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Paediatrics (Y4) > 11- Paediatric Neurology > Flashcards

11- Paediatric Neurology Flashcards

1
Q

seizures background

A

A sudden and temporary change in the electrical and chemical activity in the brain which leads to a change in a persons movement, behaviour, level of awareness and or feelings

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2
Q

causes of seizures

A
  • Epileptic seizure
  • Infection on the brain
  • Strokes
  • Tumours
  • Hypoglycaemia
  • Febrile convulsions
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3
Q

epileptic seizures vs other seizures

A
  • Epileptic when there is no apparent reason that the electrical and chemical activity has changed
  • More than 2 unprovoked seizures more than 24 hours apart
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4
Q

epilepsy background

A

Umbrella term for a condition where there is a tendency to have seizures.
- Seizures are transient episodes of abnormal electrical activity in the brain

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5
Q

types of epileptic seizures

A

Many types of seizures, with different treatments
o Generalised tonic-clonic seizures
o Absence seizure
o Atonic sieurs
o Myoclonic seizure
o Infantile spasm

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6
Q

epilepsy investigations

A

Good history – exclude vasovagal and identify type of seizure

EEG – can show typical patterns in different forms of epilepsy and support diagnosis

  • Perform EEG after the second simple tonic-clonic seizure
  • Children can have 1 simple seizure before being diagnosed with epilepsy

MRI brain can be used to visualise structure of the brain e.g. Exclude tumours.

  • When the first seizure is in a child under 2
  • Focal seizure
  • No response to first line anti-epileptic medications

Additional

  • ECG to exclude cardiac problem
  • Blood electrolytes
  • Blood glucose e.g. exclude hypoglycaemia
  • Blood cultures, urine cultures and LP
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7
Q

general precautions for people with epilepsy

A
  • Take showers rather than baths
  • Be very cautious with swimming unless seizures are well controlled and they are closely supervised
  • Be cautious with heights
  • Be cautious with traffic
  • Be cautious with any heavy, hot or electrical equipment
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8
Q

generalised tonic-clonic seizures backgroun

A
  • Classic epileptic seizure.
  • There is loss of consciousness and tonic (muscle tensing) and clonic (muscle jerking) movements.
  • Typically the tonic phase comes before the clonic phase.
  • There may be associated tongue biting, incontinence, groaning and irregular breathing.
  • After the seizure there is a prolonged post-ictal period where the person is confused, drowsy and feels irritable or low
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9
Q

management of tonic clonic seizures

A
  • First line: sodium valproate
  • Second line: lamotrigine or carbamazepine
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10
Q

absence seizures background

A

Absence seizures typically happen in children.

Presentation
- The patient becomes blank, stares into space and then abruptly returns to normal.
- During the episode they are unaware of their surroundings and won’t respond.
- These typically only lasts 10 to 20 seconds. Most patients (more than 90%) stop having absence seizures as they get older.

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11
Q

management of absence seizure

A

sodium valproate or ethosuximide

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12
Q

focal seizure background

A
  • Focal seizures start in the temporal lobes.
  • They affect hearing, speech, memory and emotions.
  • There are various ways that focal seizures can present:
    o Hallucinations
    o Memory flashbacks
    o Déjà vu
    o Doing strange things on autopilot
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13
Q

management of focal seizure

A

One way to remember the treatment is that the choice of medication is the reverse of tonic-clonic seizures:

  • First line: carbamazepine or lamotrigine
  • Second line: sodium valproate or levetiracetam
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14
Q

atonic seizures background

A
  • Atonic seizures are also known as drop attacks.
  • They are characterised by brief lapses in muscle tone.
  • These don’t usually last more than 3 minutes.
  • They typically begin in childhood. They may be indicative of Lennox-Gastaut syndrome.
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15
Q

Lennox-Gastaut syndrome

A

a severe condition characterized by recurrent seizures (epilepsy) that begin early in life.

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16
Q

management of atonic seizures

A
  • First line: sodium valproate
  • Second line: lamotrigine
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17
Q

Febrile convulsions

A
  • Seizures which occur in children during fever
  • Not caused by epilepsy or any neurological pathology
  • Between ages of 6 months and 5 yo
  • Prognosis: excellent
  • 1/3 will have another febrile convulsion
  • Slightly increases risk of epilepsy in future
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18
Q

breath holding spell

A
  • Involuntary episodes where child holds their breath, usually triggered by something upsetting or scaring them
  • 6-18 months
  • Child has no control over breath holding
  • Not harmful in long term and does not lead to epilepsy

Types
- Cyanotic breath holding spells
- Pallid breath holding spells (reflex anoxic seizures)

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19
Q

Cyanotic breath holding spells

A

occur when the child is really upset, worked up and crying. After letting out a long cry they stop breathing, become cyanotic and lose consciousness. Within a minute they regain consciousness and start breathing. They can be a bit tired and lethargic after an episode.

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20
Q

Reflex Anoxic Seizures

A

Reflex anoxic seizures occur when the child is startled. The vagus nerve sends strong signals to the heart that causes it to stop beating. The child will suddenly go pale, lose consciousness and may start to have some seizure-like muscle twitching. Within 30 seconds the heart restarts and the child becomes conscious again.

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21
Q

management of breath holding spells

A
  • Exclude other pathology
  • Reassure and educate parents
  • Links to iron def anaemia -> treat if required
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22
Q

general mangeemnt of epilepsy

A

Aim is to be on the minimum anti-epileptic medication to be seizure free. Ideally monotherapy.

MOA of anti-epileptics: raise the seizure threshold therefore reducing the likelihood of patients having a seizure-> requires titration

1) First line: Sodium valproate
2) Second line: Carbamazepine
3) Phenytoin
4) ethosuximide
5) lamotrigine

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23
Q

Sodium valproate

A

Most forms of epilepsy except focal
- MOA: Increases activity of GABA
Side effects
- Teratogenic (should be avoided in girls unless unsuitable for alternatives)
- Liver damage and hepatitis
- Hair loss
- Tremor

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24
Q

carbamazepine

A
  • Indication: Focal seizures
    Side effects
  • Agranulocytosis
  • Aplastic anaemia
  • Induced P450- drug inter
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25
Q

phenytoin

A

Side effects
- Folate and vit D def
- Megaloblastic anaemia
- Osteomalacia

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26
Q

Ethosuximide

A

Side effects
- Night terrors
- Rashes

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27
Q

Lamotrigine

A

Side effects
- SJS
- Leukopenia

28
Q

management of seizure

A
  • Put the patient in a safe position (e.g. on a carpeted floor)
  • Place in the recovery position if possible
  • Put something soft under their head to protect against head injury
  • Remove obstacles that could lead to injury
  • Make a note of the time at the start and end of the seizure
  • Call an ambulance if lasting more than 5 minutes or this is their first seizure.
29
Q

Status Epilepticus background

A
  • It is a medical emergency.
  • It is defined as a seizure lasting **more than 5 minutes **or 2 or more seizures without regaining consciousness in the interim.
30
Q

management of status epilepticus

A

In the hospital (take an ABCDE approach):
1) Secure the airway
2) Give high-concentration oxygen
3) Assess cardiac and respiratory function
4) Check blood glucose levels
5) Gain intravenous access (insert a cannula)
6) IV lorazepam, repeated after 10 minutes if the seizure continues
7) If the seizures persist the final step is an infusion of IV phenytoin. At this point intubation and ventilation to secure the airway needs to be considered, along with transfer to the intensive care unit if appropriate.
8) Rapid sequence induction with thiopental

Medical options in the community
- Buccal midazolam
- Rectal diazepam

31
Q

fainting/syncope

A
  • Transient loss of consciousness characterised by fast onset and spontaneous recovery
  • Caused by a reduced perfusion in the brain
  • Syncope is usually self-limiting- being horizontal will fix low blood pressure
  • Beware of people who have been held in an upright position

A syncopal fall describes a blackout and can be cardiovascular or neurogenic

32
Q

pathophysiology of fainting

A

to pump blood back to head

33
Q

causes of fainting/syncope

A
  • Cardiac
    o Arrhythmia
    o Postural hypotension /POTS
    o Hypertrophic cardiomyopathy
    o Cardiac failure
  • Non cardiac
    o Vasovagal
    -> Vagal activation causes vasodilation
    -> Stress/anxiety/ coughing/ pooing
    o Hypoglycaemia
    o Anaphylaxis
    o Shock
34
Q

investigations for syncope

A

Cardiac
- Rate
- Rhythm
- Murmurs
- ECG (24hr tape) e.g. long QTR Syndrome
- Lying and standing BP (postural hypotension)

Blood glucose

35
Q

History questions for syncope

A

– What they were doing at the time of the fall?
– Do they recall falling?
– Did they injure themselves?
– Did they feel dizzy or faint prior to falling?
– Has this happened before?
– How often do they fall?
– If a syncopal fall (blackout) did they bite their tongue or were incontinent of urine
– Beware of those that may be confabulating – do you need to check cognition prior to assessing?
– How quickly did they recover?
– How long were you on the floor for?

