Canine and Feline Epilepsy. Luisa De Risio
of the brain should be performed before considering CSF collection.
MRI of the brain can reveal changes suggestive of inflammatory CNS disease such as multifocal, diffuse or sometimes focal lesions within the brain parenchyma that typically appear hyperintense on T2-weighted and FLAIR images, iso- to hypointense on T1-weighted images and show variable contrast enhancement sometimes with meningeal involvement following administration of contrast medium. The MRI findings sometimes may support the ante-mortem diagnosis of a particular aetiology (e.g. FIP). The MRI features of various inflammatory CNS diseases have been reviewed (Hecht and Adams, 2010b). Sensitivity and specificity of high-field MRI for classifying brain diseases as inflammatory are 86.0 and 93.1% without provision of clinical data and 80.7 and 95.4% with provision of clinical data, respectively (Wolff et al., 2012). Sensitivity and specificity of high-field MRI are lower for detection of specific inflammatory CNS aetiologies (Wolff et al., 2012).
Treatment
Treatment of CNS infections depends on the identification of the aetiologic agent and selection of the appropriate antimicrobial or anti-fungal agent (see Tables 5.5–5.9). Treatment of viral CNS infections is mostly supportive and symptomatic. Treatment of non-infectious inflammatory CNS disorders involves immunosuppressive medications. Anti-epileptic treatment of both acute and late PES is performed as for other types of structural brain disorders (see section on encephalitic-related seizures, introduction to this chapter and Chapters 12–24). Interactions between AEMs and other medications to treat the CNS infection/ inflammation should be carefully considered. In animals with increased intracranial pressure secondary to CNS inflammation, treatment and monitoring should be performed similarly to what has been described for animals with traumatic brain injury (see management of traumatic brain injury).
Prognosis
Prognosis is variable and dependent on the underlying aetiology, extent and severity of the CNS inflammation and associated neurological deficits, and promptness of diagnosis and treatment (when available).
Canine distemper
Canine distemper (CD) is a common polysystemic disease of dogs that may infect the CNS. CD is caused by canine distemper virus (CDV), an RNA virus that belongs to the genus Morbillivirus, family Paramyxoviridae (Martella et al., 2008; Greene and Vandevelde, 2012). Although the incidence of CD has decreased since the introduction of the modified-live CDV vaccines in the 1950s, it is still a common CNS disorder worldwide, primarily in unvaccinated dogs but also occasionally in dogs with a vaccinal history as immunity to virulent CDV is not absolute after vaccination. Dogs that are not immunized regularly may lose their protection and become infected following stress, immunosuppression or contact with diseased animals. CDV is quickly inactivated in the environment and transmission mainly occurs by direct animal-to-animal contact or by exposure to infectious aerosol. The virus enters the new host by the nasal or oral route and promptly starts replication in the lymphoid tissues (Martella et al., 2008). Eight to 9 days after infection, CDV spreads by cell-associated viraemia to the epithelial cells in most organs and CNS tissue. Transient fever, loss of appetite, lethargy, ocular and nasal discharge and tonsillitis may be observed. At this stage, the outcome of the infection and the severity of the clinical signs vary markedly depending on strain virulence, environmental conditions and the dog’s age and immune status. If the dog develops a strong immune response, the virus is cleared from most tissues and the animal shows no clinical signs of infection. If the immune response is intermediate by day 9 to 14 post-infection, the virus is able to reach the epithelial tissues (resulting mainly in respiratory and gastrointestinal signs) and the CNS. The respiratory and gastrointestinal signs may resolve as antibody titre increases. However, CDV may persist for extended periods in the uvea, neurons, urothelium and in some cutaneous areas such as the foot pads. The CNS signs are generally delayed and hyperkeratosis is observed in some dogs. Dogs unable to mount an adequate immune response by day 9 to 14 post-infection undergo viral spread to many tissues, develop severe and rapidly progressive clinical signs and die.
Clinical signs
Several clinical syndromes associated with distemper have been recognized in dogs:
ACUTE DISTEMPER. Acute distemper occurs in susceptible young dogs unable to mount an adequate immune response. Respiratory and gastrointestinal signs predominate and are often exacerbated by secondary bacterial infections resulting in mucopurulent conjunctivitis, chorioretinitis, rhinitis, coughing, dyspnoea, pneumonia, diarrhoea and vomiting. Neurologic signs (mainly seizures) may occur later in the clinical course but dogs may die before these signs develop. Histological findings are consistent with a polioencephalomyelitis.
Table 5.3. Viral diseases of the CNS in dogs and cats (Lackay et al., 2008; Gunn-Moore and Reed, 2011; Lorenz et al., 2011; Addie, 2012; Bowen and Greene, 2012; Greene and Vandevelde, 2012; Greene et al., 2012; Henke and Vandevelde, 2012; Tipold and Vandevelde, 2012; Wensman et al., 2012).
Fig. 5.6. Mix-breed dog with pseudorabies. The dog is stuporous. Note the hypersalivation. The intense pruritus has caused cutaneous hyperemia and abrasions on the left side of the face.
CHRONIC DISTEMPER ENCEPHALOMYELITIS. Chronic distemper encephalomyelitis occurs in young dogs that survive the acute stages of the disease and in mature dogs without signs of systemic disease. Animals vaccinated against CDV may be affected. Enamel hypoplasia and hyperkeratosis of the foot pads and nose may be observed in dogs that survive subclinical or subacute infections. Neurological signs are commonly progressive and include obtundation, head tilt, nystagmus, ataxia (usually vestibular and/or cerebellar), paresis, constant repetitive myoclonus (constant repetitive sudden involuntary contractions, followed immediately by relaxation of a specific muscle group) involving head or appendicular muscles, and generalized or focal seizures. Constant repetitive myoclonus may persist while the animal is asleep. The so-called ‘chewing gum fits’ described in dogs with CDV are characterized by rhythmic biting movements of the mandible and may represent a form of focal seizures associated with temporal lobe polioencephalomalacia. Visual deficits can occur due to chorioretinitis and optic neuritis. Histo-logical findings are characterized by severe demyelinating meningoencephalomyelitis.
Lesions are most common in the cerebellum, cerebellar peduncles, cervical spinal cord, optic tracts and periventricular white matter.
OLD DOG ENCEPHALITIS. Old dog encephalitis is a rare form of CD that appears to be a manifestation of chronic viral infection after years of latent brain infection. There are no related systemic signs. The most common initial neurological sign is visual impairment. Other neurologic signs are progressive and include personality changes, obtundation, compulsive circling and head-pressing against objects. Histological findings are characterized by perivascular mononuclear cuffs, microglial proliferation, astrogliosis, neuronal degeneration and neuronophagia mostly within the cerebral cortex. Necrosis of cerebral grey matter may be observed.
Clinical signs may also be associated with combined infections (e.g. Toxoplasma gondii or Neospora caninum).