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

The authors describe a case of botulism in a 3-month-old infant infected with Clostridium botulinum type A. Symptomatology developed within four days, persisted for two weeks, then regressed. Symptoms were paresis of face muscles, hyporeactive pupils, loss of succion and deglutition, axial hypotonia, weakness of peripheral muscles, lability of the autonomic nervous system with acute episodes of bradycardia and constipation. Anomalies of the electroen-cephalogram and of the auditory evoked responses suggest that the toxin penetrated the central nervous system. Treatment was symptomatic, without need for assisted ventilation. It was not possible to detect the source of infection.
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PMID:[Botulism in infancy]. 266 93

A case of hypoglycemic hemiparesis in a fifteen-year-old girl with insulin dependent diabetes mellitus (IDDM) is described. The initial presentation included left facial paresis and muscular weakness of the left upper and lower extremities, associated with a blood glucose level of 31 mg/dL. The patient recovered completely after a glucose infusion. Her neurological examination became normal within 24 hours and remained so for a follow-up period of 6 months. Hypoglycemic hemiparesis is rarely described in children and adolescents.
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PMID:Hypoglycemic hemiplegia in an adolescent with insulin-dependent diabetes mellitus: a case report and a review of the literature. 266 69

The strength of 12 muscle groups of the arm was measured to determine the distribution of upper motor neuron weakness in man. Three groups of subjects were studied: 14 intact volunteers (both sides recorded), 10 patients with unilateral arm paresis (both sides recorded) and 6 patients with severe paralysis of the arm (the 'intact' arm only measured). On the side contralateral to the causative lesion the pattern of weakness was not the same in all patients. Shoulder muscles were relatively spared while the wrist and finger flexors were relatively severely affected, the difference being statistically significant. In hemiparetic and hemiplegic patients the strength of muscles ipsilateral to the lesion was reduced compared with normal controls. These observations refine previous clinical descriptions of upper motor neuron weakness and have implications for its pathophysiology.
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PMID:The distribution of muscular weakness in upper motor neuron lesions affecting the arm. 273 Oct 28

During the second stage of an illness caused by Borrelia burgdorferi, a young woman developed a myopathic syndrome characterised by severe muscular pains, incapacitating weakness of the proximal limb and the neck, as well as the bulbar muscles and elevated serum CK levels. Muscle biopsy revealed a non-inflammatory necrotising myopathy. B. burgdorferi infection was confirmed by a considerable rise of specific IgG antibodies. A course of high dose steroids alleviated the myalgias, but paresis began to improve only after treatment with antibiotics. Our observations confirm that B burgdorferi can cause, through an undertermined mechanism, a necrotising myopathy, in addition to the wide spectrum of already known neurological complications.
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PMID:Myositis during Borrelia burgdorferi infection (Lyme disease). 279 56

A 38-year-old man with severe canal stenosis at the level of the atlas is reported. The clinical manifestations were muscular weakness and wasting of the upper limbs and spastic paresis of the lower limbs, which all progressed slowly. The atlas was hypoplastic and its retrodental space was narrow. The spinal cord was markedly compressed between the odontoid process and the posterior arch of the atlas. The clinical manifestations improved after a posterior laminectomy of the atlas.
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PMID:Marked canal stenosis at the level of the atlas. 279 28

The patient, a man aged 57, was admitted to our clinic on May 1, 1987, because of severe vertigo and unsteadiness in standing. Since the age of 55 he had been suffered from hypertension and atrial fibrillation. In September, 1986, he experienced vertigo but recovered soon without therapy. On April 25, 1987, while working, he noticed severe vertigo, nausea and vomiting. He was admitted to a hospital, and then transferred to our clinic. On admission, he was alert and the mentality was normal. Slight ptosis abducent nerve paresis, hypalgesia on the forehead, nose and cheek, facial paresis of peripheral type and hypacusis were detected on the left side. No anisocoria was observed. Sweating was impaired over the left side of the face. Elevation of the soft palate was limited on the left side and the tongue deviated to the left on protrusion. Dysarthria was detected. Though there was no muscular weakness in the extremities, incoordination and dysmetria were noted in the left arm and leg. He could not stand up because of vertigo and unsteadiness. There was no sensory disturbance in the trunk and extremities. Deep tendon reflexes were well elicited and no pathological reflex was observed. These clinical manifestations, except for the ipsilateral palatal and lingual disturbances, were typical of the lateral inferior pontine syndrome caused by occlusion of anterior inferior cerebellar artery, and the lesion was clearly demonstrated by horizontal and coronal MRI. The palatal and lingual disturbances might be due to the involvements of the corticobulbar tracts of the 10th and 12th nerves after the fibers had decussated.
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PMID:[Lateral inferior pontine syndrome: a case report]. 280 19

