Increased cerebral blood flow velocities assessed by transcranial Doppler examination is associated with complement activation after cardiopulmonary bypass.

The role of complement activation on the cerebral vasculature after cardiopulmonary bypass (CPB) is unclear. The goal of the study was to assess whether heparin-coated CPB reduces complement activation, and influences cerebral blood flow velocities (CBFV). Twenty-four patients undergoing coronary surgery were randomly allocated to non-coated (NC-group) or heparin-coated (HC-group) CPB. Complement activation was assessed by measuring sC5b-9. Transcranial Doppler (TCD) was performed on middle cerebral arteries before and after CPB. Systolic (SV), diastolic (DV) and mean (MV) CBFV were measured. Significant increase of sC5b-9 (p=0.003) was observed in the NC-group and CBFV increased after CPB (SV by 27%, p=0.05; DV by 40%, p=0.06; MV by 33%, p=0.04) whereas no changes were detected in the HC-group. TCD values were higher in the NC-group than in the HC-group (SV, p=0.04; DV, p=0.03; MV, p=0.03) although cardiac index, systemic vascular resistance, haematocrit and pCO(2) were similar. Postoperative SV, DV and MV were significantly correlated with sC5b-9 (r=0.583, p=0.009; r=0.581, p=0.009; r=0.598, p=0.007, respectively). Increased CBFV after CPB are correlated to the level of complement activation and may be controlled by heparin-coated circuits.

[Cerebral metabolism and brain injury]. / Métabolisme énergétique et agression cérébrale.

Brain energy metabolism and signal transduction are intimely intricated. At the cellular level this is reflected by the interdependent metabolism of glutamate and glucose and the energetic compartmentalization between astrocytic glycolysis and neuronal metabolism. Astrocytes appear to have a particular importance in brain metabolism by regulating microcirculation and the repartition of energetic substrates in function of synaptic activity. The high level of O(2) consumption compared to the mass of tissue confers a particular vulnerability of brain to oxidative stress. The synthesis of glutathione, the main anti-oxidant of brain, appears to be dependent of the regulation of synaptic glutamate concentration by astrocytes. Deficiencies of astrocytes functions appear to play a key role in the physiopathology of brain injury.

[Conventional and diffusion magnetic resonance imaging in the acute phase of severe traumatic brain injury]. / Apports de l'IRM conventionnelle et de l'IRM de diffusion à la phase aiguë du traumatisme crânien grave.

Neuro-imaging is essential for the initial evaluation and subsequent control in the acute stage of severe head injury. In these indications tomodensitometry (TDM) has a pivotal role. Despite the well recognized contribution of magnetic resonance imaging (MRI) to the investigation of most of acute neurological pathologies, MRI is not still a routine procedure for the initial investigation of patients with acute head injury. The superiority of morphological and functional MRI on TDM in this indication is discussed.

Persistent carotid-vertebrobasilar anastomoses: how and why differentiating them?

The persistent carotid-vertebrobasilar anastomoses (PCVBA) can be explained by an interruption of the vertebrobasilar system (VBS) embryogenesis. We present two very rare cases of persistent anastomoses: a hypoglossal artery and a type I proatlantal artery, insisting on the angiographic criteria allowing differentiation. After a brief review of the embryogenesis of the VBS, we describe the different types of persistent anastomoses (hypoglossal, type I and II proatlantal, trigeminal and otic arteries). We will insist on the potential risks, not well-known, but typical of each anastomosis. PCVBA usually are incidental findings but imaging follow-up may be required since aneurysms may develop.

[Treatment of cerebral oedema]. / Traitement de l'oedème cérébral.

Progress in brain imaging, monitoring and physiopathology allows the identification of brain oedema from brain swelling, determination of its interstitial or intracellular nature, as well as blood-brain barrier permeability and the evaluation of the impact on cerebral haemodynamic. Common treatment of all types of cerebral oedema is based on prevention of self-sustained disorders due to increased intracranial pressure resulting in ischemic cerebral oedema. The specific treatment of each type of cerebral oedema is reviewed. Optimization of conventional anti-oedematous strategies is based on the precise determination of the nature of the cerebral oedema and of the blood-brain barrier status.

Doppler study of middle cerebral artery blood flow velocity and cerebral autoregulation during a simulated ascent of Mount Everest.

OBJECTIVE: To explore cerebral hemodynamics in 8 healthy volunteers in a hypobaric chamber up to the altitude of Mount Everest after a progressive stepwise decompression to 8,848 m. METHODS: Physiological, clinical, and transcranial Doppler data were collected after at least 3 days at 5,000, 6,000, and 7,000 m and within 4 hours of reaching 8,000 m and returning to sea level. RESULTS: Three subjects were excluded at 8,000 and 8,848 m because of acute neurological deficits. Heart rate increased; mean arterial pressure remained stable; PaO2 and PaCO2 decreased with altitude; hemoglobin (Hb) and hematocrit (Ht) increased; arterial O2 content decreased over 6,000 m; middle cerebral artery blood flow velocity (MCAv) increased only during acute exposure to 8,000 m; and the corresponding pulsatility (PI) and resistivity indices (RI) decreased over 5,000 m. PI and RI correlated with heart rate. The transient hyperemic response (THR) of MCAv to common carotid compression was depressed at 8,000 m. CONCLUSIONS: At 8,000 m, the increase in MCAv seemed to reflect the normal hemodynamic response to acute hypoxia. The decrease of THR at this altitude could be an indication of impaired cerebral autoregulation. The role of impaired cerebral autoregulation in the genesis of acute neurologic deficits, observed at 8,000 m and above in 3 subjects, remains speculative.

Cerebral hemodynamics during arterial and CO(2) pressure changes: in vivo prediction by a mathematical model.

The aim of this work was to analyze changes in cerebral hemodynamics and intracranial pressure (ICP) evoked by mean systemic arterial pressure (SAP) and arterial CO(2) pressure (Pa(CO(2))) challenges in patients with acute brain damage. The study was performed by means of a new simple mathematical model of intracranial hemodynamics, particularly aimed at routine clinical investigation. The model was validated by comparing its results with data from transcranial Doppler velocity in the middle cerebral artery (V(MCA)) and ICP measured in 44 tracings on 13 different patients during mean SAP and Pa(CO(2)) challenges. The validation consisted of individual identification of 6 parameters in all 44 tracings by means of a best fitting algorithm. The parameters chosen for the identification summarize the main aspects of intracranial dynamics, i.e., cerebrospinal fluid circulation, intracranial elastance, and cerebrovascular control. The results suggest that the model is able to reproduce the measured time patterns of V(MCA) and ICP in all 44 tracings by using values for the parameters that lie within the ranges reported in the pathophysiological literature. The meaning of parameter estimates is discussed, and comments on the main virtues and limitations of the present approach are offered.