Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperintense globus pallidus on T1-weighted MRI is present in most patients with advanced liver disease. We evaluated the relationship between the signal intensity of the globus pallidus and clinical or laboratory data of 77 patients eligible for liver transplantation. There was a significant correlation between the intensity of the signal and the Child-Pugh score (as indication of severity of liver disease), presence of postural tremor, previous episodes of variceal bleeding or hepatic encephalopathy, prothrombin activity, serum aspartate and alanine aminotransferase, bilirubin, and the indocyanine green (ICG) hepatic clearance, a very sensitive marker of liver function. The multivariate analysis disclosed that the ICG hepatic clearance and previous episodes of variceal bleeding were independently associated with the signal intensity in the globus pallidus. MRI repeated in 21 patients 10 to 20 months after transplant showed a disappearance of the lesion in all cases. We conclude that the hyperintense globus pallidus is secondary to the severity of the liver disease, and is reversible when liver function returns to normal.
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PMID:Hyperintense globus pallidus on T1-weighted MRI in cirrhotic patients is associated with severity of liver failure. 842 13

We report on four patients with unilateral tremor stemming from cerebrovascular accidents. In two patients with proven lesions of the thalamus, the tremor was irregular and, in addition, there was dystonic posturing of the affected arm. Tremor and dystonic posturing had appeared after the stroke. In the other two patients tremor had occurred immediately at the onset of the stroke and lasted only a few days. The tremors were of small amplitude and high frequency, and lesions could not be found on CT or MRI in these two patients. None of our patients showed signs of the so-called rubral tremor.
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PMID:Tremor due to stroke. 847 86

We have developed a new operational method for stereotactic functional neurosurgery using MRI stereotaxy combined with microelectrode recording. MRI stereotaxy shows us the individual variations of thalamic configurations. The tentative target points were determined using the MRI stereotaxy assisted software system which revised the distortion of MRI images. Consequently, the accuracy and safety of the microelectrode recording were increased. This, in turn, increased the accuracy of stereotactic thalamotomy while producing encouraging operational outcomes. The effectiveness of stereotactic thalamotomy for Parkinson's disease was confirmed by these excellent operative results. The symptoms improved and the dosage of medications, including L-DOPA, decreased. Furthermore, our results indicate that the distributing area of deep sensory neurons in the thalamus extended more posteriorly and upward than previously expected. Therefore, the functional and anatomical similarity between the human and monkey thalamus was reaffirmed. In this report, based on the above data, we reevaluated the neural mechanism of tremor and the role of stereotactic functional neurosurgery for Parkinson's disease.
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PMID:[A new operational method of functional neurosurgery combining micro-recording and MRI stereotaxy for the treatment of Parkinson's disease]. 847 65

Two men, aged 63 and 71 years, developed a gross action tremor and dysesthesias several months after an intracerebral hemorrhage. CT and MRI showed a small hemorrhage in the posterior region of the lateral nucleus of the thalamus in each patient. The tremor occurred on movement, had frequencies of 2.5-4.5 Hz and the amplitude varied depending on the joint position of the limb. Ceruletide (a cholecystokinin analog) 0.8 micrograms/kg i.m. produced a marked reduction in the action tremor and improved motor function. This effect appeared 10-15 min after the injection, and lasted for up to 4 weeks. It is suggested that ceruletide may be of value in the treatment of action tremors following a thalamic lesion.
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PMID:Ceruletide therapy in action tremor following thalamic hemorrhage. 848 85

A fifteen-year-old male was admitted to our hospital because his thyroid function showed a lack of TSH suppression in the face of elevated thyroid hormone. This patient complained of heat intolerance, palpitation and hand tremor. Peripheral indices of thyroid hormone action indicated a hypermetabolic state. Serum TSH did not respond sufficiently to TRH stimulation, suggesting TSH-secreting pituitary adenoma. However, sellar CT scan and MRI images did not demonstrate any pituitary adenoma. Moreover, the serum TSH alpha-subunit concentration was not high and serum TSH was partially suppressed by the administration of T3. Furthermore, the results of single stranded conformation polymorphism (SSCP) suggested the existence of mutation(s) in the exon 7 of T3 receptor beta (TR beta) gene of this patient. These findings support the diagnosis of pituitary resistance to thyroid hormone.
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PMID:A case of hyperthyroidism due to pituitary resistance to thyroid hormone. 852 48

