Blocking Out the Pain
Nerve blocks are procedures during which an anesthetic agent is introduced or injected to interrupt nerve impulses.1 Two of the most used medical dictionaries (Taber’s2 and Gould’s3) include electricity as a means to produce nerve block. The term ‘electric nerve block’ was coined by Dr. Jenkner4 several years ago to describe the use of electrical impulses to create a nerve block instead of injecting an anesthetizing agent into the site.
Electric nerve blocks (ENBs) represent a long tradition of the use of electricity in medicine5 along with electrocardiography (EKG), electroencephalography (EEG), electromyography (EMG), transcutaneous electrical nerve stimulation (TENS) for low back pain, electroconversion therapy (ECT) for depression, dorsal column stimulators (DCS) for chronic pain control, bone growth stimulators after orthopedic surgery, and neuromuscular stimulation for disuse atrophy — all capitalizing on the electrical properties of the human body.
The utilization of electrodes to produce high frequency electrical impulses to create numbness in a localized area requires correct medical diagnoses and knowledge of the physiologic mechanism of ENBs to optimize outcomes. Pain nerves typically repolarize — i.e., get ready to fire again — at a frequency slower than 1/1000 sec. Thus, the absolute minimum blocking frequency must be 1,000 Hz or greater; typically 4,000 to 20,000 Hz is used. Such frequencies prevent the pain nerves from repolarizing and firing repeatedly and instead achieve a neural blockade (nerve block). The efficacy of nerve blocks is illustrated by Hardy, et al6 in performing surgery while blocking sensory nerve impulses with electricity.
Electrical energy at the optimum frequencies (4,000 to 20,000 Hz) penetrates and conveys more energy to the neurons because of the lower impedance at these frequencies7 and has an intra-neuronal effect on cyclic adenosine mono-phosphate (cAMP) activity. cAMP is an intracellular second messenger which transmits signals for cell activity. Knedlitschek, et al8 showed that intracellular cAMP is depleted after being subjected to 4,000 Hz of electrical energy at adequate voltage (see figure 1). The steep initial decrease in cellular cyclic AMP (adenosine monophosphate) is consistent with these molecules being used by the cell for metabolism.
Note that the data presented in figure 1 was the result of an electrical treatment at 1 volt and a frequency of 4,000 Hz over a period of 3 minutes. The result was a 28 percent depletion of the available cyclic AMP. A typical ENB treatment with a duration of 8 to 20 minutes would be expected to completely expend the cAMP supply.8
Bowman9 has shown that frequencies in the range of 4,000 to 20,000 Hz result in interruption of nerve firing (see figure 2). Wyss10 has shown that these frequencies also result in sustained depolarization. Both of these phenomena are, by definition, nerve blocks, which result from voltage gated channels being kept open. There is an electrical energy threshold that must be exceeded for nerve block to occur. At optimal frequency and sufficient voltage, nerve firing completely stops even when being simultaneously stimulated.9
This study summarizes 3,527 ENB treatments performed by the author, with the vast majority of the treatments resulting in significant, immediate improvement in pain as measured by verbal response scores (VRS). Figure 3 groups patients into treatment outcomes with the criteria calculated as a percentage improvement (the after-VRS score subtracted from the before-VRS score, then divided by the before-VRS score). Histograms 1 thru 6 reflect the “improvement percentage” groupings which are commonly used in electromedical literature.7
Group 1 patients, reflecting about 1 percent of the population, reported negative improvement though none had any visible consequence of the ENB treatment. Group 2 patients (about 8 percent of the total) reported exactly the same verbal pain score before and after treatments. The remainder of the patients (groupings 3 thru 6) reported pain improvements ranging up to 100%. Those patients reporting improvement less than 50 percent comprised 38 percent of the total; those patients reporting at least 50 percent improvement comprised 62 percent of the total.
The remainder of this article will focus on the electromedical treatment of the sciatic nerve utilizing electric nerve blocks and will serve as an example to explore the important concepts applicable to ENBs in general. The sciatic nerve illustration has several advantages in that there are no nearby complicating structures, chemical nerve blocks are infrequently used, and other treatments are typically not successful.
Neuroanatomy of the Sciatic Nerve
The sciatic nerve is the finger-sized confluence of the nerve fibers that comes mainly from the L4, L5, and S1 nerve roots and courses through the lumbosacral plexus inside the pelvis to exit at the sciatic notch. It then passes under and perpendicular to the piriformis muscle posterior to the hip joint on its way down the leg. This nerve bundle splits into the common peroneal and tibial nerves just superior to the popliteal fossa. There is a concentration of sympathetic fibers on, and in, the sheath of these lumbosacral nerve roots and the sciatic nerve itself.
Pathophysiology of Sciatic Nerve Pain
The primary pathology of sciatic nerve pain almost certainly involves malfunctioning sympathetic C-fibers7 and probably the A-delta fibers. While mechanical impact resulting in motor and sensory nerve damage may be a causal factor, fiber damage and/or irritation from other sources can also occur. In fact, it is suspected that nerve pain my indicate that small fiber damage may be present even when electromyographic and nerve conduction studies of the motor (A-alpha) and sensory (A-beta) nerve fibers appear normal.
Primary Indicated Diagnoses
Blocking nerve signals along the sciatic nerve, or the sympathetic C-fibers and A-delta fibers that coat it, is a logical treatment for a number of conditions, including: