Pulsed magnetic fields as rTMS in migraine headache helps promote normal brain electrophysiology in headache syndromes of all types. 10% of U.S. males and 20% of U.S. females experience migraine headache at least once per 3 months. 2% of the worlds population experience headache 15 days per month. With such widespread populations you’d think that a simple, non-invasive non pharmacological solution like rTMS / pulsed electromagnetic field therapy would have garnered more interest by the media and medical community.

During research while updating the migraine bibliography we learned that in 2013 the FDA approved the first home rTMS system for migraine pain. It appears no one knows of this as I’ve never seen mention of an FDA approved rTMS other than for “treatment resistant” depression.

Magnetic PEMF Therapy for Migraine Headaches

We believe beneficial effects of pulsed electromagnetic fields / rTMS is attributable to MoreATP, which explains the healing effects of frequency specific pulsed electromagnetic fields (PEMF) therapy. Particularly where pulse repetition rate approximates 10 Hz.

We are fairly sure most pulsed electromagnetic therapies lead to enhanced cellular energy parameters through some heretofore undisclosed mechanism…an alternative cellular energy pathway. However, where pulse repetition rate is within 5 Hz and 15 Hz nearly all reported effects are simply due to enhanced organic ATP production. The abundance of cellular energy allows the body to correct it’s brain hyper or under excitability while allowing blood to flow more evenly distributed.

“When the solution is simple…God is answering” ~ Albert Einstein

The magnetic therapy headache bibliography is offered for educational purposes only and not as promotional material for our pulsed magnetic technology.

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Magnetic Therapy Migraine Headache – Pulsed Electromagnetic Field Therapy via rTMS Bibliography

To read the abstracts, copy and paste the title of the study into the search window at Pubmed .

rTMS in Alleviating Mild TBI Related Headaches – A Case Series.
Leung A, Fallah A, Shukla S, Lin L, Tsia A, Song D, Polston G, Lee R.
Pain Physician. 2016 Feb;19(2):E347-54.
PMID: 26815263 Free Article
Repetitive Transcranial Magnetic Stimulation in Managing Mild Traumatic Brain Injury-Related Headaches.
Leung A, Shukla S, Fallah A, Song D, Lin L, Golshan S, Tsai A, Jak A, Polston G, Lee R.
Neuromodulation. 2015 Nov 10. doi: 10.1111/ner.12364. [Epub ahead of print]
PMID: 26555886
[Clinical Application and Safety of rTMS in Japan and Overseas].
Kito S.
Seishin Shinkeigaku Zasshi. 2015;117(2):103-9. Review. Japanese.
PMID: 26514049
Treatment of Chronic Facial Pain Including Cluster Headache by Repetitive Transcranial Magnetic Stimulation of the Motor Cortex With Maintenance Sessions: A Naturalistic Study.
Hodaj H, Alibeu JP, Payen JF, Lefaucheur JP.
Brain Stimul. 2015 Jul-Aug;8(4):801-7. doi: 10.1016/j.brs.2015.01.416. Epub 2015 Feb 7.
PMID: 25979838
rTMS in Alleviating Mild TBI Related Headaches – A Case Series.
Leung A, Fallah A, Shukla S, Lin L, Tsia A, Song D, Polston G, Lee R.
Pain Physician. 2016 Feb;19(2):E347-54.
PMID: 26815263 Free Article
Repetitive Transcranial Magnetic Stimulation in Managing Mild Traumatic Brain Injury-Related Headaches.
Leung A, Shukla S, Fallah A, Song D, Lin L, Golshan S, Tsai A, Jak A, Polston G, Lee R.
Neuromodulation. 2015 Nov 10. doi: 10.1111/ner.12364. [Epub ahead of print]
PMID: 26555886
[Clinical Application and Safety of rTMS in Japan and Overseas].
Kito S.
Seishin Shinkeigaku Zasshi. 2015;117(2):103-9. Review. Japanese.
PMID: 26514049
Treatment of Chronic Facial Pain Including Cluster Headache by Repetitive Transcranial Magnetic Stimulation of the Motor Cortex With Maintenance Sessions: A Naturalistic Study.
Hodaj H, Alibeu JP, Payen JF, Lefaucheur JP.
Brain Stimul. 2015 Jul-Aug;8(4):801-7. doi: 10.1016/j.brs.2015.01.416. Epub 2015 Feb 7.
PMID: 25979838
Clin Neurophysiol. 2014 Oct;125(10):2090-9. doi: 10.1016/j.clinph.2014.01.028. Epub 2014 Feb 14.
Modulation of visual evoked potentials by high-frequency repetitive transcranial magnetic stimulation in migraineurs.
Omland PM1, Uglem M2, Engstrøm M3, Linde M3, Hagen K3, Sand T3.

This one is surprising particularly since it was done at 10 Hz and we’ve had such good success with migraine sufferers. Perhaps do to so much field amplitude at 80% motor threshold (about 10-15 times our current v.5 maximum setting). We don’t care why you buy your EP, you’ve got a 90 days satisfaction guarantee.

J Clin Diagn Res. 2014 Sep;8(9):MM01-2. doi: 10.7860/JCDR/2014/9377.4886. Epub 2014 Sep 20.
Poor Tolerance of Motor Cortex rTMS in Chronic Migraine.
Teo WP1, Kannan A2, Loh PK3, Chew E4, Sharma VK5, Chan YC5.
Cephalalgia. 2014 May;34(6):464-72. doi: 10.1177/0333102413515340. Epub 2013 Dec 10.
Randomized, proof-of-principle clinical trial of active transcranial magnetic stimulation in chronic migraine.
Conforto AB1, Amaro E Jr, Gonçalves AL, Mercante JP, Guendler VZ, Ferreira JR, Kirschner CC, Peres MF.
J Neurol. 2013 Nov;260(11):2793-801. doi: 10.1007/s00415-013-7072-2. Epub 2013 Aug 21.
High-rate repetitive transcranial magnetic stimulation in migraine prophylaxis: a randomized, placebo-controlled study.
Misra UK1, Kalita J, Bhoi SK.
Abstract
Repetitive transcranial magnetic stimulation (rTMS) is an emerging treatment for pain but there is no class 1 study on its role in migraine prophylaxis. In this study we report the efficacy and safety of high-rate rTMS in migraine prophylaxis. Adult migraine patients having >4 attacks/month were randomized to high-rate rTMS or sham stimulation. Stimulation in the form of 10 Hz rTMS, 600 pulses in 10 trains were delivered to the hot spot of the right abductor digiti minimi in 412 s. Three sessions were delivered on alternate days. The outcome was defined at 1 month. The primary outcome measures were reduction in headache frequency and severity >50 % as assessed by the Visual Analogue Scale (VAS). The secondary outcome measures were functional disability, rescue medication and adverse events. Fifty patients each were randomized to rTMS or sham stimulation. The baseline characteristics of rTMS and sham stimulation groups were similar. At 1 month, headache frequency (78.7 vs. 33.3 %; P = 0.0001) and VAS score (76.6 vs. 27.1 %; P = 0.0001) improved significantly in the patients receiving rTMS compared to those in the sham stimulation group. Functional disability also improved significantly in rTMS group (P = 0.0001). Only one patient following rTMS developed transient drowsiness and was withdrawn from the study. This study provides evidence of the efficacy and safety of 10 Hz rTMS in migraine prophylaxis.
Neurol Sci. 2013 May;34 Suppl 1:S109-12. doi: 10.1007/s10072-013-1385-x.
Refractory migraine: the role of the physician in assessment and treatment of a problematic disease.
Colombo B, Dalla Libera D, Dalla Costa G, Comi G.
Cephalalgia. 2013 Apr;33(5):316-22. doi: 10.1177/0333102412473372. Epub 2013 Jan 11.
