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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Critical care of a patient with SAH should focus on the prevention or immediate treatment of the common sequelae of this disorder that adversely affect outcome: vasospasm, rebleeding, hydrocephalus, seizures, and associated medical problems. The frequency of rebleeding can be lessened by early surgical or endovascular intervention. The extent of SAH on the CT scan can identify those patients at highest risk for vasospasm, and all patients must be closely monitored in the ICU with serial neurological examinations and transcranial Doppler studies. Regional CBF examinations and continuous EEG may also be helpful. Calcium channel blocking agents and volume expansion are recommended prophylatically for all patients. Aggressive hypertensive, hemodilutional, hypervolemic therapy (including pulmonary artery catheter placement) is indicated for symptomatic vasospasm. Transluminal angioplasty can be used in selected patients with vasospasm refractory to these measures. Hydrocephalus can occur in the days, weeks, or months following SAH and is treated effectively with external (acute hydrocephalus) or internal cerebrospinal fluid diversion. Seizures, which can cause intracranial and systemic hypertension, high cerebral metabolic demand, and delayed neurological injury, should be prevented with prophylactic use of anticonvulsants. In addition, early recognition and treatment of associated medical complications are critical. Novel endovascular approaches, meticulous surgical technique, and aggressive ICU care will undoubtedly lead to improved outcome following aneurysmal SAH.
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PMID:Critical care of patients with subarachnoid hemorrhage. 782 84

The quantitative autoradiographic [14C]-iodoantipyrine technique was applied to measure the effects of a 30-min period of pentylenetetrazol (PTZ)-induced status epilepticus (SE) on local cerebral blood flow (LCBF) in rats 10 (P10), 14 (P14), 17 (P17), and 21 (P21) days after birth. The animals received repetitive, timed injections of subconvulsive doses of PTZ until SE was reached. At P10, SE induced a 32 to 184% increase in the rates of LCBF affecting all structures studied. In P14- and P17 PTZ-treated rats, LCBF values significantly increased in two-thirds of the structures belonging to all systems studied and were not changed by SE in the parietal cortex, dorsal hippocampus, and dentate gyrus. At P21, rates of LCBF were still increased in 48 of the 73 structures studied; however, LCBF values were decreased by SE in most cortical areas, the hippocampus, and the dentate gyrus. CBF and cerebral metabolic rate for glucose (CMRglc) remained coupled in both controls and PTZ-exposed rats. Our results show that changes in LCBF with seizures are age dependent. At the most immature ages, P10 and P14, both LCBF and local CMRglc (LCMRglc) values are largely increased by long-lasting seizures. At P17 and P21, the blood flow response to SE becomes more heterogeneous, with specific decreases in the hippocampus and cortex at P21. The absence of mismatch between LCBF and LCMRglc in PTZ-exposed rats at all ages may explain at least partly why the immature brain is more resistant to seizure-induced brain damage than the adult brain.
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PMID:Effects of pentylenetetrazol-induced status epilepticus on local cerebral blood flow in the developing rat. 786 Jun 61

Our previous studies on cerebral metabolic activity in genetic absence epilepsy rats from Strasbourg (GAERS) were in favor of decreased functional activity during absences and normal or increased interictal activity. To ascertain that hypothesis, in the present study we performed continuous measurements of CBF in both children with typical absence epilepsy and GAERS, using Doppler ultrasonography and laser-Doppler flowmetry, respectively. CBF fluctuations during absences were recorded in four children between 5 and 6 years of age and 16 adult GAERS. In both children and animals, CBF measured in the middle cerebral artery and cortical capillaries, respectively, significantly decreased by a median value of 20-24% under basal levels during spontaneous absences. In GAERS, CBF levels were continuously decreased during haloperidol-induced absence status epilepticus, while they were not affected by ethosuximide. Conversely, convulsive seizures induced in rats either by kainate or picrotoxin led to a 175-664% increase in CBF levels. In conclusion, the present data show that during spontaneous absences, CBF decreases under basal levels in both cortical capillaries (GAERS) and the middle cerebral artery (children). Moreover, these fluctuations occur in vessels with normal vascular reactivity, are not mediated by changes in PO2, PCO2, or arterial blood pressure, and represent rather a response to reduced metabolic demand.
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PMID:Absence seizures induce a decrease in cerebral blood flow: human and animal data. 853 May 47

