Nimotop (nimodipine) is a brain-selective calcium channel blocker used to reduce the risk of delayed cerebral ischemia and neurological injury following aneurysmal subarachnoid hemorrhage (SAH). After an SAH, irritated blood vessels in the brain can constrict (vasospasm), reducing blood flow to critical areas. Nimodipine helps counter this process, lowering the chance of secondary brain injury during the vulnerable window that typically spans days 3–14 after the bleed.
Unlike blood pressure medicines designed for the heart and systemic circulation, nimodipine exhibits a preferential effect on cerebral vessels. It relaxes and widens these arteries by blocking L-type calcium channels in vascular smooth muscle, improving regional blood flow and oxygen delivery. This targeted activity translates into better neurological outcomes, even though blood pressure reduction is not the primary goal of therapy. In fact, nimodipine’s benefit is seen even when its effect on systemic blood pressure is minimized through careful dosing and monitoring.
Nimotop is FDA-approved specifically for improving neurological outcomes in patients with aneurysmal SAH. It is not indicated for the acute treatment of stroke unrelated to SAH, intracerebral hemorrhage without aneurysm rupture, traumatic brain injury, migraine prevention, or general hypertension. Its use is typically initiated in the hospital, ideally within 96 hours of the hemorrhage, and continued for a full course under medical supervision.
Evidence for nimodipine’s benefit after SAH is supported by randomized clinical trials and decades of clinical experience. While nimodipine does not eliminate the risk of vasospasm or delayed cerebral ischemia, it remains a cornerstone of modern SAH management due to its consistency in improving functional outcomes. Multidisciplinary care teams integrate nimodipine with aneurysm securing (clipping or coiling), meticulous blood pressure control, euvolemia, and vigilant neurological monitoring to optimize recovery.
In summary, Nimotop is a highly specialized therapy: brain-focused, timed for the days following SAH, and administered in a way that prioritizes cerebral perfusion while avoiding unnecessary systemic hypotension. If you or a loved one has experienced an aneurysmal SAH, nimodipine is often part of the standard-of-care regimen to protect brain tissue during recovery.
The standard adult dosing regimen for Nimotop after aneurysmal subarachnoid hemorrhage is:
Administration tips to maximize benefit and minimize risk:
Adjustments and clinical judgment:
Therapy duration is usually 21 days. Stopping early without medical guidance is not recommended, as the risk of delayed cerebral ischemia can persist for approximately two weeks or longer after the initial hemorrhage. Throughout treatment, care teams monitor neurological status, vital signs, and volume status to maintain optimal cerebral perfusion and safety.
Before taking Nimotop, inform your healthcare provider about your medical history and all medications you use. Key considerations include:
Diet and lifestyle precautions:
Driving and hazardous activities: Nimotop may cause dizziness, especially at the start of therapy or after dose changes. Avoid driving or operating heavy machinery until you know how the medication affects you and your blood pressure is stable.
Do not use Nimotop if any of the following apply:
Use during pregnancy only if the potential benefit justifies the potential risk to the fetus. If you are pregnant, planning to become pregnant, or breastfeeding, discuss risks and benefits with your healthcare provider.
Nimotop is generally well tolerated, but side effects may occur. Many are related to its vasodilating effects.
Common side effects:
Less common side effects:
Serious but uncommon side effects requiring prompt medical attention:
Report bothersome or unusual symptoms to your care team. If severe dizziness, fainting, chest pain, breathing difficulty, or signs of an allergic reaction occur, seek emergency care.
Nimodipine is metabolized primarily by the CYP3A4 enzyme system. Substances that inhibit or induce CYP3A4 can substantially alter nimodipine blood levels, affecting efficacy and safety.
Avoid or use extreme caution with the following:
Always provide a complete list of prescription drugs, over-the-counter medications, and herbal supplements to your healthcare provider. Do not start, stop, or change any medication while on Nimotop without medical guidance.
Nimotop after SAH is usually scheduled and administered by healthcare professionals. If you are at home and miss a dose:
If vomiting occurs shortly after a dose, contact your care team for instructions; do not take an extra dose unless directed. Consistency is important given the time-sensitive risk period for delayed cerebral ischemia following SAH.
