sTBL served as an equivalent alternative to small group interactive seminars for imparting knowledge and teaching CR skills, and was particularly advantageous for teaching CR in the setting of a complex neurologic topic. Furthermore, students reported a strong preference for the sTBL approach, making it a promising tool for effectively teaching neurology.
BackgroundIn the field of Neurology good clinical reasoning skills are essential for successful diagnosing and treatment. Team-based learning (TBL), an active learning and small group instructional strategy, is a promising method for fostering these skills. The aim of this pilot study was to examine the effects of a supplementary TBL-class on students’ clinical decision-making skills.MethodsFourth- and fifth-year medical students participated in this pilot study (static-group comparison design). The non-treatment group (n = 15) did not receive any additional training beyond regular teaching in the neurology course. The treatment group (n = 11) took part in a supplementary TBL-class optimized for teaching clinical reasoning in addition to the regular teaching in the neurology course. Clinical decision making skills were assessed using a key-feature problem examination. Factual and conceptual knowledge was assessed by a multiple-choice question examination.ResultsThe TBL-group performed significantly better than the non-TBL-group (p = 0.026) in the key-feature problem examination. No significant differences between the results of the multiple-choice question examination of both groups were found.ConclusionsIn this pilot study participants of a supplementary TBL-class significantly improved clinical decision-making skills, indicating that TBL may be an appropriate method for teaching clinical decision making in neurology. Further research is needed for replication in larger groups and other clinical fields.
but preserved repetition and naming. Comprehension was impaired. She was unable to read or write. Verbal memory and visuospatial processing were intact. She exhibited symmetric parkinsonism characterized by rigidity, bradykinesia, resting tremor, and impaired postural reflexes (Supporting Information Video is available online). Brain MRI showed asymmetric frontal atrophy ( Fig. 1A). She reached a state of akinetic mutism at age 69 and died at age 70.Plasma progranulin levels were 27 ng/ml (normal threshold < 61 ng/ml). 1 GRN sequencing showed a novel heterozygous deletion (g.1642_1645delTGAG) in the 3' flanking region of exon 7 (IVS7 1 1delTGAG), a highly conserved region in vertebrates ( Supplementary Figure). In silico analysis predicted that the wild-type sequence is localized in a donor splice site, which is abolished by the deletion. Microtubule Associated Protein Tau (MAPT) and Chromosome 9 Open Reading Frame 72 (C9ORF72) were negative.At autopsy, the fresh brain weighed 900 grams. Macroscopically, there was severe atrophy of the frontal and temporal lobes. Histologically, there was severe neuronal loss and gliosis involving the neocortex, caudate nucleus, putamen, globus pallidus, hippocampus, dentate nucleus, substantia nigra, and inferior olivary nucleus. Moderate to severe TDP-43-immunoreactive neuronal cytoplasmic inclusions as well as dystrophic neurites were observed in the frontal, parietal, and temporal cortices, cingulate gyrus, precuneus, thalamus, subthalamic nucleus, hippocampus, entorhinal cortex, and inferior olivary nucleus (Fig. 1B). These findings are consistent with TDP-43 Type A pathology. 2 Tau immunohistochemistry revealed rare neurofibrillary tangles, tau-immunoreactive neurons and neuropil threads in the putamen, substantia innominata, pyramidal layer of the hippocampus, and entorhinal cortex. Alpha-synuclein was absent.Progranulin expression was absent in the frontal and temporal cortices by semiquantitative real-time polymerase chain reaction expression analysis (Fig. 1C) and strongly reduced in the inferior frontal (216 fold reduction) and temporal lobes (25.7 fold reduction).In the family, the variant (and low progranulin plasma levels) segregated with dementia ( Fig. 1D): a sister diagnosed with frontotemporal dementia at 72 years of age, and another with language impairment and gait imbalance at 74 years of age (II:1, II:3). One sister without the GRN mutation developed Parkinson's disease without cognitive impairment (after 8 years from onset) at 53 years (II:6). Another sister (II:2) had clinical amnestic mild cognitive impairment, 3 but did not convert to dementia at 18 months of follow-up.In conclusion, rapidly progressive nvPPA and parkinsonism was associated in this patient with the novel GRN mutation g.1642_1645delTGAG (IVS711delTGAG). We showed that this variant segregates with dementia in the family and is associated with reduced progranulin plasma levels and TDP-43 histopathology.
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