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- Prazosin -
General Information:
Names:
Wikipedia entry:
Dr. Ray Shahelien entry:
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Observations:
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Prazosin is a centrally active antagonist of the
α1-adrenoreceptor (α1-AR) in the noradrenergic system. This
drug is used for a number of applications, not just
hypertension.
The noradrenergic system plays an
important role in learning and memory. Moderate levels of
norepinephrine released under control conditions strengthen
prefrontal cortical functions via actions at post-synaptic α-2A
adrenoceptors with high affinity for norepinephrine, while high
levels of norepinephrine release during stress impair prefrontal
cortex (PFC) cortical functions via α1 and possibly β1 receptors
with lower affinity for norepinephrine. Thus, levels of
norepinephrine determine whether prefrontal cortical or
posterior cortical systems control behavior and thought. The
successful use of atypical antipsychotics is thought to be
related to their α1- and 5HT2A-blocking properties.
Aggressive behavior is associated with
an increase in the number of α1-adrenoceptors in AD patients.
Two successful trials for treating AD
agitation and aggression with Prazosin:
PRAZOSIN FOR THE TREATMENT
OF BEHAVIORAL SYMPTOMS IN ALZHEIMER’S DISEASE PATIENTS WITH
AGITATION AND AGGRESSION
Am J Geriatr Psychiatry. Author manuscript; available in
PMC 2010 September 1.
Published in final edited form as:
Am J Geriatr Psychiatry. 2009 September; 17(9): 744–751.
doi: 10.1097/JGP.0b013e3181ab8c61.
This study provides preliminary support for the efficacy
of the alpha-1 AR antagonist prazosin as a novel treatment for
behavioral symptoms in AD patients with agitation and
aggression.
PMCID: PMC2842091 NIHMSID: NIHMS181108
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2842091
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2842091/pdf/nihms181108.pdf
Two larger trials are now recruiting
(as of October, 2010):
Changes in noradrenergic neurons appear
to be similar in AD and Lewy body patients.
It is
therefore conceivable that prazosin might help LBD patients who
are sensitive to antipsychotics.
Long-lasting
memories
of aversive or stressful events have been associated with the
noradrenergic system activation. Traumatic stressors are thought
to lead to excessive norepinephrine release and α1-AR engagement.
Animal research suggests that high levels of α1-AR stimulation
should weaken PFC inhibitory functions and strengthen amygdala
function, the profile observed in posttraumatic stress disorder
(PTSD). The high CNS noradrenergic outflow in PTSD is thought to
stimulate α1-adrenergic regulation of the prefrontal cerebral
cortex, disrupting cognitive processing and increasing fear
responses.
Trauma-related
nightmares
in
PTSD
rarely
respond
to
pharmacologic
treatment.
However,
low
doses
of
prazosin
have
been
found
to
substantially reduced nightmares and moderately or markedly
reduced overall PTSD severity and function in previously
treatment-resistant combat veterans. Given an hour before bedtime,
low doses of prazosin reduce light sleep, normalize REM sleep, and
increase total sleep time. An additional daytime dose was found to
reduce residual daytime symptoms of civilian trauma victims.
The drug
is now commonly used for this application, and there are quite a
few clinical trials ongoing, as well.
Some of
our members are dealing with ADLOs who suffer from PTSD. And I've
gotten the impression that the AD worsens the PTSD symptoms. So
perhaps prazosin may offer them some relief, too.
Fatigue
is the most common side effect.
Note that
the levels of prazosin that are reported to be effective for
treating PTSD are much lower than those that are used to treat
hypertension.
For those
who are interested, here is an overview of the way in which
various drugs for treating insomnia, parasomnias, and circadian
rhythm disorders are thought to work:
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Known sources:
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Natural sources:
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References:
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Updated: July 2, 2012
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