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PubMed1987

Trauma and multiple sclerosis. An hypothesis.

An obligatory event in the pathogenesis of the multiple sclerosis plaque appears to be an increase in the permeability of the blood-brain barrier. Neuropathological observations of the brain of persons suffering from concussion after relatively minor head injury, as well as of animals subjected to experimental brain injury, have shown that alterations of the blood-brain barrier constitute a common result of such trauma. It is postulated that the alterations of the blood-brain barrier secondary to trauma of the brain or spinal cord of patients with already established multiple sclerosis may result in an exacerbation or recurrence of a previously symptomatic plaque, in the appearance of symptoms from a silent lesion, or in the formation of a new plaque in such an area of selected vulnerability. In other persons injury to the nervous system may cause the development of multiple sclerosis plaques in the previously damaged areas when the disease has its onset after the trauma. There is no evidence to support the idea that trauma ever causes multiple sclerosis.

Adult↗

PubMed1990

Selective loss of nigral neurons in Pick's disease: a morphometric study.

Loss of neurons from the substantia nigra (SN), which is often encountered in Pick's disease, was quantitatively analyzed in 13 cases of Pick's disease and 19 age-matched controls. On sections from the upper and lower portions of the SN, the pigmented zone (zona compacta) and the non-pigmented zone (zona reticulata) were delineated, and these zones were partitioned into quarters: medial, mid-medial, mid-lateral and lateral. Neuronal loss was fairly severe and more evident in the upper section of the SN (-40%), especially in the mid-medial and lateral quarters. In the lower section (neuronal loss: -28%), the medial quarter was most severely affected. Non-pigmented neurons were preserved. Fibrillary gliosis was denser in the zona reticulata, where neuronal loss was minimal. These findings revealed a selective vulnerability of nigral neurons according to their topography and pigmentation and suggests the primary involvement of some neuronal groups (especially the pigmented neurons) of the SN in Pick's disease.

Aged↗

PubMed1993

Fluorescent histochemical localization of lipid peroxidation during brain reperfusion following cardiac arrest.

Rats were subjected to cardiac arrest and resuscitation, 90 min of reperfusion, and in situ perfusion fixation. Thiobarbituric acid (TBA) was included in the aldehyde-free perfusion fixative, the TBA reaction was driven in situ by heating, and fluorescence microscopy was utilized to characterize the location of products of the TBA reaction. Absorbance-difference spectra were performed on butanol-extracted brain homogenates to confirm in situ formation of TBA adducts with aldehydic products of lipid peroxidation. Nissl-stained sections revealed good cellular fixation without shrinkage artifacts. Fluorescence was not seen microscopically when TBA was omitted from the perfusion fixative, and little fluorescence was present in normal brains or brains after ischemia only. However, after 90-min reperfusion, intense granular fluorescence was seen in the neuronal perikarya (especially at the base of the apical dendrite) of numerous pyramidal neurons in cortical layers 5 and 6 and in the pyramidal layer of Ammon's horn in the hippocampus. The nuclei of these cells exhibited no fluorescence. Fluorescence was also present in some striatal neurons, but was absent in the adjacent radial bundles. Neither glia nor white matter exhibited similar fluorescence. These observations indicate that neurons in the selectively vulnerable zones of the cortex and hippocampus are early and specific targets of lipid peroxidation during post-ischemic reperfusion.

Animals↗

PubMed1986

Laminar distribution of neocortical senile plaques in senile dementia of the Alzheimer type.

A prospective longitudinal study was undertaken in a geriatric hospital on women over 75 years of age, clinically diagnosed as either intellectually normal or having senile dementia of the Alzheimer type (SDAT) of varying degrees of severity. Mental impairment was assessed prospectively. Fifteen brains from this population were studied to evaluate quantitatively the distribution of senile plaques (SP) in relation to cortical lamination. SP density in four neocortical areas (first temporal gyrus; supramarginal gyrus calcarine area; precentral gyrus) was significantly correlated with the degree of mental impairment. SP distribution in the cortical layers was evaluated by an indirect method and appeared to be fairly constant from one case to another. Significantly higher SP densities were observed in layers II and III of the temporal and occipital samples, while minimal values were noted in layer I. Lower densities of SP were found in layers V and IV of the occipital and temporal lobes. These data suggest a selective vulnerability of some areas of cortical projections in SDAT.

