- Email: [email protected]
Narcolepsy with cataplexy and parkinson’s disease – A case report
e174
Abstracts / Sleep Medicine 14S (2013) e165–e238
suggested that different breathing patterns before sleep onset were demonstrated between mixed apnea and pure obstructive apnea. We aim to investigate the respiratory signal patterns among 3 subtypes of obstructive sleep apnea (OSA). Materials and methods: We enrolled 60 patients who were not only diagnosed with OSA by polysomnography but also underwent nasal continuous positive airway pressure (CPAP) therapy more than at least 6 months. Ten healthy subjects were also included. Patients were divided into 3 types of OSA: pure-OSA (obstructive apnea 100%), predominant- OSA (70% 100%), mixed-OSA (mixed apnea > 30% of total apneuic events). Respiration signal was calculated as respiratory interval, which means time difference between discrete respirations during 30 s. Stable sleep time, which was defined by two conditions, was extracted from total sleep duration. First, respiration rate has to fit within 1220 per minute. Second, respiration interval was ranged from 3 to 5 s. We compared the synchrony of thorax-abdominal movements during sleep among 3 OSA subtypes and healthy subjects. Results: Out of 60 patients, 50 (90%) patients were male. Mean age was 56.3¡3/410.5 years and mean apnea–hypopnea index (AHI) was 41.7¡3/416.0/h. The proportion of stable sleep time was significantly decreased in both predominant-OSA and mixed-OSA groups (P < 0.05), compared to pure-OSA group. The value of respiratory interval in mixed OSA showed significant higher variance, compared to 2 subtypes of OSA (P < 0.01). Furthermore, significant disharmony between thorax and abdominal movement was demonstrated in patients with mixed-OSA. Conclusion: We reports that mix-OSA reveals not only unstable respiratory pattern but also desynchronized movement of thorax and abdominal wall during sleep, compared to patients with pureOSA or predominant-OSA and normal subjects. Current study provides some evidence for the different pathophysiology of respiration according to OSA subtypes. http://dx.doi.org/10.1016/j.sleep.2013.11.406
Occurrence of sleep disordered breathing in acromegaly L. 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, Hypertension Research Department, Russia 2 Pavlov St Petersburg State Medical University, Russia 3 Almazov Federal Heart, Blood and Endocrinology Centre, Research Department of Clinical Endocrinology with the course of Neuroendocrinology, Russia
Introduction: To assess the occurrence, severity and type of sleep disordered breathing in patients with acromegaly. Materials and methods: Thirty three patients [5 males and 28 females, mean age – 55 (95% CI 51.1–61.2) years, body mass index 28.7 (95% CI 27.2–30.3) kg/m2] with active form of acromegaly lasting for 3 (95% CI 0.9–36.4) months on average (since the diagnosis was verified) underwent full polysomnography (Embla N7000, MedCare, USA). The assessment of sleep disordered breathing was performed according to the Scoring rules of American Academy of Sleep 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 episodes per hour of sleep [median 3.2 (95% CI 1.7–4.4) episodes/h], in 6 subjects [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 52 and 62 years (AHI 23.1 and 16 episodes/h) had moderate obstructive sleep apnea (OSA) and 14 patients [3 males and 11 females, median
age 55 (95% CI 53.0–64.8) years] had severe sleep disordered breathing 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, median age 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 mixed apnea. Those with severe apnea had higher values of BMI that was 31.7 (95% CI 28.9–34.3); 28.4 (95% CI 24.4–31.7) and 25.5 (95% CI 23.8–28.0) kg/m2 in patients with severe, mild apnea and in subjects without sleep breathing disorders, respectively (v2 = 8.7; p = 0.03). In two females with moderate sleep apnea BMI was 29.7 and 28.7 kg/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 obstructive sleep apnea, are highly prevalent among patients with acromegaly, affecting almost 2/3 of patients that exceeds general population statistics. The severity of sleep disordered breathing is associated with BMI that might be a contributing factor, but the search for other potential 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 case report M. Krcmarova, P. Dusek, P. Kovalska, B. Roth, K. Sonka Department of Neurology, First Faculty of Medicine, Charles University in Prague, General University Hospital in Prague, Czech Republic
Introduction: Narcolepsy with cataplexy (NC) is a sporadic neurological disease with prevalence 0.02–0.067% and it is caused by the loss of hypocretin neurons in lateral hypothalamus. NC is associated with HLA DQB1*06:02 allele. Parkinson‘s disease (PD) is a degenerative disorder manifested by hypokinetic-rigid syndrome, caused by degeneration of dopamine-producing cells in the substantia nigra pars compacta. The prevalence of PD is 0.1–0.2%. In addition to cardinal motor symptoms (akinesia, rigidity, tremor and postural instability), autonomic and sensory disturbances as well as cognitive, behavioral and 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 patient was treated by phenmetrazin and imipramin or clomipramin. In 1995 the patient was retired and her narcoleptic symptoms became less prominent. The patient stopped the therapy and dropped out from the contact with our department. Hypokinetic-rigid syndrome with symmetric rigidity and akinesia in upper extremities and mild gait difficulty with instability was diagnosed when the patient was 83 year old. Patient’s symptoms stabilized after pramipexol 0.7 mg bid initiation. At the age of 85, the patient reported disturbing hypersomnia and frequent falls, which led to reevaluation in our department. Patient reported frequent daytime sleep attacks with variable duration. The sleepiness was present in rest as well as during social activities. The falls, mostly backwards were not caused by emotions nor associated with decreased muscle tone. Sometimes these were preceded by lightheadedness and pre-syncopal syndromes, but mostly were related to gait instability. Patient did not report hypnagogic hallucinations or sleep paralysis. Night PSG revealed frequent PLMS, severe sleep apnea (AHI 43), MSLT confirmed narcolepsy (short sleep latency and 2 SOREMPs), HLA typing showed haplotype HLA DQB1*06:02. Clinical examination showed typical parkinson’s syndrome (motor subscale of UPDRS 28) with
Abstracts / Sleep Medicine 14S (2013) e165–e238
good response to dopaminergic treatment and the diagnosis of idiopathic PD was established. Conclusion: We report this case because the co-occurrence of NC and 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 of sleep D. Kumar, N. Dedic, C. Flachskamm, J. Deussing, M. Kimura Max Planck Institute of Psychiatry, Germany
Introduction: Two L-type Ca2+ channels (Cav1.2 & Cav1.3) are expressed in the mouse brain with Cav1.2 contributing to a major proportion (85%). The expression of L-type Ca2+ channels is greatly densed in the suprachiasmatic nuclei, a neuronal area capable of functioning as autonomous clock and as a generator of circadian rhythms. Although one of the most important aspects regarding the circadian rhythm is the sleep–wake cycle, yet the role of Cav1.2 in the sleep–wake cycle is unclear. Therefore, we investigated whether 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 by means of EEG and EMG recordings in Cav1.2 (+/ ) mice and their wild-type littermates under baseline and sleep deprivation conditions (6 h by gentle handling). Results: Under basal condition, Cav1.2 (+/ ) mice showed increased sleep onset latency but subsequent hypersomnolence as compared to wild-type. The hypersomnolence observed in these mice was characterized by higher slow wave activity. Moreover, these heterozygous mice also exhibited drastically shorter wake episodes in the dark period, due to an increased number of NREM sleep episodes. Analysis of sleep architecture further revealed that these mice showed frequent transitions from wake to NREM sleep and vice versa. After sleep deprivation, the sleep onset latency decreased drastically and the trend for higher NREM sleep was observed in Cav1.2 (+/ ) mice. Conclusion: Our results demonstrate that depletion of Cav1.2 significantly impacts circadian sleep regulation indicated by increased NREM sleep and decreased time spent in wake in the dark period. However, homeostatic regulation of sleep was unaltered. It has been reported that L-type Ca2+ channels are involved in wake-promoting effects of hypocretin1. Therefore, decreased wakefulness in Cav1.2 (+/ ) mice suggests that a depletion of Cav1.2 might attenuate the hypocretin 1 mediated excitation of wake-related neurons. The alpha-1 subunit of L-type Ca2+ channels (Cav1.2) is encoded by the CACNA1C gene. Genome-wide association studies (GWAS) have suggested that polymorphisms in the CACNA1C gene are associated with sleep disorders, e.g., insomnia and narcolepsy. Increased sleep onset latency and fragmented sleep architecture displayed by Cav1.2 (+/ ) mice might be signs of symptomatic sleep disorders but further studies are needed to elucidate this. Nevertheless, several GWAS studies have significantly associated 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 sleep quality and stress T. Kushnir 1, S. Israeli-Tedgi 2, J. Urkin 3 1 Ben-Gurion University of the Negev, Faculty of Health Sciences, Israel 2 Ben-Gurion University of the Negev, Faculty of Health Sciences, Public Health Israel 3 Ben-Gurion University of the Negev, Faculty of Health Sciences, Medical Education, Israel
e175
Introduction: Background: Childbirth and the responsibilities of parenting require a great deal of energy. Sleep disturbances that are common in the postpartum period, are important correlates of fatigue and could affect energy levels. Postpartum fatigue (PPF) is the most common unpleasant symptom following childbirth. It is an overwhelming sense of energy loss, exhaustion and decreased capacity for physical and mental work following childbirth. There have been no direct studies of PPF and its correlates among fathers. Aims: To compare 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 were attending routine pediatric appointments in community clinics. We excluded women with postnatal depression (based on Edinburgh Postnatal Depression Scale). A self reporting questionnaire assessed: postpartum fatigue (FCS), sleep quality (PSQI), stress (PS) and postnatal depression (EPDS). Results: PPF levels of fathers and wives were highly correlated (r = 0.644, p < .001). There were no significant differences in PPF between fathers and wives. Among fathers sleep quality was strongly correlated with stress (r = 0.690, p < .001) and PPF (r = 0.633, p < 0.01). Multicollinearity was not found. In a multiple regression analysis with sleep quality and stress as independent predictors 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 reduction confirmed that stress mediated the association between sleep quality 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 levels of PPF. It is well known that most mothers in the post-partum period suffer from PPF. Our results indicate that this phenomenon may be common among fathers too. Thus PPF may adversely affect both mothers’ and fathers’ quality of life. Our results also suggest that among the fathers sleep issues probably raised stress levels which in turn increased PPT levels. This possibility requires further systematic confirmation. Further systematic studies are needed to uncover the extent and correlates of PPF and the interconnections between the factors implicated in this phenomenon among fathers. Acknowledgement: We acknowledge the help of Dr. Nir Madjar who greatly contributed to the statistical analysis. http://dx.doi.org/10.1016/j.sleep.2013.11.410
Period lengths of temperature and melatonin circadian rhythms in delayed sleep phase disorder G. Micic 1, L. Lack 1, N. Lovato 1, H. Burgess 2, S. Ferguson 3 1 Flinders University of South Australia, School of Psychology, Australia 2 Rush University Medical Center, Circadian Rhythms Research Laboratory, Australia 3 Central Queensland University, Appleton Institute, Australia
Introduction: Delayed Sleep Phase Disorder (DSPD) is characterized as an abnormally delayed sleep period. The currently assumed aetiology is simply a phase-delay in individuals’ biological body clocks. However, DSPD cases treated to produce a corrective phase advance are very prone to relapse. It has been suggested that this may be due to an abnormally long period length (time taken to complete one cycle of the rhythm). Circadian period lengths of endogenous core body temperature and salivary melatonin were measured to investigate this premise. Materials and methods: Following rigorous screening procedures, nine healthy controls and nine persons with DSPD were selected for a 80-h protocol consisting of an ultradian modified constant rou-
Abstracts / Sleep Medicine 14S (2013) e165–e238
suggested that different breathing patterns before sleep onset were demonstrated between mixed apnea and pure obstructive apnea. We aim to investigate the respiratory signal patterns among 3 subtypes of obstructive sleep apnea (OSA). Materials and methods: We enrolled 60 patients who were not only diagnosed with OSA by polysomnography but also underwent nasal continuous positive airway pressure (CPAP) therapy more than at least 6 months. Ten healthy subjects were also included. Patients were divided into 3 types of OSA: pure-OSA (obstructive apnea 100%), predominant- OSA (70% 100%), mixed-OSA (mixed apnea > 30% of total apneuic events). Respiration signal was calculated as respiratory interval, which means time difference between discrete respirations during 30 s. Stable sleep time, which was defined by two conditions, was extracted from total sleep duration. First, respiration rate has to fit within 1220 per minute. Second, respiration interval was ranged from 3 to 5 s. We compared the synchrony of thorax-abdominal movements during sleep among 3 OSA subtypes and healthy subjects. Results: Out of 60 patients, 50 (90%) patients were male. Mean age was 56.3¡3/410.5 years and mean apnea–hypopnea index (AHI) was 41.7¡3/416.0/h. The proportion of stable sleep time was significantly decreased in both predominant-OSA and mixed-OSA groups (P < 0.05), compared to pure-OSA group. The value of respiratory interval in mixed OSA showed significant higher variance, compared to 2 subtypes of OSA (P < 0.01). Furthermore, significant disharmony between thorax and abdominal movement was demonstrated in patients with mixed-OSA. Conclusion: We reports that mix-OSA reveals not only unstable respiratory pattern but also desynchronized movement of thorax and abdominal wall during sleep, compared to patients with pureOSA or predominant-OSA and normal subjects. Current study provides some evidence for the different pathophysiology of respiration according to OSA subtypes. http://dx.doi.org/10.1016/j.sleep.2013.11.406
Occurrence of sleep disordered breathing in acromegaly L. 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, Hypertension Research Department, Russia 2 Pavlov St Petersburg State Medical University, Russia 3 Almazov Federal Heart, Blood and Endocrinology Centre, Research Department of Clinical Endocrinology with the course of Neuroendocrinology, Russia
Introduction: To assess the occurrence, severity and type of sleep disordered breathing in patients with acromegaly. Materials and methods: Thirty three patients [5 males and 28 females, mean age – 55 (95% CI 51.1–61.2) years, body mass index 28.7 (95% CI 27.2–30.3) kg/m2] with active form of acromegaly lasting for 3 (95% CI 0.9–36.4) months on average (since the diagnosis was verified) underwent full polysomnography (Embla N7000, MedCare, USA). The assessment of sleep disordered breathing was performed according to the Scoring rules of American Academy of Sleep 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 episodes per hour of sleep [median 3.2 (95% CI 1.7–4.4) episodes/h], in 6 subjects [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 52 and 62 years (AHI 23.1 and 16 episodes/h) had moderate obstructive sleep apnea (OSA) and 14 patients [3 males and 11 females, median
age 55 (95% CI 53.0–64.8) years] had severe sleep disordered breathing 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, median age 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 mixed apnea. Those with severe apnea had higher values of BMI that was 31.7 (95% CI 28.9–34.3); 28.4 (95% CI 24.4–31.7) and 25.5 (95% CI 23.8–28.0) kg/m2 in patients with severe, mild apnea and in subjects without sleep breathing disorders, respectively (v2 = 8.7; p = 0.03). In two females with moderate sleep apnea BMI was 29.7 and 28.7 kg/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 obstructive sleep apnea, are highly prevalent among patients with acromegaly, affecting almost 2/3 of patients that exceeds general population statistics. The severity of sleep disordered breathing is associated with BMI that might be a contributing factor, but the search for other potential 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 case report M. Krcmarova, P. Dusek, P. Kovalska, B. Roth, K. Sonka Department of Neurology, First Faculty of Medicine, Charles University in Prague, General University Hospital in Prague, Czech Republic
Introduction: Narcolepsy with cataplexy (NC) is a sporadic neurological disease with prevalence 0.02–0.067% and it is caused by the loss of hypocretin neurons in lateral hypothalamus. NC is associated with HLA DQB1*06:02 allele. Parkinson‘s disease (PD) is a degenerative disorder manifested by hypokinetic-rigid syndrome, caused by degeneration of dopamine-producing cells in the substantia nigra pars compacta. The prevalence of PD is 0.1–0.2%. In addition to cardinal motor symptoms (akinesia, rigidity, tremor and postural instability), autonomic and sensory disturbances as well as cognitive, behavioral and 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 patient was treated by phenmetrazin and imipramin or clomipramin. In 1995 the patient was retired and her narcoleptic symptoms became less prominent. The patient stopped the therapy and dropped out from the contact with our department. Hypokinetic-rigid syndrome with symmetric rigidity and akinesia in upper extremities and mild gait difficulty with instability was diagnosed when the patient was 83 year old. Patient’s symptoms stabilized after pramipexol 0.7 mg bid initiation. At the age of 85, the patient reported disturbing hypersomnia and frequent falls, which led to reevaluation in our department. Patient reported frequent daytime sleep attacks with variable duration. The sleepiness was present in rest as well as during social activities. The falls, mostly backwards were not caused by emotions nor associated with decreased muscle tone. Sometimes these were preceded by lightheadedness and pre-syncopal syndromes, but mostly were related to gait instability. Patient did not report hypnagogic hallucinations or sleep paralysis. Night PSG revealed frequent PLMS, severe sleep apnea (AHI 43), MSLT confirmed narcolepsy (short sleep latency and 2 SOREMPs), HLA typing showed haplotype HLA DQB1*06:02. Clinical examination showed typical parkinson’s syndrome (motor subscale of UPDRS 28) with
Abstracts / Sleep Medicine 14S (2013) e165–e238
good response to dopaminergic treatment and the diagnosis of idiopathic PD was established. Conclusion: We report this case because the co-occurrence of NC and 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 of sleep D. Kumar, N. Dedic, C. Flachskamm, J. Deussing, M. Kimura Max Planck Institute of Psychiatry, Germany
Introduction: Two L-type Ca2+ channels (Cav1.2 & Cav1.3) are expressed in the mouse brain with Cav1.2 contributing to a major proportion (85%). The expression of L-type Ca2+ channels is greatly densed in the suprachiasmatic nuclei, a neuronal area capable of functioning as autonomous clock and as a generator of circadian rhythms. Although one of the most important aspects regarding the circadian rhythm is the sleep–wake cycle, yet the role of Cav1.2 in the sleep–wake cycle is unclear. Therefore, we investigated whether 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 by means of EEG and EMG recordings in Cav1.2 (+/ ) mice and their wild-type littermates under baseline and sleep deprivation conditions (6 h by gentle handling). Results: Under basal condition, Cav1.2 (+/ ) mice showed increased sleep onset latency but subsequent hypersomnolence as compared to wild-type. The hypersomnolence observed in these mice was characterized by higher slow wave activity. Moreover, these heterozygous mice also exhibited drastically shorter wake episodes in the dark period, due to an increased number of NREM sleep episodes. Analysis of sleep architecture further revealed that these mice showed frequent transitions from wake to NREM sleep and vice versa. After sleep deprivation, the sleep onset latency decreased drastically and the trend for higher NREM sleep was observed in Cav1.2 (+/ ) mice. Conclusion: Our results demonstrate that depletion of Cav1.2 significantly impacts circadian sleep regulation indicated by increased NREM sleep and decreased time spent in wake in the dark period. However, homeostatic regulation of sleep was unaltered. It has been reported that L-type Ca2+ channels are involved in wake-promoting effects of hypocretin1. Therefore, decreased wakefulness in Cav1.2 (+/ ) mice suggests that a depletion of Cav1.2 might attenuate the hypocretin 1 mediated excitation of wake-related neurons. The alpha-1 subunit of L-type Ca2+ channels (Cav1.2) is encoded by the CACNA1C gene. Genome-wide association studies (GWAS) have suggested that polymorphisms in the CACNA1C gene are associated with sleep disorders, e.g., insomnia and narcolepsy. Increased sleep onset latency and fragmented sleep architecture displayed by Cav1.2 (+/ ) mice might be signs of symptomatic sleep disorders but further studies are needed to elucidate this. Nevertheless, several GWAS studies have significantly associated 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 sleep quality and stress T. Kushnir 1, S. Israeli-Tedgi 2, J. Urkin 3 1 Ben-Gurion University of the Negev, Faculty of Health Sciences, Israel 2 Ben-Gurion University of the Negev, Faculty of Health Sciences, Public Health Israel 3 Ben-Gurion University of the Negev, Faculty of Health Sciences, Medical Education, Israel
e175
Introduction: Background: Childbirth and the responsibilities of parenting require a great deal of energy. Sleep disturbances that are common in the postpartum period, are important correlates of fatigue and could affect energy levels. Postpartum fatigue (PPF) is the most common unpleasant symptom following childbirth. It is an overwhelming sense of energy loss, exhaustion and decreased capacity for physical and mental work following childbirth. There have been no direct studies of PPF and its correlates among fathers. Aims: To compare 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 were attending routine pediatric appointments in community clinics. We excluded women with postnatal depression (based on Edinburgh Postnatal Depression Scale). A self reporting questionnaire assessed: postpartum fatigue (FCS), sleep quality (PSQI), stress (PS) and postnatal depression (EPDS). Results: PPF levels of fathers and wives were highly correlated (r = 0.644, p < .001). There were no significant differences in PPF between fathers and wives. Among fathers sleep quality was strongly correlated with stress (r = 0.690, p < .001) and PPF (r = 0.633, p < 0.01). Multicollinearity was not found. In a multiple regression analysis with sleep quality and stress as independent predictors 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 reduction confirmed that stress mediated the association between sleep quality 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 levels of PPF. It is well known that most mothers in the post-partum period suffer from PPF. Our results indicate that this phenomenon may be common among fathers too. Thus PPF may adversely affect both mothers’ and fathers’ quality of life. Our results also suggest that among the fathers sleep issues probably raised stress levels which in turn increased PPT levels. This possibility requires further systematic confirmation. Further systematic studies are needed to uncover the extent and correlates of PPF and the interconnections between the factors implicated in this phenomenon among fathers. Acknowledgement: We acknowledge the help of Dr. Nir Madjar who greatly contributed to the statistical analysis. http://dx.doi.org/10.1016/j.sleep.2013.11.410
Period lengths of temperature and melatonin circadian rhythms in delayed sleep phase disorder G. Micic 1, L. Lack 1, N. Lovato 1, H. Burgess 2, S. Ferguson 3 1 Flinders University of South Australia, School of Psychology, Australia 2 Rush University Medical Center, Circadian Rhythms Research Laboratory, Australia 3 Central Queensland University, Appleton Institute, Australia
Introduction: Delayed Sleep Phase Disorder (DSPD) is characterized as an abnormally delayed sleep period. The currently assumed aetiology is simply a phase-delay in individuals’ biological body clocks. However, DSPD cases treated to produce a corrective phase advance are very prone to relapse. It has been suggested that this may be due to an abnormally long period length (time taken to complete one cycle of the rhythm). Circadian period lengths of endogenous core body temperature and salivary melatonin were measured to investigate this premise. Materials and methods: Following rigorous screening procedures, nine healthy controls and nine persons with DSPD were selected for a 80-h protocol consisting of an ultradian modified constant rou-