Neuropathic Pain

By M. Costigan, J. Scholz, Clifford J. Woolf. Annual Review of Neuroscience, 2009

1,892 citations recorded by the source corpus.

Neuropathic pain is triggered by lesions to the somatosensory nervous system that alter its structure and function so that pain occurs spontaneously and responses to noxious and innocuous stimuli are pathologically amplified. The pain is an expression of maladaptive plasticity within the nociceptive system, a series of changes that constitute a neural disease state. Multiple alterations distributed widely across the nervous system contribute to complex pain phenotypes. These alterations include ectopic generation of action potentials, facilitation and disinhibition of synaptic transmission, loss of synaptic connectivity and formation of new synaptic circuits, and neuroimmune interactions. Although neural lesions are necessary, they are not sufficient to generate neuropathic pain; genetic polymorphisms, gender, and age all influence the risk of developing persistent pain. Treatment needs to move from merely suppressing symptoms to a disease-modifying strategy aimed at both preventing maladaptive plasticity and reducing intrinsic risk.

Subfields: Cognitive Neuroscience, Neurology, Physiology

View Paper: https://www.semanticscholar.org/paper/8847f0ae621881747b30b0c798714f47a6b55cd4

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cognitive Neuroscience

1. Javeria Ali Hashmi
2. Marwan N. Baliki
3. Clifford J. Woolf
4. G. Moalem-Taylor
5. P. Austin
6. Apkar Vania Apkarian
7. T. S. Jensen
8. N. Finnerup

In Neurology

1. G. Moalem-Taylor
2. P. Austin
3. Clifford J. Woolf
4. T. S. Jensen
5. N. Finnerup
6. Apkar Vania Apkarian
7. Marwan N. Baliki

In Physiology

1. Clifford J. Woolf
2. G. Moalem-Taylor
3. P. Austin
4. Marwan N. Baliki
5. N. Finnerup
6. Javeria Ali Hashmi
7. T. S. Jensen
8. Apkar Vania Apkarian

Citations in the corpus

• Report Nociceptive Sensitization Reduces Predation Risk (2014, neutral): “Indeed, in clinical contexts long-lasting sensitization and pain are often assumed to be maladaptive rather than adaptive [19, 25].”
• The neuro-immune balance in neuropathic pain: involvement of inflammatory immune cells, immune-like glial cells and cytokines. (2010, positive): “…neurons, IFN-γ is heavily implicated in activation of microglia, and ablation of the IFN-γ signalling in IFN-γ−/− or IFN-γR−/− mice severely impairs both activation of microglia and development of pain hypersensitivity following peripheral nerve injury (Costigan et al., 2009a; Tsuda et al., 2009).”
• Central sensitization: Implications for the diagnosis and treatment of pain (2010, background): “pathic and dysfunctional pain disorders in patients [53,258].”
• Shape shifting pain: chronification of back pain shifts brain representation from nociceptive to emotional circuits. (2013, background): “between cortico-mesolimbic reorganization with the peripheral and spinal cord reorganization that has been extensively documented in animal models (Julius and Basbaum, 2001; Costigan et al., 2009).”
• The evidence for pharmacological treatment of neuropathic pain (2010, background): “It is unlikely that this complexity can be squeezed into a ‘‘crude rating scale of global pain intensity” [21].”