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Reflex absence epilepsy induced by gait
Epilepsy & Behavior 22 (2011) 395–397
Contents lists available at ScienceDirect
Epilepsy & Behavior j o u r n a l h o m e p a g e : w w w. e l s ev i e r. c o m / l o c a t e / ye b e h
Case Report
Reflex absence epilepsy induced by gait Ji-Ho Lin a, b, Hann-Yeh Shyu c, Chien Chen d, e, Shang-Yeong Kwan d, e,⁎, Tai-Tong Wong d, e, Kai-Ping Chang d, e, Chun-Hing Yiu d, e a
Department of Neurology, Taipei General Hospital, Department of Health, Executive Yuan, Taipei, Taiwan Institute of Brain Science, National Yang-Ming University School of Medicine, Taipei, Taiwan Section of Neurology, Department of Medicine, Armed Forces Taoyuan General Hospital, Yuan, Taiwan d Pediatric Epilepsy Surgery Group, Veterans General Hospital—Taipei, Taipei, Taiwan e National Yang-Ming University School of Medicine, Taipei, Taiwan b c
a r t i c l e
i n f o
Article history: Received 12 June 2011 Accepted 21 June 2011 Available online 3 August 2011 Keywords: Absence epilepsy Electroencephalogram Movement-induced Gait Reflex epilepsy
a b s t r a c t Reflex epilepsy is characterized by seizures that are precipitated by a specific identifiable factor. We describe here the case of a 21-year-old man with notable absence epilepsy since the age of 11 who experienced generalized convulsions 2 years after onset (in the absence of antiepileptic therapy) and reflex absence seizures triggered by walking 7–10 steps. To our knowledge, this case report is the first describing reflex absence epilepsy seizures induced by gait. © 2011 Elsevier Inc. All rights reserved.
1. Introduction Seizures associated with reflex epilepsy are reliably precipitated by a specific identifiable factor. The International League Against Epilepsy (ILAE) [1] describes reflex epilepsies as “epilepsies characterized by specific modes of seizure precipitation.” However, a recent classification proposal [2] redefines reflex epilepsy syndromes as “syndromes in which all epileptic seizures are precipitated by sensory stimuli.” Reflex seizures may be classified as those occurring in generalized or in focal epilepsy syndromes [3]. Reflex seizures can also be classified according to seizure trigger [4]. The seizure-precipitating mechanism of movement-induced epilepsy has been noted in connection with tonic seizures [5,6]. Moreover, reflex absence seizures (ASs) have been reported to occur in association with somatosensory stimuli (tapping) [7], visual stimuli (photosensitivity, pattern sensitivity) [8,9], complex visual stimuli and language processes (reading) [8], and high-level processes (thinking and talking about driving) [10]. Here, we describe the case of a 21-year-old man with notable absence epilepsy since the age of 11, with generalized convulsions 2 years after onset (in the absence of antiepileptic therapy), in whom ASs could be easily evoked by walking 7–10 steps. To our
⁎ Corresponding author at: Epilepsy Division, Neurological Institute, Veterans General Hospital—Taipei, No. 201, Sect. 2, Shih-Pai Road, Taipei 11217, Taiwan. Fax: + 886 2 2875 7579. E-mail address: [email protected] (S.-Y. Kwan). 1525-5050/$ – see front matter © 2011 Elsevier Inc. All rights reserved. doi:10.1016/j.yebeh.2011.06.030
knowledge, this is the first report of reflex absence epilepsy induced by gait. 2. Case report In February 2009, a right-handed 21-year-old man presented to our epilepsy clinic for frequent brief episodes of absentmindedness throughout the day and generalized convulsions two or three times a month. He was born at full term by spontaneous delivery with normal birth weight and without birth asphyxia. No later brain injury was noted, except a traffic accident without significant trauma at the age of 2. The developmental milestones were normal, and the family history was unremarkable. He graduated from senior high school with poor grades (attributed by the patient to poor memory). Neurological examination findings were normal. The first episode of absentmindedness was noted at the age of 11. The brief episode, lasting 5–6 seconds, occurred many times daily with subtle bilateral tremor-like hand movements. Although no prolonged loss of consciousness occurred, the patient could not recall memories and details occurring during the episode. The patient underwent traditional Chinese medicine therapy for these episodes; however, no significant improvement was noted. At 13 years of age, a generalized convulsion occurred, which lasted 2–3 minutes with the head deviating to the left side and subsequent postictal drowsiness. Following this event, generalized convulsions occurred with a fluctuating pattern of once a day for several days continuously or two or three times per month; the precipitating factors were
396
J.-H. Lin et al. / Epilepsy & Behavior 22 (2011) 395–397
