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Year 5 Medicine for Finals > Neurology > Flashcards

Neurology Flashcards

1
Q

What is the pyramidal pattern of weakness?

A

What you see is what is strong.
Upper limb flexion is stronger than extension - so the arm is flexed in towards the body.
Lower limb extension is stronger than flexion - so the knee is extended, there is plantar flexion and foot inversion.

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2
Q

Which brachial plexus nerve root is involved in shoulder abduction and adduction?

A

C5 - deltoid

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3
Q

Which brachial plexus nerve root does elbow flexion and extension?

A

C6 - brachioradialis

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4
Q

Which nerve root does wrist extension and flexion (dorsiflexion and palmar flexion)?

A

C7 - wrist extensors - radial nerve

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5
Q

Which nerve root is involved in finger extension?

A

C8 - long extensors

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6
Q

Which nerve root is involved in finger abduction?

A

T1 - small muscles

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7
Q

High BROWS is a mnemonic to remember the contraindications for thrombolysis, what are they?

A 
High BP <140
Bleeding
Recent surgery
Over 80
Woke with symptoms (don't know time of onset) 
Stroke in the last 3 months
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8
Q

What is the significance of someone doing a pincer grip which forms an O or oval shape, rather than a triangle?

A

It can signify an ulnar nerve palsy

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9
Q

What are the causes of a positive prayer sign?

A
  1. Rheumatoid arthritis
  2. Carpal tunnel syndrome
  3. Scleroderma
  4. Dupuytren’s contracture
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10
Q

What are the causes of a peripheral neuropathy?

A 
A - alcohol
B - B12 deficiency
C - CKD
D - diabetes, drugs 
E - every vasculitis
\+ cancer, Lyme disease and Charcot-Marie- Tooth
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11
Q

What is Charcot-Marie-Tooth?

A

It is an inherited (most common is autosomal dominant but also has autosomal recessive modes) peripheral neuropathy, typically involving distal limb muscle waiting and sensory loss, with proximal progression over time. It is due to demyelination leading to uniform slowing of conduction velocity.

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12
Q

By what age is the slow onset of Charcot-Marie-Tooth?

A

10 years of age - muscle weakness and wasting from the feet, and gradually affecting the lower leg. It can lead to the classic ‘inverted champagne bottle’ of the legs.

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13
Q

What are the differentials for Charcot MT?

A
  1. Friedreich’s ataxia
  2. Acquired neuropathies e.g. B12 deficiency, diabetes
  3. Vasculitis
  4. Amyloidosis
  5. MND
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14
Q

What tests can be done to exclude some causes of neuropathy and investigate peripheral neuropathies?

A
  1. FBC - anaemia
  2. TFTs
  3. LFTs
  4. Vit B12
  5. Folate
  6. Antinuclear antibodies
  7. Serum and urine protein electrophoresis
  8. CSF
  9. Muscle biopsy
  10. MRI of the brain and spinal cord
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15
Q

Over 50% of patients with Charcot MT develop foot and ankle problems, which one is by far the most common?

A

Cavovarus deformity - it develops as a flexible deformity but becomes fixed by adulthood.

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16
Q

What is the treatment for cavovarus deformity?

A

Soft tissue surgery - plantar fasciotomy, tendon transfers

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17
Q

What are the cerebellar signs and what mnemonic is helped to remember them?

A 
DANISH
D - dysdiadokokinesis 
A - ataxia
N - nystagmus
I - intention tremor
S - slurred speech
H - hypotonia
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18
Q

How can you test for cerebellar speech?

A

Ask the patient to say one of the following:

  • West Register Street, Edinburgh
  • Baby hippopotamus
  • British constitution
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19
Q

What two conditions in particular do you want to exclude in someone presenting with features of a stroke?

A
  1. Hypoglycaemia

2. SAH (CT angio +/- LP)

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20
Q

While awaiting an urgent CT head, what can be done to manage someone presenting with a stroke (in which hypoglycaemia has been excluded)? (5)

A

Assess and treat:

  1. Fever
  2. Sugar (4-11mmol/l)
  3. Swallowing
  4. Bloods - including PT, APTT
  5. ECG - AF and LV+
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21
Q

What is given to all patients with a confirmed ischaemic stroke?

A

300mg aspirin

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22
Q

Why is someone with an ischaemic stroke meant to have a CT scan 24 hours after the first one?

A

Incase there is haemorrhage transformation

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23
Q

When is thrombolysis indicated for someone presenting with a stroke?

