PACES Flashcards

1
Q

What does temporalis muscle wasting indicate?

A

consider Lower motor neurone Facial nerve (e.g. Bells palsy)

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2
Q

What happens when a person with myotonic dystrophy tries to shake hands with someone?

A

They struggle to release the grip easily

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3
Q

When you present in neurology, try and be anatomical in pattern detection - give examples

A

Symmetrical vs asymmetrical
Proximal vs distal
Pyramidal vs extrapyramidal

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4
Q

Why is a symmetrical finding important to note?

A

It suggests there is a general pathology such as a syndrome as opposed to a nerve/nerve root

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5
Q

In myotonic dystrophy what would you like to do to complete the exam?

A
cardiovascular exam 
check blood sugar 
FH 
EMG 
genetic testing
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6
Q

What neuro pts tend to come to exams?

A
Parkinsons
Charcot marie tooth 
Myotonic dystrophy 
MS 
Peripheral neuropathy
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7
Q

What is associated with Myotonic dystrophy?

A
  1. Cataracts (buzz word: loss of red reflex in both eyes)
  2. Dysphagia (from weakness)
  3. Cardiac (cardiomyopathy and heart block - may need a pacemaker)
  4. Diabetes mellitus
  5. Hypogonadism (gynaecomastia/ testicular atrophy)
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8
Q

What investigations would you like for myotonic dystrophy?

A
  1. Lung function tests - to check for neuromuscular respiratory insufficiency
  2. ECG or echo (conduction block and cardiomyopathy)
  3. Fasting glucose for DM
  4. Slit lamp test for cataracts
  5. SALT assessment
  6. EMG: may show ‘dive-bomber’ potentials (this is pathopneumonic)
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9
Q

What cataracts do you get with myotonic dystrophy?

A

Christmas tree cataracts = pathopneumonic

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10
Q

What is the treatment for myotonia?

A

Phenytoin for the myotonia
but the weakness has no treatment
(avoid statins)

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11
Q

What type of genetic goup does myotonic dystrophy fall into?

A

autosomal dominant with genetic anticipation (trinucleide repeat)

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12
Q

What is genetic anticipation?

A

When a condition presents earlier and is more severe in the later generations

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13
Q

Conditions with genetic anticipation

A

Myotonic dystrophy
Huntingdon’s chroea
Freidrick’s ataxia

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14
Q

What are the differentials for bilateral ptosis?

A
  • Myaesthenia gravis
  • Myotonic dystrophy
  • Bilateral Horner’s and bilateral 3rd nerve palsy (although these would be very rare
  • congenital
  • Neurosyphillis (but isn’t really seen anymore)
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15
Q

What is the cause for Argyll Robetson pupil?

A

Syphillis

Diabetes

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16
Q

What is an Argyll Robertson pupil?

A

A pupil which does not constrict when exposed to bright light but does constrict when focusing on a near object

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17
Q

What is the antibody against in myaesthenia gravis?

A

Acetylcholine receptor on the post synaptic membrane

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18
Q

What tumours are associated with myasthenia gravis?

A

Thymoma (look for on a CT scan)

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19
Q

Why do pts with myasethenia struggle to chew food?

A

It is a repeated movement

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20
Q

What is the treatement for myasthenia gravis?

A

Pyridostigmine (Ach-esterase inhibitors)
2nd line: add immunosuppression (steroids)
- consider thymectomy

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21
Q

What is the diagnostic test for myasthenia gravis?

A

The Tensilon test

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22
Q

What is another name for the tensilon test?

A

Edrophonium test

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23
Q

Lambert-Eaton myasthenic syndrome (LEMS)- what is the anti body against in this condition?

A

pre-synaptic membrane antibody to the Ca2+ receptor

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24
Q

LEMS is a _____ syndroem associated with ___ cancer

A

Paraneoplastic

small cell lung cancer

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25
Q

How do you differentiate between LEMS and Myasthenia gravis?

A

LEMS - has no eye involvement and you also get stronger the more you do something (they start of weak and get stronger)

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26
Q

What is the treatment for small cell lung cancer?

A

Poor prognosis - as there is no surgical cure, there is chemo but only extends the lifespan a few years
- this is because by the time it is detected it is often metastasised

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27
Q

What are the differentials for proximal myopathy?

A
  1. Diabetic amyotrophy (painful quads wasting) - will not see irl, but comes up in SBA - it is unilateral proximal myopathy
  2. Cushings
  3. Thyrotoxicosis
  4. Hypocalcaemia/osteomalacia - hence kidney failure can cause it as a secondary complication), vit D def (osteomalacia can cause it)
  5. Polymyositis
  6. Polymyalgia rheumatic
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28
Q

What blood test is important to order in any muscular pathology?

