Journal Scan - Sleep Medicine
Andrew N. Wilner, MD, FAAN, FACP
From
Sleep Medicine
October 28, 2005 (Volume 7, Number 2)
A Preliminary Study of Sleep-Disordered Breathing in Major Depressive Disorder
Deldin PJ, Phillips LK, Thomas RJ
Sleep Med. 2005;Oct 28; [Epub ahead of print]
The incidence of sleep-disordered breathing was evaluated with a home monitoring device in patients with major depressive disorder compared with controls.
Study Design
The investigators studied 19 people (15 women, 4 men; mean age, 34; body mass index, 26) with major depression and 15 controls (10 women, 5 men, mean age 34, body mass index 24). At baseline, patients with depression had statistically higher scores on the Beck Depression Inventory (BDI) (P < .01) and the Spielberger Trait Anxiety Inventory (STAI-T) (P < .01) than controls. Patients with major depression also had significantly higher scores on the Pittsburgh Sleep Quality Index (PSQI) (P = 0.001) and lower sleep efficiency (P = .010) than controls. However, scores on the Epworth Sleepiness Scale (ESS) did not significantly differ between the 2 groups. A home polysomnography system (Stardust) recorded body position, oximetry, heart rate, respiratory rate and effort, and nasal airflow. Airflow was measured with a nasal cannula pressure transducer rather than a thermistor.
Results
Respiratory parameters that differed significantly between people with major depressive disorder and controls included major flow limitation events (P = .02), the percentage of major flow limitation events accompanied by a desaturation of at least 3% (P = .01), and average oxygen saturation (P = .02). In addition, 5 of 19 (26%) of the depressed patients had greater than 5 major flow limitation events/hour. Antidepressant medication or sedative hypnotics did not appear to be responsible for these differences.
Conclusion
Compared with controls, patients with major depressive disorder have symptoms of sleep-disordered breathing, increased PSQI scores, lower sleep efficiency, an increased number of major flow limitations, major flow limitations with oxygen saturation, and decreased oxygen saturation.
Commentary
Patients with obstructive sleep-disordered breathing may have symptoms of depression that respond to treatment of their breathing disorder. Conversely, patients with depression may have sleep-disordered breathing. This pilot home study reveals significant differences in reported and measured sleep variables between patients with major depression and controls. These findings suggest that patients with major depressive disorder should be screened for symptoms of obstructive sleep-disordered breathing and studied with polysomnography when indicated. If significant breathing limitations are discovered, these should be treated along with the depression. The hypothesis that treatment of minor breathing disorder symptoms may improve depressive symptoms in patients with major depressive disorder should be tested. Future studies should include a larger number of patients and matched controls. Although the use of a nasal cannula pressure transducer is innovative, standard polysomnographic techniques would allow a more direct comparison of the magnitude of sleep-disordered breathing in patients with major depressive disorder to other populations.
January 2006 (Volume 7, Number 1)
An Efficacy, Safety, and Dose-Response Study of Ramelteon in Patients With Chronic Primary Insomnia
Erman M, Seiden D, Zammit G, Sainati S, Zhang J
Sleep Med. 2006;7:17-24
The study authors report the results of a double-blind, randomized, placebo-controlled study of ramelteon, a novel agent for chronic primary insomnia.
Study Design
One hundred seven patients (64% women, 36% men; mean age, 37.7) with chronic insomnia for at least 3 months enrolled in this double-blind, randomized, placebo-controlled, crossover study of 4 doses of ramelteon (4 mg, 8 mg, 16 mg, and 32 mg). Each patient participated in each of the 5 study arms, which lasted 2 days, and were separated by a 5- to 12-day washout period. Polysomnography was performed after each dose of medication (or placebo).
