Syncope in adults: Management and prognosis

INTRODUCTION — Syncope is a clinical syndrome in which transient loss of consciousness (TLOC) is caused by a period of inadequate cerebral nutrient flow, most often the result of an abrupt drop of systemic blood pressure [1-4]. Typically, the inadequate cerebral nutrient flow is of relatively brief duration (8 to 10 seconds) and, by definition, syncope is self-limited. Unfortunately, the term "syncope" is often misapplied to encompass any form of abrupt collapse which may or may not be accompanied by TLOC, including seizures and concussions; such overbroad usage should be avoided as it deflects diagnostic focus from causes of cerebral hypoperfusion (algorithm 1) [5]. (See "Syncope in adults: Clinical manifestations and initial diagnostic evaluation".)

Issues relating to the treatment and prognosis of syncope in adults will be reviewed here. The pathogenesis and etiology of syncope, and the clinical manifestations and diagnostic evaluation of patients with syncope, are discussed elsewhere. (See "Syncope in adults: Epidemiology, pathogenesis, and etiologies" and "Syncope in adults: Clinical manifestations and initial diagnostic evaluation".)

TREATMENT — Treatment is based upon the underlying cause of syncope (table 1 and table 2) and is directed at preventing recurrence and/or, in some cases, death. A brief review of the available treatment options for each of the possible underlying disorders is presented below.

Responding to prodromal symptoms — Syncope may or may not be preceded by prodromal symptoms warning of an imminent faint, depending on the cause of syncope [6,7]. Certain symptoms may evolve during a short period before an imminent collapse, and recognition of these prodromal symptoms may permit the affected individual to react and both prevent evolution of the episode into a full faint and avoid TLOC hazards such as accidents and injury. Appropriate reactions may include pulling off to the side of the road if driving, lying down or sitting down if standing to avoid a fall, and lowering the head if feeling near faint.

Prodromes are common in young patients with reflex syncope, but seem to occur less often, or are less well recollected, in older individuals. Typical prodromes warning of imminent vasovagal faints include feeling hot or cold, feeling sweaty, pallor, nausea, and palpitations. Prodromes may also provide warning with certain cardiac syncope events (eg, chest pain with ischemia, palpitations with tachycardias), but not with others (eg, abrupt atrioventricular [AV] block or prolonged pauses). It may be helpful to ask bystanders if the affected individual expressed any symptoms before the collapse occurred; such symptoms may not be recalled by the "fainter" (particularly the older fainter) after the fact.

Patients with reflex (ie, vasovagal) syncope who experience prodromal symptoms are advised immediately respond to the warning by moving to a safe position (seated or ideally supine) and if possible, initiating physical isometric counterpressure maneuvers such as leg-crossing and/or lower body muscle tensing. The pathophysiology of these faints includes an abrupt initial drop of venous return leading to diminished stroke volume and cardiac output [8]. Counterpressure maneuvers reduce translocation of blood to dependent parts of the body and thus help maintain stroke volume and cardiac output [9,10].

Examples of physical counterpressure maneuvers include:

●Leg-crossing with simultaneous tensing of leg, abdominal, and buttock muscles

●Handgrip, which consists of maximum grip on a rubber ball or similar object

●Arm tensing, which involves gripping one hand with the other while simultaneously abducting both arms

Physical counterpressure maneuvers may also be helpful for patients with symptomatic orthostatic hypotension. An important risk of undertaking these maneuvers (particularly standing with legs crossed and muscles tensed) is postural instability, particularly for individuals who are frail or older. These maneuvers are discussed in detail separately. (See "Reflex syncope in adults and adolescents: Treatment", section on 'Recognizing symptoms and taking action'.)

Immediate (emergency) treatment of syncopal patients — For witnessed syncope, the immediate treatment of a patient with syncope or presyncope includes the following:

●Assist the patient to the ground, chair, or stretcher to avoid traumatic injury. When necessary, remove the patient from any potential external dangers (eg, high places, water, electrical wires, etc).

●Lay the patient supine, with legs elevated if possible to enhance venous return to the heart and thereby restore adequate cerebral perfusion.

●Assess vital signs, namely a pulse and evidence of respiration, to distinguish cardiac arrest from syncope.

