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3A > Neuro > Flashcards

Neuro Flashcards

1
Q

Which medications may worsen myasthenia gravis

A

Beta blockers
Several antibiotics
Lithium and anti malarials
anticholiergics- oxybutynin

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2
Q

What disease may present with worsening neuro symptoms after exercise

A

multiple sclerosis (uhtoff’s phenomenon)

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3
Q

Describe optic neuritis

A

inflammation of the optic nerve - leads to pain and changes in vision such as reduced visual acuity

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4
Q

First line treatment of focal seizures

A

lamotrigine or levetiracetam

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5
Q

first line treatment of absence seizures

A

ethosuximide

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6
Q

Where would a lesion causing disinhibition be expected to be located in the brain?

A

the prefrontal cortex

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7
Q

If presenting within 4.5 hours and having confirmed occlusion on imaging, what should be the treatment?

A

thrombolysis and thrombectomy

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8
Q

When can antiepileptic medication be stopped?

A

after being seizure free for >2 years.
Drugs are stopped over 2-3 months

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9
Q

Treatment of muscle spasticity in ms

A

baclofen or gabapentin

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10
Q

How do retinal artery strokes present q

A

amaurosis fugax- transient darkening of vision

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11
Q

Most common organism associated with Guillain - Barre syndrome

A

Campylobacter jejuni

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12
Q

How long do cluster headaches typically last

A

15 minutes to 2 hours

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13
Q
A
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14
Q

What are acoustic neuromas?

A

Slow growing tumours of the Schwann cells that surround the auditory nerve (vestibulocochlear nerve)
Also called vestibular schwannomas

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15
Q

Where are acoustic neuromas located?

A

At the cerebellopontine angle

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16
Q

At what age do acoustic neuromas typically present?

A

40-60

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17
Q

If someone has bilateral acoustic neuromas what is suggested?

A

Neurofibromatosis type II

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18
Q

Presentation of acoustic neuromas

A

Unilateral hearing loss
Intermittent dizziness and vertigo
Sensation of fullness in the ear
Facial numbness- due to tumour compressing the facial nerve
Unilateral tinnitus
Swallowing difficulty
Cerebellar symptoms if compression of brain stem

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19
Q

Two complications of acoustic neuromas

A

Facial nerve palsy
Obstructive hydrocephalus

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20
Q

How are acoustic neuromas diagnosed

A

Audio gram
MRI
CT head

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21
Q

Treatment of acoustic neuromas

A

1st line- focussed radiation or surgery

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22
Q

What is neurofibromatosis

A

A genetic condition causing nerve cell tumours (neuromas) to develop throughout the nervous system

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23
Q

Genetics of neurofibromatosis type I

A

Mutation in a gene on chromosome 17 which codes for a protein called neurofibromin (a tumour suppressor protein)

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24
Q

What is the inheritance of neurofibromatosis type I

A

Autosomal dominant

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25
Q

Genetics of neurofibromatosis type II

A

A mutation in a gene on chromosome 22 which encodes for the tumour suppressor protein Merlin

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26
Q

What is anterior cord syndrome?

A

incomplete spinal injury that affects the anterior 2/3 of the spinal cord

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27
Q

Causes of anterior cord syndrome

A
  • Occlusion of the anterior spinal artery and ischaemia to the are that the ASA supplies
  • direct injury or trauma
  • spinal canal mass
  • radiation myelopathy
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28
Q

Causes of occlusion to to the anterior spinal artery

A

iatrogenic - cross clamping of the aorta during thoracic or abdominal aortic aneurysm repair
severe hypotension
atherothrombotic disease
vasculitis
cocaine

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29
Q

What spinal cord tracts are damaged in anterior cord syndrome?

A

corticospinal tract
spinothalamic tract
descending autonomic tract

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30
Q

presentation of anterior cord syndrome

A

bilateral motor deficit below the level of the lesion
bilateral loss of pain and temperature
autonomic dysfunction- urinary incontinence, abnormal blood pressure
preserved posterior columns - position, vibration and light touch

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31
Q

How is anterior cord syndrome diagnosed?

A

MRI- shows pencil like intensities

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32
Q

Treatment of anterior cord syndreom

A

IV methylprednisolone shown to improve outcome if used in first 23 hours

Thrombolysis if embolic cause
immunosuppression if vasulitis

Surgery - laminectomy for spinal decompression

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33
Q

Prognosis of anterior cord syndrome ?

A

poor

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34
Q

Complications of anterior cord syndrome

A

respiratory failure
autonomic dysreflexia
spasticity
urinary incontinence
complications of immobility- DVT, pressure ulcers.

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35
Q

What is bells palsy

A

sudden onset unilateral facial nerve paralysis

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36
Q

Who is at increased risk of bells palsy

A

pregnant women

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37
Q

Aetiology of bells palsy

A

unknown- though to be linked with viral illnesses in particular herpes simplex virus type 1

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38
Q

Is the forehead involved in the paralysis of bells palsy?

A

yes the forehead is paralysed
This is because it is a lower motor neurone lesion- upper motor innervation is bilateral so if upper lesion it will be spared

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39
Q

presentation of bells palsy

A

unilateral facial paralysis including the forehead
postauricular pain (ear pain)
altered taste
dry eyes
hyperacusis

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40
Q

Why may there be a change of taste in bells palsy

A

the facial nerve supplies the anterior two thirds of the tongue- the chorda tympani branch

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41
Q

How does bells palsy present on examination

A

asymmetrical smile
loss of the nasolabial folds
drooping eyebrow
drooping corner of the mouth

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42
Q

what is bell’s sign

A

upward movement of the eye maintained on attempt to close the eye

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43
Q

Treatment of bells palsy

A

if presenting within 72 hours of onset prednisolone may be given (50mg for 10 days)
lubricating eye drops
eye tape for at night

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44
Q

Why might you get hyperacusis in bells palsy?

