Neuroimaging in epilepsy Flashcards
CT
Computed tomography (CT) is widely available and used in emergency rooms. With multiple detector helical CT, high spatial resolution can be obtained in all dimensions allowing 3D recon- structions and operator selected multiplanar reformats in any plane. CT may be the only option in patients who cannot obtain MRI due to contraindications such as patients with pace- makers, defibrillators, specific metal prostheses (e.g., cochlear implants), ferromagnetic aneur- ysm clips, metallic foreign bodies within eyes, and shrapnel or bullets located near vascular structures. There may be other barriers in obtaining a conventional MRI in unstable or uncooperative patients, or patients with signifi- cant claustrophobia or morbid obesity. CT scans provide better details about bony structures and can easily detect hemorrhages, calcifications, strokes after 24 h, and large tumors. However, CT may fail to recognize commonly encountered lesions in patients with epilepsy such as hip- pocampal atrophy, hippocampal sclerosis, corti- cal dysplasias, or low-grade gliomas (LGG).
MRI
MRI is a noninvasive test, which does not cause exposure to ionizing radiations and is considered safe across all age groups. It possesses excellent spatial resolution down to millimeters. MRI scanners with higher magnetic strengths (3-, 4-, or 7-Tesla) have proliferated over the past dec- ade. The typical MRI epilepsy protocol includes multiplanar diffusion, T2-weighted, FLAIR, gradient echo, or susceptibility-weighted images of the brain. This protocol is supplemented with a 3D volumetric T1-weighted acquisition and oblique coronal plane FLAIR and T2-weighted images orthogonal to the long axis of the tem- poral lobes. Gadolinium administration may have utility in certain patient populations with seizures or when there is clinical suspicion for infectious, inflammatory, or neoplastic etiologies.
The presence or absence of lesion(s) and their location on brain MRI helps identify patients who may be good surgical candidates for lesionectomy, corticectomy, topectomy, corpus callosotomy, or hemispherectomy. For example, patients with medically refractory seizures and hippocampal sclerosis should be evaluated for either standard anterior temporal lobe resection or selective amygdalohippocampectomy. A le- sionectomy of a cavernoma with or without corticectomy is a reasonable option if anti-seizure medications are not effective in controlling seizures. A more aggressive surgical approach, such as a functional hemispherectomy, may be warranted in patients with Sturge Weber syndrome, Rasmussen’s encephalitis, large porencephalic cyst due to previous traumatic or ischemic insult, hemimegalencephaly, or Dyke– Davidoff–Masson syndrome (congenital or acquired). Neuroimaging may have a direct influence on therapeutic options that neurologists offer to their patients; e.g., a scan supporting a diagnosis of Tuberous Sclerosis (TS) in an infant with infantile spasms may justify the use of vigabatrin or m-TOR inhibitors over adrenocor- ticotrophic hormone (ACTH). Not all structural lesions are epileptogenic; therefore, it is prudent to correlate incidental findings on MRI with clinical history, seizure semiology, and EEG data.
MTS
Mesial temporal sclerosis: Temporal lobe epilepsy (TLE) is the most common form of focal epilepsy. Mesial TLE is more prevalent than neocortical epilepsy and often intractable to anti-seizure medications. The most common identifiable lesion on MRI brain is mesial tem- poral sclerosis (MTS; Fig. 21.1). In patients with TLE, subtle anatomic features of the medial temporal lobes and pathologies such as MTS or incomplete hippocampal inversion (Fig. 21.2) are best appreciated in an oblique coronal plane. This orientation is orthogonal to the long axis of the temporal lobe and reduces volume averaging problems for the thin laminar appearance of the hippocampus. Oblique coronal temporal high-resolution T2-weighted and FLAIR are the best sequences to diagnose MTS. This entity is characterized by (1) hippocampal atrophy, (2) increased T2 signal, and (3) abnormal mor- phology or loss of internal architecture of hip- pocampus. In 10% of the cases, MTS can be bilateral (Fig. 21.3). Secondary findings may include dilatation of the temporal horn of the lateral ventricle, loss of gray–white matter differentiation in the temporal lobe or decreased white matter in the adjacent temporal lobe (e.g., collateral eminence and temporal stem). There can be atrophy of the ipsilateral fornix and mammillary body (Fig. 21.4). High-resolution 3D T1WI are also useful when performing hip- pocampal volumetric analyses. However, para- central lesions are more evident on axial sequences. Figure 21.5 shows a less common case of temporal lobe seizures from a temporal lobe encephalocele involving the subjacent sphenoid wing.
