Stroke In Dogs Research Articles

Heat stroke indogs: Literature review.

Heat stroke isaclinical emergency secondary toasevere temperature increase due tothe inefficiencies ofheat dissipation mechanisms, causing central nervous system dysfunctions, which may lead tomultiple organ dysfunction syndrome. Heat disturbances can beclassified as"classic" or"exertional" ones and several predisposing factors are involved intheir development. This review provides abroad approach tothe pathophysiologicalmechanisms ofthis syndrome, and the diagnostic and treatment methods tofacilitate their approach inclinical routine and increase the survival rate ofpatients.

The Effects of Various Weather Conditions as a Potential Ischemic Stroke Trigger in Dogs.

Stroke is the fifth leading cause of death in the United States, and is the leading cause of serious, long-term disability worldwide. There are at least 795,000 new or recurrent strokes each year, and approximately 85% of all stroke occurrences are ischemic. Unfortunately, companion animals are also at risk for ischemic stroke. Although the exact incidence of ischemic stroke in companion animals is unknown, some studies, and the veterinary information network (VIN), report that approximately 3% of neurological case referrals are due to a stroke. There is a long list of predisposing factors associated with the risk of ischemic stroke in both humans and canines; however, these factors do not explain why a stroke happens at a particular time on a particular day. Our understanding of these potential stroke “triggers” is limited, and the effect of transient environmental exposures may be one such “trigger”. The present study investigated the extent to which the natural occurrence of canine ischemic stroke was related to the weather conditions in the time-period immediately preceding the onset of stroke. The results of the present study demonstrated that the change in weather conditions could be a potential stroke trigger, with the strokes evaluated occurring after periods of rapid, large fluctuations in weather conditions. There are currently no epidemiological data on the seasonal variability of ischemic stroke in dogs, and determining whether canine stroke parallels human stroke would further validate the use of companion dogs as an appropriate naturally occurring model.

Evaluation of Three Hydration Strategies in Detection Dogs Working in a Hot Environment.

Physical activity in hot environments can increase the risk of heat stress or heat stroke in dogs. Heat tolerance is influenced by acclimatization to the environment, physical fitness, and hydration state. Three common strategies to promote hydration in working dogs are free access to water (W), oral electrolyte solutions (OESs), and administration of subcutaneous fluids (SQs). None of these methods have been compared for safety or efficacy in a working environment. In a cross-over design, seven vehicle-screening canines were randomly assigned to each of the three hydration strategies during working shifts at the Sarita, TX checkpoint. Physical, behavioral, and biochemical parameters were collected before, during, and after a work shift (mean 5.7 ± 0.8 h). Dogs were given 10 mL/kg oral W, 10 mL/kg chicken flavored OES, or 15 mL/kg of SQs initially followed by controlled access to W or OES. The dogs drank 15.61 ± 4.47 mL/kg/h of W and OES when in the OES group, compared to 7.04 ± 3.42 and 5.56 ± 4.40 mL of W, for the W and SQ groups, respectively. The median environmental temperature was 84.8°F (29.3°C). The median humidity was 70%. Based on mixed effects linear modeling, dogs in the OES and SQ groups had significantly higher total CO2, and lower packed cell volume and total plasma protein at the end of the day. Creatinine increased a small but significant amount in the SQ group and decreased in the OES group. Searching behaviors were independent of hydration strategy but highly related to the dog specific factors of sex, breed, and activity level. Under conditions of controlled activity in moderate heat and humidity, dogs accustomed to the work and the environment were more likely to increase fluid consumption and hydration when provided a flavored OES. Potential benefits of OES and SQ were indirect and no adverse effects were documented for any of the hydration strategies tested.

Canine model of ischemic stroke with permanent middle cerebral artery occlusion: clinical features, magnetic resonance imaging, histopathology, and immunohistochemistry

