• Lipophilic dihydropyridine Ca++ antagonist
  • Improves outcome after SAH ( reduced incidence & severity of cerebral ischaemia)
  • Moderate cerebral vasodilation not thought to be mechanism of action
  • Mainly limits intracellular Ca++ influx and so reduces ischaemic damage
  • Good PO absorption


  • SAH Significantly better prognosis.
  • 60% of SAH die (in 6 month) if no Neurosurgery i.e. delayed ischaemia
  • Delayed ischaemia = confusion, level conc. ± localizing signs.
  • Spasm generally on day 2-3 (max spasm frequency on day 6-8)

Causes of cerebral ischaemia post SAH

Cerebral Art Narrowing

Vasospasm, thrombosis, embolism from aneurysmal clot, atheroma, tentorial herniation compressing post cerebral art, antifibrinolytic therapy


Antihypertensive drugs, arrhythmia, low cardiac output, medullary compression


Dehydration, hyponatraemia

High ICP

Rebleed, hydrocephalus, IC haematoma, cerebral hyperaemia/oedema, giant aneurysm


Hyperglycaemia, epilepsy

ABG abnormal

Hypoxia, hypercapnia


Latest nimodipine trial = BRANT (Br Aneurysmal Nimo Trial)

  • Nimodipine 60mg 4 hourly - cerebral ischaemia = 22%
  • Placebo - cerebral ischaemia = 33%
  • Poor outcomes 4-0% lower in Nimodipine group
  • Higher doses no better

Head injury

  • No improvement

Stroke - TRUST study

  • 1215 patients = no indication for Nimodipine use

Cognitive impairment

  • Some studies show trend improvement in dementia


  • No improvement

Adverse Rxns

  • Small ↓ BP (mild)
  • Flushing
  • Occasional jaundice

Content by Dr Íomhar O' Sullivan 12/06/2007. Last review Dr ÍOS 15/06/21