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


[This question was introduced by a member of our project research team, based on a similar case report in the literature.]

A 1986 article titled "Association Between Regularly Occurring Partial Seizures and Thyroid Function" in the Journal Epilepsia presents a case report of a 28 year-old man with regularly occurring complex-partial seizures with regular intervals. His seizures occurred in what the authors refer to as a "remarkably regular pattern." They were typically clustered in periods of 2-4 days, with up to 10 seizures a day and then 5-6 weeks of seizure-free intervals.

The authors proceeded with a longer term (244 day) study to investigate the causes of the rhythmicity, to determine if there was a correlation between his seizure periods and biological parameters. They found he had an increased concentration of thyroxine (T4, a thyroid hormone) during each of his seizure clusters.

An excerpt from the article (bold emphasis added): "A fluctuation in thyroxine level is of special interest in the study of seizure-provoking factors because of the known excitatory effect of thyroxine. Thyrotoxicosis can cause both generalized and partial epileptic seizures (Jabbari and Huott, 1980). In our patient, however, the variations were within the reference range. This may still be of importance since in focal epilepsy there is often a defect in the blood-brain barrier. Since only free and albumin-
bound T4, [-5% of total T4, (Spaulding and Utiger,198l)] normally is capable of passing through the blood-brain barrier (Pardridge, 1981), a defect in this barrier may allow up to a 20-fold higher T4, concentration to reach the epileptogenic focus."

The authors did have some reservations, and they did not present their results as totally conclusive.

From our review of the literautre around hypertension, we noted:
Chronic hypertension is known to have disruptive effects on the blood brain barrier. See Mueller and Heistad (1980).

Based on the above, the following hypothesis was proposed: pregnancy triggers hypertension; hypertension causes issues with blood brain barrier; compromised blood brain barrier leads to increased sensitivity to thyroxine; higher concentrations of thyroxine passing through the blood brain barrier triggers seizures.

Follow Up:

A consulting researcher reviewed the question and agreed this hypothesis is logical and worth exploring, and also noted that the BBB and epilepsy are connected. The consulting neurologist also thinks this is a plausible hypothesis.

The suggestion was made to look into ongoing thyroid testing similar to what they performed in Taubøll et al. (1986).

This hypothesis also led to the suggestion that other tests should be repeated on a similar schedule. If any type of increased sensitivity is triggering seizures, then a one-time test is not enough. The results may be normal, but the question isn't "normal" but variations/patterns of levels and their potential correspondence to the seizure events.


Is there a pattern of increases in free thyroxine that would potentially explain the timing of the seizure clusters?

Action Plan:

We are trying to get in touch with Dr. Taubøll. We've sent emails to his hospital and university email addresses, but we haven't heard back yet.

The consulting neurologist suggests addressing this concern by addressing blood brain barrier permeability. Previous experimental research was mentioned regarding the use of tetracycline to decrease permeability, but the research lost funding and did not reach the next phase. The suggestion was made to research other alternatives (e.g. nutritional supplements, herbal remedies, meta protease blockers).

A consulting researcher asked if we are looking into statins? At present we are researching statins as a possible treatment option.

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