Neuronal migrational disorders
Hetero- topias are neuronal migrational disorders (NMDs) where gray matter gets arrested as neurons migrate from periventricular regions toward pia during embryonic stages. High-resolution 3D T1-weighted volumetric imaging provides superior gray–white contrast that is critical to identify subtle cortical malfor- mations in patients with epilepsy (Fig. 21.6). Higher magnetic strengths (3- or 7-Tesla) can detect very subtle cortical dysplasias.
Heterotopias can either be focal, nodular, or multifocal (as in TS) or preferentially involve one hemisphere as in hemimegalencephaly. Subcortical band heterotopias (SBH) are typi- cally periventricular, bilateral nodular collections of gray matter with relatively smooth margins, which gives the appearance of a double cortex. Pachygyria is abnormal tissue in the right loca- tion with abnormal sulcation and gyration of the mantle which is typically > 8 mm thick (Fig. 21.7a). Polymicrogyria (PMG) is either two- or four-layered cortex, which is less than 5– 7 mm (Fig. 21.7b). PMG is commonly associ- ated with hypoxic-ischemic injury, or prenatal cytomegalovirus (CMV) infection.
FCDs are classified into three categories (Type I, II, and III) and further divided into various subtypes (Table 21.1). In a fully myelinated brain, FCD type I may be characterized by subtle blur- ring of the gray–white junction with typically normal cortical thickness, moderately increased white matter signal hyperintensities on T2/FLAIR images and decreased signal intensity on T1-weighted images. FCD Type IIA cortical dysplasias are characterized by marked blurring of the gray–white junction on T1 and T2-FLAIR images due to hypomyelination or dysmyelination of the subcortical white matter with or without cortical thickening. Here, the increased white matter signal changes on T2, WI, and FLAIR images frequently tapers toward the ventricles (aka the “transmantle sign”) which marks the involvement of radial glial neuronal bands. This radiological feature differentiates FCD from low-grade tumors. Type II lesions are more commonly seen outside the temporal lobe with predilection for the frontal lobes. Type III FCD is typically associated with another principal lesion such as hippocampal sclerosis, tumor, a vascular malformation, or other acquired pathology during early life.
Other important NMDs include lissencephaly, which is characterized by smooth brain surface and abnormal gyration, which varies between agyria and pachygyria. Lissencephaly with posteriorly
predominantly gyral abnormalities is caused by mutation in LIS1 gene (Fig. 21.8). Anteriorly predominant lissencephaly in heterozygous males and subcortical band heterotopia (SBH) in heterozygous females are caused by mutations of the XLIS (double cortex gene on chromosome X). Schizencephaly is another rare form of MCD which is characterized by the presence of a transcortical cleft that can extend from ventricles to the pia with open or fused lips, and often polymicrogyria is seen on the lips of the schizen- cephaly (Fig. 21.9). Hemimegalencephaly is the unilateral hamartomatous excessive growth of all or part of one cerebral hemisphere at different phases of embryologic development. MRI in these cases reveals an enlarged hemisphere with increased white matter volume, cortical thicken- ing, agyria, pachygyria, polymicrogyria or lissen- cephaly, and blurring of the gray–white matter junction. Often, a large, ipsilateral irregularly shaped ventricle may be seen.
