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Neuroscience Y2S2 > Neurobiology of Disease 11 > Flashcards

Neurobiology of Disease 11 Flashcards

1
Q

Define ‘stroke’. (2)

A

Acute onset of neurological deficits (lasting for more than 24hrs)

due to a disturbance in blood supply.

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2
Q

Approximately 15 million people suffer strokes each year.

Describe the prognosis for people having a stroke, in terms of what proportion will die, recover, and have lasting deficits. (3)

A

1/3 will die

1/3 will recover

1/3 will have lasting deficits

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3
Q

Give (and describe where required), five non-modifiable risk factors for stroke. (5)

A

Age

Atrial fibrillation

Gender - women less likely up until menopause

Ethnicity - black and Asian people more likely

Family history

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4
Q

Give 6 modifiable risk factors for stroke. (6)

A
  • Hypertension
  • Diabetes
  • Hyperlipidaemia
  • Smoking
  • Obesity
  • Carotid artery disease
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5
Q

Give the two major classes of stroke. (2)

What percentage of stroke cases fall into each category?

A

Ischaemic (85%)

Haemorrhagic (15%)

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6
Q

Haemorrhagic stroke accounts for 15% of stroke cases.

Give two types of haemorrhagic stroke, and state what percentage of total stroke cases fall into each category. (2)

A

Intracerebral (10%)

Subarachnoid (5%)

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7
Q

Ischaemic stroke accounts for 85% of stroke cases.

Give two types of ischaemic stroke, and state what percentage of stroke cases fall into each category. (2)

A

Thrombotic (55%)

Embolic (30%)

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8
Q

A large vessel occlusion is able to cause an ischaemic stroke.

Is a large vessel occlusion a thrombotic or embolic type of stroke? (1)

A

Can be either

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9
Q

A lacunar occlusion is able to cause an ischaemic stroke.

Is a lacunar occlusion a thrombotic or embolic type of stroke? (1)

A

thrombotic

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10
Q

What do we mean by ‘thrombotic’ stroke and ‘embolic’ stroke, when referring to ischaemic stroke? (2)

A

THROMBOTIC
- artery or blood vessel slowly becomes blocked over time

EMBOLIC
- clot forms elsewhere in the body and travels to the brain

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11
Q

Give four specific symptoms of a haemorrhagic stroke. (4)

A
  • Thunderclap headache
  • Seizures
  • Nausea
  • Unilateral weakness
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12
Q

Give five specific symptoms of an anterior circulation ischaemic stroke. (5)

A
  • Hemiplegia/paresis
  • Hemisensory loss
  • Dysphagia
  • Aphasia
  • Hemianopia
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13
Q

Give four specific symptoms of a posterior circulation ischaemic stroke. (4)

A
  • Unilateral limb weakness
  • Ataxia
  • Dysarthria
  • Isolated hemianopia
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14
Q

Ataxia is a symptom sometimes seen in posterior circulation ischaemic strokes.

Ataxia points to which brain region being involved in stroke? (1)

A

Cerebellum

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15
Q

Isolated hemianopia is a symptom of a posterior circulation ischaemic stroke.

Describe what is meant by isolated hemianopia, and why it is a specific symptom of a posterior circulation stroke. (2)

A

Hemianopia not associated with any other symptoms

With other symptoms, it would almost certainly be an anterior stroke, but isolated would be posterior

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16
Q

Give six non-specific symptoms of stroke. (6)

A
  • Confusion
  • Drowsiness
  • Dizziness
  • Nausea
  • Double vision
  • Incontinence
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17
Q

Describe what is meant by a ‘lacunar infarction’. (1)

A

Small, strategic strokes in penetrating arteries that feed subcortical structures.

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18
Q

A lacunar infarction is sometimes described as a series of ‘small, strategic strokes’.

What is meant by a ‘strategic’ stroke? (1)

A

Small infarct has a large knock-on effect due to its location

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19
Q

True or false? Explain your answer if appropriate. (1)

Lacunar infarcts almost always present with motor symptoms due to effects on the basal ganglia.

A

False - as many as 80% are clinically silent

*However they can affect basal ganglia

*And if symptoms are present, they do tend to be motor

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20
Q

Name the symptom/syndrome that is most commonly experienced in a lacunar infarction. (1)

A

Motor hemiplegia syndrome

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21
Q

Some people with lacunar infarctions present with motor hemiplegia syndrome.

