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

RNA expression profiles in rat brain were examined 24 h after ischemic stroke, intracerebral haemorrhage, kainate-induced seizures, insulin-induced hypoglycemia, and hypoxia and compared to sham- or untouched controls. Rat oligonucleotide microarrays were used to compare expression of over 8000 transcripts from three subjects in each group (n = 27). Of the somewhat less than 4000 transcripts called 'present' in normal or treated cortex, 5-10% of these were up-regulated 24 h after ischemia (415), haemorrhage (205), kainate (187), and hypoglycemia (302) with relatively few genes induced by 6 h of moderate (8% oxygen) hypoxia (15). Of the genes induced 24 h after ischemia, haemorrhage, and hypoglycemia, approximately half were unique for each condition suggesting unique components of the responses to each of the injuries. A significant component of the responses involved immune-process related genes likely to represent responses to dying neurons, glia and vessels in ischemia; to blood elements in haemorrhage; and to the selectively vulnerable neurons that die after hypoglycemia. All of the genes induced by kainate were also induced either by ischemia, haemorrhage or hypoglycemia. This strongly supports the concept that excitotoxicity not only plays an important role in ischemia, but is an important mechanism of brain injury after intracerebral haemorrhage and hypoglycemia. In contrast, there was only a single gene that was down-regulated by all of the injury conditions suggesting there is not a common gene down-regulation response to injury.
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PMID:Genomic responses of the brain to ischemic stroke, intracerebral haemorrhage, kainate seizures, hypoglycemia, and hypoxia. 1209

The prevalence of diabetes increase in the elderly. Ageing is one of the most important factors contributing to development of glucose intolerance (insuline resistance). NHANES II data showed that in the poppulation over 65 years 18.7% has got overt diabetes and 22.8% glucose intolerance. Similar data were obtained among ageing inhabitants of the city of Bialystok (downtown). The criteria of diagnosis of diabetes in the elderly are the same like in the younger population. However, in the elderly the clinical symptoms are not characteristic and scanty (limited). The period without symptoms is long. Very often, the diabetes is diagnosed for the first time in patient with the heart infarct, brain stroke, diabetic foot or even hyperosmolar coma. There may occur two critical situations in the elderly diabetic persons, namely non-ketotic hyperosmolar coma and hypoglycameia. The non-ketotic hyperosmolar coma is a result of a considerable elevation in the blood concentration of glucose, sodium and urea. This, in turn, is a consequence of osmotic diuresis which is non balanced by elevation in the volume of water intake. Factors facilitating development of the coma include: nontreated diabetes, infirmity, inadequate care, diuretics, stroke, hyperthermia. Hypoglycaemia in the elderly is a very serious problem. It can cause arrhythmia, a rise in the blood pressure, unconsciousness, falls and injuries. The most often reason of hypoglycaemia in the elderly are: long-acting derivatives of sulphonylurea, treatment with insulin and irregular meals. The major aims of treatment of diabetes in the elderly are: reduction of hyperglycaemia, reduction in the development of complications and minimizing of the risk of hypoglycaemia. An elderly patient with diabetes should have each year a check-up which would include examination of the eyes, kidneys, feet. The elderly patient with diabetes is often crippled, indolent and lives often alone. Therefore, such a patient should be taken care of by a team of people. The most important role in the team should be played by a family physician and a social nurse.
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PMID:[Diabetes mellitus in the elderly]. 1218 66

The diagnosis of acute stroke remains a clinical diagnosis in the initial phases of patient evaluation. There is a differential diagnostic process to the abrupt onset of focal neurologic deficit that characterizes an acute stroke. "Is this a CNS event?" might be the initial question posed by the clinician. The stroke mimics of systemic problems such as hypoglycemia, hyperglycemia, and other encephalopathies are considered. Certainly consideration of hypoglycemia, which is common, easily detectable, and correctable, should occur in every stroke patient encounter. Any witnesses that suggest a convulsive episode should raise suspicion of the presence of an ictal or postictal phenomena. Next, if a CNS event is believed to exist, the different stroke subtypes are considered along with other CNS events that may simulate stroke. The standard acute neuroimaging with noncontrast CT scanning uncovers some mass lesions mimicking stroke and confirm a stroke subtype in other patients. Ischemic stroke, like other common diseases, does have uncommon manifestations. Acute stroke is considered in neurologic syndromes in which abrupt onset of symptoms figure prominently, particularly in patients with cerebrovascular risk factors.
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PMID:Stroke mimics and chameleons. 1237 62

Transient hypoglycemic hemiparesis is a rare but important presentation of hypoglycemia that is frequently misdiagnosed as stroke. This is a case of an 18-year-old black female with type 1 diabetes who presented to the emergency department with recurrent acute episodes of hemiparesis that resolved completely after dextrose infusion. It is the intention of the authors to increase awareness of this disorder which, if misdiagnosed, could result in permanent neurological damage. Current theories on the etiology of this disorder are discussed.
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PMID:Transient hypoglycemic hemiparesis. 1244 4