A

CK

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29
Q

What condition can be assocaited with PMR?

A

temporal arteritis

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30
Q

What signs do you get with hypocalcaemia?

A
CATS go numb 
Convulsions 
Arrhythmia 
Tetany 
and
numbness
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31
Q

How can you confirm miosis in a and e?

A

Put some 4% eye drops and the eye fails to dilate

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32
Q

What are the differentials for Horner’s syndrome?

A

Apical lung pathology (invades the sympathetic plexus):

  • Pancoast’s tumour
  • Thyroid mass
  • Mediastinal mass
  • Cervical rib
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33
Q

What is the name for this:
On looking to the right, the right eye abducts normally but the left eye is unable to adduct. The right eye has a nystagmus

A

Intranuclear ophthalmoplegia

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34
Q

What is the best way to detect nystagumus in intranuclear ophthalmoplegia (INO)

A

Start at the point between the eyebrows to use your peripheral vision

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35
Q

Where is the lesion in intranuclear ophthalmoplegia?

A

In the medial longitudinal fasciculus

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36
Q

What is normal in Intranuclear ophthalmoplegia?

A

Convergence - the eye can look inwards

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37
Q

What is the most likely cause of Intranuclear ophthalmoplesia?

A

MS - lesion in the medial longitudinal fasiculus (a stroke could also cause it if the stroke location affects the (MLF)

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38
Q

What eye conditions are associated with MS?

A

INO

Optic nerve damage

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39
Q

What are the signs of optic nerve damage?

A

Central scotoma
RAPD (relative afferent pupillary defect)
Colour and visual acuity loss
optic atrophy

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40
Q

What is a central scotoma?

A

A blind spot that covers the centre of ones vision

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41
Q

What is the eponymous name for a RAPD?

A

Marcus gun

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42
Q

What are the DDx for RAPD?

A

Optic neuritis

Total retinal detachment

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43
Q

In INO is the nystagmus in the affected or the normal eye?

A

The normal eye

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44
Q

What is Lhermittee’s phenomenon?

A

Electric shocks going down their back when they bend their neck forwards

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45
Q

What is Uthoff’s phenomenon?

A

Heat making the neuro symptoms worse

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46
Q

What is this phenomenon? -

Heat making the neuro symptoms worse

A

Lhermitte’s

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47
Q

What is this pneumenon?

Electric shocks going down their back when they bend their neck forwards

A

Uthoff’s

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48
Q

What causes Uthoff’s phenomenon?

A

Neurological condution is reduced at higher temps

In demyelination - the problem is the speed of conduction, so it get exacerbated in heat

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49
Q

What are DDx for demyelination?

A
  • HIV
  • CIDP (chronic inflammatory demyelinating polyneuropathy)
  • multiple myeloma
  • MGUS
  • Charcot Marie Tooth (type 1 and 3 are demyelinating)
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50
Q

What is chronic inflammatory demyelinating polyneuropathy a fancy name for?

A

Chronic Guillaine barre syndrome

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51
Q

Why does a patient with a 3rd nerve eye palsy need urgent CT angiogram of the brain?

A

Because a cause is Posterior communicating artery aneurysm (PCAA) - the posterior communicating artery runs right next to the 3rd nerve

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52
Q

What is Trousseau’s sign?

A

For hypocalcaemia- when you inflate the BP cuff, they get a painful contraction of the MCP joint on the same side as well as ADduction of the thumb

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53
Q

What is Webber syndrome?

A

3rd nerve palsy on one side and hemiplegia on the other side - it is caused by a midbrain infarct or bleed

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54
Q

What artery is involved with Webber’s syndrome?

A

The posterior cerebral artery

also near the 3rd cranial nerve nucleus

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55
Q

Which fracture in the brain causes rhinorrhoea and why?

A

Basal skull fracture - you get CSF leaking from the nose

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56
Q

How can you tell between a surgical or medical third nerve palsy?

A

surgical - the pupil is blown

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57
Q

Why does a surgical 3N palsy cause the pupil to be blown?

A

The entire nerve is compressed
as well as the parasympathetic fibres which run alongside the 3rd CN are affected - the cause of this could be an aneurysm for example and hence is a surgical
(the pupil wall also not respond to light and accommodation and the eye will be down and out)

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58
Q

What are the causes of a medical 3rd nerve palsy?

A

Mononeuritis multiplex - caused by Diabetes or HTN
(mononeuritis multiplex means inflammation of a single nerve)
- MS/demyelination can also causes a mononeuritis multiplex
- mass lesion or compression along the route/course of the nerve

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59
Q

Why can the pupil still constrict in a medical cause of 3N palsy?

