CNS 1, 2 and 3 Flashcards

1
Q

What is the falx cerebri?

What is the cerebellar vermis?

What is the olfactory bulb?

What is the tentorium cerebelli?

A

The central fold of the brain- sulcus

Falx cerebri- central area of fold- sulcus

Cerebellar vermis- most caudal part of the brain

Olfactory bulb- front of brain- rostral

Tentorium cerebelli- fold between cerebellum and rest of brain

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2
Q

What is the telencephalon?

What is the mesencephalon

What is the diencephalon?

A

Telencephalon- cerebral cortex and basal nuclei

Mesencephalon- periaqueductal grey matter

Diencepalin- hippocampus and thalamus

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3
Q

What kind of neurons are in the dorsal and ventral horns of the spinal cord?

What surrounds the central grey matter?

A

Dorsal- grey matter- sensory

Ventral- grey matter- motor

White matter surrounds

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4
Q

What does this image show?

What is its function of it?

A

Choroid plexus

Produces CSF

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5
Q

What lines the ventricular system?

How many ventricles is it made up of?

What is and what is the function of CSF?

A

Lined by ependyma

four communicating ventricles each with a choroid pleuxus

CSF- blood ultrafiltrate continuously produced within ventricles drained by the saggital sinus

CSF acts as a cushion and provides nutrients to neuroparenchyma

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6
Q

Which of the following cells do not belong the CNS?:

  • Oliogodendroglia
  • Microglia
  • Ependyma
  • Schwaan cells
  • Astrocytes
A

Schwaan cells

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7
Q

What are neurons structurally composed of?

A

Large nucleus with a prominent nucleus

Soma or perikaryon with prominent RER

Dendrites- multiple receiving information from myriad

Axon- single, projecting signal from the soma to the effector cell

High variation in shape and dimension

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8
Q

What is the purposes of astrocytes?

A
  • Creation and maintenance of the integrity of the BBB
  • Uptake and recycling of neurotransmitters
  • Maintenance of extracellular pH and osmotic pressure
  • Supporting metabolic demands of neurones
  • Supporting migration of neurons during neurogenesis
  • Protoplasmic and fibrillar
  • Express GFAP as intermediate filament
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9
Q

How do oligodendrocytes appear?

A

Small cells with round picnotic nucleus

Interfascicular (white matter) and satellite oligodendrocytes (grey)

Responsible for production of myelin in CNS

Long and complex membrane projection to compose myelin sheaths

In H and E surrounded by clear halo (lipids)

Schwann cells- PNS

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10
Q

What are microglia?

What is their function?

A

Resident macrophage-like cells in the CNS

12% of cells

Active immune surveillance

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11
Q

What are the layers of the head from bone to brain?

A
  • Bone
  • Dura mater- thick and rich in collagen
  • Arachnoid
  • Pia mater- thin later
  • Brain
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12
Q

What is malacia?

What is neuropil?

What is satellitiosis?

A

Malacia- necrosis of the CNS

Neuropil- area of nervous system composed mostly of unmyelinated axons

Satellitosis- abnormal clustering of one type of cell around another

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13
Q

Why are neurons susceptible to damage?

A
  • Stable, full of developed and extremely specialised cells
  • Lack of proliferating activity
  • High metabolic demands
  • Low capacity of ‘metabolic adaptation’
  • The majority of neurons extend their processes far from perikaryon
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14
Q

How do neurons become damaged and how do they react?

A

Neuron damage-
Excitotoxicity- leads to red hypoxic neurons
Oxidative stress and decreases antioxidants

Reaction-

  • Chromatolysis
  • Red dead neurons
  • Apoptosis
  • Intracytoplasmic accumulation
  • Vacuolation
  • Intranuclear and intracytoplasmic inclusions
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15
Q

What is astrogliosis and astrocytosis?

How do astrocytes respond to damage?

A

Astrogliosis- increase in number- hypoplasia

Astrocytosis- increase in cell volume- hypertrophy

Cell swelling, cell hypertrophy, scar tissue formation

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16
Q

What happens when oligodendrocytes are damaged?

A

Damage alters the cell membrane and causes-

impaired function or defective myelin formation- primary demyelination

myelin destruction and phagocytosis- secondary demyelination

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17
Q

What are the different types of CNS oedema, what causes them and what is their outcome?

A

Cytocxic-
cause- altered cellular metabolism
outcome- intracellular accumulation of fluid

Vasogenic-
cause- vascular injury with a breakdown of the BBB
outcome- extracellular accumulation of fluid- cerebrocortical white matter

Hydrostatic-
cause- elevated ventricular hydrostatic pressure
outcome- extracellular accumulation fluid

Hypo-osmotic
cause- osmotic imbalances plasma v extracellular, microenvironments
extracellular and intracellular accumulation of fluid

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18
Q

What are the different vascular lesions that can affect the CNS?

