Neuropath- Part 3

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Mawad
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309062
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Neuropath- Part 3
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2015-10-07 23:05:45
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vetmed neuropath
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vetmed neuropath
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  1. Neural tube formation is from the __________.
    neural plate
  2. Proliferation of the lining of the neural tube results in the establishment of ________________.
    neuronal and glial stem cell populations
  3. Due to the complexity of the ____________ derivatives, the greatest proliferative and migrational activity is in the ___________; this creates significant potential for developmental defects.
    prosencephalic; rostral neural tube
  4. Neuroblasts arise from stem cells at the ____________ and migrate along __________ toward the ______ surface.
    ventricular surface; radial glia; pial
  5. Neuronal cell adhesion molecule (NCAM) and nerve growth factor are factors produced by ___________ that mediate the process of neuroblast proliferation and migration.
    radial glia
  6. What are repercussions of failure of development of the diencephalon?
    no optic nerve and no retina or lens
  7. Development of the brain is complete at birth with the exception of ____________; the degree of development determines...
    cerebellum; whether the animal is ambulatory at birth or not.
  8. Period of neuronal maturation leads to ___________ of structures.
    postnatal enlargement
  9. Defect characterized by abnormal tissue organization (dysplasia), reduction in mass (hypoplasia), or total lack of formation (aplasia).
    structural defect
  10. Defect that may not initially evident upon gross or histologic evaluation, but clinical abnormalities may  be present.
    functinoal defect
  11. ________________ represent a change that is present at birth, typical of __________ malformations.
    Congenital structural defects; cerebral
  12. Cerebellar defects can be... (2)
    congenital or arise in postnatal period (due to its delayed maturation).
  13. Defect determined by a particular genotype.
    heritable defect
  14. When do heritable defects become evident?
    at birth (congenital) or in the postnatal period
  15. __________ defects tend to be more unique in their expression than for __________ defects.
    Heritable; acquired
  16. Acquired defects occur due to exposure to ______________.
    radiomimetic agents
  17. Radiomimetic agents destroy ____________; therefore, morphologic expression may be ____________.
    rapidly dividing cells; similar for diverse agents
  18. 4 types of radiomimetic agents.
    viruses, toxins, radiation, Cu deficiency
  19. Describe the continuum that manifests as absence of tissue.
    hypoplasia <--> segmental aplasia <--> aplasia
  20. Tissue disorganization.
    dysplasia
  21. Determinants of tissue alteration. (2)
    magnitude of insult, timing of insult
  22. Earlier insults result in...
    more severe abnormalities.
  23. Abnormalities of neural tube closure.
    dysraphism
  24. CNS tisues orchestrate the development of the ____________ of the brain and spinal cord; therefore, dysraphic states are accompanied by defects in ______________, known as __________.
    bony encasement; cranial vault/vertebrae; schisis
  25. Spinal dysraphism.
    myelodysplasia
  26. 4 examples of myelodysplasia.
    duplication/displacement of ventral fissue, misplaces grey matter, hydromyelia, syringomyelia
  27. Dilation of the central canal.
    hydromyelia
  28. Formation of blind-ended pouches that extend from the central canal and are not lined by ependymal cells.
    syringomyelia
  29. Secondary defect in the vertebral arches.
    spina bifida
  30. With spina bifida, the functional defect is inferred by abnormal induction of the _____________; the ____________ may be lacking/hypoplastic, reulting in increased vertebral laxity and causing _____________.
    bony encasement; dorsal vertebral arches; dynamic cord compression
  31. Lack of fusion of the vertebral arches, often accompanied by a dermal sinus/tract that communicates with the central canal and containing CSF.
    occult spina bifida
  32. Disorder in which CNS structures protrude through the defect in the vertebral arch.
    cystic spina bifida
  33. Cystic spina bifida, meningocoele is when...
    only the meninges protrude.
  34. Cystic spina bifida, meningomyelocele, is when...
    meninges and spinal cord protrude.
  35. Dynamic cord compression results from ___________; ____________ is generally the most severe sequel.
    vertebral laxity; Wallerian degeneration
  36. _____________ may result from CNS invasion by bacteria through dermal sinuses that accompany spina bifida.
