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July2010 Vol.47 Issue:      3 (Supp.) Table of Contents
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Clinical Relevance of Obstructive Sleep Apnea in Epilepsy

Ann A. Abd El Kader2, Hala A. Shaheen1, Amira M. El Gohary2,

Neveen M. El-Fayoumy2, Lamia M. Afifi2

 

Departments of Neurology1, Fayoum University; Neurophysiology2, Cairo University; Egypt

 



ABSTRACT

Background: The extent and clinical relevance of the association between epilepsy and obstructive sleep apnea (OSA) are not fully understood. Objective: This study was conducted to look for the frequency of obstructive sleep apnea in epileptic patients; in comparison to a control group; and its relation to clinical and polysomnographic data. Methods: We studied the clinical characteristics of epilepsy, sleep history and polysomnographic recording of 50 epileptics and 20 age and sex matched normal volunteers. Results: Out of 50 patients with epilepsy 7 patients (14%) were found to have obstructive sleep apnea and this was statistically higher than in the control group. Focal epilepsy type, frontotemporal lobe localization and history of snoring were significantly higher in patients with obstructive sleep apnea. Seizure frequency positively correlates with apnea and hypopnea index in REM. In epileptic patients with OSA, apnea hypopnea index positively correlates with percentage of S1 of total sleep time and hypopnea index in NREM. History of snoring, older age and focal type of epilepsy were significant predictors of obstructive sleep apnea in epileptics. Conclusions: Obstructive sleep apnea is frequent in epileptic patients, particularly those with focal epilepsy and history of snoring. We recommend precise inquire and investigations about sleep apnea in all epileptics even those without sleep complaint. [Egypt J Neurol Psychiat Neurosurg. 2010; 47(3): 461-469]

 

Key Words: Epilepsy, obstructive sleep apnea, polysomnography.

 

 

Correspondence to Hala A. Shaheen, Department of Neurology, Fayoum University, Egypt.

Tel.: +20107965888. Email shaheen.hala@yahoo.com    





INTRODUCTION

 

Epilepsy is common disease. About 1/3 of affected epileptics continue to have seizures despite appropriate treatment with antiepileptic drugs1. Reducing factors which may promote seizures could lead to new and more effective treatment strategies2. Obstructive sleep apnea (OSA) is a widely underdiagnosed condition that is associated with significant morbidity and mortality3,4 due to intermittent anatomical blockage of the upper airway and consequential reduction or cessation of airflow during sleep5 with subsequent cortical arousal, sleep fragmentation and decrease time spent in deeper sleep stages6. Common symptoms suggestive of OSA include snoring, restless sleep, daytime fatigue and sleepiness7. Previous studies reported that the appearance of OSA symptoms coincided with a clear increase in seizure frequency or the first appearance of status epileptics8. OSA leads to increased risk of cardiac, respiratory, and metabolic conditions, including hypertension, stroke and congestive heart failure9. Moreover OSA is postulated as a cause of sudden unexpected death in epileptics10. The identification and appropriate treatment of OSA may

have far-reaching consequences in controlling seizure and improving patient's quality of life11. Continuous positive airway pressure (CPAP) treatment was found to improve seizure control in patients with epilepsy and obstructive sleep apnea. Clinicians must be aware of the relationship of these two disorders and keenly question epilepsy patients about symptoms of sleep apnea12.

 

Aim of work

This study was carried out to look for the frequency of sleep apnea in epileptic patients in comparison to a control group. Apnea relation to clinical data as seizure type, seizure control, sleep history and other clinical and polysomnographic findings had been also searched for.

 

PATIENTS AND METHODS

 

This is a retrospective case control study of 50 epilepsy patients and 20 normal controls performed in the departments of neurology, neurophysiology, Cairo University; Fayoum University; Egypt. We studied their clinical data including detailed epilepsy and sleep history and the polysomnography.

