A 63-year-old man with arterial hypertension suffered from depression and suicidal wish after a cerebrovascular accident and transitory left hemiparesis. He was urgently admitted to hospital in severe metabolic acidosis which caused renal failure and coma, ending fatally within two days. At necropsy calcium oxalate crystals were found in the renal tubules and cerebral vessel walls with chemically induced meningoencephalitis. From these findings glycol poisoning was diagnosed. There was a lethal concentration of ethylene glycol in the urine. The toxic effects of ethylene glycol are due to its metabolites. The oxalate crystals are primarily of diagnostic importance.
In the current classification basal encephaloceles are grouped together with real transsphenoidal encephaloceles. But those encephaloceles extending only into but not through the sphenoid sinus seem to represent a specific clinical entity and therefore should be regarded as a rare subgroup of sphenoidal encephaloceles. One personal case and six cases from the literature are reviewed, the own case being associated with an empty sella turcica. The initial sign is rhinorrhea, almost invariably. The association with other intracranial anomalies is uncommon. The extradural transsphenoidal or transethmoidal midline approach accompanied by a shunting procedure today is the most suitable method of surgical treatment.
In this review, the value of assessing proliferation parameters in surgically resected pituitary tumour tissue is analyzed. Histological examination of basal dura biopsies identifies invasive growth even when intraoperatively not apparent to the surgeon. Determination of DNA-polymerase activity, Ki-67 immunohistochemistry and DNA-flow-cytometry shows a clear difference in the proliferative potential of enclosed and invasive pituitary adenomas. Among the various endocrinologically differentiated groups ACTH-secreting adenomas associated with Nelson's syndrome and thyrotropinomas were the most rapidly proliferating. At present, however, our results reveal that the prognosis of an individual patient cannot be reliably predicted on the basis of such studies.
Between 1975 and 1991, 40 patients with newly diagnosed medulloblastoma of the posterior fossa were treated at the authors' institutions. After aggressive surgical resection 39/40 patients (98%) received craniospinal radiation therapy (RT), including a local boost. A group of 29 patients was treated with adjuvant chemotherapy. The estimated overall 5-year survival and 5-year relapse-free survival (RFS) probabilities were 75% and 65%, respectively. The 5-year survival was significantly prolonged for patients treated after 1981 as compared to those treated between 1975 and 1980 (80% vs 64%, p = .02). However, multivariate analysis identified the adequate coverage of the target volume by external RT as the only significant variable (p = .0031). The extent of resection, stage according to Chang, radiation dose to the posterior fossa (< 55 Gy vs > or = 55 Gy) and the use of chemotherapy did not significantly influence survival and RFS. The initial site of recurrence was the posterior fossa with or without disseminated central nervous system (CNS) disease in 5 patients, the CNS without posterior fossa in 4 patients, and the bone marrow in 2 patients. An isolated frontal relapse occurred in 1 patient. We conclude that quality control of RT plays a decisive role in the long-term outcome of patients with medulloblastoma.
Summary BACKGROUND AND OBJECTIVE With regard to intracranial tumours, elevated hCG in CSF or serum has been considered to be specific for germ‐cell tumours. Recently however, elevated hCG has also been shown to be present In cyst fluid and CSF of patients with craniopharyngiomas. While germ‐cell tumours are generally non‐cystic, the aim of our study was to determine the significance of hCG In cystic intracranial lesions. DESIGN in a prospective study, hCG Immunoactivity and subunits of hCG were measured in cyst fluid, CSF, and serum of patients harbouring intracranial cyst lesions. PATIENTS AND MEASUREMENTS hCG immunoactivity was measured in cyst fluid and serum samples of 42 patients. CSF samples were available from 12 patients with craniopharyngiomas. In order to fully characterize the hCG immunoactivity, we used immunoradiometric assays for total hCG activity (measuring both intact hCG and the free β‐subunit of hCG), and those specific for intact, dimeric hCG (hCG), free β‐subunit of hCG (hCGP) and free α‐subunit. Furthermore, immunostaining of tumour tissue was performed using monoclonal antibodies directed against the free β‐subunit of hCG. RESULTS Total hCG immunoactivity was markedly elevated in cyst fluid of all 17 craniopharyngiomas (range 36·7–4558 IU/I; normal <5IU/I). Moderately elevated levels of hCG in cyst fluid were detected In three of four pituitary adenomas, in two metastases from lung cancer and in two arachnoid cysts. hCGβ was detected in cyst fluid from all hCG positive cysts, while specific determination of intact (dimer) hCG and α‐subunit mostly yielded negative results. No hCG immunoactivity was found in cystic giiomas, meningiomas or haemangioblastomas. hCG was elevated in CSF of two patients with craniopharyngiomas, but no hCG immunoactivity was detected in any serum sample. Subtle immunostaining of epithelial cell groups was shown in five of ten craniopharynglomas. Clear immunostaining for hCGβ was also found in scattered epithelial cells of one pituitary adenoma. CONCLUSIONS hCG immunoactivity in cystic intracranial lesions is due mainly to hCGβ. Measurement of hCG immunoactivity in cyst fluid can be helpful in the differential diagnosis of intracranial cystic lesions, if surgery is restricted to cyst decompression and no histology is available. High levels suggest a craniopharyngioma.
