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Phase 3A Revision > Neuro > Flashcards

Neuro Flashcards

1
Q

Features of migraine

A

Typically lasts 4-72 hours
Unilateral headache: poudning or throbbing
Nausea + vomiting
Photopboia
Phonophobia
With/without aura

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2
Q

Common triggers of migraine

A

CHOCOLATE
Chocolate (Cheese)
Hangover
Oral contraceptive
Caffeine
Orgasm
Anxiety/Alcohol
Travel
Exercise

Others: periods, injury, being hungry, smoking etc

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3
Q

Medical management of acute migraine

A

Paracetamol
Triptans - sumatriptan 50mg as soon as migraine starts
NSAIDs
Antiemetics for vomiting

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4
Q

Medications for migraine prophylaxis

A

Propanolol (preferred in women of child-bearing age)
Topiramate (teratogenic and can reduce effect of hormonal contraceptives)
Amitryptyline

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5
Q

ABCD2 score

A

Used to predict risk of stroke after a TIA
Age >60 years = 1
Blood pressure >140/90 = 1
Clinical features:
- Unilateral weakness = 2
- Speech disturbance without weakness = 1
Duration of symptoms
- >60 minutes = 2
- 10-60 minutes = 1
- <10 minutes = 0
Diabestes = 1

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6
Q

Risk of stroke following TIA using ABCD2

A

0-3 = 1%
4-5 = 4%
6-7 = 8%

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7
Q

Prevention of stroke in patients with TIA

A

If scoring >/= 4 –> 300mg Aspirin immediately, specialist assessment within 24 hours of onset
</= 3 = low risk –> 300mg aspirin, refer to be seen by specialist and investigated within 1 week of onset

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8
Q

TIA

A

Transient neurological dysfunction secondary to ischaemia without infarction
(Traditional definition = symptoms resolve completely within 24 hours of onset)

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9
Q

Amaurosis fugax

A

Sudden loss of vision in one eye
Caused by infarct in retinal artery/ies or in ophthalmic artery
Described as black curtain coming across the vision
Important differential = migraine

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10
Q

Presentation of TIA

A

Sudden, focal neurological deficit e.g.
Unilateral weakness or sensory loss
Dysphagia
Ataxia, vertigo or incoordination
Amaurosis fugax
Homonymous hemianopia
Cranial nerve defects

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11
Q

Blood tests in TIA

A

FBC
HBA1c
ESR
U+Es
Bone profile
LFTs
Lipid profile
Routine coag/clotting screen
INR (if on warfarin)

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12
Q

Main investigation in TIA

A

MRI head with diffusion-weighted imaging
CT used if MRI unavailable

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13
Q

Other investigations in TIA

A

ECG - arrhythmias
Echo - only used if suspicion of heart disease or confirmed stroke
Carotid dopplers

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14
Q

Level of carotid stenosis required for endarterectomy

A

> 70%
Only offered if patient is not severely disabled

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15
Q

Crescendo TIA

A

> 1 TIA in the last week - severe risk for future stroke

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16
Q

Acute management of TIA

A

300mg aspirin (continued for two weeks)
Clopidogrel 300mg if aspirin contraindicated/not tolerated
Immediate admission for imaging if on an anticoagulant, or has a bleeding disorder

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17
Q

Long-term therapy for TIA

A

Clopidogrel 75mg od (aspirin if cannot have clopidogrel)
Statin (atorvastatin 20-80mg od) in all patients
Consider anti-coagulation for AF
Modification of other risk factor e.g. anti-hypertensives

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18
Q

Triad of Parkinson’s disease

A

Resting tremor
Rigidity
Bradykinesia

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19
Q

Pathophysiology of PD

A

Progressive decrease in dopamine produced by substantia nigra in the basal ganglia - responsible for coordinating habital movement, voluntary movement, and learning specific movement patterns

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20
Q

Presentation of PD

A

Stooped posture
Facial masking
Forward tilit
Reduced arm swing
Pill-rolling tremor (at rest, worse if distracted)
Cogwheel rigidity
Bradykinesa
- Micrographia
- Shuffling gait
- Difficulty initiating movements
- Difficulting turning
- Hypomimia

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21
Q

Other features of PD

A

Depression
Sleep disturbance + insomnia
Anosmia
Postural instability
Cognitive impairment + memory problems

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22
Q

Differences between parkinson’s tremor + benign essential tremor

A

PD = asymmetrical, lower frequency, worse at rest, improves with intentional movement, no change with alcohol
BET = symmetrical, higher frequency, improves at rest, worse with intentional movement, improves with alcohol

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23
Q

Management of benign essential tremor

A

Primidone
Propanolol
Deep brain stimulation if refractory to drug treatment and causes severe functional impairment

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24
Q

Scan that can be used to identify Parkinson’s disease/atypical parkinsonian disorders

A

DAT scan
Shows evidence of nigrostriatal degeneration

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25
Q

Parkinson’s-plus syndromes

A

Multiple system atrophy –> autonomic + cerebellar dysfunction
Dementia with Lewy bodies
Progressive supranuclear palsy
Corticobasal degeneration

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26
Q

Management of PD

A

Levodopa (dopamine cannot cross BBB)
Given with something to improve half-life (peripheral decarboxylase inhibitors) e.g. carbidopa, benserazide –>
Co-benyldopa, or co-careldopa

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27
Q

Side-effects of levodopa treatment

A

Efficacy decreases over time
On-off effect at end of dose
Nausea/GI upset
Dyskinesias: dystonia, chorea, athetosis
Psychosis
Compulsive behaviours

