Subarachnoid haemorrhage-induced vasospasm is defined as the reduction in the diameter of the cerebral artery lumens, which is associated with microcirculatory disorders 42 and structural anomalies of the vessel walls. Vasospasm is related to the presence of blood in the subarachnoid spaces but its pathophysiology remains unclear. It begins by a prolonged contraction of the smooth muscle with modifications of the vascular wall, including hyperplasia of the intimae, subendothelial fibrosis, smooth muscle cell proliferation and collagen deposits 37. It is most commonly symptomatic in young subjects, current smokers, and those with a history of hypertension or diabetes 10. It might be more common in severe cases of subarachnoid haemorrhage (SAH) with a poor clinical grade early in its course, but these relationships are variable according to the series and are being debated. Vasospasm is the most common complication of SAH and is the main cause of delayed morbidity and mortality. It usually occurs 4 to 14 days after the initial accident, with a peak incidence at 7 days. Its rate of occurrence varies according to the authors from 40 to 70% 38. It is symptomatic in 17 to 40% of cases 10. In addition, while some vasospasms are they may be the cause of ischemic lesions 39. Due to the development of new minimally invasive techniques (transcranial Doppler, PET scan, MRI diffusion-perfusion sequences), patients with SAH are now routinely evaluated for vasospasm. The therapeutic management usually includes a preventive approach with calcium inhibitors, and curative measures with hypertension and hypervolaemia. Percutaneous angioplasty possibly associated with local vasodilator injection is effective but is not free of risk and its indication should be debated. While it is accepted that a significant spasm associated with a severe neurological deficit should benefit from a curative treatment, it is not known how to deal with severe asymptomatic vasospasms or those accompanied only by minor alterations in consciousness (confusion, disorientation, etc.). Following SAH, a significant number (50%) of patients without physical disability present with a real psychological disability in the form of a astheno-emotional syndrome. These disorders, which are difficult to quantify, are probably underestimated. One hypothesis is that the vasospasm, though asymptomatic, could play a role in the occurrence of this syndrome. The reduced perfusion pressure resulting from the spasm may be responsible for diffuse cerebral lesions through neuronal depopulation.