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Neuro Flashcards

1
Q

What is Charcot-Marie-Tooth disease?

A

an autosomal dominant inherited disease that affects the peripheral motor + sensory nerves

There are various types with different genetic mutations + different pathophysiology

they cause dysfunction in the myelin or the axons

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2
Q

Charcot-Marie-Tooth disease

when do symptoms start to appear

A

before 10 years but can be delayed until 40 or later

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3
Q

Charcot-Marie-Tooth disease

Signs (7)

A
  1. Pes cavus (high foot arches)
  2. distal muscle wasting causing ‘inverted champagne bottle legs’
  3. weakness in the lower legs, esp loss of ankle dorsiflexion
  4. weakness in the hands
  5. reduced tendon reflexes
  6. reduced muscle tone
  7. peripheral sensory loss
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4
Q

What are the causes of peripheral neuropathy?

A 
ABCDE
Alcohol 
B12 deficiency 
Cancer + CKD
Diabetes + Drugs (isoniazid, amiodarone, cisplatin 
Every vasculitis
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5
Q

Charcot-Marie-Tooth disease

Mnx

A

Purely supportive:

  • neurologists + geneticists
  • physios
  • occupational therapists
  • podiatrists
  • orthopaedic surgeons to correct disabling joint deformities
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6
Q

Tuberous Sclerosis

Cause

A

mutations in either
- TSC1 gene on Ch9 which codes for hamartin

  • TSC2 gene on Ch16 which codes for tuberin

Hamartin + tuberin interact with each other to control the size + growth of cells.

Abnormalities in one of these proteins leads to abnormal cell size + growth

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7
Q

Tuberous Sclerosis

characteristic feature

A

hamartomas: benign neoplastic growths of the tissue that they origin from

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8
Q

Tuberous Sclerosis

where do hamartomas commonly affect?

A
  • skin
  • brain
  • lungs
  • heart
  • kidneys
  • eyes
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9
Q

Tuberous Sclerosis

skin signs (6)

A
  • ash leaf spots
  • Shagreen patches
  • Angiofibromas
  • Subungual fibromata
  • Cafe-au-lait spots
  • Poliosis
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10
Q

Tuberous Sclerosis

ash leaf spots?

A

depigmented areas of skin shaped like an ash leaf

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11
Q

Tuberous Sclerosis

Shagreen patches

A

thickened, dimpled, pigmented patches of skin

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12
Q

Tuberous Sclerosis

Angiofibromas

A

small skin coloured or pigmented papules that occur over the nose + cheeks

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13
Q

Tuberous Sclerosis

Subungual fibromata

A

fibromas growing from the nail bed

usually circular painless lumps that grow slowly + displace the nail

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14
Q

Tuberous Sclerosis

Poliosis

A

isolated patch of white hair on the head, eyebrows, eyelashes or beard

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15
Q

Tuberous Sclerosis

neuro features (2)

A
  • epilepsy

- learning disability + development delay

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16
Q

Tuberous Sclerosis

other features (5)

A
  1. rhabdomyomas in the heart
  2. gliomas (tumours of the brain + spinal cord)
  3. polycystic kidneys
  4. lymphangioleimyomatosis: abnormal growth in smooth muscle cells, often affecting the lungs)
  5. retinal hamartomas
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17
Q

Tuberous Sclerosis

typical presentation

A

a child presenting with epilepsy found to have skin features of tuberous sclerosis

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18
Q

Tuberous Sclerosis

mnx

A

supportive

monitor + treat complications such as epilepsy

no trx for the underlying gene defect

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19
Q

Facial Nerve Palsy

what is it

A

isolated dysfunction of the facial nerve

typically presents with a unilateral facial weakness

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20
Q

Facial Nerve Palsy

where does the facial nerve exit the brainstem

A

at the cerebellopontine angle

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21
Q

Facial Nerve Palsy

where does the facial nerve pass through to get to the face

A

temporal bone and parotid gland

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22
Q

Facial Nerve Palsy

what are the 5 branches of the facial nerve

A

To Zanzibar By Motor Car

Temporal 
Zygomatic 
Buccal 
Marginal mandibular 
Cervical
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23
Q

Facial Nerve Palsy

name 3 functions of the facial nerve

A
  1. motor
  2. sensory
  3. parasympathetic
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24
Q

Facial Nerve Palsy

motor function of the facial nerve

A

supplies:

  • the muscles of facial expression
  • stapedius in the inner ear
  • the posterior digastric, stylohyoid + platysma muscles in the neck
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25
Q

Facial Nerve Palsy

sensory function of the facial nerve

A

carries taste from the anterior 2/3 of the tongue

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26
Q

Facial Nerve Palsy

parasympathetic function of the facial nerve

A

provides the parasympathetic supply to the submandibular + sublingual glands and the lacrimal gland (stimulating tear production)

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27
Q

Facial Nerve Palsy

patient w/ a new onset upper motor neurone facial nerve palsy mnx

A

refer urgently w/ suspected stroke

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28
Q

Facial Nerve Palsy

patient w/ a new onset lower motor neurone facial nerve palsy immediate mnx

A

reassured and managed in the community

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29
Q

Facial Nerve Palsy

each side of the forehead has UMN innervation by ____ of the brain

A

both sides

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30
Q

Facial Nerve Palsy

each side of the forehead has LMN innervations from ___ of the brain

A

one side

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31
Q

Facial Nerve Palsy

UMN lesion forehead

A

forehead will be spared

pt can move their fod on the affected side

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32
Q

Facial Nerve Palsy

LMN lesion forehead

A

fod will not be spared

pt cannot move their forehead on the affected side

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33
Q

Facial Nerve Palsy

unilateral UMN lesion causes (2)

A
  • strokes

- tumours

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34
Q

Facial Nerve Palsy

bilateral UMN lesion causes (2)

A

rare:

  • Pseudobulbar palsies
  • MND
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35
Q

Facial Nerve Palsy

Bell’s palsy cause

A

idiopathic

unilateral LMN facial nerve palsy

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36
Q

Facial Nerve Palsy

Bell’s palsy mnx presenting within 72 hours of developing sx

A

Prednisolone either:

  • 50mg for 10d
  • 60mg for 5d followed by a 5d reducing regime of 10mg/day

lubricating eye drops and tape

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37
Q

Facial Nerve Palsy

why give lubricating eye drops and tape in Bell’s palsy

A

to prevent the eye drying out + being damaged

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38
Q

Facial Nerve Palsy

Bell’s palsy pt develops pain in the eye

A

need an ophthalmology review for exposure keratopathy

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39
Q

Facial Nerve Palsy

what is Ramsay-Hunt Syndrome caused by

A

varicella zoster virus

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40
Q

Facial Nerve Palsy

Ramsay-Hunt Syndrome presentation

A

unilateral LMN facial nerve palsy

painful + tender vesicular rash in the ear canal, pinna + around the ear on the affected side. Can extend to the anterior 2/3 of the tongue + hard palate

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41
Q

Facial Nerve Palsy

trx of Ramsay-Hunt Syndrome

A

initiate within 72hrs:

  • Prednisolone
  • Aciclovir

lubricating eye drops

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42
Q

Facial Nerve Palsy

infection causes of LMN facial nerve palsy (4)

A
  • otitis media
  • malignant otitis externa
  • HIV
  • Lyme’s disease
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43
Q

Facial Nerve Palsy

Systemic disease causes of LMN facial nerve palsy (5)

A
  • diabetes
  • sarcoidosis
  • leukaemia
  • multiple sclerosis
  • guillain-barré syndrome
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44
Q

Facial Nerve Palsy

tumour causes of LMN facial nerve palsy

A
  • acoustic neuroma
  • parotid tumours
  • cholesteatomas
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45
Q

Facial Nerve Palsy

trauma causes of LMN facial nerve palsy (3)

A
  • direct nerve trauma
  • damage during surgery
  • base of skull fractures
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46
Q

Huntington’s Chorea

inheritance pattern

A

autosomal dominant

causes a progressive deterioration in the nervous system

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47
Q

Huntington’s Chorea

when do sx usually begin

A

30-50yrs

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48
Q

Huntington’s Chorea

where is the genetic mutation

A

in the HTT gene on Ch4

a ‘trinucleotide repeat disorder’

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49
Q

Huntington’s Chorea

what is genetic ‘anticipation’

A

a features of trinucleotide repeat disorders

where successive generation have more repeats in the gene resulting in:

  • earlier age of onset
  • increased severity of disease
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50
Q

Huntington’s Chorea

presentation

A

insidious, progressive worsening of symptoms

beings with: cognitive, psychiatric + mood problems

then movement disorders

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51
Q

Huntington’s Chorea

what are the movement disorder sx

A
  • chorea
  • eye movement disorders
  • dysarthria: speech difficulties
  • dysphagia (swallowing difficulties)
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52
Q

Huntington’s Chorea

what is chorea

A

involuntary, abnormal movements

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53
Q

Huntington’s Chorea

dx

A

made in a specialist genetic centre using a genetic test for the faulty gene

involves pre-test and post-test counselling

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54
Q

Huntington’s Chorea

mnx

A

supporting the person + family:

  • MDT
  • effectively breaking bad news
  • speech + language therapy
  • genetic counselling
  • advanced directives
  • end of life care planning

discontinue unnecessary meds to minimise adverse effects

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55
Q

Huntington’s Chorea

what medications can suppress the disordered movement

A
  • antipsychotics (olanzapine)
  • benzos (diazepam)
  • dopamine-depleting agents (tetrabenazine)
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56
Q

Huntington’s Chorea

prognosis

A

life expectancy is around 15-20 years after the onset of symptoms

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57
Q

Huntington’s Chorea

what is death due to

A

respiratory disease eg. pneumonia as patient becomes more susceptible and less able to fight off illnesses

suicide

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58
Q

Neurofibromatosis

what is it

A

a genetic condition that causes nerve tumours (neuromas) to develop throughout the nervous system

benign but causes neuro and structural problems

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59
Q

Neurofibromatosis

what are the types of Neurofibromatosis and which is more common

A

Neurofibromatosis type 1 is more common than Neurofibromatosis type 2

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60
Q

Neurofibromatosis

where is the NF1 Gene found

A

on Ch17

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61
Q

Neurofibromatosis

what does the NF1 gene code for

A

a protein called neurofibromin

which is a tumour suppressor protein

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62
Q

Neurofibromatosis

NF1 gene inheritance pattern

A

autosomal dominant

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63
Q

Neurofibromatosis

NF1 criteria

A

CRABBING
at least 2/7 features indicate dx:

Café-au-lait spots: ≥6 measuring ≥5mm in children or ≥15mm in adults

Relative with NF1

Axillary or inguinal freckles

BB - Bony dysplasia such as Bowing of a long bone or sphenoid wing dysplasia

Iris hamartomas (Lisch nodules): ≥2 yellow brown spots on iris

Neurofibromas: ≥ or 1 plexiform neurofibroma

Glioma of the optic nerve

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64
Q

Neurofibromatosis

inx

A

none required to make a definitive dx. Based on clinical criteria

genetic testing if in doubt

X-rays to investigate bone pain and lesions

CT + MRI: lesions in brain, spinal cord etc

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65
Q

Neurofibromatosis

mnx

A

control symptoms, monitor disease and treat complications

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66
Q

Neurofibromatosis

3 main complications

A
  1. renal artery stenosis causing HTN
  2. malignant peripheral nerve sheath tumours
  3. GI stromal tumour
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67
Q

Neurofibromatosis

other complications

A
  • migraines
  • epilepsy
  • ADHD
  • scoliosis of the spine
  • vision loss secondary to optic nerve gliomas
  • brain tumours
  • spinal cord tumours w/ assc neurology
  • increased risk of cancer
  • leukaemia
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68
Q

Neurofibromatosis

where is the NF2 gene found

A

Ch22

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69
Q

Neurofibromatosis

what does the NF2 gene code for

A

a protein called merlin, a tumour suppressor protein important in Schwann cells

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70
Q

Neurofibromatosis

what can mutations in the NF2 gene lead to the development of?

A

Schwannomas (benign nerve sheath tumours of the Schwann cells)

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71
Q

Neurofibromatosis

NF2 inheritance pattern

A

autosomal dominant

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72
Q

Neurofibromatosis

what are NF2 most associated with?

A

acoustic neuromas: tumours of the auditory nerve innervating the inner ear

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73
Q

Neurofibromatosis

NF2: sx of an acoustic neuroma

A
  • hearing loss
  • tinnitus
  • balance problems
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74
Q

Neurofibromatosis

what may bilateral acoustic neuromas present as?

A

NF2

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75
Q

Neurofibromatosis

mnx of NF2

A

surgery to resect tumours although risk of permanent nerve damage

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76
Q

Stroke

new definition of TIA

A

transient neurological dysfunction secondary to ischaemia without infarction

old definition: symptoms of a stroke that resolve within 24hrs

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77
Q

Stroke

What is a crescendo TIA

A

2 or more TIAs within a week

this carries a high risk of developing in to stroke

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78
Q

Stroke

what clinical scoring tool is used

A

ROSIER: recognition of stroke in emergency room

stroke is likely if the pt scores anything above 0

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79
Q

Stroke

mnx

A
  • admit to specialist stroke centre
  • exclude hypoglycaemia
  • immediate CT to exclude haemorrhage
  • aspirin 300mg and continue for 2w
  • thrombolysis with alteplase given within 4.5hrs
  • if not, thrombectomy within 24hrs
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80
Q

Stroke

what is alteplase

A

a tissue plasminogen activator that rapidly breaks down clots and can reverse the effects of stroke

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81
Q

Stroke

why should BP not be lowered during a stroke

A

this risks reducing the perfusion to the brain

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82
Q

mnx of TIA

A

start 300mg aspirin daily

secondary prevention measures for CVD

referred and seen within 24hrs by a stroke specialist

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83
Q

Stroke

gold standard imaging technique

A

diffusion-weighted MRI

CT is an alternative

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84
Q

Stroke

which imaging would you use to assess for carotid stenosis

A

carotid US

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85
Q

Stroke

what should be considered if there is carotid stenosis

A

endarectomy (remove plaques)

or carotid stenting (widen lumen)

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86
Q

secondary prevention of stroke

A
  • clopidogrel 75mg OD
  • artovastatin 80mg (not started immediately)
  • carotid endarterecomy or stenting in patients with carotid artery disease
  • treat modifiable RFs
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87
Q

Parkinson’s Disease

what is it

A

a condition where there is a progressive reduction of dopamine in the basal ganglia leading to disorders of movement

sx are characteristically asymmetrical

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88
Q

Parkinson’s Disease

what is the classic triad

A
  1. Resting tremor
  2. Rigidity
  3. Bradykinesia
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89
Q

Parkinson’s Disease

what is the basal ganglia responsible for

A
  • coordinating habitual movements:
    walking
    looking around
  • controlling voluntary movements
  • learning specific movement patterns
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90
Q

Parkinson’s Disease

which part of the basal ganglia produces dopamine

A

substantia nigra

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91
Q

Parkinson’s Disease

what is dopamine essential for

A

the correct functioning of the basal ganglia

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92
Q

Parkinson’s Disease

describe the typical pt

A

older man aged around 70

  • stooped posture
  • facial masking
  • forward tilt
  • reduced arm swing
  • shuffling gait
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93
Q

Parkinson’s Disease

describe the tremor

A
  • frequency of 4-6Hz (occurs 4-6 times/s)
  • pill rolling tremor
  • more pronounced at rest
  • improves on voluntary movement
  • worsens if pt is distracted
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94
Q

Parkinson’s Disease

why is it called cogwheel rigidity

A

tension in their arm that gives way to movement in small increments (like little jerks)

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95
Q

Parkinson’s Disease

what does bradykinesia describe

A

their movement gets slower and smaller

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96
Q

Parkinson’s Disease

how can bradykinesia be presented

A
  • handwriting decreases in size
  • shuffling gait
  • difficulty initiating movement
  • difficulty turning round when standing, takes lots of little steps
  • hypomimia (reduced facial movements + facial expressions)
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97
Q

Parkinson’s Disease

other features that may affect pts

A
  • depression
  • insomnia
  • anosmia (loss of smell)
  • postural instability
  • cognitive impairment + memory problems
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98
Q

describe a benign essential tremor

A
  • symmetrical
  • 5-8Hz
  • improves at rest
  • worse with intentional movement
  • no other Parkinson features
  • improves with alcohol
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99
Q

Parkinson’s Disease

name some Parkinson’s-plus syndromes

A
  • Multiple System Atrophy
  • Dementia with lewy bodies
  • Progressive Supranuclear Palsy
  • Corticobasal Degeneration
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100
Q

Parkinson’s Disease

what is Multiple System Atrophy

A

rare condition where the neurones of multiple systems in the brain degenerate

The degeneration of the basal ganglia lead to a Parkinson’s presentation.

