Question:
I saw a news program--Primetime or 20/20 about two or three years ago
reporting the case of this man. The entire time I was watching it I
thought--this guy has Lyme disease and it is affecting the area of the brain
that controls sleep. ( I use to sleep all the time during early Lyme-- now I am
lucky if I get to sleep at all. Nothing seems to help on the nights I can't
sleep.-- a sleep disorder!?!) During the news program --they interviewed his
doctors --the doctors said that even with the most powerful sleep medications
-this man could not sleep toward the end of his life. It took the doctors
sometime to believe the man when he said he wasn't sleeping. He got the run
around and was detoured via the psych route--they finally brought him in for
a sleep study and the doc said--like he was making some huge discovery--the man
had been telling the docs he could not sleep for some time now--anyway the doc
says something like--"Guess what Mr._____--- was not sleeping." DUH! It took
them long enough. They did not listen to him. I told one of the doctors I
saw in Fairfield, Conn. that I was not sleeping. You know what he said --you
will fall asleep when you need to--he didn't tell me it might be for good.
Remember- when you read the following--there is some BIG controversy over
whether prions cause any disease. The jury is still out on that one--depending
on which "expert" you consult. I am sure the docs. never considered Lyme in
the differential diagnosis. Why would they since they are all being told how
rare it is. This case was reported by someone from the University of Chicago.
Steere doesn't even know Lyme disease exists in the Boston area.
Answer:
I have had lyme for a while although I dont remember a bite
or a rash. I do have very bad arthritis and have no cartiladge in either knee
which makes walking impossible. I am taking temazepam for sleep due to bipolar
disorder which I have had for many years. I have noticed for the past few
months that I cant sleep untill 4or 5 am any more which makes getting my son up
for school unbearable. Can you advise me on what to do or what to read? It is
really upsetting me knowing that once my kids are alseep I simply sit in my
chair watching the sun come up.
I have difficulty sleeping and have found some success with Ambien. I have
tried many things but like Ambien because it seems to leave no morning
hang-over. It has by no means solved all my sleep trouble, but has allowed me
to get a few hrs now and then.
I used Ambien, too, for a major sleep disorder and it did give me sleep,
but too often 7 hours when I knew I needed 9. My Lyme psychiatrist
solved that problem by prescribing Restoril. I wouldn't say it's
stronger; it just gives me the longer rest I know I require to heal.
I'm on IVs (13 wks.).
I see many more studies with-what else- tax dollars on this one. I give it a
resounding ten more lifetimes until the " experts" conclude "we reallly don't
know but another study on.... will bring us closer..to the yawn bs yawn bs yawn
bs...bs yawn."
http://www.biomednet.com/biomednews/conf/sfn98/Monday/story_7.html
Monday Nov. 9
Report from the 1998 society for Neuroscience Meeting
Of Prusiner And Prions
by Emily Green
Fittingly enough, for the opening day's special lecture of the 1998 Society for
Neuroscience Annual Meeting, the special guest, neurologist Stanley B Prusiner
of the University of California at San Francisco, came bearing a special
pathogen: the prion. Since 1982, Prusiner has famously contended that the
prion, a mutant isoform of a normal cellular protein called PrP, is the agent
for a host of neuro-degenerative diseases. These include scrapie in sheep,
bovine spongiform encephalopathy (BSE) in cattle and a newcomer that appears to
be caused by the same agent as BSE and has in the last four years claimed 28
human victims in Britain and France: new variant Creutzfeldt-Jakob Disease
(nvCJD).
