suggested that different breathing patterns before sleep onset weredemonstrated between mixed apnea and pure obstructive apnea.We aim to investigate the respiratory signal patterns among 3 sub-types of obstructive sleep apnea (OSA).

Materials and methods: We enrolled 60 patients who were notonly diagnosed with OSA by polysomnography but also underwentnasal continuous positive airway pressure (CPAP) therapy more thanat least 6 months. Ten healthy subjects were also included. Patientswere divided into 3 types of OSA: pure-OSA (obstructive apnea100%), predominant- OSA (70% �100%), mixed-OSA (mixedapnea > 30% of total apneuic events). Respiration signal was calcu-lated as respiratory interval, which means time difference betweendiscrete respirations during 30 s. Stable sleep time, which wasdefined by two conditions, was extracted from total sleep duration.First, respiration rate has to fit within 12�20 per minute. Second,respiration interval was ranged from 3 to 5 s. We compared the syn-chrony of thorax-abdominal movements during sleep among 3 OSAsubtypes and healthy subjects.

Results: Out of 60 patients, 50 (90%) patients were male. Mean agewas 56.3¡3/410.5 years and mean apnea–hypopnea index (AHI) was41.7¡3/416.0/h. The proportion of stable sleep time was significantlydecreased in both predominant-OSA and mixed-OSA groups(P < 0.05), compared to pure-OSA group. The value of respiratoryinterval in mixed OSA showed significant higher variance, comparedto 2 subtypes of OSA (P < 0.01). Furthermore, significant disharmonybetween thorax and abdominal movement was demonstrated inpatients with mixed-OSA.

Conclusion: We reports that mix-OSA reveals not only unstablerespiratory pattern but also desynchronized movement of thoraxand abdominal wall during sleep, compared to patients with pure-OSA or predominant-OSA and normal subjects. Current study pro-vides some evidence for the different pathophysiology of respirationaccording to OSA subtypes.

http://dx.doi.org/10.1016/j.sleep.2013.11.406

Occurrence of sleep disordered breathing in acromegalyL. Korostovtseva 1, A. Semenov 1, D. Vaulina 2, S. Kravchenko 2,U. Tsoy 3, Y. Sviryaev 1

1 Almazov Federal Heart, Blood and Endocrinology Centre, HypertensionResearch Department, Russia2 Pavlov St Petersburg State Medical University, Russia3 Almazov Federal Heart, Blood and Endocrinology Centre, ResearchDepartment of Clinical Endocrinology with the course of Neuroendo-crinology, Russia

Introduction: To assess the occurrence, severity and type of sleepdisordered breathing in patients with acromegaly.

Materials and methods: Thirty three patients [5 males and 28females, mean age – 55 (95% CI 51.1–61.2) years, body mass index28.7 (95% CI 27.2–30.3) kg/m2] with active form of acromegaly last-ing for 3 (95% CI 0.9–36.4) months on average (since the diagnosiswas verified) underwent full polysomnography (Embla N7000, Med-Care, USA). The assessment of sleep disordered breathing was per-formed according to the Scoring rules of American Academy ofSleep Medicine (2009).

Results: In eleven (34%) females [median age 46 (95% CI 35.7–61.2) years] apnea/hypopnea index (AHI) was less than 5 episodesper hour of sleep [median 3.2 (95% CI 1.7–4.4) episodes/h], in 6 sub-jects [one male and 5 females, median age 59 (95% CI 51.4–76.3)years] – 12.9 (95% CI 8.2–14.8) episodes/h. Two females aged 52and 62 years (AHI 23.1 and 16 episodes/h) had moderate obstructivesleep apnea (OSA) and 14 patients [3 males and 11 females, median

age 55 (95% CI 53.0–64.8) years] had severe sleep disordered breath-ing with median AHI 53 (95% CI 46.9–66.4) episodes/h (v2 = 30;p < 0.001). Among them 12 subjects [3 males and 9 females, medianage 59 (95% CI 53.9–67.6) years] demonstrated OSA, and 2 patients(one 50-year-old male and one 53-year-old female) had mixedapnea. Those with severe apnea had higher values of BMI that was31.7 (95% CI 28.9–34.3); 28.4 (95% CI 24.4–31.7) and 25.5 (95% CI23.8–28.0) kg/m2 in patients with severe, mild apnea and in subjectswithout sleep breathing disorders, respectively (v2 = 8.7; p = 0.03).In two females with moderate sleep apnea BMI was 29.7 and 28.7kg/m2. BMI positively correlated with the severity of sleep apnea(q = 0.8; p < 0.001) and negatively – with mean oxygen saturation(q = �0.9; p < 0.001) and the size of adenoma (q = �0.5; p < 0.05).

Conclusion: Sleep disordered breathing, and mostly obstructivesleep apnea, are highly prevalent among patients with acromegaly,affecting almost 2/3 of patients that exceeds general population sta-tistics. The severity of sleep disordered breathing is associated withBMI that might be a contributing factor, but the search for otherpotential contributing factors is required in this group of patients.

