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July2007 Vol.44 Issue:      2 Table of Contents
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A Study of Postictal Sleep Architecture in Epileptic Patients

Ann Abdel-Kader1, Hatem Samir2, Mona Nada1, Aya Farouk1,Lamia Afifi1, Amira Labib1

Departments of Neurophysiology1, Neurology2, Cairo University

 



ABSTRACT

 Background: The relationship between sleep and epilepsy is complicated and reciprocal; an understanding of the influences of each on the other has important clinical implications. The post-ictal state precisely could produce profound changes in the sleep-wake cycle, and it frequently causes disruption in sleep architecture. Objective: To assess sleep architecture postictally, within a maximum period of 48 hours in epileptic patients. Methods: Post-ictal assessment of sleep architecture using polysomnographic recording and long-term video EEG monitoring was applied for twenty epileptic patients with non-symptomatic generalized or localization-related epilepsies as well as for 10 age and gender matched controls. All patients were submitted to full clinical, laboratory and radiological assessment. Results: Epileptic patients had significantly less number of awakenings, higher percentages of S2, lower percentages of SWS from total sleep time and shorter latency to SWS as compared to the control. Patients with generalized epilepsies had significantly higher periods of sleep latency to S2 as compared to patients with focal seizures and those on polytherapy had significant shorter sleep latency to S2, with significant higher apnea index in NREM sleep compared to those on monotherapy. Conclusion: Post-ictal state appears to disrupt the regulation of sleep architecture, which mainly recognized in the NREM sleep.

(Egypt J. Neurol. Psychiat. Neurosurg., 2007, 44(2): 661-673)

 




INTRODUCTION

 

The relationship between sleep and epilepsy is complicated and reciprocal, and the understanding of the influence of each on the other is of important clinical implications1. Seizures could affect sleep macroarchitecture and might produce excessive daytime sleepiness (EDS) in patients with epilepsy2. In addition; seizures occurrence could have profound effects that last much longer than the post-ictal period3.

Many studies aimed to analyze the influence of sleep and its stages on the behavior of seizures, but very few look into the opposite effect of seizures on the structure of sleep4. Structural sleep analysis confirms the presence of a disturbance of sleep stability in patients with epilepsy5; however, the exact nature of sleep disturbances in epilepsy has not yet been fully defined6. This sleep disturbance could be attributed to many factors that include the occurrence of a seizure by itself, the type of seizures, the received anti-epileptic drugs or the underlying disease process7.

Epilepsy might affect sleep architecture by producing an increase in wake time after sleep onset and stage shifts, an increase in stage 1 and 2 non-rapid eye movement (NREM) sleep and sleep latency, and a decrease in sleep spindle density and REM sleep are also observed2.

Seizures can also cause prolonged reductions in the amount of REM sleep8. Furthermore; Vignatelli et al.9 reported that nocturnal seizures could be associated with sleep fragmentation, reduced sleep efficiency, pathologic level of EDS and disturbed sleep quality. On the other hand; Hallbook et al.10  in their study on the effect of ketogenic diet on sleep quality in children with therapy-resistant epilepsy found an increase in total sleep, total night sleep and decrease in REM sleep; they added that these deleterious effects were reverted ketogenic diet owing to a more seizures control.

In addition to the previously recognized abnormalities; REM sleep behavior disorder (RBD) episodes diagnosed by standard clinical and video-polysomnographic findings were detected in epileptic patients; however, the real extent of this comorbidity is not yet established Manni et al.11.

The objective of this study was to assess sleep architecture and evaluate sleep disturbance postictally, within a maximum period of 48 hours in a group of 20 patients, previously known to be epileptic.

