TITLE:
The Primary Motor Cortex Stimulation Attenuates Cold Allodynia in a Chronic Peripheral Neuropathic Pain Condition in Rattus norvegicus
AUTHORS:
Priscila Medeiros, Sylmara Esther Negrini-Ferrari, Ana Carolina Medeiros, Lais Leite Ferreira, Josie Resende Torres da Silva, José Aparecido da Silva, Norberto Cysne Coimbra, Renato Leonardo de Freitas
KEYWORDS:
Peripheral Neuropathic Pain, Chronic Pain, Sciatic Nerve, Chronic Constriction Injury, Cold Allodynia, Primary Motor Cortex Stimulation, Antinociception
JOURNAL NAME:
World Journal of Neuroscience,
Vol.9 No.3,
August
1,
2019
ABSTRACT: Background: The primary motor
cortex (M1) stimulation (MCS) is a useful tool for attenuation of
the peripheral neuropathic pain in patients with pharmacologically refractory
pain. Furthermore, that neurological procedure may also cause antinociception
in rodents with neuropathic pain. Cold allodynia is a frequent clinical finding
in patients with neuropathic pain, then, we evaluated if an adapted model of
neuropathy induced by chronic constriction injury (CCI) of the ischiadicus nervus (sciatic nerve) produces cold allodynia in an animal model of chronic pain. In
addition, we also investigated the effect of the electrical stimulation of the
M1 on chronic neuropathic pain condition in laboratory animals. Methods: Male Wistar rats were used. An adapted model of peripheral mononeuropathy
induced by CCI was carried out by placing a single loose ligature around the
right sciatic nerve. The acetone test was used to evaluate the cold allodynia
in CCI or Sham (without ligature) rats. The MCS (M1) was performed
at low-frequency (20 μA, 100 Hz) during 15 s by
deep brain stimulation (DBS-Thomas Recording device) 21 days after CCI or Sham
procedures. The cold allodynia was measured before and immediately after the
neurostimulation of M1 in the following time-window: 0, 15 and 30
min after MCS. Results: Cold
allodynia threshold increased in animals with chronic neuropathic pain
submitted to the acetone test 21 days after the CCI surgery. The M1-stimulation
by DBS procedure decreased the cold allodynia immediately and until 30 min
after M1-stimulation in rats with chronic neuropathic pain. Conclusion: The current
proposal for a CCI model by a single loose ligature of the sciatic nerve can be
employed as an experimental model of chronic neuropathic pain in rats submitted
to peripheral nervous system injury. The M1-stimulation produced
antinociception in rats with chronic neuropathic pain. Thus, we reinforced that
the MCS decreases cold allodynia in laboratory animals submitted to persistent
sciatic nerve constriction and can be a more reasonable procedure for the
treatment of chronic intractable neuropathic pain.