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Catatonia: How to identify and treat it: Features that overlap with other syndromes make the diagnosis easy to overlook.

Is catatonia a rare condition that belongs in the history books, or is it more prevalent than we think? If we think we don't see it often, how will we recognize it? And how do we treat it? This article reviews the evolution of our understanding of the phenomenology and therapy of this interesting and complex condition.

History of the concept

In 1874, Kahlbaum (1,2) was the first to propose a syndrome of motor dysfunction characterized by mutism, immobility, staring gaze, negativism, stereotyped behavior, waxy flexibility, and verbal stereotypies that he called catatonia. Kahlbaum conceptualized catatonia as a distinct disorder, (3) but Kraepelin reformulated it as a feature of dementia praecox. (4) Although Bleuler felt that catatonia could occur in other psychiatric disorders and in normal people, (4) he also included catatonia as a marker of schizophrenia, where it remained from DSM-I through DSM-IV. (3) As was believed to be true of schizophrenia, Kraepelin considered catatonia to be characterized by poor prognosis, whereas Bleuler eliminated poor prognosis as a criterion for catatonia. (3)

In DSM-IV, catatonia was still a subtype of schizophrenia, but for the first time it was expanded diagnostically to become both a specifier in mood disorders, and a syndrome resulting from a general medical condition. (5,6) In DSM-5, catatonic schizophrenia was deleted, and catatonia became a specifier for 10 disorders, including schizophrenia, mood disorders, and general medical conditions. (3,5-9) In ICD-10, however, catatonia is still associated primarily with schizophrenia. (10)

A wide range of presentations

Catatonia is a cyclical syndrome characterized by alterations in motor, behavioral, and vocal signs occurring in the context of medical, neurologic, and psychiatric disorders. (8) The most common features are immobility, waxy flexibility, stupor, mutism, negativism, echolalia, echopraxia, peculiarities of voluntary movement, and rigidity. (7,11) Features of catatonia that have been repeatedly described through the years are summarized in Table 1 (8,12,13) (page 19). In general, presentations of catatonia are not specific to any psychiatric or medical etiology. (13,14)

Catatonia often is described along a continuum from retarded/stuporous to excited, (14,15) and from benign to malignant. (13) Examples of these ranges of presentation include (5,12,13,15-19):

Stuporous/retarded catatonia (Kahlbaum syndrome) is a primarily negative syndrome in which stupor, mutism, negativism, obsessional slowness, and posturing predominate. Akinetic mutism and coma vigil are sometimes considered to be types of stuporous catatonia, as occasionally are locked-in syndrome and abulia caused by anterior cingulate lesions.

Excited catatonia (hyperkinetic variant, Bell' s mania, oneirophrenia, oneroid state/ syndrome, catatonia raptus) is characterized by agitation, combativeness, verbigeration, stereotypies, grimacing, and echo phenomena (echopraxia and echolalia).

Malignant (lethal) catatonia consists of catatonia accompanied by excitement, stupor, altered level of consciousness, catalepsy, hyperthermia, and autonomic instability with tachycardia, tachypnea, hypertension, and labile blood pressure. Autonomic dysregulation, fever, rhabdomyolysis, and acute renal failure can be causes of morbidity and mortality. Neuroleptic malignant syndrome (NMS)--which is associated with dopamine antagonists, especially antipsychotics--is considered a form of malignant catatonia and has a mortality rate of 10% to 20%. Signs of NMS include muscle rigidity, fever, diaphoresis, rigor, altered consciousness, mutism, tachycardia, hypertension, leukocytosis, and laboratory evidence of muscle damage. Serotonin syndrome can be difficult to distinguish from malignant catatonia, but it is usually not associated with waxy flexibility and rigidity.

Several specific subtypes of catatonia that may exist anywhere along dimensions of activity and severity also have been described:

Periodic catatonia. In 1908, Kraepelin described a form of periodic catatonia, with rapid shifts from excitement to stupor. (4) Later, Gjessing described periodic catatonia in schizophrenia and reported success treating it with high doses of thyroid hormone. (4) Today, periodic catatonia refers to the rapid onset of recurrent, brief hypokinetic or hyperkinetic episodes lasting 4 to 10 days and recurring during the course of weeks to years. Patients often are asymptomatic between episodes except for grimacing, stereotypies, and negativism later in the course. (13,15) At least some forms of periodic catatonia are familial, (4) with autosomal dominant transmission possibly linked to chromosome 15q15. (13)

