PEMF Studies 2

SHORT COMMUNICATION

Non-invasive electromagnetic field therapy produces rapid and substantial pain reduction in early knee osteoarthritis: a randomized double-blind pilot study

Fred R. Nelson• Raimond Zvirbulis • Arthur A. Pilla

Received: 16 August 2011/Accepted: 11 March 2012 © Springer-Verlag 2012

Abstract This study examined whether a non-thermal, non-invasive, pulsed electromagnetic field (PEMF), known to modulate the calmodulin (CaM)-dependent nitric oxide (NO)/cyclic guanosine monophosphate (cGMP) signaling pathway, could reduce pain in early knee OA. This ran­domized, placebo-controlled, double-blind pilot clinical study enrolled 34 patients. Patient selection required initial VAS C4, 2 h of standing activity per day, and no recent interventions such as cortisone injections or surgery. Results showed VAS pain score decreased in the active cohort by 50 ± 11 % versus baseline starting at day 1 and persisting to day 42 (P < 0.001). There was no significant decrease in VAS versus baseline at any time point in the sham cohort (P = 0.227). The overall decrease in mean VAS score for the active cohort was nearly threefold that of the sham cohort (P <0.001). The results suggest that non-thermal, non-invasive PEMF therapy can have a significant and rapid impact on pain from early knee OA and that larger clinical trials are warranted.

Keywords Knee OA PEMF Calmodulin NO signaling

F. R. Nelson (&) R. Zvirbulis

Department of Orthopaedic Surgery, Henry Ford Hospital, CFP 644, 2799 West Grand Blvd., Detroit, MI 48202, USA e-mail: fnelson1@hfhs.org

A. A. Pilla

Department of Biomedical Engineering, Columbia University, New York City, NY, USA

A. A. Pilla

Department of Orthopedics, Mount Sinai School of Medicine, New York, NY, USA


Introduction

PEMF have been employed for the conservative treatment of knee OA with varied success [1]. A recent meta-analysis concluded PEMF improved clinical scores and function in patients with osteoarthritis of the knee and should be con­sidered as adjuvant therapies in their management [2]. It has recently been suggested that PEMF signals can act as first messengers in the CaM-dependent signaling pathways that orchestrate the release of cytokines and growth factors in cellular responses to injury [3]. This has enabled PEMF signals to be successfully configured a priori to modulate such tissue repair pathways [4–13]. A therapeutic target for the relief of knee OA pain is the CaM-dependent nitric oxide (NO)/cyclic guanosine monophosphate (cGMP) cascade [14], which can modulate blood, as well as lymph flow [15]. This same pathway also modulates the release of inflam­matory cytokines, such as interleukin-1beta (IL-1b) [16] and growth factors such as basic fibroblast growth factor (FGF-2) and vascular endothelial growth factor (VEGF) [17].

PEMF signals have been shown to modulate the CaM­dependent NO signaling cascades in articular chondrocytes [9] and other cells [3] using CaM antagonists, and NO and downstream inhibitors. These signals have also been reported to accelerate cutaneous wound repair by 59 % and Achilles’ tendon repair by 69 % at 21 days in rat models; angiogenesis as quickly as 7 days in a thermal myocardial necrosis rat model, wherein L-NAME, a nitric oxide syn­thase inhibitor, blocked the PEMF effect [5]; and rapidly decrease post-operative pain concomitant with an equally rapid reduction of IL-1b in the wound bed in a double-blind, randomized, human clinical trial [10]. This study was, thus, designed to determine whether PEMF, config­ured to modulate the CaM/NO/cGMP signaling pathway, would reduce pain in early knee osteoarthritis.

Rheumatol Int

Materials and methods

This double-blind, placebo-controlled, randomized pilot study was approved by the Institutional Review Board at Henry Ford Hospital and all enrolled patients gave informed consent. The primary outcome measure was VAS pain score on a 0–10 cm scale with respect to baseline in each cohort. Although consensus guidelines suggest a 20 % decrease in VAS as the minimum clinically relevant difference in knee OA pain [18], a 40 % difference was chosen as the clinically desirable outcome. Thus, prior to the start of this study, a sample size analysis, assuming a 40 % (±35 % SD) decrease in pain scores from PEMF treatment, suggested a minimum of 14 patients per group were needed. Patient selection required that subjects have knee pain for at least 3 months with an imaging study that confirmed articular cartilage loss, an initial VAS score C4, and at least 2 h of daily standing activity in a physical occupation. Patients with rheumatoid arthritis, gout, and pregnancy were excluded. Patients with cortisone injec­tions, surgery, or an effective viscosupplementation series within the past 6 months were excluded. Patients with implanted electronic devices were excluded. Patients on disability or with third party claims were excluded. Since all patients were actively employed, NSAID use was unrestricted. PEMF therapy was the only addition to the current standard of care.

