OBJECTIVE: Sleep disorders are common and may coexist with a variety of diseases, including epilepsy, with important implications for the clinical management of the latter. Sleep fragmentation and deprivation, and hypoxia associated to sleep disordered breathing (SDB) may contribute to the occurrence of seizures. On the other hand, antiepileptic drugs may worsen SDB by reducing the muscle tone of the upper airways, and increasing the arousal threshold. There is evidence indicating that treatment of the SDB can reduce both frequency and intensity of seizures. This study aimed at further understanding the relationship between SDB and epilepsy, particularly the influence of SDB on epileptogenicity - as evaluated by a quantitative analysis of interictal epileptogenic activity. METHODS: Eight consecutive patients affected by partial epilepsy associated to SDB (OSAS or an association between chronic obstructive pulmonary disease-- COPD - and snoring) underwent two nocturnal polysomnographies (PSG)-- before and after ventilatory therapy with CPAP (in 6 patients with OSAS) or oxygen (in two patients with COPD and snoring). Spiking was quantified during the first sleep cycle in both PSG studies, and spiking rates were calculated both for the entire sleep cycle and for each separate sleep phase (NREM 1, NREM 2, NREM 3-4, REM and wake time after sleep onset - WASO). RESULTS: In all patients, the improvement of the SDB after ventilatory treatment--as demonstrated by a reduction of the respiratory disturbances index (RDI) - was associated to a reduction of spiking rates, both in the entire cycle and in relationship to slow wave sleep. This reduction was particularly marked in patients with higher spiking rates in baseline conditions. CONCLUSION: Our data show that SDB treatment reduces the interictal epileptogenic activity, suggesting that SDB plays a role in increasing epileptogenicity. Further studies will be necessary to clarify the mechanisms whereby this reduction in epileptogenicity occurs, although improved sleep stability seems to play an important role. The presence of an underlying SDB in patients with refractory epilepsy should be investigated.
OBJECTIVE:Sleep disorders are common and may coexist with a variety of diseases, including epilepsy, with important implications for the clinical management of the latter. Sleep fragmentation and deprivation, and hypoxia associated to sleep disordered breathing (SDB) may contribute to the occurrence of seizures. On the other hand, antiepileptic drugs may worsen SDB by reducing the muscle tone of the upper airways, and increasing the arousal threshold. There is evidence indicating that treatment of the SDB can reduce both frequency and intensity of seizures. This study aimed at further understanding the relationship between SDB and epilepsy, particularly the influence of SDB on epileptogenicity - as evaluated by a quantitative analysis of interictal epileptogenic activity. METHODS: Eight consecutive patients affected by partial epilepsy associated to SDB (OSAS or an association between chronic obstructive pulmonary disease-- COPD - and snoring) underwent two nocturnal polysomnographies (PSG)-- before and after ventilatory therapy with CPAP (in 6 patients with OSAS) or oxygen (in two patients with COPD and snoring). Spiking was quantified during the first sleep cycle in both PSG studies, and spiking rates were calculated both for the entire sleep cycle and for each separate sleep phase (NREM 1, NREM 2, NREM 3-4, REM and wake time after sleep onset - WASO). RESULTS: In all patients, the improvement of the SDB after ventilatory treatment--as demonstrated by a reduction of the respiratory disturbances index (RDI) - was associated to a reduction of spiking rates, both in the entire cycle and in relationship to slow wave sleep. This reduction was particularly marked in patients with higher spiking rates in baseline conditions. CONCLUSION: Our data show that SDB treatment reduces the interictal epileptogenic activity, suggesting that SDB plays a role in increasing epileptogenicity. Further studies will be necessary to clarify the mechanisms whereby this reduction in epileptogenicity occurs, although improved sleep stability seems to play an important role. The presence of an underlying SDB in patients with refractory epilepsy should be investigated.
Authors: Sheela Toprani; Kimford J Meador; Chelsea P Robalino; Carrie Anne Brown; Abigail G Matthews; Elizabeth E Gerard; Patricia Penovich; Evan Gedzelman; Jennifer Cavitt; Sean T Hwang; Laura A Kalayjian; Maria Sam; Alison Pack; Page B Pennell Journal: Neurology Date: 2022-07-19 Impact factor: 11.800
Authors: Silvia Miano; Maria Chiara Paolino; Rosa Peraita-Adrados; Marilisa Montesano; Salvatore Barberi; Maria Pia Villa Journal: Sleep Date: 2009-04 Impact factor: 5.849
Authors: H Helakari; J Kananen; N Huotari; L Raitamaa; T Tuovinen; V Borchardt; A Rasila; V Raatikainen; T Starck; T Hautaniemi; T Myllylä; O Tervonen; S Rytky; T Keinänen; V Korhonen; V Kiviniemi; H Ansakorpi Journal: Neuroimage Clin Date: 2019-03-12 Impact factor: 4.881