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Phase 3a > Neurology > Flashcards

Neurology Flashcards

1
Q

Which body parts fall into the territory of the anterior cerebral artery in the sensory and motor cortices?

A

Trunk, legs, feet

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2
Q

Which body parts fall into the territory of the middle cerebral artery in the sensory and motor cortices?

A

Arms, head and neck

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3
Q

What fasciculi are within the dorsal column? Which is medial and which is lateral?

A 
Medial = Gracile fasciculus
Lateral = Cuneate fasciculus
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4
Q

What sensory/motor role does the dorsal column have?

A

Fine touch + proprioception (sensory)

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5
Q

Where does the sensory input for the gracile fasciculus of the dorsal column come from?

A

Lower limbs

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6
Q

Where does the sensory input for the cuneate fasciculus of the dorsal column come from?

A

Upper limb

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7
Q

What are the 3 neurones involved in the dorsal column tract?

A

Dorsal root ganglion - gracile/cuneate nucleus (medulla)
Gracile/cuneate nucleus - ventral posterolateral thalamus
ventral posterolateral thalamus - post-central gyrus

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8
Q

Describe the path of the first neurone in the dorsal column tract

A

Sensory neurones in limbs and dorsal root gangion outside spinal cord
Enters gracile and cuneate fasciculi in spinal cord
Goes up to ipsilateral gracile and cuneate nuclei in medulla oblongata

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9
Q

Describe the path of the second neurone in the dorsal column tract

A

Gracilie/cuneate nuclei - decussates in pyramids
Travels through medial lemniscus of the pons
Reaches ventral posterolateral nucleus of thalamus

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10
Q

Describe the path of the third neurone in the dorsal column tract

A

Ventral posterolateral nucleus of thalamus to post-central gyrus in brain (sensory cortex)

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11
Q

What role does the spinothalamic tract have?

A

Pain, temperature and crude touch (sensory)

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12
Q

Where are the 3 neurons in the spinothalamic tract?

A

Sensory neuron/dorsal root gangion - dorsal horn of grey matter
Dorsal horn - contralateral thalamus
Thalamus - post-central gyrus

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13
Q

Describe the path of the 1st neuron of the spinothalamic tract

A

Sensory neuron/dorsal root ganglion
Enters spinal cord through Lissauer’s fasciculus
Ascends in spinal cord by 1 or 2 segments
Synapses in dorsal horns of grey matter

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14
Q

Describe the path of the 2nd neuron of the spinothalamic tract

A

Dorsal horn of grey matter - decussates in Anterior White Commissure at same level
Ascends through spinal cord and brain stem
Synapses at thalamus (contralateral to dorsal horn)

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15
Q

Describe path of 3rd neuron of spinothalamic tract

A

Thalamus to post-central gyrus

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16
Q

What is the role of the corticospinal tract?

A

Axial and limb motor

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17
Q

What is the role of the lateral corticospinal tract?

A

Limb motor

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18
Q

What is the role of the anterior corticospinal tract?

A

Axial motor

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19
Q

Describe the path of the lateral corticospinal tract

A

Pre-central gyrus (motor cortex) - internal capsule - brainstem
75-90% corticospinal tract decussate at pyramids (lateral corticospinal)
Descend through spinal cord and synapse at anterior horn cell
Lower motor neuron from anterior horn cell to limb muscles

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20
Q

Describe the path of the anterior corticospinal tract

A

Pre-central gyrus (motor cortex) - internal capsule - brainstem
10-25% do not decussate at pyramids (anterior corticoospinal)
Descend to level in spinal cord where decussates through anterior white commissure
Synapses at contralateral anterior horn cell
Lower motor neuron from anterior horn cell to axial muscles

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21
Q

Give 4 nerve endings for fine touch

A

Pacinian corpuscle
Meisner’s corpuscle
Ruffini endings
Merkel endings

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22
Q

What 3 tests do you do for a mini neurological exam?

A

General appearance + vital signs
GCS
Lateralising signs
Pupil reflexes

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23
Q

What are the 3 domains of the Glasgow Coma Scale?

A

Best Motor Response
Best Verbal Response
Best Eye-opening Response

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24
Q

Which of the 3 domains of the Glasgow Coma Scale is the best prognostically?

A

Best Motor Response

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25
Q

What might you do if patient is unconscious to assess them?

A

Collateral history
Mini Neurological Exam
GCS
Pupils

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26
Q

What are the criteria for the scores on BMR of GCS?

A 
6 = obeys commands
5 = Localises to pain
4 = Flexes to pain
3 = spastic flexion/withdrawal (don't use)
2 = Extends to pain
1 = None
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27
Q

What do lateralising signs tend to indicate? Give examples of lateralising signs

A

One hemisphere lesion

E.g. gaze paresis, inattention to one side, upper limb drift, asymmetrical flexion/extension

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28
Q

What causes a fixed dilated pupil?

A

Compression of parasympathetic fibres on outside of CN3, usually over petrous temporal bone

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29
Q

What shape does a subdural bleed show on imaging? Why?

A

Crescent-shaped

Low pressure venous blood causes slow bleed

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30
Q

What shape does an extradural bleed show on imaging? Why?

A

Convex shaped

Needs high pressure arterial blood to peel periosteal dura off cranium

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31
Q

What does a subarachnoid haemorrhage present with?

A

Sudden onset, severe headache - pressure on meninges
Nausea, vomiting, stiff neck, photophobia, restless, agitation
May have seizures

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32
Q

What symptom might an occipital lobe lesion cause?

A

contralateral visual defect

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33
Q

What might occur with dominant parietal lobe syndrome?

A

Confusion
Difficulty writing and reading (agraphia)
Difficulty with mathematics (acalculia)
Visuospatial impairment - 3D (agnosia)
Apraxia - inability to comprehend verbal commands and motor impairment
Contralateral sensory impairment

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34
Q

Where is Broca’s area? What is its role?

A

Dominant hemisphere frontal lobe (usually left)

Speech production

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35
Q

Where is Wernicke’s area? What is its role?

A

Dominant hemisphere temporal lobe (usually left)
Surrounds auditory cortex, close to lateral fissure
Comprehension of speech

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36
Q

What might frontal lobe lesions present with?

A

Bilateral lesion = personality

Unilateral lesion = hemiparesis

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37
Q

What might temporal lobe lesions present with?

A

Memory loss - verbal memory loss if dominant hemisphere, non-verbal if non-dominant

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38
Q

What is the general role of the basal ganglia? How might problems present?

A

General role = control of movement and reward
Too much control = rigidity
Too little = chorea

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39
Q

What is the most likely cause of sudden onset hemiparesis? Where do most of these originate?

A

Stroke

More are ischaemic - embolic from carotid bifurcation (75%) or from heart (25%)

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40
Q

What would occur if a middle cerebellar artery stroke happened? What happens instead?

A

MCA stroke = unconscious

Most strokes in this territory are perforator artery emboli affecting internal capsule

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41
Q

Where is the lesion in myelopathy?

A

Spinal cord

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42
Q

What are the features of the A fibres in peripheral nerves?

A

Long, fast, myelinated

Role: proprioception, vibration, fine touch

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43
Q

What are the features of the C fibres in peripheral nerves?

A

Short, slow, non-myelinated

Role: pain, crude touch, temperature

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44
Q

Which nerve fibres are affected first in diabetic peripheral neuropathy? What test of sensation is most sensitive for peripheral neuropathy?

A

A fibres - long fibres affected first

Therefore - VIBRATION test - picks up neuropathy before symptoms/numbness appears

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45
Q

What is the most common cause of spinal cord lesions?

A

Disc osteophytes from arthritis

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46
Q

Give a rhyme for proximal muscle weakness. What are the presenting features?

A

Can’t do hair, stair, chair
Weak grasp, handwriting and flapping gait - finer movements lost first
Fatigue

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47
Q

Where is the lesion in a radiculopathy?

A

Nerve root - initial segment of a nerve leaving the spinal cord

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48
Q

Where is the most common cervical radiculopathy? Give the dermatome and myotome distributions of these nerve roots.

A

C6 and C7
C6 dermatome = thumb, myotome = biceps
C7 dermatome = middle and index finger, myotome = triceps

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49
Q

Where are the most common lumbar radiculopathies? What are the dermatomes and myotomes affected for these nerve roots?

A

L5 and S1
L5 dermatome = big toe, dorsal foot
Myotome = dorsiflexion of foot (stand on heels)
S1 dermatome = ltitle toe, lateral and sole of foot
Myotome = plantar flexion foot

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50
Q

What features might suggest cerebellar lesion?

