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CNS Flashcards

1
Q

List the Neural tube closure defects (dysraphia)

A
  • Anencephaly and prosencephalic hypoplasia
  • Meningoencephalocele and cranium bifidum
  • Meningomyelocele and spina bifida
  • Hydromyelia
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2
Q

what is the term for total abscence of the brain

A

Anencephaly

the term is used even though a small portion of the
brain persists
– often the medulla is present and occasionally some of
the mesencephalon

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3
Q

What are the lesions of anencephaly

A
  • absence of the cerebral hemispheres
    • failure of forebrain fusion
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4
Q

Prosencephalic hypoplasia is common in which animals

A

pigs and lambs

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5
Q

failure of bilateral separation of the primitive single telencephalic cavity into two hemispheres

A
  • cerebral aplasia(procencephalic hypoplasia)
  • there is absence of the cerebral hemispheres
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6
Q

what are the lesions of proncephalic hypoplasia

A
  • a single central ventricle
  • absence of the longitudinal fissure, the corpus
  • callosum, olfactory bulb and optic tracts
  • brain stem and cerebellum are normal
  • associated with cyclopia
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7
Q

protrusion of the brain (along with the meninges)
through a defect in the cranium (cranium bifidum)

A

Encephalocele

related to suture lines
– almost always median
– the skin forms the hernia sac
– spinal bifida refers to the defect in the spine

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8
Q

protrusion of the fluid filled
meninges

A
  • meningocele
  • it is fluid filled
  • miningocele and enencephalocele can be inherite in bothpgs and brunnete cats and has been associated with treatment of griseofuscin in pregnant queen
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9
Q

define microencephaly

A
  • it is an abnormally small brain
  • cerebrum is mostly affected
  • is a defect in cerebral corticogenesis due to decreased migration of germinal epithelial cells
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10
Q

defect in cerebral corticogenesis due to increased migration of germinal epithelial cells (errosrs of cerbal gyri)

A

macroencephaly

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11
Q

which area of the brain is most affected by microencephaly

A

cerebrum

deficiency of cerebral gray and white matter

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12
Q

abnormally flattened and narrowed frontal part
of the cranium with frontal bones thicker than normal are lesions of……..

A

Microencephaly

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13
Q

list the viruses that causes Microencephaly

A
  • Akabane virus in lambs
  • BVD virus in calves
  • Border disease virus in lambs
  • Hog cholera virus in piglets
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14
Q

abnormally large brain or excessive volume of the
intracranial contents

A

Macroencephaly (megalencephaly)

tend to be asymmetrical with exaggerated degrees
of heterotopia (displacement of an organ from its
normal position)

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15
Q

presence of clusters of
nerve cells at a site where they are normally
absent (e.g., subcortical white matter)

A

Cortical dysplasia

incomplete migration of neuroblasts during
fetal life
• usually associated with dysplastic development of
the cortex

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16
Q

lack of formation of secondary or tertiary gyri

A
  • Macrogyri
  • large, smooth gyri analogous to those of the brains of lower organisms are formed
  • dysplasia and distortion of cortical architecture
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17
Q

congenital anomality with small numerous convulutions

A

Microgyria (polymicrogyria)

normal gyral pattern is lost in affected areas

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18
Q

what are the lesions of microgyria

A
  • asymmetrical or patchy
  • abruptly demarcated from normal cortex
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19
Q

discuss morphological characteristics of Ulegyria

A
  • imparts a wrinckled appearence to the cortex
  • it arises as a consequence of scarring and atrophy to otherwise topographically normal gyri
  • there is focal laminar necrosis caused by prolonged ischemia /anoxc injury in the perinatal period
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20
Q

convulations almost absesnt in

A

Lissencephaly (agyria)

there is absence of primary gyri

brain surface is almost perfect smooth

excessively thin membrane

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21
Q

what are the morphological characteristics of lissencephaly

A
  • there is absence of primary gyri
  • brain surface is almost perfect smooth
  • excessively thin membrane
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22
Q

what causes lissencephaly

A

defective neuronal migration

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23
Q

lissencephaly occurs in which dog breed

A

Lhasa Apso dogs

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24
Q

excessively broad brain convolutions result in which cerebral corticogenesis defect

A

Pachygyria (macrogyria)

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25
Q

Pachygyria (macrogyria) lesions

A
  • Excessive broad brain convulsions resulting from fewer secondary gyri
  • increased depth of the gray matter underlying the smooth part of the cortex
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26
Q

abnormal accumulation of fluid in the ventricles of
the brain and sub-meningeally

A

hydrocephalus

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27
Q

internal hydrocephalus is common in which animals

A

brachycephalic breeds and in aged animals

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28
Q

hydrocephalus in which fluid accumulates in the ventricles

A

internal hydrocephalus

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29
Q

hydrocephalus in which fluid accumulates in the sub-arachnoid space

A

external hydrocephalus

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30
Q

etiology of Congenital hydrocephalus

A
  • idiopathic
  • intra-uterine viral infections
  • nutritional deficiencies
  • familial in pigs
  • malformation of the cranium

obstruction mostly develops as the consequence of a
periductal gliosis of the aqueduct of Sylvius

