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July2005 Vol.42 Issue:      2 Table of Contents
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The Relationship between Sleep and Epilepsy (A Clinical and Neurophysiological Study)

H. Elwan1, M. El-Tamawy1, S. Salem2, Mona T. El-Ghoneimy3
Departments of Neurology1, Neurophysiology2, Neurosurgery3,Cairo University

ABSTRACT

A reciprocal relationship is observed between sleep and epilepsy. The sleep effect on epilepsy is both protective and facilitating. On the other hand, epilepsy causes alteration of sleep organization. The aim of this work was to highlight the sleep pattern in patients with idiopathic generalized and complex partial epilepsy, to detect the effect of antiepileptic drugs (AEDs) on sleep macrostructure, and to observe sleep influence on epileptic activity. To achieve this aim we selected 30 untreated adult epileptic patients: 15 with temporal lobe epilepsy (TLE) and 15 with generalized tonic clonic seizures (GTCS), and reassessed them after three months of carbamazepine (CBZ) and sodium valproate (VPA) monotherapy respectively. Ten control subjects were also included. Subjects underwent clinical assessment, magnetic resonance imaging (MRI) for brain (for patients), conventional daytime electroencephalograrm (EEG) recording, assessment of sleep architecture as well as sleep interictal discharge (IID) using  video-polysomnographic recording, and assessment of daytime sleepiness using Epworth sleep scale (ESS). Results showed that untreated epileptic patients with TLE experienced more sleep abnormalities compared to controls, more sleep abnormalties were observed in patients with TLE compared to those with GTCS but this difference was not statistically significant. No statistically significant difference was found between patients with TLE and those with GTCS as regards sleep parameters before or after treatment. CBZ and VPA monotherapy have restorative and normalizing effects on sleep pattern, non-rapid eye movement (NREM) sleep has a facilitating effect on IID especially lighter stages (stage I and II), while rapid eye movement (REM) sleep has anti-epileptogenic effect. Untreated epileptic patients had significant excessive daytime sleepiness compared to controls, chronic CBZ and VPA monotherapy improve subjective daytime sleepiness, and that sleep EEG monitoring is more sensitive than daytime EEG recording.

(Egypt J. Neurol. Psychiat. Neurosurg., 2005, 42(2): 311-322).




INTRODUCTION

 

A reciprocal effect is observed between sleep and epilepsy. Sleep effect on epilepsy is both protective and facilitating; reciprocally epilepsy alters sleep organization and architecture¹.

       Sleep, particularly non-rapid eye movement (NREM) sleep, increases interictal epileptiform activity. Sleep increases certain seizure types as well as the rate of generalization of partial seizures. On the other hand, rapid eye movement (REM) sleep seems to suppress seizures. Also, lack of sleep and sleep disturbances, seem to be precipitating and exacerbating factors for seizures².

On the other side, structural sleep analysis confirms the presence of a disturbance of sleep stability in patients with epilepsy¹. This may be due to the occurrence of a seizure by itself, the type of seizure, the antiepileptic drug used, and/or the underlying disease process³. Nocturnal sleep fragmentation and excessive daytime sleepiness often complicate the clinical picture of epilepsy4.

   

SUBJECTS AND METHODS

 

Subjects:

This study was conducted on 40 subjects including 30 untreated epileptic patients and 10 control subjects. Patients were subdivided into: group 1 (n.15) with TLE, 6 males and 9 females, with a mean age of 23.9±5.9 years and group 2 (n.15) with GTCS, 8 males and 7 females, with a mean age of 26.2±4.3 years. Patients were further classified according to receiving AEDs into: group A, before treatment, and group B, after receiving AEDs. The control group (group 3): included 10 healthy subjects, 7 males and 3 females, with mean age of 25.4±4.7 years.

