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July2005 Vol.42 Issue:      2 Table of Contents
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Migrainous Vertigo: Clinical and Vestibular Evoked Myogenic Potential (VEMP) Findings

Azza A Ghali1, Enaas A Kolkaila2
Departments of Neuropsychiatry1, Audiology Unit, ENT2, Tanta University

ABSTRACT

Migrainous vertigo (MV) is one of the most common cause of episodic vertigo and is increasingly recognized among neurologist and migraine specialist. Although MV is not included currently in the classification of the International Headache Society (IHS), specific criteria has been proposed and utilized in clinical trials. The aim of this study is to evaluate clinical presentation, VEMP findings in MV. It was also designed to compare the VEMP findings in migrainous patients with and without vertigo and  lastly to test the sensitivity of VEMP in diagnosing MV. The study included thirty eight patients diagnosed as migraine headache according to IHS, and 18 healthy control subjects matched the patients′ age and sex. Patients were divided into 2 groups: group I included 20 patients had migraine with vertigo. They underwent a Structured Interview for the diagnosis of MV. Sixteen patients of group I scored 7 and diagnosed as MV, 4 patients did not score 7 and excluded from the study (they had basilar artery migraine). The other group (group II) included 18 patients who had migraine without vertigo. All the patients submitted to full neurological assessment including: full history taking, and basic neurological examination, and full audiological assessment including: full audiological history, otological examination, basic audiological evaluation, and VEMP test. Clinical assessment of the symptoms of MV, comparison of the VEMP data between the patients and control group as well as between group I and group II patients were done. It was concluded that MV can be considered as a distinctive entity, Structured Interview is helpful in the diagnosis of MV and VEMP has a role in the diagnosis of MV.

(Egypt J. Neurol. Psychiat. Neurosurg., 2005, 42(2): 341-350).

 




INTRODUCTION

 

                Migraine is defined by the International Headache Society (IHS) as an intermittent, recurrent unilateral disabling headache associated with nausea and sensitivity to sounds and light1.

                Patients with migraine frequently have vestibular complaints ranging from frank vertigo to less specific symptoms of dizziness, unsteadiness and head motion intolerance2. The clinical association of migraine and vertigo has been supported by case controlled studies. These studies showed that migraine is more common in patients presenting with vertigo than in age and gender matched controls3, and inversely, vertigo is more common in patients with migraine than in controls4.

Although migraine related Vertigo is not included currently in the classification of International Headache Society5, yet its specific criteria have been proposed and utilized in clinical trials6,7. A uniform nomenclature to describe patients with migraine related vertigo has not been adopted yet. Different names have been used, such as migrainous vertigo (MV), benign recurrent vertigo, migraine associated dizziness, migraine induced dizziness, migraine related vestibulopathy and vestibular migraine2. In 2004, von Brevern et. al.8  and also Neuhauser and  Lemert9 defined MV as a vestibular syndrome that is caused by migraine and is presented with attacks of spontaneous or positional vertigo lasting seconds to days and inconsistent temporal relationship to headache and other migrainous features. Migrainous vertigo (MV) is one of the most common cause of episodic vertigo and is increasingly recognized among neurologist and migraine specialist8.

In recent years, a new method of inducing recording short-latency vestibular evoked myogenic potential (VEMP) has been developed10.  VEMP is a non-invasive test for vestibular function. It is a series of electrical waves that are generated by vestibular pathway in response to acoustic stimulation11. The pathway of VEMP is induced by loud sound, transmits through the middle ear, the saccule, the inferior vestibular nerve and the vestibulospinal tract and finally terminating in the cervical muscles12. It has been shown that the first peak of the VEMP is the compound action potential of the vestibular nerve fibers synchronously activated by the stimulus13.   

                This work was designed to evaluate the clinical presentation and VEMP findings in MV. It was also designed to compare the VEMP findings in migrainous patients with and without vertigo and  lastly to test the sensitivity of VEMP in diagnosing MV.

