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Phase 2a > Neurology > Flashcards

Neurology Flashcards

1
Q

What do the ascending tracts do?

A

Carry sensory information from the body, up SC to the brain

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2
Q

What are the ascending tracts?

A

Dorsal column-medial lemniscus and spinothalamic

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3
Q

What does the dorsal column-medial lemniscus tract do?

A

Carries info about vibration, proprioception, fine touch

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4
Q

What does the spinothalamic tract do?

A

Carries info about crude touch, pain, temperature and pressure

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5
Q

What do the descending tracts do?

A

Carry motor info from the brain to the body

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6
Q

What are the descending tracts made up of?

A

UMNs and LMNs

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7
Q

What are the 2 types of descending tracts?

A

Pyramidal and extra-pyramidal

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8
Q

What do pyramidal tracts do?

A

Control fine, voluntary muscle movements

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9
Q

What are the 2 types of pyramidal tracts?

A

Anterior corticospinal and lateral corticospinal

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10
Q

What do the anterior corticospinal tracts do?

A

Control muscles of the trunk

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11
Q

What do the lateral corticospinal tracts do?

A

Control muscles of the extremities

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12
Q

What do the extra-pyramidal tracts do?

A

Control larger muscles for balance, posture, coordination

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13
Q

Name a condition that shows both UMN and LMN signs.

A

MND

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14
Q

What do UMNs do?

A

Transmit info from brain to brainstem/spinal cord

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15
Q

What do LMNs do?

A

Transmit info from brainstem/spinal cord to skeletal muscles

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16
Q

What are the UMN signs?

A

Hypertonia - spastic paralysis
Brisk reflexes - hyperreflexia
+ve Babinski’s sign

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17
Q

What causes UMN signs?

A

Any damage to brain/brainstem/white matter of spinal cord

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18
Q

Give some examples of conditions which present with UMN signs.

A

Stroke, infection, tumour

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19
Q

What are the LMN signs?

A

Hypotonia - flaccid paralysis
Reduced/absent tendon reflexes
Muscle wasting
Fasciculations

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20
Q

What causes LMN signs?

A

Any damage to axons leaving the spinal cord or the anterior horn of the spinal cord

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21
Q

Give some examples of conditions which present with LMN signs.

A

Peripheral neuropathy, spinal cord injury

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22
Q

What are the 2 types of stroke?

A

Haemorrhagic and ischaemic

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23
Q

What percentage of strokes are haemorrhagic?

A

20%

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24
Q

What percentage of strokes are ischaemic?

A

80%

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25
Q

What conditions are classed as ischaemic events?

A

TIAs and ischaemic strokes

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26
Q

What conditions are classed as strokes?

A

Ischaemic stroke, intracerebral haemorrhage and subarachnoid haemorrhage

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27
Q

What conditions are classed as haemorrhagic events?

A

Intracerebral haemorrhage
Subarachnoid haemorrhage
Subdural haematoma
Extradural haematoma

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28
Q

What are the risk factors for ischaemic stroke?

A

Alcohol
Obesity
AF
Carotid stenosis
Other CVS disease
CVS risk factors

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29
Q

What CVS risk factors predispose you to ischaemic stroke?

A

HTN, smoking, diabetes, hypercholesterolaemia

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30
Q

Why is AF a risk factor for ischaemic stroke?

A

Stasis of blood in poorly contracting atria = thrombus formation

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31
Q

What CVS diseases predispose you to ischaemic stroke?

A

Valvular disease, angina, previous MI, PVD

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32
Q

What arteries can be affected in an anterior circulation stroke?

A

Anterior cerebral and middle cerebral arteries

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33
Q

The area of the somatosensory cortex supplied by the ACA is responsible for which parts of the body?

A

Genitals
Hip
Trunk
Neck
Head
Lower limbs

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34
Q

The area of the somatosensory cortex supplied by the MCA is responsible for which parts of the body?

A

Entire arms
Eyes
Nose
Face
Mouth
Pharynx

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35
Q

How does an ACA occlusion stroke present?

A

Contralateral hemiparesis
Sensory loss in lower limbs
Executive dysfunction + emotional disturbance
Akinetic mutism

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36
Q

How does an MCA occlusion present?

