Catatonia: Definition, Causes, Signs, Symptoms, Diagnosis, Treatment and Prognosis

It is a state of psychomotor immobility and behavioral abnormality manifested by stupor.

It was first described in 1874 by Karl Ludwig Kahlbaum, in German: Die Katatonie oder das Spannungsirresein (catatonia or Tension Insanity).


Although catatonia has historically been linked to schizophrenia (catatonic schizophrenia), it is now known that catatonic symptoms are nonspecific and can be seen in other mental and neurological disorders.

In the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM):

Catatonia is not recognized as a separate disorder. Still, it is associated with psychiatric conditions such as schizophrenia (catatonic type), bipolar disorder, post-traumatic stress disorder, depression and other mental disorders, narcolepsy, and drug abuse or overdose (or both ).

It can also be seen in many medical disorders, including infections (such as encephalitis), autoimmune disorders, focal neurological lesions (including strokes), metabolic disturbances, alcohol withdrawal, and sudden or excessively rapid withdrawal from benzodiazepines.

In the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders, various medical conditions can cause catatonia, especially neurological disorders: encephalitis, cerebrovascular disease, neoplasms, and head injury.


On the other hand, metabolic conditions: include homocystinuria, diabetic ketoacidosis, hepatic encephalopathy, and hypercalcemia.

It can be an adverse reaction to the prescribed medication. It has similarities to encephalitis, lethargic, and neuroleptic malignant syndrome.

There are a variety of treatments available; benzodiazepines are a first-line treatment strategy.

Electroconvulsive therapy is also used sometimes. There is increasing evidence for the effectiveness of NMDA receptor antagonists for benzodiazepine-resistant catatonia.

Antipsychotics are sometimes used but require caution as they can worsen symptoms and have serious adverse effects.

Signs and symptoms

Catatonia can be stuporous or excited.

Stuporous catatonia is characterized by immobility. People may have rigid postures (stupor), inability to speak (mutism), and waxy flexibility, in which they hold positions after being placed in them by another person.

The mutism can be partial, and they can repeat nonsensical phrases or speak only to repeat what another person says.

People with stuporous catatonia may also show stereotyped and repetitive movements (stereotypy). Excited catatonia is characterized by bizarre, untargeted hyperactivity and impulsivity.

Catatonia is a syndrome that can occur in various psychiatric disorders, including major depressive disorder, bipolar disorder, schizophrenia, schizoaffective disorder, schizophreniform disorder, brief psychotic disorder, and substance-induced psychotic disorder.

It appears as Kahlbaum syndrome (immobile catatonia), malignant catatonia (neuroleptic malignant syndrome, toxic serotonin syndrome), and exciting forms (delusional mania, catatonic excitement, dreaming). It has also been recognized as grafted into autism spectrum disorders.


According to the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders, “catatonia associated with another mental disorder (Catatonia specifier)” (code 293.89 [F06.1]) is diagnosed if the clinical picture is dominated by at least three of the following:

  • Stupor (no psychomotor activity, not actively related to the environment).
  • Catalepsy (passive induction of a posture held against gravity).
  • Waxy flexibility (i.e., allow examiner positioning and maintain position).
  • Mutism (i.e., no or very little verbal response [exclude if aphasia is known]).
  • Negativism (opposition or lack of response to external instructions or stimuli).
  • Posture (spontaneous and active maintenance of a posture against gravity).
  • Mannerisms (that is, impartial and detailed caricature of everyday actions).
  • Stereotypy (that is, repetitive, abnormally frequent movements not directed at a goal).
  • External stimuli do not influence agitation.
  • Make faces (that is, make a face like children).
  • Echolalia (that is, imitating the speech of another).
  • Echopraxia (that is, mimicking the movements of another person).