●Observe for other signs (eg, pallor, diaphoresis, seizure-like or jerky muscular movements, etc) that may assist in establishing the etiology. Note whether eyelids are open, closed, or fluttering.

●Call for additional assistance if needed.

●Attempt to arouse the patient. Do not try to raise the patient up until the patient indicates readiness to do so. Raising the patient too soon may trigger a recurrence of the transient loss of consciousness.

For patients who are identified to be hypotensive not directly caused by excessive bradycardia or asystole, raising the legs and providing fluid resuscitation (eg, intravenous saline infusion) are the first steps for treatment. Orthostatic hypotension associated with evidence of volume depletion should improve following volume expansion. Orthostatic hypotension due to an autonomic neuropathy may not be entirely reversed with fluids, but in most cases some benefit will be achieved and, consequently, a trial of fluid resuscitation is appropriate. (See "Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock", section on 'Intravenous fluids' and "Treatment of orthostatic and postprandial hypotension".)

Patients who are identified to have symptomatic bradycardia or high-grade AV block (ie, Mobitz type II second-degree AV block or third-degree [complete] AV block) may or may not be hypotensive when medical care is initiated. For hypotensive patients, atropine followed by temporary cardiac pacing are usually the initial treatments. If these steps are not available or effective, and depending on the severity of hypotension, isoproterenol or dobutamine infusion may help to increase heart rate. Severe hypotension may require treatment with parenteral vasoconstrictors. (See "Advanced cardiac life support (ACLS) in adults", section on 'Bradycardia' and "Third-degree (complete) atrioventricular block", section on 'Unstable patients' and "Second-degree atrioventricular block: Mobitz type II", section on 'Unstable patients'.)

Therapies to prevent syncope recurrences — Therapies directed toward prevention of syncope recurrences are highly variable depending upon the suspected etiology of the syncope [1,2,11,12].

Reflex syncope — Vasovagal syncope is the most common condition in this category in all age groups and, if recurrent, may necessitate attempts at reducing susceptibility. Unfortunately, vasovagal events are unpredictable, and no therapy has been proven consistently effective for recurrent vasovagal syncope. The treatment of reflex syncope is presented in detail separately. (See "Reflex syncope in adults and adolescents: Treatment".)

Carotid sinus syncope — Carotid sinus hypersensitivity is a physical finding in which carotid massage results in a marked pause (generally 5 seconds or greater) and/or vasodepressor hypotensive effect [1,2]. Carotid sinus hypersensitivity is a common finding, especially in older men, and does not warrant treatment if asymptomatic.

If carotid sinus hypersensitivity is found to cause syncope or near-syncope, then the condition is deemed to be a particular subtype of reflex syncope known as carotid sinus syndrome (CSS). As with reflex syncope in general, initial treatment measures include reassurance and education regarding the nature, risks, and prognosis of the condition. The patient should be advised to avoid accidental mechanical manipulation of the carotid sinuses (eg, abrupt turning of the neck, tight collars). In CSS patients, medications that may induce hypotension (such as vasodilator therapy) should be discontinued or reduced when feasible. Pacemakers are helpful in many patients with CSS in whom the cardioinhibitory response (ie, bradycardia or asystole) is prominent, but are not as beneficial in individuals with a predominant vasodepressor response. The treatment of CSS is discussed in detail separately. (See "Carotid sinus hypersensitivity and carotid sinus syndrome".)

Situational syncope — Situational syncope, as the name suggests, comprises a group of reflex syncope conditions that occur in or are triggered by particular circumstances. For example, cough syncope, micturition syncope, and swallow syncope are examples in which the trigger is apparent. Treatment, however, may be difficult as it entails minimizing the impact that these common circumstances have on susceptible individuals.

Orthostatic hypotension — Orthostatic hypotension (OH) is a very common cause of lightheadedness or syncope accompanying movement to upright posture. It may be the result of volume depletion, neurologic disorders, or the effects of drugs (eg, vasodilators, diuretics). OH may be considered to comprise two clinical forms [13,14].

●The "immediate" (sometimes also referred to as the "initial") form occurs momentarily after arising and may occur in all age groups, including healthy individuals.

