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Neuro Pathology Flashcards

1
Q

List the 8 unique histopathologic rxns seen in nervous tissue.

A
  1. Chromatolysis
  2. Demyelination
  3. Wallerian degeneration
  4. Satellitosis
  5. Neuronophagia
  6. Perivascular cuffing
  7. Malacia
  8. Neuronal inclusion bodies
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2
Q

What are pale areas in neuronal cytoplasm due to dispersion of Nissl’s substance are known as?

A

Chromatolysis

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3
Q

Which NS cell types can divide?

Implications?

A

Glial cells

(Only these cells can become tumors.

Neurons CANNOT)

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4
Q

Distemper virus shows an affinity for which NS cell type?

A

Oligodendrocytes

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5
Q

Which supporting cell type produces myelin?

A

Oligodendrocytes

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6
Q

Which supporting cell type controls

CSF movement?

A

Astrocytes

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7
Q

Which 2 NS cell types may become neoplastic?

A
  • Glial cells
  • Ependymal cells
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8
Q

What condition describes disruption & phagocytic removal of myelin?

Which cells in the PNS can fix this?

A
  • Demyelination
  • Schwann cells
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9
Q

What is the term for destruction of the axon & myelin sheath following trauma or toxic injury?

Where can it regenerate?

A
  • Wallerian Degeneration
  • PNS
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10
Q

What is the term for the accumulation of glial cells around damaged neurons?

Which type of glial cells mainly?

A
  • Satellitosis
  • Microglia
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11
Q

What is the term for MØic phagocytosis

of necrotic neurons?

A

Neuronophagia

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12
Q

What is the term for accumulation of polymorphonuclear or mononuclear leukocytes in Virchow-Robin spaces?

A

Perivascular cuffing

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13
Q

What type of leukocytes are suppurative?

A

polymorphonuclear

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14
Q

What type of leukocytes are non-suppurative?

A

Mononuclear

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15
Q

What does malacia refer to?

A

softening & liquefaction of NS tissue from necrosis of neurons & glial cells

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16
Q

What do Cowdry Type A inclusion bodies look like?

What virus are they often associated with?

A
  • eosinophilic
  • usually single & displaced nucleolus
  • Herpes virus
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17
Q

What do Cowdry Type B inclusion bodies look like ?

What 2 viruses are they associated with?

A
  • Eosinophilic
  • often multiple & necleolus is NOT displaced
  • Polio & Adenovirus
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18
Q

What is Cerebral/spinal dural osseous metaplasia (Ossifying pachymeningitis) & who gets it?

A
  • ovoid, thin whitish to mottled red metaplastic plates of bone (due to hemopoietic tissue)
  • incidental finding in old dogs
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19
Q

List the 5 congenital anomalies that are the result of neural tube closure defects (dysraphia).

A
  • Anencephaly
  • Cerebral aplasia (prosencephalic hypoplasia)
  • Meningoencephalocele
  • Meningomyelocele
  • Hydromyelia
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20
Q

Pathogenesis of Anecephaly?

A
  • absence of the cerebral hemispheres w/ failure of forebrain fusion
  • Medulla & mesencephalon usually still persists
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21
Q

Congenital anomalies resulting from injury during the last trimester of gestation are due to what?

A

prominent inflammatory changes

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22
Q

List the 2 Neuronal Migration disorders.

A
  • Lissencephaly
  • Hydrocephalus
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23
Q

Pathogensis of Prosencephalic Hypoplasia?

Who gets?

(AKA Cerebral aplasia)

A
  • Failure of bilateral seperation of hemispheres resulting in a SINGLE central ventricle
  • NO cerebral hemispheres
  • Pigs & lambs
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24
Q

Pathogensis of Meningoencephalocele?

A
  • protrusion of brain & meninges through a defect in the cranium
    • almost always median, along suture lines
  • associated with crania bifidum
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25
Q

Pathogenesis of Meningomyelocele?

Who gets?

A
  • protrustion of Spinal cord & meninges
  • associated with spina bifida
  • Brachycephalic breeds of dog
  • Manx cats
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26
Q

Pathogenesis of Hydromyelia?