Brain tumors
Brain tumors: Approximately 20–40% of the adults with primary brain tumors experience one seizure prior to the tumor diagnosis, and another 20–45% will suffer from seizures during the course of the illness [1]. This incidence rate varies depending on the tumor type, the grade of the tumor, and its location. Seizures are more common in slow growing tumors such as meningiomas, gangliogliomas (GGs), dysemby- oplastic neuroepithelial tumors (DNETs), or dif- fuse low-grade tumors such as Grade II astrocytomas, oligodendrogliomas, and oligoas- trocytomas (Table 21.2). Typically, the low-grade umors do not enhance on Gd-administration. The
most common location is temporal lobe, followed
by the parietal, frontal, and occipital lobes. Ganglions typically present with temporal lobe epilepsy, presumably due to the temporal lobe being a favored location.
Gangliogliomas are closely related to gangliocy- tomas, which contain essentially only mature neural ganglion cells, and ganglioneurocytoma, which in addition have small mature neoplas- tic neurons. On MRI, these tumors may show cystic changes or calcifications.
DNETs are cortically based benign neoplastic cortical malformations, which may show sub- cortical extension in approximately 30% of tumors giving them a triangular appearance (Fig. 21.11). These tumors appear as well-defined lobulated, and solid tumors that are hyperintense on T2WI and may erode the over- lying calvarial bone or show microcystic chan- ges. The most common location is tempora (60%) followed by temporal lobes (30%). Meningiomas are the most common extra-axial tumors of the central nervous system. They are nonglial neoplasms that originate from the arachnoid cap cells of the meninges and have characteristic imaging findings, although there are many variants (Fig. 21.12). GBMs are aggressive malignant tumors that are associated with significant vasogenic edema and heteroge- neous enhancement. The overall incidence of seizures in Grade IV glioblastoma multiforme (GBM) patients, without considering the loca- tion, has been reported between 25 and 50% at presentation and another 20–30% during the course of the disease [2]. Metastatic lesions tend to have a smaller risk for seizures, one exception being metastatic melanoma.
Perfusion-weighted imaging is a useful tool, which involves several image acquisitions during the first pass of a bolus of contrast agent. This method allows the radiologist to determine the relative cerebral blood volume (rCBV). In gen- eral, the underlying principle is the greater the rCBV, the higher the grade of tumor. Lack of notable flow indicates a nonneoplastic etiology with abnormal signal intensity, such as demyelination. Of note, mixed oligoden- drogliomas can have low rCBV. Besides the prognostic information it provides, perfusion-weighted imaging can increase the yield of brain biopsy and help in differentiating recurrent neoplasm from radiation necrosis. On perfusion MRI, GBMs typically show increased regional blood flow (Fig. 21.13).
Another interesting but rare kind of focal congenital tumor is hypothalamic hamartoma (HH). These tumors are typically associated with ictal spells of laughter without mirth or gelastic seizures (Fig. 21.14). HH are composed of cytologically normal, small, and large neurons, which are organized in poorly demarcated clus- ters of variable size and density. These tumors are categorized by the Delalande classifications I–IV. Type I has a horizontal orientation and may be lateralized on one side; Type II has a vertical orientation and an intraventricular location; Type III is a combination of types I and II; Type IV is a giant hamartoma.