A

IPSILATERAL dysdiadochokinesia, ataxia, nystagmus, intention tremor, slurred speech, hyperreflexia (drunk)

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51
Q

Where are the most common sites for compression if these cranial nerves are affected together?

a) CNIII, IV, VI
b) CNVII, VIII
c) CNIX, X, XI, XII

A

a) cavernous sinus
b) petrous part of temporal bone
c) jugular foramen

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52
Q

What are features of an intracranial mass?

A

epilepsy
focal neurological signs
raised intracranial pressure - headache, dizziness, nausea, vomiting, blurred vision

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53
Q

What is the commonest cause of proximal myopathy? How might you test for proximal myopathy clinically?

A

Corticosteroid use e.g. transplant, chemotherapy, autoimmune

Stand on one leg and squat

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54
Q

If there is a lesion at a disc level, which nerve root will be affected?

A

Nerve root below

e.g. disc lesion at C6/C7 - present with C7 radiculopathy

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55
Q

What are other ways of saying “long tract signs”?

A

UMN, pyramidal, descending tract, corticospinal tract signs

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56
Q

Give some examples of long tract signs

A 
spastic gait
hypertonia, hyperreflexia
clonus + babinski
cross-adductors
Hoffman's sign
loss of fine finger movements
Deltopectoral reflex
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57
Q

What frequency is vibration sensation measured at?

A

128Hz

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58
Q

Where should pain stimulus in Best Motor and Best Eye response for GCS be done?

A

to CN distribution so not to elicit spinal reflex

e.g. behind ear and mastoid bilaterally

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59
Q

What is the formula for cerebral perfusion pressure? What should cerebral perfusion pressure be?

A

CPP = mean arterial pressure - intracranial pressure

Should be 60-70mmHg

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60
Q

Describe the relationship between intracranial volume and intracranial pressure

A

Little increase in ICP with increasing volume until decompensates
Then exponential large increase in ICP with small increase in volume

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61
Q

How long do the majority of seizures last for?

A

1-2 minutes

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62
Q

Give the management of a seizure

A

Time it! Insert nasopharyngeal airway and oxygen mask, monitor O2 sats
If >10 minutes - IV midazolam
Loading dose: IV phenytoin, valproate, levotiracetam 15 min infusion with cardiac monitoring

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63
Q

Give post-seizure management

A

U+Es
Possibly CT head
Beware of peri-ictal aspirations and risk of LRTI

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64
Q

What drug can you use for acute management of raised ICP?

A

Mannitol - 100ml 10% or 50ml 20%

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65
Q

When might hydrocortisone cover be given?

A

If on long-term corticosteroids, cover with hydrocortisone to prevent adrenal crisis

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66
Q

When might dexamethasone be given? What cautions need to be taken?

A

Given peri-operatively for tumour neurosurgery
Discontinue after 2 weeks (avoid Cushings)
Monitor blood glucose - risk hyperglycaemia
Beware of steroid psychosis

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67
Q

What risks do anticoagulants and anti-platelets have in neurology? How would you manage these?

A

Increased risk intracranial haemorrhage and chronic subdural bleeds
If pathology found, stop meds, and reverse acutely
Discuss with haematologist and only re-start if agreed by neurosurgeon

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68
Q

Give the pathophysiology of cranial diabetes insipidus. Give management

A

Decreased ADH secretion - can be feature of hypopituitarism
Excessive diuresis, thirst and hypernatraemia
Give diuresis post-surgery
Fluid-balance chart, drink to thirst, consider desmopressin

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69
Q

Why might hyponatraemia occur in neurology?

A

Water moves into plasma from cells e.g. cerebral oedema, raised ICP
Brain injury releases natriuretic peptides causing “cerebral salt wasting”
SIADH

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70
Q

What are the effects of hyponatraemia?

A

potentially life-threatening >48hrs or severe
Seizures, coma, cardio-respiratory arrest
Chronic: falls, gait problems, concentration and cognitive decline, osteoporosis

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71
Q

How would you manage hyponatraemia?

A

IV crystalloid and consider mineralocorticoid
If SIADH, either fluid restriction OR sodium replacement
Careful - Too rapid Na replacement risks central pontine myelinosis

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72
Q

How might you manage neuropathic pain?

A

Trial and error with neurotropics
Gabapentin + pre-gabalin for radicular pain
Carbamazepine - trigeminal neuralgia
Topirimate - chronic refractive head pain

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73
Q

Give the total capacity of the CSF and of the ventricles

A

CSF total = 120ml

Ventricles = 20ml

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74
Q

Give 3 functions of CSF

A

Protection (cushion)
Buoyancy - reduces pressure on base of brain
Environment for brain function and neurotransmission e.g. low K

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75
Q

What lines the ventricles and what produces CSF?

A

Ependymal cells

Choroid plexus produces CSF

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76
Q

What foramen connects 1st and 2nd ventricles to the 3rd?

A

Foramen of Monro

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77
Q

Where is the 3rd ventricle and what connects it to the 4th ventricle?

A

Between left and right thalamus

Connects to 4th via CEREBRAL AQUEDUCT

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78
Q

Where is the 4th ventricle and how does it drain to spinal canal and subarachnoid cisterns?

A

4th ventricle between pons and medulla

Drains laterally via Foramina of Luschka and foramen of Magendie medially

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79
Q

Give some presenting features of myelopathy

A

Back pain
Long tract signs - UMN signs
Loss of fine finger movements
Radiating limb pain

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80
Q

Give features of vertebral syndrome

A

Lower back pain - dull, aching

Radiating pain not as far as radiculopathy

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81
Q

Give features of radiculopathy

A

Sensory loss/pain in dermatome AND/OR motor loss in myotome

Possible back pain

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82
Q

What difference in presentation is there between L5 radiculopathy and common peroneal nerve palsy?

A

L5 radiculopathy - weakness on foot inversion

common peroneal nerve palsy - weakness on foot eversion

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83
Q

Give the features of Brown-Sequard syndrome

A

Lesion in one half of spinal cord
Ipsilateral UMN weakness below lesion
Ipsilateral loss of fine touch, proprioception and vibration below lesion
Contralateral loss of pain, temp and crude touch 1-2 segments below lesion

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84
Q

What is paracellar syndrome and what features present?

A

Pituitary tumour or mass in pituitary cellar
Upward pressure on optic chiasm - bitemporal hemianopia
Hypopituitarism

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85
Q

What are the 2 types and relative prevalence of strokes?

A

Ischaemic (85%)
Haemorrhagic (15%)
(also can be due to systemic hypoperfusion)

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86
Q

What is the WHO definition of a stroke

A

Clinical syndrome consisting of RAPIDLY developing clinical signs of focal (or global in coma) disturbance of cerebral function lasting MORE THAN 24 HRS or leading to death with no apparent cause other than a VASCULAR origin

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87
Q

Given common symptoms of an anterior/carotid circulation stroke

A

Weakness (face, legs, arms)
Impaired speech/language
Amaurosis fugax

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88
Q

Give common symptoms of a posterior circulation stroke

A 
Dysarthria
Dysphagia
Diplopia
Dizziness
Ataxia
Diplegia
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89
Q

Give the 3 types of ischaemic stroke

A

Embolic
Thrombotic
Systemic hypoperfusion

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90
Q

What does the acute CT scan show after a stroke? Why might a repeat CT be done after 48hrs?

A

Acute - bleeds/haemorrhagic stroke

Ischaemia appears normal, but after 48hrs may see dark patches

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91
Q

What arteries supply anterior circulation?

A

Internal carotid arteries - ACA and MCA

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92
Q

What arteries supply posterior circulation?

A

Posterior cerebral artery and vertebral arteries

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93
Q

What arteries connect anterior and posterior circulations?

A

Posterior communicating arteries

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94
Q

What criteria defines a total anterior circulation infarct?

A

Contralateral weakness/sensory loss
Homonymous Hemianopia/visual inattention
Higher cortical dysfunction - dysarthria, dysphasia

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95
Q

What criteria defines a partial anterior circulation infarct?

A

2 of the following:
Contralateral weakness/sensory loss
Homonymous hemianopia/visual inattention
Higher cortical dysfunction - dysarthria, dysphasia

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96
Q

What are the presenting features of a posterior circulation infarct?

A 
Cranial nerve palsy
Contralateral sensory/motor deficit (pyramidal lesion)
Cerebellar dysfunction
Isolated homonymous hemianopia
Bilateral events - reduced GCS
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97
Q

What is a lacunar infarct?