A

a branch of the facial nerve branches off in the facial canal to supply the stapedius muscle of the inner ear

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45
Q

why is eye care important in bells palsy

A

to prevent exposure keratopathy

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46
Q

What are brain abscesses?

A

localised focal necrosis of brain tissue with inflammation- usually due to bacterial infection

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47
Q

RF of brain abscesses

A

right to left shunt cardiac defects, bronchiectasis, immnosupression

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48
Q

causes of brain abscesses

A

direct implantation- head trauma leading to fracture and contamination
iatrogenic procedures
local extension of infection from adjacent areas - ear infection, dental abscess, paranasal sinusitis
haematogenous spread - organ infection

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49
Q

why do right to left shunt cardiac defects increase the likelihood of brain abscesses

A

means that the blood bypasses the filtration in the lungs so pathogens are more likely to spread

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50
Q

How do brain abscesses present

A

fever
progressively worsening focal neurology
headache

increased ICP - can lead to early morning headache, nausea and vomiting, papilloedema

mental status changes
seizures

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51
Q

How are brain abscesses diagnosed?

A

MRI or CT scan- initially will not be able to distinguish with space occupying lesions and infarcts but after 4-5 days a capsule will form

LP if no signs of raised ICP

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52
Q

how are brain abscesses treated?

A

antibiotic therapy: IV 3rd generation cephalosporin and metronidazole

Surgery: craniotomy and debridement of the abscess

dexamethasone for raised ICP

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53
Q

What are the most common cancers that metastasise to the brain

A

lung, breast, colorectal and prostate

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54
Q

what is the most common primary brain tumour in adults

A

glioblastomas

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55
Q

How do glioblastomas present on imaging?

A

solid tumours with central necrosis and a rim

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56
Q

prognosis of glioblastomas

A

1 year

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57
Q

What is the second most common brain tumour in adutls

A

meningioma

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58
Q

pathophysiology of meningiomas

A

most commonly benign
arise from the arachnoid cap cells of the meninges
Cause symptoms due to compression rather than invasion

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59
Q

Explain the relation ship between the location of cerebellar lesions and the signs produced

A

unilateral cerebellar lesion will cause ipsilateral signs

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60
Q

causes of cerebellar disease

A

Genetic inherited disorders- Freidreich’s ataxia
Neoplasms- cerebellar haemangioma
Stroke
alcohol- thiamine deficiency
MS
hypothyroidism
drugs- phenytoin, lead poisoning

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61
Q

Signs of cerebellar disease

A

dysdiadochokinesia
ataxia- limb and truncal
nystagmus
intention tremor
slurred speech
hypotonia

DANISH

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62
Q

Describe a benign essential tremor

A

a fine tremor affecting all voluntary muscles
most notable usually in the hands but can also affect other areas- head, jaw, vocal

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63
Q

Describe the features of a benign essential tremor that make it differ from parkinsons

A
  • fine tremor (6-12Hz)
  • usually absent at rest and worse with intentional movements
  • worse when tired, stressed or after caffeine
  • can be suppressed with drugs such as alcohol and benzodiazepines
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64
Q

Diagnosis of benign essential tremor- what tests might you do to rule out other causes

A

CT or MRI
serum ceruloplasmin and 25 hour urinary copper- wilsons
thyroid function tests

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65
Q

1st line treatment of benign essential tremro

A

propranolol or primidone

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66
Q

2nd line treatment of benign essential tremor

A

gabapentin, alprazolam or topiramate

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67
Q

what procedures may be done to treat benign essential tremor if medications are unsuccessful

A

deep brain stimulation
focused US thalamotomy
gamma knife thalamotomy

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68
Q

Where is an extradural haemorrhage located?

A

between the dura mater and the inner surface of the skull

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69
Q

what is the most common cause of extradural haematoma

A

skull fracture due to skull trauma in the temporoparietal region (over the pterion) leading to rupture of the middle meningeal artery

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70
Q

What % of extra dural haematomas are caused by rupture of the middle meningeal artery?

A

75%

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71
Q

Presentation of a extradural haematoma

A

previous head trauma
lucid period - lasting minutes to hours- followed by progressively decreasing consciousness
headache
nausea and vomiting
confusion
neurological signs - cranial, motor or sensory nerve deficits

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72
Q

What is cushings triad

A

a physiological response to raised ICP which aims to improve perfusion

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73
Q

presentation of cushings triad

A

hypertension
bradycardia
irregular breathing pattern

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74
Q

diagnosis of an extradural haematoma

A

CT scan- shows a biconvex lemon shaped lesion that cannot extend past the suture lines
may have midline shift and brain herniation

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75
Q

cause sof extradural haematomas other than middle meningeal artery trauma

A

AV malformations
bleeding disorders

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76
Q

treatment of extradural haematomas

A

correct anticoagulation (reversal agents)
reduce ICP = mannitol
IF small bleed then conservative
if acute- burr hole craniotomy

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77
Q

definitive treatment for extradural haematome

A

BURR HOLE CRANIOTOMY

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78
Q

COMPLICATIONS OF EXTRADURAL HAEMATOMAS

A

INFECTION- WOUND OR SURGERY
CEREBRAL ISCHAEMIA
SEIZURES
COGNITIVE IMPAIRMENT
HEMIPARESIS
HYDROCEPHALUS
BRAINSTEM INJURY

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79
Q

what is giant cell arteritis

A

a chronic vasculitis characterised by granulomatous inflammation in the walls of the medium and large arteries- most commonly the branches of the carotid artery (temporal, ophthalmic and occipital)

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80
Q

What condition is giant cell arteritis associated with

A

polymyalgia rheumatica

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81
Q

age of patients affected by giant cell arteritis

A

mainly those over 50 (peak in 70s)

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82
Q

Presentation of giant cell arteritis

A

rapid onset of:
unilateral headache,
scalp tenderness,
jaw claudication,
blurred vision,
systemic illness (fever, anorexia)
a tender palpable temporal artery

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83
Q

What visual disturbances may occur in giant cell arteritis

A

vision loss, diplopia, amaurosis fugax

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84
Q

what is the pathophysiology of visual disturbances in giant cell arteritis

A

anterior ischaemia optic neuropathy resulting from occlusion of the posterior ciliary artery (causes ischaemia of the optic nerve head)

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85
Q

what is seen on fundoscopy in giant cell arteritis

A

a swollen pale disc and blurred margins

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86
Q

Investigations for giant cell arteritis

A

Raised inflammatory markers - ESR >50
Temporal artery biopsy - shows multinucleated giant cells, may not be present if skip lesions
Duplex Ultrasonography - hypoechoic halo sign and stenosis of the temporal artery

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87
Q

Diagnostic criteria of giant cell arteritis

A

Three of the following:
- aged >/= 50
- new headache
- temporal artery abnormality
- elevated ESR (>50)
- abnormal temporal artery biopsy

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88
Q

How is giant cell arteritis treated ?

