Dr. Mena also noted a phenomenon of “hyperfrontality” (increased blood flow in the frontal lobes), which was common in young children, a routine finding in the old-fashioned hyper-ADD child. It quickly became apparent that the key to “neuroimmune” was the obvious shutting down of blood flow, shutting down of function.
This compares to what happens when a child or adult has a cold/upper respiratory infection, a virus we know does not go to the brain. We will feel “zoney,” “spacey,” tired, and achy. That is our immune system shutting down blood flow to key parts of the brain (the temporal lobes, limbic system, amygdala) to “protect” them. Then when we’ve recovered, four to seven days laters, those areas open back up, the immune system calms down, and we feel better physically and mentally.
Upon scanning adults and then children who have done many anecdotal, proposed therapies, it became very disturbing to find either diffuse areas of hypoperfusion or multiple areas of hyperperfusion in areas of the brain that had up to that time always been presenting as normal, not directly affected by this disease process itself. For me, it has been a very upsetting but striking confirmation that doing things in a random manner to the whole brain (or body), doing procedures that would never be considered physiologic in a child (or adults) not only is unlikely to help, but also has the possibility of creating additional harm or dysfunction.
NeuroSPECT: Assessment of Abnorma1 Distribution of Rcbf in CFIDS versus “Autistic Syndrome Children.”
Michael Goldberg, Ismael Mena, Bruce. Miller, and Carmen Thomas.
Dept. of Nuclear Medicine, Imaging Center, Harbor UCLA Medical Center, Torrance, CA36.
The study was done to compare our preliminary NeuroSPECT finding in twenty-five children diagnosed “autistic syndrome/PDD” with thirteen children previously scanned with CFS/CFIDS. This was compared to a normal database.
In the findings points that stood out were that “autistic” children often had increased blood flow in the frontal lobes (part of this may be physiologic in young children), and there were characteristically low areas of flow in the temporal and occipital lobes and cerebellum. These changes were significant compared to normals. Interesting, comparatively, the children with CFIDS also showed temporal-lobe hypoperfusion (as noted previously, a key point, the literal hallmark, of this disorder), along with decreased flow in the parietal lobes and part of the frontal lobes.
With this striking insight, it was our conclusion “that the common observation of temporal lobe hypoperfusion in adults and children with CFS/CFIDS, may define ‘autism’ as a disorder of impaired relations with the surrounding environment determined by the temporal hypofunction leading as a consequence to a diaschetic hypofunction of visual cortex and cerebellum.” In English that means we were looking at a significant overlap of areas of dysfunction in the brain between these disorders, providing us with an objective, explainable reason for the dysfunctions being reported “mysteriously” in these children. We were looking at anatomical markings, defining autism/PDD dysfunction, correlating to models proposed by behavioral neurologists. We tried to encourage further evaluation of this phenomenon with a focus on the likely immune dysregulation that could be causing it. It was our hope that the NeuroSPECT could open the door a more physiologic/medical approach to these processes in children. Sadly that is not what has occurred.
With this research, back in 1995, I put forth at an “autistic” conference our emerging hypothesis: Temporal lobe dysfunction is the primary source of dysfunction in many/most cases of autism, CFS/CFIDS, NIDS, and some/ many cases of ADHD. The decrease in blood flow and function is secondary to immune system “activation” and/or “dysregulation”.
With refinements and the recognition for the increased and disturbing role of a complex viral process (still with immune system primary, the virus/ viruses secondary to that), the statement remains a very realistic, very logical explanation for understanding and dealing with this disaster. Why the “system” has not decided so is the enlarging mystery and ongoing disaster.
Our early work culminated in 1999 with the publication of our finding on NeuroSPECT showing the similarities and differences of the disorders being called autism, ADHD, OCD, and other neurocognitive disorders including CFS/CFIDS in adults and then children. I remain very thankful for meeting researchers like Dr. Ismael Mena, Dr. Bruce Miller, then years, now decades ahead of their time. In these various learning fields today, without documented imaging, newer ways to document and understand the differences, the confusions and potential mistakes with therapy remain abundant. With increased incidence of learning disorders comes a greater need to understand and define the dysfunction in these children by objective, “functional” quantifications.
Being exposed to the use of NeuroSPECT early opened the doors to an understanding of these evolving strange disorders called autism, ADHD, OCD, and more. In these seemingly mysterious, supposedly development-based disorders, there were similar patterns of significant frontal and temporal lobe dysfunction. Perhaps some of the misdirection, the mistakes begin made today are explainable by the ongoing lack of insight in research studies to what is really happening in the brain, what is changing or not changing with medication. Thanks to the work with NeuroSPECT, experts way beyond me were able to say early on that something was wrong, that our findings were not consistent with the ideas, the images of “autism.” Early along it became obvious that in the hands of a researcher like Dr. Bruce Miller, one could understand and explain areas of the brain that were working and not working, and the dysfunctions that resulted. I wonder how we can now be in the twenty-first century and yet not demand data like this on any study regarding cognitive dysfunction and any study looking at what we call “neurotropic” agents.