A familial form of catatonia has been described that has a poor response to standard therapies (benzodiazepines and electroconvulsive therapy [ECT]), but in view of the high comorbidity of catatonia and bipolar disorder, it is difficult to determine whether this is a separate condition, or a group of patients with bipolar disorder. (5)

Late (ie, late-onset) catatonia is well described in the Japanese literature. (10) Reported primarily in women without a known medical illness or brain disorder, late catatonia begins with prodromal hypochondriacal or depressive symptoms during a stressful situation, followed by unprovoked anxiety and agitation. Some patients develop hallucinations, delusions, and recurrent excitement, along with anxiety and agitation. The next stage involves typical catatonic features (mainly excitement, retardation, negativism, and autonomic disturbance), progressing to stupor, mutism, verbal stereotypies, and negativism, including refusal of food. Most patients have residual symptoms following improvement. A few cases have been noted to remit with ECT, with relapse when treatment was discontinued. Late catatonia has been thought to be associated with late-onset schizophrenia or bipolar disorder, or to be an independent entity.

Untreated catatonia can have serious medical complications, including deep vein thrombosis, pulmonary embolism, aspiration pneumonia, infection, metabolic disorders, decubitus ulcers, malnutrition, dehydration, contractures, thrombosis, urinary retention, rhabdomyolysis, acute renal failure, sepsis, disseminated intravascular coagulation, and cardiac arrest. (11,12,16,20,21) Mortality approaches 10%. (12) In children and adolescents, catatonia increases the risk of premature death (including by suicide) 60-fold. (22)

Not as rare as you might think

With the shift from inpatient to outpatient care driven by deinstitutionalization, longitudinal close observation became less common, and clinicians got the impression that the dramatic catatonia that was common in the hospital had become rare. (3) The impression that catatonia was unimportant was strengthened by expanding industry promotion of antipsychotic medications while ignoring catatonia, for which the industry had no specific treatment. (3) With recent research, however, catatonia has been reported in 7% to 38% of adult psychiatric patients, including 9% to 25% of inpatients, 20% to 25% of patients with mania, (3,5) and 20% of patients with major depressive episodes. (7) Catatonia has been noted in .6% to 18% of adolescent psychiatric inpatients (especially in communication and social disorders programs), (5,8,22) some children, (5) and 6% to 18% of adult and juvenile patients with autism spectrum disorder (ASD). (23) In the medical setting, catatonia occurs in 12% to 37% of patients with delirium, (8,14,17,18,20,24) 7% to 45% of medically ill patients, including those with no psychiatric history, (12,13) and 4% of ICU patients. (12) Several substances have been linked to catatonia; these are discussed later. (11) Contrary to earlier impressions, catatonia is more common in mood disorders, particularly mixed bipolar disorder, especially mania, (5) than in schizophrenia. (7,8,17,25)


Conditions associated with catatonia have different features that act through a final common pathway, (7) possibly related to the neurobiology of an extreme fear response called tonic immobility that has been conserved through evolution. (8) This mechanism may be mediated by decreased dopamine signaling in basal ganglia, orbitofrontal, and limbic systems, including the hypothalamus and basal forebrain. (3,17,20) Subcortical reduction of dopaminergic neurotransmission appears to be related to reduced [GABA.sub.A] receptor signaling and dysfunction of N-methyl-D-aspartate (NMDA) receptors with glutaminergic excess in striato-cortical or frontal cortico-cortical systems. (13,20,26,27)

Up to one-quarter of cases of catatonia are secondary to medical (mostly neurologic) factors or substances. (15) Table 2 (5,13,15) (page 20) lists common medical and neurological causes. Medications and substances known to cause catatonia are noted in Table 3. (5,8,13,16,26)

Catatonia can be a specifier, or a separate condition

DSM-5 criteria for catatonia are summarized in Table 4. (28) With these features, catatonia can be a specifier for depressive, bipolar, or psychotic disorders; a complication of a medical disorder; or another separate diagnosis. (8) The diagnosis of catatonia in DSM-5 is made when the clinical picture is dominated by [greater than or equal to] 3 of the following core features (8,15):

* motoric immobility as evidenced by catalepsy (including waxy flexibility) or stupor

* excessive purposeless motor activity that is not influenced by external stimuli

* extreme negativism or mutism

* peculiarities of voluntary movement such as posturing, stereotyped movements, prominent mannerisms, or prominent grimacing

* echolalia or echopraxia.

