Background
Catatonia is a state of apparent unresponsiveness to external stimuli in a person who is apparently awake. The condition is difficult to differentiate from diffuse encephalopathy and nonconvulsive status epilepticus. (See DDx, Presentation, and Workup.)
Psychomotor manifestations of catatonia[1] analyzed by latent class techniques have been divided into 4 classes, as follows[2] :
- Automatic
- Repetitive/echo
- Withdrawal
- Agitated/resistive
Catatonia is not a diagnosis. Rather, catatonia is a descriptive term for a presentation observed in a wide variety of disorders. While there exists a vast differential diagnosis for catatonia, the identification of treatable causes, such as nonconvulsive status epilepticus, is crucial to the administration of the needed interventions. When faced with a patient with catatonia, the clinician must first rule out treatable causes. (See Etiology, Presentation, Workup, Treatment, and Medication.)
See the PowerPoint presentation Catatonia (PPT), by James Robert Brasic, MD, MPH, for more information on catatonia.
Complications
The following complications are associated with catatonia (see Prognosis, Treatment, and Medication):
- Trauma - During an excited state, patients with catatonia may cause serious, even fatal, injuries to themselves and others; they may cause marked destruction of property
- Refusal to eat - Patients with catatonia may refuse to eat; death may result unless parenteral nutrition and fluids are administered on an involuntary basis
- Autonomic instability - Patients with catatonia may experience autonomic instability manifested by hyperthermia, hypertension, and tachycardia; medical intervention is required.
- Neuroleptic malignant syndrome - If this condition occurs, medical consultation is appropriate.
- Pulmonary embolism - Risk of fatal pulmonary embolism is increased in catatonia; to prevent thromboembolic disease, check fibrin D-dimer levels (if people with catatonia demonstrate evidence of early coagulation activation, then hematologic consultation is appropriate[3]
- Other - Patients with catatonia are at risk of complications from the underlying neurologic, psychiatric, medical, and obstetric causes of catatonia
Etiology
Catatonia likely represents a heterogeneous group of etiologies. Some hypotheses have been proposed about the pathophysiology of catatonia.
Deficits in fetal cortical development
Deficits in fetal cortical development may result in schizophrenia and other developmental disorders.[4] These deficits, in turn, likely produce dysfunction in cortical and subcortical glutamatergic pathways, resulting in the symptoms and signs of catatonia.[5]
Developmental disorders
Individuals with mental retardation, autism,[6] {{197} other pervasive developmental disorders,[6, 7, 8] or other developmental disabilities may be particularly vulnerable to developing catatonia.[7, 8, 9, 10]
Imbalances in the excitatory:inhibitory ratio (EIR) model
Baguley proposes that alterations in interrelated networks at the spinal and brainstem level produce catatonia.[11]
Dopaminergic blockade
The administration of agents that block postsynaptic dopamine receptors is associated with the onset of catatonia in some individuals.
Agonists of dopamine D1 and D2 receptors relieve catalepsy, a sign of catatonia in rats, suggesting that these agents may be effective pharmacologic interventions. Additionally, the effectiveness of electroconvulsive treatment (ECT) for catatonia suggests that dopaminergic modulation may play a role in the development and amelioration of catatonia.
Glutamatergic dysfunction
The effectiveness of amantadine in the treatment of catatonia suggests that at least some individuals with catatonia manifest glutamatergic dysfunction.
Decreased binding to gamma-aminobutyric acid (GABA)-A receptors in the left sensorimotor cortex has been observed in some subjects with catatonia. The favorable responses of some patients with catatonia to benzodiazepines and zolpidem, agonists of GABA-A, suggest that this is a likely site of dysfunction in some cases of catatonia.[12] Potentiation of the action of GABA by benzodiazepines suggests that some individuals with catatonia may have a functional deficit of GABA.
