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

In five baboons and 11 cats cerebral ischaemia was produced either by inflating an epidural balloon and or by ligating major arteries supplying the brain. Fifteen of the animals developed intracranial hypertension after cerebral ischaemia. If ICP were high, but still significantly lower than MABP, elevation of MABP by noradrenaline infusions was accompanied by a proportional increase of ICP. However, the increase of ICP was lower than that of MABP so that CPP was raised. CBF measured by the 133Xenon clearance technique was significantly increased by arterial hypertension in eight cases. The proportional increase of CPP and CBF by elevation of arterial blood pressure was substantially greater, the lower ICP was immediately after ischaemia. There was no effect of MABP in cases in which ICP equalled MABP.
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PMID:Effect of systemic arterial blood pressure on cerebral blood flow in intracranial hypertension. 81 13

Regional cerebral blood flow (rCBF) was measured in three patients after relief of elevated intracranial pressure and restoration of normal cerebral perfusion pressure. Two patients, studied within 4 hours after closed head injury were found to have marked impairment of cortical blood flow and elevation of cerebrovascular resistance. We suggest that this picture is indicative of impending brain death, and may be the result of a long period of severe cerebral ischemia. The third patient, who had a shorter period of intracranial hypertension occurring during anaesthetic induction, responded to reduction of ICP quite differently with a transient relative hyperaemia. The physiopathological explanations for these two different types of flow response and their possible clinical significance are discussed.
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PMID:rCBF in impending brain death. 118 10

We have previously developed a reproducible model of transient forebrain ischaemia in rats by bilateral carotid artery occlusion combined with temporary increase of ICP. With this model, reversibility of the energy metabolism and intracellular pH (pHi) was investigated by 31P-MRS during 120 min of recirculation in three groups of, respectively, 30, 60, and 120 min of ischaemia. With the induction of ischaemia, ATP and phosphocreatine (PCr) disappeared, and measurement of pHi showed severe acidosis in all rats. In the 30 min ischaemia group, both energy metabolism and pHi recovered almost completely. In the 60 min ischaemia group, ATP recovered to 74% of control values, but pHi showed full recovery. In the 120 min ischaemia group, ATP recovered to about 50% of control values, and recovery of pHi was variable. Showing logarithmical changes during recirculation in ATP and PCr, the rate of metabolic recovery was fast during 60 min of recirculation, but it decreased and reached plateau thereafter in all groups. Recovery of pHi was affected by ATP levels, and was precipitously accelerated as ATP levels exceeded 50% of pre-ischaemic values. These results suggest that prolongation of the duration of ischaemia limits the restoration of the energy state, and the quality of pHi recovery after cerebral ischaemia is affected by the degree of ATP recovery during 60 min of recirculation.
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PMID:Reversibility of energy metabolism and intracellular pH after cerebral ischaemia evaluated by 31P-MRS. 136 56

Barbiturates reduce cerebral activity which again reduce the cerebral metabolic rate probably by activating chloride channels and potentiating GABA's effects on these channels. Protection of the brain against hypoxia might theoretically occur by this mechanism, by vasoconstriction or by inhibiting calcium or glutamate. The barbiturates appear to have a positive effect in head-injury patients with high ICP uncontrollable by conventional therapy (in one study 5% of patients with a GCS < or = 7), and in animal studies of regional ischemia. No effect has been established in complete cerebral ischemia (cardiac arrest). The barbiturates have a depressant effect on the cardiovascular and respiratory systems, and the patients require intensive care. Thus there are some indications in the literature that the barbiturate treatment itself causes complications, and it is possible that this might cancel a potential beneficial effect in some patients. Clinically, the barbiturates are effective anticonvulsants, can be used in an attempt to control an elevated ICP uncontrollable by conventional means, and during transient ischemic episodes in the operating room with adequate monitoring and support systems already in place.
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PMID:Barbiturates in neuroanesthesia and neuro-intensive care. 184 34

Bolus injections of lidocaine are commonly used during neuroanesthesia to prevent or treat ICP elevations caused by tracheal or painful stimuli. Lidocaine can also be employed in case of hard intracranial hypertension, when the usual therapy fails. With continuous perfusion, at high doses, of this agent, a state of lidocaine anesthesia can be induced which is more readily reversible than barbiturate anesthesia. A simultaneous anticonvulsant therapy is mandatory because of the well-known epileptogenicity of lidocaine. Closed cardiovascular monitoring is also needed to detect early signs of cardiotoxicity. Experimental works point to the effectiveness of i.v. lidocaine to prevent ischemic lesions secondary to a cerebral artery occlusion. This protective effect may result from some properties exhibited by lidocaine and not by thiopental: stabilisation of transmembrane ionic fluxes, inhibition of leucocytes intravascular sticking and tissular migration. So, i.v. lidocaine seems help to preserve or improve cerebral perfusion pressure and in cases when the latter decrease below the critical threshold, to protect against cerebral ischemia.
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PMID:[Use of intravenous lidocaine in neuro-anesthesia and neuro-resuscitation]. 184 10

