The management of neuropathic pain

Schwarz, Jacob; Naff, Neal J.

doi:10.1016/j.nec.2004.01.001

Cited by 6 publications

(7 citation statements)

References 60 publications

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“…Neuropathic pain also may occur after nerve injury [8-11], and whereas the injured tissue does usually repair, the neuropathic pain frequently persists [12-14]. One mechanism that is considered to underlie the abnormal pain after nerve damage involves regenerating nerve fibers.…”

Section: Introductionmentioning

confidence: 99%

Alteration of Primary Afferent Activity following Inferior Alveolar Nerve Transection in Rats

et al. 2010

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BackgroundIn order to evaluate the neural mechanisms underlying the abnormal facial pain that may develop following regeneration of the injured inferior alveolar nerve (IAN), the properties of the IAN innervated in the mental region were analyzed.ResultsFluorogold (FG) injection into the mental region 14 days after IAN transection showed massive labeling of trigeminal ganglion (TG). The escape threshold to mechanical stimulation of the mental skin was significantly lower (i.e. mechanical allodynia) at 11-14 days after IAN transection than before surgery. The background activity, mechanically evoked responses and afterdischarges of IAN Aδ-fibers were significantly higher in IAN-transected rats than naive. The small/medium diameter TG neurons showed an increase in both tetrodotoxin (TTX)-resistant (TTX-R) and -sensitive (TTX-S) sodium currents (INa) and decrease in total potassium current, transient current (IA) and sustained current (IK) in IAN-transected rats. The amplitude, overshoot amplitude and number of action potentials evoked by the depolarizing pulses after 1 μM TTX administration in TG neurons were significantly higher, whereas the threshold current to elicit spikes was smaller in IAN-transected rats than naive. Resting membrane potential was significantly smaller in IAN-transected rats than that of naive.ConclusionsThese data suggest that the increase in both TTX-S INa and TTX-R INa and the decrease in IA and Ik in small/medium TG neurons in IAN-transected rats are involved in the activation of spike generation, resulting in hyperexcitability of Aδ-IAN fibers innervating the mental region after IAN transection.

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Section: Introductionmentioning

confidence: 99%

Alteration of Primary Afferent Activity following Inferior Alveolar Nerve Transection in Rats

et al. 2010

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“…Central sensitisation. 41,44 Central sensitisation is a state of increased sensitivity of dorsal horn neurons so that their activation threshold is reduced. It follows the activation of the N-methyl D-aspartate (NMDA) receptor by the neurotransmitter glutamate and the subsequent influx of calcium through the voltage-gated calcium channels into the neuron.…”

Section: Mechanisms Of Neuropathic Painmentioning

confidence: 99%

“…A complex set of intracellular events following this calcium influx lead to altered gene expression and long-term neuronal changes, and a more sensitive nervous system. 42,44 Expression of the voltage-gated calcium channels is increased following nerve injury. 6,45 Clinical support for this phenomenon arises from the analgesic efficacy of α2-δ voltagegated calcium channels antagonists (see later) in patients with NP disorders.…”

Section: Mechanisms Of Neuropathic Painmentioning

confidence: 99%

“…Despite the best care and trials of therapy, NP will remain inadequately relieved for 40-60% of patients, and 10-15% of NP patients are regarded as truly refractory to all forms of pharmacotherapy. 44,47,51,65 Nerve block procedures may, in selected patients, be of value earlier in the course of NP, e.g. sympathetic nerve blocks in early complex regional pain syndrome, to facilitate physiotherapy and rehabilitation.…”

Section: Interventional Pain Managementmentioning

confidence: 99%

“…peripheral, spinal cord and motor cortex stimulation, intrathecal drug delivery systems and ablative neurosurgical procedures. 44 The best success rates in this category are for trigeminal ganglion balloon decompression and microvascular decompression, both procedures for trigeminal neuralgia.…”

Section: Interventional Pain Managementmentioning

confidence: 99%

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Neuropathic pain—Current concepts

Meyer

2008

South African Family Practice

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Neuropathic pain (NP) represents a common and diverse group of disorders with peripheral and/or central nervous system damage or dysfunction. Many patients report intractable and severe pain that is resistant to simple analgesics. The diagnosis of NP is primarily based on clinical evaluation rather than diagnostic tests. Distinct pain qualities in the patient's history and findings on clinical examination, such as hyperalgesia and other sensory findings in an area correlating with the patient's pain pattern are important in diagnosis. Various screening tools may assist in the diagnosis of NP.A number of pathophysiological mechanisms have been identified in NP, including sodium-and calcium-channel upregulation and spinal cord hyperexcitability (central sensitisation).Appropriate management includes evaluation of the functional impact of NP, patient education and reassurance. A multi-model biopsychosocial approach that includes various nonpharmacological modalities is recommended. Appropriate pharmacological management is based on evidence-based recommendations that provide guidance for selecting first-, second-and third-line medications, alone or in combination. It is hoped that future treatment advances will improve the care of patients who live with NP.

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Failed Back Syndrome

Schwarz¹,

Naff²

2006

Current Therapy in Neurologic Disease

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The management of neuropathic pain

Cited by 6 publications

References 60 publications

Alteration of Primary Afferent Activity following Inferior Alveolar Nerve Transection in Rats

Alteration of Primary Afferent Activity following Inferior Alveolar Nerve Transection in Rats

Neuropathic pain—Current concepts

Failed Back Syndrome

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