in Boston, MA. He is a psychoanalytic psychotherapist in private practice in Tampa, FL.

Understanding psychosis and schizophrenia

Dementia Praecox or the Group of Schizophrenias.

Prevalence of hallucinations and their pathological associations in the general population

Trauma and psychosis: an analysis of the National Comorbidity Survey

Schizophrenia: the sacred symbol of psychiatry

Recent conceptions and misconceptions of schizophrenia

On myths and countermyths: more on Szaszian fallacies

Letter to the editor: schizophrenia does not represent the extreme of a normally distributed trait

How does schizophrenia as a pathology differ from normal human experience?

Schizophrenia: A Difference of Kind

Roger S. McIntyre, MD, FRCPC, of the University of Toronto and the University Health Network presented on inflammation in individuals with mood disorders at the 2021 Neuroscience Education Institute (NEI) Congress Friday, November 5, in Colorado Springs, Colorado.

In his presentation, titled “Inflamed in the Brain: The Role of Inflammation in Psychiatry,” McIntyre discussed the physiology of the inflammatory system and how inflammation correlates in individuals with mood disorders, as well as some common anti-inflammatory interventions for these individuals. He stated that there is a high prevalence of inflammation in individuals with mood disorders such as depression and bipolar disorder: About 25% to 30% of individuals with major depressive disorder (MDD) or bipolar disorder have a CRP of higher than 3 mg per liter, and 50% have a CRP of higher than 1. Using COVID-19 as an example, he reported that individuals with MDD or bipolar disorder were more likely to contract, be hospitalized, and die due to COVID-19. Further, one-third of outpatients and one-half of inpatients with COVID-19 have since developed a neurologic or psychiatric disorder.

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