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MRCPCH Clinicals > Neurology > Flashcards

Neurology Flashcards

1
Q

What is cerebral palsy?

A

A static encephalopathy

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2
Q

How often is intrapartum hypoxia the cause of CP?

A

10% of cases

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3
Q

What are the types of CP in order of commonness?

A

Spastic (90%)
Dyskinetic (6%)
Ataxic (4%)

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4
Q

How common is cerebral palsy?

A

2 in 1000

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5
Q

What kind of lesion causes spastic CP?

A

UMN - usually periventricular leukomalacia

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6
Q

What are the clinical features of spastic CP?

A

Velocity dependent spasticity
Brisk deep tendon reflexes
Extensor plantar responses

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7
Q

What are the three subtypes of spastic CP?

A

Hemiplegia
Quadriplegia
Diplegia

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8
Q

What are the clinical features of dyskinetic CP?

A

Involuntary movements
Chorea
Athetosis
Dystonia

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9
Q

What is athetosis?

A

Slow, writing movements

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10
Q

What kind of lesion causes dyskinetic CP?

A

Mostly HIE

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11
Q

What lesions can cause ataxic CP?

A

Mostly genetic

If brain injury, signs are on the same side as the lesion

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12
Q

What are the clinical features in ataxic CP?

A

Early trunk and limb hypotonia
Poor balance
Later incoordinate movements, intention tremor and ataxic gait

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13
Q

How is cerebral palsy diagnosed?

A

Clinical
MRI
EEG if seizures

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14
Q

Which conditions are associated with CP?

A 
Intellectual impairment (50%)
Epilepsy (45%)
Speech and language disorders
Ophthalmological defects
Hearing impairment
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15
Q

How is CP managed?

A

Gabapentin
Botox for hypertonicity
Intrathecal baclofen
Selective dorsal rhizotomy

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16
Q

What is baclofen?

A

GABA analogue

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17
Q

What features do frontal seizures have?

A

Clonic movements
Asymmetrical tonic seizures
Atonic

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18
Q

What features can temporal lobe seizures have?

A 
Strange warning feelings or aura
Lip smacking
Plucking at a clothing
Walking in a non-purposeful manner
Deja vu and jamais vu
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19
Q

What features might an occipital lobe seizure have?

A

Distortion of vision

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20
Q

What features can a parietal lobe seizure have?

A

Contralateral dysaesthesias

Distorted body image

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21
Q

When does West syndrome usually present?

A

4-6 months

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22
Q

What do the seizures in West syndrome look like?

A

Infantile spasms - violent flexing of the head, trunk and limbs followed by extension of the arms

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23
Q

Which skills will be affected in West syndrome?

A

Often social first, but most will lose other skills too

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24
Q

How many children with West syndrome have an underlying neurological cause?

A

2/3

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25
Q

What does the EEG show in West syndrome?

A

Hypsarrhythmia - high voltage slow waves and multifocal sharp wave discharges

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26
Q

How is West syndrome treated?

A

Steroids, vigabatrin, sometimes ACTH

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27
Q

How many respond to treatment in West syndrome?

A

30-40%

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28
Q

What is the prognosis for West syndrome?

A

Most will develop a learning disability or epilepsy

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29
Q

When does Lennox-Gastaut syndrome usually present?

A

1-3 years

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30
Q

What kind of seizures are seen in Lennox-Gastaut syndrome?

A

Drop attacks
Tonic seizures
Atypical absences

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31
Q

How is development affected in Lennox-Gastaut syndrome?

A

Neurodevelopmental arrest or regression

Behavioural disorder

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32
Q

What is the prognosis like in Lennox-Gastaut syndrome?

A

Poor - many relate to a pre existing or other complex neurological disorder

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33
Q

When does childhood absence epilepsy usually present?

A

4-12 years

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34
Q

How is development affected in childhood absence epilepsy?

A

Usually not affected, but can interfere with schooling

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35
Q

Does childhood absence epilepsy affect more girls or boys?

A

2/3 are female

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36
Q

How can seizures be induced in childhood absence epilepsy?

A

Hyperventilation

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37
Q

What does the EEG show in childhood absence epilepsy?

A

Generalised 3Hz spike and wave discharge, bilaterally synchronous during and sometimes between episdoes

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38
Q

What’s the prognosis for childhood absence epilepsy?

A

Good

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39
Q

What drugs can be used in childhood absence epilepsy?

A

Sodium valproate
Ethosuximide
Lamotrigine

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40
Q

What does BECTS stand for?

A

Benign epilepsy with centrotemporal spikes

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41
Q

When does BECTS usually present?

A

4-10 years

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42
Q

What kind of seizures are seen in BECTS?

A

Tonic clonic seizures in sleep
Simple focal seizures with awareness of abnormal feelings in the tongue and distortion of the face
May involve the vocal tract with guttural sounds, hemifacial sensorimotor symptoms, hypersalivation and speech arrest

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43
Q

What does the EEG show in BECTS?

A

Focal sharp waves from the Rolandic or centrotemporal area

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44
Q

What is the management for BECTS?

A

Might not even need treatment - almost all remit in adolescence

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45
Q

What is early onset benign childhood occipital epilepsy also known as?

A

Panayiotopoulous syndrome

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46
Q

When does Panayiotopoulous syndrome present?

A

1-14 years

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47
Q

How does Panayiotopoulous syndrome present in younger children?

