Biomedical subjects
Publications and source records attributed to M Lammens.
We report an autopsy proven case of acute hemorrhagic leukoencephalitis. There was a very rapid evolution leading to death in less than 24 hours. CT of the brain revealed widespread hypodensities in both frontal lobes. In the cerebrospinal fluid as well as in the peripheral blood, there was a moderate leucocytosis. The literature is reviewed.
Two patients developed acute sensorimotor polyneuropathy after intoxication with lithium carbonate. Nerve conduction studies, electromyography, and sural nerve biopsy proved it to be an axonal neuropathy. Recovery of muscle strength, reflexes, and sensory function started weeks after discontinuation of lithium therapy. One patient fully recovered within a year. In the literature we found nine other cases of lithium polyneuropathy.
Many lesions along the visual pathway from the retina to the occipital cortex can cause a horizontal hemianopia. The anatomy of the visual pathway is reviewed in an attempt to clarify how and where this visual field defect develops. A case is presented in which two ischemic occipital infarcts caused a bilateral inferior horizontal hemianopia and complex visual hallucinations. Previous cases of occipital lesions resulting in an altitudinal hemianopia are reviewed.
Hypothermia, defined as a core temperature less than 35 degrees C has multiple causes and several neurological consequences. The cases of three patients with definite multiple sclerosis since more than a decade are reported, who presented with several episodes of coma and hypothermia. Systematic neuropathologic examination of the hypothalamus in one case did not reveal any abnormality.
Morphometrical investigation of brain nuclei in dementia of the Alzheimertyme and in other types of dementia has been done for the last 10 years. The N. Basalis of Meynert (Acetylcholine pathway) has been screened rather extensively by several groups. The L. Coeruleus (Nor-adrenergic pathway) also has been fairly well documented. The N. Raphe Dorsalis however-an important relay nucleus in the serotonergic pathway-was only studied cytometrically by a few groups. Other nuclei were not investigated systematically f.e. N. Accumbens; this nucleus might play an important role however in memory disturbances via Gabaergic influence on excitatory amino acids. This quantitative study focuses on those less well studied brain areas. A cytometrical analysis (cell counts-cell sizing) was performed on serial sections in clinically well-documented cases of different types of dementia: Alzheimer, Pick, Huntington, Jakob-Creutzfeldt. Results were compared with controls and for the N. Accumbens also with the values obtained in the brain of catatonic schizophrenics. The cell sizing and counting was done on cresylviolet sections, on modified Bielschowsky-stained sections and on Peroxidase-Anti-Peroxidase (P.A.P.) treated sections with a polycloncal antibody against Alzheimer Paired Helical Filaments (PHF). Our results show that the nerve cell degeneration in those nuclei is quite different in the diverse types of dementia, pointing to a disease specific physiopathology.
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Bombesin (a tetradecapeptide), the C-terminal nonapeptide of bombesin (bombesin-NP), and litorin (a parent nonapeptide), each stimulated amylase secretion from rat pancreatic fragments. These responses were not affected by atropine. The concentrations that produced half-maximal stumulation of secretion were 0.25 nM for bombesin, 0.30 nM for bombesin-NP, and 0.07 nM for litorin, as compared to 0.12 nM for caerulein and 0.80 muM for the cholinergic agent carbamylcholine. When used at maximal concentrations, bombesin, bombesin-NP, and litorin showed no action on cyclic AMP levels in the presence of 5 mM theophylline. By contrast, caerulein and secretin increased cyclic AMP levels by 27 and 208%, respectively. Bombesin, bombesin-NP, and litorin did not activate adenylate cyclase in a purified pancreatic plasma membrane preparation, whereas caerulein and secretin increased this activity 20 and 16-times, respectively...
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Thickening of the dura in continuity with a convexity meningioma was noted on T1-weighted magnetic resonance (MR) images in seven patients. In five cases the corresponding CT image of the lesions was typical of meningioma. In two other cases the CT image of the lesions was atypical, owing to cyst formation in one and extensive edema in the other. After intravenous injection of paramagnetic contrast medium in four patients, the thickened dura demonstrated contrast enhancement at a variable distance from the tumor. In three patients the thickened dura was confirmed surgically. Pathology, available in one case, showed the thickened dura to correspond to tumoral extension within or around the dura. Magnetic resonance demonstration of thickening of the dura in continuity with a mass at the cerebral convexity may prove to be of importance in the differentiation of atypical lesions on CT and MR, especially with lower field magnets. Moreover, it could provide useful information to the neurosurgeon for more complete resection of the tumor.
Magnetic resonance was performed in five patients with obstructive hydrocephalus due to surgically proven colloid cyst of the third ventricle. On T1-weighted images two lesions were homogeneously hyperintense and another homogeneously isointense with the surrounding brain parenchyma. On T2-weighted images these three lesions were strongly hypointense except for a hyperintense rim at the periphery. At surgery in these patients the cyst was thin walled and filled with viscous colloidal material. In two patients the content of the lesion was composed of two layers. The outer layer was hyperintense and the inner layer hypointense in one patient. In the other patient the periphery of the lesion was isointense with central hypointensity. On T2-weighted images the content of both lesions was hyperintense at the periphery with central hypointensity. In these last two patients at surgery the cyst was thin walled too. However, two clearly different components could be found in the cyst content: an outer component composed of amorphous material and cellular debris and an inner component consisting of viscous material.
