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3a PTS - PM - ZTF > Neurology > Flashcards

Neurology Flashcards

1
Q

Features of migraine

A

Severe, unilateral, throbbing headache
Typically lasts 4-72 hours
Associated with nausea, photonics and phonophobia
1/3 of patients experience aura (visual (transient hemianoptic disturbance or a spreading scintillating scotoma), progressive, last 5-60 min)

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2
Q

Migraine: epidemiology (gender)

A

3 times more common in women

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3
Q

Common triggers for a migraine attack

A

Chocolate / Cheese / Citrus fruits
Combined Oral Contraceptive Pill / Hormonal (menstruation)
Alcohol (especially red wine)
Lights
Lack of food / dehydration / Tiredness / Stress

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4
Q

Migraine diagnostic criteria (5)

A
  1. At least FIVE attacks fulfilling the criteria
  2. Two classic features: unilateral, pulsating, moderate-severe pain, aggravation by routine physical activity
  3. At least ONE: nausea/vomiting and/or photophobia/phonophobia
  4. Lasts 4-72 hours
  5. Not attributed to another disorder
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5
Q

General rule of migraine acute vs prophylactic management

A

5-HT receptor agonists (e.g. triptans) are used in acute treatment, 5-HT receptor antagonists are used in prophylaxis (e.g. propranolol, amitriptyline)

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6
Q

1st line treatment of acute migraine

A

Oral triptan + NSAID
Or
Oral triptan + paracetamol

Antiemetics e.g. metoclopramide for vomiting - can lead to EPSEs

Aged 12-17: consider nasal triptans

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7
Q

Options for medical prophylaxis of migraines

A

Propranolol
Amitriptyline
Topiramate (AVOID in women of childbearing age)

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8
Q

Menstrual migraine treatment

A

Frovatriptan or zolmitriptan 2.5mg BD around menstruation

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9
Q

‘Complementary medicine’ option for migraine prophylaxis

A

Acupuncture

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10
Q

Vitamin supplement useful in migraine prophylaxis

A

Vitamin B2 (riboflavin)

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11
Q

Hemiplegic migraine features

A

can mimic stroke - act fast

Typical migraine symptoms
Sudden or gradual onset
Hemiplegia (unilateral weakness of limbs)
Ataxia
Changes in consciousness

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12
Q

Contraception contraindicated in patients with migraine with aura

A

COC (due to increased risk of stroke)

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13
Q

1st line pain relief migraine in pregnancy

A

1st line: Paracetamol 1g

2nd line: NSAIDs can be used in first and second trimester, avoid aspirin and opioids e.g. codeine

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14
Q

Red flag aura symptoms

A

Motor weakness
Double vision
Visual symptoms affecting only one eye
Poor balance
Decreased level of consciousness

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15
Q

Most common cause of primary headache in children

A

Migraine without aura

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16
Q

ABCD2 score

A

Risk of stroke after a suspected TIA

Age > 60
BP > 140/90
Clinical features
Duration
Diabetes diagnosis

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17
Q

TIA definiton

A

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

(No longer time based definition)

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18
Q

Clinical features of TIA

A

Stroke symptoms that typically resolve within 1 hour
- Unilateral weakness or sensory loss
- Aphasia or dysarthria
- Ataxia, vertigo
- Visual problems

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19
Q

Immediate management of TIA

A

Aspirin 300mg daily (unless contraindicated or already on aspirin)

Referral for specialist assessment within 24 hours if TIA occurred in last 7 days
If > 7 days ago, refer for assessment within 7 days

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20
Q

Initial management of patient with suspected TIA who is on warfarin/a DOAC or has a bleeding disorder

A

Admit immediately for imaging to exclude haemorrhage

Aspirin 300mg is contraindicated

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21
Q

Investigations to assess the underlying cause of TIA or stroke (2)

A

All patients should have an urgent carotid doppler to assess for carotid artery stenosis

ECG to assess for atrial fibrillation

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22
Q

Surgical intervention where there is significant carotid artery stenosis (> 70%)

A

Carotid endarterectomy

Note: only available if the patient is not severely disabled

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23
Q

Preferred modality in patients with suspected TIA who require brain imaging

A

MRI brain with diffusion-weighted imaging

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24
Q

1st and 2nd line secondary prevention for TIA or stroke

A

1st: Clopidogrel 75mg once daily + Atorvastatin 20-80mg daily

2nd: Aspirin + dipyridamole (anti-platelet) + Atorvastatin 20-80mg daily

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25
Q

Crescendo TIA

A

Two or more TIAs within a week - indicate a high risk of stroke

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26
Q

4 pathological causes of disruption of blood supply to the brain

A

Thrombus or embolus
Atherosclerosis
Shock
Vasculitis

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27
Q

1st line radiological investigation for suspected stroke

+ signs for ischaemic vs haemorrhagic

A

Non-contrast CT head scan

Ischaemic signs: hyperdense artery corresponding with the responsible arterial clot

Haemorrhagic signs: hyperdense material (blood) surrounded by low density (oedema)

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28
Q

ROSIER score

A

Recognition of stroke in the ER

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29
Q

Management of stroke (4)

A

Exclude hypoglycaemia
Immediate CT scan
Aspirin 300mg daily for 2 weeks (once haemorrhage is excluded)
Admission to specialist stroke centre

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30
Q

Indications for IV thrombolysis with alteplase in stroke management

A

Within 4.5 hours of onset of stroke symptoms

Haemorrhage has been definitely excluded

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31
Q

Indication for thrombectomy in the management of ischaemic stroke

A

Within 6-24 hours

Offer to patients where there is confirmed occlusion of the proximal anterior circulation and if there is potential to salvage brain tissue (scans show limited infarct core volume)

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32
Q

Indication for thrombectomy with IV thrombolysis

A

Within 4.5 hours

Confirmed occlusion of proximal posterior circulation (basilar or PCA) and potential to salvage brain tissue (i.e. scans show limited infarct core volume)

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33
Q

Parkinson’s triad

A

ASYMMETRICAL:

