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 motor function of the pharyngo-oesophageal (PO) segment during swallowing in terms of tonicity, relaxation and peristalsis was evaluated in 25 patients with a posterior cricopharyngeus impression. Functional abnormalities were common. Defective tonicity was present in 11 patients. Relaxation was normal in all patients except at the level of the cricopharyngeal muscle. Abnormal peristalsis was present in 19 patients as weakness, paresis or abnormal timing. The impression of the cricopharyngeus was effaced during the late stage of swallowing due to collapse proximal and distal to the cricopharyngeus. It was not due to successive distension at the level of the cricopharyngeus. In 11 patients there was some retention of barium proximal to the cricopharyngeus after the passage of the barium bolus. This was due to weakness in the inferior pharyngeal constrictor and/or an abnormal timing of the peristalsis whereby contraction of the cricopharyngeus occurred before peristalsis in the inferior pharyngeal constrictor had cleared the pharynx of barium. The observations indicate that bulging of the cricopharyngeal muscle is only one aspect of a profoundly altered motor function of the PO segment.
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PMID:The cricopharyngeus revisited. 375 82

Twenty-six patients with essential blepharospasm were treated with botulinum toxin by injection. The onset of protractor weakness in all patients ranged from one to five days following treatment. Maximal weakness developed within 12 days. There was a variable and gradual return of protractor strength over eight to 29 weeks in most patients and, with it, a return of spasm. Twenty-five patients received some degree of functional relief following initial injection. In most patients, however, the post-injection result could not be stabilized and repeat injections have been necessary to control recurrent spasms. There was one treatment failure. Three patients treated by injection following previous neurectomy and myectomy appeared to have a reduced requirement for subsequent injections. Complications included transient ptosis in six patients and mild exposure symptoms in four patients. Extraocular muscle paresis did not occur. There were no systemic side effects from the botulinum toxin injections.
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PMID:Botulinum toxin for the treatment of essential blepharospasm. 380 85

Moderate unilateral weakness of shoulder and hip muscles and limb-kinetic apraxia were observed in 11 patients with frontal lobe lesions on the side opposite to the neurological deficits. On the CT scans, the posterior border of the lesions lay anterior to the precentral gyrus, thus involving the premotor cortex but not the primary motor cortex. In 9 cases, the lesions were caused by a brain infarct, in 2 cases by a tumour. In 1 patient the lesion was purely subcortical. Whereas the paresis affected all hip muscles, in the shoulder mainly those movements associated with abduction and elevation of the arm were disturbed. The EMG showed considerable delays for the preactivation of proximal arm muscles during rapid arm movements, thus interfering with the normal proximal-distal sequencing of muscle action. Limb-kinetic apraxia only became apparent during tasks requiring certain coordinations between both arms or legs. Bimanual interaction was normal. Two patients with proximal hemiparesis and small lesions in the precentral gyrus which have been examined for comparison showed no limb-kinetic apraxia and different distributions of the paretic shoulder girdle muscles. In view of the long-standing controversies as to the functional role of the premotor cortex and the question of specific deficits after lesions of this area, the relevant literature is reviewed.
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PMID:Lesions of premotor cortex in man. 392 94