 

 Inclusion criteria:

1.      Adult patients with GTCS and TLE with or without secondary generalization.

2.      Normal MRI brain.

3.      No previous AED treatment.

 

Exclusion criteria:

1.      Symptomatic epilepsy.

2.      Focal neurological deficits or psychiatric illness.

3.      Patients with DM or other endocrinal disorder, chest or ENT disease.

4.      Hepatic or renal patients.

5.      Female patients receiving oral contraceptive pills.

6.      Patients who developed seizure on the night of recording or the preceding 24 hours.

7.      Patients with known or suspected sleep disorders.

8.      Patients who were non compliant to treatment at follow up assessment.

 

Methods:

 

All subjects underwent:

§            Proper history taking according to standardized epilepsy sheet of convulsive disorders clinic, Cairo University hospitals.

§            Sleep history, and checklist to identify the sleep/wake problem5 to exclude patients with sleep disorders.

§            Assessment of daytime sleep using Epworth Sleepiness Scale (from 0 –24, where 0 means never)6.

§            Thorough general medical and neurological examination.

§            Complete blood count, liver and kidney functions tests, fasting and 2 hours postprandial blood sugar.

§                       MRI brain for patients.

§                       Neurophysiological tests which included:

a.     Conventional daytime electro-encephalography (EEG)

b.     Video-polysomnographic study (14 EEG channels, 2 EOG, 1 submental EMG channel, and 1 ECG channel).

The recording was analysed as regards: sleep latency duration in minutes, first REM sleep latency, REM sleep duration in minutes, NREM sleep stages (I, II, III, and IV) duration in minutes, duration and number of waking after sleep onset (WASO), and sleep efficiency (percentage of time asleep from sleep onset until awakening)7.

§            Follow up of patients after treatment  with Carbamzepine (CBZ) 400-600 mg/day (for TLE), and sodium valproate (VPA) 400-800 mg/day (for GTCS), for an interval of three months,  where patients underwent:

a.     The same battery of questionnaires and investigations, excluding MRI brain.

b.     Serum drug level assessment by obtaining trough samples.

 

Statistical methods

Numerical data were expressed as mean ± standard deviation (SD), median, minimum and maximum. Qualitative data were expressed as frequency and percentage. Chi-square test was used to examine the relation between qualitative variables.  For quantitative data, comparison between two groups was done using independent t-test or Mann-Whitney test. Comparisons between more than two groups were done using ANOVA test or Kruskal-Wallis test. Correlation between variables was tested using Spearman correlation test.  A P-value less than 0.05 was considered significant and less than 0.01 considered as highly significant.

 

RESULTS

 

I. Sleep parameters:

Before treatment:

·                     NREM:

Six percent of patients with TLE (1A) had absent stage III, while 20% had absent stage IV. In patients with GTCS (2A) 13% had absent stage IV. Untreated patients with TLE (group 1A) and GTCS (2A) had shorter mean duration of stage IV  and longer sleep latency compared to controls with the difference reaching statistical significance on comparing the former but not the latter group (Fig.1).

·                     REM:

Out of the 30 untreated epileptic patients 15 patients (50%) had no REM. Those patients who experienced REM in groups 1A and  2A had a shorter  mean duration of REM stage  than  control group (group 3), but  these differences did  not reach statistical significance. REM mean duration did not correlate with sleep efficiency or seizure duration or frequency.

·                     WASO and Sleep Efficiency:

Patients with TLE (1A) and GTCS (2A) had statistically significant longer mean duration of WASO than control group (P= 0.000 & P= 0.034 respectively).  Also, mean sleep efficiency percent was statistically significantly lower in group 1A and 2A compared to controls (P= 0.000 & P= 0.004 respectively) (Fig.2). No correlation was detected between the number and duration of  WASO or sleep efficiency and seizure frequency or duration.

·          Though TLE patients group had longer sleep latency, shorter mean REM duration, higher number and longer mean duration of waking after sleep onset (WASO), and less sleep efficiency compared to untreated GTCS group, yet these differences did not reach degree of statistical significance.

 

After treatment for 3 months:

·                     NREM:

Stage IV was restored in 1 patient with GTCS (1B) after VPA monotherapy. Stages III and IV became statistically significantly longer in TLE patients (2B) after CBZ therapy compared to untreated group (1A) (P = 0.29 & P = 0.034 respectively) (Fig. 3). Whereas no such difference was observed in patients with GTCS before and after treatment.

