nervous system Flashcards

1
Q

macroscopic structure of the brain

A

-gyri are the mountains and sulci are the valleys between.
-they are widened due to loss of tissue (polio (grey), or malaysia (necrosis)
- if there is brain edema the brain will appear more flat.

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2
Q

meninges

A

made of:
-dura mater: adhered to periosteum of cranium bone.
-arachnoid mater: below there is subarachaoid fluid between the pia matter. sends vili into the fluid which absorb fluid and absorb back into circulation. cushion. if excess fluid brain can herniate.
-pia mater

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3
Q

grey and white matter

A

-grey matter (outside): neuronal cell bodies
-white matter (inside): axons and myelin. containing cell bodies known as nuclei

in spinal cord:
-grey matter (inside) composed of two dorsal and two ventral horns. dorsal (sensory) and ventral roots (motor)
-white matter: outside (dorsal, ventral
and lateral funiculi)

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4
Q

cells in brain

A
  • Astrocytes
    Functions:
    1. Repair: Astrocytes swell and divide and produce too many foot process
    (glial scar)
    2. Support + important component of the blood brain barrier)

Oligodendroglia
- Function: The myelinating cells within the CNS

  • Microglial cells
  • Function: The phagocytic cells of
    the CNS
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5
Q

the BBB

A
  • Allows oxygen carbon
    dioxide and water to
    pass
  • Prevents
    neurotransmitters
    hormones, toxins ..etc
    from entering the brain

-made of tight junctions, basement membrane where endo cells sit is very thick, astrol cell foot processes which cover things as they enter brain.

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6
Q

brain response to injruy

A

-very suspectable due to long neurons (most suseptible, BV are least)
-in CNS if you cut axon there is no regeneration, but in PNS there is regeneration.
5. There are few fibroblasts in the brain. Brain wounds heal by proliferation of astrocytic foot processes.
6. The cranial cavity is nearly filled by the brain, its coverings, and fluids.
There is very little room for expansion

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7
Q

how do neurons of the brain respond to injury

A

Neurones
* If there is degeneration within
axons, neuronal cell body
respond by
CHROMATOLYSIS

  • Chromatolysis: is a change in appearance of the cell body brought about by the dispersal of the rough endoplasmic reticulum
    (Nissl granules) gets a glassy appearance.
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8
Q

injured axons response to injruy

A
  • Injured axons undergo
    Wallerian degeneration**
  • Axons form linear and
    bulbous swellings distal to
    the site of injury. These
    enlargements are termed
    axonal spheroids.
  • The myelin sheath also
    becomes dilated.
  • The site of injury is invaded
    by macrophages which
    remove debris
  • Schwan cells proliferate to
    bridge the gap
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9
Q

how are necrotic neurons removed

A
  • Necrotic neurones
    are removed by
    process known as
    neurophagia
    (microglial cells) or
    by cell lysis
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10
Q

astrocyte response to injury

A
  • Cytoplasmic swelling
    and hypertrophy
  • cell division, and the
    laying down of
    intermediate filaments in cell processes
    -histo: you will see astrocytes with cytoplasm so (activated) = Gemistocytic astrocytes= damage to brain.
    -Alzheimer’s type II astrocytes: in hepatic encepholatophy
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11
Q

olgiodendrocytes response to injury

A

Oligodendrocytes are cells responsible for mylenating axons

  • Respond to injury by cell swelling and hypertrophy.
  • Degeneration and necrosis
    of oligodendrocytes leads to
    demyelination

Demyelination: Two types
1. Primary: due to loss of
oligodendrocytes (ex. canine distemper)
2. Secondary: due to loss
of axons (most common)

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12
Q

microglial cells response to injury

A
  • Become gitter cells
  • Gitter cells: swollen lipid laden macrophages that are formed after microglial
    cells and monocytes phagocytize dead neurons and myelin
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13
Q

brain infarction (necrosis)

A

-There is low connective tissue in the brain and lot of lipid
* This causes infarcted areas to become soft.
* Infarcted areas within the grey matter tend to be red (more vascularized) while infarction within the white matter tends to be pale (less vascularized)
* After the removal of necrotic debris; if infarcted area is less then 1mm
it is filled with a glial scar. If larger than 1mm it becomes cystic