To study quantitative alterations in regional cerebral blood flow (rCBF) accompanying seizures, and to assess the utility of ictal activation PET scanning as a noninvasive clinical tool for localization of epileptogenic foci, we used pentylenetetrazole (PTZ) to induce seizures during 15O-water positron emission tomography (PET) CBF measurement in 15 patients with uncontrolled complex partial seizures (CPS) who had been referred for surgical evaluation. Continuous EEG monitoring was performed during the PET scans. After baseline scans were obtained, each patient was injected with 150-300 mg PTZ. Two patients had generalized tonic-clonic seizures (GTCs). CBF increases were asymmetrical. Two patients (in 1 the seizure occurred spontaneously, without PTZ injection) who had CPS had bitemporal 70-80% increases in CBF. Thalamic CBF increased during both CPS and GTCS. Five patients had an increase in focal EEG interictal abnormality, accompanied by focal flow decreases in 3. PTZ injection not accompanied by clinical seizures did not increase CBF. Partial seizures may be associated with bilateral increases in CBF, and subcortical gray regions are involved in ictal activation.
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PMID:Effect of seizures on cerebral blood flow measured with 15O-H2O and positron emission tomography. 876 21

Fifty-eight patients with drug-resistant partial epilepsy were studied preoperatively by interictal rCBF measurements using 99mTc-HMPAO and a dedicated brain SPECT camera (Tomomatic 64). Follow-up of seizure outcome, using the "Engel score", was at least 3 years. The data were analyzed in a blinded set-up, first visually and subsequently quantitatively by an automatic regional analysis. By visual analysis 95% of the patients were considered abnormal in one part of the brain, of whom 27% were abnormal on CT, 45% on MRI and 98% on scalp EEG. Using a quantitative regional analysis subdividing each hemisphere into 17 larger regions, 85% of the patients had an abnormal rCBF compared to an age-matched control population of healthy volunteers (using the Wilcoxon 2-sample test with Bonferroni's correction). The average number of abnormal regions of interest was 4.7. The percentage of patients with abnormal SPECT-CBF or the total number of abnormal regions of interest (ROIs) per patient showed no correlation to duration of epilepsy or seizure load (number of seizures per year x epilepsy duration) or seizure type. Neither were the rCBF changes prognostic for the outcome as measured by the Engel score. In 20 patients ictal SPECT of rCBF was additionally performed. In 2 cases it added further information to the patient evaluation.
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PMID:Interictal SPECT of rCBF is of clinical utility in the preoperative evaluation of patients with partial epilepsy. 888 60

In a previous study, we reported that the sustained increase in CBF concomitant with seizures induced by kainate is mainly due to the potent vasodilator nitric oxide (NO). However, the production site of NO acting at cerebral vessels was undetermined. In the present study, we investigated whether NO responsible for the cerebral vasodilation is of either neuronal or endothelial origin. We used a putative selective inhibitor of neuronal NO synthase, 7-nitro indazole (7-NI). CBF was measured continuously in parietal cortex by means of laser Doppler flowmetry in awake rats. Systemic variables and electroencephalograms were monitored. Kainate (10 mg/kg i.p.) was given to rats previously treated with saline (n = 8) or 7-NI (25 mg/kg i.p., n = 8) or L-arginine (300 mg/kg i.p., n = 8) followed 30 min later by 7-NI (25 mg/kg i.p.). Under basal conditions, 7-NI decreased CBF by 27% without modifying the mean arterial blood pressure. Under kainate, 7-NI prevented significant increases in CBF throughout the seizures despite sustained paroxysmal electrical activity. L-arginine, the substrate in the production of NO, prevented any decrease in CBF under 7-NI in basal conditions and partially, but nonsignificantly, reversed the cerebrovascular influence of 7-NI during seizures. In a separate group of rats (n = 6), inhibition of cortical NO synthase activity by 7-NI was assayed at 73%. The present results show that neurons are the source of NO responsible for the cerebrovascular response to seizure activity after kainate systemic injection.
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PMID:Nitric oxide of neuronal origin is involved in cerebral blood flow increase during seizures induced by kainate. 897 91

