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  • 1
    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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  • 2
    Electronic Resource
    Electronic Resource
    Metabolites of 5-fluorouracil, ·-fluoro-‚-alanine and fluoroacetic acid, directly injure myelinated fibers in tissue culture (1996)
    Springer
    Acta neuropathologica 92 (1996), S. 8-13 
    Details
    ISSN: 1432-0533
    Keywords: Key words Cerebellar tissue culture ; 5-Fluorouracil ; derivatives ; α-Fluoro-β-alanine ; Fluoroacetic acid ; Myelin injury
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The neurotoxicity of two 5-fluorouracil (5-FU) derivatives, tegafur (FT) and carmofur (HCFU), which selectively induce leukoencephalopathy involving the cerebral white matter in humans and vacuolation of myelinated fibers in dogs and cats, was examined in vitro. The common metabolites of these drugs, α-fluoro-β-alanine (FBAL) and fluoroacetic acid (FA), were added to the medium of cultured murine cerebellar myelinated fibers. On day 1 of exposure to 7 μM FBAL and FA, which corresponds to their blood concentrations 2 h after oral administration of 10 mg · kg–1 HCFU to dogs that induced central nervous system vacuolation after 30 days, partial splits of the myelinic intraperiod line were observed by electron microscopy. On days 4–7, phase contrast microscopy revealed spindle-shaped swelling and granulation of myelin and electron microscopy demonstrated prominent dissociation of the myelinic intraperiod line with monolocular and multilocular vacuolation. More severe changes, such as myelin loss, were found in cultures exposed to a higher concentration (70 μM) of FBAL and FA, but no remarkable neuronal, astrocytic or oligodendrocytic changes occurred. Quantitative evaluation of myelin injury by electron microscopy revealed significant toxicity of FBAL and FA, at concentrations of 7 and 70 μM, on day 4. However, groups treated with 0.7 μM FBAL and FA, 5-FU (7 μM) and controls exposed to β-alanine and acetic acid concentrations of 0.7, 7 and 70 μM showed no marked injury. We concluded that these anticancer drug metabolites injure myelin fibers directly, resulting in vacuolation due to myelin splitting and destruction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050482
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  • 3
    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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  • 4
    Electronic Resource
    Electronic Resource
    An experimental study of the pathogenesis of the selective lesion of the globus pallidus in acute carbon monoxide poisoning in cats (1983)
    Springer
    Acta neuropathologica 61 (1983), S. 232-238 
    Details
    ISSN: 1432-0533
    Keywords: Selective lesion of the globus pallidus ; Acute carbon monoxide poisoning ; Cerebral local blood flow ; Hydrogen clearance method
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Twenty-eight mature cats were exposed to 0.3% carbon monoxide (CO) gas for 90–193 min using artificial ventilation. The systemic blood pressure (BP), venous pressure (VP), blood flow of the left common carotid artery (CF), and blood gas were monitored. The local blood flow (LBF) of the globus pallidus, putamen, or claustrum was measured by the hydrogen clearance method. Pallidal lesions were found histologically in 14 cats. The period of CO inhalation and the time thereafter were divided into the following four stages in the animals with pallidal lesions. Stage 1: Initial phase with rapid increase in the CF and LBF, and rapid decrease in the BP. Stage 2: Middle phase with slow decrease in the BP, CF, and LBF. Stage 3: Terminal phase with rapid decrease in the BP, CF, and LBF. Stage 4: Recovery phase. The changes in stage 3 were not so prominent in the animals without pallidal lesions. The LBF of the globus pallidus of the animals with lesions decreased to 67.3±20.7% of the initial value at the terminal stage of CO inhalation, while it was 188±46.7% in those without lesions. The difference was statistically significant (P〈0.01). The LBF of the putamen or claustrum in the animals with lesions in the globus pallidus was 140±24.6% at this stage, and it was significantly higher than that of the globus pallidus (P〈0.01). Other factors, such as CO inhalation time, degree of acidosis, and terminal CO-Hb concentration, did not correlate with the occurrence of the pallidal lesion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00691991
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  • 5
    Electronic Resource
    Electronic Resource
    Cortical cerebellar degeneration with testicular neoplasm (1985)
    Springer
    Acta neuropathologica 66 (1985), S. 170-172 
    Details
    ISSN: 1432-0533
    Keywords: Cortical cerebellar degeneration ; Testicular neoplasm ; Paraneoplastic syndrome
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Cortical cerebellar degeneration was found in a 28-year-old man with testicular neoplasm. The patient, who had undergone a left orchidectomy for the testicular tumor, developed progressive cerebellar symptoms with mental changes 7 months later. The autopsy revealed the spread of a malignant germ cell tumor of the testis, and cortical cerebellar degeneration in the central nervous system (CNS) which was characterized by almost complete loss of Purkinje cells and degeneration of the both dentate nuclei and superior cerebellar peduncles. The present case is the first of cortical cerebellar degeneration combined with testicular neoplasms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00688695
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  • 6
    Electronic Resource
    Electronic Resource
    The pathogenesis of carbon monoxide encephalopathy in the acute phase—Physiological and morphological correlation (1981)
    Springer
    Acta neuropathologica 54 (1981), S. 1-10 
    Details
    ISSN: 1432-0533
