Fun facts about syncope
Syncope (n.) from the Greek, for “cessation.” As in, cessation of consciousness. I wanted to talk about syncope today because I was reminded of a funny thing that happened several years ago. While in medical school, I watched my younger brother, Alex, graduate from his basic training as a US marine. Besides how breathtaking the ceremony was and the pride I felt for my younger brother, something stood out to me. Or rather, did not stand out. Several of the graduating cadets collapsed while standing at attention. Where once there was a stone-faced soldier standing at attention before the small crowd of family and friends, there was now a limp pile of flaccid muscle that had folded into the concrete quad. And this would not be unusual, but why did this happen?
In this week’s episode, we discuss the interesting clinical manifestations of syncope, some of the more esoteric neurologic causes, and then why it happens that our elite and physically fit US military personnel will frequently pass out after simply standing? So let’s review some interesting factoids.
Fact no. 1. The average duration of syncope is about 12 seconds. That’s 12 seconds of unresponsiveness. I used to think that if a patient collapsed and lost consciousness for more than 5-10 seconds, then maybe it was an epileptic or cataplectic event. But it turns out that half of patients who syncopize will remain on the ground and immobilized for longer than 12 seconds. And when you think about it pathophysiologically, if cerebral perfusion is not restored, then impaired consciousness can last even longer.
Fact no. 2. Headaches may happen. Not just from falling and hitting your head. But actual neck pain from hypoperfusion to the suboccipital or posterior cervical muscles has been reported–the so called “coat-hanger headaches.” Also, migraines are known to cause syncope as well. But treating the migraines don’t necessarily prevent the associated syncope in adults. Not sure why…
Fact no. 3. Syncope can look like seizure. Experts have reported that some degree of shaking can occur in up to 90% of patients. Syncope should always be in your differential diagnosis for convulsions, even when seizure is most suspected. So how can we distinguish the two? Well I found this table that has a little bit of information you might find useful.
But why does syncope occur? Pathophysiologically, syncope is at its core a neurologic process from impaired cerebral blood flow. Specifically the blood flow to the ascending reticular activating system of the brainstem, and possibly the bilateral cerebral hemispheres. The nervous system unconsciously modulates blood pressure and cerebral perfusion via the carotid sinus and aortic arch baroreceptors, which sense changes in blood pressure and convey this information via the glossopharyngeal and vagus nerves to the nucleus of the solitary tract in the brainstem.
Fact no. 4. Standing will eliminate 500-1000 cc’s of peripheral blood from your circulation and deposit it into the gravity-dependent capacitance beds of the lower extremities and the abdomen. That’s nearly 20% of your circulating blood. Just, gone. As long as you have intact sympathetic circuitry, the body will quickly compensate for this loss of venous return by increasing systemic vascular resistance, and neurohumoral responses mediated by vasopressin will increase circulating plasma volume and cardiac output on a longer time scale. So most people are unaffected by this, unless they are already at greater risk of impaired venous return (e.g., dehydration), or they have impaired autonomic circuitry (e.g., poorly controlled diabetes).
So what are these other unusual causes of dysautonomia? In no particular order…
- Liver or kidney failure
- Nutritional deficiency (e.g., B12)
- Hereditary amyloidosis (e.g., transthyretin gene mutation)
- Primary amyloidosis
- Sjogren’s syndrome (Sicca)
- Familial dysautonomia
- Paraneoplastic autonomic neuropathies
- Autoimmune pandysautonomia (anti-ganglionic acetylcholine receptor antibody)
What does any of this have to do with the military graduation and how does it explain how those soldiers passed out?
It turns out that it’s a combination of factors, most of which we’ve already covered. Reduction in cardiac preload (from dehydration and venous pooling, as well as extravasation of plasma after extended durations of standing) and poor autonomic compensation (maximized sympathetic output, impaired cerebral autoregulation) are all it takes to prevent enough blood to get to the brain. Only 20% of circulating blood is directed to the brain, so this organ can’t stand to lose much more before it says “to hell with you” and then it employs a survival mechanism to drop the head to the level of the heart.
At the conclusion of our show this week, we spoke a bit about prognosis with syncope. A third of patients will syncopize at least one more time in the near future. And besides self-injury, what are some of the more worrisome consequences of syncope? Well, as a neurologist, there have been several interesting cohort studies that have identified a risk of dementia in patients with orthostatic hypotension. Now, you might be thinking—well, Jim, autonomic dysfunction is not uncommon in the elderly to begin with, and we also see it commonly in several other syndromes associated with dementia, particularly Parkinson Disease and several of the Parkinson-plus synucleinopathies like Dementia with Lewy Bodies and Multiple Systems Atrophy. Or, you might think that orthostatic hypotension may increase your risk of impaired brain perfusion, causing the slow accumulation of infarcts and a vascular dementia. But, what is interesting is that orthostasis increases your risk of Alzheimer Disease (AD). And so does hypotension. The thought here is that insufficient perfusion will increase the buildup of beta-amyloid plaques, and these result in AD. Obviously, we also worry about the converse. With uncontrolled hypertension, you’re at a greater risk of vascular dementia. So you’ve got to find that happy medium to keep that happy brain. 🙂
BrainWaves audio and online content are intended for educational purposes only and should not be used for routine clinical decision making. That being said, it’s always a good idea to stay hydrated and avoid locking your knees if you’re going to be standing up for quite a while.
- Freeman R. Clinical practice. Neurogenic orthostatic hypotension. The New England journal of medicine. 2008;358:615-24.
- Grubb BP. Neurocardiogenic syncope and related disorders of orthostatic intolerance. Circulation. 2005;111:2997-3006.
- Wolters FJ, Mattace-Raso FU, Koudstaal PJ, Hofman A, Ikram MA and Heart Brain Connection Collaborative Research G. Orthostatic Hypotension and the Long-Term Risk of Dementia: A Population-Based Study. PLoS Med. 2016;13:e1002143.
- Sonnesyn H, Nilsen DW, Rongve A, Nore S, Ballard C, Tysnes OB and Aarsland D. High prevalence of orthostatic hypotension in mild dementia. Dement Geriatr Cogn Disord. 2009;28:307-13.