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Phase 3A > Neurology > Flashcards

Neurology Flashcards

1
Q

what is syncope

A

an abrupt and transient loss of consciousness associated with loss of postural tone that follows a sudden fall in cerebral perfusion.

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2
Q

types of syncope

A

neurogenic, orthostatic (autonomic: drugs, autonomic failure), cardiac (arrythmias, valvular heart disease)

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3
Q

what is neurogenic syncope

A

inappropriate activitation of cardio-inhibitory and vasodepressor reflex leading to hypotension

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4
Q

types of neurogenic syncope

A 
Vasovagal syncope
Reflex syncope with specific precipitants
- Micturition syncope
- Cough syncope
Carotid sinus hypersensitivity
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5
Q

what is epilepsy

A

Tendency to have recurrent seizures

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6
Q

what is a seizure

A

Clinical manifestation of disordered electrical activity in the brain (paroxysmal discharge of cerebral neurones)

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7
Q

syncope triggers

A

Stress/fear, prolonged standing, heat, venepuncuture,

cough, micturition

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8
Q

seizure trigger

A

Sleep deprivation, flashing lights, menstruation,

alcohol and alcohol withdrawal

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9
Q

syncope prodrome

A 
Hot, visual crowding and loss, feel faint, can
feel dizzy (looks pale)
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10
Q

seizure prodromes

A

Aura gustatory, auditory,

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11
Q

features of syncope

A 
quick onset 
short duration
rare/brief convulsions
pale 
no incontinence/ tongue biting unless full bladder
quick recovery
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12
Q

features of seizure

A 
may have aura 
2 - 3 minutes duration 
convulsions 
- GTC, myotonic jerks, focal motor fits 
incontinence/tongue biting

recovery: confusion, headache, not recognise family/friends, needs rest

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13
Q

feature of non epileptic attack

A

can last for 30 minutes
convulsions: wild shaking, wax and wane, pelvic thrusting, closed eyes

recovery: atypically quick for prolonged seizure time

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14
Q

PMH syncope

A

Previous faints

Cardiac causes include bradycardias (heart block), tachycardias (eg VT) and obstructive lesions eg aortic stenosis.

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15
Q

PMH seizure

A

Perinatal illnesses, education achievements, previous serious head injury/neurosurgery, neonatal seizures (prolonged), meningitis. If late onset (age >40) think stroke or tumours

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16
Q

NEAD PMH

A

previous Hx of unexplained medical symptoms

hx childhood abuse

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17
Q

investigations for blackout

A 
heart exam: aortic stenosis
ECG
blood tests (FBC)
brain imaging 
EEG

syncope: 24hr tape, tilt table, autonomic function tests

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18
Q

types of EEG in seizure investigation

A 
inter-ictal
provocation (hyperventilation, photosensitivity)
sleep deprive EEG
prolonged EEG
video telemetry
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19
Q

when is imaging used in seizures

A

focal onset
new onset + >25
MRI 1st line

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20
Q

pathophysiology of seizures

A

During a seizure there is a prolonged depolarisation of a group of neurones, which spreads to adjacent or connected neurones

There is a failure of inhibitory (GABA) neurotransmission

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21
Q

class of seizure

A

focal
simple partial
complex partial, secondary generalised tonic clonic

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22
Q

types of generalised seizures

A

idiopathic generalised
myoclonic jerks
absence
primary generalised tonic clonic

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23
Q

pathophysiology of NEA

A

often a manifestation of stress, may be associated with childhood abuse; other medically unexplained symptoms

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24
Q

types of focal seizures and their aetiology

A

simple partial seizure (remains conscious)

  • strange sensations (aura)
  • jerking movements
  • Jacksonian march

complex partial seizure (impaired consciousness)

secondary generalised tonic clonic seizures

usually have a structural cause

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25
Q

types of general seizures

A

tonic: fall backwards
atonic: fall forwards
clonic: convulsions
tonic-clonic
myoclonic: muscle twitches
absence seizure: associated with 3/s spike + wave o EEG

