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Central pain, defined as “pain associated with lesions
of the central nervous system,”1 is a
type of neuropathic pain whose features are summarized in Table
38-1, as discussed by many authors.2–9 Central
pain of spinal cord origin is essentially a young man’s
disease, usually resulting from trauma, whereas central pain of
brain origin is usually the result of stroke.
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One of the amazing things about central pain is that the clinical
picture is similar in a patient with a cord lesion so slight it
produces no clinically detectable sensory loss to that seen after
complete cord transection.10–13 Furthermore,
stroke pain after a lesion so massive that it essentially produces
a hemispherectomy is similar to that after a stroke with no persisting
sensory loss. Furthermore, only a certain percentage of patients
with apparently identical lesions develop central pain.
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A chief problem is that the mechanism of this pain is poorly
understood, making attempts at treatment difficult to rationalize.
It must be remembered that the most common feature is the steady, constant,
burning, dysesthetic or aching element for which there is no laboratory
model. Patients must serve as models, because only they can tell
us what they feel.
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As has been mentioned, not every patient who suffers cord damage
develops central pain; the reported incidence ranges from 6% to
94%.9,14–24 The etiology is usually
trauma. In a personal series of 127 patients,25 65% were
victims of trauma, 12% suffered from iatrogenic lesions,
9% from inflammatory lesions, 6% from neoplastic
lesions, 4% from congenital lesions, 2% from vascular
lesions, and 2% from skeletal pathology. The location of
lesions in these patients was as follows: cervical, 42%;
T1 to T9, 21%; and T10 to L2, 37%. Thirty-two
percent of lesions were clinically complete, 64% were incomplete,
and 4% of patients had no clinically detectable sensory
loss. Etiology and level or completeness of lesion did not correlate
with presence, severity, or quality of pain, except as discussed
subsequently.