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Year 6 > Neuro > Flashcards

Neuro Flashcards

1
Q

Summarise Motor component in GCS

A
  1. Obeys commands
  2. Localises to pain
  3. Withdraws from pain
  4. Abnormal flexion to pain (decorticate posture)
  5. Extending to pain
  6. None
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2
Q

Summarise Verbal response in GCS

A
  1. Orientated
  2. Confused
  3. Words
  4. Sounds
  5. None
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3
Q

Summarise Eye opening in GCS

A
  1. Spontaneous
  2. To speech
  3. To pain
  4. None
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4
Q

How much does spontaneous eye opening score?

A

4

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5
Q

How much does eye opening to speech score?

A

3

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6
Q

How much does eye opening to pain score

A

2

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7
Q

How much does a verbal response of sounds score?

A

2

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8
Q

How much does a verbal response of words score?

A

3

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9
Q

How much does a verbal response of confused words score?

A

4

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10
Q

How much does localising pain score?

A

5

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11
Q

How much does withdrawing from pain score?

A

4

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12
Q

How much does abnormal flexion in response to pain score?

A

3

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13
Q

How much does extension to pain score?

A

2

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14
Q

features of temporal lobe seizure

A

May occur with or without impairment of consciousness or awareness

An aura occurs in most patients
typically a rising epigastric sensation

also psychic or experiential phenomena, such as déjà vu, jamais vu

less commonly hallucinations (auditory/gustatory/olfactory)

Seizures typically last around one minute

automatisms (e.g. lip smacking/grabbing/plucking) are common

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15
Q

features of frontal lobe seizures [4]

A

Head/leg movements
posturing
post-ictal weakness
Jacksonian march

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16
Q

features of parietal lobe seizures [4]

A

Paraesthesia
electric shock type sensations
hallucinations
dizziness.

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17
Q

features of occipital lobe seizures

A

floaters/ flashes

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18
Q

key features of MND

A

asymmetric limb weakness is the most common presentation of ALS

the mixture of lower motor neuron and upper motor neuron signs

wasting of the small hand muscles/tibialis anterior is common
fasciculations

the absence of sensory signs/symptoms

vague sensory symptoms may occur early in the disease (e.g. limb pain) but ‘never’ sensory signs

doesn’t affect external ocular muscles

no cerebellar signs

abdominal reflexes are usually preserved

sphincter dysfunction if present is a late feature

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19
Q

which MND has the best prognosis

A

progressive muscular atrophy

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20
Q

which MND has the worst prognosis

A

progressive bulbar palsy

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21
Q

which MND has UMN signs only

A

Primary Lateral Sclerosis

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22
Q

which MND has UMN and LMN signs

A

Amyotrophic Lateral Sclerosis

UMN in the legs
LMN in the arms

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23
Q

which MND has LMN signs only

A

Progressive muscular atrophy

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24
Q

abx for cerebral abscess

A

cephalosporin plus metronidazole

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25
Q

adverse reaction of carbamazepine

A

SJS

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26
Q

first line treatment for MS related spasticity

A

baclofen
gabapentin

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27
Q

drug treatment for MS related fatigue

A

amantidine

once other problems (e.g. anaemia, thyroid or depression)

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28
Q

CN 5 affected by acoustic neuroma causing

A

absence of corneal reflex

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29
Q

which cranial nerves can be affected by an acoustic neuroma

A

5,7, 8

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30
Q

CN 8 affected by acoustic neuroma causing [3]

A

unilateral tinnitus
unilateral sensory hearing loss
vertigo

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31
Q

drugs that predispose to Idiopathic intracranial Hypertension [5]

A

COCP
tetracyclines
steroids
retinoids
lithium

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32
Q

nerve roots for Klumpke

A

C8-T1

the lowest branch

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33
Q

nerve root for Horner’s

A

T1

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34
Q

treatment for spasticity in MS

A

baclofen or gabapentin

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35
Q

how does a chronic bleed present on CT head?

A

hypodense

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36
Q

how does an acute bleed present on CT head?

A

hyperdense

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37
Q

how is an acute subdural managed?

A

Small or incidental acute subdurals can be observed conservatively. Surgical options include monitoring of intracranial pressure and decompressive craniectomy.

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38
Q

how is a chronic subdural managed?

A

an incidental finding or if it is small in size with no associated neurological deficit can be managed conservatively with the hope that it will dissolve with time.

