Can You Have a Series of Syncope Episodes Within a Year Then Never Have Them Again

• Journal List
• Postgrad Med J
• v.82(972); 2006 Oct
• PMC2653900

Postgrad Med J. 2006 Oct; 82(972): 630–641.

How to avert a misdiagnosis in patients presenting with transient loss of consciousness

Received 2006 Feb 21; Accepted 2006 May 9.

Abstract

Daily in the UK, frontline medical and paramedical staff are required to manage patients with "plummet ?cause". This universal colloquialism refers to patients who take had an abrupt loss of postural tone. Some of these patients would have had a "coma" or a transient loss of consciousness (T‐LOC). The three most important causes of T‐LOC are syncope, epilepsy and psychogenic blackouts. Determining the correct crusade is an of import challenge; if the initial clinical diagnosis is wrong, investigations may be misdirected, and the final diagnosis and treatment incorrect. Syncope is much more common than epilepsy and may nowadays with symptoms akin to the latter. This fact is not well appreciated and frequently leads to misdiagnosis. This commodity deals with the clinical features of the iii primary causes of blackouts, the value of investigations in arriving at a diagnosis and the problem of misdiagnosis. Pathways for managing patients presenting with blackouts are suggested.

Keywords: blackouts, syncope, epilepsy, psychogenic blackouts, misdiagnosis

Every 24-hour interval in the UK, many medical and paramedical staff providing acute care are called upon to manage patients with "collapse ?cause". This universal colloquialism refers to those who have had an abrupt loss of postural tone. Patients become unaware of, or unresponsive to, their surroundings considering of several reasons, but for the purpose of this article, we will consider those who have briefly lost consciousness, and refer to this transient loss of consciousness as T‐LOC. Patients oftentimes refer to T‐LOC equally a "coma". There are several causes of T‐LOC; determining the correct crusade is an important challenge. If the initial clinical diagnosis is wrong, investigations may be misdirected, and the final diagnosis and treatment incorrect.

T‐LOC is common, affecting as many as 50% of people at some stage of life. It causes 3% of casualty attendances and 1% of admissions to hospital.¹ Reasons why examining the clinical evidence and arriving at a correct diagnosis is challenging in patients with T‐LOC include the inability of many patients to assist with an accurate description, the lack of or unreliability of witnesses, and the recovery of the patient and normality of vital signs past the time they are examined. Subsequent tests are usually normal, both bedside and laboratory, when the patient is examined, and is by then asymptomatic. The clinical history is often the only useful or unequivocal information. Patients may be able to offering just a recollection of their symptoms immediately before and after a blackout (just may after find other features, eg, urinary incontinence, a bitten tongue). Some patients, especially elderly people, may deny T‐LOC because of retrograde amnesia. This is seen in 30% of patients aged ⩾65 years who collapse.ⁱⁱ However, in such patients, it is important to determine whether the collapse is due to a fall. Falls may be a crusade of "collapse ?cause"; still, past definition,³ they are not synonymous with T‐LOC. Typically, falls are due to factors such as arthritis, unsteadiness of gait, postural hypotension due to drugs and attempting to ambulate without practiced back up. Measures aimed at falls may non aid those collapsing due to T‐LOC.

T‐LOC has 3 master underlying mechanisms:

1. Transient global impairment of cognitive perfusion (ie, syncope, oft resulting from a sudden change in eye charge per unit, heart rhythm or claret pressure)

2. An excessive and inappropriate discharge from cortical neurones (ie, epilepsy)

3. Apparent T‐LOC due to psychogenic causes.

Syncope is overall much more common than epilepsy.^{4 ,5} It is not widely recognised that a witness will commonly report limb twitching, rolling of the eyes and urinary incontinence as features of syncope. It is often assumed that these features denote epilepsy,⁶ only convulsive movements occur in syncope when cognitive neurones are irritated by anoxia, due to lack of oxygenated blood perfusing the brain. Most commonly, this results in myoclonic jerking of the limbs, hence the term "convulsive syncope". Failure to sympathise these mutual features of convulsive syncope may lead to many wrong diagnoses, unnecessary administration of antiepileptic drugs, and considerable homo and fiscal toll.^five Syncope tin therefore produce an apparent "seizure", but this should non be taken to mean that the convulsive effects of cognitive hypoperfusion are epileptic.

Box 1: Definitions

• T‐LOC: transient loss of consciousness

• Collapse: sharp loss of postural tone, with or without T‐LOC

• Syncope: T‐LOC due to global impairment of cerebral perfusion causing collapse

• Epilepsy: an excessive asynchronous discharge of cortical neurones, leading to a clinical outcome

• Psychogenic blackouts: a crusade of apparent T‐LOC without bear witness of epilepsy or syncope, or other organic affliction

• Fall: an event whereby a person comes to residual on the footing or some other lower level with or without loss of consciousness

Although the clinical history tin can exist misleading, over‐reliance on bedside or laboratory testing may besides crusade confusion. All patients should undergo a thorough physical examination and electrocardiography (ECG) (and echocardiography (Echo)) if concrete exam is not completely normal)^seven to exclude structural heart disease (SHD). Withal, it is usual for patients with T‐LOC to be asymptomatic between episodes, and investigations between episodes are usually normal.⁸

This article volition describe the definitions, clinical presentation, concrete findings and investigations of T‐LOC (blackouts). We highlight the specific problem of the misdiagnosis of epilepsy, and advise intendance pathways that can be used to assess, diagnose and manage patients with blackouts, thus helping to reduce a misdiagnosis.