This study determined whether stroke and other types of insults produced a gene expression profile in blood that correlated with the presence of neuronal injury. Adult rats were subjected to ischemic stroke, intracerebral hemorrhage, status epilepticus, and insulin-induced hypoglycemia and compared with untouched, sham surgery, and hypoxia animals that had no brain injury. One day later, microarray analyses showed that 117 genes were upregulated and 80 genes were downregulated in mononuclear blood cells of the "injury" (n = 12) compared with the "no injury" (n = 9) animals. A second experiment examined the whole blood genomic response of adult rats after global ischemia and kainate seizures. Animals with no brain injury were compared with those with brain injury documented by TUNEL and PANT staining. One day later, microarray analyses showed that 37 genes were upregulated and 67 genes were downregulated in whole blood of the injury (n = 4) animals compared with the no-injury (n = 4) animals. Quantitative reverse transcription-polymerase chain reaction confirmed that the vesicular monoamine transporter-2 increased 2.3- and 1.6-fold in animals with severe and mild brain injury, respectively, compared with no-injury animals. Vascular tyrosine phosphatase-1 increased 2.0-fold after severe injury compared with no injury. The data support the hypothesis that there is a peripheral blood genomic response to neuronal injury, and that this blood response is associated with a specific blood mRNA gene expression profile that can be used as a marker of the neuronal damage.
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PMID:Blood genomic expression profile for neuronal injury. 1262 6

Cause(s) of death in patients with diabetes mellitus (DM) admitted to a tertiary care hospital in North India was analysed from classified information in patients' death records and case file. Of the 306652 total admissions from 1991 to 1999, 21584 patients died (7.04%), 592 of whom (355 men and 237 women) had DM (2.7%). Information from 92 patients with diabetes could not be retrieved and six patients with hyperglycemia of short duration (two with gestational DM, three with post-transplant diabetes and one with stress hyperglycemia) were excluded. Of the 494 patients, 456 (92.3%) had T2DM and 38 (7.7%) had T1DM. Four hundred and forty patients had diabetes related mortality: infections (230, 46.5%), cardiovascular events (86, 17.4%), chronic renal failure (CRF) (48, 9.7%), stroke (30, 6%), diabetic ketoacidosis (DKA) (15, 3%), hyperosmolar coma (11, 2.2%), and hypoglycemia (5, 1%), while others (54 patients) had diabetes unrelated deaths. Cause of death could not be ascertained in six patients (1.2%). Death was attributed to a single cause in 301 (60.9%), to two causes in 175 (35.4%) and to three or more causes in 12 (2.4%) patients. Analysis of the cause of death in DM versus hospital in-patients in general, showed infection (P<0.02), coronary artery disease (CAD) (P<0.001), and CRF (P<0.001) to be more frequent in diabetes.
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PMID:Mortality in diabetes: a retrospective analysis from a tertiary care hospital in North India. 1270 20

The effects of hypoglycaemia during hyperinsulinaemia, occurring under various pathophysiological conditions, on the cardiovascular regulatory system and vasculature are largely unknown. The aim of the present study was to investigate regulatory and haemodynamic responses to acute hyperinsulinaemia and consequent hypoglycaemia in 18 healthy subjects. Blood sampling and 5 min ECG and blood pressure recordings were performed at baseline and during the euglycaemic and hypoglycaemic phases of a hyperinsulinaemic clamp. Heart rate variability (HRV) and blood pressure variability (BPV) were assessed by using power spectral analysis, and baroreflex sensitivity (BRS) was assessed using the cross-spectral method. Stroke volume was assessed from the non-invasive blood pressure signal by the arterial pulse contour method. Euglycaemic hyperinsulinaemia did not change plasma catecholamine concentrations, HRV, BPV, BRS, heart rate, blood pressure, stroke volume, cardiac output or peripheral resistance. However, hyperinsulinaemic hypoglycaemia resulted in an 11.7-fold increase in the plasma adrenaline concentration (from 0.19+/-0.03 to 1.68+/-0.32 nmol/l; P <0.001), and a modest 1.3-fold increase in the plasma noradrenaline concentration (from 1.74+/-0.22 to 2.02+/-0.19 nmol/l; P <0.05) compared with baseline. Furthermore, we observed significant decreases in diastolic blood pressure (from 68+/-3 to 60+/-3 mmHg; P <0.05) and peripheral resistance (from 24.1+/-1.2 to 18.5+/-1.1 mmHg.min(-1) x l(-1); P <0.01). Stroke volume and cardiac output increased markedly from the euglycaemic to the hypoglycaemic period only ( P <0.01 for both). Hypoglycaemia did not influence HRV, BPV or BRS. Our findings indicate that hyperinsulinaemic hypoglycaemia is characterized by a significant increase in the plasma adrenaline concentration and by decreases in peripheral resistance and blood pressure. Counter-regulation during hyperinsulinaemic hypoglycaemia involves selective adrenomedullary sympathetic activation, and does not influence cardiac parasympathetic regulation or baroreflex control of heart rate.
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PMID:Effects of euglycaemic and hypoglycaemic hyperinsulinaemia on sympathetic and parasympathetic regulation of haemodynamics in healthy subjects. 1277 92

