Introduction

Presentation with a ‘collapse’, ‘blackout’ or ‘funny turn’, with or without impairment of awareness and responsiveness, is common in older people and there is a wide differential diagnosis (Table 62.1). The commonest a etiologies are epileptic seizures, the various types of syncope and cerebral vascular disease. Epileptic seizures and cerebral vascular disease are discussed in other chapters; this chapter deals with syncope and some of the less common a etiologies, such as psychogenic non-epileptic attacks.

Table 62.1 Differential diagnosis of blackouts and funny turns.

The information required to reach the correct diagnosis is usually contained within the history from the patient and from witnesses, and an adequate history will often obviate the need for extensive investigations. Difficulties arise most commonly when no witness account is available. When an attack has been witnessed, attempts should be made to contact a witness, even if he/she was a bystander not previously known to the patient. If a witness has not accompanied the patient to the consultation, a witness account can usually be obtained by making use of that important investigative tool, the telephone, and ringing the relative, friend, care assistant, shop assistant and so on, involved. General practitioners or ambulance personnel called to attend a patient who has collapsed can provide crucial diagnostic evidence, as they are in a position to interview witnesses while the features of the episode are fresh in their minds.

Diagnosis can sometimes be difficult. Pending clarification by the occurrence of further attacks, diagnostic uncertainties may persist even after specialist referral and investigation. It is usually better to accept this diagnostic uncertainty, explaining it to the patient and relatives, than to plunge for a specific diagnosis which may be incorrect and lead to inappropriate treatment and management. In particular, problems arise when non-epileptic attacks are labelled as epileptic. The patient then has to come to terms with an erroneous diagnosis to which significant stigma is still attached, and receives unnecessary antiepileptic drug treatment, possibly with adverse effects.

Syncope

Syncope can be defined as loss of consciousness due to transient impairment in blood flow to the brain. The term ‘presyncope’ can be used to describe symptoms of impending syncope. It is impaired flow to the brainstem and thalamus that is most likely to result in loss of consciousness, and thus adequacy of flow in the posterior (vertebrobasilar) circulation usually determines whether syncope will occur. The impairment in blood flow can occur for a variety of reasons, and it is important to recognize this since the different causes of syncope have differing symptoms and signs. A classification of syncope is given in Table 62.2. The incidence of the different causes of syncope changes with age. In the older patients, areflexic syncope, cardiac syncope and carotid sinus syndrome become increasingly frequent. It is a common problem, accounting for 0.77% of A&E department attendances, with admission rates increasing with age (Sun et al., 2004). A specialist syncope and falls service will improve the diagnosis and outcome (Kenny et al., 2002).

Table 62.2 Classification of syncope.

Mechanisms Underlying Syncope

A sudden fall in blood pressure and syncope can occur due to the following:

Syncope can also occur due to transiently reduced perfusion of the brain in ‘respiratory syncope’, when there is a transient increase in intrathoracic and intracranial pressure (e.g. cough syncope). Finally, a transient reduction in perfusion of the brainstem may also occur in cerebrovascular disease and occasionally present as syncope, for example, vertebrobasilar transient ischaemic attacks (TIAs). In elderly patients, there may be a combination of these mechanisms.

In reflex syncope a fall in blood pressure occurs due to (1) bradycardia and a reduced cardiac output (cardioinhibitory response), (2) vasodilatation in muscle and a reduced peripheral resistance (vasodepressor response), or (3) a combination of these mechanisms (mixed response) (Barcroft et al., 1944; Brigden et al., 1950). In vasovagal syncope, these responses can be distinguished by tilt testing, and in the elderly vasodepressor responses are much more frequent than in younger patients (Galetta et al., 2004). Recognition of this is important as insertion of a cardiac pacemaker is not likely to prevent attacks in patients with vasodepressor responses. In vasovagal syncope there is also reflex vasoconstriction in skin, causing pallor and reflex sweating. The trigger for these reflex responses is usually either ‘psychological’ (e.g. a response to fear, sight of trauma, pain) (Roddie, 1977) or low venous pressure detected by mechanoreceptors in the great veins and heart (e.g. prolonged standing, haemorrhage) (Abboud, 1989). Anoxia can be a trigger, and it is important in the context of anaesthesia and air travel (Sharpey-Schafer, 1956; Bourne, 1957). Non-massive pulmonary embolism may present as syncope, probably by triggering a vasovagal reflex (Castelli et al., 2003). In the carotid sinus syndrome syncope is thought to be triggered by activation of a ‘hypersensitive’ carotid sinus, and can be provoked by carotid sinus massage; again cardioinhibitory, vasodepressor and mixed responses occur. In micturition syncope, the trigger is the sudden loss of the pressor stimulus of a distended bladder (Taylor, 1963), occurring usually when the patient has got up to micturate at night, the skin is vasodilated, and the upright posture has just been assumed (contrary to common belief, ‘straining’ is not an important factor).

