Imaging of Neuromodulation and Surgical Interventions for Epilepsy

Abstract

About one-third of epilepsy cases are refractory to medical therapy. During the past decades, the availability of surgical epilepsy interventions has substantially increased as therapeutic options for this group of patients. A wide range of surgical interventions and electrophysiologic neuromodulation techniques are available, including lesional resection, lobar resection, thermoablation, disconnection, multiple subpial transections, vagus nerve stimulation, responsive neurostimulation, and deep brain stimulation. The indications and imaging features of potential complications of the newer surgical interventions may not be widely appreciated, particularly if practitioners are not associated with comprehensive epilepsy centers. In this article, we review a wide range of invasive epilepsy treatment modalities with a particular focus on their postoperative imaging findings and complications. A state-of-the-art treatment algorithm provides context for imaging findings by helping the reader understand how a particular invasive treatment decision is made.

FIG 1.

Intractable epilepsy decision tree for surgical intervention. Noninvasive investigations indicate whether a patient is a candidate for surgical resection of unilobar lesions or MTS, or whether an intracranial EEG study is needed for further localization (ie, MCD, diffuse or multifocal lesions, normal MR imaging findings, or discordant investigations). For those with unilobar lesions, surgical treatment is based on whether the functional cortex (defined as verbal memory, sensorimotor cortex, and language regions) is involved, determined by functional electrical stimulation mapping. RNS and possibly LITT are used to treat MTS in those with preserved hippocampal function, as opposed to temporal lobectomy for those with poor hippocampal memory. Nonfocal multifocal or network-onset seizures are treated by RNS, DBS, or VNS. Fxn cortex indicates functional cortex; HC fxn, hippocampal function; MCD, malformation of cortical development; Wada, intracarotid amobarbital testing.

FIG 2.

Postelectrode placement with sagittal MIP (A) from axial CT images (B) demonstrating a subdural electrode grid over an eloquent region (eg, visual-spatial region) and subdural strip and depth electrodes. To determine the exact localization of right temporoparietal seizure onset, we coregistered CT scans to MR images (C) because electrode positions are better identified on CT. A depth electrode is placed into the subependymal heterotopia to assess whether seizures are originating there (arrow).

FIG 3.

Electrode complications in 2 patients include edema (A) and subarachnoid hemorrhage (B), possibly related to vascular injury on FLAIR axial images (arrow points to adjacent electrode). Imaging findings of the electrode tracts (arrow) include hemosiderin on gradient recalled-echo imaging (C) and contrast enhancement on axial T1WI (not shown here).

FIG 4.

Staged functional hemispherectomy. Initial functional hemispherectomy for hemimegalencephaly consisted of left frontal, parietal, and temporal lobe resections and disconnection of most of the rest of the left hemisphere from the contralateral hemisphere and deep gray matter (A). Persistent seizures from the occipital lobe and insula indicated incomplete disconnection (arrows in A, axial T2WI) necessitating further resection of these structures (arrowheads in B, axial T2WI). Hemorrhage and hemosiderosis are complications of larger resections, as seen on axial SWI (C).

FIG 5.

Corpus callosotomy. Disconnection of cerebral hemispheres posteriorly by posterior corpus callosotomy (arrowheads) is shown on sagittal (A) and axial (B) T1WI and coronal T2WI (C). Sagittal images may be inadequate for confirming complete disconnection if the plane of the resection undulates.

FIG 6.

LITT, coronal imaging. Left hippocampal LITT performed in a patient with intractable epilepsy arising from left MTS because of left language dominance. Immediate post-LITT contrast MR imaging (A) shows a catheter (as a central black dot) with surrounding enhancement (black arrowhead) on postcontrast T1W1. The ablated region has enlarged 3 weeks later (B–D). The central zone of coagulative necrosis (white arrow) is hyperintense on precontrast T1WI (B) and hypointense on T2WI (C) signal. These are surrounded by a peripheral zone of necrotizing edema (white arrowhead), which is hypointense on T1WI and hyperintense on T2WI. The peripheral zone is delineated by a rim (black arrow) of signal void on T2WI that enhances on postcontrast imaging (D), defining the ablated area. Vasogenic edema (curved white arrow) can be seen around the ablated region (hyperintense on T2WI and hypointense on precontrast T1WI). Note the focal central CSF intensity signal on B–D from fluid in the laser catheter track.

FIG 7.

FGATIR, ANT localization. An 11-year-old child needing DBS because of bilateral poorly localized focal epilepsy despite left hippocampal sclerosis on MR imaging. ANT (black arrows) can be localized superior to the mammillothalamic track (white arrows), delineated on FGATIR parasagittal (A), axial (B), and coronal (C) images. The FGATIR sequence nulls white matter in this track.

FIG 8.

DBS complications in a patient without epilepsy. Left foot weakness and dysarthria occurred 3 months after bilateral DBS for refractory essential tremor. Coronal T2 FLAIR image demonstrates a nonhemorrhagic cyst with vasogenic edema surrounding the right electrode and no restricted diffusion or enhancement to suggest infection. This rare inflammatory DBS electrode complication was treated with steroids, resulting in regression of the cyst and vasogenic edema 7 weeks later (not shown here).