This document discusses imaging in medial temporal lobe epilepsy. It begins by explaining why MRI is important for detecting epileptogenic lesions in refractory cases. It then describes the anatomy of medial temporal lobe structures like the hippocampus and amygdala. The document discusses how hippocampal sclerosis appears on MRI, including features like gliosis, neuronal loss, and atrophy. It also covers other imaging modalities that can help lateralize the seizure focus, such as hippocampal volumetry, relaxometry, MRS, PET, and SPECT. In conclusion, MRI is the best way to diagnose mesial temporal sclerosis by identifying hippocampal hyperintensity and atrophy.

1. IMAGING IN MEDIAL TEMPORAL EPILEPSY
DR.SARATH MENON.R,MD(Med.),DNB(Med.),MNAMS
DM RESIDENT
DEPT.OF NEUROSCIENCES
AIMS,KOCHI

2. WHY WE NEED TO KNOW IMAGING IN MTE?
 In medically refractory epilepsies
 A Dedicated MRI protocol helps us to detect an
epileptogenic lesion in 80% cases.
 Resection of the lesion can lead to seizure freedom in
many such cases.

5. RADIOLOGICAL ANATOMY OF MEDIAL TEMPORAL
LOBE STRUCTURES
 Medial temporal lobe structures –
 amygdala
 hippocampus
 Surrounding hippocampal
region ( perirhinal, parahippocampal and entorhi
nal)

6. HIPPOCAMPUS
 Club-shaped structure divided into three parts: head, body,
and tail.
 In coronal plane form an S-shaped configuration.
 Consists of two interlocking C-shaped structures: the
cornu ammonis and the dentate gyrus.
 Gray matter of the hippocampus is an extension of the
subiculum of the parahippocampal gyrus.

12. Note head digitations, subiculum,
subsectors of Ammon’s horn,
dentate gyrus, alveus,
fimbria, stratum radiatum and
collateral white matter

13.  On MRI, the hippocampal head is seen in the same
coronal plane as the interpeduncular cistern
Coronal T2 at the level of the
interpeduncular
cistern showing the amygdala (large
square), uncal fissure (large dot),
hippocampal
head (small dot)

14.  The body of the hippocampus is seen at the level of
the midbrain (Fig. 7). It is ovoid in shape and is the
most uniform portion. It lies inferior to the choroidal
fissure and is separated from the parahippocampal
gyrus by the hippocampal fissure.
Coronal T2 WI at the level of the
midbrain,
demonstrating the ovoid hippocampal
body (small sqaure) under the
choroidal fissure
(circle).

15.  The tail of the hippocampus is located at or behind
the midbrain where it is seen adjacent to the crura
of the fornices
Coronal T2 WI just posterior to the
midbrain illustrating the fornix (line)
and hippocampal tail (square).

16. DEFINITION OF MTS
Mesial temporal sclerosis -coined by Falconer & colleagues –
by neuronal loss and gliosis involving principally the
hippocampus and amygdala, or both, but occasionally
extending to other mesial temporal structures or even
throughout the temporal lobe, and leading to generalized
atrophy and gliosis.

17.  Hippocampal sclerosis :
 Gliosis and neuronal loss that particularly affects the
CA1, and CA4 or Sommer’s sectors, the dentate
gyrus, and the subiculum.
 Ammon’s horn sclerosis
 abnormalities restricted to the areas CA1 and CA4.
 Amygdalar sclerosis

18.  HS is unilateral in about 80% of cases
 Most frequent lesional pattern :
 Ammon’s horn sclerosis in the CA1 and CA4 sections
 Less frequent patterns include widespread cell loss in the
hippocampus
 Severity of cell loss may vary but it is usually >50% in
association with gliosis

19. IMAGING IN MTE
 MRI is far superior to CT
 Use cuts oriented in two orthogonal planes along the long axis
of the body of the hippocampus and at a right angle to this
 Prevents from obtaining oblique images of the hippocampus,
which can be difficult to interpret due to partial volume effects.
 High resolution MRI (slice thickness 1.5 mm) is the method of
choice

20. MRI EPILEPSY PROTOCOL
T1WI
Superior for cortical thickness and the interface between grey and white
matter.
FLAIR
Look very carefully for cortical and subcortical hyperintensities on the FLAIR,
which can be very subtle.
T2* or SWI
Helpful when searching for haemoglobin breakdown products as in
posttraumatic changes and cavernomas, or to look for calcifications in tuberous
sclerosis, Sturge-Weber, cavernomas and gangliogliomas.

21. Imaging Sequence Utility
T1WI sagittal Images for the localisation of the
hippocampus
Coronal high-resolution T2
WI and FLAIR perpendicular
to hippocampal axis
(3 - 4 mm)
A spoiled gradient
recalled (SPGR) echo
sequence using 1.5 mm cuts
in the oblique coronal Plane .
Provides a high-resolution T1-
weighted volume
data set which can be
reformatted
in any plane,
can also be used to measure
hippocampal volumes
co-register functional data.