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31
Q

what are the lesions of congenital hydrocephalus

A
  • dilated ventricles or the duct system

• dome-shaped, thin-boned and enlarged cranium

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32
Q

discuss Acquired hydrocephalus

A
  • seen most commonly as an internal hydrocephalus
  • obstruction of flow due to an accumulation of and organization of exudate
  • progressive
  • ** no malformation of the cranium**
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33
Q

Acquired hydrocephalus etiopathogenesis

A
  • bacterial meningitis

– most cases are acutely fatal

  • granulomatous meningitis

– TB, cryptococcosis, FIP

  • intracranial neoplasms
  • parasitic cysts
  • cholesteatoma (cholesterolinic granuloma) in

horses

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34
Q

what are the lesions of acquired hydrocephaly

A
  • may be difficult to observe in neonates where the brain is soft and easily collapses
  • pressure atrophy of the septum pellucidum and hippocampus
  • ventricular dilatation
  • pressure atrophy of cerebrocortical white matter
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35
Q

• Encephaloclastic defects

A

destructive lesions of the
brain

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36
Q

types of Encephaloclastic defects

A
  • Hydranencephaly (diffuse)
  • Porencephaly (focal)
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37
Q

complete or almost complete absence of the cerebral
hemispheres in a cranium of normal size and
formation

A

Hydranencephaly

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38
Q

discuss leptomeninges

A
  • normal position
  • form sacs enclosing CSF (the fluid occupies space normally occupied by the parenchyma)
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39
Q

residual lesion of full-thickness necrosis of the
cerebral hemisphere associated with fetal viral
infections

A

Hydranencephaly

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40
Q

which congenital cranial defect is common in calves in association with cerebellar hypoplasia
•and can also be found in lambs of ewes vaccinated during pregnancy for
bluetongue

A

Hydranencephaly

•and can also be found in lambs of ewes vaccinated during pregnancy for bluetongue

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41
Q

cysts or cavities in the wall of the cerebral
hemisphere (cystic cavitation of the brain)

A

Porencephaly

  • typically involves the white matter of the cerebral hemispheres
  • cyst communicates with the subarachnoid space and or lateral ventricle
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42
Q

etiogenesis of porencephaly

A
  • congenital anomaly
  • remnants of destructive lesions

– viral infections (Border disease, hairy shaker
disease, BVD)

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43
Q

which parasite can cause similiar lesions as porencephaly

A

taenia multiceps

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44
Q

what causes cerebral hypoplasia

A
  • usually following intra-uterine viral infections
  1. feline panleukopenia >> ataxia in kittens
  2. BVD/MD
  3. hog cholera vaccination
  4. Border disease
  5. rat virus, hamster osteolytic virus
  • can be inherited
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45
Q

what are the gross lesions of Cerebellar hypoplasia

A
  • normal in size and appearance or small nubbin of tissue
  • lack of normal development of the layers of the cerebelum
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46
Q

microscopic lesions of Cerebellar hypoplasia

A
  • loss of purkinje cells
  • granular layer narrowed and deficient in cells
  • molecular layer usually normal
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47
Q

premature or accelerated degeneration of formed
elements of the cerebellum

A

cerebellar atrophy

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48
Q

discuss characteristics of cerebellar atrophy

A
  • Purkinje cells appear particularly susceptible
  • lambs (“daft lambs” in England and Canada)
  • dogs
  • cats
  • various breeds of cattle, piglets, and foals
  • **degeneration and loss of Purkinje cells and granule **cells **
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49
Q

11 week old blue terrier is presented with ataxia and dysmetria .which inheritive cranial disease o you suspect

A

Hereditary striatonigral and cerebello-olivary degeneration

seen between 9 and 16 weeks of age

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50
Q

Purkinje cell axonal swelling in the cerebellar granular layer + degeneration and loss of Purkinje cells are all lesions of

A

Bovine familial convulsions and ataxia

  • it is heritable disorder of purebred and crossbred Aberdeen Angus cattle in the UK
  • clinicalsigns are episodic suizuresin new born and young calvesand granual development of ataxia with spasticity and hypermetria in calves surviving bouts of suizures extending over 2-3 months
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51
Q

what are the clinical signs of bovine familial convulsions and ataxia

A
  • intermittent episodic seizures in newborn and young calves

• gradual development of ataxia with spasticity and
hypermetria in calves surviving bouts of seizures
extending over 2-3 months

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52
Q

cerebellar degeneration and ataxia of horses in New
Caledonia

A

Gomen disease

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53
Q

lesions of gomen disease

A
  • folial atrophy in the cerebellar vermis
  • thinning of the cerebellar molecular layer and loss of Purkinje and granule cells
  • deposition of a pigment resembling lipofuscin in many of the surviving Purkinje cells and in the neurons of the brain and spinal cord
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54
Q

displacement of the tongue of the cerebellar vermis, medulla and caudal 4th ventricle through the foramen magnum into the spinal canal

A

Arnold-Chiari malformation

  • a developmental defect of the cerebellum and brain stem associated with hydrocephalus
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55
Q

discuss Dandy-Walker syndrome

A
  • it isa midline defect of the cerebellum where vermis is largely absent

– cerebellar hemispheres widely separated by a
large fluid-filled cyst in an enlarged caudal
fossa