·                     Sleep latency

Mean duration became shorter after treatment in both groups 1 and 2, however, the difference was statistically significant only in group 1B compared to 1A (P=0.002) (Table 2). No correlation was found between the dose and serum levels of CBZ and VPA and sleep latency.

·                     REM

Eight patients, out of 27, restored REM stage after treatment (3 patients were excluded at follow up assessment because of noncompliance) (Table 1). Mean REM duration and latency did not significantly differ amongst patients before and after treatment.

·                       WASO and Sleep Efficiency:

Mean WASO number and duration decreased and mean sleep efficiency % increased significantly after treatment in both groups (Tables 2 & 3).

·            No statistically significant difference was observed between patients receiving CBZ and those receiving VPA regarding various neurophysiological sleep parameters.

 

II. Interictal EEG parameters:

·                       Type of discharge:

Focal EEG changes were formed of sharp waves, and slow waves with sharp contour, while generalized discharges were formed of generalized paroxysmal discharge (spike and wave discharge, and polyspikes).

·                       Wake and sleep EEG recording:

Nineteen patients had interictal discharge (IID) during sleep EEG while waking conventional daytime EEG revealed IID in 11 patients indicating higher activation of IID during sleep compared to state of wakefulness. During sleep recording, higher activation of IID occurred in the light stages of NREM sleep (stage I and II).  None of either group had epileptic discharge during REM sleep, implicating facilitatory effect of NREM sleep (Table 4).

·                       Sleep EEG before and after treatment:

The number of patients experiencing IID dropped from 19 out of 30 (63.3%) to 10 out of 27 (37%) (Fig. 4).

 

III. Clinical seizure activity:

Forty percent of patients with GTCS had their fits exclusively during sleep while 13.3% of patients with TLE had exclusively nocturnal fits (Table 5).

 

IV.  Epworth Sleep Scale (ESS):

The mean ESS score was significantly higher in untreated epileptic patients (group A) compared to controls. Mean ESS score significantly decreased after VPA and CBZ monotherapy  (group B) (Fig.5).

ESS score correlated positively with WASO in untreated patients (r= 0.44 &P= 0.18) (Fig. 6), whereas no correlation was found between ESS score and REM sleep mean duration or seizure frequency or duration (r= 0.175 & P= 0.354, r= 0.254 & P= 0.176 respectively).


 

 

Fig. (1): Comparison between groups (1A), (2A), and (3) as regards sleep

latency and stage IV NREM sleep duration.

 

 

 

Fig. (2): Comparison between groups (1A), (2A), and controls as regards

WASO and sleep efficiency.

 

Fig. (3): Comparison between groups (1A) and (1B) as regards NREM sleep stages.

 

Table 1. Number & percent of patients having REM stage before and after treatment.

 

No. & percent of patients in group (A)

with REM (n. 30)

No. & percent of patients in group (B)

with REM (n. 27)

1A

6/15     

(40%)

1B

10/12

(83.3%)

2A

9/15    

(60%)

2B

13/15

(86.7)

Total

15/30  

(50%)

Total

23/27

(85%)

 

 

Table 2.  Comparison between groups (1A) and (1B) as regards sleep efficiency, sleep latency, and WASO number and duration.

 

 

No.

Mean±SD

P value

Sleep efficiency    (1A)

                              (1B)

12

12

78.36±10.16

88.33±8.36

 

0.002**

Sleep latency        (1A)

                              (1B)

12

12

35.91±16.64

18.25±6.98

 

0.003**

WASO (No.)        (1A)

                              (1B)

9

9

2.44±0.72

1.77±.66

 

0.022*

WASO (min.)       (1A)

                              (1B)

9

9

76.33±25.09

41.11±13.28

 

0.001**

* Significant                  ** Highly Significant

 

Table 3. Comparison between patients group (2A) and group (2B) as regards sleep efficiency and number of WASO.  

 

 

No.

