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ED fellowship paeds > Neuro > Flashcards

Neuro Flashcards

1
Q

Discuss diagnositc criteria for febrile siezures

A

1) Convulsion associated with an elevated temperauter greater than 38 degrees
2) a child older than 6 months and younger than 5 years
3) absence of CN infection or inflammation
4) Absence of acute systemic metabolic abnormality that my produce convulsions
5) no history of previous afebrile seizures

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2
Q

Discuss simple and complex febrile seizures

A

Simple

  • generalised tonic clonic seizure
  • duration of less than 15 minutes
  • complete recovery within 1 hour
  • do not recur within the same febrile illness

Complex

  • focal features at onset or during the seizure
  • duration greater than 15 minutes
  • incomplete recovery within 1 hour
  • recurrence within the same febrile illness

Recurrence rate depends on the age of the child; the younger the child at the time of the initial seizure, the greater the risk of a further febrile seizure (1 year old 50%; 2 years old 30%

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3
Q

Discuss criteria for discharge for febrile seizures

A
  • Returned to a normal neurological state following a simple febrile seizure
  • serious bacterial infection excluded or adequetly treated
  • underlying illness managed appropriately
  • patients aware of first aid advise and management of possible subsequent seizures
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4
Q

Discuss DDX of altered mental state in children

A

Vascular events

  • stroke
  • AVM with bleed

Infection

  • menigitis
  • sepsis
  • encephalitis

Trauma

Tox

Anatomic or structrual
-Mass or tumor

Metabolic derangements

GIT
-Intusseception

Seizures

AEIOU TIPS
A- ammonia, alcohol, atypical migraine, abuse 
E: electrolyte, epilepsy, encephalitis 
I: insulin (hypo), intussusception, inborn erros of metbaolism 
O- oxygen (hypoxia), opiates, overdose
U- uremia
T- trauma, tumor 
I: infection 
P: poisoning, psych 
S: seziure, sepsis, subarach
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5
Q

Discuss IX of altered mental state in children

A

Bedside: BGL and ECG
Bloods: FBC, LFT, U&E , VBG

Advanced imaging based on the presence of focal neurology and history and exam

Special consideration should be made regarding the need for more invasive diagnostic procedures such as lumbar puncture

In infants under 3 months the difficulties in assessing this population often necessitates are more thorough investigation. including urine and CSF sampling

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6
Q

Discuss caustive pathogens by age group for meningitis

A

Newborns: GBS, EColi, listeria monocytogens

Infants and children: Strep pneumo, N meningitidis, H influaenzae

Adolescents and young adults: N menigitidis, s. pneumo

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7
Q

Discuss Empiric AB by age

A

0-28 days -> Amp 50mg/kg TDS + Gentamycin 5mg/kg + Cefotaxime 50mg/kg TDS

28days - 3months: Amp or vanc + cefotaxime or ceftriazxone

> 3months: ceftriaxone + vanc

Aciclovir 10mg/kg or 500mg/m2

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8
Q

Define seizure (provoked vs non provoked) + define epilepsy

A

A paroxysmal event characterized by temporary involuntary changes in the patient cuased by abnormal and excessive activity of a group of cortical neurons.

They can be classified as unprovoked or provoked. Provoked have a clear identifiable trigger such as fever, metabolic derangement and trauma

Unprovoked seizures have no clear precedent

Epilepsy is commonly defined as the occurrence of two or more unprovoked seizures

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9
Q

Discuss DDX of seizures in children

A

Fever
- viral infection, menigitis, encephalitis, brain abcess

Trauma
- Cerebral contusion, haemorrhage, impact seizure (if occuring within 1 hour of impact does not signify significant underlying injury or risk of developing epilepsy)

Tox
-Drug intoxication or withdrawal

metabolic
-hypoglycaemia, hyponatraemia, hypernatraemia, hypomagnesemia, hypophosphatemia, hepatic or renal disorders, inborn errors of metabolism

Neoplastic

Vascular

  • AVM
  • Sub arach, cerebral venous thrombosis

Neurocutaneous
-neurofibromatosis, tuberous sclerosis, sturge weber syndrom

neurodegen

  • hypoxia
  • VP shunt malfunction
  • CP
  • derebral dysgenesis
  • primary epilepsy
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10
Q

