Results of Diagnostic Investigations and Long-Term Outcome of 33 Dogs with Brain Infarction (2000-2004)

Abstract

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.

Recurrent cerebrovascular accidents caused by intravascular lymphoma in a dog

“…In dogs with suspected brain infarcts, diagnostic investigations usually include MRI of the brain, CSF analysis (cell count, cytology and total protein measurement), haematology, serum biochemistry, urinalysis, thyroid and adrenal profiles, survey thoracic and abdominal radiographs, abdominal and cardiac ultrasonography, coagulation profile and blood pressure measurements. Our case underwent all usual diagnostic investigations except for an adrenal profile 17. In the UK, Angiostrongylus vasorum is considered endemic and is a recognised cause of intracranial haemorrhage secondary to coagulopathy 22.…”

“…There is no consensus defining the characteristics and criteria to diagnose cryptogenic ischaemic strokes in human beings,21 which explains the wide prevalence range. In dogs, 45 per cent of cases of ischaemic brain infarcts are cryptogenic 17. Thus, the percentage of cryptogenic ischaemic strokes in dogs is overall higher than in human beings.…”

“…There are more than 200 known causes of ischaemic stroke in human beings,18 whereas in canine medicine, the most common causes include hyperadrenocorticism, chronic kidney disease, hypothyroidism and hypertension 17. In human beings, symptomatic brain infarcts of undetermined cause are termed ‘cryptogenic ischaemic strokes’ 18.…”

Cerebellar ischaemic infarct: a rare complication of pancreatitis

“…Vascular complications occur in approximately 25 per cent of human patients with pancreatitis; the exact incidence is unknown 1. Cerebral infarction secondary to pancreatitis has been reported in a person 2. To the authors’ knowledge, this is the first description of suspected thromboembolism secondary to pancreatitis resulting in central neurological signs in a dog.…”

Intracranial infarcts in two cats with suspected thoracic limb and pulmonary neoplasia

“…A CVA is a clinical manifestation characterised by the sudden onset of clinical signs following either intracranial blood vessel rupture (haemorrhagic CVA) or occlusion of the vessels (ischaemic CVA) (Garosi and others 2005). In the veterinary literature, several reports document the occurrence of CVAs secondary to both haemorrhagic and ischaemic lesions in dogs (Joseph and others 1988, Garosi and others 2005, 2006, Irwin and others 2007, Gonçalves and others 2011, Berg and Joseph 2003). In cats, only two reports discussed CVAs (Cherubini and others 2007, Altay and others 2011).…”