Computed tomography-based morphometric analysis of cervical pedicles in Indian population: a pilot study to assess feasibility of transpedicular screw fixation.

BACKGROUND: Cervical transpedicular screw fixation is safe and is probably going to be the gold standard for cervical spine fixation. However, cervical transpedicular screw use in the Asian population can be limited as the transverse diameter in this group of patients may not be adequate to accommodate the 3.5-mm pedicular screw thus injuring the vital structures located in the close proximity of the pedicles. Thus lateral mass fixation remains the mainstay of treatment. The present study evaluated the transverse cervical pedicle diameter of C2-C7 vertebrae in a pilot study in 27 Indian subjects using computed tomography (CT) imaging and evaluated the feasibility of transpedicular screw fixation in them. AIMS: To evaluate the feasibility of transpedicular screw fixation in the Indian population. SETTINGS AND DESIGN: The cervical pedicle diameter size differs between the Asian and non-Asian population. The authors studied the transverse pedicle diameter of the C2-C7 of the cervical spine in the Indian population using CT measurements. This cross-sectional study was carried out at a tertiary care centre for a period of four months from October 2010 to December 2010. MATERIAL AND METHODS: Measurements of cervical pedicles in the subjects were performed on the CT workstation from the CT images taken at 2.5-mm interval. The transverse pedicle diameter was defined as the outermost diameter of the pedicle, taken perpendicular to the axis of the pedicle at the narrowest point and measured in millimeters±0.1 mm. STATISTICAL ANALYSIS: Descriptive statistics was used to represent percentage of transverse diameter of cervical pedicles less than 5 mm in male and female subjects at C2-C7 levels. Since there is no previous study done in India, we initiated the study with sample size of 27 as a pilot study. The statistical analysis was performed using SPSS software. RESULTS: The mean transverse diameters of the cervical pedicles of C2, C3, C4, C5, C6 and C7 in males were 5.3, 5.3, 5.3, 5.6, 5.6 and 6.1 mm respectively and ranged between 5.3 to 6.1 mm. The mean transverse diameters of the cervical pedicles of C2, C3, C4, C5, C6 and C7 in females were 5.1, 4.6, 4.7, 4.7, 5.3 and 5.6 mm respectively and ranged between 4.6 to 5.6 mm. Between 2.1% and 55.7% of pedicles in our male population and between 5.5% and 74.3% pedicles in our female population was smaller than 5.0 mm in transverse diameter and thus cannot have fixation with a 3.5 mm screw using this technique. CONCLUSIONS: We found that the transverse pedicle diameter of cervical pedicles in the Indian subjects is smaller compared to the Western population. Although transpedicular screw fixation has stronger pullout strength compared to lateral mass fixation, its use must be considered carefully and individually. Preoperative CT evaluation is a must before transpedicular fixation in the cervical spine, especially in the Indian female population. As an option 2.7-mm screws can be devised for the Indian population giving a wider safety margin.

Evaluation of nature and extent of injuries during Dahihandi festival.

BACKGROUND: Injuries related to the Hindu festival of Dahihandi where a human pyramid is formed and a pot of money kept at a height is broken, celebrated in the state of Maharashtra, have seen a significant rise in the past few years. The human pyramid formed is multi-layered and carries with it a high risk of injury including mortality. AIMS: To evaluate the nature, extent and influencing factors of injuries related to Dahihandi festival. SETTINGS AND DESIGN: We present a retrospective analysis of patients who presented in a tertiary care center with injuries during the Dahihandi festival in the year 2010. MATERIALS AND METHODS: 124 patients' records were evaluated for timing of injury, height of the Dahihandi pyramid, position of the patient in the multi-layered pyramid, mode of pyramid collapse and mechanism of an injury. A binary regression logistic analysis for risk factors was done at 5% significance level. STATISTICAL ANALYSIS: Univariate and multi-variate binary logistic regression of the risk factors for occurrence of a major or minor injury was done using Minitab™ version 16.0 at 5% significance. RESULTS: Out of 139 patients presented to the center, 15 were not involved directly in the formation of pyramid, rest 124 were included in the analysis. A majority of the patients were above 15 years of age [110 (83.6%)]. 46 (37.1%) patients suffered major injuries. There were 39 fractures, 3 cases of chest wall trauma with 10 cases of head injuries and 1 death. More than half of the patients [78 (56.1%)] were injured after 1800 hours. 73 (58.9%) injured participants were part of the pyramid constructed to reach the Dahihandi placed at 30 feet or more above the ground. 72 (51.8%) participants were part of the middle layers of the pyramid. Fall of a participant from upstream layers on the body was the main mechanism of injury, and majority [101 (81.5%)] of the patients suffered injury during descent phase of the pyramid. CONCLUSIONS: There is a considerable risk of serious, life-threatening injuries inherent to human pyramid formation and descent in the Dahihandi festival. Safety guidelines are urgently needed to minimize risk and prevent loss of human life.