Resting tremor is one of the characteristic features of Parkinson's disease. However, there are a number of patients who typically have resting tremor alone for at least 5 years without development of other parkinsonian signs or symptoms. The etiology of an isolated resting tremor is still obscure. Recently, positron emission tomography was used to study these patients with isolated resting tremor, and demonstrated a markedly decreased striatal uptake of fluoro-dopa to the range of Parkinson's disease. These findings suggested the existence of a separate subtype, namely, tremulous Parkinson's disease with a manifestation of resting tremor alone. In order to confirm the existence of this subgroup of tremulous Parkinson's disease and further investigate its morphological changes and the usefulness of magnetic resonance imaging, we collected 5 patients who typically have resting tremor for at least 8 years in the absence of other features of Parkinson's disease. MRI was performed and the results of the images showed typical findings of Parkinson's disease with smudging or decreased distance between substantia nigra and red nucleus. Quantitative analysis also demonstrated a significant decrease of the above-noted distance when the resting tremor group was compared to the essential tremor group. Therefore, patients with an isolated resting tremor can have morphological abnormalities in addition to functional disturbances shown by positron emission tomography. To our knowledge, this is the first paper to report that resting tremor is a variant of Parkinson's disease rather than essential tremor, by using a double-blind method, with magnetic resonance imaging to support.
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PMID:Resting tremor only: a variant of Parkinson's disease or of essential tremor. 858 89

Primary orthostatic tremor (OT), a clinical syndrome in which a rapid (14 to 16 Hz), regular lower limb tremor causes unsteadiness on standing, may be associated with a postural upper limb tremor of similar frequency. We used H2 15O PET to analyze the abnormal pattern of cerebral activation associated with the postural upper limb tremor in four patients with primary OT. Patients had regional cerebral bloodflow (rCBF) measured during involuntary tremor while maintaining a posture with their outstretched right upper limb and again at rest. Tremor was associated with abnormal bilateral cerebellar and contralateral lentiform and thalamic activation. These findings were evident on group analysis of pooled PET data after transformation into standard stereotactic space and in single subjects when PET images were coregistered with structural MRI of the brain. At rest, cerebellar blood flow was significantly increased bilaterally in OT when compared with age- and sex-matched controls. We have previously demonstrated similar abnormal bilateral cerebellar activation in essential and writing tremors and conclude that abnormal bilateral overactivity of cerebellar connections is a common feature of tremulous disorders.
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PMID:A positron emission tomography study of primary orthostatic tremor. 861 76

A variety of clinical and experimental findings suggest that parkinsonian resting tremor results from the involuntary activation of a central mechanism normally used for the production of rapid voluntary alternating movements. However, such central motor loop oscillations have never been directly demonstrated in parkinsonian patients. Using magnetoencephalography, we recorded synchronized and tremor-related neuromagnetic activity over wide areas of the frontal and parietal cortex. The spatial and temporal organization of this activity was studied in seven patients suffering from early-stage idiopathic Parkinson's disease (PD). Single equivalent current dipole (ECD) analysis and fully three-dimensional distributed source solutions (magnetic field tomography, MFT) were used in this analysis. ECD and MFT solutions were superimposed on high-resolution MRI. The findings indicate that 3 to 6 Hz tremor in PD is accompanied by rhythmic subsequent electrical activation at the diencephalic level and in lateral premotor, somatomotor, and somatosensory cortex. Tremor-evoked magnetic activity can be attributed to source generators that were previously described for voluntary movements. The interference of such slow central motor loop oscillations with voluntary motor activity may therefore constitute a pathophysiologic link between tremor and bradykinesia in PD.
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PMID:Central motor loop oscillations in parkinsonian resting tremor revealed by magnetoencephalography. 862 83

We report a 32-year-old man who developed cerebellar ataxia and a posterior fossa mass 12 years after the radiation therapy for a cerebellar arteriovenous malformation (AVM). The patient was well until 19 years of the age when he had an acute onset of vertigo and vomiting. A spinal tap was performed and the CSF was bloody. He was admitted to another hospital where an arteriovenous malformation was found in the cerebellum by angiography. Four years after the onset, he developed tingling sensation in the distribution of the second division of the right trigeminal nerve. He was admitted to the neurosurgery service of our hospital where the cerebellar AVM was confirmed. He was transferred to University of California where Bragg peak stereotaxic radiotherapy was successfully performed; this utilizes high energy alpha-ray produced by a cyclotron. Three years after the radiotherapy, marked reduction in the size of the AVM was confirmed by angiography. Twelve years after the onset of his initial symptom, he noted unsteadiness of gait. He was readmitted to our neurosurgery service where obstructive hydrocephalus was found. He was treated by ventriculoperitoneal shunting and placement of a Ommaya reservoir. After these therapy, he noted marked improvement in his gait and ataxia. However, in 1993, his unsteadiness of gait recurred, and he was again admitted to our neurosurgery service on June 20, 1993. On admission, T1-weighted MRI revealed a slightly low signal intensity mass lesion in the right cerebellar hemisphere compressing the brain stem; a spotty high signal intensity lesion and another small low intensity lesion were seen within the mass. Vertebro-basilar angiograms revealed upward displacement of the superior cerebellar arteries. No arteriovenous nidus was visualized. On July, 3rd, the cyst was surgically drained and the Ommaya reservoir was removed. Post-operative course was uneventful, however, he developed head tremor after the surgery. Neurologic examination on July 20, 1993 revealed an alert and well oriented man in no acute distress. General physical examination was unremarkable. Neurologic examination revealed no dementia; higher cerebral functions appeared intact. The optic discs were flat, and visual fields were intact. Ocular movements were full but convergence was restricted. Horizontal gaze nystagmus was noted more in the right lateral gaze. Pupils were intact. Facial sensation and facial muscles were intact. Hearing was normal. His voice was of nasal quality. Pharyngeal reflex was diminished. The tongue showed deviation to the left without atrophy. Head tremor at 5 c/s was noted. He was able to stand with support but was unable to walk. No muscle atrophy or weakness was noted. The finger-to-nose and the heel-to-knee tests showed dysmetria and decomposition more on the right. Rapid alternating movements were ataxic on the right. Muscle tone was diminished on the right. Muscle stretch reflexes were normally elicited and were symmetric. The plantar response was flexor bilaterally. Sensation was intact. On July 21, a posterior fossa exploration was performed. After the surgery, he was treated with 30 mg/day of alotinolol which showed no effect on his head tremor. He was then treated with gradually increasing doses of clonazepam; when he received 8 mg/day of clonazepam, his tremor showed marked improvement. He was discussed in a neurologic CPC on the nature of the posterior fossa lesion and his tremor. Opinions were divided between delayed radiation necrosis and a radiation-induced brain tumor. The chief discussant arrived at the conclusion that the patient had delayed radiation necrosis compressing the brain stem and cerebellar hemispheres. Regarding the nature of his tremor, he thought that his head tremor was of cerebellar type of postural tremor. Histologic examination of the biopsied specimen revealed accumulation of relatively fresh blood constituents in the deep area of the cerebellum forming a mass. Most of the
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PMID:[A 32-year-old man who developed a posterior fossa mass 12 years after the radiation therapy for cerebellar arteriovenous malformation]. 867 25