A
  • excess CSF in spinal cord canal
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27
Q

Lesions of Prosencephalic hypoplasia?

(Cerebral aplasia)

A
  • absence of cerebral hemispheres
  • single central ventricle
  • cyclopia → severe cases (pigs & lambs)
  • Abscence of telencephalon
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28
Q

DDX of Cerebral aplasia?

(2)

A
  • Anencephaly
  • Hydraencephaly
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29
Q

Pathogenesis of Meningocele?

Who gets?

A
  • protrusion of fluid-filled meninges
  • Pigs → inherited
  • Cats → Burmese or pregant queens TXed w/ Griseofulvin
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30
Q

Etiopathogenesis of Lissencephaly (agyria)?

A
  • Lhasa Apso
  • absence of 1° gyri → “smooth brain”
  • excessively thin cerebral cortex
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31
Q

List the 3 different types of Hydrocephalus.

A
  • Internal → ventricles
  • External → sub-arachnoid space
  • Communicating → ventricles + sub-arachnoid space

(where the fluids accumulates)

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32
Q

List the 3 animals in which Hydrocephalus is of no clincal signifcance.

A
  • Early fetus
  • Aged animals
  • Brachycephalic breeds
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33
Q

How is Hydrocephalus ex vacuo different from Hydrocephalus?

A

due to compensatory enlargement of CSF spaces

NOT the result of increased CSF pressure

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34
Q

Etiopathogenesis of Congenital Hydrocephalus?

A
  • idiopathic & develops during fetal life
  • associated w/ Malformation
  • To due:
    • intra-uterine infections
    • nutritional deficiency
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35
Q

Eitopathogenesis of Acquired Hydrocephalus?

A
  • most often internal hydrocephalus → obstructed CSF flow
  • Progressive w/ NO cranial malformation
  • Sequel to: inflammation, cholesteatoma, neoplasia & parasitic cysts
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36
Q

Pathogenesis of Hydrocephalus?

A
  • increased production of CSF
  • obstruction of CSF flow
  • defective absorption of CSF
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37
Q

Lesions of Congenital vs. Acquired Hydrocephalus.

TQ

A

Congenital

  • Lateral ventricular distention
  • enlarged cranium

Acquired

  • Lateral ventricular distention
  • NO cranial malformation
  • Pressure atrophy → white matter + cerebral cortex
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38
Q

Etiopathogenesis of Hydranencephaly?

A
  • Etiology → Viral infections
  • Path → results from severe encephaloclastic (destructive) effects
  • Lesions:
    • Ø cerebral hemispheres
    • membranous CSF
    • Leptomeninges filled sacs
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39
Q

Pathogenesis of Porencephaly?

A
  • Path:
    • less severe case of hydranencephaly
    • destructive process in PRENATAL life
  • Lesions:
    • Cysts
    • White matter defects of cerebral hemispheres
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40
Q

Etiopathogenesis of Cerebellar Hypoplasia?

A
  • Etiology → Viral or Inherited
    • Feline panleukopenia
    • BVD
    • CHV
  • Path→ malformation of cerebellum w/ loss of Perkinje & Granular cells
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41
Q

Etiopathogenesis of Syringomyelia

A
  • Etiology → rare, except Weimaraner
  • Path→malformation of the spinal cord
    • tubular cavity (syrinx) that extends over several LUMBAR segments
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42
Q

Lesions of Syringomyelia

(3)

A
  • Cysts in central Gray Matter
  • NOT lined by ependymal cells
  • Weimaraner → hopping gait
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43
Q

Pathogenesis of Abiotrophy

(Cerebellar atrophy)

A
  • 1° metabolic defect/degeneration → premature apoptosis
  • involves only cerebellar cortex or multisystem
  • Non-inflammatory dz.
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44
Q

Lesions of Abiotrophy

A
  • Loss of Purkinje & Granular cells
  • Seen in basal ganglia → caudate nuclei, putamen, olivary nuclei, & substania nigra
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45
Q

Give 5 examples of TSE’s (prion dz) & species they affect.

A
  • Scrapie → small rumis
  • BSE → cattle
  • FSE → cats (BSE in cats)
  • CWD → free ranging deer
  • Transmissible mink encephalopathy
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46
Q

Lesions of

Transmissible Spongiform Encephalopathies

(TSE).

