International Journal of Neuroscience

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Treatment with Electromagnetic Fields Reverses

the Long-Term Clinical Course of a Patient with
Chronic Progressive Multiple Sclerosis
Reuven Sandyk
To cite this article: Reuven Sandyk (1997) Treatment with Electromagnetic Fields Reverses
the Long-Term Clinical Course of a Patient with Chronic Progressive Multiple Sclerosis,
International Journal of Neuroscience, 90:3-4, 177-185, DOI: 10.3109/00207459709000637
To link to this article: http://dx.doi.org/10.3109/00207459709000637

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Intern J Nearoscience. Vol. 90(3-4).pp 177-186

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Clinical Note

TREATMENT WITH ELECTROMAGNETIC

FIELDS REVERSES THE LONG-TERM
CLINICAL COURSE OF A PATIENT
WITH CHRONIC PROGRESSIVE
MULTIPLE SCLEROSIS
REUVEN SANDYK
Department of Neuroscience at the Institute f o r Biomedical Engineering and
Rehabilitation Services of Tour0 College, Dix Hills, NY, 11746. U.S.A.
( R e c e i v e d in f i n a l f o r m

30

J a n u a r y

It is estimated that 10-20% of patients with multiple sclerosis (MS) have a chronic progressive (CP)
course characterized by an insidious onset of neurological deficits followed by steady progression of
disability in the absence of symptomatic remission. To date no therapeutic modality has proven
effective in reversing the clinical course of CP MS although there are indications that prolonged treatment with picotesla electromagnetic fields (EMFs) alters the clinical course of patients with CP MS.
A 40 year-old woman presented in December of 1992 with CP MS with symptoms of spastic paraplegia, loss of trunk control, marked weakness of the upper limbs with loss of fine and gross motor hand
functions. severe fatigue, cognitive deficits, mental depression, and autonomic dysfunction with neurogenic bladder and bowel incontinence. Her symptoms began at the age of 18 with weakness of the
right leg and fatigue with long distance walking and over the ensuing years she experienced steady
deterioration of functions. In 1985 she became wheelchair dependent and it was anticipated that within
1-2 years she would become functionally quadriplegic. In December of 1992 she began experimental
treatment with EMFs. While receiving regularly weekly transcortical treatments with AC pulsed
EMFs in the picotesla range intensity she experienced during the first year improvement in mental
functions, return of strength in the upper extremities, and recovery of trunk control. During the second
year she experienced the return of more hip functions and recovery of motor functions began in her
legs. For the first time in years she can now initiate dorsiflexion of her ankles and actively extend her
knees voluntarily. Over the past year she started to show signs of redevelopment of reciprocal gait.
Presently, with enough function restored in her legs, she is learning to walk with a walker and is able
to stand unassisted and maintain her balance for a few minutes. She also regained about 80% of functions in the upper limbs and hands. Most remarkably, there was no further progression of the disease
during the 4 years course of magnetic therapy. This patients clinical recovery cannot be explained on
the basis of a spontaneous remission. It is suggested that pulsed applications of picotesla EMFs
affect the neurobiological and immunological mechanisms underlying the pathogenesis of CP MS.

Keywords: Multiple sclerosis; electromagnetic fields; chronic progressive multiple sclerosis; clinical
course
Correspondence to: Professor Reuven Sandyk, M. D., M. Sc., P. 0. Box 453, Roslyn Heightst, NY
11577-0453, U.S.A.
177

1 9 9 7 )

