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Summary Book Neurology Flashcards

1
Q

What is the anatomical structures of the upper motor neuron pathway?

A

Cerebrum Hemispheres, Cerebellum, Brain Stem, Spinal Cord

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2
Q

What is the anatomical structures of the lower motor neuron pathway?

A

Anterior Horn Cell, Roots, Nerves, Neuromuscular Junction, Muscles

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3
Q

What neurological deficits are seen with issues with the cerebrum hemispheres?

A

Contralateral motor and sensory loss

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4
Q

What neurological deficits are seen with issues with the cerebellum?

A

Ipsilateral past-pointing and ataxia, as well as nystagmus

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5
Q

What neurological deficits are seen with issues with the brain stem?

A

Autonomic features, cranial nerve palsy, crossed limb signs

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6
Q

What neurological deficits are seen with issues with the spinal cord?

A

If cervical then bilateral upper and lower limbs affected, if thoracolumbar then bilateral lower limbs and if conus medullaris then bilateral lower limb with bladder and bowel dysfunction

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7
Q

What neurological deficits are seen with issues with the anterior horn cells?

A

Mixed upper and lower features in same region

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8
Q

What neurological deficits are seen with issues with the roots?

A

Ipsilateral, single limb involved with lower motor signs and often painful

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9
Q

What neurological deficits are seen with issues with the nerve plexus?

A

Ipsilateral, single limb, painful, not attributable to single nerve or level

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10
Q

What neurological deficits are seen with issues with the peripheral nerve?

A

Discrete deficit in one limb, one dermatome

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11
Q

What neurological deficits are seen with issues with the neuromuscular junction?

A

Generalised weakness, fatigable on repetitive testing, minimal sensory involvement

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12
Q

What neurological deficits are seen with issues with the muscles?

A

usually symmetrical in all limbs, sometimes with wasting, pattern usually proximal / limb girdle or distal

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13
Q

Conditions which affect the cerebrum hemispheres?

A

Stroke, MS, cerebral abscess, AVM, tumour

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14
Q

Conditions which affect the cerebellum?

A

Alcohol, stroke, AVM, tumour, paraneoplastic, sarcoidosis, multiple sclerosis, vitamin B12 deficiency, multiple system atrophy, congenital (spinocerebellar ataxia - dominant, Fredrich’s ataxia - recessive)

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15
Q

Conditions which affect the brain stem?

A

Stroke, MS/NMOSD, Bickerstaff

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16
Q

Conditions which affect the cervical spinal cord?

A

Trauma, MS/NMOSD, syringomyelia, cord compression, stroke

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17
Q

Conditions which affect the thoracolumbar spinal cord?

A

Trauma, compression, cord stroke, epidural abscess

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18
Q

Conditions which affect the conus medullaris?

A

Trauma, malignant cord compression, abscess

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19
Q

Conditions which affect the anterior horn cells?

A

MND, past polio

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20
Q

Conditions which affect the roots?

A

Degenerative disease, malignant compression

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21
Q

Conditions which affect the nerve plexus?

A

Trauma, malignant infiltration, paraneoplastic, inflammatory

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22
Q

Conditions which affect the peripheral nerve?

A

Extrinsic compression, metabolic, endocrine, toxic, drug, induced, vasculitis

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23
Q

Conditions which affect the neuromuscular junction?

A

Drug induced, MG, ES

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24
Q

Conditions which affect the muscles?

A

Myositis, muscular dystrophy, acquired myopathy, metabolic / mitochondrial myopathy

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25
Q

Upper motor neuron signs

A

Increased tone, clonus, increased reflexes, upgoing plantar

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26
Q

Lower motor neuron signs

A

Decreased tone and reflexes

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27
Q

Which cranial nerves enter the midbrain?

A

3 and 4

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28
Q

Which cranial nerves enter the pons?

A

5, 6, 7 and 8

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29
Q

Which cranial nerves enter the medulla?

A

9, 10, 11 and 12

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30
Q

Define Neuromyelitis Optica Spectrum Disorder

A

Inflammation of CN2, with painful eye movements, AQP4/MOG positive

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31
Q

Investigations for myopathies

A

Autoimmune screen + anti-Jo1 + biopsy of muscle

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32
Q

Causes of myopathies

A

Inflammatory (inclusion body myositis, sarcoidosis), Autoimmune (dermatomyositis, polymyositis), Metabolic (alcohol), Neoplastic, Degenerative (critical illness), Iatrogenic (steroids, statins), Congenital (Becker muscular dystrophy, Duchenne’s muscular dystrophy, myotonic dystrophy, facioscapulohumeral, limb girdle), Endocrine (acromegaly, thyroid issues, hypercortisolism)