36
Q

Differentials of headaches

A
  • Haemorrhage
  • Meningitis
  • Tumour
  • Glaucoma
  • GCA
37
Q

types of headache

A

primary or secondary

38
Q

primary headache

A

due to the headache condition itself – will have normal clinical exam
- Non life-threatening or sight thretening

39
Q

secondary headache

A

will have a rash or neurological effect
- Life-threatening
 SoL (tumour or haemorrhage)
 Meningitis
- Sight threatening
 Giant cell arteritis
 Acute glaucoma

40
Q

examples of primary vs secondary headaches

A
  • In red requireds urgent referral to ENT
41
Q

red flags for headaches

A

SNOOP
* S – Systemic signs and disorders – meningitis or hypertension
* N – Neurological symptoms – glaucoma and SOL
* O – Onset new or changed and patient over 50 – brain metastases
* O – onset in thunderclap presentation – haemorrhage
* P – papilledema, pulsatile tinnitus, positional provocation precipitated by exercise – raised ICP

42
Q

examination required for headache

A
  • Must perform pull peripheral and CN examination and vital signs when pt presents with headache
43
Q

tension headache background

A
  • F>M
  • Common
  • Teenagers and adults
44
Q

RF for tension headache

A
  • Stress and mental tension are common triggers
  • Fatigue
45
Q

pathophysiology for tension headache

A
  • Due to tension in muscles of head and neck – occipitofrontalis
  • Unusual for >50 to have first onset
46
Q

presentation of tension-type headache

A

Normal clinical examination
Band like pattern of mild ache around head
Acronym
- S – bilateral frontal, sometime occipital – radiates to neck
- Q – squeezing like a band – non pulsatile
- I – mild to moderate
- T – worse at end of day, can be recurrent >15 in a month is chronic
- A – stress, poor posture, lack of sleep
- R – simple analgesia
- S – possible slight nausea

47
Q

management of tension type headache

A
  • Simple analgesia e.g. paracetamol and ibuprofen
  • Reduce stress -relaxing activities e.g. exercise, yoga and massage
  • Avoid dehydration
  • Cut down on caffeine
  • Change pillow
48
Q

migraine background

A

Migraines are a complex neurological condition that cause headache and other associated symptoms.

They occur in “attacks” that often follow a typical pattern.

There are several types of migraine:
- Migraine without aura
- Migraine with aura
- Silent migraine (migraine with aura but without a headache)
- Hemiplegic migraine
- Abdominal migraine

49
Q

Pathophysiology of migraine

A
  • Various mechanism and theories developed
  • No simple explanation for why migraines occur and it may be a combination of structural, functional, chemical, vasc and inflame factors
50
Q

Pathophysiology of migraine

A
  • Various mechanism and theories developed
  • No simple explanation for why migraines occur and it may be a combination of structural, functional, chemical, vasc and inflame factors
51
Q

presentation of migraine

A

Migraines present differently to tension headaches. Symptoms tend to be:

  • Unilateral
  • More severe
  • Throbbing in nature
  • Take longer to resolve
    Migraines are often associated with:
  • Visual aura
  • Photophobia and phonophobia
  • Nausea and vomiting
  • Abdominal pain
52
Q

management of migraines

A

Management
* Rest, fluids and low stimulus environment
* Paracetamol
* Ibuprofen
* Sumatriptan
* Antiemetics, such as domperidone (unless contraindicated)

53
Q

Prophylactic treatments to reduce severity for chronic migraine sufferers

A
  • Propranolol (avoid in asthma)
  • Pizotifen (often causes drowsiness)
  • Topiramate (girls with child bearing potential need highly effective contraception as it is very teratogenic).
54
Q

