Le Fort I osteotomy approach to the skull base.

Horizontal osteotomy allows the surgeon to safely down-fracture the maxilla for wide exposure of the central skull base. This surgical approach is easily extended posteriorly in the midline to include the clivus and the arch of C1, providing 8 cm of horizontal anterior exposure and 5 cm of posterior. Wide operative exposure and a low rate of complications afford superior functional and cosmetic preservation in removing tumors of the central cranial base.

Stomal complications and airflow line problems of the Communi-Trach I cuffed talking tracheotomy tube.

There have been no reports of stomal complications and airflow line problems associated with a cuffed talking tracheotomy tube. However, the results of this study showed that stomal complications, in the form of pressure necrosis and wound extension, and problems with airflow line kinking occurred with a 40% and 80% frequency, respectively. Solutions to both difficulties are discussed.

Prolonged intubation vs. tracheotomy: complications, practical and psychological considerations.

The charts of 52 adult patients who underwent tracheotomy (49 after intubation) were reviewed to identify early complications of both endotracheal intubation and tracheotomy. The complication rate of endotracheal intubation was 57%, and of tracheotomy, 14%. None of the complications of tracheotomy was serious. Sixty critical-care nurses were surveyed about their attitudes regarding prolonged endotracheal intubation and tracheotomy. A large majority preferred tracheotomy for patients who require airway support, for several reasons. First, they felt that tracheotomy patients were more comfortable and, therefore, required less sedation and restraint. Second, the patients could communicate more effectively. Third, airway care was simplified. Ninety-two percent of nurses stated that they would prefer a tracheotomy for themselves or a loved one if more than 10 days of ventilatory support were required. We conclude that tracheotomy can be performed safely in this group of patients, and that it offers significant practical and psychological benefits compared to prolonged endotracheal intubation.

The role of spinal cord cyclic AMP in the acoustic startle response in rats.

Drugs thought to increase intracellular levels of cAMP were infused intrathecally into the subarachnoid space of the lumbar spinal cord, and the effects on the acoustic startle response in rats were measured. Intrathecal infusions of the cAMP analogs dibutyryl cAMP or 8-bromo cAMP (12.5-100 micrograms) produced marked, dose-dependent increases in startle amplitude compared to the infusion of artificial cerebrospinal fluid (CSF). Local infusions of dibutyryl cAMP at more rostral levels of the spinal cord or brain failed to mimic the excitatory effect seen following lumbar intrathecal infusion. No excitation of startle was seen following intrathecal infusion of cAMP itself, ATP, 5'-AMP, or dibutyryl cGMP. A weak excitation of startle was seen following intrathecal, but not intraventricular, infusion of the water-soluble adenylate cyclase activator forskolin 7-deacetyl-7-O-hemisuccinic acid (forskolin-DHA; 5.0-100 micrograms, in artificial CSF), whereas forskolin itself [0.01-200 micrograms, in dimethyl sulfoxide (DMSO)] was without consistent effect. Finally, intrathecal infusion of the selective phosphodiesterase inhibitor Rolipram (12.5-200 micrograms) produced a marked excitation of startle similar in magnitude to the effects produced by cAMP analogs. The excitatory effects of intrathecally infused dibutyryl cAMP, 8-bromo cAMP, forskolin-DHA, or Rolipram support a functional link between spinal cord cAMP and the acoustic startle reflex. Possible sites of cAMP action on startle are discussed.

Behavior and binding: desensitization to alpha 1-adrenergic stimulation of acoustic startle is associated with a decrease in alpha 1-adrenoceptor binding sites.

Desensitization of the excitatory effects of alpha 1-adrenergic agonists on acoustic startle occurred 6 h after intrathecal administration of the alpha 1-adrenergic agonist, phenylephrine. This desensitization was associated with a decrease in alpha 1-adrenoceptor sites in the lumbar spinal cord.

Behavior and binding: correlations between alpha 1-adrenergic stimulation of acoustic startle and alpha 1-adrenoceptor occupancy and number in rat lumbar spinal cord.

