Affected individuals may experience a temporary loss of consciousness or “blackout,” a condition known as syncope. There may be a gradual build up to an episode of syncope or it can occur suddenly.
A serious complication of OH is the risk of falling, which can lead to physical damage such as a broken hip or other broken bones. The constant dropping and raising of blood pressure associated with OH has also been identified as a risk factor in the development of stroke and other cardiovascular diseases.
Symptoms of OH on standing have been aggravated by raised ambient heat, such as hot weather, hot shower, hot tub, or when an affected individual has a fever. OH is often more common and more severe in the morning. Some individuals with NOH develop postprandial hypotension, which is defined as the development or worsening of hypotension approximately 30 minutes to 2 hours after eating a meal, particularly large meals high in carbohydrates.
OH can be caused by certain chemotherapy drugs which can cause an autonomic neuropathy. A common cause of OH is the decrease in volume of circulating blood (hypovolemia) resulting from excessive use of medications that increase urination and sodium loss (diuretics), or from drug therapy that widens blood vessels (vasodilators) for the treatment of high blood pressure, heart failure or chest pains (i.e., calcium blockers and nitrates). Commonly used vasodilator drugs include levodopa for Parkinson’s disease...
Some individuals with NOH may also have high blood pressure when lying down (supine hypertension). Supine hypertension complicates treatment options for affected individuals.
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aspergerian13
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Interesting subject. My experience is of having near syncope immediately after exercise. More precisely, I walk 4 miles at 4mph and have no trouble until I stop. Then after a few seconds I begin to feel faint. This lasts just a few seconds. I've only actually fainted once, but I must have experienced a near faint about 50 times. My first aid is to walk on the spot, drink water and eat crisps for their salt.
Though its under the heading rare conditions it seems some degree of hypotension is common in PD due to the involvement of the autonomic nervous system.
Yes, and levodopa is a vasodilator enhancing the likelihood of orthostatic hypotension and syncope. Postprandial blood flow ma also be a contributing factor in some pwp.
"Conclusions Acute OH occurs frequently when starting dopamine agonist therapy in Parkinson's disease, but is frequently not appreciated by patients. Knowledge of acute blood pressure responses may be useful when making decisions regarding agonist titration schedules in clinical practice.
"MEDICATIONS used to treat Parkinson's disease (PD), including levodopa,1 may result in orthostatic hypotension (OH). Dopamine agonists can markedly reduce blood pressure, and precipitous changes can occur even with the first dose.2 Dopamine agonists lower blood pressure primarily by venous and arterial dilation through inhibition of the sympathetic nervous system.3 Because apomorphine hydrochloride and bromocriptine mesylate decrease blood pressure in normotensive and hypertensive subjects,4 dopamine agonists have been used in the treatment of high blood pressure.5 In PD, OH has been a well-recognized adverse effect of all available dopamine agonists, including bromocriptine, pergolide mesylate, and the newer agents, pramipexole dihydrochloride and ropinirole hydrochloride.6,7 These studies reported OH as an adverse event associated with the administration of dopamine agonists at any point rather than as an acute effect of starting the medication. We studied the frequency and severity of acute changes in supine and standing blood pressure readings when patients took their first dose of a dopamine agonist. An acute change in blood pressure strongly suggests a direct dopamine agonist effect rather than an underlying illness (dehydration or infection) or concurrent medication (antihypertensive or antiparkinsonian) that may have resulted in an adverse event being reported in previous studies. This information would be useful when making decisions regarding subsequent titration and dosing schedules, to assure patient safety and drug tolerability."
An important contribution to this thread. I discontinued ropinirole several years ago, never used much per day. As my levodopa ingestion per day increased, I was risking c heart effects. Perhaps someone can find a comparison of rates between ropinirole use and high-end levodopa ingestion.
There seems to be spectrum of pathologies related to orthostatic hypotension. An individual pwp does not manifest all pathologies within that spectrum. Cite 12 in the article you linked is:
Neurogenic orthostatic hypotension: pathophysiology, evaluation, and management.
This doesn't particularly thrill me, since Sinemet does make it possible for me to deal with many PD symptoms, where, at least, I can manage to get around. All medicines have side effects, that is a given.
Aspergerian, Sorry but I’m not sure what particular point you are making but I do think that nOH (neurogenic orthostatic hypotension) is perhaps not well understood by many of us. Also i cant find the spectrum of pathologies related to OH.
OH (Orthostatic hypotension) is a symptom of autonomic dysfunction which probably 90% of pwp have.
My understanding is that OH is part of PD for many of us and it can be made worse by our drugs, especially levadopa eg sinemet and dopamine agonists eg ropinerole.
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Help with research... identifying the cause of orthostatic hypotension & autonomic dysfunction
Any suggestions to manage orthostatic hypotension?
Blood Pressure 
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