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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using single photon emission computed tomography (SPECT), cerebral blood flow was studied in eight patients with gradual deterioration in the level of consciousness after subarachnoid haemorrhage. Four had cerebral ischaemia and four had acute hydrocephalus. In patients with cerebral ischaemia, single photon emission computed tomography scanning showed multiple regions with decreased uptake of technetium-99M labelled d,l-hexamethyl-propylene amine oxime (99mTcHM-PAO) mainly in watershed areas. In patients with acute hydrocephalus, decreased uptake was seen mainly in the basal parts of the brain: around the third ventricle, around the temporal horns of the lateral ventricles, and in the basal part of the frontal lobe. After serial lumbar puncture, there was improvement of the uptake of 99mTc HM-PAO in these basal areas in three (convincingly in two and slightly in the other) of the four patients accompanied by clinical improvement in these three patients. These results suggest that patients with acute hydrocephalus and impaired consciousness after SAH, in contrast to patients with cerebral ischaemia, have decreased cerebral blood flow predominantly in the basal parts of the brain.
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PMID:Single photon emission computed tomography in patients with acute hydrocephalus or with cerebral ischaemia after subarachnoid haemorrhage. 188 May 9

Neurologically critically ill patients, more often than others, are unable to communicate and, for a crucial period of time, have the vital functions of their brains hidden in the "black box" of the cranial vault behind a curtain of ambiguity and immobility. Customarily--and naively--we have relied upon beside clinical observations to pierce these barriers. Recent insights lead us to conclude that these "neurochecks" no longer suffice. This article has surveyed four major monitoring systems relied upon by neurointensivists to evaluate the pathophysiology of their patients. Of these, ICPM has the longest clinical track record. It provides a quantitative measure of the brain's capacity to withstand ICP and helps us monitor interventions to reduce it. To utilize this information intelligently requires an understanding of the principles of ICC, CPP, ICP wave morphology, and the hardware available. NICU-CEEG is a more recent introduction but, in principle, it transfers from the laboratory and operating suite to the ICU bedside, established correlations among electrophysiology, CBF, and CM. Digital EEG has allowed us to overcome significant logistical barriers and made NICU-CEEG a practical ICU tool. Early but impressive data suggest that NICU-CEEG has a significant clinical impact in patients with ACI, uncontrolled seizures, or coma. It also has revealed that NICU patients have a surprisingly high incidence of NCS, which may adversely affect their outcome. TCD has contributed greatly to diagnosis and management of SAH vasospasm. It also can be applied with benefit to patients with increased ICP, and has promising value in patients with ACI. It may prove beneficial in monitoring unstable cerebral embolization. Several bedside methods for monitoring CBF are available, but they require refinement to become true monitoring systems. These methods have revealed clinically important insights in patients with head trauma, SAH vasospasm, and ACI. Methods for directly monitoring CM and CMRo2 are improving our understanding of the brain's responses to injury, and becoming increasingly relevant to bedside management. SjvO2 can detect cerebral ischemia caused by overzealous hyperventilation and accelerated ICP. ICO holds promise as a noninvasive transcranial method for assessing Scvo2. We soon may see a scalp array of such detectors, similar to an EEG "montage," that allows us to assess multiregional Scvo2. To be useful, a clinical method should raise questions for further investigation. If the neurophysiologic monitoring systems described here provide us with some answers and lead us to ask useful new questions, they will prove their benefit to our patients.
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PMID:Neurophysiologic monitoring in the neuroscience intensive care unit. 747 20

Many patients survive SAH with minimal neurologic deficits but are at risk for developing further neurologic insult from ischemia resulting from cerebral vasospasm. Nursing care of the patient experiencing vasospasm is challenging. The nurse who is knowledgeable about the signs and symptoms of cerebral ischemia and necessity for continually reviewing the patient's neurologic status can initiate prompt treatment to prevent further ischemic damage. Recognition of this critical problem is the first step toward combating its ominous effects.
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PMID:Cerebral vasospasm: early detection and intervention. 805 86

