Cerebral lesion of Epilepsy MRI image give

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I now have all the information and image URLs needed. Let me compile a comprehensive answer with all the MRI images of cerebral lesions in epilepsy.

Cerebral Lesions in Epilepsy - MRI Findings

Source: Grainger & Allison's Diagnostic Radiology (Chapter 59 - Epilepsy Imaging)

Overview

MRI is the gold standard for identifying structural brain lesions in epilepsy, with ~85% sensitivity for lesion detection in intractable epilepsy. The main role of MRI is to identify an underlying brain abnormality, characterise the pathological substrate, and guide surgical planning.
Dedicated MRI Protocol for Epilepsy includes:
  • 3D T1 (1 mm isotropic)
  • T2/STIR axial + coronal (≤3 mm)
  • FLAIR axial + coronal (≤3 mm)
  • Haemosiderin/calcium-sensitive sequence (GRE/SWI)

Categories of Epileptogenic Cerebral Lesions

1. Malformations of Cortical Development (MCD)

Account for up to 50% of paediatric and 25% of young adult intractable epilepsy cases.

Focal Cortical Dysplasia (FCD) / Abnormal Gyration

MRI shows abnormal cortex with:
  • Thickened cortex or abnormal gyri
  • Faint cortical T2 hyperintensity
  • Blurring of grey-white matter differentiation
  • Abnormal sulci
Fig. 59.11 - Focal Cortical Dysplasia (right sylvian fissure/insula):
MRI showing abnormal cortex with abnormal gyri around the right sylvian fissure, with faint cortical T2 hyperintensity and blurring of grey-white matter differentiation in the right insula

Band Heterotopia

Neurons in abnormal locations (subcortical band of grey matter). Mild form of lissencephaly. Shows same signal as cortical grey matter on all sequences.
Fig. 59.12 - Band Heterotopia (bilateral cerebral hemispheres):
MRI with axial and coronal T1, axial FLAIR, and coronal T2 images showing band-like appearances of grey matter signal within the white matter of both cerebral hemispheres

2. Tuberous Sclerosis Complex

~90% of patients develop seizures; 25-30% develop intractable epilepsy.
MRI findings:
  • Cortical/subcortical tubers - hyperintense on T2/FLAIR
  • Subependymal nodules on lateral ventricular walls
  • Subependymal giant cell astrocytomas (can cause hydrocephalus)
  • White matter radial migration lines
Fig. 59.13 - Tuberous Sclerosis:
Axial FLAIR MRI images showing hyperintense cortical-subcortical tubers in both cerebral hemispheres, subependymal tumour at the foramen of Monro, and radial migration lines in the white matter

3. Sturge-Weber Syndrome (Vascular/Neurocutaneous)

Facial port-wine stain + ipsilateral meningeal angiomatosis. Clinically: intractable seizures, hemiparesis, hemianopsia.
MRI findings:
  • Pial angiomas (predominantly hypointense) in parieto-occipital regions
  • Cortical calcifications on T2*/GRE
  • Ipsilateral cerebral hemisphere atrophy
  • Enlarged choroid plexus
Fig. 59.14 - Sturge-Weber Syndrome:
MRI showing a predominantly hypointense pial angioma in the right cerebral hemisphere with smaller hemisphere volume; T2* gradient-echo images showing signal change from pial angiomata

4. Hippocampal Sclerosis

The most common abnormality in temporal lobe resections for intractable epilepsy. Pathology: neuronal loss + gliosis. MRI identifies up to 90% of cases.
MRI findings:
  • Hippocampal volume loss (best seen on coronal T1)
  • Increased T2/FLAIR signal in the small hippocampus
  • Loss of internal hippocampal architecture
  • Atrophy of ipsilateral mammillary body and fornix
  • Dilatation of adjacent temporal horn
Surgery is curative in up to 70% of patients.
Fig. 59.15 - Hippocampal Sclerosis (right):
Coronal MRI images showing loss of volume of the right hippocampus on high-resolution T1-weighted images and increased T2 signal on coronal FLAIR images, reflecting neuronal loss and gliosis

5. Tumours (Epilepsy-Associated Neoplasms)

Found in ~4% of epilepsy patients; ~70% are in the temporal lobe.
Common types: Low-grade astrocytoma, Ganglioglioma, DNET, Oligodendroglioma, Pleomorphic xanthoastrocytoma

DNET (Dysembryoplastic Neuroepithelial Tumour)

  • Cortically based, multicystic, low-grade
  • Occurs in children/young adults
  • T1: heterogeneously hypointense with cystic component
  • T2: heterogeneously hyperintense
  • No contrast enhancement (in most cases)
Fig. 59.16 - DNET in left medial temporal lobe:
Three axial MRI brain scans showing a DNET in the left medial temporal lobe involving the hippocampus: T1 hypointense with cystic component, no contrast enhancement, and heterogeneous T2 hyperintensity

fMRI for Surgical Planning (Tumour-Related Epilepsy)

Fig. 59.17 - fMRI Motor Mapping (tumour adjacent to motor cortex):
fMRI using a motor task showing primary motor cortex of both cerebral hemispheres, with a right hemisphere tumour lying posterior and adjacent to the right-sided primary motor area

6. Post-Traumatic Epilepsy

Head injury leaves haemosiderin deposits and gliosis (especially in frontal and temporal lobes), which are epileptogenic. MRI (SWI/GRE) is best for detecting haemosiderin.
Fig. 59.18 - Post-Traumatic Epilepsy:
Axial MRI images of a patient with post-traumatic epilepsy showing haemosiderin deposits or gliosis in the frontal/temporal regions

Summary Table

Lesion TypeKey MRI FindingsEpilepsy Prevalence
Focal Cortical DysplasiaThick cortex, blurred GM-WM junction, T2 hyperintensityUp to 50% pediatric intractable
Band HeterotopiaSubcortical grey matter bands, same signal as cortexLess common; often drug-resistant
Tuberous SclerosisTubers (T2/FLAIR bright), subependymal nodules, migration lines~90% have seizures
Sturge-WeberPial angioma (hypointense), cortical calcification, hemisphere atrophyIntractable in most
Hippocampal SclerosisVolume loss + T2 signal ↑ on coronal FLAIRMost common temporal lobe epilepsy lesion
DNETCortical cystic mass, T2 bright, no enhancementLow-grade, young adults
Post-traumatic gliosisHaemosiderin (SWI dark), gliosis (T2 bright)Depends on injury severity
  • Grainger & Allison's Diagnostic Radiology, Chapter 59 (Epilepsy Imaging), pp. 1494-1497
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