Online ISSN : 1687-8329

    




Quick Search 
 
Author  
Year    
Title  
Vol:  

 
 
April2011 Vol.48 Issue:      2 Table of Contents
Full Text
PDF


Event-Related Potentials in Sleep-Related Breathing Disorders and Insomnia

Sadek M. Helmy1, Shahira M. Mostafa2, Hala R. El-Habashy2,

Amira M. El-Gohary2, Eman A. Maher2

 

Departments of Neurology1, Clinical Neurophysiology2, Cairo University; Egypt

 



ABSTRACT

Background: Since sleep may affect information processing and therefore event related potentials, an increased P300 latency and reduced amplitude are expected to be present when sleep is disrupted and shortened. Objective: To assess event related potentials (ERPs) in patients with sleep related breathing disorders (SRBDs) and insomnia, and the association between the severity of subjective and objective sleep alterations and the changes in ERPs. Methods: Thirty patients with SRBDs and insomnia were subjected to polysomnography (PSG), visual and auditory ERPs testing twice; pre and post sleep. Results: We found significant decrease in ERPs latencies, and increase in their amplitudes in the morning in the control group, but not in patients. Evening ERPs were not significantly different among the groups. Morning ERPs in sleep related breathing disorders had longer latencies and smaller amplitudes. Evening to morning comparison revealed the subtle ERPs abnormalities in insomnia. No significant correlation was found between the changes of ERPs in patients and their Epworth sleepiness scale scores and the PSG data. Conclusion: Normal uninterrupted sleep greatly enhances ERPs. Multiple P300 measurements especially in the morning provide more sensitive marker for assessment of sleep effects on attention processes. The difference between evening and morning ERPs is a very sensitive parameter and can detect subtle abnormalities especially in insomnia patients. Neither subjective nor objective estimates of sleep continuity can strongly explain the changes in ERPs. [Egypt J Neurol Psychiat Neurosurg.  2011; 48(2): 129-137]

 

Key words: event-related potentials, insomnia, P300, sleep related breathing disorders





INTRODUCTION

 

The hypothesis that sleep may play a role in the process of memory formation and cognition dates back to the report of Jenkins and Dallenbach in 1924, claiming that recall performance improves following an intervening period of sleep1.

Event-related potentials (ERPs) have been used as a neurophysiologic marker of information processing, discrimination and working memory. Some recent data have shown that ERPs and P300 amplitude and latency may be affected by the sleep-onset period, sleep deprivation and experimental sleep fragmentation. These data suggest that sleepiness, sleep loss and sleep fragmentation may affect attention-dependent and attention-independent processing and, therefore, cognitive functioning2.

Few studies have investigated the use of ERPs in sleep related breathing disorders (SRBDs). Mixed results were reported with some evidence for an increased P300 latency to visual3 and auditory4 stimuli or no effect on auditory P300 latency5. Some studies have6 and some have not3 found SRBDs patients to have reduced auditory P300 amplitude.

 

As for insomnia, the role of ERPs in assessing daytime function is much more controversial. Some studies supported hypoarousal theory and found evidence of an increased P300 latency and decreased amplitude in insomnia7,8. Other studies supported hyperarousal theory and presented evidence of increased P300 amplitude at sleep onset9,10.

This study aims at 1) Comparing evening to morning ERPs in controls, insomnia and SRBDs patients to explore the impact of good or bad sleep on ERPs. 2) Shedding the light on ERPs affection in patients with SRBDs and insomnia. 3) Assessing the association between the severity of subjective and objective sleep alterations and the changes in amplitude and latency of ERPs.

 

SUBJECTS AND METHODS

 

Patients Group

Thirty patients were selected from Kasr El-Aini Outpatient Clinic and Sleep Laboratory of the Clinical Neurophysiology Unit in the period between May 2009 and May 2010.

I)      Insomnia patients: Fifteen adult patients (9 females and 6 males), clinically diagnosed as chronic primary insomnia according to the international classification of sleep disorders 200511, were included. Patients complained of unsatisfactory sleep, which involved difficulty in initiating sleep, frequent or lengthy awakenings, early awakening, inadequate total sleep time or poor quality of sleep. Symptoms occurred at least 5 nights/week for 6 months or more.

