Tarlov cysts are fluid-filled sacs that commonly develop on the spinal nerve roots, most frequently in the sacrum, the triangular bone at the base of the spine. The fluid inside these cysts is cerebrospinal fluid (CSF). While many Tarlov cysts are small and never cause problems, the reasons why some form and expand to become symptomatic remain a topic of scientific debate. Understanding the development of these cysts requires separating the initial structural formation from the subsequent mechanisms of enlargement and symptom onset.
Primary Theories of Structural Formation
The existence of the cyst structure itself is explained by two primary theories: congenital and acquired.
The congenital theory posits that these cysts result from developmental irregularities present from birth. This view suggests defects in the arachnoid layer of the spinal cord’s protective coverings allow a pocket of CSF to form along the nerve root sheath. These cysts may represent arachnoidal proliferations or a ballooning of the dural sac, creating structural weaknesses that predispose the individual to cyst development.
The acquired theory argues that the cysts develop later due to various external or internal factors. Dr. Isadore Tarlov, who first described the cysts, proposed that trauma or hemorrhage could cause a blockage of venous drainage in the nerve root sheath. This blockage could lead to cystic degeneration and the formation of a fluid-filled sac. Other acquired causes include inflammation, infection, or a traumatic spinal injury that causes a CSF leak.
Current understanding suggests that the structural vulnerability may be congenital, but the actual expansion into a detectable cyst may be acquired. Connective tissue disorders, such as Marfan syndrome, are sometimes associated with Tarlov cysts, supporting the idea of a pre-existing structural weakness. Regardless of the origin, the structure must have an opening that allows CSF to enter the nerve root sheath.
The Role of Cerebrospinal Fluid Pressure
Once the structural sac exists, its enlargement and the resulting pressure on the nerve are driven by cerebrospinal fluid dynamics. The leading explanation for cyst growth involves a “ball-valve” or “one-way valve” mechanism at the connection point between the cyst and the subarachnoid space. This mechanism means that CSF is forced into the cyst during fluctuations in spinal fluid pressure but cannot easily exit.
CSF pressure naturally fluctuates with everyday activities like coughing, sneezing, straining, or changes in body position. These transient increases in pressure force CSF past the valve and into the cyst, causing gradual expansion. Since the valve restricts the fluid’s return, the pressure inside the cyst can become higher than the pressure in the surrounding spinal canal. This increased internal hydrostatic pressure compresses the nerve root fibers within the cyst, leading to pain and neurological symptoms.
The constant flow of CSF into the cyst, combined with the one-way valve effect, explains why symptoms often worsen with activities that increase abdominal or spinal pressure. This mechanism differentiates symptomatic, valved cysts from non-valved cysts, which communicate freely with the subarachnoid space and maintain equal pressure. Chronic pressure from an enlarging cyst can also lead to the erosion and remodeling of the surrounding sacral bone.
External Triggers and Symptom Onset
External events are often cited as a cause, but they are more accurately described as triggers that convert a pre-existing, asymptomatic cyst into a symptomatic one. These events do not create the initial structural defect but cause a sudden increase in CSF pressure, leading to rapid cyst expansion or inflammation. Physical trauma, such as a fall or car accident involving the tailbone area, is frequently linked to the sudden onset of symptoms.
Procedures like epidural injections or the physical stress of childbirth have also been documented as triggers. These events can dramatically increase the pressure within the spinal canal, forcing CSF into the cyst and causing immediate nerve compression. Trauma might also cause microscopic tears or inflammation that temporarily blocks the outflow of CSF, effectively creating or tightening the one-way valve.
The onset of pain is often correlated with the timing of a triggering event, even if the underlying cyst was present for years. This distinction highlights that treatment must address the mechanics of fluid pressure and nerve root compression, rather than focusing on the initial structural formation.