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Neurology Flashcards

1
Q

Features of tuberous sclerosis

A

Skin
- Ash leaf spots
- Nail fibroma
- Freckling
- Adenoma sebaceum (angiofibromas on face in butterfly distribution)

Brain
- Tumour
- Seizures
- Developmental delays/retardation

Others:
- Renal cysts
- Teeth pitting

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2
Q

Brainstem signs

A
  • Cranial nerve abnormalities with contralateral UMN signs
    (because cranial nerves III-XII arise from brainstem; I-II arise from cerebrum)
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3
Q

Causes of decorticate vs decerebrate positioning

A
  • Decorticate: cerebrum
  • Decerebrate: brainstem (worse prognosis)
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4
Q

Features of decorticate vs decerebrate positioning

A

Decorticate = flexor
- Arms flexed
- Fists clenched
- Legs extended and turned inwards
- Scores 3/6 in GCS

Decerebrate = extensor
- Elbows extended
- Arms and legs extended
- Head arched back
- Clenched teeth
- Scores 2/6 in GCS

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5
Q

Upper motor neurone vs lower motor neurone- which anatomical area differentiates between them

A
  • Anterior horn cell (UMN above, LMN below)
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6
Q

Signs of UMN vs LMN

A

Upper motor neurone
- Increased tone (spasticity)
- Pyramidal pattern weakness (flexors stronger than extensors in arm, vice versa in legs)
- Increased weakness
- Up-going plantars
- Clonus

Lower motor neurone
- Decreased tone
- Wasting and weakness
- Reduced reflexes
- Fasciculations

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7
Q

Signs of spinal cord lesion

A
  • Bilateral upper motor neurone signs
  • Sensory level
  • Sphincter disturbance
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8
Q

Signs of brainstem lesion

A
  • Dysarthria
  • Dysphagia
  • Cerebellar signs
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9
Q

Signs of nerve root lesion

A
  • LMN signs in dermatomal/myotomal distribution
    (nerve root = leave spinal cord at different levels e.g. C1, C2 etc– each nerve root has sensory component = dorsal nerve root, and motor component = ventral)
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10
Q

Signs of polyneuropathy

A
  • LMN signs
  • Worse distally (legs worse than arms)
  • Sensory signs
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11
Q

Signs of neuromuscular junction lesion

A
  • Weakness with normal sensation
  • Usually proximal
  • Fluctuates e.g. time of day/during examination
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12
Q

Difference between spasticity and rigidity

A
  • Spasticity = increased resistance initially but then gets better (velocity-dependent– clasp-knife) == pyramidal (cerebrum)
  • Rigidity = increased resistances constantly == extrapyramidal (basal ganglia/cerebellum)
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13
Q

Shoulder abduction - muscle, nerve root and nerve

A
  • Deltoid
  • C5-6
  • Axillary nerve
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14
Q

Shoulder adduction - muscle, nerve root and nerve

A
  • Lat dorsi and pec major
  • C6-8
  • Thoracodorsal nerve
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15
Q

Elbow flexion - muscle, nerve root and nerve

A
  • Biceps
  • C5-6
  • Musculocutaneous nerve
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16
Q

Elbow extension - muscle, nerve root and nerve

A
  • Triceps
  • C6-8
  • Radial nerve
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17
Q

Wrist extension - muscle, nerve root and nerve

A
  • Extensor carpi radialis longus, extensor carpi ulnaris
  • C5-8
  • Radial and posterior interssseous nerves
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18
Q

Wrist flexion - muscle, nerve root and nerve

A
  • Flexor carpi radialis, fl exor carpi ulnaris
  • C6-7
  • Radial and ulnar nerves
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19
Q

Finger extension - muscle, nerve root and nerve

A
  • Extensor digitorum
  • C7-8
  • Posterior interosseous nerve (branch of radial nerve)
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20
Q

Finger flexion - muscle, nerve root and nerve

A
  • Flexor digitorum superficialis and profundus
  • C8
  • Median and ulnar nerves
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21
Q

Thumb opposition, flexion, abduction - nerve root and nerve

A
  • C8-T1
  • Median nerve
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22
Q

Spastic gait - features and cause

A
  • Scissoring
  • Narrow-based
  • Stiff
  • Toes-scuffing

Cause = spastic paraparesis

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23
Q

Hemiparetic gait - features and cause

A
  • Circumducting
  • Scuffing of one foot

Cause = stroke

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24
Q

Extrapyramidal gait - features and cause

A
  • Shuffling/slow
  • Festinant (rapid fall steps as if about to fall over)
  • Poor arm swing
  • Bradykinesia (ask pt to touch thumb and index finger repeatedly quickly)

Cause = Parkinson’s

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25
Q

Apraxic gait - features and cause

A
  • Gait ignition failure
  • Upright posture with short steps

Cause = fronto-parietal lesion (Vascular parkinsonism) or normal-pressure hydrocephalus

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26
Q

High-stepping gait - features and cause

A
  • Foot-drop

Cause = neuropathy, myopathy, antalgic

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27
Q

Why is UMN lesion forehead sparing?

A
  • The muscles of the upper half of the face (frontalis, corrugator and orbicularis) are innervated bilaterally by corticobulbar fibres
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28
Q

Fasciculations in tongue

A
  • MND (tongue must be rested in floor of mouth)
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29
Q

Motor scoring for GCS

A
  • 6: obeys commands
  • 5: towards pain
  • 4: away pain
  • 3: decorticate (flexor)
  • 2: decerebrate (extensor)
  • 1: none
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30
Q

Reflex nerve roots

A
  • Ankle: S1-2 (button my shoe)
  • Knee: L3-4 (kick the door)
  • Biceps: C5-6 (pick up the sticks)
  • Triceps: C7-8 (open the gate)
    1234567!
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31
Q

What is Hoffman sign

A
  • Flick middle finger DIP –> see flexion of thumb/fingers = UMN
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32
Q

Causes of peripheral neuropathy

A

Metabolic/endocrine
- Diabetes
- Hypothyroidism
- Uraemia

Toxic
- Alcohol
- Chemotherapy

Inflammatory
- CIDP
- Vasculitis

Paraneoplastic
- Lung cancer
- Paraproteinaemia

Congenital— only say if there are motor signs/wasting!
- Charcot-Marie-Tooth

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33
Q

Dorsal column tested by

A
  • Light touch
  • Vibration
  • Proprioception
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34
Q

Spinothalamic tested by

A
  • Pinprick
  • Temperature
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35
Q

Hip flexion - muscle, nerve root and nerve

A
  • Iliopsoas
  • L1-3
  • Femoral nerve
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36
Q

Hip extension - muscle, nerve root and nerve

A
  • Gluteus maximus
  • L5-S1
  • Inferior gluteal nerve
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37
Q

Knee flexion - muscle, nerve root and nerve

A
  • Hamstrings
  • L5-S1
  • Sciatic nerve
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38
Q

Knee extension - muscle, nerve root and nerve

A
  • Quadriceps femoris
  • L3-4
  • Femoral nerve
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39
Q

Ankle dorsiflexion - muscle, nerve root and nerve

A
  • Tibialis anterior
  • L4-5
  • Deep peroneal
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40
Q

Ankle plantarflexion - muscle, nerve root and nerve

A
  • Gastrocnemius
  • S1
  • Tibial nerve
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41
Q

Ankle inversion - muscle, nerve root and nerve

A
  • Tibialis posterior
  • L4-S1
  • Tibial nerve
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42
Q

Ankle eversion - muscle, nerve root and nerve

A
  • Peroneus longus/brevis
  • L5
  • Superficial branch of common peroneal nerve
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43
Q

Contractures signify

A
  • Long-standing spasticity
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44
Q

Waddling gait

A
  • Proximal myopathy
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45
Q

Stamping gait

A
  • Proprioceptive loss (patient figures out where their feet are by resulting sensory/auditory clues)
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46
Q

