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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
What is haemorrhagic conversion?
BBB is so damaged the red blood cells can pass
26
Name the three main arteries that supply the brain
Anterior, middle and posterior cerebral artery
27
Where does the anterior cerebral artery supply?
Midline portions of the frontal lobe and superior medial parietal lobes
28
Where does the middle cerebral artery supply?
Lateral cerebral cortex, it arises from the ICA and continues into the lateral sulcus where it branches - anterior temporal lobes and insular cortices
29
Where does the posterior cerebral artery supply?
Occipital lobe
30
Define cerebrovascular injury
Any abnormality of the brain caused by pathological process of blood vessels
31
Name four pathological processes of blood vessels
- brain ischaemia and infarction - haemorrhage - vascular malformations - aneurysms
32
Name two types of ischaemia
Global and focal
33
What is global ischaemia?
Systemic compromise to the circulation, cannot be compensated for by auto-regulation e.g cardiac arrest
34
What is focal ischaemia?
Restriction of blood flow to a localised area of the brain typically due to a vascular obstruction
35
What must MAP fall to for auto-regulatory mechanisms to no longer compensate?
15mmHg
36
What areas of the brain are most sensitive to ischaemia?
Watershed areas at the periphery that are least well supplied
37
Where in the brain are neurons most sensitive?
Neocortex, hypocampus, purkinje cells
38
Define stroke
Sudden disturbance of cerebral function of vascular origin that causes death or lasts over 24 hours
39
What percentage of strokes are infarcts/haemorrhagic?
84% infarction | 16% haemorrhage
40
Describe a thrombotic stroke?
Thrombosis in atherosclerotic segment most commonly the middle cerebral artery
41
Describe an embolic stroke
Atheroma in ICA and aortic arch usually from the heart or more proximal atherosclerotic segments
42
Name some rarer causes of infarction
- osteophytes - vasculitis - septal defects
43
State the risk factors for cerebral infarction
Atheroma, hypertension, high cholesterol, heart disease, drugs, smoking, structural defects
44
In the first 12 hours after a stroke what pathology is seen?
Little visible
45
12-24 hours after infarction what is seen?
Macro - Pale soft swollen ill defined margins | Mirco - red neuron, oedema and swelling
46
24-48 hours after infarction what is seen?
Increasing neutrophils, extravasation of RBC, activation of astrocytes and microglia
47
2-14 days after an infarction what can be seen?
Macro - Brain becomes gelatinous and friable, reduction in surrounding tissue, oedema demarcates the lesion Micro - predominantly microglial cells, gliosis and myelin breakdown
48
What can be seen several months after an infarction?
Liquification, cavity formation lined by dark grey tissue | Phagocytosis and increasing cavitation and gliotic scar formation
49
What can cause a haemorrhagic infarct?
Disruption to BBB Deterioration of tissue due to infarction Intentional reperfusion through damaged vessels
50
Depending on the affected artery what is the clincial presentation of haemorrhagic infarct
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
What is the pathological consequence of hypertension?
Lacunar infarcts, multi-infarct dementia, aneurysm formation and rupture, intracerebral haemorrhage, hypertensive encephalopathy
52
What are lacunar infarcts?
Small lake like infarcts that vary in size, occur with occlusion of small penetrating vessels e.g lenticular striate branches - basal ganglia
53
What can accumulation of lacunar infarcts lead to?
Mulit-infarct dementia
54
Describe hypertensive encephalopathy
Severe hypertension, overlap of symptoms with raised ICP, headache, vomiting, altered balance, confusion, seizures, coma
55
What are the pathological findings of hypertensive encephalopathy?
Global cerebral oedema Tentorial and tonsilar herniation Arteriolar fibrinoid necrosis Petechiae (extravastation of RBC)
56
What intracranial haemorrhages can occur spontaneously?
Intracerebral Sub-arachnoid Haemorrhagic infarct
57
What intracranial haemorrhages can occur due to trauma?
``` Extra-dural/sub-dural Haematoma Contusion Intracerebral haemorrhage Sub-arachnoid haemorrhage ```
58
What causes an intracerebral haemorrhage?