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33
Q

Key sign of Duchenne’s muscular dystrophy

A

Calf pseudohypertrophy

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34
Q

Key signs of Muscular dystrophy

A

Myotonia, frontal bossing, ptosis

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35
Q

Two categories of peripheral neuropathy

A

Axonal (75%) and Demyelinating

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36
Q

Features of demyelinating peripheral neuropathy

A

Proximal predominant, neuropathic tremor, loss of proprioception, muscle wasting

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37
Q

General causes of peripheral neuropathy

A

Compression, diabetes, EtOH, uraemia, heavy metal, paraneoplastic, vitamin B12 deficit, congenital (charot mary tooth), iatrogenic (chemotherapy), infective (Guillain barre syndrome), inflammatory (sarcoidosis) and autoimmune (polyarteritis nodosa, systemic lupus erythematous, rheumatoid arthritis)

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38
Q

Causes of painful peripheral neuropathy

A

Vitamin B deficiency, heavy metal, paraneoplastic

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39
Q

Nerves of pectoralis

A

pectoral, C6, c7, c8

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40
Q

Nerves of tricep

A

radial, c6, c7, c8

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41
Q

Nerves of bicep

A

musculocutaneous, c5, c6

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42
Q

Nerves of brachioradialis

A

medial, c5, c6

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43
Q

Nerves of flexor digitorum

A

median and ulnar, c7, c8, c9

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44
Q

Nerves of adductor

A

obturator, l2, l3, l4

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45
Q

Nerves of knee - quadriceps femoris

A

femoral, l2, l3, ;4

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46
Q

Nerves of ankle - soleus / gastrocnemius

A

sciatic / tibial, s1, s2

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47
Q

Nerves of plantar

A

plantar

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48
Q

Causes of bilateral foot drop

A

motor neuron disease, hereditary neuropathy (charot marie tooth), hereditary motor dystrophy (myotonic)

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49
Q

Presentation of foot drop due to common peroneal

A

inversion preserved, sensory loss of dorsum of foot, reflexes normal

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50
Q

Presentation of foot drop due to L5 root nerve palsy

A

inversion preserved, sensory loss of dorsum of foot, reflexes normal, weakness of hip extension / knee flexion / inversion and eversion of ankle, decreased sensation of lateral calf and dorsum of foot

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51
Q

Presentation of foot drop due to sciatica (l4,5) (s1,2)

A

weakness of knee flexion and below knee, no ankle jerk, decreased sensation of lateral thigh and below knee

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52
Q

Presentation of foot drop due to femoral nerve palsy (l2,3,4)

A

weakness of knee extension and hip flexion, decreased sensation of inner thigh, decreased knee flexion

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53
Q

Presentation of motor neurone disease

A

upper and lower motor neurone signs in same region, initially asymmetric weakness confined to one segment, late signs of respiratory muscle weakness and cardiomyopathy, 25 to 40% cognitive features with frontotemporal behaviour and executive dysfunction, sensory exam unremarkable

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54
Q

Signs of pseudo bulbar disease

A

upper motor neuron, laryngospasms, trismus, brisk jaw jerk, small spastic tongue, slow + monotonous speech, emotional lability

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55
Q

Signs of bulbar disease

A

lower motor neuron, dysarthria, dysphagia, flaccid tongue, nasal twang

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56
Q

5 types of motor neuron disease syndromes

A
  1. Primary Lateral sclerosis (isolated UMN), 2. Progressive Muscular Atrophy (isolated LMN), 3. Progressive Bulbar Palsy (U + LMN disorder of cranial nerves), 4. Flail Arm / Leg Syndrome (progressive LMN weakness of proximal arm and distal leg), 5. ALS (amyotrophic) plus - plus atypical features (pain, ocular motility disturbance, tremor, extra-pyramidal symptoms (akathisia = urge to move, tardive dyskinesia = involuntary movement, dystonia = involuntary muscle contraction, parkinsonism), ataxia, autonomic dysfunction
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57
Q

Causes of acute mononeuritis multiplex

A

diabetes mellitus, vasculitis (systemic lupus erythematous, polyarteritis nodosa (medium vessel), rheumatoid arthritis)

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58
Q

Causes of chronic mononeuritis multiplex

A

infection (leprosy), multiple compressive neuropathies, sarcoidosis

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59
Q

Examination findings for myotonic dystrophy

A

hand (finger grip, percussion myotonia, repeated grip improves), face (frontal balding, cataracts, temporal-mandibular wasting, ptosis), neck (decreased muscle power and rom), cardio (conductive defects - PPM, displaced apex - cardiomyopathy), hypogonadism - gynaecomastia

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60
Q

First cranial nerve

A

olfactory - smell

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61
Q

Second cranial nerve

A

optic - vision

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62
Q

Third cranial nerve

A

Oculomotor - pupil constriction, accommodation, moves eyes up / down / medially, opens eyelids

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63
Q

Fourth cranial nerve

A

trochlear - supplies superior oblique muscle - moves eye down and inward

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64
Q

Fifth cranial nerve

A

trigeminal - sensation to face, muscles of mastication

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65
Q

Sixth cranial nerve

A

abducens - supplies lateral rectus - moves eye laterally

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66
Q

Seventh cranial nerve

A

facial - supplies muscles of facial expression, taste (anterior 2/3), closes eyelids

