Abstract
Hippocampal sclerosis is the commonest cause of drug-resistant epilepsy in adults,
and is associated with alterations to structures and networks beyond the hippocampus.
In addition to being a cause of epilepsy, the hippocampus is vulnerable to damage
from seizure activity. In particular, prolonged seizures (status epilepticus) can
result in hippocampal sclerosis. The hippocampus is also vulnerable to other insults
including traumatic brain injury, and inflammation. Hippocampal sclerosis can occur
in association with other brain lesions; the prevailing view is that it is probably
a secondary consequence. In such instances, successful surgical treatment usually
involves the resection of both the lesion and the involved hippocampus.
Experimental data have pointed to numerous neuroprotective strategies to prevent hippocampal
sclerosis. Initial neuroprotective strategies aimed at glutamate receptors may be
effective, but later, metabolic pathways, apoptosis, reactive oxygen species, and
inflammation are involved, perhaps necessitating the use of interventions aimed at
multiple targets.
Some of the therapies that we use to treat status epilepticus may neuroprotect. However,
prevention of neuronal death does not necessarily prevent the later development of
epilepsy or cognitive deficits. Perhaps, the most important intervention is the early,
aggressive treatment of seizure activity, and the prevention of prolonged seizures.
Keywords
hippocampal sclerosis - status epileptics - epilepsy - neuroprotection
