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SYMPTOMS AND SIGNS
Transient loss of
consciousness (excluding
epilepsy)
Sanjiv Petkar
Adam Fitzpatrick
Paul Cooper
Abstract
Patients are often referred suffering from a ‘Collapse cause’. In some
of these patients, the ‘collapse’ would have been caused by or associated
with loss of consciousness. The three main and common causes
of transient loss of consciousness (T-LOC) are syncope, epilepsy and
non-epileptic attack disorder (NEAD). The term T-LOC excludes patients
in whom the loss of consciousness is induced by trauma or is prolonged
(e.g. metabolic disorders like hypoglycaemia and hyponatremia). Among
the causes of T-LOC, syncope, which is a symptom with many underlying
causes, is much more prevalent than either epilepsy or NEAD. This article
will deal predominantly with syncope and how it can be differentiated
from epilepsy and NEAD.
Keywords blackouts; collapse; epilepsy; implantable loop recorders;
psychogenic blackouts; syncope; transient loss of consciousness
loss of consciousness or in some instances, even coma (from the
Greek ‘koma’, meaning deep sleep). T-LOC also excludes those
in whom the loss of consciousness occurs as a result of trauma
(e.g. concussion, intracerebral bleed). It is worth mentioning that
transient ischaemic attacks are rarely associated with T- LOC,
being typically characterized by neurological deficit without loss
of consciousness, as opposed to syncope in which patients experience
loss of consciousness without a neurological deficit.
Definitions
The European Society of Cardiology defines syncope as ‘a
transient, self-limited loss of consciousness, usually leading to
collapse. The onset of syncope is relatively rapid, and the subsequent
recovery is spontaneous, complete, and usually prompt.
The underlying mechanism is transient global cerebral hypoperfusion’.
2 Syncope is a symptom, not a diagnosis, the many causes
of which are listed in Table 1.
An ‘epileptic seizure’ is defined by the International League
Against Epilepsy (ILAE) and the International Bureau of Epilepsy
(IBE) as a ‘transient occurrence of signs and/or symptoms due to
an abnormal excessive or asynchronous neuronal activity in the
brain’. 3 A diagnosis of ‘epilepsy’ is reserved for those patients
who have recurrent ‘epileptic seizures’.
NEAD are ‘unintentional paroxysms of altered sensation,
movement, perception, or emotion that clinically resemble
epileptic seizures but are not accompanied by epileptiform neurophysiological
changes’. 4
Introduction
It is common to come across patients referred having had a ‘Collapse
cause’. ‘Collapse’, which has many causes, is a sudden
and often unannounced loss of postural tone, often, but not necessarily
accompanied by loss of consciousness. In those patients
in whom ‘Collapse’ is caused or associated with loss of consciousness,
the duration of this ‘mental state that involves complete
or near-complete lack of responsiveness to people and other
environmental stimuli’ can vary. 1 Transient loss of consciousness
(T-LOC) or blackout is commonly caused either by syncope,
epilepsy or a non-epileptic attack disorder (NEAD). Intoxication,
metabolic abnormalities e.g., hypoglycaemia or hyponatremia,
central nervous system diseases, acute neurologic injuries such
as stroke, and hypoxia are often associated with more prolonged
Sanjiv Petkar MRCP is a Clinical Research Fellow and Honorary Associate
Specialist at the Manchester Heart Centre, Manchester Royal Infirmary,
UK. Competing interests: Dr Petkar’s present position is funded by a
grant to the University from Medtronic Inc.
Adam Fitzpatrick BSc FRCP FACC is Consultant Cardiologist at the
Manchester Heart Centre, Manchester Royal Infirmary, UK. Competing
interests: none.
Paul Cooper FRCP is Consultant Neurologist at the Greater Manchester
Centre for Neurosciences, Hope Hospital, Salford, UK. Competing
interests: none.
