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CVSOH 4 > Nervous System Pathology > Flashcards

Nervous System Pathology Flashcards

1
Q

What is the terminology used in neurology?

A

Encephal- = brain
Myel- = spinal cord
Polio- grey matter
Leuko- = white matter
Meningo- = meninges
Radiculo- = spinal nerve roots
Malacia = softening of tissue, due to necrosis

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2
Q

What term would indicate there is inflammation affecting the meninges, brain and spinal cord?

A

Meningoencephalomyelitis

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3
Q

What term would indicate there is softening/necrosis affecting the grey matter of the brain?

A

Polioencephalomalacia

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4
Q

What does the nucleus contain in a neurone?

A

Nucleus cytoplasm contains nissi substance which is mostly endoplasmic reticulum so produces proteins

Neurophil is a dense interwoven nerve fibres including unmyelinated axons and dendrites and glial cells processes

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5
Q

What is not present in the CNS histologically?

A

There are no fibroblasts in the CNS, there are in the meninges but not in grey or white matter

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6
Q

How is the peripheral nerve structured?

A

Axon can extend out from spinal cord or to spinal cord in nerves. Nerve has lost an lots of axons within it. Protective sheath called endoneurium. Bundles of neurones together called fascicle with surrounding perineurium. Outer sheath of the peripheral nerve is epineurium.

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7
Q

What is the effect of neuronal high energy demand?

A
  • Oxygen and glucose so need perfusion all the time
  • Limited energy reserve capacity – don’t really have reserve capacity so need supply constantly. Most sensitive neurones will start dying in 10 minutes without supply
  • Lost neurones are not replaced (or clinically)
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8
Q

What are the cell body changes in response to injury?

A

Degeneration = chromatolysis

Necrosis = acidophilic, neuronal necrosis

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9
Q

What are the axonal changes in response to neuronal damage?

A

Axonal degeneration (Wallerian degeneration)

Axonal regeneration

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10
Q

What is chromatolysis?

A

Degenerative change affecting the cell body called chromatolysis – cell is still alive but is is degenerating and is not functioning to full potential

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11
Q

What are the microscopic features of chromatolysis in neurones?

A
  • Swelling of the cell body
  • Dispersion or loss of Nissl substance – purple pigment loss, clearing of site
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12
Q

What is the result of chromatolysis?

A

Reversible or may progress to cell death which will cause neuronal necrosis

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13
Q

What is acidphilic neuronal necrosis?

A

Cell body change following irreversible injury, often in the CNS, especially conditions affecting energy supply (ischaemia). Changes seen 6-8 hours after

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14
Q

What are the microscopic features of acidophilic neuronal necrosis

A
  • Deeply eosinophilic staining
  • Swollen or shrunken and angular
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15
Q

What is the result of acidophilic neuronal necrosis?

A

Death of the cell body results in degeneration of the axon

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16
Q

Outline axonal/wallerian degeneration.

A
  1. Axonal injury and damage
  2. Distal to the site of injury – axon undergoes degeneration along its length
  3. Proximal to injury site – if myelinated, axon degenerates back to the next node of Ranvier
  4. The cell body undergoes chromatolysis
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17
Q

What happen within a few hours/days of axonal/wallerian degeneration?

A

Axonal swellings, fragmentation of the axon and myelin. Need to clear this up so phagocytes start to come in to do this but this can take weeks/months/years

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18
Q

Can axons regenerate following degeneration?

A

Depends on a variety of factors, including whether the axon is in the peripheral nervous system or central nervous system. If PNS, may be able to get some regeneration depending on conditions.

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19
Q

What is required for axonal regeneration in the peripheral nervous system?

A

Requires the cell body to be intact and integrity of the endoneurial tube distal to the site of injury

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20
Q

Outline how axons regenerate in the peripheral nerves?

