Nimotop: Uses, Dosage & Side Effects
A calcium channel blocker (nimodipine) used to prevent and treat cerebral vasospasm following aneurysmal subarachnoid hemorrhage
Quick Facts
Key Takeaways
- Nimotop (nimodipine) is the only calcium channel blocker with proven clinical benefit in improving neurological outcomes after aneurysmal subarachnoid hemorrhage (SAH).
- Treatment must begin within 96 hours of the hemorrhage and continue for 21 consecutive days, with tablets taken every 4 hours (6 times daily).
- Nimodipine preferentially targets cerebral blood vessels, helping to prevent vasospasm and reduce the risk of delayed ischemic brain damage.
- The most important side effect to monitor is hypotension (low blood pressure), which requires regular blood pressure checks during treatment.
- Significant drug interactions exist with CYP3A4 inhibitors and inducers – always inform your medical team about all medications you are taking.
What Is Nimotop and What Is It Used For?
Nimotop is a prescription medication containing nimodipine, a member of the dihydropyridine class of calcium channel blockers. Unlike other calcium channel blockers that primarily target the heart and peripheral blood vessels, nimodipine has a unique preferential selectivity for the smooth muscle cells in cerebral (brain) arteries. This property makes it particularly valuable in the management of cerebrovascular conditions, most notably the prevention of vasospasm after subarachnoid hemorrhage.
Subarachnoid hemorrhage (SAH) occurs when blood leaks into the space between the brain and its surrounding membranes, most commonly due to the rupture of a cerebral aneurysm. Following the initial bleed, one of the most feared complications is cerebral vasospasm – a sustained narrowing of the cerebral arteries that typically develops between 3 and 14 days after the hemorrhage. This vasospasm can severely reduce blood flow to the brain, leading to delayed cerebral ischemia (DCI) and potentially devastating neurological damage, including stroke, cognitive impairment, and death.
Nimodipine works by blocking L-type voltage-gated calcium channels in the smooth muscle cells of cerebral arteries. By preventing the influx of calcium ions, which are essential for muscle contraction, nimodipine relaxes the arterial walls and helps to maintain adequate blood flow to the brain. The drug’s high lipophilicity (fat solubility) allows it to cross the blood-brain barrier readily, achieving therapeutically relevant concentrations in the cerebral vasculature and cerebrospinal fluid.
The evidence supporting the use of nimodipine after SAH is robust. The landmark British Aneurysm Nimodipine Trial (BRANT), published in the British Medical Journal in 1989, demonstrated a significant reduction in the incidence of cerebral infarction and poor neurological outcomes in patients treated with oral nimodipine compared to placebo. Subsequent meta-analyses and systematic reviews, including a Cochrane review, have confirmed these findings. Nimodipine remains the only pharmacological agent with strong evidence for improving outcomes after aneurysmal SAH, and its use is recommended with a Class I, Level A recommendation by the American Heart Association/American Stroke Association (AHA/ASA).
It is important to understand that while nimodipine reduces the incidence of poor outcomes attributed to vasospasm, the exact mechanism by which it provides neuroprotection is still being investigated. Some researchers believe that its benefits may extend beyond vasospasm prevention to include direct neuroprotective effects on neurons, potentially through reduction of calcium-mediated excitotoxicity and improvement of microcirculation. Research into these mechanisms continues to be an active area of neuroscience inquiry.
Nimotop is approved specifically for the prevention and treatment of ischemic neurological deficits following aneurysmal subarachnoid hemorrhage. It is not a general-purpose antihypertensive medication and should not be used as a substitute for other calcium channel blockers in the treatment of high blood pressure or other cardiovascular conditions.
What Should You Know Before Taking Nimotop?
Before beginning treatment with Nimotop, it is essential that your medical team conducts a thorough assessment of your medical history, current medications, and overall clinical status. Nimodipine, like all prescription medications, carries specific risks and contraindications that must be carefully evaluated to ensure safe and effective treatment.
Contraindications
Nimotop must not be used in the following circumstances:
- Hypersensitivity: Known allergy to nimodipine, other dihydropyridine calcium channel blockers, or any of the excipients in the formulation.
- Severe hepatic impairment: Patients with severe liver disease (e.g., Child-Pugh Class C cirrhosis) should not take nimodipine, as the drug is extensively metabolized by the liver and impaired metabolism can lead to dangerously elevated blood levels.
