Catatonia

Rebekah Jakel MD PhD (Dr. Jakel of Duke University has no relevant financial relationships to disclose.)
Mark A Stacy MD (Dr. Stacy of Duke University Medical Center received research support from Parkinson Study Group and consultation fees from Allergan, Eli Lilly, Merz, and Osmotica.)
Joseph Jankovic MD, editor. (Dr. Jankovic, Director of the Parkinson's Disease Center and Movement Disorders Clinic at Baylor College of Medicine, received research funding from Allergan, Allon, Ceregene, Chelsea, EMD Serono, Impax, Ipsen, Lundbeck, Medtronic, Merz, and Teva, and compensation for his services as a consultant or an advisory committee member by Allergan, Auspex, EMD Serono, Lundbeck, Merz, Neurocrine Biosciences, and Teva.)
Originally released January 10, 1995; last updated November 17, 2016; expires November 17, 2019

This article includes discussion of catatonia and Gjessing syndrome. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.

Overview

Catatonia is a complex syndrome that has undergone considerable evolution since it was initially described as a type of schizophrenia. This condition is now thought to result from a number of medical and psychiatric conditions and is 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. In this updated summary, current data regarding pharmacologic treatments that alter the GABA/glutamate balance other than benzodiazepines are discussed.

Key points

 

• Catatonia is a constellation of symptoms, or a syndrome, characterized by motor manifestations and mental status changes, including hyperreflexia, immobility, negativism, mutism, and withdrawal.

 

• Catatonia can be associated with a psychiatric condition, such as schizophrenia or an affective disorder, or it can be associated with a wide array of medical illnesses.

 

• 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.

 

• Studies of families with inherited vulnerability to catatonia have identified possible loci of interest on chromosomes 15q15 and 22q13.

 

• Catatonia is primarily treated by addressing the underlying medical condition and with benzodiazepines or electroconvulsive therapy.

 

• 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" (Gelenberg 1976). Kraepelin later suggested that catatonia should be classified phenomenologically, with the other forms of dementia praecox: hebephrenia and paranoia (Fein and McGrath 1990). Bleuler's work resulted in the term "catatonia," which became synonymous with behavioral immobility and withdrawal, a symptom often linked to schizophrenia (Joseph 1992).

In the mid-1970s, investigators reemphasized the association of catatonia with affective disorders, as well as an idiopathic or primary disorder (Abrams and Taylor 1976; Gelenberg 1976; Benegal et al 1993; Peralta et al 1997). Furthermore, there was increasing recognition of “secondary” catatonia, which develops in association with organic causes such as neurologic disease (including tumors), drug intoxication, and other metabolic disorders (including paraneoplastic syndromes) (Carroll et al 1994; Arora and Praharaj 2007; Kaestner et al 2007). Finally, 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 (Philbrick and Rummans 1994). On a broader scale, catatonia has been linked to other neuropsychiatric syndromes such as delirium, serotonin syndrome, and neuroleptic malignant syndrome (Anderson 1991; White and Robins 1991; Joseph 1992; Van Den Eede and Sabre 2004; Fink and Taylor 2006; Petho et al 2008; Fink and Taylor 2009; Ungvari et al 2009; Lee 2010). In a review, Wijemanne and Jankovic emphasized 2 subtypes of this disorder (Wijemanne and Jankovic 2015). 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 (Stober et al 2000).

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