II)     Sleep related breathing disorders patients: Fifteen adult patients (8 males and 7 females) complaining of chocking or gasping during sleep, snoring, excessive daytime sleepiness or recurrent awakenings that are not better explained by other factors were recruited. Only patients with an apnea hypopnea index in the range of 5-30 i.e., patients with mild and moderate apnea hypopnea according to standard recommendations (The Report of American Academy of Sleep Medicine Task Force, 1999)12, were included.

 

Exclusion criteria: 1) Presence of other sleep disorders such as narcolepsy, restless legs syndrome, or primary periodic limb movement. 2) Previous diagnosis of psychiatric or neurologic disease or evidence at clinical and medical examination of a neurologic or psychiatric disorder. 3) Intake of any drugs that could affect sleep or cognition such as stimulants, hypnotics, benzodiazepines and antidepressants. 4) Subjects with apnea hypopnea index less than 5 and more than 30, for SRBD patients.

 

Control Group: Fifteen age and sex matched healthy subjects served as the control group.

 

Methods

All patients and controls were subjected to the following battery of assessment:

1)      Sleep history by a one week sleep diary prior to the examination to monitor subject’s sleep-wake schedules.

2)      General examination including chest and abdominal examination to exclude general medical conditions that could affect cognition.

3)      Complete history taking and full neurological examination.

4)      Epworth Sleepiness Scale (ESS)13 to assess the level of subjective sleepiness in the patients.

5)      The PSG was carried out for patients only, over a night for at least eight hours.

Recorded Channels: According to Rechtschtaffen and Kales, 196814: two EOG channels, four EEG channels (C4–A1, O2-A1, C3,-A2, O1-A2) applied according to the international 10-20 system of electrode placement, a submental EMG channel, an ECG channel, continuous EMG of the right and left tibialis anterior muscles, one channel for airflow monitoring, two channels for ventilatory effort monitoring, two channels for arterial oxygen (O2) saturation and for pulse detection,  one channel for body position detection and one channel for upper airway sounds detection.

PSG measurements used were as follows: Sleep onset, sleep efficiency [(TST/Time in bed) x100], number of awakenings, arousal index (Number of arousals per hour), Apnea/Hypopnea index (AHI) & Oxygen desaturation index (ODI): Apneas were defined as cessation of the oronasal airflow, lasting ≥ 10 sec. Hypopneas were defined as airflow reduction of > 50%, compared to a 10sec. peak amplitude during the preceding 2 min., lasting ≥ 10 sec. and associated with either oxygen desaturation of ≥ 3% or an arousal15.

6)      Event related potentials: Visual and auditory event related potentials administered twice, pre-sleep and at least 1 hour following morning awakening (to avoid sleep inertia which affects cognitive performances for about 1 hour after awakening).

 

Machine used to record the responses was Nihon Kohden; Neuropak MEB-9200G/K EP/EMG measuring system (Neuropak M1) 4-channels version 08.11.

The active electrode was applied at Cz of the 10-20 International System of Electrode Placement. Both the reference electrode and the ground were applied to mastoid and FPZ; respectively. The electrodes impedance was kept below 5 KOhms. The gain was initially set to 50 mV per (vertical) division, monitor time was 0.12 sec. and the band pass was 0.1–50 Hz. 

For the auditory ERPs, the hearing threshold for each subject was determined. A total of 200 auditory stimuli (bursts) were presented to the ears through earphones with intensity of 60 dB above the hearing threshold. 80% of tones were 2 kHz in frequency (background tones) whereas the remaining 20% were 8 kHz (target tones). The subject was instructed to raise the right hand as quickly as possible whenever hearing the infrequent tones. These tones were presented randomly intermixed at a rate of 0.5/sec. The tones were applied so as no two target tones came in succession. 

For the visual ERPs, a total of 200 visual stimuli were presented to the eyes through goggles. 80% of stimuli were presented regularly to one eye (non target stimulus) whereas the remaining 20% were presented to the other eye (target stimulus) randomly intermixed at a rate of 0.5/sec. The subject was instructed to raise the right hand as quickly as possible whenever seeing the infrequent stimulus.

To verify reproducibility of the responses, the procedure was repeated at least once. The responses were displayed on a screen and could be printed out.

The P300 wave was defined as the most positive point of the average waveform to the target tones after 250 msec. and before 600 msec. The latency was calculated as the time taken to reach the peak of the component (in milliseconds).

