Recent Publications by CFE Educators

Representatives of 114 academic departments of obstetrics and gynecology in North America completed a written questionnaire in 1977 designed to assess undergraduate educational programs. Respondents reported increases in numbers of departments and faculty per department and decreases in the length and number of students per clerkship in comparison with a 1968 survey. Small-group discussion, lecture, and professional patients were preferred instructional modalities of faculty and students. Evaluation procedures and faculty development activities are reported and discussed in relation to prior surveys of departments of obstetrics and gynecology.

Dendritic activity in guinea pig hippocampal CA1 and CA3 pyramidal neurons was examined by using an in vitro preparation. Histologically confirmed intradendritic recordings showed that dendrites had an average input resistance of 47.0 M omega and average membrane time constant of 33.3 msec. Active spike responses could be evoked by intracellular injection of outward current or by the activation of synaptic inputs. The predominant activity was burst firing. A typical intracellularly recorded dendritic burst consisted o spikes on a slowly increasing depolarizing potential. The spike components of the burst were of two distinct types: low threshold, fast spikes; and high threshold, slow spikes. Tetrodotoxin (1 microgram/ml) blocked the fast spikes, but slow spikes could still be evoked with direct intracellular stimulation. In contrast to dendritic responses, direct depolarization of CA1 somata did not give rise to burst generation. Orthodromic stimuli evoked large-amplitude excitatory postsynaptic potentials, followed by inhibitory postsynaptic potentials in dendrites of CA1 and CA3 neurons. In two instances, simultaneous recordings were obtained from coupled pairs of elements that were presumed to be soma and dendrite of the same CA3 pyramidal neuron. Depolarization of either element led to burst generation at that site, and the underlying slow depolarization appeared to evoke a burst at the other site. This potential postsynaptic amplifying mecahnism was not ordinarily functional because even suprathreshold orthodromic activation did not normally evoke bursting in dendrites.

The anatomy, physiology, and pharmacology of an intrinsic neural network that monitors and modulates the activity of pain-transmitting neurons is reviewed. This system can be activated by opiate administration or by electrical stimulation of discrete brainstem sites. Evidence is presented that its pain-suppressing action is mediated in part by endogenous opiatelike compounds (endorphins). This pain suppression system is organized at three levels of the neuraxis: midbrain, medulla, and spinal cord. Activation of neurons in the midbrain periaqueductal gray matter (by electrical stimulation, opiates, and possibly psychological factors) excites neurons of the rostral medulla, some of which contain serotonin. The medullary neurons, in turn, project to and specifically inhibit the firing of trigeminal and spinal pain-transmission neurons. As part of a negative feedback loop, the output of the pain transmission neurons, i.e., pain itself, is an important factor in activating the pain-suppression system. A neural model which incorporates the experimental findings is proposed, and the clinical implications of the model are discussed.

Characteristics of best and worst clinical teachers in medicine are described by a random sample of medical school faculty, residents, and third- and fourth-year students at the University of Washington. The responses were factor analyzed and examined to determine whether the ratings were systematically influenced by professional role, faculty department, and teaching method. Best clinical teachers are described as being enthusiastic, clear and well organized, and adept at interacting with students and residents. Worst clinical teachers lack these skills and are characterized by negative personal attributes. Using analysis of variance, the investigator found no significant differences in ratings on the three variables examined. Six of the seven hypothesized dimensions of clinical teaching were confirmed by factor analysis. The results are discussed in relation to faculty development and evaluation of clinical teaching.

In this study the authors examined the efficacy of using student ratings of teaching effectiveness in multiinstructor courses. Specific issues addressed included student ability to identify differences in faculty teaching effectiveness, the consistency of student rating obtained immediately following each lecture with those obtained at the conclusion of the course, and the relationship between individual faculty ratings and overall course ratings. A random sample of students rated each of 14 lectures in a psychopathology course using a 13-item rating scale immediately after each lecture and again at the end of the course. Results indicated that differences in faculty teaching effectiveness are measurable, ratings of individual faculty are relatively stable over over time, and rating of individual faculty are separable from those of the course as a whole. Implications of this research for use of student ratings are also discussed.

In decerebrate cats, electrical stimulation of nucleus raphe magnus (NRM) of the medulla produced marked inhibition of spinal neurons in lumbosacral dorsal horn. Only neurons with high threshold inputs were inhibited. These cells were located in lamina I and in or near laminae V and VI. The duration of inhibition produced was related to the stimulus train length. An ipsilateral lesion of the dorsolateral funiculus at L1 markedly reduced the inhibition of neurons caudal to the lesion. Although NRM stimulation was the most effective, inhibition from more lateral sites could be obtained at higher stimulus intensities. NRM induced inhibition is probably mediated by a direct projection via the dorsolateral funiculus to spinal dorsal horn laminae I, II, V and VI. The results are discussed in relation to proposed mechanisms underlying the analgesia produced by NRM stimulation.