Nitric Oxide

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Oxidative Medicine and Cellular Longevity
Oxid Med Cell Longev. 2017; 2017: 2181942.
Published online 2017 Sep 12. doi:  10.1155/2017/2181942
PMCID: PMC5613626

Benign Effect of Extremely Low-Frequency Electromagnetic Field on Brain Plasticity Assessed by Nitric Oxide Metabolism during Poststroke Rehabilitation

Natalia Cicho,corresponding author 1 Piotr Czarny, 2 Micha Bijak, 1 Elbieta Miller, 3 , 4 Tomasz liwiski, 5 Janusz Szemraj, 2 and Joanna Saluk-Bijak 1
1Department of General Biochemistry, Faculty of Biology and Environmental Protection, University of Lodz, Pomorska 141/143, Lodz, Poland
2Department of Medical Biochemistry, Medical University of Lodz, Mazowiecka 6/8, Lodz, Poland
3Department of Physical Medicine, Medical University of Lodz, Pl. Hallera 1, Lodz, Poland
4Neurorehabilitation Ward, III General Hospital in Lodz, Milionowa 14, Lodz, Poland
5Department of Molecular Genetics, Laboratory of Medical Genetics, Faculty of Biology and Environmental Protection, University of Lodz, Lodz, Pomorska 141/143, Lodz, Poland
corresponding authorCorresponding author.
Academic Editor: Tanea T. Reed
Author information Article notes Copyright and License information
Received 2017 May 12; Revised 2017 Jul 2; Accepted 2017 Aug 14.

Abstract

Nitric oxide (NO) is one of the most important signal molecules, involved in both physiological and pathological processes. As a neurotransmitter in the central nervous system, NO regulates cerebral blood flow, neurogenesis, and synaptic plasticity. The aim of our study was to investigate the effect of the extremely low-frequency electromagnetic field (ELF-EMF) on generation and metabolism of NO, as a neurotransmitter, in the rehabilitation of poststroke patients. Forty-eight patients were divided into two groups: ELF-EMF and non-ELF-EMF. Both groups underwent the same 4-week rehabilitation program. Additionally, the ELF-EMF group was exposed to an extremely low-frequency electromagnetic field of 40Hz, 7mT, for 15min/day. Levels of 3-nitrotyrosine, nitrate/nitrite, and TNF? in plasma samples were measured, and NOS2 expression was determined in whole blood samples. Functional status was evaluated before and after a series of treatments, using the Activity Daily Living, Geriatric Depression Scale, and Mini-Mental State Examination. We observed that application of ELF-EMF significantly increased 3-nitrotyrosine and nitrate/nitrite levels, while expression of NOS2 was insignificantly decreased in both groups. The results also show that ELF-EMF treatments improved functional and mental status. We conclude that ELF-EMF therapy is capable of promoting recovery in poststroke patients.

1. Introduction

Cardiovascular diseases, including ischemic stroke (IS), are a serious problem of the modern age, killing 4 million people each year in Europe []. Stroke is caused by ischemia of brain tissue. Brain structure damage occurring during ischemia/reperfusion is due to the generation of significant amounts of reactive oxygen species and inflammatory mediators []. Damage to brain tissue as a result of a stroke cannot be undone. However, the most important part of poststroke therapy is immediate and long-term rehabilitation, considering the enormous plasticity of the brain []. Although extremely low-frequency electromagnetic field (ELF-EMF) therapy is not a standard treatment in the poststroke rehabilitation, some authors suggest its increased positive effect on patients []. ELF-EMF treatment is based on regeneration, osteogenesis, analgesics, and anti-inflammatory action. Its biological effect is related to processes of ion transport, cell proliferation, apoptosis, protein synthesis, and changes in the transmission of cellular signals []. The regenerative and cytoprotective effect of ELF-EMF is based on mechanism associated with nitric oxide induction, collateral blood flow, opioids, and heat shock proteins [].

Nitric oxide (NO) is an unstable, colourless, water-soluble gas with a short half-life (3–6sec). The compound has one unpaired electron, which makes it a highly reactive free radical. It is characterized by the multiplicity of action in the body, in both physiological and pathological conditions []. Synthesis of NO in the organism is catalysed by nitric oxide synthase (NOS), occurring in three isoforms: neuronal (nNOS), inducible (iNOS), and endothelial (eNOS), encoded by different genes whose expression is subject to varying regulation. The constituent isoforms of NOS are eNOS and nNOS, whose activity is associated with concentration of calcium ions and the level of calmodulin in a cell, as well as with hypoxia, physical activity, and the level of certain hormones, that is, oestrogens []. In contrast, because it is closely related with the calmodulin, iNOS does not require a high concentration of calcium ions but is regulated by various endogenous and exogenous proinflammatory factors [].

The two-stage synthesis of NO consists of the oxidation of L-arginine to N-hydroxy-L-arginine and, under the influence of NOS and oxygen, formation of L-citrulline and release of NO. All isoforms of NOS require the same cofactors: nicotinamide adenine dinucleotide phosphate (NADPH), flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), tetrahydrobiopterin (BH4), iron protoporphyrin IX (heme), and O2[].

Nitric oxide is one of the most important signal molecules, involved in both physiological and pathological processes. One of the major functions of NO is as a potent vasodilation, increasing the blood flow and regulation of blood pressure, which has been used in clinical practice for many years. Deficiency of this compound is observed in various disorders of many systems: cardiovascular, gastrointestinal, respiratory, and genitourinary []. The beneficial effects of NO lie in its platelet inhibition, macrophage cytotoxicity (antibacterial, antiviral, and antiparasitic), and protection of the mucosal lining of the digestive system. On the other hand, excessive expression of iNOS can be disadvantageous, for example, during sepsis. The adverse action of NO is associated with the production of superoxide anions and subsequent generation of peroxynitrite and hydroxyl radicals, which are highly toxic [].

In the central nervous system, NO as a neurotransmitter regulates cerebral blood flow, as well as neurogenesis and synaptic plasticity. Furthermore, neuronal death is caused by high concentrations of NO by caspase-dependent apoptosis process and promotion of inflammation. Elevated levels of nitric oxide promote necrosis by energy depletion. On the basis of these mechanisms, NO is involved in the etiology of many neurological diseases, such as major depression, schizophrenia, epilepsy, anxiety, and drug addiction [].

Our study was designed to investigate the effect of ELF-EMF on the metabolism of NO, as a signal molecule in the central nervous system, in the rehabilitation of acute poststroke patients.

2. Materials and Methods

2.1. Blood Sample Collection

Blood samples were collected into CPDA1-containing tubes (Sarstedt, Nümbrecht, Germany). Immediately upon doing so, a portion of the sample was frozen at 80°C and the rest of the samples centrifuged to isolate the plasma (15min, 1500g) at 25°C. Blood samples were collected twice, at an interval of 14 days before and after a standard 10 sessions of therapy. For additional analysis of 3-nitrotyrosine levels, the blood samples were collected three times, at an interval of 28 days: before treatment, after 10 treatments, and after 20 treatments. All blood samples were taken in the morning (between 7am and 9am) under patient fasting condition and stored using the same protocol.

2.2. Subject Presentation

Forty-eight poststroke patients were enrolled in the study. Participants were randomly divided into two groups: ELF-EMF (n = 25) and non-ELF-EMF (n = 23). Patients with metal and/or electronic implants (pacemakers, etc.) were excluded from the ELF-EMF group, for safety reasons. The ELF-EMF group had already undergone ELF-EMF therapy with specific parameters (40Hz frequency, magnetic induction of 5mT (B), rectangular and bipolar waveforms) (Figure 1), which was conducted using a Magnetronic MF10 generator (EiE Elektronika i Elektromedycyna, Otwock, Poland). The parameters were selected on the basis of the fact that low-intensity stimuli improve the vital functions of the body. In addition, rectangular pulses are more intense than sinusoidal and trapezoid, while bipolar pulses show more range of changes than unipolar pulses []. The ELF-EMF and non-ELF-EMF groups were treated for the same amount of time (15minutes). The non-ELF-EMF subjects were given only sham exposure. The pelvic girdle of the patients was exposed to the electromagnetic field, because exposure of the head to ELF-EMF can affect the activation of the epilepsy focus in the brain. The same therapeutic program was used for both subject groups. This consisted of aerobic exercise (30min), neurophysiological routines (60min), and psychological therapy (15min). Poststroke patients with moderate stroke severity according to NIHSS scores of 4.9 ±3.1 in the ELF-EMF group (aged 48.8 ±7.7) and 5.4 ±2.9 (aged 44.8 ±8.0) in the non-ELF-EMF group were enrolled in the study. Table 1 shows the clinical and demographic characteristics. Participants with haemorrhagic stroke, dementia, chronic or significant acute inflammatory factors, decreased consciousness, and/or neurological illness other than stroke in their medical prestroke history were excluded. The subjects had undergone neurorehabilitation for 4 weeks in Neurorehabilitation Ward III of the General Hospital in Lodz, Poland, as well as internal and neurological examinations. The Bioethics Committee of the Faculty of Biology and Environmental Protection of The University of Lodz, Poland, approved the protocol with resolution numbers 28/KBBN-U/II/2015 and 13/KBBN-U/II/2016. All participants provided written informed consent prior to participation. Depression was screened in both groups using the Geriatric Depression Scale (GDS). Cognitive status was estimated in a Mini-Mental State Examination (MMSE), and functional status using the Barthel Index of Activities of Daily Living (ADL). The GDS, ADL, and MMSE were administered either on the same day as the blood sampling or on the afternoon before.

Figure 1

ELF-EMF description. B=5mT; T = 1.3sec.

Table 1

Clinical demographic characteristics.

