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Child Health > Neurology > Flashcards

Neurology Flashcards

1
Q

Vasovagal syncope pathophysiology

A 
Stimulus—> vagus nerve—> PNS
Vasodilation of cerebral vessels
Decreased pressure in cerebral circulation 
Hypoperfusion of brain tissue
Loss of consciousness
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2
Q

Prodrome symptoms vasovagal syncope

A 
Hot or clammy
Sweaty
Heavy
Dizzy or light-headed
Vision going blurry or dark 
Headache
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3
Q

Signs and symptoms during vasovagal syncope

A

Collateral history
Suddenly losing consciousness and falling to the ground
Unconscious on ground for a few seconds to a minute as blood returns to their brain
Twitching, shaking or convulsion activity

Incontinence

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4
Q

Postictal period

A

Prolonged period of confusion, drowsiness, irritability, disorientation

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5
Q

Causes of primary syncope

A

Dehydration
Missed meals
Extended standing in warm environment
Vasovagal response to stimulus

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6
Q

Secondary causes of syncope

A 
Hypoglycaemia
Dehydration
Anaemia
Infection
Anaphylaxis
Arrhythmias (electrolyte abnormalities)
Valvular heart disease
Hypertrophic obstructive cardiomyopathy
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7
Q

Syncope features

A

Prolonged upright position before the event
Lightheaded before event
Sweating before event
Blurring or clouding of vision before the event
Reduced tone during the episode
Return of consciousness shortly after falling
No prolonged post-ictal period

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8
Q

Seizures features

A 
Epilepsy aura (smells, tastes, deja vu) before event
Head turning or abnormal limb positions
Tonic clonic activity
Tongue biting
Cyanosis 
Lasts >5 minutes
Prolonged post-ictal period
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9
Q

Types of seizures

A 
Generalised tonic-clonic seizures
Focal seizures
Absence seizures
Atonic seizures
Myoclonic seizures 
Infantile spasms
Febrile convulsions
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10
Q

Generalised tonic-clonic seizures

A

Loss of consciousness
Tonic: muscle tensing followed by
Clonic: muscle jerking
Tongue biting, incontinence, groaning, irregular breathing
Post-ictal period: confused, drowsiness, irritable or low

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11
Q

General tonic-clonic seizures management

A

First line: sodium valproate

Second line: lamotrigine or carbamazepine

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12
Q

Focal seizures features

A 
Temporal lobes: hearing, speech, memory, emotions
Hallucinations
Memory flashbacks
Deja vu 
Doing strange things on autopilot
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13
Q

Focal seizures management

A

First line: carbamazepine or lamotrigine

Second line: sodium valproate, levetiracetam

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14
Q

Absence seizures features

A 
Typical in children 4-8
Blank
Stares into space
Returns to normal abruptly 
Unaware of surroundings during episode
Last 10-20seconds
Most patients stop as they get older
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15
Q

Absence seizures management

A

First line: sodium valproate or ethosuximide

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16
Q

Atonic seizures features

A 
Drop attacks 
Brief lapses in muscle tone
<3 minutes
Typically begin in childhood
Indicative of Lennox-Gastaut syndrome
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17
Q

Management of atonic seizures

A

First line: sodium valproate

Second line: lamotrigine

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18
Q

Myoclonic seizures features

A

Brief muscle contractions
Sudden jump
Patients awake during episode
Part of juvenile myoclonic epilepsy

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19
Q

Myoclonic seizures management

A

First line: sodium valproate

Second line: lamotrigine, levetiracetam, topiramate

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20
Q

Lennox-Gastaut syndrome

A 
Extension of infantile spasms 
Onset 1-5 years
Atypical abscess, falls, jerks
90% moderate-severe mental handicap 
EEG: slow spike
Ketogenic diet may help
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21
Q

Benign rolandic epilepsy

A

Most common in childhood M>F

Paraesthesia (e.g. unilateral face), usually on waking up

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22
Q

Juvenile myoclonic epilepsy (Janz syndrome)

A

Onset: teens, F:M = 2:1
Infrequent generalised seizures, often in morning/following sleep deprivation
Daytime absences
Sudden, shock like myoclonic seizures (these may develop before seizures)
Usually good response to sodium valproate

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23
Q

Infantile spasms features

A 
West’s syndrome
Infancy->6months
Clusters of full body spasms 
M>F
Flexion of head, trunk, limbs-> extension of arms (Salaam attack); last 1-2secs, repeat up to 50times
Progressive mental handicap
EEG: hypsarrhythmia
Usually 2nd to serious neurological abnormality (e.g. TS, encephalitis, birth asphyxia) or may be cytogenetic
Poor prognosis
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24
Q