Epinephrine, vasodilation and hemoconcentration in syncopal, healthy men and women.

Healthy young people may become syncopal during standing, head up tilt (HUT) or lower body negative pressure (LBNP). To evaluate why this happens we measured hormonal indices of autonomic activity along with arterial pressure (AP), heart rate (HR), stroke volume (SV), cardiac output (CO), total peripheral resistance (TPR) and measures of plasma volume. Three groups of normal volunteers (n = 56) were studied supine, before and during increasing levels of orthostatic stress: slow onset, low level, lower body negative pressure (LBNP) (Group 1), 70 degrees head up tilt (HUT) (Group 2) or rapid onset, high level, LBNP (Group 3). In all groups, syncopal subjects demonstrated a decline in TPR that paralleled the decline in AP over the last 40 s of orthostatic stress. Ten to twenty seconds after the decline in TPR. HR also started to decline but SV increased, resulting in a net increase of CO during the same period. Plasma volume (PV, calculated from change in hematocrit) declined in both syncopal and nonsyncopal subjects to a level commensurate with the stress, i.e. Group 3 > Group 2 > Group 1. The rate of decline of PV, calculated from the change in PV divided by the time of stress, was greater (p < 0.01) in syncopal than in nonsyncopal subjects. When changes in vasoactive hormones were normalized by time of stress, increases in norepinephrine (p < 0.012, Groups 2 and 3) and epinephrine (p < 0.025, Group 2) were greater and increases in plasma renin activity were smaller (p < 0.05, Group 2) in syncopal than in nonsyncopal subjects. We conclude that the presyncopal decline in blood pressure in otherwise healthy young people resulted from declining peripheral resistance associated with plateauing norepinephrine and plasma renin activity, rising epinephrine and rising blood viscosity. The increased hemoconcentration probably reflects increased rate of venous pooling rather than rate of plasma filtration and, together with cardiovascular effects of imbalances in norepinephrine, epinephrine and plasma renin activity may provide afferent information leading to syncope.

Gender differences in autonomic cardiovascular regulation: spectral, hormonal, and hemodynamic indexes.

The autonomic nervous system drives variability in heart rate, vascular tone, cardiac ejection, and arterial pressure, but gender differences in autonomic regulation of the latter three parameters are not well documented. In addition to mean values, we used spectral analysis to calculate variability in arterial pressure, heart rate (R-R interval, RRI), stroke volume, and total peripheral resistance (TPR) and measured circulating levels of catecholamines and pancreatic polypeptide in two groups of 25 +/- 1.2-yr-old, healthy men and healthy follicular-phase women (40 total subjects, 10 men and 10 women per group). Group 1 subjects were studied supine, before and after beta- and muscarinic autonomic blockades, administered singly and together on separate days of study. Group 2 subjects were studied supine and drug free with the additional measurement of skin perfusion. In the unblocked state, we found that circulating levels of epinephrine and total spectral power of stroke volume, TPR, and skin perfusion ranged from two to six times greater in men than in women. The difference (men > women) in spectral power of TPR was maintained after beta- and muscarinic blockades, suggesting that the greater oscillations of vascular resistance in men may be alpha-adrenergically mediated. Men exhibited muscarinic buffering of mean TPR whereas women exhibited beta-adrenergic buffering of mean TPR as well as TPR and heart rate oscillations. Women had a greater distribution of RRI power in the breathing frequency range and a less negative slope of ln RRI power vs. ln frequency, both indicators that parasympathetic stimuli were the dominant influence on women's heart rate variability. The results of our study suggest a predominance of sympathetic vascular regulation in men compared with a dominant parasympathetic influence on heart rate regulation in women.

Time-frequency representation of epicardial electrograms during ventricular fibrillation.

