Nimotop (nimodipine) is a calcium channel blocker specifically formulated for the prevention and treatment of neurological deficits due to cerebral vasospasm following subarachnoid hemorrhage (SAH) from ruptured intracranial berry aneurysms. Its high selectivity for cerebral arteries allows it to exert a targeted effect, improving blood flow in compromised brain regions without causing significant systemic hypotension. Administered orally, it represents a critical component of post-SAH neuroprotective management, supported by extensive clinical evidence demonstrating its efficacy in reducing the incidence and severity of ischemic deficits. This specialized agent is a cornerstone of neurocritical care protocols aimed at mitigating secondary brain injury.

Features

• Active Pharmaceutical Ingredient: Nimodipine 30 mg
• Pharmacologic Class: Dihydropyridine Calcium Channel Blocker
• High Lipophilicity for Superior Blood-Brain Barrier Penetration
• Selective Cerebrovascular Activity with Minimal Peripheral Vasodilation
• Available in 30 mg Soft Gelatin Capsules for Oral Administration
• Specific Formulation Optimized for Neurological Indications

Benefits

• Reduces the incidence and severity of ischemic neurological deficits resulting from cerebral vasospasm.
• Improves cerebral blood flow to vulnerable regions of the brain following a subarachnoid hemorrhage.
• Contributes to better overall neurological outcomes and functional recovery post-SAH.
• Offers a targeted therapeutic approach with a well-established efficacy and safety profile in neurocritical care.
• Helps mitigate the risk of delayed cerebral ischemia, a major cause of morbidity and mortality after aneurysm rupture.

Common use

Nimotop is exclusively indicated for the improvement of neurological outcome by reducing the incidence and severity of ischemic deficits in patients with subarachnoid hemorrhage (SAH) from ruptured congenital intracranial berry aneurysms who are in good neurological condition post-ictus (e.g., Hunt and Hess Grades I-III). Its use is prophylactic and therapeutic, aimed at preventing the cerebral arterial spasm that typically occurs 4 to 14 days after the initial bleed. It is a standard of care in post-neurosurgical and neurocritical care management protocols following securing of the aneurysm (via clipping or coiling) to prevent secondary brain injury.

Dosage and direction

The dosage of Nimotop is 60 mg (two 30 mg capsules) every 4 hours for 21 consecutive days, commencing within 96 hours of the subarachnoid hemorrhage. Oral administration is mandatory; the capsules must be swallowed whole with a glass of water. If the patient is unable to swallow, a hole should be carefully pierced in both ends of the capsule with an 18-gauge needle and the contents emptied into a syringe. The contents must then be withdrawn into the syringe and administered via nasogastric tube, followed by flushing the tube with 30 mL of normal saline. Dosage should be reduced to 30 mg every 4 hours in patients with hepatic cirrhosis or significantly impaired liver function. Therapy must be continued for the full 21-day course regardless of the patient’s early neurological status.

Precautions

Blood Pressure Monitoring: Nimodopine can cause hypotension. Blood pressure should be monitored closely during initiation and throughout the therapy, especially in patients with pre-existing hypotension or those on other antihypertensive agents. Hepatic Impairment: Nimodipine is extensively metabolized by the liver. Patients with liver disease require a dosage reduction and careful monitoring for increased drug exposure and adverse effects. Cardiovascular Disease: Use with caution in patients with severe heart failure or significantly impaired left ventricular function. Gastrointestinal Absorption: Absorption may be significantly reduced by substances that increase gastric pH (e.g., cimetidine). Concomitant administration should be avoided. Porphyria: Nimodipine should be used with extreme caution, if at all, in patients with a history of porphyria, as it may precipitate an attack.

Contraindications

• Known hypersensitivity to nimodipine, any other calcium channel blocker, or any component of the capsule formulation.
• Concomitant administration with strong CYP3A4 inhibitors such as ketoconazole, itraconazole, clarithromycin, or ritonavir, due to the high risk of significantly increased nimodipine plasma levels and severe hypotension.
• Patients with cardiogenic shock or decompensated heart failure.
• Use in patients with a history of porphyria is generally contraindicated.

