Online ISSN : 1687-8329

    




Quick Search 
 
Author  
Year    
Title  
Vol:  

 
 
January2012 Vol.49 Issue:      1 Table of Contents
Full Text
PDF


Habituation and Genetic Predisposition to Migraine

Aktham I. Alemam

Department of Neurology, Minoufiya University; Egypt

 



ABSTRACT

Background: Habituation of the nociception-specific blink reflex (nBR) was found to be reduced interictally in migraine patients. This reduction may be due to inherited susceptibility that is involved in migraine, as determining a critical threshold, and also it may be responsible for interictal nervous system dysfunction. Objective: To search for an abnormal habituation pattern of the nBR in healthy asymptomatic subjects who have a first degree relative affected by migraine, and to compare them with healthy volunteers and migraine patients. Methods: The study was done on 25 patients suffering from migraine without aura (MO), 25 subjects  having at least one first degree relative who suffers from migraine (HV-F), and 27 subjects without family history of migraine (HV). We elicited the nBR by stimulating the right supraorbital region with a custom-built electrode. Habituation was measured as the percentage area-under-the-curve decrease in 10 consecutive blocks of five averaged rectified responses. Results: The  nBR habituation was clearly reduced in MO and HV-F compared to HV. Percentage area under the curve decreased between the 1st and the 10th block by 54.08 % in HV, 23.71 % in MO (P = 0.001) and 27.42 % in HV-F (P = 0.049). A positive intra-individual correlation was found between attack frequency and habituation in MO (r = 0.621; P = 0.010). Migraine patients have interictally a deficient habituation of the nBR which is inversely related to attack frequency. Habituation deficit  was more evident in asymptomatic individuals with a family history of migraine. Conclusion: Deficient nBR habituation could thus be a trait marker for the genetic predisposition to migraine. A longitudinal follow-up study may be needed for healthy subjects at high risk to compare the genotypes. [Egypt J Neurol Psychiat Neurosurg.  2012; 49(1): 27-32]

 

Key Words: Migraine, habituation, blink reflex.

 

Correspondence to Aktham I. Alemam, Department of Neurology, Minoufiya University, Egypt.

Tel: +20109084905        E-mail: e_aktham@yahoo.com




INTRODUCTION

 

Besides the cerebral cortex, current knowledge on migraine pathophysiology assigns an important role to both peripheral and central portions of the trigemino-vascular system. It is generally accepted that the migraine headache is associated with activation of the latter system1. Researchers have tried to verify if the same lack of cortical habituation may exist also at the subcortical trigeminal level.

        Migraine attacks are characterized by a particular sensitivity to visual and auditory external stimuli2. Some studies suggested that hypersensitivity to external  stimuli may persist between migraine attacks3. Habituation is a well – known physiological process which consists of a decreased responsiveness by repetition of the same stimuli and which may reflect an adaptive mechanism to protect against sensory over stimulation. For each sensation modality, like as for nociception, there is an interictal lack of habituation4. This habituation deficit concerns not only with  the cortical responses but also some brainstem reflexes such as the nociceptive blink reflex (nBR)5.

Studying trigeminal reflexes is a useful method for investigating the functional state of the trigeminal brain stem complex6. The blink reflex (BR), in particular, has been shown to be highly sensitive to changes in trigeminal activity. It was found that migraineurs have an interictal habituation deficit of the BR7. The nBR is elicited by a special stimulation electrode with high current density activating rather selectively Aδ fibers and has only a R2 component8,9. While the classical blink R2 reflex habituates normally in migraine patients10, habituation of the nBR is reduced interictally11.

The inherited susceptibility and environmental factors may be interrelated in migraine12. Genetic load can be seen as determining, on the one hand, a critical threshold, and on the other hand, it may be responsible for interictal nervous system dysfunction. 

The habituation deficit of cortical evoked potentials may have a familial character and was proposed as an endophenotypic marker of migraine13,14.