Other disorders (additional code 293.89 [F06.1] was used to indicate the presence of comorbid catatonia):

  • Catatonia is associated with an autism spectrum disorder.
  • Catatonia associated with the schizophrenia spectrum and other psychotic disorders.
  • Catatonia associated with a brief psychotic disorder.
  • Catatonia is associated with the schizophreniform disease.
  • Catatonia associated with schizoaffective disorder.
  • Catatonia is associated with a substance-induced psychotic disorder.
  • Catatonia is associated with bipolar and related disorders.
  • Catatonia associated with major depressive disorder.
  • Catatonic disorder due to another medical condition.

If catatonic symptoms are present but do not form the catatonic syndrome, a drug- or substance-induced etiology should first be considered.


Stupor: it is an apathetic and immobile state in which one is unconscious or does not react to external stimuli. Motor activity is almost non-existent. People in this state make little or no eye contact with others and can be mute and rigid.

One could stay in one position for an extended period and then go directly to another place immediately after the first position.

Catatonic arousal: is a state of constant agitation and excitement without purpose. People in this state are highly hyperactive, although, as mentioned above, the activity appears to be purposeless.

The individual may also experience delusions or hallucinations. It is commonly cited as one of psychiatry’s most dangerous states of mind.

Malignant catatonia: it is an acute onset of excitement, fever, autonomic instability, and delirium and can be fatal.

A subset of catatonic patients develops a severe level of metabolic decompensation. For reasons that are not entirely clear, this condition has created its niche in psychiatric terminology.

This is not merely a matter of nosology, as these cases are pretty severe and can have lethal results. Many physicians fear that malignant catatonia is the final common pathway for intractable and misunderstood issues.

Patients who do not respond to treatment progress to fatal metabolic conditions. However, the astute clinician can minimize the damage. Prompt support and therapeutic intervention (usually with electroconvulsive therapy) can save lives.

Patients in the chronic arousal phase are clinically challenging. They burn out quickly and risk injuring themselves and their caregivers. These patients can develop rhabdomyolysis, fever, and kidney failure.

These patients are also at risk for heart failure. Treatment for such patients generally involves electroconvulsive therapy, supportive metabolic care, and possibly moderate sedation with barbiturate or lorazepam.

Immobile and rigid catatonics are often at risk for malignant syndrome. While standing, sitting, or lying down for prolonged periods, they accumulate lymphatic and vascular fluids with the possible separation of proteins from the aqueous serum.

Immobile catatonics are at risk for pulmonary embolism, edema, and dehydration of moist membranes. Dry sclera puts the eyes at risk for ulceration and infection. Prolonged stiffness leads to rhabdomyolysis and kidney failure.

Many cases of immobile catatonia develop a fever. While malignant catatonia can be an adjective and a diagnostic term, it is always severe and life-threatening.

Some cases of malignant catatonia develop from improper treatment of the early stages of catatonia, while others develop rapidly. Most physicians now recommend immediate intervention with electroconvulsive therapy.

The cases described above rarely respond to other interventions and continue to deteriorate with supportive care alone.

Rating scale

Fink and Taylor developed a catatonia rating scale to identify the syndrome. A test for benzodiazepine or barbiturates verifies the diagnosis.

The diagnosis is validated with rapid benzodiazepines or electroconvulsive therapy (ECT). Although their use has been proven, barbiturates are no longer commonly used in psychiatry; hence the option of benzodiazepines or electroconvulsive therapy.

Differential diagnosis

The differential diagnosis of catatonia is extensive. Many conditions present with dysregulation and stupor of movement. A thorough medical examination and a detailed neurological evaluation are vital at the first contact with the patient.

This should be accompanied by blood tests, including a complete metabolic panel, blood count and analysis, electrolytes, kidney and liver function tests, a toxicology test, and a battery of common hormonal values.

MRI brain imaging and an EEG (to rule out non-convulsive status epilepticus) are required. Some cases with a fever or elevated neutrophil count will require a cerebrospinal fluid exam.

After these exams, a helpful screening test such as the one developed by Peralta may be used to evaluate psychiatric symptoms.

With these methods, most cases of catatonia can be safely evaluated and treated. Gelenberg published a more detailed pathway of differential diagnosis in 1976.