A

= occlusion of deep penetrating arteries

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98
Q

Why does a lacunar infarct not present with higher cortical features?

A

Only affect small volumes of SUB-cortical white matter so does not present with cortical features e.g. dysarthria, dysphasia, visual field loss

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99
Q

What syndromes are common in lacunar infarcts?

A 
pure motor hemiparesis
Ataxic hemiparesis
"clumsy hand" + dysarthria
pure hemisensory loss
Mixed sensorimotor
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100
Q

Why do small lacunar infarctions cause large clinical syndromes?

A

White matter infarcts - nerve fibres narrowed down so small area has large clinical consequences

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101
Q

What is the acute management of a stroke?

A

ABCDE + bloods (including BM!)
Hx: TIME of onset, risk factors, contraindications to thrombolysis, blood pressure, NIHSS
Urgent CT head (no contrast within 1h) BEFORE thrombolysis/aspirin
Thrombolysis/thrombectomy OR Aspirin 300mg

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102
Q

What might be the next stage and long-term management of a stroke?

A

Investigate cause (full history, exam, investigations)
Screen and prevent complications (infection, sores)
Secondary prevention (lifestyle, meds, surgery)
Rehabilitation (PT/OT/SLT)

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103
Q

What is the NIHSS?

A

National Institute of Health Stroke Scale
Score 0-42
Grades severity of stroke and can use to monitor response to acute treatment

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104
Q

How might ischaemic regions appear on an acute CT?

A

May not be visible
Subtle blurring and decreased attenuation of grey-white junction due to oedema may be early sign
May see hyperdense vessel - sign of intravascular clots e.g. MCA

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105
Q

What type of infarcts are MRIs better at viewing?

A

Posterior circulation infarcts

Lacunar infarcts

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106
Q

Give the indications for thrombolysis post-stroke

A

Within 4.5 hours of symptom onset

Non-haemorrhagic stroke on CT

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107
Q

Give some contra-indications for thrombolysis

A 
Haemorrhagic stroke/bleed current or previous
anti-coagulation/coagulopathy
pregnancy
high blood pressure
Aneurysm
Severe liver disease, varices, portal HTN
Seizures at presentation
Hypo/erglycaemia
Intracranial neoplasm history
Rapidly improving symptoms
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108
Q

What is given for thrombolysis? How should you follow up this treatment?

A

IV Tissue Plasminogen Activator (ALTEPLASE 0.9mg/kg)
Monitor blood pressure and complications of bleeding
24hr CT to check for haemorrhagic transformation

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109
Q

Give the indications and methods for thrombectomy

A

Indications - within 6 hours of symptom onset in anterior circulation, later if basilar thrombosis.
Methods - CT angiography to remove clot, can be used alongside thrombolysis

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110
Q

What are the 2 parts of ischaemic cerebral tissue called and which is more likely to survive when blood supply returns?

A 
Ischaemic core (central) surrounded by Ischaemic Penumbra (outer)
Core dies 1st, but penumbra may live if blood supply returned
The smaller the core, the better
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111
Q

What investigations might you do to investigate the cause of the stroke?

A

Bloods: FBC, UE, ESR, Lipids, LFTs, CRP, clotting, glucose/Hba1c
ECG + 72 hour tape (paroxysmal AF)
Carotid Doppler USS (carotid stenosis)
Echo (endocarditis/valvular disease)
MRI (confirm diagnosis, infarcts) or delayed CT if not tolerated

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112
Q

What appears white in a

a) T1 weighted image?
b) T2 weighted image?

A

a) fat

b) water

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113
Q

What is the best type of MRI for detecting acute infarcts?

A

Diffusion-weighted MRI - infarct appears WHITE

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114
Q

What type of MRI is matched with DW MRIs to detect infarcts?

A

ADC - infarct appears BLACK
Match black lesion to white lesion on DW MRI
DWI-ADC match

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115
Q

Give examples of MDT management post-stroke

A

nursing

PT, OT, SLT, dietitian, orthoptics

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116
Q

What lifestyle advice might you give someone after a stroke?

A 
smoking cessation
limit alcohol and drug use
dietary modifications
exercise
driving advice
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117
Q

What medications might you give as secondary prevention for strokes?

A

Anti-platelets - Aspirin 300mg for 2 weeks, then Clopidogrel lifelong
Anticoagulation: if have AF (HASBLED vs CHADSVASC score to determine this)
Anti-hypertensives: if haemorrhagic, be careful if ischaemic - aim <130/80
Statins - aim 40% decrease in non HDL cholesterol

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118
Q

How might you surgically manage extracranial carotid stenosis?

A

If 70-99% occluded - carotid endarterectomy

If 50-69% occluded - consider CEA or carotid artery stenting

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119
Q

How could you manage malignant MCA syndrome?

A

Decompressive hemicraniotomy

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120
Q

How could you manage posterior circulation infarct surgically?

A

External ventricular drainage or Posterior fossa decompression to prevent risk of hydrocephalus

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121
Q

What are the different methods of management for haemorrhagic stroke?

A

Manage hydrocephalus
Reversal of anticoagulation
Blood pressure control

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122
Q

What are the indications for medical and surgical management of haemorrhagic stroke?

A

Small deep haemorrhages, lobar haemorrhage without hydrocephalus, rapid neurological deterioration, large haemorrhage and significant comorbidities before stroke, GCS <8, posterior fossa haemorrhage

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123
Q

What are the indications for reversal of anticoagulation in haemorrhagic stroke management?

A

Primary intracerebral haemorrhage and taking anticoagulants with elevated INR

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124
Q

What are the indications for rapid blood pressure lowering in acute management of haemorrhagic stroke?

A

Within 6 hours symptom onset
systolic BP 150-220
Consider if >6hrs or BP>220
Aim systolic 130-140 within 1h and maintain for 7 days

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125
Q

What are the contraindications to rapid blood pressure lowering in management of haemorrhagic strokes?

A

Underlying structural cause
GCS<6
Awaiting neurosurgery for haematoma
Massive haematoma with poor prognosis

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126
Q

What medications can be used for reversal of anticoagulation in haemorrhagic stroke management?

A

Warfarin - Beriplex and vit K
LMWH - protamine
DOACs - Beriplex partial
Dabigatran - Idaruciumab

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127
Q

What causes can mimic stroke presentations?

A 
Seizures
Tumours/abscess
Migraine
Metabolic
Functional
Myelopathy, peripheral neuropathy, cranial nerve
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128
Q

What might you want to determine about the distribution and pattern of muscle weakness and why?

A

Proximal (muscle) or distal (nerve)
Symmetrical (genetic/metabolic) or asymmetrical
Mono or poly
Cranial involvement (bulbar/ophthalmoplegia)
Variability (fatigueability/relapse-remission)
Sensory deficit?

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129
Q

Give clinical features of Motor neurone disease and exclusion criteria

A

UMN (+LMN)
No sensory deficit or sphincter disturbance
Never affects eye movements

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130
Q

What are the 4 types of motor neuron disease? Which is the most common?

A

Most common = amyotrophic lateral sclerosis (ALS)
Progressive bulbar palsy
Progressive muscular atrophy
Primary lateral sclerosis (rare)

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131
Q

What are the pathophysiological features of MND?

A

Loss of motor neurones in cortex, cranial nerve nuclei and anterior horn cells

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132
Q

Where are the loss of motor neurones in ALS and what symptoms appear?

A

Loss motor neurons in motor cortex AND anterior horn cell
UMN+LMN signs
Worse prognosis if bulbar onset, older age, reduced FVC

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133
Q

Where are the loss of neurons in progressive bulbar palsy?

A

Cranial nerves 9-12

UMN (corticobulbar) and LMN (bulbar)

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134
Q

Where are the loss of neurons in progressive muscular atrophy? What type of signs do you see?

A

Anterior horn cell loss

LMN signs only

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135
Q

Where is loss of neurons in primary lateral sclerosis and what signs do you get?

A

Loss of Betz cells in motor cortex
Mainly UMN
Pseudobulbar palsy
Spastic leg weakness

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136
Q

What is the classical presentation of someone with MND?

A 
Usually >40 (median 60yrs)
Stumbling spastic gait
Footdrop +/- proximal myopathy
Weak grip/shoulder abduction
Aspiration pneumonia
UMN+LMN, potential bulbar signs
Frontotemporal dementia in 25%
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137
Q

How is MND diagnosed?