Hyponatremia, natriuresis, and a decrease in plasma volume of greater than 10% occurs in approximately 50% of the patients with aneurysmal SAH, perhaps due to SIADH and CSWS. However, fluid restriction, as indicated in SIADH, might result in vasospasm and cerebral infarction in these patients. Maintaining intravascular volume seems to be important in SAH; several reports suggest that cerebral ischemia can be reversed by use of volume expanders. Fludrocortisone has been shown to reduce natriuresis, which may help maintain plasma volume in patients with SAH. Adequate oral salt intake also appears to have possible therapeutic benefit in these patients. However, it remains unproven whether fludrocortisone results in a decreased incidence of cerebral ischemia. Larger controlled trials are needed to ascertain the impact of fludrocortisone on prevention of cerebral ischemia in patients with SAH.
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PMID:Fludrocortisone in the treatment of subarachnoid hemorrhage-induced hyponatremia. 916 63

The mechanisms underlying the loss of consciousness following the SAH can be only hypothesized at present time. The more convincing hypothesis appears to be the role of a cerebral circulatory insufficiency. Such an hypothesis stems from the following chain of events: 1) immediate increase of the intracranial pressure; 2) simultaneous constriction of the arteries of the poligone of Willis (early vasospasm); 3) decrease of the cerebral perfusion pressure; 4) cerebral ischemia. Different cerebral regions can be affected by the ischemia according to the prevalent location of the SAH, as for instance brain stem or telencephalon; consequently, different pathophysiological modalities can be responsible for the consciousness impairment. The entity of the SAH and of the consequent events responsible for the cerebral ischemia, influence the severity and reversibility of the loss of consciousness.
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PMID:[Physiopathology of non-traumatic subarachnoid hemorrhage: loss of consciousness]. 977 36

The objective of our study was to examine the course of intracranial pressure (ICP) in patients with SAH Hunt and Hess grades I-II and to analyze the relationship between ICP, cerebral perfusion pressure (CPP) and cerebral blood flow (CBF). Twenty-three patients were studied. ICP, arterial blood pressure (ABP) and CPP were continuously recorded. The measurements of CBF with single-photon emission computed tomography (SPECT) were performed in fifteen patients, who showed TCD flow velocities exceeding 120 cnlJsec. In the first two days after SAH four patients (15%) showed a normal ICP, six (25%) patients had a moderate increase of ICP ranged from 15 to 25 mm Hg and thirteen (60%) patients had ICP values higher than 25 mm Hg. Seven of these patients, with ICP values higher than 40 mm Hg, showed clinical signs of delayed ischaemia. After the treatment with osmotic diuretic, ICP decreased and a clinical improvement was observed with the exception of one patient. In this patient, the SPECT study showed middle cerebral hypoperfusion concordant with the clinically ischaemic hemisphere. Our study showed the utility of the monitoring of these parameters in patients with lower grade SAH, because it allows the modulation of the therapeutic approach and defines the onset of neurological deficits secondary to cerebral ischaemia in all grades of SAH.
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PMID:Intracranial pressure, cerebral perfusion pressure, and SPECT in the management of patients with SAH Hunt and Hess grades I-II. 977 88

This article reviews established, emergent, and potential applications of continuous EEG (CEEG) monitoring in the Neuroscience Intensive Care Unit (NICU) and Emergency Department. In each application, its goal as a neurophysiologic monitor is to extend our powers of observation to detect abnormalities at a reversible stage and to guide timely and physiologically sound interventions. Since this subject was reviewed 5 years ago, the use of CEEG monitoring has become more widespread. In a modern NICU, it is no longer novel to have CEEG data contributing to management decisions. A well-trained CEEG monitoring team is important for its optimal implementation. In the diagnosis and management of convulsive and nonconvulsive status epilepticus, its value appears established. It is finding benefit in the early diagnosis and management of precarious cerebral ischemia, including severe acute cerebral infarctions and post-SAH vasospasms. In comatose patients, it can provide diagnostic and prognostic information which is otherwise unobtainable. More recently, it has been found advantageous for targeting management of acute severe head trauma patients. Networking technology has facilitated the implementation and oversight of CEEG monitoring and promises to expand its availability, credibility, and effectiveness. The maturing of CEEG use is reflected in preliminary efforts to assess its cost benefit, cost effectiveness, and impact on patient outcomes.
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PMID:Continuous EEG monitoring in the neuroscience intensive care unit and emergency department. 1008 89

