Laura-
I seem to have largely put that dragon to rest, at least for now. Unfortunately I cannot point to one specific thing and cry "AhHa!". I will, however, list what I can think of-
1) The symptoms seemed to abate when I began two drugs - propranolol and perindopril. The latter is an ACE inhibitor. These are relatively new frontiers for PD.

This will get you started on the ACE inhibtor trail-


1. Aust N Z J Med. 2000 Feb;30(1):48-53.

The angiotensin converting enzyme (ACE) inhibitor, perindopril, modifies the
clinical features of Parkinson's disease.

Reardon KA, Mendelsohn FA, Chai SY, Horne MK.

Neurosciences Department, Monash Medical Centre, Melbourne, Vic.

BACKGROUND: Animal studies have demonstrated an interaction within the striatum
between the angiotensin and dopaminergic systems. In rats, the angiotensin
converting enzyme (ACE) inhibitor, perindopril, crosses the blood brain barrier
and increases striatal dopamine synthesis and release. In humans, angiotensin
type 1 receptors have been found on dopaminergic neurons in the substantia nigra
and striatum. In Parkinson's disease, there is a marked reduction of these
receptors associated with the nigrostriatal dopaminergic neuron loss.
AIMS: We performed a double blind placebo controlled crossover pilot study in
seven patients to investigate the effect of the ACE inhibitor, perindopril on the
clinical features of moderately severe Parkinson's disease.
RESULTS: After a four week treatment period with perindopril, patients had a
faster onset in their motor response to L-dopa and a reduction in 'on phase' peak
dyskinesia, p=0.021 and p=0.014 respectively. Patients also reported more 'on'
periods during their waking day in their movement diary, p=0.007. Perindopril was
well tolerated without any significant postural hypotension or renal dysfunction.
CONCLUSIONS: These results suggest that ACE inhibitors such as perindopril may
have a place in the management of motor fluctuations and dyskinesia in
Parkinson's disease and justify further study.


PMID: 10800878 [PubMed - indexed for MEDLINE]

And another


1. J Neurochem. 1999 Jul;73(1):214-9.

Effect of chronic angiotensin-converting enzyme inhibition on striatal dopamine
content in the MPTP-treated mouse.

Jenkins TA, Wong JY, Howells DW, Mendelsohn FA, Chai SY.

Howard Florey Institute of Experimental Physiology and Medicine, University of
Melbourne, Parkville, Victoria, Australia.

We have previously shown that chronic treatment with the angiotensin-converting
enzyme inhibitor perindopril increased striatal dopamine levels by 2.5-fold in
normal Sprague-Dawley rats, possibly via modulation of the striatal opioid or
tachykinin levels. In the present study, we investigated if this effect of
perindopril persists in an animal model of Parkinson's disease, the
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mouse. C57BL/6 mice
were treated with the neurotoxin (30 mg/kg/day intraperitoneally) for 4 days and
then left for 3 weeks to allow the degeneration of striatal dopaminergic
terminals. At this time, the mice exhibited a 40% decrease in striatal dopamine
content and an accompanying 46% increase in dopamine D2 receptor levels compared
with control untreated mice. The dopamine content returned to control levels, and
the increase in dopamine D2 receptor levels was attenuated in mice treated with
perindopril (5 mg/kg/day orally for 7 days) 2 weeks after the last dose of MPTP.
When the angiotensin-converting enzyme inhibitor was administered (5 mg/kg/day
for 7 days) immediately after the cessation of the MPTP treatment, there was no
reversal of the effect of the neurotoxin in decreasing striatal dopamine content.
Our results demonstrate that perindopril is an effective agent in increasing
striatal dopamine content in an animal model of Parkinson's disease.


PMID: 10386973 [PubMed - indexed for MEDLINE]

Now, go to Wikipedia and check for ACE Inhibitors and perhaps "perindopril". That will, in turn, put you within reach of the actions of renin and aldosterone - the hormones that regulate potassium levels by sucking it up into the cell.

Speaking of the potassium shift. Remember how it usually affects young, Asian men? And do you remember that the most common trigger is a heavy carb load before sleep? Well, keep that in mind and go to Wikipedia and read "Sleep paralysis" and then "Sudden Unexpected Death Syndrome".

" Jump to: navigation, search

Sudden unexpected death syndrome, or Sudden unexpected nocturnal death syndrome (SUNDS), or Sudden Unknown Death Syndrome is sudden unexpected death of adolescents and adults, often during sleep.[1] Sudden unexplained death syndrome was first noted in 1977 among Hmong refugees in the US.[2][3] The disease was again noted in Singapore, when a retrospective survey of records showed that 230 otherwise healthy Thai men died suddenly of unexplained causes between 1982 and 1990:[4] In the Philippines, where it is referred to in the vernacular as bangungot, SUNDS affects 43 per 100,000 per year among young Filipinos. Most of the victims are young males.[5]"

"SUNDS has been cloaked in superstition. Filipinos believe ingesting high levels of carbohydrates just before sleeping causes bangungot."




It is very interesting reading. Once you get past it I'd like to know what you think.

-Rick