A

Periods of unresponsiveness, eye deviation, vomiting and autonomic features

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48
Q

How does Panayiotopoulous syndrome present in older children?

A

Headache and visual disturbance, distortion of images, hallucinations; can have syncope-like unresponsiveness and behaviour change

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49
Q

What might the seizures in Panayiotopoulous syndrome lead to?

A

Autonomic status

Hemiconvulsions or generalised convulsions

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50
Q

What does the EEG show in Panayiotopoulous syndrome?

A

Interictal EEG shows multifocal, high amplitude, sharp and slow-wave complexes

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51
Q

What is the prognosis in Panayiotopoulous syndrome?

A

Remits in childhood with AEDs rarely needed

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52
Q

When does juvenile myoclonic epilepsy present?

A

Adolescence-adulthood

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53
Q

What kind of seizures are seen in juvenile myoclonic epilepsy

A

Myoclonic

But GTCs and absences can occur, mostly shortly after waking

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54
Q

What does the EEG show in juvenile myoclonic epilepsy?

A

3-6Hz generalised polyspike and wave discharge

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55
Q

What’s the prognosis in juvenile myoclonic epilepsy?

A

Remission unlikely, but tends to respond to treatment

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56
Q

What drugs can be used in juvenile myoclonic epilepsy?

A

Sodium valproate
Benzodiazepines
Lamotrigine

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57
Q

Which drug can worsen seizures in juvenile myoclonic epilepsy?

A

Carbamazepine

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58
Q

What are 2 common mutations causing neonatal seizures?

A

ERBBB4, SCN1A

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59
Q

When do genetically caused neonatal seizures tend to present?

A

Before day 10

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60
Q

What is the clinical triad for genetic neonatal seizures?

A

Myoclonius
Then focal fits
Then tonic infantile spasms

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61
Q

What’s the prognosis for neonatal genetic seizures?

A

Very poor - devastating psychomotor and developmental regression, bilateral pyramidal signs

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62
Q

Wat is Ohtahara syndrome?

A

A syndrome causing seizures in the neonatal period with many causes; age-dependent reaction to an insult that can progress to West syndrome or Lennox-Gastaut

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63
Q

Which cerebral malformations can cause Ohtahara syndrome?

A 
Aicardi
Linear sebaceous naevus syndrome
Porencephaly
Hemimegaloencephaly
Focal cortical dysplasia
Cerebral dysgenesis
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64
Q

What are the two main genetic causes of Ohtahara syndrome?

A

GLUT1 deficiency syndrome

MECP2 mutation

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65
Q

What are the clinical features of Ohtahara syndrome?

A

Tonic spasms lasting 1-10 seconds, often in clusters up to 100 times per day

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66
Q

What does the EEG show in Ohtahara syndrome?

A

Burst suppression

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67
Q

What ist he prognosis for Ohtahara syndrome?

A

50% mortality in weeks or months; survivors have severe cognitive/neurological deficits

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68
Q

How can Ohtahara syndrome be treated?

A

No AED consistently effective - can also try vitamins or surgery

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69
Q

How are benign familial seizures inherited?

A

Autosomal recessive

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70
Q

When is the onset of benign familial seizures?

A

Day 4-7

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71
Q

What are the clinical features of benign familial seizures?

A

Brief seizures

Can involve apnoea, deviation of head/eyes, tonic-clonic, autonomic changes

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72
Q

What is the prognosis for benign familial seizures?

A

Tend to remit in days-months, normal intelligence long-term

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73
Q

How can benign familial seizures be treated?

A

Acute: phenobarbitone, benzodiazepines, phenytoin
Preventative: keppra, valproate, carbamazepine

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74
Q

What are the commonest causes of early myoclonic encephalopathy?

A 
Inborn errors of metabolism
Non-ketotic hyperglycinaemia
Menkes disease
Zellweger syndrome
Methylmalonic acidaemia
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75
Q

Which is an important treatable cause of early myoclonic encephalopathy?

A

Pyridoxine-dependent epilepsy, which will respond well to pyridoxine supplementation

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76
Q

When do malignant migrating partial seizures in infancy present?

A

3 months

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77
Q

What kind of seizures are seen in malignant migrating partial seizures in infancy?

A

Mutlifocal - tonic and/or clonic, can have autonomic features
Frequent, almost continuous seizures

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78
Q

What other problems are malignant migrating partial seizures in infancy associated with?

A

Psychomotor regression

Quadriplegia

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79
Q

What is the prognosis in malignant migrating partial seizures in infancy?

A

Poor - most AEDs are ineffective and may die by 12 months

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80
Q

What is Fukuyama-Watanabe-Vigevano syndrome also called?

A

Benign familial infantile seizures and non-familial infantile seizures

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81
Q

What is the difference between the familial and non-familial form of Fukuyama-Watanabe-Vigevano syndrome?

A

Not much - other than that the non-familial forms’ gene abnormalities occur de novo and familial cases may have longer fits with altered consciousness, motor arrest, clonic seizures, automatisms

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82
Q

When does Fukuyama-Watanabe-Vigevano syndrome present?

A

5 months

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83
Q

What kind of seizures are seen in Fukuyama-Watanabe-Vigevano syndrome?

A

Focal, brief diurnal seizures that occur in clusters of -10 daily for 1-3 days, then recur in 1-3 months

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84
Q

When does myoclonic epilepsy of infancy usually present?

A

6 months-3 years

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85
Q

What kind of seizures are seen in myoclonic epilepsy of infancy?

