Articles: brain-pathology.
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Experimental neurology · Jul 1984
Synaptic density in chronic animals with experimental neurofibrillary changes.
Synaptic density was quantitated in the cerebral cortex and subiculum of rabbits with experimental neurofibrillary changes. Animals were subjected to subcutaneous injection of aluminum tartrate for 90 days, and synapses stained with ethanolic phosphotungstic acid were analyzed in animals killed 100, 200, or 300 days postinjection with aluminum tartrate. ⋯ In contrast, animals killed 100 days postinjection revealed the same synaptic density as their control. The data suggest that the synaptic depopulation associated with experimental neurofibrillary changes is a gradual process, and such changes are demonstrable only long after the initial appearance of neurofibrillary changes.
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Acta Psychiatr Scand Suppl · Jan 1984
Case ReportsHereditary diffuse leucoencephalopathy with spheroids.
The clinical, genetic, and morphological features of a previously unknown progressive neuropsychiatric disease are presented. By genealogical investigation of the background of an uncharacteristic case of presumed organic psychosis, we traced 71 relatives from four generations. The anamnestic data showed various combinations of psychiatric symptoms (depression, anxiety, aggressiveness, and severe dementia), neurological symptoms (impaired balance with retropulsion, hyperkinesia, and epilepsy), and somatic symptoms (gastrointestinal disorders, arthritis, and gynaecological problems) in 17 (11 dead and 6 living) members of the family. ⋯ The bilateral, frontal, fronto-parietal, and temporal locations of the most pronounced, diffusely demarcated lesions corresponded fairly well to the symptoms of an organic psychosyndrome with its main substrate in the forebrain. For this new clinico-pathological entity, the name "hereditary diffuse leucoencephalopathy with spheroids" (HDLS) is proposed. As a working hypothesis, it is suggested that not only genetic, but also immunological and possible endocrine factors may contribute to the development of the disease.
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Histology or necropsy records of 13 children with accidental or therapeutically induced salicylate intoxication were examined for the presence of hepatic and cerebral pathology findings characteristic of Reye's syndrome. Liver sections stained with haematoxylin and eosin showed intrahepatocytic microvesiculation (10 of 12 children) and absence of significant inflammation or necrosis (10 of 12 children). ⋯ Liver tissue stained with the periodic-acid/Schiff method showed complete absence of stainable glycogen in 5 of 6 children. 9 of 12 children for whom information was available had cerebral oedema. It is concluded that the light-microscopy hepatic findings and the gross cerebral findings for the majority of these children with salicylate intoxication are the same as those for children with Reye's syndrome.
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Traumatic coma was produced in 45 monkeys by accelerating the head without impact in one of three directions. The duration of coma, degree of neurological impairment, and amount of diffuse axonal injury (DAI) in the brain were directly related to the amount of coronal head motion used. Coma of less than 15 minutes (concussion) occurred in 11 of 13 animals subjected to sagittal head motion, in 2 of 6 animals with oblique head motion, and in 2 of 26 animals with full lateral head motion. ⋯ Coma lasting 16 minutes to 6 hours occurred in 2 of 13 of the sagittal group, 4 of 6 in the oblique group, and 4 of 26 in the lateral group, these animals had less neurological disability and less DAI than when coma lasted longer than 6 hours. These experimental findings duplicate the spectrum of traumatic coma seen in human beings and include axonal damage identical to that seen in sever head injury in humans. Since the amount of DAI was directly proportional to the severity of injury (duration of coma and quality of outcome), we conclude that axonal damage produced by coronal head acceleration is a major cause of prolonged traumatic coma and its sequelae.