- Concomitant use with strong CYP3A4 inhibitors: Co-administration with potent CYP3A4 inhibitors such as ketoconazole, itraconazole, ritonavir, and nelfinavir is contraindicated due to the risk of markedly increased nimodipine plasma concentrations.
- Concomitant use with rifampicin: Rifampicin is such a powerful CYP3A4 inducer that it can reduce nimodipine levels to below therapeutic concentrations, effectively rendering the treatment ineffective.
- Concomitant use with phenobarbital, phenytoin, or carbamazepine: These anticonvulsants are potent CYP3A4 inducers that substantially reduce nimodipine effectiveness.
Warnings and Precautions
The following situations require particular caution and careful monitoring during Nimotop treatment:
- Hypotension: Nimodipine lowers blood pressure through its vasodilatory effects. Patients with pre-existing low blood pressure or those receiving other antihypertensive medications are at increased risk of clinically significant hypotension. Blood pressure should be monitored at least every 2 hours during the initial treatment period and regularly thereafter.
- Raised intracranial pressure: In patients with generalized cerebral edema or severely raised intracranial pressure, nimodipine should be used with extreme caution, as any reduction in blood pressure may compromise cerebral perfusion pressure and potentially worsen brain injury.
- Hepatic impairment: Patients with mild to moderate liver disease require dose reduction due to reduced drug metabolism. Liver function tests should be monitored during treatment.
- Renal impairment: While nimodipine is primarily eliminated via hepatic metabolism, renal function should be monitored, particularly in critically ill patients who may have multi-organ involvement.
- Cardiovascular conditions: Caution is advised in patients with recent (within 4 weeks) myocardial infarction, unstable angina, congestive heart failure, or significant aortic stenosis.
Pregnancy and Breastfeeding
Nimotop should generally be avoided during pregnancy unless the clinical situation is life-threatening and no safer alternative exists. Animal reproductive studies have demonstrated teratogenic effects at high doses, including skeletal malformations and fetal growth restriction in rats and rabbits. No adequately controlled studies have been conducted in pregnant women. If treatment is considered essential, the potential risks must be carefully weighed against the benefits on a case-by-case basis.
Nimodipine and its metabolites are excreted in breast milk at concentrations approaching those found in maternal plasma. Due to the potential for pharmacological effects on the nursing infant, breastfeeding is not recommended during treatment with Nimotop. If breastfeeding is desired after treatment is completed, it is advisable to wait until nimodipine has been fully cleared from the body (at least 5 half-lives, or approximately 2 days after the last dose).
Nimodipine oral solution and tablets must NEVER be administered intravenously. Fatal cases have been reported when nimodipine oral solution was inadvertently injected intravenously. If an intravenous formulation is required, it must be the specifically manufactured IV preparation, administered via a central line with appropriate monitoring. Always verify the route of administration before giving nimodipine.
How Does Nimotop Interact with Other Drugs?
Drug interactions represent one of the most important clinical considerations when prescribing Nimotop. Because nimodipine is extensively metabolized by cytochrome P450 3A4 (CYP3A4) enzymes in the liver and intestinal wall, any drug that significantly affects CYP3A4 activity can alter nimodipine plasma concentrations, potentially leading to either toxicity or therapeutic failure.