noted to be nervousness, fatigue, hunger, playing on the computer, and taking long baths. Simultaneously, although brief episodes of absentmindedness occurred many times daily as before, the patient noted that they were more easily triggered by walking several steps. At 16 years of age, the patient was brought to a medical center in southern Taiwan, where EEG (including 3 minutes of hyperventilation and intermittent photic stimulation) and MRI of the brain revealed no abnormalities. He was prescribed antiepileptic drugs (AEDs), that is, valproate (500 mg twice daily) and lamotrigine (100 mg twice daily); however, seizure control did not improve. The patient was therefore admitted to our epilepsy clinic for further evaluation. During hospitalization in our clinic, the patient underwent video/ EEG monitoring. Initially, the patient was advised to lie on the bed; however, no event could be identified in the first 48 hours. Subsequently, the patient insisted that the event was easily triggered by walking; two brief episodes of absentmindedness were accordingly noted with clinical confirmation based on EEG findings of generalized 3-Hz spike-and-wave (SW) complexes lasting 3 and 4 seconds, respectively, while the patient walked to and fro five to seven steps in the ward (Fig. 1). No postictal confusion could be identified. The interictal background was normal. Hyperventilation, intermittent photic stimulation, thinking about walking, imitation of walking when lying on the bed, and tapping the soles of the feet alternately could not trigger the same event. Therefore, reflex absence epilepsy induced by movement (gait) was diagnosed. The AEDs were accordingly changed to valproate (750 mg twice daily) and levetiracetam (500 mg bid). Thus far, a marked improvement in seizure control has been noted: the generalized convulsions decreased to one or two events per 4 to 5 months and the severity of the episodes of absentmindedness decreased (improvement of up to 70% as declared by the patient's father).
3. Discussion Absence seizures have been reported to occur in association with somatosensory stimuli (tapping) [7], visual stimuli (photosensitivity, pattern sensitivity) [8,9], complex visual stimuli and language process (reading) [8], and high-level processes (thinking and talking about driving) [10]. However, to our knowledge, our case report is the first to describe reflex absence epilepsy induced by gait. The identification of a patient with reflex epilepsy depends on the physician's awareness and the observations of the patient and witnesses. The epileptogenic trigger must occur often enough in everyday life so that the patient suspects its relationship to the resulting seizures [9]. Our patient was aware that the ASs were being more easily triggered by walking several steps. Video/EEG monitoring verified the trigger mechanism by both clinical and EEG criteria; that is, ASs consistently followed the action of walking several steps. Wieser [11] hypothesized that in humans, a certain “critical mass” of cortical area is involved in normal excitation (the stimulus of reflex seizures) with synchronization and subsequent spreading of excitation. This hypothesis can also explain the conditioning and deconditioning of reflex epileptic seizures. In reflex epilepsies, Wolf observed that seizure evocation depends on the involvement of multiple processes associated with a functional rather than a topographic anatomy [12]. In seizures induced by a specific stimulation (reading, thinking, photic stimulation, etc.), the relatively localized trigger induces generalized or bilateral EEG abnormalities and seizures. The recruitment that produces these seizures need not be confined to physically contiguous brain tissue or fixed neuronal links. Instead, it may depend on the activity of a function-related network of both established and plastic links between brain regions that are modified by the effects of factors related to the specific stimulation [12]. In our
Fig. 1. While the patient walked to and fro five to seven steps in the ward, brief absentmindedness was associated with the EEG finding of sudden bursts of generalized high-voltage 3-Hz spike-and-wave complexes for 3–4 seconds.
J.-H. Lin et al. / Epilepsy & Behavior 22 (2011) 395–397
patient, the action of walking might have recruited the established links of the function-related network of ASs. However, the relationship between the plastic links associated with ASs and walking remain unknown. Although generalized tonic–clonic seizures often develop during adolescence [1], the relationship between the simultaneity of generalized convulsions and the trigger (in this case, gait) of ASs is also unknown. To our knowledge, our case report is the first to describe reflex absence epilepsy induced by gait. The relationship between an established type of seizure (AS), the simultaneous occurrence of generalized convulsions, and the trigger stimulus—gait—needs to be further elucidated. References [1] Proposal for revised classification of epilepsies and epileptic syndromes. Commission on Classification and Terminology of the International League Against Epilepsy. Epilepsia 1989;30:389–99.
