Role of MRI in Epilepsy
Laurens De Cocker, Felice D’Arco and Philippe Demaerel and Robin Smithuis
Publicationdate September 1, 2012
In many patients with epilepsy antiepileptic drug treatment is unable to control the seizures.
Using a dedicated MRI-protocol, it is possible to detect an epileptogenic lesion in 80 percent of these patients.
Resection of these lesions can lead to seizure freedom in many patients.
We will discuss the MRI protocol and the typical findings in the most common epilepsy-associated diseases.
Common causes of Epilepsy
The illustration summarizes the most common causes of seizures in patients with medically uncontrollable epilepsy.
Some of these lesions are readily identifiable.
Meso temporal sclerosis and focal cortical dysplasia are the most common causes and can only be depicted with a dedicated protocol.
The table also summarizes epileptogenic lesions that are detected in patients with uncontrollable seizures.
Mesial temporal sclerosis is the most common cause of intractable epilepsy.
In medication refractory epilepsia the most common location of the epilectogenic lesion is temporal lobe (60%), frontal lobe (20%) and parietal lobe (10%), periventricular (5%) and occipital (5%).
Seizures and Epilepsy
Seizures are common. About 4 percent of all people will have at least one seizure during their lifetime.
In patients with a first ever seizure imaging will mostly show no brain-abnormalities, because the seizure is provoked by fever, drugs, dehydration or sleep deprivation.
The term epilepsy is used, when there are recurrent unprovoked seizures.
About 60 percent of patients with epilepsy can be controlled with antiepileptic drugs.
Most patients with uncontrollable seizures have complex partial seizures.
Partial seizures – also called focal seizures – are seizures which affect only a part of the brain at onset. They usually start in the temporal lobe.
In simple partial seizures the person remains conscious.
A simple partial seizure can be a precursor to a larger seizure and then it is called an aura .
A complex partial seizure affects a larger part of the hemisphere and the person may lose consciousness.
If a partial seizure spreads from one hemisphere to the other this will give rise to a secondarily generalised seizure.
The person will become unconscious and may have a tonic clonic seizure.
MRI epilepsy protocol
The table shows a dedicated epilepsy protocol.
Some will also use Inversion Recovery and not use contrast on a routine base.
Superior for cortical thickness and the interface between grey and white matter.
On T1WI look for grey matter occuring in an aberrant location as in gray matter heterotopia.
Look very carefully for cortical and subcortical hyperintensities on the FLAIR, which can be very subtle.
Since FLAIR may show false-positive results due to artefacts, the abnormalities should be confirmed on T2WI.
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.
Mesial temporal sclerosis
Mesial temporal sclerosis (MTS) is a specific pattern of hippocampal neuronal loss accompanied by gliosis and atrophy.
The etiology is unknown, but there is a relationship between MTS and prolonged febrile seizures earlier in life, complicated delivery and developmental processes.
In 15% of patients another developmetal abnormality can be found, mostly focal cortical dysplasia.
This is called dual pathology.
MTS is the most common cause of partial complex epilepsy in adults and is also the most common etiology in young adult patients undergoing surgery.
Surgical removal of visible MRI changes associated with unilateral mesial temporal sclerosis leads to seizure freedom in up to 80% of cases.
Coronal T2W and FLAIR images are the most sensitive for detecting MTS.
On axial slices mesial temporal sclerosis is commonly overlooked.
Bilateral mesial temporal sclerosis is difficult to detect due to the lack of comparison with the unaffected contralateral hippocampus.
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.
Mesial temporal sclerosis may occur in association with other pathology, especially focal cortical dysplasia.
This is called dual pathology .
The images show mesial temporal sclerosis with a hyperintense and shrunken hippocampus (red arrows), and secondary enlargement of the left temporal horn of the left laterale ventricle.
Also notice associated subcortical hyperintensity in the left temporal lobe indicating focal cortical dysplasia.
Left mesial temporal sclerosis. Subtle gliosis of left hippocampus (blue arrow) and atrophy (yellow arrow).
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).
The patient was succesfully treated with amygdalo-hippocampectomy on the left.
Differential 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)
The imaging findings in status epilepticus can mimick mesotemporal sclerosis.
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.
DNET 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, which we will discuss in a moment.
The coronal contrast-enhanced T1WI shows an enlarged hippocampus without uptake of contrast medium.
