[Measuring cerebral vasoregulation--the possible clinical implications]. / Het meten van de cerebrale vasoregulatie--mogelijke klinische implicaties.

Cerebral vessels can keep cerebral perfusion more or less constant. This process is called cerebral vasoregulation and can be measured using different neuromonitoring techniques, which will be discussed in this overview. Cerebral perfusion deficits after brain damage caused by a cerebrovascular accident (CVA), subarachnoid haemorrhage (SAH) or severe traumatic skull and brain injury (TSBI) can be detected early and better understood by using these techniques. In current clinical guidelines on the treatment of CVA, SAB and TSBI, impaired cerebral vasoregulation is often assumed. However, there is a need to measure cerebral vasoregulation status at the individual level, with follow-up over time. Some vasoregulation techniques inform the clinician about subtle local regulation disorders ('snapshot' assessment). Other techniques are suitable for the global long-term monitoring of vasoregulation ('monitoring' assessment) where the results could serve as feedback for treatment interventions. Appropriate use of the techniques in daily clinical practice requires standardisation of the methods available for the monitoring of cerebral vasoregulation. Presently, use is mostly restricted to the research setting.

Near infrared spectroscopy for the detection of desaturations in vulnerable ischemic brain tissue: a pilot study at the stroke unit bedside.

BACKGROUND AND PURPOSE: There is uncertainty whether bilateral near infrared spectroscopy (NIRS) can be used for monitoring of patients with acute stroke. METHODS: The NIRS responsiveness to systemic and stroke-related changes was studied overnight by assessing the effects of brief peripheral arterial oxygenation and mean arterial pressure alterations in the affected versus nonaffected hemisphere in 9 patients with acute stroke. RESULTS: Significantly more NIRS drops were registered in the affected compared with the nonaffected hemisphere (477 drops versus 184, P<0.001). In the affected hemispheres, nearly all peripheral arterial oxygenation drops (n=128; 96%) were detected by NIRS; in the nonaffected hemispheres only 23% (n=30; P=0.17). Only a few mean arterial pressure drops were followed by a significant NIRS drop. This was however significantly different between both hemispheres (32% versus 13%, P=0.01). CONCLUSIONS: This pilot study found good responsiveness of NIRS signal to systemic and stroke-related changes at the bedside but requires confirmation in a larger sample.