If the patient is confused, has an associated neurological deficit or has severe imaging findings then surgical decompression with burr holes is required.

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39
Q

investigation of choice for acoustic neuroma

what else is done alongside this?

A

gadolinium-enhanced MRI of cerebellopontine angle

with audiogram

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40
Q

which vessel is occluded in Lateral Medullary Syndrome?

A

posterior inferior cerebellar artery.

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41
Q

what are the cerebellar features of Lateral Medullary Syndrome

A

ataxia
nystagmus

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42
Q

what are the brainstem features of Lateral Medullary Syndrome?

A

ipsilateral: dysphagia, facial numbness, cranial nerve palsy e.g. Horner’s

contralateral: limb sensory loss

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43
Q

what is Lateral Medullary Syndrome also known as ?

A

Wallenberg’s Syndrome

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44
Q

what is the preferred method of nutrition for patients with Motor Neurone Disease?

A

percutaneous gastrostomy tube (PEG

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45
Q

examples of 5HT-3 antagonists [2]

A

ondansetron
palonosetron

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46
Q

adverse effects of 5HT-3 antagonists [2]

A

prolonged QTc
constipation

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47
Q

where do 5HT-3 antagonists act

A

CTZ in medulla oblongata

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48
Q

mode of inheritance of charcot Marie tooth

A

Autosomal dominant

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49
Q

features of charcot Marie tooth [4]

A

motor symptoms mainly
distal muscle wasting
pes cavus, clawed toes
high stepping gait due to foot drop

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50
Q

how long can’t someone drive for an unprovoked/first seizure with no abnormal scans

A

6 months

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51
Q

how long can’t someone drive for an seizure with abnormal scans

A

12 months

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52
Q

how long can’t someone drive if they have multiple TIAs over a short period.

A

3 months

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53
Q

how long can’t someone drive if they have had a stroke or TIA with no neurological deficits

A

1 month

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54
Q

how long can’t someone drive if they have had a craniotomy e.g. for meningioma

A

1 year

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55
Q

how long can’t someone drive for single episode of syncope that was explained and treated

A

4 weeks

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56
Q

how long can’t someone drive for single episode of syncope that was not explained

A

6 months

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57
Q

how long can’t someone drive for two or more episodes of syncope

A

12 months

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58
Q

first line treatment for essential tremor

A

propanolol

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59
Q

differences between essential and Parkinsonian tremor

A

Essential: mildly asymmetrical, action tremor

Parkinsons: very asymmetrical, rest tremor

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60
Q

mode of inheritance of essential tremor

A

autosomal dominant

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61
Q

what is secondary progressive MS

A

describes relapsing-remitting patients who have deteriorated and have developed neurological signs and symptoms between relapses

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62
Q

what is primary progressive MS

A

progressive deterioration from onset

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63
Q

visual symptoms of MS [4]

A

optic neuritis
optic atrophy
Uthoffs phenomenon
internuclear ophthalmoplegia

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64
Q

motor symptoms of MS [1]

A

spastic weakness

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65
Q

Sensory symptoms of MS [4]

A

Pins and needles
Lhermitte’s phenomenon
trigeminal neuralgia
numbness

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66
Q

Cerebellar symptoms of MS

A

ataxia
tremor

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67
Q

associated symptoms of Bells palsy [4]

A

hyperacusis
dry eyes
altered taste
post-auricular pain

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68
Q

when should Bell’s palsy patients be referred to urgently ENT

A

if treatment does not improve symptoms after 3 weeks

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69
Q

Hypo on CT ?shade

A

dark

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70
Q

4 pillars of Parkinsons

A

Bradykinesia
Resting tremor
Postural instability
Rigidity

additional symptoms are Parkinsons+

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71
Q

muscles innervated by the ulnar nerve [5]

A

medial two lumbricals
aDductor pollicis
interossei
hypothenar muscles: abductor digiti minimi, flexor digiti minimi
flexor carpi ulnaris

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72
Q

what is a cause of ulnar nerve neuropathy

A

Cubital Tunnel Syndrome

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73
Q

Three meds that can be given after the second dose of IV lorazepam in acute seizure management

A

Phenytoin
Sodium valporate
Levetiracetam (mostly used)

