Some psychological conditions (anxiety disorder, somatic symptom disorder, conversion disorder) may cause symptoms resembling syncope. A number of psychological interventions are available.Low blood sugar can be a rare cause of syncope.Narcolepsy may present with sudden loss of consciousness similar to syncope. Diagnostic approach
A medical history, physical examination, and electrocardiogram (ECG) are the most effective ways to determine the underlying cause of syncope. Guidelines from the American College of Emergency Physicians and American Heart Association recommend a syncope workup include a thorough medical history, physical exam with orthostatic vitals, and a 12-lead ECG. The ECG is useful to detect an abnormal heart rhythm, poor blood flow to the heart muscle and other electrical issues, such as long QT syndrome and Brugada syndrome. Heart related causes also often have little history of a prodrome. Low blood pressure and a fast heart rate after the event may indicate blood loss or dehydration, while low blood oxygen levels may be seen following the event in those with pulmonary embolism. Routine broad panel laboratory testing detects abnormalities in <2–3% of results and is therefore not recommended.Based on this initial workup many physicians will tailor testing and determine whether a person qualifies as high-risk, intermediate risk or low-risk based on risk stratification tools. More specific tests such as implantable loop recorders, tilt table testing or carotid sinus massage may be useful in uncertain cases. Computed tomography (CT) is generally not required unless specific concerns are present.
In normal physiologic female hormonal cycling, at 7 days past ovulation, high levels of estrogen and progesterone produced from the corpus luteum inhibit GnRH, FSH, and LH at the hypothalamus and anterior pituitary. If fertilization does not occur in the post-ovulation period the corpus luteum disintegrates due to a lack of human chorionic gonadotropin (hCG). This would normally be produced by the embryo in the effort of maintaining progesterone and estrogen levels during pregnancy. Therapeutically, clomifene is given early in the menstrual cycle. It is typically prescribed beginning on day 3 and continuing for 5 days. By that time, FSH levels are rising steadily, causing the development of a few follicles. Follicles, in turn, produce the estrogen, which circulates in serum. In the presence of clomifene, the body perceives a low level of estrogen, similar to day 22 in the previous cycle. Since estrogen can no longer effectively exert negative feedback on the hypothalamus, GnRH secretion becomes more rapidly pulsatile, which results in increased pituitary gonadotropin release. (More rapid, lower amplitude pulses of GnRH lead to increased LH and FSH secretion, while more irregular, larger amplitude pulses of GnRH leads to a decrease in the ratio of LH to FSH.) Increased FSH levels cause the growth of more ovarian follicles, and subsequently rupture of follicles resulting in ovulation. Ovulation occurs most often 6 to 7 days after a course of clomifene.