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RACP Clinical Short > Neurology Short Case > Flashcards

Neurology Short Case Flashcards

1
Q

Investigations for floppy strong

A

TFTs
Urine metabolic screen
Serum lactate
CT Brain
Karyotype and microarray

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2
Q

Inherited causes of floppy strong

A

Central cause - UMN lesion
Genetic e.g. PWS, T21
Structural e.g. lissencephaly
Neurodegenerative e.g. Tay-Sachs, MPS, Zellweger
Neurocutaneous e.g. Sturge Weber
Metabolic e.g. amino acidopathies

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3
Q

Acquired causes of floppy strong

A

Central cause - UMN lesion
Static encephalopathy, prematurity
Infection e.g. TORCH, meningitis, encephalitis
Ischaemia
Trauma
Endocrine e.g. hypothyroidism, hypopituitarism

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4
Q

Causes of floppy weak

A

Peripheral cause - LMN lesion
Anterior horn: SMA
Peripheral nerve: GBS, hereditary motor/sensory neuropathy
NMJ: myasthenia, infantile botulism
Muscle: congenital or infantile muscular dystrophy, congenital myopathies (e.g. central, core, nemaline rod)

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5
Q

Complications of hypotonia

A

Ophthalmoplegia
Aspiration
Head lag
Scoliosis
Weak cry, cough, chest infections
Constipation
Hip dislocation

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6
Q

Investigations for floppy weak

A

CK
EMG and nerve conduction studies
Muscle biopsy
Exome sequence on microarray

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7
Q

Central/UMN clinical signs

A

Decreased alertness, not age appropriate
Hypertonia +/- clonus
Normal or decreased power
Hyperreflexic + Babinski
Normal or decreased sensation
Decreased coordination
Features of spasticity; some spontaneous/antigravity movements

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8
Q

Peripheral/LMN clinical signs

A

Normal alertness
Hypotonia
Decreased power
Hyporeflexic
Decreased sensation
Normal or decreased coordination

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9
Q

UMN lesion differentials according to location

A

Spine: unlikely unilateral, no facial changes, sensory changes at level
Brainstem: arm/leg weakness, facial weakness on opposite side
Subcortical: arm/leg weakness, facial weakness on same side
Cortical: arm/leg weakness, facial weakness on same side, cortical signs (visual fields, aphasia)

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10
Q

LMN lesion/neuromuscular DDx according to location

A

Anterior horn cell: SMA, polio
Peripheral nerve: GBS, CMT
Neuromuscular junction: myasthenia gravis, botulism
Muscular dystrophy: congenital myopathies (central/core/nemaline), dystrophies (DMD/BMD/FSHD), congenital muscular or myotonic dystrophy

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11
Q

Anterior horn cell signs

A

Normal extraocular/face strength
**Tongue fasciculations +++
Proximal > distal and LL > UL power
Hyporeflexic or absent reflexes

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12
Q

Types of SMA

A

SMA 1 - never sit
SMA 2 - sit but not stand, mini myoclonus
SMA 3 - stand and walk

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13
Q

Peripheral nerve signs

A

Normal extraocular/face strength
**Distal weakness (++)
Hyporeflexic or absent reflexes
Wasting
High stepping gait
Distal sensory loss
Tremor in CMT

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14
Q

Neuromuscular junction signs

A

**Ptosis and ophthalmoplegia
Decreased extraocular and face strength
Proximal or distal weakness
Hyporeflexic
Fatiguability

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15
Q

Myopathy signs

A

Normal extraocular strength
Decreased face strength
Proximal weakness
Hyporeflexic
Fish tented mouth
Ophthamoplegia
Facial/bulbar involvement
Normal CK
Myotonia

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16
Q

Muscular dystrophy signs

A

Normal extraocular strength
Decreased face strength
Proximal weakness
Hyporeflexic
Increased CK

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17
Q

Congenital myotonic dystrophy signs

A

Normal extraocular strength
Decreased face strength
Proximal or distal weakness
Absent reflexes
Tented upper lip open mouth, high arched palate

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18
Q

Causes of chorea (irregular rapid movements)

A

Pathology in corpus striatum
Inherited: CP, Wilson’s, neurodegenerative (Lecsh Nyhan, Huntington’s), ataxia telangiectsia
Acquired
Infective: Sydenham’s, EBV
Immune: SLE
Drugs

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19
Q

Causes of athetosis (slow writhing movements of proximal extremities)

