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Neurology > Cerebrovascular Injury & Stroke > Flashcards

Cerebrovascular Injury & Stroke Flashcards

1
Q

What are the two types of damage that can occur to nerve cells?

A

Rapid necrosis - acute functional failure

Slow atrophy - gradual dysfunction

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2
Q

What is another name for acute neuronal injury?

A

Red neuron

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3
Q

Describe what is meant by the term red neuron

A

Occurs in the context of hypoxia/ischaemia, 12-24 hours after an irreversible insult to the cell
Cell shrinks, angulation of nuclei, loss of nucleolus, intensity of red cytoplasm due to eosinophilia

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4
Q

How do cells respond to axonal injury?

A
  • increased protein synthesis, leads to cell body swelling and enlarged nucleolus
  • chromatolysis, margination and loss of Nissi granules
  • degeneration of axon and myelin sheath distal to injury
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5
Q

What is simple neuronal atrophy?

A

Process that affects functionally related sets of neurons, shrunken angulated and loss of neurons. Small dark nuceli with reactive gliosis and lipofuscin pigment - chronic degeneration

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6
Q

What are inclusions?

A

Variety of structural abnormalities that appear to accumulate with age or in viral infections

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7
Q

How do oligodendrocytes react to injury?

A

Have low anti-oxidant reserves and high intracellular iron which makes them sensitive to oxidative injury

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8
Q

What does damage to oligodendrocytes result in?

A

Reduced conduction and exposure of axons to injury

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9
Q

State the role of astrocytes

A
  • ionic, metabolic and nutritional homeostasis
  • conjunction with endothelium to maintain BBB
  • main cells involved in repair and scar formation in CNS
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10
Q

Describe gliosis

A

Astrocytes undergo hyperplasia and hypertrophy - nucleus enlarges, becomes vesicular with a prominent nucleolus and the cytoplasm expands

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11
Q

What do old lesions in the CNS look like?

A

Nuclei are small and dark and lie in a dense network of glial fibrils. Translucent, firm and circumscribed.

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12
Q

Why are the ependymal cells associated with infection?

A

As bacteria can pass from one cell to another via CSF and local proliferation can produce ependymal granulations

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13
Q

How do microglia respond to injury?

A

Proliferate, recruit inflammatory mediators and aggregates - around damaged tissue

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14
Q

Name the two types of microglia

A

M2 - actue anti-inflammatory

M1 - chronic pro-inflammatory

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15
Q

State some causes of cerebrovascular injury

A 
Hypoxia 
Trauma 
Toxic insult 
Metabolic abnormalities 
Nutritional deficiencies 
Infections 
Genetic abnormalities 
Ageing
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16
Q

How much can cerebral blow flow increase?

A

two fold

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17
Q

What percentage of body resting oxygen consumption goes to the brain?

A

20%

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18
Q

If the brain is deprived of oxygen what can happen?

A

Mitochondrial inhibition of ATP synthesis so ATP reserves are consumed within a few mins

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19
Q

What is excitotoxicity?

A

Process by which neurons are damaged due to the overactivation of excitatory pathways

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20
Q

If energy fails, describe the exitotoxicity pathway

A

Neuronal depolarisation - glutamate release
Inhibition of astrocyte reuptake - failure of glutamate uptake
Both of which cause a glutamate storm and subsequent calcium release
1. Mitochondrial dysfunction
2. Oxidative stress
3. Protease activation

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21
Q

Name three types of oedema

A
  • cytotoxic
  • ionic
  • vasogenic
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22
Q

Describe cytotoxic oedema

A

Osmotically active sodium and chloride ions move into cells and take water, no swelling occurs e.g. intoxication

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23
Q

Describe ionic oedema

A

Dysfunction of blood brain barrier extracellular space is devoid of sodium ion sand so sodium, chloride and water moves across BBB e.g SIADH

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24
Q

Describe vasogenic oedema

A

Deterioration and breakdown of BBB due to disruption of tight junctions allowing albumin and other proteins to cross therefore water follows e.g trauma, tumour

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25
Q

What is haemorrhagic conversion?

A

BBB is so damaged the red blood cells can pass

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26
Q

Name the three main arteries that supply the brain

A

Anterior, middle and posterior cerebral artery

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27
Q

Where does the anterior cerebral artery supply?

A

Midline portions of the frontal lobe and superior medial parietal lobes

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28
Q

Where does the middle cerebral artery supply?

A

Lateral cerebral cortex, it arises from the ICA and continues into the lateral sulcus where it branches - anterior temporal lobes and insular cortices

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29
Q

Where does the posterior cerebral artery supply?

