Neuropath- Part 4

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Neuropath- Part 4
2015-10-11 13:10:44
neuropath vetmed

vetmed neuropath
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  1. With fibrocartilgaenous embolization of the spinal cord, perfusion of the _________ of the spinal cord is infarcted by ___________ by fibrocartilage, called ___________.
    grey matter; vascular embolism; poliomalacia
  2. In the spinal cord, grey matter and white matter are perfused by...
    completely distinct end-arterial systems.
  3. Embolism of the ventral spinal artery results in _________; embolism of the longitudinal venous sinus results in ____________.
    pale infarct; hemorrhagic infarct
  4. The origin of fibrocartilage causing fibrocartilagenous embolization of the spinal cord is thought to originate from the __________; in dogs, this is correlated to ___________.
    intervertebral disc; degenerative disc disease
  5. Degenerative disc disease is characterized by ___________ of the ___________ and neovascularization of the ____________, forcing fragments of disc material into the vessels, where they form _________.
    fibrocartilagenous metaplasia; nucleus pulposus; annulus fibrosus; emboli
  6. How do you diagnose fibrocartilagenous embolism of the spinal cord?
    MUST identify fibrocartilage for definitive diagnosis because poliomalacia is NOT pathognomonic
  7. What are 2 differentials for poliomalacia?
    fibrocartilagenous embolism of the spinal cord, ischemia-reperfusion injury of the spinal cord
  8. A bacterial disease of cattle caused by Histophilus somni.
    thrombotic meningoencephalitis
  9. Histophilus somni causes bacterial localization in ____________, causing... (3)
    CNS vessels; vasculitis, thrombosis, an malacia.
  10. What are the 2 events that occur with Histophilus somni infection causing thrombotic meningoencephalitis?
    • 1. initiation of bacteremia from resp tract
    • 2. infection of endothelium causes fibronecrotic vasculitis with secondary thrombosis in multiple organ systems
  11. What is grossly evident in the brain and spinal cord with thrombotic meningoencephalitis?
    multifocal hemorrhagic infarcts
  12. __________ is the basis for the majority of adverse effects secondary to trauma.
  13. Mild trauma may not cause CNS damage in domestic species because of... (2)
    cushion of facial bones, less cranial rotational acceleration during falls in quadrupeds (as compared to bipeds)
  14. Loss of consciousness following transient deformation of axons.
  15. With severe concussion, the lesion is diffuse _______ injury characterized by _______ degeneration and necrosis distributed throughout the _________.
    axonal; axon; brainstem
  16. With severe concussion, lesions tend to be worse on the side that was _________ upon impact.
  17. Petechial hemorrhage of leptomeningeal vessels.
  18. What are the 2 types of contusion?
    coup- bruising on side of impact; contrecoup- bruising on side opposite of impact
  19. Stationary head is struck by a moving object, causing differential acceleration of the skull, CSF, and brain.
    coup contusion
  20. Moving head strikes a stationary object, causing differential loss of momentum of the skull, CSF, and brain and a sudden dramatic rise in pressure differential in the leptomeminges.
    contrecoup contusion
  21. Cutting or tearing of parenchyma and the associated blood vessels.
  22. Laceration can be caused by... (3)
    displacement of bone fracture margins, penetrating wound, differential brain-vault accelerations in neonates
  23. The stretching of a blood vessel until it breaks.
  24. What injury usually occurs when a horse rears up and falls backwards?
    dramatic posterior movement of the brain that stretches the optic nerves, inducing hemorrhage
  25. Hemorrhage results in __________, which are __________ that can trigger the __________.
    hematoma formation; space-occupying masses; edema cycle
  26. Hematomas cause an increase in __________.
    intracranial pressure
  27. Local hemorrhage has a ____________ on brain vasculature, resulting in _________.
    vasoconstrictive; tissue infarction
  28. Arteriospasm is a __________ of the CNS vasculature to __________.
    delayed response; hemorrhage
  29. _________________ may initiate or potentiate ateriospasms.
    Hemorrhage into the subarachnoid space
  30. The patency of arterioles in the CNS is an active process, requiring __________ products from the endothelial cells, which include... (2)
    vasodilatory; endothelial relaxation factor (ERF), prostacyclin (PG12)
  31. Subarachnoid hemorrhage releases oxyhemoglobin, leading to production of ___________, which causes accumulation of substances that promote ___________.
    free radicals; vasoconstriction (arteriospasms)
  32. Arterial spasms result in... (3)
    edema, hemorrhage, and tissue infarction.
  33. Arteriospasms may progress anterior and posterior to the spinal cord lesion, resulting in ______________; there is a _____-shaped leading margin; it can ultimately result in ________.
    ascending/descending myelomalacia; cone; death
  34. The extent of injury due to vascular compression in the spinal cord is a function of... (3)
    the rapidity in which the mass compromises the vascular supply, the degree of vascular compromise, and the presence or absence of associated hemorrhage.
