SLEEP 2011 Abstract Supplement

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B. Clinical Sleep Science VII. Neurological Disorders and Sleep and Case3 showed prolonged percentages of stage 3-4 sleep. Some neuropatological changes might be related to these sleep changes. 0629 SLEEP DISORDERED BREATHING AND OTHER SLEEP DYSFUNCTION IN MYOTONIC DYSTROPHY TYPE 2 Yang Q, Sander H, Grewal R, Rosen D, Kabolizadeh K, Maganti S, Farheen A, Bhat S, Gupta D, Chokroverty S Sleep Medicine, JFK Medical Center, Edison, NJ, USA Introduction: Myotonic dystrophy type 2 (DM2) is a recently described hereditary myotonic dystrophy which is differentiated from myotonic dystrophy type 1 (DM1) by different genetic mutations. Sleep disordered breathing (SDB) has not been described in DM2 but is known to occur in DM1. Methods: We are presenting six patients (four women and two men ages 51-63 years) with symmetric muscle weakness involving proximal more than distal muscles and thenar eminence percussion myotonia. Major sleep complaints included chronic insomnia, snoring, excessive daytime sleepiness and dream-enacting behavior (DEB) in one woman. Results: Genetic testing was consistent with a diagnosis of DM2. Electromyography showed myopathic findings and myotonia. Overnight polysomnography (PSG) disclosed obstructive sleep apnea in four patients and REM behavior disorder (RBD) in one woman (REM without atonia and excessive phasic muscle bursts associated with dream enacting behavior). Other PSG findings included absent REM sleep in one and alpha-REM-spindle mixture in another who also had paradoxical movements in the respiratory effort channels suggesting increased upper airway resistance. Conclusion: These sleep abnormalities (RBD in one and sleep disordered breathing in five patients) with DM2 are novel observations. 0630 AN INVESTIGATION OF SPONTANEOUS CORTICAL SLOW OSCILLATIONS DURING NREM SLEEP USING 256-CHANNEL EEG IN NON-EPILEPTIC AND EPILEPTIC SUBJECTS Gilbert TT 1 , Luu P 1 , Holmes M 3 , Tucker D 1,2 1 Brain Electrophysiology Laboratory, Electrical Geodesics, Inc., Eugene, OR, USA, 2 Psychology, University of Oregon, Eugene, OR, USA, 3 Neurology, Regional Epilepsy Center, Harborview Medical Center, Seattle, WA, USA Introduction: Cortical slow oscillations (CSO) (
B. Clinical Sleep Science VII. Neurological Disorders and Sleep headache over one year’s time were analyzed. As a part of their evaluation, those patients were queried regarding their sleep, and, if appropriate, were studied with polysomnography in an accredited sleep disorders center. Patients with changes on the neurologic exam suggestive of cervical radiculopathy were examined with EMG-NCV testing. Results: Of the 700 patients who had a diagnosis of headache on initial evaluation, 491 (70%) also had sleep diagnoses. Of these patients with sleep diagnoses, 277 (56%) completed polysomnography examinations. 76% of the polysomnography group had upper airway resistance syndrome (UARS) or obstructive sleep apnea (OSA). Striking in the polysomnography group patients was the presence of concomitant cervical radiculopathy (73 %). Of the patients with cervical radiculopathy, 50% or more of total sleep time was spent in non-supine sleep, despite request by the technologist to sleep supine. Conclusion: 1. Headache is strongly associated with sleep disordered breathing. 2. Cervical radiculopathy is strongly associated with sleep disordered breathing, confirming a previous study. 3. Non-supine sleep provoked by sleep disordered breathing may play a previously unrecognized role in headache and cervical radiculopathy. 0633 SEIZURE REDUCTION FOLLOWING NASAL CONTINUOUS POSITIVE AIRWAY PRESSURE THERAPY FOR CO-MORBID OBSTRUCTIVE SLEEP APNEA IN EPILEPSY St. Louis EK 1 , Berth W 2 , Zimmerman B 3 , Dyken ME 2 , Granner MA 2 1 Department of Neurology, Mayo Clinic, Rochester, MN, USA, 2 Department of Neurology, University of Iowa Hospitals and Clinics, Iowa City, IA, USA, 3 Department of Biostatistics, University of Iowa College of Public Health, Iowa City, IA, USA Introduction: Co-morbid OSA is frequent in epilepsy, and treatment with nCPAP may reduce seizure frequency but the degree of impact on seizure outcomes remains unclear. We hypothesized that seizure frequency would be reduced by nasal continuous positive airway pressure (nCPAP) therapy in epilepsy patients with co-morbid obstructive sleep apnea (OSA). We aimed to analyze the impact of nCPAP therapy on seizure frequency. Methods: We retrospectively analyzed 184 epilepsy patients who underwent polysomnography between 1/1/00-5/30/09. Demographic, seizure frequency, antiepileptic drug load, and PSG variables were recorded. Seizure frequency was compared between epilepsy patients with OSA (apnea-hypopnea index (AHI)>5/hour) who were compliant with nCPAP and those who either deferred nCPAP or were non-compliant. Group comparisons were analyzed with 2-tailed T-tests or Wilcoxon signed rank tests in JMP or SAS (Chicago, IL). Results: 110 (60%) epilepsy patients had OSA. Average AHI was 22.4 ± 20.8. Forty-three patients received nCPAP. Of 33 patients having pre- and post-nCPAP data, seizure frequency decreased significantly (t=2.138, p=0.04). 