Bradykinesia
Tremor
Rigidity

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34
Q

Bradykinesia presentation in Parkinson’s

A

Movement gets slower and smaller:

  • Short, shuffling steps with reduced arm swinging
  • Difficulty in initiating movement e.g. standing to walking
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35
Q

Tremor presentation in Parkinson’s

A

Most marked at REST
3-5 Hz
Worse when stressed or tired
Improves with voluntary movement
Typically ‘pill-rolling’, i.e. thumb and index finger

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36
Q

Rigidity presentation in Parkinson’s

A

‘Cogwheel’ due to superimposed tremor / resistance to passive movement of joint

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37
Q

Psychiatric features in Parkinson’s (4)

A

Depression (most common - 40%)
Dementia
Psychosis
Sleep disturbances

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38
Q

What can autonomic dysfunction in Parkinson’s cause

A

Postural hypotension

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39
Q

Parkinsonism vs Parkinson’s

A

Parkinsonism:
Motor symptoms are generally RAPID onset and BILATERAL
Rigidity and rest tremor are UNCOMMON

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40
Q

Who can diagnose Parkinson’s disease

A

A specialist with expertise in movement disorders

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41
Q

1st line treatment for Parkinson’s where the motor symptoms are affecting the patients QOL

A

Levodopa

(Co-carelodopa/Co-beneldopa)

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42
Q

Treatment for Parkinson’s where motor symptoms are not affecting patients QOL

A

Dopamine agonist (non-ergot derived)
Levodopa
Monoamine Oxidase B inhibitor

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43
Q

Which antiparkinson drug is associated with the greatest improvement in symptoms and ADLs but has more motor complications

A

Levodopa

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44
Q

Which antiparkinsonian medication has the highest chance of inhibition disorders

A

Dopamine agonist therapy

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45
Q

What is levodopa usually combined with to prevent peripheral metabolism

A

Peripheral decarboxylase inhibitors e.g. carbidopa or benserazide

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46
Q

Types of dyskinesias (side effect of levodopa at peak dose)

A

Dystonia
Chorea
Athetosis

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47
Q

Adverse effects of levodopa (5)

A

Dry mouth
Orthostatic hypotension
Palpitations, Psychosis
Anorexia

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48
Q

2 phenomenons regarding levodopa use

A

End-of-dose wearing off: symptoms worsen towards end of dosage interval resulting in decline of motor activity

On-off phenomenon: normal function during ‘on’ period, weakness and restricted mobility during ‘off’ period

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49
Q

Levodopa is an example of a critical medicine, what does this mean?

A

Must not be acutely stopped

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50
Q

What can be given as a rescue medicine if levodopa cannot be given orally

A

Dopamine agonist patch
- to prevent acute dystonia

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51
Q

Mechanism of action of COMT inhibitors

A

COMT enzyme metabolises levodopa in both the body and brain

COMT inhibitors extend the effective duration of levodopa by slowing down the breakdown in the brain

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52
Q

What kind of drug is entacapone

A

COMT inhibitor

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53
Q

Indication for the use of dopamine receptor agonists and Monoamine oxidase-B inhibitors in Parkinson’s

A

Less effective than levodopa in reducing symptoms, therefore used to delay the use of levodopa and then used in combination with levodopa to reduce the dose of levodopa required

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54
Q

Examples of ergot-derived dopamine receptor agonists (2nd line to non ergot-derived)

A

Bromocriptine
Carbergoline

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55
Q

Complications of the use of ergot-derived dopamine receptor agonists e.g. bromocriptine

A

Pulmonary, retroperitoneal and cardiac fibrosis

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56
Q

Example of MAO-B inhibitor

A

Selegiline
Rasagiline

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57
Q

Action of Monoamine oxidase enzymes

A

Break down neurotransmitters such as dopamine, serotonin and adrenaline

MAO-B is specific to dopamine

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58
Q

Prognosis of MND

A

Poor - 50% of patients die within 3 years

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59
Q

Riluzole mechanism in MND

A

prevents stimulation of glutamate receptors = slows progression/prognosis of disease

only licensed medication to treat MND

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60
Q

ALS presentation

A

Age around 60 / Male

Asymmetric progressive weakness (limbs, trunk, face, speech)
Mixture of lower motor neuron and upper motor neuron signs
Absence of sensory signs

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61
Q

What motor features are preserved in MND

A

External ocular muscles
Cerebellar signs
Abdominal reflexes

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62
Q

Diagnosis of MND

A

Clinical diagnosis based on presentation and exclusion of other neuropathies (nerve conduction studies are normal)

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63
Q

Lower motor neurone signs

A

Muscle wasting
Reduced tone
Fasciculations (twitches in the muscles)
Reduced reflexes

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64
Q

Upper motor neurone signs

A

Increased tone or spasticity
Brisk reflexes
Upgoing plantar reflex

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65
Q

Which muscles are primarily affected in progressive bulbar palsy

A

Muscles of talking and swallowing (the bulbar muscles)

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66
Q

Most common cause of meningitis in neonates (0-3 months)

A

Group B Streptococcus (usually contracted during birth from GBS bacteria that live harmlessly in the mothers vagina)

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67
Q

Most common cause of bacterial meningitis in children and adults

A

Streptococcus pneumoniae (pneumococcus)
Neisseria meningitidis (gram negative meningococcus)

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68
Q

Causal organisms of meningitis in: > 60 years

A

Streptococcus pneumoniae
Neisseria meningitidis
Listeria monocytogenes

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69
Q

Causal organisms of meningitis in: immunosuppressed

A

Listeria monocytogenes

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70
Q

Explain the lumbar puncture results of a bacterial sample

A

Appearance: cloudy (proteins)

Protein: high (bacteria release proteins)

Glucose: low (bacteria eat up the glucose) - typically < 1/2 plasma glucose

WCC: high (immune system releases neutrophils in response to bacteria)

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71
Q

What level is a lumbar puncture needle inserted

A

L3-L4

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72
Q

Explain the lumbar puncture results of a viral sample

A

Appearance: clear
Protein: mildly raised/normal (viruses may release a small amount of protein)
Glucose: normal (viruses don’t use glucose: 60-80% of plasma glucose present)
WCC: high (immune system releases lymphocytes in response to viruses)

