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Neurology Flashcards

1
Q

What is cerebral palsy?

A

Abnormality of movement and posture
→ activity limitation attributed to non-progressive disturbances that occurred in developing fetal or infant brain

  • Term used for brain injuries up to 2yo
  • After this called acquired brain injury
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2
Q

What are motor disorders of CP often accompanied by disturbances in? (7)

A
  • Cognition
  • Communication
  • Behaviour
  • Perception
  • Sensation
  • Seizure disorders
  • Secondary msk problems
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3
Q

Causes of cerebral palsy?

A

80% antenatal in origin:

  • Vascular occlusion
  • Cortical migration disorders
  • Structural maldevelopment of brain during gestation
  • Genetic syndromes
  • Congenital infection

10% due to hypoxic­ischaemic injury during delivery:

10% postnatal in origin:

  • Meningitis/encephalitis/ encephalopathy
  • Head trauma from accidental or non­ accidental injury
  • Symptomatic hypoglycaemia
  • Hydrocephalus
  • Hyperbilirubinaemia
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4
Q

Early features of CP? (7)

A
  • Abnormal limb +/or trunk posture & tone in infancy
  • Delayed motor milestones
  • → May be accompanied by slowing of head growth
  • Feeding difficulties, with oromotor incoordination, slow feeding, gagging & vomiting
  • Abnormal gait once walking achieved
  • Asymmetric hand function <12m of age
  • Primitive reflexes may persist and become obligatory
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5
Q

3 types of CP?

A
  • Spastic (90%)
  • Dyskinetic (6%)
  • Ataxic (4%)
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6
Q

What is the sequence of normal motor development? With median and limit ages

A

Pushes up on arms and holds head up - 1.5m, 3m
Sits supported, head up with rounded back - 3m, 6m
Sits unsupported, arms free - 6m, 9m
Pulls to standing - 9m, 13m
Stands or walks independently - 12m, 18m

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7
Q

What is the commonest cause of developmental problems?

A

Cerebral palsy

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8
Q

What is spastic CP?

A
  • Damage to UMN (pyramidal or corticospinal tract) pathway
  • Limb tone increased (spasticity)
  • → Associated brisk deep tendon reflexes and extensor plantar responses
  • Tone in spasticity is velocity dependent→ faster muscle is stretched → greater resistance
  • This elicits a dynamic catch which is hallmark of spasticity
  • Increased limb tone may suddenly yield under pressure in ‘clasp knife’ fashion
  • Limb involvement described as unilateral or bilateral
  • Spasticity tends to present early - may be seen in neonatal period
  • Sometimes initial hypotonia, esp of head and trunk
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9
Q

3 types of spastic CP?

A

Hemiplagia
- Unilat involvement of arm and leg

Quadriplegia
- All 4 limbs affected, often severely

Diplegia
- All 4 limbs affected, but legs > arms

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10
Q

Features of hemiplegia in spastic CP?

A
  • Unilateral involvement of arm and leg
  • Arm affected > leg → face spared
  • Present at 4–12m of age with fisting of affected hand, flexed arm, pronated forearm, asymmetric reaching or hand function
  • Subsequently tiptoe walk (toe–heel gait) on affected side may show
  • Affected limbs may initially be flaccid + hypotonic → increased tone soon emerges as predominant sign
  • PMH may be normal - unremarkable birth history with no evidence of hypoxic-­ischaemic encephalopathy
  • In some, condition is caused by neonatal stroke
  • Larger strokes may cause hemianopia of same side as affected limbs
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11
Q

Features of quadriplegia in spastic CP?

A
  • All 4 limbs affected, often severely
  • Trunk involved with tendency to opisothonus (extensor posturing), poor head control and low central tone
  • Often associated with seizures, microcephaly and moderate/ severe intellectual impairment
  • May have been a hx of perinatal HIE
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12
Q

Features of diplegia in spastic CP?

