Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A rare case of mesenchymal chondrosarcoma originating from the thoracic spinal dura was reported. A 10-year-old girl complained of paresis of the right leg in June 1977. Then she became unable to walk early in August, and a complete paraparesis developed on August 18. She was admitted to our department on August 22. On admission she had complete paraparesis, bilateral ankle clonus, upward plantar reflexes, sensory disturbance below T7, shincter disturbance and neck stiffness. Plain thoracic X-ray revealed bilateral decalcification of pedicles of T6. Myodil myelography showed a complete block between T6 and lower end of T7 vertebrae. Bilateral laminectomy from T3 to T8 was performed. A tumor originating from the spinal dura was located in the right dorsal extradural space. The tumor was totally removed together with a small area of the affected dura. Light microscopy showed mesenchymal chondrosarcoma. Her recovery from neurological deficiencies was excellent and now she can run 14 months after surgery. Metastasis or recurrence has not yet been seen.
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PMID:[A case of mesenchymal chondrosarcoma originating from the spinal dura (author's transl)]. 49 58

Cervical radiculopathy unaccompanied by pain or sensory disorder but manifested only by paresis, atrophy, fasciculation, and reflex loss is unusual. Three such cases are presented. Considerable diagnostic difficulty may arise in distinguishing patients presenting with these features from those who have primary motor neuron disease. Two additional case reports demonstrate that this distinction is not always possible. Diagnosis, management, and prognosis are discussed. Differentiation between motor neuron disease and spondylosis will avert needless surgery in the former group and will result in beneficial, sometimes curative surgery in the latter group.
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PMID:Cervical spondylotic radiculopathy producing motor manifestations mimicking primary muscular atrophy. 53 45

Sixteen cases of juvenile, non-progressive muscular atrophy localized in the hand and forearm were seen at our neurology out-patient clinic for the past 8 years. The analyses of these 16 cases disclosed characteristic features as follows: 1) juvenile onset 2) male preponderance 3) unique distribution of muscular atrophy and weakness in the hand and forearm. 4) insidious onset, initial progressive period and subsequent non-progressive course 5) tendon reflexes of the arms are hypoactive in half of the cases 6) no pathological reflexes 7) cold paresis 8) no definite sensory disturbance 9) no cranial nerve involvement 10) neurogenic patterns on EMG According to these features, this clinical entity carrying good prognosis must be differentiated from several diseases associated with similar muscular atrophy of extremities, especially amyotrophic lateral sclerosis which is notorious as a fetal disease.
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PMID:[Juvenile, non-progressive muscular atrophy localized in the hand and forearm. Report of 16 cases (author's transl)]. 54 13

A 73-year-old woman suffering from the acute onset monoparesis of her right arm which followed the skin eruption with mild sensory disturbance of right C4-6 level, was reported. Electrophysiological examinations revealed the brachial plexus neuritis and axonal degeneration of the proximal portion, with the evidence of herpes zoster infection. Her paresis of the right arm gradually improved without any medication during her hospital course. It was concluded that herpes zoster should be considered to be one of the causes of acute onset brachial plexopathy.
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PMID:[Monoparesis due to the brachial plexus neuritis by herpes zoster virus--report of a case]. 181 97

A 67-year-old woman with medial medullary infarction is reported, including clinical manifestations, MRI and angiographical findings, and results of evoked potentials. She suffered from contralateral hemiplegia and disturbance of deep sensation. Motor paresis of the tongue was absent. Magnetic resonance imaging revealed a lesion in the medial portion of the medulla oblongata. The 17 cases previously reported with medial medullary infarction are reviewed. Only 3 cases had triad of medial medullary infarction, contralateral hemiparesis, deep sensory disturbance, and ipsilateral hypoglossal paresis. Therefore, lesion detection is necessary to diagnose medial medullary infarction. Most infarctions limited to the upper third of the medulla were caused by occlusions of vertebral arteries or their branches and prognosis was good. In contrast, infarctions in the lower two thirds were caused by occlusions of anterior spinal arteries and their branches and the prognosis was poor. Thus localization of the lesion using MRI plays an important role to predict the prognosis.
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PMID:[Medial medullary infarction demonstrated by MRI]. 218 65

We report a case of AML (M 4) with eosinophilia who developed meningeal relapse and transverse myelopathy. A 37-year-old woman was admitted to our hospital because of lymphadenopathy and ecchymosis. One week prior to admission, she noticed swelling of the cervical lymph nodes and bleeding tendency. On admission, low-grade fever, gingival swelling, generalized lymphadenopathy, and ecchymosis on the lower legs were found. A white blood cell count was 93,900/microliters with 82% blast cells, and a platelet count was 24,000/microliters. A bone marrow was composed of 45.3% myeloblasts, 27% monocytes and 7.1% eosinophils. Chromosome analysis revealed inv(16). The diagnosis of M4Eo was made. About one year after she gained complete remission, she was readmitted because of disturbance of urination. There was a sign of transverse myelopathy at the seventh vertebral level, and blast cells were detected in the cerebrospinal fluid. Despite of radiation and chemotherapy, paresis of lower extremities and sensory disturbance were persistent, and the patient died on 52th hospital day.
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PMID:[Acute myelomonocytic leukemia with Inv(16) (p13 q22) relapsed in transverse myelopathy]. 221 77

