Abstracts

Rationale: The development of abnormal involuntary movements is infrequent and an under-reported side effect of certain anti-epileptic drugs (AED). Potential pathologic mechanisms vary with the responsible AED and for the most part are unknown. This study describes two patients who developed hyperkinetic movements shortly after addition of a first generation AED in an adult and a newer generation AED in a child.Methods: Description of two patients who developed abnormal movements and underwent assessment with continuous video-EEG monitoring (cEEG). The first patient is a 68 year old man with history of idiopathic Parkinson s disease who was transferred to our institution from a nursing home due to sudden onset of abnormal movements two weeks after initiation of levetiracetam followed by the addition of phenytoin. The second case is a 3 year old child with trisomy 21 and history of infantile spasms who was admitted with sudden onset movements after reinitiating vigabatrin. Results: The first patient was diagnosed 2 weeks prior to the onset of abnormal movements with focal onset seizures and levetiracetam therapy was initiated. He was observed on cEEG to have sub-clinical seizures which prompted the addition of phenytoin with subsequent resolution of the seizures. However, he developed repetitive facial grimacing, dystonic oral puckering, blepharospasm and right upper extremity dystonia, none of which had EEG correlate. The patient s movements subsided within a week after tapered discontinuation of phenytoin. The second patient had exhausted his vigabatrin supply and was managed with clonazepam for two weeks prior to presentation. Vigabatrin was restarted and within 24 hours, the child began having abnormal movements characterized as generalized chorea, lip smacking, blepharospasm, and facial spasms. An MRI of the brain was negative for any structural or new lesions. He underwent cEEG that demonstrated no electrographic ictal correlate with his movements. The child was weaned off vigabatrin. Although there has been attenuation, his movements have persisted at 4 months follow up. Conclusions: These two cases suggest that patients with underlying central nervous system pathology are prone to developing AED associated abnormal movements. This type of side effect can increase healthcare utilization. Treating physicians should be aware of this potential consequence when starting certain AED. Educating patients and caregivers can facilitate early detection and reporting of drug-induced abnormal movements.