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Phase 2a > Neurology 4 > Flashcards

Neurology 4 Flashcards

1
Q

What scan should you do for an acute neuro presentation (except for spine)? Why?

A

CT head. Takes 2-3 mins whereas an MRI takes about 40 mins and has more safety issues.

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2
Q

What scan should you do for anything to do with the spine or anything to do with MS?

A

MRI, even in acute presentations involving the spine e.g. cauda equina

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3
Q

Why is a CT of the spine not very useful?

A

Doesn’t show discs/nerves/nerve roots etc.

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4
Q

Where does the spinal cord end?

A

L1/2

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5
Q

What is at the bottom of the spinal cord?

A

Cauda equina - bundle of nerve roots from the lumbar/sacral levels that branch off the bottom of the spinal cord

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6
Q

What causes cauda equina?

A

Lumbar disc herniation = most common
Spinal stenosis e.g. degeneration from ankylosing spondylitis
Trauma, tumours, abscesses

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7
Q

How is cauda equina treated?

A

Surgical decompression ASAP

Treat underlying cause - antibiotics for abscess, chemo for malignancy etc.

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8
Q

How is cauda equina investigated?

A

MRI spine

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9
Q

How does cauda equina present?

A

Bowel + bladder dysfunction (incontinence/loss of sphincter control)
Saddle paraesthesia - feels strange sitting/wiping
Bilateral leg weakness/loss of reflexes
Aching back pain with sciatica (radiates down leg)
Sexual dysfunction

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10
Q

What are the 3 cardinal symptoms of brain tumours?

A

Signs of raised ICP
Progressive focal neurological deficits
Epileptic seizures

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11
Q

What are the less common symptoms of brain tumours?

A

Constant headache
N+V
Drowsiness
Change in personality/behaviour

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12
Q

Describe the headache seen in a brain tumour.

A

Often nocturnal, worse on waking, coughing, straining, bending forward and lying down

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13
Q

What are primary brain tumours?

A

Brain is original site of tumour

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14
Q

Where do primary tumours metastasise to?

A

Don’t metastasise outside of CNS

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15
Q

What are the types of primary brain tumours?

A

Gliomas
Meningiomas
Others - pituitary, CN, haematopoietic (lymph cells)

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16
Q

What is the most common primary brain tumour?

A

Glioma

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17
Q

What is a glioma?

A

Tumour of the glial cells in the brain/spinal cord e.g. astrocytoma, oligodendroglioma

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18
Q

What is a meningioma?

A

Tumour growing from cells of the meninges, usually benign

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19
Q

What are secondary brain tumours?

A

Sites the cancer has spread to i.e. metastases?

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20
Q

What are the most common cancers to metastasise to the brain?

A

Lung, breast, kidney, GI tract and skin

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21
Q

How do you investigate a brain tumour?

A

Brain imaging - CT/MRI

Brain biopsy/surgery

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22
Q

How is a brain tumour treated?

A

Often non-curative
Radio/chemotherapy - limited use
Consider palliative care

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23
Q

What can a glioma progress to?

A

Glioblastoma when it gets to grade 4 = really bad

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24
Q

When should you suspect a brain tumour when a patient presents with a headache?

A 
New onset headache + history of cancer
Cluster headache
Seizure
Significantly altered consciousness, memory, confusion
Papilloedema
Other abnormal neuro exam
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25
Q

What are the signs of raised ICP?

A

Papilloedema
Focal neurological signs
Loss of consciousness
New onset seizures

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26
Q

What are the symptoms of raised ICP?

A

Headache
Drowsiness
Vomiting

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27
Q

What nerves are affected in a polyneuropathy?

A

Lots of nerves affected all over body

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28
Q

What nerves are affected in a mononeuropathy?

A

Just one nerve

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29
Q

How does polyneuropathy present?

A

Slowly progressive
Sensory symptoms
Motor symptoms e.g. weakness
Trophic changes

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30
Q

What are the sensory symptoms of a polyneuropathy?

A

Loss of touch/proprioception/pain/temp, paraesthesia

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31
Q

What are the trophic changes in a polyneuropathy?

A

Dry scaly pigmented skin with ulcers/callouses

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32
Q

What causes polyneuropathy?

A

Diabetes and CMT disease

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33
Q

How does mononeuropathy present?

A

Upper limb nerves mostly affected at compression points

Sensory/motor symptoms in dermatome and myotome supplied by nerve

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34
Q

What causes mononeuropathy?

A

Most common = median nerve entrapment at wrist (CTS)

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35
Q

What are the other peripheral nerve causes of weakness?