Dysfunction in neurotransmission of noradrenaline and serotonin
In inbred rats with catalepsy, Alekhina and colleagues (1993) reported decreases of noradrenaline and increases of serotonin in the striatum and diencephalon.
Animal models have been developed to study the pathophysiology of catatonia. Uzbay reports that administration of a nonspecific inhibitor of nitric oxide synthase, N(G)-nitro-L-arginine methyl ester (L-NAME), to ethanol-dependent rats being withdrawn from ethanol precipitates catatonia.[13]
Moreover, L-arginine, a precursor of nitric oxide, does not reverse the catatonia precipitated by L-NAME. Therefore, nitric oxide does not mediate the production of the catatonia. These findings suggest that dysfunction of dopaminergic, serotonergic, and glutamatergic systems may play a role in the production of catatonia in ethanol-dependent rats.
Frontal anomalies
Kahlbaum noted lesions of the Sylvian fossa and the second and third frontal gyri on autopsy of patients who died with catatonia.[14] These regions modulate executive functions and the inhibition of voluntary acts.
Disorders associated with catatonia
To facilitate assessment of the cause of catatonia, associated conditions and factors are categorized as neurologic, psychiatric, psychological, medical, and obstetric in the Table, below.
Table. Causes of Catatonia by Category (Open Table in a new window)
| Category | Causes |
| Neurologic conditions | Neuroleptic malignant syndrome[15] Administration of agents that block postsynaptic dopamine receptors* Administration of sibutramine,[16] withdrawn from US market October 8, 2010 Withdrawal of lorazepam and other sedatives Akinetic-rigid syndrome Arachnoid cyst in right parietal region Astrocytoma Atrophy of left amygdala[17] Autistic disorder[6, 7, 8, 18, 19, 20, 21, 22, 23] {{197} Basilar artery thrombosis Bilateral hemorrhagic lesions of temporal lobes Cerebellar catalepsy Cerebral hemorrhage Cerebral infarct Cerebrovascular disease Cortical venous thrombosis Central pontine myelinolysis Cortical basal ganglionic degeneration Dystonia Encephalitis (herpes, Trypanosoma cruzi) Encephalopathy (Borrelia burgdorferi, human immunodeficiency virus [HIV] infection, Wernicke encephalopathy) Familial fatal insomnia[24] Fibromuscular dysplasia with dissection of basilar artery Frontal lobotomy Head injury Huntington disease Hydrocephalus Hypopituitarism secondary to postpartum hemorrhage Idiopathic recurring stupor Inherited neurometabolic disorders Locked-in syndrome Meningitis, tuberculous Meningoencephalitis Multiple sclerosis[25, 26] Neurosyphilis Nonconvulsive status epilepticus Pervasive developmental disorders[7, 8, 22] Pallidoluysian atrophy Paraneoplastic encephalitis[27] Parkinsonism Postencephalitic parkinsonism Progressive multifocal leukoencephalopathy Progressive supranuclear palsy Schizencephaly Seizures (complex with partial symptomatology) Stiff-man syndrome Stroke Stupor Subarachnoid hemorrhage Subdural hematoma Substance intoxication (alcohol, disulfiram, organic fluorides, phencyclidine) Subthalamic mesencephalic tumor Surgical removal of cerebellar tumor Tay-Sachs disease Temporal lobe epilepsy Tuberous sclerosis Tumors (corpus callosum, glioma of third ventricle, supraventricular diffuse pinealoma) Vegetative state Von Economo encephalitis Wilson disease |
| Psychiatric conditions | Acute stress disorder Anorexia nervosa Autistic disorder[6] Brief reactive psychosis with catatonia Conversion disorder Hysteria Major depression, single episode with catatonic features Mood disorders Neuroleptic malignant syndrome[15] Posttraumatic stress disorder Schizophrenia Substance intoxication (3,4-methylenedioxymethamphetamine [ie, "ecstasy"], alcohol, amphetamine, phencyclidine, substance withdrawal, hypnotic-sedative, lorazepam) |
| Psychological factors | Immigration Experiencing rejection of an expression of love Visit to relative in another country |