 

SUBJECTS AND METHODS

 

Patient Selection and Enrollment Criteria. This was a case-control study that aimed to assess sleep architecture post-ictally in 20 patients known to be epileptic and on antiepileptic drugs. They had either generalized epilepsies (n=9) or localization-related epilepsy with or without secondary generalization (n=11). Eight of them were males (40%) and 12 were females (60%). Their age ranged from 15 to 30 years, with a mean of 21.35±5.83 years. Patients were recruited from epilepsy outpatient clinic of Kasr El-Aini hospitals. All patients were eligible for the present study when they develop a fit within the previous 48 hours before the polysomnographic recording. Ten normal age and gender matched healthy subjects served as a control group.

Exclusionary Criteria. (1) Patients with mental retardation or psychiatric disorders; (2) patients with organic brain syndromes, co-morbid medical diseases, pain or substance use disorders that could affect sleep architecture; (3) patients presented with status epilepticus.

Patient Evaluation. All patients enrolled in this study were submitted to thorough clinical assessment with a detailed epilepsy history from patients and eye-witness relatives. Sleep disturbance was evaluated according to Parkes12 from patients and one of their close relatives.

Laboratory Assessment. Complete blood picture, liver and kidney function tests as well as thyroid function tests and electrolytes measurements were done for all patients.

Polysomnographic Recording. A full polysomnography (PSG) was carried out for epileptic patients and for controls over a full night. It included electroencephalography (EEG), electro-oculography (EOG), electromyography (EMG), electrocardiography (ECG), airflow cannula, ventiltary effort belts, oxygen saturation, body position, snoring microphone and tibialis anterior muscle recording. Somnologica software was used. Sleep stages were scored according to the standard scoring system for sleep stages by Rechtschaffen and Kales13.

Long-term video EEG monitoring. Video-Polygraphic monitoring was done using a Schwarzer GmbH, Medical diagnostic equipment and a digital video-camera (Panasonic AG6040). EEG electrodes were placed according to the international 10-20 system using a cap to which the electrodes were adherent.

Statistical Analysis. Data management was performed using with the Statistical Package for Social Sciences (version 10.0, 1999; SPSS Inc. Chicago, IL, USA). Descriptive Statistics: Mean±SD, median, number and percentage. Chi-square test was used in comparison between the sex of cases and controls. Comparisons between the measurements in two groups were done using Mann-Witney test. For more than two groups, Kruskal-Wallis test, a nonparametric one way analysis of variance followed by Sheffe's multiple comparisons test. Pearson's correlation coefficient was calculated for the association between the different numerical measurements14. All p-values are two-sided. P‑values < 0.05 were considered significant.

 

RESULTS

 

Demographic Data. There were twenty patients included in this case-control study; all of them had an established diagnosis of epilepsy. Ten age and gender matched normal subjects were included as a control group. No statistical significant difference between patients and control groups regarding demographic data (Table 1).

Patients Characteristics. According to the ILAE classification15 and on the basis of clinical and EEG results, 9 patients had generalized epilepsies (4 had generalized tonic clonic seizures “GTCS”, 3 had absences, and 2 had myoclonus), while 11 patients had localization-related epilepsy with or without secondary generalization. Seizures severity was assessed according to the National Hospital Seizure Severity Scale (NHS3) of epilepsy16, where each patient had got a score with a patient's minimum score was 5 and a maximum score was 22. Duration of epilepsy ranged from 2 months to 23 years. Nine of our patients were on monotherapy (Carbamazepine, Diphenylhydantoin or Sodium Valproate); while 11 patients were subjected to polytherapy in the form of different combinations of the same previous drugs. Basic clinical characteristics of included patients are shown in table (2).

Regarding EEG findings; all patients had abnormal EEG findings, 9 of them had generalized epileptogenic changes; whereas, 11 patients had focal epileptogenic changes, out of them, 5 had focal epileptogenic changes per se (2 with right focus and 3 with left focus) and 6 had focal epileptogenic dysfunction together with secondary generalization (all had left focus except one who had bilateral foci) (Table 3).

