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Neuro Flashcards

1
Q

causes of abnormal motor development

A

central (CP), myopathy, spinal cord lesion (spina bifida), global developmental delay

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2
Q

what is cerebral palsy

A

abnormality in posture and tone, brain injuries before 2 years.

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3
Q

CP are the lesions progressive

A

no, clinical manifestations emerge over time

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4
Q

causes of CP antenatal

A

placental insufficiency- occlusion, chromosomal, genetic, infection

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5
Q

causes of CP

A

antenatal 80%, hypoxic-ischaemic encephalopathy 10%, postnatal 10%

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6
Q

causes of CP postnatal

A

meningitis, encephalitis, encephalopathy, hypoglycaemia, kernicterus, hydrocephalus

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7
Q

how does CP present

A

abnormal posture and tone, delayed motor milestones, feeding difficulties, abnormal gait, hand asymmetry before 1y

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8
Q

what happens to primitive reflexes in CP

A

may persist and become obligatory

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9
Q

what are the 3 types of CP

A

spastic, dyskinetic and ataxic

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10
Q

what signs are seen in spastic CP

A

UMN lesion so increased tone, brisk reflexes, extensor plantar responses. tone is velocity dependent so clasp knife can be seen. initial hypotonia at birth

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11
Q

3 main types spastic CP

A

hemiplegia, diplegia, quadriplegia

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12
Q

how does hemiplegic spastic CP present

A

unilateral involvement arm and leg; fisting affecting hand, flexed arm, pronated forearm, asymmetric hand function; tip toe walking. birth history may be normal

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13
Q

how does quadriplegic spastic CP present

A

all 4 limbs involved, severe, trunk involved- opisothonus, poor head control, low central tone.

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14
Q

what is quadriplegic assoc with and what can happen in birth to lead to it

A

seizures, microcephaly, intellectual impairment. hypoxic-ischaemic encephalopathy

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15
Q

how does diplegic spastic CP present

A

all 4 limbs involved but legs more than arms so hand function may appear normal. abnormal walking.

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16
Q

what can happen to cause diplegic

A

periventricular brain damage

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17
Q

what is asymmetrical hand function before 12m likely to be due to

A

hemiplegic spastic CP

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18
Q

what tracts are affected in spastic CP

A

pyramidal and corticospinal tracts

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19
Q

what is damaged in dyskinetic CP

A

basal ganglia, extra pyramidal

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20
Q

how does dyskinetic CP present

A

abnormal involuntary movements more obvious with active movement and stress. tone is variable. chorea, athetosis, dystonia. intellect can be unimpaired

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21
Q

what is ataxic CP

A

early trunk and limb hypotonia, poor balance, delayed motor development

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22
Q

what are the causes of ataxic CP

A

most genetically determined. if brain injury- signs on same side as lesion. cerebellum

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23
Q

causes of headache

A

tension- tight band like headache, common in adolescents usually with abdominal pain; migraine; raised ICP; sinusitis; benign intracranial hypertension

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24
Q

symptoms raised ICP

A

headache worse on lying down and when waking up, vomiting especially in the morning, visual field defects, CN 6 palsy, gait abnormalities, papilloedema (late sign)

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25
Q

causes of hydrocephalus

A

congenital, arnold-chiari malformation, subarachnoid haemorrhage, meningitis

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26
Q

features of hydrocephalus

A

large head circumference, sutures separated, bulging anterior fontanelle, if left untreated- setting sun sign and signs of increased ICP

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27
Q

what signs can be seen from anterior fontanelle

A

closes around 1 and a half. bulging- raised ICP, sunken- dehydrated

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28
Q

what is microcephaly

A

head circumference below 2nd centile

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29
Q

causes of microcephaly

A

familial (take mean of parents), congenital infection, brain injury- meningitis, hypoxia, hypoglycaemia, accompanise CP and seizures; autosomal recessive- developmental delay

