Meningioma and associated cerebral infarction in three dogs.

BACKGROUND: In dogs, meningiomas mostly cause chronic progressive clinical signs due to slow tumor growth. CASE PRESENTATION: In contrast, three dogs were presented with the history of chronic generalized tonic-clonic seizures and peracute deterioration with sudden onset of neurological deficits in accordance with an extensive unilateral forebrain lesion. Magnetic resonance imaging examinations of the dogs revealed a well-delineated extraaxial T2W hyperintense mass in the rostral forebrain with homogeneous contrast enhancement. Additionally, an intraaxial, well-demarcated, unilateral lesion was apparent in the parenchyma supplied by the middle cerebral artery. In two cases, necropsy revealed meningothelial meningioma in the rostral fossa and marked eosinophilic neuronal necrosis, a sign of ischemia, focal malacia, edema and gliosis in the temporal lobe and hippocampus because of a focal thrombosis of the middle cerebral artery. In the third case symptomatic treatment resulted in improvement of clinical signs enabling a good quality of life for the patient. CONCLUSIONS: In dogs with structural epilepsy caused by meningioma, acute deterioration of clinical signs can be associated with ischemic infarctions as a potential complication.

Acute cerebrovascular event in a dog with polycythemia vera.

A 1-year-old neutered male Labrador retriever mixed breed dog was referred for peracute onset of ataxia and seizures. Hematocrit at presentation was 84%. Magnetic resonance imaging of the brain revealed a lesion in the right caudate nucleus consistent with infarction. Postmortem findings were consistent with polycythemia vera and presumed secondary cerebral infarction.

Événement cérébrovasculaire aigu chez un chien atteint de polycythémie vraie. Un Labrador retriever mâle âgé de 1 an a été référé pour l'apparition suraiguë d'ataxie et de crises d'épilepsie. L'hématocrite était de 84 % à la présentation. L'imagerie par résonance magnétique du cerveau a révélé une lésion dans le noyau caudé droit compatible avec à un infarcissement. Les résultats post mortem étaient conformes à une polycythémie vraie et à un infarcissement cérébral secondaire présumé.(Traduit par Isabelle Vallières).

Facilitation of ultrasonic microvesicles on homing and molecular mechanism of bone marrow mesenchymal stem cells in cerebral infarction patients.

OBJECTIVE: Cerebral infarction, or ischemia brain stroke, is a common cerebrovascular disease. Bone marrow mesenchymal stem cells (BMSCs) are widely used to treating ischemia disease such as cardiac infarction. Ultrasonic microvesicles may help the targeting of exogenous factors via localized energy blast. Therefore, this study aims to investigate the effect of ultrasonic microvesicles on the homing of BMSCs on artery thrombosis and the associated molecular mechanisms. MATERIALS AND METHODS: Rat BMSCs were isolated and cultured. Rats were divided into sham, model, BMSCs, and microvesicles groups. Cerebral infarction model was prepared by ligation of cervical artery and middle cerebral artery. 3×106/kg BMSCs were transplanted via tail veins. Microvesicles were used for assisting BMSCs infusion. Sex-determining region Y (SRY) gene expression was measured by Real-time PCR, while 2,3,5-triphenyltetrazolium chloride (TTC) staining was employed for describing the area of cerebral infarction. The activity of caspase 3 was assayed by test kit. Vascular endothelial growth factor (VEGF), nuclear factor kappa B (NF-κB) mRNA/protein levels, were quantified by Real-time PCR, and Western blotting, respectively. RESULTS: Microvesicle group had significantly elevated SRY expression (p<0.05 compared to BMSCs group). Transplantation of BMSCs remarkably decreased cerebral infarction area, caspase 3 activity or NF-κB expression, and increased VEGF expression (p<0.05 compared to model group). Microvesicle induced BMSCs had more potent effects (p<0.01). CONCLUSIONS: Ultrasound microvesicle facilitated homing of BMSCs in cerebral infarction, and improved infarction disease via up-regulating VEGF expression, inhibiting NF-κB expression, and modulating apoptosis.