    Bacterial meningomyelitis
  37. Amorphous mass of dysplastic cerebral tissue overlies the hindbrain, and eyes are absent.
    anencephaly (aplasia)
  38. How is anencephaly associateed with cranioschisis?
    cranioschisis- cranium fails to close--> brain is exposed to aminos--> brain degenerates--> anencephaly
  39. Partial aplasia/hypoplasia of the brain.
    microcephaly
  40. Disorder that results from an insult that affects a small number of cells over a wide distribution, resulting in subtle reductions in cerebral mass.
    cerebral hypoplasia
  41. 3 types of cerebral hypoplasia.
    polymicrogyria (increased # of small gyri), pachygyria (decreased # of thicker gyri), lissencephaly (lack of gyri)
  42. Lissencephaly is normal in __________.
    rabbits/rodents/manatees
  43. Cavitating lesions resulting from pannecrosis usually occur as a result of ___________.
    radiomimetic agents
  44. Extensive lesion resulting from complete destruction of the periventriculat germinal zone of the telencephalon.
    hydrancephaly
  45. Mild, multifocal insult resulting in cavities within the neocortex that may communicate with the subarachnoid space or ventricular system.
    porencephaly
  46. What is an example of an insult that causes cavitating lesions due to failure of support axons?
    Cu deficienccy in small ruminants and pigs
  47. With Cu deficiency in small ruminants, there is an inability of neurons to develop or maintain ______________, and possibly death of ____________, resulting in __(2)__.
    axonal processes; death of cerebral cortical neurons; porencephaly or hydranencephaly
  48. Cu-dependent enzyme necessary for phospholipid synthesis; thus, Cu deficiency causes decreased phospholipid production and compromised myelination.
    cytochrome c oxidase
  49. Cu-dependent enzyme that confers protection against oxygen radicals;; important b/c superoxide anion generation is increased during neuronal differentiation.
    superoxide dismutase
  50. Cu deficiency during the first weeks of life leads to... (2)
    enzootic ataxia, anemia
  51. Diffuse symmetric reduction of CNS myelin sheaths and a decrease in oligodendrocytes.
    dysmyeliniogenesis/hypomyelinogenesis
  52. Myelin formation begins in the ___________ of gestation and proceeds into _________; therfore, earaly onset injuries primarily affect the __________, whereas later onset injuries are most extensive in the ___________.
    middle; postnatal life; brain; spinal cord
  53. _________ myelin is unaffected in heritable forms of dys/hypomylinogenesis.
    PNS (b/c schwann cells are not affected)
  54. Describe embryogenesis of the cerebellum.
    neural tube closure--> neuroblast proliferation into the alar plate--> dorsal neuroblast migration from the alar plate to form the rhombic lip
  55. Central migration/proliferation of neuroblasts of the cerebellum forms the... (3)
    roof of the 4th ventricle, cerebellar roof nuclei, and Purkinje cells.
  56. Outer migration and proliferation of neuroblasts of the cerebellum forms the... (2)
    external granular layer, internal granular layer
  57. The protracted development of the cerebellum leads to...
    prolonged susceptibility to mitolytic insults.
  58. Insults to cerebellar neuroblasts can lead to... (2)
    lack of rhombic lip formation, laminar hypoplasia
  59. Lack of rhombic lip formation can result in... (2)
    agenesis (complete aplasia), segmental aplasia
  60. Laminar hypoplasia leads to loss of the _____________ and subsequently loss of _____________; _____________ is also evident as a dysplastic change.
    external granular layer; internal granular layer; mixing of Purkinje cells and surviving granular cells
  61. Viral agents causing cerebellar defects. (2)
    parvovirus (panleuk in cats), BVDv
  62. Parvovirus infection in utero or early post-natal period leads to ___________.
    laminar hypoplasia
  63. BVDv infection at __________ leads to fetal death; at _________, leads to microphthalmia/cerebral defects.
    <100 days; 100-170 days
  64. Defects in specific lysosomal enzymes, resulting in the accumulation of the substrate of that defective enzyme.
    lysosomal storage disease
  65. Lysosomal storage disease is generally the result of ______________, but ____________ is also a possibility.
    hereditary defect in enzyme structure; enzyme inhibitors may be acquired
  66. Describe defects associated with lysosomal storage disease.
    defects is generalized, with accumulations of enzyme substrate found in phagocytic cells of the spleen, liver, bone marrow, and lymph nodes
  67. With lipidosis, a _____________ disease, accumulation is predominantly within _________.
    lysosomal storage; neurons
  68. Describe the diagnosis of lysosomal storage disease. (3)
    immunohistochemistry, biochemical characterization of fibroblast primary cultures, measurement of enzyme activity with and without inhibitor
  69. Lysosomal storage disease can cause __________.
    demyelination
  70. With galactocerebrosidosis, a _____________ disease, accumulation is...
    lysosomal storage; NOT primarily in neurons.
