Empty sella syndrome

What is Empty sella syndrome?
Statistics on Empty sella syndrome
Risk Factors for Empty sella syndrome
Progression of Empty sella syndrome
How is Empty sella syndrome Diagnosed?
Prognosis of Empty sella syndrome
How is Empty sella syndrome Treated?
Empty sella syndrome References
Drugs/Products Associated with Empty sella syndrome

What is Empty sella syndrome?

Empty sella syndrome is the absence of the pituitary gland on radiological imaging of the sella turcica. The pituitary gland is partly surrounded by a bony structure called the sella turcica ("Turkish saddle"). When the pituitary gland is not visible on CT or MRI scans of the sella turcica, the condition is referred to as empty sella syndrome. 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 walls of the sella. When the sella is empty because the pituitary gland has regressed following an injury such as head trauma or an event such as surgery or radiation therapy, the condition is called secondary empty sella syndrome.

Statistics on Empty sella syndrome

One study observed empty sella in 48% of children with GH deficiency or multiple pituitary hormone deficiencies compared to only 2% of children with normal pituitary function.

Risk Factors for Empty sella syndrome

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 walls of the sella.

When the sella is empty because the pituitary gland has regressed following an injury such as head trauma or an event such as surgery or radiation therapy, the condition is called secondary empty sella syndrome.

Progression of Empty sella syndrome

Primary empty sella syndrome is most often an incidental finding during radiological imaging of the brain. Pituitary function is usually normal, and patients do not have any symptoms. The hormone prolactin is mildly elevated in 10% to 15 % of patients, and the elevated prolactin may interfere with normal function of the testes or ovaries.Patients with an empty sella syndrome due to destruction of the pituitary gland have signs and symptoms caused by partial or complete loss of pituitary gland functions. The causes and symptoms of pituitary insufficiency are reviewed in the article on hypopituitarism.Empty sella syndrome is often associated with abnormal pituitary function in children. Isolated deficiency of growth hormone (GH) is most common, but other pituitary hormones may also be deficient. Classically the affected patients in in primary empty sella syndrome are obese women with a history of multiple pregnancies.

How is Empty sella syndrome Diagnosed?

Tests of pituitary gland function may be performed to make sure that the gland is working normally. This testing is reviewed in the article on hypopituitarism.

Prognosis of Empty sella syndrome

Primary empty sella syndrome does not have adverse health consequences, and it does not alter life expectancy.The specific cause of pituitary gland injury and the effects of hypopituitarism contribute to the outcome with secondary empty sella syndrome.

How is Empty sella syndrome Treated?

Primary empty sella syndrome:

No specific treatment if pituitary function is normal

Medication to lower prolactin levels if the prolactin level is high and interfering with function of the gonads. Secondary empty sella syndrome:

Therapy is directed at replacing hormones that are deficient as a result of abnormal pituitary gland function. See the article on hypopituitarism for a complete review.

Medications such as bromocriptine that suppress prolactin production are effective in correcting the problem.

Empty sella syndrome References

[1] Empty sella syndrome as retrieved from www.nlm.nih.gov on 29/12/2003[2] Kumar, P. Clark, M. Clinical Medicine 5th Ed. W.B. Saunders 2002[3] Robbins, S.L., Cotran, R.S., Kumar, V. Robbins Pathologic Basis of Disease 5th ed. W.B. Saunders 1995.[4] Robbins, S.L., Cotran, R.S., Kumar, V. Robbins Pathologic Basis of Disease 6th ed. W.B. Saunders 1999.