Neuro Flashcards

1
Q

What would you prescribe for Mx of Bell’s palsy?

A

Prednisolone
Lubricating eye drops/artificial tears

NB aciclovir has now been found to show no additional benefit

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2
Q

Features of multiple system atrophy

A
  1. Parkinsonism
  2. Autonomic disturbance (atonic bladder, postural hypotension, erectile dysfunction)
  3. Cerebellar signs - e.g. ataxic gait

NB 2 types of MSA
MSA-P - predominant Parkinsonian features
MSA-C - predominant cerebellar features

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3
Q

When do you start anti-epileptic medication?

A

After the second epileptic seizure

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4
Q

Second line medication for generalised tonic-clonic seizures

A

Lamotrigine, carbamazepine

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5
Q

First line for focal seizures

A

Carbamazepine

Lamotrigine

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6
Q

What is a big possible adverse reaction when combining sodium valporate and lamotrigine?

A

Steven-Johnson’s syndrome

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7
Q

What is a quick and easy bedside test to perform to confirm that the fluid draining from the nose is CSF?

A

Glucose test

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8
Q

Two drugs used to decreased frequency of migraine attacks (prophylaxis)

A
  • Propanolol or topiramate
  • Propanolol is preferred in women of childbearing age as can be teratogenic and can reduce efficacy of hormonal contraceptives
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9
Q

Acute treatment of cluster headache

A

Subcutaneous sumatriptan + 100% O2

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10
Q

Prophylaxis of cluster headache

A

Verapamil

some also recommend tapering dose of prednisolone

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11
Q

Motor neurone disease - what is the result of nerve conduction studies?

A

Normal (diagnosis is clinical, but studies help exclude a neuropathy)

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12
Q

Which anti-epileptic drug is associated with weight gain?

A

Sodium valporate

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13
Q

Autonomic dysreflexia

A

This clinical syndrome occurs in patients who have had a spinal cord injury at, or above T6 spinal level.

Briefly, afferent signals, most commonly triggered by faecal impaction or urinary retention (but many other triggers have been reported) cause a sympathetic spinal reflex via thoracolumbar outflow. The usual, centrally mediated, parasympathetic response however is prevented by the cord lesion.

The result is an unbalanced physiological response, characterised by extreme hypertension, flushing and sweating above the level of the cord lesion, agitation, and in untreated cases severe consequences of extreme hypertension have been reported.

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14
Q

3 key features/triad in normal pressure hydrocephalus?

A

Ataxia, urinary incontinence and dementia

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15
Q

A 74-year-old man is brought into the emergency department by his wife. She has noticed a change in his behaviour. Although he never used to drink he has started to buy expensive whisky. He has also spent lots of time at a local bookmaker’s and his wife is very concerned that he lost a lot of money gambling.

His medical history consists of prostatic hyperplasia, osteoarthritis, and Parkinson’s disease.

Which class of drug is he most likely to have been recently prescribed?

A

Dopamine agonist (more associated with impulsive behaviour than L-dopa)

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16
Q

Management of tetanus

A
  1. supportive therapy including ventilatory support and muscle relaxants
  2. intramuscular human tetanus immunoglobulin for high-risk wounds (e.g. compound fractures, delayed surgical intervention, significant degree of devitalised tissue)
  3. metronidazole is now preferred to benzylpenicillin as the antibiotic of choice
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17
Q

Blood vessel associated with:

  1. Extradural haemorrhage
  2. Subdural haemorrhage
A
  1. Middle meningeal artery

2. Bridging veins between cortex and venous sinuses

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18
Q

Important blood tests apart from routine ones to do for confusion screen

A

TFTs (hypothyroidism), B12, Folate, GLUCOSE, bone profile (hypercalcaemia)

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19
Q

Which anaesthetic drug would a patient with myasthenia gravis be resistant to?

A

Suxamethonium!

This is a depolarising NMBD - it acts by binding to and activating the receptor, at first causing muscle contraction, then paralysis. Again, due to a decreased number of available receptors, MG patients are typically resistant to depolarising NMBDs and may require significantly higher doses.

20
Q

Which anaesthetic drug would a patient with MG be more sensitive to?

A

Rocuronium is a non-depolarising NMBD, acting as an antagonist the post-synaptic receptor and leaving fewer receptors available for acetylcholine. In MG, there are already fewer functional receptors available and therefore patients with MG will be more sensitive to rocuronium and will require a lower dose for paralysis.

21
Q

Mechanism of action of neostigmine

A

ACholinesterase inhibitor

22
Q

Lambert Eaton syndrome is associated with which type of malignancy?

A

Small-cell lung cancer

23
Q

Management of trigeminal neuralgia

A
  1. Carbamazepine
  2. Refer to neurology 2ww if red flag symptoms (could be tumour or vascular compression to trigeminal nerve) or if not responding to treatment
24
Q

Medication for meningococcal septicaemia

A
  1. IV cefotaxime/ceftriaxone ± amoxicillin
  2. Dexamethasone recommended to avoid neurological sequelae

do NOT LP if patient is septicaemic!

