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BackgroundClinical assessment of catatonia includes the use of diagnostic systems, like the Diagnostic and Statistical Manual 5 (DSM-5) and International Classification of Disease Manual 10 (ICD-10), or screening tools such as the Bush Francis Screening Instrument (BFCSI)/Bush Francis Catatonia Rating Scale (BFCRS) and Braunig’s Catatonia Rating Scale. In this study, we describe the inter-rater reliability (IRR), utilizing the BFCSI, BFCRS and DSM-5 to screen for catatonia. MethodData from 10 participants recruited as part of a larger prevalence study were used to determine IRR by five assessors after they were trained in the application of the 14-item BFCSI, 23-item BFCRS and DSM-5 to assess catatonia in new admissions. Krippendorff α was used to compute the IRR, and Spearman’s correlation was used to determine concordance between screening tools. The study was performed at a 35-bed acute mental health unit in Dora Nginza Hospital, Nelson Mandela Bay Metro. Participants were mostly involuntary admissions under the Mental Health Care Act of 2002 and between the ages of 13 and 65 years and older.ResultsThe majority (8, 80%) were 35 years or less and males (8, 80%). At least six (60%) of the ten participants were found to have catatonia based on the BFCSI/BFCRS and DSM-5 criteria.The BFCRS (complete 23-item scale) had the greatest level of inter-rater agreement with an α=0.798, while the DSM-5 had the lowest level of inter-rater agreement with an α=0.565. The highest correlation coefficients were observed between the BFCRS and BFCSI.ConclusionThe BFCSI and BFCRS were found to be sensitive tools for screening for catatonia with high IRR and high correlation coefficients, while the DSM 5 showed some deficiencies in screening for catatonia with low IRR and lowest correlation with the other two tools.

Catatonia is a psychomotor abnormality caused by neurological, medical or severe psychiatric disorders and substances. Its prevalence ranges from less than 10% to just above 60%. Diagnosis may be influenced by the screening tools used. Screening of new admissions to a mental health unit for catatonia was undertaken using three instruments to determine prevalence of catatonia. Participants ranged from age 16 years and over. Recruitment took place from September 2020 to August 2021. The setting was a mental health unit within a general hospital in Nelson Mandela Metro, South Africa. Five assessors were trained by the principal investigator to apply the Bush Francis Screening Instrument (BFCSI), the Bush Francis Catatonia Rating Scale (BFCRS), and the Diagnostic and Statistical Manual 5 (DSM-5), to assess participants. Clinical and demographic data were collected using a specially designed datasheet. Data analysis was performed to identify significant associations between presence or absence of catatonia and clinical and demographic data. Up to 241 participants were screened and 44 (18.3%) had catatonia. All 44 cases were identified through the BFCSI while the DSM-5 identified only 16 (6.6%%) of the 44 cases even though the remaining 28 (63.6%) participants still required treatment for catatonic symptoms. The DSM-5 diagnostic criteria excluded staring, which was the commonest sign of catatonia identified through the BFCSI [n = 33 (75%)]. Close to half (21; 47.7%) of those with catatonia on the BFCSI had schizophrenia. The rest had bipolar disorder (12; 27.3%), substance-induced psychotic disorder (7; 15.9%) and no specified diagnosis in one (1; 2.6%). The BFCSI was very effective at identifying catatonia while the DSM-5 was inadequate, missing close to 64% (28 of 44) of cases. Predictors of catatonia in this sample were a younger age and being male. A prevalence of 18.3%, indicates that assessment for catatonia should be routinely conducted in this and similar settings.

