Recent discussion of viral issues and the brain

[Guest guest]

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.