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Scientific Documentation and Analysis of
the Autonomic Regulation in a Case of
Facioscapulohumeral Muscular Dystrophy
Post Ken Ware NeuroPhysics Therapy
Ken Ware1, Elio Conte2,3*, Riccardo Marvulli2,4, Giancarlo Ianieri2,4,
Marisa Megna2,4, Enrico Pierangeli2, Sergio Conte2, Leonardo Mendolicchio2
and Flavia Pellegrino2
DOI:10.4236/wjns.2015.52018
ABSTRACT
This is a study on autonomic neuroscience. In a previous paper in Ware et al. [1], we studied a
subject affected from facioscapulohumeral muscular dystrophy before and after Ken Ware
NeuroPhysics Therapy (NPT). Using the non linear methodology of the Generalized Mutual
Information (GMI) analysis of Sensory Motor Rhythm, we produced detailed results evidencing that
the mentioned NPT involved a net improvement of the patient under his subjective psychological
condition, and in particular, under the neurological and sensory motor profile. We quantified with
accuracy the improvement that the subject realized during such treatment. Of course, previous
studies of several authors have evidenced that muscular dystrophies are strongly linked to a profound
ANS disfunction. Therefore, the aim of the present study was to analyze the ANS of the subject before
and after the treatment. We performed analysis in time as well as in frequency domains using
nonlinear methods. The basic result of the paper was that, according to our analysis, the subjects
started with a serious ANS disfunction before NPT and that a net improvement was obtained after this
therapy. The results of all the examined parameters that were strongly out of normal range before the
treatment verified they had returned within normal range post NPT.
Keywords: Autonomic neuroscience; HRV analysis; Ken Ware NeuroPhysics Therapy; (NPT);
facioscapulohumeral muscular dystrophy; ANS dysfunction.
1. INTRODUCTION
When speaking about Heart Rate Variability (HRV), we have to start considering such basic
foundations. Baro-receptor activity is received from the Nucleus Tractus Solitarius (NTS) that provides
to transmit on one hand the signal to Nucleus Ambiguous/Dorsal Motor Nucleus (NA/DMN) integrated
by the hypothalamus action which generates finally parasympathetic heart rhythm modulation and on
the other hand the signal to Rostral Ventro-lateral Medulla oblongata (RVLM) that integrates
hypothalamus contribution generating orthosympathetic heart rhythm modulation. A complete scheme
of the complex arrangement may be found in Conte [2].
On the basis of this scheme, the HRV may be considered as an analysis that on one hand gives
important information about the fitness of the heart to respond to the autonomic nervous system
(ANS) modulation, and on the other hand (and it is here the important feature relating the present
paper) gives direct indication on the manner in which some central brain structures of dominant
_____________________________________________________________________________________________________
1The International Neuro Physics Functional Performance Institute, Energy Circuit, Robina, Australia.
2School of Advanced International Studies on Applied Theoretical and Non Linear Methodologies of Physics, Bari, Italy.
3Department of Basic Sciences, Neuroscience and Sense Organs, University of Bari Aldo Moro, Bari, Italy.
4Department of Physical Medicine and Rehabilitation, University of Bari Aldo Moro, Bari, Italy.
*Corresponding author: E-mail: elio.conte@fastwebnet.it;
relevance are explicating their basic function when inducing heart rhythm modulation. In this sense,
we may say that HRV dynamics is the “mirror image” of the psycho-physiological mechanisms
involved in some central brain regions. By this way, we conclude that HRV studies represent currently
a non invasive marker not only to explore the cardiovascular system but also to indirectly investigate
some important neurological involved functions.
To support this thesis, we have to quote here a recent neuroimaging study [3]. This study was
conducted by Julian F. Thayer, Fredrik Åhs, Mats Fredrikson, John J. Sollers and Tor D. Wager who
evidenced the existing main relationship between Hear Rate (HR) and regional brain blood flow.