The amplitude was measured in microvolts from the peak of component to the prestimulus baseline (0-100 millisecond prior to the stimulus onset).

 

Statistical Analysis

The Kruskal-Wallis test was used to determine the statistical significance between evening and morning ERPs in control, insomnia and SRBDs groups. It was also used when comparing evening ERPs in insomnia and SRBDs groups and control group, and when comparing morning ERPs in insomnia and SRBDs groups and control group, and when comparing evening to morning difference in insomnia and SRBDs groups to control group.  Spearman rank order correlation: The relationship between evening-to-morning changes in ERP amplitude and latency, sleepiness at the Epworth Sleepiness Scale score, indices of sleep continuity and sleep fragmentation were calculated using Spearman rank order correlation coefficient.

 

RESULTS

 

I.             Clinical Results

1.      Insomnia sleep complaints: The commonest sleep complaint among insomnia patients was inadequate total sleep or poor quality of sleep, other sleep complaints and their ratios are illustrated in Table (1).

2.      SRBDs sleep complaints: Snoring was the commonest sleep complaint among SRBDs patients, other complaints and their ratios are illustrated in Table (2).

 

II.           Epworth Sleepiness Scale Scores

Excessive daytime sleepiness was assessed in insomnia patients, SRBDs patients and controls by Epworth Sleepiness Scale. The range for controls was (1-5), Insomnia patients (1-6) and SRBDs (2-16). Means and standard deviations among different groups are illustrated in Table (3).

 

III.          Polysomnographic Findings among Insomnia Patients and SRBDs

-        Sleep Architecture: The mean and standard deviation of sleep onset, sleep efficiency and number of awakenings in insomnia and SRBDs patients are illustrated in Table (4).

-        Arousal and respiratory indices: The mean and standard deviation of arousal, apnea hypopnea and oxygen desaturation indices in insomnia and SRBDs patients are illustrated in Table (5).

IV.          Event Related Potential Results

:putnam: :putnam: :putnam: :putnam: :putnam: :putnam: :putnam: :putnam: :putnam: :putnam: :putnam: :putnam: :putnam: :putnam: :putnam: :putnam: :putnam: :putnam: :putnam:

:putnam: :putnam: :putnam: :putnam: :putnam: :putnam: :putnam: :putnam: :putnam: :putnam: :putnam: :putnam: :putnam: :putnam: :putnam: :putnam: :putnam: :putnam: :putnam:

1.            Evening to morning comparison of ERP values.

The mean and standard deviation of visual and auditory P300 latencies and amplitudes in the evening and in the morning among controls, insomnia and SRBD patients are illustrated in Tables (6, 7, 8); respectively.

There were statistically significant differences between evening and morning ERPs in control group in all measured ERPs parameters (p<0.0005) (Table 6).

The only statistically significant parameter between evening and morning ERPs in insomnia patients was visual P300 amplitude (p=0.0067) (Table 7).

There were no statistically significant differences between evening and morning ERPs in SRBDs patients (Table 8).

2.      Evening ERPs comparison between patients and control.

The mean and standard deviation of visual and auditory P300 latencies and amplitudes in the evening in insomnia and SRBDs patients in comparison to controls are illustrated in Table (9). There was no statistical significance among patients and controls in any parameter of evening measurements.

3.      Morning ERPs comparison between patients and control.

The mean and standard deviation of visual and auditory P300 latencies and amplitudes in the morning in insomnia and SRBDs in comparison to controls are illustrated in Table (10).

For insomnia patients the only statistically significant parameter in morning ERPs was the visual latency (p=0.0006). Morning ERPs of SRBDs patients were statistically significant with respect to controls in visual P300 latency (p-value=0.0006), auditory P300 latency (p< 0.0001) and auditory amplitude (p=0.0023).

4.      Evening-to-morning ERP difference (Evening ERPs minus morning ERPs) comparison between patients and control.

The mean and standard deviation of evening to morning differences in visual P300 latencies and amplitudes, auditory P300 latencies and amplitudes in insomnia and SRBDs and the p-values in comparison to controls are illustrated in Table (11).

