Pain
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Evidence has been accumulated suggesting that a dysfunction in pain inhibitory systems, i.e. in 'diffuse noxious inhibitory controls' (DNIC)-like mechanisms, might be-amongst other factors-responsible for the development of anatomically generalized chronic pain like fibromyalgia. The aim of the present study was to look for similar impairments in chronic tension-type headache (CTTH) as a regionally specific pain syndrome. Twenty-nine CTTH patients and 25 age- and sex-matched healthy control subjects participated in the study. ⋯ This group difference was present during the 'pain' as well as the 'heat' condition. Furthermore, the electrical detection and pain thresholds were affected in this group-specific manner both at the forearm and at the temple. These findings suggest that patients with CTTH suffer from deficient DNIC-like pain inhibitory mechanisms in a similar manner, as do patients with anatomically generalized chronic pain like fibromyalgia.
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Comparative Study
Prolonged rhythmic gum chewing suppresses nociceptive response via serotonergic descending inhibitory pathway in humans.
Serotonergic (5-HT) neurons are implicated in modulating nociceptive transmission. It is established that 5-HT neuronal activity is enhanced by rhythmic behaviors such as chewing and locomotion in animals. We thus hypothesized that 5-HT descending inhibitory pathways may be enhanced by rhythmic behavior of gum chewing in humans. ⋯ The WB 5-HT level obtained 30 min after cessation of chewing was significantly greater than the pre-chewing level. Serotonin transporters have recently been discovered at the blood-brain barrier, suggesting that the rise in blood 5-HT may possibly reflect an increase in 5-HT level within the brain. The present results support our hypothesis that the rhythmic behavior of chewing suppresses nociceptive responses via the 5-HT descending inhibitory pathway.
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Comparative Study
A human experimental capsaicin model for trigeminal sensitization. Gender-specific differences.
Migraine is much more common in women (18%) than in men (6%). Menstrual migraine in female migraineurs also varies from 7 to 19%. The main goals of the present study were (1) to investigate gender specific differences in an experimental capsaicin model of trigeminal sensitization (a proposed mechanism of migraine) and (2) to explore the influence of menstrual cycle phases. ⋯ A significant difference was found in the capsaicin-evoked pain distribution with a greater response in menstrual phase compared to the luteal phase (P<0.01) and men (P<0.0001). Capsaicin induced trigeminal sensitization and evoked gender specific sensory and vaso-motor responses, with menstruating females generally showing the strongest manifestations. The model may be further applied to explore mechanisms of human trigeminal sensitization.
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Comparative Study
Multilevel somatosensory system disinhibition in children with migraine.
Although migraine is characterised by an abnormal cortical excitability level, whether the central nervous system is hyper- or hypo-excitable in migraine still remains an unsolved problem. The aim of our study was to compare the somatosensory evoked potential (SEP) recovery cycle, a marker of the somatosensory system's excitability, in a group of 15 children suffering from migraine without aura (MO) (mean age 11.7+/-1.6 years, five males, 10 females) and 10 control age-matched subjects (CS) (mean age 10.9+/-2.1 years, six males, four females). We calculated the SEP's latency and amplitude modifications after paired electrical stimuli at 5, 20 and 40 ms interstimulus intervals (ISIs), comparing it with a single stimulus condition assumed as the baseline. ⋯ Since, the SEP recovery cycle depends on the inhibitory interneuron function, our findings suggest that a somatosensory system disinhibition takes place in migraine. This is a generalized phenomenon, not limited to the cerebral cortex, but concerning also the cervical grey matter. The SEP recovery cycle reflects the intracellular concentration of Na(+), therefore, the shortened recovery cycle in our MO patients suggests a high level of intracellular Na(+) and a consequent depolarized resting membrane potential, possibly due to an impaired Na(+) -K(+) ATPase function in migraine.
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Reactivation of latent varicella zoster virus (VZV) within sensory trigeminal and dorsal root ganglia (DRG) neurons produces shingles (zoster), often accompanied by a chronic neuropathic pain state, post-herpetic neuralgia (PHN). PHN persists despite latency of the virus within human sensory ganglia and is often unresponsive to current analgesic or antiviral agents. To study the basis of varicella zoster-induced pain, we have utilised a recently developed model of chronic VZV infection in rodents. ⋯ VZV infection induced increased behavioral reflex responsiveness to both noxious thermal and mechanical stimuli ipsilateral to injection (lasting up to 10 weeks post-infection) that is mediated by spinal NMDA receptors. These changes were reversed by systemic administration of gabapentin or the sodium channel blockers, mexiletine and lamotrigine, but not by the non-steroidal anti-inflammatory agent, diclofenac. This is the first time that the profile of VZV infection-induced phenotypic changes in DRG has been shown in rodents and reveals that this profile appears to be broadly similar (but not identical) to changes in other neuropathic pain models.