  • roof of the cyst consists of ependyma, a disorganized layer of glial tissue, and an outer layer of leptomeningeal
    tissue
    – an expanded 4th ventricle forms the floor of
    the cyst
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56
Q

total absence of the spinal cord

A

Amyelia

usually associated with anencephaly

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57
Q

Segmental aplasia and hypoplasia of the spinal cord

A

Myelodysplasia

  • lumbar region most frequently affected

• some cases are associated with fetal Akabane
virus infection

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58
Q

discuss Perosomus elumbus in calves and lambs

A
  • Myelodysplasia
  • partial agenesis of the spinal cord and there is failure of induction of the related vertebrae
  • cranial part of the body is normal
  • _ vertebral axis ends at the caudal thoracic region_
  • lumbar, sacral, and coccygeal vertebrae areabsent
  • spinal cord ends in the thoracic region in a blind vertebral canal
  • caudal part of the body remains attached to the cranial part by soft tissue only
  • arthrogryposis limbs
  • muscular atrophy
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59
Q

spinal cord ends in the thoracic region in a blind vertebral canal and caudal part of the body remains attached to the cranial part by soft tissue only

A

Perosomus elumbus in calves and lambs

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60
Q 
tubular cavitation (syrinx) of the spinal cord
 extending over several segments
A

Syringomyelia

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61
Q

Weimaraner is presented with the clinical signs below, what do you suspect

  • affected dogs are unable to completely extend the hind limbs
  • crouched posture
  • hind limbs are moved together in progression

(symmetrical hopping gait)

A

Syringomyelia

lesions are not observed until about the 8th month
of life

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62
Q

gross lesions of Syringomyelia

A
  • cavitations in the lumbar segments
  • may or may not be visible to the naked eye
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63
Q

microscopic lesions of syringomyelia

A
  • cavitations in the central gray matter (dorsal and

lateral to the central canal)

  • not lined by ependymal cells
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64
Q

simple dilatation of the central canal of the spinal
cord

A

Hydromyelia

the cavity is connected with the central canal and lined by ependymal cells

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65
Q

a syndrome of pelvic limb gait disturbance in young
dogs (“bunny-hopping” or “kangaroo-gait”)

A

Myelodysplastic and dysraphic lesions in Weimaraner
dogs

inherited in a co-dominant mode with variable
penetrance
• lethal in the homozygous state

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66
Q

lesions of Myelodysplastic and dysraphic lesions in Weimaraner dogs

A
  • a range of dysraphic defects:
  • anomalies of the dorsal septum (may be absent)
  • hydromyelia
  • duplication or displacement of the central canal
  • anomalies of extent and distribution of the central gray matter
  • anomalies of the ventral horns
  • deficiency of the ventral median fissure
  • ± thoraco-lumbar scoliosis, depression of the sternum, abnormal hair streams in the dorsal cervical region
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67
Q

pathogenesis of Myelodysplastic and dysraphic lesions in Weimaraner dogs

A

primary lesion is related to aberrantly positioned
mantle cells ventral to the central canal in the
floor plate area

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68
Q

absence of the dorsal portions of the vertebrae

A

Spina bifida

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69
Q

spina bifida is mostly found in which animals

A
  • this defect occurs most frequently in

brachycepahlic breeds of dogs and is inherited
in Manx cats

sacrococcygeal agenesis occurs in association
with spina bifida in Manx cats, claves, dogs, and
sheep

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70
Q

a condition where neurulation does not occur,

the neural plate remaining open; the defect involves
the whole of the vertebral axis with
anencephaly an expected accompaniment;
there is virtual amyelia , neural tissue
being present only as soft red masses in
the residual groove

A

Total myeloschisis

  • a type of spinal bifida
  • local myeloschisis is a localized defect due to failure of closure of the neural tube
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71
Q

a cystic swelling protrudes through the
vertebral defect i.e

A

Spina bifida cystica

example is when meninges protrude (meningocele),
the roof of the cyst comprises skin and
condensed meninges, including dura mater

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72
Q

discuss Spina bifida with meningomyelocele

A
  • the cyst tends to be broad-based
  • failure of dehiscence of the neural crest from surface ectoderm provides for a central area without epithelial covering
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73
Q

lesions of dermoid sinus in Rhodesian Ridgeback dogs

A
  • incomplete separation of the neural tube from the overlying dorsal midline ectoderm allows persistence of a sinus connecting the skin surface to the supraspinatus ligament,
  • or it may extend as deep as the dura mater of the spinal cord
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74
Q

what are the viruses associated with congenital malformations in calves

A

BVD

BD

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75
Q

what are the viruses associated with congenital malformations in LAMBS

A
  • vaccination
         – RVF, bluetongue
  • Wesselsbron disease
         – natural infection and vaccination
  • Border disease
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76
Q

list diases that causes intracytoplasmic neuronal vacuolization

A
  1. scrapie
  2. bovine spongiform encephalopathy(BSE)
  3. toxicity)→solanum spp, myotoxicosis,aspirgillus, clavatus
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77
Q

disappearance of the nissel substances from the cell body

A

chromocytolysis

it is associate with cytoplasmic swelling

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78
Q

characteristics of chromatolysis

A
  • irregular vacuolation of the neutrophil
  • restricted to white matter and nerve
  • moth eaten appearance, status spongioform
  • reduced staining capacity of the affected tissue→rarefaction
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79
Q

loss of myelin due to disoders of myelin in supporting cells such as schwann and oligodendritic cells