A PEMF signal consisting of a 7 ms burst of 6.8 MHz sinusoidal waves repeating at 1 burst/s delivering a peak induced electric field of 34 ± 8 V/m in the knee from the portable battery operated device shown in Fig. 1 (Palermo, Ivivi Health Sciences, LLC, San Francisco, CA), was used for 15 min twice daily. Each device had an inaccessible counter which recorded the total number of treatments for each patient. The device was light weight and patients could easily position the coil directly over the knee, even over clothing. Once manually activated, treatment was automatically applied for 15 min. Manual activation was required for each treatment.

Randomization was performed by the blinded assign­ment of devices according to their serial numbers. Device randomization was performed by the manufacturer (Ivivi Health Sciences, LLC) and all devices with the randomi­zation code were sent to the Epidemiology Dept at Henry Ford Hospital, from which assignment to patients was controlled. Sham devices were activated with a switch, just as active devices, and both sham and active units had blinking indicator lights. The PEMF signal from these devices does not produce heat or cause any other sensation in tissue. The average in situ magnetic field induced by the PEMF signal employed in this study is at least 1,000- fold below the ambient magnetic field and cannot be detected using standard Gauss meters. Therefore, only

Fig. 1 The non-thermal pulsed radio frequency PEMF device used in this randomized, double-blind clinical study on knee OA pain. The device consists of a single loop wire coil with integrated amplifier (Palermo, Ivivi Health Sciences, San Francisco, CA) that delivers a PRF signal configured to modulate the CaM/NO/cGMP signaling pathway, which consisted of a 7-ms burst of a 6.8 MHz sinusoidal carrier repeating at 2 bursts/s, delivering a peak induced electric field amplitude of 34 ± 8 V/m in the knee. The device is portable and easily positioned by the patient over the knee with the VelcroTM strap. The number displayed is the number of PEMF treatments

measurements with specialized laboratory equipment, not readily available to the patient or health care practitioner, could determine whether a device was active. General unblinding occurred after all data were collected.

PEMF signal parameters were verified for each device by a third party, who had no contact with patients, at the beginning and end of treatment, with a calibrated field probe (model FCC-301-1-MR1, Fischer Custom Commu­nications, Torrance, CA) connected to a calibrated 100-MHz oscilloscope (model 2358, Tektronix, Beaverton, OR).

Patients were required to self-report maximum daily VAS pain scores on an unmarked horizontal 10 cm line (0 is no pain and 10 is worst possible pain) at baseline (day 0), daily for the first 14 days, then daily from day 29 to day 42. The 2-week gap in VAS data collection was designed to assess for possible accommodation to PEMF therapy. By not reporting VAS scores for 2 weeks, patients would be more likely not to remember their last score. Results were analyzed using the Student’s t test or one-way repeated measures ANOVA with Holm–Sidek post hoc analysis, as appropriate (Sigmastat 3.0, SPSS). Intent-to-treat analysis using last data carried forward [19] was employed for patients who did not complete the study. Significance was accepted at P B 0.05. Data are displayed ± SEM.

Rheumatol Int

Results

The portable PEMF devices were well tolerated. No adverse events were reported. Device verification for each patient at the end of treatment revealed all devices to be functioning as randomized. No signal variations or deteri­orations were noted in the active devices. The mean ± SD of the total number of treatments delivered by all devices in this study was 80 ± 9 compared with the expected 84, suggesting that devices were used as prescribed by all patients. There were no significant baseline differences in mean age, body mass index (BMI), or Kellgren–Lawrence (K-L) radiographic scores, between active and sham cohorts, as shown in Table 1.