UMN signs with spastic scissoring gait- where is the lesion

A
  • Above C4
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47
Q

Poor visual acuity in young patient

A
  • Optic atrophy in MS?
  • If very poor acuity, think neuromyelitis optica (inflammation of optic nerve/spinal cord)
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48
Q

Elderly patient with brisk upper limb reflexes, wasting of the small muscles of the hands and a sensory neuropathy

A
  • Could be dual pathology! Compressive cervical myelopathy with diabetes
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49
Q

Triad in normal pressure hydrocephalus

A
  • Gait apraxia
  • Urine incontinence
  • Cognitive impairment
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50
Q

Causes of hemiparesis

A

Intracranial
- Stroke: MCA (arm > leg), ACA (leg > arm)
- SOL
- Demyelination/inflammation

Spinal cord = Brown-Sequard
- Trauma
- Tumour (neurofibroma)
- Abscess

Others
- Todd’s paresis after seizure
- Hemiplegic migraine

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51
Q

Difference between paresis and plegia

A
  • Paresis = weakness
  • Plegia = paralysed
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52
Q

Causes of spastic paraparesis and a sensory level

A
  • Cord compression (disc/tumour/abscess)
  • Cord infarction
  • Transverse myelitis (infection/autoimmune/paraneoplastic)
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53
Q

Causes of spastic paraparesis and dorsal column loss (joint position sense and vibration)

A
  • Demyelination (MS)
  • Subacute combined degeneration of cord (B12 deficiency)
  • Friedrich’s Ataxia (degeneration of spinal cord + demyelination)
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54
Q

Causes of spastic paraparesis and spinothalamic loss (pain and temperature)

A
  • Syringomyelia (cysts in cord)
  • Anterior spinal artery infarction (affects descending spinothalamic tracts)
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55
Q

Features of anterior spinal artery infarction

A
  • Paralysis below lesion (corticospinal tracts)
  • Loss of pain/temperature below lesion (spinothalamic tracts)
  • Retained vibration/proprioception (dorsal columns not affected as they are posterior)
  • Autonomic dysfunction (retention/incontinence etc)
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56
Q

Causes of spastic paraparesis and cerebellar signs

A
  • Demyelination (MS)
  • Friedreich’s ataxia
  • Spinocerebellar ataxia (degeneration)
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57
Q

Causes of spastic paraparesis and bilateral UMN signs in arms

A
  • Bilateral strokes
  • Cervical lesion above C5
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58
Q

Features of flaccid paraparesis (LMN lesion)

A
  • Wasting of upper limbs (hands): Charcot-Marie-Tooth/other neuropathy
  • Pes cavus: peripheral neuropathy
  • No sensory signs: GBS, CIDP (Chronic Inflammatory Demyelinating Polyradiculoneuropathy), MND
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59
Q

Features of flaccid paraparesis (LMN lesion)

A
  • Wasting of upper limbs (hands): Charcot-Marie-Tooth/other neuropathy
  • Pes cavus: peripheral neuropathy
  • No sensory signs: GBS, CIDP (Chronic Inflammatory Demyelinating Polyradiculoneuropathy), MND
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60
Q

Causes of proximal myopathy

A
  • Polyradiculopathy (reduced reflexes): Chronic Inflammatory Demyelinating Polyradiculoneuropathy and GBS
  • Inflammatory: dermatomyositis
  • Neuromuscular junction: Myasthenia Gravis/Lambert-Eaton Syndrome
  • Endocrine: hypothyroidism
  • Others: polymyalgia rheumatica/fibromyalgia
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61
Q

Cause of pronator drift

A
  • UMN lesion affecting corticospinal tract: supinator muscles in the upper limb are weaker than the pronator muscles, and as a result, the arm drifts downward and the palm turns toward the floor
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62
Q

Causes of sensory loss

A

Central
- Cord: transection/hemisection/anterior artery syndrome
- Brain: parietal, thalamic, brainstem

Peripheral
- Radiculopathy: dermatomal
- Peripheral nerve: asymmetrical (mononeuropathy) and symmetrical (polyneuropathy)

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63
Q

Areas of brain which determine speech

A
  • Broca’s = expressive dysphasia (frontal lobe of dominant hemisphere)
  • Wernicke’s = receptive dysphasia (temporal lobe of dominant hemisphere)
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64
Q

Causes of dysphasia

A

Affects Broca’s (expressive - frontal) and Wernicke’s (receptive - temporal)
- MCA stroke
- SOL
- Degenerative (frontotemporal dementia)

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65
Q

Ptosis dilated vs ptosis constricted

A
  • Ptosis dilated = surgical 3rd nerve palsy
  • Ptosis constricted = Horner’s Syndrome
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66
Q

Features of right 3rd nerve palsy

A
  • Right eye down and out, cannot adduct (unopposed action of superior oblique IV and lateral rectus VI)
  • Ptosis worse on adducting

Extra points: test for normal IV nerve by asking to look medially–> eye will intort (turn down towards nose)

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67
Q

Features of right 4th nerve palsy

A
  • Right eye up and out, moves up further when abducts
  • Diplopia downwards (6th nerve = diplopia on abduction)
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68
Q

Features of right 6th nerve palsy

A
  • Right eye turned medially, cannot abduct
  • Diplopia on abduction (4th nerve = diplopia downwards)
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69
Q

Causes of ptosis

A
  • 3rd nerve palsy (dilated)
  • Horner’s (constricted)
  • Myasthenia gravis (worse at the end of the day)
  • Myotonic dystrophy
  • Senile ptosis/eyelid lesion = commonest in real world!
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70
Q

Weakness of eye movements in multiple directions

A
  • “Complex ophthalmoplegia” (myasthenia, thyroid, ocular myopathy)
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71
Q

Features of internuclear ophthalmoplegia

A
  • Eye on affected side cannot adduct
  • Eye on opposite side has nystagmus when abduct
  • (Damage to medial longitudinal fasciculus in the brainstem)
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72
Q

How to check for ocular myasthenia

A
  • Look upwards– will complain of diplopia after a few seconds
  • Icepack to eyes for 2 mins- ptosis will improve
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73
Q

Can’t move both eyes up

A
  • Supranuclear Palsy
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74
Q

Can’t move both eyes laterally

A
  • Lateral gaze palsy (pontine lesion)
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75
Q

In resting position
- Lateral nystagmus
- Upbeat nystagmus
- Downbeat nystagmus

A
  • Lateral nystagmus = unilateral vestibular lesion
  • Upbeat nystagmus = cerebellar/brainstem
  • Downbeat nystagmus = craniocervical junction lesion (Arnold-Chiari = cerebellar tonsils move down into foramen magnum; demyelination; syringobulbia)
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76
Q

When looking at examiner’s finger and then nose, affected eye is slow to adduct and left behind

A
  • Mild Internuclear Ophthalmoplegia
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77
Q

Cause of small vessel (lacunar) vs large vessel occlusion in stroke

A
  • Small vessel = atherosclerosis
  • Large vessel = embolus
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78
Q

Areas of brain affected by lacunar strokes

A
  • Deep white matter: corona radiata, internal capsule (corticospinal tracts), basal ganglia
  • Does not affect cortex so no cortical deficits (no dysphasia)
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79
Q

Types of lacunar stroke

A
  • Pure motor
  • Pure sensory
  • Sensorimotor
  • Ataxic hemiparesis
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80
Q

ACA supplies what areas of brain

A
  • Frontal and medial-parietal areas
  • Includes motor/sensory areas for lower limbs
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81
Q

MCA supplies what areas of brain

A
  • Whole lateral surface of the frontal, parietal and temporal lobes + auditory cortex
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82
Q

PCA supplies what areas of brain

A
  • Inferior, occipital, cerebellum
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83
Q

Features of ACA stroke

A
  • Leg weakness/sensory loss (worse than arm)
  • Urine incontinence
  • Face spared
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84
Q

