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Printable Handouts
Navigable Slide Index
- Introduction
- Topics
- Topic 1: neurogenic Orthostatic Hypotension
- Orthostatic Hypotension in PD
- Correlates of OH in PD
- In PD, OH greatly increases risk of falls
- In PD, OH increases cognitive impairment
- In PD, OH impairs quality of life
- Fatigue associated with cardiac sympathetic lesion
- OH is associated with supine hypertension
- In PD, OH worsens survival
- No effect of levodopa treatment
- Take-home #1
- Algorithmic approach to OH
- Neurogenic Orthostatic Hypotension
- Valsalva BP and HR: normal
- Baroreflex-sympathoneural and cardiovagal failure
- Primary' CAF syndromes are synucleinopathies
- Valsalva BP in nOH syndromes
- Take-home #2
- Topic 2: the heart of PD
- Cardiac sympathetic neuroimaging in synucleinopathies
- Myocardial catecholamine deficiency in PD
- Profound myocardial NE deficiency in PD
- 18F-DA PET in synucleinopathies
- Post-mortem validation of 18F-DA PET
- An apparent paradox
- The 'sick-but-not-dead' concept
- Treatment implications - main points
- Treatment implications
- Decreased vesicular uptake indexes in LBDs
- Accelerated 18F loss & decreased vesicular storage
- Vesicular storage defect due to synucleinopathy
- 18F-DA & 11C-MRB PET to assess vesicular storage
- Decreased vesicular storage in PD+OH
- Decreased vesicular storage in PD
- Topic 3: future trends
- 18F-DA PET separates PD+OH from MSA-P
- Tri-phasic loss of cardiac NE and putamen DA
- Cardioselective sympathetic noradrenergic lesion (1)
- Cardioselective sympathetic noradrenergic lesion (2)
- Phenoconversion of PAF to PD+OH or DLB
- LB PAF entails central LBD
- PAF evolving to DLB and pre-terminal PD
- SNS ganglion in PAF evolving to DLB and pre-terminal PD
- SNS alpha-synuclein in PAF evolving to DLB
- Three SNS - innervated skin constituents
- Intra-neuronal alpha-synuclein and vesicular storage defect in LB nOH
- Post-mortem alpha-synuclein and THir in PD
- Post-mortem skin SMG, cardiac aS and NE in PD
- Take-home #3
- Principles of management
- Education (1)
- Education (2)
- Elevate the head of the bed
- The osmopressor response
- Drug treatment
- Midodrine and phenylephrine
- L-DOPS and L-DOPA
- Take-home #4
- The intramural NINDS PDRisk study
- Low 18F-DA predicts central LBDs
- Body-first' progression
- Model predictions about treatment effects
- Take-home #5
- Conclusions
- Acknowledgements
Topics Covered
- Neurogenic orthostatic hypotension in Parkinson’s Disease
- Baroreflex-sympathoneural and cardiovagal failure
- Differentiation of PD+OH from MSA-P
- ‘Sick-but-not-dead’ phenomenon
- Alpha-synucleinopathy
- Causes of cardiac noradrenergic deficiency
- Sympathetic denervation
- Using cardiac sympathetic neuroimaging for identifying central LBDs early
- Future trends
Links
Series:
Categories:
Therapeutic Areas:
Talk Citation
Goldstein, D.S. (2023, September 28). Cardiovascular involvement in Parkinson’s disease [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 21, 2024, from https://doi.org/10.69645/LQUX6575.Export Citation (RIS)
Publication History
Financial Disclosures
- Dr. David S. Goldstein has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
Other Talks in the Series: Periodic Reports: Advances in Clinical Interventions and Research Platforms
Transcript
Please wait while the transcript is being prepared...
0:00
Hello everyone. I'm
Dave Goldstein.
I'm the Chief of the
Autonomic Medicine Section
in the Division of
Intramural Research at
the National Institute of
Neurological
Disorders and Stroke
at the National Institutes
of Health in Bethesda,
Maryland, in the USA.
Today, I'm going
to be lecturing on
cardiovascular involvement
in Parkinson's disease.
0:28
There are three general
topics for today's lecture.
One is on neurogenic
orthostatic hypotension,
a characteristic feature of
Parkinson's with
autonomic failure.
Then, I'm going to go into
the sympathetic
innervation of the heart,
which plays a major role in
the cardiovascular abnormalities
that are found in Parkinson's.
Then, I'll finish with
future trends as I see
them in this area.
1:01
Two general areas under
neurogenic orthostatic hypotension
that I'll be covering.
One is on the clinical and
prognostic significance
and the second is on how you
identify orthostatic
hypotension as neurogenic.
Concerning orthostatic
hypotension.
1:18
The frequency of orthostatic
hypotension and
Parkinson's varies
remarkably among studies.
This is because of
different referral patterns
to different types of centers.
For instance, a neurology center
will see the movement
disorder and
may underestimate
the frequency of
orthostatic hypotension
because of dependence
on complaints.
Many patients with Parkinson's
orthostatic hypotension
don't have any symptoms of
orthostatic hypotension.
Orthostatic hypotension
in Parkinson's can be
an early finding
in this situation
and can be misdiagnosed as
multiple system atrophy or
pure autonomic failure.
We'll be going over some of
the clinical correlates
that are related
to the treatment considerations
for Parkinson's with
orthostatic hypotension.
I'll provide evidence that
orthostatic hypotension in
Parkinson's Disease occurs
independently of
Levodopa treatment.
However, dopaminergic
drugs such as
Levodopa decrease blood pressure
when the person is standing.
Orthostatic hypotension
in Parkinson's
is often associated with
supine hypertension and this
poses a treatment dilemma.
Some of the special
treatment considerations
that we'll be reviewing are
that orthostatic hypotension in
Parkinson's usually is
worse in the morning.
It's associated with heat
intolerance, post-exercise,
drop in blood pressure,
and post-prandial hypotension
after eating a large meal.
Acute water ingestion can
raise the blood pressure,
and this provides a useful
tact as we'll get into it.
Finally, I'll discuss
the importance
of determining whether
the patient has
denervation super sensitivity
because this would drive
the choice of drug used
to treat orthostatic
hypotension.