Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PBL SEM 3 > CASE 5 - stroke > Flashcards

CASE 5 - stroke Flashcards

1
Q

which CNs attach directly to the forebrain?

A

olfactory and optic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is anosmia?

A

loss of sense of smell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what supplies muscles of mastication?

A

trigeminal motor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what supplies muscles of facial expression?

A

facial motor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

tensor tympani vs stapedius innervation

A
  • tensor tympani = V3 branch (mandibular branch of trigeminal)
  • stapedius = nerve to stapedius (branch of VII in facial canal)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what supplies the anterior 2/3 of the tongue?

A

facial nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what supplies the posterior 1/3 of the tongue?

A

glossopharyngeal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the nerve involved in the cough reflex?

A

vagus nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what nerve is involved in sneezing?

A

trigeminal nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

which CNs have parasympathetic fibres?

A

III, VII, IX, X

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what nerve innervates the parotid gland?

A

IX - glossopharyngeal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what nuclei are involved in the PS parts of the CNs?

A
  • III = Edinger-Westphal
  • VII = superior salivatory
  • IX = inferior salivatory
  • X = dorsal motor nucleus of vagus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are Broca’s and Wernicke’s areas connected by?

A

arcuate fasciculus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

where is Broca’s area?

A

in inferior frontal gyrus (in frontal lobe above lateral fissure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what happens if broca’s is damaged?

A

words dont come out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is Wernicke’s area for?

A

interpretation of auditory information, language comprehension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

where is Wernicke’s area?

A

near back of temporal lobe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

which dorsal column carries fibres for the lower limbs?

A

fasciculus gracilis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

where do 3rd order neurones have their cell bodies?

A

thalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

which side of the brain is dominant for language?

A

left

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what type of neurones does the spinothalamic tract contain?

A

2nd order

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what do axons pass in in the spinothalamic tract?

A

spinal lemniscus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

do axons in the spinothalamic tract ascend in the ipsilateral or contralateral tract?

A

contralateral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

where do most fibres terminate in the spinothalamic tact?

A

ventral posterior nucleus of the thalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what do lesions in the spinothalamic tract lead to?

A

impairment of pain, temperature, touch and pressure sensitivity on the contralateral side

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

lateral vs ventral spinothalamic tract

A

lateral — pain and temperature
ventral — touch and pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what do axons ascend in in the dorsal columns?

A

medial lemniscus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

do axons ascend in the ipsilateral or contralateral dorsal column to the medulla?

A

ipsilateral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

where do axons of the dorsal columns terminate?

A

nucleus gracilis/cuneatus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what do lesions of dorsal columns lead to?

A

loss of discriminative touch ipsilaterally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what can cause lesions in the dorsal columns?

A

tabes dorsalis, vitamin B12 def

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what do motor nuclei in the brainstem contain?

A

cell bodies of LMN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what do sensory nuclei in the brainstem contain?

A

2nd order neuroens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

describe the pathophysiology of a cerebral infarct

A
  1. sudden cessation of blood supply to neurones — hypoxic cells
  2. drop in ATP — failure of Na+/K+ pump
  3. Na+ begins to accumulate in cell
  4. oedema in cells - swell and burst
  5. increase in intracranial pressure as cells swell and burst 00 further reduces blood supply
  6. increase in Na+ causes constant depolarisation of neurones in the affected area
  7. increase in Glu in synapse (as reuptake relies on ATP)
  8. failure of NMDAR — allows excessive levels of Ca++ into cell
  9. free radicals released — necrosis
  10. cytokines released — inflammation — adds to oedema and general tissue swelling in region
  11. Ca++ can also directly lead to apoptosis in the penumbra
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what is oxidative stress?

A
  • the overproduction of reactive O2 species
  • drives inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

describe the process of oxidative stress

A
  • reduction in ATP
  • mitochondria membranes collapse
  • reactive O2 species (H2O2) released
  • acted upon by free radicals such as superoxide, causing them to release hydroxide radicals
  • these are extremely toxic
  • leads to changes within cell
  • leads to oxidation of proteins and lipids
  • eventually CELL DEATH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what do damaged neurones release?

