Neurological Examination In Neonates, Infants, And Young Children, Including Those With Neurological Diseases
A systematic age-appropriate assessment of mental status, cranial nerves, tone, posture, primitive reflexes, developmental milestones, and motor function in young children to detect and characterize neurological abnormalities.
Neurological Examination in Neonates, Infants, and Young Children
This lecture (GC 148, by Dr. Sophelia Chan) is about adapting the standard adult neurological examination to patients who cannot cooperate, follow commands, or describe symptoms — neonates, infants, and young children. The fundamental challenge is: how do you systematically localise a neurological lesion in a patient who can't talk to you? The answer is a structured approach that relies heavily on observation first, then hands-on examination, and uses age-appropriate tools like primitive reflexes, postural reactions, and developmental milestones as neurological markers.
How This Fits Into Exams and Clinical Practice
- This is a core OSCE and written-exam topic. You may be asked to describe how to examine a neonate or infant neurologically, list primitive reflexes and their disappearance ages, differentiate UMN from LMN signs, or recognise raised ICP in a child. [1]
- It integrates with developmental milestones (CFB PAE02), paediatric emergencies (GC 145), seizures (GC 081), and "Where is the lesion?" (GC 094).
- Past papers repeatedly ask about parameters for general well-being of a child and neurological assessment — this lecture answers those questions directly. [2][3]
"Names, Games, Interacting, Parents' help, Warm hands, Praise, Gentle voice, Toys" [1]
Why This Matters
A frightened, crying child is un-examinable. If you can't calm the child, you get unreliable findings — increased tone from struggling, absent reflexes from distraction. Building rapport isn't just being nice; it's a clinical prerequisite. This is tested in OSCEs: examiners watch whether you engage the child before touching them.
Practical approach:
- Names: Learn the child's name AND what the parents call them (nickname). Use it.
- Games: Make the exam a game — "Let's see who can squeeze harder" (power testing).
- Parents' help: Let the child sit on a parent's lap. Parents can hold limbs for you.
- Warm hands: Cold hands = crying child = failed exam.
- Praise: Reward cooperation: "You're so brave!"
- Gentle voice: Never raise your voice. Speak softly, slowly.
- Toys: Use to assess visual tracking (CN II, III, IV, VI), fine motor (picking up small objects), and as distraction.
The exam has six components: (1) General Observation/Inspection, (2) Conscious State/Alertness, (3) Cranial Nerves, (4) Motor System, (5) Sensory System, (6) Cerebellar System [1]
This structure is identical in concept to the adult exam but the methods differ dramatically by age group. The lecture explicitly gives four age-based columns: Neonates, Infants, Younger Children, Older Children.
3. Age-Specific Examination — Detailed Breakdown
Check OFC and plot on centile chart; assess head shape; look for dysmorphism and deformity; examine skin and external genitalia [1]
| Component | What to Look For | Why It Matters |
|---|---|---|
| OFC (Occipitofrontal Circumference) | Measure and plot on centile chart | Microcephaly (below 2nd centile) → brain malformation, congenital infection, genetic syndrome. Macrocephaly (above 98th centile) → hydrocephalus, storage disease, familial |
| Head shape | Plagiocephaly, brachycephaly, scaphocephaly, craniosynostosis | Premature suture fusion restricts brain growth. Moulding from birth resolves; persistent asymmetry does not |
| Anterior fontanelle | Bulging → raised ICP. Sunken → dehydration. Size (normally closes 12–18 months) | Open fontanelle in neonates/infants is a unique clinical window — absent in older children and adults |
| Dysmorphism | Face, hands, feet, spine | Suggests genetic/chromosomal disorder (e.g., Down syndrome, Williams syndrome) — may explain neurological findings |
| Skin | Café-au-lait spots (NF1), hypopigmented macules/ash leaf spots (tuberous sclerosis), port-wine stain (Sturge-Weber), midline hairy patch over spine (spina bifida occulta) | Neurocutaneous syndromes are HIGH YIELD — the skin tells you about the brain |
| External genitalia | Ambiguous genitalia, undescended testes | Associated with certain genetic syndromes (Prader-Willi, congenital adrenal hyperplasia) |
| Older children additionally | Heart, abdomen examination | Hepatosplenomegaly in storage diseases; cardiac defects in syndromes |
AVPU: A = Alert, V = Responds to voice, P = Responds to pain, U = Unresponsive [1]
Glasgow Coma Scale (GCS) is modified for children ≤ 4 years [1]
Why two scales?