DSM-5 criteria for the diagnosis of catatonia are more restrictive than DSM-IV criteria. As a result, they exclude a significant number of patients who would be considered catatonic in other systems. (29) For example, DSM-5 criteria do not include common features noted in Table 1 (8,12,13) (page 19), such as rigidity and staring. (14,29) If the diagnosis is not obvious, it might be suspected in the presence of >1 of posturing, automatic obedience, or waxy flexibility, or >2 of echopraxia/echolalia, gegenhalten, negativism, mitgehen, or stereotypy/vergiberation. (12) Clues to catatonia that are not included in formal diagnostic systems and are easily confused with features of psychosis include whispered or robotic speech, uncharacteristic foreign accent, tiptoe walking, hopping, rituals, and odd mannerisms. (5)

There are several catatonia rating scales containing between 14 and 40 items that are useful in diagnosing and following treatment response in catatonia (Table 5, (8,13,15,29) page 22). Of these, the Kanner Scale is primarily applied in neuropsychiatric settings, while the Bush-Francis Catatonia Rating Scale (BFCRS) has had the most widespread use. The BFCRS consists of 23 items, the first 14 of which are used as a screening instrument. It requires 2 of its first 14 items to diagnose catatonia, while DSM-5 requires 3 of 12 signs. (29) If the diagnosis remains in doubt, a benzodiazepine agonist test can be instructive. (9,12) The presence of catatonia is suggested by significant improvement, ideally assessed prospectively by improvement of BFCRS scores, shortly after administration of a single dose of 1 to 2 mg lorazepam or 5 mg diazepam IV, or 10 mg Zolpidem orally. Further evaluation generally consists of a careful medical and psychiatric histories of patient and family, review of all medications, history of substance use with toxicology as indicated, physical examination focusing on autonomic dysregulation, examination for delirium, and laboratory tests as suggested by the history and examination that may include complete blood count, creatine kinase, serum iron, blood urea nitrogen, electrolytes, creatinine, prolactin, anti-NMDA antibodies, thyroid function tests, serology, metabolic panel, human immunodeficiency virus testing, EEG, and neuroimaging. (8,15,16)

A complex differential diagnosis

Manifestations of numerous psychiatric and neurologic disorders can mimic or be identical to those of catatonia. The differential diagnosis is complicated by the fact that some of these disorders can cause catatonia, which is then masked by the primary disorder; some disorders (eg, NMS) are forms of catatonia. Table 6 (5,8,12,19,26,30) lists conditions to consider.

Some of these conditions warrant discussion. ASD may have catatonia-like features such as echolalia, echopraxia, excitement, combativeness, grimacing, mutism, logorrhea, verbigeration, catalepsy, mannerisms, rigidity, staring and withdrawal. (8) Catatonia may also be a stage of deterioration of autism, in which case it is characterized by increases in slowness of movement and speech, reliance on physical or verbal prompting from others, passivity, and lack of motivation. (23) At the same time, catatonic features such as mutism, stereotypic speech, repetitive behavior, echolalia, posturing, mannerisms, purposeless agitation, and rigidity in catatonia can be misinterpreted as signs of ASD. (8) Catatonia should be suspected as a complication of longstanding ASD in the presence of a consistent, marked change in motor behavior, such as immobility, decreased speech, stupor, excitement, or mixtures or alternations of stupor and excitement. (8) Freezing while doing something, difficulty crossing lines, or uncharacteristic persistence of a particular behavior may also herald the presence of catatonia with ASD. (8)

Catatonia caused by a neurologic or metabolic factor or a substance can be difficult to distinguish from delirium complicated by catatonia. Delirium may be identified in patients with catatonia by the presence of a waxing and waning level of consciousness (vs fluctuating behavior in catatonia) and slowing of the EEG. (12,15) Antipsychotic medications can improve delirium but worsen catatonia, while benzodiazepines can improve catatonia but worsen delirium.

