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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A family--mother and 2 sons--with a heredodegenerative neurological disease is described. The disease started with bilateral optic atrophy, central scotoma, and color blindness during the second decade. This was followed by a quiescent period until additional neurological symptoms appeared, around the age of 50 years in the case of the mother and 40 and 30 years, respectively, in the sons. The additional symptoms were ataxia, spastic paresis, clonic jerks, grand mal seizures, psychia lability, and slight dementia. The disease was progressive, resulting in permanent hospitalization within a few years. The mother died at the age of 63 years and the sons at 46 and 43 years of age. Neuropathological examination revealed lesions histopathologically characteristic of subacute necrotizing encephalomyelopathy (SNE, Leigh disease), and their distribution in the brain and brainstem also conformed to this disease. On the basis of the clinical course and neuropathological findings, we consider that these 3 patients represent the first reported familial cases of the adult form of SNE.
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PMID:Familial subacute necrotizing encephalomyelopathy of the adult form (adult Leigh syndrome). 23 Jul 81

The management of patients with isolated oculomotor nerve palsies (OMPs) who have normal pupils and no other signs of neurological disease is a controversial issue. A more precise delineation of the clinical course of isolated OMPs may help to determine whether neuroradiologic evaluation is indicated in these cases. We studied 41 patients with isolated third cranial nerve palsies, emphasizing the times of progression and resolution of the oculomotor nerve dysfunction. The average interval from onset to development of maximal ophthalmoplegia failed to differentiate between a microvascular etiology (3.3 days) or posterior communicating artery aneurysm (3 days). Of the 28 patients with diabetic or idiopathic palsies, regardless of pupillary involvement, 68% had improvement of the oculomotor paresis within 4 weeks, 96% within 8 weeks, and 100% within 12 weeks of the onset of symptoms. Our study suggests that patients with pupil-sparing OMPs should be considered for extensive neuroradiologic evaluation only if there is deterioration or failure to improve within 4 to 8 weeks.
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PMID:Evolution of oculomotor nerve palsies. 153 96

The sparing effect of neurological damage on the development and progression of several arthritic conditions has been documented. We describe the first 2 cases of unilateral remitting seronegative symmetrical synovitis with pitting edema (RS3PE) syndrome in individuals with neurologic disorders. Case 1 suffered from birth trauma resulting in paresis of the right upper extremity and developed RS3PE syndrome in the nonaffected extremities. Case 2 developed RS3PE syndrome on the nonparetic side 7 years after a cerebrovascular accident resulting in hemiparesis.
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PMID:Remitting, seronegative (A) symmetrical synovitis with pitting edema--two cases of RS3PE syndrome. 818 58

Vacuolar degeneration was constantly induced in the CNS of 4-week-old ICR mice by intracerebral or intranasal inoculation of JHM-CC virus, a small plaque mutant of mouse hepatitis virus (JHM). Most animals showed no symptoms or only mild hindlimb paresis. Irrespective of clinical manifestations, the virus was isolated from the CNS up to days 14 to 16. Viral antigen expression in the CNS tissue was most extensive around days 5 to 7 and became undetectable on day 14. Viral antigens were localized almost exclusively to neurons, and the temporal sequence of viral antigen distribution after intranasal inoculation clearly indicated the virus spread through the olfactory and limbic systems into the brainstem and spinal cord, and possible cell-to cell transmission of the virus within the CNS. Vacuolar changes, most conspicuous in the brainstem and spinal cord, were steadily progressive up to 4 weeks after infection, but became indistinct by 4 months. Although the distribution of vacuolar lesions largely agreed with that of viral antigen-positive cells, the severity of vacuolation did not correlate with that of inflammation. Intramyelinic splitting, periaxonal edema, and swollen neurites were major ultrastructural substrates for vacuolar changes. This model could provide a better understanding of new types of neurologic disorders associated with viral infections, including vacuolar myelopathy in AIDS.
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PMID:Vacuolar degeneration in mice infected with a coronavirus JHM-CC strain. 216 Oct 91

We report 10 patients with primary hypoparathyroidism. Age at onset varied from 7 months to 52 years (mean 28); 7 were female. Diagnosis was established at a mean of 4.1 years after the appearance of clinical manifestations. Unexplained hypocalcemia (mean 5.3 mg/dl) and hyperphosphatemia (mean 6.4 mg/dl) were present in all patients. Prevalent symptoms included tetany (9 patients), seizures (5) and hypocalcemic cataracts (4). Clinical manifestations may be grouped into 5 types 1) tetany; 2) seizures; 3) other neurologic disorders (basal ganglia calcification, pseudotumor of the brain, ataxia, nystagmus, hypertonus, paresis); 4) disorders of the lens including fully developed cataracts and 5) skin alterations like psoriasis and others. Some of these run on acute course (seizures, tetany), others a subacute one (skin alterations) while others are rather chronic (cataract and other neurologic disorders). Seizures and electroencephalographic disorders predominate in younger patients while tetany is more prevalent in older subjects.
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PMID:[Idiopathic hypoparathyroidism, a syndrome with various clinical expressions: analysis of 10 cases]. 251 14

