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

Cleidocranial dysostosis (CCD) is a rare congenital disorder characterized by the heredity, the disturbance of the ossification of the skull and clavicles, and dental anomaly. The entity of CCD was established by Marie and Sainton in 1898. In Japan about 150 cases have been reported since Haneda's first report in 1933. Recently we experienced a rare case of CCD associated with the temporal arachnoid cyst. The patient was a 61-year-old male who had suffered from mild spastic paresis of the left upper extremity since his childhood. One morning he suddenly noticed motor weakness of the left upper and lower extremities and was transferred to our hospital. On admission we observed the left hemiparesis (MMT 3/5), the left central type facial palsy, and the left long tract signs. Physical examination disclosed frontal bossing, depression of the forehead, sloped shoulders, cone-shaped thorax, and thoracic scoliosis. Plain skull radiograph showed persistent metopic suture and frontal fontanelle, many wormian bones around coronal and lambdoid sutures. Plain radiographs of the systemic bones also showed typical features of CCD such as dysplasia of the lateral third of the bilateral clavicles, deformities of the cervical vertebral bodies, thoracic scoliosis, and wide symphysis. CT scan disclosed the right putaminal hemorrhage, the right temporal arachnoid cyst, enlargement of the right middle fossa, thinning of the temporal bone adjacent to the arachnoid cyst. It also showed the atrophy of the right cerebral peduncle and midbrain. Surgical treatment was performed to remove the hematoma and release the cyst. Several neurological disorders associated with CCD have been reported such as epilepsy, mental retardation, spastic paresis etc.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of cleidocranial dysostosis associated with arachnoid cyst]. 343 33

A 16-year-old woman was admitted to our hospital because of abdominal pain, paresis of extremities, and muscle weakness. Bartter's syndrome was suspected because of the features of the hypokalemia, hyperaldosteronism, hyperreninemia, increased concentration of plasma angiotensin I & II, the defect in distal fractional reabsorption of chloride and normotension. The concentrations of the plasma angiotensin II and aldosterone, however, were decreased to normal levels after admission probably due to a decrease in the salt intake because of the regular hospital diet. Furthermore, the hyperplasia of the juxtaglomerular apparatus was not found. Therefore, at first we thought we were dealing with another disease, that is pseudo-Bartter's syndrome, which is caused by different pathogenesis. Gill et al. reported that the defect in distal fractional reabsorption of chloride was a characteristic feature in the diagnosis of the Bartter's syndrome. Thus, we tried to explain the clinical symptoms and diagnosis of this case as the Bartter's syndrome according to the theory of Gill et al. If the defect of chloride reabsorption was the only pathogenesis of the Bartter's syndrome, other symptoms seen in our case could be thought of as secondary (or new) changes. Therefore, this case could be differentiated from the pseudo-Bartter's syndrome or the "true" Bartter's syndrome because of the clinical symptoms and the defect in chloride reabsorption.
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PMID:[A case of Bartter-like syndrome with abdominal pain, paresis of the extremities and muscle weakness]. 343 14

Botulinum Toxin A injected into the levator palpebrae superioris produces a flaccid ptosis of the upper lid and provides a safe and effective protection for the cornea to aid healing in indolent ulceration or as prophylaxis when there is fifth or seventh cranial nerve damage. Fifteen patients have received this treatment. Levator paresis, producing ptosis for a mean of 2-3 weeks and recovering in a mean of 8.1 weeks was successfully produced in all patients and complete corneal healing was produced in 80% of patients. The major side effect was weakness of the superior rectus muscle which occurred in 80% of cases and lasted a mean of 6 weeks.
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PMID:Botulinum toxin A induced protective ptosis. 344 41