A
  • Schwann cells start to proliferate and form columns within the endoneurial tube and axonal sprouts start to grow from the axon stump
  • Axonal sprouts enter the columnsof Schwann cells and guide it along the column and grow along the length of the endoneurial tube
  • The regenerated fibre can become remyelinated – but this is slow at 1-4mm per day. This is just to regenerate might not even get function back which would take even longer
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21
Q

What are the outcomes of when there is damage to the whole fascicle, for example, transection?

A
  • Want these to line up with original
  • This might allow axonal regeneration with function restoration
  • Other outcomes, axon regenerates but does not complete and function not restore
  • Could also have the wrong endoneurial tube lined up and cause axonal regeneration with inappropriate function
  • May have unsuccessful regeneration, such as fibrous tissue formation between them or there is loss of integrity of the endoneurial tube and axon cannot regeneration and you get neuronal atrophy
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22
Q

Why is there no or very limited axonal regeneration in the CNS?

A
  • Lack of scaffold – endoneurium, basement membrane
  • Oligodendrocytes do not form columns as Schwann cells do in the PNS
  • Axon sprouting is inhibited
  • The CNS has very limited capacity for functional recovery following axon injury
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23
Q

What might be helpful in indicating a likely cause or type of infectious agent for neuronal damage?

A

The type of inflammatory infiltrate (and distribution)

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24
Q

What is the dominant types of inflammatory cells present with suppurative inflammation?

A

Neutrophils

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25
Q

What are the possible causes of suppurative inflammation?

A

Bacteria, some fungi, non-infectious steroid-responsive meningitis arteritis in dogs

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26
Q

What are the dominant inflammatory cell types present in non-suppurative/mononuclear inflammation?

A

Lymphocytes
Plasma cells
Monocytes

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27
Q

What are the possible causes of non-suppurative/mononuclear inflammation?

A

Viruses, protozoa, some bacterial, non-infectious diseases

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28
Q

What are the dominant inflammatory cell types present in granulomatous inflammation?

A

Macrophages

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29
Q

What are the possible causes of granulomatous inflammation?

A

Some bacteria, fungi, parasites, foreign bodies, and some immune mediated diseases

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30
Q

What are the dominant inflammatory cells type present with oesinophilic inflammation?

A

Eosinophils

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31
Q

What are some possible causes of eosinophilic inflammation?

A

Parasitic infections, some fungal infections

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32
Q

What is the role of phagocytes in healing the CNS?

A
  • Phagocytes to remove debris
  • Microglia (phagocytic, macrophage-like) – expand and get bigger and turn into macrophage like cell and functions
  • May be supplemented by macrophages derived from blood monocytes
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33
Q

What is the role of astrocytes in healing the CNS?

A
  • Do not have fibroblasts to lay down collagen
  • Astrocytes proliferate and hypertrophy with larger and more complex processes to form a matrix
  • Encapsulate and fill spaces, and may form a ‘scar’
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34
Q

Name 5 causes of swelling in the brain.

A

Space occupying lesion
Congestive brain swelling
Vasogenic oedema
Interstitial oedema
Swelling of cells present in the brain

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35
Q

How does congestive brain swelling occur?

A
  • Unregulated vasodilation of blood vessels in the brain after traumatic injury
  • Dilated blood vessels take up more space
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36
Q

How does vasogenic oedema occur?

A

Increased vascular permeability (disruption of blood brain barrier) – inflammation, trauma, cerebral hypertension, neoplasms

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37
Q

How does interstitial oedema occur?

A

Increased hydrostatic pressure within the ventricular system causing CSF fluid to move into the periventricular tissues – hydrocephalus

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38
Q

How does swelling of cells in the brain occur?

A

Glial cells, neurones, vascular endothelium

  • Caused cytotoxic oedema and is the same as hydropic change
  • Cell swelling with increased intracellular fluid
  • Caused by altered cellular metabolism with reduced energy for metabolic processes – often due to ischaemia
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39
Q

How is swelling of the brain recognised?

A

Fixed space that cannot expand so:

  • Less pronounced sulci
  • Flattening of the gyri due to pressing against the skull
  • Will either burst or try escape through a hole
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40
Q

What is the tentorium cerebelli?

