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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Micrographia due to focal cerebral disorder is very rare. We described a patient with micrographia due to a left putaminal infarction. Following an infarction involving the left putamen and corona radiata, a 58-year-old right-handed man developed micrographia with the right hand, right facial palsy, right hand clumsiness and slight aphasia. Micrographia finally disappeared by the seventh month. No parkinsonian features were noted. Our case suggests that micrographia is a disorder of the motor control system of handwriting which exists in the contralateral putamen, and has no relation with extrapyramidal signs like rigidity, tremor or akinesia.
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PMID:[A case of micrographia with the right hand due to left putaminal infarction]. 259 41

A three-year-old boy with a progressive history of headache, vomiting and ataxia in the course of 2 months, was admitted on August 1983, when he was lethargic. Neurological examination revealed dysphagia, scanning speech and tremor in the bilateral hand. CT scan showed a very large enhanced mass in the center of posterior fossa with central necrosis in it and the dilatation of whole ventricular system. Suboccipital craniectomy was immediately performed and the tumor that occupied the vermis and invaded into both cerebellar hemisphere was subtotally removed. Postoperative irradiation was well performed: 4140 rads to the whole brain and 3162 rads to the spinal cord. However, 5 months later, facial palsy in the left side and progressive ataxia became prominent. CT scan showed multiple enhanced masses in the left trigonum and right anterior horn of the lateral ventricles and in the left cerebellopontine angle. In spite of chemotherapy, the patient had a down-hill course, especially after the ventricular hemorrhage, and died on June 9th, 1984. Histologically, the tumor had a lobulated appearance with an aggregation of tumor cells encircled by vascular septae. The cells within lobules generally had vesicular nuclei, which were arranged in parallel row. Occasionally smaller hyperchromatic cells with scant cytoplasm were present along the vascular septae. Reticulin was present within the septa, but was not observed within the lobules. Scattered astrocytic cells and processes were identified within the lobules by the immunoperoxidase technique for GFAP. The fibrillary cytoplasmic processes within the lobules were stained by immunoperoxidase technique for neurofilament (68K).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of cerebellar neuroblastoma]. 361 40

A 54-year-old housewife became ill with transient diplopia followed by facial paralysis, tremor of the right hand and a progressively worsening disturbance in gait. Four years after the first appearance of the disease bilateral hypacusia, paralysis of the right hypoglossal nerve, dysarthria, severe spastic tetraparesis with ataxia, urinary retention and an organically induced character change were present. Lumbar puncture fluid contained 51/mm3 lymphocytes and 1164 mg/dl protein. Immunoglobulin A, G and M, synthesised locally, could be detected in cisternal fluid. The serum had a high antibody titre against Ixodes ricinus-Borrelia antigen and the same antibodies, formed locally, were present in the lumbar fluid. The neurological deficiencies improved markedly under parenteral penicillin treatment and the antibody titre decreased. The detection of Borrelian antibodies, especially those synthesised locally in the CSF, enabled an aetiological diagnosis to be made in seven other patients aged 18-47 years in whom the disease had been present for 1 to 8 years. These patients likewise presented symptoms characteristic of a disseminated disease of the CNS, with spastic pareses and evidence in the spinal fluid of chronic inflammation and disruption of CSF barriers in particular. This progressive encephalomyelitis differs from the common and spontaneously healing meningo-polyneuritis (Garin-Bujadoux-Bannworth), the usual manifestation of erythema chronicum migrans of the nervous system, in its progressive nature, its invasion of the CNS and the possible long lasting severe damage when not specifically treated.
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PMID:[Progressive Borrelia encephalomyelitis. Chronic manifestation of erythema chronicum migrans disease of the nervous system]. 400 60

A 36-year-old Japanese woman was admitted to our hospital, because of facial palsy, ophthalmoplegia, cerebellar ataxia, and rhythmic myoclonus of the neck. About a few weeks before admission, she developed symptoms of common cold and general fatigue. Her laboratory data were unremarkable, and her CSF was normal. Serum levels of antibodies to gangliosides were within normal limits. Her MRIs of the brain and neck were normal. Both somatosensory evoked cortical potential study and auditory evoked brainstem response study were normal. She was diagnosed as postinfectious brainstem encephalitis, and the administration of corticosteroid was started. After the treatment, her symptoms improved. To our knowledge, it is rare to see myoclonus to the neck without palatal tremor in patients with brainstem encephalitis.
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PMID:[Rhythmic involuntary movement of the neck in a patient with brainstem encephalitis]. 1065