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73
Q

Complications of meningitis

A

Hearing loss
Seizures and epilepsy
Cognitive impairment and learning disability
Memory loss
Cerebral palsy, with focal neurological deficits such as limb weakness or spasticity

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74
Q

Most common causes of viral meningitis

A

Herpes simplex virus (HSV)
Enterovirus
Varicella zoster virus (VZV)

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75
Q

Management of viral meningitis

A

Tends to be milder than bacterial and often only requires supportive treatment

Acyclovir can be used to treat HSV or VZV

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76
Q

Post exposure prophylaxis for close prolonged contact of bacterial meningitis 7 days before onset

A

Single dose of ORAL ciprOflOxacin

(Rifampicin can be used but ciprofloxacin is preferred)

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77
Q

Management of suspected meningococcal disease in a primary care setting

A

Urgent stat injection (IM or IV) of benzylpenicillin

+ dexamethasone to reduce complications

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78
Q

Red flag of a non-blanching rash in children accompanied by headache, fever, neck stiffness

A

Meningococcal septicaemia - indicates that the infection has caused DIC and subcutaneous haemorrhages

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79
Q

Typical symptoms of meningitis

A

Fever
Neck stiffness
Vomiting
Headache
Photophobia
Altered conciousness
Seizures

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80
Q

2 special tests to look for meningeal irritation

A

Kernigs test
Brudzinskis test

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81
Q

Antibiotic management of bacterial meningitis

A

Over 3 months: IV cefotaxime or ceftriaxone

Under 3 months: IV cefotaxime + amoxicillin (to cover listeria)

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82
Q

Which medication is given in meningitis management to reduce the frequency and severity of hearing loss and neurological damage

A

Dexamethasone - 4 times daily for 4 days to children over 3 months

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83
Q

Circumstances where lumbar puncture should be delayed in the investigation of meningitis

A

Signs of severe sepsis or a rapidly evolving rash
Severe respiratory/cardiac compromise
Significant bleeding risk
Signs of raised intracranial pressure

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84
Q

4 signs of raised intracranial pressure

A

Focal neurological signs
Papilloedema
Continuous or uncontrolled seizures
GCS <12

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85
Q

Who should not receive IV dexamethasone in the management of meningitis

A

Septic shock
Meningococcal septicaemia
Immunocompromised

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86
Q

When would neuroimaging be indicated in suspected bacterial meningitis

A

Raised ICP - otherwise not normally indicated

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87
Q

Most common cause of foot drop

A

Common peroneal nerve lesion causing weakness of the foot dorsiflexor muscles

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88
Q

Risk of having a stroke with AF score

A

CHADSVAS
Congestive heart failure
Hypertension
Aged 75 years or older
Diabetes mellitus
Stroke (previous)
Vascular disease
Age 65-74
Sexual category (female)

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89
Q

Total anterior circulation stroke (TACS) criteria

Bamford classification of ischaemic stroke

A

Stroke affecting both the MCA and ACA

Diagnosis requires all 3 of the following:
Unilateral weakness of face, arm and leg
Homonymous hemianopia
Higher cerebral dysfunction e.g. dysphasia

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90
Q

Posterior circulation stroke key symptoms

A

Dizziness
Diplopia
Dysarthria
Dysphagia
Dystaxia

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91
Q

what are Lewy Bodies

A

alpha synuclein cytoplasmic inclusions

seen in LBD, Parkinson’s + Alzheimer’s

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92
Q

Lilluptian bodies

A

Lewy body dementia associated visual hallucinations, classically of small creatures/children/figures

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93
Q

Lewy body dementia vs parkinson’s disease dementia

A

Lewy Body Dementia: starts at the top and eventually descends to the substantia nigra / dementia and movement disorder develop within a year of each other

Parkinson’s Disease Dementia: inclusions affect the substantia nigra (to cause the movement disorder) before ascending to involve the paralimbic and neocortical areas to result in dementia / movement disorder and dementia develop a year apart

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94
Q

Fronto-temporal dementia features

A

Onset before 65
Insidious onset
cognitive impairment
personality change
repetitive checking behaviour
disinhibition
Memory loss is a late feature

Constructional apraxia i.e. failure to draw interlocking pentagons may be a key feature in the early stages

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95
Q

3 variants of frontotemporal dementia

A

Behavioural variant (60%), characterised by loss of social skills, personal conduct awareness, disinhibition, and repetitive behaviour

Semantic dementia (20%), characterised by an inability to remember words for things, calling them ‘thingy’

Progressive non fluent aphasia (20%), where the patient can’t verbalise; their speech is laboured and difficult

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96
Q

Risk factor for frontotemporal dementia

A

repetitive head injury

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97
Q

Pick’s disease

A

one cause of FTD / diagnosed on post-mortem where “Pick’s bodies” (accumulations of TAU protein that stain with silver) are found in the neurons

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97
Q

Second most common cause of dementia

A

Vascular dementia

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98
Q

Dementia assessment tools recommended by NICE for the non-specialist setting

A

10-point cognitive screener (10-CS)
6-Item cognitive impairment test (6CIT)

AMTS and MMSE are also widely used but not recommended by NICE

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99
Q

Primary care blood screening for dementia

A

FBC, U&E, LFTs, calcium, glucose, ESR/CRP, TFTs, vitamin B12 and folate levels

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100
Q

Secondary care primary investigation for dementia

A

Neuroimaging (exclude other reversible conditions e.g. subdural haematoma) and provide aetiological information

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101
Q

Dementia most likely to present with fluctuating cognition

A

Lewy Body Dementia

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102
Q

Which medication should be avoided in LBD

A

Neuroleptics may cause irreversible parkinsonism

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103
Q

When should antipsychotics be used in Alzheimer’s patients

A

patients at risk of harming themselves or others, or when the agitation, hallucinations or delusions are causing them severe distress

antipsychotics in AD are associated with a sig. risk of increased mortality

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104
Q

Middle cerebral artery presentation (4)

