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)

Vitreous hemorrhage is relatively common following subarachnoid hemorrhage, but rarely occurs after accidental head injury. In this paper, we report a rare case of vitreous hemorrhage after an accidental head injury with chest compression. A 4-month-old girl was held in her father's arms. After he fell down, she struck her head and her chest was compressed by her father's body. She soon became pale and was immediately transported to our center complaining of disturbance of consciousness on February 6, 1993. On admission, she was semicomatose and had a generalized convulsion. Computed tomography (CT) scan showed a subdural hematoma, although no fracture was detected on the plain X-ray film. Bilateral vitreous hemorrhage was also observed. The anterior fontanelle pressure was a high 330 mmH2O. The patient was treated conservatively with agents to promote hemostasis and reduce the intracranial hypertension. She was discharged after one month with normal consciousness and improved vision. The follow-up CT scan revealed subdural hematoma, hemorrhagic infarction (suggesting rupture of the pontine veins), and cerebral atrophy, corresponding to those of the shaken baby syndrome. Her chest was compressed by her father's body. The anterior fontanelle pressure was a high 330 mmH2O. These findings suggest that shaking or abrupt deceleration, acute intrathoracic hypertension and acute intracranial hypertension, caused retinal hemorrhage, and that extensive retinal hemorrhage possibly resulted in vitreous hemorrhage.
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PMID:[Vitreous hemorrhage after accidental head injury with chest compression--case report]. 787 84

Olivary pseudohypertrophy (OH) and its chronological change was examined by MR images in two patients with brainstem vascular disease. Patient 1 was a 63-year-old woman who developed an infarction in the red nuclei associated with "top of the basilar" syndrome. Two months later, she showed 2-4 c/s rhythmic myoclonus (rubral tremor) involving four extremities. Palatal myoclonus was absent. MR images of the inferior olives did not demonstrate a significant lesion in 10 days after the onset, but showed OH in 6 months, and then their size attained a maximum in 10 months after. On T2-weighted (T2) images and proton-density-weighted (PD) images obtained at 20 and 24 months, OH gradually became irregular but discrete in their intensity, and the intensity had also decreased to some extent. Rhythmic myoclonus had subsided to some extent after 20 to 24 months. Patient 2 was a 62-year-old woman who had a small hemorrhage in the pontine tegmentum. She developed 2.5 c/s vertical ocular myoclonus without palatal myoclonus two months after the onset. MR images showed OH in 6 and 8 months after the onset. On T2 and PD images obtained at 20 months, the image of OH gradually developed to become irregular in intensity and slightly atrophic in size. The ocular myoclonus somewhat reduced in their intensity 12 months after the onset. These serial changes in MR images were considered to correspond to the chronological changes of the pathology of OH. Appearance and subsidence of the myoclonic movement was also considered to correlate to the sequential changes of MR images of OH.
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PMID:[Chronological changes in MR imaging of inferior olivary pseudohypertrophy--report of two cases]. 789 37

The authors have reported a clinical trial of an autologous cervical sympathetic ganglion transplanted into the brain of a parkinsonian patient. A 45-year-old woman presented with bradykinesia and a gait disturbance for 8 years under L-dopa treatment. The patient underwent stereotactic transplantation of the right stellate ganglion into the right putamen. She showed marked amelioration of bradykinesia and gait disturbance 1 month after the operation, and she was able to conduct her activities of daily living without requiring L-dopa administration. The patient continued to improve gradually until 3 months after the operation. Two years after surgery, the patient functions independently as a housewife. The right hand tremor, however, became slightly worse after the operation, but it was transient. The patient developed a permanent right-sided Horner's syndrome after resection of the cervical sympathetic ganglion. Taken together with our previous data obtained from animal experiments, this case suggests that the autologous cervical sympathetic ganglion can be donor tissue for neural transplantation in Parkinson's disease.
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PMID:Autologous transplantation of the cervical sympathetic ganglion into the parkinsonian brain: case report. 793 40

