Autistic Spectrum Disorders and Neurotherapy Ron J. Swatzyna, Ph.D.

Autistic Spectrum Disorders (ASD) are the fastest growing group of developmental disabilities in the United States, with a 10% to 17% annual growth rate (US Department of Education, 1999). These disorders are usually diagnosed in childhood and have a tendency to radically alter family dynamics. Children with ASD often present with extremely complex psychological and behavioral issues that change with developmental levels, making successful treatment very challenging. Although behavioral therapy (Smith et al., 2000; Sallows & Graupner, 2005) and psychopharmacology (Siegel, 1996) have been viewed as traditional treatment options for ASDs, they have demonstrated limited success. Parents of ASD children can easily become frustrated, isolated, and overwhelmed.

To better understand why "traditional" treatments have met with limited success, it is important that ASDs be viewed as neurodevelopmental brain disorders. The brains of children with ASDs are different in two important ways: metabolic function and neuroregulation (Coben, 2005b, 2005c). This article will explain why medicine and/or behavioral therapy do little to effectively improve these two dysfunctional states.

Metabolic Function/Connectivity

Neuronal metabolism refers to how well the brain cells are metabolizing glucose, which ultimately is tied to blood flow. When this metabolism ceases, cell death occurs.

Brain imaging techniques reveal that ASD brains have a significant reduction in metabolism in the prefrontal cortex area (McAlonan, 2002). ASD brains have also been found to have poor blood flow to both of the adjacent temporal lobes (Boddaert et al., 2004). The combination of reduced metabolism in the prefrontal cortex and poor blood flow in the temporal lobes inhibits the brain's ability to communicate effectively and may account for many of the symptoms seen in ASD children.

The human brain begins developing during the prenatal period and continues through the school years, reaching full development in late adolescence. During the prenatal period, the child's brain begins the dual process of getting cells to where they need to be and growing the structures needed to link to other nerve cells (Shonkoff and Phillips, 2000).

Communication within and between lobes of the brain is critical to optimal functioning. Each site of the brain should communicate with the rest of the brain to a certain extent, depending upon its need. However, if there is too much communication between sites, the individual will be very rigid and inflexible (Walker, 2002). On the other hand, if there is too little communication between certain sites, the processing of information will be slowed or inhibited. The brains of ASD patients have distinctive dysfunctional communication patterns and developmental processes.

It has been suggested that in ASD children, something goes awry in the process of brain development. Most researchers in the field believe that the problem occurs between the ages of six months and two years. As one researcher state, "The most consistent finding [in ASD children] is that of enlarged brains, likely due to white matter expansion, which is abnormal. This sets off a series of neural connectivity and other problems" (Coben, 2007). During this critical stage, instead of splitting into individual lobes and hemispheres, the development of the frontal area of ASD brains is stunted and differentiation occurs at a much slower rate. The stunted independent development of the frontal brain region creates two connectivity problems: too much communication in the frontal lobes, and too little communication between the frontal and all other brain regions.

When the frontal lobes are too undifferentiated or "glued together," this creates other communication problems. In this regard, the development of communication with other brain regions is greatly inhibited. Recent research supports previous findings that showed disconnections between two or more brain regions, particularly long-range connectivity. This study finds that long-range connectivity disconnection may actually start with maladaptive connections within brain regions (Wilson et al., 2007). In turn, maladaptive connections affect neuronal regulation in unique ways in ASD brains.

Neuroregulation/Electrical Distribution

Neuroregulation refers to how the power is distributed in the brain. Reduced metabolism and blood flow produce distinct patterns of electrical activity specific to the areas affected. In survival situations, the human brain is a highly sensitive and reactive organ and the electrical distribution changes instantly in order to respond to internal cues or environmental stimuli. However, in ASD brains, these patterns become somewhat fixed. ASD brains have four common patterns of dysfunctional electrical distribution dependent upon the individual. Four subtypes of Autism have been identified:

  • Over Focused/Over Aroused Pattern (High Beta)
  • Abnormal EEG/Seizure Pattern
  • High Delta/Theta
  • Low Voltage/Metabolic

Each of these patterns can provide quantifiable biological markers that are indicative of ASD. However, even though these patterns are made very evident using a topographical brain mapping procedure called quantifiable electroencephalogram (qEEG), the diagnosis of ASD should not be made without clinical correlation and psychiatric evaluation.

QEEG-Guided Neurotherapy for ASD

The qEEG identifies dysfunctional electrical activity and connectivity problems in a person's brain and demonstrates them in a topographical brain map. Brain maps are the representation of how the patient's brain compares to a normal population of like individuals using a statistical method called Z-scoring. Improvement in core ASD symptoms is achieved as these dysfunctional patterns are normalized using computerized audio and visual feedback given to the patient (35 to 40 sessions on average). In many cases, medications can be reduced and possibly eliminated as the brain becomes more functional (Hirshberb, 2004). Studies have demonstrated a significant improvement in ASD core measures of attention, executive and visual perceptual function, and language skills (Jarusiewicz, 2002; Cohen, 2005). Additionally, there have been no adverse effects reported using neurotherapy. In general, neurotherapy statistically has been found to work well in approximately 70% to 80% of ASD cases (Coben & Padolsky, 2007). However, it has been documented that using qEEG-guided neurotherapy appears to increase the success rate to 90 percent. Lastly, the positive changes appear to be lasting unless the brain incurs additional trauma, which has the potential to render it dysfunctional again.

Psychotherapy, behavioral therapy, and psychopharmacology interventions work well for many childhood disorders, but children with ASD experience little success with these traditional approaches. Thanks to the technological advances of qEEG and the research over the past ten years, we may now have a better understanding of why these cases are so challenging. QEEG-guided neurotherapy is an efficacious non-medication treatment option for children with ASD because it can normalize the dysfunctional patterns, restore normal functioning, and in many cases eliminate the need to medicate the symptoms.

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