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74
Q

mode of inheritance of tuberous sclerosis

A

autosomal dominant

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75
Q

how do symptoms present in alcoholic neuropathy

A

sensory symptoms before motor symptoms

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76
Q

which part of the spinal tracts are affected first in B12 deficiency

A

Dorsal columns (joint position and vibration)

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77
Q

Main treatment of degenerative cervical myelopathy

A

decompressive surgery

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78
Q

what sign is positive in degenerative cervical myelopathy

A

Hoffman’s sign

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79
Q

features of degenerative cervical myelopathy

A

pain in the neck, arms, and legs

loss of sensory, motor (fine, dexterity) and autonomic function

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80
Q

what is degenerative cervical myelopathy often misdiagnosed as

A

carpal tunnel syndrome

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81
Q

what causes autonomic dysreflexia?

A

patients who have had a spinal cord injury at, or above T6 spinal level.

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82
Q

What may trigger autonomic dysreflexia?

A

most commonly triggered by faecal impaction or urinary retention

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83
Q

features of autonomic dysreflexia [4]

A

extreme hypertension
flushing
sweating above the level of the cord lesion

agitation

and in untreated cases severe consequences of extreme hypertension have been reported, e.g. haemorrhagic stroke.

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84
Q

treatment of autonomic dysreflexia

A

Management of autonomic dysreflexia involves removal/control of the stimulus and treatment of any life-threatening hypertension and/or bradycardia.

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85
Q

what site of the brain are vestibular schwannomas found?

A

cerebellopontine angle

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86
Q

features of vestibular schwannomas [4]

A

vertigo
hearing loss
tinnitus
an absent corneal reflex and cranial nerves pathology (5,7,8)

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87
Q

which part of the spine convey the sensation of fine touch, proprioception and vibration

A

dorsal column

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88
Q

are UMN or LMN signs seen in poliomyelitis?

A

affects anterior horns resulting in lower motor neuron signs

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89
Q

MoA of acetozolamide

A

carbonic anhydrase inhibitor

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90
Q

treatment of myasthenic crisis

A

IVIG and plasmapheresis

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91
Q

which malignancy is associated with myasthenia gravis

A

thymoma

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92
Q

first line treatment of myasthenia gravis

A

pyridostigmine (long acting acetylcholinesterase inhibitor)

neostigmine

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93
Q

why can extradural haematoma present with fixed dilated pupil

A

uncal herniation compresses CNIII

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94
Q

which brain bleed features a lucid interval

A

extradural

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95
Q

differentiating factor between Huntingtons and frontotemporal dementia

A

Huntingtons has motor symptoms while FTD does not

96
Q

features of Anterior Inferior Cerebellar Artery (AICA) i.e. Lateral Pontine Syndrome stroke

A

ipsilateral auditory deficits e.g. deafness
vertigo and vomiting
ipsilateral facial paralysis
ipsilateral cerebellar dysfunction.

This is due to the involvement of the facial and vestibulocochlear nerves within the brainstem and cerebellum.

97
Q

how does mononeuritis multiplex present

A

acute or subacute loss of sensory and motor function of individual nerves.

The pattern of involvement is asymmetric, however, as the disease progresses, deficit(s) becomes more confluent and symmetrical, making it difficult to differentiate from polyneuropathy.

98
Q

3 neurological features of tuberous sclerosis

A

developmental delay
epilepsy (infantile spasms or partial)
intellectual impairment

99
Q

which sensory modality is lost in syringomyelia

A

temperature due to compression of spinothalamic tracts

100
Q

investigations for syringomyelia

A

MRI spine and brain

101
Q

what effect does dopamine have on prolactin

A

inhibitory

102
Q

treatment of symptomatic or persistent syringomyelia

A

shunt

103
Q

adverse effects of levodopa [7] DOPAMINE

A

Dyskinesia
‘On-off’ effect
Postural hypotension and psychosis
Arrhythmias
Mouth dryness
Insomnia
Nausea & vomiting
EDS

reddish discolouration of urine upon standing

104
Q

Risk factor for Bell’s Palsy

A

women and pregnancy

105
Q

main investigation for degenerative cervical myelopathy

A

MRI of the cervical spine

106
Q

complication of DCM

A

recurrence at adjacent spinal levels

needs referral back to spinal surgery

107
Q

MS has UMN or LMN signs?