Infantile spasms, West syndrome management

A

Prednisolone

Vigabatrin

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25
Q

Investigations epilepsy

A

EEG, after 2nd tonic-clonic
MRI brain
ECG to exclude heart problems
Blood electrolytes: sodium, potassium, calcium, magnesium
Blood glucose: hypoglycaemia, diabetes
Blood cultures, urine cultures, lumbar puncture

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26
Q

When should MRI brain be considered in epilepsy

A

First seizures in <2 years
Focal seizures
No response to first-line anti-epileptic medications

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27
Q

General advice for epilepsy

A 
Showers > baths
Cautious with swimming
Cautious with heights
Cautious with traffic
Cautious with heavy, hot or electrical equipment
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28
Q

Sodium valproate side effects

A

Teratogenic, contraception advice
Liver damage and hepatitis
Hair loss
Tremor

First line for most except focal seizures
Increases activity of GABA

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29
Q

Carbamazepine side effects

A

Agranulocytosis
Aplastic anaemia
Induces P450 system- many drug interactions

First line for focal seizures

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30
Q

Phenytoin Side effects

A 
Folate and vitD deficiency
Megaloblastic anaemia (folate deficiency)
Osteomalacia (vitD deficiency)
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31
Q

Ethosuximide side effects

A

Night terrors

Rashes

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32
Q

Lamotrigine side effects

A

Stevens-Johnson syndrome or DRESS syndrome

Leukopenia

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33
Q

DRESS syndrome

A

Drug reaction with eosinophilia and systemic symptoms

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34
Q

Management of seizures

A

Put patient in safe position
Place in recovery position
Put something soft under head
Remove obstacles that could lead to injury
Make a note of time at start and end
Call ambulance if >5 minutes or first seizures

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35
Q

Status epilepticus definition

A

Seizures >5minutes or
>3 seizures in one hour
>=2 seizures within a 5 minute period without the person returning to normal between them

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36
Q

Management of status epileptic in hospital

Initial management

A 
Secure airway
High-concentration oxygen
Assess cardiac and respiratory function
Check blood glucose levels
Gain IV access
IV lorazepam, repeat after 10minutes if seizure continues
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37
Q

Management of status epilepticus in hospital if seizures persist after initial management

A

Infusion of IV phenobarbital or phenytoin
Intubation and ventilation
Transfer to ICU

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38
Q

Options in community to treat status epilepticus

A

Buccal midazolam

Rectal diazepam

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39
Q

Febrile seizure definition

A

Seizure associated with a febrile illness
Not caused by CNS infection
No previous neonatal seizures or previous unprovoked seizure
Not meeting criteria for acute symptomatic seizure
6months-6years

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40
Q

Febrile seizures epidemiology

A

12-18months peak incidence

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41
Q

Febrile seizure pathophysiology

A

Viral infections: URTI, LRTI, otitis media, UTI most common

Also gastroenteritis and fever post-vaccination associated

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42
Q

Febrile seizures risk factors

A

FH
Socio-economic causes
Seasonal: viruses more common in winter
Zinc and iron deficiency

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43
Q

Clinical features of febrile seizures

A

Fever >38
Age 6months-6 years
Tonic-clonic seizure
Symptoms of infection

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44
Q

Simple febrile seizure

A

<15 minutes
Generalised tonic-clonic
Isolated event- doesn’t recur within the same febrile illness
Post-ictal state: uneventful recovery from seizure

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45
Q

Complex febrile seizure

A

> 15 minutes
Focal, or focal with secondary generalisation
Recurrence within 24 hours of the same febrile illness
May suffer from Todd’s paresis

46
Q

Febrile status epilepticus

A

Subgroup of complex febrile seizures
Duration >30minutes
Multiple seizures lasting 30 minutes with no recovery between each one

47
Q

History of febrile convulsions

A 
Has child been vaccinated
Are they at school?
Previous treatment with antimicrobials
Any history of trauma or toxin ingestion
Any family history
Developmental history
48
Q

Examination in febrile convulsions

A 
Find source of infection
External ear examination with auroscope- look for signs of otitis externa or otitis media 
Throat examination- for signs of URTI (inflamed tonsils)
Full respiratory examination- for signs of LRTI
Check fontanelles 
Brudzinskis or Kernigs sign
Nuchal rigidity (neck stiffness)
Mental status of child
Full neurological examination
Cardiovascular examination
Abdominal examination
Urine dipstick and microscopy
Superficial infective skin lesions
49
Q