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67
Q

Eight cranial nerve

A

Vestibulocochlear - hearing and balance

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68
Q

Nineth cranial nerve

A

Glossopharyngeal - taste (posterior 1/3), swallowing and salivation

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69
Q

Tenth cranial nerve

A

Vagus - parasympathetic supply to eye / heart / gut / lungs / larynx (vocal cords)

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70
Q

Eleventh cranial nerve

A

Accessory - sternocleidomastoid and trapezius

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71
Q

Twelfth cranial nerve

A

Hypoglossal - tongue muscles

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72
Q

Causes of positive jaw jerk reflex (deviates to weakness)

A

Peripheral - shingles and Sjogren’s, Central - MS, cerebellopontine angle tumour (acoustic neuroma, meningioma)

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73
Q

Which nerves travel through the cerebellopontine angle?

A

5,6,7,8

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74
Q

Sounds for testing lip, tongue and vocal cord function

A

lip = me, tongue = la, vocal cord = ee

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75
Q

Causes of unilateral ptosis

A

congenital, Horner’s, myasthenia gravis, third nerve palsy

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76
Q

Causes of bilateral ptosis

A

congenital, Horner’s, myasthenia gravis, myotonic dystrophy, neurosyphilis

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77
Q

Sign of positive relative afferent pupillary defect

A

dilation with direct light

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78
Q

Retinal causes of relative afferent pupillary defect

A

infective (CMV, HSV), neoplastic (melanoma), structural (detachment), vascular (ischaemic diabetic retinopathy; or central artery or vein occlusion)

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79
Q

Optic causes of relative afferent pupillary defect

A

glaucoma, optic neuropathy

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80
Q

How does intranuclear ophthalmoplegia present?

A

dissociative conjugate eye movements - impaired adduction of ipsilateral eye and abduction nystagmus of contralateral eye

81
Q

Causes of intranuclear ophthalmoplegia

A

lesion of medial longitudinal fasciculus (connects cn 3 and 6), drug toxicity (barbiturates, phenytoin, tricyclic antidepressants), inflammatory / demyelinating (multiple sclerosis), inflammatory / non-demyelinating (systemic lupus erythematous), neoplastic (brainstem tumour - pontine glioma), nutritional (wernickes encephalopathy), vascular (brainstem infarct). Medial medullary syndrome or cavernous sinus lesion (both CN 3,4,6). Miller fisher syndrome. Myasthenia gravis.

82
Q

Presentation of second nerve palsy

A

Reduced visual acuity, visual field defect, asymmetric optic nerve function, abnormalities on fundoscopy

83
Q

Causes of second nerve palsy

A

compressive (tumours - meningioma / glioma / pituitary adenoma; graves disease), hereditary (lebers hereditary optic neuropathy), infiltrative (tumours - carcinoma / lymphoma / myeloma; sarcoidosis), inflammatory / demyelinating (multiple sclerosis, neuromyelitis optica), inflammatory / non-demyelinating (autoimmune - bechets / GPA / SLE / systemic sclerosis; infection - lyme or syphilis), ischaemic - giant cell arteritis, nutritional - b12 deficiency, paraneoplastic - small cell and non-small cell lung cancer, traumatic, drugs (amiodarone, ethambutol, tobacco)

84
Q

Anatomy of pupillary light reflex

A

cranial nerve 2 is the afferent / sensory limb, parasympathetic of cranial nerve 3 is the motor / efferent limb

85
Q

Presentation of third nerve palsy

A

eye down and out

86
Q

Causes of third nerve palsy

A

compression (posterior communicating artery aneurysm (dilated unreactive pupil)), ischaemic (diabetes, hypertension), brainstem tumours, temporal lobe coning (cerebral oedema with infection or infarction; or intracranial haemorrhage)

87
Q

Presentation of fourth nerve palsy

A

eye is upward and out

88
Q

Causes of fourth nerve palsy

A

congenital, ischaemic (diabetes, hypertension), trauma

89
Q

Presentation of sixth nerve palsy

A

eye is medial

90
Q

Causes of sixth nerve palsy

A

ischaemic (diabetes, hypertension), trauma

91
Q

Which pathologies constrict and which dilate pupils?

A

Constrict = horners and narcotics; dilate = CN3 lesions and amphetamines

92
Q

Causes of unilateral ptosis

A

cranial nerve 3 lesion with dilated pupil; horners with constricted pupil

93
Q

Causes of bilateral ptosis

A

myotonic dystrophy, myasthenia gravis, mitochondrial myopathy, diabetes, thyroxine, miller fischer syndrome (GBS) with ataxia and areflexia and complex ophthalmoplegia

94
Q

Causes of motor only weakness

A

myasthenia gravis, motor neuron disease, inflammatory myopathy (polymyositis, dermatomyositis, inclusion body myositis), multifocal motor neuropathy (unilateral, LMN, autoimmune = anti-GM1)

95
Q

Causes of weakness with sensory component

A

guillian barre, chronic inflammatory demyelinating polyneuropathy, multiple sclerosis, transverse myelitis (bilateral UMN signs), mononeuritis multiplex (asymmetrical - paraproteins / paraneoplastic / vasculitis), metabolic toxicities

96
Q

Predominately motor peripheral neuropathy

A

guillian barre syndrome, chronic inflammatory demylinating polyneuropathy, hereditary motor and sensory neuropathy (charoct marie tooth), diabetes, lead poisoning, multifocal motor neuropathy

97
Q

Predominately sensory peripheral neuropathy

A

diabetes, paraneoplastic - lung, B6 toxicity, B12 deficiency, sjogrens syndrome, syphilis

98
Q

What do these phrases test? Yellow lorry, baby hippopotamus, we see three grey geese.

