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MRCPCH Clinicals > Neurology > Flashcards

Neurology Flashcards

1
Q

How to examine facial nerve?

A

Open and close eyes against resistance
Puff out cheeks and whistle
Smile and show teeth
Frown

Offer to check BP
Ears for infection
Any rashes ?erythema migrans
Assess hearing - acoustic neuroma 
Any exposure keratitis
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2
Q

How do lower motor facial nerve palsies present?

A

Ipsilateral upper and lower face

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3
Q

How do upper motor facial nerve palsies present?

A

Contralateral lower face affected

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4
Q

What causes a lower motor neurone facial nerve palsy?

A 
Bell’s palsy
Chronic serous otitis media
Viral infections: EBV, mumps
Ramsay Hunt syndrome: herpes zoster vesicles in ear canal
Lyme disease
GBS - bilateral
Trauma
Tumours/leukaemia
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5
Q

What causes upper motor neurone facial nerve palsy?

A

CP
Tumours
Moebius syndrome - strabismus and immobile face

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6
Q

How is facial nerve palsy managed?

A

BP
Test for Lyme disease, varicella and leukaemia

Eye care - tape shut at night and use artificial tears

Steroids if <7 days

Should have some recovery by 3 weeks, MRI head if not recovered in 3 months

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7
Q

What is pseudo-bulbar palsy?

A

Bilateral supranuclear upper motor neurone lesions of CN IX-XII

Poor tongue and pharynx movement
Associated with spastic quadriplegic CP

Stiff, spastic tongue
Dry voice and dysarthria
Preserved gag reflexes
Exaggerated jaw jerk

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8
Q

How does a third nerve palsy present?

A

Ptosis
Downwards and lateral gaze
Pupil dilation - no reaction to light or accommodation

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9
Q

How does 4th nerve palsy present?

A

Upward deviation of eye
Head tilt to unaffected side
Unable to look out or down

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10
Q

How does 6th nerve palsy present?

A

Unable to abduct eye

Convergent paralytic squint

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11
Q

How does Horner syndrome present?

A

Partial ptosis
Pupil constriction - normal light reflexes as controlled by parasympathetic nerves
Anhydrosis
Enopthalmous

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12
Q

What causes Horner’a syndrome?

A

Can be congenital - associated with heterochromia

Central - causes anhidrosis of face, arm and trunk

  • brain tumour
  • MS
  • encephalitis

Preganglionic - facial anhidrosis
- Klumpkes paralysis

Postganglionic - no anhidrosis

  • cluster headache
  • carotid artery’s dissection
  • cavernous sinus thrombosis
  • otitis media
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13
Q

How is power graded?

A

0: no contraction
1: flicker or trace of contraction
2: active movement with gravity eliminated
3: active movement against gravity
4: active movement against gravity and resistance
5: normal power

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14
Q

What is the nerve innervation of the arm reflexes?

A

Biceps - C5/6
Supinator - C5/6
Triceps - C6/7

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15
Q

What is the innervation of the leg reflexes?

A

Knee - L3/4
Ankle - S1
Plantar - S1

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16
Q

What causes neuromuscular disease?

A

Anterior horn cells

  • SMA
  • Poliomyelitis

Nerve fibre

  • Charcot Marie Tooth
  • GBS
  • leukodystrophy
  • poison

Neuromuscular junction
- myasthenia gravis

Muscle

  • Duchenne/Becker/Facioscapulohumeral/limb girdle dystrophy
  • myotonic dystrophy
  • inflammatory: polymyositis, dermatomyositis
  • metabolic: glycogen storage disease
  • thyroid
  • steroids
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17
Q

How does SMA type 3 present?

A 
5-15yrs with waddling gait
Proximal muscle weakness
Difficultly climbing stairs
Gower’s positive
Reduced tone/power/reflexes
Tongue fasciculations
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18
Q

How does Charcot-Marie-Tooth present?

A 
Damage to peritoneal and tibial nerves
Foot drop
Distal wasting
Pes caves
Sensory involvement - proprioception and vibration

Treat with ankle orthoses

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19
Q

How does Duchenne present?

A

X-linked recessive - can be familial link but 1/3 are new mutation

Delayed walking, waddling gait, tip toe walking, falls and difficulty with stairs
Calf hypertrophy
Reduced reflexes except ankle reflexes
Associated with cognitive impairment

20
Q

How is Duchenne managed?

A

Genetics to confirm + genetic counselling for family
Resp - NIV
Cardiology - LVF and arrhythmia
Ortho - scoliosis
Gait - walking frame and then wheelchair
Neuro - cognitive impairment and speech delay

Steroids
PT/OT

21
Q

How does Becker present?

A

Less cardiac/resp involvement and present later

22
Q

How does facioscapulohumeral dystrophy present?

A

Facial and shoulder girdle muscle weakness
Face is expressionless
Winging of the scapula

23
Q

How does limb girdle muscular dystrophy present?

A

Onset in late childhood
Begins with shoulder weakness, progresses to hips and then distally
Toe walking, waddling gait and then requires wheelchair

24
Q

How does Guillain Barre Syndrome present?

A

10-14 days post viral illness

ASCENDING flaccid paralysis
MOTOR > sensory
Reduced power/reflexes/tone - plantar reflexes —> flexion

Involvement of cranial nerves - ptosis and facial nerve palsy (bilateral)

25
Q

How is Guillain Barre Syndrome diagnosed?

