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Background: Myofascial trigger points (MTrPs) present with mechanical hyperalgesia and allodynia. No etectro- physiological evidence exists as to the excitability of muscle spindle afferents at myofascial trigger points MTrPs. The purpose of this current study was to explore whether an H-reflex response could be elicited from intramuscular electrical stimulation. If so, to assess the possibility of increased reflex response at MTrPs. Methods: The H-reflex latency and the conduction velocity were first determined from electrical stimulation of the tibial nerve in 13 healthy subjects. Then an intramuscular monopolar needle electrode was inserted randomly into a latent MTrP or a non-MTrP in the gastrocnemius muscle. Electrical stimuli at different intensities were delivered via the intramuscular recording electrode to the MTrP or non-MTrP. Results: The average conduction velocity (44.3 ± 1.5 mIs) of the electrical stimulation of tibial nerve was similar (p>0.05) with the conduction velocity (43.9 ± 1.4 m/s) of intramuscular electrical stimulation. The intramuscular H-reflex at MTrPs was higher in amplitude than non-MTrPs (p<0.001). The reflex threshold was lower for.MTrPs than non-MTrPs (p<0.001). Conclusion: The current study provides first electrophysiological evidence that intramuscular electrical stimulation can evoke H-reflex, and that higher H-reflex amplitude and lower H-reflex threshold exist at MTrPs than non-MTrPs respectively, suggesting that muscle spindle afferents may be involved in the pathophysiology of MTrPs. [ABSTRACT FROM AUTHOR]

Cluster headache (CH) is one of the most severe forms of headache, but the number of effective treatments is still limited. Recently, we reported the case of a drug-resistant CH patient responsive to the rotigotine transdermal patch, which is used in the treatment of Parkinson's disease. This report formed the basis for a case series where other drug-resistant CH patients were treated with rotigotine. Here are the results of this study. Twenty-two CH patients underwent the treatment. Eight were episodic cluster headache (ECH) patients and 14 were chronic cluster headache (CCH) patients. Of the eight ECH patients, four reported that their CH had been stopped by the treatment. Of the 14 CCH patients, 11 were considered responders to the treatment (5 experienced a full resolution of headache, and 6 had a headache reduction of at least 50% in terms of mean monthly number of attacks). Our case series confirms the previous observation that rotigotine could be helpful in the treatment of CH. It may even influence the monoaminergic system that has a key role in the pathogenesis of CH. [ABSTRACT FROM AUTHOR]

Background: It is unclear whether cortical hyperexcitability in chronic migraine with medication overuse headache (CM-MOH) is due to increased thalamocortical drive or aberrant cortical inhibitory mechanisms. Methods: Somatosensory evoked potentials (SSEP) were performed by electrical stimulation of the median nerve (M), ulnar nerve (U) and simultaneous stimulation of both nerves (MU) in 27 patients with CM-MOH and, for comparison, in 23 healthy volunteers (HVs) of a comparable age distribution. We calculated the degree of cortical lateral inhibition using the formula: 100 – [MU/(M + U) × 100] and the level of thalamocortical activation by analyzing the high frequency oscillations (HFOs) embedded in parietal N20 median SSEPs. Results: Compared to HV, CM-MOH patients showed higher lateral inhibition (CM-MOH 52.2% ± 15.4 vs. HV 40.4% ± 13.3; p = 0.005), which positively correlated with monthly headache days, and greater amplitude of pre-synaptic HFOs (p = 0.010) but normal post-synaptic HFOs (p = 0.122). Conclusion: Our findings suggest that central neuronal circuits are highly sensitized in CM-MOH patients, at both thalamocortical and cortical levels. The observed changes could be due to the combination of dysfunctional central pain control mechanisms, hypersensitivity and hyperresponsiveness directly linked to the chronic intake of acute migraine drugs. [ABSTRACT FROM AUTHOR]

Background Migraine is the most prevalent neurological disorder worldwide and ranked sixth among all diseases in years lived with disability. Overall preventive anti-migraine therapies have an effect in one patient out of two at the most, many of them being endowed with disabling adverse effects. No new disease-modifying drugs have come into clinical practice since the application to migraine of topiramate and botulinum toxin, the latter for its chronic form. There is thus clearly a need for more effective treatments that are devoid of, or have acceptable side effects. In recent years, scientific progress in migraine research has led to substantial changes in our understanding of the pathophysiology of migraine and paved the way for novel non-drug pathophysiological-targeted treatment strategies. Overview Several such non-drug therapies have been tested in migraine, such as oxidative phosphorylation enhancers, diets and non-invasive central or peripheral neurostimulation. All of them are promising for preventive migraine treatment and are quasi-devoid of side effects. Their advantage is that they can in theory be selected for individual patients according to their pathophysiological profile and they can (and probably should) be combined with the classical pharmacological armamentarium. Conclusion We will review here how knowledge of the functional anatomy and physiology of migraine mechanisms holds the key for more specific and effective non-pharmacological treatments. [ABSTRACT FROM AUTHOR]

