Olanzepine-induced tardive dyskinesia

Tardive dyskinesia is a serious and common motor side-effect of treatment with traditional neuroleptics, with an unknown pathophysiological basis. It affects 20-30% of patients on long-term neuroleptic therapy, with elderly patients being at higher risk (American Psychiatric Association, 1994).

Olanzapine is an atypical antipsychotic agent with a reported lack of propensity to cause tardive dyskinesia (Beasley et al, 1999). Recently, it has been suggested that olanzapine can improve tardive dyskinesia in some patients (Littrell et al, 1998; Jaffe & Simpson, 1999). Other authors, however, have shown that the prolonged use of olanzapine can instead be associated with tardive dyskinesia/dystonia (Ananth & Kenan, 1999; Dunayevich & Strakowski, 1999). Here we report the case of a patient who experienced tardive dyskinesia after only few months of treatment with olanzapine.

A 62-year-old housewife with an unremarkable past medical history, sought out-patient treatment in June 2000 for anxiety, insomnia, difficulty thinking and concentrating, and frequent episodes of aggressive behaviour. She was evaluated by neurologists, and was submitted to routine biochemical investigations (unremarkable), a computerised tomography scan (normal), and the Mini-Mental State Examination (24/30). Olanzapine (10 mg/day) was started and this was the sole medication continued thereafter. The patient soon experienced a subjective improvement. Three to four months later she noticed slight involuntary movements of the tongue and jaw. Despite these symptoms, she continued taking olanzapine until it was eventually stopped 1.5 years later (December 2001).

She was admitted to our hospital in March 2002. On examination, she displayed marked and distressing involuntary movements of the tongue and jaw, grimacing, and mild choreic movements in the upper limbs. Extensive biochemical, neuropsychological and imaging work-up was negative. A diagnosis of drug-induced tardive dyskinesia was thus made, other causes of dyskinesia excluded and therapy with vitamin E, lorazepam and tiapride initiated.

In this case, the tardive dyskinesia was most likely a result of olanzapine administration. The age of the patient may have favoured the early appearance of involuntary movements after initiation of the therapy, even though olanzapine has been claimed to carry a low risk for tardive dyskinesia and other extrapyramidal symptoms (Beasley et al, 1999).

As olanzapine is increasingly being used in elderly subjects for behavioural disturbances and/or insomnia in the absence of psychosis, our report underlines the need for a careful assessment for tardive dyskinesia and other movement disorders in patients (and in particular elderly patients) taking this atypical neuroleptic.