The aim of this study was to search for an abnormal habituation pattern of the nBR in healthy asymptomatic subjects who have a first degree relative affected by migraine, and to compare them with healthy volunteers and migraine patients.

 

PATIENTS AND METHODS

 

Patients

The study was done in the department of neurology, Minoufiya University Hospitals. It was approved by the local medical ethics committee and a written informed consent was taken from all subjects. It was done on 25 patients suffering from migraine without aura (MO: mean age: 23.8 years; 17 women, 8 men) according to Headache Classification Subcommittee of the International Headache Society, 20042. Exclusion criteria for patients included:

1-        Presence of any other pathology explaining the headache (either diagnosed clinically or by further investigations in the doubtful cases).

2-        Intake of prophylactic or abortive drugs for migraine on a regular basis.

3-        Intake of caffeine or alcohol containing beverages less than 4 hours before the recording.

 

The patients were compared to 52  healthy volunteers without personal history of migraine or any other  recurrent headache. They were recruited among  relatives of patients consulting our Neurology Clinic. They were separated in two groups of comparable age and sex distribution: 27 subjects without family history of migraine (HV: mean age: 24.6 years; 17 women, 10 men) , and  25 subjects  having at least one first degree relative who suffers from migraine (HV-F: mean age: 25.8 years; 16 women, 9 men).

 

Methods

The nociception-specific blink reflex was elicited according to the methods described by Kaube et al.8 and Katsarava et al.9. A custom-built planar concentric electrode  providing a high current density at low intensities was used to stimulate the supraorbital region. Recordings in patients were obtained interictally at least 2 days after the last and before the next migraine attack. With surface electrodes, we recorded bilaterally, over orbicularis oculi muscles, 10 blocks of  five  rectified EMG responses with an interblock interval (IBI) of 2 minutes. The 2-minutes IBI was chosen because it produces the most pronounced habituation in normal subjects9. The first sweep of each block was excluded from further analysis to avoid contamination with a startle response.

Individual pain thresholds were determined with two ascending and descending sequences of successive current intensities between 0.2 and 2mA in 0.1mA increments. Areas under the curve (AUC) of the R2 response were analyzed in each sweep off-line after demeaning, rectification and averaging between 27 and 87 ms5. We measured the area under the curve (the response area: RA) in µV × ms.15. Each block was analyzed separately. Mean values for each block were calculated. The data were normalized as a percentage deviation from the mean value of five consecutive sweeps.

Habituation of the nBR R2 was defined as the percentage change of the R2 area between the 1st and the 10th block of recordings. Since the study by Katasarva et al., that showed reduced nBR habituation interictally in migraineurs, was based on five responses obtained with short interstimulus intervals (ISIs)16, we also measured the amplitude change in the five sequential responses recorded in the 1st block with an ISI of 15-17 seconds.

 

Statistical Analysis

Results are presented as means ± standard deviations. Group differences in mean pain threshold and nBR latency were calculated with one-way analysis of variance (ANOVA). Habituation of the nBR responses was assessed by ANOVA for repetitive measurements with Scheffé's post hoc analysis, considering the different blocks (2 to 10) as within subject factors and the diagnostic groups (HV, MO and HV-F) as between subject factors. Results were considered significant at P<0.05.

 

RESULTS

     

No significant difference was found in mean perception or pain threshold between the three subject groups on either side of the forehead, or between the left and right side in any group. So, the mean stimulus intensities (1.5 × pain threshold) used for studying the nBR were similar between groups: 2.15±0.51 mA for HV; 2.11±0.72 mA for HV-F and 2.21±0.84 mA for MO.

Mean R2 latency was slightly shorter in migraineurs than in both groups of healthy volunteers (MO: 37.62±5.78 ms; HV: 41.81±7.45 ms; HV-F: 39.88±4.61 ms), but these differences were not significant [F(1,35) = 2.926, P = 0.10 versus HV; F(1,34) = 1.171, P = 0.29 versus HV-F] (Figure 1).

