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)

The pseudoclaudication syndrome, now a well known neurological entity, can simulate intermittent claudication of arterial origin in its clinical appearance. Walking and sometimes simply standing upright for a while can cause transitory pain, numbness or weakness in the legs. The symptoms are caused by entrapment of the cauda equina fibers. Intermittent bladder paresis with total inability of micturition despite urgency to void may sometimes be a prominent feature of the syndrome, a fact that seems to be less well known as seen from a review of the literature.
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PMID:Intermittent bladder paresis in the pseudoclaudication syndrome. 126 26

A 41 year old man developed a myolysis with myoglobinuria during a period of high fever. The clinical signs were severe myalgia with general muscular weakness without manifest localized paresis. Electromyographically a diffuse generalized floride myopathy was found. Besides the extreme increase of CPK, a myoglobinuria was already macroscopically visible, which caused an acute renal failure. The treatment included corticosteroids and hemodialysis. An illness of several weaks was followed by complete recovery. As other known factors leading to myoglobinuria have been excluded, and the complement fixation reaction for Herpes simplex was more than 1:80, a viral-toxic etiology of this disease might be considered.
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PMID:[Acute myoglobinuria accompanied by renal failure in high febril infection (author's transl)]. 126 94

We present a very rare case of 7 year-old-girl who had a pontine glioma with supratentorial meningeal involvement. She complained severe headache with meningeal irritation. She showed fluctuating cranial nerve impairment of the both abducens and glosopharyngeal nerves but no signs of weakness or facial paresis. She also reported two episodes of generalized convulsion with unconsciousness during admission. MRI disclosed a hypointensity intrinsic brainstem mass with an enhancing exophytic component in the prepontine cistern and a sharp contrast uptake is disclosed in the left-meninges of the supratentrial structures. An open biopsy was performed and diagnosed as a high grade astrocytoma.
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PMID:[Brainstem glioma with supratentorial meningeal dissemination--a case report]. 128 96

We reported a 49-year-old mother and her 28-year-old son with autosomal dominantly inherited bulbar spinal muscular atrophy (AD-BSMA). They showed progressive bulbar paresis, muscle wasting and weakness dominant in the proximal groups of limb muscles, and finger tremor. Onset of illness was in adult life. In laboratory examinations, elevated creatine kinase in serum and neurogenic changes either in EMG or muscle biopsy were noted. The son had neither gynecomastia nor abnormal sexual hormone levels which were observed in the sex-linked recessive bulbar spinal muscular atrophy (SR-BSMA). Elongation due to the CAG repeats at the androgen receptor gene of the X chromosome in SR-BSMA was not detected. In conclusion, it is clear that AD-BSMA is different from SR-BSMA on the basis of clinical and genetical aspects.
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PMID:[A mother and her son with autosomal dominant bulbar spinal muscular atrophy]. 130 Feb 63

A dimethoate-poisoned woman gradually developed a moderately severe cholinergic crisis that was readily treated by atropine. After being symptom-free for nearly two days, she suffered from sudden life-threatening respiratory paresis and weakness of the facial, extraocular, neck flexor and proximal limb muscles. Muscarinic symptoms were absent. Cholinesterase inhibition was severe, and EMG revealed marked decrements at low rates of repetitive nerve stimulation, and increments at a high rate. The clinical course was compatible with the Intermediate Syndrome. This syndrome seems due to persistent cholinesterase inhibition presumably leading to combined pre- and postsynaptic impairment of neuromuscular transmission. Inadequate pralidoxime therapy is proposed but not established as contributory. Prolonged monitoring of respiratory function in patients poisoned by particular organophosphate agents is mandatory.
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PMID:The intermediate syndrome in organophosphate poisoning: presentation of a case and review of the literature. 132 92

