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

Two cases of progressive hemiplegia were closely followed by daily clinical examination. In both, the CT scan and CSF were normal on admission. In both, objective aggravation occurred in three or more steps over four days, progressing from minor finger clumsiness to total paralysis of the arm. In both cases a second CT scan a day after appearance of hemiplegia demonstrated a lacune in the corona radiata just above the internal capsule. In one case an intravenous digital subtraction angiogram demonstrated patency of the middle cerebral artery during the course of the progression. In the other case, serial study with transcranial Doppler ultrasound documented the continued patency of the middle cerebral artery. These two cases demonstrate that it is not necessary to postulate transient occlusion of the middle cerebral artery as an essential mechanism for progressive lacunar infarction.
Stroke
PMID:Progressive lacunar infarction with demonstrated patency of the middle cerebral artery. 376 48

Lactate dehydrogenase activities were determined in CSF from 350 patients suffering from various neurological diseases. Reference values were established as 0-26 U/l. Slight elevations of CSF LDH activities were observed in patients with the following disorders: brain metastasis and spinal epidural metastasis from solid carcinomas, primary central nervous system tumours, cerebrovascular accident, polyneuropathy and head injury. Marked elevations were observed incidentally in patients in these groups and in a considerable number of patients with bacterial meningitis and with leptomeningeal spread from solid or haematologic malignancies. When other diagnostic information is available for the proper estimation of the pre-test likelihood of disease, CSF LDH activities exceeding 50 U/l are suggestive for meningeal carcinomatosis.
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PMID:Cerebrospinal fluid lactate dehydrogenase activities in patients with central nervous system metastases. 380 33

Since its first discovery in 1948, serotonin (5-HT) has been the subject of considerable interest. Its potent vasoactivity led to the hypothesis that altered serotonin metabolism was responsible for the pathophysiology of cerebrovascular disease (infarction & hemorrhage) with documentation of elevated levels of serotonin in CSF. If (5-HT) serotonin-mediated release is ultimately responsible for cerebral edema, vasospasm and infarction in experimental and human stroke, then an opportunity exists to pharmacologically block these effects with serotonin-antagonizing agents. This hypothesis has been tested in the laboratory with several agents that inhibit biogenic amines resulting in promising data suggesting a reduction in damage and disability. Since the "natural history of human stroke" results in a 30-40% mortality within the first three weeks, an aggressive new attempt should be directed to increasing the number of survivors in this initial period of high risk. In this regard Sansert (methysergide) was considered worthy of clinical trials.
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PMID:Methysergide (Sansert) treatment in acute stroke. Community pilot study. 389 38

The present study identifies several factors that govern brain pathologic response to marked hypoxia. None of 13 cats exposed to 25 minutes of marked hypoxia (FiO2 = 3.4%; PaO2 = 17 +/- 3 mm Hg, S.D.) that maintained mean arterial blood pressure (MABP) greater than 65 mm Hg were brain injured after reoxygenation and long term survival. In contrast, 12 of 13 exposed to the same hypoxia but that experienced reductions in MABP less than 45 mm Hg for 4 +/- 1 minutes developed a pattern of brain injury closely resembling that of humans surviving in a persistent vegetative state after cardiorespiratory arrest. Higher serum glucose and lactate concentrations and lower blood pH values significantly correlated with development of hypotension during hypoxia. Four of 8 cats exposed to 21 minutes of marked hypoxia followed by 4 minutes of 100% N2 breathing that also led to hypotension similarly developed brain injury. Among the hypoxic/hypotensive cats the magnitude of the hyperglycemic response to hypoxia as modulated by 0, 1, or 2 days of preexposure fasting, strongly correlated with occurrence and extent of brain damage. Peak cisterna magna CSF lactate concentrations 10 to 30 minutes into recovery distinguished those animals that remained brain-intact (less than 13 mM) from those that developed brain damage (greater than 15 mM) with 100% accuracy. Seven cats developed delayed cardiogenic shock 3 to 12 hours into the recovery period. This outcome was predicted by blood pH values less than 6.70 shortly after resuscitation while all 27 surviving cats exhibited values greater than 6.80.
Stroke
PMID:Brain injury from marked hypoxia in cats: role of hypotension and hyperglycemia. 393 1

The given study aimed to answer the question about the realization in clinical practice of the possibility of the timely identification of the degree of intracranial hypertension in patients with cerebral stroke under continuous monitoring of the intracranial volume/pressure ratios by means of examination of CSF changes and CT of the head. On the basis of an analysis of the interrelationship between the severity of neurologic deficit, findings of CT of the head and the results of examination of the cerebral hemodynamics the authors evaluated the informativeness of the main parameters of monitoring the intracranial volume/pressure ratios in the acute stage of cerebral stroke. It has been found that only prolonged registration of the mean and pulse pressure of the CSF in combination with "testing the reserve of the intracranial volume" may ensure the timely detection of disorders of the homeostasis of the craniospinal reservoir and the selection of the most effective means of their correction.
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PMID:[Intracranial hypertension in the acute stage of a stroke (spinal fluid dynamic and computer-tomographic studies)]. 395 89