A

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

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105
Q

Anterior cerebral artery key presentation

A

Contralateral hemiparesis and sensory loss
Lower extremity > Upper

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106
Q

Horner’s syndrome features

A

Unilateral
Anhidrosis (absence of sweating of the face)
Miosis (constricted pupil)
Ptosis (drooping eyelid)
Enophthalmos (inset eye)

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107
Q

Which lung cancer tumour can lead to Horner’s syndrome

A

Pancoast (apical) tumour compressing the sympathetic chain

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108
Q

Pharmacological medication in Alzheimer’s

A

1st line:
Acetylcholinesterase inhibitors (donepezil, galantamine and rivastigmine)

Severe (as an add on) or if Acetylcholinesterase i are contraindicated: Memantine (NMDA receptor antagonist)

NICE does not recommend antidepressants for mild to moderate depression in dementia patients

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109
Q

Trigeminal neuralgia features

A

unilateral
brief electric shock-like pains, abrupt in onset and termination, limited to one or more divisions of the trigeminal nerve
the pain is commonly evoked by light touch, including washing, shaving, smoking, talking, and brushing the teeth (trigger factors)

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110
Q

Red flag signs in trigeminal neuralgia

A

Onset before 40
Family history of MS
Optic neuritis
Sensory changes
Deafness
Bilateral pain

refer to neurology

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111
Q

1st line treatment trigeminal neuralgia

A

Carbamazepine

if contraindicated or not tolerated, refer to neurology

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112
Q

Mixed dementia (2 most common types)

A

AD and VD

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113
Q

Non-ergot derived dopamine agonists examples

A

Ropinirole
Rotigotine

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114
Q

Major non-modifiable risk factor for TIA

A

Age - risk doubles every decade after 55

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115
Q

Huntington’s disease genetic features (4)

A
  1. Autosomal dominant
  2. Trinucleotide repeat disorder (repeat CAG expansion)
  3. Defect in huntingtin gene on chromosome 4
  4. Anticipation
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116
Q

Huntington’s disease pathophysiology

A

Results in degeneration of cholinergic and GABAergic neurons in the striatum of the basal ganglia

117
Q

Clinical features of Hungtington’s disease

A

Features typically develop after 35 years of age
Chorea
Personality changes (e.g. irritability, apathy, depression) and intellectual impairment
Dystonia
Saccadic eye movements

118
Q

Progressive supranuclear palsy

A

Parkinson plus condition
Typically reduced movement and vertical gaze palsy

119
Q

Wernicke’s encephalopathy triad

A

Confusion
Opthalmoplegia (may present as CN6 palsies/nystagmus)
Ataxia (broad-based gait)

120
Q

Korsakoff syndrome symptoms

A

Retrograde amnesia
Anterograde amnesia
Confabulation
Loss of insight

occurs when Wernicke’s is left untreated

121
Q

Which motor neuron lesion ‘spares’ the upper face

A

upper motor neuron lesion

122
Q

Bell’s palsy

A

lower motor neuron facial nerve (VII) palsy (forehead affected on ipsilateral side)

Dumbell’s are heavy = low

123
Q

Temporal arteritis

A

Also known as giant cell arteritis

idiopathic vasculitis affecting medium and large sized vessel arteries

124
Q

What disorder does temporal arteritis overlap with in 50% of cases

A

Polymyalgia rheumatica: aching, morning stiffness in proximal limb muscles (not weakness)

125
Q

Features of temporal arteritis

A

Typical patient is > 60 years old
Usually rapid onset (e.g. < 1 month)
Headache
Jaw claudication
Vision (amaurosis fugax can occur)
Tender, palpable temporal artery

126
Q

2 investigations in temporal arteritis

A

Raised inflammatory markers (ESR and CRP)
Temporal artery biopsy (skip lesions)

127
Q

1st line Treatment temporal arteritis

A

urgent high dose steroids should be given as soon as the diagnosis is suspected and before the temporal artery biopsy
- no visual loss = high-dose prednisolone
- evolving visual loss = IV methylprednisolone given first then prednisolone

give bone protection with bisphosphonates as treatment requires long course of steroids

128
Q

Causative organism of the gastroenteritis that precedes guillain-barre syndrome

A

Campylobacter jejuni

129
Q

Characteristic features of Guillain-barre syndrome

A

Progressive, symmetrical weakness of all the limbs
Classically ascending i.e. the legs are affected first
Very few + mild sensory signs

130
Q

Guillain-Barre 1st line treatment

A

IV immunoglobulins

2nd line: plasma exchange

131
Q

Investigation guillain-barre

A

Nerve conduction studies
Lumbar puncture (raised protein, normal WCC, normal glucose)

132
Q

Convergent squint

A

commonest form of childhood squint

hypermetropia (long sightedness) causes the image to focus behind the retina when the eye is at rest
excessive accommodation brings the image into focus but causes squint

133
Q

Cluster headache features

A

Intense sharp, stabbing pain around one eye:
- once or twice a day / 15 mins - 2 hours
- typically lasts 4 - 12 weeks
- redness, lacrimation, lid swelling
- ptosis, miosis

134
Q

Common trigger for cluster headaches

135
Q

Investigation of choice cluster headache

A

MRI with contrast

underlying brain lesions are sometimes found

136
Q

Acute management of cluster headache

A

100% oxygen + subcutaneous triptan

triptans are C/I in CAD

137
Q

Prophylaxis management of cluster headache

138
Q

Antibodies found in myasthenia gravis

A

Anti-acetylcholine receptor (positive in 85-90%)

139
Q

2 associations myasthenia gravis

A

Thymomas
Autoimmune disorders

140
Q

Key symptoms of myasthenia gravis

A

Fatiguability
Ptosis
Diplopia
Facial weakness

141
Q

Investigations myasthenia gravis

A

Single fibre electromyography
CT thorax (thymoma)
Antibodies to Ach-receptors
CK = normal

142
Q

1st line drug myasthenia gravis

A

Pyridostigmine (long acting acetylcholinesterase inhibitor)

