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Finals Revision > Neurology > Flashcards

Neurology Flashcards

1
Q

What is Multiple Sclerosis?

A

An inflammatory demyelinating disorder of the CNS characterised by plaques disseminated in time and space

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2
Q

What mediates the demyelination in MS?

A

T cells

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3
Q

How does pyramidal dysfunction in MS present?

A

Increased tone, spasticity, weakness

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4
Q

Where is the weakness in MS?

A

Extensors of upper limbs, flexors of lower limbs

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5
Q

What sensory symptoms may be present in MS?

A

Pins & needles/numbness
Pain
Trigeminal neuralgia

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6
Q

What is Lhermitte’s syndrome?

A

Paraesthesia of the limbs on neck flexion

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7
Q

What cerebellar symptoms may be present in MS?

A

Ataxia, intention tremor, nystagmus, past pointing, pendular reflexes, dysdiadochokinesia, dysarthria

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8
Q

What visual symptoms may be present in MS?

A

Optic neuritis, optic atrophy, internuclear ophthalmoplegia, Uhtoffs phenomenon

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9
Q

What is Uhtoff’s phenomenon?

A

Worsening of vision due to increased body temperature

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10
Q

What other symptoms may be present in MS?

A

Fatigue, urinary incontinence, sexual dysfunction, intellectual deterioration

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11
Q

What are the types of MS?

A

Relapsing remitting
Relapsing progressive
Primary progressive
Secondary Progressive

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12
Q

What is the commonest type of MS?

A

Relapsing remitting

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13
Q

What investigations should be done if you suspect MS?

A

Bloods (FBC, PV, CRP, autoantibodies, B12, folate - all negative)
MRI
CSF

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14
Q

What does an MRI in MS show?

A

T2 weighted MRI shows plaques disseminated in time and space

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15
Q

What does electrophoresis of CSF show in MS?

A

Oligoclonal bands of IgG

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16
Q

What does neurophysiology show in MS?

A

Delayed evoked potentials

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17
Q

What criteria is used to diagnose MS?

A

McDonald Criteria

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18
Q

How should an acute exacerbation of MS be treated?

A

Methylprednisolone (oral or IV)

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19
Q

What are some first line disease modifying therapies for MS?

A

Beta-interferon
Copaxone
Tecfidera

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20
Q

How is fatigue managed in MS?

A

Amantadine

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21
Q

How is spasticity managed in MS?

A

Baclofen/gabapentin

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22
Q

How is oscillopsia managed in MS?

A

Gabapentin/memantine

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23
Q

How is emotional lability managed in MS?

A

Amitriptyline

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24
Q

What is motor neurone disease?

A

An untreatable and rapidly progressive neurodegenerative condition characterised by selective loss of motor neurones

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25
Q

What symptoms do you get in MND?

A

UMN and LMN signs

No sensory loss, no sphincter disturbance, no eye movements affected

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26
Q

What is the commonest type of MND?

A

Amyotrophic lateral scleorsis

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27
Q

What nerves do pseudobulbar palsy/bulbar palsy affect?

A

CN IX-XII

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28
Q

What investigations should be done for MND?

A

MRI (normal)
Nerve conduction studies (normal)
EMG

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29
Q

What does EMG show in MND?

A

Fasciculations and fibrillations

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30
Q

What drug prolongs life in MND and for how long?

A

Riluzole - anitglutaminergic drug prolongs life by 3 months

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31
Q

What drugs can be used for symptomatic relief in MND?

A

Quinine/baclofen for cramps
Baclofen/gabapentin for spasticity
Propantheline/botox for drooling
Supplements/gastronomy for nutrition

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32
Q

What does curare poisoning cause?

A

Blockage of acetylcholine receptors at NMJ leading to no muscle contraction (can mean no respiration)

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33
Q

What is botulism?

A

Caused by botilinum toxin, which blocks release of acetylcholine, causing flaccid paralysis

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34
Q

What is Lambert-Eaton Myaesthenic syndrome?

A

Antibodies against pre-synaptic calcium channels

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35
Q

What is LEMS associated with?

A

Small cell lung cancer

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36
Q

What are the symptoms of LEMS?

A

Weakness of limbs (improves with exercise), autonomic involvement, hyporeflexia

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37
Q

What investigations would you do for LEMS?

A

Bloods (increased autoantibodies)

EMG (shows improvement of potentials after use)

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38
Q

How is LEMS treated?

