Articles: neuropathic-pain.
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SUMMARY Spinal cord stimulation (SCS) as treatment for chronic neuropathic pain has developed into an important therapeutic strategy. However, several studies indicate that as many as 30-50% of patients do not respond sufficiently to technically well-functioning SCS. Experimental studies have revealed some of the possible neuronal systems and transmitters involved in SCS. ⋯ Relevant data exist for intrathecal baclofen as an adjuvant to SCS, but trials with clonidine and adenosine have also been performed. Available basic studies indicate that other substances might also prove useful in future trials. The present data thus only announce the beginning of 'drug-enhanced spinal stimulation'.
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SUMMARY Trigeminal neuropathic pains have presented diagnostic and therapeutic challenges to providers. In addition, knowledge of pathophysiology, current classification systems, taxonomy and phenotyping of these conditions are incomplete. While trigeminal neuralgia is the most identifiable and studied, other conditions are being recognized and require distinct management approaches. ⋯ Trigeminal neuropathic pain is managed medically based on the guidelines for other neuropathic pain conditions. Burning mouth syndrome is also treated with a number of neuropathic medications, both topical and systemic. In all these conditions, patients need to be thoroughly educated about their condition, involved in its management, and be provided with supportive and adjunctive treatment resources.
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Expert Rev Clin Pharmacol · May 2011
ReviewTargeting N-methyl-D-aspartate receptors for treatment of neuropathic pain.
Neuropathic pain remains a major clinical problem and a therapeutic challenge because existing analgesics are often ineffective and can cause serious side effects. Increased N-methyl-d-aspartate receptor (NMDAR) activity contributes to central sensitization in certain types of neuropathic pain. NMDAR antagonists can reduce hyperalgesia and allodynia in animal models of neuropathic pain induced by nerve injury and diabetic neuropathy. ⋯ However, patients with postherpetic neuralgia respond poorly to NMDAR antagonists. Recent studies on identifying NMDAR-interacting proteins and molecular mechanisms of increased NMDAR activity in neuropathic pain could facilitate the development of new drugs to attenuate abnormal NMDAR activity with minimal impairment of the physiological function of NMDARs. Combining NMDAR antagonists with other analgesics could also lead to better management of neuropathic pain without causing serious side effects.
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Annals of neurosciences · Apr 2011
ReviewEmerging role of WNK1 in pathologic central nervous system signaling.
WNK1 (with no lysine (K)) is a widely expressed serine/threonine protein kinase. The role of this kinase was first described in the kidney where it dynamically controls ion channels that regulate changes in cell volume. WNK1, through intermediates oxidative stress-responsive kinase-1 (OSR1) and STE20/SPS1-related proline/alanine-rich kinase (SPAK), phosphorylates the inwardly directed Na(+)-K+-Cl(-)--cotransporter 1 (NKCC1) and the outwardly directed K(+)-Cl(-)-cotransporter 2 (KCC2), activating and deactivating these channels, respectively. ⋯ Growing evidence implicates WNK1 playing a critical role in pathologic nervous system signaling where changes in intracellular ion concentration in response to γ-aminobutyric-acid (GABA) can activate otherwise silent pathways. This review will focus on current research about WNK1, its downstream effectors and role in GABA signaling. Future perspectives include investigating WNK1 expression in the CNS after spinal cord injury (SCI), where altered neuronal signaling could underlie pathological states such as neuropathic pain (NP).
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Introduction In order to develop valid experimental human pain models, i.e., models potentially reflecting mechanisms underlying certain expressions of clinical pain conditions, similarities and discrepancies of symptoms/signs must first and foremost be evaluated comparing the two. In a situation where symptoms/signs appear to be similar, a potential pitfall with surrogate models would be that pathophysiological mechanisms in clinical conditions and experimental models might differ, i.e., one symptom/sign may be due to several different mechanisms. Symptoms and signs caused by intradermally injected capsaicin have been suggested to reflect aspects of the clinical phenomenology of neuropathic pain, e.g., dynamic mechanical allodynia. ⋯ Only 3/9 healthy subjects reported brush-evoked pain after capsaicin injection, a finding that may be related to this group reporting less spontaneous pain than the patients after injection. A hyperexcitable nervous system due to the contralateral clinical condition may also have a bearing on the frequent finding of capsaicin-induced allodynia in the patients (8/9). Implications The low prevalence of tactile allodynia in healthy volunteers makes the capsaicin model an unattractive strategy.