Compared to controls, there were three statistically significant parameters in both insomnia and SRBDs patients: visual P300 latency (Insomnia: p<0.0001, SRBDs: p<0.0001), auditory P300 latency (Insomnia: p=0.001, SRBDs: p<0.0001), and auditory amplitude (Insomnia: p=0.004, SRBDs: p< 0.0001).

 

V.           Correlation Results

Spearman correlation analysis of evening to morning differences in ERPs latencies and amplitudes with diurnal sleepiness (ESS) and nocturnal polysomnographic data of insomnia and SRBDs patients showed no relation between ERPs and either ESS or polysomnographic findings (Tables 12 and 13).


 

 

Table 1. Sleep complaints among insomnia patients.

 

Complaints

No. of patients

Percent (%)

Inadequate total sleep or poor quality of sleep

5

33.3

Difficulty initiating sleep

4

26.7

Frequent or lengthy awakenings

3

20

Early awakening

3

20

Total

15

100

 

Table 2. Sleep complaints among SRBDs patients.

 

Complaints

No. of patients

Percent (%)

Snoring

7

46.6

Choking or gasping during sleep

4

26.6

Excessive daytime sleepiness

3

20

Recurrent awakenings

1

6.8

Total

15

100

 

Table 3. ESS results among insomnia patients, SRBDs patients and controls.

 

 

Mean±SD

P-value

Insomnia

2.8 ± 01.

0.9

SRBDs

9.13 ± 4.45

0001*

Control

2.73±1.33

<0.67

* p-value significant at < 0.05

 

Table 4. Sleep architecture in patients with insomnia and SRBDs.

 

Variable

Group

Mean±SD

Sleep efficiency%

Insomnia

66.37±11.48

SRBDs

85.43±9.45

Number of awakenings

Insomnia

11.53±3.48

SRBDs

4.267±4.69

Sleep onset in minutes

Insomnia

33.073±21.17

SRBDs

11.675±4.82

 

Table 5. Arousal and respiratory indices in insomnia patients and SRBDs.

 

Variable

Group

Mean±SD

Arousal index.

Insomnia

2.22±0.97

SRBDs

8.21±3.86

Apnea+hypopnea index.

Insomnia

1.61±1.39

SRBDs

15.25±9.14

ODI

Insomnia

0.067±0.26

SRBDs

3.83±5.19

Table 6. Evening to morning comparison of ERPs values in control group.

 

 

Evening

(Mean±SD)

Morning

(Mean±SD)

p-value

Visual latency

435.07±44.9

334.47±37.1

<0.0001*

Visual amplitude

17.90±2.8

24.43±4.4

<0.0001*

Auditory latency

432.93±55.4

332.6±45.6

<0.0001*

Auditory amplitude

18.26±4.1

26.02±5.9

0.0003*

* p-value significant at < 0.05

 

Table 7. Evening to morning comparison of ERPs values in Insomnia patients.

 

 

Evening

(Mean±SD)

Morning

(Mean±SD)

p-value

Visual latency

404.87±51.3

394±47.5

0.55

Visual amplitude

17.05±4.3

22.75±6.2

0.0067*

Auditory latency

404.8±46.5

368.2±53.7

0.056

Auditory amplitude

20.66±3.4

23.5±4.2

0.052

* p-value significant at < 0.05

 

Table 8. Evening to morning comparison of ERPs values in SBRDs patients.

 

 

Evening

(Mean±SD)

Morning

(Mean±SD)

p-value

Visual latency

444.47±75.4

471.93±64.2

0.29

Visual amplitude

16.89±5.7

19.94±8.4

0.25

Auditory latency

463.93±67.5

470.73±55.4

0.77

Auditory amplitude

17.45±9.4

16.4±9.4

0.76

* p-value significant at < 0.05

 

Table 9. Evening ERPs comparison between insomnia and SRBDs, and controls.

 

 

Group

Evening

(Mean±SD)

p-value

Visual latency

Insomnia

404.87±51.3

0.097

SRBDs

444.47±75.4

0.68

Control

435.07±44.9

 

Visual amplitude

Insomnia

17.05±4.3

0.52

SRBDs

16.89±5.7

0.54

Control

17.90±2.8

 

Auditory latency

Insomnia

404.8±46.5

0.14

SRBDs

463.93±67.5

0.18

Control

432.93±55.4

 

Auditory amplitude

Insomnia

20.66±3.4

0.09

SRBDs

17.45±9.4

0.76

Control

18.26±4.1

 

* p-value significant at < 0.05

Table 10. Morning ERPs of insomnia and SRBDs in comparison with control.

