• vasospasms (VSPs) in SAH are provoked by the blood in the subarachnoid space. The breakdown products lead to changes in the artery wall involving cytokines, inflammatory response, free radical production, and others ⇒ resulting in artery contraction or structural changes with thickening of the vessel wall [Dorsch, 1995].
  • VSPs appear on days 3-4, with a peak on days 5-9; VSPs may persist for up to 3-4 weeks
    • when detected < 3 days after SAH,  a previous episode of bleeding can be assumed
  • VSPs appear most commonly in the artery with a ruptured aneurysm
  • occurrence in up to 70% of patients with SAH, about 1/3-1/2 are symptomatic – leading to Delayed Ischemic Deficit (DID), which is the leading cause of neurological deficits (focal deficits, encephalopathy) and mortality in SAH patients [Dorsch, 2002]
  • patients at risk for developing spasms:
    • at a younger age
    • with more blood in the SA space (see Fisher grade)
    • with worse baseline clinical status (higher Hunt-Hess score)
    • with late treatment initiation
  • early diagnosis and correct treatment of VSP can prevent or at least minimize the development of DID
Vasospasms in subarachnoid hemorrhage
  • a clinical syndrome manifested by cognitive changes and/or focal neurological impairment lasting ≥ 1h and/or cerebral infarction
  • present in approximately 30% of patients with SAH  (Yamaki, 2019)
  • multifactorial etiology
    • vasospasms (VSP)
    • intracranial hypertension, cerebral edema, and impaired vascular autoregulation
    • presence of cortical spreading depression ⇒ microvascular dysfunction
    • micro-thrombosis due to activation of the coagulation cascade and due to inhibition of the fibrinolysis (microemboli are detectable by TCD/TCCD)
  • exclude another cause of clinical deterioration (rebleeding, hydrocephalus, intracranial hemorrhage, etc.)

Vasospasms Classification

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Clinical presentation

  • worsening of headaches and neck stiffness
  • confusion, disorientation, decreased consciousness
  • new focal neurological deficits
  • fever

Vasospasms Detection


  • TCD/TCCD allows repeated bedside monitoring  ( → TCCD diagnosis of vasospasms)
    • in VSP, a typical velocity increase of > 50 cm/s or 25%/24h can be detected
  • the progression of intracranial hypertension can be assessed → see here


  • NCCT excludes recurrent bleeding, obstructive hydrocephalus, or edema progression
  • CTA reveals the extent and severity of vasospasms
  • CT perfusion (CTP) allows assessment of the risk of DID ⇒ in the territory of the affected artery; there is a prolonged transit time (TTP, MTT) and, in severe cases, a decrease in regional perfusion (CBF) or blood volume (CBV) appears → pattern of ischemic injury  Vasospasm on CTA with hypoperfusion proved by CT perfusion    [Binaghi, 2007]
  • MRI outperforms CT in the evaluation of vasospasm-induced ischemia (DWI)
  • it has better sensitivity to small hemorrhages as well (GRE / SWI)
  • MRA and MR perfusion detect VSPs and assess their hemodynamic significance  MCA vasospasm on MRA


  • considered as the “gold standard”
  • the typical finding on DSA is a segmental narrowing of the artery
  • detection of vasospasms in peripheral, less easily visualized vessels remains a limiting factor
Vasospasm on DSA


  • individual approach
  • take these factors into account:
    • the severity of vasospasm
    • presence of significant hypoperfusion in distal circulation
    • dynamics
    • number and localization of VSP (focal or diffuse, single or multiple VSP)
    • signs of hyperperfusion
    • signs of intracranial hypertension
    • clinical status

Maintaining Cerebral Perfusion

  • effect of 3H therapy (Hypertension, Hypervolemia, and Hemodilution) is not proven
    • a review of controlled trials showed no positive impact of 3H therapy or its components on increasing cerebral blood flow) [Dankbaar, 2010]
  • maintain normovolemia with CVP at 10-12 cm H2O  (mm Hg) or pulmonary artery wedge pressure (PAWP) at 14-20 mmHg
  • maintain the hematocrit at 30-35% to optimize blood viscosity
  • SBP should be maintained preoperatively ≤ 130-140 mmHg, postoperatively 150-175 mmHg
  • administer inotrope agents and vasopressors if MAP < 90 mm Hg

Drug therapy

  • nimodipine and cilostazol are likely the most effective treatments for preventing morbidity and mortality  (Dayyani, 2022)
  • clazosentan, nicardipine, and magnesium have beneficial effects on delayed cerebral ischemia and vasospasms, but they were not found to reduce mortality or disability (Dayyani, 2022)
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Angioplasty, local application of vasodilatory drugs

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Thrombolytic therapy

  • meta-analysis suggests a clinically relevant beneficial effect of subarachnoid clot removal achieved by intracisternal tPA injections. (Amin-Hanjani, 2004]
    • ARR of 14.4% for delayed ischemic neurological deficit
  • therapy is associated with an increased risk of intracranial bleeding
  • clinical trials are needed to establish the safety and efficacy of this approach
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Vasospasms in subarachnoid hemorrhage
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