  71. Galactocerebroside is primarily a _________ component; thus, galaltocerebrosidosis is a disease of ____________, and the predominant accumulation is in ___________, which for _________.
    myelin; oligodendroglia; microglia; gitter cells
  72. Glycoproteinosis looks similar to ___________; __________ is more common.
    lipidosis; lipidosis
  73. Lysosomal storage disease characterized by accumulation of an autoflourescent lipopigment; more of a lipid transport problem than a storage problem.
    ceroid lipofuscinosis
  74. An increase in the CSF volume in the brain, reflecting an imbalance in the rates of production vs resorption.
    hydrocephalus
  75. 2 types of hydrocephalus.
    communicating hydrocephalus (less common b/c don't live long enough to develop), internal (obstructive) hydroephalus
  76. Physical alteration of the arachnoid granulations such that CSF resorption into the venous circulation occurs at a slow rate.
    communicating hydrocephalus
  77. Communicating hydrocephalus can be caused by... (3)
    vit A deficiency, meningitis/meningoencephalitis (inflammatory exudate matts arachnoid villi down), neoplastic involvement of arachnoid villi
  78. For CSF to reach the arachnoid villi from it origin in the choroid plexus of the lateral ventricles, efficient passage through __(3)__ must be unhindered; when it is hindered, it is called ___________.
    interventricular foramen, mesencephalic aqueduct, lateral apertures of fourth ventricle; internal (obstructive) hydrocephalus
  79. Internal hydrocephalus caused by obstruction of the interventricular foramen is _________; it can be caused by... (3)
    least common (b/c large size); mass involving ipsilateral choroid plexus, mass in the vicinity of the foramen.
  80. Internal hydrocephalus caused by obstruction of the mesencephalic aqueduct is __________; it can be caused by... (3)
    most common (small size, long length); hereditary stenosis, inflammatory lesions causing scarring/stricture, mass effects of inflammation/neoplasms
  81. Hereditary stenosis causing internal hydrocephalus is the most common congenital anomaly of ________, especially those with __________.
    dogs; bradycephalic skulls
  82. Internal hydrocephalus caused by obstruction of the lateral apertures of the 4th ventricle is __________; it is caused by... (3)
    second most common; congenital malformation, mass in choroid plexus/brainstem, meningitis with involvement of the choroid plexus
  83. Hydrocephalus causes __________, which leads to... (4)
    increase in intracranial pressure; expansion of fontanelles (in young), herniation of brain (mature-fontanelles ossified), ventricular expansion due to tissue atrophy, tearing of periventricular white matter/death
  84. Transependymal edema of periventricular white matter results in ___________; there is also ________ loss of _________, resulting in __________.
    demyelination; ischemia; cortical neurons; atrophy of grey and white matter (ventricular expansion)
  85. Ventricular enlargement may decrease __________ and allow ___________.
    interventricular pressure; a new equilibrium of CSF production
  86. Causes of diminished tissue perfusion. (7)
    embolism, thrombosis, trauma, external compression, vasculopathy/vasculitis, arteriospasm, interruption of systemic BP
  87. Decreased perfusion is most important because...
    lack of waste removal and nutrient supply. (to a lesser extent- hypoxia)
  88. Hypoxia in the brain is relatively ________ and manifests as __________.
    well-tolerated; reversible neurotransmitter imbalances
  89. Tissue death resulting from  ischemia.
    infarction
  90. Irreversible and complete arteriolar/arterial occlusion.
    pale infarct
  91. Incomplete arterial occlusion, transient complete arterial occlusion, vasculitis, occlusion of vein.
    hemorrhagic infarct
  92. CNS infarcts are less common in vetmed species than humans because...
    there is a greater degree of circulatory redundancy.
  93. Factors determining the severity of infarction. (3)
    caliber of affected vessel, severity and rapidity of obstruction, degree of end artery involvement which reflects the degree of collateral circulation

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