There was no significant side difference in first block nBR response area or in its habituation over 10 blocks in any of the three groups (Table 1).  The response area in the first block of stimuli was greater in healthy controls than in migraineurs  or healthy volunteers with an affected first degree relative, but this difference did not reach statistical significance [F (1,35) = 1.564, P = 0.22 versus MO; F(1,33) = 0.826, P = 0.39; (Table 1).

 

 

Figure 1. Comparison among the groups

regarding the mean R2 latency.

 

Table 1. R2 response area in the first block of averaged responses (mV_ms).

 

Subject group

Ipsilateral

Contralateral

Healthy

subjects

(HV; n =27)

1. 06 ±0.69

0.87±0.60

Healthy

+1st degree migraine

(HV-F; n =25)

0.89±0.59

0.64±0.42

Migraine

without aura

(MO; n =25)

0.85±0.47

0.62±0.42

One-way ANOVA

NS

NS

 

In HV there was a strong habituation with an amplitude decrease exceeding 50% between the first and the 10th block of five averagings. This contrasted with a less than 30% habituation in the MO [F(1,35) = 13.323, P = 0.001 versus HV] and HV-F [F(1,32) = 4.71, P = 0.049 versus HV] groups (Table 2).

Habituation steadily increased in successive blocks in all the three groups of subjects up to the 10th block of stimuli. The difference in the degree of nBR RA habituation between healthy volunteers and the other two groups, however, was already significant in the second block of five averagings: 25.2% habituation in HV, –8.9% (i.e. potentiation) in HV-F [F(1,33) = 7.810, P = 0.010 versus HV] and 1.9% habituation in MO [F(1,35) = 5.151, P = 0.037 versus HV]. Habituation of the R2 response area of ipsi- and contralateral nBR in 10 blocks of five averagings (interstimulus interval: 15–17ms; interblock interval: 2min) expressed as percentage of the 1st block.

Table  2. Habituation of the R2 response area in the last  block of averaging relative to the 1st block (%).

 

Subject group

Ipsilateral

Contralateral

Healthy

subjects

(HV; n =27)

55.07±23.49

54.08±22.49

Healthy

+1st degree migraine

(HV-F; n =25 )

26.79±45.05

 

27.42±40.82*

Migraine

without aura

(MO; n =25)

25.77±21.33**

23.71±24.82**

One-way ANOVA

*P   = 0.049

**P  =0.001

*P= 0.044    

**P = 0.001

 

        A positive intra-individual correlation was found between attack frequency and habituation in MO (r = 0.598; P = 0.010).  Single response areas within the 1st block of stimuli and their habituation in individual subjects greatly varied. There was nonetheless a significant reduction in habituation between the first and fifth response in the HV-F group. For instance, on the ipsilateral side the amplitude change was -37.5% (potentiation) in HV-F, compared to +42.1% (habituation) in HV [F(1,33) = 4.760; P = 0.04]. Habituation was also lower in MO (30.5%) than in HV, but this difference was not significant [F(1,35) = 0.811; P = 0.45].

 

DISCUSSION

     

Several studies have searched for different biochemical and neurophysiological abnormalities that  are able to explain the permanent perpetuation of the migraine attacks, which, if present, should also be detectable in the pain-free period, representing underlying dysfunctions. Patients with migraine were observed to show an increased cortical bioelectrical activity with respect to normal subjects. Early investigators observed increased amplitudes of visual responses evoked by light flashes or by pattern-reversal stimulation in migraineurs between attacks. However, the question arose whether this excessive increase in amplitude could be due to an insufficient habituation and whether the latter could be a more general abnormality in processing incoming information in migraineurs brain16.       