 

 

Patients:

Inclusion Criteria: Patients with idiopathic epilepsy and normal general and neurological examination were included in this study.

Exclusion Criteria: Patients with seizures secondary to drugs, infection, neoplasia, demyelination, metabolic illness, degenerative diseases and patients with history of drug intake that could affect sleep such as hypnotics or sedatives or those with history of psychiatric or medical disease were excluded from the study.

Control group: We also studied the clinical and polysomnographic data of 20 healthy age and sex matched individuals with no neurological, psychiatric or systemic disorders and not receiving any medication that may affect sleep.

 

Methods:

Clinical assessment:

The following clinical data were analyzed:

-        Patients’ data: Including age, sex and Body Mass Index (BMI) were analyzed.

-        A BMI of 30 kg/m2 is widely recognized as a cut-off point for obesity13.

-        Age of the patients ranged from 4.5 to 55 years. Mean age of the patients and the control group was matched {19.57±10.11 versus 23.40±15.80, P (0.696)}. Also sex was matched {patients (F/M) 25/25 versus 8/12 control; P (0.449)} and number of obese {patients 6 (12%) and control subjects 6 (30%); P (0.088)}.

-        The patients were divided into 2 subgroups according to apnea/hypopnea index: Group (1) patients without OSA and group (2) patients with OSA.

 

Epilepsy History:

Included age of onset of epilepsy, disease duration and type of epilepsy. According to International League Against Epilepsy (ILAE) classification14 patients were classified as (generalized, focal, focal with secondary generalization). Clinical and EEG data were used for further localization into lobes. Attacks characteristics as seizure frequency, circadian distribution of attacks, history of status epilepticus and antiepileptic drugs were also searched for. Fits were considered controlled if seizure frequency is ≤ once/month and uncontrolled if it is > once/month.

 

Sleep History:

Repeated awakenings during sleep, sleepy in the morning, nocturnal snoring and cessation of breathing were looked for in the patients and control records.

Electroencephalogram (EEG) Assessment:

The EEG tracings were analyzed as regards frequency, amplitude and symmetry of the background activity, as well as the presence of any abnormalities.

 

Polysomnography (PSG):

A full PSG for epileptic patients and for controls were analyzed. It was done over a full night using a Schwarzer Epos 32 GmbH, medical diagnostic polysomnogram Schwarzer Germany and Somnologica software. It included Electro-encephalography, Electroculogram,  ECG, chin and leg EMG, airflow monitoring cannula placed in the nostrils and over the mouth, ventilatory effort monitoring, recorded via strain gauges, and a body position sensor were also used. Apnea is defined as cessation of the oronasal airflow, lasting ≥ 10 sec. Hypopnea was defined as airflow reduction of > 50%, compared to 10 sec peak amplitude during the preceding 2 min, lasting ≥ 10 sec and accompanied with EEG signs of arousal and persistence of thoraco-abdominal movements denoted obstructive apnea/ hypopnea. Degree of apnea was considered mild if Apnea hypopnea index ≥ 5; moderate ≥15; severe: ≥ 30. Total sleep time (TST), Sleep efficiency ([TST/Time in bed] X 100), percentage of each stage in total sleep time (SI, SII, slow wave deep sleep (SWS) & rapid-eye-movement (REM) sleep, number of awakenings, arousal index (number of arousals per hour) and periodic limb movement (PLM) index were also measured. Sleep was scored following the International and American Sleep Disorders Association criteria15.

 

Statistical Analysis:

Statistical package for social science (SPSS) version 15 was used for data management and analysis. Quantitative data were expressed as mean and standard deviation. While qualitative data were expressed as number and percentage. Chi-square test was used for comparison between qualitative variables groups. Independent sample T test was used for normally distributed quantitative variables. Kruskal Walls and non parametrical Mann-Whitney test were used for none normally distributed quantitative variables. Pearson's correlation coefficient was calculated for the association between the different numerical measurements. The logistic regression analysis was done to test for significant predictors of OSA among epileptics. P-values ≤ 0.05 was considered significant.