A

A bone that separates the kill and membranes parts/dura mater

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41
Q

What happens in subtentorial herniation?

A
  • Swelling of the brain can result in displacement of parts of the brain
  • The cerebellum has been removed to demonstrate bilateral herniating off the medial cerebral hemispheres under the tentorium cerebelli
  • Causes cerebellar herniation/coning of the cerebellar vermis
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42
Q

How does coning of the cerebellar vermis occur?

A

Compression of the medulla oblongata, displacement of the caul cerebellum through the foramen magnum resulting in flattening of the caudal cerebellar vermis

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43
Q

How do circulatory diseases present in the nervous system?

A

Haemorrhage and/or malacia as a result of ischaemia

CNS has high requirement for energy – 20% of an animal’s energy requirements. Neurones in the cerebral cortex with the highest metabolic rate can die within a few minutes (6-10 minutes) of cessation of blood flow

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44
Q

What are the the regions most sensitive to hypoxic-ischaemic injury?

A
  • Cerebral cortex (results in laminar cerebrocortical necrosis)
  • Hippocampus and various nuclei
  • Cerebellar Purkinje cells
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45
Q

What is the gross appearance of necrosis in the brain?

A

Yellowish areas more indicative of necrosis than haemorrhage

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46
Q

What are the possible causes of haemorrhage in the nervous system?

A

Vascular injury, altered vascular integrity (including rupture) or vascular degeneration associated with:
- Trauma
- Inflammatory disease, vasculitis
- Infarction or ischaemic injury
- Toxic/metabolic disease
- Neoplastic disease

Coagulopathies

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47
Q

What are the causes of localised ischaemia?

A
  • Loss of vascular integrity
  • Vascular obstruction e.g. thrombosis from localised vascular injury, embolic disease (non-neoplastic or neoplastic)
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48
Q

What are the causes of global ischaemia in the nervous system?

A

Globally reduced CNS perfusion or global hypoxia:

  • Cardiac arrest, hypovolaemic shock, hypotension
  • Severe anaemia
  • Asphyxiation (including during parturition)
  • Anaesthetic accidents (loss of oxygen supply, airway obstruction)
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49
Q

Why might post mortem ischaemic changes not show up on histology?

A

Changes have occurred at cellular level but not at histological level until 4-6 hours after

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50
Q

What are the causes of non-symmetrical multifocal haemorrhagic/ischaemic lesions?

A
  • Trauma
  • Inflammatory disease – infectious, immune-mediated
  • Vascular disease – vasculitis, infarctions, coagulopathy
  • Neoplastic disease
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51
Q

What are the causes of symmetrical multifocal haemorrhagic/ischaemic lesions?

A
  • Metabolic/toxic
  • Global hypoxia
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52
Q

What are the causes of focal haemorrhagic/ischaemic lesions?

A
  • Trauma
  • Focal infarction or inflammation
  • Spontaneous blood vessel rupture
  • Neoplastic disease
53
Q

Name the possible routes of infectious agents into the nervous system.

A

Haematogenous
Via CSF
Direct extension from surrounding tissues or rarely penetrating injury
Intraneural extension along peripheral nerves - listeria, rabies

54
Q

How do infectious agent spread haematogenously to the nervous system?

A
  • Septic thromboemboli
  • Infection of endothelial cells or blood monocytes
  • Through the choroid plexus, may gain entry to CSF through the ventricular system
55
Q

How do infectious agents enter the nervous system from surrounding tissues/penetrating injury?

A
  • Nasal cavity and sinuses, middle/inner ear by vestibulocochlear nerve, bone in skull and vertebrae
  • Meninges often good at preventing things getting across meninges, but can happen, more likely to be epidural and not getting through meninges
56
Q

What are the characteristics of bacterial nervous system infections?

A
  • More common in farm animals
  • Often suppurative inflammation
  • Distribution patterns can range from widespread meningitis and/or encephalitis to localised infection e.g. abscess
57
Q

What is the epidemiology of bacterial suppurative/purulent meningitis?