Polysomnographic Results. All patients had their sleep record done within a period that did not exceed 48 hours from the last fit they experienced. The median duration was 25.8 hours (minimum: 5 hours and maximum: 48 hours). Comparing the PSG results of patients versus the control group, we found that in the post-ictal sleep; patients had higher percentages of sleep efficiency, lower numbers of awakenings, lower percentages of awake from sleep period, higher percentages of S2 from total sleep time (TST) and lower percentage of SWS from TST than that of control subjects with statistically significant difference (Figs. 1, 2 and 3).

We detected 3 patients (15%) without REM sleep during their all night sleep video EEG. Also; there was a tendency for patients to have shorter latencies of their post-ictal sleep than that of control subjects; yet it didn't reach statistical significance (Table 4).

In epileptic patients; correlation of sleep indices to duration of epilepsy and severity of attacks revealed no statistical significant difference (P>0.05).

Upon comparing sleep indices in relation to type of EEG changes, we found that patients with generalized epilepsies had a longer latency to S2 as compared to those with focal or focal with secondary generalization. This was statistically significant with a P-value of 0.009 (Table 5).

Regarding the antiepileptic drugs (AEDs); patients on polytherapy had shorter sleep latencies to S2 and higher apnea index in NREM sleep as compared to those on monotherapy with statistically significant difference (P<0.05), as shown in table (6).


 

 

Table 1. Demographic data of included patients and control subjects.

 

 

Patients group (n=20)

Control group (n=10)

P-value

Age (mean±SD)

21.35±5.83

21.70±4.62

0.843

Sex (F/M)

12/8

4/6

0.301

 

Table 2. Basic clinical characteristics of included patients.

 

 

No

Age(Y)

Sex

Age of onset (Y)

Type of fit

Severity

Last fit (H)

Treatment

1

2

3

4

5

6

7

8

9

10

11

12

13

14

15

16

17

18

19

20

18

25

29

21

28

20

18

17

20

30

18

15

24

16

14

15

22

30

15

32

M

F

M

F

F

F

F

M

M

F

F

M

M

F

F

F

F

M

M

F

10

22

12

1

8

7

13

6

15

7

8

1

20

0.5

7

13

13

16

14

28

Focal

GTCs

Absence

Focal

Focal

Focal

Myoclonus

Focal

GTCs

Absence

Absence

GTCs

GTCs

Focal

Focal

Focal

Myoclonus

Focal

Focal

Focal

18

17

16

10

16

16

5

17

24

15

7

22

16

7

16

9

17

11

18

10

48

48

24

24

48

5

24

24

24

7

6

48

24

24

24

24

24

6

12

48

Poly

Mono

Poly

Poly

Poly

Poly

Mono

Poly

Poly

Mono

Mono

Mono

Mono

Poly

Poly

Poly

Mono

Poly

Mono

Mono

 

Table 3. EEG findings of included patients.

 

No.

EEG Abnormalities

Type

Laterality

Site

1

2

3

4

5

6

7

8

9

10

11

12

13

14

15

16

17

18

19

20

Focal

Generalized

Generalized

Focal

Focal with 2ry generalization

Focal

Generalized

Focal

Generalized

Generalized

Generalized

Generalized

Generalized

Focal with 2ry generalization

Focal with 2ry generalization

Focal with 2ry generalization

Generalized

Focal

Focal with 2ry generalization

Focal with 2ry generalization

Left

-

-

right

left

left

-

left

-

-

-

-

-

both

left

left

-

right

left

left

Fronto-temporal

-

-

Fronto-temporal

Fronto-temporal

Frontal

-

Fronto-temporal

-

-

-

-

-

Frontal

Fronto-temporal

Fronto-temporal

-

Fronto-temporal

Fronto-temporal

Fronto-temporal

 

 

Table 4. Polysomnographic findings in both patient and control groups.

 

Measurements

Patients (n=20)

Controls (n=10)

P-value

Median

Min.

Max.