A 65-year-old female had polyglucosan body myopathy, usually called "polysaccharide storage myopathy" that presented with increasing distal paresis and only slight weakness of the proximal limb girdle musculature. Muscle biopsy revealed dystrophic changes that could have been mistaken for muscular dystrophy, and the characteristic light as well as electron microscopic features of polyglucosan bodies varying in number at the three sites of muscle biopsies studied (deltoid, quadriceps femoris, and anterior tibial muscle). In addition, there were occasional nonspecific paracristalline mitochondrial inclusions. No abnormal polyglucosan deposits were found in the sural nerve biopsy. Morphometric evaluation of nerve fiber cross sectional areas revealed some degree of demyelination and remyelination, and of nerve fiber degeneration and regeneration. Unlike a series of 10 unselected control sural nerves with Renaut bodies, hypomyelinated nerve fibers were more numerous adjacent to Renaut bodies. This is the first case of polyglucosan body myopathy in which the axon/myelin ratio and the axonal circularity factor in the sural nerve is evaluated and in which a definite lack of polyglucosan bodies or other abnormal glycogen storage products in a peripheral nerve is documented.
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PMID:Adult polyglucosan body myopathy with subclinical peripheral neuropathy: case report and review of diseases associated with polyglucosan body accumulation. 285 83

The development of organophosphorus-induced delayed neurotoxicity (OPIDN) was studied in the European ferret (Mustela putorius furo). A single oral or dermal dose of 250, 500, or 1000 mg tri-o-tolyl phosphate (TOTP)/kg body weight was administered to adult male ferrets. Corn oil served as the vehicle in the oral test and 95% ethanol was the vehicle in the dermal test. At 48 h posttreatment, half the animals in each group were killed by cervical dislocation for assessment of whole-brain neuropathy target esterase (NTE) activity. The remaining 5 animals per group were observed and examined neurologically on a daily basis for a subsequent 54 d. All ferrets dosed dermally with 1000 mg TOTP/kg body weight developed clinical signs characteristic of OPIDN ranging from ataxia to partial paresis. Ferrets administered 250 and 500 mg TOTP/kg body weight via the dermal route displayed variable degrees of hind limb weakness and ataxia. Of the animals dosed orally, only those in the 1000 mg TOTP/kg body weight group showed clinical signs indicative of OPIDN. These signs did not progress beyond mild ataxia. Small amounts of axonal degeneration were noted in the dorsolateral part of the lateral funiculus and in the fasciculus gracilis of spinal cords in ferrets receiving dermal doses of 1000 mg TOTP/kg body weight. Whole-brain neuropathy target esterase activity was also maximally inhibited (46%) in animals receiving 1000 mg TOTP/kg dermally. These results suggest that the ferret is a species that is susceptible to OPIDN.
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PMID:Delayed neurotoxic effects of tri-o-tolyl phosphate in the European ferret. 291 34

Based on statistical analysis of 97 chronic low back patients, a pelvic list model has been proposed explaining the correlation between leg length discrepancies (LLD) and sciatica. This model suggests that asymmetrical pronation patterns (one pedal arch dropping more than the contralateral pedal arch) initiates a forward downward rotation within the sacroiliac joint. Entrapment of the sciatic nerve between the piriformis muscle and sacrospinous ligament occurs. Clinically, paresis is observed: numbness, weakness and eventually paralysis of the affected limb. Based on this work, the authors have comprised a classification dividing LLD into two main categories: functional and anatomical. Functional LLD have been subdivided into two types of lists: static and dynamic. Treatment based on a combination of chiropractic and podiatric therapy is presented with a 6-month follow-up. Analysis of the success in this tandem approach is very promising. Concurrently, a chondromalacia model is proposed explaining the pathomechanical events associated with oblique tracking patellar syndrome. The authors suggest that excessive pronation is the causative factor directing asynchronous rotation between the shank and femur. This forces the patella out of its normal tracking groove, which, in turn, generates erosion between the inferior margin of the patella and femoral epicondyles.
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PMID:Excessive pronation: a major biomechanical determinant in the development of chondromalacia and pelvic lists. 297 5

Three patients developed prominent neurologic symptoms and signs associated with Schoenlein-Henoch purpura. A 7 1/2-year-old boy was seen with status epilepticus after a 2-week history of generalized headaches, irritability, and intermittent colicky abdominal pain. A left hemiparesis and a left homonymous hemianopia with a right gaze preference that were present on initial examinations gradually resolved, but a mild left arm paresis persisted. Cutaneous, renal, and joint involvement followed initial CNS manifestations. The second patient, a 7-year-old girl, had a complex partial seizure with secondary generalization and a postictal hemiparesis seven days after presentation with classic signs of Schoenlein-Henoch purpura. Behavioral changes were noted during the acute phase of the illness. The third patient, a 13-year-old boy, developed signs of a left brachial plexopathy and transient weakness of his right leg during a complicated course of Schoenlein-Henoch purpura. Review of the world literature indicates that headaches and mental status changes are the most frequent neurologic complications of Schoenlein-Henoch purpura, followed by seizures, focal neurologic deficits, mononeuropathies, and polyradiculoneuropathies. The vasculitis of Schoenlein-Henoch purpura can involve the nervous system and may add significantly to the morbidity of the illness.
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PMID:Neurologic manifestations of Schoenlein-Henoch purpura: report of three cases and review of the literature. 298 37


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