Can steroids cause increased intracranial pressure?

October 10, 2025 •

5 min read

While corticosteroids are often used to treat inflammation, a well-documented but rare side effect is the development of benign intracranial hypertension, a condition where steroids can cause increased intracranial pressure. This elevated pressure, also known as pseudotumor cerebri, frequently manifests during dose reduction or withdrawal of the medication, not during treatment.

Quick Summary

Steroids can cause a rare form of intracranial hypertension, often triggered by withdrawal or dose reduction. This condition, known as pseudotumor cerebri, involves elevated cerebrospinal fluid pressure, leading to symptoms like severe headaches and vision problems. It primarily affects specific patient demographics, and careful monitoring is essential during steroid tapering.

Key Points

Withdrawal Risk: Steroid-induced increased intracranial pressure (ICP), known as pseudotumor cerebri, most often occurs when reducing or stopping steroid medication.
CSF Dynamics: The mechanism involves disrupting the normal production and absorption of cerebrospinal fluid (CSF).
Adrenal Insufficiency: Steroid withdrawal can lead to adrenal insufficiency, a hormonal imbalance that is linked to a rise in ICP.
Key Symptoms: Watch for severe headaches, blurred or double vision, and pulsatile tinnitus, especially during a steroid taper.
High-Risk Patients: Young, obese women on long-term, high-dose therapy are particularly susceptible.
Expert Management: Any steroid tapering must be carefully managed by a healthcare provider to prevent rebound effects.
Not for IIH Treatment: Steroids are not a routine treatment for IIH, as their withdrawal can cause rebound pressure.

Understanding Steroid-Induced Intracranial Hypertension

Increased intracranial pressure (ICP) is a serious medical condition characterized by a buildup of pressure inside the skull. While it can arise from various causes, including head injuries and tumors, it is also a known, albeit rare, side effect of certain medications, including corticosteroids. The condition is often referred to as benign intracranial hypertension (BIH) or pseudotumor cerebri (PTC) when medication is the culprit. The most concerning aspect is that this issue frequently appears not during active steroid use but during the withdrawal or dose-reduction phase, presenting a significant challenge for both patients and clinicians.

Mechanisms Behind Steroid-Induced ICP

The exact mechanisms by which steroids influence intracranial pressure are still under investigation, but several hypotheses have been proposed based on clinical observations and research. The primary theories point towards a disruption of cerebrospinal fluid (CSF) homeostasis, which is the delicate balance of CSF production and absorption within the brain.

Disruption of CSF Dynamics: Studies suggest that corticosteroids can alter the normal circulation and absorption of CSF. It's believed that they may increase resistance to CSF flow, leading to a buildup of fluid and pressure. Conversely, acute withdrawal of steroids is thought to cause a decrease in CSF absorption, further contributing to the pressure spike.
Hormonal Influence: The body's endocrine system plays a role in CSF volume regulation. The use of long-term corticosteroids can suppress the body's natural adrenal function, leading to adrenal insufficiency upon withdrawal. This hormonal imbalance is a potential trigger for increased ICP. Mouse model studies have confirmed that steroid withdrawal in a state of adrenal insufficiency can induce raised ICP.
Fluid Retention: While less specific to the brain, fluid retention is a known side effect of steroids. In susceptible individuals, this general fluid increase might contribute to elevated intracranial pressure.

Steroid Withdrawal and Rebound Intracranial Hypertension

The most significant risk period for developing intracranial hypertension is when a patient is tapering off or abruptly discontinuing steroid therapy. This is known as rebound intracranial hypertension. The body, having adapted to the high dose of corticosteroids, struggles to regulate CSF dynamics effectively when the medication is reduced or stopped. Case reports have documented this phenomenon in patients receiving long-term high-dose steroids for various conditions, including multiple sclerosis and inflammatory bowel disease. Even inhaled corticosteroids have been linked to this risk, as seen in a case of a child who developed PTCS after withdrawal of inhaled glucocorticoids.

Risk Factors and Clinical Presentation

Certain patient demographics and preexisting conditions increase the risk of developing steroid-induced intracranial hypertension. These risk factors overlap significantly with those for idiopathic intracranial hypertension (IIH).

Obesity: Excessive weight is a major risk factor for IIH and is also associated with steroid-induced intracranial pressure, particularly in young women.
Gender and Age: Young, fertile women are the most commonly affected demographic. In prepubescent children, the occurrence rate is equal between boys and girls.
Duration and Dosage: Prolonged, high-dose steroid therapy increases the risk of developing this side effect upon withdrawal.
Other Medications: Some other medications, such as tetracycline antibiotics and high-dose vitamin A derivatives, can also cause intracranial hypertension, and their concomitant use with steroids may further increase risk.