Thirty four patients started treatment. Of these, 19 (14F, 5M) were shams, and 15 (10F, 5M) were actives. The imbalance in treatment groups was due to initial drop outs

Table 1 Baseline patient demographics

Index

Active

Sham

 
Age 55.5 ± 2.5 58.4 ± 2.5
BMI 33.5 ± 1.9 34.7 ± 1.7
K-L 2.7 ± 0.33 2.9 ± 0.25

Fig. 2 Randomized pilot

clinical trial on PEMF effect on knee OA pain: patient flow chart


(entered patients not starting treatment), the total number of available randomized devices, and the sequential dis­tribution of devices over time. Given there were no sig­nificant differences in baseline parameters between the cohorts, the imbalance was not a factor. All enrolled patients received PEMF treatment to day 14. Thereafter, 3 active and 7 sham patients dropped out of the study by day 42, citing lack of perceived benefit as the reason, confirmed by VAS scores. Patient flow is outlined in Fig. 2.

The results for all enrolled patients show the PEMF signal caused 50 ± 11 % decrease in mean maximum VAS versus mean baseline VAS for the treated group starting on day 1, persisting to day 42 (P < 0.001). There was no significant decrease in mean maximum VAS compared with mean start VAS at any time point in the sham group (P = 0.227). The overall decrease in VAS scores from baseline was 2.7 ± 0.57 (P < 0.001) for the active group versus 1.5 ± 0.41 (P = 0.168) for the sham group. There was no significant difference in mean start VAS between the active and sham groups (Active = 6.8 ± 0.31, Sham = 7.1 ± 0.34, P = 0.430). A summary of mean intra-cohort VAS scores from baseline to day 42 for all patients is shown in Fig. 3. Inter-cohort VAS scores are compared in Table 2. As may be seen, the overall pain decrease in the active cohort was approximately 60 % by Assessed for eligibility (n = 59) Did not meet inclusion criteria or did not start (n = 25) Randomized (n = 34)

Rheumatol Int

0 5 10 15 20 25 30 35 40 45 PEMF Treatment Days

Fig. 3 Effect of a radio frequency PEMF signal, configured, a priori, to target the CaM/NO/cGMP signaling pathway, on pain from early stage knee OA. This is a repeated measures intra-cohort comparison which shows this signal caused a nearly 60 % reduction in mean VAS pain scores within the first 3 days for the active cohort, which persisted to day 42 for all enrolled active patients. There was no significant difference in mean VAS scores for the sham cohort at any time point, or in mean baseline VAS scores for the active and sham cohorts

Table 2 Mean VAS pain scores: inter-cohort comparisons

Day Mean VAS active Mean VAS sham

P value

Baseline 6.85 ± 0.33 7.18 ± 0.31 0.481
3 4.13 ± 0.48 6.84 ± 0.43 0.008*
14 4.08 ± 0.60 6.21 ± 0.50 0.011*
29 4.22 ± 0.66 6.11 ± 0.52 0.041*,a
42 4.19 ± 0.71 6.11 ± 0.54 0.036*,a

* Significantly different a Intent-to-treat

day 42 (P < 0.001), whereas in the sham cohort pain decrease was only 18 % (P = 0.206). Thus, even assuming a placebo effect, pain decrease was approximately three­fold greater in the active cohort, within the first 3 days of PEMF treatment.

Discussion

The results from this randomized, double-blind, placebo-controlled study demonstrate that non-thermal, non-inva­sive PEMF, when configured to dose CaM-dependent NO/ cGMP signaling, has a significant and rapid impact on pain from early knee OA. The intervention is novel since the patient population treated did not have end stage disease and were required to be on their feet at least 2 h a day. The PEMF treatment time is short (15 min), and use of the device did not interfere with work or off-work activities. Review of patient notes reveals that the majority of patients in the active group were convinced the PEMF treatment had a functionally significant impact on their pain. It is noted that more than twice as many sham versus active patients opted out of the study after the initial 14-day phase.