- AVPU is a rapid bedside screen — used in emergencies (the first 30 seconds of assessment).
- GCS provides a numeric score for monitoring trends over time and communicating severity.
Modified Paediatric GCS (from the lecture slides)
| Component | Response (≥ 4 years) | Score | Response (≤ 4 years) | Score |
|---|---|---|---|---|
| Eye Opening | Spontaneous | 4 | Spontaneous | 4 |
| To verbal stimuli | 3 | To verbal stimuli | 3 | |
| To painful stimuli | 2 | To painful stimuli | 2 | |
| No response | 1 | No response | 1 | |
| Verbal | Oriented and converses | 5 | Alert, babbles, jargoning, usual words | 5 |
| Confused conversation | 4 | Less than usual babbling/words | 4 | |
| Inappropriate words | 3 | Cries only to pain | 3 | |
| Incomprehensible sounds | 2 | Moans to pain | 2 | |
| No response | 1 | No response | 1 | |
| Motor | Obeys verbal commands | 6 | Spontaneous or obeys commands | 6 |
| Localises stimuli | 5 | Localises pain or withdraws to touch | 5 | |
| Withdraws | 4 | Withdraws from pain | 4 | |
| Abnormal flexion (decorticate) | 3 | Abnormal flexion (decorticate) | 3 | |
| Extension (decerebrate) | 2 | Extension (decerebrate) | 2 | |
| No response | 1 | No response | 1 |
Exam Trap: Paediatric GCS Verbal Scale
The verbal scale for ≤ 4 years is completely different from adults. "Alert, babbles, jargoning, usual words" = 5 (NOT "oriented"). Students lose marks by using adult descriptors for infants. Know that a pre-verbal infant who babbles normally gets a V5. [1]
Key thresholds:
- GCS ≤ 8 → intubate (cannot protect airway) [5]
- Decorticate posturing (flexion, GCS Motor 3) → lesion above red nucleus (cortical/subcortical)
- Decerebrate posturing (extension, GCS Motor 2) → lesion below red nucleus (brainstem) — worse prognosis
3.3 Cranial Nerves
The lecture presents a comprehensive CN review applicable to paediatrics. The key adaptation: in neonates and infants, formal CN testing is impossible — you rely on observation of spontaneous behaviour. [1]
| Age | What You Can Assess | Method |
|---|---|---|
| Neonate | Facial symmetry of expression; spontaneous eye opening; ptosis | Observe while crying, feeding, at rest |
| Infant | Symmetrical face on crying; eye opening; visual following; making sounds; feeding (bulbar function) | Observe + use a toy/light for tracking |
| Younger child | Symmetrical face; eye opening; visual follow; simple words; feeding | Observe + interactive games |
| Older child | Similar to adult cranial nerve exam | Formal testing possible |
| CN | Test | Key Points |
|---|---|---|
| I (Olfactory) | Smell testing | Rarely tested in young children; can use familiar scents |
| II (Optic) | Vision, fundal exam | In infants: fix and follow (from 3 months). Formal VA testing uses Sheridan-Gardiner or Cardiff cards. Fundoscopy for papilloedema (raised ICP) [6] |
| III, IV, VI | Pupillary response, visual acuity, visual field, eye movement | Track a toy/light. CN VI palsy is a false localising sign of raised ICP (stretches over petrous bone) [1] |
| V (Trigeminal) | Facial sensation (light touch), corneal reflex (with VII), jaw jerk (normally absent), muscles of mastication | Observe feeding (masseter function) in infants |
| VII (Facial) | Facial symmetry, smile, puff cheeks, close eyes, wrinkle forehead, taste (anterior tongue) | Observe for asymmetry during crying — this is the key infant test. UMN lesion spares forehead; LMN affects all |
| VIII (Vestibulocochlear) | Hearing: finger rubs, whispered words; Rinne & Weber | In neonates: startle response to sound. Formal audiometry later. Vestibulo-ocular reflex testing |
| IX (Glossopharyngeal), X (Vagus) | Palatal elevation ("Ahh"), gag reflex, posterior tongue | Observe swallow/feeding in infants |
| XI (Accessory) | SCM/trapezius | Shrug shoulders, turn head — only in cooperative children |
| XII (Hypoglossal) | Tongue bulk, fasciculation, deviation | Observe during feeding. Deviation → ipsilateral LMN lesion |
High Yield: CN VI as False Localising Sign
The 6th cranial nerve (abducens) palsy is a classic false localising sign of raised ICP. The nerve has a long intracranial course and is stretched when ICP rises, causing lateral rectus palsy (inability to abduct the eye). This does NOT mean the lesion is at the pons — it can be anywhere causing raised ICP. [1]
CNs V, VII, IX, X, XII: Dysarthria or dysphagia — If multiple lower CNs are affected, think bulbar palsy (LMN) vs pseudobulbar palsy (bilateral UMN). [1]
3.4 Motor System
This is the most complex and highest-yield section of the paediatric neurological exam.