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26
Q

cardiac syncope aetiology

A

Conditions that predispose to transient tachyarrhythmias

Bradyarhythmias

Cardiac ischaemia

Structural heart disease

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27
Q

ECG signs of cardiac syncope

A

long QT interval
Wollf-Parkinson-White syndrome: short PR interval, delta wave
Brugada Syndrome
arrythmogenic right ventricular dysplasia
Heart block

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28
Q

other causes of transient loss of consciousness

A

hypoglycaemia

acute hydrocephalus

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29
Q

investigations for transient loss of consciousness

A 
ECG
CT acute assessment of seizures 
MRI epilepsy 
EEG
record an event
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30
Q

Management of epilepsy

A

anticonvulsant medication

Blood monitoring

<1y reviews

vagus nerve stimulation/deep brain stimulation

inform DVLA

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31
Q

anticonvulsants used for generalised seizures

A

1st line sodium valproate

2nd line lamotrigine (if pregnant)

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32
Q

anticonvulsants for focal seizures

A

carbamazepine or lamotrigine

2nd line: sodium valproate

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33
Q

classification of tension headache

A

episodic: <15/month
chronic: more than 15 days each month; likely to be medication induced or associated with depression

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34
Q

presentation of tension headache

A

generalised headache
pressure or tightness
may radiate to neck

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35
Q

differential diagnosis for headache

A 
migraine
giant cell arteritis (temporal arteritis)
trigeminal neuralgia 
cluster headache 
subarachnoid haemorrhage 
encephalitis 
space occupying lesion
cervical spondylosis 
sinusitis 
idiopathic intracranial hypertension
carbon monoxide poisoning
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36
Q

management of tension headache

A

reassurance, manage any underlying stress/depression, physiotherapy

simple analgesics:

  1. ibuprofen
  2. other NSAIDs e.g. naproxen as a rescue course

tricyclic antidepressants: amitryptiline

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37
Q

side effects of tricyclic antidepressants

A

can’t see, can’t pee, can’t spit, can’t shit

  • blurry vision
  • problems passing urine
  • DRY MOUTH
  • constipation
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38
Q

classifications of migraine

A

migraine without aura
migraine with aura
hemiplegic migraine
chronic migraine

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39
Q

epidemiology of migraine

A

6% of men

18% of women

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40
Q

presentation of migraine

A

lasts between 4 and 72 hours

2 of:
unilateral
pulsating 
moderate-severe pain
aggravated by routine activity

+ at least one of:
nausea/vomiting
photophobia/ phonophobia

aura: visual or sensory disturbance
premonitory phase
tiredness, irritability, depression and problems concentration

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41
Q

examinations in headache

A

optic fundi
blood pressure
head and neck
head circumference in children

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42
Q

red flag symptoms in headache requiring urgent investigation

A

papilloedema
new seizure
significant PMH (cancer esp. lung and breast, neurofibromatosis, immunodeficiency)
other neurological signs: confusion/LOC

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43
Q

complications of migraine

A

associated with ischaemic or haemorrhagic stroke

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44
Q

management of migraine

A
  1. simple analgesics+/- antiemetics (aspirin, ibuprofen, prochlorperazine)
  2. rectal analgesia/ rectal anti-emetic
  3. triptans (5HT1-receptor agonists) e.g. sumatriptan, naratriptan
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45
Q

contraindication to triptans

A

uncontrolled hypertension

coronary heart disease or cerebrovascular disease

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46
Q

epidemiology of cluster headaches

A

1 in 1000

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47
Q

difference between episodic and chronic cluster headaches

A

episodic CH have pain free periods lasting a month or longer/ year

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48
Q

features of cluster headaches

A

occur in bouts; typically at night

intense pain which comes suddenly and reaches full intensity in ~10 minutes

usually centered behind/around the eye, temple or forehead

unilateral

typically lasts 45-90minutes

causes restlessness, associated features: ipsilateral lacrimation, rhinorrhoea, swelling, sweating, partial Horner’s, oedema

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49
Q

triggers for cluster headaches

A

alcohol
histamine
heat, excercise, solvents
disruption to sleep patterns

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50
Q

management of cluster headaches

A

general: abstain from alcohol, stop smoking, good sleep hygiene

acute attack: subcutaneous sumatriptan, oxygen

prophylaxis: verapamil (ECG monitoring), prednisolone
surgery: trigeminal nerve blockade