These authors indicated in detail that the more significant involved brain regions were represented
from the amygdala and from the ventromedial pre-frontal cortex. In detail, these authors identified the
medial pfc (MPFC) (right pregenual cingulate), the MPFC (right subgenual cingulate) and the SLEA
(left sublenticular extended amygdala/ventral striatum).
Our conclusion is that such results evidence the importance of the HRV studies in exploring cognitive
as well as emotive functions in clinical conditions of subjects affected from psychological disorders as
well as psychiatric pathologies. This is not a restriction of course since, as we will attempt to evidence
in the present paper, the heart rate variability analysis may be considered of importance also in the
study of subjects affected from neuromuscular pathologies.
In 2003, we started to analyze HRV in different experimental conditions. And in the course of several
years of studies we have also introduced novel methods [4-6] of analysis in order to obtain valuable
quantifications of the VLF, LF, and HF bands where in particular the quantification obtained in the LF
band is related mainly to the modulation due to the orthosympathetic activity while the HF band
relates more directly parasympathetic activity and respiration.
The aim of the present study is to evaluate HRV and thus ANS disfunction in a subject affected from
Facioscapulohumeral Muscular Dystrophy and to estimate its improvement after that the subject has
been submitted to a treatment that we have called NPT that is due to Ken Ware and that we have
explained in detail recently elsewhere [1].
We may reassume briefly the reason to investigate here the ANS disfunction before and after Ken
Ware NPT. As previously outlined in Ware et al. [1], Duchenne (DMD) and Becker (BMD) muscular
dystrophies are disorders due to complete or partial loss of dystrophin protein. The presence of
persistent sinus tachycardia, atrial and ventricular arrhythmias, sweating and chills has suggested an
ANS involvement in these disorders. Yotsukura et al. [7,8] first described an impairment of ANS in 55
DMD, characterized by an increase in sympathetic activity and a reduction in parasympathetic output.
ANS impairment was confirmed also by studies that were developed by Lanza et al. [9] and by Inoue
et al. [10,11]. In a study developed from Vita in 2001 [12], 20 BMD patients were investigated with a
battery of six cardiovascular autonomic tests and power spectral analysis of HRV. Although 11
patients revealed abnormal findings at some cardiovascular tests, none of them had a definite auto-
nomic damage, as indicated by two or more abnormal tests. This clinical observation suggested
therefore that autonomic involvement did not represent a major finding in BMD. In 2006, the
prognostic value of HRV for sudden death was evaluated in a population of 30 BMD patients and
dilated cardiomyopathy compared with a control group of normal subjects [13]. The important result
was that an increment of sympathetic tone in BMD was observed, characterized by a lower HRV in
the frequency and time domains and a higher mean heart rate than in the control group.
When distinguishing the case of the myotonic dystrophy (DM) in the myotonic dystrophy type 1 (DM1)
and type 2 (DM2) with different clinical phenotypes, we find that in such conditions we have indication
of ANS involvement such as heart rhythm conduction disturbances, orthostatic hypotension, disorders
of sweating, ab-normal gut movements, and dysfunction of genitourinary apparatus as studied in
particular from Aminoff et al. [14]. Very important results may be found in Inoue et al. [10] Melacini et
al. [15], Ewing and Clarke [16], van Ravenswaaij-Arts et al. [17], Olofsson et al. [18], den Heijer et al.
[19], Pierangeli et al. [20], Di Leo et al. [21], Rakoèevi´c-Stojanovi´c et al. [22], Politano et al. [23],
Hardin et al. [24], Magrì et al. [25], Fregonezi et al. [26].
2
Facio Scapulo Humeral Muscular Dystrophy (FSHD) is the third most frequent form of muscular
dystrophy. In Della Marca et al. [27], HRV was evaluated in 55 FSHD patients and evidenced the
presence of autonomic modifications, characterized by a slight increase in sympathetic activity and a
progressive decrease in parasympathetic output, which became more evident with the progression of
the disease.