A

Myoclonic jerks which are spontaneous or reflex, usually with head nodding and upper limbs flinging outward. Brief duration often with intact consciousness

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86
Q

What can myoclonic epilepsy of infancy be treated with?

A

Valproate

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87
Q

What is the defect behind benign familial neonatal-infantile seizures?

A

Sodium channelopathy

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88
Q

When do benign familial neonatal-infantile seizures usually present?

A

2 days to 7 months

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89
Q

What kind of seizures are seen in benign familial neonatal-infantile seizures?

A

Focal

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90
Q

What is the prognosis for benign familial neonatal-infantile seizures?

A

Can resolve by 12 months

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91
Q

Which AEDs are used for myoclonic epilepsy in non progressive disorders e.g. Prader-Willi

A

Valproate
Benzodiazepines
Ethosuximide
ACTH

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92
Q

What is Dravet syndrome also known as?

A

Severe myoclonic epilepsy of infancy

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93
Q

What mutation is Dravet commonly associated with?

A

SCN1A

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94
Q

When is the usual onset of Dravet syndrome?

A

6 months

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95
Q

What seizures are seen in Dravet syndrome?

A 
Status
Hemimotor status plus pallor, automatisms
Clusters of absences
Head turning and flexed upper limbs
Myoclonic by 4 years
Atonic seizures
Non-convulsive status
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96
Q

What can be the precipitants for seizures in Dravet syndrome?

A

Visual induced
Hyperthermia
Water
Carbamazepine

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97
Q

How does Dravet affect development?

A

Normal development initially followed by developmenta/neurocognitive regression, with evolving ataxia and pyramidal signs

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98
Q

Which AEDs can be used in Dravet?

A 
Valproate
Topiramate
Clobazam
Keppra
Stiripentol
Cannabidiol
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99
Q

What is Doose syndrome also known as?

A

Epilepsy with myoclonic-atonic seizures

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100
Q

How commonly is there a family history of seizures in Dose syndrome?

A

Family history of febrile seizures in 50%, epilepsy in 1/3

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101
Q

When is the usual onset of Doose syndrome?

A

6 months to 6 years

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102
Q

Is Doose syndrome more common in girls or boys?

A

Boys

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103
Q

Which kinds of seizures are seen in Doose syndrome?

A

Febrile and afebrile GTCs
Months later, myoclonic-atonic seizures
Can have pure atonic or absence, and non-convulsive status
1/3 have status at some point

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104
Q

What is Gastaut type epilepsy also known as?

A

Late-onset childhood occipital epilepsy

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105
Q

What is Gastaut type epilepsy?

A

A self-limiting childhood seizure susceptibility syndrome

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106
Q

What kind of family history is there in Gastaut type epilepsy?

A

Epilepsy or migraine

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107
Q

When is the usual onset of Gastaut epilepsy?

A

15 months to 19 years

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108
Q

What kind of seizures are seen in Gastaut type epilepsy?

A

Pure occipital seizures with visual hallucinations (e.g. confetti or sequins), blindness or a combination
Short duration, frequent
Preserved consciousness
Can have other features e.g. head turning, blinking

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109
Q

What does the interictal EEG show in Gastaut type epilepsy?

A

Occipital paroxysms

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110
Q

What is the AED of choice in Gastaut type epilepsy?

A

Carbamazepine

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111
Q

What can develop if Gastaut type epilepsy isn’t treated?

A

GTCs

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112
Q

How common is a family history in epilepsy with myoclonic absences?

A

1/5

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113
Q

When is the usual onset of epilepsy with myoclonic absences?

A

1-12 years

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114
Q

Does epilepsy with myoclonic absences affect more boys or girls?

A

Boys

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115
Q

What are the clinical features of epilepsy with myoclonic absences?

A 
Rhythmic Myoclonic jerks with tonic contraction, usually unilateral
Impairment of consciousness
Short
Frequent
>75% will have another seizure type
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116
Q

What does the EEG show in epilepsy with myoclonic absences?

A

Generalised or multifocal spike and slow wave

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117
Q

How many children with epilepsy with myoclonic absences will have a learning disability?

A

70%

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118
Q

What’s the prognosis like in epilepsy with myoclonic absences?

A

Often difficult to treat

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119
Q

What kind of seizures is carbamazepine useful for?

A

Partial seizures

GTCs

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120
Q

What are the side effects of carbamazepine?

A 
Ataxia
Sedation
Leukopenia
Thrombocytopenia
Rash
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121
Q

Which seizures is sodium valproate useful for?

A

All

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122
Q

What are the side effects of sodium valproate?

A 
Nausea and vomiting
Abdo pain
Tremor
Hair loss
Thrombocytopenia
LFT abnormalities
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123
Q

Which seizures is lamotrigine useful for?

A

All

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124
Q

What are the side effects of lamotrigine?

A

Rash

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125
Q

What kinds of seizures is vigabatrin useful for?

A

Partial seizures

West syndrome

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126
Q

What are the side effects of vigabatrin?

A

Sedation

visual field constriction

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127
Q

What kind of seizures is ehtosuximide useful for?

A

Absences

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128
Q

What are the side effects of ethosuximide?

A

GI disturbance

Rash

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129
Q

Which kind of seizures is gabapentin useful?

A

Partial

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130
Q

What are the side effects of gabapentin?

A

Sedation

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131
Q

Which kind of seizures is oxcarbazpine useful for?

