Lidocaine and similar local anesthetics are effective for treating pain that emanates from damaged nerves, according to a systematic review of current evidence.
Neuropathic pain, which can occur with chronic diseases or conditions, is frequently unresponsive to treatment and worsens over time.
“Intravenous lidocaine and oral derivatives relieve pain from damage to the nervous system,” found authors Ivo W. Tremont-Lukats, M.D., of the M.D. Anderson Cancer Center in Houston, and colleagues. They add that the drugs, “were safe in controlled clinical trials for neuropathic pain, were better than placebo and were as effective as other analgesics.” [Read more]

J Orthop Sci. 2005;10(3):315-20.
We studied the efficacy of mexiletine as a sodium channel blocker for neuropathic pain by investigating the effect of mexiletine on the pathological ectopic firing pattern in a chronic constriction nerve injury (CCI) model. The experiment was conducted with 60 male Wistar rats. The CCI model was created by loosely ligating the sciatic nerve. After breeding 7 days, the frequency and pattern of ectopic firing antidromically recorded from the sural nerve and the amplitude of antidromic sensory nerve-evoked potential were analyzed. The CCI rats were given an intravenous injection of normal saline and mexiletine (5 or 15 mg/kg). Mexiletine significantly suppressed spontaneous firing frequency, an on-off firing pattern that consisted of cyclic bursting spikes and ectopic firing generation under the hypoxic condition. Mexiletine did not influence the amplitude of A-delta component in the antidromic sensory nerve-evoked potential. Mexiletine suppressed ectopic firing by blocking activity of the abnormal sodium channel at the nerve-injured site and dorsal root ganglion without blocking nerve conduction. This study suggests that mexiletine is useful for treating neuropathic pain in peripheral neuropathy.

From Bioscience Technology: Researchers say they have developed a way to block the signals responsible for neuropathic pain. The group used a disabled form of the herpes simplex virus (HSV) as a vector to deliver genes to the nucleus of neural cells in rats.
“We use the vector to provide targeted gene delivery to the nervous system,” says David Fink, MD, professor of neurology, University of Michigan Medical School, Ann Arbor, and a neurologist at the VA Ann Arbor Healthcare System, who co-directed the research study. “In this case, we’re not trying to correct a genetic defect. Our goal is simply to deliver a gene to sensory nerve cells, so its product can be used to block transmission of pain signals from damaged nerves to the brain.”

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From Current Pain and Headache Reports 2005, 9:178-183
The treatment of painful polpyneuropathies has begun to improve over the past several years. This is based on an evolving understanding of the pathogenesis related to the development of diabetic neuropathy and other diseases that may lead to peripheral nerve injury. Consensus on evaluation strategies for patients presenting with pain has furthered our ability to define neuropathic pain and accompanying signs and symptoms that may respond to particular therapeutic approaches. Recent therapeutic advances in medical management have demonstrated improved outcomes in pain relief. This, along with lower side effect-related issues, has led to improved compliance and patient satisfaction. The assessment and treatment of comorbid conditions, which include sleep, anxiety, and depression, have further advanced the management of painful polyneuropathies in patients. New antiepileptics, antidepressants, and topical therapies have contributed to improved patient outcomes.