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Sudden alteration of consciousness is a common presenting symptom in a variety of clinical contexts, from the emergency room to the outpatient clinic. The vast majority of events can be categorized as either seizure or syncope or the proverbial “fit” versus “faint.” This chapter aims to provide a practical framework to help the clinician distinguish between these two diagnoses. When evaluating a patient with a history of transient loss of consciousness, clinicians should spend the majority of their efforts on interviewing the patient and eyewitnesses, eliciting the symptoms and signs in a step-by-step fashion in order to understand the order and tempo of the events as they unfolded.
DIFFERENTIATING SYNCOPE FROM SEIZURE
is defined as a transient loss of consciousness due to insufficient blood flow to the brain. Epileptic seizures
are defined as transient alteration in brain function due to abnormal electrocerebral activity. The most important clinical features distinguishing these two conditions are the following: (1) precipitating stimuli or situations, (2) prodromal symptoms before losing awareness, and (3) the postevent recovery (Table 5.1
Although many patients and witnesses will use terms such as “passing out” or “fainting” to describe either condition, it is important to delve further and elicit a first-person narrative of the patient’s actual experience, carefully parsing out what the patient means when using these words.
Syncope typically occurs when patients are upright (standing or sitting) and can be triggered by exercise, coughing, bearing down (Valsalva maneuver), venipuncture, prolonged standing, or pain. Presyncope begins with a sense of unwellness accompanied by light-headedness and nausea. Patients may feel weak and unsteady on their feet, followed by a decreased awareness or detachment from their environment. Immediately before losing consciousness, patients experience a “graying of the vision” and/or “muffling” of ambient sounds. Eyewitnesses will often note that the patients appear pale or ashen, diaphoretic, and tachypneic. Sometimes an attack can be aborted if the patients lie down quickly or lower the head below the level of the heart. Once patients lose consciousness, they will lose tone in the muscles of their trunk and legs and they will limply collapse to the floor. On the ground, the limbs are flaccid and patients continue to appear pale and sweaty. The period of unconsciousness is generally brief, lasting only seconds up to 1 to 2 minutes. If the degree of decreased cerebral perfusion is profound enough, patients may display a few jerking movements of the limbs (“convulsive syncope”) but this is also typically very brief (lasting only a few seconds). Generally, the pulse and blood pressure quickly return to normal with the patients in the recumbent position; and they rapidly regain consciousness and quickly become oriented and aware of their surroundings. Patients will often realize that they have fainted and remember details of the event up until the moment of losing consciousness. They might experience mild fatigue or brief disorientation after the event, but this should not last more than a few minutes.
The clinical manifestations of seizures vary widely, depending on brain volume and neuroanatomic location of activation. Seizures can occur day or night, regardless of whether the patient is awake or asleep, and usually are not triggered by a precipitating stimuli or environment. Sometimes, a seizure may begin with the patients reporting an “aura” or warning. These subjective experiences might be described as a sense of déjà vu (a sense of reliving a familiar experience), a noxious smell, sudden anxiety, or tingling over one side of the body. Eyewitnesses might find the patients unresponsive to their direct questions, staring into space, or stopping what they were previously doing (behavioral arrest). Some patients exhibit oral or manual automatisms (lip smacking, chewing, rubbing of their hands, picking at their clothes). If a focal seizure then secondarily generalizes (electrical activity starting off in one area of the brain but then spreading to both hemispheres of the brain), the patients’ head and eyes may suddenly and forcibly turn to one side, with stiffening of the limbs, frothing at the mouth, cyanosis of the lips, followed by rhythmic jerking of the limbs. Most secondarily generalized seizures last between 1 and 2 minutes in duration and rarely over 5 minutes in duration, but afterwards, the patients may be confused and disoriented for minutes to hours. Patients may report lateral tongue biting and urinary incontinence after some seizures.
CAUSES OF SYNCOPE
NEURALLY MEDIATED REFLEX SYNCOPE
The most common type of syncope, accounting for over half of cases, is reflex syncope, also known as neurocardiogenic syncope
. In this form of syncope, an external factor or set of circumstances (apprehension of pain, cough, head turning etc….) leads to bradycardia, hypotension, or a mixture of both phenomena. Reflex syncope is divided into two main categories: vasovagal syncope and carotid sinus syncope (Table 5.2
Vasovagal syncope, the most common type of reflex syncope, is caused by a brief loss of neurally mediated circulatory control and is generally associated with a benign prognosis. Vasovagal syncope can be subdivided into three major categories: postural, central, and situational. In the postural form of vasovagal syncope, a common patient narrative might describe a young person attending a hot and crowded school assembly or concert, standing for a long period of time and having skipped a recent meal and ingested
some alcohol. In cases of centrally mediated vasovagal syncope, the trigger may involve sudden pain (commonly in the setting of venipuncture), apprehension of pain, or emotional shock immediately preceding the fainting episode. Less commonly, syncope occurs in specific situations or appears to be temporally related to specific triggers. Older men may report symptoms soon after arising from bed and emptying a distended bladder. Some young people describe recurrent syncope after exercise. Others describe syncope after coughing, laughing, or sneezing. It is not unusual for a history of vasovagal syncope to run in families. Surprisingly, despite the prevalence of this condition, the underlying pathophysiology of vasovagal syncope remains a mystery. Physiologists have yet to identify why an emotional state or coughing or prolonged standing can lead to a sudden decrease in blood pressure or why vasovagal syncope can recur frequently in some individuals, rarely in others.
TABLE 5.1 Clinical Features Distinguishing Syncope from Seizure
Before a Spell
Trigger (change in position, prolonged standing, emotion, Valsalva, exercise)
Sweating, light-headedness, graying of vision, and/or nausea
Occurring out of sleep
Aura (déjà vu olfactory hallucination, unilateral symptoms)
During a Spell
Common (generalized tonic-clonic seizures)
Duration of loss of consciousness
A few rhythmic jerking movements of the limbs, lasting <15 s
Prolonged stiffening of the limbs (tonic), transitioning to rhythmic jerking of the limbs (clonic), lasting ˜1-2 min
Automatic behavior (lip smacking, picking, patting)
Common (focal dyscognitive seizures)
Tongue biting (lateral)
After a Spell
Rare, <30 s
Common, several minutes or longer
Diffuse muscle pain
Common, hours to days
Creatinine kinase (CK) elevation
Common (especially after 12-24 h)
Focal neurologic signs
Amnesia for the event
Less common (sometimes seen in elderly)
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