Objectives: It is unclear whether the electrophysiological effects of erenumab, a monoclonal antibody against the calcitonin gene-related peptide receptor, occur only at the periphery of the trigeminal system or centrally and at the cortical level. Methods: We prospectively enrolled 20 patients with migraine who had failed at least two preventative treatments. We measured the nociceptive blink reflex and non-noxious somatosensory evoked potentials in all participants. The area under the curve and habituation of the second polysynaptic nociceptive blink reflex component (R2) as well as the amplitude and habituation of somatosensory evoked potentials N20-P25 were measured. Electrophysiological data were collected at baseline (T0), 28 days (T1), and 56 days (T2) before each injection of erenumab (70 mg). Results: Erenumab reduced the patients' mean monthly headache days, headache intensity, and acute medication intake considerably at T1 and T2 (all p < 0.05). The nociceptive blink reflex area under the curve was considerably lower at T1 and T2 than at baseline without changing the habituation slope. At T2, there was a significant increase in the delayed somatosensory evoked potentials amplitude reduction (habituation) but not in the initial cortical activation. Conclusion: Our findings showed that erenumab, in addition to its well-known peripheral effects, can induce central effects earlier in the brainstem and later in the cortex. We cannot rule out whether these results are due to a direct effect of erenumab on the central nervous system or an indirect effect secondary to peripheral drug modulation. [ABSTRACT FROM AUTHOR]

Background: Merging of sensory information is a crucial process for adapting the behaviour to the environment in all species. It is not known if this multisensory integration might be dysfunctioning interictally in migraine without aura, where sensory stimuli of various modalities are processed abnormally when delivered separately. To investigate this question, we compared the effects of a concomitant visual stimulation on conventional low-frequency somatosensory evoked potentials and embedded high-frequency oscillations between migraine patients and healthy volunteers. Methods: We recorded somatosensory evoked potentials in 19 healthy volunteers and in 19 interictal migraine without aura patients before, during, and 5 min after (T2) simultaneous synchronous pattern-reversal visual stimulation. At each time point, we measured amplitude and habituation of the N20-P25 low-frequency-somatosensory evoked potentials component and maximal peak-to-peak amplitude of early and late bursts of high-frequency oscillations. Results: In healthy volunteers, the bimodal stimulation significantly reduced low-frequency-somatosensory evoked potentials habituation and tended to reduce early high-frequency oscillations that reflect thalamocortical activity. By contrast, in migraine without aura patients, bimodal stimulation significantly increased low-frequency-somatosensory evoked potentials habituation and early high-frequency oscillations. At T2, all visual stimulation-induced changes of somatosensory processing had vanished. Conclusion: These results suggest a malfunctioning multisensory integration process, which could be favoured by an abnormal excitability level of thalamo-cortical loops. [ABSTRACT FROM AUTHOR]

This document is a letter to the editor commenting on a study about the lack of reproducibility of resting-state functional MRI findings in migraine with aura. The authors of the letter propose that further investigation is needed to enhance our understanding of migraine, particularly in terms of changes in functional network integration. They also point out that the comparisons made in the study are not appropriate and that the methods and testing of previous research are not adequately displayed. The authors suggest that well-designed multicentric studies with homogenous groups of patients could improve the replicability of neuroimaging studies on migraine. They also emphasize the need for an expert's consortium to recommend best practices in neuroimaging research. [Extracted from the article]

Objective: To study the effects of trains of repetitive transcranial magnetic stimulation (rTMS) over the motor cortex in patients with chronic migraine (CM) with or without medication overuse (MOH).Subjects and Methods: Thirty-two patients (CM [n = 16]; MOH [n = 16]) and 16 healthy volunteers (HVs) underwent rTMS recording. Ten trains of 10 stimuli each (120% resting motor threshold) were applied over the left motor cortex at 1 Hz or 5 Hz in random order. The amplitude of motor evoked potential (MEP) was evaluated from electromyographic recording in the first dorsal interosseous muscle. The slope of the linear regression line for the 10 stimuli for each participant was calculated using normalized data.Results: rTMS-1 Hz had a normal depressive effect on MEP amplitude in all groups. rTMS-5 Hz depressed instead of potentiating MEP amplitudes in MOH patients, with a significantly different response from that in HVs and CM patients. The slope of the linear regression of MEP amplitudes was negatively correlated with pain intensity in CM patients, and with the duration of overuse headache in MOH patients.Conclusions: This different plastic behaviour suggests that MOH and CM, despite exhibiting a similar clinical phenotype, have different neurophysiological learning processes, probably related to different pathophysiological mechanisms of migraine chronification. [ABSTRACT FROM AUTHOR]

