1. Radiological imaging of epilepsy.
DR/ ABD ALLAH NAZEER. MD.

2. Epilepsyis a chronic neurological disorder characterized by
spontaneous and recurrent seizures due to excessive and
abnormal electrical activity of cortical neurons. It affects about
1% of population.
Epilepsy diagnosis is purely clinical but neuroimaging,
especially structural magnetic resonance (MR), plays a key role
to rule out (and characterize) anatomic abnormalities and for
treatment planning.
Seizures are divided into generalized and partial. Generalized
seizures usually originate in both cerebral hemispheres and
most of them have a good response to antiepileptic drugs.
Partial seizures (focal) most likely originate in one anatomical
region and are classified as simple (when there is no loss of
consciousness) and complex (when loss of consciousness is
associated).

10. The role of CT in the assessment of epilepsy has considerably
diminished and is viewed as supplementary or supportive.
CT can be used as an initial screening method for excluding a brain
neoplasm as a cause for seizure activity, but usually MRI is more
appropriate in addition to avoiding irradiation.
CT is ideal for identifying the presence and extent of intracranial
calcification, but this has a limited impact on patient management.
CT is not as sensitive as MRI at identifying small lesions and more
subtle structural changes such as those involving the temporal
lobe and focal cerebral dysplasia.
There is also a role in the acute phase of status epilepticus, when
cerebral edema secondary to hypoxia or anoxia is suspected.
C.T

11. Hippocampal sclerosis (mesial temporal sclerosis).
Mesial temporal sclerosis is the most common epileptogenic
abnormality found after surgery in several series of epilepsy (65%)
and the most important cause of refractory epilepsy.
The most important MRI findings in hippocampal sclerosis are
atrophy and increased signal intensity in long TR sequences . There
are also other findings that we should look for because, although
they are less important, they can help us to support the diagnosis.
These findings are: the loss of the internal hippocampus
architecture (which is best viewed with 3T machines), fornix and
ipsilateral mammillary body atrophy (usually long-standing cases),
ipsilateral temporal horn dilation, decreased of para-hippocampal
white matter and reduced temporal lobe volume. In 8-20% cases of
hippocampal sclerosis, dual pathology will be found, i.e.
hippocampal sclerosis associated to other epileptogenic lesion,
which is usually located outside the hippocampus.

12. Lesions most commonly associated are cortical
development abnormalities, but tumours, post-
traumatic gliosis or infectious residual lesions can
be found. In up to 65% of cases of hippocampal
sclerosis, white matter of the temporal pole has a
subtle signal alteration (hyperintensity signal on
FLAIR images) sometimes with gray-white matter
junction blurred. It is important to identify these
structural alterations that may be associated with
hippocampal sclerosis because lesionectomy and
hipocampectomía (when possible) have a greater
benefit in seizure control.

13. Hippocampal sclerosis are atrophy and increased signal intensity.

15. Left hippocampal sclerosis.

17. Right hippocampal sclerosis with right temporal cortical dysplasia.

18. Malformations of cortical development (MCD)
Second cause of anatomic abnormality found in surgical series of
patients with chronic epilepsy. MCD are particularly common
when the beginning of the crisis occurs in childhood. They occur as
a result of defects in the different phases of cortical development:
1. Proliferation / Apoptosis of neuroblasts from the germinal
matrix.
2. Migration (radial, tangential).
3. Organization of the cortex in sheets with neural network and
synapses formation.
About 15% of patients with MCD have seizures refractory to
medical treatment and surgery may be the definitive treatment. In
the case of diffuse alterations, surgical treatment is ineffective,
contrary to focal lesions. In general, the degree of damage is
related to the extension of the malformation.
Barcovich classification of MCD provides four groups depending on
the stage of development predominantly affected:

20. Malformations of cortical development (MCD)

21. GROUP I (malformations due to abnormal proliferation or apoptosis).
- MICROCEPHALY.
It may be primary (genetic) or secondary.
- HEMIMEGALOENCEPHALY (HE).
FOCAL CORTICAL DYSPLASIA (FCD) TYPE II. It associated with
subtle focal changes which sometimes apparent microscopically. Seizures
with type 11 FCD is high. Type1 FCD may or not present with epilepsy.
- TUBEROUS SCLEROSIS.
AD inherited disorder with classic clinical triad: facial
angiofibromas, mental retardation
and refractory seizures. Underlying pathogenetic: cortical tubers,
subependymal nodules and subependymal giant cell astrocytomas.
- TUMORS.
Ganglioglioma. Desmoplastic infantile ganglioglioma.
Gangliocytoma.
Disembrioplastic neuroepithelial tumour.

22. Extreme Microcephaly, Diffuse Agyria, Agenesis of Corpus Callosum,
Cerebellar Hypoplasia with Dandy-Walker Malformation:

23. Hemimegalencephaly with enlarged, dysmorphic LT. hemisphere, enlarged l
left lateral ventricle with heterotopia and abnormal white matter.