Features of MCA stroke

A
  • Arm weakness/sensory loss (worse than legs)
  • Homonymous hemianopia (optic radiations in parietal and temporal lobes)
  • Dysphasia if dominant hemisphere involved (Broca’s = frontal and Wernicke’s = temporal)
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85
Q

Components of posterior circulation

A

Vessels supplied by the 2 vertebral arteries
- Basilar artery (pons and superior/inferior cerebellum)
- Posterior inferior cerebellar artery (PICA)
- Anterior inferior cerebellar artery (AICA)
- Superior cerebellar artery (SCA)
- Posterior cerebellar artery (PCA)

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86
Q

Features of PICA occlusion (Wallenberg’s Syndrome = Lateral Medullary)

A
  • Ipsilateral pinprick loss in face (trigeminal nerve)
  • Ipsilateral Horner’s (descending sympathetic tract)
  • Ipsilateral cerebellar signs (inferior cerebellar peduncle)
  • Contralateral pinprick loss in trunk/limbs (spinothalamic)
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87
Q

Features of AICA occlusion (Lateral Pontine Syndrome)

A
  • Ipsilateral sensory and motor loss in face (LMN facial droop as affects CN 7 which is in pons)
  • Contralateral pinprick loss in trunk/limbs
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88
Q

Features of PCA stroke

A
  • Homonymous hemianopia with macular sparing = central vision intact (occipital pole at site of rich anastomosis between MCA/PCA)
  • Cortical blindness
  • Contralateral pain/temperature loss (thalamic damage)
  • Weber’s Syndrome (medial midbrain): ipsilateral CNIII palsy and contralateral hemiplegia
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89
Q

Most common site for spinal cord infarction

A
  • Anterior spinal artery (anterior 2/3 of cord)– at upper thoracic cord (watershed area)
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90
Q

Features of spinal cord infarction

A
  • Acute flaccid paraparesis (becomes spastic later on)
  • Loss of pain/temperature (spinothalamic) but preserved vibration/proprioception (dorsal column)
  • Loss of sphincter control
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91
Q

Cause of basal ganglia haemorrhage (deep) vs lobar haemorrhage

A
  • Basal ganglia = HTN
  • Lobar = structural abnormality (AVM/tumour), vascular abnormality (vasculitis/amyloid angiopathy)
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92
Q

Causes of subarachnoid haemorrhage

A
  • Genentic: PCKD, Marfan’s, Ehlers-Danlos, pseudoxanthoma elasticum
  • Smoking
  • HTN
  • Drugs: cocaine, meth
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93
Q

Features of hydrocephalus in ICH

A
  • New 6th nerve palsy (false-localising- nerve is stretched)
  • Cushing’s triad (rise in BP, bradycardia, wide pulse pressure)
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94
Q

Differential diagnosis for stroke

A
  • Viral encephalitis
  • Migraine (aphasia/hemiparesis)
  • Epilepsy (Todd’s paresis post-seizure) = instant symptoms (stroke takes a few mins)
  • SOL
  • Functional (weakness unlikely to be pyramidal i.e. flexors won’t be weaker than extensors)
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95
Q

Investigation if CT head normal but still suspect subarachnoid haemorrhage

A
  • LP 12hrs after symptoms to let xanthochromia to form
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96
Q

Treatment for subarachnoid haemorrhage

A
  • Nimodipine 60mg PO every 4hrs for 2 weeks = prevents cerebral vasospasm
  • Neurosurgery: endovascular coiling/clipping
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97
Q

Treatment of TIA/minor ischaemic stroke as per 2023 guidelines

A
  • Clopidogrel and aspirin 300mg loading then DAPT 75mg for 3 weeks –> clopidogrel 75mg OD

(If not appropriate for DAPT, just give clopidogrel 300mg loading dose –> 75mg OD)

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98
Q

Criteria for referral for carotid endarterectomy

A
  • Symptomatic stenosis 50% or more
    (symptomatic stenosis = acute focal neurology ipsilateral to stenosis)
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99
Q

Stroke-specific MRI sequences

A
  • DWI with SWI (susceptibility-weighted images)
  • T2-weighted
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100
Q

Thrombolysis criteria if stroke occurred >4.5hrs ago (2023 guidelines)

A
  • Can thrombolyse within 9hrs of onset/9hrs of midpoint of sleep if wake-up symptoms

AND

  • CT/MRI perfusion scan shows salvageable tissue (mismatch ratio greater than 1.2, a mismatch volume greater than 10 mL, and an ischaemic core volume <70 mL)
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100
Q

Thrombolysis criteria if stroke occurred >4.5hrs ago (2023 guidelines)

A
  • Can thrombolyse within 9hrs of onset/9hrs of midpoint of sleep if wake-up symptoms

AND

  • CT/MRI perfusion scan shows salvageable tissue (mismatch ratio greater than 1.2, a mismatch volume greater than 10 mL, and an ischaemic core volume <70 mL)
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101
Q

Thrombectomy criteria if stroke occurred 6hrs ago- anterior circulation strokes (ACA+MCA) (2023 guidelines)

A

ICA/M1 occlusion with NIHSS 6+ and pre-stroke MRS 0/1

AND

  • 6-12hrs: ASPECTS 3+, irrespective of the core infarct size
  • 12-24hrs: ASPECTS 3+ and CT or MRI perfusion mismatch of greater than 15 mL, irrespective of the core infarct size.
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102
Q

Thrombectomy criteria if stroke occurred 6hrs ago- posterior circulation strokes (PCA) (2023 guidelines)

A
  • Within 12hrs
  • Vertebral/basilar occlusion
  • NIHSS 10+
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103
Q

What is valvular AF

A
  • Mitral stenosis/artificial valves
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104
Q

Cause of Multiple Sclerosis

A
  • Genetic susceptibility
  • EBV/HHV6 increases risk (?)
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105
Q

Features of Multiple Sclerosis

A

2 episodes separated in time and space

  • Optic neuritis = often presenting symptom (pain behind eye on movement –> reduced acuity/red-green colour blind/RAPD)
  • Diplopia (INO or 6th nerve palsy)
  • Cord involvement: sensory changes/paraparesis (legs)/urine and bowel dysfunction
  • Lhermitte’s sign: neck flexion –> electric shock from neck to limbs (cervical cord lesions)
  • Uhthoff’s sign: symptoms worse when body temp rises (hot shower)
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106
Q

Types of Multiple Sclerosis

A
  • Clinically isolated syndrome: 1 clinical episode –> gadolinium-enhancing/T2 weighted lesion 30 days later = relapsing-remitting MS
  • Relapsing-remitting MS: usually 1 relapse per year (85% present like this)
  • Secondary-progressive MS: gradual decline without clear relapses (80% of RRMS develop this after 20yrs)
  • Primary-progressive MS: 15% present with this gradually progressive disorder
107
Q

Investigations in Multiple Sclerosis

A
  • Exclude mimics: autoimmune screen, B12, treponemal serology (syphilis)
  • MRI with gadolinium: hyperintense lesions on T2 = periventricular and corpus callosum white matter demyelination (corpus callosum joins 2 hemispheres)- can see old and new lesions
  • LP: unmatched oligoclonal bands (in CSF but not in serum) and mildly raised WBCs
  • Visual evoked potentials: delayed conduction but normal amplitude = optic neuritis
108
Q

Management of Multiple Sclerosis- acute relapse

A
  • IV methylprednisolone 1g OD for 3 days (5days if severe)
  • Screen for precipitating infection before starting methylpred!
  • Check glucose
  • Plasma exchange if very severe
109
Q

Management of Multiple Sclerosis- chronic

A
  • MDT approach: physio, SLT, OT, incontinence nurses
  • DMARDs: interferon beta-1a, glatiramer, natalizumab (risk of PML)
  • Urine frequency: oxybutynin (anticholinergic)
  • Sensory symptoms: gabapentin/duloxetine
  • Muscle tone/spasms: baclofen
110
Q

