Effects of Blood Pressure on Brain Tissue Pulsation Amplitude in a Phantom Model.

OBJECTIVE: The precise mechanism and determinants of brain tissue pulsations (BTPs) are poorly understood, and the impact of blood pressure (BP) on BTPs is relatively unexplored. This study aimed to explore the relationship between BP parameters (mean arterial pressure [MAP] and pulse pressure [PP]) and BTP amplitude, using a transcranial tissue Doppler prototype. METHODS: A phantom brain model generating arterial-induced BTPs was developed to observe BP changes in the absence of confounding variables and cerebral autoregulation feedback processes. A regression model was developed to investigate the relationship between bulk BTP amplitude and BP. The separate effects of PP and MAP were evaluated and quantified. RESULTS: The regression model (R2 = 0.978) revealed that bulk BTP amplitude measured from 27 gates significantly increased with PP but not with MAP. Every 1 mm Hg increase in PP resulted in a bulk BTP amplitude increase of 0.29 µm. CONCLUSION: Increments in BP were significantly associated with increments in bulk BTP amplitude. Further work should aim to confirm the relationship between BP and BTPs in the presence of cerebral autoregulation and explore further physiological factors having an impact on BTP measurements, such as cerebral blood flow volume, tissue distensibility and intracranial pressure.

The Effects of Hypocapnia on Brain Tissue Pulsations.

Hypocapnia is known to affect patients with acute stroke and plays a key role in governing cerebral autoregulation. However, the impact of hypocapnia on brain tissue pulsations (BTPs) is relatively unexplored. As BTPs are hypothesised to result from cerebrovascular resistance to the inflow of pulsatile arterial blood, it has also been hypothesised that cerebral autoregulation changes mediated by hypocapnia will alter BTP amplitude. This healthy volunteer study reports measurements of BTPs obtained using transcranial tissue Doppler (TCTD). Thirty participants underwent hyperventilation to induce mild hypocapnia. BTP amplitude, EtCO2, blood pressure, and heart rate were then analysed to explore the impact of hypocapnia on BTP amplitude. Significant changes in BTP amplitude were noted during recovery from hypocapnia, but not during the hyperventilation manoeuvre itself. However, a significant increase in heart rate and pulse pressure and decrease in mean arterial pressure were also observed to accompany hypocapnia, which may have confounded our findings. Whilst further investigation is required, the results of this study provide a starting point for better understanding of the effects of carbon dioxide levels on BTPs. Further research in this area is needed to identify the major physiological drivers of BTPs and quantify their interactions with other aspects of cerebral haemodynamics.

Brain Tissue Pulsation in Healthy Volunteers.

It is well known that the brain pulses with each cardiac cycle, but interest in measuring cardiac-induced brain tissue pulsations (BTPs) is relatively recent. This study was aimed at generating BTP reference data from healthy patients for future clinical comparisons and modelling. BTPs were measured through the forehead and temporal positions as a function of age, sex, heart rate, mean arterial pressure and pulse pressure. A multivariate regression model was developed based on transcranial tissue Doppler BTP measurements from 107 healthy adults (56 male) aged from 20-81 y. A subset of 5 participants (aged 20-49 y) underwent a brain magnetic resonance imaging scan to relate the position of the ultrasound beam to anatomy. BTP amplitudes were found to vary widely between patients (from ∼4 to ∼150 µm) and were strongly associated with pulse pressure. Comparison with magnetic resonance images confirmed regional variations in BTP with depth and probe position.

Acute ischemic stroke diagnosis using brain tissue pulsations.

Healthy brain tissue pulsates with the cardiac cycle, but whether brain tissue pulsations (BTPs) are impaired by tissue ischemia due to ischemic stroke is currently unclear. This study is the first to explore the clinical potential of measuring BTPs using ultrasound in acute ischemic stroke patients. BTPs were measured in 24 healthy volunteers (aged 52-82 years) and 14 acute ischemic stroke patients (aged 51-86 years) using a novel Transcranial Tissue Doppler (TCTD) method. Measurements were quick to perform and were well tolerated by all subjects. A mixed-methods approach was used for blinded analysis of recordings. This identified qualitative disruption of BTPs in acute stroke patients, which were used to create an analysis checklist. Blinded BTP analysis by novices using the checklist resulted in high sensitivity but low specificity for stroke detection. Quantitative analysis also identified differences between stroke and healthy participants, including weaker BTPs in stroke patients. This first study reporting BTP characteristics in acute ischemic stroke revealed weaker brain tissue pulsations and waveform disruption in acute stroke patients. However, further clinical evaluation using a larger sample size is required to confirm these findings and to explore whether TCTD monitoring might be beneficial for clinical neuromonitoring.