Vascular malformations
Vascular malformations: Vascular malfor- mations can be either high flow or low flow. High flow malformations include arteriovenous malformations (AVMs), which can be parenchymal, dural, or mixed. In contrast, low flow vascular malformations are cerebral cav- ernous malformations (CCMs), developmental venous anomaly (DVA), or mixed vascular malformations (Fig. 21.15). CCMs have a unique “popcorn” appearance with hemorrhages of different ages. They may be bright on CT due to pooling of blood within the cavernoma. The most characteristic feature is blood products of different ages with an area of hyperintensity representing methemoglobin surrounded by a hypointense ring of hemosiderin on T2W MRI. Gradient echo (GRE) sequences are useful to detect CCMs and may show low or minimal enhancement on Gd. MRI brain is superior to CT scan to look for the nidus of an AVM which is hyperdense compared to adjacent brain (Fig. 21.16). It is easier to appreciate fast flow voids on T2WI due to fast flow and enlarged draining veins may be seen. Phase contrast MR angiography can help subtract the hematoma components in patients who present with acute hemorrhage into an AVM. CTA can demonstrate feeding arteries, nidus, and draining veins visi- ble, which resembles a “bag of worm” appear- ance. The exact anatomy of feeding vessels and draining veins is often difficult to delineate, and thus angiography remains necessary. Digital subtraction angiography (DSA) remains the gold standard in delineating the location and number of feeding vessels supplying the central nidus and the pattern of venous drainage (superficial or deep). The susceptibility-weighted images (SWI) are particularly sensitive to iron content in the brain, both in cortical layers and in blood vessels and identify hemosiderin in CCMs, old infarcts or old contusions.
Infectious/inflammatory disorders
Infectious/Inflammatory disorders: A common etiology for seizures in all age groups, both in the developing and developed world, includes infec- tions of the nervous system. A wide variety pathogens including viral, bacterial, fungal, para- sitic, and other opportunistic pathogens can cause CNS disease in humans. Though gold standard of diagnosis remains either biopsy or CSF analysis, neuroimaging can aid in rapid diagnosis by help- ing identify typical lesion patterns. While it is outside the scope of his chapter to comprehen- sively discuss CNS infections, we have attempted to list typical radiology findings with common CNS infections associated with epilepsy in Table 21.3. More recent MRI techniques, such as DWI and MRS also aid in diagnosis by providing additional information, which is discussed in rel- evant sections in this chapter. Briefly, restricted diffusion helps in differentiation of progenitor abscesses from ring-enhancing lesions of other etiology. Also, the presence of lactate and cytosolic amino acids and the absence of choline on MRS are seen in the cases of pyogenic abscesses. Autominnune encephalitides can also be associated with seizures. Figure 21.17 illus- trates an example of progressive volume loss and denudation of the overlying cortex Rasmussen’s syndrome is one kind of autoimmune encephalitis associated with intractable unilateral seizures, progressive hemiparesis or weakness on one side, and intellectual dysfunction.
Neurocutaneous Syndromes (Phacomatoses)
These are a group of inherited disorders charac- terized by hamartomas and neoplasms through- out the body along with involvement of the nervous system and skin. The neuroradiological features of common phacomatoses, namely, Tuberous sclerosis (TS), Neurofibromatosis (NF1 and NF2), and Sturge Weber syndrome (SWS) are summarized in Table 21.4.
Figure 21.18 illustrates a few salient neuro- radiological features of TS and SWS in patients with medically refractory seizures.
Trauma: Traumatic brain injury (TBI), espe- cially severe closed skull injury and penetrating dural injury have been well documented to cause post-traumatic epilepsy [3]. Patients with pro- longed loss of consciousness, post-traumatic amnesia, or hemorrhage in the brain (subarach- noid hemorrhage, subdural, epidural, intra- parenchymal, and intraventricular) are at a higher risk of developing immediate (onset within 24 h), early (onset within a week), or late-onset epilepsy. The findings on imaging vary from contusions, with or without diffuse axonal injury (DAI), or hemorrhages in different locations (Table 21.5). T2WI and the FLAIR images are sensitive to edema in the brain, while GRE and SWI are very sensitive to microhemorrhages. Figure 21.19 shows temporal encephalomalcia as a result of TBI. SWI and DWI are the best sequences to detect DAI. Tong et al. group showed that number of hemorrhagic DAI lesions seen on SWI was six times greater than that on conventional T2-weighted 2D GRE imaging and the volume of hemorrhage was approximately twofold greater.
