Week 12 - Neurology Flashcards

1
Q

What are the names of the 12 cranial nerves?

A
I- olfactory
II- optic 
III- oculomotor
IV- trochlear
V- trigeminal
VI- abducens
VII- facial 
VIII- vestibulocochlear
IX- glossopharyngeal
X- vagus
XI- spinal accessory
XII- hypoglossal
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2
Q

What is the component & function of the olfactory nerve?

A
  • Component: Sensory

- Function: Smell

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3
Q

What is the tract of olfactory nerve?

A

Olfactory cells of nasal mucosa –> Olfactory bulbs –> pyriform cortex

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4
Q

What is the component & function of the optic nerve?

A
  • Component(s): Sensory

- Function: Vision

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5
Q

What is the tract of optic nerve?

A

Retinal ganglion cells –> optic chiasm –> thalamus –> primary visual cortex in occipital lobe

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6
Q

What 4 examinations should you do to assess the optic nerve?

A
  1. Optic discs with ophthalmoscope
  2. Pupillary responses
  3. Visual acuity (using Snellen chart)
  4. Visual fields & blind spot (tested by confrontation)
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7
Q

What are the 2 components & functions of the oculomotor nerve?

A
  • Component 1: Motor
  • Function 1: movement of eyeball & lens accommodation
  • Component 2: Parasympathetic
  • Function 2: pupil constriction
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8
Q

What are the 2 nuclei locations of the oculomotor nerve?

A
  1. Midbrain oculomotor

2. Midbrain Edinger-Westphal

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9
Q

What structures are innervated by the motor component of the oculomotor nerve?

A
  • Inferior oblique, superior, medial & inferior recti muscles
  • Levator palpebrae superioris
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10
Q

What structures are innervated by the parasympathetic component of the oculomotor nerve?

A

Ciliary muscle & pupillary constrictor muscles

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11
Q

What is the component & function of the trochlear nerve?

A
  • Component: Motor

- Function: Moves eyeball

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12
Q

What is the nucleus location of the trochlear nerve?

A

Midbrain (inferior colliculus)

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13
Q

What structure is innervated by the trochlear nerve?

A

Superior oblique muscles

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14
Q

What eye movements does the Superior oblique muscles provide?

A

Depresses the adducted eye & intorts the abducted eye

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15
Q

What cranial nerve has the longest intracranial course?

A

Trochlear nerve

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16
Q

What 2 cranial nerves decussate to contralateral side?

A

II and IV

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17
Q

What is the component & function of the abducens nerve?

A
  • Component: Motor

- Function: Eyeball movement

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18
Q

Where is the nucleus located for the abducens nerve?

A

Pons

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19
Q

What structure is innervated by the abducens nerve?

A

Lateral rectus muscles

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20
Q

What type of disorder is internuclear opthalmoplegia?

A

Disorder of conjugate gaze- failure of adduction of affected eye with nystagmus on lateral gaze in contralateral eye

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21
Q

Describe internuclear opthalmoplegia?

A
  • Unilateral or bilateral
  • Results from lesion of medial longitudinal fasiculus (connects III & VI nerve nuclei)
  • Commonly seen in multiple sclerosis
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22
Q

What are the 4 clincial features of Horner’s syndrome?

A
  1. Miosis
  2. Ptosis
  3. Apparent enopthalmos
  4. Anhidrosis
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23
Q

What does horner’s syndrome result from?

A

Ipsilateral disruption of cervical / thoracic sympathetic chain

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24
Q

List 8 causes of Horner’s syndrome?

A
  1. Congenital
  2. Brainstem stroke
  3. Cluster headache
  4. Apical lung tumour
  5. Multiple sclerosis
  6. Carotid artery dissection
  7. Cervical rib
  8. Syringomyelia
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25
Q

What are the 2 components of the trigeminal nerve?

A
  1. Motor

2. Sensory input from face

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26
Q

Where is the nucleus for the sensory input component of the trigeminal nerve?

A

Pons & medulla

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27
Q

What structures are innervated by the trigeminal nerve?

A

Face (ophthalmic, mandibular & maxillary divisions) & anterior 2/3 of tongue

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28
Q

What is the function & nucleus location of the motor component of the trigeminal nerve?

A
  • Function: Mastication

- Nucleus location: Pons

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29
Q

What 3 structures are innervated by the motor component of the trigeminal nerve?

A
  1. Masseter
  2. Temporalis
  3. Medial & lateral pterygoids
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30
Q

Describe Herpes zoster ophthalmicus?

A
  • Pain may precede vesicles
  • Lifetime risk of 1%
  • V2 / V3 rarely affected
  • Elderly and immuno-compromised at risk
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31
Q

How is Herpes zoster ophthalmicus treated?

A

Oral aciclovir

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32
Q

What are the 3 components of the facial nerve?

A
  1. Motor
  2. Sensory
  3. Parasympathetoc
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33
Q

What is the nucleus location of the motor component of the facial nerve?

A

Pons

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34
Q

What is the function of the motor component of the facial nerve?

A

Muscles of expression

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35
Q

What is the nucleus location of the sensory & parasympathetic components of the facial nerve?

A

Medulla

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36
Q

What is the function of the sensory component of the facial nerve?

A

Taste

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37
Q

What structure is innervated by the sensory component of the facial nerve?

A

Anterior 2/3 of the tongue

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38
Q

What is the function of the parasympathetic component of the facial nerve?

A

Salivation & lacrimation

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39
Q

What does an upper motor neurone lesion cause in the face?

A

Weakness of inferior facial muscles

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40
Q

What does a lower motor neurone lesion cause in the face?

A

Weakness of superior & inferior facial muscles

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41
Q

Describe the corneal reflex?

A

Lightly touch cornea with cotton wool

  • Afferent: V
  • Efferent: VII
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42
Q

What does the corneal reflex test?

A

Pontine function

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43
Q

What are the 2 functions of the sensory vestibulocochlear nerve?

A
  1. Balance

2. Hearing

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44
Q

Where is the nucleus located for the vestibulocochlear nerve?

A

Pons & medulla

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45
Q

What structures are innervated for the balance component of the vestibulocochlear nerve?

A

Nerve endings within semi-circular canals –> cerebellum & spinal cord

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46
Q

What structures are innervated for the hearing component for the vestibulocochlear nerve?

A

Cochlear –> auditory cortex in the temporal lobes

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47
Q

What are the 2 tests for assessing the vestibulocochlear nerve?

A
  1. Rinne’s test

2. Weber’s test

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48
Q

What are the 3 components of the glossopharyngeal nerve?

A
  1. Sensory
  2. Motor
  3. Parasympathetic
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49
Q

Where is the nucleus located for the sensory & motor component the glossopharyngeal nerve?

A

Medulla

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50
Q

What is the function of the parasympathetic component of the glossopharyngeal nerve?

A

Saliva production

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51
Q

What are the 3 functions of the sensory component of the glossopharyngeal nerve?

A
  1. Taste
  2. Proprioception for swallowing
  3. Blood pressure receptors
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52
Q

What 3 structures are innervated by the sensory component of the glossopharyngeal nerve?

A
  1. Posterior 1/3 of tongue
  2. Pharyngeal wall
  3. Carotid sinus
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53
Q

What are the 2 functions of the motor component of the glossopharyngeal nerve?

A
  1. Swallow & gag reflex

2. Lacrimation

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54
Q

What 2 structures are innervated by the motor component of the glossopharyngeal nerve?

A
  1. Pharyngeal muscles

2. Lacrimal glands

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55
Q

What structure is innervated by the parasympathetic component of the glossopharyngeal nerve?

A

Parotid glands

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56
Q

Describe a Glossopharyngeal palsy?

A

Deviation of uvula away from the side of the lesion

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57
Q

What are the 3 components of the vagus nerve?

A
  1. Sensory
  2. Motor
  3. Parasympathetic
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58
Q

Where is the nuclear location of the sensory & motor components of vagus nerve?

A

Medulla

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59
Q

What are the 3 functions of the sensory component of the vagus nerve?

A
  1. Chemoreceptors
  2. Pain receptors (dura)
  3. Sensation
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60
Q

What are the 3 structures innervated by the sensory component of the vagus nerve?

A
  1. Blood oxygen concentration, carotid bodies
  2. Respiratory & digestive tracts
  3. External ear, larynx & pharynx
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61
Q

What are the 4 functions of the motor component of the vagus nerve?

A
  1. Heart rate & stroke volume
  2. Peristalsis
  3. Air flow
  4. Speech & swallowing
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62
Q

What are the 4 structures innervated by the motor component of the vagus nerve?

A
  1. Pacemaker & ventricular muscles
  2. Smooth muscles of the digestive tract
  3. Smooth muscles in bronchial tubes
  4. Muscles of larynx & pharynx
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63
Q

What are the structures innervated by the parasympathetic component of the vagus nerve?

A

Smooth muscles & glands of the same areas innervated by motor component, as well as thoracic & abdominal areas

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64
Q

What is the component & function of the spinal accessory nerve?

A
  • Component: Motor

- Function: head rotation & shoulder shrugging

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65
Q

What is the nucleus location of the spinal accessory nerve?

A

Medulla

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66
Q

What 2 structures are innervated by the spinal accessory nerve?

A
  1. Sternocleidomastoid

2. Trapezius muscles

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67
Q

What is the component & function of the hypoglossal nerve?

A
  • Component: Motor

- Function: speech & swallowing

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68
Q

What is the nucleus location of the hypoglossal nerve?

A

Medulla

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69
Q

What structure is innervated by the hypoglossal nerve?

A

Tongue

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70
Q

What 4 nerves are affected in a cavernous sinus lesion?

A
  1. III
  2. IV
  3. V (1st and 2nd divisions),
  4. VI
    (Horner’s syndrome)
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71
Q

What 4 nerves are affected in a superior orbital fissure lesion?

A
  1. III
  2. IV
  3. V (1st division)
  4. VI
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72
Q

What 3 nerves are affected in a cerebellopontine angle lesion?

A
  1. V
  2. VII
  3. VIII
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73
Q

What 3 nerves are affected in a jugular foramen lesion?

A
  1. IX
  2. X
  3. (XI)
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74
Q

What 4 nerves are affected in a bulbar/pseudobulbar palsy?

A
  1. IX
  2. X
  3. XI
  4. (XII)
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75
Q

What are the 3 upper limb nerves?

A
  1. Median nerve
  2. Ulnar nerve
  3. Radial nerve
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76
Q

What is the most common cause of radial nerve palsy?

A
  • Entrapment of nerve at spiral groove

- ‘Saturday night palsy’

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77
Q

What are the 2 factors of presenting symptoms in a radial nerve palsy?

A
  • Wrist & finger drop

- Usually painless

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78
Q

What weakness is associated with Extensor carpi radialis longus?

A

Wrist extension

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79
Q

What weakness is associated with Extensor digitorum communism?

A

Finger extension

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80
Q

What weakness is associated with Brachioradialis?

A

Elbow flexion in mid-pronation

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81
Q

What is the most common cause of ulnar nerve palsy?

A

Entrapment at ulnar groove (medial epicondyle of humerus)

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82
Q

What are the 3 presenting symptoms of ulnar nerve palsy?

A
  1. May be history of trauma at elbow
  2. Sensory disturbance & weakness “weak grip”
  3. Usually painless
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83
Q

What weakness is associated with 1st dorsal interosseus?

A

Index finger abduction

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84
Q

What weakness is associated with Abductor digiti minimi?

A

Pinkie abduction

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85
Q

What weakness is associated with Flexor carpi ulnaris?

A

Wrist flexion

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86
Q

What weakness is associated with Adductor pollicis?

A

Thumb adduction

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87
Q

What is the most common cause of median nerve palsy?

A

Entrapment within carpal tunnel at wrist

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88
Q

What are the 3 presenting symptoms of median nerve palsy?

