(Fig 1) (Fig 3). Lewy bodies were also found within neurons of the substantia innominata and of the locus ceruleus.The cerebral cortex in general showed no cytoarchitectural abnormalities or changes in the nerve fibers or glia (except for the expected scarring at the biopsy site). Adja¬ cent to many of the nerve cells, espe¬ cially in the frontal and insular cortex, there were hyaline eosinophilic bodies of rounded or irregular contour, which in their appearance and staining properties resembled the swollen axons seen else¬ where; but they differed from the Lewy bodies (Fig 4). These structures, identified as juxtaneuronal axonal swellings, could also be found in the cerebral biopsy speci¬ men. In the hippocampus, many of the pyramidal neurons showed granulovacuolar degeneration.

BACKGROUND Pituitary carcinomas are rare adenohypophysial neoplasms, the definition, diagnosis, therapy, and prognosis of which are controversial. METHODS Pituitary carcinomas were defined as primary adenohypophysial neoplasms with documented craniospinal and/or systemic metastases. The authors report a clinicopathologic study of 15 examples examined by light microscopy, immunohistochemistry, and image analysis. Both proliferative activity and p53 tumor suppressor gene expression were studied. RESULTS The study group consisted of 15 patients, including 8 males and 7 females ranging in age from 34‐71 years (mean, 56 years). Of these patients, seven had adrenocorticotropic hormone (ACTH)‐producing tumors (four in the context of Nelson's syndrome), seven had prolactin‐producing tumors, and one had a nonfunctioning tumor. No evidence of diabetes insipidus was seen in any case. Fourteen tumors were initially considered macroadenomas. Of the ten cases for whom tumor extent was known, all had invasive tumors. The interval from the initial diagnosis of adenoma to that of carcinoma ranged from 0.3 to 18.0 years (mean, 6.6 years; median, 5.0 years); the longest mean interval (15.3 years) occurred for patients with Nelson's syndrome. The latency was twice as long for ACTH‐producing tumors as for prolactin (PRL) cell tumors (9.5 vs. 4.7 years). All carcinomas showed a greater tendency toward systemic metastasis than craniospinal metastasis; the rate of systemic metastasis was 71% for PRL cell tumors and 57% for ACTH‐producing tumors. Thirteen percent of tumors showed both patterns of metastasis. Fully 50% of primary tumors and the majority of metastases showed nuclear pleomorphism and/or hyperchromasia. The mean mitotic, MIB‐1, and proliferating cell nuclear antigen indices for primary tumors and metastases were as follows: 2/10 high‐power field (hpf), 2.6% and 11%, respectively; 6/10 hpf, 7.8% and 16%, respectively. Staining for p53 protein was noted in 57% of primary tumors and 88% of metastatic tumors; a relative increase in p53 expression in metastases was noted in 83%. All but one of the primary and metastatic tumors were aneuploid. The most common treatments were radiation therapy and, for PRL cell carcinomas, dopamine agonist administration. Both treatments provided only palliation. Eighty percent of the patients died of metastatic disease 7 days to 8 years after the diagnosis of carcinoma; of these, 66% died within 1 year. At last follow‐up, 20% of patients were alive with metastases 9‐18 months after diagnosis. CONCLUSIONS Nearly all pituitary carcinomas present as functioning, microscopically atypical or mitotically active, invasive macroadenomas. By definition, after an interval related to their immunotype, all metastasize. The tumors show a greater tendency toward systemic metastasis than craniospinal metastasis and are associated with poor prognosis. Radiation and dopamine agonist therapy generally provide only palliation. Proliferation indices and p53 expression tend to be higher in metastases than in ...

Subcortical arteriosclerotic encephalopathy, a chronic vascular dementia with hydrocephalus, was characterized pathologically in five patients by severe thickening of small vessels and by diffuse regions of white matter loss with gliosis. Lacunar infarcts were also present. The clinical picture in 11 patients was characterized by: (1) persistent hypertension and systemic vascular disease; (2) acute strokes; (3) subacute accumulation of focal neurologic symptoms and signs over weeks to months; (4) long plateau periods; (5) lengthy clinical course; (6) dementia; (7) prominent motor signs and pseudobulbar palsy and; (8) hydrocephalus. The pathogenesis of subcortical arteriosclerotic encephalopathy is unknown; possible mechanisms include diffuse ischemia and fluid transudation with subsequent gliosis related to subacute hypertensive encephalopathy.

Although damage to the veins of Batson's epidural plexus is usually considered the origin of bleeding in traumatic lumbar puncture, a lesion of these veins would not explain the cases in which postmortem examination shows blood confined to the subdural and subarachnoid spaces. In two patients who had lumbar punctures a few days before death, there was subarachnoid hematoma of the cauda equina at autopsy. In one of these cases, the radicular vessels were shown to be the source of bleeding. Spinal subarachnoid and subdural hemorrhages after lumbar puncture may be due to laceration of radicular vessels by the spinal needle.

Five infantile and one adult case of Sturge-Weber disease were studied pathologically. The calcification occurring under the leptomeningeal angiomatosis increased with advancing age. Light and electron microscopy of two cases showed the smallest, and therefore possibly the earliest, calcifications occurred in perithelial cells. It is hypothesized the cause of calcification is anoxic injury to endothelial, perithelial and possibly glial mitochondria due to stasis and abnormal vessel permeability in the cerebral vessels composing the Sturge-Weber angioma.