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MSRA 2022 > Neurology > Flashcards

Neurology Flashcards

1
Q

What is the target time range for thromebectomy in an ischaemic stroke?

A

ideally within 6 hours - however recently expanded to be possible within 16 hours according to results of DAWN . + DEFUSE trials

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2
Q

What is the target time for thrombolysis in ischaemic stroke?

A

WITHIN 4 HOURS

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3
Q

What does the term anticipation mean as it pertains to trinucleotide repeat disorders such as Huntington’s disease?

A

You get earlier onset of the disease in successive generations

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4
Q

What is Bell’s Palsy and what is it’s typical presentation?

A

Idiopathic unilateral lower motor neurone facial nerve palsy.

Presents with unilateral facial drooping + weakness INCLUDING the forehead (UMN facial nerve lesions spare the forehead) + dry eyes + altered taste + may have post-auricular pain in ~ 50%.

More common in pregnancy. Typical age = 20-40 yrs.
Some association with herpes simplex but often unknown aetiology.

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5
Q

What is the recommended treatment of Bell’s Palsy?

A

If present <72 hours of symptom onset = consider oral prednisolone (either 50mg for 10 days or 60mg for 5 days then a reducing dose)
Artificial tears to lubricate eye and prevent exposure keratitis.
If unable to close the eye at bedtime then to cover with microporous tape.
Antivirals not routinely recommended - consider in liaison with specialist if severe.

Refer to ENT or neurologist if no improvement after 3 wks OR if have signs of abnormal facial nerve reinnervation (gustatory sweating or jaw winking)

Most make full recovery in ~ 3 months.

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6
Q

What is the 1st line management of suspected TIA presenting in primary care?

A

If any ongoing neurology or crescendo TIA (recurrent TIAs with increasing freq, duration or severity) = CT before any antiplatelet / anticoag.

If neurology resolved + TIA within the last 7 days = stat high dose Aspirin 300mg OD and arrange urgent specialist review within 24 hrs. Normally then switched to clopidogrel after seeing the specialist.

Exceptions to giving the high dose Aspirin after suspected TIA = *bleeding/clotting disorder or on an anticoagulant (must scan first) * already on maintenance dose antiplatelet - continue current dose until seen by specialist * TIA > 7 days ago (instead get specialist assessment within the next 7 days)

Start atorvastatin (20 - 80mg) after 48hrs from symptom onset.

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7
Q

Management of ischaemic stroke in the emergency setting?

A

1) If FAST +ve on admission = urgent CT Head
2) Once haemorrhage excluded, if < 4.5 hrs and no contraindications = consider thrombolysis with Alteplase = (15mg IV bolus followed by a weight-determined IV infusion)
3) Consider thrombectomy (+/- thrombolysis) in those with: * a pre-stroke functional status <3 on the modified Rankin scale
AND
* an NIHSS stroke score >5
AND
* either <6 hrs of symptoms onset in a confirmed proximal anterior circulation infarct (confirmed by CT or MR angiography) OR <24 hrs of symptoms onset in proximal ant/posterior circulation occlusion WITH imaging suggestive of potential to salvage brain tissue (ie limited infarct core volume)
4) Can resume high dose Aspirin after 24 hrs of Alteplase
5) Make the switch from high dose Aspirin to Clopidogrel / anticoagulation depending on the NIH Stroke Scale Score: THE HIGHER THE SCORE THE LONGER YOU STAY ON HIGH DOSE ASPIRIN
NIHSS <8 = switch day 3-5
NIHSS 8-15 = switch day 6-8
NIHSS >15 = switch day 12-14
Dual Antiplatelet therapy (Aspirin + Clopidogrel for upto 90 days or Aspirin + Ticagrelor for upto 30 days) may be recommended by specialist e.g if high risk of recurrence or significant intracranial stenosis before switch to antiplatelet monotherapy.

6) Start high intensity statin (Atorvastatin) after 48 hrs of ischaemic stroke EVEN IF CHOLESTEROL LEVELS NORMAL)

DO NOT GIVE WARFARIN IN THE ACUTE PHASE OF AN ISCHAEMIC STROKE

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8
Q

What are the side effects of sodium valproate?