The results of this study showed that habituation of the nBR is significantly reduced interictally in migraineurs compared to healthy volunteers, and this was in line with those reported by Katsarava et al.11. The intrablock habituation values were smaller in migraineurs than in healthy volunteers, but this difference was not significant, possibly because the standard deviations were too large and groups too small. The difference in the habituation of nBR response area between patients and healthy volunteers was significant as early as the 2nd block of averages. It increased with repetition of stimuli and tended to become maximal in the 10th block, a time at which habituation was found to be maximal in normal subjects9. Di Clemente et al. found that the first nBR response had a tendency to be lower in migraineurs than in healthy subjects. This observation was inconsistent with an abnormality involving trigeminal nucleus sensitization and rather suggested that the reflex could be hypoexcitable in-between attacks5,17. The question of hypo- or hyperexcitability is still debated regarding the pathophysiology of interictal habituation deficit observed in migraineurs18. The habituation of the blink reflex is reduced interictally in migraine patients during short 7,11. as well as long time courses5,17.

Few correlations have been found between neurophysiological results and frequency of migraine attacks. Our results showed positive intra-individual correlation between attack frequency and habituation in MO.  In another study, it was found that in episodic migraine, the habituation deficit of BR decreased with increasing attack frequency which suggested that it was unlikely to be due to trigeminal sensitization5,17. This does not seem to be the case in chronic migraine patients who displayed a lower degree of blink reflex habituation when studied outside an attack19. Additionally, de Tommaso et al.  studied laser-evoked cortical responses and proved that the habituation deficit  found interictally in migraineurs was positively correlated with attack frequency 20 . In a magnetoencephalographic recording of somatosensory evoked potentials, the amplitude increase in migraineurs was linked to the frequency of attacks 21.

All these results are in contrast with our finding of a negative correlation between the habituation deficit on the nBR and attack frequency. It could, however, be related to the fact that nBR short-term habituation 11, parallel to habituation of evoked cortical potentials22, normalizes during the attack period. The patients with high-attack frequencies may be at greater risk of being recorded in closer vicinity to an attack.

The classical R2 is essentially normal interictally, but it is less influenced by the warning of the stimulus in migraine 10 and, at short IBI, its habituation was found reduced in migraineurs who developed an attack within 3 days after the recording7. The rather low nBR amplitude interictally in migraineurs, contrasts with the 680% nBR RA increase reported during the migraine attack23. This may reflect ictal sensitization of spinal trigeminal nucleus neurons24. The low nBR amplitude did not favor such sensitization and rather suggested that the R2 interneurons and circuit could be hypoexcitable in-between migraine attacks. Lack of habituation might be a consequence of reduced serotoninergic transmission25,26. leading to a decreased preactivation level.

The pathophysiology of this habituation deficit may be related to an altered serotoninergic transmission. The serotoninergic system plays an important role in the endogenous pain control system and has been implicated in migraine pathophysiology  25 . Strong intensity dependence of auditory evoked potentials in migraine habituation pattern tends to normalize with fluoxetine prophylaxis which is a serotonin re – uptake inhibitor27.      

This study showed that asymptomatic subjects with a first degree migrainous relative gave the same nBR abnormalities as patients with full-blown migraine between attacks. Compared to healthy volunteers without a family history of migraine, they tended to have smaller first block nBR response areas and reduced nBR habituation. Their degree of habituation was intermediate between that of healthy controls who habituated more and that of migraineurs who habituated less, but the difference was  significant respective to the former, but not to the latter. Healthy subjects at risk also had a significant reduction of habituation within the 1st block of five responses, which differed from the findings in migraineurs.

Some migraine phenotypes appear to be complex genetic disorders, where additive genetic effects (susceptibility genes) and environmental factors are interrelated 28. Various gene polymorphisms may be more prevalent in migraineurs than in controls. Although certain rare migraine subtypes such as familial hemiplegic migraine are monogenic diseases, there is increased evidence that the common forms of migraine are polygenic multifactorial diseases, where the genotype determines a migraine threshold which is modulated by internal (e.g. hormonal) and environmental factors28-30.