A

In medical causes it is the vascular supply of the nerve which is affected but the parasympathetic occulomotor fibres have their own blood supply and so may be spared- the pupil can still react to light and accommodation but will be down and out

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60
Q

which 3N palsy is more likely to have a complete ptosis (rather than a partial one? - surgical or medical?

A

Surgical (complete compression of the nerve, hence dilated pupil and complete ptosis)

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61
Q

What are causes for dilated pupil 3N palsy (i.e. a surgical 3N palsy?

A

tumour
dissection
Posterior communicating artery aneurysm- this is the classic cause (PCAA)

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62
Q

How can you describe a 3N palsy in PACES terms?

A

the globe is down and out in the primary position

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63
Q

Why is it important to find out when the diplopia (double vision) is the worst?

A

If it is complex ophthalmoplegia with multiple muscle groups involved it can help work out the differential

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64
Q

If someone has diplopia and you cover up the affected eye, which of the two images should disappear?

A

The outer image of the two

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65
Q

If someone has a 3rd nerve palsy what investigations are good to check?

A
  1. the BP
  2. the capillary glucose
  3. examine for 4th N palsy
  4. if the pupil is dilated - then CT scan and angiography
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66
Q

If someone has a medical 3N palsy what is the management?

A

conservative - self-resolving in 3 months, can give them prism glasses in then mean time (to correct the double vision)

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67
Q

What is the job of the 4th cranial nerve?

A

to move the eye down and in

think - trying to read a book

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68
Q

Which cranial nerves does cavernous sinus syndrome invovle?

A

III
IV
V1 (first division of the 5th nerve)
VI

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69
Q

When should you consider cavernous sinus syndrome?

A

If there is 3rd and 4th nerve palsy

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70
Q

How can you check for a 4th nerve palsy in a patient who has a 3rd nerve palsy?,

A

Ask the patient to look down and you will notice the eye adduct slightly (by looking at the capillaries of the inner eye and noticing that they move into the eye socket

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71
Q

In a simple 4th nerve palsy in what position will the eye be?

A

Up and out (in the primary position)

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72
Q

If someone has a 3n Palsy why is it so important to check for a 4th nerve palsy too?

A

to make sure there is nothing in the cavernous sinus

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73
Q

What does ‘It’s a 4th nerve palsy…. Look away!’ - help you to remember?

A

The pateint will have a head tilt AWAY from the side of the 4th nerve (away from the affected side)

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74
Q

In a 4th nerve palsy, when will the diplopia be worst?

A

when they look down and in (depress and adduction) - i.e. when trying to read a book or trying to walk down stairs
- it is worst at this point because the action of the 4th nerve is to look down and in and they are unable to (which is why the eye is up and out in the primary positon)

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75
Q

What is the most common cause of 4th nerve palsy and why?

A

Trauma this is because the fourth nerve runs along the tentorium along the base of the skull

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76
Q

What are causes of 4th nerve palsy?

A

Trauma
mononeuritis multiplex
Congenital

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77
Q

What are the causes of mononeutritis multiplex?

A

Diabetes
HTN
MS
Infection - Lyme disease, syphillis
Autoimmune disorders - small vessel vasculitis (e.g. polyarteritis nodosua), SLE, RA
Malignancy- haematological malignancy or anitbodies from paraneoplastic syndromes

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78
Q

How can you detect a 6th nerve palsy

A

When they look to the side, the affected eye cannot look laterally
e.g. upon looking right, the right eye cannot loow to the right

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79
Q

What are the most common causes of 6th Nerve palsy?

A

HTN and DM

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80
Q

What is a false localising sign?

A

6th nerve is the longest intracranial nerve and so anything which raises the intracranial pressure , the 6th nerve will feel the stretch first - this could Mean that a 6th nerve palsy on the right side does not necessarily mean the issue was on the right (e.g. It could be a tumour on the left causing raised intracranial pressure and that just happens to develop a right-sided 6th nerve palsy)

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81
Q

What should you do once a 6th nerve palsy has been detected?

A
  1. Examine CN 7 and 8 for nerve palsys and examine the cerebellar system -to check for cerebellarpontine angle tumour (CPA)
  2. Fundoscopy - check for papilloedema (sign of raised ICP)
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82
Q

What is the cerebellar pontine angle and why is it important ?

A

It is space where the 6th nerve runs through and is there is a tumour there it can cause a 6th nerve palsy

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83
Q

What are the DDx for a 6th nerve palsy?

A
DM and HTN 
ICP 
Demyelination (MS) 
Mass 
Vascular
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84
Q

Why is the forehead spared in an Upper motor neurone cause of facial nerve palsy?

A

Because both hemispheres a supply nerve to the facial muscles (in the top half of the face)

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85
Q

What is Bell’s phenomenon?

