Biomedical subjects

W R Schäbitz

Publications and source records attributed to W R Schäbitz.

15 recordsLinked to original sources

PubMed2002

[Cerebrotendinous xanthomatosis, a treatable metabolic disorder].

Cerebrotendinous xanthomatosis (CTX) is a rare autosomal recessive disorder of bile acid synthesis which can be clinically diagnosed and specifically treated. It is an underdiagnosed disorder worldwide.Here,we describe two women who were diagnosed with CTX during their forties after symptoms had already developed 15 years earlier. Both patients showed gait ataxia, spastic paraparesis, polyneuropathy, bilateral premature cataracts, tendon xanthomas, and cognitive deficits. One of the patients had also chronic diarrhea. The deficiency of the mitochondrial enzyme sterol 27-hydroxylase results in a virtual absence of chenodeoxycholic acid. This leads to excessive production of cholestanol and cholesterol and accumulation of these sterols in many tissues, especially the eye lens, central nervous system,and tendons. The determination of a high cholestanol serum level allows the diagnosis,which can be confirmed through genetic analysis. Early diagnosis of CTX is important, since an effective therapy is available. Long-term therapy with chenodeoxycholic acid is effective for CTX, mainly in prevention of further deterioration.

Adult↗

PubMed2002

Neuroprotective effect of delayed moderate hypothermia after focal cerebral ischemia: an MRI study.

BACKGROUND AND PURPOSE: In contrast to early hypothermia, the effects of delayed hypothermia in focal cerebral ischemia have not been widely addressed. We examined the influence of delayed hypothermia on secondary ischemic injury, MRI lesion size, and neurological outcome after transient focal cerebral ischemia in a rat model. METHODS: Rats (n=30) were subjected to transient middle cerebral artery occlusion (MCAO, 120 minutes) by use of the intraluminal filament model. Animals of the treatment group (n=12) were exposed to whole-body hypothermia of 33 degrees C for 5 hours starting 3 hours after MCAO, whereas the control group (n=18) was kept at 37 degrees C throughout the whole experiment. The normothermia- and hypothermia-treated animals were investigated daily by using the Menzies neurological score. Serial MRI was performed 1, 3, and 6 hours after MCAO and on days 1, 2, 3, and 5. After the final MRI scan, the rats were euthanized, and brain slices were stained by 2,3,5-triphenyltetrazolium chloride. RESULTS: Delayed hypothermia resulted in a significant increase of survival rate and a significant improvement of the Menzies score. Moreover, a significant decrease in the extent of hyperintense volumes in T2-weighted scans and a reduction of cerebral edema as calculated from T2-weighted scans throughout the examination period were obvious. The extent of cerebral infarct volume and cerebral brain edema examined by MRI was consistent with 2,3,5-triphenyltetrazolium chloride staining. CONCLUSIONS: Our results suggest that even delayed postischemic hypothermia can reduce the extent of infarct volume and brain edema after transient focal cerebral ischemia.

Animals↗

PubMed2001

[Value of MRI in intracerebral and subarachnoid hemorrhage].

Intracranial hemorrhage (ICH) accounts for 15% of all strokes. In hyperacute emergency assessment, CT is the diagnostic standard for differentiating between hyperacute ICH and ischemic stroke. At this stage, MRI is considered to be of little value for the diagnosis of ICH or subarachnoidal hemorrhage (SAH). We review the current literature and characterize the role of MRI in the diagnosis of ICH and SAH as well as hyperacute stroke in general: While MRI is considered superior to CT in the diagnosis of subacute and chronic ICH/SAH, in hyperacute ICH this is still a matter of debate. MRI signal characteristics of ICH depend on hemoglobin degradation. Deoxyhemoglobin is the MRI substrate for demonstration of blood due to its paramagnetic properties causing signal loss on susceptibility weighted images (T2*-WI). Preliminary data, however, suggest that the sensitivity of modern stroke MRI protocols is sufficiently high for hyperacute ICH and SAH and may render additional information with regard to the etiology of ICH or SAH. Further interest is focused on perihemorrhagic pathophysiologic processes, which may help to improve therapeutic decision making in patients with ICH.

Cerebral Hemorrhage↗

PubMed2001

Hypoxic brain damage after intramuscular self-injection of diclofenac for acute back pain.

