Articles: neuralgia.
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Injury to central or peripheral nervous system causes neuropathic pain. Initially it affects the sensory nerves, then the motor nerves. In crush or traumatic injuries the sensory or motor nerves are affected simultaneously and the symptoms develop simultaneously. ⋯ The treatment modality can be subdivided into pharmacological pain management and interventional pain management. The following groups of drugs can be used either singularly or in combination in pharmacological pain management: Analgesics, anticonvulsants, antidepressants and miscellaneous group. Interventional pain management can be done by: Neural blockade, electric stimulation and implantable devices.
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Gabapentin is an anti-epileptic drug (AED) that was approved in 1993 for the adjunct treatment of complex partial seizures (CPS) with and without generalization. Although the mechanism of action of gabapentin has not been fully elucidated, it has been shown to be effective not only as an adjunct AED in patients with CPS, but also in children with epilepsy, many pain syndromes (most notably neuropathic pain), and several other neurological diseases. The efficacy of the drug as an AED In both adults and children has been mostly seen when used as an adjunct with other AEDs. ⋯ Also, the dosing of the drug in children has been complicated by negative behavioral adverse effects. Overall, gabapentin has a low incidence of adverse effects, a pharmacokinetic profile that limits its drug interactions, and limited effects on cognition when compared to traditional AEDs. The dosing of the drug is dependent on the disease state targeted, the number of specific therapeutic drugs used, and the renal function of the patient.
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Severe neurogenic pain still constitutes a major problem since it is often resistant to conventional therapy. During the last 30 years electric activation of pain inhibitory mechanisms through stimulation both of peripheral nerves and of central nervous circuits has been used to great advantage. The simplest method of stimulation, transcutaneous electric nerve stimulation (TENS), is extensively used by physiotherapists as well as in pain clinics. ⋯ TENS originally served as a screening method to identify patients suitable for spinal cord stimulation therapy (SCS). The main indication is severe neuropathic pain of peripheral origin, but SCS has also been found valuable in extremity ischemia as well as in refractory angina pectoris. The most severe cases of neuropathic pain may benefit from intracranial stimulation via electrodes placed stereotactically in the posteromedial thalamus or epidurally over the motor cortex.
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This review addresses the issue of how axotomy of peripheral nerve fibers leads to pain and hyperalgesia. The point of axotomy (the nerve injury site), the dorsal root ganglia, and the dorsal horn of the spinal cord are candidate sites for generation of the pain signal that is likely to be critical for maintaining the neuropathic pain state. This review considers neuropathic pain from a "systems" perspective, tracing concepts of neuropathic pain from the work of Henry Head to the present. ⋯ These abnormalities in the intact nociceptor, which arise in the context of Wallerian degeneration, probably play a role in creating or maintaining the abnormal pain state. These considerations probably also apply to the understanding of pain arising in other neuropathies. The findings relative to the "intact" nociceptor provide a rationale by which to understand how therapies distal to the nerve injury site may diminish pain.
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Damage to peripheral nerves triggers a cascade of events in axotomized sensory neurones that are generally believed to be responsible for the generation of neuropathic pain. Recent data in animal models show that alterations in the properties of undamaged neurones that project into a damaged nerve can also play an important role. These new findings could explain some of the enigmatic clinical signs and symptoms of pain following nerve injury such as the spread of symptoms into areas not affected by the primary lesion. The basis by which uninjured nerves could be affected is a reduced supply of neurotrophic factors, an abnormal interaction in the Remak bundles of partially denervated Schwann cells and unmyelinated axons, or the byproducts of Wallerian degeneration.