The case of a patient is reported who suffered from disturbed concentration and memory and constructive apraxia. She had only mild neuropsychological deficits at the first examination. T2-weighted MRI presented extensive focal white matter changes. A brain biopsy showed changes typical for Alzheimer's disease (AD). The extent of the white matter lesions was surprising compared to the mild clinical signs she had. This case confirms that AD may result in prominent white matter disease caused by incomplete infarction or demyelination.
Cytomegalovirus (CMV) causes several neurological diseases in the late stages of AIDS, but their ante-mortem diagnosis is problematic.Clinical criteria (defining a presumptive diagnosis) and polymerase chain reaction $4 (PCR) assay from cerebrospinal fluid (CSF) were blindly used to predict the involvement of CMV in neurological disorders of 164 consecutive AIDS patients undergoing a lumbar puncture.During the follow-up, a definite diagnosis based on viral culture of CSF, clinical outcome and/or CNS histology was allowed in 88 patients, 27 (16 %) of whom had a proven CMV related neurological disease.The concordance between the presumptive and definite diagnosis was of 60 %, inducing a moderate agreement kappa index of 0.40.In contrast, the sensitivity and specificity of PCR were respectively of 89 and 94 %, with a positive and negative predictive values of 86 and 95 %.Cytomegalovirus related neurological diseases appeared thus as a frequent complication of AIDS, and detection of viral DNA in CSF by means of PCR seems a reliable tool for their diagnosis, allowing its use for therapeutic decisions 20 99mTC-HMPAO LEUCOCYTE SCINTIGRAPHY IN DIAGNOSIS
Organ perfusion with bloodless solutions is an established clinical method for protecting the heart against ischemic damage. In our study, we evaluated the effects of intraischemic bloodless brain perfusion on postischemic ultrastructural neuronal changes in a model of severe incomplete forebrain ischemia produced by hemorrhagic hypotension combined with temporary carotid occlusion in the rat. Four groups of rats were compared. During an ischemic insult of 30 min, the brains of two groups were perfused via both external carotids with either a normosmolar normothermic magnesium-enriched perfusate (MgSO4, 30 mM; NaCl, 37 mM; mannitol, 180 mM; n = 10) or a normothermic normal saline solution (n = 9) at a rate of 6 ml/h. Two other groups (ischemia without perfusion, n = 8; no ischemia and no perfusion, n = 7) served as controls. After 30 min of ischemia, withdrawn blood for hemorrhagic hypotension was reinfused, the carotid arteries reopened, and the brains reperfused for 2 h. After perfusion-fixation, qualitative and quantitative evaluation of postischemic cell changes of hippocampal CA1 neurons was performed by electron microscopy. Brain perfusion with the magnesium-containing solution significantly protected neurons against ischemic cell changes and provided an ultrastructural pattern similar to that seen in the nonischemic control group. In contrast, brain perfusion with normal saline solution did not result in neuronal protection. We conclude that intraischemic intracarotid brain perfusion with magnesium-enriched perfusate protects hippocampal neurons significantly against ischemic cell changes in the early reperfusion period after transient severe forebrain ischemia.