The organic conditions that occur with catatonia are many and can be innumerable. Such a list may include but is not limited to those listed here.

Metabolic conditions include diabetic ketoacidosis, parathyroid adenoma, pellagra, and homocystinuria. Neurological disorders can cause catatonia; Akinetic mutism is an excellent example.

Fink recommended that a lorazepam switch test can provide a confirmatory diagnosis in the presence of average laboratory values. Most cases of catatonia will respond to 2-4 mg of lorazepam intravenously.

The injection will generally produce regular motor activity and restore mental clarity within minutes or two. This reduction in symptoms is brief, lasting 20 to 30 minutes before the patient gradually returns to a rigid stupor.

A breathing apparatus must be available, and active clinical surveillance is used to prevent respiratory depression or suffocation.

Neuroleptic malignant syndrome: Among the differential entities, a discussion of the neuroleptic malignant syndrome (NMS) is warranted. This serious medical condition is caused by antipsychotic medication and was first reported in 1956.

It has been associated with virtually all conventional antipsychotics and some atypical antipsychotics. The historical incidence of neuroleptic malignant syndrome has been around 2%.

Patients with neuroleptic malignant syndrome generally present with fever, muscle stiffness, and altered mental status. In some cases, akathisia sometimes looks more promising than stiff.

Patients can develop delirium and mutism during neuroleptic malignant syndrome, closely resembling idiopathic catatonia.

The white blood cell count and creatine phosphokinase test are often elevated in neuroleptic malignant syndrome, and rhabdomyolysis is frequently seen.

Hypertensive crises and metabolic acidosis are common. The fever is caused by the blockage of dopamine in the hypothalamus. It is believed that calcium in the sarcoplasmic reticulum may cause muscle stiffness.

Neuroleptic Malignant Syndrome is a medical emergency. It can lead to death if it is not treated. Most patients will need the support of an intensive care unit to provide adequate hydration, ventilation, and temperature regulation.

Drug treatments have not been uniformly successful. Bromocriptine and dantrolene are beneficial in some cases.

Early studies reported up to 30% mortality rates, but recent data suggest that early recognition and treatment can reduce this to less than 10%.

Some authors have suggested that catatonia and neuroleptic malignant syndrome may be disorders of the same essential spectrum, but the data for this position are less than robust.

The similarity of presentation, the high potential for mortality, and the occurrence in similar populations (psychotic patients) make the importance of clinical surveillance even more vital.

History and commentary

Catatonia is a motor dysregulation syndrome associated with a variety of diseases. Black described the term’s derivation from the Greek kata (down) and tonnes (tension or tone).

Papathomopoulus and Knoff offered another origin: that of the alternative meaning of kata (completely), which as a prefix strengthens the verb Otieno (tension, stretch) and renders katateino.

In early lectures, the syndrome was described in German as Spannungsirresein to connote “the madness of tension.” Etymology aside, the hallmark of catatonia syndrome is stupor accompanied by psychomotor disorders.

The American Psychiatric Association’s Diagnostic and Statistical Manual (DSM5) documents a current specification of the catatonic syndrome and reports that catatonia can be found in various disorders.

The diagnostic and statistical manual criteria include three symptoms from the following list of twelve: stupor, catalepsy, waxy flexibility, mutism, negativism, posture, gestures, stereotypy, agitation, grimacing, echolalia, and echopraxia.

Other common symptoms are motor resistance to simple commands, posture, stiffness, automatic obedience, and repetitive movements. This specification is clinically helpful and is a significant improvement on the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV).

Diagnostic parsimony has been a long time coming. It is noteworthy that many signs and symptoms of catatonia have been reported. This may be due, in part, to the growing science of psychiatry and the zeal for naming and classifying numerous bizarre and bizarre behaviors.

These early and often colorful descriptions of catatonia demonstrate that this group of symptoms has been recognized as a syndrome for quite some time.

Before the late 19th century, various terms were used to describe conditions characterized by stupor and alternation with excitement in English medical literature. The first case reports shared a common theme of psychosis with psychomotor symptoms.

