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  • 1
    Electronic Resource
    Electronic Resource
    Heterotopic brain tissue in the submandibular region and lung (1978)
    Springer
    Acta neuropathologica 43 (1978), S. 217-220 
    Details
    ISSN: 1432-0533
    Keywords: Extracranial heterotopia of brain tissue ; Nasal glioma ; Anencephaly ; Meningoencephalocele
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Two cases of extracranial heterotopia of the brain are reported. Case 1, in an otherwise normal female baby, had a brain heterotopia in the submandibular region. Case 2, in a still-born female baby with anencephaly, had the heterotopia in the lung. The lesion in case 1 is believed to be an encephalocele that has been pinched off through a cleft in the bone or through a foramen of the skull; the pathogenesis is similar to that of the so-called “nasal glioma”. Concerning the pathogenesis of case 2, contrary to the generally supported embolism theory, observation of serial sections of the tumor in the lung favors the aspiration theory according to which amniotic brain tissue fragments, which are dislocated into the amnion because of nonclosure of the ventricle or following destruction of the fetal brain, are aspirated by fetal respiratory movements in the 4th to 6th month of intrauterine life.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00691581
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  • 2
    Electronic Resource
    Electronic Resource
    An autopsy case of acute porphyria with a decrease of both uroporphyrinogen I synthetase and ferrochelatase activities (1984)
    Springer
    Acta neuropathologica 64 (1984), S. 6-11 
    Details
    ISSN: 1432-0533
    Keywords: Acute porphyria ; Porphyric neuropathy ; Axonal degeneration ; Uroporhyrinogen I synthetase ; Ferrochelatase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary An autopsy case of a 37-year-old woman with acute porphyria is reported. The patient began to complain of severe menstrual pains, and later developed serious peripheral neuropathy and various autonomic nervous symptoms. The autopsy revealed a marked loss and degeneration of axons and myelin sheaths in the peripheral nervous system (PNS), and prominent central chromatolysis of the spinal anterior horn cells. The predominant process of the peripheral neuropathy appeared to be axonal degeneration. Biochemical analysis showed a marked increase of delta-aminolevulinic acid (ALA), porphobilinogen, uroporphyrin, and coproporphyrin in the urine, and an increase of coproporphyrin and protoporphyrin in the stools and blood. In the analysis of the enzymatic activities of the liver and bone narrow, the activity of ALA synthetase (ALA-S) was markedly increased, and the activities of both uroporphyrinogen I synthetase (URO-S) and ferrochelatase were decreased. It was characteristic in this case that the enzymatic abnormalities found in both acute intermittent porphyria (AIP) and variegate porphyria (VP) coexisted. Biochemical analysis of the sciatic nerve showed an increase of ALA-S activity and a decrease of both URO-S and ALA dehydrase activities. This was the first report that indicated the presence of abnormal activities of the heme biosynthetic enzymes in the peripheral nerves of porphyric patients. The possibility was discussed that these enzymatic abnormalities of the heme biosynthesis in the peripheral nerve itself might be strongly related to the pathogenesis of the porphyric neuropathy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00695599
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  • 3
    Electronic Resource
    Electronic Resource
    A study of experimental cyanide encephalopathy in the acute phase —Physiological and neuropathological correlation (1984)
    Springer
    Acta neuropathologica 64 (1984), S. 99-107 
    Details
    ISSN: 1432-0533
    Keywords: Cyanide encephalopathy ; Selective white matter lesion ; Cerebral local blood flow
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A study was performed to elucidate the significance of various physiological factors contributing to the pathogenesis of experimental cyanide encephalopathy, such as the systemic arterial blood pressure, venous pressure, common carotid blood flow and local blood flow of the cerebral grey and white matters, and blood gas including pH. The histology and topography of the brain damage was also analysed. Twenty-one cats were divided into four groups. The animals in groups 1, 2 and 3 were subjected to continuous infusion of 0.2% sodium cyanide solution and to the ensuing hypotension below 100 mm Hg by administering a ganglion-blocking drug and by respiratory arrest. Severe damage developed in the deep cerebral white matter, corpus callosum, pallidum and substantia nigra, but the damage of the cerebral cortex and hippocampus was not remarkable. The animals in group 4 that were subjected to cyanide infusion without significant hypotension (above 100 mm Hg), but to the same degree of acidosis as that of the the other groups, had similar morphological changes, but to a lesser degree. On the basis of our physiological and morphological findings, we speculated that the pathophysiological factors of tissue hypoxia and subsequent hypotension operated in cyanide leucoencephalopathy. The topographic selectivity seemed to be related to the characteristic cerebral vascular system, and the severity of the white matter lesions was related to the intensity of both hypoxia and hypotension during cyanide infusion, but not to the extent of acidosis, total dose of cyanide or duration of its infusion per se.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00695572
