We systematically reviewed the literature to describe the “natural” history of medically treated temporal lobe epilepsy (TLE). No population-based studies recruiting incident cases of TLE irrespective of age exist. Prospective, population-based studies were limited to those recruiting only childhood-onset TLE or those reporting TLE as a subgroup of cohorts of focal epilepsies. Few studies have been performed in the “MRI era” limiting information on natural history secondary to specific pathologies. Available data suggests that TLE is highly variable, with unpredictable transient remissions and low rates of seizure freedom (30 to 50%). Etiology and failure of first and second drug seem to be the most important predictors for treatment prognosis. The role of initial precipitating injuries remains speculative, as imaging information of related events is either missing or conflicting. Prospective cohorts of new-onset TLE with long-term followup using advanced MRI techniques, timely EEG recordings, and assessments of psychiatric comorbidities are needed. 1. Introduction Temporal lobe epilepsy (TLE) is the most frequent medically refractory epilepsy syndrome seen in epilepsy outpatient clinics. It has received considerable attention in recent years owing to the remarkable rates of remission that can be achieved through surgical intervention [1]. Mesial temporal lobe epilepsy (mTLE) associated with hippocampal sclerosis (mTLE-HS), a condition that can be detected by modern magnetic resonance imaging (MRI) techniques with a high sensitivity and specificity, is now the most common indication for epilepsy surgery. To date, therapeutic advances in TLE have far outpaced our understanding of the natural history of the disorder. According to a recent International League Against Epilepsy (ILAE) commission report [2], the natural history of mTLE-HS is characterized by key features such as a history of an initial precipitating injury and a presence of a latent and/or silent period. Prior publications have attempted to assess the course and prognosis of TLE, mTLE, and mTLE-HS using sophisticated electroencephalography (EEG), MRI, and histological techniques trying to identify the “natural” history of all types of TLE. Almost all these studies are limited by the fact that their perspective comes from tertiary care centers and surgical series [3]. The ideal natural history study requires a large prospective cohort of patients with new-onset TLE undergoing extensive structural and functional testing with a followup of >10 years. We conducted a systematic review of the
References
[1]
S. Wiebe, W. T. Blume, J. P. Girvin, and M. Eliasziw, “A randomized, controlled trial of surgery for temporal-lobe epilepsy,” New England Journal of Medicine, vol. 345, no. 5, pp. 311–318, 2001.
[2]
H.-G. Wieser, “ILAE Commission on Neurosurgery of Epilepsy: ILAE Commission Report. Mesial temporal lobe epilepsy with hippocampal sclerosis,” Epilepsia, vol. 45, no. 6, pp. 695–714, 2004.
[3]
A. T. Berg, “The natural history of mesial temporal lobe epilepsy,” Current Opinion in Neurology, vol. 21, no. 2, pp. 173–178, 2008.
[4]
J. Last, A Dictionary of Epidemiology, Oxford Press, New York, NY, USA, 1983.
[5]
C. G. Spooner, S. F. Berkovic, L. A. Mitchell, J. A. Wrennall, and A. S. Harvey, “New-onset temporal lobe epilepsy in children: lesion on MRI predicts poor seizure outcome,” Neurology, vol. 67, no. 12, pp. 2147–2153, 2006.
[6]
M. Manford, Y. M. Hart, J. W. A. S. Sander, and S. D. Shorvon, “National General Practice Study of Epilepsy (NGPSE): partial seizure patterns in a general population,” Neurology, vol. 42, no. 10, pp. 1911–1917, 1992.
[7]
W. A. Hauser and L. T. Kurland, “The epidemiology of epilepsy in Rochester, Minnesota, 1935 through 1967,” Epilepsia, vol. 16, no. 1, pp. 1–66, 1975.
[8]
M. Sillanp？？ and D. Schmidt, “Natural history of treated childhood-onset epilepsy: prospective, long-term population-based study,” Brain, vol. 129, no. 3, pp. 617–624, 2006.
[9]
M. E. Morita, L. Conz, C. V. Maurer-Morelli et al., “Long term follow up of familial mesial temporal lobe epilepsy,” Journal of Epilepsy and Clinical Neurophysiology, vol. 14, no. 3, pp. 111–113, 2008.
[10]
K. Aso and K. Watanabe, “Limitations in the medical treatment of cryptogenic or symptomatic localization-related epilepsies of childhood onset,” Epilepsia, vol. 41, supplement 9, pp. 18–20, 2000.
[11]
B. M. Soeder, U. Gleissner, H. Urbach et al., “Causes, presentation and outcome of lesional adult onset mediotemporal lobe epilepsy,” Journal of Neurology, Neurosurgery and Psychiatry, vol. 80, no. 8, pp. 894–899, 2009.
