Neuropathic pain

Arises from a lesion or disease affecting the somatosensory system.

Most commonly stems from impairment within the peripheral nervous system pathways, painful perpheral neuropathy, radiculopathy, complex regional pain syndrome, postherpetic neuralgia.

Less commonly, such pain can develop from disease that affects the brain, brainstem, or spinal cord.

Referred to as central neuropathic pain that can result from any type of injury to the CNS including vascular, ischemic, hemorrhagic, infectious, such as abscess, encephalitis, myelitis, demyelinating, traumatic, or neoplastic.

Can result from syrinx formation in the spinal cord or brainstem.

Central neuropathic pain is most commonly a sequelae of stroke, multiple sclerosis, or spinal cord injury.

Randomized clinical trials reveal no more than 50% of patients with NP have clinically meaningful pain relief, which is almost only partial in nature.

Prevalence of pain in population based studies 7-8% (Smith BH).

Can adversely affect ones quality of life including physical and emotional functioning.

Impairs sleep and depresses individual’s mood.

Pain caused by a primary lesion or dysfunction of the nervous system.

Divided into central or peripheral types with abnormal somatosensory processing.

Infers abnormal neural plasticity associated with an overt injury to neural structures, as part of a recognized pathological syndrome or associated with burning, shooting pain or electrical sensation of an abnormal quality.

Causes include: infections, inflammatory diseases, metabolic abnormalities, nerve compression, trauma, toxin or drug exposure and tumors.

Most common reasons for NP pain are radiculopathies, diabetes, nerve trauma, including postsurgical neuralgia.

Herpes zoster, spine degeneration, and stroke are common causes in elderly causing NP.

Described as burning, electrical shock or shooting pain.

Cutaneous allodynia, pain caused by nonnoxious stimuli, is frequently associated with paresthesias and abnormal perception of sensory stimulus in the skin.

Clinical examination may show sensory changes in a peripheral nerve or in a radicular distribution.

Mechanism of pain include injury to peripheral nerves leading to hyperexcitability of peripheral nociceptors which leads to afferent input to central neurons which cause increased sensitization and pain intensification.

Management includes drugs, nerve blocks and ablative neurosurgical procedures in refractory cases.