Научная статья "Некоторые аспекты влияния нарушений сна на течение эпилепсии" на английском языке из журнала "Астана медициналы? журналы", специальный выпуск №4/2015 

I.Akchurina 1 , S.Savinov 2 , N.Djainakbaev 1 , R.Abedimova 1 , I.Sitnikov 2 , Z.Utebekov 2 , I.Bondareva 2 , N. Mikhailova 2 , G.Esimova 2 , T.Sinitsina 2

1 Kazakh-Russian Medical University, Almaty 1

2 SVS Laboratory of epilepsy, convulsive diseases research and family monitoring named after V.M. Savinov, Almaty 2

SOME ASPECTS OF IMPACT SLEEP DISTURBANCES ON EPILEPSY COURSE

Аbstract

Sleep and epilepsy are closely interconnected. Sleep disturbances increase epileptiform discharges detection as well as quality of life. According to general statistics more than 10% patients with epilepsy are resistant to a treatment, so in our opinion it is necessary to take into account all aspects of their life to increase a rate of pharmaco resistance.

At SVS Laboratory of epilepsy, convulsive diseases research and family monitoring named after V.M. Savinov was investigated a group of adult patients with different epilepsy forms suspected of having syndrome of obstructive sleep apnea (SOAS).

Apnea is common for children population, but due to complexity of children investigation and necessity of getting parental agreement, here will be discussed data of adult patients.

SOAS were treated with different methods. After treatment the patients underwent all night EEG and was estimated seizure frequency. According to our data these patients had improvement in frequency interictal discharges in sleep as well as in seizure frequency, decrease of daytime sleepiness.

Key words: sleep disturbance, epilepsy, pharmacoresistance, apnea, excessive day time sleepiness, snoring.

ACTUALITY

The interaction between epilepsy and sleep is complex and clinically relevant. Over a century ago, Gowers (1885) the first classified seizure occurrence as diurnal, nocturnal and diffuse [1]. After the introduction EEG and PSG, the epilepsy-sleep interaction was studied more thoroughly and proved.

Sleep can activate epileptiform EEG abnormalities, especially interictal epileptiform discharges are more facilitated during non-rapid-eye-movement (NREM) sleep due to synchronized EEG pattern. Circadian seizure distribution mainly depends on the seizure type and etiology. For example, absence seizures occur only in the waking state and seizures in autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) occur only during sleep [2].

One of the most striking examples on how sleep can activate epileptiform discharges is the syndrome of continuous spike-wave activity during slow-wave sleep (CSWS).

Moreover, sleep deprivation is well-recognized to activate epileptiform activity, although it remains controversial whether the activating effect of sleep deprivation are due to increased neuronal excitability or simply to the lack of sleep [2,3]. Seizures, both, diurnal and nocturnal, are thought to disrupt sleep structure, [5] that mostly appears in reduction and instability of rapid-eye-movement sleep. Furthermore, less total sleep time and sleep efficiency, more sleep fragmentation, longer sleep latency and increased stage shifts and awakening are reported.

It appears that the occurrence of seizures does not only depend on the sleep-wake cycle, but may depend on circadian, 24-hour rhythmicity. Seizures have been shown to have an uneven distribution over the day, depending on the lobe of seizure origin [6].

Epilepsy itself as well as its treatment may disrupt sleep [1]. This may result in chronic sleep deprivation that have detrimental effect on seizure control, causing a vicious circle.

The most studied syndrome causing sleep disruption is SOAS. According to a literature its comorbidity with epilepsy vary from 41 to 80%. Moreover, according to Chihorek et al. the patients with epilepsy and SOAS have lower seizures control in contrast with group of patient with successfully treated SOAS where was documented seizure and day-time sleepiness reduction in 45 % patients without changes in antiepileptic treatment. [7-11]

OBJECTIVES

To perform a literature review of impact sleep disturbances on epilepsy course. To analyze impact of SOAS on epilepsy in group of patients. To introduce world approach to sleep disturbances by example of OSA and how could it improve epilepsy course.

PATIENTS AND METHODS

The patients with resistant different aetiology epilepsy suspected of SOAS. 150 pharmacoresistant patients aged 35-61 were selected. For exclusion pseudoresistancy they were examined and consulted by epileptologists. All night EEG monitoring with ECG registration, AED serum level , MRI have been done.