A

Yellow lorry - tongue. Baby hippopotamus - lips. Grey geese - palate.

99
Q

What do these sounds test? Pa, Ta, Ka

A

Pa - mouth. Ta - tongue. Ka - palate.

100
Q

Why count to 30 in speech exam?

A

Fatigue in myasthenia gravis.

101
Q

Speech findings for bulbar disorder and causes.

A

Lower motor neuron, slow, low volume, tongue and facial, atrophy. Caused by motor neuron disease, cranial nerve 7/9/10/12 issues, myasthenia gravis, muscular dystrophy.

102
Q

Speech findings for cerebellar disorder and causes

A

Ataxia with irregular rhythm and pitch. Caused by spinal cerebellar ataxia, multiple sclerosis, alcohol, tumour, paraneoplastic disorder

102
Q

Speech findings for pseudo bulbar disorder and causes

A

Upper motor neuron, slow, strangulated, positive jaw jerk, hyperactive gag, emotionally labile. Caused by bilateral lacunar internal capsule strokes, multiple sclerosis, amyotrophic lateral sclerosis

103
Q

Speech findings for extra-pyramidal disorder and causes

A

Rapid, low-volume and monotone speech. Caused by parkinson’s disease.

104
Q

Anatomical area of receptive aphasia

A

Wernicke in posterior part of first temporal gyrus in dominant lobe

105
Q

Anatomical area of expressive aphasia

A

Broca in posterior part of third frontal gyrus

106
Q

Area and description of conductive aphasia

A

Isolated inability to repeat phrases with receptive and expressive intact. Located in arcuate fasciculus (temporal lobe).

107
Q

Area and description of nominal aphasia

A

Difficulty recalling or recognising nouns of objects. Located in angular gyrus (temporal lobe). Also noted in encephalopathies and space occupying lesion.

108
Q

What is the role and physiology of the spinothalamic tracts?

A

Sensation of pain and temperature. Fibres enter, ascend and decussate in the spinal cord (usually 2 levels above entry).

109
Q

What is the role and physiology of the dorsal columns?

A

Vibration and proprioception. Fibres ascend and decussate in medulla.

110
Q

What is the role and physiology of the corticospinal tracts?

A

Motor. Descending pathway.

111
Q

Describe the symptoms of anterior cord syndrome

A

Bilateral loss of motor, pain and temperature sensation below level of injury. Intact vibration and proprioception. Hyperflexion injury or disruption of anterior spinal artery.

112
Q

Describe the symptoms of central cord syndrome

A

Sensory and motor deficit. Upper extremities affected more than lower extremities. Hyperextension injury. Classically in older patients who have underlying cervical disease.

113
Q

Describe the symptoms of brown-sequard syndrome

A

Ipsilateral loss of motor, vibration and proprioception. Contralateral loss of pain and temperature. Penetrating trauma or lateral compression.

114
Q

Describe dyskinesia and outline inherited and acquired causes

A

Involuntary repetitive movements. Inherited causes: huntington’s disease, wilsons disease and spinocerebellar ataxia. Acquired causes: SLE, sydenham’s chorea, thyrotoxicosis and dopamine blockers.

115
Q

Key features of parkinson’s disease

A

pill rolling tremor (often unilateral), bradykinesia, lead pipe (elbow) + cogwheel (wrist) rigidity, difficultly initiating voluntary movements, festinating gate, mask like face, monotone speech, micrographia.

116
Q

Describe parkinson’s plus syndrome

A

Similar features to parkinson’s except has poor response to levodopa, symmetry and early onset dementia/hallucinations

117
Q

Key features of multiple system atrophy

A

autonomic dysfunction, cerebellar ataxia, UMN

118
Q

Key features of progressive supranuclear palsy

A

gaze palsy (vertical first), axial rigidity

119
Q

Key features of corticobasal degeneration

A

limb apraxia, dystonia, myoclonus

120
Q

Causes of hemiparesis and presentation, also with ACA vs MCA

A

Caused by stroke, tumour, abscess, demyelination or post ictal (Todd’s). Presents with fixed flexion of upper limb, increased tone and increased reflexions. ACA >legs, MCA >arms/face.

