Cases reported "Hypertrophy"

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1/9. Natural course of combined limb and palatal tremor caused by cerebellar-brain stem infarction.

    After infarction of the left superior cerebellar peduncle and dentate nucleus, a patient developed tremor of the left upper limb beginning on the twelfth day followed by palatal tremor appearing 10 months after infarction. Surface electromyogram revealed a difference in the frequency of the tremor in the upper limb and soft palate. When the palatal tremor appeared, brain magnetic resonance T2-weighted images revealed high signal intensity of the contralateral, right inferior olivary nucleus. Subsequently, when the amplitude of palatal tremor became less severe, the high olivary signal intensity subsided whereas the hypertrophy of the nucleus remained. This patient provides useful information on the pathogenesis of skeletal and palatal tremor with brain stem or cerebellar lesions based on the differences in the onset and frequency of tremors and morphologic changes in the inferior olive.
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2/9. Limb myorhythmia in association with hypertrophy of the inferior olive: report of two cases.

    We report on 2 patients who uncommonly developed isolated limb myorhythmia in association with inferior olive hypertrophy (IOH) after an acute stroke in the brain stem. A slow tremor presented in the proximal upper limbs predominantly when at rest. It was aggravated by outstretched arms and by active hand movements. The surface electromyogram (EMG) recorded simultaneous activities over the agonist and antagonist muscles with a rate of 3.5 Hz and 2.5 Hz in 2 patients respectively. In the first patient, bilateral limb myorhythmia presented 12 months after the brain stem stroke, and both inferior olives were hypertrophic. In the second patient, unilateral limb myorhythmia developed in the left hand 7 months after right pontine hemorrhage, and only the right inferior olive was hypertrophic. These findings indicate that limb myorhythmia commencing after brain stem insult is anatomically and temporally related to hypertrophy of the contralateral inferior olive. Based on our 2 patients and previously reported cases, we propose that a possible causal relationship exists between limb myorhythmia and contralateral IOH, although its pathophysiological mechanisms remain to be established. We suggest that, similar to palatal myoclonus, isolated limb myorhythmia is within the clinical spectrum of IOH.
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3/9. Palatal myoclonus and inferior olivary lesions: MRI-pathologic correlation.

    In a patient with palatal myoclonus, MR imaging demonstrated bilateral hyperintense lesions in the ventral part of the medulla. Microscopic examination of the inferior olives showed gliosis, enlargement and vacuolation of the neurons, and demyelinization.
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4/9. Progressive supranuclear palsy with hypertrophy of the olives. An immunocytochemical study of the cytoskeleton of argyrophilic neurons.

    In a patient with progressive supranuclear palsy (PSP) and hypertrophy of the olives, neurons with different forms of argyrophilic degeneration were detected by means of Bodian's silver staining method, i.e., neurofibrillary tangle-bearing neurons in the basal ganglia and brain stem, ballooned argyrophilic neurons in the brain stem, and hypertrophied neurons in the olives. In these cells, the cytoskeleton was investigated to ascertain whether neurons with different cytoskeletal changes contained phosphorylated neurofilaments (P-Nf) in the perikaryon. This study, carried out using two monoclonal antibodies that recognize phosphorylated epitopes of the neurofilament high molecular weight subunits, showed that hypertrophied olivary neurons, most ballooned neurons and a small aliquot of tangle-bearing neurons were labelled. The immunostaining of hypertrophied and ballooned neurons was localized in the whole perikaryon and dendrites, whereas that of tangle-bearing neurons was confined to the tangle. These findings were reproduced in five additional patients (one with hypertrophy of the olives, four with PSP) and demonstrated that, in PSP, the mechanism responsible for tangle formation does not affect the ability of neurons to accumulate P-Nf. This fact suggested that perikaryonal P-Nf accumulation is likely to be part of the cell reaction to abnormal conditions affecting the neuronal cytoskeleton.
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5/9. hypertrophy of the inferior olivary nucleus. A clinico-pathological observation.

    The clinico-pathological findings in a 61-year-old man, who suffered from branchial and skeletal myoclonus, appearing six months after a brainstem infarction are reported. Of all the drugs which are usually thought to be effective in the treatment of myoclonus, only valproic acid brought some relief. The necropsy revealed bilateral hypertrophy of the olives, together with bilateral pontine tegmental and rubral infarctions, without involvement of the olivary pathway.
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6/9. hypertrophy of the olivary nucleus. An ultrastructural study.

    The fine structure of the hypertrophic olive is reported in a case of progressive supranuclear palsy, the cause of which would be attributed to extensive symmetrical lesions in the dentate nuclei of the cerebellum and central tegmental tracts of the pons. Ultrastructurally, the enlarged neurons and their processes showed massive aggregations of neurofilaments, large accumulations of concentric laminated bodies, and occasional abnormal neurofibers (paired helical filaments and straight tubules). Their implications are briefly discussed in relation to olivary hypertrophy. Eosinophilic globules were seen in a neuron. Glomeruloid bodies were not seen.
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7/9. Unilateral symptomatic palatal myoclonus: MRI evidence of contralateral inferior olivary lesion.

    Symptomatic palatal myoclonus is a rare syndrome of segmental myoclonus which is thought to occur after damage to certain brainstem or cerebellar structures. We report two patients with unilateral PM, who showed hypertrophy of the inferior olivary nucleus on magnetic resonance imaging. In the first patient this was due to a left pontine tegmental hemorrhage, and a right-sided oculo-palato-facial myoclonus developed one month after the episode. The second one had a basilar artery occlusion with ischemic infarcts at the basis pontis, dorso-lateral aspects of the left pons, and left cerebellar dentate nucleus, as well as the occipital lobe. A delayed left oculopalatal myoclonus was recognized 3 months later. Interruption of the "dentato-rubro-olivary pathway" by the lesion with ensuing neuronal loss, cytoplasmic vacuolation, and astrocytic proliferation in the inferior olive, together with an increase of water content as mobile proton may cause the MR signal abnormalities in patients with unilateral symptomatic palatal myoclonus.
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8/9. Post-traumatic segmental myoclonus associated with bilateral olivary hypertrophy.

    We present clinical and magnetic resonance (MR) findings in three patients with segmental myoclonia occurring 11-18 months after severe brainstem injury. Palatal myoclonus and vertical ocular myorhythmia were present in all three patients and synchronous involuntary movements of the upper extremities ("wing beating") in two patients. MR-imaging showed multiple post-traumatic lesions within the dentato-rubro-olivary pathway ("myoclonic triangle"), associated with bilateral enlargement and increased signal intensity of the inferior olives. The signal abnormality was more prominent on proton density weighted images than on T2-weighted images, suggesting underlying pathological changes different from typical gliosis.
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9/9. Midbrain tremor and hypertrophic olivary degeneration after pontine hemorrhage.

    A severe rest tremor arose in a patient's right arm 9 months after a pontine tegmental hemorrhage. Magnetic resonance studies at 4 and 10 months showed residual hemosiderin in the pons and increasing hypertrophic olivary degeneration (HOD) affecting primarily the left olive. The tremor was refractory to pharmacotherapy (clonazepam, propranolol, and levodopa), but was reduced after implantation of a thalamic stimulator device. Although pontine hemorrhage is among several common causes of HOD, it has not previously been appreciated as a cause of midbrain ("rubral") tremor. A disynaptic dentatorubroolivary tract associated with tremor and monosynaptic dentatoolivary tract associated with HOD may both be components of the rubroolivocerebellorubral loop implicated in midbrain tremor. Their proximity makes the combination of tremor and HOD after pontine tegmental damage plausible and even likely.
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