Aged↗

PubMed1987

Regional cerebral blood flow of acute carbon monoxide poisoning in cats.

The mechanism of selective vulnerability of the cerebral white matter and pallidum in acute carbon monoxide (CO) poisoning was experimentally investigated by measuring regional cerebral blood flow (rCBF) with the iodo-[14C]antipyrine method. A CO group consisting of five cats was exposed to 0.2%-0.3% CO gas and the rCBF was measured when moderate systemic hypotension (70-80 mm Hg) occurred; because systemic hypotension of this level during exposing to 0.2%-0.3% CO gas induces typical cerebral lesions of acute CO poisoning in almost all cats [Okeda et al. Acta Neuropathol (Berl) 54:1-10 (1981)]. Controls were a hypotension group of three cats with moderate systemic hypotension induced for 1 h without CO exposure, and a control group of five cats which inhaled only air for 2 h. The rCBF of each structure in the CO and hypotension groups was evaluated as a percentage of that of the control group. The rCBF of the CO group exhibited a wide range (68%-127%) according to the structures examined, and the mean (94.6%) was large compared with that (range: 53%-82%, mean: 67.4%) of the hypotension group. In the CO group, the examined brain structures where divided in two groups according to the rCBF values; low-value structures and high-value structures. There was significant (P less than 0.05) difference between rCBFs of both the structure groups. The cerebral white matter and pallidum belonged to low-value structures, and these rCBFs did not show any significant difference from those of other structures in this structure group.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

PubMed1985

Polyarteritis nodosa and peripheral neuropathy. Ultrastructural study of 13 cases.

Peripheral nerves from 13 patients suffering from polyarteritis nodosa with multiple mononeuropathy were studied by light and electron microscopy. In the majority of cases, the vascular lesions were associated with Wallerian-like degeneration. Myelinated fibers presenting a normal axon with a disproportionately thin myelin sheath were less numerous. Unusual abnormalities consisted of swollen axons with an accumulation of organelles. Unmyelinated fibers were also damaged. A quantitative estimation of myelinated fibers loss did not show any selective vulnerability of either the large or the small diameter group.

Adult↗

PubMed1989

Changes in the hippocampus and the cerebellum resulting from hypoxic insults: frequency and distribution.

Detailed neurohistological studies were undertaken on 35 cases of cardiac arrest, 17 of hypoglycaemia and 16 of status epilepticus. It was found that the frequency and pattern of selective vulnerability in the hippocampus were similar following cardiac arrest, hypoglycaemia and status epilepticus with the exception that the lateral limb of the dentate fascia was more frequently involved in hypoglycaemia than in the other two groups of cases. Within each group, however, CA1 was the most vulnerable. The cerebellum was less frequently affected in hypoglycaemia and status epilepticus than after cardiac arrest. These findings are compared with recent experimental studies in the rodent which have suggested that the pattern of neuronal damage in each of the three conditions is different.

Cerebellum↗

PubMed1985

Low dose of barbiturates for prevention of hippocampal lesions after brief ischemic episodes.

Male Mongolian gerbils were subjected to bilateral carotid occlusion for 5 and 10 min, followed by 7 days of recirculation. After this interval, serial sections were made of the posterior region of the dorsal hippocampus, and the number of surviving neurons was determined per mm length of CA1 sector. In halothane-anesthetized animals only 21.1% of CA1 neurons survived 5-min ischemia, but this percentage could be raised to 78.6% when animals were pretreated with 25 mg/kg pentobarbital before ischemia. Pretreatment with 50 mg/kg pentobarbital before 5-min ischemia or pretreatment with 25 mg/kg pentobarbital before 10-min ischemia did not reduce CA1 lesions. It is concluded that a non-anesthetic dose of barbiturates is able to prevent selective vulnerability of CA1 sector, but that this effect is limited to the initial 5 min of ischemia.

