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Seizures after epilepsy surgery
Epilepsy Research 56 (2003) 101–104
Seizures after epilepsy surgery夽 C. Drees, K. Chapman, Hans O. Lüders∗ Department of Neurology, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA Received 20 September 2003; received in revised form 4 October 2003; accepted 5 October 2003
Abstract This article reviews types and prognostic significance of seizures that occur after epilepsy surgery, so-called postsurgical seizures. © 2003 Published by Elsevier B.V. Keywords: Epilepsy; Surgery; Seizures
1. Introduction Epilepsy surgery is a standard treatment for intractable focal epilepsy. Seizure freedom after resection varies based on location and type of underlying pathology. While patients with temporal lobe epilepsy and discrete lesions have a very good outcome, i.e.— seizure freedom in 60 to >90% of patients (Berkovic et al., 1995; Engel, 1996; Salanova et al., 1999; Wiebe et al., 2001), epilepsy surgery in other brain regions is less successful (Berkovic et al., 1995; Malla et al., 1998; Park et al., 2002; Tigaran et al., 2003; Wingkun et al., 1991). In patients, in whom surgery fails, seizures usually recur within 6–12 months after surgery (Falconer and Serafetinides, 1963; Lüders et al., 1994; Malla et al., 1998; Park et al., 2002; Wingkun et al., 1991). This review will discuss the
夽 Summary of a presentation at the International Spring Epilepsy Research Conference, Georgetown, Cayman Islands, April 26–May 3, 2003. ∗ Corresponding author. Tel.: +1-216-444-5507; fax: +1-216-444-0230. E-mail address: [email protected] (H.O. Lüders). URL: http://www.clevelandclinic.org/neurology.
0920-1211/$ – see front matter © 2003 Published by Elsevier B.V. doi:10.1016/j.eplepsyres.2003.10.002
different types of seizures that occur after epilepsy surgery. Seizure control at 6 months was found to be a good predictor of outcome (Lüders et al., 1994), though traditionally most authors report outcome after 2 years of follow-up (Engel, 1987; Falconer and Serafetinides, 1963; Salanova et al., 1999). Long-term observations, however, document that seizure recurrence continues to increase progressively with longer follow-up (Engel, 1987; Falconer and Serafetinides, 1963; Lüders et al., 1994; Paillas et al., 1983; Salanova et al., 1999). 2. Postsurgical seizures Following epilepsy surgery, three types of seizures are distinguished: - Habitual seizures, - Non-habitual seizures, - Neighborhood seizures. 2.1. Habitual seizures Habitual seizures are defined as seizures that have a semiology which is identical to the presurgical
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seizures. In studies that recorded actual seizure semiology, they are the most common seizure type: Wingkun 74%, Park 70% (Park et al., 2002; Wingkun et al., 1991). Habitual seizures are thought to recur because of an incomplete or inadequate resection of the epileptogenic zone or maturing foci in close proximity to the previous epileptogenic zone producing a similar clinical ictal expression (Lüders et al., 1994; Paillas et al., 1983; Salanova et al., 1999; Wingkun et al., 1991). In these patients, surface ictal EEG still tends to point to the same seizure origin. However, the EEG pattern tends to vary as compared to the presurgical ictal EEG, likely due to the postsurgical skull defect and removed tissue. Habitual seizures may occur immediately after surgery, or within the following months and years. Usually, they recur within the first year (Falconer and Serafetinides, 1963; Park et al., 2002; Salanova et al., 1999; Wingkun et al., 1991). Rarely, patients have a recurrence of habitual seizures after a prolonged seizure-free period which may last for more than 5 or 10 years (Berkovic et al., 1995; Paillas et al., 1983; Salanova et al., 1999; Wingkun et al., 1991). Recurrences of habitual seizures within the first year are more likely to become persistent and intractable (Wingkun et al., 1991), however, after the first year and late recurrences after more than a decade are easily treated with medication and not likely to become refractory to medication (Falconer and Serafetinides, 1963; Paillas et al., 1983; Wingkun et al., 1991). The reverse phenomenon is called “running down” and implies the gradual disappearance of habitual seizures. The term was introduced by Rasmussen and is seen in 14% of patients 2–10 years after epilepsy surgery (Rasmussen, 1983; Salanova et al., 1999). This may represent the natural evolution of the epilepsy, possibly promoted by surgical resection of a significant portion of the epileptogenic zone. One study (Salanova et al., 1996) found that patients who were seizure free postoperatively had smaller epileptogenic areas compared to those who showed a “running down” phenomenon. The authors suggested that the remaining epileptogenic area has a higher threshold for seizure generation and eventually is insufficient to cause clinical seizures. The reason for this to occur is unclear, but one may speculate that this occurs due to maturing of inhibitory pathways or death of excitatory connections.
