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When taking a history, the examiner should always determine by examination or ask the Central Pain patient whether the pain under discussion is dysesthetic or not. If the pain is not dysesthetic, hyperpathia will apply to it.

Hyperpathia is quite different from dysesthetic pain. It follows a gradient which is the opposite of dysesthesia, a gradient which increases proximally on the body. This gradient which increases where touch sensation is most retained and where dysesthesia is least, and the fact that the pain is not bizarre but rather retains the ordinary character, seems to suggest hyperpathia might merely be a failure of inhibition.

This is in contrast to dysesthesia, which is of wildly different character from nociceptive pain, so different as to defy explanation. Some have thought this suggests that dysesthesia is:

• A signal which does not have the modeling and integration an intact thalamus applies to incoming pain signals;
• A chemical disorder in synaptic neurotransmission which garbles the pain signal
• Devor's "crossed afterdischarge" or a chemical spreading of injury (the humoral ephapse or cross stimulation of neighboring pain neurons by the process of an injured neuron leaking excitatory chemicals as it attempts to perform transmission) reaching damaging levels as it ascends in the pain tracts. This third view is a little more complicated to state, but is very attractive in view of the fact that evoked dysesthetic burning requires peripheral stimulation.

There is known to be both a thalamic and a neuronal component to Central Pain. Scientists do not know which aspects are causative and which are consequential.

In hyperpathia, we encounter another type of delay in Central Pain, which is known as "delay with overshoot". This term has been used for many years to describe a functional, but not necessarily anatomical, injury to the spinothalamic tracts. It involved some unproven suppositions about the anatomical seat of hyperpathia, and so continues now as merely a clinical term to describe the lowered threshold for pain, which then breaks through suddenly into overwhelming pain, when stimulus reaches the pain threshold.

"Delay with overshoot" is not a delay of time, but rather an elevated threshold for pain. This means that a noxious stimulus will not be detected as soon as in people without Central Pain, but when the patient reach the pain threshold, the pain overshoots wildly and an overblown response is noted. Although the overshoot phenomenon is easy to demonstrate with pin prick, it is almost impossible to grade pressure with a sharp pin gradually enough to demonstrate the delay portion of "delay with overshoot." Von Frey hairs will invariably demonstrate some sensory deficit, often subclinical, (and therefore missed by conventional testing) in the areas of most intense burning. Patients also report a "windup-like" pain in Central Pain, a phenomenon of progressive impact of successive pin pricks.

• Situation: Central Pain patient has central subligamentous herniation of a lumbar disk. Physician concludes it is not large enough to be significant, but recommends hydromassage and exercize.

Error: The physician neglected to consider hyperpathia, markedly increased pain from normally painful situations. Pain fibers from the sinuvertebral nerve fill the posterior longitudinal ligament (PLL) is packed full of pain fibers from the sinuvertebral nerve, which double back into the canal from the spinal root. The disc itself may have relatively few pain fibers. Large herniations may therefore not be painful. A central herniation against the PLL may have considerable pain, and in a patient with hyperpathia, may be very severe. Just as pain in a normal person does not correlate well with the size of the herniation, it correlates even less well in someone with hyperpathia.

If the patient has Central Pain kinesthetic dysesthesia, exercise is not viable therapy. Also, the temperature of hydromassage may evoke the dysesthetic burning.

• Situation: Physician tests sensation in a Central Pain patient with an open safety pin and concludes the testing is normal, since the patient responds painfully to the pin everywhere.

Error: Central Pain patients have hyperpathia. The examiner has missed the difference in increased susceptibility to pin prick on the trunk as compared to feet and hands. Normally, the feet and hands are areas of increased sensibility. The increase to pin prick sensation as one goes proximally is the exact opposite of the dysesthetic burning, which usually increases distally. The gradient in dysesthesia corresponds to areas of subtle loss of touch sensation, hyperpathia is diminished in these areas.