Samuel Reyes-Long
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Alfonso Alfaro-Rodríguez
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Jose Luis Cortes-Altamirano
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Eleazar LaraPadilla
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Elizabeth Herrera-Maria
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...
Background:
Botulinum toxin type A (BoNT-A) is widely employed for cosmetic purposes and in the treatment
of certain diseases such as strabismus, hemifacial spasm and focal dystonia among others. BoNT-A effect mainly acts at the
muscular level by inhibiting the release of acetylcholine at presynaptic levels consequently blocking the action potential in
the neuromuscular junction. Despite the great progress in approval and pharmaceutical usage, improvement in displacing
BoNT-A to other pathologies has remained short. Patients under diagnosis of several types of cancer experience pain in a
myriad of ways; it can be experienced as hyperalgesia or allodynia, and the severity of the pain depends, in some degree, on
the place that the tumor is located. Pain relief in patients diagnosed with cancer is not always optimal, and as the disease
progresses, transition to more aggressive drugs, like opioids is sometimes unavoidable. In recent years BoNT-A employment in cancer has been explored, as well as an antinociceptive drug; experiments in neuropathic, inflammatory and acute
pain have been carried out in animal models and humans. Although its mechanism has not been fully cleared evidence has
shown that BoNT-A inhibits the secretion of pain mediators (substance P, Glutamate, and calcitonin gene related protein)
from the nerve endings and dorsal root ganglion, impacting directly on the nociceptive transmission through the anterolateral and trigeminothalamic systems.
Aim:
Collect available literature regarding molecular, physiological and neurobiological evidence of the BoNT-A in cancer
patients suffering from acute, neuropathic and inflammatory pain in order to identify possible mechanisms of action in
which the BoNT-A could impact positively in pain treatment.
Conclusion:
BoNT-A could be an important neo-adjuvant and coadjuvant in the treatment of several types of cancer, diminish pro-tumor activity and secondary pain.
Regulation of Calcitonin Gene-Related Peptide Secretion From Trigeminal Nerve Cells by Botulinum Toxin Type A: Implications for Migraine Therapy