A 
Metabolic - B12 deficiency
Uraemia
Thyroid
Alcohol
Toxins
Drugs
Paraneoplastic
Guillain Barre
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36
Q

What pattern of neuropathy does vasculitis normally present with?

A

Asymmetrical sensorimotor, often patchy distribution

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37
Q

How do you investigate neuropathy?

A

Mostly clinical
Bloods - FBC, U+Es, ESR, glucose, TFTs, LFTs, B12, folate
Vasculitic antibodies if vasculitis suspected e.g. ANA, ANCA, anti-dsDNA, RhF etc.
Nerve conduction studies

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38
Q

How is neuropathy managed?

A

Neuropathic analgesia options = gabapentin, pregablin, amitriptyline

Treat underlying cause e.g. diabetes control, steroids if vasculitis/inflammatory

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39
Q

How does CTS present?

A

Pain and parasthesia in thumb, index and middle finger
Wakes people from sleep in morning
Can’t open jars

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40
Q

What nerve is affected in CTS?

A

Median nerve = C6-T1

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41
Q

What causes CTS?

A

Entrapped at wrist e.g. sleeping position

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42
Q

How does an ulnar nerve mononeuropathy present?

A

Pain and parasthesia in little and ring fingers and forearm

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43
Q

What are the nerve roots of the ulnar nerve?

A

C8-T1

44
Q

What causes an ulnar nerve mononeuropathy?

A

Entrapped at cubital tunnel at elbow - elbow fracture/arthritis

45
Q

How does a common peroneal nerve mononeuropathy present?

A

Foot drop

Sensory deficit over dorsum of foot

46
Q

What are the nerve roots of the common peroneal nerve?

A

L4-S2

47
Q

What causes a common peroneal nerve mononeuropathy?

A

Compressed against head of fibula

48
Q

How does a radial nerve mononeuropathy present?

A

Can’t extend fingers or wrist > wrist drop

49
Q

What causes a radial nerve mononeuropathy?

A

Falls - spiral fracture of humerus

Sitting/sleeping with arm on chair/underneath someone = ‘Saturday night palsy’

50
Q

What are the nerve roots of the radial nerve?

A

C5-T1

51
Q

What is Guillain Barre Syndrome (GBS)?

A

Demyelinating disease of the PNS

52
Q

What causes GBS?

A

Unknown

53
Q

What triggers GBS?

A

Usually triggered by infections - bacteria, viruses

54
Q

What bacteria commonly cause GBS?

A

Campylobacter jejuni, mycoplasma pneumoniae

55
Q

What viruses commonly cause GBS?

A

Cytomegalovirus, EBV

56
Q

What are the features of GBS?

A

Progressive onset limb weakness/paralysis (LMN signs)
Numbness/tingling
CN and autonomic nerves may be involved

57
Q

How does GBS present?

A

Ascending pattern - starts distally and spreads proximally

Usually symmetrical

58
Q

How are the CN involved in GBS?

A

Diplopia, difficulty speaking, bulbar palsy

59
Q

How are the autonomic nerves involved in GBS?

A

Constipation, urinary incontinence etc.

60
Q

How is GBS diagnosed?

A

Clinical - tests can be normal in early disease
LP
Nerve conduction tests and EMG studies - shows slowing of motor conduction

61
Q

What does a LP show for GBS?

A

CSF shows increase in protein or albumin without raised white cells, normal glucose

62
Q

What is a key complication of GBS?

A

Involvement of respiratory muscles > respiratory depression > risk of death

63
Q

What must be monitored in GBS?

A

FVC serially (spirometry)

64
Q

How is GBS treated?

A

Aimed at reducing symptoms
Supportive therapy - physio, feeding tubes, heparin to prevent DVT
Immunosuppressants - IV IG reduces duration and severity of paralysis
Plasmapheresis

65
Q

What is plasmapheresis?

A

Plasma filtered to eliminate bad antibodies

66
Q

What is the prognosis for GBS?

A

Slowly recover over weeks-months as there is regrowth of myelin
20% have permanent neurological damage

67
Q

What happens in a CNIII palsy?

A

Loss of motor function to extraocular muscles (except superior oblique and lateral rectus) + parasympathetic supply responsible for pupillary constriction

68
Q

How does CNIII palsy present?

A

Down and out appearance
Ptosis
Mydriasis

69
Q

What is Horner’s syndrome?

A

Damage to sympathetic nerves of face

70
Q

How does Horner’s syndrome present?

A

Unilateral

Miosis - constricted pupil
Anhidrosis - loss of sweating
Partial ptosis - dropping upper eyelid

71
Q

How does Bell’s palsy present?