 

 

Group

Morning

(Mean±SD)

p-value

Visual latency

Insomnia

394±47.5

0.0006*

SRBDs

471.93±64.2

<0.0001*

Control

334.47±37.1

 

Visual amplitude

Insomnia

22.75±6.2

0.4

SRBDs

19.94±8.4

0.077

Control

24.43±4.4

 

Auditory latency

Insomnia

368.2±53.7

0.06

SRBDs

470.73±55.4

<0.0001*

Control

332.6±45.6

 

Auditory amplitude

Insomnia

23.5±4.2

0.19

SRBDs

16.4±9.4

0.0023*

Control

26.02±5.9

 

* p- value significant at < 0.05

 

Table 11. ERPs evening to morning difference of insomnia and SRBDs in comparison with control.

 

 

Group

Evening-Morning

(Mean±SD)

p-value

Visual latency

Insomnia

10.86±8.92

<0.0001*

SRBDs

-27.46±59.82

<0.0001*

Control

100.6±32.79

 

Visual amplitude

Insomnia

-5.70±4.46

0.59

SRBDs

-3.04±7.25

0.11

Control

-6.52±3.79

 

Auditory latency

Insomnia

36.6±37.67

0.0001*

SRBDs

-6.8±32.51

<0.0001*

Control

100.33±39.59

 

Auditory amplitude

Insomnia

2.83±4.40

0.004*

SRBDs

1.051±2.40

<0.0001*

Control

-7.74±4.25

 

* p-value significant at < 0.05

 

Table 12. Correlation of ERP parameters with ESS and sleep parameters in insomnia patients.

 

 

Visual Latency Difference

Auditory Latency Difference

Auditory Amplitude Difference

Rho

p-value

Rho

p-value

Rho

p-value

ESS

0.07

0.80

-0.29

0.28

-0.13

0.63

Sleep Efficiency

0.038

0.893

0.223

0.423

0.069

0.807

No. of  Awakening

-0.376

0.167

-0.169

0.546

-0.32

0.23

Sleep Onset

0.09

0.75

0.35

0.20

-0.32

0.24

When Rho lies around ± 1= perfect degree of association between the two variables.

* p -value significant at < 0.05

 

Table 13. Correlation of ERP parameters with ESS and sleep parameters in SRBDs patients.

 

 

Visual

Latency Difference

Auditory

Latency Difference

Auditory

Amplitude Difference

Rho

p-value

Rho

p-value

Rho

p-value

ESS

-0.139

0.62

0.447

0.098

0.224

0.428

Sleep Efficiency

-0.097

0.7315

0.261

0.3475

0.350

0.2009

No.of  Awakening

-0.099

0.7263

0.246

0.3765

-0.240

0.3879

Sleep Onset

0.398

0.1419

-0.416

0.1226

0.268

0.3344

Arousal Index

0.079

0.78

0.325

0.2368

-0.036

0.8994

AH Index

-0.104

0.7124

0.129

0.6476

-0.168

0.5499

OD Index

-0.034

0.9031

-0.129

0.6463

-0.334

0.2238

*When Rho lies around ± 1= perfect degree of association between the two variables.

* p- value significant at < 0.05


DISCUSSION

 

Up to our knowledge, our study is the first to use both visual and auditory ERPs to determine their sensitivity in detecting cognitive deficits in SRBDs and insomnia.

To explore the impact of good or bad sleep on ERPs, evening to morning ERPs were first compared in the three groups (controls, insomnia and SRBDs). In control group, the comparison revealed significant decrease in visual and auditory latencies and significant increase in visual and auditory amplitudes. These results confirm that normal uninterrupted sleep greatly enhances ERP parameters which match the findings of previous studies2. 

In contrast to the control group, comparing evening to morning ERPs in insomnia and SRBDs groups showed neither decrease in morning visual and auditory ERPs latencies nor increase in their amplitudes except for the visual ERPs amplitude in the insomnia group, which showed a significant increase in the morning (p-value=0.0067). These findings suggest that poor quality of sleep negatively impacts the ERPs of insomnia and SRBDs patients and consequently their cognition. This agrees with Kingshott et al.16, who reported a decrease in P300 amplitude after experimental sleep fragmentation and disagrees with Cote et al.17, who reported no changes in P300 amplitude after experimental sleep fragmentation.