Over a period of two years a 26-year-old man active in sports developed progressively more marked pain in the area of the left lateral tibial edge and signs of foot flexor paresis after physical exertion. These symptoms lasted for several hours. Finally there also developed sensory dysfunction in the area of the deep peroneal nerve. Electrophysiological tests revealed normal peroneal nerve conduction velocity but denervation signs in the anterior tibial muscle. In view of the diagnosis of an exercise-induced incomplete chronic anterior tibial syndrome a fasciotomy was performed revealing connective-tissue thickening of the fascial compartment which was clearly compressed. The sensory disorder in the left foot regressed within a few weeks and the patient has been symptom-free since.
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PMID:[Exercise-induced partial damage of the n. peroneus profundus]. 236 36

Four Japanese cases of postpolio progressive muscular atrophy (PPMA) of late onset were clinically studied to characterize their clinical features and discussed upon the epidemiologic viewpoint. Four male patients were included with mean age of 43.5 (30-59) years on examination, diagnosed as PPMA after the criteria by Alter (1982) and Dalakas (1986). All suffered from polio at age 10 month to 8 years (mean: 3y) between 1931 and 1957 with residual motor paresis in one limb or two. Twenty-eight to 55 (mean: 40.3) years later, subsequent muscle weakness and atrophy appeared in the limb seemingly unaffected by the initial polio attack. Marked fasciculations and occasional myalgias were noticed without sensory disturbance and bulbar as well as upper motor neuron signs. Laboratory examinations revealed moderate elevations of serum CK and protein content in SCF. No significant elevation of polio virus antibody titers was found in both serum and CSF. Electromyography showed neurogenic changes of various degrees by muscle tested. Muscle CT disclosed patchy distribution of atrophied muscles with fatty replacement in all extremities. Spinal cord MRI images were unremarkable. Scatters of small grouped atrophy and fiber type grouping were noticed on muscle biopsy specimens. These findings summarized in our cases are generally compatible with those of hereby reported PPMA cases. On reviewing the western literature and the great epidemic of polio around 1960 in Japan, an increasing number of patients with PPMA can be anticipated in near future; possibly in 10 years.
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PMID:[Postpolio late progressive muscular atrophy--clinical and epidemiologic analyses in 4 Japanese cases]. 238 7

A 24-year-old female was admitted to our hospital on Aug. 20 in 1986 because of blurred vision and right pupillary dilatation. She had sometimes noticed headache later than 1976, and blurred vision without headache several times a year later than 1983. She had been told her right pupil dilated when she had complained of blurred vision. Neurological examination revealed abnormal findings as follows; diminished sense of smell in the right side, anisocoria (R 8 mm, L 5 mm), bilateral hippus, hypesthesioalgesia in her right face, left trunk and left arm. The pupils were round and contracted promptly to light. Accommodation reflex and ciliospinal reflexes were normal. Neither blepharoptosis nor external ocular muscle paresis were observed. Deep tendon reflexes were normal. Planter responses were flexor. There was no meningeal irritative sign. No abnormal findings were obtained in blood and urine, chest X-p, brain enhanced CT scan, EEG, and cerebral angiography except for slight degree of anemia. Serum TPHA was negative. However, the cell count of cerebrospinal fluid (CSF) was 18/mm3 (Ly 100%) and decreased to 9/mm3 (Ly 100%) in nine days. Protein content and glucose level of CSF were normal. Pupils were not constricted by 0.125% pilocarpine instillation. Loss of smell and sensory disturbance disappeared within three days and her pupils became isocoric by five days after admission. The patients of episodic unilateral mydriasis without apparent cause had relatively same clinical features as "unilateral springing pupil" proposed by Hallett et al. (1970). Except for mydriasis, they had no abnormal findings of neurological and laboratory examinations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Recurrent episodic unilateral mydriasis with pleocytosis in the cerebrospinal fluid--a case report]. 259 48

Somatosensory and motor functions of both hands were examined in 10 patients with unilateral parietal cortex lesions as revealed by computerized tomography. Tests of elementary somatosensory functions comprised surface sensibility, vibration, and position sense. For evaluation of complex somatosensory functions, the recognition of surface textures and object forms was tested. Motor performance was examined by measuring force and position control as well as manipulative and explorative motor behaviour. All patients showed varying degrees of sensory disturbance. Although the patients had no or minor paresis, they all had motor deficits concerning force control, fine movements, and manipulation with the hand contralateral to the lesion. Patients with more posteriorly located parietal lesions revealed predominantly severe disturbances of complex sensibility, precision grip, manipulation, and explorative finger movements. The characteristic and consistent feature of the disturbed motor behaviour was the loss of the purposive nature of the motor acts which were no longer adequate for the tasks (tactile apraxia). Paresis or ataxia could not account for this deficits.
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PMID:Role of the parietal cortex for sensorimotor transformation. Evidence from clinical observations. 275 92


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