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14
Q

brain edema

A

-4 mechanims all look the same, brain appears flattened, sulci and gyri seem same level
Brain swelling with swollen
flattened gyri and less distinct
sulci
* Brain edema is always very
significant clinically as there is
very little space for the brain to
expand
* It can lead to herniation

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15
Q

Brain edema (4 types, mechanisms)

A
  1. Vasogenic edema:
    - Extracellular accumulation of fluid
    - Most common type of edema in the CNS
    - The underlying mechanism is
    a breakdown of the blood-
    brain barrier
  2. Cytotoxic edema:
    - Accumulation of fluid intracellularly
    in neurons, astrocytes,
    oligodendroglia, and endothelial cells
    - BBB is intact
  3. Hydrostatic edema
    Elevated ventricular hydrostatic pressure.
    Fluid moves across the ependyma of the ventricular wall and
    accumulates extracellularly in the periventricular white matter.
  4. Hypo-Osmotic Edema
    * Occurs after overconsumption of water (water intoxication), leading to
    dilution of the osmolality of the plasma, happens when osmolarity changes.
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16
Q

cytotoxic edema mechanism

A

Hypoxia > loss of Na extrusion mechanism (active) > Na enters cells and extracellular water follows Depletion of extracellular space of Na and water
> Fluid moves from the systemic circulation to the brain through intact BBB
> > Brain edema

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17
Q

Meningoencephalocele and Cranium Bifidum

A

-malformation of CNS
-Meningoencephalocele if cyst of menigies under skin
- Cranium Bifidum if with brain involvment sticking out

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18
Q

Lissencephaly

A

-malformation of CNS
-brain has no gyri
-has deficits, seizers
Breed: Lhasa Apso

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19
Q

Hydraencephaly causes

A

-large fluid replacing brain parenchyma if large portion hydranecephaly.
* Fluid filled brain cavities are termed porencephaly (small cavity) or hydraencephaly.
-congenital or in utero infection, parvo, BVD, or copper deficiency in ruminants

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20
Q

Cerebellar hypoplasia causes

A

Causes:
-could be congenital or in utero infections
-Calves: pestivirus (BVD)
-Kittens: panleukopenia virus
-Puppies: canine parvovirus
-Piglets: classic swine fever virus

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21
Q

Hydrocephalus ( not Hydraencephaly ) what it is and types

A
  • Accumulation of
    cerebrospinal fluid resulting
    in dilation of ventricles and/
    or the subarachnoid space (e
    which causes pressure
    atrophy of the brain.
  • Two types: Communicating
    and non-communicating. MOST COMMON
  • Non-communicating (due to
    obstruction)

-unilateral: one side larger than other.
-bilateral both sides effected.

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22
Q

Congenital hydrocephalus causes

A

-usually the communicating type
-will see swollen head clinically
Causes:
-Hereditary (Brachycephalic dog breeds)
-In utero viral infections

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23
Q

Acquired hydrocephalus

A

-usually older animals secondary to lesion in brain.
-Main cause is obstruction
Ex. Cholesterol granuloma in horses. Or
-Loss of brain tissue (less common and usually less pronounced lesion)
Ex. polioencephalomalacia

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24
Q

Hydromyelia

A

-CSF fluid accumulating in spinal cord.
-Abnormal dilation of the central canal
of the spinal cord that leads to the formation of a cavity in which CSF may accumulate

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25
Q

Syringomyelia

A

-Fluid filled cyst within the
spinal cord separate from
the central canal and not
lined by ependymal cells.
-cyst in spinal cord outside the spinal canal

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26
Q

inflammation of brain different terminology

A

-encephalitis: inflammation of brain
-menigitis: inflammation of meneges
-Radiculoneuritis: nerve roots of spinal cord inflammation
- Ganglioneuritis: inflammation of the ganglia
- Choroid plexus: Choroditis

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27
Q

portal of entry to the brain

A
  • Direct extension (extension
    from inner ear, nasal sinuses through the
    cribriform plate or bones)
  • Hematogenous
  • Retrograde axonal transport (rabies and listeria)
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28
Q

brain abscess causes

A

-caused by bacteria
- Direct extension or from the blood or soft tissue around.
- Streptococcus, E.coli,
Staphylococcus
Corynebacterium Klebsiella

29
Q

Meningitis and Neonatal
Septicemia

A

-Common especially in neonates
(blood born infection)
***in calf either streptococcus or ecoli secondary to septicemia.