2.3. Magnetronic MF10 Devices

ELF-EMF therapy was performed by a Magnetronic MF10 generator as per accepted guidelines. This device is able to produce pulses in rectangular, trapezoid, and sinusoidal shapes. The pulses were applied using an AS-550 applicator (EiE, Otwock, Poland), which has the following properties: 550 mm in diameter, 270mm in length, and 5 layers of 187 turns of 1.45mm twin-parallel wires. Magnetic induction was set at 5mT. The electromagnetic field intensity was not uniformed; its distribution is vertical, while the induction coils are set horizontally. Induction of the electromagnetic field of 5mT is present at the geometric center of the applicator, and the value increases in the proximity to the surface about 7mT. Other factors that could affect EMF were eliminated (electronic measuring instruments occurring in rehabilitation room and other electronic equipment).

2.4. Immunodetection of 3-Nitrotyrosine by c-ELISA

Levels of 3-NT-containing proteins in plasma were determined using a modified c-ELISA method, as described by Khan et al. []. 96-well microtiter plates were coated with nitro-fibrinogen (nitro-Fg) (1mg/mL) and kept overnight at 4°C. Concentrations of nitrated proteins inhibiting the binding of anti-nitrotyrosine antibodies were assessed from the standard curve (10–100nM nitro-Fg equivalents) and expressed as nitro-Fg equivalents [].

2.5. Nitrate/Nitrite Estimation

Plasma samples were diluted twice before the measurement of nitrate/nitrite concentration using a Nitrate/Nitrite Colorimetric Assay Kit (Cayman Chemical Company, USA), based on the two-step Griess method. In the first step, the nitrate is converted to nitrite with nitrate reductase, while in the second step, after addition of the Griess reagent, the nitrite is converted to a deep purple azo compound. The absorbance measurement was performed at 540nm in a 96-well microplate reader (SPECTROstarNano, BMG Labtech, Ortenberg, Germany) [].

2.6. Determination of NOS2 Expression in Whole Blood Samples

RNA was isolated from the frozen whole blood samples (?80°C), in accordance with the manufacturer’s protocol using TRI Reagent® (Sigma-Aldrich, USA). The aqueous phase was purified in accordance with the manufacturer’s protocol using an InviTrap Spin Universal RNA Mini Kit (Stratec Biomedical Systems, Germany). The purity and quantity of isolated RNA were assessed using a Synergy HTX Multi-Mode Microplate Reader equipped with a Take3 Micro-Volume Plate and connected to a PC running Gen5 Software (BioTek Instruments Inc., Winooski, VT, USA). Isolated RNA (20ng/L) was transcribed onto cDNA with a High-Capacity cDNA Reverse Transcription Kit (Applied Biosystems™, Waltham, MA, USA). Quantitative assays were executed using a TaqMan Hs01075529_m1 probe for human NOS2 genes and an Hs02786624_g1 for endogenous control, which was GAPDH (Life Technologies). Reactions were carried out using a TaqMan Universal Master Mix II, without UNG (Life Technologies) in a BioRad CFX96 real-time PCR system (BioRad Laboratories, Hercules, CA, USA), all in accordance with the manufacturers’ protocols. Relative expression of NOS2 was obtained using the equation 2Ct, where Ct is the threshold cycle (Ct) value for the target gene minus Ct values obtained for the housekeeping gene GAPDH [].

2.7. Determination of TNF?

Measurements of human tumour necrosis factor alpha (TNF?) in plasma samples were made with a Human TNF? ELISA development kit (MABTECH, Cincinnati, OH, USA), in accordance with the manufacturer’s protocol. The combination of two coating antibodies (TNF3 and TNF4) were used for the analysis. The absorbance was measured at 450nm, and TNF?.

Oxidative Medicine and Cellular Longevity

2.8. Data Analysis

Biochemical and clinical data were expressed as mean ±SD. All measurements were executed in duplicate. Output value (100%) was determined for each measured parameter of each patient before treatment. Data from tests performed on the same study subjects after therapy constituted a percentage of the output value. Percentage values were presented as mean ± SD. Statistical analyses were performed using the Statistica 12 statistical software (StaftSoft Inc.). A Shapiro-Wilk test was used to analyse for normality. A paired Student t-test was used to the calculate differences between the values obtained for subjects before and after therapy, whereas unpaired Student t-test or Mann–Whitney U tests were used to determine differences between the ELF-EMF and non-ELF-EMF groups. p values of 0.05 were accepted as statistically significant for all analyses.

3. Results

Our comparative analysis demonstrated an increased level of 3-nitrotyrosine (3-NT) (p< 0.05) (Figure 2) and an elevated nitrate/nitrite concentration (p < 0.01) (Figure 3) in the plasma of patients from the ELF-EMF group. The gain in the 3-NT level was significantly higher with an increased amount of sessions (Figure 2). In the non-ELF-EMF group, we saw that the effect of rehabilitation on nitrative stress was largely weaker and not statistically significant (p > 0.05) (Figures (Figures22 and and3).3). The 3-NT level increased more in the ELF-EMF group than in the non-ELF-EMF after 10 treatments (68% versus 17%, p < 0.05) (Figure 2). The level of nitrate/nitrite in the non-ELF-EMF group even decreased after 10 treatments (although not statistically significantly) (Figure 3).

Figure 2

The comparison of 3-NT levels in plasma proteins obtained from the ELF-EMF group versus those from the non-ELF-EMF group. Statistical significance between the ELF-EMF and non-ELF-EMF groups: B versus D (p < 0.05).

Figure 3

The comparison of nitrate/nitrite levels in plasma proteins obtained from the ELF-EMF group versus those from the non-ELF-EMF group. Statistical significance between ELF-EMF and non-ELF-EMF groups: B versus D (p < 0.05).

In the next set of experiments, we determined the effect of magnetotherapy on gene expression in the whole blood samples of NOS2 mRNA. Its expression was unmeasurable in 35% of subjects from both the ELF-EMF and non-ELF-EMF groups. We observed a statistically insignificant decrease in the level of NOS2 mRNA expression after treatment in both the ELF-EMF and non-ELF-EMF groups (Figure 4).

Figure 4

The comparison of NOS2 mRNA expression obtained from the ELF-EMF group versus that from the non-ELF-EMF group.

Subsequently, we determined the concentration of proinflammatory cytokine TNF?. We found that the concentration of TNF? was comparable before treatment in both the ELF-EMF and non-ELF-EMF-groups. The cytokine level did not change in either groups after rehabilitation (Figure 5).

Figure 5

The comparison of TNF? levels in plasma proteins obtained from the ELF-EMF group versus those from the non-ELF-EMF group.

The ADL, MMSE, and GDS were used to evaluate the functional and mental status of poststroke patients undergoing rehabilitation. We demonstrated that treatment using ELF-EMF improves their clinical parameters, particularly in cognitive and psychosomatic functions.

Motor abilities estimated by ADL score changed at similar levels in both groups, with the observed improvement being statistically significant in all rehabilitated patients (p < 0.001) (Table 2).

Table 2

Clinical parameters: ADL, MMSE, and GDS measured in the ELF-EMF and non-ELF-EMF groups. Data presented as the delta of a clinimetric scale before and after the standard series of treatments ADL=the increase of ADL; MMSE= the 

The baseline MMSE values before treatment in both groups were comparable, but statistically different (p < 0.05) after rehabilitation. After 2 weeks of rehabilitation, MMSE parameters improved markedly in the ELF-EMF group (p = 0.002), while a small increase in the non-ELF-EMF group was not statistically significant (p = 0.2) (Table 2).

Depression syndrome expressed by GDS improved significantly in both groups after rehabilitation. However, the GDS value reached about a 60% lower result in the ELF-EMF group than in the non-ELF-EMF group (p = 0.018), starting from a similar base level in both groups (p > 0.05) (Table 2).

4. Discussion

In this study, we provide the evidence that application of extremely low-frequency electromagnetic field increases nitric oxide generation and its metabolism, as well as improving the effectiveness of poststroke ischemic patients’ treatments.

Ischemic stroke is one of the major causes of morbidity and mortality in the world’s population and is one of the main causes of long-term disability. The mechanisms of neurological function recovery after brain injury associated with neuroplasticity (cortical reorganization) are still insufficiently understood. Poststroke neurorehabilitation is designed to provide external stimuli, improving the effectiveness of compensatory plasticity [].

In the central nervous system, NO is both a pre- and postsynaptic signal molecule. The activity of NO is associated with a cGMP-mediated signalling cascade. The presynaptic excitatory action of NO is related to the phosphorylation of synaptophysin by the cGMP-dependent protein kinase G (PKG) pathway and the subsequent potentates of glutamatergic neurotransmission []. On the other hand, NO causes a neurotransmission inhibition through gamma-aminobutyric acid- (GABA-) ergic synaptic communication. It is associated with ion exchange and regulation of membrane excitation []. Moreover, NO as an important vasodilation factor mediates neurovascular coupling. The enlargement of vessel diameter is caused by increasing metabolic consumption as a result of neuronal activity. Neurovascular coupling maintains functional and structural brain integrity [].

This study was designed to investigate the impact of ELF-EMF on the metabolism of nitric oxide in the rehabilitation of acute poststroke patients.

