This is a portable ECG device that can record the wearers heart rhythms during daily activities over an extended period of time. Since fainting usually does not occur upon command, a Holter monitor can provide a better understanding of the hearts activity during fainting episodes. For people with more than two episodes of syncope and no diagnosis on "routine testing", an insertable cardiac monitor might be used. It lasts 28–36 months and is inserted just beneath the skin in the upper chest area. Imaging
Echocardiography and ischemia testing may be recommended for cases where initial evaluation and ECG testing is nondiagnostic. For people with uncomplicated syncope (without seizures and a normal neurological exam) computed tomography or MRI is not generally needed. Likewise, using carotid ultrasonography on the premise of identifying carotid artery disease as a cause of syncope also is not indicated. Although sometimes investigated as a cause of syncope, carotid artery problems are unlikely to cause that condition. Additionally an electroencephalogram (EEG) is generally not recommended. A bedside ultrasound may be performed to rule out abdominal aortic aneurysm in people with concerning history or presentation. Differential diagnosis
Other diseases which mimic syncope include seizure, low blood sugar, and certain types of stroke. While these may appear as "fainting", they do not fit the strict definition of syncope being a sudden reversible loss of consciousness due to decreased blood flow to the brain. Management
Management of syncope focuses on treating the underlying cause. This can be challenging as the underlying cause is unclear in half of all cases.
The mutations are inherited in an autosomal recessive pattern can be either homozygous or, less frequently, compound heterozygous loss-of-function. Affected males exhibit a broad spectrum of presentation including atypical genitalia (ranging from female appearing to undervirilized male), hypospadias, and isolated micropenis. The internal reproductive structures (vasa deferentia, seminal vesicles, epididymides and ejaculatory ducts) are normal but testes are usually undescended and prostate hypoplasia is common. Males with the same mutations in SRD5A2 can have different phenotypes suggesting additional factors that are involved in clinical presentation. Females with the same mutations in SRD5A2 as affected males (as seen in siblings) are unaffected and have normal female phenotypes and reproductive function.Virilization of genitalia with voice deepening, development of muscle mass occur at puberty in affected males and height is not impaired. Gynecomastia is uncommon and bone density is normal in contrast to 46,XY DSD from other causes such as partial androgen insensitivity syndrome and 17β-hydroxysteroid dehydrogenase 3 deficiency. Hair on the face and body is reduced and male pattern baldness does not occur. Mechanism
5α-Reductase type 2 (5αR2) is an enzyme, encoded by the SRD5A2 gene, that is expressed in specific tissues in the male body from fetal development to adulthood. The enzyme catalyzes the transformation of testosterone (T) to 5α-dihydrotestosterone (DHT) intracellularly. DHT is the most potent ligand to the androgen receptor (AR).