Page 809 - Problem-Based Feline Medicine

36 – THE CAT WITH SEIZURES, CIRCLING AND/OR CHANGED BEHAVIOR 801

● Seizures preceded by an aura (behavioral changes or months. A regressive course may occur with self-
a few seconds or minutes before the onset of ictus) limiting conditions. Other progressive (or regres-
or followed by localized post-ictal motor deficits sive) neurological signs and deficits, and abnormal
(e.g. hemiparesis) are partial, even if they appear to CSF and/or brain imaging findings reflecting an
be generalized from their onset. active disease process are also likely to be present.
● Idiopathic (genetic) epilepsy causes primary gener-
Other static neurological signs (e.g. personality
alized seizures that begin in young adult cats that have
changes) and/or thalamocortical deficits (e.g. menace,
no other neurological signs and deficits (see page
facial sensation, postural reactions) may or may not be
816).
present, depending on the size and location of the
● Intoxications typically cause an acute onset of severe
lesion.
convulsive status epilepticus or cluster seizures that is
usually preceded by signs of other body systems (e.g.
Diagnosis vomiting) as well as diffuse neurological signs (e.g.
mental depression, hyperexcitability, tremors). There
There may be a history of neurological signs a few to
are no periods of normalcy in between the seizures,
several months before the seizure onset (initial cerebral
which continue until appropriate treatment is provided
insult). These signs should have improved or resolved;
or until death occurs (see page 812).
if not, an active brain disease is likely.
● Metabolic causes produce a high initial seizure fre-
Neurological examination may be normal or reveal quency. Metabolic causes may be excluded when
thalamocortical deficits that are often subtle; the there are no other signs of metabolic disorders pre-
responses obtained from both sides of the body must be ceding and following the seizures (e.g. severe and
carefully compared. classical signs of hepatoencephalopathy, hypocal-
cemic tremors – tetany, hypoglycemic weakness and
CSF analysis is usually normal. Mild non-specific
confusion). They can also be excluded when there are
degenerative changes such as an increased proportion of
partial seizures or focal (unilateral, asymmetrical)
macrophages despite a normal leukocyte count may
neurological signs or deficits. Metabolic diseases, like
sometimes persist for months after the initial cerebral
intoxications, produce generalized seizures and bilat-
insult (e.g. trauma, ischemic encephalopathy).
eral and symmetrical neurological dysfunction.
Brain imaging may identify an inactive lesion; mag-
netic resonance imaging (MRI) is more sensitive than
Treatment
computed tomography.
Aggressive but rational anti-epileptic drug therapy is
In many cases with clinical evidence of likely sympto-
mandatory if there is more than one single seizure
matic epilepsy (e.g. partial seizures, non-progressive
every 6–8 weeks.
focal thalamocortical deficits), the underlying cause
● Start phenobarbital 1.5–2.5 mg/kg PO q 12 h.
remains unknown because the CSF analysis and brain
– Measure serum phenobarbital concentration 14
MRI are normal. Such epilepsy previously classified as
days after treatment initiation and after any
cryptogenic (hidden cause) is now called “likely symp-
dosage modification. Measure trough level, that
tomatic” epilepsy.
is, just prior to next treatment. Adjust the dosage
to obtain an optimal phenobarbital concentration
Differential diagnosis
of 100–130 μmol/ml (23–32 μg/ml) using the
Exclusion of other causes of seizures is often possible formula: optimal dosage = optimal phenobarbi-
based on the history and clinical examination, even tal concentration ÷ actual phenobarbital concen-
before any ancillary tests are performed. tration × actual dosage.
● Active brain diseases often cause a higher initial ● Add diazepam (0.5–1.0 mg/kg q 12 h) if seizures
seizure frequency, including cluster seizures and are not well controlled (if > 1 seizure/6–8 weeks)
status epilepticus, and a rapid progression toward despite an optimal phenobarbital concentrations 14
high-frequency seizures within the first few weeks days after treatment initiation or change in drug dose.