© 2005 The European Society of Cardiology. Published by Elsevier Ltd. All rights reserved.
EDITORIAL
Explaining syncope: Faints need not confuse
Department of Neurology and Clinical Neurophysiology, Leiden University Medical Centre PO Box 9600, 2300 RC Leiden, The Netherlands
Manuscript submitted 2 February 2005. Tel.: +31 71 526 3960; fax: +31 71 5248 253. E-mail address: j.g.van_dijk.neur{at}lumc.nl
Key Words: syncope, diagnosis, transient loss of consciousness
Feeling for words
Many physicians frequently have to deal with ‘syncope’ and its differential diagnosis, so they may be expected to have a practical working knowledge of what it is, for what it can be mistaken, and how to proceed from a working hypothesis. In medicine, a ‘practical working knowledge’ is more often the result of experience than of a formal medical education. It would be good if this knowledge could simply be directly taught to others, but it is surprisingly difficult to convey a working knowledge clearly enough for others to find it equally workable. Putting knowledge into words requires much thought, and often forces discovery of truths previously unknown, explaining why teaching is such a good learning experience. Syncope is an excellent example of a concept that one may be able to work with and yet cannot define precisely, as a simple thought experiment may reveal: please stop reading until you have formulated the best definition of syncope you can.
Chances are that your definition is similar to the following: ‘syncope is a transient loss of consciousness, with loss of postural control causing patients to fall’. If so, you are in good company, as similar definitions can be found in many textbooks and papers. It appears to contain three key features: unconsciousness, falling, and a transient nature. There are in fact only two, as a loss of consciousness is not compatible with actively sitting or standing or being upright.1 If your definition was limited to these elements, logic dictates that you label every condition that fulfils these criteria as syncope. Thus, concussion is syncope, a subarachnoid haemorrhage may present with syncope, and a textbook tonic–clonic generalized epileptic seizure will also be classified by you as syncope. But if these conditions do not fit your concept of syncope, and I certainly expect most physicians feel this way about epileptic seizures, your definition needs rethinking and sharpening.
Thinking it through
The Task Force on Syncope of the European Society of Cardiology (ESC) [1,
2] faced the same problem: a way had to be found to include loss of consciousness due to arrhythmia, orthostatic hypotension or the ‘common faint’, while excluding psychogenic attacks of feigned unconsciousness and epileptic seizures. Here is the result: ‘Syncope is... defined as a transient, self-limited loss of consciousness, usually leading to falling. The onset of syncope is relatively rapid, and the subsequent recovery is spontaneous, complete, and usually prompt. The underlying mechanism is a transient global cerebral hypoperfusion.’
The Task Force's solution was to introduce a pathophysiological cause to the definition in the form of cerebral hypoperfusion. This represents the first of two major improvements over other definitions. At first, this addition may appear impractical as ‘cerebral hypoperfusion’ is not a straightforward clinical entity that can be established through history taking, in contrast to the rest of the definition. Would it not have been better to keep the definition all clinical? The simple truth is that there are no clinical features that distinguish between the conditions felt to be ‘syncopal’ while excluding the others (or if there are, they are unknown). This realization meant that ‘syncope’ should only be used when it is at least probable that the cause of a spell of unconsciousness is cerebral hypoperfusion. The second major improvement was that this necessitated a term to use when the nature of the spell is as yet unclear. The chosen term was ‘Transient Loss Of Consciousness’ (TLOC), with four features: loss of consciousness, a transient and self-limited nature, and it must not be due to an external cause. The last item is meant to exclude concussion that can usually be recognized easily. ‘TLOC’ can be used in a classification or epidemiological setting to encompass all disorders that share this presentation, including syncope as well as epileptic seizures. It can also be used to describe individual attacks that cannot yet be specified, with the advantage that it forces physicians to keep an open mind regarding the cause. The Task Force's work illustrated how sharpening a definition of syncope made the whole problem of temporary unconsciousness spring into focus.
Different angles
Two reviews on syncope provided a wholly different approach to syncope: one in the New England Journal of Medicine [3], and a more recent one in the British Medical Journal [4]. In the first one syncope was ‘defined as a sudden loss of consciousness associated with the inability to maintain postural tone, followed by spontaneous recovery’. The study was retrospective and spanned for 17 years. Can we be certain that this definition was in fact used? One group of causes was categorized as ‘neurologic’ and included syncope due to stroke, transient ischaemic attack, and seizure, suggesting at first glance that the definition was taken literally. The first indication that this was not so is how concussion was classified.
Concussion should fall under the given definition of ‘syncope’, but there were only 48 cases of ‘syncope due to concussion’, which appears to be very low in view of the large number of person-years. The inclusion of seizures, stroke and TIAs point to a TLOC-like concept, but it is equally doubtful that all such cases were included. Even more important is that TIAs do not cause unconsciousness in the vast majority of cases, making it clear that the physicians who used ‘syncope’ at the time did not do so in a consistent manner.
Although the BMJ paper focused on ‘neurocardiogenic’ syncope, a definition and classification of syncope itself was provided. Syncope was defined as ‘a transient loss of consciousness, with loss of posture (that is, falling)’. Causes of ‘syncope’ were cardiac, metabolic, psychiatric and neurological. The latter group included ‘seizure disorders’ (epilepsy), suggesting that their definition equalled TLOC as defined above, with one exception: the ESC Task Force excluded concussion from the definition of TLOC, as this rarely features in the diagnosis of syncope or seizures. But concussion is not listed as a cause of syncope in the BMJ paper, meaning that either the list was incomplete or the definition lacked something. A comparison of the listed causes of ‘syncope’ with the ESC classification (Fig. 1) reveals how well the provided definition fitted the problem.