Animals↗

PubMed1982

Autonomic neurons of the sacral spinal cord in amyotrophic lateral sclerosis, anterior poliomyelitis and "neuronal intranuclear hyaline inclusion disease": distribution of sacral autonomic neurons.

Further evidence is presented that the Onuf's nucleus (or "colonne en torsade" of Laruelle) and the intermediolateral nucleus of the sacral cord share common selective vulnerability with the thoracolumbar intermediolateral nucleus in ALS, anterior poliomyelitis and "neuronal intranuclear hyaline inclusion disease". Sparing of the sacral nuclei in the motor neuron diseases and neuronal loss of the nuclei in the multisystem atrophy are correlated well with normal and disturbed vesicorectal function. The clinicopathological evidence strongly supports the view that the Onuf's nucleus represents autonomic neurons much as the intermediolateral nucleus.

Adult↗

PubMed1978

Topographic distribution of neurofibrillary tangles and granulovacuolar degeneration in hippocampal cortex of aging and demented patients. A quantitative study.

Topographic analysis was performed of the distribution of Alzheimer's neurofibrillary tangles and the granulovacuolar degeneration of Simchowicz in the hippocampal cortex of patients with Alzheimer's dementia and mentally normal aged controls. A semiautomated scanning stage microscope was linked potentiometrically to an XY pen recorder in order to plot cytoarchitectonic "scattergrams" from the sequentially screened hippocampal formations. The density of both lesions per cubic mm of pyramidal cortex was quantified by measuring the area of each of six "zones", using a digitizer and programmable calculator. In elderly normal brains as well as those of Alzheimer's disease, the statistically most representative ranking order of predilection for neurofibrillary tangles (in decreasing severity) was: entorhinal cortex greater than subiculum greater than H1 greater than end-plate greater than presubiculum greater than H2. For granulovacuolar degeneration the best rank order was: subiculum greater than H1 greater than H2 greater than end-plate greater than entorhinal cortex greater than presubiculum. The notable similarities of both such orders of predilection to the well-recognized "selective vulnerability" of certain hippocampal neurones in clinical conditions of hypoxia, ischemia and epilepsy suggest some common, focally accentuated cytotoxic mechanism may underlie all these regional predispositions.

Age Factors↗

PubMed1975

Experimental cerebral ischemia in mongolian gerbils. I. Light microscopic observations.

Light microscopic observations were carried out on Mongolian gerbils (Meriones unguiculatus) subjected to a partial cerebral ischemia by occlusion of the left common carotid artery at the neck. About 30% of gerbils developed an ischemic injury in the ipsilateral hemisphere and their brains revealed the following histopathologic features: 1. the changes were related to the intensity (duration) of the ischemic insult and to the time elapsed following release of the occlusion. The ischemic lesions appear to progress after re-establishment of the circulation and this presents one facet of a "maturation" phenomenon which seems to be a general principle applicable to various parameters of ischemic injury. The rate of "maturation" of the lesions is related to the intensity of the ischemic insult, a lesser intensity resulting in longer development of lesions. 2. The changes were either focal or diffuse in character. The former were assumed to be directly related to a vascular involvement; among the latter the topistic distribution of the hippocampal changes suggested a feature of selective vulnerability. 3. An indirect indication of neuronal recovery was surmised from observations on animals sacrificed after different periods following occlusions of the same duration. Also capable of recovery was a "reactive change" observed in the H3 neurons of the hippocampus. This change was characterized by central chromatolysis and resembled the "rimäre Reizung" of Nissl.

