Fig. 5.57  Callosotomy via laser ablation. Coronal T2-weighted MRI shows the ablation zone with concentric areas of different signal characteristics in the right aspect of the corpus callosum body (arrow). Several other lesions were created along the corpus callosum

5.3.14\ Anterior Temporal Lobectomy

5.3.14.1\ Discussion

Anterior temporal lobectomy is performed for intractable seizures, particularly those caused by mesial temporal sclerosis. Varying degrees of temporal lobe resection can be performed, and a balance between minimizing the risk of postoperative deficits versus maximizing the likelihood of seizure control is sought. In general, the length of the resection is up to 4 cm in the dominant hemisphere and up to 6 cm in the nondominant hemisphere (Figs. 5.58 and 5.59).

There are certain imaging findings that can be encountered following temporal lobectomy. For example, increased enhancement of the choroid plexus has been reported in over 80% of cases of temporal lobectomies performed for seizure treatment within the first week of surgery. The pattern of enhancement is sometimes nodular or mass-like and can be mistaken for more serious

pathology (Fig. 5.60). Concomitant enlargement of the choroid plexus occurs in the majority of cases, likely secondary to reactive hyperemia. An enlarged choroid plexus can also herniate into the surgical defect in the floor of the lateral ventricle temporal horn or atrium. Over time, gliosis forms along the edges of the resection cavity, which appears as increased signal and parenchymal volume loss (Fig. 5.61). Gliosis is commonly encountered and does not appear to be a signifi-

cant mechanism of recurrent epilepsy in patients with a seizure-free period after surgery. In addition, decreased fractional anisotropy is frequently observed ipsilateral to the surgery (Fig. 5.62). The decrease is especially pronounced among patients with postoperative visual field deficits. Due to the course of the posterior cerebral artery adjacent to the medial margin of the anterior temporal lobectomy, the vessel is potentially at risk of injury and consequent infarction (Fig. 5.63).

Fig. 5.58  Dominant hemisphere anterior temporal lobectomy. Axial T2-weighted MRI shows a left anterior temporal lobe surgical defect measures 4.0 cm in the anteroposterior dimension

Fig. 5.59  Nondominant hemisphere anterior temporal lobectomy. Axial T2-weighted MRI shows a right anterior temporal lobe surgical defect that measures 6.0 cm in the anteroposterior dimension

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a

b

Fig. 5.60  Choroid plexus changes. Initial postoperative coronal contrast-enhanced T1-weighted MRI (a) shows right temporal lobectomy with herniation of the choroid plexus, which displays mass-like enhancement (arrow). Coronal contrast-enhanced T1-weighted MRI sequence obtained 3 months later (b) shows decreased swelling and enhancement of the choroid plexus changes (arrow)

D.T. Ginat et al.

Fig. 5.61  Postoperative gliosis. The patient has a history of mesial temporal sclerosis. Preoperative axial FLAIR image (a) shows increased signal and decreased size of

the left hippocampus (arrow). Postoperative axial FLAIR image (b) shows new high signal and volume loss along the left anterior temporal lobectomy margins (encircled)

Fig. 5.63  Posterior cerebral artery territory infarction. Axial FLAIR image (a) shows evidence of recent right anterior temporal lobectomy and high signal in the right

medial occipital lobe (arrow). ADC map (b) shows corresponding restricted diffusion (arrow)