In our study, we demonstrate that poststroke rehabilitation increases the level of 3-NT and nitrate/nitrite concentrations. Due to its vasodilating and proangiogenic effects, NO serves as a protective function during cerebral ischemia. Su et al. investigated the role of simvastatin-regulated TRPV1 receptors (transient receptor potential vanilloid type 1) in NO bioavailability, activation of eNOS, and angiogenesis in mice. They demonstrated that simvastatin causes an influx of calcium ions through the TRPV1-TRPA1 (transient receptor potential ankyrin 1) pathway, which then causes activation of CaMKII (Ca2+/calmodulin-dependent protein kinase II). This then enhances the formation of the TRPV1-eNOS complex, which also includes CaMKII, AMPK (5AMP-activated protein kinase), and Akt (protein kinase B), which leads to activation of eNOS, production of NO, and thus the promotion of endothelial angiogenesis []. There have been numerous reports of the protective effects of NO against inflammation and oxidative stress []. Transgenic eNOS-deficient mice demonstrated a more extensive infarct of the middle cerebral artery (MCA), compared to controls []. NO effects on the regulation of endothelial integrity, anti-inflammatory and anti-apoptotic effects, as well as maintenance of cerebral blood flow, inhibition of platelet aggregation, and reduction of leukocyte adhesion []. Khan et al. studied structurally different NO donors as agents of cerebrovascular protection in experimentally induced stroke in rats. They showed that NO donors promote cerebral blood flow through S-nitrosylation and may be an effective drug for acute stroke [].

Furthermore, Greco et al. proved the protective effect of nitroglycerin (donors of NO) on cerebral damage induced by MCA occlusion in Wistar rats. They observed a significant reduction in stroke volume in preinjected rats compared to their control group, which confirms the protective effect of nitroglycerin in vivo. They speculated that the mechanism of action is associated with the generation of a complex chain of phenomena, triggering activation of apoptosis and subsequent activation of antiapoptotic responses [].

The biological action of ELF-EMF is still being investigated. It is suggested that ELF-EMF has an impact on the physicochemical properties of water, the liquid crystal structure generated by cholesterol, and its derivatives []. Changes in ion balance caused by ELF-EMF appeal to the structure of tissue with piezoelectric and magnetostrictive properties, free radicals, diamagnetic molecules, and uncompensated magnetic spins of paramagnetic elements []. Therefore, ELF-EMF causes depolarization of cells having the ability to spontaneously depolarize, predominantly through Ca2+ influx []. In our previous study, we investigated the effect of ELF-EMF on oxidative stress in patients after ischemic stroke. We demonstrated that ELF-EMF causes activation of antioxidant enzymes [], which leads to reduction of the oxidative modification of plasma protein (this is detailed in an article published in Advances in Clinical and Experimental Medicine). As a highly reactive molecule, NO can also regulate the level of oxidative stress. Through the covalent interaction, NO influences the activity of various enzymes. Mechanisms of this modulation can be varied: NO reacts with coenzymes and active centers containing metal ions and interacts with cysteine residues of proteins [].

In the current study, we observed that in the ELF-EMF group, the level of plasma 3-NT was increased (Figure 2). The formation of 3-NT in protein molecules occurs in vivo by the action of nitrating agents on the polypeptide chain. The formation of 3-NT is mainly attributed to NO and superoxide anions (O2??), which react rapidly to form peroxynitrite (ONOO?). This is one of the major oxidizing and nitrating agents produced in vivo in acute and chronic inflammation, as well as in ischemia/reperfusion. Endothelial cells, macrophages, and neutrophils release large amounts of NO and O2?. Thus, increased amounts of NO contribute to the creation of 3-NT [].

To investigate the effect of ELF-EMF on NO metabolism, we determined nitrate/nitrite concentrations in plasma. We showed that in the ELF-EMF group, the level of nitrate/nitrite compounds in plasma increased after treatment (Figure 3), and these results correspond with the data presented by Chung et al. []. The authors investigated the effects of ELF-EMF (60Hz, 2mT) on the level of NO, biogenic amines, and amino acid neurotransmitters in the hippocampus, cortex, thalamus, cerebellum, and striatum in rats. They found a significant increase in NO concentration in the hippocampus, thalamus, and striatum. Moreover, ELF-EMF also caused a change in the level of biogenic amines and amino acid neurotransmitters in the brain. However, the observed effect and range were different, depending on the brain area. Balind et al. determined the effect of ELF-EMF (50Hz, 0.5mT) on oxidative stress in gerbils with induced cerebral ischemia. They measured the level of NO using the Griess reagent and showed an increased level of NO, provoked by electromagnetic fields. Moreover, ELF-EMF reduces oxidative stress generated during cerebral ischemia, thus leading to a decrease in the damaged brain tissue [].

NO is produced from L-arginine with the involvement of nitric oxide synthase. Three NOS isoforms are expressed in different tissues. Although, in the blood, only NOS2 is expressed, in 35% of the subjects in both the ELF-EMF and non-ELF-EMF groups, mRNA expression of NOS2 was under detection. In the remaining patients, the expression of NOS2 had not significantly changed after treatment. The NOS2 gene in fact encodes for iNOS, which is primarily activated during inflammation. In order to exclude deeper inflammation, we measured the concentration of TNF?, one of the main proinflammatory cytokines. TNF? is a pleiotropic cytokine that is involved in nearly all phenomena of inflammatory responses: initiating chemokine synthesis, promoting the expression of adhesion molecules, promoting the maturation of dendritic cells, and inducing the production of inflammatory mediators and other proinflammatory cytokines []. TNF? stimulates collagenase synthesis in synovial fibroblasts and synovial cartilage chondrocytes and activates osteoclasts, leading to joint cartilage damage, hypertrophy, bone resorption and erosion, and angiogenesis. It also activates monocytes and macrophages, enhancing their cytotoxicity and stimulating cytokine production. Chemokines and growth factors are responsible for T cell proliferation, proliferation and differentiation of B lymphocytes, and the release of inflammatory cytokines by the lymphocytes. Moreover, in the hypothalamus, TNF? stimulates prostaglandin E and IL-1 synthesis []. Pena-Philippides et al. investigated the effect of pulsed electromagnetic fields on injury size and neuroinflammation in mice after middle cerebral artery occlusion (MCAO). They found, using magnetic resonance imaging (MRI), that EMF reduced infarct size, as well as changed expression of genes encoding pro- and anti-inflammatory cytokines in the hemisphere with ischemic injury. After EMF exposure, genes encoding IL-1 and TNF superfamily were downregulated, while IL-10 expression was upregulated. Thus, the authors suggested that application of EMF to poststroke patients could have been beneficial through anti-inflammatory effect and reduction of injury size [].

On the basis of our results, we suggest that the observed increase in NO level is associated with nNOS and/or eNOS activities, but not with iNOS expression. Our research is consistent with evidence shown by Cho et al., who established that ELF-EMF (60Hz, 2mT) increased the expression and activation of nNOS in rat brains [].

The activities of nNOS and eNOS depend on calcium ions. There are many reports that the biological effect of ELF-EMF is related to the control of calcium channels []. In view of these findings, the observed mechanism of increased NO generation and metabolism may be associated with calcium-ion flux.

Additionally, we noticed that ELF-EMF treatment enhances the effectiveness of poststroke rehabilitation (Table 2). Some researchers suggest that electromagnetic fields have a beneficial effect on ischemic/reperfusion injury, and in some places, therapeutic programs using ELF-EMF are considered to be standard therapy for poststroke patients []. The beneficial effects of ELF-EMF include the following: improvement in the transport of cellular and mitochondrial membranes; normalization of blood rheological values; counteraction of tissue oxidation; intensification of regenerative processes; stimulation of axon growth in undamaged neurons; intensification of neuronal dissociation and differentiation; reduction of stress-induced emotional reactions and free radicals; acceleration of the return of fibre function in functional disorders; reduction of periapical scarring; and increase of the level of energetic substances in the brain tissue and erythrocytes []. Grant et al. estimated the impact of low-frequency pulsed electromagnetic field on cerebral ischemia in rabbit. They observed using MRI that exposure to electromagnetic field caused extenuation of cortical ischemia oedema and reduction of neuronal injury in cortical area [].

In conclusion, ELF-EMF therapy increases the metabolism and generation of NO, which has both neuroprotective and cytotoxic properties. An increase in NO level is probably associated with nNOS and/or eNOS activities, but not with iNOS expression, which increases mainly during inflammation. We suggested that in poststroke patients, NO demonstrated a protective effect due to significant improvement in patient functional status. Thus, our studies promote the validity of this method in poststroke rehabilitation therapy.

Acknowledgments

This study was supported by the Department of General Biochemistry, Faculty of Biology and Environmental Protection, University of Lodz (no. 506/1136), and Laboratory of Medical Genetics, Faculty of Biology and Environmental Protection, University of Lodz (no. B161100000004601), and Grants for Young Scientists and PhD Students, Faculty of Biology and Environmental Protection, University of Lodz (B1611000001145.02).

Conflicts of Interest

The authors declare that there is no conflict of interest regarding the publication of this article.

