Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aetiopathogenesis of haemorrhagic shock encephalopathy syndrome (HSES) remains unclear and after concern that a novel environmental agent was the cause, the British Paediatric Association and the Public Health Laboratory Service Communicable Disease Surveillance Centre in 1983 initiated surveillance of this condition in the British Isles. After 1986 cases were ascertained via the British Paediatric Surveillance Unit 'active' reporting scheme; this report presents the findings for 1985-8. Sixty five patients were reported, of whom 52 satisfied the criteria for inclusion. Of those whose outcome was known, 24 (46%) died, 18 had severe neurological damage, and six survived apparently intact. Epidemiological features of note were: the median age of 15 weeks (range 3-140); statistically significant clustering of admission times suggesting a peak onset period at night; lack of geographic clusters, of secular trends and, except for a slight excess in winter months, of seasonality. Clinical and pathological features followed a highly consistent pattern, suggesting that HSES is an individual clinical entity distinguishable from conditions with similar presentations, such as septicaemia and Reye's syndrome. There was no microbiological or epidemiological evidence to support the emergence of a novel environmental agent. Many of the features of HSES were, however, the same as those described in heat stroke and we suggest that the two conditions are the same even though there is usually no history of overt overheating.
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PMID:Haemorrhagic shock encephalopathy syndrome in the British Isles. 850 85

The pathogenetic mechanism of the mitochondrial tRNA(LeuUUR) gene mutation responsible for the MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes) syndrome was investigated in transformants obtained by transfer of mitochondria from three genetically unrelated MELAS patients into human mitochondrial DNA (mtDNA)-less (rho 0) cells. Marked defects in mitochondrial protein synthesis and respiratory activity were observed in transformants containing virtually pure mutant mtDNA, as compared to the parent of the rho 0 cells (the 143B cell line) or to transformants containing exclusively wild-type mtDNA, derived from one of the patients or a maternally related asymptomatic individual. A striking protective effect against the mutation was exerted in the transformants by levels of residual wild-type mtDNA above 6%. The MELAS mutation occurs within the mtDNA binding site for a protein factor (mTERF) that promotes termination of transcription at the 16S rRNA/tRNA(LeuUUR) gene boundary. A marked decrease in affinity of purified mTERF for the mutant target sequence was observed in in vitro assays. By contrast, RNA transfer hybridization experiments failed to show any significant change in the steady-state amounts of the two rRNA species, encoded upstream of the termination site, and of the mRNAs encoded downstream, in the transformants carrying the MELAS mutation.
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PMID:MELAS mutation in mtDNA binding site for transcription termination factor causes defects in protein synthesis and in respiration but no change in levels of upstream and downstream mature transcripts. 158 55

Myocardial imaging with beta-methyl-p-(123I)-iodophenyl-pentadecanoic acid (123I-BMIPP), a new radiopharmaceutical designed to evaluate myocardial fatty acid metabolism, was performed in 7 patients with mitochondrial myopathy to detect their myocardial damages in comparison with 201Tl myocardial imaging. These patients were divided into 4 chronic progressive external ophthalmoplegia (CPEO) cases, 2 mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) cases and 1 myoclonus epilepsy with ragged-red fibers (MERRF). In visual assessment, we observed more myocardial segments with decreased uptake of 123I-BMIPP compared to 201Tl in MELAS cases than in CPEO cases. The mean myocardial uptake of 123I-BMIPP was higher than that of 201Tl in CPEO cases. On the other hand, in MELAS and MERRF cases, the mean myocardial uptake of 123I-BMIPP was lower than that of 201Tl. Abnormal findings suggesting myocardial damages were observed in echocardiogram and/or in electrocardiogram in MELAS and MERRF cases, while no such abnormal findings were observed in CPEO cases. Along with the previously reported experimental result that the impairment of rat myocardial mitochondria decreased myocardial uptake of 125I-BMIPP, these results suggest that 123I-BMIPP may be useful to detect myocardial damages in patients with mitochondrial myopathy.
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PMID:[Clinical study on myocardial imaging with beta-methyl-p-(123I)-iodophenyl-pentadecanoic acid in patients with mitochondrial myopathy]. 160 40

