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Tuesday, August 12, 2025

Intracranial hypertension


Definition and Classification

Intracranial hypertension (IH) refers to an abnormal elevation of pressure within the skull. This can result from an increase in the volume of brain tissue, blood, or cerebrospinal fluid (CSF). When no secondary cause such as tumor, infection, venous sinus thrombosis, or hydrocephalus is found, the condition is classified as idiopathic intracranial hypertension (IIH), also known as pseudotumor cerebri.

IIH is most common in women of childbearing age, particularly those between 20 and 50 years old, with a higher incidence in individuals with obesity or recent significant weight gain.

Pathophysiology

The intracranial compartment maintains a fixed volume as described by the Monro–Kellie doctrine. Any increase in brain tissue, blood, or CSF without compensatory decrease in another component will lead to a rise in intracranial pressure (ICP).

In IIH, mechanisms proposed include:

  • Impaired CSF absorption at the arachnoid villi

  • Increased venous sinus pressure due to stenosis or thrombosis

  • Possible mild overproduction of CSF by the choroid plexus

  • Obesity-related increase in intra-abdominal and intrathoracic pressures leading to impaired venous return from the brain

Sustained elevation in ICP reduces cerebral perfusion pressure, potentially leading to optic nerve damage and vision loss.

Clinical Presentation

Common symptoms include:

  • Headache: diffuse, daily, often worse in the morning or with Valsalva maneuvers such as coughing or straining

  • Transient visual obscurations: brief episodes of visual blurring or blackout, often precipitated by posture changes

  • Persistent visual blurring or loss of peripheral vision

  • Pulsatile tinnitus: perception of a rhythmic whooshing sound in the ears

  • Diplopia: often due to abducens nerve palsy

  • Nausea and vomiting in more severe cases

Signs on examination:

  • Papilledema (optic disc swelling)

  • Constricted visual fields on perimetry

  • Possible sixth nerve palsy causing horizontal diplopia

Diagnosis

Diagnosis is based on:

  1. Neuroimaging – Magnetic resonance imaging (MRI) of the brain with MR venography to exclude mass lesions, hydrocephalus, and venous sinus thrombosis. Findings may include empty sella, flattened posterior globe, distension of perioptic subarachnoid space, and venous sinus narrowing.

  2. Lumbar puncture – Opening pressure above 25 cm H₂O in adults, with normal CSF composition, confirms raised ICP in IIH.

  3. Ophthalmologic evaluation – Visual acuity testing, automated perimetry, and fundus photography to assess papilledema and monitor progression.

Management Principles

The primary goals are to prevent visual loss, reduce intracranial pressure, and relieve symptoms. Management combines lifestyle modification, medical therapy, and surgical interventions when necessary.

Lifestyle Modification

  • Weight loss: Target loss of 6–10% of body weight is often sufficient to induce remission in IIH.

  • Dietary control: Low-calorie diet, reduced salt intake, and avoidance of excessive fluid intake.

  • Discontinuation of causative medications: Stop or replace agents known to cause IH such as high-dose vitamin A derivatives and tetracyclines.

Medical Therapy

1. Acetazolamide

  • Mechanism: Carbonic anhydrase inhibitor reducing CSF production

  • Initial dose: 250–500 mg orally twice daily

  • Titration: Increase by 250 mg every few days to weeks depending on tolerance

  • Maximum dose: Up to 4 g/day in divided doses

  • Common side effects: Paresthesias, fatigue, gastrointestinal upset, metallic taste, kidney stones, metabolic acidosis

  • Monitoring: Electrolytes, renal function, and acid–base status

2. Furosemide

  • Mechanism: Loop diuretic reducing fluid volume and mildly reducing CSF production

  • Dose: 20–40 mg orally once or twice daily, adjusted based on response and tolerance

  • Often combined with acetazolamide in refractory cases

  • Side effects: Electrolyte disturbances, dehydration, hypotension

3. Topiramate

  • Mechanism: Weak carbonic anhydrase inhibitor with additional benefits for migraine control and weight loss

  • Dose: Initiate at 25 mg orally at night, titrate to 50–100 mg twice daily as tolerated

  • Side effects: Cognitive slowing, paresthesias, weight loss, kidney stones

  • Useful in patients with coexisting migraine

4. Corticosteroids

  • Not recommended for routine management due to side effects and lack of sustained benefit

  • May be used short term in fulminant cases to preserve vision before surgery

  • Example: Methylprednisolone 250–500 mg IV daily for a few days

Osmotic Therapy for Acute ICP Reduction

Used in acute or fulminant cases, usually in hospital:

Mannitol

  • Dose: 0.25–1 g/kg IV bolus over 15–30 minutes, repeated every 4–6 hours as needed

  • Effect: Rapid osmotic shift reducing brain water content

Hypertonic saline

  • Concentrations: 3%, 7.5%, or higher depending on protocol

  • Dose: Typically 2–5 mL/kg of 3% saline over 10–20 minutes in acute settings

  • Monitoring: Serum sodium, osmolality, and fluid balance

These therapies are short-term measures while definitive treatment is arranged.

Surgical and Interventional Management

Reserved for cases with vision-threatening papilledema or those refractory to maximal medical therapy.

1. Optic Nerve Sheath Fenestration (ONSF)

  • Small incision made in the optic nerve sheath to relieve pressure

  • Indicated primarily for vision preservation

  • Can be unilateral or bilateral

2. Cerebrospinal Fluid Shunting

  • Lumboperitoneal shunt or ventriculoperitoneal shunt to divert CSF to the peritoneal cavity

  • Reduces ICP and relieves symptoms

  • Risks include infection, shunt obstruction, overdrainage, and need for revisions

3. Venous Sinus Stenting

  • Indicated when venous sinus stenosis is documented and contributes to ICP elevation

  • Stent placement restores venous outflow, reduces venous pressure, and improves CSF absorption

4. Bariatric Surgery

  • Considered for obese patients unable to achieve weight loss through lifestyle measures

  • Often results in sustained remission of IIH symptoms

Fulminant IIH

This is a rapidly progressive form with acute visual loss over days to weeks, requiring urgent intervention:

  • Immediate hospital admission

  • High-dose acetazolamide (2–4 g/day)

  • IV methylprednisolone short course as bridge therapy

  • Early surgical intervention such as ONSF or CSF shunting

Monitoring and Follow-Up

  • Ophthalmologic review: Frequent visual field testing and optic disc assessment

  • Neurology review: Monitor headache control, medication side effects, and ICP symptoms

  • Dose adjustment: Reduce acetazolamide gradually once papilledema resolves and vision stabilizes

  • Long-term care: Continued lifestyle modifications to prevent recurrence

Prognosis

With timely diagnosis and treatment, most patients retain useful vision. However, a subset may develop permanent visual field loss. Recurrence is possible, particularly with weight regain or re-exposure to precipitating factors.




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