A systematic headache history must identify features of raised intracranial pressure: morning predominance, Valsalva aggravation (coughing, straining, bending), and postural visual symptoms. Transient visual obscurations—brief greying-out on position change—are pathognomonic of papilloedema. You must also screen for IIH risk factors (young woman, elevated BMI, certain medications) and exclude other secondary causes (trauma, infection, medication overuse).

The examination must focus on detecting papilloedema (the hallmark sign of raised ICP) and excluding focal neurological deficits that would suggest a structural lesion. Fundoscopy is mandatory in any patient with headache and visual symptoms. Visual field testing by confrontation can detect enlarged blind spots. Cranial nerve examination should focus on CN II (visual acuity, fields, pupils) and CN VI (abducens palsy is a false-localising sign of raised ICP). A full neurological examination excludes focal deficits and meningism.

Once papilloedema is identified, urgent neuroimaging (MRI preferred) is mandatory before lumbar puncture to exclude mass lesion, hydrocephalus, or venous sinus thrombosis—all of which can cause papilloedema but contraindicate LP. If imaging is normal, LP with opening pressure measurement and CSF analysis confirms the diagnosis: opening pressure >25 cm H₂O with normal CSF constituents meets modified Friedman criteria for IIH. Baseline bloods exclude metabolic and endocrine causes. Formal ophthalmology assessment with perimetry quantifies visual field loss for monitoring.

The differential for headache with papilloedema includes any cause of raised intracranial pressure. Idiopathic intracranial hypertension (IIH) is the leading diagnosis in a young woman with elevated BMI, normal neuroimaging, and elevated LP opening pressure with normal CSF. Space-occupying lesions (tumour, abscess) are excluded by normal MRI. Cerebral venous sinus thrombosis is excluded by MR venography. CNS infection (meningitis, encephalitis) is excluded by normal CSF. Migraine and tension-type headache do not cause papilloedema. Medication overuse headache is a consideration given daily paracetamol use, but cannot explain objective papilloedema.

Holly meets the modified Friedman criteria for idiopathic intracranial hypertension: (1) papilloedema confirmed on fundoscopy, (2) normal neurological examination except for cranial nerve abnormalities, (3) normal brain MRI with no hydrocephalus or mass, (4) elevated LP opening pressure >25 cm H₂O (Holly's is 29 cm H₂O), and (5) normal CSF composition. IIH is a diagnosis of exclusion—secondary causes must be ruled out. The typical patient is a young woman of childbearing age with elevated BMI, which matches Holly's demographic. Untreated IIH can lead to permanent visual loss from optic nerve damage, making prompt diagnosis and management critical.

IIH management has three goals: (1) prevent permanent visual loss, (2) relieve symptoms, and (3) address underlying risk factors. Weight reduction is the most effective long-term intervention—even 5-10% weight loss can reduce ICP and induce remission. Acetazolamide is first-line pharmacotherapy, reducing CSF production via carbonic anhydrase inhibition. Urgent ophthalmology referral is mandatory for serial visual field monitoring to detect progressive optic nerve damage. Neurology referral guides disease-modifying therapy and escalation (e.g. optic nerve sheath fenestration or VP shunt if medical therapy fails). Patient education about red-flag symptoms (sudden vision loss, severe headache) is essential.