Neurology - Nerve Injury Flashcards

1
Q

What is Bell’s palsy?

A

An acute, unilateral, idiopathic facial nerve (CN VII) paralysis.

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2
Q

Features of Bell’s palsy.

A

LMN facial nerve palsy - forehead affected.

Patients may also notice:
- post-auricular pain
- altered taste
- dry etes
- hyperacusis

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3
Q

Management of Bell’s palsy.

A
  • oral prednisolone within 72 hours of presentation
  • antivirals

Eye care:
- prescription of artificial tears
- close eye at night with microporous tape

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4
Q

Follow-up of Bell’s palsy.

A

Urgent referral to ENT if no improvement within 3 weeks.

Long-standing Bell’s palsy may require plastic surgery involvement.

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5
Q

Prognosis of Bell’s palsy.

A

Most people make a full recovery within 3-4 months.

If untreated, 15% of patients can have permanent moderate to severe weakness.

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6
Q

What is trigeminal neuralgia?

A

A pain syndrome characterised by severe unilateral pain.

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7
Q

Features of trigeminal neuralgia.

A

Unilateral facial pain:
- electric shock-like
- evoked by light touch

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8
Q

Causes of trigeminal neuralgia.

A

Most commonly idiopathic.

Compression by tumours or vascular issues may cause trigeminal neuralgia.

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9
Q

Red flag symptoms and signs suggestive of a serious underlying cause of trigeminal neuralgia.

A
  • sensory changes
  • deafness or other ear problems
  • pain in opthalmic region only
  • bilateral pain
  • optic neuritis
  • onset <40 years
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10
Q

Management of trigeminal neuralgia.

A

Carbamazepine first line.

Failure to respond to treatment or atypical features should prompt referral to neurology.

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11
Q

Features of vestibular schwannoma.

A

CN VIII: vertigo; unilateral sensorineural hearing loss; unilateral tinnitus.

CN V: absent corneal reflex.

CN VII: facial palsy.

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12
Q

Management of vestibular schwannoma.

A

Urgent referral to ENT - the tumour is often slow growing, benign and observed initially.

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13
Q

Investigations of vestibular schwannoma.

A

MRI of the cerebellopontine angle.

Audiometry.

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14
Q

Management of vestibular schwannoma.

A
  • surgery
  • radiotherapy
  • observation
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15
Q

What is Erb’s palsy?

A

Damage to C5, C6 nerve roots caused by breech presentation.

Winged scapula; external rotation of shoulder and wrist flexion.

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16
Q

What is Klumpke’s palsy?

A

Damage to T1 nerve root caused by traction.

Loss of intrinsic hand muscles.

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17
Q

What is carpal tunnel syndrome?

A

Compression of the median nerve within the carpal tunnel.

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18
Q

Symptoms of carpal tunnel syndrome.

A
  • paraesthesia in thumb, index and middle finger
  • ascending symptoms
  • shaking hand relieves sx
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19
Q

Examination of carpel tunnel syndrome.

A

Tinel’s sign: tapping causes paraesthesia.

Phalen’s sign: flexion of wrist causes paraesthesia.

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20
Q

Causes of carpal tunnel syndrome.

A
  • idiopathic
  • pregnancy
  • oedema (e.g. heart failure)
  • lunate fracture
  • rheumatoid arthritis
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21
Q

Electrophysiology of carpal tunnel syndrome.

A

Motor and sensory prolongation of action potential in median nerve.

Can do nerve conduction studies.

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22
Q

Treatment of carpal tunnel syndrome.

A

Conservative:
- corticosteroid injection
- wrist splint at night

Surgical decompression if sx are severe (ie. flexor retinaculum division).

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23
Q

Divisions of the sciatic nerve.

A
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24
Q

MOA for common peroneal nerve injury.

A
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25
Q

Feature of common peroneal nerve injury.

A

FOOT DROP.

  • weakness of foot dorsiflexion
  • weakness of foot eversion
  • weakness of extensor hallucis longus
  • sensory loss over dorsum of foot and lower lateral leg
  • wasting of anterior tibial and peroneal muscles
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26
Q

What nerve is affected in meralgia paraesthetica?