Background Clinical assessment of catatonia includes the use of diagnostic systems, such as the Diagnostic and Statistical Manual, Fifth Edition (DSM-5) and the International Classification of Disease, Tenth Revision (ICD-10), or screening tools such as the Bush Francis Catatonia Screening Instrument (BFCSI)/Bush Francis Catatonia Rating Scale (BFCRS) and the Braunig Catatonia Rating Scale. In this study, we describe the inter-rater reliability (IRR), utilizing the BFCSI, BFCRS, and DSM-5 to screen for catatonia. Methods Data from 10 participants recruited as part of a larger prevalence study (of 135 participants) were used to determine the IRR by five assessors after they were trained in the application of the 14-item BFCSI, 23-item BFCRS, and DSM-5 to assess catatonia in new admissions. Krippendorff’s α was used to compute the IRR, and Spearman’s correlation was used to determine the concordance between screening tools. The study site was a 35-bed acute mental health unit in Dora Nginza Hospital, Nelson Mandela Bay Metro. Participants were mostly involuntary admissions under the Mental Health Care Act of 2002 and between the ages of 13 and 65 years. Results Of the 135 participants, 16 (11.9%) had catatonia. The majority (92 [68.1%]) were between 16 and 35 years old, with 126 (93.3%) of them being Black and 89 (66.4%) being male. The BFCRS (complete 23-item scale) had the greatest level of inter-rater agreement with α = 0.798, while the DSM-5 had the lowest level of inter-rater agreement with α = 0.565. The highest correlation coefficients were observed between the BFCRS and the BFCSI. Conclusion The prevalence rate of catatonia was 11.9%, with the BFCSI and BFCRS showing the highest pick-up rate and a high IRR with high correlation coefficients, while the DSM-5 had deficiencies in screening for catatonia with low IRR and the lowest correlation with the other two tools.

Critics of electroconvulsive therapy argue that the treatment's efficacy is unproven by random controlled trial comparisons with sham treatments. Their reviews fail to consider sham and random controlled trial studies completed in 1950s, the data republished here.

IntroductionCatatonia arises from serious mental, medical, neurological or toxic conditions. The prevalence range depends on the setting and the range is anything from 7% to 63% in other countries. South African prevalence rates are currently unknown. The proposed study is a quantitative descriptive study using the Bush Francis Catatonia Screening Instrument as a screening tool with a data capturing information sheet to extract clinical information from patient folders. The study will investigate: (1) prevalence of catatonia, (2) clinical and demographic correlates associated with catatonia, (3) predictors of catatonia, (4) response to treatment and (5) subjective experience of catatonia.Methods and analysisThe setting is an acute mental health unit (MHU) within a regional, general medical hospital in Nelson Mandela Bay, South Africa, which accepts referrals from within the hospital and from outlying clinics. Participants will be recruited from inpatients in the MHU from beginning of September 2020 to end of August 2021. Most admissions are involuntarily, under the Mental Health Care Act of 2002 with an age range of 13 to over 65 years. Participants who screen positive for catatonia will be followed up after discharge for 3 months to measure outcomes. Primary outcomes will include the 12-month prevalence rate of catatonia, descriptive and other data on presentation and assessment of catatonia in the MHU. Secondary outcomes will include data on treatment response, participants’ report of their subjective experience of catatonia and predictors of catatonia. Descriptive statistics, multivariate binomial logistic regression and univariate analyses will be conducted to evaluate associations between catatonia and clinical or demographic data which could be predictors of catatonia. Survival analysis will be used to examine the time to recovery after diagnosis and initiation of treatment. The 95% CI will be used to demonstrate the precision of estimates. The level of significance will be p≤0.05.Ethics and disseminationThe study has received ethical approval from the Research and Ethics Committees of the Eastern Cape Department of Health, Walter Sisulu University and Nelson Mandela University. The results will be disseminated as follows: at various presentations and feedback sessions; as part of a PhD thesis in Psychology at Nelson Mandela University; and in a manuscript that will be submitted to a peer-reviewed journal.

Catatonia is a motor and mood disorder of behavior increasingly recognized in systemic medically ill. Neuroleptic malignant syndrome, delirious mania, self injurious behaviors in autism, and limbic encephalitis are conditions in which ECT-responsive catatonia is increasingly recognized and effectively treated.

For more than a century, catatonia has been considered a marker of the Kraepelin/Bleuler concept of schizophrenia. However, over the past half-century, it has been increasingly recognized as a separate entity, independently diagnosable and treatable. This chapter explores the diagnosis, treatment, and biological underpinnings of catatonia. Initially, it lists certain motor behaviours whose presentation might indicate catatonia, according to the Catatonia Rating Scale (CRS) such as mutism, delirium, and repetitive rhythmic acts. Through the intravenous administration of certain drugs, such as benzodiazepines, barbiturates, or gamma-aminobutyric acid (GABA) agonists, the effect on the patient’s CRS score is used to confirm the diagnosis. The treatment history of catatonia prior to the discovery of the efficacy of benzodiazepines and induced grand mal seizures (electroconvulsive therapy) is broached, such as chemically induced seizures and amobarbital. Finally, its different presentations are discussed, along with its consideration as a biological fear response.

