The sensitivity of transcranial cortical magnetic stimulation in detecting pyramidal tract lesions in clinically definite multiple sclerosis

Mayr, Norbert; Baumgartner, Christoph; Zeitlhofer, J.; Deecke, Lüder

doi:10.1212/wnl.41.4.566

Cited by 62 publications

(40 citation statements)

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“…This is entirely in keeping with our observations that CFS patients are supersensitive to ACh and show an exaggerated GH release response when challenged with pyridostigmine, an acetylcholinesterase (AChE) inhibitor that increases intrasynaptic ACh (Chaudhuri et al, 1997a). The recent reports of prolonged central motor conduction time in both CFS and MS (Hilgers et al, 1998;Ravenborg et al, 1992;Mayr et al, 1991) are again further evidence for a common pathogenic mechanism of fatigue. These data, together with our research ®ndings of abnormal REE in CFS, transient low level antibodies to voltage-gated potassium channels in the sera of 25 per cent of CFS patients and the relationship between CTX and the development of CFS, cannot be explained rationally except as a channelopathy.…”

Section: Is Cfs An Acquired Channelopathy?supporting

confidence: 88%

Chronic fatigue syndrome is an acquired neurological channelopathy

Chaudhuri

Behan

1999

Hum. Psychopharmacol. Clin. Exp.

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Many symptoms of chronic fatigue syndrome (CFS), including severity of fatigue, may be periodic, fluctuant and induced by physical and mental activities, including trauma and stress. The fatigue in CFS is distinct from the fatigue of neuromuscular disorders but is similar to that found in disorders of the central nervous system such as multiple sclerosis, Parkinson's disease and multiple system atrophy. Though fatigue is a common symptom of depressive disorders, it is now clear that CFS patients differ from patients with major depression in their symptoms, biologic markers such as steroid metabolism and response to standard antidepressant drug therapy. In this paper, we propose dysfunctional ion channels in the cell membranes as the key abnormality in CFS which may also be responsible for the altered neuroendocrine functions reported in this condition. In our hypothesis, changes in the neuronal ion channel function from time to time offers a rational basis to explain fluctuating fatigue and related symptoms in CFS. Finally, ion channel abnormality leading to selective neuronal instability may be the common disease mechanism in CFS and other paroxysmal disorders affecting brain functions such as migraine and epilepsy. Copyright © 1999 John Wiley & Sons, Ltd.

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Section: Is Cfs An Acquired Channelopathy?supporting

confidence: 88%

Chronic fatigue syndrome is an acquired neurological channelopathy

Chaudhuri

Behan

1999

Hum. Psychopharmacol. Clin. Exp.

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“…13,15,19,25 They are useful for monitoring disease activity in patients with primary and secondary progressive MS 17 and may help predict the natural evolution of the disease. 9 However, little is known of the utility or otherwise of MEPs in experimental autoimmune encephalomyelitis (EAE), a preclinical model of MS with motor system involvement that can be induced in various strains of rodents.…”

Section: Accepted 14 September 2005mentioning

confidence: 99%

Motor evoked potentials in a mouse model of chronic multiple sclerosis

et al. 2005

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We tested cortical motor evoked potentials (cMEPs) as a quantitative marker for in vivo monitoring of corticospinal tract damage in a murine multiple sclerosis model (experimental autoimmune encephalomyelitis, EAE). The cMEPs, previously standardized in naive C57BL/6 developing and adult mice, were studied longitudinally in adult EAE mice. Central conduction times (CCTs) increased significantly shortly before the earliest clinical signs developed (10 days postimmunization, dpi), with peak delay in acute EAE (20-40 dpi). In clinically stable disease (80 dpi), CCTs did not increase further, but cMEP amplitude declined progressively, with complete loss in >80% of mice at 120 dpi. Increase in CCT correlated with presence of inflammatory infiltrates and demyelination in acute EAE, whereas small or absent cMEPs were associated with continuing axonal damage in clinically-stabilized disease and beyond (>80 dpi). These results demonstrate that cMEPs are a useful method for monitoring corticospinal tract function in chronic-progressive EAE, and provide insight into the pathological substrate of the condition.

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“…In addition, the reported diagnostic sensitivities of iSP measurements showed large variation, ranging from 80% in early RRMS [14] and 74% in a mixed sample of RRMS and chronic progressive MS [13] to 46% in a mixed sample of RRMS and secondary progressive MS [12]. In contrast, TMS measurements of central motor conduction time (CMCT) are now a diagnostic standard to assess the integrity of the corticospinal tract in patients with definite MS, and many studies reported consistently diagnostic sensitivities between 60% and 80% for both upper and lower limbs [19][20][21][22].…”

Section: Introductionmentioning

confidence: 99%