Neuro Flashcards

1
Q

Stroke: ACA

A

Contralateral hemiparesis and sensory loss, lower extremity > upper

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2
Q

Stroke: MCA

A

Contralateral hemiparesis and sensory loss, upper extremity > lower
Contralateral homonymous hemianopia
Aphasia - difficulty with language or speech

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3
Q

Stroke: PCA

A

Contralateral homonymous hemianopia with macular sparing (preserves vision in the centre of the visual field)
Visual agnosia ( cannot recognise objects)

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4
Q

Stroke: Basilar artery

A

Locked in syndrome

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5
Q

Stroke: retinal/ ophthalmic artery

A

Amaurosis fugax

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6
Q

What is a lacunar stroke?

A

present with either isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia
strong association with hypertension
common sites include the basal ganglia, thalamus and internal capsule

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7
Q

Acute management of a stroke (what are the guidelines)

A

aspirin 300mg orally or rectally should be given as soon as possible if a haemorrhagic stroke has been excluded

regards to atrial fibrillation, the RCP state: ‘anticoagulants should not be started until brain imaging has excluded haemorrhage, and usually not until 14 days have passed from the onset of an ischaemic stroke’

if the cholesterol is > 3.5 mmol/l patients should be commenced on a statin. Many physicians will delay treatment until after at least 48 hours due to the risk of haemorrhagic transformation

BM’s, Sats, hydration and temperature should be normal

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8
Q

What are the guidelines regarding thrombolysis for acute ischaemic strokes?

A

Thrombolysis with alteplase should only be given if:
it is administered within 4.5 hours of onset of stroke symptoms (unless as part of a clinical trial)
haemorrhage has been definitively excluded (i.e. Imaging has been performed)

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9
Q

What are the guidelines regarding thrombectomy for acute acute ischaemic strokes?

A

Offer thrombectomy as soon as possible and within 6 hours of symptom onset, together with intravenous thrombolysis (if within 4.5 hours), to people who have:
acute ischaemic stroke and
confirmed occlusion of the proximal anterior circulation demonstrated by computed tomographic angiography (CTA) or magnetic resonance angiography (MRA).

Offer thrombectomy as soon as possible to people who were last known to be well between 6 hours and 24 hours previously (including wake-up strokes):
confirmed occlusion of the proximal anterior circulation demonstrated by CTA or MRA and
if there is the potential to salvage brain tissue, as shown by imaging such as CT perfusion or diffusion-weighted MRI sequences showing limited infarct core volume

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10
Q

What are the secondary prevention guidelines for stroke?

A

Recommendations from NICE include:
clopidogrel is now recommended by NICE ahead of combination use of aspirin plus modified-release (MR) dipyridamole in people who have had an ischaemic stroke
Aspirin plus MR dipyridamole is now recommended after an ischaemic stroke only if clopidogrel is contraindicated or not tolerated, but treatment is no longer limited to 2 years’ duration
MR dipyridamole alone is recommended after an ischaemic stroke only if aspirin or clopidogrel are contraindicated or not tolerated, again with no limit on duration of treatment

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11
Q

What are NICE guidelines regarding the mx of Parkinson’s disease?

A
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12
Q

What are the nice guidelines for Parkinson’s mx?

A

For first-line treatment:
if the motor symptoms are affecting the patient’s quality of life: levodopa
if the motor symptoms are not affecting the patient’s quality of life: dopamine agonist (non-ergot derived), levodopa or monoamine oxidase B (MAO‑B) inhibitor

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13
Q

Which parkinsons drug is best for motor symptoms and ADOLS mx?

A

Levadopa anyday over Dpamine agonists or MAO-B inhibitors

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14
Q

What parkinsons drug can cause the the most motor complications and which one is the one that causes the most adverse events (sleepiness hallucinations etc):

A

Motor: Levodopa is the worst for side effects
Adverse events: Dopamine agonists

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15
Q

Side effects of levadopa

A

Dry mouth
Anorexia
Palpitations
Psychosis
Postural HTN
Dyskinesias ( dystonia, chorea and athetosis)

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16
Q

What is a TIA?