Central vestibular disease in a blue and gold macaw (Ara ararauna) with cerebral infarction and hemorrhage.

A 24-year-old female blue and gold macaw (Ara ararauna) was presented for an acute onset of left head tilt. On examination, the macaw was dehydrated and had a 120-degree left head tilt, decreased proprioception of the left pelvic limb, and intermittent vertical nystagmus. Results of hematologic testing and biochemical analysis revealed severe leukocytosis with lymphopenia and heterophilia and a high uric acid concentration. Radiographs showed bilateral intertarsal joint osteoarthritis and a healed ulnar fracture. Magnetic resonance imaging of the brain revealed focal T2 and fluid-attenuated inversion recovery hyperintense lesions in the right cerebral hemisphere and in the midbrain. The midbrain lesion showed susceptibility artifact on the T2* sequence, suggesting hemorrhage. In the T2* sequence, iron accumulation (as seen with hemorrhage) distorts the magnetic signal, resulting in the production of a susceptibility artifact, which can then be visualized as a region of hypointensity. The bird was hospitalized but died despite intensive care. Necropsy revealed multiple cerebral vascular lesions including an acute cerebral infarct, a ruptured midbrain aneurysm, and multifocal systemic atherosclerosis. To our knowledge, this is the first report of a cerebral aneurysm in a bird. This report correlates the clinical presentation, imaging, and histopathologic findings in a macaw with central vestibular disease and demonstrates how advanced imaging techniques can identify hemorrhagic lesions through the T2* sequence.

Feline cerebrovascular disease: clinical and histopathologic findings in 16 cats.

Sixteen cats with cerebrovascular disease confirmed via histology to be of nontraumatic and nonneoplastic origins are described. In addition, the anatomy of the arterial supply of the cat's brain is reviewed. It is suggested that this unique arterial design may influence the incidence of cerebrovascular accidents in this species. Of the 16 cats reviewed, seven cats had ischemic infarctions, five had hemorrhagic infarctions, and four were diagnosed with intracranial hemorrhage. The median age was 8 yr and 9.5 yr in cats with infarctions and intracranial hemorrhages, respectively. Clinical signs were severe, acute, consistent with the localization of the cerebrovascular lesion, and influenced by underlying pathology. Four cats with infarction showed lateralized neurologic signs. Four cats with infarctions were diagnosed with pulmonary disease antemortem and three cats had hyperthyroidism. Cerebrospinal fluid analysis and computed tomography scans were available in two cats. None of the infarctions were grossly visible. All cats with hemorrhagic infarcts had severe liver pathology and nephritis was identified in four cats. Hypoxia was a feature in four cats and one cat suffered cardiac failure. In conclusion, the clinical picture is influenced by the type of cerebrovascular disease, the localization of the intracranial lesions, and any underlying pathology.

Presumptive caudal cerebellar artery infarct in a dog: clinical and MRI findings.

Clinical signs and magnetic resonance imaging findings of a caudal cerebellar artery infarct are reported for the first time in a dog. Clinical signs were characterised by a peracute, non-progressive, right-sided central vestibular syndrome with paradoxical right-sided head tilt. Magnetic resonance images were consistent with a territorial, non-haemorrhagic, ischaemic lesion affecting the caudo-ventral part of the right cerebellar hemisphere, mainly involving the right paramedian lobe, the ansiform lobe and the caudal cerebellar peduncle. Bloodwork results were suggestive of an underlying hypercoagulable state, although the concomitant presence of a histologically confirmed mammary gland adenocarcinoma could have also been related to the cerebellar vascular obstruction through metastatic emboli formation. Posterior-inferior cerebellar artery infarction is the human equivalent of caudal cerebellar artery infarct in dogs.

Septicemia, endocarditis, and cerebral infarction due to Staphylococcus aureus in a harp seal (Phoca groenlandica).