A

The eyes rolling up when you ask the patient to close them (this is seen in Bells palsy (LMN facial palsy)

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86
Q

Why do patients with facial nerve get hyperacusis

A

Strapedius muscle reduces vibration to protect from loud noises- if it is not working then patients get hyperacusis

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87
Q

Which part of taste does the facial nerve supply?

A

Anterior 2/3rds

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88
Q

What are the causes of facial nerve palsy?

A
  1. Viral/idiopathic
  2. Damage to the nerve - facial trauma
  3. Infection (herpes Zoster)
  4. Compression/ mass lesion e.g. Parotic tumour/ tumour in the cerebellarpointine angle
  5. Otitis media (check ear with otoscope)
  6. Forceps delivery (trauma)
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89
Q

What is the most common cause of an UMN facial nerve palsy?

A

Stroke

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90
Q

Why do facial nerve palsy patients require referral to ENT?

A

To rule out cholesteatoma and acoustic neuroma (MRI brain)

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91
Q

What is the management of LMN facial palsy?

A

Self-limiting - recovery in 6 months
Eye drops and patch (because or corneal irritation or corneal scarring)
Steroids (if presented within 72 hours)
Referral to ENT surgeon for further assessment

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92
Q

What is the first sign of a cerebellarpointine angle lesion?

A

loss of corneal reflex

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93
Q

What are the signs of cerebellarpontine lesion?

A
  1. loss of corneal reflex
  2. failure to ABduct eye (6th nerve palsy)
  3. sensorineural hearing loss (8th nerve)
  4. Facial sensation loss
  5. Cerebellar signs
    the nerves involved = 5 to 8
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94
Q

What are the complications of facial nerve palsy?

A

Synkinesis of facial muscles

crocodile tears phenomena

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95
Q

What is synkinesis?

A

Wrong muscle groups activated

-if you want to close your eyes, you might clench your jaw instead

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96
Q

What is crocodile tears phenomena?

A

When they are eating, instead of salivating, they cry because the facial nerve has healed badly

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97
Q

What are the features of MS in PACES?

A
  1. Hemiplegia - similar to stroke
  2. Female
  3. Catheterised
  4. Eye signs
  5. Cerebellar signs
  6. Ataxic (unable to to hell-toe walk)
  7. UMN signs - pyramidal weakness (flexors stronger in the arms and in the legs extensors stronger) and brisk reflexes
  8. Dorsal column disease- reduced vibration, proprioception, Romberg’s positive
How well did you know this?
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2
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98
Q

What is the best way to pick up ataxia in PACES?

A

Heel-toe walk

99
Q

What is Romberg’s test?

A

Ask themselves to close their eyes - they will unstable, because they are using visual input to stabilise themselves, which is what Rombergs means

100
Q

If there are cerebellar signs, dorsal column signs and pyramidal weakness then what is the condition?

A

demyelinating condition such as MS

101
Q

If suspecting MS, make sure to suggest fundoscopy - what are you looking for?

A

Pale disc - optic neuritis

102
Q

In MS, what are you looking for on LP?

A

IgG Oligoclonal bands

103
Q

What are the features of organophosphate poisoning?

A
Constricted pupils 
Hypersalivation 
Sweating 
Diarrhoea 
Bradycardia 
(treatment is atropine)
104
Q

Why do the pupils constrict in organophosphate poisoning?

A

Because they are acetylecholinesterase inhibitors

105
Q

In Opiate overdose why do you check CK level?

A

You can get Rhabdomyolysis

106
Q

What are the differentials of bitemporal hemianopia?

A

Pituitary tumour and Craniophayngioma

107
Q

Which drug can cause cerebellar syndrome?

A

Phenytoin toxicity

in the Q it may mention an enzyme inhibitor/ a patient with epilepsy

108
Q

What is the pneumonic for causes of cerebellar signs (i.e. the DANISH signs)?

A

PASTRIES

109
Q

Expand the PASTRIES pneumonic for cerebellar signs

A
P - paraneoplastic 
A - alcohol 
S - multiple sclerosis 
T - tumour 
R -  rare (e.g. Freidreich's ataxia) 
I - Iatrogenic (classically phenytoin)  
E - endocrine - hypothyroidism 
S - stroke
110
Q

How can nystagmus help you localise a cerebellar lesion?

A

The fast saccade is towards the lesion

111
Q

What gait do you get in Freidreich’s ataxia and why?

A

Stamping gait as there is loss of proprioception and vibration

112
Q

What conditions cause UMN and LMN signs?

A

Freidreich’s ataxia

Motor neuron sign

113
Q

What does synkinesis mean in reference to Parkinson’s disease?