Definitions

Syncope is derived from the Greek "syn" meaning "with" and "kopto" meaning "I cut" or "I interrupt". The European Gild of Cardiology defines syncope every bit "a transient, self‐express loss of consciousness, usually leading to collapse. The onset of syncope is relatively rapid, and the subsequent recovery is spontaneous, complete, and unremarkably prompt. The underlying mechanism is transient global cerebral hypoperfusion."⁷ Reflex syncope, the most common crusade of syncope, has many synonyms—for case, vasovagal, neurocardiogenic, vasodepressor, neurally mediated hypotension and bradycardia syndrome, emotional fainting, pallid breath‐holding spells, pallid infantile syncope, reflex anoxic seizure, reflex asystolic syncope and malignant vasovagal syncope. All these terms imply the same process. Syncope may be caused by the triggering of inappropriate reflex hypotension, with a variable degree of bradycardia, or fifty-fifty transient asystole; hence the much simpler term, reflex syncope. The exact trigger of the afferent arc of this reflex is unknown, only the efferent arc, which arises in the brain stalk vasomotor and cardioinhibitory centres, results in an abrupt withdrawal of sympathetic outflow to resistance vessels (in particular, skeletal muscle arterioles) and sharp vagal hypertonia.⁹

The International League Confronting Epilepsy^ten and the International Agency of Epilepsy define an epileptic seizure as a transient occurrence of signs and/or symptoms due to abnormal excessive or asynchronous neuronal activity in the brain.

They go on to define epilepsy every bit a "disorder of the brain characterised by an enduring predisposition to generate epileptic seizures and by the neurobiological, cerebral, psychological and social consequences of this condition".¹⁰ Thereby, a single epileptic seizure that a person experiences may never recur, and the diagnosis of epilepsy should be reserved for those patients with recurrent epileptic seizures.

Blackouts are likewise seen in patients in whom there is no evident organic cause. These phenomena take also been given many names, including pseudoseizure, psychogenic seizure, non‐epileptic seizure, non‐epileptic attacks, hysterical epilepsy, hysteroepilepsy, hysterical seizures, conversion fits, pseudoattacks, doxogenic seizures and paroxysmal somatoform disorder. These episodes tin be described as "unintentional paroxysms of altered sensation, move, perception, or emotion that clinically resemble epileptic seizures merely are not accompanied by epileptiform neurophysiological changes".¹¹ Cardiologists tend to use the term "psychogenic blackouts" when referring to this group of patients, whereas neurologists usually adopt "psychogenic non‐epileptic attacks".

Epidemiology

Syncope is mutual across all historic period groups, with nearly 1 in ii people experiencing a blackout in their lifetime.² The Framingham Study reported a 10.5% incidence of at to the lowest degree 1 syncopal event over a 17‐year period.¹² The incidence of syncope does non remain constant, but increases sharply at age >70 years, with farther increases in women aged >80 years. Among elderly people confined to long‐term care, the annual incidence of syncope is reported to be as high as vi%.¹³ Population‐based studies have shown that among all the causes of syncope, reflex syncope is the near common mechanism.⁷

Epilepsy, on the other hand, while being the most common chronic disabling neurological status in the UK, is much less common than syncope. Available data bespeak an annual incidence of 40–70 episodes per 100 000 people in adult countries, with a lifetime prevalence of 5–10 per g. The incidence is high in childhood, decreases in adulthood and rises again in older people.¹⁴ Roughly thirty 000 new cases of epilepsy are seen every year in the Britain, with a prevalence of 0.7–1.0%⁵ (up to 600 000 people).

A psychogenic blackout, or psychogenic not‐epileptic attack disorder (NEAD), often coexists with epilepsy, and can exist encountered in equally many as 20% of patients with epilepsy.^{15 ,16 ,17} The incidence is reported to range from 3 to v per 100 000 people.^{xviii ,19 ,20} Most patients are women, begin to take symptoms in their late teens or early 20s, and as many equally 80% have a history of medically unexplained symptoms.¹⁷ Other described adventure factors for NEAD are depression and personality disorder,^{21 ,22} poor coping strategies, acute stress or loss,²³ sexual and physical abuse,^{24 ,25} previous head injury^{26 ,27 ,28} and asthma.²⁹

Recurrences

Recurrences occur approximately in 1 in 3 patients with syncope, with nearly recurrences occurring in the first ii years after the onset of symptoms.³⁰ Although recurrences themselves are non shown to be associated with increased bloodshed or sudden death rates, morbidity among such patients is higher and their quality of life is lower.⁷ More than 1 in 10 patients with recurrent syncope experience fractures and soft‐tissue injuries directly as a event of plummet,³¹ and functional impairment was found to exist similar to chronic illnesses such as rheumatoid arthritis, low‐back pain and psychiatric disorders.³² Also, recurrent syncope is negatively correlated with overall perception of health.³³

Of all the patients diagnosed with epilepsy, one tertiary of patients accept <1 seizure per year, one third have ane–12 seizures per year, and the balance have >ane seizure per month.³⁴ Remission, or existence free of seizures for 5 years, either with or without treatment, is seen in seventy% of adults and children. Early on and long‐term remission tin be predicted past the number of seizures in the first vi months afterwards presentation.^five

