PubMed Health⌕ Search

Biomedical subjects

Robert C Basner

Publications and source records attributed to Robert C Basner.

10 recordsLinked to original sources
PubMed2005

Effects of levetiracetam on sleep in normal volunteers.

BACKGROUND: Epilepsy patients commonly suffer from sleep disturbances, and these can exacerbate memory dysfunction and seizures. Sleep can be affected by seizures, independent sleep disorders, or anticonvulsant drugs. Levetiracetam is a novel anticonvulsant effective for the treatment of partial seizures. We studied the effects of levetiracetam (LEV) on sleep using polysomnography in normal subjects. METHODS: Subjects (aged 18-40) were screened for freedom from sleep disorders, excessive daytime sleepiness, and depression. Screening overnight polysomnography was performed, followed by baseline polysomnography. Subjects were randomized to placebo or LEV, titrated to 1000 mg twice daily over 9 days. Polysomnography was repeated on Treatment Day 28. Differences between baseline and treatment in the drug and placebo groups were compared using single-factor ANOVA. RESULTS: Seventeen subjects were enrolled; 14 completed the study (8 placebo, 6 LEV). All subjects who remained on LEV were able to tolerate the target dose. There were no significant differences between the placebo and drug groups with respect to baseline sleep characteristics. When baseline polysomnography was compared with treatment polysomnography, there were no differences in the change in sleep efficiency, sleep latency, total sleep time, REM latency, or percentages of REM, stage 1, stage 2, or slow wave sleep. There was an increase in the number of awakenings in the drug group that was significant compared with placebo. CONCLUSION: These results suggest that LEV does not have major effects on sleep structure.

Adolescent↗
PubMed2005

Increased sympathetic and decreased parasympathetic cardiovascular modulation in normal humans with acute sleep deprivation.

Cardiovascular autonomic modulation during 36 h of total sleep deprivation (SD) was assessed in 18 normal subjects (16 men, 2 women, 26.0 +/- 4.6 yr old). ECG and continuous blood pressure (BP) from radial artery tonometry were obtained at 2100 on the first study night (baseline) and every subsequent 12 h of SD. Each measurement period included resting supine, seated, and seated performing computerized tasks and measured vigilance and executive function. Subjects were not supine in the periods between measurements. Spectral analysis of heart rate variability (HRV) and BP variability (BPV) was computed for cardiac parasympathetic modulation [high-frequency power (HF)], sympathetic modulation [low-frequency power (LF)], sympathovagal balance (LF/HF power of R-R variability), and BPV sympathetic modulation (at LF). All spectral data were expressed in normalized units [(total power of the components/total power-very LF) x 100]. Spontaneous baroreflex sensitivity (BRS), based on systolic BP and pulse interval powers, was also measured. Supine and sitting, BPV LF was significantly increased from baseline at 12, 24, and 36 h of SD. Sitting, HRV LF was increased at 12 and 24 h of SD, HRV HF was decreased at 12 h SD, and HRV LF/HF power of R-R variability was increased at 12 h of SD. BRS was decreased at 24 h of SD supine and seated. During the simple reaction time task (vigilance testing), the significantly increased sympathetic and decreased parasympathetic cardiac modulation and BRS extended through 36 h of SD. In summary, acute SD was associated with increased sympathetic and decreased parasympathetic cardiovascular modulation and decreased BRS, most consistently in the seated position and during simple reaction-time testing.

Adolescent↗
PubMed2005

Effects of antihypertensives on arterial responses associated with obstructive sleep apneas.