The purpose of this study was to identify time-related changes in clinical, MRI, histopathologic, and immunohistochemical findings associated with ischemic stroke in dogs. Additionally, the association of cerebrospinal fluid (CSF) and tissue levels of interleukin (IL)-6 with clinical prognosis was assessed. Ischemic stroke was induced by permanent middle cerebral artery occlusion (MCAO) in nine healthy experimental dogs. The dogs were divided into three groups according to survival time and duration of the experimental period: group A (survived only 1 day), group B (1-week experimental period), and group C (2-week experimental period). Neurologic status was evaluated daily. Magnetic resonance imaging (MRI) was performed according to a predetermined schedule. Concentration of IL-6 in CSF was measured serially after ischemic stroke. Postmortem examination was performed for all experimental dogs. During histopathological examination, variable degrees of cavitation and necrosis due to neuronal cytopathic effects, such as pyknotic nuclei and cytoplasmic shrinkage, were observed on the affected side of the cerebral cortex in all dogs. Immunohistochemistry specific for IL-6 showed increased expression in the ischemic lesions. CSF IL-6 concentrations and ischemic lesion volumes 1 day after ischemic stroke were significantly higher in group A compared to groups B and C.

Presumptive Ischemic Brain Infarction in a Dog with Evans’ Syndrome

A ten-year-old neutered female mixed breed dog was referred for pale mucous membrane and acute onset of right prosencephalic clinical signs. Brain magnetic resonance imaging was suggestive for right middle cerebral artery ischemic stroke. Based on cell blood count, serum biochemistry and serologic tests and flow cytometric detection of anti-platelets and anti-red blood cells antibodies, a diagnosis of immunomediated haemolytic anemia associated with thrombocytopenia of suspected immunomediated origin was done. Immunosuppresive therapy with prednisone was started and the dog clinically recovered. Two months later complete normalization of CBC and serum biochemistry was documented. The dog remained stable for 7 months without therapy; then she relapsed. CBC revealed mild regenerative anemia with spherocytosis and thrombocytopenia. A conclusive Evans’ syndrome diagnosis was done and prednisone and cyclosporine treatment led to normalization of physical and CBC parameters. The dog is still alive at the time the paper submitted. Possible thrombotic etiopathogenetic mechanisms are illustrated in the paper and the authors suggest introducing Evans’ syndrome in the differential diagnosis list for brain ischemic stroke in dogs.

Spontaneous ischaemic stroke in dogs: clinical topographic similarities to humans

Translation of experimental stroke research into the clinical setting is often unsuccessful. Novel approaches are therefore desirable. As humans, pet dogs suffer from spontaneous ischaemic stroke and may hence offer new ways of studying genuine stroke injury mechanisms. The objective of this study was to compare clinical symptoms and infarct topography of naturally occurring ischaemic stroke in pet dogs with human ischaemic stroke. Medical records and magnetic resonance imaging (MRI) of 27 dogs with spontaneous ischaemic stroke were retrospectively investigated with respect to clinical symptoms and infarct topography. Symptomatology and MRI characteristics were compared with humans. Seventy per cent were diagnosed with middle cerebral artery (MCA) occlusions. Motor dysfunction or sensory-motor dysfunction was reported in 78%, including specific signs of contra-lateral motor dysfunction in 11 of 27 (40%). Seizures were reported in 15 of 27 cases (56%). Spontaneously occurring ischaemic stroke in dogs share characteristics with human ischaemic stroke in terms of clinical symptoms and infarct topography. Investigating pet dogs with spontaneous ischaemic stroke may provide an alternative approach to the research of stroke injury mechanisms as they occur naturally, and should be further investigated.

Effects of continuous haemofiltration on serum enzyme concentrations, endotoxemia, homeostasis and survival in dogs with severe heat stroke

AimTo examine the effectiveness of continuous haemofiltration as a treatment for severe heat stroke in dogs. MethodsDogs were randomly allocated to a control or continuous haemofiltration group (both n=8). Heat stroke was induced by placing anaesthetised dogs in a high temperature cabin simulator. Upon confirmation of heat stroke (rectal temperature>42°C, mean arterial pressure (MAP) decrease>25mmHg), dogs were removed from the chamber and continuous haemofiltration was initiated and continued for 3h for dogs in the continuous haemofiltration group. Dogs in the control group were observed at room temperature. ResultsRectal temperature, haemodynamics, pH, blood gases and electrolyte concentrations rapidly returned to baseline in the continuous haemofiltration group, but not the control group. After 3h, rectal temperature was 36.68±0.51°C in the continuous haemofiltration group and 39.83±1.10°C in the control group (P<0.05). Continuous haemofiltration prevented endotoxin and all serum enzyme concentrations from increasing and caused malondialdehyde concentrations to decrease. After 3h, endotoxin concentrations were 0.14±0.02EUml−1 in the continuous haemofiltration group and 0.23±0.05EUml−1 in the control group (P=0.003), while malondialdehyde concentrations were 4.86±0.61mmoll−1 in the continuous haemofiltration group and 8.63±0.66mmoll−1 in the control group (P<0.001). Five dogs died in the control group within 3h, whereas no dogs died in the continuous haemofiltration group. ConclusionsContinuous haemofiltration rapidly reduced body temperature, normalised haemodynamics and electrolytes, improved serum enzyme concentrations and increased survival in dogs with heat stroke. Continuous haemofiltration may be an effective treatment for heat stroke.

