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exercise is more suggestive of cardiomyopathy or primary electrical disturbance such as
Wolff-Parkinson-White syndrome or right ventricular dysplasia.

Cerebrogenic cardiac dysfunction has also been observed. Arrhythmias, conduction block,
and repolarisation ECG abnormalities have been reported in up to 56% of epileptic seizures.
Abnormalities appear to be more common in nocturnal, prolonged, and generalised seizures
than in focal seizures or those occurring during wakefulness28-32.

Differentiation
The differentiation between epileptic seizures and syncopal attacks can be difficult.
Typically, patients with epilepsy have more episodes of loss of consciousness and a longer
history than patients with syncope. Clinical features that are most strongly predictive of
syncope of any cause versus seizures are a postural component, a prior history of presyncopal
episodes with unpleasant situations, diaphoresis, dyspnoea, chest pain, palpitations, a feeling
of warmth, nausea, and vertigo. Patients are also more likely to have hypertension and
ischaemic heart disease.

In a study evaluating the utility of a diagnostic questionnaire, epilepsy was predicted by the
presence of tongue biting, urinary incontinence, prodromal déjà vu, post-ictal confusion,
mood disturbance, muscle pain, headaches, witnessed convulsive movements, head turning
and cyanosis17. The application of the questionnaire resulted in a diagnostic accuracy of 86%,
suggesting that the careful evaluation of the history from the patient and witness is of
principal importance in attaining the correct diagnosis. It is important to note that syncope
due to primary cardiac disease may present with sudden collapse and have a less well defined,
or often completely absent, prodromal period compared to vasovagal syncope18,16,33.

In patients with syncope, neurological and cardiological examinations are frequently
unrewarding. Further investigations may be necessary and are dependent on the history
obtained. Extensive investigation is not mandatory, however, in patients with, for example, a
typical history of neurocardiogenic syncope. A 12-lead ECG should, however, be undertaken
in all patients. Patients with an abnormal cardiological examination or 12-lead ECG or those
patients with a family history of sudden cardiac death or a personal history that is atypical for
neurocardiogenic syncope, for example, episodes during exercise, while lying flat or with
palpitations, warrant more extensive cardiac investigations including a transthoracic
echocardiogram, prolonged ECG monitoring and, frequently, tilt-table testing.

In conditions such as Brugada syndrome, the ECG abnormalities may be intermittent. Serial
ECGs in undiagnosed syncope may, therefore, be helpful. In patients with infrequent
episodes, one- to seven-day prolonged, Holter-type, ECG recordings have a yield of less than
1%11 and implantable loop recorders, which can monitor cardiac rhythm for up to 18 months,
are more appropriate, with a yield in unexplained syncope of up to 50%34-36. Autonomic
function testing, and more specifically tilt-table testing (for example, 70º tilt for 45 minutes)
also has high sensitivity (approaching 70%) for identifying patients with a syncopal tendency,
particularly in patients over the age of 50 years with recurrent syncope and no structural
cardiac pathology37,38, but reproducibility has been reported to be poor39. Measures to induce
syncope, such as isoprenaline, provoke syncope more rapidly and provide additional
sensitivity (1015%), but at the expense of reduced specificity40.

Prognosis and treatment
The prognosis and treatment of syncope is entirely dependent on the underlying aetiology.
Structural heart disease significantly increases the risk of death in patients with syncope11.
For example, patients with syncope and severe left ventricular failure have a one-year
mortality rate of 45% compared to a similar group of patients with cardiac failure but no
syncope10,26,27. In contrast, patients with neurocardiogenic syncope, aged 45 years or less,