Browse by Audience
Arrhythmic fluctuations in neural activity occur at many levels of the nervous system. Such activity does not have a characteristic temporal periodicity but can exhibit statistical similarities, most commonly power-law scaling behavior, which is indicative of scale-free dynamics. The recurrence of scaling laws across many different systems and its manifestation in behavior has prompted a search for unifying principles in human brain function. With this in mind, a focused search for abnormities in scale-free dynamics is of considerable clinical relevance to migraine and other clinical pain disorders. Here we examined the scale-free properties of the resting-state fMRI signal in the broadband frequency range known to be related to spontaneous neural activity (0.01-0.1Hz). In a large cohort of episodic migraine patients (N=40), we observed that the strength of long-range temporal correlations in the fMRI signal (captured by the scaling exponent α) was significantly higher in the sensorimotor network compared to healthy controls. Increases in the scaling exponent were positively correlated with fMRI signal variance and negatively correlated with patient's self-reported headache intensity. These changes in the fMRI signal suggest that the temporal structure of amplitude fluctuations carries valuable information about the dynamic state of the underlying neuronal networks and ensuing sensory impairments in migraine. The demonstrated scaling laws pose a novel quantitative approach for examining clinically relevant inter-individual variability in migraine and other pain disorders.
Learn More >Routine assessment of photophobia in the clinical setting may underestimate the presence and severity of this condition. We aimed to develop and validate a questionnaire to improve evaluation of the impact of photophobia on activities of daily living, and to determine the relationship of this questionnaire to psychophysical assessment of light sensitivity thresholds.
Learn More >ATP1A2 has been identified as the genetic cause of familial hemiplegic migraine type 2. Over 80 ATP1A2 mutations have been reported, but no data from Chinese family studies has been included. Here, we report the first familial hemiplegic migraine type 2 Chinese family with a novel missense mutation.
Learn More >Various features of the cerebral cortex and white matter have been extensively investigated in migraine with aura (MwA), but the morphological characteristics of subcortical structures have been largely neglected. The aim of this study was to identify possible differences in subcortical structures between MwA patients and healthy subjects (HS), and also to determine the correlations between the characteristics of migraine aura and the volumes of subcortical structures.
Learn More >ATP-sensitive potassium (K ) channel opener levcromakalim induces migraine attacks in migraine patients. Underlying mechanisms responsible for headache and migraine induction after levcromakalim infusion are unknown.
Learn More >A significant proportion of women report a reduction of symptoms over time-even without treatment-yet the natural progression of vulvodynia and which factors may explain decrease vs persistence of pain remain unclear.
Learn More >To assess patterns and impact of small nerve fiber dysfunction and pathology in patients with fibromyalgia syndrome (FMS).
Learn More >Neuropathic pain is evoked by aberrant sensory processing in the peripheral or central nervous system, which is characterized by persistent pain, tactile allodynia, or hyperalgesia. Neuroinflammation is associated with the initiation and maintenance of persistent pain in both the peripheral and central nervous systems. Hydrogen sulfide plays important regulatory roles in different physiological and pathological conditions. Therefore, we investigated the effect of hydrogen sulfide on allodynia, hyperalgesia and cytokine release in rats with neuropathic pain and the related regulatory mechanism. Neuropathic pain was established by chronic constriction injury (CCI) of the sciatic nerve in rats. Nuclear factor erythroid-2 (NF-E2)-related factor 2 (Nrf2) siRNA, hemin, Sn-protoporphyrin (SnPP)-IX and/or NaHS were administered to rats with neuropathic pain, and the spinal cord was collected to detect the expression of Nrf2, hemeoxygenase-1 (HO-1), nuclear factor-kappa B (NF-κb) and the cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6 and high mobility group box (HMGB)-1 by Western blot (WB) analysis, reverse transcription polymerase chain reaction (RT-PCR), immunofluorescence or enzyme-linked immunosorbent assay (ELISA). Mechanical allodynia, thermal hyperalgesia and the number of paw lifts were measured at different time points after operation. In the present research, neuropathic pain induced Nrf2 and HO-1 expression in the microglial cells of the spinal cord; Nrf2 and HO-1 were necessary to alleviate the hyperalgesia of CCI-induced rats; NaHS mitigated the hyperalgesia and allodynia induced by the CCI operation; and NaHS mitigated the excessive release of the cytokines TNF-α, IL-1β, IL-6 and HMGB1 via the Nrf2/HO-1 pathway in the microglial cells of the spinal cord. These results indicated that NaHS exhibited antinociceptive and anti-inflammatory effects that were associated with the activation of the Nrf2/HO-1 pathway in the spinal cord of rats with neuropathic pain.
Learn More >Sodium channel Na1.7 controls firing of nociceptors, and its role in human pain has been validated by genetic and functional studies. However, little is known about Na1.7 trafficking or membrane distribution along sensory axons, which can be a meter or more in length. We show here with single-molecule resolution the first live visualization of Na1.7 channels in dorsal root ganglia neurons, including long-distance microtubule-dependent vesicular transport in Rab6A-containing vesicles. We demonstrate nanoclusters that contain a median of 12.5 channels at the plasma membrane on axon termini. We also demonstrate that inflammatory mediators trigger an increase in the number of Na1.7-carrying vesicles per axon, a threefold increase in the median number of Na1.7 channels per vesicle and a ~50% increase in forward velocity. This remarkable enhancement of Na1.7 vesicular trafficking and surface delivery under conditions that mimic a disease state provides new insights into the contribution of Na1.7 to inflammatory pain.
Learn More >To estimate the prevalence of co-occurring pain sites among older adults with persistent back pain and associations of multisite pain with longitudinal outcomes.
Learn More >