Mesial temporal sclerosis (MTS) is characterized by atrophy and neuronal loss in the hippocampus. It is the most common cause of temporal lobe epilepsy. Imaging findings include a shrunken hippocampus with hyperintensity on T2-weighted MRI. MTS most often presents with complex partial seizures in older children and young adults. Anteromedial temporal lobectomy is an effective treatment for reducing seizures in patients with drug-resistant temporal lobe epilepsy due to MTS.

1. Mesial temporal Sclerosis
Islah Raoof

2. Introduction
• Temporal lobe epilepsy (TLE) is the most common form of partial complex
epilepsy and can occur with or without mesial temporal sclerosis.
Terminology
• Mesial temporal sclerosis (MTS), also known as hippocampal sclerosis (HS) is
the most common overall localization-related form of epilepsy (32-41). Its most
common manifestation is complex partial seizures.

3. Etiology
• A variety of events such as trauma or infection may precipitate intractable
complex partial seizures (32-42). The end result is MTS.
• Although the precise pathophysiology of how and why MTS develops is
unclear, inflammatory processes or prolonged seizures with hippocampal
hypoxic-ischemic injury are considered the most likely candidates.

4. Pathology
• MTS is characterized grossly by atrophy of the hippocampus and adjacent
structures (32-41). The hippocampal body (85- 90%) is the most commonly
affected site, followed by the tail (60%) and head (50%). Approximately 15-
20% of cases are bilateral but usually asymmetric.
• The CA1 and CA4 areas are the most susceptible to hypoxic- ischemic
damage, but all regions of the hippocampus can be affected.
• Neuronal loss with chronic astrogliosis is the typical histologic finding.

5. Clinical Issues
Epidemiology
• Nearly 10% of all individuals experience a seizure in their lifetime.
• Two-thirds of these are nonrecurrent febrile/nonfebrile seizures. Peak prevalence is
bimodal (< 1 year and > 55 years of age). One-third of patients develop repeated
seizures ("epilepsy").
• Approximately 20% of patients with epilepsy have complex partial seizures. Of these,
35-50% are pharmacoresistant and are refractory to anticonvulsant therapy.
• Current estimates based on a USA population of 325 million indicate that as many as
143,000-191,000 patients suffer from drug-resistant HS-TLE.
• MTS is one of the most common types of localization-related epilepsy and accounts
for the majority of patients undergoing temporal lobectomy for seizure disorder.

6. Clinical Issues
Demographics, Presentation & Treatment options
• Demographics. MTS is a disease of older children and young adults. There is
no sex predominance.
• Presentation. Most patients with MTS present with complex partial seizures
lasting 1-2 minutes. Preceding "auras" with fear, anxiety, and associated
autonomic symptoms are common.
• Treatment Options. Anteromedial temporal lobectomy is the most common
treatment for MTS with drug-resistant TLE and is successful in reducing or
eliminating seizures in 70-90% of patients.

7. Imaging
MR Findings
• Imaging markers of MTS are found in 60-70% of patients with TLE.
• True coronal IR or 3D SPGR sequences show a shrunken hippocampus with
atrophy of the ipsilateral fornix and widening of the adjacent temporal horn
and/or choroid fissure (32-43).
• Abnormal T2/FLAIR hyperintensity with obscuration of the internal
hippocampal architecture is typical (32-42).
• MTS typically does not enhance following contrast administration.

8. Imaging
MR Findings
• DWI shows increased diffusivity on ADC and hyperintensity on DWI (T2 "shine-through"). The
spectroscopic hallmark of TLE is reduced NAA in the epileptogenic focus, presumably secondary
to neuronal loss.
• Cho and Cr are typically unchanged. In MTS, NAA is reduced—and not just in the hippocampus.
• Widespread alterations in extrahippocampal and even extratemporal regions can be
demonstrated in MTS.
• High- resolution DTI shows evidence of diffusion abnormalities of the ipsilateral fimbria-fornix,
parahippocampal WM bundle, and the uncinate fasciculus and is helpful in predicting
postoperative seizure outcome.
• Resting-state fMR demonstrates that the inferior cingulum bundle undergoes degeneration in
tandem with ipsilateral hippocampal volume loss.

9. Imaging
Nuclear Medicine Findings
• FDG PET is one of the most sensitive imaging procedures for diagnosing MTS.
• Temporal lobe hypometabolism is the typical finding (32-43).
• SPECT shows hyperperfusion in the epileptogenic zone during seizure activity;
hypoperfusion in the interictal period is common.
Angiography.
• In the past, most patients with intractable TLE who were candidates for temporal lobe
resection underwent a Wada test (intracarotid amobarbital test) to evaluate language
lateralization and assess risk for postoperative memory disorders.
• With new noninvasive techniques such as resting fMR mapping, the utilization of Wada
testing is declining precipitously. It is no longer used in many epilepsy centers.

12. Differential Diagnosis
• The major differential diagnosis of MTS is status epilepticus. Status epilepticus
can be subclinical and may cause transient gyral edema with T2/FLAIR
hyperintensity and/or enhancement in the affected cortex as well as the
hippocampus.
• A low-grade glioma (WHO grade II astrocytoma, oligodendroglioma, or
oligoastrocytoma) in the temporal lobe can cause drug-resistant TLE. Gliomas
are usually T2/FLAIR hyperintense and cause mass effect, not volume loss.
• Cortically based neoplasms associated with TLE include dysembryoplastic
neuroepithelial tumor (DNET).

13. • DNET typically is a well-demarcated, "bubbly" mass that is often associated
with adjacent cortical dysplasia.
• Cortical dysplasia is isointense with GM but frequently causes T2
hyperintensity in the underlying temporal lobe WM.
• Cystic-appearing lesions in the temporal lobe that are hyperintense on T2WI
include prominent perivascular spaces, hippocampal sulcus remnants, and
choroid fissure cysts. These "leave me alone" lesions all behave like CSF and
suppress on FLAIR.