Abstract

Akathisia is frequently reported to be caused by neuroleptic drugs and sometimes by certain other agents such as fluoxetine. Benzodiazepines are a common treatment. The principal mechanism of akathisia is thought to be neurochemical, probably dopaminergic with serotonin also playing an important role. It is not usually thought to be related to benzodiazepine-caused disinhibition. Four episodes of atypical or paradoxical benzodiazepine-induced akathisia in three patients are reported and analyzed. All four episodes of akathisia were atypical because they were caused by clonazepam, clorazepate, or lorazepam. In one patient neither thiothixene nor lorazepam caused akathisia, but clonazepam and clorazepate did. In another patient both lorazepam and fluoxetine caused akathisia. It is also noted that all three patients had a history of traumatic brain injury and seizure disorder. The data support the hypothesis that atypical benzodiazepine-induced akathisia exists. Its mechanism may be different from neuroleptic-induced akathisia, but may still involve serotonergic systems or the forced normalization phenomenon. The similarity of these cases to reports of benzodiazepine-induced disinhibition raises the possibility that in some patients they may be the same entity.

Highlights

  • Akathisia, a combination of motor restlessness and psychic anxiety, is often reported after treatment with high potency neuroleptic drugs such as haloperidol and thiothixene and has other causes

  • We report four episodes of akathisia caused by clonazepam, clorazepate and lorazepam, benzodiazepine drugs, in three patients with traumatic encephalopathy and seizure disorders

  • It is noteworthy that the first patient did not experience cognitive or motor akathisia prior to or after the week of clonazepam even when she was on a potent neuroleptic

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Summary

INTRODUCTION

A combination of motor restlessness and psychic anxiety, is often reported after treatment with high potency neuroleptic drugs such as haloperidol and thiothixene and has other causes. We report four episodes of akathisia caused by clonazepam, clorazepate and lorazepam, benzodiazepine drugs, in three patients with traumatic encephalopathy and seizure disorders. The patient's psychotic symptoms responded well to this approach but she reported sedation and mild cognitive impairment from the thiothixene. Lorazepam was restarted at 1.5 mg/day, and subsequently gradually increased to 9 mg/day At that dose she reported almost complete symptom control, once again without any akathisia. Both these symptoms resolved if she self-medicated with additional lorazepam She suffered from akathisia and increased visual hallucinations and paranoia. She reported that the clorazepate activated and agitated her.

His seizures had been difficult to control on tegretol and
DISCUSSION
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