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101
Q

Parkinson’s Disease

what features other than parkinson presentation does Multiple System Atrophy have

A

autonomic dysfunction:

  • postural hypotension
  • constipation
  • abnormal sweating
  • sexual dysfunction

cerebellar dysfunction:
- ataxia

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102
Q

Parkinson’s Disease

how is a dx made

A

clinically by a specialist

NICE recommend using the UK Parkinson’s Disease Society Brain Bank Clinical Diagnostic Criteria.

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103
Q

Parkinson’s Disease

what is Levodopa

A

synthetic dopamine

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104
Q

Parkinson’s Disease

why is levodopa often combined with another drug

A

the other drug stops levodopa being broken down in the body before it gets the chance to enter the brain

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105
Q

Parkinson’s Disease

what drug is levodopa often combined with

A

peripheral decarboxylase inhibitors e.g. carbidopa and benserazide

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106
Q

Parkinson’s Disease

what is in co-benyldopa

A

levodopa and benserazide

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107
Q

Parkinson’s Disease

what is in co-careldopa

A

levodopa and carbidopa

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108
Q

Parkinson’s Disease

when is levodopa used

A

often reserved for when other treatments are not managing to control symptoms.

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109
Q

Parkinson’s Disease

what do patients develop when levodopa dose is too high

A

patients develop dyskinesia:

abnormal movements associated with excessive motor activity.

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110
Q

Parkinson’s Disease

levodopa SE’s

A

dyskinesias:

  • dystonia
  • chorea
  • athetosis
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111
Q

Parkinson’s Disease

levodopa SE’s: what is dystonia

A

excessive muscle contraction leads to abnormal postures or exaggerated movements

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112
Q

Parkinson’s Disease

levodopa SE’s: what is chorea

A

abnormal involuntary movements that can be jerking and random.

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113
Q

Parkinson’s Disease

levodopa SE’s: what is athetosis

A

involuntary twisting or writhing movements usually in the fingers, hands or feet

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114
Q

Parkinson’s Disease

what are COMT inhibitors

A

inhibitors of catechol-o-methyltransferase

e.g. entacapone

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115
Q

Parkinson’s Disease

how do COMT inhibitors work

A

COMT enzyme metabolises levodopa in both the body and brain.

Entacapone is taken with levodopa (and a decarboxylase inhibitor) to slow breakdown of the levodopa in the brain.

It extends the effective duration of the levodopa.

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116
Q

Parkinson’s Disease

what are dopamine agonists

A

they mimic dopamine in the basal ganglia and stimulate the dopamine receptors

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117
Q

Parkinson’s Disease

what are dopamine agonists used for

A

to delay the use of levodopa and are then used in combination with levodopa to reduce the dose of levodopa that is required to control symptoms

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118
Q

Parkinson’s Disease

SE of dopamine agonists

A

pulmonary fibrosis

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119
Q

Parkinson’s Disease

examples of dopamine agonists

A
  • Bromocryptine
  • Pergolide
  • Cabergoline
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120
Q

Parkinson’s Disease

what are Monoamine Oxidase-B inhibitors

A

Monoamine oxidase enzymes break down neurotransmitters: dopamine, serotonin and adrenaline

monoamine oxidase-B enzyme is more specific to dopamine

block this enzyme and therefore help increase the circulating dopamine.

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121
Q

Parkinson’s Disease

when are monoamine oxidase-B inhibitors used

A

to delay the use of levodopa and then in combination with levodopa to reduce the required dose.

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122
Q

Parkinson’s Disease

examples of monoamine oxidase-B inhibitors

A

Selegiline

Rasagiline

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123
Q

Epilepsy

inx and why

A

EEG: can show typical patterns in different forms of epilepsy and support dx

MRI brain: diagnoses structural problems and other pathology e.g. tumour

ECG: exclude heart problems

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124
Q

Epilepsy

presentation of tonic-clonic seizures

A
  • loss of consciousness
  • tonic (muscle tensing)
  • clonic (muscle jerking) episodes
  • tongue biting
  • incontinence
  • groaning
  • irregular breathing
  • post-ictal period
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125
Q

Epilepsy

what is the post-ictal period

A

where the person is confused, drowsy and feels irritable or depressed

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126
Q

Epilepsy

mnx of tonic-clonic seizures

A

1st line: sodium valproate

2nd line: lamotrigine or carbamazepine

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127
Q

Epilepsy

where do focal seizures start

A

in temporal lobes

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128
Q

Epilepsy

presentation of focal seizures

A
  • hallucinations
  • memory flashbacks
  • deja vu
  • doing strange things on autopilot
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129
Q

Epilepsy

trx for focal seizures

A

1st line: carbamazepine or lamotrigine

2nd line: sodium valproate or levetiracetam

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130
Q

Epilepsy

mnx of absence seizures

A

1st line: sodium valproate or ethosuximide

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131
Q

Epilepsy

what are atonic seizures

A

aka drop attacks

brief lapses in muscle tone lasting <3 min

typically begin in childhood

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132
Q

Epilepsy

what may atonic seizures be indicative of

A

Lennox-Gastaut syndrome

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133
Q

Epilepsy

mnx for atonic seizures

A

1st line: sodium valproate

2nd line: lamotrigine

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134
Q

Epilepsy

presentation of myoclonic seizures

A
  • sudden brief muscle contractions like a sudden ‘jump’
  • remains awake
  • typically happen in children in juvenile myoclonic epilepsy
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135
Q

Epilepsy

mnx of myoclonic seizures

A

1st line: sodium valproate

other options: lamotrigine, levetiracetam or topiramate

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136
Q

Epilepsy

what are infantile spasms

A

aka West syndrome

clusters of full body spasms

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137
Q

Epilepsy

when do infantile spasms begin

A

in infancy at around 6m

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138
Q

Epilepsy

1st line treatments for infantile spasms

A

prednisolone

vigabatrin

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139
Q

Epilepsy

how does sodium valproate work

A

by increasing the activity of GABA

which has a relaxing effect on the brain

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140
Q

Epilepsy

SEs of sodium valproate

A
  • Teratogenic
  • liver damage + hepatitis
  • hair loss
  • tremor
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141
Q

Epilepsy

SEs of carbamazepine

A
  • agranulocytosis
  • aplastic anaemia
  • induces the P450 system so there are many drug interactions
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142
Q

Epilepsy

SEs of phenytoin

A
  • folate and vit D deficiency
  • megaloblastic anaemia (folate deficiency)
  • osteomalacia (vit D deficiency)
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143
Q

Epilepsy

SEs of Ethosuximide

A
  • night tremors

- rashes

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144
Q

Epilepsy

Lamotrigine SEs

A
  • Stevens-Johnson sydrome or DRESS syndrome

- Leukopenia

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145
Q

Status Epilepticus

definition

A

seizures lasting >5m

or >3 seizures in 1 hr

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146
Q

Status Epilepticus

mnx in the hospital

A

ABCDE

  • secure airway
  • high conc o2
  • assess cardiac + resp function
  • check blood glucose levels
  • gain IV access

IV lorazepam 4mg, repeated after 10min if the seizure continues

if persists: IV phenobarbital or phenytoin

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147
Q

Status Epilepticus

medical options in the community

A

buccal midazolam

rectal diazepam

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148
Q

Brain Tumours

presentation

A
  • focal neurological sx

- raised ICP

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149
Q

Brain Tumours

pt has had an unusual change in personality and behaviour; Where is the tumour

A

in the frontal lobe

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150
Q

Brain Tumours

what is a key finding on fundoscopy which indicates raised ICP

A

papilloedema

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151
Q

Brain Tumours

causes of raised ICP

A
  • brain tumours
  • intracranial haemorrhage
  • idiopathic intracranial hypertension
  • abscesses or infection
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152
Q