We present a case of hypoxic brain damage that occurred after intramuscular injection of diclofenac due to a severe anaphylactic reaction. A 38-year-old nurse treated herself for acute lower back pain with 100 mg diclofenac intramuscularly. Five minutes later, she collapsed and developed coma and respiratory arrest. After cardiopulmonary resuscitation she was transferred to hospital. On admission she was comatose and received controlled ventilation of the lungs. Magnetic resonance imaging and computerized tomography showed signs of hypoxic brain injury and the patient died from central cardiopulmonary failure 7 days later. Intramuscular treatment with non-steroidal anti-inflammatory drugs such as diclofenac has rare but potentially severe side-effects. Therefore, intramuscular injections are inappropriate and should be replaced with oral or rectal treatment, which has similar absorption profiles.

Acute Disease↗

PubMed2001

Neurometabolic changes during treatment with moderate hypothermia in a patient suffering from severe middle cerebral artery infarction.

Microdialysis is a means of measuring neurochemical changes in the extracellular space and has been applied in acute brain trauma, subarachnoid hemorrhage and stroke patients. In this study, we monitored neurochemical changes in the extracellular space using microdialysis in a patient with left-sided hemispheric infarction treated with moderate hypothermia (33 degrees C). Microdialysis probes were obtained from the infarcted and noninfarcted hemisphere during hypothermia and rewarming. Concentrations of extracellular substances in the infarcted hemisphere (glutamate, glycerine, lactate/pyruvate) decreased with hypothermia and remained stable (glutamate) or increased (glycerine, lactate/pyruvate) during rewarming. Concentrations of these substances in the noninfarcted hemisphere remained at normal levels. Microdialysis monitoring of therapeutic hypothermia in severe hemispheric infarction might be a useful additional monitoring tool to assess the status of the brain and to predict further deterioration.

Adult↗

PubMed2001

Delayed neuroprotective effect of insulin-like growth factor-i after experimental transient focal cerebral ischemia monitored with mri.

BACKGROUND AND PURPOSE: Insulin-like growth factor (IGF) treatment has been shown to have trophic and neuroprotective effects in vitro and in vivo in different lesion models. IGF-I has potent neuroprotective effects after hypoxic-ischemic injury and global ischemia. The role of IGF-I in focal cerebral ischemia is only partially understood. Therefore, in the present study, we evaluated, by applying MRI monitoring, whether a clinically relevant systemic administration of IGF-I can achieve a long-lasting neuroprotective effect. METHODS: Male Wistar rats underwent transient occlusion of the right middle cerebral artery for 1 hour by using the suture occlusion model. Animals then were intraventricularly treated with 33.33 microg IGF-I/d for 3 days (group A, the IGF-I group [n=13]; group B, the placebo group [n=14]) or subcutaneously treated with 200 microg IGF-I/d for 7 days (group D, the IGF-I group [n=10]; group E, the placebo group [n=10]). Groups C and F served as sham-operated controls (n=5 and n=3, respectively). Treatment was begun 30 minutes after occlusion of the middle cerebral artery. Subcutaneously treated animals underwent MRI studies (diffusion-weighted imaging, perfusion imaging, and T2-weighted imaging) beginning 60 minutes after vessel occlusion at 6 hours and at days 1, 2, 5, and 7 after ischemia. The animals were weighed and neurologically assessed daily (rating scale ranged from 0, indicating no deficit, to 5, indicating death). On the third day (intraventricular trial) and on the seventh day (subcutaneous trial), animals were euthanized, and brain sections were stained with triphenyltetrazolium chloride. RESULTS: The mean infarct volume was 52.9+/-25.2 mm(3) in intraventricularly treated animals versus 146.4+/-62.2 mm(3) in control animals (P<0.01) and 42.2+/-17.9 mm(3) in subcutaneously IGF-I-treated animals versus 73.1+/-38.1 mm(3) in control animals (P<0.05). Apparent diffusion coefficient-derived lesion volume at 60 minutes after occlusion was 40.4+/-23.7 mm(3) versus 38.3+/-19.3 mm(3) (P=NS), increased to 168.3+/-49.55 mm(3) versus 105.5+/-33.8 mm(3) (P<0.05) at 24 hours, and then decreased to 55.8+/-30.3 mm(3) versus 23.3+/-20.2 mm(3) (P<0.05) for control and IGF-I-treated animals, respectively. The T2-weighted-derived ischemic lesion volume at 24 hours after occlusion was 236+/-49.2 mm(3) versus 115.9+/-56.8 mm(3) (P<0.05) and decreased to 115.9+/-26.2 mm(3) versus 75.7+/-35.8 mm(3) (P<0.05) at day 7 for control and IGF-I-treated animals, respectively. The relative regional cerebral blood volume was reduced to 50% before reperfusion in all regions of interest except for region of interest 1 (vessel territory of anterior cerebral artery), recovered during reperfusion, but was not different between the control and the growth factor-treated group at any imaging time point. There was no significant difference in weight loss. There was less neurological deficit after ischemia in intraventricularly and subcutaneously IGF-I-treated animals compared with control animals (P<0.05). CONCLUSIONS: Continuous treatment with intraventricularly and subcutaneously administered IGF-I achieved a long-lasting neuroprotective effect as early as 24 hours after ischemia as measured by MRI. Therefore, IGF-I may represent a new approach to the treatment of focal cerebral ischemia.