An adult, wild-collected, male harp seal (Phoca groenlandica) was transferred from a rehabilitation center to a display facility because of unilateral phthisis bulbi and decreased use of the right forelimb, which precluded its release. In quarantine, the animal demonstrated limited use of the right forelimb, which acutely progressed to complete disuse of the limb accompanied by intermittent lethargy. One month after transfer, the animal was found dead on exhibit. Necropsy showed septic arthritis of the right scapulohumeral joint, valvular endocarditis with systemic bacterial thromboembolism, and infarction of the cerebrum and myocardium. Culture of the blood and affected joint space revealed Staphylococcus aureus. Bacterial polymerase chain reaction of formalin-fixed tissues from the heart and brain were also positive for S. aureus. Staphylococcus aureus infection should be considered as an additional cause of endocarditis and embolic encephalitis in seals.

Pontine infarction in a dog with unilateral involvement of the trigeminal motor nucleus and pyramidal tract.

An unusual case of unilateral trigeminal neuronopathy in a dog is reported, in which the motor nucleus of the trigeminal nerve and the ipsilateral corticospinal tract were destroyed, apparently by a cerebrovascular accident (stroke). Hemiplegia did not occur. Neuropathological changes are described, including remyelination by Schwann cells in the central nervous system. The case illustrates the importance of central nervous system post-mortem examination when establishing causes of cranial nerve paralysis.

Noninfectious complications due to vascular access ports (VAPs) in Yucatan minipigs (Sus scrofa domestica).

Vascular access ports (VAPs) for studies requiring intermittent or continuous infusion and frequent sampling are well accepted and widely used in large animal species. However, the use of medical devices such as VAPs to facilitate sample collection can lead to complications. Noninfectious complications of VAP implantation can result from thrombotic or mechanical obstructions, other mechanical problems, and animal-associated complications. To facilitate our research, we surgically implanted VAPs in the right external jugular vein of 6 adult male and 3 female Yucatan miniswine (age, 12 mo) to enable collection of blood samples every 30 min for 8 h and then every 8 h for as long as 60 d. The VAPs were operational an average of 35.6 d (range, 29 to 56 d) and had an overall success rate of 77.8% with 7 of 9 VAPs functional. In these 7 animals, 53.1 samples on average (range, 28 to 95 samples) were collected from each VAP. Rates of noninfectious complications were 60% for thrombotic events and 40% for nonthrombotic events over the course of this study.

Differences in infarct evolution between lipopolysaccharide-induced tolerant and nontolerant conditions to focal cerebral ischemia.

OBJECT: Although brain tissue may be protected by previous preconditioning, the temporal evolution of infarcts in such preconditioned brain tissue during focal cerebral ischemia is largely unknown. Therefore, in this study the authors engaged in long-term observation with magnetic resonance (MR) imaging to clarify the difference in lesion evolution between tolerant and nontolerant conditions. METHODS: Bacterial lipopolysaccharide (LPS; 0.9 mg/kg) was administered intravenously to induce cross-ischemic tolerance. Focal cerebral ischemia was induced 72 hours later in spontaneously hypertensive rats. Serial brain MR images were obtained 6 hours, 24 hours, 4 days, 7 days, and 14 days after ischemia by using a 7.05-tesla unit. Lesion-reducing effects were evident 6 hours after ischemia in the LPS group. Preconditioning with LPS does not merely delay but prevents ischemic cell death by reducing lesion size. Lesion reduction was a sustained effect noted up to 14 days after ischemia. Reduction of local cerebral blood flow (ICBF) in the periinfarct area was significantly inhibited in the LPS group, which was correlated with endothelial nitric oxide synthase (eNOS) expression. CONCLUSIONS: Significant preservation of ICBF in the periinfarct area, which is relevant to sustained upregulation of eNOS, could be a candidate for the long-term inhibiting effect on infarct evolution in the LPS-induced tolerant state.

Cerebral infarction and meningoencephalitis following hot-iron disbudding of goat kids.