Prediction of the presence of OSA have been made on the base of clinical features, body mass index as an independent predictor of the presence of OSA (BMI >30 – predictor of high probability of OSA), criteria developed by Flemons and coworkers used an adjusted neck circumference classifying patients as low, moderate, or high probability and Berlin questionnaire that consist of three categories: category 1 concerns snoring an witnessed apnea, category 2 concerns being sleepy/tired/fatigued more than three or four times a week or nodding off while driving a vehicle, and category 3 concerns the presence of hypertension.

To estimate excessive day time sleepiness Epworth scale was used. The sum of all questions provides the severity of sleepiness.

Table 1.

Picture 1

RESULTS

After exclusion a pseudoresistant patients or candidates for surgical treatment, were selected a group of 48 patients, 18 female and 31 male patients suspected for having OSA (32% of general population), who suffered from focal symptomatic or probably symptomatic temporal lobe or frontal lobe epilepsy not responsible for basic antiepileptic treatment. Age range from 45 to 68 years, seizures frequency from 2 per month up to multiple per day. The patients underwent all night EEG. Afterwards they were referred for PSG. According to PSG conclusions 21 (43%) of male patients and 7 (14,6%) of female patients has obstructive or mixed apneas with AHI 5-30/hr. As a cause 15 (11 – males, 4 female) has otolaryngologic problems, 8 patients had obesity (3 m, 5 f), and 5 cigarette heavy smokers (20 and more cigarettes per day).

More significant efficacy in treatment OSA was achieved in patients with otolyringologic pathology (nasal septum deformation, long soft palate and uvula, chronic rhinitis or tonsillitis), comparing with obese patients and heavy smokers. After resolving or reducing apneas AHI <=15 (in 11 patients - 7 mails, 4 females – 42% of pharmacoresistant patients with OSA) improvement in seizure frequency and EEG was achieved without changes of AED therapy in all patients, 2 of them was seizure free at least 6 month.

CONCLUSION

1. Sleep is powerful activator of epileptiform discharges. Seizures frequency is higher during sleep in patients with frontal lobe origin. Whereas temporal seizures tend to occur during day time (according to the literature).

2. Approach to the patient should be from the position of whole organism taking into consideration possible comorbidity that can worsen epilepsy course and results of antiepileptic treatment.

3. Such factors as pharmacoresistance to AED, high body mass index, excessive day time sleepiness should alert the physicians to the possibility of underlying sleep disturbance (e.g. Syndrome obstructive sleep apnea etc.) and to motivate them for further investigation before making a decision of surgical treatment. Because sleep improvement can lead to seizure frequency and interictal discharges reduction.

4. This small study demonstrates a necessity further more detailed investigation of this issue with working up certain recommendations and protocols for approach to patient with epilepsy and sleep disturbances.

REFERENCES

1. Bazil C.W., Malow B.A., Sammaritano M.R. Sleep and epilepsy: the clinical spectrum//Elsevier Science B.V. – 2002.

2. Foldvary-Schaefer N., Grigg Damberger M. Sleep and epilepsy//Semin Neurol. – 2009. – V. 29 (4). – P. 419-428.

3. The relationship between sleep and epilepsy: evidence from clinical trials and animal models/ Matos G., Andersen M., Cristina do Valle A., Tufik S.// J Neurol Sc. – 2010. – V. 295. – P. 1-7.

4. Gutter Th. De Weerd A.W. Effects of daytime secondarily generalized epileptic seizures during the following night// Epilepsy Behav. – 2012. – V. 25. – P. 289–294.

5. Diurnal rhythms in seizures detected by intracranial electrocorticographic monitoring: an observational study/ Hofstra W.A., Spetgens W.P., Leijten F.S., de Weerd A.W. // Epilepsy Behav. – 2009. – V. 14 (4). – P. 617-621.

6. Selim R. Benbadis, Lynn Liu CPAP : A treatment for epilepsy? //Neurology. – 2007. – V. 6. – P. 1814. DOI 10.1212/01.wnl.0000279381.88385.e9

7. Obstructive sleep apnea is common in medically refractory epilepsy patients/ Malow B.A., Levy K., Maturen K., Bowes R.// Neurology. – 2000. – V. 55. – P. 1002-1007.

8. Identification and treatment of obstructive sleep apnea in adults and children with epilepsy: a prospective pilot study/ Malow B.A., Weatherwax K.J., Chervin R.D., Hoban T.F. et al.// Sleep Med. – 2003. – V. 4. – P. 509-515.