BACKGROUND: Many patients with obstructive sleep apnea syndrome (OSAS) have complicated with hypertension and may be prescribed with antihypertension medications to control their blood pressure. But whether antihypertension medications can also decrease arterial stiffness or control the blood pressure increasing following obstructive events is not well described. This study aimed to investigate whether antihypertensive medications can ameliorate the changes in arterial stiffness and blood pressure associated with OSA. METHODS: Sixty-one OSAS patients [13 women, 48 men, mean age (53.4 +/- 12.3) years], 26 normotensive patients (N), 7 hypertensive patients on no antihypertension medications (H), and 28 hypertensive patients on various combination antihypertension therapy (HM), were prospectively diagnosed with standard nocturnal polysomnography. Beat-to-beat blood pressure was continuously recorded from the radial artery by applanation tonometry during baseline sleep. As a measure of arterial stiffness, arterial augmentation index (AAI) was calculated as the ratio of augmented systolic blood pressure (SBP) to pulse pressure and expressed as a percentage for the following conditions: awakening, the first 10 ("early apnea") and last 10 ("late apnea") cardiac cycles of obstructive events (apnea or hypopnea), and the first 15 cardiac cycles following event termination ("post apnea") for all events with nadir O2 saturation <or= 89%. RESULTS: Systolic blood pressure (SBP) post-apnea [(142.74 +/- 13.06) mmHg (N), (137.06 +/- 26.56) mmHg (H), (136.94 +/- 14.1) mmHg (HM)] was significantly increased from awakening [(135.76 +/- 14.76) mmHg (N), (135.58 +/- 23.17) mmHg (H), (129.77 +/- 14.00) mmHg (HM)], early apnea [(130.53 +/- 12.65) mmHg (N), (124.47 +/- 24.97) mmHg (H), (126.04 +/- 13.12) mmHg (HM)], and late apnea [(129.8 +/- 12.68) mmHg (N), (124.78 +/- 25.15) mmHg (H), (124.48 +/- 13.82) mmHg (HM)] respectively (P < 0.001, repeated measures ANOVA). AAI was significantly increased for the N group (P < 0.001) from awakening to late apnea [(10.45 +/- 2.62)% vs (14.43 +/- 3.21)%] and from early apnea to late apnea [(10.61 +/- 2.34)% vs (14.43 +/- 3.21)%], and also for H group (P < 0.05) from awakening to late apnea [(11.23 +/- 3.87)% vs (16.32 +/- 8.02)%] and from early apnea to late apnea [(11.75 +/- 3.79)% vs (16.32 +/- 8.02)%]. Meanwhile, no significant differences in AAI among awakening, early apnea, late apnea, and post-apnea conditions were found in HM group. CONCLUSIONS: The current data demonstrate that systemic blood pressure increases significantly during the post-apneic phase of OSAS, compared with that during awakening and intra-apnea phases even with the use of combined antihypertensive therapy which could normalize BP during awakening in the hypertensive patients. However, increases in arterial stiffness during obstructive events could be ameliorated by combined antihypertension medications.

Adult↗
PubMed2004

The effect of ventilation on spectral analysis of heart rate and blood pressure variability during exercise.

Heart rate variability (HRV) and systolic blood pressure variability (BPV) during incremental exercise at 50, 75, and 100% of previously determined ventilatory threshold (VT) were compared to that of resting controlled breathing (CB) in 12 healthy subjects. CB was matched with exercise-associated respiratory rate, tidal volume, and end-tidal CO(2) for all stages of exercise. Power in the low frequency (LF, 0.04-0.15 Hz) and high frequency (HF, >0.15-0.4 Hz) for HRV and BPV were calculated, using time-frequency domain analysis, from beat-to-beat ECG and non-invasive radial artery blood pressure, respectively. During CB absolute and normalized power in the LF and HF of HRV and BPV were not significantly changed from baseline to maximal breathing. Conversely, during exercise HRV, LF and HF power significantly decreased from baseline to 100% VT while BPV, LF and HF power significantly increased for the same period. These findings suggest that the increases in ventilation associated with incremental exercise do not significantly affect spectral analysis of cardiovascular autonomic modulation in healthy subjects.

Adult↗
PubMed2004

Pupil staging and EEG measurement of sleepiness.

The goal of this multi-method study was to examine the validity (accuracy) of the pupillometric Alertness Level Test (ALT) as a physiologic measure of sleepiness. The study used a pooled-time series-correlation design with 16 untreated narcolepsy (8 F, 8 M), 16 untreated obstructive sleep apnea (OSA) (7 F, 9 M) and 16 healthy control (8 F, 8 M) subjects. Participants underwent EEG/polysomnography testing using standard Multiple Sleep Latency Test electrode placement concurrent with the 15 min pupillometric ALT. EEG data were examined to determine if theta power (4-7 Hz) increased during 2-s periods of proportional pupil size decreases (pupil Stage 1, 95% or more of maximal pupil size to Stage 4, 65-74% of maximal size). Printed EEG records also were visually scored. Self-report sleepiness measures included the Pittsburgh Sleep Quality Index, the Profile of Mood States and the Epworth Sleepiness Scale. Within subject groups, theta power ratios significantly increased across pupil stages for the sleep disorder groups but not for controls (theta activity increased 42% for narcoleptic and 36% for OSA subjects). Between subject groups, the amount of theta activity was significantly greater for narcoleptic and OSA subjects than that for controls. Visual EEG scoring and self-report measures were usually consistent with objective findings. The ALT is convenient, easily repeatable and less technically demanding than EEG sleepiness measures, and it deserves more comprehensive testing as a valid measure of sleepiness.