I78

K.SANDYK

It is estimated that 10-7,OCic of multiple sclerosis (MS) patients have a chronic

progressive (CP) course (Smith & Scheinberg, 1985: Whitaker & Benveniste,
1990). The CP course is characterized by an insidious onset of slowly progressive
disability in which remissions do not occur (Kraft et al., 1977; Smith & Scheinberg,
1985). CP course tends to have a later age of onset (Noseworthy et al., 1983) and
typically first presents with motor disturbances involving gait and limb weakness
(Minderhoud et al., 1988). CP MS is associated also with a higher incidence of
cognitive deficits (Heaton et al., 1985: Beatty et al., 1989; Franklin et al., 1989).
In patients with CP MS, onset of the disease before age 35 years and the occurrence
of symptoms primarily of a sensory nature are associated with a more favorable
prognosis (Smith & Scheinberg. 1985). On the other hand, early onset of motor
signs including weakness. spasticity. or cerebellar symptoms is associated with a
poorer prognosis. Pyramidal or cerebellar signs present within 5 years of the disease
onset are felt to be a strong indicator of subsequent poor prognosis which appears
slightly worse for men than for women (Leibowitz et al., 1969; Kurtzke et al., 1977;
Smith & Scheinberg, 1985). Presently, no pharmacologic treatment modality has
demonstrated long term beneficial effects on the core symptoms of MS and there is
no available specific therapeutic modality effective for CP MS (Bauer, 1978;
Hughes. I99 1: Rudick et al., 1992). In addition, no therapeutic modality has shown
long term beneficial effect in reversing the course of the disease in patients with CP
MS (Giesser. 1985: Ellison et al., 1994).Transcortical application of picotesla range
electromagnetic fields (EMFs) is a safe and highly effective modality for the
symptomatic treatment of MS (Sandyk. 1992; Sandyk & Derpapas, 1993; Sandyk
& Iacono, 1993: Sandyk & Dann. 1994: 1995; Sandyk, 1995 a; b; Sandyk, 1996;
Sandyk. in press a ) and is presently the only modality which has demonstrated
symptomatic improvement and reversal of the clinical course of the disease in
patients diagnosed with CP MS.

CASE REPORT
This 40 year old wonian pharmacist presented in December of 1992 with a history
of CP MS with resultant spastic paraplegia. loss of trunk control, profound
weakness of the upper extremities with loss of hand functions, neurogenic bladder. loss of' bowel control with incontinence, impaired cognitive functions and
mental depression. Additional symptoms included intermittent difficulties with
breathing, chronic fatigue. extreme sensitivity to heat and mental stress and
rwrlling with rubor of the legs, feet and hands. Her initial symptoms emerged at
age 18 when she began to experience weakness of the right leg and fatigue with
long distance walking. Over the ensuing years she gradually developed increasing

EMF AND CHRONIC PROGRESSIVE MULTIPLE SCLEROSIS

179

disability with spastic paraparesis, ataxia of gait, weakness in the upper limbs, and
loss of bladder and bowel control. An MRI scan obtained in 1987 revealed multiple subcortical and upper spinal demyelinating lesions. Pattern Reversal VEP
studies obtained in April of 1993 showed prolonged PlOO latencies bilaterally,
greater on the left than on the right (1 17 ms and 115 ms, respectively) suggesting
delayed conduction in the prechiasmal segments of the central visual pathways.
Since 1985 she has been confined to a wheelchair. She had very limited functions
of her arms and hands being unable to cut her food, comb or wash her hair or dress
herself. Upon stress or increasing fatigue her hands would claw. Being unable to
move and shift her body position during sleep was a major distressing symptom.
Her prognosis was considered extremely unfavorable and it was anticipated that
within 1-2 years she would become quadriplegic and require full time care.
In December of 1992 the patient began experimental treatment with transcortical applications of picotesla intensity EMFs. Since then she has received weekly
treatments which are administered in a quiet and artificially illuminated room that
is magnetically unshielded. EMFs are administered extracranially via an array of
24 coils embedded in a plate which, during treatment, is placed over the patients
cranial vertex. The EMFs are administered using the Sandyk Electromagnetic
StimulatorSM,TM
which emits an AC pulsed EMF of 7.5 picotesla flux density.
A session comprises two successive treatments each of 25 minutes duration separated by an interval of 15 minutes. A 4.2 Hz sinusoidal wave is employed in the
first treatment and a 4.2 Hz trapezoidal wave is administered in the second application. During the first year the patient reported improvement in mental functions
particularly in mood, memory and concentration. I am in control of my emotions
and I dont cry as often as I used to. Her dream recall was restored and in the
summer of 1993 she began reading books for the first time in 10 years. She also
experienced improvement in motor functions predominantly increased muscle
strength in the upper limbs with recovery of trunk control enabling me to sit up
straight and conduct myself as a healthy person would. rather than sitting in a
slumped over position. During the second year she experienced the return of
more hip functions and motor recovery began in her legs. Spasticity in the lower
limbs was reduced about 50% and for the first time in years she can now initiate
dorsiflexion of her ankles and actively extend her knees voluntarily. She has even
started to show signs of redevelopment of reciprocal gait. A VEP study repeated
in June of 1995 showed normal PlOO latencies in both eyes (107 ms on the left
side and 105 ms on the right side). Presently, with enough function restored in her
legs, she is learning to walk with a walker and is able to stand unassisted and
maintain her balance for a few minutes. She continued to regain strength in her
upper extremities and is now able to cut her food again, comb and wash her hair,
dress herself and cook for her family. Her bladder and bowel control have

