Read with caution!

This post was written during early stages of trying to understand a complex scientific problem, and we didn't get everything right. The original author no longer endorses the content of this post. It is being left online for historical reasons, but read at your own risk.

I just found this narrative case study of FFI in the archives of the New York Times — published in 2001.  Title: “To sleep no more.”

While it supplies only the science needed to tell the story, it’s an interesting insight into how this disease finally got recognized, named, and linked up with the work Stanley Prusiner was doing on prions.  Not an easy read, and this line broke my heart:

As for Gambetti himself [of the National Prion Disease Surveillance Center at Case Western Reserve University, Cleveland OH], he predicts a cure for F.F.I. within 10 years.

Reads a little differently when the ten-year mark has just passed us by.  But hopefully he wasn’t too far off!  Other tidbits:

”The good thing,” he [Pierluigi Gambetti] told me, ”is that research on prion diseases doesn’t have to be targeted to F.F.I. to work for F.F.I.”

We cannot live without sleep. At the same time, these catastrophic results are brought about by very limited cerebral damage — and this almost exclusively to the thalamus. Vast portions of the brain are untouched. This finding has shocked pathologists and sleep researchers and opened up new possibilities for aiding normal insomniacs. ”If I were the director of the N.I.H. I would pour money into F.F.I. research,” said William Dement, who founded the sleep disorders clinic at Stanford University. ”You might get a cure for insomnia. At the very least we could make our sleeping pills infinitely safer and more practical.” We would no longer need to affect billions of receptors the way we do now, said Dement, to bring about the desired result: safe, deep sleep.