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  • 4
    Electronic Resource
    Electronic Resource
    Chronic manganese poisoning: A neuropathological study with determination of manganese distribution in the brain (1986)
    Springer
    Acta neuropathologica 70 (1986), S. 273-278 
    Details
    ISSN: 1432-0533
    Keywords: Chronic manganese poisoning ; Pallidal lesion ; Distribution of manganese
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary An autopsy case of a 52-year-old man suffering from chronic manganese poisoning (CMP) is reported with determination of the manganese distribution in the brain. The patient had been working in a manganese ore crushing plant since 1965. In 1967 he began to complain of difficulties in walking and diminished libido. Later, he developed various neuro-psychiatric symptoms including euphoria, emotional incontinence, masked face, monotonous speech, “cock-walk”, increased muscle tone, weakness of upper and lower extremities, tremor of the eye lids, and exaggeration of knee jerks. The major neuro-pathological change was degeneration of the basal ganglia, in which the pallidum was severely affected. The pallidum discolsed a loss and degeneration of nerve cells, which was especially marked in the medial segment, a prominent decrease of myelinated fibers, and moderate astrocytic proliferation. The substantia nigra was intact. Distribution of manganese in the brain of the present case of CMP was determined using flameless atomic absorption spectrometry and compared with control cases and also a case of Parkinson's disease (PD). There was no significant difference between the control cases and the case of PD in average concentration of manganese and its ditribution in the brain. The present case of CMP showed no elevation in average concentration of manganese in the brain. However, there were some changes in its distribution. Thus, the continuance of neurological disorders in CMP is not linked to an elevated manganese concentration itself in the brain. CMP appears to be different from PD in neuropathology and manganese behavior in brain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00686083
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  • 5
    Electronic Resource
    Electronic Resource
    Blood-brain barrier disruption and exacerbation of ischemic brain edema after restoration of blood flow in experimental focal cerebral ischemia (1988)
    Springer
    Acta neuropathologica 76 (1988), S. 62-70 
    Details
    ISSN: 1432-0533
    Keywords: Focal cerebral ischemia ; Blood-brain barrier ; Ischemic brain edema ; Regional cerebral blood flow ; Cerebral reperfusion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The mechanism of exacerbation of ischemic brain edema after blood flow restoration was studied in 20 cats under ketamine and alpha-chloralose anesthesia. Regional cerebral blood flow was measured by the hydrogen clearance method, and the left middle cerebral artery (MCA) was occluded for 6 h in group A, and for 3 h with subsequent 3 h recirculation in group B. Severity of brain edema was assessed by specific gravity measurement of tissue samples taken from coronal brain sections at the MCA area, while severity of blood-brain barrier (BBB) disruption was determined by measuring the amount of extravasated serum albumin by using [125I]albumin and tissue-uptake method in the same samples as those used for gravimetry. Structural and ultrastructural change was correlated with the severity of ischemic brain edema and BBB disruption. The results obtained showed that: (i) ischemic brain edema observed in group A was not associated with BBB opening to serum proteins; (ii) ischemic edema in group B was exacerbated significantly after recirculation in correlation with serum protein extravasation in most of the postischemic area; (iii) in the severely edematous area, serum protein extravasation reached a plateau and morphological examination at this type of area revealed cell membrane disruption especially of astrocytes, with leakage of intracellular substances. Our study indicated that the increase of extracellular osmotic pressure due to leakage of serum proteins via the disrupted BBB and of intracellular substances via the ischemically injured cell membrane into the extracellular space is the mechanism responsible for edema fluid accumulation in exacerbated ischemic brain edema.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687681
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  • 6
    Electronic Resource
    Electronic Resource