DD febrile seizures

A 
CNS infection
Delirium
Syncope
Epilepsy 
Intracranial space occupying lesions, brain tumours or intracranial haemorrhage
Electrolyte abnormalities
Trauma
50
Q

Febrile convulsions investigations
If child >1
Or symptoms of intracranial infection

A 
General observations
Clear source of infection 
Bedside testing- urinalysis
Bloods: FBC, CRP, U&E, calcium, glucose, magnesium, blood cultures
Stool cultures
Lumbar puncture
Imaging: CXR
CT/ MRI/ EEG in complex seizures
51
Q

Red flags of CNS infection

A

Complex febrile seizures
History of lethargy, irritability or decreased feeding
Prolonged post-ictal altered consciousness or neurological deficit >1 hour
Any physical signs of meningitis/ encephalitis
Previous/ current treatment with antibiotics which may have masked full clinical presentation of meningitis
Incomplete immunisation in children 6-18months against Haemophilus influenza B and streptococcus pneumoniae

52
Q

Acute management febrile seizure

A 
A-E
Monitor child and prevent injury 
Keep child well-hydrated
Paracetamol or ibuprofen 
In-depth explanation
53
Q

Treatment febrile seizure >5 minutes

A

Benzodiazepine rescue

54
Q

Febrile seizures risk factors for recurrence

A

Age <18 months at onset
Shorter duration of fever before seizure (<1 hour)
Relatively lower grade of fever associated with seizure (<40degrees)
Multiple seizures during the same febrile illness
Day nursery attendance
FH of febrile seizure in a first degree relative

55
Q

Risk of epilepsy after febrile seizure

A

FH epilepsy
Complex focal seizure
Neurodevelopmental impairment

56
Q

Breath holding spells

A 
Breath holding attacks
Involuntary episodes
Trigger: something scaring or upsetting them 
Occur 6-18months of age
Not harmful in long term

Cyanosis breath holding spells
Pallid breath holding spells

57
Q

Cyanotic breath holding spells

A

Occur when child is really upset, worked up, crying
Stop breathing after letting out a long cry
Become cyanosis and lose consciousness
Regain consciousness within a minute and start breathing again
Tired and lethargic after an episode

58
Q

Reflex anoxic seizures

A

Occur when child is startled
Vagus nerve sends strong signals to heart that causes it to stop breathing
Child will suddenly go pale, lose consciousness, seizure-like muscle twitching
<30seconds heart restarts and child becomes conscious again

59
Q

Management of breath holding spells

A

Treat iron deficiency anaemia

60
Q

Causes of headache in children

A 
Tension headaches
Migraines
ENT infection
Analgesic headache
Problems with vision
RICP
Brain tumours
Meningitis
Encephalitis
Carbon monoxide poisoning
61
Q

Tension headaches features

A

Mild ache across forehead
Pain/pressure in band-like pattern around head
No visual changes or pulsating sensations
Typically symmetrical

Symptoms in young children:
Quiet, stop playing, turn pale or become tired
Resolve quickly in children compared with adults
Within 30 minutes

62
Q

Triggers for tension headaches

A

Stress, fear or discomfort
Skipping meals
Dehydration
Infection

63
Q

Management tension headaches

A 
Reassurance
Analgesia
Regular meals
Avoid dehydration
Reduce stress
64
Q

Migraines types

A 
Migraine without aura
Migraine with aura
Silent migraine
Hemiplegic migraine
Abdominal migraine
65
Q

Symptoms of migraines

A

Unilateral
More severe
Throbbing in nature
Take longer to resolve

66
Q

Migraine associations

A

Visual aura
Photophobia and phonophobia
Nausea and vomiting
Abdominal pain

67
Q

Management of migraines in children

A 
Rest, fluids and low stimulus environment
Paracetamol 
Ibuprofen 
Sumatriptan 
Antiemetic, domperidone
68
Q

Migraine prophylaxis

A

Propanolol (avoid in asthma)
Pizotifen (drowsiness SE)
Topiramate: teratogenic

69
Q

Abdominal migraine

A 
Young children
Occur before the develop traditional migraines 
Central abdominal pain >1 hour
N/v
Anorexia
Headache
Pallor
70
Q

Sinusitis

A 
Headache
Inflammation in sinuses
Facial pain
Tenderness over affected sinuses
Sinusitis resolves within 2-3weeks 
Mostly viral
71
Q

Causes of neonatal hypotonia

A

Neonatal sepsis
Werdnig-Hoffman disease (spinal muscular atrophy TY1)
Hypothyroidism
Prader-Willi