Discuss episodic disorders that may mimic siezure activity

A
  • Breath holding spells
  • rigors
  • GORD
  • migraine
  • sleep disorders
  • ALTE
  • Panic attack
  • Psychogenic seizures
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11
Q

Discuss breath holding spells

A

Common in chlidren aged 6months to 6 years
occur when the child is frightened or distressed - minor accident or fright or when scolded
Most will have first episode of breath holding before 18 months and will grow out of them by the time they are six years old

Two main types
Blue spells ( cyanotic) - the child will
-cry and scream
-breathe out forecefully
-hold there breath and develop central cyanosis
-may become floppy and hav eLOC

Pale spells

  • Open mouth as if to cry but no sound comes out
  • faint and look very pale
  • have period where thier arms and legs become stiff or lose contgrol of thiere bladder and bowel
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12
Q

Define BRUE

A

Brief resolved unexplained event
Occurs in an infant less than 12 months
-duration >1 minute usually 20-30 seconds
- sudden onset accompanied by a return to a baseline state
-Characterized by >1 of the following
–Cyanosis or pallor
– Absent or decreased or irregular breathing
–marked change in tone
–Aletered level of conciousness

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13
Q

Discuss risk stratification for BRUE

A

Low risk occurs when there are no concerning features on history or exam and all of the following are met

  • > 60 days
  • born >32 weeks of gestation and corrected gestation age >45 weeks
  • no CPR
  • First event
  • event lasted < 1 minute
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14
Q

Discuss IX and disposition

A

Low risk BRUE does not require any investigation and can be safely discharged home with safety netting

If not low risk should be admitted for observation

  • ECG
  • NPA for viruses and pertusis
  • BGL
  • FBC and UEC if clinically indicated
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15
Q

Discuss management of seizure in childrenq

A

A: at risk of apnoea and hypoventialtion if siezure continue so prep for intubation and assistance
B: supllemental o2 should be applied aiming spo2 >94%
C: catious fluid due to risk of ICP
D: Treat hypoglycaemia with 2ml/kg of 10% dex
E: Treat hyponatraemia with 3ml/kg of 3% hypertnoic aiming to increase sodium by 3-7 mmol/l acutely and the rest slowly
Hypernatraemia is treated over 48 horus
Hypocalcaemia treated with 10% calcium gluconate 100mg/kg
Tox as per toxin – isoniazid is particualry resistant to standard anticonvulsants and should be treated with pyridoxine 1G IV for every gram of isoniazid

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16
Q

Discuss Treatment of status

A

Initial drug of choice is benzos
-Midaz 0.2 mg/kg IM, IN, buccal, 0.15mg/kg IV, can give 2 doses

After 2 doses of benzo risk of respiratory depression increases and second line should be given

Can use Levetiracetam, valproate or phenytoin as second line agent - ESETT and ConSEPT trials found all three to be equally efficacy and nil statistically signifaicnt increase in adverse effects for any of them

Levetiracetam at 40mg/kg as second line

In patient with ongoing siezures despite second line threapy preparation for continous infusions of midaz,prop or phenobarb should be readied – will need intubatuion

Use a different second line if patient already on antiepileptics and compliant

Non convulsive epilepsy is treated as above but more difficult to recognize and may need EEG for diagnosis

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17
Q

Discuss common causes of neonatal seizure

A 
Hypoxic ischaemic encephalopathy 
CNS infection 
Intracranial haemorrhage 
Trauma (accidental and non accidental) 
Cerebral infarction 
Chromosomal or congenital brain abnormalities 
inborn errors of metabolism or other metabolic derangements 
Drugs intox or withdrawals
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18
Q

Discuss IX of neonatal siezures

A 
BGL
FBC U&E
Metabolic testing
VBG
Ammonia

Because clinical assessment of rmeningitis is not reliable in young infants, lumbar punction should be performed and fluid sent for Cell, protein and glucose determinations, MCS + herpes simplex PCR

Advanced imaging should also be performed CT or MRI
In the unstable neonate a head ultrasound can be performed

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19
Q

Discuss management of neonatal seixzures

A

ABCD

Empirical antibiotics amp + gent + cefotaxime as well as acyclovir 20mg/kg TDS if herpes encephalitis is a clinical consern

