Local cerebral blood flow assessment using transcranial Doppler ultrasonography in a dog with brain infarction in the right middle cerebral artery territory.

A 12-year-old neutered male Chihuahua was diagnosed with acute brain infarction in the right middle cerebral artery (MCA) territory. Transcranial Doppler ultrasonography (TCD) was performed to assess the local cerebral blood flow at the time of diagnosis and after 4 and 31 hr. Initially, the right MCA retained blood flow but with a lower cerebral blood flow velocity (CBFV; 14.9 cm/sec) than the left MCA (27.9 cm/sec). The TCD vascular resistance variables were higher in the right than in the left MCA. An increase in the CBFV and a decrease in TCD vascular resistance variables were observed, consistent with improvements in neurological symptoms. TCD can be a non-invasive, and easy-to-use modality for bedside monitoring of cerebral edema and infarction.

Multiple infarcts and hemorrhages in the central nervous system of a dog with cerebral amyloid angiopathy: a case report.

BACKGROUND: ß-amyloid (Aß) can accumulate in the brain of aged dogs, and within vessels walls, the disease is called cerebral amyloid angiopathy (CAA). In humans, Alzheimer's disease and CAA are strongly correlated with cerebrovascular disease. However, in dogs, this association has not been extensively studied yet. The present report highlights the pathological and clinical features of a concomitant cerebrovascular disease and amyloid precursor protein (APP) accumulation in the brain of a dog. CASE PRESENTATION: A female, 16-year-old, Standard Poodle with a one-year history of cognitive deficits presented with an acute onset of right-sided postural reaction deficit and circling, left-sided head tilt, positional nystagmus, and ataxia. Due to poor prognosis the dog was euthanized, and pathological examination of the brain revealed an acute lacunar infarction within the thalamus extending to rostral colliculus. Additional findings included subacute and chronic areas of ischemia throughout the brain and areas of hemorrhage within the medulla. Immunolabeling revealed APP deposition within intraparenchymal vessels of frontal, temporal and occipital cortex, hippocampus, diencephalon, mesencephalon and myelencephalon, besides meningeal vessels walls. Glial fibrillary acidic protein (GFAP) immunolabeling showed marked astrocytosis around the acute area of infarction and within chronic areas of ischemia. Histological examination of the brain along with immunohistochemistry results showed a concomitant APP, which is an Aß precursor, accumulation within the neuroparenchyma and vessels (CAA) with histological evidences of a cerebrovascular disease in an aged dog. CONCLUSIONS: This report shows that APP accumulation in the brain can occur concomitantly to a severe cerebrovascular disease in a dog. Further studies are necessary to elucidate if cerebrovascular disease is associated with Aß accumulation in the brain of dogs.

Bilateral Symmetrical Idiopathic Necrotizing Encephalopathy: A New Syndrome in Sprague-Dawley Rats.

This article describes the occurrence of a bilaterally symmetrical encephalopathy in Sprague-Dawley rats, which occurred over the period 2005 to 2012 in our laboratory in both untreated control rats and rats treated with different pharmacologically active compounds. The acute brain lesions consisted of degeneration/necrosis in the ventral areas of the brain mostly with little inflammatory response; in the more rare chronic cases there were numerous lipid-laden macrophages. The areas most consistently affected were the crus cerebri, the ventral midbrain, the pyramids, and the internal capsule. Other areas less frequently affected were the mammillary bodies, the fimbria, the olfactory tubercles, the optic tracts, and the ventral hippocampus. All available data, including clinical signs, gross pathology, clinical pathology, diet, breeding, and housing were collected and are presented. Our investigations did not elucidate the pathogenesis of the lesions, although the infarction-type changes are suggestive of a vascular etiology. To our knowledge, this particular lesion with its consistent distribution pattern has not been reported in the rat literature and its publication is therefore important to the toxicological pathology community, because an unbalanced group distribution in a toxicology study could potentially confound the safety assessment of a compound.

Presumed brain infarctions in two dogs with systemic leishmaniasis.

Clinical signs and magnetic resonance imaging findings of multiple brain infarcts in two dogs infected with Leishmania spp. are reported. Clinical signs of intracranial dysfunction were peracute and there was no further deterioration. Magnetic resonance images of the brain were consistent with multifocal, non-haemorrhagic, ischaemic lesions. Routine serum biochemistry revealed hyperproteinaemia and hyperglobulinaemia. Serum antibody titres were highly positive for Leishmania infantum and Leishmania amastigotes were seen within bone marrow macrophages in both cases. Canine leishmaniasis can cause cerebrovascular alterations, such as vasculitis, that might predispose dogs to brain infarcts.