A

high dose corticosteroids:
- if no visual disturbances then high dose prednisolone
- if visual disturbances IV methylprednisolone prior to starting oral pred

Bone protection due to steroids- bisphosphonates

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89
Q

What is guillain-barre syndrome

A

an acute inflammatory demyelinating polyneuropathy that affects the peripheral nervous system- an acute symmetrical ascending weakness and potentially sensory symptoms

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90
Q

pathophysiology of guillain barre

A
  • immune mediated demyelination of the peripheral nerves
  • usually triggered by an infection (campylobacter jejuni)
  • The antibodies to the infectious organism also attack the nerves due to molecular mimicry
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91
Q

Presentation of guillain barre syndrome

A

progressive symmetrical weakness of all limbs- ascending (legs before arms)
reflexes are usually reduced or absent
Sensory symptoms tend to be mild - may have some paraesthesia
May have cranial nerve involvement - diplopia, bilateral facial nerve palsy
May have autonomic involvement- urinary retention, diarrhoea

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92
Q

How soon after an infection does guillain barre usually present?

A

3 weeks after a gastroenteritis like illness- usually campylobacter

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93
Q

How is guillain barre diagnosed?

A

lumbar puncture- rise in protein by normal white cell count
Nerve conduction studies- decreased motor nerve conduction velocity due to demyelination, prolonged distal motor latency, increased F wave latency

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94
Q

How is guillain barre treated?

A

IV immunoglobulins - first line
plasmapheresis
DVT prophylaxis - TEDS and LMWH

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95
Q

What needs to be monitored in patients with guillain barre

A

FVC- can cause respiratory failure

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96
Q

What is Miller-Fisher syndrome

A

A variant of Guillain-Barre syndrome
Associated with ophthalmoplegia, areflexia and ataxia
Usually associated with anti-GQ1b antibodies

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97
Q

What is Horner’s syndrome?

A

A condition that affects one half of the face causing ptosis, miosis and facial anhidrosis
Occurs due to a disruption of the sympathetic nerve supply

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98
Q

Causes of Horner’s syndrome

A

can be central lesions, pre-ganglionic lesions and post- ganglionic lesions
Central lesions: strokes (lateral medullary syndrome), MS, pituitary or basal ganglia tumours, basal meningitis, syringomyelia, spinal cord tumours
Pre-ganglionic lesions: apical lung tumours (pancoast), lymphadenopathy, trauma, thyroidectomy
post-ganglionic lesions: carotid artery dissection, carotid aneurysm, cavernous sinus thrombosis, cluster headache

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99
Q

If a central lesions has caused horners syndrome, how will it present?

A

anhidrosis will occur on the face, arm and trunk

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100
Q

if a pre-ganglionic lesion has causes horners syndrome, how will it present?

A

anhidrosis will only affect the face

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101
Q

if a post ganglionic lesion has causes horner’s syndrome, how will it present?

A

no anhidrosis

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102
Q

How can you remember the different causes of horners

A

Central- The 4 S’s (stroke, multiple Sclerosis, Syringomyelia, Spinal cord tumours)
Pre-ganglionic- the 4 T’s (pancoast Tumour, Thyroidectomy, Trauma, Top of cervical rip)
Post-ganglionic- the 4 C’s (carotid artery aneurysm, carotid artery dissection, cavernous sinus thrombosis, cluster headache)

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103
Q

What additional feature will congenital horner’s syndrome have?

A

heterochromia

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104
Q

How is horners syndrome diagnosed?

A

usually a clinical diagnosis however can be confirmed with cocaine or apraclonidine drops

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105
Q

How can cocaine drops confirm the diagnosis of horners syndrome?

A

cocaine blocks the reuptake of noradrenaline at the nerve synapse. In a normal eye will lead to pupillary dilation however in horners where there is impaired sympathetic innervation it will have no affect

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106
Q

How can apraclonidine drops confirm the diagnosis of horners syndrome?

A

apraclonidine is an alpha-adrenergic agonist- it usually causes pupillary constriction however in horners it causes dilation as there is alpha 1 supersensitivity

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107
Q

What drops can be used to localise the lesion in horners syndrome

A

hydroxyamphetamine- in 1st and 2nd order lesions it will lead to dilation, in 3rd it will have no effect

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108
Q

Does horners syndrome present on the contralateral or ipsilateral side of the face to the lesion?

A

ipsilateral

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109
Q

What is lateral medullary syndrome?

A

a type of stroke caused by infarction of the posterior inferior cerebellar artery

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110
Q

how does lateral medullary syndrome present?

A

cerebellar features: ataxia and nystagmus
Brainstem features:
- ipsilateral dysphagia, facial numbness, Horners
- contralateral limb sensory loss

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111
Q

what is encephalitis?

A

inflammation of the brain parenchyma caused by an infection- mainly viral

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112
Q

What are the most common causes of viral encephalitis

A

HSV 1 or 2, varicella zoster virus, arbovirus, enteroviruses

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113
Q

most common cause of encephalitis in adults

A

HSV type 1

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114
Q

what part of the brain is most commonly effected in encephalitis

A

the temporal and inferior frontal lobes

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115
Q

How does encephalitis present

A

fever
headache
seizures
vomiting
focal features- aphasia
peripheral unrelated features- cold sores

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116
Q

How is encephalitis diagnosed?