A

primary demyelination

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80
Q

give an example of a secondary demyelination

A

wallerian degeneration

  • it follows a severe axonal damage.
  • it reflects death of an exon
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81
Q

describe wallerian degeneration

A
  1. axon and myelin are disrupted at the point of injury and the fiber dies back several nodes and the distal section dies
  2. then fragmentation of the axon and sheath occurs in a few days
  3. debris are then removed by phagocytosis within a few weeks
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82
Q

hereditary or congenital defects of Cu def. in lambs (swayback)

A

dysmyelination and dysmyelinogenesisis

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83
Q

the condition whare myelination is not complete at birth

A

nota bene

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84
Q

what are the clinical signs of nota bela in neonates with incomplete myelination at birth

A
  1. neonates cannot walk
  2. brain is very soft with severe brain edema
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85
Q

what are the clinical sings of neonates with nearly complete myelination at birth

A

allows neonates to run(foals)

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86
Q

edema of the myelin and disruption at the intraperiod line of the myelin sheath

A

spongioform myelinopathies

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87
Q

list the familial or heditory disease

A
  1. primary neuronal degeneration
  2. spongy degeneration
  3. mitochondrial encephalopathy
  4. degenerative myelopathy
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88
Q

what causes abiotrophy neurodegeneration

A
  • it is a primary premature neuronal degeneration
  • it is not secondary to toxin or infectious agents
    *
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89
Q

an arabian horse gets ataxic and dysmetria before maturity. which disease do you suspect

A

cerebellar abiotrophy

  • it also affects dogs
  • it is distinct from cerebellar hypoplasia
  • affected animals appear normal after birth
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90
Q

cerebellum can be normal or shrunken in which disease

A

cerebellar abiotrophy

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91
Q

what are the lesions of cerebellar abiotrophy

A

cerebellum can be normal or shrunken

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92
Q

what are the histological lesions of cerebellar abiotrophy

A
  • neuronal degenraration and loss
  • reactive gliosis ( production of dense fibrous network of neuroglia in areas of damage)
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93
Q

lesions of neuroxonal dystrophy

A

axonal swelling of the brain stem, cerebellum and spinal cord

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94
Q

axonal degeneration and secondary demyelination in the white matter of the spinal cord

A

degenerative leukomyelopathy

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95
Q

discuss changes seen in acute nerve necrosis

A
  • initial degeneration
  • neuronal swelling central dissolution of nissel substance

n.bas long as the cell body is intact then damage is reversible

96
Q

discuss acute nerve necrosis due to damaging injury

A
  • condensation of the cytoplasm
  • intennse cytoplasmic eosinophilia of the neuron
  • the nucleus becomes pyknoticand the entire cell may fragmentand get phagocytised
97
Q

what causes acute nerve necrosis

A
  • ischemia
  • acute toxicity
  • infection
98
Q

this type of nerve degeneration is seen as cellular atrophy and hyperchromasia or by the presence of cytoplasmic vacuolizationand increase intracellular filaments and proteins

A

chronic nerve degeneration

99
Q

what are the characteristics of chronic nerve cell injury

A
  • cellular atrophy and hyperchromasia
  • cytoplasmic vacuolization
  • increased intracellula filaments and proteins
  • further injury⇒ contraction of the cell body, the cytoplasm becomes basophilic rather than eisinophilic.
  • prolonged injury⇒nucler pyknosis and fragmentation
100
Q

pale areas in neuronal cytoplasm due to dispersion of nissle substances

A

chromatolysis

101
Q

destruction of axon and myelin sheath following trauma or toxic injury

A

wallerian degeneration

102
Q

accumulation of glial cells around damaged neurons

A

satellitosis

103
Q

accumulation of polymorphonuclear (supperative) or mononuclear (non supperative)leukocytes in perivascular spaces

A

perivascular cuffing

104
Q

thin,whittish mottled red enlongated plates often containing bone marrow

A

cerebral and spinal dural metaplasia

it causes pressure on the spinal cord and nerve roots resulting in wallerian degeneration

105
Q

what is the condition where there is failure of bilateral separaton of the primitive telecenphalic cavity into 2 hemispheres and there is absence of the cerebral hemispheres

A

cerebral aplasia

106
Q

what are the characteristic lesions of cerebral aplasia

A
  • absence of cerebral hemispheres
  • there is a single central ventricle
  • abscence of
  • the longitudinal fissure,
  • corpus collosum,
  • olfactory bulb
  • optic tracts
  • severe cases may have central proboscis and a single eye
107
Q

potrution of the of the brain through a defect in the cranium

A

encephalocele

it is related to the suture lines and are almost always median, the skin forms the hernia sac

108
Q

portrution of the fluid filled meninges

A

meningocele

109
Q

a pregnant queen was treated with griseofuscin. what are you mostly concerned with

A

encencephaly and meningiocele

110
Q

what is macrogyri

A

lack of formation of secondary or tertiary gyri

111
Q

what are the lesions of macrogyri

A

large,smooth gyri analogy with those of the brains of lower organisms

there is dysplasia and distorsion of cortical architecture

112
Q

abscence of primary gyri

A

lissencephaly (agyria)

convulsions are almost entirely absent and the brain surface may be smooth (smooth brain) eccept for slight grooves in which the meningeal surfaces are situated