A

By EXCLUSION
Brain/cord MRI to exclude structural
LP to exclude inflammatory
Nerve conduction studies - detect loss of motor neurones and exclude mimicking motor neuropathies

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138
Q

What is the prognosis of MND?

A

Poor, <3 years in 50% patients

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139
Q

How would you manage MND?

A

MDT approach
Riluzole - NMDA receptor antagonist, improves survival slightly
Supportive

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140
Q

What supportive measures might you need to do for someone with MND?

A

excess saliva - positioning, suction, oral care, anti-muscarinics, botulinum toxin A
dysphagia - blend food, gastrostomy
Spasticity - baclofen, exercise, orthotics
communication - SLT, alternative methods
palliative care - from diagnosis!
ventilation - if wanted, only increases prognosis few months

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141
Q

Give 3 branches of peripheral nerve disease

A

Polyneuropathy
Mononeuropathy
Mononeuritis multiplex

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142
Q

Give some causes of polyneuropathy

A 
Peripheral neuropathy
Guillain-Barre Syndrome
Lead poisoning
Charcot-Marie tooth
Leprosy
143
Q

Give features of peripheral neuropathy

A

Chronic and progressive
Starts in longer nerves (vibration, proprioception sense)
Starts in legs first, “glove and stocking”
Sensory/LMN/both signs - numbness, pain, difficulty handling small objects/fine motor loss
Trophic changes - hair loss, shiny skin, calluses, nail changes, cold, pallor

144
Q

What are the common causes of peripheral neuropathy?

A 
Commonest = DIABETES
20% = idiopathic
145
Q

What are some less common causes of peripheral neuropathy?

A 
B12 or folate deficiency
Alcohol/toxins/drugs
hereditary neuropathies
paraneoplastic syndromes
metabolic - uraemia, thyroid
146
Q

How would you manage peripheral neuropathy?

A

Treat cause - e.g. diabetes, deficiencies, alcohol XS
PT + OT - orthotics
Splinting joints to prevent contractures in prolonged paralysis

147
Q

Give features of Guillain-Barre syndrome

A

Subacute <6 weeks
Ascending paralysis/numbness/areflexia
Sensory loss and LMN signs
Post-infectious autoimmune response

148
Q

What investigations would you do for Guillain-Barre syndrome and what would you see?

A

NCS - demyelination

LP - raised protein, normal or decreased WCC (cyto-albuminologic dissociation)

149
Q

How would you treat Guillain-Barre syndrome?

A

IV Ig
Supportive measures
Monitor FVC

150
Q

Give some features of Charcot-Marie tooth disease

A

Hereditary motor and sensory neuropathy (HMSN)
Muscle weakness/sensory loss in feet, legs and hands
Abnormal gait
High arched or very flat feet
Usually presents age 5-15
Managed: supportive, OT/PT, walking aids

151
Q

Describe the distribution and presentation of mononeuritis multiplex. How might you localise the site of lesions?

A

Random distribution of mononeuropathies (2 or more)
Subacute presentation <6 weeks
Electromyography

152
Q

Give the causes of mononeuritis multiplex

A

vasculitides
Connective tissue disorders e.g. SLE, RA, sarcoidosis
Leprosy

153
Q

What is the commonest mononeuropathy?

A

Carpal tunnel - median neuropathy

154
Q

What other common mononeuropathies occur in the upper limb?

A

Ulnar neuropathy - compression at elbow

Radial neuropathy - compression in axilla

155
Q

What is the are the comonest mononeuropathies of the leg?

A

Common peroneal neuropathy - fibular head

Lateral cutaneous thigh neuropathy - anterolateral burning thigh pain - inguinal ligament

156
Q

What are the signs of common peroneal nerve palsy?

A

Footdrop
Dorsal foot sensory loss
Weak ankle dorsiflexion and EVERSION

157
Q

Give the pathophysiology of myasthenia gravis

A

Autoantibodies to nicotinic post-synaptic acetylcholine receptors at neuromuscular junction - both B and T cells implicated

158
Q

Where does spasticity tend to develop when there is UMN/pyramidal weakness?

A

In stronger muscle groups
arms = flexors
legs = extensors

159
Q

Describe spasticity

A

Increased tone
Velocity-dependent - faster movement = greater resistance, until gives way
Clasp-knife response

160
Q

Describe spasticity

A

Increased tone
Velocity-dependent - faster movement = greater resistance, until gives way
Clasp-knife response

161
Q

Which groups are more likely to have myasthenia gravis?

A

<50 = women (thymic hyperplasia), >50 = men (thymic atrophy or thymoma)
Autoimmune conditions

162
Q

Give presenting features of myasthenia gravis

A

Slowly progressive or relapsing muscular fatigue. Fatigue increases on repetition of movement of VOLUNTARY muscles
Order of muscles affected: extraocular, bulbar, face, neck, limb girdle, trunk
Ptosis, diplopia, “peek sign” - orbicularis fatiguability
Myasthenic snarl on smiling
Voice fades when counting to 50 - dysphonia
Normal reflexes

163
Q

What can exacerbate myasthenia gravis symptoms?

A 
pregnancy
hypokalaemia
infection
over-treatment
change of climate
emotion
exercise
gentamicin or tetracyclines or quinine or beta blockers
opiates
164
Q

What investigations could you do in someone presenting with myasthenic features?

A

Anti-AchR antibodies (90%) or MuSK Abs
Electromyography - decreasing muscle response to repeated nerve stimulation
CT thorax to exclude thymoma
Ice on eyelid test (not diagnostic)
Tensilon test - rare (inject edrophonium)

165
Q

How would you treat myasthenia gravis?

A

Pyridostigmine (Achesterase inhibitor) for symptoms
Prednisolone + osteoporosis prophylaxis
OR azathioprine/methotrexate/mycophenolate
Thymectomy (with or without thymoma can be helpful)

166
Q

What is myasthenic crisis?

A

Life-threatening weakness of respiratory muscles

Can be caused by infection, natural disease or overdosing cholinergic meds (pyridostigmine)

167
Q

How would you manage a myasthenic crisis?

A

Monitor FVC, ventilatory support if needed
Plasmapheresis or IV Ig
Treat cause
Call anaesthetics and urgent neurology review

168
Q

What is the pathophysiology of Lambert-Eaton myasthenic syndrome (LEMS)?

A

Paraneoplastic or autoimmune production of antibodies to Ca channels on pre-synaptic membrane of neuromuscular junction

169
Q

What clinical features might you see in LEMS?

A

Gait difficulty before eye signs
Autonomic involvement (dry mouth, constipation, impotence)
Hyporeflexia and weakness, symptoms and EMG amplitude improve after exercise

170
Q

What are common causes of proximal myopathy?

A

Steroids
Statins
Metabolic and endocrine
Myotonic dystrophy

171
Q

What are less common causes of proximal myopathy?

A

Duchenne’s, Becker’s, muscular dystrophies
Inflammatory muscle disease (polymyositis, dermatomyositis)
Mitochondrial disorders

172
Q

What are features of proximal myopathy?

A 
Gradual onset
Preserved reflexes, no fasciculation
Can't do hair, stairs, chairs
Muscle wasting
Facial and neck weakness (sometimes)
Contractures
(Scoliosis)
(Eye movement disorders)
173
Q

How would you investigate suspected proximal myopathy?

A

CK (Duchenne’s),ESR, AST, LDH, CRP
EMG
(Muscle biopsy)
(genetic testing)

174
Q

How would you treat proximal myopathy?

A

Remove cause/medications
Supportive (OT, PT, back, renal, diet)
Immunosuppressants if inflammatory

175
Q

Give some features of Duchenne’s muscular dystrophy

A

Proximal myopathy, commonest of muscular dystrophies, X-linked recessive
Presents 4 yrs old clumsy walking, difficulty standing and respiratory failure
Pseudohypertorphy in calves
Raised serum CK
Supportive treatment and ventilatory support

176
Q

Give some features of Becker’s muscular dystrophy

A

Proximal myopathy, less common of muscular dystrophies, X-linked recessive
Presents later and milder than Duchenne’s
Better prognosis

177
Q

Give some features of Faciospaculohumeral muscular dystrophy (FSHD, Landouzy-Dejerine)

A

Proximal myopathy, common as Duchenne’s, autosomal dominant
Onset 12-14
Inability to puff out cheeks, or raise arms above head

178
Q

What is a myotonic disorder? What is the commonest form and its 2 types?