A

TREAT UNDERLYING CANCER. Steroids, azaithioprine, pyridostigmine, immunoglobulins

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39
Q

What is Myaesthenia Gravis?

A

Autoimmune condition against post-synaptic acetylcholine receptors

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40
Q

Who commonly gets Myaesthenia Gravis?

A

Commonly females in 3rd decade of life or Males in 6th/7th decade

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41
Q

What are symptoms of Myaesthenia Gravis?

A

Muscular fatigue, eye signs (e.g. ptosis, diplopia), gets worse throughout day. Voice deterioration as they speak.

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42
Q

What can exacerbate symptoms of Myaesthenia Gravis?

A

Pregnancy, change of climate, emotion, exercise, certain medications

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43
Q

What investigations can be done for Myaesthenia Gravis?

A

Bloods (autoantibodies)
Tensilon test
Neurophysiology (decreased response to nerve stimulation over time)

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44
Q

How is Myaesthenia Gravis treated?

A

Pyridostigmine for symptom control
Steroids/azaithioprine/methotrexate for immunosuppression
Thymectomy may be needed if disease not well controlled by anticholinesterases

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45
Q

What is Myaesthenic crisis?

A

Weakness of respiratory muscles during a relapse which can be life threatening

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46
Q

How is a myaesthenic crisis treated?

A

Plasmapheresis or IV Immunoglobulins

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47
Q

What makes up the triad of meningism?

A

Fever, headache and neck stiffness

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48
Q

What are the key symptoms of meningitis?

A

Meningism, photophobia, confusion, agitation, seizure, non-blanching purpuric rash

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49
Q

What is Kernig’s sign?

A

Pain and resistance on passive extension of the knee with flexed hip

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50
Q

What are some viral causes of meningitis?

A

ECHO virus, coxsackie virus, herpes simplex

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51
Q

What are the common bacterial causes of meningitis in neonates?

A

Listeria, Group B strep, E coli

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52
Q

What is the commonest bacterial cause of meningitis in children?

A

Haemophilus influenzae

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53
Q

What is the commonest bacterial cause of meningitis in those aged 10-21?

A

Neisseria Meningitidis

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54
Q

What are the common bacterial causes of meningitis in those over 21?

A

Strep pneumoniae and neisseria meningitidis

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55
Q

What are the common bacterial causes of meningitis in the elderly?

A

Strep pneumoniae, Listeria

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56
Q

What is aseptic meningitis?

A

Inflammation of the meninges with no pus

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57
Q

What are some causes of an aseptic meningitis?

A

TB, HIV, syphilis, vasculitis, drug induced

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58
Q

What investigations should you consider in someone with suspected meningitis?

A

Bloods (FBC, U&Es, coag screen, glucose, cultures), throat swab, CXR if suspect TB, LP is diagnostic

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59
Q

When is a lumbar puncture contraindicated?

A

Immunocompromised
Papilloedema
Focal neurological signs

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60
Q

On LP, which organisms show neutrophilia?

A

Bacterial

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61
Q

On LP, which organisms show lymphocytes?

A

Viral and TB

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62
Q

What are protein and glucose like in viral meningitis?

A

Normal

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63
Q

What are protein and glucose like in bacterial meningitis?

A

High protein, low glucose

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64
Q

What is the empirical antibiotic treatment for bacterial meningitis?

A

IV ceftriaxone 2g BD + Dexamethasone 10mg IV QDS

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65
Q

What antibiotic should be added if you suspect listeria as a cause of bacterial meningitis?

A

Amoxicillin IV 2g 4hrly (Chloramphenicol if allergic)

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66
Q

Who should be contacted if there is a case of bacterial meningitis?

A

Public Health

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67
Q

What is the contact prophylaxis for bacterial meningitis?

A

500mg ciprofloxacin orally

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68
Q

What is encephalitis?

A

Inflammation of the brain parenchyma

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69
Q

What are the common causes of encephalitis?

A

Herpes simplex, varicella zoster, CMV/HIV

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70
Q

How does encephalitis present?

A

Similar to meningitis but may also be odd behaviours or aphasia (if temporal lobe affected)

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71
Q

What investigations should be done for encephalitis?

A

LP - CSF shows lymphocytosis. Do PCR for HSV

MRI - may show ‘temporal lobe enhancement’

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72
Q

What is temporal lobe enhancement on MRI a sign of?