Detection of cerebral metabolites in a canine model of ischemic stroke using 1H magnetic resonance spectroscopy

Proton magnetic resonance spectroscopy (1H MRS) provides in vivo biochemical information on tissue metabolites. The purpose of this study was to investigate the serial metabolic changes of 1H MRS in the cerebrum of ischemic dogs. An ischemic stroke was induced in five health laboratory beagle dogs by permanent middle cerebral artery occlusion using a silicone plug. 1H MRS was serially performed three times with a 1.5-T MR system: before, three days after and 10days after the stroke. Immunohistochemical staining was performed to determine the expression of neuronal nuclei (NeuN) and glial fibrillary acidic protein (GFAP) at both the ipsilateral and contralateral cerebral cortex. Reduced levels of N-acetyl-asparate (p<0.05), choline (Cho), creatine (Cr) and myo-inositol (mI), and a marked increase in the lactate (Lac) level (p<0.01) were found at three days after the stroke. At 10days after the stroke, the levels of Lac significantly increased (p<0.01); however, the other metabolites were partially elevated. The changes of Cr, Cho and mI were not statistically significant (p>0.05) when the before and after stroke values were compared. There was a significant loss of NeuN and GFAP immunoreactivity at the ischemic core. 1H MRS may be to a useful diagnostic tool for the evaluation of ischemic stroke in dogs.

Immune mediated destruction of platelets in dogs with heat stroke: A prospective study

Summary Objective: Severe thrombocytopenia is a common sequelae to heat stroke in dogs. So far it has been hypothezised that it is due to disseminated intravascular coagulation. We hypothezised that it is due to immune mediated destruction via antiplatelet antibodies. Material and methods: Prospective evaluation of dogs with heat stroke from May 2005 to August 2008. Dogs that developed severe thrombocytopenia within 5 days of admission were included in the study. All dogs were treated with a standardized treatment protocol. In addition, they received either immunoglobulins or prednisolone. Results: Six dogs were presented with heat stroke during that time period. Four developed a severe thrombocytopenia. All four dogs tested positive for antiplatelet antibodies and did not have elevated D-Dimers at that time. Platelet count in three dogs recovered fully, one dog was euthanized due to liver and renal failure. Conclusion: In those cases thrombocytopenia was due to immune mediated destruction not due to DIC. Clinical rele-vance: Due to the severity of the thrombocytopenia and the high risk for bleeding in those patients, immunosuppressive therapy in addition to DIC prophylaxis should be discussed.

Minimally invasive neuroradiologic model of preclinical transient middle cerebral artery occlusion in canines

Stroke is currently the third leading cause of death in the United States, with approximately 780,000 Americans affected by a new or recurring stroke each year. Although a variety of therapeutic approaches have shown promise in small-animal models of stroke, the vast majority of clinical trials to test the efficacy of such modalities have failed. To bridge the translational gap between laboratory and clinical research, we developed a preclinical model of acute ischemic stroke in dogs. Using a minimally invasive endovascular approach, a platinum coil was intravascularly guided through the vertebrobasilar system under C-arm fluoroscopy to occlude the M1 segment of the middle cerebral artery (MCA) for 1 h. The approach included femoral artery catheterization to access the MCA and therefore eliminated the occurrence of head trauma associated with other preclinical stroke models relying on transorbital or craniectomy approaches. After 1 h of focal MCA ischemia, the coil was retrieved to cause reperfusion, which was verified by arteriograms. At 24 h, T2-weighted coronal magnetic resonance (MR) images were acquired and processed for three-dimensional reconstruction of the brain and its vasculature. Infarction, limited to the area at risk, was noted. Two independent observers calculated the mean percentage hemispherical lesion volumes as follows: observer 1, 30.9 +/- 2.1%; observer 2, 31.2 +/- 4.3%. Infarct-affected changes in histology were determined by hematoxylin and eosin as well as by Fluoro-Jade staining. This work reports the successful development of a powerful preclinical model of stroke that lends itself to the study of biologic mechanisms as well as to testing experimental therapeutics.