143
Q

3 components of GCS

A

Motor response e.g. 2 = extending to pain, 6 = obeys commands
Verbal response e.g. 3 = words, 5 = orientated
Eye opening e.g. 2 = to pain, 4 = spontaneous

144
Q

Uhthoff’s phenomenon

A

Small increases in body temperature can temporarily worsen current or pre-existing symptoms of MS e.g. reduced visual acuity after exercise

145
Q

Most common presentation of MS

A

Optic neuritis

demyelination of the optic nerve = unilateral reduced vision

146
Q

4 features of optic neuritis

A
  1. Central scotoma (enlarged central blind spot)
  2. pain with eye movement
  3. Impaired colour vision
  4. Relative afferent pupillary defect (affected eye pupil constricts more when shining a light in the contralateral eye than when shining light in the affected eye)
  5. Typically resolves in days or weeks
  6. Phosphenes (images of light or colour whilst eye closed)
  7. Optic disc swelling
  8. Unilateral presentation
147
Q

Treatment optic neuritis

A

High dose steroids

148
Q

4 examples of focal weakness in MS

A

Incontinence
Horner syndrome
Facial nerve palsy
Limb paralysis

149
Q

4 examples of focal sensory symptoms in MS

A

Trigeminal neuralgia
Numbness
Paraesthesia (pins and needles)
Lhermitte’s sign

150
Q

MS: Clinically isolated syndrome

A

First episode of demyelination and neurological signs/symptoms

Patients with CIS may never have another episode or may go on to develop MS - lesions on MRI scan have poorer prognosis for MS diagnosis

151
Q

Most common pattern of MS when first diagnosed

A

Relapsing-remitting

152
Q

Secondary progressive MS

A

Relapsing-remitting disease that turns into a progressively worsening disease (symptoms with incomplete remissions)

153
Q

Primary progressive MS

A

Worsening disease and neurological symptoms from point of diagnosis without relapses and remissions

154
Q

Investigations that support a clinical diagnosis of MS

A

MRI brain + spinal with contrast - high signal T2 lesions, periventricular plaques

Lumbar puncture - oligoclonal bands in CSF

155
Q

Management of acute relapse in MS

A

High dose steroids (e.g. oral or IV methylprednisolone)

156
Q

1st line DMARD for MS

A

Natalizumab

157
Q

Management of specific problems in MS:
1. Fatigue
2. Spasticity
3. Bladder dysfunction
4. Oscillopsia (visual fields appear to oscillate)

A
  1. Exclude anaemia, thyroid, depression then offer trial of amantadine
  2. Baclofen and Gabapentin
  3. KUB ultrasound to assess bladder emptying, significant residual volume = intermittent self catheterisation, if no significant residual volume = anticholinergics
  4. Gabapentin
158
Q

Common non-specific early feature of MS

A

Lethargy (75%)

159
Q

Risk factors subarachnoid haemorrhage

A

Smoking
Cocaine use
Excess alcohol intake
Ehlers Danos syndrome
Polycystic kidney disease
Coarctation of the aorta

160
Q

What can be given in cauda equina syndrome before surgery to reduce malignant compression

A

High dose dexamethasone (reduces oedema around the tumour site)

161
Q

Most common cause of cauda equina syndrome

A

Central disc prolapse (typically L4/L5 or L5/S1)

162
Q

Features of cauda equina syndrome

A

Low pack pain
Bilateral sciatica
Reduced sensation in perianal area
Decreased anal tone
Urinary dysfunction (incontinence is a late sign)

163
Q

Investigation cauda equina syndrome

A

Urgent MRI

164
Q

Management cauda equina syndrome

A

Surgical decompression

165
Q

1st line investigation in suspicion of pituitary tumour

A

CT head - quick and easily available, to then triage patient

166
Q

Most common cause of vertigo

A

Benign paroxysmal positional vertigo

167
Q

Average age of onset BPPV

168
Q

BPPV features

A

Vertigo triggered by change in head position
May be associated w nausea
Lasts 10-20 seconds
Positive Dix-Hallpike manoeuvre (pathgnomonic) i.e. rotatory nystagmus

169
Q

Vestibular neuronitis

A

Inflammation of the vestibular portion of CN8
Causes vertigo
Often develops following a viral infection

170
Q

Features of vestibular neuronitis

A

Recurrent vertigo attacks lasting hours or days
Nausea and vomiting
Horizontal nystagmus
No hearing loss or tinnitus

171
Q

key differential diagnosis in vertigo

A

Posterior circulation stroke

172
Q

Labyrinthitis vs vestibular neuritis

A

Labyrinthitis = hearing impairment

173
Q

4 A’s of alzheimer’s presentation

A

Amnesia
Aphasia
Agnosia (naming an object)
Apraxia

174
Q

What causes brown-sequard syndrome

A

Lateral hemisection of the spinal cord

175
Q

3 features of brown-sequard syndrome

A
  1. Ipsilateral weakness below lesion
  2. Ipsilateral loss of proprioception and vibration sensation
  3. Contralateral loss of pain and temperature sensation
176
Q

what movement worsens a benign essential tremor

A

Arms outstretched (postural tremor)

177
Q

Management of benign essential tremor

A

1st line: propranolol

If C/I: reassure + explain treatment isn’t possible

178
Q

3 other features outside of the core features of PD

A
  • Handwriting gets smaller and smaller (micrographia)
  • Reduced facial movements and expressions (hypomimia)
  • Soft speech (hypophonia)
179
Q

4 causes of brain abscess

A

Sepsis form middle ear
Trauma or surgery to the scalp
Penetrating head injuries
Embolic events from endocarditis

180
Q

features of raised intracranial pressure

A

Headache (dull, persistent)
Vomiting
Focal neurology (CN III/CN VI)
Nausea, papilloedema on fundoscopy, seizures
Cushing’s triad (wide pulse pressure, bradycardia, irregular breathing)

181
Q

Brain abscess investigations

182
Q

Brain abscess management

A

Craniotomy
IV antibiotics (IV 3rd gen cephalosporin + metronidazole)
ICP management e.g. dexamethasone