Objective To examine the psychological substrate of catatonia. Method Reviewing the historical descriptions and explanations of catatonic behaviours by clinicians from its delineation in the 19th century to the present. Results Patients with catatonia are often haunted by fears and terrors; this has not been widely appreciated, and certainly was lost from view in the days when catatonia was considered a subtype of schizophrenia. The report contributes to resolving a major question in catatonia: is the mind in stupor inactive, as the blank state that we picture in anesthetized patients, or is the mind active, so preoccupied as to exclude all other influences. The main finding Persistent fear occupies the mind of catatonic patients. Conclusion The signs of catatonia are adaptations to persistent fear, akin to tonic immobilization. The relief afforded by sedation supports this interpretation.

Inducing grand mal seizures (electroshock, electroconvulsive therapy) developed as an effective treatment to alleviate the psychosis of dementia praecox. Clinicians quickly recognized that seizures also relieved depressed moods, suicide risk, catatonia, manic excitement, and delirium. It is an unheralded, often stigmatized, medical achievement. Seizures may be induced chemically or with electric or magnetic currents. Grand mal seizures must be repeated for persistent benefits. Not all seizures are equally effective. Effective seizures are marked by bilateral electroencephalographic brain wave changes and neuroendocrine discharges from hypothalamic-pituitary glands. Treatments are remarkably safe, with zero mortality. Immediate effects on memory are common but are almost always transient. They are not a practical deterrent to the treatments, although they are widely cited to reject its use. The stigmatization of induced seizures that places it as a “last resort” therapy is wasteful and unethical. It offers a remarkable opportunity for advancement in neuroscience. This review contains 4 figures, 3 tables, and 90 references. Key words: anesthesia, bipolar disorder, catatonia, delirium, electroconvulsive therapy, electroencephalography, major depression, melancholia, neuroendocrine, seizures

The W.H.O. Expert Committee on Drug Dependence lists more than 100 compounds under international narcotics control, presumably as drugs with high dependence liability in man. Many of the compounds studied by the methods are defined as drugs of dependence, and it is the purpose of this report to summarize these data, to classify the electroencephalogram (EEG) events in man, and to attempt a justification of ‘dependence’ in EEG terms. For drugs of dependence, particularly those with high abuse potential, the central effects following their injection, ingestion, or inhalation are rapid in onset and usually short in duration. It is characteristic of the use of dependence-producing drugs that the most rapid introduction is preferred—inhalation and intravenous administration being preferred to oral, intramuscular, or subcutaneous routes. Lysergide, mescaline, amphetamine, meth-amphetamine, and cocaine are hallucinogens with similar central and behavioral effects. Drugs of dependence are of diverse structure and origin, with few behavioral effects in common.

The symptoms of catatonia—stupor, staring, mutism, food refusal, grimacing, negativism, odd movements, rigidity, posturing, “waxy flexibility,” and stereotypies—have always existed. But they were described under different terms, such as catalepsy, acute delirium, hysteria, and “homesickness” and were not linked together as part of the same disorder. People once had a terrible fear of being buried alive, for example, dreading that stuporous catatonia might be misrecognized as death. Yet what people considered “demonic possession” has almost always been viewed in medicine as a group of legitimate illnesses—different illnesses with different treatments, such as catalepsy, ecstasy, stupor, tics, chorea, and melancholia.

Reports of fatal febrile, hypertensive, tachycardic neurotoxic cases followed quickly on the introduction of potent new neuroleptic drugs in the 1970s. Patients became mute, rigid, posturing, and staring, showing the signs of catatonia. Labeled the neuroleptic malignant syndrome (NMS), attention was first given to neuroleptic blockade of dopamine receptors as the cause, but treatments with dopamine agonists (bromocriptine) and muscle relaxants (dantrolene) offered little benefit. When catatonia was recognized, treatments with benzodiazepines (lorazepam, diazepam) and induced seizures (electroshock, ECT) led to clinical relief and the saving of lives. The recognition of NMS as catatonia stimulated a revision of the century-long view of catatonia as a form of schizophrenia, with calls for catatonia to be considered independent of schizophrenia.