In the present study we quantified changes in dominant frequency, which is reciprocal of activation interval or cycle period, during ventricular fibrillation (VF). We used a Smoothed Pseudo Wigner Distribution (SPWD) to estimate time-frequency representations of epicardial electrograms recorded in swines. We used a sock with 64 electrodes spaced equally to record electrograms during 30 seconds of electrically induced VF. Results from 29 trials in three animals showed a mean dominant frequency of 6.64 Hz. We observed considerable variation in dominant frequencies during VF. Temporally, the frequencies varied by as much as +/- 1.24 Hz (2 standard deviations). Spatial variation in frequencies was +/- 1.20 Hz. Cycle periods were computed as the reciprocal of dominant frequencies obtained from the SPWD. These cycle periods were verified to be numerically similar to the cycle periods estimated using activation times detected from differentiated electrograms. Results of recent studies by others have shown that cycle periods during VF are correlated with refractory periods. Our results show that a non-stationary analysis technique such as the SPWD can be used to track spatio-temporal variation in cycle periods. These changes can be used to investigate spatio-temporal variation in cellular properties such as the effective refractory periods during VF. The substantial temporal variation in dominant frequencies that we observed suggest the possibility that the excitable gap at any epicardial location also varies considerably from one instance to another during a VF episode.

Time averaged spatial distribution of epicardial dominant frequencies during ventricular fibrillation.

Recent evidence suggests that the dominant frequencies during ventricular fibrillation (VF) may be used as indicators of dispersion in repolarization and in activation patterns. In the present study, we quantified dominant frequencies from multiple epicardial electrodes to investigate if there are differences in the averaged frequencies within the electrograms recorded from the left and the right ventricles. Further, we quantified whether the difference in average frequency between the two ventricles changed during 30 seconds of VF. Results from eighteen trials in two pigs showed that during the entire duration of VF the average dominant frequencies of all electrodes over the left ventricle were higher than those over the right ventricle (p < 0.005). The dominant frequencies are reciprocal of cycle periods or activation intervals during VF. Our results show that on average, activations in the left ventricle occurred at a faster rate than those in the right ventricle. Activation intervals at any site are determined by the refractory period at that site and the arrival time of next activation. Although differences in cellular properties may have contributed to the observed differences in activation intervals between the ventricles, it is possible that activation arrival times may be different as well. It is possible that the increased tissue mass of the left ventricle may increase the probability that any site will get excited at a faster rate after it is recovered from previous activation.

False positive head-up tilt: hemodynamic and neurohumoral profile.

OBJECTIVES: This study examined differences in mechanisms of head-up tilt (HUT)-induced syncope between normal controls and patients with neurocardiogenic syncope. BACKGROUND: A variable proportion of normal individuals experience syncope during HUT. Differences in the mechanisms of HUT-mediated syncope between this group and patients with neurocardiogenic syncope have not been elucidated. METHODS: A 30-min 80 degrees HUT was performed in eight HUT-negative volunteers (Group I), eight HUT-positive volunteers (Group II) and 15 patients with neurocardiogenic syncope. Heart rate and blood pressure (BP) were monitored continuously. Epinephrine and norepinephrine plasma levels, as well as left ventricular dimensions and contractility determined by echocardiography, were measured at baseline and at regular intervals during the test. RESULTS: The main findings of this study were the following: 1) All parameters were similar at baseline in the three groups; and 2) During tilt: a) the time to syncope was shorter in Group III than in group II (9.5 +/- 3 vs. 17 +/- 3 min p < 0.05); b) there was an immediate, persisting drop in mean BP in Group III; c) the decrease rate of left ventricular end-diastolic dimensions was greater in Group III than in Group II or Group I (-1.76 +/- 0.42 vs. -0.87 +/- 0.35 and -0.67 +/- 0.29 mm/min, respectively, p < 0.05); d) the leftventricular shortening fraction was greater in Group III than in the other two groups (39 +/- 1 vs. 34 +/- 1 and 32 +/- 1%, respectively, p < 0.05); and e) although the norepinephrine level remained comparable among the groups, there was a significantly higher peak epinephrine level in Group III than in Group II and Group I (112.3 +/- 34 vs. 77.6 +/- 10 and 65 +/- 12 pg/ml, p < 0.05). CONCLUSIONS: Mechanisms of syncope during HUT appeared to be different in normal volunteers and patients with neurocardiogenic syncope. In the latter, there was evidence of an impaired vascular resistance response from the beginning of the orthostatic challenge. Furthermore, in the patients there was more rapid peripheral blood pooling, as indicated by the echocardiographic measurements of left ventricular end-diastolic changes, leading to more precocious symptoms. In syncopal patients, the higher level of plasma epinephrine probably mediated the increased cardiac contractility and possibly contributed to the impaired vasoconstrictive response.

Comparison of heart rate and arterial pressure spectra during head up tilt and a matched level of LBNP.

