This is one of a set of hypotheses we are considering involving a disruption in the blood brain barrier. See also BBB & Thyroid and BBB, Other.


[This question was asked by a PhD student in immunology, contributing through the Facebook page.]

Did you check the option that the bacteria is currently in the brain, and that is why blood work IgG came out normal? Immune system changes due to pregnancy may have altered the permeability of the Blood-Brain-Barrier, allowing for bacteria or something that triggers it to enter the brain tissue. These changes may have also decreased the brain's immune system (Glia cells) ability to fight it off. The relative closeness of the temporal lobe to the Circadian clock area might suggest that the nocturnal nature of the seizures is due to melatonin effects, and blood pressure changes are due to effects of the bacteria on the Hypothalamus.

Follow Up:

A consulting researcher reviewed the question and agreed this hypothesis is logical and worth exploring. He suggested a brain CT, MRI with contrast,
or lumbar puncture followed by PCR to check for bacterial involvement. (See reference regarding detecting infections via a molecular biology method following lumbar puncture.

Up to this point the patient has been resistant to undergoing a lumbar puncture, but it may become necessary. Other suggestions for non-invasive procedures to investigate this hypothesis include looking into the possibility that there is a contrast agent for MRI or PET that can detect the bacteria (biomarkers? general inflammation?). If we take the non-invasive approach, we need to consult a radiologist about limitations of the machines (resolution, signal to noise ratio, etc.).

The advantage of the lumbar puncture is that we can investigate other triggers, e.g. thyroxine levels. However, these other levels might be elevated only during a seizure or ongoing high blood pressure.


Is there an MRI or PET contrast agent that would detect bacteria?

Do the antibiotics affect the brain (cross the BBB, spread in the tissue, etc.)?

If there is bacterial involvement, are the seizures a direct result of the bacteria itself or perhaps a toxin it secretes (goes to when should you see improvement if bacteria is cleared by antibiotics but toxin is not)?

If there is bacterial involvement, is there also an interaction with another trigger?

Does bacterial involvement (with or without interaction with another trigger) explain the timing of the seizure clusters?

Action Plan:

This hypothesis has been taken under serious consideration. At this point, the suggested procedures are being considered but no tests have been scheduled.

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