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Twenty-three biopsies from patients with the typical symptoms of intermetatarsal neuroma (so-called Morton's metatarsalgia) were compared histologically and semi-quantitatively with 25 plantar nerves from the intermetatarsal space III/IV gained at autopsies from cases where no problems in the forefoot had been recorded. The histomorphological examination of the nerves from autopsies revealed the same findings as were found in the biopsies. Thus, qualitatively, the nerves from patients could not be distinguished from those gained at autopsy. The only difference was the diameter of the resected nerves: semi-quantitative analysis of the nerves showed that the 17 thinnest ones were all from autopsies and the five thickest ones from biopsies of symptomatic patients. At medium diameters, however, there was wide overlap of the two groups. The study yielded a specificity of the swelling of 80 % and a sensitivity of 78%. From these results it must be concluded that diagnostic MRIs or ultrasonography, are unnecessary for decision-making about operative treatment and are not superior to exploratory local anaesthesia. Since histomorphological findings in intermetatarsal neuroma (so far accepted as the gold standard for confirmation of that diagnosis) were the same as findings in autopsied (normal) specimens, the value of postoperative histological examination is questioned. It merely proved that the nerve has been resected.

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Light microscopic immunohistochemical investigations were performed on neurofibrillary tangles (NFT) in four histologically confirmed cases of Alzheimer's disease (AD) and in five patients with a progressive supranuclear palsy (PSP). The antibody panel included antisera to the neuronal microtubule-associated protein, tau, and to isolated paired helical filaments (PHF), as well as mouse monoclonal antibodies (MAbs) to phosphorylated epitopes on high and medium molecular weight neurofilament subunits (RT97 and BF10, respectively). Paraffin sections were also impregnated with the Gallyas silver method, which specifically stains tangles and cortical neuropil threads in AD, but does not stain normal neurofilaments. All tangles in PSP and AD showed consistent immunostaining with antibodies to tau protein and isolated PHF, regardless of their localization. MAbs RT97 and BF10, however, did not stain or only weakly stained, subcortical tangles in PSP and AD, whereas most cortical NFT in AD were intensely immunostained. All tangles in PSP were as heavily impregnated with Gallyas as they were in AD. Furthermore there were extensive networks of Gallyas-positive, tau- and PHF-immunoreactive neurites in subcortical gray areas containing NFT, and bundles of positive axons in white matter tracts interconnecting subcortical nuclei of PSP. Our studies indicate a much more extensive disruption of fibrillar proteins in PSP subcortical neurons than previously reported. They furthermore indicate a very similar antigenic profile of NFT in PSP and AD, as far as subcortical neurons are concerned.

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