J. Rosenbluth et al., EFFECTS OF CEREBELLAR LESIONS ON TONIC SEIZURES, TREMOR AND LIFE-SPANIN MYELIN-DEFICIENT RATS, Brain research, 650(1), 1994, pp. 85-92
In common with other dysmyelinating mutants, the myelin-deficient rat
displays an action tremor and tonic seizures culminating in the death
of the animals at similar to 23-26 days. We find that deep lesions of
the cerebellar vermis alleviate the manifestations of the myelin defic
iency significantly. Such lesions introduced at 20 days or later elimi
nate both tremor and seizures for periods up to 10 days. Lifespan is p
rolonged to nearly 30 days, on average, and to 35 days in some cases.
Shallow lesions of the vermis or lateral lobe lesions have relatively
little effect. Based on these observations we suggest that the cerebel
lum contributes not only to the action tremor but also to the tonic se
izures characteristic of central myelin deficiency. Spontaneous activi
ty originating in myelin-deficient fiber tracts may be carried to the
cerebellum and processed there to produce a highly amplified and/or sy
nchronized output to broad areas of the neuraxis. Deep lesions of the
vermis presumably interfere with cerebellar output and compromise the
cerebellar contribution to the seizures. Tonic seizures and other 'par
oxysmal attacks' also occur commonly in human demyelinating diseases i
ncluding multiple sclerosis [11]. Manipulation of cerebellar output of
fers a potential approach to the control of such spontaneous activity.