We present the case of an acute neurotoxic reaction with severe extrapyramidal features associated with commencement of citalopram in a patient without a prior history of Parkinson's disease or neuroleptic exposure.

A 77-year-old woman was admitted to a rural hospital with dehydration secondary to antibiotic-associated diarrhoea following treatment for a chest infection. Her past history included type two diabetes mellitus on insulin, a transient ischaemic attack, parotid carcinoma with left facial paralysis, ischaemic heart disease, atrial fibrillation, and mastectomy for breast carcinoma with resultant lymphoedema of her right upper limb.

There was no definite prior history of Parkinsonism but subtle extrapyramidal features were present on admission with reduced mobility, swallowing difficulty, psychomotor slowing, and increased tone with cogwheeling in the left upper limb. Modified Mini-Mental State examination revealed cognitive impairment with a score of 64/100. Medications on admission consisted of digoxin, enalapril, simvastatin, Penmix insulin, aspirin, and cefuroxime. She improved with rehydration with normal saline and cessation of her antibiotics.

Ten days after admission, she was commenced on citalopram10 mg daily for depressive symptoms. Over the next 4 days, she deteriorated significantly, with hypoactive delirium and markedly worsened extrapyramidal signs. She developed marked bradykinesia and rigidity of the limbs, associated with decreased coordination of swallowing, monosyllabic speech, and decreased self-cares. She was no longer able to follow requests.

She continued to deteriorate with decreased level of consciousness, increased rigidity with cogwheeling, and sustained clonus at the ankles with positive Babinski responses. There was no myoclonus, hyper-reflexia, fever, or autonomic dysfunction. Her citalopram was stopped 3 days after commencement. She was commenced on lorazepam for possible catatonia.

Investigations showed normal electrolytes and creatine kinase but mildly raised liver function tests. Full blood count and erythrocyte sedimentation rate were normal. C-reactive protein was 10 mg/L. She was transferred to a tertiary hospital for further investigation and treatment.

A magnetic resonance imaging (MRI) brain scan showed generalised cortical, posterior fossa, and brainstem atrophy with no sign of ischaemic or neoplastic processes or hydrocephalus. Lumbar puncture was attempted twice but was unsuccessful. Over the next 3 days she developed dystonic posturing of the upper limbs. She continued to have rigidity in both upper limbs. A psychiatry of the elderly specialist did not find any evidence to suggest major depression or catatonia, and the lorazepam was stopped 5 days after commencement. A normal electroencephalogram (EEG) excluded status epilepticus.

Over the following 7 days, the patient improved, becoming more communicative and alert. Tone remained increased in the upper limbs. She was commenced on levodopa, which had no noticeable effect. This was discontinued.

The patient was transferred back to the peripheral hospital 10 days later where she continued to recover over the next month becoming alert and orientated. She also communicated freely and was mobile with a low frame under supervision. She was noted to have persisting increased tone in the upper limbs, although this was improving. Unfortunately at this time (when she appeared to have returned almost to her pre-morbid level of functioning) she had an acute left middle cerebral artery infarct with a right hemiparesis and severe global aphasia. MRI scan confirmed a large left inter parietal/temporal lobe infarct.

Although extrapyramidal motor disorders are well reported with serotonin uptake inhibitors (SSRIs)1–4 there have been very few reports with citalopram5–7 being thought to have a low potential for extrapyramidal side effects.8 The extrapyramidal effects of SSRIs are thought secondary to an indirect modulatory effect of dopaminergic function through inhibitory serotonergic input.3

This appears to be a case of a neurotoxic reaction with severe extrapyramidal features (Parkinsonism and dystonia) and delirium probably resulting from citalopram. There were no other features to support serotonin syndrome. The relatively rapid onset of extrapyramidal symptoms following commencement of an SSRI is consistent with other reports.2–4 The patient may possibly have had pre-existing cerebral Lewy body disease, a condition in which toxic reactions to neuroleptic drugs (thought to involve brain dopaminergic/serotonergic dysfunction) are common.9

Clinicians need to be aware of possible extrapyramidal reactions from SSRIs, as early recognition and management is essential to prevent potentially significant adverse outcomes.