A

Pathology in putamen (same causes as chorea)
Inherited: CP, Wilson’s, neurodegenerative (Lecsh Nyhan, Huntington’s), ataxia telangiectasia
Acquired
Infective: Sydenham’s, EBV
Immune: SLE
Drugs

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20
Q

Causes of dystonia (abnormal posturing)

A

Inherited: CP, Wilson’s, dopa responsive, Hallevorden-Spatz, Huntington’s
Acquired: drugs

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21
Q

Causes of static tremor (present with rest and gone with action)

A

Wilson’s
Hallervorden-Spatz
Huntington’s

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22
Q

Causes of postural tremor (throughout range of movement)

A

Thyrotoxicosis
Phaeochromocytoma
Wilson’s
Familial
Cushing’s syndrome
Hypoglycaemia

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23
Q

Causes of intention tremor (end of movement only)

A

Cerebellar lesions (multiple sclerosis, stroke,
mass lesion), drugs, chronic alcoholism, Wilson’s

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24
Q

Causes of myoclonus (sudden, disorganised, irregular contraction of muscle/muscle group)

A

Primary seizure disorder
Structural brain abnormalities e.g. Aicardi
Degenerative e.g. neurocutaneous, Tay Sachs, WIlson’s
Ishcaemic
Infections e.g. HIV encephalopathy, SSPE
Metabolic e.g. amino acidopathies

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25
Q

Key cerebellar signs

A

Ipsilateral to side of lesion (cross twice in brainstem)
Dysdiadochokinesis
Past pointing/dysmetria; dyssynergia
Ataxic gait - wide-based, veer towards affected side, difficulties heel-toe walking
Nystagmus
Dysarthria (scanning), explosive speech
Hypotonia, pendular reflexes
Head titubation, truncal ataxia
Romberg’s +ve

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26
Q

Causes of ataxia (broad categories)

A

Cerebellar
Vestibular (acute labyrinthitis)
Dorsal-column loss
Peripheral neuropathy

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27
Q

Investigations for cerebellar pathology

A

Urine dipstick: glycosuria in AT and FA (Friedreich’s Ataxia)
Imaging: CT/MRI - if no lesion, then genetic/metabolic evaluation
Bloods: FBE, UEC, toxicology screen (blood/urine), metabolic screen (amino acids, lactate, pyruviate, ammonia, pH, ketones)
Other: LP, urine catecholamines for neuroblastoma (VMA/HVA) with chest/abdo imaging

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28
Q

Clinical features of Friedreich’s Ataxia

A

Ataxia, pes cavus, hammer toes, kyphoscoliosis, sensorineural hearing loss, HOCM

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29
Q

Clinical features of ataxia telangiectasia

A

Telangiectasia of bulbar, pinnae, nares, flexures
Impaired cognition
Ear/lung infection
Clubbing
Leukaemia/lymphoma
Gonadal atrophy

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30
Q

Causes of cerebellar ataxia

A

Chemical: EtOH, phenytoin, CBZ, lead
Hypoxic/vascular: CP, cerebellar CVA/bleed/AVM
Infection: abscess, meningitis, encephalitis
Neoplastic: cerebellar, posterior fossa (medulloblastoma, astrocytoma), neuroblastoma
Physical: trauma, structural (Dandy-Walker, Chiari malformation, agenesis of cerebellar vermis), raised ICP
Inflammatory: acute cerebellitis, Miller-Fisher variant of GBS (ataxia, ophthalmoplegia, areflexia)
Genetic: AT, FA, Angelman’s, Bardet-Biedl
Endocrine/metabolic: leukodystrophies, Wilson’s, lysosomal storage, peroxisomal
Nutritional: vitamin E deficiency

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31
Q

Causes of ataxia from posterior column loss

A

Subacute combined degeneration of the cord - B12 deficiency (also get peripheral neuropathy, absent ankle reflexes, doral column loss, atrophy, dementia)
Diabetes
Hypothyroidism
Tabes dorsalis (untreated syphilis)

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32
Q

Causes of peripheral neuropathy

A

DAM IT BICH
Drugs: isoniazid, vincristine, phenytoin, nitrofurantoin, cisplatin, heavy metals, amiodarone
Alcohol
Metabolic: diabetes, CRF, neurodegenerative
Infective: GBS
Tumour: lymphoma, leukaemia
B12 deficiency
Idiopathic
Connective tissue disease: SLE, PAN
Hereditary: HSMN