Brain Tumours

what are the concerning features of a headache that should prompt further examination and inx (5)

A
  • constant
  • nocturnal
  • worse on waking
  • worse on coughing, straining or bending forward
  • vomiting
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153
Q

Brain Tumours

presenting features of raised ICP

A
  • altered mental state
  • visual field defects
  • seizures (particularly focal)
  • unilateral ptosis
  • 3rd and 6th nerve palsies
  • papilloedema
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154
Q

Brain Tumours

what is papilloedema

A

swelling of the optic disc secondary to raised ICP

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155
Q

Brain Tumours

what will fundoscopy show in papilloedema

A
  • blurring of the optic disc margin
  • elevated optic disc (vessels curve over a raised disc)
  • loss of venous pulsation
  • engorged retinal veins
  • haemorrhages around optic disc
  • Paton’s lines (creases in the retina around the optic disc
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156
Q

Brain Tumours

types

A
  • secondary metastases
  • gliomas
  • meningiomas
  • pituitary tumours
  • acoustic neuroma aka vestibular schwannoma
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157
Q

Brain Tumours

what are the common cancers that metastasise to the brain

A
  • lung
  • breast
  • renal cell carcinoma
  • melanoma
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158
Q

Brain Tumours

what are gliomas

A

tumours of the glial cells in the brain or spinal cord

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159
Q

Brain Tumours

what are the 3 types of gliomas (from most to least malignant)

A
  • Astrocytoma (glioblastoma multiforme in the most common)
  • Oligodendroglioma
  • Ependymoma
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160
Q

Brain Tumours

how are gliomas graded

A

1-4

1: most benign
4: most malignant

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161
Q

Brain Tumours

what are meningiomas

A

tumour growing from the cells of the meninges in the brain and spinal cord

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162
Q

Brain Tumours

are meningiomas benign

A

mostly, however takes up space –> raised ICP –> neuro sx

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163
Q

Brain Tumours

are pituitary tumour benign

A

tend to be

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164
Q

Brain Tumours

what visual defect can occur with pituitary tumours and why

A

bitemporal hemianopia

large ones can press on the optic chiasm

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165
Q

Brain Tumours

describe the visual change in bitemporal hemianopia

A

loss of the outer half of the visual fields in both eyes

166
Q

Brain Tumours

what can pituitary tumours cause

A

hypopituitarism or release excess hormones leading to:

  • acromegaly
  • hyperprolactinaemia
  • cushing’s disease
  • thyrotoxicosis
167
Q

Brain Tumours

what is an acoustic neuroma

A

tumours of the Schwann cells surrounding the auditory nerve that innervates the inner ear

168
Q

Brain Tumours

where do acoustic neuromas occur around

A

the cerebellopontine angle

169
Q

Brain Tumours

classic sx of acoustic neuroma (3)

A
  • tinnitus
  • hearing loss
  • balance problems

can also be associated with facial nerve palsy

170
Q

Brain Tumours

what may a bilateral acoustic neuroma suggest

A

neurofibromatosis type 2

171
Q

Brain Tumours

mnx options

A
  • palliative care
  • chemo
  • radiotherapy
  • surgery
172
Q

Brain Tumours

trx of pituitary tumours

A
  • trans-sphenoidal surgery
  • radiotherapy
  • bromocriptine
  • somatostatin analogues
173
Q

Brain Tumours

how does bromocriptine help in the trx of pituitary tumours

A

it blocks the prolactin-secreting tumour

174
Q

Brain Tumours

how does somastostatin analogues (e.g. ocreotide) help in the trx of pituitary tumours

A

they block growth hormone-secreting tumours

175
Q

Parkinson’s

impulse control disorders are more common in which medication

A

dopamine agonists

176
Q

Intracranial Bleeds

what are the layers of the brain from top to bottom

A 
skull 
dura mater
arachnoid mater 
subarachnoid space 
pia mater 
brain
177
Q

Intracranial Bleeds

RFs (6)

A
  • head injury
  • HTN
  • aneurysms
  • ischaemic stroke can progress to haemorrhage
  • brain tumours
  • anticoagulants such as warfarin
178
Q

Intracranial Bleeds

key feature

A

sudden onset headache

179
Q

Intracranial Bleeds

presentation

A
  • sudden onset headache
  • seizures
  • weakness
  • vomiting
  • reduced consciousness
  • other sudden onset neuro sx
180
Q

Intracranial Bleeds

what does the Glasgo Coma Scale assess

A

level of consciousness

181
Q

Intracranial Bleeds

GCS: eyes

A 
4 = spontaneous 
3 = speech 
2 = pain 
1 = none
182
Q

Intracranial Bleeds

GCS: verbal

A 
5 = orientated 
4 = confused 
3 = inappropriate words 
2 = sounds 
1 = nothing
183
Q

Intracranial Bleeds

GCS: motor

A 
6 = obeys commands 
5 = localises pain 
4 = normal flexion 
3 = abnormal flexion 
2 = extends 
1 = none
184
Q

Intracranial Bleeds

what is a subdural haemorrhage caused by

A

rupture of the bridging veins in the outermost meningeal layer

185
Q

Intracranial Bleeds

where does a subdural haemorrhage occur

A

between the dura mater and arachnoid mater

186
Q

Intracranial Bleeds

CT scan findings in a subdural haemorrhage

A
  • crescent shaped

- they can cross over the cranial sutures

187
Q

Intracranial Bleeds

whom do subdural haemorrhages occur most frequently in

A

the elderly and alcoholics

188
Q

Intracranial Bleeds

why do the elderly and alcoholics more frequently get subdural haemorrhages

A

they have more atrophy in their brains making vessels more likely to rupture

189
Q

Intracranial Bleeds

what is the cause of extradural haemorrhages

A

rupture of the middle meningeal artery

190
Q

Intracranial Bleeds

where do extradural haemorrahges occur

A

in the temporo-parietal region

between the skull and dura mater

191
Q

Intracranial Bleeds

what fracture are extradural haemorrhages associated with

A

fracture of the temporal bone

192
Q

Intracranial Bleeds

CT scan findings in extradural haemorrhages

A
  • bi concave shape

- limited by the cranial sutures

193
Q

young pt with traumatic head injury that has ongoing headache. Periods of improved neuro sx and consciousness followed by rapid decline over hours. What is it

A

extradural haemorrhage as the haematoma gets large enough to compress the intracranial contents

194
Q

Intracranial Bleeds

what is an intracerebral haemorrhage

A

bleeding into the brain tissue. presents similarly to an ischaemic stroke

195
Q

Intracranial Bleeds

where can intracerebal hameorrhages be

A
  • Lobar intracerebral haemorrhage
  • Deep intracerebral haemorrhage
  • Intraventricular haemorrhage
  • Basal ganglia haemorrhage
  • Cerebellar haemorrhage
196
Q

Intracranial Bleeds

how can intracerebral haemorrhages occur

A
  • spontaneously
  • result of bleeding into an ischaemic infarct
  • tumour
  • rupture of an aneurysm
197
Q

Intracranial Bleeds

what is a subarachnoid haemorrhage

A

bleeding in to the subarachnoic space

198
Q

Intracranial Bleeds

where do subarachnoids occur

A

where the CSF is located, between the pia mater and the arachnoid membrane

199
Q

Intracranial Bleeds

what is the usual cause of a subarachnoid haemorrhage

A

rupured cerebral aneurysm

200
Q

sudden onset occipital headache. Occurs during weight lifting or sex. Thunderclap headache. What is it

A

subarachnoid haemorrhage

201
Q

Intracranial Bleeds

what is a subarachnoid associated with

A

cocaine and sickle cell anaemia

202
Q

Intracranial Bleeds

principles of mnx

A
  • Immediate CT head to establish the diagnosis
  • Check FBC and clotting
  • Admit to a specialist stroke unit
  • Discuss with a specialist neurosurgical centre to consider surgical treatment
  • Consider intubation, ventilation and ICU care if they have reduced consciousness
  • Correct any clotting abnormality
  • Correct severe hypertension but avoid hypotension
203
Q

MND

what is it

A

an umbrella term for when motor neurones stop functioning

NO SENSORY SX

204
Q

MND

what is the most common MND (Stephen Hawking)

A

Amyotrophic lateral sclerosis (ALS)

205
Q

MND

what is the 2nd most common

A

Progressive bulbar palsy

206
Q

MND

what muscles are primarily affected in progressive bulbar palsy

A

talking and swallowing muscles

207
Q

MND

name 4 MNDs

A
  • progressive muscular atrophy
  • primary lateral sclerosis
  • amyotrophic lateral sclerosis
  • progressive bulbar palsy
208
Q

MND

degeneration in?