-Can be caused by direct
extension (bone)

-Meninges will appear cloudy and congested and you may see pus

Causes meningitis +/- encephalitis and lesions of septicaemia

  • Escherichia coli, Streptococcus spp., Salmonella spp., Pasteurella spp.,
    and Haemophilus spp
30
Q

herpesvirus (viral disease of CNS)

A

Neurotropic herpes viruses enter the CNS principally by retrograde axonal transport;
however, entry by hematogenous spread via viremia may occur.

The can hide in neurons (Ganglia) and lie their dormantly (we call this viral latency)

Ganglioneuritis is always present IN RABIES AND HERPES VIRUS ONLY

Equine herpesvirus 1 myeloencephalopathy’
Bovine herpesvirus-1
Pseudorabies in pigs

31
Q

rabies viral disease of CNS

A
  • Cause is lyssavirus
  • Zoonotic (bats are carries)
  • Infection is usually through biting
  • Reach the brain via retrograde
    axoplasmic transport system
    -no gross lesions ONLY HISTO, * Non suppurative encephalitis
    +/- eosinophilic and inclusion bodies.
  • Ganglioneuritis is always present
32
Q
  1. Cryptococcus Neoformans fungal disease of CNS
A

Has a particular affinity for the CNS, common cats.
* Enters the leptomeninges and
subarachnoid space by direct extension through the cribriform
plate after a nasal or sinus infection or hematogenously

  • This fungi has thick mucinous capsule protects the organism from host defenses

-gross: soap like bubble lesion in brain, if you see in cat always cryptococcus.

33
Q

fungal infections of CNS

A
  1. Other fungi (Coccidioides
    immitis, Blastomyces
    dermatitidis, Histoplasma
    capsulatum)

Reach the brain by
hematologic spread (usually from the lung).

Produce granulomatous
lesions everywhere

34
Q

diseases of CNS caused by protozoa

A
  1. Neospora
    * Affinity for the CNS
    * Can affect the CNS in utero leading to abortion
    * And can affect the CNS
    after birth
  2. Equine Protozoal Encephalomyelitis
    (Sarcocystosis)
    - Cause is Sarcocystis neurona.
    - Affects horses brainstem/ spinal cord
  3. Toxoplasma
    * Cat is the definitive host
    * Multisystemic infection +/- nervous system
    * Abortion
35
Q

-Feline Ischemic Encephalopathy

A

parasites in brain insect larvae
: migration of Cuterebra (fly) larva after entry into the brain via the nasal cavity.

Gross: Unilateral necrosis of the white and grey matter from larvae blocking BF.

36
Q

parasites in CNS cestodes dog

A

-Coenurus cerebralis
-Larval form of the dog
tapeworm Multiceps multiceps,
-most commonly infests sheep/ ruminants
-Form cyst in the brain

37
Q

Transmissible Spongiform Encephalopathies
Disease caused by Prions

A

-Cause is PRoteinaceous
Infectious OrgaNism (PRIOIN) a misfolded protein. and becomes resistant to degradation.
seen in neurons.

ex. Scrapie: Sheep
Bovine Spongiform Encephalopathy
Feline Spongiform Encephalopathy
Chronic Wasting Disease

38
Q

hepatic encephalopathy affecting brain

A

-Cause: Acute and
chronic liver failure
and hepatic atrophy
associated with
congenital or
acquired vascular
shunts–>
very high AMMONIA toxic to brain–> hepatic encephalopathy.

-histo in all species but horse will see: spongy change (vacuolation) and formation of Alzheimer’s type II astrocytes.

39
Q

lead toxicity to CNS

A

-Most common toxicosis in cattle

-Mostly from discarded car batteries

-Seasonal: April till Sept
-Leads to poilioencephalomalacia
(laminar cortical necrosis of the grey matter=polio)
-gyri are thin and sulci are widened.
-for toxicities test fresh liver sample

40
Q

Salt Toxicity (Sodium chloride) in the CNS

A
  • “Water deprivation syndrome”
    -High salt in diet (direct) and/or water deprivation (indirect)
    -Pigs most commo, Cattle and sheep also
    -Pathogenesis: unable to remove excess Na from brain (energy dependent)
    -test grain see if high salt.
    -histo see: eosinophilic
    meningoencephalitis and
    polioencephalomalacia
41
Q

Tetanus CNS toxicity

A

Tetanus
Cause: Cl. Tetani
* Penetrating wound (Nails)->Bacteria release Tetanospasmin
(toxin) transported by retrograde
axoplasmic flow–>
* Tetanospasmin blocks the release
of inhibitory neurotransmitters
such as glycine and GABA.

