Reviewing the case for compromised spinal inhibition in neuropathic pain.
M A GradwellR J CallisterBrett Anthony GrahamPublished in: Journal of neural transmission (Vienna, Austria : 1996) (2019)
A striking and debilitating property of the nervous system is that damage to this tissue can cause chronic intractable pain, which persists long after resolution of the initial insult. This neuropathic form of pain can arise from trauma to peripheral nerves, the spinal cord, or brain. It can also result from neuropathies associated with disease states such as diabetes, human immunodeficiency virus/AIDS, herpes, multiple sclerosis, cancer, and chemotherapy. Regardless of the origin, treatments for neuropathic pain remain inadequate. This continues to drive research into the underlying mechanisms. While the literature shows that dysfunction in numerous loci throughout the CNS can contribute to chronic pain, the spinal cord and in particular inhibitory signalling in this region have remained major research areas. This review focuses on local spinal inhibition provided by dorsal horn interneurons, and how such inhibition is disrupted during the development and maintenance of neuropathic pain.
Keyphrases
- neuropathic pain
- spinal cord
- human immunodeficiency virus
- chronic pain
- spinal cord injury
- multiple sclerosis
- antiretroviral therapy
- hepatitis c virus
- cardiovascular disease
- oxidative stress
- hiv infected
- pain management
- type diabetes
- systematic review
- white matter
- papillary thyroid
- genome wide
- resting state
- hiv aids
- squamous cell carcinoma
- hiv positive
- adipose tissue
- lymph node metastasis
- skeletal muscle
- brain injury
- trauma patients
- squamous cell
- rectal cancer