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.

The magnetic resonance imaging (MRI) findings of presumed cerebrovascular accident in 12 dogs are described. Fourteen lesions were seen, commonly (11 of 14) within the gray matter of the cerebellar hemispheres or vermis. Thirteen lesions were hyperintense on T2-weighted images (in 11 dogs) and one was hypointense. Eleven of 14 lesions were within the region supplied by the rostral cerebellar artery or one of its main branches and there was no, or minimal, mass effect. Contrast enhancement was only seen in six lesions and was mild in all. Gradient-echo images provided additional information in two dogs. The appearance of infarction in dogs with diffusion-weighted images (DWI) is similar to that in humans, and provided supportive evidence for the diagnosis of infarction in five dogs. The use of gradient-echo and DWI is recommended for the evaluation of suspected cerebrovascular accidents in dogs. Six of the 12 affected animals were spaniels or spaniel crosses, suggesting a possible breed predisposition.

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.

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.

This report describes three dogs with intracranial haemorrhage secondary to severe coagulation defects associated with Angiostrongylus vasorum infection. The initial case was diagnosed at necropsy, with two subsequent cases diagnosed antemortem and successfully treated. The dogs ranged in age from 14 months to four years and were presented for evaluation of a severe, subacute onset of suspected cerebral disease. Magnetic resonance imaging performed on all three dogs was suggestive of multiple areas of intraparenchymal brain haemorrhage. Coagulation assays showed a consumptive coagulopathy resembling chronic disseminated intravascular coagulation. Postmortem examination of the initial case confirmed the presence of multiple intracranial and extracranial haemorrhages. An unexpected finding was that of a marked multifocal nematode infection of the lungs with an associated vasculopathy. The parasites were confirmed to be A vasorum. In the two other dogs, faecal examination by Baermann technique confirmed A vasorum infection. Both dogs were treated with fenbendazole and one was additionally given a plasma transfusion. Repeated coagulation assays were normal within one week. Neurological examinations were normal for both dogs within six weeks. This case series indicates that A vasorum infection should be considered as a possible aetiology of intracranial haemorrhage in dogs.

Ischemia and infarction of the spinal cord is a known cause of acute spinal injury in dogs. Currently, the diagnosis of spinal cord infarction in small animals is based on history, clinical signs, and the exclusion of other differentials with radiography and myelography. It is a diagnosis only confirmed through necropsy examination of the spinal cord. The aim of this paper is to describe the Magnetic resonance imaging (MRI) findings of the spinal cord of dogs with suspected spinal cord infarcts to utilize this technology for antemortem support of this diagnosis. This retrospective study evaluated the spinal MR examinations of 11 dogs with acute onset of asymmetric nonpainful myelopathies. All patients except one (imaged at 2 months) were imaged within 1 week of clinical signs and managed conservatively with minimal medical and no surgical intervention. They were followed clinically for a minimum of 4 months after discharge. MR findings in all dogs were characterized by focal, intramedullary, hyperintense lesions on T2-weighted images with variable contrast enhancement similar to what is reported in humans. Though it could not be used to diagnose spinal cord infarction definitively, MRI was useful in excluding extramedullary spinal lesions and supporting intramedullary infarction as a cause of the acute neurologic signs. Together with the history and clinical examination findings, MRI is supportive of a diagnosis of spinal cord infarction.

BackgroundThe prognostic value of early magnetic resonance imaging (MRI) in dogs after traumatic brain injury (TBI) remains unclear.ObjectivesDetermine whether MRI findings are associated with prognosis after TBI in dogs.AnimalsFifty client‐owned dogs.MethodsRetrospective study of dogs with TBI that underwent 1.5T MRI within 14 days after head trauma. MRI evaluators were blinded to the clinical presentation, and all images were scored based on an MRI grading system (Grade I [normal brain parenchyma] to Grade VI [bilateral lesions affecting the brainstem with or without any lesions of lesser grade]). Skull fractures, percentage of intraparenchymal lesions, degree of midline shift, and type of brain herniation were evaluated. MGCS was assessed at presentation. The presence of seizures was recorded. Outcome was assessed at 48 h (alive or dead) and at 3, 6, 12, and 24 months after TBI.ResultsSixty‐six percent of the dogs had abnormal MRI findings. MRI grade was negatively correlated (P < .001) with MGCS. A significant negative correlation of MRI grade, degree of midline shift, and percentage of intraparenchymal lesions with follow‐up scores was identified. The MGCS was lower in dogs with brain herniation (P = .0191). Follow‐up scores were significantly lower in dogs that had brain herniation or skull fractures. The possibility of having seizures was associated with higher percentage of intraparenchymal lesions (P = 0.0054) and 10% developed PTE.Conclusions and Clinical ImportanceSignificant associations exist between MRI findings and prognosis in dogs with TBI. MRI can help to predict prognosis in dogs with TBI.

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.