A

UMN only as it affects the CNS

108
Q

a positive straight leg raise test indicates which pathology

A

disc herniation

109
Q

which movement of the shoulder is most painful in adhesive capsulitis

A

Limited external rotation of the shoulder

110
Q

features of viral encephalitis[5]

A

fever
headache
psychiatric symptoms e.g. new onset somnolence
seizures
vomiting

111
Q

key investigation for viral meningitis

A

CSF PCR

main: HSV-1, VZV, enteroviruses

112
Q

which lobes are typically affected in viral encephalitis

A

temporal and inferior frontal lobes

113
Q

what is the timeframe for thrombolysis in acute ischaemic stroke

A

within 4.5 hours from onset of symptoms

114
Q

what timeframe should thrombectomy be offered alongside thrombolysis in acute ischaemic stroke

who can this be offered to

A

within 6 hours from onset of symptoms

confirmed occlusion of the proximal anterior circulation demonstrated by computed tomographic angiography (CTA) or magnetic resonance angiography (MRA)

115
Q

which nerve is affected in Saturday night palsy

A

radial nerve

116
Q

when is aspirin given after alteplase in acute stroke treatment

A

within 24 hours

117
Q

drug given in MND to extend life

A

riluzole

118
Q

TIA:investigations

A

carotid USS
MRI (not CT)
BP, ECG, bloods for risk factor

119
Q

management of TIA (w/o AF)

A

aspiring 300mg 14 days

ongoing: clopi+ statin 1st line;
aspirin+ dipyridamole+ statin 2nd line

Referral for specialist assessment within 24 hours (within 7 days if more than 7 days since the episode)
Diffusion-weighted MRI scan is the imaging investigation of choice.

120
Q

what degree of carotid stenosis requires an endarectomy

A

> 50%

121
Q

how is long term stroke prophylaxis determined

A

presence of AF:

NO AF –> clopi + statin ; aspirin+ dipyridamole+ statin

AF –> apixaban, rivaroxaban

122
Q

which index is used to monitor functional status and improvement post-stroke

A

Barthel index

123
Q

management of subarachnoid haemorrhage [3]

A

nimodipine (CCB, 21 days)
coiling
surgical clipping

124
Q

first line treatments for Parkinsons Disease [3]

A

levodopa (co-careldopa)
MAO-I e.g. selegiline
DA agonist e.g. ropinirole

125
Q

which antiemetic can be used in PD

A

domperidone (does not cross BBB unlike the other DA antagonists)

126
Q

what chemical is raised in true CNS seizure

A

prolactin

127
Q

acute management of migraine [2]

A

triptan (aura)
NSAID/paracetamol (no aura)

128
Q

prophylaxis of migraine

A

topimirate
propanolol

129
Q

acute management of cluster headache

A

100% oxygen and SC triptan

130
Q

prophylaxis of cluster headache

A

verapamil

131
Q

which antibodies are investigated for in MS

A

Anti-MBP (myelin basic protein)

NMO-IgG (neuromyelitis optica) → Devic’s syndrome

132
Q

chronic management of MS [2]

A

DMARDs:
* IFN-beta
* Glatiramer

Biologicals:
* Natalizumab (anti-VLA-4 AB)
* Alemtuzumab (anti-CD52)

133
Q

treatment of MS related pain

A

amitriptyline

134
Q

treatment of MS related tremor

A

clonazepam

135
Q

long term management of myasthenia gravis [2 lines]

A

immunosuppression:
1st line- prednisolone
2nd line- azathioprine, MMF etc

136
Q

which cancers are associated with Lambert Eaton Syndrome [3]

A

SCLC
breast
ovarian

137
Q

what antibody is produced in Lambert Eaton Syndrome

A

against presynaptic voltage-gated calcium channel (VGCC) in the peripheral nervous system

138
Q

what occurs with repeated muscle contraction in Lambert Eaton Syndrome

A

increase in muscle strength

139
Q

investigation of Lambert Eaton Syndrome

A

EMG
Incremental response to repetitive electrical stimulation

140
Q

management of Lambert Eaton Syndrome [2]