2.2. Non-habitual seizures In some instances, seizure semiology changes postsurgically from habitual seizures to a new clinical type. There are different mechanisms that may lead to non-habitual postsurgical seizures: (a) Resection of the presurgical symptomatogenic zone with persistence of the epileptogenic zone can alter seizure semiology. For example, surgery for a patient with right foot clonic seizures may include resection of the primary motor (M1) foot area and postsurgically the patient might continue to have right arm clonic seizures. (b) Partial resection of the epileptogenic zone or of selected essential seizure-propagating pathways, which were defining the presurgical seizure semiology, may change the clinical picture. Seizures may then propagate through different pathways (Spencer, 1988). This mechanism may be responsible for the frequent occurrence of postsurgical auras which tend not to evolve into seizures with motor manifestation or loss of consciousness even when antiepileptic medication is withdrawn (Fried et al., 1995; Malla et al., 1998). This is particularly frequent in patients with temporal lobe epilepsy who postsurgically remain only with typical abdominal auras (Fried et al., 1995; Lund and Spencer, 1992). It is hypothesized that a portion of the epileptogenic zone was not removed and is the origin for seizures that can still reach the insula, generating abdominal auras. However, the usual spread of seizures that produces automatisms and loss of awareness is no longer possible after surgery. A similar mechanism may be responsible, if a temporal lobectomy simplifies or eliminates aura features of residual complex partial seizures in patients who had undergone surgery for temporal lobe epilepsy (Blume and Girvin, 1997). The patients loose the symptomatogenic zone or essential pathways for the generation of their aura and, yet, the network to produce other features of their temporal lobe seizures is intact. A similar phenomenon is the documented relative increase of secondary generalized seizures in patients after temporal lobectomy (Henry et al., 2000). In animal experiments, secondary
C. Drees et al. / Epilepsy Research 56 (2003) 101–104
generalization requires extension of the ictal discharge into the pons and mesencephalon (Gale, 1992). Selected brain regions that connect the amygdalo-hippocamus with the pontomesencephalic regions (rostral piriform cortex (area tempestas), the insula, and the septal area) are usually not resected during a standard temporal lobectomy. It is possible, therefore, that seizures preferentially spread through these pathways after temporal lobectomy giving rise to a relatively higher proportion of secondary generalizations (Henry et al., 2000). (c) Postsurgical maturation or uncovering of additional epileptogenic zones may create a new type of seizures. One of the problems of defining the extent of the epileptogenic zone is the fact that it may be more extensive than the actual seizure onset zone (Lüders and Awad, 1992). Therefore, after surgery the “potentially epileptogenic zone” may give rise to seizures which may have a different semiology when compared to presurgical seizures. On the other hand, we know that maturation of the epileptogenic zone may take an extended period of time before causing seizures. For example, patients with cortical dysplasia, may be seizure free for decades before seizure onset, though their lesions are congenital. Therefore, it is conceivable that a new epileptogenic zone may develop after surgery as part of the maturation process of the epileptogenic focus (Lüders et al., 1994). This new epileptogenic zone may then give rise to postsurgical seizures that have a new semiology. Alternatively, the surgical scar can also mature into a new epileptogenic zone with the same consequences (Falconer and Serafetinides, 1963). 2.3. Neighborhood seizures The term “neighborhood seizure” was coined by Penfield and implies the occurrence of focal simple motor seizures immediately (1–2 weeks) after temporal lobe surgery, often without loss of consciousness (Falconer and Serafetinides, 1963; Penfield and Jasper, 1954). They constitute 20–58% of seizures experienced by patients in the postoperative period: Bengzon 20%, Falconer 45%, Garcia 47%, Malla 21%, Tigaran 58% (Bengzon et al., 1968; Falconer
