Just Accepted by International Journal of Neuroscience

ELECTROMAGNETIC HYPERSENSITIVITY:
EVIDENCE FOR A NOVEL NEUROLOGICALSYNDROMEDavid E. McCarty, M.D., Simona Carrubba, Ph.D., Andrew L.
Chesson, Jr., M.D., Clifton Frilot, II, Ph.D., Eduardo Gonzalez-Toledo,
M.D., Andrew A. Marino, Ph.D.
doi:10.3109/00207454.2011.608139

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ABSTRACT
Objective: We sought direct evidence that acute exposure to environmental-strength
electromagnetic fields could induce somatic reactions (EMF hypersensitivity).
Methods: The subject, a female physician self-diagnosed with EMF hypersensitivity,
was exposed to an average (over the head) 60-Hz electric field of 300 V/m(comparable to typical environmental-strength EMFs) during controlled provocation
and behavioral studies.
Results: In a double-blinded EMF provocation procedure specifically designed tominimize unintentional sensory cues, the subject developed temporal pain,
headache, muscle-twitching, and skipped heartbeats within 100 s after initiation of
EMF exposure (P < 0.05). The symptoms were caused primarily by field transitions(off-on, on-off) rather than the presence of the field, as assessed by comparing thefrequency and severity of the effects of pulsed and continuous fields in relation tosham exposure. The subject had no conscious perception of the field as judged byher inability to report its presence more often than in the sham control.
Discussion: The subject demonstrated statistically reliable somatic reactions in
response to exposure to subliminal EMFs under conditions that reasonably excluded
a causative role for psychological processes.
Conclusion: EMF hypersensitivity can occur as a bona fideenvironmentally-inducible neurological syndrome.

© 2011 Informa Healthcare USA, Inc. This provisional PDF corresponds to the article as it appeared upon acceptance. Fully
formatted PDF and full text (HTML) versions will be made available soon.
DISCLAIMER: The ideas and opinions expressed in the journal’s Just Accepted articles do not necessarily reflect those of Informa Healthcare (the Publisher), the Editors
or the journal. The Publisher does not assume any responsibility for any injury and/or damage to persons or property arising from or related to any use of the material
contained in these articles. The reader is advised to check the appropriate medical literature and the product information currently provided by the manufacturer of eachdrug to be administered to verify the dosages, the method and duration of administration, and contraindications. It is the responsibility of the treating physician or other
health care professional, relying on his or her independent experience and knowledge of the patient, to determine drug dosages and the best treatment for the patient.
Just Accepted have undergone full scientific review but none of the additional editorial preparation, such as copyediting, typesetting, and proofreading, as have articles
published in the traditional manner. There may, therefore, be errors in Just Accepted articles that will be corrected in the final print and final online version of the article.
Any use of the Just Accepted articles is subject to the express understanding that the papers have not yet gone through the full quality control process prior to publication.

ELECTROMAGNETIC HYPERSENSITIVITY: EVIDENCE FOR A NOVELNEUROLOGICAL SYNDROMETEDDavid E. McCarty, M.D.a, Simona Carrubba, Ph.D.a, Andrew L. Chesson, Jr., M.D.a,

Department of Neurology, LSU Health Sciences Center, Shreveport, LA, USAb

School of Allied Health Sciences, LSU Health Sciences Center, Shreveport, LA, USA

c

EP

a

Department of Radiology, LSU Health Sciences Center, Shreveport, LA, USAC*Corresponding author. Address: Department of Neurology, LSU Health Sciences

AC

Center, P.O. Box 33932, Shreveport, LA 71130-3932, USA. Tel.: 1-318-675-6177.

ST

E-mail address: amarino@lsuhsc.edu

Running head: Electromagnetic Sensitivity
Keywords:

Electromagnetic fields, Evoked potentials, Hypersensitivity, Provocation

study, Sensory transduction, Sleep study.

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Clifton Frilot II, Ph.D.b, Eduardo Gonzalez-Toledo, M.D.c, Andrew A. Marino, Ph.D.a,*‐1–

ABSTRACTObjective: We sought direct evidence that acute exposure to environmental-strength
electromagnetic fields could induce somatic reactions (EMF hypersensitivity).

