What Is Neuropathic Pain?

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>>>>Since neuropathic pain seems to be unheard of to some, and not experienced

by some, I thought I would send this again. ~>Becky M.

www.mmhc.com/cg/suppl/neuropathic/

What Is Neuropathic Pain?

Neuropathic pain is simply that pain which results from injury to the peripheral

or central nervous system. For the purposes of this review, neuropathic pain is

addressed mainly in terms of the peripheral nervous system; however, damage to

other portions of the nervous system, particularly in the spinal cord or

thalamus, can also produce neuropathic pain. Neuropathic pain can be regarded as

a maladaptive pain occurring from damage to the peripheral nerves by a variety

of possible mechanisms. These causes may be metabolic in origin and include the

following:

* Diabetes or renal failure

* Trauma such as from a crushing or penetrating injury

* Ischemia from a variety of vascular diseases

* Toxicity from alcohol, arsenic, medications, or a variety of other substances

* Hereditary conditions such as Charcot-Marie-Tooth disease

* Infections such as HIV, syphilis, or Lyme disease

* Immune-mediated conditions such as Guillain-Barre syndrome and chronic

immune-related neuropathies

Depending upon the etiology and particular response to the etiology,

pathophysiologic mechanisms produce either stimulus-independent or

stimulus-evoked pain, resulting in the syndrome of neuropathic pain (Figure 1).2

The pain generated in neuropathic pain syndrome can be quite varied from person

to person and, in fact, quite varied in the same person depending on time of

day, activity level, mood state, or a number of other variables.

Stimulus-Independent Pain

Stimulus-independent pain can be a mechanism of peripheral neuropathic pain

associated with spontaneous activity in the primary sensory neurons or in

injured axons. By a complex mechanism of sodium channel excitability, chemical

release at postganglionic sympathetic terminals, and increased excitability in

dorsal horn neurons due to reduced inhibitory input from the nerve injury,

a state of neuropathic pain can be independent and spontaneous—much to the

distress of the patient.

Attempts at neurosurgical lesions and anesthetic blocks have long been tried,

usually with temporary or often negligible benefit.

The lack of optimal benefit probably is due to the plasticity of the peripheral

and central nervous systems, which can bypass a focal lesion. In fact, recent

evidence has shown that unilateral nerve injury in a postherpetic state can be

associated with bilateral neuron damage.

Stimulus-Evoked Pain

Stimulus-evoked pain is quite distressing to patients with neuropathic

pain. This pain typically is due to a mechanical stimulation, such as light

touch or any form of pressure that triggers a mechanical hyperalgesia. This

hyperalgesia can be interpreted as an increased excitability compared to a

normal response from sensory input. An exaggerated and persistent stimulation

often mediated through C-fiber sensory neurons causes sensitization of the

dorsal horn neurons. This sensitization causes stimulation that normally would

be innocuous to become irritating and painful. The term allodynia best describes

this exaggerated response of pain perception to injured nerve fibers that is

typically stimulus-evoked. Recently, loss of sensory neurons within the

epidermis of patients with postherpetic neuralgia that caused allodynia has been

positively correlated with sensory defects.

Potential treatment of neuropathic pain from peripheral injury should

consider central nervous system (CNS) changes in the spinal cord and the brain.

Changes in the CNS can alter the function, chemistry, and sometimes the actual

structure of neurons.

With such changes, long-lasting or even permanent neuropathic pain can result.

Therefore, treatment options for peripheral nerve injuries of a significant

nature need to consider treatment directed at changes of the CNS as well.

Clinical reorganization with alterations of cortical spatial maps also has been

detected after nerve injury, contributing to phantom pain.