A

Herpes Simplex Encephalitis

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73
Q

How is Herpes Simplex Encephalitis treated?

A

IV Aciclovir

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74
Q

How does a brain abscess present?

A

Raised ICP, focal neurological signs, fever

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75
Q

How is a brain abscess diagnosed?

A

CT head

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76
Q

How is a brain abscess treated?

A

Surgically - crainiotomy and debridement

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77
Q

What is progressive multifocal leukoencephalopathy caused by?

A

JC virus which causes widespread demyelination

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78
Q

What are some risk factors for PML?

A

Immunosuppression, autoimmune disease, MS drugs

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79
Q

How is PML investigated?

A

LP shows JC virus DNA

MRI shows focal white matter lesions

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80
Q

What is Parkinsons disease?

A

Progressive neurodegenerative condition caused by degeneration of dopaminergic neurons in the substantia nigra

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81
Q

What is the biggest risk factor for Parkinson’s Disease?

A

Age

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82
Q

What are the 3 main motor symptoms of Parkinson’s Disease (Parkinsonism)?

A

Bradykinesia
Tremor
Rigidity

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83
Q

How does bradykinesia present in Parkinsons?

A

Slowness of movement with progressive loss of amplitude, decreased facial expression (mask like expression), soft speech, micrographia, shuffling gait, decreased arm swing

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84
Q

What is the tremor like in Parkinsons?

A

4-7hZ pill rolling resting tremor, worse when stressed/tired. Usually disappears when doing something

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85
Q

How does the rigidity present in Parkinsons?

A

Increased tone

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86
Q

What is cogwheel rigidity?

A

Felt at the wrist, the result of the tremor imposed on hypertonia

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87
Q

What are some non-motor symptoms of Parkinsons?

A

Anosmia, visual hallucinations, REM sleep disorder, depression, drooling, constipation

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88
Q

What is the first line treatment for Parkinsons if QOL is severely affected by motor symptoms?

A

Levodopa

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89
Q

What is the first line treatment for Parkinsons if QOL not severely affected by motor symptoms?

A

Dopamine agonist, levodopa or MAO-B inhibitor

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90
Q

What is a risk if a medication is missed in Parkinsons disease?

A

Neuroleptic Malignant Syndrome

91
Q

How does neuroleptic malignant syndrome present?

A

Pyrexia, rigidity, tachycardia, increased CK, leucocytosis

92
Q

How is neuroleptic malignant syndrome treated?

A

IV fluids and dantrolene

93
Q

What are some side effects of levodopa?

A

Nausea and vomiting, dyskinesia, sudden off days, psychosis

94
Q

What is an example of a dopamine agonist?

A

Ropinorole (non-ergo_

Bromocriptine (ergo)

95
Q

What are some side effects of dopamine agonists?

A

Daytime somnomelence, impulse disorders, pulmonary fibrosis

96
Q

What is an example of an MAO-B inhibitor and how does it work?

A

Selegiline - inhibits dopamine breakdown

97
Q

What is an example of a COMT inhibitor and when is it used?

A

Entacapone. Used in conjunction with levodopa to increase its effect (e.g. synimet)

98
Q

How is psychosis treated in Parkinsons?

A

Quetiapine

99
Q

How is an REM sleep disorder in Parkinsons treated?

A

Clonazepam/Melatonin

100
Q

What is the presentation of essential tremor?

A

Symmetrical, postural tremor with a higher frequency than PD. Intensifies with use. Autosomal dominant

101
Q

How does Multiple System Atrophy present?

A

Jerky, postural tremor, cerebellar signs, parkinsonism, pyramidal signs, urinary retention/incontinence, postural hypotension, impotence

102
Q

How is MSA differed from PD?

A

Autonomic involvement

103
Q

‘MRI shows hot cross bin sign’

A

MSA - due to cerebellar and pontine atrophy

104
Q

How does progressive supranuclear palsy present?

A

Parkinsonism plus psuedobulbar palsy, neck dystonia, supranuclear ophthalmoplegia, gait and balance issues

105
Q

How does corticobasal degeneration present?

A

Rigidity and weakness of one limb, apraxia, loss of powerful movement, sensory disturbance

106
Q

What is fragile X tremor ataxia syndrome and how does it present?

A

Late onset neurodegenerative disorder. Causes cerebellar ataxia, postural/intention tremor, dysautonomia and cognitive decline

107
Q

What drugs may cause parkinsonism?