 

SUBJECTS AND METHODS

 

                Subjects of this study were selected from the Outpatient Clinic of Neuropsychiatry Department, Tanta University Hospital. From patients complaining of headache, 38 patients were diagnosed as having migraine headache according to the classification of IHS5.

                The exclusion criteria included: basilar artery migraine, vertigo due to other possible neurological causes (e.g. epileptic vertigo, transient ischemic attacks, motion sickness), Meniere’s disease and Inner ear diseases as well as any other audiological complaint.

 

The selected patients were divided into two groups:

Group I: included 20 patients of migraine with vertigo. These patients then underwent Structured Interview (Appendix 1) for the diagnosis of MV. This Structured Interview was adapted from Marcus et al.7, and translated into Arabic. It included 7 questions. The patient has to answer yes for each question in order to get a score and then to proceed to the next question. Thus, the diagnosis of MV is considered positive if the score of the interview is 7. Finally, patients who had a score of 7 in the interview (16 patients) were included in this study. On the other hand, patients who did not have a score of 7 were excluded from this study. The excluded patients were four with basilar artery migraine.

Group II: included 18 patients who had migraine without vertigo. Furthermore, the study included 18 healthy control subjects who matched the patients in age and gender. Subjects in the control group had no history of headache, vertigo, any audiological or neurological problems.

 

All subjects were submitted to the following:

1.      Neurological Evaluation: which included: full history taking of the following items: age and gender, age onset of migraine and vertigo and temporal relationship of both, frequency of the attacks (occasional, one or twice/month, once or twice/week, or daily)14, severity of the attacks (grade I: patient still able to perform normal work activity, grade II: unable to perform normal work but bed rest is unnecessary, grade III: bed rest is necessary)15, duration of migrainous  symptoms (short duration less than 2 hours, or longer duration more than 2 hours), duration of vertiginous symptoms (from minutes to hours), site and laterality of headache, migrainous symptoms associated with the vertigo (e.g. headache, photophobia, phonophobia), types of vertiginous symptoms (head motion intolerance, positional vertigo, rotational vertigo), family history of migraine, and finally history of drug intake (for drugs affecting vestibular system). Basic neurological examination: including cranial nerve examination, coordination tests, motor and sensory system evaluation was done.

2.             Audiological Assessment: including:

A.     Full audiological history and otological examination.

B.     Basic audiological evaluation: including pure tone audiometry for the octave frequencies ranging from 250Hz through 8000Hz., speech audiometry (including both Speech Reception Threshold and Word Discrimination score) as well as Immittancemetry (including both tympanogram and acoustic reflex threshold determination).

3.      Vestibular Evoked MyogenicPotential (VEMP): vestibular evoked potential in response to monoaurally delivered rarefaction clicks16. The response was recorded using surface electrodes over the isometrically contracting sternocleidomastoid (SCM) muscle. Subjects were seated on a comfortable armchair, they were instructed to rotate their head to the opposite side of the stimulated ear in order to activate the ipsilateral (SCM) muscle. They were also instructed to maintain steady muscle contraction throughout the test. The position of active electrode was chosen to be on the middle part of the SCM muscle in order to obtain consistent recordings17. While, the negative electrode was placed on the clavicle (middle part) and the reference on the forehead. The stimuli were delivered through a headphone with the intensity of 95dBnHL and a repetition rate of 1/sec. The analysis time for each stimulus was 50msec. The signals were amplified and band filtered between 30 and 3000Hz (Smart – EP TM, Intelligent Hearing System, USA). Response to 128 stimuli was averaged and each response was obtained three times to ensure reproducibility17. Positive VEMP was defined as an initial positive polarity (p13) approximately 13 msec after stimulus onset, and subsequent negative polarity (n23), beginning at 23 msec. This biphasic wave represented the largest response wave within an analysis of 50 msec, without defining the criterion for its amplitude16.

RESULTS

 

                Fifty two subjects were included in this study. Eighteen subjects as a control. They were seven males and eleven females. Their age ranged from 23 to 45 years with the mean of 33.1±6.9 years.