Of more relevance to Prusiner's own research are the 17 other human variations
of these invariably fatal neuro-degenerative disorders, called transmissible
spongiform encephalopathies (TSEs): sporadic Creutzfeldt-Jakob Disease (CJD),
fatal familial insomnia (FFI), kuru and Gerstmann-Straussler-Schenker Syndrome
(GSS). While these are the rarest of killers, at best claiming one in a
million, the spectre of BSE appearing in humans in Britain and the extreme
nature of the claims Professor Prusiner has made for the prion since coining
the term in 1982 have vaulted them to the forefront of neurology and molecular
genetics. Even his fiercest critics, including retired neuro-pathologist Hugh
Fraser of the Neuropathogenesis Unit (NPU) in Edinburgh, insist, "He deserves
enormous credit for elucidation of PrP and the advancement of protein
chemistry." And enormous credit he has received. Last year Professor Prusiner
received the Nobel Prize for Medicine for promoting the notion that TSEs are a
school of diseases with distinct strains that, unlike viruses and bacteria, do
not necessarily involve an agent with an independent genome. In fact, as he
conceded in his lecture, for the prion to satisfy epidemiological evidence,
TSEs would have to be not simply novel, but positively acrobatic: spontaneous,
inheritable and transmissible, too.
His address to the Society, titled "Molecular Biology of Prions Causing
Neurodegeneration - A Scientific Odyssey from Heresy to Orthodoxy", set out a
multi-disciplinary barrage of evidence to argue just that. Working to the whir
and click of the projector, Professor Prusiner quickly trotted through his
ascent through the field - his first encounter with a CJD patient in 1972, his
attempts to isolate TSE agents using mice, his switch to hamsters for their
faster incubation times, isolation of the PrP protein from unwieldy mass of
diseased brain using a succession of detergent and enzyme purification
techniques, the genetic sequencing of PrP in its normal form, the discovery of
what appeared to be strain-specific mutations at tell-tale codons in the
roughly 210 amino acid sequence of PrP, the importance of cleavage sites where
the protein breaks during misfolding in the disease process, then molecular
assaults using transgenic mice to explore which polymorphisms might signal a
genetic predisposition to TSEs.
It was an address that jumped scientific specialisms in a manner bespeaking a
mightily endowed lab, but one which, vaulting dramatically from discipline to
discipline, left much of the audience behind. For the neuro-pathologists, there
were beautifully stained samples of amyloid plaques in slides of diseased
brains, for cell biologists there was a quick explanation of the life cycle of
the prion from its birth in the cell center, its traverse to the cell membrane
where it may serve in synaptic function. And then, for the biochemists, there
were the illustrations of the mis-folding of diseased PrP, and hypothetical
mechanisms whereby the prion might somehow come in contact with an as yet
undefined co-factor, probably a second protein - "Protein X" - after which
domino mis-folding is initiated and PrP converted to prions.
For the molecular geneticists, there were his lab's latest immuno assays using
antibodies to investigate structural variations in the amino acid sequence of
PrP that may correspond to TSE strains. These are reported in the October
edition of Nature Medicine (Safar et al., vol 4, no 10, pp1157-1165).
Finally, there was rich fodder for his critics. "We have created prions de
novo," he told the audience, repeating it three times lest its importance
escape the uninitiated. This would take care of the spontaneous part of the
prion hypothesis. The claim is not new, and first arose over a GSS trial in
which Prusiner claimed that transgenic mice spliced up with a GSS mutation
spontaneously developed disease which in turn proved transmissible. In June of
this year, at the only independent lab to attempt to repeat the work, molecular
geneticist Jean Manson of the NPU in Edinburgh found GSS transgenic mice lived
up to 750 days of age with "no signs of neurological disease" while the
inoculated animals succumbed relatively quickly, supporting the idea that the
disease is transmissible, but not necessarily spontaneous (Statement No. 59,
BSE Inquiry, http://www.bse.org.uk).
By way of more red flags for his detractors, Prusiner took pains twice to
emphasize: "The prion has no nucleic acid." To be precise, while it has a gene
telling it to be a protein, unlike any known pathogen, the prion as proposed by
Prusiner does not require the help of disease-specific nucleic acid to
propagate. And, propagate the TSE agent does as anyone familiar with the BSE
epidemic can testify. . Whether or not the prion can propagate via its
hypothetical chain of chemical conformation outside slide shows at scientific
meetings remains one of the hottest arguments in modern science. However, this
Sunday morning, the argument was not audible, and did not involve Professor
Prusiner. The last words of his exactly hour-long address were: "There is no
time for questions."
