Tass Lab Research
The goal of our computational research - the bedrock of our approach - is to predict how we might counteract abnormal neuronal synchrony by inducing desynchronization, in this way restoring physiological information processing and symptom reduction. Several brain disorders are characterized by abnormal neuronal synchronization processes. In these disorders, instead of being involved in normal physiological task- and context-dependent information processing, large numbers of neurons are engaged in or influenced by detrimentally synchronized neuronal activity leading to an array of symptoms. The goal of our computational research is to predict how we might counteract abnormal neuronal synchrony by inducing desynchronization, in this way restoring physiological information processing and symptom reduction. Accordingly, we develop stimulation techniques that aim at creating desynchronization which persists long after the cessation of stimulation. It should be noted that we do not aim at suppressing neuronal activity or at inducing artificial neural rhythms.
We use real-time High Density (HD) Electroencephalography (EEG) in order to optimize and calibrate therapeutic neuromodulation techniques, such as vibrotactile stimulation or sound stimulation applying the data analysis techniques we have developed to study disease-related brain dynamics and stimulation-induced changes of brain dynamics, e.g., neural synchronization processes and interactions of different brain areas and neural rhythms.
Deep brain stimulation
Deep brain stimulation (DBS) is the standard therapy for patients suffering from medically refractory Parkinson’s disease (Benabid et al., 2009). For this treatment, depth electrodes are implanted in targeted areas of the brain and electrical pulses are continuously administered at high frequencies (> 100Hz) (Benabid et al., 2009). DBS may cause side effects as the stimulation of the targeted areas impacts fibers that run through that areas. It can also adversely impact surrounding regions of the brain. Accordingly, it is desirable to reduce the total amount of current delivered to the brain tissue.
Through Dr. Tass’s research it was found that CR deep brain stimulation (CR-DBS) caused long-lasting therapeutic after-effects in parkinsonian monkeys (Tass et al. 2012, Wang et al, 2016). After 2 h of CR-DBS per day, delivered to the subthalamic nucleus (STN), on five consecutive days (Tass et al, 2012). In contrast, classical DBS did not induce any sustained effects after the stimulation was discontinued.
Vibrotactile stimulation for the treatment of Parkinson’s disease and stroke
Our computational studies predicted that CR stimulation can be delivered non-invasively, i.e. without implanting electrodes in patients’ brains (Popovych & Tass 2012; Tass & Popovych 2012). There are different ways that brain tissue can be stimulated non-invasively. Currently, we are focusing on two approaches that use pre-existing neuronal pathways that deliver sensory information to particular brain areas. One of these approaches is vibrotactile CR stimulation (Tass 2017). Instead of administering bursts of electrical pulses through implanted electrodes, we deliver brief vibratory stimuli, e.g., to the fingertips. The weak and non-painful vibratory stimuli are administered through mechanical stimulators mounted in a glove. In a first in man study performed together with Dr. Bronte-Stewart and her team Parkinson’s patients received 12 hours of vibrotactile CR stimulation on their fingertips over three consecutive days (Syrkin-Nikolau et al. 2018). Vibrotactile CR stimulation turned out to be safe and tolerable. Furthermore, vibrotactile CR improved patients’ gait and bradykinesia. Remarkably, patients were improved even one and four weeks after stimulation was stopped, suggesting cumulative and long-lasting effects of vibrotactile CR stimulation.
Acoustic stimulation for tinnitus therapy
Another non-invasive approach is acoustic CR stimulation for the treatment of chronic subjective tinnitus. For this treatment, pure tones adapted to the patient’s dominant tinnitus pitch are administered according to the CR algorithm (Tass et al., 2012). In a proof of concept study in patients with chronic subjective tinnitus it was shown that acoustic CR treatment was safe, well-tolerated and caused a significant decrease of tinnitus loudness, annoyance and pervasiveness of symptoms (Tass et al., 2012). Therapeutic effects achieved in 12 weeks of treatment persisted through a preplanned 4-week therapy pause and showed sustained long-term effects after 10 months of therapy, with a 75 % responder rate. EEG recordings performed before and after 12 weeks of CR treatment revealed a number of CR-induced changes of brain activity: Neuronal synchrony was significantly reduced in a tinnitus-associated network of brain areas (Tass et al. 2012, Admachic et al. 2012, Adamchic et al. 2014a). Abnormal interactions between different brain areas (Silchenko et al. 2013) and between different brain rhythms (Adamchic et al., 2014b) were significantly reduced. Already short epochs of acoustic CR stimulation specifically counteract the abnormal brain wave pattern characteristic for tinnitus sufferers. Short (16 min) epochs of acoustic CR stimulation caused the longest significant reduction of delta (slow waves, 1.0-4.0 Hz) and gamma (30.0-48.0 Hz) and increase of alpha (8.0-13.0 Hz) power in the auditory cortex region (Adamchic et al., 2017).