Results
One hundred three patients completed the study. Latency to persistent sleep (LPS) as measured by polysomnography was 37.7 minutes with placebo. Compared with placebo, all doses of ramelteon resulted in statistically significant reductions in LPS: LPS was 24 minutes with ramelteon 4 mg, 24.3 minutes with ramelteon 8 mg, 24 minutes with ramelteon 16 mg, and 22.9 minutes with ramelteon 32 mg (P < .001 for all doses). In addition, subjective sleep latency was 57 minutes with placebo compared with 43.9 minutes with ramelteon 16 mg (P = .040). Total sleep time as measured by polysomnography was 400.2 minutes with placebo. Total sleep time was longer with all ramelteon doses compared with placebo: 411 minutes with ramelteon 4 mg (P ≤ .050), 412.9 minutes with ramelteon 8 mg (P ≤ .010), 411.2 minutes with ramelteon 16 mg (P ≤ .050), and 418.2 minutes with ramelteon 32 mg (P ≤ .001). Ramelteon did not improve wake after sleep onset or subjective sleep quality. Next-day performance was not adversely affected by ramelteon, as measured by word list memory and digit symbol substitution tests. The most common adverse events were headache, somnolence, and sore throat.
Conclusion
Ramelteon significantly reduces LPS and increases total sleep time as measured by polysomnography without adverse next-day effects.
Commentary
A variety of drugs are used for the treatment of insomnia, including GABAA benzodiazepine receptor sedative hypnotics (eszopiclone, zaleplon, and zolpidem), benzodiazepines, sedating antidepressants, antipsychotics, and over-the-counter antihistamines. Ramelteon is a novel pharmacologic agent that acts as a highly selective agonist on MT1/MT2 receptors in the suprachiasmatic nucleus. MT1 receptors may mediate the suppressive effect of melatonin and MT2 receptors affect phase shifting. Thus, it appears that the primary target of ramelteon is the body's chronoregulation of sleep rather than providing sedation as a fortuitous side effect of other actions. Results from this study show that ramelteon significantly improved objectively measured sleep latency and total sleep time without residual next-day effects, thereby suggesting that ramelteon will be an important pharmacologic agent for many patients with sleep-onset insomnia.
Abstract
From
Epilepsia
January 2006 (Volume 47, Number 1)
Effect of Levetiracetam on Nocturnal Sleep and Daytime Vigilance in Healthy Volunteers
Cicolin A, Magliola U, Giordano A, Terreni A, Bucca C, Mutani R
Epilepsia. 2006;47:82-85
In this article, statistically significant increases in total sleep time, sleep efficiency, and stages II and IV of nonrapid eye movement (NREM) sleep were observed with levetiracetam compared with placebo in 14 healthy volunteers after 3 weeks of treatment.
Study Design
Fourteen healthy adult volunteers (7 men, 7 women; mean age, 28.9 years) participated in a double-blind, placebo-controlled, crossover study of levetiracetam (≤ 2000 mg/day) or placebo for 3 weeks separated by a 4-week washout period. The Epworth Sleepiness Scale was performed at baseline. Polysomnography was performed 1 week after a steady-state dose of levetiracetam (2000 mg/day) was reached. Subsequently, subjects completed the Epworth Sleepiness Scale and Multiple Sleep Latency Test.
Results
Statistically significant reductions were observed after treatment with levetiracetam in total sleep time (P = .01), REM (P = .004), wake after sleep onset (P = .004), and the number of stage shifts (P = .001). Sleep efficiency (P = .004) and time spent in NREM stages II (P = .001) and IV (P = .001) significantly increased. There were no significant differences in Epworth Sleepiness Scale scores, the mean sleep time per night based on sleep logs, REM latency, or Multiple Sleep Latency Test scores. Mean levetiracetam serum concentrations were 14.9 ± 4.7 mcg/mL.
Conclusion
Levetiracetam has beneficial effects on sleep without resulting in excessive daytime somnolence in healthy volunteers.