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30
Q

what is macrocephaly

A

head circumference >98th centile

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31
Q

causes of macrocephaly

A

tall stature, familial, hydrocephalus, raised ICP, tumour, chronic subdural haematoma

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32
Q

what is a febrile seizure

A

seizure accompanied by fever in absence of intracranial infection due to meningitis/encephalitis

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33
Q

what happens in febrile seizure

A

usually brief generalised tonic clonic, usually early in infection when temperature is rising rapidly

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34
Q

what age is febrile seizure likely

A

6m-5y

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35
Q

how many patients will have further febrile seizures and what will make further seizures more likely

A

30-40%. more likely if younger child, started earlier on in the illness, family history, lower temperature when the convulsion occured

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36
Q

what is the chance of developing epilepsy with febrile convulsions

A

1-2% in simple seizures. 4-12% if it is complicated by having focal signs, prolonged seizures, repeated in the same illness

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37
Q

in febrile convulsion what must you always consider

A

bacterial cause eg meningitis as classical features may not be present if patient is

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38
Q

if history of prolonged seizures what can be given

A

rectal diazepam or buccal midazolam.

39
Q

what is the normal length of a febrile convulsion and above which you would get worried

A

5 mins

40
Q

causes of paroxysmal events in children

A

breath holding attacks, reflex anoxic seizures (head trauma, cold food, fright, fever), syncope, BPPV, pseudoseizures, epilepsy, induced illness (NAI), cardiac- prolonged QT

41
Q

what are examples of generalised seizures

A

arise from both hemispheres. generalised tonic-clonic, myoclonic, atonic, absence

42
Q

what is the most common focal seizure and what does it present with

A

temporal- aura, lip smacking and other automatisms, deja vu

43
Q

what does frontal present with

A

motor/pre motor. clonic movements, asymmetrical tonic can be seen

44
Q

what does parietal present with

A

altered sensation- dysaesthesia, distorted body image

45
Q

what investigations should be done in child with seizures

A

EEG, 24h ambulatory EEG, video telemetry, MRI/CT to exclude brain lesions (tumour, infarct, malformation), PET to see hypometabolism

46
Q

what is West syndrome

A

infantile spasms. occurs 4-6m. triad- spasms, learning difficulties and hypsarrhythmia on EEG. multiple bursts 20-30 spasms lasting 1-2s each

47
Q

what can you use to treat West syndrome

A

vigabatrin and corticosteroids. poor prognosis

48
Q

what is Lennox-Gastaut syndrome

A

slightly later onset seizures- 1-3years. drop attacks- astatic seizures, tonic, atypical absences. neurodevelopmental arrest. poor prognosis

49
Q

what is childhood absence epilepsy and when does it come on

A

4-12 year olds. absence- for seconds not longer than a minute, then may twitch eyelids or hand. developmentally normal, females 2/3.

50
Q

how could childhood absence be induced in the clinic

A

hyperventilation

51
Q

what is the prognosis of childhood absence

A

good, 5% develop tonic clonic in adults

52
Q

when does juvenile-myoclonic epilepsy set in and what happens in it

A

adolescence- adult. myoclonic but can have clonic and absences. learning unimpaired. remission unlikely

53
Q

what is the most common syndrome and is it generalised or focal

A

rolandic- benign epilepsy with centro-temporal spikes. focal

54
Q

what is benign epilepsy with centro temporal spikes (rolandic) and does it remit by adolescence

A

4-10 years. facial movements and strange movements of the lips. remits by adolescence

55
Q

what AED can make absence and myoclonic seizures worse

A

carbamazepine

56
Q

first line in tonic clonic

A

valproate, carbamazepine

57
Q

first line in absence and myoclonic

A

valproate

58
Q

first line in focal

A

carbamazepine, valproate, lamotrigine

59
Q

second line tonic clonic

A

lamotrigine, topiramate

60
Q

second line absence and myoclonic

A

lamotrigine

61
Q

second line focal

A

topiramate, levetiracetem, gabapentin

62
Q

other options other than AED for seizures

A

ketogenic diet, VNS, surgery

63
Q

what is status epilepticus

A

> 30 mins of seizure. lorazepam IV if access, rectal diazepam/buccal midazolam if not. if no response- phenytoin