Eugen Bleuler, professor of psychiatry in Zurich, renamed Kraepelin’s dementia praecox as “schizophrenia” in 1908. He retained catatonia as a subtype. Bleuler’s dementia praecox was a much milder and broader condition than the downhill course toward dementia that Kraepelin had described: it could strike at any moment in life, not just in youth, and often ended in partial recovery. Ultimately, Kraepelin’s and Bleuler’s efforts gave rise to an immense “schizophrenia” literature, an industry that continues today, an outpouring that can be compared only to the enormous “hysteria” industry that existed before DSM-III abolished the diagnosis in 1980. The effect is striking: one moment the profession believes implicitly in a disease so huge as to dominate the literature; the next moment the disease no longer exists.

For the many varieties of catatonia, all medical ministrations were applied with little success until sodium Amytal (amobarbital) was shown to be specifically successful beginning in the 1930s. Induced seizures as treatments for psychoses in 1930s were also found to effectively relieve catatonia. These treatments were so successful, and the incidence of catatonia so reduced, that questions were raised whether and why catatonia had disappeared. By 1980s, the benzodiazepines were offered as replacements for barbiturates. The specificity of benzodiazepines in relieving up to 80 percent of catatonia cases, with ECT successful in the remainder, encouraged belief that catatonia was best seen as a unique systemic medical illness. Solving the puzzle of catatonia is one of medicine’s unheralded treatment triumphs.

The long history of catatonia is presently resolved into a systemic syndrome, identified by symptoms and signs, verified by tests, and fully resolved by defined means. Our skills in relieving catatonia are as successful as our treatment for neurosyphilis. Catatonia is best seen as a systemic medical, not a psychiatric disorder. Unresolved fear is a core feature in its pathophysiology. There are difficulties distinguishing catatonia from melancholia; the prompt resolution of both with induced seizures presents a challenge in understanding them. Are they related? Melancholia’s neuroendocrine abnormalities offer direction to neuroscience studies of catatonia and of the mechanism of electroconvulsive therapy (ECT).

For almost a century, catatonia was considered only as a sign of schizophrenia and cases were classified as “schizophrenia, catatonic type,” as in DSM-III in 1980. Awareness that catatonia was an identifiable syndrome independent of schizophrenia and treatable with approaches not effective in relieving schizophrenia led to the development of rating scales to identify catatonia, benzodiazepine challenge tests to verify the diagnosis, and efficient protocols to successfully treat the syndrome. By 1994, in DSM-IV, catatonia was also identified as a syndrome secondary to a medical condition and assigned a unique identification number. By 2013, in DSM-5, the class of catatonic schizophrenia was deleted, and catatonia was recognized as an identifiable, verifiable, and treatable behavior syndrome.

Initially, the stuporous, excited (delirious mania), and febrile neurotoxic forms (neuroleptic malignant syndrome) of catatonia were recognized as distinctive. As catatonia became systematically defined by symptoms identified in lists of symptom rating scales, verified by benzodiazepine challenge tests, and validated by responses to treatments by benzodiazepines (lorazepam, diazepam) and electroconvulsive therapy (ECT), other syndromes met these criteria—anti-NMDAR encephalitis, self-injurious behavior (SIB), selective mutism, pervasive refusal syndrome, and akinetic mutism, among others. Such classification brought these syndromes within the catatonia variants, relieved by catatonia treatments. Such identification is feasible when clinicians consider the medical (Sydenham) model of diagnosis, the process of identification by symptoms, verification by objective tests, and validation by response to specific treatments.

Emil Kraepelin, professor of psychiatry first in Heidelberg then Munich, originated modern psychiatric diagnosis. So it was a fateful error when, in 1899, Kraepelin made catatonia a “subtype” of schizophrenia (which Kraepelin called “dementia praecox”). He did so on the basis of what Kraepelin considered a downhill course and outcome. Catatonia thus disappeared into the schizophrenia tent and ceased to be an independent disease entity. There it remained for the next century. It was because of Kraepelin’s immense prestige that his disease classification has survived virtually until the present. Kraepelin thus saved catatonia from extinction as a diagnosis, but at the cost of ensuring that it would be diagnosed only in “schizophrenics.” Clinicians who did not think their patients had schizophrenia would miss the catatonia diagnosis.