  • NO gross or histo lesions and NO
    confirmatory tests available
42
Q

Botulism CNS toxicity

A

Botulism
Cause: neurotoxin of Clostridium
botulinum
-Horses mainly
-Toxin inhibits (blocks) of the release of acetylcholine results in flaccid paralysis of muscles
-No gross or histo lesions

43
Q

plant toxins (locoweed posioning) path

A

Astragalus, Oxytropis, and Swainsona poisoning (all have swainsonine) –> chronic ingestion–> enzyme inhibition causing lysosomal storage disease. (mannosidosis)–> abnormal accumulation of molecules in the brain–> neuronal swelling and death

-yellow star thistle poisoning: ingestion of plant leads to syndrome Nigropallidal
encephalomalacia”
This a horse disease.

44
Q

moldy corn disease (leukoencephalomalacia)

A

-ingestion of moldy feeds, corn, that has fungus Fusarium moniliforme.
-toxin produced fumonisin B1
* The white matter of the brain
undergoes necrosis
(Leukoencephalomalacia)
* Fumonisin B1 interferes with
sphingolipid biosynthesis

45
Q

Ischemic Myelopathy (fibrocartilaginous emboli)

A
  • Cause: Herniation of degenerative disk material into the
    vasculature.
  • The herniated material blocks blood supply and cause a
    large area of necrosis
  • Always acute sudden onset of neurological deficit
  • Associated with exercise and/or trauma
46
Q

Hypomyelination and Dysmyelination

A

Hypomyelinogenesis is a process in which
there is underdevelopment of myelin.
* Dysmyelination refers to the formation of
biochemically defective myelin.
-young dog or cat with neurological defitcist and no infecttious or systemic disease think this and check the breed.
* Viruses and hereditary conditions
Just now that there are breed specific abnormalities.

47
Q

traumatic injury

A
  • first skin brusing then ->Bone damage
  • Grossly detectable hemorrhage
  • Tearing of CNS tissue. Tearing
    results in tissue necrosis and
    neuronal loss.
  • Epidural, subdural, and
    subarachnoid space, under
    the pia mater (subpial), and in
    the brain
48
Q

compressive lesions of the brain

A
  • Brain:
    Neoplasms, abscesses,
    granulomas can compress
    the brain causing herniation
  • Spinal cord:
    Intramedullary compression:
    Neoplasms, abscesses,
    granulomas can compress the
    spinal cord (less common)
    -Extramedullary compression
    can be caused by
    intervertebral disk herniation
    in the dog; cervical stenotic
    myelopathy (wobbler
    syndrome) more common
49
Q

Medulloblastoma

A

-Cell of origin: primitive cells
originating in the neuroepithelial
roof of the fourth ventricle that
give rise to the external granular
cell layer.
* Young animals, with tumor below the cerebellum**

50
Q

Choroid Plexus Papillomas and Carcinomas

A
  • Tumor within the ventricular system from the choroid
    plexus
    -mass inside ventricle
51
Q

Astrocytoma

A

Astrocyte is the cell of origin
* Often not very well demarcated
* Often the pyriform lobe is involved
**if dog and puriform lobe is involved = astrocytoma

52
Q

Oligodendrogliomas

A
  • Oligodendrocyte is the
    cell of origin
  • They are usually well
    demarcated
    -looks like a round O tumor in brain
53
Q

Meningiomas

A
  • The most common
    intracranial tumor in the
    cat.**
  • Tumor on top of the brain, within skull. not a brain tumor but compresses the brain
54
Q

Metastatic tumors to the brain

A
  • Hematogenous
  • Mammary carcinomas,
    hemangiosarcomas (red), melanomas (dark brown)
    -usually logged in grey white matter junction due to BV
55
Q

horse CNS viral infections

A

-all cause non-suppurative inflammation
1. Equine Encephalomyelitis: grey matter and some spinal cord
2. West Nile:
Cause: Flavivirus Flaviviridae
Grey matter is primarily affected
(lower brainstem and ventral horns
of the thoracolumbar spinal cord).
3. Equine Herpesvirus-1 Myeloencephalopathy
Cause: EHV-1
CNS disease affects adults mainly.
Ganglia is affected in addition to the grey and white matter for the brain and spinal cord
Vasculitis is a common finding