Animals↗

PubMed1991

Excitatory and inhibitory amino acid changes in ischemic brain regions in spontaneously hypertensive rats.

Excitatory (glutamate, aspartate) or inhibitory amino acids (gamma-aminobutyric acid: GABA, taurine) and glutamine contents were examined in acutely induced cerebral ischemia in spontaneously hypertensive rats. At 20 min ischemia most of these amino acids remained unchanged, but glutamine significantly decreased by 14% in the CA3 hippocampal subfield. At 60 min ischemia glutamate significantly decreased by 14% in the CA3, aspartate by 17-26% in the CA3, cingulate cortex, septum and striatum. In contrast, GABA significantly increased by 48-106% in the cortices (frontal, parietal and cingulate), striatum and nucleus accumbens, but insignificantly in hippocampal subfields. Likewise, taurine increased in the parietal cortex and nucleus accumbens. Glutamine showed heterogeneous changes (increase in the nucleus accumbens and decrease in the CA3). Amino acid levels change during ischemia, but their changes are varied in each area, implying that different reaction of amino acids may explain the selective vulnerability to cerebral ischemia.

Amino Acids↗

PubMed1988

Neurochemical effects of prenatal treatment with ochratoxin A on fetal and adult mouse brain.

Ochratoxin A (OA) is a mycotoxin produced by several storage fungi, such as Aspergillus ochraceus and several Penicillium species. OA (3 mg/kg) was given intraperitoneally to pregnant mice on day 11 of gestation (day 1 = day of insemination), and neurochemical changes in brains of their offspring were examined at fetal and adult stages. OA treatment produced retardation of intrauterine growth as well as microencephaly and reductions in total weight and DNA content of fetal brains. Specific activities of lysosomal enzymes in fetal brains began to increase by the 2nd day after treatment and to reach peak activities by the 3rd or 4th day after injection, indicative of cell death in the developing brains. Examination of brain regions of offspring three months after birth revealed that both tissue weight and DNA content were reduced to 80% of control in cerebral hemispheres (CHs; cerebral cortex and subjacent white matter, hippocampus, and amygdala) and to 90% of control in remainder of the brain (BGDM; basal ganglia, diencephalon, and mesencephalon). Total content of noradrenaline (NA), dopamine (DA) 5-hydroxytryptamine (5-HT) in treated CH showed about 15% reduction, although, expressed on a tissue weight basis, concentrations of these monoamines were increased by about 15%. Total DA content in BGDM was also reduced to 85% of controls, but total content of NA and 5-HT in BGDM and pons-medulla oblongata did not change. These results suggest that synaptogenesis of monoamine neurons in the cerebrum is impaired by prenatal treatment with OA, and that dopaminergic neurons show a slight selective vulnerability to the toxin.

Animals↗

PubMed1990

Ischemia in the dorsal hippocampus is associated with acute extracellular release of dopamine and norepinephrine.

The cerebral dialysis technique was employed to monitor extracellular concentrations of dopamine (DA), norepinephrine (NE), dihydroxyphenylacetic acid (DOPAC), and homovanillic acid (HVA) in the dorsal hippocampus of gerbils before and after cerebral ischemia induced by carotid artery occlusion. Extracellular concentrations of DA and NE in the dorsal hippocampus increased from baseline levels of less than 35 fmol/collection interval to 180 and 200 fmol/collection, respectively, within 36 minutes following carotid artery ligation (n = 8 animals). Extracellular concentrations of the DA metabolites, DOPAC and HVA, did not change significantly following carotid artery ligation. These data demonstrate that ischemia in the dorsal hippocampus is associated with a mared release of DA and NE. This release may contribute to the selective vulnerability of the dorsal hippocampus to neuronal damage during ischemia.

Animals↗

PubMed1978

Loss of pigment-laden stellate cells: a severe alteration of the isocortex in juvenile neuronal ceroid-lipofuscinosis.

