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Sleep attacks mimicking epileptic seizures and pseudoseizures
Sleep Attacks
Mimicking Epileptic and Pseudoseizures
Beth A. Malow,
Seizures
Gail A. Fromes, and Linda M. Selwa
Common treatable sleep disorders resulting in excessive daytime sleepiness may resemble or contribute to spells of altered responsiveness. These spells may mimic epileptic seizures or other paroxysmal disorders. Three patients presented with paroxysmal spells of altered responsiveness that were attributed initially to epileptic seizures or pseudoseizures. One patient had a history of childhood epilepsy and was referred for the concern of recurrent seizures. In another patient, antiepileptic drugs (AEDS) were prescribed for suspected epileptic seizures without an improvement in spells. After their physicians obtained a history of excessive daytime sleepiness, snoring, and/or restless leg symptoms, patients were evaluated with polysomnography, multiple sleep latency tests, electroencephalograms (EEG), and video-EEG monitoring. Sleep studies were diagnostic of obstructive sleep apnea, periodic limb movement disorder, and probable narcolepsy. In all patients, spells of altered responsiveness and excessive daytime sleepiness improved or resolved with treatment of the sleep disorder or discontinuation of AEDS. Patients presenting with paroxysmal spells of altered responsiveness and excessive daytime sleepiness should be evaluated for sleep disorders. Identification and treatment of an underlying sleep disorder may contribute to resolution of their spells. Key Words: Seizures-Pseudoseizures-Sleep disorders-Periodic limb movementsabstructive sleep apnea. 0 1997 by Elsevier Science Inc. All rights reserved.
Patients with excessive daytime sleepinessresulting from a sleep disorder may experience sleep attacks that resemble spells of altered responsiveness. Sleepiness, however, is not commonly considered in the evaluation Received February 24, 1997; accepted May 2, 1997. From the Clinical Neurophysiology Laboratory, Department of Neurology, University of Michigan Medical School, Ann Arbor, MI, U.S.A. Address correspondence and reprint requests to Beth A. Malow, M.D., Assistant Professor, Department of Neurology, University Hospital, Room 8D8702, 1500 E. Medical Center Drive, Ann Arbor, MI 48109-0117, U.S.A. J. Epilepsy 1997;10:232-235 0 1997 by Elsevier Science Inc. All rights reserved. 655 Avenue of the Americas, New York, NY 10010
of such spells. We report clinical and neurophysiologic findings in three patients, one with a prior history of epilepsy, who presented with paroxysmal spells of altered responsiveness. All were diagnosed with sleep disorders and improved with treatment.
Methods The
three
patients
reported
in this
case series
were seen by one or more of the aluthors from
0896-6974/97/$17.00
PII SO896-.6974(97)00057-l
SLEEP ATTACKS
Table 1. Patient 1 2 3
Study PSG /MSLT CPAP, 7 cm water
PSG/MSLT PSG CPAP, 11 cm water
MIMICKING
SElZURES
Polysomnography and MSLT results
RDI
m02
PLMI
15.7 7.8 28.6 68 5.7
74% 84% 84 54 86
13.4 n/a 84.5 41.3 n/a
Arousals
with PLMs
MSL
SOREMs
rare
2
4/4
frequent frequent
4.3
o/4
PSG, polysomnogram; MSLT, multiple sleeplatency test; CPAP, continuous positive airway pressure;RDI, respiratory disturbance index, apneasand hypopneas per hour of sleep;“’mO,, minimum oxygen saturation, PLMI, periodic limb movement index, periodic limb movements per hour of sleep;bn/a, not available; PLMIs were not quantified for individual levels of CPAP; MSL, mean sleeplatency in minutes; SOREMs, sleep onset REM periods. “In our laboratory, an apnea is defined as a decreasein airflow or effort to 20% or less of baselinefor 110or more seconds.A hypopnea is defined by a decreasein airflow or effort that is accompaniedby either electroencephalographic sitns of arousal (11) or a 4% or greater decrease in oxygen saturation. OSA is diagnosed if the RDI > 10. In our laboratory, periodic limb movementsare defined by movementsin the anterior tibialis channelof 0.5-5 seconds in duration, in trains of at least three movements with intermovement intervals of 4-120 seconds.