A

Teratogenic
Weight gain / ^ appetite
Alopecia
Ataxia
Hepatotoxicity
Pancreatitis
Thrombocytopenia

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9
Q

What are the order of drug treatments to initiate in Parkinson’s disease?

A

1st line = Levodopa
If still has symptoms of dyskinesia despite this then = offer a choice of either
- non-ergot dopamine agonist -> ropinirole, rotigotine, pramipexole
- MAO-B inihibitor - Rasagilline, Selegilline
- COMT inhibitor - Entacapone, Tolcapone

If these fail to improve things:
can add in an ergot dopamine agonist -> Bromocriptine, Cabergoline, Pergolide

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10
Q

What is the typical presentation of an abducens nerve injury?

A

aBducens = aBduction
= responsible for ipsilateral lateral gaze
When damaged = horizontal diplopia on lateral gaze + eyes appeared cross-eyed (convergent squint / esotropia_

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11
Q

What are the actions of the oculomotor nerve on the eye?

A

Pupil constriction (carries the parasympathetic fibres)
Upper eyelid elevation (levator palpebrae superior)
Looking up and medial adduction of the eyeball

Defect = down + out, with a droopy eyelid, dilated pupil

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12
Q

What is the typical presentation of an oculomotor nerve lesion?

A

Ipsilateral *ptosis (eyelid drooping) * pupil dilation * eye is ‘down + out’ due to loss of superior movement and adduction

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13
Q

What are the actions of the trochlear nerve on eye movements?

A

Superior oblique muscle
= allows the eye to look down and to externally and internally rotate from that position

Trochlear - Trotting down the stairs
Classically get double vision when looking down the stairs

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14
Q

What is the typical presentation of a trochlear nerve palsy?

A

VERTICAL double vision that is worse when looking down or looking AWAY from the side of the lesion
(ie double vision when looking down + to the left witha right-sided nerve lesion)

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15
Q

What is the triad for Wernicke’s encephalopathy?

A

1) Altered mental status (confusion -> coma)
2) Ophthalmoplegia
3) Cerebellar dysfunction (ataxic gait)

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16
Q

What is the safest anti-epileptic in women of childbearing age (ie to switch them to if they are on valproate and TTC)

A

Carbamazepine (+high dose folic acid)

(carbamazepine is the safest choice of anti-epileptic in pregnancy but is still teratogenic) so if they have been fit free for 2 or more years then ideally stop anti-epilepics =)

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17
Q

When can you consider stopping anti-epileptic medication in a women TTC?

A

If they have been fit free for 2 YEARS or MORE
(Still start folic acid)

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18
Q

What does Rinne positive mean?

A

It means that there is a NORMAL response to the rinnes test
Ie that air conduction was louder than bone conduction

If bone conduction was louder, they would be rinne negative, suggestive of conductive hearing loss

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19
Q

What is the typical presentation of myasthenia gravis?

A

Progressive weakness, chiefly of the facial, periocular, bulbar and girdle muscles -> presents with FATIGUABLE weakness ie fatiguable eyelid drooping, difficulty chewing + swallowing.

Autoimmune condition associated with IgG antibodies against acetylcholine receptors.

20
Q

What is the typical presentation of carpal tunnel syndrome?

A

= median nerve palsy
Loss of sensation / pins and needles over thumb, index and middle finger +/- thenar eminence atrophy

21
Q

What is the typical presentation of ulnar nerve compression?

A

Weakness and loss of sensation in the little and ring finger = claw hand

22
Q

What is the typical presentation of a radial nerve palsy?

A

Wrist drop and loss of sensation over dorsal aspect of hand

23
Q

What is the typical presentation of de quervains tenosynovitis?

A

Pain and stiffness in the thumb / difficulty moving the thumb

24
Q

What is West’s syndrome?

A

Infantile spasms involving drawing up of the knees
leads to progressive learning difficulties

Associated with perinatal asphyxia, metabolic abnormalities, encephalitis and cerebral abnormalities

25
Q

What is the typical presentation of Juvenile myoclonic epilepsy (Janz syndrome)?

A

Myoclonic jerks usually in the morning that can make people seem that they are clumsy
Daytime absences
Infrequent more generalised seizures (also usually on waking)

26
Q

What is the advised pre-hospital management of suspected meningitis in children?