Group I: included 16 patients with migrainous vertigo. They were six males and ten females. Their age ranged from 22 to 45 years with the mean of 32.6±7.1

Group II: included 18 patients having migraine without vertigo. They were seven males and eleven females. Their age ranged from 23.8 to 44.2 years with the mean of 33.6±7.5 years.

                 Regarding to the clinical evaluation of group I (patients with migrainous vertigo), the assessment of the temporal relationship between age of onset of both migraine and vertigo revealed that in two cases the vertiginous attacks preceded migrainous attacks and in one case both of them started together. While in the rest of cases the migraine attacks preceded vertigo attacks. Frequency of MV was:1 or 2/month in 7 cases, 1 or 2/week in 7 cases, daily in one case and occasional in one case. Severity of the attacks was graded and revealed that: 2 cases had grade I, 9 cases had grade II and 5 cases had grade III. Duration of migraine symptoms was classified into: short in 7 cases and long in 9 cases. While, duration of vertiginous symptoms during migraine attacks was-in most of the cases-minutes. Site and laterality revealed that 3 cases had bifrontal headache, 7 cases had right frontal headache and 6 cases had left frontal headache (Table 1). As regards the presence of aura only 5 case had no aura. The most common migrainous symptoms were photophobia and headache. Furthermore, the most common vestibular symptoms in patients with MV were positional vertigo, head motion intolerance and rotational vertigo or a combination of them (Table 2).

                As regards the results of VEMP test, none of the subjects in the control and group II (migraine without vertigo) demonstrated absent VEMP in either ear. On the other hand, In group I (migraine with vertigo) three cases showed absent VEMP in both ears, four cases showed absent  VEMP in the right ear only, while one case showed absent response in the left ear. Comparing the results of VEMP test in both ears among the three tested groups was done using ANOVA test (Table 3). The results were statistically significant (p<0.001). Tukey’s test was then applied to detect the significant cell. Its results revealed that VEMP waves in group I (migraine with vertigo) were significantly delayed than control group and group II (migraine without vertigo). Moreover, there was no significant difference between the control group and group II (migraine without vertigo) (Figs. 1 and 2).

                In order to test the sensitivity of VEMP to detect vestibular affection in migrainous patients, ROC curve was done (Table 4). The results revealed that sensitivity of VEMP test ranged from (87.5 to 93,7). While, the specificity ranged from (88 to 100). Moreover, the accuracy of this test ranged from (97 to 98.8).


 

Table 1. Clinical Data of Patients in group I (with migrainous vertigo).

 

Clinical Data

No

Percent

 

Temporal relationship

Migraine First

13

81.25%

Vertigo first

2

12.5%

Together

1

6.25%

 

Frequency of the attacks

Per month

7

43.75%

Per week

7

43.75%

Daily

1

6.25%

Occasional

1

6.25%

 

Severity

I

2

12.5%

II

9

56.25%

III

5

31.25%

 

Duration

MA     short

            Long

7

43.75%

9

56.25%

VA    Hours

         Minutes

4

25%

12

75%

 

Site

RF

7

43.75%

LF

6

37.5%

BF

3

18.75%

MA= migrainous attacks,       VA= vertigo attacks,               BF=bifrontal,          RF= right frontal,    LF= left frontal

 

Table 2. Presentations of MV during the attacks.

 

Symptoms

 

No

Percent

 

Vestibular Symptoms

PV

10/16

62.5%

HMI

10/16

62.5%

RV

6/16

37.5%

 

Presence of Aura

With Aura

11/16

68.75%

Without Aura

5/16

31.25%

 

Migrainous Symptoms during vertiginous attacks

Phonophobia

9/16

56.25%

Photophobia

12/16

75%

Headache

10/16

62.5%

Nausea

9/16

56.25%

Vomiting

5/16

31.25%

PV = positional vertigo,                          HMI = head motion intolerance,                            RV = rotational vertigo

Table 3. Comparison of VEMP findings in control and patients (group I & II).