A

Partial/generalised

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132
Q

What are the side effects of oxcarbazepine?

A

Sedation

Rash

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133
Q

What kind of seizures is topiramate useful for?

A

All

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134
Q

What are the side effects of topiramate?

A

Sedation
Anorexia
Paraesthesiae

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135
Q

What kind of seizures are clobazam and clonazepam useful for?

A

All

136
Q

What are the side effects of clobazam and clonazepam?

A

Sedation

137
Q

What kind of seizures is phenytoin useful for?

A

All

138
Q

What are the side effects of phenytoin?

A

Nausea and vomiting
Diarrhoea
Rash
Peripheral neuropathy

139
Q

What kind of seizures is phenobarbital useful for?

A

All

140
Q

What are the side effects of phenobarbital?

A

Sedation

141
Q

What kind of seizures is keppra useful for?

A

Partial

142
Q

What are the Side effects of keppra?

A

Sedation

143
Q

What kind of seizures is tiagabine useful for?

A

Partial

144
Q

What are the side effects of tiagabine?

A

Sedation

145
Q

What is the management of status?

A

2x benzos
Rectal paraldehyde
Phenytoin
RSI

146
Q

How many neural tube defects are preventable with maternal folate supplementation?

A

70%

147
Q

What are some non-folate causes of neural tube defects?

A 
High BMI
Temperature elevation
Diabetes
Anti epileptics
T13, 18 and 21
Waardenburg syndrome
Joubert syndrome type 1
148
Q

What is the risk of recurrence for a mother who has had a child with a neural tube defect?

A

1 in 100-200; triple the baseline risk

149
Q

What are the different kinds of neural tube defects?

A 
Spina bifida occulta
Anencephaly
Encephalocoele
Meningocoele
Myelomeningocoele
150
Q

What is the defect in spina bifida occulta?

A

Failure of closure of the vertebral arch

151
Q

What is the defect in anencephaly?

A

Failure of closure of the rostral aspect of the neural tube

152
Q

What is the prognosis in anencephalic pregnancies?

A

75% will be stillborn

153
Q

What is the defect in an encephalocoele?

A

Protrusion of cerebral tissue through midline cranial defect located in frontal or occipital regions

154
Q

What is the defect in meningocele?

A

Cyst formed by herniation of meninges, usually over dorsum of spine

155
Q

What are the possible sequelae of a meningocoele

A

Neurological disability is minimal, but risk of bacterial meningitis

156
Q

What is the defect in a myelomeningocoele?

A

Herniation of meninges, nerve roots, and spinal cord through the dorsal vertebral defect

157
Q

What are the possible sequelae of a myelomeningocoele?

A

Motor and sensory defects below the lesion, including sphincter disturbance
Hydrocephalus can occur

158
Q

What particular malformation might be associated with a myelomeningocoele?

A

Arnold-Chiari

159
Q

What are the options for bladder dysfunction from neural tube defects?

A

Anticholinergics
Alpha adrenergics
Intermittent catheterisation
Botox

160
Q

What are the features of the Arnold-Chiari II malformation?

A

Downward displacement of the cerebellar tonsils and vermis through the foramen magnum
Elongation and kinking of the medulla
Caudal displacement of the cervical spinal cord and medulla
Obliteration of the cisterna magna

161
Q

What are the possible consequences of an Arnold-Chiari II malformation?

A

Descent of hindbrain through foramen magnum - can cause compression of brainstem, cerebellar dysfunction, medullary respiratory centre dysfunction, malfunction of IX and X nerves, hydrocephalus

162
Q

What are the clinical features of an Arnold-Chiari II malformation?

A 
Swallowing problems
GORD
Dysarthria
OSA
Stridor
Weakness or spasticity of upper limbs
Clumsiness or poor coordination
Many others!
163
Q

How is the Arnold-Chiari II malformation managed?

A

Surgically:
Decompression of the medulla and upper cervical cord
Insertion of a dural patch to increase the size of the dural sac
Cervical laminectomy

164
Q

What is a syringomyelia?

A

Cavity which communicates with the central canal of the spinal cord

165
Q

With is hydromyelia?

A

Dilatation of the central canal of the spinal cord

166
Q

What malformation is associated with Syringohydromyelia?

A

ArnoldChiari II

167
Q

What clinical features are associated with Syringohydromyelia?

A

Scoliosis
Lower limb weakness and deformities
Upper limb weakness
Back pain

168
Q

How can a syringohydromyelia be treated?

A

Shunt from syrinx to peritoneal cavity

169
Q

What are the causes of scoliosis in myelomeningocele?

A 
Congenital malformation
Syringohydromyelia
Tethered cord
Shunt failure
Spinal muscle weakness
170
Q

How common is tethered cord in myelomeningocele?

A

Present in virtually all, but only causes problems requiring intervention in 1/3

171
Q

What are the symptoms of tethered cord?

A 
Often during growth spurts
Gait changes (crouched)
Back or lower limb pain
Worsening of motor function
Change in sensory level
Change in bladder or bowel habit
Progressive deformity of spine or lower limbs
172
Q

How is spinal muscle atrophy inherited?

A

Autosomal recessive

173
Q

What gene is responsible for spinal muscular atrophy?

A

5q11-13

174
Q

What is the defect in spinal musuclar atrophy?

A

Degeneration of anterior horn cells due to mutation in the survival motor neurone gene

175
Q

What is the general clinical picture in spinal muscular atrophy?