Commentary
Sleep disruption and excessive daytime sleepiness commonly occur in people with epilepsy. Nocturnal seizures may disrupt sleep and may not be remembered by the patient. Antiepileptic drugs often have a sedating effect and may contribute to daytime somnolence. Less commonly, antiepileptic drugs may have alerting properties and result in insomnia, as may be seen with felbamate (Felbatol, MedPointe, Somerset, New Jersey) and lamotrigine (Lamictal, GlaxoSmithKline, Research Triangle Park, North Carolina). Consequently, it is reassuring that levetiracetam (Keppra, UCBPharma, Brussels, Belgium), another "new" antiepileptic drug, appears to consolidate sleep. A lack of effect on the Epworth Sleepiness Scale suggests that daytime somnolence is not increased. Because sleep deprivation may exacerbate seizures, sleep disruption should be minimized in people with epilepsy. Replication of these results in people with epilepsy would lead to the recommendation that levetiracetam should be considered in people with epilepsy who have sleep difficulties due to their antiepileptic drugs.
Abstract
From
Sleep and Biological Rhythms
June 2005 (Volume 3, Number 2)
Dreaming and Schizophrenia: A Common Neurobiological Background?
Gottesmann C
Sleep Biol Rhythms. 2005;3:64-74
This article probes the physiologic similarities between the rapid eye movement (REM) dream state and schizophrenia.
Study Design
In a wide-ranging discussion, the study author compares the physiology of the REM dream state with the pathophysiology of schizophrenia.
Results
The study author observes that 40-Hz electroencephalographic (EEG) activity, which occurs during REM sleep, is uncoupled over the cortical areas. This uncoupling may parallel a "problem of connectivity" that occurs with schizophrenia. Decreased blood flow occurs in the dorsolateral prefrontal cortex during REM sleep and in schizophrenia. Hallucinations that occur in schizophrenia may be due to a decrease in sensory constraints, which also occur during REM sleep. The study author speculates that the failure of inhibitory cortical neurotransmitters could allow the individual to remember "useless memories" created during REM dreams, perhaps leading to schizophrenia. Dopamine levels are decreased during REM sleep compared with waking, which could correlate with the negative symptoms of schizophrenia, which may also be due to reduced levels of dopamine.
Conclusion
Dreams, with their disjointed, at times illogical, and time-distorted imagery, harbor similarities with the psychotic mentation of schizophrenia. In addition, a decrease in the neurotransmitter dopamine appears to play an important role in REM sleep as well as in the negative symptoms of schizophrenic psychosis. The study author postulates that REM sleep could become an experimental model for schizophrenia.
Commentary
Although dreams have fascinated humankind for millennia, the study of dreams is fraught with technically challenging methodologic problems. Dreams that occur during REM sleep represent a normal physiologic phenomenon, but at least superficial similarities exist with the abnormal state of schizophrenia. The study author articulates some commonalities underlying the physiology of dreams and the pathology of schizophrenia. However, it is premature to establish REM sleep as a neurobiological model for schizophrenia. Continued research may lead to an increased understanding of the creation of dreams and perhaps provide insights leading to novel treatments for schizophrenia.
From
Journal of Neurology, Neurosurgery & Psychiatry
January 2006 (Volume 77, Number 1)
Effects of Sleep Deprivation on Cortical Excitability in Patients Affected by Juvenile Myoclonic Epilepsy: A Combined Transcranial Magnetic Stimulation and EEG Study
Manganotti P, Bongiovanni LG, Fuggetta G, Zanette G, Fiaschi A
J Neurol Neurosurg Psychiatry. 2006;77:56-60
The study authors measured the effects of sleep deprivation with magnetic stimulation and electroencephalography (EEG) in 10 patients with juvenile myoclonic epilepsy (JME) and in 10 controls.
Study Design
Ten patients with JME (8 women, 2 men; ages 16-33) were compared with 10 controls (5 women, 5 men; ages 18-30). Eight of the patients were treated with phenobarbital and valproate, whereas the other two did not receive treatment. Subjects were studied with EEG and magnetic stimulation presleep and postsleep deprivation. Patients were sleep-deprived in the hospital from midnight until morning. Stimulation was over the presumed hand area of the motor cortex and recorded from the contralateral thenar eminence. Epileptic activity was quantified on the basis of 30 minutes of EEG recording before and after sleep deprivation.
