scholarly journals Clinical and Neurophysiological Effects of Botulinum Neurotoxin Type A in Chronic Migraine

Toxins ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 392
Author(s):  
Mariarosaria Valente ◽  
Christian Lettieri ◽  
Valentina Russo ◽  
Francesco Janes ◽  
Gian Luigi Gigli

Chronic pain syndromes present a subversion of both functional and structural nociceptive networks. We used transcranial magnetic stimulation (TMS) to evaluate changes in cortical excitability and plasticity in patients with chronic migraine (CM) treated with botulinum neurotoxin type A (BoNT/A). We enrolled 11 patients with episodic migraine (EM) and 11 affected by CM. Baseline characteristics for both groups were recorded using single- and paired-pulse TMS protocols. The same TMS protocol was repeated in CM patients after four cycles of BoNT/A completed in one year. At baseline, compared with EM patients, patients with CM had a lower threshold in both hemispheres (right hemisphere: 46% ± 7.8 vs. 52% ± 4.28, p = 0.03; left hemisphere: 52% ± 4.28 vs. 53.54% ± 6.58, p = 0.02). In EM, paired-pulse stimulation elicited a physiologically shaped response, whereas in CM, physiological intracortical inhibition (ICI) between 1 and 3 ms intervals was absent at baseline. On the contrary, increasing intracortical facilitation (ICF) was observed for all interstimulus intervals (ISIs). In CM, cortical excitability was partially reduced after BoNT/A treatment, along with a significant decrease observed in MIDAS score (from 20.7 to 9.8; p = 0.008). The lower motor threshold in CM reflects a higher cortical hyperexcitability. The lack of physiological ICI in CM could indicate sensitisation of the trigeminovascular system. Although reduced, this type of response is still observable after treatment, despite a marked clinical improvement. Our study suggests a long-term alteration of cortical plasticity due to chronic pain.


Toxicon ◽  
2021 ◽  
Vol 190 ◽  
pp. S70
Author(s):  
Sudhakar R. Subramaniam ◽  
Greg Nicholson ◽  
Brian B. Cai ◽  
Amy D. Brideau-Andersen ◽  
Ron S. Broide


Toxicon ◽  
2021 ◽  
Vol 190 ◽  
pp. S63
Author(s):  
Susana Rosa ◽  
Bruno Guimarães ◽  
Joana Martins ◽  
José Luís Mesquita ◽  
Margarida Freitas ◽  
...  




Toxicon ◽  
2015 ◽  
Vol 93 ◽  
pp. S8-S9 ◽  
Author(s):  
Anna Rita Bentivoglio


2000 ◽  
Vol 68 (5) ◽  
pp. 2587-2593 ◽  
Author(s):  
John A. Chaddock ◽  
John R. Purkiss ◽  
Lorna M. Friis ◽  
Janice D. Broadbridge ◽  
Michael J. Duggan ◽  
...  

ABSTRACT Clostridial neurotoxins potently and specifically inhibit neurotransmitter release in defined cell types by a mechanism that involves cleavage of specific components of the vesicle docking/fusion complex, the SNARE complex. A derivative of the type A neurotoxin fromClostridium botulinum (termed LHN/A) that retains catalytic activity can be prepared by proteolysis. The LHN/A, however, lacks the putative native binding domain (HC) of the neurotoxin and is thus unable to bind to neurons and effect inhibition of neurotransmitter release. Here we report the chemical conjugation of LHN/A to an alternative cell-binding ligand, wheat germ agglutinin (WGA). When applied to a variety of cell lines, including those that are ordinarily resistant to the effects of neurotoxin, WGA-LHN/A conjugate potently inhibits secretory responses in those cells. Inhibition of release is demonstrated to be ligand mediated and dose dependent and to occur via a mechanism involving endopeptidase-dependent cleavage of the natural botulinum neurotoxin type A substrate. These data confirm that the function of the HC domain of C. botulinumneurotoxin type A is limited to binding to cell surface moieties. The data also demonstrate that the endopeptidase and translocation functions of the neurotoxin are effective in a range of cell types, including those of nonneuronal origin. These observations lead to the conclusion that a clostridial endopeptidase conjugate that can be used to investigate SNARE-mediated processes in a variety of cells has been successfully generated.





Toxicology ◽  
2015 ◽  
Vol 335 ◽  
pp. 79-84 ◽  
Author(s):  
Ivica Matak ◽  
Zdravko Lacković


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