Neuropathic pain whether based on an injury or a result of a form of dysfunction from the nervous system is still a condition which better treatment options are still being researched. Neuropathic pain can even be divided further into peripheral and central neuropathic pain. While peripheral pain may result from a disease, a more central neuropathic pain may result from damage to brain or spinal cord. [] Despite numerous medications in the market and therapy treatments which patients endure, neuropathic pain remains a formidable opponent. Areas of clinical research today that work with neuropathic pain, has focus in areas which include use of ion modulators. Within the past decade itself treatment for neuropathic pain by targeting ion gated
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Change in the level of expression otherwise distribution of sodium channels is strongly correlated with neuropathic pain. It is understood that an increase in sodium channel density then lowers the nociceptive threshold. The neurons then have a tendency to move towards action potential initiation and propagation. Ion channel modulators then inhibit increasing activity. Blockade of the sodium ion channel stops the process where action potential initiation is most frequent. Local anesthetics have been a common therapeutic approach. Infusions of lidocaine has demonstrated relief of pain symptoms associated with diabetic neuropathy in certain patients. While effective the idea of intravenous infusions is not an easily accessible mode of delivery, especially for patients with a chronic condition. Mexiletine, analogues to lidocaine has shown to be a better alternative. As an oral intake, benefits included being a sodium ion channel blockade. Through clinical trials however the medication is rather inconsistent and has often lead to GI distress and other side effects as a result of drug to drug interaction. Topical lidocaine in the form of a patch (5%) when used at recommended dosage has been shown that there is no need for titration and there is no …show more content…
As the molecular characterization of medications made improves so will the significance of a mechanism based approach to treatment which will vary from patient to patient. With current understanding of sodium gated ion channels, one must remember that different causes or injuries that result in neuropathic pain may also result in changes of certain expression of sodium ion channel genes. However, based on review done it is understood that sodium ion channel expression in DRG neurons changes after an injury and thus changes in sodium channel expression alters excitability within the cells themselves. Research on the exact role of each of the sodium channel subtype in relation to the pathophysiology of DRG neurons and pain is still currently underway. In my opinion further development of sodium ion channel blockades will be a promising strategy for a phrenological treatment of neuropathic
Change in the level of expression otherwise distribution of sodium channels is strongly correlated with neuropathic pain. It is understood that an increase in sodium channel density then lowers the nociceptive threshold. The neurons then have a tendency to move towards action potential initiation and propagation. Ion channel modulators then inhibit increasing activity. Blockade of the sodium ion channel stops the process where action potential initiation is most frequent. Local anesthetics have been a common therapeutic approach. Infusions of lidocaine has demonstrated relief of pain symptoms associated with diabetic neuropathy in certain patients. While effective the idea of intravenous infusions is not an easily accessible mode of delivery, especially for patients with a chronic condition. Mexiletine, analogues to lidocaine has shown to be a better alternative. As an oral intake, benefits included being a sodium ion channel blockade. Through clinical trials however the medication is rather inconsistent and has often lead to GI distress and other side effects as a result of drug to drug interaction. Topical lidocaine in the form of a patch (5%) when used at recommended dosage has been shown that there is no need for titration and there is no …show more content…
As the molecular characterization of medications made improves so will the significance of a mechanism based approach to treatment which will vary from patient to patient. With current understanding of sodium gated ion channels, one must remember that different causes or injuries that result in neuropathic pain may also result in changes of certain expression of sodium ion channel genes. However, based on review done it is understood that sodium ion channel expression in DRG neurons changes after an injury and thus changes in sodium channel expression alters excitability within the cells themselves. Research on the exact role of each of the sodium channel subtype in relation to the pathophysiology of DRG neurons and pain is still currently underway. In my opinion further development of sodium ion channel blockades will be a promising strategy for a phrenological treatment of neuropathic