22.  Volumetric pulse sequences with reformatting of thin
sections
 Parallel and perpendicular to the long axis of the
hippocampi represent a valid tool.
 FIRMS:fast inversion recovery pulse sequence with
white matter signal suppression
 Since CSF artifacts are incompletely suppressed on
FLAIR

23. OTHER MODALITIES
 MR Hippocampal Volumetry
 MR Hippocampal T2 Relaxometry
 MRS
 SPECT
 PET

24. MRI IN MTE
MRI has the ability to detect subtle
alterations in cortical architecture &
changes in signal intensity
most sensitive and specific imaging
technique for non-invasive identification
of these epileptogenic foci

26. ATROPHY AND HIGH SIGNAL IN MTE
The coronal T2WI and FLAIR images show right-sided mesial temporal
sclerosis.
Notice the volume loss, which indicates atrophy and causes secondary
enlargement of the temporal horn of the lateral ventricle.
The high signal in the hippocamous reflects gliosis.

27. 35-year-old patient with refractory temporal lobe epilepsy.
MR shows subtle hyperintensity of the left hippocampus on the axial
FLAIR (blue arrow) and atrophy of the left hippocampus on coronal
images (yellow arrow).

28. Right sided
hippocampus
showing- Smaller
in size
Loss of internal
structure
Bright on T2

29. a Rotated coronal FSE T2-weighted image at hippocampal body.
b Reformatted coronal image after corrections of head rotation better shows
left hippocampal atrophy (arrow)

30. Left amygdalo-hippocampal sclerosis.
Coronal FLAIR (a) and axial FSE T2-weighted
(b) images show hyperintense
lesion involving the amygdala and head of
hippocampus on the left.

31. Bilateral hippocampal sclerosis. Axial
FLAIR (c) and oblique coronal FSE T2-
weighted (d) images show hyperintense
signal involving the head and body of both
hippocampi, more
evident on the right

32.  Atrophy of the ipsilateral fornix and mamillary body
 Increased signal and or atrophy of the anterior thalamic nucleus
 Atrophy of the cingulate gyrus
 Increased signal and / or reduction in volume of the amygdala
 Reduction in volume of the subiculum
 Dilatation of temporal horn and temporal lobe atrophy

33.  Collateral white matter and entorhinal cortex atrophy
 Thalamic and caudate atrophy
 Ipsilateral cerebral hypertrophy
 Contralateral cerebellar hemiatrophy
 Loss of grey-white matter interface in the anterior
temporal lobe
 Reduced white matter volume in the parahippocampal
gyrus

34. HIPPOCAMPAL ATROPHY WITH DILATED TEMPORAL HORN
Fig. 1. Coronal FLAIR demonstrating atrophy of the right hippocampal
head with dilatation of the temporal horn.

35. LOSS OF GREY WHITE DIFFERENTIATION
Coronal T1WI displaying
loss of grey white matter
differentiation in the region
of the right hippocampal
head.

36. HIPPOCAMPAL AND FORNIX ATROPHY
Coronal FLAIR sequences exhibiting atrophy of the right
hippocampal body and tail as well as the right
fornix.

37. Oblique coronal FSE T2-weighted image
shows digitation loss in the hippocampal
head (arrow).
b Left hippocampal sclerosis. Oblique
coronal FSE T2-weighted image shows
atrophy of ipsilateral mammillary body
(arrow).

38. c Right hippocampal sclerosis.
Oblique coronal FSE T2-
weighted image shows thinning
of ipsilateral posterior fornix
(arrow).
Left hippocampal sclerosis.
Oblique coronal inversion recovery
images. Note enlargement of
ipsilateral ventricular temporal
horn (asterisk, d),
small ipsilateral mammillary
body (arrow, d), and
narrowed collateral white matter
on the left, consistent
with atrophy of the hippocampus
without apparent signal
abnormality.

39. SIGNIFICANCE OF SECONDARY FEATURES
 Important findings related to pathophysiology,diagnosis
and prognosis
 One should think about mesial temporal sclerosis as a
process involving diffuse regions of the brain rather than
as one limited to the hippocampus.
 Lateralization of mesial temporal sclerosis.
 Inpatients with subtle primary findings of unilateral
mesial temporal sclerosis, these secondary imaging
features help improve diagnostic confidence
 In bilateral hippocampal abnormalities, secondary
findings can determine the more important side to resect.

