Journal of Pediatric Neurosciences
: 2011  |  Volume : 6  |  Issue : 1  |  Page : 19--26

Neuroimaging in epilepsy

Shahina Bano1, Sachchida Nand Yadav2, Vikas Chaudhary3, Umesh Chandra Garga2,  
1 Department of Radiodiagnosis, Govind Ballabh Pant Hospital & Maulana Azad Medical College, New Delhi, India
2 Department of Radiodiagnosis, Dr. Ram Manohar Lohia Hospital and PGIMER, New Delhi, India
3 Department of Radiodiagnosis, Employees' State Insurance Corporation (ESIC) Model Hospital, Gurgaon, Haryana, India

Correspondence Address:
Shahina Bano
Room No: 603, Doctor«SQ»s Hostel, Govind Ballabh Pant Hospital, New Delhi - 110 002


Epilepsy is the most common neurological disease worldwide and is second only to stroke in causing neurological morbidity. Neuroimaging plays a very important role in the diagnosis and treatment of patients with epilepsy. This review article highlights the specific role of various imaging modalities in patients with epilepsy, and their practical applications in the management of epileptic patients.

How to cite this article:
Bano S, Yadav SN, Chaudhary V, Garga UC. Neuroimaging in epilepsy.J Pediatr Neurosci 2011;6:19-26

How to cite this URL:
Bano S, Yadav SN, Chaudhary V, Garga UC. Neuroimaging in epilepsy. J Pediatr Neurosci [serial online] 2011 [cited 2019 Nov 18 ];6:19-26
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A seizure is defined as a paroxysmal alteration in neurologic function due to excessive electrical discharge from the central nervous system. Epilepsy is defined as a condition of recurrent seizures, and medical intractability as recurrent seizures despite optimal treatment under the direction of an experienced neurologist over a 2-3-year period. Determining the underlying cause of a patient's seizure is the fundamental goal in the workup of epilepsy. Imaging of the brain provides valuable information in this regard. The main purposes of neuroimaging in epilepsy patients are to identify underlying structural or metabolic abnormalities that require specific treatment and to aid in formulating a syndromic or etiological diagnosis. Neuroimaging is even more important for those patients who have medically intractable seizures. Advances in technology to localize epileptogenic focus, especially with high resolution magnetic resonance imaging (MRI), have substantially improved the success of surgical treatment.

Structural disorders associated with seizure and detected on imaging can be categorized into the following groups [Figure 1],[Figure 2],[Figure 3],[Figure 4],[Figure 5],[Figure 6],[Figure 7],[Figure 8],[Figure 9],[Figure 10],[Figure 11],[Figure 12],[Figure 13],[Figure 14],[Figure 15],[Figure 16],[Figure 17],[Figure 18],[Figure 19],[Figure 20],[Figure 21]: hippocampal or mesial temporal sclerosis, cortical developmental malformations or neuronal migration disorders (cortical dysplasias, heterotopias, hemimegalencephaly, lissencephaly, schizencephaly, pachygyria, polymicrogyria, Rasmussen encephalitis), phakomatoses (Tuberous sclerosis, Sturge Weber syndrome, neurofibromatosis), vascular abnormalities (arteriovenous malformation, cavernous hemangiomas), infections (tuberculoma, neurocysticercosis), neoplasms (ganglioglioma, dysembryoplastic neuroepithelial tumor, low-grade gliomas, and cerebral metastasis in adults), stroke, post-traumatic epilepsy and miscellaneous conditions (gliosis, encephalocele).{Figure 1}{Figure 2}{Figure 3}{Figure 4}{Figure 5}{Figure 6}{Figure 7}{Figure 8}{Figure 9}{Figure 10}{Figure 11}{Figure 12}{Figure 13}{Figure 14}{Figure 15}{Figure 16}{Figure 17}{Figure 18}{Figure 19}{Figure 20}{Figure 21}

The role of imaging, in particular MRI, in dysembryoplastic neuroepithelial tumor (DNET) is important as this condition is encountered in significant number of patients undergoing surgery for intractable epilepsy. DNETs are benign tumors of young adults. Temporal lobe is the most common location, followed by frontal and parietooccipital lobes. Imaging [Figure 20] and [Figure 21] shows a predominantly cortical based gyral or nodular configuration mass, appearing hypodense on NCCT, hypointense on T1WI, hyperintense on T2WI and showing contrast enhancement in about 20-50% cases. They may resemble a simple or complex cyst showing peripheral ring enhancement or soap bubble appearance, respectively. These lesions lack edema and mass effect, and there is little or no white matter extension. Hemorrhage and calcification are uncommon. Diffusion-weighted imaging (DWI) and corresponding ADC mapping shows no diffusion restriction. MR spectroscopy (MRS) finding is non-specific although an elevated choline peak may be present. Important differential diagnosis include ganglioglioma and low-grade astrocytoma. [1],[2]

 Imaging Modalities

This article highlights the specific role of various imaging modalities in patients with epilepsy, and their practical applications in the management of epileptic patients.

