Clinical Features of Gulf War Syndrome and Autism

There is considerable and growing evidence that chronic microglial activation plays a major role in numerous neurological conditions including Alzheimers dementia, Parkinsons disease, ALS, strokes, and inflammatory brain diseases. The release of toxic elements from activated microglia, such as cytokines and excitotoxins, is known to produce neurodegeneration. Peripheral immune stimulation has been shown to activate CNS microglia, and when excessive can lead to neurodegeneration and cognitive defects commonly associated with both the Gulf War Syndrome (GWS) and autism. This paper summarizes the mechanism linking these two disorders with excessive immune stimulation secondary to overvaccination. Following the first Gulf War, tens of thousands ofAmerican and British veterans began to suffer from numerous complaints, which have become known as the Gulf War Syndrome (GWS). These included recurrent fevers, cognitive difficulties, neuropsychiatric problems, polyarthralgias, chronic fatigue syndrome, and numerous allergies where none existed before. In addition, an increase in birth defects has been documented in the offspring of Gulf veterans, including tricuspid valve insufficiency, aortic valve stenosis, renal agenesis or hypoplasia, and hypospadias. One recent study documented reduced cerebrovascular flow and impaired ability to handle complex cognitive tasks in a substantial number of these veterans. Another study found that cognitive symptoms correlated closely with immune dysfunction in Gulf War veterans, but not with nonveteran chronic fatigue controls. The Gulf War veteran was exposed to as many as 17 inoculations over a very short period. In many ways, behavioral problems associated with this syndrome resemble astheno-emotional disorder, which is characterized by fatigue with prolonged mental activity, stress intolerance, decreased concentration and short term memory, headache with mental processing, irritability, and sensitivity to sounds or lights. The anatomic substrate of this syndromeascribed to the hippocampus, limbic connections, temporal lobes, and parts of the frontal lobesoverlaps those most damaged by neuroinflammation and attendant excitotoxicity