TE
D

Methods: The subject, a female physician self-diagnosed with EMF hypersensitivity,

was exposed to an average (over the head) 60-Hz electric field of 300 V/m (comparable

studies.

EP

Results: In a double-blinded EMF provocation procedure specifically designed tominimize unintentional sensory cues, the subject developed temporal pain, headache,muscle-twitching, and skipped heartbeats within 100 s after initiation of EMF exposureC(P < 0.05). The symptoms were caused primarily by field transitions (off-on, on-off)ACrather than the presence of the field, as assessed by comparing the frequency andseverity of the effects of pulsed and continuous fields in relation to sham exposure. The
subject had no conscious perception of the field as judged by her inability to report its

ST

presence more often than in the sham control.
Discussion: The subject demonstrated statistically reliable somatic reactions in
response to exposure to subliminal EMFs under conditions that reasonably excluded acausative role for psychological processes.

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to typical environmental-strength EMFs) during controlled provocation and behavioral

Conclusion: EMF hypersensitivity can occur as a bona fide environmentally-inducible
neurological syndrome.

‐2–

INTRODUCTION
Man-made electromagnetic fields (EMFs) such as those produced by cell
phones, powerlines, or computers are ubiquitous in the general and workplaceTED

environments. About 3–5% of the population subjectively associates acute or subacuteexposure to EMFs with departures from normal function or feeling (EMF

been attributed to somatization disorders [3, 4].

EP

A possible nonpsychological basis for EMF hypersensitivity was provided by thediscovery of the ability of human beings to detect weak EMFs, as evidenced by theoccurrence of field-onset and field-offset brain potentials [5], and the induction ofCsteady-state changes in brain electrical activity that persisted during the presence of theACfield [6]. The underlying mechanism of field sensory transduction appears to be anelectric-force-sensitive ion channel [7]. Animal studies suggest that the electroreceptor
cells and/or afferent processing cells are located in the brain stem [8, 9].

ST

Despite the physiological and biophysical evidence that could explain at least
some cases of human somatic responses to EMFs without invoking psychologicalprocesses [5-9], direct evidence of nonpsychological EMF hypersensitivity is lacking.
Our purpose was to determine whether EMFs could produce symptomatic responses in

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hypersensitivity) [1, 2]. The prevalence of self-reported EMF hypersensitivity has usuallya putatively hypersensitive subject, while appropriately controlling for chance,
confounders, and somatization.

‐3–

METHODS
Subject
In the context of ongoing human, animal, and biophysical studies involving EMF

TED

sensory transduction in our laboratory, we were contacted by a 35-year-old female

physician with multiple neurologic and somatic symptoms including headaches, hearing

musculoskeletal complaints, all of which she reported could be precipitated by exposureEP

to environmental EMFs and abated by withdrawal from the fields. Among theenvironmental triggering sources she identified were cell phones, computers,
powerlines, and various common electrical devices. During extensive interviews sheACsources could provoke her symptoms.

C

credibly explained the reasons for her belief that EMFs from common environmental

After she agreed to medical tests appropriate for evaluating her medical
condition, she was admitted as a patient on the neurology service and underwent aSTphysical exam including a comprehensive neurologic exam, a clinicalelectroencephalogram (EEG) exam, a noncontrast magnetic-resonance (MR) imagingof the brain, an overnight sleep study (with video and expanded EEG montage) in which
the resulting polysomnogram was scored in accordance with standardized rules [10], a

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and visual disturbances, subjective sleep disturbances and nonrestorative sleep, andstandard laboratory evaluation of serum electrolytes and blood chemistries, liverfunction tests, serum fasting cortisol, and complete blood count, and direct evaluationsof her EMF sensitivity in a series of EMF provocation and behavioral studies (seebelow). The institutional review board at the LSU Health Sciences Center approved all
experimental procedures, and the subject gave her written informed consent.