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28
Q

Other options for management of PD

A

Catechol-o-methyltransferanse (COMT) inhibitors e.g. entacapone - extends effective duration of levodopa
Non-ergot derived dopamine agonists e.g. ropinirole
Ergot-derived dopamine agonists e.g. bromocriptine, pergolide, carbergoline: prolonged use –> pulmonary fibrosis
Monoamine oxidase-B inhibitors e.g. selegiline, rasagiline

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29
Q

What drugs may induce Parkinsonism

A

Anti-psychotics
Antiemetics e.g. metoclopramide
Lithium
Methyldopa
Antiepileptic drugs
Calcum channel blockers

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30
Q

Four most common forms of MND

A

Amyotrophic lateral sclerosis
Progressive bulbar palsy - affects more swallowing + talking
Progressive muscular atrophy
Primary lateral sclerosis

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31
Q

Presentation of MND (ALS)

A

Signs of LMN disease
Signs of UMN disease
NO SENSORY PROBLEMS
Progressive weakness and wasting of limbs (symmetrical) - starts at hands and spreads. May begin unilateral, but will become bilateral
No pain usually
Important: Loss of muscle tone + spasticity rarely seen together

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32
Q

Signs of UMN disease

A
  • Increased tone or spasticity
  • Brisk reflexes
  • Upgoing plantar responses
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33
Q

Signs of LMN disease

A
  • Muscle wasting
  • Reduced tone
  • Fasciculations
  • Reduced reflexes
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34
Q

Presentation of progressive bulbar palsy

A

Problems with speech and swallowing
Dysphagia
Dysarthria
Nasal regurgitation
Choking
Tongue may be immobile, or wasted + fasciculating
Progressive

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35
Q

Progressive muscular atrophy

A

Typically only affects LMNs of upper limbs

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36
Q

Spinal muscular atrophy

A

Characterised by wasting and weakness of mucles

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37
Q

Management of ALS

A

Riluzole - used to improve prognosis, but only by a few months. Sodium channel blocker. Most effective in patients with bulbar signs
Baclofen - GABA agonist, helps reduce spasticity
Amitriptyline/propantheline for drooling
Ventilation support

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38
Q

Important features that differentiate MND from other similar diseases

A

Bladder never affected
No sensory signs
Ocular muscles never affected

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39
Q

Commonest causative agents of bacterial meningitis (general population)

A

Neisseria meningitidis (gram negative diplococci)
Streptococcus pneumoniae
(also haemophilus influenzae in 3months - 6 years)

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40
Q

Commonest causative agent of bacterial meningitis in neonates

A

Group B streptococcus

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41
Q

Common causative agents of bacterial meningitis in children 0-3 months

A

E coli
Listeria monocytogenes

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42
Q

Presentation of meningitis

A

Fever
Neck stiffness
Vomiting/poor feeding
Hedache
Photophobia
Altered conciousness
Seuizures (infective causes)

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43
Q

Signs of meningitis

A

Tachycardia
Kernig’s sign - flex hip with knee flexed, extend knee. Spasm in hamstrings = +ve
Brudzinski’s sign = passively flex neck. Flexion of hip and/or knee = +ve
Fever (if infective)

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44
Q

Late signs of meningitis (in children)

A

Bulging fontanelle
Neck stiffness
Opisthotonos (arched back)
Rash (bacterial causes only) –> petechial + non-blancing (suggests septicaemia)
Fall in BP

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45
Q

Which children should receive an LP to rule out meningitis

A

Under 1 months presenting with fever
1-3 months with fever + unwell
Under 1 years with unexplained fever and other features of serious illness

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46
Q

Management of bacterial meningitis in community

A
  • IM or IV benzylpenicillin
  • Transfer to hospital
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47
Q

Management of bacterial meningitis in hospital

A
  • Blood culture, LP for CSF prior to antibiotics where possible
  • Meningococcal PCR testing
  • <3 months old –> cefotaxime + amoxicillin (cover listeria)
  • > 3 months –> ceftriaxone
    • vancomycin if possible of penicillin resistant pneumococcal infection
  • Steroids e.g. dexamethasone to prevent long-term deficitns
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48
Q

Post-exposure prophylaxis for bacterial meningitis

A

Single dose of ciprofloxacin (given orally)
Ideally given within 24 hours of initial diagnosis
Anyone with prolonged contact within 7 days prior to onset of illness

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49
Q

Commonest causes of viral meningitis

A

Herpes simplex virus
Enterovirus
Varicella zoster virus

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50
Q

Management of viral meningitis

A

Often just supportive management
Aciclovir if HSV

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51
Q

CSF findings in bacterial meningitis

A

Cloudy
High protein
Low glucose
High WCC (neutrophils)
Culture +ve for bacteria

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52
Q

CSF findings in viral meningitis

A

Clear
Protein mildly raised or normal
Normal glucose
High WCC (lymphocytes)
Negative culture

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53
Q

Complications of meningitis

A

Hearing loss
Seizures + epilepsy
Cognitive impairment + learning disability
Memory loss
Focal neurological deficits e.g. limb weakness or spasticity