Second, ERPs in insomnia and SRBDs were compared to controls. In SRBDs, neither latency nor amplitude differences were observed before sleep (evening) in comparison to control group. In contrast, when measurements were taken in the morning and after final awakening, significant increase in visual and auditory P300 latencies together with significant decrease in auditory P300 amplitude were observed in SRBDs compared to controls. This concludes that for SRBDs patients multiple P300 measurements especially in the morning provide more sensitive assessment of their performance. This clarifies, as well, the conflicting results in previous studies. P300 parameters are greatly influenced by the subject’s level of arousal18 and hence vary along the day. At one time, they may be similar to controls and at another time, they may be significantly different.

For insomnia patients, the condition is different. Evening as well as morning P300 measurements were not significantly different compared to control subjects, with the exception of the visual P300 morning latency, which showed significant delay. This finding disagrees with previous studies 9, 10 who found increased P300 amplitude in primary insomnia patients compared to control group, supporting the hyperarousal theory. Also, our findings differ partly from those who reported a decrease in the P300 amplitude (hypoarousal) among insomnia patients7,8.

The differences between evening to morning (evening-morning) ERPs was also calculated for the insomnia and SRBD patients and compared to controls. The subtle P300 abnormalities among insomnia patients were unmasked and significant increase in visual and auditory P300 latencies with a significant decrease in auditory P300 amplitude were revealed. However, visual P300 amplitude again failed to show significant difference.

For SRBDs, the comparison confirmed the changes detected in the morning ERPs and there was significant increase in visual and auditory P300 latencies together with decreased auditory amplitudes. Still visual P300 amplitude failed to show significant difference. Our results agree with others   regarding SRBDs only2.

Visual ERPs amplitude failed in nearly all comparisons to show any significant abnormality, which is most probably due to its known varying nature and its great dependence on stimulus characteristics19.

One of the main aims of this study was to find the relation between P300 parameters and factors explaining their variations in patients with sleep disorders. Although sleepiness, sleep quality, sleep fragmentation and reduced sleep efficiency are potential causes of P300 variation20; it is still unclear whether P300 amplitude and latency are directly affected by the duration and quality of sleep or they simply co-vary.

Since insomnia is defined as a complaint of unsatisfactory sleep, which may involve difficulty initiating sleep, frequent or lengthy awakenings, inadequate total sleep time or poor quality of sleep, we chose to correlate the following corresponding polysomnographic parameters (sleep onset, number of awakening, sleep efficiency) to the significant ERP findings (visual P300 latency difference, auditory P300 latency and amplitude differences). While for SRBDs extra three polysomnographic parameters (arousal index, AH index, OD index) are assumed to be the underlying causes of cognitive deficits, therefore, they were correlated as well to the ERPs most significant parameters.

Neither objective estimates of sleep continuity nor indices of sleep breathing disorders or oxygen desaturation could strongly explain the changes in the magnitude of P300, which agree with previous studies2.   

Correlating the most significant parameters (visual P300 latency difference, auditory P300 latency and amplitude differences) in insomnia and SRBDs to their scores in Epworth sleepiness scales, reflecting their subjective estimate of day time sleepiness, again failed to show any significant correlation, which also agrees with other researchers17,21,22, who found no significant correlation between P300 and subjective and objective measures of sleepiness.

Based on these findings, we can conclude that individual vulnerability, motivation, and the individual’s ability to compensate for attention and alertness deterioration may contribute to memory and attention processing. Some patients can perform extra compensatory effort to overcome their cognitive deficits resulting from obvious poor sleep quality (as assessed by ESS and polysomnography) while others cannot despite their mild sleep problems. This agrees with the ‘cognitive reserve’ theory23.

Also we can conclude that subjective estimates of sleep impairment as ESS are not reliable tools to evaluate the magnitude of day time dysfunction in insomnia and SRBDs patients.

Our results suggest also that other factors besides sleep may be involved in attention, memory dysfunction and P300 variations. We cannot exclude a possible circadian effect on presleep-to-postsleep P300 measurement, that insomnia and SRBDs patients cannot follow due to their sleep problems.

