P. 558

An Urban Experience
H. Gredal1
1University of Copenhagen, Copenhagen, Denmark
Hanne Gredal
DVM, PhD, Associate professor
Dept. of Veterinary Clinical Sciences, University of Copenhagen
Dyrlægevej 16, 1870 Frederiksberg C, Denmark
A stroke is broadly de ned as a focal neurological impairment of sudden onset lasting more than 24
hours and of presumed vascular origin1. Such vascular accidents may be caused by either an acute brain haemorrhage (haemorrhagic stroke) or a thrombus/ thromboemboli causing an area of infarction in the brain (ischaemic stroke).
In humans, stroke is a leading cause of death accounting for approximately 5 million deaths every year1. Although the prevalence is much lower in dogs, it is still an important cause of acute intracranial signs. In dogs, as well as humans, ischaemic stroke appears to be far more common than haemorrhagic stroke, which is why the main focus of the talk will be on ischaemic stroke.
The vascular supply of the brain
The cerebral blood supply is maintained by a circular arterial system, called the circle of Willis, which is
placed on the ventral aspect of the brain. Paired arteries originating from the internal carotid arteries form the rostral part of this circle, whereas the caudal components originate from the basilar artery. The circle of Willis sends off three paired arteries: the rostral cerebellar artery (RCA), the middle cerebral artery (MCA), and the caudal cerebral artery (CCA). Two paired arteries maintain the blood supply to the cerebellum: the rostral cerebellar artery (RCeA) and the caudal cerebellar artery (CCeA). The anatomical appearance of the cerebellar arteries
is subject of some variation, but the RCeA usually originates from the caudal communicating artery of the circle of Willis, whereas the CCeA originates from the basilar artery.
Clinical signs – What to look out for?!
In line with the de nition and aetiology of ischaemic stroke, the clinical picture in dogs is characterised by acute onset of intracranial signs with no prior warning; this is a key clinical feature! Clinical signs may be
progressive within the  rst 24 hours due to an expanding peri-infarct oedema, but usually do not develop further beyond this time frame.
The speci c neurological signs depend on the site of infarction, and may therefore vary widely. Ischaemic stroke in dogs has been reported in relation to almost any of the brain arteries, but especially in relation to the rostral cerebellar artery causing e.g. ataxia, head tilt, nystagmus, and decreased menace response2,3.
Thromboembolic occlusion of the MCA, which happens to be the artery most commonly affected in humans,
is also a relatively common site of ischaemic stroke
in dogs4. The MCA supplies the majority of the lateral surface of the cerebrum. Clinical signs associated with infarction of this area in dogs include seizures, mental changes, hemiparesis and ataxia4.
Another relatively commonly reported site of infarction in dogs is the thalamus, which is supplied by perforating arteries from the caudal part of the circle of Willis or the RCeA5. Three clinical syndromes associated with three different sites of thalamic infarction have been identi ed, namely: 1) paramedian lesions causing vestibular dysfunction, 2) extensive dorsal lesions causing vestibular ataxia, circling and contralateral menace response de cits, and 3) ventrolateral lesions causing circling and contralateral proprioceptive de cits5.
As opposed to ischaemic stroke, the clinical signs of a haemorrhagic stroke may progress beyond the 24h time frame, if an underlying cause of haemostatic dysfunction is not corrected, and bleeding continues. Furthermore, speci c clinical ‘syndromes’ are not recognised for cerebral haemorrhages, as these can occur at random sites and do not restrict to speci c parenchymal structures in the same manner as ischaemic infarcts do. In fact, multifocal bleedings may be present if natural haemostasis is compromised6.
Diagnostic work-up – How to diagnose a stroke
In essence, any dog with peracute onset of focal, non- progressive brain dysfunction should raise a suspicion of stroke. However, as the neurological signs always depend on the site of pathology, several differential diagnoses, including focal in ammatory disease or other space-occupying lesions, idiopathic vestibular disease, and trauma-associated haematomas, may cause similar de cits. Obviously, the history should reveal information of a possible trauma, and brain tumours usually present with a more insidious onset, although acute bleeding in relation to the tumour or sudden changes in intracranial pressure may cause peracute signs.

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