A

Occipital lobe

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30
Q

Define cerebrovascular injury

A

Any abnormality of the brain caused by pathological process of blood vessels

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31
Q

Name four pathological processes of blood vessels

A
  • brain ischaemia and infarction
  • haemorrhage
  • vascular malformations
  • aneurysms
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32
Q

Name two types of ischaemia

A

Global and focal

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33
Q

What is global ischaemia?

A

Systemic compromise to the circulation, cannot be compensated for by auto-regulation e.g cardiac arrest

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34
Q

What is focal ischaemia?

A

Restriction of blood flow to a localised area of the brain typically due to a vascular obstruction

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35
Q

What must MAP fall to for auto-regulatory mechanisms to no longer compensate?

A

15mmHg

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36
Q

What areas of the brain are most sensitive to ischaemia?

A

Watershed areas at the periphery that are least well supplied

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37
Q

Where in the brain are neurons most sensitive?

A

Neocortex, hypocampus, purkinje cells

38
Q

Define stroke

A

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

39
Q

What percentage of strokes are infarcts/haemorrhagic?

A

84% infarction

16% haemorrhage

40
Q

Describe a thrombotic stroke?

A

Thrombosis in atherosclerotic segment most commonly the middle cerebral artery

41
Q

Describe an embolic stroke

A

Atheroma in ICA and aortic arch usually from the heart or more proximal atherosclerotic segments

42
Q

Name some rarer causes of infarction

A
  • osteophytes
  • vasculitis
  • septal defects
43
Q

State the risk factors for cerebral infarction

A

Atheroma, hypertension, high cholesterol, heart disease, drugs, smoking, structural defects

44
Q

In the first 12 hours after a stroke what pathology is seen?

A

Little visible

45
Q

12-24 hours after infarction what is seen?

A

Macro - Pale soft swollen ill defined margins

Mirco - red neuron, oedema and swelling

46
Q

24-48 hours after infarction what is seen?

A

Increasing neutrophils, extravasation of RBC, activation of astrocytes and microglia

47
Q

2-14 days after an infarction what can be seen?

A

Macro - Brain becomes gelatinous and friable, reduction in surrounding tissue, oedema demarcates the lesion
Micro - predominantly microglial cells, gliosis and myelin breakdown

48
Q

What can be seen several months after an infarction?

A

Liquification, cavity formation lined by dark grey tissue

Phagocytosis and increasing cavitation and gliotic scar formation

49
Q

What can cause a haemorrhagic infarct?

A

Disruption to BBB
Deterioration of tissue due to infarction
Intentional reperfusion through damaged vessels

50
Q

Depending on the affected artery what is the clincial presentation of haemorrhagic infarct

A

Carotid Artery - contralateral weakness/sensory loss
Middle cerebral artery - contralateral face and arm
Anterior cerebral artery - weakness/sensory loss in contralateral leg
Vertebro-basilar artery - vertigo, atoxia, dysarthria, dysphagia

51
Q

What is the pathological consequence of hypertension?

A

Lacunar infarcts, multi-infarct dementia, aneurysm formation and rupture, intracerebral haemorrhage, hypertensive encephalopathy

52
Q

What are lacunar infarcts?

A

Small lake like infarcts that vary in size, occur with occlusion of small penetrating vessels e.g lenticular striate branches - basal ganglia

53
Q

What can accumulation of lacunar infarcts lead to?

A

Mulit-infarct dementia

54
Q

Describe hypertensive encephalopathy

A

Severe hypertension, overlap of symptoms with raised ICP, headache, vomiting, altered balance, confusion, seizures, coma

55
Q

What are the pathological findings of hypertensive encephalopathy?

A

Global cerebral oedema
Tentorial and tonsilar herniation
Arteriolar fibrinoid necrosis
Petechiae (extravastation of RBC)

56
Q

What intracranial haemorrhages can occur spontaneously?

A

Intracerebral
Sub-arachnoid
Haemorrhagic infarct

57
Q

What intracranial haemorrhages can occur due to trauma?

A 
Extra-dural/sub-dural 
Haematoma
Contusion 
Intracerebral haemorrhage 
Sub-arachnoid haemorrhage
58
Q

What causes an intracerebral haemorrhage?

A 
Aneurysms
Vascular Malformations 
Systemic coagulation disorders/iatrogenic coagulation 
Open heart surgery 
Neoplasm
59
Q

Where do intracerebral haemorrhages due to neoplasm most commonly occur?

A

Basal ganglia including the thalamus

Cerebral white matter and cerebellum

60
Q

What does a intracerebral haematoma due to neoplasm look like?

