Neurology Flashcards

1
Q

What would you examine on a kid with a headache? [6]

A
Growth parameters (height, weight, OFC, BP)
Sinuses & teeth
Visual acuity, fields and fundoscopy
Listen for cranial bruit
Focal neurological signs
Cognitive/emotional status
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2
Q

Headaches in kids fall into 4 groups:

A
  • Migraines
  • TTHs
  • Raised ICP
  • Analgesic Overuse
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3
Q

Pointers to childhood migraine
Site, character, duration
Associated sx [4]
Relieving [1]

A

Hemicranial, throbbing & pulsatile headache lasting 0.5-few hours
Associated abdominal pain, nausea, vomiting
Presence of an aura
Relieved by rest and quiet, often photo/phonophobic
Also useful to look for FH

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4
Q

How would you diagnose a tension type headache? [3]

A

Constant ache
Diffuse and symmetrical
Band like distribution

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5
Q

Management migraine
Acute attacks [2]
Preventative drugs if occurs 2 or more times a month [2]

A

Give them simple analgesics for acute attacks

  • NSAID
  • Nasal triptan in 12-17 yo

Preventative

  • Propranolol
  • Topiramate
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6
Q

TTH Mx
Principles [3]
Acute treatment, give 3 options
Prophylaxis [2]

A

Reassure the parent it’s nothing sinister. MDT: attention to underlying chronic physical, psychological or emotional problems. Encourage use of simple analgesia in acute attacks. Discourage chronic use of analgesics

  1. acute treatment: aspirin, paracetamol or an NSAID are first-line
  2. prophylaxis: NICE recommend ‘up to 10 sessions of acupuncture over 5-8 weeks’
  3. low-dose amitriptyline is widely used in the UK for prophylaxis against tension-type headache.
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7
Q

How would you spot a medication overuse headache [2]

A

High use of PCM/NSAIDs (more problematic if with compound analgesics e.g. cocodamol)

Pain returns before they can have another dose

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8
Q

What would be red flags of a raised ICP headache? [5]

A
  • Wakens them from sleep
  • Aggravated factors (these raise ICP) e.g. coughing, toilet straining or bending over
  • Altered conscious level, memory loss, cognitive loss
  • Focal neuro signs
  • Papilloedema
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9
Q

Headaches are diagnosed clinically, when would you want to use imaging? [6]

A

1) Cerebellar dysfunction e.g. ataxia
2) Raised ICP
3) New focal deficit e.g. new squint
4) Seizures
5) Personality change
6) Unexplained deterioration in schoolwork

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10
Q

Presentation of fits/falls/funny turns - differentials? [6]

A

1) Epilepsy
2) Acute Symptomatic seizures e.g. febrile convulsion
3) Reflex Anoxic Seizures
4) Syncope
5) Parasomnias e.g. night terrors
6) Psychogenic Seizures

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11
Q
Reflex anoxic seizures
Ep 
Define
Triggers [3]
Symptoms and signs [3]
Ix [2]
Mx
A

Ep: 6m/o-2y/o

Brief (15s) periods of asystole
Triggers: pain, anxiety, fear

Sy/Si:

  • Pallor +/- hypotonia
  • rigidity, upward eye deviation, clonic movements, urinary incontinence
  • but NOT tongue biting

Ix:

  • serum ferritin (ensure >50ng/mL)
  • if unsure of dx can refer to specialist for vagal excitation tests under continuous ECG and EEG monitoring

Mx: reassurance benign

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12
Q

What is an Acute Symptomatic Seizure or non-epileptic seizure?

Name 6 and indicate which is most common

A

A response to an acute insult e.g. hypoglycaemia, infection or hypoxia

Reflex anoxic seizure
Syncope
Parasomnias
Psychogenic seizures 
*Febrile Convulsion
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13
Q

What can you use to diagnose epilepsy? [7]

A

Mostly a clinical diagnosis!!!

