Estimating the motor unit number of the flexor carpi ulnaris muscle with MScanFit MUNE.

INTRODUCTION/AIMS: MScanFit motor unit number estimation (MUNE) is a promising method for motor unit estimation and is reported to have good reliability in distal and small muscles. In this study, we investigated the reliability of MScanFit MUNE in a proximal forearm muscle, the flexor carpi ulnaris. METHODS: Twenty healthy volunteers were included in this study, and 15 participants were re-evaluated in a second session. The ulnar nerve was stimulated at the elbow and a compound muscle action potential (CMAP) scan from the flexor carpi ulnaris (FCU) muscle was recorded from each arm. CMAP, MUNE, and other motor unit parameters were obtained. Reproducibility was evaluated using intraclass correlation coefficients (ICCs). RESULTS: The average MUNE from 40 FCU muscles was 90.9 (standard deviation: 16.4). MScanFit MUNE and CMAP were not significantly different between the dominant and non-dominant sides. The ICC indicated good reliability between sessions for each side (0.81 and 0.8, respectively). DISCUSSION: Our results indicate that MScanFit MUNE is a feasible method with good reproducibility for MUNE of the FCU muscle.

Short latency afferent inhibition: comparison between threshold-tracking and conventional amplitude recording methods.

Short-latency afferent inhibition (SAI), which is conventionally measured as a reduction in motor evoked potential amplitude (A-SAI), is of clinical interest as a potential biomarker for cognitive impairment. Since threshold-tracking has some advantages for clinical studies of short-interval cortical inhibition, we have compared A-SAI with a threshold-tracking alternative method (T-SAI). In the T-SAI method, inhibition was calculated by tracking the required TMS intensity for the targeted MEP amplitude (200 uV) both for the test (TMS only) and paired (TMS and peripheral stimulation) stimuli. A-SAI and T-SAI were recorded from 31 healthy subjects using ten stimuli at each of 12 inter-stimulus intervals, once in the morning and again in the afternoon. There were no differences between morning and afternoon recordings. When A-SAI was normalized by log conversion it was closely related to T-SAI. Between subjects, variability was similar for the two techniques, but within-subject variability was significantly smaller for normalized A-SAI. Conventional amplitude measurements appear more sensitive for detecting changes within-subjects, such as in interventional studies, but threshold-tracking may be as sensitive as detecting abnormal SAI in a patient.

CGRP receptor antagonist MK-8825 attenuates cortical spreading depression induced pain behavior.

BACKGROUND AND OBJECTIVE: The present study aimed to investigate the effects of selective calcitonin gene related peptide (CGRP) receptor antagonist (MK-8825) on cortical spreading depression (CSD) induced pain behavior and anxiety in freely-moving rats, and neuronal activation in the correlated anatomical regions. METHODS: CSD was induced while keeping all meningeal layers and BBB intact and MK-8825 was administered in two different doses. Regional cerebral blood flow (rCBF), arterial pressure and DC shift were recorded. Behavioral studies were conducted in freely-moving rats. Spontaneous behavior, mechanical allodynia, ultrasonic vocalization, and anxiety were evaluated. Immunohistochemistry of c-fos, CGRP, calcitonin receptor like-receptor (CLR) and receptor activity modifying protein 1 (RAMP1) were studied. RESULTS: MK-8825 did not block DC shifts in the cerebral cortex and accompanied hemodynamic response. CSD significantly induced freezing and grooming behavior in freely-moving rats. MK-8825 reversed increased episodes of freezing, grooming, wet dog shake and head shake behavior. MK-8825 increased CSD-induced reductions in von Frey thresholds, but did not change elevated plus maze results. MK-8825 blocked c-fos induction by CSD in the brainstem trigeminal nucleus caudalis (TNC) and reticular nucleus of thalamus (TRN) but not in the amygdala. Immunofluorescence analysis showed no co-localization of CGRP, CLR or RAMP1 with c-fos positive cells. CONCLUSION: CGRP receptor antagonist MK-8825 dose dependently attenuated CSD-induced trigeminal nerve mediated pain response without altering CSD waves and accompanied rCBF response. While blocking TNC activation, MK-8825 did not exert any effect on amygdala and anxiety behavior. CGRP receptor antagonists may also modulate thalamo-cortical gating.

Somatosensory temporal discrimination remains intact in tension-type headache whereas it is disrupted in migraine attacks.

Background and objective Somatosensory temporal discrimination was recently reported as prolonged during migraine attacks, which is consistent with disrupted sensorial perception in migraine. However, knowledge about central sensory processing in tension-type headache is still lacking. This prospective, controlled study aimed to investigate somatosensory temporal discrimination thresholds in tension-type headache. Methods The study included 10 tension-type headache patients, 10 migraine patients and 10 healthy volunteers without headache. Somatosensory temporal discrimination thresholds were evaluated during the headache attacks of tension-type headache and migraine patients. Results Somatosensory temporal discrimination thresholds of tension-type headache patients (39.0 ± 5.5 ms for the right hand and 40.6 ± 4.6 ms for the left hand) were significantly lower than those of episodic migraine patients (137.1 ± 35.8 ms for the right hand and 118.4 ± 34.3 ms for the left hand, p < 0.0001 and p < 0.0001 respectively), and comparable to those of healthy volunteers (38.6 ± 5.3 ms for the right hand and 38.3 ± 7.2 ms for the left hand, p = 0.79 and p = 0.45 respectively). Conclusion Central sensory processing, as tested by somatosensory temporal discrimination, was remarkably disrupted during the headache attacks in migraineurs, whereas it remained intact in the tension-type headache patients.