Maternal drugs, e.g. benzodiazepines
Maternal myasthenia gravis

72
Q

Neurological conditions causing hypotonia

A

Central hypotonia:
Cerebral palsy
Brain and spinal cord injury
Serious infections; meningitis, encephalitis

Peripheral hypotonia:
Muscular dystrophy 
Myasthenia gravis
Spinal muscular atrophy
Charcot-Marie-Tooth disease: affects myelin
73
Q

Non-neurological causes of hypotonia

A 
Down’s syndrome
Prader-Willi
Tay-Sachs disease
Congenital hypothyroidism
Marfan syndrome and Ehlers-Danlos 
Connective tissue disorders
Premature
74
Q

Causes of hypotonia in larger life

A

Multiple sclerosis

Motor neurone disease

75
Q

Extradural haematoma pathophysiology

A

Collection of blood between skulls and dura
Caused by low-impact trauma
Collection in temporal region, pterion, middle meningeal artery
Haematoma expands
Uncus of temporal lobe herniates around tentorium cerebelli
Compression of parasympathetic fibres of CN3
Biconvex (or lentiform), hyperdense collection around the brain surface
Limited by suture lines of the skull

76
Q

Extradural haematoma presentation

A

Loses, briefly regains, loses again consciousness
After low impact head injury
Lucid interval
Fixed and dilated pupil from compression of parasympathetic fibres CN3

77
Q

Management of extradural haematoma

A

Craniotomy

Evacuation of haematoma

78
Q

Subdural haematoma pathophysiology

A

Collection of blood deep to dural layer of meninges
High-impact injury
Bridging veins
Crescent collection on CT
Midline shift or herniation
Shaken baby syndrome in infants as they have fragile bridging veins

79
Q

Subdural haematoma management

A

Surgical decompression with burr holes

80
Q

Subdural haematoma signs and symptoms

A

Confusion
Reduced consciousness
Neurological deficit

81
Q

Subarachnoid haemorrhage causes

A 
Head injury (traumatic SAH)
Absence of trauma (spontaneous SAH)
Intracranial aneurysm: Berry aneurysm, adult polycystic kidney disease, Ehlers-Danlos, coarctation of aorta 
AV malformation
Pituitary apoplexy 
Arterial dissection
Mycotic (infective) aneurysm 
Perimesencephalic (idiopathic venous bleed)
82
Q

Classic presenting feature of SAH

A 
Headache: thunderclap 
N/V
Meningism 
Coma
Seizures
Sudden death 
ECG changes: ST elevation
83
Q

SAH diagnosis

A

CT head: acute blood
Lumbar puncture: if CT negative, 12 hours following onset of symptoms to allow for Xa tho chronic to develop
Referral to neurosurgery

CT intracranial angiogram

84
Q

SAH treatment

A

Craniotomy and clipping
Bed rest
Control BP
Avoid straining to prevent re-bleed
21 days of nimodipine to treat vasospasm, treat with hyper volar is, induced-hypertension, haemodilution
Hydrocephalus is treated with external ventricular drain (CSF diverted into a bag at bedside) or long-term ventriculo-peritoneal shunt

85
Q

Complications of aneurysms SaH

A

Re-bleeding: most common in first 12 hours, need repeat CT
Vasospasm: delayed cerebral ischaemia, 7-14days after onset
Hyponatraemia: SIADH
Seizures
Hydrocephalus
Death

86
Q

Muscular dystrophy

A

Genetic conditions that cause gradual weakening and wasting of muscles

87
Q

Types of muscular dystrophy

A 
Duchennes muscular dystrophy
Becker’s muscular dystrophy
Myotonic dystrophy
Facioscapulohumeral muscular dystrophy
Oculopharyngeal muscular dystrophy
Limb-girdle muscular dystrophy
Emery-dreifuss muscular dystrophy
88
Q

Gowers sign

A

Technique to stand up from a lying position
Proximal muscle weakness
Pelvic weakness
Use hands on their legs to help them stand up

89
Q

Management of muscular dystrophy

A 
No curative treatment
Occupational therapy
Physiotherapy
Medical appliances 
Manage complications: spinal scoliosis and heart failure
90
Q

Duchennes muscular dystrophy pathophysiology

A

Caused by defective gene for dystrophin on the X-chromosome
Dystrophin helps hold muscles together at cellular level
X-linked recessive

91
Q

Duchennes muscular dystrophy presentation

A 
Boys present at 3-5years 
Weakness in muscles around pelvis 
Progressive weakness
Eventually all muscles will be affected
Wheelchair bound by teenage years
Life expectancy 25-35
Good management of cardiac and respiratory complications 
Associated with dilated cardiomyopathy
Calf pseudohypertrophy
92
Q