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51
Q

what is giant cell arteritis

A

systemic immune-mediated vasculitis affecting medium-sized and large-sized arteries, particularly the carotid artery and its extracranial branches

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52
Q

epidemiology of giant cell arteritis

A

M:F 2/3:1
0.2% of population
peak incidence is in 60-80years

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53
Q

risk factors for GCA

A

personal or family history of polymyalgia rheumatica
european descent
over 60

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54
Q

presentation of GCA

A

temporal headache
scalp tenderness
jaw claudication
visual disturbances: blurred vision, diplopia, amaurosis fugax, visual loss

systemic symptoms: anorexia, weight loss, fatigue, malaise etc.

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55
Q

signs of GCA

A

fundoscopic evidence of ischaemic disease

temporary artery tenderness on palpation, decreased pulsation

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56
Q

investigations in GCA

A

ESR/CRP
FBC: anaemia, thrombocytosis
LFTs may be elevated
temporal artery biopsy

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57
Q

management of GCA

A

high dose prednisolone or IV methylprednisolone if there are visual symptoms

low dose aspirin + PPI (+ osteoporosis prophylaxis)

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58
Q

complications of GCA

A

loss of vision
aneurysms
CNS disease e.g. seizures + cerebral vascular accidents
steroid related complications

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59
Q

what are steroid related complications

A 
osteoporosis 
corticosteroid myopathy 
bruising 
insomnia/restlessness/hypomania
hypertension 
diabetes
fluid retention
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60
Q

risk factors for stroke/TIA

A 
hypertension
smoking 
diabetes mellitus 
heart disease e.g. AF
peripheral arterial disease 
polycythaemia 
carotid artery occlusion 
combined oral contraceptive pill 
excessive alcohol 
clotting disorders
hyperlipidaemia
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61
Q

aetiology of TIA

A

emboli usually from carotid bifurcation

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62
Q

examinations and investigations in TIA

A

neurological exams
(attentiveness and verbal fluency)
BP in both arms, listen for carotid bruits, check peripheral pulses

Bloods: FBC, ESR, U+E, fasting lipids and glucose, LFTs, TSH, coagulation studies
ECG: AF, MI or myocardial ischaemia
CT imaging
Carotid imaging

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63
Q

management of TIA

A

lifestyle advice

clopidogrel: 300mg loading dose; 75mg daily

statin therapy: atorvastatin

BP lowering therapy: thiazide like diuretic, calcium channel blocker or ACE inhibitor

carotid endarterectomy

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64
Q

DVLA management for TIA

A

1st TIA: do not drive for 1 month

2nd TIA in short period: 3 months free from attacks + inform DVLA

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65
Q

features that influence risk of stroke after TIA

A 
ABCD2 score 
age > 60 
high blood pressure 
clinical features of weakness
duration of symptoms > 60 minutes 
diabetes
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66
Q

what is a stroke

A

clinical syndrome caused by disruption of blood supply to the brain, characterised by rapidly developing signs of focal or global disturbance of cerebral functions, lasting for more than 24 hours or leading to death

67
Q

types of strokes

A

infarction: 85%; 80% of these are anterior circulation
haemorrhagic: 10% primary; 5% SAH

68
Q

differential diagnosis for stroke

A

Todd’s paresis
TIA
hypoglycaemia

69
Q

screening tool for stroke

A

FAST

70
Q

Stroke presentation

A

cerebral hemisphere

  • contralateral hemiplegia/sensory loss
  • homonymous hemianopia
  • dysphagia

posterior circulation

  • motor deficits
  • ipsilateral cranial nerve dysfunction; contralateral motor/sensory tract dysfunction
  • ataxia, imbalance, vertigo, nausea/vomiting
  • diplopia
  • locked in syndrome: complete infarction of pons

lacunar infarcts
- basal ganglia, internal capsule, thalamus and pons

71
Q

stroke investigations

A

FBC - polycythaemia, thrombocytopenia

sickle cell disease test

ESR

hypo/hyperglycaemia, hyperlipidaemia

ECG

CT/Brain imaging
CT contrast angiography

72
Q

when should a CT be done

A

within 24 hours

immediately if:
on anticoagulants/bleeding tendency
GCS<13
unexplained progressive or fluctuating symptoms
papilloedema, neck stiffness or fever; severe headache

