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).
Treatment
Treatment of CVA focuses on prevention of secondary brain injury or complications, such as increased ICP (see management of traumatic brain injury) or seizures, and on the underlying disease. For further details on all the aspects of CVA treatment the reader is directed to more comprehensive descriptions (Garosi, 2010). Anti-epileptic treatment is performed as for other types of structural brain disorders (see section on post-stroke seizures and epilepsy, introduction to this chapter and Chapters 12–24).
Prognosis
Most dogs recover within weeks after the onset of ischaemic CVA with only supportive care (Garosi et al., 2005a). Prognosis depends on the severity of the neurological dysfunction, occurrence of complications and the underlying cause of CVA, if identified. In a retrospective study on 33 dogs with MRI or histologic diagnosis of ischaemic CVA, no association was identified between type (lacunar or territorial) or location (telencephalic, thalamic/midbrain, cerebellar) of infarct and patient outcome. Dogs with concurrent medical conditions had significantly shorter survival times than those with no identifiable medical condition and were significantly more likely to suffer from recurrent neurologic signs because of subsequent infarcts. In a retrospective study on 75 dogs with an MRI diagnosis of nontraumatic intracranial haemorrhage, outcome was poor in the majority of dogs with hypertension (Lowrie et al., 2012).
Table 5.1. Change of appearance of intracranial haemorrhage over time (Bradley, 1993; Thomas et al., 1997).
Box 5.2. Diagnostic investigations to identify the underlying aetiology of ischaemic or haemorrhagic CVA.
Diagnostic investigations to identify the underlying aetiology of ischaemic CVA:
• Serial blood pressure measurements;
• Haematology;
• Serum biochemistry profile;
• Urinalysis;
• Urine protein/creatinine ratio;
• Serum antithrombin III activity;
• D-dimers;
• Thromboelestography;
• Infectious disease testing (e.g. serology, PCR);
• Endocrine testing for hyperadrenocorticism, thyroid diseases, diabetes mellitus and pheochromocytoma;
• Thoracic radiographs;
• Abdominal ultrasound;
• Echocardiography and electrocardiography.
Diagnostic investigations to identify the underlying aetiology of haemorrhagic CVA:
• Serial blood pressure measurements;
• Haematology;
• Serum biochemistry profile;
• Buccal mucosa bleeding time;
• Prothrombin time (PT);
• Activated partial thromboplastin time (APTT);
• Infectious disease testing (e.g. serology, PCR);
• Thoracic radiographs;
• Abdominal ultrasound;
• Faecal analysis to investigate parasitic infestation (such as A. vasorum).
Post-stroke epilepsy has a negative effect on stroke recovery and quality of life in people (Arntz, 2013).
Inflammatory/infectious
Inflammatory disease of the CNS can be classified as infectious (when caused by a known or suspected infectious agent) or immune-mediated (when the underlying aetiology is unknown and an immune-mediated process is suspected). A degree of CNS inflammation may occur also with brain neoplasia, infarction or trauma. This section will focus on infectious and presumed immune-mediated disorders. Inflammatory disease of the CNS may affect the brain parenchyma (encephalitis), the meninges (meningitis) and the spinal cord (myelitis). Inflammatory CNS disorders commonly affect young to middle-aged animals, although animals of any age and gender can be affected. Certain infectious disorders occur exclusively or predominately in certain geographic areas (Nghiem and Schatzberg, 2010). The majority of reported inflammatory CNS diseases in dogs and cats are outlined in Tables 5.3, 5.4, 5.6, 5.7, 5.8, 5.10 and 5.11. Additional information is provided in the text for selected disorders. The suggested references should be consulted for more detailed information on each disorder.
Clinical signs
Signs of systemic involvement may (e.g. certain viral diseases or mycotic disorders) or may not (e.g. cerebral abscess, neurotropic infections, immune-mediated encephalitis) be present. Ophthalmologic examination may reveal fundic changes or uveitis.
Neurological signs in animals with inflammatory CNS disease often have an acute to subacute onset, are progressive and reflect multifocal or diffuse involvement of the CNS. However, focal neurological deficits can also occur (e.g. cerebral abscess, fungal granuloma). Seizures commonly occur in animals with forebrain involvement.
Encephalitis-related seizures and post-encephalitic epilepsy
Seizures can occur during the active stage of cerebral inflammation, disappear after the inflammation/infection has resolved, they may persist, or they may first manifest in the post-encephalitic period after the inflammation/infection has resolved (see Schwartz-Porsche and Kaiser, 1989; Michael and Solomon, 2012; Chapter 3). The exact risks of developing encephalitis-associated seizures are poorly understood, but appear to relate to the pathogen, the degree of cortical involvement and the cytokine-mediated inflammatory