A

= tonic muscle spasm, long chains central nuclei within muscle fibres
Myotonic dystrophy - DM1 and DM2
DM1 more common and severe, both types autosomal dominant
Mexiletine may help with disabling myotonia, genetic counselling

179
Q

What is the MRC grading for power?

A 
5 = normal power
4 = active movement against gravity and resistance
3 = active movement against gravity
2 = active movement with gravity eliminated
1 = flicker movement/contraction
0 = no movement/contraction
180
Q

What is subacute combined degeneration of spinal cord?

A

B12 deficiency

Affects dorsal column first - proprioception

181
Q

Which way does someone tend to fall in an ataxic gait?

A

towards the side of the lesion

182
Q

What are the 3 broad differentials for transient loss of consciousness (TLOC)?

A
  1. syncope
  2. epileptic seizure
  3. non-epileptic (psychogenic)
183
Q

What causes syncope as a whole category?

A

Transient global cerebral hypoperfusion

184
Q

What are the 3 types of syncope?

A

Reflex
Cardiogenic
Orthostatic hypotension

185
Q

What are the 3 types of reflex syncope?

A

vasovagal
situational - micturition, exercise
carotid sinus hypersensitivity

186
Q

What causes vasovagal syncope? aka neurocardiogenic

A

Reflex bradycardia +/- peripheral vasodilation

Provoked by emotion, pain, standing too long

187
Q

What are the typical features of vasovagal syncope?

A

Onset over seconds - not instant
Prodromal symptoms (nausea, pallor, sweating, narrowing of vision)
Brief clonic jerking possible, but no tonic clonic
Duration - 2mins
Rapid recovery
(3Ps - precipitating, prodrome, posture)

188
Q

What are the typical features of situation syncope?

A 
Clear precipitant - cough, effort/exercise, micturition
onset over seconds
prodromal symptoms
may jerk but not tonic-clonic
Duration - 2 mins
Rapid recovery
189
Q

What are the typical features of carotid sinus hypersensitivity?

A

Baroreceptors in carotid sinus hypersensitive - reflex bradycardia + vasodilation on minimal stimulation e.g. head turning or shaving
Same as vasovagal in features

190
Q

What are the features of cardiogenic syncope?

A

Transient arrhythmias or structural stenosis causing tachycardia or bradycardia
No warning except palpitations, falls to ground
Pale, slow or absent pulse
Recovery within seconds, patient flushes, pulse speeds up
Anoxic clonic jerks may occur in prolonged LOC
May happen several times a day and in any posture

191
Q

What are some other causes of blackouts outside of syncope, epilepsy and pscychogenic causes? What features might you see?

A

Hypoglycaemia - tremor, hunger, light-headed
Anxiety - hyperventilation, tremor, sweating, tachy, weakness, light-headed, no LOC
Drop attacks - sudden drops without LOC (narcolepsy, catoalexy, acute hydrocephalus)
Factitious blackouts - pseudoseizures, Munchausens

192
Q

What is an epileptic seizure?

A

Clinical manifestation of abnormal electrical discharge in the brain

193
Q

What is epilepsy?

A

Tendency to recurrent epileptic seizures

194
Q

What are the features of an epileptic seizure?

A

Attacks when asleep or lying down
Aura, (identifiable triggers?), sudden onset
Altered breathing + cyanosis
Typical tonic-clonic movements (symmetrical)
Jerking changing frequency
Urinary incontinence
Tongue-biting - lateral
Duration <3mins
Prolonged post-ictal drowsiness/confusion - 15 mins
Amnesia
Transient focal paralysis (Todd’s palsy)

195
Q

Why is TIA not a differential for TLOC?

A

TIA is a focal hypoperfusion whereas TLOC indicates GLOBAL hypoperfusion!

196
Q

Give the features of a non-epileptic seizure

A 
May be trigger e.g. anxious, stress
No prodrome or sparingly described
Jerking not synchronous, random, constant frequency
Rhythmic pelvic movements, head side to side
Eyes often close
May bite tongue but often tip of tongue
Duration >3 mins (longer than GES)
May feel tired after
197
Q

What is your first investigation following a TLOC?

A

ECG - rule out cardiac causes e.g. heart block, arrhythmias, long QT
May do ambulatory ECG/24 hr ECG to see transient arrhythmia

198
Q

What other investigations might you do after ECG for TLOC?

A 
U+E, FBC, Mg, Ca, glucose
Tilt-table test (exclude cardiac cause first)
Echocardiogram
EEG/sleep EEG
CT/MRI
199
Q

What are the 3 classifications of focal seizures?

A

Simple - no LOC
complex - impaired consciousness, often temporal
Starts partial then evolves to bilateral generalised convulsive seizure

200
Q

What are the different types of generalised seizures?

A 
Absence seizures
Tonic-clonic
Myoclonic
Atonic - sudden loss muscle tone, no LOC
Infantile spasms
201
Q

Give some features of temporal lobe focal seizures

A

Impaired awareness + complex motor e.g. lip smacking, chewing, swallowing, manual movements
Dysphasia, deja vu, jamais vu
Emotional disturbance
Olfactory, gustatory, auditory hallucinations, delusions
Post-ictal confusion

202
Q

Give some features of frontal lobe focal seizures

A 
Posturing or peddling movements of legs
Focal motor seizure starting with thumb/face (Jacksonian march)
Motor arrest
Subtle behavioural disturbances
Dysphasia or speech arrest
Post-ictal Todd's palsy
203
Q

Give some features of parietal lobe focal seizures

A

Sensory disturbances - tingling, numbness, pain (rare)

Motor symptoms if spreads to pre-central gyrus

204
Q

Give some features of occipital lobe focal seizures

A

Visual phenomena - spots, line, flashes

205
Q

What is amaurosis fugax?

A

Occlusion of retinal artery causing unilateral progressive vision loss
“like a curtain descending”

206
Q

What can cause TIAs?

A

Carotid emboli
Cardiac emboli
Hyperviscosity - polycythaemia, SCD, myeloma
Vasculitis - rare non-embolic cause

207
Q

How would you manage a TIA?

A

Control CVD RFs - antihypertensives, statins, diabetic medication, smoking cessation
Antiplatelets - aspirin 300mg 2 wks, then clopidogrel 75mg OD
Anticoagulation if cardiac emboli
Carotid endarterectomy in 2wks if 1st TIA and can tolerate (preferred to carotid angioplasty with stent)
Advise not to drive for 1 month

208
Q

What tool gives the risk for a stroke following a TIA?

A

ABCD2 score

209
Q

What is a TIA?

A

= transient ischaemic attack

ischaemic/embolic neurological event with symptoms lasting less than 24 hours

210
Q

What factors are considered on ABCD2 score?

A 
Age >60
Blood pressure >140/90
Clinical: unilateral weakness, speech disturbance without weakness
Duration: symptoms 10-59 mins or >1h
Diabetes
211
Q

What is a high risk score on the ABCD2?

A

4+ = high risk, see specialist within 24h

212
Q

What are the typical features of meningitis?

A 
Rapid onset headache
Fever
Photophobia
Stiff neck
Purpuric rash
Coma
213
Q

What are the typical features of encephalitis?

A

Rapid onset headache
Fever
Odd behaviour
Fits or reduced consciousness

214
Q

Give the differentials for a rapid onset headache

A 
Subarachnoid haemorrhage
Meningitis
Encephalitis
Post-coital headache
Cluster headaches
215
Q

Give the features of venous sinus thrombosis

A

subacute, gradual onset headache

papilloedema

216
Q

Give the features of sinusitis

A

Dull, constant headache over frontal or maxillary sinuses with tenderness
Ethmoid or sphenoid pain is deep in midline at nose root, common with coryza
Postnasal drip
Pain worse on bending over
Lasts 1-2 weeks

217
Q

Give the features of intracranial hypotension

A

CSF leakage e.g. iatrogenic after LP, epidural

Headaches worse on standing

218
Q

How would you manage intracranial hypotension due to CSF leak post-LP?

A

Epidural blood patch over leak

Conservative management with IV fluids and caffeine fails

219
Q

Give the features of a tension headache

A

Tight band
Bilateral
Non-pulsatile
Scalp muscle tenderness

220
Q

Give the features of migraines

A

Prodrome - precedes by days (mood changes, tired)
Visual or other aura lasting 15-30 mins, followed by
(1h unilateral, throbbing headache)
Nausea, vomiting, photophobia, phonophobia
Allodynia

221
Q

Give some examples of visual aura experience in migraines

A 
Chaotic distorting
Melting and jumbling of lines
Dots
Zigzags
Scotomata (blind spots)
Hemianopia
222
Q

What aura might you get with migraines other than visual

A

Paraesthesiae spreading from fingers to face
Dysarthria, ataxia, ophthalmoplegia, hemiparesis
Dysphasia or paraphasia

223
Q

What are some triggers of migraines?