Major Interactions
| Drug / Class | Mechanism | Effect | Recommendation |
|---|---|---|---|
| Ketoconazole, itraconazole | Strong CYP3A4 inhibition | Marked increase in nimodipine levels | Contraindicated – do not co-administer |
| Ritonavir, nelfinavir | Strong CYP3A4 inhibition | Potentially dangerous increase in nimodipine levels | Contraindicated – do not co-administer |
| Rifampicin | Potent CYP3A4 induction | Nimodipine rendered virtually undetectable | Contraindicated – do not co-administer |
| Phenytoin, carbamazepine, phenobarbital | CYP3A4 induction | Substantially reduced nimodipine levels | Contraindicated – do not co-administer |
| Erythromycin, clarithromycin | Moderate CYP3A4 inhibition | Significant increase in nimodipine levels | Avoid – use azithromycin as alternative |
| Grapefruit juice | Intestinal CYP3A4 inhibition | Increased nimodipine bioavailability | Avoid grapefruit during treatment |
Minor Interactions
| Drug / Class | Mechanism | Effect | Recommendation |
|---|---|---|---|
| Other antihypertensives | Additive vasodilation | Enhanced blood pressure lowering | Monitor BP closely; adjust doses as needed |
| Beta-blockers | Combined cardiovascular effects | Increased risk of hypotension and bradycardia | Monitor heart rate and BP carefully |
| Fluoxetine | CYP3A4 inhibition (moderate) | Increased nimodipine exposure | Monitor for increased side effects |
| Nortriptyline | Unknown | Increased nortriptyline plasma levels reported | Monitor for tricyclic side effects |
| Cimetidine | CYP inhibition | Moderate increase in nimodipine levels | Consider alternative H2 blocker |
| Valproic acid | CYP inhibition (mild) | Modest increase in nimodipine exposure | Monitor; usually clinically manageable |
In the neurocritical care setting, it is particularly important to be aware of interactions with anticonvulsants, as seizures are a common complication of subarachnoid hemorrhage. The traditional anticonvulsants phenytoin, carbamazepine, and phenobarbital are all potent CYP3A4 inducers and are contraindicated with nimodipine. If anticonvulsant therapy is required, alternatives such as levetiracetam (Keppra), which does not significantly affect CYP3A4, are preferred.
Patients in the ICU setting may receive multiple medications simultaneously, including antibiotics, sedatives, analgesics, and vasoactive agents. A thorough drug interaction review should be performed before starting nimodipine and whenever new medications are added to the regimen. Hospital pharmacy teams play a crucial role in identifying and managing potential interactions in this complex patient population.
What Is the Correct Dosage of Nimotop?
Adults
Standard Adult Dosage
60 mg (two 30 mg tablets) every 4 hours, 6 times daily, for 21 consecutive days. Treatment should be initiated as early as possible, ideally within 96 hours (4 days) of the onset of subarachnoid hemorrhage. The total daily dose is 360 mg.
The dosing schedule requires tablets to be taken approximately every 4 hours around the clock, which means patients typically take their doses at times such as 6:00, 10:00, 14:00, 18:00, 22:00, and 02:00. In hospital settings, nursing staff will administer the medication on schedule. Maintaining a strict dosing interval is important to ensure consistent therapeutic blood levels throughout the 21-day treatment period.
Nimodipine tablets should be swallowed whole with a small amount of liquid. They should not be crushed, chewed, or broken. For patients who are unable to swallow (which is common in neurologically impaired SAH patients), nimodipine oral solution may be administered via nasogastric tube. In some countries, an intravenous formulation is also available for patients who cannot receive oral medication.
| Patient Group | Dose | Frequency | Duration | Notes |
|---|---|---|---|---|
| Adults (standard) | 60 mg (2 × 30 mg) | Every 4 hours | 21 days | Start within 96 hours of SAH |
| Hepatic impairment | 30 mg (1 × 30 mg) | Every 4 hours | 21 days | Mild–moderate impairment; severe is contraindicated |
| Low body weight (<70 kg) | 30 mg (1 × 30 mg) | Every 4 hours | 21 days | If blood pressure drops significantly |
| Significant hypotension | 30 mg (1 × 30 mg) | Every 4 hours | 21 days | Reduce dose if systolic BP falls below 100 mmHg |
Children
The safety and efficacy of nimodipine in children and adolescents under 18 years of age have not been established. Subarachnoid hemorrhage from aneurysm rupture is rare in the pediatric population. When SAH does occur in children, the decision to use nimodipine is made on a case-by-case basis by the treating pediatric neurosurgeon and neurointensive care team, often extrapolating from adult data with appropriate weight-based dose adjustments. There are no specific pediatric dosing guidelines from regulatory authorities.
Elderly
No specific dose adjustment is generally required for elderly patients based on age alone. However, older patients are more likely to have hepatic impairment, renal dysfunction, and concomitant cardiovascular diseases that may necessitate dose reduction and more intensive monitoring. The risk of hypotension is also higher in elderly patients, and blood pressure should be monitored frequently. As SAH predominantly affects adults aged 40–65, a significant proportion of patients receiving nimodipine are middle-aged or older.
