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neurology Flashcards

1
Q

mx of tension-type headache?

A

acute- aspirin, paracetamol, NSAID
prophylaxis- acupuncture
amitriptyline

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2
Q

features of migraine?

A

severe, unilateral throbbing headache

associated with nausea, photophobia, phonophobia

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3
Q

diagnostic criteria for migraine? ABCDE

A

At least 5 attacks fulfilling criteria B-D:
B- attacks lasting 4-72 hours
C- 2 of the following characteristics:
- unilateral location
-pulsating quality
- moderate or severe pain headache
- aggravation by or causing avoidance of routine physical activity
D- during headache at least one of the following:
1. Nausea and/or vomiting
2. Photophobia and phonophobia
E- not attributed to any other disorder

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4
Q

triggers for migraine

A 
Chocolate
Hangovers
Orgasms
Cheese
Oral contraceptives- CI'd if aura
Lie-ins
Alcohol
Tumult
Exercise
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5
Q

mx of acute migraine?

A

1st line- oral triptan and NSAID or paracetamol

metoclopramide or prochlorperazine

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6
Q

prophylaxis of acute migraine?

A

if 2+ attacks a month
Topiramate or propranolol
acupuncture
riboflavin

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7
Q

what is wrong with topiramate?

A

cleft palate and reduces effectiveness

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8
Q

RFs for cluster headache?

A

male, smokers

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9
Q

features of cluster headaches?

A

Unilateral pain around one eye- episodes last 15 minutes-2 hours
Restless and agitation
Eye- redness, lacrimation, lid swelling, miosis, ptosis
Rhinorrhoea

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10
Q

mx of cluster headaches?

A

100% O2
sub cut triptan (sumatriptan)
prophylaxis- verapamil, short course prednisolone may help

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11
Q

what is trigeminal neuralgia?

A

a pain syndrome characterised by severe unilateral pain

majority are idiopathic but could have serious underlying cause such as tumour

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12
Q

features of trigeminal neuralgia?

A

a unilateral disorder of brief electric-shock like pains, abrupt in onset and termination, limited to one or more divisions of the trigeminal nerve

triggers= washing, shaving, brushing teeth

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13
Q

RFs for trigeminal neuralgia?

A

hypertension, >50

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14
Q

Ix of trigeminal neuralgia?

A

MRI

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15
Q

mx of trigeminal neuralgia?

A

1st line= carbamazepine

failure to respond needs prompt referral to neurology

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16
Q

RFs of GCA?

A

over 50s, associated with polymyalgia rheumatica

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17
Q

features of GCA?

A 
scalp tenderness
jaw claudication
pulseless temporal arteries
temporal pulsating headache
amaurosis fugax
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18
Q

ix of GCA?

A

ESR
raised CRP, platelets, alk phos, reduced Hb
temporal artery biopsy

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19
Q

mx of GCA?

A

Steroids- prednisolone 60mg

PPI and bisphosphonates

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20
Q

complications of GCA?

A

Visual loss

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21
Q

signs of raised ICP?

A 
Worse walking, bending forwards, lying down, coughing
associated with vomiting
papilloedema
focal signs
seizures
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22
Q

layers of meninges of the brain

A

Dura mater
Arachnoid mater
Subarachnoid space
Pia mater

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23
Q

causes of SAH?

A 
Berry aneurysm- associated with adult PKD, Ehlers Danlos syndrome, coarctation of the aorta
AV malformation
Pituitary apoplexy
Arterial dissection
Mycotic aneurysms
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24
Q

features of SAH?

A 
Thunderclap headache
N&V
Meningism: photophobia, neck stiffness
Coma
seizures
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25
Q

Ix of SAH?

A

CT head
LP- done if CT is negative, perform 12 hours after symptom onset to allow development of xanthochromia (RBC breakdown)
refer to neurosurgery as soon as SAH confirmed

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26
Q

Tx of SAH?

A

CT intracranial angiogram
clipping of aneurysm
vasospasm is prevented with nimodipine
external ventricular drain for hydrocephalus
maintain cerebral perfusion with dexamethasone to decrease cerebral oedema

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27
Q

causes of subdural haemorrhage?

A

tearing of bridging veins between the venous sinuses and the cortex
causes increased ICP

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28
Q

RF for subdural haemorrhage?