A
  • Haematogenous bacterial infection
  • Predisposing factors can include lack of colostrum and poor hygiene (high levels of bacterial challenge)
58
Q

What are the clinical signs and PM findings of bacterial suppurative/purulent meningitis?

A
  • Meninges – cloudy, opaque, hyperaemia
  • Purulent or fibrinopurulent exudate may pool in sulci, and on the ventral aspect of the brain
  • Variable degrees of swelling of the brain
  • May have concurrent infections at other sites e.g. joints (polyarthritis) and, in calves – eyes (endophthalmitis)
  • Streaks of white
59
Q

What are some possible complications of purulent/suppurative meningitis?

A

Involvement of the choroid plexus (chroiditis) and ependyma (cells lining the ventricular system) can lead to accumulation of pus in the ventricles (suppurative ventriculitis) and abscess formation

60
Q

What can happen if brain swelling is severe enough?

A

If severe enough it could cause cerebellar herniation (cerebellar coning)

60
Q

Describe abscess formation in CNS tissues due to local extension.

A
  • Choroid plexus infections
  • Meningitis (rare cause of abscesses)
  • Extension from inner or middle ear infections
  • Extension of infection from the cribriform plate, paranasal sinuses or pituitary fossa
  • Penetrating wounds, or foreign bodies (rare)
60
Q

Describe abscess formation in CNS tissues due to haematogenous spread.

A
  • Sources of thromboembolism e.g. endocarditis
  • Bacterial emboli occurring during septicaemia
  • Brain abscess caused by spread of Strep equi in a case with strangles
60
Q

Describe abscess formation in the epidural space due to haematogenous spread.

A

Septic embolism. Sources of thromboembolism e.g. endocarditis

61
Q

Describe abscess formation in the epidural space due to local extension.

A
  • Paranasal sinuses (into cranium)
  • Penetrating/traumatic wounds including bite wounds (cats) or contaminated spinal needles
  • Tail biting (pigs)
  • Tail docking (lambs)
  • Vertebral osteomyelitis
  • Foreign bodies
62
Q

What is a consequence of spinal epidural abscesses?

A

Compression of the spinal cord

63
Q

What is listerial encepahlitis/listeriosis?

A
  • Ruminants
  • Listeria monocytogenes in spoiled silage
  • Invades oral mucosa, infects cranial nerve(s) e.g. trigeminal and spreads to the brainstem
  • (Meningo)encephalitis in brainstem and/or spinal cord
64
Q

What are the clinical signs of listerial encephalitis/listeriosis?

A

head tilt and circling behaviour

65
Q

How is listerial encephalitis/listeriosis diagnosed?

A

Requires culture (of brainstem) and/or histopathology to diagnose

66
Q

How is listerial encephalitis/listeriosis diagnosed on histopathology?

A

Microabscesses aggregations of neutrophils and mononuclear inflammatory cells

Perivascular cuffing by inflammatory cells (non-suppurative)

67
Q

Name 2 manifestations of viral infection in the nervous system.

A

Viral encephalitis

Pre/perimatal infections - some viruses can cause congenital malformations

68
Q

Describe viral encephalitis.

A
  • Typically non-suppurative inflammation
  • May have neuronal necrosis
  • Some viruses produce inclusion bodies - rabies (Negri bodies)
  • Some viruses cause vasculitis - FIP, EHV1
69
Q

Describe the epidemiology of fungal infections in the CNS?

A
  • Opportunistic
  • Haematogenous spread or occasionally local extension to the brain
70
Q

Name 3 fungal infections of the CNS.

A

Aspergillus
Candida
Cryptococcus spp

71
Q

What is the effect of fungal infections in the CNS?

A
  • Inflammatory response typically pyogranulomatous or granulomatous
  • Fungal hyphae often cause vasculitis with thrombosis and infarction
72
Q

Name and describe a helminth parasitic infection of the CNS.