Animals↗

PubMed2001

Hemorrhagic transformation of ischemic brain tissue: asymptomatic or symptomatic?

BACKGROUND AND PURPOSE: The term symptomatic hemorrhage secondary to ischemic stroke implies a clear causal relationship between clinical deterioration and hemorrhagic transformation (HT) regardless of the type of HT. The aim of this study was to assess which type of HT independently affects clinical outcome. METHODS: We used the data set of the European Cooperative Acute Stroke Study (ECASS) II for a post hoc analysis. All patients had a control CT scan after 24 to 96 hours or earlier in case of rapid and severe clinical deterioration. HT was categorized according to radiological criteria: hemorrhagic infarction type 1 and type 2 and parenchymal hematoma type 1 and type 2. The clinical course was prospectively documented with the National Institutes of Health Stroke Scale and the modified Rankin Scale: The independent risk of each type of HT was calculated for clinical deterioration at 24 hours and disability and death at 3 months after stroke onset and adjusted for possible confounding factors such as age, severity of stroke syndrome at baseline, and extent of the ischemic lesion on the initial CT. RESULTS: Compared with absence of HT, only parenchymal hematoma type 2 was associated with an increased risk for deterioration at 24 hours after stroke onset (adjusted odds ratio, 18; 95% CI, 6 to 56) and for death at 3 months (adjusted odds ratio, 11; 95% CI, 3.7 to 36). All other types of HT did not independently increase the risk of late deterioration. CONCLUSIONS: Only parenchymal hematoma type 2 independently causes clinical deterioration and impairs prognosis. It has a distinct radiological feature: it is a dense homogeneous hematoma >30% of the ischemic lesion volume with significant space-occupying effect.

Age Factors↗

PubMed2000

The N-methyl-D-aspartate antagonist CNS 1102 protects cerebral gray and white matter from ischemic injury following temporary focal ischemia in rats.

BACKGROUND AND PURPOSE: Cerebral white matter is as sensitive as gray matter to ischemic injury and is probably amenable to pharmacological intervention. In this study we investigated whether an N-methyl-D-aspartate (NMDA) antagonist, CNS 1102, protects not only cerebral gray matter but also white matter from ischemic injury. METHODS: Ten rats underwent 15 minutes of temporary focal ischemia and were blindly assigned to CNS 1102 intravenous bolus injection (1. 13 mg/kg) followed by intravenous infusion (0.33 mg/kg per hour) for 3.75 hours or to vehicle (n=5 per group) immediately after reperfusion. Seventy-two hours after ischemia, the animals were perfusion fixed for histology. The severity of neuronal necrosis in the cortex and striatum was semiquantitatively analyzed. The Luxol fast blue-periodic acid Schiff stain and Bielschowsky's silver stain were used to measure optical densities (ODs) of myelin and axons, respectively, in the internal capsule of both hemispheres, and the OD ratio was calculated to reflect the severity of white matter damage. RESULTS: Neuronal damage in both the cortex and the striatum was significantly better in the drug-treated group than in the placebo group (P<0.05). The OD ratio of both the axons (0.93+/-0.08 versus 0.61+/-0.18; P<0.01) and the myelin sheath (0.95+/-0.07 versus 0.67+/-0.19; P=0.01) was significantly higher in the CNS 1102 group than in the placebo group. The neurological score was significantly improved in the drug-treated group (P<0.05). CONCLUSIONS: The NMDA receptor antagonist CNS 1102 protects not only cerebral gray matter but also white matter from ischemic injury, most probably by preventing degeneration of white matter structures such as myelin and axons.

Animals↗

PubMed2000

Intravenous brain-derived neurotrophic factor reduces infarct size and counterregulates Bax and Bcl-2 expression after temporary focal cerebral ischemia.

