Cerebellar tonsillar ectopia shares many of the same symptoms as CSF leak, but originates either congenitally or from trauma, including whiplash strain to the dura.An alternate method of locating the site of a CSF leak is to use heavily T2-weighted MR myelography. This has been effective in identifying the sites of a CSF leak without the need for a CT scan, lumbar puncture, and contrast and at locating fluid collections such as CSF pooling. Another highly successful method of locating a CSF leak is intrathecal contrast and MR Myelography.Contrast-enhanced brain MRI with sagittal reformats can assess for the following:
Subdural fluid collections
Enhancement of the meninges
Engorgement of venous structures
Pituitary swelling
Sagging of the brainFor suspected spinal CSF leaks, spine imaging can be used to guide treatment. Assay
Fluid dripping from the nose (CSF rhinorrhoea) or ears (CSF otorrhea) should be collected and tested for the protein Beta-2 transferrin which would be highly accurate in identifying CS fluid and diagnosing a cranial CSF leak. CSF analysis
Patients with CSF leaks have been noted to have very low or even negative opening pressures during lumbar puncture. However, patients with confirmed CSF leaks may also demonstrate completely normal opening pressures. In 18–46% of cases, the CSF pressure is measured within the normal range. Analysis of spinal fluid may demonstrate  lymphocytic pleocytosis and elevated protein content or xanthochromia. This is hypothesized to be due to increased permeability of dilated meningeal blood vessels and a decrease of CSF flow in the lumbar subarachnoid space.
Metabolism
Prasterone is also reversibly transformed into its active metabolite prasterone sulfate (DHEA-S) by steroid sulfotransferase (specifically SULT1E1 and SULT2A1), which in turn can be converted back into prasterone by steroid sulfatase. Interconversion takes place in both adrenal and peripheral tissues.It is transformed into androstenedione by 3β-hydroxysteroid dehydrogenase (3β-HSD), and into androstenediol by 17β-hydroxysteroid dehydrogenase (17β-HSD). Then, androstenedione and androstenediol can be converted into testosterone by 17β-HSD and 3β-HSD, respectively. Subsequently, testosterone can be metabolized into dihydrotestosterone by 5α-reductase.In addition, androstenedione and testosterone can be converted into estrone and estradiol by aromatase, respectively. Dose-response of hormone levels
At a high dosage of 1,600 mg/day orally for 4 weeks, treatment of postmenopausal women with prasterone has been found to increase serum levels of DHEA by 15-fold, testosterone by 9-fold, DHEA-S, androstenedione, and DHT all by 20-fold, and estrone and estradiol both by 2-fold.Although prasterone can reliably increase testosterone levels in women, this isnt similarly the case in men. A high dosage of 1,600 mg/day prasterone in men for 4 weeks was found to increase DHEA and androstenedione levels but did not significantly affect testosterone levels. Dosing
In clinical studies of prasterone supplementation, dosages have ranged from 20 to 1,600 mg per day.In people with adrenal insufficiency, oral dosages of 20 to 50 mg/day prasterone have been found to restore DHEA and DHEA-S levels to physiological levels seen in young healthy adults.