Syncope, seizures and stress

STRESS MEDICINE, VOL. 3: 41-49 (1987)

Symposium on ‘The Heart, the Brain and Stress’ SYNCOPE, SEIZURES AND STRESS

HAROLD STEVENS. PhD, MD 3301 New Mexico Avenue, NW, Washington, DC, 20016, USA

SUMMARY The episodic attack may reflect either cardiogenic or neurogenic mechanisms and not all seizures are due to epilepsy but rather can be caused by acute cerebral ischaemia. Cerebral ischaemia may result from vaso-vagal syncope or vago-vagal syncope, the latter being associated with an abrupt fall in blood pressure. Many events may precipitate syncope and convulsions: rectal examinations, micturition syndrome, tussive syncope, ingestion of food and liquids (i.e. the Banquet Syndrome) are some examples. Sudden death may occur due to stress, the causal mechanisms usually involving the cardiovascular system. Cardiac dysrhythmia is frequently implicated. Stress may incude a broad variety of autonomic responses mediated often through the vagal system resulting in syncope, seizures and fatal collapse. The higher nervous system may also modify autonomic electrical activity of the heart with the same consequences.

KEY WoRDS-cerebral Ischaemia, Convulsions. Rectal examinations, Food and Drink, Alcohol, Cardiac Arrest, Vaso-vagal, Vago-vagal.

One of the most compelling problems in medicine is determining the aetiology of paroxysmal disorders; that is to say, the signs and symptoms that occur in episodic bursts. These are very common, with protean manifestations extending over a broad spectrum of patterns, for example attacks of dizziness, headache, periodic weakness, paraesthesias, transient confusion, amnesia, episodic dyscontrol, dementia, syncope and seizures.

The sole source of diagnostic data may be the patient’s description of the fleeting episode. Physical examination often is normal, laboratory tests negative or misleading. The diagnostic waters may be further muddied by the patient’s unsolicited conviction that the attack was due to stress. Sometimes it is. Paradigmatic of this diagnostic challenge is the differential diagnosis of syncope and seizures, either of which may be associated with or precipitated by stress. The episodic attack may reflect either cardiogenic or neurogenic mechanisms.

Report of a Symposium organized by the Arizona Heart Institute, Phoenix, Arizona, U.S .A. on February 14th, 1986.

ATTACKS OF UNCONSCIOUSNESS

When an otherwise healthy subject collapses, hyperventilation syndrome is frequently inferred, often induced by obvious immediately preceding stressful stimuli, or chronic stress may underlie the episode. The differential diagnosis is aided by the established observation that complete syncope is uncommon in hyperventilation and true seizures are very rare. However, a misleading history of ‘passing out’ may be offered by the patient, implying a seizure disorder. But further analysis is needed, since not all convulsions are due to epilepsy. Some are caused by acute cerebral ischaemia, which in turn may be triggered by a broad variety of intrinsic and extrinsic stimuli simulating reflex epilepsy, that is, seizure disorder precipitated by some more or less specific stimulus in a susceptible person, for example photic epilepsy, musicogenic epilepsy, reading epilepsy, etc. A large number of non-epileptic syndromes have been encountered, including postural hypotension, dumping syndrome, tussive syndrome, “trumpeter’s” syncope, syncope with pain, with swallowing, with yawning, with rectal, vaginal

Received 16 July 1986 0748-8386/87/010041-09$05 .OO 0 1987 by John Wiley & Sons, Ltd.

42 H . STEVENS

and otologieal examinations, and micturition syndrome; the last is often associated with seizure phenomena including psychomotor patterns. I .

Differential diagnosis Differentiation between seizures due to cer-

ebral ischaemia and those due to epilepsy is often difficult although distinctive clinical and EEG characteristics have been identified.3. The convulsion due to cerebral ischaemia is usually brief, recovery rapid and postictal phenomena rare. But the ischaemic seizure pattern varies considerably and the literature reflects disagreement among the few who have studied this phenomenon.s Since a physician is rarely present during an attack, refined details of the seizure are not usually available to the clinician, who is confronted with the diagnostic issue of reflex epilepsy versus syncope. The EEG may be helpful in this pre- dicament.