July-October somnography;
1995. All patients underwent multiple
sleep latency
poly-
tests (MSLTs)
were also performed on the day after polysomnography according to standard criteria (1) in patients 1 and 2. Patient 3 did not have an MSLT performed because he underwent a split-night trial of continuous positive airway pressure (CPAP). Overnight sleep recordings were performed on 21-channel polygraphs or l&channel computerized electroencephalogram (EEG) polysomnography systems (SASSSY, Telefactor Corporation, West Conshohocken, PA) and EEG, electrooculography (EOG), submental electromyogram (EMG), nasal-oral airflow, respiratory effort, pulse oximetry, and anterior tibialis EMG were recorded. Patients 2 and 3 underwent 16-channel continuous video-EEG monitoring (Telefactor Corporation) in an epilepsy inpatient unit. Patient 1 This 33-year-old woman had childhood absence epilepsy treated with ethosuximide and phenobarbital. Medications were discontinued during adolescence without recurrent seizures. Her clinic visit was prompted by the concern that her seizures had recurred. She had almost daily spells of diminished concentration during meetings at work. These spells, however, were not accompanied by loss of consciousness and instead involved a sensation of fighting off sleepiness. After driving for many hours on a business-related trip, she felt extremely sleepy and pulled over to the side of the road to nap. She admitted to having had similar episodes in her twenties following her daughter’s birth. She had gained 40 pounds in 3 years and had been told
that she snored. She had occasional hypnogogic hallucinations but denied sleep paralysis or cataplexy and was taking no medications. She denied restless leg symptoms. EEG showed a normal waking background and brief 3-3.5 Hz generalized spike-wave discharges without clinical manifestations, consistent with prior studies. Polysomnography was diagnostic of mild obstructive sleep apnea (OSA) and an MSLT showed a shortened mean sleep latency and four sleep-onset rapid eye movement (REM:) periods, consistent with probable coexisting narcolepsy (10) (Table 1). Human leukocyte antigen (HLA) testing was positive for HLA-DR2 (DR15 subtype). A CPAP trial improved OSA (Table 1). The patient remained excessively sleepy, however, despite nightly CPAP use and was begun on methylphenidate (Ritalin), which markedly improved daytime alertness and resolved spells. She continues to take methylphenidate 30 mg daily and to use CPAP every night. Patient 2 This 90-year-old man presented with a l-year history of episodic lapses in consciousness when he was alone and engrossed in reading or accounting. During
one
of these
spells,
he fractured
his
left
femur and required surgical repair. A Holter monitor revealed significant bradycardia and a permanent pacemaker was placed without alleviation of symptoms. He had no history of epilepsy, head trauma with loss of consciousness, or incontinence, although he did have frequent leg movements and difficulty maintaining sleep. He described sleeping J EPILEPSY,
VOL. IO, NO. 5, 1997
233
B. A. MALOW
ET AL.
4-5 hours per night, noting “restlessness and jerking” of his legs while in bed. Long-term video-EEG monitoring, performed to exclude epileptic seizures as a cause of his spells, did not capture any episodes of diminished awareness. Polysomnography was diagnostic of periodic limb movement disorder (PLMD) and OSA; an MSLT was consistent with excessive daytime sleepiness (Table 1). Between the second and third naps of the MSLT, the patient was sitting in a chair reading. He called for help and was found lying on the floor. He reported that he had felt tired and suddenly weak and then slid to the ground. Because he stated that he had experienced similar episodes at home on multiple occasions, his spells were attributed to sleepiness due to OSA, restless legs syndrome, and PLMD. He was reluctant to try CPAP for OSA and was not a candidate for surgical intervention. He was agreeable to treatment with carbidopa-levodopa (Sinemet) up to 50/200 mg nightly for PLMD with associated restless legs syndrome. He had excellent initial improvement in his daytime sleepiness and falling spells. His spells recurred intermittently and worsened again when his gerontologist decreased carbidopa-levodopa to 25/100 mg nightly.