The link between genetic determinants and abnormal information processing may exist in migraine31. One of the migraine interictal electrophysiological abnormalities is a marked intensity dependence of auditory evoked cortical potentials (IDAP), which is obtained after stimulations of increasing intensities (25).  The IDAP habituation was investigated in 20 pairs of migraineurs, i.e. parents and their children. Children tended to have more abnormal values than parents32.

Another interictal abnormality tested was the contingent negative variation (CNV). It is a slow cortical potential related to higher mental functions, used to study habituation in migraine. Its early component showed that habituation was markedly decreased or even abolished in patients affected by migraine without aura between attacks 33.  Siniatchkin et al, observed strong correlations according to the amplitude and habituation of the early CNV component (iCNV) between children suffering from migraine and their parents with migraine and between young migraineurs and their healthy parents who have a positive family history of migraine 32. Moreover, lack of habituation of the iCNV was found in asymptomatic subjects with a positive family history of migraine, defined ‘‘at risk”, and the amplitude of the iCNV correlated significantly with the relative number of subjects suffering from migraine in the family 34.  The same observation was present with nociceptive blink reflex in a group of healthy asymptomatic subjects having a 1st degree relative affected by migraine 5.

The previous studies and our results raise the possibility that subjects with a familial predisposition for migraine may present a presymptomatic neurophysiological abnormality in response habituation, i.e. the same habituation deficit as migraine patients. A longitudinal follow-up study may be conducted for healthy subjects at high risk and to compare the genotypes. This may help to determine which factors such as personality traits, life events, environment or co-morbidity can protect subjects with a family history of migraine against developing migraine.

 

[Disclosure: Author reports no conflict of interest]

 

REFERENCES

 

1.      Burstein R., Yarnitsky D, Goor-Aryeh I, Ransil BJ, Bajwa ZH. Association between migraine and cutaneous allodynia. Ann Neurol. 2000; 47: 614-24.

2.      Headache classification Committee: The international classification of headache disorders. Cephalalgia 2004; S1: 88- 101.

3.      Mulleners WM, Chronicle EP, Palmer JE, Koehler PJ,. Vredeveld JW. Visual  cortex excitability in migraine with and without aura. Headache. 2001; 41: 565-72. 

4.      Valeriani M, de Tommaso M, Restuccia D, Le Pera D, Guido M, Iannetti GD, et al. Reduced habituation to experimental pain in migraine patients. A CO (2) laser evoked potential study. Pain. 2003; 105: 57-64.

5.      Di Clemente L, Coppola G, Magis D, Fumal A, De Pasqua V, Di Piero V, et al. Interictal habituation deficit of the nociceptive blink reflex: An endophenotypic marker for presymptomatic migraine? Brain. 2007; 130, 765-70.

6.      Esteban A. A neurophysiological approach to brainstem reflexes. Blink reflex. Neurophysiologie Clinique. 1999. 29; 7-38.

7.      De Marinis M, Pujia A, Natale L, D'arcangelo E, Accornero N. Decreased habituation of the R2 component of the blink reflex in migraine patients. Clin Neurophysiol. 2003; 114: 889-93.

8.      Kaube H, Katsarava Z, Kaufer T, Diener HC, Ellrich J. A new method to increase nociception specificity of the human blink reflex. Clin Neurophysiol. 2000; 111: 413-6.

9.      Katsarava Z, Ellrich J, Diener HC, Kaube H. Optimized stimulation and recording parameters of human “nociception specific” blink reflex recordings. Clin Neurophysiol. 2002a; 113: 1932-6.

10.    De Tommaso M, Murasecco D, Libro G, Guido M, Sciruicchio V, Specchio LM, et al.  Modulation of trigeminal reflex excitability in migraine: effects of attention and habituation on the blink reflex. Int J Psychophysiol. 2002;44: 239-49.