Juvenile neuronal ceroid-lipofuscinosis is associated with a moderate numerical decrease of isocortical neurons. From Nissl preparations, it is not apparent, whether this neuronal rarefication occurs at random or affects specific types of cortical neurons. Lipopigment preparations facilitate the distinction between pyramidal and stellate cells. In juvenile neuronal ceroid-lipofuscinosis, they reveal an almost complete to total loss of small pigment-laden stellate cells. This type of local circuit neurons, scattered throughout the corpuscular and pyramidal layer in varying numbers and patterns of distribution, is common to all isocortical regions. Its pronounced and selective vulnerability in this lysosomal disease may be causally related to the marked functional impairment of the brain.

Adolescent↗

PubMed1983

Sequence-dependent toxicity and small bowel mucosal injury in neonatal mice treated with low doses of 5-azacytidine and X-irradiation at the late organogenesis stage.

A combined treatment of pregnant mice on day 12 of gestation with both azacytidine and X-irradiation in low doses induces sequence-dependent histological effects. These effects, in turn, induce different symptomatic signs if evaluated either prenatally or neonatally. In the azacytidine treatment/X-irradiation sequence the malformations of the fetal forebrain are predominant. Consequently, these dams show a high incidence in the stillbirth rate. Conversely, the X-irradiation/azacytidine treatment schedule leads only to a mild brain hypoplasia, and does not cause an increased stillbirth rate. In these offspring, however, a severe impairment of small bowel epithelial proliferation capacity was found. This is linked to an outstanding neonatal mortality within 48 h after birth. The pathogenesis of these sequence-dependent effects can be attributed to a selective vulnerability of cells in different stages of the generation cycle. This comprises a high degree of cytolethality affecting the S/G2-stage cells in azacytidine/X-irradiation treatment and the G1/S-stage cells in the reverse combinations (Schmahl 1979). The present observations show the validity of a teratological assay in providing a detailed analysis of the cell kinetic responses after combined noxious influences.

Animals↗

PubMed1991

Environmental-occupational risk factors and familial associations in multiple system atrophy: a preliminary investigation.

We studied 60 patients with multiple system atrophy and autonomic failure and 60 control subjects matched for age, sex and race. Their psychosocial history, pedigree and occupation were obtained by personal interview. An inventory of autonomic and neurologic symptoms was obtained from 148 first-degree relatives of the patients and 80 controls by a self-administered questionnaire. Patients with multiple system atrophy had significantly more potential exposures to metal dusts and fumes, plastic monomers and additives, organic solvents, and pesticides than the control population. The potential exposures were determined in most subjects by their reported usual occupation. Clinical symptoms of multiple system atrophy were reported by a significantly larger group of patients' relatives than controls. These findings are possibly consistent with the hypothesis that multiple system atrophy develops as a result of a genetically determined selective vulnerability in the nervous system. Specific neuronal systems may become targets for environmental insults or toxins, and the disease state may occur when ageing neuronal systems can no longer sustain functional capacity. This preliminary study supports the need to further explore possible environmental, occupational, and familial contributions to the aetiology of multiple system atrophy.

Environment↗

PubMed1995

Pathogenesis of diencephalic lesions in an experimental model of Wernicke's encephalopathy.

The relationship of thiamine deficiency to Wernicke's encephalopathy has been well established. The biochemical bases and physiologic mechanisms responsible for the pathologic changes and their selective distribution within the brain remain controversial. The present paper reviews recent biochemical, histopathological and pharmacological evidence of a glutamate-mediated excitotoxic mechanism of neuronal loss in pyrithiamine-induced thiamine deficiency (PTD), a rat model of Wernicke's encephalopathy. A mechanistic model involving the unique combination of thiamine deficiency-induced impairment of energy metabolism, increased release of histamine, and multidirectional glutamate inputs is presented to explain the selective vulnerability of thalamic nuclei to excitotoxic lesions in the PTD model.

Animals↗