A

Progressive weakness and wasting of skeletal muscles

176
Q

What is SMA Type 1 also known as?

A

Werdnig-Hoffman disease

177
Q

When does SMA type 1 present?

A

Antenatally as diminished foetal movements, or in early infancy

178
Q

What signs might be seen in spinal muscular atrophy?

A 
Arthrogryposis
Lack of antigravity power in hips
Symmetrical weakness, proximally>distally, trunk and limbs
Absent deep tendon reflexes
Intercostal recession
Fasciculation of the tongue
Unable to sit or walk
179
Q

What is the prognosis of SMA type I?

A

Bad - death is from respiratory failure at about 10 months

180
Q

When is the usual onset of SMA type II?

A

After 3 months

181
Q

What are the clinical features of SMA type II?

A

Can sit but not walk

Prone to early scoliosis

182
Q

What is the prognosis of SMA type II?

A

Depends on degree of respiratory muscle involvement

183
Q

What is SMA type III also known as?

A

Kugelberg-Welander disease

184
Q

What are the features of SMA type III?

A

Can walk, but some proximal weakness

Tendon jerks may not be absent

185
Q

What is Charcot-Marie-Tooth disease also known as?

A

Peroneal muscular atrophy

186
Q

What are the clinical features of Charcot-Marie-Tooth?

A

Slowly progressive distal weakness with areflexia
Foot drop often the main early problem
In later stages (up to decades later): hand weakness, joint deformity, distal sensory loss

187
Q

What are the differences between Freidreich’s ataxia and HMSNs?

A

Areflexia in HMSN
More clear ataxia in Freidreich’s
HMSN have abnormal motor conduction, whereas Freidreich’s have sensory neuropathy

188
Q

What are the three most common types of Charcot-Marie-Tooth?

A

1: demyelinating
2: axonal
3: hypertrophic
And X-linked forms

189
Q

What are the features of type 1 charcot-Marie-Tooth?

A

Low motor neurone conduction velocity

1st decade onset

190
Q

What are the features of type 2 Charcot-Marie-Tooth disease?

A

Normal motor neuron conduction velocity

2nd to 3rd decades

191
Q

What are the features of type 3 Charcot Marie Tooth?

A

Low motor neurone conduction velocity

1st year onset

192
Q

What is the most common disease of the NMJ?

A

Myasthenia gravis

193
Q

What is the defect in myasthenia gravis?

A

Antibodies against postsynaptic acetylcholine receptors

194
Q

What are the clinical features of myasthenia gravis?

A

Affects extra ocular muscles first, then proximal limbs and bulbar muscles
Weakness which gets worse over the course of the day

195
Q

How is Myasthenia Gravis diagnosed?

A

Edrophonium test
EMG (confirms neuromuscular block)
Anti-ACh receptor antibodies

196
Q

How is Myasthenia Gravis treated?

A

Anticholinesterases
Immunosuppressants
Thymectomy
Plasma exchange or IVIG

197
Q

What is the cause of Sydenham chorea?

A

Immune reaction triggered by group A strep infection

198
Q

What is the prognosis for Sydenham chorea?

A

75% have resolution of chorea within 6 months

199
Q

What is the defect in anti-NMDA receptor encephalitis?

A

Antibodies to the NMDA receptor - usually after an intercurrent illness or mycoplasma infection

200
Q

What are the clinical features of anti NMDA receptor encephalitis?

A

Movement disorder e.g. chorea, dystonia
Autonomic instability
Neuropsychiatric symptoms
Seizures

201
Q

How do you treat anti-NMDA receptor encephalitis?

A 
Steroids
Immunoglobulin
Plasma exchange
Cyclophosphamide
Rituximab
202
Q

What is subacute sclerosis panencephalitis?

A

Slow viral infection caused by atypical response to measles infection

203
Q

What are the risk factors for subacute sclerosis pan encephalitis?

A

Exposure to measles in first 2 years

Natural measles infection vs immunisation

204
Q

What are the clinical features of subacute sclerosing panencephalitis?

A

Subtle deficits first
Increasing memory difficulties
Worsening disabilities: seizures, motor difficulties, learning disability

205
Q

What is the median interval between measles and subacute sclerosis panencephalitis?

A

8 years

206
Q

What is the gene for neurofibromatosis type 1?

A

NF1 gene on 17q11.2

207
Q

What does the NF1 gene code for?

A

Neurofibromin 1, a cytoplasmic protein found throughout the nervous system

208
Q

What are the diagnostic criteria for NF1?

A

Need 2 or more:
≥6 cafe au last spots, >5mm in prepubertal patients or >15mm in post pubertal patients
≥2 neurofibromas or one plexiform neurofibroma
Axillary or inguinal freckling
Optic glioma
≥2 iris hamartomas (Lisch nodules)
Typical osseous lesions e.g. sphenoid dysplasia
1st degree relative affected

209
Q

What are the neurological manifestations of NF1?

A

Macrocephaly
Learning disability
Epilepsy
Optic gliomas

210
Q

What are the non-diagnostic features of NF1?

A

Scoliosis
Hypertension
Pulmonary stenosis
Tumours: brainstem and cerebellar gliomas

211
Q

Which gene codes for neurofibromatosis type 2?

A

NF2 gene on 22q11.2

212
Q

What are the diagnostic criteria for neurofibromatosis type 2?

