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definitions of non-convulsive status epilepticus should include: unequivocal electrographic
seizure activity; periodic epileptiform discharges or rhythmic discharge with clinical seizure
activity; and rhythmic discharge with either clinical or electrographic response to treatment.
There is uncertainty about the relevance of periodic lateralised epileptiform discharges
(PLEDs). This is most notable following severe encephalitis or hypoxic injury in which
discharges can occur with such periodicity so as to be confused with periodic discharges seen
following prolonged status epilepticus. Some have argued that such discharges represent
ongoing seizure activity, and should be treated thus. The general consensus, however, is that
a multitude of aetiologies can underlie PLEDs, and that they should only be treated as
epileptic if there is other evidence of ictal activity.

Neuronal damage and non-convulsive status epilepticus

It has long been recognised that ongoing electrographic seizure activity can result in neuronal
damage, so-called excitotoxic neuronal damage. This damage occurs in animal models of
non-convulsive status epilepticus. These animal models, however, involve the induction of
status epilepticus in non-epileptic animals with either powerful chemoconvulsants or
prolonged high frequency repetitive stimulation. This is very different from the human
situation. Furthermore, non-convulsive status epilepticus in humans tends to have lower
frequency discharges, which if reproduced in animal models produces substantially less
neuronal damage.

Another important finding has been that epileptic animals, animals pretreated with
antiepileptic drugs (AEDs) and young animals are all resistant to chemoconvulsant induced
neuronal damage. Thus young age, AEDs and prior history of epilepsy probably all confer
some degree of neuroprotection. Lastly, in humans non-convulsive status epilepticus often
results from an acute precipitant such as an encephalitis and, in such circumstances, the status
epilepticus only minimally contributes to any resultant pathology.

There have been reports of prolonged memory problems, hemiparesis and death occurring
following complex partial status epilepticus although, in most of these cases, the outcome
relates to the underlying aetiology. Indeed, the degree to which non-convulsive status
epilepticus contributes to neuronal damage in humans is unclear. Since aggressive treatment
is not entirely benign, and can lead to hypotension and respiratory arrest, then the best
approach to treatment will only be determined in randomised studies of aggressive versus
more conservative management.

Specific forms of non-convulsive status epilepticus

Typical absence status epilepticus
This entity needs to be distinguished from complex partial status epilepticus and atypical
absences seen in mental retardation. This term should perhaps be reserved for prolonged
absence attacks with continuous or discontinuous 3 Hz spike and wave occurring in patients
with primary generalised epilepsy. The EEG, however, may also include irregular spike and
wave, prolonged bursts of spike activity, sharp wave or polyspike and wave.

Although absence epilepsy has its peak in childhood and commonly remits in adolescence,
absence status epilepticus commonly occurs in later life. Absence status epilepticus can be
divided into childhood absence status epilepticus (those usually already receiving treatment),
late-onset absence status epilepticus with a history of primary generalised seizure (often a
history of absences in childhood) and late-onset absence status epilepticus developing de
novo (usually following drug or alcohol withdrawal).