121
Q

Causes of pseduo bulbar palsy

A

stroke-bilateral, MND, MS, CJD

122
Q

Causes of bulbar palsy

A

MND, myasthenia gravis, GBS, myotonic dystrophy

123
Q

Describe symptoms of posterior (dorsal) column syndrome

A

bilateral loss of proprioception and vibration only, preserved power (corticospinal) and sensation/temp (spinothalamic)

124
Q

What sensation level corresponds to the nipple and the navel?

A

T4 = nipple. T10 = navel.

125
Q

Presentation of frontal lobe stroke

A

expressive (broca’s) dysphasia, disinhibition, loss of smell, repeating words

126
Q

Presentation of temporal lobe stroke

A

receptive (wernicke’s) dysphasia, superior quadrantanopia, not recognise sounds/faces

127
Q

Presentation of parietal lobe stroke

A

sensory inattention, inability to follow 3 step commands, inferior quadrantanopia, can’t read letters or perform calculations

128
Q

Presentation of occipital lobe stroke

A

homonymous hemianopia, cortical blindness/visual agnosia

129
Q

Presentation of cerebellar stroke

A

gait or truncal ataxia (leaning towards lesion), nystagmus, dysmetria, past pointing, intentional tremor

130
Q

Presentation of medullary stroke

A

double vision, vertigo, vomiting, nystagmus, leans towards stroke

131
Q

Presentation of lateral medullary syndrome (wallenbergs)

A

Occlusion of PICA. Sensory only (4S). 1. Ipsilateral loss of pain/temp in face (sensory nucleus of 5th cranial nerve). 2. Contralateral loss of pain/temp in limbs (spinothalamic pathway). 3. Ipsilateral cerebellar signs (limb ataxia, vertigo, dysarthria (spinocerebellar pathway)). 4. Ipsilateral horners (sympathetic pathway).

132
Q

Presentation of medial medullary syndrome (think motor)

A

Occlusion in perforators off vertebral/proximal basilar. Mostly motor (4M). 1. Ipsilateral loss of CN 3,4,6,12 (divisible by 12, tongue deviates towards lesion and complex ophthalmoplegia) (motor nucleus). 2. ipsilateral inter-nuclear ophthalmoplegia (MLF). 3. Contralateral weakness of the arm and leg (motor corticospinal tract). 4. Contralateral loss of vibration and proprioception in the arm and leg (medial lemniscus).

133
Q

Presentation of PCOM aneurysm

A

CN 3 palsy with headache

134
Q

Which nerve damage causes claw hand

A

Ulnar nerve, inability to extend fingers at interphalangeal joints, causing flexion (4th and 5th fingers). Also weakness of abducting/adducting of fingers, adducting of thumb, wasting of small muscles and loss of sensation in 4th/5th fingers. C8-T1.

135
Q

Which nerve damage causes ape hand

A

Median nerve, inability to oppose thumb. Wasting of thenar eminence (abductor pollicus), weakness of 2 and 3 finger flexion (benediction sign), weakness of thumb abduction, sensory loss over palmar aspect of first three fingers and tinel’s and phalen’s positive. C6-T1.

136
Q

Which nerve damage causes wrist drop

A

Radial nerve, inability to extend the hand or fully extend forearm. Weakness of wrist extension, first and middle finger extension, forearm supination (if lesion from spinal groove), and elbow extension (if lesion in axilla). Also loss of sensation over snuff box/thumb. C5-8.

137
Q

Two causes of wrist drop

A
  1. radial nerve lesion = also weak finger extension + supernation of forearm (affecting brachioradialis). 2. C7 nerve root damage = also weak wrist flexion and elbow extension
138
Q

Three causes of small hand wasting

A
  1. Anterior horn cells (spinal cord) = generalised wasting of the hand, LMN signs, caused by MND, spinal muscular atrophy and polio, 2. Brachial plexus (nerve root C8-T1) = pancoast tumour (check for horners), cervical rib, radiculopathy and trauma. 3. Peripheral nerve originating from C8 to T1 = eg. ulnar or median nerve palsy (check for hand claw + weakness in nerve distribution), caused by muscular dystrophy (myopathic facies).
139
Q

Presentation of complete brachial plexus lesion (plexopathy)

A

LMN lesion sign which affects whole arm, sensory loss throughout arm, ?associated horners

140
Q

Presentation of nerve root (radiculopathy) eg C5/6 lesion

A

Loss of shoulder movement and elbow flexion, sensory loss over lateral arm/forearm.

141
Q

Features and causes of motor neuropathy

A

Distal wasting and weakness with depressed reflexes. GBS/CIPD, porphyria, lead, drugs (vincristine, nitrofurantoin, isonazid).

142
Q

Features and causes of sensation neuropathy

A

Loss of hair, reduced sensation or proprioception (distal > proximal), ataxia due to sensory losses. Small fibre neuropathy = touch, pain, temperature loss, autonomic dysfunction = DM, EtOH. Large fibre neuropathy = vibration and proprioception loss (B12 def > dorsal spino-cerebellar tract).

