“A Comparison of the Clinical Effectiveness of Specific Neurostimulation and Photobiomodulation Modalities with Therapeutic Nutrition in the Treatment of Peripheral Neuropathy”

John Hayes Jr1,2, Shannon Boyce1 and Nicholas A Kerna3*
1NeuropathyDR®, USA
2University of Science, Arts and Technology, Montserrat, USA
3SMC–Medical Research, Thailand
*Corresponding Author: Nicholas A Kerna, POB47 Phatphong, Suriwongse Road, Bangkok, Thailand 10500.
Received: April 19, 2020; Published: May 13, 2020

Abstract: Peripheral neuropathy (PN) is a severe condition with numerous comorbidities. Approximately 4% of adults and the elderly develop polyneuropathy of various etiologies. The incidence of PN likely increases with age and multiple facets of declining health. Many pharmacological agents are inadequate in treating PN, and some have significant side effects. Thus, other treatment options, methods, and modalities to treat PN should be advanced and explored. This retrospective study reports a comparison of the clinical effectiveness of specific neurostimulation and photomodulation (low-level laser therapy) modalities with therapeutic nutrition in the treatment of the symptoms of PN. Most participants reported some level of symptom relief with each of the treatment components, while neurostimulation provided nearly universal relief of all PN symptoms in the participants surveyed.

Keywords: Low-Level Laser; Neurostimulation; Peripheral Neuropathy; Photobiomodulation; Therapeutic Nutrition

John Hayes, Jr., MD is co-founder of NeuropathyDR® and co-designer of the NDGen® neurostimulator used in this study. Sources of sup- port for the work: self-funded by NeuropathyDR®. Shannon Boyce, J.D. acknowledges a proprietary interest in the NDGen® neurostimula- tor used in this study. Nicholas A. Kerna, PhD, MD, MPH, DNBCE, declares that his contribution to this paper was written in the absence of any commercial or financial relationship that could be construed as a potential conflict of interest.

The NDGen® neurostimilator is an advanced FDA-approved electrotherapy neurostimulator that combines adjustable waveforms (shape, pulse width, and duration) with unique physician-determined programming. It is wearable, portable, and utilizable for both neuropathic pain control and neuropathy treatment. The development of the NDGen® neurostimulator was the result of research findings and best practices in electrotherapy as well as multi-treatment clinical testing and reporting [23,24]. The NDGen® neurostimilator was co-designed by John Hayes, Jr., MD of the United States.

The NeuropathyDR® Nutrition Plan is a carbohydrate-controlled plant-based [20], low-allergenicity diet combined with broad-spectrum and neurotropic-targeted oral and topical nutrient supplementation.

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Non-Pharmacologic Care and Management of Neuropathy