Phenobarbital is the most common first line agent for neonatal seizures loading of 20mg/kg with additional 5mg/kg every 15-30 minutes to a max of 30mg/kg - can use benzo as first line particularly if there is to be a delay for phenobarb

NEOLEV2 trial showed superioty of phenobar to levirtarcetam as first line – if phenobarb failed seconda line agents are particularly poor and infants will likely progress to intubation - can use phenytoin, keprra or valproate

If refractory to all treatment pyridoxine 100mg IV should be considered

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20
Q

Discuss disposition for children with seizures ( non infant)

A

Most can be safely discharged home after appropriate invesitgation of first unprovoked seizure

2/3rds of children with a first unprovoked siezure never experience a recurrence - the risk of recurrence is increased with abnormalities in neuroimaging or EEG, family history of epilepsy, remote symptomatic seizure, first seizure occuring during sleep or Todds paralyis - if none of thees the 5 year recurrence i 21%

As such anticonvulsants are generally not started unless there are 2 unprovoked seizure

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21
Q

Discuss Red flags for headach presentation in children

A 
Sudden onset severe 
Occurrence with straining or exertion 
associated with neurological symptoms 
change in normal headache pattern 
nocturnal awakening
bilaterall occipital headaches
22
Q

Discuss DDX of secondary headaches

A

Trauma

  • Intracranial bleed
  • concussion
  • skull fracture

Structural

  • neoplasm
  • AVM
  • Congenital malformation
  • hydrocephalus

Systemic

  • HTN
  • Metabolic (Diabetes and ketoacidosis)
Infection 
-meningitis
abcsess
-encephalitis 
-sinusitis 
-influenza
-pyelo 
-GAS

Toxic

  • medications
  • ingestion
23
Q

Discuss Acute headaches

A

Common problem in children and adolescents and accompanies many infectious processes

In the absence of other signs of CNS involvement (nuchal rigidity, alteration in LOC, focal neurolgocial finding) headaches in febrile children usually do not constitute evidence of infection.

Although far less common AVM can be a trigger for a new severe headache - intracranail AVM are structually unstable and prone to rupture - in children with acute sudden onset headache in the absence of trauma ICH should be considered

Other DDX for acute headache include

  • Opthalmogic conditions
  • sinusitis
  • dentition
  • ottits media
24
Q

Briefly discuss acute weakness in children

A

Challenging presentation
in the preverbal child only symptoms may be regression in motor milestones
Ataxia can be the predominate feature

Trauma can present as weakness and NAI needs to be considered in appropriate circumstanes

INsepction should be mad for bites and ticks, rashes (enteroviral rashes are usually scattered macular papular but may be petechial or hand foot and mouth) investigation for signs of NAI should be made

25
Q

Describe Gowers sign

A

Sign indicative of proximal muscle weakness
child is lain on his or her back and asked to stand
positive sign is seen when the child does not sit up but rolls over onto her front gets up on all fours and then climbs to his or her legs using her hands

26
Q

List predictors of the necessacity for ICU level care with acute weakness

A

Bulbar pulsy -(lower motor lesion of CN 9,10,12)

  • absent gag reflex
  • toungue wasted and fasciculates
  • palatal movememtn absent
  • jaw jerk absent
Vital capacity <20 ml/kg
>30% reduction in vital capacity 
flaccid quadriparesis 
rapidly progressive weakness 
autonomic CVS instability
27
Q

Describe GBS

A

Acute polyradiculopathy. Group of diseases with two main pathological mechanisms

  • demyelination and axonal degeneration
  • Primarily lower MND affecting the myelin sheath with variable damage to axones.
  • It is a immune mediated reaction usually to a recent infection.
  • Common infection include (campylobacter, mycoplasma, EBV, coxsacki, influenzae, echovirus and CMV)
28
Q

Discuss clinical features of GBS

A

Usually present with weakness, falls regression of motor milsetones or ataxia.
Also commonly complain of muscle pain.
CN involvment in 50% of cases with 7th nerve being most common

Miller Fisher variant presents with oculomotor palsies, ataxia and areflexia.

Classic history is one of a generalised viral respiratory or GIT illness in the preceding 2 weeks. Parasethesia may be initial symptom followed by ascending and symmetrical weakness.
-papilloedema is rare but can occur in GBS
-paralysis of resp muscles is common and must be monitored for
Sympathetic nervous systme involvement can produce perfuse sweating, hypertension and disturbances of pshincter function.