NOTE: Dedicated research into genetic mutations that give rise to FSHD suggest that sporadic DUX4
expression is the primary factor for the onset and progression of this particular form of muscular
dystrophy; Haynes,Bomsztyk et al. [30]. However to consider the measurable reversal of the typical
FSHD related compromised motor/muscular functions of this reliable FSHD patient who is the focus of
this study within 4 days of NPT, as previously outlined in Ware et al. [1], followed by similar outcomes
for other FSHD patients during a 4 day Ken Ware NPT regime as recorded, Ware [31], raises valid
questions over the reliability of reports on findings that nominate DUX4 mutations as being the
primary contributing factor for the onset and continual progression of losses of motor/muscular
functions and degeneration that is symptom topic of FSHD. It requires future investigation as the
obvious question is; if mutation in DUX4 is the controlling factor in FSHD, how is it possible for the
behavior of DUX4 to be altered in such small time frames during the 4 day NPT process to allow for
the significant reversal of high order FSHD symptoms. The FSHD patient who is the focus of this
report has continued to make progressive functional improvements through the continued application
of non-invasive NPT protocols in defiance of the DUX4 paradigm.
Emery-Dreifuss Muscular Dystrophy (EDMD) is genetically heterogeneous since it may be caused by
a mutation in the STA gene encoding emerin (X-linked inheritance) or as AD trait determined by
mutations in the LMNA gene encodinglamin A/C. Scintigraphic studies [28] evidenced a diffuse and
severe decrease in accumulation of MIBG in the heart, suggesting an abnormality in the cardiac
sympathetic nerve terminals in the patient.
Miyoshi muscular dystrophy (MMD) is caused by mutation in the gene encoding the protein dysferlin.
In 1994, Tomoda et al. [29] performed accurate autonomic studies in 2 MMD affected girls, including
laser doppler flowmetry, study of the component analysis of the cardiographic R-R interval and
sympathetic skin response (SSR). They demonstrated marked abnormalities such as sensitive
vasoconstrictive response, a suppressed peak of low frequency components, and an absence of
SSR, compared with healthy controls.
We retain to have delineated a sufficient picture of the importance of evaluation of HRV and ANS
disfunction in muscular dystrophy. The present paper is a case report. We give the results on ANS
renormalization in a severe case of muscular dystrophy after the treatment that is introduced by Ware
and discussed and analyzed in detail by us elsewhere [1].
2. MATERIALS, METHODS AND THE NPT TREATMENT
As it was outlined by us in detail in Ware et al. [1] the case is of a subject 60-year-old-male suffering
for more than 30 years from the rare form of Muscular Dystrophy, Facioscapulohumeral Muscular
Dystrophy (FSHD). (FSHD) is a genetic muscle disorder in which the muscles of the face, shoulder
blades and upper arms are among the most affected. EEG, ECG, EMG were all recorded
simultaneously using BioRadio 150 technology. EEG was recorded in channel 8 with electrodes
placed at C3-F3 of the left hemisphere. ECG was recorded in Channel 7 with electrodes placed at V1
and V2. An appropriate software by BioPac sytem enabled us to obtain the relative R-R intervals for
HRV analysis. The patient was recorded for 5 minutes at rest before therapy in order to perform
quantitative estimations before and after the treatment. The exercise equipment used is specialized
exercise equipment supplied to the International NeuroPhysics Functional Performance Institute by
“Synergy Fitness (http://synergyfitness.com.au/gallery/15/Synergy_4_Pin_Loaded) and was described
in detail min [1]. In sub-stance this treatment that we have called the Ken Ware NeuroPhysics
Therapy (NPT) does not involve physical manipulation of the treated individual. Usually early phase
equipment is the leg press (which may be substituted with the seated leg curl), lateral pull down, and
pectoral exercise, the pec dec. Each exercise machine is loaded with a very light weight, mostly
representative of the equipment’s minimum lifting loads. Most movements have only two degrees of
freedom (df) (up-down or forward-back). Only one machine used in the early phase of treatment has 4
3
df, namely the pec dec. The initial treatment in our case, involved four models of variable resistance
exercise equipment, which were selected in consideration to the level of ability of the patient. No
stretching or warm-up exercises are permitted to preserve a patient’s system normal resting state,
innocent of perturbations until the (NPT) starts. The initial assessment session(s) evidences the
patient’s chronic system condition and how it interacts with and evaluates its environments in general.