Differential for Multiple Sclerosis

A
  • Autoimmune: SLE, Sjogren’s, Behcet’s, sarcoid
  • Vascular: recurrent TIA, antiphospholipid
  • Metabolic: B12
  • Infectious: HIV encephalitis, syphilis, PML, Lyme disease
  • Mitochondrial: MELAS (Mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes )
111
Q

What is Neuromyelitis Optica and treatment

A
  • Demyelination of cord/optic nerves (antibody directed against aquaporin-4 = can be found in serum)
  • Severe optic neuritis
  • Treatment: IV immunoglobulin and plasma exchange in the acute setting –> steroids and immunosuppressants
112
Q

Features of Parkinson’s Disease tremor

A
  • UNILATERAL pill-rolling
  • Worsening by distraction (count from 100 to 1) or repetitive movements of other hand
  • Disappears on movement
113
Q

Causes of drug-induced Parkinsonism

A
  • Dopamine antagonist antipsychotics (haloperidol)
  • Anti-emetics (metoclopramide = dopamine antagonist)
  • Phenothiazines (prochlorperazine)
  • Valproate
114
Q

Features of Progressive Supranuclear Palsy (PSP)

A
  • Can’t look up
  • Falls (backwards)
  • Frontalis overactivation
  • Axial rigidity (neck and trunk)
115
Q

Features of Multi-System Atrophy

A

Autonomic disturbance
- Incontinence
- Postural hypotension
- Impotence

Cerebellar ataxia

116
Q

Features of corticobasal degeneration

A
  • Unilateral apraxia/pyramidal signs
  • Myoclonus (brief muscle twitching)
  • Dystonic posturing
117
Q

Features of essential tremor

A
  • “Yes-yes” head movements
  • On movement
  • Relieved by alcohol/beta-blockers
118
Q

Features of demyelinating tremor

A
  • Present in posture (holding arms out) or action
  • Absent in rest
119
Q

Causes of bilateral cerebellar disorder

A
  • Demyelination
  • Bilateral strokes/SOL in posterior fossa
  • Paraneoplastic (onconeural antibodies)

Remember PASTRIES
- Paraneoplastic
- Alcohol
- Sclerosis (MS)
- Tumour (posterior fossa)
- Rare (Friedrich’s Ataxia = young, spinocerebellar ataxia = old)
- Iatrogenic (phenytoin, lithium)
- Endocrine (hypothyroidism, Wilson’s)
- Stroke (brainstem)

120
Q

Features of spinocerebellar ataxia (apart from cerebellar signs)

A

May look like well patient with mild cerebellar signs
- Varied modes of inheritance, degenerative
- Old (Friedrich’s ataxia will be young)
- UMN signs
- Peripheral neuropathy
- Ophthalmoplegia

121
Q

Features of Friedrich’s Ataxia (apart from cerebellar signs)- including pathogenesis and mode of inheritance

A
  • Degeneration of spinal cord + demyelination
  • Autosomal recessive deficiency of frataxin protein- onset 8-15yrs so will be wheelchair-bound (whereas spinocerebellar ataxia patient will be old)
  • Spastic paraparesis
  • Pes cavus
  • Leg wasting with absent reflexes and upgoing plantars
  • Dorsal column signs (loss of vibration/proprioception)
  • HOCM risk (need regular echos)
122
Q

Features of Miller-Fisher Syndrome

A
  • Ophthalmoplegia
  • Ataxia
  • Absent lower limb reflexes

(Auto-immune post-infectious- anti-GQ1b ganglioside
antibody)

123
Q

Signs of spinal cord disorders

A
  • Spastic paraperetic gait (scissoring narrow toes scuffing)
  • Pyramidal weakness
  • Hyper-reflexia with upgoing plantars
  • Sensory level about L1
  • Catheter
124
Q

Predominant sensory signs vs predominant motor signs in spinal cord disorder

A
  • Sensory: inflammatory myelitis (HIV/syphilis)- also B12 deficiency as affects posterior cord
  • Motor: cord compression
125
Q

Asymmetrical spinal cord signs

A
  • Cord compression
  • Myelitis
126
Q

Causes of inflammatory cord lesions

A
  • MS: commonest transverse myelitis in young
  • Post-infectious acute disseminated encephalomyelitis (ADEM)- MMR, varicella
  • Autoimmune: SLE, Sjogren’s, vasculitis
  • Neuromyelitis optica (optic neuritis with long segments of myelitis)

Get sensory level with mostly sensory signs

127
Q

Features of subacute combined degeneration of cord (SCD)

A
  • Bilateral dysaesthesiae (unpleasant sensation when touched)
  • Loss of posterior column modalities = dorsal column (light touch, vibration, proprioception)
  • Brisk knee jerks + absent ankle jerks + upgoing plantars
  • Spastic paraparesis lower limbs

Causes: B12 deficiency (also copper/Vitamin E)

128
Q

Features of hereditary spastic paraparesis

A

Heterogenous group of disorders (autosomal dominant/recessive/X-linked)
- Slowly progressive gait disturbance
- Spasticity worse than weakness
- Hyper-reflexia with upgoing plantars
- Complicated form: neuropathy, retinopathy, cognitive issues

129
Q

Causes and features of bulbar palsy

A

LMN lesion of cranial nerves 9-12
- MND
- Myasthenia
- Neuropathy (GBS)

Features
- Nasal speech (palatal weakness)
- Tongue wasting/fasciculations
- Can’t handle secretions
- Dysphagia

130
Q

Causes and features of pseudobulbar palsy

A

UMN lesion of cranial nerves 9-12 (affecting supply to tongue/oropharynx)
- MS
- Brainstem stroke
- MND

Features
- Hot potato speech (tongue doesn’t move as spastic)
- Slow tongue movements
- Brisk jaw jerk
- Emotional labile (sudden laughter/crying)

131
Q

Causes of mixed UMN and LMN signs

A
  • Dual pathology (cervical myelopathy and peripheral neuropathy)
  • Cervical radiculomyelopathy (affects nerve root and cord)
  • MND
  • Syringomyelia
  • Subacute combined degeneration of cord
132
Q

Signs of cervical myelopathy with peripheral neuropathy

A

Mixed UMN and LMN in old person
- Surgical scars on neck
- Brisk reflexes if severe myelopathy with mild neuropathy
- No signs above neck

133
Q

Features of cervical radiculomyelopathy

A

Degeneration of c-spine –> compression of the exiting nerve roots (radiculopathy) and cord (myelopathy)

Get mixed UMN and LMN signs
- Wasting and pyramidal weakness
— C5-6: flaccid weakness biceps/supinators with loss of these reflexes
— C7-T1: wasting of the triceps, forearm or intrinsic hand muscles
- Brisk reflexes (clasp knife)
- Spasticity
- Sensory loss in radicular distribution

134
Q

Types of MND

A
  • Amyotrophic Lateral Sclerosis (ALS): UMN and LMN (corticospinal tracts mainly –> spastic paraparesis)
  • Primary Lateral Sclerosis (PLS): UMNs- best prognosis
  • Progressive Muscular Atrophy (PMA): LMNs (speech/swallowing issues –> worse prognosis)
135
Q

Treatment for MND

A
  • MDT: SLT/dietitian for feeding
  • Riluzole increases survival by 2-3 months (causes nausea/deranged LFTs)
  • Baclofen for muscle spasms
  • Monitor respiratory function (may need NIV)
  • Screen for frontotemporal dementia
136
Q

Features of syringomyelia

A

Cyst in central spinal canal (syringobulbia is when brainstem affected)
- Loss of pain/temperature but preserved light touch/vibration/proprioception (affects decussating spinothalamic fibres in the central grey matter with preservation of the dorsal columns)
- “Hanging/cape-like” sensory loss in upper body but not legs
- Wasting/weakness intrinsic hand muscles (C8-T1)
- Charcot joints