143
Q

Causes of combined sensory motor neuropathy

A

alcohol, diabetes, drugs, GBS/CIDP, paraproteins, vasculitis, uraemia (CRF), HMSN (CMT/SMA), paraneoplastic disease, HIV, mononeuritis multiplex, hypothyroidism, amyloid/sarcoid

144
Q

Investigations for peripheral neuropathy

A

HbA1c, B12, folate, TFT, FBP, UEC, QEP/SFLC, CK, ANA/ANCA, HIV, NCS, EMG

145
Q

What would a cerebellopontine angle tumour compress, cause and be caused by?

A

Compresses pons CN 5-8. Causes reduced facial sensation (CN 5 palsy), weakness of muscle mastication (CN 5), cannot abduct eye (CN 6 palsy), facial weakness upper and lower face (CN 7 palsy, LMN), hearing loss (CN 8 palsy). Caused by acoustic neuroma, meningioma, basilar artery aneurysm, brain mets.

146
Q

Differentiate LMN and UMN causes of facial nerve palsy (CN 7)

A

Forehead sparing (central cause - brainstem stroke with CN 5/6/8 palsies or MND). Affects forehead (LMN, check for vesicles - Ramsay-Hunt, or idiopathic as in Bell’s - 95% of time, also cerebellopontine angle/parotid tumour, MG/GBS)

147
Q

Causes of bilateral facial palsy

A

GBS, MG, myotonic dystrophy, MND

148
Q

Signs of syringomyelia (spinal cord cyst), differentiate anterior horn, lower horn and below lesion.

A

Typically C8-T1, surgical scar on neck, loss of pain and temperature sensation (spinothalamic tract). Anterior horn = LMN signs (fasciculations, small hand wasting, reduced reflexes) in upper limb. Lateral horn = horners syndrome. Below lesion = UMN signs in lower limb.

149
Q

Signs of cervical myelopathy

A

wasting of arm and hand muscles, pyramidal weakness in upper limb, sensory loss throughout C5-C7 distribution, reduced bicep jerk, increased tricep jerk, myelopathy hand sign (outward movement of 4th and 5th fingers), hoffman positive and spastic paraparesis in lower limb.

150
Q

Describe and list signs of motor neuron disease

A

Neuronal loss at all levels of motor system including cortex > brainstem > anterior horn cells. Bulbar signs = dysarthria with nasal speech, can be pseudobulbar or bulbar weakness. LMN signs = proximal and distal wasting of all limbs, fasciculations of all limbs. UMN signs = hypertonia and hyper-reflexia throughout and ankle clonus.

151
Q

Describe disease, presentation and causes of horners syndrome

A

Damage to sympathetic nerves from spinal cord to face. Has pupil constriction (miosis), ptosis (overcome by upward gaze), ipsilateral anhidrosis of face and no ocular palsy (normal eye movement). Central causes = MS, brainstem lesion (lateral medullary syndrome), syringomyelia. Peripheral causes = pancoast tumour, cervical rib, carotid artery dissection, lymphoma, brachial nerve injury.

152
Q

Describe the orders of horners syndrome and there respective causes

A

1st order = brainstem to c spine = trauma, stroke, syringomyelia. 2nd order = nerve root, lung apex = cervical rib, plexus injury, tumour. 3rd order = carotid artery, cavernous sinus orbital = dissection, herpes zoster, base of skull mass

153
Q

Presentation and diagnosis of guillian barre / CIDP / MFS

A

Motor/sensory with diminished reflexes. Bilateral weakness (distal legs, proximal arms), reduced peripheral sensation/paraesthesia, reduced/absent reflexes, bulbar weakness (especially miller fisher), respiratory/diaphragm weakness. Diagnose with CSF (high protein, anti-ganglioside Ab) and NCS (demyelination with delayed conduction).

154
Q

Presentation and diagnosis of myasthenia gravis

A

Face and neck motor weakness with fatiguability and bulbar. Ptosis (made worse on sustained upward gaze), bilateral facial and neck muscle weakness, bulbar weakness with swallow and nasal voice (not in LEMS), proximal limb weakness (arms > legs) with fatiguability, difficulty breathing. Tests = acetylcholine/musk receptor abs, tensilon (cholinergic test) test to see for improvement. EMG = reduced muscle action potential amplitude and increased fibrillation.

155
Q

Presentation and diagnosis of multiple sclerosis

A

Ocular = internuclear ophthalmoplegia, rapid afferent pupillary defect, reduced visual acuity, optic atrophy (pale optic disc). Motor (UMN) = pyramidal weakness, increased tone/spasticity, increased reflexes. Sensory = reduced dorsal column signs (vibration and proprioception) and Lhermitte’s sign. Cerebellar = reduced upper and lower limb coordination, ataxia and slurred speech. Tests = MRI, Visual Evoked Response, LP (oligoclonal band).

156
Q

Signs of cerebellar syndrome

A

DANISH. Dysdiadochokinesia, ataxia (upper and lower limbs), nystagmus, intention tremor, slurred speech, hypotonia/hyporeflexia.

