The Neurologist 2016;21:32-33)T he etiology of chorea is heterogeneous, 1 however, chorea associated with chronic subdural hematoma (SDH) is rare. [2][3][4][5] We report a patient with bilateral chorea associated with chronic SDH which was surgically treated.
CASE REPORTA 76-year-old woman with previous history of seronegative rheumatoid arthritis treated with hydroxychloroquine was admitted later, with the onset about a month earlier of bilateral involuntary movements and mental confusion. Initially, the patient showed especially fidgeting and irritability that preceded the development of the movement disorders. With time, chorea highlights with hyperkinetic movements, such as myoclonic jerks and dystonia at the head, first left upper and lower limb and then in all extremities. Objective neurological examination performed at the admission in our department showed a good state of space-time orientation, good ability to perform calculations, and no praxis disorders. However, in about a month, we observed severe axial choreic involuntary movements, first left upper and lower limb and then in all 4 limbs. Brain computed tomography (CT) scan showed the presence of a layer of subdural chronic-type hematoma with contralateral shift of the midline of about 12 mm with slight herniation of the right cerebellar tonsil in the right frontotemporoparietal cortex (Fig. 1). One day later she underwent a small temporoparietal craniotomy, incision of the dura mater with blood leakage at high pressure. At the end of surgery, progressive reexpansion of the brain was rapidly highlighted. Within a few days, involuntary movements were completely regressed to achieve a complete normalization of the clinical neurological examination. Another brain CT scan performed 1 month later was normal (Fig. 2).
DISCUSSIONThe presence of choreic syndrome secondary to an SDH is rare but not that uncommon. It is possible that the cause is the high-pressure load to the basal nuclei in a possible anomaly of neurotransmitters and possibly also because of transient ischemia that the high hematoma pressure may cause. 4,6-9 In fact the high pressure may lead to a severe compression and distortion of the encephalon and subcortical structures, in particular, the caudate.The mechanism responsible of parkinsonism in chronic SDH patients is not well understood. Various hypotheses may be argued including mechanical pressure on the basal ganglia, either directly from the overlying hematoma or indirectly by torsion or displacement of the brain structure 10 ; midbrain compression caused by the uncal herniation through the tentorial notch 11 ; decreased number of dopaminergic receptors in the striatum secondary to mechanical pressure 12 ; and finally, circulatory disorders within the basal ganglia as a consequence of displacement and compression of the anterior choroidal artery. 4 FIGURE 1. First brain computed tomography. FIGURE 2. Second brain computed tomography.From the