137
Q

Features of conus medullaris vs cauda equina lesion

A

Conus medullaris (end of spinal cord) = central disc herniation, demyelination, tumour
- Early sphincter loss
- Saddle anaesthesia
- Upgoing plantars (conus contains UMNs)

Cauda equina = extrinsic compression (prolapsed intervertebral disc), inflammation, infection (HSV)
- Radicular pain
- Unilateral LMN signs (flaccid weakness, absent reflexes)

138
Q

Causes of unilateral LMN facial droop

A
  • Bell’s Palsy
  • Ramsey-Hunt: herpes zoster reactivation in the geniculate ganglion–> vesicles over the external auditory meatus/in ear canal
  • SOL: cerebellar pontine angle (CPA) lesion e.g acoustic neuroma in NF2
139
Q

Features of T1 radiculopathy

A
  • Horner’s Syndrome (disrupts sympathetic pathway to the
    cervical sympathetic ganglia)
140
Q

Causes of radiculopathy (nerve root damage)

A
  • Disc herniation (usually L5-S1 = sciatica)
  • Cervical/lumbar spondylosis (degeneration) + osteophytes
  • Compression: schwannoma, abscess, met
  • Inflammation: ADEM, GBS
141
Q

Causes of brachial plexopathy

A
  • Brachial neuritis: inflammatory- sudden pain–> patchy sensory loss and winged scapula
  • Cancer: Pancoast tumour
  • Thoracic outlet syndrome: cervical rib/structural abnormality –> slowly progressive unilateral atrophic weakness of intrinsic hand muscles and numbness in the distribution of the ulnar nerve
142
Q

Features of brachial plexopathy

A
  • Muscle weakness and atrophy.
  • Reduced reflexes in weak muscles.
  • Sensory loss which commonly involves the axillary nerve distribution (regimental patch C7)
143
Q

Causes of lumbar plexopathy

A
  • Diabetic amyotrophy (L2-4): wasted quadriceps (may be asymmetrical), severe proximal leg/hip pain and weakness, not much sensory symptoms
  • Compression (haematoma/abscess/tumour)
  • Radiotherapy: slowly progressive weakness and sensory loss of leg
144
Q

Features of median nerve palsy

A

Affects LOAF muscles of hand (T1)
- Lateral 2 lumbricals: index/middle finger
- Opponens pollicus: make “O” with thumb to fingers
- Abductor pollicis brevis: thumbs up
- Flexor pollicis brevis: thumb flexion

Sensation to lateral 2/3 of palm

145
Q

Tests for carpal tunnel (median nerve)

A
  • Tinel’s: tap flexor retinaculum –> tingling along median nerve
  • Phalen’s: keep this position for 1min
146
Q

Causes of carpal tunnel

A
  • Work-related
  • Pregnant
  • Diabetes
  • Hypothyroid
  • Acromegaly
147
Q

Signs of ulnar nerve palsy

A
  • Claw hand
  • Sensory loss of little finger and ulnar half of ring finger
148
Q

Signs of radial nerve palsy

A
  • Wrist drop: weakness of wrist extension and elbow extension
  • Can’t straighten fingers
149
Q

Signs of common peroneal nerve palsy (L4/5)

A
  • Foot-drop (high-stepping gait)
  • Weakness of ankle dorsiflexion and eversion of the foot.
  • Reduced sensation anterior shin and dorsum foot
150
Q

Causes of peripheral neuropathy (sensori-motor)

A
  • Charcot-Marie-Tooth
  • GBS/CIDP
  • Drugs: chemotherapy, isoniazid, amiodarone
  • Critical illness neuropathy
  • Vasculitis
151
Q

Causes of peripheral neuropathy (motor)

A
  • Inflammatory: GBS
  • Diabetic amyotrophy
  • Critical illness neuropathy
  • Heavy metals (lead)
  • Congenital: spinal muscular atrophy
152
Q

Causes of peripheral neuropathy (sensory)

A
  • Alcohol
  • B12/folate deficiency
  • Diabetes
  • Uraemia
  • Drug: isoniazid, chemotherapy, amiodarone
153
Q

Causes of peripheral neuropathy (mononeuritis multiplex)

A
  • Vasculitis: Eosinophilic granulomatosis with polyangiitis (Churg-Strauss), Granulomatosis with Polyangiitis (Wegener’s)
  • Sarcoid
  • Sjogren’s
154
Q

Drug-induced peripheral neuropathy (sensori-motor)

A
  • Anti-tuberculosis drugs (isoniazid, ethambutol)
  • Antibiotics (metronidazole, nitrofurantoin)
  • Anti-cancer (cisplatin, vincristine)
  • Anti-arrhythmics (amiodarone)
  • Anti-convulsants (phenytoin)
155
Q

Differential diagnosis for motor peripheral neuropathy

A
  • NMJ disorder: myasthenia, Lambert-Eaton
  • Distal myopathy: myotonic dystrophy (frontal balding/cataracts/facial wasting); inclusion body myositis (loss of wrist/finger flexion > extension)
156
Q

Myasthenia gravis age of onset

A
  • Bimodal (women in 20s, men in 60s)
157
Q

Myasthenia gravis antibodies

A
  • Anti-acetylcholine receptor
  • Anti-muscle specific kinase
158
Q

Myasthenia gravis- other conditions to co-exist

A
  • Thymoma in 15%
  • Pernicious anaemia
  • SLE
  • Vitiligo
  • RA
159
Q

Myasthenia gravis features

A
  • Proximal muscle weakness- fatigable
  • Ptosis and diplopia - worse at end of day/when eyes kept in same position (hold upward gaze to see if ptosis develops)
  • Bulbar weakness (dysphagia, jaw weakness, slow hoarse voice)
  • Paradoxical breathing = respiratory muscle weakness- check FVC!!!
160
Q

Myasthenia gravis investigations

A
  • Anti-acetylcholine receptor and anti-muscle specific kinase antibodies
  • Single-fibre EMG on repetitive stimulation (will have decrementally reduced response - opposite occurs in Lambert-Eaton)
  • CT chest
  • FVC <1.5L = HDU, <1.2L = ITU
161
Q

Drugs which worsen myasthenia gravis

A
  • Aminoglycosides
  • Quinine
  • Beta-blockers
  • Phenytoin
  • Neuromuscular blockade anaesthetic agents (rocuronium)
162
Q

Myasthenia gravis management (acute and chronic)

A
  • Pyridostigmine (cholinesterase inhibitor) - can add glycopyrrolate to reduce muscarinic effects (oral secretions, bradycardia)
  • Prednisolone –> azathioprine if pyridostigmine not effective (anti-muscle specific kinase antibodies)— steroids can initially worsen myasthenia so severe patients need admission for steroid titration

Acute:
- IV immunoglobulin + plasma exchange
- High-dose pred (1mg/kg)

163
Q

Differential for myasthenia gravis

A

Ophthalmoplegia
- Thyroid eye disease
- Cranial nerve palsy
- GBS

Bulbar and respiratory weakness
- MND

Proximal limb weakness
- Lambert-Eaton
- Myopathy
- Inflammatory myositis

164
Q

Lambert-Eaton Syndrome cause and mechanism

A
  • Anti-voltage gated calcium channel antibodies –> reduced release of ACh from the pre-synaptic terminal
  • 50% cancer (small cell, lymphoproliferative), 50% autoimmune (thyroid, RA)
165
Q

Lambert-Eaton Syndrome features

A
  • > 40yrs
  • Pelvic girdle weakness (unlike Myasthenia)
  • Reduced reflexes, which temporarily improve after contraction of relevant muscle (do reflexes before and after testing power!)
166
Q