The objective, “functional” quantification by NeuroSPECT offered an easy explanation for the progressive process of the autistic syndrome that occurs frequently between fifteen and twenty-four months of age. It is this immune-mediated, abnormal shutdown of blood flow in the brain that affects the language and social skills area of the brain and central nervous system function. The dysfunction/lack of blood flow can eventually lead to injury of nerve cells. This evolves into part of the explanation for the increasing number of children with abnormal brain waves and the large numbers of autistic syndrome children having concurrent seizures and epilepsy. (See the discussion on seizures.) Consistently on NeuroSPECT (in early studies, with “clean” children, those not on other therapies or remedies) we saw the following: decreased left temporal lobe function (explaining and pinpointing areas of severe speech and language dysfunction), and decreased right temporal lobe function explaining areas needed for social interaction and social integration with our environment and others. Finally (to our surprise) we repeatedly saw abnormal cerebellar involvement, explaining the appearance of so many children with usually fine and sometimes gross motor difficulties. As noted elsewhere, the issues of fine or gross motor abnormalities were not expected or discussed in the literature of the 1940s, 1950s, or 1960s, or ever noted in expected finding or criteria for autism, a major indicator that this is not the same thing.
We found autism, pervasive developmental disorder (PDD), attention deficit hyperactivity disorder (ADHD), and obsessive-compulsive disorder (OCD) involve significant frontal and temporal lobe dysfunction. This conclusion is based on NeuroSPECT work now in progress on children afflicted with these disorders. We have been using NeuroSPECT to image cerebral abnormalities of perfusion/function in autism, ADHD, OCD, and other neurocognitive disorders. With the increased focus and presentation of children labeled autistic syndrome/PDD has come a greater need to understand and define the dysfunction in these children by objective functional quantification, which is now possible with new imaging technology such as NeuroSPECT.
This offers an explanation for the process of the autistic syndrome that occurs sometime between fifteen and twenty-four months of age. The immune-mediated, abnormal shutdown of blood flow in the brain affects the language and
social skills area of the brain and central nervous system function. The dysfunction caused by the lack of blood flow can eventually lead to injury of nerve cells. This is a possible explanation for the abnormal brain waves and the large numbers of autistic syndrome children suddenly being labeled as Landau-Kleffner.
We are seeing abnormal NeuroSPECT scans. There is hypoperfusion in the temporal lobes (primary dysfunction), hypoperfusion in the occipital/ parietal lobes, and hypoperfusion in the cerebellum. Sadly we are finding scalloping and thinning (in some); this is actual loss of brain tissue and explains LKS and abnormal EEGs. These same children and adults have normal MRIs, and normal CAT scans.
With the NeuroSPECT, one could begin to explain various issues of learning difficulties and multiple variations of attention deficit dysfunction beginning to evolve at that time. (As noted earlier, the variations are now far more common than the classical, typical hyper-ADD child; again maybe because this has nothing to do with our original ideas of ADD/ADHD.) A key point from this work was that most of these children had normal MRIs and normal CAT scans. How can we expect to obtain new information and develop a new understanding of these disorders if we are in the twenty-first century but want to continue to use twentieth-century tools—tools, which became very good at defining the black-and-white structure of the brain, but do not give any idea of how those apparently intact areas are really functioning? Without that insight, without that understanding, this book—and the real chance to understand these mysterious disorders now, not in another decade or two—would not be possible. It is my hope that this book leads to a demand for technology application and answers now for so many children and adults with these interconnected disorders.
7
HOW EVALUATION AND TREATMENT BEGIN: THE GOLDBERG APPROACH
Intro to Therapy: An Overview of The Goldberg Approach
MY BACKGROUND IN BASIC SCIENCE, CLINICAL logic, research, and the ongoing support and evolution for the idea of a complex neuroimmune, complex viral disorder / NIDS has evolved into an overall approach to therapy called The Goldberg Approach. This approach has evolved over many years and is a starting point to evaluate its application for patients with autism/ASD, ADHD, and chronic fatigue (in a more formal protocol, it can potentially create an expedited pathway to evaluate new pharmaceutical agents or other potential therapeutic choices). Until new pharmaceutical solutions evolve, this has become a multistep (similar to multiantibiotic therapy now common for ulcers) combined therapy approach.
Step one is always dietary elimination (including most nonpharmaceutical supplements). The key to helping the immune system is not how many different products and things can one throw into it, but rather how many negative stimuli (primarily foods or other non-pharmaceutically pure ingested products) you can remove from the immune system, in turn allowing the immune system the first chance to start to become healthier. While so many studies focus on the effects of pharmaceuticals, they fail to realize that food may be the biggest drug of all.
It is important to remember that since this disease did not start metabolically, you are not going to cure a patient by dietary manipulations alone, but it is a major first step to helping a child (or an adult) with these disorders (and likely many others).