A
  1. History of intermittent nocturnal pain, numbness & tingling- often relieved by shaking hand
  2. Patient may complain of “weak grip”
  3. Positive Tinel’s sign / Phalen’s test
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89
Q

What weakness is associated with Lumbricals I+II?

A

Flexion at MCP joints

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90
Q

What weakness is associated with Opponens pollicis?

A

Thumb opposition

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91
Q

What weakness is associated with Abductor pollicis brevis?

A

Thumb abduction

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92
Q

What weakness is associated with Flexor pollicis brevis?

A

Thumb flexion

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93
Q

What is the most common cause of median nerve II anterior interosseous branch palsy?

A

Trauma to forearm

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94
Q

What are the 3 presenting symptoms of median nerve II anterior interosseous branch palsy?

A
  1. History of forearm pain
  2. Patient may complain of “weak grip” of keys
  3. Positive Tinel’s sign / Phalen’s test
  4. You cannot do OK sign
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95
Q

Is there any sensory change associated with median nerve II anterior interosseous branch palsy?

A

NO

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96
Q

What weakness is associated with pronator Quadratus?

A

Flexion at MCP joints

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97
Q

What weakness is associated with Flexor Pollicus Longus?

A

Thumb flexion

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98
Q

What weakness is Flexor Digitorum Profundus (lateral)?

A

Thumb flexion

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99
Q

What 3 upper limb palsy’s have sensory changes?

A
  1. Radial nerve palsy
  2. Ulnar nerve palsy
  3. Median nerve palsy
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100
Q

What muscles are innervated by the radial nerve?

A

Tennis back hand

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101
Q

What muscles are innervated by the median nerve?

A

Forearm flexors (LOAF)

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102
Q

What muscles are innervated by the ulnar nerve?

A

Other hand muscles + Smaller ones (axillary, musculocutaneous)

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103
Q

What are the 3 thigh nerves?

A
  1. Femoral
  2. Obturator
  3. Sciatic
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104
Q

What muscles are innervated by the femoral nerve?

A

Quads

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105
Q

What muscles are innervated by the obturator nerve?

A

Adduction muscles

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106
Q

What muscles are innervated by the sciatic nerve?

A

Hamstrings

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107
Q

What is the most common cause of femoral nerve palsy?

A

Haemorrhage / trauma

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108
Q

What are the 3 presenting symptoms of femoral nerve palsy?

A
  1. Weakness of Quadriceps
  2. Weakness of Hip flexion
  3. Numbness in medial shin
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109
Q

What weakness is associated with quadriceps?

A

Knee Extension

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110
Q

What weakness is associated with Illiopsoas?

A

Hip flexion

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111
Q

What weakness is associated with Adductor Magnus?

A

Hip adduction

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112
Q

What are the 2 tibial/back lower leg nerves?

A
  1. Gastrocnemius

2. Soleus

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113
Q

What are the 2 peroneal/front lower leg nerves?

A
  1. Tibialis anterior

2. Peroneal

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114
Q

What is the most common cause of peroneal nerve palsy?

A

Entrapment at fibular head

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115
Q

What are the 3 presenting symptoms of peroneal nerve palsy?

A
  1. May be history of trauma, surgery or external compression
  2. Acute onset foot drop + sensory disturbance
  3. Usually painless
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116
Q

What happens to the foot in a peroneal nerve palsy?

A

Foot drop will occur but you shall still be able to invert your foot because its innervated (L5) differently

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117
Q

What weakness is associated with Tibialis anterior?

A

Ankle dorsiflexion

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118
Q

What weakness is associated with Extensor hallucis longus?

A

Great toe extension

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119
Q

What is mononeuritis multiplex?

A
  • Painful, asymmetrical, asynchronous sensory and motor peripheral neuropathy involving isolated damage to at least 2 separate nerve areas
  • Multiple nerves in random areas of the body can be affected
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120
Q

What are 6 common causes of mononeuritis multiplex?

A
  1. Diabetes
  2. Vasculitic- Churg Strauss, polyarteritis nodosa
  3. Rheumatological- Rheumatoid arthritis, Lupus, Sjogren’s syndrome
  4. Infective- Hepatitis C, HIV
  5. Sarcoidosis
  6. Lymphoma
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121
Q

What are 2 examples of polyneuropathy?

A
  1. Peripheral neuropathy

2. Guillain-Barre Syndrome

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122
Q

What is an example of a muscle/neuromuscular junction disorder?

A

Mysathenia gravis

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123
Q

What are the 3 functions of the peripheral nervous system?

A
  1. Sensory input to CNS
  2. Motor output to muscles
  3. Innervation of viscera
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124
Q

Where in the PNS does the incoming sensory information enter via?

A

Posterior root

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125
Q

Where in the spinal cord does the motor information exit via?

A

Anterior root

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126
Q

What is the collection of nerve cell bodies in PNS called?

A

Ganglia

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127
Q

What are the 2 types of large fibres (myelinated)?

A
  1. Motor nerves

2. Proprioception, vibration & light touch

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128
Q

What are the 2 types of thinly un/myelinated fibres?

A
  1. Light touch

2. Pain & temperature

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129
Q

Describe the 6 processes occurring at the neuromuscular junction & muscle?

A
  1. Action potential
  2. Voltage-gated Ca2+ channels open
  3. Ca2+ influx causes neurotransmitter-filled vesicles to fuse with cell membrane
  4. ACh released into synaptic cleft & binds to receptors, causing ion channels to open
  5. ACh binds to the postsynaptic receptors & causes the influx of Na+, which depolarises the cell
  6. Postsynaptic muscle cell depolarises, causing the opening of voltage-gated Ca2+ channels. The influx of Ca2+ initiates muscle contraction
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130
Q

Describe the motor presentation of neuropathy?

A

Weakness / muscle atrophy

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131
Q

Describe the 2 types of sensory presentations for neuropathy?

A
  1. Large (myelinated) fibres –> sensory ataxia, loss of vibration sense +/- numbness & tingling
  2. Small (thinly myelinated/ unmyelinated) fibres –> impaired pinprick, temperature, painful burning
    numbness & tingling
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132
Q

List the 4 autonomic presentations of neuropathy?

A
  1. Postural hypotension
  2. Erectile dysfunction
  3. GI disturbance
  4. Abnormal sweating
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133
Q

What happens to the tendon reflexes during a neuropathy?

A

May be reduced or absent

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134
Q

Describe Length-dependent axonal neuropathy?

A
  • Diffuse involvement of peripheral nerves
  • Age > 50 years
  • Length dependent: starts in toes / feet
  • Symmetrical
  • Slowly progressive
  • No significant sensory ataxia
  • Any weakness is distal & mild
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135
Q

What is the typical presentation of Length-dependent axonal neuropathy said to look like?

A

Glove & stocking pattern

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136
Q

List 11 causes of Length-dependent axonal neuropathy?

A
  1. Diabetes
  2. Alcohol
  3. Nutritional: Folate / B12 / thiamine /B6 deficiency
  4. Immune mediated
  5. Metabolic / endocrine
  6. Drugs
  7. Infectious
  8. Inherited
  9. Neoplastic: Myeloma
  10. Paraneoplastic
  11. Critical illness
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137
Q

List 4 immune mediated causes of Length-dependent axonal neuropathy?

A
  1. Rheumatoid arthritis
  2. Lupus
  3. Vasculitis
  4. Polyarteritis nodosa
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138
Q

List 2 metabolic/endocrine causes of Length-dependent axonal neuropathy?

A
  1. Renal failure

2. Hypothyroidism

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139
Q

List 4 drugs which cause Length-dependent axonal neuropathy?

A
  1. Isoniazid
  2. Cisplatin
  3. Amiodarone
  4. Gold
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140
Q

List 2 infections causing Length-dependent axonal neuropathy?

A
  1. HIV

2. Hepatitis B & C

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141
Q

List 2 inherited conditions causing Length-dependent axonal neuropathy?

A
  1. Charcot-Marie-Tooth

2. Hereditary neuropathy with liability to pressure palsy (HNPP)

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142
Q

Describe the presentation of peripheral neuropathy?

A
  • Pain in feet
  • Worse at night, irritated by bedsheets
  • Long duration (years)
  • Gradually worsening
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143
Q

What are 2 risk factors for peripheral neuropathy?

A
  1. Excessive drinking (increased GGT)

2. Diabetes (increased HBA1c)

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144
Q

Describe the presentation of Guillain-Barré syndrome?

A
  • Progressive (ascending) weakness over days
  • Flaccid, quadraparesis with areflexia +/- respiratory / bulbar / autonomic involvement
  • Some aching low back pain
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145
Q

Describe the CSF in Guillain-Barré syndrome?

A
  • Acellular
  • No organisms on microscopy or culture
  • Raised protein
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146
Q

What is Guillain-Barré syndrome?

A

Acute inflammatory demyelinating neuropathy

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147
Q

Describe the aetiology of Guillain-Barré syndrome?

A

Post-infectious autoimmune (campylobacter, CMV, EBV)

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148
Q

How is Guillain-Barré syndrome treated?

A

Intravenous immunoglobulin or apheresis

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149
Q

What is Chronic inflammatory demyelinating neuropathy (CIDP)/ chronic Guillain-Barré syndrome treated with?

A

Steroid & IVIG responsive

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150
Q

Describe the Proximal limb weakness in muscle disease?

A

Difficulty raising arms above head, arising from seated position

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151
Q

Describe the Facial weakness in muscle disease?

A

Characteristic myopathic facies, drooling

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152
Q

List the 2 Eye symptoms in muscle disease?

A
  1. Ptosis

2. Ophthalmoplegia (paralysis of the muscles within/surrounding the eye)

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153
Q

List the 2 bulbar symptoms in muscle disease

A
  1. Dysarthria

2. Dysphagia

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154
Q

List the 2 neck & spine symptoms in muscle disease?

A
  1. Head drop

2. Scoliosis

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155
Q

Describe the respiratory symptoms in muscle disease?

A

Breathlessness (especially on lying flat)

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156
Q

List the 2 myocardial symptoms in muscle disease?

A
  1. Exercise intolerance

2. Palpitation

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157
Q

List the 6 causes of muscle disease?

A
  1. Muscular dystrophies
  2. Metabolic muscle disorders
  3. Mitochondrial disorders
  4. Myotonic dystropies
  5. Inflammatory muscle disorders
  6. Neuromuscular junction disorders
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158
Q

List the 4 Muscular dystrophies causing muscle disease?

A
  1. Dystrophinopathies (Duchenne / Becker)
  2. Fascioscapulohumeral (FSH)
  3. Dystrophy
  4. Limb girdle
  5. Oculopharyngeal
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159
Q

List the 2 metabolic muscle disorders causing muscle disease?

A
  1. Glycogen storage diseases

2. Defects of fatty acid metabolism

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160
Q

List the 3 inflammatory muscle disorders causing muscle disease?

A
  1. Polymyositis
  2. Dermatomyositis
  3. Inclusion body myositis
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161
Q

List the 2 neuromuscular junction disorders causing muscle disease?

A
  1. Myasthenia gravis

2. Lambert Eaton syndrome

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162
Q

Describe the pathogenesis of Myasthenia gravis?

A

Autoimmune disorder: antibodies to acteylcholine receptor at post- synaptic NMJ

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163
Q

What are the 2 Myasthenia gravis associations?

A
  1. Other autoimmune disorders

2. May be associated with thymic hyperplasia or thymoma

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164
Q

Who is commonly affected by Myasthenia gravis?

A

Affects young women in 20’s & older men in 70’s

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165
Q

Describe the clinical signs of Myasthenia gravis?

A

Fatiguable weakness of ocular, bulbar, neck, respiratory &/or limb muscles

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166
Q

Describe the investigations for Myasthenia gravis?

A
  • Antibodies to AChR present in 85% of cases

- Single fibre EMG & repetitive nerve stimulation also abnormal

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167
Q

How is Myasthenia gravis managed?

A

Pyridostigmine (anti-acetylcholine esterase) & immunosuppressive therapies (eg. steroids & IV Immunoglobulin)

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168
Q

What is the commonest type of peripheral neuropathy?