Lambert-Eaton Syndrome management

A
  • Treat underlying cause
  • Amifampridine +/- pyridostigmine
167
Q

Indication of thymectomy in Myasthenia Gravis

A
  • Anti-AchR receptor +ve patients with generalized disease under the age of 60 (ocular myasthenia may not need thymectomy)
168
Q

Causes of muscle disorder

A
  • Inflammatory (autoimmune)
  • Dystrophy: congenital defect in components of muscle fibre
  • Metabolic
  • Secondary: drugs (steroids/statins), endocrine (hypothyroid), systemic (ICU illness)
169
Q

Red urine/+ve erythrocytes with muscle weakness

A
  • Myoglobinuria = McArdle’s Syndrome, a glycogen storage disease (deficiency of myophosphorylase –> glycogen not broken to glucose for use in muscles)
170
Q

Causes of distal > proximal weakness in myopathy

A
  • Inclusion body myositis: flexors of forearm and quadriceps.
  • Facioscapulohumeral dystrophy: scapular winging and sparing of deltoid, involvement of anterior tibial
    compartment may cause foot drop.
  • Myotonic dystrophy: frontal balding, hatchet facies, ptosis
171
Q

Cause of facial weakness with external ocular muscle weakness in myopathy

A
  • Grave’s disease.
  • Mitochondrial disorders –look for ptosis, deafness, retinitis pigmentosa
  • Myasthenia Gravis
172
Q

Causes of facial weakness without external muscle weakness in myopathy

A
  • Myotonic dystrophy: frontal balding, hatchet facies, ptosis
  • Facioscapulohumeral dystrophy –winging, wasting of upper arm, foot drop
173
Q

Features of myotonic dystrophy (including mode of inheritance)

A
  • Most common adult dystrophy (autosomal dominant with genetic anticipation)
  • Myotonia: fail to relax after voluntary contraction (after shaking hand)
  • Percussion myotonia: percuss thenar eminence–> thumb flexion
  • Frontal balding
  • Bilateral ptosis
  • Wasting of the masseters–> narrowing of lower half of face (‘hatchet face’)
  • Distal > proximal weakness and areflexia (first affects hand/extensor elbow)
  • Complications: conduction block, cardiomyopathy, diabetes
174
Q

Complications of myotonic dystrophy

A
  • Cardiac involvement, with bradycardia, AV block, or heart failure –this is a frequent cause of death
  • Low IQ
  • Cataracts.
  • Diabetes mellitus
  • Testicular atrophy.
175
Q

Cause of myotonic dystrophy

A
  • Autosomal dominant
  • Expansion of an unstable trinucleotide repeat on chromosome 19q (type 1) or chr 3 (type 2)
  • Genetic anticipation = earlier onset and more severe with subsequent generations
  • PROM = Proximal myotonic dystrophy (milder, proximal weakness mainly, no cardiac/IQ issues)
176
Q

Cause of Duchenne’s vs Becker’s muscular dystrophy (including mode of inheritance)

A
  • X-linked mutation in dystrophin gene
  • Always male as X-linked
  • Duchenne’s = no dystrophin; Becker’s = abnormal dystrophin
177
Q

Features of Duchenne’s vs Becker’s muscular dystrophy

A

Duchenne’s
- Onset 3-10yrs
- Proximal weakness legs and lower trunk
- Calf pseudohypertrophy
- Dilated cardiomyopathy/low IQ
- Wheelchair by 12yrs –> dead by 20s

Becker’s
- Onset 10-40yrs
- Milder, often still walking as adults
- Fewer IQ and cardiac issues than Duchenne’s
- Diagnosis: raised CK, EMG consistent with myopathy,
muscle biopsy and dystrophin gene testing

178
Q

Features of facioscapulohumeral dystrophy (including mode of inheritance)

A
  • Autosomal dominant, onset 6-20yrs
  • Facial weakness
  • Cannot raise arms above head
  • Winged scaplulae (scapulae are pushed off the back due to weakness of serratus anterior)
179
Q

Features of dermatomyositis

A
  • Proximal myopathy legs > arms
  • Myalgia
  • Heliotrope rash rash and upper trunk
  • Gottron’s papules
  • Periorbital oedema
  • Associated with adenocarcinoma/gynae tumour
  • Antibody mediated
180
Q

Features of polymyositis

A
  • Proximal symmetrical weakness
  • Older people
  • No skin lesions
  • Cell-mediated (CD8)
181
Q

Features of inclusion body myositis

A
  • Older white males
  • Distal muscle weakness (flexion worse than extensors)
182
Q

Management of myotonic dystrophy

A
  • MDT approach!
  • Phenytoin may help myotonia
  • No anaesthetic as too high risk of resp distress
  • Treat complications (heart block, diabetes)
183
Q

Causes of ptosis

A

Unilateral
- 3rd nerve palsy
- Horner’s - look for ipsilateral scars = trauma (endarterectomy) or Pancoast tumour

Bilateral
- Myotonic dystrophy
- Myasthenia gravis

184
Q

Cerebellar lesion - ipsilateral or contralateral signs?

A
  • Ipsilateral (tracts do not decussate in cerebrum)
185
Q

Nystagmus in cerebellar lesion vs VIII nerve palsy- which direction?

A

Cerebellar
- Fast phase TOWARDS lesion and maximal when looking TOWARDS lesion

VIII nerve palsy
- Fast phase AWAY lesion and maximal when looking AWAY lesion

186
Q

Causes of hand muscle wasting

A

Anterior horn cell (motor neurone which projects from anterior grey matter of cord to muscle)
- MDN
- Syringomyelia
- Cervical cord compression (C7-C8)

Brachial plexus
- Cervical rib (extra rib above 1st rib)
- Pancoast tumour
- Trauma

Peripheral nerve
- Median and ulcer nerve palsies combined
- Peripheral neuropathy

Muscle
- Disuse atrophy (RA)

187
Q

Management of Parkinson’s Disease

A

MDT approach and manage non-motor symptoms! Involve Parkinson’s Nurse/support groups

Medical
- Dopamine agonist (pergolide): use for younger patients as less side-effects (nausea/hallucinations) and save L-Dopa until later
- L-Dopa with Dopa-decarboxylase inhibitor (co-careldopa = carbidopa/levodopa): nausea/dyskinesia and effect wears off after a few years
- MAO-B inhibitor (selegiline): stops dopamine breakdown

Surgical
- Deep Brain Stimulation (neurostimulator inserted onto brain to fire impulses to globus pallidus)

188
Q

Features of Charcot-Marie-Tooth (a.k.a Hereditary Sensory Motor Neuropathy)- including differences between 2 types and mode of inheritance

A
  • Type 1 = demyelinating; Type 2 = axonal– so do nerve conduction studies!
  • Autosomal dominant– mention FH when asked what you would do after examination
  • Stocking sensory loss
  • Inverted champagne bottle legs
  • Pes cavus
  • Hand wasting (dorsal interossei and thenar eminences)
  • Weakness of ankle dorsi-flexion and toe extension
  • Gait: high-stepping (foot drop) and stamping (reduced proprioception)
189
Q

Associating features with Freidrich’s Ataxia

A
  • Sensorineural deafness
  • HOCM
  • Optic atrophy
190
Q

Causes of upgoing plantars and absent knee jerks

A
  • Combined UMN/LMN: cervical spondylosis with peripheral neuropathy
  • Friedrich’s ataxia
  • Subacute combined degeneration of cord
  • MND
191
Q

Cause of Bell’s Palsy

A
  • Swelling/compression of facial nerve –> demyelination and temporary conduction block (?due to HSV-1)
192
Q

Management of Bell’s Palsy

A
  • If within 3days of onset: pred 60mg for 5days, then taper by 10mg every day
  • Eye protection: artificial tears, tape eye closed at night
  • Ophthalmology if persistent eye symptoms
  • ENT referral if no improvement after 3 weeks
193
Q