In persons with knee OA, bone attrition, bone marrow lesions, synovitis/effusion, and meniscal tears are all cau­ses of knee pain [20]. Effusion (edema) is one manifesta­tion of the inflammatory response to bone injury attributable to knee OA. The rapid onset response in the active group is remarkably similar to that reported for a similarly configured PEMF signal, which produced approximately 2.5-fold reduction in pain from breast reduction surgery within 5 h post-op [10]. That study also showed IL-1fl, a master inflammatory cytokine, was con­comitantly reduced by approximately 2.5-fold in the wound bed. Certainly, there are no data from this study, which directly support a PEMF effect on CaM-dependent NO signaling. However, it is reasonable to speculate that the effect of PEMF on knee OA pain reported here could involve modulation of CaM-dependent NO signaling which is known to rapidly reduce edema (effusion) [15]. This is consistent with the rapid effects of similar PEMF signals reported on edema from ankle sprains in randomized studies [21, 22] and could explain the rapidity of the PEMF effect in this patient population.

The persistence of pain reduction in active patients to day 42 suggests daily use of PEMF produced a sustained anti-inflammatory effect, perhaps via down-regulation of IL-1fl, which may slow the progression of knee OA. Obviously, this pilot study was not designed to assess the effect of this PEMF treatment on OA per se in this patient population. However, it is useful to consider evidence suggesting that PEMF could attenuate the effects of the prolonged inflammation caused by IL-1fl. Thus, weak electric fields partially reversed the decrease in the pro­duction of extracellular matrix caused by exogenous IL-1fl in full-thickness articular cartilage explants from osteoar­thritic adult human knee joints [23]. Similar studies showed the decreased production of proteoglycans caused by exogenous IL-1fl was reversed by PEMF in bovine artic­ular cartilage explants [24]. There are also reports that PEMF can increase proliferation in chondrocyte cultures [9, 25]. Finally, there are reports which suggest that PEMF can affect the progression of OA [26] and heal cartilage defects in animal models [27, 28].

The rapid and substantial effect of non-thermal, non­invasive PEMF therapy on knee OA pain in this double-blind, randomized, placebo-controlled pilot clinical study are promising enough to warrant further larger studies designed to confirm the PEMF effect on pain, in which standard clinical measures of function, as well as effusion and inflammatory markers are included. Once confirmed, use of this PEMF therapy may provide an important simple and economical adjunct for the non-invasive, non-phar­macological treatment of OA.

Acknowledgments The authors gratefully acknowledge partial support of this work by the Department of Orthopaedic Surgery, Henry Ford Hospital, Detroit Michigan, and Ivivi Health Sciences, LLC, San Francisco, CA, who manufactured the PEMF devices uti­lized in this study.

Conflict of interest FN and RZ have no association with Ivivi Health Sciences. AAP is a basic science consultant to Ivivi Health Sciences and had no contact with patients in this study.

References

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2. Vavken P, Arrich F, Schuhfried O, Dorotka R (2009) Effective­ness of pulsed electromagnetic field therapy in the management of osteoarthritis of the knee: a meta-analysis of randomized controlled trials. J Rehabil Med 41:406–411

3. Pilla AA, Fitzsimmons RJ, Wu J, Rohde C, Casper D (2011) Electromagnetic fields as first messenger in biological signaling: application to calmodulin-dependent signaling in tissue repair. Biochem Biophys Acta 1810:1236–1245

4. Pilla AA (2006) Mechanisms and therapeutic applications of time-varying and static magnetic fields. In: Barnes F, Greene­baum B (eds) Biological and medical aspects of electromagnetic fields. CRC Press, Boca Raton, pp 351–411

5. Nelson FR, Brighton CT, Ryaby J, Simon BJ et al (2003) Use of physical forces in bone healing. J Am Acad Orthop Surg 11(5):344–354

6. Strauch B, Herman C, Dabb R, Ignarro LJ, Pilla A (2009) Evi­dence-based use of pulsed electromagnetic field therapy in clin­ical plastic surgery. Aesthet Surg J 29:135–143

7. Brighton CT, Wang W, Seldes R, Zhang G et al (2001) Signal transduction in electrically stimulated bone cells. J Bone Joint Surg 83A:1514–1523

8. Aaron RK, Boyan BD, Ciombor DMCK, Schwartz Z et al (2004) Stimulation of growth factor synthesis by electric and electro­magnetic fields. Clin Orthop 419:30–37

9. Callaghan MJ, Chang EI, Seiser N, Aarabi S et al (2008) Pulsed electromagnetic fields accelerate normal and diabetic wound healing by increasing endogenous FGF-2 release. Plast Reconstr Surg 121:130–141