Among other neurologic syndromes that can be confused with catatonia, locked-in syndrome consists of total immobility except for vertical extraocular movements and blinking. In this state, patients attempt to communicate with their eyes, while catatonic patients do not try to communicate. There is no response to a lorazepam challenge test. Stiff man syndrome is associated with painful spasms precipitated by touch, noise, or emotional stimuli. Baclofen can resolve stiff man syndrome, but it can induce catatonia. Paratonia refers to generalized increased motor tone that is idiopathic, or associated with neurodegeneration, encephalopathy, or medications. The only motor sign is increased tone, and other signs of catatonia are absent. Catatonia is usually associated with some motor behaviors and interaction with the environment, even if it is negative, while the coma vigil patient is completely unresponsive. Frontotemporal dementia is progressive, while catatonia usually improves without residual dementia. (30)

Benzodiazepines, ECT are the usual treatments

Experience dictates that the general principles of treatment noted in Table 7 (12,15,23,31) apply to all patients with catatonia. Since the first reported improvement of catatonia with amobarbital in 1930, (6) there have been no controlled studies of specific treatments of catatonia. (13) Meaningful treatment trials are either naturalistic, or have been performed only for NMS and malignant catatonia. (5) However, multiple case reports and case series suggest that treatments with agents that have anticonvulsant properties (benzodiazepines, barbiturates) and ECT are effective. (5)

Benzodiazepines and related compounds. Case series have suggested a 60% to 80% remission rate of catatonia with benzodiazepines, the most commonly utilized of which has been lorazepam. (7,13,32) Treatment begins with a lorazepam challenge test of 1 to 2 mg in adults and 0.5 to 1 mg in children and geriatric patients, (9,15) administered orally (including via nasogastric tube), IM, or IV. Following a response ([greater than or equal to] 50% improvement), the dose is increased to 2 mg 3 times per day. The dose is further increased to 6 to 16 mg/d, and sometimes up to 30 mg/d. (9,11) Oral is less effective than sublingual or IM administration. (11) Diazepam can be helpful at doses 5 times the lorazepam dose. (9,17) A Zolpidem challenge test of 10 mg orally or via nasogastric tube has also been utilized. (15) Response is brief and is usually followed by lorazepam, although Zolpidem up to 40 mg/d has been used for ongoing treatment. (9)

One alternative benzodiazepine protocol utilizes an initial IV dose of 2 mg lorazepam, repeated 3 to 5 times per day; the dose is increased to 10 to 12 mg/d if the first doses are partially effective. (16) A lorazepam/ diazepam approach involves a combination of IM lorazepam and IV diazepam. (11) The protocol begins with 2 mg of IM lorazepam. If there is no effect within 2 hours, a second 2 mg dose is administered, followed by an IV infusion of 10 mg diazepam in 500 ml of normal saline at 1.25 mg/hour until catatonia remits.

An Indian study of 107 patients (mean age 26) receiving relatively low doses of lorazepam (3 to 6 mg/d for at least 3 days) found that factors suggesting a robust response include a shorter duration of catatonia and waxy flexibility, while passivity, mutism, and auditory hallucinations describing the patient in the third person were associated with a poorer acute response. (31) Catatonia with marked retardation and mutism complicating schizophrenia, especially with chronic negative symptoms, may be associated with a lower response rate to benzodiazepines. (20,33) Maintenance lorazepam has been effective in reducing relapse and recurrence. (11) There are no controlled studies of maintenance treatment with benzodiazepines, but clinical reports suggest that doses in the range of 4 to 10 mg/d are effective. (32)

ECT was first used for catatonia in 1934, when Laszlo Meduna used chemically induced seizures in catatonic patients who had been on tube feeding for months and no longer needed it after treatment. (6,7) As was true for other disorders, this approach was replaced by ECT. (7) In various case series, the effectiveness of ECT in catatonia has been 53% to 100%. (7,13,15) Right unilateral ECT has been reported to be effective with 1 treatment. (21) However, the best-established approach is with bitemporal ECT with a suprathreshold stimulus, (9) usually with an acute course of 6 to 20 treatments. (20) ECT has been reported to be equally safe and effective in adolescents and adults. (34) Continued ECT is usually necessary until the patient has returned to baseline. (9)

ECT usually is recommended within 24 hours for treatment-resistant malignant catatonia or refusal to eat or drink, and within 2 to 3 days if medications are not sufficiently effective in other forms of catatonia. (12,15,20) If ECT is initiated after a benzodiazepine trial, the benzodiazepine antagonist flumazenil is administered first to reverse the anticonvulsant effect. (9) Some experts recommend using a muscle relaxant other than succinylcholine in the presence of evidence of muscle damage. (7)

Alternatives to benzodiazepines and ECT. Based on case reports, the treatments described in Table 8 (13,15,17,20,25) (page 24) have been used for patients with catatonia who do not tolerate or respond to standard treatments. The largest number of case reports have been with NMDA antagonists, while the presumed involvement of reduced dopamine signaling suggests that dopaminergic medications should be helpful. Dantrolene, which blocks release of calcium from intracellular stores and has been used to treat malignant hyperthermia, is sometimes used for NMS, often with disappointing results.