To investigate the cat as a test animal for organophosphorous compound-induced delayed neurotoxicity, tri-o-cresyl phosphate (TOCP) was applied directly on the unprotected back of the neck of young adult cats. Single dermal doses, ranging from 250 to 2000 mg/kg TOCP, or subchronic daily administration of 1 to 100 mg/kg produced delayed neurotoxic effects in the cat. Severity of delayed neurotoxicity depended on the dose and duration. Clinical signs were characterized by hindlimb weakness, ataxia, and paresis. Electromyographic abnormalities resulting from acute denervation were observed in most cats that developed a neurologic deficit. No changes were seen in the motor nerve conduction, thus suggesting that the deficits were in the terminal branch rather than being diffuse lesions in the peripheral nerves. These results correlated well with histopathologic results showing lesions in the most distal portion of the longest tracts in both central and peripheral nervous systems. In the spinal cord, histopathologic studies showed that the ascending tracts of the upper cervical levels and descending tracts of the lumbosacral regions were affected most frequently. Although this study shows that the cat, like the chicken, is susceptible to TOCP-induced delayed neurotoxicity, it demonstrates two differences between the cat and the chicken: greater sensitivity of the cat to the acute effect of TOCP, and greater extent of recovery or improvement of the cat from delayed neurotoxicity. This recovery was demonstrated by: improvement of clinical signs, gain in body weight, disappearance of electromyographic abnormalities, and regeneration of peripheral nerves. Dermal administration of a single 100-mg/kg dose or subchronic 0.5-mg/kg doses of TOCP did not produce delayed neurotoxicity.
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PMID:Electromyographic, neuropathologic, and functional correlates in the cat as the result of tri-o-cresyl phosphate delayed neurotoxicity. 395 42

Sclerosteosis is a rare, potentially lethal, autosomal recessive, progressive craniotubular sclerosing bone dysplasia with characteristic facial and skeletal features. The temporal bone changes include a marked increase in overall size, extensive sclerosis, narrowing of the external auditory canal, and severe constriction of the internal auditory meatus, fallopian canal, eustachian tube, and middle ear cleft. Attenuation of the bony canals of the 9th, 10th, and 11th cranial nerves, reduction in size of the internal carotid artery, and severe obliteration of the sigmoid sinus and jugular bulb also occur. Loss of hearing, generally bilateral, is a frequent symptom. It often manifests in early childhood and initially is expressed as sound conduction impairment. Later, a sensorineural hearing loss and loss of vestibular nerve function often develop. Impairment of facial nerve function is another feature occasionally present at birth. In the beginning, a unilateral intermittent facial weakness may occur which eventually progresses to a bilateral permanent facial paresis. The histologic examination of the temporal bones from a patient with sclerosteosis explains the mechanisms involved in the progressive impairment of sound conduction and loss of cochlear, vestibular, and facial nerve function. There is a decrease of the arterial blood supply to the brain and an obstruction of the venous drainage from it. The histopathology reveals the obstacles to decompression of the middle ear cleft, ossicular chain, internal auditory and facial canals, and the risks, and in many instances the contraindications, to such procedures. On the other hand, decompression of the sigmoid sinus and jugular bulb should be considered as an additional life-saving procedure in conjunction with the prophylactic craniotomy recommended in all adult patients.
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PMID:Sclerosteosis involving the temporal bone: histopathologic aspects. 395 65

A patient developed weakness in the upper limbs, eventually causing brachial diplegia with only slight paresis of the legs after rapid correction of severe hyponatraemia. Pseudobulbar palsy, mental confusion and urinary incontinence were also present. CT scan showed a zone of lucency in the pons. Clinical recovery occurred and the zone of lucency had disappeared 12 months after the appearance of the neurological signs.
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PMID:Brachial diplegia in central pontine myelinolysis. 397 43

Electrophysiological aspects of thiamine depletion in the rat induced by dietary deficiency are described. Behavioral changes as well as qualitative and quantitative alterations in the sensitivity of cerebellar Purkinje cells to iontophoretically-applied 5-hydroxytryptamine (5-HT) were observed. Thiamine-deficient rats were characterized essentially by ataxia, piloerection, paresis, apparent weakness, and hypothermia after 4-6 weeks on a thiamine-free diet. Basal Purkinje cell firing frequency was unaffected by thiamine deficiency. The response of Purkinje cells to iontophoretically-applied 5-HT was solely inhibitory in deficient rats. In control rats, however, responses to 5-HT were excitatory, biphasic, or inhibitory. Neurons in the thiamine-deficient animals were more sensitive to the inhibitory effects of 5-HT, as demonstrated by a significant parallel shift to the left of the dose-response curve. Durations of 5-HT effects were similar in both groups. Dose-response relationships for GABA-induced inhibition of Purkinje cell firing from thiamine deficient and control rats did not differ from one another. These data demonstrate a relatively selective effect of thiamine depletion on cerebellar serotonergic neurotransmission assessed electrophysiologically. We believe there is up-regulation of 5-HT receptors on Purkinje cells caused by thiamine deficiency-induced impairment of indoleamine input to the cerebellum from raphe and related nuclei.
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PMID:Enhanced sensitivity of cerebellar Purkinje cells to iontophoretically-applied serotonin in thiamine deficiency. 398 3

