Once catatonia is recognized, the clinician should consider psychiatric catatonia as a matter of exclusion, especially with unfamiliar patients or new onset. A variety of systemic, neurologic, and toxic conditions may produce a catatonic syndrome. Catatonia arising from psychiatric illness and that secondary to general medical conditions or toxicities shows a similar pattern and severity of catatonic signs.25,26
The laboratory workup should vary based on clinical factors. Brain imaging is encouraged, since strokes, hematomas, and space-occupying lesions can all present with new-onset catatonia25,27,28 and such patients may worsen if exposed to prolonged treatment with benzodiazepines. Other tests to consider include blood chemistries, hematology, electroencephalography, toxicology, and possibly lumbar puncture. The scope of investigation will depend on the age of the patient, psychiatric history, severity and duration of the catatonic state, and the promptness of response to initial treatment.
No specific genetic, pathologic, neurochemical, or structural mechanisms have been elucidated in catatonia, although promising information is becoming available.
Familial clustering of catatonia suggests a genetic component that lacks classic Mendelian inheritance. For example, in a study of 25 catatonia patients, Barnes and colleagues4 found familial clustering in probands with overt psychiatric disorders as well as in patients whose catatonia appeared idiopathic or associated with a general medical condition. Molecular studies of periodic catatonia show familial aggregation and initial evidence for genetic linkage to chromosome 15.29
Neurochemical studies in catatonia have focussed primarily on dopamine(Drug information on dopamine) and -aminobutyric acid (GABA).30 Attention has been directed to these systems because of clinical similarities between catatonia and basal ganglia disorders in which these transmitters are implicated. In addition, effective biologic treatments, such as amobarbital(Drug information on amobarbital), benzodiazepines, and ECT, have direct or indirect actions on these neurochemical systems. Northoff30 found elevated levels of the dopamine metabolite homovanillic acid in a series of inpatients with catatonia, and higher levels predicted a positive initial response to lorazepam(Drug information on lorazepam) during the first 24-hour period of treatment. Anecdotal reports of a positive treatment response to zolpidem(Drug information on zolpidem), which shares strong GABA-A agonism with lorazepam, led Carroll31 to hypothesize a role for GABA-A receptor dysfunction in catatonia.
The treatment response in catatonia is typically one of complete resolution. Benzodiazepines and ECT are the most recommended modalities in current usage. Amobarbital has a longer history of clinical use, dating from the early 1930s. Only 1 randomized placebocontrolled double blind trial for initial treatment has been published.32 This study of 20 mute patients compared intravenous amobarbital with saline infusions in a crossover design. There was no change among 14 saline trials, but 10 of 20 patients responded to amobarbital (scores on a 5-point arousal scale improved 56% within 10 minutes).
In an open trial with 13 acute catatonic patients, Bush and colleagues20 reported that 2 mg of intravenous lorazepam reduced catatonia scores on the BFCRS by 60% within 10 minutes. Numerous case series and prospective open trials over the past 20 years with parenteral or oral benzodiazepines such as lorazepam show a response rate of 60% to 80% within hours or days, but there are no published randomized controlled trials for acute catatonia.33 Despite this, the consistent response in these studies along with extensive clinical experience has led to a consensus favoring benzodiazepines as initial treatment. A parenteral benzodiazepine challenge has been encouraged as initial treatment for catatonia.20,33