Chronic pain treatment with intravenous lidocaine

Petersen, Palle; Kastrup, Jens; Zeeberg, I.; Boysen, Gudrun

doi:10.1080/01616412.1986.11739753

Cited by 48 publications

(26 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, it is reasonable to predict that painful sensations will result from ectopic impulses generated in pain ¢bres, although the authors are not aware of such reports. It may be relevant that systemic injections of lignocaine are typically e¡ective in treating pain in MS patients (Petersen et al 1986), consistent with an underlying mechanism involving sodium channels (see above).…”

Section: (V) Painmentioning

confidence: 99%

The pathophysiology of multiple sclerosis⋮ the mechanisms underlying the production of symptoms and the natural history of the disease

Smith

McDonald

1999

Phil. Trans. R. Soc. Lond. B

290

181

View full text Add to dashboard Cite

The pathophysiology of multiple sclerosis is reviewed, with emphasis on the axonal conduction properties underlying the production of symptoms, and the course of the disease. The major cause of the negative symptoms during relapses (e.g. paralysis, blindness and numbness) is conduction block, caused largely by demyelination and inflammation, and possibly by defects in synaptic transmission and putative circulating blocking factors. Recovery from symptoms during remissions is due mainly to the restoration of axonal function, either by remyelination, the resolution of inflammation, or the restoration of conduction to axons which persist in the demyelinated state. Conduction in the latter axons shows a number of deficits, particularly with regard to the conduction of trains of impulses and these contribute to weakness and sensory problems. The mechanisms underlying the sensitivity of symptoms to changes in body temperature (Uhthoff's phenomenon) are discussed. The origin of ‘positive’ symptoms, such as tingling sensations, are described, including the generation of ectopic trains and bursts of impulses, ephaptic interactions between axons and/or neurons, the triggering of additional, spurious impulses by the transmission of normal impulses, the mechanosensitivity of axons underlying movement–induced sensations (e.g. Lhermitte's phenomenon) and pain. The clinical course of the disease is discussed, together with its relationship to the evolution of lesions as revealed by magnetic resonance imaging and spectroscopy. The earliest detectable event in the development of most new lesions is a breakdown of the blood–brain barrier in association with inflammation. Inflammation resolves after approximately one month, at which time there is an improvement in the symptoms. Demyelination occurs during the inflammatory phase of the lesion. An important mechanism determining persistent neurological deficit is axonal degeneration, although persistent conduction block arising from the failure of repair mechanisms probably also contributes.

show abstract

Section: (V) Painmentioning

confidence: 99%

The pathophysiology of multiple sclerosis⋮ the mechanisms underlying the production of symptoms and the natural history of the disease

Smith

McDonald

1999

Phil. Trans. R. Soc. Lond. B

290

181

View full text Add to dashboard Cite

show abstract

“…Expression on afferent neurons has made VGSCs attractive targets to regulate the flow of nociceptive signals to the spinal cord. Nonselective inhibitors of VGSCs, such as local anesthetics, have been used for the treatment of acute and pathological pain, but the therapeutic appeal of these agents is limited due to undesirable side effects (Petersen et al, 1986;Bach et al, 1990;Chaplan et al, 1995;Mao and Chen, 2000). Thus, there has been a growing interest in developing channel blockers that are selective for one VGSC subtype over all others for use in pain management and potentially limiting adverse events.…”

mentioning

confidence: 99%

A Selective Nav1.8 Sodium Channel Blocker, A-803467 [5-(4-Chlorophenyl-N-(3,5-dimethoxyphenyl)furan-2-carboxamide], Attenuates Spinal Neuronal Activity in Neuropathic Rats

McGaraughty¹,

Chu²,

Scanio³

et al. 2008

The Journal of Pharmacology and Experimental Therapeutics

View full text Add to dashboard Cite

We have recently reported that systemic delivery of A-803467 [5-(4-chlorophenyl-N-(3,5-dimethoxyphenyl)furan-2-carboxamide], a selective Na v 1.8 sodium channel blocker, reduces behavioral measures of chronic pain. In the current study, the effects of A-803467 on evoked and spontaneous firing of wide dynamic range (WDR) neurons were measured in uninjured and rats with spinal nerve ligations (SNLs). Administration of A-803467 (10 -30 mg/kg i.v.) reduced mechanically evoked (10-g von Frey hair) and spontaneous WDR neuronal activity in SNL rats. In uninjured rats, A-803467 (20 mg/kg i.v.) transiently reduced evoked but not spontaneous firing of WDR neurons. The systemic effects of A-803467 in SNL rats were not altered by spinal transection or by systemic pretreatment with the transient receptor potential vanilloid type 1 (TRPV1) receptor agonist, resiniferatoxin, at doses that impair the function of TRPV1-expressing fibers. To determine sites of action,

show abstract

“…Similarly, studies examining the analgesic effects of lidocaine in patients with chronic neuropathic pain report relief sometimes lasting weeks from single infusions [27,28]. In the study by Attal et al [12] of lidocaine in peripheral neuropathic pain, the analgesic effects of lidocaine were no longer statistically significant beyond 24 hours.…”

Section: Therapeutic Lidocaine Infusionsmentioning

confidence: 97%

Intravenous lidocaine for neuropathic pain: Diagnostic utility and therapeutic efficacy

Carroll

2007

Curr Pain Headache Rep

View full text Add to dashboard Cite

Lidocaine is a use-dependent sodium channel blocker that produces analgesia when administered intravenously to patients with neuropathic pain. This article reviews the role and limitations of intravenous lidocaine infusions for neuropathic pain. Lidocaine infusions rarely provide relief that persists significantly beyond the duration of the infusion. Diagnostically, systemic lidocaine may help establish the presence of neuropathic pain and the responsivity to oral sodium channel blockade. However, the data supporting diagnostic infusions remain sparse. Therapeutically, infusions should generally be restricted to patients with neuropathic pain who are unable to take oral medication.

show abstract

Chronic pain treatment with intravenous lidocaine

Cited by 48 publications

References 7 publications

The pathophysiology of multiple sclerosis⋮ the mechanisms underlying the production of symptoms and the natural history of the disease

The pathophysiology of multiple sclerosis⋮ the mechanisms underlying the production of symptoms and the natural history of the disease

A Selective Nav1.8 Sodium Channel Blocker, A-803467 [5-(4-Chlorophenyl-N-(3,5-dimethoxyphenyl)furan-2-carboxamide], Attenuates Spinal Neuronal Activity in Neuropathic Rats

Intravenous lidocaine for neuropathic pain: Diagnostic utility and therapeutic efficacy

Contact Info

Product

Resources

About