A
  • All 4 limbs, but legs affected much more than arms
  • → Hand function may appear relatively normal
  • Motor difficulties in arms most apparent with functional use of hands
  • Walking is abnormal
  • Diplegia associated with preterm birth due to periventricular brain damage
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13
Q

What is dyskinesia and 3 types of dyskinetic movements?

A

Movements which are involuntary, uncontrolled, occasionally stereotyped, and often more evident with active movement or stress

Chorea – irregular, sudden and brief non­repetitive movements

Athetosis – slow writhing movements occurring more distally such as fanning of fingers

Dystonia – simultaneous contraction of agonist and antagonist muscles of trunk and prox muscles often giving twisting appearance

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14
Q

Other features of dyskinetic CP?

A
  • Intellect may be relatively unimpaired
  • Often present with floppiness, poor trunk control and delayed motor development in infancy
  • Abnormal movements may only appear towards end of 1st y of life
  • Signs due to damage/dysfunction in basal ganglia or associated pathways (extrapyramidal)
  • Past→ commonest cause hyperbilirubinaemia (kernicterus) due to Rh disease of newborn
  • Now → hypoxic­ ischaemic encephalopathy at term
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15
Q

Features of ataxic CP?

A
  • Most genetically determined
  • When due to acquired brain injury (cerebellum or connections), signs occur on same side as lesion but usually relatively symmetrical
  • Early trunk and limb hypotonia, poor balance and delayed motor development
  • Incoordinate movements, intention tremor and ataxic gait may be evident later
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16
Q

3 elements of CP management?

A

Physiotherapy

Drugs
- Diazepam as muscle relaxant

Orthopaedic surgery

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17
Q

Prevalence of epilepsy?

A

0.5%

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18
Q

Causes of epilepsy? (7)

A 
Idiopathic (70-80%)
Cerebral dysgenesis/malformation
Cerebral vascular occlusion
Cerebral damage eg congenital infection, HIE, IVH
Cerebral tumour
Neurodegenerative disorders
Neurocutaneous syndromes
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19
Q

Features of generalised seizures? (5)

A
  • Onset in both hemispheres
  • Always loss of consciousness
  • No warning
  • Symmetrical seizure
  • Bilaterally synchronous seizure discharge on EEG or varying asymmetry
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20
Q

Types of generalised seizures? (5)

A 
Absence
Myoclonic
Tonic
Tonic-clonic
Atonic
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21
Q

Features of absence seizures?

A
  • Transient loss of consciousness
  • Abrupt onset and termination
  • Unaccompanied by motor phenomena except for some flickering of eyelids and minor alteration in muscle tone
  • Absences may be typical (petit mal) or atypical
  • Often can be precipitated by hyperventilation
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22
Q

Features of myoclonic seizures?

A
  • Brief, often repetitive, jerking movements of limbs, neck or trunk
  • Non-epileptic myoclonic movements also seen physiologically in hiccoughs (myoclonus of diaphragm) or on passing through stage II sleep (sleep myoclonus)
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23
Q

Features of tonic seizures? (1)

A

Generalised increase in tone

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24
Q

Features of tonic-clonic seizures?

A
  • Rhythmical contraction of muscle groups following tonic phase
  • In rigid tonic phase, children may fall to ground, sometimes injuring themselves
  • They don’t breathe and become cyanosed
  • Followed by clonic phase, with jerking of limbs
  • Breathing irregular, cyanosis persists and saliva may accumulate in mouth
  • May be biting of tongue and incontinence of urine
  • Seizure usually lasts few secs→mins, followed by unconsciousness or deep sleep up to several hrs
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25
Q

Features of atonic seizures?

A

Often combined with myoclonic jerk, followed by transient loss of muscle tone causing sudden fall to floor or drop of head

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26
Q

Features of frontal focal seizures?

A
  • Involve motor or premotor cortex
  • May → clonic movements, which may travel proximally (Jacksonian march)
  • Asymmetrical tonic seizures can be seen, which may be bizarre and hyperkinetic and can be mistakenly dismissed as non­epileptic events
  • Atonic seizures may arise from mesial frontal discharge
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27
Q

Features of temporal lobe focal seizures?

