Marjan Nabili

Real-Time Detection and Monitoring of Acute Brain Injury Utilizing Evoked Electroencephalographic Potentials.

Rapid detection and diagnosis of a traumatic brain injury (TBI) can significantly improve the prognosis for recovery. Helmet-mounted sensors that detect impact severity based on measurements of acceleration or pressure show promise for aiding triage and transport decisions in active, field environments such as professional sports or military combat. The detected signals, however, report on the mechanics of an impact rather than directly indicating the presence and severity of an injury. We explored the use of cortical somatosensory evoked electroencephalographic potentials (SSEPs) to detect and track, in real-time, neural electrophysiological abnormalities within the first hour following head injury in an animal model. To study the immediate electrophysiological effects of injury in vivo, we developed an experimental paradigm involving focused ultrasound that permits continuous, real-time measurements and minimizes mechanical artifact. Injury was associated with a dramatic reduction of amplitude over the damaged hemisphere directly after the injury. The amplitude systematically improved over time but remained significantly decreased at one hour, compared with baseline. In contrast, at one hour there was a concomitant enhancement of the cortical SSEP amplitude evoked from the uninjured hemisphere. Analysis of the inter-trial electroencephalogram (EEG) also revealed significant changes in low-frequency components and an increase in EEG entropy up to 30 minutes after injury, likely reflecting altered EEG reactivity to somatosensory stimuli. Injury-induced alterations in SSEPs were also observed using noninvasive epidermal electrodes, demonstrating viability of practical implementation. These results suggest cortical SSEPs recorded at just a few locations by head-mounted sensors and associated multiparametric analyses could potentially be used to rapidly detect and monitor brain injury in settings that normally present significant levels of mechanical and electrical noise.

Surface Acoustic Wave devices for ocular drug delivery

In this work we are reporting on the development of a novel Surface Acoustic Wave (SAW) device based on MEMS technology for drug delivery in the treatment of ocular diseases. The miniaturized SAW drug delivery device will be placed on the eye surface to allow non-invasive long-term drug application based on the programmed timeline and electronic control of a drug regiment. This novel drug delivery method is expected to lead to better clinical outcomes in the treatment of various eye diseases, and improved patient compliance with therapy. The device can be programmed for delivery of precise amounts of drugs at predetermined times over several months, and will use acoustic streaming to push the drug outside of the reservoir. Our modeling results were obtained using COMSOL multiphysics program and Coventor microfluidic simulator. Different force values were applied to investigate the force necessary to push the drug through the outlet.

A simple animal model for cerebral vasculature rupture due to exposure to intense pressure waves

Understanding the threshold of microvasculature rupture in the central nervous system is critical to evaluating the safety of transcranial therapeutic ultrasound procedures, and treatment planning for blast traumatic brain injury. The goal of this study is to determine the threshold for microvasculature rupture in a simple animal model, as a function of the characteristics of the incident pressure-pulse train. An earthworm model was chosen, as a first step in a sequence of increasingly complex models, and because of its readily accessible large vessel. Following anesthetization, the earthworms were sonicated with 3.3 MHz pulse trains from a high-intensity focused ultrasound (HIFU) transducer. A variety of pulse durations, repetition rates, and amplitudes were considered. The pulse duty cycle was kept low (0.0001 to 0.001) to minimize thermal effects. In cases where rupture occurred within 10 min of exposure, the rupture time was recorded. A noticeable threshold for microvascular damage was observed at a peak negative pressure of about 20 MPa. Beyond this pressure, rupture times decreased rapidly with increasing acoustic pressure. The threshold for damage is likely due to the onset of cavitation, though the mechanisms affecting the rupture time require further study.