  1. Fitzsimmons RJ, Gordon SL, Kronberg J, Ganey T, Pilla A (2008) A pulsing electric field (PEF) increases human chondro­cyte proliferation through a transduction pathway involving nitric oxide signaling. J Orthop Res 26:854–859
    1. Rohde C, Chiang A, Adipoju O, Casper D, Pilla AA (2010) Effects of pulsed electromagnetic fields on IL-1f3 and post operative pain: a double-blind, placebo-controlled pilot study in breast reduction patients. Plast Reconstr Surg 125:1620–1629
    2. Pilla AA, Muehsam DJ, Markov MS, Sisken BF (1999) EMF signals and ion/ligand binding kinetics: prediction of bioeffective waveform parameters. Bioelectrochem Bioenerg 48:27–34
    3. Pilla AA (2007) A weak PEMF signal is the first messenger for tissue growth and repair. In: Proceedings, bioelectromagnetics society 29th annual meeting, Kanazawa, Japan, June 10–15, p 468
    4. Hancock CM, Riegger-Krugh C (2008) Modulation of pain in osteoarthritis: the role of nitric oxide. Clin J Pain 24:353–365
    5. Bredt DS (2003) Nitric oxide signaling specificity—the heart of the problem. J Cell Sci 116:9–15
    6. Ren K, Torres R (2009) Role of interleukin-1beta during pain and inflammation. Brain Res Rev 60:57–64
    7. Madhusoodanan KS, Murad F (2007) NO-cGMP signaling and regenerative medicine involving stem cells. Neurochem Res 32:681–694
    8. Bellamy N, Kirwan J, Boers M, Brooks P et al (1997) Recom­mendations for a core set of outcome measures for future phase III clinical trials in knee, hip and hand osteoarthritis. Consensus development of OMERACT III. J Rheumatol 24:799–802
    9. Sheiner LB, Rubin DB (1995) Intention-to-treat analysis and the goals of clinical trials. Clin Pharmacol Ther 57:6–15
    10. Torres L, Dunlop DD, Peterfy C, Guermazi A, Prasad P, Hayes KW, Song J, Cahue S, Chang A, Marshall M, Sharma L (2006) The relationship between specific tissue lesions and pain severity in persons with knee osteoarthritis. Osteoarthritis Cartilage 14:1033–1040
    11. Pilla AA (1999) State of the art in electromagnetic therapeutics: soft tissue applications. In: Bersani F (ed) Electricity and mag­netism in biology and medicine. Plenum, New York, pp 871–874
    12. Pennington GM, Danley DL, Sumko MH, Bucknell A, Nelson JH (1993) Pulsed, non-thermal, high-frequency electromagnetic energy (DIAPULSE) in the treatment of grade I and grade II ankle sprains. Mil Med 158:101–104
    13. Brighton CT, Wang W, Clark CC (2008) The effect of electrical fields on gene and protein expression in human osteoarthritic cartilage explants. J Bone Joint Surg Am 90:833–848
    14. De Mattei M, Pasello M, Pellati A, Stabellini Get al (2003) Effects of electromagnetic fields on proteoglycan metabolism of bovine articular cartilage explants. Connect Tissue Res 44:154–159
    15. De Mattei M, Caruso A, Pezzetti F, Pellati A et al (2001) Effects of pulsed electromagnetic fields on human articular chondrocyte proliferation. Connect Tissue Res 42:269–279
    16. Ciombor DM, Aaron RK, Wang S, Simon B (2003) Modification of osteoarthritis by pulsed electromagnetic field—a morphologi­cal study. Osteoarthritis Cartilage 11:455–462
    17. Benazzo F, Cadossi M, Cavani F, Fini M et al (2008) Cartilage repair with osteochondral autografts in sheep: effect of bio­physical stimulation with pulsed electromagnetic fields. J Orthop Res 26:631–642
    18. Boopalan PR, Arumugam S, Livingston A, Mohanty M, Chit­taranjan S (2011) Pulsed electromagnetic field therapy results in healing of full thickness articular cartilage defect. Int Orthop 35:143–148

PEMF studies: Sandyk R; Research Bibliography: covers peer reviewed literature since 1980.

