Differing roles for parvalbumin neurons after nerve injury

Neuropathic pain is abnormal, persistent pain that is caused by injury to the somatosensory system. It commonly involves damage to the peripheral nerves as a result of physical trauma, metabolic diseases such as diabetes, infections such as HIV or shingles, or toxicity induced neuropathies as a result of cancer treatments. Neuropathic pain is common, with epidemiological studies suggesting that around 18-30% of American, European and Australian adults suffer from chronic pain. This leads to significant disabilities and suffering. People with chronic pain complain of spontaneous pains that may be electric-shock like or continuous. Often coexisting with these are abnormal, evoked sensations such as tactile allodynia (pain in response to innocuous stimuli e.g., light brush or pressure) and cold allodynia (pain in response to innocuous cooling), or hyperalgesia (increase pain in response to an already noxious stimulus), as well as ataxia and proprioceptive deficits. The management of these conditions is often suboptimal for two main reasons: firstly, an incomplete knowledge of the mechanisms that are involved (and which of them are the most important). Secondly, patients often have compliance issues with pharmacological medications (Attal, 2012). Both peripheral and central neuronal mechanisms contribute to the pathophysiology and since the turn of the century particular emphasis has focussed on the role of glial cells in pain (West et al., 2015).