Weakness may evolve rapidly wihtin hours but usually takes 1-2 weeks to reach max, then in the 2nd -4th week recovery is apparent with most having fully recovered in 2 months,

Painful ++ in children as compared to adults

29
Q

Discuss DDX of GBS

A 
Tick paralysis 
snake envenomation 
spinal cord lesions 
periodic paralysis 
infant botulism 
poisoning (lead, organophosphate) 
Vasculitis 
Myosisits 
Polio
30
Q

Discuss IX of GBS

A

Isolated protein in CSF is the classical finding

Nerve conduction studies characteristically show increased latency and conduction block.

31
Q

Discuss management of GBS

A 
ABCD
A: indications for intubation for GBS should be actively sort to avoid resp arrest and include 
-Vital capacity <20ml/kg
-Max inspiratory pressure <30 cm h2o
-max expiratory pressure <40cm h2o 
-tidal volume <5ml
-A sustained incrase of PCo2 
-A increased resp rate 
-increasing oxygen requirement 
-An increased use of accessory muscles and paraxocial diaphragm movement these reflex restrictive lung chest wall movement and low lung volumes.

Less emergent treatment include IVIG, plasma exchange

32
Q

Discuss infant botulism

A

Caused by release of the botulinum toxin into the bloodstream from clostridium botulinum bacteria.

Part of the toxin enters the terminal bouton of chjolinregic motor nerves and enzymatically disables the mechanisms by which ACH containing vesciles attach to the cell membrane.

Risk factors include exposure to honey in the first 6 months should not be exposed in the first year of life

Diagnosis is characterised

  • age group almost always less than 6 monhts
  • nature of onset: infants always start wtih bulbar pasies because that is where the blood supply is greatest; this is a descending paralysis
  • fatigability but lack of reversibility with edrophonium or neostigimine
  • absence of fever
  • absence of an altered mental status
  • absence of sensory defects
  • noraml CSF

Treatment is by supportive care and administartion of butulinum antitoxin. ABS are not recommended unless there is underlying secondary infection.
If ABS are used aminoglycosides should be avoided as they can make paralysis worse

Can also get botulism at a later date from consuption of food in which there is preformed toxin and from wound botulism (very rare)

33
Q

Discuss spinal cord lesions causing acute weakness in children

A

Transverse myelitis

  • Aetiology is uncertain, hypothesis include microbial antigen cross reaction with neural elements, bacterial superantigen inflammation and direct microbial invasion.
  • Usually hsa a rapid onset of predominantly lower limb weakness and altered sensation. Neck stiffness and fever are present early in most cases along with low back pain.
  • the sensory level is usually around the mid thoracic region below which pain light touch and temperature sensations are impaired.
  • Bladder and bowel disturbance is common
  • Tone is usually flaccid early in the illness with decreased reflexes
  • 60% of cases will achieve full recovery
  • MRI is IX of choice
  • Treatment complciated

SPinal cord space occupying lesions

CNS Tumors

AVM

  • usually occur in the thoracic region
  • may cause symptoms via compression or stealing circulation from the nearby cord
  • history is usually subacute unless a haemorrahge or ischaemia has intervened

Epidura abscess

  • rare in children
  • usual presentation is with back pain and rigidity, fever leucocytosis and a raised ESR
  • THese may be followed by spinal neurological signs
  • MRI is the investigation of choice
34
Q

Describe the basic hardware of CSF shunt

A

Proximal tube which take CSF from the lateral ventricle through brain tissue and a small burr hole to the outer surface of the skull

At or near this point there is usually a silicone reservoir dome that can be used for sampling and/or pumping.