A

Length-dependent axonal neuropathy

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169
Q

What neuropathy is a medical emergency?

A

Guillain-Barré syndrome

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170
Q

What is a primary headache?

A

Headache with no underlying cause ie. migraine, tension-type headache, cluster headache

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171
Q

What is a secondary headache?

A

Secondary to underlying cause
ie. Subarachnoid haemorrhage, space-occupying lesion, meningitis, temporal arteritis, high / low intracranial pressure, drug-induced

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172
Q

What 2 important features of the onset of a headache do you need to find out through the history?

A
  1. Time to maximal symptoms

2. Circumstances at onset

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173
Q

What 4 important features of the severity & quality of pain in a headache do you need to find out through the history?

A
  1. Pain scale 0 – 10
  2. Throbbing / pulsatile / ‘vice-like’ / stabbing
  3. Location / radiation of pain
  4. Presence of aura / prodrome
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174
Q

What 8 associated features are common in a migraine headache?

A
  1. Photophobia
  2. Phonophobia
  3. Osmophobia
  4. Nausea & vomiting
  5. Movement sensitivity
  6. Mood disturbance
  7. Diarrhoea
  8. Autonomic disturbance- lacrimation, conjunctival injection, nasal stuffiness
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175
Q

What associated feature is common in a cluster headache?

A

Periorbital autonomic disturbance

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176
Q

What are the 2 different ages at onset for headaches?

A
  1. Migraine usually starts in childhood / early adulthood

2. Age >50 years more likely to have secondary cause

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177
Q

List 6 triggers/ exacerbating/ relieving factors for a headache?

A
  1. Posture
  2. Valsalva
  3. Cough
  4. Alcohol
  5. Stress
  6. Sex/exertion
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178
Q

Describe the family history associated with headaches?

A

Upto 80% of migraineurs have 1st-degree relative with migraine

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179
Q

List the 3 social/employment histories associated with headaches?

A
  1. Alcohol
  2. Smoking
  3. Caffeine
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180
Q

List the 3 mediation histories associated with headaches?

A
  1. Prescribed & OTC analgesia
  2. Preventative drugs
  3. Recreational drugs
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181
Q

What else is associated with headaches?

A

Co-morbid depression / sleep disturbance

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182
Q

What does the red flag mnemonic “SNOOPT” stand for, suggesting a secondary headache?

A
  • Systemic symptoms
  • Neurological signs or symptoms
  • Older age at onset
  • Onset is acute (under 5 minutes)
  • Previous headache history is different / absent
  • Triggered headache (valsalva or posture)
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183
Q

What are the 4 specific red flag situations suggesting a secondary headache?

A
  1. Cancer
  2. Pregnancy
  3. Post-partum
  4. HIV /immunosupression
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184
Q

Describe the usual clinical examination of a patient with headache?

A

No abnormal signs will be present, abnormal signs suggest secondary cause

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185
Q

List the 6 general/systemic clinical examination findings in a patient with headache?

A
  1. Reduced conscious level
  2. BP / pulse
  3. Pyrexia
  4. Meningism
  5. Skin rash
  6. Temporal artery tenderness
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186
Q

List the 4 cranial nerve clinical examination findings in a patient with headache?

A
  1. Pupillary responses
  2. Visual fields +/- blind spot
  3. Eye movements
  4. Fundoscopy
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187
Q

List the 4 upper motor neurone signs in a patient with headache?

A
  1. Pronator drift
  2. Increased tone
  3. Brisk reflexes
  4. Extensor plantar response
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188
Q

List the 4 cerebellar signs in a patient with headache?

A
  1. Nystagmus
  2. Past-pointing
  3. Dysdiadochokinesis
  4. Broad-based ataxic gait
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189
Q

What gender is more prone to migraines?

A

Females

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190
Q

What 2 things do most patients with migraines have?

A
  1. Positive family history

2. Report triggers ie. hormonal, weather, stress, hunger, sleep disturbance, exertion, alcohol excess, foods

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191
Q

What are the 2 types of migraines?

A
  1. Migraine without aura (70%)

2. Migraine with aura (30%)

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192
Q

Describe the pathophysiology of a migraine?

A
  • Primary dysfunction in brainstem sensory nuclei (V, VII – X)
  • Pain results from pain sensitive cranial blood vessels & their innervating trigeminal fibres
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193
Q

Describe the pathophysiology of an aura in migraines?

A

Cortical spreading depression

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194
Q

What is activated in a migraine headache?

A

Trigeminovascular system (with CGRP & other neuropeptides)

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195
Q

List the 4 phases of a migraine as time goes on?

A
  1. Prodrome
  2. Aura
  3. Headache + associated features
  4. Postdrome
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196
Q

Describe prodromes in migraines?

A
  • Reported by 40-60%
  • Up to 48 hours before headache
  • Variable symptoms: mood disturbance / restlessness / hyperosmia / photophobia / diarrhoea
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197
Q

Describe aura’s in migraines?

A
  • Recurrent reversible focal neurological symptom (eg. visual, sensory, motor)
  • Develops over 5-20 mins & lasts <60 mins
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198
Q

Describe the 2 different types of aura’s occurring in migraines?

A
  1. Visual aura is most common

2. Sensory aura often starts in hand & migrates up arm

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199
Q

List the 4 different types of visual aura’s?

A
  1. Zigzag fortification spectrum
  2. Visual field loss
  3. Negative scotoma
  4. Positive scotoma
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200
Q

Describe the type of headache felt in a migraine?

A
  • Commonly throbbing or pulsatile
  • Moderate-severe intensity
  • Gradual onset, duration 4-72hrs
  • Unilateral in 60%, can radiate
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201
Q

What are the 2 complications of a migraine?

A
  1. Medication overuse headache (MOH)

2. Chronic migraine- headache on 15+ days per month

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202
Q

What are the 3 lifestyle managements for a migraine?

A
  1. Avoid triggers
  2. Reduce caffeine / alcohol intake
  3. Encourage regular meals & sleep patterns
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203
Q

What are the 3 acute managements for migraines?

A
  1. Simple analgesia (Paracetamol, Aspirin, NSAIDs)
  2. Triptans (Sumatriptan)
  3. +/- antiemetic (domperidone, metoclopramide)
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204
Q

What are the 3 prophylaxis managements for migraines?

A
  1. Beta-blockers (Propanolol)
  2. Tricyclic antidepressants (Amitriptyline, Dosulepin, Nortriptline)
  3. Anti-epilepsy drugs (Topiramate, Sodium Valproate)
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205
Q

What is the definition of a thunderclap headache?

A

Abrupt-onset of severe headache which reaches maximal intensity <5mins (& lasts >1hr)

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206
Q

What is the diagnosis of a thunderclap headache?

A

Should be considered as subarachnoid haemorrhage (SAH) until proven otherwise

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207
Q

What % of thunderclap headaches are due to a subarachnoid haemorrhage?

A

Approx 15%

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208
Q

List the 7 other causes of a thunderclap headache?

A
  1. Intracerebral haemorrhage
  2. Arterial dissection (vertebral or carotid)
  3. Cerebral venous sinus thrombosis
  4. Bacterial meningitis
  5. Rare- spontaneous intracranial hypotension, pituitary apoplexy
  6. Primary headaches (migraine, exertional headache, cluster headache)
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209
Q

What 7 blood tests would you do to investigate a thunderclap headache?

A
  1. U+E
  2. LFT
  3. Glucose
  4. Full blood count
  5. Coagulation screen
  6. CRP
  7. Blood cultures if pyrexial
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210
Q

What 4 investigations would you do for a thunderclap headache?

A
  1. Bloods
  2. 12-lead ECG
  3. Urgent CT brain- blood visible in >95% of SAH within first 4 hours
  4. Lumbar puncture- performed after 12 hours to look for xanthochromia
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211
Q

What is the normal intracranial pressure (ICP)?

A

7-15mmHg

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212
Q

What is Monroe-Kellie doctrine?

A

Any increase in 1 component results in reduction of other 2

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213
Q

What is the Cerebral perfusion pressure (CPP)?

A
  • Net pressure gradient causing blood to flow into the brain

- CPP= mean arterial pressure - ICP

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214
Q

For what 2 reasons is a raised ICP a problem?

A
  1. Global brain perfusion is reduced when ICP is elevated

2. Cerebral metabolism is reduced

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215
Q

List the 6 possible herniation effects of a raised ICP?

A
  1. Uncal
  2. Central (transtentorial)
  3. Cingulate (subfalcine)
  4. Transcalvarial
  5. Upward transtentorial (upward cerebellar)
  6. Tonsillar (downward cerebellar)
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216
Q

Describe the history of a patient with raised pressure headaches?

A
  • Worse on lying flat, improved on sitting / standing up
  • Worse in the morning
  • Persistent N/V
  • Worse on valsalva & physical exertion
  • Transient visual obscurations with change in posture
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217
Q

List the 6 examination findings in someone with a raised pressure headache?

A
  1. Optic disc swelling- papilloedema
  2. Impaired visual acuity / colour vision
  3. Restricted visual fields / enlarged blind spot
  4. IIIrd nerve palsy
  5. VIth nerve palsy
  6. Focal neurological signs
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218
Q

What are the 4 causes of a raised ICP?

A
  1. Mass effect- tumour, infarction with oedema etc
  2. Increased venous pressure
  3. Obstruction to CSF flow/absorption- hydrocephalus, meningitis
  4. Idiopathic intracranial hypertension
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219
Q

Describe the presentation of a low CSF pressure headache?

A

Headache worse on sitting / standing up and relieved by lying down, results from CSF leakage

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220
Q

What are the 2 causes of a low CSF pressure headache?

A
  1. Post-lumbar puncture

2. Spontaneous intracranial hypotension

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221
Q

What is the updated definition of a stroke (2013)?

A

Central nervous system infarction (includes brain, spinal cord & retinal cells attributable to ischaemia), based on objective evidence of focal ischaemic injury in a defined vascular distribution or clinical evidence of the former with other aetiologies excluded

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222
Q

What 3 things happen when a stroke occurs?

A
  1. Blood flow stopped
  2. Neurones depolarised- instant onset of early symptoms
  3. Brain tissue dies
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223
Q

List the 8 arteries in the brainstem?

A
  1. Anterior communicating artery
  2. Anterior cerebral artery
  3. Internal carotid artery
  4. Middle cerebral artery
  5. Posterior communicating artery
  6. Basilar artery
  7. Posterior cerebral artery
  8. Vertebral artery
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224
Q

List the 4 features of an acute onset stroke?

A
  1. Weakness: leg/ face & arm/ hemiparesis
  2. Dysphasia
  3. Visual disturbance: right homonymous heminopia
  4. Acute light-headedness (past-pointing, nystagmus)
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225
Q

What 2 cerebral arteries cause weakness in leg/face & arm/hemiparesis in stroke?

A
  1. Anterior cerebral artery

2. Middle cerebral artery

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226
Q

What is Broca’s area responsible for?

A

Fluid speech production

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227
Q

What is Wernicke’s area responsible for?

A

Understanding speech

228
Q

What 2 cerebral arteries cause dysphagia in stroke?

A
  1. Anterior cerebral artery

2. Middle cerebral artery

229
Q

What 2 cerebral arteries causes visual disturbance in stroke?

A
  1. Posterior cerebral artery

2. Middle cerebral artery

230
Q

What is the cerebellum responsible for?

A

Coordination of movements

231
Q

What cerebral artery causes acute light-headedness in stroke?

A

Posterior cerebral artery

232
Q

What are the 2 different types of stroke & how common are they?

A
  1. Haemorrhage (15-20%)

2. Ischaemic (80-85%)

233
Q

What is the definition of an ischemic stroke?

A

An episode of neurological dysfunction caused by focal cerebral, spinal, or retinal infarction

234
Q

List the 4 causes of ischaemic stroke?

