Mal de debarquement syndrome (MdDS) is a disorder of phantom perception of self-motion of unknown cause. The purpose of this work was to describe the quality of life (QOL) of patients with MdDS and to estimate the economic costs associated with this disorder. A modified version of a QOL survey used for another neurological disease (multiple sclerosis; MSQOL-54) was used to assess the impact of MdDS on QOL in 101 patients. The estimated economic costs were based on self-reported direct and indirect costs of individuals living in the United States using Medicare reimbursement payment rates for 2011 in 79 patients. Patients with MdDS reported a poor overall QOL as indicated by a mean composite QOL score of 59.26 ± 1.89 (out of 100). The subcategories having the lowest QOL rating were role limitations due to physical problems (18.32 ± 3.20), energy (34.24 ± 1.47), and emotional problems (36.30 ± 4.00). The overall physical health composite score including balance was 49.40 ± 1.69, and the overall mental health composite score was 52.40 ± 1.83. The cost to obtain a diagnosis was $2,997 ± 337, which included requiring an average of 19 physician visits per patient. The direct cost of MdDS medical care was $826 ± 140 per patient per year, which mainly included diagnostic imaging and physician visits. The indirect costs (i.e., lost wages) were $9,781 ± 2,347 per patient per year. Among 65 patients who were gainfully employed when they acquired MdDS, the indirect costs were $11,888 ± 2,786 per patient per year. Thus, the total annual cost of the disorder ranged from $11,493 ± 2,341 to $13,561 ± 2,778 per patient per year depending on employment status prior to developing MdDS. MdDS negatively and dramatically impacts QOL, and also imposes a substantial economic burden on MdDS patients. These findings underscore the need for further basic and clinical research on MdDS.

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The goal of this project was to determine the effects of elevated temperature on preload‐dependent and independent regulation of left ventricular developed pressure (LVDP) in Langendorff‐perfused, electrically paced (420 bpm), Sprague‐Dawley rat hearts. LVDP responses to steady‐state isoproterenol (ISO) infusions (10−8 M) were determined at 37, 38, 39, and 40ºC. Preload‐dependent LVDP was determined at 37 and 40ºC. ISO‐induced LVDP and preload‐dependent LVDP time controls were conducted in a separate group at 37ºC. The percent increase in LVDP during ISO infusion significantly decreased to 42±6(SE) mmHg at 40ºC, compared to 55±9, 55±6, and 53±7 mmHg at 37, 38, and 39ºC, respectively. No significant differences were observed in corresponding time controls (50±6, 47±3, 56±4, and 56±5 mmHg). Preload‐dependent LVDP decreased across the experimental protocol, but there were no temperature effects. These data indicate that intrinsic heart contractility is not altered by moderate heating but is compromised at very high temperatures (40ºC). Furthermore, local temperature does not alter the inherent preload‐dependent LVDP.Funded by a NIOSH Education and Research Center Grant #T42/OH008432‐05.

To determine if sub‐occipital release (SOR) modulates sympathetic control during basal conditions and in conditions with acutely increased activity, 9 healthy subjects (5 male, 4 female) participated in 2 protocols: 1) cold stress (15°C water perfused through a high‐density tube‐lined suit for 20 min) to increase sympathetic tone and 2) normothermia (34°C). In each thermal condition, subjects received in random order, SOR and yaw sham (30 cycles/min) for 2 min. Measurements included: heart rate (HR; ECG); mean arterial blood pressure (MAP; photoplethysmography); cutaneous vascular conductance (CVC; laser‐Doppler flux/MAP); stroke volume (SV; Modelflow); systemic vascular resistance (SVR; Modelflow); and low frequency (LF; 0.04‐0.15 Hz) spectral power (Fast‐Fourier Transform). Cold stress increased MAP (SOR: 90±2 to 98±2; yaw: 87±2 to 99±2 mmHg) and SVR (SOR: 15±2 to 17±2; yaw: 15±2 to 17±2 units), decreased CVC (SOR: 0.52±0.22 to 0.26±0.14; yaw: 0.46±0.15 to 0.24±0.11 units, normothermia to cold stress, respectively), and did not significantly change HR or SV. Blood pressure and laser‐Doppler flux LF spectral power also increased during cold stress. No significant differences were observed between SOR and yaw during normothermia or cold stress. These data indicate that cold stress increases sympathetic noradrenergic tone but SOR does not have the capability to modulate these variables. Grant Funding Source: Supported by a grant from the American Osteopathic Association