This case report explores a rare occurrence of Idiopathic Intracranial Hypertension (IIH) in conjunction with COVID-19 infection, a scenario that has received minimal attention in the literature to date. A 49-year-old female with no significant medical history presented with rapidly progressing bilateral vision loss and was found to have grade 3 bilateral optic disc edema alongside a positive COVID-19 diagnosis. Despite the absence of traditional risk factors for IIH, such as obesity or a prior history of similar symptoms, the patient's clinical presentation suggested a possible link between her IIH and COVID-19 infection. Diagnostic workup included normal cerebrospinal fluid analysis and MRI findings, except for an empty sella turcica. The patient underwent successful bilateral endoscopic optic nerve decompression surgery following medical management that included mannitol, dexamethasone, low molecular weight heparin, acetazolamide, vitamin D3 supplementation, ivermectin, and oxygen therapy. Significant symptomatic improvement was observed postoperatively. This case highlights the necessity for heightened awareness among clinicians regarding the potential for COVID-19 to precipitate or exacerbate IIH, underlining the importance of considering IIH in the differential diagnosis of COVID-19 patients presenting with neurological symptoms to prevent irreversible outcomes. Further research is encouraged to investigate the relationship between COVID-19 and IIH, which could offer new insights into their management and preventative strategies.
Idiopathic Intracranial Hypertension (IIH) emerges as a perplexing clinical entity characterized by elevated intracranial pressure without an identifiable cause, presenting a myriad of symptoms including headache, vision loss, and pulsatile tinnitus. The cornerstone of its diagnosis rests on neuro-imaging to exclude mass lesions and lumbar puncture findings that reveal a normal cerebrospinal fluid (CSF) composition. Notably, IIH demonstrates a significant association with obesity and predominantly impacts women in their reproductive years. A hallmark of IIH, papilledema, accentuates the severity of the condition by revealing optic disc edema, a consequence of optic nerve compression and obstructed axoplasmic flow.1-4
In the context of the global COVID-19 pandemic, the intersection between IIH and COVID-19 infection remains scarcely reported, marking an area ripe for exploration. This case report unfolds a rare instance of IIH concomitant with COVID-19 infection, endeavoring to illuminate the potential for the virus to act as an aggravating factor in the pathophysiology of IIH. Through this detailed account, we aim to enhance the medical community's understanding of the interplay between COVID-19 and IIH, potentially guiding more nuanced approaches to diagnosis and management in these challenging clinical scenarios.
On September 25, 2021, a 49-year-old female was urgently admitted to the emergency department, presenting with a concerning clinical picture that had evolved over two years but had notably worsened in the preceding week. Initially, the patient reported experiencing intermittent headaches of increasing severity. However, a more alarming symptom emerged over the last week: a precipitous decline in visual acuity, progressing to complete bilateral vision loss by the day prior to her hospital admission. Upon clinical evaluation, the patient demonstrated hand movement close to face (HMCF) visual acuity in both eyes, indicative of severe visual impairment. Further ophthalmological assessment revealed grade 3 bilateral optic disc edema, a critical finding that underscored the urgency of her condition, while no additional neurological deficits were noted. Complicating her clinical scenario was the confirmation of COVID-19 infection, diagnosed via a rapid antigen test upon admission. This case thereby presents a complex interplay between sudden visual loss, idiopathic intracranial hypertension, and concurrent COVID-19 infection, highlighting a unique and challenging clinical presentation.
The investigative journey commenced with a cerebrospinal fluid (CSF) analysis, which unveiled normal levels of protein and glucose, effectively excluding infectious etiologies. An MRI scan of the brain brought to light an empty sella turcica, a finding devoid of other intracranial anomalies. Notably, a modest elevation in D-dimer levels was observed, suggesting a slight pro-thrombotic predisposition, an aspect warranting careful consideration given the patient's clinical context.
Upon confirmation of her COVID-19 status, the patient was admitted to the specialized COVID ward, where a multidimensional therapeutic strategy was initiated. This regimen included mannitol for osmotic diuresis, dexamethasone as an anti-inflammatory agent, low molecular weight heparin for anticoagulation, acetazolamide to reduce cerebrospinal fluid production, vitamin D3 supplementation, and ivermectin, along with supplementary oxygen therapy to manage COVID-19 symptoms.
Faced with the acute threat of irreversible vision loss due to severe papilledema, the medical team opted for bilateral endoscopic optic nerve decompression surgery, performed in the department of otorhinolaryngology. This procedure aimed to alleviate the pressure on the optic nerves in an effort to preserve the patient's remaining visual function.
In the postoperative phase, the patient was administered high-dose prednisolone, with a careful, gradual reduction in dosage over the following week. This postoperative management was meticulously planned to mitigate inflammation and support recovery, marking a crucial phase in the patient's treatment trajectory.
This comprehensive and tailored approach underscores the intricate challenges and considerations in managing a case of Idiopathic Intracranial Hypertension in the setting of concurrent COVID-19, highlighting the importance of a multidisciplinary strategy to safeguard and optimize patient outcomes.
