Brain, Vol. 125, No. 6, 1348-1357,
June 2002
© 2002 Guarantors of Brain
Generation of symptomatic palatal tremor is not correlated with inferior olivary hypertrophy
Departments of 1 Pathology and 2 Neurology, Research Institute for Brain and Blood Vessels-Akita and 3 Department of Neurological Science, Institute of Brain Science, Hirosaki University School of Medicine, Hirosaki, Japan
Correspondence to: Makoto Nishie, MD, Department of Neurological Science, Institute of Brain Science, Hirosaki University School of Medicine, 5 Zaifu-cho,Hirosaki, 036-8562, Japan E-mail: m-nishie{at}sd5.so-net.ne.jp
Although the generation of symptomatic palatal tremor (SPT) is thought to derive from the abnormal activity of hypertrophic inferior olivary neurones, the actual mechanism of SPT has not yet been elucidated. We therefore investigated the relationship between SPT and the pathological process of inferior olivary hypertrophy (IOH). We examined 16 autopsied subjects with cerebrovascular lesions of the dentate-olivary tracts. We analysed the size of the olives, the number of olivary neurones, synaptic, axonal and astrocytic changes in the olives and the clinical course in the subjects. SPT was observed in eight patients, in seven of whom it appeared 12 months after interruption of the afferents then progressed to reach a peak
12 years from the onset. SPT persisted for the rest of the subjects lives without decreasing in severity. Neuronal hypertrophic change began 2030 days after the onset of the causative lesions and reached maximum size, accompanied by prominent astrocytosis and synaptic and axonal remodelling, 67 months later. The number of olivary neurones decreased to <10% of that in controls in patients who survived >6 years. Despite the persistence of SPT, both the myelin and the axons of efferent fibres from olivary neurones were severely degenerated in patients who survived several years. Therefore, the appearance of SPT may depend on the hyperactivity of olivary neurones released from inhibitory inputs until the peak of both IOH and SPT. However, the persistence of peak intensity and distribution of established SPT is probably due to both the disturbance of natural rhythmicity in the body and the lack of feedback from the abnormal movement resulting from the dysfunction of the olive.
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
J. S. Kim, S. Y. Moon, K. -D. Choi, J. -H. Kim, and J. A. Sharpe Patterns of ocular oscillation in oculopalatal tremor: Imaging correlations Neurology, April 3, 2007; 68(14): 1128 - 1135. [Abstract] [Full Text] [PDF] |
||||
![]() |
Y. Yakushiji, R. Otsubo, T. Hayashi, K. Fukuchi, N. Yamada, Y. Hasegawa, and K. Minematsu Glucose utilization in the inferior cerebellar vermis and ocular myoclonus. Neurology, July 11, 2006; 67(1): 131 - 133. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Samuel, N. Torun, P. J. Tuite, J. A. Sharpe, and A. E. Lang Progressive ataxia and palatal tremor (PAPT): Clinical and MRI assessment with review of palatal tremors Brain, June 1, 2004; 127(6): 1252 - 1268. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. I. Seok, H. Yi, Y. M. Song, and W. Y. Lee Metronidazole-Induced Encephalopathy and Inferior Olivary Hypertrophy: Lesion Analysis With Diffusion-Weighted Imaging and Apparent Diffusion Coefficient Maps Arch Neurol, December 1, 2003; 60(12): 1796 - 1800. [Abstract] [Full Text] [PDF] |
||||