Patient
3
This 47-year-old man with coronary artery disease, noninsulin dependent diabetes mellitus, hypercholesterolemia, and hypertension presented with a 5-month history of spells involving inattention, diminished responsiveness, and occasional falls. Spells lasted several minutes, were preceded by a sensation of physical and mental slowness, and were followed by sleepiness and occasional headache. While mowing his lawn, he felt groggy and hit a tree. Head magnetic resonance imaging (MRI) with angiography, EEG, in-patient electrocardiogram (ECG) telemetry, Holter monitoring, and cardiac catheterization were normal. The frequency of his spells increased from once every 2 weeks to once a day during treatment with phenytoin (Dilantin) and gabapentin (Neurontin) for presumed seizures. He had stopped working because of the frequency of his spells. Because his spells did not respond to antiepileptic drugs (AEDS) and no other cause was found, his referring physician suspected pseudoseizures and referred him for long-term video-EEG monitoring. When evaluated at our institution during longterm monitoring, he stated that he slept as little as 234
j EPILEPSY,
VOL. 20, NO. 5, 1997
2-3 hours on most nights because of crawling sensations in his legs while trying to fall asleep. He was receiving levodopa-carbidopa 25/1.00 mg for PLMD. Other medications included insulin, glipizide (Glucotrol), gemfibrozil (Lopid), nifedipine (Procardia), fluoxetine (Prozac), and zolpidem (Ambien) for insomnia. Long-term video-EEG monitoring captured several typical spells consisting of diminished responsiveness with only partial ability to follow commands. In several spells that occurred while standing, he would lower himself to the bed or to the ground. Many spells were preceded by pacing or rubbing of his legs; when these behaviors were discussed with him at a later time, he said he was attempting to relieve his restless leg symptoms. The EEG preceding, during, and after a spell was consistent with drowsiness; no spells were associated with ictal EEG changes and no interictal epileptiform activity was recorded. Blood glucoses obtained immediately after these spells were normal. Polysomnography was diagnostic of OSA and PLMD (Table 1). Total sleep time was 5 hours and 17 minutes and sleep efficiency was 73%. Because of the severity of OSA, CPAP was initiated in the second half of the night with a g,ood response (Table 1). PLMs persisted after CPAP was applied. The patient was discharged on CPAP. Phenytoin, gabapentin, fluoxetine, and zolpidem were discontinued and clonazapam (Klonopin), 0.5 mg at bedtime, was added to carbidopa-levodopa for treatment of restless legs syndrome and PLMD. At follow-up in clinic 8 months later, he was using CPAP regularly and had only one recurrent spell occurring in the setting of sleep deprivation. Symptoms of insomnia and daytime sleepiness had resolved and he had returned to work full-time.