Is β endorphin related to migraine headache and its relief?
Misra UK, Kalita J, Tripathi GM, Bhoi SK.
Neurol Res. 2012 Jul;34(6):547-51. doi: 10.1179/1743132812Y.0000000045. Epub 2012 Jun 20.
High frequency repetitive transcranial magnetic stimulation (rTMS) is effective in migraine prophylaxis: an open labeled study. Misra UK, Kalita J, Bhoi SK.
Effects of repetitive transcranial magnetic stimulation on somatosensory evoked potentials and high frequency oscillations in migraine. Coppola G, De Pasqua V, Pierelli F, Schoenen J.
Abstract
OBJECTIVE:
To evaluate the effect of high rate repetitive transcranial magnetic stimulation (rTMS) in migraineprophylaxis in medically refractory patients.
METHODS:
Migraine patients above 15 years of age, having more than 7 attacks/month and refractory to at least two prophylactic drugs were included. The patients were evaluated for migraine frequency, severity, functional disability, number of rescue medications and migraine index. Three sessions of alternate day 10 Hz rTMS comprising of 600 pulses in 10 trains were delivered to left frontal cortex. The response was evaluated at the end of session and weekly for 4 weeks.
RESULTS:
Fifty-one patients aged 16-61 years and 45 females were treated. Fifty (98%) patients had more than 50% reduction of headache frequency at the end and 1 week after rTMS and the improvement persisted till the fourth week in 80.4% patients. The headache frequency, severity, functional disability,migraine index, and rescue medications significantly reduced at all time points, but the maximum benefit was observed in the first 2 weeks. There were no serious adverse events.
CONCLUSION:
High rate rTMS in left frontal cortex is effective and well tolerated for migraine prophylaxis.
Cephalalgia. 2012 Jul;32(9):700-9. doi: 10.1177/0333102412446313. Epub 2012 May 31. Headache. 2010 Jul;50(7):1153-63. Epub 2010 Jun 10.
Transcranial magnetic stimulation for migraine: a safety review.
Dodick DW, Schembri CT, Helmuth M, Aurora SK.
Mayo Clinic, Phoenix, AZ, USA.
Cephalalgia. 2010 Jan;30(1):46-52.
High-frequency transcranial magnetic stimulation on motor cortex of patients affected by migraine with aura: a way to restore normal cortical excitability?
Brighina F, Palermo A, Daniele O, Aloisio A, Fierro B.
Dipartimento Universitario di Neuroscienze Cliniche, University of Palermo, Palermo, Italy.
Neurotherapeutics. 2010 Apr;7(2):204-12.
Transcranial magnetic simulation in the treatment of migraine.
Lipton RB, Pearlman SH.
Department of Neurology, Montefiore Headache Center, Albert Einstein College of Medicine, Bronx, New York 10461, USA
CNS Spectr. 2007 Dec;12(12):921-5.
Unexpected reduction in migraine and psychogenic headaches following rTMS treatment for major depression: a report of two cases.
O’Reardon JP, Fontecha JF, Cristancho MA, Newman S.
University of Pennsylvania, Transcranial Magnetic Stimulation Laboratory, Philadelphia, PA, USA.
Cereb Cortex. 2008 Mar 27. [Epub ahead of print]
Homeostatic Metaplasticity of the Motor Cortex is Altered during Headache-Free Intervals in Migraine with Aura.
Antal A, Lang N, Boros K, Nitsche M, Siebner HR, Paulus W.
Department of Clinical Neurophysiology, Georg-August University, 37073 Göttingen, Germany.
Preconditioning of the human primary motor cortex (M1) with transcranial direct current stimulation (tDCS) can shape the magnitude and direction of excitability changes induced by a subsequent session of repetitive transcranial magnetic stimulation (rTMS). Here, we examined this form of metaplasticity in migraine patients with visual aura and healthy controls. In both groups, facilitatory preconditioning of left M1 with anodal tDCS increased the mean amplitudes of motor-evoked potentials (MEPs) elicited in the contralateral hand, whereas inhibitory preconditioning with cathodal tDCS produced a decrease in amplitude. Following cathodal tDCS, a short train of low-intensity 5-Hz rTMS antagonized the suppression of the mean MEP amplitude in both groups. In contrast, the homeostatic effects of 5-Hz rTMS differed between groups when rTMS was given after anodal tDCS. In controls 5-Hz rTMS induced a marked decrease in MEP amplitudes, whereas in migraineurs rTMS induced only a modest decrease in MEP amplitudes, which were still facilitated after rTMS when compared with baseline amplitudes. These findings indicate that short-term homeostatic plasticity is altered in patients with visual aura between the attacks.
PMID: 18372292 [PubMed – as supplied by publisher]
Clin Neurophysiol. 2008 Mar;119(3):504-32. Epub 2007 Dec 11.
The clinical diagnostic utility of transcranial magnetic stimulation: report of an IFCN committee.
Chen R, Cros D, Curra A, Di Lazzaro V, Lefaucheur JP, Magistris MR, Mills K, Rösler KM,Triggs WJ, Ugawa Y, Ziemann U.
Division of Neurology, Toronto Western Research Institute, University of Toronto, 7MC411, Toronto Western Hospital, 399 Bathurst Street, Toronto, Ont., Canada M5T 2S8. robert.chen[@]uhn.on.ca
The review focuses on the clinical diagnostic utility of transcranial magnetic stimulation (TMS). The central motor conduction time (CMCT) is a sensitive method to detect myelopathy and abnormalities may be detected in the absence of radiological changes. CMCT may also detect upper motor neuron involvement in amyotrophic lateral sclerosis. The diagnostic sensitivity may be increased by using the triple stimulation technique (TST), by combining several parameters such as CMCT, motor threshold and silent period, or by studying multiple muscles. In peripheral facial nerve palsies, TMS may be used to localize the site of nerve dysfunction and clarify the etiology. TMS measures also have high sensitivity in detecting lesions in multiple sclerosis and abnormalities in CMCT or TST may correlate with motor impairment and disability. Cerebellar stimulation may detect lesions in the cerebellum or the cerebellar output pathway. TMS may detect upper motor neuron involvement in patients with atypical parkinsonism and equivocal signs. The ipsilateral silent period that measures transcallosal inhibition is a potential method to distinguish between different parkinsonian syndromes. Short latency afferent inhibition (SAI), which is related to central cholinergic transmission, is reduced in Alzheimer’s disease. Changes in SAI following administration of cholinesterase inhibitor may be related to the long-term efficacy of this treatment. The results of MEP measurement in the first week after stroke correlate with functional outcome. We conclude that TMS measures have demonstrated diagnostic utility in myelopathy, amyotrophic lateral sclerosis and multiple sclerosis. TMS measures have potential clinical utility in cerebellar disease, dementia, facial nerve disorders, movement disorders, stroke, epilepsy, migraine and chronic pain.
PMID: 18063409
Schmerz. 2008 Feb;22 Suppl 1:17-21.
[Cortical dysbalance in the brain in migraineurs–hyperexcitability as the result of sensitisation?]
[Article in German]
Stankewitz A, May A.
Institut für systemische Neurowissenschaften, Universitätsklinikum Hamburg-Eppendorf, Martinistrasse 52, 20246, Hamburg, Germany.
A cortical dysbalance has a pivotal role in the pathophysiology of migraine. Numerous electrophysiological and transcranial magnetic stimulation (TMS) studies have investigated the interictal excitability level in migraineurs and have shown a consistent lack of habituation during repetitive stimulation. There is some controversy in the current literature over whether this deficit is based on a lowered or an elevated preactivation level. However, the current discussion may be misguided. It seems that multiple external and intrinsic factors influence the level of cortical excitability and the frequency and intensity of attacks: Habituation is specific neither to migraine nor even to pain; the same phenomenon is found in tinnitus patients, for example. Cortical hyperexcitability is presumably the result of chronicity and the concomitant central sensitisation process.