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[2] Engel Jr J. A proposed diagnostic scheme for people with epileptic seizures and with epilepsy: report of the ILAE Task Force on Classification and Terminology. Epilepsia 2001;42:796–803. [3] Engel Jr J. Report of the ILAE classification core group. Epilepsia 2006;47:1558–68. [4] Panayiotopoulos CP. Epilepsies characterized by seizures with specific modes of precipitation (reflex epilepsies). In: Wallace SJ, editor. Epilepsy in children. London: Chapman & Hall; 1996. p. 355–75. [5] Burger LJ, Lopez RI, Elliott FA. Tonic seizures induced by movement. Neurology 1972;22:656–9. [6] Pierelli F, Di Gennaro G, Gherardi M, Spanedda F, Marciani MG. Movementinduced seizures: a case report. Epilepsia 1997;38:941–4. [7] DeMarco P. Reflex petit mal absence? Clin Electroencephalogr 1990;21:74–6. [8] Matricardi M, Brinciotti M, Paciello F. Reading epilepsy with absences, televisioninduced seizures, and pattern sensitivity. Epilepsy Res 1991;9:145–7. [9] Zifkin B, Andermann F. Epilepsy with reflex seizures. In: Wyllie E, editor. Wyllie's treatment of epilepsy: principles and practice. 5th ed. Philadelphia: Lippincott Williams & Wilkins; 2011. p. 305–16. [10] Bencze KS, Troupin A, Prockop LD. Reflex absence epilepsy. Epilepsia 1988;29:48–51. [11] Wieser H. Seizure-inducing and preventing mechanism. In: Beaumanoir A, Gastaut H, Naquet R, editors. Reflex seizures and reflex epilepsies. Geneva: Editions Médecine et Hygiène; 1989. p. 49–60. [12] Wolf P. Fron seizures to syndromes. In: Wolf P, editor. Epileptic seizures and syndromes. London: John Libbey; 1994. p. 39–40.
Contents lists available at ScienceDirect
Epilepsy & Behavior j o u r n a l h o m e p a g e : w w w. e l s ev i e r. c o m / l o c a t e / ye b e h
Case Report
Reflex absence epilepsy induced by gait Ji-Ho Lin a, b, Hann-Yeh Shyu c, Chien Chen d, e, Shang-Yeong Kwan d, e,⁎, Tai-Tong Wong d, e, Kai-Ping Chang d, e, Chun-Hing Yiu d, e a
Department of Neurology, Taipei General Hospital, Department of Health, Executive Yuan, Taipei, Taiwan Institute of Brain Science, National Yang-Ming University School of Medicine, Taipei, Taiwan Section of Neurology, Department of Medicine, Armed Forces Taoyuan General Hospital, Yuan, Taiwan d Pediatric Epilepsy Surgery Group, Veterans General Hospital—Taipei, Taipei, Taiwan e National Yang-Ming University School of Medicine, Taipei, Taiwan b c
a r t i c l e
i n f o
Article history: Received 12 June 2011 Accepted 21 June 2011 Available online 3 August 2011 Keywords: Absence epilepsy Electroencephalogram Movement-induced Gait Reflex epilepsy
a b s t r a c t Reflex epilepsy is characterized by seizures that are precipitated by a specific identifiable factor. We describe here the case of a 21-year-old man with notable absence epilepsy since the age of 11 who experienced generalized convulsions 2 years after onset (in the absence of antiepileptic therapy) and reflex absence seizures triggered by walking 7–10 steps. To our knowledge, this case report is the first describing reflex absence epilepsy seizures induced by gait. © 2011 Elsevier Inc. All rights reserved.