79% reported seizure reduction and 61% were responders (having a 50% or greater seizure reduction), and this effect held when antiepileptic drugs were unchanged or reduced (n=18, p=0.01). In patients who did not receive or comply with nCPAP therapy, there was no significant difference in seizure frequency (n=28, t=-1.411, p=0.17). Conclusion: nCPAP treatment significantly reduces seizure frequency, and the degree of seizure improvement appears comparable to the effect of adjunctive antiepileptic drug therapy. Further prospective studies of the impact of co-morbid OSA in epilepsy patients on seizure burden and interictal state factors crucial to quality of life (i.e., mood state, vulnerability to antiepileptic drug adverse effects, and sleepiness/vigilance) are warranted. Support (If Any): University of Iowa Carver College of Medicine Medical Student Summer Research Award; Mentored Clinical Research Scholar Program at Iowa (K12 RR017700-05); Grant Number 1 UL1RR024150 from the National Center for Research Resources (NCRR) 0634 VAGUS NERVE STIMULATION THERAPY ENHANCES OBSTRUCTIVE RESPIRATIONS DURING SLEEP Simmons JH 1,2 , Barlow S 1,2 1 Sadler Clinic Sleep Disorders Center, The Woodlands, TX, USA, 2 CSMA, Houston, TX, USA Introduction: Vagus Nerve Stimulator (VNS) therapy has been used in medication resistant Epilepsy with improved outcomes and utilization has increased over the past decade. In our center we have OSA patients with epilepsy that have VNS devices and have recognized many of these patients have periodic obstructive breathing patterns that correspond to their VNS stimulation settings. We sought to confirm this association and to also determine optimal methods of treating both the patients seizures and OSA rather than one at the detriment of the other. Methods: The study was done in two parts. First, we reviewed all of our patients who have both VNS devices for the treatment of their epilepsy and who underwent NPSG testing. Next, assessment was done to identify if there was an association between the VNS stimulation pattern and the occurrence of OSA. In one patient modifications were made in the VNS settings during NPSG testing to clearly confirm the association between VNS stimulation and OSA occurrence and then modifications were made on the VNS stimulation settings to identify parameters that stopped producing OSA. Results: Eight patients met our criteria of which six demonstrated OSA. All six demonstrated OSA in a pattern that correlated to the VNS stimulation rate. PAP titration was performed and initially prevented OSA from occurring during sleep. In three patients over time OSA worsened. Repeat titrations were performed and a clear pattern of periodic OSA was identified that was not adequately treated by prior CPAP pressures. To address the above observation one patient thus far was further evaluated by a repeat PAP titration. During the study, clear periodic obstructive apneas again occurred in accordance with her VNS settings. Stimulator parameters were modified to identify parameters that would not precipitate OSA. Lowering the stimulation rate from 25Hz down to 10 Hz resolved the precipitation of OSA during the study. Conclusion: We claim that OSA is a potential complication of VNS therapy. This can be managed adequately but must be recognized when present. VNS stimulation parameters may require modification to optimize OSA treatment. We will present the clinical significance of these findings in relation to treating both OSA and Epilepsy. Further study is clearly needed on this topic since VNS is a useful treatment in Epilepsy patients. 0635 NOCTURNAL SEIZURES AND DYSREGULATION IN THE AUTONOMIC NERVOUS SYSTEM Kawai M 1 , Thapalia U 1 , Ohki N 2 , Verma A 1 1 Neurology/Neurophysiology, Neurological Institute, The Methodist Hospital, Houston, TX, USA, 2 NoruPro Light Systems, , Kokubunnji city, Japan Introduction: There are several reports that nocturnal seizures and sudden unexpected death in epileptic patients (SUDEP) is related. Correlation of autonomic nervous system (ANS) dysregulation and SUDEP has been recognized. Heart rate variability (HRV) has been utilized to evaluate ANS. High frequency (HF) component (0.15-0.4 Hz) of HRV is known to represent parasympathetic modulation. HF tends to appear steadily in normal NREM sleep. Temporal correlation between ANS and nocturnal seizure is not known well. Complex demodulation analysis of HRV allows us to detect dynamic changes in HF with temporal resolution of 6.25 seconds, whereas other analyses (i.e. fast Fourier transform) have that of 1-2 minutes. Methods: All of the nocturnal seizures captured in our epilepsy monitoring unit from January 2008 to September 2010 were reviewed retrospectively. Electrocardiogram data were analyzed with complex A219 SLEEP, Volume 34, Abstract Supplement, 2011
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