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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intramuscular blood vessels were examined with succinate dehydrogenase stain in skeletal muscle biopsy specimens from 6 patients with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS). Almost all arteries had large granular deposits with high succinate dehydrogenase activity in their walls. Electron microscopic examination of serial frozen sections of these biopsies showed that the smooth muscle cells of the strongly succinate dehydrogenase-reactive blood vessels contained markedly proliferated mitochondria, characteristic of patients with MELAS. The presence of strongly succinate dehydrogenase-reactive blood vessels in muscle biopsy specimens provides an important clue toward understanding the underlying pathogenetic mechanism in patients with MELAS as well as another approach to the diagnosis of this disorder.
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PMID:Strongly succinate dehydrogenase-reactive blood vessels in muscles from patients with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes. 189 63

The total sequences of mitochondrial DNA were determined in two patients with juvenile-onset mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) due to Complex I deficiency. Patients 1 and 2 had three and two unique point mutations, respectively, causing replacement of phylogenically conserved amino acids. A transition from G to A was found at nucleotide position 5601 in the alanine tRNA gene of Patient 2, and a transition from A to G was found at 3243 in the leucine (UUR) tRNA gene of both patients. The latter mutation located at the phylogenically conserved 5' end of the dihydrouridine loop of the tRNA molecule, and was present in two patients with adult-onset MELAS and absent in controls. These results indicate that a mass of mtDNA mutations including the A-to-G transition in the tRNA(Leu) gene is a genetic cause of MELAS.
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PMID:Mitochondrial DNA mutations in mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS). 189 74

EEG was studied in 25 children and adolescents with mitochondrial encephalomyopathies, defined on the basis of clinical, biochemical and morphological criteria. Twenty cases conformed to well-known mitochondrial syndromes: Alpers syndrome [6], Leigh syndrome [2], MERRF (myoclonus epilepsy and ragged red fibers) syndrome [3], MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) syndrome [5] and Kearns-Sayre syndrome [4]. Many patients were followed for several years with repeated EEG. In all, 112 EEG records were included in the study. A common feature of all the mitochondrial encephalomyopathic syndromes was slowing of the alpha rhythm. Epileptic discharges were seen in most syndromes. In spite of the small number of cases in each group, in Alpers, MERRF and MELAS syndromes we found sequential EEG patterns which seemed to be typical of the respective syndromes. In contrast, in Kearns-Sayre syndrome, a slow background rhythm was the only consistent finding. We conclude that EEG, especially repeated recordings, may be of help in the diagnostic evaluation of mitochondrial encephalomyopathies.
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PMID:EEG findings in children and adolescents with mitochondrial encephalomyopathies: a study of 25 cases. 192 9

A six-month-old boy with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome developed repeated crops of purpuric macules on his soles and palms, which were histologically identified as hemorrhage into the dermis without inflammatory infiltrates. Transmission electron microscopy of the skin eruptions revealed various stages of endothelial degeneration in the dermal capillaries associated with consequent extravasation of erythrocytes. The degenerative change was characterized by swollen and vacuolated mitochondria which showed disintegration of their cristae. These morphological changes in the mitochondria of the endothelial cells resembled those seen in skeletal muscle fibers. Similar changes were also noted in other tissues of the skin, such as the axons of myelinated peripheral nerves and some of the keratinocytes in the epidermis. Although these fine structural features are difficult to differentiate from artifacts, abnormal mitochondria could result in functional disturbance particularly in the tissues that require relatively high kinetics, and thus contribute the symptoms of myopathy, encephalopathy, acidosis and stroke-like episodes.
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PMID:Purpuric cutaneous manifestations in mitochondrial encephalomyopathy. 193 57

A 32 year-old diabetic woman presented with an acute coma followed by epileptic seizures, aphasia and constructive apraxia. No ischemic lesion was demonstrated by CT scan and carotid angiograms. The other investigations showed sensorineural hearing loss, retinal degeneration, calcifications of the basal ganglia and lactic acidosis. The follow-up was marked by pseudo-dementia with personality disorders, memory deficits, behavioural changes, migrainous and epileptic features. Although there was no sign of muscular deficiency, a muscular biopsy showed characteristic ragged-red fibers and mitochondrial abnormalities at electron microscopy. The muscular biopsy enables us to classify this case as a mitochondrial encephalopathy similar to the MELAS syndrome. The stroke-like episodes are probably caused by a specific angiopathy involving the mitochondria of brain vessels.
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PMID:[Mitochondrial encephalopathy affecting only the central nervous system]. 196 61

We describe 5 patients with a relapsing encephalopathy in association with Hashimoto's disease and high titers of anti-thyroid antibodies. The presentation is usually with a subacute onset of confusion, alteration in conscious level, and focal or generalized seizures. The relapsing course, association with myoclonus or tremulousness, and episodes of stroke-like deterioration are characteristic features. The long-term prognosis is favorable with steroid therapy, though additional immunosuppressive therapy may be required. Neurologic investigation typically shows a diffusely abnormal EEG, high CSF protein level without pleocytosis, and normal brain CT and cerebral angiogram. Isotope brain scan may show patchy abnormal uptake. Hashimoto's encephalopathy should be recognized as a definite neurologic entity and added to the list of CNS complications of thyroid disease.
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PMID:Hashimoto's encephalopathy: a steroid-responsive disorder associated with high anti-thyroid antibody titers--report of 5 cases. 199 66