Patients with NEAD have considerable disability, but early diagnosis and psychotherapeutic intervention have been shown to reduce undue infirmary omnipresence and avoid unnecessary anticonvulsant handling.³⁵ Ettinger et al ³⁶ followed upwards 43 patients with videoelectroencephalogram‐documented diagnosis of non‐epileptic seizures, and found that only 1 in five patients was episode gratuitous at 6–9 months of follow‐upwardly. Roughly half of the patients studied had improved, 20% of patients reported no alter in their symptom frequency and almost ten% reported an increase in frequency of episodes. Patients currently having many friends, and good relationships with friends every bit a child, were more probable to be episode complimentary. Not surprisingly, patients with pending litigation were less probable to experience a reduction in frequency of their symptoms. Psychiatric comorbidities, including personality disorders, were associated with a poor long‐term outcome.¹⁵

Prognosis

The prognosis of syncope depends on the underlying cause (box 2). SHD (eg, symptomatic aortic stenosis, hypertrophic cardiomyopathy and arrhythmogenic correct ventricular dysplasia, old myocardial infarction) greatly increases the risk of death in patients with syncope.⁷ Patients with advanced heart failure, New York Heart Clan Form III–IV, mean ejection fraction of 20% and syncope were institute to have a 45% take chances of sudden decease at i year when compared with those without syncope.³⁷ Similarly, patients with syncope caused by ventricular tachycardia in the setting of astringent left ventricular dysfunction accept a very poor prognosis.³⁸ In contrast, patients with reflex syncope, age <45 years, no SHD, a normal electrocardiogram, supraventricular tachycardia or ill sinus syndrome have a relatively good prognosis. Patients with syncope due to an unknown cause—that is, those with a benign cause besides every bit those with an undiagnosed cardiac crusade—have an intermediate risk of increased mortality and sudden cardiac death.⁷

Box 2: Causes of syncope

Syncope is a cardiovascular disorder. Causes can thus be divided into the following:

Cardiac causes

Due to underlying structural heart affliction

• Aortic stenosis

• Hypertrophic cardiomyopathy

• Arrhythmogenic right ventricular dysplasia

• Severe ischaemic left ventricular dysfunction

• Some forms of congenital centre defect

• Left atrial myxoma

• Pulmonary embolism

Due to an arrhythmia

• Tachyarrhythmias—for case, ventricular tachycardia, ventricular fibrillation, polymorphic ventricular tachycardia, Brugada syndrome, long‐QT syndrome, pre‐excited atrial fibrillation, supraventricular tachycardia

• Bradycardias—for example, atrioventricular block, sinus node disease

Vascular causes

Reflex causes

• Vasovagal syncope

• Carotid sinus hypersensitivity

Situational causes

• Cough syncope

• Micturition syncope, etc

Postural causes

• Orthostatic hypotension

• Postural orthostatic tachycardia syndrome

The United kingdom of great britain and northern ireland National General Exercise Study of Epilepsy³⁹ was a prospective, population‐based study on patients with newly diagnosed epilepsy, in which a accomplice of 792 patients was followed up for a median duration of 11.8 years. The standardised mortality for this group of patients was twice that of the normal population. The increase in mortality was most noticeable in the first few years after diagnosis. Subgroups that were associated with a college risk of death were patients with acute symptomatic epilepsy, generalised tonic–clonic seizures and in whom epilepsy was due to congenital neurological defects. Similar findings, of increased bloodshed, were mirrored in a Dutch cohort of patients with epilepsy followed up for a mean of 28 years.⁴⁰ Unlike patients with newly diagnosed epilepsy, in whom most deaths are due to the underlying cause (eg, tumour, vascular affliction), in patients with chronic epilepsy, the cause is sudden unexpected death in epilepsy (SUDEP).⁴¹ SUDEP is divers as "sudden, unexpected, witnessed or unwitnessed, nontraumatic and nondrowning decease in individuals with epilepsy, with or without prove for a seizure, and excluding documented status epilepticus, in which mail‐mortem examination does not reveal a toxicological or anatomical crusade for death".⁴² Young age, generalised tonic–clonic seizures, uncontrolled epilepsy, learning disability, seizures occurring during sleep and poor adherence to antiepileptic drug regimen are run a risk factors for SUDEP. It is estimated that approximately 500 lives are lost per yr in the UK due to SUDEP.⁴³

Box 3: Common abnormalities on electrocardiograms in patients with arrhythmic syncope

• Bifasicular block (left‐bundle or right‐bundle branch block combined with left inductive or left posterior fasicular block)

• Other intraventricular conduction abnormalities (QRS duration ⩾0.12 due south)

• Sinus bradycardia <40 beats/min

• Sinoatrial block or sinus pauses >three s in the absence of negatively chronotropic drugs

• Mobitz 2d‐caste or third‐caste atrioventricular block

• Alternate left‐bundle and right‐bundle branch block

• Ventricular tachycardia

• Long‐QT syndrome

• Brugada syndrome

• Wolff–Parkinson–White syndrome

• Negative T waves in right precordial leads, and ε waves suggestive of arrhythmogenic right ventricular dysplasia