    Keywords: Carbon monoxide encephalopathy ; Selective topography of CNS lesion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Experimental studies were performed to elucidate the significance of various physiological factors contributing to the pathogenesis of carbon monoxide (CO) encephalopathy, such as systemic blood pressure (BP), common carotid artery blood flow (CF), local blood flow (LBF) of the brain and blood gas including pH, and to analyse the morphological character of the cerebral white matter lesions in the acute phases with light and electron microscopes; 14 adult cats were exposed to 0.3% CO/air gas under respiratory control for 1 h and 17 min to 2 h and 50 min and killed 1.5 h to 3 weeks later. During the 1st h the CF and LBF increased along with the concentration of CO haemoglobin and the BP showed slight decrease in all the CO-exposed cats. After the 1st h, the BP dropped progressively as well as the CF and LBF. The LBF of the cortex and white matter changed in parallel, but often that of the latter approximated or exceeded that of the former in the cerebrum. During CO exposure, acidosis occurred in all the cats and haemoconcentration resulted in almost all of the cats. In all the cats except one which showed the least BP drop, lesions occurred selectively in the cerebral white matter and in six or seven cats focal coagulation necrosis or ischaemic changes occurred in the nerve cells in the bilateral pallidum, substantia nigra, and hippocampus similar to human patients. The cerebral white matter lesions were suggestive of those caused by circulatory disturbance. The severity of the white matter damage showed a good positive correlation with the intensity of the BP drop, but not with other factors, such as the duration of CO-exposure, CO-haemoglobin level, acidosis, or haemoconcentration. On the basis of such physiological and morphological findings, we have found the following to be essential for the selective damage of the cerebral white matter rather than the cerebral cortex or white matter of other regions of the CNS: (1) the coexistence of the initial phase of increase in and the succeeding decrease in the cerebral blood flow and (2) the anatomical finding that the cerebral white matter is supplied by its own long nourishing arteries with small amounts of capillary beds and a thinner media compared with that of the subarach-noidal artery.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00691327
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  • 7
    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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  • 8
    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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  • 9
    Electronic Resource
    Electronic Resource
    An experimental study of the pathogenesis of Grinker's myelinopathy in carbon monoxide intoxication (1983)
    Springer
    Acta neuropathologica 59 (1983), S. 200-206 
    Details
    ISSN: 1432-0533
    Keywords: Grinker's myelinopathy ; Carbon monoxide intoxication
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The change of Grinker's myelinopathy in carbon monoxide (CO) poisoning occurs not only in patients with the clinically diphasic type of CO-poisoning but is also found around the destructive lesions in patients with the acute form of CO-poisoning. The distribution of this myelinopathy is similar to that of the acute form of CO-poisoning. The cerebral change of experimental acute CO-encephalopathy is a sort of hypoxic-ischemic encephalopathy. Based on these findings an experiment was conducted to analyze the pathogenesis of Grinker's myelinopathy as follows: 43 cats were separated into four groups. Group A was subjected at first to inhalation of 0.3% CO/Air gas lasting for 2 h and then 2 or 3 days later to hypotension ranging from 60 to 90mm Hg for 1 h under the state of slight hypoxia (PaO2: 50–80 mm Hg). Group B was also exposed to CO-gas and hypotension similarly to Group A, but hypoxia was not imposed during hypotension. Groups C and D were subjected only to hypotension and to CO-gas, respectively. Myelin pallor was found selectively in the cerebral white matter of all cats of Group A and 18 of the 23 cats of Group B, and the subcortical U-fibers and perivascular myelin were spared. This was similar to Grinker's myelinopathy. The myelin pallor was investigated by light and electron microscopy and considered to be due to edema and separation of the myelin sheath and axon. In Groups C and D such a change was either absent or only slight. The conditions necessary for the onset of Grinker's myelinopathy were discussed, and it was proposed that the patients recovering from acute CO-poisoning should be kept in hospital for several weeks so that their blood pressure and blood gas could be monitored continuously.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00703204
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  • 10
    Electronic Resource
    Electronic Resource
    Regional cerebral blood flow of acute carbon monoxide poisoning in cats (1987)
    Springer
    Acta neuropathologica 72 (1987), S. 389-393 
    Details
    ISSN: 1432-0533
    Keywords: Regional cerebral blood flow ; Carbon monoxide ; Acute carbon monoxide poisoning ; Selective vulnerability
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 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 group according to the rCBF values; low-value structures and high-value structures. There was significant (P〈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. The rCBF of the cerebral white matter was significantly lower than that of the cerebellar white matter. From these findings and our previous observations using the hydrogen clearance and rheological methods, the mechanism of the selective vulnerability of the pallidum and cerebral white matter in acute CO poisoning is discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687271
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