Mode of inheritance in tuberous sclerosis and neurofibromatosis

A
  • Autosomal dominant
194
Q

Causes of Horner’s pupil

A

Follow sympathetic tract’s anatomical course:

Brainstem
- Stroke (Wallenberg’s)
- MS

Spinal cord
- Syrinx

Neck
- Pancoast’s
- Trauma (endarterectomy)
- Aneurysm

195
Q

Causes of 3rd nerve palsy

A

Medical = Ms – normal pupil
- Mononeuritis multiplex (diabetes)
- Midbrain stroke (Weber’s)
- Midbrain demyelination (MS)
- Migraine

Surgical = Cs – dilated pupil (affects superficial pupillary fibres)
- Communicating artery aneurysm (posterior)
- Cavernous sinus pathology (affects III-VI): tumour
- Cerebral uncus herniation

196
Q

How to categorise embolic causes of stroke

A

Cardiac
- AF
- Mural thrombus
- Valvular

Vascular
- Carotid stenosis (ant. circulation)
- Vertebral disease (post. circulation)

197
Q

Diagnostic criteria for neurofibromatosis type 1

A

2 or more of:
- 6+ café au lait macules (>15mm diameter)
- 2+ neurofibromas
- Freckling in axillary or inguinal regions.
- 2+ Lisch nodules.
- Optic glioma.
- Distinctive osseous lesion, such as sphenoid dysplasia or thinning of long bone cortex
- 1st -degree relative with NF-1.

  • Also scoliosis
198
Q

Diagnostic criteria for neurofibromatosis type 2

A
  • Bilateral 8th cranial nerve masses
  • 1st-degree relative with NF-2 and either a unilateral 8th nerve mass or 2 of: neurofibroma, meningioma, glioma, schwannoma or juvenile
    posterior subcapsular lenticular opacity.

Also get:
- Renal artery stenosis
- UIP fibrosis

199
Q

Differences between neurofibromatosis type 1 and type 2

A
  • Type 2 less skin: fewer cafe-au-laits, no axillary freckling/Lisch nodules
  • Type 2 presents with more central issues: hearing loss, tinnitus, ataxia (acoustic neuromas)
200
Q

3 causes of HTN in neurofibromatosis

A
  • Renal artery stenosis
  • Phaeochromocytoma
  • Coarctation of the aorta
201
Q

TIA affecting ACA: features

A
  • Emotional changes (frontal)
  • Dysphasia (frontal - Broca’s area)
  • Contralateral weakness (frontal)
202
Q

TIA affecting MCA: features

A
  • Dysphasia (frontal- supplied by ACA and MCA)
  • Contralateral weakness (frontal)
  • Sensory loss (parietal)
  • Visual field loss and neglect (parietal and temporal lobes)
203
Q

TIA affecting PCA: features

A
  • Contralateral visual field loss and neglect (occipital)
  • Weakness and sensory loss
204
Q

TIA affecting vertebrobasilar arterial system: features

A
  • Nausea, vomiting, vertigo, visual disturbance, dysarthria, ataxia, weakness and/or sensory disturbance.
205
Q

Risk of stroke post-TIA

A
  • 2-day stroke risk of ~4 %
  • 7-day stroke risk of ~5.5 %
  • 30-day stroke risk of ~7.5 %
  • 90-day stroke risk of ~9 %
206
Q

If CT head is performed within this timeframe, a LP is not needed to confirm subarachnoid haemorrhage

A
  • 6 hours (if done after 6 hours, need to do LP after 12 hours to exclude xanthochromia)
207
Q

Signs of Turner Syndrome

A
  • Webbed neck
  • Shortened 4th/5th metacarpals
  • Absent sexual characteristics
  • Cubitus valgus
  • Widely spaced nipples
208
Q

Signs of DiGeorge Syndrome

A
  • Long face
  • Low-set ears
  • Cleft palate
209
Q

Cause of Brown-Sequard Syndrome

A
  • Unilateral cord lesion
210
Q

Features of Brown-Sequard Syndrome

A
  • Ipsilateral motor loss below (corticospinal injury)
  • Ipsilateral vibration/proprioception loss below (dorsal column)
  • Contralateral pain/temperature loss below (spinothalamic)

Because spinothalamic decussates at level of cord, whereas others decussate in brainstem!

211
Q

Chromosomes affected in Neurofibromatosis Type 1 vs Type 2

A
  • Type 1: chromosome 17
  • Type 2: chromosome 22
212
Q

Acronym for Parkinson’s Disease symptoms

A

TRAP CDS
- Tremor
- Rigidity
- Akinesia
- Postural instability
- Cognitive (hallucinations)
- Digestive (constipation/retention)
- Sleep (REM sleep disorder = muscles don’t relax = act out dreams)

213
Q

Treatment for cervical myelopathy

A
  • MDT approach
  • Decompressive surgery (neurosurgery)
214
Q

Examination special tests for meningitis

A
  • Neck stiffness must be checked while supine!
  • Brudzinksi: you lifting their head off bed will cause involuntary knee/hip flexion
  • Kernig: lift up knee bent at right angle–> extending the knee would cause pain
215
Q

When need CT head before doing LP in meningitis

A
  • Focal neurology
  • Altered consciousness
  • Papilloedema
  • Known cancer
  • HIV
216
Q

Features of Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)

A
  • Symmetrical
  • Loss of reflexes
  • Loss of vibration sense
  • Proximal and distal muscle weakness
217
Q

Purpose of nerve conduction studies in peripheral neuropathy

A

Differentiate between axonal and demyelinating
- Axonal: reduced amplitude and length dependent (occur distally first)
- Demyelinating: reduced conduction velocity and non-length dependent

218
Q

Examination tests which check for small nerve fibres vs large nerve fibres

A
  • Small = pinprick
  • Large = vibration
219
Q

Heel-to-toe walking tests for

A
  • “Midline gait ataxia”
220
Q

Horizonal saccades vs vertical saccades

A
  • Horizontal = internuclear ophthalmoplegia
  • Vertical = supranuclear palsy
221
Q

Complications of methylprednisolone

A
  • Insomnia
  • Personality change/mania
  • Rise in BMs
  • GI ulceration
  • Avascular necrosis of hip
222
Q

Causes of spastic paraparesis

A

Demyelinating
- MS = most common

Trauma
- Cord compression

Vascular
- Spinal stroke (cord infarction)
- Bilateral cerebral strokes

Congenital
- Motor neurone disease
- Cerebral palsy
- Spinocerebellar ataxia

Infective
- Transverse myelitis
- Abscess causing cord compression

223
Q

Important distinction you need to make with ataxic patient

A

Cerebellar vs sensory
- Cerebellar: dysarthria and nystagmus
- Sensory: sensation and proprioception loss— sensory is central (dorsal column damage) or peripheral (neuropathy)… or both (B12)

224
Q

Areas in brain which control speech

A
  • Broca’s (expressive - frontal)
  • Wernicke’s (receptive - temporal)
225
Q

Differentials for Motor Neurone Disease

A
  • Multifocal motor neuropathy with conduction block (inflammatory– no UMN/sensory signs– needs IVIG)
  • Spinal muscular atrophy (congenital loss of motor neurones)
  • Kennedy Disease (X-linked recessive, peri-orbital fasciculations)
226
Q

Complications of Down’s Syndrome

A
  • Atrial-septal defect/mitral regurgitation
  • Acute leukaemia
  • Early Alzheimer’s
  • Duodenal atresia
  • Cataracts
227
Q

Bedside investigations for diabetic peripheral neuropathy

A
  • L/S BP (autonomic dysfunction)
  • Urine dip
  • Fundoscopy
228
Q

How to classify lower motor neurone conditions affecting motor function

A

Anterior horn cell disorder
- MND

Motor nerve disorder
- Multifocal motor neuropathy

229
Q

Pathophysiology of poliomyelitis

A
  • Destruction of motor neurones –> inflammation around destroyed neurones
230
Q