Severe head injury can result in a high mortality rate or irreversible brain damage. One technique used to induce traumatic brain injury (TBI) is exposure of the brain to fluid percussion pressure while monitoring the increase in intracranial pressure (ICP). Since brain injury is a multifactorial, pathological, time-dependent state, the multiparametric monitoring approach was adopted for studying fluid percussion effects on the rat brain. A multiprobe assembly (MPA) connected to the brain in vivo (right hemisphere) enabled the simultaneous monitoring of CBF, NADH redox state, extracellular K+, Ca2+, H+ levels as well as DC potential, ECoG and ICP. The animal was connected to the monitoring system and exposed to TBI after a recuperation period of at least 3 hours after the end of the operation. Two typical responses to TBI were recorded in our preliminary experiments. When severe injury was induced, ischemic depolarization (ID) developed, whereas mild or moderate injury led to repetitive spreading depression (SD) cycles. The relationship between the ID and SD observed under TBI is important to the understanding of the mechanism of brain injury. ICP before injury was between 2-6 mm Hg and increased to 20-22 mm Hg 2-3 minutes after the ID. After severe head injury, ICP remained high and in some cases increased to critical values causing death of these animals. Some animals developed seizures at various stages after the TBI. Hyperbaric oxygenation was used as a therapeutic tool to treat severely injured animals. These preliminary results suggest that it is feasible and practical to use the MPA approach for monitoring the brain after TBI.
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PMID:Continuous multiparametric monitoring of brain activities following fluid-percussion injury in rats: preliminary results. 898 34

We divided eight patients with Sturge-Weber syndrome into two groups, depending on the presence or absence of clinical progression, and investigated differences in brain hemodynamics between the groups by measuring regional cerebral blood flow (rCBF) before and after acetazolamide activation using stable xenon computed tomography. The most evident difference between the groups was acetazolamide vaso-reactivity (delta CBF) in the primarily healthy area remote from lesion. delta CBF on the contralateral side and in distant areas on the affected side was significantly lower in the group with progression group (unpaired t-test), although both groups had similar delta CBF values in the area of primary lesion. This remote hemodynamic compromise might aggravate the clinical condition. Operations were performed on three patients with progressive disease, resulting in good seizure control with anticonvulsants and a variable degree of improvement in neurological symptoms and vasoreactivity. The neurological improvement appeared to correlate with the size of the resected area and the increase in delta CBF after surgery.
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PMID:Hemodynamic compromise as a factor in clinical progression of Sturge-Weber syndrome. 920 57

Converging evidence suggests that partial epileptic seizures can cause a circumscribed increase of CBF. However, quantified studies of ictal perfusion changes verified by intracranial EEG are still needed to better evaluate the relationships between CBF changes and the underlying electrical activity. We studied, in 10 patients undergoing a SEEG for epilepsy surgery, the local perfusion changes measured by [15O]-H2O PET during focal epileptic discharges induced by intracerebral electrical stimulation. CBF measurements under SEEG control were performed at rest and during stimulations eliciting, or not, subclinical or mild symptomatic epileptic discharges. PET and magnetic resonance imaging slices parallel to the AC-PC plane were matched for anatomical identification of cortical regions. Individual normalized CBF difference images between rest and stimulation (with or without induced discharge) were analysed by a hierchical description and multiscale detection method. Only CBF changes at p < 0.01 were considered significant. No significant CBF change was observed on test-retest at rest or during ineffective stimulations. Among the 12 elicited discharges, of which 11 involved mainly the temporal lobe, 8 were associated with a focal CBF increase (16-55 p. 100), there was no CBF change in 3, and a significant CBF decrease was observed in 1 (64 p. 100). These latter 4 discharges were restricted to mesio-temporal lobe structures. PET data were analysed in the same 10 anatomical areas during each of the 12 discharges. In 70.5 p. 100 of the 61 regions explored by SEEG, PET and depth EEG findings were consistent, showing either a CBF change in a discharging area, or no CBF change in a region unaffected by the discharge. Areas of increased CBF indicated an underlying epileptic discharge in almost 100 p. 100 of the cases. Discrepancies between SEEG and PET concerned almost always discharging regions showing no ictal CBF changes. A focal CBF increase detected at the seizure onset is a reliable marker of an underlying epileptic discharge. However, the extent of the CBF changes can be more restricted than that of the electrical discharge, and ictal discharges restricted to the mesial temporal cortex can be overlooked by CBF studies.
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PMID:[Modification of ictal cerebral blood flow studied by positron emission tomography (PET) and stereoelectroencephalography (SEEG)]. 1047 62


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