We examined sclerotic changes of the medullary arteries in 110 nonneuropsychiatric patients ranging in age from the second to the ninth decades, in 20 patients with subcortical arteriosclerotic encephalopathy (Binswanger's disease), and in 20 patients with dementia of the Alzheimer type. The principal sclerotic change was fibrohyaline thickening of the wall, which began to appear during the late fourth decade, increased in incidence gradually with age, and was most severe in patients with subcortical arteriosclerotic encephalopathy. Morphometry showed that the sclerotic changes of the medullary arteries were most prominent in the frontal lobe, followed by the parietal, occipital, and temporal lobes, in both the nonneuropsychiatric and demented groups. The sclerotic rate in the frontal lobe of patients with dementia of the Alzheimer type was slightly higher than that in the nonneuropsychiatric patients (p less than 0.05) but far less than that in the patients with subcortical arteriosclerotic encephalopathy (p less than 0.001). The sclerotic rate correlated well with the degree of ischemic white matter changes as well as with blood pressure.
Stroke 1991 Apr
PMID:Medullary arteries in aging and dementia. 202 72

We used 31P nuclear magnetic resonance spectroscopy to study the cerebral metabolic function of eight patients with severe postischemic anoxic encephalopathy secondary to cardiac arrest. Spectroscopy was performed at 18 +/- 13 and 64 +/- 20 hours after resuscitation. Glasgow Coma Scale scores at the time of initial and repeat spectroscopy were 3.6 +/- 1.2 and 3.5 +/- 1.2, respectively. In those patients whose spectra were of adequate quality to monitor pH, all demonstrated tissue alkalosis in at least one brain region. The mean brain pH at initial spectroscopy was 7.14 +/- 0.09 and was significantly alkalotic when compared with age- and sex-matched normal controls (pH = 6.98 +/- 0.04, p less than 0.0001). Five of the eight patients showed at least one region of persistent alkalosis at repeat spectroscopy, whereas one patient demonstrated severe acidosis with a pH of 6.42. Spectra demonstrated marked metabolic heterogeneity, ranging from normal in appearance to complete obliteration of all high-energy phosphates with only inorganic phosphate remaining.
Stroke 1991 Apr
PMID:Nuclear magnetic resonance spectroscopy study of human brain after cardiac resuscitation. 202 76

The total sequence data for mitochondrial DNA (mtDNA) revealed distinct clustering of point mutations (pms) in mtDNA among one patient with myoclonus epilepsy with ragged-red fibers (MERRF), two patients with Parkinson's disease (PD), two patients with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS), and one patient with fatal infantile cardiomyopathy (FICM). Among 33 to 62 pms found in each patients, sequentially diverged five clusters of pms were detected and designated as C-1 to C-5. C-1, consisted of fourteen pms, existed in the MERRF patient, C-1 and C-2 (nine pms) in one PD patient, C-1 to C-3 (seven pms) in another PD patient, C-1 to C-4 (one pm) in one MELAS patient and C-1 to C-5 (three pms) in another MELAS patient and the FICM patient. From these clustering of pms, a phylogenetic tree of mitochondrial encephalomyopathies (ME) was constructed. This tree clearly indicated that the ME and PD patients are members of the same gene family, and the MELAS and FICM patients are each others' closest relative. Each patient's unique pms (14 to 28 pms) were detected and, from their characteristic features, the types of the mutations specific for the disease were classified as mit- + syn- for MERRF, mit- + p- for PD, and syn- + mit- for MELAS. An inverse relation was found between the total number of pms and life span of the MELAS and FICM patients.
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PMID:Distinct clustering of point mutations in mitochondrial DNA among patients with mitochondrial encephalomyopathies and with Parkinson's disease. 202 3

Regular drug treatment in mild hypertension (diastolic blood pressure 90-104 mm Hg) reduces death from stroke, and other non-coronary vascular events. The optimum strategy remains sequential monotherapy with the lowest effective dose, with drug combinations as an option. A beta-adrenoceptor blocker or low-dose thiazide is good value treatment for many patients. beta-Blockers are good for young (under 50 years), anxious non-smoking men, men after myocardial infarction, and renal failure patients. Older persons over about 65 years, women, smokers, stroke victims, and liver disease patients should generally take a thiazide or calcium ion-channel blocker. Pregnant women and untreated gouty patients should avoid diuretics. Calcium blockers and angiotensin-converting enzyme inhibitors are preferable in severe or insulin-dependent diabetes and renal failure, and angiotensin manipulators or thiazides in heart failure or peripheral vessel disease. Hyperlipidaemia should not generally exclude thiazides or beta-blockers. Some hypertensive stroke patients without encephalopathy may not need antihypertensive drug treatment for the first 24-48 hours. Drug treatment should be tailored to individuals according to their general condition, physiological age, and any concurrent disease or medication. Unwanted drug reactions should not deter patients from fulfilling social and economic goals. The desired treatment end-point is a diastolic pressure of 85-89 mm Hg, but a compromise is usual in poorly motivated young men, and the elderly.
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PMID:Optimising drug management of individuals with cryptogenic hypertension. 202 55


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