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Re: Recent discussion of viral issues and the brain

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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.

>

>

>

>

>

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