By using tilt table technique and studying sim- ultaneous EEGs, EKGs and cerebral blood flow, we found that the clinical phenomena observed during rapidly induced hypotension simulate a classical seizure. They were more or less stereo- typed.6 The subject developed a sequential pattern of signs usually beginning with slight pallor than sweating. A subjective and objective state of relaxation was observed in most cases, but in a few subjects marked anxiety and restlessness appeared in the stage of sweating. Conversely, many patients who were apprehensive prior to the induction of hypotension became quite composed and reported on being questioned, and also spon- taneously, a feeling of lassitude and equanimity. Further depression of blood pressure produced staring and a fixity of expression often followed by abrupt onset of unconsciousness or convulsions. The latter were usually mild, generalized and brief. Although the EEG patterns of generalized slowing or generalized amplitude suppression distinguishes syncope from seizure elec- trographically, this brief transient experimental dysrhythmia is not present between attacks in either seizure patients or experimental subjects.

Etiology As stated, history is the most important single

source of valid data in making a differential diagnosis between syncope and epilepsy. Diagnostic error can be attributed to several causes:

(1) Faulty history or minimizing the elements in history. It is important to inquire into the details of activity and environment of the patient immediately preceding the onset of the attack. The most important question is, ‘What were you doing at the time of the attack?’

(2) Tendency to overread EEGs. (3) Universal tendency to explain precipitating

factors in a seizure as stress. (4) The ease and efficacy of anticonvulsant

treatment increases the bias in favour of diagnos- ing familiar and treatable disorders.

(5) Unfamiliarity with case and mechanism of cerebral ischaemia.

This diagnostic dilemma of syncope vs seizure associated with stress is illustrated by the following case:

This 15-year-old healthy girl engaged in a swimming competition was found floating on the sur- face of a pool by the lifeguard. Her last rec- ollection was standing on the edge of the pool. She came to in the hospital and was reported to have had a seizure. Past history was negative and there was no history nor evidence of head trauma or use of medication. Physical and neurological examination, EEG and EKG were normal. Phenytoin was temporarily prescribed, dis- continued, and there have been no further epi- sodes.

Although syncope or seizures in response to stress may be caused through the mediation of hyperventilation inducing decreased cerebral blood flow by virtue of cerebrovascular constriction secondary to hypocapnia, other mechanisms must be considered. In this instance, the patient had stood on the edge of the pool, hyper- ventilated, preliminary to diving, a common but dangerous practice. By brisk hyperventilation serum COz is lowered, diminishing the natural drive to breathe. The ensuing cerebral anoxia and underwater blackout may cause the swimmer to drown.7 About five times the oxygen requirement at quiet sitting is needed during active swimming. The exercising muscles go into oxygen debt but the brain requires a constant and adequate supply of oxygen to utilize glucose through the Krebs cycle. The fall in blood carbon dioxide tension diminishes or obliterates the impulse to breathe and acts directly on the cerebral arteries, causing active constriction and reduction in cerebral blood flow. The combination of these effects alters cerebral metabolism and promotes cerebral dysfunction with loss of consciousness.

SYNCOPE AND SEIZURES 43

An additional risk in swimmers is the potential cerebral anoxia caused by an overactive diver’s reflex. The latter is readily demonstrable in diving ducks but also in other animals, including man. It is an automatic oxygen-conserving reflex triggered by exposing the face to water, producing bradycardia gradually in 10 secSx It is mediated through the ophthalmic branch of the trigeminal nerve. The reflex bradycardia may also be acti- vated in anticipation of d i ~ i n g . ~ By virtue of the oxygen conservation effect, due to the bradycardia, together with the respiratory suppression induced by hyperventilation, Japanese and Korean sponge divers may remain submerged for up to 2 min while foraging as deep as 80 ft.l0 According to Wolf and others,” this reflex bradycardia, if overdone, may lead to serious arrhythmias, cardiac arrest and even death.

CEREBRAL ISCHAEMIA

Surprisingly little interest has been paid to seizures due to cerebral ischaemia even though as expected this phenomenon was known by and intrigued Gowers.I2 He studied the possible association between impaired cardiac function and epilepsy and observed that an abnormal con- dition of the heart was noted in 93 cases of epilepsy. He added that he rarely failed to exam- ine the heart in epileptics and observed ‘a slow degradation of cerebral nutrition in consequence of the imperfect blood supply is another possible explanation for epilepsy’ and added ‘in some cases the disease may originate in the medulla, the cardiovascular centers of which are sometimes manifestly disturbed in their action in cases of organic heart disease’. More recently Schott et af.13 found that 20 per cent of patients referred to a neurological department in a 6-month period with possible idiopathic epilepsy were sub- sequently discovered to have cardiac arrhythmias that caused or significantly contributed to their symptoms.