A
  • NO INFLAMMATION!!
  • Cytoplasmic vacuoules & astrocytosis
  • + Spongiform changes
  • PrPSC protein
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47
Q

How do you DX TSE’s?

A
  • Abnormal protein + lesions → OBEX of brainstem
  • IHC → before CNS lesions
    • 3rd eyelid, tonsils, retropharyngeal LN
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48
Q

Etiopathogenesis of Globoid Cell Leukodystrophy
(a Lysosomal Storage dz)

A
  • Etiology → inherited defect of galactocerebroside-B-galactosidase
  • Path → Accumulation of Galactocerebroside
    • MØs (microglial cells) → Globoid cells
    • neurotoxic → CNS signs (@ 2-7 mo. old)
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49
Q

Lesions of Globoid Cell Leukodystrophy

A
  • WHITE matter becomes gray & soft
  • PAS (+) globoid type MØs
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50
Q

4 things that can cause Brainstem Lesions

A
  • Prions → obex
  • Listeriosis → medulla & pons
  • Shiga-like toxin from E. coli
  • Cu deficiency
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51
Q

Vit. E deficiency in birds affects what area of the brain?

A

Cerebellum

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52
Q

Acute Pb toxicity in Dogs affects what 2 regions of the brain?

A

Cerebrum & Cerebellum

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53
Q

Broad etiology of Malacia

(necrosis of CNS tissue)

A
  • Vascular
  • Hypoxia
    • horse → post anesthesia
  • Toxins
  • Infections
  • Nutritional
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54
Q

List the Toxins that can cause Malacia and

the form of malacia seen with each.

A
  • Yellow Star Thistle → nigropallidal
  • Pb, Salt, Se → poliomyelomalacia
  • Moldy corn → leukoencephalomalacia
    • HORSE
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55
Q

List the 2 protozoal infections that cause malacia.

A
  • Theileriosis
  • Babesiosis
    • DOGS
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56
Q

What CNS disease is seen in Sheep as a result of

C. perfringens D infection?

A

Focal Symmetrical Encephalomalacia

(FSE)

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57
Q

What 2 Nutritional deficiencies lead to malacia?

A
  • Vitamin → cerebral hypoxia
    • A, B1, E
  • Mineral
    • Copper
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58
Q

What 4 things cause Focal Malacia?

A
  • FSE
  • Equine leukoencephalomalacia
  • Equine Nigropallidal encephalmalacia (YST toxicity)
  • Avian encephalomalacia (Vit E deficiency)

(associated w/ a specific toxin)

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59
Q

Susceptibility of cell types to

Laminar Cortical Necrosis (due to hypoxia) ?

A

Neurons > Oligodendrocytes>Astrocytes> Microglia

(NOAM)

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60
Q

2 things that cause Cerebrocortical necrosis (a form of laminar cortical necrosis)

A
  • Chronic Pb poisoning → cattle
  • Thiamine deficiency → cats & cattle
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61
Q

What causes Bilateral Polioencephalomalacia?

(form of laminar cortical necrosis)

A

Acute Se toxicity→ pigs

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62
Q

What are 2 causes of Polioencephalomalcia?

A
  • Salt toxicity → pigs
  • Thiamine deficiency → cats & cattle
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63
Q

Pathogenesis of Laminar Cortical Necrosis

A

Softening of the cerebrocortical GREY matter based on susceptibility of cells to hypoxia.

64
Q

Lesions of Malacia

A
  • Acute → swollen gyri
  • Subacute (2-5 d) & Chronic (7-14 d) → Liquefaction
    • yellow/green/brown, flat gyri
    • brain edema
65
Q

Sequelae of Malacia

A
  • Gitter cells
  • chronic liquefaction
66
Q

Hyperemia refers to an increase in ______ blood flow & is an ______ process.

A
  • Aterial
  • Active
67
Q

Congestion referes to an increase in _____ blood flow & is a _____ process.

A
  • Venous
  • Passive
68
Q

Give some examples of things that can cause Ischemia/Hypoxia in the CNS.