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and Serafetinides, 1963; Garcia et al., 1991; Malla et al., 1998; Tigaran et al., 2003). It has been assumed that these seizures were due to surgical irritation, edema, hemorrhage, or infection, and may have been facilitated by falling anticonvulsant levels (Falconer and Serafetinides, 1963; Tigaran et al., 2003). However, decreased levels of antiepileptic medication was not a frequent factor in recent studies (Malla et al., 1998; Park et al., 2002; Wingkun et al., 1991). Among other postoperative seizures, “neighborhood seizures” are usually a minority. “Neighborhood seizures” have to be distinguished from “acute postoperative seizures”, a term used by some authors referring to seizures of all types in the first postoperative week (Malla et al., 1998; Park et al., 2002; Tigaran et al., 2003). They are experienced by 20–49% of patients: Malla 20%, Park 25%, Tigaran 26%, Wingkun 29%, Lüders 38%, Garcia 49% (Garcia et al., 1991; Lüders et al., 1994; Malla et al., 1998; Park et al., 2002; Tigaran et al., 2003; Wingkun et al., 1991). The occurrence of postoperative seizures is associated with a worse prognosis (Garcia et al., 1991; Lüders et al., 1994; Malla et al., 1998; Park et al., 2002; Tigaran et al., 2003), but it does not preclude seizure freedom. About one third to one half of patients with seizures in the first postoperative week may still become seizure free: Park 33%, Falconer 42%, Tigaran 47%, Lüders 51% (Falconer and Serafetinides, 1963; Lüders et al., 1994; Park et al., 2002; Tigaran et al., 2003). The classical “neighborhood seizure” has traditionally been regarded as less ominous (Engel, 1987; Penfield and Jasper, 1954). Newer observations seem to support this: Malla et al. (1998) describe that 75% of patients with postoperative focal motor seizures, auras, and generalized tonic–clonic seizures eventually became seizure free. However, acute postoperative seizures that are similar or identical to habitual seizures—which occur in 46–85% of patients with postoperative seizures: Bengzon 46%, Garcia 59%, Wingkun 85% (Bengzon et al., 1968; Garcia et al., 1991; Wingkun et al., 1991)—have a poor prognosis with respect to outcome (Lüders et al., 1994; Malla et al., 1998; Park et al., 2002; Wingkun et al., 1991). Fourteen to forty-four percent of patients with acute postoperative habitual seizures might still become seizure free (Garcia et al., 1991; Malla et al., 1998).
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The majority of studies (Lüders et al., 1994; Malla et al., 1998; Tigaran et al., 2003) investigating acute postoperative seizures found that it made no difference in ultimate outcome whether seizures occurred within the first 24 h or later in the first week. Only one investigation reports that patients with a single seizure or seizures restricted to the first postoperative day were more likely to become seizure free compared to those who had multiple seizures or seizures later in the week (Garcia et al., 1991).
3. Conclusion The great majority of patients who had epilepsy surgery will be either seizure free or have habitual seizures arising from the vicinity of the cortical resection. Habitual seizures may recur up to 10 years after surgery. Occasionally, a “running down” phenomenon, a tapering off of seizures, is observed. “Neighborhood seizures” occurring in the immediate postoperative period are infrequent and have limited prognostic significance, though, in the majority of investigations acute postoperative seizures, particularly early habitual seizures, are associated with an overall worse prognosis regarding seizure outcome. Isolated auras and secondary generalized seizures are relatively more frequent and occurrence of non-habitual seizures can be observed after surgery.
References Bengzon, A.R., Rasmussen, T., Gloor, P., Dussault, J., Stephens, M., 1968. Prognostic factors in the surgical treatment of temporal lobe epileptics. Neurology 18, 717–731. Berkovic, S.F., McIntosh, A.M., Kalnins, R.M., Jackson, G.D., Fabinyi, G.C.A., Brazenor, G.A., Bladin, P.F., Hopper, J., 1995. Preoperative MRI predicts outcome of temporal lobectomy: an actuarial analysis. Neurology 45, 1358–1363. Blume, W.T., Girvin, J.P., 1997. Altered seizure patterns after temporal lobectomy. Epilepsia 38, 1183–1187. Engel Jr., J., 1987. Outcome with respect to epileptic seizures. In: Engel Jr., J. (Ed.), Surgical Treatment of the Epilepsies. Raven Press, New York, pp. 553–571. Engel Jr., J., 1996. Surgery for seizures. New Engl. J. Med. 334, 647–652. Falconer, M., Serafetinides, E., 1963. A follow-up study of surgery in temporal lobe epilepsy. J. Neurol. Neurosurg. Psychiatry 26, 154–165.
