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Applied Neuroanatomy > Principles and Cerebrovascular Disease > Flashcards

Principles and Cerebrovascular Disease Flashcards

1
Q

What is the dura?

A

the tough fibrous outer layer which bridges crevices and is attached to the skull

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2
Q

What is the arachnoid?

A

delicate sealed bag for CSF - bridges crevices - impermeable to salt and water

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3
Q

What ropes across the subarachnoid space?

A

arachnoid trabeculae

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4
Q

Where is the cerebral artery branch?

A

embedded in the pia - susceptible to tearing and damage

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5
Q

What is the pia mater?

A

delicate - next to brain and dips into crevices

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6
Q

What are the main cellular components of the CNS?

A 
nerve cells
glial cells
blood vessels
microglia
connective tissue - meninges
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7
Q

What are the glial cells?

A

astrocytes, oligodendrocytes, ependyma

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8
Q

What can damage the cells of the CNS?

A 
hypoxia
trauma
toxic insult
metabolic abnormalities
nutritional deficiencies
infections
ageing
genetic abnormalities
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9
Q

What are the neuronal responses to injury?

A

acute neuronal injury
simple neuronal atrophy
sub-cellular alterations
axonal reactions

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10
Q

Why are neurons particularly susceptible to hypoxic damage?

A

due to activation of glutamate receptors -> Ca overload

can’t use anaerobic glycolysis

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11
Q

Why would you be better drowning in cold water?

A

slows metabolic processes and cell death down

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12
Q

What is the axonal reaction?

A

the reaction within the cell body that is associated with injury to the axon

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13
Q

What is the responses to axonal injury?

A
  • increased RNA and protein synthesis
  • swelling of the cell body
  • peripheral displacement of the nucleus
  • enlargement of the nucleolus
  • anterograde degeneration of the axon - distal to site of injury
  • breakdown of myelin sheat
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14
Q

How do astrocytes react to injury?

A

proliferation (gliosis)

reactions leading to cell death or degeneration

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15
Q

What is the process gliosis?

A

where astrocytes undergo hyperplasia and hypertrophy
nucleus is enlarged, becoming vesicular and the nucleolus is prominent
cytoplamsic expansion with extension of ramifying processes

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16
Q

What can be seen on old lesions of gliosis?

A

nuclei become small and dark and lie in a dense net of processes - fibrils
comparable to scar formation

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17
Q

What is injury to oligodendrocytes a feature of?

A

demyelinating diseases

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18
Q

How do oligodendrocytes react to injury?

A

very limited response

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19
Q

where are ependymal cells found?

A

lining the ventricular system

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20
Q

What is disruption of ependymal cells associated with?

A

local proliferation of sub-ependymal astrocytes producing small irregularities on the ventricular surfaces - ependymal granulations

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21
Q

What can produce changes in ependymal cells?

A

infectious agents i.e. viruses

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22
Q

How do microglia respond to injury?

A
  • proliferate
  • develop elongated nuclei
  • forming aggregates about small foci of tissue necrosis
  • congregate around portions of dying neurons
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23
Q

How long does brain need to lose blood supply before there is irreversible damage?

A

4 minutes

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24
Q

How much CO and O2 does the brain receive?

A

15% of CO and 20% of O2

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25
Q

How is blood flow maintained in the brain?

A

autoregulatory mechanisms

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26
Q

Where does the blood supply in the brain come from?

A

internal carotid arteries and vertebral arteries

27
Q

Why is the circle of willis protective?

A

occlusion of any one pathway does not stop flow to one area unlike when blood flow is deeper into the brain

28
Q

Where is the circle of willis?

A

base of the brain

29
Q

What does occlusion to the anterior cerebral artery lead to?

A

contralateral sensory loss in foot and leg

paresis of arm and foot, relative sparing of thigh and face

30
Q

Where does the anterior cerebral artery lead?

A

frontal lobe

31
Q

What happens with occlusion to the middle cerebral artery?

A

hemiparesis
hemisensory loss
aphasia/dysphasia - loss of language or vocal chord function
apraxia

32
Q

what does the brain stem consist of?