The role of the cerebellum in motor imagery.

OBJECTIVE: Although it is well documented that the cerebellum plays a role in motor imagery (MI), its exact role in MI is still obscure. Since motor imagery and execution of movement share common pathways, and the cerebellum has an inhibitory effect on the motor cortex, we speculated that the cerebellum also has an inhibitory role on MI. METHODS: To test this hypothesis, 12 healthy individuals aged 27-47 years (mean age 33.3 years) were enrolled in the study. Subjects were asked to imagine two different tasks, one complex (MI-c) and one simple (MI-s) motor task. The intensity of anodal cerebellar transcranial direct current stimulation (ctDCS) was set at 2 mA for 20 min. Sham ctDCS consisted of 30s current stimulation. RESULTS: MI-s resulted in significantly increased log MEP amplitude during MI, compared with control MEP amplitude,(p=0.000). The increase in log MEP amplitude during MI disappeared after anodal ctDCS. Before sham ctDCS, both MI-s and MI-c resulted in log MEP amplitude increases (p=0.000). This facilitator effect of both MI-c and MI-s on log MEP amplitude was also persistent after sham ctDCS (p=0.000). CONCLUSIONS: The study demonstrates for the first time that the cerebellum has an inhibitory effect on MI. SIGNIFICANCE: Combining ctDCS with MI significantly modulates corticomotor excitability.

Somatosensory temporal discrimination is prolonged during migraine attacks.

BACKGROUND AND OBJECTIVE: Symptoms and signs of sensorial disturbances are characteristic features of a migraine headache. Somatosensory temporal discrimination measures the temporal threshold to perceive two separate somaesthetic stimuli as clearly distinct. This study aimed to evaluate somaesthetic perception in migraine patients by measuring the somatosensory temporal discrimination thresholds. METHODS: The study included 12 migraine patients without aura and 12 volunteers without headache. Somatosensory temporal discrimination threshold (STDT) values were measured in the face (V3) and hands (C7) during a lateralized headache attack and the headache-free interictal period. The disease duration, pain intensity, phonophobia, photophobia, nausea, vomiting, and brush allodynia were also recorded during the migraine attack. RESULTS: STDT values were within normal limits and not different between the control group and the interictal period in migraine patients. Compared to the headache-free period, STDT values during the attack were significantly prolonged in the contralateral hand (C7) (155.7 ± 84.2 vs 40.6 ± 16.1 ms [P < .001]), ipsilateral hand (C7) (88.6 ± 51.3 vs 31.4 ± 14.2 ms [P < 0.001]), contralateral face (V3) (65.5 ± 35.4 vs 37.6 ± 22.2 ms [P = .006]) and ipsilateral face (V3) (104.1 ± 44.5 vs 37.5 ± 21.4 ms [P < 0.001]) according to the lateralization of the headache. Ictal STDT values of the contralateral hand and ipsilateral face were significantly increased compared to that of the ipsilateral hand and contralateral face (155.7 ± 84.2 ms vs 88.6 ± 5.1.3 ms [P = .001], 104.1 ± 44.5 ms vs 65.5 ± 35.4 ms [P = 0.001]). No allodynia was detected in the areas that were tested for somatosensory temporal discrimination. The visual analog scale scores were correlated with the somatosensory temporal discrimination thresholds of the contralateral hand (r = 0.602, P = .038), whereas no correlation was detected between the somatosensory temporal discrimination thresholds and disease duration, brush allodynia in the forehead, phonophobia, photophobia, nausea and vomiting. CONCLUSION: The study demonstrates for the first time that somatosensory temporal discrimination thresholds are elevated during migraine attacks. A transient disruption of the central processing of somaesthetic stimuli during the lateralized migraine attack may provide additional information to understand the mechanisms of the cognitive and sensory perception impairment associated with migraine headache and may have diagnostic value.

Pathophysiology of Migraine.

Migraine is a serious health problem which impair quality of life. It is the second most common primary headache that affects approximately more than %10 people in general population. Migraine pathophysiology is still unclear. Increasing results of studies suggest to migraine pathophysiology is related with primary neuronal mechanisms. Migraine pain starts in which region of brain and what brain regions are activated in different stages is unenlightened. There is evidences that growing number of studies which using new imaging techniques as positron emission tomography (PET) and functional magnetic resonans imaging (fMRI) show that migraine and cluster headaches are related with neuronal structures and vasodilatation. There are four phases to a migraine. The prodrome phase, aura, the attack, and the postdrome phase. Some datas obtained from last ten years indicate that cortical excitability has increased in interictal phase too. For many years, studies in rodents show trgimenial nerve is activated and it leads to vasodilatation and neurogenic inflammation in the headache phase. Although the majority of patients encountered in clinical practice are migraine without aura or chronic migraine, experimental studies of the migraine pathophysiology are focusing on the aura model which is used cortical spreading depression.