A systematic history must now distinguish primary from secondary headache and identify modifiable risk factors. IIH (idiopathic intracranial hypertension) classically affects young women with elevated BMI. Key historical features include: absence of prior migraine, medications that can raise ICP (oral contraceptives, vitamin A, tetracyclines, corticosteroids), and absence of systemic symptoms suggesting infection or malignancy. Document analgesic use to screen for medication overuse headache, though objective signs (papilloedema) cannot be explained by this alone.

The examination must focus on detecting papilloedema (the hallmark sign of raised ICP) and excluding focal neurological deficits that would suggest a mass lesion. Fundoscopy is mandatory in any patient with progressive headache and visual symptoms. Test visual acuity, visual fields (confrontation), and cranial nerves II–VI. Cranial nerve VI palsy is a false-localising sign of raised ICP. Assess for meningism (neck stiffness) to exclude CNS infection. The absence of focal deficits supports IIH over a structural lesion.

Bilateral papilloedema mandates urgent investigation to confirm raised ICP and exclude secondary causes. Neuroimaging (MRI brain preferred) must be performed before lumbar puncture to exclude mass lesion, hydrocephalus, and cerebral venous sinus thrombosis – all of which contraindicate LP or alter management. Once imaging is normal, lumbar puncture with opening pressure measurement is diagnostic: opening pressure >25 cm H₂O with normal CSF constituents confirms IIH. Bloods (FBC, U&E, TFT) exclude anaemia, electrolyte disturbance, and thyroid disease.

The differential for headache with papilloedema includes: (1) Idiopathic intracranial hypertension (IIH) – young woman, elevated BMI, normal imaging, elevated LP opening pressure with normal CSF; (2) Cerebral venous sinus thrombosis – excluded by MR venography; (3) Intracranial mass – excluded by normal MRI; (4) CNS infection (meningitis/encephalitis) – excluded by normal CSF and absence of fever/meningism. Migraine and tension-type headache do not cause papilloedema and are excluded by objective findings. Medication overuse headache is a consideration given daily paracetamol use, but cannot explain papilloedema or raised ICP.

Holly meets the modified Friedman criteria for IIH: (1) symptoms and signs of raised ICP (headache, papilloedema, visual obscurations); (2) no focal neurological deficits except CN VI palsy (absent here); (3) normal neuroimaging; (4) elevated LP opening pressure (>25 cm H₂O in non-obese, >28 in obese) with normal CSF composition; (5) no other cause identified. Her LP opening pressure of 29 cm H₂O, bilateral papilloedema, and normal MRI/CSF confirm the diagnosis. IIH is a diagnosis of exclusion but, once confirmed, requires prompt treatment to prevent permanent visual loss from chronic papilloedema.

IIH management has three pillars: (1) Weight reduction – 5–10% body weight loss can reduce ICP and induce remission; this is the most effective long-term intervention. (2) Acetazolamide – first-line pharmacotherapy; reduces CSF production via carbonic anhydrase inhibition. Start 500 mg BD, titrate to effect (max 2–4 g/day). (3) Urgent specialist referral – ophthalmology for serial visual field monitoring (to detect progressive optic nerve damage) and neurology for disease management and escalation decisions. If vision deteriorates despite medical therapy, surgical options include optic nerve sheath fenestration or ventriculoperitoneal shunt. Counsel on the risk of permanent vision loss and the importance of adherence and follow-up.