Biomedical subjects
Publications and source records attributed to H J Gertz.
A 59-year-old patient suffered during three months from depressive episode. Thereafter he developed depressive attacks of 30 to 60 minutes duration, reoccurring weekly to every third week. The patient could be treated successfully with Carbamacepine.
To elucidate the pathogenetic significance of neurofibrillary tangles in Alzheimer's disease, the dendritic tree of tangle-bearing and unaffected pyramidal cells of area CA1 of the hippocampus was morphometrically examined. Golgi-stained neurons were assessed which were deimpregnated and counterstained with Congo red to visualize neurofibrillary tangles. The study revealed that tangle-bearing neurons have more extensive apical dendritic trees than tangle-free neurons. It is concluded that metabolic processes associated with the formation of neurofibrillary tangles may increase neurotrophic activity on a single cell level and counteract the cellular degeneration process.
A 19-year-old man suffering from a first episode of schizophrenia developed a neuroleptic malignant syndrome (NMS) after administration of haloperidol and levomepromazine. After five weeks of neuroleptic treatment he died of an unknown cause. Histological examination of the brain revealed a low melanin content in neurons in the substantia nigra (SN). Since neuromelanin in SN is the end-product of nonenzymatic dopamine degradation, the amount of melanin probably depends on the overall amount of dopamine produced during life. Thus, dopamine production must have been low in the reported case. In addition, ectopic neurons were found in subcortical white matter.
Neurons of the substantia nigra show severe morphological changes in Parkinson's disease. Pathological alterations of cell bodies have been described, whereas those of neuronal processes have hardly been investigated. Golgi impregnation has been the chosen method for demonstrating neuronal processes and dendritic and somatic spines. We therefore used the Golgi-Braitenberg method to qualitatively and semi-quantitatively study the substantia nigra of eight patients with Parkinson's disease compared with eight control cases. Golgi impregnation of substantia nigra neurons was good in all control cases. In full agreement with the analysis of Braak and Braak (1986) three neuronal types within the substantia nigra were found. In cases of Parkinson's disease, severe pathological changes such as decrease of dendritic length, loss of dendritic spines and several types of dendritic varicosities were found only in the melanin-containing pars compacta neurons. Pars reticulata nerve cells were intact. These findings support the predominant role played by the dopaminergic efferent pathway in the degenerative process. The afferent pathway was not affected. This suggests that the substantia nigra lesion is primary in Parkinson's disease. Loss of neurons found in H & E sections corresponded to a lesser amount of impregnated pars compacta neurons in cases with Parkinson's disease when compared to controls. Evidences exist that the duration of the disease may be related to the extent of pathologically altered Golgi-impregnated pars compacta cells. The amount of Lewy bodies in H & E sections corresponded to the quantity of round varicosities in impregnated pars compacta neurons. These round dendritic varicosities were considered to be Lewy body inclusions.(ABSTRACT TRUNCATED AT 250 WORDS)
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Reported in this paper is a case of a fetus delivered in the 24th week of pregnancy whose intracranial space was found to be almost totally filled up by a choroid plexus papilloma. Co-expression of vimentin and cytokeratin 8, 18 of the epithelium was immunocytochemically observed, as had been also described in normal fetal choroid plexus.
A shortening of sleep duration is going along with aging. Several somatic diseases and different psychiatric disorders, which increasingly occur in old people cause sleep disorders. Thus patients suffering from disturbed sleep must be examined carefully before treatment. Benzodiazepines and Clomethiazol are potent and save drugs for sleep disorders in the aged. Antidepressants and neuroleptics should be applicated only for sleep disorders caused by underlying psychiatric diseases.
Samples of 14 brains of autopsied patients suffering from dementia of the Alzheimer type were examined. In Congo red-hemalum stained 14-microns-thick sections of the hippocampus 15 tangle-bearing and 25-30 unaffected nerve cells of area CA1 per case were measured for cell size and nucleolar size utilizing an interactive image processing unit. In affected cells tangle size was measured too. There was no significant difference in neuron size and nucleolar size between affected and unaffected cells. In tangle-bearing cells nucleolar size and cell size were not correlated with tangle size. Since nucleolar volume can serve as an indicator of RNA synthesis of a cell, tangles themselves seem not to disturb nerve cell metabolism.
