Canine and Feline Epilepsy. Luisa De Risio
rel="nofollow" href="#ulink_72975c18-da71-5425-9d64-9b079e24f768">Fig. 5.2a–e), the age of the infarct (e.g. recent, organizing), the presence of secondary haemorrhage, the pathogenesis of the stroke (e.g. thrombotic, embolic, haemodynamic) and the suspected underlying aetiology.
Haemorrhagic CVA can be classified according to the anatomical site of the haemorrhage (e.g. epidural, subdural, Fig. 5.3a–d; subarachnoid; intraparenchymal, Fig. 5.4a–f; intraventricular), size of the lesion (e.g. small, large) and the age of the lesion or the suspected underlying aetiology (Wessmann et al., 2009). Several disorders can predispose to ischaemic or haemorrhagic CVA (Box 5.1).
The most commonly reported concurrent medical conditions in dogs with ischaemic CVA include hyperadrenocorticism, chronic renal disease, hypothyroidism and hypertension (Garosi et al., 2005a). Reported concurrent medical conditions in dogs with haemorrhagic CVA include Angiostrongylus vasorum infection, primary or secondary brain tumours, hypertension, hyperadrenocorticism, chronic renal disease and hypothyroidism (Lowrie et al., 2012). A concurrent medical condition has been identified in approximately 50% and 44% of dogs with ischaemic and haemorrhagic strokes, respectively (Garosi et al., 2005a; Lowrie et al., 2012).
Reports of ischaemic or haemorrhagic strokes in cats are limited (Cherubini et al., 2007; Altay et al., 2011). Reported concurrent medical conditions include hyperthyroidism, hypertrophic cardiomyopathy, hepatic and renal disease (Altay et al., 2011). The term feline ischemic encephalopathy has been used to describe cases of peracute onset of neurological signs (including seizures) consistent with a unilateral (focal) forebrain lesion caused by ischaemia associated with Cuterebra larval migration through the cerebrum. It has been suggested that the migrating parasite or the host response leads to vasospasm in the cerebral vasculature, typically the middle cerebral artery, resulting in focal cerebral ischaemia (Glass et al., 1998; Williams et al., 1998).
Clinical signs
Neurological signs in animals with CVA have typically a peracute (6 h) to acute (7–24 h) onset and are nonprogressive or rapidly progressive and subsequently regressive in their evolution. Progression of neurological signs for 24 to 72 h can occur due to worsening cerebral oedema and haemorrhage. Once the neurological signs plateau, they gradually improve in most cases but CVA can be fatal. In animals with ischaemic CVA neurological signs commonly refer to a focal and unilateral intracranial anatomic neuro-localization (Garosi, 2010). In animals with haemorrhagic strokes, neurological signs may refer to more than one intracranial neuroanatomic localization (e.g. forebrain, brainstem or cerebellum) as the haemorrhage usually involves the territory of more than one artery and intracranial pressure (ICP) may be increased. In animals with CVA affecting the forebrain, seizures can occur immediately or several weeks later and are often recurrent (see section on poststroke seizures and epilepsy) (Garosi et al., 2005a; Lowrie et al., 2012). Ocular fundic examination should be performed in all animals with suspected CVA as it may reveal tortuous retinal vessels (suggestive of systemic hypertension) haemorrhage (suggestive of coagulopathy or systemic hypertension) or papilledema (suggestive of increased ICP) (Garosi, 2010).
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