Precipitating causes Many cases of cerebral ischaemia eventuating

in convulsions have been encountered in clinical practice. Two general categories are presented as clinical examples: one, vasovagal syncope; and two, vagovagai syncope. I4 Vasovagal syncope is probably the explanation for most cases of simple

fainting. Vagovagal attacks are usually associated with an abrupt fall in blood pressure, rapid pulse, pallor and syncope. An unlimited variety of precipitating factors may be responsible, but in cases where the same stimulus produces the same sequence eventuating in syncope and convulsion very often reflex epilepsy is erroneously mis- constructed.

The following is an example. A 49-year-old lawyer was examined by a der- matologist because of a penile lesion. While wait- ing he felt lightheaded, flushed, attempted to put his clothes on, tried to get to the door but knew that he couldn’t. He lost consciousness, and convulsion was observed associated with urinary incontinence. There were four other previous seizures all in the same context, that is, during a rectal examination. In an attempt to study this patient, he was hospitalized; EEG tracings and blood pressure recordings were made during proctoscopic examination. A typical attack was promptly induced with insertion of the proc- toscope and blood pressure fell to 5010. Sub- sequently he remained asymptomatic but under- standably loath to permit examination for treatment of his haemorrhoids which was the justification for the proctoscopic examination. He died of colon cancer two years later. Was he a victim of stress-induced immunity suppression?

The induction of cardiac dysrhythmia by barium enema has been documented frequently, especially in elderly patients. Eastwood found ECG changes to be common (46 per cent) with over one-third of patients having potentially serious dy~rhthmia.’~ The danger of rectal examination in patients with myocardial infarction has been agonized over by many clinicians but remains an unresolved issue. Dr Tinsley R. Har- rison says, ‘I have never done rectal examination on patients with acute infarction therefore have no personal experience’. According to Dr Paul Dudley White, ‘It is wise to postpone rectal examination in acute cases for the first two or three days’. Dr M. Masters writes, ‘I can see no reason for not performing a gentle digital rectal examination in a patient with an acute myocardial infarction’. David L. Earnest considered the rectal examination in myocardial infarction to be safe and also necessary.lh

Other probable examples of vagovagal syncope with or without seizures are micturition syndrome and tussive syncope. In the former instance the Valsalva maneuver is considered to be the under- lying mechanism.2 In three cases reported by Pro-

44 H . STEVENS

zan and others, T-wave changes, sinus arrest and nodal rhythm occurred in all three patients but not in a control series. It was concluded that cardiac standstill and subsequent arrhythmia in phase 4 of valsalva maneuver is a cause of syncope in micturition syndrome and possibly in other conditions associated with the valsalva maneuver ,I7 including tussive syncope.'X The latter was initially considered by Charcot to be a form of 'laryngeal epilepsy'19 but according to Sharpey-Schafer,20 it is the result of an acute cerebral ischaemia. He considered it to be common. The Valsalva maneuver may also cause decreased coronary artery flow2' and fatal asthma .22

SYNCOPE AND FOOD

Kopald and others23 described a 43-year-old den- tal technician who suffered attacks of syncope precipitated frequently with ingestion of a bolus of food or liquid and which consistently occurred when carbonated beverages were swallowed. This produced substernal tightness within 3 sec followed by marked pallor and sinus bradycardia. They attributed this concatenation to diffuse oesophageal spasm which caused reflex vagovagal syncope. Similar instances have been reported, three due to an oesophageal diverticulum with attacks triggered by ~ w a l l o w i n g . ~ ~ ~ 25 Instances of reflexly induced syncope mediated through the vagal system have occasionally been described in pharyngeal, oesophageal or pharyngeal-- bronchial and mediastinal lesions,26 during SUC- tioning, bronchoscopy and oesophagoscopy , also in pleural puncture and ocular p re~su re .~ . 27-30

An analogous syndrome and mechanism was recently reported in a patient with frequent seizures and status-epilepticus due to phrenic nerve stimulation following implantation of an electrical pacemaker.28 Dramatic improvement resulted after a phrenic nerve crush. Symptoms reap- peared after regeneration of the phrenic nerve and were again controlled by division of the nerve. The EEG remained normal.