A
  • Most common of all epilepsies
  • May result in strange warning feelings or aura with smell & taste abnormalities and distortions of sound & shape
  • Lip­smacking, plucking at clothing and walking in non­purposeful manner (automatisms) may be seen, following spread to pre­motor cortex
  • Déjà­vu and jamais­vu described (intense feelings of having been, or never having been, in same situation before)
  • Consciousness can be impaired and length of event longer than typical absence
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28
Q

Name a feature of occipital lobe focal seizures?

A
  • Cause distortion of vision
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29
Q

Name a features of parietal love focal seizures?

A
  • Cause contralateral 
dysaesthesias (altered sensation), or distorted body image
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30
Q

Ix used in epilepsy?

A 
EEG
MRI/CT - not routinely
Functional imaging - PET/SPECT
Metabolic Ix
Genetic Ix

Yet normally diagnosis is from detailed hx

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31
Q

First line treatment for

a) tonic-clonic
b) absence
c) myoclonic
d) focal seizures?

A

a) valproate
b) valproate, ethosuxamide
c) valproate
d) carbemazepine, lamotrigine

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32
Q

3 types of non-pharmacological treatment for epilepsy?

A

Ketogenic (fat) based diet
Vagal nerve stimulation
Surgery

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33
Q

Common SEs of

a) Valproate
b) Carbamazepine
c) Lamotrigine

A

a) Wt gain, hair loss, idiosyncratic liver failure (rare)
b) Rash, neutropenia, hyponatraemia, ataxia, liver enzyme induction
c) Rash

34
Q

What is status epilepticus?

A

Seizure lasting 30mins
or
Repeated seizures for 30mins without recover of consciousness

35
Q

RFs for SUDEP?

A

SUDEP = sudden unexpected death in epilepsy

RFs:

  • Poor seizure control
  • Seizures during sleep
36
Q

What % of children have a febrile seizure?

A

3%

  • 10% risk if first degree relative
  • 30-40% will have further episode
37
Q

Features of febrile seizure?

A
  • Occurs early in viral infection when temp rising rapidly
  • Seizures brief, and generalised tonic-­clonic seizures
  • About 30–40% will have further febrile seizures
38
Q

What factors increase risk of child having second febrile seizure? (4)

A
  • Younger child
  • Shorter the duration of illness before seizure
  • Lower temp at time of seizure
  • Positive FH
39
Q

Chance of developing epilepsy following febrile seizure?

A

1-2%
- Slight increased risk

Yet if complex seizure (focal, prolonged or repeated in same illness) –> 4-12% risk

40
Q

Examination/Ix for febrile seizure?

A

Look for cause of fever

  • Usually viral
  • Look for sx of bacterial e.g. meningitis
  • → Infection screen (inc blood cultures, urine culture and lumbar puncture for CSF) may be necessary
  • If child unconscious or has CV instability, LP CI and abx should be started immediately
41
Q

Management of febrile seizures?

A
  • Parents need reassurance and info
  • Advice sheets given to parents
  • Antipyretics not shown to prevent febrile seizures and tepid sponging no longer recommended
  • Family taught 1st aid management of seizures
  • If hx of prolonged seizures (>5min), rescue therapy with rectal diazepam or buccal midazolam supplied
  • Oral prophylactic anti­epileptic drugs not used as they do not reduce recurrence rate of seizures or risk of epilepsy
  • EEG not indicated as does not serve as guide for treatment; nor does it predict seizure recurrence
42
Q

Causes of non-epileptic seizures?