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18. Désy O., Carignan D., Caruso M., de Campos-Lima P. O. Methanol induces a discrete transcriptional dysregulation that leads to cytokine overproduction in activated lymphocytes. Toxicological Sciences2010;117(2):303–313. doi: 10.1093/toxsci/kfq212. [PubMed] [Cross Ref]
19. Allman C., Amadi U., Winkler A. M., et al. Ipsilesional anodal tDCS enhances the functional benefits of rehabilitation in patients after stroke. Science Translational Medicine2016;8(330):p. 330re1. doi: 10.1126/scitranslmed.aad5651.[PMC free article] [PubMed] [Cross Ref]
20. Wang H. G., Lu F. M., Jin I., et al. Presynaptic and postsynaptic roles of NO, cGK, and RhoA in long-lasting potentiation and aggregation of synaptic proteins. Neuron2005;45:389–403. doi: 10.1016/j.neuron.2005.01.011. [PubMed] [Cross Ref]
21. Yang Y. R., Jung J. H., Kim S. J., et al. Forebrain-specific ablation of phospholipase C?1 causes manic-like behavior. Molecular Psychiatry2017 doi: 10.1038/mp.2016.261. [PubMed] [Cross Ref]
22. Fekete C. D., Goz R. U., Dinallo S., et al. In vivo transgenic expression of collybistin in neurons of the rat cerebral cortex. The Journal of Comparative Neurology2017;525(5):1291–1311. doi: 10.1002/cne.24137. [PubMed] [Cross Ref]
23. Ungvari Z., Tarantini S., Hertelendy P., et al. Cerebromicrovascular dysfunction predicts cognitive decline and gait abnormalities in a mouse model of whole brain irradiation-induced accelerated brain senescence. Geroscience2017;39(1):33–42. doi: 10.1007/s11357-017-9964-z. [PMC free article] [PubMed] [Cross Ref]
24. Su K. H., Lin S. J., Wei J., et al. The essential role of transient receptor potential vanilloid 1 in simvastatin-induced activation of endothelial nitric oxide synthase and angiogenesis. Acta Physiologica (Oxford, England) 2014;212(3):191–204. doi: 10.1111/apha.12378. [PubMed] [Cross Ref]
25. Cirino G., Fiorucci S., Sessa W. C. Endothelial nitric oxide synthase: the Cinderella of inflammation? Trends in Pharmacological Sciences2003;24:91–95. doi: 10.1016/S0165-6147(02)00049-4. [PubMed] [Cross Ref]
26. Huang Z., Huang P. L., Ma J., et al. Enlarged infarcts in endothelial nitric oxide synthase knockout mice are attenuated by nitro-L-arginine. Journal of Cerebral Blood Flow and Metabolism1996;16:981–987. doi: 10.1097/00004647-199609000-00023.[PubMed] [Cross Ref]
27. Li H., Forstermann U. Nitric oxide in the pathogenesis of vascular disease. The Journal of Pathology2000;190:244–254. doi: 10.1002/(SICI)1096-9896(200002)190:3<244::AID-PATH575>3.0.CO;2-8. [PubMed] [Cross Ref]
28. Khan M., Jatana M., Elango C., Paintlia A. S., Singh A. K., Singh I. Cerebrovascular protection by various nitric oxide donors in rats after experimental stroke. Nitric Oxide2006;15(2):114–124. doi: 10.1016/j.niox.2006.01.008. [PubMed][Cross Ref]
29. Khan M., Sekhon B., Giri S., et al. S-Nitrosoglutathione reduces inflammation and protects brain against focal cerebral ischemia in a rat model of experimental stroke. Journal of Cerebral Blood Flow and Metabolism2005;25:177–192. doi: 10.1038/sj.jcbfm.9600012. [PubMed] [Cross Ref]
30. Greco R., Amantea D., Blandini F., et al. Neuroprotective effect of nitroglycerin in a rodent model of ischemic stroke: evaluation of Bcl-2 expression. International Review of Neurobiology2007;82:423–435. doi: 10.1016/S0074-7742(07)82024-1.[PubMed] [Cross Ref]
31. Sulpizio M., Falone S., Amicarelli F., et al. Molecular basis underlying the biological effects elicited by extremely low-frequency magnetic field (ELF-MF) on neuroblastoma cells. Journal of Cellular Biochemistry2011;112:3797–3806. doi: 10.1002/jcb.23310. [PubMed] [Cross Ref]
32. Yi G., Wang J., Wei X., et al. Effects of extremely low-frequency magnetic fields on the response of a conductance-based neuron model. International Journal of Neural Systems2014;24(1, article 1450007) doi: 10.1142/S0129065714500075. [PubMed][Cross Ref]
33. Brisdelli F., Bennato F., Bozzi A., Cinque B., Mancini F., Iorio R. ELF-MF attenuates quercetin-induced apoptosis in K562 cells through modulating the expression of Bcl-2 family proteins. Molecular and Cellular Biochemistry2014;397(1-2):33–43. doi: 10.1007/s11010-014-2169-1. [PubMed] [Cross Ref]
34. Morgado-Valle C., Verdugo-Díaz L., García D. E., Morales-Orozco C., Drucker-Colín R. The role of voltage-gated Ca2+ channels in neurite growth of cultured chromaffin cells induced by extremely low frequency (ELF) magnetic field stimulation. Cell and Tissue Research1998;291(2):217–230. [PubMed]
35. Cichon N., Bijak M., Miller E., Saluk J. Extremely low-frequency electromagnetic field (ELF-EMF) reduces oxidative stress and improves functional and psychological status in ischemic stroke patients. Bioeletromagtetics2017;38(5):386–396. doi: 10.1002/bem.22055. [PubMed] [Cross Ref]
36. Wink D. A., Miranda K. M., Espey M. G., et al. Mechanisms of the antioxidant effects of nitric oxide. Antioxidants & Redox Signaling2001;3(2):203–213. doi: 10.1089/152308601300185179. [PubMed] [Cross Ref]
37. Ronson R. S., Nakamura M., Vinten-Johansen J. The cardiovascular effects and implications of peroxynitrite. Cardiovascular Research1999;44:47–59. [PubMed]
38. Chung Y. H., Lee Y. J., Lee H. S., et al. Extremely low frequency magnetic field modulates the level of neurotransmitters. The Korean Journal of Physiology and Pharmacology2015;19(1):15–20. doi: 10.4196/kjpp.2015.19.1.15. [PMC free article][PubMed] [Cross Ref]
39. Rauš B. S., Selakovi? V., Radenovi? L., Proli? Z., Jana? B. Extremely low frequency magnetic field (50 Hz, 0.5 mT) reduces oxidative stress in the brain of gerbils submitted to global cerebral ischemia. PLoS One2014;9(2, article e88921) doi: 10.1371/journal.pone.0088921. [PMC free article] [PubMed] [Cross Ref]
40. Wu P., Jia F., Zhang B., Zhang P. Risk of cardiovascular disease in inflammatory bowel disease. Experimental and Therapeutic Medicine2017;13(2):395–400. doi: 10.3892/etm.2016.3966. [PMC free article] [PubMed] [Cross Ref]
41. Godos J., Biondi A., Galvano F., et al. Markers of systemic inflammation and colorectal adenoma risk: meta-analysis of observational studies. World Journal of Gastroenterology2017;23(10):1909–1919. doi: 10.3748/wjg.v23.i10.1909.[PMC free article] [PubMed] [Cross Ref]
42. Pena-Philippides J. C., Yang Y., Bragina O., Hagberg S., Nemoto E., Roitbak T. Effect of pulsed electromagnetic field (PEMF) on infarct size and inflammation after cerebral ischemia in mice. Translational Stroke Research2014;5(4):491–500. doi: 10.1007/s12975-014-0334-1. [PubMed] [Cross Ref]
43. Cho S. I., Nam Y. S., Chu L. Y., et al. Extremely low-frequency magnetic fields modulate nitric oxide signaling in rat brain. Bioelectromagnetics2012;33(7):568–574. doi: 10.1002/bem.21715. [PubMed] [Cross Ref]
44. Walleczek J. Electromagnetic field effects on cells of the immune system: the role of calcium signaling. The FASEB Journal1992;6:3177–3185. [PubMed]
45. Grassi C., D’Ascenzo M., Torsello A., et al. Effects of 50 Hz electromagnetic fields on voltage-gated Ca2+ channels and their role in modulation of neuroendocrine cell proliferation and death. Cell Calcium2004;35:307–315. doi: 10.1016/j.ceca.2003.09.001. [PubMed] [Cross Ref]
46. Piacentini R., Ripoli C., Mezzogori D., Azzena G. B., Grassi C. Extremely low-frequency electromagnetic fields promote in vitro neurogenesis via upregulation of Cav1-channel activity. Journal of Cellular Physiology2008;215:129–139. doi: 10.1002/jcp.21293. [PubMed] [Cross Ref]
47. Gobba F., Malagoli D., Ottaviani E. Effects of 50 Hz magnetic fields on fMLP-induced shape changes in invertebrate immunocytes: the role of calcium ion channels. Bioelectromagnetics2003;24:277–282. doi: 10.1002/bem.10102. [PubMed][Cross Ref]
48. Craviso G. L., Choe S., Chatterjee P., Chatterjee I., Vernier P. T. Nanosecond electric pulses: a novel stimulus for triggering Ca2+ influx into chromaffin cells via voltage-gated Ca2+ channels. Cellular and Molecular Neurobiology2010;30:1259–1265. doi: 10.1007/s10571-010-9573-1. [PubMed] [Cross Ref]
49. Sieroñ A., Cieslar G. Use of magnetic fields in medicine – 15 years of personal experience. Wiadomo?ci Lekarskie2003;56:434–441. [PubMed]
50. Wolda?ska-Oko?ska M., Czernicki J. Effect of low frequency magnetic fields used in magnetotherapy and magnetostimulation on the rehabilitation results of patients after ischemic stroke. Przegla?d Lekarski2007;64(2):74–77. [PubMed]
51. Capone F., Dileone M., Profice P., et al. Does exposure to extremely low frequency magnetic fields produce functional changes in human brain? Journal of Neural Transmission (Vienna) 2009;116(3):257–265. doi: 10.1007/s00702-009-0184-2.[PubMed] [Cross Ref]
52. Miecznik A., Czernicki J., Krukowska J. Influence of magnetic field of different characteristics on blood pressure in patients with back pain syndromes and hypertensive disease. Acta Bio-Optica et Informatica Medica2001;7(1-2):9–13.
53. Di Lazzaro V., Capone F., Apollonio F., et al. A consensus panel review of central nervous system effects of the exposure to low-intensity extremely low-frequency magnetic fields. Brain Stimulation2013;6(4):469–476. doi: 10.1016/j.brs.2013.01.004.[PubMed] [Cross Ref]
54. Grant G., Cadossi R., Steinberg G. Protection against focal cerebral ischemia following exposure to a pulsed electromagnetic field. Bioelectromagnetics1994;15(3):205–216. [PubMed]

Measurements of human tumour necrosis factor alpha (TNF?) in plasma samples were made with a Human TNF? ELISA development kit (MABTECH, Cincinnati, OH, USA), in accordance with the manufacturer’s protocol. The combination of two coating antibodies (TNF3 and TNF4) were used for the analysis. The absorbance was measured at 450nm, and TNF? concentration was expressed as pg/mL [].