Causes of syncope
Reflex syncope
• Vasovagal syncope
• Carotid sinus syncope
• Situational syncope (e.g. post micturition, post exercise,
postprandial, cough, swallow, visceral pain)
Orthostatic hypotension
Cardiac arrhythmias as a primary cause
• Sinus node dysfunction (including tachy-brady syndrome)
• Atrioventricular conduction disease
• Ventricular tachycardia and supraventricular tachycardia
• Inherited syndromes, e.g. long QT syndrome, Brugada
syndrome, arrhythmogenic right ventricular dysplasia (ARVD)
• Implanted device (e.g. pacemaker) malfunction
Structural cardiac or cardiopulmonary disease
• LV dysfunction
• Obstructive valvular heart disease, e.g. aortic stenosis
• Remote or acute myocardial infarction/ischaemia
• Obstructive cardiomyopathy
• Acute aortic dissection
• Pericardial disease/tamponade
• Pulmonary embolism/pulmonary hypertension
Adapted from The Task Force on Syncope, Europace 2004; 6: 467–537. 2
Table 1
MEDICINE 36:10 531 © 2008 Published by Elsevier Ltd.

SYMPTOMS AND SIGNS
Epidemiology
Syncope is a common problem with an estimated prevalence of
42% during the life of a person living 70 years. 2 It shows a bimodal
age distribution with a high incidence in young populations
(median age 15 years), with a second peak in older patients ≥75
years of age. Females are more prone to syncope than men. The
prognosis of syncope depends on its cause. Reflex syncope, the
commonest cause of syncope, has a mortality which is near to
0%, 2 while cardiac syncope is an independent predictor of mortality
and sudden death. In patients with advanced heart failure
and a mean ejection fraction of 20%, the one-year mortality can
reach as high as 45%. 2
Pathophysiology
A sudden cessation of cerebral blood flow for 6 to 8 seconds, a
decrease in systolic blood pressure to 60 mmHg, or a 20% drop in
cerebral oxygen delivery, has been shown to be enough to cause
complete loss of consciousness. 2 A number of control mechanisms
are critical in maintaining adequate cerebral oxygen delivery:
• cerebral autoregulation
• local metabolic and chemical control
• arterial baroreceptor induced adjustments of heart rate, cardiac
contractility, and systemic vascular resistance
• intravascular volume regulation by salt and water intake, hormones
and the renal system.
Whatever the mechanism, a transient global cerebral hypoperfusion
to critical values induces a syncopal episode. As
opposed to healthy younger individuals, 2 ageing alone has
been shown to be associated with a decrease in cerebral blood
flow, 5 and therefore, the risk of failure of these compensatory
mechanisms is likely to be greatest in the elderly or critically
ill patients.
On standing, 0.5 to 1.0 litre of blood shifts to the venous
capacitance vessels below the diaphragm. On continued standing,
a further 10 to 15% of the plasma volume is lost due to
the higher transmural capillary pressure in the dependent parts
of the body. 6 Both of these mechanisms result in a decrease in
stroke volume and cardiac output. A fall in the mean arterial
pressure is prevented by compensatory mechanisms, including
vasoconstriction of the resistance and capacitance vessels. These
adjustments are mediated entirely by the autonomic nervous system
through, mainly, baroreceptors in the aortic arch and carotid
sinuses and mechanoreceptors in the heart and the lungs. Failure
of the above compensatory mechanisms is thought to result
in syncope. 2 The initial trigger of reflex syncope is unknown,
although the relay in the brainstem and the afferent arc are well
understood. 7
Evaluation
The initial evaluation of a patient with syncope consists of a
careful history, physical examination, including orthostatic
blood pressure measurements, and a standard 12-lead electrocardiogram
(ECG). 8 Studies have shown that based on this initial
evaluation, a diagnosis of syncope could be made with certainty
in between 50–63% of patients, 9,10 thus avoiding the need for
additional testing.