Fried, I., Spencer, D.D., Spencer, S.S., 1995. The anatomy of epileptic auras: focal pathology and surgical outcome. J. Neurosurg. 83, 60–66. Gale, K., 1992. Subcortical structures and pathways involved in convulsive seizure generation. J. Clin. Neurophysiol. 9, 264– 277. Garcia, P.A., Barbaro, N.M., Laxer, K.D., 1991. The prognostic value of postoperative seizures following epilepsy surgery. Neurology 41, 1511–1512. Henry, T.R., Drury, I., Schuh, L.A., Ross, D.A., 2000. Increased secondary generalization of partial seizures after temporal lobectomy. Neurology 55, 1812–1817. Lüders, H., Awad, I., 1992. Conceptual considerations. In: Lüders, H. (Ed.), Epilepsy Surgery. Raven Press, New York. Lüders, H., Murphy, D., Awad, I., Wyllie, E., Dinner, D.S., Morris III, H.H., Rothner, A.D., 1994. Quantitative analysis of seizure frequency 1 week and 6, 12, and 24 months after surgery of epilepsy. Epilepsia 35, 1174–1178. Lund, J.S., Spencer, S.S., 1992. An examination of persistent auras in surgically treated epilepsy. Epilepsia 33 (Suppl.), 95. Malla, B.R., O’Brien, T.J., Cascino, G.D., So, E.L., Radhakrishnan, K., Silbert, P., Marsh, R., 1998. Acute postoperative seizures following anterior temporal lobectomy for inctractble partial epilepsy. J. Neurosurg. 89, 177–182. Paillas, J.E., Gastaut, H., Sedan, R., Bureau, M., 1983. Long-terms results of conventional surgical treatment for epilepsy. Delayed recurrence after a period of 10 years. Surg. Neurol. 20, 189– 193. Park, K., Buchhalter, J., McClelland, R., Raffel, C., 2002. Frequency and significance of acute postoperative seizures following epilepsy surgery in children and adolescents. Epilepsia 43, 874–881. Penfield, W., Jasper, H.H., 1954. Epilepsy and the Functional Anatomy of the Human Brain. Churchill, London, p. 781. Rasmussen, T.B., 1983. Surgical treatment of complex partial seizures: results, lessons and problems. Epilepsia 24 (Suppl.), 65–76. Salanova, V., Andermann, F., Rasmussen, T., Olivier, A., Quesney, L., 1996. The running down phenomenon in temporal lobe epilepsy. Brain 119, 989–996. Salanova, V., Markand, O., Worth, R., 1999. Longitudinal follow-up in 145 patients with medically refractory temporal lobe epilepsy treated surgically between 1984 and 1995. Epilepsia 40, 1417–1423. Spencer, S., 1988. Cortical and intercortical seizure spread. In: Meldrum, B., Ferrendelli, J., Wieser, H. (Eds.). Anatomy of Epileptogenesis. John Libbey, London, pp. 139–154. Tigaran, S., Cascino, G.D., McClelland, R.L., So, E.L., Richard, M.W., 2003. Acute postoperative seizures after frontal lobe cortical resection for intractable partial epilepsy. Epilepsia 44, 831–835. Wiebe, S., Blume, W.T., Girvin, J.P., Eliasziw, M., 2001. A randomized, controlled trial of surgery for temporal-lobe epilepsy. New Engl. J. Med. 345, 311–318. Wingkun, E.C., Awad, I.A., Lüders, H., Awad, C.A., 1991. Natural History of recurrent seizures after resective surgery for epilepsy. Epilepsia 32, 851–856.
