Cases reported "Tremor"

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1/68. Function of the cerebellum in Parkinsonian rest tremor and Holmes' tremor.

    We describe a patient who developed Parkinson's disease (PD) 17 years after resection of his right cerebellum because of a Lindau tumor. He showed a classic 4.3-Hz resting tremor on the left side but a 3.1-Hz resting, postural, and intention tremor on the right side compatible with midbrain tremor (Holmes' tremor). We conclude that the generator of the tremor in PD cannot be located within the olivocerebellar loop. The cerebellum, however, seems to modulate the tremor frequency of parkinsonian rest tremor and may prevent the rest tremor from transforming into a postural and goal-directed tremor.
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2/68. 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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3/68. Posteroventral pallidotomy for midbrain tremor after a pontine hemorrhage. Case report.

    This 49-year-old man gradually developed a disabling action tremor in the proximal right upper extremity 8 months after suffering a pontine tegmental hemorrhage. The intraoperative microrecording in the nucleus ventralis intermedius (VIM) of the left thalamus revealed tremor-synchronous grouped discharges with a vigorous (2.7 Hz) action tremor predominantly in the shoulder and upper arm. High frequency electrical stimulation in the VIM did not affect the tremor. A posteroventral pallidotomy (PVP) was performed and resulted in the successful alleviation of all tremor activity. Posteroventral pallidotomy is known to alleviate parkinsonian tremors, especially those occurring in the contralateral lower extremity, trunk, and proximal segment of the contralateral upper extremity. The authors consider the pallidoreticular pathway to be an important tremor-mediating pathway for the proximal segment of the upper extremities and believe it can be controlled more effectively by PVP than by VIM thalamotomy, as demonstrated by the PVP-induced resolution of the midbrain tremor observed in this case.
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4/68. Childhood head tremor.

    We report here four children (three girls, one boy) with head tremor followed longitudinally, ages 15 months to 11 years, with follow-up over 1 to 8 years. Each demonstrated onset of head tremor between the ages of 5 and 10 months. In each case head tremor was characterized by a predominant "yes-yes" or "no-no" movement of the head. In two of the children the movement was slightly skewed with chin movement toward the shoulder. Oscillations were at a frequency of about 1 to 2 Hz. They were accentuated when sitting upright without head support, increased at times of movement, and dissipated while lying flat or sleeping. The children were unable to voluntarily suppress the action and did not experience any sensation of movement. Three of the children had shuddering spells prior to onset of head tremor. Two children have developed mild dystonic posturing of the legs when intently concentrating. Their general and neurologic examinations were normal. Normal investigations included brain magnetic resonance imaging and computed tomography, urine amino acids and organic acids screening, serum lactate, erythrocyte sedimentation rate, antinuclear antibodies, and ceruloplasmin and copper levels. A family history of tremor was present in two children, maternal epilepsy in one child, and infantile shuddering occurred in the father of one child. Therapy included trials of selective and nonselective beta-adrenergic blockers, alpha-adrenergic agonists, anticholinergics, anticonvulsants, and amantadine. One child responded well to both timolol and trihexyphenidyl. A second child responded moderately to primidone. Two have not been treated. Two have had head tremor spontaneously remit. We conclude from this small series of children with head tremor that it can evolve from a prior history of shuddering spells, occurs in the context of a positive family history of tremor, and can be accompanied by the development of a mild dystonia. Therapeutic response is variable to multiple agents. Spontaneous remission occurs, suggesting a benign course.
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5/68. Irregular jerky tremor, myoclonus, and thalamus: a study using low-frequency stimulation.

    High-frequency thalamic stimulation alleviates tremor in Parkinson's disease (PD) and essential tremor (ET). The origin of thalamic myoclonus is unexplained and the effects of low-frequency thalamic stimulation on movement control are still unknown. We studied the effects of stimulation at a low frequency of 15 Hz in five drug-free patients (3 PD, 2 ET) 6 months after thalamic implantation of quadripolar electrodes (unilateral in four patients, bilateral in one patient). Clinical, electrophysiological, and videotaped assessment, using a monopolar 15 Hz frequency (3 V, 90 micros) stimulation current applied simultaneously through two adjacent contacts of the electrode, was performed. We observed myoclonus and irregular jerky tremor in the upper limb contralateral to the site of stimulation. The jerks lasted less than 200 ms, were irregular and not synchronous with stimulation, were superimposed on rest or postural tremor, and increased in response to tactile, proprioceptive, or vibratory stimuli. The fact that this complex movement disorder can be induced by low-frequency stimulation in the ventral intermediate nucleus (Vim) of the thalamus suggests that it results, at least partly, from dysfunction of the Vim and possibly adjacent nuclei of the thalamus.
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6/68. The treatment of essential voice tremor with botulinum toxin A: a longitudinal case report.

    The purpose of this study was to evaluate the effects of bilateral botulinum toxin injection into the thyroarytenoid (TA) muscles of a patient with essential voice tremor. Acoustic and aerodynamic data were collected weekly over a 16-week period. Flexible nasolaryngoscopy was performed prior to injection and 2, 6, 10, and 16 weeks postinjection. Perceptual analyses of the acoustic and nasolaryngoscopic data were performed. A reduction in frequency tremor and, to a lesser extent, amplitude tremor was observed during the 1-10 week period. Estimated laryngeal resistance decreased after injection and was accompanied in perceptual measures by a reduction in vocal effort, laryngeal tremor, and supraglottic hyperfunction. Essential voice tremor can be successfully attenuated with bilateral percutaneous injection of botulinum toxin A into the vocalis muscle.
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7/68. dopamine deficiency in rubral tremor caused by midbrain hemangioma: case report.

