Cerebral vasospasm following subarachnoid haemorrhage
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
- thromboxane A2
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.
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.
Treatment and prognosis
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:
Triple H therapy
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.
Calcium channel blockers
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
- 1. Mascia L, Del Sorbo L. Diagnosis and management of vasospasm. (2009) F1000 medicine reports. doi:10.3410/M1-33 - Pubmed
- 2. Jennifer A. Frontera, Andres Fernandez, J. Michael Schmidt, Jan Claassen, Katja E. Wartenberg, Neeraj Badjatia, E. Sander Connolly, Stephan A. Mayer. Defining Vasospasm After Subarachnoid Hemorrhage. (2009) Stroke. 40 (6): 1963. doi:10.1161/STROKEAHA.108.544700 - Pubmed
- 3. Tosaka M, Okajima F, Hashiba Y et-al. Sphingosine 1-phosphate contracts canine basilar arteries in vitro and in vivo: possible role in pathogenesis of cerebral vasospasm. Stroke. 2001;32 (12): 2913-9. Stroke (link) - Pubmed citation
- 4. Pennings FA, Bouma GJ, Ince C. Direct observation of the human cerebral microcirculation during aneurysm surgery reveals increased arteriolar contractility. Stroke. 2004;35 (6): 1284-8. doi:10.1161/01.STR.0000126039.91400.cb - Pubmed citation
- 5. Bevan JA, Bevan RD, Walters CL et-al. Functional changes in human pial arteries (300 to 900 micrometer ID] within 48 hours of aneurysmal subarachnoid hemorrhage. Stroke. 1998;29 (12): 2575-9. Stroke (link) - Pubmed citation
- 6. Kassell NF, Sasaki T, Colohan AR et-al. Cerebral vasospasm following aneurysmal subarachnoid hemorrhage. Stroke. 16 (4): 562-72. Stroke (link) - Pubmed citation
- 7. Abruzzo T, Moran C, Blackham KA et-al. Invasive interventional management of post-hemorrhagic cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage. J Neurointerv Surg. 2012;4 (3): 169-77. doi:10.1136/neurintsurg-2011-010248 - Pubmed citation
- 8. Thomas JE, Rosenwasser RH, Armonda RA et-al. Safety of intrathecal sodium nitroprusside for the treatment and prevention of refractory cerebral vasospasm and ischemia in humans. Stroke. 1999;30 (7): 1409-16. Stroke (link) - Pubmed citation
- 9. Onoue H, Tsutsui M, Smith L et-al. Expression and function of recombinant endothelial nitric oxide synthase gene in canine basilar artery after experimental subarachnoid hemorrhage. Stroke. 1998;29 (9): 1959-65. Stroke (link) - Pubmed citation
- 10. David M. Yousem, Robert I. Grossman. Neuroradiology. p.138-139 (2018) ISBN: 9780323045216
Stroke and intracranial haemorrhage
stroke and intracranial haemorrhage
- general discussions
- scoring and classification systems
- by region
- hemispheric infarcts
- frontal lobe infarct
- parietal lobe infarct
- temporal lobe infarct
- occipital lobe infarct
- internal capsule infarct
- ataxic hemiparesis syndrome: MCA perforators or basilar artery perforators
- lacunar infarct
- thalamic infarct
- striatocapsular infarct
- cerebellar infarct
- midbrain infarct
- Brissaud-Sicard syndrome
- facial colliculus syndrome
- Gasperini syndrome: basilar artery or AICA
- inferior medial pontine syndrome (Foville syndrome): basilar artery
- lateral pontine syndrome (Marie-Foix syndrome): basilar artery or AICA
- locked-in syndrome: basilar artery
- Millard-Gubler syndrome: basilar artery
- Raymond syndrome: basilar artery
- medullary infarct
- acute spinal cord ischaemia syndrome
- hemispheric infarcts
- by vascular territory
- anterior cerebral artery infarct
- anterior choroidal artery infarct
- anterior inferior cerebellar artery infarct
- basilar artery infarct
- middle cerebral artery infarct
- posterior cerebral artery infarct
- posterior inferior cerebellar artery infarct
- superior cerebellar artery infarct
- treatment options
- by region or type
- basal ganglia haemorrhage
- cerebellar haemorrhage
- cerebral contusions
- cerebral microhaemorrhage
- haemorrhagic venous infarct
- haemorrhagic transformation of an ischaemic infarct
- hypertensive intracranial haemorrhage
- intraventricular haemorrhage (IVH)
- lobar haemorrhage
- pontine haemorrhage
- extra-axial haemorrhage
- extradural versus subdural haemorrhage
- extradural haemorrhage (EDH)
- intralaminar dural haemorrhage
- subdural haemorrhage (SDH)
- subarachnoid haemorrhage (SAH)
- intra-axial haemorrhage
- ischaemic stroke