Give three locations where the infarct may have occurred in these patients. (3)

A
  • Internal capsule
  • Basal ganglia
  • Pons
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22
Q

Give a specific type of stroke (including the blood vessel involved) which is the most common. (1)

Give two symptoms commonly experienced in this type of stroke. (2)

A

Middle cerebral artery infarction

Contralateral hemiplegia

Contralateral hemisensory loss

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23
Q

How is a stroke usually diagnosed? (2)

A
  • Neurological examination
  • Followed by neuroimaging (usually CT)
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24
Q

Describe how an ischaemic and a haemorrhagic stroke would appear on a CT scan. (2)

A
  • CT not good for detecting ischaemic stroke, but subtle signs may be visible (loss of basal ganglia definition and sulcal effacement)
  • Haemorrhage looks brighter/whiter than brain tissue (intracerebral often look very angular and wedge-shaped)
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25
Q

Give two subtle signs of acute ischaemic stroke that could be picked up on a CT scan. (2)

A
  • Loss of basal ganglia definition
  • Sulcal effacement
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26
Q

What is the mortality rate in haemorrhagic stroke? (1)

A

45%

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27
Q

Give a complication of haemorrhagic stroke seen in about 30% of patients. (1)

Describe how this complication may impact on brain function. (1)

A

Vasospasm

Could cause subsequent ischaemic stroke or pathological variations in blood flow

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28
Q

Give three general treatment approaches for haemorrhagic stroke. (3)

A
  • Pain management
  • Surgery to repair bleed
  • Lowering blood pressure if required
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29
Q

Give two surgical interventions that could be used to treat haemorrhagic stroke. (2)

A

Clipping the bleed

Coiling (filling aneurysm with coils of wire to stop bleeding)

30
Q

Give two general options for treating ischaemic stroke. (2)

A

Thrombolysis

Thrombectomy

31
Q

Name the medication, and the type of medication, which is used for thrombolysis treatment of ischaemic stroke. (1)

A

Alteplase (which is a tissue plasminogen activator - tPA)

32
Q

Give the time limit for treating ischaemic stroke with thrombolysis. (1)

A

Has to be given within 3hrs

(can sometimes go up to 4.5hrs)

33
Q

Give the time limit for treating ischaemic stroke with thrombectomy. (1)

A

Has to be done within 6hrs

34
Q

True or false? Explain your answer. (1)

There is no evidence that thrombolysis is effective for treating ischaemic stroke later than 4.5hrs after onset.

A

False - it has been previously been used to restore middle cerebral artery patency after 6hrs of stroke onset

However - it is not used in clinical practice after 4.5hrs

35
Q

Describe a typical stroke lesion, in terms of areas of blood flow. (4)

A

Core is middle of lesion with very little/no blood flow (<12ml/100g/min)

Penumbra around core (12-22ml/100g/min)

Benign oligemia around penumbra (>22ml/100g/min)

Normal tissue with normal bloodflow (50-54ml/100g/min)

36
Q

A stoke lesion is usually made up of the core, penumbra, and benign oligemia.

Describe the tissue viability of each of these areas. (3)

A

Core - tissue is dead

Penumbra - at high risk of death but can still be saved with timely intervention

Benign oligemia - at risk, but is likely to spontaneously recover

37
Q

Why does stroke have to be treated quickly? (3)

A

Around the core of the lesion (which is dead tissue), the penumbra also has reduced blood flow

The penumbra tissue is at risk but can still be saved if intervention is applied quickly

If intervention is delayed, the core of the stroke lesion will extend to incorporate the penumbra and the tissue can no longer be saved

38
Q

True or false? Explain your answer if appropriate. (1)

In a stroke lesion, the penumbra is the area around the core of dead tissue.
The penumbra can spontaneously recover, despite the fact that it too has reduced blood flow.

A

False - the benign oligemia is likely to spontaneously recover, the penumbra only recovers if intervention is given quickly

39
Q

What is the main pathological event which happens in stroke and kills most brain tissue? (1)

A

Excitotoxicity

40
Q

Describe the time course of stroke in terms of the pathological events which occur. (4)

A
  • Extremely high levels of excitotoxicity occur first, over minutes to hours
  • Peri-infarct depolarisations also occur quickly, over minutes to hours
  • Inflammation then reaches a peak over hours-days
  • In the subsequent days, apoptosis occurs
41
Q

True or false? Explain your answer if appropriate. (1)

In stroke, the fate of cells is determined within the first couple of hours of symptom onset.

A

False - cells which looked like they were going to survive early on can undergo apoptosis over the next few days

42
Q

Explain what causes the high levels of excitotoxicity seen early on in stroke pathology. (3)

A
  • Energy substrates cannot be delivered to neurones
  • Energy failure leads to ion pump failure and inability of the neurones to maintain their membrane potential
  • So neurones depolarise and release glutamate into the extracellular space, which binds to NMDA and causes excitotoxicity
43
Q

Explain how excitotoxicity causes cell death in stroke. (3)

A
  • Glutamate causes Na and Ca to enter cells
  • Na causes depolarisation and cell swelling
  • Ca causes enzyme induction, ROS production, membrane degradation, DNA damage, mitochondrial damage, and apoptosis
44
Q

Explain why inflammation occurs in stroke. (3)

A

Excitotoxicity in neurones causes increased ROS, cell damage, and apoptosis

And this process releases inflammatory mediators

Which activate microglia and any leukocytes which have infiltrated brain tissue, causing inflammation

45
Q

Describe how peri-infarct depolarisations are caused during stroke. (3)

A

When a cell is stimulated by glutamate and depolarises (excitotoxicity), K ions and glutamate are released into the extracellular space

And these can act on nearby neurones causing them to depolarise

So a wave of depolarisation and excitotoxicity spreads from the core of the lesion

46
Q

Apart from neurones, give four other cell types which may be affected by the inflammatory response to stroke. (4)

A
  • Leukocytes (which infiltrate into brain tissue)
  • Microglia
  • Astrocytes
  • Oligodendrocytes
47
Q

How are microglia affected by the inflammatory response in the brain, which occurs during/after stroke? (2)

A

Inflammatory mediators activate microglia,

when then go on to produce more inflammatory mediators.