73
Q

acute stroke management

A

stabilise

anti-platelet therapy: aspirin once haemorrhagic stroke has been excluded

thrombolytic treatment within 4.5 hrs (alteplase)

thrombectomy (within 6 hours of symptom onset)

74
Q

what are requirements for alteplase and what are contraindications

A
  1. within 4.5 hr window
  2. haemorrhagic stroke has been excluded
  3. access to neuroimaging to monitor progress
contraindications
- seizure + stroke 
- stroke/head trauma in 3 months
-SAH symptoms 
- previous Intracranial haemorrhage 
-intracranial neoplasm or surgery 
arteriovenous malformatiom or anuerysm 
bleeding disorder/anticoagulation treatment
75
Q

characteristic features of parkinsons

A

bradykinesia
tremor at rest
rigidity

76
Q

pathogenesis of PD

A

degeneration of dopaminergic neurons in substantia nigra

77
Q

epidemiology and risk factors for PD

A

1-2% of over 60

RF: age, male, pesticide exposure

78
Q

other features of PD

A

shuffling gait, trouble turning, stoop

fixed facial expression + infrequent blinking

micrograthia

non-motor disturbance: sleep disorder, orthostatic hypotension, constipation and urinary disturbance, quiet voice

79
Q

complications of PD

A 
falls
bed sores
contractures
bowel and bladder disorders
poor nutrition 
depression
dementia
80
Q

specialists involved in PD management

A 
neurologist 
GP
PD specialist nurses
physiotherapists 
occupational therapists 
speech and language therapists 
psychologists/psychiatrists 
nutritionists
81
Q

management of PD

A

symptoms that don’t affect QoL/early disease: dopamine agonists, monoamine-oxidase-B inhibitors, amantadine or anticholinergics

symptoms that affect quality of life: levodopa

Deep brain stimulation

comorbidities

  • psychotherapy/support groups
  • TCA for sleep disturbance (nortriptyline)
  • SSRI for apathy (not used if using selegiline)
    dementia: cholinesterase inhibitor
82
Q

side effects of levodopa

A

nausea and dizziness; rare

83
Q

examples of dopamine agonists and their side effects

A

pramipexole, ropinirole

nausea/diziness
compulsive behaviours

84
Q

example of monoamine-oxidase-B inhibitors

A

rasagiline

selegiline

85
Q

what is dementia

A

Syndrome caused by various brain disorders leading to memory loss and decline in other aspects of cognition and leading to difficulties with ADL

86
Q

symptom categories in dementia

A

o Cognitive impairment: (short term) memory, language, attention, thinking, orientation, calculation and problem-solving difficulties
o Psychiatric and behavioural disturbances: changes in personality, emotional control, social behaviour; depression, agitation, hallucination and delusions
o Difficulties with ADL: e.g. driving, shopping, eating, dressing

symptoms should go back at least several months

87
Q

what is mild cognitive impairment

A

decline in cognitive function but does not affect ADL, often a pre-dementia state

88
Q

epidemiology of dementia

A

7% in over 65

89
Q

common causes of dementia

A 
o	Alzheimer’s disease 50%
o	Vascular dementia 25%
o	Dementia with Lewy bodies 15%
o	Frontotemporal dementia <5%
o	Mixed dementia
o	Parkinson’s disease (Preceded by Parkinson symptoms)

o Potentially treatable causes (substance misuse, hypothyroidism, space occupying intracranial lesion, syphilis, vitamin B12 deficiency, normal pressure hydrocephalus, folate deficiency, pellagra)
o Genetic causes e.g. familial autosomal dominant AD

90
Q

what needs to be done for a dementia diagnosis

A

comprehensive history + exam; collateral history

assess attention + concentration, orientation to time, place and person; short and long term memory; praxis; language function; executive function; psychiatric symptoms

exclude medicine related causes or reversible organic causes

cognitive impairment screen: mini mental state exam, montreal cognitive assessment test
6 item cognitive impairment test, GP assessment of cognition, 7 minute screen