‐4–

EMF Exposure
The subject sat in a comfortable wooden chair with her eyes closed, and uniaxial

TE
D

60-Hz (unless noted otherwise) sinusoidal electric fields were generated by applying a
voltage to parallel 49-cm square metal plates spaced 36 cm apart (Figure 1). The

no visual or auditory stimuli. The background electric field (the field present irrespectiveEPof whether or not a voltage was applied to the parallel plates) was about 1 V/mthroughout the region occupied by the subject (HI-3603, Holaday, Eden Prairie, MN,
USA). The plate arrangement did not produce magnetic fields. The continuously-presentCbackground 60-Hz magnetic field was 0.1 mG, and the geomagnetic field wasAC599.8 mG, 68.4° below the horizontal component (component along the direction of theapplied field, 360.5 mG) (MAG-03, Bartington, GMW, Redwood City, CA, USA). Highfrequency signals from cell-phone towers and other distant antennae (1–10 GHz) wereST

less than 0.1 µW/cm2 (the background fields in the sleep-study room were similar)(Spectran, Aaronia, Euscheid, Germany).
In the provocation studies the electric field was applied for 100-s intervals with aduty cycle of 50% and a repetition rate of 10 Hz, which resulted in alternating field-on

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equipment that controlled the field was located outside the subject’s view and emitted

and field-off pulses of 100 ms (pulsed field); a continuous field (100% duty cycle) wasused in one of the provocation studies. Duty cycle, pulse structure, and interval length
were regulated by a microcontroller programmed to produce the desired signals. Whenthe duty cycle was 50% the actual EMF stimuli consisted of: 1) 10 onset stimuli persecond x 100 s = 1000 field-onset stimuli per interval; 2) an equal number of field-offset‐5–

stimuli; 3) the presence of the EMF for a total of 50 s. When the duty cycle was 100%
there was only 1 field-onset stimulus and 1 field-offset stimulus, and the EMF waspresent for 100 s. In the behavioral studies the electric field was applied in trials

Field StrengthEP

The applied electric field was significantly distorted by the subject’s body,resulting in strong inhomogeneities in the field surrounding the subject. To overcome
the problem of measuring the external field, we used Maxwell’s laws to calculate it atCevery point in the subject’s vicinity. The subject was modeled as an electrically isolated

AC

composite of rectangular solids representing the trunk and lower extremities, and an
ellipsoid representing the head. The assumed conductivity was 1 S/m. The total electricfield at every point was determined for VAC = 100 V using finite-element analysis

ST

consisting of approximately 106 elements; a more detailed mesh was automaticallygenerated in the head region (Multiphysics, Comsol, Los Angeles, CA, USA). The peak
external electric field was about 1000 V/m (Figure 1); the average field was about 300
V/m around the head, and less than 50 V/m around the body. The peak and average

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repetition rate) and a 10-s field-free control epoch.

TED

consisting of a 2-s epoch when a pulsed field was applied (50% duty cycle, 10-Hz

field strength and duration of exposure were far below the levels generally recognized
as capable of producing physiological effects in human subjects [11].
The external electric field resulted in an induced internal electric field in the brainin accordance with physical law. The strength of the induced brain electric field wascomparable to that induced by environmental-strength power-frequency electric and‐6–magnetic fields [12, 13].

Somatic Responses

TED

A pulsed field (50% duty cycle) was applied for 100 s in ten independent field-

exposure intervals. The controls were ten 100-s sham-exposure intervals during which arandomly. The environmental conditions during the field-exposure and sham-exposureEPintervals were identical except that the wires carrying the plate voltage weredisconnected during the sham-exposure intervals. At the end of each interval thesubject was questioned by an interviewer blinded to whether or not the field had beenCapplied and asked to describe any symptoms she developed during the interval,

ACwhether or not the symptoms had persisted into the interview period. She was queriedusing descriptive terms she had employed. Whenever she reported symptoms,
commencement of the next interval was delayed until she reported that they had

STabated.