The major utility of computed tomography (CT) scanning is in the initial evaluation of seizures, particularly in trauma, hemorrhage, infarction, tumors, calcified lesions and major structural changes. In perioperative patients, it is the imaging technique of choice as it can detect the bleed, hydrocephalus and assess electrode placement. However, the overall sensitivity of CT in patients with epilepsy is low (~ 30%), and because of poor resolution in the temporal fossa, CT is of no use in detecting mesial temporal sclerosis, the most common pathology in intractable temporal lobe epilepsy. [3]

MRI, with its excellent spatial resolution, soft tissue contrast, and multiplanar capabilities, is the imaging modality of choice in investigating patients with seizure disorder. The sensitivity of MRI in identifying epileptogenic foci in patients with medically refractory patients has been reported to be more than 80%. However, in patients with idiopathic generalized epilepsy, MRI has not been shown to be useful. The correlation of the MRI finding with clinical and electroencephalography (EEG) findings are essential to avoid false positive localization of epileptogenic focus. [4]

Routine scanning protocol for a patient with refractory epilepsy may include axial or coronal T1 and T2-weighted imaging, fluid-attenuated inversion recovery (FLAIR) imaging, and 3D volume acquisition sequences. Common 3D acquisition sequences include high-resolution T1-weighted magnetization prepared rapid acquisition gradient echo (MPRAGE) and fast spoiled GRASS (3D-FSPGR), where GRASS is gradient recalled echo acquisition in steady state. T1-weighted sequences are used to define the brain anatomy, and T2-weighted or FLAIR sequences are used to detect the brain pathologies. High-resolution 3D volume acquisition provides good T1-weighted contrast between gray and white matter and helps to detect subtle cortical dysplasias and internal structure of hippocampus in case of mesial temporal sclerosis. [5],[6],[7] For optimal assessment of hippocampus the imaging should be in hippocampal axis (oblique coronal plane) with thin slices and good signal-to-noise ratio. The application of contrast agent is indicated if there is suspicion of primary or metastatic tumor, infection or inflammatory lesion.

The specialized protocol includes quantitative volumetry and T2 relaxometry, MRS, functional MRI (fMRI), DWI and diffusion tensor imaging (DTI), and magnetic source imaging (MSI).

High resolution T1-weighted 3D volume gradient echo sequences are also used for quantitative measurement of volume of any particular region of interest. In the case of epilepsy this is usually the hippocampus. Volumetric analysis of the hippocampus can be performed both in adults and children with epilepsy, to detect more subtle volume deficits (atrophy) that may be missed by visual assessment alone. Volumetric measurements can be performed manually or with half or fully automated software, however, needs good knowledge of anatomical details. Longitudinal studies done to assess the progression of volumetric changes correlate with the seizure-associated damage. [8] T2 relaxometry is the quantitative determinant of the T2 relaxation time. To achieve this, several T2-weighted images are acquired at different echo times, and with these values an exponential decay curve is obtained to estimate the T2 decay rate of the imaged tissue. The tissues that have prolonged T2 are considered abnormal. In epileptic patients with hippocampal sclerosis, signal increase on T2-weighted images is typically observed in the hippocampus. The measured values of the hippocampal volume and the T2 times are correlated with each other, indicating that a marked volume loss is associated with a significant increase in T2 relaxation, reflecting the complex pathology of hippocampal sclerosis. [9]

Proton MR spectroscopy (MRS) has proven to be a sensitive measure to detect metabolic dysfunction in patients with temporal lobe epilepsy (TLE), particularly mesial temporal sclerosis (MTS) involving hippocampus. Twenty percent of patients with TLE have normal structural MRI scan and the findings in children generally tend to be more subtle than those in adults. MRS metabolite abnormalities may be found even in the absence of detectable structural abnormalities. NAA, NAA/Cho, NAA/Cr, and NAA/(Cho+Cr) all are decreased in atrophic hippocampi, as well as in nonatrophic hippocampi with abnormal EEG findings. Reduced N-acetylaspartate concentration suggests neuronal loss or dysfunction. TLE patients may also show increased choline and myoinositol signals, suggestive of gliosis. Studies of patients during or immediately after seizures (within 6 hours) may also show lactate increase in the epileptogenic focus. MRS also has promising role in the evaluation of patients with extratemporal epilepsy (frontal lobe epilepsy). [10],[11] In patients with structural MR evidence of malformations of cortical development (MCD) or neuronal migration disorders (NMD), MRS provides insight into both the pathology and true extent of the disease processes. Abnormally decreased NAA/Cr and Cho/Cr ratios have been noted in these lesions, as well as in the normal appearing brain contralateral to the lesion, when compared with gray and white matter of neurological controls. [12,13] MRS is of particular importance in patients with brain tumors. The characteristic elevation of choline makes MRS a valuable tool for the diagnosis of tumors and their differentiation from other lesions. There is also evidence that MRS can differentiate between tumor types. [14] Neurotransmitter MRS studies have potential therapeutic impact in seizure patients. Glutamate and γ-amino-butyric-acid (GABA) can be measured using MRS editing techniques. Intracellular glutamate concentrations remain elevated in the epileptogenic hippocampus and neocortex, and contribute to the epileptic state by increasing cellular excitability. [15]

