MR imaging reveals signs of temporal lobe epilepsy


Seizures are paroxysmal events caused by abnormal, excessive, hypersynchronous discharges from an aggregate of neurons in the central nervous system. Epilepsy describes a condition in which a chronic, underlying process produces recurrent seizures. It can be caused by anything that disturbs the normal pattern of neuron activity. Illness, brain damage, and abnormal brain development, for example, can all lead to seizures. Epilepsy may also result from changes in non-neuronal brain cells called glia. These cells regulate concentrations of chemicals in the brain that can affect neuronal signaling.

Seizures are paroxysmal events caused by abnormal, excessive, hypersynchronous discharges from an aggregate of neurons in the central nervous system. Epilepsy describes a condition in which a chronic, underlying process produces recurrent seizures. It can be caused by anything that disturbs the normal pattern of neuron activity. Illness, brain damage, and abnormal brain development, for example, can all lead to seizures. Epilepsy may also result from changes in non-neuronal brain cells called glia. These cells regulate concentrations of chemicals in the brain that can affect neuronal signaling.

Seizure classification is essential for directing diagnosis, selecting an appropriate therapy, and providing prognostic information. Seizures are usually described as focal or generalized. These two categories can be further subdivided (Table 1).

Partial seizures, episodes in which activity is restricted to discrete areas of the cerebral cortex, are often associated with structural abnormalities of the brain. Generalized seizures involve diffuse regions of the brain simultaneously and may result from cellular, biochemical, or structural abnormalities that have a more widespread distribution.

Approximately 50% of patients with epilepsy have partial epilepsy. The temporal lobe is the most epileptogenic region of the brain, and so partial epilepsy often originates here. The true prevalence of temporal lobe epilepsy is not known, however, because most cases are classified by clinical history and interictal electroencephalogram findings, rather than neuroradiological imaging.

Temporal lobe epilepsy, the most common form of partial epilepsy in adults, is often unaffected by medical treatment. The condition was defined in 1985 as characterized by recurrent unprovoked seizures originating from the medial or lateral temporal lobe. Symptoms consist of simple partial seizures without loss of awareness (with or without aura) and complex partial seizures (i.e., with loss of awareness).


The most frequent neuropathologic substrate in adult patients with temporal lobe epilepsy is hippocampal sclerosis involving the limbic system. The limbic system may be understood as four concentric arches (Figure 1):

- limbic lobe including the cingulate and hippocampal gyri, which together arch around the corpus callosum, and callosal and hippocampal fissures;

- space containing cerebrospinal fluid, and callosal and hippocampal fissures;

- intralimbic gyrus of Brocca: a tract of arched fibers (cingulum) connecting the cingulate and hippocampal gyri; and

- fornix (fimbriae).

The anterior extremity of the hippocampal gyrus adopts the form of a hook (uncus), which is separated from the apex of the temporal lobe by a slight fissure, the incisura temporalis. Although superficially continuous with the hippocampal gyrus, the uncus forms a part of the rhinencephalon morphologically.

The hippocampus is a 5-cm-long curved eminence that extends throughout the entire length of the lateral ventricle's inferior cornu. Its lower end is enlarged and has two or three rounded elevations that give it a pawlike appearance (pes hippocampi). A transverse section through the hippocampus would show that this eminence is produced by the folding of the hemisphere wall to form the hippocampal fissure.

The hippocampus is made up of complex interfolded gray layers of dentate gyrus and cornu ammonis. Cornu ammonis is divided into four parts (CA1 to CA4), one of which (CA4) is fully covered by the dentate gyrus. Cornu ammonis is continuous with the subiculum, which merges with the parahippocampal gyrus. A thin layer of white matter extends between the cornu ammonis and dentate gyrus (stratum radiatum) to form the alveus, which is continuous with the fimbria hippocampi.

Less common structural lesions include tumors, vascular malformations, developmental anomalies, gliosis, infection, cortical encephalomalacia and scarring, trauma, and ischemia. Assessment of the epileptogenic network is primarily based on clinical and EEG data.


Ictal recordings from patients with typical temporal lobe epilepsy usually exhibit rhythmic, sharp theta activity in the 5 to 7-Hz range. Activity is generally greatest in the sphenoidal and basal temporal electrodes on the side of seizure origin. Interictal EEG should be performed in all patients with suspected temporal lobe epilepsy. One-third of these patients will have bilaterally independent temporal interictal epileptiform abnormalities. Interictal abnormalities, consisting of spike/sharp and slow complexes, are usually located in the anterior temporal (F7/F8 and T3/T4 electrodes) or basal temporal region (T9/T10 and F9/F10 electrodes).