183
Q

Causative organism of 95% of cases of encephalitis in adults

184
Q

Features of encephalitis

A

first features: fever + lethargy
headache
psychiatric symptoms (typically temporal and inferior frontal lobes affected e.g. irritability or focal seizures)
vomiting
Focal features e.g. aphasia

peripheral lesions have no relation to the presence of HSV encephalitis

185
Q

Investigations encephalitis

A

Lumbar puncture/CSF: lymphocytosis, elevated protein, PCR for HSV, VZV and enteroviruses

Neuroimaging (MRI)
EEG

186
Q

Management encephalitis

A

IV aciclovir in all cases of suspected encephalitis

187
Q

Shingles pathophysiology

A

Following primary infection with varicella-zoster virus (VZV/chickenpox), the virus lies dormant in the dorsal root or cranial nerve ganglia

Herpes zoster infection/shingles is caused by reactivation of the varicella-zoster virus (VZV)

188
Q

Shingles risk factors

A

Increasing age
HIV (x 15)
Other immunosuppressive conditions (steroids, chemo)

189
Q

Features of shingles

A

Prodromal period: burning pain over affected dermatome for 2-3 days

Rash: painful erythematous, macular rash over affected dermatome, quickly becomes vesicular, UNILATERAL

190
Q

When is shingles no longer infectious

A

When the vesicles have crusted over (usually 5-7 days following onset)

191
Q

Management of shingles

A

Antivirals within 72 hours (unless <50 with mild symptoms) e.g. aciclovir
reduces incidence of post-herpetic neuralgia

Analgesia:
1st line: paracetamol and NSAIDs
2nd line: neuropathic agents e.g. amitriptyline
3rd line: oral corticosteroids (in first 2 weeks only in immunocompetent adults)

192
Q

Complications of shingles

A

Post-herpetic neuralgia (most common)
Herpes zoster opthlamicus (trigeminal nerve)
Herpes zoster oticus (Ramsay Hunt syndrome): ear lesions + facial paralysis

193
Q

Most common form of brain tumour

A

Metastatic brain cancer often multiple and not treatable with surgical intervention

194
Q

Tumours that most commonly spread to the brain

A

Lung (most common)
Breast
Bowel
Skin (melanoma)
Kidney

195
Q

What kind of spread to metastases spread to the brain

A

Haematogenous spread

196
Q

Most common primary tumour in adults

A

Glioblastoma

197
Q

Presentation of vestibular schwannoma (acoustic neuroma)

A

Vertigo (CN VIII)
Unilateral sensorineural hearing loss (CN VIII)
Unilateral tinnitus (CN VIII)
Absent corneal reflex (CN V)
Facial nerve palsy (CN VII)

198
Q

Condition most commonly associated with bilateral vestibular schwannomas

A

Neurofibromatosis type 2

199
Q

Vestibular schwannoma investigation of choice

A

MRI of the cerebellopontine angle

200
Q

4 endocrinology pathologies caused by pituitary tumours

A

Acromegaly (GH)
Hyperprolactinaemia (prolactin)
Cushing’s (ACTH and cortisol)
Thyrotoxicosis (TSH and thyroid hormone)

201
Q

Symptoms of cerebellar disease

A

DANISH

Dysdiadochokinesia
Ataxia
Nystagmus
Intention tremor
Slurred speech
Hypotonia

Unilateral lesions cause ipsilateral signs

202
Q

Causes of cerebellar disease

A

PASTRIES
Paraneoplastic (e.g. secondary to lung cancer)
Alcohol
Stroke,
Trauma
Rarer causes
Inherited
Epilepsy treatment (phenytoin)
Multiple Sclerosis

203
Q

4 risk factors for hypoxic-ischaemic encephalopathy (Intra partum asphyxia)

A

Prolapsed cord
Placental abruption
Trauma
Cephalopelvic disproportion

204
Q

Who is Bell’s palsy most common in

A

Pregnant women

205
Q

2 treatments for Bell’s palsy

A
  1. Oral prednisolone within 72 hours of onset
  2. Eye care (drops, lubricants) to prevent exposure keratopathy

Antivirals may be of small benefit

206
Q

When should someone with Bell’s palsy be referred to ENT

A

No sign of paralysis improvement after 3 weeks

207
Q

Causes of most Extradural haematoma

A

Low impact trauma (blow to head/fall) to the temporal region

208
Q

Vessel affected in Extradural haematoma

A

Middle meningeal artery

209
Q

Classical presentation Extradural haematoma

A

Patient who initially loses, briefly regains and then loses again consciousness after a low impact head injury

Fixed and dilated pupil (temporal lobe herniates and the parasympathetic fibres of CNIII are compressed)

regain in consciousness = lucid interval

210
Q

Imaging signs Extradural haematoma

A

Biconvex (lentiform) hyperdense collection around the surface of the brain
Limited by the suture lines of the skill

211
Q

Definitive treatment Extradural haematoma

A

Craniotomy and evacuation of the haematoma

212
Q

Most common cause of spontaneous SAH

A

Intracranial aneurysm (saccular ‘berry’ aneurysm) - 85%

213
Q

Presentation subarachnoid haemorrhage

A

Headache: Occipital, worst ever, sudden-onset, thunderclap
Meningism (photophobia, neck stiffness)
Nausea and vomiting
ECG changes inc ST elevation
Star shaped lesion on CT

214
Q

Management if subarachnoid haemorrhage is suspected but a CT head is done within 6 hours of symptom onset and is normal

A

Do not do a lumbar puncture, consider alternative diagnosis

215
Q

Management if subarachnoid haemorrhage is suspected but a CT head is done more than 6 hours of symptom onset and is normal

A

Lumbar puncture (at least 12 hours following onset to allow xanthochromia)
- Other findings include normal or raised opening pressure

216
Q

How is vasospasm prevented in subarachnoid haemorrhage

A

Nimodipine

217
Q

Definitive treatment subarachnoid haemorrhage

A

Most patients will have a coil (interventional neuroradiology) but some may require craniotomy and clipping (neurosurgery)