Common symptoms of increased intracranial pressure include:

Headache: A constant, throbbing headache, often worse in the morning or when coughing/straining.
Vision Problems: Blurry vision, double vision (diplopia), or transient visual obscurations (temporary graying out of vision).
Papilledema: Swelling of the optic nerve head, a key sign found during an eye exam.
Nausea and Vomiting: Unexplained nausea and vomiting.
Tinnitus: A pulse-synchronous ringing or buzzing in the ears.

Management and Treatment

If steroid-induced intracranial hypertension is suspected, a medical evaluation is crucial. Diagnosis typically involves a physical examination, ophthalmological assessment for papilledema, and sometimes a lumbar puncture to measure CSF pressure. Once diagnosed, management focuses on resolving the elevated pressure and managing symptoms.

Controlled Steroid Tapering: The primary management strategy is to continue or reintroduce steroids at a controlled, gradual tapering schedule to prevent sudden hormonal shifts. The rate of withdrawal must be carefully managed by a healthcare professional.
Pharmacologic Intervention: Medications that help reduce CSF production, such as acetazolamide, may be used to manage the pressure.
Surgical Intervention: In severe cases, particularly where vision is threatened, surgical options like optic nerve sheath fenestration or CSF shunting may be considered.

Crucially, corticosteroids should not be used for routine IIH treatment, as their withdrawal can cause a rebound effect.

Comparison of Steroid-Induced and Idiopathic Intracranial Hypertension


Feature	Steroid-Induced Intracranial Hypertension	Idiopathic Intracranial Hypertension (IIH)
Cause	Primarily related to the withdrawal or dose-reduction of steroid medication.	Cause is unknown, but strongly linked to obesity.
Timing of Onset	Often occurs during the tapering or discontinuation phase of therapy.	Onset is not linked to medication withdrawal but can be exacerbated by steroid use.
Demographics	More common in young obese women, but can affect patients receiving long-term steroid therapy, including children.	Primarily affects obese women of childbearing age.
Mechanism	Disruption of glucocorticoid-mediated CSF dynamics and adrenal insufficiency.	Exact mechanism is unclear, but linked to CSF flow and hormonal factors.
Treatment	Careful re-tapering of steroids and management with diuretics like acetazolamide.	Weight loss, diuretics (acetazolamide), and potentially surgery in severe cases.

Conclusion

While corticosteroids are powerful and vital medications for many conditions, their potential to cause increased intracranial pressure, particularly during withdrawal, is a serious risk that requires careful consideration. The association is well-documented in medical literature and is not limited to oral medications but can also occur with prolonged use of inhaled steroids. For patients on long-term steroid therapy, particularly those in high-risk groups, careful monitoring and a professional, gradual tapering plan are essential to mitigate the risk of rebound intracranial hypertension. Early recognition of symptoms and prompt medical consultation are crucial for effective management and for preventing long-term complications, such as permanent vision loss.

MedlinePlus offers detailed information on idiopathic intracranial hypertension.

Potential Complications

Vision Loss: Untreated, chronic papilledema can lead to damage to the optic nerve and potentially permanent vision loss.
Neurological Deficits: While rare, severe cases can lead to seizures, confusion, and other neurological issues.
Diagnostic Delay: Because symptoms like headaches are common, steroid-induced intracranial hypertension can be misdiagnosed or overlooked, leading to delays in appropriate treatment.
Relapse Risk: Patients with steroid-induced ICP may be at risk for a relapse of their original condition, especially if the steroid dosage is reduced too quickly.

Frequently Asked Questions

While the withdrawal phase is the most common trigger, some cases of intracranial hypertension have been reported during active corticosteroid treatment, particularly in young, obese women. However, the risk is significantly higher upon dose reduction or cessation.

Steroid-induced pseudotumor cerebri is often reversible with appropriate management, which typically involves carefully re-tapering the steroid dose and possibly using other medications to lower intracranial pressure. However, if left untreated, it can cause irreversible vision loss due to damage to the optic nerve.

No, cases of increased intracranial pressure have been associated with various forms of corticosteroids, including inhaled and even excessive topical application, although these occurrences are considered rare.

The onset of symptoms can vary, but it typically occurs shortly after the steroid dose is reduced or stopped. In some cases, it may appear within days to weeks of the change in medication.

One of the most important signs is papilledema, or swelling of the optic nerve head, which is visible during an ophthalmic examination. This indicates pressure on the optic nerve from the elevated intracranial pressure.

Yes. Since obesity is a significant risk factor for both idiopathic and steroid-induced intracranial hypertension, weight management can help reduce overall risk. Weight loss has been shown to improve symptoms in many cases of IIH.

If you experience severe headaches, vision changes, or other symptoms suggestive of increased intracranial pressure while tapering steroids, you should contact your doctor immediately. Abruptly stopping steroids can be dangerous, so any changes to your medication regimen should be made under medical supervision.