Cerebral vasospasm following subarachnoid haemorrhage

Dr Dan J Bell and A.Prof Frank Gaillard et al.

Cerebral vasospasm following subarachnoid haemorrhage is a major complication of subarachnoid haemorrhage (SAH). It is overtaking rebleed as the major cause of mortality and morbidity in the subgroup of patients with SAH who reach the hospital and receive medical care.

It is seen in 40-70% of SAH patients on vascular imaging, and becomes clinically apparent in 20-30% of patients, typically from the 4th to 10th day post bleed 1.

Vasospasm can be clinically silent. However, symptomatic vasospasm is defined as new focal neurological symptoms or deterioration of the level of consciousness attributable to vasospasm-induced ischaemia after other aetiologies have been ruled out 2. As such, symptomatic vasospasm is often referred to as 'delayed cerebral ischaemia' in the medical literature 2.

About half of the symptomatic patients will show severe permanent neurological deficits or die 1.

After decades of research the exact mechanism(s) responsible remain elusive although a number of candidate agents are demonstrated to play a role. These include:

  • NO (nitrous oxide)
  • endothelin 1 
  • oxyhaemoglobin
  • others:
    • thrombin
    • serotonin
    • thromboxane A2
    • noradrenaline
    • sphingosine-1-phosphate

Most likely the 'true' pathway involves multiple agents interacting with each other, both biochemically and via changes in gene expression, accounting for the delay of onset.

Oxyhaemoglobin, highest in concentration in arterial blood, appears to simultaneously up-regulate the expression of endothelin 1 (ET-1) and reduce the efficacy of NO.

This results in alteration of normal vascular tone, resulting in narrowing of the large vessels. Increasingly it is also becoming apparent that small calibre vessels which are in contact with CSF blood are narrowed also - down to 15 micrometres -  far too small to be visualised on angiography, let alone CTA/MRA.  

The result, if severe enough, is to reduce perfusion of brain parenchyma resulting in ischaemic symptoms, infarction, and its sequelae. 

The degree of vasospasm is difficult to predict but correlates with the original Fisher scale and more accurately with the modified Fisher scale.

Vasospasm associated with subarachnoid haemorrhage is usually characterised by diffuse narrowing without intervening regions of normal vessel calibre 10. It is often centred at the arterial bifurcation 10, giving the appearance of enlargement of said bifurcation.

Aggressive, early and prophylactic treatment can markedly reduce the incidence of vasospasm but often requires early securing of the ruptured aneurysm. Three main modalities are employed:

Haemodilution, Hypertension, Hypervolaemia to maintain adequate cerebral perfusion pressure is achieved with hydration and inotropes if necessary. This often requires admission to a neurological intensive care unit with a central venous catheter and intracranial pressure (ICP) monitoring.

Nimodipine is the best known and most widely used calcium channel blocker, which dilate vessels especially leptomeningeal collateral.

In severe cases, intra-arterial therapy can be beneficial. Intra-arterial delivery of a calcium channel blocker such as nimodipine or verapamil has replaced previously used drugs such as papaverine. They are administered by slow bolus injection into the relevant vascular territory via a standard diagnostic catheter, with careful monitoring of blood pressure. Treatment may need to be repeated daily for 3-5 days.

Balloon angioplasty is a more invasive neurointerventional technique requiring a guiding catheter and placement of an endovascular microballoon over a guidewire across the affected segment. Expanding the balloon disrupts the smooth muscle fibres within the vessel wall. There is a risk of vessel dissection or rupture. Once treated the spasm does not usually recur.

Other experimental treatments include:

  • intrathecal sodium nitroprusside
  • mechanical (surgical) evacuation of subarachnoid blood
  • intrathecal fibrinolytic
Stroke and intracranial haemorrhage
Share article

Article information

rID: 4534
Synonyms or Alternate Spellings:
  • Cerebral vasospasm (post SAH)
  • Cerebral vasospasm following SAH

Support Radiopaedia and see fewer ads

Cases and figures

  • Drag
    AP
    Case 1
    Drag here to reorder.
  • Drag
    Right side
    Case 2
    Drag here to reorder.
  • Drag
    Case 3
    Drag here to reorder.
  • Drag
    Severe narrowing ...
    Case 4
    Drag here to reorder.
  • Updating… Please wait.
    Loadinganimation

    Alert accept

    Error Unable to process the form. Check for errors and try again.

    Alert accept Thank you for updating your details.