 

[Disclosure: Authors report no conflict of interest]

 

REFERENCES

 

1.        Mograss M, Godbout R, Guillem F. The ERP old-new effect: A useful indicator in studying the effects of sleep on memory retrieval processes. Sleep. 2006; 29(11): 1491-500.

2.        Sforza E, Haba-Rubio J. Event-related potentials in patients with insomnia and sleep-related breathing disorders: evening-to-morning changes. Sleep. 2006; 29(6): 805-13.

3.        Kotterba S, Rasche K, Widdig W, Duschaa C, Blombacha S, Schultze-Werninghausb G, et al. Neuropsychological investigations and event-related potentials in obstructive sleep apnea syndrome before and during CPAP-therapy. J Neurol Sci. 1998; 159(1): 45-50.

4.        Walsleben J, Squires NK, Rothenberger VL. Auditory event related potentials and brain dysfunction in sleep apnea. Electroencephalogr Clin Neurophysiol. 1989; 74(4): 297-311.

5.        Afifi L, Guilleminault C, Colrain IM. Sleep and respiratory stimulus specific dampening of cortical responsiveness in OSAS. Respir Physiol Neurobiol. 2003; 136(2–3): 221-34.

6.        Rumbach L, Krieger J, Kurtz D. Auditory event-related potentials in obstructive sleep apnea: effects of treatment with nasal continuous positive airway pressure. Electroencephalogr Clin Neurophysiol. 1991; 8(5): 454-7.

7.        Anderer P, Saletu B, Saletu-Zyhlarz G, Gruberb D, Metkab M, Huberb J, et al. Brain regions activated during an auditory discrimination task in insomniac postmenopausal patients before and after hormone replacement therapy: low-resolution brain electromagnetic tomography applied to event-related potentials. Neuropsychobiology. 2004; 49(3): 134-53.

8.        Bruder GE, Towey JP, Stewart JW, Friedman D, Tenke C, Quitkin FM. Event-related potentials in depression: influence of task, stimulus hemifield and clinical features on P3 latency. Biol Psychiatry. 1991; 30(3): 233–46.

9.        Devoto A, Violani C, Lucidi F, Lombardo C. P300 amplitude in subjects with primary insomnia is modulated by their sleep quality. J Psychosom Res. 2003; 54(1): 3-10.

10.     Regestein QR, Dambrosia J, Hallett M. Daytime alertness in patients with primary insomnia. Am J Psychiatry. 1993; 150(10): 1529-34.

11.     American academy of sleep medicine. The International classification of sleep disorders, revised. Diagnostic and coding manual. Rochester, MN: American Academy of Sleep Medicine; 2005.

12.     American academy of sleep medicine task force. Sleep-related breathing disorders in adults: Recommendations for syndrome definition and measurement techniques in clinical research. Sleep. 1999; 22: 667-89.

13.     Johns MW. A new method for measuring daytime sleepiness: The epworth sleepiness scale. Sleep. 1991; 14: 540–45.

14.     Rechtschaffen A, Kales A. A manual of standardized terminology, techniques and scoring system for sleep stages of human subjects. Brain Information Service, University of California. 1968. Quoted from: Kubicki S, Hermann WM, Hoeller L, Haag C. On the distribution of REM and NREM sleep under two benzodiazepines with comparable receptor affinity but different kinetic properties. Pharmacopsychiatry. 1987; 20: 270-7.

15.     Guilleminault C, Abad VC. Review of rapid eye movement behavior sleep disorders. Curr Neurol Neurosci Rep. 2004; 4(2): 157-63.

16.     Kingshott RN, Cosway RJ, Deary IJ, Douglas NJ. The effect of sleep fragmentation on cognitive processing using computerized topographic brain mapping. J Sleep Res. 2000; 9(4): 353-57.

17.     Cote KA, Milner CE, Osip SL, Ray LB, Baxter KD. Waking quantitative electroencephalogram and auditory event-related potentials following experimentally induced sleep fragmentation. Sleep. 2003; 26(6): 687-94.

18.     Colrain IM, Campbell K. The use of evoked potential in sleep research. Sleep Medicine Rev. 2007; 11: 277-93.

19.     Elkholy S, Topographical mapping on P300 event related potentials in cerebrovascular accidents patients, MD thesis in Clinical Neurophysiology, Faculty of Medicine, Cairo University; 1995.