The main findings in unilateral INO are paresis of adduction in the eye on the side of the lesion (for conjugate but not vergence eye movements) and abduction nystagmus in the eye on the side opposite to the lesion. A skew deviation (eye usually higher on the side of the lesion) or a dissociated, mixed vertical-torsional nystagmus, with the eye beating down on the side of the lesion, may also occur. The main findings in bilateral INO are paresis of adduction in both eyes, bilateral abduction nystagmus and, in the vertical plane, impaired gaze-holding, vestibular responses and smooth tracking. Abduction nystagmus in INO may have a number of causes; probably most common are a gaze-evoked nystagmus superimposed on adduction weakness and adaptation to adduction weakness. Most of the findings in INO can be explained by interruption of projections from abducens internuclear neurones, mediating adduction, and from the vestibular nuclei, mediating both canal- and otolith-induced reflexes as well as vertical gaze holding and pursuit. Extension of the lesion to structures near but outside the MLF, or involvement of cell bodies intermixed with MLF fibres, may also be important in the pathogenesis of the abduction nystagmus and the occasional slowing of abducting saccades.
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PMID:Internuclear ophthalmoplegia: pathophysiology and diagnosis. 134 79

Recurring episodes of extreme leg weakness and associated mortality were documented in a turkey flock at 8 to 15 weeks of age. Flock mortality attributed to posterior paresis was approximately 12%, or 4800 of 40,000 turkeys. Four of six open-confinement units were affected. Gross and histological examinations revealed no significant lesions. Immunology and virology were uninformative. There were no significant differences in serum chemistry between clinically affected and normal turkeys. Testing of feed, water, soil, and tissues revealed no common toxicants. Isolation and supportive care for affected turkeys, both in the laboratory and in the field, frequently resulted in full recovery. Injection of a test group of affected turkeys with Type C botulism antitoxin appeared to enhance recovery. However, repeated attempts to detect botulism toxin in serum, liver, or cecal contents using mouse bioassay procedures were unsuccessful.
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PMID:Recurrent transient paresis in a turkey flock. 141 11

A parathion-poisoned patient with prolonged cholinesterase inhibition due to impaired hepatic metabolism and urinary excretion is reported. An intermediate syndrome characterized by respiratory paresis, weakness in the territory of several motor cranial nerves and of proximal limb and neck flexor muscles, persisted for 3 weeks. During this whole period, cholinesterase remained markedly reduced. Serial EMGs with repetitive nerve stimulation pointed to a combined pre- and postsynaptic disorder of neuromuscular transmission. Electron microscopy of an intercostal muscle biopsy showed focal degeneration at the poorly branched postsynaptic folds, and was considered to be nonspecific.
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PMID:Intermediate syndrome due to prolonged parathion poisoning. 145 89

Selenium toxicosis was diagnosed in feeder pigs on a central Michigan farm. Use of a commercial supplement, found to contain approximately 20 times the intended Se concentration, resulted in a Se concentration of 8.1 mg/kg of the complete feed. This was fed for 34 days during which daily feed consumption decreased approximately 35%, several pigs developed weakness and forelimb paresis, and 1 pig died. The highest serum Se concentration measured was 1,550 ng/ml (normal range, 140 to 190 ng/ml). Normal feed consumption returned when an alternative feed was provided. Mean serum Se concentrations of representative pigs, monitored over the subsequent 26 days, decreased from 905 to 258 ng/ml. Histologic examination of a recovering pig revealed skeletal and cardiac myopathy and bilaterally symmetric malacia of the gray matter of the ventral horns of the spinal cord. During the developing toxicosis, the pigs consumed an estimated 11.4 mg of Se/pig/d.
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PMID:Selenium toxicosis in feeder pigs. 150 Mar 26

A prolonged type of organophosphate toxicity, previously characterized as the Intermediate Syndrome, has been recognized in 6 out of 7 prospectively studied patients poisoned by insecticide containing parathion and methyl parathion in equal proportions. The clinical characteristics included respiratory paresis, weakness in the territories of several motor cranial nerves, neck flexors and proximal limb muscles, and depressed tendon reflexes, all lasting for several days or weeks. Electromyography in the early stages disclosed diverse types of impaired neuromuscular transmission. EMG normalization preceded clinical recovery. Severe plasma butyrylcholinesterase and erythrocyte acetylcholinesterase inhibition persisted along with the occurrence of Intermediate Syndrome-related symptoms. We conclude that combined parathion and methyl parathion poisoning is more likely to induce Intermediate Syndrome than parathion poisoning alone. The mechanisms underlying this difference remain obscure. The Intermediate Syndrome shows clinical and electromyographic hallmarks of combined postsynaptic impairment of neuromuscular transmission.
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PMID:Prolonged toxicity with intermediate syndrome after combined parathion and methyl parathion poisoning. 151 8


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