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Study Aims: We assessed clinical and early electrophysiological characteristics, in particular Generalized Periodic Epileptiform Discharges (GPEDs) patterns, of consecutive patients during a 1-year period, hospitalized in the Intensive Care Unit (ICU) after resuscitation following cardiac arrest (CA)., Patients and Methods: Consecutive patients resuscitated from cardiac arrest (CA) with first EEG recordings within 48hours were included. Clinical data were collected from hospital records, in particular therapeutic hypothermia. Electroencephalograms (EEGs) were re-analyzed retrospectively., Results: Sixty-two patients were included. Forty-two patients (68%) were treated with therapeutic hypothermia according to international guidelines. Global mortality was 74% but not significantly different between patients who benefited from therapeutic hypothermia compared to those who did not. All the patients who did not have an initial background activity (36/62; 58%) died. By contrast, initial background activity was present in 26/62 (42%) and among these patients, 16/26 (61%) survived. Electroencephalography demonstrated GPEDs patterns in 5 patients, all treated by therapeutic hypothermia and antiepileptic drugs. One of these survived and showed persistent background activity with responsiveness to benzodiazepine intravenous injection., Conclusion: Patients presenting suppressed background activity, even when treated by hypothermia, have a high probability of poor outcome. Thorough analysis of EEG patterns might help to identify patients with a better chance of survival., (Copyright © 2014 Elsevier Masson SAS. All rights reserved.)

Objective: We investigated the expression in rabbit basilar arteries of cyclooxygenase (COX)-2, which is the inducible isoform of the enzyme of prostaglandin (PG) production, and the concentrations of the proinflammatory cytokine tumor necrosis factor alpha (TNFalpha) and representative PGs in the cerebrospinal fluid (CSF) after experimental subarachnoid hemorrhage (SAH)., Methods: Seven sets of basilar arteries were removed from control rabbits and from rabbits killed 1 and 3 days after induced SAH. The arteries were subjected to identical simultaneous immunolabeling for examination with a confocal microscope. One-half of each artery was stained for the constitutive form COX-1 and the other half for COX-2. CSF was sampled in control animals and at 6 hours, 1 day, and 3 days for assays of TNFalpha, PGE2, and 6-keto-PGF1 (metabolite of PGI2)., Results: COX-1 immunoreactivity in the endothelial layer was similar in the three groups. Weak endothelial COX-2 immunoreactivity was found in arteries of control animals. COX-2 staining was higher in the group killed at 3 days compared with the control group (P < 0.05). The levels of PGE2 and 6-keto-PGF1alpha in the CSF peaked significantly at 6 hours, then decreased at 3 days to the basal level (PGE2) or significantly lower (6-keto-PGF1). TNFalpha was undetectable in control CSF, significantly higher (P < 0.001) at 6 hours, and undetectable at 3 days., Conclusion: After SAH, endothelial COX-1 immunoreactivity does not change, whereas overexpression of COX-2 occurs at 3 days. This induction does not seem linked to TNFalpha production, nor is it responsible for early raised levels of PGE2 and PGI2 in the CSF. We suggest that the role of induced COX-2 may be to modify gene expression and hence alter the properties of the vessel wall after SAH.