Mean±SD

P value

Sleep efficiency    (2A)

                              (2B)

15

15

80.78±13.42

92.56±7.90

 

0.001**

WASO  (NO.)      (2A)

                              (2B)

12

12

3.25±1.48

1.66±0.88

 

0.006**

                  * Significant                  ** Highly Significant

Table 4. Number and percent of patients with IID during wake and sleep EEG recording.

 

State during recording

No. of patients with IID

% of patients with IID

Wakefulness

11

36.4

Sleep

19

63.3

NREM stage I

17

56.7

NREM stage II

18

60

NREM stage III

15

50

NREM stage IV

11

36.4

REM

0

0

 

 

 

 

Fig. (4): Percentage of interictal discharge (IID) in patients groups before and after treatment.

 

 

Table 5. Diurnal distribution of fits in groups 1A & 2A.

 

Group

Exclusively Nocturnal Fits

Exclusively Diurnal Fits

Random Ffits (nocturnal &  diurnal)

1A (n.15)

2 (13.3%)

9 (60%)

4 (26.7%)

2A (n.15)

6 (40%)

2 (13.3%)

7 (46.7%)

 

 

 

Fig. (5):  Comparison between patients groups (A & B) and control group as regards ESS.

 

 

 

Fig. (6):  Correlation between ESS and WASO number in patients group (A).


DISCUSSION

 

The relationship between sleep and epilepsy is interchanging. So, as the epileptic phenomena may induce sleep pattern modifications, sleep also can strongly influence seizure activity and interictal EEG changes. These mutual effects have been noted in idiopathic generalized epilepsies as well as partial epilepsies with or without secondary generalization. This relationship, between sleep and epilepsy, can be influenced by pharmacological treatment as AEDs, which are able to control seizures as well as to modify hypnic structure7,8.

In this study, only the untreated TLE patients group had statistically significant lower duration stage IV, and statistically highly significant higher mean WASO duration, longer sleep latency, and lower sleep efficiency compared to normal controls.  This goes in concordance with other studies9,10. Also, patients with TLE, both untreated and treated, had more sleep abnormalities compared to patients with  untreated GTCS though this difference  did not reach statistically significant values. This goes in agreement with Touchon et al.11, who found more marked sleep abnormalities in patients with TLE compared to those with generalized epilepsy with a significant increase in number and duration of WASO and decrease in sleep efficiency. A possible explanation for increased sleep abnormalities in TLE group could be attributed to the fact that involvement of temporal structures in epilepsy induces disturbed sleep patterns favoring waking and light sleep12.

The untreated patients with GTCS had statistically significant higher duration of WASO, and statistically highly significant lower sleep efficiency compared to controls.  Similar findings were reported by Dadmehr et al.13. The disturbed sleep in generalized and partial seizure patients have different character, possibly reflecting generally altered cerebral excitability by afferent stimuli in the former situation, and the more localized effects of limbic or cortical hyperactivity in the latter13.

Fifty percent of patients in this series had no REM sleep during their all night sleep EEG before treatment and 14.81% had no REM sleep after treatment. Absence of REM sleep among epileptic patients was also observed by other studies7. Absence of REM sleep in some of the untreated epileptic patients could be part of disrupted sleep in epileptics related to the disease itself, while the reported increase in its occurrence noticed after treatment could be attributed to the normalizing and restorative effect of CBZ and VPA on sleep, decreased interictal discharge, and improvement of sleep continuity.

In this series, more patients had IID during sleep EEG recording than during daytime recording indicating higher activation of IID during sleep. This goes in agreement with several studies14-16. The presence of lower EEG activity during wakefulness may be explained on the basis of increased 5-HT during wakefulness which is protective against epilepsy while decreased activity during sleep may have a facilitatory effect (though this remains controversial)17. During sleep EEG recording, increased activation of IID occurred in NREM sleep stages with the highest activation occurring during the light stages of sleep (stage I and II) in both groups. None of either group had epileptic discharge during REM sleep. These findings were also observed by many other studies18-26. This could be attributed to the facilitating effect of NREM sleep on IID especially light stages (stage I and II) which is associated with EEG synchronization23 and reflects the antiepileptic role of REM sleep.