Focal Cortical Dysplasia
- Subcortical white matter hyperintensities
- Blurred grey-white matter interface
Focal cortical dysplasia is a congenital abnormality where the neurons fail to migrate in the proper formation in utero.
MRI findings may be very subtle or may even be negative, therefore a high index of suspicion is mandatory!
The most common findings are cortical or subcortical hyperintensities especially seen on FLAIR-images.
These are often found at the bottom of a deep sulcus.
Another finding is a blurred interface between grey and white matter, because the white matter looks a little bit like gray matter because it contains neurons that did not reach the cortex.
The images show typical focal cortical dysplasia.
There is cortical thickening and blurring of the grey/white matter junction on T1WI (left).
The FLAIR image on the right shows the subcortical hyperintensity.
The images demonstrate cortical and subcortical signal abnormalities on T2WI and FLAIR in the left temporal lobe indicating focal cortical dysplasia.
Notice associated T2/FLAIR hyperintense and shrunken hippocampus as a result of mesial temporal sclerosis, i.e. dual pathology.
Another case of focal cortical dysplasia.
Notice the hypoplastic left temporal lobe with cortical thickening (arrow) and atrophy of the white matter.
Axial T1WI, T2WI and FLAIR-images of a 15 year old boy with epilepsy.
Notice thickening and hyperintensity of the cortex of the left superior frontal gyrus.
The FLAIR-images also show high signal in the subcortical white matter.
These findings are typical for focal cortical dysplasia.
Sometimes the hyperintensity is seen extending from the subcortical area to the margin of the ventricle.
This is called the transmantle sign.
This finding represents the arrested neuronal migration.
Images of a 27-year-old male with refractory occipital lobe epilepsy.
Coronal FLAIR and axial T2WI show T2-hyperintense cortical thickening and high signal in cortex and subcortical region.
Notice subcortical hyperintensity extending to the right ventricle indicating transmantle sign (blue arrow).
Transmantle sign seen in another patient with focal cortical dysplasia.
Cortical and glial scars – Ulegyria
54-year-old patient with a history of perinatal asphyxia and longstanding refractory partial epilepsia. Left parietal scar in the parasagittal watershed area resulting in a shrunken cortex.
Cortical and glial scars usually result from meningitis or birth injury.
Ulegyria is a specific type of scar.
It is defined as cerebral cortex scarring due to perinatal ischemia.
Ulegyria typically affects full term infants.
In these infants there is greater perfusion to the apex of the gyri than to the cortex at the depth of the sulci.
The resulting pattern is that of a shrunken cortex in which the deep portions of the gyri are more shrunken than the superficial portions, leaving pedunculated gyri on long stalks with a mushroom appearance.
Ulegyria must be differentiated from microgyria.
MR will shows tissue loss and gliosis underneath a shrunken cortex.
The shrunken cortex is best appreciated on a 3D-T1WI because of its high resolution and the superior delineation of the cortex, while FLAIR will show the hyperintensity associated with the gliosis.
Therefore always use the FLAIR-sequence to search for hyperintensities in an epileptic patient and subsequently correlate these findings with the cerebral cortex in the affected area on high resolution T1WI.
Cavernoma is also known as cavernous malformation or cavernous angioma.
It is a benign low flow vascular malformation with a tendency to bleed.
75 percent occur as solitary sporadic lesions and 10-30 percent occur as multiple lesions.
Cavernomas consist of locules of variable size that contain blood products in different stages of evolution which produces a popcorn appearance.
A complete hemosiderin rim surrounds the lesion, but not when there is a recent bleeding.
Unenhanced CT may show a hyperdense nodule or calcification, but in 50% of cases cavernomas will be occult on CT.
T2WI and T2* gradient echo show multiple cavernomas.
Notice the popcorn appearance with peripheral rim of hemosiderin on the T2WI.
The lesions are almost completely black on the gradient echo due to blooming artefacts.
T2* and susceptibility weighted imaging (SWI) markedly increase the sensitivity of MRI to detect small cavernomas.
The five black dots in the left cerebral hemisphere on the T2* are also cavernomas and are not visible on the T2WI.
Cavernomas are associated with developmental venous anomalies (DVA’s).
The unenhanced CT shows a small calcification in the right lentiform nucleus.
Enhanced CT shows a venous anomaly draining the cavernoma into the right internal cerebral vein.
Coronal T2WI shows the venous anomaly as a curvilinear flow void.