In areflexic syncope, the loss of the baroreceptor reflexes that normally keep the blood pressure stable despite changes in posture can occur for a wide variety of causes. These include autonomic neuropathy (in diabetes, Shy–Drager syndrome, Guillain–Barré syndrome, etc.) and spinal cord disease (in particular, traumatic cervical cord lesions) (Bannister, 1988). The baroreceptor responses tend to become more ‘sluggish’ in the elderly, causing an increased tendency to postural syncope with age. This can be exacerbated by a large range of medications, by dehydration, and by some conditions affecting the central nervous system (e.g. Parkinson’s disease). Caird et al. (1973) found a postural fall in blood pressure of more than 20 mmHg in about 30% of a large elderly population, and a fall of more than 40 mmHg in 10%. Drugs implicated included ganglion blockers, diuretics, phenothiazines, antihistamines, antidepressants, benzodiazepines, barbiturates and antiparkinsonian drugs. Davidson et al. (1989) emphasized the role of drugs given for cardiovascular disease in causing syncope, in particular, nitrates, β-blockers and nifedipine. Donepezil may increase the risk of syncope. Orthostatic hypotension and syncope are common in the elderly following haemodialysis.

Cardiac syncope occurs in association with complete heart block (Stokes–Adams attacks), but also with other severe bradyarrhythmias, asystole, and paroxysmal tachyarrhythmias (e.g. ventricular tachycardia). The commonest underlying condition is sinoatrial node dysfunction (sick sinus syndrome), with intermittent sinus arrest or sinus node exit block. If it is associated with atrioventricular block, paroxysmal tachycardia may also occur (tachy–brady syndrome). In the older patient, the arrhythmias will occur most commonly in the context of ischaemic heart disease. Cardiac syncope also occurs with ventricular outflow tract obstruction due to aortic stenosis or hypertrophic cardiomyopathy and may be associated with exertion.

A number of different mechanisms contribute to respiratory syncope (Sharpey-Schafer, 1953; McIntosh et al., 1956; De Maria et al., 1984). The rise in intrathoracic pressure associated with coughing, playing a wind instrument, weight lifting, or performing the Valsalva manoeuvre will be associated with a decrease in venous return to the heart, reduced cardiac output and fall in blood pressure. With cough syncope, which can occur after just one or several paroxysms of coughing, this will be only a brief response. Two additional mechanisms are of probable importance. First, the very high intrathoracic pressure transient is transmitted via the carotid artery to the baroreceptors, causing a more prolonged reflex fall in blood pressure. Second, the very high pressure transients are also transmitted via the venous system to the intracranial cavity, reducing cerebral perfusion pressure. Yet another mechanism is likely to contribute to syncope associated with hyperventilation; the fall in carbon dioxide partial pressure causes vasodilatation in muscle and reduced peripheral resistance.

Vertebrobasilar ischaemia may occasionally present as syncope, but there will usually be additional neurological symptoms. The underlying a etiology might either be embolic or related to critical changes in flow distal to atheromatous disease. With the latter the symptoms may be related to changes in posture.

Clinical Manifestations of Syncope

The usual image of a syncopal attack is of a subject feeling dizzy, going pale, falling with loss of awareness and then recovering rapidly within about 30 s. This sequence of events certainly occurs, but the variety of other manifestations of syncope of different types needs to be emphasized. The motor manifestations are particularly prone to cause diagnostic error and will be discussed first, followed by the other clinical features. In the elderly, presentation may be with a history of falls or drop attacks with no recall of loss of consciousness (Kenny et al., 2001).