A

treat the underlying cancer
immunosuppression

141
Q

is sensation normal or abnormal in MND

A

normal

142
Q

is eye movement normal or abnormal in MND

A

normal till very late

143
Q

treatment of drooling in MND

A

amitriptyline

144
Q

gait in Unilateral UMN lesion and Bilateral UMN lesion

A

unilateral –> circumducting gait

bilateral –> scissoring gait

145
Q

tone in UMN lesion

A

increased

146
Q

reflexes in UMN lesion

A

increased

147
Q

power in UMN lesion

A

decreased in pyramidal distribution (voluntary muscle control)

legs: ext > flex
arms: flex > ext

148
Q

Babinski and Hoffman in UMN lesion

A

both positive

149
Q

what is the difference between pyramidal and extrapyramidal tracts

A

In summary, while both pyramidal and extrapyramidal tracts contribute to motor control, the pyramidal tracts are more directly involved in voluntary, skilled movements, while the extrapyramidal tracts play a modulatory role in regulating posture, muscle tone, and involuntary movements. The term “extrapyramidal” is historical and refers to the tracts that do not pass through the pyramids of the medulla.

150
Q

which form of hypertonia is extra-pyramidal

A

rigidity “lead-pipe” like that seen in Parkinson’s

increased tone throughout ROM independent of velocity

151
Q

which form of hypertonia is pyramidal

A

spasticity “clasp knife”

increased velocity dependent tone, more rigid at the start

152
Q

Hoffman reflex: how do you illicit it and what does it cause

A

flick middle digit IP joint → adduction of thumb + flexion of index digit)

153
Q

tone in LMN lesion

A

decreased

154
Q

reflexes in LMN lesion

A

decreased

155
Q

power in LMN lesion in legs and arms: extensor or flexor

A

legs: extensor > flexor
arms: flexor > extensor

156
Q

which type of motor neurone lesion presents with wasting ad fasciculations

A

LMN lesion

157
Q

motor predominant causes of peripheral neuropathy [5]

A

GBS (AIDP)
polio
CIDP
porphyria
lead poisoning

158
Q

sensory predominant causes of peripheral neuropathy [4]

A

diabetes mellitus
alcohol
vit B12 def
isoniazid

159
Q

investigations for Charcot Marie Tooth (+HSMN, peroneal muscular dystrophy)

A

nerve conduction studies: reduced conduction velocity and amplitude

160
Q

Signs of cerebellar syndrome: DANISH

A

D- Dysdiadochokinesia, dysmetria, dysarthira
A- Ataxia
N- Nystagmus
I- Intention tremor
S- slurred Speech
H- Hypotonia

161
Q

What quandranopia does a pituitary tumour cause

A

superior

162
Q

what quadranopia does a craniopharngioma cause

A

inferior

163
Q

where in the brain does a superior quadranopia originate

A

temporal [PITS]

164
Q

where in the brain does a inferior quadranopia originate

A

parietal [PITS]

165
Q

how does Weber syndrome present

A

ipsilateral third nerve palsy with contra-lateral hemiplegia due to midbrain stroke

166
Q

pupil size in surgical third nerve palsy

A

dilated

167
Q

treatment of paroxysmal hemicrania

A

indomethacin

168
Q

head ache with fluctuating consciousness suggests

A

subdural

169
Q

what should be done in suspected stroke/TIA before administering aspirin

A

non contrast CT head to exclude haemorrhagic stroke

170
Q

treatment of acute pulmonary oedema that goes into hypotension/cardiogenic shock [2]

A

dobutamine
norepinephrine (if dobutamine doesn’t work)

171
Q

viral meningitis vs encephalitis

A

viral meningitis: neck stiffness, photophobia etc, self limiting

encephalitis: more ill, temporal lobe seizure

172
Q

contraindications to aspirin 300mg in TIA

A
  • already taking regular aspirin
  • bleeding disorder or taking anticoagulant –> need urgent CT
  • aspirin CI
173
Q

treatment of absence seizures

A

ethosuximide

174
Q

secondary prevention of TIA

A

1st line: clopi + statin
2nd line: aspirin + dipyridamole + statin

175
Q

visual symptoms of TIA

A

amaurosis fugax
homonymous hemianopia
diplopia

176
Q

how can you distinguish flexing and localising pain in GCS assessment

A

To be counted as localising, the arm must be brought above the clavicle, else it should be scored as ‘flexing’

177
Q

investigations for HSV encephalitis

A

CSF: lymphocytosis, elevated protein
PCR for HSV
CT: medial temporal and inferior frontal changes (e.g. petechial haemorrhages) - normal in one-third of patients
MRI is better
EEG pattern: lateralised periodic discharges at 2 Hz

