Recent Publications by CFE Educators

Faculty play an important role in the delivery of quality instruction in the ambulatory setting. As medical schools and residency programs move more clinical training to ambulatory care settings, more faculty must be recruited and trained. Medical educators have attempted to prepare faculty to teach in ambulatory care settings by conducting faculty development programs. This study documents the current practices of a sample of 14 peer-nominated medical educators who conduct this type of faculty development program. The authors conducted telephone interviews to learn what these educators taught, how they conducted and evaluated their programs, and the theoretical framework guiding their selection of program content and format. Results show that these faculty development programs were delivered almost exclusively in the workshop format, and that there was remarkable similarity in the topics and strategies used. Evaluation was generally limited to satisfaction ratings. Based on the results of this study, the authors recommend that faculty development programs that now emphasize the teaching encounter itself should give equal emphasis to (1) the importance of pre-instructional planning; (2) teaching faculty how to employ post-instructional techniques such as reflection; and (3) training learners and clinic staff to collaborate with faculty in the learning process.

The authors surveyed a group of distinguished clinical teachers regarding episodes of failure that had subsequently led to improvements in their teaching. Specifically, they examined how these teachers had used reflection on failed approaches as a tool for experiential learning. The respondents believed that failures were as important as successes in learning to be a good teacher. Using qualitative content analysis of the respondents' comments, the authors identified eight common types of failure associated with each of the three phases of teaching: planning, teaching, and reflection. Common failures associated with the planning stage were misjudging learners, lack of preparation, presenting too much content, lack of purpose, and difficulties with audiovisuals. The primary failure associated with actual teaching was inflexibly using a single teaching method. In the reflection phase, respondents said they most often realized that they had made one of two common errors: selecting the wrong teaching strategy or incorrectly implementing a sound strategy. For each identified failure, the respondents made recommendations for improvement. The deliberative process that had guided planning, teaching, and reflecting had helped all of them transform past failures into successes.

Although the neurokinin-1 (NK-1)/substance P (SP) receptor is expressed by neurons throughout the spinal dorsal horn, noxious chemical stimulation in the normal rat only induces internalization of the receptor in cell bodies and dendrites of lamina I. Here we compared the effects of mechanical and thermal stimulation in normal rats and in rats with persistent hindpaw inflammation. Electron microscopic analysis confirmed the upregulation of receptor that occurs with inflammation and demonstrated that in the absence of superimposed stimulation, the increased receptor was, as in normal rats, concentrated on the plasma membrane. In general, noxious mechanical was more effective than noxious thermal stimulation in inducing NK-1 receptor internalization, and this was increased in the setting of inflammation. Although a 5 sec noxious mechanical stimulus only induced internalization in 22% of lamina I neurons in normal rats, after inflammation, it evoked near-maximal (98%) internalization in lamina I, produced significant changes in laminae III-VI, and expanded the rostrocaudal distribution of neurons with internalized receptor. Even non-noxious (brush) stimulation of the inflamed hindpaw induced internalization in large numbers of superficial and deep neurons. For thermal stimulation, the percentage of cells with internalized receptor increased linearly at >45 degrees C, but in normal rats, these were restricted to lamina I. After inflammation, however, the 52 degrees C stimulus also induced internalization in 25% of laminae III-IV cells. These studies provide a new perspective on the reorganization of dorsal horn circuits in the setting of persistent injury and demonstrate a critical contribution of SP.

In normal animals, peripheral nerve injury produces a persistent, neuropathic pain state in which pain is exaggerated and can be produced by nonpainful stimuli. Here, mice that lack protein kinase C gamma (PKCgamma) displayed normal responses to acute pain stimuli, but they almost completely failed to develop a neuropathic pain syndrome after partial sciatic nerve section, and the neurochemical changes that occurred in the spinal cord after nerve injury were blunted. Also, PKCgamma was shown to be restricted to a small subset of dorsal horn neurons, thus identifying a potential biochemical target for the prevention and therapy of persistent pain.

To assess the contribution of PKA to injury-induced inflammation and pain, we evaluated nociceptive responses in mice that carry a null mutation in the gene that encodes the neuronal-specific isoform of the type I regulatory subunit (RIbeta) of PKA. Acute pain indices did not differ in the RIbeta PKA mutant mice compared with wild-type controls. However, tissue injury-evoked persistent pain behavior, inflammation of the hindpaw, and ipsilateral dorsal horn Fos immunoreactivity was significantly reduced in the mutant mice, as was plasma extravasation induced by intradermal injection of capsaicin into the paw. The enhanced thermal sensitivity observed in wild-type mice after intraplantar or intrathecal (spinal) administration of prostaglandin E2 was also reduced in mutant mice. In contrast, indices of pain behavior produced by nerve injury were not altered in the mutant mice. Thus, RIbeta PKA is necessary for the full expression of tissue injury-evoked (nociceptive) pain but is not required for nerve injury-evoked (neuropathic) pain. Because the RIbeta subunit is only present in the nervous system, including small diameter trkA receptor-positive dorsal root ganglion cells, we suggest that in inflammatory conditions, RIbeta PKA is specifically required for nociceptive processing in the terminals of small-diameter primary afferent fibers.