A
  • progressive degeneration of BOTH UMN + LMN

- sensory neurones are spared

209
Q

MND

RFs

A
  • genetic component
  • smoking
  • exposure to heavy metals
  • certain pesticides
210
Q

60yr old man w/ affected relative.

insidious, progressive weakness of the muscles throughout the body affecting the limbs, trunk, face and speech

what is it

211
Q

MND

where is the weakness first noticed

A

in the upper limbs

212
Q

MND

may there be increased fatigue

A

yes when exercising

213
Q

MND

what may pts complain of

A

clumsiness, dropping things or tripping over

dysarthria (slurred speech)

214
Q

MND

signs of LMN disease

A
  • muscle wasting
  • reduced tone
  • fasciculations
  • reduced reflexes
215
Q

MND

signs of UMN disease

A
  • increased tone or spasticity
  • brisk reflexes
  • upgoing plantar responses
216
Q

MND

dx

A

clinical presentation and excluding other conditions that can cause motor neurone sx

217
Q

MND

is there effective trx for halting or reversing the progression of the disease

218
Q

MND

medical mnx

A
  • Riluzole
  • Edaravone
  • NIV
219
Q

MND

what can Riluzole do

A

slow the progression of the disease and extend survival by a few months in ALS

220
Q

MND

where is Edaravone used

A

in the US, not the UK

221
Q

MND

how does NIV help

A

used at home to support breathing at night

improves survival and QoL

222
Q

MND

how to support the person + family

A
  • effectively breaking bad news
  • MDT
  • advanced directives: document pt’s wishes
  • end of life care planning
223
Q

MND

what do pts usually die from

A

resp failure or pneumonia

224
Q

what is myasthenic crisis characterised by

A

acute respiratory failure characterised by:

  • FVC<1L
  • negative inspiratory force (NIF) of 20 cm H2O or less
  • need for ventilatory support
225
Q

Myasthenia Gravis

what is it

A

an autoimmune condition that causes muscle weakness that get progressively worse with activity and improves with rest

226
Q

Myasthenia Gravis

at what age are pts usually affected by it

A

woman <40

man >60

227
Q

Myasthenia Gravis

what is it strongly linked with

A

thymomas (tumours of the thymus gland)

228
Q

Myasthenia Gravis

pathophysiology

A

ACh receptor antibodies bind to post synaptic NMJ receptors

this prevents ACh from being able to stimulate the receptor and trigger muscle contraction

229
Q

Myasthenia Gravis

why is there more muscle weakness the more muscles are used

A

As the receptors are used more during muscle activity, more of them become blocked up.

This leads to less effective stimulation of the muscle with increased activity.

230
Q

Myasthenia Gravis

pathophysiology: what further worsens sx

A

ACh receptor antibodies also activate the complement system within the NMJ, leading to damage to cells at the postsynaptic membrane

231
Q

Myasthenia Gravis

dx

A

test directly for antibodies:

  • ACh receptor antibodies (85%)
  • Muscle-specific kinase (MuSK) antibodies (10%)
  • low-density lipoprotein receptor-related protein 4 (LRP4) antibodies (<5%)
232
Q

Myasthenia Gravis

what do the proteins MuSK and LRP4 do

A

creation and organisation of the ACh receptor

233
Q

Myasthenia Gravis

characteristic feature

A

weakness that gets worse with muscle use and improves with rest

sxs minimal in the morning and worst at the end of the day

234
Q

Myasthenia Gravis

which muscles are most affected

A

proximal muscles and small muscles of the head and neck

235
Q

Myasthenia Gravis

why is there diplopia

A

extraocular muscle weakness

236
Q

Myasthenia Gravis

why is there ptosis

A

Eyelid weakness causing drooping of the eyelids

237
Q

Myasthenia Gravis

signs and sx

A
  • diplopia
  • ptosis
  • Weakness in facial movements
  • Difficulty with swallowing
  • Fatigue in the jaw when chewing
  • Slurred speech
  • Progressive weakness with repetitive movements
238
Q

Myasthenia Gravis

examination to elicit fatiguability in the muscles

A
  • Repeated blinking will exacerbate ptosis
  • Prolonged upward gazing will exacerbate diplopia on further eye movement testing
  • Repeated abduction of one arm 20 times will result in unilateral weakness when comparing both sides
239
Q

Myasthenia Gravis

what to look for and test in examination

A

check for a thymectomy scar

test for FVC

240
Q

Myasthenia Gravis

what test can be helpful where there is doubt about dx

A

Edrophonium Test

241
Q

Myasthenia Gravis

what is the Edrophonium Test

A
  • IV edrophonium chloride (or neostigmine)
  • edrophonium blocks cholinesterase enzymes in the NMJ
  • ACh levels increase
  • briefly relieves weakness. This establishes dx
242
Q

Myasthenia Gravis

trx

A
  • Reversible acetylcholinesterase inhibitors (usually pyridostigmine or neostigmine)
  • Immunosuppression (e.g. prednisolone or azathioprine)
  • Thymectomy
243
Q

Myasthenia Gravis

trx if standard trx not effective

A

Rituximab

targets B cells and reduces the production of antibodies

244
Q

Myasthenic Crisis

what is it

A

often triggered by another illness such as a respiratory tract infection

life-threatening complication of myasthenia gravis

245
Q

Myasthenic Crisis

why may pts require BiPAP (non-invasive ventilation) or full intubation and ventilation

A

weakness in the muscle of respiration can result in resp failure

246
Q

Myasthenic Crisis

medical trx

A

immunomodulatory therapies such as IV immunoglobulins and plasma exchange

247
Q

what is Bulbar palsy

A

a ‘lower motor neurone’ lesion affecting cranial nerves 9, 10 and 12. This causes impairments in speech and swallowing.

248
Q

Bulbar palsy

clinical features

A
  • absent or normal jaw jerk reflex
  • absent gag reflex
  • flaccid fasciculating tongue
  • nasal quiet speech
  • signs suggestive of the cause e.g. limb fasciculations of MND
249
Q

Bulbar palsy

causes

A
  • MND (progressive bulbar palsy variant)
  • myasthenia gravis
  • Guillain-Barré syndrome
  • brainstem stroke (the lateral medullary syndrome)
  • syringobulbia
250
Q

Hallucinations (auditory/gustatory/olfactory), Epigastric rising/Emotional, Automatisms (lip smacking/grabbing/plucking), Deja vu/Dysphasia post-ictal)

Where is the likely site of the seizure onset

A

Temporal lobe (HEAD)

251
Q

Head/leg movements, posturing, post-ictal weakness, Jacksonian march

Where is the likely site of the seizure onset

A

Frontal lobe (motor)

252
Q

Paraesthesia

Where is the likely site of the seizure onset

A

Parietal lobe (sensory)

253
Q

Floaters/flashes

Where is the likely site of the seizure onset

A

Occipital lobe (visual)

254
Q

CT: Hyper-attenuation within the superior sagittal sinus

what is it

A

Intracranial Venous Thrombosis in the superior sagittal sinus

255
Q

a lesion in which lobe would cause contralateral homonymous superior (upper) quadrantanopia

A

temporal lobe

PITS

256
Q

a lesion in which lobe would cause contralateral homonymous inferior (lower) quadrantanopia

A

parietal lobe

PITS

257
Q

a lesion in which lobe would cause contralateral homonymous hemianopia

A

occipital lobe

258
Q

what medication is useful for managing tremor in drug-induced parkinsonism?

