Syncope And Related Paroxysmal Spells

Paroxysmal spells are non-epileptic, paroxysmal events that may mimic epileptic seizures but are not associated with rhythmic discharges of cortical neurons typical of seizures. They clinically manifest as a transient loss of consciousness, often occurring suddenly, with or without a prodrome. Paroxysmal spells can be caused by psychological disorders such as substance abuse and psychiatric disease or physiological events such as hypoglycemia, traumatic brain injury, and syncope. Psychological Conditions Data suggest that men with psychiatric disease have an increased incidence of syncope or paroxysmal events of unknown etiology. This data should lead clinicians to consider screening for psychiatric disorders in patients with transient loss of consciousness they cannot identify with a clear etiology. Among patients with a history of substance use disorder, 45% have been found to have unexplained syncope. This suggests that prior and current substance use is also associated with increased incidence of transient loss of consciousness of unknown etiology. Patients evaluated in the emergency department or even hospitalized with syncope of unknown etiology may benefit from toxicology screening and possible detoxification referral. Hypoglycemia Hypoglycemia is defined as low blood sugar with associated symptoms. In patients without diabetes mellitus, this is usually manifested at glucose levels below 50 mg/dl. To diagnose hypoglycemia, symptoms and blood sugar must improve with exogenous glucose. Hypoglycemia can affect the central nervous system, leading to lightheadedness, nausea, flashes of light, focal neurological deficits, transient loss of consciousness, and seizure. It is, therefore, paramount that patients with any paroxysmal spell or syncope receive a fingerstick glucose. Traumatic Brain Injury Traumatic brain injury is an intracranial impairment, often due to external forces. These forces may include blunt or penetrating trauma to the head, causing acceleration/deceleration injury to the cerebral cortex. Intracerebral bleeding, lacerations, and diffuse axonal injuries may result. Injuries, such as an epidural hematoma, may cause a brief state of loss of consciousness, with rapid return of, usually, altered consciousness. Other injuries, such as large subdural hematoma or diffuse axonal injury may cause worsening mentation and coma over hours to days. This is a result of increased intracranial pressure, leading to decreased cerebral perfusion pressure, and finally, neuronal ischemia. Diagnosis is by clinical history and CT imaging, although MRI may be more specific for secondary trauma. Management is to reduce intracranial pressure and edema. Syncope As most paroxysmal events are syncopal, the remainder of this discussion will focus primarily on syncope. Physiologically, syncope is a transient loss of consciousness as a result of cerebral hypoperfusion. As such, syncope varies from other etiologies of loss of consciousness in that it does not include head trauma or a post-ictal state. Syncope instead results in complete and rapid resolution of mental status. It may have myoclonic jerking, but no generalized tonic-clonic movement. Rather than a disease, syncope is a symptom of an underlying pathology ranging from benign to life-threatening. Patients are often divided into "low-risk" and "high-risk" groups. The etiology, epidemiology, evaluation, treatment, and management of these patients vary greatly. In the United States, hospitalization costs for syncope are estimated to be $5300 per admission and more than $2 billion annually. These costs are higher than those of chronic obstructive pulmonary disease and asthma combined. As extensive workups can be costly, time-consuming, and often unnecessary, a growing cadre of management tools has been devised to evaluate patients with syncope. These tools are tailored to determining the etiology of the syncopal event and treating dangerous, high-risk, syncope patients.