PMID: 18228046
J Neurol Sci. 2008 Jan 15;264(1-2):93-6. Epub 2007 Aug 27.
Clinical correlates of phosphene perception in migraine without aura: an Asian study.
Lo YL, Lum SY, Fook-Chong S, Cui SL, Siow HC.
Department of Neurology, National Neuroscience Institute, Singapore General Hospital, Outram Road, Singapore 169608, Singapore. lo.yew.long[@]sgh.com.sg
INTRODUCTION: Although controversy exists with regard to the presence of hypoexcitability versus hyperexcitability of the visual cortex in migraine patients, there remain a group who do not perceive phosphenes (P-). However, its clinical implications have not been systematically addressed. In this study, we hypothesize that P- patients classified as migraine without aura (MO) have distinct clinical features. METHODS: Twenty-nine Asian MO patients (7 men; mean age: 44; median: 45; range: 25 to 65) were consecutively entered into the study. Visual cortex transcranial magnetic stimulation (TMS) was performed in the migraine interictum. RESULTS: Of the 19 patients, 19 (66%) were able to perceive phosphenes (P+), while 10 (34%) were not able to after repeated TMS (P-). P- patients had significantly higher headache frequency (p=0.008) and pain score (p=0.002) compared with P+ patients. In addition, there was significant positive correlation of phosphene threshold with pain score (r=0.52, p=0.02) in P+ patients. There was no significant difference between P+ and P- patients in terms of age (t-test, p=0.6). CONCLUSIONS: Our study is inkeeping with the hypothesis that interictal visual cortex excitability is reduced in relation to the severity of migraine in Asian MO patients, and lack of phosphene perception may be related to significantly elevated thresholds beyond the output of TMS stimulators.
PMID: 17720202
CNS Spectr. 2007 Dec;12(12):921-5.
Unexpected reduction in migraine and psychogenic headaches following rTMS treatment for major depression: a report of two cases.
O’Reardon JP, Fontecha JF, Cristancho MA, Newman S.
University of Pennsylvania, Transcranial Magnetic Stimulation Laboratory, Philadelphia, PA, USA. oreardon[@]mail.med.upenn.edu
Our objective is to report a coincident reduction in headache pain in patients treated with repetitive transcranial magnetic stimulation (rTMS) for major depressive disorder (MDD). Two patients with a Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition diagnosis of MDD, non-responsive to prior antidepressant treatment who were enrolled in a sham-controlled, double-blind study of rTMS for MDD. After the study, it was revealed that both were in the active-treatment arm. Both patients suffered from near daily headaches and kept logs of headache frequency and severity before, during, and after the study. Headache pain was significantly reduced under double-blind conditions with rTMS treatment, but returned to baseline following cessation of rTMS treatment. Ultimately, when receiving rTMS post-study as a maintenance intervention for MDD (approximately 2 rTMS sessions/week), the positive effects on headache amelioration were sustained. Headache pain is frequently comorbid with mood disorders and has been reported as the most common side effect with rTMS. In these subjects, rTMS was, in fact, associated with relief of depressive symptoms and preexisting headache pain. This indicates that rTMS may be beneficial for both disorders in some patients.
PMID: 18163038
Pain. 2007 Nov;132(1-2):124-31. Epub 2007 Jun 14.
Shortened cortical silent period in facial muscles of patients with migraine.
Curra A, Pierelli F, Coppola G, Barbanti P, Buzzi MG, Galeotti F, Serrao M, Truini A, Casali C, Pauri F, Cruccu G.
Department of Neurological Sciences, La Sapienza University, Rome, Italy. antonio.curra[@]uniroma1.it
Despite intensive neurophysiological research, evidence is lacking to show whether abnormal cortical excitability in migraine reflects a primary cortical disturbance or reduced control by thalamo-cortical loops. One way to contribute to the scientific discussion on this topic is to deliver transcranial magnetic stimulation (TMS) and test the cortical silent period (SP) recorded in facial muscles. The facial-muscle SP is a purely cortical phenomenon that reflects the excitability of inhibitory interneurons, and can disclose changes in cortical inhibition even in patients without documented primary lesions of the motor cortices. To test the interictal excitability of cortical motor inhibitory interneurons in migraine, we investigated the facial-SP in patients with migraine with and without aura between attacks. In 26 patients and 15 age-matched controls, high-intensity magnetic stimuli were delivered with a round coil centered at the vertex during a maximal muscle contraction. Electromyographic responses were recorded from surface electrodes placed over the subjects’ perioral muscles. Facial SPs were significantly shorter in patients than in controls. The SP shortening provides neurophysiological evidence showing hypoexcitability of cortical inhibitory neurons in patients with migraine between attacks. Despite a possible primary deficit of cortical inhibitory interneurons in migraine, we favor the interpretation of a secondary disfacilitation by hypoactive thalamo-cortical loops. Based on this interpretation, the interictal reduced cortical inhibition documented by the shortened SP could be considered the motor counterpart of the reduced preactivation excitability level in the sensory cortices purported to explain why cortical evoked responses habituate poorly in patients with migraine.
PMID: 17574759
Cephalalgia. 2007 Jul;27(7):833-9. Epub 2007 May 10.
Transcranial direct current stimulation reveals inhibitory deficiency in migraine.
Chadaide Z, Arlt S, Antal A, Nitsche MA, Lang N, Paulus W.
Department of Clinical Neurophysiology, Georg-August University, Göttingen, Germany.
The issue of interictal excitability of cortical neurons in migraine patients is controversial: some studies have reported hypo-, others hyperexcitability. The aim of the present study was to observe the dynamics of this basic interictal state by further modulating the excitability level of the visual cortex using transcranial direct current stimulation (tDCS) in migraineurs with and without aura. In healthy subjects anodal tDCS decreases, cathodal stimulation increases transcranial magnetic stimulation (TMS)-elicited phosphene thresholds (PT), which is suggested as a representative value of visual cortex excitability. Compared with healthy controls, migraine patients tended to show lower baseline PT values, but this decrease failed to reach statistical significance. Anodal stimulation decreased phosphene threshold in migraineurs similarly to controls, having a larger effect in migraineurs with aura. Cathodal stimulation had no significant effect in the patient groups. This result strengthens the notion of deficient inhibitory processes in the cortex of migraineurs, which is selectively revealed by activity-modulating cortical input.
PMID: 17498207
Headache. 2007 Jul-Aug;47(7):996-1003; discussion 1004-7
Brainstem dysfunction in chronic migraine as evidenced by neurophysiological and positron emission tomography studies.
Aurora SK, Barrodale PM, Tipton RL, Khodavirdi A.
Swedish Headache Center, 1101 Madison #200, Seattle, WA 98104, USA.
Brain Res Bull. 2007 May 30;72(4-6):208-14. Epub 2007 Jan 24.
Safety aspects of transcranial direct current stimulation concerning healthy subjects and patients.
Poreisz C, Boros K, Antal A, Paulus W.
Department of Clinical Neurophysiology, Georg-August University, Robert Koch Strasse 40, 37075 Göttingen, Germany.
Headache. 2007 Mar;47(3):364-70.
Intracortical inhibition and facilitation in migraine–a transcranial magnetic stimulation study.
Siniatchkin M, Kröner-Herwig B, Kocabiyik E, Rothenberger A.
Department of Child Neurology, University of Kiel, Kiel, Germany.