Although infrequent, recovery of pituitary function after necrosis of a pituitary adenoma is not an exceptional event. We report the case of a 32-year-old woman with previous surgery for an adrenal mass and signs of hypercortisolism which failed to revert postoperatively. She then developed pituitary apoplexy followed by hypopituitarism, as confirmed by hormonal measurements. Magnetic resonance imaging (MRI) showed evidence of a pituitary macroadenoma with signs of necrosis, impinging on the optic chiasm, which was excised by the trans-sphenoidal approach. Nine months later, hormone tests indicated a near total recovery of pituitary functions. The patient had a successful pregnancy three years later. After a 5-year follow-up, she remained clinically asymptomatic, with moderate reduction in cortisol and blunted growth hormone (GH) response to hypoglycemia and MRI failed to disclose any residual tumor, except for a partial arachnoidocele.
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PMID:[Pregnancy after spontaneous necrosis of a pituitary macroadenoma]. 1451 45

A 47-year-old man presented with severe clinical hypoglycaemia. He had long-standing insulin-dependent diabetes with previously good glycaemic control. Intense headaches and vomiting initiated hospitalization. A brain computed tomography (CT) scan was normal, and a lumbar puncture showed elevated cerebrospinal fluid (CSF) protein [0.67 g/L; normal range (NR) 0.15-0.45 g/L], suggesting resolving viral meningitis. Routine thyroid function tests were abnormal (free thyroxine 10.6 pmol/L, NR 9-22.5 pmol/L; thyroid-stimulating hormone 0.16 mU/L, NR 0.35-5 mU/L). In the absence of evident thyroid therapy, the laboratory policy required an urgent cortisol assay to be added; this was very abnormal (42 nmol/L), suggesting hypopituitarism. Later analysis showed that concentrations of gonadotrophins and adrenocorticotrophin were low. An urgent pituitary magnetic resonance imaging scan revealed an unsuspected pituitary tumour with recent haemorrhage (pituitary apoplexy). The patient was given intravenous hydrocortisone and then stabilized on oral hydrocortisone, thyroxine and mesterolone. He made a full recovery and the hypoglycaemia resolved. The normal brain CT scan was falsely reassuring and the CSF protein was not due to viral meningitis but to haemorrhage into the pituitary tumour. If laboratory policy had not required the urgent cortisol assay be added, the diagnosis of hypopituitarism would have been delayed or even missed altogether. This could have led to the death of the patient.
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PMID:The role of the biochemistry department in the diagnosis of pituitary apoplexy. 1502 11

Diffusion-weighted nuclear magnetic resonance (NMR) imaging (DWI) is sensitive to the random translational motion of water molecules due to Brownian motion. Although the mechanism is still not completely understood, the cellular swelling that accompanies cell membrane depolarization results in a reduction in the net displacement of diffusing water molecules and thus a concomitant reduction in the apparent diffusion coefficient (ADC) of tissue water. Cerebral regions of reduced ADC appear hyperintense in a DWI and this technique has been used extensively to study acute stroke. In addition to cerebral ischemia, reductions in the ADC of cerebral water have been observed following cortical spreading depression, ischemic depolarizations (IDs), transient ischemic attack (TIA), status epilepticus, and hypoglycemia. Although the mechanism responsible for initiating membrane depolarization varies in each case, the ensuing cell volume changes follow a similar pattern. Water ADC values are also affected by the presence and orientation of barriers to translational motion (such as cell membranes and myelin fibers) and thus NMR measures of anisotropic diffusion are sensitive to more chronic pathological states where the integrity of these structures is modified by disease. Both theoretical prediction and experimental evidence suggest that the ADC of tissue water is related to the volume fraction of the interstitial space via the electrical conductivity of the tissue. The implication is that acute neurological disorders that exhibit electrical conductivity changes should also exhibit ADC changes that are detectable by DWI. A qualitative correlation between electrical conductivity and the ADC of water has been demonstrated in a number of animal model studies and the results indicate that reduced ADC values are associated with reductions in the extracellular volume fraction and increased extracellular tortuosity. The close relationship between ADC changes and cell volume changes in various pathological states suggests that NMR measurements are also sensitive to chemical communication between cells through the extracellular space (i.e., extrasynaptic or volume transmission, VT).
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PMID:Nuclear magnetic resonance (NMR) measurement of the apparent diffusion coefficient (ADC) of tissue water and its relationship to cell volume changes in pathological states. 1518 24


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