Evoked potentials and transcranial magnetic stimulation in migraine: published data and viewpoint on their pathophysiologic significance

Schoenen, Jean; Ambrosini, Anna; Sándor, Péter; Noordhout, Alain Maertens De

doi:10.1016/s1388-2457(03)00024-5

Cited by 182 publications

(190 citation statements)

References 144 publications

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“…The well-established genetic basis of some familial hemiplegic migraine phenotypes has provided a unique opportunity for studies of the cellular migraine mechanisms (Tottene et al, 2009). The cortex of migraineurs is believed to be hyperexcitable due to impaired habituation, which may explain the increased vulnerability to CSD in these patients (Schoenen et al, 2003). Likewise, the basic pathology of CSD is an increase in excitability of cortical neurons, which is brought about by the cooperative action of persistent Na + currents plus NMDA receptor-controlled currents.…”

Section: Migrainementioning

confidence: 99%

Clinical Relevance of Cortical Spreading Depression in Neurological Disorders: Migraine, Malignant Stroke, Subarachnoid and Intracranial Hemorrhage, and Traumatic Brain Injury

Lauritzen

Dreier

Fabricius

et al. 2010

J Cereb Blood Flow Metab

652

547

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Cortical spreading depression (CSD) and depolarization waves are associated with dramatic failure of brain ion homeostasis, efflux of excitatory amino acids from nerve cells, increased energy metabolism and changes in cerebral blood flow (CBF). There is strong clinical and experimental evidence to suggest that CSD is involved in the mechanism of migraine, stroke, subarachnoid hemorrhage and traumatic brain injury. The implications of these findings are widespread and suggest that intrinsic brain mechanisms have the potential to worsen the outcome of cerebrovascular episodes or brain trauma. The consequences of these intrinsic mechanisms are intimately linked to the composition of the brain extracellular microenvironment and to the level of brain perfusion and in consequence brain energy supply. This paper summarizes the evidence provided by novel invasive techniques, which implicates CSD as a pathophysiological mechanism for this group of acute neurological disorders. The findings have implications for monitoring and treatment of patients with acute brain disorders in the intensive care unit. Drawing on the large body of experimental findings from animal studies of CSD obtained during decades we suggest treatment strategies, which may be used to prevent or attenuate secondary neuronal damage in acutely injured human brain cortex caused by depolarization waves.

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Section: Migrainementioning

confidence: 99%

Clinical Relevance of Cortical Spreading Depression in Neurological Disorders: Migraine, Malignant Stroke, Subarachnoid and Intracranial Hemorrhage, and Traumatic Brain Injury

Lauritzen

Dreier

Fabricius

et al. 2010

J Cereb Blood Flow Metab

652

547

View full text Add to dashboard Cite

show abstract

“…Once considered solely a vascular event, current research supports a combination of both neural and vascular causes [16][17][18][19][20]. Many studies report the biochemical reaction and clinical effects of medications in migraine [21].…”

Section: Introductionmentioning

confidence: 97%

Transcranial magnetic stimulation for migraine: clinical effects

et al. 2006

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The objective was to assess the impact of transcranial magnetic stimulation (TMS) on pain and the autonomic nervous system (ANS) in migraine. Fortytwo people [mean age 41.43±11.69 (SD) years, 36 females] were randomised into high vs. low TMS stimulation groups and received 2 brief pulses of TMS. Thirty-three (33/42) individuals had heart-rate variability assessed, before and after stimulation. No group effects were found. Pain decreased by 75%; 32% of people after 1 treatment reported no headache after 24 h. Mean heart rate decreased from 79.05±10.27 to 72.89±11.35 beats/min. The low-frequency (LF) and the high-frequency (HF) areas derived from power spectral analyses increased [mean 6522±1277 to 8315±1009 beats/min 2 (LF) (p=0.001) and mean 5600±1568 to 8755±3071 beats/min 2 (HF) (p=0.001)]. The LF:HF ratio decreased from mean 1.31±0.51 to 1.13±0.48 (NS). TMS produces immediate, sustained reductions in pain and modification of the ANS.