Results
At baseline, JME patients had significantly decreased short-latency intracortical inhibition (SICI) values compared with controls (P < .001). This effect was larger in the 2 untreated patients than those on antiepileptic drugs. Sleep deprivation further decreased SICI values in patients with JME, but not in controls (P < .001). At baseline, short-latency intracortical facilitation (SICF) did not differ between patients and controls. However, sleep deprivation significantly increased SICF in patients with JME, but not in controls (P < .005). Motor threshold (MT) was significantly reduced by sleep deprivation in patients with JME, but not in controls (P < .001).
Conclusion
Several variables measured by magnetic stimulation were significantly affected by sleep deprivation in patients with JME: SICI decreased; SICF increased; and MT decreased.
Commentary
Every textbook on epilepsy mentions sleep deprivation as a "trigger" for seizures, yet little is known about the pathophysiology of this phenomenon. This study reveals that sleep deprivation can significantly modify the results of several variables (SICI, SICF, and MT) elicited by magnetic stimulation that represent primary motor cortex excitability. Of interest, patients treated with antiepileptic drugs had less prominent changes in SICI. If these results are routinely reproducible, this paradigm could prove extremely valuable in pursuing our understanding of the pathophysiology of epileptic activity and in providing a platform for the evaluation of new antiepileptic drugs. (Drugs that have the greatest effects on magnetic excitability parameters would merit further study.)
This study suffers from several basic technical limitations. The small population includes adults and children who may well differ in cortical excitability. The subjects were not sex-matched and were poorly age-matched. In addition, 8 patients were treated with antiepileptic drugs, whereas 2 were not. In such a small study, these variables should be eliminated. Future studies should endeavor to provide age- and sex-matched controls, control for treatment, and focus on adults or children. Further, although the text clearly states that SICI decreased, the table and figure reveal an apparent increase and are difficult to interpret. The EEG results were also not clearly reported relative to sleep deprivation.
Abstract
Supported by an independent educational grant from Takeda.
Saludos Cordiales
Dr. José Manuel Ferrer Guerra
From
Sleep Medicine
October 28, 2005 (Volume 7, Number 2)
A Preliminary Study of Sleep-Disordered Breathing in Major Depressive Disorder
Deldin PJ, Phillips LK, Thomas RJ
Sleep Med. 2005;Oct 28; [Epub ahead of print]
The incidence of sleep-disordered breathing was evaluated with a home monitoring device in patients with major depressive disorder compared with controls.
Study Design
The investigators studied 19 people (15 women, 4 men; mean age, 34; body mass index, 26) with major depression and 15 controls (10 women, 5 men, mean age 34, body mass index 24). At baseline, patients with depression had statistically higher scores on the Beck Depression Inventory (BDI) (P < .01) and the Spielberger Trait Anxiety Inventory (STAI-T) (P < .01) than controls. Patients with major depression also had significantly higher scores on the Pittsburgh Sleep Quality Index (PSQI) (P = 0.001) and lower sleep efficiency (P = .010) than controls. However, scores on the Epworth Sleepiness Scale (ESS) did not significantly differ between the 2 groups. A home polysomnography system (Stardust) recorded body position, oximetry, heart rate, respiratory rate and effort, and nasal airflow. Airflow was measured with a nasal cannula pressure transducer rather than a thermistor.
Results
Respiratory parameters that differed significantly between people with major depressive disorder and controls included major flow limitation events (P = .02), the percentage of major flow limitation events accompanied by a desaturation of at least 3% (P = .01), and average oxygen saturation (P = .02). In addition, 5 of 19 (26%) of the depressed patients had greater than 5 major flow limitation events/hour. Antidepressant medication or sedative hypnotics did not appear to be responsible for these differences.
Conclusion
Compared with controls, patients with major depressive disorder have symptoms of sleep-disordered breathing, increased PSQI scores, lower sleep efficiency, an increased number of major flow limitations, major flow limitations with oxygen saturation, and decreased oxygen saturation.
