Hostname: page-component-cd9895bd7-gvvz8 Total loading time: 0 Render date: 2024-12-28T01:37:03.209Z Has data issue: false hasContentIssue false
  • English
  • Français

Cortical Relay Time for Long Latency Reflexes in Patients with Definite Multiple Sclerosis

Published online by Cambridge University Press:  16 February 2016

Cengiz Tataroglu ,
Ahmet Genc ,
Egemen Idiman ,
Raif Cakmur  and
Fethi Idiman
Cengiz Tataroglu*
Affiliation:
Department of Neurology, Mersin University, Faculty of Medicine, Mersin
Ahmet Genc
Affiliation:
Department of Neurology, Dokuz Eylul University, Faculty of Medicine, Izmir, Turkey
Egemen Idiman
Affiliation:
Department of Neurology, Dokuz Eylul University, Faculty of Medicine, Izmir, Turkey
Raif Cakmur
Affiliation:
Department of Neurology, Dokuz Eylul University, Faculty of Medicine, Izmir, Turkey
Fethi Idiman
Affiliation:
Department of Neurology, Dokuz Eylul University, Faculty of Medicine, Izmir, Turkey
*
Mersin University, Faculty of Medicine, Department of Neurology, 33079 Mersin, Turkey
Rights & Permissions [Opens in a new window]

Abstract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.
Background:

Long latency reflexes (LLR) include afferent sensory, efferent motor and central transcortical pathways. It is supposed that the cortical relay time (CRT) reflects the conduction of central transcortical loop of LLR. Recently, evidence related to the cortical involvement in multiple sclerosis (MS) has been reported in some studies. Our aim was to investigate the CRT alterations in patients with MS.

Methods:

Upper extremity motor evoked potentials (MEP), somatosensory evoked potentials (SEP) and LLR were tested in 28 patients with MS and control subjects (n=22). The patients with MS were classified according to the clinical form (relapsing-remitting [R-R] and progressive groups). The MS patients with secondary progressive and primary progressive forms were considered as the “progressive” group. CRT for LLR was calculated by subtracting the peak latency of somatosensory evoked potentials (SEP) and that of motor evoked potentials (MEP) by transcranial magnetic stimulation from the onset latency of the second component of LLR (LLR2) (CRT = LLR2 – [MEP latency + N20 latency])

Results:

Cortical relay time was calculated as 7.4 ± 0.9 ms in control subjects. Cortical relay time was prolonged in patients with MS (11.2 ± 2.9 ms) (p<0.0001). The latencies of LLR, MEP and SEP were also prolonged in patients with MS. Cortical relay time was not correlated with disease severity and clinical form in contrast to other tests.

Conclusions:

Our findings suggested that CRT can be a valuable electrophysiological tool in patients with MS. Involvement of extracortical neural circuits between sensory and motor cortices or cortical involvement due to MS may cause these findings.

Type
Original Article
Information
Canadian Journal of Neurological Sciences , Volume 31 , Issue 2 , May 2004 , pp. 229 - 234
Copyright
Copyright © The Canadian Journal of Neurological 2004