    Adult pigment type (Peiffer) of sudanophilic leukodystrophy (1989)
    Springer
    Acta neuropathologica 78 (1989), S. 533-542 
    Details
    ISSN: 1432-0533
    Keywords: Sudanophilic leukodystrophy ; van Bogaert and Nyssen's disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Two autopsy cases of siblings with the adult pigment (Peiffer) type of sudanophilic leukodystrophy (SLD), which demonstrated the full-blown stage (case 1) and early stage (case 2) of demyelination, were examined. Numerous brown pigments deposited in demyelinated cerebral areas were characterized histochemically and ultrastructurally as lipofuscin and ceroid. Under the electron microscope formation of blebs due to myelin splitting associated with deposition of multilamellar myeloid bodies within them was a prominent feature in the demyelinated cerebral areas of case 2 as compared with case 1. However, various features of myelin degradation such as thinning, partial or complete circumferential myelin loss, and deposition of electron-dense material on the interperiodic lines were found in both cases. Blebs occurred in all layers of myelin, and axons were compressed by these blebs or the hydropically swollen inner lips of oligodendroglias. Oligodendroglias were relatively well preserved in the demyelinated and nondemyelinated areas in case 2, although the cytoplasm was hydropic. Many spheroids were present in demyelinated areas and were irregularly distributed in both cases. The peripheral nerves in case 1 presented essentially the same changes as those in the brain, although those in case 2 were not affected. Morphometrically, the results showed that hypomyelination was not the mechanism for this pigment type of SLD. One possible cause may be an accelerated ageing of the metabolic process of myelin turnover.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687716
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  • 7
    Electronic Resource
    Electronic Resource
    Experimental neurotoxicity of 5-fluorouracil and its derivatives is due to poisoning by the monofluorinated organic metabolites, monofluoroacetic acid and α-fluoroβ-alanine (1990)
    Springer
    Acta neuropathologica 81 (1990), S. 66-73 
    Details
    ISSN: 1432-0533
    Keywords: 5-Fluorouracil ; Monofluoroacetic acid ; α-Fluoro-β-alanine ; Neurotoxicity ; Vacuolation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Two metabolites of 5-fluorouracil (FU), monofluoroacetic acid (FA) and α-fluoro-β-alanine (FBAL), were continuously administered into the left ventricle of the brain in cats for up to 1 month to investigate the mechanissm of neurotoxicity of FU and its derivatives. The cumulative doses of FU and FBAL over a 1-month period were 1.5–45 mg (20 cats) and 0.2–4.8 mg (21 cats), respectively. As controls for each experimental group, acetic acid (AA) and β-alanine (BAL) were administered. In terms of survival time in relation to the cumulative dose and molecular weight, FBAL was more toxic than FA. Neuropathologically, two types of change, vacuoles and necrosis/softening-like change, were found. The vacuoles were 20–50 μm in diameter, and distributed mainly in the cerebellar nuclei, white matter and the tectum and tegmentum of the brain stem in both experimental groups. Electron microscopically, these vacuoles were due to splitting of the myelin intraperiod line or separation between the axon and the innermost layer of myelin. Necrosis/softening-like change occurred preferentially in the FBAL group and was located symmetrically in the superior and inferior colliculi, oculomotor nuclei and thalamus. Both types of neuropathological change, especially those in the FBAL group, were similar to those found in cats orally administered with FU and its derivatives. It was, therefore, concluded that the subacute and chronic neurotoxicity of FU and its derivatives in dogs and cats is due to intoxication with the monofluorinated organic metabolites, FA and FBAL, and that the direct action of FA and FBAL on myelin and the action of FBAL on energy metabolism or vessels of the mid brain were proposed as the main pathogenetic factor involved.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00662639
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  • 8
    Electronic Resource
    Electronic Resource
    Menkes' kinky hair disease: morphological and immunohistochemical comparisonof two autopsied patients (1991)
    Springer
    Acta neuropathologica 81 (1991), S. 450-457 
    Details
    ISSN: 1432-0533
