The Neurofeedback / Medical Treatment of Peripheral Neuropathy

– William E. Baumzweiger, M.D. & Victoria Ibric, MD, PhD, BCIAC

This article describes the treatment of peripheral neuropathy though a combination of Neurofeedback (NF) and medical management. The clinical course of peripheral neuropathy is difficult to predict, and its treatment, through any NF, medical or combination modalities may also be difficult to predict.

The human nervous system is both wonderfully and woefully complex, with the peripheral nervous system, being the first line of defense. The peripheral nerves are part of the sum of the entire nervous system and its associated immune and vascular mechanisms. There are genetic factors, behavioral and psychosocial factors that impact the nervous system as well. The brain’s vulnerability and its response to injury can be extremely gratifying in the short term but less-than-forgiving in the long term. For example, a staff psychiatrist colleague who worked at Cedars-Sinai died last month with Post Polio Syndrome. I knew him as a healthy adult in his mid thirties and early forties. All I ever saw was that he had a very mild limp when he was rather tired. He never commented on his childhood polio. It returned, beginning as a neuropathy in his late 40’s. This, I believe, shows that later in life, subsequent injuries, environmental contamination or even neurogenetic propensity in another part of the peripheral nervous system may generate yet other clinical peripheral neuropathic symptoms. Long forgotten excessive exercise such as running or soccer injuries may predispose one to mild lower leg neuropathy. An occult brachial plexus injury can result in a dual peripheral neuropathy or simultaneous reflex sympathetic dystrophy associated with the precipitating peripheral neuropathy.

It is therefore critical that we not underestimate the complexity or give up on the treatment of peripheral neuropathy. The nervous system is, in its own way, unforgiving. Its retrograde consequences, as we get older, can have a profound impact on our health and life. Predisposing factors, that had affected the nervous system years before the injury that created disability, can reappear at the beginning of a new disease process, becoming a precipitating factor to the new illness.

The authors worked with such a complex situation occurring in 2000. This patient, a 62 year-old male, presented a left frontal epidural abscess that required treatment with Gentamycin, a known neurotoxic antibiotic. After 5 days the Gentamycin was changed to Vancomycin, but the neuropathic precipitant was enough to generate a syndrome that seriously affected the patient. The patient developed severe pain in the feet and legs and less severe, but clearly present, dysesthetic pain above the legs, as well as over the rest of the entire body. He also developed profound fatigue.

It appeared at first, that all of these symptoms and signs were part of a single over-all disease process. The physicians treating the condition viewed it as a single entity and they prescribed Kadian, Gabatril, Lexopro, and Trazadone. The patient was also given significant doses of pain medication that impaired him cognitively. In parallel to the above-mentioned medication, an intense NF training program was started. One piece of history came to the surface here: the patient, from the age of 13 into his thirties, had been an avid runner.

Even under pain medication, the patient reported high levels of pain, expressed by the VAS (visual analog scale) for both legs up to the thigh, bilaterally. The treatment regimen continued for four and a half years. Continued application of a Neurofeedback cum medication combination for the neuropathy brought other problems to the surface. This revealed an underlying divergence of VAS readings showing tendencies that might not have become evident during a shorter course of treatment.

One could say that the clinical problem was simply the Gentamycin. On the other hand, the rest of the patient’s body was not nearly as dysesthetic as the thighs, calves and feet, suggesting that predisposing factors had indeed been a part of the picture. Over 3 years of treatment the patient completed more than 180 NF sessions, primarily using inhibit protocols for the lower frequencies over the frontal and temporal areas, which were obviously presenting high amplitudes and great variability on the mind-mirror screen of the ROSHI I instrument. This patient had the highest Neural Efficiency Index (NEI) readings that we have ever seen in a patient. (NEI expresses the threshold value for each frequency band or single frequency). Continued NF training helped him lower the NEI’s and had produced a marked improvement in his symptomatology by mid-2004.

The disjunction of the pain in the lower legs and feet compared with the rest of the body demonstrated the combined effect of milder predisposing events with the precipitating event. This kind of complication should be looked for in all cases of NF treatment of peripheral neuropathy.

By mid-2004 the patient developed new symptoms: left temporo-mandibular muscle tension with trigeminal dysesthesia, as a consequence of a treatment with Septocaine, a newer type of dental anesthetic. Despite the fact that it is known to be a neurotoxin, this was given to the patient in the left mandible for the placement of a Titanium stub. The Septocaine immediately caused an acute pain with VAS as high as 9/10. Gradually this left hemi-cranial new pain became persistent daily, and extremely debilitating. In addition, Septocaine administration reactivated other peripheral neuropathic symptoms. Depakote reduced the pain from 9/10 to 6/10, and while NF continued for another 15 sessions, patient’s left hemi-cranial pain perception was lowered to 5/10.

A qEEG was done in January 2005, as a part of the experimental group of patients in an ongoing research project. This qEEG was analyzed before, during and after ROSHI light or electromagnetic closed loop-EEG sessions. This qEEG showed reduced connectivity in the left frontocentral and bilateral posterior fields, as the right side presented hypercoherent delta while the patient was on ROSHI with light closed loop EEG. Ectopic elevations of 7-10Hz were also observed bilaterally over the fronto-temporal regions, and ectopic midline (Fz, Cz) with elevation of 7-8 Hz amplitudes.

Regarding the NF training, we can mention only that it was very complex and the protocols were changed according to the symptoms presented at each visit. The protocols addressed either reduction of amplitudes of the lower frequencies over the frontal or sensory-motor areas, or of the above mentioned coherence issues. During several visit, 2 or 3 protocols were interchanged. The frequency of sessions was decreased as the time went on, from daily trainings to 2-3 per week, and now only once a week or every other week, as needed for reinforcement purposes. Corrections in the electrical presentation were accompanied by a substantial reduction of the pain perception to a VAS of 2-3/10, improvement in the quality of life, due to reduced fatigue. In parallel the patient was able to reduce his medications.

The Septocaine episode re-enforces the earlier message that an injured nerve, like an injured psyche, will respond with signs and symptoms of lesser or greater intensity to a new insult. Just as with our feelings, our nervous system might remember benevolence for a time, but never forget an injury.

Instead of conclusions we’d like to mark the following 4 points:

Point One: Neuropathies may occur when a predisposed nervous system is affected by a precipitating exposure, creating a more or less prolonged neuroimmune dysfunction. Neuroelectrical and laboratory findings can usually be found to define its underlying process. MRI and newly advancing state of the art equipment may also be useful in further defining the syndrome.

Point Two: A treatment is required for each component of the peripheral neuropathy. Some treatments can be pain relievers. Other therapies are available and combinations of treatments must be considered. One thing that they have in common is that the period of treatment can be lengthy.

Point Three: After improvement of the initial neuropathic syndrome, the patient may be excessively vulnerable to a new neuropathic syndrome. The new must be approached as actively as the prior neuropathy.

Point Four: Medical approach (anti-inflamatories, pain killers, anti-depressants, and axiolytics) and physical therapy (massage and saunas) are beneficial in neuropathic pain treatment but they have to be flexible and proactive. The addition of a NF program can enhance the chance of recovery from the devastating consequences of a neuropathic pain syndrome. The number of NF sessions can be very extensive and complex, but the benefits are rewarding.