A

Coenurus cerebralis in brain of sheep (coenurosis)

Space occupying lesion – progressive clinical signs such as circling, depression, head-pressing

73
Q

Name 2 protozoan parasitic infections of the CNS.

A

Neospora caninum
Toxoplasma gondii

74
Q

What is the effect of protozoan parasitic infections of the CNS in older and juvenile animals?

A

Older animals - myositis, CNS and peripheral nerve inflammation

Juvenile:
- Predilection for lumbosacral nerves
- Progressive hind limb paralysis with atrophy of hind limb muscles

75
Q

What is microsporidia and its effect?

A

Encephalitozoon cuniculi

Rabbits – primarily affects CNS and kidneys. Cause foci of granulomatous inflammation within the brain

76
Q

What are the pathological processes involved in non-infectious, immune-mediated neurological inflammatory diseases?

A

Inflammation and/or malacia

77
Q

What are the non-infectious, immune-mediated neurological inflammatory diseases of dogs?

A
  • Necrotizing meningoencephalitis (NME)
  • Necrotizing encephalitis (NE)
  • Eosinophilic meningoencephalitis (EME)
  • Steroid-responsive meningitis-arteritis (SRMA)
  • Granulomatous meningoencephalitis (GME)
78
Q

Name a non-infectious, immune-mediated neurological inflammatory diseases of horses?

A

Polyneuritis equi (cauda equina neuritis)

79
Q

What the general considerations of trauma and compressive injuries to the CNS?

A
  • Trauma can cause compression, stretching, twisting, sheering and tearing of tissues
  • Traumatic injury may affect the neurological tissues and the vasculature (can cause secondary effects that can be more severe than the primary)
80
Q

What is the effect of a contusion in the CNS?

A

Impact causing transient deformation. Damage to the vasculature causes haemorrhage, but the architecture of the nervous tissue remains intact

81
Q

What is the effect of a laceration in the CNS?

A

Traumatic injury in which there is disruption of the tissue

82
Q

What is the effect of a compression in the CNS?

A

Persistent deformation of the tissue

83
Q

Describe how trauma can result in brain haemorrhage/contusion at different points of the brain.

A
  • Brain has inertia within skull and can move independently in the skull but is cushioned by CSF
  • If haemorrhage occurs at site adjacent to where site of injury occurred = coup injury
  • Contrecoup – haemorrhage on area of the brain opposite to the impact site
  • If both, we have coup-contrecoup
84
Q

What is a primary brain injury?

A

Initial forces may cause injury to nervous tissues and vasculature (haemorrhage and oedema)

85
Q

How does a secondary brain injury occur?

A
  1. Altered blood flow (perturbed autoregulation) and pressure (catecholamine release) -> oedema
  2. Vascular injury -> ischaemia -> necrosis, inflammation and oedema
  3. Haemorrhage (space occupying lesion) -> increased intracranial pressure -> oedema and ischaemia
  4. Brain swelling may result in herniation
86
Q

What is ascending/descending haemorrhagic myelomalacia?

A

Occasionally following a contusion of the spinal cord, haemorrhage and necrosis may extend up or down the spinal cord from the site of injury

87
Q

What are the posisble causes of compression of the brain or spinal cord?

A
  • Malformations and malarticulation of vertebrae
  • Fractures or luxations
  • Neoplasia
  • Abscesses (e.g. epidural abscess)
  • Intervertebral disc disease e.g. herniations, discospondylitis
88
Q

What is neuropraxia from peripheral nerve trauma?

A
  • Compressive injury causes local demyelination
  • Causes a physiological conduction block at site of injury
  • Return to function takes hours to months
89
Q

What is axonotmesis from peripheral nerve trauma?

A
  • Axon disruption but preservation of the connective tissues
  • Wallerian degeneration occurs distal to the injury
  • Regeneration may take months to years
90
Q

What is neurotmesis from peripheral nerve trauma?