●The "delayed" or "classic" form tends to occur in older patients and/or those with neurologic disorders (eg, Parkinson disease, autonomic failure, diabetic neuropathy). The classic form may be more hazardous, as TLOC may not begin until the patient is sufficiently far from support (such as a chair or sofa) that they have nothing to hold on to in order to diminish the severity of the collapse. Injury is far more prevalent in the classic form.

Causes and evaluation of orthostatic hypotension are discussed further separately. (See "Mechanisms, causes, and evaluation of orthostatic hypotension".)

Identifying the underlying cause of OH is crucial to determine appropriate preventive treatment. OH associated with evidence of volume depletion should be treated with volume expansion and avoidance of precipitating factors (such as diuretic use). In the absence of volume depletion, OH is most often due to administration of vasodilator or negative chronotropic drugs; other cases may be due to autonomic neuropathy, with causes including diabetes mellitus, alcohol abuse, and other toxins. In the latter group (ie, autonomic dysfunction), supine hypertension is a common limiting factor. Long-term management of OH is complicated by the associated risk of supine hypertension in many of these patients, and is discussed in detail separately. (See "Treatment of orthostatic and postprandial hypotension".)

Medication-induced syncope — Recurrent syncope resulting as a side effect of therapy with certain medications is often preventable. Most, but not all, of medication-induced syncope are orthostatic. Effective interventions should, if possible, include the elimination of the offending medication, substitution of an alternative agent, dose adjustment, or altering the timing of drug administration.

As examples:

●Orthostatic complications:

•Patients with OH, particularly if taking one or more medications (eg, antihypertensives, vasodilators) that may exacerbate orthostasis (table 3).

•Patients with volume depletion who are taking diuretics.

●Nonorthostatic complications:

•Patients with bradyarrhythmias and/or heart block who are taking beta blockers, calcium channel blockers, other antiarrhythmic drugs and/or digoxin.

•Patients with tendency to long QT syndrome who are prescribed QT-prolonging drugs may develop collapse due to torsades de pointes. (See "Congenital long QT syndrome: Treatment" and "Acquired long QT syndrome: Clinical manifestations, diagnosis, and management".)

Cardiac syncope — Syncope of cardiac origin is most often due to tachy- and bradyarrhythmias (with causes including genetically determined channelopathies and various types of structural cardiac diseases). Less commonly, "mechanical" disturbances may trigger hypotension and syncope (eg, severe aortic stenosis with inadequate cardiac output on exertion).

Arrhythmias — Patients with syncope and documented ventricular tachyarrhythmias are often candidates for drug or device therapy aimed at both preventing recurrences and addressing concerns regarding sudden cardiac death (SCD).

Documented, suspected, or induced ventricular tachycardia — Syncope in patients with ventricular tachycardia (VT) may reflect an increased risk of SCD or hemodynamic collapse in the setting of structural heart disease. Patients with structural cardiac disease, syncope, and documented ventricular arrhythmias are at high risk for recurrent VT and/or SCD. Therapy with ablation and/or an implantable cardioverter-defibrillator (ICD) is indicated in most such patients [1]. Additionally, ICD therapy is an option for some patients who have syncope due to an unknown cause but have underlying structural heart disease that places them at risk of SCD. While ICD therapy plays an important role in preventing sudden death, it may not protect against syncope recurrences. A full discussion of the secondary prevention of SCD due to VT is presented separately. (See "Secondary prevention of sudden cardiac death in heart failure and cardiomyopathy".)

Supraventricular arrhythmias — While many patients with a supraventricular tachycardia (SVT) will develop symptoms, usually palpitations, chest discomfort, or dyspnea, syncope is much less often encountered, as most SVTs are hemodynamically well tolerated. However, syncope may occur at the onset of SVT when the vascular compensatory mechanisms to maintain blood pressure take time to become active. In some patients, usually older adults, syncope may occur when SVT terminates and a pause ensues, since return to an adequate rhythm may be delayed due to overdrive suppression.