178
Q

how long do cluster headache clusters lasts

how long do the episodes last

A

4 to 12 weeks

15 mins to 2 hours

179
Q

investigation required for cluster headaches

A

MRI with contrast to check for SOL

180
Q

cerebellar lesions: which side do they present on

A

symptoms are on ipsilateral side

181
Q

posterior circulation lesions [3]

A

ataxia
vertigo
isolated homonymous hemianopia

includes vertebral arteries

182
Q

anterior circulation lesions

A

middle and anterior cerebral arteries

183
Q

investigating thunderclap headache [3]

A

CT head
LP
CT angio

184
Q

when is aspirin used in stroke

A

24h after thrombolysis or stat if no thrombolysis is planned

185
Q

what signs are expected in lesions below L2 eg caudal equina

A

LMN signs

186
Q

where do dorsal column fibres cross

A

medulla

187
Q

where to spinothalamic tract fibres cross

A

spinal level

188
Q

overall management of stroke [4]

A

Exclude hypoglycaemia
Immediate CT brain to exclude haemorrhage
Aspirin 300mg daily for two weeks (started after haemorrhage is excluded with a CT)
Admission to a specialist stroke centre where thrombolysis may be initiated

189
Q

what two conditions need to be screened for when finding the underlying cause of stroke

A

carotid artery stenosis and atrial fibrillation

therefore do carotid imaging and ECG/monitoring

190
Q

when is anticoagulation for stroke w/ AF started

A

after haemorrhage has been excluded and 2 weeks of aspirin has been taken

191
Q

Weber’s syndrome

which branch?

A

Ipsilateral CN III palsy
Contralateral weakness of upper and lower extremity

posterior cerebral artery
no cerebellar signs

192
Q

Posterior inferior cerebellar artery (lateral medullary syndrome, Wallenberg syndrome)

A

Ipsilateral: facial pain and temperature loss
Contralateral: limb/torso pain and temperature loss
Ataxia, nystagmus

193
Q

Broca’s dysphasia: 3 features

which lobe

A

speech non-fluent
comprehension normal
repetition impaired

frontal lobe

194
Q

Parkinsonism with associated autonomic disturbance (atonic bladder, postural hypotension) points towards ….

A

Multiple System Atrophy

erectile dysfunction: often an early feature
postural hypotension
atonic bladder
cerebellar signs

There are 2 predominant types of multiple system atrophy
1) MSA-P - Predominant Parkinsonian features
2) MSA-C - Predominant Cerebellar features

195
Q

treatment of myoclonic seizures in females

A

levetiracetam

196
Q

treatment of tonic or atonic seizures in females

A

lamotrigine

197
Q

features of MCA stroke [3]

A

Contralateral hemiparesis and sensory loss, upper extremity > lower
Contralateral homonymous hemianopia
Aphasia

198
Q

features of PCA stroke [2]

A

Contralateral homonymous hemianopia with macular sparing
Visual agnosia

199
Q

features of retinal artery stroke

A

amaurosis fugax

200
Q

features of Basilar artery stroke

A

locked in syndrome

201
Q

GBS: UMN or LMN signs?

A

LMN

202
Q

2 investigations in GBS

A

lumbar puncture –> rise in protein with a normal white blood cell count (albuminocytologic dissociation) - found in 66%

nerve conduction studies –> decreased motor nerve conduction velocity (due to demyelination

203
Q

drug useful for managing tremor in drug-induced parkinsonism

A

procyclidine (anti-musc)

204
Q

Parkinson’s drug associated with pulmonary and cardiac fibrosis

A

dopamine receptor agonist
bromocriptine, ropinirole, cabergoline, apomorphine

205
Q

Parkinsons drug that loses effect over time

A

levodopa

206
Q

drugs that cause impulse control disorders and excessive daytime somnolence

A

dopamine receptor agonists e.g. bromocriptine, ropinirole, cabergoline, apomorphine

207
Q

most common primary tumour in adults

A

glioblastoma multiform

poor prognosis

208
Q

second most common primary brain tumour in adults

A

meningioma

209
Q

Tumours that most commonly spread to the brain include

A

lung (most common)
breast
bowel
skin (namely melanoma)
kidney

210
Q

Definition of TIA

A

a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction

otherwise its a stroke

211
Q

treatment of focal seizures [2]

A

first line: lamotrigine or levetiracetam
second line: carbamazepine, oxcarbazepine or zonisamide