Two cases of a rare peripheral neurological disease (neuralgic amyotrophy of the lower extremity) are presented, with clinical symptoms (severe sciatic pain with motor paresis) that pose differential diagnostic difficulties against a hernia of a lumbar disk. Because of a tendency to heal by itself, the disease has a good prognosis. The diagnosis is based on a process of exclusion of herniated disks, lesions of the lumbar plexus in tumors or after radiation therapy, hematoma of the psoas after coagulation disturbances, birth, or trauma, and nutritive disruptions of the nervous system as in diabetes mellitus. Knowledge of the symptoms of this--in orthopedics--mostly unknown disease and critical interpretation of the clinical and medical-technical data are important to avoid wrong indications for surgery.
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PMID:Neuralgic amyotrophy of the lumbar area. Case report. 278 27

Physical fitness through exercise is the rage of today. Almost everybody is indulging in various forms of exercise from weight lifting to marathons. These regimens presuppose a normal muscle metabolism. However, a significant number of so-called normals end up with the symptoms of cramps, fatigue, and, in advanced cases, myoglobinuria. Exercise forms the mainstay of rehabilitation of patients with neurologic disorders manifesting as paresis or paralysis, and certain rheumatologic or metabolic problems are also handled via the medium of exercise therapy. It is, thus, imperative that there should be a clear understanding of normal muscle composition and metabolic responses. We will summarize the histology, histochemistry, physiology and metabolic responses of normal muscle to exercise and put this information in perspective in the light of various muscle disorders.
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PMID:Metabolic response to exercise and muscle disease. 293 40

A survey of the literature of neurological manifestations associated with the acquired immune deficiency syndrome (AIDS) shows a broad disease spectrum affecting approximately one third of the patients in large hospital series. The complications include focal cerebral lesions caused by abscesses, lymphomas, leucoencephalopathy or infarcts as well as encephalitis, meningitis and myelitis. Most opportunistic infections of the central nervous system presumably are caused by toxoplasma gondii, cytomegalovirus and cryptococcus neoformans. One tenth of all patients have neurological disease as their initial symptom of AIDS. The diagnosis should always be considered in patients at risk and in males with an unusual neurological history or with a peculiar CT scan of the brain. Besides the opportunistic complications of AIDS, LAV/HTLV-III itself probably attacks the nervous system and gives rise to concomitant lesions of the long tracts of the spinal cord with ataxia, paresis and spasticity and to subacute encephalopathy and peripheral nerve abnormalities as well.
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PMID:Neurological complications and concomitants of AIDS. 303 38

This study, initiated in June 1987, describes the epidemiology of bovine spongiform encephalopathy (BSE), a recently described novel neurological disease of domestic cattle first identified in Great Britain in November 1986. Records suggested that the earliest suspected cases occurred in April 1985. There was variability in the presenting signs and the disease course, but the majority of cases developed behavioural disorders, gait ataxia, paresis and loss of bodyweight; pruritus was not a predominant sign. The form of the epidemic was typical of an extended common source in which all affected animals were index cases. The use of therapeutic or agricultural chemicals on affected farms presented no common factors. Specific genetic analyses eliminated BSE from being exclusively determined by simple mendelian inheritance. Neither was there any evidence that it was introduced into Great Britain by imported cattle or semen. The study supports previous evidence of aetiological similarities between BSE and scrapie of sheep. The findings were consistent with exposure of cattle to a scrapie-like agent, via cattle feedstuffs containing ruminant-derived protein. It is suggested that exposure began in 1981/82 and that the majority of affected animals became infected in calfhood.
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PMID:Bovine spongiform encephalopathy: epidemiological studies. 321 47

In a cross-sectional population study of Danish patients with AIDS 16 of 23 had clinical signs of neurological disease with muscle weakness or ataxia of the lower limbs as the dominant manifestation. Tibial and median nerve conduction was mildly slowed in a few patients and 15 had widening of cerebral ventricles at CT. However, all had prolonged latency of cortical evoked response following tibial nerve stimulation mainly due to slowing through the spinal cord. The prolongation of the latency of the evoked cortical responses was most pronounced in patients with lower limb ataxia and/or paresis. It is concluded that affection of the long tracts of the spinal cord are closely associated with the human immunodeficiency virus infection.
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PMID:Myelopathy in AIDS. A clinical and electrophysiological study of 23 Danish patients. 335 13


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