Median

Min

Max

Sleep onset (min)

22.7

3.0

229.5

14.2

0.5

72.2

0.356

Sleep latency to S1 (min)

34.3

4.1

238.5

45.8

5.5

477.5

0.692

Sleep latency to S2 (min)

28.8

0.5

230.0

20.0

0.5

177.2

0.487

Sleep latency to SWS (min)

48.5

11.0

254.0

112.7

28.5

240.0

0.050

REM latency from sleep onset (min)

170.0

12.5

412.0

243.0

5.5

385.5

0.435

% of S1 from TST

8.8

1.0

29.8

7.1

0.5

43.2

0.202

% of S2 from TST

57.2

31.9

77.1

48.7

17.9

59.3

0.013*

% of SWS from TST

22.8

6.5

58.1

35.5

0.8

66.5

0.014*

% of REM from TST

8.6

1.9

18.3

9.9

2.5

20.5

0.643

% of awake from sleep period

11.8

2.6

45.6

38.4

12.3

73.2

0.001*

Sleep efficiency (%)

88.3

54.4

97.4

61.6

26.8

87.7

0.001*

Number of awakenings

10.0

0.0

22.0

17.5

7.0

26.0

0.027*

PLM index

0.0

0.0

0.9

0.5

0.0

13.1

0.089

Apnea index: in REM

0.0

0.0

1.5

0.0

0.0

0.0

0.203

Apnea index: in NREM

0.2

0.0

1.4

0.0

0.0

14.2

0.712

Hypopnea index: in REM

0.0

0.0

15.3

0.0

0.0

14.1

0.944

Hypopnea index: in NREM

0.5

0.0

6.2

0.7

0.0

8.1

0.494

 

 

Table 5. Sleep indices in relation to type of EEG changes.


 

Measurements

Focal

(n=5)

Focal with 2ry generalization (n=6)

Generalized

(n=9)

P-value

Median

Min

Max

Median

Min

Max

Median

Min

Max

Sleep onset (min)

11.5

3.0

29.5

13.0

4.1

30.0

52.8

14.5

229.5

0.058

Sleep latency to S1 (min)

74.5

11.0

201.5

13.0

4.1

39.0

52.8

14.5

238.5

0.112

Sleep latency to S2 (min)

17.5b

0.5

37.0

22.1b

0.8

32.0

57.8a

23.7

23.0

0.009*

Sleep latency to SWS (min)

32.3

11.0

119.0

37.1

13.8

58.5

82.5

30.7

254.0

0.087

REM latency from sleep onset (min)

230.0

117.0

363.0

73.5

43.5

292.8

178.8

12.5

412.0

0.414

% of S1 from TST

5.7

1.0

24.2

10.3

6.0

24.2

10.4

3.4

29.8

0.312

% of S2 from TST

61.4

31.9

69.4

60.2

45.1

67.5

53.9

40.7

77.1

0.409

% of SWS from TST

26.6

6.5

58.1

18.7

11.2

22.3

23.3

11.6

45.4

0.143

% of REM from TST

9.0

1.9

14.1

12.0

6.6

18.3

5.7

1.9

16.4

0.263

% of a wake from sleep period

15.9

5.5

32.2

11.8

2.6

43.3

10.3

5.4

45.6

0.973

Sleep efficiency (%)

84.2

67.8

94.5

88.2

56.7

97.4

89.7

54.4

94.6

0.973

Number of awakenings

7.5

2.0

17.0

13.0

4.0

18.0

9.0

0.0

22.0

0.287

PLM index

0.1

0.0

0.2

0.0

0.0

0.3

0.0

0.0

0.9

0.989

Apnea index: in REM

0.0

0.0

0.8

0.0

0.0

1.5

0.0

0.0

0.0

0.171

Apnea index : in NREM

0.4

0.0

1.4

0.2

0.0

0.8

0.2

0.0

0.8

0.538

Hypopnea index: in REM

0.0

0.0

3.1

0.0

0.0

15.3

0.0

0.0

7.3

0.352

Hypopnea index: in NREM

0.7

0.0

1.6

0.4

0.2

6.2

0.5

0.0

2.2

0.697

* Group medians sharing same letter are not significantly different than each other.

Table 6. Sleep indices in relation to therapy.