A

If you want to exacerbate a symptom, ask them to do something on the other side
e.g. to exacerbate a tremor on the left hand ask them to tap their knee using their right hand

114
Q

What would you do to complete the examination of Parkinson’s syndrome ?

A

DH
Lying and standing BP (checking for MSA)
Examine the cranial nerve (Checking for PSP)

115
Q

What are the differntials of Parkinsons disease?

A
Drug-induced 
MSA 
PSP 
Lewy body dementia 
CBD
116
Q

What drugs can cause Parkinsonism?

A

Metoclopramide

Antipsychotics

117
Q

How do you diagnose motor neurone disease?

A

It is a clinical diagnosis (the tests will be negative if you do them)

118
Q

In MND, where do you classically get UMN signs and LMN signs?

A

UMN in the lower limb,

LMN in the upper limb

119
Q

What are the differentials for bulbar palsy?

A

MND
Syringobulbia
Polio
Guillaine-Barre Syndrome

120
Q

What are the features of subacute combined degeneration of the spinal cord?

A

Peripheral neuropathy

Dorsal column loss - upgoing plantars and loss of ankle jerk

121
Q

if you had a patient with profound B12 deficiency, what should you consider?

A

IBD - diarrhoea

Pernicious anaemia

122
Q

What condition can B12 deficiency cause?

A

Subacute combined degeneration (progressive degeneration of the spinal cord due to B12 defiency)

123
Q

Where is the lesion in lateral medullary syndrome?

A

PICA - posterior, inferior cerbellar artery

124
Q

What are the features of lateral medullary syndrome?

A

Ipsilateral Horner’s syndrome, cerebellar
Ipsilateral cranial nerve: trigeminal pain and temperature
Contralateral pain and temperature below the lesion

125
Q

What is the rule of 4s when it comes to cranial nerve?

A

4 in each section
(outside) - CN 1 + 2 /Midbrain CN3 + 4
Pons CN 5, 6, 7, 8
Medulla 9, 10, 11, 12

126
Q

What is the rule of 12s when it comes to cranial nerves?

A

The factors of 12 run laterally 3, 4, 6, 12

The non-factors of 12 run medially

127
Q

What is the rule of S and M (sensory and motor)?

A

The motor tracts travel medially 3,4,6,12
M = M
The sensory tracts travel laterally 5,7,8,9,10,11

128
Q

To detect foot drop, how should you ask the patient to walk?

A

On their heels

129
Q

Every small muscle of the hand is supplied by the ulnar nerve except for which?

A
LOAF muscles 
Lateral lumbricals (radial lumbricals) 
Opponens pollicis 
Abductor pollicis brevis 
Flexor pollicis brevis
130
Q

What test do you want to do in a peripheral neuropathy?

A

A nerve conduction study

131
Q

Peripheral neuropathy can be sensory, motor or autonomic - state which are more likely to be sensory

A

DM
Alcohol
B12
Hypothyroid

132
Q

Peripheral neuropathy can be sensory, motor or autonomic - state which are more likely to be motor

A

Chronic guillaine Barre

Lead poisoning

133
Q

What are the features of ulnar nerve palsy?

A

Claw hand
The 3rd and 4th digits are hyperextended
ulnar deviation of the little finger (wartenberg’s sign)

134
Q

What is the ulnar paradox?

A

The higher the lesion is, the less deformity they have

135
Q

If there is loss of sensation over the hypothenar eminence what does that mean?

A

The ulnar nerve injury is above the wrist

136
Q

What are the causes of carpel tunnel syndrome?

A
Acromegaly 
Diabetes mellitus 
Amyloid (due to multiple myeloma) 
Hypothyroid
Pregnancy
137
Q

Lucid interval - suggest what head injury?

A

Extradural

138
Q

What is the classic presentation of subdural haemorrhoage?

A

Recurrent falls

Gradual decline

139
Q

What haemorrhage causes a lens-like haematoma?

A

Extradural - like a lemon
Lemons are extra
(Convex)
look for midline shift

140
Q

What shape is a subdural on CT scan?

A

Crescent (Concave)

look for midline shift

141
Q

Why are alcoholics and elderly patients more at risk of subdurals?

A

They have cortical atrophy- so there is a bit more space in the brain - more easy for the veins to be ripped and damaged

142
Q

Parkinsonism features + sudden memory deterioration _ urinary incontinence suggests what condition? (Wet, Wacky and Wobbly)

A

Normal pressure hydrocephalus

Incontinence, Dementia, gait abnormality

143
Q

What does hydrocephalus mean?

A

Enlarged ventricles on brain imagine

144
Q

What causes normal pressure hydrocephalus?

A

Failure to reabsorb CSF in the subarachnoid space (e.g. long term complication after meningitis or subarachnoid haemorrrhage)

Look for signs of raised ICP - papilloedema on fundoscopy

145
Q

What is the treatment for normal pressure hydrocephalus?