157
Q

Unilateral causes of cerebellar syndrome

A

Ipsilateral to lesion. Cerebellar stroke, lesion and trauma. MS

158
Q

Bilateral causes of cerebellar syndrome

A

Toxin (alcoholic, drugs = phenytoin, lithium), hereditary ataxia (fredreich’s ataxia, spinocerebellar ataxia, ataxia -telangiectasia), paraneoplastic syndrome (anti-hu, yo, ri), endocrine (wilson’s, hypothyroidism), vitamin e def.

159
Q

Presentation of myotonic dystrophy

A

LMN, with sensation spared. Myopathic facies (wasting of facial muscles), fontal balding, bilateral ptosis, slow releasing hand grip, thenar thumb reflex, distal limb wasting and weakness, reduced muscle tone (possibly fasciculations), bilateral foot drop with high stepping gait, systemic features (valvular disease (mitral regurgitation), cardiomyopathy (CCF signs), PPM (arrythmia), respiratory distress (home o2)).

160
Q

Presentation of facioscapulohumeral muscular dystrophy

A

Bilateral ptosis, wasting of temporal / masseter muscles, myopathic facies with weakness of facial muscles (eyes, mouth, neck), scapula winging with severe proximal upper limb weakness and wasting (lower limb also affected)

161
Q

Differentials of bilateral spastic weakness

A
  1. MS (ocular and cerebellar signs). 2. Motor neuron disease (LMN, bulbar involvement, muscle wasting, nil sensory). 3. Hereditary (Fredrich’s) ataxia (upper and lower limb cerebellar signs, muscle wasting, pas caves, weakness and kyphosis). 4. Hereditary spastic paraplegia (spasticity of the legs only, UMN signs (increased tone, hyper-reflexia, clonus). 5. Cord lesion / transverse myelitis (sensory level affected, scars). 6. B12 Deficiency (proprioception/ vibration, sensory loss, ataxia, UMN (spasticity/hyper reflexes) and rhombergs)
162
Q

Presentation of charcot marie tooth

A

LMN, sensation affected. Most common inherited neurological disorder (auto-dominant). Symmetrical distal wasting hand and feet (champagne bottle legs). Reduced distal sensation, clawing of hands and feet, pes cavus, absent reflexes, ataxic high step gait (foot drop), thickened peripheral nerves (onion skinning).

163
Q

Causes of pes cavus

A

muscular dystrophy, cerebral palsy, MND, CIDP, spinal cord injury

164
Q

Presentation of Friedrich’s Ataxia

A

Cerebellar syndrome with muscle wasting. Most common hereditary ataxia (autosomal recessive mutation in FXN gene). Broad based ataxic gait, upper limb ataxia, slurred speech, bilateral nystagmus with hypermetric saccade, distal muscle wasting, weakness in pyramidal distribution (extensors arms, flexor legs), impaired vibration or proprioception, reduced reflexes (spasticity in later stages), pes cavas, scoliosis, cardiomegaly. Similar signs in spinocerebellar ataxia.

165
Q

Causes of unilateral weakness

A

Cortical lesion (UMN - stroke, tumour, MS), nerve root palsy (LMN), isolated nerve compression (radial nerve), multifocal motor neuropathy (MMN)

166
Q

Causes of distal weakness

A

peripheral neuropathy (DM/B12/EtOH/vasculitis), hereditary myopathy (myotonic dystrophy/duchenne), hereditary neuropathy (CMT/SMA), motor neuron disease (with UMN), IBM (hands however proximal weakness in lower limb), syringomyelia (usually LMN signs)

167
Q

Causes of proximal weakness

A

NMJ (myasthenia gravis - motor only), autoimmune (CIDP/GBS - motor, sensory, areflexic, distal legs, proximal arms), endocrine (thyrotoxicosis, cushings), inflammatory myopathies (PM), drugs (steroids/statins), metabolic myopathies (electrolytes), vasculitis

168
Q

Give 4 examples of parkinson plus syndrome

A

Lewy body dementia, PSP, MSA, cortical basal degeneration

169
Q

Give symptoms of Lewy body dementia

A

early onset with hallucinations

170
Q

Management of parkinsons

A
  1. Levodopa. 2. Dopamine agonists - effective in early disease to decrease dyskinesia but increases cognition issues. 3. Catechol-o-methyl transferase inhibitors which prevent levodopa breakdown by enzymes. 4. Surgery - thalamotomy / pallidotomy
171
Q

Difference in lack of coordination caused by dorsal column and cerebellar

A

Dorsal column (proprioception) - ataxia with eyes closed, as well as decreased vibration and proprioception. Cerebellar - always ataxic, also nystagmus and poor coordination in both upper and lower limbs.

