Several additional syndromes show clinical overlap with catatonia. Like Fisher,4,10 we believe akinetic mutism, an extreme form of the abulic syndrome caused by neurological injury, to be a neurologic version of catatonia. Hypoactive delirium may overlap or coexist with catatonia. It is extremely important to confirm a delirious patient is not also suffering from a catatonic episode, because neuroleptics can worsen simple catatonia, resulting in malignant catatonia. Decreased eyeblink and resistance to eye and mouth opening may hint at a catatonia nested in delirium.
To assess catatonia, a few steps can be routinely followed (Table 3). Once the diagnosis of catatonia is made, a definable etiology must be sought. In addition to mood disorders and schizophrenia-spectrum disorders, catatonia can be seen in up to 20% of patients with autism-spectrum disorders. Case reports have described catatonia secondary to obsessive compulsive disorder, PTSD, and personality disorders.
Up to 50% of cases of catatonia may be due to a host of neuromedical syndromes. These include paraneoplastic and limbic encephalitidies (especially anti-NMDA receptor antibody encephalitis), ictal and post-ictal states, posterior reversible encephalopathy syndrome, and lupus. Substances associated with catatonia include dopamine-blocking agents, tacrolimus, disulfiram, and phencyclidine, among others. Finally, catatonia can occur as an isolated clinical syndrome without an obvious underlying cause; this phenomenon is known as recurrent idiopathic catatonia.
Management and treatment
With severe threat, challenges to brain function can emerge via circuit disconnection or modulatory dysfunction and result in catatonia. This view may underlie the effectiveness of benzodiazepine GABAA agonism, of NMDA-R antagonism, and of electroconvulsive therapy (ECT). These treatments show effects on GABA, dopamine, acetylcholine, and glutamate within cortico-striato-thalamo-cortical loops. (For an outline of a proposed catatonia treatment algorithm, please see Figure 2.)
All treatments for catatonia are off-label uses, as there is no FDA-approved drug indicated for catatonia. In 1983, lorazepam was described as a successful treatment for catatonia and later became the first-line treatment for the catatonic syndrome.11,12 A lorazepam challenge (using 2-mg intravenous [IV] lorazepam) can be a helpful diagnostic test. Although a negative response does not rule out catatonia, many patients will show improvement with a single dose. Following the challenge, a standing dose of 2 mg every 4 to 6 hours is typical; some patients may require titration to as much as 30 mg daily, especially in cases with malignant features.
Doses should be held only for respiratory depression due to oversedation and not for sedation alone, as the regularity of dosing is important for full lysis. IV lorazepam is preferred over other routes or benzodiazepine types because of its quick onset, preference for the GABA-A receptor, and long duration of effect.
Dr Beach is Assistant Professor of Psychiatry and Residency Training Director, Massachusetts General Hospital, Harvard Medical School; Dr Francis is Professor of Psychiatry, Associate Director of Residency Training, and Director of Neuromodulation Services, Penn State Medical School, Hershey Medical Center, Hershey, PA; Dr Fricchione is Professor of Psychiatry, Mind Body Medical Institute and Associate Chief of Psychiatry, Massachusettes General Hospital, Harvard Medical School, Boston, MA. Drs Fricchione and Beach have received funding through the David Judah Fund for catatonia research.
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