11.    Katsarava Z, Giffin N, Diener HC, Kaube H. Abnormal habituation of “nociceptive” blink reflex in migraine – evidence for increased excitability of trigeminal nociception. Cephalalgia. 2003; 23: 814-9.

12.    Gervil M, Ulrich V, Kaprio J, Olesen J, Russell MG. The relative role of genetic and environmental factors in migraine without aura. Neurology. 1999; 53: 995-9.

13.    Sándor PS, Áfra J, Proietti-Cecchini A, Albert A, Schoenen J. Familial influences on cortical evoked potentials in migraine. Neuroreport. 1999; 10: 1235-8.

14.    Siniatchkin M, Kirsch E, Kropp P, Stephani U, Gerber WD. Slow cortical potentials in migraine families. Cephalalgia. 2000; 20: 881-92.

15.    Ellrich J, Treede RD. Characterization of blink reflex interneurons by activation of diffuse noxious inhibitory controls in man. Brain Res. 1998; 803: 161-8.

16.    Ambrosini A, de Noordhout AM, Sandor PS, Schoenen J. Electrophysiological studies in migraine: A comprehensive review of their interest and limitations. Cephalalgia. 2003; 23(Suppl. 1): 13-31.

17.    Di Clemente L, Coppola G, Magis D, Fumal A, De Pasqua V, Schoenen J. Nociceptive blink reflex and visual evoked potential habituations are correlated in migraine. Headache. 2005; 45: 1388-93.

18.    Coppola G, Ambrosini A, Di Clemente L, Magis D, Fumal A, Gérard P, et al. Interictal abnormalities of gamma band activity in visual evoked responses in migraine: An indication of thalamocortical dysrhythmia? Cephalalgia. 2007; 27: 1323-30.

19.    De Marinis M, Pujia A, Colaizzo E, Accornero N. The blink reflex in ‘‘chronic migraine”. Clin Neurophysiol. 2007; 118: 457-63.

20.    De Tommaso M, Lo Sito L, Di Fruscolo O, Sardaro M, Pia Prudenzano M, Lamberti P, et al. Lack of habituation of nociceptive evoked responses and pain sensitivity during migraine attack. Clin Neurophysiol. 2005; 116: 1254-64.

21.    Lang E, Kaltenhauser M, Neundorfer B, Seidler S. Hyperexcitability of the primary somatosensory cortex in migraine – a magnetoencephalographic study. Brain. 2004; 127: 2459-69.

22.    Schoenen J, Ambrosini A, Sandor PS, De Noordhout A. Evoked potentials and transcranial magnetic stimulation in migraine: published data and viewpoint on their pathophysiologic significance. Clin Neurophysiol. 2003; 114: 955-72.

23.    Kaube H, Katsarava Z, Prywara S, Drepper J, Ellrich J, Diener HC. Acute migraine headache. Possible sensitization of neurons in the spinal trigeminal nucleus? Neurology. 2002; 58: 1234-8.

24.    Katsarava Z, Lehnerdt G, Duda B, Ellrich J, Diener HC, Kaube H. Sensitization of trigeminal nociception specific for migraine but not pain of sinusitis. Neurology 2002b; 59: 1450-3.

25.    Wang W, Timsit-Berthier M, Schoenen J. Intensity dependence of auditory evoked potentials is pronounced in migraine: an indication of cortical potentiation and low serotonergic neurotransmission? Neurology. 1996; 46: 1404-9.

26.    Juckel G, Molnar M, Hegerl U, Csepe V, Karmos G. Auditory evoked potentials as indicator of brain serotonergic activity – first evidence in behaving cats. Biol Psychiatry. 1997; 41: 1181-95.

27.    Ozkul Y, Bozlar S. Effects of fluoxetine on habituation of pattern reversal visually evoked potentials in migraine prophylaxis. Headache. 2002; 42: 282-7.

28.    Montagna P. Molecular genetics of migraine headaches: a review. Cephalalgia. 2000; 20: 3-14.

29.    Sandor PS, Ambrosini A, Agosti RM, Schoenen J. Genetics of migraine: Possible links to neurophysiological abnormalities. Headache. 2002; 42: 365-77.