PET
PET is a noninvasive, diagnostic imaging tech- nique for measuring the metabolic activity of cells in the human body. PET studies character- ize genotype–phenotype interactions because this technique directly measures neurometabolic changes and receptor binding. PET produces images of the body by detecting the radiation emitted from radioactive substances. These sub- stances are injected into the body and are usually tagged with a radioactive atom (11C, 18Fl, 15O or 13N) that has short decay time (Table 21.6). The radioactivity localizes in the appropriate areas of the body and is detected by the PET scanner.
Different colors and/or degrees of brightness on a PET image represent different levels of tis- sue or organ function. For example, as healthy tissue uses glucose for energy, it accumulates some of the tagged glucose, which shows up on PET images. However, epileptogenic tissue dur- ing interictal phases utilizes less glucose than healthy normal tissue, and thus, it appears less bright than normal tissue on the PET images (Fig. 21.20). 18F FDG-PET is particularly helpful in identifying subtle FCDs. FDG is useful for tumor grading because most high-grade tumors, such as high-grade gliomas, medulloblastoma, and primary central nervous system lymphoma, have high concentrations and activity of glucose transporters (GLUTs). Most low-grade tumors have lower concentrations of GLUTs and can usually be distinguished from high-grade glio- mas by the lower FDG uptake on PET [4]. FDG-PET is a useful tool in distinguishing post-radiation necrosis from tumor progression, both in high-grade gliomas and brain metastases. In general, recurrent tumor is FDG avid, and radiation necrosis is not FDG avid.
SISCOM
SISCOM is a novel neuroimaging technique that couples MR images with nuclear medicine SPECT (Single-Photon Emission Computed Tomography) scans to identify areas of increased perfusion with respect to regional cerebral flow (rCBF). It is commonly used as a tool in pre-surgical evaluation to localize the seizure focus in both pediatric and adult patients with refractory epilepsy [5]. Technically, radiotracer injections (typically Tc-99 m) are administered during an ictal event that allows computation of variations in rCBF between ictal and inter-ictal states. Studies by multiple groups have validated SISCOM as a valuable tool that offers improved localization of seizure focus by visualization of the region of hyperperfusion and thus higher neuronal activity (40–86%). Further, SISCOM findings serve as a guide for further intracranial monitoring, electrode place- ment, and in determining the extent of surgical resection, which in turn offers a higher proba- bility of post-surgical seizure freedom [6–8]. Occasionally, incongruous findings have been reported between intracranial vEEG and SISCOM in post-surgical patients [5]. These likely reflect an altered blood flow pattern in these patients rather than the actual seizure onset zone. However, SISCOM still exists as a valuable tool in pre-surgical planning in both identification of the ictal zone and guiding surgical resection. For the clinician, though, it is essential to remember that the complete workup must be tailored to each individual patient.
A separate chapter is devoted to MEG but is mentioned briefly here. MEG measures small electrical currents arising inside the neurons of the brain, which produce very weak magnetic fields in the range of femto and pica Tesla. Patients wear a helmet with an array of 100+ sensitive magnetic field measurement devices. The measurement devices are called Superconducting Quantum Interference Devices (SQUIDS). MEG has a high resolution in both space (2–3 mm) and time (<1 ms). The skull and the tissue surrounding the brain affect the magnetic fields measured by MEG much less than they affect the electrical impulses measured by electroencephalogram. MEG is usually per- formed with simultaneous EEG. For Magnet Source Imaging (MSI), information from MEG and MRI is coregistered to form magnetic source localization images that provide detailed struc- tural–unctional information of the brain. MSI helps in characterization and localization of epileptiform activity and pre-operative mapping of brain areas supporting sensory, motor, and language function (Fig. 21.21). MSI is compli- mentary to PET, fMRI, and EEG as it provides unique information on the spatiotemporal dynamics of brain activity.