A 
Febrile seizures
Metabolic 
- Hypoglycaemia
- Hypocalcaemia/hypomagnesia
- Hypo/hypernatraemia
Head trauma
Meningitis/encephalitis
Poisons/toxins
43
Q

What are the causes of ‘funny turns’? (7)

A 
Breath holding attacks
Reflex anoxic seizures (head trauma, cold food, fright, fever)
Syncope
Migraine
Benign paroxymal vertigo
Cardiac arrhythmia
Paroxymal movement disorders
44
Q

What is a breath holding attack?

A
  • Occurs in some toddlers when upset
  • Child cries, holds breath and goes blue
  • May briefly lose consciousness
  • Recover rapidly
  • Drug therapy unhelpful
  • Behaviour modification e.g. distraction may help
45
Q

What is a reflex anoxic seizure?

A

Trigger event e.g. head trauma, cold food, fright or fever
Child becomes v pale and falls to floor
Hypoxia may induce tonic-clonic seizure
Episodes are due to cardiac asystole from vagal inhibition
Seizure is brief and child rapidly recovers
Ocular compression under controlled conditions often –> asystole and paroxysmal slow-wave discharge on EEG

46
Q

What do people with ataxia usually have difficulty with? (5)

A
  • Balance and walking
  • Speaking
  • Swallowing
  • Tasks that require high degree of control, e.g. writing and eating
  • Vision

→ Exact sx and their severity vary depending on type of ataxia a person has

47
Q

Features of cerebellar ataxia? (6)

A
  • Unsteady wide-based gait (truncal atxia)
  • Dysdiadochokinesis
  • Intention tremor
  • May be scanning dysarthria (speech problem)
  • May be +ve Romberg’s test
  • Nystagmus
48
Q

Types of ataxia?

A

Acquired

Hereditary

  • Friedreich ataxia
  • Ataxia telangiectasia

Idiopathic late onset cerebellar ataxia (ILOCA)

49
Q

Causes of acquired ataxia?

A

Acute

  • Post-infectious
  • Toxins
  • Tumours
  • Trauma
  • Vascular (stroke)

Recurrent

  • Toxin ingestion
  • Basilar artery migraine

Chronic

  • Brain tumours
  • Hydrocephalus
  • Nutritional
  • MS
50
Q

What is Friedreich ataxia?

A
  • Autosomal recessive condition
  • → Worsening ataxia, distal wasting in legs, absent lower limb reflexes but extensor plantar responses, pes cavus and dysarthria
  • Similar to hereditary motor sensory neuropathies, but impairment of joint position and vibration sense, extensor plantars and often optic atrophy
  • Cerebellar component becomes more apparent with age
  • Kyphoscoliosis & cardiomyopathy can → cardiorespiratory compromise and death at 40–50y
51
Q

What is ataxia telangiectasia?

A
  • Autosomal recessive condition
  • Mild delay in motor development in infancy and oculomotor problems (oculomotor dyspraxia), with difficulty with balance and coordination becoming evident at school age
  • Subsequent deterioration - dystonia and cerebellar signs
  • Many children require wheelchair for mobility in early adolescence
  • Telangiectasia develops in conjunctiva, neck and shoulders from 4yo
52
Q

Name the types of brain tumour? (5)

A 
Astrocytoma (40%)
Medulloblastoma (20%)
Ependymona (8%)
Brainstem glioma (6%)
Craniopharyngoma (4%)
53
Q

S+S of raised ICP in children and adolescents? (5)

A
  • Headache – worse in morning

  • Vomiting – esp on waking in morning
  • Behaviour/personality change

  • Visual disturbance

  • Papilloedema
54
Q

S+S of raised ICP in infants? (5)

A
  • Vomiting

  • Separation of sutures/tense fontanelle
  • Increased head circumference

  • Head tilt/posturing
  • Developmental delay/ regression
55
Q

Ix for brain tumour?

A

MRI

- Never do LP w/o neurosurgical advice if suspicion of raised ICP

56
Q

In what anatomical position is a brain tumour not safe to biopsy?

A

Brainstem

57
Q

What conditions can cause developmental regression? (5)

A 
Battens disease
Rett's syndrome
Leukodystrophies
Wilson's disease
Subacute sclerosis panencephalitis (SSPE)
58
Q

What is Battens disease?