A

MRI brain and spine - normal

LP - high protein

Nerve conduction studies - abnormal

26
Q

How is Guillain Barre treated?

A

Monitor with daily spirometry - may require ventilation
Can have CV autonomic involvement

IVIG/plasma exchange
PT and rehab

27
Q

Causes of a floppy infant?

A

Central

  • encephalopathy
  • CP
  • IVH
  • neurometabolic

Spinal cord

  • spina bifida
  • cord transection
  • tumour/haematoma

Anterior horn cell
- SMA/polio

Nerve fibre
- GBS

Neuromuscular
- transient myasthenia gravis, congenital myasthenia

Muscle

  • congenital myopathy
  • congenital myotonic dystrophy
  • congenital musclar dystrophy
  • Pompes

Other

  • Downs/Prader Willi
  • hypothyroid/hypercalcaemia
28
Q

How does SMA 1/2 present?

A

Present within first year

Normal face
Frog like posture
Bell shaped chest - see saw respiration

Reduced tone/power/reflexes
Fasciculations

Never sit - die of resp failure 12-18 months
Never stand - may require NIV

29
Q

How does congenital myotonic dystrophy present?

A 
Reduced fetal movements
Floppy infant
Facial diplegia with triangular fancies
Resp problems
Associated with talipes and hip problems
High mortality
30
Q

How does myotonic dystrophy present in the older infant?

A 
Myotonic, expressionless, immobile face
Hypotonia
Poor muscle bulk
Weakness
Normal/reduced reflexes

AVOID GENERAL ANAESTHETIC

31
Q

What causes ataxia?

A

Acute

  • infectious: chickenpox, measles, mycoplasma
  • structural: tumour, hydrocephalus
  • drugs: phenytoin
  • metabolic
  • vascular: basilar artery thrombosis

Intermittent

  • migraine
  • epilepsy

Chronic

  • perinatal e.g. encephalopathy
  • cerebellar: Dandy Walker
  • spinocerebellar degeneration: Friedrichs ataxia
  • ataxia telangectasia
  • metabolic: leukodystrophy, Wilson’s, abetalipoproteinaemia
32
Q

How does Friedrichs ataxia present?

A 
Progressive, presents before 15th birthday
Ataxia and dysarthria
Lower limb weakness, absent reflexes
Up going planters
Pes cactus
Nystagmus
Romberg positive

Cardiac: hypertrophic cardiomyopathy

33
Q

How does ataxia telangiectasia present?

A

Cerebellar ataxia
Telangiectasia of conjunctiva and behind ears

Malignancy
Low IgA and IgG

34
Q

What is spina bifida associated with?

A 
Associated with hydrocephalus - regular head circumference and imaging if indicated
Learning difficulties
Scoliosis
Urine and faecal incontinence
Foot ulcers
35
Q

What clinical features are seen in NF1?

A 
Visual fields, lisch nodules, ptosis and pro ptosis
Macrocephaly
Scoliosis
Irregularly shaped, brown macules
Axillary freckling
Blood pressure
36
Q

How is NF1 diagnosed?

A

2 of:

First degree relative
Axillary/inguinal freckling
Gliomas - brain or optic
Lisch nodules >1
Osseous lesions - kyphoscoliosis, tibial bowing, sphenoid dysplasia
Neurofibromas
>6 cafe au lait >5mm / >15mm
37
Q

What is the prognosis of NF1?

A

Learning disabilities
Monitor tumours as can become malignant
Risk of developing phaeochromocytoma, Wilms, thyroid cancer

38
Q

How is NF2 diagnosed?

A

Bilateral acoustic neuromas

1st degree relative
Unilateral acoustic neuroma
Schwannoma
Neurofibromas
Meningitis
Glioma
39
Q

Which professionals are involved in NF?

A

Paediatrician - monitor growth, BP, scoliosis
Paeds surgeons - excision of neurofibromas
Ortho - scoliosis
ENT and audiologist - acoustic neuromas
Plastic surgeons

Ophthalmologist
SLT
Geneticist
Psychology

40
Q

How does tuberous sclerosis present?

A

Skin

  • ash leaf lesions (need Woods lamp)
  • adenoma sebaceous (warty lesions along nasal folds)
  • periungal fibromas
  • shagreen patches
  • cafe au lait

Teeth
- teeth pits

Eyes
- hamartomas

GI
- rectal polyps

CNS

  • Astrocytomas
  • tubers
  • subependymal nodules

Kidney

  • PCK
  • lipomas

Cardiac
- rhabdomyoma

Resp
- interstitial lung disease

41
Q

How is tuberous sclerosis investigated?

A

BP
Renal ultrasounds

Echocardiogram
ECG

EEG and MRI head

42
Q

How does Sturge Weber present?

A

Facial naevus
Can have glaucoma

CNS involvement - intracranial calcification, ipsilateral angiomas, contralateral hemiparesis, LD and GDD

43
Q

What is incontinentia pigmenti ?

A 
Girls
Hyperpigmented, whirled lesions across body
Seizures, LD, spasticity
Ocular
Peg shaped teeth
44
Q

How does hypomelanosis of Ito present?

A

Whirled, hypopigmentation

Seizures, LD, hemiplegia

45
Q

What is posterior fossa syndrome?

A

Secondary to medulloblastoma treatment
Cerebellar mutism

Hemiparesis
Mutism
Supranuclear cranial nerve palsy

MRCPCH Clinicals (5 decks)

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