Vascular involvement in biopsied muscle specimens from 11 patients with chronic progressive external ophthalmoplegia (CPEO) with ragged-red fibers (RRF) was studied. Almost none of 69 intramuscular arteries examined were strongly stained with succinate dehydrogenase (SDH) except one patient who had 2 SSV (strongly SDH-reactive blood vessels) in his muscle biopsy. Although RRF and focal cytochrome c oxidase (CCO) deficiency in muscle fibers were the common histochemical changes in muscle biopsy specimens from CPEO patients, all mitochondria in both endothelial and smooth muscle cells of the arteries had normal morphology except for the two SSV and all mitochondria in the blood vessels had normal CCO activity by electron cytochemistry. The findings obtained from the present study were quite different from those in mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS), and myoclonus epilepsy associated with ragged-red fibers (MERRF) in which the striking vascular involvement with SSV is the most common and major abnormality in muscle biopsy specimens. To study vascular involvement in mitochondrial encephalomyopathies is the one of very important clues to understand the pathophysiology of phenotypic expressions in mitochondrial encephalomyopathies.
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PMID:[Vascular pathology in chronic progressive external ophthalmoplegia with ragged-red fibers]. 161 73

Current neurologic assessments consider idling neurons and ischemic penumbras to be metabolically lethargic and electrically nonfunctional or nonviable. Diagnosis, prognosis, and therapeutics of central nervous system dysfunctions require differentiation between viable and nonviable neurons. It is necessary to develop and document efficacious and safe techniques for reactivating idling neurons. The authors present a case study of a near drowning 12 years earlier. Areas of cortical hypometabolism were identified by using SPECT imaging in conjunction with hyperbaric oxygen therapy (HBOT). Delayed imaging after HBOT (1 hour, 1.5 atm abs) suggested viable but metabolically lethargic neurons. After HBOT (80 1-hour treatments, monoplace chamber, 1.5 atm abs), marked improvements in cognitive and motor functioning were demonstrated. The data support the hypothesis that idling neurons and ischemic penumbras, when given sufficient oxygen, are capable of reactivation. Thus, changes in tracer distribution after a single exposure to HBOT may be a good prognostic indicator of viable neurons. HBOT may be valuable not only in recovery from anoxic encephalopathy but also from other traumatic and nontraumatic dysfunctions of the central nervous system, including stroke. HBOT in conjunction with physical and rehabilitative therapy may help reactivated idling neurons to remain permanently active.
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PMID:Identification of hypometabolic areas in the brain using brain imaging and hyperbaric oxygen. 161 42

Urinary infections caused by Staphylococcus are attributed usually to Staphylococcus epidermidis or Staphylococcus saprophyticus. 8 cases of urinary infection due to S. haemolyticus are discussed: 5 adults all of them over 66 years, diagnosed respectively of diabetes, cancer and stroke. Three children diagnosed of febrile syndrome, encephalopathy and enterocolitis associated with urinary infection. S. haemolyticus was identified through the determination of 19 biochemical parameters. The antibiograms performed showed that all S. haemolyticus isolated were sensible to vancomycin, nitrofurantoin and trimethoprim/sulfamethoxazole. It is concluded that S. haemolyticus is an opportunistic pathogen that is present on immunodepressed hosts, that is why is advisable to perform a more in-depth characterization of the S. epidermidis isolated in urine, especially in persistent pathologic processes.
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PMID:[A Staphylococcus haemolyticus study in urinary infections. An analysis of 8 cases]. 162 88

Dysphagia is more frequently observed in patients with neurologic diseases (stroke, bulbar or pseudo-bulbar syndrome, amyotrophic lateral sclerosis, cranial trauma). Furthermore, the presence of this pathology is obviously more frequently noted in the light of the increase in the length of the human life span. It has become evident that alternative feeding procedures such as the nasogastric tube or gastrostomy may bring about complications and deprive patients of the oral phase of deglutition which plays a leading role in stimulating digestive functions. The Authors report a systematic research on the rehabilitation aspects of neurogenous dysphagia. All the patients studied underwent a neurological examination and oropharyngeal functional evaluation using echo-videorecording of the oral phase of deglutition and fluoro-videorecording of the pharyngeal phase. The data obtained allowed for the selection of five patients considered suitable for the rehabilitation program. One of them had a multi-infarct encephalopathy, two a spastic hemiplegia f.b.c., a fourth a cerebellar syndrome and the last a sequela of meningioma removal of the ponto-cerebellar angle with peripheral paralysis of the right VII, IX, X, XI cranial nerves. This last patient also underwent a crico-pharyngeal myotomy. Therapy consisted in making the patient sensitive to swallowing movements and in training them to assume a compensatory posture as well as functional rehabilitation of the organs involved in deglutition. The first datum emerging from the study is the lack of etiological homogeneity found in the cases treated with evident variability in different deglutition organ impairment, even though there was the common denominator of the dysphagia symptom. With regard to the results obtained, there was a complete resolution in one patient, while in the other four there was such an improvement as to allow the patients a safe autonomous oral assumption of food. The positive results obtained are not only linked to the recovery of damaged organs, but also to the development of compensatory strategies such as the choice of appropriate food consistency and the assumption of postures which protect the respiratory tract from aspiration and favor crico-pharyngeal relaxation.
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PMID:[Rehabilitation of oro-pharyngeal dysphagia of neurogenic etiology using radiological examination: preliminary results]. 163 72