Video-EEG monitoring is used to define the site of the seizure's focus and to correlate abnormal electrophysiologic activity with behavioral manifestations. Routine scalp or scalp-sphenoidal recordings are usually sufficient for localization. Intracranial EEG with placement of intracranial subdural electrodes is done only for surgical candidates, when MRI and other noninvasive EEG data cannot locate the seizure site. The presence of structural abnormalities in the temporal lobe will support clinical and EEG data in establishing a diagnosis. MRI also helps discriminate between different subgroups of patients presenting with specific pathologies and may help predict prognosis. MRI is therefore the neuroimaging modality of choice for temporal lobe epilepsy.

T1-weighted, T2-weighted fast spin-echo, and FLAIR MR sequences should be performed routinely with thin slices of no more than 4 mm. Gradient recall images and T1-weighted MRI with 1 to 2-mm thick slices are useful for better anatomic and morphometric studies. Observation of a vascular malformation or tumorlike mass should be followed by T2-weighted gradient recall imaging, or contrast-enhanced T1-weighted MRI.

When interpreting the images, we use the hippocampal plane as the reference plane. This passes through the planes of both hippocampi and is parallel to the plane of the left lateral (sylvian) fissure. Images perpendicular to this plane are perpendicular to the hippocampal bodies.

Further investigation will be needed if the severity of disease indicates that surgery is required and MRI cannot detect the lesion. Interictal SPECT, invasive electroencephalography, and/or FDG-PET may be performed.

MR spectroscopy, diffusion-weighted MRI, and perfusion studies may have a role in presurgical localization of functionally important cortical areas, though they are not yet used routinely.

Therapy for patients subject to seizures is almost always multimodal. Strategies include treatment of underlying causal or contributory conditions, avoidance of precipitating factors, suppression of recurrent seizures through anti-epileptic medication or surgery, and attention to a variety of psychological and social issues.

Around 47% to 60% of new-onset partial seizures are controlled effectively by traditional anti-epileptic drugs such as phenytoin, phenobarbital, carbamazepine, or valproate. Approximately one-third of patients with epilepsy do not respond to treatment with a single drug and must be prescribed a combination. If none of these traditional medications work, addition of a newer drug may be tried. Candidates that show similar, if not better, efficacy than traditional anti-epileptic drugs include topiramate, lamotrigine, levetiracetam, oxcarbezapine, and zonisamide.

About 40% of patients continue to have seizures in spite of using three different anti-epileptic drugs. Surgery can be extremely effective in reducing seizure frequency or even stopping seizures in such cases, and it is important to identify potential candidates for surgery. Anterior temporal lobectomy is the definitive treatment for medically intractable temporal lobe epilepsy. Patients whose epilepsy is not responding to drug treatment but who cannot undergo resective brain surgery may be offered vagus nerve stimulation instead. This can result in a reduction of 25% to 28% in seizure frequency.1


Mesial temporal sclerosis, also known as hippocampal sclerosis, is the most common cause of temporal lobe epilepsy found at surgery. It describes a pathologic alteration of the hippocampus, with loss of at least 50% of the neurons, with or without sclerosis. Classic hippocampal sclerosis is characterized by a neuronal depopulation in the CA1 and CA3 regions. Complete hippocampal sclerosis affects all sectors, while end-folium sclerosis concerns CA4 alone. Pathology may extend to the subiculum, amygdala, fornix, and mamillary body. Surgical resection of the hippocampus is the only reliable method for treating patients with medically refractory epilepsy due to temporal lobe sclerosis.

Primary MRI findings of temporal lobe epilepsy are hippocampal atrophy, hyperintensity, and loss of internal architecture. Patients with these findings have a 70% to 90% chance of relief from seizures after temporal lobectomy (Figure 2).

Secondary MRI findings, which may help diagnose mesial temporal sclerosis, can involve the temporal region (loss of digitation pattern, temporal horn dilatation, temporal lobe atrophy, collateral white matter atrophy, bilateral entorhinal cortex atrophy, changes in anterior temporal white matter) and extratemporal locations (fornix atrophy, mamillary body atrophy, talamus atrophy, and caudate atrophy).11 High-resolution MRI shows hippocampal atrophy in 87% of patients with temporal lobe epilepsy by visual analysis alone. Hippocampal atrophy is bilateral in 10% to 15% of cases. Increased T2-weighted signal intensity in the hippocampus may be seen on FLAIR, and this finding is also consistent with hippocampal sclerosis.