It took many years before the science of descriptive psychopathology evolved to get a clearer picture of catatonia.

Most clinical historians would agree that Karl Kahlbaum conducted the first disciplined and systematic investigation to define catatonia as a discrete syndrome.

He followed a group of patients from his office at the Riemer Sanitarium in Germany in the late 19th century. His early descriptions of the condition focused on motor symptoms of mutism, catalepsy (waxy flexibility), verbigeration, stereotypes, and negativism.

It is clear that, in addition to Kaltbaum’s important specification of the catatonic syndrome, his work supported multi-causality and did not consider its presentation as indicative of a single disease entity.

He described it in various patients with different primary conditions, including depression, mania, and overt psychosis. He presented this work at academic conferences in 1866 and a classic monograph in 1874.

Many physicians modeled their concept of the syndrome after its description and identified it as coexisting with various disorders.

Although the first doctors began to recognize catatonia, its clinical picture was confused by the observations of patients with chronic and deteriorating diseases.

This shared understanding reflects the available evidence of the times: that catatonia led to a uniformly poor outcome, similar to a demented illness.

When Kraepelin considered the condition, recognition of variability between possible courses was prevented. This was not irrational, given the state of the science, the severity of the disease (s) resulting in institutionalization, and the lack of effective treatments for mental disorders.

The sampling of available cases to those of hospitalized patients created a bias towards inevitable decline. Kraepelin noted the deteriorating course of his patients and concluded that catatonia was one of the three primary forms of early dementia, along with the paranoid and disorganized types.

Eugene Bleuler reorganized the criteria for dementia precocious and included milder and less chronic presentations. Having distinguished it from uniformly progressive disorders, he renamed the condition schizophrenia.

Similar to the Kraepelin classifications of praecox dementia, Bleuler’s focus on ambivalence, autism, and affect disorders resulted in the inclusion of catatonic syndrome as a subgroup of schizophrenia.

While Kraepelin went on to define catatonia as a type of insane illness, both he and Bleuler recognized that the syndrome could be found in different kinds of psychosis.

Other physicians increasingly identified catatonia as a medical condition in many settings.

The subsequent significant development toward a modern understanding of catatonia came as more physicians recognized its association with affective disorders.

In 1913, Kirby had reported clear cases of catatonia in patients with manic depressive illness, and Kleist’s early work supported the notion of association of catatonic with mood disorders.

An emerging body of work supported the recognition that catatonia was not simply a form of schizophrenia but could be found in mood disorders, as well as a variety of medical conditions.

Once again, this progress in informing our modern knowledge of catatonia, specifically its common association with affective disease, was left relatively unnoticed, probably overshadowed by interest in infectious diseases that affect the brain.

These conditions could confuse the inexperienced clinician by the nature and severity of your psychomotor symptoms. The first prospective studies revealed that untreated catatonia had a high mortality rate in various settings.

Underlying medical conditions could easily explain this.

Despite the evolutionary consensus that catatonic syndromes are often associated with medical illnesses, physicians in the psychoanalytic school remained focused on rational explanations.

Rigorous medical examinations were often neglected. A review of the analytical literature reveals case reports of catatonia but few scientific studies. Considering catatonia as a defense mechanism with sensorimotor regression was a probable psychoanalytic interpretation.

The analytical concepts of catatonia were practically impossible to confirm. Not surprisingly, early psychoanalysts had difficulty treating catatonia.

Kahlbaum’s descriptive work was developed to include longitudinal observations of his patients.

However, this work was compromised by common institutional diseases, such as pneumonia and tuberculosis, which made long-term follow-up of the natural history of catatonic syndrome difficult.

Similarly, the works of Kraepelin and Hoch documented attempts to collect longitudinal data, but these efforts also suffered from the limitations of the medical therapies of the time.

Gjessing described a condition he referred to as periodic catatonia in the 1930s. Gjessing cited Kraepelin as estimating that about 2% of psychiatric hospital admissions in the early 20th century would be of this type.

