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Mechanisms of Neuropathic pain

Mechanisms Of Neuropathic Pain

(ĐTĐ) – Neuropathic pain is a type of pain which is caused by damage to or dysfunction of the nervous system. Neuropathic pain cannot be explained by a single disease process or a single specific location of damage.

Neuropathic pain may be associated with abnormal sensations called dysesthesias, which occur spontaneously and allodynias that occur in response to external stimuli. Neuropathic pain may have continuous and/or episodic (paroxysmal) components. The latter are likened to an electric shock. Common qualities of neuropathic pain includes burning or coldness, “pins and needles” sensations, numbness and itching. Nociceptive pain is more commonly described as aching.

As much as 7% to 8% of the population is affected and in 5% it may be severe. Neuropathic pain may result from disorders of the peripheral nervous system or the central nervous system (pain and spinal cord). Thus, neuropathic pain may be divided into peripheral neuropathic pain, central neuropathic pain, or mixed (peripheral and central) neuropathic pain.

Central neuropathic pain is found in spinal cord injury, multiple sclerosis, and some strokes. Fipomyalgia, a disorder of chronic widespread pain, is potentially a central pain disorder and is responsive to medications that are effective for neuropathic pain.4

Aside from diabetes (see Diabetic neuropathy) and other metabolic conditions, the common causes of painful peripheral neuropathies are herpes zoster infection, HIV-related neuropathies, nutritional deficiencies, toxins, remote manifestations of malignancies, genetic, and immune mediated disorders or physical trauma to a nerve trunk.

Neuropathic pain is common in cancer as a direct result of cancer on peripheral nerves (e.g., compression by a tumor), or as a side effect of chemotherapy, radiation injury or surgery.


The starting point for neuropathic pain is a lesion or dysfunction within the somatosensory system. Current knowledge regarding the mechanisms of neuropathic pain is incomplete and is biased by a focus on animal models of peripheral nerve injury.


Under normal circumstances, pain sensations are carried by unmyelinated and thinly myelinated nerve fibers, designated C-fibers and A-delta fibers respectively. After a peripheral nerve lesion, a neuroma may develop at the stump. The neurons become unusually sensitive and develop spontaneous pathological activity, abnormal excitability, and elevated sensitivity to chemical, thermal and mechanical stimuli. This phenomenon is called “peripheral sensitization”.


The dorsal horn neurons give rise to the spinothalamic tract (STT), which constitutes the major ascending nociceptive pathway. As a consequence of ongoing spontaneous activity arising in the periphery, STT neurons develop an increased background activity, enlarged receptive field and increased responses to afferent impulses, including normally innocuous tactile stimuli. This phenomenon is called central sensitization. Central sensitization has been proposed as an important mechanism of persistent neuropathic pain.

Other mechanisms, however, may take place at the central level after peripheral nerve damage. The loss of afferent signals induces functional changes in dorsal horn neurons. A decrease in the large fiber input decreases activity of interneurons inhibiting nociceptive neurons i.e. loss of afferent inhibition. Nociceptive pain can be described as the one that can occur in our everyday life as an aftermath of a simple insult or injury. The mechanism for such type of pain can be generated by transduction, which converts the stimulus into electrical activity in specialized nociceptive primary afferent nerves. Hypoactivity of the descending antinociceptive systems or loss of descending inhibition may be another factor. With loss of neuronal input (deafferentation) the STT neurons begin to fire spontaneously, a phenomenon designated “deafferentation hypersensitivity.”Non-neural glial cells may play a role in central sensitization. Peripheral nerve injury induces glial to releasing glial proinflammatory cytokines and glutamate which, in turn influence neurons.

Mechanisms at light-microscopic and submicroscopic levels

The phenomenon described above are dependent on changes at light-microscopic and submicroscopic levels. Aberrant regeneration, altered expression of ion channels, changes in neurotransmitters and their receptors as well as altered gene expression in response to neural input are at play.

Source: Wikipedia

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