A retrospective study of 75 consecutive cases of spontaneous cerebellar haemorrhage was undertaken in order to evaluate the clinical features and natural history of this condition. A wide spectrum of clinical findings contributed to the poor clinical diagnostic accuracy of 23 per cent, with common misdiagnoses including brainstem stroke and vestibular or labyrinthine disturbance. Presentation with, or the later development of stupor or coma strongly correlated with poor outcome (severe disability or death; p = 0.002). The characteristics of conscious patients who remained stable were compared with those who subsequently deteriorated. The initial conscious state (alert, drowsy or confused), severity of symptoms and ataxia, and the size of haemorrhage on CT scan were not reliable prognostic indicators. However, the presence of bilateral gaze paresis, anarthria (present in eight cases), limb weakness, a systolic blood pressure above 200 mmHg and moderate hydrocephalus significantly correlated with a poor outcome. The presence of these signs warrants consideration of urgent surgical intervention at the time of diagnosis. Since no clinical or radiological findings excluded the possibility of further deterioration, careful monitoring in an intensive care unit is necessary within the first 48 h in those conscious patients who are likely to remain stable. Guidelines for making the clinical diagnosis and for selecting those patients who will require transfer to adequately equipped centres are suggested.
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PMID:Cerebellar haemorrhage--diagnosis and treatment: a study of 75 consecutive cases. 344 85

This report deals with what is to be known in applying ENG in the everyday office. From vestibular, visual and proprioceptive informations central neural processing evolve to stabilize images on the retina. ENG can perform an analysis of these systems, alone or interacting. Anatomical, neurophysiological backgrounds and experimental pathophysiology results are first described. The methodic rule of anamnesis is emphasized and the non instrumental examination is outlined. Concerning the technical aspects and the ENG achievement, some nonlinearities are stressed. Next, procedure of eye movements recording, oculomotor and vestibular testing are described. Alertness, stimulation order, gaze direction and drugs influence the response. The nystagmus responses are evaluated by quantitative parameters and morphological aspects. The variability of these implies the multiplication of the pathological arguments. Peripheral vestibular disturbances lead to labyrinthine paresis or paralysis and to nystagmus directional preponderance, sometimes alone, often combined. Thermic predominance may be associated and cause of some interpretation difficulty. Diagnosis of central neurological disturbances is submitted to four conditions: only specific criteria selection; complete oculomotor and vestibular testing; graduated conclusions in function of the criteria number; no etiological but only functional or topographical diagnosis. Central vestibular syndromes lead also to labyrinthine weakness or nystagmus directional preponderance but, first at all, to specific criteria who are: saccadic, pursuit and horizontal optokinetic abnormalities, central spontaneous or positional nystagmus, failure of fixation suppression, hyperreflexia, perverted nystagmus, slowing of the nystagmus fast phases, slowing-down of the nystagmus slow phases, anisonystagmus, vertical optokinetic deficits and retraction nystagmus. Finally, these dysfunctions incidence in personal observations with some multi or unifocal central pathologies is described and the correspondent more characteristic findings are outlined.
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PMID:[Electronystagmography aspects of peripheral and central vestibular syndromes]. 349 58

A rare case of extracranial internal carotid occlusion with a coexisting ipsilateral internal carotid aneurysm is reported. A 50-year-old male had a sudden onset of severe headache, vomiting and right motor weakness on May 14, 1984. Two days later the patient was transferred to our hospital. On admission he was alert but presented with nuchal rigidity and right moderate hemiparesis. He had an episode of a blunt head injury 12 years previously, but no history of hypertension, diabetes mellitus or cerebral stroke. A computed tomography revealed mild subarachnoid hemorrhage and mild ventricular dilatation. A cerebral angiography did not demonstrate any aneurysms but it revealed occlusion of the right internal carotid artery at the cervical bifurcation. The repeated angiography on May 31 disclosed a saccular aneurysm arising anteromedially at the level of the junction of the right posterior communicating artery and the internal carotid artery. The cervical internal carotid artery remained occluded at the same site. The middle cerebral artery was supplied through the well-developed posterior communicating artery, and the right anterior cerebral artery was supplied through the anterior communicating artery. Clipping of the aneurysm was attempted but it was forcibly trapped because of premature bleeding on June 5. The right V-P shunt was performed for the progressive ventricular dilatation on June 12. The patient was discharged with no paresis on June 20. It has been well known that the uni- or bilateral carotid occlusion, whatever the origins are, are often associated with cerebral aneurysms.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Extracranial internal carotid occlusion and coexisting ipsilateral intracranial internal carotid aneurysm]. 361 34

