eeg-mgr 1.pdf

7/29/2019 eeg-mgr 1.pdf

1/8

ournal of Neurological Sciences (Turkish) Table of Contents

NOROL BIL D 18: 1 , 2001 http://www.med.ege.edu.tr/norolbil/2001/NBD14401.html

Research Article

PATTERN REVERSAL VISUAL EVOKEDPOTENTIALS AND EEG IN MIGRAINE PATIENT

WITH- AND WITHOUT VISUAL AURA*

Aysun SOYSAL, Turan ATAY, Fikret AYSAL, Musa OZTURK, Yavuz ALTUNKAYNAK, Sevim BAYB

Baki ARPACI

akirkoy State Hospital for Neurological & Psychiatric Diseases, Departments of Neurology I-II,tanbul, Turkey

BSTRACT

order to investigate possible electrophysiological changes in migraine, we evaluated pattern revesual evoked potentials (PRVEP) and EEG findings of 13 patients with visual aura (MWA) and 20atients without visual aura (MWOA) during interictal period as well as in a control group of 21 normbjects.

hen compared with the controls, the P100 latencies of PRVEPs aroused by full-field, right- and lefemi-field stimulation of both eyes were significantly longer in MWOA patients in all recordingectrodes. Similarly, the P100 latencies of PRVEPs in MWA patients were also significantly longer ose of controls except for O2 recordings with left hemi-field stimulation, and O1/O2/Oz recordingth full-field stimulation of right eye. On the other hand, EEG abnormalities were observed in only MWA and in three of MWOA patients.

though controversial results have been reported in the literature, our results suggest that there iseuronal dysfunction in migraine which can be elicited with VEP studies.

ey-words: Migraine, visual evoked potentials, EEG.

TRODUCTION

It has been postulated that local ischemia due to focal cerebral vasospasm is responsible for theprodromal neurologic deficits in migraine patients(1,5,15,16,17). Cerebral blood flow (CBF)studies in patients having migraine with aura (MWA) have shown a reduction of regional CBF inone occipital pole during or just before the aura (1, 5,17). The reduction of regional CBF spreadsforward at a rate of 2 to 3 mm per minute or may stop at a point and it is correlated with the

PATTERN REVERSAL VISUAL EVOKED POTENTIALS AND EEG IN MIGRAINE PATIENTS WITH- AND WITHOUT VISUAL AURA

le:///C|/wwwhome/2001/NBD14401.html (1 of 8) [19.03.2001 10:47:53]
http://www.med.ege.edu.tr/norolbil/http://www.med.ege.edu.tr/norolbil/2001/2001_1.htmlhttp://www.med.ege.edu.tr/norolbil/2001/2001_1.htmlhttp://www.med.ege.edu.tr/norolbil/

7/29/2019 eeg-mgr 1.pdf

2/8

symptoms of migraine (1, 5,17). It has been reported that the reduction of CBF is limited tooccipital regions in patients with pure visual aura whereas more widespread CBF reduction mayalso cause symptoms in extremities (17). Migraine without aura (MWOA) is accompanied by a20% or less reduction of CBF. More severe reduction of CBF (i.e. 50% or more) may lead toMWA (15,16,17). The CBF changes in migraine is very similar to " cortical spreading depression(SD)" observed by Leao in animal studies (1,5,15,16,17). This phenomenon can be elicited inexperimental animals by stimulation of cerebral cortex, and consists of a slow wave ofdepolarization followed by repolarization. Temporary abolishment of the EEG and changes incortical pH also occur. The process is reversible and spreads at a rate of 2 to 4 mm per minute (1,5,17). The similarity between the SD described by Leao and CBF changes in migraine have led tothe hypothesis that migraine may have a physiological basis in form of a SD (12).

Visual evoked potentials (VEP) recorded at the scalp are caused by the activation of occipitalneurons and represents the summation of dendritic synaptic potentials of these neurones (4).Therefore, VEP studies have commonly been performed in migraine cases. On the other hand,there are some studies in the literature suggesting hyperexcitability in occipital areas (8). In orderto investigate possible electrophysiological changes in migraine, we evaluated pattern reversalvisual evoked potentials (PRVEP) and EEG findings in migraine patients with- and without visualaura as well as in a healthy control group.