30.    Haan J, Kors EE, Vanmolkot KR, van den Maagdenberg AM, Frants RR, Ferrari MD. Migraine genetics: an update. Curr Pain Headache Rep. 2005; 9: 213-20.

31.    Sandor PS, Afra J, Proietti-Cecchini A, Albert A, Schoenen J. Familial influences on cortical evoked potentials in migraine. Neuroreport. 1999; 10: 1235-8.

32.    Siniatchkin M, Kirsch E, Kropp P, Stephani U, Gerber W. D. Slow cortical potentials in migraine families. Cephalalgia. 2000c; 20: 881-92.

33.    Kropp P, Gerber WD. Contingent negative variation during migraine attack and interval: Evidence for normalization of slow cortical potentials during the attack. Cephalalgia. 1995; 15(2): 123-8.

34.    Siniatchkin M, Kropp P, Gerber WD. Contingent negative variation in subjects at risk for migraine without aura. Pain. 2001; 94(2): 159-67.


 

 

الملخص العربي

 

التعود والاستعداد الوراثي للصداع النصفي

 

في مرضى الصداع النصفي، وجد أن التعود في الفعل التغميض المنعكس ينخفض فيما بين النوبات، وأن هذا الانخفاض قد ينشأ عن حساسية وراثية تدخل في أسباب الصداع النصفي سواء بتحديد العتبة الحرجة، أو الاضطراب الوظيفي للجهاز العصبي فيما بين النوبات.

وتهدف هذه الدراسة إلى البحث عن نمط غير طبيعي من التعود فى الفعل المنعكس التغميضى في الأشخاص الذين ليس لديهم أعراض الصداع النصفي ولكن لديهم قريب من الدرجة الأولى يعانى منه، ومقارنته بمتطوعين أصحاء ومرضى الصداع النصفي.

وقد أجريت الدراسة على 25 مريضا يعانون من الصداع النصفي من دون هالة(المجموعة الأولى)، و 25 شخصا لدى كل منهم قريب من الدرجة الأولى يعانى من الصداع النصفي (المجموعة الثانية)، حيث تمت مقارنتهم ب 27 شخصا من الأصحاء والذين ليس لديهم تاريخ عائلي للصداع النصفي (المجموعة الثالثة). وقد تم استخدام الفعل التغميضى المنعكس عن طريق تنبيه منطقة أعلى الحاجب الأيمن ، كما تم قياس نسبة انخفاض التعود للمنطقة تحت المنحنى في 10 كتل متتالية  كل منها يتكون من خمس استجابات مصححة.

وقد أظهرت الدراسة انخفاض تعود الفعل التغميضى المنعكس بشكل واضح في المجموعتين الأولى والثانية مقارنة بالثالثة، حيث  انخفضت نسبة المساحة تحت المنحنى ما بين الكتلة الأولى والعاشرة 54.08% في المجموعة الثالثة و 23.71% في المجموعة الأولى و 27.42% فى المجموعة الثانية. وقد أظهرت المجموعة الثانية أعلى نسبة اضطراب عن طريق التقوية بدلا من التعود في الكتلة الثانية، كما أن انخفاض التعود كان أكثر وضوحا في هذه المجموعة، وكذلك لوحظ وجود ارتباط إيجابي بين معدل النوبات والتعود داخل مجموعة الأفراد الذين يعانون من الصداع النصفي.

وتخلص هذه الدراسة إلى أن انخفاض تعود الفعل التغميضى المنعكس قد يكون علامة للاستعداد الوراثي للصداع النصفي مما يفتح الباب أمام عمل دراسة طولية لمتابعة الأشخاص ذوى الاحتمال العالي لحدوث الصداع النصفي للمقارنة بين التراكيب الوراثية.



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

Powered By DOT IT