Commentary
Patients with obstructive sleep-disordered breathing may have symptoms of depression that respond to treatment of their breathing disorder. Conversely, patients with depression may have sleep-disordered breathing. This pilot home study reveals significant differences in reported and measured sleep variables between patients with major depression and controls. These findings suggest that patients with major depressive disorder should be screened for symptoms of obstructive sleep-disordered breathing and studied with polysomnography when indicated. If significant breathing limitations are discovered, these should be treated along with the depression. The hypothesis that treatment of minor breathing disorder symptoms may improve depressive symptoms in patients with major depressive disorder should be tested. Future studies should include a larger number of patients and matched controls. Although the use of a nasal cannula pressure transducer is innovative, standard polysomnographic techniques would allow a more direct comparison of the magnitude of sleep-disordered breathing in patients with major depressive disorder to other populations.
January 2006 (Volume 7, Number 1)
An Efficacy, Safety, and Dose-Response Study of Ramelteon in Patients With Chronic Primary Insomnia
Erman M, Seiden D, Zammit G, Sainati S, Zhang J
Sleep Med. 2006;7:17-24
The study authors report the results of a double-blind, randomized, placebo-controlled study of ramelteon, a novel agent for chronic primary insomnia.
Study Design
One hundred seven patients (64% women, 36% men; mean age, 37.7) with chronic insomnia for at least 3 months enrolled in this double-blind, randomized, placebo-controlled, crossover study of 4 doses of ramelteon (4 mg, 8 mg, 16 mg, and 32 mg). Each patient participated in each of the 5 study arms, which lasted 2 days, and were separated by a 5- to 12-day washout period. Polysomnography was performed after each dose of medication (or placebo).
Results
One hundred three patients completed the study. Latency to persistent sleep (LPS) as measured by polysomnography was 37.7 minutes with placebo. Compared with placebo, all doses of ramelteon resulted in statistically significant reductions in LPS: LPS was 24 minutes with ramelteon 4 mg, 24.3 minutes with ramelteon 8 mg, 24 minutes with ramelteon 16 mg, and 22.9 minutes with ramelteon 32 mg (P < .001 for all doses). In addition, subjective sleep latency was 57 minutes with placebo compared with 43.9 minutes with ramelteon 16 mg (P = .040). Total sleep time as measured by polysomnography was 400.2 minutes with placebo. Total sleep time was longer with all ramelteon doses compared with placebo: 411 minutes with ramelteon 4 mg (P ≤ .050), 412.9 minutes with ramelteon 8 mg (P ≤ .010), 411.2 minutes with ramelteon 16 mg (P ≤ .050), and 418.2 minutes with ramelteon 32 mg (P ≤ .001). Ramelteon did not improve wake after sleep onset or subjective sleep quality. Next-day performance was not adversely affected by ramelteon, as measured by word list memory and digit symbol substitution tests. The most common adverse events were headache, somnolence, and sore throat.
Conclusion
Ramelteon significantly reduces LPS and increases total sleep time as measured by polysomnography without adverse next-day effects.
Commentary
A variety of drugs are used for the treatment of insomnia, including GABAA benzodiazepine receptor sedative hypnotics (eszopiclone, zaleplon, and zolpidem), benzodiazepines, sedating antidepressants, antipsychotics, and over-the-counter antihistamines. Ramelteon is a novel pharmacologic agent that acts as a highly selective agonist on MT1/MT2 receptors in the suprachiasmatic nucleus. MT1 receptors may mediate the suppressive effect of melatonin and MT2 receptors affect phase shifting. Thus, it appears that the primary target of ramelteon is the body's chronoregulation of sleep rather than providing sedation as a fortuitous side effect of other actions. Results from this study show that ramelteon significantly improved objectively measured sleep latency and total sleep time without residual next-day effects, thereby suggesting that ramelteon will be an important pharmacologic agent for many patients with sleep-onset insomnia.