A

LP- lymphocytosis, elevated proteins,
PCR of CSF = test for HSV, VZV etc
Neuroimaging- MRI shows hyperintense lesions
EEG

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117
Q

How is encephalitis treated?

A

IV aciclovir in all cases

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118
Q

complications of encephalitis

A

memory loss, muscle weakness, personality change, vision loss, hydrocephalus

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119
Q

inheritance of huntingtons

A

autosomal dominant

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120
Q

genetics of huntingtons

A

trinucleotide repeat of the CAG triplet in the huntingtin gene on chromosome 4
>40 repeats leads to HD, reduced penetrance may be seen in those with 36 to 39 repeats

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121
Q

what is anticipation

A

a phenomenon where the disease presents earlier in successive generations due to increases repeats

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122
Q

pathophysiology of huntingtons

A

degeneration of the cholinergic and GABAergic neurones in the striatum of the basal ganglia

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123
Q

how does huntingtons present?

A
  • chorea
  • personality change- irritability, apathy, depression
  • intellectual impairment
  • dystonia
  • incoordination
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124
Q

at what age does huntingtons typically present ?

A

35

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125
Q

How can huntingtons disease be treated?

A

no cure
- symptomatic treatment of chorea- tetrabenazine, antipsychotics
- antidepressants
- consider dopamine agonist for bradykinesia and rigidity

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126
Q

what is menieres disease?

A

a disorder of the inner ear of unknown cause characterised by excessive pressure and progressive dilation of the endolymphatic system

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127
Q

how does menieres disease present?

A

a triad of hearing loss, tinnitus and vertigo
Aural fullness
May have drop attacks and nystagmus
symptoms are typically unilateral initially and the progress to bilateral

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128
Q

How is menieres disease diagnosed?

A

clinical evaluation
May use audiometry- bone and air conduction
MRI to rule out other causes

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129
Q

How is menieres disease treated?

A

diuretics may help reduce endolymph fluid
Low salt diets- reduce endolymph
Prophylactic betahistine
in acute attacks- prochlorperazine

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130
Q

How are attacks prevented in menieres

A

lifestyle changes and betahistine

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131
Q

how are acute attacks treated in menieres

A

prochlorperazine

132
Q

describe episodes of vertigo associated with menieres

A

sudden onset unprovoked attacks lasting 20 mins to several hours
May be associated with nausea and vomiting.

133
Q

describe how hearing loss presents in menieres disease

A

initially fluctuates and occurs with vertigo attacks
Gradually becomes more permanent
Sensorineural hearing loss
affects lower frequencies first

134
Q

What is motor neurone disease?

A

A neurodegenerative condition of unknown cause which can affect the lower and upper motor neurones

135
Q

What is the most common type of motor neurone disease?

A

amylotrophic lateral sclerosis (up to 80% of cases)

136
Q

Describe ALS

A

loss of motor neurones in the motor neurones of the motor cortex and the anterior horn of the spinal cord
Typically has lower motor neurone signs in the arms and UMN signs in the legs

137
Q

Types of MND

A

amylotrophic lateral sclerosis
primary lateral sclerosis
progressive muscular atrophy
progressive bulbar palsy

138
Q

Desribe primary lateral sclerosis

A

loss of Betz cells in the motor cortex- will only have upper motor neurone signs

139
Q

Describe progressive muscular atrophy

A

loss of the anterior horn cells- lower motor neurone signs only
Affects distal muscles before proximal

140
Q

Describe progressive bulbar pasly

A

affects cranial nerves IX to XII - leads to palsy of the tongue, muscles of chewing and facial muscles

141
Q

which MND has the worse prognosis

A

progressive bulbar palsy

142
Q

How does MND present

A
  • asymmetrical limb weakness
  • mix of lower and upper motor neurone signs
  • foot drop
  • loss of dexterity
  • slurred speech
  • muscle wasting- small hand muscles
  • No sensory signs
143
Q

what symptoms will not be present in motor neurone disease>

A

no sensory disturbance
no ocular muscle disturbance
No sphincter dysfunction
no cerebellar sigms

144
Q

how is MND diagnosed?

A

clinical
May use nerve conduction studies- normal motor conduction
EMG- reduced action potentials and increased amplitude
MRI to rule out cervical cord compression and myelopathy

145
Q

Which drug can be used to prolong life in MND

A

riluzole- prolongs life by about 3 months
Respiratory support- non invasive ventilation at night
symptomatic baclofen for spasticity
Nutrition support- may need PEG tube

146
Q

What is the median survival of MND from symptom onset

A

3-5 years

147
Q

what is normal pressure hydrocephalus?

A

a condition characterised by the symptoms of hydrocephalus without significantly elevated CSF pressure

148
Q

triad of normal pressure hydrocephalus

A
  • urinary incontinence
  • dementia
  • gait abnormality
149
Q

theory of the pathophysiology of normal pressure hydrocephalus

A

thought to be due to reduced CSF absorption at the arachnoid villi or reduced blood perfusion to the basal ganglia

150
Q

Aetiology of normal pressure hydrocephalus

A

can be idiopathic or secondary to conditions such as SAH, meningitis, head trauma

151
Q

how is normal pressure hydrocephalus diagnosed?

A

imaging- will show ventriculomegaly in the absence of, or out of proportion to sulcal enlargement
LP- shows normal pressure

152
Q

how is normal pressure hydrocephalus diagnosed?