Seizures after epilepsy surgery夽 C. Drees, K. Chapman, Hans O. Lüders∗ Department of Neurology, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA Received 20 September 2003; received in revised form 4 October 2003; accepted 5 October 2003
Abstract This article reviews types and prognostic significance of seizures that occur after epilepsy surgery, so-called postsurgical seizures. © 2003 Published by Elsevier B.V. Keywords: Epilepsy; Surgery; Seizures
1. Introduction Epilepsy surgery is a standard treatment for intractable focal epilepsy. Seizure freedom after resection varies based on location and type of underlying pathology. While patients with temporal lobe epilepsy and discrete lesions have a very good outcome, i.e.— seizure freedom in 60 to >90% of patients (Berkovic et al., 1995; Engel, 1996; Salanova et al., 1999; Wiebe et al., 2001), epilepsy surgery in other brain regions is less successful (Berkovic et al., 1995; Malla et al., 1998; Park et al., 2002; Tigaran et al., 2003; Wingkun et al., 1991). In patients, in whom surgery fails, seizures usually recur within 6–12 months after surgery (Falconer and Serafetinides, 1963; Lüders et al., 1994; Malla et al., 1998; Park et al., 2002; Wingkun et al., 1991). This review will discuss the
夽 Summary of a presentation at the International Spring Epilepsy Research Conference, Georgetown, Cayman Islands, April 26–May 3, 2003. ∗ Corresponding author. Tel.: +1-216-444-5507; fax: +1-216-444-0230. E-mail address: [email protected] (H.O. Lüders). URL: http://www.clevelandclinic.org/neurology.
0920-1211/$ – see front matter © 2003 Published by Elsevier B.V. doi:10.1016/j.eplepsyres.2003.10.002
different types of seizures that occur after epilepsy surgery. Seizure control at 6 months was found to be a good predictor of outcome (Lüders et al., 1994), though traditionally most authors report outcome after 2 years of follow-up (Engel, 1987; Falconer and Serafetinides, 1963; Salanova et al., 1999). Long-term observations, however, document that seizure recurrence continues to increase progressively with longer follow-up (Engel, 1987; Falconer and Serafetinides, 1963; Lüders et al., 1994; Paillas et al., 1983; Salanova et al., 1999). 2. Postsurgical seizures Following epilepsy surgery, three types of seizures are distinguished: - Habitual seizures, - Non-habitual seizures, - Neighborhood seizures. 2.1. Habitual seizures Habitual seizures are defined as seizures that have a semiology which is identical to the presurgical
102
C. Drees et al. / Epilepsy Research 56 (2003) 101–104
seizures. In studies that recorded actual seizure semiology, they are the most common seizure type: Wingkun 74%, Park 70% (Park et al., 2002; Wingkun et al., 1991). Habitual seizures are thought to recur because of an incomplete or inadequate resection of the epileptogenic zone or maturing foci in close proximity to the previous epileptogenic zone producing a similar clinical ictal expression (Lüders et al., 1994; Paillas et al., 1983; Salanova et al., 1999; Wingkun et al., 1991). In these patients, surface ictal EEG still tends to point to the same seizure origin. However, the EEG pattern tends to vary as compared to the presurgical ictal EEG, likely due to the postsurgical skull defect and removed tissue. Habitual seizures may occur immediately after surgery, or within the following months and years. Usually, they recur within the first year (Falconer and Serafetinides, 1963; Park et al., 2002; Salanova et al., 1999; Wingkun et al., 1991). Rarely, patients have a recurrence of habitual seizures after a prolonged seizure-free period which may last for more than 5 or 10 years (Berkovic et al., 1995; Paillas et al., 1983; Salanova et al., 1999; Wingkun et al., 1991). Recurrences of habitual seizures within the first year are more likely to become persistent and intractable (Wingkun et al., 1991), however, after the first year and late recurrences after more than a decade are easily treated with medication and not likely to become refractory to medication (Falconer and Serafetinides, 1963; Paillas et al., 1983; Wingkun et al., 1991). The reverse phenomenon is called “running down” and implies the gradual disappearance of habitual seizures. The term was introduced by Rasmussen and is seen in 14% of patients 2–10 years after epilepsy surgery (Rasmussen, 1983; Salanova et al., 1999). This may represent the natural evolution of the epilepsy, possibly promoted by surgical resection of a significant portion of the epileptogenic zone. One study (Salanova et al., 1996) found that patients who were seizure free postoperatively had smaller epileptogenic areas compared to those who showed a “running down” phenomenon. The authors suggested that the remaining epileptogenic area has a higher threshold for seizure generation and eventually is insufficient to cause clinical seizures. The reason for this to occur is unclear, but one may speculate that this occurs due to maturing of inhibitory pathways or death of excitatory connections.