Neurological aspects Several cases of vagovagal syncope have been

reported in connection with glossopharyngeal n e ~ r a l g i a . ~ * - ~ ~ The first was by Riley and others in 1942.28, 33, 36-41 The syndrome consists of

severe pain in one tonsilar area occurring spon- taneously, induced by swallowing followed immediately by fainting and convulsions. EKG recorded during the syncopal attack reflects bradycardia or asystoly. Complete relief of pain and syncope is usually obtained by cocainization of the tonsilar fossa or by sectioning the glossopharyngeal nerve. Belladonna derivatives relieve the syncope and the seizures.

Distension, distortion or compression of the oesophagus and also of the stomach has been reported as a cause of syncope and seizures, and experimental techniques have in a few instances documented this pa th~genes i s .~~ . 25, 40, 42 Soma Weiss and others42 reported a 58-year-old patient who suffered convulsions when he ate food or drank liquid. His convulsions would last 1-5 min. Making him drink water and alternatively dis- tending a balloon in his oesophagus caused heart- block and ventricular standstill. Similarly, Mor- rison and S ~ a u m , ~ " employing a balloon in the oesophagus and stomach, could produce pain and/or cardiac standstill with subsequent relief with deflation. The patient found that belching would give him relief. Atropine was successful in mitigating the symptoms, as it was in a 2-year- old child with apnoeic seizures.43

Beverages Beer, like other carbonated beverages, is a

particularly competent precipitating cause of vagovagal syncope. Carbonated beverages, particularly ginger ale, can effect massive ballooning and displacement of the a phenomenon exploited by paediatric radiologists to obtain clear urograms.*'. 45 The ingested soft drink, usually Pepsi Cola, releases carbon dioxide which distends the stomach and pushes aside the over- lying bowel, whose plexiform shadow would otherwise overlie the renal silhouette.

The banquet syndrome An analogous vagovagal mechanism that may

eventuate in syncope, seizures or even death is the banquet syndrome. A diner may collapse in the midst of a meal or after finishing the meal, usually with some premonitory symptoms such as weakness, dizziness, sweating, pallor, etc. He may be able to report his imminent collapse in time for fellow diners to place him in a recumbent posirion. Faecal incontinence and brief con-


vulsions may ensue. Multiple mutually reinforcing phenomena may

operate to incapacitate the diner, who often is seated at the head table. Contributing aetiological factors may be vagal stimulation by gastric distension causing bradycardia, with decreased cardiac output and consequent cerebral ischaemia. Associated decreased blood volume is due to inbi- bition of fluid into the gastrointestinal tract for digestive purposes. Hypoglycaemia and hypo- kalaemia may be superadded burdens and analogous to the concatenation in the dumping syn- d r ~ m e . ~ ~ Decreased coronary blood flow averaging 21 per cent, with T-wave depression, was demonstrated in dogs in whom the dumping syndrome was induced by injecting 200 cc of 50 per cent glucose into the proximal jejunum.

Public speaking has also triggered cardiac dysrhythmia. Ventricular premature beats emerged in six of 23 healthy individuals and in five of seven patients with coronary artery disease preliminary to or during public speaking.

Alcohol Alcoholic beverages provided during a cocktail

hour enhance the gastric diste‘nsion and also increase the volume of gastric secretion and the inhibition of fluid into the gastrointestinal tract. If wine is drunk, the diner may be further vic- timized by the histamine bodies often found in wine, especially red wine. Further assault on his circulatory integrity may be induced by pre- servatives and other additives, including nitrites, sulphites and sodium glutamate. Cimetidine has been recommended to neutralize the histaminic effect found in red The banquet attendee may also be a victim of what Dr Paul Dudley White calls the “tight girdle syndrome”.4x He observed that a tight girdle on a rather stout woman may displace the diaphragm and heart upwards resulting in dyspnoea and other symptoms. He considered the tight girdle syndrome ‘doubtless a residual of the popularity of the wasp waist that was in style a couple of generations ago, pictured in many of the fashion magazines of the epoque. Perhaps now that women have been liberated, they may also be free of the feeling that they need tight girdles’.