A

The original definition of a TIA was time-based: a sudden onset of a focal neurologic symptom and/or sign lasting less than 24 hours, brought on by a transient decrease in blood flow. However, this has now changed as it is recognised that even short periods of ischaemia can result in pathological changes to the brain. Therefore, a new ‘tissue-based’ definition is now used: a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction.

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17
Q

What are the features of a TIA

A

Resolve within1-24hrs however are:

unilateral weakness or sensory loss.
aphasia or dysarthria
ataxia, vertigo, or loss of balance

visual problems:
sudden transient loss of vision in one eye (amaurosis fugax)
diplopia
homonymous hemianopia

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18
Q

What would you do if you came across someone with a sus TIA?

A

give aspirin 300 mg immediately, unless
1. the patient has a bleeding disorder or is taking an anticoagulant (needs immediate admission for imaging to exclude a haemorrhage)
2. the patient is already taking low-dose aspirin regularly: continue the current dose of aspirin until reviewed by a specialist
3. Aspirin is contraindicated: discuss management urgently with the specialist team

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19
Q

Investigations for a TIA!!!!!!

A

NICE recommend that CT brains should not be done ‘unless there is clinical suspicion of an alternative diagnosis that CT could detect’
MRI (including diffusion-weighted and blood-sensitive sequences) is preferred to determine the territory of ischaemia, or to detect haemorrhage or alternative pathologies
Carotid doppler!

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20
Q

How would you treat a confirmed TIA?

A

Clopidogrel is recommended first line
Aspirin + dipyramidole for those patients who cannot.

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21
Q

Features of a third nerve palsy ?

A

eye is deviated ‘down and out’
ptosis
pupil may be dilated (sometimes called a ‘surgical’ third nerve palsy)

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22
Q

Causes of a third nerve palsy?

A

DM , Vasculitis, PCA aneurysm (ASSOCIATED WITH PAIN!!!!!)
MS?

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23
Q

How do we classify seizures?

A
  1. Where seizures begin in the brain
  2. Level of awareness during a seizure (important as can affect safety during seizure)
  3. Other features of seizures
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24
Q

What is a focal seizure?

A

these start in a specific area, on one side of the brain
the level of awareness can vary in focal seizures. The terms focal aware (previously termed ‘simple partial’), focal impaired awareness (previously termed ‘complex partial’) and awareness unknown are used to further describe focal seizures
further to this, focal seizures can be classified as being motor (e.g. Jacksonian march), non-motor (e.g. déjà vu, jamais vu; ) or having other features such as aura

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25
Q

Gen seizures what are they ?

A

these engage or involve networks on both sides of the brain at the onset
consciousness lost immediately. The level of awareness in the above classification is therefore not needed, as all patients lose consciousness
generalised seizures can be further subdivided into motor (e.g. tonic-clonic) and non-motor (e.g. absence)

tonic-clonic (grand mal)
tonic
clonic
typical absence (petit mal)
atonic

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26
Q

What is Bells palsy? What is it caused by and who does it affect?

A

Bell’s palsy may be defined as an acute, unilateral, idiopathic, facial nerve paralysis. The aetiology is unknown although the role of the herpes simplex virus has been investigated previously. The peak incidence is 20-40 years and the condition is more common in pregnant women.

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27
Q

What are the features of Bell’s palsy?

A

lower motor neuron facial nerve palsy - forehead affected
in contrast, an upper motor neuron lesion ‘spares’ the upper face
patients may also notice post-auricular pain (may precede paralysis), altered taste, dry eyes, hyperacusis

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28
Q

Mx of bells palsy?