A

DAMPs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

describe the sterile inflammation process in the brain

A

= inflammation in the absence of a pathogen

  • damaged neurones release DAMPs
  • recognised by brain resident microglia and infiltrating monotypes via pathogen recognition receptors
  • upregualtion of receptors on cell surface and release of cytokines and chemokines (reactive O2 species, TNFa, IL-1B, MMPs etc)
  • damage to basement membrane and BBB when vessel wall damaged — vWF released — blood flow reduced even more
  • migration of neutrophils and other immune cells into brain tissue — release contents (cytokines, proteases, ROS) which damage neurones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what is affected by a small-vessel (lacunar) infarct?

A
  • involve small penetrating vessles that supply the deep structures
  • these include basal ganglia, thalamus and internal capsule, brainstem
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what are lacunar infarcts usually associated with?

A

small-vessel disease caused by chronic hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what is the result of an occlusion in the anterior cerebral artery?

A

paralysis and sensory loss in contralateral leg and perineum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what is the result of an occlusion in the middle cerebral artery?

A

contralateral paralysis (mostly in lower face and arm), general somatosensory deficits, speech deficits (aphasia) if dominant hemisphere affected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what is the result of an occlusion in the basilar artery?

A

coma followed by death due to resp failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what is the result of an occlusion in the posterior cerebral artery?

A

blindness, contralateral homonymous hemianopia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what is locked-in syndrome and what is it caused by?

A
  • patient aware and awake but virtually all motor neurones are paralysed — thus patient cannot move
  • usually the eyes are the only structures not affected
  • caused by an upper brainstem infarct
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what is pseudo bulbar palsy?

A
  • result of a lower brainstem infarct
  • results in bilateral impairment of the 9th-12th cranial nerves
  • dysarthria and dysphagia
47
Q

what is wallenberg syndrome due to and present with?

A
  • a neurological disorder that is due to damage to the lateral portion of the medulla
  • aka. lateral medullary syndrome or posterior inferior cerebellar artery thrombosis
  • typically due to ischaemia in a vertebral artery or posterior inferior cerebellar artery
  • presents with acute vertigo and other cerebellar signs
48
Q

what type of infarct is often symptomless?

A

lacunar

49
Q

the most common stroke is caused by an infarction where?

A

in the internal capsule following a thromboembolism in a MCA branch

50
Q

lacunar infarct symptoms

A
  • affects deep arteries of brain
  • often symptomless
  • may present with very localised symptoms such as purely motor/sensory
  • pure motor strokes (face, arm and leg) in the posterior limb of internal capsule
  • pure sensory stroke (thalamus)
  • ataxic hemiparesis (weakness and ataxia affecting the same side) due to a pontine lesion
  • clumsy hand/dysarthria due to a lesion in the pons or in its internal capsule
51
Q

anterior circulation infarct symptoms

A
  • amaurosis fugax/retinal infarction
  • hemiparesis
  • hemisensory loss
  • hemianopia (optic tract and radiation)
  • dysphasia
  • sensory and visual inattention
52
Q

posterior circulation infarct symptoms

A
  • ataxia
  • cranial nerve involvement
    • diplopia, facial sensory loss, dysphargia,
      dysarthria
  • hemiparesis (may be bilateral)
  • hemisensory loss (may be bilateral)
  • contralateral hemianopia (occipital lobe)
  • cortical blindness — basilar artery occlusion
53
Q

you are most likely to lose consciousness and have a headache (usually of sudden onset) with what type of stroke?

A

intracranial haemorrhage

54
Q

an intracranial haemorrhage is nearly always the result of what?

