neurologic disorders
Neuropathic Pain
Etiology of Neuropathic Pain
Neuropathic pain may result from efferent activity (sympathetically maintained pain) or from interruption of afferent activity (deafferentation pain). Peripheral nerve injury or dysfunction can result in neuropathic pain. Examples are Mononeuropathies (involve a single nerve [eg, Brachial Plexus and Lumbosacral Plexus Disorders (involve multiple nerves within a particular neural plexus; typically caused by trauma, inflammation, or nerve compression, as by a tumor) Polyneuropathy (involve multiple nerves, often throughout the body; typically caused by various metabolic disorders, paraproteinemias, toxic exposures [eg, alcohol, chemotherapy]), hereditary predisposition, or, rarely, immune mediated mechanisms—see tables Mechanisms of neuropathic pain are complex and involve changes At the peripheral nociceptor and nerve level At the dorsal root ganglion In central nervous system (CNS) nociceptive pathways and terminal structures At the peripheral nerve and nociceptor level, injury results in inflammation and in activation and over-representation of cation channels, particularly sodium channels. These changes reduce the threshold for activation and increase the response to noxious stimuli. In chronic states, the peripheral nerve continuously triggers nociceptive ectopic signals to the CNS. This bombardment of continuous peripheral nociceptive input leads to changes in receptive nociceptors (central sensitization); they are primed, interpret pain from minor stimuli (including nonpainful stimuli [allodynia]) as substantial pain, and interpret that pain as coming from a wider area than it is. These changes can be reversed, at least for a time, if the peripheral nociceptive input can be interrupted. Central neuropathic pain syndromes(pain caused by dysfunction of somatosensory pathways in the CNS) can result from any CNS lesion, but these syndromes most commonly occur after stroke, result from spinal cord injury, or are associated with a multiple sclerosis demyelinating plaque. To be considered central neuropathic pain, the pain must occur in the area clinically affected by the CNS lesion; however, it does not need to involve the entire affected area. Central neuropathic pain develops only if the spinothalamic tract (pinprick, temperature sensation) malfunctions. If pinprick and temperature sensation are normal in the area of pain suspected to be central neuropathic pain, another pain source should be considered. The cause of pain in neurologically impaired patients is more commonly musculoskeletal (eg. shoulder pain related to arm paresis after a stroke or an upper extremity overuse syndrome in wheelchair-bound patients with a spinal cord injury). Deafferentation painis due to partial or complete interruption of peripheral or central afferent neural activity. Examples are Postherpetic neuralgia None Central pain (pain after CNS injury) Complications (pain felt in the region of an amputated body part) Mechanisms are unknown but may involve sensitization of central neurons, with lower activation thresholds and expansion of receptive fields. Neuropathic pain syndromes are sometimes associated with overactivity of the sympathetic nervous system. The sympathetic overactivity does not cause neuropathic pain, but it can contribute to its clinical features and severity. The pain that results is called sympathetically maintained pain, which depends on efferent sympathetic activity. Complex Regional Pain Syndrome (CRPS) sometimes involves sympathetically maintained pain. Other types of neuropathic pain may have a sympathetically maintained component. What triggers sympathetic overactivity in some neuropathic pain states and not others is unknown. Mechanisms probably involve abnormal sympathetic-somatic nerve connections (ephapses), local inflammatory changes, and changes in the spinal cord. 