A
  • High systemic BP
  • High ICP
  • Reperfusion injury
  • Leukocyte products
  • Free radicals
  • Ca2+
  • L-glutamate (excitotoxin)
  • Lactic acidosis
69
Q

Which age group is more resistant to hypoxia?

Why?

A
  • Neonates
  • lower metabolic activity
  • can utilize lactate
  • high [ascorbate] may be protective
70
Q

4 things that affect Cerebral Metabolic Activity?

A
  • Systemic BP
  • Vascular patency
  • ICP
  • Autoregulation
71
Q

Etiology of CNS Ischemia/Hypoxia in

Horse, Dog & Cat?

A
  • Horse → Anesthesia related syndrome
  • Dog → Fibrocartilaginous Embolic Myelopathy (FCEM)
  • Cat → Feline Ischemic Encephalopathy due to Cuterebra
72
Q

Lesions of CNS Ischemia?

A
  • Generalized → ischemic encephalopathy
    • (necrosis of neurons & glial cells)
  • Localized → infarcts
73
Q

Sequelae of Circulatory Distrubances to the CNS?

(5)

A
  • Neuronal edema
  • Swelling
  • Contracture
  • Cytoplamsmic eosinophilia
  • Karyolysis
74
Q

List examples of things that affect the INTEGRITY of the BVs and lead to CNS Hemorrhage?

A
  • Viruses → ICH, HC, ASF, MCF
  • Histophilus somni (bacT)
  • Protozoa
  • Trauma
75
Q

List some examples of things that affect the COAGLABILITY of the blood in the CNS?

A
  • Thrombocytopenia
  • DIC
76
Q

Sites of Hemorrhage?

A
  • ICH in dogs → midbrain & medulla
  • FSE in sheep → internal capsule, thalamus, pons
  • Thiamine deficiency in cats → inferior colluculi
77
Q

What are the possible consequences of

CNS Hemorrhage?

A
  • depends on exact location of hemorrhage
  • Can act as SOLs → increased ICP
  • Local edema
  • Internal or external hydrocephalus
  • Epilepsy → from organized thrombi & blood clots
78
Q

What is the most important single change that accompanies ALL intracerebral lesions?

What is it’s etiology?

TQ

A
  • Edema
  • increased ICP due to:
    • inflammation
    • hypoxia
    • ischemia
    • toxins
79
Q

Differentiate Localized Edema of the CNS

from Generalized Edema of the CNS.

A

Localized

  • SOLs
  • Vague outline
  • if Chronic → faint yellow discoloration

Generalized

  • due to systemic conditions
  • diffuse inflammation
  • Toxemias/Intoxications
80
Q

What can cause Generalized Edema of the CNS in cattle & sheep?

A

Cerebrocortical necrosis (CNN)

81
Q

What are the gross lesions of Intracellular/Cytotoxic Edema?

A
  • fluid accumlation in the astrocytes (intracellularly)
  • NOT moist
  • NOT oozy
82
Q

What are the gross lesions seen in Vasogenic edema?

A
  • Extracellular accumulation of fluid
  • Moist
  • Oozy
83
Q

Gross appearance of the brain followin edema?

A
  • flat gyri
  • shallow sulci
  • lipping
84
Q

What is the definition and etiology of Lipping?

A
  • herniation of cerebellum through foramen magnum
  • Hydrocephalus
  • Cerebrum impacted against tentorium
  • Compressed brain stem
85
Q

Sequelae of CNS Edema?

A
  • Brain sweling
  • Brain distortion
  • Herniation
  • Brain stem injury
86
Q

Etiology of a Thromboembolism

A
  • Reduced diameter of arteries entering brain parenchyma
  • Jxn of grey & white matter→ capillaries loop back into cortex
87
Q

What is the lesion associated with a Thromboembolism?

A

OCCLUSIVE

(not ischemic)

88
Q

Give the typical causes of a Thromboemobolism

in the various domestic animal species

A
  • Cat → Atrial or Aortic thrombosis
  • Dog → cartilaginous or nucleus pulposis emboli → FCEM
  • Bacterial emboli
    • Pig → Erysipelas & Pasteurellosis
    • Horse → Sleepy foal dz.
    • Ruminants → Pasteurellosis
  • ALL → BM emboli after a long bone fx, Septicemias, tumors, etc.
89
Q

Definition of Meningitis?

