Search

Objective: Normal-pressure hydrocephalus (NPH) is a potentially treatable syndrome with abnormal cerebrospinal fluid dynamics. Meningeal fibrosis and/or obliteration of the subarachnoid space has been suggested as the pathoanatomic basis. The purpose of the present study was to investigate whether meningeal fibrosis causes increased resistance to cerebrospinal fluid outflow (R(out)) and/or increased B-wave activity and whether pathological changes in the brain parenchyma after brain compliance, causing increased B-wave activity., Methods: The study involved a group of 38 consecutively studied patients with clinical and radiological evidence of idiopathic NPH, for whom a frontal brain biopsy was obtained. For 29 patients, hydrodynamic criteria of NPH were fulfilled and a ventriculoperitoneal shunt was performed., Results: Meningeal fibrosis was found in 12 of 25 biopsies containing arachnoid tissue, but no correlation with R(out) or B-waves was found. Pathological parenchymal changes, most often Alzheimer's disease (10 cases) or vascular changes (10 cases), were found in 21 biopsies, but no correlation with B-waves or R(out) was found., Conclusion: The results suggest that leptomeningeal fibrosis is not the only pathoanatomic basis of increased R(out) and/or B-wave activity in patients with NPH and that various degenerative changes in the parenchyma may be responsible for the altered cerebrospinal fluid dynamics characteristic of NPH.

In a series of 571 acoustic neuromas, 23 were identified as cystic tumors. An immunohistochemical study including nervous system-associated protein (S-100), glial fibrillary acidic protein (GFAP), neurofilament protein (NF), laminin, fibronectin, vimentin, factor VIII (von Willebrand factor)-related antigen, and the nuclear antibody Ki-67 was performed. The cyst walls contained numerous S-100-positive fibrils distributed throughout the whole extent of the walls. Laminin, fibronectin, and vimentin were predominantly located around the vessel walls, factor VIII was found inside the vessels. GFAP-positive lamellae occurred in 50% of the cases near the surface of the cyst walls. Ki-67 is an antigen associated with cell proliferation. The density of Ki-67-positive cells was found to be 36 times lower in 16 noncystic controls than in the 23 cystic neuromas, indicating that the increase in tumor size in cystic acoustic neuromas may be caused by expansion of the cysts and not by an actual increase in the growth rate of the tumor cells. The data achieved in this series may contribute to better planning of the surgical approach. Because of the risk of sudden expansion of cystic elements, a wait-and-see policy should not be applied to patients with cystic acoustic neuromas.

In order to develop an in vivo model for growth of acoustic schwannomas, we studied tumor specimens from 10 patients, transplanted into a subcutaneous pocket of 67 nude mice. The number of tumors which survived or grew was 63 (94%). Obvious macroscopic growth was observed in 22 (33%), status quo in 28 (42%), and regression of tumor size in 13 (19%). The tumor disappeared in 4 cases (6%). Serial implantation was not possible due to the small amount of neuroma tissue in the surviving tumors. In animals with obvious macroscopic growth, neovascularization was clearly demonstrated. The presence of Schwann cells in the implants was confirmed immunohistochemically. The proliferative activity in the original and implanted tumors was evaluated by the proliferating cell nuclear antigen (PCNA) and Ki-67 nuclear antigen stainings and showed good correlation between primary tumors and implants. This in vivo tumor model will open new opportunities to study the biology of acoustic tumors and to test different therapeutic modalities.

Tumor configuration and attenuation on CT scan with contrast enhancement or gadolinium-DTPA-enhanced MR depends upon tumor histology. Various elements are responsible for the density on CT or MR, e.g. blood vessels, fatty tissue, connective tissue, calcium, necrotic tissue, hemorrhage and intra- or extratumoral cyst formation. In a series of 571 acoustic neuromas we found 23 cystic tumors. The diagnosis was based on neuro-imaging examination, confirmed at surgery and finally verified histologically. Eight tumors with small or large cysts were diagnosed by CT or MR scan as intratumoral, and 15 with large cysts were diagnosed as extratumoral. We found a good correlation between the histology of cystic acoustic neuromas and the CT or MR scans. The tumors were predominantly hypodense, corresponding to the cystic areas, but also iso- or hyperdense areas were observed, corresponding to other tissue types. Antoni type B tissue and xanthomatous areas were found in all 23 cases.