The relationship between alterations in alpha 1-adrenoceptors and behavioral effects of alpha 1-adrenergic agonists were investigated in a localized region of the rat central nervous system. Direct infusion of the alpha 1-adrenergic agonists, D-amphetamine or phenylephrine. into the subarachnoid space of the lumbar cord (intrathecal administration) increased the amplitude of the acoustic startle reflex, The magnitude of this behavioral facilitation correlated highly with the degree of alpha 1-adrenoceptor occupation measured by [3H]prazosin binding in lumbar spinal tissue. Using an in vitro estimate of receptor occupation, maximal potentiation of startle occurred following approximately 30% occupation of the receptors, using either D-amphetamine or phenylephrine. Intrathecal administration of 6-OHDA produced a 95% decrease in spinal norepinephrine and markedly enhanced the behavioral response to intrathecal phenylephrine as well as the number of alpha 1-adrenoceptors. The correlation between the time course of the behavioral and binding changes was 0.99. No change in receptor affinity (KD) or receptor occupation by phenylephrine was found after 6-OHDA. The data indicate that receptor binding parameters do have predictive value for behavior, especially if localized regions of the nervous system, critical to the behavior, are analyzed.

Spinal modulation of acoustic startle: opposite effects of clonidine and d-amphetamine.

Direct infusion of d-amphetamine (25--400 micrograms) or phenylephrine (12.5--50 micrograms) onto the spinal cord (intrathecal administration) increased acoustic startle amplitude. These effects were blocked by IP injection of the alpha 1-adrenergic antagonist WB-4101, but not the serotonin antagonist cyproheptadine. In contrast, intrathecal administration of clonidine (0.9--12.5 micrograms) markedly depressed startle. This effect was not blocked by IP administration of WB-4101 or cyproheptadine, but was blocked by IP or intrathecal administration of the alpha 2-adrenergic antagonist yohimbine (5 mg/kg), which by itself increased startle. Moreover, intrathecal yohimbine (100 micrograms) attenuated the depressant effect of IP clonidine, indicating that the spinal cord partially mediates the depressant effects on startle after systemic administration of clonidine. Thus clonidine does not behave like an alpha 1-agonist on acoustic startle, even when introduced directly onto the spinal cord. Conditions under which clonidine produces excitatory or depressant behavioral effects are discussed.

5-Methoxy-N,N-dimethyltryptamine: spinal cord and brainstem mediation of excitatory effects on acoustic startle.

The effects of different doses (0.03, 0.06, 0.12, 0.25, 1.0, 2.0, 4.0, and 8.0 mg/kg body weight) of 5-methoxy-N,N-dimethyltryptamine (5-MeODMT) were tested on the acoustic startle reflex in rats. Beginning at 0.12 mg/kg, 5-MeODMT increased startle monotonically up to the highest dose used. 5-MeODMT still increased startle in acutely decerebrate rats or when infused directly onto the spinal cord. The excitatory effects of a high systemic dose of 5-MeODMT were completely blocked by cinanserin, cyproheptadine, and propranolol, but not by parachlorophenylalanine, alpha-methyl-p-tyrosine, haloperidol, sotalol, or phenoxybenzamine. The results were discussed in terms of a new theory, which suggests that stimulation of serotonin receptors in the spinal cord enhance startle whereas serotonin receptors in the forebrain inhibit startle.

Conditioned fear and startle magnitude: effects of different footshock or backshock intensities used in training.

In Experiment 1 four groups of rats received 30 light-shock pairings using footshock intensities of either .2, .4, .8, or 1.6 mA. One day later all rats were tested for startle by presenting tones in the presence or absence of the light CS. Potentiated startle (the difference between startle on light-tone vs tone-alone trials) was nonmonotonically related to the shock intensity used in training, with the greatest potentiation at intermediate shock levels. Experiment 3 demonstrated a similar relationship when backshocks instead of footshocks were used. In Experiment 2 rats were trained with either a moderate or high shock and then given an extended extinction-test session 1 day later. The moderate-shock group showed a gradual decline in potentiated startle over extinction. The high-shock group showed a nonmonotonic extinction curve where potentiation progressively increased toward the middle of extinction and dissipated thereafter. The results suggest that acoustic startle bears an inverted U-shaped relationship to fear and are discussed in relation to other studies concerned with this issue.