PAIN

Pain is the chief reason people visit doctors.   It stands to reason that anyone treating pain (or being treated for it!) would like to know what works best.  And there shouldn’t be any doubt about it, should there?

Yet that is not the case.  There is enormous confusion throughout health care and on the part of the public as to what genuinely works best.  All of us age, experience illness and eventually die.  Don’t we owe it to ourselves give our best to one another while we are still here in these bodies?

Therapies which stimulate healing of the underlying tissue trauma causing pain are few and far between.  Shouldn’t such methods be the first ones given?

Laser and PEMF can reach and heal deep pain at the source and may be ideal therapies because:

  1. They stimulate cellular and tissue healing.
  2. Most sources of pain and the nerves for its perception are well within reach of their tissue healing, anti-inflammatory and analgesic effects.
  3. Efficacy and safety demonstrated in a broad range of conditions over many years. [1]

Laser therapy can penetrate five centimeters to effectively reach the source of almost any pain in soft tissue, vertebrae and joints. Besides its properties to stimulate tissue regeneration, laser therapy can also block neural transmission by C fibers (dull, difficult to locate pain) and A delta fibers (sharp, easy to pinpoint pain).  Laser therapy may provide immediate relief even for many individuals whose pain has seemed unremitting and intractable.

Pulsed electromagnetic fields (PEMF) which pass though tissue as if it were transparent can penetrate the whole body, inducing electrical currents and stimulating healing

anywhere they are applied.  PEMF has been shown to reduce inflammation and stimulate tissue repair in a broad range of conditions with beneficial effects documented at cellular, tissue, system and whole body levels.  An added advantage is that treatment can be unattended so highly cost-effective for patients.  Combined treatment with laser and PEMF may give better results than either method on its own.  Even chronic pain which has not responded to other methods may be rapidly alleviated by laser and PEMF.

 The Nature of Pain

Pain is information.   If you are experiencing it, there is always a reason.  It is wise to honor an inner voice telling us to avoid what is painful.  Much current practice for “managing” pain, if it involves aggressively stretching and manipulating tendons, ligaments and tissues already pushed beyond their limits, goes against what our bodies are telling us.   Dismissing the failure of this approach as the fault of the patient or an inherent problem within the brain or central nervous system may be no more than a poor excuse for inappropriate treatment.

Soft tissue takes time and rest to heal.    Would anyone treat a broken ankle by forcefully bending and twisting it?  Actively resting + appropriate laser and / or PEMF are a sound approach to support the healing of soft tissue injuries, arthritis and pain in general.

Laser Therapy Research

Pulsed Electromagnetic Field Therapy Research

Chronic pain and disability can be prevented.

When acute pain is inadequately or incorrectly treated, it frequently becomes chronic. Chronic pain is the leading cause of disability.  If appropriate laser and pulsed electromagnetic field therapies were to be administered at the outset of injury, much disability, chronic pain and the high medical costs and suffering associated with them can be avoided.

Lasers and PEMF have been shown to improve and even to reverse many chronic inflammatory conditions. Even better, they have demonstrated much greater safety than current methods. We have been spending three out of four of every health care dollars in the US to “manage” chronic inflammatory conditions.   Why “manage” what you can heal? [2] Laser and other forms of photomedicine and PEMF promise better clinical outcomes in pain and many other inflammatory conditions and a healthier, happier, far more cost-effective future.

[1] Pulsed electromagnetic field therapy research is well worth viewing and available HERE.

[2] $2.6 trillion  was spent on health care in the U.S. in 2010 and approximately $1.95 trillion to “manage” chronic inflammatory conditions.

Copyright 2011-2017 by David Rindge.  All rights reserved.

Pain

Pain is the chief reason people visit doctors.   It stands to reason that anyone treating pain (or being treated for it!) would like to know what works best.  And there shouldn’t be any doubt about it, should there?

Yet that is not the case.  There is enormous confusion throughout health care and on the part of the public as to what genuinely works best.  Therapies which stimulate healing of the underlying tissue trauma causing pain deserve to be on the front line and should be the first methods applied, not the last.

Laser and PEMF can reach and heal deep pain at its source.

Laser and pulsed electromagnetic fields (PEMF) are ideal therapies in pain because:

  1. They stimulate cellular and tissue healing.
  2. Most sources of pain as well as the nerves critical for its perception are well within reach of their tissue healing, anti-inflammatory and analgesic effects.
  3. Efficacy, affordability and track record for safety.

Laser therapy can penetrate five centimeters to effectively reach the source of almost any pain in soft tissue, vertebrae and joints. Besides its properties to stimulate tissue regeneration, laser therapy can also block neural transmission by C fibers (dull, difficult to locate pain) and A delta fibers (sharp, easy to pinpoint pain).  Laser therapy may provide immediate relief even for many individuals whose pain has seemed unremitting and intractable.

Pulsed electromagnetic fields (PEMF) which pass though tissue as if it were transparent can penetrate the whole body, inducing electrical currents and stimulating healing anywhere they are applied.  PEMF has been shown to reduce inflammation and stimulate tissue repair in a broad range of conditions with beneficial effects documented at cellular, tissue, system and whole body levels.  An added advantage is that treatment can be unattended so highly cost-effective for patients.  Combined treatment with laser and PEMF may give better results than either method on its own.  Even chronic pain which has not responded to other methods may be rapidly alleviated by laser and PEMF.

 The Nature of Pain

Pain is information.   If you are experiencing it, there is always a reason.  It is wise to honor an inner voice telling us to avoid movement which is painful.  Much current practice for “managing” pain, if it involves aggressively stretching and manipulating tendons, ligaments and tissues already pushed beyond their limits, goes against what our bodies are telling us.   Dismissing the failure of this approach as the fault of the patient or an inherent problem within the brain or central nervous system may be no more than a poor excuse for inappropriate treatment.

Soft tissue takes time and rest to heal.    Would anyone treat a broken ankle by forcefully bending and twisting it?  Actively resting + energy-based methods are a sound approach to support the healing of soft tissue injuries, arthritis and pain in general.

Laser Therapy Research

Pulsed Electromagnetic Field Therapy Research

Chronic pain and disability can be prevented.

When acute pain is inadequately or incorrectly treated, it frequently becomes chronic. Chronic pain is the leading cause of disability.  If appropriate laser and pulsed electromagnetic field therapies were to be administered at the outset of injury, much disability, chronic pain and the high medical costs and suffering associated with them can be avoided.

Lasers and PEMF have been shown to improve and even to reverse many chronic inflammatory conditions. Even better, they have demonstrated much greater safety than current standard practice. We have been spending three out of four of every health care dollars in the US to “manage” chronic inflammatory conditions.   Why “manage” what you can heal? [1] Laser and other forms photomedicine and PEMF promise better clinical outcomes in pain and in many other inflammatory conditions and a healthier, happier, far more cost-effective future.

[1] $2.6 trillion  was spent on health care in the U.S. in 2010 and approximately $1.95 trillion to “manage” chronic inflammatory conditions.

Copyright 2011-2017 by David Rindge.  All rights reserved.

Pain

by David Rindge

Pain is the chief reason people visit doctors.   It stands to reason that anyone treating pain (or being treated for it!) would like to know what works best.  … And there shouldn’t be any doubt about it, should there?

Yet that is not yet the case.  There is enormous confusion both in the medical community and on the part of the public as to what genuinely works best.  Therapies which stimulate healing of the underlying tissue trauma causing pain deserve to be on the front line and should be the first methods applied, not the last.

Laser and PEMF can reach and heal deep pain at its source.

Laser and pulsed electromagnetic field therapy are ideal Neural Targets of the Head and Necktreatments for pain because:

  1.  They stimulate cellular and tissue healing.
  2.  Most sources of pain as well as the nerves critical for its perception are well within reach of their tissue healing, anti-inflammatory and analgesic effects.
  3.  Efficacy, affordability and track record for safety.

Laser therapy can penetrate five centimeters to effectively reach the source of almost any pain in soft tissue, vertebrae and joints. Besides its properties to stimulate tissue regeneration, laser therapy can also block neural transmission by C fibers (dull, difficult to locate pain) and A delta fibers (sharp, easy to pinpoint pain).  Laser therapy may provide immediate relief even for many individuals whose pain has seemed unremitting and intractable.

Pulsed electromagnetic fields (PEMF) which pass though tissue as if it were transparent can penetrate the whole body, inducing electrical currents and stimulating healing anywhere they are applied.  PEMF has been shown to reduce inflammation and stimulate tissue repair in a broad range of conditions with beneficial effects documented at cellular, tissue, system and whole body levels.  An added advantage is that treatment can be unattended so highly cost-effective for patients.  Combined treatment with laser and PEMF may give better results than either method on its own.  Even chronic pain which has not responded to other methods may be rapidly alleviated by laser and PEMF.

