Catatonia is a complex syndrome that has undergone considerable evolution since it was initially described as a subtype of schizophrenia. This condition is now thought to result from multiple medical and psychiatric conditions and may be more often linked to affective disorders than schizophrenia. Increasingly, early recognition is thought to be a good prognostic factor, and the diagnosis should be considered in patients who suddenly develop an acute to subacute change in behavior associated with hyperkinetic and hypokinetic movement disorders. Patients most often benefit from treatment with benzodiazepines or electroconvulsive therapy in addition to treatment of the underlying clinical condition; however, there is a paucity of randomized, controlled trials to guide therapeutics. In this updated article, current reports on the association of catatonia with SARS-CoV-2 (COVID-19) are discussed.
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• Catatonia is a constellation of symptoms, or a syndrome, characterized by motor manifestations and mental status changes, including posturing, hyperreflexia, immobility, negativism, mutism, and withdrawal.
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• Catatonia can be associated with psychiatric conditions, such as schizophrenia and affective disorders, or with a wide array of medical illnesses.
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• Imaging studies suggest that changes in cortical and basal ganglia structures are related to motor manifestations; multiple neurotransmitter systems are implicated and include GABAergic, dopaminergic, and glutamatergic pathways.
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• Studies of families with inherited vulnerability to catatonia have identified possible loci of interest on chromosomes 15q15 and 22q13.
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• Catatonia is primarily treated by addressing the underlying condition and with benzodiazepines or electroconvulsive therapy.
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• Pharmacotherapies that modulate the balance between excitatory and inhibitory pathways can be considered as alternative treatments when benzodiazepines or electroconvulsive therapy are not effective or accessible.
Historical note and terminology
Since its original description, catatonia has remained a poorly defined clinical condition that is characterized by disturbed motor behavior initially described in the presence of severe mental illness. In 1874, the term "catatonia" was coined by Kahlbaum to describe a syndrome "with a cyclic, alternating course in which mental symptoms are consecutively as follows: melancholy, mania, stupor, confusion, and eventually, dementia" (52). Kraepelin later suggested that catatonia should be classified phenomenologically with the other forms of dementia praecox: hebephrenia and paranoia (45). Bleuler's work resulted in the term "catatonia," which became synonymous with behavioral immobility and withdrawal, a symptom often linked to schizophrenia (67).
In the mid-1970s, investigators reemphasized the association of catatonia with affective disorders, as well as an idiopathic or primary disorder (01; 52; 17; 113). Furthermore, there was increasing recognition of “secondary” catatonia, which develops in association with organic causes such as neurologic disease (including tumors), drug intoxication or withdrawal, and other metabolic disorders, including paraneoplastic syndromes (27; 10; 69).
Malignant catatonia represents the most severe form of this syndrome and is more often seen in the presence of organic illness, illicit or therapeutic drug toxicity, or other metabolic encephalopathy (115). On a broader scale, catatonia has been linked to other neuropsychiatric syndromes such as delirium, serotonin syndrome, and neuroleptic malignant syndrome (09; 152; 67; 147; 46; 114; 47; 144; 79). In a review, Wijemanne and Jankovic emphasized 2 subtypes of this disorder (153). Malignant catatonia has a much poorer prognosis and is associated with rapid onset, fever, hypertension, and without the distinguishing features of involuntary movements, which is similar to neuroleptic malignant syndrome. Periodic catatonia is characterized by recurrent episodes of illness lasting 4 to 10 days that may occur over many years. This condition appears to be less frequent than the malignant form and has been reported as an autosomal dominant disorder linked to chromosome 15q15 (138).