Rathke Cleft Cysts (RCCs) are relatively uncommon fluid-filled sacs that develop near the pituitary gland, a small organ responsible for regulating many of the body’s hormones. These cysts are often discovered unexpectedly during imaging for unrelated conditions. Understanding how these cysts behave is important for individuals diagnosed with them, as their presence raises questions about potential growth and the risk of developing symptoms. This discussion focuses on the nature of these cysts, their potential for size change, and the resulting clinical consequences.
Defining Rathke Cleft Cysts
A Rathke Cleft Cyst originates from the embryological structure known as Rathke’s pouch, which is a key component in the development of the pituitary gland. During fetal development, this pouch normally regresses. If the remnants of this cleft persist and accumulate fluid, a Rathke Cleft Cyst forms, a process that is present from birth. The cyst is situated within the sella turcica, a bony cavity at the base of the skull that houses the pituitary gland. These lesions are classified as non-cancerous, or benign, and are filled with a mucus-like or gelatinous fluid. Because of their location, many small cysts remain entirely asymptomatic and are only found incidentally on magnetic resonance imaging (MRI). Their clinical significance is tied directly to their size and proximity to surrounding neural and endocrine structures.
Understanding Cyst Size Change
The most pressing question for many individuals is whether a Rathke Cleft Cyst will grow. For the majority of diagnosed cysts, the size remains stable or may even show signs of regression over time. However, a small minority of cysts will demonstrate significant growth, typically driven by the accumulation of fluid or, less commonly, a hemorrhage within the cyst cavity. Studies suggest that the median growth rate can be around 2.1 millimeters per year in patients under observation. A growth rate of 3 millimeters or greater annually is associated with a clinically significant increase in the risk of developing pituitary dysfunction. Factors like a younger age (under 35) and active smoking have been identified as potentially accelerating the rate of cyst enlargement. The mechanism of growth is not cell proliferation, but rather an increase in the internal fluid pressure that causes the cyst wall to expand.
When Growth Causes Symptoms
When a Rathke Cleft Cyst grows large enough, it begins to exert pressure on the surrounding confined structures, leading to recognizable symptoms. The most common consequence is the compression of the normal pituitary gland tissue, which can disrupt the production of hormones. This compression may result in various hormonal deficiencies, such as hypothyroidism, hypogonadism, or a reduction in cortisol production. Another frequent clinical issue arises from the cyst pressing upward on the optic chiasm, the point where the optic nerves cross. This compression often causes visual field defects, typically manifesting as a loss of peripheral vision. Symptoms like frequent headaches are also common, likely due to the pressure the enlarging mass places on the internal structures of the skull. In rare instances, rapid enlargement from internal bleeding can cause acute symptoms resembling pituitary apoplexy, a serious medical event.
Monitoring and Treatment Approaches
Clinical management of a Rathke Cleft Cyst depends almost entirely on whether it is causing symptoms. For cysts that are discovered incidentally and are not producing any clinical effects, the standard approach is one of observation, often referred to as watchful waiting. This typically involves regular follow-up MRI scans, perhaps annually for the first few years, to monitor the cyst’s size and stability. If the cyst grows or if the patient develops symptoms such as vision loss, severe headaches, or significant hormonal dysfunction, surgical intervention is generally recommended. The preferred surgical technique is the transsphenoidal approach, a minimally invasive procedure performed through the nasal cavity. The primary goal of this surgery is to drain the cyst fluid and remove a portion of the cyst wall to prevent fluid reaccumulation, rather than attempting a complete removal that might risk damaging the pituitary gland. Hormone replacement therapy may be necessary to correct any underlying endocrine deficiencies, even after successful surgical decompression.