Observe: Resting posture, active voluntary movement, muscle bulk [1]
| Finding | Significance |
|---|---|
| Frog-leg posture (hips abducted, knees flexed) | Hypotonia — LMN disease (e.g., SMA, neonatal myopathy) |
| Fisting beyond 3 months | Spasticity — UMN disease (e.g., cerebral palsy) |
| Asymmetric posture | Hemiplegia — unilateral brain lesion |
| Paucity of spontaneous movement | Either weakness (LMN) or depression of consciousness |
| Muscle bulk | Wasting → LMN/myopathy; Pseudohypertrophy (e.g., calf enlargement) → Duchenne muscular dystrophy |
Examine: Muscle tone, Deep tendon reflexes, Primitive reflexes (neonates/infants), Postural reactions (infants), Motor milestones [1]
Muscle Tone:
- Tested by passive movement of joints and feeling resistance
- Hypotonia ("floppy baby"): the child drapes over your hand during ventral suspension, has head lag on pull-to-sit
- Causes: SMA, congenital myopathy, Down syndrome, Prader-Willi, metabolic disorders, cerebellar disease
- Hypertonia: increased resistance to passive movement
- Spasticity (velocity-dependent, "clasp-knife") → UMN
- Rigidity (constant, "lead-pipe" or "cogwheel") → extrapyramidal
- In cerebral palsy: may present initially as hypotonia in infancy, then evolve to spasticity
Deep Tendon Reflexes (DTRs):
- Tested with a reflex hammer at the same sites as adults (biceps, triceps, knee, ankle)
- Hyperreflexia → UMN lesion
- Hyporeflexia/Areflexia → LMN lesion
- Clonus (sustained rhythmic jerking at ankle) → UMN lesion
Behaviour, Head control, Moro, Stepping, Galant, Ventral & Vertical Suspension [1]
-
Ventral suspension: Hold baby prone (face down) over your hand supporting the chest
- Normal neonate: head held momentarily in line with body, limbs slightly flexed
- Hypotonic baby: drapes limply like an inverted "U"
- Hypertonic baby: extends stiffly
-
Vertical suspension: Hold baby upright under the axillae
- Normal: baby held with legs slightly flexed
- Hypotonic baby: slips through your hands ("slip-through sign")
3 months: ventral and vertical suspension. 6 months: active weight bearing, lateral propping postural reaction. 12 months: forward parachute and a few steps of toddler gait. [1]
| Age | Motor Milestone | Neurological Significance |
|---|---|---|
| 3 months | Good head control in ventral and vertical suspension | Tests cervical motor function and tone |
| 6 months | Active weight bearing on legs; lateral propping (protective extension to sides) | Tests trunk stability, emerging postural reactions |
| 12 months | Forward parachute reflex; first steps (toddler gait) | Tests integration of motor, cerebellar, and vestibular systems |
Postural (Protective) Reactions:
- These are secondary reflexes that emerge as primitive reflexes disappear [4]
- Parachute reflex: infant held in ventral suspension and suddenly tilted forward → arms extend protectively
- Appears around 8–9 months; persists throughout life
- Asymmetric parachute → hemiplegia on the non-extending side
- Lateral propping: infant pushed gently sideways while sitting → extends arm to the side to prevent falling
- Appears around 6 months
- Absent/asymmetric → motor pathology
Primitive reflexes: most are gone by 6 months of age; ALL are gone by 1 year of age [1]
This is one of the most frequently examined topics in paediatrics.
