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U N I T 1 0
Nervous System
The pain may be persistent or intermittent. The diag-
nosis depends on the mode of onset, the distribution of
abnormal sensations, the quality of the pain, and other
relevant medical conditions (e.g., diabetes, hypothyroid-
ism, alcohol use, rash, or trauma). Injury to peripheral
nerves sometimes results in pain that persists beyond the
time required for the tissues to heal. Peripheral patho-
logic processes (e.g., neural degeneration, neuroma
formation, and generation of abnormal spontaneous
neural discharges from the injured sensory neuron) and
neural plasticity (i.e., changes in CNS function) are the
primary working hypotheses to explain persistent neu-
ropathic pain.
Treatment methods include measures aimed at restor-
ing or preventing further nerve damage (e.g., surgi-
cal resection of a tumor causing nerve compression,
improving glycemic control for diabetic patients with
painful neuropathies) and interventions for the pal-
liation of pain. Although many adjuvant analgesics are
used for neuropathic pain, pain control often is difficult.
The initial approach in seeking adequate pain control is
to try these drugs in sequence and then in combination.
The adjuvant analgesics can be divided into three gen-
eral classes according to the pain they are used to treat:
burning, tingling, or aching pain; stabbing or shoot-
ing pain; and neurogenic pain. For pain that is burn-
ing, tingling, or aching, tricyclic antidepressants and the
α
2
-adrenergic agonist clonidine frequently are used. For
the stabbing or shooting pain of neuralgias, antiseizure
medications or baclofen, a drug used in the treatment of
spasticity, may be used.
32
Nonpharmacologic therapies
such as electrical stimulation of the peripheral or spinal
nerves can be used for radiculopathies and neuralgias.
As a last resort, neurolysis or neurosurgical blockade
sometimes is used.
Neuralgia
Neuralgia is characterized by severe, brief, often repeti-
tive attacks of lightninglike or throbbing pain. It occurs
along the distribution of a spinal or cranial nerve and
usually is precipitated by stimulation of the cutaneous
region supplied by that nerve.
Trigeminal Neuralgia.
Trigeminal neuralgia, or tic
douloureux, is one of the most common and severe neu-
ralgias. It is manifested by facial tics or spasms and char-
acterized by paroxysmal attacks of stabbing pain that
usually are limited to the unilateral sensory distribution
of one or more branches of the trigeminal cranial nerve
(CN V), most often the maxillary or mandibular divi-
sions.
32,33
Although intermittent, the pain often is excru-
ciating and may be triggered by light touch, movement,
drafts, and eating. Considerable controversy remains
regarding the pathophysiology of trigeminal neuralgia,
but it is thought to be related to neurovascular com-
pression. It also occurs secondary to major neurological
diseases such as multiple sclerosis or tumor formation.
33
Treatment of trigeminal neuralgia includes pharma-
cologic and surgical modalities. Other interventions
include avoidance of precipitating factors (e.g., stimula-
tion of trigger spots) and eye injury due to irritation;
provision for adequate nutrition; and avoidance of
social isolation. Carbamazepine, an antiseizure drug,
is recognized as a first-line agent for treatment of tri-
geminal neuralgia. There is also some research showing
the addition of lamotrigine, an anti-convulsant medica-
tion, to the treatment plan may be helpful.
33
Surgical
release of vessels, dural structures, or scar tissue sur-
rounding the semilunar ganglion or root in the middle
cranial fossa often eliminates the symptoms. If not, per-
cutaneous blocking or partial destruction of peripheral
branches of the trigeminal nerve with heat, glycerol, or
balloon compression may be used. Gamma knife radio-
surgery, one of the newest techniques, involves imaging
of the trigeminal nerve root entry zone, and radiation of
the trigeminal nerve. There has also been recent interest
in the use of botulinum toxin as a treatment modality.
33
Postherpetic Neuralgia.
Herpes zoster (also called
shingles
) is caused by the same herpes virus (varicella-
zoster virus) that causes chickenpox and is thought to
represent a localized recurrent infection by the varicella-
zoster virus that has remained latent in the dorsal root
ganglia since the initial attack of chickenpox
34
(see
Chapter 46). Reactivation of viral replication is associ-
ated with a decline in cellular immunity, such as occurs
with aging. Thus, the probability of developing herpes
zoster increases strikingly with aging, and most cases
occur in the elderly. Impaired cellular immunity also
increases the risk.
During the acute stage of herpes zoster, the reacti-
vated virus travels from the affected sensory ganglia and
peripheral nerve to the skin of the corresponding derma-
tomes, causing a unilateral localized vesicular eruption
and hyperpathia (i.e., abnormally exaggerated subjec-
tive response to pain).
Persons with postherpetic neuralgia may suffer from
constant pain (“burning, aching, throbbing”), intermit-
tent pain (“stabbing, shooting”), and stimulus-evoked
pain (allodynia). Persons with allodynia often suf-
fer from excruciating pain after the slightest touch to
affected skin by such things as cold wind or clothing.
These subtypes of pain may interfere with sleep and
basic activities of living, causing chronic fatigue, depres-
sion, anorexia, weight loss, and social isolation.
Early treatment of shingles with antiviral drugs such
as acyclovir or valacyclovir that inhibit herpes virus
deoxyribonucleic acid (DNA) replication may reduce the
severity of herpes zoster. Initially, postherpetic neuralgia
can be treated with a topical anesthetic agent, lidocaine–
prilocaine cream or 5% lidocaine gel. A tricyclic antide-
pressant medication, such as amitriptyline or desipramine,
may be used for pain relief. Regional nerve blockade (i.e.,
stellate ganglion, epidural, local infiltration, or peripheral
nerve block) has been used with limited success.
A live attenuated vaccine is now available for preven-
tion of herpes zoster in adults 60 years of age and older.
The vaccine is not indicated for treatment of herpes zoster
or postherpetic neuralgia.
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