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CANDF1  -  candidiasis, familial 1

Homo sapiens

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Disease relevance of CMCT


Psychiatry related information on CMCT


High impact information on CMCT

  • A novel percutaneous magnetic stimulator was used to stimulate the motor cortex painlessly and CMCT was calculated by subtracting the onset latency of muscle responses obtained by electrical stimulation over the C7/T1 interspace from that obtained from stimulation over the scalp [1].
  • The results suggest that prolonged CMCT is related to spinal cord lesion load and that, over time, changes in the CMCT occur only when spinal cord lesion load increases [2].
  • A 12 month longitudinal study has been performed on 118 subjects following first-ever stroke to determine changes in central motor conduction time (CMCT) to upper limb muscles [7].
  • Measurements of CMCT were made as described in the accompanying article (Heald et al., 1993, Brain, 116, 1355-1370), in which the following three groups of patients were recognized within 12-72 h after the onset of symptoms: normal response group, delayed response group and no response group [8].
  • Additional methods including analysis of oligonucleotides following chemical blocking of uridylate residues with CMCT and analysis of products of incomplete enzymatic digestion are also discussed [9].

Biological context of CMCT

  • We determined central motor conduction time (CMCT) (motor cortex to root C-8 and motor cortex to root S-1) as well as the amplitude of the compound muscle action potentials in the hypothenar and the abductor hallucis muscles on both sides in 44 patients with definite MS [10].
  • Motor evoked potentials (MEPs) were used to measure central motor conduction time (CMCT) and the triple stimulation technique (TST) was applied to assess conduction deficits [11].
  • No correlation was found between CMCT (R and L) and chronologic age, duration of disease, peroneal motor nerve conduction velocity [12].
  • The patients with full hand strength recovery and the normal controls were also tested by means of the 9-hole peg test.RESULTS: Motor threshold (MT), MEP amplitude and central motor conduction time (CMCT) of the affected side were significantly different from those of the normal side and of the control subjects [13].
  • Abnormalities in CMCT may be the third electrophysiological diagnostic criterion in FA, after reduced amplitude of nerve action potentials and absent H reflex [14].

Anatomical context of CMCT

  • OBJECTIVE: Diagnostic value of central motor conduction time (CMCT) to upper and lower limbs in cervical cord lesions was investigated [15].
  • Abnormal CMCT correlated to cord compression and to upper motor neuron involvement [15].
  • A less predictable pattern of weakness and CMCT change in corona radiata infarction may be attributed to a less definite organisation of motor pathways compared with the internal capsule [16].
  • The greatest number of abnormalities was disclosed by measurement of CMCT followed by SEPs after tibial nerve stimulation [17].
  • We report the results of a clinical and central motor conduction time (CMCT) study in 16 patients with internal capsule and 17 with computed tomography (CT)-proven corona radiata infarction [16].

Associations of CMCT with chemical compounds

  • The two groups of patients had clinical signs, CMCT changes and reduced MEP amplitude reflecting relevant cortico-spinal disorder [18].
  • CMCT from cortex to C8/T1 segments (APB) was 4.68 +/- 0.6 msec and between cortex and C5/C6 (biceps) 4.24 +/- 0.42 msec [19].

Other interactions of CMCT

  • In the second one, the 4 explored PTs showed a slowed conduction, but in addition, CMCT difference between the CLT and CCT was longer than normal [20].
  • As to the diagnosis of MS, the reliability of a prolonged central motor conduction time (CMCT) was 0.83 (0.73 to 0.93), while the reliability of a normal CMCT was 0.75 (0.61 to 0.98) [21].
  • Central motor conduction time (CMCT) in patients with hyperreflexia was significantly delayed compared to that in patients with GBS and areflexia (p < 0.001), and the delayed CMCTs were significantly improved in the recovery periods (p < 0.001) [22].
  • Three patients also underwent transcranial bifocal electric cortical stimulation (TES) and MEPs were recorded from the APB muscle, and CMCT, MEP threshold and amplitude were measured [23].

Analytical, diagnostic and therapeutic context of CMCT

  • Threshold to transcranial magnetic stimulation was determined by standard methods and CMCT was measured using the F-wave method [24].
  • A longitudinal study was performed on 118 first-ever stroke patients to evaluate neurophysiological measurements of central motor conduction time (CMCT) in the period immediately following stroke as predictors of functional outcome and mortality at 12 months [8].
  • For example, the CMCT system has the potential to improve the safety of guiding cochlear implant electrodes within the inner ear and assist the placement of inner ear microcatheters for delivery of gene modification therapy or administration of neurotrophic factors [25].
  • Central motor conduction time (CMCT) after transcranial magnetic stimulation (TMS) of the cortex, electromyography and nerve conduction velocity were performed in 24 patients with multiple system (MSA) and late onset cerebellar atrophy (LOCA) (often olivopontocerebellar atrophy--OPCA -) [26].
  • Central motor conduction time (CMCT) calculated from scalp and spine MEP was the most sensitive diagnostic test [27].