This rare variety of the syndrome was characterized by phases of catatonic symptoms that rapidly alternated with completely asymptomatic periods.

Gjessing reported cases in which patients were regular one day, then catatonic the next, only to return to an asymptomatic phase the next day.

Case reports of recurrent brief episodes of catatonia followed by total remission remain in the literature today.

Treatment of periodic catatonia was often unusual. Gjessing was one of the doctors who tried treatments for catatonia. He followed patients over the years and considered them candidates for metabolic studies.

His research detected changes in nitrogen levels in the blood that correlate with the stages of stupor and arousal. Gjessing found a benefit in treating many of these patients with thyroxine in addition to electroconvulsive therapy.

In modern times, the use of thyroxine in catatonia has almost disappeared. Notions of cyclical changes in the nitrogen balance have been largely abandoned. Some research has suggested that periodic catatonia may have a unique genetic basis.

The results of family studies support this. Genetic analysis indicates possible loci on chromosome 15q15 and chromosome 22q13.

Early treatment involved little more than supportive care. Feeding was carried out using a nasogastric tube, and cold baths regulated body temperature.

Treatment for the syndrome evolved with barbiturates and electroconvulsive therapy (ECT) in the late 1920s.

As tranquilizers and electroconvulsive therapy became increasingly popular treatments for all psychiatric disorders, it became clear that they were beneficial for catatonic patients.

At first, intravenous barbiturates were used for interviews as patients became more lucid 20-30 minutes after injection.

These windows of clarity also allowed time to address seriously ill patients’ dietary and hygienic needs.

Prognosis and course of catatonia

As more effective medical treatments were established for both catatonic syndrome and the concurrent diseases historically encountered, the possibility of conducting level-field cohort studies with other medical conditions eventually became possible.

Hamilton, in 1962, observed that catatonia seemed to have two types of results, depending on its affective or psychotic comorbidity. He reported that when it was associated with mood disorders, it ran an episodic course and often went into full recovery for long periods.

On the other hand, he noted that the catatonia associated with schizophrenia typically entered prolonged periods of stupor, interrupted by an alert state that was characterized by poor hygiene, asocial behavior, and disorganized activity.

Of the catatonic patients diagnosed with schizophrenia, Hamilton reported that about 32% improved significantly over time, while the other 68% continued on a deteriorating course with early death.

Publications of other prognostic studies reported recovery in only 20% and 40% of cases, with the remaining instances continuing with ongoing psychosis and personality disintegration.

As in previous reports, patients with affective disorders fared better than those diagnosed with schizophrenia. However, work published up to 1966 demonstrated high overall mortality for catatonia, even when modern treatments were available.

In the early 1970s, physicians at the University of Iowa investigated a large retrospective cohort. This was made possible by the Iowa Psychopathic Hospital, where records of nearly 20,000 psychiatric patients hospitalized between 1920 and 1934 were kept.

Patient signs and symptoms were carefully documented in these records, producing detailed descriptions of behavior.

Such precise information allowed reconstruction and retrospective diagnosis using Investigative Diagnostic Criteria (RDC).

The evaluations were found to have very high kappa coefficients or inter-rater reliability.

In addition to analyzing data from chart revisions, Iowa patients could often be contacted and followed over time to monitor the course and progression of their disease.

As the hospital catchment area was a primarily rural setting, many families were tied to their geographic location for their livelihood, often agriculture. This made patients less likely to move and be available to contact for decades.

Patients born in the late 19th century could be followed with remarkable ease for much of the 20th century.

In some cases, surviving family members provided additional histories of patients’ functioning, adding to a large amount of data available to categorize disease course and recovery.

From the resulting analyses of this rich database, the Iowa group provided compelling evidence that catatonia cases were associated with affective illness with a frequency similar to schizophrenia.

Morrison selected letters from the Iowa project for further study. He focused on catatonia and found exciting results: in his group of catatonic subjects, 40% were found to have recovered.

Factors associated with improvement were mood disorder diagnosis, acute onset, and treatment with electroconvulsive therapy.