  35. 4 types of masses that can cause compression of the spinal cord and vasculature.
    herniated intervertebral disc material, epidural abscess, neoplasm, displaced/subluxated vertebral body
  36. What limits the field of damage created by a focal compressive insult on the spinal cord?
    extensive anastomoses b/w vessels; the white matter is supplied by circumferential anastomotic network of vessels that penetrate the leptomeninges
  37. What is the hallmark pathologic response to compression?
    wallerian degeneration
  38. Wallerian degeneration is a __________ indicator of ___________.
    morphologic; loss of function
  39. The presence and distribution of Wallerian degeneration can be used to... (2)
    substantiate loss of CNS function, localize the insult underlying the functional deficit
  40. Cranial to the insult, Wallerian degeneration is localized to the ____________, the __(2)__ funiculi.
    ascending white matter tracts; dorsal and dorsolateral
  41. Caudal to the insult, Wallerian degeneration is localized to the ____________, the __(2)__ funiculi.
    descending white matter tracts; ventral and ventromedial aspects of the lateral
  42. At the site of the insult, Wallerian degeneration may affect _____________.
    all white matter tracts
  43. Compromised circulation affects _________ tracts first because they are the first to be ___________ and because they have the highest ___________.
    ventral; compressed; metabolic demands
  44. __(2)__ tracts are affected with more severe compression that affects perfusion.
    Lateral and dorsal
  45. Although not usual, loss of function can occur in the absence of ____________.
    Wallerian degeneration
  46. Grey matter of the spinal cord is supplied blood by the ____________; occlusion of this vessel is observed in states of ___________.
    ventral spinal a.; severe compression
  47. Gelatinous mass acting as the shock-abosrber b/w vertebral bodies.
    nucleus pulposus
  48. Displacement of nucleus pulposus into the spinal canal causes ______________.
    spinal cord compression
  49. Fibrous container of the nucleus pulposus.
    annulus fibrosus
  50. The annulus fibrosis is thinnest/weakest at its __________ aspect; reinforcement here is provided by __(2)__.
    dorsal; dorsal spinal ligament and conjugal ligaments (thoracic)
  51. Herniation in the intervertebral disc tends to occur _________ in the __(2)__ regions.
    dorsally; cervical and lumbosacral regions
  52. In chondrodystrophic breeds, __________ of the degenerative nucleus, often with ___________, results in loss of this shock-absorptive function; this leads to ______________ through a relatively normal annulus and ________, massive cord compression.
    chondroid metaplasia; mineralization; explosive herniation; sudden
  53. In non-chondrodystrophic breeds, ____________ degeneration of the _________ allows ________, incomplete protrusion of the __________; it can ultimately lead to ___________.
    age-dependent; annulus; slow; nucleus; Wallerian degeneration
  54. Equine cervical vertebral instability/stenotic myelopathy usually occurs in... (signalment)
    young TB and standardbreds.
  55. With equine cervical vertebral instability/stenotic myelopathy, instability of the cervical vertebrae is the result of a ______________; there is _________ cord compression upon __________ of the cervical column.
    progressive degeneration of the articular facets; dynamic; flexion/extension
  56. With equine CVI/SM, lesions of the articular facets cause changes that include... (3)
    overgrowth of articular cartilage, osteochondritis dissecans, +/- progression to DJD.
  57. With equine CVI/SM, ventroflexion results in overriding of the ___________ relative to the ___________, thus compressing the ___________; usually occurs at ________ [level of the spine].
    posterior vertebral body; anterior body; ventral; C3-4
  58. Cervical vertebral malarticulation of dogs occurs in __________ breeds; there is _________ compression of the ________ aspect of the cord during ___________.
    rapidly-growing; dynamic; dorsal; extension
  59. Equine cervical static stenosis occurs in ______________ [signalment].
    young quarterhorses
  60. With equine cervical static stenosis, there is primary __________, resulting in compensatory responses that cause___________ of the spinal canal and _____________.
    cervical  vertebral joint laxity; narrowing; static cord compression
  61. Compression that occurs with equine cervical static stenosis is due to... (2)
    sclerosis of the dorsal lamina, hypertrophy of the yellow ligament/ligamentum flavum
  62. Compression associated with equine cervical static stenosis is often at the level of _______ and is at the ________ aspect (i.e. the _________ funiculus); pathologic changes are restricted to ____________.