20.     Campbell KB, Colrain IM. Event-related potential measure of the inhibition of the information processing, the sleep onset period. Int J Psychophysiology. 2002; 46:197-214.

21.     Zhang X, Wang Y, Li S, Huang X, Cui L. Early detection of cognitive impairment in patients with obstructive sleep apnea syndrome: an event-related potential study. Neurosci Lett. 2002; 325: 99-102.

22.     Inoue Y, Nanba K, Kojima K, Mitani H, Arai H. P300 abnormalities in patients with severe sleep apnea syndrome. Psychiatry Clin Neuroscience. 2001; 55: 247-8.

23.     Scarmeas N, Stern Y. Cognitive reserve and lifestyle. Journal of Clinical and Exp Neuropsychol. 2003; 25: 625-33.


 

 

الملخص العربى

 

للنوم تأثير كبير على وظائف كثيرة في المخ ومنها الذاكرة والانتباه ودرجة الوعي والإدراك. ولذلك فانه من المتوقع أن يتأثر الجهد المرتبط بالحدث من حيث زمن الكمون ومقدار الجهد باضطرابات النوم وتقطعاته.

وعليه فان هذه الرسالة تهدف إلي: 1) مقارنة قياسات الجهد المرتبط بالحدث صباحا بقياسات المساء في الأشخاص ذو النوم الطبيعي وفي مرضى الأرق وفي مرضى اضطرابات التنفس المرتبطة بالنوم. 2) اختبار حساسية الجهد المرتبط بالحدث في تشخيص اضطرابات الإدراك عند مرضى الأرق ومرضى اضطرابات التنفس المرتبطة بالنوم. 3) إلقاء الضوء على العلاقة بين تغيرات الجهد المرتبط بالحدث ونتائج معمل النوم و إحساس المريض بالنعاس.

ولإتمام هذه الدراسة فانه تم إخضاع 15 مريضا بالأرق و 15 مريضا باضطرابات التنفس المرتبطة بالنوم لاختبارات معمل النوم والجهد المرتبط بالحدث مرتين، الأولى مساء قبل النوم والثانية صباحا عند الاستيقاظ وكذلك تم تكوين مجموعة ضابطة مكونة من 15 شخص طبيعي. وتم قياس مقدار الجهد و كمون موجة بـ 300 في المرضى والمجموعة ضابطة.

وقد تبين من هذه الدراسة أن قياسات الجهد المرتبط بالحدث في الصباح قد تحسنت بشكل ملحوظ في المجموعة الضابطة مقارنة بالمساء في حين لم تتحسن في المرضى. كذلك لم تسفر مقارنة قياسات الجهد المرتبط بالحدث في المساء عن أي اختلافات بين المرضى والمجموعة الضابطة في حين أن قياسات الجهد المرتبط بالحدث في الصباح في مرضى اضطرابات التنفس المرتبطة بالنوم كانت أسوأ بكثير من المجموعة الضابطة ولم تسفر مقارنة قياسات الجهد المرتبط بالحدث في الصباح عن أي اختلافات بين مرضى الأرق والمجموعة الضابطة. وبحساب الفرق بين قياسات الصباح والمساء ومقارنته في الثلاث مجموعات تأكدت نتائج مرضى اضطرابات التنفس المرتبطة بالنوم وكشف الستار عن مشاكل الوعي في مرضى الأرق. وقد تبين عدم وجود ترابط بين نتائج الجهد المرتبط بالحدث وبين شعور المريض بالنعاس ونتائج معمل النوم مما يوحي أن هناك اختلاف بين قدرة الأشخاص على التغلب على مشاكل النوم.

وعليه فإننا نستخلص أن النوم الطبيعي يحسن بوضوح زمن كمون ومقدار الجهد المتعلق بالحدث وأن القياسات المتعددة ل بـ 300 خاصة في الصباح تكون أكثر حساسية في الكشف عن اضطرابات الإدراك والوعي وأن حساب الفرق بين قياسات الصباح والمساء يكشف التأثرات البسيطة لدى مرضى الأرق.



2008 � Copyright The Egyptian Journal of Neurology,
Psychiatry and Neurosurgery. All rights reserved.

Powered By DOT IT