A

uncontrolled chronic hypertension

55
Q

describe a subarachnoid haemorrhage

A
  • sudden bleeding into the subarachnoid space surrounding the brain
  • causes severe headache with stiffness of the neck
  • possibly loss of consciousness
  • risk factors : hypertension, smoking, alcohol, situations with a sudden elevation in BP
56
Q

describe an intracerebral haemorrhage

A
  • due to bursting of blood vessels within the brain itself
  • can lead to a haematoma
  • a very large haematoma can displace brain structures — causes herniation syndromes
57
Q

describe an aneurysm and how it causes an increase in intracranial pressure

A
  • due to weakness of blood vessels such that one part of it balloons out and dilates
  • blood collects in these berry-like swellings and often in the circle of willis
  • aneurysm bursts and bleeds into subarachnoid space causing an increase in intracranial pressure
58
Q

what may the increased intracranial pressure following a haemorrhage lead to?

A

a loss of blood supply to affected tissue with resulting infarction

59
Q

what is the secondary injury following a haemorrhage?

A

toxic products in haematoma (eg. thrombin, Hb, heme, iron) — damage surrounding brain tissue

60
Q

blood can also leak into the ventricular system following a haemorrhage, causing what?

A

acute hydrocephalus

61
Q

what is herniation?

A

when the brain is compressed against fixed tissue compartments of the skull

62
Q

what are symptoms of a transient ischaemic attack?

A
  • weakness, numbness or paralysis in face, arm or leg, typically on one side of the body
  • slurred or garbled speech or difficulty understanding others
  • blindness in one or both eyes or double vision
  • vertigo or loss of balance or coordination
63
Q

what is a sub dural haematoma (SDH)?

A

accumulation of blood in sub dural space following rupture of a vein

64
Q

what are the risk factors for stroke?

A
  • untreated hypertension — damage to arterial walls
  • atrial fibrillation — increases likelihood of thrombus formation due to turbulent blood flow
  • smoking — increases BP and damages arterial walls making them more vulnerable to atherosclerotic plaques
  • diet — high cholesterol, salt, fat
  • diabetes
  • existing ischaemic heart disease
  • age — atherosclerosis increases with age and arteries become stiffer
  • gender — men at greater risk
  • family history — eg high BP and diabetes
  • heaving drinking — increases BP
  • rates higher in asian and black african populations than in caucasians
65
Q

what is the result of an infarct in the ophthalmic artery?

A

amaurosis fugax = temporary loss of vision in one or both eyes dye to a lack of blood flow to the retina

66
Q

a blockage in where causes contralateral face-arm or face-arm-leg weakness, contralateral sensory changes, contralateral visual field defects, aphasia and neglect?

A

MCA

67
Q

what is neglect?

A
  • usually caused by large strokes in MCA territory
  • when the brain doesnt receive info from one side of the body
68
Q

an infarct in what causes contralateral leg weakness?

A

ACA

69
Q

the severity of carotid stenosis can be estimated with what?

A

Doppler ultrasound and magnetic resonance angiography (MRA)

doppler : a stethoscope, placed just below the angle of the jaw, will pick up a whooshing sound (bruit)

70
Q

what is the treatment for carotid stenosis?

A

carotid endarterectomy = a surgical procedure to remove the build up of plaque causing a narrowing in a carotid artery

71
Q

what is the purpose of investigations in stroke?

A
  • confirm the clinical diagnosis and distinguish between haemorrhage and thromboembolic infarction
  • look for underlying causes and to direct therapy
  • to exclude other causes eg. tumour
  • source of embolus should be sought (eg.carotid bruit)
72
Q

infarctions always show up as what shape on both CT and MRI?

A

wedge shaped

73
Q

how does a haemorrhage appear on CT? does this change with time?

A

white — the longer it has been present the darker it becomes

74
Q

how can you roughly estimate the length of time the haemorrhage has been present with a CT scan?

A
  • by the density of blood on the scan
  • the longer blood is present, the more of its products are broken down and removed, and thus density is reduced
  • macrophages in particular will break down blood products
75
Q

what kind of scans detect abnormalities much earlier than on normal CT and MRI (esp infarctions) and why?