A

Proven ischaemic stroke within 4.5 hours of onset of symptoms, without any contraindications for thrombolysis e.g. age over 80, recent surgery, hypertension (all the high BROWS).

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24
Q

If someone presents with a stroke and it is found to be haemorrhagic (10%), what is the management?

A
  1. Reverse anticoagulation
  2. Restore BP homeostasis
  3. If required - vitamin K and prothrombin complex
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25
Q

What is the typical anti platelet regimen for someone with an ischaemic stroke?

A

Aspirin 300mg daily for 2 weeks then switch to clopidogrel for maintenance at 75mg daily
(alternatives for clopidogrel include aspirin or dipyramidamole 200mg BD)

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26
Q

If a patient who has had an ischaemic stroke also has long-term AF, what is the management?

A

After two weeks of aspirin 300mg daily, consider anticoagulation instead of anti platelet therapy

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27
Q

NICE 2019 guidelines for a large vessel clot indicate mechanical thrombectomy when?

A

If the clot in the large vessel has a limited infarct volume, offer mechanical thrombectomy up to 6 hours

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28
Q

What is the rationale for thrombolysis?

A

Salvaging the ischaemic penumbra - so limit the infarct site

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29
Q

What is the rationale for blood pressure treatment in haemorrhage stroke?

A

Intracerebral haemorrhage –> autonomic dysfunction –> hypertension –> haematoma expansion –> worse outcomes

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30
Q

What are the features of carpal tunnel syndrome? (5)

A
  1. Arm pain and hand tingling
  2. Often worse at night
  3. Most commonly idiopathic in middle aged women
  4. Tinels and Phalens test
  5. Motor sign: weakness and wasting of abductor pollicis brevis
31
Q

The mnemonic RAPID TTT can be used to remember the causes of carpal tunnel…apparently. So what are the causes of carpal tunnel?

A 
R - rheumatoid arthritis
A - acromegaly
P - pregnancy
I - idiopathic 
D - diabetes
T - trauma
T - tendons (tendonsynovitis of flexor tendons) 
T - thyroid - hypothyroid
32
Q

What are the four signs of an ulnar nerve palsy? (4)

A
  1. Weakness of pincer grip - forms an O not a triangle
  2. Sensory loss over 5th finger and the ulnar half of the 4th finger
  3. Weakness and wasting of the first dorsal interosseous
  4. Partial claw hand (weakness of medical lumbricals)
33
Q

How do you test the upper limb roots in terms of movement against resistance?

A 
C5 = chicken arms
C6 = ski poles 
C7 = wrists cocked back in a fist 
C8 = flat hand wrist cocked back 
T1 = fingers splayed
34
Q

According to NICE guidelines 2019, what is the management for a TIA - after initial clinical assessment to confirm most likely a TIA (i.e. no residual loss of function)

A
  1. Aspirin 300mg stat + specialist assessment within 24 hours
  2. No driving for one month
  3. Urgent carotid imaging
  4. > 50% stenosis = endarterectomy
  5. <50% stenosis = best medical treatment e.g. antiplatelet usually clopidogrel and lifestyle management e.g. BP
  6. No CT head unless on anticoagulants
  7. Do not used ABCD risk stratification
35
Q

How is stroke defined?

A

A sudden neurological event of vascular origin, but excluding SAH, that lasts more than 24 hours.

36
Q

What are the two classifications used in the oxford classification of strokes - based on clinical impressions?

A

They are either ‘syndromes’ or ‘infarcts’ e.g. TACI or TACS There are two important distinctions:

  1. Site of lesion - anterior or posterior circulation
  2. Whether the lesion is due to a major vessel thrombosis or to occlusion of a deep perforating artery, affecting the thalamus, internal capsule or corona radiata. These lesions are more localised ‘lakes’ of infarcted brain and are called lacunes or lacunar infarcts.
37
Q

1 in how many people will have a recurrent stroke within a year?

A

1 in 6

38
Q

What is the overall risk of death within a year of having a stroke?

A

1 in 4, and then 2 of those 4 will be dependent living and 1 in 4 independent.

39
Q

What are the 4 main subtypes of stroke?

A
  1. TACI
  2. PACI
  3. POCI
  4. LACI
40
Q

What is a TACI? (3 features all present)

A

Total anterior circulation infarct - this has the highest mortality (60%) and a very poor change of making a good recovery.
Comprises of three features, all of which are present:
1. Contralateral hemiparesis (usually severe)
2. Contralateral homonymous hemianopia
3. High cortical dysfunction (dysphasia or dyspraxia or inattention)

41
Q

What is a PACI?