A

there is consensus that all patients should receive oral prednisolone within 72 hours of onset of Bell’s palsy
Eye care - artificial tears and tape etc
If no improvement in 3 weeks urgent ENT referral

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29
Q

What is a cluster headache and what is its pattern?

A

The name relates to the pattern of the headaches - they typically occur in clusters lasting several weeks, with the clusters themselves typically once a year.
Men 3:1 and smokers more common

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30
Q

Features of cluster headaches?

A

Features
pain typical occurs once or twice a day, each episode lasting 15 mins - 2 hours
clusters typically last 4-12 weeks
intense sharp, stabbing pain around one eye (recurrent attacks ‘always’ affect same side)
patient is restless and agitated during an attack
accompanied by redness, lacrimation, lid swelling
miosis and ptosis in a minority

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31
Q

Acute and prophylaxis treatment of cluster headaches?

A

acute: 100% oxygen (80% response rate within 15 minutes), subcutaneous triptan (75% response rate within 15 minutes)
prophylaxis: verapamil is the drug of choice. There is also some evidence to support a tapering dose of prednisolone
NICE recommend seeking specialist advice from a neurologist if a patient develops cluster headaches with respect to neuroimaging

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32
Q

What is Myasthenia gravis?

A

Myasthenia gravis is an autoimmune disorder resulting in insufficient functioning acetylcholine receptors. Antibodies to acetylcholine receptors are seen in 85-90% of cases*. Myasthenia is more common in women (2:1)

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33
Q

What are the features of MG?

A

Fatigability which improves with rest:
Extraocular muscle weakness + diplopia
Proxismal muscle weakness (head and neck)
Ptosis
Dysphagia

34
Q

What is MG associated with?

A

Thymomas! and other autoimmune disorders

35
Q

What Ix would you do for MG?

A

single fibre electromyography: high sensitivity (92-100%)
Autoantibodies - to acetylcholine receptors

36
Q

Mx of MG?

A

Pyridostigmine - first line. Can lead to horrible diarrhoea

Most patients on some sort of long term immunosuppression

37
Q

What is a status epilepticus?

A

Status epilepticus is defined as:
a single seizure lasting >5 minutes, or
>= 2 seizures within a 5-minute period without the person returning to normal between them

38
Q

How would you manage status epilepticus?

A

ABC + blood glucose!
First-line drugs are IV benzodiazepines such as diazepam or lorazepam
in the prehospital setting PR diazepam or buccal midazolam may be given
in hospital IV lorazepam is generally used. This may be repeated once after 10-20 minutes
If ongoing (or ‘established’) status it is appropriate to start a second-line agent such as phenytoin or phenobarbital infusion

39
Q

How would you manage GBS?

A

IVig + plasma exchange

40
Q

What is GBS? What is it caused by?

A

Guillain-Barre syndrome describes an immune-mediated demyelination of the peripheral nervous system often triggered by an infection (classically Campylobacter jejuni).

41
Q

What are the characteristic features of GBS?

A

The characteristic features of Guillain-Barre syndrome is progressive, symmetrical weakness of all the limbs.
the weakness is classically ascending i.e. the legs are affected first
reflexes are reduced or absent
sensory symptoms tend to be mild (e.g. distal paraesthesia) with very few sensory signs

42
Q

Ix for GBS?

A

Lumbar puncture - rise in protein but normal WBC count
Decreased motor nerve conduction - due to demyelination

43
Q

How do you manage migraines acutely?

A

first-line: offer combination therapy with an oral triptan and an NSAID, or an oral triptan and paracetamol

44
Q

What is the prophylactic tx of migraines?

A

NICE advise either topiramate or propranolol ‘according to the person’s preference, comorbidities and risk of adverse events’. Propranolol should be used in preference to topiramate in women of child bearing age

45
Q

Temporal love focal seizure mnemonic?

A

HEAD
Hallucinations (auditory/gustatory/olfactory), Epigastric rising/Emotional, Automatisms (lip smacking/grabbing/plucking), Deja vu/Dysphasia post-ictal)

46
Q

Frontal lobe seizure features?

