The Myth of Autism
How a Misunderstood Epidemic Is Destroying Our Children
Dr. Michael J. Goldberg
Elyse Goldberg
Dr. Ismael Mena
Copyright © 2011 by Dr. Michael J. Goldberg
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Table of Contents
Title Page
Copyright Page
FOREWORD
INTRODUCTION
1 - IN THE BEGINNING
2 - HOW CAN THIS BE ANYTHING BUT AN ILLNESS?
3 - CHANGING LETTERS: ADD? ADHD? MIXED ADHD? QUIET ADD?
4 - A HISTORY OF MEDICAL RESEARCH
5 - THE EVIDENCE
6 - NEUROSPECT: A NEW TOOL
7 - HOW EVALUATION AND TREATMENT BEGIN: THE GOLDBERG APPROACH
8 - MISTAKES AND MISDIRECTIONS
9 - THE ROLE OF ALLERGENS AND DIET
10 - TIPS TO HELP GET THROUGH THE DAY (DEPENDING ON BEHAVIORAL AGE)
11 - THE 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 nonspecific 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. This brain scan graphically illustrates the difficulty of normal brain function when “holes” are present.
NeuroSPECT scan 2.5 years later, after treatment with The Goldberg Approach (see chapter 7). While brain function is not normal, it is significantly improved.
Conclusion: this disorder and its complications can be changed.
FOREWORD
SINCE 1994, DR. MICHAEL GOLDBERG AND I have collaborated during my tenure as Director of the Department of Nuclear Medicine at Harbor-UCLA Medical Center in Torrance, California. The development of quantitative functional imaging techniques at our laboratory was instrumental for a long-standing collaboration in the challenging field of autism that Dr. Goldberg suspected from very early to be the consequence of an inflammatory 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 fifteen years we have participated actively in the development of quantitative software in order to assess brain perfusion by means of NeuroSPECT. The development of this imaging software has achieved results by comparing against a normal, age-matched database and expressed in standard deviations above or below the normal mean. (The 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. The colors red, pink, and white are 2, 3, and 4 standard deviations above normal mean, respectively). The 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). This highly accurate way of assessing brain perfusion, and therefore of brain function, is performed with the radiopharmaceutical Tc99m HMPAO, Ceretec, that provides stability of distribution and concentration in the brain parenchyma after the first two minutes of IV injection with a 1 percent / hour loss only.
THE MYTH OF AUTISM
The NeuroSPECT findings of cerebral cortical and subcortical perfusion in chronic fatigue syndrome (CFS) and in pervasive developmental disorders, namely, autism, have enabled us to define common features among these two disorders. 1, 2, 3, 4 I’ve included these findings, in brief, to give the reader a sense of the extensive research that informs The 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. There 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 fissure, 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 some times also hypoperfusion in the lentiform nuclei. The findings of subgenual hypoperfusion, anterior cingulate hypoperfusion, and increased thalamic perfusion are indicative of the presence secondary depression. The 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. These findings suggest severe inflammatory 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 significantly 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 deficit 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. They 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.
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sp; In 1995, Mountz, Tolbert, Lill, Katholi, and Liu5 reported their HMPAO findings in six children with severe autism and demonstrated with semiquantitative techniques temporal and parietal hypoperfusion with lateralization to the left hemisphere.
Georges, Costa, Coniz, Ring, and Ell reported in four autistic adults with Tc-99 HMPAO diminished rCBF in temporal and frontal lobes. The temporal abnormality appears to be confirmed mostly in adults, adolescents, and children suffering of autism. Thus, damage to temporal lobe in an early developmental stage may result in autistic manifestations.
The results are otherwise heterogeneous, denoting the presence of occipital hypoperfusion and cerebellar hypoperfusion mostly in the mesial aspects corresponding to the vermis area. This 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.
In Asperger’s syndrome the hypoperfusion defects appear predominantly in occipital lobes in the paramedial aspects and also in the cerebellar vermis.
In both chronic fatigue syndrome and autism the multifocal areas described—strikingly in the occipital lobes and always more extensively in temporal lobes—suggest strongly the inflammatory nature of both disorders, at vascular or cellular level (vasculatis versus cellular damage), thus opening expectations for early diagnosis and hopefully for treatment for these and other potentially related crippling diseases.
Ismael Mena, MD
Emeritus Professor Radiological Sciences
UCLA School of Medicine
Doctor Honoris Causa
University d’Auvergne, France
Department of Nuclear Medicine
Clinica Las Condes
Santiago, Chile
INTRODUCTION
WHEN I GRADUATED FROM UCLA MEDICAL School as a pediatrician in 1972, I was told if I had even one autistic child in my practice it would be unusual. Today most of my practice (250–300 active patients at any time) is composed of children and young adults diagnosed on the autistic spectrum, something we were never prepared for in medical school. General pediatrician practices now have between six and twelve children on the spectrum or with significant learning difficulties. I have heard from parents that their pediatricians were as unprepared as I was for this onslaught. So how is it that in thirty years the rate of “autism” in American children has gone from nonexistent to affecting nearly 1 percent of the total population or even higher?
To understand this change, let me give you some history. After I failed handwriting in the third grade, my teacher joked that I should become a doctor. Growing up, I enjoyed math and science, liked working with people and children, and did not envision myself in a lab with test tubes, so medicine, and in particular pediatrics, became my goal. I was extremely thankful to be accepted into UCLA Medical School, and I remain thankful for the wonderful training, for my internship and residency in pediatrics spent at Los Angeles County–University of Southern California Medical Center, with rotations through Children’s Hospital of Los Angeles. What I learned within these institutions gave me an excellent background in infectious disease, immunology, allergies, and more. The professors and the medical system to which I was exposed formed a dynamic, exciting system. There was still the expectation that a physician would use a combination of clinical skills and emerging technologies to help advance their understanding and take their research to new levels. Medicine was viewed as a frontier that needed to be consistently explored. This expectation was quickly dropped when it came to researching the causes of a rising disease called autism.
