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)

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

We present a case of progressive bulbar paresis in a 2-year-old child, with appropriate autopsy findings. A review of previously reported cases and a comparison with more extensive literature in Werdnig-Hoffmann disease suggest that Fazio-Londe disease is not unique, but belongs in the spectrum of progressive lower motor neuron disease.
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PMID:Progressive bulbar paresis in childhood. 124 98

Motor neurone disease (MND) was studied in relation to various determinants in a case-control study covering nine counties in southern Sweden. A questionnaire about occupational exposures, medical history, lifestyle factors etc was given to all cases in the age range 45-79 and to a random sample of 500 population controls in the same age range. The questionnaires were answered by 92 cases and 372 controls, a response rate of 85% and 75% respectively. Among men high Mantel-Haenszel odds ratios (MHORs) were obtained for electricity work (MHOR = 6.7, 95% confidence interval (95% CI) 1.0-32.1), welding (MHOR = 3.7, 95% CI 1.1-13.0), and impregnating agents (MHOR = 3.5, 95% CI 0.9-13.1). Heritability with regard to a neurodegenerative disease or thyroid disease seemed to predispose to a risk of developing MND (OR = 2.1, 95% CI 1.0-4.3). The highest OR was found for the combination of such heritability, exposure to solvents, and male sex (OR = 15.6, 95% CI 2.8-87.0), a combination that occurred for seven cases and three controls. Hereditary factors and external exposures had a different distribution among cases with the spinal type of MND than among cases with involvement of the pyramidal tract or bulbar paresis also.
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PMID:A case-control study of motor neurone disease: its relation to heritability, and occupational exposures, particularly to solvents. 146 80

Nine puppies suffered from progressive paresis with muscle wasting, hyporeflexia and extensor rigidity. CK-activity in serum was elevated and electrodiagnostic findings were indicative of lower motor neuron disease. Although lesions were also found in the CNS, additional neurological signs were rare, but CSF examination revealed the presence of inflammatory lesions. On pathologic examination, all animals had a disseminated necrotizing myositis. In addition, a disseminated encephalomyelitis was found as well as, in 2 cases, a neuritis. In the lesions of 6 animals protozoal organisms were found which were immunocytochemically identified as Neospora caninum. Our results show that the protozoal myositis-encephalitis syndrome in puppies can be diagnosed in the clinic with high probability. A clinical differentiation between toxoplasmosis and Neospora caninum infection is presently difficult.
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PMID:[The clinical diagnosis of protozoal myositis syndrome (Neospora caninum) of puppies]. 188 44

Herpes zoster may, in some instances, cause motor paralysis as well as the usual sensory and cutaneous manifestations. It is suggested that the presence of electromyographic denervation potentials be used as the criterion of muscle paresis in order to avoid mistaking atrophy of disuse for true lower motor neuron disease. Use of the proper physical therapy procedures hastens the recovery of function and may serve to retard denervation atrophy and fibrosis in patients with muscle paralysis.
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PMID:Muscle paralysis in herpes zoster. 582 75

Two patients with amyotrophic lateral sclerosis proved postmortem had nystagmus in addition to typical clinical signs of motor neuron disease. The first patient had gaze-evoked rotatory nystagmus that was followed by horizontal nystagmus in the primary position with supranuclear paresis of horizontal gaze and upgaze. The second patient had rotatory nystagmus that was evoked by lateral gaze, with normal range of eye movements. Nystagmus is so rare in motor neuron disease that these observations may imply another disease, but postmortem examination did not provide any other explanation. These two cases add to the increasing evidence that motor neuron disease comprises a heterogeneous group of disorders.
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PMID:Nystagmus in motor neuron disease: clinicopathological study of two cases. 646 63

The case of a progressive bulbar paresis in a nine and a half year old child is reported. The first symptoms were present at birth; however, the subsequent evolution was very low. Lesion of the motor nuclei of the V, VII, IX, XII, cranial nerves was evident on electromyographic investigation. Damage to the acoustic brain stem pathway was documented by the brain stem evoked potentials although audiometry was normal. No other neuronal systems or districts appeared to be damaged. The case suggests Fazio-Londe disease, although the involvement (albeit partial) of the auditory pathways recalls Van Laere syndrome. This supports the view that motor neuron disease in infancy is not an autonomous entity but a variant in a wide spectrum of progressive neuronal diseases.
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PMID:Progressive bulbar paralysis in childhood: a case report. 686 38