A

Lateral femoral cutaneous nerve.

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27
Q

Risk factors for meralgia paraesthetica.

A
  • obesity
  • pregnancy
  • tense ascites
  • trauma
  • iatrogenic (ie. spinal surgery)
  • gymnastics
  • idiopathic
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28
Q

Symptoms of meralgia paraesthetica.

A

Upper lateral aspect of thigh:
- burning, tingling, shooting pain
- numbness
- deep muscle ache
- aggravated by standing; relieved by sitting

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29
Q

Signs of meralgia paraesthetica.

A

Reproduce sx by deep palpation below the ASIS.

Altered sensation over upper lateral aspect of thigh.

No motor weakness.

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30
Q

Path of the radial nerve.

A
  1. Lies posterior to the axillary artery.
  2. Enters the arm between the brachial artery and long head of triceps.
  3. Spirals around the radial groove in the proximal humerus.
  4. Descends down the lateral epicondyle of the humerus.
  5. Lies deeply between brachialis and brachioradialis.
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31
Q

Radial nerve innervation (m).

A
  • triceps
  • aconeus
  • brachioradialis
  • extensor carpi radialis
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32
Q

Radial nerve innervation - posterior interosseous branch (m).

A
  • supinator
  • extensor carpi ulnaris
  • extensor digitorum
  • extensor indicis
  • extensor digiti minimi
  • extensor pollicis longus and brevis
  • abductor pollicus longus
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33
Q

Radial nerve innervation (s).

A
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34
Q

Features of damage to radial nerve.

A
  • wrist drop
  • sensory loss to dorsal aspect of the 1st and 2nd metacarpals

If damaged in the axilla, paralysis of triceps also occurs.

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35
Q

What is thoracic outlet syndrome?

A

Compression of:
- brachial plexus
- subclavian artery
- subclavian vein

at the site of the thoracic outlet.

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36
Q

Causes of thoracic outlet syndrome.

A
  • neck trauma
  • cervical rib
  • scalene muscle hypertrophy
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37
Q

Presentation of neurogenic TOS.

A
  • painless muscle wasting of hand muscles
  • sensory symptoms

NB: autonomic nerve involvement causes cold hands, blanching and swelling.

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38
Q

Presentation of vascular TOS.

A

Subclavian a. compression: painful arm claudication, ulceration and gangrene.

Subclavian v. compression: painful arm swelling with distended veins.

39
Q

Examination of TOS.

A
  • neurological examination
  • MSK examination
40
Q

Differentials for TOS.

A
  • cervical radiculopathy
  • shoulder injury
  • carpal tunnel syndrome
41
Q

Investigations of TOS.

A
  • chest and cervical spine plain films (?obvious osseous abnormalities)
  • MRI (?cervical root lesion)
  • venography / angiography (?vascular TOS)
  • anterior scalene block to confirm neurogenic TOS
42
Q

Treatment of TOS.

A

Conservative for neurogenic TOS:
- education
- rehabilitation
- physiotherapy

Surgical decompression is warranted where conservative management has failed, or first line in vascular TOS.

43
Q

Function of ulnar nerve (m).

A
  • medial two lumbricals
  • aDductor pollicis
  • interossei
  • hypothenar muscles
  • flexor carpi ulnaris
44
Q

Function of ulnar nerve (s).

A
45
Q

Ulnar nerve damage at wrist.

A

Claw hand:
- hyperextension of MCPJ
- flexion and DIPJ and PIPJ (FDP spared)

46
Q

Ulnar nerve damage at elbow.

A

Claw hand:
- hyperextension of MCPJ

Looks less severe, but is a more significant nerve injury.

47
Q

L3 nerve root compression - features.

A

-Sensory loss over anterior thigh
-Weak hip flexion, knee extension and hip adduction
-Reduced knee reflex
-Positive femoral stretch test

48
Q

L4 nerve root compression - features.

A
  • Sensory loss anterior aspect of knee and medial malleolus
  • Weak knee extension and hip adduction
  • Reduced knee reflex
  • Positive femoral stretch test
49
Q

L5 nerve root compression - features.