The specific activities and equipment used at the beginning of treatment are expanded after initial
sessions’ effects area assessed and systematically modulated as necessary, through the unique
applications and qualities of NPT. In the next treatment phase, additional exercises that are slightly
more complex to perform, but with still very lightly weighted, are added to the patients program, again
depending on ability or disability. Some of these pieces of equipment have many ( df); the handles are
attached to cables that can move in any direction. The patients are at this time (re) introduced to so-
called “cardio” exercises (this nuisance term promoted by the exercise industry un-holistically implies
the cardiovascular system is separate, requiring its own form of exercise). In the reinforcement and
maintenance phase of the program, additional equipment with prescribed repetitions and weights is
introduced. Individuals in treatment perform the following activities with trained coaching support. In
conclusion, we may identify six phases of the treatment.
The first phase is devoted the subject to learn to relax physically, mentally, and emotionally.
The second phase is finalized to adjust position for proper contact points and symmetrical balance on
equipment.
The third phase is devoted to maintain up right posture.
In the fourth and fifth phases, the subject closes the eyes and performs ultra-slow movements.
Finally, the sixth phase is devoted to form and to operationalize the intention to distribute effort and
energy throughout the brain/body system. For further detail the reader is addressed to ref. [1].
3. THE RESULTS
As previously outlined, we performed HRV analysis starting with an ECG recorded at 960 Hz. We
used linear and non linear methods. As previously discussed, studies in literature have evidenced
relationship between low-frequency power (Power Spectral Density, PSD) of heart rate variability and
muscle sympathetic nerve activity (MSNA). We studied HRV before, during the treatment, and days
after the treatment.
By using Fourier transform (FFT or DFT), one obtains balancing inspection of the ANS modulation in
HRV in the three VLF, LF and HF bands. The VLF Band relates hormonal activity, thermoregulation
and possibly the rennin-angiotensin system, the LF band relates mainly the orthosympathetic activity
and, finally, the HF band relates instead the parasympathetic activity in the frequency domain.
Let us explore the DFT results evaluating the ANS condition of the subject at rest before starting the
treatment. We identify this at rest section as Lat Pull1bt. Let us give a look at the tachogram and to
the DFT spectrum as they are reported in Fig. 1.
4
Fig. 1. Tachogram obtained after ECG recording, PSD Spectrum (msec2/Hz) with three
delineated bands, VLF, LF and HF
Fig. 1 evidences that we are in the presence of a subject with very exaggerated beat – to - beat
variations and the presence of an arrhythmia to be classified. In the PSD spectrum peaks are
represented in the three bands all having abnormal amplitudes in the three bands respectively.
Let us give a look at the results of the quantitative analysis. The bpm (beats per minute) of the subject
resulted to be 68.7 bpm where we consider a normal range included between 59 and 96 bpm. Soon
after we examined the variance results from the reconstructed tachogram starting with the given R-R
time series. Usually, we attribute a great relevance to such index since it informs us directly on the
variability induced on the heart rhythm by the ANS modulation and on the availability of the sinus node
to respond to ANS activity. The value resulted of 135.5 mseconds and we adopt as normal range the
interval 20 - 60 mseconds in the age range of 50 - 70 years old. This result indicated an exaggerated
variability in heart rhythm induced from some kind of arrhythmia. The Total Power (PSD) resulted to
be 18,397 msec2/Hz with natural logarithmic value of 9.81. Usually, we consider as normal range the
interval 6.0 - 8.1. Therefore, we concluded for the presence of an exaggerated modulation total value
exceedingly the normal prefixed value. The VLF band gave us the value of 3207 msec2/Hz with Ln
value of 8.07 and the normal range is considered usually to be between 4.5 and 6.4. The obtained
value results showed exaggerated exceeding of the established normal range ...
