Since the negative results of the international Bypass Study, extracranial-intracranial (EC-IC) bypass surgery is infrequently employed in the treatment of patients with cerebral ischemia. Newly ...acquired evidence concerning the pathophysiology of cerebral ischemia, however, has facilitated the identification of a small subgroup of patients with "hemodynamic" cerebral ischemia. Characteristically, these patients demonstrate severely impaired cerebrovascular reserve capacity due to occlusive disease and insufficient collateral blood supply. Over an 8-year period, 28 patients were defined by clinical and laboratory criteria as suffering from hemodynamic cerebral ischemia. All patients had recurring episodes of focal cerebral ischemia due to unilateral internal carotid artery occlusion. Computerized tomography (CT) scans either were normal or showed evidence of border zone infarction. The cerebrovascular reserve capacity was studied using 133Xe single-photon emission CT and acetazolamide challenge and was found to be significantly impaired in all patients. Based on these criteria, superficial temporal artery-middle cerebral artery anastomosis was performed to augment collateral flow to the ischemic hemispheres. Two patients died from myocardial infarction, one 4 days and the other 2 months postoperatively. One patient died from massive brain infarction and another suffered a postoperative stroke with incomplete recovery, resulting in a major morbidity and mortality rate of 14%. Minor morbidity included one patient with a subdural hematoma who subsequently recovered completely. The postoperative course was uneventful in 23 patients (82%). Over a mean follow-up period of almost 3 years, no patient had another episode of brain ischemia. Bypass patency was confirmed by postoperative angiography in 26 patients. Follow-up studies of cerebral blood flow (CBF) and cerebrovascular reserve capacity showed significant improvement of the latter while the resting CBF was essentially unchanged. In view of these findings, the authors conclude that EC-IC bypass surgery constitutes appropriate therapy for a subgroup of patients with recurrent focal cerebral ischemia, defined using the strict selection criteria employed in this study.
The goal of this study was the development of a simple bedside test to assess cerebrovascular reserve capacity using transcranial Doppler sonography. We studied 33 normal persons at rest and after ...stimulation of cerebral blood flow with 1 g acetazolamide. Their mean +/- SD increase in blood flow velocity in 54 middle cerebral arteries 10 minutes after stimulation was 24.4 +/- 9.2 cm/sec. We tried to validate the increase in blood flow velocity as cerebrovascular reserve capacity in 21 patients with obstructive carotid artery disease and symptoms of cerebral ischemia. The patients were studied using transcranial Doppler sonography and xenon-133 dynamic single-photon emission computed tomography after acetazolamide stimulation. Their increases in blood flow velocity (delta FV) and increases in cerebral blood flow (delta CBF) correlated significantly in both hemispheres (asymptomatic: Y = 0.32X + 10.65, r = 0.45, p = 0.04; symptomatic: Y = 0.36X + 2.28, r = 0.59, p = 0.004). There was no significant difference between the slopes of the regression lines. Blood flow velocity and cerebral blood flow at rest were not correlated. The increase in blood flow velocity after acetazolamide stimulation offers a simple and reliable method for assessing cerebrovascular reserve capacity.
The beneficial effect of decompressive craniectomy in the treatment of head trauma patients is controversial. The aim of our study was to assess the value of unilateral decompressive craniectomy in ...patients with severe traumatic brain injury.
We retrospectively investigated 49 patients who underwent decompressive craniectomy. Intracranial pressure, cerebral perfusion pressure, therapy intensity level, and cranial computed tomographic scan features (midline shift, visibility of ventricles, gyral pattern, and mesencephalic cisterns) were evaluated before and after craniectomy. The gain of intracranial space was calculated from cranial computed tomographic scans. Patient outcome was graded using the Glasgow Outcome Scale.
Thirty-one patients (63.3%) underwent rapid surgical decompression within 4.5 +/- 3.8 hours after trauma; in 18 patients (36.7%), delayed surgical decompression was performed 56.2 +/- 57.0 hours after injury. Patients younger than 50 years or patients who underwent rapid surgical decompression had a significantly better outcome than older patients or patients who underwent delayed surgical decompression. Craniectomy significantly decreased midline shift and improved visibility of the mesencephalic cisterns. The state of the mesencephalic cisterns correlated with the distance of the lower border of the craniectomy to the temporal cranial base. Alterations in intracranial pressure, cerebral perfusion pressure, and therapy intensity level were not significant. The overall mortality of the patients corresponded to the reports of the Traumatic Coma Data Bank (1991).
Although there was a significant decrease in midline shift after craniectomy, this did not translate into decompressive craniectomy demonstrating a beneficial effect on patient outcome.
Our aim was to demonstrate the feasibility of an angiographically controlled rat model for the study of macrocirculatory and microcirculatory changes of the anterior intracranial circulation after ...subarachnoid hemorrhage.
Subarachnoid hemorrhage was induced by transorbital injection of 0.3 mL of nonheparinized autologous arterial blood into the chiasmatic cistern. Changes in regional cerebral blood flow were continuously recorded with the use of laser-Doppler flowmetry over the parietal cortex. Angiographic verification of middle cerebral artery diameter was performed by carotid catheterization at baseline and 2 days after injection of blood or artificial cerebrospinal fluid. We monitored intracranial and systemic blood pressure during and after injections.