 

 

Mean±SD

ANOVA

F

P-value

R(P13)

Control

12.21±0.97

82.33

<0.001*

Group I

17.74±2.06

Group II

13.24±0.58

R(N23)

Control

22.45±0.78

46.75

<0.001*

Group I

28.31±3.08

Group II

23.8±0.82

L(P13)

Control

12.14±0.96

97.93

<0.001*

Group I

16.88±1.54

Group II

12.69±0.52

L(N23)

Control

22.61±1.71

103.35

<0.001*

Group I

30.02±2.1

Group II

23.82±0.80

* Significant and at 0.05

* Tukey's test results:            - Control Vs Group I <0.001*, - Control Vs Group II > 0.05,  - Group I Vs Group II < 0.001*

* Group I = migrainous vertigo &  Group II = migraine without vertigo                               * R= right ear,  L= left ear

 

Table 4. ROC curve data of VEMP test.

 

Variable

Cut Off

Sensitivity

Specificity

+PV

-PV

Accuracy

Rp13

13.9

93.7

100

100

90

97

Rn23

23.5

87.5

100

100

90

97.5

Lp13

13.9

87.5

100

100

94.7

98.8

Ln23

23.4

93.7

88

88.2

94.1

98

 

Rp13= right p13,    Rn23= right n23,     Lp13= left p13,      Ln23= left n23,                      

+PV= positive predictive value, - PV= negative predictive value

 

Fig. (1):  Results of VEMP by ANOVA test.


 

Fig. (2): Examples of VEMP response in a normal subject and a subject from group II

 (migraine without vertigo) and a subject from group I (migrainous vertigo).

 

 


DISCUSSION

 

Although migrainous vertigo MV is considered to be uncommon and atypical presentation of migraine, yet it is important to recognize this syndrome. This is due to the fact that treatment was successful in relieving all or most of the symptoms, even in subjects who had been unwell for years18.

The clinical evaluation of patients with MV revealed that in most of our patients migraine predate the vertiginous attacks except in 2 cases were vertigo predated migraine and in one case both appeared at same time. This finding agrees with Bir et al.19 and Thakar et al.20.

All patients reported migrainous complaints during the vertiginous attacks, photophobia and headache were the most frequent. However, these migrainous symptoms should be specifically inquired about, as patients may do not volunteer them. It has to be mentioned that some authors20-21 reported that many patients may experience attacks of vertigo for years before development of migrainous symptoms. This points to the importance of applying the Structured Interview to help in early diagnosis of MV.

The absence of VEMP in some cases of MV and the significant delay in VEMP waves in the rest of this group agrees with Liao & Young22. The significant delay of VEMP waves MV patients is considered to be due to affection of vestibular apparatus in MV patients.

Many speculations were presented to explain the vestibular dysfunction in migraine. The first speculation relates the spreading depression affecting brainstem structures to the short lasting episodes of MV23. Vasospasm of the internal auditory artery could also explain vestibular dysfunction in migraine24 similar to retinal vasospasm observed in retinal migraine25. Thirdly, functional imaging studies using PET during acute migraine attacks have identified activation of brainstem regions in projection to locus coeruleus and dorsal raphe nucleus, suggesting that these neural structures are involved in the initiation of migraine attacks. As the vestibular nuclei receive noradrenergic projections from locus coeruleus26 and serotonergic input from the dorsal raphe nucleus27, it is conceivable that activation of these structures in migraine also affect central vestibular processing28. Similarly, calcitonin gene-related peptide and other neuropeptides that are released during migraine attacks have a neuromodulatory role in the peripheral and central vestibular system29. Lastly, it has been proposed that defects of ion channel are involved in migraine. Accordingly, a channelopathy could account for central and peripheral vestibular dysfunction21. This is based on the fact that other paroxysmal disorders that are often presented with both migraine and vertigo have been found to result from mutations in the calcium channel gene CACNAIA, namely familial hemiplegic migraine and episodic ataxia type II30.

The specificity of VEMP test points to its importance in clinical application to exclude cases without MV. While being highly sensitive, VEMP is useful in diagnosing MV.

