Additionally there is:

CT scan 
MRI scans

Classification
There are two types of empty sella syndrome: primary and secondary. Primary empty sella syndrome occurs when a small anatomical defect above the pituitary gland increases pressure in the sella turcica and causes the gland to flatten out along the interior walls of the sella turcica cavity. Primary empty sella syndrome is associated with obesity and increase in intracranial pressure in women. In most cases, especially in people with primary empty sella syndrome, there are no symptoms and it does not affect life expectancy or health. Some researchers have estimated that less than 1% of affected people ever develop symptoms of the condition. Secondary empty sella syndrome is the result of the pituitary gland regressing within the cavity after an injury, surgery, or radiation therapy. Individuals with secondary empty sella syndrome due to destruction of the pituitary gland have symptoms that reflect the loss of pituitary functions, such as intolerance to stress and infection. Differential diagnosis
The major differential to consider in empty sella syndrome is intracranial hypertension, of both unknown and secondary causes, and an epidermoid cyst, which can mimic cerebrospinal fluid due to its low density on CT scans, although MRI can usually distinguish the latter diagnosis. Treatment
In terms of management, unless the syndrome results in other medical problems, treatment for endocrine dysfunction associated with pituitary malfunction is symptomatic and thus supportive; however, surgery may be needed in some cases. References
Further reading
Disorders, National Organization for Rare (2003). NORD Guide to Rare Disorders. Lippincott Williams & Wilkins. ISBN 9780781730631.
Either free in the cytoplasm or inside a parasitophorous vacuole, microsporidia develop by sporogony to mature spores. During sporogony, a thick wall is formed around the spore, which provides resistance to adverse environmental conditions. When the spores increase in number and completely fill the host cell cytoplasm, the cell membrane is disrupted and releases the spores to the surroundings. These free mature spores can infect new cells thus continuing the cycle. Diagnosis
The best option for diagnosis is using PCR.Diagnosis with Microsporidia can be done through gram-positive, acid-fast spores in stool and biopsy material with morphologic demonstration of the organism. Initial detection through light microscopic examination of tissue sections, stools, duodenal aspirates, nasal discharges, bronchoalveolar lavage fluids, and conjunctival smears. Definitive diagnosis can also be achieved through fluorescein-tagged antibody immunofluorescence or electron microscopy, and species identification can be done through PCR. Classification
Although it is classified as a protozoal disease in ICD-10, their phylogenetic placement has been resolved to be within the Fungi, and some sources classify microsporidiosis as a mycosis, however, they are highly divergent and rapidly evolving. Treatment
Fumagillin has been used in the treatment. Another agent used is albendazole.Because of its severe mortality risk in immunocompromised individuals, two main agents are used: Albendazole, which inhibits tubulin, and Fumagillin, which inhibits methionine aminopeptidase type two. References
External links
CDCs microsporidiosis info page.