Cases reported "Tremor"

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1/5. 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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keywords = olive
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2/5. 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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keywords = olive
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3/5. Palatal tremor of cortical origin presenting as epilepsia partialis continua.

    Palatal tremor (PT) is frequently caused by brainstem lesions. The inferior olive plays a major role in the pathophysiologic mechanisms involved. We report a case of PT of cortical origin presenting as epilepsia partialis continua. EEG showed continuous left frontocentral epileptiform discharges and both single photon emission computed tomography (SPECT) and positron emission tomography (PET) showed focal hypoperfusion and hypometabolism in the corresponding location.
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keywords = olive
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4/5. 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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keywords = olive
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5/5. Action palatal tremor in a patient with primary intestinal lymphoma.

    We report the case of a 59-year-old man with primary intestinal T-cell non-Hodgkin's lymphoma who developed abnormal facial twitching synchronous with small palatal movements induced by attempts at speaking or swallowing. At rest, the electromyogram (EMG) showed no spontaneous muscular activity. phonation triggered trains of synchronous, rhythmic EMG bursts at a frequency of 3-4 Hz lasting 10-20 s, with an average burst of 150 ms, which simultaneously involved palatal, facial, and neck muscles bilaterally with left-sided predominance. An enhanced blink reflex recovery curve was observed after stimulation of either side. Backaveraging electroencephalographic study revealed no activity that was time locked with the jerks. Axial T2-weighted magnetic resonance imaging showed an increased signal intensity and bilateral enlargement of the inferior olives. No antineuronal-specific antibodies were found in the blood or in the cerebrospinal fluid. All of these clinical findings were consistent with a symptomatic palatal tremor (PT). Because it was triggered by activation of cranial muscles, we termed this movement disorder action PT. To our knowledge, this is the first report of symptomatic PT displaying these features.
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keywords = olive
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