A

MOTOR
Head/leg movements, posturing, post-ictal weakness, Jacksonian march.

47
Q

Parietal lobe seizure features? Occipital lobe?

A

Paraesthesia - parietal
Floater and flashes- occipital

48
Q

What is the epi of MND?

A

Motor neuron disease is a neurological condition of unknown cause which can present with both upper and lower motor neuron signs. It rarely presents before 40 years and various patterns of disease are recognised including amyotrophic lateral sclerosis, progressive muscular atrophy and bulbar palsy.

49
Q

What features point towards a diagnosis of MND?

A

fasciculations
the absence of sensory signs/symptoms*
the mixture of lower motor neuron and upper motor neuron signs
wasting of the small hand muscles/tibialis anterior is common
Often no cerebellar or ocural signs

50
Q

What is wenickes aphasia?

A

This area ‘forms’ the speech before ‘sending it’ to Broca’s area. Lesions result in sentences that make no sense, word substitution and neologisms but speech remains fluent - ‘word salad’
Comprehension is impaired

51
Q

Brocas aphasia?

A

Due to a lesion of the inferior frontal gyrus. It is typically supplied by the superior division of the left MCA

Speech is non-fluent, laboured, and halting. Repetition is impaired

52
Q

Acute mx of MS?

A

High dose steroids (e.g. oral or IV methylprednisolone) may be given for 5 days to shorten the length of an acute relapse. Shortens relapse does not cure

53
Q

MS long term meds?

A
  1. Natalizumab - monoclonal antibody
    Others????
    Beta interferon no longer thought of as effective?
54
Q

What is the symptom pattern of parkinsons?!!!

A

Asymmetrical
Classic triad of: bradykinesia, termor and rigidity
You cannot have parkinsons without bradykinesia!!!!!

55
Q

Features of parkinsons?

A

Bradykinesia: hypokinesia, short shuffling steps with reduced arm swing, difficulty starting mvmnt
Pill rolling tremor that is worse when stressed or tired - improves with voluntary movement (3-5hz)
Lead pipe/cogwheel rigidity
Essential ones above

You can also have: mask like facies (lack of facial expressions), micrographia, REM and Parkinsons +++???

56
Q

Investigations for a stroke when not TIA?

A

non-contrast CT head to determine what therapy to start

57
Q

MS ix?

A

CSF: Oligoclonal bands
MRI: High signal T2 lesions, plaques

58
Q

MS features?

A

75% present with sig lethargy
Visual: Optic neuritis, Uhtoffs (worsening vision after heat)
Sensory: Lhermittes (paraesthesia in limbs on neck flexion), trigeminal neuralgia, numbness
Cerebellar: ataxia + tremor
Other: spastic weakness (mostly legs), sexual dysfunction and urinary incontinence

59
Q

What is optic neuritis?

A

Optic neuritis occurs when swelling (inflammation) damages the optic nerve — a bundle of nerve fibers that transmits visual information from your eye to your brain. Common symptoms of optic neuritis include pain with eye movement and temporary vision loss in one eye.

60
Q

How can you differentiate acute and chronic subdural haematomas on CT?

A

Acute: hyperdense bright crescent shape whilst chronic is darker hypodense crescent shape.

61
Q

How do we manage MND?

A

Riluzole which prolongs life by 3 months then resp care.
PEG for nutrition
However 50% will still die in 3 years

62
Q

How can you differentiate a pseudoseizure from a true epi seizure?

A

Pseudo is morelikely: When not alone, crying after seizure, gradual onset.
Epileptic seizures: Tongue biting + raised serum PROLACTIN

63
Q

Patterns of damage for radial nerve?

A

Patterns of damage
wrist drop
sensory loss to small area between the dorsal aspect of the 1st and 2nd metacarpals

64
Q

What is trigeminal neuralgia?

