Chapter 20 The Surgery of Temporal Lobe Epilepsy II—Surgical Complications and Long-Term Adverse Effects
Earlier in this book the effect of temporal lobectomy on seizure frequency (the “seizure outcome”) was outlined. There is no doubt whatsoever that this operation, when carried out for epilepsy, can have a profoundly beneficial effect by reducing or eliminating seizures and by raising the patient’s quality of life. Indeed, the operation can transform a person handicapped by continuing seizures into a normally and fully functioning member of society.
Of all therapies for epilepsy, the positive effect of surgery can be the most impressive. However, its success should not lead one to ignore the potential downsides, and there are complications and adverse outcomes of temporal lobe surgery, which are often not stressed sufficiently. Like all treatment, the decision of whether or not to undergo surgical therapy depends on a balance between risk and benefit, and it is important that all patients undergoing temporal lobe surgery are given enough information to make an informed decision on both aspects of the risk–benefit equation. The decision to undergo surgery must always be an individual choice, and in similar situations, different individual patients will make different choices. A knowledge of the risks of surgery is essential and should be communicated accurately to the individual. This is particularly important in temporal lobe epilepsy surgery, where the surgery is elective, the seizures that have the best outcome (mild partial seizures without secondary generalization) are often not the cause of great disability themselves, and there are various alternative therapeutic options. On the latter point, it has been recently shown that the introduction of new medications, even in patients with chronic epilepsy unresponsive to previous drugs, has a significant chance of long-term benefit.1,2 Furthermore, medical options increase over time; for instance, at the present time, a series of novel drug therapies in the drug development pipeline carry significant promise.
This chapter outlines the adverse outcomes that must be considered when deciding on temporal lobe surgical therapy. These can be divided into four main categories: (1) operative complications, (2) neurological complications, (3) effects on memory functioning, and (4) psychiatric and other cognitive functions’ adverse effects.
The mortality rate of epilepsy surgery is usually quoted to lie between 0.5% and 1.0%. In the Kings/Maudsley series between 1976–2001, there were 451 temporal lobe resections with 2 perioperative deaths (0.44%), due cerebral edema of uncertain cause (1 case) and cerebral hemorrhage 2 weeks after the operation due to anticoagulation for a DVT (1 case).3 In the large series from Montreal, a recent review reported that there were no deaths in 526 operations.4 In the current authors’ analysis of 737 cases of temporal lobe surgery in the literature (see Chapter 19), there were two postoperative deaths (wound infection with osteomyelitis)5 and six late deaths, three seizure related6,7 and in three cases no details were given.5,8 It should not be forgotten, when considering the mortality of surgery, that the death rate in epilepsy (with active seizures) is two to three times increased in people with epilepsy, and the rate of death of patients on surgical waiting lists for epilepsy surgery is about 1 case per 100 per year.9 The death rate of epilepsy after surgery has been found to be reduced, especially if seizures are controlled, in some studies10 but not in others.11 The risk of death due to surgery is clearly dependent on the underlying etiology. Operations for mesial temporal sclerosis or benign tumors, for instance, have very low mortality, whereas there is a greater risk for operations on vascular lesions and particularly arteriovenous malformations (AVMs). In two large series of surgically treated AVM, although at all cerebral sites and with any presentation, the operative mortality was 11%.12,13
Infection following epilepsy surgery occurs in most series at a rate below 1%, although is higher where intracranial recordings are carried out. In one series of 122 implantation procedures, operative complications included the need for repeated surgery for additional electrode placement (5.7%); wound infection (2.4%); cerebrospinal fluid leak (1.6%); and subdural hematoma, symptomatic pneumocephalus, bone flap osteomyelitis, and strip electrode fracture requiring operative retrieval (one patient [0.8%] each). There were four cases of transient neurological deficit (3.3%) and no permanent deficit or death associated with invasive monitoring.14 In Olivier’s series of 560 patients, meningitis was reported once, subdural abscess twice, and scalp infections five times. Hemorrhage along the track of the recording electrodes is another hazard, with a risk usually quoted at 1%.14
Neurological complications following temporal lobe surgery are well summarized by Polkey (2004) (Table 20-1).15 A visual field loss—usually an homonymous superior quadrantanopia—is a common sequel of an extensive temporal lobectomy, due to damage to Meyers loop of the geniculocalcarine tract (see Figure 20-1). How common this complication is following more restricted operations is unclear but is certainly underestimated. Manji and Plant assessed 24 patients following temporal lobe surgery for epilepsy using sensitive methods and found a field deficit in 13 (54%).16 A proportion of these deficits might have been missed on more routine evaluation. In this series, details of the extent of resection were not given, but the surgery was carried out by experienced epilepsy surgeons using orthodox means.
|III nerve palsy||<1%|
1987 figures from Van Buren 1993; 1993 figures from Pilcher 1993 (cited by Polkey 2004).