218
Q

4 complications of aneurysmal SAH

A

Re-bleeding (Ix: repeat CT)
Hydrocephalus (Mx: external ventricular drain)
Vasospasm
Hyponatraemia (caused by SIADH)

219
Q

Predictive factors in SAH

A

Conscious level on admission
Age
Amount of blood visible on CT head

220
Q

Definition of acute, subacute and chronic subdural haematoma

A

Acute = within 48 hours of injury (rapid neurological deterioration)
Subacute = days to weeks post-injury
Chronic = weeks to months (patients may not recall a specific head injury, common in elderly)

221
Q

4 neurological symptoms subdural haematoma

A

Altered mental status
Focal neurological deficits e.g. nystagmus
Headache
Seizures

222
Q

4 physical examination findings subdural haematoma

A

Papilloedema
Pupil changes (unilateral dilated pupil - compression of CNIII)
Gait abnormalities (ataxia or weakness)
Hemiparesis or hemiplegia

223
Q

Behavioural and cognitive changes in subdural haematoma

A

Memory loss
Personality changes
Cognitive impairment

224
Q

Who is most at risk of subdural haematomas

A

Elderly and alcoholic patients - brain atrophy with fragile or taut bridging veins

225
Q

CT imaging acute vs chronic subdural haematoma

A

Both will be crescent in in shape, not restricted by suture lines and compress the brain ‘mass effect’

Acute = hyperdense/bright (fresh blood)
Chronic = hypodense/dark (old blood)

226
Q

Most likely operation for symptomatic chronic subdural bleeds

A

Burr hole evacuation

227
Q

Neurofibromatosis inheritance pattern

A

Autosomal dominant

228
Q

Ménière’s disease

A

Disorder of the inner ear of unknown cause
Characterised by excessive pressure and progressive dilation of the endolymphatic system

Common in middle-aged adults

229
Q

Features of Ménière’s disease

A

Recurrent episodes of vertigo, tinnitus and sensorineural hearing loss
Aural fullness/pressure
Nystagmus
Positive Romberg test
Lasts minutes to hours
Typically unilateral

230
Q

Management Ménière’s disease (4)

A

ENT assessment
Inform DVLA
Buccal or IM prochlorperazine for acute attacks (same as vestibular neuritis)
Betahistine and vestibular rehabilitation for prophylaxis

231
Q

Chronic fatigue syndrome diagnostic definition

A

At least 3 months of disabling fatigue affecting mental and physical function more than 50% of the time in the absence of other disease which may explain symptoms

232
Q

Screening tests for chronic fatigue (name 4)

A

FBC, U&E, LFT, glucose, TFT, ESR, CRP, calcium, CK, ferritin, coeliac screening, urinalysis

233
Q

Advice regarding physical activity and exercise in a patient with chronic fatigue syndrome

A

do not advise people with ME/CFS to undertake exercise that is not part of a programme overseen by an ME/CFS specialist team

should only be recommended if patients ‘feel ready to progress their physical activity beyond their current activities of daily living’

234
Q

Features of narcolepsy

A

Typical onset = teenage years
Hypersomnolence (excessive sleep)
Cataplexy (sudden loss of muscle tone triggered by emotion)
Sleep paralysis
Vivid hallucinations going to sleep or waking up

235
Q

Investigations narcolepsy

A

Multiple sleep latency EEG

236
Q

Management narcolepsy

A

Daytime stimulants e.g. modafinil
Nighttime sodium oxybate

237
Q

Peripheral neuropathies which cause predominantly sensory loss

A

Diabetes
Leprosy
Alcoholism
Vitamin B12 deficiency

238
Q

Radiculopathy definition

A

Conduction block in the axons of a spinal nerve or its roots with motor and sensory affects, most commonly due nerve compression

239
Q

5 causes of Radiculopathy

A

Intervertebral disc prolapse
Degenerative diseases of the spine
Fracture
Malignancy (commonly metastatic)
Infection

240
Q

Damage to ulnar nerve presentation

A

‘Claw hand’
Wasting and paralysis of intrinsic hand muscles and hypothenar muscles
Sensory loss to the medial 1 1/2 fingers

241
Q

2 presentations of radial nerve damage

A

Wrist drop
Sensory loss to small area between dorsal aspect of the 1st and 2nd metacarpals

242
Q

Which nerve is affected in carpal tunnel syndrome

A

Median nerve

243
Q

Presentation carpal tunnel syndrome

A
  1. Pain/pins and needles in thumb, index, middle finger
  2. Patient classically has to shake hand at night to obtain relief
244
Q

Examination findings in carpal tunnel syndrome (4)

A
  1. Weakness of thumb abduction
  2. Wasting of thenar eminence
  3. Tinel’s sign (tapping causes paraesthesia)
  4. Phalen’s sign (flexion of wrist causes symptoms)
245
Q

4 causes of carpal tunnel syndrome

A

Idiopathic
Pregnancy
Oedema e.g. HF
Rheumatoid arthritis

246
Q

Electrophysiology findings carpal tunnel syndrome

A

Motor and sensory axon action potential prolongation

247
Q

Treatment mild-moderate carpal tunnel syndrome

A

6 week trial:
Wrist splints at night (particularly helpful in transient conditions such as pregnancy)
Corticosteroid injection

Severe/no improvement: surgical decompression

248
Q

4 features of anterior cord syndrome

A

Bilateral weakness
Bilateral loss of pain and temperature
Autonomic dysfunction (abnormal BP)
Bladder dysfunction

249
Q

2 causes of anterior cord syndrome

A

Vascular/ischaemia (thromboembolism, aortic disease, hypotension)

Pathology to spinal cord (tumour, trauma, disc hernia)

250
Q

3 visual symptoms in posterior cerebral artery stroke

A

Diplopia
Contralateral homonymous hemianopia with macular sparing
Visual agnosia

251
Q

Posterior inferior cerebellar artery stroke

A

Loss of temperature and pain sensation to the ipsilateral face and Contralateral trunk and limbs
Slurring of speech and ataxic gait

