Neuropathy is characterized by abnormalities in the function of sensory and motor nerves. The Combined Electrochemical Technique (CET) has been shown to stimulate the growth of epidermal nerves (c and unmyelinated A-delta) fibers.
In the process of treating sensory neuropathy, our group has treated a subset of patients with foot drop (peroneal motor nerve dysfunction) which has also responded to the protocol. Foot drop is an abnormality in which the forefoot cannot be elevated (flexion of ankle) due to irritation,
weakness or damage to the common fibular nerve, the sciatic nerve, or paralysis of the muscles in the anterior portion of the lower leg. Foot drop is a common and distressing problem that can lead to falls and injury. As a result, individuals with foot drop scuff their toes along the ground or bend their knees to lift their foot higher than usual to avoid the scuffing, which causes what is called a “steppage” gait. Foot drop can be unilateral or bilateral and it is a symptom of an underlying problem that is either temporary or permanent, depending on the cause. Causes may include: peripheral neuropathies, stroke, neurodegenerative disorders of the brain that cause muscular problems, such as multiple sclerosis and cerebral palsy; motor neuron disorders such as polio, some forms of spinal muscular atrophy and amyotrophic lateral sclerosis, injury to the nerve roots, such as in spinal stenosis; peripheral nerve disorders such as peripheral neuropathy or Charcot-Marie-Tooth disease; local compression or damage to the peroneal nerve as it passes across the fibular bone below the knee; and muscle disorders, such as muscular dystrophy or myositis. Although the most frequent cause is a (common) peroneal neuropathy at the neck of the fibula, other causes include anterior horn cell disease, lumbar plexopathies, L5 radiculopathy and partial sciatic neuropathy. Even when the nerve lesion is clearly at the fibular neck, there can be a variety of causes not immediately obvious; habitual leg crossing may well be the most frequent cause and most patients tend to improve when they stop this habit. A meticulous neurological evaluation may help to locate the anatomical site of the lesion. Nerve conduction and electromyography studies are useful adjuncts in localizing the site of injury, establishing the degree of damage and predicting the degree of recovery. Foot drop can be a temporary condition in some cases or can become permanent if therapeutic action is not implemented early. Chronic foot drop is very difficult to reverse. One of our patients was told it would be four years, if at all, before he recovered. Case reports below reveal several different outcomes.
Program – Materials and Methods
We routinely see patients with varying types and stages of painful peripheral neuropathy, including diabetic peripheral neuropathy (DPN), chemotherapy-induced peripheral neuropathy (CIPN), and idiopathic peripheral neuropathies.
The range of patient symptoms seen at the clinic has included:
- Decreased sensation, numbness, or tingling in the top of the foot or the outer part of the upper or lower leg
- Foot that drops (unable to hold the foot up)
- Toes drag while walking and general walking problems
- Weakness of the ankles or feet
- Loss of muscle control in the lower legs and feet
- Atrophy of the foot or foreleg muscles
- Difficulty lifting up the foot and toes and making toe-out movements
Our approach for these patients revolves around specific parameter electronic cell signaling treatment(EST), a critical component of functional nerve stimulation.
Treatment aims to influence regenerative neural bioprocesses by a variety of mechanisms including a profound anti-inflammatory effect, an increase in cyclic adenosine monophosphate (cAMP), enhanced nerve regeneration (speed), and reduction of edema and pressure on the nerve.
Approximately six percent of our neuropathy patients present with common peroneal nerve motor dysfunction (foot drop). Common peroneal nerve dysfunction may be part of a generalized distal symmetric neuropathy also involving the tibial branch of the sciatic nerve. More commonly these distal symmetric neuropathies are sensory only, but this small percentage of patients also has motor involvement. Damage to the nerve destroys the myelin sheath that covers the axon (branch of the nerve cell), or it may destroy the whole nerve cell. There is a loss of feeling, muscle control, muscle tone, and eventual loss of muscle mass because the nerves aren't stimulating the muscles. Each patient was treated according to our standard neuropathy protocol; programming parameters included, in patients with foot drop, specific neuromuscular re-education parameters in addition to sensory programming parameters. Patients were treated three days each week, including ankle blocks and EST (CET) on Monday and Friday, and electric cell signaling treatment (EST) only on Wednesday. Those patients who had no sensory neuropathy symptoms were treated without the ankle block. Programs for patients with sensory neuropathy symptoms could be delivered simultaneously with the sensory neuropathy programs; patients without sensory symptoms were delivered with the specific neuromuscular re-education programs. Recovery of motor function was graded on the standard 0-5 scale; full recovery is rated 5/5, which represents the ability of the patient to resist the maximum opposite pressure from an examiner with normal muscle strength. 4/5 represents the ability of a patient to flex a muscle against gravity, but the action can be overcome by the examiner. 3/5 represents and inability to flex the muscle even against gravity.
Summary:
Our treatment experience indicates that the overall outcome depends most importantly on the actual pathological cause of the problem. The authors have successfully treated these patients with motor nerve dysfunction by healing the pathology in about 85% of the cases. Depending on the severity of the patient, treatment may require 2-3 months for the surrounding tissue to stabilize, peroneal nerve to regrow and finally to improve both motor and sensory function.
With some patients who have suffered from long term, severe peroneal nerve damage, complete restoration may remain elusive and the disability may be permanent. However, even in these difficult cases, we have managed to alleviate the accompanying associated pain and inflammation and regain at least 50% of the motor nerve function. The authors have presented multiple mechanisms, which demonstrate initial facilitation, biosystem stabilization and then quick resolution of the inflammatory process to prevent it from leading to chronic inflammation and chronic pain. Continued treatments with protocol driven, specific-parameter electric signals are then employed to stimulate axon regeneration, neuromuscular training and overall muscle strengthening. While significantly complex, all concepts above fit together when taken into the context of cell signaling cAMP. Through this and the other mechanisms discussed, cellular derangements are returned to normal in optimum physiological time.
Conclusion:
This is the first study to report the use of EST in the treatment of foot drop. Because of virtually no risk related to this treatment, it has the potential to make a significant impact on the patients with this difficult to treat neurological problem. The successful treatment of foot drop in a significant percentage of the population would reduce falls and other morbidity. All current treatments for foot drop are much less effective and much more costly.
Electric cell signaling treatment (EST) involves physical science and not chemistry. Therefore, it is considerably more natural and physiological to the human body. While we believe that additional studies involving EST as a treatment for the functional recovery in foot drop are important, there appears to be enough evidence to encourage the primary or adjuvant use of EST for this condition.