Duchennes muscular dystrophy management

A

Oral steroids: slow progression of muscle weakness as much as two years
Creatine supplementation: slight improvement in muscle strength
Genetic trials are ongoing

93
Q

Beckers muscular dystrophy presentation

A

Similar to Duchennes
Dystrophin gene is less severely affected and maintains some function
Symptoms appear 8-12years
Some patients require wheelchairs in their last 20s or 30s
Others able to walk with assistance into later adulthood
Management similar to Duchennes

94
Q

Features of myotonic dystrophy

A

Progressive muscle weakness
Prolonged muscle contractions
Cataracts
Cardiac arrhythmias

Unable to let go after shaking hand, unable to release doorknob grip

95
Q

Facioscapulohumeral muscular dystrophy

A

Usually presents in childhood with weakness around face
Progressing to shoulders and arms
Classic initial symptom: sleeping with eyes initially open, weakness in pursing their lips
Unable to blow their cheeks our without air leaking from their mouth

96
Q

Oculopharyngeal muscular dystrophy

A

Usually presents in late adulthood
Weakness of ocular muscles (around eyes)
Weakness of pharynx (around throat)
Typically presents with bilateral ptosis, restricted eye movements, and swallowing problems
Muscles around limb girdles are also affected to varying degrees

97
Q

Limb-girdle muscular dystrophy

A

Usually presents in teenage years

With progressive weakness around limb girdles (hips and shoulders)

98
Q

Emery-Dreifuss muscular dystrophy

A

Usually presents in childhood with contracture
Most commonly in the elbows and ankles
Contractures: shortening of muscles and tendons that restrict the range of movement in limbs
Patients also suffer with progressive weakness and wasting of muscles, starting with the upper arms and lower legs

99
Q

Raised intracranial pressure pathophysiology

A

Normal ICP is 7-15mmHg in adults in the supine position
Cerebral perfusion pressure is the net pressure gradient causing cerebral blood flow to the brain
CPP= mean arterial pressure - ICP

100
Q

RICP causes

A 
Idiopathic intracranial hypertension 
Traumatic head injuries 
Infection: meningitis
Tumours
Hydrocephalus
101
Q

RICP features

A 
Headache
Vomiting
Reduced level of consciousness
Papilloedema
Cushings trial: widening pulse pressure, bradycardia, irregular breathing
102
Q

RICP investigations and monitoring

A

Neuro imaging: CT/ MRI
Invasive ICP monitoring
Catheter placed into lateral ventricle of brain to monitor the pressure
May also be used to take collect CSF samples and also to drain small amounts of CSF to reduce the pressure
Cut-off of >20mmHg is often used to determine if further treatment is needed to reduce the ICP

103
Q

RICP management

A

Investigate and treat underlying cause
Head elevation to 30degrees
IV mannitol for osmotic diuresis
Controlled hyperventilation, reduce pCO2-> vasoconstriciton of cerebral arteries-> reduced ICP. Rapid, temporary lowering of ICP

Removal of CSF:
Drain from intraventricular monitor
Repeated lumbar puncture
Ventriculoperitoneal shunt

104
Q

Spinal muscular atrophy

A

Rare autosomal recessive condition
Progressive loss of motor neurones
Progressive muscular weakness
Affects LMN in spinal cord

105
Q

Spinal muscular atrophy signs

A 
LMN signs 
Fasciculations
Reduced muscle bulk 
Reduced tone
Reduced power
Reduced or absent reflexes
106
Q

SMA TY1

A

Onset in first few months of life

Usually progressing to death within 2 years

107
Q

SMA TY2

A

Onset within the first 18 months

Most never walk, but survive into adulthood

108
Q

SMA TY3

A

Onset after the first year of life
Most walk without support, but subsequently loose that ability
Respiratory muscles are less affected and life expectancy is close to normal

109
Q

SMA TY4

A

Onset in 20s
Most will retain ability to walk short distances
May require wheelchair for motility
Everyday tasks can lead to significant fatigue
Respiratory muscles and life expectancy aren’t affected

110
Q

Management of spinal muscle atrophy

A

MDT management
Physiotherapy: maximising strength in muscles and retaining respiratory function. Splints, braces and wheelchairs can be used to maximise function
Respiratory support with non-invasive ventilation, may be required to prevent hypoventilation and resp failure

SMA TY1: may require a tracheostomy with mechanical ventilation

Percutaneous endoscopic gastrostomy: unsafe swallow

Child Health (20 decks)

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