9. Treating obstructive sleep apnea in adults with epilepsy: a randomized pilot trial/ Malow B.A., Foldvary-Schaefer N., Vauhn B.V. et al.//Neurology. – 2008. – V. 71. – P. 572-577.

10. Obstructive sleep apnea in a clinical series of adult epilepsy patients: frequency and features of the comorbidity/ Manni R., Terzaghi M., Arbasino C. et al.// Epilepsia. – 2003. – V. 44 (6). – P. 836-840.

11. Chihorek A.M., Bou-Khalil B., Malow B.A. Obstructive sleep apnea is associated with seizure occurrence in older adults with epilepsy//Neurology. – 2007. – V. 69. - 1832-1827.

Т?ЙІН

Акчурина Я.Е. 1 , Савинов С.В. 2 , Джайнакбаев Н.Т. 1 , Абедимова Р.А. 1 , Ситников И.Ю. 2 , Утебеков Ж.Е. 2 , Бондарева И.В. 2 , Михайлова Н.В. 2 , Есимова Г.Н. 2, Синицина Т.Н. 2

1 ?аза?-Ресей Медицина Университеті, Алматы

2 В.М. Савинов атында?ы эпилепсия ж?не тырыспалы мемлекеттердін лабораториясы, Алматы

?Й?Ы Б?ЗЫЛЫСТАРЫНЫ? ЭПИЛЕПСИЯ А?ЫМЫНА КЕЙБІР ?СЕР ЕТУ АСПЕКТТЕРІ

В.М. Савинова атында?ы эпилепсияны, тырысу салдарын ж?не жан?ялы? мониторингті окып білу SVS зертханасы базасында, ?рт?рлі жаста?ы, ?рт?рлі эпилепсия т?рлерімен ауыратын топтарга ?й?ы кезіндегі обструктивті апноэ к?дігі бар нау?астар?а зерттеулер ж?ргізілді.

Апноэ балаларда да, улкендерде де бай?алады, біра? балалар?а тексеруді ж?ргізуді? ?иынды?ы ата-аналарыны? міндетті т?рде р??саты керектігіне байланысты улкен жаста?ы нау?астарды? м?леметтері келтірілген. Осы нау?астарды? кейбірі толы? тексерістен ж?не диагноз на?тылан?аннан кейін ?й?ы кезіндегі апноэ ?арсы емдеу та?айындалды. Апноэ то?та?ан кезде ?за? мерзімді ЭЭГ т?сіріліп, талмаларды? жиілігі ба?аланды. Аны?тал?аны, апноэдан емделген нау?астарды? ?й?ы кезіндегі эпилептиформды белсенділікті? т?мендеуі, талмалар саныны? азаюы. Сонымен ?атар жалпы жа?дайыны? жа?саруы к?ндізгі ?й?ышылды?ты? азаюымен байланысты.

РЕЗЮМЕ

Акчурина Я.Е. 1 , Савинов С.В. 2 , Джайнакбаев Н.Т. 1 , Абедимова Р.А. 1 , Ситников И.Ю. 2 , Утебеков Ж.Е. 2 , Бондарева И.В. 2 , Михайлова Н.В. 2 , Есимова Г.Н. 2 , Синицина Т.Н. 2

1 Казахстанско-Российский Медицинский Университет, Алматы

2 SVS Лаборатория изучения эпилепсии, судорожных состояний и семейного мониторинга им. В.М. Савинова , Алматы

НЕКОТОРЫЕ АСПЕКТЫ ВЛИЯНИЯ НАРУШЕНИЙ СНА НА ТЕЧЕНИЕ ЭПИЛЕПСИИ

На базе SVS Лаборатории изучения эпилепсии, судорожных состояний и семейного мониторинга им. В.М. Савинова (Алматы), были проведены исследования группы пациентов с различными формами эпилепсии, разных возрастов, у которых было подозрение на наличие синдрома обструктивного апноэ во время сна. Апноэ наблюдалось как у детей, так и у взрослых, но учитывая сложности проведения исследований у детей в связи с необходимостью разрешения родителей в данном случае приводятся данные по пациентам старшего возраста.

Некоторые из этих пациентов после обследования и уточнения диагноза получали лечение по предотвращению апное во сне. После устранения апноэ был проведен длительный ЭЭГ мониторинг и оценена частота приступов. Выяснилось, что у пролеченных от апноэ пациентов уменьшилось количество приступов, снизился индекс эпилептиформной активности во сне и значительно улучшилось общее состояние за счет уменьшения дневной сонливости.