A

ventriculoperitoneal shunting
carbonic anhydrase inhibitors - acetazolamide
serial lumbar punctures

153
Q

management of a TIA if within 24 hours of onset

A

300mg of aspirin immediately
urgent assessment within 24 hours by a stroke specialist

154
Q

management of a TIA if more than 7 days after symptoms

A

should be seen by a stroke specialist within 7 dyas

155
Q

treatment options for spasticity in MS

A

baclofen and gabapentin are first line

156
Q

what key causes of status epilepticus should be ruled out first

A

hypoxia and hypoglycaemia

157
Q

what is autonomic dysreflexia

A

a clinical syndrome in patients who has a spinal cord injury at or above T6 spinal level
Most commonly triggered by faecal impaction or urinary retention
Presents as an unbalanced sympathetic response with unbalanced parasympathetic response

158
Q

how does autonomic dysreflexia

A

extreme hypertension
flushing and sweating above the lesion
agitation

159
Q

What is paroxysmal hemicrania?

A

severe attacks of severe unilateral headache in the orbital, supraorbital or temporal region
These are often associated with autonomic features and usually last less than 30 minutes and can occur multiple times a day

160
Q

Treatment of paroxysmal hemicrania

A

indomethacin

161
Q

When should patients with bells palsy be referred to ENT

A

if no improvement after 3 weeks refer urgently to ENT

162
Q

why can a subdural haematoma cause a third nerve pasly?

A

increased ICP can lead to herniation which can compress the third cranial nerve

163
Q

how does a third nerve palsy present?

A

down and out eye position (abducted and depressed)
ptosis
dilated pupil- cannot constrict in response to light

164
Q

first line radiological investigation for suspected stroke

A

non contrast CT

165
Q

first line treatment for focal seizures

A

lamotrigine or levetiracetam

166
Q

What is wernicke’s aphasia

A

receptive aphasia- impaired comprehension, fluent speech, inability to repeat back phrases
think W- what?

167
Q

What is broca’s aphasia

A

expressive aphasia- speech is non-fluent however will be able to comprehend

168
Q

where in the brain is Wernicke’s area

A

superior temporal gyrus

169
Q

where in the brain is brocas area

A

inferior frontal gyrys

170
Q

what migraine phophylactic is associated with cleft lip and palate

A

topiramate

171
Q

if a parietal lesion where will visual defects be?

A

inferior

172
Q

If a temporal lesion where will visual defects be?

A

superior

173
Q

If there is evidence of infarction on imaging can a TIA be diagnosed?

A

no - TIA can only be diagnosed if there is no evidence of acute infarction on imagn

174
Q

How are acute relapses of MS treated?

A

high dose steroids (methylprednisolone)

175
Q

first line treatment of absence seizures

A

ethosuximide

176
Q

What is Weber’s syndrome

A

a form of midline stroke characterised by ipsilateral cranial nerve III palsy and contralateral hemiparesis

177
Q

what screening tool is used to assess stroke symptoms in an acute setting

A

ROSIER

178
Q

how does juvenile myoclonic epilespy present?

A

seizures in the morning/ following sleep deprivation

179
Q

what blood test can be used to determine if a seizure has been a true seizure or a pseudoseizure

A

prolactin

180
Q

what radiculopathy causes loss of sensation on the dorsal aspect of the thumb and index finger

A

c6

181
Q

Causes of cauda equina

A

lumbar disc herniation- most common cause
lumbar stenosis
trauma
abscesses
malignancy
spondylolisthesis
congential cause (spinal bifida)
epidural haematoma

182
Q

presentation of cauda equine

A

lower back pain
radicular pain
leg weakness
difficulty walking
saddle anaesthesia
bowel or bladder dysfunction
erectile dysfunction

183
Q

diagnosis of cauda equina

A

urgent whole spine MRI
CT myelography if cant have MRI

184
Q

treatment of cauda equine

A

emergency surgery for cord decompression

185
Q

complications of cauda equina

A

premanent paralysis
sensory loss
bladder and bowel dysfunction
sexual dysfunction

186
Q

RF for SAH

A

hypertension
polycystic kidney disease
smoking
excessive alcohol intake
aged 45-70
cocaine use
connective tissue disorders- Marfans, Ehlers danlos

187
Q

pathophysiology of SAH

A

rupture of a berry aneurysm - 85% occur in the circle of willis

Rarer causes- AV malformations, vasculitis, arterial dissection, venous thrombosis

188
Q

complication of SAH

A

vasospasm causing ischaemic injury

189
Q

presentation of SAH

A

thunderclap headache- occipital, worse headache ever
may have preceding sentinel headache
neck stiffness
photophobia
nausea and vomiting
new symptom of altered brain function - reduced consciousness, seizure
coma

190
Q

examination findings of SAH

A

isolated pupil dilation with loss of light reflex
ophthalmoscopy may show intraocular haemorrhage
oculomotor nerve impairment

191
Q

Investigations for a SAH

A

urgent CT - hyperattentuated- hyperdense bright blood distributes in the basal cisterns, sulci and potentially the ventricular system

LP- xanthochromia, used if >12 hours since onset if CT was normal after 6 (CT less reliable after 6 hours)

CT angiography - to show the cause of SAH

192
Q

Treatment of SAH

A

initial- nimodipine to reduce vasospasm

definitive- endovascular coiling r neurosurgical clipping

193
Q

complications of SAH

A

hydrocephalus, electrolyte disturbance, seizures, hyponatraemia

194
Q

what is brudzinski’s sign

A

flexing of the neck causes hip and knee flexion

195
Q

what is kernig’s sign

A

extending leg from 90 degrees elicits pain

196
Q

how does optic neuritis present

A

graying or blurring of vision in one eye
may have pain on moving eye and loss of colour discrimination (particularly red)

197
Q

acute management of myasthenia gravis

A

pyridostigmine

198
Q

management of myasthenic crisis

A

plasma exchange, IV Ig

199
Q

where are most adult brain tumours located

A

supratentorial

200
Q

where are most paediatric brain tumours located

A

infratentorial

201
Q

What condition is associated with myasthenia gravis

A

thymomas

202
Q

pathophysiology of myasthenia gravis

A

antibodies against the nicotinic Ach receptors on the post-synaptic membrane which block the binding of Ach preventing the end plate potential becoming large enough to trigger muscle contracti

203
Q

How does myasthenia gravis present

A

muscle fatiguability
ocular symptoms- diplopia, ptosis (may be worse with prolonged upwards gaze)
fatiguable chewing
expressionless face (myasthenic sneer)

204
Q

how is myasthenia gravis diagnosed?

