Intracranial hypertension and cerebrovascular autoregulation: novel insights and clinical implications

Neurological conditions such as ischaemic or haemorrhagic stroke, traumatic brain injury (TBI), and hypoxic-ischaemic encephalopathy after cardiac arrest, all impact cerebral perfusion. Recovery depends on optimization or adequate restoration of cerebral perfusion; therefore, understanding its determinants remains crucial. Cerebral blood flow (CBF) is primarily driven by cerebral perfusion pressure (CPP), defined by the difference between mean arterial pressure (MAP) and intracranial pressure (ICP). CPP is the main modifiable determinant of cerebral perfusion and can be manipulated through MAP and ICP. ICP represents the hydrostatic pressure exerted by the components inside the cranial vault, and its monitoring is essential for guiding cerebral perfusion management. Invasive ICP monitoring is the gold standard, via an external ventricular catheter or an intraparenchymal probe.1 However, these should be avoided or used with great caution in patients receiving anticoagulant therapy. If invasive monitoring is unavailable or contraindicated, non-invasive methods—including transcranial doppler ultrasonography, optic nerve sheath diameter measurement, automated pupillometry, or near-infrared spectroscopy—can be used to estimate ICP. However, these methods are less accurate than invasive techniques and only provide temporal measurements.