A

Well demarcated SOL, formed by an area of parenchyma haematoma, softening of adjacent tissue with surrounding oedema - herniation and shifts are common

61
Q

Which condition is commonly associated with amyloid angiopathy?

A

Alzheimers

62
Q

Describe amyloid angiopathy

A

Beta amyloid sheets are deposited in the cerebral and meningeal vessels - reduces compliance and ability to cope with pressure

63
Q

When do vascular malformations usually occur?

A

During angiogenesis

64
Q

Name some vascular malformations

A

Arteriovenous - MCA teritory
Cavernous angiomas
Venous angiomas
Capillary telangectases

65
Q

Describe arteriovenous malformations

A

Smooth muscle hypertrophy, reduced compliance and shunting from artery to vein

66
Q

How do vascular malformations present?

A

Bleeding, headaches, seizures, focal neurological deficits

67
Q

What vascular malformations are at most risk of bleeding?

A

Ateriovenous

Cavernous angiomas

68
Q

Where do 90% of sub-arachnoid haemorrhages occur?

A

Territory of ICA - bifurcation at circle of Willis

69
Q

Name the risk factors for sub-arachnoid haemorrhage

A
  • Acquired degenerative lesion
  • PCKD
  • Collagen gene abnormality
70
Q

Describe the morphology of a sub-arachnoid haemorrhage

A

Blood in sub-arachnoid space, presence of aneurysm, infarction of brain parenchyma due to arterial spasm, mass effect due to haematoma, increased ICP, hydrocephalus

71
Q

Describe the clinical presentation of a sub-arachnoid haemorrhage

A

Abrupt onset, headache, vomiting, loss of consciousness, high mortality, blood in CSF, midline shifts, herniation and hydrocephalus

72
Q

Name some stroke mimics

A

Seizure, sepsis, toxic/metabolic, SOL, pre/syncope, confusion/delirium, dementia

73
Q

Describe a CT of a stroke

A

Blood is white, only useful straight after haemorrhage

74
Q

Describe a MRI of a stroke

A

Diffusion weighted will show infarct - little differentiation between grey/white matter, blood will appear white and static in a blocked artery

75
Q

Define penumbra

A

Cells that are still alive but at risk of death

76
Q

What is the management for acute cerebrovascular syndrome?

A

Thrombolysis
Endovascular therapy
Anti-platelets

77
Q

Describe thrombolysis

A

IV tissue plasminogen activator, systemic treatment acts to break down clots - dose based on weight needs to be given less than 4.5 hours after onset - high risk of bleeding

78
Q

Describe endovascular therapy

A

Interventional radiology - catheter passed through groin to the brain to pull out the clot, only used for proximal vessels - no risk of bleeding

79
Q

What antiplatelet therapy is given after a stroke?

A

Aspirin ASAP
CT to exclude a bleed
Mild - aspirin + clopidogrel for up to 3 weeks

80
Q

What reduces risk of DVT?

A

Intermittent pneumatic compression

81
Q

What must be given to a patient after a TIA?

A

Statin and anti-platelet

82
Q

How is hypertension treated after a haemorrhage?

A

IV GTN

83
Q

What can reverse anti-coagulation?

A

Vitamin K - warfarin

DOACs have no licensed reversible drug but prothrombin complex is advised

84
Q

What are the four key types of stroke depending on location of damage?

A

Total Anterior Circulation Syndrome
Partial Anterior Circulation Syndrome
Lacunar Syndrome
Posterior Circulation Syndrome

85
Q

What makes up the anterior circulation?

A

Internal carotid
Middle cerebral
Anterior cerebral

86
Q

How will TACS present?

A

Hemiplegia
Homonymous hemianopia
Cortical signs - neglect, dysphagia

87
Q

What is partial anterior circulation syndrome?

A

2/3 features of TACS
- isolated cortical dysfunction
Pure motor/sensory signs

88
Q

Where do lacunar infarcts occur?

A

Deeper parts of the brain - basal ganglia/thalamus

Small perforating arteries

89
Q

What arteries are affected in posterior circulation syndrome?

A

Vertebral and basilar

90
Q

What are the symptoms of PCS?

A

Ipsilateral cranial nerve palsy with contralateral motor and/or sensory deficit
Bilateral motor and/or sensory deficit
Cerebellar dysfunction
Isolated homonymous visual field defect

91
Q

When does a syndrome become more specific?

A

When ischaemia/haemorrhage is determined

92
Q

What can happen if a stroke occurs on the right?

A

Neglect

Spatial awareness

Neurology (29 decks)

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