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The four cardiac causes of ‘syncope’ also feature as syncope in the ESC classification, but not all as ‘cardiac’. Arrhythmia and structural cardiac disease are obviously cardiac in nature, but this does not hold for orthostatic hypotension. What is cardiac about the inadequacy of the sympathetic nervous system to keep up peripheral vascular resistance in autonomic failure? It also does not hold for reflex syncope. The theory that the afferent signal triggering the reflex is carried by cardiac C-fibres in some types of syncope has been disproved, and was in fact never invoked for other types of reflex syncope such as micturition syncope or carotid sinus stimulation.
Metabolic causes of ‘syncope’ are stated as hypoxia, hypoglycaemia and hyperventilation. In defence of hypoxia one may argue that cerebral hypoxia is the cause of unconsciousness in cerebral hypoperfusion, but it is likely that hypoxia is mentioned as a primary mechanism. Choking on an object or a severe attack of asthma are primary causes of hypoxia, but the resulting unconsciousness takes longer to develop and longer to resolve than in syncope. Moreover, these conditions are not necessarily self-limited. A similar reasoning applies to hypoglycaemia. In the ESC classification, these conditions do not fall under the headings of syncope or TLOC. As for hyperventilation, it should be understood that there is no formal proof that it is possible to lose consciousness by hyperventilating, and this does not seem likely. The clinical features attributed to the ‘hyperventilation syndrome’ cannot be attributed to the act of hyperventilation, and suggest panic attacks, that do not look like syncope.
The psychiatric causes of ‘syncope’ contain conditions that are not associated with loss of consciousness, and cannot therefore be considered as syncopal under any definition. There is no way to lose consciousness through a direct mental mechanism. Psychiatric disorders can cause true syncope, but always indirectly: examples are voluntary induction through the ‘fainting lark’, reflex syncope through fear, and orthostatic hypotension due to drugs. The ESC solution was to label such conditions as ‘apparent syncope’ and not as syncope or TLOC.
This leaves ‘neurological syncope’. Some forms of generalized epilepsy cause loss of consciousness, and may therefore logically be regarded as ‘syncope’ under the definition provided in the paper (in the ESC classification these are recognised as TLOC and not as syncope). The inclusion of TIAs is most unfortunate: carotid artery TIAs almost always cause neurological deficit without loss of consciousness, while syncope causes loss of consciousness without neurological deficit. Only vertebrobasilar TIAs might cause loss of consciousness, but there too neurological deficit is very prominent. The subclavian steal syndrome is classified as syncope by the ESC, as it can cause loss of consciousness due to cerebral hypoperfusion. The inclusion of normal pressure hydrocephalus is odd. This disorder causes dementia, incontinence and a gait disorder. The latter may cause falling, but the falls are not due to loss of consciousness and therefore not syncope.
Sharpening or blurring?
In summary, using a definition of syncope that has not been thought through can result in a collection of disorders that are syncope, that may look like syncope but do not cause loss of consciousness, that do cause unconsciousness but do not resemble syncope, or that merely cause a fall. The consequences of using such unclear terms have not been measured, but can only be harmful. Can this help in formulating a differential diagnosis? Can it help to teach colleagues or medical students what syncope and related disorders are all about? The result may be the opposite of what was intended; instead of providing colleagues with a workable knowledge by sharpening their focus it is possible that crucial concepts such as epilepsy and syncope become even more blurred than they are already. At present, many studies on syncope do not provide a definition of syncope, and in many other cases the provided definitions were apparently not used, or not completely, or not always, or in differing patients. That is hardly science, and it is not the basis for patient care. Deblurring is the only solution.
Footnotes
1Some may argue that, as consciousness refers to the awareness of one self and one's surroundings, any state in which this is not the case represents unconsciousness [meaning that absence seizures would represent loss of consciousness]. In practice, however, the term unconsciousness is restricted to a low state of arousal, i.e. a sleep-like state. Epileptologists use ‘altered’ or ‘impaired’ to describe consciousness in absence seizures, but not ‘lost’. Hence, we may say that loss of consciousness is not compatible with standing. 
2A member of the Task Force on Syncope of the European Society of Cardiology, and is in favour of the definition and classification of syncope formulated by that Task Force.
References
[1] Brignole M, Alboni P, Benditt D, Bergfeldt L, Blanc JJ, Bloch Thomsen PE, et al. Guidelines on management (diagnosis and treatment) of syncope. Eur Heart J 2001; 22: 1256–1306.
[2] Brignole M, Alboni P, Benditt D, Bergfeldt L, Blanc JJ, Bloch Thomsen PE, et al. Guidelines on management (diagnosis and treatment) of syncope – update 2004. Europace 2004; 6: 467–537.
[3] Soteriades ES, Evans JC, Larson MG, Chen MH, Chen L, Benjamin EJ, et al. Incidence and prognosis of syncope. N Engl J Med 2002; 347: 878–885.
[4] Chen-Scarabelli C and Scarabelli TM. Neurocardiogenic syncope. Br Med J 2004; 329: 336–341.
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