A
  1. Atherosclerotic cerebrovascular disease 20%
  2. Small vessel disease “lacunes” 25%
  3. Cardiac embolism 20%
  4. Cryptogenic 30%
235
Q

What are the 4 classifications according to the Oxfordshire Community Stroke Project Classification?

A
  1. Total Anterior Circulation Syndrome (TACS)
  2. Partial Anterior Circulation Syndrome (PACS)
  3. Posterior Circulation Syndrome (POCS)
  4. Lacunar Syndrome (LACS)
236
Q

Describe Total Anterior Circulation Syndrome (TACS)?

A
  • Hemiparesis + Higher cortical dysfunction + hemianopia

- Usually proximal MCA or ICA occlusion

237
Q

Describe Partial Anterior Circulation Syndrome (PACS)?

A
  • Isolated higher cortical dysfunction OR
  • Any 2 of hemiparesis, higher cortical dysfunction, hemianopia
  • Usually branch MCA occlusion
238
Q

Describe Posterior Circulation Syndrome (POCS)?

A
  • Isolated hemianopia OR
  • Brainstem syndrome
  • Can include perforating arteries, PCA or cerebellar arteries
239
Q

Describe Lacunar Syndrome (LACS)?

A
  • Pure motor stroke OR pure sensory stroke OR sensorimotor stroke OR ataxic hemiparesis OR clumsy hand-dysarthria
  • Perforating artery / small vessel disease
240
Q

What is the definition of stroke caused by intracerebral haemorrhage?

A

Rapidly developing clinical signs of neurological dysfunction attributable to a focal collection of blood within the brain parenchyma or ventricular system that is not caused by trauma

241
Q

List the 8 causes of an intracranial bleed?

A
  1. Trauma
  2. Small vessel disease
  3. Amyloid angiopathy
  4. Abnormalities in blood vessels
  5. Blood clotting deficiencies
  6. Haemorrhagic transformation of an infarct
  7. Tumours
  8. Drug usage: cocaine, amphetamin
242
Q

List the 3 different treatment approaches for ischaemic stroke?

A

ALL IN STROKE UNIT:

  1. IV Thrombolysis
  2. Thrombectomy ± IV thrombolysis Aspirin
  3. Hemicranectomy
243
Q

List the 2 different treatment approaches for an intracranial bleed (haemorrhagic stroke)

A

ALL IN STROKE UNIT:

  1. Blood pressure control
  2. Neurosurgical evacuation
244
Q

What are the 3 available hyper-acute treatments proven to be effective for stroke?

A
  1. Thrombolysis- within 4.5 hrs of symptom onset
  2. Thrombectomy- within 6-8 hrs of symptom onset
  3. Admission to a stroke unit
245
Q

List 7 cerebrovascular risk factors which explains around 85% of all ischaemic stroke?

A
  1. High blood pressure
  2. Obesity
  3. Low physical activity
  4. Poor fatty diet
  5. Smoking
  6. Poverty
  7. Genetics
246
Q

List 5 common secondary prevention methods for reducing cerebrovascular risk factors?

A
  1. Weight loss
  2. Stop smoking
  3. Lower BP
  4. Blood thinners
  5. Healthy diet
247
Q

Describe the formation of an aneurysm?

A
  • Haemodynamic stress
  • Extensive inflammatory & immunological
    reactions are common in unruptured intracranial aneurysms & may be related to aneurysm formation & rupture
248
Q

What can cerebral artery aneurysms cause?

A

Subarachnoid bleeding

249
Q

What can a ruptured middle cerebral artery aneurysm cause?

A

Secondary right/left temporal haematoma

250
Q

What can a ruptured distal middle cerebral artery aneurysm cause?

A

Secondary acute subdural haemorrhage

251
Q

What % of sub-arachnoid haemorrhages are non-aneurysmal?

A

15-20%

252
Q

Describe a sub-arachnoid haemorrhages?

A
  • Majority angiogram negative & follow
    benign course
  • Small number due to other causes e.g. AVM, neoplasia
253
Q

List the 5 predisposing factors to an aneurysmal sub-arachnoid haemorrhages?

A
  1. Smoking
  2. Female sex
  3. Hypertension
  4. Positive family history
  5. ADPCK, Ehlers Danlos, coarctation of the aorta
254
Q

Describe the history of an aneurysmal sub-arachnoid haemorrhages?

A
  • Sudden onset headache
  • LOC, seizures, visual, speech & limb disturbance
  • Sentinel headache
255
Q

List the 6 clinical examination features of an aneurysmal sub-arachnoid haemorrhages?

A
  1. Photophobia
  2. Meningism
  3. Subhyaloid hemorrhages
  4. Vitreous haemorrhages (Terson’s syndrome)
  5. Speech & limb disturbance
  6. Pulmonary edema
256
Q

Describe the WFNS grading system?

A
  • GCS 15: Grade 1
  • GCS 13-14 without deficit: Grade 2
  • GCS 13-14 with deficit: Grade 3
  • GCS 7-12: Grade 4
  • GCS 3-6: Grade 5
257
Q

What is the purpose of a CT investigation for a sub-arachnoid haemorrhage (SAH)?

A
  • Confirms diagnosis
  • Clues to aetiology
  • Identifies complications: infarction, haematoma, hydrocephalus
  • Prognostic: Fisher grade
258
Q

List the 8 investigations for a sub-arachnoid haemorrhage (SAH)?

A
  1. Lumbar puncture- xanthochromia (bilirubin vs oxy Hb)
  2. CT angiography
  3. Magnetic resonance angiography
  4. Digital subtraction angiography- stroke, diabetics
  5. Hyponatraemia
  6. ECG changes
  7. Elevated Troponin levels
  8. Echocardiography- “tako tsubo
    cardiomyopathy”
259
Q

Describe resuscitation for a sub-arachnoid haemorrhage (SAH)?

A
  • Bed rest
  • Fluids: 2.5-3.0 L Normal saline
  • Anti-embolic stockings
  • Nimodipine: 60 mg q 4Hr oral /NG or 2.5-10
    ml/hr IV via central line
  • Analgesia
  • Doppler studies
260
Q

What are the 3 management options for a sub-arachnoid haemorrhage (SAH)?

A
  1. Surgical clipping
  2. Endovascular (coils, stents & glue)
  3. Conservative
261
Q

List the 6 complications of Endovascular treatment for a sub-arachnoid haemorrhage (SAH)?

A
  1. Rehaemorrhage
  2. Delayed ischaemia
  3. Hydrocephalus
  4. Hyponatraemia
  5. ECG changes, LVF (Tako-tsubo cardiomyopathy)
  6. LRTI, PE, UTI
262
Q

List the 4 situations when Rehaemorrhage incidence is highest?

A
  1. Immediately following initial bleed
  2. 5-10% over 1st 72 hrs
  3. Higher in poor grade patients
  4. Larger aneurysms
263
Q

List the 3 treatments for hydrocephalus?

A
  1. External ventricular drainage
  2. Lumbar puncture
  3. Shunt
264
Q

Describe delayed ischaemia in SAH?

A
  • Day 3-10
  • Progressive deterioration in LOC associated
    with new deficit
  • Angiographic spasm
265
Q

What are the 4 treatments for delayed ischaemia in SAH?

A
  1. Fluid management (CVP, colloid infusions)
  2. Nimodipine
  3. Inotropes
  4. Angioplasty (balloon angioplasty, intra
    arterial Nimodipine)
266
Q

What are the 3 treatments for hyponatraemia in SAH?

A
  1. Establish volume status
  2. Hypertonic saline
  3. Fludrocortisone
267
Q

List the 6 cardiopulmonary complications of hyponatraemia in SAH?

A
  1. Sympathetic stimulation & cathecolamine release can lead to myocardial injury
  2. Elevations of Troponin I can occur in 35%
  3. Arrythmias (35%)
  4. Wall motion abn (25%)
  5. Sudden death 12%
  6. Myocardial function normal in 1-3 d
268
Q

Describe seizures after initial aneurysm rupture?

A
  • Often an manifestation of re-rupture
  • Short course (3-7 d) may be useful in patients
    with heavy blood load, parenchymal clots, infarcts or > 65 undergoing surgery
269
Q

What does SAH induce?

A

Prothrombotic state (DVT ~2-18%)

270
Q

Describe the DVT prophylaxis in SAH?

A
  • Timing with aneurysm occlusion is controversial
  • Probably safer to use Sequential Compression
    Devices initially then LMWH after aneurysm secure
271
Q

What 2 things does consciousness reflect?

A
  1. Level of arousal (RAS)

2. Presence of cognitive behaviour (cerebral hemispheres)

272
Q

List 11 factors that can affect consciousness

A
  1. Trauma
  2. Elevated ICP
  3. Fever
  4. Hypothermia
  5. Seizure
  6. Hypotension/severe hypertension
  7. Hypoxia
  8. Hypercapnia
  9. Sepsis
  10. Metabolic
  11. Medications (eg sedatives)
273
Q

What are the 3 subscales of the glasgow coma scale (GCS)?

A
  1. Eyes (4 eyes)
  2. Verbal (V=5)
  3. Motor (M6 motorway)
274
Q

Describe the eyes subscale of the glasgow coma scale (GCS)?

A
4 - Spontaneous
3 - to verbal command 
2 - to pain
1 - none
- Cannot be assessed if eyes are swollen
275
Q

Describe the verbal subscale of the glasgow coma scale (GCS)?

A
5 - oriented(T/P/P)
4 - confused
3 - inappropriate words
2 - incomprehensible sounds
1 - none
- Append􏰀 "T􏰁" to score if patient is intubated
276
Q

Describe the motor subscale of the glasgow coma scale (GCS)?

A
6 - Obeys commands 
5 - Localizes pain
4 - Normal Flexion
3 - Abnormal flexion
2 - Extension
1 - None
- Cannot be assessed if patient has received muscle relaxants. Or spinal injury
277
Q

What are 3 different ways to clinically inflict pain in order to assess a patients conscousness level (motor GCS)?

A
  1. Trapezius squeeze
  2. Sternal rub
  3. Supraorbital pressure
278
Q

The coma is an inability to do what 3 things?

A
  1. Obey commands
  2. Speak
  3. Open eyes to pain
279
Q

Describe the modified verbal subscale of the GCS for young children?

A
BEST VERBAL RESPONSE (1-5)
1 - none
2 - restless, agitated
3 - persistently irritable
4 - consolable crying
5 - appropriate words, smiles, fixes/follows
280
Q

Describe the verbal subscale of the GCS for a 0-23 month baby?

A
5 - smiles/ coos/ cries/ appropriately
4 - cries/ consolable crying/ screams
3 - irritable/ inconsolable
2 - grunts/ agitated
1 - none
281
Q

Describe the verbal subscale of the GCS for a 2-5year old child?

A
5 - appropriate words/ phrases
4 - inappropriate words
3 - cries/ screams
2 - grunts
1 - none
282
Q

Describe the verbal subsclae of the GCS for a >5year old child?

A
5 - orientated
4 - confused
3 - inappropriate
2 - incomprehensible 
1 - none
283
Q

Describe the 3 severity types of GCS head injuries?

A
  • Minor= 14-15
  • Moderate= 9-13
  • Severe= <8
284
Q

Describe the prevalence & incidence of Multiple Sclerosis (MS)?

A
  • Scotland has the highest incidence and prevalence of MS in the world
  • Highest prevalence in Orkney islands (1 in 243)
  • Lower prevalence near the equator
  • Rare in China
285
Q

What is multiple sclerosis?

A

Idiopathic Inflammatory Demylinating Disease of the CNS

286
Q

Describe the 2 types of deficits caused by multiple sclerosis?

A
  1. Acute episodes of inflammation are associated with focal neurological deficits
  2. Demylination results in loss of neurological function: Weak leg, Visual loss, Urinary incontinence
287
Q

Describe the timeframe of deficits developing in multiple sclerosis?