Motor Manifestations

A detailed study of vasovagal syncope in normal young volunteers led to important insights into the variety of clinical manifestations of syncope, which is relevant to the differential diagnosis of blackouts at any age. Lempert et al. (1994) induced vasovagal syncope in 56 of 59 volunteer medical students, by asking them to hyperventilate while squatting, and then to stand up performing the Valsalva manoeuvre. They carefully documented the manifestations with video recording. It was only a minority of subjects that lay still after falling, 90% having some asynchronous myoclonic jerks of the limbs. In a few, the jerks were quite vigorous for several seconds, such that the attack might be mistaken for a generalized clonic seizure. Some displayed other motor activity, such as limb-posturing, head-turning, complex movements, eye deviation and eyelid flicker, that might be misinterpreted as manifestations of partial epileptic seizures. Vocalization was frequent.

Similar findings of a very high frequency of myoclonic movements in syncope have also been reported in cardiac syncope (Aminoff et al., 1988). The opportunity to make these observations of the features of cardiac syncope has arisen with patients with recurrent ventricular arrhythmias treated with implantation of an automatic defibrillator, in whom syncope has been deliberately induced by induction of the arrhythmia to test the defibrillator. Simultaneous electroencephalogram (EEG) recording has shown no evidence of associated epileptiform activity. The variety of clinical manifestations of syncopal attacks has also been documented in attacks induced by use of a tilt table (Passman et al., 2003).

In vasovagal and cardiac syncope, therefore, the classic image of the patient falling, lying still for some seconds and then coming round is unusual, and much more often there are jerks and other motor manifestations. In these types of syncope it can be argued that the fall in blood pressure was very sudden and marked, and that this may have predisposed to the myoclonus. There is anecdotal evidence that the patient who faints, and who is propped up on falling rather than falling flat on the ground, is more likely to have myoclonic movements, presumably associated with a more prolonged and severe fall in blood pressure, and rarely the hypoxia may provoke an epileptic seizure. It may be that myoclonic movements are less common in patients with areflexic syncope and postural hypotension, in whom the presyncopal symptoms will often permit preventive measures, the fall in blood pressure is less catastrophic and the blood pressure will be immediately restored once they have fallen.

Other Clinical Features

The various trigger factors for the different types of syncope have been described in the preceeding text, and their importance will be discussed further in the section on diagnosis.

Warning symptoms, before loss of awareness, are common with reflex and areflexic syncope, but are absent in some patients (or not recalled). The symptoms of light-headedness, dizziness and blurring of vision are familiar to most people on standing up from a hot bath too suddenly. Additionally, there may be nausea, ‘hot and cold’ feelings, feelings of depersonalization or distance from the surroundings and buzzing in the ears. In the Lempert et al. (1994) study, described earlier, the students often described having had visual and auditory disturbances. Palpitations, dyspnoea and chest pain may occur (Graham and Kenny, 2001). Warning symptoms in cardiac syncope are less frequent and can consist just of a brief premonition as well as better-defined dizziness. A history of palpitations is usually sought, but positive responses are often difficult to interpret and negative responses are not diagnostically useful.

Marked pallor and clamminess are prominent features of vasovagal syncope due to the reflex vasoconstriction in skin and reflex sweating. In contrast, patients with areflexic syncope and postural hypotension may have relatively little colour change in association with their attacks, there is no sweating and the skin remains warm. Patients with cardiac syncope become pale owing to the marked reduction in cardiac output, and sometimes there is subsequent flushing when the output is restored (but this sequence is not sufficiently consistent or specific to be diagnostically very helpful).

If the opportunity arises to feel the pulse early in vasovagal and other causes of reflex syncope, it will be weak and there will be a reflex bradycardia. In contrast, in areflexic syncope there will be no change in heart rate. In cardiac syncope the heart rhythm changes could, of course, be diagnostic, but it is rare for a chance to arise to feel the pulse in an attack.

Not all syncopal attacks are associated with complete loss of either responsiveness or awareness. In the Lempert et al. (1994) study, 13 of the 56 subjects had a fall associated with only partial loss of awareness, and sometimes with confused behaviour that might be mistaken for a partial epileptic seizure. These phenomena are also well recognized in patients with postural hypotension and areflexic syncope.

Incontinence may occur with syncope of any type, and is not useful in differential diagnosis. Tongue biting is extremely rare, but has been reported as a consequence of the fall.

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