CASE HISTORY: Twelve of 150 goat kids, 4-10 days old, died 3 days after disbudding with a hot iron. Another 18 kids had been ill the previous day but survived following antibiotic therapy. Five of the dead kids were necropsied. PATHOLOGICAL FINDINGS: There was necrosis and haemorrhage of the skin, subcutaneous tissues and frontal bone at disbudding sites in all five kids examined post mortem. Beneath disbudding sites in 4/5 kids there were bilateral, dark red, often cavitated areas of necrosis extending deep into the frontal cortex of the brain. Histologically, these areas consisted of coagulation necrosis, haemorrhage, vascular thrombosis and suppurative inflammation. Numerous bacteria, predominantly large Gram positive rods, were present in the necrotic brain tissue. In the remaining kid, bilateral areas of yellow discolouration and flattening of gyri in frontal lobes corresponded histologically to extensive polioencephalomalacia. A mixed growth of aerobes and anaerobes was cultured from the brain of one kid with suppurative lesions. CLINICAL RELEVANCE: Thermal disbudding of neonatal kids is widely practised in dairy goat herds and is considered the method of choice for disbudding in New Zealand. However, the skull of goat kids is much thinner than that of calves and the safety margin for thermal injury to the brain is markedly reduced. This report highlights the risks associated with the technique and its potential as a welfare issue.

Optimal blood glucose levels while using insulin to minimize the size of infarction in focal cerebral ischemia.

OBJECT: Insulin has been shown to ameliorate cerebral necrosis in global and, more recently, in focal cerebral ischemia. The goal of this study was to determine the relationship between this neuroprotective effect and blood sugar levels in a rat model of focal ischemia. METHODS: Thirty-four rats were subjected to 80 minutes of transient middle cerebral artery occlusion at a mean arterial blood pressure of 60 mm Hg and a temperature of 37 degrees C. Insulin (3.5 IU/kg) was administered 1 hour before (12 rats) and 20 minutes after (12 rats) ischemia; 10 animals served as controls. A quantitative histopathological study conducted after 1 week of survival showed that insulin was not beneficial in reducing the size of the infarction or selective neuronal necrosis in the penumbra when administered before or after ischemia. In addition to infarction, six animals from the insulin-treated groups had bilateral selective neuronal necrosis in the hippocampus or the neocortex. A nonlinear regression analysis in which glucose levels were compared with both cortical necrosis and total infarction yielded a U-shaped curve with a nadir for cerebral necrosis that lay in the 6- to 7-mM blood glucose range. The increased brain damage induced by insulin occurred in animals with very low blood sugar values in the range of 2 to 3 mM. CONCLUSIONS: These results in rats indicate that if insulin is used following ischemia, blood glucose levels should be maintained at approximately 6 to 7 mM. From these data one can infer that hypoglycemia of less than 3 mM should be avoided in situations of focal cerebral ischemia in which insulin is used. Additional animal studies and clinical trials in humans are needed to study the effects of insulin on ischemia.

Diagnosis and treatment of a cerebral infarct in a chimpanzee (Pan troglodytes).

A 29-yr-old chimpanzee (Pan troglodytes) presented after an acute onset of right facial and forearm paresis that progressed to paralysis within 24 hr, with subsequent development of right leg paresis. Magnetic resonance imaging (MRI) of the head revealed an abnormal region of increased signal intensity in the left frontal, parietal, and temporal cerebral hemispheres, corresponding to the vascular territory of the middle cerebral artery, with resultant compression of the left lateral ventricle. The findings were consistent with a cerebral infarct (stroke). MRI is the most sensitive test for early detection of cerebral changes due to ischemia and was essential in obtaining a diagnosis in this case. The chimpanzee responded well to treatment with long-term anticoagulant aspirin and a short, tapered course of prednisone and regained full gross motor function.

MR imaging findings in a dog with intravascular lymphoma in the brain.

Intravascular lymphoma (malignant angioendotheliomatosis, angiotrophic lymphoma) is a rare neoplastic disorder in dogs. The literature contains few reports in dogs and a single report in a cat. Intravascular lymphoma is characterized by an intravascular proliferation of malignant lymphocytes. This unique angiocentric distribution of neoplastic cells leads to the characteristic clinicopathologic feature of thromboses and infarctions. In people, intravascular lymphoma has a predilection for vessels in the central nervous system (CNS) and skin. Typically, affected patients have episodic symptoms that coincide with the timing of infarctions. This report details the clinicopathologic description and magnetic resonance (MR) images of a dog with intravascular lymphoma that resulted in multiple CNS infarctions. Abnormalities identified with MR imaging consisted of multifocal hyperintensities observed in pre-contrast T1-weighted, T2-weighted, intermediate-weighted, and FLAIR pulse sequences. Lesions were most conspicuous on the FLAIR images. In addition, there was mild enhancement of the lesions seen in post-contrast T1 weighted images.