A

traumatic head injury
cerebral atrophy/increasing age
alcoholism
anticoagulation meds

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29
Q

Signs and symptoms of subdural haemorrhage?

A

acute- raised ICP, confusion, seizure

chronic- cognitive decline, personality change, headache

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30
Q

Ix of subdural haemorrhage?

A

CT- gold standard

diffusely spreading crescent shaped mass

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31
Q

mx of subdural haemorrhage?

A

neurosurgery- monitor ICP and decompressive craniotomy

if chronic and no neuro deficit- can be managed conservatively

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32
Q

what is an extra dural haemorrhage?

A

collection of blood between the dura mater and bone

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33
Q

symptoms of extra dural haemorrhage?

A

briefly consciousness after a low impact injury then lucid interval:
then altered consciousness, severe headache, N&V, confusion, seizures
may lead to rapid increase in intra-cranial pressure- ipsilateral pupil dilatation, signs of brainstem injury/ compression

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34
Q

Ix of extradural haemorrhage?

A

CT- hyperdense biconvex (lemon shape) adjacent to skull

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35
Q

mx of extradural haemorrhage?

A

craniotomy and clot evacuation

give mannitol if raised ICP

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36
Q

causes of encephalitis?

A

viral infection- HSV 1&2, VZV, EBV, CMV, HIV, measles and mumps
Secondary to bacterial meningitis, TB, malaria, listeria etc

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37
Q

symptoms of encephalitis?

A

features of a viral infection
LOC
behavioural change
focal neurological deficit

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38
Q

Ix of encephalitis?

A

LP and CSF studies (PCR)- moderate increase in protein level. lymphocytes and decreased glucose
bloods and cultures

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39
Q

mx of encephalitis?

A

if viral- aliclovir IV high dose for 14 days
IM benpen in meningitis
anti-seizure meds

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40
Q

what is guillain barre syndrome?

A

an immune mediated demyelination of the peripheral nervous system often triggered by an infection (classically campylobacter jejuni)

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41
Q

features of GBS?

A 
Progressive weakness in all 4 limbs
some sensory signs
history of gastroenteritis
areflexia
CN involvement e.g. diplopia
autonomic involvement e.g. urinary retention, diarrhoea
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42
Q

Ix of GBS?

A

LP- rise in protein found with a normal WCC
nerve conduction studies
if resp muscle involvement -> ITU admission

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43
Q

mx of GBS?

A

IVIG for 5 days

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44
Q

causes of epilepsy?

A 
idiopathic
CP
tuberous sclerosis
mitochondrial diseases
head injury
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45
Q

types of epilepsy?

A

primary generalised- LOC, bilateral discharges, no ofcal brain abnormality
partial/focal- one hemisphere involved.

partial seizure is focal structural abnormality until proven otherwise

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46
Q

types of primary generalised epilepsy?

A

-tonic-clonic- stiffness and rigidity followed by rhythmic jerking. can have tongue biting and incontinence. post-ictal confusion and todd’s paralysis

  • tonic
  • clonic
  • absence
  • myoclonic
  • atonic
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47
Q

name some non-epileptic causes of seizures?

A

febrile convulsions
Alcohol withdrawal seizures
Psychogenic non-epileptic seizures

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48
Q

types of focal seizures?

A

focal aware
focal impaired awareness
awareness unknown
focal to bilateral seizure (secondary generalised)

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49
Q

features of temporal lobe seizure?

A 
HEAD
Hallucinations (auditory, olfactory, gustatory)
Epigastric rising/emotion
Automatisms (lip smacking)
Deja vu/ dysphasia (Wernicke's area)
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50
Q

features of frontal lobe seizure? (motor)

A

head/leg movements
posturing
post-ictal weakness
Jacksonian march (up and down motor homunculus)

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51
Q

features of parietal lobe seizures? (sensory)

A

paraesthesia

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52
Q

features of occipital lobe seizures? (visual)

A

floaters/flashes

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53
Q

Ix of epilepsy?

A

EEG and MRI

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54
Q

mx of epilepsy?

A

1st line for generalised seizures- sodium valproate 2nd line lamotrigine
1st line for partial seizures- carbamazepine

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55
Q

driving and epilepsy?

A

cannot drive for 6 moths following a seizure, 12 months if established epilepsy

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56
Q

How can epilepsy meds contraindicate other meds e.g. warfarin?