A

Partical anterior circulation infarct - two of the three features of TACI present, typically includes:

  1. High cortical dysfunction and
  2. Contralateral weakness or sensory loss
    - the deficit is often incomplete, e.g. face and arm or arm and leg
42
Q

What is a POCI and what are the features?

A

Posterior circulation infarct

  • high risk of late recurrence (1 in 5 within a year)
  • any of the three main possibilities:
    1. Contralateral homonymous hemianopia OR
    2. Cerebellar signs OR
    3. Brainstem signs (e.g. Horner’s or conjugate gaze palsy or ipsilateral cranial nerve lesion with contralateral hemiparesis)
43
Q

What is a LACI, and what are the features that should be absent?

A

Lacunar infarct
Four features are ABSENT
1. No high cortical dysfunction as cortex not affected
2. No homonymous hemianopia as lesion away from optic radiation
3. No drowsiness
4. No brainstem signs

44
Q

What are the different type of lacunar syndrome? (5)

A
  1. Pure motor stroke (posterior limb of internal capsule)
  2. Pure sensory stroke (posterior thalamus)
  3. Sensorimotor stroke (internal capsule)
  4. Dysarthria-clumsy hand syndrome (middle of internal capsule)
  5. Contralateral hemiballismus (rare-subthalamic nucleus infarct)
45
Q

When examining the eyes - if a central scotoma is identified, what does this indicate in terms of the optic nerve?

A

Demyelination of the optic nerve - they will also have red colour desaturation

46
Q

On examination of the eyes, what do you need to do? (6)

A
  1. Inspection - squint, pupils, trauma
  2. Visual acuity
  3. Fields
  4. External ocular movements
  5. Fundi
  6. Pupils
47
Q

What are the causes of optic neuropathy? (6)

A
  1. Demyelination (optic neuritis)
  2. Trauma
  3. Compression e.g. pituitary tumour
  4. Ischaemic - diabetes and cranial arteritis (GCA)
  5. Toxic e.g. methanol, ethambutol
  6. Secondary to papilloedema e.g. essential intracranial hypertension
48
Q

What are the signs of optic neuropathy? (5)

A
  1. Pale disc (optic atrophy)
  2. Loss of visual acuity
  3. Loss of red colour vision
  4. Central scotoma
  5. Afferent pupillary defect
49
Q

In an upper motor neurone palsy e.g. stroke, why is there sparing of the upper part of the face? (forehead sparing)

A

Because there is bilateral cortical representation of the upper part of the face (there is upper motor neurone input from both cerebral hemispheres)
AVOID THE WORD ‘INNERVATION’

50
Q

What is the management for Bells palsy according to NICE guidelines? (5)

A
  1. Eye drops during the day, eye ointment at night
  2. Microporous tape at night to close eyelid
  3. High dose steroids if seen within 72 hours (e.g. prednisolone 60mg daily for 5 days then reduce)
  4. Do not use antivirals
  5. If residual weakness after 6 months, consider referral to plastics
51
Q

Parkinsons disease has a quadrad of clinical features (previously was triad), what is it?

A
  1. Tremor
  2. Rigidity
  3. Bradykinesia
  4. Loss of postural reflexes (falling over)
52
Q

What questions are important to ask in Parkinson’s history? (6)

A
  1. ADLs
  2. Depression
  3. Handwriting - micrographia
  4. Buttons and shoe laces?
  5. Turning over in bed at night?
  6. Getting in and out of car?
53
Q

How can you assess for unilateral internuclear ophthalmoplegia?

A

The link between abduction and adduction of the eye is the medial longitudinal bundle. So, asking someone to look left, both eyes should move left - one is abducting na the other is adducting - the abducting eye will show nystagmus (this is the ok eye) but the adducting eye will not be able to move nasally. - there is failure of adduction on the side of the lesion. The nystagmus occurs as the brain is trying to make images line up.

54
Q

Why does internuclear ophthalmoplegia occur?

A

When there is demyelination - most commonly in MS, but also could be alcohol - wernicke’s encephalopathy.

55
Q

Why is the pupil so often spared in diabetes?