Following three months of CBZ and VPA monotherapy in patients with TLE and GTCS respectively, marked improvement of sleep parameters occurred including shorter sleep latency, restoration of REM sleep, decreased number and duration of WASO and increased sleep efficiency indicating normalization of disturbed sleep patterns. These findings are in agreement with other studies27-30. CBZ effect on sleep may be due to increased dopamine turnover by CBZ at therapeutic doses31 as the reduction of dopamine activity seems to facilitate sleep32. Also shorter sleep latency after CBZ montherapy may be due to its serotonergic mechanism, where pharmacological evidence suggested that serotonin may have a role in sleep induction. The effect of VPA on GABA may have a modulating and stabilizing effect on excitatory neurotransmitters, also GABA is responsible for induction and maintenance of SWS33.

Excessive daytime sleepiness (EDS) is an important symptom that needs to be quantified, Johns33 documented that ESS is the most discriminating test of daytime sleepiness. It is a simple questionnaire measuring the general level of daytime sleepiness, called here the average sleep propensity. This is a measure of the probability of falling asleep in a variety of situations34. In the present study, significantly higher ESS score was found in untreated epileptic patients group compared to normal controls in accordance with Drake et al.35. Daytime sleepiness was not significantly different between untreated TLE patients and untreated GTCS in accordance with other studies36,37, implicating that there was no real relationship between sleep disorders and types of epilepsy. Our results revealed significant improvement in daytime drowsiness as measured by ESS in the GTCS patients group after VPA monotherapy and in the TLE patients group after CBZ monotherapy in concordance with some studies30,38, however, other studies stand in disagreement with these results, where one study39 found higher degree of drowsiness in epileptic children on VPA monotherapy compared to age and sex matched controls, and another study40 that found objective daytime sleepiness in epileptic patients on chronic CBZ monotherapy, however, they compared their patients to normal controls. On the other hand Gigli et al.41, observed no increase in daytime sleepiness in epilepsy patients taking controlled release CBZ. Our findings can be explained on the basis of improvement of sleep quantity and quality as measured by increased sleep efficiency, decreased WASO, and decreased sleep latency, which were observed in this study and also in the study by Ehrenberg et al.30, together with seizures improvement, low VPA and CBZ doses and serum level, and absence of sleep disorders other than EDS, in our series, which in turn increased daytime somnolence, going in agreement with Cortesi et al.39 and Foldvary42.

A significant positive correlation between ESS score and WASO number in the untreated patients group was observed going in concordance with other studies43,44 which also found that number of arousals correlated significantly with sleepiness index suggesting that the number and type of nocturnal arousals play an important role in subsequent daytime sleepiness. On the other hand, Bonnani et al.40 observed that their patients showed a daytime tendency to fall asleep in absence of any abnormalities of nocturnal sleep pattern. 

There is lack of significant correlation between seizure frequency and EDS in our study. In addition, duration of the disease did not change results significantly. Similar results are reported by other studies45,38.

 

Conclusion:

Sleep disturbances are well-documented associations in epileptic patients. Patients with TLE have more sleep abnormalities compared to those with GTCS and to normal subjects. NREM sleep has a facilitating effect on IID especially lighter stages (stage I and II), while REM has anti-epileptogenic effect.  Forty percent and 13.3% of seizures in patients with GTCS and TLE respectively are exclusively nocturnal. Chronic CBZ and VPA therapy have restorative and normalizing effects on sleep pattern in idiopathic epilepsies, in addition to improving subjective daytime sleepiness. Untreated epileptic patients had significant excessive daytime sleepiness compared to controls. ESS correlated well with WASO numbers. Sleep EEG monitoring is more sensitive than daytime EEG recording.