DWI
DWI adds spatially encoding magnetic gradients to the standard MRI sequence to make the image sensitive to the translational motion of water molecules. In the absence of T2 weighting, the “bright regions” represent decreased water diffu- sion, and “dark regions” represent increased water diffusion. Hence an acute stroke with cytotoxic edema and slow water diffusion will appear very bright. However, a T2-bright tissue, such as edema or gliosis from a late subacute or chronic infarct, also can appear bright on a diffusion trace image (this is called “T2 shine through”). In apparent diffusion coefficient (ADC) maps calculated from the diffusion-weighted images, the intensity of pixels is more directly proportional to extent dif- fusion, and the T2 weighting is removed from the data. A bright signal on DWI and dark signal on ADC supports the evidence of cytotoxic edema seen with infarctions (Table 21.7). A focus of increased signal intensity on DWI with a normal ADC signal suggests vasogenic edema and refer- red to as “T2 shine through.”
DTI
DTI is based on the basic principle that the dif- fusion of water molecules in the brain is restricted by intracellular and extracellular membranes, particularly myelin. The image intensities are inversely related to the relative mobility of water molecules in tissue and the direction of motion. Anisotropy is a measure of the orientation dependent water diffusion within an image voxel, e.g., CSF has a fractional ani- sotropy of near zero, whereas highly coherent white matter has a fractional anisotropy near 1. The diffusion data can also be given color codes based on principal direction of diffusion, and the intensity of color is proportional to the fractional anisotropy. The transverse axis (x-axis) is repre- sented by red color; the green color depicts anterior posterior (y axis), and blue is designated to superior inferior (z-axis). DTI tractography then uses fractional anisotropy and the principal orientation of diffusion with the voxel to char- acterize the coherent white matter bundle 3D orientations with the brain and spinal cord. Thus, tractography allows accurate diagnosis of even subtle congenital and acquired lesions that might disrupt the axonal organization.
Practical applications of DTI and tractography in epilepsy include precise delineation of white matter tracts in the brain, especially in identifi- cation of eloquent white matter tracts, such as the arcuate fasciculus adjacent to neoplasms or epileptogenic regions [9, 10]. Another area where tractography has significant implications is in mapping of optic radiations during pre-surgical planning of anterior temporal lobe resection pro- cedures. Here, pre-operative tractography can demonstrate the anterior extent of Meyer’s loop, which is variable between people and cannot be visualized on traditional MRI studies. Thus, one can predict the extent of visual field defects that might happen post-surgery. DTI has relatively poor spatial resolution and is less sensitive to injury at crossing fibers and close to gray–white matter junction [11, 12].
MRS
In the field of epilepsy, MRS acts as a valuable tool by complementing MRI. While conventional MRI is very helpful in studying anatomy, MRS offers a noninvasive means to determine the biochemical and metabolic characteristics of the tissue of interest. Though both are based on similar principles, MRS uses signal from protons to estimate the concentration of metabolites, chiefly N-acetyl aspartate (NAA), choline (Cho), creatine (Cr), and lactate in brain tissue. 1H spectroscopy, most widely used, is useful for assessment of markers of neuronal loss such as NAA, products of anaerobic metabolism such as lactic acid, and direct measures of primary excitatory and inhibitory neurotransmitters. 31P spectroscopy is directed toward the characteri- zation of the bio energetic status of the tissue of interest phosphocreatine (PCr), adenosine triphosphate (ATP), and phosphoinositol (Pi).
Applications of MRS in epilepsy imaging are widespread. In patients with hippocampal scle- rosis, the MRS shows evidence of neuronal dys- function such as decreased NAA and decreased NAA/Cho and NAA/Cr ratios and decreased myoinositol (MI) in ipsilateral temporal lobe and increased lipid and lactate soon after a seizure [13]. Conventionally, MRS has been used in characterization and differentiation of masses that appear equivocal on MRI. MRS can help differ- entiate between dysplastic versus neoplastic masses, recurrent brain neoplasm versus radiation injury, or between an abscess versus a tumor [14]. Further, MRS has also been used to screen for inborn errors of metabolism such as Canavan’s disease and creatine deficiency. There is a typi- cally decreased NAA/Cr ratio in patients with dysplastic cortex as in hemimegalencephaly. Interestingly, multiple studies have now validated MRS as a tool in identifying the seizure focus, thus making it useful in the evaluation of both focal and generalized epilepsy. Work by numer- ous groups has shown specific metabolic abnor- malities that are confined to the seizure zone [15, 16]. Inter-ictal changes include increased inor- ganic phosphate (Pi), increased pH, and decreased phosphomonoesters, a decreased PCr/Pi ratio together with a decrease in NAA (reduction of 22% ipsilateral to seizure focus). Also, an increase in lactic acid is usually seen post-ictally. While MRS has been reported to have localizing value by numerous groups (65–96% chances of lateralization in TLE by proton MRS and 65–75% value in TLE by phosphorus MRS), research is still ongoing to determine the value of MRS in localization of the epileptogenic focus.