A
  • Sensory loss dorsum of foot
  • Weakness in foot and big toe dorsiflexion
  • Reflexes intact
  • Positive sciatic nerve stretch test
50
Q

S1 nerve root compression - features.

A
  • Sensory loss posterolateral aspect of leg and lateral aspect of foot
  • Weakness in plantar flexion of foot
  • Reduced ankle reflex
  • Positive sciatic nerve stretch test
51
Q

Management of prolapsed disc.

A
  • analgesia (NSAIDs + PPI)
  • physiotherapy
  • exercise

NB: if sx persist >6 weeks, referral for consideration of MRI if appropriate.

52
Q

What type of nerve injury does diabetes usually result in?

A

Sensory loss

53
Q

Distribution of diabetic neuropathy.

A

Glove and stocking distribution.

Lower legs affected first due to long length of sensory neurones supplying the area.

54
Q

Management of diabetic neuropathy.

A

First line: amitriptyline, duloxetine, gabapentin, pregabalin.

Tramadol may be used as a rescue therapy for exacerbations of neuropathic pain.

55
Q

Gastrointestinal neuropathic complications of diabetes.

A

Gastroparesis:
- occurs secondary to autonomic neuropathy
- symptoms include erratic blood glucose control, bloating and vomiting
- management options include metoclopramide, domperidone or erythromycin (prokinetic agents)

Chronic diarrhoea:
- often occurs at night

Gastro-oesophageal reflux disease:
- caused by decreased lower esophageal sphincter (LES) pressure

56
Q

What is neuropathic pain?

A

Pain which arises following damage or disruption to the nervous system.

57
Q

Examples of causes of neuropathic pain.

A
  • diabetic neuropathy
  • trigeminal neuralgia
  • prolpased intervertebral disk
58
Q

First line management of neuropathic pain.

A
  • amitriptyline
  • duloxetine
  • gabapentin
  • pregabalin

If the first-line drug treatment doesn’t work, try one of the other three drugs.

NB: tramadol can be used as rescue therapy for acute exacerbations.

59
Q

Sensory innervation to the face.

A

Trigeminal nerve:
- opthalmic branch (Va)
- maxillary branch (Vb)
- mandibular branch (Vc)

60
Q

Differentials for facial pain.

A
  • trigeminal neuralgia
  • sinusitis
  • dental problems (e.g. abscess)
  • tension-headache
  • migraine
  • giant cell arteritis
61
Q

What is cervical spondylosis?

A

A degenerative osteoarthritis condition affecting the cervical spine.

Results in narrowing of the spinal canal and resultant neurological dysfunction.

62
Q

Features of cervical spondylosis.

A
  • motor weakness
  • sensory loss
  • bladder / bowel dysfunction
  • neck pain
  • ataxic gait
  • UMN lesion in legs
63
Q

Complications of cervical spondylosis.

A
  • radiculopathy
  • myelopathy
64
Q

What is Guilliain-Barre syndrome?

A

Immune mediated demyelination of the peripheral nervous system, often triggered by infection (ie. Campylobacter jejuni).

65
Q

Presentation of Guillain-Barre syndrome.

A

Initially back/leg pain.

Progressive, symmetrical weakness of all limbs:
- weakness is ascending
- reflexes are absent or reduced
- sensory symptoms are mild

66
Q

Investigations for Guillain-Barre syndrome.

A
  • lumbar puncture (rise in protein, normal WCC)
  • nerve conduction studies (decreased motor nerve conduction velocity)
67
Q

Name some drugs that cause peripheral neuropathy.

A
  • amiodarone
  • isoniazid
  • vincristine
  • nutrofurantoin
  • metronidazole
68
Q

Causes of peripheral neuropathy - predominantly motor loss.

A
  • Guillain-Barre syndrome
  • lead poisoning
  • diphtheria
  • chronic inflammatory demyelinating polyneuropathy (CIDP)
  • hereditary sensorimotor neuropathies (HSMN)
69
Q

Causes of peripheral neuropathy - predominantly sensory loss.