| Medical conditions | Acquired immunodeficiency syndrome (AIDS) Acute intermittent porphyria Addison disease Bacterial septicemia Bronchorrhea Carcinoid tumors Diabetic ketoacidosis Encephalopathy (hepatic, HIV infection ? related, Wernicke) Fever of unknown cause Heat stroke Hepatic failure Hereditary coproporphyria Homocystinuria Hypercalcemia Hyperparathyroidism Hyperthyroidism Hyponatremia Hypothermia Intestinal atony Malaria Neuroleptic malignant syndrome[15] Poisoning (carbon monoxide, tetraethyl lead) Renal failure Substance intoxication (alcohol, cyclosporine, disulfiram, organic fluorides, phencyclidine) Syndrome of inappropriate antidiuretic hormone (SIADH) Syphilis Systemic lupus erythematosus Thermal injury Thrombotic thrombocytopenic purpura Tuberculosis Typhoid fever Uremia Von Economo encephalitis |
| Obstetric conditions | Hypopituitarism secondary to postpartum hemorrhage |
| *The administration of agents that block postsynaptic dopamine receptors is associated with the onset of catatonia in some individuals. | |
Neuroleptic malignant syndrome[15]
Neuroleptic malignant syndrome is characterized by the introduction of or a dose increase in a neuroleptic medication, a temperature greater than 38⁰ C, and heart rate greater than 100 beats per minute or diastolic blood pressure greater than 100mm Hg. The triad of fever, tachycardia, and rigidity is typical of the syndrome, which is associated with death in about one fifth of cases.
A similar etiology for catatonia and the neuroleptic malignant syndrome after exposure to antipsychotic medications, including typical and atypical neuroleptics, is suggested by the similar clinical presentation; ie, elevated temperature, rigidity, delirium, and dysregulation of the autonomic nervous system.
Although apparently uncommon, the neuroleptic malignant syndrome has been reported in up to 12.2% of people exposed to neuroleptic medication. Nielsen and Nielsen reported the occurrence of the neuroleptic malignant syndrome after a single dose of neuroleptic medication.[28]
Latah betul
Latah betul ("real latah" or "true latah") is a phenomenon present in Malaysia characterized by the apparent loss of control over behavior and by echolalia, echopraxia, and automatic obedience.
Winzeler surveyed ethnic groups in different regions of Malaysia to present demographic and epidemiologic data about the condition. None of the individuals under 10 years of age exhibited latah in any of the groups examined. Latah was much more common in women. Mature women were the most common group to exhibit latah. People who developed latah exhibited it for the rest of their lives.
People who developed latah in Malaysia often associated the onset with frightening experiences (in life and in dreams) and with sorcery.[29] Simons[30] and Tanner and Chamberland[31] have published videotapes of individuals with latah to facilitate its recognition by individuals from other cultures who are unfamiliar with the condition.
The occurrence of latah betul in older women in particular cultures in Southeast Asia suggests that some individuals in the affected ethnic groups may have a vulnerability to develop the condition. This is reminiscent of other neuropsychiatric disorders with a genetic basis. The histories of persons with latah betul suggest that extreme stress may precipitate the onset of the disorder in some individuals. Thus, environmental influences may facilitate the development of latah betul in those with an inborn predisposition to express the phenotype of latah betul.
Evaluation of people with latah betul by clinicians experienced with movement disorders may facilitate the application of the standard nomenclature for movement disorders, mental disorders, and other medical conditions to categorize latah betul. The published reports of latah betul suggest the diagnosis of catatonia. Research by individuals trained in the diagnosis of neuropsychiatric disorders will facilitate the understanding of latah betul and its place in a lexicon of diseases.