A

anti-muscarinics: procyclidine, benzotropine, trihexyphenidyl (benzhexol)

259
Q

what is the difference between foot drop and L5 radiculopathy

A

L5 radiculopathy presents with foot drop and an inability to both invert and evert the foot.

in foot drop you can invert the foot

260
Q

Guillain-Barré Syndrome

pathophysiology

A

molecular mimicry

B cells create antibodies against the antigens on the pathogen that causes the infection

the antibodies also match the proteins on the nerve cells

may target proteins on the myelin sheath of the motor nerve cell or the nerve axon.

261
Q

Guillain-Barré Syndrome

what usually triggers it

A

infection from campylobacter jejuni, cytomegalovirus and Epstein-Barr virus.

262
Q

Guillain-Barré Syndrome

presentation

A
  • Symmetrical ascending weakness
  • Reduced reflexes
  • may be peripheral loss of sensation or neuropathic pain
  • may progress to the cranial nerves and cause facial nerve weakness
263
Q

Guillain-Barré Syndrome

when do sx start from the preceding infection

264
Q

Guillain-Barré Syndrome

what criteria can be used for dx

A

The Brighton criteria

265
Q

Guillain-Barré Syndrome

what inx can support the dx

A
  • nerve conduction studies

- LP

266
Q

Guillain-Barré Syndrome

what will nerve conduction studies show

A

reduced signal through the nerves

267
Q

Guillain-Barré Syndrome

what will CSF show in the LP

A

raised protein with a normal cell count and glucose

268
Q

Guillain-Barré Syndrome

mnx

A
  • IV immunoglobulins
    2nd line: plasma exchange
  • supportive care
  • VTE prophylaxis
269
Q

Guillain-Barré Syndrome

what is the leading cause of death

270
Q

Guillain-Barré Syndrome

when may pts need intubation, ventilation and admission to ICU

A

severe cases with resp failiure

271
Q

Headaches

red flags

A
  • Fever, photophobia or neck stiffness (meningitis or encephalitis)
  • New neuro sx (haemorrhage, malignancy, stroke)
  • Dizziness (stroke)
  • Visual disturbance (temporal arteritis, glaucoma)
  • Sudden onset occipital headache (subarachnoid haemorrhage)
  • Worse on coughing, straining (raised ICP)
  • Postural, worse on standing, lying or bending over (raised ICP)
  • Severe enough to wake the pt from sleep
  • Vomiting (raised ICP or CO poisoning)
  • History of trauma (intracranial haemorrhage)
  • Pregnancy (pre-eclampsia)
272
Q

Headaches

what may papilloedema indicate on fundoscopy

A

raised ICP due to brain tumour, intracranial HTN or an intracranial bleed

273
Q

Headaches

mnx for sinusitis

A
  • usually resolves within 2-3 w
  • nasal irrigation with saline can be helpful
  • steroid nasal spray of prolonged sx
274
Q

Headaches

presentation of cervical spondylosis

A
  • neck pain worse with movement

- headache

275
Q

Headaches

what are the 3 branches of the trigeminal nerve

A
  • Ophthalmic (V1)
  • Maxillary (V2)
  • Mandibular (V3)
276
Q

Headaches

presentation of trigeminal neuralgia

A
  • intense facial pain
  • few sec - hours
  • electricity-like shooting pain
277
Q

Headaches

triggers for trigeminal neuralgia

A
  • cold weather
  • spicy food
  • caffeine
  • citrus fruits
278
Q

Headaches

1st line mnx for trigeminal neuralgia

A

carbamazepine

other option: Surgery to decompress or intentionally damage the trigeminal nerve

279
Q

Headaches

what condition is trigeminal neuralgia associated with

A

multiple sclerosis

280
Q

Headaches

cause of trigeminal neuralgia

A

thought to be caused by compression of the nerve

281
Q

Headaches

presentation of cluster headaches

A
  • severe, unbearable unilateral headaches, usually around the eye. red swollen, watering
  • pupil constriction
  • eyelid drooping
  • nasal discharge
  • facial sweating
282
Q

Headaches

how long would a cluster headache occur

A

15 min- 3 hours

cluster attacks: e.g. 3-4 attacks a day for weeks or months followed by a pain-free period lasting 1-2 years

283
Q

Headaches

what can cluster headaches be triggered by

A

alcohol, strong smells and exercise

284
Q

Headaches

acute mnx for cluster headache

A
  • SC 6mg sumatriptan

- High flow 100% oxygen for 15-20 min

285
Q

Headaches

prophylaxis mnx for cluster headache

A
  • Verapamil
  • Lithium
  • Prednisolone (a short course for 2-3 weeks to break the cycle during clusters)
286
Q

Migraines

what are the 4 types

A
  • Migraine without aura
  • Migraine with aura
  • Silent migraine (migraine with aura but without a headache)
  • Hemiplegic migraine
287
Q

Migraines

how long do they last

288
Q

Migraines

sx

A
  • mod-severe intensity
  • pounding/throbbing
  • unilateral (can be bi)
  • photophobia
  • phonophobia
  • with or without aura
  • nausea and vomiting
289
Q

Migraines

what is aura

A

the visual changes associated with migraines:

  • sparks
  • blurring
  • lines across
  • loss of different visual fields
290
Q

Migraines

what can a hemiplegic migraine mimic

291
Q

Migraines

sx of a hemiplegic migraine

A
  • typical migraine sx
  • sudden or gradual onset
  • hemiplegia (unilateral weakness of limbs)
  • ataxia
  • changes in consciousness
292
Q

Migraines

triggers

A
  • stress
  • blind lights
  • strong smells
  • food (choc, cheese, caffeine)
  • dehydration
  • menstruation
  • abnormal sleep patterns
  • trauma
293
Q

Migraines

what are the 5 stages

A
  • premonitory/ prodromal
  • aura
  • headache
  • resolution
  • postdromal
294
Q

Migraines

medical mnx

A
  • Paracetamol
  • Triptans (e.g. sumatriptan 50mg as the migraine starts)
  • NSAIDs (e.g ibuprofen or naproxen)
  • Antiemetics if vomiting occurs (e.g. metoclopramide)
295
Q

Migraines

how do triptans work

A

5HT (serotonin) receptors agonists:

  • Smooth muscle in arteries to cause vasoconstriction
  • Peripheral pain receptors to inhibit activation of pain receptors
  • Reduce neuronal activity in the central nervous system
296
Q

Migraines

conservative mnx

A

avoid triggers

acupuncture?

297
Q

Migraines

medical prophylactic mnx

A

1st line: propranolol or amitriptyline

  • topiramate
298
Q

what is pseudobulbar palsy

A

a bilateral lesion affecting the corticobulbar tracts (running from the motor cortex to the motor nuclei of cranial nerves 9, 10, and 12 in the medulla)

299
Q

2 week history of dysphagia, difficulty speaking, and emotional lability. On physical examination there is slow “hot-potato” speech and a brisk jaw jerk reflex. what is it

A

pseudobulbar palsy

300
Q

Lambert-Eaton Myasthenic Syndrome

which pts tend to get this

A

patients with small-cell lung cancer.

301
Q

Lambert-Eaton Myasthenic Syndrome

pathophysiology

A

antibodies are produced against voltage-gated calcium channels in small cell lung cancer (SCLC) cells.

they also target and damage voltage-gated calcium channels in the presynaptic terminals of the NMJ

302
Q

Lambert-Eaton Myasthenic Syndrome

presentation

A
  • proximal leg muscle weakness
  • diplopia
  • ptosis
  • slurred speech and dysphagia
  • autonomic dysfunction
  • reduced reflexes
303
Q

Lambert-Eaton Myasthenic Syndrome

what happens to tendon reflexes

A

reduced reflexes but

they become temporarily normal for a short period following a period of strong muscle contraction

e.g. maximally contract the quads for a period, then have their reflexes tested immediately afterwards, and display an improvement in the response

this is POST-TETANIC POTENTIATION

304
Q

Lambert-Eaton Myasthenic Syndrome

medical mnx

A

Amifampridine (blocks voltage-gated K channels in the presynaptic cells which prolongs the depolarisation of the cell membrane and assists Ca channels in carrying out their action)

other:

  • prednisolone, azathioprine
  • IV immunoglobulins
  • plasmapheresis
305
Q

parkinson sx + arm flailing around. Dx?

