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Migraine is one of the most prevalent and disabling medical illnesses. Preventive drugs are used to reduce the frequency, severity, and duration of attacks. Most patients were no longer on their medication due to contraindications or poor clinical response. Therefore, there is need for novel prophylactic agents for migraine. New preventive treatments are those of the class of calcitonin gene related peptide (CGRP)-targeting therapies. We aimed to assess the real level of therapeutic innovation of these new drugs.
Learn More >Neuropathic pain (NP) in head and neck cancer (HNC) patients represents a treatment challenge. Most studies investigating drugs against NP are conducted in patients suffering with diabetic neuropathy or postherpetic neuralgia, while data are limited in cancer pain management. Additionally, regarding cancer therapy-related NP, most of the studies do not focus on HNC patients. The aim of this review is to identify the studies on systematically administered medication for NP management that included HNC patients under radiotherapy.
Learn More >Despite the worldwide prevalence and severe complications of type 2 diabetes mellitus (T2DM), the pathophysiological mechanisms underlying the development of diabetic polyneuropathy (DPN) are poorly understood. Beyond strict control of glucose levels, clinical trials for reversing DPN have largely failed. Therefore, understanding the pathophysiological and molecular mechanisms underlying DPN is crucial. Accordingly, this study explored biochemical and neuropathological deficits in a rat model of T2DM induced through high-fat diet (HFD) feeding along with two low-dose streptozotocin (STZ) injections; the deficits were explored through serum lipid, neurobehavioral, neurophysiology, neuropathology, and immunohistochemistry examinations. Our HFD/STZ protocol induced (1) mechanical hyperalgesia and depression-like behaviors, (2) loss of intraepidermal nerve fibers (IENFs) and reduced axonal diameters in sural nerves, and (3) decreased compound muscle action potential. In addition to hyperglycemia, which was correlated with the degree of mechanical hyperalgesia and loss of IENFs, we observed that hypertriglyceridemia was the most dominant deficit in the lipid profiles of the diabetic rats. In particular, SEPT9, the fourth component of the cytoskeleton, increased in the satellite glial cells (SGCs) of the dorsal root ganglia (DRG) in the T2DM-like rats. The number of SEPT9(+) SGCs/DRG was correlated with serum glucose levels and mechanical thresholds. Our findings indicate the putative molecular mechanism underlying DPN, which presumably involves the interaction of SGCs and DRG neurons; nevertheless, further functional research is warranted to clarify the role of SEPT9 in DPN.
Learn More >Inflammation is the body's mechanism to trigger the immune system, thereby preventing bacteria and viruses from manifesting their toxic effect. Inflammation plays a vital role in regulating inflammatory mediator levels to initiate the wound healing process depending on the nature of the stimuli. This process occurs due to chemical release from white blood cells by elevating blood flow to the site of action, leading to redness and increased body temperature. Currently, there are numer-ous Non-steroidal anti-inflammatory drugs (NSAIDs) available, but these drugs are reported with adverse effects such as gastric bleeding, progressive kidney damage, and increased risk of heart at-tacks when prolonged use. For such instances, alternative options need to be adopted. The introduc-tion of voltage-gated ion channel blockers can be a substantial alternative to mask the side effects of these currently available drugs. Chronic inflammatory disorders such as rheumatoid and osteoarthri-tis, cancer and migraine, etc., can cause dreadful pain, which is often debilitating for the patient. The underlying mechanism for both acute and chronic inflammation involves various complex re-ceptors, different types of cells, receptors, and proteins. The working of voltage-gated sodium and calcium channels is closely linked to both inflammatory and neuropathic pain. Certain drugs such as carbamazepine and gabapentin, which are ion channel blockers, have greater pharmacotherapeutic activity for sodium and calcium channel blockers for the treatment of chronic inflammatory pain states. This review intends to provide brief information on the mechanism of action, latest clinical trials, and applications of these blockers in treating inflammatory conditions.