This is the first history of the psychiatric illness called catatonia, virtually forgotten by medicine yet often present in severely ill patients. The main symptoms of catatonia affect movement and thought, including staring, stupor, mutism, food refusal, negativism, and even psychosis. These symptoms are age-old, but they were brought together in the single term “catatonia” by German psychiatrist Karl Kahlbaum in 1874. Yet, 30 years later, catatonia disappeared from view as an independent illness, turned into a “subtype” of dementia praecox (schizophrenia). There, catatonia remained submerged from view for almost a century, rediscovered again as a disease of its own in the 1990s. Today, catatonic symptoms are seen in around one in ten admissions to a psychiatric emergency department. Untreated, catatonia may have a fatal outcome. Interest today has been increasing because of the discovery that, unlike schizophrenia, catatonia responds readily to therapy, with the symptoms vanishing without a trace. The authors argue that catatonia may be a response to fear and alarm triggered by trauma; during a stupor, patients often experience terrifying images and thoughts. Edward Shorter is a medical historian who has written widely about psychiatry. Max Fink is a clinician whose writings on melancholia, catatonia, and convulsive therapy have been internationally recognized.

Catatonia is a syndrome that is identifiable, verifiable, and eminently treatable, unlike other disorders in the roster of psychiatric diseases. Catatonia is not a form of “schizophrenia,” and, although it may “piggyback” on other diseases, it is also a disease in its own right. Today, catatonia is often not recognized; clinicians and the public are more familiar with the term as a subtype of “schizophrenia.” Failure to diagnose it is very common. This introduction documents the earliest descriptions of the disorder and its treatment and gives a brief history of the acceptance of the term “catatonia” by the psychiatric discipline. The authors emphasize the importance of recognizing the symptoms of catatonia and appreciating how straightforward its treatment is. Proper recognition is important because catatonia may be life-threatening, so diagnosing and treating it properly are matters of importance.

In a debate about a possible psychology of catatonia, those who argued that patients’ minds were blank during stupor vied against those who saw that stuporous patients were filled with fear and apprehension. The latter won out. It became clear that sometimes a fearful or traumatic event itself sufficed to trigger catatonia. The “blank slate” school were led by Karl Kleist in Frankfurt and a group of German neurologists. Karl Leonhard, an acolyte of this school, authored an elaborate classification of catatonia. The “fear and apprehension school” were led by a number of psychologically minded psychiatrists in Germany and France. A wide international variety of clinical observations confirm the role of fear, including the formation of catatonic symptoms in people experiencing extreme stress.

The acute onset of excited, aggressive, and destructive states, often febrile, described as Bell’s mania and Stauder’s delirium are hallmarks in the literature. Death is frequent. Subjects are disoriented, and delirious with catatonia signs of mutism, posturing, and repetitive speech. Treatments were ineffective until multiple daily induced seizures (ECT) were shown to be life-saving. A syndrome of nostalgia was also described in French and German armies among subjects pining to death. Delirious mania and its fatal variants were a rock-solid part of traditional psychiatric diagnosis. By the 1960s, almost everywhere in the UK and Europe, fatal delirious mania or pernicious catatonia was an accepted part of psychiatric diagnostics that a clinician would ignore at the patient’s peril.

Even as researchers became aware that the neuroleptic drug–induced neurotoxic syndrome was best treated as catatonia, signs of catatonia were found more often among depressed and manic populations than among the schizophrenic. Catatonia as a sign of schizophrenia was challenged, with calls for catatonia to be recognized as a systemic independent syndrome. In 1987, James Lohr and Alexander Wisniewski laid a heavy thumb on the independent-disease side of the scales in a book, citing evidence that catatonia represents a distinct entity, but that it should be diagnosed on the basis of motor signs alone. These challenges questioned the connection of catatonia to schizophrenia. The increasing reports of deaths as a consequence of treating catatonia with potent neuroleptics stimulated interest in effective treatments and forced the separation of catatonia from schizophrenia.

In 1874, Karl Kahlbaum, a German psychiatrist in an obscure private hospital, pulled various symptom pictures together into a single diagnosis: “catatonia.” Kahlbaum had earlier pioneered the modern classification of illness with his concepts of course and outcome as demarcating the various disease entities. He thought that, similar to neurosyphilis, catatonia had a common cause and common clinical course but, unlike neurosyphilis, often a relatively benign outcome. He believed the illness progressed in fixed stages. At the same time, Kahlbaum’s associate, Ewald Hecker, described madness in young people (“hebephrenia”), which became the forbearer of “schizophrenia.” Kahlbaum’s ideas were not immediately accepted: there was a core of true believers, but many psychiatrists in the Atlantic community did not readily take up the diagnosis and remained skeptical that Kahlbaum had done anything other than repackage familiar symptoms in a new and unfamiliar box.