A
  • Usually develop gradually, last for more than 24 hours & may gradually improve over days to week
  • Later untreated disease patients may become progressively more disabled
288
Q

What are the 4 subtypes of multiple sclerosis?

A
  1. Relapsing remitting Multiple Sclerosis
  2. Primary Progressive Multiple Sclerosis
  3. Secondary progressive Multiple Sclerosis
  4. Benign Multiple Sclerosis
289
Q

What 4 syndromes may develop into multiple sclerosis?

A
  1. Optic Neuritis
  2. Clinically Isolated Syndromes
  3. Transverse Myelitis
  4. Radiologically isolated syndromes
290
Q

What is Optic Neuritis?

A
  • Painful visual loss that comes on over a few days
  • Inflammation of optic nerve & damaged myelin
  • May resolve after a few weeks
291
Q

What % of optic neuritis develops into MS by 5/15 years?

A
  • 30% develop MS by 5 years

- 50% develop MS by 15 years

292
Q

What does the risk of MS in optic neuritis depend on?

A

MRI scan & oligoclonal bands

293
Q

What is transverse myelitis?

A

Inflammation of the spinal cord, with many causes other than MS

294
Q

What are 3 symptoms of transverse myelitis?

A
  1. Weakness
  2. Sensory loss
  3. Incontinence can be only symptom
295
Q

What are clinically isolated syndromes?

A
  • Single episode of neurological disability due to focal CNS inflammation
  • Can include optic neuritis & transverse myelitis
296
Q

On what 2 occasions can clinically isolated syndromes occur?

A
  1. May be a first attack of MS

2. Can happen after infection & not related to MS

297
Q

Describe the diagosis of multiple sclerosis?

A

Is diagnosed when there is evidence of 2 or more episodes of demylination disseminated in space & time

298
Q

What are the 5 causes of multiple sclerosis?

A
  1. We don’t know
  2. Genetic Factors
  3. Sunlight/vitamin D exposure
  4. Viral trigger- possibly EBV
  5. Multifactorial- smoking
299
Q

List 8 situations when you would suspect multiple sclerosis?

A
  1. Neurological symptoms that develop over a few days
  2. History of transient neurological symptoms lasting for >24 hours & spontaneously resolved
  3. ‘Hidden’ relapses
  4. Optic Neuritis/Visual Disruption
  5. ‘Bell’s Palsy’
  6. ‘Labyrinthitis’
  7. Sensory Symptoms
  8. Bladder symptoms in young man/woman without children
300
Q

List 7 situations when you would suspect something else other than multiple sclerosis?

A
  1. Sudden onset
  2. Peripheral signs- areflexia, glove & stocking distribution, muscle wasting, fasiculations
  3. Major cognitive involvement
  4. Reduced level of consciousness
  5. Prominent seizures
  6. Pyrexia/evidence of infection
  7. Normal MRI scan
301
Q

What is radiologically isolated syndrome?

A
  • MRI scan performed in patients who does not have symptoms or signs of MS
  • Incidental finding that looks like MS
302
Q

What is the problem with radiologically isolated syndrome?

A

May develop MS (but may not) so can cause unnecessary distress for patient

303
Q

How can you diagnose multiple sclerosis?

A

With 1 scan of MRI brain & cervical spine with gadolinium contrast

304
Q

What result can indicate dissemination in space?

A

Evidence of demylination in 2 regions (periventricular & spinal cord)

305
Q

What result can indicate dissemination in time?

A

If enhancing & non-enhancing areas of demylination are seen

306
Q

What are 4 additional investigations for multiple sclerosis (other than MRI & gadolinium contrast)?

A
  1. Lumbar puncture
  2. Bloods- exclude other conditions
  3. Visual evoked potentials
  4. CXR- exclude sarcoidosis
307
Q

List the 4 CSF tests in a lumbar puncture?

A
  1. CSF oligoclonal bands (need matched blood sample)
  2. CSF cell counts- exclude mimics
  3. CSF glucose (matched blood sample)
  4. CSF protein
308
Q

What are oligoclonal bands?

A

Immunoglobulin bands seen in blood & spinal fluid after protein electrophoresis, supports diagnosis of MS but can be seen in other conditions

309
Q

What CSF result suggests immunoglobulin production in CNS?

A

Presence of oligoclonal bands in CSF but not blood

310
Q

List 6 blood tests that we would do in suspected multiple sclerosis to exclude other causes?

A
  1. B12/Folate
  2. Serum ACE
  3. Lyme serology
  4. ESR/CRP - should be normal
  5. ANA/ANCA/Rheumatoid Factor
  6. Aquaporin-4 antibodies (if transverse myelitis/optic neuritis)
311
Q

What is visual evoked potentials?

A
  • Measure conduction of nerve signals in optic nerve to look for subclinical optic neuritis
  • Conduction will be slower if a patient has had optic neuritis in the past
312
Q

What is the definitive diagnostic test for MS?

A
  • There is NONE!

- Clinical diagnosis is based on weight of evidence from history, examination & investigation

313
Q

What 3 things should neurologists do for a patient with multiple sclerosis?

A
  1. Review history, examination & investigation results
  2. Consider differential diagnosis & explain things to patient
  3. Start treatment if appropriate & organise routine review
314
Q

Describe the effect multiple sclerosis has on a patients life?

A
  • Many are normal
  • Significant proportion become progressively more disabled
  • Difficult to prognosticate
  • May present to general medicine with neurological deterioration or with other medical problems
  • Seldom admitted to acute neurology units
315
Q

What is a relapse of multiple sclerosis?

A

Usually involves a new neurological deficit that lasts for more than 24 hours in the absence of pyrexia or infection

316
Q

What is a pseudo-relapse of multiple sclerosis?

A

The reemergence of previous neurological symptoms or signs related to an old area of demylination in the context of heat or infection

317
Q

Describe the treatment of a multiple sclerosis relapse?

A
  • Not all need treatment
  • Steroids may speed up recovery from relapse with no effect on progression of disease
  • If appropriate patient should get physiotherapy +/- occupational therapy
318
Q

When should steroids NOT be given for multiple sclerosis relapse treatment?

A

If any evidence of infection

319
Q

What management occurs sometimes in relapsing-remitting MS?

A
  • Plan to organise MRI with contrast to look for active disease & change treatment
  • If patient is on treatment for Relapsing Remitting MS the nurses should be informed as patient may be eligible for new treatment
320
Q

Describe the steroid regime for relapse multiple sclerosis?

A
  • 1g of IV methylprednisilone for 3 days
    OR
  • 500mg of oral methylprednisilone for 5 days AND
  • PPI for gastroprotection
321
Q

When should steroids be prescribed in relapse multiple sclerosis?

A

Ideally prescribe at 9AM to avoid sleep disruption

322
Q

What are the 2 powerful drugs for multiple sclerosis?

A
  1. Alemtuzumab

2. Natalizumab

323
Q

What is the dose of Alemtuzumab for multiple sclerosis?

A

2 short courses over a year then further treatment if needed

324
Q

Describe the effect & risks of Alemtuzumab for multiple sclerosis?

A
  • Stops relapses in 40% of patients
  • High risk of secondary autoimmune problems (thyroid, ITP, Goodpastures)
  • May improve disability
325
Q

What is the dose of Natalizumab for multiple sclerosis?

A

Monthly infusions

326
Q

Describe the effect & risks of Natalizumab for multiple sclerosis?

A
  • Very effective treatment for relapses

- Serious risk of fatal PML if infected with JC virus

327
Q

What are the 2 oral treatments for Multiple sclerosis?

A
  1. Fingolimod

2. Dimethyl Fumarate

328
Q

Describe the dose of Fingolimod for Multiple sclerosis?

A

Daily tablet

329
Q

Describe the effect & risks of Fingolimod for Multiple sclerosis?

A
  • Less effective than natalizumab or alemtuzumab
  • Risk of infections
  • May slow heart rate
330
Q

Describe the dose of Dimethyl Fumarate for Multiple sclerosis?

A

Twice daily tablet

331
Q

Describe the effect & risks of Dimethyl Fumarate for Multiple sclerosis?

A
  • Less effective than fingolimod
  • Low white cell counts
  • Risk of infections
332
Q

Describe Cladribine for multiple sclerosis treatment?

A
  • Old chemotherapy drug
  • 2 short courses of tablets (8 days) over 2 years
  • Targets B-cells
  • May stop MS activity for many years
333
Q

Describe Beta interferon, copaxone (older treatments) for multiple sclerosis?

A
  • Less effective than fingolimod or monoclonal antibodies
  • Patients do not like injections
  • May prolong life in some patients (long term data up to 16 years available)
  • Less people disabled over 20 years
334
Q

Describe primary progressive multiple sclerosis?

A
  • At least 1 year of disease progression
  • MRI scan supports diagnosis of MS
  • Oligoclonal bands support diagnosis of MS
335
Q

Describe secondary progressive multiple sclerosis?

A

RRMS in past but now progressive disease without relapses or inflammation on scan

336
Q

Describe the treatment for progressive multiple sclerosis?

A
  • No licenced DMT at present
  • Focus on treating symptoms
  • Hope that treating RRMS will reduce progression to SPMS
337
Q

What is the potential treatment for PPMS?

A

Ocrelizumab

338
Q

What is the potential treatment for SPMS?

A

Siponimod

339
Q

What is Biotin?

A
  • Dietary supplement

- High dose vitamin

340
Q

Describe the use of Biotin for multiple sclerosis?

A
  • May lead to some symptom relief & mild improvement power
  • Ongoing large clinical trials
  • Gives energy to damaged nerve cells
341
Q

Describe the rehabilitation & symptom management for multiple sclerosis?

A
  • No disease modifying treatment for secondary progressive MS
  • Control bladder, fatigue, mood, spasticity, mobility symptoms
342
Q

What is the definition of dementia?

A

Progressive cognitive decline

343
Q

What are the 3 main factors of dementia?

A
  1. Interfere with the ability to function at work or at usual activities
  2. Represent a decline from previous levels of functioning & performing
  3. Not explained by delirium or major psychiatric disorder
344
Q

The cognitive/behavioural impairment of dementia involves a minimum of 2 out of what 4 domains?

A
  1. Memory
  2. Executive function
  3. Language
  4. Apraxia/ Visuospatial
345
Q

What are the 3 simple questions for assessing dementia?

A
  1. Does this patient have cognitive impairment?
  2. If so, what cognitive domains are involved?
  3. What is the likely pathological process?
346
Q

What cognitive symptoms are normal?

A

Occasional memory lapses- 18% of 35yr old controls report Memory problems, 13% need to take notes to help remember

347
Q

What is the purpose of the brains frontal lobe?

A

Executive function/language

348
Q

What is the purpose of the brains temporal lobe?

A

Memory, language

349
Q

What is the purpose of the brains parietal lobe?

A

Visuospatial, praxia

350
Q

What is the golden rule when taking a history from someone with potential dementia?

A

Take history from patient & always from next of kin

351
Q

Describe the characteristic problems of someone with dementia?

A
  • Impaired ability to acquire & remember new information
  • Symptoms include: repetitive questions or conversations, misplacing personal belongings, forgetting events or appointments, getting lost on a familiar route
352
Q

Describe the characteristic executive function problems of someone with dementia?

A
  • Impaired reasoning & handling of complex tasks, poor judgment
  • Symptoms include: poor under- standing of safety risks, inability to manage finances, poor decision-making ability, inability to plan complex or sequential activities
353
Q

Describe the characteristic visuospatial problems of someone with dementia?

A
  • Impaired visuospatial abilities
  • Symptoms include: inability to recognize faces or common objects or to find objects in direct view despite good acuity, inability to operate simple implements, or orient clothing to the body
354
Q

Describe the characteristic language problems of someone with dementia?

A
  • Impaired language functions (speaking, reading, writing)
  • Symptoms include: difficulty thinking of common words while speaking, hesitations, speech, spelling, & writing errors
355
Q

What are 2 simple cognitive bed-side assessments for dementia?

