Improvement of students' communication skills through targeted training and the use of simulated patients in dental education-a prospective cohort study.

BACKGROUND: Good communication between patients and practitioners is essential, especially during dental procedures, as these treatments are often associated with increased nervousness and anxiety. The aim of this study was to investigate, implement and evaluate a concept for communication skills training by using targeted training in combination with simulation patients in dental education. METHODS: Students (n = 34) were assigned to four small groups receiving targeted training consisting of two parts. A lecture about the theoretical basics of communication skills and two practical sessions with simulation patients. During this training, one of the students performed the conversation with the patient. Immediately after self-assessment was obtained, the simulation patient, the remaining students and the lecturer provided feedback. Additionally, anonymous surveys were administered to the students at the beginning of the semester, immediately after the training and at the end of the course. RESULTS: The students rated the learning of communication skills as important for later professional life at all times. After targeted training followed by subsequent use in simulated patients, there was a significant improvement in communication skills (p < 0.001). The number of open-ended questions asked to patients after attending the course significantly increased (p = 0.0245). The communication training was considered useful, especially in small groups. CONCLUSION: The implementation of targeted training with subsequent use in simulated patients significantly contributed to the students' improvement in communication skills. The concept offers a good opportunity to better prepare students for interaction with patients, both in their studies and in their upcoming professional lives.

Thalamus pathology in multiple sclerosis: from biology to clinical application.

There is a broad consensus that MS represents more than an inflammatory disease: it harbors several characteristic aspects of a classical neurodegenerative disorder, i.e. damage to axons, synapses and nerve cell bodies. While the clinician is equipped with appropriate tools to dampen peripheral cell recruitment and, thus, is able to prevent immune-cell driven relapses, effective therapeutic options to prevent the simultaneously progressing neurodegeneration are still missing. Furthermore, while several sophisticated paraclinical methods exist to monitor the inflammatory-driven aspects of the disease, techniques to monitor progression of early neurodegeneration are still in their infancy and have not been convincingly validated. In this review article, we aim to elaborate why the thalamus with its multiple reciprocal connections is sensitive to pathological processes occurring in different brain regions, thus acting as a "barometer" for diffuse brain parenchymal damage in MS. The thalamus might be, thus, an ideal region of interest to test the effectiveness of new neuroprotective MS drugs. Especially, we will address underlying pathological mechanisms operant during thalamus degeneration in MS, such as trans-neuronal or Wallerian degeneration. Furthermore, we aim at giving an overview about different paraclinical methods used to estimate the extent of thalamic pathology in MS patients, and we discuss their limitations. Finally, thalamus involvement in different MS animal models will be described, and their relevance for the design of preclinical trials elaborated.

Thalamus Degeneration and Inflammation in Two Distinct Multiple Sclerosis Animal Models.

There is a broad consensus that multiple sclerosis (MS) represents more than an inflammatory disease: it harbors several characteristic aspects of a classical neurodegenerative disorder, i.e., damage to axons, synapses, and nerve cell bodies. While several accepted paraclinical methods exist to monitor the inflammatory-driven aspects of the disease, techniques to monitor progression of early and late neurodegeneration are still in their infancy and have not been convincingly validated. It was speculated that the thalamus with its multiple reciprocal connections is sensitive to inflammatory processes occurring in different brain regions, thus acting as a "barometer" for diffuse brain parenchymal damage in MS. To what extent the thalamus is affected in commonly applied MS animal models is, however, not known. In this article we describe direct and indirect damage to the thalamus in two distinct MS animal models. In the cuprizone model, we observed primary oligodendrocyte stress which is followed by demyelination, microglia/astrocyte activation, and acute axonal damage. These degenerative cuprizone-induced lesions were found to be more severe in the lateral compared to the medial part of the thalamus. In MOG35-55-induced EAE, in contrast, most parts of the forebrain, including the thalamus were not directly involved in the autoimmune attack. However, important thalamic afferent fiber tracts, such as the spinothalamic tract were inflamed and demyelinated on the spinal cord level. Quantitative immunohistochemistry revealed that this spinal cord inflammatory-demyelination is associated with neuronal loss within the target region of the spinothalamic tract, namely the sensory ventral posterolateral nucleus of the thalamus. This study highlights the possibility of trans-neuronal degeneration as one mechanism of secondary neuronal damage in MS. Further studies are now warranted to investigate involved cell types and cellular mechanisms.