CHAPTER 62 Standard Temporal Lobectomy
Historical Background
The standard temporal lobectomy developed concurrently with the identification of the temporal lobe epilepsy syndrome and the emergence of electroencephalography (EEG) in the 1940s and 1950s. Much of the credit belongs to Penfield and Jasper at the Montreal Neurological Institute (MNI).1 When Herbert Jasper joined the MNI in 1937, he brought the technique of EEG with him. By this time, Penfield and his partner William Cone had been performing surgery for epilepsy since Penfield arrived in 1928. As EEG became more established in the evaluation and diagnosis of focal epilepsy through the work of Jasper and Gibbs, the classification and study of temporal lobe epilepsies was under way. Through the close friendship of Jasper and Penfield, the MNI became a leader in the late 1930s in the surgical treatment of epilepsy. In 1941, Jasper and Kershman proposed a classification of epilepsy based on EEG waves.2 In this report, they described the localization of psychomotor phenomena from within the deep regions of the temporal lobe. Despite increasing awareness of the role of the mesial temporal lobe in these seizures, the lack of understanding about the function of this tissue and the inability of the surgeon to “see” the lesion at the time of resection led to reluctance on Penfield’s part to remove these structures.1 In 1950, Penfield reported his success in anterolateral temporal resections.3 In this series of 68 patients, 10 had partial removal of the uncus, and only 2 had hippocampal resections. EEG abnormalities were recorded from the temporal lobe in this group of patients, but an underlying substrate had not been identified. At the same time, Percival Bailey and Ernest Gibbs reported a series of 25 patients from the University of Illinois program who underwent temporal resection guided by EEG.4 Similar to Penfield’s series, these patients did not have hippocampal resections.
The second phase in the development of the modern surgical strategy to treat temporal lobe seizures took place in the 1950s as the role of the mesial temporal lobe structures in the pathogenesis of the epilepsy became better understood. This occurred as a number of scientists began to study the connections of the mesial temporal lobe to the rest of the brain and through the use of stimulation studies to reproduce seizure semiology in animals and humans.5–8 In 1952, Penfield and Baldwin published a classic monograph describing their technique for anterolateral temporal lobectomy including the hippocampus and amygdala.9 They reported that the most frequent pathologic abnormality in two of three of their cases was an atrophic lesion termed incisural sclerosis. Falconer in a report in 1953 recognized a connection with febrile seizures and introduced a modification allowing for en bloc resection of the hippocampus, which allowed the pathologists to study the tissue.10 With the advent of neuroimaging, modifications to the technique reported by Penfield have been made to address specific pathology seen preoperatively. Despite these modifications, the operation developed and introduced by innovative neurosurgeons in the early 20th century remains one of the most successful operations for the treatment of epilepsy today.
Identification of Surgical Candidates: The Concept of Pharmacoresistance and Medical Intractability
The indications for epilepsy surgery generally include the presence of focal epilepsy resistant to treatment with an adequate trial of anticonvulsant therapy. The precise definition of an adequate anticonvulsant trial is open to interpretation, but a study by Kwan and Brodie produced useful information regarding the efficacy of anticonvulsant therapy in newly diagnosed epilepsy.11 This study suggests that after three medications fail to control seizures, further success is unlikely, and other options should be considered. Consider also the paper by Wiebe and associates, comparing temporal lobectomy to optimal medical therapy in a group of patients with temporal lobe epilepsy.12 In this prospective randomized trial, surgical therapy in combination with medical therapy was far superior to ongoing medical therapy alone. These papers lend credence to the idea that patients with ongoing epilepsy despite a trial with a few anticonvulsants should be expeditiously evaluated for possible epilepsy surgery.
Preoperative Evaluation
Video Electroencephalography Monitoring
The diagnosis and type of epilepsy should be confirmed through prolonged video-scalp EEG monitoring in a dedicated epilepsy monitoring unit (EMU).13 Scalp EEG recording is a noninvasive monitoring technique that can sample extensive areas of the brain to give the best overview of the general distribution of interictal and ictal epileptic activities. It gives an excellent overview of the approximate location and extent of the epileptogenic area. Most epileptic patients with TLE (between 85% and 100%) show epileptiform discharges on their interictal scalp EEG recordings.14,15 Both the localization and pathologic type of the epileptogenic lesion within the temporal lobe affect the scalp localization (and lateralization) of interictal and ictal EEG patterns. In addition, video recordings and analyses permit the characterization of the seizure semiology that may be helpful in the localization and lateralization of the ictal onset zone.
