Latency Relationships Between Cerebral Blood Flow Velocity and Intracranial Pressure
Pulsatile intracranial pressure (ICP) is a key to the understanding of several neurological disorders in which compliance is altered, e.g., hydrocephalus. A recently proposed model suggests that ICP pulse is a standing wave and not a transmitted wave. The
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Abstract Pulsatile intracranial pressure (ICP) is a key to the understanding of several neurological disorders in which compliance is altered, e.g., hydrocephalus. A recently proposed model suggests that ICP pulse is a standing wave and not a transmitted wave. The present work, aimed at obtaining a better understanding of the pulsatility in the cranium, tries to test the following hypotheses: first, ICP pulse onset latency would be lower than that of cerebral blood flow velocity (CBFV) pulses measured at a distal vessel; second, CBFV pulse at different intracranial arteries will have different pulse onset latencies, and hence they are not generated as a standing wave. The dataset used in the present study consists of ICP and CBFV signals collected from 60 patients with different diagnoses. The results reveal that the ICP pulse leads CBFV for 90% of the patients regardless of the diagnosis and mean ICP value. In addition, we show that CBFV pulse onset latency is roughly determined by the distance of the measurement point to the heart. We conclude that the ICP signal is not generated as a standing wave and that ICP pulse onset may be related to the arteries proximal to the heart. Keywords Intracranial pressure • Cerebral blood flow velocity • Pulse onset latency • Pulsatility
S. Asgari Department of Neurosurgery, Neural Systems and Dynamics Laboratory, The David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA P.M. Vespa Neurocritical Care Program, Department of Neurosurgery, The David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA M. Bergsneider and X. Hu () Department of Neurosurgery, Neural Systems and Dynamics Laboratory, The David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA Biomedical Engineering Graduate Program, Henry Samueli School of Engineering and Applied Science, University of California, Los Angeles, CA 90095, USA e-mail: [email protected]
Introduction For three decades, many clinical investigators have indicated that abnormalities of intracranial pulsations could play an important role in the pathophysiology of several neurological conditions (e.g., hydrocephalus) and have consequently employed the intracranial pressure (ICP) response to cardiac pulsations for characterization of compliance [5, 7, 10, 20]. In 1981, Foltz underlined the significance of intraventricular cerebral spinal fluid (CSF) pulsatility as the cause of hydrocephalus by showing that the power of intraventricular CSF pulsations is augmented by four times in chronic hydrocephalus [13, 14]. Since then, several interesting models of normal CSF pulsations have been proposed that relate CSF pulsatile flow to ICP, cerebral blood flow (CBF) or arterial blood pressure (ABP). While each model has its own specific set of assumptions, all of them suggest a major role of pulsatility in the cranium [4, 12, 14]. In 2000, Bateman reported decreased pulsatility at the cortical veins; measured for the first time in hydrocephalus patients, using mag
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