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The Journal of Neurophysiology Vol. 87 No. 4 April 2002, pp. 2084-2094
Copyright ©2002 by the American Physiological Society

Departments of Neurosurgery and Neurology, Johns Hopkins Hospital, Baltimore, Maryland 21278-7713
Lenz, F. A.,
C. J. Jaeger,
M. S. Seike,
Y. C. Lin, and
S. G. Reich.
Single-Neuron Analysis of Human Thalamus in Patients With
Intention Tremor and Other Clinical Signs of Cerebellar Disease. J. Neurophysiol. 87: 2084-2094, 2002. Tremor that occurs as a result of a cerebellar lesion,
cerebellar tremor, is characteristically an intention tremor. Thalamic activity may be related to cerebellar tremor because transmission of
some cerebellar efferent signals occurs via the thalamus and cortex to
the periphery. We have now studied thalamic neuronal activity in a
cerebellar relay nucleus (ventral intermediate
Vim) and a pallidal
relay nucleus (ventralis oral posterior
Vop) during thalamotomy in
patients with intention tremor and other clinical signs of cerebellar
disease (tremor patients). The activity of single neurons and the
simultaneous electromyographic (EMG) activity of the contralateral
upper extremity in tremor patients performing a pointing task were
analyzed by spectral cross-correlation analysis. EMG spectra during
intention tremor often showed peaks of activity in the tremor-frequency
range (1.9-5.8 Hz). There were significant differences in thalamic
neuronal activity between tremor patients and controls. Neurons in Vim
and Vop had significantly lower firing rates in tremor patients than in
patients undergoing thalamic surgery for pain (pain controls). Other
studies have shown that inputs to Vim from the cerebellum are
transmitted through excitatory connections. Therefore the present
results suggest that tremor in these tremor patients is associated with
deafferentation of the thalamus from cerebellar efferent pathways. The
thalamic X EMG cross-correlation functions were studied for cells
located in Vim and Vop. Neuronal and EMG activity were as likely to be significantly correlated for cells in Vim as for those in Vop. Cells in
Vim were more likely to have a phase lag relative to EMG than were
cells in Vop. In monkeys, cells in the cerebellar relay nucleus of the
thalamus, corresponding to Vim, are reported to lead movement during
active oscillations at the wrist. In view of these monkey studies, the
present results suggest that cells in Vim are deafferented and have a
phase lag relative to tremor that is not found in normal active
oscillations. The difference in phase of thalamic spike X EMG activity
between Vim and Vop may contribute to tremor because lesions of
pallidum or Vop are reported to relieve cerebellar tremor.

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