Getting to Grips with Canine Stroke
World Small Animal Veterinary Association Congress Proceedings, 2017
Hanne Gredal, DVM, PhD
Associate Professor, Department of Veterinary Clinical Sciences, University of Copenhagen, Dyrlregevej, Frederiksberg C, Copenhagen, Denmark

A stroke is broadly defined as a focal neurological impairment of sudden onset lasting more than 24 hours and of presumed vascular origin.1 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 year.1 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 cerebella r 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 definition 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 first 24 hours due to an expanding peri-infarct oedema, but usually do not develop further beyond this time frame.

The specific neurological signs depend on the site of infarction, and may therefore vary widely. lschaemic 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 response.2,3

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 dogs.4 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 ataxia.4

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 RCeA.5 Three clinical syndromes associated with three different sites of thalamic infarction have been identified, namely: 1) Paramedian lesions causing vestibular dysfunction, 2) extensive dorsal lesions causing vestibular ataxia, circling and contralateral menace response deficits, and 3) ventrolateral lesions causing circling and contralateral proprioceptive deficits.5

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, specific clinical ‘syndromes’ are not recognised for cerebral haemorrhages, as these can occur at random sites and do not restrict to specific parenchymal structures in the same manner as ischaemic infarcts do. In fact, multifocal bleedings may be present if natural haemostasisis compromised.6

Diagnostic Work-up - How to Diagnose a Stroke

In essence, any dog with peracute onset of focal, non­progressive 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 inflammatory disease or other space-occupying lesions, idiopathic vestibular disease, and trauma-associated haematomas, may cause similar deficits. 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.

The basic diagnostic work-up of a suspected stroke includes a clinical and neurological examination, haematology and serum biochemistry, and haemostatic parameters, such as APTT, PT and thromboelastography (TEG), fibrinogen and D-dimer, if possible.

Eventually, the diagnosis of a stroke, ischaemic or haemorrhagic, is based on magnetic resonance imaging (MRI) of the brain.

With ischaemic stroke, signal changes on MRI are mainly due to the cellular changes caused by ischaemia and a growing brain oedema. Conventional MRI typically reveals a well-demarcated lesion, which confines to a known arterial territory. There is usually no or only little mass effect, and the lesion is characterised by a hypo­ or isointense signal on T1-weighted images (WI), and a hyperintense signal on T2-WI and fluid-attenuated inversion recovery (FLAIR). There is usually only very little contrast enhancement with ischaemic stroke.2,7

With haemorrhagic stroke, the signal changes on MRI are primarily related to the oxygen saturation of haemoglobin causing a shift in the paramagnetic signal of the iron ions as haemoglobin is degraded through several forms (oxy-, deoxy-, and methaemoglobin) over time. Accordingly, an acute haemorrhage (<24h) typically appears hypo- to isointense on T1-WI, and hyperintense on T2-WI, but hypointense in both T1-WI and T2-WI at 24–72h. From 3–7 days, a haemorrhage is usually hyperintense in T1-WI and hypointense in T2-WI. As opposed to ischaemic stroke, the lesion is typically less well demarcated, and some mass effect may be visuals.

Treatment and Prognosis

At present, there is no specific treatment for stroke in dogs. Supportive care, aiming at preventing secondary brain damage, and optimising rehabilitation should be conducted. If any underlying diseases are identified, these should obviously be addressed.8 Fortunately, most dogs with ischaemic stroke seem to have a good prognosis, especially if they survive the first 30 days.9 Survival is, however, dependent on the site of infarction, and the prognosis is therefore guarded in dogs with severe brainstem and mid-brain signs.8

In dogs surviving the acute state of ischaemic stroke, marked improvement is usually seen within the first 30 days, and complete or nearly complete motor function is regained within 1–3 months. The possibility of recurrent episodes is, however, described.8

For haemorrhagic stroke the identification and treatment of a possible underlying cause of haemostatic dysfunction is crucial. Such conditions may result in multiple concurrent lesions, which may explain why haemorrhagic stroke is apparently associated with a less favourable outcome than ischaemic stroke.6


1.  World Health Organization. WHO STEPS Stroke Manual: The WHO STEPwise approach to stroke surveillance. 2006.

2.  McConnell JF, Garosi L, Platt SR, et al. Magnetic resonance imaging findings of presumed cerebellar cerebrovascular accidents in twelve dogs. Veterinary Radiology & Ultrasound. 2005;46:1–10.

3.  Thomsen B, GarosiL, Skerritt G, Rusbridge C, Sparrow T, Berendt M, Gredal. Neurological signs in 23 dogs with suspected rostral cerebellar ischaemic stroke. Acta Veterinaria Scandinavia. 2016;58:40. DOI 10.1186/s13028-016-0219-2.

4.  Gredal H, Skerritt GC, Gideon P, Arlien-Soeborg P, Berendt M. Spontaneous ischaemic stroke in dogs: clinical topographic similarities to humans. Acta Neurologica Scandinavica. 2013 DOI: 10.1111/ane.12092.

5.  Gonçalves R, Carrera I, Garosi L, et al. Clinical and topographic magnetic resonance imaging characteristics of suspected thalamic infarcts in 16 dogs. The Veterinary Journal. 2011;188:39–43.

6.  Lowrie M, De R1sio L, Dennis R, Uabres-Diaz F, Garosi L. Concurrent medical conditions and long-term outcome in dogs with nontraumatic intracranial haemorrhage. Veterinary Radiology & Ultrasound. 20 12;53:381–388.

7.  Wessmann A, Chandler K, Garosi L. Ischaemic and haemorrhagic stroke in the dog. The Veterinary Journal. 2009;180:290–303

8.  Garosi L, JF,Platt SR, Barone G, Baron JC, de Lahunta A, Schatzberg SJ. Results of diagnostic investigations and long-term outcome of 33 dogs with brain infarction (2000–2004). Journal of Veterinary Internal Medicine. 2005;19:725–731.

9.  Gredal H, Toft N, Westrup U, Motta L, Gideon P, Arlien-Seborg P, Skerritt, Berendt M. Survival and clinical outcome of dogs with ischaemic stroke. The Veterinary Journal. 2013;196:408–413.


Speaker Information
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Hanne Gredal, DVM, PhD
Dept. of Veterinary Clinical Sciences
University of Copenhagen
Dyrlregevej, Frederiksberg C, Denmark

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