We used a pulsed field because we expected it would result in a stronger
symptomatic response compared with a continuous field [9, 14]. To test this reasoning
we performed a second study to assess whether the subject developed a differential

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field was not applied. The order of the field and sham intervals was determined

symptomatic response to the pulsed and continuous fields. The subject was exposed or
sham exposed for 100-s intervals, and immediately after each interval was interviewed
as described above. A sham field (S), continuous field (C) (100% duty cycle), andpulsed field (P) (50% duty cycle, 10 Hz) were applied, and the SCP pattern was
repeated five times. The subject was blinded regarding the use of different EMFs; from‐7–

her perspective the laboratory procedures were identical to those followed in the firststudy. The interviewer was aware that the effects of C and P fields were beingTE
D

compared, but was blinded regarding the actual sequence of the fields.

Behavioral Responses

the combined processes of conscious awareness of the EMF followed by a somatizationEP

reaction based on a fear that EMFs were harmful. We approached the issue by
determining whether the subject could consciously perceive a field when it waspresented in multiple independent trials. A field having the same strength and spatial

C

distribution as previously (Figure 1) was applied in a series of trials each of whichACconsisted of a 2-s epoch during which a pulsed field (50% duty cycle, 10-Hz repetitionrate) was applied and a 10-s field-free control epoch. Eight independent sequenceswere employed, each with 30–50 trials. In three sequences the frequency was 60 Hz, inST

two it was 1 kHz, and in three others the respective frequencies were 10 kHz, 100 kHz,and 500 kHz.

The subject held a small plastic box that housed a buzzer, a button labeled YES
and another button labeled NO. In the middle of each on and off epoch the buzzer

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We considered the possibility that any symptomatic response might be a result of

emitted a 4-kHz tone at 60 dB which lasted 100 ms, and she was instructed to press the
YES or NO button whenever she heard the tone, depending on whether or not she had
any conscious sensation of a field at that moment. Employing a custom-designed virtual
instrument (LabView, National Instruments, Austin, TX, USA), we determined thenumber of YES and NO responses in the presence and absence of the field in each‐8–sequence. In addition, 4 sham sequences (minimum of 30 trials in each) wereconducted in which a field was not applied. The subject had no knowledge that an off-on
pattern was being used in the field sequences or that some sequences consisted ofTEDsham exposure.

The frequencies of the somatic and behavioral responses in the presence andEPabsence of the field were evaluated using the chi-square test (2 x 2 tables) or theFreeman-Halton extension of the Fisher exact probability test (2 x 3 tables) [15].

C

RESULTSAC

Clinical Studies

The patient’s physical examination was unremarkable. The presence of frequent
subjective awakenings from sleep, sometimes with unintended gross motor activity suchSTas muscle twitching and leg jerking, prompted clinical concern for a sleep-related
movement disorder, parasomnia, or nocturnal epilepsy. The polysomnogram revealed
significant sleep fragmentation and discontinuity (Table 1), but no evidence of significant
sleep-disordered breathing, nocturnal epilepsy, or abnormal REM-related atonia.

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Statistics

Periodic limb movements were noted, but did not appear to be a major sleep-disrupting

force.

Standard and 24-hour video-accompanied EEG recordings revealed normalappearing background rhythms and no epileptiform activity. EEG performed in thepresence of active cellular telephone use provoked a right-sided headache, but‐9–

produced no unusual EEG waveforms. The MR image revealed evidence of corticaldysplasia in the right temporal lobe, and right parietal polygyria, both without intervalchange when compared with a study performed 19 months earlier. LaboratoryTED

evaluation for common metabolic/endocrine problems and blood count abnormalities

Somatic Responses

EP

The sequence and characteristics of the symptomological and behavioral
experiments are shown in Table 2.