Functional MRI
Functional MRI is a noninvasive imaging tech- nique that has grown in popularity over the past two decades. Its role has been increasingly rec- ognized in clinical practice to lateralize language and motor functions. The intracarotid sodium amobarbital angiographic procedure (the “Wada”) and intraoperative cortical stimulation mapping procedures are still the clinical gold standards to localize the epileptogenic zone and map the functional areas of the brain. However, these mapping techniques have their own limita- tions due to afterdischarges and seizures produced by stimulation. The spatial resolution of fMRI is great, but the temporal resolution is suboptimal for dissecting out the different functional areas of the brain that are related to a particular task.
Fig. 21.3 Coronal FLAIR (a), T2-weighted (b) and 3D T1-weighted demonstrate bilateral hippocampal body hyperintensity, laminar blurring, and volume loss, respectively. Findings are consistent with bilateral hippocampal sclerosis
Fig. 21.4 Oblique coronal T2 demonstrates obvious volume loss and laminar blurring of the right hippocampal head (arrow, panel a) consistent with right hippocampal sclerosis and right fornix atrophy (b). There is a small
gray matter heterotopia in the lateral wall of the right lateral ventricle, best seen on the coronal double-inversion recovery image (arrow, panel c) compared to companion T2 and T1-weighted MRI (b and d)
Fig. 21.5 Axial and coronal T2-weighted MRI, and coronal FLAIR demonstrate a small encephalocele that involves a focal portion of the fusiform gyrus cortex extending into the right foramen ovale (arrows). The MRI
abnormality is not always associated with seizures, but should be considered suspicious. In this case, the finding was concordant with semiology and EEG
Fig. 21.6 Coronal FLAIR MRI (a) and serial axial FLAIR MRI of the frontal lobes (b) demonstrating subtle gray–white blurring and FLAIR hyperintensity in the left
anterior cingulate gyrus and adjacent left medial frontal gyrus (arrows) from a pathologically proven cortical dysplasia
Fig. 21.7 a Coronal 3D T1-weighted (A) and axial FLAIR MRI (B) demonstrate broad, simplified gyri with relatively shallow sulci in the bifrontal regions compared to the temporal and parietal regions consistent with pachygyria. b Coronal and axial FLAIR (A and B), sagittal, and axial post-contrast 3D T1 (C and D) MRI
show abnormal cortex that appears thickened extending from the posterior right Sylvian fissure (arrow). The fissure is lengthened with a vertical orientation toward the vertex (arrow, panel C). Findings consistent with unilat- eral polymicrogyria
Classification of FCD
Fig. 21.8 MRI brain axial T2-weighted image shows lissencephaly agyria and smooth brain. Especially poste- riorly in a patient with LIS1 mutation
Fig. 21.9 CT brain axial image shows a cleft in the left hemisphere consistent with schizencephaly
Meningioma
Isointense on T1 and T2; homogeneous enhancement with Gd, extra-axial, dural tail, and CSF cleft sign
Ganglioma
Cyst with enhancing mural nodule/solid; calcifications in *50%
Fig. 21.10 Axial FLAIR (a), T2-weighted (b), pre-contrast (c), and post-contrast T1-weighted MRI (d) demonstrating solid and cystic mass in the left posteromedial temporal lobe with focal areas of contrast enhancement most consistent with ganglioglioma. CT also often demonstrates focal calcification
Fig. 21.11 Axial T2- and T1-weighted MRI (a and b) demonstrate bubbly T2 bright lesion in the left superior frontal gyrus with minimal mass effect that does not enhance (contrast not shown). In a patient with seizures, these findings are most consistent with dysembyroblastic neuroepithelial tumor (DNET)