Whereas first-generation antipsychotics definitely increase the risk of catatonia and second-generation antipsychotics (SGAs) probably do so, SGAs are sometimes necessary to treat persistent psychosis in patients with schizophrenia who develop catatonia. Of these medications, clozapine may be most desirable because of low potency for dopamine receptor blockade and modulation of glutamatergic signaling. Partial dopamine agonism by aripiprazole, and the potential for increased subcortical prefrontal dopamine release resulting from serotonin 5HT2A antagonism and 5HT1A agonism by other SGAs, could also be helpful or at least not harmful in catatonia. Lorazepam is usually administered along with these medications to ameliorate treatment-emergent exacerbation of catatonia.

There are no controlled studies of any of these treatments. Based on case reports, most experts would recommend initiating treatment of catatonia with lorazepam, followed by ECT if necessary or in the presence of life-threatening catatonia. If ECT is not available, ineffective, or not tolerated, the first alternatives to be considered would be an NMDA antagonist or an anticonvulsant. (20)

Course varies by patient, underlying cause

The response to benzodiazepines or ECT can vary from episode to episode (11) and is similar in adults and younger patients. (22) Many patients recover completely after a single episode, while relapse after remission occurs repeatedly in periodic catatonia, which involves chronic alternating stupor and excitement waxing and waning over years. (11) Relapses may occur frequently, or every few years. (11) Some cases of catatonia initially have an episodic course and become chronic and deteriorating, possibly paralleling the original descriptions of the natural history of untreated catatonia, while malignant catatonia can be complicated by medical morbidity or death. (4) The long-term prognosis generally depends on the underlying cause of catatonia. (5)

Clinical Point

In general, presentations of catatonia are not specific to any psychiatric or medical etiology

Clinical Point

Periodic catatonia refers to recurrent, brief hypokinetic or hyperkinetic episodes lasting 4 to 10 days

Clinical Point

Catatonia is more common in mood disorders, particularly mixed bipolar disorder, than in schizophrenia

Clinical Point

Up to one-quarter of cases of catatonia are secondary to medical (mostly neurologic) factors or substances

Clinical Point

Some psychiatric and medical disorders can mimic and/or cause catatonia, which can make the differential diagnosis complex

Clinical Point

Treatment with agents that have anticonvulsant properties (benzodiazepines, barbiturates) and ECT are effective

Clinical Point

In case series, the effectiveness of electroconvulsive therapy for catatonia has been 53% to 100%

Bottom Line

Much more common than many clinicians realize, catatonia can be overlooked because symptoms can mimic or overlap with features of an underlying medical or neurologic disorder. Suspect catatonia when one of these illnesses has an unexpected course or an inadequate treatment response. Be alert to characteristic changes in behavior and speech. A benzodiazepine challenge can be used to diagnose and begin treatment of catatonia. Consider electroconvulsive therapy sooner rather than later, especially for severely ill patients.

Clinical Point

Most experts would recommend initiating treatment of catatonia with lorazepam, followed by ECT if necessary

Clinical Point

Many patients with catatonia recover completely after a single episode


Dr. Steven L. Dubovsky receives grant or research support from Allergan, Janssen, Neurim, Neurocrine, and Tower Foundation. Dr. Amelia N. Dubovsky reports no financial relationships with any company whose products are mentioned in this article, or with manufacturers of competing products.

Steven L. Dubovsky, MD Professor and Chair Department of Psychiatry State University of New York at Buffalo Buffalo, New York Adjoint Professor of Psychiatry and Medicine University of Colorado Aurora, Colorado

Amelia N. Dubovsky, MD Assistant Professor Department of Psychiatry University of Washington Seattle, Washington
Related Resources

* Gibson RC, Walcott G. Benzodiazepines for catatonia
in people with schizophrenia and other serious mental
illnesses. Cochrane Database Syst Rev. 2008;(4):CD006570.

