Idiopathic Intracranial Hypertension (IIH) in a Patient on Tirzepatide: Cure or Culprit? A Case Report

Malagi AD, Modi K, Sonwane AC, Sethi BK and Modi KD

Published on: 2026-06-27

Abstract

Idiopathic intracranial hypertension (IIH) is a syndrome of elevated intracranial pressure commonly associated with obese females of reproductive age group. Incidence of IIH is approximately 0.9 in 100.00 and 3.5/100.00 in females of 15 to 44 years of age. Diagnosis is usually done by the modified Dandy criteria which includes signs and symptoms of raised ICP with absence of localizing findings on neurological examination, no evidence of deformity or obstruction of ventricular system and increased CSF pressure (> 250mm in adults and >280 mm in children), with neuroimaging signs of increased ICP and no other apparent secondary causes of intracranial hypertension present. The role of incretin based therapy in the management of IIH is emerging. We report a case of IIH observed during tirzepatide therapy raising discussion about its role in IIH.

Keywords

Idiopathic Intracranial Hypertension (IIH); Tirzepatide therapy; Type 2 Diabetes Mellitus

Introduction

Idiopathic intracranial hypertension (IIH) is a syndrome of elevated intracranial pressure commonly associated with obese females of reproductive age group. Incidence of IIH is approximately 0.9 in 100,00 and 3.5/100,00 in females of 15 to 44 years of age [1]. Diagnosis is usually done by the modified Dandy criteria which includes signs and symptoms of raised ICP with absence of localizing findings on neurological examination, no evidence of deformity or obstruction of ventricular system and increased CSF pressure (> 250mm in adults and >280 mm in children), with neuroimaging signs of increased ICP and no other apparent secondary causes of intracranial hypertension present [2]. The role of incretin based therapy in the management of IIH is emerging. We report a case of IIH observed during tirzepatide therapy raising discussion about its role in IIH.

Case Report

A 33-year-old female, with history of hypertension and type 2 Diabetes Mellitus for 3 years presented to us for obesity management. She was already on semaglutide 0.5 mg weekly for 2 months along with Metformin (1000mg/d), Empagliflozin (25mg/d), Olmesartan (20mg/d) and Amlodipine (5mg/d). Her baseline body mass index (BMI) was 46kg/m2 with normal blood pressure (130/90 mmHg) and adequate glycemic control (HbA1c 6.6%). She lost about 2 kgs in the 2 months and was switched to 5 mg weekly tirzepatide for better weight management and dose was escalated from 5 mg to 10 mg in 3 months. She achieved a total weight loss of 7.9 kgs in 5 months. For a 3 day history of headache and vomiting, she was evaluated where fundoscopy showed evidence of bilateral papilledema with normal IOP. The visual field chart showed right-eye hemianopia and left-eye inferior quadrantanopia. MRI brain was normal except for globe flattening in both eyes. CSF opening pressure was elevated (26 cm of H2O), with normal biochemistry and cytology. Diagnosis of IIH was made and for the time being tirzepatide was discontinued and acetazolamide 250 mg twice a day was initiated and later on increased to 500 mg thrice a day. Her older fundus photography taken 1 year back as a diabetes work up also showed early papilledema in left eye while right eye fundus was normal. This was missed due to early stage. Subsequently, ophthalmology follow-up revealed pressure and papilledema in an improving trajectory and patient was advised to continue acetazolamide for 10 more days.

Figure 1: Sequential images of fundus showing blurring of disc margins (early changes, prior to tirzepatide therapy), grade 4 papilledema (while on tirzepatide for 6 months), and resolving papilledema (on Acetazolamide/Off tirzepatide for 4 months.

Discussion

According to current clinical data GLP-1 and dual GIP/GLP-1 RAs are being studied as potential therapeutic agents in IIH by demonstrating significant efficacy in reducing ICP related symptoms like headache frequency, papilledema and visual disturbances [3]. It has been shown that GLP-1 receptors in the choroid plexus alter Na/K-ATPase activity directly influencing CSF production and they also act by reducing intracranial venous pressure through sustained weight loss [4]. In our case, obesity is more likely the culprit for IIH as fundus scan 8 months before starting tirzepatide also shows early papilledema which was somehow missed due to early changes. Decision to restart tirzepatide is a topic of discussion. The purpose of reporting this case is the settings of obesity and tirzepatide therapy where progressive IIH was observed.

Conclusion

IIH occurring during tirzepatide therapy is likely coincidental in patients with obesity. This case highlights the importance of getting a baseline fundus examination before starting GLP-1 or dual GIP/GLP-1 RAs agonist. Further data is needed to prove any therapeutic or causal relation.

International Journal of Endocrinology and Diabetes