  • History
  • Video recordings
  • ECG
  • Interictal/Ictal EEG
  • MRI (For malformations)
  • Genetics (Familial & single gene disorders e.g. Tuberous Sclerosis)
  • Metabolic tests if ass with developmental delay
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14
Q

Which cause and type of epilepsy is most common

A

Mostly it’s idiopathic

Mostly generalised

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15
Q

What factors are important when determining drug treatment for epilepsy? [4]

A
  • Age
  • Gender
  • Seizure type
  • Epilepsy type
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16
Q
Anti-epileptic drugs (AED) should only be considered if diagnosis is clear even if this means delaying treatment. What are the AEDs given for:
Tonic clonic [2]
Absence [2]
Myoclonic [2]
Partial
A
  1. Tonic clonic
    - Sodium valproate or lamotrigine
  2. Absence
    - Sodium valproate or ethosuximide
  3. Myoclonic
    - Sodium valproate or levetiracem

Partial: carbamazepine

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17
Q

What are the major SEs of Anti-Epileptic Drugs (AEDs)? [4]

A

CNS - Drowsiness, impacted learning, cognition & behaviour

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18
Q

Invasive procedures for epilepsy [2]

A

Some forms respond to Vagus Nerve Stimulation or Epilepsy surgery

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19
Q

What signs would suggest a neuromuscular disorder in a walking child? [4]

A
	Baby ‘floppy’ from birth
	Alert but paucity of limb movements
	Delayed motor milestones
•	Slips from hands
•	Able to walk but frequent falls
	Pes cavus (hammer) and waddling gait
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20
Q

What is pes cavus and hammer toes indicative of?

A

Charcot Marie Tooth Disease

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21
Q
How can you differentiate a neuropathy from a myopathy?
Site of weakness
Motor/sensory involvement
Reflexes
\+ 2 other distinguishing factors
A

Myopathy:

  • Proximal weakness
  • Purely motor
  • Preserved reflexes
  • Contractures
  • ~Myocardial dysfunction

Neuropathies:

  • Distal weakness
  • ~sensory involvement
  • Loss of reflexes
  • ~Fasciculations
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22
Q

List some of the major neuromuscular disorders in kids? [4]

A

Muscular dystrophies e.g. Duchenne’s
Spinal Atrophy
Myasthenia Gravis

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23
Q

How is Duchenne’s MD inherited? What gene mutation is involved?

A

X-linked –> female carriers and male suffers

Xp21 - the dystrophin gene

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24
Q

How would you expect Duchenne’s MD to present? [6]

Specific manifestation in teens [1]

A
Delayed gross motor skills
Symmetrical proximal weakness
Waddling gait
Calf hypertrophy
Gowers sign
~ Cardiomyopathy
Resp involvement in teens
25
Q

How do you confirm Duchenne’s? [2]

A

Gower’s sign (required but not specific)

Raised CK (>1000)

26
Q

How do we treat Duchenne’s?

A

Steroids

27
Q

Febrile convulsions
Define [2]
Ep
Ax [3]

A

Define:
- Event occurring in infancy or childhood associated with fever [1] but without evidence of intracranial infection or defined cause of seizure [1]
Ep: 3m/o-5y/o
Ax: viral infection, otitis media, tonsillitis

28
Q

Febrile convulsions

Describe the 2 forms that it can present with

A

• Simple:
- single tonic-clonic seizure lasting <15mins
- occurring as temperature rises rapidly in acute febrile illness
- brief post-ictal period of drowsiness/irritability/confusion
- full recovery within 1h
• Complex:
- partial onset or focal features (movement limited to 1 side of body or 1 limb)
- >15mins duration
- recurrence in 24h or within same febrile illness, seizure recurrence within 1h or prolonged post-ictal drowsiness or transient hemiparesis (Todd’s palsy)

29
Q

Management of febrile convulsions
Immediate [4]
Examinations [4]

A

o Monitor duration, protect from injury by cushioning head, check airway and place in recovery position when seizure stopped
o If seizure >5mins, give IM lorazepam?

o Observe until recovered and examine and manage any injury

Ex:

  • GCS, focal neuro deficit
  • temp post seizure (>38oC)
  • fluid status
  • signs of underlying febrile illness
30
Q

Febrile convulsions Ix [5]

A
FBC, ESR
Glucose
U&amp;E
Coagulation screen
Blood cultures and urine MC&amp;S if no source found
31
Q

Mx when confirmed dx febrile convulsion [6]

A

Parental advice and education

  • Not the same as epilepsy; risk child developing subsequent epilepsy
  • About 1 in 3 have another febrile seizure
  • Rare beyond 6 yo
  • First aid advice and call ambulance if >5min
  • PCM will not reduce seizure reccurrence but can make child more comfortable
32
Q

Features of seizures in a history
Preceding
During seizure [5]
Post seizure [2]