A

—> diffusion MRI scans
- exploits the fact that damaged cells fill with water and thus contain more water than normal cells in the early stages of damage

76
Q

a level over what detected with a carotid doppler scan usually requires a carotid endarterectomy to reduce future stroke risk?

A

> 60%

77
Q

how is ECG used in stroke?

A

check for AF and for any abnormal heart ischaemic disorders

78
Q

what is a key characterstic on an ECG for atrial fibrillation?

A

no p waves

79
Q

when measuring brachial BP on both sides, a difference of >20mmHg indicates what?

A

subclavian artery stenosis

80
Q

describe the NIH stroke scale

A
  • national institute of health stroke scale
  • 11 items, each with a potential score of 0-4
  • higher score = higher level of impairment
  • individual scores are summed up to a total score. maximum score is 42 and minimum is 0
  • 0 = no stroke symptoms
  • 1-4 = minor stroke
  • 5-15 = moderate stroke
  • 16-20 = moderate to severe stroke
  • 21-42 = severe stroke
81
Q

describe the Glasgow coma scale

A
  • assesses level of consciousness
  • patient given a score between 3 (indicating deep unconsciousness) and either 14 (original scale) or 15 (the more widely used modified or revised scale)

3 = coma/dead
15 = fully conscious

82
Q

describe the MRC scale for muscle strength

A
  • patient’s effort is graded on a scale of 0-5:
    > grade 5 = muscle contracts normally against full resistance
    > grade 4 = muscle strength is reduced but muscle contraction can still move joint against resistance
    > grade 3 = muscle strength is further reduced such that the joint can be moved only against gravity with the examiner’s resistance completely removed. eg. the elbow can be moved from full extension to full flexion starting with the arm hanging down at the side
    > grade 2 = muscle can move only if the resistance of gravity is removed. eg. the elbow can be fully flexed only if the arm is in the horizontal plane
    > grade 1 = only a trace or flicker of movement is seen or felt in the muscle or fasciculations are observed in the muscle
    > grade 0 = no movement is observed
83
Q

UMN lesion symptoms

A
  • hypertonia
  • no change in muscle mass
  • no fasciculations
  • hyperreflexia
  • normal nerve conduction
  • +ve babinski
  • pseudobulbar palsy
84
Q

LMN lesion symptoms

A
  • hypotonia
  • muscle wasting
  • fasciculations
  • hyporeflexia / areflexia
  • abnormal nerve conduction
  • no babinski sign
  • bulbar palsy
  • sensations remain intact
85
Q

pseudobulbar palsy vs bulbar palsy

A
  • bulbar = LMN lesion of CNs IX, X and XII
  • pseudobulbar = UMN lesion of CNs IX, X and XII — corticobulbar tracts affected — bilateral tract damage must occur for clinically evident disease as the muscels are bilaterally innervated
86
Q

why is there a hypertonia in UMN lesion?

A

increase in alpha motor neurone firing

— inhibitory medially reticulospinal nuclei lost so therefore there is more activation of LMNs

87
Q

why do you get hyperreflexia in UMN lesion?

A

increase in gamma motor neurone firing — increased sensitivity of muscle spindles — more stretch reflex

88
Q

spasticity vs rigidity

A
  • spasticity = velocity dependent and is only resistant in one direction
  • rigidity = seen in parkinson’s disease — not velocity or direction dependent
89
Q

intrafusal vs extrafusal fibre innervation

A

intrafusal = yMN
extrafusal = aMN

90
Q

what type of paralysis is seen in UMN and LMN?

A

UMN = spastic paralysis
LMN = flaccid paralysis

91
Q

why do you get hypo/areflexia in LMN lesion?

A

decrease in gamma MN firing — decreased sensitivity of muscle spindles — decreased stretch reflex activity

92
Q

how does aspirin work? how is it used in stroke?

A
  • inhibits cyclo-oxygenase, which converts arachidonic acid to prostaglandins and thromboxanes
  • thromboxane, under normal circumstances, binds platelet molecules together to create a patch over damaged walls of blood vessels. this platelet clump can become too large and block blood flow
  • aspirin, an anti-thrombotic drug, is an immediate treatment after an ischaemic stroke to reduce the likelihood of having another stroke
93
Q

what is aspirin contraindicated in?