The question of a relation between the presence of the field and the occurrenceCof symptoms was directly addressed by interviewing the subject immediately followingAC

100-s field-exposure or sham-exposure intervals; both the interviewer and the subject
were blinded regarding the exposure condition. During the interviews the subject
reported a range of symptoms including localized pain in her jaw, ear, or the side of herSThead, a more diffuse head pain, and muscle pain or twitching in the hip, neck, and back.
Sometimes she qualified the symptom as “strong” or “mild,” and sometimes she denied
all symptoms. We grouped the symptoms related to localized head pain as “temporalpain,” those related to diffuse head pain as “headache,” and those related to muscle

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was unremarkable.

effects as “muscle pain/twitching.” Symptoms reported more rarely were indicatedexplicitly (Table 3a). The subject consistently reported pronounced symptoms that
occurred during the field intervals, particularly in intervals 7, 13, 14, 15, and 18. In thesham intervals she reported no symptoms in intervals 4, 6, 8, 16, 20, weak temporal‐ 10 –

pain in intervals 2, 3, 19, and a weak headache in intervals 10 and 12. The field andsham distributions of symptoms differed significantly (P < 0.05) (Table 3b).
In a second study, the relative role of EMF changes (number of onsets andTED

offsets) and steady-state presence of the EMF was directly addressed by interviewing

the subject immediately following 100-s exposure intervals in which either a pulsed field

previously and reported symptoms in both field intervals (Table 4a). The symptoms

EP

triggered by the pulsed field were more intense compared with the sham control(P < 0.05) (Table 4b); the symptoms triggered by the continuous field did not differ fromthe sham control (P = 0.16). The subject reported no symptoms in 4 of 5 sham intervals

ACC(intervals 1, 4, 10, 13).

Behavioral Responses

The possible influence of conscious awareness of the EMF on the development

STof symptoms was investigated by assessing whether the subject could consciously
perceive the field. A total of 300 independent trials involving carrier frequencies of 60 Hz
to 500 kHz were used; the controls consisted of 150 sham trials. The results did notdepend on the carrier frequency, and consequently the data was combined for analysis

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or a continuous field was presented. She was queried regarding her symptoms as(Table 5).

The subject failed to respond to the tone 7 times while the field was on and 7

times while it was off, resulting in a total of 293 responses for each of the two
conditions. There were no missed responses in the sham trials. The overall yes
response rate in the field trials was (51/586) x 100 = 8.7%. The occurrence of a yes‐ 11 –

response was significantly associated with the presence of the field (P < 0.05) (Table5a), but the sensitivity of the yes responses was low ([32/(32 + 261)] x 100 = 11%). The
yes response rate in the sham trials was slightly higher than that seen in the field trials

TE
D([27/273 = 9.9%]) (Table 5b).

Appropriately controlled provocation studies are required to establish theEPexistence of EMF hypersensitivity and to understand the relative importance of

psychological and nonpsychological processes in mediating any observed symptoms. A
working laboratory definition of EMF hypersensitivity formulated in symptomologicalCterms is therefore needed to permit recognition of hypersensitivity reactions when theyACoccur. In previous provocation studies the assumption was made that true
hypersensitive subjects would exhibit more or less the same symptoms in response torepeated provocations. The assumption led to experimental designs that involvedSTaveraging across exposed and control groups, which is an inherently insensitive
statistical procedure for detecting real but variable responses [3, 4]. The assumption isparticularly inapplicable to EMF hypersensitivity because intra- and inter-subject
variability are its salient features [1, 2]. We defined EMF hypersensitivity as theJU

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DISCUSSION

occurrence of any medically recognized symptom in response to provocation using anenvironmentally relevant EMF; there was no requirement that the same symptom mustreoccur when the EMF provocation was repeated. This definition avoided the problem ofmasking real effects and more appropriately matched the laboratory procedure to the
known characteristics of EMF hypersensitivity [1, 2]. We focused on a single self-‐ 12 –

reported subject and employed a procedure in which she served as her own control.
While controlling for artifacts, chance, and somatization, the question whether she
reliably exhibited any symptomatic responses to an EMF was addressed; the alternativeTED

hypothesis was that she did not exhibit EMF-triggered symptoms. The laboratory

conditions were controlled in such a way that a putative role of psychological processes