40. THE ATROPHIC-GLIOTIC CHANGES CAN
INVOLVE
 part of the hippocampal formation
 patchy areas, and
 extend to the temporal neocortex
 Structures outside the temporal lobe
 insula; frontobasal and opercular cortex, a lesion termed pararhinal sclerosis
 Atrophy of the whole ipsilateral temporal lobe
 Hippocampal sclerosis can be bilateral

42. D/D OF HIPPOCAMPAL HYPERINTENSITY
Hippocampal hyperintensity on T2WI or FLAIR images with volume loss is
diagnostic for mesial temporal sclerosis in the appropriate clinical setting.
Hippocampal hyperintensity without volume loss is seen in:
Status epilepticus
Low grade tumors (astrocytoma, DNET)
Encephalitis

43. STATUS EPILEPTICUS
In status epilepticus a hyperintense hippocampus can be seen, but there is swelling
and no atrophy.
Axial FLAIR, axial DWI and coronal T2WI demonstrate a hyperintense
hippocampus with a slightly compressed temporal horn of the lateral ventricle
consistent with hippocampal edema.
DWI shows diffusion restriction due to cytotoxic edema in the acute stage of the
status epilepticus.

44. DNET
NET mimicking mesial temporal sclerosis
Axial T2WI shows hyperintense, but enlarged hippocampus with a bubbly
appearance.
This is typical for a DNET or dysembryoplastic neuroepithelial tumor,
The coronal contrast-enhanced T1WI shows an enlarged hippocampus without
uptake of contrast medium.

45. HIPPOCAMPAL VOLUMETRY
 Requires side-to-side ratios & absolute volumes corrected for
intracranial volume, which must be compared with appropriated age-
matched controls from the same laboratory
Limitations
 Time-consuming.
 Relies on subjective definition of the hippocampal boundaries
 May fail to detect bilateral changes [201].
 May be normal in a small subgroup of patients with abnormal signal
in one hippocampus as determined by preoperative MRI and
pathologically proven HS

46.  Normally, both hippocampi are of equal volume
 with a slight prevalence of the right side
 Any asymmetry greater than 0.3 cm is abnormal
 Volumetry can detect up to 90% of cases of HS compared to
about 80% by visual assessment

47. T2 RELAXOMETRY
 Quantitative MRI may be also used to detect
hippocampal Gliosis
 Actual quantitative measurements of T2 relaxation time
through the hippocampal body may permit the
recognition of unilateral or bilateral involvement in
patients with apparently normal MRI scans obtained
by classical techniques

48.  As a result of neuronal loss, the extra cellular space is
enlarged and thus diffusion of water molecules is greater
on the affected side, resulting in increased values on
the affected side (higher signal on ADC).
 Conversely, due to neuronal dysfunction and swelling,
diffusion is restricted following a seizure, and thus
values are lower.

49. DTI
 Diffusion tensor imaging may reveal focal temporal
anisotropy in patients with temporal lobe epilepsy

50.  The NAA decline has been considered to reflect neuronal loss
 Patients with TLE have reduced NAA in the ipsilateral
hippocampus compared with NAA in the contralateral side
lateralizing the seizure focus in TLE.
 Myo-Inositol is found primarily in astrocytes.
 Elevation of myoinositol would be expected in areas of
astroglial cell proliferation
 Decreased NAA / Cho and NAA / Cr ratios
 Increased lipid and lactate soon after the seizure

51. PET SCAN IN MTE
 Inter ictal period metabolism in the region of seizure
focus decreases compared to normal brain regions.
 Intra ictal period the seizure focus usually shows
abnormally increased metabolism, which can also help
identify the location of seizure activity.
 PET imaging for epilepsy is usually used as a tool for
possible surgical candidates.

52.  PET is of great assistance in lateralizing the seizure
focus in patients with temporal lobe epilepsy and a
normal MRI
 Bilateral temporal hypometabolism suggests bilateral
temporal pathology and possibly a poorer prognosis
following temporal lobe surgery

53. Coronal interictal MR/FDG-PET fusion image shows hypometabolic
activity in the right temporal pole (arrow).

54. SPECT
 If the radiotracer is injected ictally, focally increased
uptake is identified in the affected temporal lobe (hot
focus).
 Interictally, the affected temporal lobe demonstrates
decreased uptake compared with that of the rest of
the brain (cold focus).
 Interictal SPECT studies may include a number of false
positive and negative results, because the precise time
course of the perfusion abnormalities is unknown.

55.  Ictal SPECT is extremely helpful in the presurgical
evaluation of temporal lobe epilepsy in selected
patients, especially those in whom ictal EEG data
is inconclusive.
 Interictal SPECT provides useful baseline
information for assessing ictal studies, while in
isolation is of minimal value

56. CONCLUSIONS
 MRI is the radiological investigation of choice for
diagnosing MTS.
 Familiarity with the regional medial temporal lobe
anatomy is important for correct MRI
interpretation.
 Coronal high-resolution FLAIR is the best
sequence to diagnose MTS, where
hyperintensity and atrophy of the hippocampus
are the most sensitive signs.

57. THANK YOU