A

Bilateral 8th nerve neurofibromas
Unilateral 8th nerve mass in association with any 2 of : meningioma, neurofibroma, schwannoma, juvenile posterior capsular cataracts
Unilateral 8th nerve tumour or other spinal or brain tumour in 1st degree relative

213
Q

How is tuberous sclerosis inherited?

A

Dominantly, with variable expression

214
Q

Which mutations are responsible for tuberous sclerosis?

A

TSC1 (9p34) and TSC2 (16p), both of which are tumour suppressor genes

215
Q

What are the clinical features of tuberous sclerosis?

A 
Seizures
Neurodevelopmental impairment
Cutaneous manifestations
Retinal hamartomas
Renal angiolipomas
Cardiac rhabdomyomas
Brain: cortical tubers and subependymal nodules with calcifications
216
Q

What are the cutaneous manifestations of tuberous sclerosis?

A

Adenoma sebaceum
Periungual fibromas
Hypopigmented patches
Shagreen patch

217
Q

What are the characteristic features of ataxia telangiectasia?

A

Conjunctival telangiectasia
Progressive cerebellar degeneration
Immunological impairment

218
Q

Where is the gene for ataxia telangiectasia?

A

11q22-23

219
Q

What are the clinical features of ataxia telangiectasia?

A

Progressive ataxia
Scleral telangiectasia
Abnormality of cell mediated and humeral immunity, causing sinopulmonary infections, high incidence of reticuloendothelial malignancy

220
Q

How is ataxia telangiectasia diagnosed?

A

Elevated alpha fetoprotein
Low IgA and IgD
Inversions and translocations on chromosomes 7 and 14
Gene mutation analysis

221
Q

What are the features of Sturge Weber syndrome?

A

Port wine stain in the distribution of the trigeminal nerve
Facial naevus
Ipsilateral leptomeningeal angioma, causing ischaemic injury to underlying cerebral cortex

222
Q

What are the consequences of Sturge Weber syndrome?

A

Focal seizures
Hemiparesis
Variable degree of intellectual deficit
Glaucoma (usually ipsilateral to the port wine stain)

223
Q

How is incontinentia pigmenti inherited?

A

Probably X linked dominant; NEMO gene

224
Q

What are the skin features of incontinentia pigmenti?

A

Erythematous papular, vesicular or bullous lesions on trunk and limbs
Then pustular lesions
Then pigmented

225
Q

What are the non-skin features of incontinentia pigmenti?

A

30-50% have neurological features e.g. seizures, encephalopathy
30% have eye lesions

226
Q

How is hypomelanosis of Ito inherited?

A

Sporadically

227
Q

What are the features of hypomelanosis of Ito?

A

Hypopigmented areas that are streaky, patchy, or whorls
Seizurs
Hemimegalencephaly (one half of cerebral cortex larger than the other)

228
Q

What is the defect in lishencephaly?

A

Brain has very few or no gyro, so the surface of the brain is smooth

229
Q

What are the clinical features of lishencephaly?

A

Severe motor and learning disability

230
Q

What are the associated mutations in lishencephaly?

A

65% associated with mutations in LIS1 gene

17p13.3 deletion - Miller-Dieker syndrome (facial abnormalities)

231
Q

What is the defect in polymicrogyria?

A

Increased numbers of small gyro, especially in the temporoparietal regions. Can be focal or generalised

232
Q

What is the defect in periventricular heterotopia?

A

Aggregation of neurone arrested in their primitive positions

233
Q

What is pachygyria and what are the consequences?

A

Thickened, abnormal cortex - depending on extent can cause cerebral-palsy like picture or epilepsy

234
Q

Which brain malformation is associated with Aicardi syndrome?

A

Agenesis of corpus callosum

235
Q

What are the features of Moebius syndrome?

A

Bilateral facial paralysis with bilateral abducens paralysis
Other lower CNs can be affected
1/4 have learning disability

236
Q

What are the features of Bell’s palsy?

A

Unilateral facial paralysis

237
Q

What’s the cause of Bell’s palsy?

A

Usually idiopathic

238
Q

What is the management of Bell’s palsy?

A

Usually recovers completely in 2-4 weeks, but steroids can be given

239
Q

What are the clinical features of a 3rd nerve palsy?

A

Down and out position of the eye; can involve pupillary reaction if parasympathetic fibres are involved

240
Q

What are the causes of a 3rd nerve palsy?

A

Closed head trauma, infection, tumour

241
Q

What are the features of a 4th nerve palsy?

A

Superior oblique palsy, which pulls the eye downwards; vertical diplopia when looking obliquely, often head tilting, and torsional diplopia

242
Q

What is the most common cause of a 4th nerve palsy?

A

Trauma

243
Q

What is the most common cause of a 6th nerve palsy?

A

Raised ICP - tumours, benign intracranial hypertension

244
Q

What are the features of a 6th nerve palsy?

A

Convergent squint and horizontal diplopia

245
Q

What are the features of the classic Dandy-Walker malformation?

A

Complete or partial Genesis of cerebellar vermis
Large cystic formation in posterior fossa due to dilatation of fourth ventricle
Hydrocephalus (may not develop until adulthood)

246
Q

What is a Dandy-Walker variant?

A

Part of vermis present, posterior fossa not enlarged

247
Q

What is megacisterna magna?

A

Complete vermis, large retrocerebellar cyst

248
Q

What is Joubert syndrome?

A

Familial agenesis of the cerebellar vermis

249
Q

What are the features of Joubert syndrome?