    To elucidate the nigrostriatal involvement in rubral tremor, we studied single photon emission computed tomography (SPECT) imaging with [2-[[2-[[[3-(4-chlorophenyl)-8-methyl-8-azabicyclo[3.2.1]oct-2- yl]methyl](2-mercaptoethyl)amino]ethyl]amino]ethanethiolato(3-)- N2,N2',S2,S2']oxo-[1R-(exo-exo)]-[99mTc]technetium ([99mTc]TRODAT-1) in a 70-year-old woman with a midbrain hemangioma. She had developed a slow tremor in her right arm and leg after an episode of hemorrhage at the age of 28. The tremor was 3 to 5 Hz in frequency at rest, which was enhanced by outstretching the limb and action. There was no rigidity or bradykinesia. Neurological examination also revealed mild palsy of the left oculomotor nerve. The magnetic resonance imaging (MRI) of the brain showed a small hemangioma in the left midbrain localized mainly in the substantia nigra. The [99mTc]TRODAT-1 SPECT imaging revealed significantly reduced [99mTc]TRODAT-1 uptake in the left caudate and putamen, but it was only mildly reduced in the right striatum. This reduction in uptake was even more severe than that of patients with Parkinson's disease, and indicated that the dopamine function was markedly impaired in the left nigrostriatal system. The tremor had not progressed over the years, and she responded moderately to treatment with levodopa. We concluded that the rubral tremor in the right extremities was probably caused by a dopamine deficiency in the left nigrostriatal system. This suggests that a dopamine deficiency secondary to the midbrain hemangioma might have contributed to the development of the rubral tremor in this patient.
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8/68. Shuddering attacks-report of four children.

    Shuddering attacks are recognized as an uncommon benign disorder occurring during infancy or early childhood. It is necessary to distinguish these episodes from epileptic seizures. The attacks seem to involve shivering movements occurring daily for several seconds without impairment of consciousness. According to the criteria for benign myoclonus of early infancy, both shuddering attacks and benign myoclonus of early infancy should be regarded as having the same nosologic entity. I studied the pathophysiology of shuddering attacks in four children between 8 and 14 months of age using a video-electroencephalographic monitoring system. In one patient the frequency of shuddering movements, which was read as contamination of the electromyography on electroencephalography during attacks, seemed to be almost the same as that as of essential tremor. Shuddering attacks have decreased in number or disappeared in all four patients, but one exhibited mild abnormalities on magnetic resonance imaging and had relatives with epilepsy, and another had a flattened sella turcica. Although previous reports suggest that these movements are benign and needless investigations should be avoided, a problem related to the development of the nervous system may be present in children with shuddering attacks.
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9/68. Thalamotomy caused by cardioversion in a patient treated with deep brain stimulation.

    deep brain stimulation (DBS) has been applied mainly for the treatment of intractable pain and involuntary movement disorders. Based on the rising numbers of patients undergoing DBS therapy, the possibility of emergent application of cardioversion for the treatment of occasional severe arrhythmia in DBS patients has also increased. However, there has been insufficient discussion about cardioversion in DBS patients. We employed a radiofrequency receiver that transmits to the brain impulses provided by an external generator through an antenna applied to the skin in front of the receiver. We experienced a patient who displayed almost complete cessation of his action tremor with thalamic stimulation. He also developed central dysesthetic pain and showed complete disappearance of his action tremor, even without stimulation, following successful application of cardioversion. It is considered that slight changes in the high-voltage electrical current or high-voltage electrical current spread induced central dysesthetic pain and almost identical effects to thalamotomy. We report for the first time a case of thalamotomy induced by cardioversion in a DBS patient. Clearly, we need to bear in mind that cardioversion has the capability to cause brain lesions in DBS patients with a radiofrequency receiver implanted subcutaneously at the anterior chest wall.
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10/68. Deep brain stimulator electrodes used for lesioning: proof of principle.

    OBJECTIVE: patients with chronically implanted deep brain stimulator (DBS) electrodes can encounter complications requiring hardware removal. We assessed the safety and efficacy of using implanted DBS electrodes to create a therapeutic lesion before their removal. methods: Revision or removal of the DBS electrodes was required in two patients who had previously undergone DBS implantation. We conducted a series of in vitro experiments to confirm that the DBS electrodes could be used to generate radiofrequency lesions and to assess the relationship between radiofrequency parameters and lesion size. With this information, and with the approval of the hospital ethical review board, implanted electrodes were used to create incremental radiofrequency lesions in the thalamus in one patient and in the subthalamic nucleus in another. The procedures were performed under local anesthesia with contiguous contacts of the DBS lead connected to the active and reference sites of the RF generator to create a bipolar lesion. RESULTS: A 51-year-old man with essential tremor and a thalamic DBS required repeated battery changes secondary to tolerance and high voltage demands. Rather than replacing the battery, a radiofrequency thalamotomy was performed by using the existing left DBS electrode. At the 6-month follow-up examination, successful lesioning provided near complete tremor control. A second patient, a 50-year-old man with Parkinson's disease who had undergone bilateral subthalamic deep brain stimulation, developed skin erosion over the DBS hardware. A subthalamic nucleus lesion was made through the right DBS electrode. Lesion position and size were confirmed with magnetic resonance imaging. CONCLUSION: Lesions can be made through chronically implanted DBS electrodes in a safe, graded fashion and can produce therapeutic benefit.
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