Acknowledgement: Authors declare no conflict of interest.

http://dx.doi.org/10.1016/j.sleep.2013.11.407

Narcolepsy with cataplexy and parkinson’s disease – A casereportM. Krcmarova, P. Dusek, P. Kovalska, B. Roth, K. SonkaDepartment of Neurology, First Faculty of Medicine, Charles Universityin Prague, General University Hospital in Prague, Czech Republic

Introduction: Narcolepsy with cataplexy (NC) is a sporadic neuro-logical disease with prevalence 0.02–0.067% and it is caused by theloss of hypocretin neurons in lateral hypothalamus. NC is associatedwith HLA DQB1*06:02 allele. Parkinson‘s disease (PD) is a degenera-tive disorder manifested by hypokinetic-rigid syndrome, caused bydegeneration of dopamine-producing cells in the substantia nigra parscompacta. The prevalence of PD is 0.1–0.2%. In addition to cardinalmotor symptoms (akinesia, rigidity, tremor and postural instability),autonomic and sensory disturbances as well as cognitive, behavioraland sleep problems can occur during the disease progression.

Materials and methods: This is a case report presentation.Results: An 86-year-old Caucasian woman suffering from NC was

diagnosed at our department in 1980s. Daytime polysomnography(PSG) was performed, demonstrating typical SOREMPs. The patientwas treated by phenmetrazin and imipramin or clomipramin. In1995 the patient was retired and her narcoleptic symptoms becameless prominent. The patient stopped the therapy and dropped outfrom the contact with our department. Hypokinetic-rigid syndromewith symmetric rigidity and akinesia in upper extremities and mildgait difficulty with instability was diagnosed when the patient was83 year old. Patient’s symptoms stabilized after pramipexol 0.7 mgbid initiation. At the age of 85, the patient reported disturbing hyper-somnia and frequent falls, which led to reevaluation in our depart-ment. Patient reported frequent daytime sleep attacks withvariable duration. The sleepiness was present in rest as well as dur-ing social activities. The falls, mostly backwards were not caused byemotions nor associated with decreased muscle tone. Sometimesthese were preceded by lightheadedness and pre-syncopal syn-dromes, but mostly were related to gait instability. Patient did notreport hypnagogic hallucinations or sleep paralysis. Night PSGrevealed frequent PLMS, severe sleep apnea (AHI 43), MSLT con-firmed narcolepsy (short sleep latency and 2 SOREMPs), HLA typingshowed haplotype HLA DQB1*06:02. Clinical examination showedtypical parkinson’s syndrome (motor subscale of UPDRS 28) with

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good response to dopaminergic treatment and the diagnosis of idio-pathic PD was established.

Conclusion: We report this case because the co-occurrence of NCand PD is very rare according to the literature.

Acknowledgement: IGA MZ ÈR: NT 13238–4/2012.

http://dx.doi.org/10.1016/j.sleep.2013.11.408

CAV1.2 calcium channel is involved in the circadian regulation ofsleepD. Kumar, N. Dedic, C. Flachskamm, J. Deussing, M. KimuraMax Planck Institute of Psychiatry, Germany

Introduction: Two L-type Ca2+ channels (Cav1.2 & Cav1.3) areexpressed in the mouse brain with Cav1.2 contributing to a majorproportion (85%). The expression of L-type Ca2+ channels is greatlydensed in the suprachiasmatic nuclei, a neuronal area capable offunctioning as autonomous clock and as a generator of circadianrhythms. Although one of the most important aspects regardingthe circadian rhythm is the sleep–wake cycle, yet the role ofCav1.2 in the sleep–wake cycle is unclear. Therefore, we investigatedwhether depletion of Cav1.2 in a transgenic mouse line Cav1.2 (+/�)would alter spontaneous sleep–wake activities.

Materials and methods: Sleep–wake patterns were monitored bymeans of EEG and EMG recordings in Cav1.2 (+/�) mice and theirwild-type littermates under baseline and sleep deprivation condi-tions (6 h by gentle handling).

Results: Under basal condition, Cav1.2 (+/�) mice showed increasedsleep onset latency but subsequent hypersomnolence as compared towild-type. The hypersomnolence observed in these mice was charac-terized by higher slow wave activity. Moreover, these heterozygousmice also exhibited drastically shorter wake episodes in the dark per-iod, due to an increased number of NREM sleep episodes. Analysis ofsleep architecture further revealed that these mice showed frequenttransitions from wake to NREM sleep and vice versa. After sleep depri-vation, the sleep onset latency decreased drastically and the trend forhigher NREM sleep was observed in Cav1.2 (+/�) mice.