A

Lumbar puncture to remove the fluid

Shunt

146
Q

Name 3 medications used to treat dementia early on

A

(acetylcholinesterase inhibitors)
Donezepil
Rivastigmine
Galantamine

147
Q

What medication is used to treat moderate-severe dementia?

A

Memantine

148
Q

What causes Wernicke’s encephalopathy?

A

Thiamine B1 deficiency (associated with alcohol use or repeated vomiting)

149
Q

What is the triad of Wernicke’s encephalopathy?

A

Confusion
Ataxia
Ophthalmoplegia (usually Nystagmus or INO or CN6 palsy)

150
Q

Damage to which part of the brain shows up on Wenicke’s encephalopathy brain MRI?

A

Mamillary bodies

151
Q

What kind of amnesia do you get with Korsakoff syndrome?

A

Retrograde as well as antegrate but retrograde is more common

152
Q

How long after a GI infection will Guillaine Barre present?

A

2-3 weeks

153
Q

Patients with Guillaine Barre can get Ascending paralysis (starting distally) along with paraesthesia
What might patients with paraesthesia say?

A

It feels like they are walking on air

154
Q

What are the autonomic disturbances you can get in Guillaine Barre and why is important to look out for them?

A

Sweating
Urinary incontinence
Cardia rhythm - important as they can get SVT (put them on a cardiac monitor to check for arrhythmia)

155
Q

What antibodies is Guillaine BS assocaited with?

A

anti-GM1 = anti-ganglioside antibodies

156
Q

What is the finding in the CSF of Guillaine Barre?

A

Increased protein in the CSF

157
Q

Why do patients with Guillaine Barre require lung function tests and ABG?

A

Once the paralysis ascends high enough and hits the resp muscles then the forced vital capacity reduces
FVC below 1.5L then consider ITU

158
Q

What investigations do you want in Guillaine Barre?

A
Stool culture (campylobacter) 
Check bulbar function (aspiration risk) 
ECG 
FVC
ABG 
LP 
Antibody testing - anti-GM1
159
Q

What is the Rx for Guillaine Barre? and when is it indicated?

A

IVIg or plamsa exchange - if they are unable to walk

160
Q

What is the other name for Guillaine Barre?

A

Acute inflammatory demyelinating polyneuropathy (AIDP)

161
Q

What is the long term consequence of Guillaine Barre?

A

It can become permanent

Chronic inflammatory demyelinating polyneuropathy (CIDP)

162
Q

When you have a first generalised tonic clonic seizure, what is the treatment?

A

NONE!

You don’t treat them only investigate

163
Q

What is the criteria to diagnose epilepsy?

A

2 unprovoked seizures more than 24 hours apart

164
Q

What is status epilepticus definition?

A

Continuous or repeated seizures over 30 mins without regaining consciousness

165
Q

How long does Todd’s paresis last?

A

<48 hours - mimicking a stroke

166
Q

Which location in the brain is associated with Partial seizures?

A

Temporal lobe

167
Q

What is the criteria to perform a CT head <1 hour at presentation into hospital?

A
  1. GCS <13 on initial assessment, or GCS <15 at 2h following injury
  2. Focal neurological deficit
  3. Suspected open or depressed skull fracture, or signs of basal skull fracture:
    - periobital ecchymoses (‘panda’ eyes/racoon sign)
    - postauricular ecchymosis (Battle’s sign)
    - CSF leak through nose/ears
    - haemotympanum.
  4. Post-traumatic seizure.
  5. Vomiting more than once.
168
Q

What is the criteria to perform a CT head <8 hour at presentation into hospital?

A

Any loss of consciousness or amnesia AND any of:

  1. age ≥65
  2. coagulopathy
  3. high-impact injury e.g:
    - struck by or ejected from motor vehicle;
    - fall >1m or >5 stairs
  4. retrograde amnesia of >30min.
169
Q

What makes a seizure complex vs simple?

A

Complex- there is impaired consciousness

170
Q

What is the treatment for seizures with automatisms?

A

Carbamezapine

171
Q

Partical seizures starting with an automatism can often progress to which seizure type?

A

Tonic -clonic

172
Q

Pseudoseisures/ psychogenic seizures - what are they? and how can you differentiate between a fake and real one?

A

They are entirely in the patients mind

  • they are awake
  • no post ictal phase
  • prolactin/lactate
  • in patient video EEG - you need to capture the event at the same time –> this is the definitive diagnosis
173
Q

Which epilepsy would you avoid carbamazepine in? a

A

Absence seizures - it can make them worse

174
Q

What is another name for absence seizures?

A

Petit mal

175
Q

What is first line for partial seizures?