A

Trigeminal neuralgia is a pain syndrome characterised by severe unilateral pain. The vast majority of cases are idiopathic but compression of the trigeminal roots by tumours or vascular problems may occur.

65
Q

What are the features of a trigeminal neuralgia?

A

a unilateral disorder characterised by 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), and frequently occurs spontaneously
small areas in the nasolabial fold or chin may be particularly susceptible to the precipitation of pain (trigger areas)
the pains usually remit for variable periods

66
Q

Mx of trigeminal neuralgia?

A

carbamazepine is first-line
failure to respond to treatment or atypical features (e.g. < 50 years old) should prompt referral to neurology

67
Q

What is wernickes encephalopathy ?

A

A classic triad of ophthalmoplegia/nystagmus, ataxia and confusion
caused by thiamine deficiency which is most commonly seen in alcoholics.

68
Q

What Ix would you do for Wernickes encephalopathy?
What tx?

A

Investigations
decreased red cell transketolase
MRI

Tx: Thiamine

69
Q

Relationship between Wernickes encephalopathy and Korsakoffs syndrome?

A

If not treated Korsakoff’s syndrome may develop as well. This is termed Wernicke-Korsakoff syndrome and is characterised by the addition of antero- and retrograde amnesia and confabulation in addition to the above symptoms.
Opthalmoplegia, ataxia and confusion

70
Q

What is Menieres disease?

A

Meniere’s disease is a disorder of the inner ear of unknown cause. It is characterised by excessive pressure and progressive dilation of the endolymphatic system.

71
Q

Features of Menieres disease?

A
  • recurrent episodes of vertigo, hearing loss and tinnitus
  • sensation of aural fullness or pressure is a common feeling
    *Symptoms are unilateral but bilateral symptoms may develop after a few years
72
Q

Mx of Menieres disease?

A

ENT assessment to confirm diagnosis
DVLA- dont drive till symptoms controlled
Acute: Buccal or IM prochlorperazine

73
Q

What is narcolepsy? What are some features?

A

Disease where patients fall asleep at inappropriate times
Features: teenage years
sleep paralysis, Cataplexy (sudden loss of muscle tone triggered by emotion).

74
Q

Mx of narcolepsy

A

Daytime stimulants such as modafinil

75
Q

What is an essential tremor?

A

Essential tremor (previously called benign essential tremor) is an autosomal dominant condition which usually affects both upper limbs.
Features:
* Postural tremor (worse if arms outstretched)
* improved by alcohol and rest

76
Q

Management of essential tremor?

A

Management
propranolol is first-line

77
Q

What do you know about Huntingtons?

A

Genetics - death in 20 years
autosomal dominant
trinucleotide repeat disorder: repeat expansion of CAG
as Huntington’s disease is a trinucleotide repeat disorder, the phenomenon of anticipation may be seen, where the disease is presents at an earlier age in successive generations
results in degeneration of cholinergic and GABAergic neurons in the striatum of the basal ganglia
due to defect in huntingtin gene on chromosome 4

78
Q

Features of Huntingtons?

A

chorea
personality changes (e.g. irritability, apathy, depression) and intellectual impairment
dystonia
saccadic eye movements

79
Q

What is lyme disease caused by?

A

Lyme disease is caused by the spirochaete Borrelia Burgdorferi, which is transmitted via Ixodes ticks in wooded areas.

80
Q

What is encephalitis?

A

Encephalitis is a histological diagnosis characterised by inflammation of the “encephalon” (or brain parenchyma).

81
Q

What is the main culprit in encephalitis?

A

Encephalitis is usually of viral aetiology, with herpes simplex virus type 1 as the most common culprit.

82
Q

Clinical features of encephalitis?

A

the cardinal feature of which is altered mental status (not as prominent in meningitis). Other suggestive features include fever, a flu-like prodromal illness, and early seizures.