 

RESULTS

 

Clinical Data

Clinical characteristics of epileptic group:

Seventeen patients (34%) had generalized epilepsy, 14 (28%) had focal and 19 (38%) had focal with secondary generalization. The seizure frequency ranged from once per 3 months to 10 per day with mean of 37.35±57.17 per month. Seizures were uncontrolled in 44 patients (88%) and 9 patients (18%) had history of status epilepticus. Circadian distribution of the attacks was diurnal in 5 patients (10%), Nocturnal in 23 (46%) and both nocturnal and diurnal in 22 (44). The mean age of onset of epilepsy was 10.47±6.82 and the mean duration was 9.16±9.12. Seven patients (14%) had not received medications yet, 18 (36) were on monotherapy and 25 (50) were on polytherapy.

 

Sleep clinical results in epileptic and control group:

The sleep complains in patients were mainly repeated awakenings during sleep and feel sleepy in the morning (Figure 1). The sleep complaint did not differ significantly between epileptic and control group (P-value 1, 0.173, 0.552, 0.286 respectively).

 

Frequency of OSA in epilepsy patients

No one of the control group had OSA whereas 7 patients (14%) of the epilepsy group had and this difference was statistically significant, (P 0.453). OSA in our patients was mild in 6 patients (12%), moderate in1 patients (2%), and there was no severe cases (Figure 2).

 

 

Comparison between clinical variables in epilepsy patients’ subgroup

Focal epilepsy type, frontal and frontotemporal lobe localization and history of snoring history of snoring was significantly higher in patients with OSA. All other clinical epilepsy, sleep and EEG findings did not differ significantly (Tables 1 and 2).

 

Polysomnography Results

Epileptic patients had significantly higher arousal index, % of S2 from TST and longer sleep onset but lower % of SWS from TST and shorter REM latency from sleep onset, in comparison to the control group (Table 3).

 

Comparison of sleep parameters in patients’ subgroup:

Patients with OSA had higher hypopnea index in REM and in NREM. They also had higher apnea hypopnea index (Table 4).

 

Correlation between apnea hypopnea index, clinical and polysomnographic data:

Only % of S1 from TST and hypopnea index in NREM positively correlates with apnea hypopnea index in epileptic patients with OSA. No other significant correlations neither with clinical nor with polysomnographic data were detected (Table 5). Seizure frequency positively correlates with apnea index in REM (r 0.537 P, 0.000) (Figure 3), and hypopnea index in REM (r 377 P 0.008).

Prediction of obstructive sleep apnea in epilepsy patients: Logistic regression analysis was done to ascertain predictive value of epilepsy and sleep parameters. History of snoring, older age and focal type of epilepsy have been found to be significant predictors of OSA in epilepsy patients, P-value (0.019, 0.031, 0.039) respectively.


 

 

Figure 1. Sleep complaint in epileptic patients and control group.

 

Figure 2. Frequency of OSA in epilepsy patients.

 

 

Table 1. Comparison between clinical variables in epileptic patients’ subgroups.

 

Clinical  variables

Group (1) Patients without OSA

No. (%)

Group (2) Patients with OSA

No. (%)

P-value

Age

Mean±SD

18.87±8.48

23.86±17.54

0.547

Age of onset

Mean±SD

10.88±6.90

8.00±6.16

0.251

Disease duration

Mean±SD

8.02±7.16

16.14±15.97

0.229

Sex

Female

23 (53.5)

2 (28.6)

0.221

Male

20 (46.5)

5 (71.4)

BMI

Increased BMI

4 (9.3)

2 (28.6)

0.192

Type of epilepsy

Generalized

17 (39.5%)

0 (0)

0.015*

Focal

17 (39.5%)

2 (28.6%)

Focal with 2nd generalization

9 (20.9%)