We present a 77-year-old woman with myoclonus and epilepsy. She was well until 35 years of age, when she noted an onset of trembling of the legs upon standing. Her symptom slowly progressed, and she felt a difficulty in standing when she was 39-year-old. She had a major motor seizure without an apparent focal onset when she was 46-year-old. She also developed tremor in her hands, and she felt difficulty in holding a glass filled with water. She was admitted to our service for the first time in 1965 when she was 51-year-old. She showed wide-based ataxic gait with truncal titubation. In finger to nose test, myoclonic jerks were induced in the upper extremities. Otherwise neurological examination was unremarkable. She was treated with primidone and phenobarbital, and was discharged for out patient follow up. Her symptoms slowly progressed, and gait and station became more difficult. Mentally she was sound. Three months prior to the present admission, she developed more difficulty in gait, and decrease in food intake. On the 14th of September in 1991, she was seen by a local physician who found an abnormal shadow in her chest X-ray, and she was admitted to our service for further work-up on September 18, 1991. On admission, the patient was a chronically ill and emaciated woman. Her blood pressure was 140/84 mmHg, heart rate 115/minutes and regular, and the body temperature 36.9 degrees C. The palpebral conjunctivae were anemic. No cervical adenopathy was noted. The lung fields were clear, and no heart murmur was audible. The abdomen was soft, and no organomegaly was present. On neurologic examination, she looked somnolent with disorientation to time and place. Her memory was poor, and she could not do well serial 7s. The disc was flat and the ocular movements appeared intact. Other cranial nerves were also unremarkable. She showed diffuse muscle wasting. She was unable to stand or walk. Maintaining the sitting position was also difficult. She was able to raise her arms, but almost unable to move her lower extremities. The precise muscle testing was impossible. No abnormal involuntary movement was seen. Finger to nose test could not be performed.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 77-year-old woman with myoclonus and epilepsy]. 812 9

We report a family with autosomal dominant parkinsonism. The propositus developed parkinsonism at a relatively young age (45 years) and came to autopsy after a 6-year illness. She had typical features of Parkinson's disease except for an absence of rest tremor, although this was present in other family members. A diagnosis of Lewy body parkinsonism was confirmed by neuropathological examination. Additional pathological features included the presence of cortical Lewy bodies and anti-ubiquitin-positive neurites in the cornu Ammonis 2 and 3 (CA2-3) region of the hippocampus. This kindred is similar both clinically and pathologically to a few previously reported pedigrees, further strengthening recent evidence of a genetic etiology of some forms of Parkinson's disease.
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PMID:Autosomal dominant Lewy body parkinsonism in a four-generation family. 828 94

We report a 20-year-old female with Hallervorden-Spatz syndrome (HSS). This patient is the product of consanguineous parents. She developed genu valgum, tendency to fall and mental deterioration at the age of 6, decrease of the number of spoken words at the age of 14, dysarthria, unsteady gait, postural tremor of the upper extremities, dystonic posture of hands and double incontinence at the age of 16. Her disease progressed slowly. Neurological examination on admission revealed severe mental retardation, optic atrophy, forced grasping, hyperactive tendon reflexes in the upper extremities and bilateral Babinski sign. An extensive laboratory investigation including the leukocyte lysosomal enzymes, serum amino acid analyses, copper studies and ceruloplasmin were almost within normal limits. MRI, T2 weighted images, showed markedly decreased signal intensity in the globus pallidus but substantia nigra and increased signal intensity in diffuse cerebral white matter. T1 weighted images showed marked atrophy of the brainstem and cerebellum. She met the diagnostic criteria for HSS by Swaiman; we diagnosed her as HSS group II. HSS is characterized by the presence of many spheroids in the central nervous system which is similar to neuroaxonal dystrophy (ND). However, clinical and pathological differences exist between HSS and ND, the precise classification of the two conditions has remained controversial. Although there are many reported cases in which both conditions overlap, this is the first reported case that simultaneously demonstrates increased iron deposition in the globus pallidus, marked atrophy of the brainstem and cerebellum and typical clinical course compatible with HSS.
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PMID:[A case of Hallervorden-Spatz syndrome with marked atrophy of the brainstem and cerebellum]. 836 59