A
  • CNS-
    • Ishaemic brain infarct
    • Ishaemic encephalopathy
    • Feline ishaemic encephalopathy
    • Haemorrhagic brain infarct
    • Haemorrhage/haematoma
    • Feline hypertensive encephalopathy
  • Atherosclerosis
  • Oedema
  • Siderocalcinosis of a vessel wall
  • Feline ishaemic encephalopathy
  • Spinal cord
19
Q

Why is the CNS highly susceptible to ischaemia?

A
  • High metabolic request
  • Impossible local storage of glycogen
  • Ishaemia starts after 60% decrease in blood flow
  • Can be global or local

A few minutes of hypoxia can lead to neuronal cell death

20
Q

What can cause an ischaemic brain infarct?

How do they appear acutely and chronically?

A

Vascular thrombosis, emboli, intracarotid injection (horses)

Acute infarction- penumbra of hyperaemia and astrocytosis with a central area of ischaemia with the pale area with red neurons and spheroids

Chronic infarction- penumbra of glial scar formation with centre of liquefactive necrosis and astrogliosis

21
Q

How do infectious agents reach the brain?

What are the different types of inflammatory patterns?

A
  • Deposition of immunocomplexes- FIP
  • Direct inflammation of endothelial cells- classical swine fever
  • ‘Trojan horse’ mechanism- virus, toxoplasma
  • Local accumulation of bacteria within vessels and consequent suppration
  • Retrograde axonal transport- listeria

Inflam patterns-

Suppurative/non-supprative
eosinophilic,
granulomatous
polioencephalitis
leukoencephalitis

22
Q

What do the following inflammations affect?:

  • Encephalitis
  • Myelitis
  • Polioencephalitis
  • Polioencephalomyelitis
  • Leucoencephalitis
  • Leucoencephalomyelitis
  • Meningoencephalititis
  • Pachimeningitis
  • Choroiditis
A
  • Encephalitis- brain
    Myelitis- spinal cord
  • Polioencephalitis- grey matter of the brain
  • Polioencephalomyelitis- grey matter of the brain and spine
  • Leucoencephalitis- white matter of the brain
  • Leucoencephalomyelitis- white matter of the brain and spine
  • Meningoencephalitis- leptomeninges and brain
  • Pachimeningitis- inflammation of the dura mater
  • Choroiditis- choroid plexus
23
Q

What is a perivascular cuff?

A

Accumulation of extravasated inflammatory cells within the perivascular space

24
Q

How are viral lesions distributed and what is their inflammatory pattern in the CNS?

A

Inflammatory pattern-
non-supprative with frequent formation of neuruonphagic nodules

Distribution-

often selectively targeting neurons or specific neuronal subpopulations (polio encephalitis/myelitis)

frequently involve meninges and choroid plexus

25
Q

What type of virus is rabies?

What is its CNS inflammatory pattern?

What is its inoculum site?

What inclusion bodies does it cause and where?
What do they tell you about the inflammation?

What are the three clinical phases?

A

RNA- Rhabdoviridae lyssavirus

Inflammatory pattern- mild non-supprative polioencephalomyelitis- incubation period variable

Inoculum site- muscle- axons- CNS

Pathognomonic presence of eosinophilic round intracytoplasmic inclusoins- negri’s body in the cytoplasm
Frequency of inclusion bodies is inversely proportional to inflammation

Three clinical phases- prodromic, excitatory, paralitic

26
Q

What is the inflammatory pattern of west nile?

Which area of the CNS is particularly affected?

A

West Nile- arbovirus

Inflammatory pattern- non-supprative polioencephalomyelitis

Grey matter of the thoracolumbar spinal cord is particularly affected
Lesions extend into the caudal brainstem

27
Q

What is the inflammatory pattern of canine distemper?

What are the acute and chronic pathological stages?

What is post vaccinal distemper?

A

Inflammatory pattern- demyelinating leukoencephalitis

Acute- pale demyelinated areas

Chronic- non-suppurative inflammation with evident cavitation

Post vaccinal distemper- non-suppurative polio encephalitis with abundant inclusion bodies occurring 2 weeks after CDV vaccination

28
Q

Describe the inflammatory pattern seen in this image

What virus causes this in sheep?

A

Inflammatory pattern- granulomatous leucencephalomyelitis

Visna- maedi-visna virus

Chronic lymphoplasmacytic infiltration- granulomatous appearance
Cavitation and malacia are frequently observes

Choroiditis and meningitis are commonly observed

29
Q

What kind of virus causes FIP?

How does FIP grossly appear?

What lesions does FIP cause in the eye?

A

Feline coronavirus

Antibody-antigen immunocomplexes deposit within the vessel wall
Immune-mediated aggression
Diffuse pyogranulomatous meningochorio-subenendimitis

Vasculitis is a histological hallmark, characteristic prevalence of plasma cells and macrophages

Pyogranulomatous lesions in the eye

30
Q

What causes louping ill and what transmits it?