113
Q

what are the lesions of lissencephaly

A
  • convulsions are almost entirely absent
  • the cerebral cortex is extremely thin
  • etiopathogenesis:defective neuronal migration
  • occurs in lhasa Apso dogs
114
Q

what causes lissencephaly

A

defective neuronal migration

115
Q

what causes cyclopia

A
  • idiopathic
  • chromosomal anomalies
  • prolonged gestation in guersey and jersey fetuses
  • veraturum califonicam
    *
116
Q

fluids builds in the ventricles

A

internal hydrocephalus

117
Q

fluids accumulates in the sub-arachnoid space

A

external hydrocephalus

118
Q

complete or almost complete absence of the cerebral hemispheres leaving only membraneous sacs filled with CSFand enclosed leptoleptomengitis

A

hydranencephaly

119
Q

how does hydranencephaly differ from hydrocephalus

A
  • the cranial cavity is complte in contrast to hydrocephalus and of normal comformation
  • the leptominingis are in their normal positions and form sacs enclosing the CSF
  • the cerebral hemispheres are largely represented by large cystic spaces or sacs.
  • there is no ependymal lining
120
Q

give examples of hydranencephaly in anmals

A
  • mostly commonly observe in calves with cerebral hypoplasia
  • lambs of ewes vaccionated uring pregnancy for bluetongue
  • hydrancencephaly is a residual lesion of full thickness necrosis of the cerebral hemisphere usually associated with fetal viral infections eg akabane virus
121
Q

cystic cavitation of the brain evolving from a destructive process in prenatal life

A

porencephaly

  • the defect typically involves the white matter of the cerebral hemispheres.the naffected brain may contain a single cyst or there may be multiple cystic lesions.
  • the cyst may communicate with the ventricular cavities or with the subrachnoid space
122
Q

what causes porencephaly

A

same as hydracephaly

. uterine virus such as BVD

123
Q

what causes cerebellar hypoplasia

A
  1. inherited in chowchow etc
  2. viruses
  • feline pannleukopenia virus
  • herpes virus in dogs
124
Q

what are the lesions of cerebellar hypoplasia

A
  • decrease in size of the cerebellum
  • with lack of development of the layers of the cerebellum
125
Q

what are the microscopic lesions of cerebellar atrophy

A

degeneration and loss of purkinje cells and granules

126
Q

what causes cerebellar atrophy

A

intrinsic metabollic defect

127
Q

a 10 week old blue kerry terrier is presented with a history of ataxia and dysmetria .what disease should be top of your differential

A

hereditary striatonigral and cerebello-olivary degeneration

128
Q

a tubular cavitation of the spinal cord which extends over several segments

A

syringomyelia

129
Q

gross lesions of syringomyelia

A

cavitations are usually found in the lumbar segments and they may or may not be visible to the naked eye.

130
Q

what are the microscopic lesions of syringomyelia

A

the cavitations are usually found in the central gray matter and they are not line by ependymal cells

131
Q

dilation of the central canal of the spinal cord

A

hydromyelia

the cavity is connected with the central canal and lined by ependymal cells.

132
Q

a waimaraners has a pelvic limb gait disturbance which is characterised by bunny hopping or kangaroo gait. which isease do you suspect

A

myelodysplastic and dysraphic lesion

133
Q

what are the lesions of myelodysplastic and dysraphic

A
  • anomalies of the dorsal septum which may be absent
  • hydromyelia
  • duplication or displacement of the central canal
  • anomalies of extent and distribution of the central gray matter
  • anomalies of the ventral horn
  • def. of the sternum
  • abnormal hair streams in the dorsal cervical region
134
Q

what are the lesions of prion diesease

A

characterised by

  • spongiform change of the neuropil
  • neuronal degeneration
  • apoptosis and loss
  • astrocytosis
  • formation of prominent cytoplasmic vacuoles
135
Q

where are histolic lesions of prion diseases found

A

brainstem espercially obex

136
Q

inherited deficiency of the catabolic enzyme galactocerebroside-B-galactosidase

A

globoid cell leukodystrophy

137
Q

what is the lesion observed in globoid cell leukodystrophy

A

macrophages(microglial cell) are transformed into globoid cells when PAS positive inclusion tubules of galactocerebroside accumulate within them

138
Q

what are the gross lesions of globoid cell leukodystrophy

A

regions of fixed white matter are gray and soft compared to normal white matter

139
Q

necrosis of the white matter

A

leukomalacia

140
Q

necrosis of the gray matter

A

poliomalacia

141
Q

necrosis of the brain as a whole

A

encephalomalacia

142
Q

necrosis of the spinal cord

A

myelomalacia

143
Q

necrosis of the brain and spinal cord

A

encelomyelomalasia

144
Q

what type of lesions do you find in hypoxia

A

laminar patter( laminar cortical necrosis)