An analysis of associated deformities in 74 patients with isolated microtia is reported. Microtia should be considered a microform of hemifacial microsomia because of similar (1) asymmetrical nature of the defects, (2) incidence and pattern of seventh nerve paresis, (3) correlation of the degree of seventh nerve weakness with grade of auricular deformity and not with the severity of mandibular hypoplasia, (4) right-sided preponderance, (5) incidence of associated cleft lip and palate, (6) male predilection, and (7) equivocal mode of inheritance. These clinical observations confirm the concept that microtia and hemifacial microsomia have the same etiopathogenesis which is not shared by mandibulofacial dysostosis.
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PMID:Microtia: a microform of hemifacial microsomia. 407 Apr 53

Twenty-three patients were seen with entrapment neuropathy in a two-and-a-half-year period. Symptoms consisted of pain, paresis, and paraesthesia in the distribution of the common peroneal nerve. Some degree of paresis was often present, which in five patients was severe enough to cause drop foot. In 20 patients decompression of the entrapped nerve at the neck of the fibula was quickly and completely successful. It is suggested that the ankle weakness which frequently follows sprains and other forced inversion injuries may often be at least partially due to entrapment of the common peroneal nerve.
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PMID:Weak ankles. A study of common peroneal entrapment neuropathy. 430 53

Mammalian exposure to toxic levels of the trialkyltin compounds, triethyltin (TET) and trimethyltin, results in pathological manifestations largely restricted to the nervous system. The remarkable features of TET toxicity are cerebral edema and muscular weakness. Rats exposed orally to TET (10-30mg TET Br/l of drinking water) progress through an increasingly compromised state beginning with mild ataxia and hindlimb weakness after one week, spastic paresis of the hindlimbs by two weeks; and hindlimb paraplegia and sensory changes by 3 weeks. Histopathological studies of chronic TET-exposed rats report minimal ultrastructural damage to distal peripheral nerves, myelin, and muscle. Chromatolytic reactions are observed in some alpha motor neurons; intramyelinic vacuolization in the ventral roots and horn is substantial by 3 weeks. Myelin vacuolization and degeneration are observed to a lesser extent in the dorsal roots of the spinal cord. Wet weights and myofiber diameters of EDL and soleus muscles are reduced during chronic TET intoxication, but no histopathology is evident using light microscopy. Conduction of compound action potentials in vivo along distal sensory fibers, ventral roots and distal motor fibers (in sciatic n.) is normal in 3 week TET rats as compared to control; however, nerve conduction velocity is decreased in the segment of the H-reflex arc involving the dorsal roots. Earlier studies by Stoner and coworkers led to suggestions that the neuromuscular junction may be preferentially affected by TET and could contribute, in part, to the symptoms of muscular weakness. In support of this hypothesis preliminary studies from our laboratory and others indicate that neurotransmission is functionally depressed at the myoneural junction following chronic TET treatment in vivo or when applied in vitro to isolated muscle preparations. Stimulated, but not unstimulated, release of acetylcholine from the vascular perfused rat phrenic nerve-hemidiaphragm preparation is decreased by TET especially at higher stimulation rates (20 Hz). In vitro administration of TET Br (10(-6)M) results in an irreversible decrease in the amplitude of evoked endplate potentials; chronic in vivo exposure to TET causes a decrease in the resting membrane potential of soleus muscle (in situ recordings) and provokes a peculiar post-stimulus (200Hz bursts) elevation of spontaneous miniature endplate potentials in isolated cut diaphragm preparations.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neuromuscular function and organotin compounds. 609 43


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