A

CHOCOLATE
C = chocolate, H = hangovers, O = orgasms, C = cheese/caffeine, O = oral contraceptive, L = lie-ins, A = alcohol, T = travel, E = exercise

224
Q

What is the diagnostic criteria for migraines with no aura?

A

> 5 headaches lasting 4-72hrs with nausea/vomiting/photo/phonophobia + 2 of
unilateral, pulsating, impairs routine activity

225
Q

How would you manage migraines?

A 
Avoid triggers (consider progesterone only/non-hormonal contraceptives in young women)
Prophylaxis = propanolol/topiramate/amitryptiline
Attack = Oral triptan + NSAID/paracetamol, anti-emetic
Other = warm or cold packs to head, rebreathing into paper bag, Butterbur extracts, riboflavin supplements, acupuncture, transcutaneous nerve stimulation
226
Q

Give some contraindications and side effects of triptans

A 
CI = IHD, coronary spasm, uncontrolled HTN, recent lithium, SSRI, ergot
SE = arrhythmias, angina, MI
227
Q

Give features of a headache due to raised ICP

A

chronic, progressive headache - worse on waking, lying, bending forward or coughing
AS - vomiting, papilloedema, seizures, false localising signs, irritability

228
Q

If suspect ICP, what investigation would you do first and why?

A

Imaging - CT/MRI FIRST before LP (risk herniation/coning)

If no abnormalities, consider idiopathic intracranial hypertension

229
Q

What medications can cause medication overuse headache/analgesic rebound headache?

A

Combined analgesics (paracetamol + codeine/opiates)
Ergotamine
Triptans
Episodic headache becomes chronic daily headache

230
Q

What are the symptoms of cluster headaches?

A

Rapid onset excruciating pain around orbit unilaterally
Eye watery and bloodshot, lid swelling
Facial flushing, rhinorrhoea, miosis or ptosis
Duration 15-180 mins, OD or BD, often nocturnal
Clusters last 4-12 weeks, then pain-free periods of months-2 years

231
Q

How would you treat cluster headaches?

A

Acute attack - 100% O2 for 15 mins via non-rebreathe mask + sumatriptan at onset
Prophylaxis - avoid triggers. Consider corticosteroidds, verapamil, lithium

232
Q

What are the symptoms of trigeminal neuralgia?

A

Intense unilateral stabbing pain lasting seconds in trigeminal nerve distribution
Often mandibular or maxillary distributions
Triggers - washing area, shaving, eating, talking, dental prostheses

233
Q

How would you manage suspected trigeminal neuralgia?

A

MRI - to exclude secondary inflammatory or structural causes
Carbamazepine, lamotrigine, phenytoin or gabapentin
Microvascular decompression

234
Q

What is the minimum GCS score and what is the maximum?

A 
Min = 3
Max = 15
235
Q

Give some common causes of coma

A 
Drugs//toxins/opiates/ethanol
Anoxia
Mass lesions e.g. bleeds, SAH
Infections (HSE, meningitis
Infarcts of brainstem
Metabolic (DKA, wernicke's)
Epilepsy
236
Q

Give less common causes of coma

A 
Tumour
Carbon monoxide
Venous sinus occlusions
Hypothermia
Psychiatric catatonia
Pituitary apoplexy
Fat embolism
237
Q

How does blood appear on CT in sub/extradural haemorrhage initially and then after some time?

A

High density or white initially

Then becomes hypodense after time

238
Q

How would you investigate for a non-haemorrhagic ass lesion?

A

CT with contrast - illuminates wall of mass

239
Q

How would an MCA infarct appear on a CT? What criteria would make it a malignant MCA infarct?

A

Reduced white-grey matter differentiation and sulcal effacement
if 2/3 artery territory infarcted = malignant

240
Q

What would you expect to see on a lumbar puncture without culture in bacterial meningitis?

A

Raised protein, decreased glucose

241
Q

What is the pathophysiology and signs for phenobarbital overdose?

A

GABA-A chloride channels open longer
Cerebellar signs and diplopia
Coma, respiratory depression, death

242
Q

What are the signs of CO poisoning?

A

headache, nausea, confusion, syncope, convulsions, coma, death
low CO levels can still kill if have IHD

243
Q

What symptoms and signs can amphetamines and other stimulants cause?

A

seizures
psychosis
ischaemic stroke, intracranial haemorrhage
angiitis (stroke, mononeuritis multiplex)
rhabdomyolosis
delirium, coma
posterior reversible encephalopathy syndrome

244
Q

What neurological events can occur shortly after ingesting cocaine?

A

Seizures, stereotypic movements (tic-like)
Anxiety, confusion, paranoia, visual hallucinations
Stroke - usually haemorrhagic

245
Q

What are the symptoms of ethanol overdose?

A

ataxia
nystagmus
dysarthria
coma

246
Q

What are the symptoms of ethanol/alcohol withdrawal

a) within 6-8hrs?
b) within 24 hrs?
c) within 3-5 days?

A

a) tremor, anxiety, nausea
b) hallucinations (visual, olfactory, auditory)
c) delirium tremens - hyperactivity (motor+sensory) and altered mental state

247
Q

How would you treat alcohol withdrawal?

A

Thiamine, then glucose, multivitamins
Benzodiazepine (Lorazepam), Chlordiazepoxide
Fluids - check hydration, K and Mg
Check clotting, monitor glucose

248
Q

What is the main concern that chronic ethanol overuse can cause? What are features of this?

A 
= Wernicke's encephalopathy
Thiamine deficiency
Ophthalmoparesis
Ataxia
Confusion
25% get Korsakoff's psychosis
249
Q

What other conditions can chronic ethano overuse cause except for WE?

A

cerebellar degeneration - LL and trunk ataxia
peripheral neuropathy
amblyopia
central pontine myelinosis (if hyponatraemia corrected too rapidly)
dementia
tremor

250
Q

What is a sub-hyaloid haemorrhage?

A

Intra-ocular bleed between retina and posterior layer of vitreous

251
Q

What features do you see in 3rd CN palsy?

A

Parasympathetic palsy = fixed dilated pupil, droopy eyelid

Sympathetic = Horner’s syndrome, partial ptosis

252
Q

What are the features of Horner’s syndrome?

A 
Loss of sympathetic oculomotor function - triad = 
Constricted pupil (miosis) 
Partial ptosis
Hemifacial sweating (anhidrosis)
Sometimes enophthalmos
253
Q

What might you see on an LP after a sub-arachnoid haemorrhage? When should a CT be done?

A

CT most sensitive within 24 hrs

LP = CSF xanthochromia (yellow due to bilirubin) - most sensitie within 2 weeks

254
Q

What are 2 common treatments for a sub-arachnoid haemorrhage?

A
  1. surgical clipping

2. Endovascular coiling

255
Q

When would maximum weakness need to occur in acute paresis?

A

Within 4 weeks

256
Q

What features may suggest a brainstem lesion for UMN weakness?

A

Cranial nerve involvement
Horner’s syndrome
Internuclear ophthalmopegia

257
Q

What features may suggest a spinal cord injury for UMN weakness?

A

Bilateral weakness
Radicular symptoms may give level
Sensory loss below level

258
Q

What are some acute causes of weakness?

A

Vascular (haemorrhagic or embolic)
Compression (haemorrhagic usually)
Hypoglycaemia

259
Q

What are some subacute causes of weakness?

A 
UMN = mass lesion, subdural, inflammatory, infection, metabolic
LMN = GBS, peripheral neuropathy, myopathy, MG, malignant meningitis
260
Q

Why is it useful to check if weakness involves dorsal and spinothalamic tracts?

A

If it does, then lesion must be beyond arterial distribution because each tract has separate arterial blood supply

261
Q

What is spinal shock?

A

Acute complete transverse lesion across spinal cord can cause spinal shock
Flaccid weakness below lesion but no UMN signs

262
Q

What are the features of spinal cord compression?

A 
UMN deficit below lesion
Sensory impairment below lesion
Possible spinal shock if acute
Lhermitte's phenomenon
Painless atonic bladder
Urgency
Impotence
Respiratory paralysis if high cervical lesion
263
Q

What are the 4 types of cancer that can metastasise to the spine?