A
  • Rare, fatal autosomal recessive neurodegenerative developmental regression disorder that begins in childhood
  • Sx occur 4-10y with gradual onset of visual problems and seizures
  • Progresses to change in behaviour, speech and regression in learning
  • May be a slow in growth and breath holding attacks
  • Eventually function will deteriorate to dementia and death
59
Q

Sx of leukodystrophies?

A
  • Group of conditions characterised by dysfunction of white matter of brain
  • Cause = incorrect growth of myelin sheath

Sx inc

  • Gradual decline in infant/child who was previously doing well
  • Progressive loss of movement, speech, vision, hearing and behaviour
60
Q

What is Wilson’s disease?

A
  • Autosomal recessive disorder
  • Incidence of 1/200,000
  • General result of condition is reduced synthesis of copper binding protein as well as defective excretion of copper in bile → accumulation of copper in liver, brain, kidney and cornea
  • Rarely presents in children <3y and can present with almost any form of liver disease including hepatitis, (fulminant or acute), cirrhosis and portal hypertension
  • Neuropsychiatric features more common after 2nd decade and inc deterioration in school performance, mood, behaviour and coordination
61
Q

3 types of hydrocephalus?

A

Obstructive
- Obstruction in ventricular system

Communicating

  • Failure to reabsorb CSF
  • CSF overproduction
  • Venous drainage insufficiency

External
- Absorption deficiency of infancy (self-limiting)

62
Q

Clinical features of hydrocephalus?

A
  • In infants (skull sutures not fused) head circumference may be disproportionately large or show XS rate of growth
  • Skull sutures separate, ant fontanelle bulges and scalp veins become distended
  • Advanced sign is fixed downward gaze or sun setting of the eyes
  • Older children –> S&S of raised ICP
63
Q

Ix for hydrocephalus? (3)

A

Cranial USS
CT/MRI
Head lentil measured on charts

64
Q

Treatment of hydrocephalus?

A

Ventriculo-peritoneal shunt

65
Q

When do anterior and posterior fontanelles close by?

A

Anterior - 12-18m

Posterior - 8w

66
Q

Definition and causes of microcephaly? (4)

A

→ Head circumference <2nd centile, may be:

  • Familial – present from birth and development often normal
  • Autosomal recessive condition – associated with developmental delay
  • Caused by congenital infection
  • Acquired after insult to developing brain, 
e.g. perinatal hypoxia, hypoglycaemia or meningitis, often accompanied by CP and seizures
67
Q

Definition and causes of macrocephaly? (9)

A

→ Head circumference >98th centile may be due to:

  • Tall stature
  • Familial macrocephaly
  • Raised ICP
  • Hydrocephalus – progressive or arrested
  • Chronic subdural haematoma
  • Cerebral tumour
  • Neurofibromatosis
  • Cerebral gigantism (Sotos syndrome)
  • CNS storage disorders eg mucopolysaccharidosis (Hurler syndrome)

→ Most are normal children and often parents have large heads

68
Q

What does rapidly increasing head size suggest?

A

Raised ICP

  • Hydrocephalus
  • Subdural haematoma
  • Brain tumour
69
Q

What is craniosynostosis?

A

Premature fusion of ≥1 sutures and may → distortion of head shape

70
Q

What are primary headaches and different types? (4)

A

Thought to be due to a primary malfunction of neurones

Types:
• Migraine
• Tension­-type headache
• Cluster headache (and other trigeminal autonomic cephalalgias)
• Other primary headaches (eg cough or exertional headache)

71
Q

Causes of secondary headaches? (8)

A
  • Head +/or neck trauma
  • Cranial or cervical vascular disorder – vascular malformation or intracranial haemorrhage
  • Non-vascular intracranial disorder – raised ICP, idiopathic HTN
  • Substance or withdrawal – alc, sovent or drug abuse
  • Infection- meningitis or encephalitis
  • Disorder of homeostasis – hypercapnia or HTN
  • Disorder of facial or cranial structures – acute sinusitis
  • Psychiatric disorder
72
Q