What is the inflammatory pattern?

Where is there particular neurotropism?

A

Flavivirus transmitted by ticks

Inflammatory pattern- non-suppurative polio encephalitis with neuronal necrosis, glial nodules and neuronphagia

Particular neurotropism for Purkinje cells

31
Q

What kind of virus causes classical swine fever?
What does it grossly cause?

What causes Hepatitis contagiosa canis?
What is its inflammatory pattern?

What causes malignant catarrhal fever?
What lesions does it cause?

A

ALL ARE EXAMPLES OF VIRAL VASCULITIS

Classical swine fever- pestivirus
disseminated, non-suppurative meningoencephalitis of swine

Hepatitis contagiosa canis- canine adenovirus 1
amophillic inclusion bodies in endothelium, vasculitis and haemorrhage

Malignant catarrhal fever- ovine herpes virus 2, alcephine herpes 1, caprine herpes 2
necrotising and mononuclear vasculitis

32
Q

What virus causes herpetic encephalomyelitis?

What is the inflammatory pattern?

A

Equine herpes virus type 1

Petechial or ecchymotic haemorrhages in the white and grey matter of the spine

Inflammatory pattern- vasculitis and thrombosis, suppurative myelitis and haemorrhages

33
Q

What does suppuration mean?

A

Recruitment of neutrophils

34
Q

What generally causes bacterial CNS infections?
Which bacteria is this not true for?

What distribution patterns are characteristic?

A

Haematogenous spreading, an extension of local inflammations

Listeria not

Both disseminated and focal/multifocal distribution patterns are characteristic

35
Q

What causes listeriosis?

How does listeria spread in the body?

What is the inflammatory pattern?

A

Listeria monocytogenes- gram +ve

Retrograde transport along axons and trans-synaptic spreading

Inflammatory pattern: multifocal to coalescing microabscesses
oral cavity to cranial nerves to the brain stem
Small leukomalacic areas

36
Q
A
37
Q

What animals can be affected by mycotic encephalitis?

What can cause encephalitis and what agents?

What is the inflammatory pattern?

A

All animal species can be effected

Often systemic mycosis or local infection

Aspergillus sp, Mucor
Yeasts- cryptococcus neoformans, candida sp

Inflammatory pattern- necrotising and suppurative- granulomatous or granulomatous meningoencephalitis/myelitis
Necrotic vasculitis and thrombosis common

Love the endothelium

38
Q

What causes encephalitozoonosis?

What is the inflammatory pattern?

How does it appear histologically?

A

Encephalitozoon cuniculi, family microsporidia
Obligate intracellular gram-positive parasite

Inflammatory pattern
Disseminated granulomatous encephalitis

Compact epitheloid macrophages
multifocal to massive dissemination throughout the encephalon

39
Q

What are the intermediate hosts for toxoplasma?

When is the myocardia always involved with toxoplasma?

What is the inflammatory pattern in young and adult animals?

A

Intermediate hosts are all warm-blooded animals, including humans while definitive hosts are cats

In young or immunocompromised animals the CNS involvement is always associated with severe myocarditis

Inflammatory pattern

Young- non-suppurative polio encephalitis with gliosis

Adult- necrotising and granulomatous encephalitis

40
Q

What is the suggested pathology of idiopathic inflammatory encephalitis?

What species are affected by granulomatous meningoencephalitis?
How does it appear?

A

An immune-mediated like reaction or an autoimmune response against specific CNS antigens has been postulated

Adult dogs- no clarified cause

Inflammatory pattern- multifocal to coalescing granulomatous meningoencephalitis
In perivascular cuffs- abundant recruitment of macrophages and lymphocytes

Image shows- granulomatous meningoencephalitis

41
Q

What are the two types of intervertebral disc herniation?

What does it cause?

A

Hensen type 1: extrusion of degenerated disc material

Hensen type 2: protrusion without rupture of the annulus fibrosis

Responsible for acute or chronic spinal cord compression with spinal cord degeneration

42
Q

What is a coup and and a contre-coup?

Describe how acceleration-deceleration injuries occur in the CNS?

A

Coup- traumatic lesion just beneath the site of impact
Contre-coup- on the opposite side

Acceleration- deceleration injuries:
Caused by sudden stop/deceleration
At the site of impact, cutaneous and cortical haemorrhage can be seen but minimal
At the contralateral haemorrhage site intensity of the lesion is much more pronounced

43
Q

Describe what a deformation or injury by blow appears like in the CNS?

A

Caused by a kinetic energy delivered with higher velocity at the impact point

Kinetic energy transforms into deformation of the skull
Large contusion and lacerations extending deeply into the neutroparenchyma at the impact site

Conreolateral haemorrhages are mild or not present