The LF band gave us a value of 7565 msec2/Hz with an Ln value of 8.93 while the normal range is
included between 5.0 and 6.9. Finally the HF band gave us a result of 6956 msec 2/Hz with an Ln
value of 8.84 in the normal range included between 4.5 and 6.7.
Also all the linear time indexes results indicated exaggerated out of normal range.
They are reported in Fig. 2.
Fig. 2. Linear time indexes of the subject at rest
The context previously delineated configures a net ANS disfunction but to clarify the problem more
deeply we need to add further investigations. This was the reason to apply and refer to the data
generated by the CZF method that we introduced in literature as explained in detail in Conte et al. [4],
Conte et al. [5], Conte [6]. The CZF method enables us to develop a detailed analysis of the heart
rhythm variability in the frequency domain evaluating in detail the variability induced from
orthosympathetic and parasympathetic modulating activities respectively. The results are reported in
the Fig. 3 and Fig. 4.
5
Fig. 3. Time series of heart rhythm variability and values of variability (msec/Hz) in the case
with absolute value (for de-tails see [4-6]). The CZF method
Fig. 4. Time series of heart rhythm variability and values of variability (msec/Hz) in the case
without absolute value (for details see [4-6]). The CZF method
The case of the CZF application with absolute value quantifies variability between each pair of
subsequent values taking the result in mseconds while the case without absolute value quantifies
such variability but accounting if the subsequent time beat value is greater or less of the previous one.
The first estimates the value of the beat to beat difference. The second approach estimates in addition
if such interval increases (acceleration of beat to beat interval) or decreases.
In red we have time dynamics and on the right we have Fourier analysis of the heart rhythm variability.
The important result that we obtain with this kind of analysis is that it evidences that in the LF band we
have a strong reduction of variability and this is to say that we have a strong dominance of
sympathetic activity while the HF band that of course characterizes the ANS modulation of the
parasympathetic activity remains in the normal range. Therefore, the results appear to be
unquestionable. The ANS heart rhythm modulation of this subject is affected from a hyper
orthosympathetic activation. This is in agreement with the results of other authors as we discussed in
detail in the introduction.
At this point it is instructive to examine also the histograms computed one time for the heart rate
(bpm) and one time for the R-R intervals. We give the results in Fig. 5 and Fig. 6 respectively.
6
Fig. 5. Histograms of HR for the subject at rest
The analysis of HR histograms also reveals the subject is affected by a profound arrhythmia with HR
values violating a normal Gaussian distribution. Mean, Median and Mode are out of the normal
requirement in a normal distribution and we observe substantially a distribution peaked about three
central values, a peak in HR about 76 (bpm), another peak about 128 (bpm) and a final distribution
about 180 (bpm) The same evaluation is obtained obviously when we consider the distribution of the
R-R values as reported in Fig. 6. We have substantially a plurimodal distribution that is always
indicative of a serious happening arrhythmia in the examined subject.
To complete the analysis we may apply the Poincaré method. We give the results in Fig. 7.
7
Fig. 6. Histograms of R-R intervals for the subject at rest
Fig. 7. Poincaré Plot relating the subject at rest
This is a well know representation in bi-dimensional phase space. Also its interpretation, obtained on
the basis of the distribution of the points and of the estimated values for SD1, SD2, ellipse area and
centroid, is well known. As confirmation also of the results previously obtained, this is a clear case of
atrial fibrillation.
8
In detail, the examination of the Poincaré plot given in Fig. 7 in conjunction with the results previously
given, enables us to classify the kind of arrhythmia of the subject. In the plot RR n/RRn+1 we identify
two locations out of the ellipse, one located in the range 310 - 496 ms and the other in the range 748 -
868 ms. The Sd1 value is reduced to about 51 ms or 9.17 n.u. (orthosympathetic activity) against the
284.63 ms or 46.66 n.u. for SD2 with SD1/SD2 = 0.1966 strongly distant from a condition of
acceptable balance parasympathetic/orthosympathetic modulation. The Ellipse Area is strongly out of
a normal range. This picture enables us to conclude that the subject is suffering of a persistent
arrhythmia to be classified as atrial fibrillation.