NEUROLOGY OF STRESS

It appears, therefore, that stress may induce a

broad variety of autonomic responses mediated often through the vagal system and may eventuate in syncope, seizures and even death. An analogous pathological process mediated through the vagus nerve further demonstrating the potency of this mechanism is the stress ulcer, elucidated by Cushing in 1932.48. 49 Burch and his colleagues drew attention to peaked T-waves, long Q-T intervals and U-waves as manifestations of central nervous system disease, primarily but not exclus- ively in subarachnoid haemorrhage patients. Cropp and Manningso reported a series of 15 patients with subarachnoid haemorrhage with ECG changes. Four of these patients died and were said to have normal heart at autopsy. The authors postulated that ECG changes were due to autonomic nervous system abnormalities arising from area 13 in the orbital frontal cortex. Similar findings were reported by Mathew et al.38 and by Hugenholtzsl in six patients with a variety of neurological lesions including metastatic cancer, cerebral emboli, subdural haematoma, multiple strokes, subarachnoid haemorrhages, etc. The authors coqcluded that this phenomenon was due to an abnormality in hypothalamic control of cardiac r epo la r i za t i~n .~~

Thus, there is a considerable body of evidence that the higher nervous system modifies autonomic electrical activity of the heart and may trigger sudden death.9. 11, 52-56 It is due to ventricular fibrillation, which is the leading cause of fatality in non-hospitalized subjects in the indu- strially developed ~ o r l d . ~ ’ The evidence for increased rislc for ventricular fibrillation due to psychophysiological factors is supported by ani- mal studies, but increasing evidence is forth- coming from human studiess8

Sudden death

The neurology of sudden death has been demonstrated in dogs who were adversely conditioned by receiving an electric shock. When stressed by placement in a sling, 70 per cent demonstrated reduction in ventricular fibrillation threshold and also when placed in the sling even when shocks were no longer a d m i n i ~ t e r e d . ~ ~

In man, data relating stress to sudden death from ventricular fibrillation have been largely inferential. Loss of a spouse has been associated with increased mortality in the surviving mate, which is higher for males than for females. Cul- tural influences also play a role.59 Sudden death

46 H . STEVENS

is 3.6 times higher among workers in the lowest working grades in Britain than among the top employment grades. The Japanese show a gradi- ent in cardiac mortality prevalence depending upon the place of residence, being lowest in native Japan, intermediate in Hawaii and highest in California, while Japanese Americans who have retained ancestral cultural practices exhibit a risk of cardiac death no different from that found in Japan.

The putative precipitating cause and cir- cumstance that immediately precedes the sudden unexplained collapse varies through a broad range that borders on the cosmic. Even banal activity such as driving in traffic through familiar routes has been associated with cardiac dysrhythmia.@’ The majority with normal hearts or a history of coronary heart disease increase their heart rates. Brief periods when the rate exceeded 140 per minute was reported in both groups. ST changes not caused by tachycardia developed in three out of 32 normal drivers. Of 24 drivers with coronary heart disease, 13 increased their ST and T abnormalities, changes being gross in six. Fur- ther, five developed multiple ventricular ectopic beats. Two coronary drivers experienced anginal pain, and the author recommended that persons in whom angina is easily provoked when driving should be advised not to drive.

Considerable anecdotal data imply a clear causative connection between stress and sudden death.6’ For example, in the Athens earthquake increased cardiac related deaths and cardiac arrhythmias were recorded when compared to controls, suggesting that in such a setting autonomic output increases and results in significant cardiopathy.6z George L. Engel cites anecdotal data to support the thesis that there is immediate direct causation of death following stress, including anniversary deaths3’, 5 5 , 6367 and voodoo deaths .63

Stress and murder In addition to grief and anger, threat and fear

have also been implicated in sudden death,65 rais- ing a vexing legal issue. Can sudden cardiac death be murder? The answer is yes, according to several authorities.68 Five such cases were reported over a period of 15 years in which a conviction of homocide had been obtained in the absence of physical contact between the assailant and the victim. For example, an elderly white female with

a past history of stroke and heart disease heard burglars breaking the window glass. While attempting to awaken her elderly sister by throw- ing pillows across the room to the other bed she suffered a fatal heart attack and died. Two subjects were apprehended in the act of the attempted break-in. The autopsy disclosed severe occlusive coronary arteriosclerosis and evidence of previous myocardial infarction as well as an old cerebral ischaemic infarct.