48
Q

The inflammatory response it the brain during/after stroke can attack oligodendrocytes.

Give three consequences of this. (3)

A
  • Demyelination
  • White matter changes
  • Axonal injury
49
Q

Describe how the neuroinflammatory response seen during/after stroke affects astrocytes. (3)

A

Astrocytes become swollen

which compromises blood brain barrier integrity (leukocyte infiltration)

and also compromises synaptic homeostasis

50
Q

Describe how leukocytes are able to contribute to the neuroinflammatory response in the brain seen during/after stroke. (2)

A

Can infiltrate brain (BBB integrity compromised by damaged astrocytes)

and produce inflammatory mediators to contribute to inflammation.

51
Q

Complete the sentence relating to cerebrovascular diseases. (1)

The same vascular risk factors that predispose an individual to stroke, also increase the risk of developing ………………..

A

Dementia

52
Q

Define ‘vascular cognitive impairment’. (1)

A

VCI is an umbrella term for many cognitive disorders that are thought to share a vascular origin.

53
Q

Some classification schemes include Alzheimer’s disease under the umbrella term of vascular cognitive impairment.

Why can AD be classed as vascular? (1)

A

As many as 50% of brains with classic Alzheimer’s pathology also show evidence of cerebrovascular disease

***This can also be classed as mixed dementia

54
Q

Give the eight major mechanisms underlying vascular cognitive impairment. (8)

i.e. how might vascular disease lead to cognitive impairment?

A
  • Cerebral amyloid angiopathy
  • Large vessel occlusion
  • White matter change
  • Enlarged perivascular spaces
  • Infarcts
  • Atrophy
  • Lobar and deep haemorrhage
  • Microbleeds
55
Q

What is cerebral amyloid angiopathy? (1)

How might this contribute to vascular cognitive impairment? (1)

A

Amyloid plaques accumulate in blood vessels

this makes blood vessels more fragile and prone to bleeding and inflammation

56
Q

Describe how cerebral vascular disease might cause white matter change in the brain, which can then cause cognitive impairment. (1)

A

WMC is associated with slight decreases in cerebral blood flow over a long period of time (eg. due to atherosclerosis in old age)

57
Q

Enlarged perivascular spaces, in other words, larger spaces around the blood vessels in the brain, may be a sign of vascular cognitive impairment.

Give four potential causes of enlarged perivascular spaces. (4)

A
  • Brain atrophy
  • Hypertension
  • Inflammation
  • Changes in perivascular flow
58
Q

Compare the neuroimaging techniques used to visualise Alzheimer’s dementia and vascular dementia. (2)

A

Can only really see AD on PET scans

Changes associated with vascular dementia can be seen using MRI

59
Q

Give four brain changes associated with vascular cognitive impairment which can be seen on an MRI scan. (4)

A
  • White matter change
  • Microbleeds
  • Enlarged perivascular spaces
  • Cerebral amyloid angiopathy
60
Q

White matter change is associated with vascular cognitive impairment.

How would white matter change show up on an MRI scan? (1)

A

Hyperintensity

61
Q

Which receptor does BDNF bind to? (1)

A

TrkB

62
Q

When BDNF binds to its receptor, name an intracellular pathway/enzyme which is activated. (1)

A

PLCy (PLC gamma)

63
Q

The precursor to BDNF, pro-BDNF, binds to which receptor? (1)

A

P75

64
Q

Give two cellular/molecular effects of pro-BDNF binding to its receptor. (2)

A
  • Cell death
  • LTD
65
Q

Which neurotransmitter in particular, is affected by BDNF? (1)

How is this neurotransmitter affected by BDNF in depression? (1)

A

Glutamate

Reduced BDNF reduces glutamatergic neurotransmission

66
Q

Describe a BDNF polymorphism which increases risk of anxiety and depression. (1)

A

Val66Met mutation

67
Q

Describe how BDNF signalling/function affects treatment response to antidepressants. (1)

Describe a piece of supporting evidence. (1)

A

Antidepressant treatment response is dependent on BDNF signalling

BDNF gene mutation or knockout animal model show attenuated response to antidepressant treatment

68
Q

Describe a hypothesis explaining how reduced hippocampal volume and HPA hyperactivation may be linked in depression. (4)

A
  • HPA hyperactivation releases more glucocorticoids
  • Hippocampus is rich in glucocorticoid receptors
  • So increased GCs may induce excitotoxicity and ROS generation
  • Leading to hippocampal neuronal loss
69
Q

Name 2 inotropic glutamate receptors or receptor subunits which are thought to be mutated and implicated in ADHD. (2)

A
  • GluN2A
  • GluN2B
70
Q

Give a metabotropic glutamate receptor which may be mutated and implicated in ADHD. (1)

A

mGluR5

Neuroscience Y2S2 (15 decks)

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