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
Pathophysiology/etiology
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 GABAA 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 25,13,15 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 ≥3 of the following core features8,15:
- 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.
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