A clinical review of cerebral vasospasm and delayed ischaemia following aneurysm rupture.

The continuation of a review of delayed vasospasm after aneurysmal subarachnoid haemorrhage, originally published in 1994 and partially updated at the ninth vasospasm conference in Turkey, is presented. Further online and physical searches have been made of the relevant literature. The incidence of delayed ischaemic deficit (DID) or symptomatic vasospasm reported in 1994 was 32.5% in over 30,000 reported cases. In recent years, 1994-2009, it was 6,775/23,806, or 28.5%. Many of the recent reports did not specify whether a calcium antagonist was used routinely, and when this was stated (usually nimodipine or nicardipine), DID was noted in 22.0% of 10,739 reported patients. The outcome of delayed ischaemia in the earlier survey was a death rate of 31.6%, with favourable outcomes in 36.2%. In recent reports, though with fewer than 1,000 patients, the outcome is possibly better, with death in 25.6% and good outcome in 54.1%. It thus appears likely that delayed vasospasm is still common but less so, and that the overall outcome has improved. This may be due to the more widespread use of calcium antagonists and more effective fluid management. A number of other mechanical and drug treatments are also mentioned.

Cerebral vasospasm following subarachnoid hemorrhage: time for a new world of thought.

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.

Direct cerebral oxygenation monitoring--a systematic review of recent publications.

This review has been compiled to assess publications related to the clinical application of direct cerebral tissue oxygenation (PtiO2) monitoring published in international, peer-reviewed scientific journals. Its goal was to extract relevant, i.e. positive and negative information on indications, clinical application, safety issues and impact on clinical situations as well as treatment strategies in neurosurgery, neurosurgical anaesthesiology, neurosurgical intensive care, neurology and related specialties. For completeness' sake it also presents some related basic science research. PtiO2 monitoring technology is a safe and valuable cerebral monitoring device in neurocritical care. Although a randomized outcome study is not available its clinical utility has repeatedly been clearly confirmed because it adds a monitoring parameter, independent from established cerebral monitoring devices. It offers new insights into cerebral physiology and pathophysiology. Pathologic values have been established in peer-reviewed research, which are not only relevant to outcome but are treatable. The benefits clearly outweigh the risks, which remains unchallenged in all publications retrieved. It is particularly attractive because it offers continuous, real-time data and is available at the bedside.

Protein S-100 and neuropsychological functioning following severe traumatic brain injury.

PRIMARY OBJECTIVE: To examine the relationship between serum concentrations of protein S-100beta and neuropsychological functioning following severe traumatic brain injury. DESIGN: Matched control group. METHODS: Blood samples were taken within 12 hours of injury and then daily up to 7 days post-injury (n=23). Within 2 weeks of emerging from post-traumatic amnesia (PTA), participants completed a battery of neuropsychological measures. These results were compared with a matched sample of healthy controls. RESULTS: Early measurement of S-100 not only reflected overall brain injury severity, but also related to neuropsychological deficits, with higher serum concentrations associated with poorer performance across most cognitive domains. PTA duration, measured by the Westmead PTA Scale, was found to be the strongest predictor of S-100 concentration (R2=0.59, p<0.001). CONCLUSIONS: These findings show that measurement of serum protein S-100 may further aid in the identification of individuals with severe TBI who are likely to experience cognitive difficulties.

Cerebral autoregulation and ageing.

Little is known about the effects of ageing on cerebral autoregulation (CA). To examine the relationship between age and CA in adults, we conducted a prospective study using a non-invasive protocol without external stimuli. We studied 32 subjects, aged 23-68 years. They were assigned to a young group (28+/-5 years) and an old group (54+/-8 years). The groups were sex-matched. Transcranial Doppler ultrasonography (TCD) was used to record bilateral middle cerebral artery flow velocities (CBFV, cm/sec). Noninvasive beat-to-beat tonometric arterial blood pressure (ABP) measurement of the radial artery was used to record spontaneous blood pressure fluctuations. The Mx, an index of dynamic cerebral autoregulation (dCA), was calculated from a moving correlation between ABP and CBFV. We did not find a correlation between age and Mx. No statistically significant difference in the Mx between the groups (0.27+/-0.23, young, vs. 0.37+/-0.24, old) was demonstrated. Age does not affect dynamic cerebral autoregulation assessed by the Mx index in healthy adult subjects. This study supports findings from previous papers wherein CA was measured with protocols which require external stimuli. Further studies are needed to determine CA in subjects above 70 years of age.

