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Abstract Details

The Magnitude of the Headpulse Biometric Signal Appears Mostly Independent of Intracranial Pressure and Systemic Blood Pressure
Neuro Trauma and Critical Care
P9 - Poster Session 9 (11:45 AM-12:45 PM)
7-004
We sought to evaluate whether the cranial accelerometry-derived HP signals were correlated with mean arterial pressure (MAP) or intracranial pressure (ICP).
Studies have identified unique characteristic changes in headpulse (HP) biometric measurements in TBI, large vessel occlusion stroke, cerebral vasospasm in subarachnoid hemorrhage, and concussion. Despite its clinical potential as a non-invasive neuromonitoring device, the origin of this signal has remained unclear.

Recordings were obtained using a device consisting of a printed circuit board with a MEMS-based triaxial accelerometer, electrocardiogram, and a microprocessor. The root mean square of the data from each axis was summed to generate a time-domain force signal composite. These values were then compared to raw MAP and ICP in 1 second increments using MATLAB2022a.

Recordings were obtained from 12 participants admitted to the neurointensive care unit with external ventricular drain (EVD) or arterial pressure monitoring. Of the 12, four had an arterial line only, four had an EVD only, and four had both. Pooled analyses of ICP values in relation to HP and MAP with HP demonstrated a negligible correlation and minimal agreement between the two metrics. Enrolled patients had a variety of neurological conditions, such as intraparenchymal hemorrhage, subarachnoid hemorrhage, post-spinal surgery, and hydrocephalus, providing no apparent explanation between the lack of correlation observed and disease condition.

Although cranial accelerometry signals were previously hypothesized to be driven by ICP or blood pressure, there was no correlation between HP amplitude and MAP or ICP. This may be due to cerebral autoregulation or may suggest the headpulse signal is a novel signal independent of ABP or ICP. We plan to evaluate HP signals in patients with impaired autoregulation to investigate the origins of the HP signals further.
Authors/Disclosures
Eliot Lee, Clinical Research Coordinator
PRESENTER
Mr. Lee has nothing to disclose.
Derrick Cheng, MD (UCSF Medical Center) Dr. Cheng has nothing to disclose.
Wade S. Smith, MD, PhD (University of California, San Francisco) Dr. Smith has stock in MindRhythm, Inc. The institution of Dr. Smith has received research support from NIH. Dr. Smith has received intellectual property interests from a discovery or technology relating to health care. Dr. Smith has received publishing royalties from a publication relating to health care.