A Tour around Syncope
(Date of publication 19 March 2004)

We are all familiar with the unfortunate Victorian heroine who falls to the ground when confronted by something unexpected and deeply shocking, such as the sight of a naked male chest. However, emotional stress is only one of many different causes of fainting, or syncope.

A brief outline of the clinical picture is given on the American Heart Association site; essentially, syncope consists of a transitory loss of consciousness and posture, usually associated with a temporarily insufficient flow of blood to the brain. According to the British Heart Foundation the condition is surprisingly common, affecting 30% of adults at some point in their lives and accounting for up to 6% of attendances at Accident and Emergency Departments.

Syncope may be neurally-mediated, or a consequence of cardiac arrhythmia or a physical obstruction to bloodflow. The most common type is vasovagal syncope, also known as neurocardiogenic or vasodepressor syncope, when the brain fails to regulate the body’s blood pressure and heart rate adequately. The basic mechanism involved is explained here . People of all ages who are otherwise healthy can be affected by this benign disorder, but it is particularly frequent in young women. Victims are almost always standing and before fainting generally experience a range of symptoms including nausea, sweating, rapid heartbeat and dizziness, which last anywhere from a few seconds to a few minutes. Once fainting occurs, the patient should be allowed to lie down, with legs elevated, until completely recovered.

A Tilt Table Test may be used to ascertain whether vasovagal syncope is responsible for fainting episodes. The patient lies down on a special table with belts and a footrest, an intravenous line is inserted, a sphygmomanometer cuff placed and ECG leads attached. Once the patient has been belted to the table, it is tilted upright to a 60-80° angle for approximately 45 minutes. If the patient faints it is considered pathognomic for vasovagal syncope. The test may be repeated after the injection of a drug that mimics the action of adrenaline, such as isoproterenol. The NASA site has a good photograph of the test in progress.

When vasovagal syncope is brought about by particular circumstances, as in the case of our hapless maiden earlier, it is termed situational syncope . The triggers which may cause fainting are very diverse, ranging from embarrassment to coughing, swallowing cold liquids to urinating. One specific example of situational syncope is carotid sinus syndrome , when fainting may be induced by looking up, turning the head, or even just wearing a tight collar. The explanation is that the carotid sinus, a dilatation of the carotid artery, has pressure detectors which feed information to the vasomotor centre in the brain stem that controls blood pressure and heart rate. If the carotid sinus becomes hypersensitive, mechanical stimulation may cause a pause in the heart beat - see the trace here - or a drop in blood pressure.

The gravitational stress of rising quickly to a standing position causes blood to pool in the legs and trunk, leading to a decrease in venous return and cardiac output, and a fall in blood pressure. In healthy individuals, autonomic reflexes are activated and rapidly normalise the blood pressure by increasing the heart rate. Where this response is impaired, however, cerebral perfusion may be reduced and lead to syncope. The condition is called postural or orthostatic hypotension, and is defined as a decrease of at least 20 mm Hg in systolic blood pressure when moving from a supine to a standing position. The most frequent cause is hypovolaemia, often induced by the excessive use of diuretics. Many other drugs can have a similar effect, as can various neurological disorders, systemic arterial hypertension and decreased receptor responsiveness as a result of ageing. A wealth of clinical information about this disorder is available from the American Academy of Family Physicians .

Syncope may also be caused by an abnormally slow heartbeat, or bradycardia (<60 beats/min). This can occur when the electrical impulses that regulate the heartbeat are disrupted as a result of ageing, cardiac disease or conditions such as hypothyroidism which impair electrical conduction, or by various medications. Electrical events in the heart during bradycardia are covered in detail in this .pdf file from the New England Journal of Medicine - some of the accompanying ECG traces look positively frightening, with pauses in atrial activity of more than 3 seconds! Treatment depends upon the symptoms experienced and underlying cause, but an artificial pacemaker may be required to increase the heart rate.

Paradoxically, the heart beating too quickly (>100 beats/min) may also lead to syncope, because the ventricles have insufficient time to fill with blood and cannot pump effectively, reducing the supply of oxygen to the brain. This is termed tachycardia and its seriousness primarily depends upon the origin of the rapid beat. In ventricular tachycardia the heartbeat is usually regular at between 150 and 200 beats per minute, with a dissociation between atrial and ventricular activity. The condition is dangerous because it may cause shock or cardiorespiratory arrest, and lead to ventricular fibrillation - the number one cause of sudden cardiac death - which is characterised by rapid, irregular and chaotic heartbeats.