Creatine Kinase BB isoenzyme (CKBB) has been shown to rise in the serum and CSF following acute cerebral injury. To test the hypothesis that brain infarct size could be estimated from the appearance and disappearance of CKBB in the serum and CSF, strokes of varying size were produced in twelve mongrel dogs by silastic emboli. The rate of disappearance, Kd of CKBB (-.00732 +/- 0.001 min-1 mean +/- SE, N = 8) was determined by injecting purified CKBB (25 IU) intravenously then measuring its disappearance. Following the embolic stroke, serum samples were taken hourly for 24 hours and then at intervals for up to 160 hours for measurement of CKBB by radioimmunoassay until the animals were sacrificed. The brains were then removed, fixed in formalin, cut in 2 mm sections and photographed. The area of the infarct was measured using high pad digitizer interfaced with an Apple computer. The infarct size was then calculated from the area and thickness. Using a one-compartment mathematical model, the infarct size was estimated from the amount of CKBB appearing in the serum, the Kd of CKBB, and the amount of CKBB depleted from tissue. The computed infarct size correlated well (r = 0.94) with the measured infarct size. This model may have value in testing therapeutic modalities in the intact animal.
Stroke
PMID:Quantification of cerebral infarct size by creatine kinase BB isoenzyme. 396 36

There continues to be a need for good animal models of experimental subarachnoid hemorrhage (SAH). The rat would be an ideal subject in which to study SAH since it is inexpensive and easier to use than the larger laboratory animals. The present study was undertaken to determine if alterations of cerebral blood flow could be produced in the rat after experimental SAH, and thereby justify using the rat as a model for further study of SAH. Rats weighing between 450 and 500 grams underwent insertion of a cannula into the cisterna magna at least 5 days prior to physiological testing. One group of rats then received a 0.3 cc injection of fresh autologous arterial blood into the cisterna magna to simulate a SAH. Another group of rats received injection of an equal volume of mock CSF (buffered saline) into the cisterna magna. A third group of rats had no subarachnoid injections. In all three groups, blood flow to the cerebral hemispheres was measured with the labeled microsphere technique. Rats with experimental SAH showed a 40% decrease of cerebral blood flow, whereas rats with saline injections showed only a 15% decrease. Control rats had no changes of cerebral blood flow. These studies demonstrate that the rat is a potential experimental model for investigations into SAH.
Stroke
PMID:Decrease in cerebral blood flow in rats after experimental subarachnoid hemorrhage: a new animal model. 396 67

Vasopressin was determined in CSF and plasma of 243 patients with different neurological and psychiatric disorders, including control patients. CSF vasopressin was significantly higher in patients with high pressure hydrocephalus, intracranial tumour, benign intracranial hypertension, intracranial haemorrhage, ischaemic stroke, and craniocerebral trauma. In patients with primary degenerative dementia, CSF vasopressin was lower than in control patients. Among patients with psychiatric disorders, CSF vasopressin was increased in manic patients, while in patients with depression CSF concentration of this hormone did not differ from that found in controls. However, an increase in CSF vasopressin level was found in patients recovering from a depression. The clinical significance of changes in CSF vasopressin concentrations in groups of patients with neurological and psychiatric disorders is still unknown.
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PMID:Cerebrospinal fluid vasopressin in neurological and psychiatric disorders. 397 21

CT contrast enhancement of the ischemic infarction, blood-CSF barrier function for albumin, and severity of neurological symptoms were evaluated at predefined intervals in 41 patients with supratentorial ischemic infarctions. Contrast enhancement was most frequently observed in the 2nd and 3rd week after the stroke. This late CT enhancement was not related to infarction size and severity of blood-CSF barrier disturbance. The rare appearance of CT enhancement in the 1st week was usually associated with extensive infarctions and accompanied by blood-CSF barrier disturbances. These barrier disturbances, which occurred with higher frequency and greater severity in extensive infarctions (peak 3rd day), generally persisted for several weeks. We suggest that contrast enhancement in the 1st week after an ischemic stroke is due to diapedesis from necrotic capillaries; the more frequently observed late enhancement might be the result of a blood-brain barrier disturbance which in turn is hypothetically attributed to increased pinocytotic activity of regenerated endothelial cells.
Stroke
PMID:CT contrast enhancement on brain scans and blood-CSF barrier disturbances in cerebral ischemic infarction. 397 65

The effect of perfusion of the cerebral ventricles with artificial cerebrospinal fluid containing carbachol on the blood flow in the caudate nucleus of the cat and the possibility to inhibit this effect by anticholinergic drugs was studied by means of the hydrogen clearance technique. After a control period during which both lateral ventricles were perfused with artificial CSF of identical composition, the drug under study was added on one side (experimental side) while the other side continued to be perfused with the control artificial CSF (control side). The blood flow on the experimental side and on the control side were compared. A dose dependent response to carbachol was observed. Lower concentrations of carbachol (10(-6) up to 10(-4)M) caused vasodilatation whereas high concentrations (10(-3)M) caused local vasoconstriction. The increase in the local blood flow caused by the low carbachol concentrations was reduced by both atropine (10(-5)M) and hexamethonium (10(-3)M). The fall in CBF observed with the high carbachol concentration was prevented by atropine (10(-5)M). It may be concluded that low, physiologically more meaningful, carbachol concentrations cause a local vasodilatation due to interaction with both muscarinic and nicotinic receptors.
Stroke
PMID:Response of local blood flow in the caudate nucleus of the cat to intraventricular administration of carbachol. 614 38


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