Heat Stroke in Dogs: a Retrospective Study of 54 Cases (1999–2004) and Analysis of Risk Factors for Death

The medical records of 54 dogs presented to the Hebrew University Veterinary Teaching Hospital and diagnosed with heat stroke were retrospectively reviewed. Data abstracted included history, clinical and clinicopathological signs at admission, treatment, disease progression, and outcome. Exertional and environmental heat stroke were present in 63% (34 of 54) and 37% (20 of 54) of the dogs, respectively, and 78% (42 of 54) were examined between June and August. The mean temperature and heat discomfort index in the particular days of heat stroke were significantly increased (P < .001, P < .001, respectively) compared with their corresponding average daily values. In 27 dogs the body temperature was > or = 41 degrees C (105.8 degrees F). Belgian Malinois (15%, odds ratio [OR] = 24, 95% confidence interval [CI95%] 8.2-64.5), Golden and Labrador Retrievers (21%, OR = 2.08, CI95% 0.95-4.2), and brachycephalic breeds (25%, OR = 1.7, CI95%], 0.81-3.21) were overrepresented, whereas small breeds (<8 kg) were underrepresented (2%, OR = 0.08, CI95%, 0.002-0.48). Thrombocytopenia (45 of 54 dogs) and prolongation of the prothrombin (PT) and activated thromboplastin (aPTT) times (27 of 47 dogs) were recorded during hospitalization. Disseminated intravascular coagulation (P = .013) and acute renal failure (P = .008), diagnosed in 28 of 54 and 18 of 54 of the cases, respectively, were risk factors for death. The overall mortality rate was 50%. Hypoglycemia (<47 mg/dL, P = .003), prolonged PT (>18 seconds, P = .05), and aPTT (>30 sec, P < .001) at admission were associated with death. Serum creatinine >1.5 mg/dL (P = .003) after 24 hours, delayed admission (>90 minutes, P = .032), seizures (P = .02), and obesity (P = .04) were also risk factors for death. Heat stroke in dogs results in serious complications and high fatality rate despite appropriate treatment.

Heat Stroke in Dogs: A Retrospective Study of 54 Cases (1999–2004) and Analysis of Risk Factors for Death

The medical records of 54 dogs presented to the Hebrew University Veterinary Teaching Hospital and diagnosed with heat stroke were retrospectively reviewed. Data abstracted included history, clinical and clinicopathological signs at admission, treatment, disease progression, and outcome. Exertional and environmental heat stroke were present in 63% (34 of 54) and 37% (20 of 54) of the dogs, respectively, and 78% (42 of 54) were examined between June and August. The mean temperature and heat discomfort index in the particular days of heat stroke were significantly increased (P&lt;.001,P&lt; .001, respectively) compared with their corresponding average daily values. In 27 dogs the body temperature was ≥41°C (105.8°F). Belgian Malinois (15%, odds ratio [OR] = 24, 95% confidence interval [CI95%] 8.2–64.5), Golden and Labrador Retrievers (21%, OR = 2.08, CI95%0.95‐4.2), and brachycephalic breeds (25%, OR = 1.7, CI95%0.81‐3.21) were overrepresented, whereas small breeds (&lt;8 kg) were underrepresented (2%, OR = 0.08, CI95%0.002‐0.48). Thrombocytopenia (45 of 54 dogs) and prolongation of the prothrombin (PT) and activated thromboplastin (aPTT) times (27 of 47 dogs) were recorded during hospitalization. Disseminated intravascular coagulation (P= .013) and acute renal failure (P= .008), diagnosed in 28 of 54 and 18 of 54 of the cases, respectively, were risk factors for death. The overall mortality rate was 50%. Hypoglycemia (&lt;47 mg/dL,P= .003), prolonged PT (&gt;18 seconds,P= .05), and aPTT (&gt;30 sec, P &lt; .001) at admission were associated with death. Serum creatinine &gt; 1.5 mg/dL (P= .003) after 24 hours, delayed admission (&gt;90 minutes,P= .032), seizures (P= .02), and obesity (P= .04) were also risk factors for death. Heat stroke in dogs results in serious complications and high fatality rate despite appropriate treatment.

