Nimotop(R) (nimodipine) 30-mg Capsules
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21-Day Therapy

Why 21-day therapy for SAH?

The risks of vasospasm and ischemic deficits extend through the third week after SAH.

  • After SAH, both vasospasm and delayed cerebral ischemia typically begin at day 3, peak between days 7 and 12, and may continue through day 21.1-7

  • Only 37% of cerebral ischemic events occur during days 7-10 after SAH; infarction may occur as late as day 40.8



  • Blood-flow velocities become maximal 7-20 days after SAH.10

  • Critically high blood-flow velocities* (>120 cm/sec) have been correlated strongly with vasospasm on angiograms.10

Nimotop® is indicated for the improvement of neurological outcome by reducing the incidence and severity of ischemic deficits in patients with subarachnoid hemorrhage from ruptured intracranial berry aneurysms regardless of their post-ictus neurological condition (e.g. Hunt and Hess Grades I-V).8

Nimotop® therapy should begin within 96 hours of the aneurysmal subarachnoid hemorrhage regardless of angiographic evidence of vasospasm. The recommended course of therapy is 21 days.8

To learn more about the efficacy of Nimotop® in clinical trials using 21-day dosage, click here.

To learn more about dosage and administration, click here


Sources:
  1. Kassell NF. Treatment outcome of SAH: comments derived from the National Cooperative Aneurysm Study.

  2. Kassell NF, Sasaki T, Colohan ART, Nazar G. Cerebral vasospasm following aneurysmal subarachnoid hemorrhage. Stroke. 1985;16:562-572.

  3. Saito I, Ueda Y, Sano K. Significance of vasospasm in the treatment of ruptured intracranial aneurysms. J Neurosurg. 1977;47:412-429.

  4. Torner JC, Kassell NF, Haley EC Jr. The timing of surgery and vasospasm. Neurosurg Clin North Am. 1990;1:335-347.

  5. Weir B, Grace M, Hansen J, et al. Time course of vasospasm in man. J Neurosurg. 1978;48:173-178.

  6. Biller J, Godersky JC, Adams HP. Management of aneurysmal subarachnoid hemorrhage. Stroke. 1988;19:1300-1305.

  7. Heros R, Zervas NT, Varsos V. Cerebral vasospasm after subarachnoid hemorrhage: an update. Ann Neurol. 1983;14:599-608.

  8. Pickard JD, Murray GD, Illingworth R, et al. Effect of oral Nimotop® on cerebral infarction and outcome after subarachnoid haemorrhage: British aneurysm Nimotop® trial. BMJ. 1989;298:636-642.

  9. Seiler RW, Grolimund P, Zurbruegg HR. Evaluation of the calcium-antagonist nimotop for the prevention of vasospasm after aneurysmal subarachnoid haemorrhage: a prospective transcranial Doppler ultrasound study. Acta Neurochir (Wein). 1987;85:7-16.

  10. Harders AG, Gilshach JM. Time course of blood velocity changes related to vasospasm in the circle of Willis measured by transcranial Doppler ultrasound. J Neurosurg. 1987;66:718-728.


DO NOT ADMINISTER NIMOTOP INTRAVENOUSLY OR BY OTHER PARENTERAL ROUTES. DEATHS AND SERIOUS, LIFE-THREATENING ADVERSE EVENTS HAVE OCCURRED WHEN THE CONTENTS OF NIMOTOP CAPSULES HAVE BEEN INJECTED PARENTERALLY

(See WARNINGS and DOSAGE AND ADMINISTRATION.)


 
  • In patients with SAH, Nimotop® controls damage with a low side effect profile.

  • Decreased blood pressure is the most common side effect, occurring in 4.4% of patients. Blood pressure should be monitored during therapy.1

  • Other side effects occurring at a low frequency of ≥1.0% include headache, nausea, and bradycardia.1

  • No clinically significant effects on hematologic factors, renal or hepatic function, or carbohydrate metabolism have been causally associated with oral nimodipine.1

  • Nimotop® does not appear to affect anesthetic management.2
 
Sources:
  1. Nimotop® (nimodipine) Capsules Prescribing Information December 2005

  2. Stullken EH, Johnston WE, Prough DS. Implications of nimodipine prophylaxis of cerebral vasospasm on anesthetic management during intracranial aneurysm clipping. J. Neurosurg. 1985; 62:200-205.



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