Missed Dose
If a dose of Nimotop is missed, it should be taken as soon as remembered, unless it is almost time for the next scheduled dose. In that case, the missed dose should be skipped and the regular dosing schedule resumed. Do not take a double dose to make up for a missed one. In the hospital setting, missed doses should be documented and reported to the medical team, as consistent dosing is critical for maintaining therapeutic blood levels during the vulnerable period after subarachnoid hemorrhage.
Overdose
Overdose with nimodipine can cause severe hypotension, tachycardia (rapid heart rate), nausea, vomiting, and potentially life-threatening cardiovascular collapse. There is no specific antidote for nimodipine overdose. Treatment is supportive and symptomatic, including intravenous fluid resuscitation, vasopressor administration (e.g., norepinephrine) to maintain blood pressure, and positioning the patient in Trendelenburg position. Gastric lavage and activated charcoal may be considered if the overdose was recent. Due to nimodipine’s extensive protein binding (approximately 98%), hemodialysis is not expected to be effective.
Nimodipine tablets should be taken at least 1 hour before or 2 hours after meals, as food can increase its absorption unpredictably and lead to higher peak plasma concentrations. However, in the acute hospital setting, clinical judgment may dictate that the critical importance of maintaining the dosing schedule takes precedence over meal timing.
What Are the Side Effects of Nimotop?
Like all medications, Nimotop can cause side effects, although not everyone experiences them. The side effects of nimodipine are predominantly related to its vasodilatory action – by relaxing blood vessel walls, it can lower blood pressure and cause symptoms associated with increased blood flow. Most side effects are mild to moderate in severity and are dose-dependent, meaning they are more likely at higher doses and often resolve or improve when the dose is reduced.
The following side effects have been reported in clinical trials and post-marketing surveillance, organized by frequency:
Common
May affect up to 1 in 10 people
- Hypotension (low blood pressure) – the most clinically significant side effect
- Headache
- Nausea
- Flushing (feeling of warmth in the face)
- Tachycardia (rapid heart rate) – usually a compensatory response to blood pressure lowering
Uncommon
May affect up to 1 in 100 people
- Bradycardia (slow heart rate)
- Dizziness
- Peripheral edema (swelling of ankles or feet)
- Gastrointestinal disturbances (abdominal discomfort, diarrhea, constipation)
- Skin rash
- Feeling of warmth throughout the body
Rare
May affect up to 1 in 1,000 people
- Thrombocytopenia (low platelet count)
- Hepatic transaminase elevations (abnormal liver function tests)
- Ileus (temporary paralysis of bowel movements)
- Allergic reactions (urticaria, angioedema)
Not Known
Frequency cannot be estimated from available data
- Severe hypotension leading to hemodynamic compromise
- Rebound vasospasm upon abrupt discontinuation (theoretical)
Hypotension is the most common and clinically important side effect of nimodipine. In the context of subarachnoid hemorrhage management, maintaining adequate cerebral perfusion pressure is paramount, and any drop in blood pressure can potentially worsen cerebral ischemia. For this reason, blood pressure is monitored very closely (often continuously via arterial line) during nimodipine treatment. If clinically significant hypotension occurs (e.g., systolic blood pressure falls below 100 mmHg or there is a drop of more than 20% from baseline), the dose should be reduced to 30 mg every 4 hours rather than discontinuing the drug entirely.
Headache is reported in some patients, which can be challenging to distinguish from the headache associated with the subarachnoid hemorrhage itself. In most cases, headache from nimodipine is a benign vasodilatory effect and resolves without specific intervention.
Hepatic effects, while rare, warrant monitoring. Transient elevations of liver enzymes (AST, ALT) have been observed during treatment. In most cases, these normalize after treatment is completed. Severe hepatotoxicity is extremely rare but has been reported in isolated post-marketing cases. Liver function tests should be monitored periodically during the 21-day treatment course, particularly in patients with pre-existing liver disease.
Long-term side effects are generally not a concern with nimodipine, as the treatment course is limited to 21 days. There is no evidence of clinically significant rebound effects or withdrawal symptoms upon completion of the treatment course, although gradual tapering has been suggested by some clinicians as a precautionary measure.
Inform your doctor or nurse immediately if you experience: a sudden drop in blood pressure accompanied by dizziness or fainting; severe headache that is different from your usual post-hemorrhage headache; rapid or irregular heartbeat; unexplained swelling; jaundice (yellowing of the skin or eyes); or any new or worsening symptoms. In the ICU setting, these parameters are typically continuously monitored.