A

tensilon test - infusion of acetylcholinesterase inhibitor will briefly improve symptoms (edrophonium)

measure AChR and MuSK antibodies

EMG

205
Q

What antibodies are associated with myasthenia gravis

A

AChR and MuSK

206
Q

Long term treatment of myasthenia gravis

A

corticosteroids (prednisolone)
Immunosuppressives (azathioprine)
thymectomy

207
Q

What is a side effect of phenytoin

A

megaloplastic anaemia due t altered folate metabolism

Others: peripheral neuropathy, gingival hyperplasia

208
Q

How does subacute degeneration of the spinal cord present?

A

hyperreflexia
loss of proprioception
loss of vibration sense

209
Q

what is the first line treatment of stroke and TIA in those who have gastric ulcers and are high risk of bleeding

A

clopidogrel

210
Q

first line treatment of trigeminal neuralgia

A

carbamazepine

211
Q

what type of MRI should be used for MS

A

MRI brain with contrast

212
Q

if clopidogrel is not tolerated what treatment can be given from secondary prevention following a stroke

A

aspirin 75mg

213
Q

1st like medications for alzheimer’s

A

donezepil

214
Q

medications that can be used for alzheimer’s disease?

A

donezepil
rivastigmine
Memantine

215
Q

if someone with dementia suffers hallucinations what medication is good ?

A

rivastigmine

216
Q

What is trigeminal neuralgia

A

severe episodic facial pain in the distribution of one of the branches of the 5th trigeminal cranial nerve

217
Q

epidemiology of trigeminal neuralgia

A

increased in women, increases with age (rare those younger than 40)

218
Q

pathophysiology of trigeminal neuralgia

A

90% thought to be caused by vascular compression of the trigeminal nerve

Causes demyelination and abnormal electrical activity in response to stimuli

219
Q

How does trigeminal neuralgia present?

A

paroxysmal attacks of pain that may be triggered by precipitating factors such as touching the face, cold wind, vibration and cleaning teeth

220
Q

What is the pain like in trigeminal neuralgia

A

electric shock like severe pain, usually unilateral, short-lived, recurrent and episodic.

221
Q

Treatment of trigeminal neuralgia

A

1st line- carbamazepine
2nd line- gabapentin, lamotrigine

222
Q

pathophysiology of wernicke’s encephalopathy

A

thiamine deficiency leadsing to decreased activity of thiamine dependent enzymes

Causes neuronal death in parts of the brain including- medial dorsal thalamic nucleus, mamillary bodies, periaqueductal grey matter, floor of the first ventricle and cerebellar vermis

223
Q

How does wernicke’s encephalopathy present?

A

triad of confusion, ataxia and ophthalmoplegia / nystagmus

224
Q

triad of korsakoff’s

A

retrograde amnesia, anterograde amnesia, confabulation

225
Q

How is wernicke’s encephalitis treated

A

thiamine
magnesium sulphate
pabrinex

226
Q

if a patient on levodopa presents with postural instability what is the most likely cause?

A

the parkinsons disease not the medication

227
Q

what is ramsey hunt syndrome?

A

shingles affecting the facial nerve

228
Q

how does ramsey hunt syndrome present?

A

ear pain, vesicles in the external auditory canal, vertigo, tinnitus

229
Q

triggers for migraines

A

chocolate
hangovers
oral contraceptive pill
cheese
orgasms
lie ins
alcohol
tumult
exercsie

230
Q

How does a migraine present

A

unilateral throbbing headache lasting 4-72 hours,
moderate to severe
associated with nausea and vomiting
photophobia and phonophobia
may have an associated aura- zig zag lines, pins and needles

231
Q

what features may occur in the prodrome of a migraine?

A

yawning
fatigue
mood changes
craving

232
Q

what classifies chronic migraines

A

occur on at least 15 days a month

233
Q

What is the criteria for migraines

A
  1. at least 5 attacks.
  2. headache lasting 4-72 hours
  3. headache has at least 2 of the following qualitites:
    - unilateral
    - pulsating
    - moderate to severe
    - aggravated by physical activity
  4. there is at least one of the following:
    - nausea +/- vomiting
    - photophobia +/- phonophobia
  5. headache cannot be attributed to another disorder
234
Q

what aura symptoms of migraine are atypical and require further investigation

A

motor weakness
double vision
visual symptoms in one eye
poor balance
decreased level of consciousness

235
Q

1st line acute treatment of a migraine

A

combination therapy of oral triptan and either paracetamol or NSAID

may add anti-emetic if not effective (e.g metoclopramide)

236
Q

prophylactic drugs for migraines

A

propranolol
topiramate
amitriptyline

237
Q

which migraine prophylactic should not be used in pregnant women

A

topiramate- teratogenic and can reduce effectiveness of prophylaxis

238
Q

what treatment can be given to women with menstrual cycle related migraines

A

frovatriptan or zolmitriptan when needed

239
Q

how does an atonic seizure present

A

sudden weakness in all muscles of the body with retained awareness

240
Q

what sign of multiple sclerosis is characterised by tingling in hands when flexing neck

A

Lhermitte’s phenomenon

241
Q

which type of seizure may be associated with plucking of clothes?

A

temporal lobe

242
Q

what is the initial management of a suspected TIA in someone on anticoagulants

A

immediate referral to emergency department for imaging

243
Q

what is the management of a brain abscess

A

IV cephalosporin + metronidazole

244
Q

how does a brain abscess present?