A

Cortico-basal degeneration (CBD)

306
Q

Parkinsonism and vertical gaze palsy. Dx?

A

Progressive supranuclear palsy

307
Q

Parkinsonism and early autonomic clinical features such as: postural hypotension, incontinence, and impotence. Dx?

A

Multiple system atrophy

308
Q

what causes Brown-Sequard syndrome

A

lateral hemisection of the spinal cord:

  • Cord trauma (penetrating injuries being the most common)
  • Neoplasms
  • Disk herniation
  • Demyelination
  • Infective/ inflammatory lesions
  • Epidural hematomas
309
Q

features of Brown-Sequard syndrome

A
  • ipsilateral weakness below lesion
  • ipsilateral loss of proprioception and vibration sensation
  • contralateral loss of pain and temperature sensation
310
Q

what are the typical findings on MRI in Huntington’s disease

A

atrophy of the caudate nucleus and putamen

311
Q

what are the typical findings on MRI in Alzeheimer’s

A

cerebral atrophy with enlarged ventricles and sulcal widening

312
Q

arm was forcefully abducted –> small hand muscle paralysis, dermatomal sensory disturbance and ptosis (possible Horner’s syndrome)

dx?

A

Klumpke’s palsy: damage to lower brachial plexus C8-T1

313
Q

cerebellar signs, tremor and rhythm abnormalities in a young patient

dx?

A

Wilson’s disease

314
Q

presentation of unilateral X and XI palsies:

  • soft palate and uvula deviation
  • weakness of head twisting and shoulder shrugging
A

Jugular foramen syndrome

315
Q

Subarachnoid Haemorrhage

where is the bleed

A

in to the subarachnoid space
where the CSF is located

between the pia mater and arachnoid membrane

316
Q

Subarachnoid Haemorrhage

what is it due to

A

a ruptured cerebral aneurysm

317
Q

Subarachnoid Haemorrhage

presentation

A
  • thunderclap headache
  • sudden onset, occpital
  • neck stiffness
  • photophobia
  • vision changes
  • neuro sx: speech, weakness, seizure, loss of conscioussness
318
Q

Subarachnoid Haemorrhage

trigger

A

strenuous activity such as weight lifting or sex

319
Q

Subarachnoid Haemorrhage

who is it more common in

A

Black patients
Female patients
Age 45-70

320
Q

Subarachnoid Haemorrhage

particularly associated with?

A
  • Cocaine use
  • Sickle cell anaemia
  • Connective tissue disorders (such as Marfan syndrome or Ehlers-Danlos)
  • Neurofibromatosis
  • Autosomal dominant polycystic kidney disease
321
Q

Subarachnoid Haemorrhage

1st line inx

A

immediate CT head

322
Q

Subarachnoid Haemorrhage

CT result

A

hyperattenuation in the subarachnoid space

323
Q

Subarachnoid Haemorrhage

when is lumbar puncture used

A

to collect a sample of the CSF if the CT head is negative.

324
Q

Subarachnoid Haemorrhage

CSF signs

A
  • raised red cell count

- xanthochromia (the yellow colour of CSF caused by bilirubin)

325
Q

Subarachnoid Haemorrhage

inx once a subarachnoid haemorrhage is confirmed to locate the source of the bleeding.

A

Angiography (CT or MRI)

326
Q

Subarachnoid Haemorrhage

mnx

A
  • supportive
  • coiling: placing platinum coils into the aneurysm and sealing it off from the artery
  • or clipping
327
Q

Subarachnoid Haemorrhage

common complication that can result in brain ischaemia following a subarachnoid haemorrhage

328
Q

Subarachnoid Haemorrhage

mnx to prevent vasospasm

A

Nimodipine

329
Q

Subarachnoid Haemorrhage

what is required to treat hydrocephalus

A

Lumbar puncture or insertion of a shunt

330
Q

Subarachnoid Haemorrhage

what can be used to treat seizures

A

Antiepileptic medications

331
Q

S1 dermatome

A

back of the thigh and some of the back of the calf

332
Q

S1 myotome

A

ankle plantarflexion.

333
Q

L2 dermatome

A

lateral upper thigh extending towards the groin

334
Q

L2 myotome

A

hip flexion

335
Q

which nerve roots does the femoral nerve come off

336
Q

L3 dermatome

A

medial side of the thigh

337
Q

L3 myotome

A

knee extension

338
Q

L4 dermatome

A

lateral aspect of the upper shin + dorsal medial foot

339
Q

L4 myotome

A

ankle dorsiflexion

340
Q

Multiple Sclerosis

what is it

A

chronic and progressive condition that involves demyelination of the myelinated neurones in the CNS

341
Q

Multiple Sclerosis

what covers the axons of neurones in the CNS

A

myelin

helps the electrical impulse move faster along the axon

342
Q

Multiple Sclerosis

what cells provide the myelin in the peripheral NS

A

Schwann cells

343
Q

Multiple Sclerosis

what cells provide the myelin in the CNS

A

oligodendrocytes

344
Q

Multiple Sclerosis

does MS affect the CNS or peripheral

A

typically the CNS (oligodendrocytes)

345
Q

Multiple Sclerosis

what does it mean when lesions are ‘disseminated in time and space’

A

lesions vary in their location over time, meaning that different nerves are affected and symptoms change over time.

346
Q

Multiple Sclerosis

cause

A

unclear but combination of:

  • Multiple genes
  • Epstein–Barr virus (EBV)
  • Low vitamin D
  • Smoking
  • Obesity
347
Q

Multiple Sclerosis

what is the most common presentation of MS

A

optic neuritis

348
Q

Multiple Sclerosis

signs and sx

A
  • optic neuritis
  • eye movement abnormalities
  • focal weakness
  • focal sensory sx
  • ataxia
349
Q

Multiple Sclerosis

why may pts present with double vision

A

lesion with the 6th CN (abducens nerve)

350
Q

Multiple Sclerosis

6th cranial nerve palsy presentation

A
  • internuclear ophthalmoplegia

- conjugate lateral gaze disorder

351
Q

Multiple Sclerosis

what is internuclear ophthalmoplegia

A

internuclear: CN nuclei that control eye movement (3,4,6) to ensure eyes move together
opthalmoplegia: Problem with muscle around eye

352
Q

Multiple Sclerosis

what is conjugate lateral gaze disorder

A

conjugate: connected

lateral gaze: where both eyes move together to look laterally to the left or right.

When looking laterally in the direction of the affected eye, the affected eye will not be able to abduct.

353
Q

Multiple Sclerosis

what focal weakness may be present

A
  • bell’s palsy
  • horner’s syndrome
  • limb paralysis
  • incontinence
354
Q

Multiple Sclerosis

what are the focal sensory sx

A
  • Trigeminal neuralgia
  • Numbness
  • Paraesthesia (pins and needles)
  • Lhermitte’s sign
355
Q

Multiple Sclerosis

what is Lhermitte’s sign

A

an electric shock sensation that travels down the spine and into the limbs when flexing the neck.

It indicates disease in the cervical spinal cord in the dorsal column.

It is caused by stretching the demyelinated dorsal column.

356
Q

Multiple Sclerosis

what is sensory ataxia

A
  • loss of proprioception
357
Q

Multiple Sclerosis

what can a positive Romberg’s test indicate

A

sensory ataxia

358
Q

Multiple Sclerosis

what is cerebellar ataxia

A

problems with the cerebellum coordinating movement.

This suggestions cerebellar lesions.