1. Introduction Seizures associated with reflex epilepsy are reliably precipitated by a specific identifiable factor. The International League Against Epilepsy (ILAE) [1] describes reflex epilepsies as “epilepsies characterized by specific modes of seizure precipitation.” However, a recent classification proposal [2] redefines reflex epilepsy syndromes as “syndromes in which all epileptic seizures are precipitated by sensory stimuli.” Reflex seizures may be classified as those occurring in generalized or in focal epilepsy syndromes [3]. Reflex seizures can also be classified according to seizure trigger [4]. The seizure-precipitating mechanism of movement-induced epilepsy has been noted in connection with tonic seizures [5,6]. Moreover, reflex absence seizures (ASs) have been reported to occur in association with somatosensory stimuli (tapping) [7], visual stimuli (photosensitivity, pattern sensitivity) [8,9], complex visual stimuli and language processes (reading) [8], and high-level processes (thinking and talking about driving) [10]. Here, we describe the case of a 21-year-old man with notable absence epilepsy since the age of 11, with generalized convulsions 2 years after onset (in the absence of antiepileptic therapy), in whom ASs could be easily evoked by walking 7–10 steps. To our
⁎ Corresponding author at: Epilepsy Division, Neurological Institute, Veterans General Hospital—Taipei, No. 201, Sect. 2, Shih-Pai Road, Taipei 11217, Taiwan. Fax: + 886 2 2875 7579. E-mail address: [email protected] (S.-Y. Kwan). 1525-5050/$ – see front matter © 2011 Elsevier Inc. All rights reserved. doi:10.1016/j.yebeh.2011.06.030
knowledge, this is the first report of reflex absence epilepsy induced by gait. 2. Case report In February 2009, a right-handed 21-year-old man presented to our epilepsy clinic for frequent brief episodes of absentmindedness throughout the day and generalized convulsions two or three times a month. He was born at full term by spontaneous delivery with normal birth weight and without birth asphyxia. No later brain injury was noted, except a traffic accident without significant trauma at the age of 2. The developmental milestones were normal, and the family history was unremarkable. He graduated from senior high school with poor grades (attributed by the patient to poor memory). Neurological examination findings were normal. The first episode of absentmindedness was noted at the age of 11. The brief episode, lasting 5–6 seconds, occurred many times daily with subtle bilateral tremor-like hand movements. Although no prolonged loss of consciousness occurred, the patient could not recall memories and details occurring during the episode. The patient underwent traditional Chinese medicine therapy for these episodes; however, no significant improvement was noted. At 13 years of age, a generalized convulsion occurred, which lasted 2–3 minutes with the head deviating to the left side and subsequent postictal drowsiness. Following this event, generalized convulsions occurred with a fluctuating pattern of once a day for several days continuously or two or three times per month; the precipitating factors were
396
J.-H. Lin et al. / Epilepsy & Behavior 22 (2011) 395–397
noted to be nervousness, fatigue, hunger, playing on the computer, and taking long baths. Simultaneously, although brief episodes of absentmindedness occurred many times daily as before, the patient noted that they were more easily triggered by walking several steps. At 16 years of age, the patient was brought to a medical center in southern Taiwan, where EEG (including 3 minutes of hyperventilation and intermittent photic stimulation) and MRI of the brain revealed no abnormalities. He was prescribed antiepileptic drugs (AEDs), that is, valproate (500 mg twice daily) and lamotrigine (100 mg twice daily); however, seizure control did not improve. The patient was therefore admitted to our epilepsy clinic for further evaluation. During hospitalization in our clinic, the patient underwent video/ EEG monitoring. Initially, the patient was advised to lie on the bed; however, no event could be identified in the first 48 hours. Subsequently, the patient insisted that the event was easily triggered by walking; two brief episodes of absentmindedness were accordingly noted with clinical confirmation based on EEG findings of generalized 3-Hz spike-and-wave (SW) complexes lasting 3 and 4 seconds, respectively, while the patient walked to and fro five to seven steps in the ward (Fig. 1). No postictal confusion could be identified. The interictal background was normal. Hyperventilation, intermittent photic stimulation, thinking about walking, imitation of walking when lying on the bed, and tapping the soles of the feet alternately could not trigger the same event. Therefore, reflex absence epilepsy induced by movement (gait) was diagnosed. The AEDs were accordingly changed to valproate (750 mg twice daily) and levetiracetam (500 mg bid). Thus far, a marked improvement in seizure control has been noted: the generalized convulsions decreased to one or two events per 4 to 5 months and the severity of the episodes of absentmindedness decreased (improvement of up to 70% as declared by the patient's father).