The subject developed symptoms in association with the presentation of a pulsedEPelectric field significantly (P < 0.05) more often than could reasonably be explained on

the basis of chance (Table 3). Several considerations suggested that the statistical link
was a true causal association with a subliminal EMF. First, the subject’s environmentC

was carefully controlled to avoid putative confounding factors. The testing took place inACan acoustically quiet environment and the presence of uncontrolled environmental
EMFs was nil. The environmental conditions during the field-exposure and shamexposure intervals were identical except that during the sham-exposure intervals, at a

STpoint far removed form the subject’s field of view, the wires carrying the plate voltage
were disconnected. A key aspect of our laboratory procedure was the elimination of
sensory cues that could serve as conscious markers of the electric field leading to asomatization reaction. All appropriate precautions were taken to eliminate potential

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could reasonably be identified.

confounders. Second, the occurrence of symptoms was significantly associated with thetype of EMF (Table 4). The symptomatic response was associated with the pulsed EMF,
which maximized occurrence of the number of transient changes in the EMF (off-on andon-off), not with the presence of the field, as expected on the basis of prior animalstudies where the issue of somatization was irrelevant [9]. Finally, in a behavioral study‐ 13 –

specifically designed to assess awareness of the field, yes response rates were 8.7%
and 9.9% in the field and sham conditions, respectively, which provided no evidence fora psychological role in the development of the subject’s symptoms. We thereforeTED

conclude with a reasonable level of certainty that the causal association we foundbetween the presence of the EMF and the subject’s symptoms was mediated by aassociation, that possibility could not be excluded. The existence of the neurologicalEP

syndrome reported here was previously suspected, but not documented.

The mechanism for the subject’s symptoms of headache, visual disturbances,and somatic musculoskeletal discomfort following exposure to EMFs is unknown. BasedC

on clinical evaluation, intermittent seizure activity is not a credible explanation, althoughACa deeper epileptic focus with partial seizure activity may have escaped the detection of
surface EEG electrodes. The abnormal findings in the subject’s medical workup
included the abnormal MR image (cortical dysplasia and polygyric changes) andST

extensive sleep discontinuity and fragmentation manifested in the overnightpolysomnogram; the possible association of these findings with the subject’s syndromeof EMF hypersensitivity is unknown.
Our aim here was to concentrate on the previously unaddressed questionJU

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subconscious neural process. Although chance was an unlikely explanation for thewhether acute exposure to weak EMF could produce real but not precisely predictablesomatic effects mediated by nonpsychological processes. Within the limitations of thestudy we concluded that we demonstrated the neurological syndrome in the subject westudied. The question of whether EMF hypersensitivity is a significant public-healthproblem was not addressed here. The EMF we employed was equivalent in strength‐ 14 –

and pulse structure to EMFs pervasively present in the environment [1, 2], and our
results were consistent with the possibility that environmental EMFs can directly trigger
clinical symptoms. Nevertheless resolution of the public-health issue depends on aTED

deeper understanding of how internal EMFs caused by environmental EMFs are related
to physiological process, and of the role of psychological factors and co-morbidities inEP

Declaration of Interest: The authors report no conflicts-of-interest. The authors
alone are responsible for the content and writing of the paper.

Levallois P, Neutra R, Lee G, Hristova L. Study of self-reported hypersensitivity

AC

1.

C

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Table 1 Polysomnography Results. Comparison with usual night, per patient: “Same as
usual.” No epileptiform activity noted during arousals associated with unintended grossmotor activity. Normal REM-related atonia. REM, rapid eye movement; WASO, wakeTE
D

NORMAL RANGE

Sleep latency

6 min

13.4 ± 10.1 [16]Stage N1 sleep

13.8%

3–8% [17]Stage N2 sleep

51.8%

44–55% [17]Stage N3 sleep

23.6%

10–15% [17]Stage R sleep

10.7%

20–25% [17]150.5 min

57–66 min [18]C

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SUBJECTWASO index

AC

REM latency

6/hr

1.3 ± 0.8 [16]40.5 min10.7 ±11 min [19]340.5 min

340.0 ± 70 [16]Sleep efficiency

88%

86.4% ± 11.6 [16]Arousal index

34.2/hr

16.8 ± 6.2 [20]PLM index

7.8/hr< 5/hr [21]0.2/hr< 5/hr [22]WASO total

ST

Total sleep timeJU

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after sleep onset; PLM, periodic limb movement; AH, apnea/hypopnea.