A

asthma

94
Q

how does diazepam work? side effects?

A
  • acts on GABA (A) receptor
  • allosteric modulator at GABA receptors
  • GABA binds between a and b subunits causing Cl- to flow into neurone and hypoerpolarise cell — major inhibitory neurotransmitter
  • diazepam binds at separate site between a and y subunits — this potentiates the action of GABA and increases Cl- influx
  • eases anxiety within 0.5-1 hours
  • side effects: sedation, respiratory depression, tolerance, dependence, impaired cognition
  • shouldn’t be prescribed for more than 4 weeks
95
Q

describe SSRIs

A

= 1st line drug
- block serotonin (5-HT) reuptake from synapse
- increases amount of 5-HT in synaptic cleft
- not addictive, may take 1-2 weeks to start working, effective in 70% of cases
- eg. escitalopram, paroxetine, sertaline
- common side effects : nausea, dry mouth, low sex drive, blurred vision, dizziness, loss of appetite, insomnia, sweating

96
Q

describe statins

A
  • eg. atorvastatin
  • competitively inhibit HMG-CoA reductase = rate limiting enzyme in the production of cholesterol in the liver
  • reduces liver production of cholesterol —> leads to more LDL receptors
  • increased removal of LDL from plasma
  • also increase HDL and lower triglycerides
  • side effects: myosotis, rhabdomyolysis (rapid breakdown of skeletal muscle — causes dark coloured urine — myoglobin released from muscle and ends up in urine — toxic for kidneys — kidney failure), altered liver function tests, complications are rare but lots of people are taking them
97
Q

what is the main trigger factor for angiogenesis?

A

vascular endothelial growth factor (VEGF)

98
Q

what is neuroplasticity?

A

the ability of the brain to modify its own structure and function following changes within the body or in the external environment

99
Q

when can someone start driving after having a stroke?

A
  • valid driving license — must wait a month after a stroke or TIA. can then start driving again if doctor is happy with the patient’s recovery
100
Q

which of the following is not a stroke symptom?

  • exaggerated Babinski reflex
  • loss of motor function
  • shortness of breath
  • slurred speech
  • sudden onset hearing-loss
A

SOB

101
Q

describe lenticulostriate arteries

A
  • arise from the initial portions of the middle cerebral artery before it enters the Sylvian fissure
  • supply large regions of basal ganglia and internal capsule
102
Q

describe anterior choroidal artery

A
  • arises from the internal carotid artery
  • its territory includes portions of the globus pallidus, putamen, thalamus, and the posterior limb of the internal capsule
103
Q

describe the recurrent artery of Heubner

A
  • arises from the initial portion of the anterior cerebral artery to supply portions of the head of the caudate, anterior putamen, globus pallidus, and internal capsule
104
Q

what is vagus nerve simulation used to treat?

A

epilepsy, depression and pain

105
Q

why is the right vagus nerve not used in vagus nerve stimulation?

A

more likely to carry fibres that supply nerves to the heart

106
Q

which neurotransmitter transmits nerve impulses from upper to lower motor neurons?

A

glutamate

107
Q

which descending spinal tract is responsible for control of facial and jaw musculature, swallowing and tongue movements?

A

corticobulbar

108
Q

which descending spinal tract is responsible for fine voluntary motor control of the limbs?

A

corticospinal

109
Q

which descending spinal tract is responsible for adjusting posture to maintain balance?

A

vestibulospinal

110
Q

which descending tract is responsible for involuntary adjustment of head position in response to visual information?

A

colliculospinal

111
Q

what is difficulty comprehending and using language known as?

A

aphasia

112
Q

what is the greatest risk factor for stroke?

A

hypertension

113
Q

which scan is most commonly used to differentiate between an ischaemic and haemorrhagic stroke?

A

CT

PBL SEM 3 (49 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions