This post originally appeared on PEMBlog back in August of 2014 and has been reposted because I think it is a really important topic.
Certainly we’ve all taken care of of the patient with the chief complaint “possible seizure.” Upon history and examination many of us will discover that the patient had syncope. So, the purpose of this post is to examine how we differentiate between convulsions in a epileptic seizure versus those that occur when a patient faints. Read on!
What actually happens when a patient faints?
There is a brief loss of consciousness that is associated with transient global cerebral hypoxia. The most common causes of syncope in the pediatric population are:
- Vasovagal (neurocardiogenic): 50% of cases that present to the ED. Often precipitated by prolonged standing and physical or emotional stress. Most patients experience the typical prodrome, which includes lightheadedness, dizziness, pallor, diaphoresis, nausea and visual changes. The reflexes that govern heart rate and vasomotor tone are exaggerated, and a drop in BP leads to global cerebral hypoperfusion.
- Breath-holding spells: Seen in toddlers and triggered by emotional stress (tantrum) or minor painful stimuli. They can lead to loss of consciousness and brief posturing or tonic-clonic convulsions. Read here for more.
- Orthostatic hypotension: This is syncope that occurs with postural changes (prolonged standing, just standing up upon being supine for a prolonged period of time). An abrupt drop in BP may result from dehydration, pregnancy (venous pooling in the lower extremities), anemia, anorexia nervosa and certain medications (diuretics and other BP meds).
Other causes for fainting include:
- SVT
- Bradycardia
- Arrhythmia
- Pulmonary hypertension
- Basilar migraine
- Seizure
- Hyperventilation
- Conversion disorder
- The choking game
- Narcolepsy
What is convulsive syncope?
A common variant of syncope that is associated with brief tonic or myoclonic activity. These convulsions are thought to occur because the brain doesn’t like to be oxygen deprived. The early stages of hypoxia appear to induce motor centers in the brainstorm reticular formation. Studies from the 1950s in experimentally induced syncope of humans showed no epileptiform activity on EEG when fainting patients convulsed. Maneuvers used to induce syncope include forced valsalva, hyperventilation + valsalva, acceleration on a centrifuge (whee!), venipuncture, ocular compression and more.
What does it look like?
Almost immediately after “passing out” patients will experience anything from twitching of the mouth to violent four extremity jerking. Myoclonic jerks are often seen. It can be multifocal and asynchronous, as opposed to the rhythmic convulsions of generalized tonic clonic epileptiform seizures.
Children that have breath holding spells often have dramatic opisthotonic posturing. Some patients will have tonic posturing early in their syncope and fall to the ground as if they were “stiff as a board” rather than slumping down. Some patients will even have complex motor movements like fumbling of the hands, arching out lip licking and more. Some patients moan and growl. If the eyes are open you may note upward turning of the eyes (rolling back in the head). This can also be accompanied by subtle downbeat nystagmus or transient deviation.
Syncopal convulsions are almost always brief, lasting less than 30 seconds. Patients DO NOT have a protracted postictal period and “come to” relatively quickly. They often recognize that they fainted, or ask “what happened.”
I’m not sure why it is filed under “Entertainment” at NeurologyNerd.com – but these videos of German students with induced syncope are incredibly demonstrative when it comes to giving you an idea of all of the different motor eccentricities of syncope. I think that it’s a must watch.
How common is it?
The short answer is VERY. The overall incidence varies quite a bit according to dozens of studies, and may depend on the precipitating cause. The initial studies were done almost 70 years ago – and though I did not read them upon initial publication I do think that our physiology has not changed, thus they still hold water. Overall the incidence falls somewhere in the range of 5-15% but could be as high as 50%. Many of these studies are retrospective reviews, case series or video-based studies of induced syncope.
Should we be more worried if the patient has convulsions with syncope?
If the patient has returned to a normal neurologic status and has a reassuring cardiac history and exam – NO. An EKG is an excellent screening test that will allow you to rule out heart block, long QTc, WPW and right heart strain form primary pulmonary hypertension. Perhaps in adults we should, as some studies have indicated that convulsive syncope may be associated with underlying arrhyhtmia (see Kanjwal, 2009 and MacCormick, 2011) – but in children and healthy adolescents there is no increased associated with cardiac pathology in convulsive syncope versus nonconvulsive fainting.
What should we tell patients and families?
I can’t think of anything more terrifying for a family to witness than a seizure. The first thing you need to do is clearly explain what you believe happened, and why you are reassured based on your H&P and available tests. Find out what the patient/family’s experiences are with seizures (maybe they have an uncle with epilepsy for instance), and dispel common myths. Use your knowledge of epidemiology and pathophysiology to discuss why neuroimaging is not warranted. And don’t say “they just fainted, they’re fine.” Of course the family wants to know that their child is OK, but their are more deft and tactful ways to do it. And, as with any other patient with syncope, discuss ways to prevent further episodes – like staying adequately hydrated, eating regular meals and recognizing the symptoms of presyncope.