145
Q

list all causes of laminar cortical necrosis

A
  • hypoxia
  • thiamine deficiency in cats/ruminants
  • salt poisoning in pigs
  • lead poisoning in cattle
146
Q

what are the lesions of CNS necrosis

A

softened to liquefied,yellow,greenish or brown color and fluorescent

147
Q

discuss lesions of acute necrosis of CNS

A
  • prominent hemorrhages
  • softened, swollen gyri
  • friable and irregular on cut surface
  • bluish red or grayish
148
Q

discuss subacute to chronic necrotic lesions of the CNS

A
  • **yellow,greenish or brown color **
  • liquefation
  • large cavities fille with gelatininous, opaque yellowish or brownish fluid
  • flattened gyri, glial scarring
  • brain edema in surrounding tissue
149
Q

what makes neonates less susceptible to hypoxia

A
  1. lower cerebral metabolic activity
  2. ability to utilise lactate
  3. high content of ascorbate which may be protective
150
Q

what potentiate reperfusion injury

A
  1. oxygen radicals
  2. ca influx
  3. glutamate neurotranmitter
  4. lactic acidosis
151
Q

what is the sequela of hypoxia-ischemia

A
  • swelling of perineunal astrocyte foot process
  • neuronal contrascture
  • cytoplasmic eosinophilia
  • nuclear pyknosis
  • karyolysis
  • cell dissolution
152
Q

list specific disorders of animals encompassed by CNS hypoxia-ischemia

A
  • Neonatal maladjastment syndrome
  • anesthesia related syndrome in horses
  • hypoglycemia
  • fibrocartilaginous embolic myelopathy
  • feline ischemic encelopathy
153
Q

what are the consequences of hemorrhages in brain or meningis

A
  • acts as space occupying lesions causing increased ICP
  • clots may cause blocks resulting in internal or extrrnal hydrocephalus
  • organised thrombi and blood clots may bt epileptogenic
    *
154
Q

discuss localised edema

A
  • it is caused by and surrounds space occupying lesions such as neoplasia, inflamation, focal necrosis,trauma and hemorrhages
  • in most cases it is extensive and contributes more to the clinical signs than the primary lesions
  • edmatous areas are swoolen and have soft ,depressed and moist appearance on cut surface.
  • there is faint yellowish discoration on the edematous tissue
155
Q

which edema reflects direct damage to osmoregulation

A

cytotoxic or intracellular edema

156
Q

what are the histological lesions of cytotoxic/intracellular edema

A

nuclear and cytoplasmic swelling and accumulation of glycogen granules witin the cells

157
Q

what are the gross lesions of cytotoxic/intracellular edema

A

brain swelling is characterised by swollen, tugid brain which is not moist on cut surface

158
Q

vasogenic edema is prominent in which part of the CNS

A

white matter

intersttial

159
Q

explain how vasogenic edema occurs

A

extracellular fluid accumulates due to vascular damage which allows the leakage of plasma and variable amounts of protein into the intersttial tissue

160
Q

describe the appearance of recent and severe edema

A
  • the brain is swollen,pale,soft and wet
  • the hemispheres droop over the edges of cut bone of the cranium prior to the removal of the brain from the cranium
161
Q

describe the appeareance of severe chronic edema

A
  • the gyri are flattened, the sulci are shallow and signs of isappearance occur
  • displacement of brain
162
Q

discuss displacement of brain due to severe compression

A
  • medulla omblongata and posterior portion of vermis herniate through the foramenmagnum.
  • this lipping in may cause internal hydrocephalus
163
Q

sequela of edema

A
  • swelling,
  • distortion
  • ,herniation,
  • brainsterm injury
164
Q

what are the lesions of equine neonatal maladjustment syndrome

A
  • schemic laminar cortical necrosis
  • necrosis in the brain stem and multiple haemorrhages through the brain
165
Q

what are the lesions of cerebrospinal angiopathy in pigs

A
  • it is edema disease of pigs
  • it is characterised by fibrinoid changes in arterioles in various areas of the body
166
Q

what are the lesions of annual rye grass toxicity

A

lesions are sparse and consists mainly of edema

167
Q

what are lesions of feline ischemic encephalopathy

A

cerebral infaction of the middle cerebral artery

168
Q

list diseases that causes cerebrospinal vasculities

A
  • sporadic bovine encephalomyelitis (SBE)
  • malignant fever (MCF)
  • lesions are aggrevated by subsequent fibrosis
169
Q

what are consequences of CNS inflammation

A
  • pronounced vascular response
  • perivascular cuffing
  • neuronal degeneration/death
  • gliosis
  • demyelination due to disease like distemper
170
Q

infectious meningoencephalities is more common in which animals

A

cats

171
Q

idiopathic inflamatory brain disorders are more common in which animals

A

dogs

172
Q

give the 3 examples of idiopathic inflammatory brain disorders in dogs

A
  1. granulomatous meningioencephalitis ⇒marked perivascular cuffing
  2. necrotising encephalitis⇒multifocal,necrotic, cavitating lesions
  3. generalised idiopathic tremors
173
Q

what are the clinical sings of histophilus infection

A

its an acute infectous disease characterised by;

  • fever, depression
  • weakness
  • ataxia
  • blindness
  • polyarthritis
  • coma
  • death
174
Q

what are the gross lesions of histophilus somni

A

lesons are single or multiple hemorrhagic foci(infacts)located in any part of the brain

175
Q

what are the microscopic lesions of histophilus somni

A

vasculitis with thrombosis and septic infaction in the brain as well as in other organs