Notice in 1989 the shift in research toward electromagnetic field therapy pemf for Parkinson’s, multiple sclerosis MS, Alzheimer’s, attention deficit disorder ADD, attention deficit hyperactivity disorder ADHD, migraine headache, cluster headache and Tourette’s syndrome.

In April 1992, notice discovery that pineal calcification may be underlying cause of several central nervous system (CNS) disorders; and that electromagnetic field therapy pemf of picotesla flux density may in fact reverse this calcification and the neurological deficits caused by it.

1: 
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No Abstract

Weak electromagnetic fields potentiate the effects of 4-aminopyridine in multiple sclerosis.
Int J Neurosci. 1996 Mar;85(1-2):125-9. No abstract available.
PMID: 8727688 [PubMed - indexed for MEDLINE]
43:
Abstract

Freezing of gait in Parkinson’s disease is improved by treatment with weak electromagnetic fields.
Int J Neurosci. 1996 Mar;85(1-2):111-24.
PMID: 8727687 [PubMed - indexed for MEDLINE]
44:
Abstract

Application of weak electromagnetic fields facilitates sensory-motor integration in patients with multiple sclerosis.
Int J Neurosci. 1996 Mar;85(1-2):101-10.
PMID: 8727686 [PubMed - indexed for MEDLINE]
45:
Abstract

Bidirectional effect of electromagnetic fields on ketanserin-induced yawning in patients with multiple sclerosis: the role of melatonin.
Int J Neurosci. 1996 Mar;85(1-2):93-9.
PMID: 8727685 [PubMed - indexed for MEDLINE]
46:
Abstract

Weak electromagnetic fields increase the amplitude of the pattern reversal VEP response in patients with multiple sclerosis.
Int J Neurosci. 1996 Mar;85(1-2):79-91.
PMID: 8727684 [PubMed - indexed for MEDLINE]
47:
Abstract

Effects of picotesla flux electromagnetic fields on dopaminergic transmission in Tourette’s syndrome.
Int J Neurosci. 1996 Feb;84(1-4):187-94. Review.
PMID: 8707481 [PubMed - indexed for MEDLINE]
48:
Abstract

Treatment with weak electromagnetic fields improves fatigue associated with multiple sclerosis.
Int J Neurosci. 1996 Feb;84(1-4):177-86.
PMID: 8707480 [PubMed - indexed for MEDLINE]
49:
Abstract

Effect of weak electromagnetic fields on the amplitude of the pattern reversal VEP response in Parkinson’s disease.
Int J Neurosci. 1996 Feb;84(1-4):165-75.
PMID: 8707479 [PubMed - indexed for MEDLINE]
50:
Abstract

Resolution of partial cataplexy in multiple sclerosis by treatment with weak electromagnetic fields.
Int J Neurosci. 1996 Feb;84(1-4):157-64.
PMID: 8707478 [PubMed - indexed for MEDLINE]
51:
Abstract

Premenstrual exacerbation of symptoms in multiple sclerosis is attenuated by treatment with weak electromagnetic fields.
Int J Neurosci. 1995 Dec;83(3-4):187-98. Review.
PMID: 8869427 [PubMed - indexed for MEDLINE]
52:
Abstract

The pineal gland, cataplexy, and multiple sclerosis.
Int J Neurosci. 1995 Dec;83(3-4):153-63. Review.
PMID: 8869424 [PubMed - indexed for MEDLINE]
53:
Abstract

Resolution of dysarthria in multiple sclerosis by treatment with weak electromagnetic fields.
Int J Neurosci. 1995 Nov;83(1-2):81-92.
PMID: 8746751 [PubMed - indexed for MEDLINE]
54:
Abstract

Reversal of alexia in multiple sclerosis by weak electromagnetic fields.
Int J Neurosci. 1995 Nov;83(1-2):69-79. Review.
PMID: 8746750 [PubMed - indexed for MEDLINE]
55:
Abstract

Long term beneficial effects of weak electromagnetic fields in multiple sclerosis.
Int J Neurosci. 1995 Nov;83(1-2):45-57. Review.
PMID: 8746748 [PubMed - indexed for MEDLINE]
56:
Abstract

Diurnal variations in vision and relations to circadian melatonin secretion in multiple sclerosis.
Int J Neurosci. 1995 Nov;83(1-2):1-6.
PMID: 8746744 [PubMed - indexed for MEDLINE]
57:
Abstract