Catatonia remained an epidemiological enigma. After the initial description of Kahlbaum syndrome, the prevalence of catatonia appeared stable for several decades.

From 1900 to 1920, catatonia was consistently found in 10% to 40% of psychiatric hospital admissions.

However, in the decades to come, catatonia was believed to be decreasing in occurrence and was on the verge of becoming a rare syndrome.

In the 1970s, doctors began trying to determine the cause of this perceived change. Several hypotheses were presented to explain this phenomenon.

The perceived decrease in hospital admissions of patients with catatonic characteristics could be related to improvements in the detection and treatment of primary diseases that potentially lead to the catatonic state.

Furthermore, it was observed that modern treatments of underlying etiologies may have prevented the development of catatonia in otherwise susceptible patients.

A similar hypothesis considers that many cases of catatonia are related to ineffective treatment of affective disorders.

Therefore, the decrease in hospital admissions for catatonia can be attributed to the increased efficacy of outpatient treatments for mood disorders.

The discovery of effective treatments for affective diseases has evolved significantly in the last 60 years, the same period in which a decrease in hospital admissions for catatonia was observed.

It should be noted that electroconvulsive therapy has been effective in treating catatonia in affective disorders for quite some time, as early as 1929.

Increasingly, clinicians found that prospectively followed catatonia patients did have affective disorders.

The works of Taylor, Abrams, and Fink demonstrated a strong tendency for catatonia to occur in psychotic depression and mania.

This finding seemed to discourage the idea of ​​catatonia arising from the delayed treatment of the most common psychiatric illness, as treatments for affective disorders have been around for quite some time.

Early age onset of psychiatric illness was observed as a risk factor for catatonic syndrome by Ungvari et al. This also seems to counter the argument that the delayed treatment caused catatonia.

In another cohort study of 568 catatonic patients, Kleinhaus and Harlap found an association with the schizophrenic diagnosis. This may be due to selection bias in a sample with many psychotic patients.

Common theories to explain the declining prevalence of catatonia have included: the use of increasingly restrictive definitions of the syndrome, more reliable exclusion criteria, and improved treatment resulting in fewer cases reaching the catatonic stage associated with advanced disease.

The use of alternative classification systems, such as the Leonhard approach, has produced significantly more cases of catatonia than the use of the Investigative Diagnostic Criteria.

It is also possible that some “false negatives” appear in which actual cases of catatonia were confused with the neuroleptic malignant syndrome.

Doctors noted a tendency for catatonic episodes to last at least six months in almost all cases studied and multiple hospital admissions.

These variables can contribute to the underestimation of catatonia in clinical systems.


Establishing the medical etiology is the first order of care for the individual with catatonia. As described above, in the case of idiopathic catatonia, a simple reduction of catatonic symptoms is desired.

Immediate discontinuation of neuroleptics is indicated. While a minimal number of success stories have been reported with clozapine, it is best to avoid using antipsychotic medications altogether.

Most of the neuroleptic drugs routinely prescribed for psychosis can worsen the psychomotor symptoms of catatonia. A small body of literature suggests that transcranial magnetic therapy may be helpful in some patients.

Regardless of etiology, patient care includes adequate hydration and other supportive measures. Concurrent care may consist of nutrition, cooling, prevention of aspiration, and consideration of thrombophlebitis prophylaxis.

Once these steps have been taken, treatment of any underlying condition should alleviate psychomotor symptoms. This approach, however, does not handle all cases as catatonia can be idiopathic.

Once medically stable, active treatment generally falls into two categories, benzodiazepine activation or electroconvulsive therapy.

Most cases will respond quite well to large doses of lorazepam (2-5 mg), administered intravenously, with care to control ventilation.

If benzodiazepine therapy fails or the patient is in an emerging situation of lethal catatonia, electroconvulsive therapy is the treatment of choice. A course of nine to twelve bilateral treatments is usually sufficient to reduce catatonic symptoms.

After completion of electroconvulsive therapy, oral lorazepam is introduced. To have a persistent response, most patients require several sessions of electroconvulsive treatment.