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54
Q

C5 myotome

A

Shoulder abduction + external rotation
Elbow flexion

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55
Q

Nerve for wrist extension

A

C6

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56
Q

Nerve for elbow extension + wrist flexion

A

C7

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57
Q

Nerve for finger flexion + thumb extension

A

C8

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58
Q

Nerve for finger abduction

A

T1

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59
Q

Nerve for hip flexion

A

L2

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60
Q

Nerve for knee extension

A

L3

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61
Q

Nerve for ankle dorsiflexion

A

L4

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62
Q

Nerve for great toe extension

A

L5

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63
Q

Nerve for ankle plantarflexion

A

S1

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64
Q

C4 dermatome

A

Over acromioclavicular joint

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65
Q

C5 dermatome

A

Laterl aspect of lower edge of deltoid

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66
Q

C6 dermatome

A

Palmar side of thumb e.g. thenar eminence

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67
Q

C7 dermatome

A

Palmar side middle finger

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68
Q

C8 dermatome

A

Palmar side little finger

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69
Q

T1 dermatome

A

Medial aspect antecubital fossa, proximal to medial epicondyle of humerus e.g. soft upper underarm, closest to body

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70
Q

Common features of non-epileptic attack

A

Arms flexing + extending
Pelvic thrusting
Sudden drop at start
Eyes closed
Prolonged seizures (>30 minutes)
Symptoms wax and wane

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71
Q

Features of simple partial seizure

A

Patient remains conscious
Isolated limb jerking
Isolated head turning (away from side of seizure)
Isolated parasthesia
Weaness of limbs may follow

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72
Q

What is Todd’s paralysis

A

Weakness of limbs following a seizure (usually a simple partial motor seizure e.g, Jacksonian)

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73
Q

Features of generalised tonic-clonic seizures

A

Loss of consciousness
Muscle tensing + muscle jerking episodes (usually this order)
Tongue biting
Incontinence
Groaning
Irregular breathing
Confused post-ictally: drowsy, irritable, depressed

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74
Q

Management of tonic-clonic seizures

A

1st line = sodium valproate
2nd line = lamotrigine/carbamazepine

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75
Q

Features of focal seizures/complex partial seizures e.g. temporal lobe seizures

A

Affects hearing, speech, memory and emotions
e.g.
Hallucinations
Memory flashbacks
Deja-vu/jamais-vu
Vertigo
Lip-smacking/other disturbances

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76
Q

Management of focal seizures

A

1st = carbamazepine or lamotrigine
2nd = sodium valproate or levetiracetam

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77
Q

Management of absence seizures

A

Sodium valproate or ethosuximide

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78
Q

Features of atonic seizures

A

Drop attacks
Brief lapses in muscle tone
Typically <3 minutes
Begin in childhood
May be associated with Lennox-Gastaut syndrome

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79
Q

Management of atonic seizures

A

1st = sodium valproate
2nd = lamotrigine

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80
Q

Definition of status epilepticus

A

Seizure >5 minutes
OR >3 seizures in 1 hour

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81
Q

Management of status epilepticus in hospital

A

Secure airway
O2 (high concentration)
Assess cardiac + resp function
Check blood glucose - rule out hypoglycaemia
Gain IV access

IV lorazepam 4mg, repeated after 10 minutes if seizures continue
–> IV phenobarbital or phenytoin

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82
Q

Options for management of status epilepticus in community

A

Buccal midazolam
Rectal diazepam

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83
Q

Medications that should be avoided in Parkinson’s disease

A

Prochlorperazine
Metoclompramide
Haloperidol
Chlorpromazine
Promazine

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84
Q

Presentation of brain abscess

A

Headache - often dull, persistent
Fever - may be absent, not swinging pyrexia
Focal neurology e.g. oculomotor/abducens palsy secondary to raised intracranial pressure

Other features of raised ICP:
- Nausea
- Papilloedema
- Seizures

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85
Q

Investigations for brain abscess

A

CT head - rim-enhancing lesion with a central cavity, surrounding oedema

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86
Q

Most common pattern for multiple sclerosis

A

Relapsing-remitting

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87
Q

Risk factors for IIH

A

Obesity
Female sex
Pregnancy
Drugs: COCP, steroids, TCAs, Vitamin A, lithium

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88
Q

Features of IIH

A

Headache
Blurred vision
Papilloedema
Enlarged blind spot
Sixth nerve palsy may be present

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89
Q

Management of IIH

A

Weight loss
Diuretcis e.g. acetazolamide
Topiramata may be used –> can also help with weight loss
Repeat LP
Surgery

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90
Q

Definition of status epilepticus

A

Single seizure lasting >5 minutes, or
>/= 2 seizures within a 5-minute period without the person returning to normal between them

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91
Q

Features of third nerve palsy

A

Eye ‘down and out’
Ptosis
Pupil may be dilated
Direct light reflex absent, consensual light reflex may be present

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92
Q

Causes of third nerve palsy

A

Diabetes mellitus
Vasculitis
Posterior communicating artery aneurysm
Cavernous sinus thrombosis
Weber’s syndrome
Multiple sclerosis

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93
Q

Features of post-concussion syndrome

A

Headache
Fatigue
Anxiety/depression
Dizziness

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94
Q

International Headache Society for migraine without aura

A

A - at least 5 attacks, fulfilling criteria B-D
B - headaches lasting 4-72 hours
C - headache has at least two of:
- Unilateral location
- Pulsating quality
- Moderate or severe pain intensity
- Aggravation by or causing avoidance of routine physical activity
D - during headahce, at least one of:
- Nausea and/or vomiting
- Photophobia + phonophobia
E - not attributred to another disorder

95
Q

Difference in presentation of migraine in children

A

Attacks may be shorter lasting
Headache more commonly bilateral
Gastrointestinal disturbance is more prominent

96
Q

Presentation of cluster headaches

A

Typically unilateral symptoms:
Red, swollen and watering eye
Miosis (pupil constriction)
Eyelid drooping (ptosis)
Nasal discharge
Facial sweating
Intense, sharp, stabbing pain around one eye

97
Q

Timing of cluster headaches

A

Pain usually once or twice a day
Each episode lasts 15 minutes - 2 hours
Clusters typically last 4-12 weeks

98
Q

Acute management of cluster headaches

A

Triptans e.g. sumatriptan 6mg injected subcutaneously
High flow 100% oxygen for 15-20 minutes

99
Q

Prophylaxis of cluster headaches

A

Verapamil
Lithium
Prednisolone

100
Q

Management of neuropathic pain

A

1st line: amitriptyline, duloxetine, gabapentin, or pregabalin
- If does not work, try one of the other three
- Typically used as monotherapy
- NB: carbamazepine used in trigeminal neuralgia
Tramadol - used as rescue therapy for exacerbations
Topical capsaicin - used or localised neuropathic pain

101
Q

Features of encephalitis

A

Fever
Headache
Altered mental status
And/or neurological deficits

May also have seizures, behavioural changes (e.g. psychotic or affective features), brainstem dysfunction, memory problems

102
Q

Pathophysiology of encephalitis

A

HSV-1 responsible for 95% cases in adults
Typically affects temporal + inferior frontal lobes

103
Q

MRI findings on encephalitis

A

Prominent swelling
Increased signal of the brain in affected areas

104
Q

Investigations in encephalitis

A

CSF: lymphocytosis, elevated protein
PCR for HSV
Neuroimaging: MRI is better, medial temporal + inferior frontal changes (or normal)
EEG: lateralised periodic discharges at 2Hz

105
Q

Management of encephalitis

A

IV aciclovir

106
Q

Withdrawing analgesia in medication overuse headache

A

Simple analgesia (e.g. paracetamol, NSAIDs) + triptans: stop abruptly
Opiods: withdraw gradually

107
Q

Features of medication overuse headaches

A

Present for 15 days/more per month
Developed or worsened whilst taking regular symptomatic medication
Higher risk in patients using opioids and triptans
May be psychiatric co-morbidity

108
Q

What to do when a PD patient cannot take oral medication

A

Levodopa can only be given orally –> use a dopamine agonist patch

109
Q

Key difference between LMN and UMN facial nerve palsy

A

UMN palsy –> forehead sparing, due to bilateral innervation of the forehead
LMN palsy –> forehead not spared

110
Q

Examples of UMN lesions causing facial nerve palsy

A

Unilateral:
Cerebrovascular accidents e.g. strokes
Tumours
Bilateral (rare):
Psuedobulbar palsies
Motor neurone disease

111
Q

Bell’s palsy

A

Unilateral LMN facial nerve palsy

112
Q

Recovery from Bell’s palsy

A

Majority of patients fully recover over several weeks
Recovery may take up to 12 months
1/3 are left with some residual weakness

113
Q

Management of Bell’s palsy

A

If patient presents within 72 hours of developing symptoms:
- 50mg prednisolone for 10 days, or
- 60mg pred for 5 days, followed by a 5-day reducing regime of 10mg/day
Antivirals may offer some benefit
Lubricating eye drops to prevent eye damage
Tape to keep eye closed at night

114
Q

Features of Bell’s palsy

A

Forehead does not rise
Drooping of eyelid - exposing eye
Loss of nasolabial fold
Patients may also notice post-auricular pain (prior to paralysis), altered taste, dry eyes, hyperacusis

115
Q

Complication of Bell’s palsy

A

Exposure keratopathy –> requires ophthalmology review

116
Q

Follow-up in Bell’s palsy

A

If paralysis shows no sign of improvement after 3 weeks –> urgent ENT referral
Plastic surgery referral may be required for patients with more long-standing weakness

117
Q

What is Guillain-Barre syndrome

A

Acute paralytic polyneuropathy
Causes acute, symmetrical, ascending weakness, as well as sensory symptoms
Usually triggered by an infection

118
Q

Infections associated with Guillain-Barre syndrome

A

Campylobacter jejuni
Cytomegalovirus
Epstein-Barr virus

119
Q

Main features of GBS

A

Symmetrical ascending weakness - starting at feet, moving up body
Reduced reflexes
May have peripheral loss of sensation, or neuropathic pain (mild sensory symptoms)

May have history of gastroenteritis

120
Q

Other features of GBS

A

Respiratory muscle weakness
May progress to cranial nerves –> facial nerve palsy, diplopia, oropharyngeal weakness
Autonomic involvements –> urinary retention, diarrhoea
Papilloedema may be present

121
Q

Investigations in GBS

A

Lumbar puncture
- Rise in protein
- Normal WBC count (albuminocytologic dissociation)
- Normal glucose
Nerve conduction studies may be performed
- Decreased motor nerve conduction velocity (demyelination)
- Prolonged distal motor latency
- Increased F wave latency

122
Q

Management of GBS

A

IV immunoglobulins
Plasma exchange (alternative to IV IG)
Supportive care
VTE prophylaxis
May require respiratory support

123
Q

What is multiple sclerosis

A

Chronic and progressive condition
Involves demyelination of the myelinated neurones in the CNS
Caused by an inflammatory process involving activation of immune cells against the myelin

124
Q

Diagnosis of MS

A

Lesions disseminated in time + space
However, if one episode of acute lesion e.g. optic neuritis, and an MRI showing a previous lesion, or positive oligoclonal bands on CSF –> can diagnose MS as these Ix show dissemination

For time dissemination: lasts longer than 24 hours + more than 1 month apart (typically)

125
Q

Typical patient affected by MS

A

2-3x more common in women
Present around 20-40 years old

126
Q

Classifications of MS

A

Relapsing-remitting
Primary progressive MS
Secondary progessive MS (50% of patients with relapsing-remitting will develop this within 15 years of onset)