OBJECTIVE: Migraine is a disease of altered cortical excitability between attacks. However, the mechanisms of abnormal excitability in migraine are insufficiently investigated. Hence, the aim of the study was to investigate intracortical inhibition/facilitation of the motor circuit in migraine. METHODS: Sixteen women suffering from migraine without aura and 15 healthy women were investigated using a suprathreshold transcranial magnetic stimulation (TMS) in the paired-pulse paradigm with long interstimulus intervals (ISI = 20, 60, 120 ms) and measurement of the cortical silent period. RESULTS: We found no differences for the cortical silent period and for the long intracortical inhibition between the groups. Concerning intracortical facilitation, this ability was significantly more pronounced in patients suffering from migraine compared with healthy controls. CONCLUSION: Migraineurs produce an increased intracortical facilitation. The results may be discussed in line of glutamatergic mechanisms in migraine, which could be related to altered facilitation.
PMID: 17371353
J Headache Pain. 2006 Oct;7(5):341-6. Epub 2006 Oct 25.
Transcranial magnetic stimulation for migraine: clinical effects.
Clarke BM, Upton AR, Kamath MV, Al-Harbi T, Castellanos CM.
Division of Neurology, McMaster University, Hamilton, Ontario, Canada.
Acta Neurol Belg. 2003 Sep;103(3):144-54.
Transcranial magnetic stimulation in migraine: a review of facts and controversies.
Fumal A, Bohotin V, Vandenheede M, Schoenen J.
Departments of Neurology and Neuroanatomy, University of Liège, B-4000 Liège, Belgium.
Med Hypotheses. 2002 Dec;59(6):703-5.
Cellular telephones and effects on the brain: the head as an antenna and brain tissue as a radio receiver.
Weinberger Z, Richter ED.
Jerusalem College of Technology, Jerusalem, Israel.
Headache and other neuropsychological symptoms occur in users of cellular telephones, and controversy exists concerning risks for brain cancer. We hypothesize these effects result from the head serving as an antenna and brain tissue as a radio receiver.
Adv Ther. 2001 May-Jun;18(3):101-9.
Impulse magnetic-field therapy for migraine and other headaches: a double-blind, placebo-controlled study.
Pelka RB, Jaenicke C, Gruenwald J.
Universitat der Bundeswehr Munchen Munich, Germany.
Headache. 1999 Sep;39(8):567-75.
Treatment of migraine with pulsing electromagnetic fields: a double-blind, placebo-controlled study.
Sherman RA, Acosta NM, Robson L.
Orthopedic Surgery Service, Madigan Army Medical Center, Tacoma, WA 98431, USA.
Headache. 1998 Mar;38(3):208-13.
Initial exploration of pulsing electromagnetic fields for treatment of migraine.
Sherman RA, Robson L, Marden LA.
Service of Orthopedic Surgery, Madigan Army Medical Center, Tacoma, Wash. 98431, USA.
Ambrosini A, Schoenen J. The electrophysiology of migraine.
Curr Opin Neurol. 2003 Jun;16(3):327-31. Review.
PMID: 12858069
Schoenen J, Ambrosini A, Sandor PS, Maertens de Noordhout A. Evoked potentials and transcranial magnetic stimulation in migraine: published data and viewpoint on their pathophysiologic significance.
Clin Neurophysiol. 2003 Jun;114(6):955-72. Review.
PMID: 12804664
Bohotin V, Fumal A, Vandenheede M, Bohotin C, Schoenen J. Excitability of visual V1-V2 and motor cortices to single transcranial magnetic stimuli in migraine: a reappraisal using a figure-of-eight coil.
Cephalalgia. 2003 May;23(4):264-70.
PMID: 12716343
Aurora SK, Welch KM, Al-Sayed F. The threshold for phosphenes is lower in migraine.
Cephalalgia. 2003 May;23(4):258-63.
PMID: 12716342
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. Review.
PMID: 12699456
Mulleners W, Chronicle E, Vredeveld J, Koehler P. Visual cortex excitability in migraine before and after valproate prophylaxis: a pilot study using TMS.
Headache. 2003 Mar;43(3):304.
PMID: 12603670 [PubMed – as supplied by publisher]
Ozturk V, Cakmur R, Donmez B, Yener GG, Kursad F, Idiman F. Comparison of cortical excitability in chronic migraine (transformed migraine) and migraine without aura. A transcranial magnetic stimulation study.
J Neurol. 2002 Sep;249(9):1268-71.
PMID: 12242552
Brighina F, Piazza A, Daniele O, Fierro B. Modulation of visual cortical excitability in migraine with aura: effects of 1 Hz repetitive transcranial magnetic stimulation.
Exp Brain Res. 2002 Jul;145(2):177-81. Epub 2002 May 09.
PMID: 12110957
Battelli L, Black KR, Wray SH. Transcranial magnetic stimulation of visual area V5 in migraine.
Neurology. 2002 Apr 9;58(7):1066-9.
PMID: 11940694
Bohotin V, Fumal A, Vandenheede M, Gerard P, Bohotin C, Maertens de Noordhout A, Schoenen J. Effects of repetitive transcranial magnetic stimulation on visual evoked potentials in migraine.
Brain. 2002 Apr;125(Pt 4):912-22.
PMID: 11912123
Mulleners WM, Chronicle EP, Vredeveld JW, Koehler PJ. Visual cortex excitability in migraine before and after valproate prophylaxis: a pilot study using TMS.
Eur J Neurol. 2002 Jan;9(1):35-40.
PMID: 11784374
Mulleners WM, Chronicle EP, Palmer JE, Koehler PJ, Vredeveld JW. Visual cortex excitability in migraine with and without aura.
Headache. 2001 Jun;41(6):565-72.
PMID: 11437892
Aurora SK, Cao Y, Bowyer SM, Welch KM. The occipital cortex is hyperexcitable in migraine: experimental evidence.
Headache. 1999 Jul-Aug;39(7):469-76.
PMID: 11279929
Mulleners WM, Chronicle EP, Palmer JE, Koehler PJ, Vredeveld JW. Suppression of perception in migraine: evidence for reduced inhibition in the visual cortex.
Neurology. 2001 Jan 23;56(2):178-83.
PMID: 11160952
Cutrer FM, O’Donnell A, Sanchez del Rio M. Functional neuroimaging: enhanced understanding of migraine pathophysiology.
Neurology. 2000;55(9 Suppl 2):S36-45. Review.
PMID: 11089518
Werhahn KJ, Wiseman K, Herzog J, Forderreuther S, Dichgans M, Straube A. Motor cortex excitability in patients with migraine with aura and hemiplegic migraine.
Cephalalgia. 2000 Feb;20(1):45-50.
PMID: 10817446
Afra J, Ambrosini A, Genicot R, Albert A, Schoenen J. Influence of colors on habituation of visual evoked potentials in patients with migraine with aura and in healthy volunteers.
Headache. 2000 Jan;40(1):36-40.
PMID: 10759901
Maertens de Noordhout A, Schoenen J. Transcranial magnetic stimulation in migraine.
Electroencephalogr Clin Neurophysiol Suppl. 1999;51:260-4. Review. No abstract available.
PMID: 10590958
Aurora SK, al-Sayeed F, Welch KM. The cortical silent period is shortened in migraine with aura.
Cephalalgia. 1999 Oct;19(8):708-12.
PMID: 10570724
Cutrer FM, O’Donnell A. Recent advances in functional neuroimaging.
Curr Opin Neurol. 1999 Jun;12(3):255-9. Review.
PMID: 10499170
Curr Opin Neurol. 2003 Jun;16(3):327-31.
The electrophysiology of migraine.
Ambrosini A, Schoenen J.
Headache Clinic, INM Neuromed, IRCCS, Pozzilli, Isernia, Italy.