  1. Measurement of central motor conduction in multiple sclerosis by magnetic brain stimulation. Hess, C.W., Mills, K.R., Murray, N.M. Lancet (1986) [Pubmed]
  2. Central motor conduction time in progressive multiple sclerosis. Correlations with MRI and disease activity. Kidd, D., Thompson, P.D., Day, B.L., Rothwell, J.C., Kendall, B.E., Thompson, A.J., Marsden, C.D., McDonald, W.I. Brain (1998) [Pubmed]
  3. Latency and duration of the muscle silent period following transcranial magnetic stimulation in multiple sclerosis, cerebral ischemia, and other upper motoneuron lesions. Haug, B.A., Kukowski, B. Neurology (1994) [Pubmed]
  4. Motor evoked potentials in the preoperative and postoperative assessment of normal pressure hydrocephalus. Zaaroor, M., Bleich, N., Chistyakov, A., Pratt, H., Feinsod, M. J. Neurol. Neurosurg. Psychiatr. (1997) [Pubmed]
  5. Autosomal dominant pure spastic paraplegia: a clinical, paraclinical, and genetic study. Nielsen, J.E., Krabbe, K., Jennum, P., Koefoed, P., Jensen, L.N., Fenger, K., Eiberg, H., Hasholt, L., Werdelin, L., Sørensen, S.A. J. Neurol. Neurosurg. Psychiatr. (1998) [Pubmed]
  6. Central motor conduction time and regional cerebral blood flow in patients with leuko-araiosis. Mochizuki, Y., Oishi, M., Takasu, T. J. Neurol. Sci. (1998) [Pubmed]
  7. Longitudinal study of central motor conduction time following stroke. 1. Natural history of central motor conduction. Heald, A., Bates, D., Cartlidge, N.E., French, J.M., Miller, S. Brain (1993) [Pubmed]
  8. Longitudinal study of central motor conduction time following stroke. 2. Central motor conduction measured within 72 h after stroke as a predictor of functional outcome at 12 months. Heald, A., Bates, D., Cartlidge, N.E., French, J.M., Miller, S. Brain (1993) [Pubmed]
  9. Approaches to sequence analysis of 125I-labeled RNA. Dickson, E., Pape, L.K., Robertson, H.D. Nucleic Acids Res. (1979) [Pubmed]
  10. The sensitivity of transcranial cortical magnetic stimulation in detecting pyramidal tract lesions in clinically definite multiple sclerosis. Mayr, N., Baumgartner, C., Zeitlhofer, J., Deecke, L. Neurology (1991) [Pubmed]
  11. Quantification of central motor conduction deficits in multiple sclerosis patients before and after treatment of acute exacerbation by methylprednisolone. Humm, A.M., Z'Graggen, W.J., Bühler, R., Magistris, M.R., Rösler, K.M. J. Neurol. Neurosurg. Psychiatr. (2006) [Pubmed]
  12. Central motor conduction time in children and adolescents with insulin-dependent diabetes mellitus (IDDM). d'Annunzio, G., Moglia, A., Zandrini, C., Bollani, E., Vitali, L., Pessino, P., Scaramuzza, A., Lanzi, G., Lorini, R. Diabetes Res. Clin. Pract. (1995) [Pubmed]
  13. Transcranial magnetic stimulation after pure motor stroke. Pennisi, G., Alagona, G., Rapisarda, G., Nicoletti, F., Costanzo, E., Ferri, R., Malaguarnera, M., Bella, R. Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology. (2002) [Pubmed]
  14. Central motor conduction to upper and lower limbs after magnetic stimulation of the brain and peripheral nerve abnormalities in 20 patients with Friedreich's ataxia. Cruz Martínez, A., Anciones, B. Acta neurologica Scandinavica. (1992) [Pubmed]
  15. Central motor conduction time to upper and lower limbs in cervical cord lesions. Brunhölzl, C., Claus, D. Arch. Neurol. (1994) [Pubmed]
  16. Central motor conduction studies in internal capsule and corona radiata infarction. Misra, U.K., Kalita, J. J. Neurol. (1997) [Pubmed]
  17. SEPs and CNS magnetic stimulation in syringomyelia. Nogués, M.A., Pardal, A.M., Merello, M., Miguel, M.A. Muscle Nerve (1992) [Pubmed]
  18. MEP recruitment curves in multiple sclerosis and hereditary spastic paraplegia. Jørgensen, L.M., Nielsen, J.E., Ravnborg, M. J. Neurol. Sci. (2005) [Pubmed]
  19. Simplified technique for recording human cortical & spinal evoked muscle potentials. Gursahani, R.D., D'souza, C., Mansukhani, K., Pandya, S.S. Indian J. Med. Res. (1990) [Pubmed]
  20. Multiple sclerosis: assessment of lesional levels by means of transcranial stimulation. Segura, M.J., Garcea, O., Gandolfo, C.N., Sica, R.E. Electromyography and clinical neurophysiology. (1994) [Pubmed]
  21. The diagnostic reliability of magnetically evoked motor potentials in multiple sclerosis. Ravnborg, M., Liguori, R., Christiansen, P., Larsson, H., Sørensen, P.S. Neurology (1992) [Pubmed]
  22. Corticospinal tract involvement in a variant of Guillain-Barré syndrome. Oshima, Y., Mitsui, T., Endo, I., Umaki, Y., Matsumoto, T. Eur. Neurol. (2001) [Pubmed]
  23. Excitatory and inhibitory mechanisms in Wilson's disease: investigation with magnetic motor cortex stimulation. Perretti, A., Pellecchia, M.T., Lanzillo, B., Campanella, G., Santoro, L. J. Neurol. Sci. (2001) [Pubmed]
  24. The natural history of central motor abnormalities in amyotrophic lateral sclerosis. Mills, K.R. Brain (2003) [Pubmed]
  25. Design, analysis and simulation for development of the first clinical micro-CT scanner. Wang, G., Zhao, S., Yu, H., Miller, C.A., Abbas, P.J., Gantz, B.J., Lee, S.W., Rubinstein, J.T. Academic radiology. (2005) [Pubmed]
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