Discussion This series illustrates the importance of considering excessive daytime sleepiness as a cause of spells of altered responsiveness, particularly when sympotoms occur preferentially in sedentary situations. The history of excessive daytime sleepiness prompted evaluation with sleep studies and eventually led to diagnosis and treatment of underlying sleep disorders. In all three patients, epileptic seizures or pseudoseizures were considered in the differential diagnosis. Patient 1, who had a history of childhood epilepsy and an abnormal EEG, was referred for the concern of recurrent seizures. Patients 2 and 3 were monitored for suspected sei-
SLEEPAl-TACKS zures or pseudoseizures. Patient 3 had been treated with AEDs and, after his spells became more frequent on medication, the possibility of pseudoseizures was considered. In each of our patients, daytime sleepiness was most likely multifactorial and due lo several sleep disorders. In patient 1, probable narcolepsy coexisting with OSA was diagnosed because four naps on her MSLT showed sleep-onset REM periods and sleepiness persisted despite nightly use of CPAP. We were unable to measure the relative impact of treating narcolepsy and OSA on daytime sleepiness in this patient. Patient 3 received simultaneous treatment for both OSA and PLMD with associated restless legs syndrome. AEDs, prescribed for a presumed seizure disorder, may have contributed to daytime sleepiness; patients taking AEDs have reported subjective sleepiness as a common adverse effect (3). Despite these limitations in establishing the specific causes of daytime sleepiness, we found that spells of altered responsiveness and excessive daytime sleepiness improved or resolved in all patients with treatment of the sleep disorder or discontinuation of AEDs. Sleep disorders are common. In addition to masquerading as epileptic seizures, sleep disorders may coexist with epileptic syndromes. OSA is particularly common, affecting 2% of women and 4% of men in the middle-aged work force (4). Identifying and treating coexisting sleep disorders in epilepsy patients has important implications for seizure control. In our series of 63 adult epilepsy patients undergoing polysomnograms in a sleep disorders laboratory over an 11-year period, 15 patients were diagnosed with OSA, prescribed CPAP, and continued to use the equipment at the time of most recent follow-up. The majority reported improvements in excessive daytime sleepiness, seizure control, or both (5). Three previous reports have documented the coexistence of epilepsy and OSA and the beneficial effect of treatment of OSA on seizure control. The first report described a patient with sleep apnea treated with tracheostomy who became seizure-free except for two exacerbations that correlated with closure of his tracheostomy stoma (6). Two recent series documented improved seizure control after treatment with CPAP, medication, tracheostomy, or positional therapy (7,s). The mechanism whereby treatment of OSA improves seizure control is unknown. OSA frequently results in sleep depriva-
MlMlCKlNG
SEIZURES
tion, a condition associated with increased seizures in epileptic (9) and nonepileptic individuals (10); resolution of sleep deprivation from frequent arousals may improve seizure control. Sudden and irresistible sleep attacks have been described in narcolepsy (2). However, any sleep disorder resulting in excessive daytime sleepiness may present with lapses into sleep. Historically, these spells may be mistaken for epileptic seizures or pseudoseizures. We recommend taking a thorough sleep history in any patient presenting with spells of altered responsiveness and considering polysomnography if a sleep disorder is suspected.
Acknowledgments:
Dr. James Spindler referred valuable history. Dr. Michael Aldrich provided helpful suggestions on the manuscript. one of the patients presented and provided
References 1. Carskadon MA, Dement WC, Mitler MM, Roth T, Westbrook PR, Keenan S. Guidelines for the multiple sleep latency test (MSLT): a standard measure of sleepiness. Sleep 3986;9:51924. 2. American Sleep Disorders Association. The International Classification of Sleep Disorders Diagnostic and Coding Manual. Rochester: American Sleep Disorders Association, 1990. 3. Beghi E. Adverse reactions to antiepileplic drugs: a multicenter survev of clinical oractice. Epilepsia 1986;27:323-30. 4. Young T, Paita M, Demisey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med 1993;328:1230-5. 5. Malow BA, Fromes GA, Aldrich MS. Usefulness of polysomnography in epilepsy patients. Neurology 1947;48:13891394. 6. Wyler AR, Weymuller EA. Epilepsy complicated by sleep apnea. Ann Neural 1981;9:403-4. 7. Devinsky 0, Ehrenberg B, Barthlen GM, Abramson HS, Luciano D. Epilepsy and sleep apnea syndrome. Yeurology 1994;44:2060-4. 8. Vaughn BV, D’Cruz OF, Beach R, Messenheimer JA. Improvement of epileptic seizure control with treatment of obstructive sleep apnoea. Seizure 1996;5:73-78. 9. Rajna P, Veres J. Correlations between night sleep duration and seizure frequency in temporal lobe epilepsy. Epilepsia 1993;34:574-9. 10. Gunderson C, Dunne I?, Feyer T. Sleep deprivation seizures. Neurology 1973;23:678-86. 11. American Sleep Disorders Association. EEG Arousals: scoring rules and examples. A preliminary report from the Sleep Disorders Atlas Task Force of the American Sleep Disorders Association. Sleep 1992;15:173-84.