Experiments were performed to test the hypothesis that subarachnoid hemorrhage (SAH) causes functionally relevant perturbations of cyclooxygenase activity in cerebral arteries. Four groups of rabbits were formed: (I) controls; (II) sham injected animals (2 ml physiological solution in the cisterna magna); (III) SAH group (2 ml blood in cisterna magna); (IV) indomethacin group (4 mg/kg i.v. 30 min before sacrifice). Animals of groups II and III were used 3 days after injection. The basilar arteries (BAs) were removed and perfused at a constant flow rate (after electrocoagulation of all branches) in vitro in a 2-ml bath at 37 degrees C. After 45 min equilibration, the arteries were subjected to a fixed protocol: first, in Krebs solution, contraction to increasing extraluminal concentrations of histamine (HA), followed by a single maximal extraluminal concentration of acetylcholine (ACh); then, after 30 min rest, the same tests were repeated in oxyhemoglobin (oxyHb) solution (extraluminal, 10-4 M). Perfusion pressure changes reflected changes in artery resistance. Although oxyHb alone increased pressure, indicating contraction of the arteries, its most important effect was to increase contraction to HA (in groups II, III, and IV but not controls) and to strongly inhibit ACh-induced relaxation in the SAH (-66.3%) and indomethacin (-46.9%) groups (III and IV) but not the control (-27.6%) group. The latter result suggests that a relaxing factor released by ACh in oxyHb solution in the control group was not present in groups III and IV. In conjunction with the results on HA, which is known to normally release prostacyclin (PGI2) from the endothelium, it is concluded that PGI2 was not or little released from arteries of the SAH group when they bathed in oxyHb solution. Alternatively, in the SAH group constrictor prostaglandins were released in response to HA and ACh in place of PGI2., (Copyright 1998 Elsevier Science B.V.)

Unlabelled: In this study, the functional and clinical evolution of the cerebral postischemic hyperperfusion (CPH) were evaluated., Methods: Forty-four noncomatose patients suffering from unilateral cerebral ischemia located in the internal carotid territories were studied. Twenty-five consecutive patients having CPH with 133Xe-SPECT cerebral blood flow (CBF) measurement and 19 patients without cerebral hyperperfusion matched for age. CBF, vasoreactivity to acetazolamide and the evolution of the clinical state, scored by the National Institutes of Health scale for stroke, were compared., Results: CPH coincided with CT-scan abnormalities in 57% of cases. The mean cerebral vasoreactivity to acetazolamide was comparable in the two groups, but there was local vasoplegia in the hyperperfused areas in 20% of CPH patients, including two cases (8%) with a steal syndrome. Comparison of the initial and late clinical scores showed no significant difference between patients with and without CPH. For patients without CPH, the interhemispheric CBF asymmetry was correlated with the initial and the late scores (p < 0.0001, r = 0.81). For the CPH group, the interhemispheric asymmetry, compensated or even inverted by the hyperperfusion, was not correlated with the initial score (ns, p = 0.051, r = 0.42) and was weakly correlated to the late score (p = 0.048, r = 0.43)., Conclusion: The cerebral hemodynamics remain normal in 80% of cases of CPH patients. The presence of CPH does not interfere with the clinical evolution. The initial and late clinical scores were not different compared to those of patients without hyperperfusion. The clinical outcome of the CPH patients cannot be accurately predicted by the interhemispheric asymmetry.

Cerebral functional imaging has been greatly improved over the last ten years by the development of noninvasive techniques using radioactive elements emitting gamma radiation. Depending on the radioactive tracer used, these single photon emission computed tomography (SPECT) techniques provide either simple imaging of the distribution of local blood flows (99m Tc or 131 I labelled molecules) or quantitative imaging of the cerebral regional blood flow (133 Xe). Because of the rapidity of these techniques and the possibility of performing repeated examinations associated with dynamic test, quantitative measurement of cerebral blood flow with 133 Xe constitutes a value investigation for cerebral ischaemia by defining the site of the lesions, the distant consequences, the haemodynamic disturbances and their course over time. It has an even more important place in the preoperative assessment of stenoses and thromboses of the supra-aortic vessels and intracranial vessels: the study of the haemodynamic reserve by induced vasodilatation (injection of acetazolamide or acetazolamide test) provides valuable information necessary for the decision to perform a revascularisation procedure. In the future, 133 Xe SPECT will certainly be useful for determining the prognosis of an ischaemic cerebral vascular accident by means of very early examinations and to demonstrate the efficacy of new treatments for cerebral ischaemia by means of repeated examinations.

A patient with cerebral vasospasm following subarachnoid hemorrhage (SAH) was investigated by serial measurement of cerebral blood flow (CBF) using the xenon-133 emission tomography method. The CBF was measured before and after acetazolamide injection. On Day 2 after SAH, there was early local hyperperfusion in the middle cerebral artery (MCA) territory, ipsilateral to the left posterior communicating artery aneurysm. The regional CBF of this arterial territory decreased slightly after acetazolamide injection, probably because of vasoplegia and the "steal" phenomenon, and thus surgery was delayed. A right hemiplegia with aphasia and disturbed consciousness occurred 4 days later (on Day 6 after SAH) due to arterial vasospasm, despite treatment with a calcium-channel blocker. The initial hyperemia of the left MCA territory was followed by ischemia. The vasodilation induced by acetazolamide administration was significantly subnormal until Day 13, at which time CBF and vasoreactivity amplitude returned to normal and the patient's clinical condition improved. Surgery on Day 14 and outcome were without complication. It is concluded that serial CBF measurements plus acetazolamide injection are useful for monitoring the development of cerebral vasospasm to determine the most appropriate time for aneurysm surgery.

The resulting changes in the regional cerebral blood flow of 18 patients suffering from idiopathic trigeminal neuralgia and treated by selective thermocoagulation of the trigeminal ganglion were measured by xenon-133 emission tomography. One hour after thermal stimulation, there was an asymmetric increase (P < 0.05) in cerebral blood flow, with a 14.7% mean increase in the ipsilateral cerebral hemisphere (P < 0.001) and a 12.7% mean increase in the contralateral side (P < 0.01). The increase in regional cerebral blood flow was not uniform but was most marked in the ipsilateral middle cerebral artery territory (P < 0.001). There was a slight decrease in cerebellar blood flow, but the reduction in the ipsilateral cerebellar lobe was less than that in the contralateral lobe (P < 0.01). The topography of the most significant changes coincided with that of the innervation of the cerebral vessels by the trigeminal nerve. Several mechanisms are involved in the increase in regional cerebral blood flow, including overall nonspecific activation of the central nervous system and local mechanisms associated with the trigeminal-vascular system.

The timing for surgery on ruptured intracranial aneurysms remains a difficult question and the choice of the day of operation depends greatly from the occurrence of a vasospasm. On a previous paper, the value of the cerebral blood flow (CBF) measurement by intravenous injection of Xenon 133 was demonstrated to be efficient for the prediction of vasospasm only when done between day 4 and day 8 after bleeding. Moreover the efficiency of the measurement was much greater if the evolution of the CBF values between D0 and D8 was considered, but this method was incompatible with early surgery. It suggested the interest of a dynamic study of the CBF by the same method. On a series of 43 patients, the comparison between basal CBF values and reactivity of CBF values to intravenous injection of 1 gram of acetazolamide for the prediction of clinical vasospasm is presented. The series comprises 32 early admitted patients (74%) and 31 operated patients (16 of them between D0 and D3 after bleeding, 15 others after D4). The efficiency of the CBF reactivity study for the prediction of the clinical vasospasm appears much greater than that of the basal CBF value, even during the first three days after bleeding, but not for the prediction of the final clinical outcome. The method is immediate and compatible with early surgery. What precisely is evaluated by this method on the physiopathology of the vasospasm remains disputable, but the operability of the patients seems to be explored.

Quantitative measurements of cerebral blood flow (CBF) by xenon-133 (133Xe) tomography, together with magnetic resonance imaging (MRI), electroencephalography (EEG), psychometric tests, and laboratory analyses were performed on 18 human immunodeficiency virus 1 (HIV-1) seropositive asymptomatic subjects. Abnormalities of cerebral perfusion were observed in 16 cases (88%). These abnormalities were particularly frequent in the frontal regions (77% of cases). MRI demonstrated leucoencephalopathy in only two cases. EEG showed only induced diffuse abnormalities in two cases. Psychometric tests showed restricted moderate disturbances in 55% of patients. These disturbances mostly concerned those sectors involved in cognitive functions and memorization. These results indicate that quantitative measurements of CBF by 133Xe-SPECT is capable of detecting abnormalities of cerebral perfusion at a very early stage (Phase II) of HIV-1 infection. These abnormalities are indications of disturbances resulting from unidentified metabolic or vascular lesions. This technique appears to be superior to MRI at this stage of the disease's development. It could provide objective information leading to earlier treatment, and prove useful in evaluating potential antiviral chemotherapy.