91
Q

diagnostic criteria for dementia

A

Affects ADL
Represents decline from previous level of function
Cannot be explained by delirium or major psychiatric disorder
Established using history, collateral history and cognitive impairment assessment
Involve impairment in at least 2 of:
 Ability to acquire and remember new information
 Judgement, ability to reason or handle complex tasks
 Visuospatial ability
 Language functions
 Personality and behaviour

92
Q

investigtions in dementia

A

o Bloods (exclude other causes): FBC, ESR, CRP, U+E, LFT, glucose, TFT, B12 and folate
o MSU
o Consider blood cultures, CXR, MRI scans and psychometric testing
o CSF examination for rapidly progressing dementia e.g. Creutzfeldt-Jakob disease

93
Q

legal aspects of dementia management

A

o Advances statements or decisions, lasting power of attorney and preferred place of care plans early on if possible
o Obliged to inform DVLA

94
Q

non-pharmacological dementia management

A

cognitive stimulation programmes, multisensory stimulation, music therapy, art therapy, pet therapy, aromatherapy, dance therapy, massage, structured exercise programmes

95
Q

pharmacological dementia management

A

acetylcholinesterase-inhibitors for mild and moderate AD (donepezil, galantamine or rivastigmine)

NMDA antagonists: memantine

oral/IM benzodiazepines for severe agitation, risperidone for psychotic symptoms

96
Q

dementia prevention

A

reduce smoking, alcohol consumption, obesity and other cerebrovascular disease risk factors e.g. hypertension + hyperlipaemia

97
Q

dementia prevention

A

reduce smoking, alcohol consumption, obesity and other cerebrovascular disease risk factors e.g. hypertension + hyperlipaemia

98
Q

what is multiple sclerosis

A

cell mediated autoimmune conditions with repeated episodes of CNS inflammation and loss of the myelin sheath

99
Q

types of MS

A

relapsing-remitting: 80%
secondary progressive MS
primary progressive MS: 10 - 15%

100
Q

MS epidemiology

A

peak incidence: 40 - 50

101
Q

McDonald criteria for MS

A

disseminated in space and tine

102
Q

presentation of MS

A

visual problems or abnormal eye movements (e.g. optic neuritis + nystagmus)

facial weakness (e.g. Bell’s Palsy)

cognitive dysfunction

paraesthesia, numbness, sensory and balance problems

autonomic dysfunction: bladder, sexual

Lhermitte’s sign and Uhthoff’s phenomenon

103
Q

MS investigations

A

bloods: FBC, inflammatory markers, HIV, B12 etc
electrophysiology: e.g. visual evoked potential

MRI: periventricular lesions, plaques, white matter abnormalities

CSF: increased immunoglobulin + oligoclonal bands

104
Q

MS management

A

inform DVLA

relapse: methylprednisolone

maintenance: interferon beta
2nd line: natalizumab

105
Q

causes of foot drop

A

most common: L5 radiculopathy
anterior horn cell disorder (e.g. MND)
peroneal nerve palsy

106
Q

main tracts in the spinal cord

A

spinothalamic: crosses in spine
- anterior tract: crude touch
- lateral tract: pain + temperature

fasciculus gracilis + cuneatus: crosses in brainstem
pressure, vibration, fine touch + proprioreception

corticospinal tract: crosses in brain stem
voluntary muscle movements

107
Q

presentation of brown sequard syndrome

A

ipsilateral hemiplegia

ipsilateral loss of proprioreception, vibration, fine touch and pressure

contralateral loss of pain temperature and crude touch 1 or 2 levels below lesion

108
Q

Horner’s syndrome

A

miosis (constriction of pupil)
ptosis (drooping of upper eyelid)
anhidrosis (absence of sweating of face)

due to damage to sympathetic nerves of the face

109
Q

upper motor neuron signs and conditions

A

spastic paresis
increased tone
increased reflexes + babinski +

MND, Stroke, spinal cord section

110
Q

lower motor neuron signs and conditions

A

flaccid paresis
decreased tone
decreased reflexes
muscle wasting, fasciculations

MND, spinal cord injury, poliomyelitis, peripheral nerve dysfunction, myasthenia gravis

