Abstract
Obsessive-compulsive disorder (OCD) secondary to structural brain pathology is rarely described in pediatric populations. This single-case report describes a child with a pineal germinoma and obstructive hydrocephalus who developed prominent obsessive-compulsive symptoms, highlighting a potentially reversible neurobiological contributor to atypical pediatric OCD. The case illustrates the temporal association between symptom evolution, neurosurgical and oncologic management, and subsequent changes in obsessive-compulsive behaviors, contributing to understanding the role of cortico-striato-thalamo-cortical (CSTC) circuit disruption in secondary OCD. A 15-year-old boy initially presented with a 12-month history of mild generalized anxiety and intermittent insomnia, which progressed over the subsequent 8 months to severe obsessive thoughts and compulsive behaviors, including checking and repetition, significantly impairing sleep and food intake. Two months prior to tertiary referral, he developed progressive neurological symptoms, including afternoon headaches, blurred vision, gait instability with falls, polyuria, enuresis, and one witnessed episode of loss of consciousness. A neurological examination demonstrated Parinaud's syndrome, hyperreflexia with ankle clonus, extensor plantar responses, past-pointing, and papilledema. Neuroimaging (CT and MRI) revealed a pineal mass causing aqueductal obstruction with hydrocephalus, periventricular edema, and a suspected vestibular schwannoma. Endoscopic third ventriculostomy with biopsy and external ventricular drainage confirmed germinoma and relieved the cerebrospinal fluid (CSF) obstruction, with postoperative imaging demonstrating restored CSF flow. The patient subsequently received chemotherapy and focal radiotherapy. Following CSF diversion, the patient's caregivers reported a marked reduction in compulsive rituals and improved sleep, with further attenuation of OCD symptoms during oncologic treatment. Residual anxiety and mild obsessive-compulsive symptoms were managed with adjunctive selective serotonin reuptake inhibitor therapy. At the 12-month follow-up, standardized assessments indicated subclinical to mild OCD, and the patient had returned to full academic participation. This case underscores the importance of considering hydrocephalus-related CSTC circuit disruption as a potential, and occasionally reversible, contributor to pediatric OCD. Recognizing hydrocephalus-associated obsessive-compulsive symptoms may significantly influence both psychiatric and neurosurgical management. Clinicians evaluating atypical or treatment-refractory pediatric OCD should consider neuroimaging to identify underlying structural causes, emphasizing the value of interdisciplinary collaboration in optimizing outcomes.