64
Q

side effect valproate

A

weight gain, hair loss

65
Q

side effect carbamazepine

A

rash, neutropenia, hyponatraemia, ataxia

66
Q

side effect lamotrigine

A

rash. steven johnson

67
Q

side effect benzos

A

sedation

68
Q

side effect topiramate

A

weight loss, drowsy, withdrawal

69
Q

how does an ataxic child present

A

abnormal gait, tremor

70
Q

how would you describe the ataxic/cerebellar gait

A

broad based, staggering/lurching, fall towards side of cerebellar lesion

71
Q

what is ataxia

A

inabillity to coordinate muscle activity- jerky and incoordination. inability to perform precise movements and loss of balance

72
Q

what is true ataxia and what are the types

A

sign of cerebellar dysfunction. sensory and cerebellar

73
Q

what is sensory ataxia

A

peripheral nerve or posterior columns damaged. wide based gait. can look normal whilst sitting, loss of position and vibration sense. positive romberg.

74
Q

what is cerebellar ataxia

A

problem in the vermis of the cerebellum. lurching, staggering gait. unable to sit balanced

75
Q

what viral infection is most implicated in ataxia

A

varicella

76
Q

acute causes of ataxia

A

drugs, trauma, post infectious immune eg GBS, tumour, labyrinthitis

77
Q

insidious ataxia

A

tumours, BPPV, hereditary- ataxia telangectasia, Friedrichs, congenital malformations- Dandy Walker, chiari malformation

78
Q

how does hemiplegic gait look

A

flexed arm, straight leg, foot makes circle round0 circumduction, upper limb flexed, lower limb extended, distal more affected than proximal so get weak fingers and foot drop

79
Q

what does diplegic gait look like

A

both arms flexed, both legs extended. tip toe walking. adduction prominent feature. can get scissoring gait

80
Q

what is the gait in patient with myopathy

A

waddling gait- lean trunk away from side of lesion, compensate for the weak pelvic muscles which cant lift hip when lift leg to take a step

81
Q

central causes of floppy baby

A

causes of developmental delay eg Downs, hypothyroid, hypocalcaemia, HIE, evolving CP

82
Q

peripheral causes of floppy baby

A

spinal muscular atrophy, MG, myopathy

83
Q

what is hydrocephalus

A

obstruction to the flow of CSF leading to dilatation of the ventricular system proximal to the site of obstruction.

84
Q

where is the obstruction in non communicating hydrocephlus

A

within ventricular system or aqueduct

85
Q

where is the obstruction in communicating hydrocephalus

A

arachnoid villi

86
Q

causes of non communicating

A

aqueduct stenosis, dandy walker, chiari

87
Q

causes of communicating

A

SAH, meningitis

88
Q

signs hydrocephalus

A

bulging ant fontanelle, scalp veins distended, downward gaze or sun setting sign

89
Q

what is needed for diagnosis neurofibramotosis type 1

A

2 or more of : 6 or more café au lait, more than one neurofibroam, axillary freckles, optic glioma, lisch nodule, bony lesions, first degree relative with NFM1

90
Q

dominant feature of NFM2

A

acoustic neuroma

91
Q

what are the lipid storage disorders causing neurodegeneration

A

tay sachs, gaucher, niemann pick

92
Q

what enzyme is deficient in tay sachs

A

hexosaminidase A. auto somal recessive. Ashkenazi Jews. developmental regression. death by 2-5 years. cherry red spot macula

93
Q

what enzyme is deficient in gaucher

A

beta glucosidase. Ashkenazi jews. splenomegaly, bone marrow suppression.

94
Q

what enzyme is deficient in niemann pick

A

sphingomyelinase. death by 4 years. feeding difficulties, failure to thrive, cherry red spot macula

Paeds (16 decks)

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