A
  1. Folstein MMSE (30)

2. Addenbrookes Cognitive assessment (100)

356
Q

What 5 things does the Addenbrookes Cognitive assessment examine?

A
  1. Memory
  2. Attention/Concentration
  3. Language
  4. Visuospatial
  5. Executive function
357
Q

What are the 2 purposes of the Addenbrookes Cognitive assessment examine?

A
  1. Severity

2. Pattern of impairment

358
Q

What is essential for all aspects of cognition?

A

Component of consciousness which allows filtering of

information to allow one to focus on a particular stimuli

359
Q

What is the pathological process of Attention/ concentration/orientation?

A

Delirium (depression)

360
Q

How is Attention/ concentration/orientation tested through Addenbrooke’s Cognitive Examination-III (ACE-III)?

A
  • Orientation
  • Serial 7s
  • Working memory facet of attention/concentration eg. Digit span
361
Q

What are the 3 parts to declarative (explicit) memory?

A
  1. Episodic (personal)
  2. Semantic (general)
  3. Working (concentration)
362
Q

What is cognitive bedside testing limited to for memory?

A

Episodic memory (or semantic memory)

363
Q

What are the 2 pathological processes for episodic memory?

A
  1. Early Alzheimer’s disease

2. Limbic encephalitis

364
Q

What 2 tests in Addenbrooke’s Cognitive Examination-III (ACE-III) assess a patients memory?

A
  1. Anterograde memory (address learning)

2. Retrograde (Historical famous figures)

365
Q

Describe the brain spread of Alzheimer􏰀s?

A
  • Classically starts in temporal lobe

- Spreads to parietal & frontal lobes

366
Q

What 3 abnormalities would be a result of bilateral removal of both hippocampus?

A
  1. Loss of new episodic memory
  2. 2yrs of retrograde amnesia
  3. Retained implicit & semantic memory
367
Q

Give an example of a disease affecting the semantic memory?

A

Dementia (variant Frontotemporal dementia)

368
Q

What does a pathological semantic memory result in?

A

Loss of knowledge about the world including words

369
Q

What 2 tests in Addenbrooke’s Cognitive Examination-III (ACE-III) assess semantic memory?

A
  1. Marked reduction category verbal fluency

2. Impairment of irregular words (dyslexia) eg. pint

370
Q

What brain lobe controls a persons behaviour/judgement?

A

Frontal lobes

371
Q

What are the 3 parts to executive function & where in the brain are they located?

A
  1. Behaviour, social awareness (Orbitofrontal)
  2. Working memory, cognitive estimates, planning (Dorsolateral prefrontal cortex)
  3. Motivation (anterior cingulate)
372
Q

What are 3 tests for executive function?

A
  1. Proverbs
  2. Verbal Fluency
  3. Estimates
  4. Planning
373
Q

What does visuospatial involve?

A
  • Visual processing: Where? What?

- Accurately Localise objects

374
Q

What history would be typical of a visuospatial pathology?

A

“Inability to recognise faces or common objects or to find objects in direct view despite good acuity, inability to operate simple implements, or orient clothing to the body”

375
Q

What are the 2 brain streams for visual processing?

A
  1. Dorsal stream= Where?

2. Ventral stream= What?

376
Q

What is dyspraxia?

A

Position of object in space

377
Q

What is visual agnosia?

A

Object recognition

378
Q

What is prosopagnosia?

A

Facial recognition

379
Q

What are the 4 Addenbrooke’s Cognitive Examination-III (ACE-III) tests assessing visuospatial-parietal lobe function?

A
  1. Pentagons
  2. Cubes
  3. 3-D letters
  4. Dots counting
380
Q

What are 4 other tests for dementia?

A
  1. Assess higher motor control, deficits result in impairment of purposeful motor skills (praxia)
  2. Pantomime gestures to command
  3. Appropriate use of everyday objects eg. Toothbrush
  4. Copying meaningless gestures
381
Q

What are the 3 parts to language?

A
  1. Speech (aphasia)
  2. Reading (alexia)
  3. Writing (agraphia)
382
Q

What are 2 examples of language disorders?

A
  1. Progressive non-fluent aphasia (variant FTD)

2. Dominant MCA territory infarction

383
Q

What are 4 Addenbrooke’s Cognitive Examination-III (ACE-III) tests assessing language?

A
  1. Naming
  2. Repetition
  3. Three stage command (comprehension)
  4. Reading
384
Q

What are the 3 distinct types of language (speech in) impairment dementia?

A
  1. Semantic variant
  2. Logopenic variant
  3. Non-fluent aphasia variant
385
Q

Describe the Semantic variant of language disorders?

A
  • Poor confrontation naming
  • Impaired single word comprehension
  • Poor object/person recognition, surface dyslexia, spared repetition
386
Q

Describe the Logopenic variant of language disorders?

A
  • Impaired single word retrieval
  • Impaired repetition, speech sound errors (phenomic)
  • Spared object/person recognition, single word recognition
387
Q

Describe the Non-fluent variant of language disorders?

A
  • Effortful, halting speech speech
  • Phenomic errors
  • Spared object/person recognition, single word recognition
388
Q

What are the 4 parts to diagnosing if a patient has dementia?

A
  1. History including functional status
  2. Relevant investigations
  3. Cognitive assessment
  4. Physical examination
389
Q

What is the likely disorder for episodic memory deficit in Addenbrooke’s Cognitive Examination-III (ACE-III)?

A

Alzheimer’s

390
Q

What is the likely disorder for semantic memory deficit in Addenbrooke’s Cognitive Examination-III (ACE-III)?

A

Semantic Dementia

391
Q

What is the likely disorder for attention/ concentration deficits in Addenbrooke’s Cognitive Examination-III (ACE-III)?

A

Delirium

392
Q

What is the likely disorder for naming/fluency deficit in Addenbrooke’s Cognitive Examination-III (ACE-III)?

A

Progressive Non fluent aphasia

393
Q

What is the likely disorder for visuospatial deficit in Addenbrooke’s Cognitive Examination-III (ACE-III)?

A

PD plus syndrome OR variants AD

394
Q

What is a seizure?

A

Episode of neuronal hyperactivity causing symptoms and signs

395
Q

What is epilepsy?

A

At least 2 unprovoked episodes of seizure

396
Q

What are the 2 types of epilepsy/seizures?

A
  1. Focal

2. Generalised

397
Q

Describe the incidence of epilepsy and seizure?

A
  • Higher in childhood, dips at 4 years old onwards

- Once you get to 55 the risk increases to as high as childhood & it continues to climb

398
Q

What are the 3 most important parts of the clinical history of someone with epilepsy?

A
  1. Patient
  2. Eye witness
  3. Investigations
399
Q

What are the 3 things to do if you see someone in a seizure?

A
  1. Keep them out of harm’s way
  2. Put them in recovery position
  3. If movements stop & no impairment of ABCs, does not need hospitalisation once recovers awareness
400
Q

List the 5 features of local epilepsy?

A
  1. History trauma / birth injury
  2. Focal aura / sequelae (including gustatory / sensory / motor features)
  3. Post-attack confusion / drowsiness
  4. Automatisms
  5. Nocturnal events
401
Q

List the 8 features of generalised epilepsy?

A
  1. Photosensitivity
  2. Age of onset 8-26
  3. Alcohol or sleep deprivation
  4. Myoclonus (especially in AM)
  5. Lack of aura
  6. Seizures within 2 Hrs of awakening
  7. Family History of IGE (1/3)
  8. EEG abnormal
402
Q

What 3 investigations are needed for someone with an episode of seizure?

A
  1. Brain Imaging- MRI
  2. EEG
  3. Systemic provocations
403
Q

Describe the EEG test for seizures?

A
  • Test takes 1 hour
  • Observe activity on EEG
  • Lying at rest
  • Hyperventilation
  • Drowsiness
  • Photic stimulation
404
Q

What does EEG stand for?

A

Electroencephalography

405
Q

What are the 2 types of EEG?

A
  1. Ambulatory

2. Video telemetry

406
Q

What are the 2 common differential diagnosis of epilepsy?

A
  1. Seizures

2. Syncope (fit)

407
Q

What are the 4 rarer differential diagnosis of epilepsy?

A
  1. Migraine
  2. Narcolepsy / cataplexy
  3. Transient Global Amnesia
  4. Panic attacks
408
Q

What is Status Epilepticus?

A

Repetitive or prolonged epileptic seizures which is a medical emergency

409
Q

What may Status Epilepticus cause?

A

Profound systemic / neuronal damage & recognised mortality

410
Q

What is the clinical definition of status epilepticus?

A
  • > 2 seizures without full recovery of neurologic function between seizures
    OR
  • Continuous seizure activity >5 mins
411
Q

What are the 3 drugs used to treat focal epilepsy?

A
  1. Lamotrigine
  2. Carbamazepine
  3. Levetiracetam
412
Q

What are the 3 drugs used to treat generalised epilepsy?

A
  1. Valproate
  2. Levetiracetam
  3. Lamotrigine
413
Q

List the 5 different brain/spinal cord cisterns?

A
  1. Spinal cistern
  2. Pontine cistern
  3. Interpeduncular cistern
  4. Superior cistern
  5. Cisterna magna
414
Q

Where is long-term memory areas located on the brain?

A

Temporal lobe

415
Q

List the 2 structures of the basal ganglia deep within the forebrain?

A
  1. Putamen

2. Caudate nucleus

416
Q

List the 5 limbic structures in the brain?

A
  1. Ventricular system
  2. Thalamus
  3. Hippocampus in the floor of the lateral ventricle
  4. Amygdala
  5. Mamillary bodies
417
Q

What are the 2 special functions of the brain?

A
  1. Vision

2. Speech

418
Q

Where do nasal retinal fibres cross?

A

Optic chiasm

419
Q

Describe the projection of visual fields?

A
  • Contralateral visual field projects onto the temporal or lateral portion of the retina
  • The ipsilateral visual field projects onto the nasal or medial portion of the retina
420
Q

What does the optic nerve carry?

A

All information from the ipsilateral eye

421
Q

What does the optic tract contain?

A

Fibres from the contralateral visual field

422
Q

What are optic radiations?

A

Projections from the lateral geniculate body to the primary visual cortex

423
Q

What would a lesion to the optic nerve of one eye lead to?

A

Monocular vision loss= complete loss of visual field of that eye

424
Q

What would a lesion in the optic chasm lead to?

A

Bitemporal hemianopia= loss of the nasal retinal fibres from both eyes which carry info about the temporal visual field

425
Q

What would a lesion in the optic tract lead to?

A

Contralateral homonymous hemianopia= lost nasal fibres from contralateral eye & the temporal fibres from the ipsilateral eye

426
Q

What would a lesion in the Meyer loop lead to?

A

Contralateral superior quadrantanopia= loss of fibres from the upper portion of the contralateral visual field from both eyes

427
Q

What would a partial lesion in the optic radiations before they are joined by fibres from the Meyer’s loop lead to?

A

Contralateral inferior quadrantanopia= affect fibres from the lower portion of the contralateral visual field from both eyes

428
Q

What would a lesion in the entire primary visual cortex on one side lead to?

A

Contralateral homonymous hemianopia= loss of the contralateral visual field from both eyes

429
Q

Describe speech formation in the brain?

A
  • Wernickes comprehends the language
  • Information is sent via Arcuate fasciculus to Broca’s area
  • Broca’s area forms what you want to say
  • Sends speech information down corticobulbar tract & into bulbar muscles
430
Q

Describe the location of speech in a right handed & left handed individual?

A
  • Right handed: dominant left hemisphere

- Left handed: around 60% left dominant % 40% right dominant

431
Q

What 2 structures makes up the brainstem tectum?

A
  1. Superior colliculus

2. Inferior colliculus

432
Q

What 3 structures makes up the brainstem pons?

A
  1. Crus cerebri (basis pendunculi)
  2. Basal pons
  3. Pyramid
433
Q

Describe the location of the arachnoid mater?

