Читать книгу Canine and Feline Epilepsy - Luisa De Risio - Страница 250

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 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).