The Nature of Pain

Pain is information.   If you are experiencing it, there is always a reason.  It is wise to honor an inner voice telling us to avoid movement which is painful.  Much current practice for “managing” pain, if it involves aggressively stretching and manipulating tendons, ligaments and tissues already pushed beyond their limits, goes against what our bodies are telling us.   Dismissing the failure of this approach as the fault of the patient or an inherent problem within the brain or central nervous system may be no more than a poor excuse for inappropriate treatment.

Soft tissue takes time and rest to heal.    Would anyone treat a broken ankle by forcefully bending and twisting it?  Actively resting + energy-based methods are a sound approach to support the healing of soft tissue injuries, arthritis and pain in general.

Laser Therapy Research

Pulsed Electromagnetic Field Therapy Research

Chronic pain and disability can be prevented.

Chronic pain is the leading cause of disability.  When acute pain is not correctly treated, it frequently becomes chronic. If appropriate laser and pulsed electromagnetic field therapies were to be administered at the outset of injury, much disability, chronic pain and the high medical costs and suffering associated with them can be avoided.

Lasers and PEMF have been shown to improve and even to reverse many chronic inflammatory conditions. Even better, they have demonstrated much greater safety than current standard practice. We have been spending three out of four of every health care dollars in the US to “manage” chronic inflammatory conditions.   Why “manage” pain when you can heal it? [1] Laser and other forms photomedicine and PEMF promise better clinical outcomes in pain and many other inflammatory conditions and a healthier, happier, far more cost-effective future for all of us.

[1] $2.6 trillion  was spent on health care in the U.S. in 2010 and approximately $1.95 trillion to “manage” chronic inflammatory conditions.

Copyright 2011-2017 by David Rindge.  All rights reserved.

To Be Prepared is Half the Victory!

Lasers, laser needles, pulsed electromagnetic fields and light emitting diodes are the right tools for healing today’s complex patients and for your practice success!

All devices pictured above and more will likely be available for you to train and practice with in this course.

David Rindge and Healing Light Seminars have been teaching and practicing with energy-based therapies since 2002. We continually update our methods and equipment as new technology and information become available.  We will only offer a device if we are continuing to use it clinically, have found it effective and to deliver good value.

Day 1 focuses on theory, biological effects and essentials for treatment success.   You have the opportunity for hands-on practice with state-of-the-art laser, laser needle acupuncture, pulsed electromagnetic field and light emitting diode therapy systems  systems for the treatment of pain, head to toe.

In Day 2, you will learn how laser, laser needle, light emitting diode and pulsed electromagnetic field therapy devices may be applied successfully in aesthetics / dermatology / facial rejuvenation, cardiovascular disease, digestive, ear and eye disorders, gynecology, for hair regrowth, neuropathy, osteoporosis, respiratory disorders, sports medicine and much more.

You will receive Laser Therapy: A Clinical Manual as part of the course.

Laser Therapy - A Clinical Manual This popular training manual by Blahnik and Rindge presents the theory and clinical application of laser therapy in clearly understandable terms with treatment protocols for more than 40 conditions.  Laser Therapy: A Clinical Manual is an important important resource in the course and a $79.00 value.  You will also receive treatment protocols for other conditions, updates and much, much more relevant material in this course.

Gain a solid understanding of the principles, technology and parameters of energy-based therapies and the skills to apply them successfully in your practice!  Our goal is to provide you with everything you need to come from knowledge and strength in your practice with laser, laser needle, pulsed electromagnetic field and light emitting diode therapies.  Learn More and Register Here.

Course Date / Location

November 4-5, 2017.  Wild Manta, 5151 South Babcock St, Palm Bay, FL 32905.  (321) 676-8606.

LEARN MORE AND REGISTER HERE

Or call 321-751-7001.

Healing Light Seminars

Training in Energy-based Therapies since 2002

14 PDAs – NCCAOM 322-5

14 CEUs Florida Acupuncturists

NCCAOM emblem

The Promise of Energy-Based Therapies in Pain

by David Rindge.

Leading Causes of Disability

Acute pain inadequately treated frequently becomes chronic.  Chronic pain is the leading cause of disability.  We spent $2.6 trillion on health care in the U.S. in 2010, 75% of it ($1.95 trillion) to “manage” chronic inflammatory conditions.  The price is too high and consumer satisfaction too low to continue as we have been.

A growing body of science and clinical experience has shown that energy-based treatments can improve outcomes in chronic pain and also suggests health care costs will be reduced.   Low intensity lasers, leds and pulsed electromagnetic fields have well documented properties to move the body through inflammation and heal injury.  Applied at the outset, these methods hold promise to prevent many, perhaps most, acute conditions from ever becoming chronic. What would be the potential health and financial benefits for all Americans – and the economy – were these treatments to be broadly implemented and reimbursable by insurance?

 

“Arthritis or rheumatism” is the #1 cause of disability = 8.6 million people.
“Back or Spine Problems” is the #2 cause of disability = 7.6 million people
16.2 million people

To see what researchers have reported about the effects of low intensity laser, led and pulsed electromagnetic field therapies to improve the underlying pathology in the #1 and #2 causes of disability, click on:

Chronic Pain is the Leading Cause of Disability

Chronic pain affects more than one out of three U.S. citizens (>100 million). Direct costs have been estimated at $100 billion[1]. Yet though over the counter and prescription pain relievers are expensive, these costs, missed work days and the like are trivial compared to the hidden financial burden, pain and suffering born by individuals and society.

Taking care of the disabled is enormously expensive. How expensive? Nobody seems to know exactly. Besides their enormous cost, current methods may do little to address the underlying causes. How much has the high cost of current health care methods contributed to America’s economic tailspin.

Can we do better?

The best possible treatments for pain would address underlying causes, be safe and affordable. Low intensity laser, led and pulsed electromagnetic field therapies have been documented to heal tissue, promote healthy function and to improve the underlying pathology in the #1 and #2 causes of disability. Therapies documented to heal damaged tissue and improve physiological function are also likely to have an endpoint. As such, they hold great promise to improve the way we care for one another – while also lowering costs. In contrast, “managing” chronic pain endlessly with prescription or over the counter medications is hugely expensive and may do little to address the underlying disease process or to improve health.

In 2010 the Patient Protection and Affordable Health Care Act (aka Obamacare) became law.  Since 2014 Americans have been required to buy insurance.  Does yours include laser, led and pulsed electromagnetic field therapies?

Energy-Based Treatments Promise to Lower Costs and Improve Quality of Care

As we spent $2.6 trillion on health care in 2010, an average of of $8,402 per person, redistributing expensive methods which have created a seemingly impossible financial burden seems unlikely to this writer to achieve the savings necessary to make the Affordable Care Act viable.   By opening to innovation, we can raise the bar in health care, improving quality and making it affordable.

Low level lasers, leds and pulsed electromagnetic fields have properties shown to move the body through inflammation to heal damaged tissue, preventing chronic illness.  Even in long-standing disease, these methods can restore function, reduce pain and improve quality of life.  How much pain, suffering and money will be spared with the implementation of these methods as first line treatments for pain in health care?  What might it mean for the health of all Americans and the economy?

 


[1] Bjordal JM, Couppe C, Chow RT, Tuner J, Ljunggren EA, A Systematic Review of Low Level Laser Therapy with Location-Specific Doses for Pain from Chronic Joint Disorders, J Physiother. 2003;49(2):107-16.


[i] From http://www.allbusiness.com/labor-employment/compensation-benefits-wages-salaries/12503910-1.html, True cost of disability is staggering.Colorado Springs Business Journal. June 5, 2009

Copyright 2013-2016 by David Rindge. All rights reserved.

Laser and NSAIDs

Lasers Med Sci. 2017 Aug 9. doi: 10.1007/s10103-017-2299-2. [Epub ahead of print]

Effects of photobiomodulation therapy and topical non-steroidal anti-inflammatory drug on skeletal muscle injury induced by contusion in rats-part 2: biochemical aspects.

Tomazoni SS1, Frigo L2, Dos Reis Ferreira TC3,4, Casalechi HL3, Teixeira S5, de Almeida P6, Muscara MN5, Marcos RL6, Serra AJ6, de Carvalho PTC4,6, Leal-Junior ECP3,4.

Author information

1
Masters and Doctoral Programs in Physical Therapy, Universidade Cidade de São Paulo (UNICID), Rua Cesário Galeno, 448/475, São Paulo, SP, 05508-900, Brazil. shaiane.tomazoni@gmail.com.
2
Biological Sciences and Health Center, Cruzeiro do Sul University (UNICSUL), São Paulo, SP, Brazil.
3
Laboratory of Phototherapy in Sports and Exercise, Nove de Julho University (UNINOVE), São Paulo, SP, Brazil.
4
Postgraduate Program in Rehabilitation Sciences, Nove de Julho University (UNINOVE), São Paulo, SP, Brazil.
5
Department of Pharmacology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, SP, Brazil.
6
Postgraduate Program in Biophotonics Applied to Health Sciences, Nove de Julho University (UNINOVE), São Paulo, SP, Brazil.