Weak electromagnetic fields improve body image perception in patients with multiple sclerosis.
Int J Neurosci. 1995 Jun;82(3-4):285-302.
PMID: 7558655 [PubMed - indexed for MEDLINE]
58:
Abstract

Improvement of body image perception in Parkinson’s disease by treatment with weak electromagnetic fields.
Int J Neurosci. 1995 Jun;82(3-4):269-83.
PMID: 7558654 [PubMed - indexed for MEDLINE]
59:
Abstract

Reversal of visuospatial deficit on the Clock Drawing Test in Parkinson’s disease by treatment with weak electromagnetic fields.
Int J Neurosci. 1995 Jun;82(3-4):255-68.
PMID: 7558653 [PubMed - indexed for MEDLINE]
60:
Abstract

Chronic relapsing multiple sclerosis: a case of rapid recovery by application of weak electromagnetic fields.
Int J Neurosci. 1995 Jun;82(3-4):223-42. Review.
PMID: 7558651 [PubMed - indexed for MEDLINE]
61:
Abstract

Weak electromagnetic fields restore dream recall in patients with multiple sclerosis.
Int J Neurosci. 1995 May;82(1-2):113-25.
PMID: 7591509 [PubMed - indexed for MEDLINE]
62:
Abstract

Resolution of Lhermitte’s sign in multiple sclerosis by treatment with weak electromagnetic fields.
Int J Neurosci. 1995 Apr;81(3-4):215-24. Review.
PMID: 7628912 [PubMed - indexed for MEDLINE]
63:
Abstract

Improvement of right hemispheric functions in a child with Gilles de la Tourette’s syndrome by weak electromagnetic fields.
Int J Neurosci. 1995 Apr;81(3-4):199-213. Review.
PMID: 7628911 [PubMed - indexed for MEDLINE]
64:
Abstract

Cholinergic mechanisms in Gilles de la Tourette’s syndrome.
Int J Neurosci. 1995 Mar;81(1-2):95-100. Review.
PMID: 7775075 [PubMed - indexed for MEDLINE]
65:
Abstract

Parkinsonian micrographia reversed by treatment with weak electromagnetic fields.
Int J Neurosci. 1995 Mar;81(1-2):83-93.
PMID: 7775074 [PubMed - indexed for MEDLINE]
66:
Abstract

Improvement in short-term visual memory by weak electromagnetic fields in Parkinson’s disease.
Int J Neurosci. 1995 Mar;81(1-2):67-82.
PMID: 7775073 [PubMed - indexed for MEDLINE]
67:
Abstract

Weak electromagnetic fields reverse visuospatial hemi-inattention in Parkinson’s disease.
Int J Neurosci. 1995 Mar;81(1-2):47-65. Review.
PMID: 7775072 [PubMed - indexed for MEDLINE]
68:
Abstract

Amantadine in Parkinson’s disease: pro and contra.
J Neural Transm Suppl. 1995;46:415-21. Review.
PMID: 8821077 [PubMed - indexed for MEDLINE]
69:
Abstract

Weak electromagnetic fields attenuate tremor in multiple sclerosis.
Int J Neurosci. 1994 Dec;79(3-4):199-212.
PMID: 7744562 [PubMed - indexed for MEDLINE]
70:
Abstract

Reversal of visuospatial hemi-inattention in patients with chronic progressive multiple sclerosis by treatment with weak electromagnetic fields.
Int J Neurosci. 1994 Dec;79(3-4):169-84.
PMID: 7744559 [PubMed - indexed for MEDLINE]
71:
Abstract

Pineal-hypothalamic tract mediation of picotesla magnetic fields in the treatment of neurological disorders.
Panminerva Med. 1994 Dec;36(4):201-5. Review.
PMID: 7603740 [PubMed - indexed for MEDLINE]
72:
Abstract

A drug naive parkinsonian patient successfully treated with weak electromagnetic fields.
Int J Neurosci. 1994 Nov;79(1-2):99-110.
PMID: 7744555 [PubMed - indexed for MEDLINE]
73:
Abstract

