A systematic headache history uses the mnemonic SOCRATES (Site, Onset, Character, Radiation, Associated symptoms, Timing, Exacerbating/relieving factors, Severity) to characterise the pain. Beyond this, you must actively explore features that point to raised intracranial pressure: morning predominance (worse after lying flat overnight), Valsalva aggravation, and postural visual symptoms.

The visual symptoms in this case are particularly important. Transient visual obscurations — brief (seconds-long) episodes of vision loss or greying-out triggered by postural change — are a hallmark of papilloedema and indicate that the optic nerve is being compromised by raised pressure. Progressive blurring suggests evolving optic nerve damage. These features distinguish raised ICP from migraine aura (which typically lasts 20-60 minutes and has positive visual phenomena like zigzag lines).

Finally, screen for IIH risk factors: female sex, reproductive age, obesity (BMI >25), oral contraceptive use, vitamin A derivatives (isotretinoin), tetracyclines, and recent corticosteroid withdrawal. Also exclude secondary causes: recent head trauma, infection, systemic symptoms suggesting malignancy.

The examination in suspected raised intracranial pressure has three priorities: (1) fundoscopy to detect papilloedema, (2) visual function assessment (acuity and fields), and (3) neurological examination to detect focal deficits or false-localising signs.

Papilloedema is the key finding. It appears as blurring of the optic disc margins, elevation of the disc, loss of the optic cup, and engorged retinal veins. It is almost always bilateral in raised ICP. Papilloedema confirms that intracranial pressure is elevated and mandates urgent investigation. Its absence does not exclude raised ICP, but its presence is diagnostic.

Visual field testing by confrontation can detect enlarged blind spots, a consequence of papilloedema. Formal perimetry is more sensitive and is essential for monitoring disease progression. Cranial nerve examination focuses on CN II (acuity, fields, pupils, fundoscopy) and CN VI (abducens), as a VI nerve palsy is the most common false-localising sign of raised ICP. A full neurological examination screens for focal deficits that would suggest a structural lesion rather than idiopathic disease.

The investigation pathway for suspected raised intracranial pressure follows a strict sequence: (1) neuroimaging, (2) lumbar puncture, (3) specialist ophthalmology and neurology assessment.

Neuroimaging (MRI brain preferred) must be performed before lumbar puncture to exclude space-occupying lesions, hydrocephalus, and cerebral venous sinus thrombosis — all of which can present with papilloedema and would make LP dangerous or alter management. MRI is superior to CT for detecting posterior fossa lesions and venous pathology. MR venography should be included if venous sinus thrombosis is a consideration.

Lumbar puncture with opening pressure measurement is diagnostic. An opening pressure >25 cm H₂O (>250 mm H₂O) in a non-obese patient, or >28 cm H₂O in an obese patient, with normal CSF constituents (cell count, glucose, protein) confirms the diagnosis of idiopathic intracranial hypertension by modified Friedman criteria. CSF analysis also excludes infection and malignancy.

Blood tests (FBC, UEC, LFTs, TFTs) are performed to screen for anaemia, renal impairment, and thyroid disease, and to establish a baseline before starting acetazolamide. Formal visual field testing (perimetry) and ophthalmology review are essential to document baseline visual function and monitor for progressive optic nerve damage, which can lead to permanent visual loss if untreated.

The differential diagnosis for headache with papilloedema includes any cause of raised intracranial pressure. The key is to systematically exclude secondary causes before diagnosing idiopathic intracranial hypertension.

Space-occupying lesions (tumour, abscess, haematoma) are excluded by normal MRI. Hydrocephalus is excluded by normal ventricular size on imaging. Cerebral venous sinus thrombosis is excluded by MR venography. Meningitis or encephalitis is excluded by normal CSF cell count, glucose, and protein, and absence of fever or meningism. Subarachnoid haemorrhage is excluded by the subacute presentation and normal CSF (no red cells or xanthochromia).

Once secondary causes are excluded, the diagnosis is idiopathic intracranial hypertension (IIH), confirmed by the modified Friedman criteria: (1) papilloedema, (2) normal neurological examination except for cranial nerve abnormalities, (3) normal brain imaging, (4) elevated LP opening pressure (>25 cm H₂O), and (5) normal CSF composition. Hollie meets all five criteria.

Primary headache disorders (migraine, tension-type headache) do not cause papilloedema or elevated opening pressure, and are therefore excluded by the objective findings in this case. Medication overuse headache is a consideration given daily paracetamol use, but cannot explain the papilloedema or raised ICP.

The diagnosis of idiopathic intracranial hypertension (IIH) is made using the modified Friedman criteria, which require all of the following:

• Papilloedema (bilateral optic disc swelling)
• Normal neurological examination except for cranial nerve abnormalities (most commonly CN VI palsy)
• Normal neuroimaging (no mass, hydrocephalus, or venous sinus thrombosis)
• Elevated lumbar puncture opening pressure (>25 cm H₂O in non-obese, >28 cm H₂O in obese patients)
• Normal CSF composition (normal cell count, glucose, and protein)

Hollie meets all five criteria: she has bilateral papilloedema, a normal neurological examination, normal MRI, an opening pressure of 29 cm H₂O, and normal CSF analysis. Her risk factors (young woman, BMI 28, sedentary occupation) are typical for IIH, which predominantly affects women of reproductive age with obesity.

IIH is a diagnosis of exclusion — secondary causes must be ruled out first. The term 'idiopathic' means no identifiable cause, though obesity is a strong modifiable risk factor. The pathophysiology is thought to involve impaired CSF absorption at the arachnoid granulations, leading to raised intracranial pressure.

The management of IIH has three goals: (1) reduce intracranial pressure, (2) preserve vision, and (3) address modifiable risk factors. Treatment is escalated based on severity of visual impairment and response to initial therapy.

First-line management:

• Weight reduction: Even 5-10% weight loss significantly reduces ICP and can lead to remission. This is the most effective long-term intervention and should be emphasised in all overweight patients.
• Acetazolamide: A carbonic anhydrase inhibitor that reduces CSF production. Start at 500 mg BD and titrate up to 1-2 g/day as tolerated. Side effects include paraesthesias, metallic taste, and (rarely) metabolic acidosis or renal stones. Monitor U&Es.
• Ophthalmology follow-up: Regular visual field testing (perimetry) and fundoscopy to monitor for progressive optic nerve damage. Frequency depends on severity (monthly if severe, 3-6 monthly if stable).

Second-line options: If acetazolamide is ineffective or not tolerated, consider furosemide or topiramate (which also has weight-loss effects). Surgical intervention (optic nerve sheath fenestration or ventriculoperitoneal shunt) is reserved for cases with rapidly progressive or severe visual loss despite maximal medical therapy.

Patient education: Explain that IIH is a chronic condition requiring long-term monitoring, that weight loss is the most important modifiable factor, and that untreated disease can lead to permanent blindness. Provide safety-netting advice to return urgently if vision worsens.