The next step, dependent on lab workup and clinical history, is prescribing an antiviral for many of the patients. The antivirals are in what we call antiherpes medications. This is partly because, as presented, potential CNS herpes viruses are obviously playing a very large role in this disorder. Unfortunately, to this day, many in the research world will debate whether the proof is absolute, even though the literature and markers overwhelmingly confirm the likely presence of herpes-related viruses. These specific antivirals are also safe to administer to children because of their mode of action (they work on a metabolic point that the Herpes virus needs for survival), as long as they are monitored and dosed appropriately. Adults with Herpes remain on them their entire lives with little if any side effects. In further research trials there will be studies of stronger antiherpetic antivirals, and if indicated, potentially other types of antivirals. The key in choosing treatments for patients with this disorder is that they must be safe.
The third step is administering an antifungal (the use of antifungals is still of great debate in some medical circles because of all the misconceptions and misrepresentations). Based on work in adults and children, we know that when the immune system is stressed, something we call delayed hypersensitivity often is not working right (delayed hypersensitivity, often called tuberculin-type hypersensitivity, is our body’s delayed response to a threat—a rash from poison oak or a reaction to an allergy skin test or tuberculosis skin test are all examples of how our healthy immune system is expected to react). When delayed hypersensitivity is not working correctly, since it is the key part of our immune system that handles yeast and fungal issues, there is a place for a potential yeast or fungal overgrowth in any patient. While a yeast overgrowth in theory may add to symptoms of fatigue, achiness, spaciness, and more the exact mechanism (a general GI overgrowth, interference with absorption versus possible release of a toxin) is debatable even today. Doing trials looking at markers based on the immune system—not based on blood, stool, or urine testing because of their notorious inaccuracy—there is a way to formerly evaluate and document when an excess of yeast, a yeast overgrowth, is likely. By administering antifungals to correct this overgrowth (again used correctly, chosen cautiously and monitored carefully), we can help balance another stressor to the immune system in patients.
Finally, based on clinical symptoms, and the now common denominator in these patients of temporal lobe hypoperfusion (to different degrees), comes the usage of an SSRI. This comes as step number four, since an SSRI was not originally designed to treat immune system dysfunction or viruses (if present). After diet control, antiviral, and if indicated, an antifungal, then I begin to look at using an SSRI. As explained many times to parents and patients, I do not use an SSRI, nor should trials be done, to treat a particular symptom (though helping temporal lobe function can help many “symptoms” seen as part of this dysfunction), especially to try to control behaviors and/or calm down or sedate a child—but because with the research and work that has evolved it is obvious that most of the origin of the symptoms and dysfunction is based in the temporal lobes of the brain. As confirmed repeatedly on NeuroSPECT, they are under working, under perfused—conveniently the temporal lobes are primarily serotonin mediated—it is logical to say that if you could take an agent and make the serotonin that is produced stay around longer constructively, that can and does help restore function to those areas (which in turn can address some “symptoms” but in a very physiologically healthy manner by helping restore function). And that is what SSRIs do. Unlike old-fashioned antidepressants that literally could sedate or affect the entire brain, an SSRI selectively works to block the reuptake of serotonin being produced naturally. Done judiciously and correctly, this has turned out to be an extremely important and positive step of The Goldberg Approach. This is visible and can be confirmed on repeat Spect scans, showing reversal of the low perfusion, and normalization to the areas of the brain that were not working right before therapy. One of the most dramatic presentations is that of a child (multiple children in fact; see case studies at the end of the book) who could not speak, but as their temporal lobe normalized, with good appropriate speech therapy, the child regained speech and language function. Not just younger children, but older children too.
The approach also encourages the role (as will be discussed) for potentially adjunctive, supportive therapies based on the individual and their particular testing or markers. Examples included usage of antibiotics for a potential strep infection, agents to help balance frontal lobe hyperperfusion such as Strattera or Wellbutrin, Tenex (often indicated for basal ganglia, lower brainstem hyperperfusion), and selectively a few others. Since the focus is children, the focus must always be on a specific need or indication, and the p
otential for long-term safety (or harm).
Combining the above steps of therapy, it has been my repeated pleasure to see children return to levels of function never predicted before. (As I have noted repeatedly to a happy parent, that success is expected and only possible in terms of a disease, never in a developmental disorder). While not every child is where I would like (the urgency to build and improve on The Goldberg Approach), I have many, many children not only in regular academic classes (at all grade levels), but children who are in honors, have graduated high school with honors, who are now in college. In a now healthy manner, these children are leading lives as my wife once commented “we would all like for any of our children.” The joy of the success stories is enormous, but cannot make up for the sadness that we continue to live in a world that does not believe we are “losing” children of that potential, but that rather mistakenly subscribes to the myth of “autism.” While not yet simple or easy, every child deserves this chance, every parent and family deserves a right to believe and hope. A key point, is in every patient who has stayed with me (unfortunately, especially in the early days, many parents gave up quite prematurely or did not follow diet, etc.) has done better, is a functioning member of the family, and no child with me has had to be admitted to a group home! Even when full success (a bright eyed, healthy child, functioning fully normally) is not possible, there is a tremendous ability to improve brain function, help improve health and quality of life for all. While in reality it is inevitable that our research world and scientific community will have to reach the same conclusion—that this is a treatable, medical disease—the parents meanwhile remain on the front lines with a firm focus and belief in these patients really being children that can be “returned” to their normal state.
The Myth of Autism Page 7