Ischaemic stroke in dogs and humans: a comparative review

Cerebrovascular accidents, also known as strokes, are one of the major causes of disability and mortality among adult humans. The increased availability of magnetic resonance imaging in veterinary medicine means they are being increasingly recognised in dogs, too. Cerebrovascular accident is defined as the sudden onset of non-progressive, focal brain dysfunction as a result of ischaemic infarction or haemorrhage. Focal ischaemic stroke is caused by interruption of the arterial blood flow to a dependent area of brain parenchyma by a thrombus or an embolus. Once the diagnosis of ischaemic stroke is confirmed, potential sources of thrombosis or embolism should be investigated and treated accordingly. Dogs with ischaemic stroke tend to recover within several weeks with supportive care only.

P-453 - Effect of TAK-218 on the neurologic and histopathologic outcome after experimental thromboembolic stroke in dogs.

P-453 - Effect of TAK-218 on the neurologic and histopathologic outcome after experimental thromboembolic stroke in dogs.

Intracarotid hydroxyethyl methacrylate solution causing stroke in dogs

Hydroxyethyl methacrylate (HEMA) has been advocated as a polymerizing solution with which to prevent deflation of detachable balloons in interventional neuroradiology. It is pertinent to know if unpolymerized HEMA would have untoward effects if accidentally released into the carotid artery by balloon rupture or deflation. Seven mongrel dogs underwent transfemoral catheterization of the common carotid artery and subsequent injection of HEMA solution in volumes of 1 cc in five dogs, 2 cc in one, and 4 cc in one. Angiography performed at the time of injection revealed evidence of intravascular thrombosis as well as possible spasm. Three surviving animals were sacrificed at 48 hours; the brains were fixed and examined histopathologically. One brain was normal and one was autolyzed and could not be examined. Five of the seven animals had histopathologically documented cerebral infarctions of varying size. No foreign substance was seen within the blood vessels to suggest intravascular polymerization. The animals injected with 2 or 4 cc HEMA solution did not survive 48 hours. Literature review reveals little documentation of the toxicology of intravascular HEMA. With its increasing popularity as a compound for polymerization in detachable balloons introduced into the brain, further investigations are warranted to understand the physical properties of the compound and potential risks of its use.

Effects of preexisting bypass graft on rCBF and SSEP's following acute stroke in dogs.

Regional cerebral blood flow (rCBF) was measured with radiolabeled microspheres in a canine model of superficial temporal artery-middle cerebral artery (STA-MCA) bypass and acute ischemia. Ischemic zone flows in seven dogs with the bypass first closed and then open showed no significant contribution of bypass flow in the intact vascular system. Following acute proximal occlusion, rCBF was preserved by bypass flow. A significant flow decrease ensued when the bypass was then clipped, confirming the adequacy of the lesion and the protective effect of the bypass. Reopening the bypass after 15 minutes of ischemia restored 76% of the previous flow. This was a significant increase from the global ischemia values, and was not statistically different from preocclusive values. Preocclusion somatosensory evoked potentials (SSEP's) in these animals showed a consistent biphasic wave at 8 to 10 msec after stimulation. This wave, with some decrease in amplitude, was preserved by bypass flow following creation of the arterial lesion. Bypass clipping abolished these ipsilateral SSEP's. Variable return of SSEP's occurred following reopening of the graft, but the recordings never reached preischemic amplitudes. This experimental study shows that, in this model, a prophylactic bypass subjected to immediate demand (with no time for "maturation") can adequately augment cortical rCBF and is superior to delayed revascularization. The data lend theoretical support to placement of a prophylactic STA-MCA bypass prior to elective carotid artery sacrifice or in surgery where the risk of acute vascular injury is high.

Effect of extracranial-intracranial bypass and pentobarbital on acute stroke in dogs.

