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PAEDIATRICS > NEUROLOGY PAEDS > Flashcards

NEUROLOGY PAEDS Flashcards

1
Q

Causes of syncope

A 
Primary 
- dehydration 
- missed meals
- extended standing in a warm environment 
- vasovagal response to a stimuli e.g. blood, pain, surprise 
Secondary 
- hypoglycaemia 
- dehydration 
- anaemia 
- infection 
- anaphylaxis 
- arrhythmias 
- valvular heart disease 
- hypertrophic obstructive cardiomyopathy
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2
Q

Key points in taking a syncope history

A

Features that distinguish between syncopal episode and seizure
After exercise? (More likely to be secondary cause)
Triggers?
Concurrent illness? Fever/signs of infection?
Injury secondary to the faint? Do they have a head injury?
Associated cardiac symptoms, such as palpitations or chest pain?
Associated neurological symptoms?
Seizure activity?
FH - cardiac problems? Sudden death?

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3
Q

Syncope: Examinations

A
  • Any physical injuries as a result of the faint
  • concurrent illness? Infection?
  • Neurological examination
  • Cardiac examination - pulse, HR, rhythm, heart sounds
  • Lying and standing BP
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4
Q

Syncope: Investigations

A

ECG - arrhythmias, QT intervals, long QT syndrome
24 hour ECG
Echocardiogram (if structural heart disease suspected)
Bloods - incl. FBC, electrolytes, blood glucose

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5
Q

Generalised Tonic clonic seizures: characteristics and treatment

A

LOC, tonic (muscle tensing), clonic (muscle jerking) movements
May be associated: tongue biting, incontinence, groaning and irregular breathing
Prolonged post-ictal period

1st line: SODIUM VALPORATE
2nd line: LAMOTRIGINE, or CARBAMAZEPINE

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6
Q

Focal seizures: characteristics and treatment

A

Start in temporal lobes
Affect hearing, speech, memory, emotions
Various ways they can present: Hallucinations, memory flashbacks, Deja vu, doing strange things on autopilot

1st line: CARBAMAZEPINE or LAMOTRIGINE
2nd line: SODIUM VALPROATE or LEVETIRACETAM
!! The reverse of generalised tonic clonic medications !!

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7
Q

Absence seizures: characteristics and treatment

A

Typically happen in children. Pt becomes blank, stares into space, the abruptly returns
During episode unaware of surroundings and wont respond
Most pt stop having these seizures when older

1st line: SODIUM VALPROATE or ETHOSUXIMIDE

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8
Q

Atonic seizures: characteristics and treatment

A

Aka drop attacks
Brief lapse in muscle tone
Usually last less than 3 mins
Typically begin in childhood, may be indicative of LENNOX-GASTAUT SYNDROME

1st line: SODIUM VALPROATE
2nd line: LAMOTRIGINE

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9
Q

Myoclonic seizures: characteristics and treatment

A

Sudden brief muscle contractions, patient remains awake
Typically happen in children as part of juvenile myoclonic epilepsy

1st line: SODIUM VALPROATE
Other options: LAMOTRIGINE, LEVETIRACETAM, TOPIRAMATE

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10
Q

Infantile spasms: characteristics and treatment

A 
aka WEST SYNDROME 
Rare, starts in infancy (around 6m) 
Clusters of full body spasms 
Poor prognosis - 1/3 die by 25, however 1/3 are seizure free 
Can be difficult to treat

1st line: PREDNISOLONE, VIGABATRIN

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11
Q

Febrile convulsions characteristics

A

Occur in children while they have a fever
Not caused by epilepsy or any underlying neurological pathology
Occur in children between the age of 6 months - 5 years

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12
Q

Epilepsy: Investigations

A

!! Good history is key !! To establish if actually seizures
N.B. Children are allowed one simple seizure before being investigated for epilepsy

EEG
MRI brain - check for any structural problems
ECG - to exclude problems with the heart
Blood electrolytes - Na, K, Ca, Mg
Blood glucose - hypoglycaemia and DM
Blood cultures, urine cultures, LP - where sepsis, encephalitis, or meningitis suspected

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13
Q

Epilepsy: General advice

A

Advise about safety precautions, managing and reporting further seizures
Avoid situations which may put the child in danger
- take showers rather than baths
- very careful with swimming unless seizures well controlled and closely supervised
- be cautious with heights, traffic, any heavy, hot or electrical equipment
- older teenagers should avoid driving

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14
Q

SODIUM VALPROATE: MOA and SE

A

Increases activity of GABA - which has a relaxing effect on the brain

SE: Teratogenic, liver damage and hepatitis, hair loss, tremor
- avoided in girls unless no other suitable alternative