We evaluated children in the first grade of a elementary school using neurological examination. With no previous knowledge of their educational performance, were invited all children attending five classes of the first grade of an elementary public school chosen randomly, in Itatiba / Sao Paulo / Brazil, whose parents assigned a Commitment Term for participation in this research. Children who missed three evaluations in different days or whose parents did not assigned the Commitment Term were excluded. The Traditional Neurological Examination (ENT) (Lefevre, 1972) was applied. It was considered for normal the measurement of the skull circumference, proposed by Diament & Rodrigues (1976), and the application of all ENT items. The data were stored in a database of the Epi6 Program (Epidemiologic Information), and analyzed by percentage calculation and by the chi2 test. The significance level was 0.05. Children evaluated were 124. The ENT results were normal in 87 (70.16%) and altered in 37 (29.83%). Among the alterations, there were observed: light tremor, light muscular hypotonia, speech acquisition delay, macrocephaly, microcephaly, hyperactivity, cranial nerve syndrome, central facial paralysis. One child presented corticospinal tract impairment syndrome of the distal lower extremities.
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PMID:[Neurologic semiology of a group of first grade students in an elementary school]. 1077 Aug 75

Cyclosporine (CsA)-associated neurotoxicity has been reported in recipients of solid organ and bone marrow transplants. These neurological side effects are usually mild and resolve with temporary reduction or withdrawal of CsA. We report a 16-year-old renal transplant recipient who developed tremor, tinnitus, and peripheral facial paralysis during oral CsA treatment. Her serum magnesium level was below the normal range and her peripheral facial paralysis did not improve with the cessation of the drug.
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PMID:Cyclosporine-associated facial paralysis in a child with renal transplant. 1217 72

A 78-year-old Korean woman was referred to Chonbuk National University Dental Hospital complaining of facial palsy and palpable mass in the right parotid gland area for 4 years. Clinical examination showed an asymmetrical facial appearance due to a 4 cmx5 cm hard, fixed, non-tender mass in the right parotid gland area, incomplete eye closure and a slight tremor at the corner of the mouth. A panoramic radiograph showed an amorphous calcified mass on the posterior mandibular ramus with thinning of the cortical plate adjacent to the mass. A sialogram showed constriction of the main duct and no further filling of striated, intercalated ducts and parenchymal areas. CT indicated an expansile mass with slight contrast enhancement involving the right parotid gland. The large mass showed necrotic areas and calcifications. A bone scan showed marked accumulation of (99)Tc(m)-methylene diphosphonate on the right posterior maxilla. Microscopic findings revealed minimal morphological alterations and rare mitotic figures within tumour cells, and the lesion was diagnosed as adenocarcinoma not otherwise specified (NOS, grade II).
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PMID:Adenocarcinoma of the parotid gland with calcification. 1277 69