Patients with severe underlying cardiac disease (eg, decompensated heart failure, etc) in whom there is insufficient cardiac reserve to tolerate the increase in heart rate may be at particular risk of collapse with tachyarrhythmias. When possible, patients with syncope due to SVT and an accessory pathway should be treated with catheter ablation. A full discussion of the treatment of SVT in patients with an accessory pathway is presented separately. (See "Treatment of arrhythmias associated with the Wolff-Parkinson-White syndrome", section on 'Treatment to prevent recurrent arrhythmias'.)

Bradyarrhythmias — In some patients with syncope, a bradyarrhythmia will be recorded at presentation. These may be due to a wide range of underlying conduction system problems, such as sinus node dysfunction, progressive disease of the specialized conduction system, and genetically determined disorders such as the muscular dystrophies. In any case, bradyarrhythmias of sufficient severity to cause syncope (eg, sinus pause, pause after SVT termination) can be infrequent and difficult to document. In such cases, it is essential to extend periods of ambulatory electrocardiogram (ECG) monitoring to capture infrequent events [14]. In general, if no reversible causes are present, definitive treatment of high-grade AV block (ie, Mobitz type II second degree AV block or third degree [complete] AV block) or prolonged pauses in a patient with documented correlation between symptoms and bradycardia necessitates permanent pacemaker placement [1]. (See "Third-degree (complete) atrioventricular block", section on 'Stable patients' and "Second-degree atrioventricular block: Mobitz type II", section on 'Stable patients' and "Sinus node dysfunction: Treatment", section on 'Symptomatic patients'.)

Rarely, a permanent pacemaker is used empirically when baseline ECG or invasive electrophysiology studies (EPS) strongly suggest a conduction abnormality as the cause for syncope as illustrated by the following examples [1]:

●Pacemaker therapy is reasonable in patients with syncope when clinically significant sinus node dysfunction is observed or provoked during EPS. However, it is unusual for EPS to be particularly useful in this setting.

●Pacemaker therapy is reasonable in patients with syncope and bifascicular or trifascicular disease on the baseline ECG if other causes have been excluded, specifically VT. Electrophysiologic study to assess severity and anatomic level of the block may be warranted. However, some studies have raised concern that empiric pacing in these settings may not prevent syncope [15,16].

●In some older adult patients, severe bradycardia is recorded (occasionally as low as 20 to 30 beats per minute), but symptoms are not reported. The appropriate role for pacemakers in this situation remains controversial.

Obstruction to left ventricular outflow — Syncope in a patient with severe aortic stenosis may be directly related to the valve disease; however, patients with severe aortic stenosis and syncope may also have syncope from another cause (eg, reflex-mediated, orthostatic hypotension, conduction system disturbance, etc) which is only indirectly attributable to the aortic valve disease itself. As with all patients who experience syncope, a thorough history and physical examination are critical in determining the etiology and subsequent management. For patients with severe aortic stenosis in whom no other etiology of syncope is identified, aortic valve replacement may be indicated, but thorough discussion with the patient and family (ie, shared decision making) is crucial. The approach to symptomatic severe aortic stenosis is discussed in detail separately. (See "Clinical manifestations and diagnosis of aortic stenosis in adults" and "Indications for valve replacement for high gradient aortic stenosis in adults".)

Syncope may also occur in patients with dynamic outflow obstruction resulting from hypertrophic cardiomyopathy (HCM). Unexplained syncope (ie, not related to neurocardiogenic/vasovagal causes) is considered a marker for increased risk of sudden death. The approach to patients with HCM and syncope is discussed in detail separately. (See "Hypertrophic cardiomyopathy: Clinical manifestations, diagnosis, and evaluation", section on 'Syncope' and "Hypertrophic cardiomyopathy: Risk stratification for sudden cardiac death", section on 'Risk stratification'.)

DRIVING RESTRICTIONS — Rules regarding driving may vary from region to region within some countries and certainly between countries. Driving restrictions are indicated for some patients at risk for recurrent syncope for the safety of themselves and others. In general, patients with untreated syncope should not drive until appropriate preventive treatment has been instituted (table 4) [1,17]. Following the institution of therapy for syncope, the duration of time patients should avoid driving varies significantly depending upon the underlying condition as well as the legal restrictions of the local, state, or national government. Because of the significant variability in legal restrictions worldwide, providers should be familiar with their local driving laws and restrictions and advise patients accordingly.

