scholarly journals Motor conduction velocity in the human spinal cord: slowed conduction in multiple sclerosis and radiation myelopathy.

1985 ◽  
Vol 48 (11) ◽  
pp. 1135-1139 ◽  
Author(s):  
S J Snooks ◽  
M Swash
Keyword(s):  
Multiple Sclerosis ◽  
Spinal Cord ◽  
Conduction Velocity ◽  
Motor Conduction Velocity ◽  
Radiation Myelopathy ◽  
Human Spinal Cord

Clinico-pathological evidence that axonal loss underlies disability in progressive multiple sclerosis

2010 ◽  
Vol 16 (4) ◽  
pp. 406-411 ◽  
Author(s):  
Emma C Tallantyre ◽  
Lars Bø ◽  
Omar Al-Rawashdeh ◽  
Trudy Owens ◽  
Chris H Polman ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Spinal Cord ◽  
Progressive Multiple Sclerosis ◽  
Axonal Loss ◽  
Motor Disability ◽  
Human Spinal Cord ◽  
Axonal Pathology ◽  
Motor Tracts ◽  
First Time

Growing evidence suggests that axonal degeneration rather than demyelination is the pathological substrate underlying chronic, irreversible disability in multiple sclerosis. However, direct evidence linking clinical disability measured in vivo with corresponding post-mortem measures of axonal pathology is lacking. Our objective in this study was to investigate the relationship between motor disability accumulated by patients with multiple sclerosis during life and the degree of axonal loss observed in their descending motor tracts after death. Human spinal cord derived at autopsy from 45 patients with multiple sclerosis was investigated. The medical records of each patient were reviewed by a multiple sclerosis neurologist to determine the degree of motor disability reached before death. Spinal cord sections were stained immunohistochemically. The degree of demyelination and the number of surviving corticospinal tract axons were measured in each patient. Patients who had accumulated higher levels of motor disability prior to death demonstrated fewer surviving corticospinal axons. Motor disability did not correlate with degree of demyelination. This study provides for the first time, direct clinico-pathological evidence that axonal loss is the pathological substrate of established disability in multiple sclerosis.

scholarly journals Increases in human motoneuron excitability after cervical spinal cord injury depend on the level of injury

2017 ◽  
Vol 117 (2) ◽  
pp. 684-691 ◽  
Author(s):  
Christine K. Thomas ◽  
Charlotte K. Häger ◽  
Cliff S. Klein
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Conduction Velocity ◽  
Spinal Injury ◽  
Cervical Spinal Cord ◽  
Motor Units ◽  
M Wave ◽  
Human Spinal Cord ◽  
Motoneuron Excitability ◽  
Cord Injury

After human spinal cord injury (SCI), motoneuron recruitment and firing rate during voluntary and involuntary contractions may be altered by changes in motoneuron excitability. Our aim was to compare F waves in single thenar motor units paralyzed by cervical SCI to those in uninjured controls because at the single-unit level F waves primarily reflect the intrinsic properties of the motoneuron and its initial segment. With intraneural motor axon stimulation, F waves were evident in all 4 participants with C4-level SCI, absent in 8 with C5 or C6 injury, and present in 6 of 12 Uninjured participants ( P < 0.001). The percentage of units that generated F waves differed across groups (C4: 30%, C5 or C6: 0%, Uninjured: 16%; P < 0.001). Mean (±SD) proximal axon conduction velocity was slower after C4 SCI [64 ± 4 m/s ( n = 6 units), Uninjured: 73 ± 8 m/s ( n = 7 units); P = 0.037]. Mean distal axon conduction velocity differed by group [C4: 40 ± 8 m/s ( n = 20 units), C5 or C6: 49 ± 9 m/s ( n = 28), Uninjured: 60 ± 7 m/s ( n = 45); P < 0.001]. Motor unit properties (EMG amplitude, twitch force) only differed after SCI ( P ≤ 0.004), not by injury level. Motor units with F waves had distal conduction velocities, M-wave amplitudes, and twitch forces that spanned the respective group range, indicating that units with heterogeneous properties produced F waves. Recording unitary F waves has shown that thenar motoneurons closer to the SCI (C5 or C6) have reduced excitability whereas those further away (C4) have increased excitability, which may exacerbate muscle spasms. This difference in motoneuron excitability may be related to the extent of membrane depolarization following SCI. NEW & NOTEWORTHY Unitary F waves were common in paralyzed thenar muscles of people who had a chronic spinal cord injury (SCI) at the C4 level compared with uninjured people, but F waves did not occur in people that had SCI at the C5 or C6 level. These results highlight that intrinsic motoneuron excitability depends, in part, on how close the motoneurons are to the site of the spinal injury, which could alter the generation and strength of voluntary and involuntary muscle contractions.