``` Aneurysms Vascular Malformations Systemic coagulation disorders/iatrogenic coagulation Open heart surgery Neoplasm ```
59
Where do intracerebral haemorrhages due to neoplasm most commonly occur?
Basal ganglia including the thalamus | Cerebral white matter and cerebellum
60
What does a intracerebral haematoma due to neoplasm look like?
Well demarcated SOL, formed by an area of parenchyma haematoma, softening of adjacent tissue with surrounding oedema - herniation and shifts are common
61
Which condition is commonly associated with amyloid angiopathy?
Alzheimers
62
Describe amyloid angiopathy
Beta amyloid sheets are deposited in the cerebral and meningeal vessels - reduces compliance and ability to cope with pressure
63
When do vascular malformations usually occur?
During angiogenesis
64
Name some vascular malformations
Arteriovenous - MCA teritory Cavernous angiomas Venous angiomas Capillary telangectases
65
Describe arteriovenous malformations
Smooth muscle hypertrophy, reduced compliance and shunting from artery to vein
66
How do vascular malformations present?
Bleeding, headaches, seizures, focal neurological deficits
67
What vascular malformations are at most risk of bleeding?
Ateriovenous | Cavernous angiomas
68
Where do 90% of sub-arachnoid haemorrhages occur?
Territory of ICA - bifurcation at circle of Willis
69
Name the risk factors for sub-arachnoid haemorrhage
- Acquired degenerative lesion - PCKD - Collagen gene abnormality
70
Describe the morphology of a sub-arachnoid haemorrhage
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
Describe the clinical presentation of a sub-arachnoid haemorrhage
Abrupt onset, headache, vomiting, loss of consciousness, high mortality, blood in CSF, midline shifts, herniation and hydrocephalus
72
Name some stroke mimics
Seizure, sepsis, toxic/metabolic, SOL, pre/syncope, confusion/delirium, dementia
73
Describe a CT of a stroke
Blood is white, only useful straight after haemorrhage
74
Describe a MRI of a stroke
Diffusion weighted will show infarct - little differentiation between grey/white matter, blood will appear white and static in a blocked artery
75
Define penumbra
Cells that are still alive but at risk of death
76
What is the management for acute cerebrovascular syndrome?
Thrombolysis Endovascular therapy Anti-platelets
77
Describe thrombolysis
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
Describe endovascular therapy
Interventional radiology - catheter passed through groin to the brain to pull out the clot, only used for proximal vessels - no risk of bleeding
79
What antiplatelet therapy is given after a stroke?
Aspirin ASAP CT to exclude a bleed Mild - aspirin + clopidogrel for up to 3 weeks
80
What reduces risk of DVT?
Intermittent pneumatic compression
81
What must be given to a patient after a TIA?
Statin and anti-platelet
82
How is hypertension treated after a haemorrhage?
IV GTN
83
What can reverse anti-coagulation?
Vitamin K - warfarin | DOACs have no licensed reversible drug but prothrombin complex is advised
84
What are the four key types of stroke depending on location of damage?
Total Anterior Circulation Syndrome Partial Anterior Circulation Syndrome Lacunar Syndrome Posterior Circulation Syndrome
85
What makes up the anterior circulation?
Internal carotid Middle cerebral Anterior cerebral
86
How will TACS present?
Hemiplegia Homonymous hemianopia Cortical signs - neglect, dysphagia
87
What is partial anterior circulation syndrome?
2/3 features of TACS - isolated cortical dysfunction Pure motor/sensory signs
88
Where do lacunar infarcts occur?
Deeper parts of the brain - basal ganglia/thalamus | Small perforating arteries
89
What arteries are affected in posterior circulation syndrome?
Vertebral and basilar
90
What are the symptoms of PCS?
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
When does a syndrome become more specific?
When ischaemia/haemorrhage is determined
92
What can happen if a stroke occurs on the right?
Neglect | Spatial awareness

Neurology (29 decks)

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