Diagnosis of hippocampal sclerosis does not necessarily mark the end of an investigation. A complete examination should cover the whole temporal lobe, and indeed the entire brain, to detect or rule out any dysplastic lesions. Mesial temporal sclerosis is associated with other potentially epileptogenic extrahippocampal anomalies in 15% of cases. This dual pathology is associated with a poor postsurgical prognosis.

Most epileptogenic neoplasms are located in the temporal lobe, just inside or near to the cortex. We have found a wide variety of tumors: low-, medium-, and high-grade gliomas, dermoid tumors, lymphoma, xantoastrocytoma, oligoastrocytoma, oligodendroglioma, and dysembryoplastic neuroepithelial tumors. These lesions all grow slowly. Metastasis is the most frequent cause of lesions associated with late-onset epilepsy in elderly patients.

It is extremely difficult to establish the histology of these lesions on the basis of their imaging features. Most present as small, well-defined masses, with scarce perilesional edema (Figure 3).

Vascular malformations, in particular cavernomas, are also linked to epilepsy. The most common form of presentation is partial-onset seizures (Figure 4). Cavernomas are large vascular spaces with no enlarged feeding artery or draining vein, and they may be associated with a venous malformation or a developmental venous anomaly. They can be single or multiple and may clot or bleed.

Diagnosis of cavernomas on MRI is easy. T2-weighted sequences show a lobulated core of T1, T2, and FLAIR signal, all rounded by a rim void of

signal. This effect is enhanced on T2-weighted gradient-echo sequences, which should be used to determine whether other cavernomas are present and to differentiate blood from angioma more clearly. Edema or gliosis (high signal on T2-weighted MRI or FLAIR) may be observed around the cavernoma.

Developmental anomalies responsible for epilepsy can be divided into three main groups:

- Differentiation disorders. Premigratory developmental abnormalities of the cerebral mantle affect stem cell differentiation. These dysplastic glioneuronal disorders are characterized by a poorly differentiated ganglionic (neuronal) cell, with abnormal connections. Such lesions are intrinsically epileptogenic. They include focal cortical dysplasia of Taylor, isolated tuber of tuberous sclerosis complex (TSC) or TSC-like neuroglial hematoma, and hemimegalencephaly.

- Migration disorders. Disorders beginning during neuronal migration disturb the normal neuronal arrangement. Resulting heterotopias can be local or diffuse, nodular or laminar, periventricular, subcortical, transcerebral, or intracortical. Agyria-pachygyria belongs to this group.

- Organization disorders. Micropoligyria, or polymicrogyria (which causes an excessive "overfolding" of the cortex), and schizencefalia are transcerebral clefts lined with cortex and pia, extending from the brain's surface to the lateral ventricles.

Visualization of the alternative developmental abnormalities differs widely on MRI (Table 2). High signal, corresponding to white matter, may be seen on FLAIR or T2-weighted sequences in cases of focal cortical dysplasia. This extends as an elongated triangle from cortex to ventricle. Affected gyrus may sometimes appear broad. The lesion may occasionally be limited to the cortex, which is typically hyperintense on FLAIR images.10

Partial-onset epilepsy can also be related to acquired focal brain lesions, resulting from inflammation, trauma, or cerebrovascular injury. MRI shows a limited area of gliosis, which appears as low signal on T1-weighted MRI and as high signal on T2-weighted MRI and FLAIR. This astrocytic gliosis is associated with loss of volume (cavitation or cleft). Hematomas produce epileptic seizures due to gliosis and production of hemosiderin, which is a potent epileptogenic substance.

Ischemia is the most frequent cause of later partial-onset epilepsy in patients older than 50. This group has a high risk of developing chronic epilepsy. Infections such as abscesses have been linked to acute seizures. Chronic scars may be a causal factor in chronic epilepsy.

DR. PALACIOS BOTE and DR. FERNANDEZ-GIL are radiologists at Infanta Cristina University Hospital in Badajoz, Spain.


1. Lowenstein DH. Seizures and Epilepsy. In: Kasper DL, Fauci AS, Longo DL, et al, eds. Harrison's Principles of Internal Medicine, 16th ed. New York: McGraw-Hill, 2005:2357-2372.

2. Pedley TA, Bazil CW, Morrell MJ. Epilepsy. In: Rowland LP, ed. Merritt's neurology, 10th ed. Philadelphia: Lippincott, Williams & Wilkins, 2000:813-832.

3. Commission on classification and terminology of the International League Against Epilepsy. Proposal for revised clinical and electroencephalographic classification of epileptic seizures. Epilepsia 1981;22:489-501.

