Orolingual Dyskinesia and Involuntary Neck Movements Caused by Phenytoin Intoxication

A widely-used antiepileptic drug, phenytoin has a number of well-observed and documented side effects when prescribed in toxic doses; these include dizziness, insomnia, meningeal irritation with pleocytosis, nystagmus, ophthalmoplegia, dysarthria, ataxia, and confusion. Besides these, various involuntary movements, such as tremor, asterixis, myoclonus, and dyskinesias have been reported in these patients so far.^1–3 Montenegro et al. identified one patient with axial and orofacial dyskinesia and two patients with choreoathetosis in a 1-year period, and literature shows that the main findings in phenytoin-intoxicated dyskinesic patients were choreoathetosis, dystonia, orofacial dyskinesia, and ballism, in decreasing order.⁴

In addition to phenytoin, other anticonvulsants that cause dyskinesia include carbamazepine, gabapentin, felbamate, and valproic acid.² The exact pathophysiology of the occurrence of involuntary movement in phenytoin intoxication is still obscure; however, the most likely mechanism seems to be a dopaminergic, cholinergic, and serotonergic imbalance within the basal ganglia system in these patients.^1–5

Brain damage has been shown to cause sensitization to the toxic effects of phenytoin.¹ Examples include bilateral striatal infarction, globus pallidus calcification, frontal abscess, serious head trauma, operated meningioma, parasagittal glioblastoma, subdural hematoma, and thalamic infarction.¹ After the diagnosis was made, withdrawal of the drug brought about complete disappearance of all the signs within a short time.

Although rarely seen, the occurrence of a new or the exacerbation of an existing movement disorder in a patient using phenytoin, regardless of serum phenytoin level, unless proven otherwise, should be evaluated as being caused by this drug, and treatment should be conducted accordingly.