Cases reported "Brain Injuries"

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1/5. Neuropathological findings associated with retained lead shot pellets in a man surviving two months after a suicide attempt.

    We describe the neuropathological findings in a 30-year-old man who died two months after attempting suicide with a shotgun. We focused our study on lesions associated with retained lead shot pellets and distant therefrom, as well as lesions distant from the principal site of injury. At the sites of the retained lead shot pellets, we found macrophage proliferation and astrocyte activation, together with axonal spheroids and signs of neuronal damage. In the remaining white matter we observed axonal swellings, astrocyte activation and rarefaction of the neuropil; regressive phenomena of the neurons were also present. All axonal spheroids immunoreacted with antibodies against APP, alphaB-crystallin, NF subunits and ubiquitin. Most reactive astrocytes were positive for GFAP and alphaB-crystallin immunostaining. Some neurons immunoreacting with alphaB-crystallin were also found. These data indicated that an important local reaction developed at the sites of lead shot retention, and mild signs of diffuse axonal damage were found throughout the brain.
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keywords = astrocyte
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2/5. glycogen-rich and glycogen-depleted astrocytes in the oedematous human cerebral cortex associated with brain trauma, tumours and congenital malformations: an electron microscopy study.

    PRIMARY OBJECTIVE: The anaerobic mobilization of astrocyte glycogen in anoxic-ischemic regions of the oedematous human cerebral cortex is analysed. methods and PROCEDURES: Seventeen cortical biopsies of patients with brain trauma, brain tumours and congenital malformations were examined by conventional transmission electron microscopy. RESULTS: glycogen-rich and glycogen-depleted, clear or dense astrocytes cell bodies were observed in anoxic ischaemic regions of different brain cortical areas in perineuronal, neuropilar and perivascular localization. glycogen-rich astrocytes showed clear or moderately dense cytoplasm and accumulation of both beta-type or monogranular glycogen granules and alpha-type or multigranular glycogen particles. Focal regions of translucent cytoplasm were observed in areas of glycogen degradation. glycogen-depleted astrocytes exhibited a clear cytoplasm and scarce amount or absence of beta-type glycogen granules. Coexisting glycogen-rich and glycogen-depleted neuropilar astrocytic processes were observed in the vicinity of degenerated myelinated axons and degenerated axodendritic contacts. glycogen-rich and glycogen-depleted perivascular astrocytic processes were also found surrounding injured and collapsed cerebral capillaries. CONCLUSION: The findings suggest astrocytic glycogen mobilization during anoxic and ischaemic conditions, revealing the important contribution of astrocytes on neuronal survival under conditions of energy substrate limitations.
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keywords = astrocyte
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3/5. extracellular fluid S100B in the injured brain: a future surrogate marker of acute brain injury?

    The authors describe the measurement of S100B protein in brain extracellular fluid (ECF) of patients with acute brain injury (traumatic brain injury and subarachnoid haemorrhage) using the technique of microdialysis. To our knowledge, this is the first report of S100B measurement in the human brain. Acute Brain Injury (ABI) is a leading cause of death and disability and the need for a practical and sensitive biochemical marker for monitoring these patients is urgent. The calcium binding astrocyte protein, S100B, may be a candidate for this role. Previous serum studies have shown S100B to be a sensitive predictor of mortality and rise in intracranial pressure in ABI, but it has never before been measured directly within the brain. The ECF reflects the local biochemistry of the brain parenchyma, and the use of intracerebral microdialysis opens up the possibility of studying many novel surrogate markers of injury in the laboratory, in addition to the conventional markers it measures at the bedside (lactate, pyruvate, glucose, and glycerol). In this preliminary report of two cases, the authors demonstrate the quantification of S100B in ECF microdialysate, and investigate whether changes in hourly S100B profile can be related to secondary brain injury. It is shown that extracellular concentrations of S100B change markedly in response to secondary brain injury. Further investigation is required to determine whether extracellular S100B measurement in ABI could assist in patient management.
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keywords = astrocyte
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4/5. Focal brain injury and upregulation of a developmentally regulated extracellular matrix protein.

    tenascin is an extracellular matrix glycoprotein expressed during both normal development and neoplastic growth in both neural and nonneural tissues. During development of the central nervous system (CNS), tenascin is synthesized by glial cells, in particular by immature astrocytes, and is concentrated in transient boundaries around emerging groups of functionally distinct neurons. In the mature CNS, only low levels of the glycoprotein can be detected. The present study demonstrates that following trauma to the adult human cerebral cortex, discrete populations of reactive astrocytes upregulate their expression of tenascin and dramatically increase their transcription of the tenascin gene. The enhanced expression of tenascin may be involved in CNS wound healing, and may also affect neurite growth within and around a brain lesion.
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keywords = astrocyte
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5/5. Electron microscopic analysis of cortical biopsies in patients with traumatic brain injuries and dysfunction of neurobehavioural system.

    Cortical biopsies of eight patients with craniocerebral trauma complicated with subdural or epidural hematoma were examined with the transmission electron microscope. The patients showed post-traumatic neurobehavioural disorders and moderate or severe vasogenic brain edema. The capillary wall displayed increased vacuolar and vesicular endothelial transport, basement membrane thickening and vacuolization and swollen astrocytic end-feet. Pericapillary and parenchymatous hemorrhages were also observed. The extracellular space appeared considerably enlarged with presence of proteinaceous hematogenous edema fluid and fibrinous organization. Pyramidal and non-pyramidal neurons showed intracellular edema featured by irregular enlargement of rough endoplasmic reticulum, nuclear envelope and golgi apparatus. The myelinated axons exhibited clear or black type axoplasmic degeneration, varicose fiber swelling, myelin sheath distortion, formation of myelin ovoids and increased amount of oligodendroglial ad-axonal layer. The dendrites also showed clear or dark and beaded shape degeneration. Synaptic degeneration was characterized by swollen and shrunken pre- and postsynaptic endings, clumping, enlargement and depletion of synaptic vesicles, synaptic membrane complex disassembly and detachment of glial ensheathment. Perivascular and perineuronal astrocytes appeared remarkably swollen. Phagocytic astrocytes were also found. Oligodendrocytes displayed hydropic and reactive changes. Reactive oligodendrocytes induced myelinolysis. The brain barrier dysfunction, the vasogenic and cytotoxic edema and the subsequent neuronal and neuroglial cell reactive and degeneration processes might represent the morphological substrate responsible for the post-traumatic neurobehavioural disorders.
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