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Imaging studies of the brain such as computed tomography (CT) and magnetic resonance imaging (MRI) are necessary to support the diagnosis of CVA, to differentiate between ischaemic and haemorrhagic CVA, and to determine the location and extent of the lesion. CT is very sensitive at detecting acute haemorrhage which appears hyperdense, but it may not detect acute ischaemia in the brain (Garosi, 2010). Conventional MRI can help detecting both ischaemic and haemorrhagic CVA, however differentiation between CVA and other intracranial diseases may be challenging in some cases (Cervera et al., 2011; Wolff et al., 2012). Sensitivity and specificity of routine (not including T2* gradient echo sequences and diffusion weighted images) high-field MRI (with or without provision of clinical data) in overall lesion detection and differentiation of CVAs from neoplastic and inflammatory brain disorders in dogs are 39% and 98%, respectively. Sensitivity and specificity of routine high-field MRI (with knowledge of clinical data) are 33% and 89%, respectively, in the diagnosis of haemorragic CVAs, and 67% and 100%, respectively, in the diagnosis of ischaemic CVAs (Wolff et al., 2012). MRI pulse sequences such as T2* gradient echo (for haemorrhagic CVAs), diffusion and perfusion weighted images (for ischaemic CVAs) and magnetic resonance angiography improve the sensitivity and specificity of the diagnosis of peracute and acute CVA (Garosi, 2010; Cervera et al., 2011).

The MRI features of ischaemic CVA include an intraparenchymal lesion within a vascular territory which:

• is well demarcated from the surrounding normal brain tissue;

• involves primarily the grey matter;

• causes minimal or no mass effect;

• compared to normal grey matter, appears:

• hyperintense on T2-weighted, fluid-attenuated inversion recovery (FLAIR) and diffusion-weighted images (DWIs) (Fig. 5.1a, b, e; 5.2a, b, e);

• hypointense on a synthesized apparent diffusion coefficient (ADC) map derived from two or more diffusion-weighted images;

• iso- to hypointense on T1-weighted images (Fig. 5.1c; 5.2c);

• shows variable contrast-enhancement (usually minimal, peripheral or heterogeneous) 7 to 10 days after onset of neurological signs.

The MRI features of haemorrhagic CVA vary depending on several intrinsic (time from ictus, oxygenation state of haemoglobin, source, size and location of haemorrhage) and extrinsic (pulse sequence and field strength) factors (Table 5.1) (Bradley, 1993; Thomas et al., 1997). Haemorrhage in areas with high ambient oxygen (ventricles; epidural, subdural and subarachnoid space) ‘ages’ more slowly than parenchymal haemorrhage, with a resultant change in time course of haemoglobin degradation. Contrast enhancement due to neovascularization in the surrounding brain tissue can occur 7–14 days after intraparenchymal haemorrhagic CVA and may be minimal, heterogenous or peripheral to ring-like.

Cerebrospinal fluid (CSF) analysis in animals with CVA is either normal, or shows aspecific changes such as mild mononuclear or neutrophilic pleocytosis, elevated protein concentration and xanthocromia. CSF should not be collected in animals with coagulopathy or increased ICP.

Once a probable diagnosis of CVA has been achieved (based on clinical presentation, MRI of the brain, and, if possible, CSF analysis), further diagnostic investigations should be performed in attempt to identify an underlying cause of ischaemic or haemorrhagic CVA (Box 5.2).

A definitive diagnosis of CVA can be reached histopathologically (Plate 3).