Guest guest Posted December 3, 2008 Report Share Posted December 3, 2008 great information. On Dec 3, 2008, at 6:50 AM, Reynolds wrote: > There were a number of people wanting a bit more information on viral > issues and the brain. > > Here's a line from one of the abstract on how nasty this viral > stuff gets: > > " study revealed active, low-level viral infection in the resected > hippocampus and temporal lobe cortex, with immunohistochemical > evidence > for infection by herpes simplex 2, principally in neurons " > > Reading through some of it you can imagine how the mercury gets in the > system, knocks the immune system out and causes a whole heap of other > cellular and biochemical damage, and then the virus's get free reign, > with the body almost putting up no fight, hence a chronic viral > infection becomes possible. But because its not acute, most of our > main stream medicos ignore it, or worse yet, deny it is possible. > > Here's some more interesting studies in case people haven't come > across > them: > > Cornford ME, McCormick GF (1997) Adult-onset temporal lobe epilepsy > associated with smoldering herpes simplex 2 infection. Neurology. 48 > (2), 425-30. PMID: 9040733 > > A 40-year-old man with chronic genital herpes simplex infection > developed partial complex temporal lobe seizures of insidious onset, > with EEG and MRI evidence of a unilateral temporal lobe destructive, > atrophic process. Extensive workup did not reveal an infectious > etiology. Three years of escalating number and severity of daily > seizures with memory loss led to temporal lobectomy. Histologic study > revealed active, low-level viral infection in the resected hippocampus > and temporal lobe cortex, with immunohistochemical evidence for > infection by herpes simplex 2, principally in neurons. In situ > hybridization confirmed the presence of herpes simplex virus in > neurons. > Anticonvulsant-resistant seizure episodes began to recur several times > daily soon after surgery, but the addition of acyclovir to the > treatment > regimen resulted in a substantial reduction in seizure occurrence, > maintained for the subsequent 2.5 years. > > DeLong GR, Bean SC, Brown FR (1981) Acquired reversible autistic > syndrome in acute encephalopathic illness in children. Arch Neurol. 38 > (3), 191-4. PMID: 6162440 > > In seeking the neurologic substrate of the autistic syndrome of > childhood, previous studies have implicated the medial temporal > lobe or > the ring of mesolimbic cortex located in the mesial frontal and > temporal > lobes. During an acute encephalopathic illness, a clinical picture > developed in three children that was consistent with infantile autism. > This development was reversible. It was differentiated from acquired > epileptic aphasia, and the language disorder was differentiated > aphasia. > One child has rises in serum herpes simplex titers, and a computerized > tomographic (CT) scan revealed an extensive lesion of the temporal > lobes, predominantly on the left. The other two, with similar clinical > syndromes, had normal CT scans, and no etiologic agent was defined. > These cases are examples of an acquired and reversible autistic > syndrome > in childhood, emphasizing the clinical similarities to bilateral > medial > temporal lobe disease as described in man, including the Klüver-Bucy > syndrome seen in postencephalitic as well as postsurgical states. > > Ghaziuddin M, Al-Khouri I, Ghaziuddin N (2002) Autistic symptoms > following herpes encephalitis. Eur Child Adolesc Psychiatry. 11 (3), > 142-6. PMID: 12369775 > > Autism is a childhood onset neurodevelopmental disorder > characterized by > reciprocal social deficits, communication impairment, and rigid > ritualistic interests, with the onset almost always before three years > of age. Although the etiology of the disorder is strongly > influenced by > genes, environmental factors are also important. In this context, > several reports have described its association with known medical > conditions, including infections affecting the central nervous system. > In this report, we describe an 11-year-old Asian youngster who > developed > the symptoms of autism following an episode of herpes encephalitis. In > contrast to previous similar reports, imaging studies suggested a > predominant involvement of the frontal lobes. At follow-up after three > years, he continued to show the core deficits of autism. This case > further supports the role of environmental factors, such as > infections, > in the etiology of autism, and suggests that in a minority of cases, > autistic symptoms can develop in later childhood. > > Barak Y, Kimhi R, Stein D, Gutman J, Weizman A (1999) Autistic > subjects > with comorbid epilepsy: a possible association with viral infections. > Child Psychiatry Hum Dev. 29 (3), 245-51. PMID: 10080966 > > This study evaluates the comorbidity of epilepsy as a variable > supporting a viral hypothesis in Autism. Data covering a 30-year > period > (1960-1989), including general population live births, autistic > births, > and incidence of viral encephalitis and viral meningitis, were > collected > for Israel. 290 autistic births were evaluated. The annual birth > pattern > of subjects with comorbid epilepsy fit the seasonality of viral > meningitis. These findings support the role of viral C.N.S. infections > in the causality of this disorder. > > I also threw in this study at the end because of the reference to > seizures, demyelination, and serotonin. > > M, Hart PN, Randall J, Lee J, Hijada D, Bratenahl CG (1977) > Serotonin levels in the blood and central nervous system of a patient > with sudanophilic leukodystrophy. Neuropadiatrie. 8 (4), 459-66. PMID: > 579443 > > A case report is presented of a boy with the infantile spasm syndrome > beginning at eight months of age. He had a clinical course marked by > increasingly severe seizures and neurological regression. After > death at > twenty-one months of age, autopsy of the central nervous system > revealed > demyelination of white matter with sparing of arcuate fibers. An > earlier > born male sibling had had a similar clinical pattern but died > without an > autopsy. During his lifetime, the patient had markedly elevated levels > of 5-hydroxyindoles (a measure of serotonin) in his blood. At autopsy, > the level of 5-hydroxytryptamine (serotonin) in four grey matter areas > of the brain was lower than those of a control who died on the same > day. > This is the first case reporting a comparison of blood and central > nervous system levels of 5-hydroxytrypamine in a child. > > > > > Quote Link to comment Share on other sites More sharing options...
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