Ninety-three mongrel dogs underwent intracranial carotid and middle cerebral artery occlusions. They were then randomized into four groups: 1) the untreated control group (no surgical or medical therapy) showed significant neurological deficit, 16% mortality, and 17% mean hemisphere infarction; 2) in the bypass group (superficial temporal to middle cerebral artery (STA-MCA) anastomosis completed within 3 hours of occlusion), neurological deficit was diminished, mortality was 7%, and mean infarction 5.66%; 3) in the pentobarbital group (single dose of pentobarbital, 35 mg/kg administered intravenously 30 minutes after occlusion), neurological deficit was essentially the same as in the previous group, there was no mortality, and mean infarction was 5.52%; and 4) in the pentabarbital/bypass group (pentabarbital dose plus STA-MCA bypass), neurological deficit was slightly lower than in previous treatment groups, there was no mortality , and mean hemisphere infarction was 1.78%. Extracranial-intracranial bypass produced an immediate 31.6% increase in regional cortical blood flow. The combination of pentobarbital postocclusive therapy and early extracranial-intracranial bypass beneficial synergism.

Extracranial-intracranial bypass in experimental cerebral infarction in dogs.

HomeStrokeVol. 9, No. 5Extracranial-intracranial bypass in experimental cerebral infarction in dogs. Free AccessAbstractPDF/EPUBAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessAbstractPDF/EPUBExtracranial-intracranial bypass in experimental cerebral infarction in dogs. S Asari, K Kinugasa, H Fujisawa, S Ohara, T Kageyama and K Matsumoto S AsariS Asari Search for more papers by this author , K KinugasaK Kinugasa Search for more papers by this author , H FujisawaH Fujisawa Search for more papers by this author , S OharaS Ohara Search for more papers by this author , T KageyamaT Kageyama Search for more papers by this author and K MatsumotoK Matsumoto Search for more papers by this author Originally published1 Sep 1978https://doi.org/10.1161/01.STR.9.5.461Stroke. 1978;9:461–464 Previous Back to top Next FiguresReferencesRelatedDetailsCited By Zaki Ghali M, Srinivasan V and Britz G (2019) Maxillary Artery to Intracranial Bypass, World Neurosurgery, 10.1016/j.wneu.2019.03.015, 128, (532-540), Online publication date: 1-Aug-2019. Karoutas G, Tsitsopoulos P, Taskos N, Karacostas D, Artemis N, Andreou A, Milonas J and Logothetis J (1987) Improvement of cerebral circulation by extracorporal collateral between the femoral and the external carotid artery in experimentally induced ischaemia, Acta Neurochirurgica, 10.1007/BF01406668, 89:1-2, (53-63), Online publication date: 1-Mar-1987. Okada Y, Shima T, Oki S and Uozumi T Experimental microsurgical embolectomy after middle cerebral artery embolization in the dog, Journal of Neurosurgery, 10.3171/jns.1983.58.2.0259, 58:2, (259-266) Azzena G, Campus G, Mameli O, Moraglia S, Padua G, Pau A, Pau S, Ruju P, Sehrbundt Viale E, Tolu E, Turtas S and Viale G (1983) Omental transposition or transplantation to the brain and superficial temporal artery-middle cerebral artery anastomosis in preventing experimental cerebral ischaemia, Acta Neurochirurgica, 10.1007/BF01406203, 68:1-2, (63-83), Online publication date: 1-Mar-1983. Lawner P, Laurent J, Simeone F and Fink E Effect of extracranial-intracranial bypass and pentobarbital on acute stroke in dogs, Journal of Neurosurgery, 10.3171/jns.1982.56.1.0092, 56:1, (92-96) September 1978Vol 9, Issue 5 Advertisement Article InformationMetrics Copyright © 1978 by American Heart Associationhttps://doi.org/10.1161/01.STR.9.5.461 Originally publishedSeptember 1, 1978 PDF download Advertisement

Effect of extracranial-intracranial vascular bypass graft on experimental acute stroke in dogs.

✓ Anastomosis of the superficial temporal artery (STA) to a middle cerebral artery (MCA) branch was completed about 2 hours after occlusion of the MCA root in 20 dogs. Occlusion of the MCA root without bypass grafting was performed in 11 control animals. All dogs were evaluated clinically. Two days to 3 months (usually 2 weeks) after surgery, STA catheter angiograms were made and the animals sacrificed by perfusion fixation. The brains were evaluated pathologically. Animals with patent or occluded STA-MCA bypass grafts fared better both clinically and pathologically than the controls. Hemorrhagic infarction and blood-brain barrier damage were common in untreated dogs and uncommon in treated animals. STA-MCA bypass grafts rarely led to occlusion of intrinsic collateral blood supply to the brain. The data suggest that prompt STA-MCA branch anastomosis might lead to restoration of neurological function and parenchymal structural integrity in certain patients with acute middle cerebral artery occlusion.