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33
Q

Causes of hemiplegia

A

SCIT
Systemic: coagulopathies (Factor V Leiden, SLE, ALL), sickle cell, NF-1
Cardiac: hypertension, cyanotic congenital heart (< 2 years - usually cerebral thrombosis, 2 years cerebral abscess), SBE, vessel abnormalities (cerebral AVMs, Sturge Webeter)
Infective: HSV encephalitis, bacterial meningitis, cerebral abscess
Traumatic: MVA, NAI

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34
Q

Signs of spinal cord involvement in hemiplegia e.g. Brown Sequard, hemicord syndrome

A

Ipsilateral arm involvement if cord level high enough
Sensory changes:
Ipsilateral light touch and proprioception
Contralateral pain and temperature

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35
Q

Signs of brainstem involvement in hemiplegia

A

Ipsilateral arm involvement
Contralateral face involvement
May have cerebellar signs
Brainstem signs depending on level: midbrain (CN III/IV), pons (V, VI, VII, VIII), medulla (IX, X, XI, XII)

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36
Q

Signs of internal capsule involvement in hemiplegia

A

Ipsilateral arm involvement
Ipsilateral face involvement
Absence of cortical signs

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37
Q

Signs of cortex involvement in hemiplegia

A

Ipsilateral arm involvement
Ipsilateral face involvement
Cortical signs: hemianopia, visual field changes, dysphasia

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38
Q

Causes of seizures

A

Idiopathic
Inherited (PWS, T21, TS, NF-1, Sturge Weber)
Acquired: structural/space occupying, infective (post meningitis/encephalitis), immune (SLE, vasculitis), metabolic, endocrine (low sugar/electrolytes)

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39
Q

Complications of seizures and medications

A

Seizures: developmental delay, aspiration
Medications: drowsiness, weight gain, gum hypertrophy, rash, cytopaenias, nausea and vomiting

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40
Q

General causes of macrocephaly

A

Large bones - bony disorders
Large brain - megalencephaly
Large ventricles/fluid - hydrocephalus

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41
Q

Bony disorders causing macrocephaly

A

Achondroplasia
Rickets
Osteogenesis imperfecta
Chronic haemolytic anaemias

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42
Q

Causes of megalencephaly

A

Generalised enlargement: Sotos, Neurocutaneous (NF, TS, Klippel-Trenauney-Weber, Sturge-Weber), Metabolic
Localised enlargement: tumours (glioma, ependymoma), abscess, subdural haematoma

43
Q

Causes of hydrocephalus

A

Obstructive: aqueductal stenosis and gliosis (secondary to neonatal meningitis, TORCH infections, haemorrhage), Vein of Galen malformation, posterior fossa malformations (Dandy-Walker, Arnold-Chiari, tumours)
Non-obstructive: reduced absorption (subarachnoid haemorrhage, leukaemic infiltrates, infections/meningitis), increased production (very rare)

44
Q

Closure of sagittal suture

A

Dolichocephaly/scaphocephaly
Long and boat shaped
Increased AP diameter
Decreased biparietal diameter
Normal intellect and neuro

45
Q

Closure of coronal suture

A

Brachycephaly
Widened biparietal diameter and high vault
Decreased AP diameter
Flat and short
Eye signs - proptosis

46
Q

Closure of unilateral lamboid/coronal suture

A

Plagiocephaly
Skewed shape
Normal intellect and neuro

47
Q

Closure of metopic suture

A

Trigonocephaly
Mid-forehead ridging
Pointed narrow appearance to forehead
Hypotelorism, colobomata, intellectual impairment and midline defects e.g. cleft

48
Q

> 4 sutures fused

A

Oxycephaly, turricephaly, acrocephaly
High, narrow, tower-shaped skull
Can cause significant neurological sequelae - raised ICP

49
Q

Investigations for microcephaly

A

Imaging: skull X-ray, CT/MRI
Bloods: TORCH serology, karyotype, NST, TSH, metabolic studies
Urine CMV
CSF: TORCH

50
Q

Signs of Horner’s syndrome

A

Partial ptosis
Miosis
ANhydrosis

51
Q

Causes of Horner’s syndrome

A

Brainstem: vascular, tumour, syringobulbia/myelia (this can be bilateral)
Neck: thyroid mass, trauma
Carotid: aneurysm, dissection
Lung mass
Post cardiac surgery

