Catatonia: Our current understanding of its diagnosis, treatment and pathophysiology

Abstract

Catatonia is a psychomotor syndrome that has been reported to occur in more than 10% of patients with acute psychiatric illnesses. Two subtypes of the syndrome have been identified. Catatonia of the retarded type is characterized by immobility, mutism, staring, rigidity, and a host of other clinical signs. Excited catatonia is a less common presentation in which patients develop prolonged periods of psychomotor agitation. Once thought to be a subtype of schizophrenia, catatonia is now recognized to occur with a broad spectrum of medical and psychiatric illnesses, particularly affective disorders. In many cases, the catatonia must be treated before any underlying conditions can be accurately diagnosed. Most patients with the syndrome respond rapidly to low-dose benzodiazepines, but electroconvulsive therapy is occasionally required. Patients with longstanding catatonia or a diagnosis of schizophrenia may be less likely to respond. The pathobiology of catatonia is poorly understood, although abnormalities in gamma-aminobutyric acid and glutamate signaling have been suggested as causative factors. Because catatonia is common, highly treatable, and associated with significant morbidity and mortality if left untreated, physicians should maintain a high level of suspicion for this complex clinical syndrome. Since 1989, we have systematically assessed patients presenting to our psychiatry service with signs of retarded catatonia. In this paper, we present a review of the current literature on catatonia along with findings from the 220 cases we have assessed and treated.

Pervasive refusal syndrome: systematic review of case reports

“…Authorities on the treatment of catatonia recommend incremental doses of lorazepam starting at 1-2 mg/day and gradually increasing up to (10-20 mg/day), and if there is no response, to administer between 10 and 20 sessions of bilateral ECT [9,15]. Rasmussen et al recommend using a smaller dose of lorazepam in young, elderly, or medically compromised patients [31]. In clinical practice, parenteral administration of lorazepam offers rapid response compared to oral administration [59].…”

Radiographic dose‐dependency study of loperamide effects on gastrointestinal motor function in the rat. Temporal relationship with nausea‐like behavior

“…Thus, only extremely high doses of loperamide might be able to induce catalepsy in laboratory animals. Interestingly, catalepsy occurs in catatonia, and, intriguingly, after excessive loperamide intake one patient developed severe catatonia that fully remitted with lorazepam …”

“…Catalepsy is characteristically induced by Thus, only extremely high doses of loperamide might be able to induce catalepsy in laboratory animals. Interestingly, catalepsy occurs in catatonia, 45 and, intriguingly, after excessive loperamide intake one patient developed severe catatonia that fully remitted with lorazepam. 46 Intraperitoneal morphine-induced mild hypothermia in mice, 35 and, in the context of surgical pain management, persistent hypothermia after intrathecal morphine (generally associated with sweating and nausea) may occur.…”

Catatonia and the immune system: a review

“…Patients treated with anti psychotics who have preexisting catatonia are at an increased risk of developing neuroleptic malignant syndrome compared with those who do not have catatonia (3·6% vs Series 0·07-1·8%). 28 Given that no clinical features exist that can reliably distinguish neuroleptic malignant syndrome from malignant catatonia, 29 some authors consider neuroleptic malignant syndrome to be a specific form of antipsychoticinduced malignant catatonia. 30 Residual cata tonia frequently remains after the resolution of the full syndrome of neuroleptic malignant syndrome.…”

“…Given that the disorder bears several similarities to catatonia, one author has suggested testing for GAD2 autoantibodies to distinguish between the two disorders. 28 The syndromes share immobility, an emotionless facial expression, and marked anxiety. Moreover, hypertonic episodes in stiff person syndrome can have psychological triggers.…”