180

R. SANDYK

improved considerably and with the use of laxatives she now maintains normal
bowel functions. Her level of energy has improved considerably and her tolerance
to stress has improved as well. Over the past year she noted return of her ability to
move and shift her body position during sleep. Most importantly, however, the
progressive course of her disease has been reversed since the initiation of treatment
with EMFs with no clinical evidence of further progression of symptoms.

DISCUSSION
This patients clinical recovery cannot be explained on the basis of a spontaneous
remission. Since the onset of her first neurologic symptoms at the age of 18 she
experienced an insidious and steady deterioration of motor, autonomic, cerebellar
and cognitive functions with no remission of symptoms and was classified with
CP MS. Recovery of symptoms during magnetic therapy occurred slowly initially
involving predominantly mental and cognitive functions and subsequently affecting motor skills with improved strength in the upper limbs, trunk and lower
extremities. As part of the recovery process she regained greater personal independence and was able to cut her food. wash and comb her hair, dress herself and
prepare meals for her family. She regained sufficient balance to stand unassisted
and over the past year was working with her physical therapist on ambulating with
a walker. Over the past 4 years the patient experienced no further deterioration of
symptoms indicating that during this period the progressive course of the disease
has been reversed by treatment with EMFs.
The pathogenesis of CP MS and specifically the neurobiological and immunological mechanisms underlying the relentless progression of symptoms in this
group of MS patients remain unknown (Weiner & Hafler, 1988). Specifically, it
is not known whether these patients represent a subcategory of disease related to
different biological or immunological mechanisms or whether they might, in fact,
have had subclinical attacks. Schuller et al. (1973) suggested that in the early
active stage of MS the lesions result directly from infection but that in the latter,
often progressive. stages, damage to the nervous system results from an autoimmune process directed against myelin tissue. Minderhoud et al. (1988) suggested
that relapsing-remitting MS shows some characteristics of an autoimmune
process, but the cause of CP MS remains unclear. Biochemically, CP MS is associated with a more extensive loss of serotonin (5-HT) neurons indicated by the
findings of significantly lower CSF 5-HIAA levels in CP patients compared to
relapsing-remitting patients (Sonninen et al., 1973). CSF 5-HIAA levels were
also lower in bedridden patients compared to controls and ambulatory MS
patients. These neurochemical changes are relevant to the pathogenesis and