Catatonia remained a subtype of schizophrenia for the next hundred years because a “Praetorian guard” around Kraepelin relentlessly flacked their teacher’s diagnoses. There was, to be sure, some initial support for Kahlbaum’s diagnosis as a separate entity, yet Kraepelin’s “textbook,” in its various editions, carried the day. Psychosis became the hallmark of schizophrenia, and catatonic patients who became psychotic simply had their diagnoses changed. In a world dominated by “schizophrenia,” catatonia was only of nodding interest. By the end of the Second World War, the term “schizophrenia” had lost whatever specificity it might once have possessed, and catatonia in schizophrenia had shed its distinctiveness as a treatable motor syndrome.

Self-injurious behaviour (SIB) is a devastating condition frequently encountered in autism spectrum disorders (ASDs) that can lead to dangerous tissue injury and profound psychosocial difficulty. An increasing number of reports over the past decade have demonstrated the swift and well tolerated resolution of intractable SIB with electroconvulsive therapy (ECT) when psychopharmacological and behavioural interventions are ineffective. The current article provides a review of the salient literature, including the conceptualization of repetitive self-injury along the catatonia spectrum, and further clarifies the critical distinction between ECT and contingent electric shock.We searched electronically for literature regarding ECT for self-injurious behaviour from 1982 to present, as the first known report was published in 1982. Eleven reports were identified that presented ECT in the resolution of self-injury in autistic or intellectually disabled patients, and another five reports discussed such in typically developing individuals. These reports and related literature present such self-injury along the spectrum of agitated catatonia, with subsequent implications for ECT.Intractable self-injury remains a significant challenge in ASDs, especially when patients do not respond adequately to behavioural and psychopharmacological interventions. ECT is well tolerated and efficacious treatment for catatonia, and can confer marked reduction in SIB along the agitated catatonia spectrum.

Background Camphor-induced and pentylenetetrazol-induced brain seizures were first used to relieve psychiatric illnesses in 1934. Electrical inductions (electroconvulsive therapy, ECT) followed in 1938. These were easier and less expensive to administer and quickly became the main treatment method. In 1957, seizure induction with the inhalant anesthetic flurothyl was tested and found to be clinically effective.For many decades, complaints of memory loss have stigmatized and inhibited ECT use. Many variations of electricity in form, electrode placement, dosing, and stimulation method offered some relief, but complaints still limit its use. Methods The experience with chemical inductions of seizures was reviewed based on searches for reports of each agent in Medline and in the archival files of original studies by the early investigators. Findings Camphor injections were inefficient and were rapidly replaced by pentylenetetrazol. These were effective but difficult to administer. Flurothyl inhalation-induced seizures were as clinically effective as electrical inductions with lesser effects on memory functions. Flurothyl inductions were discarded because of the persistence of the ethereal aroma and the fears induced in the professional staff that they might seize. Conclusions Persistent complaints of memory loss plague electricity induced seizures. Flurothyl induced seizures are clinically as effective without the memory effects associated with electricity. Reexamination of seizure inductions using flurothyl in modern anesthesia facilities is encouraged to relieve medication-resistant patients with mood disorders and catatonia.

Suicide is a leading cause of death among psychiatric patients, and a leading cause of death from all causes in people younger than 30 years. The rapid relief of severe depression, mania, and psychosis by electroconvulsive therapy (ECT) is accompanied by the rapid reduction in suicide drive. Electroconvulsive therapy use is, however, inhibited by fear of electricity, unreasoned prejudice, legislative restrictions, and the limited availability of trained professionals and adequate facilities. This review assesses the experience with ECT in persons with suicide risk and recommends the consideration of ECT in treatment algorithms to reduce suicide rates.