In recent years there are a considerable increase in alcohol consumption in Taiwan, which may have been accompanied by increased incidence of alcohol-related physical disease. This study was designed for an understanding of neurological problems in chronic alcoholic patients. One hundred and five cases of chronic alcoholics with neurological problems were collected. All had taken more than 100 g alcohol daily for more than 8 years. They were all males, with a mean age of 47.0 +/- 1.3 years, mean daily alcohol consumption of 185.1 +/- 9.0 g (mean +/- S.E.). These chronic alcoholic patients showed various neurological problems. Patients showing typical clinical features of alcoholic neurological disease are now rather rare. Most of the patients had manifestations of more than one problems: polyneuropathy (74.3%), alcoholic tremor (37.1%), hallucinosis (30.5%), myopathy (26.7%), head injury (24.8%), withdrawal seizures (18.1%), Wernicke encephalopathy (15.2%), paranoia (13.3%), and stroke (15.2%). Furthermore, we divided all the patients into 5 categories, they were: encephalopathy, 59 cases (56.2%); stroke, 16 cases (15.2%); cerebellar degeneration, 12 cases (11.4%); neuropathy, 78 case (74.3%); and myopathy, 28 cases (16.7%). The daily alcohol consumption and duration of daily drinking were different significantly (p less than 0.05) among five different syndrome categories.
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PMID:Neurological problems in chronic alcoholics. 165 33

Peripheral neuropathy has attracted relatively little attention in mitochondrial myopathy. However, mitochondrial myopathies are clinically heterogeneous disorders that can affect multiple systems including peripheral nerves other than the skeletal muscle. In addition to the survey of the literature, we studied 6 cases of mitochondrial myopathy with peripheral neuropathy; 3 cases of oligo-systemic involvement confined mainly to skeletal muscles and peripheral nerves, and 3 cases of multi-systemic involvement diagnosed as myoclonus epilepsy with ragged-red fibers (MERRF) or mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS). This study suggests that peripheral neuropathy may be relatively common and has similar clinical and laboratory features in a broad spectrum of mitochondrial myopathies. The clinical manifestation is usually of mild sensorimotor neuropathy with frequent subclinical involvement. Sensory disturbances are more evident than manifestations of motor neuropathy which is usually subclinical. It is also noteworthy that there exist some cases of oligo-systemic involvement, which present with peripheral neuropathy as main clinical manifestations. Electrophysiological findings include decreased nerve conduction velocities and neuropathic electromyograms. Peripheral nerves show loss of myelinated fibers, particularly of large ones, and the remaining fibers have disproportionately thin myelin sheaths with or without onion-bulb formation. Thus the pathological process is axonal degeneration with demyelination resulting from involvement of both neurons (axons) and Schwann cells.
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PMID:Peripheral neuropathy of mitochondrial myopathies. 166 Jan 82

The authors present the results of surgical treatment of patients with concomitant extra-intracranial and bilateral lesions of the carotid arteries. The patients underwent 163 operations for establishment of extra-intracranial microanastomosis (EICMA) including reconstruction of the extracranial segments with EICMA establishment (75 cases). In 66 cases, EICMA was performed for contralateral stenosis of the internal carotid artery (ICA). Of these, 22 patients later underwent carotid endarterectomy. In 14 patients, EICMA was established as the first stage before reconstruction of the iliofemoral segment. The operation was also performed in 8 patients with occlusion of the median cerebral artery or with the crimp of the carotid arteries. Examinations that included ultrasound dopplerography, transcranial dopplerography, studies of the cerebral blood flow according to 133Xe clearance and angiography were carried out. A study was made of the long-term results of the surgical treatment (from 0.5 to 5 years). It has been discovered that to estimate indications for surgical treatment, it is necessary that the data on the regional blood flow (RBF) be taken into account. In patients with stable cerebral hemodynamics according to the RBF that characterizes an uneventful course of ICA occlusion and in the decompensated type most typical of patients with pronounced postinsult neurological dificit, the establishment of EICMA is not indicated. Surgical treatment is most desirable in ICA occlusion (with preliminary reconstruction of the extracranial segments provided they are impaired) and in patients with unstable cerebral hemodynamics most typical of patients with transitory ischemic attacks, dyscirculatory encephalopathy, and minor brain stroke with chiefly mild residual phenomena of ischemic brain stroke.
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PMID:[Tactics and indications for surgical treatment of patients with combined extra- and intracranial lesions of the carotid arteries]. 166 89


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