Plaques, symptoms, and the remitting course of multiple sclerosis

Namerow, Norman S.; Thompson, Lawrence R.

doi:10.1212/wnl.19.8.765

Cited by 46 publications

(13 citation statements)

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“…Several studies using evoked po tentials and tissue imaging have shown that lesions of MS may be present in completely asymptomatic patients for months and even years. As Namerow and Thompson [17] stated in 1969: 'One should be clear in dif ferentiating the disease process per se from the cause of symptoms, since the two may at times be quite independent. Central ner vous system demyelination and functional incapacity are not synonymous.'…”

Section: Date Of Onsetmentioning

confidence: 99%

Analysis of the ‘Epidemic' of Multiple Sclerosis in the Faroe Islands

Poser

Hibberd²,

Benedikz³

et al. 1988

Neuroepidemiology

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The claim has been made that British troops introduced multiple sclerosis (MS), a transmissible disease, into the Faroe Islands during World War II, causing a three-tier epidemic which resulted in the appearance of 32 cases from 1943 until 1973. Assumptions underlying this hypothesis include the belief that the disease was absent from the Faroe Islands before 1940, the view that ascertainment of cases was complete and that Faroese patients who had either been born in Denmark or had been away from the Islands for 3 or more years before the onset of the disease had to be excluded. All the calculations were based on the presumed date of appearance of the first symptoms of MS. We reject the hypotheses of an epidemic and of the transmissibility of MS for several reasons. The most important one is that the date of onset of illness bears no relationship to the probable date of acquisition, which is widely believed to occur between the ages of 5 and 15 years. The criteria for exclusion of cases are arbitrary and instead of the accepted 32 cases, we believe that 42 cases should be counted in all analyses, including at least 2 with onset of illness before 1940. Only 15 of these 42 were in the age range 5–14 years during the British occupation. We cannot accept the statement that the disease was unknown in the Faroes before 1940 and believe that case ascertainment was incomplete in the Islands, which share close geographic, ethnic, and environmental similarities with other North Sea countries of high MS incidence. The theory of transmission is unconvincing and the characteristics of the putative agent unrealistic. The extremely high incidence of disease, which has statistical significance, is based on a very small number of cases in a very small population, and is of very doubtful biological significance.

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Section: Date Of Onsetmentioning

confidence: 99%

Analysis of the ‘Epidemic' of Multiple Sclerosis in the Faroe Islands

Poser

Hibberd²,

Benedikz³

et al. 1988

Neuroepidemiology

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“…There is abundant clinical evidence that the symptoms of central demyelination can remit, or never appear (as in 'benign' multiple sclerosis), without remyelination being involved (Namerow & Thompson, 1969;Mackay & Hirano, 1967;McAlpine, …”

Section: (C) Continuou8 Conductionmentioning

confidence: 99%

The internodal axon membrane: electrical excitability and continuous conduction in segmental demyelination.

Bostock¹,

Sears²

1978

The Journal of Physiology

313

104

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SUMMARY1. Longitudinal action currents were recorded from single, undissected myelinated nerve fibres in intact, perfused ventral roots of normal rats and ones treated with diphtheria toxin to produce demyelination.2. Closely spaced recording electrodes (120 jsm), signal averaging and the use of a calibrating current through the root permitted membrane currents to be determined over 240 ,sum lengths of nerve. Contour plotting was used to plot membrane current density as a function of space and time.3. The previous result of Rasminsky & Sears (1972) of delayed saltation in demyelinated nerve fibres was confirmed.4. In addition a new phenomenon of continuous conduction was observed, along distances of up to 14 times the afferent internodal distance. The continuous spatial distribution of inward current in these cases showed that electrical excitability was distributed along the internodes.5. Internodal excitability was also revealed in demyelinated fibres by extra foci of inward current judged to be internodal on the basis of the spacing of the other (nodal) foci.6. Continuous conduction occurred at velocities in the range of 1*1-2 3 m/sec or roughly 1/20th-1/40th of the velocities expected for normal stretches of the same fibres.7. The continuous conduction was attributed to conduction along lengths of demyelinated axon. This was supported by estimates of 0-86 and 1-5 ,F/cm2 for membrane capacity from the foot of a continuously conducted action potential.8. The implications of internodal electrical excitability in demyelinated nerve fibres are discussed in relation to (a) recent estimates of the density of sodium channels in intact and homogenized normal nerves, (b) the pathophysiology of demyelinating disease.

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“…Clinical and experimental observations both suggest that, under some conditions, conduction may proceed without interruption, albeit at a reduced conduction velocity, through regions of total demyelination. Pathological studies, for example, have demonstrated that some demyelinated plaques may be asymptomatic (Ghatak et al, 1974), and that the distribution of plaques may be more widespread than would be predicted from the clinical deficits (Namerow and Thompson, 1969). One implication of these observations is that conduction may be preserved along at least some of the demyelinated axons.…”

mentioning

confidence: 99%

Conduction through demyelinated plaques in multiple sclerosis: computer simulations of facilitation by short internodes.

Waxman¹,

Brill²

1978

Journal of Neurology, Neurosurgery & Psychiatry

171

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S U M M A R Y Clinical and laboratory observations both suggest that it may be possible for action potentials to traverse, in a continuous manner and without interruption, demyelinated zones along some axons. This continuous mode of conduction requires the presence of sufficient numbers of sodium channels in the demyelinated region. One of the factors which will tend to prevent such conduction is the impedance mismatch at sites of focal demyelination, which may result in a reduction in current density sufficient to cause conduction failure. As part of an effort to examine the conditions which would promote conduction into, and beyond, the demyelinated region, we examined, using computer simulations, the effects of reduction in length of the proximal internodes closest to the demyelinated region. Our results indicate that reduction in length of the two internodes closest to the demyelinated region, to approximately one-third of normal length or less, will facilitate conduction beyond the plaque. The results suggest that reductions in internode length, which have been histologically observed along some demyelinated fibres, may have functional significance in terms of facilitating conduction past focally demyelinated zones.

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Plaques, symptoms, and the remitting course of multiple sclerosis

Cited by 46 publications

References 0 publications

Analysis of the ‘Epidemic' of Multiple Sclerosis in the Faroe Islands

Analysis of the ‘Epidemic' of Multiple Sclerosis in the Faroe Islands

The internodal axon membrane: electrical excitability and continuous conduction in segmental demyelination.

Conduction through demyelinated plaques in multiple sclerosis: computer simulations of facilitation by short internodes.

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