Citation: Kerna NA, Flores JV, Holets HM, Akabike LU, Chen MH, Solomon EO, Pruitt KD, Hayes Jr J, Waugh S. “Non-Pharmacologic Care and
Management of Neuropathy”. EC Neurology 13.2 (2021): 67-76.
Abstract
According to the International Association of the Study of Pain (IASP), neuropathic pain is caused by a primary lesion or dysfunction of the nervous system. The lesion may be peripheral, spinal, or supra-spinal and is differentiated from other types of pain due
to sensory symptoms caused by a compromised peripheral or central nervous system. Neuropathic pain is further delineated as
“evoked pain” or “rest pain”, the latter typically observed in spinal cord injury patients. Neuropathies can be cranial, autonomic, or
focal.
The major types and categories of neuropathies include chronic degenerative neuropathy, post-traumatic neuropathy, diabetic
neuropathy, stroke-related neuropathy, and peripheral neuropathy. Common comorbidities include Alzheimer’s disease and Parkinson’s disease. Neuropathic conditions are diagnosed by a patient’s medical history, examination, and when indicated, electromyography (EMG) and the nerve conduction velocity (NCV) test. This research explores non-pharmacologic care and management of
specific neuropathies, particularly nutrition, and nutritional supplementation, and photobiomodulation therapy (PBMT), also known
as low-level laser therapy (LLLT). Comparisons are given regarding these modalities and conventional treatments. Although research
into the efficacious applications of nutrition, nutritional supplements, and photobiomodulation therapy is in its relative infancy, these
modalities seem promising when used alone or, in combination and or as conjunctive therapies with conventional treatments.
Keywords: Alzheimer’s Disease; Demyelination; Diabetic Neuropathy; Neuropathic Pain; Nutritional Supplements; Parkinson’s Disease;
Vitamins
Nicholas A Kerna1,2*, John V Flores3,4, Hilary M Holets3,4, Lawrence U Akabike5, Mark H Chen6, Emmaneulla Olubumni
Solomon7, Kevin D Pruitt8, John Hayes Jr9 and Shain Waugh10
1
SMC–Medical Research, Thailand
2
First InterHealth Group, Thailand
3
Beverly Hills Wellness Surgical Institute, USA
4
Orange Partners Surgicenter, USA
5
Larrico Enterprises, LLC, USA
6
For Your Health, LLC, USA
7
Obafemi Awolowo University, Nigeria
8
Kemet Medical Consultants, USA
9
NeuropathyDR®, USA
10Fettle Path, USA
*Corresponding Author: Nicholas A Kerna, (mailing address) POB47 Phatphong, Suriwongse Road, Bangkok, Thailand 10500.
Contact: medpublab+drkerna@gmail.com.
Received: December 28, 2020; Published: Janaury 30, 2021

Discussion

Neuropathic pain is classified as evoked pain or rest pain (pain at rest). The latter is observed commonly in patients with spinal cord
injury. Symptoms of evoked pain include pressure hyperalgesia, allodynia, and heat hyperalgesia, whereas those of rest pain include
numbness, burning and pricking pain, and electric-shock-like pain. Neuropathic pain intensity is often determined using a visual analog
scale (VAS) scoring system [5].
Cranial neuropathy
Cranial neuropathy, also known as multiple cranial neuropathies, is a common clinical neurological condition. Diagnosis of cranial neuropathy is challenging due to its complex etiology. Typically, dysfunction of or damage to any of the 12 cranial nerves can result in cranial
neuropathy. Infections, autoimmune diverticulitis, and neoplasms can also lead to the condition [6,7].
Autonomic neuropathy
Autonomic neuropathy is a condition in which involuntary nerve fibers are affected, in addition to peripheral nerve dysfunctions.
Mostly, the conditions are mild and asymptomatic. In a few instances, myelinated nerve fibers are involved. These conditions are often
associated with diabetes mellitus, metabolic alkalosis, immune-mediated autonomic neuropathy like para-neoplastic syndrome, various
inherited autonomic neuropathies, autonomic neuropathies of infectious origin, and toxic autonomic neuropathies. The syndrome’s clinical features include gastrointestinal, cardiovascular, urogenital, sudomotor, pupillomotor, and thermoregulatory impairments. Diagnostic
procedures and physiological and laboratory tests help estimate autonomic function and monitor outcomes in most patients [8].
Focal neuropathy
This neuropathy occurs when a single (or group of nerves) at a particular site is affected. The etiology is varied, ranging from acute
traumatic nerve injuries to chronic compressions. Although differential diagnosis is challenging, an accurate diagnosis can be determined
by a detailed medical history, clinical examination, and targeted physiologic examination. Imaging techniques, such as magnetic resonance imaging and monographs, provide essential information. Morphological data in complicated cases helps delineate the diagnosis.
Further, the diagnostic process has become more direct due to the availability of state-of-the-art electrodiagnostic procedures [9,10].
Peripheral neuropathy is sometimes considered a category of focal neuropathy, which will be discussed in a later section.
Major types/categories of neuropathies
Chronic degenerative neuropathy
Patients with chronic degenerative neuropathy, also known as chronic inflammatory demyelinating polyneuropathy (CIDP), often
present with nerve swelling and irritation (inflammation), resulting in a loss of strength or sensation [11].
In this condition, nerves outside the brain and spinal cord are involved, commonly affecting both sides of the body. As damage to the
nerve cell’s myelin sheath leads to degeneration, the condition is considered autoimmune. Moreover, CIDP is associated with multiple
disorders, such as chronic hepatitis, diabetes mellitus, bacterial infection, HIV, compromised immunity, inflammatory bowel syndrome,
systemic lupus erythematosus (SLE), cancer of the lymph system, hyperthyroidism, and use of anticancer medications [11,12]. Although
there are data on the disease pathogenesis, the exact triggering factors remain unclear.

