Neurology Flashcards

1
Q

what is cerebral palsy?

A

Disorder of developmental delay, due to a non-progressive fixed cerebral lesion in early childhood.

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2
Q

Causes of Cerebral palsy

A

Most are idiopathic
of those which have a cause..
80% antenatal : TORCH, abndomal brain development, stroke during labour
10% perinatal: Hypoxic ischeamic encephalopathy, Intrapartum trauma
10% postnatal - neonatal hypoglycaemia, hyperbilirubineamia, cerebral infarct, meconium aspiration, CNS infections.

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3
Q

Risk factors of cerebral palsys?

A

increased maternal and paternal age, multiple pregnancy, first child.

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4
Q

Classification of cerebral palsy

A

Gross motor function classification score (GMFCS)
1. Walk without limitation
2. Walk with limitation
3. Walk with equipment assistance, can utilize and control wheelchair. Some independence in standing transfers
4. Self mobility with powered motor assistance
Severe control limitations, required physical assistance ad transport mechanically.

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5
Q

Presentation of crerbal palsy

A

Signs of developmental delay, delayed motor milestones.
Difficulty feeding
abnormal posture, increased muscle tone
persistent primitive reflexes
recurrent chest infectsios, constipation, reflux.
abnormal walking - tip toe walking or circumduction gait.

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6
Q

What are the 3 main types of cerebral palsy and their features?

A

Spastic (80%)
- stiff and tight muscles
- will have hemiplegia, diplegia r quadriplegia (most common)
- will have circumduction gait if hemiplegic, will have scissoring gait of diplegic and tiptoe walking
Dyskienetic
- damage to basal ganglia
-withering involuntary movements, unusual posture.
- often normal intellectual development
Ataxic
- damage to cerebellum, shaky movements, poor balance.
- wide baised gait, unsteady trunk.

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7
Q

Conditions commonly associated with cerebral palsy

A

epilepsy, recurrent chest infections, deafness, learning disability, unsafe swallows, stunted growth.

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8
Q

Investigations and diagnosis for crerbral palsy

A
developmental assessment
clinical diagnosis
exclusion of other causes:
bloods - FBC, U&Es, CK, TFTs, Vit D
imaging: MRI spine, Bone scan, hearing test
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9
Q

RED flags for developmental delay

A
persistent primitive reflexes
not walking by 18 months
exclusive toe walking
hand preference before 18 months
not babbling by 12 months
no understanding commands by 18 months
fixed squint
not fixing and following by 6 weeks
lack of social smile at 6 months
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10
Q

Management of cerebral palsy

A

MDT involvement with occupational therapists, SALT, physiotherapists, dieticians, peads.
Aims - to promote independence.
splints and mobility aids
Spacisity aids

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11
Q

Treatments for Spacisity

A

Baclofen - lots of side effects (nightmares, dizziness, anxiety)
Botox - to block acetylcholine to the muscle to stop contractions.
orthopaedic involvement, dorsal risotomy

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12
Q

who gets febrile convulsions? how common are they?

A

3% of children, most common in children between the ages of 6 months and 6 years.

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13
Q

causes of febrile convulsions

A

fever, often due to viral infectiosn (URTI, OM or tonsillitis most commonly).

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14
Q

features of simple vs complex/atypical febrile convulsion

A

simple: tonic clonic, lasts less than 15 mins, only happens once within an illness
complex: lasts more than 15 mins, may recur within the same illness, can be focal (very concerning).

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15
Q

Epilepsy risk with febrile convulsions

A

Population risk is 1/100
Simple <15 mins - 1/50 risk of developing epilepsy
Complex >15 mins 1/20 risk of developing epilepsy

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16
Q

Presentation of febrile fit

A

Before: history of febrile illness, temp above 38.5, lymph node enlargement
During: LOC, generalised tonic clonic
After: no neurological signs, will have post ictal phase

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17
Q

Investigations for febrile convulsions

A

Find source of infection!

Sepsis screen: LP, blood culture, CXR, urine dip, bloods (FBC, U&Es, CRP, ESR)

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18
Q

Management of febrile convulsions

A

seizure management - A-E. time seizure, remove danger, put in the recovery position.
if fit continues for over 5 mins use buccal midazolam.
Find and treat source of infection
Management of pyrexia - paracetamol, hydration.

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19
Q

education for parents for febrile convulsions

A

1/3 risk of recurrence with future infections,
call an ambulance of the fit id lasting over 15 mins.
1-2% risk of epilepsy development.
red flags - of severe infection and when to seek help.

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20
Q

Red Flags for febrile convulsions sepsis

A
Colour - pale, mottled, 
No response to social skills
Weak or high pitch continuous cry
Signs of respiratory distress, grunting, tachypnoea, recessions, 
Non-blanching rash
focal signs.
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21
Q

what is a rigor?

A

shaking associated with fevers, no post-ictal phase, can happen at any age, may be peripherally shut down.

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22
Q

presentation of breath holding attacks

A

episodic apnoea, precipitated by crying usually due to pain or anger. red face, limbs extended, may later become cyanosed and briefly LOC.
will have a RAPID full recovery. No post-ictal signs.

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23
Q

What age of children have breath holding attacks?

A

common in children under three, usually between 6-18 months. will resolve by school age.

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24
Q

investigations and management of breath holding attacks

A

Clinical diagnosis - no signs of fitting, full rapid recovery after attacks. families often asked to record events.
Reassurance to parents no medical management needed.
When attacks happen, parents ignore, may need to put in recovery position.

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25
Q

Risk factors for epilepsy

A

FH, SGA, HIE, febrile convulsions, head trauma, bleeds to brain.

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26
Q

Presentation of epileptic seizure

A

Before: Prodrome - changes in mood, sleep deprivation. can have localising features eg preceding aura or motor symptoms.
During: either generalised (tonic (stiff) , clonic (jerk), tonic clonic, absence, myoclonic) or partial seizure ( focal symptoms, preceding aura)
After: post ictal phase - headaches, confusion, dysphasia, amnesia

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27
Q

Investigations and diagnosis of epilepsy

A

diagnosis: ned 2 unprovoked seizure over 24 hours apart. History is key
investigations: look for causes.
Bloods: U&Es, bone profile - important to check calcium, potassium and sodium.
Imaging - need head MRI to rule out space occupying lesion.
ECG to identify any cardiac cause.

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28
Q

antiepileptic mediation used in tonic clinic seizures

A

Carbamazepine, valproate, lamotrigine

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29
Q

antiepileptics used in absence seizures

A

Lamotrigine, valproate, ethosuximide.

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30
Q

Management for epilepsy (not acute)

A

Antiepileptic medication - depends on seizure type.
Keep fit diary
precautions with swimming, no baths.
Inform school, may have slow progress, can have developmental delay.

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31
Q

Acute epileptic fit management

A

1) A-E approach. Airway manoeuvre if respiratory distress, give O2 if available, recovery position, prevent harm
2) Time seizure - wait 5 mins
Benzodiapipine if over 5 mins
3) 2nd dose if over 15 mins
4) Phenytoin infusion if over 25 mins
5) If status epilepticus can do RSI and PICU transfer.

32
Q

Causes of seizures

A

CNS infections
electrolyte disturbence - sodium, potassium and calcium.
idiopathic
cerebral insult - bleed, space occupying lesion
Most are idiopathic.

33
Q

What is benign Rolandic epilepsy? who gets it?

A

20% of childhood epilepsies, usually boys aged 4-10, nocturnal mouth salivation and grunting, will grow out if it in adolescence.

34
Q

What is West syndrome? who gets it?

A

Infantile spasms, occur in 4-8 month olds. myoclonic spasms on walking, poor developmental progress, poor prognosis with severe developmental delay.

35
Q

what is Juvenile myoclonic epilepsy? who gets it?

A

Early morning tonic clonic seizures and absence seizures, jerking of the upper limbs, can be triggers by sleep deprivation, alcohol and flashing lights. more common ages girls, ages 8-20.

36
Q

causes of pseudo-fits / non-epileptic attacks

A

syncope, hallucinations, sleep disturbance disorders,.
most commonly due to anxiety, panic attcks.
be aware of Muchcausens syndrome and fabrictaed illness.

37
Q

presentation of pseudo seizures

A

Before: usually have emotional or social stimuli

During: Mimic tonic clonic seizers, but normal tone. not lasting more than 2 mons, no oxygen de-saturation.

After: no post ictal phase.

38
Q

Management and investigations of pseudo-fits

A

Investigations - gold standard is video of fit, rule out pathological causes, may need further imaging etc.
Management - reassure parents, exloanstion of possible triggers wat to do when out occurs. recovery position, red flags for when to call for ambulance. referral for psychological therapies.

39
Q

Causes of headaches in children

A

Stress headache
cluster headaches
Infections - meningitis, encephalitis, sinusitis, Dental causes
Raised ICP headache - Neoplastic - space occupying lesions, Trauma: post-concussive headaches, haemorrhage
Migraine headache

40
Q

Red flags for headaches in children

A
Acute presentation
children <3 years old
Progressive chronic headaches.
Focal neurology
headache on walking
Vomiting
Neck stiffness
Hypertension
41
Q

What is Cushing’s triad?

A

A triad of raised ICP

bradycardia, irregular breathing, hypertension.

42
Q

Investigations/examinations for child presenting with headache

A

Full detailed history.
CN, PNS mental status, examination
Temperature and BP.
imaging needed if focal signs, sudden onset, signs of raised ICP or meningism.

43
Q

Red flags for head injuries

A
sign of NAI - retinal haemorrhages, inconsistent history. 
signs of skull fracture
bleeding from ears, clear fluid from eyes of nose. 
problems understanding or speaking
loss of balance
drowsiness for more than 1 hour
vomiting
seizures.
44
Q

criteria for needing CT within 1 hour for head truama

A
- LOC > 5 mins
, abnormal drowsiness- amnesia
- >3 episodes of vomiting
- suspicion of NAI
- signs of basal skull fracture
- tense fontanelle
- post traumatic seizure with no Hx of epilepsy
-Focal neurological signs
45
Q

3 signs of basal skull fractures

A

panda eyes, hemotympanum, bruising behind the ear (battles sign)

46
Q

Paediatric GCS

A

Eye opening - score /4
- very similar to adult

Verbal response - score / 5
- normal developmental
verbal response is highest score. lowers, depending on crying to stimuli.

Movement - score/6
- movement normal to development, purposefully. abnormal flexion or extension in response to pain.

47
Q

risk factors for hydrocephaulus

A

PTB, pre-eclampsia, alcohol use in pregnancy, reduced antenatal care, neural tube abnormalities.

48
Q

Causes of hydrocephalus

A

obstructive: prenatal causes - congenital abnormality, toxoplasmosis, Chiari malformation
post natal causes: stenosis following meningitis, intracranial bleed or tumour, aqueduct stenosis

meningitis, SAH, something which causes excess CSF, increased viscosity of CSF, SAH, meningitis.

49
Q

Presentation of hydrocephalus infants and in older children

A

infants: irritability, vomiting, impair consciousness, increased head circumference, tense fontanelle, dilated scalp veins, increased limb tone.

older children: headaches, vomiting, papilledema, large head, can have uni- or bi-lateral CN 6 nerve palsy eyes turn inwards)

50
Q

what is the sun-setting sign? what dose it indicate?

A

both eyes deviate downwards, upper lids retracted.

Sign of infantile severe hydrocephalus.

51
Q

Management of hydrocephalus

A

Plot head circumference to see rate of expansion.
Head CT w/ contrast or USS to see ventricular enlargement,
Treat cause
symptomatic pressure relief
LP external ventricular drain or surgery to produce shunt.

52
Q

How common are migraines in children? what are the risk factors?

A

most common cause of primary headache in children.

increased risk with: HF, stress, girls in menarche.

53
Q

presentation of migraine

A

bilateral or unilateral pulsatile headache that lets from 1-72hrs.
associated symptoms: photophobia, N/V, phonophobia, relived by sleep.
Aura (with only 10%) - sensory or motor disturbance, loss of visual field.

54
Q

Management of migraine

A

Reassurance, identification of triggers through a dairy, simple analgesics, anti-emetics if needed.

Rescue treatments: Triptan (serotonin agonist)

Prophylactic measures: Propranolol or Topiramate (na+ channel blocker)

55
Q

What is plagiocephaly? who does it effect and how common is it?