J EPILEPSY, VOL. 10, NO. 5, 1997
235
Mimicking Epileptic and Pseudoseizures
Beth A. Malow,
Seizures
Gail A. Fromes, and Linda M. Selwa
Common treatable sleep disorders resulting in excessive daytime sleepiness may resemble or contribute to spells of altered responsiveness. These spells may mimic epileptic seizures or other paroxysmal disorders. Three patients presented with paroxysmal spells of altered responsiveness that were attributed initially to epileptic seizures or pseudoseizures. One patient had a history of childhood epilepsy and was referred for the concern of recurrent seizures. In another patient, antiepileptic drugs (AEDS) were prescribed for suspected epileptic seizures without an improvement in spells. After their physicians obtained a history of excessive daytime sleepiness, snoring, and/or restless leg symptoms, patients were evaluated with polysomnography, multiple sleep latency tests, electroencephalograms (EEG), and video-EEG monitoring. Sleep studies were diagnostic of obstructive sleep apnea, periodic limb movement disorder, and probable narcolepsy. In all patients, spells of altered responsiveness and excessive daytime sleepiness improved or resolved with treatment of the sleep disorder or discontinuation of AEDS. Patients presenting with paroxysmal spells of altered responsiveness and excessive daytime sleepiness should be evaluated for sleep disorders. Identification and treatment of an underlying sleep disorder may contribute to resolution of their spells. Key Words: Seizures-Pseudoseizures-Sleep disorders-Periodic limb movementsabstructive sleep apnea. 0 1997 by Elsevier Science Inc. All rights reserved.
Patients with excessive daytime sleepinessresulting from a sleep disorder may experience sleep attacks that resemble spells of altered responsiveness. Sleepiness, however, is not commonly considered in the evaluation Received February 24, 1997; accepted May 2, 1997. From the Clinical Neurophysiology Laboratory, Department of Neurology, University of Michigan Medical School, Ann Arbor, MI, U.S.A. Address correspondence and reprint requests to Beth A. Malow, M.D., Assistant Professor, Department of Neurology, University Hospital, Room 8D8702, 1500 E. Medical Center Drive, Ann Arbor, MI 48109-0117, U.S.A. J. Epilepsy 1997;10:232-235 0 1997 by Elsevier Science Inc. All rights reserved. 655 Avenue of the Americas, New York, NY 10010
of such spells. We report clinical and neurophysiologic findings in three patients, one with a prior history of epilepsy, who presented with paroxysmal spells of altered responsiveness. All were diagnosed with sleep disorders and improved with treatment.
Methods The
three
patients
reported
in this
case series
were seen by one or more of the aluthors from
0896-6974/97/$17.00
PII SO896-.6974(97)00057-l
SLEEP ATTACKS
Table 1. Patient 1 2 3
Study PSG /MSLT CPAP, 7 cm water
PSG/MSLT PSG CPAP, 11 cm water
MIMICKING
SElZURES
Polysomnography and MSLT results
RDI
m02
PLMI
15.7 7.8 28.6 68 5.7
74% 84% 84 54 86
13.4 n/a 84.5 41.3 n/a
Arousals
with PLMs
MSL
SOREMs
rare
2
4/4
frequent frequent
4.3
o/4
PSG, polysomnogram; MSLT, multiple sleeplatency test; CPAP, continuous positive airway pressure;RDI, respiratory disturbance index, apneasand hypopneas per hour of sleep;“’mO,, minimum oxygen saturation, PLMI, periodic limb movement index, periodic limb movements per hour of sleep;bn/a, not available; PLMIs were not quantified for individual levels of CPAP; MSL, mean sleeplatency in minutes; SOREMs, sleep onset REM periods. “In our laboratory, an apnea is defined as a decreasein airflow or effort to 20% or less of baselinefor 110or more seconds.A hypopnea is defined by a decreasein airflow or effort that is accompaniedby either electroencephalographic sitns of arousal (11) or a 4% or greater decrease in oxygen saturation. OSA is diagnosed if the RDI > 10. In our laboratory, periodic limb movementsare defined by movementsin the anterior tibialis channelof 0.5-5 seconds in duration, in trains of at least three movements with intermovement intervals of 4-120 seconds.