Cavernoma in the postcentral gyrus on T1WI, T2WI and SWI.
Notice popcorn appeance and blooming artefact.
Notice the hemosiderin coating of the precentral gyrus consistent with superficial siderosis due to prior hemorrhage of the cavernoma (red arrowheads).
Differential diagnosis of microbleeds
In patients with multiple small black dots the differential diagnosis is:
- Cerebral amyloid angiopathy (CAA)
Asymmetric microbleeds in peripheral location seen in normotensive older person with lobar hemorrhage. CAA is commonly seen in demented patients.
- Hypertensive microhemorrhages
Microbleeds in hypertensive patients younger than CAA ( Diffuse axonal injury (DAI)
Posttraumatic hemorrhages in corpus callosum, subcortical white matter and brainstem.
Diffuse axonal injury (DAI)
A 46 year old biker presented with seizures after being hit by a car.
CT-image shows only minimal subarachnoidal hemorrhage (arrow).
MRI was performed several weeks after the injury because of a change in personality.
T2*-images show multiple hemosiderin depositions at the interface between grey and white matter, consistent with diffuse axonal injury (DAI).
Notice that the location of the microbleeds is different from the peripheral located CAA-bleeds.
Epilepsy associated tumours
All brain tumors may present with epilepsy, but there are some typically epilepsy associated tumors.
These tumours share the following characteristics:
- They arise in a cortical location.
- Often located in the temporal lobe.
- Closely related to developmental malformations.
- Typically seen in adolescents and young adults.
- Characterized by a benign behaviour, a slow growth, a sharp delineation and usually show absence of edema.
- Show signs of chronicity, such as bone remodeling and scalloping of the adjacent skull.
Ganglioglioma in the right occipital lobe presenting as a cystic mass with rim enhancement. Notice calcification on CT.
- Typically presents as cyst with enhancing mural nodule, but may be entirely solid
- Calcification in up to 50%
Ganglioglioma is the most common tumor associated with temporal lobe epilepsy.
Calcification is common in ganglioglioma and is an important distinguishing factor from DNET and pleomorphic xanthoastrocytoma.
Ganglioglioma in a young child. Note large cyst with enhancement of mural solid tissue.
Schizencephaly is a cleft in the brain that connects the lateral ventricle to the subarachnoid space.
The cleft is lined by polymicrogyric gray matter.
Open-lip schizencephaly is characterized by separation of the cleft walls.
Closed-lip schizencephaly is characterized by cleft walls in apposition to each other.
Patients have seizures and hemiparesis, which is proportional to the size of the cleft and are more common in the open-lip type.
First study the images and then continue reading.
This patient has a bilateral schizencephaly.
There is an open-lip type on the right and a closed-lip type on the left (red arrow).
Notice the track of grey matter in the left hemisphere on the axial image.
The differential diagnosis of schizencaphaly is porencephaly, which is also a cleft, but it is not lined by grey matter.
by Abdel Razek AA et al.
AJNR. 2009 Jan;30(1):4-11
by Barkovich J et al.
by Barkovich AJ.
Neuroradiology 2010 52:479-487
by Bien CG, et al
Brain 2002; 125:1751-1759.
by Bien CG et al
Brain 128(pt 3):454-71,2005
by Chiapparini L, et al
Neuroradiology 2003; 45:171-183.
by Chinchure S et al
Neurol India 2010 May-Jun,58(3):361-70
by Demaerel P
JBR-BTR 2008 Nov-Dec;91(6):254-7
by Flores-Sarnat L
J Child Neurol 2002; 17:373-384
by Hanefeld F, Kruse B, Holzbach U, Christen HJ, Merboldt KD, Hanicke W, Frahm J. J Magn Reson Imaging 2008 aug,28(2):300-7
by Kim SJ et al.
Pediatr Neurol 27(4):282-8,2002
by Maria BL, et al
J Child Neurol 1998; 13:606-618.
by Martin N, et al
Neuroradiology 1990; 31:492-497
by Montenegro MA et al
Arch Neurol 2002; 59:1147-1153
by Radhakrishnqn R et al
Journ Clin Imag Sci 2011; 1(2):1-11
by Urbach H et al
JNR 2004 Jun-Jul;25(6):916-26
by Tortori-Donati P, Rossi A
by Woermann FG, Vollmar C
Epilepsy Behav 2009 May;15(1):40-9