Abstract
Mesial temporal sclerosis is one of the most common pathologies seen in patients with
temporal lobe epilepsy. Complex partial seizures arise from the mesial (deepest) part
of the temporal region. This region includes the amygdala and the hippocampus. The
etiology of mesial temporal sclerosis is still uncertain and controversial. The most
popular mechanism implicated in this pathology involves glutamate, an amino acid whose
release results in excessive excitability. This model is documented both in animals
and in humans. The other mechanism describes neuronal death from seizure induced gene
expression and seizure induced energy metabolism deficits. There are many theories
linked to the development of this lesion. It is seen as a rare pathological finding
in children less than 10 years of age, but it is not uncommon in adolescence. Clinical
studies are suggestive of the occurrence of lesions in children with prolonged febrile
seizures. The other etiologies include perinatal ischemic insult, hypoglycemia, intrauterine
hypoxia, and status epilepticus resulting in hypoxia and edema in the hippocampus.
Magnetic resonance imaging is the modality of choice for the detection of the lesion,
which demonstrates scarring in the mesial temporal region. The coronal high-resolution
fluid-attenuated inversion recovery is known to be one of the best sequences, since
sensitivity is high to detect the hyperintensity and atrophy of the hippocampus. The
use of magnetic resonance imaging is crucial for the pre-surgical work up for epilepsy.
Specific surgical procedures including anterior temporal lobectomy tailored towards
resection of the mesial temporal lesion have a much higher rate of success in intractable
epilepsy patients. Seizure freedom is seen in 70–95% of patients undergoing resective
surgery as compared with 25% of medically treated cases.
Keywords Mesial temporal sclerosis - temporal lobe epilepsy - temporal lobectomy - MRI - EEG