56
Q

metabolic diseases of horse

A

1: Equine Degenerative Myeloencephalopathy
Axonal degeneration in the white matter of
the spinal cord (mainly) and brain (less
affected)
Young horses
No compressive lesions

  1. Cholesterol granuloma
    * Seen mainly in horses
    * Concretions within the ventricular system
    * Usually an incidental finding but can cause hydrocephalus if
    obstruction occurs
57
Q

Listeria monocytogenes ruminants

A

-they eat silage with listeria, have injury in oral cavity, goes through 5 nerve through retrograde axonal transport to the medulla oblongata
-gross lesions may occur in the medulla oblongata and pons, always examine/ culture the brainstem if you suspect this.

58
Q

Thrombotic Meningoencephalitis (TME)
Bovine disease

A

Cause: Histophilus somni
Results in four main lesions: Pneumonia,
polyarthritis, myocarditis, and
meningoencephalitis.
Neutrophilic vasculitis > thrombosis > infarction in multiple organs including the brain.

-red arreas of infarction following BV

59
Q

Bovine Malignant Catarrhal Fever

A

Cattle bison and deer
Cause is ovine herpesvirus-2
Sheep are carriers
Lymphocytic vasculitis in the brain, spinal cord and any organ
-you also see erosions in the GI with swollen lymph nodes and urinary bladder as well as
corneal edema

60
Q

Maedi-Visna adult sheep

A

-Cause is lentivirus
(retroviridae)
-Nonsuppurative
encephalitis with primary
demyelination
-can effect multiple systems:
1. Interstitial pneumonia (maedi and ovine progressive pneumonia)
2. Encephalomyelitis (visna of sheep)
3. Arthritis
4. Mastitis

61
Q

Caprine Arthritis Encephalitis

A

-Goat disease
-CAE virus which is a lentivirus (retroviridae)
-CNS lesions are usually seen in younger animals (2-4 months of age)
-Arthritis is seen in adults that survive

62
Q

Polioencephalomalacia

A
  • Pilio refers to the grey matter and malacia means necrosis
  • Ruminant disease
    Four causes
    1. Lead poisoning (most common)
    2. Salt toxicity or water deprivation
    3. High water sulfur
    4. Thiamin deficiency

-Grossly causes narrowing of
gyri and widening of sulci
-Grey matter may fluoresce
under UV light
-The gyri are narrow due to
neuronal necrosis

63
Q

Copper deficiency
* Sheep and goats

A
  • Two syndromes
    1. Swayback: congenital form (brain and spinal cord are affected, cavitation due to malacia)
  1. Enzootic ataxia: delayed form i.e.,
    seen 6 months after birth (only brain stem and spinal cord are affected)
    need histology to see lesinos
64
Q

Cl. Perfringens type D

A
  • Enterotoxemia in multiple
    spp
  • In sheep neurologic
    manifestations can be seen
  • Brain: bilateral symmetric
    hemorrhage and malacia of
    basal nuclei and thalamus
65
Q

canine distemper

A

Cause: morbillivirus
Multisystem dz
-Brain: non suppurative inflammation
-Eosinophilic intranuclear inclusion bodies in the nervous system
-Primary demyelination

66
Q

Thiamin Deficiency

A

-Dog and cat dz
* Thiamin is an absolute dietary
requirement
* They eat fish containing
thiaminase or diet deficient in
thiamin
* Gross and microscopic lesions
are bilaterally symmetric and
commonly involve brainstem
nuclei

67
Q

Reticulosis Granulomatous
Meningoencephalitis (GME)

A
  • Inflammatory dz of unknown etiology
  • Small toy breed dogs (poodles, terrier breeds), 1-6 years of age, with a higher prevalence in females
  • BRAIN STEM is mainly affected
  • Optic form of the dz: optic nerve and retina are affected.
68
Q

FIP cats

A

-Causes is feline coronavirus
-Noneffusive form more frequently result in leptomeningitis,
chorioependymitis, focal encephalomyelitis

69
Q

edema disease pigs

A
  1. Edema disease
    -Affects growing, healthy
    feeder pigs (4 to 8 weeks)
    -Cause: Escherichia coli
    producing a Shiga-like toxin
    -Lesions are secondary to
    endothelial damage by
    toxin > edema