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About SAH

Epidemiology

Risk Factors

Clinical Manifestations

Diagnosis

Classification of SAH

Therapeutic Measures
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Risk Factors

Although the overall stroke rate decreased between 1945 and 1984, there was no apparent change in incidence of SAH during this period, suggesting an inability to identify and manage risk factors for SAH.1


Unruptured aneurysms. Large autopsy studies suggest that approximately 11 million persons in the U.S. have or will have unruptured intracranial aneurysms-the most definitive risk factor for SAH.1 The annual risk of SAH in these patients is estimated at I %-2%.2 Since the risk continues from year to year, a young person with an incidental intracranial aneurysm has about an even chance of having a major SAH during the next 20-30 years.3 The risk of SAH increases when the size of the unruptured aneurysm exceeds 3-5 mm in diameter. Guidelines published by the AHA Stroke Council recommend surgical clipping of unruptured aneurysms larger than 5-7 mm in patients who have acceptable surgical risk.2

Genetic factors. The risk of SAH is fourfold higher in first-degree relatives of SAH patients than in the general population.4 Epidemiological studies indicate that 7%o-20% of patients with SAH have first- or second-degree relatives with unruptured aneurysms. Although these findings suggest potential genetic linkage in SAH, the identity of specific genetic loci as well as their effect on the etiology of aneurysms and SAH remains unknown. Intracranial aneurysms have been associated with a number of inherited connective tissue disorders; these include polycystic kidney disease, Marfan's syndrome, and Ehlers-Danlos syndrome. However, current guidelines do not advocate angiographic screening for unruptured aneurysms among these high-risk patients.2

Smoking. Cigarette smoking is the only factor that has been consistently and strongly associated with increased risk of SAH.2 Cigarette smoking increases risk of symptomatic vasospasm after SAH.5 People who quit smoking appear to have reduced SAH risk relative to current smokers, with the time since smoking cessation being inversely related to SAH risk.6,7

Hypertension. Although hypertension is a recognized risk factor for hemorrhagic stroke, little information is available on whether elevated blood pressure increases risk of aneurysmal SAH. It should be recognized that improvements in blood pressure control over the past 20 years have not been paralleled by a reduced incidence of SAH.2 Guidelines published by the AHA Stroke Council strongly recommend blood pressure control as a means of reducing stroke of varying etiology.2

Increased age. Most clinical series of SAH show a peak incidence in the fifth and sixth decades of life. When corrected for age distribution within the population, the rate increases with age.8

Female gender. Epidemiologic studies show that SAH is the only type of hemorrhagic stroke that is more common in women than in men,9 but prospective studies do not support this finding.8 In a meta-analysis of SAH incidence studies between 1960 and 1994, Linn et al. found a significant effect of sex in 6 studies that analyzed men and women separately, but the higher risk for women was based on only one-fifth of all patients in their review, which prevented them from confirming these findings.10 Labor and delivery (but not pregnancy per se) may increase the risk of SAH, according to a study of maternal deaths in Minnesota between 1950 and 1973.11 In this study SAH was found to be the eighth-leading cause of maternal death, accounting for 4.4% of the 843 deaths, and aneurysmal rupture has been cited as a factor in 12%-25% of maternal deaths.

Other factors. Several other factors, including alcohol or binge drinking and drug abuse, have been associated with increased risk of SAH in case reports or cohort studies.6,12,13



Back to Epidemiology Next: Clinical Manifestations


Sources:
  1. Weibers WO, Torner JC, Meissner MD. Impact of unruptured intracranial aneurysm on public health in the United States. Stroke 1992;23:1416-1419.

  2. Mayberg MR, Batjer HH, Dacey R et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage: a statement for healthcare professionals from a special writing group of the Stroke Council, American Hearth Association. Stroke 1994;25:2315-2328.

  3. Heros RC, Zervas NT. Subarachnoid hemorrhage. Annu Rev Med. 1983;34:367-375.

  4. Schievink WI. Genetics of intracranial aneurysms. Neurosurgery 1997;40:651-662.

  5. Lasner TM, Weil RJ, Riina HA, et al. Cigarette smoking-induced increase in the risk of symptomatic vasospasm after aneurysmal subarachnoid hemorrhage. J Neuroseurg 1997;87:381-384.

  6. Longsrreth WT Jr, Nelson LM, Koepsell TD, van Belle G. Cigarette smoking, alcohol use, and subarachnoid hemorrhage. Stroke 1992;23:1242-1249.

  7. Kawachi I, Colditz GA, Stampfer MJ, et al. Smoking cessation and decreased risk of stroke in women. JAMA 1993;269:232-236.

  8. King JT Jr. Epidemiology of aneurysmal subarachnoid hemorrhage. Neuroimag Clin North Am 1997;7;659-668.

  9. Davis P. Stroke in women. Curr Opin Neurol 1994;7:36-40.

  10. Linn FHH, Wijdick EFM, van der Graaf Y, Weerdesteyn-van Vliet FAC, Bartelds AIM, van Gijn J. Prospective study of sentinel headache in aneurysmal subarachnoid hemorrhage. Stroke 1992;23:1242-1249.

  11. Barno A, Freeman DW. Maternal deaths due to spontaneous subarachnoid hemorrhage. Am J Obstet Gynecol 1976;125:384-392.

  12. Gill JS, Shipley MJ, Tsementzis SA, et al. Alcohol consumption: a risk factor for hemorrhagic and non-hemorrhagic stroke. Am J Med 1991;90:489-497.

  13. Oyesiku NM, Colohan AR, Barrow DL, Reisner A. Cocaine-induced aneurysmal rupture: an emergent factor in the natural history of intracranial aneurysms? Neurosurgery 1993;32:518-526.

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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