The objective of this study was to evaluate histologically the toxicity of human beta-endorphin on the rat central nervous system after intrathecal administration. Animals received a single injection of 5 micrograms (n = 9) or 50 micrograms (n = 10) on each of four consecutive days, while others received 50 micrograms (n = 8) as a single dose. The control groups received either physiologic saline (n = 10) during each of four consecutive days or had sham operations (n = 4). Tests for nociception (tail-flick latency), motor function, and reflexes (righting reflex, eye-blink reflex, and inclined plane) were performed 5, 15, 30, 60, and 120 min after injection. Both dosages produced a dose-dependent impact on these parameters. In the 50-micrograms group, there were no significant differences in analgesia between the first and the fourth doses injected. The 50-micrograms dose produced catalepsy in some animals. All changes returned to baseline within 24 h. One animal in the 50-micrograms group developed hind limb paralysis after a single injection. Histologic sections from brain, brain stem, and spinal cord were prepared. No changes in histology were found except for that in the paretic animal, which had anoxic changes in the hippocampus and other cortical areas. Human beta-endorphin produced no neurotoxicity. The effect on nociception, reflexes, and motor function confirmed the results of previous studies.

Objective: We assessed pituitary histology in patients with Cushing's disease., Design: Systematic histological assessment of pituitary tissue removed at surgery., Patients: Thirty-six consecutive patients cured from Cushing's disease by transsphenoidal neurosurgery., Measurements: Microscopical examination of all available tissue removed at operation., Results: After selective removal of tissue supposed to represent an adenoma in 25 patients this could be histologically verified in 18. In the 11 patients who had undergone a total hypophysectomy an adenoma could be demonstrated in three patients only, despite a systematic search of the entire pituitary gland. Only in 21 of the 36 cured patients (58%) could an adenoma be verified., Conclusions: Combining the present results with previous reports there is strong reason to believe that in some patients with Cushing's disease no histological lesion in the pituitary is verifiable.

The immunoprofile of 76 human pituitary adenomas was studied with particular reference to the occurrence of entrapped, non-neoplastic pituitary cells. This phenomenon was defined as unevenly distributed, usually peripherally located cells forming less than 1% of the total cell population. The stellate contour of such passively incorporated cells departed from the more rounded shape of most principal, neoplastic cells. Thirty-six of the adenomas studied comprised one or more types of entrapped elements. According to the hormone produced, prolactin-(PRL-)cells most commonly occurred as a minor "foreign" component (seen in 23 of the adenomas), whereas growth hormone-(GH-) and adrenocorticotropic hormone-(ACTH-)cells rarely were trapped (seen in 5 and 4 of the adenomas. Entrapped follicle stimulating hormone-(FSH-), luteinizing hormone-(LH-), and thyroid-stimulating hormone-(TSH-)cells assumed an intermediate position (seen in 14, 17 and 15 of the adenomas, respectively).

Acoustic neuromas are more frequent, larger, and more vascular in women, and their growth rate increases during pregnancy. Estrogen receptors were claimed to be demonstrated in these neoplasms for the first time in 1981. Since then, numerous diverging studies, using various biochemical and histochemical methods, have been published on the contents of estrogen and progesterone receptors in acoustic neuromas. We determined the content of estrogen and progesterone receptors by means of an immunohistochemical method, using monoclonal antibodies, which has proved to be reliable, reasonably sensitive, and clinically relevant in other tissues, especially in breast carcinomas. No estrogen or progesterone receptors could be found in 18 consecutive acoustic neuromas from 7 men and 11 women, ranging in age from 26 to 73 years. The results do not support preoperative hormone treatment of acoustic neuromas.

The ethanol withdrawal syndrome in man and animals is characterized by signs of CNS hyperactivity although a direct measurement of a physiological variable reflecting this CNS hyperactivity has never been performed in untreated man or in animals. We induced ethanol dependence in the rat by means of intragastric intubation with a 20% w/v ethanol solution, thus keeping the animals in a state of continuous severe intoxication for 3--4 days; during the subsequent state of withdrawal characterized by tremor, rigidity, stereotyped movements and general seizures a 25% increase in cerebral oxygen consumption (CMRO2) could be measured; this increase was not due to catecholamines originating from adrenal medulla as adrenomedullectomized animals showed a similar increase in CMRO2 (28%); the withdrawing animals showed a corresponding cerebral blood flow (CBF) increase. The elevated CMRO2 and CBF could be reduced to normal by administration of a beta-adrenergic receptor blocker (propranolol 2 mg/kg i.v.), and hence the increased CMRO2 during ethanol withdrawal could be related to catecholaminergic systems in the brain, e.g. the noradrenergic locus coeruleus system which is anatomically well suited as a general activating system. This interpretation is supported by the earlier neurochemical finding of an increased cerebral noradrenaline turnover during ethanol withdrawal. The exact mechanism underlying the increased cerebral oxygen consumption during ethanol withdrawal and the effect of propranolol on cerebral function during this condition remains to be clarified.