BACKGROUND AND PURPOSE: Pretreatment with intraventricular brain-derived neurotrophic factor (BDNF) reduces ischemic damage after focal cerebral ischemia. In this experiment we studied the effect of intravenous BDNF delivered after focal cerebral ischemia on neurological outcome, infarct size, and expression of proapoptotic and antiapoptotic proteins Bax and Bcl-2, respectively. METHODS: With the use of the suture occlusion technique, the right middle cerebral artery in rats was temporarily occluded for 2 hours. Thirty minutes after vessel occlusion, BDNF (300 microg/kg per hour in vehicle; n=12) or vehicle alone (n=13) was continuously infused intravenously for 3 hours. After 24 hours the animals were weighed and neurologically assessed on a 5-point scale. The animals were then killed, and brains underwent either 2,3,5-triphenyltetrazolium chloride staining for assessment of infarct volume or paraffin embedding for morphology and immunohistochemistry (Bax, Bcl-2). RESULTS: Physiological parameters (mean arterial blood pressure, PO(2), PCO(2), pH, body temperature, glucose) and weight revealed no difference between groups. Neurological deficit was improved in BDNF-treated animals versus controls (P:<0.05, unpaired, 2-tailed t test). Mean+/-SD infarct volume was 229.7+/-97.7 mm(3) in controls and 121.3+/-80.2 mm(3) in BDNF-treated animals (P:<0.05, unpaired, 2-tailed t test). Cortical infarct volume was 155.5+/-78.5 mm(3) in the placebo group and 69.9+/-50.2 mm(3) in the BDNF-treated group (P:<0.05, unpaired, 2-tailed t test). Subcortical infarct volume was 74.1+/-30.6 mm(3) in the placebo group and 51.1+/-26.8 mm(3) in the BDNF-treated group (P:=NS). Bax-positive neurons were significantly reduced in the ischemic penumbra in BDNF-treated animals (P:<0.05, unpaired, 2-tailed t test), whereas Bcl-2-positive neurons were significantly increased in this area (P:<0.001, unpaired, 2-tailed t test). CONCLUSIONS: This study demonstrates a neuroprotective effect of BDNF when delivered intravenously after onset of focal cerebral ischemia. As shown here, one possible mechanism of action of neuroprotection of BDNF after focal ischemia appears to be counterregulation of Bax/Bcl-2 proteins within the ischemic penumbra.

Animals↗

PubMed1999

Synergistic effects of a combination of low-dose basic fibroblast growth factor and citicoline after temporary experimental focal ischemia.

BACKGROUND AND PURPOSE: Basic fibroblast growth factor (bFGF) and citicoline (cytidine 5'-diphosphate choline, an endogenous compound that stabilizes membrane function) have demonstrated neuroprotective effects after focal cerebral ischemia. Both agents are candidates for future stroke therapy in humans. For evaluation of synergistic effects of bFGF and citicoline, a low-dose combination of both compounds was tested against each compound alone and placebo. METHODS: Four groups of Sprague-Dawley rats (n=12 per group) underwent 90 minutes of focal cerebral ischemia with the use of the suture model of middle cerebral artery occlusion. Animals were randomly and blindly assigned to one of the following treatment groups: placebo, low-dose citicoline (250 mg/kg IP daily for 4 days), low-dose bFGF (10 microg/kg per hour IV for 3 hours), and the combination of both (250 mg/kg citicoline and 10 microg/kg per hour bFGF). Triphenyltetrazolium chloride staining was used after 4 days to determine postmortem infarction. Neurological scores were assessed on a daily basis. RESULTS: The premature mortality rate was 41.7% in the placebo and citicoline groups, 33.3% in the bFGF group, and 25% (P=NS) in the combination group. The mean neurological score on day 4 was 3.1+/-1.6 (placebo), 3.1+/-1.6 (citicoline), 2.9+/-1.5 (bFGF), and 2.4+/-1.4 (combination) (P=NS). The mean volume of infarction was significantly reduced in the combination group (136. 5+/-25.4 mm3) versus placebo (172.6+/-48.9 mm3; P=0.036, Fisher test), versus citicoline alone (186.0+/-35.7 mm3; P=0.005, Fisher test), and versus bFGF alone (176.0+/-49.2 mm3; P=0.023, Fisher test). CONCLUSIONS: These results demonstrate synergistic effects of a low-dose combination of the growth factor bFGF and citicoline after temporary experimental focal cerebral ischemia and furthermore support the effectiveness of a combination treatment regimen for the management of acute stroke.