A

they can induce/inhibit the P450 system affecting metabolism of other drugs

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57
Q

epilepsy and pregnancy?

A

sodium valproate is teratogenic

breastfeeding is generally considered safe

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58
Q

epilepsy and contraception?

A

they both reduce the effectiveness of eachother

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59
Q

how does sodium valproate work and AEs?

A

increases GABA activity
AEs- weight gain and increased appetite, alopecia, ataxia, tremor, hepatitis, pancreatitis, thrombocytopenia, P450 enzyme inhibitor

60
Q

how does carbamazepine work? and AEs

A

binds to sodium channels increasing their refractory period

AEs- P450 inducer, dizziness and ataxia, drowsiness, agranulocytosis, SIADH, visual disturbances

61
Q

SE of lamotrigine?

A

stevens- johnson syndrome

62
Q

how does phenytoin work?

A

binds to sodium channels and increases their refractory period
AEs- P450 inducer, dizziness and ataxia, drowsiness, hirsutism, megaloblastic anaemia, peripheral neuropathy, osteomalacia, lymphadenopathy

63
Q

management of status epilepticus?

A

ABCDE
check BG levels

benzodiazepines e.g. diazepam (rectally or intranasally or sublingual) or lorazepam (IV) 4mg

wait 10 mins

phenytoin, sodium valproate and phenobarbital IV

GA in no response within 30 mins

64
Q

what should be checked to rule out other causes of status epilepticus?

A

BG

PaO2

65
Q

what is Parkinson’s disease?

A

degeneration of the dopaminergic neurons in the substantia nigra
symptoms are classically symmetrical
development of lery bodies

66
Q

features of PD?

A

Bradykinesia
tremor- 3-5Hz, most at rest
rigidity- cog wheel or lead pipe

mask-like facies
flexed posture
micrographia
fatigue
REM sleep behaviour disorder
psych disturbance
67
Q

diagnosis of PD?

A

clinical

MRI will be normal initially but then show atrophy

68
Q

mx of PD?

A

If motor symptoms are affecting QOL-> 1st line levodopa
if they aren’t -> dopamine agonist e.g. ropinirole or MAOB inhibitor

Combine drugs
Can add COMT inhibitor

69
Q

what is levodopa?

A

usually combined with a decarboxylase inhibitor to prevent peripheral metabolism of levodopa to DA to reduce AEs

  • reduces effectiveness with time (usually by 2 years)
70
Q

AEs of levodopa?

A 
dyskinesia (involuntary writhing movements)
on-off effect
dry mouth
anorexia
palpitations
postural hypotension
psychosis
drowsiness

Don’t stop suddenly -> can cause acute dystonia

71
Q

AEs and monitoring of dopamine receptor agonists?

A

bromocriptine, ropinirole
prior to tx- ECHO, ESR, CXR, creatinine

AEs- impulse control disorder, excessive daytime sleepiness, hallucinations, nasal congestion, postural hypotension

72
Q

how do MAO-B inhibitors work?

A

e.g. selegiline
inhibits the breakdown of DA
AEs- postural hypotension, AF

73
Q

how do COMT inhibitors work?

A

e.g. entocapone, tolcapone
stops breakdown of DA
AEs- can cause liver damage

74
Q

name some parkinson plus syndromes?

A

Progressive supra-nuclear palsy
Multiple system atrophy
Corticobasal degeneration
Lewy body dementia

75
Q

features of progressive supra-nuclear palsy?

A 
early postural instability and falls
vertical gaze palsy
rigidity of limbs < trunks
no tremor
symmetrical
76
Q

features of multiple system atrophy?

A

early autonomic features (postural hypotension, bladder dysfunction)
cerebellar signs
no tremor

77
Q

features of corticobasal degeneration?

A

akinetic rigidity involving one limb

78
Q

features of lewy body dementia?

A

dementia before motor symptoms= LBD

dementia one year after motor symptoms= PD

79
Q

what is huntington’s disease?

A

AD neurodegenerative condition
trinucleotide repeat disorder: CAG
results in degeneration of cholinergic and GABAergic neurons in the striatum of the basal ganglia

80
Q

features of huntington’s disease?

A 
typically after 35 years of age
chorea
personality change
dystonia
saccadic eye movements
81
Q

diagnosis of huntington’s disease?

A

CT/MRI
clinical
genetic testing

82
Q

mx of huntington’s disease?