Epidemiology
Occurrence in the United States
The current frequency of catatonia in the United States is unknown. A few studies have noted a decrease in the frequency of catatonia in parts of the United States over the past century. A variety of biases may influence the results of the few epidemiologic studies of catatonia.
In a university hospital in New York in 1994, the incidence of catatonia was 7% of psychiatric inpatients.[32] However, the study was performed at a tertiary care referral hospital known for the treatment of catatonia, so the population likely was not representative of the general population.
International
The current frequency of catatonia in international populations is unknown. The few epidemiologic studies report vastly different rates. These suggest that the occurrence of catatonia may differ greatly from one location to another.
On the other hand, studies suggest that many cases of catatonia may remain undiagnosed. Thus, results may be confounded by an ascertainment bias. In other words, catatonia may be diagnosed less frequently in developing countries than it is in industrialized countries, because clinicians fail to identify the condition in their patients.
The prevalence of catatonia among inpatients of psychiatric hospitals is 11.4% in Colombia,[33] 13.5% in India,[34] 16.9% in Spain,[35] and 9.6% in Wales.[34] In a forensic psychiatric hospital in France, the prevalence of catatonia was 13.1%.[36] In Colombia, treatment apparently is not administered to many patients with catatonia until they have reached an advanced stage of the condition.
Benegal and colleagues reported that catatonia appears to be more common in India than in Europe and North America.[37]
In contrast to studies in Colombia, India, and Spain, reports in several other locations have suggested that the occurrence of catatonia in the general population decreased dramatically in the past century. In Great Britain, the incidence of catatonia dropped from 6% of admissions to a hospital in the 1850s to 0.5% in the 1950s.[38]
In a psychiatric clinic in Chile, a decrement in the proportion of patients with schizophrenia who manifested catatonia was observed from 1964-1984. In Finland, the percentage of patients with schizophrenia displaying catatonia decreased from 37% in 1933-1935 to 11% in 1953-1955.[39] In Canada, catatonia was present in 10% of inpatient psychiatric admissions in 1993.
Race-, sex-, and age-related demographics
The frequency of catatonia in specific races is unknown. Ungvari and colleagues noted the need to investigate the role of ethnic, cultural, and social influences in the development of catatonia.[40]
In Monroe County, New York, the female-to-male ratio was 1.3:1 for catatonic schizophrenia and 1.1:1 for all forms of schizophrenia during the period 1960-1969.[41] In 1972-1973, a female-to-male ratio of 1.3:1 was observed among inpatients with catatonia admitted to 2 psychiatric units in a municipal hospital in New York City.[42] Catatonia is rare in preadolescent children. Although rare in children, catatonia has been reported in adolescents and adults. The prognosis in adolescents is poor.
Prognosis
Carroll noted that studies of catatonia have reported recovery rates from 12% to more than 40% regardless of the treatment administered.[43] A response to benzodiazepines has been reported in more than 70% of patients with catatonia who undergo treatment. Failure to institute treatment early in the course of catatonia is associated with a poor prognosis.