Objective Catatonia, a disorder of movement and mood, was described and named in 1874. Other observers quickly made the same recognition. By the turn of the century, however, catatonia was incorporated as a type within a conjured syndrome of schizophrenia. There, catatonia has lain in the psychiatric classification for more than a century. Method We review the history of catatonia and its present status. In the 1970s, the tie was questioned when catatonia was recognized among those with mood disorders. The recognition of catatonia within the neuroleptic malignant syndrome offered effective treatments of high doses of benzodiazepines and electroconvulsive therapy (ECT), again questioning the tie. A verifying test for catatonia (the lorazepam sedation test) was developed. Soon the syndromes of delirious mania, toxic serotonin syndrome, and the repetitive behaviors in adolescents with autism were recognized as treatable variations of catatonia. Results Ongoing studies now recognize catatonia among patients labeled as suffering from the Gilles de la Tourette's syndrome, anti-NMDAR encephalitis, obsessive–compulsive disease, and various mutisms. Conclusion Applying the treatments for catatonia to patients with these syndromes offers opportunities for clinical relief. Catatonia is a recognizable and effectively treatable neuropsychiatric syndrome. It has many faces. It warrants recognition outside schizophrenia in the psychiatric disease classification.

For more than 50 years, research in convulsive therapy has been focused on the impact of electricity and seizures on memory and not on brain chemistry or neurophysiology. Brief pulse and ultra-brief pulse currents replaced sinusoidal currents. Electrode placements were varied, energy dosing was altered, and electricity was replaced by magnetic currents.The published experiences and archival records of seizures induced by camphor, pentylenetetrazol, and flurothyl are reviewed and compared with the changes induced by electricity.The clinical efficacy of chemically induced seizures is equal to that of electrical inductions. Seizure durations are longer, and impairment of cognition and memory is less. Electroconvulsive therapy replaced chemical treatments for ease of use, not for greater efficacy or safety.The brain seizure, not the method of induction, is the essential element in the efficacy of convulsive therapy. Seizure induction with chemicals avoids the direct effects of electricity on brain functions with lesser effects on cognition. Reexamination of chemical inductions of seizures as replacements for electricity is encouraged.

To the electrophysiologist accustomed, in his animal experiments, to probing with his electrode into the nervous system and even into the nerve cell itself, it remains a matter of astonishment that so many of the brain's secrets escape across the wall of the skull to electrodes fixed to the scalp of man. That they indeed do so is testimony to the fact that the brain's electrical activity is a most sensitive indicator of its function. In this fact lies the attraction of electroencephalography for its devotees.

Objective We sought to examine the relationship of seizure threshold (ST) to age and other demographic characteristics in a large sample where ST was determined by the dose titration (DT) method. We also compared the resulting stimulation levels to estimates predicted by an age-based formula, the half-age (HA) method.

Bailine S, Fink M, Knapp R, Petrides G, Husain MM, Rasmussen K, Sampson S, Mueller M, McClintock SM, Tobias KG, Kellner CH. Electroconvulsive therapy is equally effective in unipolar and bipolar depression. Objective: To determine the relative efficacy of electroconvulsive therapy (ECT) in the treatment of bipolar (BP) and unipolar (UP) depressive illness and clarify its role in BP depression. Method: Patients referred for ECT with both UP and BP depressions. [classified by Structured Clinical Interview for DSM (SCID-I) criteria for history of mania] were included in a multi-site collaborative, double-masked, randomized controlled trial of three electrode placements – right unilateral, bifrontal or bitemporal – in a permutated block randomization scheme. Results: Of 220 patients, 170 patients (77.3%) were classified as UP and 50 (22.7%) as BP depression in the intent-to-treat sample. The remission and response rates and numbers of ECT for both groups were equivalent. Conclusion: Both UP and BP depressions remit with ECT. Polarity is not a factor in the response rate. In this sample ECT did not precipitate mania in depressed patients. Treatment algorithms for UP and BP depression warrant re-evaluation.

Catatonia is a motor dysregulation syndrome described by Karl Kahlbaum in 1874. He understood catatonia as a disease of its own. Others quickly recognized it among diverse disorders, but Emil Kraepelin made it a linchpin of his concept of dementia praecox. Eugen Bleuler endorsed this singular association. During the 20th century, catatonia has been considered a type of schizophrenia. In the 1970s, American authors identified catatonia in patients with mania and depression, as a toxic response, and in general medical and neurologic illnesses. It was only occasionally found in patients with schizophrenia. When looked for, catatonia is found in 10% or more of acute psychiatric admissions. It is readily diagnosable, verifiable by a lorazepam challenge test, and rapidly treatable. Even in its most lethal forms, it responds to high doses of lorazepam or to electroconvulsive therapy. These treatments are not accepted for patients with schizophrenia. Prompt recognition and treatment saves lives. It is time to place catatonia into its own home in the psychiatric classification.