A

‘Flat head syndrome’. distortion of the skull, commonly seen at 2-3 months of age.
Effects 1/100 infants.
More common in twins, PTB, breech, prolonged labour,.

56
Q

Types of plagiocephaly

A

Synostosis (one or more fused suture) or mon- synostosis (no fusion) plagiocephaly

57
Q

what is craniosynostosis? when should it occur?

A

it is the premature union of skull bones. it should occur at the age of 4.

58
Q

differentials for plagiocephaly?

A

congenital muscular torticollis - tightening of the SCM. need to check through examination.

59
Q

Management of plagiocephaly

A

counselling parents: does not effect brain development or cause any brain abnormalities.
sleeping - sleep on one side, not on tummies.
physiotherapy - if finding it hard to turn head in one direction can use physiotherapy techniques.

60
Q

management of Crainiosyntosis

A

corrective surgery

61
Q

what are tics? how common are they nd who gets them?

A

Sudden and co-ordinated partial involuntary movements developed in one part of the body.
occurs in 1/10 children, more common in boys, ages 8, improving with adolescence.

62
Q

causes of tics

A

random, but associated with stress, boredom, anxiety, tiredness.

Tourette’s syndrome has strong genetic links

63
Q

Presentation of Transient tic disorder, chronic tic disorder and Tourette’s disorder

A

Transient: Tics happen once or come and go, lasts less than a year

Chronic: tics last for more than 1 year, only occurs in motor or vocal tics

Tourette’s: lasts for more than 1 year, must have BOTH moor and vocal tics, breaks in tics does not exceed 3 moths.

64
Q

Management of Tics

A

Encourage family to ignore and avoid re-enforcement of tics.
Reduce stress, encourage good sleep pattern.

Can refer for behavioural therapy.

65
Q

Causes of Duchenne’s muscular dystrophy

A

X linked genetic condition.

mutation of the dystrophin gene Xp21. Either spontaneous or trough maternal - fetal transmission.

66
Q

Presentation of Duchenne’s muscular dystrophy

A

developmental delay reaching milestones.
imbalance in strength of knees and hips.
Gowers sign - patient climbs up body to stand (poor power in legs)
will have diminished tendon reflexed and hypotonia.

67
Q

Prognosis of Duchenne’s muscular dystrophy

A

Progressive disease, wheelchair bound by the age of 12, causes death by cardiac or respiratory dysfunction in 20s/30s

68
Q

Investigations for muscular dystrophy

A

CK levels - will be 50-100X the normal range

Muscle biopsy

69
Q

Management of muscular dystrophy

A
  • Stage 1: whilst walking - glucocorticoid therapy, physiotherapy, optimatsion of bone health
  • Stage 2: wheelchair bound - cardiac and respiratory surveillance, physiotherapy
  • Stage 3: later stages - respite care, optimise complications, palliative care, NIV for coughing and airway clearance.
70
Q

Risk factors for spina bifida

A

FH, lack of folic acid during pregnancy, diabetes, alcohol exposure, valproate or carpamezapine use in pregnancy, girls.

71
Q

Most common form of spina bifida?

A

spina bifida occulta - mildest, gap between the vertebrae.

72
Q

Define myelomeningocele, rachischis, and meningocele

A

All types of spina bifida

Myelomeningocele: most severe type, spinal canal open, meninges from sac.
meningocele: meninges push out through the spine, chord stays inside.
Rachichisis: severe, spine open, commonly also with anencephaly

73
Q

Presentation of spina bifida

A

Most commonly found antenatally or on newborn examination.
Check vertebra, lumps or tufts on SC.
later presentation: hydrocephalus, weakness o paralysis of legs, bowel and urinary incontinence, loss of temperature sensation of lower limbs.

74
Q

what is used in prenatal screening to detect spina bifida

A

AFP - will have raised levels in amniotic fluid.

can uses AFP and AcH to differentiate between ventral wall defects and NT defects.

75
Q

Management of spina bifida

A

Foetal surgery - repair defect before 26 weeks.
Post natal surgery - within first few days of life
prognosis depends on severity. neurological damage will be irreversible.

76
Q

when does damage in spina bifida occur?

A

days 17-30 during embryogenesis during the formation and closure of the neural tube.