MATERIALS and METHODS

Thirty-three migraine patients assembled from the Headache Outpatient Clinic of Bakirkoy StateHospital for Neurological & Psychiatric Diseases, Departments of Neurology I-II, and 21age-matched healthy volunteers were included in the study. Out of 33 patients, 13 had visual aura(MWA). The diagnosis was made according to the classification proposed by the InternationalHeadache Society (11). The mean age of MWA-, MWOA- and control group was 33.9 9.28(18-50), 37.9 10.5 (20-57) and 36.4 9.22 (22-54), respectively. All patients and controls werefemale and none of the patients was in migraine attack during the study. Neurological andophtalmological examinations were normal in both patients and controls. The duration of thedisease was 1-25 and 1-30 years in MWA and MWOA group, respectively. The frequency ofattacks was 1-4/month in both groups. The duration of the attacks was 12-60 hours in MWA and6-60 hours in MWOA group. All patients included in the study had their last migraine attack at

least one week prior to the EEG and VEP recordings, and they were still under prophylactictherapy. EEG and VEP recordings were made on the same day for each patient.

EEG recordings along with hyperventilation and photic stimulation were performed using a 24+8channel Medelec (Profile) device. Different montages were evaluated.

VEP studies were performed using a Medelec Sapphire 4ME device. Ag/AgCl disc electrodeswere used. Active electrodes were placed to O1, O2 and Oz (according to 10-20 system), andreferred to Fz. Electrode impedance was kept below 2 k. The filter bandpass was 1-50 Hz.Pattern reverse stimulation was performed in a dark room by a 16x16 checkerboard pattern 70cm away from the nasion with 2 Hz frequency and 100% contrast. Full-field, right and lefthemi-field pattern reverse stimuli were consecutively given to the right- and left eye. At least 100

artefact-free responses were averaged and two runs were performed for each patient. The P100latencies and the peak to peak N75/P100 amplitudes of VEP were measured. Results werecompared with students t-test.

RESULTS

No statistical difference was found between MWA- and MWOA patients and control group inrespect to the mean age (p=0.704 and p=0.380, respectively).

One patient with MWA- and another one in MWOA group exhibited mild slowing in EEG activityon frontal areas. One patient in MWOA group showed theta activities on the left frontal region,while another one had slow wave paroxysms on the left hemisphere.



7/29/2019 eeg-mgr 1.pdf

3/8

7/29/2019 eeg-mgr 1.pdf

4/8

7/29/2019 eeg-mgr 1.pdf

5/8

7/29/2019 eeg-mgr 1.pdf

6/8

stimulation of the hemifield (19). Connolly et al. reported increased amplitudes of VEP responsesin migraine patients, and the authors suggested that this finding might reflect occipitalhyperexitability (6). Polich reported a statistically unsignificant increase in LP100 and VEPamplitudes compared with the controls (13). Mariani found significantly longer LP100 in MWA butnormal LP100 and VEP amplitudes in MWOA (13). Nyrkes study showed an interhemisphericasymmetry in classic migraineurs and postulated that the changes may reflect increasedfunctional lability of the occipital visual cortex (14). Diener reported that the use of -blockersresulted in a significant decrease in VEP amplitudes in migraine patients (7). Some other studiesdemonstrated no difference in VEP latencies and amplitudes of migraineurs compared with thecontrols (9, 20, 21). Some authors reported decreased magnesium (Mg) serum levels andincreased VEP amplitudes in migraine patients (3,10,18,22). After Mg treatment, VEP amplitudesand/or the frequency of migraine attacks were decreased (3,10). These data seem to suggest thatlow brain Mg level and higher VEP amplitudes can both be an expression of neuronalhyperexitability of the visual pathways and a lowered threshold for migraine attacks. On the otherhand, fra et al. demonstrated that during long period of PRVEP, the amplitudes of VEPresponses were progressively decreased in control subjects, but remained stable in both MWAand MWOA group (2). The authors postulated that these findings represented an interictalhabituation deficit in cortical information processing which might suggest a lactate accumulation insensory cortex.