52
Q

Approximate visual acuities in normal child

A

6 months - 6/30
18 months - 6/9
24 months - 6/6

53
Q

Causes of ptosis

A

Neurogenic: CN 3 palsy (ptosis and large pupil), Horner’s (ptosis plus small pupil - most commonly post cardiac surgery)
Myogenic: myasthenia (fatiguability), myotonic dystrophy, congenital ptosis

54
Q

Ages and stages of vision in babies

A

Neonates: turn head to diffuse light source
6 weeks: face or large coloured object
3 months: eyes converge for finger play
4 months: follows objects through 180 degrees, turning their head
5 months: reach for toy and regard small raisin on table
6 months: move eyes together in all directions
9 months: able to pick up raisin, plays peek a boo

55
Q

Causes of absent light reflex but intact accommodation

A

Midbrain lesion - Argyll Robertson pupil
Ciliary ganglion lesion - Adie’s pupil
Parinaud syndrome
Bilateral afferent pupil deficits

56
Q

Causes of absent convergence but intact light reflex

A

Cortical lesion (cortical blindness)

57
Q

Small pupils

A

Horner’s
Argyll Robertson (neurosyphilis)
Pontine lesion
Narcotics

58
Q

Dilated pupils

A

Drugs
Third nerve lesion
Adie’s syndrome
Trauma
Surgical: lens transplant, iridectomy
IFM (iritis)
Congenital

59
Q

Adie pupil

A

Efferent parasympathetic pathway affected
Dilated pupil
Decreased light reaction
Slow accommodation
No ptosis
Often young women
Decreased reflexes

60
Q

Argyll Robertson pupil

A

Lesion in midbrain - syphilis
Constricted pupil
Decreased light reaction
Normal accommodation
No ptosis

61
Q

Horner’s pupil

A

Sympathetic chain lesion
Constricted pupil
Normal light and accommodation reaction
Ptosis present

62
Q

Ptosis with normal pupils

A

NMJ: myasthenia, botulism
Muscle: MD, FSHD, thyrotoxic myopathy
Congenitl

63
Q

Ptosis with small pupils

A

Nerve: Horner’s, syphilis

64
Q

Ptosis with large pupils

A

III nerve palsy

65
Q

Causes of cataracts

A

Hereditary: myotonic dystrophy
Acquired: irradiation, trauma, metabolic (e.g. steroids, diabetes)

66
Q

Causes of papilloedema

A

Space occupying lesion
Hydrocephalus
Benign intracranial hypertension
Hypertension
Central retinal vein thrombosis
Central venous sinus thrombosis

67
Q

Papilloedema characteristics

A

Both eyes
Swollen optic disc
Normal acuity (early)
Normal colour vision
Large blind spot
Peripheral construction

68
Q

Papillitis (optic neuritis) characteristics

A

Usually one eye and sudden
Swollen optic disc
Poor acuity
Decreased colour vision (especially red)
Central scotoma
Pain on eye movements

69
Q

Causes of optic neuropathy

A

TIIME
Toxic: ethambutol, chloroquine
Immune: MS
Infective
Endocrine: diabetes
Metabolic: decreased B12

70
Q

Visual field defect for pituitary defect

A

Bitemporal hemianopia

71
Q

Visual field defect for optic tract to occipital cortex defect

A

Homonymous hemianopia

72
Q

Visual field defect for temporal lobe defect

A

Superior quadrantanopia

73
Q

Visual field defect for parietal lobe defect

A

Inferior quadrantanopia

74
Q

Visual field defect for optic nerve defect

A

Complete blindness of ipsilateral eye

75
Q

Visual field defect for defect in midline chiasmal region

A

Bitemporal nasal hemianopia

76
Q

CN III palsy features

A

Complete ptosis (partial if incomplete lesion)
Eye down and out
Dilated pupil - not reactive to light and accommodation
Exclude IV nerve if III palsy present

77
Q

Causes of CN III palsy

A

UMN: vascular, tumour, demyelination
LMN: compression (nasopharyngeal carcinoma, basal meningitis, orbital lesions), infarction (DM)

78
Q

CN VI palsy features

A

Failure of lateral movement

79
Q

Causes of CN VI palsy

A

UMN: vascular, tumour, demyelination
LMN: trauma, raised ICP

80
Q

Causes of jerky nystagmus

A

Horizontal: vestibular, cerebellar (both to side. of lesion), internuclear ophthalmoplegia, toxins
Vertical: brainstem/cerebellar lesion (up - lesion in floor of 4th ventricle, down - lesion in foramen magnum), drugs (EtOH, phenytoin)

