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Special Issue "Botulinum Toxin for Neuropathic Pain Treatment"
Deadline for manuscript submissions: closed (30 June 2019).
Prof. Dr. Antonella Giannantoni Website E-Mail
Department of Medical and Surgical Sciences and Neurosciences; Functional and Surgical Urology Unit; University of Siena, Azienda Ospedaliero-Universitaria Santa Maria alle Scotte, Siena, Italy
Interests: Functional Urology, Female Urology, Neuro-Urology, Oncological Urology
Botulinum neurotoxin (BoNT), derived from Clostridium botulinum, has been used worldwide for the treatment of neurologic disorders, such as dystonia or spasticity, and for cosmetic purposes. The neurotoxin has eight antigenically different serotypes, and its main mechanism of action is the inhibition of acetylcholine release at presynaptic nerve terminals, with a resulting reduction of muscle fiber activity.
In recent times, the therapeutic use of BoNT, and particularly of BoNT/A, has expanded to cover different clinical conditions characterized by neuropathic pain (NP), such as chronic migraine, lower back pain, myofascial pain, trigeminal neuropathy, temporo-mandibular joint disorders, osteoarthritis, pelvic pain, and bladder painful syndrome.
NP, which is pain caused by a lesion or a disease of the somatosensory system, affects 6–8% of the general population and exerts a great impact on patients’ quality of life. Despite its high prevalence, NP is still difficult to diagnose and treat, as it is not a unique disease but a syndrome covering a wide spectrum of different pathologies with complex clinical presentations and multiple signs and symptoms. The pathophysiology of NP involves both the peripheral and the central nervous systems and includes changes in the excitability of peripheral nerves and dorsal root ganglions (peripheral sensitization), changes in spinal cord neurons, the descending pain-controlling systems, and abnormal brain plasticity (central sensitization).
Although BoNT/A action on NP is still mainly considered to be of peripheral origin, recent findings showed that the neurotoxin is axonally transported to central sensory regions and suggested that its antinociceptive action is centrally mediated. Yet, the process by which BoNT/A is able to induce pain relief is not clear, and many additional questions remain to be answered on the mechanism of BoNT/A antinociceptive action at both peripheral and central levels and on the effectiveness of the neurotoxin in the treatment of different pain syndromes. Studies addressing these questions are welcomed.
Prof. Dr. Antonella Giannantoni
Manuscript Submission Information
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a double-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Toxins is an international peer-reviewed open access monthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.
- Botulinum toxin
- neuropathic pain
- chronic pain syndromes
- substance P
- calcitonin gene-related peptide