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Lecture 13
Normal Histology & Common Pathologic Conditions of the CNS
Question | Answer |
---|---|
What structure is identified with the luxol fast blue? | Histochemical stain for myelin |
What structures are identified with the bielschowsky silver stain? | Histochemical stain for axons and neurites |
What is nissel substance? | Prominent rough endoplasmic reticulum of a neuron |
What areas of the brain contain neurons espeically vulnerable to hypoxic injury? | (1) CA1 area (Sommer's sector) of hippocampus (2) Pyramidal neurons in layers 3 and 5 of the neocortex (3) Purkinje cells in the cerebellum |
Microscopic changes seen in 1 hour after hypoxic-ischemic injury | (1) Microvacuolation of cytoplasm (Mitochondrial swelling) (2) Perineuronal vacuolation (astrocytic processes swelling) |
Microscopic changes seen in 4-12 hours after hypoxic-ischemic injury | Appearance of red neuron: (1) Neuronal cytoplasm eosinophilia (Nissel bodies disappear) (2) nucleus piknosis (3) disappearance of nucleoli |
Microscopic changes seen in 15-24 hours after hypoxic-ischemic injury | Neurtophil leukocytes infiltration begins |
Microscopic changes seen in 2 days after hypoxic-ischemic injury | Macrophage infiltration |
Microscopic changes seen in 5 days after hypoxic-ischemic injury | Neutrophil infiltration ceases |
Microscopic changes seen in 1 week after hypoxic-ischemic injury | Proliferation of astrocytes |
What diseases is characterized by Cowdry A type intranuclear inclusion? | (1) CMV (2) Herpes simplex virus |
Intracytoplasmic inclusion of neurons in Alzheimer's disease | Neurofibrillary tangles |
Intracytoplasmic inclusion of neurons in Parkinson's disease | Lewy bodies |
Intracytoplasmic inclusion of neurons in ALS | Bunina bodies |
Intracytoplasmic inclusion of neurons in Rabies | Negri bodies |
Proliferation of astrocytes in ares of CNS damage | Gliosis or Astrocytosis |
An acute response of astrocytes to injury | Gemistocytic astrocytosis |
An chronic response of astrocytes to injury | Fibrillary astrocytosis |
A major intermediate filament present in the cytoskeleton of astrocytes, ependymal cells, and oligodendrocytes | Glial fibrillary acidic protein (GFAP) |
Cells that produce myelin in the CNS | Oligodendrocyte |
What type of cells provide lining of the ventricles? | Epndymal cells provide lining of the ventricles and play a major role in maintenance of the CSF-brain barrier. |
What is the function of choroid plexus epithelium? | Choroid plexus epithelium produce cerebrospinal fluid. |
What is the normal level of white blood cells in CSF? | <5 cells/mm3 |
What is the normal range of glucose in CSF? | 40-70 mg/dL |
What is the normal amount of protein in CSF? | 15-25 mg/dL |
What are the major sites of CSF blockage? | (1) Foramen of Monro (2) 3rd ventricle (3) Aqueduct of Sylvius (4) Foramina of Luschka and Magendie (5) Basal cisterns/subarachnoid spaces |
What is the function of activated microglia? | (1) Brain damage repair (2) recruitment of hematogenous monocytes (3) antigen-presenting cells |
A condition of excessive CSF within the ventricular system due to alteration of production, flow, or absorption of CSF. | Hydrocephalus |
Excessive CSF within the ventricular system due to alteration of production or absorption of CSF in the absence of CSF-flow obstruction. | Communicating hydrocephalus |
A condition characterized by dilation of hte ventricular system with a compensatory increase in CSF volume secondary to brain parenchyma loss (atrophy) | Hydrocephalus ex vacuo |
Consequences of increased intracranial pressure | (1) compression of normal structure of the nervous tissue (2) ischemia and infarction (3) cranial nerve palsies (4) herniation |
Herniation of cingulate gyrus under the falx cerebri | Subfalcine herniation |
Hernication of the uncus and mesial temporal horn under the tentorium cerebelli | Transtentorial or uncal herniation |
Herniation ofhte cerebellar tonsils through the foramen magnum | Tonsillar herniation |
What is the sequelae of subfalcine herniation? | Compression of branches of the anterior cerebral artery resulting in infarcts. |
What type of herniation would result in ipsilateral papillary dilation and impairment of ocular movements? | Transtentorial or uncal herniation |
Brainstem hemorrhage secondary to brainstem compression from cerebral herniation. | Duret hemorrhage |
What is a seriousl consequence of tonsillar herniation? | Tonsillar herniation is life-threatening because of compression of vital respiratory and cardiac centers in the medulla oblongata. |
A notch in the cerebral peduncle due to displacement of the brainstem against the incisura of the tentorium by a transtentorial herniation resulting in hemiparesis ipsilateral to the herniation side. | Kernohan's notch |