172
Q

What causes shuffling gait

A

parkinsons

173
Q

What causes spastic gait

A

hereditary spastic paraplegia, subacute combined degeneration, spinal cord lesion

174
Q

What causes wide based gait

A

cerebellar and posterior column

175
Q

What causes high stepping gait

A

distal weakness

176
Q

What causes waddling gait

A

proximal weakness

177
Q

Components of parkinsons exam

A

mask like facies with lack of blinking, gait, resting tremor, rigidity, glabellar, ocular ROM, writing, frontal reflexes, postural hypotension

178
Q

Components of cerebellar exam

A

gait (s1 toes, l4/5 heels), rhombergs, lower limb sx, upper limb sx, nystagmus, speech (hippopotamus), truncal ataxia, other neuro

179
Q

Causes of ischaemic stroke

A

Cardiac embolism 20%, large artery occlusion 20%, subcortical lacunar infarct- hypertension 25%, cryptogenic 30%, vasculitis/ genetic/ sinus thrombosis 5%

180
Q

Management of ischaemic stroke

A

Thrombolysis if within 4.5 hours. Thrombectomy if 18 hours. Aspirin (+clopidogrel) 6weeks. Anticoagulation for AF. Statin. BP control. Rehab.

181
Q

Investigations for stroke

A

CT / MRI / carotid ultrasound. Ecg / holter/ consider ECHO. Ix connective tissue disorders or antiphospholipid syndrome if younge.

182
Q

Risk factors for stroke

A

Age, smoking, hypertension, diabetes, high lipids, AF, previous strokes

183
Q

Presentation of posterior stroke

A

Bilateral weakness (basilar), medullary, cerebellar signs, bilateral vision loss

184
Q

Management of Guillian Barre Syndrome and CIDP

A

IVIG for GBS, steroids for CIDP. Plasma exchange. Ventilation.

185
Q

Investigation findings for GBS

A

Infection- campylobacter, mycoplasma, CMV, EBV, HIV. Raised protein levels in CSF. Slowed motor conduction and reduced sensory action potentials on nerve conduction studies and EMG. Reduced FVC. Anti-ganglione antibodies (anti-GM1, anti-GQ1b in Miller Fisher)

186
Q

Presentation of Guillian Barre Syndrome

A

Ascending muscle weakness, absent reflexes, sensory loss (more dorsal column - vibration and proprioception), breathing difficulties, bulbar symptoms (speech/ swallowing difficulties), autonomic neuropathy (postural hypotension and arrhythmias)

187
Q

Management of Myasthenia Gravis

A

Pyridostigmine (acetylcholinesterase inhibitor). Steroids. Immunosuppressant if steroids fail (azathioprine, ciclosporin, MMF). IVIG or rituximab. Thymectomy. Treat underlying infection or cease aggrevating drug.

188
Q

Antibodies for Myasthenia Gravis

A

Acetylcholine receptor antibodies, 80 to 90% positive. MUSK, 40% of those seronegative to acetylcholine receptor antibodies. Voltage gated calcium channel antibodies - Eaton Lambert secondary to small cell lung cancer (mostly upper limb, no bulbar)

189
Q

Investigations for Myasthenia Gravis

A

Antibodies. Electomyogram (reduced action potentials amplitudes). Thymoma screening. Lung volume testing (exclude reduced FVC).

190
Q

Risk factors for Myasthenia Gravis

A

Previous thymoma or thymectomy. Autoimmune condition, SLE or RA

191
Q

Presentation of Myasthenia Gravis

A

Occular (90%), ptosis, diplopia (muscle fatigue - peek sign). Bulbar - dysarthria, dyaphagia. Neck weakness. Proximal muscle weakness with fatigue in exertion with recovery at rest. Reflexes and sensation present.

192
Q

Presentation of Multiple Sclerosis

A

Spastic paresis. Parasethesia. Posterior column loss. Visual disturbance (optic neuritis with cortical vision loss, eye pain, diplopia). Relevant afferent pupillary defect. Intranuclear opthalmaplegia. Cerebellar triad (ataxia, dysarthria, tremor). Urinary urgency and faecal incontinence. Depression, dementia, seizures, vertigo. Aggravating factors like heat, infection and pregnancy. Lhemittes sign - electric shocks in upper limb with neck flexion (c spine lesion).

193
Q

Complications of Multiple Sclerosis

A

Immobility, visual loss, incontinence, social disability.

194
Q

Management of Multiple Sclerosis

A
  1. Supportive treatment- baclofen for bladder or muscle spasticity, amitryptyline for urinary urgency, duloxetine for facial spasms, support groups, IV methylprednisolone for acute flares. 2. Immunotherapy. 3. Natalizumab (alpha4 integren antibody, good for RR MS, can cause progressive multifocal leukoencephalopathy). 4. Ocrelizumab (monoclonal for CD20). 5. Fingolimod / siponimod - sphingosine 1 phosphate receptor inhibitor lymphopenia. 6. Teriflunomide- pyrimidine synthesis inhibitor (leflunomide) causes GI symptoms and hair loss
195
Q

McDonald criteria

A
  1. MRI demonstrates more than 1 T2 lesion within the periventricular, infratentorial, spinal cord or juxtacortical regions. 1. New lesions over space and time.
196
Q

Investigations for multiple sclerosis

A

McDonald criteria. Oligoclonal antibodies or raised IgG in CSF. Visual provoked responses are delayed.

197
Q

Risk factors for multiple sc

A

Smoking, far from equator, family history

BPT (11 decks)

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