A

no cure

chorea- benzodiazepines, valproic acid, tetrabenazine

83
Q

what is motor neuron disease?

A

cause is unknown

presents with upper and lower motor neuron signs

84
Q

clues which point towards a diagnosis of MND?

A

Fasisculations
the absence of sensory S&S
mixture of LMN and UMN signs
wasting of the small hand muscles/ tibialis anterior is common

85
Q

types of MND?

A

1) Amytrophic lateral sclerosis- (50%)- typically presents with LMN signs in arms and UMN signs in legs. Associated with fronto-temporal dementia
2) Primary lateral sclerosis- UMN signs only
3) Progressive muscular atrophy- LMN signs only, affects distal muscles before proximal, carries best prognosis

4) progressive bulbar palsy- palsy of the tongue, muscles of chewing/swallowing and facial muscles due to loss of function of brainstem motor nuclei
- carries worse prognosis

86
Q

diagnosis of MND?

A

Clinical
nerve conduction studies
EMG
MRI to exclude cervical cord compression and myelopathy

87
Q

mx of MND?

A

Riluzole- prevents stimulation of glutamate receptors. Used mainly in amytrophic lateral sclerosis. Prolongs life by about 3 months

Resp care- NIV e.g. BiPAP at night
Spasms- baclofen

88
Q

prognosis of MND?

A

50% die within 3 years

89
Q

what is MS?

A

Chronic cell-mediated autoimmune disorder characterised by demyelination in the CNS

90
Q

epidemiology of MS?

A

3x more common in women
age 20-40 years
more common at higher altitude

91
Q

types of MS?

A
  • Relapsing-remitting disease- (85%) acute attacks (last 1-2 months) followed by periods of remission
  • secondary progressive disease- neurological S&S between relapses
  • primary progressive disease (10%)
92
Q

diagnosis of MS?

A

2 OR MORE RELAPSES AND EITHER
OBJECTIVE CLINICAL EVIDENCE OF 2 OR MORE LESIONS OR
OBJECTIVE CLINICAL EVIDENCE OF 1 LESION TOGETHER WITH REASONABLE HISTORICAL EVIDENCE OF A PREVIOUS RELAPSE

93
Q

Features of MS?

A

Visual- optic neuritis, optic atrophy, Uhthoff’s phenomenon (worsening symptoms following increased body temp), internuclear ophthamoplegia

Sensory- pins and needles, numbness, trigeminal neuralgia, Lhermitte’s syndrome (paraesthesia in limbs on neck flexion)

Motor- spastic weakness

Cerebellar- ataxia, tremor

Others- urinary incontinence, sexual dysfunction, intellectual deterioration

94
Q

Ix of MS?

A

MRI- periventricular plaques
CSF- oligoclonal bands, IgG
Visual evoked potentials- delayed, but well preserved waveform

95
Q

mx of MS?

A

Acute relapse- oral or IV methylprednisolone for 5 days

Disease modifying drugs- DMARDS (beta-interferon), glatiramer acetate, natalizumab, fingolimod

96
Q

mx of specific problems of MS- fatigue, spasticity, bladder dysfunction?

A

fatigue- CBT, mindfulness, amantadine
spasticity- baclofen and gabapentin, PT, diazepam, cannabis and botox
bladder dysfunction- self-catheterisation, anticholinergics e.g. doxizosin

97
Q

what is myasthenia gravis?

A

an autoimmune affecting the neuromuscular junction

affects acetylcholine receptors- antibodies against them

98
Q

associations with myasthenia gravis?

A 
thymomas
autoimmune antibodies (pernicious anaemia, thyroid, RA, SLE), thymic hyperplasia
99
Q

features of myasthenia gravis?

A 
muscle fatiguability
extraocular muscle weakness: diplopia
ptosis
dysphagia
peek sign= can't keep eyes closed for long
100
Q

Ix of myasthenia gravis?

A 
single fibre electromyography
CT thorax to exclude thymoma
CK normal
auto-antibodies- anti-AChR or anti-MuSK
Tensilon test- IV edrophonium reduces muscle weakness temporarily
101
Q

mx of myasthenia gravis?

A

long-acting anticholinesterase inhibitors e.g. pyridostigmine
immunosuppression e.g. prednisolone initially
thymectomy

102
Q

mx of myasthenic crisis?