Possible side effect

The most common side effects are related to its pharmacological action as a vasodilator, though its cerebroselectivity limits systemic effects. Cardiovascular: Hypotension (dose-related), flushing, edema, tachycardia, bradycardia, palpitations. Gastrointestinal: Nausea, diarrhea, abdominal discomfort. Neurological: Headache, dizziness. Dermatological: Rash, pruritus. Other: Dyspnea, muscle cramps/cpain. Serious adverse reactions include profound hypotension, which requires medical intervention, and rare instances of ileus and hepatitis.

Drug interaction

Nimodipine is a substrate of the CYP3A4 enzyme system. Concomitant use with strong inhibitors or inducers of this enzyme can lead to significant interactions.

• Strong CYP3A4 Inhibitors (CONTRAINDICATED): Ketoconazole, itraconazole, clarithromycin, ritonavir, nefazodone. These drugs drastically increase nimodipine plasma concentrations, leading to a high risk of severe hypotension and cardiovascular adverse events.
• Moderate CYP3A4 Inhibitors (Use with Caution): Diltiazem, verapamil, fluconazole, erythromycin. May increase nimodipine levels; blood pressure must be monitored closely, and a dosage reduction may be necessary.
• CYP3A4 Inducers: Phenytoin, carbamazepine, phenobarbital, rifampin, St. John’s Wort. These drugs may decrease nimodipine plasma levels, potentially reducing its efficacy.
• Other Antihypertensives: Beta-blockers, ACE inhibitors, other calcium channel blockers. Concomitant use can have an additive hypotensive effect.
• Alpha-blockers (e.g., prazosin): May potentiate the hypotensive effect of nimodipine.

Missed dose

If a dose is missed, it should be taken as soon as it is remembered. However, if it is almost time for the next scheduled dose, the missed dose should be skipped, and the regular dosing schedule resumed. The patient should not take a double dose to make up for the missed one. Maintaining the strict 4-hourly schedule is important for efficacy, so healthcare providers should implement measures (e.g., strict medication administration records) to minimize missed doses in the inpatient setting.

Overdose

Overdose would be expected to manifest as significant, profound hypotension and reflex tachycardia due to excessive peripheral vasodilation. Other symptoms could include bradycardia, dizziness, drowsiness, nausea, and gastrointestinal disturbances. In case of suspected overdose, medical attention must be sought immediately. Management is primarily supportive and symptomatic. This includes placing the patient in a supine position with legs elevated, vigorous intravenous fluid administration, and careful monitoring of vital signs and urinary output. The use of vasopressors (e.g., dopamine or norepinephrine) may be necessary to support blood pressure. As nimodipine is highly protein-bound, dialysis is not likely to be of benefit.

Storage

Store Nimotop capsules at controlled room temperature, 20°C to 25°C (68°F to 77°F), with excursions permitted between 15°C and 30°C (59°F and 86°F). Protect from light and moisture. Keep the bottle tightly closed and out of reach of children. Do not freeze. Do not use beyond the expiration date printed on the packaging.

Disclaimer

This information is intended for educational and informational purposes only for healthcare professionals and does not constitute medical advice. It is not a substitute for professional medical judgment, diagnosis, or treatment. The content is derived from the manufacturer’s prescribing information but may not be exhaustive. Always refer to the full official prescribing information before initiating or monitoring therapy. Dosage and treatment decisions must be made by a qualified physician based on the individual patient’s clinical condition, contraindications, and potential drug interactions.

Reviews

“Nimotop remains a foundational, evidence-based therapy in our neuro-ICU for post-aSAH management. Its targeted cerebrovascular effect is evident in practice, and we observe a tangible reduction in symptomatic vasospasm in patients who complete the full course. The main challenge is diligent BP monitoring, but the benefit in neurological preservation is unequivocal.” – Neurocritical Care Specialist, Academic Medical Center.

“While the administration logistics for non-oral patients can be cumbersome, the clinical data supporting nimodipine’s use is robust. It’s one of the few drugs with a clear, proven benefit in improving outcomes after a devastating subarachnoid hemorrhage. It’s a staple in our post-operative orders for aneurysm patients.” – Vascular Neurosurgeon.