Neurons in rostral ventromedial medulla and the periaqueductal gray modulate dorsal horn nociceptive transmission. Endogenous peptides implicated in this modulation include enkephalin (ENK), which is antinociceptive, and cholecystokinin (CCK), which has anti-opioid effects. In this study double-label fluorescence immunocytochemistry demonstrated somata and terminals with ENK- or CCK-like immunoreactivity in these regions. Although the distribution of CCK- and ENK-immunoreactive terminal fields overlapped significantly, co-localization was rare. Furthermore, CCK- and ENK-immunoreactive somata had different morphologies and distinct distributions. The overlap of CCK- and ENK- immunoreactive terminals arbors provides a morphological substrate for an antagonistic interaction of CCK and ENK within brainstem pain modulating circuits, as has been demonstrated in the spinal cord.

Withdrawal from morphine evokes increases in Fos-like immunoreactivity in the spinal cord, particularly in the superficial dorsal horn, laminae I/II. To determine the origin of the increased Fos-like immunoreactivity, we selectively targeted central or peripheral opioid receptors with naloxone-methiodide, an antagonist that does not cross the blood-brain barrier, or induced withdrawal after eliminating possible sources of input to the superficial dorsal horn. To induce tolerance, we implanted rats with morphine or placebo pellets (75 mg, six pellets over three days). On day 4, withdrawal was precipitated and after 1 h, the rats were killed, their spinal cords removed and 50 microm transverse sections of the spinal cord immunoreacted with a rabbit polyclonal antiserum directed against the Fos protein. In placebo-pelleted rats, none of the different procedures, viz. spinal transection, unilateral dorsal rhizotomy (L4-S2), neonatal capsaicin treatment or direct intrathecal opioid antagonist injection, induced expression of the Fos protein. However, both spinally transected and rhizotomized withdrawing animals showed significant increases in Fos-like immunoreactivity in laminae I/II, compared to intact withdrawing rats. Neonatal treatment with capsaicin, which eliminates C-fibres, did not alter Fos-like-immunoreactivity. Selective withdrawal of morphine from peripheral opioid receptors by naloxone-methiodide did not induce Fos-like immunoreactivity in the lumbar spinal cord greater than that recorded in nonwithdrawing rats. However, intrathecal injection of naloxone-methiodide increased Fos-like immunoreactivity in laminae I/II and the ventral horn to a greater extent than did subcutaneous injection of naloxone. We hypothesize that the increased Fos expression after systemic withdrawal in spinally-transected rats results from a loss of descending inhibitory control that is activated during withdrawal. The increase in withdrawal-induced Fos-like immunoreactivity after rhizotomy may be secondary to loss of inhibitory controls exerted by large diameter primary afferents or to deafferentation-induced reorganization in the dorsal horn. Since capsaicin did not alter the magnitude of Fos-like immunoreactivity in withdrawing rats, we conclude that hyperactivity of opioid receptor-laden C-fibres is not a necessary contributor to the withdrawal-induced increase in Fos-like immunoreactivity in laminae I and II. Taken together with the results recorded after intrathecal injection of naloxone-methiodide in tolerant rats, we conclude that the pattern of lumbar spinal cord Fos expression following systemic withdrawal is primarily a consequence of increased activity in opioid receptor-containing circuits intrinsic to the dorsal horn and that the magnitude of Fos expression is normally dampened by supraspinal and primary afferent-derived inhibitory inputs.

To identify time-efficient and educationally effective methods for teaching in ambulatory care and managed care settings, the authors studied four exemplary preceptors who taught family medicine clerks in managed care clinics. They interviewed all four preceptors and observed three of them. All of these preceptors claimed to practice more efficiently with students than without them. Analysis of 33 patients encounters involving students revealed that each of the five students observed spent an average of 12.0 minutes conducting a history and physical examination, 2.2 minutes presenting the case to the preceptor, 7.9 minutes observing the preceptor reviewing and/or repeating the examination with the patient, and 1.8 minutes receiving direct instruction and feedback from the preceptor. The total time per patient encounter was 23.7 minutes, 11.7 minutes of which directly involved the preceptor. The authors then compared these 33 encounters with encounters involving the preceptors alone; these encounters took an average of 10.6 minutes of the preceptors' time. The 1.1-minute difference between the amount of time preceptors spent in encounters involving students and the amount of time they spent in encounters on their own was not statistically significant as measured by t-test (p .05). However, in calculating this time difference, possible time saved by students' assistance with charting was not accounted for. In interviews the preceptors identified three major instructional strategies for time-efficient teaching; planning and preparing; teaching with patients; and charting, giving feedback, and reflecting. Students described these preceptors as enthusiastic teachers and good role models; however, they also felt that their first two years of education had not prepared them for seeing patients in fast-paced ambulatory care settings. The challenge for medical schools is to better prepare both students and preceptors for learning and teaching in productivity driven ambulatory care and managed care environments.