A

Episodic hyperpnoea
Ataxia
Cognitive impairment

250
Q

What is periventricular leukomalacia?

A

Bilateral necrosis of periventricular white matter with ensuing gliosis

251
Q

What are the consequences of periventricular leukomalacia?

A

Interruption of the fibres responsible for lower limb and optic function –> spastic diplegia and visual impairment

252
Q

Which nerves are affected in Erb’s palsy?

A

C5-6

253
Q

Which muscles are affected in Erb’s palsy?

A 
Deltoid
Serratus anterior
Supraspinatus
Infraspinatus
Biceps
Brachioradialis
254
Q

What are the clinical features of Erb’s palsy?

A

Arm is flaccid, adducted, and internally rotated

Elbow is extended, wrist flexed

255
Q

Which nerves are affected in a Klumpke paralysis?

A

C8-T1

256
Q

What are the features of a Klumpke paralysis?

A

Intrinsic hand muscles are affected leading to flexion of wrist and fingers
Cervical sympathetic involvement can lead to ipsilateral Horner syndrome

257
Q

What is the defect in Friedreich’s ataxia?

A

Spinocerebellar degeneration - abnormality of a gene for frataxin, which is involved in modulation of mitochondrial function

258
Q

How is Friedreich’s ataxia inherited?

A

Autosomal recessive

259
Q

Where is the gene for Friedreich’s ataxia?

A

9cen-q21

260
Q

What are the clinical features of Friedreich’s ataxia?

A 
Onset 1st or 2nd decade
Loss of proprioception
Increasing impairment of cerebellar function
Development of pis caves, nystagmus
Cardiomyopathy
Usually not ambulant by 20s or 30s
261
Q

How is Friedreich’s ataxia treated?

A

Symptomatic
Physiotherapy
Antioxidant treatment e.g. idebenone may be of benefit in delaying cardiac deterioration

262
Q

What is dystonia?

A

Abnormal muscle tone without pyramidal involvement

263
Q

What is dystonia musculorum deforming also known as?

A

Torsion dystonia

264
Q

How is torsion dystonia inherited?

A

Autosomal dominant with incomplete penetrance

265
Q

What is the gene for torsion dystonia?

A

9q34 in Jewish families; another unidentified gene in others

266
Q

When is the usual onset of torsion dystonia?

A

After 5 years

267
Q

What are the clinical features of torsion dystonia?

A

Can be focal or generalised
Can be task specific e.g. when walking forwards but not backwards
Often gradually spreads to other parts of the body

268
Q

How is torsion dystonia treated?

A

High dose anticholinergics

Sometimes L-dopa

269
Q

What is the cause of dopa-responsive dystonia?

A

Idiopathic

270
Q

What are the clinical features of dopa-repsonsive dystonia

A

Can start in first 5 years

Symptoms vary throughout the day

271
Q

Where is the gene for dopa-responsive dystonia?

A

14q22.1-q22.2

272
Q

How is dopa responsive dystonia treated?

A

Lifelong L-dopa

273
Q

What is the most common cause of childhood muscular dystrophy?

A

Duchenne

274
Q

What is the defect in Duchenne muscular dystrophy?

A

Mutation in the dystrophin gene on the X chromosome

275
Q

What is the natural history of Duchenne?

A 
Diagnosis around 5 years
Delayed motor milestones
Proximal skeletal muscle weakness
Waddling gait
Difficulty climbing stairs
Motor regression
Wheelchair bound by 12
Decline in respiratory function and cardiomyopathy
276
Q

What is the life expectancy in Becker muscular dystrophy?

A

67

277
Q

When does wheelchair dependency happen in Becker?

A

between 3rd and 7th decade

278
Q

How is Duchenne inherited?

A

X-linked recessive, but 1/3 are de novo mutations

279
Q

How common is Duchenne?

A

1 in 3600-6000 male births

280
Q

What is the defect in Duchenne?

A

Absence of dystrophin makes the muscle membrane vulnerable from shearing stresses, leading to degeneration of muscle fibres

281
Q

How is Duchenne diagnosed?

A

Array CGH
Next generation sequencing
Muscle biopsy
Prenatal diagnosis with CVS or amnio also possible

282
Q

What are the examination findings in Duchenne

A 
Small muscle bulk
Pseudohypertrophy of calves
Equinus deformity of feet
Gait abnormalities
Gower's manoeuvre
Proximal weakness
283
Q

Which gait abnormalities might be seen in Duchenne?

A

Knee-locking gait
Trendelenburg gait
Lordosis
Easier to walk on toes than heels

284
Q

What is a Trendelenburg gait?

A

Weak hip flexors mean the leg is swung forward, and the pelvis tilts down on the unsupported side

285
Q

What is the instruction for Gower’s manoeuvre?

A

Ask to lie supine then get up

286
Q

How is Duchenne managed?

A 
Steroids
Physio
OT
Surgery as needed for fractures, tonotomies, scoliosis
NIV
ACE inhibitors or beta blockers
287
Q

How is Emergy-Dreifuss muscular dystrophy inherited?

A

X-linked; Xq28

288
Q

What are the features of Emery-Dreifuss muscular dystrophy?

A

Mild proximal muscular weakness
Joint contractures
Cardiac involvement and sudden cardiac death

289
Q

How is facioscapulohumeral muscular dystrophy inherited?

A

AD - 4q35

290
Q

What are the features of facioscapulohumeral muscular dystrophy?