Background Previous functional MRI studies have revealed that ongoing clinical pain in different chronic pain syndromes is directly correlated to the connectivity strength of the resting default mode network (DMN) with the insula. Here, we investigated seed-based resting state DMN-insula connectivity during acute migraine headaches. Methods Thirteen migraine without aura patients (MI) underwent 3 T MRI scans during the initial six hours of a spontaneous migraine attack, and were compared to a group of 19 healthy volunteers (HV). We evaluated headache intensity with a visual analogue scale and collected seed-based MRI resting state data in the four core regions of the DMN: Medial prefrontal cortex (MPFC), posterior cingulate cortex (PCC), and left and right inferior parietal lobules (IPLs), as well as in bilateral insula. Results Compared to HV, MI patients showed stronger functional connectivity between MPFC and PCC, and between MPFC and bilateral insula. During migraine attacks, the strength of MPFC-to-insula connectivity was negatively correlated with pain intensity. Conclusion We show that greater subjective intensity of pain during a migraine attack is associated with proportionally weaker DMN-insula connectivity. This is at variance with other chronic extra-cephalic pain disorders where the opposite was found, and may thus be a hallmark of acute migraine head pain. [ABSTRACT FROM AUTHOR]

Background: We studied lateral inhibition in the somatosensory cortex of migraineurs during and between attacks, and searched for correlations with thalamocortical activity and clinical features.Participants and Methods: Somatosensory evoked potentials (SSEP) were obtained by electrical stimulation of the right median (M) or ulnar (U) nerves at the wrist or by simultaneous stimulation of both nerves (MU) in 41 migraine without aura patients, 24 between (MO), 17 during attacks, and in 17 healthy volunteers (HVs). We determined the percentage of lateral inhibition of the N20-P25 component by using the formula [(100)-MU/(M + U)*100]. We also studied high-frequency oscillations (HFOs) reflecting thalamocortical activation.Results: In migraine, both lateral inhibition (MO 27.9% vs HVs 40.2%; p = 0.009) and thalamocortical activity (MO 0.5 vs HVs 0.7; p = 0.02) were reduced between attacks, but not during. In MO patients, the percentage of lateral inhibition negatively correlated with days elapsed since the last migraine attack (r = -0.510, p = 0.01), monthly attack duration (r = -0.469, p = 0.02) and severity (r = -0.443, p = 0.03), but positively with thalamocortical activity (r = -0.463, p = 0.02).Conclusions: We hypothesize that abnormal migraine cycle-dependent dynamics of connectivity between subcortical and cortical excitation/inhibition networks may contribute to clinical features of MO and recurrence of attacks. [ABSTRACT FROM AUTHOR]

Background: Neurophysiological investigations have demonstrated that there are unique fluctuations in the migraine brain functional activity between the ictal and interictal periods. Here we investigated the possibility that there are fluctuations over time also in whole brain morphometry of patients affected by episodic migraine without aura (MO). Methods: Twenty-four patients with untreated MO underwent 3T MRI scans during (n=10) or between attacks (n=14) and were compared to a group of 15 healthy volunteers (HVs). We then performed voxel-based-morphometry (VBM) analysis of structural T1-weighted MRI scans to determine if changes in brain structure were observed over the course of the migraine cycle. Results: Interictally, MO patients had a significantly lower gray matter (GM) density within the right inferior parietal lobule, right temporal inferior gyrus, right superior temporal gyrus, and left temporal pole than did HVs. Ictally, GM density increased within the left temporal pole, bilateral insula, and right lenticular nuclei, but no areas exhibited decreased GM density. Conclusions: These morphometric GM changes between ictal and interictal phases suggest that abnormal structural plasticity may be an important mechanism of migraine pathology. Given the functional neuroanatomy of these areas, our findings suggest that migraine is a condition associated with global dysfunction of multisensory integration and memory processing. [ABSTRACT FROM AUTHOR]

The article discusses a study which concludes that the predisposition and recurrence of episodic cluster headache (ECH) is attributed to the malfunctioning of the posterior hypothalamus and of the nociceptive processing and the sensitization of the trigeminal pain system resulting in the descending aminergic controls. It is mentioned that lateralized pathological abnormalities were observed in the nociceptive-specific blink reflex (BR) in the ECH patients.

Background Previous functional MRI studies have revealed that ongoing clinical pain in different chronic pain syndromes is directly correlated to the connectivity strength of the resting default mode network (DMN) with the insula. Here, we investigated seed-based resting state DMN-insula connectivity during acute migraine headaches. Methods Thirteen migraine without aura patients (MI) underwent 3 T MRI scans during the initial six hours of a spontaneous migraine attack, and were compared to a group of 19 healthy volunteers (HV). We evaluated headache intensity with a visual analogue scale and collected seed-based MRI resting state data in the four core regions of the DMN: Medial prefrontal cortex (MPFC), posterior cingulate cortex (PCC), and left and right inferior parietal lobules (IPLs), as well as in bilateral insula. Results Compared to HV, MI patients showed stronger functional connectivity between MPFC and PCC, and between MPFC and bilateral insula. During migraine attacks, the strength of MPFC-to-insula connectivity was negatively correlated with pain intensity. Conclusion We show that greater subjective intensity of pain during a migraine attack is associated with proportionally weaker DMN-insula connectivity. This is at variance with other chronic extra-cephalic pain disorders where the opposite was found, and may thus be a hallmark of acute migraine head pain. [ABSTRACT FROM AUTHOR]