The Neuropathology Task Force of the Consortium to Establish a Registry for Alzheimer's Disease (CERAD) has developed a practical and standardized neuropathology protocol for the postmortem assessment of dementia and control subjects. The protocol provides neuropathologic definitions of such terms as "definite Alzheimer's disease" (AD), "probable AD," "possible AD," and "normal brain" to indicate levels of diagnostic certainty, reduce subjective interpretation, and assure common language. To pretest the protocol, neuropathologists from 15 participating centers entered information on autopsy brains from 142 demented patients clinically diagnosed as probable AD and on eight nondemented patients. Eighty-four percent of the dementia cases fulfilled CERAD neuropathologic criteria for definite AD. As increasingly large numbers of prospectively studied dementia and control subjects are autopsied, the CERAD neuropathology protocol will help to refine diagnostic criteria, assess overlapping pathology, and lead to a better understanding of early subclinical changes of AD and normal aging.

The objective of this trial was to determine the efficacy of echinomycin (1.2 mg/m2) administered on a weekly times four schedule in the treatment of patients with recurrent or progressive central nervous malignancies despite adequate radiotherapy. Thirty-five patients were registered on study. The majority of patients (20) had glioblastoma multiforme. Ten had anaplastic astrocytoma. Eight patients had received prior nitrosoureas. SWOG performance status was 1 in 11 patients and 2 in 22. The median age was 51 years (25-75 years). One patient had a partial remission (3%:95% confidence interval: 1%-16%). Twenty two patients had progressive disease. The median survival was 5.9 months. Toxicity was primarily gastrointestinal with nausea and vomiting in 13 patients and nausea only in 11 patients. Hepatotoxicity occurred in 10 patients. Echinomycin given at this dose and schedule is not effective in treating patients with recurrent or progressive glioblastoma multiforme or anaplastic astrocytomas.

A lipolytic enzyme has been demonstrated by means of a cytochemical technique and by direct chemical assay in granulomatous tissues of guinea pigs with encephalomyelitis and demyelinization resulting from the injection of an emulsion comprised of brain tissue and adjuvants, including Mycobacterium butyricum. Combined histologic and cytochemical studies showed that the lipolytic enzyme was present in the cytoplasm of a large proportion of the reactive histiocytes in the granulomatous tissue around the site of injection in the diseased animals, and that the enzyme-containing histiocytes were even more numerous in the inflamed regional lymph nodes. In control experiments, when emulsions lacking either brain tissue or M. butyricum were injected in previously normal guinea pigs, the experimental condition did not develop; under these circumstances the lipolytic enzyme was found in only a small proportion of the cells of the granulomatous tissue around the injection sites, and it was almost negligible in the regional lymph nodes of these animals. It was absent from the cells of the lymph nodes of normal animals, and from the cells of talcum and aluminum hydroxide granulomas produced experimentally in guinea pigs. The lipolytic enzyme may be a factor in the pathogenesis of the experimental encephalomyelitis and demyelinization.

✓ In three patients intrasellar cysts were found without epithelial lining but containing thick dark brown fluid. The clinical course and histological findings suggested intermittent hemorrhage and infarction of the adenohypophysis as the probable etiology. The surgical importance of differentiating these lesions from cystic craniopharyngiomas and pituitary adenomas has been stressed in a discussion of the diagnostic characteristics. Wide surgical drainage is recommended as the treatment of choice. Evidence points to a possible relationship of these cysts to the “empty sella syndrome.”