2.2. Non-habitual seizures In some instances, seizure semiology changes postsurgically from habitual seizures to a new clinical type. There are different mechanisms that may lead to non-habitual postsurgical seizures: (a) Resection of the presurgical symptomatogenic zone with persistence of the epileptogenic zone can alter seizure semiology. For example, surgery for a patient with right foot clonic seizures may include resection of the primary motor (M1) foot area and postsurgically the patient might continue to have right arm clonic seizures. (b) Partial resection of the epileptogenic zone or of selected essential seizure-propagating pathways, which were defining the presurgical seizure semiology, may change the clinical picture. Seizures may then propagate through different pathways (Spencer, 1988). This mechanism may be responsible for the frequent occurrence of postsurgical auras which tend not to evolve into seizures with motor manifestation or loss of consciousness even when antiepileptic medication is withdrawn (Fried et al., 1995; Malla et al., 1998). This is particularly frequent in patients with temporal lobe epilepsy who postsurgically remain only with typical abdominal auras (Fried et al., 1995; Lund and Spencer, 1992). It is hypothesized that a portion of the epileptogenic zone was not removed and is the origin for seizures that can still reach the insula, generating abdominal auras. However, the usual spread of seizures that produces automatisms and loss of awareness is no longer possible after surgery. A similar mechanism may be responsible, if a temporal lobectomy simplifies or eliminates aura features of residual complex partial seizures in patients who had undergone surgery for temporal lobe epilepsy (Blume and Girvin, 1997). The patients loose the symptomatogenic zone or essential pathways for the generation of their aura and, yet, the network to produce other features of their temporal lobe seizures is intact. A similar phenomenon is the documented relative increase of secondary generalized seizures in patients after temporal lobectomy (Henry et al., 2000). In animal experiments, secondary
C. Drees et al. / Epilepsy Research 56 (2003) 101–104
generalization requires extension of the ictal discharge into the pons and mesencephalon (Gale, 1992). Selected brain regions that connect the amygdalo-hippocamus with the pontomesencephalic regions (rostral piriform cortex (area tempestas), the insula, and the septal area) are usually not resected during a standard temporal lobectomy. It is possible, therefore, that seizures preferentially spread through these pathways after temporal lobectomy giving rise to a relatively higher proportion of secondary generalizations (Henry et al., 2000). (c) Postsurgical maturation or uncovering of additional epileptogenic zones may create a new type of seizures. One of the problems of defining the extent of the epileptogenic zone is the fact that it may be more extensive than the actual seizure onset zone (Lüders and Awad, 1992). Therefore, after surgery the “potentially epileptogenic zone” may give rise to seizures which may have a different semiology when compared to presurgical seizures. On the other hand, we know that maturation of the epileptogenic zone may take an extended period of time before causing seizures. For example, patients with cortical dysplasia, may be seizure free for decades before seizure onset, though their lesions are congenital. Therefore, it is conceivable that a new epileptogenic zone may develop after surgery as part of the maturation process of the epileptogenic focus (Lüders et al., 1994). This new epileptogenic zone may then give rise to postsurgical seizures that have a new semiology. Alternatively, the surgical scar can also mature into a new epileptogenic zone with the same consequences (Falconer and Serafetinides, 1963). 2.3. Neighborhood seizures The term “neighborhood seizure” was coined by Penfield and implies the occurrence of focal simple motor seizures immediately (1–2 weeks) after temporal lobe surgery, often without loss of consciousness (Falconer and Serafetinides, 1963; Penfield and Jasper, 1954). They constitute 20–58% of seizures experienced by patients in the postoperative period: Bengzon 20%, Falconer 45%, Garcia 47%, Malla 21%, Tigaran 58% (Bengzon et al., 1968; Falconer
103
