some conditions there may be completely normal clinical examinations. This is the rule in trigeminal and glossopharyngeal neuralgias and it occurs more than occasionally in post-herpetic neuralgia. But some patients, particularly with what appear to be small-fiber neuropathies or specific nerve injuries, who describe their pains with the aforementioned typical neuropathic pain adjectives, also have normal examinations. There is the temptation to attri- bute their pain complaints to functional etiologies; however, at least from a logical perspective, that cannot always be the case, and if they are known to have a particular disease such as diabetes, or suffered an injury in which nerve damage is likely, pain may be their only manifestation of neural dys- function. In such situations and, of course, in most cases in which further diagnostic information would be helpful, ancillary testing can be used.
Any consideration of the utility of ancillary tests to support the diagnosis of specific neuropathic pain mechanisms must take into account several fac- tors: (1) Currently, available tests only evaluate nervous system structures and functions presumed to be relevant to pain perception and transmission; from their results the presence, extent, and mechanisms of neuropathic pain are, at best, inferred. This situation is somewhat similar to testing for diabe- tes mellitus with peripheral nerve, ophthalmologic, and renal studies with- out the availability of plasma glucose levels. (2) There is a spectrum of clinical and physiological manifestations of neural injury within each disor- der, with chronic pain occurring in only a small percentage of affected patients. For example, neuropathic pain occurs in w16% of patients with diabetes mellitus and a third of those with diabetic neuropathy ; post-her- petic neuralgia, defined as chronic pain present 4 or more months after res- olution of the acute herpes zoster (shingles) rash, occurs in 13% to 20% of patients ; and following direct nerve injury, as occurs during venipunc- ture, persistent pain is rare, perhaps occurring in 1:1,500,000 procedures . (3) The causes of this clinical variability are less than certain, but the presence of pain is presumed to reflect damage to the small myelinated (Ad-) and unmyelinated (C-) fibers within peripheral nerves . As these fiber types also mediate other clinical functions that are measurable, eg, appreciation of painful stimuli, temperature perception, and autonomic activity, many tests have focused on demonstrating defects in these modal- ities to verify Ad- or C-fiber damage.
Neurophysiologic testing, principally nerve conduction studies and elec- tromyography, are frequently used in suspected disorders of the peripheral nervous system. The usual techniques, with surface electrodes for nerve stimulation and evoked potential recording, measure activity of the largest and fastest conducting sensory and motor myelinated nerve fibers (Aab-).