111
Q

causes of spinal cord compression

A 
trauma
tumour 
prolapsed intervertebral disc (L4/L5, L5/S1)
epidural or subdural haematoma
inflammatory disease 
infection
cervical spondylitic myelopathy
112
Q

spinal cord compression presentation

A

muscle weakness/ paralysis

sensory loss, Lhermitte’s sign

abnormal tendon reflexes

sphincter and autonomic disturbances

113
Q

spinal cord compression investigations

A

MRI

114
Q

Management of spinal cord compression

A

lie patient flat in neutral alignment

dexamethasone

symptomatic treatment

surgery/radiotherapy

115
Q

what is a dermatome

A

an area of skin supplied by a single spinal nerve

116
Q

cranial nerve 5 dermatomes

A

CN5: V1 – ophthalmic branch – top of the head
V2 – maxillary branch – nares to the top lip
V3 – mandibular branch – bottom lip to jaw

117
Q

C5 - T1 dermatomes

A 
C5 – lateral antecubital fossa
 C6 – thumb
 C7 – middle finger
 C8 – little finger
 T1 – medial antecubital fossa
118
Q

L1 - S1 dermatomes

A 
L2 – mid anterior thigh
 L3 – medial femoral condyle
 L4 – medial malleolus
 L5 – dorsum of 3rd metatarsal phalangeal joint
 S1 – lateral heel
119
Q

myotomes

A 
C4 – shoulder shrugs
C5 – shoulder abduction and external rotation; elbow flexion
C6 – wrist extension
C7 – elbow extension and wrist flexion
C8 – thumb extension and finger flexion
T1 – finger abduction
L2 – hip flexion
L3 – knee extension
L4 – ankle dorsiflexion
L5 – great toe extension
S1 – ankle plantarflexion
S4 – bladder and rectum motor supply
120
Q

causes of mononeuropathy

A 
mechanical 
entrapment 
diabetes
hypothyroidism
rheumatoid arthritis
vitamin deficiency 
vasculitis
121
Q

types of mononeuropathies

A 
carpal tunnel syndrome
ulnar neuropathy 
thoracic outlet syndrome
tarsal tunnel syndrome
radial nerve compression
lateral femoral cutaneous nerve compression
sciatic nerve damage
common peroneal nerve
122
Q

S1 dermatome, myotome and reflex

A

myotome: plantar flexion; stand on toes
dermatome: little toe, lateral side of foot, sole
reflex: ankle jerk

123
Q

C5/C6 dermatome myotome reflex

A

elbow flexion
thumb
biceps

124
Q

C7 dermatome myotome reflex

A

elbow extension
middle finger
triceps

125
Q

C8. T1 dermatome myotome

A

little finger, + forearm

hand

126
Q

C8. T1 dermatome myotome

A

little finger, + forearm

hand

127
Q

investigations for mononeuropathies

A

nerve conduction studies
electromyography
USS

128
Q

management of mononeuropathies

A

conservative: NSAIDs, splinting, local steroid injections

surgery

129
Q

common causes of peripheral neuropathy

A

diabetes

idiopathic

130
Q

uncommon causes of peripheral neuropathy

A 
Deficiency states e.g. B12 /Folate
Alcohol/Toxins/Drugs
Hereditary Neuropathies 
Paraneoplastic Syndromes
Metabolic abnormalities e.g. uraemia/thyroid
131
Q

what is mononeuritis multiplex and what are potential causes

A

Individual nerves picked off randomly
Subacute presentation
Inflammatory/Immune mediated

Causes
Vasculitides
Connective tissue disorders
e.g Sarcoid

132
Q

commmon mononeuropathies and their entrapment

A

Median nerve entrapment at the wrist most common (Carpal Tunnel Syndrome)

Ulnar nerve at elbow common

Radial nerve in axilla common

Common peroneal nerve in leg most common

133
Q

neuropathy investigation

A 
History and examination
\+/-Neuropathy screen
\+/-Vasculitic screen
\+/-EMG/NCS
\+/-CSF study
\+/-nerve biopsy
134
Q

what tests are part of a neuropathy screen

A 
FBC ESR
U+E, glucose, TFT, CRP, Serum electorophoresis
B12 Folate
Anti Gliadin
(TPHA, HIV)
135
Q

what tests are part of a vasculitic screen

A

FBC, ESR
U+ECr, CRP
ANA, ENA, ANCA, anti dsDNA, RhF, Complement, Cryoglobulins

136
Q

neuropathy treatment

A 
20% idiopathic with no treatment
Neuropathic analgesic (gabapentin,pregabalin amitrptyline)