Bonnot and colleagues reported that children with childhood schizophrenia and catatonia have more severe symptoms and a longer duration of illness than do children with childhood schizophrenia without catatonia. They concluded that catatonia has deleterious effects beyond mere motor symptoms in children with schizophrenia.[44] Catatonia in adolescents also has a poor prognosis, with these patients experiencing striking morbidity and mortality.[45]
Morbidity and mortality
In Monroe County, New York, the age-adjusted relative risk of death for people with catatonic schizophrenia was 3-fold greater that of the county population during the period 1960-1969. However, the risk of death was no higher than for other forms of schizophrenia or other types of mental illness.[41]
Among 35 young people with catatonia in France aged 12-18 years, most continued to manifest psychiatric morbidity at follow up from 1-10 years. There were 3 deaths, including 2 suicides. As stated above, morbidity and mortality in adolescents with catatonia is marked.[45]
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| Category | Causes |
| Neurologic conditions | Neuroleptic malignant syndrome[15] Administration of agents that block postsynaptic dopamine receptors* Administration of sibutramine,[16] withdrawn from US market October 8, 2010 Withdrawal of lorazepam and other sedatives Akinetic-rigid syndrome Arachnoid cyst in right parietal region Astrocytoma Atrophy of left amygdala[17] Autistic disorder[6, 7, 8, 18, 19, 20, 21, 22, 23] {{197} Basilar artery thrombosis Bilateral hemorrhagic lesions of temporal lobes Cerebellar catalepsy Cerebral hemorrhage Cerebral infarct Cerebrovascular disease Cortical venous thrombosis Central pontine myelinolysis Cortical basal ganglionic degeneration Dystonia Encephalitis (herpes, Trypanosoma cruzi) Encephalopathy (Borrelia burgdorferi, human immunodeficiency virus [HIV] infection, Wernicke encephalopathy) Familial fatal insomnia[24] Fibromuscular dysplasia with dissection of basilar artery Frontal lobotomy Head injury Huntington disease Hydrocephalus Hypopituitarism secondary to postpartum hemorrhage Idiopathic recurring stupor Inherited neurometabolic disorders Locked-in syndrome Meningitis, tuberculous Meningoencephalitis Multiple sclerosis[25, 26] Neurosyphilis Nonconvulsive status epilepticus Pervasive developmental disorders[7, 8, 22] Pallidoluysian atrophy Paraneoplastic encephalitis[27] Parkinsonism Postencephalitic parkinsonism Progressive multifocal leukoencephalopathy Progressive supranuclear palsy Schizencephaly Seizures (complex with partial symptomatology) Stiff-man syndrome Stroke Stupor Subarachnoid hemorrhage Subdural hematoma Substance intoxication (alcohol, disulfiram, organic fluorides, phencyclidine) Subthalamic mesencephalic tumor Surgical removal of cerebellar tumor Tay-Sachs disease Temporal lobe epilepsy Tuberous sclerosis Tumors (corpus callosum, glioma of third ventricle, supraventricular diffuse pinealoma) Vegetative state Von Economo encephalitis Wilson disease |
| Psychiatric conditions | Acute stress disorder Anorexia nervosa Autistic disorder[6] Brief reactive psychosis with catatonia Conversion disorder Hysteria Major depression, single episode with catatonic features Mood disorders Neuroleptic malignant syndrome[15] Posttraumatic stress disorder Schizophrenia Substance intoxication (3,4-methylenedioxymethamphetamine [ie, "ecstasy"], alcohol, amphetamine, phencyclidine, substance withdrawal, hypnotic-sedative, lorazepam) |
| Psychological factors | Immigration Experiencing rejection of an expression of love Visit to relative in another country |
| Medical conditions | Acquired immunodeficiency syndrome (AIDS) Acute intermittent porphyria Addison disease Bacterial septicemia Bronchorrhea Carcinoid tumors Diabetic ketoacidosis Encephalopathy (hepatic, HIV infection ? related, Wernicke) Fever of unknown cause Heat stroke Hepatic failure Hereditary coproporphyria Homocystinuria Hypercalcemia Hyperparathyroidism Hyperthyroidism Hyponatremia Hypothermia Intestinal atony Malaria Neuroleptic malignant syndrome[15] Poisoning (carbon monoxide, tetraethyl lead) Renal failure Substance intoxication (alcohol, cyclosporine, disulfiram, organic fluorides, phencyclidine) Syndrome of inappropriate antidiuretic hormone (SIADH) Syphilis Systemic lupus erythematosus Thermal injury Thrombotic thrombocytopenic purpura Tuberculosis Typhoid fever Uremia Von Economo encephalitis |
| Obstetric conditions | Hypopituitarism secondary to postpartum hemorrhage |
| *The administration of agents that block postsynaptic dopamine receptors is associated with the onset of catatonia in some individuals. | |
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