Stress in the young Sudden death may occur in a young healthy

person.69 James reported the postmortem finding in an 18-year-old who died while playing football, similar to the case reported of a 14-year-old boy who suddenly dropped dead while playing soccer. The circumstances under which a healthy young athlete dies suggests that stress is a companion if not a cause of a fatality.69 The vulnerability of fatal cardiac dysrhythmia in an athelete is considered to be due to a combination of vagal over- stimulation superimposed on an abnormal sinus node artery.70 In the case of the 18-year-old athlete, microscopy disclosed this defect with sinus node artery markedly narrowed by bizarre medial hyperplasia. This histopathological entity has been evoked to explain sudden death in Lang- Nielsen disease, that is, congenital deafness associated with prolonged Q-T interval and sudden death.39, 71-73

A curious analogous lesion is found in Dob- erman Pinschers, a highly bred species of dog.74 In a postmortem study of 11 Doberman Pinschers that died suddenly an identical cardiac lesion was found in 10. There was a nearly complete focal degeneration of the bundle of His which was associated with cartilage and bone formation in the adjacent central fibrous body. The cause of these lesions is considered to be luminal nar- rowing of the local small coronary arteries, which may constitute a hereditable defect. It is postulated that sudden unexpected death in these dogs may be due to a form of Adams-Stokes attacks.

Another line of evidence that the central nervous system is responsible for or participates in lethal cardiac arrest is found in the reports of unexplained deaths of young ambulatory epilep- t i c ~ . ~ ~ , 75-78 Eight such cases were examined postmortem, showing no evidence of recent or old myocardial d i ~ e a s e . ~ ’ The mechanism of death in


these epileptic patients was considered to be a combination of pulmonary oedema and ventricular arrhythmia. Prolonged sinus arrest was reported in a 23-year-old man lasting 9 sec at the time of a clinically observed seizure. There was no demonstrable cardiac d i~ease , ’~ as in a patient in whom photic stimulation provoked spike and wave discharges usually with myoclonus.40 Con- tinued photic stimulation on two occasions resulted in cardiac arrest accompanied by an anoxic seizure, followed once by a convulsion. The cardiac arrest reaction was treated by beller- gal and the epileptic phenomenon by pheno- barbital. It was concluded that this patient was suffering from two affections, namely, epileptic seizures and increased vagal excitability. Both affections could be provoked by photic stimulation.

CONCLUSIONS

In summary, not all seizures are due to epilepsy. Some are due to cerebral ischaemia, secondary to cardiac dysrhythmia due to stress. Other or additional psychophysiological mechanisms should be investigated, particularly the possibility of excessive autonomic nervous system discharge, not necessarily due to stress. A large variety of mechanisms may trigger cerebral ischaemic seizures. Two general categories are considered: (1) vasovagal, and (2) vagovagal, the latter sometimes triggered by a wide variety of provocative circumstances, for example by swallowing, which may be associated with demonstrable oesophageal or glossopharyngeal nerve lesions, or by distension of the gut. Anticonvulsant medication in vagovagal attacks is ineffectual. Atropine may be beneficial. Prognostically, three categories can be identified: (1) syncope due to cardiac mechanism; (2) due to neurogenic mechanism; and (3) undetermined. Prognosis is worse in number one.

The most important source of valid diagnostic data is the history, with particular emphasis on the answer to the all-important inquiry, ‘What were you doing at the time of the attack?’ This principle is illustrated by the following:

A 54-year-old trumpet player suddenly lost consciousness while playing concert A in a sustained fortissimo in Beethoven’s 7th Symphony. He had amnesia for a few seconds, continued to play but did not fall. Three such attacks have occurred in the last 15 years. He has learned to share parts

of a long and loud high passage with his assistant, has had no further attacks but reports that he frequently has to catch and briefly support his more eager but less skilled students who have not yet learned the art of blowing in moderation.

It is well known among professional trumpeters that playing high and loud notes for more than a few seconds may cause dizziness or occasionally a blackout, since greater pressures across the vibrating aperture are needed in trumpet playing than in any other commonly used in~trument .~’ The circulatory effects are those of a formidable valsalva maneuver.

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Syncope, seizures and stress