127
Q

Visual manifestations of MS

A

Optic neuritis
INO: disorder of conjugate lateral gaze (failure to adduct eg. look right, right eye abducts, left eye remains central)
Abducens nerve palsy eg. look right, right eye fails to abduct

128
Q

Features of optic neuritis

A
  • Visual loss
  • Blurred vision
  • Pain behind eye, and on movement
  • Central scotoma (enlarged blind spot)
  • Poor colour differentiation (dyschromatopsia –> typically cannot see red)
  • Poor visual acuity
  • Relevant afferent pupillary defect
  • Optic nerve swelling seen on fundoscopy
129
Q

Motor + coordination manifestations of MS

A

Progressve paraparesis
UMN signs: spasticity, reduced power, hyper-reflexia
Transverse myelitis: sensory + motor symptoms below level of lesion in spine, with potential bladder/bowel involvement
Cerebellar syndrome: ataxia, slurred speech, intention tremor, nystagmus, vertigo + clumsiness

130
Q

Sensory + autonomic manifestations of MS

A

Paraesthesia
Pain
Heat sensitivity (Uhthoff phenomenon)
Sexual dysfunction
Bladder + bowel dysfunction

131
Q

Uhthoff’s phenomenon

A

Neuro symptoms are exacerbated by increases in body temperature

132
Q

Lhermitte’s sign

A

A sign on physical examination seen in MS
Shooting pain some patients expereicne when in neck flexion

133
Q

Cognitive + psychological manifestations of MS

A

Cognitive impairment
Depression –> can also affect memory, attention + concentration
Fatigue

134
Q

What is an MS attack

A

An episode of neurological symptoms that relate to an inflammatory demyelinating lesion
Lasts >24 hours, with or without recovery
Must be more than 30 days between attacks to count as separate episodes

135
Q

Clinically isolated syndrome

A

First episode of demyelination + neurological signs + symptoms
Cannot diagnose MS from this as lesions must be ‘disseminated in time + space’

136
Q

Investigations in MS

A

MRI scans - demonstrate lesions
Lumbar puncture - detect oligoclonal bands in CSF (more than seen in serum, not specific to MS)

137
Q

Non-MS causes of optic neuritis

A

Sarcoidosis
Systemic lupus erythematous
Diabetes
Syphilis/HIV
Measles
Mumps
Lyme disease
B12 deficiency

138
Q

Management of acute relapse MS

A

High dose steroids e.g. oral or IV methylprednisolone for 5 days
Used to shorten duration of relapse, not alter degree of recovery

139
Q

Management of MS

A

DMARDs + biologic therapy
Natalizumab
Fingolimod
Beta-interferon
Glatiramer acetate

140
Q

Myasthenia Gravis

A

Autoimmune condition causing muscle weakness that gets progressively worse with activity and improves with rest
Disorder of neuromuscular junctions - prevention of binding of ACh to receptors
Typically affects women <40 years old, and men >60

141
Q

Tumoir associated with myasthenia gravis

A

Thymoma (tumour of thymus gland)

142
Q

Muscle weakness in myasthenia gravis

A

Weakness that gets worse with muscle use, and improves with rest - symptoms typically worse at end of day
Symptoms mostly affect proximal muscles + small muscles of head + neck

143
Q

Presentation of myasthenia gravis

A

Diplopia (extraocular muscles)
Ptosis (eyelid weakness)
Weakness in facial movements
Difficulty swallowing
Fatigue in jaw with chewing
Slurred speech
Progressive weakness with repetitive movements

144
Q

How to elicit signs of myasthenia gravis on examination

A

Repeated blinking –> exacerbate ptosis
Prolonged upward gazing –> exacerbate diplopia on further eye movement testing
Repeated abduction of one arm 20 times –> unilateral weakness when comparing sides
Test forced vital capacity

145
Q

Diagnosis of myasthenia gravis

A

ACh-receptor antibodies (85% patients)
Muscle-specific kinase antibodies (MuS)
LRP4 antibodies (low-density lipoprotein receptor-related protein 4)
CT/MRI thymus - look for thymoma
Edrophonium test

146
Q

Edrophonium test

A

Patients given IV dose of edrophonium chloride (or neostigmine)
Prevents breakdown of acetylcholine in NMJ
Briefly + temporarily relieves weakness

147
Q

Management of myasthenia gravis

A

Reversible acetylcholinesterase inhibitors (pyridostigmine or neostigmine)
Immunosuppression e.g. prednisolone or azathioprine
Thymectomy (even if no thymoma)
Rituximab - reduces production of antibodies

148
Q

Myasthenic crisis

A

Severe complication of myasthenia gravis
Causes an acute worsening of symptoms, often triggered by another illness e.g. resp tract infection
Can lead to respiratory failure –> may required ventilation
Perform bedside FVC + arterial blood fas analysis
Immunomodulatory therapies: IVIG and plasma exchange

149
Q

Drugs that may exacerbate myasthenia

A

Penicillamine
Quinidine, procainamide
Beta-blockers
Lithium
Phenytoin
Antibiotics: gentamicin, macrolides, quinolones, tetracyclines

150
Q

Ptosis + dilated pupil vs. constricted pupil

A

Dilated = third nerve palsy
Constricted = Horner’s

151
Q

Presentation of Horner’s syndrome

A

Ptosis
Miosis
Anhidrosis

May also have enopthalmos
Light + accomodation reflexes not affected

152
Q

What is Horner’s syndrome

A

Caused by damage to sympathetic nervous system supply to the face

153
Q

Central causes of Horner’s syndrome

A

Central lesions cause anhidrosis of trunk + arm as well as face (4Ss)
- Stroke
- Multiple Sclerosis
- Swelling (tumours)
- Syringomyelia (cyst in spinal cord)