Animals↗

PubMed1997

Intraventricular brain-derived neurotrophic factor reduces infarct size after focal cerebral ischemia in rats.

Brain-derived neurotrophic factor (BDNF), acting through the high-affinity receptor tyrosine kinase (TrkB), is widely distributed throughout the central nervous system and displays in vitro trophic effects on a wide range of neuronal cells, including hippocampal, cerebellar, and cortical neurons. In vivo, BDNF rescues motorneurons, hippocampal, and substantia nigral dopaminergic cells from traumatic and toxic brain injury. After transient middle cerebral artery occlusion (MCAO), upregulation of BDNF-mRNA in cortical neurons suggests that BDNF potentially plays a neuroprotective role in focal cerebral ischemia. In the current study, BDNF (2.1 micrograms/d) in vehicle or vehicle alone (controls) was delivered intraventricularly for 8 days, beginning 24 hours before permanent middle cerebral artery occlusion by intraluminal suture in Wistar rats (n = 13 per group). There were no differences in physiological variables recorded during surgery for the two groups. Neurological deficit (0 to 4 scale), which was assessed on a daily basis, improved in BDNF-treated animals compared with controls (P < 0.05; analysis of variance and Scheffe's test). There were no significant differences in weight in BDNF-treated animals and controls during the experiment. After elective killing on day 7 after MCAO, brains underwent 2,3,5-triphenyltetrazolium chloride staining for calculation of the infarct volume and for histology (hematoxylin and eosin and glial fibrillary acid protein). The mean total infarct volume was 83.1 +/- 27.1 mm3 in BDNF-treated animals and 139.2 +/- 56.4 mm3 in controls (mean +/- SD; P < 0.01, unpaired, two-tailed t-test). The cortical infarct volume was 10.8 +/- 7.1 mm3 in BDNF-treated animals and 37.9 +/- 19.8 mm3 in controls (mean +/- SD; P < 0.05; unpaired, two-tailed t-test), whereas ischemic lesion volume in caudoputaminal infarction was not significantly different. These results show that pretreatment with intraventricular BDNF reduces infarct size after focal cerebral ischemia in rats and support the hypothesis of a neuroprotective role for BDNF in stoke.

Animals↗

PubMed1996

The effects of prolonged treatment with citicoline in temporary experimental focal ischemia.

Potential therapeutic effects of cytidine 5-diphosphocholine (citicoline), a key intermediary in the biosynthesis of the membrane phospholipid, phosphatidylcholine, are presumably related to enhanced phospholipid synthesis in the ischemic brain. We evaluated prolonged citicoline treatment in a temporary focal ischemia model. Using the suture occlusion model, we induced 2 hours of temporary ischemia in 30 Sprague-Dawley rats. The rats were randomly and blindly assigned to receive intraperitoneally 500 mg/kg citicoline (HD), 100 mg/kg citicoline (LD) or physiologic saline as the control group once daily for 7 days (n = 10 per group) beginning at the time of reperfusion. Neurological scoring (0-5 scale) was performed daily. After elective sacrifice on day 7, or earlier if death occurred prematurely, the brains underwent 2,3,5-triphenyltetrazolium chloride (TTC) staining for calculation of corrected infarct and edema volume. The mean corrected infarct volume in the HD group was 125 +/- 45.2 mm3 (mean +/- SD), significantly smaller than controls, 243.5 +/- 88.6 mm3 (p < 0.01, Scheffe's-test). The LD group infarct volume was 200.2 +/- 62.8 mm3 (N.S.). The mean amount of brain edema in the HD group was 46.4 +/- 45.6 mm3 was smaller than the controls, 92.3 +/- 54.4 mm3 and the LD group, 84.9 +/- 71.7 mm3 (N.S.). Mortality before day 7 in the HD was 30% while it was 50% in the two other groups. The neurologic score on day 7 was 2.5 +/- 1.8 in the HD group, 3.3 +/- 1.8 in the LD group and 3.4 +/- 1.7 in controls (N.S.). These results demonstrate that extended high dose citicoline treatment significantly reduced infarct volume in this temporary focal ischemia model and that there was a trend toward reducing brain edema and mortality. These effects may be related to membrane stabilization and inhibition of free fatty acid release.

Animals↗

PubMed1996

Decompressive craniectomy in a rat model of "malignant" cerebral hemispheric stroke: experimental support for an aggressive therapeutic approach.