5 (71.4)

Seizure frequency

Mean±SD

33.29±45.45

62.29±106.74

0.460

Uncontrolled

37 (86)

7 (100)

0.576

Controlled

6 (14)

0 (0)

Status epilepticus

Yes

7 (16.3)

2 (28.6)

0.595

Circadian rhythm

Diurnal

5 (11.6)

0

 

0.596

Nocturnal

19 (44.2)

4 (57.1)

Nocturnal and diurnal

19 (44.2)

3 (42.9)

Medication

No

7 (16.3)

0

 

0.366

Monotherapy

16 (37.2)

2 (28.6)

Polytherapy

20 (46.5)

5 (71.4)

Depakin and/or Epanutin

32 (74.4)

4 (57.1)

0.384

Other drugs

11 3 (25.6)

3 (42.9)

BMI Body mass index, OSA obstructive sleep apnea, SD standard deviation

*Significant at p<0.05

 

 

Table 2. Comparison between sleep and EEG in epileptic patients’ subgroups.

 

Clinical sleep and EEG variables

Group (1)

No. (%)

Group (2) No. (%)

P-value

Sleep history

Repeated awakenings

20 (46.5)

3 (42.9)

1.000

Snoring

1 (2.3)

2 (28.6)

0.048*

Sleepy in the morning

19 (44.2)

2 (28.6)

0.684

EEG findings and seizure localization

Normal

10 (23.3)

0

 

 

 

0.034*

Frontal

4 (9.3)

4 (57.1)

Frontal with 2nd generalization

5 (11.6)

0

Frontotemporal

18 (41.9)

3 (42.9)

Frontotemporal with 2nd generalization

5 (11.6)

0

Temporoccipital with 2nd generalization

1 (2.3)

0

Generalized

9 (20.9)

0

Seizure lateralization

Right

5 (11.6)

2 (28.6)

0.154

Left

19 (44.2)

5 (71.4)

Generalized

9 (20.9)

0

Normal

10 (23.3)

0

*Significant at p<0.05

 

Table 3. Comparison of polysomnographic parameters in patients and control.

 

Polysomnographic data

Patients

Mean±SD

Controls

Mean±SD

P-value

Sleep onset in min.

33.05±45.26

16.69±21.71

0.014*

Sleep efficiency %

82.74±12.60

78.39±8.8

0.163

No. of awakenings

11.22±6.06

13.10±5.34

0.322

Sleep latency to S1

75.49±95.02

70.24±141.21

0.077

Sleep latency to S2

48.21±59.14

33.79±51.46

0.056

Sleep latency SWS

70.99±63.24

95.79±82.80

0.317

Sleep latency REM

153.36±108.67

219.83±91.63

0.019*

% of S1 from TST

9.64±7.61

8.98±7.41

0.640

% of S2 from TST

55.88±14.62

40.53±13.11

0.000**

% of SWS from TST

23.27±12.33

37.30±14.50

0.000**

% of REM from TST

11.44±8.55

13.18±5.54

0.298

Arousal index

8.18±11.35

1.13±0.68

0.001**

Periodic Leg Movement index

0.58±1.15

0.26±0.33

0.712

Apnea index REM

0.54±1.78

0.00±0.00

0.118

Apnea index in NREM

0.38±0.49

3.04±7.16

0.292

Hypopnea index in REM

3.04±7.16

1.54±4.43

0.530

Hypopnea index in NREM

1.02±1.43

0.66±0.97

0.621

Apnea hypopnea index

1.92±2.94

1.03±1.32

0.467

Apnea hypopnea index

1.92±2.94

1.03±1.32

0.467

NREM Non-Rapid eye movement, REM Rapid eye movement, SD standard deviation, SWS short wave sleep, TST total sleep time

*Significant at p<0.05 **Significant at p<0.01

 

Table 4. Comparison of polysomnographic parameters in patients’ subgroup.

