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Authors' Reply:

We thank Dr Kasahata and his colleagues for confirming the induction of Gallyas-positive neurons in ischemic foci. The cytological changes described in their patient seem to be in agreement with our series on cerebral infarcts (1). They demonstrate the use of this distinction in ruling out progressive supranuclear palsy in their patient with progressive supranuclear palsy-like clinical features. Since ischemic complications are very frequent in human autopsy brains, awareness of this potential pitfall may improve the accuracy of histological diagnoses. It remains to be clarified, however, whether these cytological features are unique to ischemia or are shared with other nondegenerative processes that may harbor tau-positive structures, such as inflammation, trauma, and demyelination (2, 3). Careful comparison of these categories by looking for possible argyrophilia and tau-like immunoreactivity in a broader disease spectrum will specify the diagnostic use and pitfalls of these findings. Furthermore, this may provide insight into the mechanisms of tau deposition induced by ischemia, possibly distinct from but partly shared with neurodegeneration.

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