How Should You Store Nimotop?
Proper storage of Nimotop is essential to maintain its potency and safety. Nimodipine is a photosensitive compound, meaning it degrades when exposed to light. This is a particularly important consideration, as improperly stored medication may have reduced effectiveness, which could compromise patient outcomes in the critical post-SAH period.
- Temperature: Store at a temperature not exceeding 30 °C (86 °F). Do not freeze. Avoid exposure to excessive heat or direct sunlight.
- Light protection: Keep the tablets in the original blister packaging and outer carton to protect from light. Do not remove tablets from the blister pack until immediately before administration.
- Moisture protection: Store in a dry place. Moisture can degrade the tablet coating and affect drug stability.
- Keep out of reach of children: Store all medications in a secure location inaccessible to children.
- Expiration date: Do not use Nimotop after the expiration date (EXP) printed on the blister pack and carton. The expiration date refers to the last day of that month.
- Disposal: Do not dispose of unused tablets via household waste or wastewater. Return unused medication to a pharmacy for appropriate disposal in accordance with local regulations.
In the hospital setting, nimodipine tablets are typically stored in the pharmacy under controlled conditions and dispensed for individual patient use. Ward-based storage should also ensure light protection, as fluorescent lighting in hospital wards can contribute to photodegradation over time. Some institutions use amber-tinted medication cups or light-protective bags to safeguard individual doses during distribution.
What Does Nimotop Contain?
Understanding the composition of Nimotop is important for patients and healthcare providers, particularly in identifying potential allergens or ingredients that may be contraindicated in specific conditions.
Active Ingredient
The active substance is nimodipine, a 1,4-dihydropyridine calcium channel antagonist. Each film-coated tablet contains precisely 30 mg of nimodipine. Nimodipine is a yellow crystalline powder that is practically insoluble in water, which contributes to its relatively low oral bioavailability and the importance of consistent dosing conditions.
Inactive Ingredients (Excipients)
| Ingredient | Role | Notes |
|---|---|---|
| Nimodipine | Active substance (calcium channel blocker) | 30 mg per tablet |
| Microcrystalline cellulose | Binder / filler | Provides tablet structure |
| Maize starch | Disintegrant / filler | Aids tablet breakdown |
| Povidone K25 | Binder | Holds tablet together |
| Crospovidone | Superdisintegrant | Ensures rapid disintegration |
| Magnesium stearate | Lubricant | Prevents sticking during manufacture |
| Hypromellose | Film-coating agent | Part of the film coat |
| Macrogol 4000 | Plasticizer (film coat) | Provides flexibility to coating |
| Titanium dioxide (E171) | Colorant / opacifier | Provides white base color |
| Iron oxide yellow (E172) | Colorant | Gives characteristic yellow color |
Appearance and Pack Sizes
Nimotop 30 mg tablets are round, yellow, film-coated tablets. They are supplied in blister packs within a cardboard outer carton. Common pack sizes include 30 tablets (sufficient for approximately 2.5 days of treatment at the standard dose) and 100 tablets. A full 21-day treatment course at the standard dose of 60 mg six times daily requires 252 tablets (12 tablets per day × 21 days). Not all pack sizes may be available in every country.
Marketing Authorization and Manufacturer
Nimotop was originally developed and marketed by Bayer AG (Leverkusen, Germany). Bayer retains the marketing authorization in many countries, although the brand may be distributed under different arrangements in certain markets. Nimodipine is also available as a generic medication in several countries following the expiration of patent protection. Generic versions must meet the same regulatory standards for quality, safety, and efficacy as the original branded product.
Frequently Asked Questions About Nimotop
Nimotop (nimodipine) is a prescription calcium channel blocker used specifically to prevent and treat ischemic neurological deficits caused by cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH). Vasospasm is a dangerous narrowing of blood vessels in the brain that can occur 3–14 days after the hemorrhage, potentially leading to stroke and brain damage. Nimodipine is the only drug proven to improve neurological outcomes after SAH and is considered the standard of care worldwide. It is not used as a general blood pressure medication.
Unlike other calcium channel blockers such as amlodipine or nifedipine that primarily target the heart and peripheral blood vessels, nimodipine has a unique preferential selectivity for cerebral (brain) blood vessels. This selectivity is due to its high lipophilicity, which allows it to cross the blood-brain barrier readily and concentrate in cerebral vascular smooth muscle. While other calcium channel blockers are used to treat high blood pressure, angina, and arrhythmias, nimodipine is specifically indicated for cerebral vasospasm after subarachnoid hemorrhage and is not interchangeable with other drugs in its class.