154
Q

Pre-ganglionic causes of Horner’s syndrome

A

Anhidrosis of face only
4Ts
- Tumour (Pancoast’s tumour)
- Trauma
- Thyroidectomy
- Top rib (cervical rib growing above first rib above clavicle)

155
Q

Post-ganglionic causes of Horner’s syndrome

A

No anhidrosis
4Cs
- Carotid aneurysm
- Carotid artery dissection
- Cavernous sinus thrombosis
- Cluster headache

156
Q

Diagnosis of Horner syndrome

A

Cocaine eye drops - causes normal eye to dilate, but no reaction of Horner syndrome pupil
Low concentration adrenaline eye drops - won’t dilate normal pupil, does dilate Horner syndrome pupil

157
Q

Key features of progressive supranuclear palsy

A

PSP = problem seeing planes = vertical gaze palsy
Parkinsonism symptoms
Dysarthria

158
Q

Key features of multi-system atrophy

A

Parkinsonism
Features of affect on other systems
e.g. postural hypotension
Ataxia
Urinary system –> incontinence/other bladder problems
Erectile dysfunction

159
Q

Causes of homonymous hemianopia

A

Incongruous defects: Lesion of optic tract
Congruous defects: lesion of optic radiation, or occipital cortex
Macula sparing: lesion of occipital cortex

160
Q

Causes of homonymous quadrantopias

A

Superior: lesion of inferior optic radiations in temporal lobe (Meyer’s loop)
Inferior: lesion of superior optic radiations in parietal lobe
PITS (parietal - inferior, temporal-superior)

161
Q

Cause of bitemporal hemianopia

A

Lesion of optic chiasm
Upper quadrant defect > lower quadrant = inferior chiasmal compression, commonly pituitary tumour
Lower > upper = superior chiasmal compression, commonly a craniopharyngioma

162
Q

Timeframe for stroke thrombolysis

A

Only consider if <4.5 hours since symptoms
Must exclude haemorrhage first

163
Q

Timeframe for stroke thrombectomy

A

Soon as possible - within 6 hours of symptom onset
Within 4.5 hours if given with thrombolysis

Can be given if known to be well between 6-24 hours previously depending on imaging

164
Q

Secondary prevention for stroke after ischaemic stroke

A

In people who have had an ischaemic stroke: clopidogrel
2nd line = aspirin + dipyridamole

165
Q

Features of anterior inferior cerebellar artery occlusion

A

Lateral pontine syndrome –>
Sudden onset vertigo + vomiting
Ipsilateral: facial paralysis, deafness, facial pain + temp loss
Contralateral: limb/torso pain + temperature loss
Ataxia
Nystagmus

166
Q

Features of anterior cerebral artery lesion

A

Contralateral hemiparesis + sensory loss
Lower extremity > upper
May have personality changes

167
Q

Features of middle cerebral artery lesion

A

Contralateral hemiparesis + sensory loss
Upper extremity > lower
Contralateral homonymous hemianopia
Aphasia

168
Q

Features of posterior cerebral artery lesion

A

Contralateral homonymous hemianopia with macular sparing
Visual agnosia - inability to recognise visually presnted objects
No facial blindness

169
Q

Features of lesion affecting branches of posterior cerebral artery supplying midbrain

A

Weber’s syndrome
Ipsilateral CN III palsy
Contralateral weakness of upper + lower extremity

170
Q

Features of lesion affecting posterior inferior cerebellar artery

A

Wallenberg syndrome/lateral medullary syndrome
Ipsilateral: facial pain + temperature loss
Contralateral: limb/torso pain, and temperature loss
Nystagmus
Ataxia

171
Q

What is a lacunar stroke

A

Stroke involving the perforating arteries around the internal capsule, thalamus and basal ganglia

172
Q

Presentation of lacunar strokes

A

Isolated: hemiparesis, hemisensory loss or hemiparesis with limb ataxia
May have have dysarthria/clumsy hand syndrome

173
Q

What is autonomic dysreflexia

A

Clinical syndrome
Occurs in patients with spinal cord at, or above, T6 level
Afferent signals, commonly triggered by faecal impaction or urinary retention, cause a sympatheitc spinal reflex
Parasympathetic response prevented by cord lesion –> unbalanced physiologiccal response

174
Q

Features of autonomic dysreflexia

A

Commonly history of constipation or urinary retention
Hx of spinal cord lesion at, or above, T6 spinal level
Extreme hypertension
Sweating + flushing above level of cord lesion
Agitation

175
Q

Red flag features for headache

A

Sudden onset headache, reaching maximum intensity within 5 minutes
Vomiting without other obvious cause
Headache worse with fever
New-onset neurological deficit/cognitive dysfunction
Change in personality
Impaired level of consciousness
Headahce triggered by cough, valsalva, sneeze or exercise
Headache changing with posture
Substantial change in characteristics of headache

176
Q

Red flag features in personal history for headache

A

Recent (last 3 months) head trauma
Compromised immunity
<20 years old with history of malignancy
Hx malignancy known to have brain metastases

177
Q

Cushing reflex

A

Response to raised ICP
–> hypertension + bradycardia

178
Q

How to calculate cerebral perfusion pressure

A

Mean arterial pressure - intracranial pressure

179
Q

Features of subdural haemorrhage

A

Caused by rupture in bridging veins between dura + arachnoid mater
CT: crescent shape, not limited by cranial sutures
(bright if acute, hypodense if chronic)