Multimodality monitoring in severe traumatic brain injury: the role of brain tissue oxygenation monitoring.

Traumatic brain injury (TBI) is a major cause of morbidity and mortality with widespread social, personal, and financial implications for those who survive. TBI is caused by four main events: motor vehicle accidents, sporting injuries, falls, and assaults. Similarly to international statistics, annual incidence reports for TBI in Australia are between 100 and 288 per 100,000. Regardless of the cause of TBI, molecular and cellular derangements occur that can lead to neuronal cell death. Axonal transport disruption, ionic disruption, reduced energy formation, glutamate excitotoxicity, and free radical formation all contribute to the complex pathophysiological process of TBI-related neuronal death. Targeted pharmacological therapy has not proved beneficial in improving patient outcome, and monitoring and maintenance of various physiological parameters is the mainstay of current therapy. Parameters monitored include arterial blood pressure, blood gases, intracranial pressure, cerebral perfusion pressure, cerebral blood flow, and direct brain tissue oxygen measurement (ptiO2). Currently, indirect brain oximetry is used for cerebral oxygenation determination, which provides some information regarding global oxygenation levels. A newly developed oximetry technique, has shown promising results for the early detection of cerebral ischemia. ptiO2 monitoring provides a safe, easy, and sensitive method of regional brain oximetry, providing a greater understanding of neurophysiological derangements and the potential for correcting abnormal oxygenation earlier, thus improving patient outcome. This article reviews the current status of bedside monitoring for patients with TBI and considers whether ptiO2 has a role in the modern intensive care setting.

Hemispheric asymmetry and temporal profiles of cerebral pressure autoregulation in head injury.

A moving correlation index (Mx-ABP) between arterial blood pressure (ABP) and mean middle cerebral artery blood flow velocity (CBFV) can be used to monitor dynamic cerebrovascular autoregulation (CA) after traumatic brain injury (TBI). In this study we examined hemispheric CA asymmetry and temporal CA profiles, their relationship with ABP and CBFV, and their prognostic relevance. Mx-ABP was calculated for each hemisphere in 25 TBI patients second-daily for as long as they were receiving sedation and analgesia. Forty-nine recordings were obtained, between one and six per patient. Four time periods were defined: immediate--postinjury days (PID) 0 and 1; early--PID 2 and 3; intermediate--PID 4 and 5, and late--PID 6 and later. GOS was estimated at discharge, GOS 4 and 5 were considered favorable (15 patients) and GOS 1-3 unfavorable outcome (10 patients). A Mx difference >0.2 was classified as hemispheric asymmetry (HA). HA was observed at least once in 12 of the 25 patients (48%) and in 18 of 49 recordings (37%). It was observed during all time periods: 35%, 43%, 25%, 43%, respectively, and was not related to outcome. There was no difference in mean CBFV or ABP between patients with and without HA. HA was not related to interhemispheric CBFV differences. A significant improvement in Mx was seen over time. Hemispheric CA asymmetry is common after traumatic brain injury. It does not bear significant clinical or predictive relevance, and it is unrelated to CBFV or ABP. CA is most profoundly disturbed during the immediate postinjury phase and improves gradually during the ICU course. Further studies are needed to investigate CA during post ICU recovery and rehabilitation.

Noninvasive cerebrovascular autoregulation assessment in traumatic brain injury: validation and utility.

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.

Therapeutic approaches to vasospasm in subarachnoid hemorrhage.

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.

Facial nerve palsy after intracisternal papaverine application during aneurysm surgery--case report.

A 61-year-old woman suffered transient mydriasis and prolonged facial nerve palsy after intracisternal papaverine application subsequent to elective clipping of an unruptured middle cerebral artery aneurysm. The mydriasis resolved within 90 minutes, but the facial nerve dysfunction persisted for 2 months before complete recovery. Prolonged irrigation of the cisterns may have washed the papaverine into contact with the facial nerve. This case supports previously reported evidence of a possible effect of topical intracisternal papaverine hydrochloride application on the facial nerve.