Abstract
From
Epilepsia
January 2006 (Volume 47, Number 1)
Effect of Levetiracetam on Nocturnal Sleep and Daytime Vigilance in Healthy Volunteers
Cicolin A, Magliola U, Giordano A, Terreni A, Bucca C, Mutani R
Epilepsia. 2006;47:82-85
In this article, statistically significant increases in total sleep time, sleep efficiency, and stages II and IV of nonrapid eye movement (NREM) sleep were observed with levetiracetam compared with placebo in 14 healthy volunteers after 3 weeks of treatment.
Study Design
Fourteen healthy adult volunteers (7 men, 7 women; mean age, 28.9 years) participated in a double-blind, placebo-controlled, crossover study of levetiracetam (≤ 2000 mg/day) or placebo for 3 weeks separated by a 4-week washout period. The Epworth Sleepiness Scale was performed at baseline. Polysomnography was performed 1 week after a steady-state dose of levetiracetam (2000 mg/day) was reached. Subsequently, subjects completed the Epworth Sleepiness Scale and Multiple Sleep Latency Test.
Results
Statistically significant reductions were observed after treatment with levetiracetam in total sleep time (P = .01), REM (P = .004), wake after sleep onset (P = .004), and the number of stage shifts (P = .001). Sleep efficiency (P = .004) and time spent in NREM stages II (P = .001) and IV (P = .001) significantly increased. There were no significant differences in Epworth Sleepiness Scale scores, the mean sleep time per night based on sleep logs, REM latency, or Multiple Sleep Latency Test scores. Mean levetiracetam serum concentrations were 14.9 ± 4.7 mcg/mL.
Conclusion
Levetiracetam has beneficial effects on sleep without resulting in excessive daytime somnolence in healthy volunteers.
Commentary
Sleep disruption and excessive daytime sleepiness commonly occur in people with epilepsy. Nocturnal seizures may disrupt sleep and may not be remembered by the patient. Antiepileptic drugs often have a sedating effect and may contribute to daytime somnolence. Less commonly, antiepileptic drugs may have alerting properties and result in insomnia, as may be seen with felbamate (Felbatol, MedPointe, Somerset, New Jersey) and lamotrigine (Lamictal, GlaxoSmithKline, Research Triangle Park, North Carolina). Consequently, it is reassuring that levetiracetam (Keppra, UCBPharma, Brussels, Belgium), another "new" antiepileptic drug, appears to consolidate sleep. A lack of effect on the Epworth Sleepiness Scale suggests that daytime somnolence is not increased. Because sleep deprivation may exacerbate seizures, sleep disruption should be minimized in people with epilepsy. Replication of these results in people with epilepsy would lead to the recommendation that levetiracetam should be considered in people with epilepsy who have sleep difficulties due to their antiepileptic drugs.
Abstract
From
Sleep and Biological Rhythms
June 2005 (Volume 3, Number 2)
Dreaming and Schizophrenia: A Common Neurobiological Background?
Gottesmann C
Sleep Biol Rhythms. 2005;3:64-74
This article probes the physiologic similarities between the rapid eye movement (REM) dream state and schizophrenia.
Study Design
In a wide-ranging discussion, the study author compares the physiology of the REM dream state with the pathophysiology of schizophrenia.
Results
The study author observes that 40-Hz electroencephalographic (EEG) activity, which occurs during REM sleep, is uncoupled over the cortical areas. This uncoupling may parallel a "problem of connectivity" that occurs with schizophrenia. Decreased blood flow occurs in the dorsolateral prefrontal cortex during REM sleep and in schizophrenia. Hallucinations that occur in schizophrenia may be due to a decrease in sensory constraints, which also occur during REM sleep. The study author speculates that the failure of inhibitory cortical neurotransmitters could allow the individual to remember "useless memories" created during REM dreams, perhaps leading to schizophrenia. Dopamine levels are decreased during REM sleep compared with waking, which could correlate with the negative symptoms of schizophrenia, which may also be due to reduced levels of dopamine.