A

o Pre-ceding events and epileptic aura (olfactory or gustatory hallucinations, visual hallucinations (flashing lights, blurred vision), déjà vu feeling, sensory disturbance (numbness, tingling, burning))
o Eyewitness account of seizure: movements, duration (>20s), lateral tongue biting, incontinence, cyanosis (arrhythmias)
o Post-seizure: post-ictal confusion or agitation, secondary injuries

33
Q

Causes of epilepsy [6]

A
Idiopathic
Genetic
Brain malformation
Brain damage
Metabolic defects
Brain tumour
34
Q

Presentation of different types of epilepsy:

  1. Generalised
    - Name 3 types
  2. Focal - what are 3 clinical features?
A

Generalised

  • Tonic clonic
  • Absence
  • Myoclonic

Focal

  • Signs assoc to one hemisphere
  • Reduced consciousness
  • Automatisms eg lip smacking, running, rubbing face
  1. focal aware (previously termed ‘simple partial’)
  2. focal impaired awareness (previously termed ‘complex partial’)
  3. awareness unknown
35
Q

Describe the difference in presentations of generalized seizures

  • Tonic clonic
  • Absence [3]
  • Myoclonic [2]
A
  • Tonic clonic: limbs stiffen and jerk forcefully
  • Absence: 4-8yo, brief 10s pauses with loss of awareness, eyes may roll back
  • Myoclonic: 1-4 yo, fall to floor
36
Q
Brain tumour
Ax [2]
Sxs [3]
Ix 
Mx [3]
A

Ax: brainstem astrocytoma, medullablastoma
Sy/Si: unexplained headache, nausea and vomiting
Ix: MRI brain
Mx: surgical resection, chemotherapy, RT

37
Q

Brain tumour: describe presentation of raised ICP [3]

A

Diplopia
Papilloedema
Headache aggravated by Valsalva or wakes up

38
Q

What are other more long term symptoms that can point to a brain tumour [4]

A

diabetes insipidus (polydipsia and polyuria), growth disturbance or failure, delayed, arrested or precocious puberty

39
Q

Red flags (meningitis or encephalitis) [7]

A
  • Irritability
  • Neck stiffness
  • Petechial rash
  • Headache
  • Photophobia
  • Prolonged post-ictal period
  • Focal neurological deficit >1h
40
Q

Encephalitis
What is the main presenting symptom?
Aetiology can be divided into infective [11] and non-infective causes [8]

A

Main presenting symptom: altered consciousness

Ax:
• Infective: HSV, mumps, VZV, rabies, parvovirus B19, toxoplasmosis, TB, malaria, Lyme disease, Rikettsia, Dengue
o Immunocompromised: CMV, EBV, HHV-6
• Non-infective: hypoglycaemia, DKA, kernicterus, hepatic failure (Reye’s syndrome), lead or other poisoning, SAH, malignancy, SLE

41
Q

Encephalitis
Presentation
Symptoms [3]
Signs [2]

Management

Complications [4]

A

Flu like prodrome
Odd behaviour
Vomiting, fever

Focal neurological deficits
Reduced GCS

Mx: antimicrobials target at causative organism eg aciclovir for HSV

Cx: Kluver-Bucy syndrome (hyper sexuality, rage, visual agnosia), auditory agnosia, autism, amnesia

42
Q

Infant presents with abnormal head size and shape. What are your 2 top differentials

A

Hydrocephalus

Microcephaly

43
Q

Hydrocephalus
Congenital causes [5]
Acquired causes [5]

A

Congenital:

  • Arnold-Chiari malformation type 1 and 2
  • Bickers-Adams syndrome,
  • Dandy-Walker malformation
  • agenesis of foramen of Monro, Vein of Galen aneurysm
  • congenital toxoplasmosis

Acquired:

  • brain tumour
  • intraventricular haemorrhage
  • meningitis
  • increased venous sinus pressure (e.g. in achondroplasia)
  • iatrogenic, idiopathic
44
Q

Hydrocephalus
Classifications [2]`
Ix [2]

A
  • Communicating: failure to reabsorb CSF e.g. post bleed/infection, Arnold-Chiari malformation
  • Non-communicating: obstruction to CSF flow e.g. tumour, congenital malformation

Investigations:

  • USS through anterior fontanelle in infants
  • CT head
45
Q

Hydrocephalus

Presentation infants: signs [5], symptoms [3], name 2 special signs

A
Infants:
Signs
- Rapid increase in OFC or OFC > 98th centile
- Suture disjunction
- Dilated scalp veins
- Tense fontanelle
- increased limb tone
Symptoms
- irritability
- poor feeding
- seizures