176
Q

what manifest listeriosis

A
  1. encephalitis or meningoencephalitis in adult ruminants
  2. septicemia with focal hepatic necrosis in young ruminants and monogastric animals
  3. septicemia and myocardial degeneration or focal hepatic necrosis in fowl
  4. abortion and prenatal infection may occur in all susceptible mammals
177
Q

what are the gross lesions of listerial ewncephalitis

A
  • usually not observed in the brain however,occassional grayish foci of malacia may be found in cross sections of the medulla
  • listeria has affirnity for the brainsterm and lesions are more severe in the medulla and pons
  • infection reach the brain though cranial nerves
178
Q

what are the microscopic lesions of listeria

A

primary lesion is circumscribed collections of mononuclear cells with/out neutrophils in close proximity to blood vessels

179
Q

discuss two morphologc patterns of enterotoxemia due to clo. perfuringins type D

A
  1. the more common pattern is hemorrhagia and softening of the basal ganglia
  2. the second pattern is characterised by lysis and liquefaction of the white matter of the frontal gyri which spares only the common ‘U’ fibers
180
Q

discuss the pathogenesis of c.perforingins type D

A

epsilon toxin→vascular injury→increase vascular permability→edema→hypoxia-ischemia→necrosis

181
Q

what feature is common in lambs with c.peforingins type D infection

A

glucosuria

182
Q

discuss the pathogenesis of edema disease of swine

A

e.coli infection→toxin(shiga like) production→angiopathy→vasculitis→edema→hypoxia-ischemia→bilateral symmetrical foci of malacia/necrosis

183
Q

discuss vascular reaction ue toviruses in CNS

A
  • perivascular cuffing by lymphocytes, plasma cellsand macrophages
  • thrombosis is rare
  • large infiltratesm may cause compresson of vessels and ischemia
184
Q

discuss neornal changes due to viral infection

A
  • usually non specific
  • neurological dearangement may be observed without any neuronal changes
185
Q

discuss effects of viral infection on the white matter

A
  1. mostly secondarily affected in viral disease
  2. cuffing,microgliosis and demyelination may occur
  3. demyelination is characteristic for certain disease e.g canine distemper
186
Q

discuss meningitis due to viral infection

A

a lymphocytic meningitis may occur focally or diffuse

187
Q

what are histological changes due to viral infection in the CNS

A
  1. vascular reaction
  2. neuronal changes
  3. cuffing,demyelination and microgliosis in the white matter
  4. meningitis
  5. inclusion bodies
188
Q

what are the gross lesions of cerebral nematodiasis

A
  • hemorrhages,
  • malacia
  • migratory tracts
  • or space occupying cysts
189
Q

which larvae parasite of rabbits and rodents can invade the CNS of dogs and cats

A

cutebra spp

190
Q

dicuss the pathogenesis of cutebral spp and resultant lesion in cats

A
  • invade the CNS of cats and dogs
  • abberant migration of the larvae
  • vascular lesion–hemorrhages,vasculitis
  • resulting in ischemic encephalopathy
191
Q

which CNs parasite affets the young adult horse

A

sarcocystosis

causes equine protozoal encephalomyelitis{EPM}

192
Q

discuss the pathogenesis of sarcocystosis

A

localization in the spinal cord >focal parasitic activation and replication>inflammation>axonal damage>axonal transection>axonal swelling and degeneraton>wallerian degeneration

193
Q

cresent shaped parasite of the CNS

A

toxoplasmosis

194
Q

what are CNS lesions of toxoplasmosis

A
  • hemorrhages
  • infacts
  • edema
  • non supperative inflammation
195
Q

what are the lesions of neoporosis in dogs, horses and cattle

A
  • dogs>polyradiculoneuritis and polymyositis
  • hoses>meningoencephalomyelitis
  • cattle>multifocal necrosis
196
Q

an oval or spherical thick walled yeast like bodies surrounded by a wide gelatinious capsule was removed was seen on a cut surface of tissue.the tissue tissue had mucinnous quality.which organism do you suspect

A

cryptococcus neoformans

197
Q

which animals are naturally deficient in thiamine

A

cats

mink

fox

198
Q

discuss the pathogenesis of thiamine deficiency

A
  • thiamine required to maintain ATP pump
  • thus in thiamine def.membrane repolarization is impaired
  • water and eleectrolyte balance is impaired
  • and thiamine pyrophosphate reduced
  • pyruvate and lactate accumulate in the tissues causing necrosis
199
Q

what causes polioencephalomalacia or CCN in ruminants

A

thiamine def.

200
Q

what are the clinical signs of thiamine def. in ruminants

A
  • incoordination
  • recumbency
  • bradycardia
201
Q

what are the lesions of thimine deficiency in cats

A
  • edema
  • perivascular dilation
  • hemorrhages and necrosis of brain tissue
    *
202
Q

what causes swayback in lambs

A

Cu def.

203
Q

what are the gross lesions of swayback in lambs

A

bilateral cerebrolateral lesions

204
Q

what are the clinical signs of Cu def. in lambs and kids

(swayback)

A

enzootic ataxia

205
Q

what are the microscopic lesions of Cu def.