and Serafetinides, 1963; Garcia et al., 1991; Malla et al., 1998; Tigaran et al., 2003). It has been assumed that these seizures were due to surgical irritation, edema, hemorrhage, or infection, and may have been facilitated by falling anticonvulsant levels (Falconer and Serafetinides, 1963; Tigaran et al., 2003). However, decreased levels of antiepileptic medication was not a frequent factor in recent studies (Malla et al., 1998; Park et al., 2002; Wingkun et al., 1991). Among other postoperative seizures, “neighborhood seizures” are usually a minority. “Neighborhood seizures” have to be distinguished from “acute postoperative seizures”, a term used by some authors referring to seizures of all types in the first postoperative week (Malla et al., 1998; Park et al., 2002; Tigaran et al., 2003). They are experienced by 20–49% of patients: Malla 20%, Park 25%, Tigaran 26%, Wingkun 29%, Lüders 38%, Garcia 49% (Garcia et al., 1991; Lüders et al., 1994; Malla et al., 1998; Park et al., 2002; Tigaran et al., 2003; Wingkun et al., 1991). The occurrence of postoperative seizures is associated with a worse prognosis (Garcia et al., 1991; Lüders et al., 1994; Malla et al., 1998; Park et al., 2002; Tigaran et al., 2003), but it does not preclude seizure freedom. About one third to one half of patients with seizures in the first postoperative week may still become seizure free: Park 33%, Falconer 42%, Tigaran 47%, Lüders 51% (Falconer and Serafetinides, 1963; Lüders et al., 1994; Park et al., 2002; Tigaran et al., 2003). The classical “neighborhood seizure” has traditionally been regarded as less ominous (Engel, 1987; Penfield and Jasper, 1954). Newer observations seem to support this: Malla et al. (1998) describe that 75% of patients with postoperative focal motor seizures, auras, and generalized tonic–clonic seizures eventually became seizure free. However, acute postoperative seizures that are similar or identical to habitual seizures—which occur in 46–85% of patients with postoperative seizures: Bengzon 46%, Garcia 59%, Wingkun 85% (Bengzon et al., 1968; Garcia et al., 1991; Wingkun et al., 1991)—have a poor prognosis with respect to outcome (Lüders et al., 1994; Malla et al., 1998; Park et al., 2002; Wingkun et al., 1991). Fourteen to forty-four percent of patients with acute postoperative habitual seizures might still become seizure free (Garcia et al., 1991; Malla et al., 1998).
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The majority of studies (Lüders et al., 1994; Malla et al., 1998; Tigaran et al., 2003) investigating acute postoperative seizures found that it made no difference in ultimate outcome whether seizures occurred within the first 24 h or later in the first week. Only one investigation reports that patients with a single seizure or seizures restricted to the first postoperative day were more likely to become seizure free compared to those who had multiple seizures or seizures later in the week (Garcia et al., 1991).
3. Conclusion The great majority of patients who had epilepsy surgery will be either seizure free or have habitual seizures arising from the vicinity of the cortical resection. Habitual seizures may recur up to 10 years after surgery. Occasionally, a “running down” phenomenon, a tapering off of seizures, is observed. “Neighborhood seizures” occurring in the immediate postoperative period are infrequent and have limited prognostic significance, though, in the majority of investigations acute postoperative seizures, particularly early habitual seizures, are associated with an overall worse prognosis regarding seizure outcome. Isolated auras and secondary generalized seizures are relatively more frequent and occurrence of non-habitual seizures can be observed after surgery.
References Bengzon, A.R., Rasmussen, T., Gloor, P., Dussault, J., Stephens, M., 1968. Prognostic factors in the surgical treatment of temporal lobe epileptics. Neurology 18, 717–731. Berkovic, S.F., McIntosh, A.M., Kalnins, R.M., Jackson, G.D., Fabinyi, G.C.A., Brazenor, G.A., Bladin, P.F., Hopper, J., 1995. Preoperative MRI predicts outcome of temporal lobectomy: an actuarial analysis. Neurology 45, 1358–1363. Blume, W.T., Girvin, J.P., 1997. Altered seizure patterns after temporal lobectomy. Epilepsia 38, 1183–1187. Engel Jr., J., 1987. Outcome with respect to epileptic seizures. In: Engel Jr., J. (Ed.), Surgical Treatment of the Epilepsies. Raven Press, New York, pp. 553–571. Engel Jr., J., 1996. Surgery for seizures. New Engl. J. Med. 334, 647–652. Falconer, M., Serafetinides, E., 1963. A follow-up study of surgery in temporal lobe epilepsy. J. Neurol. Neurosurg. Psychiatry 26, 154–165.
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