    Keywords: Menkes' kinky hair disease ; Confronting cisternae complex ; Somatic sprout ; Cactus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary An autopsied patient with Menkes' kinky hair disease, who showed unusually long survival until the age of five years with typical neuropathological changes, was examined for distribution of neuronal depletion in the cerebral cortex, and the cerebellar changes were compared morphologically and immunohistochemically with those found in a younger patient (1 year 8 months old) reported previously. Neuronal loss in the cerebral cortex in the both cases, which was illdefined and unassociated with gliosis, was preferentially distributed in the fifth and sixth layers, especially of the gyral bottom in almost all lobes in the older case. Therefore, this change was thought to be secondary to local ischemia caused by mechanical distortion at the stage of gyrus formation in addition to abnormal development. Ultrastructurally, a prominent increase of confronting cisternae (CC) complexes was found in the perikaryon and processes of Purkinje cells in both cases, and in the older patient CC complexes were arranged more densely and were transformed into concentric lamellar structures in the swollen dendrites. Immunohistochemically, the stainability of neurofilaments (NF, 200 kDa) in Purkinje cells, with or without somatic sprouts was faint or negative in the older patient compared with the marked or moderate positivity in the younger patient and age-matched controls. Empty baskets were absent and NF-positive axonal terminals and synaptophysin-positive granules on Purkinje cells were markedly decreased in both cases. These changes suggest that Purkinje cells degenerate progressively with time and that basket cells also are simultaneously involved.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00293467
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  • 9
    Electronic Resource
    Electronic Resource
    Comparative study on pathogenesis of selective cerebral lesions in carbon monoxide poisoning and nitrogen hypoxia in cats (1982)
    Springer
    Acta neuropathologica 56 (1982), S. 265-272 
    Details
    ISSN: 1432-0533
    Keywords: Carbon monoxide encephalopathy ; Nitrogen hypoxia ; Selective white matter lesion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Since in a previous study hypoxia and subsequent hypotension were considered to be essential for the pathogenesis of carbon monoxide encephalopathy (CO-encephalopathy), experiments were conducted to see whether a combination of nitrogen hypoxia and subsequent systemic hypotension of similar degree and duration as in the previous experimental CO poisoning could induce the same lesion in the CNS of cats. The partial pressure of blood oxygen was reduced to less than 26 mm Hg by increasing the concentration of nitrogen in N2/O2 gas to be inhaled in 1.5 h and then the aortic blood pressure (BP) was reduced to 60–80 mm Hg by blood depletion and ganglion-blockage for 1 h. In 11 of the 15 cats, lesions were produced in the CNS which were similar by light and electron microscopy to those in CO-encephalopathy. In control groups which were treated by hypoxemia only, hypotension only or a combination of CO2-gas inhalation and hypotension without hypoxemia, such lesions were not found in the cerebral white matter. Considering the pathogenesis of lesions in the cerebral white matter in both nitrogen hypoxia and CO-poisoning, two factors, i.e., hypoxemia and subsequent systemic hypotension, are common and essential. Further, the enormous vasodilation in the cerebral white matter induced by hypoxemia and subsequent drop in BP seem to cause a more severe circulatory disturbance in the cerebral white matter than in the cortex.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00691257
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  • 10
    Electronic Resource
    Electronic Resource
    Experimental study on pathogenesis of the fetal brain damage by acute carbon monoxide intoxication of the pregnant mother (1986)
    Springer
    Acta neuropathologica 69 (1986), S. 244-252 
    Details
    ISSN: 1432-0533
    Keywords: Fetal carbon monoxide intoxication ; Pregnancy ; Fetus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The pathogenesis of fetal brain damage caused by acute maternal carbon monoxide (CO) intoxication was experimentally investigated in cats; 11 pregnant cats in various gestational stages were exposed to 0.2–0.3% CO/air gas for 76–150 min; thereafter, 29 live and stillborn neonates and 14 fetuses removed by cesarian section were observed pathologically. In the full-term or late-gestational-stage fetuses and neonates, the most vulnerable areas were the cerebral white matter and brain stem, followed by the basal ganglia and thalamus, and then the cerebral cortex. No changes were found in the cerebellum. From the distribution and nature of the brain changes, a hypoxic-ischemic mechanism was proposed as the pathogenesis of fetal brain damage. In the fetuses or neonates in middle and early gestational stages, the frequency and severity of the brain changes were generally lower than in those in the late gestational stage, and the cerebral white matter and basal ganglia were most often involved, but the thalamus, brain stem and the cerebral cortex were spared. The severity and extent of the brain changes were not the same among all littermates, but varied from normal to severely damaged animals. Among the maternal physiological factors measured during the CO exposure, only the severity of acidosis was correlated with the grade of fetal brain damage.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00688300
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