LENTICULAR NUCLEUS LESION IN IDIOPATHIC DYSTONIA DETECTED BY TRANSCRANIAL SONOGRAPHY

We report the transcranial sonography (TCS) findings of the basal gang lia in 86 patients with dystonic disorders including idiopathic dyston ia (facial, cervical, upper limb, and generalized dystonia), drug-indu ced tardive dystonia, dopa-responsive dystonia, and kinesigenic dyston ia. The TCS was focused on alterations of the lenticular, caudate, rap he nuclei, and the thalamus. Seventy-five percent of patients with idi opathic cervical and 83% of those with idiopathic upper limb dystonia had a hyperechogenic lesion of the middle segment of the lenticular nu cleus on the side opposite to the clinical dystonic symptoms. The ipsi lateral side was also affected in 20%. In facial dystonia, only one-th ird of the patients revealed lenticular nucleus lesions. The mean area of the lenticular nucleus lesion opposite to the clinically affected side was 30 mm(2) in cervical dystonia, 17 mm(2) in upper limb dystoni a, and 7.5 mm(2) in facial dystonia. These lenticular abnormalities we re significantly more frequent (p < 0.001) and their areas were signif icantly greater (p < 0.001) compared with a control group of 50 patien ts afflicted with radiculopathy. There was a significant correlation o f the severity of symptoms with the intensity of lenticular nucleus hy perechogenicity in patients with cervical and upper limb dystonia (p < 0.05). Increased caudate nucleus echogenicity was present in 20% of p atients with cervical and upper limb dystonia, mostly contralateral to the clinically affected side, and raphe abnormalities were present in 7% of all patients with idiopathic dystonia. In contrast, there were no abnormalities of the lenticular nucleus or thalamus in nonidiopathi c dystonias. We conclude that idiopathic dystonia is associated with l esions in the basal ganglia, particularly the lenticular nucleus, that can be visualized by TCS. An alteration of the basal ganglia matrix m ay be the pathologic basis of idiopathic dystonia with secondary affli ction of striatopallidothalamic pathways.