Semiology and Electroencephalography Patterns in Mesial Temporal Lobe Epilepsy Due to Hippocampal Sclerosis or Mesial Temporal Mass Lesions (Neoplasms or Cavernomas)
Hippocampal sclerosis is one of the most common pathologic substrates in patients with TLE. Patients with mesial TLE show a characteristic electroclinical syndrome that typically consists of a rising abdominal sensation aura that may be followed by mouth and hand automatisms and possible ictal contralateral hand dystonic posturing. The presence of postictal speech difficulties may help in lateralizing the seizure onset zone to the dominant hemisphere for language. Patients with TLE due to hippocampal sclerosis show slowing in the ipsilateral temporal electrodes and interictal epileptic sharp waves that are usually mapped to the anterior temporal lobe.16 In addition, in less than 50% of these patients, sharp waves mapped to the contralateral anterior temporal lobe electrodes are found. Patients with mesial TLE due to amygdalohippocampal tumors or cavernomas are more likely to exhibit less localized sharp waves and less likely to have contralateral epileptiform abnormalities.
Semiology and Electroencephalography Patterns in Neocortical Temporal Lobe Epilepsy Due to Cortical Dysplasia or Temporal Mass Lesions (Neoplasms or Cavernomas)
Imaging
Magnetic resonance imaging (MRI) of the brain, fluorodeoxyglucose (FDG) positron emission tomography (PET), ictal radionuclide blood flow studies (e.g., single-photon emission computed tomography [SPECT]), and functional MRI are the main neuroimaging tests that are used in the preoperative evaluation of patients with pharmacoresistant epilepsy that is suspected to arise from the temporal lobe. The typical MRI sequence involves thin-slice coronal T1-weighted imaging, fluid-attenuated inversion recovery (FLAIR) coronal sequences, and T2-weighted coronal sequences. Typical findings of mesial temporal sclerosis include atrophy of the affected hippocampus and increased signal intensity on the FLAIR and T2 sequences. One must always carefully study the remainder of the temporal lobe because dual pathology occurs in about 10% to 30% of mesial temporal sclerosis cases.17–19 Findings suggestive of dual pathology include blurring of the temporal pole gray-white interface or enlargement or distortion of the cortical ribbon. These are important findings that may influence the choice of surgical procedure.
The metabolism of the brain is studied with the use of interictal PET scanning. In this procedure, a radionuclide (18FDG) is injected, and computed tomography (CT) scanning is performed. This test gives the clinician a picture of how the brain takes up glucose. Originally designed for TLE, the test is said to be 70% specific when hypometabolism is seen in one of the temporal lobes.20
The localization of language is now possible by noninvasive functional MRI, which is slowly replacing the more invasive intracarotid sodium amobarbital testing. One possible advantage of the latter is the ability to test memory function at the same time, although recent reports suggest that cognitive functional MRI may offer an important, noninvasive, preoperative assessment of hippocampal memory function.21–23
Neuropsychological and Psychosocial Preoperative Evaluations
Neuropsychological testing and psychosocial and psychiatric evaluations are also completed during the initial work-up. Neuropsychological information is important because the temporal lobes play a role in emotion, language, and memory. In fact, patients with TLE are often aware of significant progressive memory and naming problems that lead them to pursue surgical intervention. Despite many years of experience in temporal lobe surgery, our understanding of function and prediction of neuropsychological deficits is still somewhat poor. During the preoperative evaluation of the TLE patient, it is important to gain a baseline measure of overall intellectual functioning as well as verbal and visual spatial memory scores. This is accomplished with standardized neuropsychological testing, which is then repeated 6 months after surgery. Preoperative and postoperative deficits in short-term memory and naming are common in patients with dominant (language-localized) TLE, and the risk for worsening must be discussed with the patient. This risk is dependent on baseline preoperative functioning and the individual substrate of the epilepsy (e.g., presence of mesial temporal sclerosis).24–26
Surgical Decision Making
For the TLE patient, decisions revolve around localizing the epilepsy to the lateral or mesial temporal lobe, the presence and nature of the epileptic lesion, and the presence of language or important short-term memory deficits. For the patient undergoing a standard temporal lobectomy, the epilepsy should be localized to the anteromesial temporal lobe, and ideally a well-defined lesion should be present (mesial temporal sclerosis, malformation of cortical development, neoplasm, cavernoma). The planned posterior extent of resection should not encroach on possible neocortical temporal lobe language areas. If the dominant temporal lobe is involved, a baseline memory or naming deficit in the presence of mesial temporal sclerosis would support the conclusion that the correct brain site was targeted, and the risk for causing further neurological deficits would be acceptably low.27,28