History alone may be sufficient in arriving at a diagnosis of the
cause of T-LOC. 11,12 Table 2 lists some of the important clinical
features of the different types of syncope. A good history also
helps to differentiate ‘convulsive syncope’, from epilepsy. If the
clinical features of ‘convulsive syncope’ (cerebral hypoperfusion
associated with abrupt T-LOC resulting in myoclonic jerks) are
not appreciated, it can lead to a misdiagnosis of epilepsy. 8 However,
the yield of history-taking may be limited in the presence of
cognitive impairment in the elderly, a feature encountered in 5%
of 65-year-olds and 20% of 80-year-olds. 13
Physical examination: care should be taken to assess the rate
and regularity of the pulse, lying and standing blood pressure,
examination for scars of previous cardiac operations, and auscultation
for heart sounds and any murmurs. Abnormalities in the
physical examination can point towards a diagnosis of syncope
due to orthostatic hypotension, an arrhythmia or structural heart
disease. On the other hand, in reflex syncope, the examination is
likely to be normal.
ECG
The diagnostic yield of electrocardiography and rhythm recordings
is low, ranging from 1 to 11%. 2,14 However, a 12-lead ECG
is a cheap and reliable test and must be done for every patient
who presents with a T-LOC. A normal 12-lead ECG is a good
prognostic indicator. Abnormalities on the ECG which suggest
or confirm the cause of T-LOC or confer higher risk, are given in
Tables 3 and 4.
Other investigations
Basic laboratory tests have only limited value in the investigation
of patients with syncope and are indicated only if a syncope-like
condition with a metabolic cause is suspected. 8
When the mechanism of syncope is not evident from the
above evaluation, further tests e.g. echocardiography, stress
Clinical features suggestive of specific causes of
syncope
Reflex syncope
• Absence of cardiac disease
• Long history of syncope
• T-LOC occurring after unpleasant sight, sound, smell or pain,
after prolonged standing or in crowded, hot places
• Nausea, vomiting associated with syncope
• T-LOC during or in the absorptive state after a meal
• Head rotation or pressure on the carotid sinus precipitating
T-LOC
• T-LOC occurring after exertion
Cardiac syncope
• Presence of severe structural heart disease
• T-LOC during exertion or supine
• T-LOC preceded by palpitation or accompanied by chest pain
• Family history of sudden cardiac death ≤40years of age
Adapted from The Task Force on Syncope, Europace 2004; 6: 467–537. 2
Table 2
MEDICINE 36:10 532 © 2008 Published by Elsevier Ltd.

SYMPTOMS AND SIGNS
ECG abnormalities suggesting an arrhythmic cause
of syncope
• Bifascicular block (left bundle branch block or right bundle
branch block combined with left anterior or left posterior
fascicular block)
• Other intraventricular conduction disturbances (QRS
duration ≥0.12 secs)
• Mobitz I second-degree atrioventricular block
• Asymptomatic sinus bradycardia (

SYMPTOMS AND SIGNS
Management
Only about two thirds of patients with a syncopal episode see
a doctor or visit hospital for evaluation. 20 In those who do seek
medical attention and when the initial evaluation leads to a certain
diagnosis, no further evaluation is needed and treatment, if
necessary, can be started. 8
Treatment of patients with syncope depends on its cause. In
all patients with reflex syncope, 8 treatment consists of:
• education and reassurance
• lifestyle measures e.g., volume expansion by salt supplements,
head–up tilt sleeping (>10°), isometric leg and arm
counter pressure manoeuvres to abort an impending attack.
In selected cases, the following may be useful:
• tilt training
• drug therapy e.g. midodrine 21
• permanent pacemaker implantation. 22
Treatment in patients with cardiac syncope, again, depends on
the cause and may include:
• drug treatment
• permanent pacemaker or implantable cardioverter defibrillator
implantation
• catheter ablation of arrhythmias
• coronary revascularization, e.g. angioplasty or coronary artery
bypass grafting
• cardiac surgery, e.g. valve replacement.
Conclusion
When managing patients with Collapsecause, in whom one
encounters a history of T-LOC, it is important to remember that
simple tools (a good history, a thorough physical examination
and a 12-lead ECG) can help to differentiate amongst the three
commonest causes of T-LOC i.e., syncope, epilepsy or NEAD. It
is, therefore, of vital importance that one is aware of the clinical
features and presentation of these three conditions. ◆
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MEDICINE 36:10 534 © 2008 Published by Elsevier Ltd.