Ischemic cerebral edema frequently develops after aneurysm surgery and may lead to severe intracranial hypertension. Of prime importance are reducing the level of ICP and preserving oligemic areas from becoming infarcted. Besides correction of factors known to worsen intracranial hypertension, several therapeutics may be of value: external CSF drainage, perfusion of mannitol, induced arterial hypertension and use of anesthetic agents with cerebral vasoconstricting capability. Hyperventilation is not recommended. Arterial hypotension and hypovolemia certainly contribute to aggravate cerebral ischemia and must be corrected. Cerebral ischemia may be reduced by two specific approaches: by improving cerebral oxygen transport in ischemic areas using arterial hypertension and calcium blockers rather than hemodilution or hypervolemia; by reducing cerebral metabolic rates with heavy anesthesia under the cover of a complete cardiovascular monitoring. In view of the large heterogenicity in cerebral lesions and physiopathological stages, a therapeutical trial appears suitable in each individual case. Criteria allowing to know if any therapeutic, used alone or in association, is beneficial include increase in blood flow in ischemic areas, reduction of ICP level and normalizing of indices like CSF or venous jugular blood lactate.
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PMID:[Treatment of ischemic cerebral edema with intracranial hypertension after neurosurgery of intracranial aneurysms]. 212 75

This review has indicated that barbiturates are useful in controlling ICP during anaesthesia in patients with intracranial hypertension. While laboratory data indicate that intraoperative administration of barbiturates during episodes of transient cerebral ischaemia, associated with surgical revascularization procedures, should be efficacious, current intraoperative results claiming benefit are anecdotal. Continuous high-dose barbiturate therapy (induced barbiturate coma) for occlusive stroke and persistently increased intracranial pressure is currently undergoing clinical trials. While it is clear that this therapy can often reduce increased ICP in head injured patients, its influence on neurological outcome remains to be determined by a multicentre trial at present in progress. Despite evidence that high-dose barbiturate therapy can reduce the area of infarction in occlusive stroke in the laboratory, organized clinical trials have not yet commenced. Until more definitive knowledge is available concerning the influence of high-dose barbiturate therapy in treating different forms of cerebral ischaemia, its application should be viewed sceptically and limited to centres willing to create an organized data base for inter-institutional evaluation of this form of treatment. If barbiturate therapy proves successful and the mechanisms involved are better understood, drugs with fewer side-effects and risks may become available to combat cerebral ischaemia.
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PMID:Barbiturates in brain ischaemia. 388 Nov 16

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

The administration of an intravenous anaesthetic agent before experimental cerebral ischaemia in animals improves the functional and histological outcome. Cerebral ischaemia may be global or focal, complete or incomplete. Intravenous anaesthetic agents reduce the cerebral metabolic demand for oxygen (CMRO2) and abolish electrophysiological activity. This reflects a discontinuation of the functional neuronal activity with maintenance of its basic metabolic activity. The oxygen spared by the decrease in consumption, while reducing the functional activity, might be used by the neurons to sustain longer periods of ischaemia. This protective effect is also observed after pretreatment with either lidocaine or volatile agents, but their potentially deleterious vasodilating effect must be considered. Ketamine has recently been shown to antagonize NMDA receptors. The protective effect of barbiturates was experimentally demonstrated more than 30 years ago. They are still used as a reference. They reduce CMRO2, optimise the ratio between oxygen consumption and oxygen delivery and thus reduce cerebral blood flow and cerebral blood volume, as a result of the decrease of the metabolic demand. This might explain why a protective effect is seen in case of global or focal hypoxia with increased intracranial pressure, while no protection is documented in case of global cerebral ischaemia, such as after cardiac arrest, where EEG is immediately flat and ICP low. However, at doses required to obtain a protective effect, barbiturates induce deleterious side effects such as severe arterial hypotension, which limits their use. Cerebrovascular and cardiac surgery or surgery of the carotids are characterised by potentially ischaemic episodes which can be predicted.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cerebral protection: contribution of intravenous anesthetic agents]. 767 77

Monitoring of ICP from the subarachnoid, intraparenchymal, or ventricular spaces can be accomplished easily and reliably. The risks and benefits of each approach should be considered when choosing the monitoring technique. The goal of ICP management is to prevent herniation and to optimize cerebral perfusion. Even transient episodes of post-traumatic cerebral ischemia due to inadequate CPP can quickly nullify all resuscitative efforts. The provision of sufficient CBF is complicated by the varying degree of disruption of pressure autoregulation commonly resulting from head trauma. Post-injury, there is a need to provide a CPP which is elevated to some extent with respect to that sufficient in uninjured brains. This generally requires a CPP of at least 70 mm Hg, which must be accomplished by maintaining an adequate MAP while controlling ICH. Although ICH can generally be controlled using methods commonly employed, the majority of these techniques have potential complications. Additionally, there is increasing evidence that significant variation exists in the pathologic processes driving ICH in individual patients. Therefore, goals such as the desired CPP and conditions such as the relative contribution of edema, cerebral hypervolemia, and ischemia to ICH should optimally be considered in a patient-specific fashion and allow a targeted approach to therapy.
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PMID:Intracranial pressure. Monitoring and management. 782 72


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