Acute ischemia in the complete territory of the carotid artery may lead to massive cerebral edema with raised intracranial pressure and progression to coma and death due to uncal, cingulate, or tonsillar herniation. Although clinical data suggest that patients benefit from undergoing decompressive surgery for acute ischemia, little data about the effect of this procedure on experimental ischemia are available. In this article the authors present results of an experimental study on the effects of decompressive craniectomy performed at various time points after endovascular middle cerebral artery (MCA) occlusion in rats. Focal cerebral ischemia was induced in 68 rats using an endovascular occlusion technique focused on the MCA. Decompressive craniectomy was performed in 48 animals (in groups of 12 rats each) 4, 12, 24, or 36 hours after vessel occlusion. Twenty animals (control group) were not treated by decompressive craniectomy. The authors used the infarct volume and neurological performance at Day 7 as study endpoints. Although the mortality rate in the untreated group was 35%, none of the animals treated by decompressive craniectomy died (mortality 0%). Neurological behavior was significantly better in all animals treated by decompressive craniectomy, regardless of whether they were treated early or late. Neurological behavior and infarction size were significantly better in animals treated very early by decompressive craniectomy (4 hours) after endovascular MCA occlusion (p < 0.01); surgery performed at later time points did not significantly reduce infarction size. The results suggest that use of decompressive craniectomy in treating cerebral ischemia reduces mortality and significantly improves outcome. If performed early after vessel occlusion, it also significantly reduces infarction size. By performing decompressive craniectomy neurosurgeons will play a major role in the management of stroke patients.

Animals↗

PubMed1995

Diffusion weighted imaging for acute cerebral infarction.

The diagnosis of acute cerebral ischemia remains difficult. Computed tomography and magnetic resonance tomography are not specific at early time points. Diffusion imaging a new technique for magnetic resonance imaging was introduced in experimental studies and shown to have much earlier sensitivity for acute ischemic infarction. Diffusion imaging demonstrated early hyperintensities within minutes after ischemic onset and correlated well with post-mortem studies of the final infarct size. On the basis of molecular motion of water, hyperintensities during ischemia on diffusion imaging are most likely related to the development of ischemia induced cytotoxic edema and to slower diffusional motion. Experimental treatment and reperfusion studies with diffusion imaging demonstrated lesion reversal in vivo. Continuous monitoring after induction of ischemia enables an in vivo demonstration of the evolution of the ischemic lesion. Quantitative analysis of the apparent diffusion coefficient may enable the differentiation of infarcted tissue in the core of the lesion from reversibly damaged tissue. Preliminary clinical studies demonstrated a superior sensitivity of diffusion imaging compared with T2-weighted imaging. Clinicians may be able in the near future to image early stroke and to assess therapy when the stroke is still evolving.

Acute Disease↗

PubMed1995

Decompressive craniectomy for cerebral infarction. An experimental study in rats.

BACKGROUND AND PURPOSE: Acute ischemia in the territory of the carotid artery can lead to massive cerebral edema with raised intracranial pressure and progression to coma and death due to uncal, cingulate, or tonsillar herniation. Thus far, only anecdotal experience with supratentorial ischemia treated by decompressive craniectomy has been reported; and there are no published experimental data dealing with this kind of therapy in acute supratentorial stroke. In this study, we present our results on the effect of decompressive craniectomy in an endovascular model of cerebral infarction in rats. METHODS: Focal cerebral ischemia was induced in 50 rats using an endovascular occlusion technique of the middle cerebral artery. Decompressive craniectomy was performed in 30 animals: in 15 animals after 1 hour and in the remaining 15 animals 24 hours after vessel occlusion. Twenty animals were not treated by decompressive craniectomy (control group). RESULTS: Mortality in the nontreated group was 35%, whereas none of the animals treated by decompressive craniectomy died. Neurological behavior, weight loss, and infarction size were all significantly better in the animals treated by decompressive craniectomy, regardless of whether they had been treated after 1 or 24 hours (P < .01). CONCLUSIONS: Our results suggest that decompressive craniectomy for cerebral ischemia not only reduces mortality but also significantly improves outcome and reduces infarction size, probably because of increased perfusion pressure through leptomeningeal collaterals. This experimental study suggests that a controlled study of decompressive craniectomy in patients with acute internal carotid or middle cerebral artery occlusion would be worthwhile. By performing decompressive craniectomy in a small, selected group of patients, neurosurgeons may play an important role in the management of these patients.

Acute Disease↗