We may now conclude our examination by using non linear analysis, estimating in detail Approximate
Entropy (ApEn), Sample Entropy (SnEp), and the Detrended Fluctuation Analysis (DFA). They are
given in Table 1.
Table 1. Estimation of approximate entropy, of sample entropy, and detrended fluctuation
analysis in the subject at rest
Approximate Entropy (ApEn) 0.194
Sample Entropy (SampEn) 0.127
Detrended fluctuation (DFA): a1 0.963
Detrended fluctuation (DFA): a2 1.536
The results are given in Table 1. It is confirmed the profound condition of great cardiovascular risk of
the subject and his serious ANS disfunction. This condition is clearly evidenced when considering the
values of ApEn and SampEn that are so distant from a valuable value near to 1. Fortunately long as
well as short range correlations as estimated by the DFA still remain in the range of an acceptable
value.
We may now proceed to examine the question of the treatment of the subject connecting in this
manner the great interest from the general neurological interest. After Ken Ware NPT, the previously
mentioned indexes change as it follows.
The Fourier transform: The subject has now 72 bpm. The most important thing is that the variability
is now of 30 mseconds that is in the normal range. The total power (PSD) is now 902 msec2/Hz (Ln =
6.8) (against the value at rest of 18,397 msec2/Hz) and is now in the normal range. The VLF band
gives a value of 464 msec2/Hz (Ln = 6.13) and is in the normal range, the LF band is 313 msec2/Hz
(Ln = 5.74) and is now in the normal range, the HF band is 94 (ln = 4.54) and still is in the normal
range. In Fig. 8, we report the tachogram and the Fourier spectrum and both the behaviors re-enter
now in the normal regime.
Please replace this figure with clear view
Fig. 8. Tachogram obtained after ECG recording after the treatment PSD Spectrum (msec2/Hz)
with three delineated bands, VLF, LF and HF
Let us start examining the results obtained by Fourier Transformation and given in Fig. 7.
9
Looking at the Fig. 8, we may appreciate under the neurological profile the valuable improvement
induced from the Ken Ware NPT treatment. The ANS modulation has totally recovered.
Also the values of the time linear indexes now result in their normal range as shown in Fig. 9.
Fig. 9. Values of linear time indexes in HRV analysis after the treatment
Also the values of the CZF method result to be totally in the normal range. It is very interesting to
examine the histograms and the Poincaré Plots. The histograms are given in Fig. 10 and Fig. 11, HR
and R-R intervals respectively.
Fig. 10. HR-Histogram distribution of the HR values after NPT treatment
The histograms now follow the expected normal distribution that we observe in a subject with missing
disfunctions.
Evaluating all such results, we may conclude that the ANS has totally recovered its modulating
function.
Let us look at the Poincaré Plot in Fig. 12.
10
Fig. 11. R-R histogram distribution of the RR values after NPT treatment
Fig. 12. Poincaré plot of the subject after NPT treatment
Looking at Fig. 12, we observe that the subject has totally recovered the characteristic distribution at
cigar of normal subjects also if still remain some extra-distribution episodes and the form of the cigar
is not so largely extended as in a health normal subject. Sd1 and SD2 values are however in the
normal range of values as well as the values of the ellipse area and centroid. In detail, the SD1 and
the SD2 values, relating the ANS modulation, enter now, as said, in the range of normal values with a
correct balancing parasympathetic-orthosympathetic action, that in fact results to be Sd1/SD2 = 0.848
11
(against the value of 0.193 at rest before of the treatment) with SD1 = 43.94 ms and 5.22 n.u. and
SD2 = 51.79 ms and 6.15 n.u.