We report a right-handed 62-year-old man with early onset familial parkinsonism. The patient was well until 24 years of the age when he noted an onset of resting tremor in his right hand. During the next four years, he noted rigidity, bradykinesia, and difficulty in walking. He was seen in another hospital at 28 years of the age, where he received left pallidotomy. Rigidity on the left side showed marked improvement. He received right pallidotomy at age 30 years. He developed right hemiplegia after this surgery. He was admitted to our hospital in March, 1983 when he was 51 years of the age. He was treated with levodopa but improvement was rather of minor degree. He was transferred to another hospital, but his motor disturbance progressed slowly, and was admitted again to our hospital in November 1990. He had 6 siblings 4 of whom including himself suffered from parkinsonism. No consanguinity was noted in parents. On admission, he appeared chronically ill but the general physical examination was unremarkable. Neurologic examination revealed an alert and mentally sound man. Hasegawa dementia scale was 28.5/32.5. Upward gaze was slightly restricted (3/5). Cranial nerve examination revealed oculogyric crisis, apraxia of eyelid opening, masked face, and small voice. He was able to stand with support; his posture showed left-ward leaning. He had right hemiparesis with moderate weakness. He showed marked bradykinesia and moderate rigidity in his left upper extremity. Fine postural tremor was noted in the left hand. Deep tendon reflexes were diminished in the upper extremities. No Babinski sign was noted. Pain sensation was somewhat diminished on the right side. Results of routine laboratory examination were unremarkable. Cranial CT scan revealed atrophy in the frontal lobe, particularly in the prefrontal area. In addition, MRI revealed T1-and-T2-low signal intensity lesions in the right ventral pallidal region and in the left ventrolateral thalamic-hypothalamic areas. He was treated with 600 mg of levodopa with benserazide and 22.5 mg of bromocriptine with mild to moderate improvement in his bradykinesia and rigidity. He was discharged in January 1991. His clinical course was complicated by intestinal obstruction in October, 1994. He was admitted to another hospital where he was operated on the obstruction on November 5, 1994. The sigmoid colon was markedly dilated but no mass was found. Postoperative course was uneventful until November 18, 1994 when he was found dead in his hospital room shortly after 4 am. The patient was discussed in neurological CPC, and the chief discussant arrived at the conclusion that the patient had young-onset familial Lewy body-negative parkinsonism. Opinions were divided between Lewy body-positive familial Parkinson's disease and Lewy body negative young onset parkinsonism. Postmortem examination revealed aspiration pneumonia, which appeared to be the cause of his death, in the right lung. Neuropathologic examination revealed loss of malanized neurons in the substantia nigra and the locus coeruleus. In the substantia nigra, neuronal loss was particularly severe in the ventrolateral area. No Lewy bodies were seen. The dorsal motor nucleus of the vagal nerve was well preserved. Stereotaxic lesions involved bilateral thalamic areas. This patient appears to represent a case of autosomal recessive juvenile parkinsonism (AR-JP). Early onset, superb response to levodopa, sleep effect, and easy development of dyskinesias and motor fluctuations characterize AR-JP. The reason why this patient did not show these clinical features is probably bilateral sterotaxic surgeries. Particularly, the second surgery was complicated by right hemiparesis. His siblings who developed parkinsonism showed typical clinical features of AR-JP.
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PMID:[A 62-year-old man with familial parkinsonism with the onset at 24 years of the age]. 870 64


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