AH index‐ 18 –

Pulsed

10

100

Sham

10

100

Pulsed5

100

Continuous

5

100

Sham

5

Pulsed300

Sham

Symptoms

Symptoms

100

ST

AC

150

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3

RESPONSE

TE
D

1

2

NO. OF
TRIALSTRIAL
DURATION(sec)

EP

EXPERIMENTELECTRIC
FIELD
CONDITIONC

Table 2 Sequence and characteristics of experiments.

‐ 19 –

1

1

Behavior

Table 3 Evaluation of the relation between presentation of a pulsed electric field and thedevelopment of symptoms. (a) Results from the individual 100-s exposure intervals. (b)CONDITIONRESULT

1

Pulsed Field

Temporal pain

2

Sham

Mild temporal pain

3

Sham

Mild temporal pain

4

Sham

No symptoms

5

Pulsed Field

Temporal pain; Headache

6

Sham

No symptoms

7

Pulsed Field

8

Sham

No Symptoms

9

Pulsed Field

Headache

10

Sham

Mild headache

11

Pulsed Field

Temporal pain

C

EP

INTERVAL
NO.

ST

AC

Skipped heartbeats; Feeling of unease

12

Sham

Mild headache

13

Pulsed Field

Muscle twitch; Feeling of unease

14

Pulsed Field

Strong headache

15

Pulsed Field

Strong headache

16

Sham

No symptoms

17

Pulsed Field

Stiff neck18

Pulsed Field

Muscle twitch; temporal pain

19

Sham

Mild temporal pain

20

Sham

No symptoms

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(a)

TE
D

Summary table.

‐ 20 –

ST

JU
EP

C

AC

FIELD
CONDITION
NONE
MILD

Sham
5
5

*Pulsed Field00*P < 0.05‐ 21 –TED

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(b)
SYMPTOMS> MILD
0

10

Table 4 Evaluation of the comparative effect of continuous and pulsed fields relative toa sham field on the development of symptoms. (a) Results from individual 100-s

RESULTSham

No symptoms

2

Continuous Field

No symptoms

3

Pulsed Field

Temporal pain

4

Sham

5

Continuous Field

6

Pulsed Field

7

Sham

8

Continuous Field

Muscle twitch

9

Pulsed Field

Severe pain

10

Sham

No symptoms

11

Continuous Field

Temporal pain

EP

1

AC

INTERVALCONDITIONNO.

No symptoms

No symptoms

C

Mild headache

ST

Mild headache

12

Pulsed Field

Headache; Muscle twitch

13

Sham

No symptoms

14

Continuous Field

Mild temporal pain

15

Pulsed Field

Mild temporal painJU

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(a)

TE
D

exposure intervals. (b) Summary table.

‐ 22 –

ST

JU
EP

C

AC

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CONDITIONNONEMILD> MILD

Sham
4
1
0

Continuous Field
2
03*Pulsed field0
2
3*P <0.05‐ 23 –TED(b)
SYMPTOMS

Table 5 Evaluation of conscious perception of a pulsed electric field. Subject’s
responses during the presence (On) and absence (Off) of the field, respectively.

OFF

Yes*

32

19

No

261

274
*P < 0.05

RESPONSE

EP

ON

TE
D

PULSED FIELD

OFF

Yes

15

12

No

135

138

AC

ON

C

SHAM

ST

(b)

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(a)‐ 24 –

Figure Legend

Figure 1. Spatial distribution of the external electric field (E) in the mid-sagittal plane. ETED

was generated by applying VAC = 100 volts to parallel metal plates while the subject waselectrically isolated (insert), and calculated at all points in the subject’s environment.

EP
C
AC
ST
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Average E surrounding the head was about 300 V/m.

‐ 25 –