scholarly journals Reduced motor conduction velocity of the ulnar nerve in spinal cord injured patients

Spinal Cord ◽  
1980 ◽  
Vol 18 (1) ◽  
pp. 21-24 ◽  
Author(s):  
Luba Stefaniwsky ◽  
David S Bilowit ◽  
Sheo S Prasad
Keyword(s):  
Spinal Cord ◽  
Ulnar Nerve ◽  
Conduction Velocity ◽  
Motor Conduction Velocity ◽  
Injured Patients ◽  
Spinal Cord Injured

Impairment of spinal cord conduction velocity in diabetic rats

Diabetes ◽  
1989 ◽  
Vol 38 (6) ◽  
pp. 730-736 ◽  
Author(s):  
R. E. Carsten ◽  
L. R. Whalen ◽  
D. N. Ishii
Keyword(s):  
Spinal Cord ◽  
Conduction Velocity ◽  
Diabetic Rats

scholarly journals CKD-506: A novel HDAC6-selective inhibitor that exerts therapeutic effects in a rodent model of multiple sclerosis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Daekwon Bae ◽  
Ji-Young Lee ◽  
Nina Ha ◽  
Jinsol Park ◽  
Jiyeon Baek ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Spinal Cord ◽  
Immune Responses ◽  
Therapeutic Potential ◽  
Autoimmune Encephalitis ◽  
Selective Inhibitor ◽  
Therapeutic Effects ◽  
Treatment Regimens ◽  
Ifn Γ ◽  
Experimental Autoimmune

AbstractDespite advances in therapeutic strategies for multiple sclerosis (MS), the therapy options remain limited with various adverse effects. Here, the therapeutic potential of CKD-506, a novel HDAC6-selective inhibitor, against MS was evaluated in mice with myelin oligodendrocyte glycoprotein35–55 (MOG35–55)-induced experimental autoimmune encephalitis (EAE) under various treatment regimens. CKD-506 exerted prophylactic and therapeutic effects by regulating peripheral immune responses and maintaining blood–brain barrier (BBB) integrity. In MOG35–55-re-stimulated splenocytes, CKD-506 decreased proliferation and downregulated the expression of IFN-γ and IL-17A. CKD-506 downregulated the levels of pro-inflammatory cytokines in the blood of EAE mice. Additionally, CKD-506 decreased the leakage of intravenously administered Evans blue into the spinal cord; CD4+ T cells and CD4−CD11b+CD45+ macrophage/microglia in the spinal cord was also decreased. Moreover, CKD-506 exhibited therapeutic efficacy against MS, even when drug administration was discontinued from day 15 post-EAE induction. Disease exacerbation was not observed when fingolimod was changed to CKD-506 from day 15 post-EAE induction. CKD-506 alleviated depression-like behavior at the pre-symptomatic stage of EAE. In conclusion, CKD-506 exerts therapeutic effects by regulating T cell- and macrophage-mediated peripheral immune responses and strengthening BBB integrity. Our results suggest that CKD-506 is a potential therapeutic agent for MS.

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