Finally, it can be concluded that MV is a separate clinical entity and that the Structured interview can be applied to diagnose this condition. Application of VEMP test in MV patients helps in diagnosing MV patients as it is an objective, simple and non-invasive test. The application of VEMP test in MV patients before and after treatment by antimigrainous drugs is recommended in future studies which will help to find out if vestibular dysfunction in these patients is reversible or not.

 

REFERENCES

 

1.      Headache Classification Committee of the International Headache Society (1988): Classification and diagnostic Criteria for headache disorders, Cranial neuralgias and facial pain. Cephalgia; 8 (Suppl. 7): 1-96.

2.      Crevits L, Bosman T (2005): Migraine-related vertigo: towards a distinctive entity. Clinical Neurology and Neurosurgery; 107: 82-87.

3.      Neuhauser H, Leopold M, von Brevern M, et al., (2001): The interrelation of migraine, vertigo and migrainous vertigo. Neurology; 56: 436-441.

4.      Bayazit Y, Yilmaz M, Mumbuc S, Kanlikana M (2001): Assessment of migraine-related cochleo vestibular symptoms. Rev Laryngol Otol Rhinol (Bord); 122: 85-88.

5.      Headache Classification Subcommittee of the International Headache Society (2004): The International Classification of Headache Disorders. 2nd edition Cephalgia; 24 (Suppl. 1): 9-160.

6.      Troost BT (2004): Vestibular migraine. Curr Pain Headache Rep. Aug; 8(4): 310-314.

7.      Marcus DA, Kapelewski C, Rudy TE, Jacob RG, Furman JM (2004): Diagnosis of migrainous vertigo: validity of a structured interview. Med Sci Monit. May; 10 (5): CR 197-201. Epub April 28.

8.      Von Brevern M, Arnold G, Lempert T (2004): Migrainous vertigo. Schmerz. Sep; 18(5) : 411-414. (English Abstract).

9.      Neuhauser H, Lempert T (2004): Vertigo and dizziness related to migraine: a diagnostic challenge. Cephalalgia. Feb; 24 (2): 81-82.

10.    Perez R, Freeman S, Sohmer H, Sichel J (2000): Vestibular and cochlear ototoxicity of topical antiseptics assessed by evoked potentials. Laryngoscope, Sep., 110 (9);1522-1527.

11.    Eliden J, Shomer H (1993): Short and middle latency vestibular evoked responses to acceleration in man. Electroenceph. Clin. Neurophysiol; 80: 140-145.

12.    Wu C, Young Y, Murofushi T (1999): Tone burst- evoked myogenic potentials in human neck flexor and extensors. Acta Otolaryngol (Stockh), 119: 741-744.

13.    Elidan J, Lin J, Honrubia V (1987): Vestibular ototoxicity of gentamicin assessed by recording of a short latency vestibular evoked response in cats. Laryngoscope, 97: 865-870.

14.    Pascual J, Berciano J, (1994): Experience in the diagnosis of headache that starts in elderly people. J Neurol Neurosurg Psychiatry; 57: 1255-1259.

15.    Olsen J, Friberg L, Olsen TS, Lassen NA (1993): Symptomatic Migraine attacks. Brain; 116: 187-202.

16.    Cheng P, Huang T, Young Y (2003): The influence of clicks versus short tone bursts on the Vestibular Evoked Myogenic Potentials. Ear & Hearing; 24: 195-197.

17.    Sheykholeslami K, Murofushi T, Kaga K (2001): The effect of sternocleidomastoid electrode location on vestibular evoked myogenic potential. Auris Nasus Larynx, Jan; 28 (1): 41-43.

18.    Waterston J (2004): Chronic migrainous vertigo. J Clin Neurosci; 11 (4), 384-388.

19.    Bir LS, Ardic FN, Kara CO, Akalin O, Pinar HS, Celiker A (2003): Migraine patients with or without vertigo: comparison of clinical and electronystagmographic findings. J Otolaryngol: 32; 234-238.

20.    Thakar  A, Anjaneyulu C, Deka RC (2001): Vertigo syndromes and mechanisms in migraine. J Laryngol  Otol; 115: 782-787

21.    Von Brevern M, Zeise D, Neuhauser H, Clarke AH, Lempert T (2005): Acute migrainous vertigo: clinical and oculographic findings. Brain, 128, 365-374.

