The researchers in this study asked whether infections with human herpesvirus 6B (HHV-6B) are associated with a common type of epilepsy called mesial temporal lobe epilepsy (MTLE). Patients with MTLE often have extensive scarring in the hippocampus, a brain region responsible for memory that lies deep within a bigger region called the temporal lobe. Hippocampal scarring and MTLE are associated with a history of fever-induced fits, and HHV-6B infection can cause such fits in young children. Most people become infected with HHV-6B (or the closely related HHV-6A) early in life. The virus then remains latent for years within the brain and elsewhere. Given these facts and a previous investigation that showed that brain tissue from several patients with MTLE contained HHV-6B, the researchers reasoned that it was worth investigating HHV-6B as a cause of MTLE.


These findings, together with those from the previous study, reveal that nearly two-thirds of patients with MTLE (but no patients with other forms of epilepsy) have an active HHV-6B infection in the brain region where their epilepsy originates. Overall, they provide strong support for the idea that HHV-6B infections might cause MTLE, particularly given the results obtained from the patient whose condition only improved after multiple brain operations had removed all the virally infected material. Furthermore, the demonstration that HHV-6B infection reduces glutamate transporter expression in astrocytes suggests that HHV-6B infection might cause astrocyte dysfunction. This dysfunction could lead to injury of the sensitive neurons in the hippocampus and trigger MTLE. Additional patients now need to be studied both to confirm the association between HHV-6B infection and MTLE and to discover exactly how this virus triggers epilepsy.

Interesting. Thanks for the link!
I re-read the linked article today and noticed something I had missed before (emphasis mine):
... The long latency between childhood febrile seizures and the appearance of persistent unprovoked seizures suggests these patients may have chronic HHV-6 infection rather than reactivated virus. The presence of chronic viral infection in these patients would be supported by the progression of hippocampal atrophy. Collectively, these data suggest an ongoing process; the latency between occurrence of an early risk factor such as febrile seizures and onset of chronic epilepsy is consistent with either persistent or reactivated infection [25,32].
An association between chronic epilepsy and persistent or reactivated HHV-6 infection of astrocytes suggests the possibility that viral infection of astrocytes are associated with changes in cell function that may contribute to disease. Astrocytes are known to interact closely with neurons and are critical in modulating synaptic transmission [49]. Astrocytes can modulate neurotransmission by maintaining low concentrations of extracellular glutamate by the glial glutamate transporters EAAT-1 and EAAT-2 [50]. Elevated extracellular glutamate, the main excitatory neurotransmitter, may be involved in epilepsy by triggering excitotoxicity through loss of glutamine synthetase [51], an enzyme that metabolizes glutamate in astrocytes, and/or by malfunctioning astrocytic glutamate transporters [50]. The CA1 and CA3 neurons lost in MTS/MTLE are particularly susceptible to glutamatergic-mediated cell death. Sclerotic hippocampi from temporal lobe epilepsy demonstrate reduced EAAT-2 immunoreactivity [52], and are prone to alternative EAAT-2 mRNA splicing [53]. A unique finding in this study is the isolation ex vivo of cultured astrocytes from patients with MTLE who are infected with HHV-6. These primary HHV-6–infected astrocytes demonstrated low levels of EAAT-2 mRNA. In support of our ex vivo findings, astrocytes infected with HHV-6 in vitro also demonstrated a remarkable decrease in EAAT-2 mRNA. Detection of high levels of HHV-6 DNA in MTLE brain tissue, isolation of HHV-6 from primary astrocytes isolated from MTLE brain tissue, and decreased expression of EAAT-2 mRNA demonstrates an association between HHV-6 infection and astrocytic dysfunction. Functional changes in virus infected glia or in glia harboring reactivated virus may lead to secondary injury of the exquisitely sensitive hippocampal neuron, and ultimately to development of MTLE and epilepsy. The potential relationship between HHV-6 astrocytic infection and MTLE deserves further investigation.

It appears that there is very high likelyhood that anyone with MTLE and an MRI result showing atrophy of the hippocampus might benefit from eliminating glutamate from the diet (via a GFCF/GARD diet).
This is something I have discussed with my doctor.You are very smart to see that. I told one Dr. about it. and he just stared at me.
WOW! Ive always had a problem with strep throat-very high fevers as a young child and I can still remember thoughts,feelings and hallucinations.I always thought high fevers could cause hallucinations-no big deal.Now Im wondering if this has contributed to my E.My docs paperwork says I have left TLE and in parenthesis it has Mtle.Very interesting.
Well any kind of virus you get growing up, nose herpes, anything, can just sit in your brain and if you get to stressed out or whatever, it is easier to have a siezure. I am not speaking for everybody of course. But it's like during flu season. The epilepsy center is full.
Interesting. Two thirds is a lot. So how do they test for it, and how do they treat it?
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