• Q waves suggesting myocardial infarction

Clinical features

The yield from bedside and laboratory examinations in patients with blackouts is shown to be depression. Typically, when simple examinations are unhelpful, more sophisticated, loftier‐tech investigations have a very low yield at a very loftier toll.⁸ Attending has to exist focused on obtaining the best possible history from patients and eye witnesses. T‐LOC is a story (often told over and over over again). Every story has a beginning, a centre and an end. The clinician should make a detailed record of events before, during and afterwards a coma. A good history provides clues to whether a coma is due to syncope or epilepsy, and may likewise help in differentiating diverse causes of syncope or epilepsy syndromes.⁷ One meta‐analysis of half dozen studies showed that a skillful history, physical exam and a 12‐lead ECG made a diagnosis of syncope in roughly 45% of patients presenting with T‐LOC.^42a In the Syncope Symptom Study,⁴⁴ all patients presenting with T‐LOC completed a questionnaire. Points were allocated for their presenting symptoms. It was reported that 94% of patients were correctly diagnosed on the footing of their presenting symptoms solitary. Epilepsy was said to have been diagnosed with 94% sensitivity and specificity. Withal, the obvious limitation of the study was that it used circular logic. Clinical features were not proved for a particular cause of T‐LOC in advance. Still, given the unhelpfulness of tests, the importance of gaining experience with detailed, consequent, history taking cannot be overemphasised.

T‐LOC precipitated by fear, severe hurting, emotional distress, instrumentation or prolonged continuing suggests reflex syncope. A prodrome of nausea, vomiting, sweating, or feeling of cold and tiredness may suggest reflex syncope. Brief myoclonic jerking of limbs starting after LOC, which itself is of brusk duration, may likewise be seen in convulsive syncope. Facial pallor is particularly important during T‐LOC. Claret drains abroad from the skin with diversion to skeletal muscle when the arterioles open up with a loss of sympathetic tone. Often patients are and then pale that witnesses say "I thought he/she was dead", and they are described every bit existence "as white as a canvass". Nausea and vomiting after the event are suggestive of reflex syncope,⁴⁵ and presumably represent reflex vagal hypertonia. Syncope occurring during or immediately later urination, defecation, coughing or swallowing is chosen "situational syncope". These situations are associated with stimulation of autonomic reflexes, such as the gag reflex, with manoeuvres that heighten intrathoracic pressure and reduce venous return during standing (in men, often when getting up to go to the bathroom in the middle of the night), or with both. Patients experiencing T‐LOC in the setting of definite SHD, or during (not after) exercise, may betoken that syncope is due to a malignant tachyarrhythmia. Arrhythmias might also cause T‐LOC while the person is supine, sometimes when preceded by palpitation. In patients with a family history of sudden cardiac death, an inherited cardiomyopathy, such as hypertrophic cardiomyopathy, or a principal electrical heart affliction, such every bit the long‐QT or Brugada syndrome, arrhythmic syncope must exist considered very likely, and every endeavour made to testify the diagnosis, considering the gamble of death is high.^seven

In dissimilarity, a diagnosis of epilepsy is more probable when there is a history of an aura, such as unusual or distinctive smell before the event. Genuine tonic–clonic movements that are prolonged and coincident with the onset of T‐LOC, rather than limb twitching (myoclonic jerks), are more suggestive of generalised epilepsy. A turn of the head at onset of lateralised clonic movements, or articulate automatisms, such as chewing or lip smacking, propose focal epilepsy. Lateral natural language biting, a suffused or cyanosed face, prolonged post‐T‐LOC confusion, or headache and agonized muscles propose generalised epilepsy, every bit does a family history of epilepsy.⁵ Epilepsy is far more likely if there is a history of brain injury,⁴⁵ and it is besides mutual in conjunction with cerebral birth trauma or hypoxia, severe learning disabilities and autism.^{5 ,46}

Psychogenic blackouts (NEAD) usually nowadays as¹⁵ dissociative seizures, factitious disorders (eg, panic disorder) or other psychiatric disorders.⁴⁷ A dissociative seizure is by far the nigh common imitator of epilepsy. Prominent motor features that wax and wane throughout a coma, long duration of blackouts (>ii min) and, on recovery, bear witness that the patient is able to call back events for a period of unresponsiveness, poor response to antiepileptic drugs and the presence of risk factors (eg, previous unexplained medical symptoms, a psychiatric history and a history of babyhood traumatic experiences) favour a diagnosis of dissociative seizure or a psychogenic cause of blackouts.¹⁵ Interestingly, about 1 in x patients with NEAD presents in apparent condition epilepticus.⁴⁸