A

Contralateral hemiparesis
Sensory loss of face + upper limb
Legs usually spared
Affects language centres if occlusion is in dominant hemisphere = dysphasia and aphasia
Contralateral homonymous hemianopia

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37
Q

How does executive dysfunction present?

A

Apathy, reduced concentration, impulsivity

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38
Q

How does akinetic mutism present?

A

Drowsy and reduced spontaneous speech (lack of movement and speech)

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39
Q

What are the language centres of the brain?

A

Wernicke’s and Broca’s areas

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40
Q

What is contralateral homonymous hemianopia?

A

(This would be an occlusion in the right hemisphere)

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41
Q

What is contralateral hemiparesis?

A

Paralysis on the opposite side of the body to the site of the occlusion

42
Q

What are fasciculations?

A

Twitches

43
Q

What is Babinski’s sign?

A
44
Q

What causes dysarthria?

A

Damage to motor speech pathway

45
Q

What conditions might cause dysarthria?

A

Stroke, tumour, MS

46
Q

What is dysarthria?

A

Slurred speech/difficulty pronouncing words so patient sounds drunk

47
Q

What is dysphasia?

A

Inability to understand or compose language

48
Q

What area is damaged in expressive dysphasia?

A

Broca’s area

49
Q

What lobe is damaged in expressive dysphagia?

A

Dominant frontal lobe

50
Q

How does expressive dysphagia present?

A

Can’t generate language - can understand what is said to them but have difficulty getting words out

51
Q

What area is damaged in receptive dysphagia?

A

Wernicke’s area

52
Q

What lobe is damaged in receptive dysphagia?

A

Dominant temporal lobe

53
Q

How does receptive dysphagia present?

A

Little/no understanding of spoken/written language - can speak fluently but usually makes no sense

54
Q

Where are the language centres found?

A

Dominant lobe

55
Q

How do you know which lobe is dominant?

A

Right handed = left lobe dominant

56
Q

What are the 2 types of dysphagia?

A

Expressive and receptive

57
Q

What vessels are involved in a posterior circulation stroke?

A

Basilar and vertebral arteries

58
Q

What areas do the basilar and vertebral arteries supply?

A

Occipital lobe, cerebellum, hippocampus, brainstem etc.

59
Q

What does a PCA stroke affecting the occipital lobe present with?

A

Contralateral homonymous hemianopia, cortical blindness

60
Q

What does a PCA stroke affecting the cerebellum present with?

A

Ataxia, nystagmus, N+V, dysarthria

61
Q

What does a PCA stroke affecting the brainstem present as?

A

CN palsies causing diplopia, facial sensory loss/weakness, dysphagia etc.

62
Q

What are lacunar strokes?

A

Small strokes due to blockages in small arteries supplying deep brain structures

63
Q

What structures might be affected by lacunar strokes?

A

Thalamus, pons etc.

64
Q

How do lacunar strokes present?

A

Cortical function is preserved

Could be purely motor, purely sensory or sensorimotor symptoms

65
Q

What are the purely motor symptoms of a lacunar stroke?

A

Weakness in contralateral arm, leg, face

66
Q

What are the purely sensory symptoms in a lacunar stroke?

A

Sudden paraesthesia in contralateral arm, leg, face

67
Q

What are the sensorimotor symptoms of a lacunar stroke?

A

Ataxia, dysarthria, clumsy hands

68
Q

What is the first line investigation for a suspected stroke? Why?

A

Immediate non-contrast CT head to rule out haemorrhage

69
Q

Why does a haemorrhage need to be ruled out for a suspected stroke?

A

Thrombolysis dissolves the clot so can cause bleeding, which is very dangerous to give to a patient with a haemorrhage

70
Q

What does an infarct look like on CT?

A

Hypodense (dark) area

71
Q

What are the 2nd line investigations for a suspected stroke?

A

Bloods - look for underlying cause/RFs

ECG - look for AF

Carotid doppler - look for carotid stenosis

CT angiography - find cause

MRI later if CT didn’t show infarct and still suspected

72
Q

What is the 1st line immediate management for an ischaemic stroke?

A

Thrombolysis with alteplase

73
Q

When must alteplase be given for a stroke?

A

Within 4.5 hours of onset of symptoms and after a haemorrhage is excluded

74
Q

What are the contraindications to thrombolysis?