Lower Body Negative Pressure (LBNP) can be used to stimulate cardiovascular regulation by inducing blood shifts similar to those produced during head up tilt (HUT). It is unclear, however, whether similar blood shifts produced by these two stresses evoke similar cardiovascular regulatory responses. Hence, we compared the autonomic components of cardiovascular responses to 50 degrees HUT and a matched level of LBNP. A level of LBNP that produced changes in calf circumference similar to those produced during the first 3 min of 50 degrees HUT was considered to be a matched level. Autonomic components of cardiovascular responses were determined by spectral analysis of heart rate and blood pressure. Results from nine subjects showed that in terms of changes in calf circumference at the end of 3 min, 50 degrees HUT and 48 mm Hg LBNP were similar (2.13% and 1.94%). During 20-min exposures to HUT and LBNP, the increase in heart rate during LBNP was greater (+7 bpm) than HUT, while blood pressure increases were similar. For heart rate and blood pressure spectra, power in the respiratory frequency region (0.25 Hz) decreased and power in the low frequency region (0.03 Hz) increased similarly during HUT and LBNP. These results indicated that 50 degrees HUT and a matched level of LBNP evoked similar autonomic responses in cardiovascular regulation, with the autonomic balance shifted toward increased sympathetic and decreased parasympathetic influence.

Override of spontaneous respiratory pattern generator reduces cardiovascular parasympathetic influence.

We investigated the effects of voluntary control of breathing on autonomic function in cardiovascular regulation. Variability in heart rate was compared between 5 min of spontaneous and controlled breathing. During controlled breathing, for 5 min, subjects voluntarily reproduced their own spontaneous breathing pattern (both rate and volume on a breath-by-breath basis). With the use of this experimental design, we could unmask the effects of voluntary override of the spontaneous respiratory pattern generator on autonomic function in cardiovascular regulation without the confounding effects of altered respiratory pattern. Results from 10 subjects showed that during voluntary control of breathing, mean values of heart rate and blood pressure increased, whereas fractal and spectral powers in heart rate in the respiratory frequency region decreased. End-tidal PCO2 was similar during spontaneous and controlled breathing. These results indicate that the act of voluntary control of breathing decreases the influence of the vagal component, which is the principal parasympathetic influence in cardiovascular regulation.

Spectral indices of cardiovascular adaptations to short-term simulated microgravity exposure.

We investigated the effects of exposure to microgravity on the baseline autonomic balance in cardiovascular regulation using spectral analysis of cardiovascular variables measured during supine rest. Heart rate, arterial pressure, radial flow, thoracic fluid impedance and central venous pressure were recorded from nine volunteers before and after simulated microgravity, produced by 20 hours of 6 degrees head down bedrest plus furosemide. Spectral powers increased after simulated microgravity in the low frequency region (centered at about 0.03 Hz) in arterial pressure, heart rate and radial flow, and decreased in the respiratory frequency region (centered at about 0.25 Hz) in heart rate. Reduced heart rate power in the respiratory frequency region indicates reduced parasympathetic influence on the heart. A concurrent increase in the low frequency power in arterial pressure, heart rate, and radial flow indicates increased sympathetic influence. These results suggest that the baseline autonomic balance in cardiovascular regulation is shifted towards increased sympathetic and decreased parasympathetic influence after exposure to short-term simulated microgravity.

Voluntary control of breathing does not alter vagal modulation of heart rate.

Variations in respiratory pattern influence the heart rate spectrum. It has been suggested, hence, that metronomic respiration should be used to correctly assess vagal modulation of heart rate by using spectral analysis. On the other hand, breathing to a metronome has been reported to increase heart rate spectral power in the high- or respiratory frequency region; this finding has led to the suggestion that metronomic respiration enhances vagal tone or alters vagal modulation of heart rate. To investigate whether metronomic breathing complicates the interpretation of heart rate spectra by altering vagal modulation, we recorded the electrocardiogram and respiration from eight volunteers during three breathing trials of 10 min each: 1) spontaneous breathing (mean rate of 14.4 breaths/min); 2) breathing to a metronome at the rate of 15, 18, and 21 breaths/min for 2, 6, and 2 min, respectively; and 3) breathing to a metronome at the rate of 18 breaths/min for 10 min. Data were also collected from eight volunteers who breathed spontaneously for 20 min and breathed metronomically at each subject's mean spontaneous breathing frequency for 20 min. Results from the three 10-min breathing trials showed that heart rate power in the respiratory frequency region was smaller during metronomic breathing than during spontaneous breathing. This decrease could be explained fully by the higher breathing frequencies used during trials 2 and 3 of metronomic breathing. When the subjects breathed metronomically at each subject's mean breathing frequency, the heart rate powers during metronomic breathing were similar to those during spontaneous breathing. Our results suggest that vagal modulation of heart rate is not altered and vagal tone is not enhanced during metronomic breathing.