References

1.Andersson, T, Siden, A, Persson, A.A comparison of motor evoked potentials and somatosensory evoked potentials in patients with multiple sclerosis and potentially related conditions. Electromyogr Clin Neurophysiol 1995;35:17–24.Google ScholarPubMed
2.Matthews, WB, Wattam-Bell, JR, Pountney, E.Evoked potentials in the diagnosis of multiple sclerosis: a follow up study. J Neurol Neurosurg Psychiatry 1982;45:303–307.CrossRefGoogle ScholarPubMed
3.Hess, CW, Mills, KR, Murray, NM, Schriefer, TN.Magnetic brain stimulation: central motor conduction studies in multiple sclerosis. Ann Neurol 1987;22:744–752.CrossRefGoogle ScholarPubMed
4.Mayr, N, Baumgartner, C, Zeitlhofer, J, Deecke, L.The sensitivity of transcranial cortical magnetic stimulation in detecting pyramidal tract lesions in clinically definite multiple sclerosis. Neurology 1991;41:566–569.CrossRefGoogle ScholarPubMed
5.Goodin, DS, Aminoff, MJ, Shih, PY.Evidence that the long latency stretch responses of the human wrist extensor muscle involves a transcerebral pathway. Brain 1990;113:1075–1091.CrossRefGoogle Scholar
6.Noth, J, Podoll, K, Friedemann, H.Long loop reflexes in small hand muscles in normal subjects and patients with Huntington’s Disease. Brain 1985;108:65–80.CrossRefGoogle ScholarPubMed
7.Deuschl, G, Strahl, K, Schenck, E, Lucking, C.Diagnostic significance of long latency reflexes in multiple sclerosis. Electroencephalogr Clin Neurophysiol 1988;70:56–61.CrossRefGoogle ScholarPubMed
8.Tarkka, IM, Larsen, TA.Short and long latency reflex responses elicited by electrical and mechanical stimulation in human hand muscle. Acta Physiol Scan 1986;128:71–76.CrossRefGoogle Scholar
9.Deuschl, G, Ludolph, A, Schenck, E, Lücking, CH.The relations between long-latency reflexes in hand muscles, somatosensory evoked potentials and transcranial stimulation of motor tracts. Electroencephalogr Clin Neurophysiol 1989;74:425–430.CrossRefGoogle ScholarPubMed
10.Michels, R, Wessel, K, Klöhn, S, Kompf, D.Long latency reflexes, somatosensory evoked potentials and transcranial magnetic stimulation: relation of the three methods in patients with multiple sclerosis. Electroencephalogr Clin Neuropysiol 1993;89:235–241.CrossRefGoogle Scholar
11.Kurusu, K, Kitamura, J.Long latency reflexes in contracted hand and foot muscles and their relations to somatosensory evoked potentials and transcranial magnetic stimulation of the motor cortex. Clin Neurophysiol 1999;110:2014–2019.CrossRefGoogle ScholarPubMed
12.McDonald, WI, Compston, A, Edan, G, et al.Recommended diagnostic criteria for multiple sclerosis: Guidelines from the International Panel on the Diagnosis of Multiple Sclerosis. Ann Neurol 2001;50:121–127.CrossRefGoogle ScholarPubMed
13.Lublin, FD, Reingold, SC.The National Multiple Sclerosis Society USA advisory Committee on Clinical Trials of New Agents in Multiple Sclerosis. Defining the clinical course of multiple sclerosis: results of an international survey. Neurology 1996;46:907–911.CrossRefGoogle ScholarPubMed
14.Kurtzke, JF.Rating neurologic impairment in multiple sclerosis: an expanded disability status scale (EDSS). Neurology 1983;33: 1444–1452.CrossRefGoogle ScholarPubMed
15.Krupp, LB, LaRocca, NG, Muir-Nash, J, Steinberg, AD.The fatigue severity scale. Application to patients with multiple sclerosis and systemic lupus erythmetosus. Arch Neurol 1989;46:1121–1123.CrossRefGoogle Scholar
16.Deuschl, G, Schenck, E, Lücking, CH.Long-latency responses in human thenar muscles mediated by fast conducting muscle and cutaneus afferents. Neurosci Lett 1985;55:361–366.CrossRefGoogle Scholar
17.Sonoo, M, Kobayashi, M, Genba-Shimizu, K, Mannen, T, Shimizu, T.Detailed analysis of the latencies of SEPcomponents. 1:selection of the best standard parameters and the establishment of the normal values. Electroencephalogr Clin Neurophysiol 1996;100:319–331.CrossRefGoogle Scholar
18.Nielsen, J, Petersen, N, Fedirchuk, B.Evidence suggesting a transcortical pathway from cutaneus foot afferents to tibialis anterior motoneurons in man. J Physiol 1997;501:473–484.CrossRefGoogle Scholar
19.Leocani, L, Colombo, B, Magnani, G, et al.Fatigue in multiple sclerosis is associated with abnormal cortical activation to voluntary movement – EEG evidence. Neuroimage 2001;13:1186–1192.CrossRefGoogle ScholarPubMed
20.Roelcke, U, Kappos, L, Lechner-Scott, J, et al.Reduced glucose metabolism in the frontal cortex and basal ganglia of multple sclerosis patients with fatigue. Neurology 1997;48:1566–1571.CrossRefGoogle Scholar
21.Bjartmar, JR, Wujek, BD, Trapp, BD.Axonal loss in the pathology of MS: consequences for understanding the progressive phase of the disease. J Neurol Sci 2003;206:165–171.CrossRefGoogle ScholarPubMed
22.Peterson, JW, Bö, L, Mörk, S, Chang, A, Trapp, BD.Transected neurites, apoptotic neurons, and reduced inflammation in cortical multiple sclerosis lesions. Ann Neurol 2001;50:389–400.CrossRefGoogle ScholarPubMed
23.Ciccarelli, O, Werring, DJ, Wheeler-Kingshott, CAet al.Investigation of MS normal-appearing brain using diffusion tensor MRI with clinical correlations. Neurology 2001;56:926–933.CrossRefGoogle ScholarPubMed
24.Ge, Y, Grossman, RI, Udupa, JK, et al.Magnetization transfer ratio histogram analysis of gray matter in relapsing-remitting multiple sclerosis. AJNR Am J Neuroradiol 2001;22:470–475.Google ScholarPubMed
25.Bakshi, R, Benedict, RH, Bermel, RA, et al.T2 hypointensity in the deep gray matter of patients with multiple sclerosis: A quantitative magnetic resonance imaging study. Arch Neurol 2002;59:62–68.CrossRefGoogle ScholarPubMed
26.Catalaa, I, Fulton, JC, Zhang, X, et al.MR imaging quantitation of gray matter involvement in multiple sclerosis and its correlation with disability measures and neurocognitive testing. AJNR Am J Neuroradiol 1999;20:1613–1618.Google ScholarPubMed