It has been suggested that there is an occipital hyperexitability, as photic stimulation provokesparoxysmal responses in epileptic patients and visual signs in migraineurs (8). In our study, onlyone patient in MWOA group exhibited paroxysmal activity suggesting neuronal hyperexitability inmigraine. EEG changes in other three patients were considered as non-specific.

Epileptic photosensitivity and migraine with visual aura could share some commonpathophysiological features. It has been postulated that primary events in migraine are in CNS butthe vascular phenomena are secondary. Considering the hypothesis about the SD in migraine,neuronal hyperexitability may provoke both the migraine- and epileptic attacks (8).

Our study demonstrated significant changes in VEP latencies. Controversial results reported inthe literature may be explained by using of different stimulation procedures and study protocols.Whatever the underlying etiology, our results suggest that there is a neuronal dysfunction inmigraine which can be elicited with VEP studies.

GRSEL AURASI OLAN VE OLMAYAN MGRENL HASTALARDA PATERN-REVERSGRSEL UYARILMI POTANSYELLER VE EEG*

ZET

Migrendeki olas elektrofizyolojik deiiklikleri incelemek iin, grsel auras olan (GA) 13 vegrsel auras olmayan (GAO) 20 migrenli hasta ile 21 normal kiiden oluan kontrol grubunda,interiktal dnemde pattern-revers grsel uyarlm potansiyel (PRGUP) yantlar ve EEGbulgular incelendi.

Kontrollarla kyaslandnda, GAO migrenli hastalarda tam alan, sa ve sol yar alan uyarmile tm kayt elektrodlarndan elde edilen PRGUP yantlarnn P100 latanslar uzundu. Benzerekilde GAl migrenli hastalarda da P100 latanslar, sol yar alan uyarm ile O2 ve sa gzntam alan uyarm ile O1/O2/Ozden kaydedilen PRGUP yantlar dnda kontrollerden anlamlolarak uzun bulundu. GAl bir hastada ve GAO hastada EEG bozukluklar saptand.

Literatrde elikili sonular bildirilmesine ramen, sonularmz migrende GUP almalar ileortaya karlabilen nronal fonksiyon bozukluu olduunu dndrmtr.

Anahtar kelimeler: Migren, grsel uyarlm potansiyeller, EEG.



7/29/2019 eeg-mgr 1.pdf

7/8

*Presented in "XI. International Congress of EMG and Clinical Neurophysiology",Sept.7-11,1999, Prague,Czech Rep.

REFERENCES

Adams RD, Victor M, Ropper AH. Headache and other craniofacial pains. In: Principles ofneurology. New York : McGraw-Hill, 1997, Sixth ed. pp : 167-93 .

1.

fra J, Cecchini AP, De Pasqua V, Albert A, Schonen J. Visual evoked potentials during longperiods of pattern-reversal stimulation in migraine. Brain 1998; 121 : 233-41.

2.

Aloisi P, Marrelli A, Porto C, Tozzi E, Cerone G. Visual evoked potentials and serum magneslevels in juvenile migraine patients. Headache 1997; 37: 383-5. (Medline abstract)

3.

Arroyo S, Lesser RP, Poon W-T, Webber WRS, Gordon B. Neuronal generators of visual evokpotentials in humans: Visual processing in the human cortex. Epilepsia 1997; 38 (5) : 600-10.

4.

Campbell JK, Caselli RJ. Headache and other craniofacial pain. In : Neurology in clinicalpractice. Eds, Bradley WG, Daroff RB, Fenichel GM, Marsden CD. Boston, Butterworth -

Heinemann, 1996, Second ed. pp : 1683 719.

5.

Connolly JF, Gawell M, Rose FC. Migraine patients exhibit abnormalities in the visual evokedpotentials. J Neurol Neurosurg Psychiatry 1982; 45: 464-67. (Medline abstract)

6.

Diener HC, Scholz E, Dichgans J, Gerber WD, Jack A, Bille A, Niederberger U. Central effecdrugs used in migraine prophylaxis evaluated by visual evoked potentials. Ann Neurol 1989; 2125-30.

7.

Donnet A, Bartolomei F. Migraine with visual aura and photosensitive epileptic seizures.Epilepsia 1997; 38 (9): 1032-34.

8.

Drake ME, Pakalnis A, Hietter SA, Padamadan H. Visual and auditory evoked potentials in

migraine. Electromyogr Clin Neurophysiol 1990; 30: 77-81. (Medline abstract)

9.