EMF AND CHRONIC PROGRESSIVE MULTIPLE SCLEROSIS

181

symptomatology of MS since 5-HT mechanisms have a key role in spinal and

supraspinal regulation of motor control as well as integration of sensory, autonomic, cognitive, affective and endocrine functions (Barasi & Roberts, 1973;
Baumgarten & Lachenmayer, 1985; Jacobs, 1991; 1994; Jacobs & Fornal, 1993;
Sirvio et al., 1994; Wallis, 1994). In addition, 5-HT is known to play an important
role in the modulation of the immune system and the integrity of the blood brain
barrier (BBB) (O'Brien et al., 1962; Jankovic et al., 1970; Essman, 1978;
Westergaard, 1980; Hall & Goldstein, 1981; Devoino et al., 1987; Sharma & Dey,
1986 a; b). It has been suggested that the BBB is a target of the pathological
process in MS and disruption of the permeability of the BBB is thought to be a
critical factor in the pathogenesis and progression of the disease (Broman, 1964;
Berger & Sheremata, 1983; Koopmans et al., 1989; Poser, 1986; 1992). Loss of
5-HT mediated control of BBB permeability may allow continued leakage of
inflammatory cells into the CNS causing destruction of the adjacent tissues with
resultant progression of symptoms. The pineal gland also influences the integrity
of the BBB through the 5-HT system (Jankovic et al., 1970; Sandyk, in press b)
and may have a critical role in the pathogenesis of MS and its clinical course. In
fact, pinealectomy enhances the development of experimental allergic
encephalomyelitis (EAE), a T-cell mediated autoimmune disease, which is widely
considered as an animal model of MS (Jankovic et al., 1970).
The mechanisms by which chronic pulsed applications of picotesla EMFs
induced recovery of this patient's neurologic deficits and reversal of her clinical
course remain unknown. In experimental animals pulsed application of EMFs was
reported to enhance neurite outgrowth and regeneration of peripheral nerves, transected spinal cord, and optic nerve (Sisken et al., 1989; Rusovan et al., 1992;
Borgens et al., 1981; Politis et al., 1988). Stimulation has been reported within a
board range of frequencies and field amplitudes (Rusovan et al., 1992). It has been
demonstrated that cerebral neuronal activity is associated with the generation of
picotesla EMFs (Cohen, 1972; Okada et al., 1987; Kyuhou & Okada, 1993) suggesting that these fields reflect a mode of neuronal communication. Low-frequency
EMFs may affect neuronal functions by changing transmembrane signal transduction processes (Luben, 1991). A model proposed by Adey (1981) implicated a role
for Ca++in 'membrane amplification' as a possible basis for susceptibility of central
neurons to weak magnetic fields. E m s may affect the release of synaptic transmission, the level of amino acid neurotransmitters and the concentrations of CAMPby
changing the permeability of Ca" and K+ channels (Kaczmarek & Adey, 1974;
Bawin & Adey, 1976; Blackman, 1988; Rudolph et al., 1988; Zecca et al., 1991;
Trabulsi et al., 1996). The modulation of intracellular Ca" concentrations by EMFs
may trigger long lasting amplification or depression of synaptic efficiency and neuronal membrane excitability (Gareri et al., 1995; Trabulsi et al., 1996). Pulsed EMF

I82

R. SANDYK

have also been shown to affect the secretion of several hormones including pineal
melatonin (Stoupel et al.. 1983: Welker et al., 1983: Wilson et al., 1986; 1989; 1992;
Semm, 1992) which affects neurotransmitter functions ( Anton-Tay et al., 1968;
Sugden, 1983; Erlich & Apuzzo. 1985; Miguez et al.. 1994)-neuronal excitability
(Bindoni & Rizzo. 1965: Roldan & Anton-Tay. 1968; Nir et al., 1969;Pazo, 1979;
Albertson et al.. 1981; Zeise & Semm, 1985). myelin production and nerve regeneration (Relkin & Schneck, 1975: Relkin et al.. 1973) and neuroimmunomodulation
(Angeli et al., 1988: Pierpaoli & Maestroni. 1988: Maestroni. 1993). Melatonin
secretion is diminished in patients with MS during periods of exacerbation of symp
toms (Sandyk & Awerbuch. 1992; 1993). a factor which may promote inununodysregulation and ongoing breakdown of the integrity of the BBB. Intermittent, pulsed
applications of picotesla EMFs is thought to boost circadian melatonin secretion.
increase 5-HT transmission. stabilize neuronal excitability. diminish T-cell mediated inflammatory responses. and promote nerve regeneration all of which may contribute to symptomatic improvement and inhibition of the progression of the disease.

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