    C5-7; dorsal; dorsal; Wallerian degeneration
  63. Craniovertebral malformation of Arab horses manifests as ____________ and increased mobility at the ____________; these changes are accommodated by a __________.
    atlanto-occipital fusion; atlantoaxial articulation; hypoplastic dens
  64. Craniovertebral malformation in Arab horses results in cord compression at the _________ aspect at the level of _________ during _________; this ultimately leads to ____________.
    ventral; C1-2; flexion; Wallerian degeneration
  65. Hemivertebrae are malformed vertebrae that result in ______ instability that may cause _______ cord compression and ____________.
    axial; thoracic; Wallerian degeneration
  66. Spina bifida and myelodysplasia cause _________ cord compression.
  67. Canine Brucella canis can cause __________ in the _________ region.
    discospondylitis; lumbar
  68. Equine idiopathic discospondylitis occurs at the ____________.
    cervical intumescence
  69. Epidural abscesses cause ___________; the ___________ prevents direct invasion of the leptomeninges and cord.
    space-occupying masses; dense fibrous dura mater
  70. Neoplastic cells are not sensitive to ____________; The process of carcinogenesis has the following steps... (3)
    growth inhibitory influences; initiation, promotion, and progression.
  71. Step of carcinogenesis in which alteration of the genetic information of a cell occurs, being fixed by a round of replication.
  72. Step of carcinogenesis in which additional rounds of replication result in a change in the phenotype pf initiated cells; the new phenotype confers a selective advantage to survival.
  73. Step of carcinogenesis in which further replication in an environment otherwise inhibitory to autonomous growth drives a survival of the fittest evolutionary process for altered cells.
  74. Why are primary nervous tissue neoplasms rare?
    adult nervous tissue is either terminally differentiated or have a low degree of replication potential; the ability to replicate is required for carcinogenesis
  75. __(2)__ calls have the greatest replication potential and therefore make up the most common primary nervous tissue neoplasms in older individuals.
    Glial and mesenchymal cells
  76. Neural progenitor cells may "escape" the differentiation process; this gives rise to __(3)__ neoplasia in ________ individuals.
    primitive neuroectodermal tumors (PNET), neuroblastoma, or mixed; younger
  77. Slowly growing mass lesions consisting of well differentiated cells.
  78. Unlike in other organ systems, benign tumors of the CNS lack ____________.
    fibrous encapsulation
  79. How can metastasis from primary CNS tumors occur?
    neoplasms arise from structures within the ventricular system and flow through CSF to seed other organ systems
  80. Space occupying masses in the CNS leads to increased ____________, which can subsequently cause __(2)__.
    intracranial pressure; initiation of the edema cycle and hydrocephalus
  81. 2 common sequelae to initiation of the edema cycle, which can occur with neoplasia in the CNS.
    necrosis and herniation
  82. How do CNS tumors cause hydrocephalus? (2)
    choroid plexus tumors may occlude the interventricular foramen or the lateral apertures of the fourth ventricle, thalamic tumors and mesencephalic tumors may occlude the mesencephalic aqueduct
  83. Hallmark of hydrocephalus is _____________, which occurs due to _____________.
    enlarged lateral ventricles; periventricular demyelination
  84. Describe the premise of histogenic classification of CNS tumors.
    these neoplasms arise via transformation of a committed cell type; classification is based on the light microscopic appearance and the expression of cell-lineage specific antigens
  85. Where are neural progenitor cells located in young (3) and mature (1) animals?
    • young: subependymal zone, external granular cell layer of the cerebellum, olfactory epithelium
    • mature: olfactory epithelium
  86. Neural progenitor cells can differentiate into __(2)__, depending on their location/environment.
    neurons or glia
  87. What are 2 types of committed blast cells?
    neuroblasts, glioblasts
  88. What is the most common primary intracranial tumor of animals?
    meningeal neoplasms
  89. __(2)__ are the primary basis for identifying a tumor type; confirmation is based on __________.
    Location and morphological features; histological examination
  90. Why do we care about histogenic classification of CNS tumors? (3)
    realistic list of DDx when evaluating imaging data on a clinical neurological case, classification is linked to biological behaviors and response to treatment
  91. What is one morphologic finding that is VERY COMMON with brain tumors of any kind?
    cerebellar herniation
  92. 2 types of mesenchymal neoplasms and how you ID them.
    primary lymphosarcoma- stain CD3+ in dogs and cats; neoplastic reticulosis- non-B, non-T leukocytic neoplasm- do not stain with lymphocyte markers but contain cells of leukocytic origin
  93. 30-50% pf a CNS neoplasms are ____________, which can be... (2)
    secondary tumors; extension from surrounding structures  or hematogenous metastasis.
  94. Hematogenous metastases frequently lodge at the ____________; often secondary to... (3)
    grey-white junction; mammary carcinoma,  lymphosarcoma, and hemangiosarcoma.
  95. Describe intradural, extramedullary tumors.
    inside the dura but not attached to it, coming from the surface of the spinal cord
  96. Meningiomas originate from the ___________; they are not attached to the ____________.
    arachnoid complex; brain parenchyma