A

mid-brain, pons, medulla

33
Q

What does the brain stem control?

A

cardio-respiratory centres

34
Q

what do bleeds on the occipital lobe cause?

A

homonymous hemianopia because of the cross over of optic nerve

35
Q

What does a stroke in the cerebellum cause?

A

ataxia
nystagmous - eye twitch in extreme visual fields
intention tremor
pendular reflexes - acts like a pendulum when it shouldnt

36
Q

what is the mortality of Cerebrovascular disease?

A

20% in the first month

37
Q

What are the potential causes of cerebrovascular disease?

A

brain ischemia and infarctions
haemorrhages
vascular malformations and developmental abnormalities

38
Q

What may cause hypoxic ischemic damage?

A

respiratory obstruction, lung and heart disease, epilepsy, cardiac arrest

39
Q

Which groups of neurons are more vulnerable to hypoxic/ischemic damage?

A

pyramidal cells of hippocampus

purkinje cells of cerebellum

40
Q

What are watershed areas?

A

junctions of arteries which are the first areas to be deprived

41
Q

When may hypoxic ischemic encephalopathy occur?

A

in any circumstance that results in global decrease in HbO2 available to the brain

42
Q

What is a stroke?

A

a sudden disturbance of cerebral function of vascular origin that causes death or lasts over 24 hours

43
Q

What are the types of stroke and their commonality?

A

infarction (84%) or haemorrhage (16%)

44
Q

What is a cerebral infarction?

A

caused by local interuption of cerebral blood flow due to thrombosis or emboli

45
Q

What is an embolis?

A

a clot that has broken off

46
Q

What are risk factors for stroke?

A

atheroma, HBP, serum lipids, obesity, diet, T2DM, heart disease, smoking

47
Q

What is the morphology of a cerebral infarct 4-12 hours later?

A

brain may appear normal

48
Q

What is the morphology of a cerebral infarct 15-20 hours later?

A

ischemic neuronal changes develop

49
Q

What is the morphology of a cerebral infarct 24-36 hours later?

A

inflammatory reaction, extravasion of RBCs and activation of astrocytes and microglia

50
Q

What is the morphology of a cerebral infarct 36-48 hours later?

A

necrotic area visible macroscopically, becomes swollen and softer than surrounding tissue

51
Q

What is the morphology of a cerebral infarct 3 days later?

A

macrophages are in the area

52
Q

What is the morphology of a cerebral infarct 1-2 weeks later?

A

liquification of tissue and gliosis

53
Q

What is the morphology of a cerebral infarct months later?

A

cavitation and completion of glial scar

54
Q

What is the most common cause of haemorrhage?

A

spontaneous

55
Q

What is a spontaneous haemorrhage??

A

rupture of a saccular aneurysm

56
Q

Where do most aneurysms occur?

A

arise at arterial bifurcation in territory or internal carotid (90%)

57
Q

What are the potential morphologies of aneurysms?

A
  • rupture of berry aneurysm - bleeds into subarachnoid space
  • intracerebral haematomas adjacent to aneurysm
  • infarcts of brain parenchymal due to arterial spasms (40%)
58
Q

What are the clinical features of haemorrhages?

A

-abrupt onset (headache, vomiting, loss of conciousness)

59
Q

What are the signs of a haemorrhage?

A

bloody CSF, meningeal signs incl. neck stiffness

60
Q

What are the complications of a haemorrhage?

A

cerebral infarcts, acute hydrocephalus, herniation

61
Q

Why may chronic hydrocephalus develop in patients surviving the initial haemorrhage?

A

due to organisation of blood in the leptomeninges and or arachnoid granulations with resultant obstruction of CSF flow

62
Q

What does hypertension cause in the brain?

A

increased atheroma
hyaline arteriosclerosis
microaneurysms
shift in autoregulatory curve to the right

63
Q

What is the pathology of hypertension in the brain?

A
  • lacunar infarcts
  • intracerebral haemorrhage
  • multi-infarct dementia
  • hypertensive encephalopathy

Applied Neuroanatomy (11 decks)

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