MOVEMENT-RELATED CORTICAL POTENTIALS PRECEDING SEQUENTIAL AND GOAL-DIRECTED FINGER AND ARM MOVEMENTS IN PATIENTS WITH CEREBELLAR ATROPHY

Citation
K. Wessel et al., MOVEMENT-RELATED CORTICAL POTENTIALS PRECEDING SEQUENTIAL AND GOAL-DIRECTED FINGER AND ARM MOVEMENTS IN PATIENTS WITH CEREBELLAR ATROPHY, Electroencephalography and clinical neurophysiology, 92(4), 1994, pp. 331-341
Citations number
56
Categorie Soggetti
Neurosciences
ISSN journal
00134694
Volume
92
Issue
4
Year of publication
1994
Pages
331 - 341
Database
ISI
SICI code
0013-4694(1994)92:4<331:MCPPSA>2.0.ZU;2-S
Abstract
To determine the influence of cerebellar involvement on the preparator y state of the cerebral cortex for voluntary movements, we studied the movement-related cortical potentials (Bereitschaftspotential, BP) pre ceding sequential and goal-directed finger and arm movements in patien ts with cerebellar atrophy (CA). The first task (paradigm 1) consisted of a sequential finger movement at a self-paced rate of every 3 sec o r longer, in which patients and control subjects pushed rapidly 7 keys on a keyboard in a sequence visually predetermined on a screen. The s econd task (paradigm 2) consisted of a goal-directed self-paced moveme nt with visual feedback on a screen. In both paradigms, control subjec ts and patients had distinct movement-related cortical potentials, but peak amplitudes (close to movement onset) were reduced in the patient group (paradigm 2), whereas in the overall analysis the mean amplitud e 600-800 msec before movement onset (NS1) was larger in the patient g roup (paradigms 1 and 2). Accordingly, the difference (NS2) between pe ak amplitude and NS1 was smaller in the patient group (paradigms 1 and 2). Whereas control subjects' peak amplitude (paradigm 2) and NS2 (pa radigm 1) were focused at Cz, this topographical differentiation was a bolished in the patient group. The onset of the BP was earlier in the patients than in the control subjects (paradigms 1 and 2). Our results suggest that pathways from the cerebellum to the cortex do play a rol e in generating movement-related cortical potentials. A strong input f rom the cerebellum seems to be crucial for the generation of a normal motor potential close to the movement onset, reflecting a specific def icit in patients with CA. Patients with CA may try to compensate for t heir motor deficits by a longer cortical activation preceding voluntar y movements (earlier onset of the BP). The increased NS1 could be the result of larger effort, by which patients try to compensate for their motor deficits as well.