Dados do Trabalho

Título

Lamotrigine-Induced Tic Disorder: case report and review of literature

Apresentação do caso

A 17 y/o male patient, with history of prematurity (GA: 27 weeks, twin pregnancy) with periventricular hemorrhage, congenital toxoplasmosis, hydrocephalus requiring ventriculoperitoneal shunting at 4 months of age. Family history is unremarkable for neurological disorders. His epileptic seizures started at 9 months of age as infantile spasms (West Syndrome), which evolved into other seizure types typical of Lennox-Gastaut Syndrome. He evolved with cerebral palsy and intellectual disability and he received continued rehabilitation services. Brain MRI showed right subinsular and basal ganglia gliosis, and dysgenesis of the corpus callosum. At age of 17 yrs, after failing numerous antiseizure medicines (ASM), he was taking valproate 500mg b.i.d. and nitrazepam 10mg t.i.d. To improve seizure control, lamotrigine (LTG) was added with gradual increase in 6 weeks to 100mg/day. After one week achieving target dose he developed complex motor and vocal tics in addition to worsening of speech. LTG was gradually withdrawn with recovery of speech and great improvement of tics, and he started ketogenic diet.

Discussão

Motor tics are rapid, brief, and recurrent movements, while phonic tics are vocalizations of sounds or words usually preceded by an urge and followed by a temporary sense of relief. Tics are rarely related to the use of ASM, however, when present, are often associated with carbamazepine and LTG, among others such as phenobarbital and phenytoin. This adverse drug reaction (ADR) is scarce in literature. In a recent review, it was observed in 1.3% of the cases and all of them were related to preexisting cerebral structural abnormalities. It is believed that LTG, through its negative presynaptic modulation of glutamate release, may lead to increased dopaminergic transmission in the striatum, inducing the manifestation of tics. Some authors consider that patients who were previously affected by tics or with a genetic predisposition or with basal nuclei circuitry dysfunction would be the most affected. These tics usually begin in 4-10 months after starting ASM and persist throughout treatment. In contrast, in our case the tics started in about 1.5 month after beginning LTG.

Comentários finais

The occurrence of tics as ADR, although rare, is important to anticipate when prescribing LTG for patients with preexisting cerebral structural disease. In most cases reported to date, tics improved or resolved completely with dose reduction or withdrawal of LTG.

Área

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