The assessment of motor vehicle accident risk among patients with a history of syncope, or, as is more often the case, a diagnosis of "syncope/collapse," is difficult in practical terms due to the rarity of events, and especially of repeat events in the same individual. Consequently, the topic remains controversial.

The likelihood of a motor vehicle crash has been estimated to be between 1.5 and 4 times higher for patients with a history of syncope compared with the general population [17-21]. In a Danish cohort of 41,039 patients with first episodes of syncope between 2008 and 2012 with a median follow-up of two years, 1791 patients (4.4 percent) experienced a motor vehicle crash at a rate that was significantly higher than the general population (20.6 compared with 12.1 per 1000 patient-years in the general population; rate ratio 1.83, 95% CI 1.74-1.91) [17,18].

While the risk of motor vehicle crash may be higher in patients with history of syncope than in the general population, a British Columbia study suggested that the crash risk in patients with presumed syncope may be similar to that for other patients presenting to emergency departments [21]. In this study of 43,589 patients visiting emergency departments (9223 with syncope and 34,366 with other conditions), the baseline motor vehicle crash rates for "syncope and collapse" and control groups were similar and higher than in the general population (12.2, 13.2, and 8.2 crashes per 100 driver-years, respectively) [21]. During the year after the index emergency department visit, crashes occurred at similar rates in the "syncope and collapse" and control groups (9.2 versus 10.1 percent; adjusted hazard ratio 0.93, 95% CI 0.87-1.01). A major limitation of the interpretation of this study and similar emergency department-based studies is that emergency department clinicians often of necessity combine "syncope and collapse" rather than restrict observations to "syncope" alone. The take-away lesson may then be that motor vehicle accidents are likely to be similarly increased in frequency among patients with an acute illness of sufficient severity to cause them to seek emergency department evaluation.

PROGNOSIS — The prognosis of the patient with syncope is in most cases directly related to the underlying etiology of the syncope and the underlying comorbidities, not the syncope itself [22-25]. As a result, patients can be categorized into different risk categories based upon cause (figure 1). Those with an underlying cardiovascular cause are at higher risk for sudden death and all-cause total mortality rates than those with a noncardiovascular cause. Overall mortality in the cardiovascular group after five years of follow-up has been reported to approach 50 percent, with a 30 percent incidence of death in the first year.

However, a major problem in determining the true mortality rate in patients with syncope is that most individuals with transient loss of consciousness do not seek medical advice. It is suspected that most individuals have a low recurrence rate of syncope and an excellent long-term survival in the absence of underlying cardiac disease or channelopathy (eg, long QT syndrome, Brugada syndrome). Underlying cardiac disease substantially increases mortality risk. Outpatients never admitted for their episodes may be at lesser risk for recurrence and have a more benign long-term prognosis than those requiring hospitalization.

Improvements in diagnostic capability have altered understanding of the prognosis associated with syncope/collapse of unknown cause. In considering syncope/collapse prognosis, it is important to differentiate studies derived from the emergency department (ED) from those obtained in presumably lower-risk, community-based studies. The ED studies have resulted in development of several risk stratification schemes mainly focused on short-term risk, as discussed separately. (See "Approach to the adult patient with syncope in the emergency department", section on 'Risk stratification'.)

In evaluation of longer-term prognostic implications of syncope of unknown cause, the Framingham study indicated that syncope/collapse of unexplained cause is accompanied by a mortality risk profile that is about halfway between low-risk vasovagal syncope patients (who had mortality rates no different than the normal population) and high-risk cardiac syncope patients (who had a much more worrisome mortality) (figure 1). However, as discussed above, given the important limitations associated with its diagnostic methodologies, the Framingham conclusions in this regard need to be reconsidered.

Contemporary evidence, while still in need of refinement, suggests that with a few exceptions (eg, channelopathies), mortality in patients with syncope/collapse of unknown cause is related less to having experienced a syncope event than to the presence and severity of underlying cardiovascular disease. For instance, a study of nationwide Danish registries identified 37,000 first hospitalizations with syncope which were compared with 185,000 nonsyncope controls [26]. Presence or absence of syncope had minimal effect on mortality over 10 years in older patients (>75 years) or younger individuals (<25 years) but did have an impact in middle-aged patients. The age-related differences are not readily explained, but tend to favor the interpretation that evolving underlying disease in middle-aged patients may be important. These data suggest that a hospitalization for syncope is a signal that warrants careful assessment of underlying cause.

