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Cerebral vasospasm (CV)

Cerebral vasospasm, is characterized by angiographic narrowing of arterial vessels, which can be symptomatic and asymptomatic 1).


Cerebral vasospasm (CVS) is the most common neurological complication after aneurysmal subarachnoid hemorrhage (aSAH) and associated with poor functional outcome and mortality.

Angiographic vasospasm is detected in 30 to 70% of patients during the first 5 to 14 days after hemorrhage 2) 3).

Among these patients, 50% with detected vasospasm in angiography suffer from delayed cerebral ischemia, of whom 15 to 20% suffer from stroke or die 4) 5).

Although the development and prevalence of cerebral vasospasm (CV) has been extensively investigated in adults, little data exist on the development of CV in children.

Children have a relatively high incidence of angiographically detectable, moderate-to-severe CV. Children rarely develop symptomatic CV and have good long-term outcomes, perhaps due to robust cerebral collateral blood flow. Criteria developed for detecting CV with TCD ultrasonography in adults overestimate the prevalence of CV in children. Larger studies are needed to define TCD ultrasonography-based CV criteria for children 6).


Mild, 120-140 cm/s

Moderate, 141-200 cm/s

Severe,>200 cm/s

Angiographic vasospasm.

Symptomatic vasospasm

Risk Factors

see Vasospasm after aneurysmal subarachnoid hemorrhage

Multivariate analysis showed that SAH Fisher scale III-IV was the most important risk factor for vasospasm followed by left ventricular hypertrophy (LVH), on electrocardiogram, cigarette smoking, and hypertension. angiographic vasospasm (AV) grade III-IV, symptomatic vasospasm (SV), and cerebral infarction occurred in 57%, 54%, and 39% of the 46 smokers with LVH, and in 43%, 49%, and 35% of the 68 patients who had both LVH and hypertension, respectively. CT-evident SAH, LVH, cigarette smoking, and hypertension are associated with vasospasm. In smokers or hypertensive patients, premorbid LVH appears to predict much more severe vasospasm 7).


A number of pathological processes have been identified in the pathogenesis of vasospasm including endothelial injury, smooth muscle cell contraction from spasmogenic substances produced by the subarachnoid blood clots, changes in vascular responsiveness and inflammatory response of the vascular endothelium.


The pathophysiology on cerebral vasospasm and delayed cerebral ischemia (DCI) remains poorly understood. Much research has been dedicated to finding genetic loci associated with vasospasm and ischemia.

In a study, endothelial nitric oxide (eNOS VNTR) and haptoglobin (Hp) polymorphisms appear to have the strongest associations with delayed ischemic neurologic deficit (DIND) and radiographic vasospasm, respectively 8).

The pathogenesis of vasospasm involves endogenous spasmogens including oxyhemoglobin and endothelin. These are believed to inhibit nitric oxide (NO) synthetase and subsequently reduce the level of endogenous vasodilators, thereby producing vasospasm 9) 10).





Vasospasm is an important cause for mortality following aneurysmal subarachnoid hemorrhage aSAH affecting as many as 70% of patients. It usually occurs between 4th and 21st days of aSAH and is responsible for delayed ischemic neurological deficit (DIND) and cerebral infarction

It is one of the factors that can most significantly worsen the prognosis despite different treatments.

Transcranial doppler (TCD) evidence of vasospasm is predictive of delayed cerebral ischemia (DCI) with high accuracy. Although high sensitivity and negative predictive value make TCD an ideal monitoring device, it is not a mandated standard of care in aneurysmal subarachnoid hemorrhage (aSAH) due to the paucity of evidence on clinically relevant outcomes, despite recommendation by national guidelines. High-quality randomized trials evaluating the impact of TCD monitoring on patient-centered and physician-relevant outcomes are needed 11).


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cerebral_vasospasm.txt · Last modified: 2018/05/08 12:48 by administrador