Posterior cerebral epilepsy: special considerations

Abstract Surgical treatment for epileptic seizures emanating from the posterior cerebral cortex (occipital, parietal, posterior temporal areas) is less common than for seizures from the anterior temporal and frontal regions. The diagnosis entails integrating the combination of clinical, electrographical, neuropsychological, and imaging studies. Extremely important is the knowledge of the pathways of possible suprasylvian spread anteriorly toward the central sulcus of the frontoparietal cortex (producing focal sensory/motor symptoms) or to the midline, reaching the supplementary motor regions (postural, bilateral asymmetrical limb girdle, focal tonic, vocalization, speech arrest, etc.). There can be infrasylvian spread to the lateral temporal cortex or, very frequently, to the mesial temporal regions such as the hippocampus and amygdala (expressing experiential phenomena and automatisms). For a patient with a single occipital lobe focus suggested by a visual aura or hemianopic field defect, for example, the anterior spread could follow different pathways and gives a clinical and electrographic appearance suggesting multiple focal seizures, thus causing confusion for less informed epileptologists. The problem of anterior spread has been known since the pioneering days of epilepsy surgery by the late Wilder Penfield, Herbert Jasper, and associates at the Montreal Neurological Institute (see case studies in the 1954 text Epilepsy and the Functional Anatomy of the Human Brain) and the extensive metrazol activation studies by Ajmone-Marsan and Ralston [C. Ajmone-Marsan, B.L. Ralston, The Epileptic Seizure: Its Functional Morphology and Diagnostic Significance. A Clinical–Electrographic Analysis of Metrazol-Induced Attacks, Charles C. Thomas, Publisher, Springfield, 1957]. These concepts have been rediscovered and elaborated upon by several investigators. In the past, as emphasized by Penfield, Jasper, and their associates, the epileptic focus was excised along with all or most of the lesion, depending on the proximity to vital cortex such as speech and motor areas. Various lesions, including tumors, cortical dysplasias, gliosis, angioma, and hippocampal sclerosis, can produce an epileptic focus, and the exact mechanism for lesion-induced epileptogenesis is still unknown. In recent years, lesionectomy alone has been performed by some investigators without searching for and excising the epileptogenic focus. These procedures have been enhanced by the development of stereotactic surgery with computer-assisted procedures. With the patient's head fixed in a frame, refined imaging studies can display on a screen three-dimensional views of the brain, vasculature, and lesion. The best results have shown a significant reduction in the number of seizures or even no seizures in about 90% of patients, but longer follow-up is needed. In some reports, patients presented with complex partial seizures, and anterior temporal lobectomy was performed to remove the secondary epileptogenic activity within the hippocampus and amygdala, structures that frequently are the destination for spread from more posterior lesions. To improve seizure control, a second surgical procedure was often necessary to remove the posterior lesion and epileptic surround. At times, intracranial electrode grids and strips were inserted during a previous craniotomy, which meant that some patients had up to three surgical procedures. In planning posterior surgery for epilepsy, it is important to individualize each case rather than follow fixed ideas about surgical management emphasized by each major epilepsy center. The following case serves as an example. While I was temporarily at the University of Washington after retiring from the Mayo Clinic, a neurologist in Spain referred a 16-year-old girl to me. The imaging studies showed a left posterior lesion (occipital, parietal, and posterior temporal). On scalp EEG recordings, a recorded seizure emanated from that area. However, the patient also had complex partial epilepsy (CPE), and interictal EEGs showed anterior temporal spikes as well as temporal intermittent rhythmic delta activity (TIRDA), which has a very high specificity for CPE [Can. J. Neurol. Sci. 16 (1989) 398]. The neuropsychological and intracarotid amobarbital studies for language and memory performed by Dr. Dodrill showed left cerebral dominance for language and no contraindications for surgery. Craniectomy was performed by Dr. George Ojemann. After the eloquent cortex for language and motor function were identified with cortical mapping procedures, electrocorticography was performed. Multicontact strip electrodes recorded epileptiform activity from the hippocampus as well as the TIRDA pattern there. Surgical resection included the left anterior temporal lobe and hippocampus. Most of the gliotic lesion was excised by tunneling from the mesial temporal region toward the lesion, preserving the convexity of the posterior cerebral cortex. This single surgical procedure tailored to the individual patient reduced postoperative morbidity and was successful because after 7 years of follow-up, there is excellent control of seizures. She recently graduated from college, drives an automobile, and has taken an internship in theater as a preliminary step toward employment. This report emphasizes both the primary focus (the posterior lesion) and the possible spread anteriorly to a secondary focus. On the basis of the clinical, imaging, electrographical, neuropsychological, and amobarbital findings, the surgical treatment should be individualized with the goal of removing, when possible, both the lesion with its primary focus and the secondary focus, optimally during a single craniotomy. “For every complex problem, there is a solution that is simple, neat, and wrong”. H.L. Mencken (1880–1956)