PURPOSE OF REVIEW: The pathophysiology of migraine is far from being understood. Electrophysiological methods are useful to investigate peripheral and central mechanisms underlying this disorder. The purpose of this review is to highlight the results of electrophysiological studies published during the last year and to examine their added value to our previous knowledge.
RECENT FINDINGS: Studies by visual and auditory evoked potentials and event-related responses suggested that lack of habituation is the principal interictal abnormality of sensory processing in migraineurs. Recently confirmed for somatosensory and laser-evoked cortical potentials and for brainstem responses, it is also responsible for the increased intensity dependence of auditory evoked potentials. This abnormality is possibly caused by a reduced cortical preactivation level due to hypofunctioning subcortico-cortical aminergic pathways. Although studies of cortical excitability by transcranial magnetic stimulation have yielded conflicting results, results obtained using habituation of pattern-reversal visual evoked potentials to explore cortical excitability changes induced by repetitive transcranial magnetic stimulation strongly favour the hypothesis that migraine is characterized by a decreased level of preactivation excitability. With regard to pain mechanisms in migraine, electrophysiological studies of trigeminal pathways using nociceptive blink and corneal reflexes have confirmed that sensitization of central trigeminal nociceptors occurs during the attack, and may even persist interictally.
SUMMARY: Scientific publications over the last year confirmed that electrophysiological methods are particularly suited to unravelling some of the pathophysiological mechanisms of migraine. To improve their future contribution, they need to be better standardized and to be correlated with behavioural, metabolic and genetic studies.
PMID: 12858069 [PubMed – in process]
Cephalalgia. 2003;23 Suppl 1:13-31.
Electrophysiological studies in migraine: a comprehensive review of their interest and limitations.
Ambrosini A, de Noordhout AM, Sandor PS, Schoenen J.
Headache Clinic, INM Neuromed, IRCCS, Pozzilli (Isernia),Italy.
Electrophysiological methods may help to unravel some of the pathophysiological mechanisms of migraine. Lack of habituation is the principal and most reproducible interictal abnormality in sensory processing in migraineurs. It is found in evoked potential (EP) studies for every stimulation modality including nociceptive stimuli, and it is likely to be responsible for the increased intensity dependence of EP. We have hypothesized that deficient EP habituation in migraine could be due to a reduced preactivation level of sensory cortices because of hypofunctioning subcortico-cortical aminergic pathways. This is not in keeping with simple hyperexcitability of the cortex, which has been suggested by some, but not all, studies of transcranial magnetic stimulation (TMS). A recent study of the effects of repetitive TMS on visual EP strongly supports the hypothesis that migraine is characterized by interictal cortical hypoexcitability. With regard to pain mechanisms in migraine, electrophysiological studies of trigeminal pathways using nociceptive blink and corneal reflexes have confirmed that sensitization of central trigeminal nociceptors occurs during migraine attacks.
PMID: 12699456
Clin Neurophysiol. 2003 Jun;114(6):955-72.
Evoked potentials and transcranial magnetic stimulation in migraine: published data and viewpoint on their pathophysiologic significance.
Schoenen J, Ambrosini A, Sandor PS, Maertens de Noordhout A.
University Department of Neurology, CHR Citadelle, Blvd du XIIemede Ligne, 1-B-4000, Liege, Belgium. jean.schoenen[@]chrcitadelle.be
Migraine is a disorder in which central nervous sytem dysfunction might play a pivotal role. Electroneurophysiology seems thus particularly suited to study its pathophysiology. We have extensively reviewed evoked potential and transcranial magnetic stimulation studies performed in migraineurs in order to identify their pathophysiologic significance. Publications available to us were completed by a Medline search. Retrieved and personal data were compared with respect to methodology and interpreted according to present knowledge on cortical information processing. Results are in part contradictory which appears to be method-, patient- and disease- related. Nonetheless, both evoked potential and transcranial magnetic stimulation studies demonstrate that the cerebral cortex, and possibly subcortical structures, are dysfunctioning interictally in both migraine with and without aura. These electrophysiologic abnormalities tend to normalise just before and during an attack and some of them seem to have a clear familial and predisposing character. Besides the studies of magnetophosphenes which have yielded contrasting results, chiefly because the method is not sufficiently reliable, most recent electrophysiologic investigations of cortical activities in migraine favour deficient habituation and decreased preactivation cortical excitability as the predominant interictal dysfunctions. We propose that the former is a consequence of the latter and that it could favour both interictal cognitive disturbances as well as a cerebral metabolic disequilibrium that may play a role in migraine pathogenesis. To summarize, electrophysiologic studies demonstrate in migraine between attacks a cortical, and possibly subcortical, dysfunction of which the hallmark is deficient habituation.
PMID: 12804664 [PubMed – in process]
Curr Opin Neurol. 2002 Jun;15(3):303-9.
The electrophysiology of migraine.
Giffin NJ, Kaube H.
Headache Group, Institute of Neurology, Queen Square, London WC1N 3BG, UK.
Migraine is currently regarded as a neurovascular disorder of trigeminal sensory processing, generated centrally, probably at the level of the brainstem. In the past, electrophysiological techniques have drawn no definite conclusions on either interictal or ictal changes in migraineurs compared with controls, largely because of methodological differences. Recently, two findings have been shown consistently: an interictal increasing lack of habituation of evoked potentials with a normalization at the start of the attack and strong intensity dependence of auditory evoked potentials. These findings substantiate migraine sufferers as having an abnormal trait interictally, with the attack characterized by a change in the state of central processing. Exploitation of these differences may be a useful tool to study the mechanism of action of drugs used for the treatment of migraine.
PMID: 12045729
Clin Neurosci. 1998;5(1):10-7.
Cortical electrophysiology in migraine and possible pathogenetic implications.
Schoenen J.
Department of Neurology, University of Liege, CHR Citadelle, Liege, Belgium. Schoenen.J[@]innet.be
According to recent evoked potential studies a fundamental, probably protective, feature of cortical information processing, i.e., response habituation during stimulus repetition, is abnormal in migraine between attacks. The deficient habituation is found for different sensory modalities and experimental paradigms: pattern-reversal visual evoked potentials (same stimulus at a constant intensity), cortical auditory evoked potentials (same stimulus at increasing intensities), and auditory event-related potential obtained in a passive “oddball” paradigm (novel stimulus). The abnormal information processing is an interictal cortical dysfunction most likely due to inadequate control by the so-called “state-setting, chemically-addressed pathways” originating in the brain stem, in particular by the serotonergic pathway, leading to a low preactivation level of sensory cortices. We propose that it may play a pivotal role in migraine pathogenesis in conjunction with the reported decrease of brain mitochondrial energy reserve, by favouring a rupture of metabolic homeostasis and biochemical shifts capable of activating the trigeminovascular system and, thus, of producing a migraine attack. We postulate that both the deficient habituation in information processing and the deranged oxygen metabolism may have behavioral correlates. Which of these abnormalities are inherited, acquired, or both remains to be determined.
PMID: 9523052
Biomed Pharmacother. 1996;50(2):71-8.
Deficient habituation of evoked cortical potentials in migraine: a link between brain biology, behavior and trigeminovascular activation?
Schoenen J.
Department of Neurology, University of Liege, Belgium.
According to recent evoked potential studies, a fundamental, probably protective, feature of cortical information processing, ie, response habituation during stimulus repetition, is abnormal in migraine between attacks. The deficient habituation is found for different sensory modalities and experimental paradigms: pattern-reversal visual evoked potentials (same stimulus at a constant intensity), cortical auditory evoked potentials (same stimulus at increasing intensities) and auditory event-related potentials obtained in a passive “oddball” paradigm (novel stimulus). The abnormal information processing is an interictal cortical dysfunction most likely due to inadequate control by the so-called “state-setting, chemically-addressed pathways” originating in the brain stem, in particular by the serotonergic pathway, leading to a low preactivation level of sensory cortices. We suggest that it may play a pivotal role in migraine pathogenesis in conjunction with the reported decrease of brain mitochondrial energy reserve, by favouring a rupture of metabolic homeostasis and biochemical shifts capable of activating the trigeminovascular system and thus capable of producing a migraine attack. We postulate that both the deficient habituation in information processing and the deranged oxygen metabolism may have behavioral correlates. Which of these abnormalities are inherited, acquired or both remains to be determined.
