Several evidences indicate that the basal ganglia may process sensory information to control movements. Motor impairment in PI) hus been in part related to deficits in the use of sensory information. In lliis regard. SHP studies from upper limb in PD have provided conflicting refills about the involvement of specific cortical responses (i.e. the frontal N il) potential which is thought to originate in SMA). Moreover, there arc no reports concerning cortical SEPs to lower limb stimulation in PI). We studied cortical SEPs to libial nerve stimulation in 14 patients affected by PI) with akinetic-rigid syndrome using multiple scalp recording electrodes. Median nerve SEPs were also evaluated in all patients. Tibial nerve cortical SEPs were altered in 11 out of 14 patients. In V out of 10 patients with bilateral akinetic-rigid syndrome SEP abnormalities were bilateral: in 2 out of 4 patients with predominant unilateral signs SEP abnormalities were bilateral in 1 patient and ipsilateral to motor impairment in the other one. Abnormalities of tibial nerve SEPs were characterized by a significant reduction in arnplitude of P.V7-N50 complex recorded over the vertex without involvement of the contralateral N37-P50 complex. Median nerve N30 frontal potential was abnormal in 5 out of 11 patients with tibial nerve SEP abnormalities. The selective attenuation of tibial nerve cortical SEPs in PI) suggests that the dysfunction of basal ganglia circuitry might interfere with sensory input processing along specific thaîamo-cortical projections. These data suggest that SEP recording procedure might be a useful loo! for diagnosing and monitoring therapeutic response in PD.
|Number of pages||1|
|Journal||Italian Journal of Neurological Sciences|
|Publication status||Published - 1997|
ASJC Scopus subject areas
- Clinical Neurology