Ichiro Okayasu

Mouth-opening Increases Upper-airway Collapsibility without Changing Resistance during Midazolam Sedation

Sedative doses of anesthetic agents affect upper-airway function. Oral-maxillofacial surgery is frequently performed on sedated patients whose mouths must be as open as possible if the procedures are to be accomplished successfully. We examined upper-airway pressure-flow relationships in closed mouths, mouths opened moderately, and mouths opened maximally to test the hypothesis that mouth-opening compromises upper-airway patency during midazolam sedation. From these relationships, upper-airway critical pressure (Pcrit) and upstream resistance (Rua) were derived. Maximal mouth-opening increased Pcrit to −3.6 ± 2.9 cm H2O compared with −8.7 ± 2.8 (p = 0.002) for closed mouths and −7.2 ± 4.1 (p = 0.038) for mouths opened moderately. In contrast, Rua was similar in all three conditions (18.4 ± 6.6 vs. 17.7 ± 7.6 vs. 21.5 ± 11.6 cm H2O/L/sec). Moreover, maximum mouth-opening produced an inspiratory airflow limitation at atmosphere that was eliminated when nasal pressure was adjusted to 4.3 ± 2.7 cm H2O. We conclude that maximal mouth-opening increases upper-airway collapsibility, which contributes to upper-airway obstruction at atmosphere during midazolam sedation.

Effect of Mandibular Position on Upper Airway Collapsibility and Resistance

It has been proposed that advancement of the mandible is a useful method for decreasing upper airway collapsibility. We carried out this study to test the hypothesis that mandibular advancement induces changes in upper airway patency during midazolam sedation. To explore its effect, we examined upper airway pressure-flow relationships in each of 4 conditions of mouth position in normal, healthy subjects (n = 9). In the neutral position, Pcrit (i.e., critical closing pressure, an index of upper airway collapsibility) was −4.2 cm H2O, and upstream resistance (Rua) was 21.2 cm H2O/L/sec. In the centric occlusal position, Pcrit was −7.1 cm H2O, and Rua was 16.6 cm H2O/L/sec. In the incisor position, Pcrit was significantly reduced to −10.7 cm H2O, and Rua was significantly reduced to 14.0 cm H2O/L/sec. Mandibular advancement significantly decreased Pcrit to −13.3 cm H2O, but did not significantly influence Rua (22.1 cm H2O/L/sec). We conclude that the mandibular incisors’ position improved airway patency and decreased resistance during midazolam sedation.

New Animal Model for Studying Mastication in Oral Motor Disorders

To identify the basic parameters of oral behavior in mice, we recorded the three-dimensional jaw movement trajectories and masseter and digastric muscle activities in freely behaving mice eating foods of various textures. Results showed that: (1) there are characteristic jaw movement patterns for food intake and mastication; (2) the pattern in a chewing cycle may be divided into opening, closing, and protruding (power) strokes; and (3) food texture affects basic patterns of jaw movement, muscle activities, and chewing rhythms. The oral motor behavior of mice appears identical to those of other experimental animals, so mice are appropriate animal models for the study of mastication.

Development of a three-dimensional jaw-tracking system implanted in the freely moving mouse

A high-resolution mandibular tracking system was designed and tested in a freely moving mouse. A sensor unit, which consisted of four small magnetic sensors, was employed to trace small magnet movements in the three-dimensional space. After the sensors output-to-displacement transformation equations were obtained from a multiple regression analysis of pre-experimental calibration data, the magnet and the sensors were transferred to the mouse, being kept at the same configuration as determined in the calibration system. In order to measure the three-dimensional jaw movements, the magnet was glued on the mandibular surface of the mouse and the sensor unit was implanted in the nasal bone. Jaw-movement trajectories were obtained as electrical signals from the sensors after being compensated by the output-to-displacement transformation equations of the sensors with a personal computer. This sensor system, applied to the freely moving mouse, could trace the jaw trajectories with an accuracy of better than 20 microm in three-dimensional space. Consequently, the typical pattern of the rhythmical jaw movements of the mouse during mastication was obtained. The mouse protruded the mandible to the most anterior position in the jaw-opening phase and retruded to it the most posterior position in the jaw-closing phase. This tracking system may also be applied to other small animals.

The involvement of brain-derived neurotrophic factor in the pattern generator of mastication

Brain-derived neurotrophic factor (BDNF) is a family of neurotrophins that plays crucial roles in neural development, survival, maintenance and regeneration both in central and peripheral nervous systems. To examine the effects of BDNF on mastication, jaw movement trajectories and masticatory muscle activities were electrophysiologically investigated in BDNF-deficient mice, compared with those of littermate wild-type mice. BDNF-deficient mice showed less number of chewing strokes and more irregular chewing pattern during mastication than wild-type mice. Masseter muscle activities of BDNF-deficient mice exhibited smaller values than those of wild-type mice. No significant difference in the cycle duration existed between these two types of the mice. These results indicate that the burst pattern is more susceptible to peripheral sensory inputs than the timing and suggest the involvement of BDNF in the control of jaw movement.