3. Discussion Absence seizures have been reported to occur in association with somatosensory stimuli (tapping) [7], visual stimuli (photosensitivity, pattern sensitivity) [8,9], complex visual stimuli and language process (reading) [8], and high-level processes (thinking and talking about driving) [10]. However, to our knowledge, our case report is the first to describe reflex absence epilepsy induced by gait. The identification of a patient with reflex epilepsy depends on the physician's awareness and the observations of the patient and witnesses. The epileptogenic trigger must occur often enough in everyday life so that the patient suspects its relationship to the resulting seizures [9]. Our patient was aware that the ASs were being more easily triggered by walking several steps. Video/EEG monitoring verified the trigger mechanism by both clinical and EEG criteria; that is, ASs consistently followed the action of walking several steps. Wieser [11] hypothesized that in humans, a certain “critical mass” of cortical area is involved in normal excitation (the stimulus of reflex seizures) with synchronization and subsequent spreading of excitation. This hypothesis can also explain the conditioning and deconditioning of reflex epileptic seizures. In reflex epilepsies, Wolf observed that seizure evocation depends on the involvement of multiple processes associated with a functional rather than a topographic anatomy [12]. In seizures induced by a specific stimulation (reading, thinking, photic stimulation, etc.), the relatively localized trigger induces generalized or bilateral EEG abnormalities and seizures. The recruitment that produces these seizures need not be confined to physically contiguous brain tissue or fixed neuronal links. Instead, it may depend on the activity of a function-related network of both established and plastic links between brain regions that are modified by the effects of factors related to the specific stimulation [12]. In our
Fig. 1. While the patient walked to and fro five to seven steps in the ward, brief absentmindedness was associated with the EEG finding of sudden bursts of generalized high-voltage 3-Hz spike-and-wave complexes for 3–4 seconds.
J.-H. Lin et al. / Epilepsy & Behavior 22 (2011) 395–397
patient, the action of walking might have recruited the established links of the function-related network of ASs. However, the relationship between the plastic links associated with ASs and walking remain unknown. Although generalized tonic–clonic seizures often develop during adolescence [1], the relationship between the simultaneity of generalized convulsions and the trigger (in this case, gait) of ASs is also unknown. To our knowledge, our case report is the first to describe reflex absence epilepsy induced by gait. The relationship between an established type of seizure (AS), the simultaneous occurrence of generalized convulsions, and the trigger stimulus—gait—needs to be further elucidated. References [1] Proposal for revised classification of epilepsies and epileptic syndromes. Commission on Classification and Terminology of the International League Against Epilepsy. Epilepsia 1989;30:389–99.
397
[2] Engel Jr J. A proposed diagnostic scheme for people with epileptic seizures and with epilepsy: report of the ILAE Task Force on Classification and Terminology. Epilepsia 2001;42:796–803. [3] Engel Jr J. Report of the ILAE classification core group. Epilepsia 2006;47:1558–68. [4] Panayiotopoulos CP. Epilepsies characterized by seizures with specific modes of precipitation (reflex epilepsies). In: Wallace SJ, editor. Epilepsy in children. London: Chapman & Hall; 1996. p. 355–75. [5] Burger LJ, Lopez RI, Elliott FA. Tonic seizures induced by movement. Neurology 1972;22:656–9. [6] Pierelli F, Di Gennaro G, Gherardi M, Spanedda F, Marciani MG. Movementinduced seizures: a case report. Epilepsia 1997;38:941–4. [7] DeMarco P. Reflex petit mal absence? Clin Electroencephalogr 1990;21:74–6. [8] Matricardi M, Brinciotti M, Paciello F. Reading epilepsy with absences, televisioninduced seizures, and pattern sensitivity. Epilepsy Res 1991;9:145–7. [9] Zifkin B, Andermann F. Epilepsy with reflex seizures. In: Wyllie E, editor. Wyllie's treatment of epilepsy: principles and practice. 5th ed. Philadelphia: Lippincott Williams & Wilkins; 2011. p. 305–16. [10] Bencze KS, Troupin A, Prockop LD. Reflex absence epilepsy. Epilepsia 1988;29:48–51. [11] Wieser H. Seizure-inducing and preventing mechanism. In: Beaumanoir A, Gastaut H, Naquet R, editors. Reflex seizures and reflex epilepsies. Geneva: Editions Médecine et Hygiène; 1989. p. 49–60. [12] Wolf P. Fron seizures to syndromes. In: Wolf P, editor. Epileptic seizures and syndromes. London: John Libbey; 1994. p. 39–40.