212
Q

which antiepileptic may exacerbate absence seizures

A

carbamazepine

213
Q

cafe au lait spots: are they pigmented and which condition

A

hyper pigmented

in Neurofibromatosis

214
Q

features of NF1 [6]

A

Café-au-lait spots (>= 6, 15 mm in diameter)
Axillary/groin freckles
Peripheral neurofibromas
Iris hamatomas (Lisch nodules) in > 90%
Scoliosis
Pheochromocytomas

215
Q

features of NF2

A

Bilateral vestibular schwannomas
Multiple intracranial schwannomas, mengiomas and ependymomas

216
Q

which portion of the tongue sensation is lost in Bell’s palsy

A

anterior two thirds

217
Q

MRI finding in normal pressure hydrocephalus

A

ventriculomegaly in the absence of, or out of proportion to, sulcal enlargement

218
Q

treatment of normal pressure hydrocephalus

A

ventriculoperitoneal shunting

219
Q

four main features of neuroleptic malignant syndrome

A

rigidity
hyperthermia
autonomic instability (hypotension, tachycardia)
altered mental status (confusion)

220
Q

what are the bloods like in NMS

A

A raised creatine kinase is present in most cases. Acute kidney injury (secondary to rhabdomyolysis) may develop in severe cases. A leukocytosis may also be seen

221
Q

treatment of Bell’s palsy

A

prednisolone within 72 hours

+ eye care

222
Q

what is a Arnold-Chiari malformation

what are 3 features

A

describes the downward displacement, or herniation, of the cerebellar tonsils through the foramen magnum. Malformations may be congenital or acquired through trauma.

Features
non-communicating hydrocephalus may develop as a result of obstruction of cerebrospinal fluid (CSF) outflow
headache
syringomyelia

223
Q

features of progressive supra nuclear palsy [4]

A
  • postural instability and falls
    patients tend to have a stiff, broad-based gait
  • impairment of vertical gaze (down gaze worse than up gaze - patients may complain of difficultly reading or descending stairs)
  • parkinsonism
    bradykinesia is prominent
  • cognitive impairment
    primarily frontal lobe dysfunction
224
Q

features of lacunar stroke [3]

A

involves perforating arteries around the internal capsule, thalamus and basal ganglia
presents with 1 of the following:
1. unilateral weakness (and/or sensory deficit) of face and arm, arm and leg or all three.
2. pure sensory stroke.
3. ataxic hemiparesis

225
Q

what must be done for bladder dysfunction in MS

A
  1. get an bladder USS
  2. if significant residual volume → intermittent self-catheterisation
  3. if no significant residual volume → anticholinergics may improve urinary frequency

anticholinergics may worsen symptoms

226
Q

what must be done for oscillopsia in MS

A

gabapentin

227
Q

features of Miller Fischer Variant [3]

A

areflexia, ataxia, ophthalmoplegia

228
Q

which aphasia? Speech is fluent but repetition is poor. Aware of the errors they are making, normal comprehension

A

Conduction aphasia

229
Q

which aphasia? Speech is non-fluent, laboured, and halting. Repetition is impaired, normal comprehension

A

Broca’s

230
Q

which aphasia has impaired comprehension

A

Wernicke’s

231
Q

which aphasia has severe expressive and receptive aphasia

A

global aphasia

232
Q

Difference between Ramsay Hunt and Bells

A

Ramsay-Hunt syndrome is caused by the varicella zoster virus (VZV). It presents as a unilateral lower motor neurone facial nerve palsy. Patients stereotypically have a painful and tender vesicular rash in the ear canal, pinna and around the ear on the affected side. This rash can extend to the anterior 2/3 of the tongue and hard palate.

i.e. abnormal ENT exam

233
Q

features of pontine haemorrhage stroke [3]

A

reduced GCS, paralysis and bilateral pin point pupils

234
Q

which vessel supplies Brocas and Wernickes area

A

middle cerebral artery

235
Q

L5 vs common peroneal lesion

A

Weakened dorsiflexion, inversion and eversion of the ankle indicates an L5 nerve lesion not a common peroneal nerve lesion

Common peroneal provides sensation over the posterolateral part of the leg and knee. It is also involved in dorsiflexion and eversion of the ankle. It is NOT however involved in the inversion of the ankle and would not cause specific paraesthesia in the first web space of the foot.

236
Q

what element is most severely impacted in dementia

A

short term memory

237
Q
A

Year 6 (19 decks)

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