Post-mortem studies interpretations

While these proposals provide useful and testable hypotheses, they are based on slim evidence from post mortem neurochemistry of schizophrenia. Since the deficits in GABAergic markers may be interpreted as demonstrating neuronal hypofunction rather than cell loss, they could equally be ascribed to a consequence of, rather than a cause of, glutamatergic abnormalities. It would be valuable to identify temporal changes in neurochemistry over the disease course, rather than end-stage information that most post-mortem studies inevitably provide, as well as more information from individuals at risk for schizophrenia. 

In the first definitive monograph on asthma, published in 1864, Sir Henry Hyde Salter concluded that the airway obstruction in asthma results from bronchoconstriction, mucus plu ng of the airway lumen, and edema of the airway wall (Salter, 1864). Salter s interpretations were probably based on clinical observations rather than on pathological examinations, because post-mortem findings were not described at that time. In fact, the initial histopathological studies of the airways of asthmatics did not recognize the presence of mucosal edema For example, in the first description of a post-mortem examination of a patient who died in status asthmaticus, Leyden concluded that the airflow obstruction resulted from mucus in the airways and that the walls [of bronchi]. ..are not essentially changed (Leyden, 1886). 

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