A
  • Axon disruption and partial or complete disruption of the connective tissues
  • Wallerian degeneration occurs distal to the injury
  • Regeneration may or may not be possible depending on severity
91
Q

What are the factors to consider with anomalies and malformations of the nervous system?

A

Genetic factors

Environmental factors:
- Viral infections
- Nutritional deficiencies
- Teratogenic chemicals, drugs, toxins
- CNS development continues in the post-natal period and may still be sensitive to teratogenic agents

92
Q

What are the possible cerebellar malformations?

A

Hypoplasia, agenesis, dysplasia

93
Q

What are the secondary causes of cerebellar malformations?

A

Usually viral infection destruction of cerebellar tissue:

  • Feline parvovirus (feline panleukopenia virus)
  • Schmallenberg virus
  • BVDV
  • Classical swine fever
94
Q

What are the clinical signs of cerebellar malformations?

A

Affects coordination - ataxia, dysmetria = inability to control range of movement, intention tremors, head tremors

95
Q

How do we measure hypoplasia or hyperplasia of the cerebellum?

A

Weigh mass – normal is 13-14% cerebellar mass of the whole brain in cats. Horses will have greater mass due to more complicated gait cycles

May not be the whole cerebellum affecting, may have segmental loss

96
Q

What is hydrocephalus?

A
  • Increased volume of CSF and enlargement of all or part of the ventricular system
  • Hydrocephalus can be congenital or acquired (acquired obstruction of CSF flow by a tumour mass or exudate)
97
Q

Where is CSF produced and where does it then go?

A

CSF is produced by choroid plexus at sites in the ventricles. CSF reabsorbed from arachnoid space into the dural venous sinuses

98
Q

What is the effect of hydrocephalus on communicating venous sinuses?

A
  • Bilateral and symmetrical dilation of the ventricular system
  • No detectable gross or microscopic lesions to account for this
99
Q

What is the effect of hydrocephalus on non-communicating venous sinuses?

A

Partial or complete obstruction of CSF flow at one or more points in within the ventricular system (intraventricular) or subarachnoid space (extraventricular)

Most common sites of obstruction:
- Between lateral and third ventricles
- Mesencephalic aqueduct
- Lateral apertures of the fourth ventricles

100
Q

What is ventriculomegaly?

A

Hydrocephalus with marked ventricular enlargement

101
Q

How does ventriculomegaly develop?

A
  • (CSF production exceeds rate of removal)
  • Increased CSF pressure proximal to site of obstruction
  • Leads to atrophy and loss of periventricular tissues
  • Extensive loss of the periventricular white matter and sparing of the cortical grey matter
102
Q

What are the typical features of congenital hydrocephalus in dogs?

A

Domed skull with thin calvaria and enlarged fontanelles

103
Q

What is compensatory hydrocephalus/ex-vacuo hydrocephalus?

A

Occurs when a disease results in loss of brain tissue creating a void (space) into which a ventricle distends, resulting in secondary compensatory enlargement of the ventricular space. Not necessarily associated with increased CSF pressure

104
Q

What is hydranencephaly?

A

Bilaterally symmetrical, extensive fluid-filled cavitary lesions with complete or almost complete absence of the cerebral hemisphere parenchyma

105
Q

How does hydranencephaly develop?

A
  • Residual cerebral cortex residual tissues and/or meninges appear as large fluid-filled sacs
  • Ependymal lining of the lateral ventricles is intact and there may be compensatory expansion of the lateral ventricles (compensatory hydrocephalus)
106
Q

What can cause hydranencephaly in ruminants?

A

Global destruction of cerebral tissues in the foetus by some viruses e.g. BVDV, Border disease, Bluetongue virus, Schmallenberg virus

107
Q

Wat is porencepahly?

A

Congenital focal fluid-filled cavitary (cystic) lesion within a cerebral hemisphere. Occasionally may be bilateral and symmetrical

108
Q

What can obstruction of CSF flow and increase of CSF pressure in the central canal of the spinal cord cause?