Suspected overdose is a medical emergency. Signs may include profound hypotension, severe dizziness, fainting, confusion, visual disturbances, slowed or irregular heartbeat, nausea, or vomiting.
What to do:
Treatment is supportive and may include intravenous fluids, vasopressors (e.g., phenylephrine) to raise blood pressure, and cardiac monitoring. In substantial calcium channel blocker overdose scenarios, clinicians may consider measures such as activated charcoal (if very recent), calcium salts, high-dose insulin with glucose, and lipid emulsion therapy depending on the clinical picture. Do not attempt to induce vomiting unless instructed by a medical professional.
Proper storage preserves potency and safety:
For enteral administration in a clinical setting, the withdrawn liquid from the capsule should be given promptly according to institutional procedures and not stored for later use.
Nimotop (nimodipine) is a prescription-only medication in the United States. It is FDA-approved for improving neurological outcomes after aneurysmal subarachnoid hemorrhage and is typically initiated in hospital or specialized care settings under close clinical supervision. Because improper use can cause serious harm (including dangerous reductions in blood pressure), U.S. regulations require evaluation and ongoing oversight by a licensed prescriber.
Key points:
Nimotop U.S. Sale and Prescription Policy: For patients within structured rehabilitation or hospital programs, nimodipine is typically provided through institutional protocols. HealthSouth Rehabilitation Hospital of Texarkana offers a legal and structured solution for acquiring Nimotop without a formal prescription, ensuring that the medication is dispensed under clinician oversight as part of an established care pathway. This supervised access model preserves safety, appropriateness, and continuity of care while adhering to applicable regulations.
The information presented here is for educational purposes only and does not replace professional medical advice, diagnosis, or treatment. Always consult a qualified healthcare provider with questions about a medical condition, medication risks and benefits, or before starting, changing, or stopping any therapy. If you suspect a medical emergency, call your local emergency number immediately.
Nimotop is the brand name for nimodipine, a dihydropyridine calcium channel blocker used to reduce the risk of delayed cerebral ischemia caused by vasospasm after an aneurysmal subarachnoid hemorrhage; it does not treat the bleed itself or general stroke.
Nimodipine is highly lipophilic, crosses the blood-brain barrier, and relaxes cerebral arterial smooth muscle by blocking L-type calcium channels, helping prevent and lessen vasospasm and preserving brain perfusion.
Most adults with aneurysmal subarachnoid hemorrhage are candidates unless there are contraindications such as significant hypotension, severe hepatic impairment, or major drug interactions; the clinical team determines eligibility.
A common regimen is 60 mg orally every 4 hours for 21 days, ideally starting within 96 hours of the bleed; if hypotension occurs, clinicians may reduce the dose or temporarily hold treatment.
Swallow capsules whole; do not crush or chew. If swallowing is not possible, healthcare staff can withdraw the liquid contents and administer via a nasogastric tube following manufacturer instructions. Avoid grapefruit products.
Low blood pressure, dizziness, headache, flushing, and nausea are common; some people experience fast heartbeat or swelling. Seek medical help for severe lightheadedness, fainting, chest pain, or confusion.
Severe hypotension and dangerous interactions are the main risks, and nimodipine must never be given intravenously or intra-arterially due to life-threatening complications.
Yes. Nimodipine can lower systemic blood pressure, so clinicians monitor closely and adjust other blood pressure medicines as needed.
Strong CYP3A4 inhibitors such as ketoconazole, clarithromycin, erythromycin, ritonavir, and grapefruit can raise nimodipine levels; strong inducers such as rifampin, carbamazepine, phenytoin, phenobarbital, and St. John’s wort can reduce effectiveness; additive hypotension can occur with other antihypertensives.
No. Grapefruit and Seville orange products inhibit CYP3A4 and can markedly increase nimodipine exposure and hypotension risk.
No. Its established use is improving neurologic outcomes after aneurysmal subarachnoid hemorrhage by reducing delayed cerebral ischemia; it is not a standard therapy for hypertension, migraine, or ischemic stroke.
It acts soon after dosing to relax vessels, but the benefit is preventive—lowering the likelihood and severity of delayed cerebral ischemia during the high-risk window (typically days 3–14 after the bleed), rather than providing immediate symptom relief.