 

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الملخص العربي

 

العلاقة بين النوم و مرض الصرع

(دراسة كهروفيسيولوجية و إكلينيكية)

 

العلاقة بين النوم ونوبات الصرع علاقة تبادلية حيث يؤثر كل منهما على الآخر،  فاضطرابات النوم ونقصه تساعد على حدوث نوبات صرع كما أن مرضى الصرع يعانون من  عدم استقرار فى النوم.̣ وقد تم تصميم هذا البحث لإلقاء الضوء على نـمط النوم لمرضى الصرع وكذلك دراسة تأثير العلاج على نمط النوم لهؤلاء المرضى.  تم إجراء الدراسة على (30) مريضاً بالصرع قبل وبعد العلاج وقسم المرضى الى مجموعة تعانى من نوبات صرع كبرى (15 مريضاً تلقوا عقار الفالبروييت)  وأخرى تعانى من مرض الصرع الجزئى المركب للفص الصدغي (15 مريضاً تلقوا عقار الكاربامازيبين)، وقد شملت الدراسة أيضاً عشرة أشخاص أصحاء (مجموعة ضابطة) مماثلين فى العمر والجنس لمجموعة المرضى .وقد خضع كل المرضى إلى بيان تاريخ تفصيلى للمرض مع فحص سريرى كامل وفحوص معملية كاملة لاستبعاد الأمراض التى قد تؤثر على النوم وتاريخ تفصيلى لاضطراب النوم وتقييم وجود نعاس فى فترة النهار (معامل ايبوارث)  واختبارات تخطيط النوم الليلى المتعدد ورسام المخ الكهربائى ورنين مغناطيسى على المخ قبل تناول مضادات الصرع، وتم إعادة هذه الفحوصات بعد مرور (3) شهور على تناول مضادات الصرع )عدا الفحوصات المعملية والرنين المغناطيسى( بالإضافة الى قياس مستوى  مضادات الصرع فى الدم .وقد أظهرت النتائج ما يلى : كان لدى مرضى الصرع الجزئى المركب للفص الصدغي قبل العلاج العدد الأكثر لمرات الاستيقاظ ليلا ًوالمدة الأطول لبداية النوم والفترة الأقل للمرحلة الرابعة للنوم الغير مصاحب بحركة العين السريعة مقارنة بالمجموعة الضابطة. وبالإضافة إلى مجموعة  مرضى الصرع الجزئى المركب للفص الصدغي فقد كان أيضا لدى مرضى نوبات الصرع الكبرى الفترات الأطول للاستيقاظ ليلاً والكفاءة الأقل للنوم مقارنة بالمجموعة الضابطة. العلاج بالكاربمازيبين لمدة (3) شهور لمرضى الصرع الجزئى المركب للفص الصدغي وكذلك العلاج بالفالبروييت لمدة (3) شهور لمرضى نوبات الصرع الكبرى أدى إلى تـحسين كفاءة النوم وتقليل عدد مرات ومدة الاستيقاظ خلال النوم وتقليل الفترة اللازمة لبداية النوم وزيادة نسبة النوم العميق (المرحلة الثالثة والرابعة) . لوحظ حدوث تغييرات رسم المخ الصرعية ما بين النوبات فى مرحلة النوم الغير مصاحب بحركة العين السريعة وخاصة فى فترات النوم الخفيف (المرحلة الأولى والثانية) بينما لوحظ عدم حدوثها فى النوم المصاحب بحركة العين السريعة. كانت  مجموعتا المرضى تعانيان من كثرة النعاس أثناء فترة النهار مقارنة بالمجموعة الضابطة قبل العلاج بينما أدى العلاج بالكاربمازيبين والفالبروييت الى تقليل النعاس أثناء النهار لكلتا المجموعتين فى حين أنه لم يكن هناك فارق ذو دلالة إحصائية بين مجموعتى المرضى بالنسبة لكثرة النعاس أثناء النهار قبل وبعد العلاج. لوحظ عدم وجود فارق ذو دلالة إحصائية بين كثرة النعاس بالنهار وعدد مرات حدوث النوبات الصرعية، فى حين وجدت علاقة طردية بين كثرة النعاس بالنهار وعدد مرات الاستيقاظ ليلاً فى مجموعتى  المرضى تحت البحث قبل العلاج.



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