22.    Liao LJ, Young YH (2004): Vestibular evoked myogenic potentials in basilar artery migraine. Laryngoscope. Jul; 114 (7): 1305-1309.

23.    Dieterich M, Brabdt T (1999): Episodic vertigo related t migraine (90 cases): vestibular migraine? J Neurol; 246: 883-892.

24.    Baloh  RW (1997): Neurotology of migraine. Headache; 37: 615-621.

25.    Killer HE, Forrer A, Flammer J (2003): Retinal vasospasm during an attack of migraine. Retina; 23: 253-254.

26.    Schuerger RJ, Balaban CD (1999): Organization of the coeruleo-vestibular pathway in rats, rabbits and monkeys. Brain Res; 30: 189-217.

27.    Halberstadt AL, Balaban CD (2003): Organization of projection from the raphe nuclei to the vestibular nuclei in rats. Neuroscience; 120: 573-594.

28.    Furman JM, Marcus DA, Balaban CD (2003): Migrainous vertigo: development of a pathogenetic model and structured diagnostic interview. Curr Opin Neurol. Feb; 16(1): 5-13.

29.    Cutrer FM, Baloh RW (1992): Migraine-associated dizziness. Headache; 32: 300-304.

30.    Ophoff  RA, Terwindt GM, Vergouwe MN, van Eijk R (1996): Familial hemiplegic migraine and episodic ataxia type II are caused by mutations in the Ca2+ channel gene CACNLIA4. Cell; 87: 543-552.

 

Appendix I

استبيان تشخيص دوار الشقيقة

1. هل تعانى من الشقيقة؟ 

·                 الشقيقة يصحبها حس شخصي يسبق النوبة؟

·                 الشقيقة بدون حس شخصي يسبقها؟

                يجب أن تكون تعرضت إلى خمس نوبات أو أكثر مصحوبة بما يلي:

                أ} عرضين من الآتي:

·                 موضع وحيد الجانب

·                 ألم نبضي

·                 ألم متوسط إلى شديد الدرجة

·                 أو يسؤ بعمل الأنشطة الروتينية

ب} عرض واحد من الآتي

·                 رهب الضوء

·                 رهب الأصوات

·                 غثيان: يجب ألا يكون مسبب بمرض معروف

                إذا كانت الإجابة( لا) فتوقف هنا أما إذا  كانت الإجابة( نعم) فانتقل إلى السؤال التالي.

2. هل تعانى أحيانا مما يأتي :

·                 دوخة بسيطة

·                 دوار شديد

·                 إحساس بحركة غير عادية و دلك مثل

v               إحساس بالمشي فوق سطح قارب

v               إحساس بأن الأشياء من حولك تبدو في حالة حركة شديدة

v               هل تشعر بأنك تدور بسرعة في حين انك ثابت

v               إحساس بعدم الاتزان حركة غير عادية غثيان أو دوار عند تحريك الرأس أو ميل للانحراف إلى الجانب عند محاولة المشي مستقيما.

إذا كانت الإجابة لا أو فقط دوخة بسيطة توقف أما إذا وجدت أعراض أخرى فانتقل إلى السؤال التالي

3. هل تم تقييم أعراض الدوخة أو الدوار أو اضطراب الاتزان الذي تعانى منها

·                 نعم ماذا كان التشخيص؟

              إذا كان التشخيص متعلق باضطراب المخ أو الأعصاب أو الإذن الداخلية توقف. أما إذا كان التشخيص غير متعلق بما سبق فانتقل إلى السؤال التالي.

4. هل تعانى من نقص سمعي مزمن أو رنين في أذنيك مع مشكلتك في الاتزان؟

إذا كانت الإجابة (نعم) لأي من السؤالين توقف. أما إذا كانت (لا) فانتقل إلى السؤال التالي.