Fig. 21.12 Axial pre-contrast (a) and post-contrast T1-weighted MRI (b) demonstrate an extra-axial mass overlying the right frontal operculum that is isointense to gray matter and shows homogeneous enhancement with dural tail consistent with meningioma
Fig. 21.13 MRI brain post-Gd T1-weighted image (a) showing ring enhancement in the right thalamus and deep gray structures with associated mass effect, midline shift, and obstructive hydrocephalus. Pathology was onsistent with glioblastoma multiforme. Perfusion MRI (b) shows increased regional cerebral blood flow at the tumor margins
Fig. 21.14 Coronal T2-weighted (a) and sagittal T1-weighted MRI (b) demonstrating ectopic gray matter along the wall of the 3rd ventricle (arrow) in adolescent patient with gelastic seizures. Findings support diagnosis of hypothalamic hamartoma
Fig. 21.16 MRI brain axial T1-weighted image (a) shows right mesial frontal arteriovenous malformation. Post-Gd T1-weighted (b) reveals enlarged draining vein
Fig. 21.17 Serial coronal FLAIR images of the left temporal lobe in an adult patient with autoimmune encephalitis. Between 2010 and 2015, there was progressive volume loss and denudation of the overlying cortex (arrow). Similar focal lobar volume loss can happen in Rasmussen encephalitis.
Fig. 21.18 Axial FLAIR (a, b) demonstrates focal T2 hyperintense masses in the cortex and subcortical white matter of the basal left temporal lobe and left inferior parietal lobule consistent with tubers. Axial pre-contrast T1 and coronal T2-weighted MRI demonstrate multiple ependymal nodules along the bilateral caudo-thalamic grooves. These lesions demonstrate subtle T1 hyperin- tensity (arrow) attributed to calcification that can be seen on CT (not shown). Video EEG suggested the adjacent tubers in the posterior basal left temporal lobe were responsible for the majority of seizures in this patient with tuberous sclerosis. Axial CT slice (c) demonstrating cortical tram-track calcification throughout most of the left cerebral hemisphere consistent with pial angiomato- sis. There is a volume loss, but with relative sparing of the left frontal operculum. Findings are consistent with Sturge Weber syndrome
Fig. 21.19 Axial FLAIR (a) and coronal 3D T1-weighted MRI
(b) demonstrating subtle encephalomalacia in the anterior right superior temporal gyrus (arrows) attributed to remote trauma in a patient with seizures and history of high-speed motor vehicle accident
Common PET ligands
Fig. 21.20 Simultaneous PET-MRI technology in a temporal lobe epilepsy patient. Coronal FLAIR demon- strates volume loss and hyperintensity in the left hippocampal head (arrow, panel a). Coronal FDG demon- strates hypometabolism that involves both medial and lateral left temporal lobe (arrow, panel b). Blended images combining MRI and FDG data can also be obtained to assist visual detection of abnormalities (here, FLAIR with color FDG map superimposed)
Fig. 21.21 Advanced imaging workup in patient with MRI-negative left temporal lobe epilepsy. Coronal MPRAGE with interictal MEG dipole cluster in the left middle temporal gyrus (blue arrow, panel a) was concordant with semiology and EEG. Task-based functional MRI of the patient performing word generation task demonstrates left language dominance (b). A re- gion-of-interest of BOLD signal in the planum temporale (presumably Wernicke’s area) demonstrated a strong correlation with performance of the task (arrow, panel c)
DWI and ADC characteristics in different disorders