Abstract

Muscle injuries trigger an inflammatory process, releasing important biochemical markers for tissue regeneration. The use of non-steroidal anti-inflammatory drugs (NSAIDs) is the treatment of choice to promote pain relief due to muscle injury. NSAIDs exhibit several adverse effects and their efficacy is questionable. Photobiomodulation therapy (PBMT) has been demonstrated to effectively modulate inflammation induced from musculoskeletal disorders and may be used as an alternative to NSAIDs. Here, we assessed and compared the effects of different doses of PBMT and topical NSAIDs on biochemical parameters during an acute inflammatory process triggered by a controlled model of contusion-induced musculoskeletal injury in rats. Muscle injury was induced by trauma to the anterior tibial muscle of rats. After 1 h, rats were treated with PBMT (830 nm, continuous mode, 100 mW of power, 35.71 W/cm2; 1, 3, and 9 J; 10, 30, and 90 s) or diclofenac sodium (1 g). Our results demonstrated that PBMT, 1 J (35.7 J/cm2), 3 J (107.1 J/cm2), and 9 J (321.4 J/cm2) reduced the expression of tumor necrosis factor alpha (TNF-?) and cyclooxygenase-2 (COX-2) genes at all assessed times as compared to the injury and diclofenac groups (p < 0.05). The diclofenac group showed reduced levels of COX-2 only in relation to the injury group (p < 0.05). COX-2 protein expression remained unchanged with all therapies except with PBMT at a 3-J dose at 12 h (p < 0.05 compared to the injury group). In addition, PBMT (1, 3, and 9 J) effectively reduced levels of cytokines TNF-?, interleukin (IL)-1?, and IL-6 at all assessed times as compared to the injury and diclofenac groups (p < 0.05). Thus, PBMT at a 3-J dose was more effective than other doses of PBMT and topical NSAIDs in the modulation of the inflammatory process caused by muscle contusion injuries.

Med Oral Patol Oral Cir Bucal. 2017 Jul 1;22(4):e467-e472.

Effect of pre-operatory lowlevel laser therapy on pain, swelling, and trismus associated with third-molar surgery.

Petrini M1, Ferrante M, Trentini P, Perfetti G, Spoto G.

Author information

1
Department of Medical, Oral and Biotechnological Sciences, University of Chieti – Italy, Via Vestini 31, 66013 Chieti, Italy materialidentari.uda@gmail.com.

Abstract

BACKGROUND:

The extraction of impacted third molars is commonly associated to pain, edema, trismus, limited jaw opening and movements. The aim of this retrospective study is to verify if pre-surgical lowlevel laser therapy (LLLT) associated with the extraction of impacted lower third molars could add benefits to the postoperative symptoms respect LLLT performed only after surgery.

MATERIAL AND METHODS:

Data from 45 patients subjected to a surgical extraction of lower third molars were pooled and divided into three groups. Patients that received only routine management were inserted in the control group. Group 1, were patients that received LLLT immediately after surgery and at 24 hours. In group 2 were included patients treated with LLLT immediately before the extraction and immediately after the end of the procedure. Data were analyzed using linear regression and descriptive statistics.

RESULTS:

Both laser-treated groups were characterized by minor events of post-surgery complications of pain, edema, trismus. The use of NSAIDs in the first 24 hours was significantly inferior in Group 2.

CONCLUSIONS:

Pre-surgical LLLT treatment seems to increase the analgesic effect of LLLT. However, trismus and edema were reduced in both laser treated groups, independently from the period of irradiation.

Lasers Med Sci. 2016 Winter;7(1):45-50. doi: 10.15171/jlms.2016.10. Epub 2016 Jan 7.

Low Level Laser Therapy Versus Pharmacotherapy in Improving Myofascial Pain Disorder Syndrome.

Khalighi HR1, Mortazavi H1, Mojahedi SM2, Azari-Marhabi S1, Moradi Abbasabadi F3.

Author information

1
Department of Oral and Maxillofacial Medicine, School of Dentistry, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
2
Department of Laser, School of Dentistry, Shahid Beheshti University of Medical Sciences, Tehran,Iran.
3
Department of Oral and Maxillofacial Pathology, Faculty of Dentistry, Qom University of Medical Sciences, Qom, Iran.

Abstract

INTRODUCTION:

Temporomandibular disorders (TMD) lead to masticatory muscle pain, jaw movement disability and limitation in mouth opening. Pain is the chief complaint in 90% of the TMD patients which leads to disability and severe socioeconomic costs. The purpose of this study was to evaluate the therapeutic effects of low level laser therapy (LLLT) compared to pharmacotherapy with NSAIDs (naproxen) in myofascial pain disorder syndrome (MPDS).

METHODS:

In this randomized controlled clinical trial, 40 MPDS patients were divided into two groups. One group received naproxen 500 mg bid for 3 weeks as treatment modality and also had placebo laser sessions. The other group received active laser (diode 810 nm CW) as treatment and placebo drug. Pain intensity was measured by visual analogue scale (VAS) and maximum painless mouth opening was also measured as a functional index every session and at 2 months follow up. Data was collected and analyzed with SPSS software. Independent t test was used to analyze the data. A P < 0.05 was considered significant.

RESULTS:

Low level laser caused significant reduction in pain intensity (P < 0.05) and a significant increase in mouth opening. In naproxen group neither pain intensity nor maximum mouth opening had significant improvement. Pain relief, in subjective VAS was observed in third session in LLLT group, but did not occur in naproxen group. Maximum mouth opening increased significantly in laser group compared to the naproxen group from the eighth session.

CONCLUSION:

Treatment with LLLT caused a significant improvement in mouth opening and pain intensity in patients with MPDS. Similar improvement was not observed in naproxen group.

Lasers Med Sci. 2017 Jan;32(1):101-108. doi: 10.1007/s10103-016-2091-8. Epub 2016 Oct 10.

Effects of photobiomodulation therapy, pharmacological therapy, and physical exercise as single and/or combined treatment on the inflammatory response induced by experimental osteoarthritis.

Tomazoni SS1, Leal-Junior EC2, Pallotta RC3, Teixeira S3, de Almeida P3, Lopes-Martins RÁ4.

Author information

1
Laboratory of Pharmacology and Experimental Therapeutics, Department of Pharmacology, Institute of Biomedical Sciences, University of São Paulo (USP), Av. Prof. Lineu Prestes, 1524, Butantan, São Paulo, SP, 05508-900, Brazil. shaiane.tomazoni@gmail.com.
2
Postgraduate Program in Biophotonics Applied to Health Sciences and Post Graduate Program in Rehabilitation Sciences, Nove de Julho University (UNINOVE), São Paulo, SP, Brazil.
3
Laboratory of Pharmacology and Experimental Therapeutics, Department of Pharmacology, Institute of Biomedical Sciences, University of São Paulo (USP), Av. Prof. Lineu Prestes, 1524, Butantan, São Paulo, SP, 05508-900, Brazil.
4
Biomedical Engineering Research and Post-Graduate Center, Mogi das Cruzes University (UMC), Mogi das Cruzes, SP, Brazil.

Abstract

Osteoarthritis (OA) triggers increased levels of inflammatory markers, including prostaglandin (PG) E2 and proinflammatory cytokines. The elevation of cytokine levels is closely associated with increased articular tissue degeneration. Thus, the use of combination therapies may presumably be able to enhance the effects on the modulation of inflammatory markers. The present study aimed to evaluate and compare the effects of photobiomodulation therapy (PBMT), physical exercise, and topical nonsteroidal anti-inflammatory drug (NSAID) use on the inflammatory process after they were applied either alone or in different combinations. OA was induced by intra-articular papain injection in the knee of rats. After 21 days, the animals began treatment with a topical NSAID and/or with physical exercise and/or PBMT. Treatments were performed three times a week for eight consecutive weeks, totaling 24 therapy sessions. Analysis of real-time polymerase chain reaction (RT-PCR) gene expression; interleukin (IL)-1?, IL-6, and tumor necrosis factor alpha (TNF-?) protein expression; and PGE2 levels by enzyme-linked immunosorbent assay (ELISA) was conducted. Our results showed that PBMT alone and Exerc + PBMT significantly reduced IL-1? gene expression (p?<?0.05) while no treatment changed both IL-6 and TNF-? gene expression. Treatment with NSAID alone, PBMT alone, Exerc + PBMT, and NSAID + PBMT reduced IL-1? protein expression (p<0.05). All therapies significantly reduced IL-6 and TNF-? protein expression (p<0.05) compared with the OA group. Similarly, all therapies, except Exerc, reduced the levels of PGE2 (p?<0.05) compared with the OA group. The results from the present study indicate that treatment with PBMT is more effective in modulating the inflammatory process underlying OA when compared with the other therapies tested.

Lasers Med Sci. 2014 Mar;29(2):653-8. doi: 10.1007/s10103-013-1377-3. Epub 2013 Jun 30.

What is the best treatment to decrease pro-inflammatory cytokine release in acute skeletal muscle injury induced by trauma in rats: low-level laser therapy, diclofenac, or cryotherapy?

de Almeida P1, Tomazoni SS, Frigo L, de Carvalho Pde T, Vanin AA, Santos LA, Albuquerque-Pontes GM, De Marchi T, Tairova O, Marcos RL, Lopes-Martins RÁ, Leal-Junior EC.

Author information

1
Postgraduate Program in Rehabilitation Sciences, Universidade Nove de Julho (UNINOVE), São Paulo, SP, Brazil.

Abstract

Currently, treatment of muscle injuries represents a challenge in clinical practice. In acute phase, the most employed therapies are cryotherapy and nonsteroidal anti-inflammatory drugs. In the last years, low-level laser therapy (LLLT) has becoming a promising therapeutic agent; however, its effects are not fully known. The aim of this study was to analyze the effects of sodium diclofenac (topical application), cryotherapy, and LLLT on pro-inflammatory cytokine levels after a controlled model of muscle injury. For such, we performed a single trauma in tibialis anterior muscle of rats. After 1 h, animals were treated with sodium diclofenac (11.6 mg/g of solution), cryotherapy (20 min), or LLLT (904 nm; superpulsed; 700 Hz; 60 mW mean output power; 1.67 W/cm(2); 1, 3, 6 or 9 J; 17, 50, 100 or 150 s). Assessment of interleukin-1? and interleukin-6 (IL-1? and IL-6) and tumor necrosis factor-alpha (TNF-?) levels was performed at 6 h after trauma employing enzyme-linked immunosorbent assay method. LLLT with 1 J dose significantly decreased (p?<?0.05) IL-1?, IL-6, and TNF-? levels compared to non-treated injured group as well as diclofenac and cryotherapy groups. On the other hand, treatment with diclofenac and cryotherapy does not decrease pro-inflammatory cytokine levels compared to the non-treated injured group. Therefore, we can conclude that 904 nm LLLT with 1 J dose has better effects than topical application of diclofenac or cryotherapy in acute inflammatory phase after muscle trauma.