Then there is a subcutaneous one way valve that is set to open at a certain pressure differential in order to avoid overshunting

The distal tubing is tunneled under the skin to the drainage site which is usually the peritoneal cavity

35
Q

Discuss complications associated with VP shunts

A 
Infection 
Malfunction 
-blocked proximal catheter
-blocked distal catheter
-loculation of lateral ventricle 
-vavle dysfunction 
-overshunting/slit ventricle syndrome 
-disconnection 
Abdominal pesudocyst 
migration of distal catheter
invasion of abdominal organs
36
Q

List signs and symptoms that on their own warrant immediate referral to neurosurgical services

A 
Buldging fontanelle
Decreased LOC 
FLuid tracking around shunt tubinh 
Signs of local infection (usually <6 months post operative)
-erythema of site
-erosion or ulceration 
-CSF leak 
-purulent drainage
Meingismus 
Peritonitis
37
Q

Discus signs and symptoms that may warrant refferal to neuro

A 
Abdominal pain 
Fever
Nausea/vomiting 
irritability 
headache 
abnormal shunt pump test 
Accelerated head growth
38
Q

Describe shunt evaluation

A

Hardware should if possible be palpated and inspected for signs of infection

Compressibility of the bulb should be test

  • incompressibility suggest distal obstruction (less common)
  • compressibility but nil refilling suggest proximal
  • Should avoid multiple test
39
Q

Discuss IX of VP shunt

A

On rare occasions needle insertion into the shunt pumping chamber is diagnostic and therapeutic- normally performed by neurosurg – May need to be done in ED for rapid deterioation in remote regions after discussion with neurosurg.

In the moribund child insertion of a 23 gauge buttfly needle at 45 degress can releive raised ICP.

Shunt series - XR of the entire shunt may demonstrate a disconnection or kinking causing blockage, Small positive studies and did not result in subsequent surgical intervention. Some ED do not do routinely

CT - preferred method of imaging.

40
Q

DIscuss presentation complaints for shunt infection and ABs of choice for same

A

Shunt malfunction 33%
fever 26%
Localised wound or shut tract inflammation 22%
abdominal pain or pseudocyts 19%

Staph epididymis is the most common causative agent and antibiotics regime should include fluclox + gram -ve cover

41
Q

Discuss briefly toxic neuopathies

A

Anticholinesterases

  • organophosphates and carbamates
  • inhibit cholinesterases allowing ach to persistently stimulate the nicotinic and muscarinic receptors which then can become refractory and thus cause weakness.
  • the weakness is usually accompanied by the cholinergic toxidrome and indeed it usually the respiratory and cardiac features that predominate.

Lead
-Lead mercury and arsenic are all known to cause neuropathies often taking the form of mononeuritis multiplex.

Chemo
-Vincristine, vinblastine and cisplastin are known to cause a peripheral neuropathy.

42
Q

Discuss breifly muscular disorders causing weakenss.

A

Infectious myositis

  • Viral infections such as influenza can cause a myositis that may may in its severest form lead to rhabdo
  • children may stop walking due to associated pain
  • weakness is only found on close examination

Juvenile dermatomyositis

  • systemic vasculitis though to be triggered by infection
  • enteroviruses and GAS
  • peak incidence is 6 years of age
  • The child may present with rash before weakness has become apparent.
  • the rash appears on sun-exposed areas especially malar region of the face and a purple discolouration of the eyelids
  • weakness come on about 2 months after the rahs and is usually very slow onset.
  • proximal muscles reveal weakness first.
  • the vasculopathy can affect any muscle group and children may present with aspiration dysphagia or hoarse voice.
  • Diagnosis is made on clinical picture associated with a raised CK. There are typical changes on biopsy and electromyogram

Metabolic/endocrine myopathies

  • Most endocrinopathies can produce weakness by several mechanisms
  • often this is just myalgia and fatigue but true myopathies can develop.
  • weakness usually responds to treatment of the underlying endocrine disorder

Periodic paralysis

  • Series of genetic ion channel disorders that leat to acute episodes of weakness lasting from 1 hour up to more than a day
  • they often come on after rest during sleep or immediately following exercise but never during
  • Diagnosis is made by mearsurement of electrolytes during an attack, response to metabolic challenge or by gene mutation identification.
43
Q

Discuss DDX of Ataxia in children

A

Post viral - acute cerebellar ataxia
Poisoning/drug intoxication

Tumours

  • -posterior fossa, brainstem
  • -paraneoplastic syndrome

Trauma including NAI

  • Haematoma
  • post concussion

Metabolic

  • hypoglycaemia
  • hyponatraemia
  • hyperammonaemia
  • inborn errors of metabolism

Infections

  • Meningitis - bacterial viral
  • Cerebral abcess
  • malaria
  • labyrinthitis
  • encephalitis

Vascular

  • stroke
  • vasculitis

Immune

  • MS
  • ADEM
44
Q

Discuss Acute cerebellar ataxia

A

Most common diagnosis of acute ataxia in children particularly between the ages of 2-7 years of age.