A 56 year old mentally disabled woman of short stature was admitted to our hospital because of severe chest pain and dyspnoea. An extended myocardial infarction in the anterior wall was clinically found and confirmed by autopsy. On admission cretinism with massive myxedema was diagnosed, which was confirmed by subsequent laboratory findings. Only at the base of the tongue thyroid tissue 3 mm in diameter was found. In the anterior lobe of the pituitary gland areas with nodular hyperplasia and microadenomas of TSH-producing cells were detected. Thyrotroph adenomas in long standing hypothyroidism are rare. There are only few reports on congenital hypothyroidism as primary underlying disease.
Is MEG source analysis able to precisely locate the primary focal epileptic activity? 22 patients with pharmacoresistant temporal lobe epilepsy were recorded during presurgical evaluation simultaneously with multichannel MEG/EEG and invasive (subdural) electrodes to evaluate the increase of information gained by MEG concerning the localization of focal epileptic activity and lesions. With this systematic study it should become clearer how often MEG can establish a diagnostic bridge between function and morphology. In addition, MEG localization accuracy of focal epileptic activity was to be validated empirically by invasive EEG recordings and postsurgical outcome. Spikes in the MEG were used for magnetic source localization, and the result was combined with magnetic resonance imaging (MRI). All patients definitely suffered from temporal lobe epilepsy and revealed a structural abnormality in MRI. 17 patients with lesions in the temporal lobe were operated meanwhile and became markedly improved or seizure free. In 7 of 8 patients with a tumor and validated operation outcome, a very close correlation of the 3D-magnetic source localization and the border of the tumor in the brain was found (distance less than 10 mm). In 8 of 9 patients with a temporal/hippocampal atrophy and validated operation outcome, dipoles of epileptiform activity were located within the atrophic lobe.(ABSTRACT TRUNCATED AT 250 WORDS)
We report the fatal outcome of bifrontal intracerebral hemorrhage after an epileptic drop attack. The importance of a prophylactic treatment is stressed, especially the use of head protectors. The possibility of a palliative surgical treatment of these patients should also be considered - the callosotomy.
Immunohistochemical expression of the three major isozymes of protein kinase C--Types I, II, and III--was studied in 32 cases of human pituitary adenomas, and the results were compared in detail with their clinical data. Immunoreactivity for the Type I and Type II isozymes was negative in tumor cells of all pituitary adenomas. Moderate to strong cytoplasmic immunoreactivity for the Type III isozyme was constantly seen in acromegaly, Cushing's disease, and nonfunctioning adenomas, which indicated overexpression of the isozyme, since only slight cytoplasmic immunoreactivity was observed in the normal human anterior pituitary cells. Among 13 prolactinomas, 5 cases showed positive immunoreactivity for Type III in all tumor cells, whereas 8 cases showed negative immunoreactivity for the isozyme in all or more than 85% of tumor cells. The sizes of the tumors in this protein kinase C Type III negative group of prolactinomas tended to be smaller than those of the Type III positive prolactinomas. Also, the negative immunoreactivity for Type III was predominantly observed in those cases where prolactinomas were relatively well controlled by continuous oral dosage of dopamine agonists before operation. These results suggest that protein kinase C Type III is closely involved in human pituitary adenomas. The exceptional negativity for the isozyme in prolactinomas may be relevant to the suppression of tumor growth by dopamine agonists.
Between 1975 and 1991, 40 patients with newly diagnosed medulloblastoma were treated at the authors' institutions. After aggressive surgical resection 39/40 (98%) received craniospinal radiation therapy with a local boost to the posterior fossa and other macroscopically involved areas. A group of 29 patients was treated with adjuvant chemotherapy. The five-year actuarial survival and event-free survival were 75% and 65%, respectively. Survival was significantly better for patients treated after 1981 as compared to those treated between 1975 and 1980 (p = .02). Younger age (two to four years) was associated with a better prognosis (p = .02). The extend of resection, Chang-stage, radiation dose to posterior fossa and the use of chemotherapy did not significantly impact on survival and relapse-free survival.
A 60-year-old woman had undergone surgery for ductal breast carcinoma. Six years after operation there was no local recurrence, but metastases were found in the liver, lungs and in a meningioma.