Citation: Kerna NA, Flores JV, Holets HM, Akabike LU, Chen MH, Solomon EO, Pruitt KD, Hayes Jr J, Waugh S. “Non-Pharmacologic Care and
Management of Neuropathy”. EC Neurology 13.2 (2021): 67-76. Non-Pharmacologic Care and Management of Neuropathy

The incidence and prevalence rates of CIDP were 1.6/100,000/year and 8.9/100,000, respectively, in a study conducted in the United
States. The disease seems to affect individuals aged 40–60 years, having male predominance [11,12].
Clinical presentation of chronic degenerative neuropathy
The symptoms are mostly symmetrical and progressive, starting from the feet and gradually moving to the arms and hands. Symptoms
include weakness of limbs, burning, tingling, pain, and numbness. There may be fatigue, dyspnoea, slurred speech, hoarseness of voice
(dysphonia), and uncoordinated movements (ataxia) in patients with advanced disease. It is crucial to differentiate CIDP from GuillainBarré syndrome, especially in patients presenting with relapse [11,12].
Post-traumatic neuropathy
Injury to the peripheral nerves is the primary cause of post-traumatic neuropathy. Accidental traumas, surgeries, and diseases can
cause mild to severe neuropathic pain. As this condition affects the productive age group, it has a considerable negative effect on the patient’s QoL. The incidence of peripheral nerve injury ranges from 2.8% to 5% [13].
Although various pathophysiological mechanisms can explain these types of pains, the differentiating factor is that post-traumatic
neuropathy begins with a spontaneous or deranged activity in the injured sensory neurons [14].
Post-surgical neuropathy is a commonly encountered variant of post-traumatic neuropathy [15].
Clinical presentation of post-traumatic neuropathy
The clinical picture revolves around pain, allodynia, dysesthesia, and hypersensitivity. Such pain and symptoms have been reported
mostly after surgeries, such as mastectomy, thoracotomy, and hernia repair [13–15].
Diabetic neuropathy
Signs and symptoms of neuropathy in diabetic patients often point to the presence of diabetic neuropathy. The condition can be either
symmetrical or asymmetrical neuropathy, but most patients (75%) often present with distal symmetrical neuropathy. Asymmetrical neuropathies likely involve cranial, thoracic, or limb nerves, resulting from an acute ischemic episode of vasa nervosa causing infarction [16].
Diabetic neuropathy, under the symmetric variant, is further classified as diabetic polyneuropathy, painful autonomic neuropathy,
painful distal neuropathy with weight loss (diabetic cachexia), insulin neuritis, polyneuropathy after ketoacidosis, polyneuropathy with
glucose impairment, and CIDP. Under asymmetrical variants, there are radiculoplexic neuropathies (lumbosacral, thoracic, cervical),
mononeuropathies, median neuropathy of the wrist, ulnar neuropathy of the elbow, peroneal neuropathy of the fibular head, and cranial
neuropathy. The predisposing factors for diabetic neuropathy are hyperglycemia, dyslipidemia, and impaired insulin signaling [17,18].

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