NEUROPATHIC PAIN
Neuropathic pain includes pain associated
with diabetic neuropathy, causalgia, phantom limbs, postherpetic neuralgia,
stroke, spinal cord injury, and multiple sclerosis. Cancer pain and chronic low
back pain may have prominent neuropathic compo-nents. Neuropathic pain tends to
be paroxysmal and sometimes lancinating with a burning quality, and is usually
associated with hyperpathia. Mechanisms of neuropathic pain are reviewed
earlier.
Because neuropathic pain is often difficult to treat, multiple
therapeutic modalities may be nec-essary. Treatment options include
anticonvulsants (eg, gabapentin, pregabalin), antidepressants (tri-cyclic
antidepressants or serotonin-norepinephrine reuptake inhibitors),
antiarrhythmics (mexiletine), α2-adrenergic
agonists (clonidine), topical agents(lidocaine or capsaicin), and analgesics
(NSAIDs and opioids). Of note, tricyclic antidepressants may have significant
anticholinergic side effects that may limit their tolerability. Secondary
amines, such as nortriptyline or desipramine, may have less severe or fewer anticholinergic
side effects than tertiary amines such as amitriptyline or imipramine. Spi-nal
opioids may be very effective for some patients. Sympathetic blocks are
effective in selected disor-ders . Spinal cord stimulation may be effective for
patients who do not tolerate or respond to other treatments.
Diabetic neuropathy is the most common type
of neuropathic pain encountered in practiceand is a major cause of morbidity.
Its pathophysi-ology is poorly understood but may be related to microangiopathy
and to abnormal activation of metabolic (polyol) pathways and glycation of
pro-teins as a consequence of chronic hyperglycemia. Diabetic neuropathy may be
symmetric (general-ized), focal, or multifocal, affecting peripheral (sen-sory
or motor), cranial, or autonomic nerves.
The most common syndrome is peripheral
polyneuropathy, which results in symmetric numb-ness (“stocking-and-glove”
distribution), pares-thesias, dysesthesias, and pain. The pain varies in
intensity, may be severe, and is often worst at night. Loss of proprioception
may lead to gait distur-bances, and sensory deficits can lead to traumatic
injuries. Isolated mononeuropathies affecting indi-vidual nerves may lead to
wrist or foot drop or to cranial nerve palsy. Mononeuropathies typically have a
sudden onset and are reversible, lasting a few weeks. Autonomic neuropathy
typically affects the gastrointestinal tract, causing diarrhea, delayed gastric
emptying, and esophageal motility disorders. Orthostatic hypotension and other
forms of auto-nomic dysfunction are common.
Treatment of diabetic neuropathy is symp-tomatic and directed at optimal
glycemic control to slow progression. Acetaminophen and NSAIDs are usually
ineffective for moderate to severe pain. Risks associated with opioids limit
their use in the treatment of this condition. Adjuvant drugs play a major role.
The combination of an antiepileptic drug and a tricyclic antidepressant may be
particu-larly effective.
Complex regional pain syndrome (CRPS) is a
neuropathic pain disorder with significantautonomic features that is usually
subdivided into two variants: CRPS 1, formerly known as reflex sympathetic
dystrophy (RSD), and CRPS 2, formerly known as causalgia. The major difference between the two is the absence or presence,
respectively, of documented nerve injury. Signs, symptoms, patho-physiology,
and response to treatment are quite similar. Previously, this condition was
thought to represent sympathetically maintained pain, but there is recent
evidence that in some cases the pain may be sympathetically independent.
CRPS is a largely underdiagnosed condi-tion
affecting at least 50,000 patients a year in the United States alone. It
affects individuals from childhood to late adulthood and may occur more
commonly in females. Patients frequently present with burning neuropathic pain
having components of hyperalgesia and allodynia. The autonomic ner-vous system
may be involved, exemplified by alter-ations in sweating (sudomotor changes),
color, and skin temperature, and by trophic changes in the skin, hair, or
nails. Decreases in strength and range of motion in the affected extremity may
be present. CRPS may develop after minimal injury, although the most common initiating
events are surgery, fractures, crush injuries, and sprains.
The pathophysiology of CRPS 1 and 2 is
prob-ably multifactorial, involving both the sympathetic nervous system and the
central nervous system. There may be changes in the cutaneous innervation after
a nerve injury, along with changes in central and peripheral sensitization.
Genetic, inflammatory, and psychological factors may all play roles. Causal-gia
(which means burning pain), first identified in injured veterans of the
American Civil War, typically follows gunshot injuries or other major trauma to
large nerves. The pain often has an immediate onset and is associated with
allodynia, hyperpathia, and vasomotor and sudomotor dysfunction. It is
exacer-bated by factors that increase sympathetic tone, such as fear, anxiety,
light, noise, or touch. The syndrome has a variable duration that can range
from days to months or may be permanent. Causalgia commonly affects the
brachial plexus, particularly the median nerve, and the tibial division of the
sciatic nerve in the lower extremity.
Patients with CRPS often respond to sympa-thetic blocks, but a
multidisciplinary therapeutic approach must be utilized to avoid long-term
func-tional and psychological disability. Some patients recover spontaneously,
but if left untreated other patients can progress to severe and irreversible
functional disability. Sympathetic blocks and intra-venous regional
sympatholytic blockade are equally effective; these blocks should be continued
until either a cure is achieved or the response plateaus. The blocks facilitate
physical therapy, which plays a central role and which typically consists of
active movement without weights and of desensitization therapy. Many patients
require a series of three to seven blocks. The likelihood of a cure is high
(over 90%) if treatment is initiated within 1 month of symptom onset and
appears to decrease over time with therapeutic delay.
Some patients benefit from transcutaneous
electrical nerve stimulation (TENS) therapy. Spi-nal cord stimulation can be
particularly effective in both acute and chronic settings. In the acute phase
of treatment, there is increasing interest in placing tunneled epidural
catheters for infusion therapy, or percutaneous electrodes for extended trials
of spinal cord stimulation, in order to help patients tolerate physical
therapy. Many patients benefit from sur-gical implantation of peripheral nerve
stimulators placed directly on the larger injured nerves.
For sympathetically maintained pain, oral α-adrenergic blockers, such as the nonselectivephenoxybenzamine or the α1-selective prazosin, may be
beneficial. Caution is advised because of the risk of orthostatic hypotension
with these agents, and dosage should be increased gradually. Anticon-vulsant and
antidepressant medications may also be beneficial.
Surgical sympathectomy in patients with chronic symptoms is frequently
disappointing, resulting in only transient relief and in some cases a new,
alternate pain syndrome. Recent research suggests that patients with pain
refractory to prior medical or procedural therapies may respond to intravenous
infusions of ketamine in a monitored setting.
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