An 8-year-old nongravid female llama with a 1-month history of progressive posterior paresis was referred because of suspected degenerative myelopathy secondary to copper deficiency or plant poisoning. Neurologic examination revealed loss of conscious proprioception and slightly depressed bilateral patellar reflexes. Electromyographic examination of hindlimb flexors and extensors did not elicit evidence of lower motor neuron disease. Possible fragmentation and mottling of the 10th thoracic vertebral body were noted radiographically. Results of a lumbar CSF tap, complete blood count, and fecal flotation were not diagnostic. In the face of poor prognosis, the llama was euthanatized. Postmortem and histologic evaluation revealed, in addition to disseminated visceral granulomas, an extradural pyogranulomatous mass compressing the cord laterally at the level of T-10. Large numbers of Coccidioides immitis were dispersed throughout the granulomas. Complement fixing antibody tests in 11 other herd members showed evidence of C immitis infection in three.
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PMID:Coccidioidomycosis in the llama: case report and epidemiologic survey. 717 54

This study investigated the potential value of eccentric (ECC) and concentric (CONC) isokinetic testing for quantifying motor deficit in patients with spastic paresis secondary to motor neuron disease. We hypothesized that, at a moderately fast (120 degrees s-1) angular velocity, spastic patients would demonstrate different ECC-CONC torque relationships from healthy controls or patients with non-spastic neuromuscular disorders. Eleven patients with motor neuron disease having clinical evidence of spasticity, and 11 disease-control patients (with non-spastic disorders, e.g. lower motor neuron disease or myopathy) underwent isokinetic testing. One healthy subject was matched to each of the 22 patients. The average torque generated during maximal voluntary ECC and CONC knee flexion (KF) and extension (KE) was measured using an isokinetic dynamometer (Kin-Com). Reliability was established (all ICC > or = 0.97) for patient torque measurements. Relative strength (% of control subject torque) in spastic patients was significantly higher for ECC than for CONC actions in both KF and KE; conversely, in non-spastic disease-control patients relative strength was not affected by the type of muscle action. The ECC/CONC average torque ratios for KE and KF at 120 degrees s-1 were significantly greater in spastic patients than controls, but did not differ from controls in non-spastic patients. In spastic patients the ECC-CONC imbalances were related to ambulatory dysfunction. In four spastic patients followed with serial testing, the disproportion between ECC and CONC voluntary capacity persisted over time.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Eccentric and concentric muscle performance in patients with spastic paresis secondary to motor neuron disease. A preliminary report. 801 93

The ultrastructural features of a recently described inherited lower motor neuron disease were studied in 5 affected pigs. Clinical signs comprised progressive ataxia and paresis of variable severity. Affected pigs, 6, 7, 15, 15, and 19 weeks of age, and 2 unrelated healthy pigs, 9 and 15 weeks of age, were anesthetized and their tissues were fixed by whole body perfusion with mixed aldehydes. From 1 or more affected pigs, samples of cervical and lumbar spinal ventral horn, lateral and ventral spinal columns, dorsal and ventral lumbar spinal nerve roots, 2 peripheral nerves (Nn. phrenicus and fibularis communis), and 2 skeletal muscles (Mm. diaphragma and tibialis cranialis) were examined ultrastructurally. There was widespread degeneration of myelinated axons in peripheral nerves and in lateral and ventral columns of lumbar and cervical segments of spinal cord. Axonal degeneration was present in ventral spinal nerve roots and was absent in dorsal spinal nerve roots sampled at the same lumbar levels. Unmyelinated axons in peripheral nerves and spinal nerve roots were unaffected. In 4 of 5 affected pigs, there were atrophic alpha motor neurons in cervical spinal cord that contained dense, round osmiophilic perikaryal inclusions up to 4 microns in diameter and round swollen mitochondria. Axonal regeneration was present in N. phrenicus of the 19-week-old affected pig that had clinical signs of longest duration (10 weeks). There was no morphologic evidence of axonal degeneration or spinal neuronal atrophy in either control pig. The ultrastructural features of this motor neuron disease distinguish it from other reported progressive spinal neuropathies of pigs.
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PMID:Ultrastructural pathology of an inherited lower motor neuron disease of pigs. 806 56


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