T-2 toxin at 0 or 15 mg/kg in 0.75 ml dimethyl sulfoxide was topically applied to 11- to 12-week-old specific-pathogen-free derived crossbred female pigs. Animals were killed on Days 1, 3, 7, or 14 after treatment. Clinical signs and morphologic changes in the skin and internal organs, as well as the residual concentrations of T-2 toxin and its metabolites in plasma, bile, urine, skin, and subcutaneous tissue, were examined. The T-2-treated pigs had signs of lethargy, anorexia, posterior weakness or paresis, and persistent fever. The skin at the site of application was red and swollen initially and progressively became dark red and then purple. By Day 7, at the margin of the exposed area, clefts had formed and were covered by serosanguinous exudate. By Day 14, the affected skin was focally separated from the underlying tissue and covered by a thick scab. The initial skin lesions were characterized as a spongiotic dermatitis and were located mainly in the dermal papillae and stratum germinativum of the epidermis. These lesions progressed to a locally extensive necrotizing dermatitis between Days 3 and 7 that was still evident at Day 14. Healing began on Day 7 and was more prominent on Day 14. Morphologic changes in the internal organs were minimal. They consisted of necrosis of single cells in the follicles of lymphoid tissues and in the exocrine pancreas.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The toxicity of T-2 toxin in swine following topical application. I. Clinical signs, pathology, and residue concentrations. 362 62

T-2 toxin at 0 (6 pigs) or 15 mg/kg (8 pigs) in 0.75 ml of dimethyl sulfoxide was topically applied to 9- to 10-week-old, male castrated, specific-pathogen-free derived pigs which were immunized subcutaneously with sheep red blood cells (SRBC) on Days 0 and 21. Whole blood and serum samples were taken periodically for clinical pathologic and immunologic evaluations. The pigs were observed daily and weighed weekly; their rectal temperatures were measured periodically. The T-2-treated pigs displayed anorexia, lethargy, posterior weakness and paresis, persistent high fever, and reduced body weight gain. Prominent neutrophilia, decreased serum glucose, albumin, and alkaline phosphatase activity, and increased serum globulin were seen in the T-2-treated group. The responses of enriched peripheral blood mononuclear cells to mitogens concanavalin A, phytohemagglutinin, and pokeweed mitogen of the T-2-treated group were significantly lower than those of the control group both at early (3 to 5 days) and late (20 to 28 days) postdosing intervals. No significant effects were noted in the hemagglutination titer to SRBC. Thus, in addition to the severe local dermal injury reported previously, topical exposure of swine to a sublethal dose of T-2 toxin, 15 mg/kg, can cause significant systemic effects on parameters such as body weight gain, rectal temperature, hematology, serum biochemistry, and cellular immune response.
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PMID:The toxicity of T-2 toxin in swine following topical application. II. Effects on hematology, serum biochemistry, and immune response. 362 63

A 6-year-old Golden Retriever was referred for evaluation of hind limb paresis and generalized weakness. Neurologic examination revealed multifocal cervical and lumbosacral spinal disease. Radiography and myelography failed to identify a lesion. Cerebrospinal fluid was markedly cellular and had a high protein concentration, consistent with myelitis or a neoplastic process. The dog did not improve with medical management. Gross and histologic examination of the brain and spinal cord revealed a thick meningeal surface characterized by polymorphic histiocytic-like cells to multinucleate giant cells. The neoplastic process was considered to be a disseminated meningeal polymorphic cell sarcoma.
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PMID:Disseminated meningeal tumor in a dog. 367 56

We describe a kindred with a rare autosomal dominant myopathy limited to the limb-girdle muscles, beginning insidiously any time from the late second through the sixth decades and followed by slow progression. Pelvifemoral precedes scapulohumeral weakness, and proximal appendicular involvement antedates limited distal paresis. Expressivity varies and includes an asymptomatic myopathy (preclinical or subclinical) and a nonmanifesting carrier state that extends well into the eighth decade. A variety of nonspecific changes are present in muscle on light, enzyme histochemical, and electron microscopic examination; of these changes, "rimmed" or autophagic vacuoles are the most characteristic. We identified one very similar previously reported genealogy. The similarities between the two unrelated families clearly establish this dystrophic process as a distinct genetic entity; their differences suggest genetic heterogeneity.
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PMID:Adult-onset autosomal dominant limb-girdle muscular dystrophy. 375 67


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