July-October somnography;
1995. All patients underwent multiple
sleep latency
poly-
tests (MSLTs)
were also performed on the day after polysomnography according to standard criteria (1) in patients 1 and 2. Patient 3 did not have an MSLT performed because he underwent a split-night trial of continuous positive airway pressure (CPAP). Overnight sleep recordings were performed on 21-channel polygraphs or l&channel computerized electroencephalogram (EEG) polysomnography systems (SASSSY, Telefactor Corporation, West Conshohocken, PA) and EEG, electrooculography (EOG), submental electromyogram (EMG), nasal-oral airflow, respiratory effort, pulse oximetry, and anterior tibialis EMG were recorded. Patients 2 and 3 underwent 16-channel continuous video-EEG monitoring (Telefactor Corporation) in an epilepsy inpatient unit. Patient 1 This 33-year-old woman had childhood absence epilepsy treated with ethosuximide and phenobarbital. Medications were discontinued during adolescence without recurrent seizures. Her clinic visit was prompted by the concern that her seizures had recurred. She had almost daily spells of diminished concentration during meetings at work. These spells, however, were not accompanied by loss of consciousness and instead involved a sensation of fighting off sleepiness. After driving for many hours on a business-related trip, she felt extremely sleepy and pulled over to the side of the road to nap. She admitted to having had similar episodes in her twenties following her daughter’s birth. She had gained 40 pounds in 3 years and had been told
that she snored. She had occasional hypnogogic hallucinations but denied sleep paralysis or cataplexy and was taking no medications. She denied restless leg symptoms. EEG showed a normal waking background and brief 3-3.5 Hz generalized spike-wave discharges without clinical manifestations, consistent with prior studies. Polysomnography was diagnostic of mild obstructive sleep apnea (OSA) and an MSLT showed a shortened mean sleep latency and four sleep-onset rapid eye movement (REM:) periods, consistent with probable coexisting narcolepsy (10) (Table 1). Human leukocyte antigen (HLA) testing was positive for HLA-DR2 (DR15 subtype). A CPAP trial improved OSA (Table 1). The patient remained excessively sleepy, however, despite nightly CPAP use and was begun on methylphenidate (Ritalin), which markedly improved daytime alertness and resolved spells. She continues to take methylphenidate 30 mg daily and to use CPAP every night. Patient 2 This 90-year-old man presented with a l-year history of episodic lapses in consciousness when he was alone and engrossed in reading or accounting. During
one
of these
spells,
he fractured
his
left
femur and required surgical repair. A Holter monitor revealed significant bradycardia and a permanent pacemaker was placed without alleviation of symptoms. He had no history of epilepsy, head trauma with loss of consciousness, or incontinence, although he did have frequent leg movements and difficulty maintaining sleep. He described sleeping J EPILEPSY,
VOL. IO, NO. 5, 1997
233
B. A. MALOW
ET AL.
4-5 hours per night, noting “restlessness and jerking” of his legs while in bed. Long-term video-EEG monitoring, performed to exclude epileptic seizures as a cause of his spells, did not capture any episodes of diminished awareness. Polysomnography was diagnostic of periodic limb movement disorder (PLMD) and OSA; an MSLT was consistent with excessive daytime sleepiness (Table 1). Between the second and third naps of the MSLT, the patient was sitting in a chair reading. He called for help and was found lying on the floor. He reported that he had felt tired and suddenly weak and then slid to the ground. Because he stated that he had experienced similar episodes at home on multiple occasions, his spells were attributed to sleepiness due to OSA, restless legs syndrome, and PLMD. He was reluctant to try CPAP for OSA and was not a candidate for surgical intervention. He was agreeable to treatment with carbidopa-levodopa (Sinemet) up to 50/200 mg nightly for PLMD with associated restless legs syndrome. He had excellent initial improvement in his daytime sleepiness and falling spells. His spells recurred intermittently and worsened again when his gerontologist decreased carbidopa-levodopa to 25/100 mg nightly.
