A neurophysiological theory for the pain mechanism of tic douloureux

Calvin, William H.; Loeser, John D.; Howe, John F.

doi:10.1016/0304-3959(77)90078-1

Cited by 118 publications

(40 citation statements)

References 22 publications

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“…This continues periodically and results in a "pacemaker." Similar rhythmogenic phenomena associated with midaxon changes in properties may be involved with neural mechanisms of pain such as trigeminal neuralgia [3]. Since wave reflection occurs in cellular discrete media as well as in continuous cables it may provide yet another mechanism for ectopic pacemakers in cardiac tissue.…”

mentioning

confidence: 93%

Reflected Waves in an Inhomogeneous Excitable Medium

Ermentrout

Rinzel²

1996

SIAM J. Appl. Math.

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mentioning

confidence: 93%

Reflected Waves in an Inhomogeneous Excitable Medium

Ermentrout

Rinzel²

1996

SIAM J. Appl. Math.

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“…The period of stimulation may be expected to increase the extracellular potassium ion concentration, favouring a role for this ion in the underlying mechanism (Kapoor et al 1993;Felts et al 1995), but other mechanisms are also possible. In some demyelinated axons, impulses can be`re£ected' from sites of demyelination (Howe et al 1976;Calvin et al 1977Calvin et al , 1982Bostock 1994), i.e. an impulse propagating through a demyelinated site can result in the formation of a second impulse which travels back along the same axon in the opposite direction.…”

Section: (Iii) Triggered Sensationsmentioning

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

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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.

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“…This theory entails demyelination of and ectopic activity in Aδ nociceptive afferents. But paroxysmal bursts of ectopic activity arising from largediameter, non-nociceptive afferents may induce a secondary central dysfunction: a repeated, abnormally high-frequency activity in tactile afferents projecting to WDR neurons in the spinal trigeminal nucleus may change their excitability and induce a persistent derangement that provokes high-frequency signals from WDR neurons and thus pain [11]. Several works supporting this hypothesis have been reported [12].…”

Section: Pain Mechanismsmentioning

confidence: 98%