To investigate the involvement of NADPH-diaphorase (NADPH-d)-containing neurons in Alzheimer's disease (AD), NADPH-d enzyme histochemistry in vibratome sections was applied to the superior frontal and superior temporal cortex and the neostriatum in 5 AD and 6 aged control brains. Overall there was a neuronal loss and atrophy in the cortex of AD. Despite slight morphological neuronal changes in the cortex of AD, we found no significant difference in the number of NADPH-d-positive neurons in both cortex and neostriatum between control and AD cases. These results provide further evidence for a selective preservation of NADPH-d neurons in AD. In order to check whether nNOS-immunoreactive neurons are identical to NADPH-d-positive neurons in the human brain, we examined the frontal and temporal cortex and neostriatum of normal human brains in serial cryostat sections. We found that nNOS-containing neurons paralleled NADPH-d-positive neurons in these brain regions. Copyrightz1999S.KargerAG,Basel
Heparan sulfate (HS), along with serum amyloid P component, has been identified in all types of amyloid investigated so far, regardless of the type of amyloid protein deposited. To assess whether unique or specific HS proteoglycans (HSPGs) may be involved in the formation of these lesions, we have investigated the accumulation of several distinct HSPG epitopes in the cerebra of patients with different forms of neurodegenerative disease. A panel composed of several antibodies revealed distinctive patterns of HSPG accumulation. In patients with dementia of the Lewy body type, the burned-out-type plaques and preamyloid-type plaques were strongly stained by both the anti-HS 'chain' and anti-HS 'stub' antibodies, but by none of the available anti-core protein antibodies. In Alzheimer's disease, the preamyloid-type plaques, dense-cored-type plaques, neuritic-type plaques and the neurofibrillary tangles were stained by the anti-'stub' antibody. The anti-'chain' and the anti-core protein antibodies, in contrast, failed to stain the preamyloid-type plaques and burned-out-type plaques, but stained the neuritic-type plaques in these patients. These data suggest differences in the types of HS and HSPG (fragments) that accumulate in amyloid lesions that may hallmark neurodegenerative disorders of different etiologies.
Defects of neuronal migration were detected in the brains of five unrelated infants with Potter syndrome (oligohydramnios sequence). These consisted of abnormal lamination of cerebral cortex, white matter heterotopias, and meningeal and molecular zone neuronal-glial ectopias. Besides, various other brain anomalies were sometimes found. They comprised one or more of the followings: abnormal gyration patterns (gyral fusion, cerebellar microgyria), cerebellar granule and Purkinje cell heterotopias, brain stem heterotopias, adysplasia of basal ganglia, gliosis, mineralization, and hydrocephalus. Detailed investigations, using standard neuropathologic stains, immunohistochemical and Golgi methods, and a new electron microscopic histochemical technique that we applied to study the developing human brain, suggest that migration defects of neurons are caused by an abnormality in their glial guides, the radial glial fibers, during the period of cortical histogenesis. We hypothesize that abnormally and precociously induced radial glial transformation into astrocytes is the pathogenic mechanism for the defects in neuronal migration. The etiological factor(s) that precipitates such abnormal glial transformation seems to be heterogeneous. Its relation to the Potter anomaly is discussed.
Prominent dural enhancement was noted in 10 (16%) of 61 superficial malignant intracranial tumors studied with contrast-enhanced MR imaging during a 2-year period. Included were six glioblastomas, three parenchymal metastases, and one case of dural metastasis. Seven patients had surgery. In four, there was extensive leptomeningeal invasion in the center of the lesion. In two of these lesions there was firm attachment of the center of the tumor to the dura, but without dural invasion despite extensive external carotid artery supply to the tumor in one case. In two cases the overlying dura was normal, and there was no leptomeningeal tumoral invasion. In the case of dural metastasis, huge nodular lesions were present along the inner aspect of the dura. In none of the cases did prominent dural enhancement adjacent to the tumor correspond with tumoral invasion or extension to the dura. Prominent dural enhancement on contrast-enhanced MR images appears to be much less frequent in malignant tumor than in meningioma, where it is seen in up to 60% of the cases. We believe this finding is more likely to represent reactive changes of the dura than tumoral invasion.
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The magnetic resonance (MR) findings in 50 surgically verified intracranial meningiomas were reviewed. An attempt was made to correlate their signal intensity on spin echo (SE) T1-weighted, proton density [N(H)], and T2-weighted images with the different histologic subtypes. The T1-weighted images were nonspecific in differentiating the subtypes of meningiomas. On proton density and T2-weighted images, more information was available, but there remained large group (46%) of meningiomas that were not classifiable. The average signal intensity scores on T1-weighted, proton density, and T2-weighted images in the different histologic subtypes were correlated with each other using the Student t test. Only one significant correlation (psammomatous-anaplastic) and three almost significant correlations (syncytial-transitional or psammomatous and transitional-psammomatous) were found. Different histologic subtypes may have a different MR appearance, but this does not suffice to reach a histologic diagnosis by MR imaging.