Features of tension-type headaches? (5)

A
  • Symmetrical headache
  • Gradual onset
  • Often described as tightness, band or pressure
  • Genetic predisposition
  • Usually no other sx
73
Q

Features of migraine w/o aura? (6)

A
  • 90% of migraine
  • Episodes may last 1–72 h
  • Headache commonly bilateral
  • Characteristically pulsatile, over temporal or frontal area
  • Often accompanied by unpleasant GI disturbance such as N+V/abdo pain and photophobia or phonophobia
  • Aggravated by physical activity
74
Q

Features of migraine with aura?

A
  • 10% of migraine
  • Headache preceded by aura (visual, sensory or motor), although aura may occur w/o headache
  • Absence of problems b/w episodes
  • Frequent presence of premonitory symptoms (tiredness, difficulty concentrating, autonomic features, etc.)
  • Most common aura = visual disturbance
  • Episodes usually last few hrs, → children often lie down in quiet, dark place
  • Sleep often relieves bout
  • Genetic predisposition
  • Bouts pos triggered by disturbance of biorhythms - late nights/early rises, stress, or winding down after stress at home or school
  • Certain foods, e.g. cheese, chocolate and caffeine, only rarely a reliable trigger
  • In girls, headaches can be related to menstruation and OCP
75
Q

Rescue treatments for headaches? (3)

A
  • Analgesia → paracetamol and NSAIDs taken early as pos in individual troublesome episode
  • Anti-emetics – prochloperazine and metoclopramide
  • Serotonin agonists eg sumatriptan – nasal preparation of this licensed for >12yo
76
Q

Prophylactic treatments for headaches? (3)

A
  • Pizotifen (5­HT antagonist) – can cause weight gain and sleepiness
  • Beta­blockers – propranolol; contraindicated in asthma
  • Sodium channel blockers – valproate or topiramate
77
Q

Red flag sx in headache for SOL? (5)

A

Worse on lying/coughing/straining
Wakes child up
Associated confusion
Associated morning or persistent nausea/vomiting
Recent change in personality, behaviour or educational performance

78
Q

Red flag physical signs in headache for SOL? (10)

A 
Growth failure
Visual field defects
Squint
Cranial nerve abnormality
Torticollis
Abnormal coordination - cerebellar lesion
Gait - UMN or cerebellar signs 
Papilloedema - late feature
Bradycardia
Cranial bruits - AV malformations
79
Q

How does a subdural haematoma occur?

A

Results from tearing of veins as they cross subdural space

  • Characteristic lesion in NAI caused by shaking or direct trauma in infants or toddlers
  • Occasionally seen after falling from considerable height
80
Q

How can you classify neuromuscular disorders (peripheral motor disorder)?

A

Disorders of anterior horn cell

  • SMA
  • Poliomyelitis

Disorders of peripheral nerve

  • Hereditary motor sensory neuropathies
  • Guillan Barre
  • Bell palsy

Disorders of neuromuscular transmission
- Myaesthenia gravis

Muscle disorders

  • Muscular dystrophies
  • Inflammatory myopathies
  • Myotonic disorders
  • Metabolic myopathies
  • Congenital myopathies
81
Q

Is neuropathy usually proximal or distal weakness?

Is myopathy usually proximal or distal weakness?

A

Neuropathy - usually distal

Myopathy - usually proximal

82
Q

Causes of a hypotonic infant?

A

Central – cortical

  • HIE
  • Cortical malformations

Central – genetic

  • Down syndrome
  • Prader-Willi syndrome

Central – metabolic

  • Hypothyroidism
  • Hypocalcaemia

Peripheral – neuromuscular

  • SMA
  • Myopathy
  • Myotonia
  • Congenital myasthenia

Paeds (15 decks)

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