The Multiple System Atrophy Coalition offered a two-day conference in late-October on various aspects of multiple system atrophy (MSA), which is a disorder similar to Parkinson’s disease (PD) (MSA is called an atypical parkinsonism disorder). One of the talks, presented by Tom Chelimsky, MD, a neurologist at Wisconsin Medical College, focused on blood pressure issues in multiple system atrophy patients, but his advice applies to Parkinson’s patients.
Dr. Chelimsky also provided advice on managing the blood pressure decrease when rising from sitting or lying down to standing. Since this symptom is common in both MSA and PD patients, these solutions apply to both groups. Treatments for low blood pressure include drinking adequate water, managing salt intake, and exercising regularly.
This talk is different from the “Neurogenic Orthostatic Hypotension” lecture I attended at the same conference (and for which I will share notes soon). Dr. Chelimsky’s lecture focused more on exercise and non-pharmacological treatments for low blood pressure issues, whereas Dr. Kompoliti’s lecture emphasized monitoring orthostatic hypotension and lifestyle choices that can be changed to help low blood pressure.
To watch this webinar, go here and click “Register Now.” Follow the instructions and email link, then return to the conference website. If you are logged in, you can access this link to view the recording.
Dr. Chelimsky’s talk begins at timestamp 1:22:59.
Here are the slides for Dr. Chelimsky’s talk: (at this time, these 28 slides can *only* be viewed or downloaded if you are logged in to the conference)
Dr. Chelimsky also put together a 5-minute video of him speaking about the pharmacological treatment (fludrocortisone, midodrine, pyridostigmine, droxidopa) and non-pharmacological treatment of orthostatic hypotension: (again, at this time, this short recording can *only* be viewed or downloaded if you are logged in to the conference)
Stanford Parkinson’s Community Outreach has a lot of resources on low blood pressure for people with Parkinson’s here.
I listened to this webinar and am sharing a summary of the talk below.
– August Besser
“Blood Pressure Issues in MSA” – Lecture Notes
Speaker: Tom Chelimsky, MD, neurologist, Medical College of Wisconsin
Conference Host: Multiple System Atrophy Coalition
October 24, 2020
Summary by August Besser, Stanford Parkinson’s Community Outreach
Does Autonomic Function Do Much?
- Imagine there is a sudden bad traffic jam.
- The first person is in a Porsche taking a pleasant stroll to the country; their blood pressure and heart rate remain steady.
- The second person, driving a SEAT, is unemployed and on their way to their first interview in a year; their blood pressure and heart rate rise and they might have a urinary/fecal urgency.
- The autonomic nervous system harmonizes the brain and the body
- These coordinating centers degenerate in Multiple System Atrophy (MSA)
Who works harder to get blood to their brain? A man or a giraffe?
- How much blood is below the heart (pump)?
- Man: 75% of their blood is below the heart
How often does MSA happen?
- Muscle system atrophy has a prevalence of 4.4 cases per 100,000 people
- 58% of MSA patients develop Parkinsonian type
- 29% of MSA patients develop cerebellar type
- Compared to Parkinson’s disease: approximately 2,000 per 100,000 people, about 500 times more common
- Synapse: the way cells talk to one another
- Axon (the talking end of the nerve cell) sends a signal to the dendrite (the listening end of the nerve cell)
Let’s focus on Orthostatic Hypotension: What is it?
- A drop in blood pressure when you stand up of > 20 systolic mm Hg or >10 diastolic mm Hg
- Symptoms: systolic drops below 100 or > 60 total drop in blood pressure
- Problem: nerves to blood vessels don’t work; vessels stay open when you stand up
- Problem: when your blood pressure falls, you may fall too!
The Baroreflex: How does it work?
- Senses change in pressure: the blood pressure drop is sensed on the venous side of the right atrium, and the pressure rise is sensed on the arterial side of the aorta and carotids
- Adjusts pressure by: vasoconstriction (increases norepinephrine) and vasodilation (increases nitric oxide)
- These are opposite systems moving blood from the gut and skin to the main circulation; the moveable blood depends on a person’s setting (e.g., digestion, hot environment, etc.)
- Causes increasing or decreasing heart rate
- In MSA, the baroreflex fails us in 2 ways: when there is a need for higher blood pressure (resulting in orthostatic hypotension), or when there is a need for lower pressure (resulting in supine hypotension)
Beware! People with MSA may not know when their blood pressure drops
So, can you do anything? Yes, LOTS
- The main failure is not selecting the wrong drug, but failure to back up the drugs with non-pharmacologic measures
- Remember: you can’t pump a dry well. Drugs primarily pump the well, salt and fluid fill the well.
Blood Pressure Restoration
A. Increasing Central Volume
- Salt loading (fill the well) may require 3 to 15 g per day
- High pressure hose with abdominal binder
- Elevate head of bed: microgravity signals kidneys to reduce total volume (less signal -> pee less at night)
B. Tighten those vessels again!
- Water drinking
- Frequent small meals (both food and insulin are strong vasodilators)
- Physical counter maneuvers
- Physical exercise: water jogging, land exercise training, core building
- Self-tilt exercises
Salt has 2 Actions
- Short term: increases the volume of blood (need 96 fluid oz water)
- Over the long haul: reduces nitric oxide synthase which dilates the blood vessels, a double negative that makes BP higher
- Start with 1 gram twice per day, and go up or down based on response
- 8-16 oz water
- Don’t include salt in it
- Cross your legs
- Sit w/legs crossed
- “Party” pose
- Daily 10-minute minimum, 30 minutes is better
- Interval training with 90 min cycle
- Can start with water jogging if balance or endurance are major problems
- Improves: mitochondrial function in the brain, motor coordination, baroreflex function, delays disease progression in Parkinson’s