4. Bonn PA, Williamson PD, Fried I, et al. Intracranial, intraaxial, space-occupying lesions in patient with intractable partial seizure: An anatomoclinical, neuropsychological, and surgical correlation. Epilepsia 1991;32:467-476.

5. Commission on classification and terminology of the International League Against Epilepsy. Proposal for classification of epilepsies and epileptic syndromes. Epilepsia 1985;26(3):268-278.

6. De Kier EL, Fulbright RK, Bronen RA. Insights into limbic lobe embryology and anatomy: dissection and MR imaging of the medial surface of the fetal human cerebral hemisphere. AJNR 1995;16:1847-1853.

7. de Lanerolle NC, Kim JH, Williamson A, et al. A retrospective analysis of hippocampal pathology in human temporal lobe epilepsy: evidence for distinctive patient subcategories. Epilepsia 2003;44(5):677-687

8. Bruton CJ. The neuropathology of temporal lobe epilepsy. Oxford: Oxford University Press, 1988:1-85.

9. Commission on classification and terminology of the International League Against Epilepsy. Proposal for revised classification of epilepsies and epileptic syndromes. Epilepsia 1989;30:389-399.

10. Raybaud C, Guye M, Mancini J, Girard N. Neuroimaging of epilepsy in children. Magn Reson Imag Clin N Am 2001;9(1):121-147.

11. Bronen R. MR of mesial temporal sclerosis: How much is enough? AJNR 1998;19(1):15-18.

12. Jack CR Jr. Epilepsy: surgery and imaging. Radiology 1993;189(3):635-646.

13. Kuzniecky R, Burgard S, Faught E, et al. Predictive value of magnetic resonance imaging in temporal lobe epilepsy surgery. Arch Neurol 1993;50(1):65-69.

14.Tien RD, Felsberg GJ, de Castro CC, et al. Complex partial seizures and mesial temporal sclerosis: evaluation with fast spin-echo MR imaging. Radiology 1993;189(3):835-842.

15. Bergin PS, Fish DR, Shorvon SD, et al. Magnetic resonance imaging in partial epilepsy: additional abnormalities shown with the fluid attenuated inversion recovery (FLAIR) pulse sequence. J Neurol Neurosurg Psychiatry 1995;58(4):439-443.

16. Cendes F, Cook MJ, Watson C, et al. Frequency and characteristics of dual pathology in patients with lesional epilepsy. Neurology 1995;45(11):2058-2064.

17. Bronen RA, Fulbright RK, Spencer DD, et al. MR characteristics of neoplasms and vascular malformations associated with epilepsy. Magn Reson Imag 1995;13(8):1153-1162.

18. Requena I, Arias M, Lopez IL, et al. Cavernomas of the central nervous system: clinical and neuroimaging manifestations in 47 patients. J Neurol Neurosurg Psychiatry 1991;54(7):590-594.

19. Casazza M, Broggi G, Franzini A, et al. Supratentorial cavernous angiomas and epileptic seizures: preoperative course and postoperative outcome. Neurosurgery 1996;39(1):26-32.

20. Stefan H, Hammen T. Cavernous haemangiomas, epilepsy and treatment strategies. Acta Neurol Scand 2004;110(6):393-397.

21. Barkovich AJ, Kuzniecky RI, Dobyns WB, et al. A classification scheme for malformations of cortical development. Neuropediatrics 1996;27(2):59-63.

22. Willmore L. Post-traumatic seizure. Neurol Clin 1993;11(4):823-834.

23. Camilo O, Goldstein LB. Seizures and epilepsy after ischemic stroke. Stroke 2004;35(7):1769-1775.

24. Chadwick D. Seizures and epilepsy after traumatic brain injury. Lancet 2000;355(9201):334-336.


Partial or focal seizures

- Simple partial (with motor, sensory, autonomic or psychic signs)

- Complex partial

- Partial with secondary generalization

Primarily generalized seizures

- Absence (petit mal)

- Tonic-clonic (grand mal)

- Tonic

- Atonic

- Myoclonic

Unclassified seizures

- Neonatal seizures and infantile spasm

Source: International League Against Epilepsy, 1981.3


Cortical thickening

Blurring of cortical-subcortical junction line

Irregularity of union zone




Cortical cleft

Radial bands

Heterotopic gray matter

Transmantle heterotopy

High homogeneous intensity in subcortical white matter

Enlarged hemisphere

Related Videos
Reimbursement Challenges in Radiology: An Interview with Richard Heller, MD
Nina Kottler, MD, MS
The Executive Order on AI: Promising Development for Radiology or ‘HIPAA for AI’?
Related Content
© 2023 MJH Life Sciences

All rights reserved.