Effects of chewing efforts on the sensory and pain thresholds in human facial skin: A pilot study

The aim of this study was to examine the effect of chewing efforts on sensory and pain thresholds of the orofacial skin of symptom-free subjects. Fourteen healthy volunteers were recruited. Using a stair-case method, the tactile detection threshold (TDT) and the filament-prick pain detection threshold (FPT) on the cheek skin (CS) and the skin overlying the palm side of the thenar skin (TS) were measured before and after chewing gum for 5 min (Time 1: T1) and keeping the jaw relaxed for 5 min (Time 2: T2) as a control. Both for the test and control situation, the TDT was higher in all measurement sites after 5 min. As for the FPT, the reactions between T1 and T2 were quite opposite: the FPT increased and/or remained stable in T1, while, it decreased at all sites in T2. There were significant session effects (T1-T2) on the FPT at the left CS (P<0.01), right CS (P<0.05) and TS (P<0.05). The increase of TDT after chewing/no chewing could be due to habituation, while the decrease of FPT observed in the control situation might be due to sensitization, respectively. This potential sensitization, however, was not observed after chewing efforts. Further studies are needed to clarify the modulating effect of masticatory function on the trigeminal sensory system.

Effect of topical lidocaine in the oral and facial regions on tactile sensory and pain thresholds

OBJECTIVE The aim of the present study was to examine the effect of lidocaine application to the face, tongue and hand on sensory and pain thresholds of symptom-free subjects. DESIGN Eighteen females (mean age 25.7 years, range 22-38) participated. Using Semmes-Weinstein monofilaments, the tactile detection threshold (TDT) and the filament-prick pain detection threshold (FPT) were measured on the cheek skin (CS), tongue tip (TT) and palm side of the thenar skin (TS). Subjects were tested in 2 sessions at a 1week interval in randomised order. Lidocaine (session A) or placebo gel (session B) was applied for 5min. The TDT and FPT were measured before and after application. RESULTS The TDT at all sites in session A significantly increased after 5min, but a significant session effect on the TDT was only found at the TT (P<0.01). On the other hand, there were significant session effects on the FPT at all sites (P<0.01). CONCLUSION These results indicate that the pain threshold (FPT) is more susceptible to local anesthetics than the sensory threshold (TDT), but further study is needed to use topical lidocaine for the control of oral and facial pain in the clinic.

Tactile sensory and pain thresholds in the face and tongue of subjects asymptomatic for oro-facial pain and headache

The aim of this study was to examine the tactile sensory and pain thresholds in the face, tongue, hand and finger of subjects asymptomatic for pain. Sixteen healthy volunteers (eight men and eight women, mean age 35·7 years, range 27-41) participated. Using Semmes-Weinstein monofilaments, the tactile detection threshold (TDT) and the filament-prick pain detection threshold (FPT) were measured at five sites: on the cheek skin (CS), tongue tip (TT), palm side of the thenar skin (TS), dorsum of the hand (DH) and the finger tip (FT). The difference between the tactile sensory and pain threshold (FPT-TDT) was also calculated. Both for the TDT and FPT, TT and DH had the lowest and highest values, respectively. As for the FPT-TDT, there were no significant differences among the measurement sites. As the difference between FPT and TDT (FPT-TDT) is known to be an important consideration in interpreting QST (quantitative sensory testing) data and can be altered by neuropathology, taking the FPT-TDT as a new parameter in addition to the TDT and FPT separately would be useful for case-control studies on oro-facial pain patients with trigeminal neuralgia, atypical facial pain/atypical odontalgia and burning mouth syndrome/glossodynia.

Management of post-hyperventilation apnea during dental treatment under monitored anesthesia care with propofol

Although hyperventilation syndrome generally carries a good prognosis, it is associated with the risk of developing severe symptoms, such as post-hyperventilation apnea with hypoxemia and loss of consciousness. We experienced a patient who suffered from post-hyperventilation apnea. A 17-year-old female who suffered from hyperventilation syndrome for several years developed post-hyperventilation apnea after treatment using the paper bag rebreathing method and sedative administration during a dental procedure. We subsequently successfully provided her with monitored anesthesia care with propofol. Monitored anesthesia care with propofol may be effective for the general management of patients who have severe hyperventilation attacks and post-hyperventilation apnea. This case demonstrates that appropriate emergency treatment should be available for patients with hyperventilation attacks who are at risk of developing post-hyperventilation apnea associated with hypoxemia and loss of consciousness.

Comparison of the hemodynamic effects of propofol and ketamine as anesthetic induction agents during high-dose remifentanil administration: a single-center retrospective comparative study

Background We hypothesized that ketamine, when administered as the anesthetic induction agent, may prevent cardiovascular depression during high-dose remifentanil administration, unlike propofol. To test our hypothesis, we retrospectively compared the hemodynamic effects of ketamine, during high-dose remifentanil administration, with those of propofol. Methods Thirty-eight patients who underwent oral surgery at the Nagasaki University Hospital between April 2014 and June 2015 were included in this study. Anesthesia was induced by the following procedure: First, high-dose remifentanil (0.3-0.5 µg/kg/min) was administered 2-3 min before anesthesia induction; next, the anesthetic induction agent, either propofol (Group P) or ketamine (Group K), was administered. Mean arterial pressure (MAP) and the heart rate were recorded by the automated anesthesia recording system at four time points: immediately before the administration of high-dose remifentanil (T1); immediately before the administration of propofol or ketamine (T2); 2.5 min (T3), and 5 min (T4) after the administration of the anesthetic induction agent. Results In Group P, the MAP at T3 (75.7 ± 15.5 mmHg, P = 0.0015) and T4 (68.3 ± 12.5 mmHg, P < 0.001) were significantly lower than those at T1 (94.0 ± 12.4 mmHg). However, the MAP values in the K group were very similar (P = 0.133) at all time points. The heart rates in both Groups P (P = 0.254) and K (P = 0.859) remained unchanged over time. Conclusions We showed that ketamine, when administered as the anesthetic induction agent during high-dose remifentanil administration, prevents cardiovascular depression.