 

Measurements

Monotherapy (n=9)

Polytherapy (n=11)

P-value

Median

Min.

Max.

Median

Min.

Max.

Sleep onset (min)

38.9

6.0

229.5

18.4

3.0

85.8

0.208

Sleep latency to S1 (min)

52.8

14.5

238.5

29.5

4.1

199.0

0.184

Sleep latency to S2 (min)

53.1

6.0

230.0

22.1

0.5

107.8

0.041*

Sleep latency to SWS (min)

52.3

11.0

254.0

37.1

13.8

121.8

0.447

REM latency from sleep onset (min)

250.3

12.5

412.0

117.0

43.5

292.8

0.102

% of S1 from TST

7.9

2.7

17.3

10.3

1.0

29.8

0.342

% of S2 from TST

56.9

40.7

77.1

57.5

31.9

69.4

0.621

% of SWS from TST

27.3

17.7

45.4

19.1

6.5

58.1

0.139

% of REM from TST

8.6

1.9

16.4

8.6

1.9

18.3

0.824

% of awake from sleep period

17.5

5.4

45.6

8.8

2.6

43.3

0.239

Sleep efficiency (%)

82.5

54.4

94.6

91.2

56.7

97.4

0.239

Number of awakenings

10.0

0.0

22.0

9.0

2.0

18.0

0.909

PLM index

0.0

0.0

0.9

0.0

0.0

0.6

0.699

Apnea index: in REM

0.0

0.0

0.8

0.0

0.0

1.5

0.632

Apnea index: in NREM

0.0

0.0

0.4

0.2

0.0

1.4

0.035*

Hypopnea index: in REM

0.0

0.0

7.3

0.0

0.0

15.3

1.000

Hypopnea index: in NREM

0.6

0.0

2.2

0.4

0.0

6.2

0.819

 

 

 

Fig. (1): Hypnogram of a 16-years old female control. S2 = 45.3% from TST. SWS = 52.1% from TST. Wake = 53.6% from total sleep period.

Fig. (2a): Digital EEG sleep recording.

 

Fig. (2b): Polysomnographic record.

Fig. (2): Female patient, 15 years old, presented by recurrent nocturnal fits in the form of GTCs with focal onset. She was on CBZ and VPA. Digital EEG sleep recording (Fig. 2a): left frontotemporal focus. PSG recording (Fig. 2b): high percentage of S2 from TST (69.4%) and low percentage of SWS from TST (6.5%).

Fig. (3a): Digital sleep EEG record.

 

Fig. (3b): Polysomnographic recording.

 

Fig. (3): Female patient, 15 years old had dialeptic seizures. She was subjected to long-term VPA treatment. Digital EEG sleep recording (Fig. 3a): generalized 3 c/s spike and wave discharges. PSG recording (Fig. 3b): high percentage of S2 from TST (77.1%) and low percentage of SWS from TST (17.7%), low percentage of REM sleep from TST (1.9%), and high percentage of sleep efficiency (94.6%)


DISCUSSION

 

The relationship between sleep and epilepsy is interchanging; so as sleep can influence seizure activity and interictal EEG changes, the epileptic phenomena may also induce sleep pattern modifications; however, the exact nature of these sleep disturbances has not yet been fully defined, and this could be attributed to methodological differences in various studies6. These mutual effects of both epilepsy and sleep have been noted in idiopathic generalized epilepsies as well as partial epilepsies with or without secondary generalization17.

The current study aimed to define sleep patterns that occur in epileptic patients post-ictally. Twenty epileptic patients were enrolled in our study (11 patients had localization-related epilepsy, and 9 patients had generalized epilepsy), they were subjected to clinical evaluation, laboratory and radiological assessment. Overnight video EEG-PSG recording was performed in the presence of one of the patient's relatives and a technician. The attendance of a technician who can record any event during monitoring was essential, this criterion can increase the diagnostic accuracy of this tool according to Foley et al.18. Our study also included age, gender and education matched control group. All patients were on conventional antiepileptic drugs (AEDs), either monotherapy (n=9), or polytherapy (n=11); the drugs were not withdrawn prior to the recording, as though this may potentially increase diagnostic yield of long-term video EEG monitoring; yet, this will carry the risk of increased fits frequency. Similar proposals established by other authorities18,19.