A

If suspected meningococcal disease (non-blanching rash) -> stat IM / IV benzylpenicillin then transfer to hospital
(only don’t give if prev anaphylactic allergy to penicillin, rash alone doesn’t count!)

If suspected non-meningococcal disease -> emergency transfer to hospital

27
Q

What is the advised in-hospital management of suspected meningitis in children?

A

Give IV Ceftriaxone immediately to children with a petechial rash + any of the following (v high risk of meningococcal disease):
- rash starts to spread
- rash becomes purpuric
- signs of bacterial meningitis / septicaemia
- child appears unwell

Inv: Bloods including whole-blood PCR for Neisseria Meningititidis (negative blood PCR does not exclude meningococcal disease), Lumbar puncture (but do not delay abx for this)
CT Head only if fluctuating GCS / focal neurology / other contraindications for LP to look for alternative pathology.

28
Q

What titre of white cells in the CSF should you start abx for in neonates and children (assuming they are stable and haven’t already been started on abx due to clinical suspicion of meningococcal disease)

A

20 cells/ microlitre or more (neonates)
5 cells/microlitre or more (children)

29
Q

What are contraindications to a LP in children (including red flags of ^ ICP and ICH)

A
  • GCS <9
  • Fluctuating GCS (drop of 3 or more)
  • Bradycardia + Hypertension
  • Focal neurology
  • Abnormal posture
  • Extensive or spreading purpura
  • Shock
  • Coagulation abnormalities
  • Respiratory insufficiemcy (LP can precipitate resp faillure) in these)
  • Until after convulsions / seizures are stabilised

DO NOT USE CT HEAD TO ASSESS FOR ^ ICP / WHETHER IT IS SAFE TO LP -> not realiable BUT if CT does show ^ ICP then don’t LP

30
Q

What is the typical presentation of Friedrich’s ataxia

A

= trinucleotide repeat on Frataxin gene = autosomal RECESSIVE inheritance (so affected individuals tend to have 2x carrier parents)

= low frataxin = reduced mitochondrial ATP production + ^ iron in cells = oxidative damage.
= affects metabolically active areas:
* Neurones -> ataxia (begins in childhood), reduced proprioception, initially affects legs then torso
* Cardiac cells -> hypertrophic cardiomyopathy
* Pancreatic B cells -> diabetes

31
Q

What is the typical presentation of Huntington’s disease?

A

= autosomal DOMINANT -> trinucleotide mutation in Huntington gene -> neurodegeneration (especially in the basal ganglia)

Typically presents in MIDDLE AGE w/ initially subtle personality / cognition changes then -> chorea (uncontrolled spasms), impaired balance/coordination, muscle rigidity, difficulty speaking / swallowing

32
Q

What is the pathology and typical presentation of Wilson’s disease?

A

Pathology = autosomal RECESSIVE defect in copper metabolism in the liver
excess copper = reactive free radicals = tissue damage

  • Low serum caeruoplasmin

Presentation = symptoms start in LATE CHILDHOOD
* Kayser-Fleischer rings = visible copper deposits in cornea
* Liver damage - acute hepatitis -> cirrhosis and liver failures -> hepatosplenomegaly
* Renal disease (damage to tubules)
* HAEMOLYTIC ANEMIA
* Basal ganglia -> movement disorders
* Cerebrum -> dementia

Tx:
* Penicillamine (binds copper)
* Zinc / Ammonium tetrathiomalybdate (reduces copper reabsorption)
* May need liver transplant

33
Q

What is the typical presentation of motor neurone disease?

A

90% are sporadic ie no family history
Normal nerve conduction
DIFFUSE FIBRILLATION + FASCICULATIONS ON EMG
Classify MND based on whether UMN or LMN or Mixed neurology.

