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| | Episodic migraine (EM) | Chronic migraine (CM) |
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| Electrophysiology | | |
| VEP | Lack of habituation and peri-ictal normalization [14] | No specific study |
| MEG | Peri-ictal normalization of visual cortical excitability, reflecting a dynamic modulation of cortical activities [15] | Persistent ictal-like visual cortex excitability [16]; in patients who remitted from CM to EM, the MEG pattern shifted to that characterizing EM between attacks, that is, decreased initial amplitude with subsequent deficient habituation [17] |
| TMS | Hyperexcitability measured by TMS indices of phosphene thresholds and magnetic suppression of perceptual accuracy [18] | Reduced visual suppression correlating with high cortical excitability [18, 19] |
| SSEP | Abnormal habituation during interictal period and central sensitization (increase of N20-P25 amplitude) during ictal period [14] | Increase of N20-P25 amplitudes recorded interictally in patients with CM compared with in patients with EM, indicating excessive cortical activation of the somatosensory pathway [20] |
| BAEP | Lack of habituation of wave IV-V, especially with symptomatic vertigo [14] | No specific study |
| LEP | Lack of habituation of N1 (generated by secondary somatosensory cortex) and N2-P2 (generated by ACC and insula) during interictal and ictal periods
Sensitization represented by increased N2-P2 amplitude in the ipsilateral headache side during ictal period [14] | Increase of amplitudes and rostral shift within ACC in patients with CM, similar to EM patients in the ictal period [21, 22] |
|
| Neuroimaging | | |
| Functional | | |
| PET | Activation of certain brain areas during ictal period indicating the involvement of specific brain areas associated with various symptoms in migraine including photophobia, nausea, and vertigo [23–26]
Ligand PET: changes of serotonin and opioid receptors and activities, indicating possible roles these neurotransmitters play and related neural plasticity associated with migraine [27, 28] | Increased cerebral metabolism at brainstem compared to the global flow and also decreased cerebral metabolism in the medial frontal, parietal, and somatosensory cortex, indicating a potential dysfunction in the inhibitory pathways [19] |
| fMRI | Greater activation of pain-matrix areas and less activation of pain inhibition areas [29] | No specific study |
| rs-fMRI | Aberrant functional connectivity mostly in pain-matrix and also involving different networks including salience, default mode, central-executive, somatomotor, and frontoparietal attention networks [29] | Aberrant functional connectivity in affective pain regions including anterior insula, amygdala, pulvinar, mediodorsal thalamus, middle temporal cortex, and periaqueductal gray [30] |
| Structural | | |
| VBM | Decrease of gay matter volume of multiple brain areas within pain-matrix [31–37] | No specific study; only two studies recruited small numbers of CM patients (11 and 3 patients each) without definite conclusions [33, 35] |
| SBM | Increase thickness of the somatosensory cortex and visual motion areas [38, 39]; no changes [40]; thickness of somatosensory cortex decrease in low frequency (1-2 days/month) and increase in high frequency (8–14 days/month) [41]; mixed results of increase and decrease of cortical thickness in other brain areas [42, 43] | No specific study |
| DTI | Changes of white matter microstructures in areas such as corpus callosum and cingulate gyrus [36, 44–50]
Dynamic alteration of fractional anisotropy noted at thalami, in relation with peri-ictal/ictal status [51] | No changes in one study recruiting both CM and EM patients [52] |
| Biochemical | | |
| MRS | Higher NAA/Cr ratio at dorsal pons, indicating possible neuronal hypertrophy; inverse correlation with headache frequency and intensity [53]
Changes of the excitatory glutamate in the ACC and insula, indicating [54] | Lower NAA/Cr as compared with EM with inverse correlation with headache frequency and intensity, indicating possible progression of neuronal loss during evolution [53] |
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