A

inflammation of meninges

90
Q

Definition of Pachymeningitis?

A

Inflammation of the Dura mater

(outer, white)

91
Q

Definition of Leptomeningitis?

A

Inflammation of Pia-arachnoid mater

(inner, thin)

92
Q

Definition of Choroiditis?

A

Inflammation of the Choroid

93
Q

Definition of Ependymitis

A

Inflammation of the ependyma

94
Q

Definition of Encephalitis?

A

Inflammation of the Brain

95
Q

Definition of Myelitis?

A

Inflammation of the Spinal Cord

96
Q

Definition of Encephalomyelitis

A

Inflammation of the Brain & Spinal cord

97
Q

4 Main lesions of CNS Inflammation?

A
  • Pronounced vascular response
  • Perivascular cuffing (PMN’s)
  • Neuronal degeneration/death
  • Gliosis
98
Q

What etiology of CNS inflammation is typically seen in cats?

A

Infectious Meningoencephalitis

99
Q

What etiology of CNS inflammation is typically seen in dogs?

A

Idiopathic Inflammatory Brain disorders

100
Q

Etiology of Suppurative/Purulent Inflammation due to bacterial infections.

(4)

A
  • Thrombotic Meningoencephalitis (TME)
  • Listeriosis
  • Enterotoxemia → C. perfringes type D
  • Edema dz → E. coli
101
Q

Etiology & lesions of

Thrombotic Meningoencephalitis?

A
  • acute Histophilis somi infection
  • Hemorrhagic foci & infarcts
  • Vasculitis w/ thrombosis (hallmark) → septic infarction → septicemia
102
Q

Etiology & Lesions of Listeriosis in Adult rumis?

A
  • Listeria monocytogenes
  • Encephalitis or meningoencephalitis
  • Affinity for brain stem → multifocal microabscesses in medulla & pons
  • Circumscribed collections of mononuclear cells (hallmark)
103
Q

Etiology & lesions of Listeriosis in Young Rumis & monogastrics?

A
  • Listeria monocytogenes
  • septicemia
  • focal hepatic necrosis
104
Q

Discuss the 2 different morphologic patterns of

Focal Symmetrical Encephalomalacia (FSE).

A
  • Hemorrrhage & softening of the basal ganglia → more common
  • Lysis & liquefaction of the white matter of the frontal gyri
105
Q

Etiopathogenesis of Enterotoxemic colibacillosis (Edema dz) in Pigs?

A
  • Shiga-like toxin production by E. coli
  • toxin → angiopathy → vasculitis → edema
  • Bilateral symmetrical necrosis of the brainstem
106
Q

C/S of Edema Dz

(Enterotoxemic Colibacillosis)

A
  • Incoordination
  • hind-limb paresis
  • tremors
  • convulsions
107
Q

List the histological changes & regions affected seen due to Nonsuppurative (viral) inflammation.

A
  • Perivascular cuffing → mononuclear cells (lymphocytes & plasma cells)
  • Neuronal degeneration
  • Gliosis & demyelination of the WHITE matter
  • Lympho (+ plasma)cytic meningitis
  • Inclusion bodies
108
Q

List the lesions associated with K9 Distemper virus.

TQ

A
  • Demyelination of WHITE matter
  • IN inclusion bodies
109
Q

Which virus has IC inclusion bodies

(aka Negri bodies)?

110
Q

Pathogenesis of

Granulomatous Meningioencephalitis (GME)?

A
  • Middle-aged/ small breed dogs (terriers, poodles)
  • marked pervascular cuffing

Forms:

  • Focal → chronic, SOLs
  • Mulitfocal/Disseminated → acute, lower brain stem, cervical SC & meninges → death w/in a wk.
  • Ocular → acute progressive or static
111
Q

Pathogenesis of Necrotizing Encephalitis

(Pug dog encephalitis/PDE)?

A
  • Pugs, Maltese, Yorkies & Chihauhuas
  • multifocal, necrotic, cavitating lesions
  • Lymphocytes predominate
112
Q

Cerebral Nematodiasis results in brain hemorrhage, malacia, migratory tracts & SOLs.