A 52-year-old woman developed severe hyponatremia following treatment for hypertension with chlorthalidone. Rapid correction of hyponatremia resulted in coma, quadriplegia and hypopnea compatible with central pontine myelinolysis. She recovered with residual facial hypomimia, bradykinesia, cogwheel rigidity and coarse resting tremor, responding to dopaminergic treatment. Her symptoms and signs, which are quite similar to idiopathic Parkinson's disease, are still responsive to treatment 7 years after onset.
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PMID:Extrapyramidal syndrome responsive to dopaminergic treatment following recovery from central pontine myelinolysis. 844 Feb 86

A family with two siblings presenting cerebral calcifications is reported. The sister was suffering from action tremor since the age of 10. The disease worsened by the age of 39. When aged 42, she was unable to walk and had severe rigidity and intellectual deterioration. She died at 43. The brother had mild debility. Action tremor started at the age of 14, without significant aggravation when seen at the age of 30. In both cases, brain CT scan showed calcifications of the dentate nuclei and cortical atrophy with ventricular enlargement. In addition, the sister had bilateral putaminal and pallidal calcifications. The other family members were unaffected and had normal CT scans. The nosology and the pathophysiology of this family report are discussed, particularly regarding the late occurrence of facial atrophy, reminiscent of the Cole-Engmann syndrome (Dyskeratosis Congenita).
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PMID:[Striato-pallido-dentate calcifications and acquired facial atrophy]. 859 48

A case is described of a patient with limb shaking in whom anticonvulsant therapy was effective for inhibiting attacks. A 70 year old female developed rhythmical involuntary limb shaking of the right upper and lower limb in April 1986. She was diagnosed as having transient ischemic attacks and was followed up under treatment with an antiplatelet drug. Subsequently, anticonvulsant therapy was also initiated on an outpatient basis. In August 1991, she was admitted with shaking of the right upper and lower limbs. Low molecular dextran was ineffective for inhibiting limb shaking attacks, but intravenous injection of diazepam was effective. Phenytoin and phenobarbital was used in combination. No limb shaking attacks occurred thereafter. The involuntary movement was the same as that observed at the onset of the disease. Though no changes were observed in the pattern of the involuntary movement, anticonvulsant therapy was effective in preventing and inhibiting attacks. This finding is inconsistent with previous reports. It is possible that epileptic factors are involved in the development of this condition.
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PMID:Effective anticonvulsant therapy in a patient with limb shaking: a case report. 860 39

Mechanism of essential tremor remains unknown. Central oscillators, postulated in thalamus, inferior olive, and spinal cord are thought to be important to form rhythmicity, and finally to stimulate spinal or medullary motor cells, leading trembling muscle contraction, tremor. Among several subtypes of essential familial tremor, including hand tremor, neck tremor, and voice tremor, essential neck tremor is a common disorder, and its pathophysiology seems different from that of typical essential hand tremor, since patients with essential hand tremor are responsive to beta blocker, whereas those with neck tremor are usually not. We experienced a 41-year-old left handed woman with essential neck tremor in whom neck titubation disappeared shortly after pontine base infarct. She was our patient in the outpatient clinic with the diagnosis of essential neck tremor. The tremor developed when she was teenage, and has been localized in the neck muscles. Alcohol intake had apparently diminished it transiently. Her mother also had the tremor in her neck. She was admitted to our hospital with sudden onset of right-sided limb weakness and speech disturbance. Neurological examination showed right hemiparesis including the ipsilateral face, scanning speech, and cerebellar limb ataxia on the same side. In addition, there was no tremor in her neck. Brain MR imaging revealed a pontine base infarct at the level of middle pons, which was consistent with paramedian artery territory. The hemiparesis and speech disturbance improved almost completely after treatment, and her neck tremor has never occurred in one year follow-up. In our patient, efficacy of alcohol imply that essential neck tremor and hand tremor had same central nervous pathway including central oscillator in common, and descending cortical fibers is seemingly associated with diminishing patient's tremor. Pathophysiology of essential neck tremor was discussed with reviewing previous literature.
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PMID:[Disappearance of essential neck tremor after pontine base infarction]. 879 10


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