The Malmo (Sweden) population-based study found no major differences in outcomes during the first 12 years of follow-up between an index unexplained syncope versus orthostatic hypotension without syncope [27]. After 12 years, mortality was higher in the syncope group, but the cause of this observation is uncertain. A report in patients with syncope and moderate left ventricular dysfunction found no mortality difference over 30 months follow-up compared with previously reported nonsyncope patients with similar severity of heart disease [28]. A meta-analysis of observational cohort studies compared mortality in a control population without syncope with that in a population with noncardiac/unexplained syncope [29]. A noncardiac/unexplained syncope history was associated with a 13 percent greater all-cause mortality (pooled adjusted hazard ratio 1.13, 95% CI 1.05-1.23) in older individuals or those with a diabetic or hypertensive history.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Syncope".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topic (See "Patient education: Syncope (fainting) (The Basics)" and "Patient education: Bradycardia (The Basics)".)

●Beyond the Basics topic (See "Patient education: Syncope (fainting) (Beyond the Basics)".)

SUMMARY AND RECOMMENDATIONS

●Patients with vasovagal syncope (the most common cause of syncope) and prodromal symptoms are instructed to move safely to a seated or supine position and perform physical isometric counterpressure maneuvers such as leg-crossing and/or lower body muscle tensing upon first recognition of premonitory symptoms. (See 'Responding to prodromal symptoms' above.)

●For witnessed syncope, the immediate treatment of a patient with syncope or presyncope includes assisting the patient to the ground or another location to avoid traumatic injury, laying the patient supine with legs elevated (if possible), assessing for vital signs, and calling for assistance. (See 'Immediate (emergency) treatment of syncopal patients' above.)

●Therapies directed toward prevention of recurrent syncope is selected based upon the suspected etiology of the syncope. (See 'Therapies to prevent syncope recurrences' above.)

●Recurrent syncope resulting as a side effect of therapy with certain medications is often preventable following elimination of the offending medication, substitution of an alternative agent, dose adjustment, or altering the timing of drug administration. (See 'Orthostatic hypotension' above.)

●No therapy has been proven consistently effective for recurrent vasovagal syncope. However, patients should be reassured about the generally benign nature of reflex syncope (while noting the risk of injury), educated to avoid potential triggers and identify warning symptoms, and instructed on how to perform physical counterpressure maneuvers at the onset of symptoms. (See 'Reflex syncope' above and "Reflex syncope in adults and adolescents: Treatment".)

●Patients with syncope and documented ventricular tachyarrhythmias are often candidates for drug or device therapy aimed at preventing sudden cardiac death (SCD). Patients with syncope and high-grade atrioventricular (AV) block (ie, Mobitz type II second degree AV block or third degree [complete] AV block) or prolonged pauses are treated with permanent pacemaker placement. (See 'Arrhythmias' above.)

●For patients with severe aortic stenosis in whom no other etiology of syncope is identified, and the syncope is suspected to be due to the severe aortic stenosis, aortic valve replacement is indicated. Similarly, unexplained syncope (ie, not related to neurocardiogenic/vasovagal causes) in patients with hypertrophic cardiomyopathy is considered a marker for increased risk of sudden death. (See 'Obstruction to left ventricular outflow' above and "Indications for valve replacement for high gradient aortic stenosis in adults" and "Hypertrophic cardiomyopathy: Risk stratification for sudden cardiac death".)

●Driving restrictions are indicated for some patients at risk for recurrent syncope for the safety of themselves and others. In general, patients with untreated syncope should not drive until appropriate preventive treatment has been instituted. Following the institution of therapy for syncope, the duration of time patients should avoid driving varies significantly depending upon the underlying condition as well as the legal restrictions of the local, state, or national government (table 4). (See 'Driving restrictions' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Brian Olshansky, MD, who contributed to earlier versions of this topic review.