Investigations: the importance of the ECG

Reflex syncope is the about mutual cause of syncope, and usually there is no SHD. Past the time a patient has been transported to hospital after such an episode, a 12‐atomic number 82 ECG is commonly normal.^vii However, although the ECG may exist normal, this is an of import negative finding. Only about 4% of patients seen in Britain neurology outpatient settings undergo an ECG, and of import findings, although rare, may be crucial. We take seen a small merely considerable number of patients with primary electrical diseases of the heart who have been misdiagnosed, leading to near tragedy. Effigy ane​ shows the ECG of a 35‐year‐old man who was misdiagnosed with an astute coronary syndrome afterward existence admitted with T‐LOC. "Failed thrombolysis" led to transfer for coronary angioplasty. His coronary arteries were normal. Neurological review for epilepsy suggested syncope. Somewhen, he was diagnosed with the Brugada syndrome and received an implantable cardioverter defibrillator. He has since had three successful device discharges for ventricular fibrillation. Figure two​ shows the ECG of a 3‐yr‐former girl with blackouts who was treated unsuccessfully for epilepsy. An ECG was finally carried out and it showed long‐QT syndrome (type Iii). She connected to black out on β‐blockers, and received an implantable cardioverter defibrillator. Since and so, episodes of non‐sustained polymorphic ventricular tachycardia are stored in the device memory. An ECG must exist carried out in each and every patient with blackouts. An abnormal ECG (see box three) is an independent predictor of cardiac syncope or increased mortality.⁷ The almost common diagnoses encountered in the accident and emergency department in patients with arrhythmic syncope are ventricular tachycardia and bradycardias.

Figure 1 An electrocardiogram of a 35‐twelvemonth‐onetime man with transient loss of consciousness who was misdiagnosed every bit having an acute coronary syndrome. The appearances are typical of the Brugada syndrome.

Effigy 2 An electrocardiogram (ECG) of a 3‐year‐old girl misdiagnosed and treated for epilepsy. The ECG shows long‐QT type Three syndrome.

Tilt‐table testing

Kenny et al ⁴⁹ introduced tilt‐tabular array testing in unexplained syncope. Although it is widely accepted, its value in the management of T‐LOC is uncertain.

Standing shifts 1000 ml of blood book into the venous capacitance vessels of the lower legs. Later on standing continuously for about ten min, increased fluid book in the legs causes a rising in capillary pressure. This causes egress of tissue fluid into the interstitial infinite, with further depletion of the intravascular volume. This in plough leads to a decrease in venous return and stroke book, and the activation of compensatory mechanisms (vasoconstriction of the resistance vessels in the splanchnic, musculocutaneous and renal vascular beds) to prevent a fall in blood pressure. During the initial phase, changes are due to aligning of sympathetic tone. Afterwards adjustments arise from recruitment of the humoral limb of the neuroendocrine system.⁵⁰ Failure of these compensatory mechanisms is thought to play a part in patients with reflex syncope and form the footing of the tilt‐tabular array test. Tilt‐positive patients accept a gradual asymptomatic fall in mean arterial blood pressure after being tilted to 60°, before the sudden collapse that reproduces syncope, whereas the mean arterial blood pressure of tilt‐negative patients gradually increases over 45 min.⁵¹ Tilt‐positive patients likewise have exaggerated reflex responses to gravitational stress simulated by lower‐body negative pressure while they are supine,⁵² simply attenuated reflex responses to gravitational stress when they are tilted to 60°.⁵³ Tilt‐positive patients are definitely dissimilar from tilt‐negative patients, at least on the day of their particular tilt response. Nonetheless, tilt responses are non consistent inside individual patients,^{54 ,55} are poorly reproducible^{56 ,57} and depend on the pre‐examination likelihood of a positive or negative tilt issue.⁵⁸

Figure three​ shows the results of tilt testing in unselected patients with T‐LOC. All comers had a depression overall yield, akin to the lowest yield reported elsewhere.⁵⁸ Older patients with recurrent blackouts and no SHD had a high yield similar to the highest yield reported.⁵⁹ This suggests that the clinical characteristics of patients tilted are the clue to their response, and that in one case again, a skilful history of blackouts is as useful as any test. Also, by inference, tilt‐tabular array testing is unlikely to discriminate effectively between unselected patients with unexplained blackouts—that is, it may not be helpful equally a discriminative tool in all comers with T‐LOC.

Figure three Results of tilting in 145 patients with transient loss of consciousness (T‐LOC). Overall positivity in all comers was about 20%. Patients who were older, had no structural heart disease (SHD) and who had recurrent T‐LOC (correct side of nautical chart) had a higher rate of positive test. Patients who were young, had SHD (usually congenital or corrected congenital heart disease) and fewer episodes had no positive tests. The pre‐examination likelihood of a positive or a negative result was determined past clinical features predicted the outcome of the examination. Adding drug provocation (isoprenaline and edrophonium showtime, in randomised way) after 45 min of baseline tilt achieved only a pocket-sized increase in yield. Drug provocation may increase the sensitivity of the examination, but at the cost of decreasing specificity.⁵⁸ SDC, sudden diminished consciousness.

At that place is i important exception to this rule. In patients with suspected psychogenic blackouts, tilt‐table testing is legitimate and very useful if accompanied by simultaneous recording of ECG, phasic blood pressure and EEG. Patients with psychogenic blackouts are suggestible to black out during tilt, even at a pre‐suggested time. However, the ECG, claret pressure and EEG may remain quite normal throughout.^sixty This is useful in making a diagnosis.

The European Society of Cardiology recommends that tilt‐table testing be carried out for diagnostic purposes in patients with a single syncopal episode in high‐run a risk settings or in people who have recurrent syncopal episodes in the absence of organic heart illness.⁷ When the history is typically of reflex syncope, tilt‐table testing adds footling to the overall diagnosis and management of the condition. Debate continues over the value of this test in assessing patients with recurrent unexplained falls, recurrent presyncope or dizziness.⁷ The value of the tilt‐tabular array test in unselected patients with blackouts may be limited.

