The history in this case is rich with diagnostic clues if you ask the right questions. Headaches due to raised ICP have a characteristic pattern: worst in the morning (due to recumbent venous pooling overnight increasing ICP), aggravated by Valsalva manoeuvres such as bending, straining, or coughing, and accompanied by nausea. Transient visual obscurations — brief (seconds) greying-out of vision on postural change — are a hallmark symptom of papilloedema from raised ICP and are distinct from the sustained visual aura of migraine. Ask specifically about these features, as patients do not volunteer them spontaneously. Probe IIH risk factors: obesity (BMI ≥30 is highest risk; BMI 28 is relevant), oral contraceptive pill, vitamin A or retinoid use, tetracyclines, and corticosteroid withdrawal. The absence of photophobia, phonophobia, and prior migraine history argues against a primary headache disorder.

The examination in this case pivots on two critical steps: fundoscopy and visual field assessment. Bilateral papilloedema is the most important single finding — it is the direct ophthalmoscopic sign of raised ICP and, in this context, is a medical near-emergency requiring same-day investigation. Enlarged blind spots on confrontation testing are a direct consequence of papilloedema. Cranial nerve VI palsy (abducens nerve) is the most common false-localising sign of raised ICP — its presence would indicate severe intracranial hypertension. Perform a full cranial nerve examination (CN II–XII), and screen for focal neurological deficits (motor, sensory, coordination) and meningeal signs — these findings would broaden the differential to include structural lesions or CNS infection. In Hollie's case, the neurological examination is otherwise normal, narrowing the diagnosis toward IIH.

The presence of bilateral papilloedema mandates urgent neuroimaging before lumbar puncture — this is non-negotiable. A space-occupying lesion or hydrocephalus must be excluded first, as LP in the setting of a mass lesion can cause fatal transtentorial herniation. MRI brain is preferred over CT for its superior sensitivity for posterior fossa lesions and venous sinus thrombosis. Once imaging is normal, a lumbar puncture with opening pressure measurement is both diagnostic and therapeutic. An opening pressure above 25 cm H₂O with normal CSF constituents confirms IIH by the modified Friedman criteria. In Hollie's case: LP opening pressure is 29 cm H₂O (elevated), CSF is acellular, glucose and protein are normal, and Gram stain is negative — this meets diagnostic criteria. Routine bloods (FBC, UEC, LFTs, TFTs) are normal and screen for metabolic and thyroid causes. A normal MRI with no venous sinus thrombosis effectively excludes the most dangerous structural mimics.

With bilateral papilloedema and an elevated LP opening pressure, the differential centres on causes of raised ICP. The key differentials to consider and systematically exclude are:

• Idiopathic intracranial hypertension (IIH): young woman, elevated BMI, no secondary cause found — leading diagnosis
• Cerebral venous sinus thrombosis (CVST): can present identically; excluded by MRI/MRV showing no thrombosis
• Intracranial mass lesion: can cause raised ICP and papilloedema; excluded by normal MRI
• CNS infection (meningitis/encephalitis): raised ICP + headache; excluded by absence of fever, meningism, and normal CSF (no cells, no organisms)
• Migraine: lacks papilloedema, photophobia/phonophobia absent, no prior history — does not explain objective findings
• Medication overuse headache: daily paracetamol use is at the threshold, but cannot explain papilloedema or elevated opening pressure

Hollie meets the modified Friedman criteria for idiopathic intracranial hypertension (IIH):

1. Signs and symptoms of raised ICP (headache, papilloedema, visual symptoms)
2. LP opening pressure ≥25 cm H₂O (Hollie: 29 cm H₂O)
3. Normal CSF constituents (no pleocytosis, normal glucose, normal protein)
4. No structural or vascular cause on neuroimaging (normal MRI including no venous sinus thrombosis)
5. No other identifiable cause (no relevant medications, no secondary disease identified)

IIH predominantly affects women of childbearing age who are overweight. Hollie's BMI of 28 and sedentary lifestyle are relevant risk factors. The most serious risk is progressive visual loss from chronic papilloedema compressing the optic nerves — this is the main target of monitoring and treatment.

Management of confirmed IIH is stepwise and targets both symptom relief and prevention of permanent visual loss:

• Weight reduction: the most effective long-term intervention; even 5–10% weight loss can normalise ICP and lead to remission. Hollie's sedentary lifestyle and BMI 28 make this the first-line modifiable intervention.
• Acetazolamide: first-line pharmacotherapy; reduces CSF production via carbonic anhydrase inhibition; start at 250–500 mg twice daily and titrate. This is recommended by Australian (RACGP/neurological specialist) and international guidelines.
• Urgent specialist referrals: ophthalmology for serial visual field testing and OCT (to detect optic nerve damage), and neurology for disease-modifying management and escalation decisions.
• Lumbar puncture: the diagnostic LP also provides immediate therapeutic ICP reduction; serial LPs can be used for acute symptomatic relief but are not a long-term solution.
• Surgical options (CSF shunting, optic nerve sheath fenestration): reserved for refractory disease or acute visual loss.
• Communication: explain the diagnosis clearly and without excessive alarm; address Hollie's fears about permanent vision loss, explain the investigation pathway, and engage her in weight management decisions.