A

The parasympathetic fibres have a separate blood supply derived from the nerve sheath vessels

56
Q

What are the clinical features of Horner’s syndrome? (5)

A
  1. Slight ptosis
  2. Constricted pupil
  3. Reduced sweating over forehead (anhydrosis)
  4. Eye may be slightly bloodshot early on
  5. Loss of alpha vasoconstrictor tone
57
Q

The 6th nerve (abducens) controls which eye muscle/movement?

A

Lateral rectus muscle

58
Q

The 4th nerve trochlear controls which eye muscle?

A

Superior oblique

59
Q

When are dopamine agonists used rather than L dopa and a dopa-decarboxylase inhibitor? (because the latter combo are known to be more effective)

A

They are sometimes used in young patients as they cause fewer motor complications.

60
Q

What are the common side effects of dopamine agonists?

A
  1. Sleepiness
  2. Hallucinations - typically visual
  3. Impulse control disorders - gambling, hyper sexuality, binge eating, obsessive shopping
61
Q

What is the mainstay of treatment for Parkinson’s disease?

A

L dopa and dopa decarboxylase inhibitor - this combination is most effective for bradykinesia and rigidity, and are less effective for tremor. There is a finite window of benefit (5 years), so it is best they are used at the right time - delay use until real functional disability occurs.

62
Q

When are COMT inhibitors used?

A

These inhibit breakdown of dopamine and are used in later PD, particularly when the end-of-dose effect is a problem

63
Q

What is multiple sclerosis (MS)?

A

It is a disease of unknown aetiology characterised by episodes of focal neurological deficit disseminated in space and time.

64
Q

What are the possibly mechanisms to cause MS (immunopathology)? (5)

A
  1. Probably autoimmune once triggered
  2. Antigens include: myelin basic protein and myelin oligodendrocyte glycoprotein
  3. Initial attack by virus leads to inflammation of the blood brain barrier
  4. This allows B cells and T cells to cross from the periphery into the brain
  5. This leads to direct damage to axons and indirect damage too (demyelination - due to damage to myelin producing oligodendrocytes)
65
Q

What are the main clinical types of MS, defined by the course of the illness? (4)

A
  1. Relapsing remitting (RRMS 80%)
  2. Primary progressive (PPMS 10%)
  3. Benign (10%)
  4. Secondary progressive
66
Q

What is the most common course of MS?

A

Relapsing remitting - whereby people experience acute attacks of neurological deficit with incomplete recovery each time. Usually after about 10 years they enter a phase of secondary progressive MS, whereby their functional status steadily declines without major acute new lesions.

67
Q

What are the main aims of disease modifying therapy in MS?

A

To reduce the number of acute attacks and delay the transition from relapsing remitting to secondary progressive

68
Q

Other than DMARDs, what other treatments can be used in MS, and when are they most effective?

A

Biologics are also increasingly being used as can reduce the number of relapses, however they are not helpful in people with progressive disease

69
Q

What are the presenting symptoms of MS?

A
  1. Sensory 40%
  2. Optic neuritis 20%
  3. Cerebellar/vertigo 20%
  4. Internuclear ophthalmoplegia (10%)
  5. Motor: usually spastic paraparesis (10%)
70
Q

What is the differential diagnosis for adult onset spastic paraparesis?

A
  1. Multiple sclerosis
  2. Amyotrophic lateral sclerosis
  3. Transverse myelitis
  4. Spinal cord compression/trauma
  5. Intramedullary structural lesions
  6. Cervical myelopathy
  7. Spinocerebellar degeneration
  8. B12 deficiency
  9. Luetic disease (syphilis) and HIV
71
Q

What are the indications for disease modifying therapies in MS? (3)

A
  1. Ambulant patient with RRMS
  2. > 2 relapses in 2 years
  3. Or one relapse plus radiological progression
72
Q

What are ‘category 1 drugs’ in treating MS?

A
  1. Beta interferon and glutarmir (given IV)
  2. Fingolimod and dimethylfumarate (PO)
    - 30% reduction in relapse rate using these
73
Q

What are the ‘category 2’ drugs in treating MS?

A
  1. Alemtuzumab (risk of autoimmune thrombocytopenia and thyroid disease)
  2. Natalizumab (risk of progressive multifocal encephalopathy)
    - >50% reduction in relapse rate
74
Q

What are the two strategies for treating MS?

A

Either:
- Induction: start with a powerful drug which may be more likely to have side effects and step down to a less risky therapy once disease controlled
OR
- Escalation: start with a lower efficacy drug, which may be less likely to have adverse effects and step up to a more powerful drug if disease not controlled

Year 5 Medicine for Finals (4 decks)

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