Injection of artificial cerebrospinal fluid in the control group did not change the diameter of the middle cerebral artery. Injection of blood caused a significant arterial narrowing of 17.5%, from 0.37 +/- 0.04 mm to 0.31 +/- 0.04 mm after 2 days (P = .0001). In the control group regional cerebral blood flow decreased to 75.9 +/- 16.8% of preinjection control but quickly recovered to 99.7 +/- 19.4%. Intracranial pressure increased for 5 minutes after the injection to a maximum of 27.3 +/- 8.9 mm Hg, accompanied by a 10% decrease in mean arterial pressure. A fall in cerebral blood flow to 53.1 +/- 26.3% in blood-injected animals that recovered to only 80.7 +/- 16.9% of baseline values during the observation period of 30 minutes was noted. A peak intracranial pressure of 45.7 +/- 11.5 mm Hg occurred 2 minutes after injection with a decrease in mean arterial pressure of 13%, resulting in a markedly lower cerebral perfusion pressure than in the control group.
An angiographically controlled model of subarachnoid hemorrhage primarily involving the anterior circulation is feasible in the rat. The resulting narrowing of the middle cerebral artery reflects moderate vasospasm and will allow further microcirculatory studies with cranial windows.
To determine whether a standardized stimulation challenge with acetazolamide will be helpful for assessing the vasodilatory capacity in patients with obstructive cerebrovascular disease.
To establish ...normative data of the cerebrovascular reserve capacity, a group of 41 control patients was investigated. The regional cerebral blood flow was measured quantitatively before and after stimulation with acetazolamide using the xenon 133 inhalation method and dynamic single-photon emission CT.
A significant increase of regional cerebral blood flow was found after administration of 1 g of acetazolamide. By doubling the dose no significant further increase was measured. We found no correlation of either baseline or stimulated flow values with age. However, a linear dependence between the stimulated flow values and their respective baseline values was observed.
The standardized challenge with acetazolamide seems to be a reliable method to determine cerebrovascular reserve capacity quantitatively.
Intraindividual variability of Doppler frequencies in the basal cerebral arteries is higher than the variability in perfusion measurements. Since Doppler frequency is dependent on vessel diameter, we ...measured intraluminal vessel diameters post mortem. In 73 human cadavers, we measured fresh pairs of rings of the terminal internal carotid artery, the anterior and the middle cerebral artery. Mean intraluminal diameters (+/- standard deviation) for the respective vessel segments were 2.8 +/- 0.49 mm (2.72 +/- 0.49 mm), 1.61 +/- 0.37 mm (1.63 +/- 0.39 mm) and 2.10 +/- 0.38 mm (2.10 +/- 0.41 mm). The left/right ratio was 1.04 +/- 0.13, 1.05 +/- 0.35 and 1.02 +/- 0.17. Intraindividual asymmetries in intraluminal vessel diameters might be an additional factor in the interpretation of intracranial Doppler frequency measurements.
In this report we describe our experience with extracranial-intracranial arterial bypass surgery in a subgroup of 9 patients (mean age at surgery 61 +/- 9 years) with bilateral carotid artery ...occlusion, unilaterally symptomatic for occlusive cerebrovascular disease of haemodynamic origin. Haemodynamic insufficiency is characterized by a severely reduced cerebrovascular reserve capacity, measured with Xe-133 D-SPECT and acetazolamide challenge. Preoperatively, the mean baseline cerebral blood flow of 54 +/- 6 ml 100 g-1 min-1 did not change after challenge (54 +/- 5 ml 100 g-1 min-1) in the symptomatic hemisphere. Immediately following surgery an improvement in cerebrovascular reserve capacity for up to 14 +/- 8 ml 100 g-1 min-1 (1-2 years control) was noted. One patient subsequently died from a perioperative stroke, another patient died three months post-operatively from a myocardial infarction. Three patients were followed up to 4 years, four for 2 years. Patients with former transient ischaemic attacks had no further attacks, symptoms from PRIND or minor stroke did not progress further, nor did new symptoms occur. Unilateral extracranial-intracranial bypass surgery has a positive effect on clinical outcome in highly selected patients with bilateral carotid artery occlusion and cerebral ischaemia of haemodynamic origin.
The aims of this study were to investigate the early changes in the mean apparent diffusion coefficient (ADC) after severe subarachnoid hemorrhage (SAH), as a marker of ischemic damage, and to ...examine the effects of moderate hypothermia, induced at various time points, on ADC changes.
ADC maps were calculated from diffusion-weighted, blipped-epi, spin echo, magnetic resonance imaging sequences (2.35-T BIOSPEC 24/40 scanner; Bruker Medizin Technik GmbH, Karlsruhe, Germany) for 21 anesthetized (0.45-1% halothane, temperature-adjusted/30% oxygen/69% nitrogen) and ventilated Wistar rats. After baseline scanning, bolus injection of 0.5 ml of autologous arterial blood or artificial cerebrospinal fluid (control group), into the cisterna magna, was performed. Serial scanning was performed for 3 hours after injection, using normothermic or hypothermic (32 degrees C) rats. In an additional series of experiments, hypothermia was initiated either immediately or 60 minutes after normothermic SAH. The water contents of the removed brains were calculated using the wet/dry weight method.
The ADC values did not change in the control group but decreased to 88.6+/-5.2% (P < 0.05 versus baseline) after SAH and remained significantly decreased throughout the experiment in normothermia. An injection of blood during hypothermia caused an initial decrease in ADC to 96.1+/-5.6% (P < 0.05 versus baseline); values continuously increased and reached normal levels within 60 minutes. Delayed hypothermia also normalized ADC values within the observation period. The brain water content in the control group was 80.3+/-0.1%, that after SAH in normothermia was 81.1+/-0.7%, and that after SAH in hypothermia was 79.3+/-0.5%.
This model of severe SAH in rats causes significant ADC changes, which are reversible by application of moderate hypothermia even when it is induced after a 60-minute delay. These findings support the concept of moderate hypothermia exerting a neuroprotective effect in severe SAH.
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