A

Carbamezapine

176
Q

What is first line for generalised seizurers?

A

Valporate

177
Q

What are the side effects of valporate?

A

Tremor and weight gain

it causes neural tube defects

178
Q

What are the side effects of carbamezapine

A

Neutropenia
SIADH (common)
enzyme inducer

179
Q

What are the side effects of phenytoin?

A

Cerebellar syndrome (in toxicity)
Gum hypertrophy
Facial coarsening

180
Q

Which AED does not interact with the CYP enzymes?

A

Levetiracetam

181
Q

If you have had a single seizure and you have not been diagnosed with epilepsy yet (and brain scan/EEG is normal) then how long do you have to wait to drive (compared to those with epilepsy)?

A

6 months

if epilepsy - then 12 months of being seizure free before you can drive

182
Q

What are 2 important considerations in epilepsy counselling?

A

Contraception

Dont bathe alone

183
Q

Which meningitis can cause a raised CSF?

A

Bacterial

TB - can be raised or normal

184
Q

How can you differentiate between TB and viral meningitis on CSF?

A

Both are lymphocyte predominant
But
TB will have reduced glucose

185
Q

What is the commonest cause of meningitis?

A

Viral

186
Q

If you see a gram negative diplococcus on blood culture, what should you think?

A

Neiseria meningococcus

187
Q

What are the 2 clinical signs for meningitis?

A

Kernig’s sign - hip and knee both flexed to 90 degrees and then extend the knee causes pain

Brudzinski’s sign - flexion of the neck causes the patients hip and knee to flex
(both are a sign meningeal irritation)

188
Q

Which patients are more likely to have strep pneumoniae as the causes of meningitis?

A

Alcoholics
Elderly
Skull fracture

189
Q

Which patients are more likely to have Listeria as the causes of meningitis?

A

Pregnancy (unpasturised dairy such as milk)
Alcoholics
Immunocompromised

190
Q

Which patients are more likely to have Cryptococcus as the causes of meningitis?

A

HIV (this is an AIDS defining illness)

191
Q

What is the most common cause of encephalitis?

A

HSV1

192
Q

How can Encephalitis present?

A

Temporal love signs - e.g. aphasia

193
Q

How can you elicit sciatic pain?

A

Straight leg raising

194
Q

What is the cause of cauda equina?

A

Disc herniation

Tumour

195
Q

What investigation is needed urgently in cauda equina?

A

MRI

196
Q

What is papilloedema?

A

Sign of raised ICP -

197
Q

What basic obs do you need for papilloedema (and state why)?

A

BP - malignant HTN

Temperature - meningitis

198
Q

What investigations for raised ICP?

A

Neuro exam + CN exam
Bloods - look for inflammation
Urgent brain imaging - if this is normal then check LP opening pressure

199
Q

Why is LP opening pressure so important to check in raised ICP if there is normal brain imaging?

A

Idiopathic/benign intracranial HTN

- papilloedema and raised ICP

200
Q

What are the causes of raised ICP?

A

SOL
Infection
Thrombosis
Hydrocephalus

201
Q

What is the opening pressure in Idiopathic/benign intracranial HTN?

A

> 25

202
Q

What drug is Idiopathic/benign intracranial HTN associated with?

A

Idiopathic/benign intracranial HTN

203
Q

What is the treatment for Idiopathic/benign intracranial HTN?

A

Ventricular periotoneal shunt

Long term - ophthalmplogy follow up - can lose their sight

204
Q

What drug is associated with Idiopathic/benign intracranial HTN?

A

COCP

205
Q

How does Cerebral venous sinus thrombosis present and what is it?

A
It is like a DVT (clot in the veins) 
Presents with Headache and papilloedema 
Signs of raised ICP 
Remember Cushing's reflex 
(Hypotension, bradycardia and irregular breathing)
206
Q

How do you diagnose a Cerebral venous sinus thrombosis?

A

MRI with MR venography

207
Q

How do you differentiate by Hx /examination between Idiopathic/benign intracranial HTN and cerebral venous sinus thrombosis?

A

Idiopathic/benign intracranial HTN - is gradual onset, central scotoma, no meningism, gradual loss of vision because of the papilloedema

Cerebral venous sinus thrombosis - more acute, meningism - normal CT head

208
Q

What is the treatment for cerebral venous sinus thrombosis?

A

LMWH

209
Q

How does spinal stenosis present?

A

Back/leg pain worse on walking
Buttock pain, paraesthesia
Eased by walking uphill/ leaning forward

210
Q

Anterior spinal artery occlusion - where is the infarct?

A

Vertebrobasilar artery

211
Q

Which sensation modalities are lost in anterior spinal artery occlusion and why?