PMID: 8761712
Brain. 2002 Apr;125(Pt 4):912-22.
Effects of repetitive transcranial magnetic stimulation on visual evoked potentials in migraine.
Bohotin V, Fumal A, Vandenheede M, Gerard P, Bohotin C, Maertens de Noordhout A, Schoenen J.
Department of Neurology, University of Liege, Liege, Belgium.
Between attacks, migraine patients are characterized by potentiation instead of habituation of stimulation-evoked cortical responses. It is debated whether this is due to increased or decreased cortical excitability. We have studied the changes in visual cortex excitability by recording pattern-reversal visual evoked potentials (PR-VEP) after low- and high-frequency repetitive transcranial magnetic stimulation (rTMS), known respectively for their inhibitory and excitatory effect on the cortex. In 30 patients (20 migraine without, 10 with aura) and 24 healthy volunteers, rTMS of the occipital cortex was performed with a focal figure-of-eight magnetic coil (Magstim). Nine hundred pulses were delivered randomly at 1 or 10 Hz in two separate sessions. Stimulus intensity was set to the phosphene threshold or to 110% of the motor threshold if no phosphenes were elicited. Before and after rTMS, PR-VEP were averaged sequentially in six blocks of 100zztieresponses during uninterrupted 3.1 Hz stimulation. In healthy volunteers, PR-VEP amplitude was significantly decreased in the first block after 1 Hz rTMS and the habituation normally found in successive blocks after sustained stimulation was significantly attenuated. In migraine patients, 10 Hz rTMS was followed by a significant increase of first block PR-VEP amplitude and by a reversal to normal habituation of the potentiation (or dishabituation) characteristic of the disorder. This effect was similar in both forms of migraine and lasted for at least 9 min. There were no significant changes of PR-VEP amplitudes after 1 Hz rTMS in migraineurs and after 10 Hz rTMS in healthy volunteers, nor after sham stimulation. The recovery of a normal PR-VEP habituation pattern after high-frequency rTMS is probably due to activation of the visual cortex and the dishabituation in healthy volunteers to cortical inhibition. We conclude, therefore, that the deficient interictal PR-VEP habituation in migraine is due to a reduced, and not to an increased, pre-activation excitability level of the visual cortex.
PMID: 11912123
Neurology. 1996 May;46(5):1404-9.
Intensity dependence of auditory evoked potentials is pronounced in migraine: an indication of cortical potentiation and low serotonergic neurotransmission?
Wang W, Timsit-Berthier M, Schoenen J.
Department of Neurology, University of Liege, Belgium.
Migraine is associated with stimulus hypersensitivity, increased evoked cortical responses, and abnormal 5-HT levels in peripheral blood. We studied cortical auditory evoked potentials (AEPs) between attacks in 35 patients suffering from migraine without aura (MO, n = 25) or with aura (MA, n = 10) and in 25 healthy volunteers. Binaural tones were delivered at 40, 50, 60, and 70 dB sensation level (SL) in a pseudorandomized order. The intensity dependence of the auditory N1-P2 component was significantly greater in MO (p = 0.003) and MA (p = 0.02) patients than in healthy controls, resulting in a much steeper amplitude/stimulus intensity function slope. When three sequential blocks of 40 averaged responses were analyzed at the 40- and 70-dB SL intensities, N1-P2 amplitude decreased in second and third blocks at both intensities in controls, but increased in migraineurs, a difference that was significant in both blocks for the 70-dB SL stimulus. The strong interictal dependence of AEPs on stimulus intensity may thus be due to potentiation (instead of habituation) of the response during repetition of the high-intensity stimulation. In concordance with previous studies of visual evoked potentials, these results confirm that migraine is characterized between attacks by an abnormality of cortical information processing, which might be a consequence of low 5-HT transmission and favor cortical energy demands.
PMID: 8628490
Cephalalgia. 1985 May;5 Suppl 2:53-8.
Visual evoked potentials and brainstem auditory evoked potentials in migraine and transient ischemic attacks.
Benna P, Bianco C, Costa P, Piazza D, Bergamasco B.
A study of brainstem auditory evoked potentials (BAEPs) and pattern reversal visual evoked potentials (VEPs), recorded in intercritical phase, was carried out in 20 subjects (10 suffering from common migraine and 10 suffering from vertebrobasilar TIA) in order to obtain a comparative evaluation of cortical-subcortical functions. The data we obtained demonstrate the presence of BAEPs alterations in patients with previous vertebrobasilar TIA: no abnormalities were found in the migraine group. VEPs parameters are normal in both groups. Our data show that the study of the so-called “stimulus-related” potentials, such as BAEPs and pattern reversal VEPs, is useful in evaluating the damage produced by any noxa, while it cannot clearly emphasize individual factors predisposing to a specific pathology, as the absence of specific alterations in migraine patients demonstrates.
PMID: 4016942
Ann Neurol. 1998 Aug;44(2):209-15.
Interictal cortical excitability in migraine: a study using transcranial magnetic stimulation of motor and visual cortices.
Afra J, Mascia A, Gerard P, Maertens de Noordhout A, Schoenen J.
Department of Neurology, CHR Citadelle, University of Liege, Belgium.
We performed transcranial magnetic stimulations of the motor and visual cortices in healthy controls (n = 27) and in patients suffering from migraine without (n = 33) or with (n = 25) aura between attacks. By using a 13-cm circular coil placed over the vertex and recordings of the first dorsal interosseus muscle, we measured thresholds (at rest and during contraction), amplitudes of motor evoked potentials and cortical silent periods. Paired stimulations with short (1-20 msec) interstimulus intervals were performed to assess intracortical inhibition. The visual cortex was stimulated with the same coil placed over the occipital scalp (7 cm above the inion) and the prevalence and threshold of phosphene production was determined. In patients with migraine with aura, motor thresholds during isometric contraction were significantly higher, whereas the prevalence of stimulation-induced phosphene production was lower compared with healthy controls. These changes were not correlated with attack frequency or disease duration. No differences were found between subject groups in thresholds at rest, motor evoked potential amplitudes, cortical silent periods, or response curves after paired stimuli. These results are in favor of cortical hypoexcitability rather than hyperexcitability in patients with migraine with aura between attacks.
PMID: 9708543
Neurology. 2002 Apr 9;58(7):1066-9.
Transcranial magnetic stimulation of visual area V5 in migraine.
Battelli L, Black KR, Wray SH.
Department of Psychology, Harvard University, Cambridge, MA 02138, USA. Battelli[@]wjh.harvard.edu
OBJECTIVE: To examine visual cortical excitability in persons with migraine using transcranial magnetic stimulation (TMS) over an extrastriate area of the brain, area V5.
BACKGROUND: Previous studies found that persons with migraine have a lower phosphene threshold than healthy control subjects with TMS delivered over the primary visual cortical area V1. The result suggests that the occipital cortex in migraineurs between migraine attacks is hyperexcitable. However, it is not known whether interictal cortical hyperexcitability is also present in areas of the association visual cortex.
METHOD: To investigate this, single-pulse TMS was delivered over visual area V5, the motion cortex, to 16 persons with migraine and visual aura, nine migraineurs without visual aura, and 16 healthy control subjects. TMS was delivered at intensities ranging from 30 to 100% of maximum stimulator output or until the participant reported seeing phosphenes (visual illusions characterized by flashes of light). Thresholds to phosphenes were obtained for each participant using a staircase procedure.
