Fig. 5.1. MRI of a 12-year-old, male West Highland white terrier with peracute onset of right-sided forebrain signs (severe obtundation, disorientation and compulsive circling to the right, left-sided hemiparesis, absent postural reactions in the left thoracic and pelvic limbs, decreased menace response on the left eye and decreased facial sensation on the left side of the face). Transverse T2W (a), FLAIR (b), T1W (c), T1WC (d) and dorsal DWI (e) images show a large sharply demarcated T2W, FLAIR and DWI hyperintense, T1W hypointense and non-contrast-enhancing area in the right cerebral cortex involving the parietal lobe and the rostral occipital cortex (e). The MRI features of this lesion are strongly suggestive of a territorial ischaemic infarct affecting the right cerebrum in the territory of the middle cerebral artery. Transverse T2W (a), FLAIR (b), T1W (c), T1WC (d) and dorsal DWI (e) images show a large sharply demarcated T2W, FLAIR and DWI hyperintense, T1W hypointense and non-contrast-enhancing area in the right cerebral cortex involving the parietal lobe and the rostral occipital cortex (e). The MRI features of this lesion are strongly suggestive of a territorial ischaemic infarct affecting the right cerebrum in the territory of the middle cerebral artery.
Box 5.1. Disorders predisposing to ischaemic or haemorrhagic CVA.
Ischaemic CVA:
• Embolus (septic, fat, air, parasites (e.g. Dirofilaria immitis), primary or secondary neoplasia, fibrocartilaginous);
• Systemic hypertension (generally associated with chronic renal disease, hyperadrenocorticism or pheochromocytoma);
• Hypercoagulable state;
• Increased blood viscosity (e.g. polycythaemia vera, multiple myeloma);
• Cardiac disease;
• Hyperlipoproteinaemia in miniature schnauzers;
• Atherosclerosis associated with primary hypothyroidism, diabetes mellitus, hyperadrenocorticism or hereditary hypercholesterolaemia.
Haemorrhagic CVA:
• Neoplasia (e.g. intravascular lymphoma, haemangiosarcoma, oligodendrogliomas, glioblastomas, ependymomas, haemangioendotheliomas);
• Coagulopathy (associated with von Willebrand’s disease, Angiostrongylus vasorum infection or neoplasia);
• Congenital or acquired vascular malformations;
• Cerebral amyloid angiopathy;
• Necrotizing vasculitis.
Fig. 5.2. MRI of a 12-year-old, male neutered, crossbreed with peracute onset of left-sided forebrain signs (severe obtundation, compulsive circling to the left, absent postural reactions in the right thoracic and pelvic limbs, decreased menace response on the right eye and decreased facial sensation on the right side of the face). Transverse T2W (a), FLAIR (b), T1W (c), T1WC (d) and dorsal DWI (e) images show a small relatively sharply demarcated area in the left thalamus, which appears hyperintense on T2W, FLAIR and DWI, iso- to hypo-intense on T1W, and non-contrast enhancing. The MRI features of this lesion are strongly suggestive of a lacunar ischaemic infarct resulting from obstruction of a small perforating artery in the left thalamus. Transverse T2W (a), FLAIR (b), T1W (c), T1WC (d) and dorsal DWI (e) images show a small relatively sharply demarcated area in the left thalamus, which appears hyperintense on T2W, FLAIR and DWI, iso- to hypo-intense on T1W, and non-contrast enhancing. The MRI features of this lesion are strongly suggestive of a lacunar ischaemic infarct resulting from obstruction of a small perforating artery in the left thalamus.
Fig. 5.3. MRI of a 13-year-old, male neutered Bouviers des Flandres with acute onset right forebrain signs and severe thrombocytopaenia. Transverse T2W (a), dorsal T2W (b), T1W (c), and T1WC (d) images show a hyperintense area within the subdural space of the right cerebral hemisphere (b) resulting in compression of the right hemisphere, midline shift and partial obliteration of the right lateral ventricle. The lesion was a subdural haemorrhage.
Fig. 5.4. MRI of a 17-month-old female spayed Staffordshire bull terrier with subacute progressive onset of right-sided forebrain signs. Transverse T2W (a), T2* GRE (b), T1W (c), T1WC (d) and FLAIR (e and f) images show an intraparenchymal area of signal change in the right parietal lobe. The lesion is hypointense on T2* GRE (b), has a hypointense centre on T2W (a), T1W (c) and FLAIR (e and f), peripheral hyperintensity on T2W (a) and FLAIR (e and f), and mild peripheral contrast enhancement on T1WC (d). These signal changes were suggestive of intraparenchymal haemorrhage in the right parietal lobe. FLAIR images (e and f) show marked hyperintensity (most likely marked secondary vasogenic oedema) within the corona radiata. The dog had positive faecal culture for Angiostrongylus vasorum.
CVA can recur and relapses are most frequent in dogs where an underlying cause is identified but it is difficult to treat (Garosi et al., 2005a).
Post-stroke seizures and epilepsy
Seizures can occur secondary to CVAs and TIAs and can be classified as early and late depending on time of occurrence (less than 7 days or more than 7 days, respectively) following stroke (or TIA). Two or more recurrent late post-stroke seizures (PSS) are referred to as post-stroke epilepsy (PSE) (Slapo et al., 2006), although some have defined PSE also as first unprovoked seizure caused by a previous stroke (Jungehulsing et al., 2013). PSS can be focal or generalized, and status epilepticus can occur. PSS have a negative effect on outcome in patients with CVAs. PSS may exacerbate secondary cerebral injury by inducing glutamate excitotoxicity, and enhancing the mismatch between energy supply and demand under ischaemic conditions, leading to breakdown of ion gradients, mitochondrial damage, and eventually an irreversible state of injury (Menon and Shorvon, 2009). Experimental studies suggest that repeated seizure-like activity in the context of cerebral ischaemia significantly increases stroke size and can impair functional recovery. In people, the incidence of early and late PSS ranges from 2% to 16%, depending on study population, stroke subtype, follow-up duration and how the authors have defined early and late PSS and PSE (Arntz et al., 2013; Conrad et al., 2013; Jungehulsing et al., 2013). Patients with intracerebral haemorrhage have the highest incidence of PSS, followed by patients with ischaemic stroke and patients with a transient ischaemic attack (Arntz et al., 2013). The overall incidence of PSE is 2–6.4% in people with CVA (Arntz et al., 2013; Graham et al., 2013). In one study, the incidence of PSE was estimated as 1.2%, 3.5%, 9.0% and 12.4% at 3 months, 1, 5 and 10 years post-CVA, respectively