Adult↗
PubMed2004

Supplemental oxygen increases arterial stiffness in chronic obstructive pulmonary disease.

STUDY OBJECTIVES: Recently, we demonstrated significantly improved baroreflex sensitivity (BRS) and autonomic balance after 31% supplemental oxygen (SuppO2) in resting patients with chronic obstructive pulmonary disease (COPD). In order to investigate whether peripheral arterial stiffness changes may play a role, we evaluated changes in peripheral arterial stiffness and BRS after SuppO2. DESIGN: Single blinded crossover design. SETTING: Pulmonary exercise testing laboratory. PARTICIPANTS: Seventy subjects with moderate to severe COPD. INTERVENTIONS: We measured arterial vascular stiffness using the augmentation index via contour analysis of the radial pulse obtained from applanation tonometry. BRS was derived using the sequence method before and after treatments with compressed air (CA) and 30% SuppO2 in 70 individuals with COPD via a counterbalanced crossover design. RESULTS: Paired t-tests indicated significant differences in oxygen saturation (SaO2) following SuppO2 when compared to CA (mean 96.0+/-2.0% SuppO2 versus mean 92.6+/-3.6% CA, P<0.001). BRS was significantly greater following SuppO2 compared to CA (mean 3.5+/-2.3 ms/mmHg SuppO2 versus mean 3.1+/-2.1 CA ms/mmHg, P<0.03). Vascular stiffness was significantly increased with SuppO2 when compared with CA (mean 13.3+/-6.1% SuppO2 versus mean 10.8+/-4.9% CA, P<0.001). CONCLUSIONS: Our findings indicate that oxygen supplementation ameliorates BRS by changes in vasomotor activity. The amelioration of the BRS into a more normal range is a move towards the restoration of more normal physiology.

Aged↗
PubMed2004

Baroreflex sensitivity in nonapneic snorers and control subjects before and after nasal continuous positive airway pressure.

HYPOTHESIS: We hypothesized that baroreflex sensitivity is decreased during wakefulness and non-rapid eye movement sleep in normotensive, nonapneic snorers who are otherwise healthy. Moreover, we hypothesized that nocturnal alterations in baroreflex sensitivity are abolished during the application of nasal continuous positive airway pressure (nCPAP). DESIGN: The sequencing technique was used to measure baroreflex sensitivity in 16 normotensive nonapneic snorers and 16 control subjects matched for age, height, weight, gender, and race. Subsequently, baroreflex sensitivity was measured in 12 of 16 snorers and 14 of 16 control subjects during the application of nCPAP. RESULTS: Mean (+/- SE) baroreflex sensitivity was reduced during sleep in the nonapneic snoring group (wakefulness, 20.99 +/- 1.46 ms/mm Hg; sleep, 15.85 +/- 1.49 ms/mm Hg), but not in the control group (wakefulness, 21.82 +/- 2.48 ms/mm Hg; sleep, 23.54 +/- 2.18 ms/mm Hg). This reduction was abolished by the application of nCPAP in the snoring group (before nCPAP therapy, 16.30 +/- 2.17 ms/mm Hg; during nCPAP therapy, 20.63 +/- 2.40 ms/mm Hg). The application of nCPAP did not alter baroreflex sensitivity in the control group (before nCPAP therapy, 23.54 +/- 2.18 ms/mm Hg; during nCPAP therapy, 22.56 +/- 1.73 ms/mm Hg). BP was not significantly different between the snoring and control groups either before or during nCPAP application. CONCLUSIONS: Our findings suggest that nocturnal alterations in baroreflex sensitivity may exist in nonapneic snoring subjects prior to alterations in other cardiovascular variables.

Adult↗
PubMed2003

High-frequency modulation of heart rate variability during exercise in patients with COPD.