Implantable loop recorder

ECG monitoring is an important tool in the examination of patients presenting with T‐LOC. Nevertheless, to rely on this investigation to confirm or rule out an arrhythmia equally the cause of symptoms, it is important to take a correlation between symptoms and ECG, which is difficult to achieve⁶¹ and is rarely achieved past conventional Holter monitoring.^{62 ,63 ,64 ,65} Indeed, in that location is a good risk that random monitoring without the recurrence of typical symptoms may lead to a false reassurance of normality in the absence of arrhythmia, or a false supposition of arrhythmic syncope when an incidental arrhythmia is found, merely in the absence of symptoms.^seven

Holter monitoring, for 1–seven days, is commonly undertaken in patients with T‐LOC and has a few apparent advantages. It is non‐invasive, with vanquish‐to‐beat ECG recording, reasonable quality and low recording costs. All the same, the diagnostic yield is around 1% for symptom–ECG correlation.^seven Most patients with T‐LOC have exceptional symptoms and a small pre‐test likelihood of blackout symptom–ECG correlation during recording. This makes Holter monitoring costly, rarely useful and potentially misleading. Prolonged periods of Holter monitoring are precluded because of poor compliance and peel irritation, which is common. External effect recorders, to exist applied to the chest during a blackout, accept a slightly higher yield,⁶⁶ just are impractical, owing to infrequent symptoms⁶⁷ and the disability of the patient to use the recorder successfully during a coma.

The implantable loop recorder (ILR) is implanted on the left side of the chest by means of a minor surgical procedure carried out under local anaesthesia. This has perceived disadvantages because it is invasive and has high unit of measurement costs. The ILR costs about £1500 per treatment, whereas a 24‐h ECG costs nigh £70 per tape. However, an ILR battery lasts betwixt 18 and 24 months. It is always capable of monitoring during that fourth dimension. It has the power to record a high‐allegiance ECG during an episode of blackout using a retrospective loop memory. This allows ILR activation afterwards consciousness is restored. The ILR gives a high symptom–ECG correlation of virtually 88% at 6 months.⁶⁸ The diagnostic yield is far higher than that of Holter monitoring, and thus information technology is definitely more than toll effective. In the Manchester Heart Middle (Manchester Uk), Holter monitoring is 4–v times equally costly per symptom/ECG correlation equally the ILR in patients who have had blackouts. The value of ILR in patients with unexplained syncope, after conventional investigations had failed, was highlighted in a recent publication by Brignole et al.⁶⁹ Patients anile ⩾65 years in this study, when compared with those anile <65 years, had a higher syncope recurrence rate and a considerably higher incidence of arrhythmias as a cause of their symptoms that were appropriately detected and treated by the ILR. Gradually, we conceptualize that the ILR will supplant other investigations in patients with blackouts, because of a much greater symptom–ECG correlation and a much greater toll effectiveness. The ISSUE Two study confirms this.⁷⁰

EEG and neuroimaging

Similar to syncope, the diagnosis of epilepsy is essentially clinical. In most cases, it is possible for medical practitioners with specialised preparation, experience and hence expertise in epilepsy to go far at a diagnosis on the basis of the history and examination of the affected people, and information obtained from eye witnesses.⁵ Once a clinical diagnosis is made, further investigations, either in the form of an EEG or encephalon imaging, are justified to make a full classification of epilepsy and the epilepsy syndromes. It is of import to recognise the limitations of these examinations in establishing a diagnosis of epilepsy. The standard EEG has a variable sensitivity and specificity, and over‐reliance on this investigation to brand a diagnosis is likely to lead to misdiagnosis considering of the number of false positives.^{five ,43 ,71} If a standard EEG is unhelpful, long‐term video or convalescent EEG may exist helpful.

Both magnetic resonance imaging (MRI) and computed tomography can identify structural abnormalities in the brain that cause sure epilepsies. Because of its higher sensitivity and specificity, MRI is the preferred method in patients with structural abnormalities. This investigation is particularly of import in those children who present with epilepsy earlier the age of two years or in machismo, in patients of whatsoever age whose history and examination propose a focal onset of epilepsy, and in the minority of patients in whom seizures go along despite first‐line handling.^{v ,72} Computed tomography tin be used to help management if facilities for an MRI are non available, or in an acute situation, to decide whether seizures are a result of an acute neurological lesion or illness.

Which patients benefit from hospitalisation?

Blackouts are the sixth virtually common reason for admission of adults anile >65 years to acute medical infirmary beds.⁷ The average length of stay for such patients is 5–17 days, and hospitalisation accounts for 74% of the cost of investigating syncope.⁷³ Currently, the strategies for assessment of a patient with a blackout vary widely among doctors and amongst hospitals. Some authors have evaluated the consequence of the introduction of in‐hospital protocols.^{74 ,75} However, a large number of inappropriate admissions and investigations still occur, increasing the toll per diagnosis.

Hospitalisation is strongly recommended when the crusade of syncope is likely to be prognostically relevant. Patients with blackouts due to an acute myocardial infarction, acute pulmonary embolism, high‐grade atrioventricular block, long‐QT syndrome, Brugada syndrome, WPW syndrome with atrial fibrillation and rapid ventricular response, ECG abnormalities suggestive of an arrhythmic cause of syncope, symptoms occurring during exercise or causing astringent injury, and patients with a family history of sudden decease, benefit from hospitalisation for either diagnosis or treatment.

Patients with isolated or exceptional blackouts, who have no evidence of SHD and any worrisome concrete injury, and have a normal resting ECG and a history typical of reflex syncope, tin can safely exist evaluated on an outpatient basis every bit the long‐term prognosis in such patients is favourable.

The misdiagnosis of epilepsy

The misdiagnosis of epilepsy is common.^{5 ,76 ,77 ,78 ,79 ,eighty ,81 ,82} It affects xx–xxx% of adults and as many as 40% of children.^{5 ,83 ,84 ,85} As epilepsy affects as many as 600 000 patients in the UK, a misdiagnosis may bear on as many as 180 000 people.^{76 ,77 ,78 ,79} Misdiagnosis of epilepsy in the UK may exist compounded by poor access to neurological assessment, and the diagnosis of epilepsy by generalists in primary and secondary care.⁷⁸ Reflex syncope affects as many as 50% of the people, just epilepsy affects only 1–ii%. Hence, many misdiagnoses of epilepsy may probably occur because of syncope, possibly considering of misinterpretation of the appearances and meaning of convulsive syncope by witnesses and medical attendants. Indeed, reports point that misdiagnosed epilepsy is due to syncope with several mechanisms.⁷⁹

A misdiagnosis of epilepsy is costly and amercement the lives of patients, families and the wider National Health Service. Direct costs are incurred every bit a result of utilisation of resource, including medical costs. These include treatment in primary care, hospital intendance, drugs, investigations and non‐medical costs, such as community and residential intendance. Indirect costs include decreased or lost productivity due to underemployment or unemployment, psychological problems due to stigmatisation by social club, and transport problems due to driving restrictions. A misdiagnosis leads many patients to receive antiepileptic drugs inappropriately, not only proving ineffective in controlling their symptoms merely also exposing them to side effects of the drugs. If prescribed to pregnant women, they can have serious agin consequences for the unborn kid.⁸⁶ In add-on, patients do not receive the advisable treatment for the condition they actually take. The economical burden to the National Health Services and to social intendance is substantial. The direct costs are estimated at £24.3–82.nine million, with the total price in the range of £130–189 1000000.⁵ Withal, this may be a considerable underestimate. Further business organization is regarding the effect of SUDEP. Patients with poorly controlled epilepsy have at least a ninefold increased gamble of sudden expiry,^{5 ,87} and the mechanism remains uncertain, other than that it is commonly preceded by plummet. A low level of fifty-fifty the simplest cardiological screening, by ECG, in patients with blackouts in Britain neurological clinics, raises concerns that some cases of SUDEP may actually exist due to unsuspected cardiac affliction and arrhythmic syncope.

That the presenting clinical features of epilepsy can be mimicked by syncope^{half dozen} is clearly not widely appreciated. Information technology is probably causeless that a patient presenting with a convulsive blackout and abnormal movements has epilepsy, and and then the history taken may be besides superficial, and the features described may too readily be attributed to a main brain dysfunction rather than to a secondary effect of cerebral hypoperfusion. In attempting to confirm this clinical impression, doctors may turn to laboratory tests. Again, it is poorly appreciated that interictal EEG/(due south) cannot reliably confirm or dominion out the diagnosis of epilepsy.⁸⁸ Although an EEG can show specific epileptiform discharges in many patients with epilepsy,⁸⁹ similar discharges can be seen in x% of patients having undergone intracranial surgery and in 3% of patients with psychiatric disorders who practise not have epilepsy.⁹⁰ It is also poorly appreciated that normal phenomena, artefacts and non‐specific abnormalities, occurring in many from the general population, are open to misinterpretation and therefore contribute to false‐positive results.⁹¹ The incidence of apparent abnormalities on EEG varies with the population studied, and tin be particularly loftier in patients attending hospital clinics, who accept other medical disorders, making them particularly prone to misdiagnosis. Epilepsy is a clinical diagnosis, and laboratory tests such as EEG are used by neurologists to define the epilepsy syndrome of a patient, not to cement a diagnosis in unselected patients with blackouts.

Driving regulations

The need for the driver of a motor vehicle to notify the Driver Vehicle and Licensing Bureau (DVLA) and the duration of the ban from driving depend on the underlying cause of collapse and the type of vehicle the driver is licensed to drive. The purpose of the ban is to reduce the hazard of an injury resulting from an blow to either the commuter or other road users. To reach this aim, the DVLA has tried to hazard stratify patients with blackouts on the basis of clinical features and investigations.⁹² The longest and almost severe ban is for patients with suspected or proved epilepsy, equally this disorder is the most common cause of plummet at the wheel of the machine, while driving. Auto or motorcycle drivers are not permitted to drive for at least 1 yr after an episode of epilepsy. Patients with blackouts who accept an abnormal ECG, clinical evidence of SHD, sustained an injury equally a event of their blackouts, symptoms occurring at the cycle (while driving), while sitting or lying, or with more than ane episode in 6 months are considered to be at loftier adventure. The DVLA needs to be notified whether any high‐take chances features are present, and driving may be banned for up to 6 months. On the other hand, no driving restrictions apply and the DVLA need not exist notified if blackouts are due to unproblematic faints—that is, there are definite provocational factors, associated with prodromal symptoms and unlikely to occur while sitting or lying. If no cause of blackouts is found despite all-encompassing investigations, the patient is not permitted to drive for half-dozen months.

Conclusion

Syncope is far more prevalent than epilepsy in the general population. Similar clinical features, especially between convulsive syncope and generalised epilepsy, mean that the misdiagnosis of epilepsy is common. After work on the NSF for Arrhythmias and Sudden Cardiac Death, the Section of Health, Great britain, has canonical intendance pathways (​ ​ ​ figs 4–seven) to assist medical or paramedical people at the first and subsequent points of contact with a blackout patient.⁹³ These pathways may aid to tackle the common problem of a misdiagnosis of epilepsy.

Figure 4 Indicate of care: ambulance service. A&E, accident and emergency; CVA, cardiovascular assault; ECG, electrocardiography; MI, myocardial infarction; TIA, transient ischaemic attack; T‐LOC, transient loss of consciousness.

Effigy 5 Betoken of care: blow and emergency section. CVA, cardiovascular attack; ECG, electrocardiography; MI, myocardial infarction; SCD, sudden cardiac expiry; TIA, transient ischaemic attack; T‐LOC, transient loss of consciousness.

Effigy half-dozen Bespeak of care: general practitioner and out of hospital. CVA, cardiovascular set on; ECG, electrocardiography; MI, myocardial infarction; SCD, sudden cardiac expiry; TIA, transient ischaemic set on; T‐LOC, transient loss of consciousness.

Figure 7 Point of care: rapid admission to clinics for patients with blackouts. CVA, cardiovascular assail; ECG, electrocardiography; GP, general practitioner; MI, myocardial infarction; TIA, transient ischaemic attack; T‐LOC, transient loss of consciousness.

Key References

• The Task Force on Syncope, European Gild of Cardiology. Guidelines on management (diagnosis and handling) of syncope—update 2004. Europace 2004;6:467–537.

• Stokes T, Shaw EJ, Juarez‐Garcia A, et al. Clinical guidelines and evidence review for the epilepsies: diagnosis and management in adults and children in primary and secondary intendance. London: Royal College of Full general Practitioners, 2004.

• Fitzpatrick A. Convalescent electrocardiographic (AECG) monitoring for evaluation of syncope. In: Benditt DG, Blanc JJ, Brignole Thou, Sutton B, eds. The evaluation and treatment of syncope. A handbook of clinical practice. New York: Blackwell, 2003: 63–70.

• Section of Health Expert Reference Groups for the National Service Framework for Arrhythmias. National Service Framework for Coronary Eye Disease. Arrhythmias and sudden cardiac death: implementation. http://www.dh.gov.uk/PolicyAndGuidance/HealthAndSocialCareTopics/CoronaryHeartDisease

• Zaidi A, Clough P, Cooper P, et al. Misdiagnosis of epilepsy: many seizure similar attacks have a cardiovascular cause. J Am Coll Cardiol 2000;36:181–4.

Self‐assessment questions (True (T)/False (F)); answers at the end of references

1. Regarding the epidemiology of blackouts:

1. Nigh one in two people experience a syncopal event in their lifetime.

2. The incidence of syncope decreases in elderly people.

3. Reflex syncope is the virtually common cause of syncope.

4. The prevalence of epilepsy in the UK is approximately 0.vii–i.0%.

5. Psychogenic blackouts oftentimes coexist in patients with epilepsy.

6. Quality of life is the aforementioned in patients with or without syncope.

7. Well‐controlled epilepsy is a chance factor for SUDEP.

two. The post-obit clinical features are suggestive of reflex syncope:

1. History of aureola.

2. Lateral tongue bitter.

3. Prolonged post‐T‐LOC confusion.

4. T‐LOC precipitated by prolonged standing or instrumentation.

5. Facial pallor during T‐LOC.

6. Brief myoclonic jerks of limbs starting later on the loss of consciousness.

three. Regarding investigations of blackouts:

1. The 12‐lead electrocardiogram (ECG) is often normal in patients with reflex syncope.

2. An abnormal resting 12‐lead ECG makes an arrhythmic cause of syncope more likely.

3. The prognosis of syncope is meliorate in patients with underlying structural heart disease.

4. Left ventricular dysfunction is a marker of sudden cardiac death.

5. Holter monitoring yields a loftier ECG–symptom correlation.

6. The results of the tilt tabular array test are highly reproducible.

7. Drug provocation during tilt tabular array testing increases the specificity of the test.

8. The implantable loop recorder (ILR) has no role in the investigation of elderly patients with blackouts.

9. A combined EEG and tilt‐table test is valuable in evaluating patients with psychogenic blackouts.

10. The battery life of an ILR is approximately 6 months.

Abbreviations

DVLA - Commuter Vehicle and Licensing Agency

ECG - electrocardiography

EEG - electroechocardiography

ILR - implantable loop recorder

MRI - magnetic resonance imaging

NEAD - not‐epileptic attack disorder

SHD - structural middle illness

SUDEP - sudden unexpected expiry in epilepsy

T‐LOC - transient loss of consciousness

Answers

(one) (A) T (B) F (C) T (D) T (E) T (F) F (G) F (ii) (A) F (B) F (C) F (D) T (Eastward) T (F) T (three) (A) T (B) T (C) F (D) T (Eastward) F (F) F (G) F (H) T (I) T (J) F

Footnotes

Competing interests: None.

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