[12]
M. Harbord and J. Manson, “Temporal lobe epilepsy in childhood: reappraisal of etiology and outcome,” Pediatric Neurology, vol. 3, no. 5, pp. 263–268, 1987.
[13]
G. Regesta and P. Tanganelli, “Temporal lobe epilepsy of adult age of possible idiopathic nature,” Seizure, vol. 11, no. 2, pp. 131–135, 2002.
[14]
D. Chao, J. A. Sexton, and L. S. Santos Pardo, “Temporal lobe epilepsy in children,” The Journal of Pediatrics, vol. 60, no. 5, pp. 686–693, 1962.
[15]
S. Currie, K. W. G. Heathfield, R. A. Henson, and D. F. Scott, “Clinical course and prognosis of temporal lobe epilepsy: a survey of 666 patients,” Brain, vol. 94, no. 1, pp. 173–190, 1971.
[16]
D. J. Dlugos, M. D. Sammel, B. L. Strom, and J. T. Farrar, “Response to first drug trial predicts outcome in childhood temporal lobe epilepsy,” Neurology, vol. 57, no. 12, pp. 2259–2264, 2001.
[17]
W. J. Kim, S. C. Park, S. J. Lee et al., “The prognosis for control of seizures with medications in patients with MRI evidence for mesial temporal sclerosis,” Epilepsia, vol. 40, no. 3, pp. 290–293, 1999.
[18]
K. E. VanLandingham, E. R. Heinz, J. E. Cavazos, and D. V. Lewis, “Magnetic resonance imaging evidence of hippocampal injury after prolonged focal febrile convulsions,” Annals of Neurology, vol. 43, no. 4, pp. 413–426, 1998.
[19]
T. Salmenper？, M. K？n？nen, N. Roberts, R. Vanninen, A. Pitk？nen, and R. K？lvi？inen, “Hippocampal damage in newly diagnosed focal epilepsy: a prospective MRI study,” Neurology, vol. 64, no. 1, pp. 62–68, 2005.
[20]
R. K？lvi？inen, T. Salmenper？, K. Partanen, P. Vainio, P. Riekkinen, and A. Pitk？nen, “Recurrent seizures may cause hippocampal damage in temporal lobe epilepsy,” Neurology, vol. 50, no. 5, pp. 1377–1882, 1998.
[21]
W. Van Paesschen, J. S. Duncan, J. M. Stevens, and A. Connelly, “Longitudinal quantitative hippocampal magnetic resonance imaging study of adults with newly diagnosed partial seizures: one-year follow-up results,” Epilepsia, vol. 39, no. 6, pp. 633–639, 1998.
[22]
R. S. N. Liu, L. Lemieux, J. W. A. S. Sander et al., “Seizure-associated hippocampal volume loss: a longitudinal magnetic resonance study of temporal lobe epilepsy,” Annals of Neurology, vol. 51, no. 5, pp. 641–644, 2002.
[23]
A. Labate, A. Gambardella, E. Andermann et al., “Benign mesial temporal lobe epilepsy,” Nature Reviews Neurology, vol. 7, no. 4, pp. 237–240, 2011.
[24]
F. Cendes, F. Andermann, P. Gloor et al., “Atrophy of mesial structures in patients with temporal lobe epilepsy: cause or consequence of repeated seizures?” Annals of Neurology, vol. 34, no. 6, pp. 795–801, 1993.
[25]
A. T. Berg, B. G. Vickrey, F. M. Testa et al., “How long does it take for epilepsy to become intractable? A prospective investigation,” Annals of Neurology, vol. 60, no. 1, pp. 73–79, 2006.
[26]
M. A. King, M. R. Newton, G. D. Jackson et al., “Epileptology of the first-seizure presentation: a clinical, electroencephalographic, and magnetic resonance imaging study of 300 consecutive patients,” The Lancet, vol. 352, no. 9133, pp. 1007–1011, 1998.
[27]
B. Pohlmann-Eden and M. Newton, “First seizure: EEG and neuroimaging following an epileptic seizure,” Epilepsia, vol. 49, supplement 1, pp. 19–25, 2008.
[28]
M. H. Schmidt and B. Pohlmann-Eden, “Neuroimaging in epilepsy: the state of the art,” Epilepsia, vol. 52, supplement 4, pp. 49–51, 2011.
[29]
B. Pohlmann-Eden, “Conceptual relevance of new-onset epilepsy,” Epilepsia, vol. 52, supplement 4, pp. 1–6, 2011.
[30]
A. M. Kanner, “Depression and epilepsy: a bidirectional relation?” Epilepsia, vol. 52, supplement 1, pp. 21–27, 2011.