Etiology & area affected??

A
  • Oestrus ovis → cranial vault
  • Hypoderma bovis → spinal cord
  • Cuterebra spp. → brain
113
Q

Etiopathogenesis of

Feline Ischemic Encephalopathy?

A
  • Cuterebra spp.
  • larvae migrate to brain → vascular lesions
  • Hemorrhage
  • Thrombosis
  • Vasculitis
114
Q

Etiopathogenesis of Sarcocystosis?

A
  • Sarcocytis neurona → EPM
  • affects Spinal Cord
  • Wallerian degeneration, encephalitis, myelitis, ataxia
115
Q

Lesions of Toxoplasmosis?

A
  • Hemorrhage
  • Infarcts
  • Edema
  • Non-suppurative inflammation
116
Q

Etiology & Lesions of Neosporosis by species?

A
  • Neospora caninum
  • Horse → Meningioencephalomyelitis
  • Dog → Polyradiculoneuritis & Polymyositis
  • Cattle (IH) → Multifocal malacia + abortion
117
Q

List the 3 examples of Fungal Dz of the brain & the lesions associated with each.

A
  • Blastomycosis → granulomatous
  • Cryptococcosis
    • Dogs → meninges & paranasal sinus
    • Cats → nasal cavity & pharynx
  • Phaeohyphomycosis (Cladophialophora bantiana)
    • Pyogranulomatous
118
Q

Which animals get Vitamin B1 (Thiamine) Deficiency?

A
  • Cat
  • Fox
  • Mink
  • Ruminants
119
Q

Etiology of Vitamin B1 (Thiamine) Deficiency?

A
  • Thiaminase in fish
  • Bracken fern
  • Horsetail
120
Q

Lesions of Vitamin B1 (Thiamine) Deficiency?

A
  • Rumis → polioencephalomalacia or central cortical necrosis (CNN) → ceberal cortex
  • Edema
  • Perivascular dilation
  • Hemorrhage
  • Laminar necrosis
121
Q

Etiology & lesions of Swayback in lambs/goats?

A
  • Copper deficiency
  • Astrogliosis
  • Chromatolysis
  • Necrosis (neuronal)
  • Degeneration (mylenated axons)
122
Q

Pathogenesis of Copper deficieny in lambs/goats?

A
  • affects the GREY & WHITE matter of brain stem & spinal cord
  • Delayed onset→ enzootic ataxia
123
Q

Vitamin E (Tocopheral) deficiency

causes what 4 things in chicks?

A
  • Encephalomalacia
  • “Crazy chick dz”
  • Exudative diathesis
  • Nutritional mm. dystropy
124
Q

Where are the lesions located in

Vitamin E (Tocopheral) deficiency?

A

focal malacia of the cerebellum

125
Q

Lesions seen in Vitamin A (Retinol) Deficiency?

A
  • Night blindness
  • Optic neuropathy
  • Vit. A is required for osteogensis
126
Q

Which areas are specifically affected by

Equine Nigropallidal Malacia (YST toxicity)?

A

Focal necrosis of:

  • Pallidus
  • Substantia nigra
127
Q

What is the most consistenly important poison in farm animals?

A

Pb toxicity

128
Q

Lesions of Pb toxicity in Cattle?

A
  • Acute → head pressing, blindness, death 12-24 hrs
  • Chronic → laminar cerebral cortical necrosis
129
Q

Lesions of Pb toxicity in Dogs?

A
  • WHITE matter edema
  • neuronal degeneration → cerebrum & cerebellum
130
Q

C/S of Selenium toxicity in Pigs?

A
  • Walking backwards
  • sitting down
131
Q

Pathogenesis & lesions of Selenium toxicity in Pigs?

A
  • acute paralytic syndrome due to bilateral poliomyeomalacia
  • Yellow discoloration & necrosis of GREY matter of Spinal cord
  • Wallerian degeneration
132
Q

4 C/S of Salt toxicity in pigs?

A
  • Blindness
  • Deafness
  • Head pressing
  • Convulsions
133
Q

Pathognomonic lesions of Salt Toxicity in Pigs?

