Objective Delayed cerebral vasospasm has long been recognized as an important cause of poor outcome after an otherwise successful treatment of a ruptured intracranial aneurysm, but it remains a pathophysiological enigma despite intensive research for more than half a century. Method Summarized in this review are highlights of research from North America, Europe and Asia reflecting recent advances in the understanding of delayed ischemic deficit. Result It will focus on current accepted mechanisms and on new frontiers in vasospasm research. Conclusion A key issue is the recognition of events other than arterial narrowing such as early brain injury and cortical spreading depression and of their contribution to overall mortality and morbidity.

No abstract

SUMMARY Twelve patients in a series of 22 with giant intracranial aneurysms demonstrated neuroradiological features of partial or total spontaneous intra-aneurysmal thrombosis. The presence of this intra-aneurysmal clot significantly altered the computed tomographic appearance of the giant aneurysm. Massive intra-aneurysmal thrombosis did not protect against subarachnoid haemorrhage and the likelihood of rupture of a clot containing giant aneurysm was not significantly different from that of a non-thrombosed giant aneurysm. Although parent artery occlusion from a thrombosed giant aneurysm, and massive aneurysmal thrombosis leading to the formation of giant serpentine aneurysm were documented, these are rare epiphenomena. The risk of embolisation from a partially thrombosed giant aneurysm, which was documented in one case, would appear to be greater than that from a non-thrombosed giant aneurysm. The findings in this series, and a review of literature, suggest that the presence of intra-aneurysmal clot in giant intracranial aneurysms has little prognostic significance and does not alter the management or outcome after treatment.

A review of the literature on cerebral vasospasm after aneurysmal subarachnoid haemorrhage (SAH) has shown that angiographic vasospasm occurs in 67.3% of cases when angiography is timed for the highest likelihood, and delayed ischaemic deficit or symptomatic vasospasm in 32.6%. The presence of vasospasm has a marked effect on overall outcome of SAH, and the outcome of delayed ischaemia itself is in about one-third death and in one-third permanent deficit. Management with fluid loading or induced hypertension and with calcium antagonists has been reported widely for both prevention and treatment, and can reduce the incidence and improve the outcome of vasospasm. Other forms of treatment including tissue plasminogen activator, aminosteroids and transluminal angioplasty also appear useful. In spite of these improved therapeutic possibilities, large numbers of patients are still being reported in whom no specific treatment is used.

The technique of hydrogen clearance by an inhalation method is discussed. The electronic instrumentation necessary to secure stability and reproducibility from the recordings is described. Clearance rates in gray matter of about 80 ml/100 gm per minute in the cortex and putamen have been obtained, and of about 20 ml/100 gm per minute in white matter.Clearance curves have invariably been monoexponential in character in white matter, and in over half the cases in the putamen. In the remainder of the putamen curves and in 60% of the cortical clearance curves, the curves could be resolved into only two exponentials. Using bicompartmental analysis, the fast-clearing components of biexponential curves in both cortex and deep nuclei gave the same figures as clearance curves of an entirely monoexponential character from these two tissues. The importance of recirculation time, concentration of hydrogen inhalation, and verification of the tissue placement by subsequent dissection are discussed. The capacity of the method to detect sudden changes in flow during clearance is described.

Delayed vasospasm as a result of subarachnoid blood after rupture of a cerebral aneurysm is a major complication. It is seen in over half of patients and causes symptomatic ischemia in about one third. If left untreated, it leads to death or permanent deficits in over 20% of patients. The essential cause and the relative contribution of true muscle spasm and other changes in the vessel wall remain uncertain. The mainstays of treatment are careful maintenance of fluid balance, induced hypervolemia and hypertension, calcium antagonists, balloon or chemical angioplasty, and, in some centers, cisternal fibrinolytic drugs. Promising future lines of treatment include gene therapy, nitric oxide donors, magnesium, sustained release cisternal drugs, and several other drugs that are under experimental or clinical trial.

Catheterization of Labbé's vein and of a pial branch of the middle cerebral artery has been performed on anesthetized baboons. Closure of the skull has enabled the reaction of the venous outflow from Labbé's vein to be monitored in response to pressure step increases in the pial arterial pressure induced by gas compression of a perfusion mixture connected to the arterial line. Rapid changes in cerebrovascular resistance with swift emergence of regulatory constancy have been shown, and the time characteristics of the resistance changes strongly suggest that they are primarily myogenic in origin. Induction of hypercapnia did not interfere with this autoregulatory mechanism to increased perfusion pressure, which indeed appeared to be more effective at raised arterial P CO 2 , but the mechanism was abolished by the induction of ischemia from middle cerebral occlusion.

A moving correlation index (Mx-CPP) of cerebral perfusion pressure (CPP) and mean middle cerebral artery blood flow velocity (CBFV) allows continuous monitoring of dynamic cerebral autoregulation (CA) in patients with severe traumatic brain injury (TBI). In this study we validated Mx-CPP for TBI, examined its prognostic relevance, and assessed its relationship with arterial blood pressure (ABP), CPP, intracranial pressure (ICP), and CBFV. We tested whether using ABP instead of CPP for Mx calculation (Mx-ABP) produces similar results. Mx was calculated for each hemisphere in 37 TBI patients during the first 5 days of treatment. All patients received sedation and analgesia. CPP and bilateral CBFV were recorded, and GOS was estimated at discharge. Both Mx indices were calculated from 10,000 data points sampled at 57.4Hz. Mx-CPP > 0.3 indicates impaired CA; in these patients CPP had a significant positive correlation with CBFV, confirming failure of CA, while in those with Mx < 0.3, CPP was not correlated with CBFV, indicating intact CA. These findings were confirmed for Mx-ABP. We found a significant correlation between impaired CA, indicated by Mx-CPP and Mx-ABP, and poor outcome for TBI patients. ABP, CPP, ICP, and CBFV were not correlated with CA but it must be noted that our average CPP was considerably higher than in other studies. This study confirms the validity of this index to demonstrate CA preservation or failure in TBI. This index is also valid if ABP is used instead of CPP, which eliminates the need for invasive ICP measurements for CA assessment. An unfavorable outcome is associated with early CA failure. Further studies using the Mx-ABP will reveal whether CA improves along with patients' clinical improvement.