Surgical treatment of refractory focal seizure has been an important and effective means for seizure control. However, the surgical outcome is dependent on precise localization of epiletogenic focus and functional areas of the brain. The fMRI, plays a very important role in preoperative localization of epileptogenic focus and assessment of cognitive function in patients with refractory epilepsy. During focal seizure, cerebral blood flow and metabolism is considerably increased. fMRI using blood oxygen level dependent (BOLD) technique can detect these cerebral hemodynamic changes. The excellent spatial resolution of fMRI helps to study cortical activation during epileptic activity and define epileptogenic focus in originally activated area. The recent development of EEG-triggered fMRI which allows interpretable electroencephalographic data to be recorded during MRI scanning, has advantage of combining the spatial resolution of imaging with the temporal resolution of electrophysiology in precise localization of seizure foci, thus increasing the rate of successful resection of the epileptogenic focus. The EEG-triggered fMRI is highly reliable, repeatable and noninvasive tool in localization of the seizure foci of patients with intractable focal seizure. Combined video-EEG and fMRI in localization of seizure foci has also shown good results. [16],[17] Long-term epileptic activity in patients with epilepsy results in atypical distribution of cognitive function areas because of reorganization of cortical language and memory areas. Accurate localization of cognitive functional areas is necessary, to avoid their resection at the time of surgery, to modify surgical approaches for those patients at risk of language and memory deficit and to predict postoperative cognitive deficit after resection of seizure foci. [18]

The diffusion-weighted signal reflects the molecular motion of water in the intra and extracellular environments. In tissue components such as CSF, molecular motion is not restricted in any direction and is known as isotropic diffusion, detected by DWI. In tissues with linear arrangement of myelinated fibers such as white matter tracts, the molecular motion is restricted to the axis along the white tracts and is known as anisotropic diffusion, detected by DTI or tractography. In epilepsy, DWI is used to assess acute cerebral ischemia, tumors or infections, while DTI has been used to assess the degree of distortion of white matter tracts in case of developmental abnormalities and other lesions responsible for seizure. Anisotropy is reduced in areas of structural abnormalities suggesting structural disorganization of white matter. [19],[20]

Magnetoencephalography (MEG), also known as MSI when combined with structural imaging, has proved to be a new noninvasive tool for localization of epileptic focus. MSI is similar to EEG, but unlike EEG it detects magnetic rather than electric signal and is more accurate for localizing abnormal focus. It is increasingly useful for presurgical localization of epileptogenic lesions and stimulus-induced normal neuronal function to minimize postoperative neurological deficits. [21]

Besides purely structural imaging techniques like MRI, functional imaging studies like interictal positron emission tomography (PET), and ictal and interictal single photon emission computed tomography (SPECT) may provide additional information in some patients and thus aid in clinical decision making. PET and SPECT are usually not indicated for the majority of patients with epilepsy but has important role in the surgical candidates. The detection of cryptogenic lesions is the main goal of functional epilepsy imaging with PET or SPECT. PET utilizes an injection of tracer 18 F-labeled deoxyglucose ( 18 FDG) to measure brain metabolism. Interictal PET shows hypometabolism in the seizure focus, especially in TLE. Ictal PET is not practical due to extremely short half-life of the radiotracers used. PET remains a diagnostic modality for presurgical localization of the focus in temporal lobe and extratemporal epilepsy when MRI is normal. [22] SPECT utilizes injection of radio-labeled tracer Technetium 99 m hexamethyl-propyleneamineoxime (Tc-HMPAO) or ethyl cysteinate dimer (Tc ECD), which has very slow distribution once in the brain. The tracer is stable for several hours, allowing delayed imaging. The most useful study for presurgical evaluation is an ictal SPECT, which usually reveals increased blood flow at site of seizure onset. Interictal studies often show relative hypoperfusion at the site of seizure onset. The substraction of the interictal from the ictal SPECT, and then coregistration of the resulting images onto MRI (substraction ictal SPECT coregistration MRI - SISCOM) has shown to increase the accuracy of this method. [23]