359
Q

Multiple Sclerosis

what is a clinically isolated syndrome

A

the first episode of demyelination and neurological signs and symptoms

cannot be diagnosed as MS as not been disseminated in time and space

360
Q

Multiple Sclerosis

what is the most common pattern

A

relapsing-remitting

361
Q

Multiple Sclerosis

relapsing-remitting: active

A

new symptoms are developing or new lesions are appearing on MRI

362
Q

Multiple Sclerosis

relapsing-remitting: not active

A

no new symptoms or MRI lesions are developing

363
Q

Multiple Sclerosis

relapsing-remitting: worsening

A

there is an overall worsening of disability over time

364
Q

Multiple Sclerosis

relapsing-remitting: not worsening

A

there is no worsening of disability over time

365
Q

Multiple Sclerosis

what is the secondary progressive pattern

A

there was relapsing-remitting disease at first, but now there is a progressive worsening of symptoms with incomplete remissions

366
Q

Multiple Sclerosis

what are the types of secondary progressive pattern

A
  • active
  • not active
  • progressing
  • not progressing
367
Q

Multiple Sclerosis

what is primary progressive pattern

A

worsening of disease and neurological symptoms from the point of diagnosis without initial relapses and remissions

sx have to be progressive >1y

368
Q

Multiple Sclerosis

what are the types of primary progressive pattern

A
  • active
  • not active
  • progressing
  • not progressing
369
Q

Multiple Sclerosis

what inx can support dx

A
  • MRI: lesions

- lumbar puncture

370
Q

Multiple Sclerosis

what would lumbar puncture show

A

oligoclonal bands in the CSF

371
Q

Multiple Sclerosis

presentation of optic neuritis

A
  • unilateral reduced vision developing over hrs - days
  • Central scotoma. This is an enlarged blind spot.
  • pain on eye movement
  • impaired colour vision
  • Relative afferent pupillary defect
372
Q

Multiple Sclerosis

causes of optic neuritis

A
  • MS
  • Sarcoidosis
  • SLE
  • Diabetes
  • Syphilis
  • Measles
  • Mumps
  • Lyme disease
373
Q

Multiple Sclerosis

mnx of optic neuritis

A

steroids and recovery takes 2-6 weeks.

374
Q

Multiple Sclerosis

mnx

A
  • MDT approach

- disease modifying drugs + biologic therapy

375
Q

Multiple Sclerosis

how to treat relapses

A

methylprednisolone

500mg PO OD 5d
or 1g IV OD 3-5d 2nd line

376
Q

Multiple Sclerosis

what can spasticity be managed with

A

baclofen, gabapentin and physiotherapy

377
Q

presentation of Internuclear ophthalmoplegia

A
  • impaired adduction of the eye on the same side as the lesion
  • horizontal nystagmus of the abducting eye on the contralateral side
378
Q

pathophysiology of Internuclear ophthalmoplegia

A

lesion in the medial longitudinal fasciculus (MLF)

379
Q

causes of Internuclear ophthalmoplegia

A
  • MS

- vascular disease

380
Q

features of cerebellar dysfunction

A

DANISH
Dysdiadochokinesia

Ataxia

Nystagmus

Intention tremor

Slurred speech

Hypotonia

381
Q

Neuropathic Pain

what is it caused by

A

abnormal functioning of the sensory nerves delivering abnormal and painful signals to the brain.

382
Q

Neuropathic Pain

what is used to assess the characteristics of the pain and examination of the affected area

A

DN4 Questionnaire

scored out of 10 fpr their pain

383
Q

Neuropathic Pain

what score indicates neuropathic pain on the DN4 questionnaire

384
Q

Neuropathic Pain

what are the four 1st line trx

A
  • Amitriptyline (TCA)
  • Duloxetine (SNRI antidepressant)
  • Gabapentin (anticonvulsant)
  • Pregabalin (anticonvulsant)

NICE: if 1 doesn’t work, stop and start an alternative until all 4 have been tried

385
Q

Neuropathic Pain

when to use tramadol

A

ONLY as a rescue for short term control of flares

386
Q

Neuropathic Pain

when to use Capsaicin cream (chilli pepper cream)

A

for localised areas of pain

387
Q

Neuropathic Pain

what is Complex Regional Pain Syndrome

A

areas are affected by abnormal nerve functioning causing neuropathic pain and abnormal sensations. It is usually isolated to one limb.

388
Q

Neuropathic Pain

what is Complex Regional Pain Syndrome often triggered by

A

an injury to the area.

389
Q

Neuropathic Pain

presentation of complex regional pain syndrome

A
  • area very painful and hypersensitive e.g. wearing clothes
  • intermittently swell, change colour, temp, flush with blood
  • abnormal sweating
  • abnormal hair growth
390
Q

Neuropathic Pain

trx of complex regional pain syndrome

A

guided by a pain specialist and is similar to other neuropathic pain.

391
Q

Which sign on MRI would support the diagnosis of encephalitis?

A

Bilateral medial temporal lobe involvement

392
Q

74 year old T1DM

L common peroneal nerve palsy leading to motor and sensory loss. recovered spontaneously after 3w

3m later: transient left-sided facial weakness - recovered spontaneously after 2w

O/E peripheral sensory loss affecting both feet

what is it

A

Mononeuritis multiplex

393
Q

what is the difference between type 1 and type 2 charcot-marie tooth disease

A

type 1: demyelinating condition which is more common (and includes the PMP22 subtype)

type 2: axonal

394
Q

what does the anterior spinal artery supply

A

the anterior 2/3 of the spinal cord (not the dorsal column)

395
Q

what is the dorsal column responsible for

A

vibration, two-point discrimination, and proprioception

396
Q

39 year old man

now + then jerks his head violently to one side

what kind of seizure could this be

397
Q

Creutzfeldt-Jakob disease

what is it

A

a group of neuro-degenerative diseases caused by prions (mis-shaped proteins).

398
Q

Creutzfeldt-Jakob disease

presentation

A
  • myoclonus
  • rapidly progressive dementia
  • psych
399
Q

Creutzfeldt-Jakob disease

what will CSF show

A

normal or abnormal proteins e.g. 14-3-3 protein

400
Q

Creutzfeldt-Jakob disease

what will EEG show

A
  • biphasic, high amplitude sharp waves (only in sporadic CJD)
401
Q

Creutzfeldt-Jakob disease

what will MRI show

A

hyperintense signals in the basal ganglia and thalamus

402
Q

Creutzfeldt-Jakob disease

dx

A

tonsil/olfactory mucosal biopsy

403
Q

Creutzfeldt-Jakob disease

mean age of onset between sporadic CJD and new variant CJD

A

sporadic CJD: 65y

new onset variant CJD: 25y

404
Q

what is cushings triad and what does it indicate

A

raised ICP

  1. bradycardia
  2. hypertension
  3. irregular/abnormal breathing.
405
Q

what is the most common cause of surgical 3rd nerve palsy

A

posterior communicating artery aneurysm, located in the circle of Willis.

406
Q

why is there hyperacusis in Bell’s Palsy

A

Paralysis of the stapedius muscle prevents its function in dampening the oscillations of the ossicles, causing sound to be abnormally loud on the affected side

407
Q

why look in the ear in Bell’s Palsy

A

Check for ramsey hunt vesicles

408
Q

what is the most important side effect to look out for for pts on Ropinirole (a dopamine agonist)

A

impulsivity

409
Q

30 year old woman has severe headache 24 hours after a spinal anaesthetic. What is the most likely diagnosis

A

low pressure headache

410
Q

73yo: 3m of increasing weakness of R hand w/ reduced sensation of forearm. Wasting of all intrinsic muscles of R hand. Weakness of finger abduction + adduction, + thumb adduction. Finger flexion is normal. Mild altered light touch sensation along ulnar aspect of forearm. Biceps, supinator + triceps reflexes are normal. The lower limbs and L arm are normal.

Where is the most likely site of the lesion causing his symptoms?

A
  • intrinsic hand muscle wasting suggests T1
  • normal reflexes and normal other arm are against a cord lesion.
  • The sensory loss on the forearm excludes median and ulnar nerve lesions.
  • T1 dermatome is often thought to be higher in the arm medially
411
Q

immediate mnx of malignant spinal cord compression

A

dexamethasone

412
Q

A 17 year old boy has repeated episodes characterised by a funny ‘racing’ sensation in his abdomen, followed by loss of awareness. His girlfriend describes that he has a vacant stare and waves his left arm around in a writhing manner during these attacks

Which is the most likely site of origin of these episodes

A

right temporal lobe

the aura implicates one of the temporal lobes

Finals (47 decks)

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