Learn More >Unlike the spontaneously appearing aura in migraineurs, experimentally, cortical spreading depression (CSD), the neurophysiological correlate of aura is induced by non-physiological stimuli. Consequently, neural mechanisms involved in spontaneous CSD generation, which may provide insight into how migraine starts in an otherwise healthy brain, remain largely unclear. We hypothesized that CSD can be physiologically induced by sensory stimulation in primed mouse brain.
Learn More >Migraine has consistently been associated with an increased risk of cardiovascular disease (CVD) events. It remains, however, unclear to what extent cardiovascular risk profiles might be linked with migraine activity status, and how these profiles relate to the development of migraine.
Learn More >Physician prescribing habits for opiates and headache therapies have not been previously evaluated in a large, matched cohort study in idiopathic intracranial hypertension (IIH). Our objective was to evaluate opiate and headache medication prescribing habits in women with IIH compared to matched women with migraine and population controls. We also investigated the occurrence of new onset headache in IIH compared to population controls.
Learn More >Alpha1-adrenoceptors are over-expressed in the epidermis of a subgroup of patients with complex regional pain syndrome (CRPS). Activating α1-adrenoceptors in epidermal cells increases production of the pro-inflammatory cytokine interleukin-6 (IL-6), a mediator of inflammation. To investigate whether this might exacerbate inflammation in CRPS, primary keratinocytes and/or dermal fibroblasts were cultured from skin biopsies obtained from the affected limb of 25 patients and a similar site in 28 controls. The fundamental pro-inflammatory cytokine, tumor necrosis factor alpha (TNFα), was administered for 24 hours to initiate inflammation. Following this, cells were incubated for 6 hours with the α1-adrenoceptor agonist phenylephrine. Exposure to TNFα induced pro-inflammatory cytokine mRNA production and protein secretion in keratinocytes and fibroblasts, and enhanced α1B-adrenoceptor mRNA expression in keratinocytes. Additional stimulation of α1-adrenoceptors with phenylephrine increased the production of interleukin-6 (IL-6) mRNA and protein secretion in both cell types. Under all conditions, gene and protein α1-adrenoceptor levels and cytokine gene expression and protein secretion were similar, overall, in patients and controls, except for abnormally high α1-adrenoceptor protein levels in the keratinocytes of three of 17 patients. These findings suggest that persistent inflammation in CRPS is not due to dysfunction of skin cells but is a normal response to extrinsic signals. After α1-adrenoceptor stimulation of keratinocytes, increases in IL-6 mRNA but not protein were proportional to basal α1-adrenoceptor protein levels. Skin cells play an important role in persistent inflammation in CRPS. Potentially, a positive feedback loop between α1-adrenoceptors and IL-6 production in skin cells contributes to this inflammatory state.
Learn More >The aim of the current study was to determine whether tension-type headache (TTH) and migraine with or without aura have altered anterior and posterior circulation compared with normal volunteers as assessed by Transcranial Doppler (TCD) ultrasonography. The study included 24 patients with chronic TTH and 37 patients with migraine (16 with aura and 21 without aura) classified according to the diagnostic criteria of the International Headache Society 2018. They were compared with a control group of 50 age- and sex-matched healthy volunteers. Each participant was examined with TCD ultrasonography of the middle, anterior and posterior cerebral and vertebral arteries (MCA, ACA, PCA, and VA) at rest. Patients in the TTH group had a significantly lower peak systolic velocity (PSV) and mean flow velocity (MFV) in the MCA compared with controls, whereas EDV and MFV in the ACA were significantly higher in the migraine without aura group than controls. Within the 3 groups of patients, the TTH group had significantly lower PSV in the MCA and PCA than the group of migraine with aura. In addition, the TTH group had significantly lower PSV and MFV in the MCA and a lower EDV in the VA than migraine patients without aura. In conclusion, the possibility of cerebrovascular changes is confirmed in the present study in both TTH and migraine without aura. The former has a low MFV in the MCA whereas the latter has a high MFV in the ACA.
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