Hemichorea and striatal infarction

We present two cases of hemichorea associated with an arterial ischaemic stroke in the controlateral striatum and we reviewed 28 similar cases in the literature. The pathogenesis of this movement disorder involves the gabaergic and enkephalinergic neurons of the striatal matrice which mainly projects on the external globus pallidus. A destruction of the striatal neurons of the indirect striato-thalamo-cortical ways may reduce their inhibitory out flow on normal inhibited thalamic and cortical structures and then create abnormal choreiform movements. The scarcity of this phenomenon can be explained by: 1) the repartition of the enkephalinergic local circuit neurons which represent but one third of the motor striatal neuronal population; 2) the type of vascularisation which often involves larger territories in the striatum and the globus pallidus or the anterior limb of the internal capsule. These abnormal movements are often transient because of the regulation of accessory striato-nigro-striatal, cortico-striato-nigro-thalamo-cortical and cortico-luysin circuits. More over, because these hypotheses and after having reviewed all such cases in literature, choreic movements to pure thalamic involvement are to be questioned.