A
  • diabetes
  • uraemia
  • alcoholism
  • B12 deficiency
  • amyloidosis
70
Q

Complication of B12 deficiency.

A

Subacute degeneration of the spinal cord.

NB: recreational nitrous oxide inhalation may also result in vitamin B12 deficiency.

71
Q

Which three structures are affected in subacute combined degeneration of the spinal cord?

A
  • dorsal column
  • lateral corticospinal tract
  • spinocerebellar tract
72
Q

Features of subacute combined degeneration of the spinal cord - dorsal column involvement.

A
  • distal tingling / burning affecting the legs > arms
  • impaired propriocepetion and vibration sense
73
Q

Features of subacute combined degeneration of the spinal cord - lateral corticospinal tract involvement.

A
  • muscle weakness, hyperreflexia and spasticity
  • UMN signs in legs first
  • brisk knee reflexes
  • absent ankle jerks
  • extensor plantars
74
Q

Features of subacute combined degeneration of the spinal cord - spinocerebellar tract involvement.

A
  • sensory ataxia
  • positive Romberg’s sign
75
Q

Features of Horner’s syndrome.

A
76
Q

Pathophysiology of Horner’s syndrome.

A

Compression of the sympathetic chain (ie. typically pancoast tumour, cervical rib) results in features of Horner’s syndrome:

  • miosis (no innervation to dilator pupillae)
  • ptosis (no innervation to LPS)
  • anhidrosis (no sympathetic stimulation of sweat glands)
77
Q

Causes of Horner’s syndrome.

A
78
Q

Causes of bilateral ptosis.

A
  • myotonic dystrophy
  • myasthenia gravis
  • syphilis
  • congenital
79
Q

Causes of unilateral ptosis.

A
  • third nerve palsy
  • Horner’s syndrome
80
Q

Features of third nerve palsy.

A
  • ptosis
  • eye deviation down and out*

*CN VI innervates lateral rectus; CN IV innervates superior oblique (LR6SO4).

81
Q

Causes of third nerve palsy.

A
  • diabetes mellitus
  • vasculitis (e.g. temporal arteritis, SLE)
  • uncal herniation
  • cavernous sinus thrombosis
82
Q

Types of aphasia.

A
  • Wernicke’s (receptive) aphasia
  • Broca’s (expressive) aphasia
  • conduction aphasia
  • global aphasia
83
Q

Cause of Wernicke’s aphasia.

A

Lesion of the superior temporal gyrus - usually supplied by inferior division of left MCA.

84
Q

Features of Wernicke’s aphasia.

A

Wernicke’s area forms the speech before sending it to Broca’s area.

Lesions result in sentences that make no sense, but speech remains fluent (ie. word salad).

Comprehension is impaired.

85
Q

Cause of Broca’s aphsia.

A

Lesion of the inferior frontal gyrus - typically supplied by the superior division of the left MCA.

86
Q

Features of Broca’s aphasia.

A

Speech is non-fluent, laboured and halting.

Repetition impaired.

Comprehesion is normal.

87
Q

Cause of conduction aphasia.

A

Stroke affecting the arcuate fasiculus - the connection between Wernicke’s and Broca’s area.

88
Q

Features of conduction aphasia.

A

Speech is fluent but repetition is poor - aware of the errors they are making.

Comprehension is normal.

89
Q

Cause of global aphasia.

A

Large lesion affecting all three of:
- Broca’s area (inferior frontal gyrus)
- Wernicke’s area (superior temporal gyrus)
- arcuate fasiculus

Resulting in a severe expressive and receptive aphasia.

90
Q

Most common primary tumours that result in MSCC.

A
  • breast
  • lung
  • prostate cancer
91
Q

Features of MSCC.

A
  • back pain (worse on lying, coughing)
  • lower limb weakness
  • sensory loss and numbness
  • areflexia at level of lesion
  • hyperreflexia below level of lesion
92
Q

Investigations for MSCC.

A
  • urgent MRI of whole spine within 24 hours of presentation
93
Q

Management of MSCC.

A
  • high dose oral dexamethasone

Urgent oncological assessment for consideration of treatment within 24 hours:
- radiotherapy
- surgery