* Newcastle University. Catatonia,

Drug Brand Names

Amantadine * Symmetrel      Flumazenil * Romazicon
Amobarbital * Amytal        Fluoxetine * Prozac
Aripiprazole * Ability      Fluvoxamine * Luvox
Azithromycin * Zithromax    Levetiracetam * Keppra
Baclofen * Lioresal         Lithium * Eskalith, Lithobid
Benztropine-Cogentin        Lorazepam * Ativan
  Carbamazepine *           Memantine * Namenda
Carbatrol, Tegretol         Methylphenidate * Ritalin
Carbidopa/levodopa *        Minocycline * Minocin
  Sinemet                   Olanzapine * Zyprexa
Ciprofloxacin * Cipro       Risperidone * Risperdal
Clozapine-Clozaril          Succinylcholine * Anectine
Dantrolene * Dantrium       Topiramate * Topamax
Dexamethasone * Decadron    Trihexyphenidyl * Artane
Dextromethorphan/           Valproate * Depakote
  quinidine * Neudexta      Ziprasidone * Geodon
Diazepam * Valium           Zolpidem * Ambien
Disulfiram * Antabuse


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Table 1
Features of catatonia

Feature                Description

Stupor                 Extreme hypoactivity and immobility.
                       Absence of movement or reaction when awake;
                       not actively relating to environment

Excitement             Purposeless hyperactivity.
                       Agitation not influenced by external stimuli

Mutism                 Extreme verbal unresponsiveness
                       in the absence of aphasia

Logorrhea              Excessive, monotonous speech

Staring                Fixed gaze at a distance, often with limited
                       tracking, little eye contact, and poor
                       blinking to threat

Posturing              Spontaneous, active maintenance
                       of rigid postures against gravity

Grimacing              Contortion of facial features

Rigidity               Maintaining stiff position
                       despite efforts to move patient

Psychological          Type of posturing involving a reclined
pillow                 position with head and shoulders raised
                       as if on a pillow, maintained for
                       extended periods

Mannerisms             Repetitive, idiosyncratic, purposeful
                       caricatures of movements or gestures,
                       such as using hands when talking

Ambitendency           Alternation between cooperation
                       with and resistance to instructions

Waxy flexibility       Patient can be positioned in uncomfortable
                       positions that patient maintains for long
                       periods with slight resistance to examiner

Automatic obedience    Exaggerated cooperation with a request or
                       excessive continuation of a requested

Mitgehen               Type of automatic obedience in which patient
                       can be positioned in any posture with minimal
                       effort, even when told to resist, but unlike
                       in waxy flexibility, body part immediately
                       returns to original position

Mitmachen              Variant of automatic obedience in which
                       body can be put into any posture despite
                       instructions to resist

Catalepsy              Maintenance of fixed sitting or standing
                       position against gravity that appears
                       uncomfortable with minimal movement
                       in response to external stimuli,
                       including pain

Motor perseveration    Persistence of a movement after
                       the original intent or command has ceased

Echopraxia             Mimicking another's movements

Echolalia              Nearly simultaneously mimicking
                       another's speech

Stereotypy             Involuntary, coordinated, rhythmic,
                       and repetitive but purposeless movement
                       or behavior, such as chewing, rocking,
                       grimacing, shrugging, hand waving, opening
                       and closing eyes, mouth and jaw movements;
                       may involve self-injurious behaviors, such
                       as self-hitting, biting, scratching; phonic
                       stereotypies include sniffing, clicking,
                       snorting, moaning, and other meaningless

Verbigeration          Verbal stereotype consisting of continuously
                       repeating (perseverating) meaningless words
                       or phrases

Aversion               Avoidance of examiner when called

Grasp                  Automatic grasping of examiner's hand

Obstruction            Sudden block of a movement

Gegenhalten            Motiveless resistance to movement by examiner
                       of part of patient's body with equal and
                       opposite force to that of examiner

Negativism             Opposition or no response to instructions or
                       external stimuli. Resistance to manipulation
                       of limbs involving doing the opposite of what
                       is asked, as opposed to simple resistance of

Social negativism      Turning away when addressed, refusing to open
(withdrawal)           eyes, closing mouth when offered food or

Combativeness          Undirected aggression unprovoked by
                       environmental threat and followed by
                       no or a facile explanation

Autonomic              Dysregulation of blood pressure,
abnormalities          pulse, respiration, temperature