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“…1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 We included patients without taking into account the period in their migraine cycle. Reactivity of the cerebral cortex, as explored by evoked potentials, was shown to vary with the migraine cycle [20]. However, there seems to be no significant variation of steady state visual EEG evoked-responses (SSVEPs) in the medium frequencies range (15-30 Hz) over the migraine cycle [7,12,21].…”

Section: Discussionmentioning

confidence: 99%

“…PD power was also significantly superior in episodic migraine as compared to chronic migraine. This could be related to the changes in visual cortex responsiveness over the migraine cycle [20,22] and between episodic and chronic migraine [23]. For instance, during stimulus repetition, EEG and magnetoencephalographic visual evoked responses lack habituation in episodic migraine between attacks, but habituate normally during attacks and in chronic migraine [24,25,26].…”

Section: Discussionmentioning

confidence: 99%

Analysis and clinical correlates of 20 Hz photic driving on routine EEG in migraine

et al. 2014

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Abstract:Enhanced photic driving (PD) during high frequency flicker stimulation, the so-called H response, is a classical feature of migraine patients between attacks, but is thought to be of poor clinical utility. Visual inspection of the EEG for its detection may not be reliable, however, and data on its possible correlations with clinical features and migraine pathophysiology are scarce.We have compared visual inspection and EEG spectral analysis to detect abnormal PD in 280 consecutive migraine patients of our headache clinic (episodic migraine without aura, n=171; chronic migraine, n=48; migraine with aura, n=61) and in a group of 24 non-migrainous neurological controls. Spectral frequency analyses were performed blindly by one of us (YF). On visual inspection, 50.4% of migraineurs were thought to have increased 20Hz PD. After spectral analysis, only 62.4% of them had PD power superior to the mean+95%CI of the control group. Sensitivity of visually identified PD was 82.24%, specificity 69.36%. Increased PD on spectral analysis was more prevalent in episodic migraine than in chronic migraine, in patients with low attack frequency, in those with ictal autonomic symptoms in addition to nausea and in those with a strong family history of migraine. We confirm therefore that 20Hz photic driving is of little diagnostic utility and its prevalence in migraine overestimated on visual inspection. Its presence on spectral analysis of the EEG, however, might be of pathophysiological interest, as it identifies subgroups of migraineurs of whom the common denominator could be lack of habituation of cortical responses during repetitive stimulation. We have compared visual inspection and EEG spectral analysis to detect abnormal PD in 280 consecutive migraine patients of our headache clinic (episodic migraine without aura, n=171; chronic migraine, n=48; migraine with aura, n=61) and in a group of 24 non-migrainous neurological controls. Spectral frequency analyses were performed blindly by one of us (YF).On visual inspection, 50.4% of migraineurs were thought to have increased 20Hz PD. After spectral analysis, only 62.4% of them had PD power superior to the mean+95%CI of the control group. Sensitivity of visually identified PD was 82.24%, specificity 69.36%.Increased PD on spectral analysis was more prevalent in episodic migraine than in chronic migraine, in patients with low attack frequency, in those with ictal autonomic symptoms in addition to nausea and in those with a strong family history of migraine.We confirm therefore that 20Hz photic driving is of little diagnostic utility and its prevalence in migraine overestimated on visual inspection. Its presence on spectral analysis of the EEG, however, might be of pathophysiological interest, as it identifies subgroups of migraineurs of whom the common denominator could be lack of habituation of cortical responses during repetitive stimulation.

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Evoked potentials and transcranial magnetic stimulation in migraine: published data and viewpoint on their pathophysiologic significance

Cited by 182 publications

References 144 publications

Clinical Relevance of Cortical Spreading Depression in Neurological Disorders: Migraine, Malignant Stroke, Subarachnoid and Intracranial Hemorrhage, and Traumatic Brain Injury

Clinical Relevance of Cortical Spreading Depression in Neurological Disorders: Migraine, Malignant Stroke, Subarachnoid and Intracranial Hemorrhage, and Traumatic Brain Injury

Transcranial magnetic stimulation for migraine: clinical effects

Analysis and clinical correlates of 20 Hz photic driving on routine EEG in migraine

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