A

headache
fever
focal neurology
conditions of raised ICP- nausea, papilloedema, seizures

245
Q

how does a brain abscess present on CT scan

A

ring enhancing lesion

246
Q

most common complication following meningitis

A

sensorineural hearing loss

247
Q

when would you offer thrombectomy alongside thrombolysis

A

when there is confirmed occlusion of the proximal anterior circulation

248
Q

what motor pattern will be seen in an anterior cerebral artery stroke

A

leg weakness but not face or speech impairment

249
Q

what should be done on all stroke patients to reduce aspiration pneumonia

A

swallow assessment to evaluate swallow function before any oral intake

250
Q

how do chronic subdural haematomas present on CT

A

hypodense (dark)

251
Q

how does third nerve palsy present?

A

ptosis, dilated pupil and down and out appearance of the eye

252
Q

how does an ulnar nerve palsy present?

A

wasting of the hypothenar muscles, loss of thumb adduction, wasting of the first web space and ulnar claw hand

253
Q

what are the components of a GCS score

A

motor response
verbal response
eye opening

254
Q

6 types of motor response scores for GCS

A

6- obeys commands
5- localises to pain
4- withdraws from pain
3- abnormal flexion to pain
2- extending to pain
1- none

255
Q

5 types of verbal response scores for GCS

A

5- orientated
4- confused
3- words
2- sounds
1- none

256
Q

4 types of eye opening response

A

4- spontaneous
3- to speech
2- to pain
1- none

257
Q
A
258
Q

If a ‘seizure’ is associated with a period of feeling light headed and sweaty before what is the likely cause

A

Vasovagal syncope

259
Q

what is myasthenic gravis

A

a chronic autoimmune condition caused by insufficiency acetyl choline receptors in the neuromuscular junction

260
Q

pathophysiology of myasthenia gravis

A

antibodies to the acetyl choline receptor on the post synaptic membrane (prevents Ach binding and causing muscle contraction)

a type II hypersensitivity reaction

261
Q

associated diseases to MG

A

thymomas in 15%
autoimmune diseases- thyroid disease, rheumatoid, SLE, pernicious anaemia

262
Q

how does MG present?

A

muscle fatiguability - muscle weakness that improves on rest and is worse towards the end of the day
- proximal muscles first
- arms more than legs

Weakness of the extraocular muscles - diplopia, ptosis (may be worse on prolonged upward gaze)

dysphagia

Facial weakness- myasthenic sneer

respiratory muscle weakness

263
Q

how is MG diagnosed?

A

antibody testing= acetylcholinesterase receptor antibody (85-90%) and anti-muscle specific- tyrosine kinase antibody (MuSK)

Gold- single fibre EMG

May also CT for thymoma

264
Q

what test can be done for MG

A

tensilon test- give patient IV edrophonium and there should be temporary improvement in symptoms (as it is an acetylcholinesterase inhibitor)

265
Q

what is the first line treatment of MG

A

pyridostigmine- long acting acetylcholinesterase inhibitor

266
Q

overview of MG treatment

A
  • pyridostigmine
  • can add immunosuppressant (prednisolone, azathioprine)
  • thymoma
267
Q

what is myasthenic crisis

A

a life threatening worsening of myasthenia causing respiratory failure

268
Q

treatment of myasthenic crisis

A

plasmapheresis
IV immunoglobulins

269
Q

what can trigger myasthenic crisis

A

warm weather, infection, surgery, stress, pregnancy, illness
medications- penacillamine, quinidine, procainamide, beta blockers, lithium, phenytoin, antibiotics (gentamycin, tetracyclines, macrolides)

270
Q

what additional tests should be done in young patients (under 55) who present with stroke with no obvious cause

A

thombophilia and autoimmune screening

271
Q

How can you distinguish between foot drop caused by common peroneal nerve pasly and that caused by L5 radiculopathy

A

in common peroneal nerve pasly there will be weakness in eversion of the feet whereas in L5 there will be weakness in inversion

272
Q

How is meningitis treated in those with penicillin allergy

A

IV chloramphenicol- cannot use IV ceftriaxone as there is cross-reactivity between penicillins and cephalosporins

273
Q

treatment of ramsey hunt

A

oral aciclovir

274
Q

How might a typical migraine aura be described?

A

transient hemianopic disturbance or a spreading scintillating scotoma (jagged crescent)

275
Q

RF for ischaemic stroke

A

age
htn
smoking,
hyperlipidaemia
dm
AF

276
Q

RF for haemorrhagic stroke

A

HTN ,
anticoagulants
age
AV malformations

277
Q

What vessels are effected in weber syndrome

A

the branches of the posterior cerebral artery that supply the midbrain

278
Q

How does Weber’s syndrome present?

A

ipsilateral cranial nerve III palsy
contralateral weakness in the upper and lower limbs

279
Q

What vessels are effected in Wallenberg syndrome (lateral medullarly syndrome)

A

posterior inferior cerebellar artery

280
Q

How does lateral medullary syndrome (Wallenberg’s) present?

A

ipsilateral loss of pain and temperature in the face
contralateral loss of pain and temperature in the limbs and torso
ataxia
nystagmus

281
Q

What artery is effected in lateral pontine syndrome

A

anterior inferior cerebellar artery

282
Q

how does lateral pontine syndrome present?

A

similar to wallenbergs but with ipsilateral facial paralysis and deafness

283
Q

How does a stroke affecting the retinal/ ophthalmic artery present?

A

amaurosis fugax

284
Q

How does a stroke affecting the basilar artery present?

A

locked in syndrome

285
Q

How does a lacunar stroke present?

A

either:
- unilateral weakness (+/- sensory loss) of face, arm or leg, or all three
- purely sensory loss
- ataxic hemiparesis

286
Q

How does a stroke affecting the anterior cerebral artery present?

A

contralateral hemiparesis and sensory loss (legs more than arms)

287
Q

how does a stroke affecting the middle cerebral artery present?

A

contralateral hemiparesis and sensory loss (arms more than legs)
contralateral homonymous hemianopia
haphasia

288
Q

how does a stroke affecting the posterior cerebral artery present ?