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15
Q

CARBAMAZEPINE: MOA and SE

A

Blocks Na Channels and reduces cell excitability

SE: Agranulocytosis (drug induced blood disorder, reduction in no. Of white blood cells), aplastic anaemia, induces P450 system in the liver - so many drug interactions

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16
Q

PHENYTOIN: MOA and SE

A

Na channel blocker

SE: Folate and VitD deficiency, Megaloblastic anaemia (folate deficiency), osteomalacia (VitD deficiency)

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17
Q

ETHOSUXIMIDE MOA and SE

A

Antagonism of pot-synaptic VG Ca channels

SE: Night terrors, rashes

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18
Q

LAMOTRIGINE

A

SE: STEVENS-JOHNSON SYNDROME or DRESS syndrome (life threatening skin reaches)
Leukopenia

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19
Q

Acute management of seizures

A

Put patient in safe position
Place in recovery position if possible
Put something soft under head
Remove obstacles that could lead to injury
Make note of time at start and end of seizure
Call ambulance if lasting more than 5 mins or first seizure

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20
Q

STATUS EPILEPTICUS: definition

A

Seizures lasting > 5 mines
Or
> 3 seizures in 1 hour

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21
Q

STATUS EPILEPTICUS: Management in hospital

A

ABCDE approach

IV LORAZEPAM - repeated after 10 mins if seizure continues
When seizure persists the final step is infusion of IV PHENOBARBITAL or PHENYTOIN

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22
Q

STATUS EPILEPTICUS: medical options in the community

A

Buccal midazolam

Rectal diazepam

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23
Q

Simple and complex FEBRILE CONVULSIONS

A

Simple: generalised, tonic clonic seizures. Last <15 mins, only occur once during a febrile illness

Complex: consist of partial or focal seizures, last > 15 mins or occur multiple times during the same febrile illness

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24
Q

Febrile convulsions: Differential diagnoses

A

Epilepsy
Meningitis, encephalitis, or another neurological infection
Intracranial space occupying lesion (e.g. tumour, haemorrhage)
Syncopal episode
Electrolyte abnormalities
Trauma (always think about non-accidental injury)

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25
Q

Breath holding spells: Types

A

Cyanotic breath holding spells

Pallid breath holding spells (aka anoxic seizures)

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26
Q

Breath holding spells: what are they

A

Involuntary episodes during which a child holds their breath, usually triggered by something upsetting or scaring them

Typically occur between 6 and 18 months

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27
Q

Cyanotic breath holding spells

A

Occur when a child is really upset, worked up and crying
They become Cyanotic and lose consciousness
Within 1 min they regain consciousness and start breathing
They can be a bit tired and lethargic after an episode

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28
Q

Reflex anoxic seizures

A

Occur when a child is startled
Vagus nerve sends strong signals to the heart that causes it to stop beating
Child will suddenly go pale, lose consciousness and may start to have seizure like muscle twitching
Within 30 seconds the heart restarts and the child becomes conscious again

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29
Q

Breath holding spells: management

A

Exclude other pathology
Reassure parents

There has been a link to iron deficiency anaemia - treating this can help

30
Q

Causes of headaches in children

A 
Tension headaches 
Migraines 
ENT infections 
Analgesic headache 
Problems with vision 
RICP 
Brain tumours 
Meningitis 
Encephalitis 
CO poisoning
31
Q

Management of Migraines in children

A 
Rest, fluids, low stimulus environment 
Paracetamol 
Ibuprofen 
Sumatriptan 
Antiemetics (e.g. domperidone)
32
Q

Migraine prophylaxis options

A

Propranolol (avoid in asthma)
Pizotifen (often causes drowsiness)
Topiramate (teratogenic)

33
Q

Abdominal Migraine

A

More common in children than adults
Central abdominal pain lasting > 1 hour
May be associated: N&V, Anorexia, headaches, pallor

May predispose to head migraines

34
Q

Causes of cerebral palsy

A

Antenatal - maternal infections, trauma during pregnancy
Perinatal - Birth asphyxia, pre-term birth
Post-natal - Meningitis, severe neonatal jaundice, head injury

35
Q

Types of cerebral palsy

A

SPASTIC - hypertonia and reduced function from damage to UMN

DYSKINETIC - problems with controlling muscle tone, with hypertonia and hypotonia, causing athetoid movements and oro-motor problems. Result of damage to the basal ganglia

ATAXIC - problems with coordinated movement resulting from damage to the cerebellum

MIXED - mix of spastic, dyskinetic and/or ataxic features

36
Q

Patterns of spastic cerebral palsy

A

Monoplegia - one limb affected
Hemiplegia - one side of body affected
Diplegia - four limbs are affected, but mostly the legs
Quadriplegia - four limbs affected more severely, often with seizures, speech disturbance and other impairments

37
Q

What does child with cerebra palsy’s gate tell us?