 

Polysomnographic data

Group (1)

patients without OSA

Mean±SD

Group (2)

patients with OSA

Mean±SD

P-value

Sleep onset in min.

35.99±47.75

23.86±17.54

0.180

Sleep efficiency %

83.00±12.00

81.13±16.92

0.856

No. of awakenings

10.91±6.20

13.14±5.05

0.165

Sleep latency to S1

84.51±99.53

20.07±14.59

0.067

Sleep latency to S2

52.38±62.10

19.00±9.46

0.130

Sleep latency SWS

77.75±65.57

29.50±15.08

0.057

Sleep latency REM

169.82±109.09

59.36±32.79

0.006*

% of S1 from TST

9.87±8.05

8.20±4.02

0.944

% of S2 from TST

55.32±14.48

59.31±7.33

0.394

% of SWS from TST

23.34±12.90

22.84±8.73

0.790

% of REM from TST

11.74±9.02

9.64±5.01

0.886

Arousal index

7.91±10.74

9.83±15.50

0.955

Periodic Leg Movement index

0.50±1.09

1.07±1.45

0.224

Apnea index REM

0.28±0.90

2.01±4.07

0.073

Apnea index in NREM

0.34±0.47

0.60±0.58

0.122

Hypopnea index in REM

0.71±2.10

16.66±10.88

0.000*

Hypopnea index in NREM

0.53±0.66

4.00±1.29

0.000*

Apnea hypopnea index

0.99±0.93

7.64±4.49

0.000*

NREM Non-Rapid eye movement, REM Rapid eye movement, SD standard deviation, SWS short wave sleep, TST total sleep time

*Significant at p<0.01

Table 5. Correlation between apnea hypopnea index and clinical & polysomnographic data of.

 

Clinical and polysomnographic data

Correlation

Coefficient

P Value

Age

-0.232

0.617

age of onset of epilepsy

-0.647

0.117

disease duration

-0.017

0.971

seizure Frequency

0.025

0.863

Number of awakening

-0.117

0.803

Sleep onset in min.

-0.139

0.729

Sleep efficiency %

0.266

0.565

Sleep latency to S1

-0.396

0.379

Sleep latency to S2

-0.049

0.926

Sleep latency SWS

0.649

0.115

Sleep latency REM

0.343

0.452

% of S1 from TST

0.758

0.048*

% of S2 from TST

-0.370

0.414

% of SWS from TST

0.005

0.992

% of REM from TST

-0.075

0.873

Arousal index

0.046

0.922

PLM index

-0.263

0.569

Apnea index REM

-0.239

0.606

Apnea index in NREM

-0.441

0.322

Hypopnea index in REM

0.068

0.884

Hypopnea index in NREM

0.771

0.043*

NREM Non-Rapid eye movement, REM Rapid eye movement, SD standard deviation, SWS short wave sleep, TST total sleep time

*Significant at p<0.05

 

Apnea index in REM

 

Figure 3. Correlation between seizures frequency and apnea index in REM.

 

 


DISCUSSION

 