Angle Orthod. 2010 Sep;80(5):925-32. doi: 10.2319/010410-10.1.

Interventions for pain during fixed orthodontic appliance therapy. A systematic review.

Xiaoting L1, Yin T, Yangxi C.

Author information

1
State Key Laboratory of Oral Disease and Department of Orthodontics, West China School of Dentistry, Sichuan University, Chengdu, China.

Abstract

OBJECTIVE:

To compare the different methods of pain control intervention during fixed orthodontic appliance therapy.

MATERIALS AND METHODS:

A computerized literature search was performed in MEDLINE (1966-2009), The Cochrane Library (Issue 4, 2009), EMBASE (1984-2009), and CNKI (1994-2009) to collect randomized controlled trials (RCTs) for pain reduction during orthodontic treatment. Data were independently extracted by two reviewers and a quality assessment was carried out. The Cochrane Collaboration’s RevMan5 software was used for data analysis. The Cochrane Oral Health Group’s statistical guidelines were followed.

RESULTS:

Twenty-six RCTs were identified and six trials including 388 subjects were included. Meta-analysis showed that ibuprofen had a pain control effect at 6 hours and at 24 hours after archwire placement compared with the placebo group. The standard mean difference was -0.47 and -0.48, respectively. There was no difference in pain control between ibuprofen, acetaminophen, and aspirin. Other analgesics such as tenoxicam and valdecoxib had relatively lower visual analog scale (VAS) scores in pain perception. Lowlevel laser therapy (LLLT) was also an effective approach for pain relief with VAS scores of 3.30 in the LLLT group and 7.25 in the control group.

CONCLUSIONS:

Analgesics are still the main treatment modality to reduce orthodontic pain despite their side effects. Some long-acting nonsteroidal anti-inflammatory drugs (NSAIDs) and cyclo-oxygenase enzyme (COX-2) inhibitors are recommended for their comparatively lesser side effects. Their preemptive use is promising. Other approaches such as LLLT have aroused researchers’ attention.

Photomed Laser Surg. 2010 Aug;28(4):553-60. doi: 10.1089/pho.2009.2576.

Acute low back pain with radiculopathy: a double-blind, randomized, placebo-controlled study.

Konstantinovic LM1, Kanjuh ZM, Milovanovic AN, Cutovic MR, Djurovic AG, Savic VG, Dragin AS, Milovanovic ND.

Author information

Abstract

OBJECTIVE:

The aim of this study was to investigate the clinical effects of lowlevel laser therapy (LLLT) in patients with acute low back pain (LBP) with radiculopathy.

BACKGROUND DATA:

Acute LBP with radiculopathy is associated with pain and disability and the important pathogenic role of inflammation. LLLT has shown significant anti-inflammatory effects in many studies.

MATERIALS AND METHODS:

A randomized, double-blind, placebo-controlled trial was performed on 546 patients. Group A (182 patients) was treated with nimesulide 200 mg/day and additionally with active LLLT; group B (182 patients) was treated only with nimesulide; and group C (182 patients) was treated with nimesulide and placebo LLLT. LLLT was applied behind the involved spine segment using a stationary skin-contact method. Patients were treated 5 times weekly, for a total of 15 treatments, with the following parameters: wavelength 904 nm; frequency 5000 Hz; 100-mW average diode power; power density of 20 mW/cm(2) and dose of 3 J/cm(2); treatment time 150 sec at whole doses of 12 J/cm(2). The outcomes were pain intensity measured with a visual analog scale (VAS); lumbar movement, with a modified Schober test; pain disability, with Oswestry disability score; and quality of life, with a 12-item short-form health survey questionnaire (SF-12). Subjects were evaluated before and after treatment. Statistical analyses were done with SPSS 11.5.

RESULTS:

Statistically significant differences were found in all outcomes measured (p < 0.001), but were larger in group A than in B (p < 0.0005) and C (p < 0.0005). The results in group C were better than in group B (p < 0.0005).

CONCLUSIONS:

The results of this study show better improvement in acute LBP treated with LLLT used as additional therapy.

J Oral Rehabil. 2008 Dec;35(12):925-33. doi: 10.1111/j.1365-2842.2008.01891.x.

Lowlevel laser therapy improves bone repair in rats treated with anti-inflammatory drugs.

Ribeiro DA1, Matsumoto MA.

Author information

1
Department of Biosciences, Federal University of Sao Paulo, UNIFESP, Santos, SP, Brazil. daribeiro@unifesp.br

Abstract

Nowadays, selective cyclooxygenase-2 non-steroidal anti-inflammatory drugs have been largely used in surgical practice for reducing oedema and pain. However, the association between these drugs and laser therapy is not known up to now. Herein, the aim of this study was to evaluate the action of anti-COX-2 selective drug (celecoxib) on bone repair associated with laser therapy. A total of 64 rats underwent surgical bone defects in their tibias, being randomly distributed into four groups: Group 1) negative control; Group 2) animals treated with celecoxib; Group 3) animals treated with lowlevel power laser and Group 4) animals treated with celecoxib and lowlevel power laser. The animals were killed after 48 h, 7, 14 and 21 days. The tibias were removed for morphological, morphometric and immunohistochemistry analysis for COX-2. Statistical significant differences (P < 0.05) were observed in the quality of bone repair and quantity of formed bone between groups at 14 days after surgery for Groups 3 and 4. COX-2 immunoreactivity was more intense in bone cells for intermediate periods evaluated in the laser-exposed groups. Taken together, such results suggest that lowlevel laser therapy is able to improve bone repair in the tibia of rats as a result of an up-regulation for cyclooxygenase-2 expression in bone cells.

Clin Orthop Relat Res. 2008 Jul;466(7):1539-54. doi: 10.1007/s11999-008-0260-1. Epub 2008 Apr 30.

Treatment of tendinopathy: what works, what does not, and what is on the horizon.

Andres BM1, Murrell GA.

Author information

1
Orthopaedic Research Institute, St George Hospital, University of New South Wales, Level 2 Research and Education Building, 4-10 South Street, Kogarah, Sydney, NSW, 2217, Australia. bandres@yahoo.com

Abstract

Tendinopathy is a broad term encompassing painful conditions occurring in and around tendons in response to overuse. Recent basic science research suggests little or no inflammation is present in these conditions. Thus, traditional treatment modalities aimed at controlling inflammation such as corticosteroid injections and nonsteroidal antiinflammatory medications (NSAIDS) may not be the most effective options. We performed a systematic review of the literature to determine the best treatment options for tendinopathy. We evaluated the effectiveness of NSAIDS, corticosteroid injections, exercise-based physical therapy, physical therapy modalities, shock wave therapy, sclerotherapy, nitric oxide patches, surgery, growth factors, and stem cell treatment. NSAIDS and corticosteroids appear to provide pain relief in the short term, but their effectiveness in the long term has not been demonstrated. We identified inconsistent results with shock wave therapy and physical therapy modalities such as ultrasound, iontophoresis and lowlevel laser therapy. Current data support the use of eccentric strengthening protocols, sclerotherapy, and nitric oxide patches, but larger, multicenter trials are needed to confirm the early results with these treatments. Preliminary work with growth factors and stem cells is promising, but further study is required in these fields. Surgery remains the last option due to the morbidity and inconsistent outcomes. The ideal treatment for tendinopathy remains unclear.

Inspire and deepen your practice!

Laser, laser needle acupuncture,light emitting diode and pulsed electromagnetic field therapies are the right tools for healing today’s complex patients and for your practice success.

4-24-17 PrePNG - Images for HLS WHITE

All devices pictured above (and more) will likely be available for you to train and practice with in this course.  Learn more about them in the links below.

Healing Light Seminars and David Rindge have been practicing, teaching and continually updating our treatment methods and equipment since 2002. Our goal, first and foremost, is to provide you with a foundation for success with energy-based therapies.  We will only offer devices we have found to be effective, well made and which we are continuing to use clinically.  Yet our goal is to ensure that you learn the parameters and methods for success whether or not you buy from us.  .

Day 1 focuses on theory, biological effects and essentials for clinical success.   You have the opportunity for hands-on practice with state-of-the-art laser, laser needle, led and pemf systems for the treatment of pain, head to toe.

In Day 2, you will learn how to apply laser, laser needles, led and pulsed electromagnetic field therapies for aesthetics / dermatology / facial rejuvenation, cardiovascular disease, digestive, ear and eye disorders, gynecology, for hair regrowth, neuropathy, osteoporosis, respiratory disorders, sports medicine and more.

You will receive Laser Therapy: A Clinical Manual as part of the course.

Laser Therapy - A Clinical Manual This popular training manual by Blahnik and Rindge presents the theory and clinical application of laser therapy in clearly understandable terms with treatment protocols for more than 40 conditions.  Laser Therapy: A Clinical Manual is an important important resource in the course and a $79.00 value.  You will also receive treatment protocols for other conditions, updates and much, much more relevant material in this course.

Gain a solid understanding of energy-based therapies.    NCCAOM 322-5, seven hours each day, Saturday and Sunday.    Learn More.

Course Dates / Location

November 4-5, 2017.  Palm Bay, FLWild Manta, 5151 South Babcock St, Palm Bay, FL 32905.  (321) 676-8606.

 

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Healing Light Seminars

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