Patient
3
This 47-year-old man with coronary artery disease, noninsulin dependent diabetes mellitus, hypercholesterolemia, and hypertension presented with a 5-month history of spells involving inattention, diminished responsiveness, and occasional falls. Spells lasted several minutes, were preceded by a sensation of physical and mental slowness, and were followed by sleepiness and occasional headache. While mowing his lawn, he felt groggy and hit a tree. Head magnetic resonance imaging (MRI) with angiography, EEG, in-patient electrocardiogram (ECG) telemetry, Holter monitoring, and cardiac catheterization were normal. The frequency of his spells increased from once every 2 weeks to once a day during treatment with phenytoin (Dilantin) and gabapentin (Neurontin) for presumed seizures. He had stopped working because of the frequency of his spells. Because his spells did not respond to antiepileptic drugs (AEDS) and no other cause was found, his referring physician suspected pseudoseizures and referred him for long-term video-EEG monitoring. When evaluated at our institution during longterm monitoring, he stated that he slept as little as 234
j EPILEPSY,
VOL. 20, NO. 5, 1997
2-3 hours on most nights because of crawling sensations in his legs while trying to fall asleep. He was receiving levodopa-carbidopa 25/1.00 mg for PLMD. Other medications included insulin, glipizide (Glucotrol), gemfibrozil (Lopid), nifedipine (Procardia), fluoxetine (Prozac), and zolpidem (Ambien) for insomnia. Long-term video-EEG monitoring captured several typical spells consisting of diminished responsiveness with only partial ability to follow commands. In several spells that occurred while standing, he would lower himself to the bed or to the ground. Many spells were preceded by pacing or rubbing of his legs; when these behaviors were discussed with him at a later time, he said he was attempting to relieve his restless leg symptoms. The EEG preceding, during, and after a spell was consistent with drowsiness; no spells were associated with ictal EEG changes and no interictal epileptiform activity was recorded. Blood glucoses obtained immediately after these spells were normal. Polysomnography was diagnostic of OSA and PLMD (Table 1). Total sleep time was 5 hours and 17 minutes and sleep efficiency was 73%. Because of the severity of OSA, CPAP was initiated in the second half of the night with a g,ood response (Table 1). PLMs persisted after CPAP was applied. The patient was discharged on CPAP. Phenytoin, gabapentin, fluoxetine, and zolpidem were discontinued and clonazapam (Klonopin), 0.5 mg at bedtime, was added to carbidopa-levodopa for treatment of restless legs syndrome and PLMD. At follow-up in clinic 8 months later, he was using CPAP regularly and had only one recurrent spell occurring in the setting of sleep deprivation. Symptoms of insomnia and daytime sleepiness had resolved and he had returned to work full-time.