Treat/remove underlying cause e.g. DM/gluten

Inflammatory neuropathy (e.g CIDP)
Prednisolone with steroid sparing agents e.g. azathioprine
Vascultic neuropathy (e.g with Wegners)
Prednisolone with immunosupressant e.g. cyclophosphamide
137
Q

migraine prophylaxis

A

1st line: beta blockers or amitryptilline

2nd line: topiramate or sodium valproate

3rd line: pizotifen (weight gain)

138
Q

percentage of recurrence after first seizure

A

20 - 45% (50%)

139
Q

organisms that can cause GBS

A

campylobacter jejuni
EBV
CMV

140
Q

presentation of GBS

A

weakness approximately 3 weeks after viral infection

ascending pattern of progressive symmetrical weakness starting from lower extremities; maximum severity in 2 weeks and onset stops

141
Q

risk factors for MS

A

previous infectious mononucleosis

vitamin D deficiency

genetics

smoking

142
Q

migraine triggers

A

CHOCOLATE: chocolate, hangovers, orgasms, cheese/caffeine, oral contraceptives, lie-ins, alcohol, travel, exercise

143
Q

what is normal pressure hydrocephalus and how does it present

A

ventricular dilatation in the absence of raised CSF pressure on lumbar puncture

wet wacky wobbly

144
Q

causes of NPH

A

subarachnoid haemorrhage
meningitis
head injury
CNS tumour

145
Q

management of NPH and complications

A

surgical insertion of CSF shunt

complications: shunt occlusions, headaches, infarct, haemorrhage, infection

146
Q

what is hydrocephalus

A

increase in CSF occupying the ventricles either due to problems of absorption or too much secretion

147
Q

symptoms of hydrocephalus

A

headache + vomiting
papilloedema
unsteady gait

6th nerve palsy
large head

148
Q

investigations and management for hydrocephalus

A

CT

surgical insertion of a shunt or external ventricular drain

149
Q

most common type of brain metastases sites

A 
breast
lung 
kidney 
melanoma
bowel
150
Q

types of brain tumours

A

secondary tumours are 10x more common than primary

high grade: glioma, glioblastoma multiforme, medulloblastoma

low grade: acoustic neuroma, pituitary tumor, craniopharyngioma

151
Q

what is horner’s syndrome

A

disruption to sympathetic nerves supplying the eye:

anhidrosis
ptosis
miosis

152
Q

Bell’s palsy

A

LMN: can’t wrinkle forehead
UMN: forehead sparing

management: steroids

153
Q

risk factors for status epilepticus

A

under 5, elderly
genetic predisposition
intellectual disability

hypoglycaemia, alcohol withdrawal

154
Q

management of status epilepticus

A

community
ABCDE
buccal midazolam (rectal diazepam)

hospital
ABCDE
IV lorazepam (x 2 if needed)
IV phenytoin or phenobarbital

155
Q

3rd nerve palsy

A

down and out

156
Q

4th nerve palsy

A

up

157
Q

6th nerve palsy

A

unable to abduct

158
Q

drugs that exacerbate myasthenia gravis

A 
antibiotics e.g. ciprofloxacin
beta-blockers 
anti-arrhytmic drugs
lithium 
statins
159
Q

investigations in MG

A

Ach-R antibody serum levels
thyroid function tests
thymus CT/MRI

160
Q

management of MG

A

pyridostigmine

corticosteroids, immunosupressives e.g. azathioprine, thymectomy

161
Q

subarachnoid haemorrhage cause and RF

A

bleeding from berry aneurysm

cocaine, smoking, hypertension, excessive alcohol

162
Q

SAH: investigation + management

A

CT: hyper- dense appearance of blood around basal cisterns

cerebral panangiography

surgical clipping or coiling

163
Q

SDH cause, RF, investigation and management

A

bridging veins

infants, elderly, alcoholism

CT

craniotomy + clot evacuation

164
Q

EDH

A

middle meningeal artery

surgical evacuation

Phase 3A (9 decks)

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