A
  • astrogliosis associated with degeneration of white matter
  • lesions of the brain sterm and spinal cord consists of chromatolysi, neuronal degeneration and necrosis of myelinated axons
206
Q

lesions of vit E def. in chicks

A
  1. encephalomalacia
  2. exudative diathesis
  3. nutritional muscular dystrophy
207
Q

what causes metabolic encephalopathies

A
  1. ionic imbalances
  2. acid base imbalances
  3. hypoglycemia
  4. hypoxia
  5. renal failure
  6. hepatic encephalopathy
208
Q

what are the gross lesions of yellow star thistle in horses

A

sharply demarcated foci of yellow discoloration and malacia

209
Q

what are the microscopic lesions of yellow star thistle

A
  • necrosis with loss of loss of axons,neurons,glia and blood vessels,
  • influx of macrophages
210
Q

what are the lesions of lead poisoning

A
  • hemorrhages and edema
  • also
  • immunosuppressive
  • irritating
  • gametotoxic
  • teratogenic
  • nephrotoxic
  • toxic to the hematopoitic system
211
Q

a calf start to stagger ,develop muscular tremers and rapidly becomes recumbant.what should be high in your differential diagnosis

A

lead poisoning

212
Q

an adult cowhas its head pressed on the tree and later becomes blind and dies from convulsions.what should be high in your differential list

A

lead poisoning

213
Q

discuss the type of necrosis seen in subacute to chronic lead poisoning

A

laminar cortical necrosiswhich is associated with ischemia and anoxia

214
Q

what causes acute paralytic syndrome(bilateral poliomyelomalacia) in pigs

A

se toxicity

215
Q

what are the gross lesions of se toxicity

A

areas of softning and yellow discoloration in the ventral spinal gray matter of the cervical and lumbar intumescences

216
Q

discuss the pathogenesis of organophosphate toxicity

A
  • either inhibition of cholineserase
  • or delayed neurotoxicity unrelatedto cholinesteraseinhibition
217
Q

a cow is presented with hyperactivity(or depression), miosis,respiratory difficulty, mm tremors or fascuculations and salivation.what should be top of your rule out list

A

organophosphate toxicity

n.b there are no gross or micro. lesions in inhibition of cholinesterase mechanism

in the delayed neurotoxicity mechanism, there is dying back neuropathy

218
Q

a pig is presented with blindness,deafness, headpressingand convulsions.the pig walks backwards and sit downwhat should be top of your rule out list

A

salt poisoning

219
Q

what are the microscopic lesions of salt poisoning in pigs

A

eosinophilic meningoencephalities and encephalomalasia

220
Q

a horse is presented with drowsiness,impaired vision,partial or complete pharyngeal paralysis,weakness, STAGGARING AND TENDENCY TO CIRCLE. what disease/condition do you suspect.

A

leukoencephalomalacia associated with moldy corn(MYCOTOXICOSIS)

221
Q

DISCUSS THE PATHOGENESIS OF LEUKOENCEPHALOMALACIA

A
  • TOXIN=FUMONISIN B1
  • vascular damage>infaction?]
  • inhibit the enzyme ceramide synthase interfering with the synthesis of sphingolipids
  • disruption of the cell membrane
  • lipid peroxidation
  • production of TNF alpha by macrophages
  • inhibition of synthesis of DNA
222
Q

what are the gross lesions of leukoencephalomalacia

A
  • necrosis of the white matter of the cerebral hemisphere
  • the malacic foci are pulpy,grayish depressions with small hemorrhages
223
Q

what are the lesions of anoxia

A

it produces neuronal necrosis and softning of the gray matter

224
Q

what are the lesions of equine wobbles

A

brownish yellow foci of malacia

225
Q

discuss mechanisms of cholesteatosis of old horses

A

inflamatory changes>cholesterol changes are found in this lesions

226
Q

most common primary NS tumer of both dogs and cats

A

meningioma

they are often located in the olfactory bulb or frontal lobe

227
Q

this tumer is well encapsulated and characterised by whorls and solid cords of spindle shaped cellsof uniform sizeand shape

A

meningioma

228
Q

this tumer is seen most freguently in dogs espercially brachycephalic breeds

A

glial tumers

229
Q

solid grayish,pooly encapsulated tumer

A

astrocytoma

  • it is the most common of the glial tumers
230
Q

what are the lesions of oligodentrioma

A
  • soft cyst like
  • it is well demarcated ,being grayish and soft
  • microscopically it is densly cellular with almost no stroma
231
Q
  • this tumer is uncommon in animals but well known in childrean
  • it is composed of of cells of unknown %
A

medulloblastoma

232
Q

well confined,soft grayish or pinkish masses unilaterally in cerebellar cortex or central in the vermis extending or compressing the 4th ventricle

A

medulloblastoma

it consists of masses of black staining cells that are round,enlongated or pyriform with oval or enlongated nuclei

233
Q

what are the characteristics of ependymoma

A
  • they are largeintraventricular masses,well demarcated,gray and freshy
  • intratumural cystic area
  • necrosis and hemorrhages may be present
  • can cause hydrocephalus
234
Q

this condition is characterised by abnormally flattened and narrowed frontal part of the cranium.and the frontal bones are thicker than normal

A

microencephaly

235
Q

what causes microencephaly

A

associated with fetal infection by akabane virus in lambs,bvd virusin calves,border virus in lambs

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