Generally less serious is supraventricular tachycardia (SVT), when the increase in heart rate, typically to between 160 and 200 beats per minute, is caused by abnormal activity in the atrium. SVT is frequently seen in people who are physically fatigued, consume large amounts of coffee, use alcohol or smoke heavily. This type of arrhythmia tends to begin and end suddenly. Specific examples include atrial flutter, caused by an aberrant circuit in the right atrium, and atrial fibrillation, the commonest form of rapid heart rhythm found in hospitalised patients, in which the cardiac impulse originates from several abnormal pacemakers in the atria. A brief summary of the mechanisms involved can be found here , but it does require prior knowledge of the electrical conduction system of the heart.

One type of SVT - sinus arrhythmia - is often seen in teenagers and young adults and rarely needs treatment, giving rise to an interesting speculation. Could the delicate sensibilities of the demure Victorian female be explained by a widespread incidence of this condition - or is a more likely explanation the tightly-laced corsets that were de rigeur at the time?

Whilst most authorities agree that there is no cure for stammering and that it can only be controlled, a whole host of different causes has been postulated. Some of the old wives tales are so positively weird - go to the bottom of this page - that one can only speculate upon their origin. How could allowing an infant to look in the mirror, cutting its hair before it learns to speak, or tickling the soles of its feet possibly affect its powers of speech?

Turning to more scientifically plausible theories, two researchers in Utrecht have put forward the Vicious Circle Hypothesis. We all constantly monitor our own speech and stop, correct errors, backtrack and start again whenever necessary, creating minor dysfluencies such as hesitations, reformulations and repetitions. This hypothesis suggests that stammerers monitor their own speech too closely, identifying trivial irregularities. The detection itself creates an error, which is detected, creates an error, and so on, making the problem worse. Evidence supporting this view is that sufferers who perform an additional task while speaking, thereby distracting their attention, stammer significantly less.

At another page on the same site, Professor Webster of Brock University, Ontario, elucidates his theory, citing the research that underpins it. He believes that the speech centre of stammerers is located in the left cerebral hemisphere - as in fluent speakers - but that it is inefficient and unusually susceptible to interference from both hemispheres. Also, there is a lack of 'left hemisphere activation bias'; in fluent speakers the left hemisphere is in a greater state of readiness than the right, but in stammerers the balance is more equal, and it is known that activity in the frontal portion of the right hemisphere is associated with negative emotions such as fear and anxiety. Thus the fundamental cause is biological but the condition is reinforced psychologically. Recent research from Germany, involving sophisticated magnetic resonance imaging, appears to corroborate this to some extent, indicating that stuttering is associated with a structural abnormality in the left side of the brain.

A widely disseminated but scientifically unproven theory is that forwarded by William Parry, who attributes stammering to the Valsalva Manoeuvre, a natural mechanism which increases air pressure in the lungs in order to help exert physical effort or expel things from the body. One example is a weightlifter 'holding his breath' as he raises a barbell above his head. Muscles throughout the body are involved, but the relevant activity is that the larynx closes tightly around the upper airway to prevent air escaping from the lungs. This theory argues that when a stammerer anticipates a difficult word is needed, the need for extra effort is registered, triggering the Valsalva Manoeuvre and causing a stuttering block.

Professor Maguire of California University takes a different view, believing that the cause is a chemical imbalance in the brain, namely an excess of dopamine in the corpus striatum. This implies that drug treatment might provide the answer; haloperidol has been shown to reduce symptoms and Professor Maguire suggests that olanzapine, which he has used successfully, could prove effective.

Information about the best currently available therapies can be found at Stammering.net. These fall into four basic categories: self-therapy, electronic devices, speech language pathologists and speech clinics. It is emphasised that stammering is not only a speech disorder, but also a communication and behavioural disorder, and it cannot be eliminated overnight. Click here for a detailed review of electronic devices, which work by manipulating the stammerer's voice and relaying it back, and the neurological mechanisms involved.

Should you be really interested in this field, and its future development, there is a new quarterly online journal, Stammering Research, which was launched in April. The goal is to provide a forum for open exchange on relevant topics and to provoke strong debate from proponents of different theoretical positions.

Finally, here is a paradox from the UK. According the Disability Discrimination Act 1995, speech therapy which encourages stammerers not to avoid difficult words or to use substitution, thereby helping them to overcome their problem, could actually make them more likely to qualify as disabled and entitled to protection under its terms. Bizarre!

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