Improvement in word-fluency performance in patients with multiple sclerosis by electromagnetic fields.
Int J Neurosci. 1994 Nov;79(1-2):75-90.
PMID: 7744553 [PubMed - indexed for MEDLINE]
74:
Abstract

Improvement by picoTesla range magnetic fields of perceptual-motor performance and visual memory in a patient with chronic progressive multiple sclerosis.
Int J Neurosci. 1994 Sep;78(1-2):53-66.
PMID: 7829292 [PubMed - indexed for MEDLINE]
75:
Abstract

Naltrexone attenuates the antiparkinsonian effects of picoTesla range magnetic fields.
Int J Neurosci. 1994 Sep;78(1-2):111-22.
PMID: 7829285 [PubMed - indexed for MEDLINE]
76:
Abstract

Rapid normalization of visual evoked potentials by picoTesla range magnetic fields in chronic progressive multiple sclerosis.
Int J Neurosci. 1994 Aug;77(3-4):243-59.
PMID: 7814217 [PubMed - indexed for MEDLINE]
77:
Abstract

Further observations on the effects of external picoTesla range magnetic fields on visual memory and visuospatial functions in multiple sclerosis.
Int J Neurosci. 1994 Aug;77(3-4):203-27.
PMID: 7814214 [PubMed - indexed for MEDLINE]
78:
No Abstract

Stephen Walter Ranson (1880-1942): a pioneer in hypothalamic research.
Int J Neurosci. 1994 Jul;77(1-2):85-8. No abstract available.
PMID: 7989164 [PubMed - indexed for MEDLINE]
79:
Abstract

Reversal of micrographia in Parkinson’s disease by application of picoTesla range magnetic fields.
Int J Neurosci. 1994 Jul;77(1-2):77-84.
PMID: 7989163 [PubMed - indexed for MEDLINE]
80:
Abstract

Improvement in word-fluency performance in Parkinson’s disease by administration of electromagnetic fields.
Int J Neurosci. 1994 Jul;77(1-2):23-46. Review.
PMID: 7989159 [PubMed - indexed for MEDLINE]
81:
Abstract

The co-occurrence of multiple sclerosis and migraine headache: the serotoninergic link.
Int J Neurosci. 1994 Jun;76(3-4):249-57.
PMID: 7960481 [PubMed - indexed for MEDLINE]
82:
No Abstract

The effects of external picotesla range magnetic fields on the EEG in Parkinson’s disease: a follow up study.
Int J Neurosci. 1994 Jun;76(3-4):227-9. No abstract available.
PMID: 7960478 [PubMed - indexed for MEDLINE]
83:
Abstract

Alzheimer’s disease: improvement of visual memory and visuoconstructive performance by treatment with picotesla range magnetic fields.
Int J Neurosci. 1994 Jun;76(3-4):185-225. Review.
PMID: 7960477 [PubMed - indexed for MEDLINE]
84:
Abstract

The relationship between melatonin secretion and serum cholesterol in patients with multiple sclerosis.
Int J Neurosci. 1994 May;76(1-2):81-6.
PMID: 7960472 [PubMed - indexed for MEDLINE]
85:
Abstract

The relationship of pineal calcification to cerebral atrophy on CT scan in multiple sclerosis.
Int J Neurosci. 1994 May;76(1-2):71-9.
PMID: 7960471 [PubMed - indexed for MEDLINE]
86:
Abstract

Relationship of nocturnal melatonin levels to duration and course of multiple sclerosis.
Int J Neurosci. 1994 Apr;75(3-4):229-37.
PMID: 8050864 [PubMed - indexed for MEDLINE]
87:
Abstract

Reversal of a visuoconstructional deficit in Parkinson’s disease by application of external magnetic fields: a report of five cases.
Int J Neurosci. 1994 Apr;75(3-4):213-28.
PMID: 8050863 [PubMed - indexed for MEDLINE]
88:
Abstract

Paroxysmal itching in multiple sclerosis during treatment with external magnetic fields.
Int J Neurosci. 1994 Mar;75(1-2):65-71.
PMID: 8050852 [PubMed - indexed for MEDLINE]
89:
Abstract

Successful treatment of respiratory dyskinesia with picoTesla range magnetic fields.
Int J Neurosci. 1994 Mar;75(1-2):91-102.
PMID: 7914186 [PubMed - indexed for MEDLINE]

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