It is a diagnosis of exclusion after consideration of more sinister causes such as tumours.
An autoimmune aetiology is likley with autoantibodies demonstrated in acute cerebellar ataxia folowing infection with varicella, EBV, mycoplasma and huan parvovirus.

45
Q

Discuss clinical features of acute cerebellar ataxia

A

Usually present with sudden onset of severe gait ataxia though a small number of cases have an insidious onset

Most have dysarthric speech.
Mild horizontal nystagmus occurs in 50% of cases

Clinical findings of
-intention tremor
-dysdiadochokinesis, hypoptonia and decreased or pendular reflexes are seen in 2/3rds
Truncal ataxia is uncommon
-unlike MS or ADEM there are no focal neurological signs

Usually beings to improve within a few days but full recovery may take from 10 days to 2 months. Patients with slower recovery are still likley to fully recover

46
Q

Discuss IX of acute cerebella ataxia

A

Aimed at excluding an alternative diagnosis as there is no specific dianostic test for acute cerebellar ataxia

CT scan is usually normal
MRI may be abnormal
LP - slight elevation of CSF cell count by4-50 slight elevation in protein

47
Q

Discuss Toxic causes of ataxia

A

Anticonvulsants

  • phenytoin
  • carbamazepine

Alcohols

  • Ethanol
  • ethylene glycol
  • isopropanol

Essential oils
-eucalyptus oil

Illicit substances

  • PCP
  • LSD
48
Q

Discuss tumor as a cause of ataxia in children

A

Cerebella lesions may present with an acute rather than insidious onset of ataxia as a result of either haemorrhage into a tumour or as a result of hydrocephalus.

Paraneoplastic syndrome may also present as ataxia

Posterior fossa tumors including medulloblastoma, astrocytoma and ependymomom are common cases of ataxia from brain tumours.

Brainstem gliomas

Clinical features suggestive of a brain tumor include

  • headache
  • vomiting
  • behavioural changes
  • papilloedema
  • CN dysfunction
49
Q

Discuss other neurological conditions presenting with ataxia

A

1) GBS in which areflexia and opthalamoplegia (in Miller-Fisher) distinguish it from acute cerebella ataxia
2) MS/transverse myelitis - not usually seen until adolescent years - present with ataxia, optic or retinal neuritis, regional paraesthesia or weakness
3) ADEM
4) seizures
5) complex migraines

50
Q

Describe ADEM

A

Post-infectious encephalomyelitis is a demyelinating disease of the CNS that typically presents as a monophasic disorder associated with multifocal neurological symptoms

Encephalopathy is a required diagnositc features and usually develops rapidly in asscoaited with multifocal neuroglocail deficits including

  • acute hemiparesis
  • cerebella ataxia
  • CN neuropathies including optic neuritis and myelopathy

Severe phase of ADEM lasts from 2-4 weeks
Most children with ADEM have mean length of Hospital stay of 13-27 days

51
Q

Briefly discuss common causes of chronic ataxia

A

CP

HEREDITARY ATAXIAS
1) Firedreichs ataxia - an autosomal recessive condition which manifest in a child less than 10 years of age with atxai and nystagmus
Usually rapid progression

2)Ataxia telangiectasia is also autosomal recessive with neurocutaneous manifestations - ataxia is predominantly truncal and becomes evident in early childhood. Occular and cutaneous telangiectasia become evident between 2-6 yeas of age

CONGENITAL MALFORMATIONS

1) cerebella aplasia/hypoplasoa
2) Dandy-Walker malforamtion
3) Arnold-Chiari malformation or vemral palsia

52
Q

Discuss pertinent history and exam finding in the ataxic child

A

HX

  • timing of ataxia
  • acute, recurrent or chornic
  • what is mainly affected - trunk vs limbs
  • other sumptoms such as headache blurred vision altered mental status
  • antecedent history such as viral illness
  • other symptoms such as parasethesia - ADEM

EXAM

  • Cerebella signs
  • GAIT

ED fellowship paeds (15 decks)

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