24. TUBEROUS SCLEROSIS.

25. TUBEROUS SCLEROSIS.

26. Ganglioglioma.

27. Gangliocytoma Associated with Focal Cortical Dysplasia

28. GROUP II (malformations due to abnormal neuronal
migration).
- LISSENCEPHALY.
MCD caused by the arrest of neuronal migration
developing cerebral cortical thickening
and smooth surface. Important overlap with band
heterotopy. In image, particularly MRI,
the cerebral hemispheres appear as "eight" or "hourglass"
Number of cortical sulci separated by broad gyres,
enlarged ventricles, truncated arborisation of the white
matter. In infants, on T2 weighted-images can
distinguish three layers:

30. LISSENCEPHALY.

31. HETEROTOPYS (HT).
Alteration / arrest migration of groups of neurons from the
periventricular germinal zone to the cortex, appearing as gray
substance anywhere outside the cortex, from the ventricles to the
meningeal coating, with size, morphology and location variable:
1. Periventricular / subependymal nodular HT (the most common). Uni
or multifocal asymmetric indentation.
2. Band HT ("double cortex"). Symmetric thick band of subcortical gray
matter.
3. Subcortical nodular HT.
• Isolated nodules. Thin surface cortex often.
• "Mass" of white matter that continues the cortex and the ventricular
surface.
4. Periventricular and subcortical HT associated.
CT and MRI show heterotopys similar to the cortex in density and signal
intensity respectively . The ipsilateral hemisphere is small and the
lateral ventricle is usually large due to underdevelopment of white
matter.

32. GROUP III (malformations due to abnormal cortical
organization)
- POLYMICROGYRIA.
MDC due to an anomaly in the late stages of neuronal
migration and cortical organization.
Convolutions formed are numerous, small, prominent and
irregular. T2-weighted MRI
has two patterns:
• <12 months: cortex with fine and small ripples, normal
thickness.
•> 18 months: thick and irregular cortex, increase of
Virchow-Robin spaces and variable cortical invagination.

33. HETEROTOPIA

34. Gray matter heterotopia.

35. Left peri-ventricular heterotopia.

37. LAMELLAR HETEROTOPIA.

38. Polymicrogyria:

41. - SCHIZENCEPHALY (E).
Alteration in cortical organization characterized by the presence of
clefts in the cerebral parenchyma, which extend from the cortical
surface to the ventricular system coating
with dysplastic gray matter. Often associated with polymicrogyria,
heterotopy and microcephaly. There are two types:
• E. "Closed lip": walls oppose one another, obliterating the
subarachnoid space. Irregular
gray matter cord extending from the cortical surface to the
ventricle.
• E. "Open-lip": CSF fills the cleft from the lateral ventricle to the
subarachnoid space.
At MRI gray matter coating can be more difficult to distinguish
from that in the "closed Lip”
The most common location is close to the pre and post-central
gyrus. More often is unilateral than bilateral. Venous
developmental anomalies are common in the cleft.

42. SCHIZENCEPHALY.

43. Schizencephaly “open-lip

44. FOCAL CORTICAL DYSPLASIA (FCD) TYPE I.
It is characterized by greater extension than the type II,
affects more than one lobe and associates loss of white
matter volume, without thickening or distortion the
cortical pattern. Juxtacortical white matter shows
discrete increase signal intensity especially in FLAIR and
effacement of the SG / SB union differentiation. These
findings are more difficult to detect than in type II FCD.
It is most commonly located in the temporal lobe and
may be associated with mesial sclerosis (dual
pathology). The surgical outcome is worse due to its
greatest extent and worse definition.

45. FCD Palmini type in the frontal lobe.

48. FCD at right parietal region.

49. Transmantle dysplasia compromising the right frontal cortex.

50. Neoplasms.
The neoplasms may also cause drug-resistant epilepsy. About 90% of
neoplasms that produce seizures will be located next to the cerebral cortex
and of these, 70% are located in the temporal lobes. They tend to be low-
grade neoplasm and slow growth usually without edema or mass effect
associated. They can produce thinning or remodeling adjacent calvarium.
Enhancement after intravenous contrast is common but may not be present.
Oligodendroglioma, ganglioglioma (neoplasm associated with
chronic epilepsy in children and young adults and that may be
associated with focal cortical dysplasia), DNET or pleomorphic
xanthoastrocytoma.
Hypothalamic hamartoma is another neoplasm that is typically
associated with gelastic epilepsy in childhood. It usually has similar
signal intensity to gray matter on all pulse sequences and typically
does not enhance after administration of intravenous contrast.
Epileptogenic hypothalamic hamartoma always affects the
mammillary bodies and also often the tuber cinereum .

51. Left temporal low-grade glioma.

52. Tuber cinereum hamartoma.

53. Oligodendroglioma.

54. Right fronto-temporal glioma.

55. Dysembryoplastic neuroepithelial tumour (DNET).

56. Vascular malformations (VM).
VM represent 5% of lesions found in series of patients
with chronic epilepsy. Mainly arteriovenous
malformations (AVMs) and cavernous malformations .
To explain the seizures that occur in patients with
AVMs two phenomena have been postulated:
1. Focal cerebral ischemia due to a steal phenomenon
due to arteriovenous shunt.
2. Gliosis and hemosiderin deposits in the parenchyma
due to subclinical bleeding.
The sensitivity of MRI in detection is nearly 100%.

57. Left temporal cavernous malformation.

58. Right parietal cavernoma.

59. Gliosis / Miscellaneous.
Gliosis is the end state of several injuries that can affect the central
nervous system, mainly: trauma, infection and stroke. The findings
are nonspecific at MRI although usually hyper-signal areas often are
present in long TR sequences, associated with loss of volume sings
(such as grooves widening and ventricular retraction) and
encephalomaly areas. Emphasize the stroke as most common cause
of epilepsy in the elderly.
There are many other diseases that can cause seizures.
-Parenchymal infectious processes (encephalitis, abscesses) with
or without meningeal involvement: may present with seizures.
- The Sturge-Weber syndrome or pial angiomatosis.
Rasmussen's encephalitis: Childhood typical chronic encephalitis
characterized by partial motor seizures and progressive cognitive and
neurological deterioration; in image is characterized by a progressive
unilateral cerebral cortical atrophy.

60. Left frontal gliosis.

61. Post-encephalitis with epilepsy.

63. Right frontal abscess.

64. Sturge Weber syndrome.