81
Q

Causes of pendular nystagmus

A

Retinal - decreased macular vision e.g. oculocutaneous albinism
Congenital nystagmus

82
Q

Features and causes of supranuclear palsy

A

Both eyes affected
Unequal pupils
No diplopia

Causes: pinealoma, MS, vascular lesions

83
Q

Causes of exaggerated jaw jerk reflex

A

UMN lesion
Pseudobulbar palsy

84
Q

CN V palsy causes

A

Central: vascular, tumour, demyelination
Peripheral
- posterior fossa: tumour, chronic meningitis
- petrous temporal bone: acoustic neuroma, meningioma, middle fossa fracture
- cavernous sinus: thrombosis, tumour

85
Q

Cause of loss of sensation in all 3 divisions of CN V

A

Ganglion or sensory root lesion

86
Q

Cause of total loss of sensation in 1 division of CN V

A

Post-ganglion lesion

87
Q

Loss of pain but intact sensation of CN V

A

Brainstem or upper cord lesion

88
Q

Loss of touch but intact pain of CN V

A

Pons/nucleus lesion

89
Q

Causes of bilateral facial weakness

A

NMJ: myasthenia
Muscle
Nerve: GBS, bilateral parotid disease, mononeuritis multiplex

90
Q

Causes of CN VII palsy

A

UMN: tumour, vascular
LMN:
Pontine (anterior horn cell) - vascular, tumour, MS
Posterior fossa - acoustic neuroma, meningioma
Petrous temporal bone - Bell’s palsy, Ramsey Hunt, fracture, otitis media
Parotid - tumour, sarcoid

91
Q

Weber’s test: if sound localises to good ear

A

Sensorineural hearing loss

92
Q

Weber’s test: if sound localises to bad ear

A

Conductive hearing loss

93
Q

Rinne’s test positive: air conduction > bone conduction

A

Sensorineural hearing loss or normal

94
Q

Rinne’s test negative: bone > air

A

Conductive hearing loss

95
Q

Causes of sensorineural deafness

A

Unilateral:
Tumour e.g. acoustic neuroma
Trauma e.g. fracture of petrous temporal bone

Bilateral:
Environmental exposure to noise
Toxicity: gentamicin, frusemide
Infection: congenital rubella
Menière’s disease

96
Q

Causes of conductive deafness

A

Wax
OM/effusion
Otosclerosis
Bony disease e.g. Paget’s

97
Q

Things that point toward lesion

A

V nerve –> jaw
XII nerve –> tongue

98
Q

Things that point away from lesion

A

X nerve –> uvula

99
Q

Causes of facial weakness

A

Cortex and brainstem: Moebius, cerebral palsy, tumour, vascular insult, infection
Posterior fossa: acoustic neuroma, meningioma, chronic meningitis
Cranial nerve: GBS, Bell’s, Ramsay Hunt, petrouts temporal bone fracture, parotic gland tumour, osteopetrosis
NMJ: myasthenia gravis, infantile botulism
Muscle: myotonic dystrophy, FSHD

100
Q

Causes of bilateral facial weakness + ptosis + ophthalmoplegia

A

Moebius, myotonic dystrophy, myasthenia gravis, infantile botulism

101
Q

Causes of bilateral facial weakness alone

A

FSHD, GBS (bilateral LMN CN7), CP (bilateral UMN CN7)

102
Q

Causes of unilateral CN7 palsy

A

UMN (spares the forehead): cortical vascular lesion or tumours
LMN:
Pontine lesions: tumours, vascular, demyelination
Posterior fossa: acoustic neuroma, meningioma, chronic meningitis
Petrous temporal bone: Bell’s, fracture, Ramsay Hunt, otitis media
Parotid gland: tumour

103
Q

Features of pseudobulbar palsy (UMN lesion of IX, X, XII)

A

Increased gag reflex
Spastic movements of tongue
Spastic dysarthria
Labile emotions
Bilateral limb UMN signs

104
Q

Features of bulbar palsy (LMN lesion of IX, X, XII)

A

Decreased gag reflex
Wasted, fasciculations of tongue
Nasal speech
Normal emotions
Signs of underlying cause

RACP Clinical Short (11 decks)

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