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Tobias ECVS > Ch 29 - Pathogenesis and Physiology of CNS disease and injury > Flashcards

Ch 29 - Pathogenesis and Physiology of CNS disease and injury Flashcards

1
Q

Descirbe the distribution of the grey matter in the spinal cord, brainstem and cerebral cortex

A
  • Spinal cord - butterfly shape in the central cord, divivding the surrounding white matter into funiculi
  • Brainstem - forms scattered nuclei with intervening tracts of white matter
  • Cerebral cortex - external layer of grey matter with white matter connecting the cortex to other regions of the CNS
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2
Q

What is grey matter and white matter?

A
  • Grey matter - high density of neuronal cell bodies
  • White matter - Axons and associated glial cells
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3
Q

Describe the ventricles of the CNS

A
  • One lateral ventricle within each hemisphere
  • Third ventricle within diencephalon
  • Fourth ventricle ventral to the cerebellum
  • CSF formed within ventricles via the choroid plexus
  • Flows from lateral ventricles, through interventricular foramina into 3rd, through mesencephalic aqueduct into 4th and then through lateral aperatures into subarachnoid space or continues caudally into central canal
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4
Q

What are the leptomeninges?

A

Arachnoid mater and pia mater

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5
Q

What are the pachymeninges?

A

Dura mater and arachnoid mater

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6
Q

Name the two forms of brain herniation

A
  • Transtentorial
  • Foramen magnum
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7
Q

What is the normal resting potential of neuronal cell membranes?

A

-80mV (inside of cell negative with respect to the outside)

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8
Q

How are action potentials generated?

A
  • Rapid depolarisation of the membrane due to an influx of Na through voltage-gated Na-channels
  • ELectrolyte oncentrations are returned to resting levels by active extrusion of Na from the cell in exchange for K, and K uptake by astrocytes
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9
Q

What cell produces myelin?

A

Oligodendrocytes

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10
Q

What is required for maintenance of a resting potential and generation/conduction of action potentials?

A
  • Energy (Na-K/ATPase)
  • Appropriate intra and extracellular electrolyte concentrations
  • Ion channel function
  • Myelin
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11
Q

What are the 2 forms of CNS perfusion autoregulation?

A
  • Pressure autoregulation - remains constant with MAP between 50-160mmHg via vasodilation during hypotension and vasoconstriction during hypertension
  • Metabolic autoregulation - astrocytes match blood flow to neuronal activity (NO, CO, K, adenosine, glutamate, arichadonic acid)
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12
Q

How does PaCO2 alter CNS perfusion?

A
  • Increases during hypercapnia
  • Decreases during hypocapnia
  • For every 1mmHg change in PaCO2, there is a 5% change in cerebral perfusion
  • PaCO2 less than 25mmHg causes vasoconstriction and potential ischaemia
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13
Q

How is cerebral perfusion pressure defines?

A

CPP = MABP - ICP

Reduction in MABP or increase in ICP can therefore impair cerebral perfusion

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14
Q

What is normal intracranial pressure?

A

8-15mmHg

Over 15 required treatment, over 30 causes significant reduction in cerebral perfusion

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15
Q

What are some mechanisms for accomodating for gradual increases in intracranial volume?

A
  • Moving CSF into subarachnoid space
  • Reducing CSF production
  • Decreasing cerebral bloodflow
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16
Q

How much is ICP decreased by a craniotomy and by a durotomy?

A
  • Craniotomy alone 15%
  • Durotomy 65%
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17
Q

What forms the blood-brain barrier?

A
  • Endothelial cell tight junctions
  • Astrocyte foot processes
  • Basal lamina
  • Pericytes
  • Perivascular microglia
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18
Q

What ABx have good penetration of the BBB?

A
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19
Q

Why is the CNS said to be ‘immunologically previledged”

A
  • Relatively isolated from the immune system by the BBB
  • Immunosuppresive parenchymal environment
  • Poorly developed lymphatic drainage
20
Q

What protective immunologic mechanisms limits entry of pathogens and other exogenous material into the CNS?

A
  • Expression of major histocompatibility complex molecules and coexpression of costimulatory molecules (B7) are necessary for cells to act as antigen-presenting cells. Endothelial cells do not express these.
  • Cell adhesion molecules are expressed only at low levels on endothelial cells (can be rapidly upregulated)
  • Perivascular macrophages and microglial cells DO express major histocompatibility complex and participate in the immune response
21
Q

What are the resident immune and phagocytic cells of the CNS?

A

Microglial cells

22
Q

Where are the 2 stem cell populations within the CNS?

A
  • Subventricular zone/olfacotry system
  • Dentate gyrus of the hippocampus
23
Q

What are the main categories of CNS injury?

A
  • Contusion
  • Compression
  • Inflammation
  • Vascular
  • Metabolic/toxic
  • Degenerative
24
Q

What causes diffuse brain injury?

A

Widespread damage to white and/or grey matter cause by brain swelling, hypoxia and diffuse axonal injury.
DIffuse axonal injury results from inertial forces causing membrane damage to axona, allowing unregulated Na entry and depolaristion, initiating secondary effects

25
Q

What is the broad definitial of secondary injury?