180
Q

Features of extradural haemorrhage

A

Typically rupture of middle meningeal artery
Can be associated with fracture of temporal bone
CT: bi-convex shape, limited by cranial sutures

Typical: young patient, traumatic head injury, ongoing headache. Period of improved neuro symptoms + consciousness followed by rapid decline

181
Q

First line radiological investigation for suspected stroke

A

Non-contrast CT head - needed to rule out intracranial haemorrhage

182
Q

Causes of raised ICP

A

Idiopathic intracranial hypertension
Traumatic head injuries
Infection e.g. meningitis
Tumours
Hydrocephalus

183
Q

Features of raised ICP

A

Headache
Vomiting
Reduced levels of consciousness
Papilloedema
Cushing’s triad: widening pulse pressure, bradycardia, irregular breathing

184
Q

Investigations for raised ICP

A

Neuroimaging to determine cause
Invasive ICP monitoring

185
Q

Management of raised ICP

A

Treat underlying cause
Head elevation to 30 degrees
IV mannitol may be used as an osmotic diuretic
Controlled hyperventilation –> aim to reduce pCO2
Removal of CSF e.g. repeated LP

186
Q

Features of intracranial venous thrombosis

A

Headache (may be sudden onset)
N+V
Reduced conciousness
Generally features of raised ICP

187
Q

Investigation for intracranial venous thrombosis

A

MRI venography = gold standard
- CT venography = alternative
D-dimer may be elevated
Non-contrast CT head often normal

188
Q

Management of intracranial venous thrombosis

A

Anticoagulation:
- LMWH acutely
- Warfarin for longer term

189
Q

Management of optic neuritis

A

Resolves in around 6 weeks
Oral steroids may speed up recovery/lessen pain

190
Q

Features of temporal lobe seizures

A

HEAD
Hallucinations
Epigastric rising/Emotional
Automatisms e.g. lip smacking/grabbing/plucking
Deja vu/Dysphasia post-ictal

191
Q

Features of frontal lobe seizures

A

Head/leg movements
Posturing
Post-ictal weakness
Jacksonian march (clonic movements travelling proximally)

192
Q

Presentation of brain abscess

A

Headache: often dull, persistent
Fever: may be absent
Focal neurology e.g. oculomotor or abducens nerve palsy, secondary to raised ICP
Other features of raised ICP: nausea, papilloedema, seizures

193
Q

Investigations of brain abscess

A

Imaging with CT scanning - ring-enhancing lesion

194
Q

Management of brain abscess

A

Surgery: craniotomy + abscess cavity debrided
IV antibiotics: 3rd gen cephalosporin e.g. ceftriaxone, and metronidazole
Intracranial pressure management e.g. dexamethasone

195
Q

Inheritance of Charcot-Marie-Tooth disease

A

Most mutations are inherited in an autosomal dominant pattern

196
Q

Features of Charcot-Marie-Tooth

A

High foot arches (pes cavus)
Distal muscle wasting –> inverted champagne bottle legs
Weakness in lower legs (loss of ankle dorsiflexion)
Weakness in hands
Reduced tendon reflexes
Reduced muscle tone
Peripheral sensory loss

197
Q

Causes of peripheral neuropathy

A

A - Alcohol
B - B12 deficiency
C - Cancer + CKD
D - Diabetes + Drugs (e.g. isoniazid, amiodarone and cisplatin)
E - Every vasculitis

198
Q

Definition of overuse of medication (for headaches)

A

Applies to opioids + triptans
Using the medication on 10 days or more per month, for 3 months or more

199
Q

Features of medication overuse headaches

A

Often tension-type headache, but can have migraine-like characteristics
Present for 15 days or more per month
Worse after exercise
Worst in the morning
Resolve within 2 months of stopping the causative medication

200
Q

Causes of bilateral facial nerve palsy

A

Sarcoidosis
Guillain-Barre syndrome
Lyme disease
Bilateral acoustic neuromas
Bell’s palsy

201
Q

What is an acoustic neuroma

A

Vestibular Scwannoma
Benign tumour of the Schwann cells surroudning the vestibulochoclear nerve
Occur at the cerebellopontine angle
Usually unilateral

202
Q

Disease associated with bilateral acoustic neruomas

A

Neurofibromatosis type II

203
Q

Presentation of acoustic neuromas

A

Typically patient aged 40-60
Gradual onset of symptoms
Unilateral sensorineural hearing loss (often first symptom)
Unilateral tinnitus
Dizziness or imbalance (vertigo)
Sensation of fullness in one ear

May also have a facial nerve palsy (CN VII)
Cranial nerve V may also be affected –> absent corneal reflex

204
Q

Management of acoustic neuroma

A

Conservative management may be appropriate
Surgery to remove the tumour
Radiotherapy to reduce growth

205
Q

Key features of normal pressure hydrocephalus

A

Urinary incontinence
Gait abnormality
Dementia

206
Q

Imaging in normal pressure hydrocephalus

A

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

207
Q

Management of normal pressure hydrocephalus

A

Ventriculoperitoneal shunting

208
Q

Most common causes of cervical myelopathy

A

Degenerative cervical spondylosis
Congenital stenosis

209
Q

Presentation of cervical myelopathy

A

Neck pain + stiffness
Extremeity paraesthesias - bilateral, non-dermatomal numbness + tingling
Bilateral weakness + clumsiness
Gait instability
Urinary retention (rare, and only appear late)