I entered private practice in Tarzana, California, with optimism and excitement. I built the third largest pediatric practice in the San Fernando Valley in Los Angeles. On a busy day, I could see up to fifty-two children. I would never let a sick child wait for an appointment if it were at all possible. I was taught preventive medicine in medical school; I was a good pediatrician if few children needed admittance to the hospital. The United States has evolved rapidly to a system where hospitals encourage admissions, however. Sadly, our collective “health” now boils down to dollars and cents.
Back then, for example, the standard practice was to postpone immunization for a child if he or she had a cold or a fever; parents would bring the child back for the shots once he or she was healthy. Economics now dictates that we limit visits. The more we bill at one time, the better, so let’s vaccinate them with everything we can give them while they are here in the office, all in the name of efficiency.
What new vaccines are being added to the roster of necessary childhood vaccinations, and why? How many readers are aware that the fairly recent decision by the Academy of Pediatrics in 1991 to give a hepatitis B vaccine in the newborn nursery1 (the most dangerous adjustment time in a baby’s life) was not made on the rational basis of medical efficacy but, in large part, due to the sticky issue of political correctness? It would not be PC to point out the limited number of cases where a child might be returning to a high-risk home, so let’s vaccinate all the infants. (For the record, I never have given that shot in the nursery, and many pediatricians now have no problem if parents elect to defer that vaccination until later.)
In the early eighties I met the woman who would become my wife. Around fifteen months after we met, Elyse developed a mysterious illness that at that time had no name—she was suffering sudden severe headaches, overwhelming fatigue, constant short-term memory issues and often periods of severe brain fog, fibromyalgia muscle and joint symptoms, fevers, and swollen glands. She visited various doctors all around the country, but she remained miserable and undiagnosed. Her blood work came back positive for an astounding number of viruses—almost every virus she was tested for excluding HIV. While she tested positive for Epstein-Barr, CMV (cytomegalovirus), HHV6, rubeola, and rubella, to name a few, it was rapidly obvious that while some of these titers might represent a potential virus to target, others were just false activation from a dysfunctional or misdirected (perhaps an unidentified virus or retrovirus) immune system. With these test results in hand, it seemed logical to suspect that some of these viruses (not as a new acute infection, but with the new concept of reactivation) were causing an impairment of her immune system or that somehow her immune system was making mistakes. Healthy patients do not run around with three or four active viruses in their bodies, or even multiple elevated titers—although some of the medical profession didn’t see any significance to the results of these blood tests, whether true viruses or just false titers, there was no direct evidence as far as they were concerned that this was causing harm (retrospectively this was a very large mistake).
She was sick and scared. As a physician I felt helpless, and we turned to prescription-grade vitamins and amino acids, thinking maybe they would help address any imbalances in her system. She took sixty-eight supplements a day, leaving little room for food with all the liquid she needed to swallow them. It was years before she would have a diagnosis. It is both sad and ironic that some of the same treatments tried on her then and others we never would have allowed (because they were potentially harmful) are being used on children today with about the same success rate of close to nothing. Of more concern is preliminary evidence (with formal study being planned) from NeuroSPECT testing showing potential increased stress to children’s brains when they undergo some of the more untested treatment ideas (including chelation, hyperbaric oxygen, and megasupplements).
We were married, and her symptoms continued. One night at dinner my son, around four years old at the time, said, “Dad, why are you sending Mom all over the country? Why don’t you just fix her?” This began my journey into the complex workings of the neuroimmune system and how it controls the body and our brains.
1
IN THE BEGINNING
IN THE EARLY EIGHTIES, I WAS starting to see a shift in the co
ncerns of the patients in my practice. Children were tired. Moms started complaining they couldn’t keep up or that they were feeling “spacey” or “zoney.” This was troubling, since early in my career I could safely joke that if a mother checked the fine print on her child’s birth certificate, she was not allowed to get sick until the child was at least eighteen years old. I had to stop saying that, since mothers were among the first being hit by what was facetiously being called the “yuppie flu.” Running viral blood titers (measurement of specific viral antibodies in their bloodstream/serum) on these patients was eye-opening. We were taught in medical school you were only supposed to have one active virus at a time, and “old” titers were supposed to be present but at low numbers. These patients were presenting with multiple viruses evident. A theory evolved that the immune system was so dysfunctional, it mistakenly thought it was fighting many viruses. How could so many moms and children be walking around and functioning with obvious evidence for some type of a severe autoimmune or viral disorder going on? After a few years, I attended the First International Congress on Chronic Fatigue in 1990 hosted by Dr. Jay Goldstein, who was beginning to define this new illness that had been given the official (but deliberately demeaning) name of Chronic Fatigue Syndrome by the Centers for Disease Control two years earlier in 1988. Dr. Goldstein and other clinicians were using the term postviral fatigue syndrome/chronic fatigue syndrome (the British still use the term ME—myalgic encephalomyelitis). The CDC made the official criteria/definition in 1988. Several years later, I had the honor of cohosting, and our journey toward understanding began in earnest. At these conferences I met many great doctors, including Dr. Nancy Klimas, who would finally offer some answers. Dr. Klimas sat my wife down and explained the immune system to her. She explained how it worked and, if you pushed the wrong buttons, how it didn’t.
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