Once electroconvulsive therapy is complete, maintenance with lorazepam and a mood stabilizer such as valproic acid is often the most successful outpatient care.

To get a proper perspective on the presentation and treatment of catatonia, it is helpful to examine real cases.

Case 1

The patient was a 37-year-old white male with a history of chronic bipolar disorder. He had no history of catatonia but had a history of psychotic mania within the past two years.

His family brought him to the hospital after an episode of depression progressed to refusal of meals, silence, and refusal to leave the bed. The initial examination found a resistive and silent man with little eye contact.

He could only leave his chair with help and stiffened when offered physical assistance. The patient provided passive resistance to attempts to move the arms and held the arms in position for 5 to 10 minutes after they were moved (waxy flexibility).

His skin was sebaceous and reddish. The students reacted to the light and the accommodation. Reflexes decreased but were the same bilaterally. Babinski’s sign was ordinary. Attempts to move limbs were met with resistance (gegenhalten).

An EKG is normal. Urinary toxicology was every day. Routine complete blood count, electrolytes, blood urea nitrogen (BUN), creatinine, and liver function tests were unremarkable.

The patient had average temperature and respiration. Their blood pressure was 132/79.

Creatinine phosphokinase (CPK) levels were normal, suggesting that the rhabdomyolysis had not started. Brain MRI revealed no abnormality. The chest radiograph was clear.

The patient was not taking any psychiatric medication. Analysis of the cerebrospinal fluid found no abnormalities.

This patient met the criteria for catatonia in the Diagnostic and Statistical Manual of Mental Disorders. They gave him a 3 mg test dose of lorazepam intravenously.

Within sixty seconds of the injection, the patient sat up in bed and asked for something to eat. He had a rational conversation for ten minutes, and then gradually, he became disorganized and finally became speechless.

In a few more minutes, he was still and finally rigid. The attending physicians considered electroconvulsive therapy to be the treatment of choice. A series of spinal radiographs, electrocardiograms, and legal permission for electroconvulsive treatment was obtained.

Once electroconvulsive treatment began, a remarkable response was observed. The patient received his first treatment of bilateral electroconvulsive therapy with a setting of 150 volts at 0.5 s in a routine procedure.

After his first treatment, the patient responded to the conversation for approximately three hours. He continued to receive this treatment every other day until nine sessions were completed.

Cognition and rigidity improved with each treatment. After the last treatment, the patient was alert, well versed, and able to ambulate. His family reported that the patient was “back to his old self.”

He has discharged with lorazepam 2 mg three times a day and fluoxetine 20 mg per day, and valproic acid 1000 mg at bedtime. A subsequent follow-up a year later found him in recovery and doing well in his community.


Catatonia is a syndrome caused by a variety of brain diseases. It has likely been a part of human pathology for centuries. Systematic observations began to appear in the literature, starting with Kahlbaum.

Their detailed descriptions allowed other clinicians to study the syndrome, culminating in developing our current understanding. Doctors and scientists have learned a considerable amount by studying the epidemiology of this syndrome.

Medical comorbidities and institutional conditions complicated the initial work. Many early cases were lost to follow-up. By the 1950s, the life cycle of patients with catatonia could be followed from onset to death.

Treatments for catatonia, such as electroconvulsive therapy and barbiturates, were introduced in the early 20th century. Ongoing research revealed many causes for this syndrome. Catatonic patients are divided into several general groups.

Of these, those with affective symptoms may experience long periods of remission. Cases diagnosed with schizophrenia tend to have a more chronic course, but some of this may be due to treatable Neuroleptic Malignant Syndrome.

Based on this review, we encourage psychiatrists to recognize catatonia as a syndrome rather than a rare disease entity. Our old school photos aside, catatonia awareness has modern clinical significance.

Numerous studies have described the prevalence among psychiatric patients ranging from 7.6 to 38%. Clinicians must be familiar with catatonia, its underlying medical conditions, and its idiopathic presentation.

A good medical history and prompt treatments are life and death.