A

Lung
Breast
Prostate
Kidney

264
Q

What are some primary tumours that could be in the spine?

A 
Neuroma
Meningioma
Glioma
Sarcoma
Ependymoma
265
Q

What are some non-compressive causes of myelopathy?

A

Inflammation
Infarction
MND
Syrinx (fluid-filled cavity in spinal cord)
AVM, spinocerebellar syndromes, radiation, fluorosis, sarcoidosis

266
Q

What supportive treatments might you do for GBS?

A

Thromboprophylaxis
Dysautonomia - 2-4hrly BP, cardiac monitor
Monitor FVC, RR
Pain - opiates, amitryptiline
Rehab - splints, pressure sores, nutrition

267
Q

What types of immunotherapy can you give for GBS?

A

IV Ig
Plasma exchange
monoclonal antibodies??

268
Q

What is status epilepticus?

A

When a seizure lasts longer than 5 minutes or when seizures occur close together with no recovery between them

269
Q

How would you manage a sub-arachnoid haemorrhage?

A

Re-examine neuro often - BP, pupils, GCS
Repeat CT if deteriorating
Keep hydrated - maintain perfusion
Nimodipine - prevent vasospasm, cerebral ischaemia
Surgery - Endovascular coiling or surgical clipping

270
Q

Give some primary and secondary causes of orthostatic hypotension

A 
Primary = MSA, PoTS
Secondary = diabetes, medication, Parkinsons
271
Q

Give some potential triggers of epileptic seizures

A

sleep deprivation
flashing lights
menstruation
alcohol/alcohol withdrawal

272
Q

How useful are EEGs in diagnosing epilepsy?

A

Not very! Should be done after ECG, bloods, imaging
Some may have abnormal epileptic wave forms inter-ictally, but some none unless during seizure
Often not useful in outpatients, send home with EEG
Can provoke seizure - sleep deprivation, hyperventilation, flashing lights
Useful if not sure if in status epilepticus

273
Q

What is the role of MRI/CT in patients with recurrent blackouts?

A

Indications: FOCAL or new onset seizures >25yrs old
MRI preferred over CT - CT if urgent e.g. bleed
None needed if GTC, MC, absence seizures

274
Q

Give pathophysiology of epileptic seizures

A

Excitatory and inhibitory phases
Prolonged depolorisation in neurones which spreads to adjacent areas +
failure of GABA transmission

275
Q

Give treatment of focal seizures

A

Carbamazepine
Lamotrigine
If refractory - vagal nerve stimulator

276
Q

Give treatment of tonic clonic seizures

A

Valproate (not if young woman)

Lamotrigine

277
Q

Give treatment of myoclonic seizures

A

Valproate
Levoteracetam
Topiramate

278
Q

What does a visual acuity of 6/60 mean?

A

Able to see clearly at 6m, but average population can see clearly at 60m distance

279
Q

Describe Marcus-Gunn pupil

A

= relative afferent pupillary defect (RAPD)
Pupil constricts less/dilates when light moved from unaffected eye to affected eye
Indirect and direct responses diminished when light in affected eye, but normal when light shines on unaffected eye
Efferent constriction is OK, problem is with afferen pathway - light detection

280
Q

What is the role of pinhole correction?

A

To exclude corneal defects, myopia, hypermetropia

281
Q

What are the different causes of relative afferent pupillary defect?

A

Optic nerve lesion or neuritis
Vascular causes
Retinal detachment or vitreous haemorrhage
Acute angle closure glaucoma

282
Q

What might you experience with retinal detachment or vitreous haemorrhage?

A

Flashes/floaters in vision
Decrease in vision
Vitreous haemorrage associated with diabetic retinopathy, macular degeneration

283
Q

What might you experience with acute angle closure glaucoma?

A

painful red eye, nausea, vomiting

284
Q

What causes anterior ischaemic optic neuropathy? What might you see on examination?

A

ischaemia of posterior choroidal artery that supplies optic nerve head (optic disc)
Swollen optic disc on fundoscopy
Think GCA

285
Q

What are the features of central retinal artery occlusion?

A

Occlusion of central retinal artery which supplies retina (branch of ophthalmic artery)
PALE optic disc
CHERRY RED SPOT on macula

286
Q

What are the features of central retinal vein occlusion?

A

Dilated branch veins
Multiple retinal haemorrhages
Cotton wool patches
STORMY SUNSET

287
Q

What are the features of optic neuritis?

A

Painful eye movements, blurred vision over few days, exacerbated by heat/exercise, afferent pupillary defect, dyschromatopsia
Inflammation of optic nerve at the optic nerve head (optic disc)
If behind optic disc - often normal in 2/3

288
Q

Give an example of a transient painless monocular loss of vision

A

Amaurosis fugax

Migraines

289
Q

Give an example of a permanent painless monocular loss of vision

A

central retinal artery occlusion

central retinal vein occlusion

290
Q

Give an example of permanent painful monocular loss of vision?

A

Optic neuritis
Acute angle closure glaucoma
Vitreous haemorrhage

291
Q

What investigation might you do to confirm optic neuritis?

A

Visual evoked potentials - EEG during light stimulus

292
Q

Give some causes of optic neuritis

A
  1. Multiple Sclerosis!

2. Lyme, syphilis, HIV, B12 deficiency, GCA

293
Q

What is the prognosis of optic neuritis?

A

50% develop MS

Vision improves over 6 weeks, may have ongoing dyschromatopsia or decreased acuity

294
Q

Give the diagnostic criteria for multiple sclerosis

A

McDonald’s criteria
Inflammatory plaques of demyelination disseminated in SPACE and TIME causing focal loss with relative preservation of axons
>30 days between attacks
>1hr duration attacks

295
Q

Describe the pathophysiology of multiple sclerosis

A

Relapse-remission part - inflammatory response causes demyelination of axons leading to relapse and remitting symptoms
Neurodegenerative part - demyelination heals poorly leading to axonal degeneration causing progressive and fixed deficits

296
Q

What are the 4 types of multiple sclerosis?

A
  1. Benign
  2. Relapsing-remitting
  3. Secondary chronic progressive
  4. Primary progressive
297
Q

What is a pseudo-relapse of MS?

A

flare-up of symptoms not due to MS, but due to other factors e.g. stress, infection

298
Q

Give some symptoms of MS

A 
Unilateral vision loss
Fatigue, cognitive impairment
Weakness (pyramidal), spastic paresis
Sensory disturbance
Cerebellar - ataxia, nystagmus, intention tremor, vertigo, dysarthria
Bladder involvement/sexual dysfunction
Lhermitte's
Uhtoff's
Cranial nerve/bulbar dysfunction - swallowing, facial movements, eye movements
299
Q

Give some signs of MS

A

UMN signs - spastic paresis, brisk reflexes
Sensory loss
Cerebellar signs
Optic atrophy, RAPD
Internuclear ophthalmoplegia
CN involvement - swallowing, face and eye movements

300
Q

Give the investigations and findings for MS

A
  1. MRI - T2 weighted - white matter lesions often peri-ventricular, or in brainstem, cerebellum, spinal cord
  2. LP - oligoclonal IgG bands
  3. Visual evoked potentials - delayed
  4. MRI with contrast - lesions in last 3 months more enhanced - to see if disseminated in time
301
Q

What is Lhermitte’s sign?

A

radiating pain from back of neck down spine to arms and legs on flexion of neck
(plaques in spinal cord cause nerve irritation)

302
Q

What is Uhtoff’s sign?

A

Worsening of neurological symptoms in demyelinating conditions due to heat

303
Q

Give short-term management of multiple sclerosis

A

RULE OUT INFECTION
1g methylprednisolone IV 24 hrs or PO for 3-5 days
(don’t use more than once a year)

304
Q

What are the short-term risks of high dose steroid treatment?

A

delirium/psychosis
immunosuppression
peptic ulcers
pancreatitis

305
Q

What is the long-term conservative management for MS?

A

Smoking cessation
Psychological support
Regular exercise
PT/OT/SLT

306
Q

What medical long-term disease-modifying management is there for MS?

A

Dimethylfumarate - mild/moderate relapse-remitting
Alemtuzumab or Natalizumab
(Interferon beta and glatiramer - not recommended)

307
Q

What medical symptomatic control is there for MS?

A

Baclofen/gabapentin - spasticity
Botulinum type A injections - tremor
Amantadine - fatigue
Tolterodine - urinary frequency/urgency
Duloxetine - bladder instability, neuropathic pain
Gabapentin, pregabalin, amitryptiline - neuropathic pain

308
Q

What do you see in internuclear ophthalmoplegia?