Meningeal layers

A

outside -> inside
Dura mater
Arachnoid
Pia Mater

55
Q

types of intracranial haemorrage

A
  • Extradural bleeds
    Can occur in children with TBI
  • Subdural bleeds
  • Subarachnoid haemorrhage
    Cerebral aneurysm- linked to ADPK, connective tissue disorder- why it can happen in younger patients
56
Q

risk factors for intracranial haemorrhage

A
  • Head injury
  • Hypertension
  • Aneurysms
  • Ischaemic stroke progressing to haemorrhage
  • Brain tumours
  • Anticoagulants
57
Q

investigations for intracranial bleeds

A
  • Glasgow coma scale
  • Imaging
    o CT
    o MRI
    o Angiography
58
Q

principles of management intracranial bleeds

A
  • Immediate CT head to establish the diagnosis
  • Check FBC and clotting
  • Admit to a specialist stroke unit
  • Discuss with a specialist neurosurgical centre to consider surgical treatment
  • Consider intubation, ventilation and ICU care if they have reduced consciousness
  • Correct any clotting abnormality
  • Correct severe hypertension but avoid hypotension
59
Q

Subdural bleeds

A

Background
- Outermost layer of meningeal layer (dura mater and arachnoid mater)

Pathophysiology
- Torn bridging veins
- Spontaneous in elderly or Alcoholic due to atrophy of brain
- Trauma

CT findings
- Crescent shape and not limited by cranial sutures)

60
Q

Extradural/epidural bleeds

A

Background
- Occurs between the skull and dura mater

Pathophysiology
- Rupture of the middle meningeal artery in temporo-parietal region e.g. associated with fracture of temporal bone

CT findings
- Bi-convex shape and limited by cranial sutures

Typical history
- Young patient with TBI that has ongoing headache
Presentation
- Prolonged headache after injury
- LOC and then lucid interval
Period of improved neurological symptoms and consciousness followed by rapid decline over hours as the haematoma get large enough to compress structures

61
Q

subarachnoid haemorrhage background

A
  • Bleeding into the subarachnoid space where CSF is located
  • Between pia mater and arachnoid membrane
  • A type of stroke 6%
  • Causes
  • Can occur in trauma
  • Usually spontaneous
  • High mortality and morbidity
62
Q

RF for subarachnoid haemorrhage

A
  • More likely in females(1.6:1)
  • More likely in black, Finnish and Japanese populations
  • Average age of onset is 50-55 yrs
  • Smoking, HTN, alcohol, cocaine
  • Fx
    Associations
  • Cocaine
  • SCC
  • Marfans or Ehlers danlos
  • Autosomal dominant polycystic kidney disease
63
Q

pathophysiology of subarachnoid haemorrhage

A
  • Ruptured cerebral aneurysm
64
Q

presentation of subarachnoid haemorrhage

A

Headache(48%) – thunderclap

  • Sudden onset
  • Often occurs during strenuous activity e.g. wright lifting or sex

Other features

  • Neck stiffness – irritation of meninges
  • Dizziness
  • Diplopia

Neurological:

  • Visual loss (anterior communicating artery aneurysm)
  • Weakness
  • Seizure
  • LoC
65
Q

investigations for subarachnoid haemorrhage

A

Investigations
First line: CT
* Hyper attenuation in subarach space due to blood

Lumbar puncture
* Only if CT head is negative
* RBC raised in CSF and Xanthochromia (yellow colour of CSF due to bilirubin)

Angiography (CT or MRI) – locate bleed

66
Q

Arteriovenous malformation (AVM)(10%)

A

Berry aneurysms

  • Aneurysms develop due to pressures on the arterial wall (vessels in subarachnoid space)
  • Usually at bifurcation points
  • Large cerebral arteries in anterior circle of Willis most affected
  • Intracranial arteries lack external elastic lamina and have thin adventitia
  • Small aneurysms(<5mm) unlikely to rupture
  • Risk factors for developing aneurysms (not conclusive)
  • Same as cardiovascular- hypertension, smoking etc
  • Alcohol++
67
Q

management of subarachnoid bleed

A

MDT approach in specialist neurosurgical unit

Anaesthetics
- If reduced consciousness: intubation and ventilation

Surgical intervention
* Repair vessel and prevent re-bleeding
1) Coiling (endovascular approach) or
2) Clipping- cranial surgery

Medical intervention
* Nimodipine – CCB
* Prevents vasospasm, preventing ischaemia
* Lumbar puncture or shunt to treat hydrocephalus
* Antiepileptic medication to treat seizures

Paediatrics (Y4) (42 decks)

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