A

Facial, scapular, humeral wasting and weakness
Slowly progressive
Other muscles can be involved
Variable expression within families

291
Q

What are the features of merosin-negative congenital muscular dystrophy?

A 
Hypotonia
Weakness
Contractures
Learning disability
Don't achieve independent walking
Absence of Mersin on muscle biopsy
292
Q

What is the difference between merosin-positive muscular dystrophy and merosin-negative?

A

Similar but merosin-positive is less severe

293
Q

What are the clinical features of congenital muscular dystrophies associated with abnormal glycosylation of alpha-dystroglycan?

A

Severe weakness

Brain malformations

294
Q

What are some examples of congenital muscular dystrophies associated with abnormal glycosylation of alpha-dystroglycan?

A

Fukuyama congenital muscular dystrophy
Muscle-eye-brain disease
Walker-Warburg syndrome

295
Q

How is myotonic dystrophy inherited?

A

AD

296
Q

What are the features of congenital myotonic dystrophy?

A 
Often unrecognised in mothers
May have preceding polyhydramnios
Facial weakness, hypotonia
Often needing respiratory support
Joint contractures, especially talipes
297
Q

What are the features of myotonic dystrophy in older children?

A

Initially facial weakness
Then weakness affecting temporals, sternomastoid, distal leg muscles
Progressive weakness
Difficulty in relaxing muscular contraction
Cardiac involvement

298
Q

How is myotonic dystrophy diagnosed?

A

Gene mutation analysis

Electromyogram (‘dive bomber’ discharges)

299
Q

What is Thomsen disease also known as?

A

Myotonia congenita

300
Q

What are the features of myotonia congenita?

A

Myotonia
Cramps
Muscular hypertrophy

301
Q

What does biopsy show in Charcot Marie Tooth?

A

Onion bulb - due to demyelination followed by attempts at remyelination

302
Q

What does the CSF show in Guillain Barre

A

Raised protein, normal white cell count

303
Q

What is cranial nerve 1?

A

Olfactory

304
Q

Is the olfactory nerve sensory or motor?

A

Sensory only

305
Q

How do you test the olfactory nerve?

A

Ask about sense of smell, smell a mint

306
Q

What is cranial nerve 2?

A

Optic

307
Q

Is the optic nerve motor or sensory?

A

Sensory only

308
Q

How do you examine the optic nerve

A 
Pupil size, shape, symmetry
Visual acuity
Direct and consensual pupillary response
Swinging torch
Accommodation reflex
Colour vision
Visual inattention
Blind spot
Visual fields
309
Q

What is cranial nerve 3?

A

Oculomotor

310
Q

What is cranial nerve 4?

A

Trochlear

311
Q

What is cranial nerve 6?

A

Abducens

312
Q

What does oculomotor supply?

A

All extra ocular muscles except superior oblique and lateral rectus
Parasympathetic fibres for pupillary constriction

313
Q

What does the trochlear nerve supply?

A

Superior oblique

314
Q

What does abducens supply?

A

Lateral rectus

315
Q

How do you examine oculomotor, trochlear, and abducens nerves?

A

Ptosis
Squint/nystagmus
Eye movement through horizontal and vertical planes

316
Q

What is cranial nerve 5?

A

Trigeminal

317
Q

What are the branches of the trigeminal and are they sensory or motor?

A

Ophthalmic - sensory
Maxillary - sensory
Mandibular - sensory and motor

318
Q

How do you test the trigeminal nerve?

A

Sensation over forehead, cheek and jaw
Clench teeth and waggle jaw against resistance
Jaw jerk and corneal reflexes

319
Q

What is cranial nerve 7?

A

Facial

320
Q

Is the facial nerve motor or sensory?

A

Motor to facial expression and stapedius

Sensory to anterior 2/3 of the tongue

321
Q

How do you test the facial nerve?

A 
Ask about change in taste or hearing
Facial asymmetry
Raise eyebrows
Close eyes tight
Blow out cheeks
Smile
Pursed lips
322
Q

What is cranial nerve 8?

A

Vestibulocochlear

323
Q

Is the vestibulocochlear nerve sensory or motor?

A

Sensory only

324
Q

How do you test the vestibulocochlear nerve?

A

Ask about hearing

Weber and Rinne

325
Q

What is the 9th cranial nerve?

A

Glossopharyngeal

326
Q

What is the 10th cranial nerve?

A

Vagus

327
Q

What does the glossopharyngeal nerve supply?

A

Motor for swallowing and speech

Sensory for posterior 1/3 of tongue

328
Q

What does the vagus nerve supply?

A

Motor to muscles involved in speech and gag reflex

329
Q

How do you test the glossopharyngeal and vagus nerves?

A

Ask about swallowing, drooling, speech and cough
Say ‘aah’ look at uvula for deviation
Gag reflex

330
Q

What is the 11th cranial nerve?

A

Accessory

331
Q

Is the accessory nerve sensory or motor?

A

Motor

332
Q

How do you test the accessory nerve?

A

Trapezius and sternomastoid - shrug shoulders and turn head against resistance

333
Q

What is the 12th cranial nerve?

A

Hypoglossal

334
Q

Is the hypoglossal nerve motor or sensory?

A

Motor

335
Q

How do you test the hypoglossal nerve?

A

Stick tongue out, look for atrophy or deviation

Push tongue into each cheek

MRCPCH Clinicals (17 decks)

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