Epilepsy and Obstructive sleep apnea (OSA) are two common disorders that can profoundly exacerbate each others16. Make matter worse OSA is notoriously underdiagnosed particularly in epilepsy patients. The routine assessment of sleep complaints with specific inquire about OSA in all epilepsy patients is rarely done in clinical practice17. Furthermore OSA cardinal symptoms; snoring and excessive daytime sleepiness; usually ascribed to the effects of the antiepileptic medications or the epilepsy itself 18. Serious consequences of OSA include hypertension, cerebrovascular accidents, myocardial infarctions19, neurocognitive deteriorations, psychiatric diseases 20 and sudden unexpected death 21. Moreover unrecognized or untreated sleep apnea worsens seizure control 22. Thus identification and appropriate treatment of OSA in epilepsy patients reduces seizure frequency and improve daytime sleepiness 23 and may have far-reaching consequences in improving epileptic patient's quality of life11. Prevalence of sleep apnea in epileptics varies in literatures. Recent reports suggest that OSA may be more common in patients with epilepsy than it was suspected16. In this study OSA was detected in 7 out of 50 epilepsy patients (14%)  versus no one in the control group; P (0.453). Similarly Milena Pavlova 200918 reported coexistence of OSA with epilepsy in 10.2% of epilepsy patients. Contradictory others reported higher percentage as Nancy F. S. and Madeleine G. D.2009 24 who reported 33% of patients with intractable partial epilepsy were found to have OSA and Malow BA et-al 199725 who reported OSA in (71%) of their epileptic patients. But this difference can be attributed to difference in patient selection as the first study included only patients with intractable focal epilepsy where higher prevalence of OSA is suspected and in the second study epileptic patients had been referred specifically for the evaluation of sleep disorders, including OSA whereas in our study we looked for OSA in all epileptic patients. The observed coexistence of OSA and epilepsy is higher than co-occurrence of both diseases expected by chance. Assuming a lifetime prevalence of 1.8% for epilepsy and 2–4% for OSA of the general population, the two diseases should co-occur by chance in approximately 0.04–0.08%6. Several mechanisms may contribute to the increased incidence of OSA in epileptic, the adverse effect of central nervous system depression of antiepileptic drugs (AEDs), possibly phenytoin effect on upper airway tone, weight gain associated with some AEDs, reduced physical activity of people with epilepsy. In our study all group (2) patients with OSA were on medications and most of them (71.4%) were on polytherapy though this did not reach statistical significance when compared to group (1) also type of medication did not differ .Small number of patients with OSA may contribute to these results.

There is also a suggestion that sleep in the epileptic brain is inherently unstable. This instability promotes seizures, and seizures, in turn, fragment sleep, thus facilitating the epileptic process. Seizures prolonged REM where OSA became worse due to atonia of respiratory musculature. In this study, seizures frequency positively correlates with apnea index in REM (r 0.537, P.000) and hypopnea index in REM (r 377, P .008). Further researches are needed to explore other causes of OSA in epilepsy.

Conversely a variety of seizure-provoking mechanisms have been proposed in patients with OSA. Cerebral hypoxemia, sleep fragmentation and sleep deprivation are all postulated 26. In this study statistically significant positive correlations were found between seizure frequency and apnea and hypopnea index in REM, all group with OSA had uncontrolled seizure and more seizure frequency and more frequent history of status though this did not reach statistically significant difference. Small sample size limits the comparability of the data. Mild degree of OSA in our patients may also be a contributing explanatory factor.

If sleep deprivation is the assumed mechanism, one might expect that seizures during both sleep and wakefulness would be facilitated in epileptic patients with OSA17.  This was the case in our study as diurnal variation of seizure did not differ significantly between patients with and without OSA. In contrast, if sleep fragmentation and frequent stage shifts resulting from apneas are responsible for provoking seizures, then seizures during sleep may be facilitated preferentially in epileptic patients with OSA27 as previous study reported that patients with seizures during sleep were more likely to have OSA they assume OSA was causal in facilitating seizures during sleep 28.

Several studies have found that one-third to one-half of the epileptic patients report excessive daytime sleepiness 28. In this study though about 1/2 patients reported frequent awakenings during night and excessive day time sleepiness; sleep complaint did not differ significantly between patients and control group or patients subgroups, only snoring was significantly prevalent in patients with OSA;. This is raising the importance of investigating epileptic patients for sleep apnea even in absence of sleep complaint. 