A

contralateral homonymous hemianopia with macular sparing
visual agnosia

289
Q

What three presentations are considered in the oxford stroke classification

A

unilateral hemiparesis and/or hemisensory loss of the face, arm , leg

homonymous hemianopia

higher cognitive dysfunction (e.g. dyphasia)

290
Q

what may be shown on CT of ischaemic stroke

A

low density white and grey matter,
hyperdence artery

291
Q

what may be shown on CT of haemorrhagic stroke?

A

hyperdence material with surrounding low dense oedema

292
Q

what should blood pressure be bought down to before thrombolysis

A

185/110

293
Q

what are some contraindications to thombolysis

A

previous intracranial haemorrhage
seizure on stroke onset
intracranial neoplasm
suspected SAH
stroke or injury in preceding 3 months
LP in previous 7 days
GI haemorrhage in preceding 3 weeks,
oesophageal varices
uncontrolled HTN

294
Q

what is the inheritance of neurofibromatosis ?

A

autosomal dominant

295
Q

what is the mutation associated with neurofibromatosis type 1?

A

a mutation on chromosome 17- encodes for the tumour suppressor protein neurofibrin

296
Q

what is the mutation associated with neurofibromatosis type 2?

A

a mutation on chromosome 22- encodes for merlin, a tumour suppressor protein which is important in schwann cells

297
Q

how does neurofibromatosis type 1 present?

A

Cafe-au-lait spots
Axillarly and inguinal freckling
Peripheral neurofibromas
Iris haematomas (Lisch nodules)
Scoliosis
phaeochromocytosis

298
Q

how does neurofibromatosis type 2 present?

A

bilateral vestibular schwannomas
mutliple intracranial schwannomas, meningiomas and ependymomas

299
Q

how may neurofibromas are indicative of neurofibromatosis ?

A

two or more or one plexiform neurofibroma

300
Q

what are two key complications of neurofibromatosis

A

GI stromal tumours
malignant peripheral nerve sheath tumours

301
Q

What is a brain abscess?

A

a localised area of necrosis in the brain tissue with associated inflammation

302
Q

Causes of brain abscesses?

A

direct implantation- from trauma or iatrogenic
local spread of infection from adjacent structures (e.g. sinusitis, otitis media)
haematogenous spread from other organ infections

303
Q

RF for brain abcesses

A

right to left shut (allows blood to bypass the lungs where infection could be filtered out)
bronchiectasis
immunsupression

304
Q

how does a brain abscess present?

A

fever
headache
progressive focal neurology

May have nausea, early morning headache, seizures, papilloedema

305
Q

How is a brain abscess diagnosed?

A

CT or MRI- shows bright ring of capsule around necrotic core

306
Q

How are brain abscesses treated?

A

surgery- craniotomy and abscess debridement
antibiotics- IV cephalosporins and metronidazole
dexamethasone

307
Q

What areas of the brain are affected in wernicke’s

A

mamillary bodies, ventricle walls, periaqueductal grey matter, floor of the 4th ventricle

308
Q

triad of wernicke’s encephalopathy

A

cognitive decline
gait ataxie
oculomotor dysfunction- nystagmus, ophthalmoplegia

309
Q

what ophthalmoplegia can occur in wernicke’s encephalopathy?

A

lateral rectus palsy
conjugate gaze palsy

310
Q

what investigations may be done for wernicke’s

A

thiamine levels
CT/MRI to rule out other causes
decreases red cell transketolase

311
Q

triad of korsakoff’s

A

retrograde amnesia
anterograde amnesia
confabulation

312
Q

What is spinal stenosis?

A

a condition where the central canal of the spine is narrowed which causes compression of the nerves and pain

313
Q

Most common cause of spinal stenosis

A

age related degenerative change

314
Q

what is the pathophysiology of how age- related degeneration causes spinal stenosis

A
  • biochemical changes in the intervertebral disc (cell death, loss of proteoglycan and water content) lead to progressive disc bulging and collapse
  • hypertrophy and osteophyte formation on the facet joints
  • thickening of the ligamentum flavum

These three features (bulging disc, facet hypertrophy and ligamentum flavum thickening) lead to narrowing of the spinal canal and compression of nerves

315
Q

How does spinal stenosis present ?

A

similar to PAD- claudication like pain of the proximal thigh and buttock
- differs from PAD as it is relieved when walking up hill and worse on stretching of the canal (e.g. walking downstairs)
- may also have neurological symptoms- burning and tingling

316
Q

How is spinal stenosis diagnosed?

A

MRI

317
Q

How is spinal stenosis treated?

A

1st line- analgesia, physio, weight loss
definitive- laminectomy

318
Q

what are myopathies?

A

diseases of the skeletal muscle (not caused by nerve disorders) that cause the muscle to become weak and wasted

319
Q

what are the three broad types of myopathies

A

hereditary
inflammatory
endocrine

320
Q

What are some examples of hereditary myopathies

A

duchenne muscular dystrophy
becker muscular dystrophy
mitochondrial myopathies
metabolic myopathies

321
Q

Give some examples of inflammatory myopathies

A

polymyositis and dermatomyositis

322
Q

what drugs can cause temporary myopathies?

A

statins, steroids

323
Q

How does polymyositis present?

A

proximal muscle weakness
Reynauds
Resp muscle weakness
dysphagia
dysphonia
interstitial lung disease

324
Q

what skin signs may be present in dermatomyositis ?

A

helitrope rash- macular periorbital rash
shawl sign- macular rash over back and shoulders
Gottron’s papules- roughened red papules over the extensor surfaces of the fingers)
Holter’s sign- erythema of the buttocks, hips and lateral thighs
photosensitive rashes

325
Q

what investigations may be done to diagnose polymyositis and dermatomyositis

A

raised creatinine kinase
raised muscle enzymes (LDH)
Anti-jo-1 and anti-mi-2
EMG
muscle biopsy

326
Q

how are dermatomyositis and polymyositis treated?

A

in the acute stage- high dose corticosteroids then wean down
DMARDs longterm

327
Q
A

3A (32 decks)

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