1Osborn AG. Meningioma and other Nonglial Neoplasms. Diagnostic Neuroradiology. Saint Louis: Mosby Year Book; 1994. p. 579-625.
2Barkovich AJ. Intracranial, Orbital, and Neck Masses of Childhood. Pediatric Neuroimaging. 4 th ed. Philadelphia: Lippincott Williams and Wilkins; 2005. p. 506-658.
3Gastaut H, Gastaut JL. Computerized transverse axial tomography in epilepsy. Epilepsia 1976;17:325-36.
4Berg AT, Shinnar S. The risk of seizure recurrence following a first unprovoked seizure: A quantitative review. Neurology 1991;41:965-72.
5Ruggieri PM, Najm IM. MR imaging in epilepsy. Neurol Clin 2001;19:477-89.
6Raybound C, Guye M, Mancini J, Girard N. Neuroimaging of epilepsy in children. Magn Reson Imaging Clin N Am 2001;9:121-47, viii.
7Barkovich AJ, Kuzniecky RI, Jackson GD, Guerrini R, Dobyns WB. Classification system for malformations of cortical development. Update 2001. Neurology 2002;57:2168-78.
8Cook MJ, Fish DR, Shoryon SD, Straughan K, Stevens JM. Hippocampal volumetric and morphometric studies in frontal and temporal lobe epilepsy. Brain 1992;115:1001-15.
9Van paesschen W, Connelly A, King MD, Jackson GD, Duncan JS. The spectrum of hippocampal sclerosis. A quantitative magnetic resonance imaging study. Ann Neurol 1997;41:41-51.
10Danielsen ER, Ross B. The clinical significance of metabolites. In: Danielsen ER, Ross B, editors. Magnetic resonance spectroscopy of Neurological Disease. New York: Marcel Dekker inc; 1999. p. 23-42.
11Kuzniecky R, Palmer C, Hugg J, Martin R, Sawrie S, Morawetz R, et al. Magnetic resonance spectroscopic Imaging in temporal lobe epilepsy: Neuronal dysfunction or cell loss? Arch Neurol 2001;58:2048-53.
12Li LM, Cendes F, Bastos AC, Andermann F, Dubeau F, Arnold DL. Neuronal metabolic dysfunction in patients with cortical developmental malformations: A proton magnetic resonance spectroscopic imaging study. Neurology 1998;50:755-9.
13Simone IL, Federico F, Tortorella C, De Blasi R, Bellomo R, Lucivero V, et al. Metabolic changes in neuronal migration disorders: Evaluation by combined MRI and proton MR spectroscopy. Epilepsa 1999;40:872-9.
14Burtscher IM, Holtas S. Proton magnetic resonance spectroscopy in brain tumors: Clinical applications. Neuroradiology 2001;43:345-52.
15Petroff OA. GABA and glutamate in the human brain. Neuroscientist 2002;8:562-73.
16Yu AH, Li KC, Piao CF, Li HL. Application of functional MRI in epilepsy. Chin Med J 2005;118:1022-1027.
17Al asmi A, Benar CG, Gross DW, Khani YA, Andermann F, Pike B, et al. fMRI activation in continous and spike triggered EEG-fMRIstudies of epileptic spikes. Epilepsia 2003;44:1328-30.
18Zhang L, Jin Z, Zeng YW, Li K, Wang Y. Preoperative brain functional mapping using fMRI in patients with intractable epilepsy. Chin J sterotact Funct Neurosurg 2004;17:257-61 .
19Romero JM, Schaefer PW, Grant PE, Becerra L, Gonzalez RG. Diffusion MR imaging of acute ischemic stroke. Neuro Imaging Clin N Am 2002;12:35-53.
20Rugg-Gunn FJ, Eriksson SH, Symms MR, Barker GJ, Duncan JS. Diffusion tensor imaging of cryptogenic and acquired partial epilepsies. Brain 2001;124:627-36.
21Gallen CC, Hirschkoff EC, Buchann DS. Magnetoencephalography and magnetic source imaging. Capabilities and limitations. Neuroimaging Clin N Am 1995;5:227-49.
22Chugani DC, Chugani HT. New directions in PET neuroimaging for neocortical epilepsy. Adv Neurol 2000;84:447-56.
23Zubal IG, Spencer SS, Imam K, Seibyl J, Smith EO, Wisniewski G, et al. Difference images calculated from ictal and interictal technetium-99m-HMPAO SPECT scans of epilepsy. J Nucl Med 1995;36:684-9.