The anatomy of the temporal lobe deserves a brief discussion at this point. The temporal lobe has well-defined anterior, lateral, basal, and mesial surfaces. The posterior boundary is arbitrary, having no obvious anatomic demarcation separating it from the parietal area. The temporal lobe is made up of five gyri and their corresponding sulci. The lateral surface lies below the sylvian fissure and extends to the floor of the middle cranial fossa. The gyri from top to bottom include the superior temporal gyrus (T1), the middle temporal gyrus (T2), and the inferior temporal gyrus (T3), which often extends onto the basal surface. The basal surface includes the inferior temporal gyrus (T3), the fusiform gyrus, and the parahippocampal gyrus. The mesial surface includes the amygdala and the parahippocampal gyrus, including the uncus. The collateral sulcus separates the fusiform and parahippocampal gyri and serves as an important reference to locate the temporal horn of the ventricle. Within the temporal horn, important anatomic structures include the inferior choroidal point (anterior choroidal artery enters the choroid plexus here), the hippocampus occupying the mesiobasal portion of the ventricle, the fornix, the choroid plexus, the choroidal fissure, and the amygdala in the anterior-superior-medial portion of the ventricle. The reader is referred to an excellent series of articles describing in detail the temporal lobe anatomy.29
Functional anatomy in the temporal lobe includes comprehensive language cortex in the dominant temporal lobe, visual field fibers (Meyer’s loop) subserving the contralateral upper quadrantic visual field information, and potential important memory and naming centers. The anatomy of language cortex in the temporal lobe can be quite variable.30,31 Cortical stimulation testing can be performed to further identify and protect lateral language cortex when posterior temporal lobe resections are anticipated on the dominant side. This can be done either intraoperatively with the patient awake or extraoperatively with implanted electrodes. After the language cortex has been identified, the temporal resection can be tailored to the patient’s individual anatomy. The standard temporal lobectomy is designed to avoid temporal lobe cortical language sites by limiting the resection of the superior temporal gyrus to 3 to 4.5 cm from the anterior temporal pole. There is some controversy as to whether even this practice is safe, and some centers advocate leaving the entire superior temporal gyrus in place. This is based on language-stimulation data suggesting the presence of language sites in the anterior 3 cm of the superior temporal gyrus in a small percentage of patients.30 Of course, these sites were not resected, and thus it is difficult to know whether they were essential language sites. Other “nonessential” language sites in the temporal lobe have been demonstrated through cortical stimulation followed by resection.32 These sites were located in the basal temporal lobe by direct cortical stimulation but left no permanent language deficit after they were resected. Insufficient data, however, are available from the limited numbers of patients reported to conclude with certainty that no patient will develop a permanent language deficit after resection of a basal temporal language site.
Visual field fibers are also located in the temporal lobe as they extend forward from the lateral geniculate body before turning posterior on their way to calcarine cortex. These fibers are located unpredictably in the roof of the temporal horn, and standard temporal lobe resections cause injury to this fiber tract in as many as 50% of cases.33 This leads to the “pie in the sky” visual field deficit with loss of peripheral vision in the opposite upper quadrant. In most cases, the visual field defect noted with careful perimetry testing is not clinically significant.
Surgical Technique
When the decision has been made to perform a standard temporal lobectomy, the technique varies little from patient to patient. The word standard implies a reproducible operation from patient to patient and even surgeon to surgeon. It is best used to treat the “standard” syndrome of mesial TLE consisting of reproducible EEG, MRI, and seizure semiology elements. The targets of this operation are the mesial temporal lobe structures that are “sclerotic”: the parahippocampus, hippocampus, and amygdala. The exact posterior extent of resection of the hippocampus to improve outcomes is unknown, but at least one prospective trial correlated improved outcome with more aggressive resection of the hippocampus.34