25
Q

Recommended drug for tension headache and possible prophylaxis Rx

A

aspirin/NSAID/paracetamol 1st line

Acupuncture prophylaxis (amytriptilline recommended before - but not anymore)

26
Q

Treatment for cluster headache (acute)

A

acute: 100% oxygen (80% response rate within 15 minutes), subcutaneous triptan (75% response rate within 15 minutes

27
Q

Treatment for cluster headache (prophylaxis)

A

Verapamil is the drug of choice. There is also some evidence to support a tapering dose of prednisolone

28
Q

Management for altitude sickness

A

Acetazolamide

29
Q

Treatment given for close contacts of patients with meningitis dx (notifiable disease)

A

Single dose oral ciprofloxacin

30
Q

Drug given for treatment of trigeminal neuralgia

A

Carbamazepine

31
Q

Polymyalgia rheumatica - what is the symptom asked

A

Early morning stiffness and aching in proximal muscles (NOT weakness!)

32
Q

Ix and management of GCA/PMR

A
  1. ABCDE
  2. Investigations - ESR/CRP, CK, consider EMG; temporal artery biopsy (may be normal - skip lesions)
  3. Treatment:
    - High dose prednisolone
    - Urgent ophthalmology referral if visual symptoms present (visual damage often irreversible)
33
Q

Treatment for SAH

A
  1. Definitive management is either through a coil (neuroradiology), or a craniotomy and clipping by neurosurgery
  2. Until treated, the patient should:
    - Kept on strict bedrest
    - Controlled BP
    - Avoid straining to prevent re-bleed
  3. Nimodipine (specific for brain vasculature) - used to prevent vasospasm (21d) + hypervolaemia + induced HTN and haemodilutation
  4. Hydrocephalus temporarily treated with an external ventricular drain (CSF diverted into a bag at the bedside), or long-term ventriculo-peritoneal shunt if required.
34
Q

Complications of SAH

A
  1. Re-bleeding
  2. Vasospam - 7-14d after onset
  3. Hyponatraemia (usually due to SIADH)
  4. Seizures
  5. Hydrocephalus
  6. Death
35
Q

MMSE scores and dementia severity

A

Max score you can get is 30

  1. 24-20 - mild dementia
  2. 13-20 - moderate dementia
  3. <12 - severe dementia
36
Q

Medical management of Alzheimer’s disease

A
  1. Mild dementia - acetylcholinesterase inhibitors (donepezil (CI in bradycardia), rivastigmine, galantamine
  2. Severe; or if above CI; or can use alongside above - memantine (NMDA receptor antagonist)

NICE do not recommend antidepressants for depressive symptoms

37
Q

What is pellagra?

A

Pellagra is a caused by nicotinic acid (niacin) deficiency. The classical features are the 3 D’s -

  1. dermatitis
  2. diarrhoea
  3. dementia

Pellagra may occur as a consequence of isoniazid therapy (isoniazid inhibits the conversion of tryptophan to niacin) and it is more common in alcoholics.

38
Q

Essential tremor vs Parkinson’s tremor

A
  1. essential - bilateral, symmetrical, postural tremor (i.e. positional or on movement), may be improved by alcohol
  2. PD - asymmetrical, present at rest
39
Q

Management for essential tremor

A
  1. Exclude organic causes of tremor e.g. thyroid, drugs, caffeine
  2. Propanolol - 1st line!
  3. Gabapentin, topiramate are alternatives
40
Q

Ddx for optic neuritis in multiple sclerosis

A

Neuromyelitis optica

presents with recurrent optic neuritis; anti-NMO antibodies positive!

41
Q

Mode of inheritance for Duchenne’s and Becker’s dystrophinopathies?

A

X-linked recessive

42
Q

2 signs that are distinct for Duchenne’s

Extra notes: Duchenne’s is dx around 4-5y/o (Becker’s 9y/o) and is a proximal myopathy

A

Gower’s sign and calf pseudohypertrophy

43
Q

What is a myasthenic crisis and how is it managed?

A

Worsening of muscle weakness leading to respiratory failure; requires intubation (if low PEF) and mechanical ventilation; may be cause by stress, infection, steroids

Mx

  1. Check FVC spirometry - intubate if low
  2. IV immunoglobulin (short onset, short offset)
  3. Plasmapharesis (long onset, longer offset)
44
Q

Long-term mx of myasthenia gravis

NB that NMJ disorders tend to show proximal weakness compared to peripheral neuropathies which show distal

A
  1. Long-acting anticholinesterase - e.g. pyridostigmine
  2. Immunosuppression - prednislone
  3. ± thymectomy
45
Q

Aetiology of Lambert Eaton syndrome

A

Antibody against pre-synaptic VGCC on peripheral nervous system; associated with small cell lung cancer

46
Q

EMG findings in MG vs Lambert Eaton

A

MG - shows fatiguability of muscle

LE - incremental response to repetitive electrical stimulation

47
Q

Mx of Lambert Eaton

A
  1. Treat underlying malignancy
  2. Immunosuppresion - steroids
  3. 3,4-diaminopyridine
  4. IV Ig and plasmapheresis may play a role