Discussion This series illustrates the importance of considering excessive daytime sleepiness as a cause of spells of altered responsiveness, particularly when sympotoms occur preferentially in sedentary situations. The history of excessive daytime sleepiness prompted evaluation with sleep studies and eventually led to diagnosis and treatment of underlying sleep disorders. In all three patients, epileptic seizures or pseudoseizures were considered in the differential diagnosis. Patient 1, who had a history of childhood epilepsy and an abnormal EEG, was referred for the concern of recurrent seizures. Patients 2 and 3 were monitored for suspected sei-
SLEEPAl-TACKS zures or pseudoseizures. Patient 3 had been treated with AEDs and, after his spells became more frequent on medication, the possibility of pseudoseizures was considered. In each of our patients, daytime sleepiness was most likely multifactorial and due lo several sleep disorders. In patient 1, probable narcolepsy coexisting with OSA was diagnosed because four naps on her MSLT showed sleep-onset REM periods and sleepiness persisted despite nightly use of CPAP. We were unable to measure the relative impact of treating narcolepsy and OSA on daytime sleepiness in this patient. Patient 3 received simultaneous treatment for both OSA and PLMD with associated restless legs syndrome. AEDs, prescribed for a presumed seizure disorder, may have contributed to daytime sleepiness; patients taking AEDs have reported subjective sleepiness as a common adverse effect (3). Despite these limitations in establishing the specific causes of daytime sleepiness, we found that spells of altered responsiveness and excessive daytime sleepiness improved or resolved in all patients with treatment of the sleep disorder or discontinuation of AEDs. Sleep disorders are common. In addition to masquerading as epileptic seizures, sleep disorders may coexist with epileptic syndromes. OSA is particularly common, affecting 2% of women and 4% of men in the middle-aged work force (4). Identifying and treating coexisting sleep disorders in epilepsy patients has important implications for seizure control. In our series of 63 adult epilepsy patients undergoing polysomnograms in a sleep disorders laboratory over an 11-year period, 15 patients were diagnosed with OSA, prescribed CPAP, and continued to use the equipment at the time of most recent follow-up. The majority reported improvements in excessive daytime sleepiness, seizure control, or both (5). Three previous reports have documented the coexistence of epilepsy and OSA and the beneficial effect of treatment of OSA on seizure control. The first report described a patient with sleep apnea treated with tracheostomy who became seizure-free except for two exacerbations that correlated with closure of his tracheostomy stoma (6). Two recent series documented improved seizure control after treatment with CPAP, medication, tracheostomy, or positional therapy (7,s). The mechanism whereby treatment of OSA improves seizure control is unknown. OSA frequently results in sleep depriva-
MlMlCKlNG
SEIZURES
tion, a condition associated with increased seizures in epileptic (9) and nonepileptic individuals (10); resolution of sleep deprivation from frequent arousals may improve seizure control. Sudden and irresistible sleep attacks have been described in narcolepsy (2). However, any sleep disorder resulting in excessive daytime sleepiness may present with lapses into sleep. Historically, these spells may be mistaken for epileptic seizures or pseudoseizures. We recommend taking a thorough sleep history in any patient presenting with spells of altered responsiveness and considering polysomnography if a sleep disorder is suspected.
Acknowledgments:
Dr. James Spindler referred valuable history. Dr. Michael Aldrich provided helpful suggestions on the manuscript. one of the patients presented and provided
References 1. Carskadon MA, Dement WC, Mitler MM, Roth T, Westbrook PR, Keenan S. Guidelines for the multiple sleep latency test (MSLT): a standard measure of sleepiness. Sleep 3986;9:51924. 2. American Sleep Disorders Association. The International Classification of Sleep Disorders Diagnostic and Coding Manual. Rochester: American Sleep Disorders Association, 1990. 3. Beghi E. Adverse reactions to antiepileplic drugs: a multicenter survev of clinical oractice. Epilepsia 1986;27:323-30. 4. Young T, Paita M, Demisey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med 1993;328:1230-5. 5. Malow BA, Fromes GA, Aldrich MS. Usefulness of polysomnography in epilepsy patients. Neurology 1947;48:13891394. 6. Wyler AR, Weymuller EA. Epilepsy complicated by sleep apnea. Ann Neural 1981;9:403-4. 7. Devinsky 0, Ehrenberg B, Barthlen GM, Abramson HS, Luciano D. Epilepsy and sleep apnea syndrome. Yeurology 1994;44:2060-4. 8. Vaughn BV, D’Cruz OF, Beach R, Messenheimer JA. Improvement of epileptic seizure control with treatment of obstructive sleep apnoea. Seizure 1996;5:73-78. 9. Rajna P, Veres J. Correlations between night sleep duration and seizure frequency in temporal lobe epilepsy. Epilepsia 1993;34:574-9. 10. Gunderson C, Dunne I?, Feyer T. Sleep deprivation seizures. Neurology 1973;23:678-86. 11. American Sleep Disorders Association. EEG Arousals: scoring rules and examples. A preliminary report from the Sleep Disorders Atlas Task Force of the American Sleep Disorders Association. Sleep 1992;15:173-84.
J EPILEPSY, VOL. 10, NO. 5, 1997
235