A

Antipsychotics, prochloperazine, metoclopramide, methyldopa

108
Q

What is Wilson’s disease?

A

Autosomal recessive disease of copper accumulation in liver and CNS

109
Q

What neurological symptoms does Wilsons disease cause?

A

Psychiatric issues, decreased IQ, decreased memory, tremor, akinesia, ataxia, movement disorders

110
Q

What is epilepsy?

A

Common neurological condition characterised by recurrent seizures

111
Q

What conditions are associated with epilepsy?

A

Cerebral palsy, tuberous sclerosis, mitochondrial diseases

112
Q

What are the two classifications of epilepsy onset?

A

Focal

Generalised

113
Q

Where does a focal seizure occur in the brain?

A

Starts in an area on one side of the brain (can spread though)

114
Q

Where does a generalised seizure occur in the brain?

A

Both sides of the brain at onset

115
Q

What can focal seizures further be classified by?

A

Awareness retained or impaired

116
Q

What motor symptoms may be seen in focal seizures?

A

Jerking, twitching, stiffening etc

117
Q

What non-motor symptoms may be seen in focal seizures?

A

Changes in sensation, emotions, smells, thinking, experiences

118
Q

What motor symptoms may be seen in generalised seizures?

A

Tonic-clonic, myoclonic etc

119
Q

What non-motor symptoms may be seen in generalised seizures?

A

Absence seizures - staring, changes in awareness, lip smacking

120
Q

What may patients experience following a seizure?

A

Post-ictal phase - flaccid, unresponsiveness, drowsiness, headache

121
Q

What investigations should be done following a patients first seizure?

A

ECG, EEG, MRI

122
Q

When is drug treatment for epilepsy introduced?

A

After the patients second seizure

123
Q

What is the first line treatment for generalised seizures?

A

Sodium valproate

124
Q

What is the first line treatment for focal seizures?

A

Carbemazepine or lamotrigine

125
Q

What is the other drug option for absence seizures?

A

Ethosuximide

126
Q

How does sodium valproate work?

A

Increases GABA activity

127
Q

What are side effects of sodium valproate?

A

Weight gain, alopecia, ataxia, tremor, hepatitis, teratogenicity, p450 inhibitor

128
Q

How does carbamazepine work?

A

Binds to sodium channels

129
Q

What are side effects of carbamazepine?

A

p450 enzyme inducer, dizziness, drowsiness, agranulocytosis, diplopia, SIADH

130
Q

How does lamotrigine work?

A

Sodium channel blocker

131
Q

What are side effects of lamotrigine?

A

Steven-Johnson-Syndrome

132
Q

What are side effects of phenytoin?

A

P450 enzyme inducer, facial coursening, anaemia, neuropathy

133
Q

What medication should be used in the community for status epilepticus? (>5mins)

A

Buccal midazolam or rectal diazepam

134
Q

What medication should be used in hospital for status epilepticus?

A

IV lorazepam repeated if necessary

IV phenobarbitol/phenytoin if ongoing

135
Q

How long are you not allowed to drive for after first seizure?

A

Car - 6 months

HGV - 5 years

136
Q

How long are you not allowed to drive for once you have a diagnosis of epilepsy?

A

Car - 5 years

HGV - 10 years

137
Q

What should be done in patients who are wanting to concieve with epilepsy?

A

Swap from valproate to lamotrigine

5mg folic acid from trying to concieve until 12 weeks

138
Q

What are red flag symptoms in headache?

A 
New onset aged over 55
Known/previous malignancies
Immunosuppression
Early morning headache
Exacerbation by coughing (raised ICP)
139
Q

What is a migraine caused by?

A

Neural and vascular influences cause changes in the brain, activating trigeminovascular dilatation. Chemicals released irritate blood vessels and nerves causing pain

140
Q

What are the features of migraine without aura?

A

Unilateral, pulsatile, moderate/severe pain, nausea, vomiting, photophobia, phonophobia
Need 5 separate attacks of duration 4-72hrs

141
Q

What are features of migraine with aura?

A

Recurrent attacks lasting minutes of unilateral fully reversible visual, sensory or other CNS symptoms then headache

142
Q

What can trigger migraines?

A

Stress, sleep (too much or too little), trauma, sensory stimulation, certain foods, exercise, heat, dehydration

143
Q

What is non-pharmacological management of migraine?

A

Avoid triggers, stress techniques, accupuncture

144
Q

What is the acute management of migraine?