A

Hemiplegic / diplegic gait: indicated UMN lesion
Broad based gait /ataxic gait: indicates cerebellar lesion
High stepping gait: indicates foot drop or LMN lesion
Waddling gait: Indicates pelvic muscle weakness due to myopathy
Antalgic gait: indicates localised pain

38
Q

Cerebral palsy: Complications and associated conditions

A 
Learning disability 
Epilepsy 
Kyphoscoliosis 
Muscle contractures 
Hearing and visual impairments 
Gastroenteritis-oesophageal reflux
39
Q

Cerebral Palsy: Management

A

MDT APPROACH: Physio, OT, SALT, Dieticians, orthopaedic surgeon, Paediatricans, social workers, support groups
Surgery may be able to release contractures or lengthen tendons
Muscle relaxants (e.g baaclofen)
Anti-epileptics
Glycopyrronium bromide (for excessive drooling)

40
Q

Causes of squints

A

Squint in otherwise healthy children are usually idiopathic
Other causes:
- hydrocephalus
- cerebral palsy
- space occupying lesions e.g. retinoblastoma
- trauma

41
Q

What is ‘Hirschberg’s test’?

A

Shine pen torch at the patient from 1m away
When they look at it observe the reflection of the light source on their cornea
Reflection should be central and symmetrical
Deviation from the centre —> squint

42
Q

What is the ‘cover test’?

A

Cover one eye and ask the patient to focus on an object in front of them
Move the cover across to the other eye and watch the movement of the previously covered eye
If this eye moves inwards (means it had drifted outwards when covered) = EXTROPIA
If it moves outwards (means it had drifted inwards when covered) = ESOTROPIA

43
Q

Management of squints

A

Visual fields develop until the age of 8 years - so treatment needs to start before then
Delayed treatment increases risk of the squint becoming permanent

OCCLUSIVE PATCH. - can be used to cover the good eye and force the weaker eye to develop.
ATROPINE DROPS - in the good eye - making it blurry
Management coordinated by ophthalmologist
Treat any underlying pathology

44
Q

Hydrocephalus: definition

A

CSF build up within brain and spinal cord
Either due to
- over production of CSF
- problem with draining or absorbing CSF

45
Q

Normal CSF anatomy/physiology

A

4 ventricles

  • 2 x lateral ventricles
  • third ventricle
  • fourth ventricle

CSF is created in the 4 x choroid plexuses (1 in each ventricle) and by the walls of the ventricles
CSF is absorbed into the venous system by the arachnoid granulations

46
Q

Causes of HYDROCEPHALUS

A

CONGENITAL:
- aqueductal stenosis —> insufficient drainage of CSF (the cerebral aqueduct that connects the third and fourth ventricles is stenosed - blocking normal flow of CSF out the 3rd ventricle —> build up in the lateral and third ventricles) - most common

  • Arachnoid cysts can block the flow of CSF if they area large enough
  • Arnold-chiari malformation (cerebellum herniates downwards through the foremen magnum)
  • chromosomal abnormalities and congenital malformations
47
Q

Hydrocephalus: Presentation

A

Cranial bones don’t fuse at sutures until about 2 yrs
Babies with hydrocephalus before this age present with enlarging head and rapidly increasing head circumference (occipito-frontal circumference)
Other signs
- budging anterior fontanelle
- poor feeding and vomiting
- poor tone
- sleepiness

48
Q

Ventriculoperitoneal shunt

A

VP shunt can be placed to drain CSF from the ventricles to another body cavity (usually perionteal cavity)
Valve helps to regulate the amount of CSF that drains from the ventricles

49
Q

VP shunt complications

A

Infection
Blockage
XS drainage
Intraventricular haemorrhage (during shunt related surgery)
Outgrowing them (generally need replacing every 2 years as child grows)

50
Q

Craniosynostosis: definition

A

When sutures close prematurely —> abnormal head shape and restriction to growth of brain

51
Q

Craniosynostosis: if left untreated

A 
Will lead to raised intracranial pressure
Developmental delay 
Cognitive impairment 
Vomiting 
Irritability 
Visual impairment 
Neurological symptoms and seizures
52
Q