Symptomatic vasospasms or delayed cerebral ischemia associated with arteriographic evidence of arterial constriction is currently the most important cause of morbidity after acute subarachnoid hemorrhage. Symptomatic vasospasm usually develops between 4 and 12 days after subarachnoid hemorrhage. There is typically a gradual deterioration of the level of consciousness accompanied by focal neurological deficits. 30% of patients who survived aneurysmal SAH develop delayed cerebral ischemia secondary to vasospasm. Vasospasm produces cerebral ischemia and infarction by hemodynamic mechanisms. Vasospasm is an important independent predictor of poor outcome after aneurysmal SAH. Other conditions than aneurysmal subarachnoid hemorrhage such as trauma, tumors, unruptured aneurysms, meningitis and ruptured AVM may be associated with vasospasm.
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PMID:[Epidemiology, clinical study and pathology of vasospasm]. 1036 47

Cerebral ischaemia and reperfusion injury may be exacerbated by leukocyte recruitment and activation. Adhesion molecules play a pivotal role in leukocyte recruitment. We report a prospective study of the potential role of the selectin family of adhesion molecules (E-, P- and L-selectin) in delayed cerebral ischaemia (DID) following aneurysmal subarachnoid haemorrhage. In patients with good grade SAH, we have compared serum concentrations of E-, P- and L-selectin, between patients who do, and do not develop delayed cerebral ischaemia. There was no difference in E-selectin concentration between the two groups (44.0 ng/ml vs. 37.4 ng/ml). Serum P-selectin concentration was significantly higher in patients with DID compared to those patients without DID (149.5 ng/ml vs. 112.9 ng/ml, p = 0.039). Serum L-selectin concentrations were significantly lower in patients with DID (633.8 ng/ml vs 897.9 ng/ml, p = 0.013). We conclude that P- and L-selectin are involved in the pathogenesis of DID following aneurysmal subarachnoid haemorrhage. The results of this study do not elucidate the exact role of each selectin in DID.
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PMID:The selectin superfamily: the role of selectin adhesion molecules in delayed cerebral ischaemia after aneurysmal subarachnoid haemorrhage. 1145 88

The Platelet Activating Factor (PAF) is believed to be the major function in human after cerebral vascular spasm and cerebral ischemia. PAF has been found to participate in cerebral vascular spasm and cerebral ischemia by the basic and clinical study. The symptom of cerebral vascular spasm and cerebral ischemia has appeared with SAH. It has not been reported that the rule and change of PAF with SAH. In the present work, the concentration of PAF in human cerebral spinal fluid (CSF) with SAH were determined by high performance layer thin chromatography. The TLC plate was coated with high performance silica gel G using V(chloroform):V(methanol):V(water) = 65:35:6 as developing solvent. The PAF was determined by TLC scanning method and detected at 630 nm. The method was applied to determine the concentration of PAF in 16 CSF samples with SAH. The samples were collected in 1-3 d, 7-10 d and 14-21 d. CSF samples were deproteinized with methanol and chloroform. After centrifugation, the chloroform layer separated was dried at room temperature with nitrogen and stored under 20 degrees C in the refrigerator. The linear range of the method was 0.5-2.5 micrograms/L with regression coefficient of 0.9990. The lower limit of detection were 50 ng/L. The recovery of the method was 98.6%. The method enables a simple, rapid and reproducible quantification of PAF with SAH.
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PMID:[High performance thin layer chromatographic (HPTLC) determination of PAF in cerebrospinal fluid of patients with subarachnoid hemorrhage(SAH)]. 1255 2


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