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Case 13 > Functional Neuroanatomy > Flashcards

Functional Neuroanatomy Flashcards

1
Q

What does stroke damage to anterior cerebral artery affect?

A

Lower limb

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2
Q

What does stroke damage to posterior cerebral artery cause?

A

Vision deficit

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3
Q

What does stroke damage to middle cerebral artery cause?

A

Loss of sensation + motor control of arm, hand, face + linguistic function on left

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4
Q

Why is the middle cerebral artery vulnerable to clots or emboli?

A

Continuation of internal carotid so clots likely to travel into it

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5
Q

What is the arterial supply of the brainstem?

A
  • Internal carotid
  • Basilar
  • Vertebral x 2
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6
Q

What is meant by contralateral circulation?

A

If one vessel damaged and supply compromised, can be taken over by another

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7
Q

What can a brainstem stroke lead to?

A
  • Involving vertebral + basilar arteries = high mortality
  • Life support functions - breathing, chewing + swallowing via cranial nerves
  • Coma due to damage to ARAS
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8
Q

What is seen in lateral medullary syndrome?

A
  • Occlusion of PICA
  • Contralateral loss of pain + temp on body (spinothalamic)
  • Ipsilateral loss of pain + temp on face (trigeminal)
  • Dysphagia, hoarseness, loss of gag reflex (nucleus ambiguous, roots of vagus + glossopharyngeal)
  • Ipsilateral Horner’s syndrome (hypothalamopsinal fibres)
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9
Q

What is the arterial supply of the brainstem?

A
  • Internal carotid
  • Basilar
  • Vertebral x 2
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10
Q

What is meant by contralateral circulation?

A

If on vessel damaged and supply compromised, can be taken over by another

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11
Q

What can a brainstem stroke lead to?

A
  • Involving vertebral + basilar arteries = high mortality
  • Life support functions - breathing, chewing + swallowing via cranial nerves
  • Coma due to damage to ARAS
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12
Q

How are glial cells different from most neuronal cells?

A

Retain ability to divide throughout lifetime

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13
Q

What do brain tumours contrain?

A

Only glial cells (gliomas) or cells of meningeal coverings of brain (meningiomas)

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14
Q

What are the roles of astrocytes?

A
  1. Control extracellular ion concentrations (esp K)

2. Remove and deactivate transmitters (esp glutamate)

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15
Q

What do oligodendrocytes form?

A

Myelin sheath

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16
Q

What is necrosis?

A
  • General cell injury

- Cell ruptures = inflam reaction

17
Q

What is apoptosis?

A
  • Programmed cell death
  • Due to loss of trophic factors needed for cell to survive
  • Via proteolytic enzymes (caspases) + DNAses
    = Apoptotic bodies = phagocytosed by microglia
  • No inflam response
  • Triggered by injury
18
Q

Summarise axonal regeneration

A
  • Triggered by IC Ca entering cytosol + activating protease which breaks down cytoskeleton
  • Schwann cells phagocytose debris + secrete tropic factors > promoting axonal growth
  • Schwann cells de-differentiate but stay within basal lamina
  • Invading macrophages secrete factors = promote Schwann cell migration + axon growth
19
Q

What is CNS response to injury?

A
  1. Blood borne monocytes + macrophages invade
  2. Microglia multiples + activate to remove debris
  3. 24hrs - oligodendrocyte precursors (OPCs) divide + hypertrophy - astrocytes follow
  4. Astrocyte process link together = barrier around lesion
  5. Meningeal like cells invade lesion forming plug
  6. Glial scar formation
20
Q

Why is there a lack of axonal regeneration?

A
  • Regrowth physically blocked by glial scar formation + chemically by inhibitory molecules:
    1. Even small lesions that don’t seem to disrupt glial structure may inhibit
    2. Regions of glial transitions may form barrier to regrowth
    3. Inhibitory molecules block growth of adult axons but not embryonic (Nogo A)
    4. Astrocytes produce inhibitors (CSPGs)
    5. Macrophages produce molecules toxic to neurons
21
Q

What is diffuse axonal injury associated with?

A
  • Coup (injury under site of impact) + contracoup (injury on side opposite area hit)
  • May remain comatose or go into persistent vegetative state (due to disturbance of ARAS in brainstem)
  • Cerebral concussion = mild form
22
Q

What is seen on the histology of DAI?

A

Damaged axons = brown using antibodies to B amyloid prescursor protein

23
Q

What are petechial haemorhages?

A
  • Often associated with DAI

- Indicate severe brain injury even in absence of any midline shift

24
Q

What are coup and contracoup injuries associated with?

A
  • Cerebral contusions (bruised brain)

- Rupture of bridging veins between brain surface + dural sinuses (slow subdural haemorrhage)

25
Q

What are haemorrhages in corpus callosum associated with?

A

DAI

26
Q

What may be the LT effect of axonal damage and haemorrhaging?

A

Loss of white matter and consequent enlargement of ventricles

27
Q

Summarise excitotoxicity (glutamate recycling)

A
  • Glutamate = main excitatory transmitter
  • Terminated by re-uptake via glutamate transporters into nerve terminals
  • Traumatic brain injury can increase EC [glutamate] levels
  • Levels may also increase if astrocyte metabolism compromised
  • Astrocytes can metabolise glucose anaerobically for prolonged periods but lactic acid builds up > if pH below 6.6 = no glycolysis = irreversible damage
28
Q

What are the cellular consequences of excitotoxicity?

A
  • NMDA + AMPA involved - glutamate receptors
  • @ resting potential NMDA channel blocked by Mg > Depolarising dendrite via AMPA unblocks NMDA
  • Na and Ca flow through NMDA = further depolarisation
  • If neuron also contains glutamate more released when APs fired
  • Some AMPA types also permeable to Ca
29
Q

What do high levels of IC Ca lead to?

A

Reduced mitochondrial ATP synthesis

30
Q

What do high levels of IC Na and Ca lead to?

A

Osmotic swelling + cell rupture

  • calpains degrade neuronal cytoskeleton
  • proteases digest structural proteins
  • phospholipases break down cell membrane
  • endonucleases cause DNA fragmentation
31
Q

Summarise the process of oxidative stress

A

In normal mitochondria = ROS

  • Reactive nitrogen species (RNS) may also be produced due to excitotoxicity + ROS
  • Mitochondria have large amounts of Ca that become elevated by excitotoxicity = production of abnormal ROS
  • ROS scavanged by antioxidants = Vit C + E + key enzymes = SOD, catakase + glutathione perioxidase
  • Excessive ROS can swamp these mechanisms = oxidation of important cell mechanisms
32
Q

What happens to mitochondrial abnormalities during ageing?

A

Accumulate due to mutations in mitochondrial DNA

33
Q

What neurodegenerative disease is mutations in SOD linked to?

A

Motor neuron disease

34
Q

What neurodegenerative disease is mutations in dopaminergic neurones linked to?

A

Parkinson’s

Case 13 (9 decks)

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