Teaching Diagnostic Reasoning to Medical Students: a four-step approach.

Diagnosis is fundamental to clinical medicine, and diagnostic errors are a serious public health problem. However, there is little consensus regarding the best approach to teaching diagnostic reasoning in medical schools. One approach ("pattern recognition") uses learned associations between patient symptoms and signs and human disorders to help experienced clinicians solve problems rapidly and efficiently. However, this approach may be ineffective when used by students with little clinical experience. Here we describe a four-step analytical approach to diagnosis that can be used by medical students before beginning clinical training. This approach complements the pattern recognition approach used by experts and can be used by students, residents in training, and attending physicians when confronting complex cases. The analytical approach also highlights critical basic science concept areas that support diagnostic reasoning and therefore warrant emphasis in medical school curricula. We propose introducing the analytical approach to medical students early in their training, coordinated with basic science instruction. Once students master relevant basic science concepts, they can use the analytical approach to diagnose disorders affecting one or more physiological systems, as a foundation for future clinical training.

Johann Friedrich Horner and the Repeated Discovery of Oculosympathoparesis: Whose Syndrome Is It?

Disruption of cranial sympathetic tone leads to the symptom complex of miosis, ptosis, and hemifacial anhidrosis. It is widely believed that this phenomenon was discovered in 1869 by the Swiss ophthalmologist Johann Friedrich Horner, and as a result, the term Horner syndrome has become synonymous with the clinical presentation. However, the syndrome that would become Horner syndrome had actually been described several times before his report. François Pourfour du Petit documented the ocular effects of sympathetic trunk lesions in animal studies in 1727. Claude Bernard identified the full clinical triad in animal studies in 1852, and as a result, the condition is sometimes called Bernard syndrome. There were also 2 previous reports of ptosis and miosis resulting from sympathetic nerve damage in humans: 1 by Edward Selleck Hare in 1838 associated with brachial plexus tumor, and the other by Silas Weir Mitchell in 1864 associated with a gunshot wound to the neck. Although Horner was the first to objectively characterize the co-occurrence of vasomotor and ocular changes in a human patient, he did not identify the etiology of the condition, discuss its relationship to the sympathetic nervous system, or reference any of the previous studies in animals or humans. It is possible that a lack of familiarity with previous investigations delayed the full appreciation of the mechanism underlying this disorder.

Opsoclonus persisting during sleep in West Nile encephalitis.

BACKGROUND: Recent outbreaks of West Nile virus infection have alerted the public to disabling paralysis as an outcome. Ocular motor involvement with West Nile virus is rare. OBJECTIVE: To describe a patient with West Nile virus encephalitis that resulted in opsoclonus-myoclonus syndrome with persistent ocular oscillation on electroencephalography during stage 2 sleep. PATIENT: A 53-year-old man who presented with viral prodrome followed by intense vertigo and encephalopathy. In addition to multifocal myoclonic jerks in the extremities, his eye movements were disrupted by bursts of high-frequency, conjugate ocular oscillations that occurred in random directions. RESULTS: Electroencephalography showed eye movement artifacts during the awake state and stage 2 sleep. Opsoclonus-myoclonus syndrome remained disabling 3 months after onset but markedly improved 8 months after onset. CONCLUSIONS: West Nile virus is another cause of opsoclonus-myoclonus syndrome that can occur in conjunction with encephalitis. The presence of an eye movement artifact on results of electroencephalography during stage 2 sleep should raise suspicion for opsoclonus.