RESULT: Significantly lower phosphene thresholds for TMS delivered over V5 were found in migraineurs as compared with control subjects. Qualitatively, the migraineurs’ experience of phosphenes were more vivid, florid, and sustained compared with that of control subjects.
CONCLUSION: Results of this study indicate that hyperexcitability of the visual cortex in migraine goes beyond visual area V1 and demonstrates for the first time a significant difference in threshold for excitability of visual area V5 in persons with migraine.
PMID: 11940694
Exp Brain Res. 2003 Jun;150(3):332-40. Epub 2003 Apr 16.
Effects of repetitive transcranial magnetic stimulation on visual evoked potentials: new insights in healthy subjects.
Fumal A, Bohotin V, Vandenheede M, Seidel L, de Pasqua V, de Noordhout AM, Schoenen J.
University Department of Neurology, CHR Citadelle Hospital, 4000 Liege, Belgium.
In a previous comparative study with migraineurs, we found in 24 normal subjects that the amplitude of the pattern-reversal visual evoked potential (PR-VEP) in the first block of 100 responses and its habituation over 6 sequential blocks were significantly decreased after 1 Hz repetitive transcranial magnetic stimulation (rTMS), while 10 Hz rTMS had no significant effect. We report here our results on the reproducibility of the rTMS effect studied in ten of these subjects by repeating the recordings for each frequency three times on different days. We have also reanalysed the data obtained in 24 normal subjects, looking separately at the results in those stimulated at an intensity equal to phosphene threshold (group 1; n=14) and those stimulated at 110% of motor threshold because of unelicitable phosphenes (group 2; n=10). We finally determined the precise duration of the rTMS effect. Despite some interindividual variability, the effects of both rTMS frequencies on first block amplitude, habituation between first and sixth block and habituation slope over the six blocks were highly reproducible. The only difference between the two groups of subjects was the effect of 1 Hz rTMS on the second measured PR-VEP component. Whereas first block amplitude of the first P1-N1 component and habituation were decreased in both groups, such a decrease was found for the second P1-N2 component only in group 1 stimulated at phosphene threshold. The dishabituation of the N1-P1 component after 1 Hz rTMS was maximal at 15 min, but lasted up to 33 min, while that of P1-N2 disappeared after 3 min. There was a non-significant trend ( p=0.06) for a reduction of first block amplitude after 10 Hz rTMS in the total group of subjects, but no effect on habituation. The inhibitory effect of 1 Hz rTMS, which reduces in healthy controls both first block PR-VEP amplitude and habituation, probably by decreasing the preactivation excitability level of the underlying visual cortex, is thus reproducible and long lasting. Long trains of 10 Hz rTMS tend to attenuate reproducibly the cortical preactivation level in normal subjects, but they do not affect habituation at all, which contrasts with their effect in migraineurs, in whom, as previously reported, they significantly correct the habituation deficit. The absence of an effect of 1 Hz rTMS on PR-VEP P1-N2 in subjects stimulated at 110% of motor threshold may be explained by the deeper anatomical location of the cortical generators of this component and the lower stimulation intensity used. Taken together our results confirm that the effect of rTMS on the underlying cortex depends on several variables such as frequency, intensity and level of cortical preactivation.
PMID: 12698314 [PubMed – in process]
Headache. 2003 Mar;43(3):303.
Modulation of trigeminal reflex excitability in migraine: effects of attention and habituation on the blink reflex.
De Tommaso M, Murasecco D, Libro G, Guido M, Sciruicchio V, Specchio L, Gallai V, Puca F.
Int J Psychophysiol. 2002 Jun;44(3):239-249
The modulation of trigeminal reflex excitability in migraine patients was evaluated during the asymptomatic phase by studying the effects of attention, habituation and preconditioning stimulus on the R2 and R3 components of the blink reflex (BR). Fifty patients suffering from migraine without aura, 20 affected by migraine with aura and 35 sex- and age-matched controls were selected. In subgroups of migraine with-aura and without-aura patients, and normal controls, the blink reflex was elicited during different cognitive situations: (a) spontaneous mental activity; (b) stimulus anticipation; (c) recognition of target numbers. In the remaining subjects, R2 and R3 habituation was evaluated by repetitive stimulation at 1, 5, 10, 15, 20, 25 and 30 s intervals. The R2 and R3 recovery curves were also computed. A reduced R3 threshold with a normal pain threshold was found in migraine with-aura and without-aura patients; the R3 component was not significantly correlated with the pain thresholds in patients and controls. The R2 and R3 components were less influenced by the warning of the stimulus in migraine without-aura and migraine with-aura patients, in comparison with the control group. A slight increase of both R2 and R3 recovery after preconditioning stimulus was also observed in migraine patients, probably caused by a phenomenon of trigeminal hyperexcitability persisting after the last attack. The abnormal BR modulation by alerting expresses in migraine a dysfunction of adaptation capacity to environmental conditions, probably predisposing to migraine. Comment: Further physiologic and functional evidence for the interictal hyperexcitability of neurons in patients with migraine, in this case trigeminal neurons involved in the blink reflex. SJT
PMID: 12603665 [PubMed – as supplied by publisher]
Curr Opin Neurol. 1998 Jun;11(3):205-9.
Brain excitability in migraine: evidence from transcranial magnetic stimulation studies.
Aurora SK, Welch KM.
Henry Ford Hospital and Health Sciences Center, Department of Neurology, Detroit, Michigan, USA.
Central neuronal hyperexcitability is proposed to be the putative basis for the physiologic disturbances in migraine. Because there are no structural disturbances in migraine, only physiologic studies can provide insight into the underlying mechanisms. Recently, transcranial magnetic stimulation has been developed as a valuable research tool and can be used to study brain function noninvasively. This article is a review of the studies done in migraine using transcranial magnetic stimulation.
PMID: 9642537
No To Shinkei. 1998 Apr;50(4):361-5.
[Superficial siderosis of the central nervous system: an electrophysiological study]
[Article in Japanese]
Shimo Y, Nohara C, Hotta M, Miwa H, Mizuno Y.
Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
Superficial siderosis of the central nervous system (SS) is a rare neurological disorder characterized by symptoms such as neurosensory hearing loss, ataxic gait, and spastic paraparesis. Recently, magnetic resonance imaging (MRI) enables us to make a clinical diagnosis. However, the exact pathophysiological mechanism underlying this disorder remains uncertain. Although iron chelation therapy has been attempted experimentally, it has not been successful and there is no effective medical treatment available. Towards the better understanding of the pathophysiological mechanism underlying SS, we performed electrophysiological studies, in which multiple evoked potential studies were included, in 3 patients with SS. Somatosensory evoked potentials (SEPs) evoked by median nerve stimulation were all normal, but those evoked by the posterior tibial nerve stimulation showed a significant delay of the latency of P40. In the auditory brainstem response (ABR) studies, there were no reproducible responses of the brainstem origin. In the blink reflex studies, R2 latency was delayed in one patient. In visual evoked potential (VEP) studies, the latency of P100 was delayed in two of three patients, unless all the patients clinically showed no visual symptom. The nerve conduction velocity studies performed in peripheral nerves of upper and lower extremities were all normal. The abnormal findings of ABR and SEP may suggest that the acoustic nerve and the posterior funiculus of the spinal cord are involved, respectively. These findings are also in a good agreement with pathological findings of SS reported in the literature. In SS, the hemosiderine accumulation is usually less severe in the visual tract; however, the delay of VEPs may suggest the latent dysfunctioning of the visual system in SS. It is suggested that multiple evoked potential study is useful for clinical evaluation of SS.