A

Haemorrhage

On anticoagulants

>4.5 hours after onset of symptoms (or unknown onset time)

Recent surgery or GI bleed

Active cancer

HTN cut off = 185/110

75
Q

What 1st line treatment is given for ischaemic stroke if thrombolysis is contraindicated?

A

Thrombectomy

76
Q

What is the second line treatment for ischaemic stroke?

A

300mg aspirin for 2 weeks/until discharge

77
Q

What is the long-term management of an ischaemic stroke?

A

Clopidogrel 75mg daily (antiplatelet) after 2 weeks of aspirin

Treat modifiable risk factors

If patient has carotid artery disease, consider for carotid endarterectomy within 2 weeks

78
Q

Give some examples of modifiable risk factors can be treated after a stroke.

A

Manage BP and diabetes

Monitor cholesterol levels - start statins

Smoking cessation, diet, exercise, weight loss

Investigate for AF - consider need for anticoagulants e.g. warfarin

79
Q

What supportive management is provided after a stroke?

A

Admit patient and must be seen by specialist within 24 hrs

BP control - keep high

O2 and glucose levels

Swallow assessment - NBM/NG tube and nutrition

Mobilise ASAP - physio and OT input

No driving for 1 month after stroke/longer if symptoms ongoing

80
Q

Why must BP be kept high immediatley after a stroke?

A

A small fall can massively reduce cerebral perfusion

81
Q

What 2 scores would we consider before starting anticoagulants in a patient with AF?

A

CHADSVASc – risk of stroke in a patient with AF

HASBLED – risk of bleeding in a patient with AF

82
Q

What is a transient ischaemic attack (TIA)?

A

Transient neurological dysfunction

83
Q

What causes a TIA?

A

Ischaemia without infarction

84
Q

How does a TIA present?

A

Presents similarly to an ischaemic stroke

Sudden loss of function for a few mins to 24 hours with complete recovery

85
Q

What is the immediate management of a TIA?

A

None

86
Q

What is the long-term management of a TIA?

A

Long-term same as stroke

300mg aspirin

Secondary prevention for CVD

Long-term clopidogrel and physio

87
Q

What is amaurosis fugax?

A

Sudden transient loss of vision in one eye like ‘a curtain coming down’

88
Q

What causes amaurosis fugax?

A

Occlusion of retinal artery

89
Q

What risk score predicts the risk of a stroke after a TIA?

A

ABCD2 score - determines management/time to see a specialist

90
Q

What is the ABCD2 score?

A

Age > 60 = 1

Blood pressure > 140/90mmHg = 1

Clinical features:

Unilateral weakness = 2

Speech disturbance without weakness = 1

Duration of symptoms:

Symptoms lasting more than 1 hour = 2

Symptoms lasting 10-59 mins = 1

Diabetes = 1

91
Q

What is a subarachnoid haemorrhage?

A

Bleeding into the subarachnoid space between arachnoid and pia mater

92
Q

What are the risk factors for SAH?

A

HTN

Smoking

XS alcohol

Cocaine

FHx

93
Q

What diseases is SAH associated with?

A

Autosomal dominant PKD

Sickle cell anaemia

Connective tissue disorders

94
Q

What causes a SAH?

A

Rupture of berry aneurysm (most common)

Arteriovenous malformation

95
Q

How does an SAH present?

A

Sudden onset ‘worst ever’ thunderclap occipital headache

Neck stiffness

Photophobia

N+V

May have signs of raised ICP - reduced consciousness

96
Q

What investigations are done for an SAH?

A

Immediate CT head

LP 12 hours after onset of symptoms if CT doesn’t confirm SAH

CT angiography once confirmed to show source of bleeding

97
Q

What would an LP show 12 hours after the onset of symptoms of an SAH?

A

Xanthochromia - yellow CSF due to presence of bilirubin (breakdown of haem)

98
Q

What does an SAH look like on CT?

A

Blood is white (hyperdense) on CT - blood in subarachnoid space, sometimes looks like a star as it fills all the sulci

99
Q

How is SAH managed?

A

ABCDE management + rapid BP lowering

Monitor GCS

Surgical = coiling or clipping

Treat complications e.g. nimodipine (CCB for vasospasm)

100
Q

What are the complications of SAH?

A

High mortality

Rebleeding

Vasospasm which can lead to ischaemia

Seizures

Hydrocephalus

Phase 2a (25 decks)

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