|
20th Congress of the European Sleep Research Society
Lisbon, Portugal
14.09.2010 - 18.09.2010 |
| Please enter your email address here in order to bring up your personal programme |
|
|
|
Sleep and healthFriday, September 17, 2010, 13:00 - 14:30Hypersomnia and coeliac diseaseD. Neutel, P. Pita Lobo, T. Mestre, R. Peralta, C. Bentes (Lisbon, PT)
Objectives: sleepiness is a common symptom noted by 5% to 15% of individuals. It may result from a wide range of medical disorders. Celiac disease (CD) is an autoimmune disorder caused by intolerance to gliadin associated with the presence of Antigladin Antibody (AA). CD is also known to have neurological manifestations. The nature of this association is still controversial. Restless legs syndrome (RLS) has been reported in CD patients presumably due to iron deficiency. We report two patients with central hypersomnia and CD.
Methods: cases reports.
Results: case 1) A 27-year-old woman with CD under a gluten-free diet, complained of excessive daytime sleepiness (EDS) with frequent paroxysms during which she fall asleep without warning and occasional sleep onset dream enacting behaviour. Sleep and gastrointestinal complains started simultaneously around the age of 20. Unremarkable physical examination. She scored 14 on Epworth Sleepiness Scale (ESS). Full PSG (with 19 EEG channels) in sleep lab showed sleep fragmentation and increased amount of slow wave sleep (SWS) (44,9%). No periodic limb movements (PLMs), cardiorespiratory disturbances or REM sleep without atonia were found. There was significant clinical improvement under modafinil. Case 2) A 54-year-old woman presented to the sleep clinic complaining of constant EDS with unrefreshing naps for more than 15 years. CD had been diagnosed one year before due to iron deficiency anemia and she was under a gluten-free diet. BMI was 26 but otherwise unremarkable physical examination. She scored 11 on ESS. Full ambulatory PSG showed an increased amount of SWS (40,3%), RDI of 9,2/h and PLMS of 12,1/h. There was no REM sleep abnormalities. There was no improvement on CPAP. None of the patients had cataplexy, sleep paralysis, hypnagogic/hypnopompic hallucinations or symptoms of RLS.
Conclusion: the association between CD and central hypersonmia may be casual. However, physiopathological links favor a causal relationship. Autoimmunity has been proposed as one of the probable mechanism of SNC lesion in CD. AA react to specific neuronal antigens in widespread SNC locations. Moreover there are reports of antihypothalamus autoantibodies and hypothalamus-hypophysary axis dysfunction in CD patients. It is therefore possible that these patients are vulnerable to damage in central sleep regulatory centers. Further research is necessary to evaluate the prevalence of central hypersomnia in CD.
|
|
|