A
  • Eosinophilic meningoencephalitis
  • Encephalomalacia
  • + laminar necrosis of cerebral cortex GREY matter
134
Q

Etiopathogenesis of Moldy Corn Toxicity?

A
  • seen in Horses
  • due to Fusmonsin B1 toxin produced by Fusarium moniliforme in corn
  • Fumonsin B1 disrupts cell membranes → lipid peroxidation → TNF-alpha is produced by MØs → Ø DNA synthesis
135
Q

Lesions associated with Moldy Corn toxicity in Horses?

A
  • Leukoencephalomalacia
  • Focal necrosis of the WHITE matter in the cerebral hemispheres
136
Q

C/S of Moldy Corn Toxicity in horses?

A
  • Weakness
  • Drowsiness
  • Staggering
  • Circling
  • Impaired vision
  • Pharyngeal paralysis
137
Q

What are the characteristics of a Coup lesion?

A
  • Stationary head
  • Focal injury
  • Hemorrhage @ point of impact
138
Q

What are the characteristics of a Contre Coup Lesion?

A
  • Moving head
  • Diffuse injury
  • Hemorrhage @ OPPOSITE side of point of impact
139
Q

What is the nucleus pulposus?

A

central semisolid mucoid CT

140
Q

What is the Annulus fibrosus?

A

thick zone of fibrous tissue surrounding the nucleus pulposus

141
Q

C/S of Intervertebral Disc Dz due to rupture of the Annulus fibrosus?

A
  • Arches back
  • Distended abdomen
  • Flaccid paraplegia of limbs
142
Q

Sequelae of Intervertebral Disc Dz?

A

Fibrocartilagnious embolic myelopathy

(FEM)

143
Q

Contrast Hansen Type I & Hansen Type II

Intervertebral Disc Dz.

A

Hansen I

  • acute rupture, multiple disks involved, early degeneration
  • Young animals (< 3 yrs)
  • Chondroystrophoid breeds

Hansen II

  • gradual rupture, less discs involved
  • Older animals
  • All breeds
144
Q

Etiopathogenesis of Cervicospinal Arthropathy (Wobbler’s)

in YOUNG horses?

A
  • malalignment & hypermotility of cervical vertebra
  • degeneration of cervical articular processes
145
Q

What is the most common brain tumor

of dogs & cats?

What 2 areas are most often affected?

A
  • Meningioma
  • Olfactory bulb or frontal lobe
146
Q

Lesions of Meningioma?

A
  • well circumscribed & encapulsated lesions
  • streams & whorls of uniform fusiform CT
147
Q

What brain tumor is common in

Brachycephalic breeds?

A

Glial tumors → astrocytoma & oligodendroglioma

148
Q

Contrast Astrocytoma & Oligdendroglioma.

A

Astrocytoma

  • MOST COMMON
  • POORLY demarcated
  • solid, greyish-white mass

Oligodendroglioma

  • less common
  • WELL demarcated
  • soft, cyst-like lesions
149
Q

List the 2 examples of Embryonal Tumors.

A
  • Medulloblastoma
  • Ependymoma
150
Q

Diagnosis of Medulloblastoma?

(rare embryonal tumor)

A

Rosette (rose-like) arrangement of cells

151
Q

2 Lesions of Epedymoma?

A
  • Large, well demaracted intravascular mass (SOL)
  • Hydrocephalus
152
Q

Give 3 examples of

Brain Metastatic (2° Tumors) Tumors that have predilection for the jxn of Grey & White matter.

A
  • Hemangiosarcoma
  • Malignant Melanoma
  • Adenocarcinoma
153
Q

What is an incidental lesion seen in horses & is NOT a true neoplasm?

A

Cholesteatoma

154
Q

Pathogenesis & lesions of

Cholesteatoma in OLD horses?

A
  • degenerative lesion of the choroid plexus
  • granulomatous inflammation w/ cholesterol crystals
  • Hydrocephalus
  • Location → lateral ventricles
155
Q

What can cause tail paralysis & loss of bladder & rectum sphincter tone?

A

Neuritis of cauda equina

Path 2 (6 decks)

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