Differential Epidural Block

Differential epidurals allow us to break down complex pain syndromes into basic anatomical and neurophysiologic groups.

A differential epidural block is a very old technique that dates back to the end of the 19th century. It relies on the fact that different types of nerves can be blocked with different concentrations of local anesthetics. Smaller nerves and unmyelinated nerves can be blocked at lower concentrations than larger nerves or nerves that are wrapped in myelin sheaths. Neuroanatomists in the late 19th and early 20th centuries also learned that the anatomical properties (size & the presence or absence of myelin sheaths) of nerves are closely correlated with their function.

 

Large myelinated nerves (Aα and Aβ fibers) usually carry motor impulses as well as sensory impulses from the skin and joints. Pain signals from the skin and subcutaneous structures are usually carried by Aβ fibers. These fibers conduct impulses very quickly and the sensations are characteristically sharp and well localized. The first neural connections made by these nerves are usually in the dorsal root ganglia, just inside the spine.

 

In contrast pain from deeper structures such as the abdominal or pelvic organs is often carried by smaller Aδ and C fibers. These fibers conduct impulses much more slowly and the sensations are most often less sharp and more poorly localized. Another important point is that Aδ and C fibers often run with nerves of the autonomic nervous system. These nerves will usually anastomose with other nerves in ganglia (collections of nerve cells) just outside of the spine.

 

During a differential epidural a small catheter (tube) is inserted into the epidural space through a needle, after which the needle is removed and the catheter secured to the skin. Medicine of varying strengths is then injected through the catheter into the epidural space at regular intervals. By noting the response of the patient an estimate can be made of the size of the fibers anesthetized and the type of pain being dealt with.

 

As an example, if a very dilute solution of lidocaine 0.25% or 0.5% is used only the smallest nerves will be anesthetized. If the patient reports pain relief, a sensation of warmth, perhaps a measureable increase in skin temperature, but no cutaneous numbness, then it is very likely that the pain is mediated by the autonomic nervous system and the source of the pain may be deeper. If pain relief comes only with cutaneous numbness, say after the administration of 1-1.5% lidocaine, then the large fibers of the sensory/motor nervous system are likely to be involved and the source of the pain may be more superficial. Finally if the patient fails to respond to even 2% lidocaine, despite intense cutaneous numbness and complete motor blockade, it is likely that one is dealing with a central pain state.

 

While this still does not tell us the exact cause and anatomic locus of the pain it does allow us to rapidly eliminate a large number of possibilities. This allows for further testing to proceed in a more rational and orderly manner.

 

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