The every-4-hour dosing schedule is based on nimodipine’s pharmacokinetic profile. After oral administration, nimodipine is rapidly absorbed and reaches peak blood levels within about 1 hour. It has a relatively short elimination half-life of approximately 8–9 hours, which means it is cleared from the body relatively quickly. Dosing every 4 hours ensures that therapeutic drug levels are maintained consistently throughout the day, providing continuous protection against vasospasm during the critical 21-day risk period. Missing doses or extending the interval can allow blood levels to fall below the therapeutic threshold.
Nimotop film-coated tablets should ideally be swallowed whole with water. Crushing or breaking the tablets can alter the drug’s release characteristics and expose the photosensitive nimodipine to light, potentially reducing its potency. For patients who cannot swallow tablets (common after subarachnoid hemorrhage), a nimodipine oral solution is available in many countries, which can be administered via nasogastric or orogastric tube. If neither option is available, consult your pharmacist about appropriate alternatives, as some preparations may be suitable for dispersal in water.
The recommendation to start nimodipine within 96 hours of subarachnoid hemorrhage is based on the clinical trial protocols that demonstrated its efficacy. Starting treatment later than 96 hours may reduce its effectiveness, as cerebral vasospasm can begin as early as day 3 after SAH. However, in clinical practice, many neurointensive care teams will still initiate nimodipine even if the window has been slightly exceeded, particularly if the patient has not yet developed vasospasm, as some benefit may still be obtained. The decision should be made by the treating medical team based on the individual clinical circumstances.
Generic nimodipine products approved by regulatory authorities (EMA, FDA, and equivalent agencies) are required to demonstrate bioequivalence with the original brand-name Nimotop. This means they must deliver the same amount of active ingredient to the bloodstream at the same rate, ensuring comparable therapeutic effects. Generic manufacturers must meet the same quality, purity, and stability standards as the original product. In clinical practice, generic nimodipine is widely used and is considered therapeutically equivalent to brand-name Nimotop.
References
- European Medicines Agency (EMA). Nimotop (nimodipine) – Summary of Product Characteristics. Last updated 2024. Available at: EMA.
- U.S. Food and Drug Administration (FDA). Nimodipine capsules/tablets – Prescribing Information. Revised 2023.
- Pickard JD, Murray GD, Illingworth R, et al. Effect of oral nimodipine on cerebral infarction and outcome after subarachnoid haemorrhage: British Aneurysm Nimodipine Trial. BMJ. 1989;298(6674):636–642. doi:10.1136/bmj.298.6674.636.
- Dorhout Mees SM, Rinkel GJE, Feigin VL, et al. Calcium antagonists for aneurysmal subarachnoid haemorrhage. Cochrane Database Syst Rev. 2007;(3):CD000277. doi:10.1002/14651858.CD000277.pub3.
- Connolly ES Jr, Rabinstein AA, Carhuapoma JR, et al. Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke. 2012;43(6):1711–1737. doi:10.1161/STR.0b013e3182587839.
- Steiner T, Juvela S, Unterberg A, et al. European Stroke Organisation Guidelines for the Management of Intracranial Aneurysms and Subarachnoid Haemorrhage. Cerebrovasc Dis. 2013;35(2):93–112. doi:10.1159/000346087.
- Diringer MN, Bleck TP, Claude Hemphill J 3rd, et al. Critical Care Management of Patients Following Aneurysmal Subarachnoid Hemorrhage: Recommendations from the Neurocritical Care Society’s Multidisciplinary Consensus Conference. Neurocrit Care. 2011;15(2):211–240.
- Allen GS, Ahn HS, Preziosi TJ, et al. Cerebral arterial spasm – a controlled trial of nimodipine in patients with subarachnoid hemorrhage. N Engl J Med. 1983;308(11):619–624. doi:10.1056/NEJM198303173081103.
- World Health Organization (WHO). WHO Model List of Essential Medicines. 23rd list, 2023. Available at: WHO Essential Medicines.
- British National Formulary (BNF). Nimodipine. National Institute for Health and Care Excellence (NICE). 2025.
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