5. هل تعانى من أعراض عدم الاتزان طوال الوقت أم أنها متقطعة؟

   إذا كنت تعانى منها طوال الوقت هل تكون شدتها متقلبة أو متغيرة؟

   إذا كانت الأعراض ثابتة أو غير متقلبة توقف أما إذا كانت متقطعة أو متقلبة في الشدة فانتقل إلى السؤال التالي.

6. كيف تتدخل نوبات عدم الاتزان و الأعراض المتقلبة في نشاطاتك اليومية؟

- الأعراض لا تتدخل (تصف بأنها خفيفة و توقف)

- الأعراض عادة تتدخل و لكن لا تمنع النشاطات اليومية (تصنف متوسطة و انتقل إلى التالي)

_ الأعراض عادة تمنع النشاطات اليومية (تصنف شديدة و انتقل إلى السؤال التالي)

7. هل حدث إحدى الأعراض الآتية على الأقل مرتين في نفس الوقت الذي تعرضت فيه لنوبات عدم الاتزان أو  عند زيادة الشدة أو تقلب أعراض الاتزان؟

1)     صداع نصفى

2)     زيادة شديدة في الحساسية إلى الإضاءة العادية للغرفة أو المحادثة الكلامية (يجب أن يقرر الشخص حاجته إلى إطفاء الأنوار أو المذياع أو جهاز التلفاز أو إسدال الستائر أو حاجته إلى الانتقال إلى غرفة كظلمة و هادئة)

3)     حس شخصي سبق ألم نصف الرأس عبارة عن هلاوس بصرية أو ضعف أو تنميل في جانب واحد من الجسم

-    إذا كان الحس الشخصي عبارة عن دوخة فان الدرجة لا تحسب

-    أما إذا كانت الإجابة نعم فان تشخيص دوار هو دوار الشقيقة

-    أما إذا كانت الإجابة لا فان التشخيص ليس دوار الشقيقة

إن تشخيص دوار الشقيقة يتم عندما إجابة المريض هي نعم على كل الأسئلة حتى السؤال السابع.

الملخص العربي

 

دوار الشقيقة: ظواهر إكلينيكية و نتائج الجهد العضلي المثار للاتزان

 

إن دوار الشقيقة واحد من أهم أسباب الدوار المعروفة.و لقد تنامي العلم به في الآونة الأخيرة بين متخصصى الأعصاب. وعلى الرغم انه إلى الآن لم يتم إدراج دوار الشقيقة كأحد أنواع الشقيقة ضمن التقسيم الدولي للصداع فان علاماته الإكلينيكية قد وضعت واستخدمت في الدراسات الإكلينيكية. وقد اعد هدا  البحث لدراسة الأعراض الإكلينيكية لمرض دوار الشقيقة وكذلك مقارنة نتائج الجهد العضلي المثار للاتزان في مرض الشقيقة المصاحب بالدوار و الغير مصاحب بالدوار. كما يهدف البحث إلى اختبار حساسية هدا الاختبار في تشخيص مرض دوار الشقيقة. وقد شمل هدا البحث 38 مريض بمرض الشقيقة و كذلك 18 شخص سليم كمجموعة ضابطة. وقد قسم المرضى إلى مجموعتين. المجموعة الأولى اشتملت على 20 مريض بالشقيقة المصحوب بالدوار وقد أخضعوا إلى استبيان لتشخيص دوار الشقيقة وقد تم استبعاد 4 مرضى بعد عمل الاستبيان. واشتملت المجموعة الثانية على 18 مريض بمرض الشقيقة بدون دوار. وأشتمل الفحص الإكلينيكي للمرضى على أخد التاريخ المرضى لدوار الشقيقة بالتفصيل وفحص عصبي كامل وفحص سمعي أولى وكذلك الجهد العضلي المثار للاتزان. وكان من نتائج هدا البحث انه يمكن اعتبار دوار الشقيقة كمرض قائم بذاته كما انه يمكن الاعتماد على الاستبيان المستخدم في تشخيص هذا المرض وقد ثبت أيضا إن الجهد العضلي المثار للاتزان له دور في تشخيص دوار الشقيقة.

 



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