Finally, from a neurological point of view, the most interesting result is given by using non linear
indexes. Let us report the results relating the Approximate Entropy (ApEn), the Sample Entropy
(SnEp) and the Detrended Fluctuation Analysis (DFA).They are given in Table 2.
Table 2. Estimation of approximate entropy, of sample entropy, and detrended fluctuation
analysis in the subject after the NPT treatment
Approximate Entropy (ApEn) 0.887
Sample Entropy (SampEn) 0.913
Detrended fluctuation (DFA): a1 0.802
Detrended fluctuation (DFA): a2 0.973
All the results are now in the normal range.
4. CONCLUSIONS
This is a case report of ANS analysis in a subject affected by muscular dystrophy. The HRV was
analyzed by using linear and non linear analysis. The analysis performed initially on the subject at rest
and before the treatment by the linear time indexes and traditional FFT were exceedingly of the
normal range.
The use of the CZF method, histograms and Poincaré plot evidenced that the subject started with a
strong orthosympathetic against parasympathetic unbalance and atrial fibrillation. After the treatment,
the patient evidenced that all the standard HRV indexes re-entered in the normal range of values in
consideration of his starting arrhythmia, and that in particular balancing orthosympathetic-
parasympathetic correct modulation was recovered.
Under the neurological profile, we have to outline here the profound correlation existing in autonomic
regulation and muscular dystrophy. In particular, the use of standard methodologies in HRV analysis,
as well as the use of the CZF method and of non linear estimations, enables us to estimate and to
correlate the ANS dysfunction with the severity of the muscular pathology. In fact, the results on EMG
analysis, published elsewhere [1] and relating to this subject, evidenced that he had a very serious
initial compromission that of course resulted to improve under the profile of the clinical and
pathophysiological conditions after Ken Ware NPT.
COMPETING INTERESTS
Authors have declared that no competing interests exist.
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31. Facioscapulohumeral Muscular Dystrophy (FSHD) Endurer Michelle Mackay Expresses
The Positive Benefits of NeuroPhysics Therapy: https://vimeo.com/163920526
Biography of author(s)
Ken Ware
The International Neuro Physics Functional Performance Institute, Energy Circuit, Robina, Australia.
https://www.neurophysicstherapy.global/
He is the Founder of Neurotricional Sciences Pty Ltd and NeuroPhysics Therapy and Research. He has been in private practice
for more than 30 years, engaging in independent and collaborative therapy based research in an effort to advance the global
understanding of the real potential the human psychophysical system has for 'self-healing' of complex psychophysical diseases
and disorders'- when given the right sets of initial conditions. His long-term devotion to and successes in assisting others to
optimize their mental and physical health has become internationally appreciated and portrayed though several international
and national media programs. His unique methods saw world renowned paraplegic wheelchair athlete John Maclean take his
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first unassisted steps in 25 years in just 3 days of NeuroPhysics Therapy, as detailed in the Sixty Minutes program titled ‘No
Limits’. He has presented his unique research and findings at various International Science Conferences, including
Neuroscience, Physics, Psychology and Life Sciences, covering a very broad scientific audience. He is co-author in relative
publications based upon the research and findings which are published in ‘Frontiers in Clinical Physiology’ - ‘World Journal of
Neuroscience’ – ‘World Journal of Cardiovascular diseases’. He is also a former Mr. Universe 1994, National powerlifting and
Bodybuilding champion and record holder. He was the recipient of Her Majesty, Queen Elizabeth’s’ ‘Australian Sports Medal’ in
2000, in recognition of his personal contributions to the development of the Australian Sporting Culture. See
also https://www.neurophysicstherapy.global/ Sixty Minutes ‘No Limits’ https://www.9now.com.au/60-minutes/2014/clip-
cin5l1ysp009f0glhj0scp5pi/b6bd8628-7a4e-409b-b692-27d462441bed
Elio Conte
School of Advanced International Studies on Applied Theoretical and Non Linear Methodologies of Physics, Bari, Italy and
Department of Basic Sciences, Neuroscience and Sense Organs, University of Bari Aldo Moro, Bari, Italy.