Imaging diagnosis--magnetic resonance imaging findings in a dog with sequential brain infarction.

An adult greyhound was evaluated on three occasions for acute, intracranial neurologic signs. Based on magnetic resonance (MR) imaging, there were T2-hyperintense and T1-hypointense, noncontrast enhancing lesions in the cerebellum, and brain stem. Using diffusion-weighted imaging (DWI), the lesions were characterized initially by restricted water diffusion. The presumptive diagnosis on each occasion was acute ischemic cerebrovascular accident leading to infarction. This allowed us to characterize the changes in appearance of infarcted neural tissue on the standard MR sequences over time, and to confirm that the DWI could be successfully used in low-field imaging. © 2012 Veterinary Radiology & Ultrasound.

Computed tomography diagnosis of eight dogs with brain infarction.

OBJECTIVE: Medical records of eight dogs presenting with acute onset of neurological signs and a diagnosis of brain infarction as determined by computed tomography (CT) imaging were reviewed. DESIGN: Retrospective single-centre case review. RESULTS: Ischaemic infarction in the territory of the rostral cerebellar artery was identified in three spaniel-breed dogs. All cerebellar infarcts were non-haemorrhagic. Telencephalic infarcts were identified in five dogs, in the territories of the middle cerebral artery (2/5) and rostral cerebral artery (3/5). One of these dogs had an ischaemic infarction, but all other infarctions appeared haemorrhagic. All dogs were geriatric (≥ 8 years old), with concurrent medical conditions identified in six dogs. One dog was euthanased after diagnosis because of the severity of its neurological signs and one dog was euthanased as a result of associated renal disease 2 months after diagnosis. Six dogs were alive at least 1 year after diagnosis. CONCLUSIONS: CT is useful in the diagnosis of cerebrovascular accident in dogs, which can present as a spectrum of images with early changes in attenuation and subtle mass effects detected after infarction. CT is particularly sensitive for detecting haemorrhagic infarction, but under-represent ischaemic and lacunar infarctions when compared with MRI.

Rostral cerebellar arterial infarct in two cats.

A 10-year-old female neutered domestic shorthair (DSH) cat and a 6-year-old female neutered Siamese cat were presented following a peracute onset of decerebellate rigidity and a cerebellar vestibular syndrome, respectively. In both cats, physical examination and routine blood tests were unremarkable, as was routine analysis of cerebrospinal fluid obtained from the DSH cat. Based on the magnetic resonance imaging (MRI) features - focal wedge-shaped lesion in the cerebellum characterised by hyperintensity in T2-weighted, T2( *)-gradient echo and fluid attenuated inversion recovery (FLAIR) images - a presumptive diagnosis of cerebellar infarct was made in both cases. In the DSH cat, the post-mortem examination confirmed the diagnosis of cerebellar infarct and additionally found acute renal infarcts and a pulmonary neoplasia. In the Siamese cat, ultrasonographic evaluation of the heart revealed a probable low-grade chronic valvular endocarditis which was thought to be a potential source of thromboembolism. This paper describes the first two cases - one confirmed and the other suspected - of cerebellar infarct in the cat. The in vivo potential diagnostic value of the MRI study is highlighted. Cerebellar infarcts should be included in the differential diagnosis of cat with a peracute onset of cerebellar signs regardless of the severity of neurological deficits.

Presumed and confirmed striatocapsular brain infarctions in six dogs.

