Regression of Pituitary Macroadenoma after Endovascular Embolization of Thoracic CSF-Venous Fistula for Symptomatic Intracranial Hypotension

Pituitary hyperemia and gland enlargement can be cardinal features of intracranial hypotension secondary to cavernous sinus and epidural venous plexus distention. This phenomenon can therefore complicate radiographic interpretation of sellar lesions when both diagnoses co-exist. We report a unique case of a rapidly enlarging pituitary macroadenoma in the setting of a thoracic CSF-venous fistula causing symptomatic intracranial hypotension.

A 53-year-old female with no previous neurosurgical history nor prior trauma presented with complaints of daily retro-orbital headache radiating to the occiput and cervical spine. Her symptoms were exacerbated by position change and valsalva maneuver. MRI brain revealed a heterogeneously enhancing solid and cystic sellar lesion measuring 1.4 × 1.1 × 1.1 cm with extension into the left cavernous sinus (Knosp Grade 2) and displacement of the left optic chiasm ([Fig. 1A]). MRI also revealed diffuse pachymeningeal enhancement and bilateral holohemispheric subdural hematomas ([Fig. 1B]) concerning for intracranial hypotension. A complete endocrinologic and ophthalmologic workup returned normal, and her suspected non-functioning pituitary macroadenoma was monitored with surveillance imaging while she underwent conservative management for spontaneous intracranial hypotension.

Fig. 1 Pituitary macroadenoma and intracranial hypotension.

Serial MRIs obtained at 4 and 7 months showed unusually rapid growth (1.6 × 1.5 × 1.2 cm to 1.7 × 1.6 × 1.2 cm) of her macroadenoma for which surgical intervention was considered. Given persistent radiographic features of intracranial hypotension ([Fig. 2]), however, she first underwent CT-guided lumbar puncture for dynamic myelogram in the decubitus positions. Imaging was consistent with a CSF-venous fistula in the inferior and posterior right T6–7 neural foramen. She underwent endovascular obliteration of the right epidural venous plexus at T6–7 via selective micro-catheterization of the right T6–7 intervertebral vein ([Fig. 3]).

Fig. 2 Sellar lesion expands rapidly in short interval.

Fig. 3 Endovascular obliteration of right T6–T7 foraminal CSF venous fistula.

Repeat MRI obtained 4 weeks postprocedurally showed near complete resolution of pachymeningeal enhancement, diencephalon sag, and foramen magnum crowding with concurrent improvement in clinical symptoms. Importantly, imaging also showed an interval decrease in the size of the patient’s pituitary macroadenoma from 1.7 × 1.6 × 1.2 cm to 1.4 × 1.3 × 1.0 cm with no further mass effect on the optic apparatus ([Fig. 4]). This lesion remained stable in size on follow-up MRI obtained 4 months after treatment with durable symptom relief.

Fig. 4 CSF–venous fistula embolization reverses intracranial hypotension and induces tumor regression.

Pituitary enlargement has been reported as a feature of intracranial hypotension and has even been misdiagnosed as tumor in this context. This report summarizes the joint presentation of a macroadenoma and intracranial hypotension that nearly prompted surgical intervention given progressive tumor enlargement in relatively short time. Endovascular treatment of a thoracic CSF-venous fistula induced durable radiographic tumor regression, suggesting that pressure disequilibrium can potentiate intratumoral venous congestion and complicate pituitary tumor management in this setting.

Publication History

Article published online:
07 February 2025