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Motor Impairment and Neuropathic Pain in Patients with Neurological Diseases:...
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Motor Impairment and Neuropathic Pain in Patients with Neurological Diseases: Pathophysiological Mechanisms and Potential Treatment Options

A special issue of Journal of Functional Morphology and Kinesiology (ISSN 2411-5142).

Deadline for manuscript submissions: closed (31 January 2018) | Viewed by 8713

Special Issue Editor

Dr. Alessandro Castorina

E-Mail Website
Guest Editor
School of Life Sciences, University of Technology Sydney, Sydney, NSW 2007, Australia
Interests: nervous system diseases; neuropharmacology; anatomy; biomolecular; musculoskeletal disorders; neuropathic pain
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurological diseases are the result of neurodegenerative processes, neuroinflammation and/or physical trauma to the central or peripheral nervous system. Patients affected by neurological diseases frequently develop comorbidities like motor impairment and neuropathic pain, which can be more debilitating than the primary neurological condition. Whilst understanding the aetiology of the neurological disease is imperative, clarifying the pathophysiological mechanisms of the associated comorbidities is progressively becoming a prioritized area. Exploring the mechanisms underlying the associated motor and sensorial dysfunctions represents a unique opportunity to gain new insights on the neurological disease, and may be the next logical step for the development of more effective therapeutical strategies. In this Special Issue, “Motor Impairment and Neuropathic Pain in Patients with Neurological Diseases: Pathophysiological Mechanisms and Potential Treatment Options” authors are encouraged to submit original research papers and/or current reviews focused on the pathophysiological mechanisms of motor impairment and/or neuropathic pain in neurological diseases and on currently available treatment options.

Dr. Alessandro Castorina
Guest Editor

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 submissions that pass pre-check are 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 single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Functional Morphology and Kinesiology is an international peer-reviewed open access quarterly 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 1600 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.

Keywords

  • motor impairment
  • neurotrauma
  • neuropathic pain
  • neurodegenerative disease
  • neuroinflammation
  • autoimmune disease
  • drugs
  • multiple sclerosis

Published Papers (2 papers)

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Research

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2890 KiB  
Article
Sonic Hedgehog and TDP-43 Participate in the Spontaneous Locomotor Recovery in a Mouse Model of Spinal Motoneuron Disease
by Rosario Gulino, Rosalba Parenti and Massimo Gulisano
J. Funct. Morphol. Kinesiol. 2017, 2(2), 11; https://doi.org/10.3390/jfmk2020011 - 19 Apr 2017
Cited by 1 | Viewed by 3920
Abstract
Several studies have attempted to repair the damaged spinal cord (SC) by stimulating neurogenesis or neuroplasticity, with limited success. Sonic hedgehog (Shh) is involved in neural induction and stem cell functioning, but recent findings also suggest its role in regeneration and functional recovery. [...] Read more.
Several studies have attempted to repair the damaged spinal cord (SC) by stimulating neurogenesis or neuroplasticity, with limited success. Sonic hedgehog (Shh) is involved in neural induction and stem cell functioning, but recent findings also suggest its role in regeneration and functional recovery. Transactive response DNA-binding protein of 43 kDa (TDP-43) is a nuclear DNA/RNA binding protein involved in transcription and RNA processing. Recent findings have reported cytoplasmic inclusions containing TDP-43 in amyotrophic lateral sclerosis. Although substantial attention has been given to the toxic effects of this protein, the functional role of TDP-43 remains largely unclear. We used a mouse model of neurotoxic motoneuron depletion to study the role of the above-described factors in the compensatory changes occurring after the lesion. The injection of cholera toxin-B saporin into the gastrocnemius muscle caused a partial motoneuron death accompanied by an impairment of locomotion. Interestingly, motor activity was significantly restored as soon as one month later. Moreover, we observed an activity-dependent modification of Shh and synaptic proteins: synapsin-I and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptors. Notably, the motor performance of lesioned animals correlated with the expression of synapsin-I and Shh. Conversely, the expression of Shh significantly correlated with the levels of synapsin-I, GluR2, and TDP-43. The results suggest that Shh and TDP-43 are crucial parts of a complex mechanism of neuroplasticity in a mouse model of SC motoneuron disease. Full article
(This article belongs to the Special Issue Motor Impairment and Neuropathic Pain in Patients with Neurological Diseases: Pathophysiological Mechanisms and Potential Treatment Options)
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Review

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14 pages, 452 KiB  
Review
Insights into the Role of Neuroinflammation in the Pathogenesis of Multiple Sclerosis
by Ghaith Al-Badri and Alessandro Castorina
J. Funct. Morphol. Kinesiol. 2018, 3(1), 13; https://doi.org/10.3390/jfmk3010013 - 13 Feb 2018
Cited by 10 | Viewed by 4323
Abstract
Multiple sclerosis (MS) is a devastating disease, and with the increasing number of cases each year, it is becoming a significant socioeconomic burden for the affected people and the entire community. The aetiology of MS is largely unknown, but genetic susceptibility, exposure to [...] Read more.
Multiple sclerosis (MS) is a devastating disease, and with the increasing number of cases each year, it is becoming a significant socioeconomic burden for the affected people and the entire community. The aetiology of MS is largely unknown, but genetic susceptibility, exposure to infections and/or environmental toxicants are recognised as risk factors. MS is characterised by the appearance of lesions/plaques in the central nervous system, caused by destruction of the myelin sheet by auto-reactive T cells. Symptoms range from mild impairment of daily motor functions to severe sensory and cognitive disabilities necessitating mobility assistance, medical and support from caregivers. Due to the progressive nature of the disease, MS is gaining more attention and research to better understand its multifaceted pathogenesis. In the present review, we focus on some of the latest research related to the neuroinflammatory component of the disease, since it appears to play a critical role in MS pathogenesis. The goal is to shed more light on this specific domain of MS, in an attempt to assist in the identification of novel treatment trajectories and management plans. Full article
(This article belongs to the Special Issue Motor Impairment and Neuropathic Pain in Patients with Neurological Diseases: Pathophysiological Mechanisms and Potential Treatment Options)
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