In our study, we found that patients with epilepsy had higher percentages of sleep efficiency than controls, they showed less number of awakenings throughout the night and lower percentages of awake from total sleep period; also patients showed a significant tendency towards light sleep than slow wave sleep (SWS), with particular increase in percentages of S2 from TST, decrease percentages of SWS with shorter periods of sleep latencies to SWS as compared to controls. These findings could be attributed to postictal drowsiness and somnolence, as our patients had their PSG recordings done directly after experiencing a fit; this result was previously emphasized by Eisensehr and Schmidt20. On the other hand this does not go in accordance with Wang et al.21, who found that epileptics had a more fragmented sleep than controls. They also stated that epileptics with interictal discharges had significantly longer total sleep time and longer REM latency than the controls. However, sleep fragmentation of epileptics in this study could be attributed to first night sleep lab effect, together with longer periods elapsed between occurrence of last fit and time of the recording, and this reduces the effect of postictal somnolence. Also Weerd et al.22 studied sleep disturbance among a group of patients having partial epilepsy and a group of healthy controls. They used sleep questionnaires that analyzed sleep over the past 4 weeks. An average of less than 7 to 8 hours sleep per night in the past 4 weeks was reported by 39% of the patients compared with 32% of the controls. Moreover, the primary analysis of the sleep diagnosis list showed significantly higher prevalence of subjective sleep disturbance among patients than among controls. This study is somehow tedious and time-consuming as the subjects take too much time completing their scores, besides the need to study specific reliable subjects who would not escape or get bored before coming to the end. On the other view; Hallbook et al.10, found an increase in total sleep, total night sleep and decrease in REM sleep in therapy-resistant epilepsy.

On comparing the 2 groups of patients; those with generalized epilepsy versus patients with localization-related epilepsy-whether alone or with secondary generalization, we found that patients with generalized paroxysms had longer latencies to S2 than those with focal epileptogenic dysfunction. This result contradicts what was found by Wang et al.21; they reported that patients with partial seizures had a significantly higher arousal number than those with generalized seizures. The number of NREM stage shifts tended to be higher in those with partial seizures than in those with generalized seizures. Similar findings were reported by Touchon et al.23, who found more marked sleep abnormalities in patients with temporal lobe epilepsy (TLE) compared to those with generalized epilepsy, with a significant increase in number and duration of waking after sleep onset and decrease in sleep efficiency. On the other view; Barreto et al.24 recognized that patients with idiopathic focal epilepsy presented a tendency toward an excessive somnolence, whereas the group with idiopathic generalized epilepsy presented sleep of poorer quality. The former group showed an increase in the total sleep time, and the latter had a reduction of stage 4 NREM sleep. The efficiency of total sleep period and of total sleep time was also lower in the group with idiopathic generalized epilepsy. This goes in accordance with Dadmehr et al.25, who found that patients with GTCs had statistically significant higher duration of waking after sleep onset (WASO) and significantly lower sleep efficiency. Also Crespel et al.26 emphasized that patients with partial seizures have been shown to have relatively normal sleep on seizure-free nights except for slightly decreased sleep efficiency with temporal lobe epilepsy.

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 latter25. The 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 sleep27. This pattern of sleep disturbance could prevail without overt seizures.

In our study, 15% of patients had no REM sleep during their all night sleep video EEG. Kawahara et al.28 found that 29.41% of their patients had no REM sleep throughout the night. This lightens the idea that most patients spend longer periods of sleep in the NREM stage, with special direction towards S2. Moreover, both, seizures and interictal epileptiform discharges (IEDs) are facilitated by NREM sleep. While deeper stages of NREM sleep activate IEDs, lighter stages of NREM sleep promote seizures. These findings were reported by Minecan et al.29, who concluded that 95% of seizures occurred in NREM sleep (61% in stage 2, 20% in stage 1, 14% in stages 3 and 4 combined), and 5% in REM sleep. However, in our study, only few patients experienced genuine epileptic fits during the recording, and these were distributed over different sleep stages.