In this study epileptic patients had higher arousal index, % of S2 from TST and longer sleep onset but lower % of SWS from TST and shorter REM latency from sleep onset. Patients with OSA had higher hypopnea index in REM and in NREM and higher apnea hypopnea index. Percent of S1 from TST positively correlates with apnea hypopnea index in epileptic in patients with OSA.  Similarly Kaleyias J et-al 200829 reported that patients with epilepsy and OSA had significantly longer sleep latency, higher arousal index, and a lower apnea-hypopnea index. But in a previous Ann Abdel-Kader et-al 200730 study, they found that patients with epilepsy had less number of awakenings, decrease % of SWS with shorter periods of sleep latencies to SWS but increase in % of S2 from TST. These findings could be attributed to postictal somnolence, as their patients had their PSG recordings done within 48 hours after the fit. There is an agreement that in epileptics there is significant tendency towards light sleep than slow wave deep sleep and it is well known that sleep apnea is not the same throughout the course of the night. It tends to be worse in (REM) sleep. REM sleep induces skeletal muscle atonia, making the upper airways more susceptible to collapse.

 

Conclusions and Recommendations

Obstructive sleep apnea is frequent in epileptics, particularly those with focal epilepsy and history of snoring. Investigating sleep apnea in all epileptics is recommended. Future large number study to determine epilepsy features that are predictive of OSA and to better establish how epilepsy increases the risk of OSA and to determine effect of CPAP treatment on epilepsy is also recommended.

 

[Disclosure: Authors report no conflict of interest]

 

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الملخص العربى

 

العلاقة الإكلينيكية بين مرض الصرع وتوقف التنفس الأنسدادى أثناء النوم

 

مدى وطبيعة العلاقة الإكلينيكية بين مرض الصرع وتوقف التنفس أثناء النوم لا تزال غير مفهومة تماما. أجريت هذه الدراسة للبحث عن مدى وجود توقف التنفس الأنسدادى أثناء النوم لدى مرضى الصرع وذلك مقارنة مع مجموعة ضابطة وعلاقة توقف التنفس أثناء النوم في مرضى الصرع بالحالة الإكلينيكية ورسم المخ المتعدد الأغراض أثناء النوم .

المرضى وطرق البحث : لقد تمت مراجعة التاريخ المرضى وخصائص الصرع، والشكاوى من النوم ورسم المخ المتعدد الأغراض أثناء النوم لـ50 مصاب بالصرع  و20 متطوعا طبيعيا.

 النتائج : وجد أن 7 مرضى (14٪) من أصل 50 مريض بالصرع لدية توقف التنفس أثناء النوم وكان هذا أعلى إحصائيا عن المجموعة الضابطة. وقد وجد أن نوع الصرع الجزئي، فى الفص الأمامي والصدغي و الشخير أعلى بكثير في المرضى الذين يعانون من توقف التنفس أثناء النوم. وقد ارتبطت عدد مرات نوبات الصرع بشكل ايجابي مع مؤشر توقف وانخفاض التنفس. وكان مؤشر توقف وانخفاض التنفس أثناء مرحلة حركة العين السريعة من النوم أعلى في مرضى الصرع الذين يعانون من توقف التنفس أثناء النوم كما أرتبط مؤشر توقف وانخفاض التنفس بشكل ايجابي مع نسبة مرحلة النوم الخفيف وقد وجد أن الشخير، وكبار السن، ونوع الصرع الجزئي يمكن أن يتنبأ بتوقف التنفس أثناء النوم في مرضى الصرع .

الاستنتاجات والتوصيات : انتشار توقف التنفس أثناء النوم في مرضى الصرع، وبخاصة الذين يعانون من الصرع الجزئي. ونوصي بالاستفسار عن توقف التنفس أثناء النوم وعمل رسم المخ المتعدد الأغراض أثناء النوم لمرضى الصرع حتى مع عدم وجود شكوى من أضطرابات النوم. كما نوصي بعمل دراسات مستقبلية على عدد كبير من المرضى لتحديد أفضل لكيفية العلاقة بين مرض الصرع وتوقف التنفس أثناء النوم وتأثير علاج وتوقف التنفس على مرض الصرع.



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