Source: References 8,12,13

Table 2
Medical and neurologic causes
of catatonia

Structural CNS disease
Infectious and anti-NMDAR encephalitis
Other CNS infections (including HIV)
Seizure disorders
Neurocognitive/neurodegenerative disorders
(eg, Lewy body dementia, Wilson disease,
Huntington disease)
Normal pressure hydrocephalus
Hypoxic brain damage
Subdural hematoma
Hypertensive encephalopathy
Bilateral globus pallidus disease
Lesions of thalamus, parietal lobe, frontal lobe
Down syndrome
Tertiary syphilis
Autoimmune/inflammatory disorders
(eg, SLE, MS)
Takotsubo cardiomyopathy
Electrolyte disorders
G6PD deficiency
Pernicious anemia
Thrombotic thrombocytopenic purpura
Liver or kidney transplantation
Wasp sting
Deep brain stimulation complication

Source: References 5,13,15

G6PD: glucose-6-phosphate dehydrogenase; HIV: human
immunodeficiency virus; MS: multiple sclerosis; NMDAR:
W-methyl-D-aspartate receptor; SLE: systemic lupus

Table 3
Medications and substances that
induce catatonia

CNS depressant intoxication and withdrawal,
including alcohol
Abrupt withdrawal of antipsychotics, including
Withdrawal of benzodiazepines and
dopaminergic drugs
Lithium toxicity
Corticosteroids (eg, dexamethasone)
Gamma hydroxybutyric acid

Source: References 5,8,13,16,26

Table 4
DSM-5 criteria for catatonia

Waxy flexibility

Source: Reference 28

Table 5
Catatonia rating scales

Bush-Francis Catatonia Rating Scale
Modified Rogers Scale
Northoff Catatonia Rating Scale
Braunig Catatonia Rating Scale
Kanner Scale

Source: References 8,13,15,29

Table 6
Differential diagnosis of catatonia

Tardive dyskinesia
Tic disorders
Neuroleptic withdrawal dyskinesias
Neuroleptic malignant syndrome
Akinetic Parkinsonism/Parkinson's disease
Locked-in syndrome
Stiff man syndrome
Partial complex seizures
Nonconvulsive status epilepticus
Frontotemporal dementia
Metabolic stupor
Malignant hyperthermia
Serotonin syndrome
Vegetative state (coma vigil)
Conversion disorder

Source: References 5,8,12,19,26,30

Table 7
Principles of treatment
of catatonia

Early treatment is important

Treat pressure ulcers in stupor and fever in
excited catatonia

Treat underlying illnesses and withdraw
unnecessary medications

Avoid high-potency antipsychotics; second-generation
antipsychotics are sometimes used
for comorbid psychosis

Restart recently discontinued dopamine

Reverse hyperthermia

Monitor for autonomic instability

Ensure adequate hydration to prevent kidney

Maintain nutrition

Initiate deep vein thrombosis/pulmonary
embolism prophylaxis

Prevent contractures and aspiration

Source: References 12,15,23,31

Table 8
Alternatives to benzodiazepines and electroconvulsive therapy

Medication             Details

Amobarbital            Response rate up to 60%

NMDA antagonists       Amantadine (also dopaminergic) 100 to 600 mg
                       Memantine 10 to 20 mg

Dopaminergic agents    Carbidopa/levodopa
                       (levodopa dose 25 to 100 mg)
                       Methylphenidate 10 to 40 mg

Anticonvulsants        Valproate (possible GABAergic mechanism)
                       600 to 4 000 mg
                       Topiramate (anti-glutaminergic) 200 mg
                       Carbamazepine (unknown mechanism)
                       100 to 1000 mg

Dantrolene             Occasionally helpful

drugs                  Minocycline
                       Lithium (multiple actions)

SSRIs                  Fluoxetine

Anticholinergic        Benztropine
agents                 Trihexyphenidyl

Second-generation      Aripiprazole 3 to 30 mg
antipsychotics         Olanzapine 2.5 to 20 mg
                       Risperidone 0.5 to 8 mg
                       Ziprasidone 40 to 160 mg
                       Clozapine 150 to 800 mg

Repetitive             Fast rTMS (may be GABAergic); 10 Hz
magnetic stimulation

Source: References 13,15,17,20,25
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Author:Dubovsky, Steven L.; Dubovsky, Amelia N.
Publication:Current Psychiatry
Article Type:Disease/Disorder overview
Geographic Code:1USA
Date:Aug 1, 2018
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