A

plasmapheresis

IVIG

103
Q

exacerbating factors for myasthenic crisis?

A 
beta blockers
penicllamine
lithium
phenytoin
Abx
104
Q

causes of dementia?

A 
alzheimer's disease
CV disease- multi-infarct dementia
lewy body dementia
huntingtons
CJD
Pick's disease
HIV
105
Q

assessment of dementia?

A

6CIT, 10-CS
GP setting- MMSE, GPCOG
Blood screen to exclude reversible causes- FBC, U&E, LFT, Ca, glucose, TFT, vit B12 and folate
Neuroimaging to excluse organic causes

106
Q

genetics of Alzheimer’s disease?

A

most cases are sporadic
5% of cases are inherited as an autosomal dominant trait
mutations in the amyloid precursor protein (chromosome 21), presenilin 1 (chromosome 14) and presenilin 2 (chromosome 1) genes are thought to cause the inherited form
apoprotein E allele E4 - encodes a cholesterol transport protein
risk factors include Down’s syndrome

107
Q

macroscopic changes of AD?

A

Widespread cerebral atrophy, particularly involving the cortex and hippocampus

108
Q

microscopic changes of AD?

A 
Cortical plaques (due to deposition of type A-Beta amyloid protein)
Intraneuronal neurofibrillary tangles (caused by anbormal aggregation of the tau protein)
109
Q

mx of alzheimer’s disease?

A

non-pharmacological- exercise, group therapy, cognitive rehab

pharmacological-
-3 acetylcholinesterase inhibitors (donepezil, galantamine, rivastigmine) 1st line

  • memantine (NMDA receptor antagonist) 2nd line
  • donepezil contraindicated in bradycardia, can cause insomnia*
110
Q

features of fronto-temporal lobar dementia?

A

onset before 65
insidious onset
relatively preserved memory and visuo-spatial skills
personality change and social conduct problems

111
Q

3 types of fronto-temporal lobar dementia?

A
  1. Pick’s disease
  2. Progressive non-fluent aphasia/ CPA-non-fluent speech
  3. Semantic dementia- fluent progressive aphasia
112
Q

features of pick’s disease?

A 
personality change
impaired social conduct
hyperorality
dis-inhibition
increased appetite
113
Q

macroscopic changes associated with pick’s disease?

A

atrophy of frontal and temporal lobes

114
Q

microscopic changes associated with pick’s disease?

A

aggregation of tau proteins
gliosis
neurofibrillary tangles
plaques

115
Q

features of lewy body dementia?

A

associated with PD
progressive cognitive impairment
parkinsonism
visual hallucinations (other features such as delusions and non-visual hallucinations may also be seen)

116
Q

Ix of lewy body dementia?

A

clinical

SPECT (DAT scan)

117
Q

tx of lewy body dementia?

A

both acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine) and memantine can be used as they are in Alzheimer’s

118
Q

RF of brain tumours?

A

ionising radiation
immunosuppression
genetic syndromes- neurofibromatosis

119
Q

types of brain tumours?

A

high grade- gliomas- astrocytomas or oligodendromas

  • primary cerebral lymphoma
  • medulloblastoma

low grade- meningioma, acoustic neuromas, neurofibromas, pituitary adenoma, pineal tumour

120
Q

features of brain tumours?

A

increased ICP

neurological focal symptoms- personality change, cognitive or behavioural symptoms, confusion

Coning can occur- herniation of cerebellar tonsils through foramen magnum -> resp depression, bradycardia, death

121
Q

diagnosis of brain tumours?

A

CT/MRI

122
Q

tx of brain surgery?

A

neurosurgery

123
Q

cause of extra dural haemorrhage?

A

fracture of temporal or parietal bone causing laceration of the middle meningeal artery
ususally young adults

124
Q

causes of cerebellar disease?

A 
PASTRIES
Paraneoplastic
Alcohol
Stroke
Trauma
Rare- Gluten's ataxia, Friedrich's ataxia
Iatrogenic- drugs e.g. phenytoin
Endocrine
SOL/MS
125
Q

what is a neurofibromatosis?

A

a genetic condition that causes nerve tumours (neuromas) to develop throughout the nervous system
2 types- NF1 most common

126
Q

features of neurofibromatosis type 1?

A

at least 2 of CRABBING.