Presentation of CRANIOSYNOSTOSIS

A

ABNORMAL HEAD SHAPE - Head shape depends on the affected cranial suture (Saggital synostosis / coronal synostosis / metopic synostosis / lambdoid synostosis )

Anterior frontanelle closure before 1 year of age
Small head in proportion to body

53
Q

Craniosynostosis: investigation and management

A

1st line: skull X-ray
2nd line: CT head with bone views can be used to confirm diagnosis or exclude it if any double on X-ray

Management: mild cases monitored and followed up over time. More severe cases require surgical reconstruction
Prognosis usually good with proper management

54
Q

Plagiocephaly and brachycephaly

A

Common conditions which cause abnormal head shapes in otherwise healthy babies
Plagio- = translates to oblique/slanted.
- Plagiocephaly refers to flattering of one area of baby’s head
Brachy- = translates to short
- Brachycephaly refers to flattering at the back of the head, resulting in a short head from front to back

55
Q

Management of Plagiocephaly/brachycephaly

A

Exclude: Craniosynostosis (palpate sutures)
Check for congenital muscular torticollis (shortening of SCM muscle on one side) - may be the reason child always lies on one side of head

Usually resolves as child grows

Measures to avoid child lying on flatterened area

  • position on rounded side for sleep
  • supervised tummy time
  • using rolled towels or other props
  • minimising time in push chairs and car seats

PHAGIOCEPHALY HELMETS - although have limitations and can cause skin problems and psychosocial problems. Not provided on NHS

56
Q

MUSCULAR DYSTROPHY: what is it

A

MS is an umbrella term for genetic conditions that cause a gradual weakening and wasting of muscles

57
Q

Types of muscular dystrophy

A

Duchennes muscular dystrophy (the main one)

Others: beckers MD, myotonic MD, Facioscapulohumeral MD, oculopharyngeal MD, Limb-girdle MD, emery-Dreifuss MD

58
Q

Gower’s sign

A

Children with proximal muscle weakness use a specific technique to stand up from a lying position = Gower’s sign

They get onto their hands and knees then push their hips up and backwards like the “downward dog” pose
They shift weight backwards and transfer their hands to their knees
Whilst keeping legs quite straight they walk hands up their legs
(They do this because the muscles around the penis are not strong enough to get their body erect without help of their arms)

59
Q

Muscular dystrophy: Management

A

No curative treatment
MDT - OT, physio, medical appliances (e.g. wheelchairs)
Surgical and medical management of complications e.g. spinal scoliosis and HF

STEROIDS have been shown to slow progression of muscle weakness by as much as 2 years
CREATINE supplementation can give slight improvement

60
Q

Genetics of duchennes muscular dystrophy

A

X linked recessive
Defective gene codes for dystrophin (a protein that holds muscles together at the cellular level)
Females usually not affected as they have a spare copy of the gene

61
Q

Beckers Muscular dystrophy

A
62
Q

Myotonic dystrophy

A
63
Q

Fascioscapulohumeral MD

A
64
Q

Oculopharyngeal MD

A
65
Q

Limb-girdle MD

A
66
Q

Emery-Dreifuss MD

A
67
Q

Spinal muscular Atrophy (SMA): what is it

A

Rare autosomal recessive condition causing progressive loss of motor neurones, causing progressive muscular weakness
Affects LMN in the spinal cord —> LMN signs

68
Q

LMN signs seen in SMA

A

Fasiculations, reduced muscle bulk, reduced tone, reduced power, reduced/absent reflexes

69
Q

Spinal muscular atrophy: categories

A

SMA type 1: onset in first few months of life, usually progressing to death within 2 years

SMA type 2: onset within first 18 months. Most never walk but survive into adulthood

SMA type 3: onset AFTER the first year of life. Most walk without support, but subsequently lose that ability. Respiratory muscles less affected and life expectancy is close to normal.

SMA type 4: onset in 20s. Most retain ability to walk short distances but require a wheelchair for mobility. Everyday tasks cause severe fatigue. Respiratory muscles and life expectancy not affected.

70
Q

Spinal muscular atrophy: management

A

No cure
Supportive and MDT approach
Physio, respiratory support (e.g. non-invasive ventilation, Type 1 SMA may require tracheostomy and mechanical ventillation)
PEG feeding if swallow unsafe

71
Q

What is Benign Rolandic epilepsy?

A

seen between the ages of 4-12

focal seizure, involving their face, drooling, and one side or one limb twitching (that can sometimes progress to secondary generalised seizure)

Before or after bedtime. It is common for children to be sleep deprived.

Good prognosis - stop by adolescence

PAEDIATRICS (18 decks)

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