Monro-Kellie 4.0: moving from intracranial pressure to intracranial dynamics

Abstract

The Monro-Kellie doctrine, introduced in the late 18th century, was a groundbreaking concept aimed at explaining the interactions between intracranial volume components. It has since become a cornerstone of brain physiology, now recognized as intracranial dynamics. Initially, the doctrine focused on physiological observations of the three incompressible components of the cranial vault: brain tissue, blood, and cerebrospinal fluid (CSF). Over the centuries, advancements in neuroscience and medical technology have deepened our understanding of intracranial pressure (ICP) regulation, its pathophysiological implications and its role in neurological disorders. This revisitation of the Monro-Kellie doctrine examines how impairments in cerebrovascular autoregulation, brain compartmentalization and the glymphatic system interact in severely brain-injured patients, calling for new management strategies when facing these critical situations. Additionally, it reinforces the need for a holistic monitoring approach to improve early diagnostics and intervention. The evolution of ICP assessment has significantly shaped the management of brain trauma, spontaneous bleeding, ischemic stroke, and hydrocephalus. With the introduction of innovative tools such as brain ultrasound, automated pupillometry and noninvasive pressure waveform monitoring, ICP management is shifting toward more accessible and continuous evaluation strategies. This review explores how blending historical principles with cutting-edge innovations is transforming neuromonitoring and enhancing patient outcomes in critical care.

Keywords: Acute brain injury; Intracranial compartmental syndrome; Intracranial compliance; Intracranial pressure; Traumatic brain injury.

Fig. 1

MONRO-KELLIE 4.0, the dynamic nature of intracranial components with their determinants for variation. The cerebrovascular autoregulation for arterial blood, the buffering reserve for venous and CSF volumes and the glymphatic activity to regulate interstitial space and consequently the brain tissue volume

Fig. 2

The ABP and ICP counterforces do not play an equal role in CPP compensation. After acute brain injuries with unknown CA impairment severity, as ICP raises, efforts on cerebral perfusion compensation by increasing ABP empirically may lead to further brain offense. ABP: arterial blood pressure, CA: cerebrovascular autoregulation, CPP: cerebral perfusion pressure, ICP: intracranial pressure

Fig. 3

Mechanisms for glymphatic system impairment in acute brain injuries. Interstitial bleedings, intracranial hypertension and decompressive craniectomy contribute for increasing vascular resistance and reducing arterial pulsation, AQP4 dysfunction, accumulation of cerebral metabolism debris, neurotoxins and citoquines. These multiple mechanisms reinforce the need for CSF drains when bleedings reach the cisterns and Virchow-Robin spaces. AQP4: aquaporin 4, BBB: brain-blood barrier, CSF: cerebrospinal fluid

Fig. 4

Noninvasive evaluation of intracranial compliance (ICC) in the emergency setting within the MK 4.0 paradigm shift. A severe TBI patient presenting a Marshal II injury at admission. ONSD ultrasound, noninvasive ICP waveform analysis and TCCD (A, B and C respectively) performed in the ER were indicative of ICC impairment, whereas NPi (D) was still favorable. Noninvasive assessment of an impending neurological deterioration. ER: emergency room, ICP: intracranial pressure, ONSD optic nerve sheath diameter, TCCD: transcranial color coded duplex, TBI: traumatic brain injury