He was born in Italy in 1946. He has been the professor of Theoretical and Nuclear Physics from 1972 (now retired) in the
following disciplines: Nuclear Physics, Theory of Radioactive Tracers, Mathematical modelling of kinetics of Radionuclides in
Humans, Environmental Radioactivity, Techniques of Radioactivity Measurements at the graduate School of Nuclear
Medicine ,University Aldo Moro of Bari, Italy where he has been also professor of Imaging Diagnostic , Informatics Technology
and Instrumentation in Medicine, at the master in Medical Radiology, professor of Theoretical Physics , of Environmental
Radioactivity and Mathematical Models of Radionuclide Metabolism in Humans at the Institute of Cybernetics in San Marino-
Italy., professor of elective didactic at the graduate course of medicine , department of Human physiology in Bari-Italy, on Linear
and non Linear Methods of Analysis of Biomedical Signals in Clinical Electrophysiology. Subsequently, he has been professor
of Clinical Psychophysiology and Linear and non Linear Methods of Analysis of Biomedical Signals at the post graduate School
of Psychiatry and , respectively, of Clinical Psychology at the department of Psychiatric and Neurological Sciences., of
Cognitive Models and of Neuroscience of the Emotions and On the use of the Biofeedback always at the University Aldo Moro
in Bari, Italy. Starting with 2009 he has been professor of Quantum Mechanics and Applications at Human Cognitive Level at
the accredited International at distance course on Quantum Cognition and of Linear and non Linear Methodologies in Heart
Rate Variability Analysis in the at distance accredited course on HRV analysis at the School of Advanced International Studies
on Applied Theoretical and non Linear Methodologies of Physics in Bari-Italy where he is also the director. He has had several
research grants at the National Research Council in years 1978-1995 and he has also had in these years the Direction of
several Laboratories of Research. He is member of the European Society of Cardiology (ESC) and component of the
international working group of ESC on Computers in Cardiology. He has particular competence in Quantum Mechanics, Chaos
Theory and Fractals, in application and analysis of electrophysiological signals in Humans. He is reviewer of the following
journals: Journal of Theoretical Biology, Annals of Biomedical Engineering, NeuroQuantology, Foundations of Physics, and
component of the Editorial Board of Austin Cardiology, Chaos and Complexity Letters, Advanced Research and Review in
Applied Sciences. He is the authors of about three hundred original published papers on international journals and about twenty
books.
Sergio Conte
School of Advanced International Studies on Applied Theoretical and Non Linear Methodologies of Physics, Bari, Italy.
He is a doctor in medicine and surgery, researcher at the School of Advanced Studies on Applied Theoretical and non Linear
Methodologies of Physics, Bari- Italy. He has a particular competence in the analysis of electrophysiological signals in humans ,
in the analysis and therapy of the disfunctions of the autonomic nervous system and in particular in Cardiology and Heart Rate
Variability, in Clinical Electrophysiology , Biofeedback transcutaneous Vagal stimulation, electromyography, Skin Conductance
Resistance, electroencephalography applied to Psychiatry, Neurology ,sports medicine therapy. He has also a particular
specialization in Chaos and Fractal theory starting with his graduate thesis entitled Analysis of the heart rate variability in the
frequency domain and through multifractals in subjects with type 2 diabetes mellitus affected by autonomic neuropathy in silent
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and full-blown clinical condition, in course of publication. He also attended a master's degree in applied nutrition and dietetics.
He is a collaborator of prof.ssa Ferda Kaleagasioglu, Department of Medical Pharmacology , University of Nicosia, Turkey in
the research for the study of HRV in subjects affected from hypercholesterolemia . He is the authors of 27 scientific publications
in collaboration appeared in international journals.
_________________________________________________________________________________
© Copyright (2020): Author(s). The licensee is the publisher (Book Publisher International).
DISCLAIMER
This chapter is an extended version of the article published by the same author(s) in the following journal.
World Journal of Neuroscience, 5: 162-173, 2015.
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