Facchinetti F, Sancez G, Borella P, Genazzani AR, Nappi G. Magnesium prophylaxis of menstmigraine : effects on intracellular magnesium. Headache 1991; 31: 298-301. (Medline abstra

10.

Headache Classification Committee of the International Headache Society. Classification anddiagnostic criteria for headache disorders, cranial neuralgias and facial pain. Cephalalgia 198( suppl 7): 1-96.

11.

Lauritzen M. Cerebral blood flow in migraine and spreading depression. In : Migraine andepilepsy. Eds, Andermann F, Lugaresi E. Boston, Butterworths, 1987, pp : 325-37.

12.

Mariani E, Moschini V, Pastorino G, Rizzi F, Severgnini A, Tiengo M. Pattern reversal visualevoked potentials (VEP-PR) in migraine subjects with visual aura. Headache 1990; 30: 435-513.

Nyrke T, Kangasniemi P, Lang AH. Transient asymmetries of steady-state visual evoked potenin classic migraine. Headache 1990; 30: 133-37.

14.

Olesen J, Bonica JJ. Headache. In : The management of pain. Eds, Bonica JJ, Loeser JD,Chapman CR, Fordyce WE. Philadelphia, Lea & Febiger, 1990, Second ed, 687-726.

15.

Olsen TS, Friberg L, Lassen NA. Ischemia may be primary cause of the neurologic deficits inclassic migraine. Arch Neurol 1987; 44: 156-61.

16.



7/29/2019 eeg-mgr 1.pdf

8/8

Olsen TS. Migraine with and without aura: The same disease due to cerebral vasospasm ofdifferent intensity. A hypothesis based on CBF studies during migraine. Headache 1990; 30: 2

72.

17.

Ramadan NM, Halvorson H, Vanda-Linde A, Levine SR, Helpern JA, Welch KMA. Low brainmagnesium in migraine. Headache 1989; 29: 590-3. (Medline abstract)

18.

Streletz LJ, Bae SH, Roeshman AM, Shatz NJ, Savino PJ. Visual evoked potentials in occipitallesions. Arch Neurol 1981; 38: 80-5. (Medline abstract)

19.

ener H, Haktanir I, Demirci S. Pattern-reversal visual evoked potentials in migraineurs wiwithout visual aura. Headache 1997; 37: 449-51.

20.

vanDijk JG, Dorresteijn M, Haan J, Ferrari MD. No confirmation of visual evoked potentialdiagnostic test for migraine. Lancet 1991; 337: 517-18.

21.

Welch KMA, DAndrea G, Tepley N, Barkley G, Ramadan NM. The concept of migraine as a sof central neuronal hyperexcitability. In : The neurologic clinics of North America. Headache

Mathew NT. Philadelphia, W.B. Saunders Company, 1990, pp : 817-28.

22.

orrespondence

. Aysun Soysal

akrky Ruh ve Sinir Hastalklar Hastanesi 1. Nroloji Klinii 34747 Bakrky/Istanbul TRKYE Phone90-212-543 65 65/423 Fax : +90-212-572 9595 E-mail [email protected]

he Online Journal of Neurological Sciences (Turkish) 1984-2001

eceived by:19.01.2001

ccepted : 21.02.2001

eer-reviewers: 3

op of the page

is page is run by Aegean Neurological Society, Ege University Faculty of Medicine, Dept. of Neurologica

rgery, Bornova, Izmir-35100TR

part of the Ege Neurological Surgery World Wide Web service.

mments and feedback: [email protected]

L: http://www.med.ege.edu.tr/norolbil

Journal of Neurological Sciences (Turkish)ISSN 1302-1664

mailto:[email protected]://www.med.ege.edu.tr/~norolbil/aegean.htmhttp://www.med.ege.edu.tr/neurosurgery/mailto:[email protected]://www.med.ege.edu.tr/~norolbilhttp://www.med.ege.edu.tr/~norolbilmailto:[email protected]://www.med.ege.edu.tr/neurosurgery/http://www.med.ege.edu.tr/~norolbil/aegean.htmmailto:[email protected]

eeg-mgr 1.pdf

Documents