OBJECTIVE: To describe the clinical and diagnostic features of the canine sensorimotor syndrome caused by striatocapsular brain infarctions (SCI). ANIMALS STUDIED: Six dogs with diagnostic imaging or postmortem evidence of SCI. PROCEDURES: Medical records of dogs with SCI were retrospectively reviewed and the signalment, history, clinical signs, antemortem clinicopathologic test results, diagnostic imaging findings, case outcomes, and pathologic findings recorded. RESULTS: All dogs had an acute onset of nonprogressive homonymous visual field deficits and contralateral general proprioceptive (GP) deficits. Contralateral hemiparesis and facial hypalgesia were noted in 5/6 dogs. CT scans were normal in 2/4 dogs, and revealed poorly defined hypoattenuating lesions in the subcortical white matter in two dogs. MRI exams were performed in 5/6 dogs and revealed unilateral, variably sized, striatocapsular lesions consistent with nonhemorrhagic infarctions. Diagnostic imaging (6/6) and postmortem examinations (2/6) suggested that SCI resulted from lesions in the vascular territories of the rostral choriodal (6/6) and lenticulostriate arteries (2/6). Diseases predisposing to infarction were not identified in 5/6 dogs. Improvements in mentation, behavior, proprioceptive deficits, and hemiparesis were seen in surviving dogs, but persistent, symptomatic sensory deficits were noted during the follow-up period. CONCLUSIONS: SCI should be considered as a differential diagnosis for dogs with acute onset, nonprogressive homonymous hemianopia, contralateral GP deficits or hemiparesis, and facial hypalgesia. MRI is the preferred modality for the antemortem imaging diagnosis of SCI. Although partial recovery occurred in all surviving dogs, visual and facial sensory disturbances persisted.

Clinical and topographic magnetic resonance characteristics of suspected brain infarction in 40 dogs.

Medical records of 40 dogs presented for evaluation of acute-onset, nonprogressive, intracranial dysfunction by means of magnetic resonance imaging (MRI) diagnosis of brain infarction were reviewed. Location of the brain infarcts was: 11 of 38, telencephalic; 8 of 38, thalamic/midbrain; 18 of 38, cerebellar; and 3 of 38, multifocal. Telencephalic infarcts developed within the territory of the middle cerebral (4/11), rostral cerebral (2/11), and striate (5/11) arteries. Thalamic/midbrain infarcts developed within the territory of perforating arteries of the caudal portion of the thalamus and rostral portion of the brainstem (8/8). All cerebellar infarcts (18/38) were within the territory of the rostral cerebellar artery or one of its branches. All infarcts appeared nonhemorrhagic, with marked contrast enhancement observed in only 3 of 38 dogs, all of which were imaged more than 7 days after the onset of signs of neurologic dysfunction. Diffusion-weighted imaging (DWI) sequences were available from 6 dogs, all imaged within 5 days of the onset of signs of neurologic dysfunction. Suspected infarcts were hyperintense on DWI sequences and were hypointense on the apparent diffusion coefficient map. Telencephalic infarcts caused abnormal mental status, contralateral postural reaction deficit, contralateral nasal hypalgesia, contralateral menace deficit, and ipsilateral circling. Thalamic/midbrain infarcts caused contralateral or ipsilateral postural reaction deficit, contralateral menace deficit, ipsilateral head tilt or turn, nystagmus, ventrolateral strabismus, and anisocoria. Cerebellar infarcts caused ipsilateral asymmetric cerebellar quality ataxia, head tilt, intermittent opisthotonus, nystagmus, and ipsilateral menace deficit with apparent normal vision.

Results of diagnostic investigations and long-term outcome of 33 dogs with brain infarction (2000-2004).

Medical records of 33 dogs presented for acute onset, nonprogressive, intracranial dysfunction that had a magnetic resonance imaging diagnosis of brain infarction were reviewed. Postmortem confirmation of brain infarction was available in 10 dogs. All dogs were evaluated by CBC, serum biochemistry, thyroid and adrenal testing, urinalysis, thoracic and abdominal imaging, and cerebrospinal fluid analysis. Results of coagulation profile and arterial blood pressure were available in 32/33 and 28/33 dogs, respectively. On the basis of the imaging findings, infarcts were classified depending on their type (territorial or lacunar) and location within the brain (telencephalic, 10/33; thalamic/midbrain, 8/33; cerebellar, 15/33). No marked associations among location or type of infarct and patient age and sex, occurrence of systemic hypertension, and the presence or absence of a concurrent medical condition were identified. Small breed dogs (< or =15 kg) were significantly more likely to have territorial cerebellar infarcts, whereas large breed dogs (>15 kg) were significantly more likely to have lacunar thalamic or midbrain infarcts. A concurrent medical condition was detected in 18/33 dogs with brain infarcts, with chronic kidney disease (8/33) and hyperadrenocorticism (6/ 33) being most commonly encountered. Of 33 dogs, 10 were euthanized because of the severity and lack of improvement of their neurologic status or the severity of their concurrent medical condition. No association was identified between type or location of infarct and patient outcome. Dogs with concurrent medical conditions had significantly shorter survival times than those with no identifiable medical condition and were significantly more likely to suffer from recurrent neurologic signs because of subsequent infarcts.