Conclusion: Our results demonstrate that depletion of Cav1.2 signif-icantly impacts circadian sleep regulation indicated by increased NREMsleep and decreased time spent in wake in the dark period. However,homeostatic regulation of sleep was unaltered. It has been reported thatL-type Ca2+ channels are involved in wake-promoting effects of hypo-cretin1. Therefore, decreased wakefulness in Cav1.2 (+/�) mice sug-gests that a depletion of Cav1.2 might attenuate the hypocretin 1mediated excitation of wake-related neurons. The alpha-1 subunit ofL-type Ca2+ channels (Cav1.2) is encoded by the CACNA1C gene. Gen-ome-wide association studies (GWAS) have suggested that polymor-phisms in the CACNA1C gene are associated with sleep disorders, e.g.,insomnia and narcolepsy. Increased sleep onset latency and frag-mented sleep architecture displayed by Cav1.2 (+/�) mice might besigns of symptomatic sleep disorders but further studies are neededto elucidate this. Nevertheless, several GWAS studies have significantlyassociated the CACNA1C gene with psychiatric disorders.

http://dx.doi.org/10.1016/j.sleep.2013.11.409

Do fathers suffer from postpartum fatigue? The roles of sleepquality and stressT. Kushnir 1, S. Israeli-Tedgi 2, J. Urkin 3

1 Ben-Gurion University of the Negev, Faculty of Health Sciences, Israel2 Ben-Gurion University of the Negev, Faculty of Health Sciences, PublicHealth Israel3 Ben-Gurion University of the Negev, Faculty of Health Sciences,Medical Education, Israel

Introduction: Background: Childbirth and the responsibilities ofparenting require a great deal of energy. Sleep disturbances that arecommon in the postpartum period, are important correlates of fatigueand could affect energy levels. Postpartum fatigue (PPF) is the mostcommon unpleasant symptom following childbirth. It is an over-whelming sense of energy loss, exhaustion and decreased capacityfor physical and mental work following childbirth. There have beenno direct studies of PPF and its correlates among fathers. Aims: Tocompare PPF levels of fathers and wives in the post delivery period;to assess the contribution of sleep quality and stress to fathers’ PPF.

Materials and methods: Participants were 50 married couples(n = 100), ages 20–40, four to six weeks post delivery. They wereattending routine pediatric appointments in community clinics.We excluded women with postnatal depression (based on EdinburghPostnatal Depression Scale). A self reporting questionnaire assessed:postpartum fatigue (FCS), sleep quality (PSQI), stress (PS) and post-natal depression (EPDS).

Results: PPF levels of fathers and wives were highly correlated(r = 0.644, p < .001). There were no significant differences in PPFbetween fathers and wives. Among fathers sleep quality wasstrongly correlated with stress (r = 0.690, p < .001) and PPF(r = 0.633, p < 0.01). Multicollinearity was not found. In a multipleregression analysis with sleep quality and stress as independent pre-dictors of PPF, the effect of sleep quality on PPF was greatly reduced(r = 0.28, p < .05). A Sobel test of the significance of this reductionconfirmed that stress mediated the association between sleep qual-ity and PPF. Thus the effect of sleep quality on fatigue was indirect.

Conclusion: In this preliminary investigation with a small sample,fathers and their wives in the post delivery period had similar levelsof PPF. It is well known that most mothers in the post-partum periodsuffer from PPF. Our results indicate that this phenomenon may becommon among fathers too. Thus PPF may adversely affect bothmothers’ and fathers’ quality of life. Our results also suggest thatamong the fathers sleep issues probably raised stress levels whichin turn increased PPT levels. This possibility requires further system-atic confirmation. Further systematic studies are needed to uncoverthe extent and correlates of PPF and the interconnections betweenthe factors implicated in this phenomenon among fathers.

Acknowledgement: We acknowledge the help of Dr. Nir Madjarwho greatly contributed to the statistical analysis.

http://dx.doi.org/10.1016/j.sleep.2013.11.410

Period lengths of temperature and melatonin circadian rhythmsin delayed sleep phase disorderG. Micic 1, L. Lack 1, N. Lovato 1, H. Burgess 2, S. Ferguson 3

1 Flinders University of South Australia, School of Psychology, Australia2 Rush University Medical Center, Circadian Rhythms Research Labora-tory, Australia3 Central Queensland University, Appleton Institute, Australia

Introduction: Delayed Sleep Phase Disorder (DSPD) is character-ized as an abnormally delayed sleep period. The currently assumedaetiology is simply a phase-delay in individuals’ biological bodyclocks. However, DSPD cases treated to produce a corrective phaseadvance are very prone to relapse. It has been suggested that thismay be due to an abnormally long period length (time taken to com-plete one cycle of the rhythm). Circadian period lengths of endoge-nous core body temperature and salivary melatonin weremeasured to investigate this premise.

Materials and methods: Following rigorous screening procedures,nine healthy controls and nine persons with DSPD were selectedfor a 80-h protocol consisting of an ultradian modified constant rou-

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