1. Murine SK poliomyelitis virus has been transferred from mouse to guinea pig with the establishment of a fixed strain of cavian passage virus. 2. The disease thus produced in guinea pigs is characterized by the occurrence of flaccid paralysis. Typical poliomyelitic lesions are found in the anterior horn of the spinal cord. 3. Guinea pigs are susceptible to infection with murine virus by the intracerebral, intravenous, intraperitoneal, and subcutaneous route; cavian passage virus produces paralysis only upon intracerebral or intravenous injection. Neither virus paralyzes guinea pigs by feeding or nasal instillation. 4. The potency of the virus (murine or cavian) in guinea pigs is considerably lower than in mice and compares with the titer of the original SK strain in monkeys. In paralyzed guinea pigs the virus is found only in the central nervous system and not in extraneural sites, such as blood or abdominal viscera. 5. Attempts to cultivate cavian passage virus in tissue culture have yielded evidence of some in vitro propagation but no passage virus has as yet been obtained by this method. 6. Cross neutralization tests with cavian passage virus in guinea pigs and with murine virus in mice have established the serological identity of the two viruses. Inactivation of cavian passage virus in guinea pigs by poliomyelitis-convalescent monkey sera is irregular. Complete neutralization has been obtained with a concentrated poliomyelitis horse serum. 7. Resistance to reinfection with potent virus can be demonstrated in convalescent guinea pigs as well as in guinea pigs which have survived a symptomless infection with either murine or cavian virus. This immunity is demonstrable by the power of the serum of such animals to neutralize the virus in vitro and by the ability of nerve tissue to dispose in vivo of the infectious agent. 8. Cavian passage virus has a limited pathogenicity for rhesus monkeys. Of a total of 35 monkeys injected intracerebrally with guinea pig passage virus 26 failed to respond with any manifest symptoms of disease; 8 monkeys showed various signs of definite involvement of the central nervous system consisting of tremor, convulsions, facial palsy, and localized pareses; 1 monkey developed typical flaccid paralysis. 9. Following injection with cavian virus the virus may be recovered from the tissues of normal monkeys but not from the tissues of convalescent monkeys shortly after a paralyzing attack of poliomyelitis due to SK or Aycock virus. 10. Immunization of monkeys with early cavian passage virus by the subcutaneous route has given no clear-cut evidence of protection against intracerebral reinfection with SK poliomyelitis virus. Neither has there been any evidence of effective interference in monkeys injected intravenously with early cavian passage virus and intracerebrally with RMV poliomyelitis virus. 11. The bearing of the experimental data upon the epidemiology of the human disease is discussed.
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PMID:STUDIES IN RODENT POLIOMYELITIS : III. EXPERIMENTAL POLIOMYELITIS IN GUINEA PIGS PRODUCED WITH THE MURINE STRAIN OF SK POLIOMYELITIS VIRUS. 1987 Dec 19

Holmes tremor is a rare movement phenomenon, with atypical low-frequency tremor at rest and when changing postures, often related to brainstem pathology. We report a 70-year-old female patient who was presented with dystonic head and upper limb tremor after brainstem hemorrhage. The patient had experienced a sudden onset of left hemiparesis and right facial paralysis. Brain magnetic resonance imaging showed an acute hemorrhage from the brachium pontis through the dorsal midbrain on the right side. Several months later, the patient developed resting tremor of the head and left arm, which was exacerbated by a sitting posture and intentional movement. The tremor showed a regular low-frequency (1-2 Hz) for the bilateral sternocleidomastoid and cervical paraspinal muscles at rest. The patient's symptoms did not respond to propranolol or clonazepam, but gradually improved with levodopa administration. Although various remedies were attempted, overall, the results were poor. We suggest that levodopa might be a useful remedy for Holmes tremor. The curative or relieving effect of the dopaminergic agent in Holmes tremor needs more research.
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PMID:Holmes tremor after brainstem hemorrhage, treated with levodopa. 2402 44

The aim of this study was to describe otitis media with effusion in seven boxers. All dogs presented with a range of clinical signs, which included head shaking, neurological dysfunction, pain on opening of the mouth and reduction in hearing ability. Otitis media was confirmed under general anaesthesia in each case by video-otoscopic identification of a bulging pars tensa and subsequent myringotomy, which revealed a tenacious mucus plug within the middle ear. Brainstem auditory evoked response thresholds were elevated in all affected ears. In three cases, CT revealed soft tissue opacity in the affected bulla. All of the affected middle ears were flushed using warm sterile saline to remove the mucus. A combination of glucocorticoid and antibiotic in EDTA tris was instilled into the middle ears. After the initial middle ear flush under general anaesthesia, topical therapy was applied into the ear canals daily by the owners using the same combination of drugs. Dembrexine, a systemic mucolytic, was administered with food daily. Six out of seven dogs were also prescribed oral prednisolone. In each case, the middle ear effusion was sterile. All clinical signs resolved with treatment, with the exception of facial paralysis in two dogs. Otitis media with effusion should be considered a cause of otitis media in boxers.
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PMID:Otitis media with effusion in the boxer: a report of seven cases. 2923 79


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