A

Ipsilateral LMN facial weakness e.g. inability to wrinkle brow, close eye, asymmetrical smile, drooping mouth
Hyperacusis (hypersensitivity to sound)

72
Q

What nerve is affected in Bell’s palsy?

A

CN VII

73
Q

What does CNVII innervate?

A

Muscles of facial expression and stapedius muscle + taste to anterior 2/3 of tongue

74
Q

How does a LMN facial nerve lesion present?

A

E.g. Bell’s palsy

Upper and lower facial paralysis

75
Q

How does a UMN facial nerve lesion present?

A

E.g. stroke

Lower facial paralysis only - forehead is spared

76
Q

What does CNIV do?

A

Innervates superior oblique

Medial rotation, depression and abduction

77
Q

What does CNVI do?

A

Lateral rectus

Abducts the eye (ABducens ABducts)

78
Q

Why is the eye down and out in CNIII palsy?

A

Unopposed action of superior oblique and lateral rectus muscles

79
Q

Why is there ptosis in CNIII palsy?

A

Loss of innervation to levator palpebrae superioris

80
Q

Why is there mydriasis in in CNIII palsy?

A

Loss of parasympathetic fibres that innervate the sphincter pupillae muscle

81
Q

What is the pathophysiology of myasthenia gravis?

A

Disorder of neuromuscular transmission due to binding of autoantibodies (anti-AChR and anti-MuSK) to the Ach receptor at NMJs.

82
Q

What does myasthenia gravis have a strong link with?

A

Thymus is abnormal in majority - strong link with thymoma

83
Q

How is myasthenia gravis investigated?

A

Bloods - serum anti-AChR/anti-MuSK
CT thymus
Crushed ice test
EMG

84
Q

What is the crushed ice test?

A

Ice applied to ptosis for few mins > if ptosis improves = indicative of MG

85
Q

What does an EMG show for MG?

A

Decremental muscle response to repetitive stimulation

86
Q

How does MG present?

A

Muscle weakness that get worse with use and improve with rest = fatigueability, especially with repetitive movements
No sensory symptoms

87
Q

What muscles are most affected in MG?

A

Proximal muscles + muscles of head/neck/eyes most affected

88
Q

What are the symptoms of MG?

A 
Diplopia
Ptosis
Myasthenic snarl on smiling (outer corners of lips don't elevate)
Weakness in facial movements
Difficulty swallowing
Dysarthria
89
Q

How is MG managed?

A

Acetylcholinesterase inhibitors e.g. pyridostigmine = 1st line
Steroids/immunosuppressants
Consider thymectomy

90
Q

What is the main complication of MG?

A

Myasthenic crisis

91
Q

What is myasthenic crisis?

A

Acute worsening of symptoms often triggered by another illness

92
Q

What can myasthenic crisis lead to?

A

Can lead to respiratory failure due to weakness of respiratory muscles > do an FVC

93
Q

How is myasthenic crisis treated?

A

May require ventilation/intubation

Treat with immunomodulatory therapies (IV Ig) and plasma exchange

94
Q

What causes Lambert-Eaton syndrome?

A

Paraneoplastic - especially small cell lung cancer

Autoimmune - antibodies against voltage gated calcium channels in presynaptic membranes > defective Ach release

95
Q

How does Lambert-Eaton syndrome present?

A

Weakness

Autonomic involvement e.g. dry mouth, incontinence

96
Q

How do you investigate Lambert-Eaton syndrome?

A

Serum auto-antibodies

EMG - incremental muscle response to repetitive stimulation (differentiates from MG)

97
Q

How is Lambert-Eaton syndrome treated?

A

Treat cancer if present
IV Ig or immunosuppressants
Symptomatic treatment - pyridostigmine

98
Q

Where does weakness affect in LES?

A

Proximal muscles around pelvic girdle +/- shoulder

99
Q

What does weakness in LES improve with?

A

Sustained/repeated exercise

100
Q

What is LES similar to?

A

MG

101
Q

Give examples of focal neurological deficit symptoms seen in brain tumours.

A

Sensory loss, ataxia, speech disturbances

102
Q

What is pyridostigmine?

A

Acetylcholinesterase inhibitor

103
Q

What improves pain in CTS?

A

Hanging arm over side of bed

104
Q

Why do people with CTS struggle to open jars?

A

Wasting of thenar muscles

105
Q

What part of the hand is not affected in CTS?

A

Palm

106
Q

Where do polyneuropathies present?

A

‘Glove and stocking’ distribution

Often symmetrical, starts in legs

107
Q

What is the non-medicated treatment for HD?

A

MDT - physio, OT, SALT

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