STUDY OBJECTIVES: To evaluate cardiac autonomic modulation in patients with COPD during peak exercise. METHODS: Fifty-three patients with COPD (mean FEV(1), 35% predicted [SD, 11% predicted]; mean PaO(2), 68 mm Hg [SD, 11 mm Hg]; mean PaCO(2), 40 mm Hg [SD, 7 mm Hg]; mean age, 61 years [SD, 10 years]; 26 women and 27 men) and 14 healthy control subjects aged 60 years (SD, 8 years) [seven women and seven men] were studied at rest and during ramped bicycle ergometry to their volitional peak. Patients were not receiving autonomic medications other than inhaled beta-agonist agents and/or anticholinergic agents. Control subjects were not receiving any medications. Cardiac autonomic modulation was assessed via time-frequency analysis (Wigner-Ville) of ECG-derived heart rate variability as the power in the low-frequency (LF) band (ie, 0.04 to 0.15 Hz) and the high-frequency (HF) band (ie, > 0.15 to 0.4 Hz) averaged from > 3 min at rest and minutes 2 through 5 of their exercise period. RESULTS: Patients with COPD had a significantly increased mean, ln-transformed HF band from rest to peak exercise (9.9 ms(2) [SD, 1.4 ms(2)] vs 10.7 ms(2) [SD, 1.4 ms(2)], respectively; p < 0.01), while the HF band was unchanged for the control group (10.7 ms(2) [SD, 1.5 ms(2)] vs 10.4 ms(2) [1.3 ms(2)], respectively; difference not significant). The mean ln-transformed LF band was significantly increased from rest to peak exercise in patients with COPD (10.9 ms(2) [SD, 1.5 ms(2)] vs 11.5 ms(2) [SD, 1.4 ms(2)], respectively; p < 0.01) and in control subjects (10.9 ms(2) [SD, 1.5 ms(2)] vs 11.5 ms(2) [SD, 1.3 ms(2)], respectively; p < 0.01). The mean LF/HF ratio was significantly decreased from rest to peak exercise in patients with COPD (3.1 [SD, 1.5] vs 2.5 [SD, 1.0], respectively; p < 0.01) and was increased in control subjects (1.9 [SD, 0.8] vs 2.4 [1.0], respectively; p < 0.01). When expressed in normalized units ([absolute power of the components]/[total power - very low frequency power] x 100), the HF band was again significantly greater during peak exercise than at rest in the patients with COPD and was unchanged during peak exercise for the control group. Autonomic changes were not significantly correlated with age, gender, body mass index, spirometry, lung volumes, resting gas exchange, or oxygen saturation during exercise. CONCLUSION: These data suggest that, in contrast to control subjects, the balance of sympathetic to parasympathetic cardiac modulation decreases in patients with COPD during maximal volitional exercise.

Aged↗
PubMed2002

Arterial stiffness increases during obstructive sleep apneas.

STUDY OBJECTIVES: Obstructive sleep apnea (OSA) appears to be an independent risk factor for diurnal systemic hypertension, but the specific biologic markers for this association have not been well established. Increased arterial stiffness is an important measure of increased left ventricular load and a predictor of cardiovascular morbidity and may precede the onset of systemic hypertension in humans. However, arterial stiffness has not been measured in association with obstructive apneas in patients with OSA, nor related to systemic blood pressure (BP) activity in this setting. Our objective was to test the hypothesis that arterial stiffness may be utilized as a sensitive measure of arterial vasomotor perturbation during obstructive events in patients with OSA, by demonstrating that (1) arterial stiffness increases acutely in association with obstructive apnea and hypopnea, and that (2) such increased stiffness may occur in the absence of acute BP increase. DESIGN: Prospective, cross-sectional. SETTING: A tertiary-care university-based sleep and ventilatory disorders center. PATIENTS: Forty-four normo- and hypertensive adult patients (11 women, 33 men) with polysomnographically diagnosed moderate to severe OSA. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Beat-to-beat BP was recorded from the radial artery by applanation tonometry during nocturnal polysomnography. Arterial augmentation index (AAI), a measure of arterial stiffness, was calculated as the ratio of augmented systolic BP (SBP) to pulse pressure and expressed as a percentage for the following conditions: awake, the first 10 ("early apnea") and last 10 ("late apnea") cardiac cycles of obstructive events, and the first 15 cardiac cycles following apnea termination ("post apnea"). Mean AAI (+/-SD) for the group was significantly increased during NREM sleep from early apnea to late apnea (12.02 +/- 2.70% vs 13.35 +/- 3.54%, p<0.05, ANOVA). During REM (analyzed in 20 patients), MI again significantly increased from early apnea to late apnea (11.75 +/- 2.81% vs 13.43 +/- 4.97%). Conversely, neither mean SBP nor mean arterial BP was significantly changed from early apnea to late apnea in NREM (SBP 130 +/- 14 mmHg vs 129 +/- 14 mmHg) or REM (SBP 128 +/- 22 mmHg vs 127 +/- 21 mmHg). CONCLUSIONS: Arterial stiffness increases acutely during obstructive apneas in both NREM and REM sleep, in the absence of measurable BP change. These data suggest that arterial stiffness may be a sensitive measure of acute arterial vasomotor perturbation in this setting and may have implications concerning cardiovascular sequelae in patients with OSA.

Adult↗