A

Simple analgesia first (aspirin/ibuprofen), triptan +/- antiemetic

145
Q

When is prophylactic treatment for migraine considered?

A

If more than 3 attacks per month/severe

146
Q

What is the prophylactic treatment of migraine?

A

Propranolol, amitriptyline

2nd line - topiramate

147
Q

Who is cluster headache common in?

A

Young men, smokers

148
Q

How does a cluster headache present?

A

Severe, unilateral headache, bloodshot red eyes, rhinorrhoea, lid swelling, lacrimation

149
Q

How often and for how long to cluster headaches occur?

A

30mins-3hrs, 1-8 times a day

150
Q

How are cluster headaches managed acutely?

A

Oxygen for 15-20 mins and subcut sumitriptan

151
Q

What is given prophylactically for cluster headaches?

A

Verapamil

152
Q

How does paroxysmal hemicrania present?

A

In elderly women. Unilateral headache and autonomic features

153
Q

How often and for how long does paroxysmal hemicrania occur?

A

Lasts 2-45mins , 1-40 times a day

154
Q

How is paroxysmal hemicrania treated?

A

Absolute response to indomethacin

155
Q

What is a SUNCT?

A

Short lived (15-120s), unilateral, neuralgiform headache with conjunctival injections and tearing

156
Q

How is SUNCT treated?

A

Lamotrigine, gabapentin

157
Q

How does trigeminal neuralgia present?

A

Severe stabbing unilateral pain in V2/3 triggered by touch

158
Q

How long and how often does trigemnial neuralgia occur?

A

1-90 seconds 10-100times a day

159
Q

How is trigeminal neuralgia managed?

A

Carbemazepine

160
Q

How does a tension headache present?

A

Recurrent, non-disabling, bilateral headache, described as a tight band, non pulsatile

161
Q

How is a tension headache managed?

A

stress relief

162
Q

What are features of a medication overuse headache?

A

Present for 15+ days of the month, developed or worsened by medication, psychiatric comorbidity common

163
Q

How is medication overuse headache managed?

A

Remove cause, advise patients to take OTC pain relief no more than 6 days a month

164
Q

How does temporal arteritis present?

A

Rapid onset unilateral headache, jaw claudication, tender, palpable pulseless temporal artery. Raised ESR

165
Q

How is temporal arteritis managed?

A

Steroids

166
Q

What is a stroke?

A

Acute onset focal neurology due to a disruption of blood supply to the brain

167
Q

What are the two main types of stroke?

A

Ischaemic and haemorrhagic

168
Q

What are risk factors for stroke?

A

Age, hypertension, smoking, hyperlipidaemia, DM, atrial fibrillation

169
Q

What which type of stroke is more common?

A

Ischaemic (85%)

170
Q

What are the two causes of ischaemic strokes?

A

Thrombotic and embolic

171
Q

If symptoms of stroke last less than 24hrs what is it defined as?

A

TIA

172
Q

What are the symptoms of a TACS?

A

Hemiparesis+/- hemisensory loss AND
homonymous hemianopia AND
higher cognitive dysfunction

173
Q

What arteries does a TACS affect?

A

Anterior circulation - middle and anterior cerebral

174
Q

What are symptoms of a PACS?

A

2 from
Hemiparesis +/- hemisensory loss
homonymous hemianopia
higher cognitive dysfunction

175
Q

What arteries does a PACS affect?

A

Middle/anterior cerebral arteries

176
Q

What are symptoms of a LACS?

A

One from
Hemiparesis
Purely sensory loss
Ataxic hemiparesis

177
Q

What arteries does LACS affect?

A

Perforating arteries (e.g. thalamus, basal ganglia etc)

178
Q

What are symptoms of POCS?

A

One from
Cerebellar/brainstem syndromes
LOC
Isolated homonymous hemianopia

179
Q

What symptoms does lateral medullary syndrome cause?

A

Ipsilateral ataxia, nystagmus, nerve palsies

Contralateral limb sensory loss

180
Q

What symptoms does Webers syndrome cause?

A

Ipsilateral CNIII palsy

Contralateral weakness

181
Q

What does a basilar artery stroke cause?

A

Locked in syndrome

182
Q

What score is used to assess stroke?

A

Rosier

183
Q

What score is used to assess TIAs?

A

ABCD2

184
Q

What is the initial investigation of stroke?

