Approximately half a million mortalities occur in the United States due to cardiac arrest alone; only a few survive from the initial shock. To improve these chances, first responders must resuscitate patients before their arrival to the hospital for proper medical treatment. Unfortunately, none of the devices on the market can be deployed to guide resuscitation by generating useful hemodynamic information to the responder. Animal studies further simulate that obtaining hemodynamic data during medical procedures such as CPR provides optimum patient outcomes. We have created a non-invasive ultrasound-controlled system that measures flow patterns of oxygenated blood within the ascending carotid artery, as a means to guide resuscitation during cardiac arrest. We designed and tested our ultrasound transducers on a water-submerged string phantom that mimics the flow properties of blood. The transducer propagates a pressure wave towards the moving string, and then records the reflected and frequency shifted wave resulting from the Doppler effect. Once the data has been collected in MATLAB, we produce a graphical user interface (GUI) containing a real-time pulsed Doppler spectrogram displaying the blood flow speeds, which are proportional to the Doppler-shifted frequencies. Our team collected data from multiple swine in-vivo to capture the flow rate in the carotid artery. We analyzed and compared the baseline, trauma, and resuscitation measurements to significant parameters such as heart rate and mean arterial pressure. Successful analysis of those pig studies will motivate retrospective human trials that, in turn, should provide sufficient results to motivate commercialization of this technology.

Previous work in my lab has shown that extracranial applications of high intensity focal ultrasound can affect the activity of specific regions in the brain, even going as far as producing specific movements in the extremities of rodents if applied to the motor cortex. With the recent discovery that activation using light stimulation of neurons whose conductive coating (myelin) has been damaged results in higher-than-normal remyelination processes, we proposed that the activation of similarly damaged neurons using high frequency focused ultrasound will also result in increased remyelination and restoration of the targeted neurons. Such a treatment could be used for various neurodegenerative diseases, including multiple sclerosis. Since multiple sclerosis is a disease which damages the myelin coating of neurons and impairs their function, this treatment could revolutionazie multiple sclerosis therapy. Earlier this year, I began work on developing such a treatment using a mouse model which induces brain lesions similar to those found in human multiple sclerosis patients. These experiments include therapies using ultrasound transducers at three different center frequencies, and effectiveness of the treatment is assessed by EEG recordings of the mouse brains during application of ultrasound, as well as MRI scans and stained brain slices of treated and control mice. This work will run through May, and by then I will be able to determine whether high frequency focused ultrasound therapy can be effective in either slowing down demyelination or speeding up remyelination in a well-known animal model of multiple sclerosis. So far we have collected about half of our mouse data, and the post-therapy MRI scans look promising but brain slice staining is currently underway, which will provide much more concrete data on the extent of remyelination.