A

A series of metabolic and biomechanical changes that cause neuronal and glial cell death

26
Q

What gene is upregulated in secondary injury and plays a central role in ongoing haemorrhage?

A
  • Trmp4 (transient membrane potential)
27
Q

List the mechanisms by which contusion causes secondary injury

A
  • Decreased perfusion and therefore energy to neurons and glial cells cause Ion pump failure (increased intracellular Ca, Na, Cl causing swelling)
  • Mechanical damage to neurons results in increased neuronal release and decreased astrocytic uptake of glutamate. Glutamate interaction with NMDA and AMPA receptors cause rapid increases in intracellular Na and Ca (more gradually)
  • Mitochondrial membranes become permeable due to ischaemia and apoptosis-inducing factor is released as well as free radicals and further decreases energy production
  • Rapidly initiates a inflammatory responce with initial inflex of neutrophila and peak macrophages in 5-7days which conincides with demyelination
28
Q

What is the result of increased intracellular Ca?

A
  • Activates intracellular proteases (calpains, caspase), which destroy the cytoskeleton and initiate programmed cell death
  • Activates phospholipase A2, initiating an inflammatory response
  • Binds intracellulr phosphates, further depleting energy sources
29
Q

What cytokines and toxic chemicals ar released by microglial cells after injury?

A
  • Cytokines: IL-1, TNFa
  • Chemicals - H2O2, NO, proteinases
30
Q

How does CNS injury effect an animals susceptibility to infection?

A
  • Circulating lymphcyte ad monocyte numbers are depressed for several days
  • Lymphocyte function is depressed for several months after spinal cord injusry and stroke
31
Q

What are the pathologic changes associated with compression?

A
  • Demyelination
  • Oedema
  • Axonal degeneration
  • Neuronal necrosis (oligodendrocytes, astrocytes, neurons and axona)
32
Q

What are the main forms for disease causing vascular obstructive lesions?

A
  • FCE
  • Feline ischaemia encephalopathy (FIE)
  • Thrombotic “stroke” in dogs
33
Q

What are the 5 broad localisations of CNS haemorrhage?

A
  • Extradural
  • subdural
  • subarachnoid
  • intraventricular
  • intraparenchymal

Secondary injusy due to compression and also similarly to contusion due to decreased energy supply

34
Q

How does the inflammatory response cause CNS dysfunction?

A
  • Inflammatory mediators can directly affect neural function
  • NO, leukotrienes and prostanoids have profound effects on the microcirculation and the integrity of the BBB
35
Q

What substance is a powerful blocker of conduction?

A

Nitrous oxide

36
Q

List some metabolic diseases of the CNS

A
  • Hypoglycaemia secondary to insulinoma
  • Hepatic encephalopathy
  • Uraemic encephalopsthy
  • PANS
37
Q

What are the most common neoplasms to metastasise to the brain?

A
  • HSA
  • melanoma
  • carcinoma
38
Q

What is the difference between cytotoxic oedema, vasogenic oedema and interstitial oedema?

A
  • Cytotoxic oedema - intracellular swelling in the presence of a normal BBB as a result of ion pump failure
  • Vasogenic oedema - Increased vascular permeability causing the accumulation of extracellular fluid, particularly within the white matter tracts
  • Interstitial oedema - Abnormal flow of CSF through the CNS associated with elevated intraventricular pressure
39
Q

What is Hansen Type 1 degeneration?

A

Progressive decrease in proteoglycan content of the nucleus pulposus with consequant dehydration and mineralisation. Loead to loss of ability to withstand pressure and causes secondary degeneration and tearing of the annulus

40
Q

What is Hansen Type II degeneration?

A

Progressive dehydration of the nucleus and replacement with fibrinoid tissue leading to an increase in stress transfer to the annulus. Annulus undergoes wear-and-tear degeneration with rupture of fibers over months-to-years and progressive protrusion

41
Q

Which cells of the CNS can be regenerated readily?

A

Glial cells (astrocytes and oligodendrocytes)
For unknown reasons, remyelination does not always occur spontaneously

42
Q

Define hydrocephalus, hydromyelia
syringomyelia.
What cause syringomyelia?

A

Hydrocephalis - accumulation of fluid within the ventricles
Hydromyelia - within the central canal
Syringomyelia - within the parenchyma of the spinal cord. Caused by diseases which alter the CSF flow such as arachnoiditis, Chiari-like malformation and elevated ICP

43
Q

What is synaptic plasticity?

A

Alteration in synapses within the brain in response to variation in the nature of their input.
- upregulation of neurotransmitter receptors
- alterations in type of postsynaptic receptors and in reliability of transmission
- Can change the types of ion channels expressed
- Formation of new synapses - may be influenced by rehab

44
Q

What is collateral sprouting?

A

A repair mechanish where a partially denervated cell will become reinnervated by branches from a functioning nerve

45
Q

How can fasting aid in CNS recovery?

A

Reduced calor intake is associated with
- reduction in reactive oxygen species and lipid peroxidation
- Increase in neuroprotective molecules suchs as BHB and antiapoptotic proteins

Tobias ECVS (110 decks)

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