# Theory of arterial acceleration: implications for transcranial Doppler monitoring in patients with severe traumatic brain injury

**Authors:** Arjen Schaafsma

PMC · DOI: 10.3389/fphys.2025.1654072 · Frontiers in Physiology · 2025-10-30

## TL;DR

This paper introduces a new theory about how arteries contract, which could improve monitoring of brain injuries using Doppler techniques.

## Contribution

The novel contribution is the theory of arterial acceleration and its implications for transcranial Doppler monitoring in traumatic brain injury.

## Key findings

- Arterial acceleration generates a peristaltic wave that enhances pulsatility index during intracranial pressure elevation.
- Sys1 component of blood pressure has better tissue penetration than Sys2 or diastole.
- The theory offers new insights into waveform morphology for ICP monitoring.

## Abstract

The theory of arterial acceleration (AA) proposes that heart contraction is supported by a temporary and short-lasting contraction in arterial smooth muscle layers. Theoretically, it relies upon a stretch induced depolarization of smooth muscle cells at the aortic notch that spreads along the branches of the arterial tree via intercellular gap junctions. This wave of depolarization leads to a short-lasting contraction in the circularly arranged smooth muscle cells and generates a peristaltic wave from proximal to distal. In blood velocity or blood pressure recordings AA underlies the Sys1 component that becomes stronger the further it travels downstream. It adds to the Sys2 component, which is the pressure wave generated by the ejection of blood volume into the aorta that pushes forward the volume already present. This Sys2 component will follow the way of least resistance. The Sys1 component has a better tissue penetration than Sys2 and/or diastole which explains why intracranial pressure (ICP) elevation is accompanied by an increase in pulsatility index (PI). According to the author, the theory of AA leads to a better understanding of wave form morphology and, thereby, provides new perspectives for research into the detection, monitoring and treatment of ICP elevation.

## Linked entities

- **Diseases:** traumatic brain injury (MONDO:0858950)

## Full-text entities

- **Genes:** SYS1 (SYS1 golgi trafficking protein) [NCBI Gene 90196] {aka C20orf169, dJ453C12.4, dJ453C12.4.1}
- **Diseases:** traumatic brain injury (MESH:D000070642)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

32 references — full list in the complete paper: https://tomesphere.com/paper/PMC12611821/full.md

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Source: https://tomesphere.com/paper/PMC12611821