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
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.