A

Ipsilateral eye cannot adduct while contralateral eye abducts with nystagmus

309
Q

What causes INO?

A

Communication between CN3 and CN6 disrupted due to lesion in medial longitudinal fasciculus

310
Q

What are the top 2 risk factors for stroke?

A
  1. Hypertension

2. Atrial Fibrillation

311
Q

What is the CHADS-VASC Score for?

A

To determine stroke risk in a patient with atrial fibrillation

312
Q

What are the parameters on the CHADS-VASC score?

A

CHF, HTN, Age, Diabetes, Stoke/TIA/VTE history, Vascular disease, Sex

313
Q

What type of seizures in status epilepticus are an emergency and which type are not?

A 
Convulsive = emergency
Non-convulsive = not emergency
314
Q

What are T1 and T2 in status epilepticus?

A 
T1 = 10 mins, where unusually prolonged
T2 = 30 mins, where expect impairment
315
Q

How would you manage status epilepticus?

A
  1. 2 doses benzodiazepines 10 mins apart (IV/buccal midazolam, IV lorazepam/diazepam)
  2. If not work - valproate or levoteracetam, consider glucose + thiamine
  3. If not work - anaesthesia
316
Q

Give mechanism of action of benzodiazepines

A

Increase frequency of chloride ion channel opening, increasing GABA inhibitory effect

317
Q

What investigations would you do for status epilepticus?

A

Toxicology, FBC, U+E, CRP, BM, Calcium
CT head (quick) especially if focal neurological signs
EEG during if not sure it’s status epilepticus

318
Q

What is true vertigo?

A

Hallucination of movement, often rotatory, of the patient and their surroundings

319
Q

What might be some associated symptoms of vertigo?

A 
Difficulty walking or standing
Relief on lying, sitting still - worse on movement
Nausea, vomiting
Pallor, sweating
Possible hearing loss, tinnitus
320
Q

Give some causes of true vertigo

A
  1. vestibular neuritis
  2. BPPV
  3. Meniere’s disease
  4. Ototoxicity
  5. Acoustic neuroma
  6. Trauma
  7. HZV
  8. Central/brainstem causes
  9. Alcohol intoxication
321
Q

What does BPPV stand for? What are its typical features?

A

Benign paroxysmal positional vertigo

  • true vertigo on head MOVEMENT, stops when head still
  • decreases over time due to brain adapting (self-terminating)
  • Fatigueable nystagmus on Hall-pike manoeuvre is diagnostic
322
Q

What manoeuvre helps to resolve BPPV?

A

Epley manoeuvre - clears debris from semicircular canals of ears

323
Q

Give another name for acute labrynthitis. What are its typical features

A 
= vestibular neuronitis
Abrupt onset severe vertigo, nausea and vomiting
Prostration
No deafness or tinnitus
Self-limiting (complete 3-4wks)
324
Q

What causes acute labrynthitis? How would you manage?

A

Virus
Vascular lesion
Mx: Reassure and sedation if severe

325
Q

What are the features of Meniere’s disease?

A

Increased pressure in endolymphatic system of inner ear
Recurrent attacks vertigo lasting >20 mins, fluctuating/permanent sensorineural hearing loss, tinnitus, aural fullness and falling to one side

326
Q

How would you manage Meniere’s disease?

A

Bed rest and reassurance in acute attacks

If prolonged - antihistamine (cinnarizine or buccal prochlorperazine if severe)

327
Q

What ototoxic drugs can cause vertigo and/or deafness?

A

Aminglycosides e.g. gentamicin
Loop diuretics
Cisplatin

328
Q

What type of tumour is an acoustic neuroma?

A

Schwannoma arising from vestibular nerve

Accounts for 80% cerebellopontine angle tumours

329
Q

How do acoustic neuromas present?

A

Unilateral hearing loss
Followed by vertigo
Can be predicted with serial MRIs, slow growth
Once progressed - CN5,6,9,10 may be affected and Ipsilateral cerebellar signs

330
Q

What kind of trauma might cause vertigo?

A

Trauma affecting petrous temporal bone or cerebello-pontine angle, may damage CN8 causing vertigo, deafness or tinnitus

331
Q

What features might you see in Herpes zoster external meatus infection?

A

Facial palsy, deafness, tinnitus and vertigo

332
Q

What test would you do to check vertigo is not from a central/brainstem lesion?

A

Dolls-eye test
Move head and ask patient to keep eyes fixed on stationary object. If eyes move with head rather than stay fixed = negative - likely vestibular system and brainstem intact??

333
Q

What are the features of congenital nystagmus?

A

Usually bidirectional, pendular (no particular beating direction)
Compensation - usually no vision effect

334
Q

What is the inheritance pattern of Friedrich’s ataxia? What are its typical features?

A

autosomal recessive
Ataxia, sensory loss arms and legs, impaired speech
Spinocerebellar degeneration

335
Q

What is the inheritance pattern of Spino-Cerebellar Ataxia? What is the commonest type and its features?

A

Autosomal dominant
SCA 6 is commonest in UK
Pure ataxia

336
Q

What inheritance pattern is ataxia telangiectasia? What are its features?

A

Autosomal recessive
Progressive ataxia starting in childhood
Susceptible to cancer and oculomotor apraxia

337
Q

Give some toxicities that may cause ataxia

A

Alcohol
Phenytoin and anti-convulsants
Lithium
Amiodarone

338
Q

What is a degenerative cause of cerebellar ataxia?

A

MSA - either MSA P or MSA C

Early onset speech impairment and autonomic decline

339
Q

What are immune-mediated causes of cerebellar ataxia?

A

post-viral cerebellitis - VZV in children
Paraneoplastic degeneration
Gluten ataxia (with/without coeliac)
Primary autoimmune ataxia

340
Q

What might down-beat nystagmus mean?

A

Obstruction in foramen magnum

341
Q

Give some features of Bell’s palsy

A

= idopathic facial nerve palsy
Abrupt onset complete unilateral facial weakness at 24-72hrs
Ipsilateral numbness or pain around the ear
Decreased taste
Hypersensitivity to sounds

342
Q

How would you differentiate between LMN (Bell’s palsy) and UMN facial weakness?

A

UMN weakness - forehead sparing as bilateral innervation

LMN weakness - no forehead sparing, unable to wrinkle forehead

343
Q

What conditions might you see a high steppage gait in?

A

Peripheral neuropathy

L5 radiculopathy, common peroneal nerve palsy

344
Q

What gait might you see in Parkinson’s disease?

A

wide base, shuffling, stooped posture, asymmetrical reduced armswing
Freezing at obstacles
Apraxia - struggle to stand and start walking

345
Q

What gait might you see in hemiplegia?

A

Arm flexed and ipsilateral leg circumduction

346
Q

What gait might you see in proximal myopathy?

A

Waddling gait

347
Q

Give the triad of extrapyramidal features of Parkinson’s disease

A
  1. Tremor
  2. Hypertonia/rigidity “cogwheel rigidity”
  3. Bradykinesia (slow movements, decrease in amplitude with repetition, festinant gait, freezing at doors and obstacles, expressionless face)
348
Q

What is the cause of Parkinson’s disease?

A

Loss of dopaminergic neurons in substantia nigra, associated with Lewy bodies in basal ganglia, brainstem and cortex
Mostly sporadic, some genetic

349
Q

Give some non-motor features of Parkinson’s

A 
Autonomic dysfunction - postural hypotension, constipation, urinary frequency/urgency, saliva dribbling
Sleep disturbance
Reduced sense of smell
Depression
Dementia
Psychosis
350
Q

How is Parkinson’s disease diagnosed?

A

Exclude cerebellar and frontotemporal disease
Clinical diagnosis and based on response to dopaminergic treatment
If suspect alternative cause - MRI or DaTscan, PET

351
Q

What is the pharmacological management for Parkinson’s disease?

A

Symptom control, not reversing disease so start late as tolerance increases and SE get worse with higher doses
Levodopa
Dopamine agonists to delay levodopa initiation - ropinirole, pramipexole
Apomorphine
Anticholinergics
MAO-B inhibitors
COMT inhibitors

352
Q

Why should you not withdraw Levodopa suddenly?

A

Acute kinesia risk

Neuroleptic malignant syndrome

353
Q

What is some non-pharmacological management of Parkinsons?

A

Deep brain stimulation (if partly dopamine-responsive)

Surgical ablation of overactive basal ganglia circuits

Phase 3a (8 decks)

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