A

Ballooned up against the dura

434
Q

Describe the location of the pia mater?

A

Adheres tightly to the surface of the spinal cord

435
Q

Describe the denticulate ligaments?

A
  • Extensions of pia that anchor the spinal cord to the dura

- Lateral denticulate ligaments separate the posterior & anterior roots

436
Q

Describe the epidural space?

A

True space between the dura & the vertebral periosteum, filled with fat & venous plexus

437
Q

Describe the dura mater?

A

Continuous with inner sheet of dura in the cranium, forms dural sac, extends to S2

438
Q

Describe the posterior root of the spinal cord?

A
  • Carrier sensory information, cell bodies are in the spinal ganglion
  • Enters the spinal cord in poster-lateral sulcus
439
Q

Describe the spinal ganglion?

A
  • Contains the nerve cell bodies of primary sensory afferents
  • Pseudounipolar neurone, there are no synapses
440
Q

Describe the anterior root?

A

Carrier motor information, exits spinal cord through anterolateral sulcus

441
Q

What does the fasciculus gracilis carry?

A

Sensory (fine touch, vibration, proprioception) from ipsilateral lower limb

442
Q

What does the fasciculus cuneatus carry?

A

Sensory (fine touch, vibration, proprioception) from the ipsilateral upper limb

443
Q

What does the spinocerebellar tract carry?

A

Proprioception from limbs to cerebellum

444
Q

What does the lateral corticospinal tract carry?

A

Motor to ipsilateral anterior horn (mostly limb musculature)

445
Q

What does the spinothalamic tract carry?

A

Pain & temperature from contralateral side of the body

446
Q

What does the anterior corticospinal tract carry?

A

Motor to ipsi- and contralateral anterior horn (mostly axial musculature)

447
Q

What does the anterior white commissure carry?

A
  • Pain & temperature fibres cross

- Anterior corticospinal tract fibres cross

448
Q

Describe the passage of sensory information in the dorsal columns?

A
  • Axons enter spinal ganglion & pass directly to ipsilateral posterior column
  • Terminate in nucleus gracilis & nucleus cuneatus
  • Cross midline as internal arcuate fibres & form medial lemniscus
  • Fibres travel in rostral medulla
  • Medial lemniscus flattens horizontally in caudal pons
  • Terminates in VPL of thalamus
  • Fibers project through internal capsule & corona radiate to terminate in the primary somatosensory cortex (post central gyrus)
449
Q

Where do fibres below/above T6 enter in the dorsal column sensory tract?

A
  • Below T6: fasciculus gracillis

- Above T6: fasciculus cuneatus

450
Q

Describe the passage of sensory information in the anterolateral spinothalamic tract?

A
  • Axons enter from spinal ganglion, travel up/down 1-2 segments in Lissauer tract & then synapse in posterior horn
  • Cross midline in anterior white commissure & ascend
  • Travels up the caudal medulla, rostral medulla, pons & midbrain
  • Terminates in the VPL of thalamus
  • Fibres project through internal capsule & corona radiata to terminate in primary somatosensory cortex (postcentral gyrus)
451
Q

Describe the passage of motor infection in the corticospinal tract?

A
  • In motor cortex descending fibres from corona radiata converge to pass through posterior limb of internal capsule
  • Descend through middle 3/5 crus cerebri (basis pedunculi) in anterior midbrain
  • Pons break up fibres
  • Descends as pyramids in anterior part of medulla
  • Medulla & spinal cord junction 85-90% decussate to form lateral corticospinal tract
  • Uncrossed fibres descend as anterior corticospinal tract
  • LCST terminates on LMNs in anterior horn
  • ACST decussate at level where they terminate on LMNs
452
Q

Describe the 5 steps in spinal reflexes?

A
  1. Ia fibre from muscle spindle senses stretching
  2. Ia fibre synapses with alpha-motor neurone in anterior horn
  3. Ia fibre synapses with inhibitory interneuron
  4. Alpha-motor neurons to extensor muscles are excited
  5. Inhibitory interneurons inhibits alpha-motor neurone of the antagonist muscle
453
Q

What 3 information is given to the cerebellum?

A
  1. Proprioception
  2. Vestibular information
  3. Environmental cues
454
Q

What 4 information is given to the basal ganglia?

A
  1. Decision to move
  2. Direction of movement
  3. Amplitude of movement
  4. Emotional body language
455
Q

What 2 things send information to the Upper Motor Neuron system?

A
  1. Basal ganglia

2. Cerebellum

456
Q

How is information passed from UMN to LMN?

A

Corticospinal tract

457
Q

What 3 tracks send information to the Lower Motor Neuron System?

A
  1. Reticulospinal tract
  2. Rubrospinal tract
  3. Vestibulospinal tract
458
Q

What are the 4 roles of the basal ganglia loops?

A
  1. Motor- movement
  2. Oculomotor- eye movement control
  3. Lateral orbito-frontal- social behaviour
  4. Dorsolateral prefrontal loop- executive functions / working memory
459
Q

Describe the posture & voluntary movement component of the basal ganglia?

A
  • Input: cortex

- Output: cortex & brainstem

460
Q

What is the mean duration from parkinson’s disease diagnosis to death?

A

15 years

461
Q

What is Parkinson’s disease primarily?

A

A “sporadic” disorder

462
Q

Describe Hereditary Parkinsonism?

A
  • Mutate protein LRRK2 on PARK8 gene at 12q12 locus

- Inherited in autosomal dominant pattern

463
Q

Describe the pathology of parkinson’s disease?

A
  • Loss of dopaminergic neurones within substantia nigra

- Surviving neurones contain Lewy bodies

464
Q

When does parkinson’s disease manifest clinically?

A

After loss of approximately 50% of dopaminergic neurones

465
Q

List the 10 suggested mechanisms for Lewy Body formation?

A
  1. Oxidative stress
  2. Mitochondrial failure
  3. Excitotoxicity
  4. Protein aggregation
  5. Interference with DNA transcription
  6. Nitric oxide
  7. Inflammation
  8. Apoptosis
  9. Trophin deficiency
  10. Infection
466
Q

Describe stage 1-2 Parkinson’s disease?

A
  • In medulla/ pons anterior olfactory nucleus

- Presymptomatic or pre- motor e.g. loss of smell

467
Q

Describe stage 3-4 Parkinson’s disease?

A
  • In midbrain: substantia nigra pars compacta

- Parkinsonism only becomes evident after extensive nigral damage

468
Q

Describe stage 5-6 Parkinson’s disease?

A
  • Neocortex involvement

- Development of PD dementia

469
Q

What are the 4 possible clinical features of parkinsonism?

A
1. Bradykinesia
\+ At least 1 of the following:
2. Muscular rigidity
3. 4-6 Hz rest tremor 
4. Postural instability
470
Q

What is Bradykinesia?

A

Slowness in initiation of voluntary movement with progressive reduction in speed & amplitude of repetitive actions

471
Q

What are the 6 non-motor symptoms of parkinsonism?

A
  1. Neuropsychiatric
  2. Autonomic
  3. Sleep
  4. Reduced olfactory function
  5. Fatigue
  6. Pain & sensory symptoms
472
Q

List the 3 neuropsychiatric symptoms of parkinsonism?

A
  1. Dementia
  2. Depression
  3. Anxiety
473
Q

List the 5 autonomic symptoms of parkinsonism?

A
  1. Constipation
  2. Urinary urgency / nocturia
  3. Erectile dysfunction
  4. Excessive salivation / sweating
  5. Postural hypotension
474
Q

List the 3 sleep symptoms of parkinsonism?

A
  1. REM sleep behaviour disorder
  2. Restless legs syndrome
  3. Daytime somnolence
475
Q

How do you diagnose Parkinson’s disease?

A

Largely clinical diagnosis

476
Q

What 5 disorders are commonly mistaken for Parkinson’s disease?

A
  1. Benign tremor disorders (eg. essential tremor)
  2. Dementia with Lewy bodies
  3. Vascular parkinsonism
  4. Parkinson plus disorders (eg. progressive supranuclear palsy, multiple system atrophy)
  5. Drug-induced parkinsonism/ tremor
477
Q

What are the 3 main investigations for Parkinson’s disease?

A
  1. Bloods: If tremor present do thyroid function tests, copper/ caeruloplasmin
  2. Structural imaging: CT / MRI brain normal in PD, abnormal in vascular parkinsonism, Parkinson plus disorders
  3. Functional imaging: of presynaptic dopaminergic function using DAT SPECT is abnormal in degenerative parkinsonism
478
Q

What is the clinical aim in parkinson’s disease?

A

Improve motor symptoms / improve QOL

No evidence of neuro-protective effect

479
Q

What are the 4 drug classes of Parkinson’s disease?

A
  1. L-dopa
  2. Dopamine agonists
  3. MAO-B inhibitors
  4. COMT- inhibitors
480
Q

Describe the mechanism of action of L-dopa?

A

Taken up by dopaminergic neurones and decarboxylated to dopamine within presynaptic terminals, half life approx 90 mins

481
Q

What is L-dopa prescribed with?

A

Dopa-decarboxylase inhibitor

482
Q

What are the 2 common preparations of L-dopa?

A
  1. L-dopa + carbidopa = Sinemet®

2. L-dopa + benserazide = Madopar®

483
Q

What are the peripheral/central adverse effects of L-dopa?

A
  • Peripheral: Nausea, vomiting, postural hypotension

- Central: confusion, hallucinations

484
Q

What are the longer term effects of L-dopa?

A
  • Approx. 50% of patients develop motor complications after 5 years L-dopa
  • Fluctuation in motor response
  • Dyskinesia: most commonly chorieform movements at peak dose
485
Q

Give 4 examples of Dopamine agonists?

A
  1. Ropinirole
  2. Pramipexole
  3. Rotigotine
  4. Apomorphine
486
Q

Describe the mechanism of action of Dopamine agonists?

A

Act directly on post-synaptic striatal dopamine receptors (D2 subtype)

487
Q

Describe how Dopamine agonists are different to L-dopa?

A
  • Longer half-life than L-dopa
  • Less efficacious than L-dopa
  • Associated with fewer motor complications than L-dopa
488
Q

How are Dopamine agonists prescribed?

A
  • As monotherapy in early disease or in combination with L-dopa
  • Longer-acting oral, transdermal & subcutaneous
489
Q

List the 4 side effects of Dopamine agonists?

A
  1. Dopaminergic side effects
  2. Somnolence
  3. Impulse control disorders (eg. pathological gambling, hypersexuality)
  4. Nightmares
490
Q

What are 2 examples of MAO-B inhibitors?

A
  1. Selegiline

2. Rasagiline

491
Q

Describe the mechanism of action of MAO-B inhibitors?

A

Prevents dopamine breakdown by binding irreversibly to monoamine oxidase

492
Q

How can MAO-B inhibitors be prescribed?

A

Monotherapy in early disease or as adjunct in later disease, well tolerated

493
Q

What are 2 examples of COMT inhibitors?

A
  1. Entacapone

2. Tolcapone

494
Q

Describe the mechanism of action of COMT inhibitors?

A

Inhibiting Catechol-o-methyltransferase results in longer L-dopa half-life / duration of action

495
Q

How can COMT inhibitors be prescribed?

A

Co-prescribed with L-dopa (available as combined table - Stalevo®) in later disease

496
Q

What are the 2 side effects of COMT inhibitors?

A

Dopaminergic + diarrhoea

497
Q

List the 3 motor problems in advanced parkinson’s disease?

A
  1. Motor complications- ‘On /off’ fluctuations, L-dopa-induced dyskinesia
  2. Poor balance/falls
  3. Speech/swallowing disturbance
498
Q

What is the cognitive problem in advanced parkinson’s disease?

A

Dementia

499
Q

What is the treatment for advanced parkinson’s disease?

A

Deep brain stimulation of subthalamic nucleus

500
Q

What are the 4 degenerative causes of parkinsonism?