A
  • Dilation of the central canal = Hydromyelia
  • Formation of fluid-filled cavities (syrinx) in the spinal cord parenchyma = Syringomyelia
109
Q

What is the effect of occipital bone malformation?

A

Caudal fossa too small to accommodate the cerebellum resulting in cerebellar herniation into foramen magnum. Changes the pressure of the CSF and the pulses that occur down the spinal cord and leads to formation of syrinx/multiple syrinxes along the spinal canal

110
Q

What are the clinical signs of occipital bone malformation?

A

Sensitivity over the neck (pain and scratching), paresis or proprioception deficits, scoliosis (spinal curvature)

111
Q

What can be a consequence of occipital bone malformation?

A
  • May cause syringomyelia affecting the cervical and/or the thoracolumbar region
  • Cavalier king Charles spaniels
112
Q

What are the consequences of metabolic and toxic disorders in the nervous system?

A

Tend to produce bilaterally symmetrical lesions in the CNS

113
Q

What are possible causes of metabolic and toxic disorders of the nervous system?

A
  • Nutritional deficiencies – copper deficiency, thiamine deficiency
  • Endogenous toxins – hepatic encephalopathy
  • Exogenous toxins – tetanus, botulism
  • Idiopathic – dysautonomia (grass sickness)
114
Q

Distinguish swayback and enzootic ataxia.

A

Swayback – congenital. Signs at birth – recumbency, ataxia, flaccid, blindness

Enzootic ataxia – delayed form seen in growing lambs
- Progressive disease with swaying and ataxia of hind limbs
- Flaccid paralysis, muscular atrophy

115
Q

What causes swayback and enzootic ataxia?

A

Low pasture copper and/or impaired absorption from gut by other elements

116
Q

What are the brain lesions apparent in swayback?

A

Bilaterally symmetrical cerebral white matter cavitation or softening

117
Q

What are the brain lesions apparent in swayback and enzootic ataxia?

A

Microscopic lesions - bilateral symmetrical white matter exonal degeneration and neuronal degeneration

118
Q

What is the condition caused by thiamine deficiency in ruminants?

A

Polioencephalomalacia/cerebrocortical necrosis (CCN)

119
Q

Why and how does thiamine deficiency arise?

A
  • Overgrowth of thiaminase-producing bacteria in the rumen
  • Ingestion of thiaminase-containing plants (e.g. bracken)
  • Decreased absorption/increased excretion in GI disease
120
Q

What is the mechanism of thiamine deficiency causing polioencephalomalacia/cerebrocortical necrosis?

A
  1. Thiamine pyrophosphate – cofactor in carbohydrate metabolism
  2. Deficiency results in depleted energy (ATP)
  3. Reduced energy causes neuronal necrosis (cortical laminae especially sensitive) and astrocyte dysfunction
  4. Bilaterally symmetrical cerebrocortical necrosis
  5. Signs can include blindness, ataxia, seizures, paddling
121
Q

How does thiamine deficiency cause cortical laminar necrosis?

A
  • Cerebral cortex swelling may cause flattened gyri
  • May have bilaterally symmetrical yellow discolouration of the grey matter where necrosis has occurred
122
Q

How can cortical laminar necrosis be visualised?

A

Lesions autofluorescence under UV light

123
Q

What are the effects of primary tumours of the CNS?

A

Rarely spread outside the CNS, but can spread within

Space occupying mass > compression, haemorrhage, obstruction, herniation

124
Q

What does a tumour located in the inner aspect of the brain or ventricular system indicate about its origin?

A

Consider tumours arising from the choroid plexus or ependyma (cells lining the ventricular system and central canal)

125
Q

What does a tumour located in the outer aspect of the brain indicate about its origin?

A

Consider meningioma

126
Q

What does a tumour located within the parenchyma indicate about its origin?

A

Astrocytoma Oligodendroglioma. Consider glial cell tumours e.g. oligodendroglioma (from oligodendrocytes), astrocytoma (from astrocytes)

CVSOH 4 (34 decks)

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