C – Café-au-lait spots (6 or more) measuring ≥ 5mm in children or ≥ 15mm in adults
R – Relative with NF1
A – Axillary or inguinal freckles
BB – Bony dysplasia such as Bowing of a long bone or sphenoid wing dysplasia
I – Iris hamartomas (Lisch nodules) (2 or more) are yellow brown spots on the iris
N – Neurofibromas (2 or more) or 1 plexiform neurofibroma
G – Glioma of the optic nerve

127
Q

mx of neurofibromatosis type 1?

A

There is no treatment of the underlying disease process or to prevent the development of neurofibromas or complications.

Management is to control symptoms, monitor the disease and treat complications.

128
Q

complications of neurofibromatosis type 1?

A

Migraines
Epilepsy
Renal artery stenosis causing hypertension
Learning and behavioural problems (e.g. ADHD)
Scoliosis of the spine
Vision loss (secondary to optic nerve gliomas)
Malignant peripheral nerve sheath tumours
Gastrointestinal stromal tumour (a type of sarcoma)
Brain tumours
Spinal cord tumours with associated neurology (e.g. paraplegia)
Increased risk of cancer (e.g. breast cancer)
Leukaemia

129
Q

what is Neurofibromatosis type 2 commonly associated with?

A

acoustic neuromas
These are tumours of the auditory nerve innervating the inner ear.
bilateral almost always indicates NF2
mx= surgery

130
Q

mx of benign essential tremor?

A

propranolol

primidone

131
Q

features of benign essential tremor?

A 
Fine tremor
Symmetrical
More prominent on voluntary movement
Worse when tired, stressed or after caffeine
Improved by alcohol
Absent during sleep
132
Q

what is lambert eaton myasthenic syndrome?

A

similar to myasthenia gravis

damage to NM junction causes progressive muscle weakness

133
Q

common cause of lambert eaton myasthenic syndrome?

A

small cell lung cancer

antibodies against voltage-gated calcium channels in SCLC cells

134
Q

medical mx of lambert eaton syndrome?

A

amifampridine allows more ACh to be released in the NM junction

135
Q

what is charcot marie tooth disease?

A

an inherited disease that affects the peripheral motor and sensory nerves

136
Q

features of charcot marie tooth disease?

A
  • high foot arches (pes cavus)
  • distal muscle wasting causing inverted champagne bottle legs
  • weakness in lower legs (ankle dorsiflexion)
  • weakness in hands
  • reduced tendon reflexes
  • reduced tone
  • peripheral sensory loss
137
Q

differentials of peripheral neuropathy?

A 
A – Alcohol
B – B12 deficiency 
C – Cancer and Chronic Kidney Disease
D – Diabetes and Drugs (e.g. isoniazid, amiodarone and cisplatin)
E – Every vasculitis
138
Q

mx of charcot marie tooth disease?

A

neurologists
PT, OT, podiatrists
ortho surgeons to correct disabling joint deformities

139
Q

What is tuberous sclerosis characterised by?

A

harmatomas- benign neoplastic growths of the tissue (skin, brain, lungs, heart, eyes)
can cause epilepsy

140
Q

skin features of tuberous sclerosis?

A 
ash leaf spots
shagreen patches
angiofibromas
café au lait spots
poliosis
141
Q

where does the facial nerve exit the brainstem?

A

cerebellopontine angle

passes through the temporal bone and parotid gland

142
Q

what are the 5 branches of the facial nerve?

A 
temporal
zygomatic
buccal
marginal mandibular
cervical
143
Q

functions of the facial nerve?

A

motor- muscles of facial expression, stapedius (ear), some neck muscles

sensory- taste anterior 2/3 tongue

parasympathetic- submandibular and sublingual salivary glands and lacrimal gland

144
Q

why is the forehead not spared in a LMN lesion?

A

each side of the forehead only has innervation from one side of the brain therefore in a lesion it can’t be supplied by the other side of the brain

145
Q

examples of unilateral and bilateral UMN lesions of the facial nerve?

A

Unilateral- CVAs, tumours

Bilateral- pseudobulbar palsies, MND

146
Q

causes of LMN facial nerve palsies?

A

Infection- otitis media, malignant otitis externa

Systemic disease- DM, sarcoidosis, leukaemia, MS, GBS

Tumours- acoustic neuroma, parotid tumour, cholesteatomas

Trauma

finals (14 decks)

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