Figure 20–1 Tractography of the visual tracts showing the visual pathways visualized in green. Note: This extraordinary image in a patient with full-field stimulation, was produced by Professor Mark Cook in Melbourne using what is probably the most advanced MRI software globally for tractography. I am indebted to Professor Cook for permission to use this image.
Penfield was the first to report a transient hemipareisis in 5% of patients undergoing temporal lobectomy. The rate of hemipareisis depends on etiology and is now lower, between 1 and 3%, in patients following temporal lobe surgery for mesial temporal sclerosis. Hemipareisis is usually due to interference with perforating vessels supplying the internal capsule or the anterior choroidal or even posterior choroidal artery, or in the case of arteriovenous malformations, to hemorrhage or infarction. A 2% rate of mild but permanent hemipareisis due to anterior choroidal artery damage was reported in the recent series by Sindou et al.17 Diencephalic infarction occasionally occurs with hemianopia, ophthalmoplegia, and speech disturbance in addition to hemipareisis or hemiplegia. A higher risk of hemiparesis is conferred in surgery on tumors or vascular malformations, and also in operations on the insula region, due to the vacular palisade overlying the insula. Clearly, the surgical technique and the experience of the surgical team are also important factors, and the rate of vascular complications is generally higher the more inexperienced the surgeon—a major reason for the current recommendation that epilepsy surgery be carried out in appropriate centers.
Cranial nerve palsy has been reported (in less than 1% of cases). The third nerve is the most vulnerable but fourth and sixth nerve palsies also occur. A facial palsy can occur and is usually transient. Facial pain is another complication, possibly more common, which can be persistent and may be due to the section of superficial nerves during the craniotomy.
Transient dysphasia in a dominant hemisphere temporal resection is not uncommon, especially if grids or strips are inserted for electrocorticography (ECoG) or mapping purposes. The dysphasia is usually maximal 1 to 3 days postoperatively and usually largely resolves within a week, although minor speech disturbance may persist for months. Permanent dysphasia may occur when a dominant temporal lobectomy is extended too far posteriorly or when a lesionectomy is carried out in or under the posterior cortex. The anatomical location of language function in patients with temporal lobe epilepsy can be extremely variable, and dysphasia may occur even if the resection avoids the conventional anatomical locations of language. The risk can be reduced but not eliminated by preoperative language mapping. It is now usual not to extend the resection of a dominant middle or superior temporal gyrus back beyond 3.5 cm (in contrast to Penfield’s original 4.5 cm resection), and this precaution significantly reduces the risk of dysphasia. More posterior or basal resections should be conducted only in units with considerable experience and usually only with preoperative language mapping. Unfortunately, at present, preoperative fMRI is not sufficiently accurate to delineate language areas safely enough, and surgeons should not take the lack of language activation in any particular location on fMRI as a sign that there is no risk of postoperative dysphasia as this location is resected.
A range of other complications has been recorded. Complications include distant hemorrhage in the cerebellum, pneumocephalus, hematoma, meningitis (2% in the series of Sindou et al.17), acute hydrocephalus requiring shunt insertion (2% in the series of Sindou et al.17), scalp infections, and wound pain. It has also to be noted that most of the large series report complication rates retrospectively, and most also depend on surgical notes. Almost certainly this will lead to an underestimation of the true complication rate, but the extent of this underestimate is unclear. The published figures, however, should certainly be considered minimum estimates.
It is probably not too much of an exaggeration to say that the neural substrates and mechanisms of human memory remain almost totally obscure, despite intense basic and clinical research in the past few decades. Indeed, much of what little has been discovered about the anatomical basis of memory is from operations on the temporal lobes in epilepsy. It has been recognized, at least from the time of Penfield, that the hippocampus is intimately involved in memory functions, but that a unilateral resection is often possible without much disturbance of memory, whereas a bilateral resection carries a significant risk for severe amnesia. Why this is and how the brain encodes or stores memories is, however, otherwise largely speculative—and although Nobel prizes have been won in this area, it has to be admitted that what knowledge there is has little utility from the clinical or practical points of view.
The effects of bilateral hippocampal and temporal resection are most famously recorded in great detail in the case of HM, whose severe permanent antegrade amnesia has been the subject of intensive study.18 Bilateral resections were then largely abandoned, but in the 1960s to 1980s, most of the work on postoperative patients (after unilateral or bilateral resections) was concerned with psychological theories of memory, which has been of little clinical or practical value. More recent work has taken a more prosaic and pragmatic emphasis on psychometric testing to identify tests that will predict the surgical outcome for memory after unilateral resection.
About one-third of patients currently suffer memory decline following temporal lobe resection. About 15% experience a slight improvement in memory; these patients are more likely to be seizure free, and the improvement is probably due to the removal of the adverse effects of seizures on memory.19 A number of factors are now generally accepted to be predictive of memory outcome and are useful considerations when counseling patients about the risk of temporal lobe surgery to memory (Table 20-2):