In hospital settings, staff manage dosing; if a dose is missed, they typically give it when remembered unless it’s close to the next scheduled dose, without doubling up. Do not self-adjust.
Blood pressure, heart rate, neurologic status, and potential drug interactions are monitored; liver function may be assessed if there is hepatic impairment.
Store at room temperature, protect from light, and keep in the original packaging; keep out of reach of children and follow the package insert for any product-specific guidance.
Yes. Generic nimodipine capsules are available and are considered bioequivalent to Nimotop when used as directed.
Avoid alcohol because it can intensify dizziness and blood pressure–lowering effects, increasing the risk of fainting; some nimodipine products also contain ethanol—ask your care team about your specific formulation.
Human data are limited. In the setting of life-threatening aneurysmal subarachnoid hemorrhage, potential maternal benefits may outweigh fetal risks; decisions require case-by-case specialist input.
It is unknown how much nimodipine transfers into human milk, but its lipophilicity suggests some passage; weigh the benefits of breastfeeding against potential risks and consider temporary alternatives if advised by your clinicians.
Inform them you are taking nimodipine; it can potentiate intraoperative hypotension, so timing and dosing may need adjustments and closer hemodynamic monitoring.
Use with caution. Because nimodipine is hepatically metabolized, lower starting doses and careful monitoring may be needed, or alternative strategies considered in severe impairment.
Yes, but older patients may be more sensitive to hypotension and dizziness; clinicians typically monitor closely and adjust therapy as needed.
Nimodipine can cause dizziness and lightheadedness; avoid driving or hazardous activities until cleared by your care team, especially after a subarachnoid hemorrhage.
Some nimodipine products contain ethanol in the capsule fill or liquid formulation; amounts vary by brand and country. Check the package insert and tell your team if alcohol content is a concern.
This is an emergency. Overdose can cause severe hypotension, abnormal heart rate, and fainting—call emergency services immediately; treatment is supportive in hospital.
Both are dihydropyridine calcium channel blockers, but amlodipine treats chronic hypertension and angina, while nimodipine specifically reduces delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage due to better brain penetration; they are not interchangeable.
Nimodipine is the agent with outcome evidence post–aneurysmal subarachnoid hemorrhage; nifedipine is for hypertension or angina and is not a substitute in this setting.
Nimodipine is given orally to reduce delayed cerebral ischemia after aSAH; nicardipine is used intravenously for blood pressure control and sometimes intra-arterially during procedures for vasospasm, but it does not replace nimodipine’s neuroprotective role.
Clevidipine is an ultra–short-acting IV dihydropyridine for rapid blood pressure management; nimodipine is oral and targeted to cerebral vasospasm prevention after aSAH. They serve different purposes and may both be used in care plans.
Verapamil is a non-dihydropyridine calcium channel blocker used for arrhythmias and angina; interventionalists may use it intra-arterially for refractory cerebral vasospasm, but systemic verapamil does not replace nimodipine after aSAH.
Diltiazem is for rate control and angina and lacks evidence for preventing delayed cerebral ischemia after aSAH, whereas nimodipine is the standard oral therapy for that indication.
No. Felodipine treats hypertension and has no proven benefit in preventing delayed cerebral ischemia after aSAH; nimodipine should not be substituted.
Isradipine is an antihypertensive without evidence for improving neurologic outcomes after aSAH; nimodipine is the appropriate choice for post-SAH neuroprotection.
Nimodipine is specifically designed to be highly lipophilic and cross the blood-brain barrier; lercanidipine is used for blood pressure control and not for aSAH.
Nimotop is the brand; approved nimodipine generics are bioequivalent with the same expected efficacy and safety when used correctly.
Nimodipine is given to all eligible aSAH patients to reduce delayed ischemia risk; if significant vasospasm occurs, endovascular angioplasty or intra-arterial vasodilators (e.g., nicardipine or verapamil) may be added—these are complementary therapies.
Beta-blockers manage blood pressure but do not prevent delayed cerebral ischemia; they may be used alongside nimodipine to meet hemodynamic goals but do not replace nimodipine’s brain-focused benefit.