A
  1. Dementia with Lewy bodies
  2. Progressive supranuclear palsy
  3. Multiple system atrophy
  4. Corticobasal degeneration
501
Q

What are the 4 secondary causes of parkinsonism?

A
  1. Drug-induced: chronic use of dopamine antagonists
  2. Cerebrovascular disease
  3. Toxins (e.g. carbon monoxide,
    organophosphates, MPTP)
  4. Post-infectious
502
Q

What 3 syndromes can bacterial microbes cause in the CNS?

A
  1. Meningitis
  2. Meningo-encephalitis
  3. Abscess
503
Q

Give 9 examples of bacterial microbes affecting the CNS?

A
  1. Meningococcus
  2. Pneumococcus
  3. Haemophilus influenzae
  4. TB Listeria
  5. Lyme
  6. Syphilis
  7. Strep sp
  8. Anaerobes
  9. Nocardia
504
Q

What 2 syndromes can viral microbes cause in the CNS?

A
  1. Encephalitis

2. Meningitis

505
Q

Give 6 examples of viral microbes affecting the CNS?

A
  1. HSV
  2. VZV
  3. Enterovirus (D-68)
  4. HIV
  5. Mumps
  6. CMV
506
Q

What 2 syndromes can fungal microbes cause in the CNS?

A
  1. Meningo-encephalitis

2. Mass lesion

507
Q

Give 3 examples of fungal microbes affecting the CNS?

A
  1. Cryptococcosis,
  2. Coccidiomycosis
  3. Aspergilloma
508
Q

What 2 syndromes can Protozoal microbes cause in the CNS?

A
  1. Mass lesion

2. Eosinophilic-meningitis

509
Q

Give 2 examples of protozoal microbes affecting the CNS?

A
  1. Toxoplasmosis

2. Helminths (Angiostrongylus, Gnathostoma)

510
Q

What is Meningitis?

A

Inflammation of meninges +/- cerebrum (meningo-encephalitis), Inflammatory CSF

511
Q

What are the 3 most common aetiologies of meningitis (from most to least)?

A
  1. Unknown
  2. Viral
  3. Bacterial
512
Q

What is the relationship between meningitis and age?

A

More common in younger population

513
Q

List the 6 signs & symptoms of meningitis (95% will have at least 2)?

A
  1. Headache
  2. Neck stiffness
  3. Reduced GCS
  4. Fever
  5. Rash purpuric +/or petechial but macular early on (meningococcal)
514
Q

Give an example of a gram positive diplococci bug causing meningitis?

A

Streptococcus pneumoniae

515
Q

Give an example of a gram negative diplococci bug causing meningitis?

A

Neisseria meningitidis

516
Q

Give an example of a gram positive rod bug causing meningitis?

A

Listeria monocytogenes

517
Q

What type of meningitis is caught through needles?

A

Staph aureus, Streptococci

518
Q

What are the 5 risk factors for pneumococcal bacterial meningitis?

A
  1. Middle ear disease
  2. Head injury (CSF leak)
  3. Neurosurgery
  4. Alcohol
  5. Immunosupression (HIV)
519
Q

What are the 2 risk factors for listeria bacterial meningitis?

A
  1. Immunosupression

2. Pregnancy

520
Q

List the 3 neurology signs of pneumococcal meningitis?

A
  • 65% focal signs
  • 24% seizures
  • 22% VIII palsy
521
Q

List the 6 adverse outcomes of bacterial meningitis?

A
  1. Pneumococcus
  2. Reduced GCS
  3. CNS signs
  4. Older age (>60 years)
  5. CN palsy (Pneumococcal)
  6. Bleeding (Meningococcal)
522
Q

What are the 5 investigations for suspected meningitis?

A
  1. History & exam- throat & cervical lymph nodes
  2. Blood cultures (blood PCR)
  3. Throat culture, Viral gargle
  4. FBC, UEs, LFTs, CRP
  5. Lumbar puncture
523
Q

What 3 things are you assessing in a lumbar puncture for suspected meningitis?

A
  1. Cell count, Gram stain, Culture & PCR
  2. Protein & Glucose
  3. Viral PCR
524
Q

What 2 abnormalities does a CT head scan exclude?

A
  1. Mass lesion / mass effect

2. Gross cerebral oedema

525
Q

What doesn’t a head CT scan exclude?

A

Raised intracranial pressure

526
Q

In what 5 situations would you do a CT scan before lumbar puncture in suspected meningitis?

A
  1. GCS ≤ 12
  2. CNS Signs
  3. Papilloedema
  4. Immunocompromised
  5. Seizure
527
Q

When would you give antibiotics for suspected meningitis?

A

Pre-CT scan

528
Q

What 7 situations contraindicate a lumbar puncture?

A
  1. Brain shift
  2. Rapid GCS reduction
  3. Resp/cardiac compromise
  4. Severe sepsis
  5. Rapidly evolving rash
  6. Infection at LP site
  7. Coagulopathy (INR => 4, platelets <40, DOAC, therapeutic LMWH)
529
Q

What is the normal CSF cells, protein, glucose & other?

A
  • Cells: 0-5/mm3, lymphocytes
  • Protein: 0.15-0.45g/l
  • Glucose: 2.8-4.2 mmol/l (>50% blood)
  • Other: Opening Pressure 7-18 cm/CSF
530
Q

What is the CSF: cells, protein, glucose & other in BACTERIAL meningitis?

A
  • Cells: Neutrophils, Lymphocytes (Listeria)
  • Protein: raised
  • Glucose: reduced <50%
  • Other: culture, PCR, blood culture
531
Q

What is the CSF: cells, protein, glucose & other in TB meningitis?

A
  • Cells: Lymphocytes
  • Protein: raised
  • Glucose: reduced <50%
  • Other: culture, PCR
532
Q

What is the CSF: cells, protein, glucose & other in VIRAL meningitis?

A
  • Cells: Lymphocytes
  • Protein: raised
  • Glucose: normal
  • Other: PCR
533
Q

What is the CSF: cells, protein, glucose & other in FUNGAL meningitis?

A
  • Cells: Lymphocytes
  • Protein: raised
  • Glucose: reduced <50%
  • Other: India ink, CrAG
534
Q

Describe the treatment of suspected bacterial meningitis?

A
  • Do not delay starting IV Antibiotics
  • Prescribe all for Meningo/Pneum & HI
  • Stratify Rx by Age ≥ 60yrs & risk factors for Listeria
535
Q

What treatment would you add if there was a high likelihood of pneumonia meningitis?

A

Steroids

536
Q

What is the definitive antibiotic therapy for meningococcal bacterial meningitis?

A
  • IV Ceftriaxone or Benzyl penicillin

- 5-7 days (3 days)

537
Q

What is the definitive antibiotic therapy for pneumococcal bacterial meningitis?

A
  • IV Ceftriaxone or Benzyl Penicillin

- 14 days (Increase duration if complications)

538
Q

What is the definitive antibiotic therapy for listeria bacterial meningitis?

A
  • IV Amoxicillin (stop Ceftriaxone)

- 21 days (Increase duration if complications)

539
Q

What are the 3 concerns with pre-hospital antibiotic therapy?

A
  1. Microbe lysis pre-hospital: Cytokine storm
  2. Exacerbation of sepsis + lack of supportive measures
  3. Neurological deterioration + Increased mortality
540
Q

Describe the regimen of corticosteroids in bacterial meningitis?

A

10mg qid Dexamethasone (with or prior to antibiotic Rx) for 4/7

541
Q

What 3 situations can lead to corticosteroids having a reduced benefit in bacterial meningitis?

A
  1. When presentation is delayed
  2. Untreated HIV
  3. Other life-threatening CNS infections are endemic (Resource poor nations)
542
Q

What is the secondary prevention of meningococcal infection?

A

Chemoprophylaxis (Ciprofloxacin or Rifampicin)

543
Q

What is the primary prevention of meningococcal infection?

A

Schedule for childhood immunisations (HIB, Pneumo)

544
Q

What 5 ages need the meningococcal vaccine?

A
  1. 2 months (primary)
  2. 3 months (primary)
  3. 4 months (primary)
  4. 12-13 months (booster)
  5. Around 14 years (booster)
545
Q

What are the 3 special cases for meningococcal vaccine?

A
  1. Travel to Sub-Saharan Africa & other high prevalence areas- ACWY recommended
  2. Asplenia, Complement deficiency: Men boosters with Men B & ACWY, HIB & Pneumo
  3. Cochlear implants- Pneumo booster
546
Q

Describe the diagnosis of viral meningitis?

A
  • Usually diagnosed only after exclusion of BM

- No confusion

547
Q

What are the 5 types of viral meningitis?

A
  1. Enterovirus
  2. HSV 2 > VZV > HSV 1
  3. HIV (seroconversion)
  4. Mumps
  5. Unidentified
548
Q

When would you consider aciclovir for viral meningitis?

A

Only if immunocompromised

549
Q

What does viral encephalitis result in?

A

Confusion, fever +/- seizures

550
Q

Describe the 3 investigation results for viral encephalitis?

A
  1. Lymphocytic CSF (normal glucose), PCR
  2. EEG: Temporal lobe
  3. MRI
551
Q

What would you prescribe for viral encephalitis?

A

Aciclovir IV 2-3 weeks (HSV, VSV)

552
Q

Describe intra-cerebral TB?

A
  • Sub-acute (weeks)
  • Often associated with other sites
  • May be “unmasked” during TB Rx
  • CSF may be normal
  • Paradoxical worsening usual
553
Q

What lesions are usual in intra-cerebral TB?

A

CN lesions usual (III, IV, VI, IX)

554
Q

What is the treatment for intra-cerebral TB?

A

One year of (isoniazid, rifampin, ethambutol, and pyrazinamide) + Steroids

555
Q

What is HIV brain disease a consequence of?

A

Unrecognised/untreated infection & marked immunodeficiency or life-style

556
Q

List 4 causes of HIV brain disease?

A
  1. Encephalitis (ARVs)
  2. Dementia
  3. Neuro-syphilis (secondary or tertiary)
  4. Opportunistic
557
Q

List 4 causes of opportunistic HIV brain disease?

A
  1. Tuberculosis
  2. Cryptococcus
  3. Toxoplasmosis
  4. JCV (Human polyomavirus 2)- Progressive multi-focal leuco-encephalopathy
558
Q

Describe Progressive focal multifocal leucoencephalopathy (PMLE)?

A
  • Progressive motor dysfunction
  • Immunocompromised
  • HIV, anti-TNF, Transplant
  • John Cunningham virus
  • May occur as part of immune reconstitution (IRIS)
559
Q

Describe the treatment of Progressive focal multifocal leucoencephalopathy (PMLE)?

A
  • No specific treatment

- Antiretroviral treatment if HIV pos

560
Q

What bug causes Intra-cerebral Toxoplasmosis?

A

Toxoplasma gondii

561
Q

Describe Intra-cerebral Toxoplasmosis?

A
  • Headache, seizures, focal CNS signs
  • Immunocompromised (HIV)
  • Multiple enhancing lesions (basal ganglia)
  • IgG & IgM (Blood), PCR (CSF)
562
Q

What is the treatment for Intra-cerebral Toxoplasmosis?

A

Sulphadiazine + Pyramethamine (restore immune function)

563
Q

What are the 3 types of Cryptococcal meningitis?

A
  1. Immunodeficiency usually (HIV)
  2. SOL
  3. Meningo-encephalitis (sub-acute)
564
Q

Describe the CSF in Cryptococcal meningitis?

A

India ink, Cryptococcal antigen (also blood), Culture

565
Q

What is the treatment for Cryptococcal meningitis?

A
  • Amphotericin B + Flucytosine

- Fluconazole

566
Q

What 2 things can cryptococcal meningitis cause?

A
  1. Raised ICP (need shunt)

2. Paradoxical worsening with antiretroviral treatment in HIV

567
Q

What 2 investigations exclude CNS infections?

A
  1. CT

2. Lumbar puncture