A

CT head to rule in/out haemorrhagic stroke

185
Q

What other investigations should be done in suspected stroke?

A

Bloods (FBC, glucose, U&Es, LFTs, coag, lipids)
ECG, echo
Carotid doppler

186
Q

What is the initial management of ischaemic stroke?

A

Thrombolysis - Alteplase

187
Q

What is the time frame for thrombolysis?

A

4.5hrs

188
Q

What antiplatelet should initially be started for ischaemic stroke and for how long?

A

Aspirin 300mg for 14 days

189
Q

How is haemorrhagic stroke managed?

A

Clot evacuation, treat underlying cause, stop anticoagulants

190
Q

What are the post-stroke preventative medications?

A

Clopidogrel 75mg lifelong
Statin lifelong
ACEi/ARB + diuretic to control blood pressure

191
Q

If a stroke patient is found to have AF, what should they be put on and with what target?

A

Warfarin with target INR 2-3

192
Q

What are some common stroke mimics?

A

Hypoglycaemia, migraine, SOL, post-ictal, demyelination, intracranial haemorrhage, functional

193
Q

Where does a subarachoid haemorrhage occur?

A

Bleed in circle of willis with blood accumulating in the subarachnoid space

194
Q

What are causes of SAH?

A

AVM, ruptured berry aneurysm (EDS, PCKD)

195
Q

How does SAH present?

A

Thunderclap headache, collapse, LOC, meningism, focal neurology

196
Q

What does CT show in SAH?

A

Grey areas with dark ventricles

197
Q

If the CT is negative in suspected SAH what should you do?

A

LP

198
Q

How is SAH managed?

A

Fluids, nimodipine to prevent vasospasm, endovascular clipping/coiling of artery

199
Q

What vessels cause and where does a subdural haemorrhage occur?

A

Bridging vessels

Between dura and arachnoid

200
Q

What are risk factors for subdural haemorrhage?

A

Increased age, alcoholics, epilepsy, anti-coagulants

201
Q

What is the cause of a subdural?

A

Trauma or commonly unable to recall an incident of trauma

202
Q

What is the presentation of a subdural haemorrhage?

A

Fluctuating consciousness, mental slowing, sleepiness, dull headache, focal neurology

203
Q

What does a subdural look like on CT?

A

Creset shaped haematoma

204
Q

How is a subdural haemorrhage treated?

A

Burr hole craniotomy

205
Q

What vessels and where does an extradural haemorrhage occur?

A

Middle meningeal artery, blood accumulates between the bone and the dura

206
Q

What are causes of extradural haemorrhage?

A

Temporal bone fracture, history of head injury

207
Q

How does extradural haemorrhage present?

A

Head injury then lucid period. Increasing headache and then sudden decline in conscioussness, confusion, seizures, vomiting, hemiparesis, focal neurology

208
Q

What does a CT head show in extradural haemorrhage?

A

Biconvex haematoma (rugby ball shaped)

209
Q

How is an extradural haematoma managed?

A

Clot evacuation and ligation of middle meningeal artery

210
Q

What are common side effects of triptans?

A

Tightness of chest, feeling of heaviness, pressure

211
Q

What diet may be helpful in epilepsy?

A

Ketogenic diet

212
Q

What is the commonest psychiatric problem in PD?

A

Depression

213
Q

What is cataplexy?

A

Sudden and transient loss of muscle tone in response to emotion

214
Q

What is the classic triad of Wernickes encephalopathy?

A

Nystagmus, ataxia and confusion

215
Q

What is the triad of normal pressure hydrocephalus?

A

Ataxia, urinary incontinence, dementia

216
Q

Obese young female with headache and blurred vision

A

Idiopathic intracranial hypertension

217
Q

What are features of syringomelia?

A

Wasting and weakness of arms
Loss of pain and temperature sensation
Loss of reflexes, upgoing plantars

218
Q

How does degenerative cervical myelopathy present?

A

Loss of fine motor function of upper and lower limbs

219
Q

‘Unilateral tinnitus and deafness’

A

Acoustic neuroma

220
Q

How is cervical myelopathy investigated?

A

MRI

221
Q

What drug is used to manage Bells palsy?

A

Prednisolone

222
Q

What is chronic inflammatory demyelinating polyneuropathy?

A

Antibody mediated demyelination of peripheral nerves

223
Q

What is the commonest long term complication of meningitis?

A

Sensorineural hearing loss

Finals Revision (22 decks)

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