Some reports have stressed that obstructive sleep apnea (OSA) and periodic limb movements (PLMs) during sleep can significantly account for sleepiness complaints in epilepsy patients, most of the AEDs can worsen OSA 30. In our study; the apnea indices had significant higher values in patients on polytherapy rather than those on monotherapy. Moreover; patients on polytherapy had shorter sleep latencies to S2 as compared to those on monotherapy with statistically significant difference (P<0.05), this result reflects the sedative effects of the combination of conventional AEDs; however, we could not obtained any results regarding each drug separately, and this is attributed to the small sample size. The effects of drugs on sleep pattern were studied by many authorities; whereas, Legros and Bazil31 stated that phenytoin increases light sleep and decreases REM sleep; the findings for carbamazepine (CBZ) are more variable, but generally it facilitates sleep, with reduction in REM sleep particularly with acute treatment32. The university of CBZ effect on sleep in epilepsy may be due to increased dopamine turnover with subsequent reduction of dopamine activity33. On the other view; valproate (VPA) significantly increases stages 3 and 4, and improves sleep efficiency and decreased arousals, indicating that VPA has a consolidating effect on sleep34. The effect of VPA on GABA may have stabilizing effect on excitatory neurotransmitters, and also GABA is responsible for induction and maintenance of SWS that leads to increase sleep efficiency35.

In conclusion we found, by means of PSG recording, that epileptic patients have evident sleep disturbances and disruption of their sleep architecture. Patients with chronic diseases who also have sleep disturbances find coping with the disease more difficult, along with a constriction of leisure time. Thus it is of utmost importance to detect, diagnose and treat the sleep disorders and not just focus on the primary disease.

 

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الملخــص العربـــى

 

يعانى مرضى الصرع من تغيرات في التكوين الكهربي للنوم وتكون هذه التغيرات أكثر وضوحاً بعد إصابتهم بالنوبات الصرعية سواء الكبرى أو الصغرى. يتم عمل رسم نوم إلى جانب رسم مخ طويل لهؤلاء المرضى لتحليل هذه التغيرات والتأكد منها.

            في هذه الدراسة، تم إجراء هذه الاختبارات لمجموعة من مرضى الصرع ومجموعة ضابطة من الأشخاص الطبيعيين. اشتمل الفحص على أربع قنوات لرسم المخ، قناتين لتسجيل حركة العين، قناتين لرسم عضلات الذقن والساق، قناة لرسم القلب، قناة لوضع جسم المريض، ثلاث قنوات لقياس حركة التنفس، قناتين لقياس نسبة تشبع الدم بالأكسجين وقياس النبض وقناة لتسجيل الأصوات في الجزء العلوي من الجهاز التنفسي.

            وقد تم إجراء الفحص لهؤلاء المرضى خلال مدة 48 ساعة من آخر نوبة صرعية ثم تم إجراء تحليل ساعات النوم التي تراوحت ما بين 6 إلى 8 ساعات لكل مريض. كما أجريت لهم فحوص إكلينيكية عصبية وتحاليل معملية لاستبعاد إصابتهم بأي أمراض أخرى مسببة للصرع.

            بعد فحص نتائج اختبارات النوم تبين أن هؤلاء المرضى يعانون من زيادة ملحوظة فى النسبة المئوية للمرحلة الثانية للنوم ذو غياب حركة العين السريعة مع انخفاض في النسبة المئوية لكل من المرحلة الثالثة والرابعة وأيضاً في عدد دقائق تنبه المريض خلال مدة النوم الكلية مما يؤدى إلى زيادة ظاهرية في النسبة المئوية لكفاءة النوم عند هؤلاء المرضى.



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