The intricate pathogenesis of Idiopathic Intracranial Hypertension (IIH) amidst the backdrop of a COVID-19 infection presents a complex puzzle, with the interplay between the two conditions offering a fertile ground for speculation and research. The potential mechanisms underpinning the emergence of IIH in this context are multifaceted, with an exacerbated inflammatory response and the possibility of cerebral venous sinus thrombosis (CVST) being prime suspects. However, it is critical to note that CVST was not detected in our patient, steering the focus towards other inflammatory or thrombotic pathways potentially exacerbated by COVID-19.5-7
Remarkably, our patient did not exhibit the conventional risk factors typically associated with IIH, such as obesity or a prior history of similar symptoms. This deviation from the norm suggests that the COVID-19 virus itself may play a pivotal role as a precipitating factor in the development of IIH. This hypothesis aligns with the broader understanding of COVID-19's systemic effects, particularly its capacity to instigate an inflammatory cascade and disrupt coagulation pathways, which could, in theory, contribute to the elevated intracranial pressure characteristic of IIH.8-10
The therapeutic intervention, specifically the decision to proceed with bilateral endoscopic optic nerve decompression surgery, was primarily motivated by the urgent need to address the acute risk of permanent vision loss. This decision underscores the critical nature of timely and decisive action in cases where IIH poses a direct threat to essential functions such as sight. The significant symptomatic improvement observed postoperatively in our patient serves as a testament to the efficacy of this surgical approach, particularly in the context of severe papilledema and impending visual compromise.11-13
This case highlights the complex interplay between COVID-19 and IIH, shedding light on the potential for COVID-19 to act as a catalyst in the development of IIH in individuals without traditional risk factors. It underscores the importance of considering a broad differential diagnosis in COVID-19 patients presenting with neurological symptoms, particularly when such symptoms deviate from the expected clinical course. Further research into the mechanisms linking COVID-19 and IIH is imperative, as it could unlock new avenues for understanding, preventing, and managing these challenging clinical scenarios.
This case underscores the critical potential for COVID-19 to act as a precipitant or exacerbator of Idiopathic Intracranial Hypertension (IIH), emphasizing the need for increased vigilance among clinicians when encountering COVID-19 patients with neurological manifestations. The interplay between COVID-19-induced coagulopathy and hyperviscosity could compromise cerebrospinal fluid absorption, highlighting the necessity of incorporating IIH into the differential diagnosis to avert permanent vision loss. This case serves as a call to action for the medical research community to delve deeper into the dynamics between COVID-19 and IIH, with the aim of uncovering novel insights that could inform both management and prevention strategies, ultimately enhancing patient care in these complex scenarios.

Fig-1: Grade I Papilledema Fig-2: Grade III Papilledema
Wall, Mark. "Idiopathic Intracranial Hypertension." Neurologic Clinics, vol. 28, no. 3, Aug. 2010, pp. 593-617. DOI: 10.1016/j.ncl.2010.03.001.
Wang, Michael T. M., et al. "Idiopathic Intracranial Hypertension: Pathophysiology, Diagnosis and Management." Journal of Clinical Neuroscience, vol. 95, Jan. 2022, pp. 172-179. DOI: 10.1016/j.jocn.2021.12.032.
Ziemska-Gorczyca, Marta, et al. "Otoneurological Symptoms in Idiopathic Intracranial Hypertension." Polish Otorhinolaryngology Review, vol. 12, no. 1, 2023, pp. 35-41. DOI: 10.5114/por.2023.117783.
Mollan, Stephen P., et al. "Current Perspectives on Idiopathic Intracranial Hypertension without Papilloedema." Life, vol. 11, no. 6, 2021, p. 472. DOI: 10.3390/life11060472.
Sriuoginys, Saulius, et al. "De Novo Presentation of Idiopathic Intracranial Hypertension (IIH) Associated With COVID-19 Infection." Neurohospitalist, vol. 12, no. 4, Oct. 2022, pp. 691-692. DOI: 10.1177/19418744221135012.
Khalid, Muhammad F., and Julia A. Micieli. "Idiopathic Intracranial Hypertension Associated with SARS-CoV-2 B.1.1.7 Variant of Concern." Canadian Journal of Neurological Sciences, vol. 49, no. 3, May 2022, pp. 472-473. DOI: 10.1017/cjn.2022.71.
Eide, Per Ketil, and Hans-Anton Hansson. "A New Perspective on the Pathophysiology of Idiopathic Intracranial Hypertension: Role of the Glia-Neuro-Vascular Interface." Frontiers in Molecular Neuroscience, vol. 15, 2022, p. 900057. DOI: 10.3389/fnmol.2022.900057.
Chen, Jun, and Mark Wall. "Epidemiology and Risk Factors for Idiopathic Intracranial Hypertension." International Ophthalmology Clinics, vol. 54, no. 1, Winter 2014, pp. 1-11. DOI: 10.1097/IIO.0000000000000006.
Khalid, Muhammad F., and Julia A. Micieli. "Idiopathic Intracranial Hypertension Associated with SARS-CoV-2 B.1.1.7 Variant of Concern." Canadian Journal of Neurological Sciences, vol. 49, no. 3, May 2022, pp. 472-473. DOI: 10.1017/cjn.2022.71. [Note: This citation is a repeat from item 6]
Adnyana, I. M. O., and C. T. L. Indah. "Idiopathic Intracranial Hypertension: From Concise History to Current Management." Egyptian Journal of Neurology, Psychiatry and Neurosurgery, vol. 59, 2023, p. 128. DOI: 10.1186/s41983-023-00499-2.
Göksu, Ekin, et al. "Endoscopic Bilateral Optic Nerve Decompression for Treatment of Idiopathic Intracranial Hypertension." Brain Sciences, vol. 11, no. 3, Mar. 2021, p. 324. DOI: 10.3390/brainsci11030324.
Thakur, Sunil, et al. "COVID-19 Associated Idiopathic Intracranial Hypertension and Acute Vision Loss." Indian Journal of Otolaryngology and Head & Neck Surgery, vol. 75, no. 2, Jun. 2023, pp. 1031-1034. DOI: 10.1007/s12070-022-03155-w.
Khalid, Muhammad F., and Julia A. Micieli. "Idiopathic Intracranial Hypertension Associated with SARS-CoV-2 B.1.1.7 Variant of Concern." Canadian Journal of Neurological Sciences, vol. 49, no. 3, May 2022, pp. 472-473. DOI: 10.1017/cjn.2022.71.