The Myth of Autism: How a Misunderstood Epidemic Is Destroying Our Children, Expanded and Revised Edition

256 Pages·2014·1.1 MB·English

by  Michael J. Goldberg

Copyright © Michael J. Goldberg 2011, 2014
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10 9 8 7 6 5 4 3 2 1
Library of Congress Cataloging-in-Publication Data is available on �le.
ISBN: 978-1-62873-717-2
eISBN: 978-1-62914-063-6
Printed in the United States of America
CONTENTS
Foreword
Introduction
1. In the Beginning
2. How Can is Be Anything But an Illness?
3. Changing Letters: ADD? ADHD? Mixed ADHD? Quiet ADD?
4. A History of Medical Research
5. e Evidence
6. NeuroSPECT: A New Tool
7. How Evaluation and Treatment Begin: e Goldberg Approach™
8. Mistakes and Misdirections
9. e Role of Allergens and Diet
10. Tips to Help Get through the Day (depending on behavioral age)
11. e Future
Appendix A
A Case Study
Appendix B
Parent Stories
Appendix C
Patient Screening/Data Questionnaire for Autism/PDD/ADHD Used at Dr. Goldberg’s
Practice
Glossary
Notes
Although the focus of this book is the autism myth, a lot of the information, studies, and conclusions can be
applied to how we understand and approach ADHD variants, CFS, and CFIDS in children and adults (and to many
other nonspeci�c psychiatric and learning labels applied to many “special needs” children today).
Initial 3-D NeuroSPECT imaging on patient with autism (see appendix A). “Holes” are multiple areas of decreased
perfusion and decreased function in the brain. is brain scan graphically illustrates the difficulty of normal brain
function when “holes” are present.
NeuroSPECT scan 2.5 years later, aer treatment with e Goldberg Approach (see chapter 7). While brain function
is not normal, it is signi�cantly improved.
Conclusion: this disorder and its complications can be changed.
FOREWORD
S
1994, D . M G I have collaborated during my tenure as
INCE R ICHAEL OLDBERG AND
Director of the Department of Nuclear Medicine at Harbor-UCLA Medical Center
in Torrance, California. e development of quantitative functional imaging
techniques at our laboratory was instrumental for a long-standing collaboration in the
challenging �eld of autism that Dr. Goldberg suspected from very early to be the
consequence of an in�ammatory process and thus amenable for treatment. Over the
years, the epidemic increase of the prevalence of this dreadful condition has
strengthened this hypothesis.
During the last �een years we have participated actively in the development of
quantitative soware in order to assess brain perfusion by means of NeuroSPECT. e
development of this imaging soware has achieved results by comparing against a
normal, age-matched database and expressed in standard deviations above or below the
normal mean. (e color gray is normal range, whereas light blue, dark blue, and green
denote hypoperfusion at 2, 3, and 4 standard deviations below the normal, age-matched
mean, respectively. e colors red, pink, and white are 2, 3, and 4 standard deviations
above normal mean, respectively). e process entails normalization of brain volume in
order to establish the comparisons mentioned above, and this is achieved by means of
the Talairach technique, which is currently performed by automatic reconstruction, thus
reaching the ultimate goal of 100 percent reproducibility of results (Segami Corp.
Neurogam Oasis). is highly accurate way of assessing brain perfusion, and therefore
99m
of brain function, is performed with the radiopharmaceutical Tc HMPAO, Ceretec,
that provides stability of distribution and concentration in the brain parenchyma aer
the �rst two minutes of IV injection with a 1 percent/hour loss only.
e NeuroSPECT �ndings of cerebral cortical and subcortical perfusion in chronic
fatigue syndrome (CFS) and in pervasive developmental disorders, namely, autism, have
1, 2, 3, 4
enabled us to de�ne common features among these two disorders. I’ve included
these �ndings, in brief, to give the reader a sense of the extensive research that informs
e Myth of Autism.
Chronic Fatigue Syndrome
Patients with CFS present during the evolution of their chronic condition signs of
small vessel disease distributed in the lateral aspects of temporal lobes, premotor areas,
and parietal lobes reaching to the convexity of the brain and also in the orbital-frontal
areas of the frontal lobes. ere is also frequent involvement of temporal lobes in the
mesial aspects, in the projection of the hippocampus, and in the inferior gyrus at the
level of the temporal poles also. In the limbic system we observe diminished function in
anterior and posterior cingulate gyri and approximately in 50 percent of patients
hypoperfusion in the subgenual area thus implying the presence of a secondary
depression. Finally there is focal hypoperfusion also in both occipital lobes in the
interhemispheric �ssure, highlighted in this patient in the posterior view and inferior
aspects of temporal and occipital lobes. In the subcortical structures there is very
frequently deep hypoperfusion of the head of the caudate nuclei, less frequently in the
dorso-ventral posterior aspects of both thalami and sometimes also hypoperfusion in
the lentiform nuclei. e �ndings of subgenual hypoperfusion, anterior cingulate
hypoperfusion, and increased thalamic perfusion are indicative of the presence
secondary depression. e caudate and posterior cingulate gyrus hypoperfusion in the
presence of hippocampus hypoperfusion are indicative in other patients of cognitive
dysfunction, which is a frequent symptom in CFS. ese �ndings suggest severe
in�ammatory changes involving, temporal, frontal, parietal lobes, occipital lobes, and
frequently caudate nuclei involvement denoting cognitive impairment.
Autism
Quantitative rCBF absolute measurements with Xenon 133 were found to be
signi�cantly higher than normal in autistic children, with maximal values in the frontal
lobes and visual cortex. Minimal perfusion was observed in the temporal lobes.
Decreased rCBF was also noted in the cerebellum and occipital lobe. Tc 99m HMPAO
images demonstrate qualitatively increased frontal (subgenual) perfusion, and also
temporal, occipital hypoperfusion. In this patient increased subgenual perfusion is
indicative of a comorbidity of attention de�cit disorder.
In other patients we have demonstrated with Tc 99m HMPAO imaging increased
frontal perfusion, and also temporal, occipital, and cerebellar hypoperfusion. In the
basal ganglia of these patients very frequently there is normal perfusion and function of
thalami, caudate nuclei, and lentiform nuclei. ey may also have many symptoms
consistent with OCD characteristics, associated with the following areas of dysfunction,
namely, inferior frontal, anterior poles of the temporal lobes (amygdala), and posterior
cingulate gyri, demonstrating increased perfusion of these areas.
In 1995, Mountz, Tolbert, Lill, Katholi, and Liu reported their HMPAO �ndings in six
children with severe autism and demonstrated with semiquantitative techniques
temporal and parietal hypoperfusion with lateralization to the le hemisphere.
Georges, Costa, Coniz, Ring, and Ell reported in four autistic adults with Tc 99
HMPAO diminished rCBF in temporal and frontal lobes. e temporal abnormality
appears to be con�rmed mostly in adults, adolescents, and children suffering of autism.
us, damage to temporal lobe in an early developmental stage may result in autistic
manifestations.
e results are otherwise heterogeneous, denoting the presence of occipital
hypoperfusion and cerebellar hypoperfusion mostly in the mesial aspects corresponding
to the vermis area. is later observation correlates with reports in the literature of
atrophy of the cerebellar vermis demonstrated by MRI technique. Further heterogeneity
in our group of patients is demonstrated by apparent comorbidity with OCD and
ADHD in these children and their typical presentation of increased perfusion in lateral
frontal lobes.