PMID: 9592826
J Neurol. 2002 Sep;249(9):1268-71.
Comparison of cortical excitability in chronic migraine (transformed migraine) and migraine without aura. A transcranial magnetic stimulation study.
Ozturk V, Cakmur R, Donmez B, Yener GG, Kursad F, Idiman F.
Dokuz Eylul University, Medical School, Department of Neurology, 35340, Izmir, Turkey. vesile.ozturk[@]deu.edu.tr
We studied the excitability of the motor cortex in patients with migraine without aura (MWOA) (n = 20) and with chronic migraine (CM) (n = 20) using transcranial magnetic stimulation (TMS). By using a 90-mm circular coil placed over the vertex and recording of the first dorsal interosseous muscle, we measured thresholds, latencies and amplitudes of motor evoked potentials and duration of cortical silent periods in patient groups and in controls (n = 20). No differences were found between groups for threshold, latency and amplitude values. However, the duration of the cortical silent period was longer in CM patients, being significantly different from both controls and MWOA. We suggest that either this difference in cortical excitability may develop during transformation from MWOA to CM or different pathophysiological mechanisms may play a role in these two headache syndromes.
PMID: 12242552
Neurology. 1997 May;48(5):1462-4.
Interictal cortical excitability to magnetic stimulation in familial hemiplegic migraine.
van der Kamp W, MaassenVanDenBrink A, Ferrari MD, van Dijk JG.
Department of Neurology and Clinical Neurophysiology, Leiden University Hospital, the Netherlands.
We studied interictal cortical excitability with magnetic stimulation in controls, in patients with migraine with aura, and in patients with familial hemiplegic migraine (FHM), in which ictal hemiparesis occurs. Amplitudes (p < 0.05) and amplitude ratios (p < 0.01) revealed heightened excitability in migraine with aura when compared to controls. In patients with FHM, mean thresholds were higher (p < 0.001) and conduction times longer (p < 0.01) than in controls. In FHM, amplitudes were lower on the ictally paretic side of the body than on the other (p < 0.05). Patients with FHM may have increased interictal cortical excitability, complicated by decreased excitability of the affected side.
PMID: 9153495
Can J Neurol Sci. 1999 Nov;26 Suppl 3:S12-9.
Pathophysiology of migraine–new insights.
Hargreaves RJ, Shepheard SL.
Merck Research Laboratories, West Point PA 9486, USA.
Current theories propose that the primary dysfunction in migraine occurs within the CNS and that this evokes changes in blood vessels within pain-producing intracranial meningeal structures that give rise to headache pain. Migraine is now thought of as a neurovascular disorder. It has been proposed that genetic abnormalities may be responsible for altering the response threshold to migraine specific trigger factors in the brain of a migraineur compared to a normal individual. The exact nature of the central dysfunction that is produced in migraineurs is still not clear and may involve spreading depression-like phenomena and activation of brain stem monoaminergic nuclei that are part of the central autonomic, vascular and pain control centers. It is generally thought that local vasodilatation of intracranial extracerebral blood vessels and a consequent stimulation of surrounding trigeminal sensory nervous pain pathways is a key mechanism underlying the generation of headache pain associated with migraine. This activation of the ‘trigeminovascular system’ is thought to cause the release of vasoactive sensory neuropeptides, especially CGRP, that increase the pain response. The activated trigeminal nerves convey nociceptive information to central neurons in the brain stem trigeminal sensory nuclei that in turn relay the pain signals to higher centers where headache pain is perceived. It has been hypothesized that these central neurons may become sensitized as a migraine attack progresses. The ‘triptan’ anti-migraine agents (e.g. sumatriptan, rizatriptan, zolmitriptan naratriptan) are serotonergic agonists that have been shown to act selectively by causing vasoconstriction through 5-HT1B receptors that are expressed in human intracranial arteries and by inhibiting nociceptive transmission through an action at 5-HT1D receptors on peripheral trigeminal sensory nerve terminals in the meninges and central terminals in brain stem sensory nuclei. These three complementary sites of action underlie the clinical effectiveness of the 5-HT1B/1D agonists against migraine headache pain and its associated symptoms.
PMID: 10563228
Neurology. 2002 Apr 23;58(8):1234-8.
Acute migraine headache: possible sensitization of neurons in the spinal trigeminal nucleus?
Kaube H, Katsarava Z, Przywara S, Drepper J, Ellrich J, Diener HC.
Institute of Neurology, National Hospital for Neurology and Neurosurgery, London, UK. holgerk[@]ion.ucl.ac.uk
Headache. 1992 Jul;32(7):345-7.
Menstrual migraine without aura: cortical excitability to magnetic stimulation.
Bettucci D, Cantello R, Gianelli M, Naldi P, Mutani R.
Department of Neurology, University School of Medicine of Novara, Italy.
The purpose of the present study was the evaluation of the excitability threshold and the central motor conduction time (CCT) studied by means of electromagnetic cortical stimulation in ten subjects affected by menstrual migraine without aura, both in the ictal and the interictal period. The patients were chosen from among a group of 254 outpatients affected by migraine, diagnosed according to the International Headache Society criteria. The control group consisted of ten healthy female subjects. As far as CCTs were concerned no differences emerged between patients and controls. However in the patient group we found a significant increase in the excitability threshold values, both in the ictal and the interictal period, and in both hemispheres. If confirmed, the increased excitability threshold may be a useful neurophysiological correlate of migraine without aura.
PMID: 1526765
Brain Res Cogn Brain Res. 2003 May;16(3):488-91.
Reductions in CI amplitude after repetitive transcranial magnetic stimulation (rTMS) over the striate cortex.
Schutter DJ, van Honk J.
Affective Neuroscience Section, Helmholtz Research Institute, Utrecht University, Heidelberglaan 2, 3584 CS Utrecht, The Netherlands. d.schutter[@]fss.uu.nl
Slow repetitive transcranial magnetic stimulation (rTMS) is a method capable of transiently inhibiting cortical excitability and disrupting information processing in the visual system. This method can be used to topographically map the functional contribution of different cortical brain areas in visual processing. An early electrophysiological component, the CI is argued to reflect early visual processing. In addition, source-localization studies have provided evidence for the assumption that the striate cortex is the underlying neural generator of CI. In the present placebo-controlled, crossover study, slow rTMS was applied in order to further investigate the relationship between the striate cortex and the CI component. Based on the inhibitory effects of slow rTMS, a reduction in CI amplitude and an increase in latency were expected. Compared to placebo stimulation, slow rTMS over the striate cortex resulted in significant decreases of the CI amplitude, but did not affect latency. The present study provides causal evidence for the involvement of the striate cortex in generating the CI component.
PMID: 12706228
Headache. 1997 Jun;37(6):383-5.
Visual evoked potentials and serum magnesium levels in juvenile migraine patients.
Aloisi P, Marrelli A, Porto C, Tozzi E, Cerone G.
Servizio di Neurofisiopatologia, University of L’Aquila, Italy.
Changes in visual evoked potentials and decreased intracellular magnesium levels have been separately described in patients affected by migraine both during the attacks and in the interictal periods. An inverse correlation between increased P100 amplitude and lowered serum magnesium levels was found in children suffering from migraine with and without aura in a headache-free period. A 20-day treatment with oral magnesium pidolate seemed to normalize the magnesium balance in 90% of patients. After treatment, the reduced P100 amplitude confirmed the inverse correlation with the serum magnesium level. These data seem to suggest the hypothesis that higher visual evoked potential amplitude and low brain magnesium level can both be an expression of neuronal hyperexcitability of the visual pathways related to a lowered threshold for migraine attacks.
PMID: 9237412

End pulsed electromagnetic field therapy for migraine headache bibliography