UMN: Pseudo-bulbar palsy (UMN signs in corticobulbar tract ie tongue and swallowing), Primary Lateral Sclerosis (UMN signs in the corticospinal pathway ie limb UMN signs)

LMN: Progressive bulbar palsy (LMN ie weak and wasted tongue with fasciculations), Progressive Spinal Muscular Atrophy (affects spinal cord = LMN signs in the limbs

Mixed: AML (Amyotrophic lateral sclerosis) = THE MOST COMMON TYPE OF MND - spastic hyperreflexia AND flaccid hyporeflexia

Drugs available for MND: Riluzole, Edavarone (slow down damage)

34
Q

what is the 1st line drug for generalised tonic clonic seizures

A

1st line = Sodium valproate
Alternative = Lamotrigine

35
Q

What is 1st line for absence seizures

A

Ethosuximide

36
Q

Definition of status epilepticus?

A

Seizure lasting over 5 mins OR 3+ seizures in 1 hr
Tx: Buccal midazolam 10mg or rectal diazepam 10-20mg
Can repeat after 10-15 minutes
Need to urgently admit if no response to initial treatment

37
Q

Treatment for guillain barre?

A

IV immunoglobulins
(steroids no use!)

38
Q

Which parkinson’s drug can cause pulmonary fibrosis?

A

bromocriptine

39
Q

typical presentation of lewy body dementia?

A

PD + cognitive decline + visual hallucinations + disordered REM sleep

40
Q

Abx choice in bacterial meningitis in adults and children (after the initial benzylpenicillin given)?

A

Children <3 months or the elderly = need listeria cover = Cefotaxime + Ampicillin
Children > 3 months + adults = cefotaxime or ceftriaxone

41
Q

Pharmaceutical Mx of Parkinson’s?

A

1st line:
if AFFECTING QUALITY OF LIFE -> Co-careldopa or co-beneldeopa
If NOT affecting their QOL -> choose between either
* Leveldopa * Non-ergot dopamine agonist (ropinirole, rotigotine, pramipexole) * MAO-B inhibitor (Rasagilline, selegilline)

2nd line: if having motor fluctuations (freezing, end of dose fluctuations) despite adequate levodopa -> add-in: a non-ergot dopamine agonist, MAO-B or a COMT inhibitor (entacapone ,tolcapone)

3rd line: should ONLY use an ergot-derived dopamine agonist IF SYMPTOMS NOT CONTROLLED WITH A NON-ERGOT DERIVED DOPAMINE AGONIST.
Ergot-derived = *Bromocriptine * Cabergoline

4th line: for ADVANCED PD only -> Apomorphine injections (need to give domperidone alongside for N+V)

To treat side-effects (assuming have modified drugs first)
To Tx daytime sleepiness: Modafinil
For postural hypotension: Midodrine
For hallucinations (assuming they DO NOT HAVE cognitive impairment): Quetiapine
REM sleep disorders: Clonazepam or melatonin

Side effects of Parkinsonian meds: sudden-onset sleepiness, psychosis, impulse control disorders (ESPECIALLY both ergot and non-ergot dopamine agonists)
Levodopa gives the most effective improvement in motor performance and less likely to have hallucinations / impulse control disorders than dopamine agonists!

Ergot-derived agonists (cabergoline + bromocriptine) -> can cause pulmonary and cardiac fibrosis -> need regular echos.

42
Q

When is an URGENT MRI indicated in cervical spondylosis?

A

iF <2O OR >55
If they have loss of sensation in more than 1 dermatome or weakness in more than 1 myotome
If they progressive pain

43
Q

Myasthenia gravis presentation?

A

PROXIMAL, SYMMETRICAL AND FATIGUABLE muscle weakness (especially corticobulbar)
due to antibodies against acetylcholine receptors

Tx -> thymectomy, pyridostigmine, azathioprine, steroids, plasma exchange

44
Q

Duchenne muscular dystrophy presentation?

A

X-linked recessive (affects boys mainly)
presents w/ progressive weakness in childhood w/ pseudohypertrophy of calves, Gower’s sign (Walking up the body on standing up)

45
Q

Motor neurone disease presentation?

A

can be limb onset, bulbar onset or respiratory onset
can be LMN, UMN or mixed (Amyotrophic lateral sclerosis) -> the most common type of motor neurone disease!)

nerve conduction studies are NORMAL, EMG shows fibrillations + fasciculations

46
Q

Which one drug is shown to have slight reduction in progression in motor neurone disease?

A

Riluzole

MSRA 2022 (23 decks)

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