A

Pain and temp as it is the anterior part of the spinal chord
(dorsal columns spared)

212
Q

How does Brown sequard syndrome present?

A

Loss of pain and temp on the opposite side (contralateral)

Loss of proprioception and vibration sense on the ipsilateral side (same side)

213
Q

What 3 medications are for acute management of migraine?

A

Sumitriptans
Anti-emetic
NSAID/paracetamol

214
Q

What medications are given for prophylaxis of frequent migraines? and which is teratogenic?

A

Propanolol (commonly used)
Pizotifen
Verapamil
Topiramate (teratogenic)

215
Q

Which patients with migraines typically receive prophylaxis?

A

More than 2 a month

216
Q

Nasal triptans can be used from which age?

A

> 12 yo

217
Q

How can asking a patient what they do when they get a headache, help to differentiate the headache type?

A

Migraine - sits down in a dark room

Cluster headaches - patients get relief by walking around

218
Q

Which conditions causes amaourgis fugax?

A
TIA 
Temporal arteritis (GCA)
219
Q

Where is the pain in cluster headaches?

A

Behind the eye

220
Q

What is the treatment for cluster headaches?

A

100% oxygen and triptans

221
Q

In subarachnoid headache - what should you be looking out for in the PMH of the pt?

A

Renal failure - it is associated with PCKD (berry aneurysms)
Tall patient - Marfan’s disease

222
Q

How do you diagnosis subarachnoid haemorrhage?

A

Non-contrast CT (if this is normal)

then do a LP for xanthcochromia (>12 hours after the headache onset as the RBCs need enough time to breakdown)

223
Q

What is the treatment of subarachnoids?

A

Neurosurgery - they clip or coil to stop the bleed

Then they are started on Nimodipine (60mg every 4 hours)

224
Q

What does Nimodipine do for subarachnoid?

A

Prevents vasospasm of the cerebral arteries

225
Q

What is the IVx of choice for Trigeminal neuralgia?

A

MRI brain - looking for something compressing the trigeminal nerve

226
Q

What is the definitive IVx for GCA?

A

Temporal artery biopsy

227
Q

Why are steroids given immediately in GCA?

A

To prevent the blindness

228
Q

What are the features of a ICP headache?

A

Worse at night and on waking
Coughing and straining
N and V
VIsual disturbance

229
Q

What is the treatment for raised ICP?

A

Mannitol and Hypertonic saline (will done in ITU

230
Q

How can you find out if it is true vertigo?

A

Is the room spining or do you feel light-headed

light-headed is more pre-syncope

231
Q

If it is true vertigo, waht other question to you need to ask?

A

Is there hearing loss

232
Q

What are the differentials for Vertigo?

A

BPPV (benign paroxysmal positional vertigo)
Meniere disease
Viral labyrinthitis (most common cause)

233
Q

Which is the vertigo differentials have hearing loss?

A

Meniere’s disease

234
Q

What are the features of meniere’s disease

A

Vertigo
Hearing loss
Tinnitus
Feeling of fullness/pressure in the ear

235
Q

Which are patients with meniere’s disease restricted from doing?

A

Driving

236
Q

How do you treat tinitus?

A

Betahistine

237
Q

What is the treatment for choice for vertigo?

A

Prochlorperazine

238
Q

What are the features of vertebrobasillar ischaemia?

A

Posterior circulation of the brain is affected - cerebellum and brain stem)
Vertigo (triggered by head position)
Hemifacial weakness and contralateral peripheral weakness/paraesthesia
(right sided ischaemia would cause right sided hemifacial numbness but the peripheral nerves for sensation and motor would have crossed by that stage so you get paraesthesia on the contralateral side in the peripheral nervous system)

239
Q

in both RA and OA there is joint swelling but the swelling feels different in what way?

A
RA = soft 
OA = hard
240
Q

In OA you can also get morning stiffness, so how can you differentiate between OA and RA with morning stiffness?

A

OA- lasts LESS 30 mins

RA - a lot longer than that

241
Q

Which bloods are normal in OA?

A

ESR, CRP, FBC, ALP = all is normal!

242
Q

What is the management of OA?

A
MDT - PT/OT 
Exercise -disuse atrophy 
Weight reduction 
NSAIDs/Cox-2 inhibitors (joint injections) 
Surgery - if severe symptoms 
Knee locking - arthroscopy and wash out
243
Q

What is the aim of the surgery in OA?

A

To reduce the pain, NOT to improve the function (although reduced pain may help them to walk further)

244
Q

What are the causes of gout?

A
  1. Increased cell turn over
    - Haemolysis
    - Psoriasis
    - Myeloproliferatives
  2. Tumour lysis syndrome
  3. Underexcretion
    - Renal failure
    - Diuretics