210
Q

Gold standard investigation for suspected cervical myelopathy

A

MRI cervical spine

211
Q

Management of cervical myelopathy

A

Typically surgical decompression + stabilisation

212
Q

Juvenile myoclonic epilepsy presentation

A

Myoclonus (jerking) in limbs
Normally bilateral myoclonus
Typically occur early in the morning or near bedtime
May have daytime absences
More common in girls + teenagers
Can progress to generalised seizures

213
Q

Benign roalndic epilepsy presentation

A

Typically children aged 4-12 years old
Partial seizures, occurring at night
Typically parasthesias (of the face)
No LOC or significant mental status change
More common in males

214
Q

What diet may be recommended in or help with epilepsy that is hard to control/is unresponsive

A

Ketogenic diet

215
Q

Genetics of Huntington’s disease

A

Autosomal dominant
Trinucleotide repeat expanded disorder (CAG)
Involves genetic mutation in the HTT gene on chromosome 4
Shows anticipation: successive generations have more repeats –> earlier age of onset, increased severity

216
Q

Presentation of Huntington’s disease

A

Insidious, progressive worsening of symptoms
Tend to present aged 30-50
Usually begins with cognitive, psychiatric or mood problems
Movement disorder then develops:
- Chorea (involuntary, abnormal movements)
- Eye movement disorders
- Dysarthria
- Dysphagia
Life expectancy around 15-20 years after symptom onset

217
Q

Medications to suppress disordered movement

A

Antipsychotics e.g. olanzapine
Benzodiazepines e.g. diazepam
Dopamine-depleting agents e.g. tetrabenazine

218
Q

Giant cell arteritis

A

Systemic vasculitis that affects medium + large arteries
Often known as temporal arteritis

219
Q

What condition is strongly associated with giant cell arteritis

A

Polymyalgia rheumatica

220
Q

Symptoms of giant cell arteritis

A

Severe unilateral headache, typically around temple + froehead
Scalp tenderness may be noticed e.g. when brushing hair
Jaw claudication
Blurred or double vision
Irreversible painless complete sight loss can occur rapidly
Systemic symptoms also possible

221
Q

Investigations of giant cell arteritis

A

Raised ESR (usually >50mm/hour)
Temporal artery biopsy - showing multinucleated giant cells

Other possible findings:
FBC: normocytic anaemia + thrombocytosis
LFTs: raised ALP
CRP rasied
Duplex USS of temporal artery –> hypoechoic halo sign.

CTA due to risk of aortic aneurysm

222
Q

Management of giant cell arteritis

A

Steroids: given before confirmation of diagnosis to reduce risk of permanent sight loss
- 40-60mg prednisolone per day (60 if jaw claudication or visual symptoms)
- Review response within 48 hours: usually rapid and significiant
Aspiring 75mg daily: decrease visual loss + strokes
PPI for gastric prevention while on steroids

223
Q

Commonest recessive type of ataxia in UK

A

Friedrich’s ataxia
Causes atrophy + thinning of dorsal root ganglia
GAA repeat disorder

224
Q

Papillitis

A

Inflammation of optic nerve head
Presents with pain on eye movement + blurred vision
Assciated with inflammatory + demyelinating disorders
Significant visual loss

225
Q

Types of manifest strabismus

A

One eye forwards with…
Esotropia: one eye inwards
Exotropia: one eye outwards
Hypertropia: one eye upwards
Hypotropia: one eye downwards

226
Q

Latent strabismus

A

Eyes are straight when both eyes are open, but deviation can be elicited when each eye is covered
Under occluder eye turning…
Esophoria - inwards
Exophoria - outwards
Hyperphoria - upwards
Hypophoria - downwards

227
Q

Causes of childhood strabismus

A

Hereditary
Refractive errors (requires glasses)
- Most common = uncorrected hypermetropia (long-sighted) and accomodative esotropia
- Anisometropia (difference in refractive error of each eye) and development of amblyopia (lazy eye)
Hydrocephalus
Cerebral palsy
Space occupying lesions
Trauma

228
Q

Amblyopia

A

Eye affected becomes passive and has reduced function compared to dominant eye (lazy eye)

229
Q

Examination of squint

A

Eye movements
Fundoscopy - rule out retinoblastoma, cataracts, or other retinal pathology
Visual acuity
Hirschberg’s test: observe reflection of light source on cornea
Cover test: watch movement of previously covered eye

230
Q

Management of strabismus etc

A

Treatment needed before age of 8 (as visual fields still developing)
Occlusive patch: cover good eye + force weaker eye to develop
Atropine drops: alternative to patch, causes blurry vision in good eye
Ophthalmology input
Correct refractive errors

231
Q

Common location of lesion in painful third nerve palsy

A

Posterior communicating artery aneurysm
Associated headache also present

232
Q

Genetics of neurofibromatosis

A

NF1: gene found on chromosome 17, codes for neurofibromin (tumour suppressor protein); autosomal dominant
NF2: chromosome 22, codes for merlin (tumour suppresor protein, esp in Schwann cells); autosomal dominant

233
Q

Criteria for neurofibromatosis type 1

A

2/7 required for diagnosis
CRABBING
C- cafe-au-lait spots (6+) 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 harmatomas (Lisch nodules) (2+), yellow-brown spots on iris
N - neurofibromas (2+) or 1 plexiform neurofibroma
G - glioma of optic nerve

234
Q

Key features of neurofibromatosis type 2

A

Mutations in this gene –> schwannomas
Associated with aucostic neuromas –>
- Hearing loss
- Tinnitus
- Balance problems
Bilateral acoustic neuromas suggests NF2
Can also develop schwannomas in brain + spinal cord
Surgical resection may be useful

Phase 3A Revision (12 decks)

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