Cerebral infarction and myocardial fibrosis in a white-handed gibbon (Hylobates lar).

A white-handed gibbon (Hylobates lar) lost the use of its right hand. Complete blood count, serum chemistry profile, electrocardiographic findings, blood pressure, and radiographic work-up were normal, but the gibbon died 2 days later. The gibbon was serologically positive for herpes simplex I and Epstein-Barr virus. Necropsy and histopathology showed acute infarction of the right cerebrum and multifocal to coalescing severe myocardial fibrosis.

Necrotizing mycotic vasculitis with cerebral infarction caused by Aspergillus niger in a horse with acute typholocolitis.

An 18-year-old Morgan mare was presented to the Veterinary Medical Teaching Hospital, University of Illinois, with a 10-day history of watery diarrhea, depression, and dysphagia. On admission, the animal was severely dehydrated, depressed, and unable to swallow and had no clinical signs of diarrhea. The respiratory and heart rate and body temperature were within normal limits. Following fluid therapy, the mare developed severe watery diarrhea and continued to be depressed, incoordinated, and dysphagic. The animal died on the fourth day after admission and was sent to the Laboratories of Veterinary Diagnostic Medicine for necropsy. Gross postmortem findings were consistent with an acute cerebral infarction in the right cerebral hemisphere, an acute necrotizing typhlocolitis, multifocal petechial and ecchymotic hemorrhages, enlarged and congested pars intermedia of the pituitary gland, and marked bilateral adrenocortical hyperplasia with multifocal areas of necrosis and hemorrhage. Histologic evaluation of the affected brain demonstrated an area of coagulative necrosis of the gray matter, with hemorrhage, vasculitis, and thrombosis. There were many fungal hyphae 3.5-6.0 microm, pale basophilic, septate, and occasionally branching at 45 degrees present in the arterial walls and throughout the necrotic tissue. Immunohistochemical analysis revealed Aspergillus niger as the etiologic agent responsible for the mycotic vasculitis and infarction in the brain. Bacteria culture and immunohistochemical staining of the colon and cecum failed to demonstrate specific pathogens.

Unilateral cerebral necrosis resembling feline ischemic encephalopathy in an African lion (Panthera leo).

In November 1996, a 14-yr-old captive male African lion (Panthera leo) had sudden onset of left-sided hemiparesis and mydriasis of the left eye. After 24 hr of supportive care, the lion showed no improvement and was euthanized. At necropsy, the right cerebral hemisphere was diffusely and irregularly swollen and malacic. Histopathology revealed extensive acute necrosis and edema of the portion of the right cerebral hemisphere that received blood from the right middle cerebral artery. Gross and histopathologic cerebral findings resembled those of feline ischemic encephalopathy.

Localization of metallothionein-I and -II in hypertrophic astrocytes in brain lesions of dogs.

To study the neurophysiological functions of metallothioneins (MTs), localization of MT-I and -II was examined immunohistochemically in a variety of brain lesions in dogs, including infarct, laminar cortical necrosis, hemorrhage, invasive growth of tumour, inflammatory lesions in granulomatous meningoencephalitis and distemper encephalitis. MT-I and -II were demonstrated in both nucleus and cytoplasm of hypertrophic astrocytes in most brain lesions examined regardless of the type, size, localization and duration of the lesions. In addition, MT expression was stronger in a population of hypertrophic astrocytes localizing inside of the surviving brain tissue rather than those localizing at the boundary between the surviving brain tissue and necrotic area, where severe inflammatory changes were developing. These results suggest that MT-I and -II may play roles not only in protection of neurons from metals and free radicals ubiquitous in the inflammatory lesions but also in repair of injured neural tissues.