Conclusion
Dreams, with their disjointed, at times illogical, and time-distorted imagery, harbor similarities with the psychotic mentation of schizophrenia. In addition, a decrease in the neurotransmitter dopamine appears to play an important role in REM sleep as well as in the negative symptoms of schizophrenic psychosis. The study author postulates that REM sleep could become an experimental model for schizophrenia.
Commentary
Although dreams have fascinated humankind for millennia, the study of dreams is fraught with technically challenging methodologic problems. Dreams that occur during REM sleep represent a normal physiologic phenomenon, but at least superficial similarities exist with the abnormal state of schizophrenia. The study author articulates some commonalities underlying the physiology of dreams and the pathology of schizophrenia. However, it is premature to establish REM sleep as a neurobiological model for schizophrenia. Continued research may lead to an increased understanding of the creation of dreams and perhaps provide insights leading to novel treatments for schizophrenia.
From
Journal of Neurology, Neurosurgery & Psychiatry
January 2006 (Volume 77, Number 1)
Effects of Sleep Deprivation on Cortical Excitability in Patients Affected by Juvenile Myoclonic Epilepsy: A Combined Transcranial Magnetic Stimulation and EEG Study
Manganotti P, Bongiovanni LG, Fuggetta G, Zanette G, Fiaschi A
J Neurol Neurosurg Psychiatry. 2006;77:56-60
The study authors measured the effects of sleep deprivation with magnetic stimulation and electroencephalography (EEG) in 10 patients with juvenile myoclonic epilepsy (JME) and in 10 controls.
Study Design
Ten patients with JME (8 women, 2 men; ages 16-33) were compared with 10 controls (5 women, 5 men; ages 18-30). Eight of the patients were treated with phenobarbital and valproate, whereas the other two did not receive treatment. Subjects were studied with EEG and magnetic stimulation presleep and postsleep deprivation. Patients were sleep-deprived in the hospital from midnight until morning. Stimulation was over the presumed hand area of the motor cortex and recorded from the contralateral thenar eminence. Epileptic activity was quantified on the basis of 30 minutes of EEG recording before and after sleep deprivation.
Results
At baseline, JME patients had significantly decreased short-latency intracortical inhibition (SICI) values compared with controls (P < .001). This effect was larger in the 2 untreated patients than those on antiepileptic drugs. Sleep deprivation further decreased SICI values in patients with JME, but not in controls (P < .001). At baseline, short-latency intracortical facilitation (SICF) did not differ between patients and controls. However, sleep deprivation significantly increased SICF in patients with JME, but not in controls (P < .005). Motor threshold (MT) was significantly reduced by sleep deprivation in patients with JME, but not in controls (P < .001).
Conclusion
Several variables measured by magnetic stimulation were significantly affected by sleep deprivation in patients with JME: SICI decreased; SICF increased; and MT decreased.
Commentary
Every textbook on epilepsy mentions sleep deprivation as a "trigger" for seizures, yet little is known about the pathophysiology of this phenomenon. This study reveals that sleep deprivation can significantly modify the results of several variables (SICI, SICF, and MT) elicited by magnetic stimulation that represent primary motor cortex excitability. Of interest, patients treated with antiepileptic drugs had less prominent changes in SICI. If these results are routinely reproducible, this paradigm could prove extremely valuable in pursuing our understanding of the pathophysiology of epileptic activity and in providing a platform for the evaluation of new antiepileptic drugs. (Drugs that have the greatest effects on magnetic excitability parameters would merit further study.)
This study suffers from several basic technical limitations. The small population includes adults and children who may well differ in cortical excitability. The subjects were not sex-matched and were poorly age-matched. In addition, 8 patients were treated with antiepileptic drugs, whereas 2 were not. In such a small study, these variables should be eliminated. Future studies should endeavor to provide age- and sex-matched controls, control for treatment, and focus on adults or children. Further, although the text clearly states that SICI decreased, the table and figure reveal an apparent increase and are difficult to interpret. The EEG results were also not clearly reported relative to sleep deprivation.
Abstract
Supported by an independent educational grant from Takeda.
Saludos Cordiales
Dr. José Manuel Ferrer Guerra
posted by Klip7 at
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