252
Q

Hoover’s sign

A

When examining a patient lying down, you place your hand under one leg and ask them to raise the contralateral leg and test whether you feel pressure against your hand

Tests for functional weakness

253
Q

Idiopathic intracranial hypertension classic patient

A

Young, overweight female

254
Q

Management of idiopathic intracranial hypertension

A

Carbonic anhydride inhibitors e.g. acetazolamide and topiramate (also helpful for weight loss)

Repeated lumbar puncture (temporary measure)

Optic nerve sheath decompression and fenestration may be needed to prevent optic nerve damage

Lumboperitoneal or ventriculoperitoneal shunt

255
Q

Tension headache features

A

Bilateral
‘Tight band’ around the head
May be related to stress

256
Q

Chronic tension headache definition

A

15 or more days per month

257
Q

Management of tension headache

A

Acute: aspirin, paracetamol or NSAID

Prophylaxis: up to 10 sessions of acupuncture over 5-8 weeks

258
Q

cerebellar hemisphere vs cerebellar vermis lesions

A

Hemisphere = peripheral (finger-nose ataxia)
Vermis = gait ataxia

259
Q

Diet used for children with epilepsy unresponsive to treatment

A

Ketogenic diet

260
Q

Medication overuse headache

A

present for 15 days or more per month
developed or worsened whilst taking regular symptomatic medication
patients using opioids and triptans are at most risk
may be psychiatric co-morbidity

261
Q

Mydriasis vs miosis

A

Dilated pupil vs constricted pupil

262
Q

Visual field defect pathway

A

Superior = temporal
Inferior = parietal
Bitemporal hemianopia = pituitary
Macular sparing = posterior

263
Q

Anti-epileptics in pregnancy

A

Lamotrigine: safe
Sodium valproate: neural tube defects
Carbamazepine: relatively safe
Phenytoin: associated with cleft palate

264
Q

Benign Rolandic epilepsy

A

4-12 years
Occur at night
Focal seizures (e.g. paraesthesia affecting the face)
Child is otherwise well
EEG: centrotemporal spikes

265
Q

Ataxic gait

A

Wide-based gait with loss of heel to toe walking

266
Q

Post-lumbar puncture headache

A

Usually develops within 24-48 hours following LP
Worsens with upright position

Treatment: blood patch, epidural saline fluids and IV caffeine

267
Q

Associated drugs with idiopathic intracranial hypertension

A

COC
Steroids
Tetracyclines
Retinoids
Lithium

268
Q

Headache red flags

A

History of malignancy + < 20
Thunderclap
New onset cognitive dysfunction
Impaired consciousness
Triggered by cough, valsalva, sneeze, exercise
Orthostatic

269
Q

Dorsal columns

A

Proprioception
Vibration sense
Tactile discrimination

270
Q

Corticospinal tracts

A

Muscle weakness
Hyperreflexia
Spasticity and persistent weakness if not treated
Babinski sign

271
Q

Spinothalamic tracts

A

Loss of pain and temperature sensation

272
Q

Oxford stroke classification 3 criteria

A
  1. Unilateral hemiparesis and/or hemisensory loss of the face, arm and leg
  2. Homonymous hemianopia
  3. Higher cognitive dysfunction e.g. dysphasia
273
Q

Total vs partial anterior circulation infarcts

A

Total:
Middle and anterior cerebral arteries
All 3 of the Oxford criteria

Partial:
Smaller arteries of anterior circ e.g. upper or lower division of MCA
2 of the Oxford criteria

274
Q

Lacunar infarcts presentation

A

Presents with 1 of the following:
1. Unilateral weakness of face, arm, leg or all three
2. Pure sensory stroke
3. Ataxic hemiparesis

275
Q

Chemoreceptor trigger zone

A

Medulla oblongata

276
Q

2 contraindications lumbar puncture

A

Any signs of raised ICP
Meningococcal septicaemia

277
Q

Management of medication overuse headache

A

Simple analgesics and triptans can be withdrawn abruptly
Opioid analgesics should be gradually withdrawn

278
Q

Key symptom of posterior communicating artery aneurysm

A

Painful third nerve palsy

279
Q

Epilepsy and the DVLA

A

All patients must not drive and must inform the DVLA
1st seizure: 6 months
Established epilepsy: can drive if seizure-free for 12 months
Withdrawal of epilepsy medication: 6 months after last dose

280
Q

Treatment for cerebral oedema in patients with brain tumours

A

Dexamethasone

281
Q

Key feature of basilar artery stroke

A

Locked-in syndrome

282
Q

Features of Weber’s syndrome (posterior cerebral artery that supply the midbrain)

A

Ipsilateral CNIII palsy
Contralateral weakness of upper and lower extremity

283
Q

Most common complication of meningitis

A

Sensorineural hearing loss

284
Q

Creutzfeldt-Jakob disease

A

Degenerative brain disorder caused by infectious prion proteins

Key features: rapidly progressive dementia and myoclonus

MRI: hyperintense signals in the basal ganglia and thalamus

285
Q

Atonic seizure

A

Sudden loss of muscle tone
Last 15 seconds or less
After effects of confusion

286
Q

Focal impaired awareness seizures

A

Emotional disturbance
Automatism e.g. lip smacking
Disturbance of consciousness/awareness
Post-ictal state/tiredness

287
Q

3rd nerve palsy vs Horner’s

A

3rd nerve: ptosis + dilated pupil/mydriasis
Horner’s: ptosis + constricted pupil/miosis

288
Q

Mechanism of action of ondansetron

A

Anti-emetic: 5-HT3 receptor antagonist in chemoreceptor trigger zone in medulla oblongata

289
Q

syncope vs epilepsy

A

Short ictal period
Stressful event participating the syncope e.g. phobia or upcoming interview
Can be associated with mild twitching or jerking

290
Q

Management options for raised intracranial pressure

A

Head elevation to 30 degrees
IV mannitol (osmotic diuretic)
Controlled hyperventilation
Removal of CSF (drain, repeated LP e.g. IIH)

3a PTS - PM - ZTF (8 decks)

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