Pain
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Understanding the role of voltage-gated sodium channels in nociception may provide important insights into pain mechanisms. Voltage-gated sodium channels are critically important for electrogenesis and nerve impulse conduction, and a target for important clinically relevant analgesics such as lidocaine. Furthermore, within the last decade studies have shown that certain sodium channel isoforms are predominantly expressed in peripheral sensory neurons associated with pain sensation, and that the expression and functional properties of voltage-gated sodium channels in peripheral sensory neurons can be dynamically regulated following axonal injury or peripheral inflammation. ⋯ Electrophysiological experiments indicate that these pain-associated mutations cause small yet significant changes in the gating properties of voltage-gated sodium channels that are likely to contribute substantially to the development of chronic pain. Equally exciting, recent studies indicate that recessive mutations in Na(v)1.7 that eliminate functional current can result in an apparent complete, and possibly specific, indifference to pain in humans, suggesting that isoform specific blockers could be very effective in treating pain. In this review we will examine what is known about the roles of voltage-gated sodium channels in nociception.
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Comparative Study
The impact of chronic low back pain on older adults: a comparative study of patients and controls.
Chronic low back pain (CLBP) is one of the most common, poorly understood, and potentially disabling chronic pain conditions from which older adults suffer. Many older adults remain quite functional despite CLBP, and because age-related comorbidities often exist independently of pain (e.g., medical illnesses, sleep disturbance, mobility difficulty), the unique impact of CLBP is unknown. We conducted this research to identify the multidimensional factors that distinguish independent community dwelling older adults with CLBP from those that are pain-free. ⋯ Significant differences were ascertained for all 22 measures. Discriminant function analysis revealed that eight measures uniquely maximized the separation between the two groups (self-reported function with the Functional Status Index and the SF-36, performance-based function with repetitive trunk rotation and functional reach, mood with the Geriatric Depression Scale, comorbidity with the Cumulative Illness Rating Scale and BMI, and severity of degenerative disc disease). These results should help to guide investigators that perform studies of CLBP in older adults and practitioners that want an easily adaptable battery for use in clinical settings.
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The pathogenesis of gastrointestinal symptoms in diabetes mellitus is complex and multi-factorial. Diabetes induced peripheral and central changes in the neuronal pain matrix may be of importance and were explored using a new multi-modal and multi-segmental sensory testing approach. The sensitivity to mechanical, thermal and electrical stimulations in the oesophagus and duodenum was assessed in 12 type-1 diabetic patients with proven autonomic neuropathy and severe gastrointestinal symptoms using a comprehensive stimulation device aiming to activate different gut nerves and pain mechanisms. ⋯ The multi-modal and multi-segmental sensory testing approach indicates that the sensory nerves are widely affected in the GI tract and generalized to nerves in all layers of the gut. Changes in the neuronal pain matrix including interactions between peripheral and central pain mechanisms may be involved in the pathogenesis of gastrointestinal symptoms in long-standing diabetes. Future targets in the treatment of gastrointestinal symptoms in diabetic patients with autonomic neuropathy could be based on modulation of the central nervous system excitability.
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Central pain following traumatic brain injury (TBI) has not been studied in depth. Our purpose was to conduct a systematic study of patients with TBI suffering from chronic central pain, and to describe the characteristics of the central pain. Groups were TBI patients with (TBIP) and without central pain (TBINP) and healthy controls. ⋯ The characteristics of the chronic pain resembled those of other central pain patients although TBIP displayed several unique features. The sensory profile indicated that damage to the pain and temperature systems is a necessary but not sufficient condition for the development of chronic central pain following TBI. Neuronal hyperexcitability may be a contributing factor to the chronic pain.