There is an age-dependent nerve cell loss in some areas of the brain, while other brain regions are stable with aging. The nucleus basalis of Meynert (NbM) is believed to be the source of cholinergic innervation of the cerebral cortex, and loss of its neurons seems to be followed by cognitive deficits. The normal age kinetics of the NbM are, therefore, of considerable importance. Sixteen autoptic human brains were examined, ages ranging from 35th week of gestation to 90 years of age. Blocks containing the NbM in its entirety were cut into 20-mu thick serial sections; every 25th section was cresyl-violet stained and underwent morphometric analysis. Nerve cell counts were slightly but significantly higher in the right hemisphere. The total number of neurons in the 9th decade was 23% below that in newborns. This decrease was statistically significant. We hypothesize that there is a threshold number of nerve cells below which cognitive failure is highly probable.
In a patient with Creutzfeldt-Jakob Disease (CJD), MRI showed increased signal intensity in striatum, thalamus, and cerebral cortex in images obtained with TR 1,600 msec, and TE 35 and 70 msec. In postmortem examination, all affected areas showed the hallmarks of CJD, such as status spongiosus, gliosis, and nerve cell loss. MRI can help to differentiate CJD from other dementing processes.
Creutzfeldt-Jakob disease (CJD) occurring in later life has a duration of about one year. Gait disturbance, myoclonic jerks, dementia and akinetic mutism occur. Post-mortem examination of the brain shows nerve cell loss, gliosis and spongiform changes of the grey matter. Clinical and neuropathological features of a case of the panencephalopathic type of CJD, with additional extensive degeneration of the cerebral white matter, are described. The panencephalopathic type of CJD is characterized clinically by a longer duration and a biphasic course.
In 7 cases of senile dementia of Alzheimer's type (SDAT) and in 7 age-matched controls, nerve cells of the medial septal nuclei (area CH1) and of the vertical limb of the diagonal band of Broca (area CH2) of the right hemisphere were counted in Cresyl-fast-violet-stained serial sections. The granular cells of the ipsilateral fascia dentata were Golgi-stained and dendritic spine density was quantified in 10-micron segments. There was a significant loss of neurons in areas CH1 and CH2 in SDAT cases compared to controls. The spine density of the granular cell dendrites was significantly reduced in the distal parts of the dendrites. In the most proximal part, where cholinergic septal fibers form synapses, the spine density was not significantly different between the two groups. We assume that collateral sprouting of undamaged inputs occurs maintaining a constant number of spines in the proximal segments despite the loss of source neurons within CH1 and CH2.
We report a proven case of CJD with prolonged clinical course and white matter involvement which consisted of severe, widespread myelin damage in the forebrain and cerebellum but with sparing of the internal capsule. Histologically, there was status spongiosus of the involved white matter with axonal loss, proliferation of hypertrophic astrocytes and scattered and perivascular foamy macrophages. White matter lesions have not been considered to be a significant feature of CJD. In the last few years, however, a few cases have been described with prominent degeneration of cerebral white matter. We believe that our findings corroborate the existence of an entity that at present may only be defined as spongiform panencephalopathy.
We give an electron microscopic description of vascular convulates, which occur along with normal brain aging. They consist of up to 10 vessels which are surrounded by a common perivascular space. We can make clear that the convolutes consist exclusively of normal arterioles. Each single vessel shows endothelial cells without pores. The media is mostly composed of a single layer of smooth muscle cells which are surrounded by adventitial cells or their processes. The adventitial cells show a high amount of lipid inclusions. From microangiographic research it is obvious that the absolute increase in length of the vessels is the main factor in the genesis of vascular convolutes. According to experimental animal studies it seems likely that recurrent hypoxic conditions lead to a considerable increase in length in the cerebral arterioles in old people.
We describe light- and electron-microscopically a new type of intracytoplasmatic inclusions within cell processes of the cerebral cortex and the underlying white matter. These structures measure 5-50 micron in diameter and consist almost exclusively of densely packed alpha- or beta-glycogen granules, which never occur together in any single structure. Within their periphery, electron-dense amorphous spots and cell organelles, especially mitochondria, were seen. No membrane-bound glycogen was observed. We propose to call them granular glycogen bodies. They occur in 4 of 7 examined postmortem specimens of the cerebral cortex of people older than 60 years of age. They were not found in 4 younger controls aged 26-48. Their appearance may reflect a distinct turnover disorder of carbohydrate metabolism, which becomes manifest under diverse pathologic conditions and in the normal aging process.