Rapidly reversible hyperprolactinemia in slit ventricle syndrome: a neuroendocrine correlate of intracranial hypertension. A case report and literature review

Abstract Background Slit Ventricle Syndrome (SVS) is characterized by symptoms of increased intracranial pressure, despite the ventricular system appearing radiologically small, thus posing a diagnostic challenge. The correlation between elevated intracranial pressure (ICP) and biochemical markers is not well established. Although increased serum prolactin has been associated with pituitary stalk dysfunction, its relationship with ICP dynamics remains unclear. Aim of the work The objective of this study is to present a rare case of SVS associated with significantly elevated and rapidly reversible hyperprolactinemia. Additionally, this work reviews the literature to explore the potential relationship between elevated serum prolactin levels and increased intracranial pressure (ICP). This investigation raises the question of whether elevated prolactin levels could serve as an adjunctive diagnostic marker for elevated ICP in specific clinical contexts. Case presentation A 13-year-old female with a history of ventriculoperitoneal shunt insertion at one year of age presented with a two-month history of progressive headaches, predominantly nocturnal, accompanied by nausea, vomiting, and diplopia. Neurological examination revealed left abducens nerve palsy. A CT scan of the brain demonstrated slit-like ventricles with the proximal shunt tube appropriately positioned inside the lateral ventricle. Fundus examination showed no papilledema. Serum prolactin was markedly elevated at 859.1 ng/mL. No obvious sellar or suprasellar mass lesion was identified on MRI brain and other causes of hyperprolactinemia were ruled out. Lumbar puncture confirmed elevated intracranial pressure with an opening pressure of 34 cm H₂O. The patient underwent navigation-guided proximal shunt revision, resulting in rapid clinical improvement. Serum prolactin levels declined to 74 ng/mL on the second postoperative day. At a three-month follow-up, the patient was neurologically intact, the ventriculoperitoneal shunt was functioning well, and the prolactin level had returned to normal at 20 ng/mL. Conclusion This case reveals a notable and reversible hyperprolactinemia linked to intracranial hypertension in SVS. The temporal association between normalization of intracranial pressure (ICP) and a decline in prolactin levels suggests a possible dynamic, pressure-mediated disruption of hypothalamic dopaminergic inhibition. Serum prolactin could serve as an adjunctive biochemical indicator of intracranial pressure in specific cases; however, its clinical utility requires further definition and validation through prospective studies.