Setting sun sign: both globes deviated downwards, upper lids retracted and white sclera visible above iris (failure of upward gaze)
Macewan’s sign: cracked pot sound on percussing head

46
Q

Hydrocephalus
Presentation in children:
- Describe an acute onset [4]
- Describe a chronic onset [4]

Mx
Complications [4]

A

Acute onset:

  • headache and vomiting
  • papilloedema
  • impaired upward gaze
  • seizures

Chronic onset:

  • unsteady gait (leg spasticity)
  • large head (although sutures closed
  • skull still enlarges due to chronic increased ICP)
  • unilateral or bilateral VI palsy due to increased ICP

Mx: ventriculopertitoneal shunt insertion
Cx: LD and epilepsy if untreated; shunt infection; CSF over-drainage

47
Q

Causes of microcephaly [7]

Definition

A

OFC <2nd centile

  • Normal variation (small child w/ small head)
  • Familial (parents w/ small head)
  • Congenital infection: toxoplasmosis, rubella, cytomegalovirus
  • Fetal alcohol syndrome
  • Hypoxic ischaemic encephalopathy (association w/ cerebral palsy)
  • Patau syndrome
  • Craniosyntosis
48
Q

Cerebral palsy
Definition [3]
Prenatal causes [4]

A

Def:

  • Permanent non-progressive (lesion static, clinical picture not) motor disorder
  • due to brain damage
  • before birth or before 2y/o

Prenatal:

  • Placental insufficiency
  • Toxaemia
  • Smoking, alcohol, drugs
  • TORCH2 infection
49
Q

Cerebral palsy
Perinatal causes [4]
Postnatal causes [2]

A

Perinatal:

  • Prematurity
  • Anoxia
  • Kernicterus
  • Erythoblastosis fetalis

Postnatal:

  • CMV or rubella infection
  • Head trauma
50
Q

Classification of CP [4]

State the affected part of the nervous system

A
  • Spastic (pyramidal system and motor cortex)
  • Athetoid/dyskinetic (extrapyramidal system (basal ganglia)
  • Ataxia (cerebellum and brainstem)
  • Other: rigid (basal ganglia and motor cortex), hemi ballistic, mixed
51
Q

Describe the gross motor function classification score (GMFCS)

A
  • I: walks w/out limitations
  • II: walks w/ limitations
  • III: walks using hand held mobility device
  • IV: self-mobility w/ limitations, may use powered wheelchair
  • V: transported in manual wheelchair
52
Q

Types of spastic CP [3]

A

Spastic CP:

  • Hemiplegia
  • Diplegia
  • Quadriplegia
53
Q

Presentation of:
hemiplegia spastic CP [3]
diplegia spastic CP [1]
quadriplegia [2]

A

o Hemiplegia: delayed walking, hand preference <1y/o, increased deep reflexes of affected limb
o Diplegia: scissor legs on picking up
o Quadriplegia: associated with seizures and reduced IQ

54
Q

Presentation of athetoid CP [4]

Presentation of ataxia CP

A

Athetoid:

  • unwanted movements and poor posture control
  • spasticity and hypotonia
  • reduced hearing, dysarthria
  • kernicterus association

Ataxia CP: hyper or hypotonia

55
Q

General clinical features of CP [4]

Investigations [3]

A
  1. Spasticity, contractures
  2. Lack of voluntary control, poor co-ordination
  3. Delayed walking
  4. Sensory impairment

XR, MRI, gait analysis

56
Q

Types of contractures [2] and the difference between them

A

Dynamic

  • Increased muscle tone
  • Hyperreflexia
  • No fixed deformity

Fixed muscle contracture

  • Persistent spasticity
  • Shortened tendon muscle units cannot be overcome
  • Fixed contractures with joint subluxation
  • Secondary bone changes
57
Q

Management of CP

  1. MDT [3]
  2. For spasticity [3]
  3. Ortho review [2]
A

MDT: Physiotherapy and OT, ortho scoliosis correction, posture management of hips and spine
Spasticity:
- Medication: Baclofen or diazepam
- Botulinum toxin injections
- Surgery: soft tissue release of adductors or hamstrings, bony realignment, osteotomy

Ortho review:

  • Annual exam
  • Hip XR
58
Q

Management of CP

Prognosis

A

persistence of >2 primitive reflexes suggests child will be non-ambulatory (moro startle reflex, parachute reflex, tonic neck reflex, neck righting reflex, extensor thrust)