Features of post-polio syndrome

A
  • Unilateral wasted shortened leg (shortening may be masked by foot drop, so straighten the foot!)
  • Progressive weakness
  • Fatigue
  • Cramping
231
Q

Side effects of Parkinson’s medications

A
  • Impulsivity
  • On-off phenomenon (esp Levodopa)
  • Dose-related dyskinesia
232
Q

Differentiate between neuromuscular junction disorder and myopathy using special investigations

A
  • NMJ: nerve conduction study shows reduced action potentials with repetitive stimulation
  • Myopathy: EMG shows denervation
233
Q

Causes of unilateral foot drop

A

Common peroneal nerve palsy
- Weak ankle dorsiflexion/inversion/eversion
- Cause: fracture fibula neck

L4/5 root lesion
- Cause: disc prolapse

Peripheral neuropathy

Sciatic nerve lesion
- Cause: hip trauma/surgery

234
Q

Causes of flaccid paresis

A

Anterior horn cell disease
- MND
- Poliomyelitis

Cauda Equina
- Disc herniation/abscess/mets

Lumbrosacral plexoplathy (usually unilateral)

Motor neuropathy
- Inflammatory (CIDP, GBS)
- Infectious (HIV, HTLV-1)
- Congenital (Charcot-Marie Tooth)

Neuromuscular Junction disorder
- Myasthenia/Lambert-Eaton/botulinism

Myopathy

235
Q

Causes of myopathy

A

Inflammatory
- Polymyositis
- Dermatomyositis

Connective tissue disease
- SLE
- Vasculitis

Endocrine
- Cushing’s
- Diabetic amyotrophy

Drugs
- Statins
- Steroids

Paraneoplastic
- Small cell lung cancer

236
Q

Pathogenesis of GBS (inc triggers)

A
  • Resp (M. pneumoniae) or GI (campylobacter)
  • Acute inflammatory demyelinating polyneuropathy
237
Q

Clinical features of GBS

A
  • Ascending flaccid paresis
  • Distal reduced reflexes
  • Distal paraesthesia
  • Patchy sensory loss (non length-dependent)

Also:
- Cranial nerves (ptosis, opthalmoplegia, bulbar weakness = CN IX to XII)
- Autonomic dysfunction
- Respiratory!

238
Q

Investigations for GBS

A
  • CSF (raised protein)
  • Anti-GM1 antibodies
  • Nerve conduction study: reduced velocity
  • FVC (<1.2L = ITU!)
239
Q

Management of GBS

A
  • IVIG +/- methylprednisolone
  • Plasma exchange
240
Q

Differential for pes cavus

A
  • Charcot-Marie-Tooth
  • Friedrich’s ataxia
  • Polio
  • Myotonic dystrophy
  • Cerebral palsy
241
Q

Pathogenesis for Motor Neurone Disease

A
  • Progressive degenerative disorder of motor neurons in the motor cortex and corticospinal tract + anterior horn cells of the spinal cord and brainstem.
  • Hence affects upper and lower motor neurones
242
Q

Investigations for Motor Neurone Disease

A
  • Bloods: paraneoplastic screen, syphilis serology, B12
  • MRI: exclude cord compression
  • Nerve conduction studies: exclude multifocal motor neuropathy
  • EMG: denervation/fibrillations.
  • Lumbar puncture may be indicated to exclude demyelination if unclear clinical picture
243
Q

Paraneoplastic antibodies

A
  • Anti-Hu, Yo, Ri, Ma
  • Urine bence-jones protein!
244
Q

Important complications of Friedrich’s ataxia

A
  • HOCM
  • Diabetes
245
Q

Myotonic dystrophy investigations

A
  • EMG: dive bomber (waxing and waning of potentials)
  • Muscle biopsy: fibre atrophy, no inflammation
  • Genetic testing (unstable trinucleotide repeat on chromosome 19q)
  • ECG: long QT/heart block
  • Echo: cardiomyopathy
246
Q

Proximal myopathy investigations

A
  • Bloods: including anti-Jo for myositis
  • Cancer screen if myositis
  • EMG: low amplitude
  • MRI muscle and biopsy: inflammation
247
Q

Origin of cranial nerves

A

1-2: cerebrum
3-4: midbrain
5-8: pons
9-12: medulla

248
Q

Features of Cavernous Sinus Syndrome

A
  • Complex ophthalmoplegia (CNs 3,4,6)
  • Fixed dilated pupil (CN 2)
  • (Super Orbital Fissure Syndrome is similar, but also has ptosis/exophthalmos)
249
Q

Features of Jugular Foramen Syndrome

A
  • Deficit of CN 9-11 (and maybe 12)
  • Due to tumour (such as glomus tumour)
250
Q

Special tests to do in Parkinson’s examination

A
  • Gait
  • Bradykinesia: thumb and index finger together
  • Writing (if no micrograthia then draw spiral - should be irregular contours)

THEN do following if time
- Supranuclear palsy: test upgaze
- Multisystem Atrophy: cerebellar signs and L/S BP
- Lewy-Body Dementia: mini-mental state examination

251
Q

Special tests to do in Myotonic Dystrophy

A
  • Close eyelids tightly –> delay in opening
  • Percussion myotonia of thenar eminence
  • CN exam to check for ptosis/ophthalmoplegia/dysarthria
  • Cardio including PPM
  • Testicular atrophy
  • Diabetes (urine dip)
252
Q

Horizontal vs vertical diplopia - cranial nerve palsies

A
  • Horizontal = 6th nerve palsy
  • Vertical = 4th nerve palsy
253
Q

Important cause of 6th nerve palsy

A
  • Raised ICP (SOL) = false-localising sign (because 6th is longest cranial nerve)
254
Q

Eyes cannot move in any direction

A

Complex Progressive External Ophthalmoplegia = mitochondrial

255
Q

Unilateral foot drop = UMN or LMN?

A
  • UMN as plantarflexion is extensor!
256
Q

Drug-induced cerebellar disorder

A
  • Lithium
  • Phenytoin
  • Carbamazepine
257
Q

Differential for unilateral wasted leg (apart from polio)

A
  • Anterior horn cell: Progressive Muscular Atrophy
  • Plexopathy (sensory loss)
  • Trauma
258
Q

Cause and features of diabetic amyotrophy

A

Lumbar plexopathy (L2-4)
- Wasted quadriceps (may be asymmetrical)
- Severe proximal leg/hip pain and weakness
- Reduced reflexes
- Not much sensory symptoms

259
Q

Seizure comes up in Comms Skills scenario- what 2 things must you ask about

A
  • Driving
  • Contraception- condoms not good enough!
  • (Also counsel about shower not bath, do not cook alone, no open water swimming)
260
Q

Causes of bilateral ptosis

A
  • Myasthenia
  • Myotonic dystrophy
  • Bilateral Horner’s
  • Chronic Progressive External Ophthalmoplegia
261
Q

Which cranial nerve is contralateral

A
  • CN 4 (trochlear)
262
Q

Features of Brown-Sequard Syndrome

A
  • Ipsilateral motor loss below (corticospinal)
  • Ipsilateral vibration/proprioception loss below
  • Contralateral pinprick/temperature loss below
263
Q

Mode of inheritance in Huntington’s

A
  • Autosomal dominant (if have mutation, you have 100% chance of getting the disease)
264
Q

Management of Huntington’s

A
  • Mainly supportive (MDT)
  • Tetrabenazine helps with chorea
265
Q

Thrombolysis absolute contraindications

A
  • BP >185/110
  • Seizure at time of onset
  • Warfarin and INR >1.7
  • DOAC in last 48hrs
  • Ischaemic stroke in last 3 months
  • Previous haemorrhagic stroke
  • Severe liver disease inc varices
  • LP in last 10 days
266
Q

Features of complicated form of Hereditary Spastic Paraparesis

A
  • Neuropathy
  • Retinopathy
  • Cognitive issues

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