No abstract

The analysis of time duration between consecutive R waves of electrocardiogram (ECG) is a standard method to evaluate the variations in heart rate. The physiological literature reveals that blood glucose levels modulate the autonomic nervous system (ANS) activity and heart rate variability (HRV) is representative of the cardiovascular autonomic function. In the research described here, a pilot investigation was carried out to investigate the relationship between HRV signal measures derived from ECG and arterial blood glucose changes in a female subject with type 1 diabetes mellitus (T1DM) subject during normoglycemic and mildly hyperglycemic conditions. A CleveLabs BioCapture wireless device was used to acquire ECG signals from a 160 Kg, 59.6 year old female volunteer with type 1 diabetes. The PhysioToolkit Software was used to extract the HRV signal and the Kubios software package was deployed to perform comprehensive HRV signal analysis. This software has an easy-to-use graphical user interface that displays the HRV signal and provides three options to calculate: Time-domain, Frequency-domain and Nonlinear Dynamics parameters from raw HRV signals. In its Frequency-domain analysis section, it provides frequency bands such as VLF (Hz), LF (Hz), and HF (Hz), with LF/HF as an index that reflects the sympathovagal balance of the ANS. ECG data were acquired for 30 minutes during normoglycemic condition and for another 30 minutes during mildly hyperglycemic conditions, while blood glucose levels were measured manually by the subject using a glucometer every 5 minutes. ECG signal segments of 5 minute durations were then processed to extract HRV signals and these in turn were analyzed to provide frequency-domain measures. The results indicated that blood glucose changes were inversely related to LF/HF. For this dataset, it was observed that mean ± std of the LF/HF decreased from 6.0 ± 1.04 to 0.91 ± 0.17 when blood glucose levels increased from 156 ± 22 mg/dl to 202 ± 29 mg/dl. Further investigation is underway to recruit more diabetic subjects to acquire a large dataset and explore the relationships between different HRV signal parameters and blood glucose changes under different gylcemic conditions in a comprehensive way.

The auditory brainstem response (ABR) is an electrophysiological test that examines the functionality of the auditory nerve and brainstem. Traumatic brain injury (TBI) can be detected if prolonged peak latency is observed in ABR measurements, since latency measures the neural conduction time in the brainstem, and an increase in latency can be a sign of pathological lesion at the auditory brainstem level. The ABR is elicited by brief sounds that can be used to measure hearing sensitivity as well as temporal processing. Reduction in peak amplitudes and increases in latency are indicative of dysfunction in the auditory nerve and/or central auditory pathways. In this study we used sixteen young adult mice that were divided into two groups: sham and mild traumatic brain injury (mTBI), with ABR measurements obtained prior to, and at 2, 6, and 14 weeks after injury. Abnormal ABRs were observed for the nine TBI cases as early as two weeks after injury and the deficits lasted for fourteen weeks after injury. Results indicated a significant reduction in the Peak 1 (P1) and Peak 4 (P4) amplitudes to the first noise burst, as well as an increase in latency response for P1 and P4 following mTBI. These results are the first to demonstrate auditory sound processing deficits in a rodent model of mild TBI.

Traumatic brain injury negatively impacts auditory processing including difficulty in hearing in background noise. In this study we used behavioral and electrophysiological outcomes to examine the effects of mTBI on perceptual auditory disorders and change in behavioral responses overtime following injury. Subjects were 16 (equal gender), 6 month old CBA/CaJ mice. All experimental protocols were approved by the University of South Florida Institutional Animal Care and Use Committee (IACUC). Mice were exposed to either sham or to mTBI administered using a controlled cortical impactor. Auditory behavioral responses were measured using acoustic startle response (ASR). Auditory brainstem response (ABR) audiograms from 8 to 32 kHz were used to measure hearing function. A gap-in-noise paradigm (70 dB SPL markers with gap durations of 2 to 64 ms) was also used to assess temporal processing. All TBI animals showed symptoms immediately following TBI: motor lethargy, poor appetite and mild weight loss, with recovery seen within 3 days. Behavioral and electrophysiological assessments were completed at 3,7, 14, 28, 35, 45, and 90 days post-TBI. Three days post-TBI, ASR functions were comparable between TBI and sham groups. For ABRs, there was a significant decrease in the amplitudes of P1 (22%) and P4 (30%), and an increase in P4 latency in the mTBI mice. These findings indicate that mTBI can result in significant long term deficits of auditory processing and the mouse model may prove to be a translational model for understanding the pathology and treatment of mTBI-induced auditory dysfunction.