Nonspecific Changes of the Central Nervous System in Normal and Experimental Material

Cammermeyer, Jan

doi:10.1016/b978-0-12-119286-0.50010-7

Cited by 29 publications

(25 citation statements)

References 298 publications

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“…rough handling of unfixed tissue (e.g., traumatic dissection, pressure) promotes this change (Cammermeyer 1978;Garman 1990); ischemia is an integral part of the process (Cammermeyer 1973); a role for neuronal excitotoxicity is suggested by the demonstration that treatment of rats with glutamate antagonists prior to formaldehyde fixation abolishes dark neuron formation following cortical biopsy (Kherani and Auer 2008 (Cammermeyer 1972), but such early lesions are usually characterized by the presence of adjacent neurons in different stages of degeneration (in contrast to the monomorphic traits of dark neuron clusters); necrotic lesions of some duration are often associated with glial changes such as reactive glia and/or activated microglia (Jortner 2006).…”

Section: Dark Neuron Artifact (Figures 134-136)mentioning

confidence: 99%

Proliferative and Nonproliferative Lesions of the Rat and Mouse Central and Peripheral Nervous Systems

et al. 2012

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Harmonization of diagnostic nomenclature used in the pathology analysis of tissues from rodent toxicity studies will enhance the comparability and consistency of data sets from different laboratories worldwide. The INHAND Project (International Harmonization of Nomenclature and Diagnostic Criteria for Lesions in Rats and Mice) is a joint initiative of four major societies of toxicologic pathology to develop a globally recognized nomenclature for proliferative and nonproliferative lesions in rodents. This article recommends standardized terms for classifying changes observed in tissues of the mouse and rat central (CNS) and peripheral (PNS) nervous systems. Sources of material include academic, government, and industrial histopathology databases from around the world. Covered lesions include frequent, spontaneous, and aging-related changes as well as principal toxicant-induced findings. Common artifacts that might be confused with genuine lesions are also illustrated. The neural nomenclature presented in this document is also available electronically on the Internet at the goRENI website (http://www.goreni.org/).

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Section: Dark Neuron Artifact (Figures 134-136)mentioning

confidence: 99%

Proliferative and Nonproliferative Lesions of the Rat and Mouse Central and Peripheral Nervous Systems

et al. 2012

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“…Variations in time from end of hypoxia-ischemia to perfusion-fixation (30 to 120 min¬ utes) affected neither incidence nor severity of brain damage. Blood gases during hypoxia-ischemia ([mean ± SE] Pa02, 20.7 ± 0.3 mm Hg; PaC02, 31.8 ± 0.7 mm Hg; and pHa, 7.37 ± 0.01) did not differ between animals with and without neuronal damage.…”

Section: Neuropathologymentioning

confidence: 99%

Brief Hypoxia-Ischemia Initially Damages Cerebral Neurons

Levy¹,

Brierley²,

Silverman³

et al. 1975

Archives of Neurology

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Rats were studied during cerebral hypoxic ischemia to determine whether neurons or blood vessels suffered the first damage. Ten or more minutes of unilateral carotid artery occlusion combined with systemic hypoxemia (PaO-2, 21 mm Hg) produced neuronal but not vascular damage in the ipsilateral cerebral hemispheres of 18 of 29 rats (62%); two and five minute stresses caused no visible neuronal abnormalities. The longer exposures produced more widespread damage, and neuronal loss and gliomesodermal reaction were evident after prolonged survival. Early neuronal changes correlated with abnormalities of motor behavior (P less than .005). Despite neuronal damage that was sometimes extensive, vascular no-reflow developed in only one of 24 animals after 20 and 30 minutes of hypoxia-ischemia. Production of neuronal and neurological abnormalities in the absence of hypotension or vascular no-reflow indicates that hypoxia-ischemia initially damaged cerebral neurons.

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“…The material was free of any signs of nervous tissue damage of the type produced by arrest ed oil emboli within one hour [Cammermeyer, 1972]; notably, there was no perivascular diffusion of iron or juxtaembolic deposition of fibrin in the brain, as occurring after 3-4 days in man [Cammermeyer, 1953] and dog [Cammermeyer and Swank, 1959], and there were no hemorrhages in the retina, as describ ed in the dog [Czerny, 1875] and the rabbit [Gubisch, 1965]. Furthermore, in the cat, the emboli occurred in both the brain and the eye in only 3 out of 10 animals, i.e., the cor relation was not sufficient to support the concept of a systemic involvement.…”

Section: Discussionmentioning

confidence: 95%

“…The embolization with oil and the stagnation of erythrocytes were so massive in the dorsal parts of both hemi spheres that the entire area had the appearance of a bilateral hemorrhagic infarction, which had escaped the effect of Bouin's fixative. Nonetheless, with few exceptions, there were no effusions of blood typical of such in farctions, and the tissue, free of dark and ischemic neurons [Cammermeyer, 1972[Cammermeyer, , 1975a, seemed to be remarkably well preserved. This animal, in which the apex of the heart had been lifted and covered with running water during incision, had two types of oilred-O-stained emboli in the brain.…”

Section: Experimental Oil Embolismmentioning

confidence: 99%

“…1971] may be explained, on the one hand, by the frequent use, until recently, of fixation by immer sion and. on the other hand, by the failure to include normal material in studies on experimental fat em bolism in which the tissues were fixed by perfusion [brain, Meriwether andWilson, 1934: Broman, 1940;Cammermeyer, 1972]. Should the simultaneous pres ence of fat emboli in the two organs be indicative of a systemic involvement, these fat emboli could be at tributed to a vital phenomenon and thus present a hazard to microcirculation in the living organism.…”

Section: Introductionmentioning

confidence: 99%

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Cerebral and retinal fat emboli in normal animals fixed by perfusion

Cammermeyer¹

1977

Cells Tissues Organs

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The brains and retinas of laboratory animals fixed by perfusion occasionally contain isolated round fat emboli, which increase in number if the two organs are covered with oil during the autopsy. These emboli, in contrast to emboli induced by intravenous injection of oil, are present in smaller numbers, occur without adjacent aggregation of erythrocytes and do not cause widening of the occluded vascular channel. The fat emboli in the normal brain are attributed to connective tissue fat aggregating on the exposed cerebral surface and flowing through openings cut in the leptomeninges and the vascular walls during removal of the brain. Their formation could not be entirely prevented by covering the brain with running water or by submerging the forepart of the animal’s body in water during the autopsy. Nevertheless, such a procedure is recommended to avoid introduction of extraneous fat when in a given experiment the question of fat embolism arises. Fat emboli demonstrable in the flattened retina of the cat and the mulatta monkey are ascribed to aspiration of retrobulbar connective tissue fat; they can be prevented by placing a ligature around the optic nerve prior to removal of the eye.

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Nonspecific Changes of the Central Nervous System in Normal and Experimental Material

Cited by 29 publications

References 298 publications

Proliferative and Nonproliferative Lesions of the Rat and Mouse Central and Peripheral Nervous Systems

Proliferative and Nonproliferative Lesions of the Rat and Mouse Central and Peripheral Nervous Systems

Brief Hypoxia-Ischemia Initially Damages Cerebral Neurons

Cerebral and retinal fat emboli in normal animals fixed by perfusion

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