| Reflex | How to Elicit | Normal Response | Disappears By | Clinical Significance |
|---|---|---|---|---|
| Stepping | Hold baby vertically, feet touching surface | Feet move in stepping motion | 2 months | Tests spinal cord and motor pathways |
| Rooting | Stroke cheek | Mouth turns to that side | 4 months | Tests CN V/VII and brainstem feeding circuits |
| ATNR (Asymmetric Tonic Neck Reflex) | Rotate infant's head to one side for 15 seconds | Extension of limbs on side turned to; flexion on opposite side ("fencing posture") | 4 months | Persistence beyond 4m → cerebral palsy or brain damage |
| Palmar grasp | Place finger in infant's palm | Flexion of fingers / makes fist | 4 months | Must disappear for voluntary grasp to develop |
| Moro | Sudden head drop / startle response | Symmetrical arm abduction then adduction with crying | 4–6 months | Asymmetric Moro → brachial plexus injury, hemiplegia, or clavicle fracture |
| Galant | Hold child prone, stroke along one side of spine | Trunk flexes toward stimulated side | 4–8 months | Tests thoracolumbar spinal segments |
| Plantar (Babinski) — extensor | Stroke sole of foot | Great toe dorsiflexes, other toes fan | Up to 1 year | Normal in infants (immature corticospinal tract). After 1 year, extensor = UMN |
High Yield: Primitive Reflex Key Rules
- Most primitive reflexes are gone by 6 months; ALL are gone by 1 year [1]
- Persistence beyond expected age → upper motor neuron pathology (e.g., cerebral palsy)
- Absence in a neonate → CNS depression (hypoxia, sedation, severe illness), neuromuscular disease
- Asymmetry of Moro reflex → brachial plexus injury (Erb's palsy), clavicle fracture, hemiplegia
- Primitive reflexes are lost in a cephalocaudal direction (head → feet) [4]
- Plantar extensor response (Babinski) is normal up to age 1 year — do NOT call it pathological in an infant!
Why do primitive reflexes exist? They are brainstem- and spinal cord-mediated reflexes present from birth because the corticospinal (pyramidal) tract is not yet myelinated. As myelination proceeds (cephalocaudal), the cortex gains inhibitory control over these reflex arcs, and they disappear. If the cortex is damaged (UMN lesion), it loses this inhibition, and primitive reflexes persist or re-emerge.
| Age | Assessment | Method |
|---|---|---|
| Neonate | Response to touch | Observe withdrawal, facial grimace, crying to tactile stimuli |
| Infant/Young child | Response to touch | Observe + gentle pin prick if tolerated |
| Older child | Light touch, pain, temperature, vibration, proprioception, cortical sensation (stereognosis, graphesthesia, two-point discrimination) | Formal adult-type testing |
Older children: Response to light touch, pain, temperature; Vibration, proprioception; Cortical sensation: stereognosis, tactile discrimination, graphesthesia [1]
Why is sensory testing limited in neonates? Because you cannot ask them what they feel. You can only observe their behavioural response to stimulation. This makes sensory localisation unreliable in very young children — another reason why motor and reflex testing are more important at this age.
| Age | Assessment | Method |
|---|---|---|
| Neonate | Nystagmus | Observe spontaneous eye movements |
| Infant/Young child | Coordination, hand tremor, nystagmus | Watch reaching for toys (dysmetria?), hand tremor |
| Older child | Finger-nose test, heel-shin test, rapid alternating movements, Romberg test, gait | Formal testing as in adults |
Gait assessment in older children: walking base, symmetry, stability, arm swing [1]
Romberg test: Stand with feet together, eyes closed. Positive = falls → implies proprioceptive or vestibular dysfunction (NOT cerebellar — cerebellar patients are already unsteady with eyes open).
This table is directly from the lecture and is extremely high yield [1]
| Feature | Upper Motor Neuron (UMN) | Lower Motor Neuron (LMN) |
|---|---|---|
| Muscle wasting | Minimal to mild | Prominent wasting |
| Muscle tone | Increased (spasticity) | Decreased (flaccidity) |
| Muscle power | Weakness | Weakness |
| Deep tendon reflexes | Hyperreflexia | Hyporeflexia / Areflexia |
| Clonus | Present | Absent |
| Babinski sign | Upgoing (extensor) | Downgoing (flexor) |
| Examples | Cerebral palsy, Stroke, Brain tumour, Congenital brain malformation | Muscular dystrophy, Myopathy, Spinal muscular atrophy, Peripheral neuropathy |
Exam Discriminator: UMN vs LMN
Students commonly confuse the tone findings. Remember: UMN = UP (tone UP, reflexes UP, Babinski UP). LMN = LOW (tone LOW, reflexes LOW, wasting prominent). The "U" in UMN = "Up". The "L" in LMN = "Low". [1]
Why does UMN cause hypertonia and hyperreflexia? The upper motor neuron (corticospinal tract) normally exerts inhibitory control on spinal reflex arcs. When the UMN is damaged, this inhibition is released → spinal reflexes become exaggerated (hyperreflexia), muscle tone increases (spasticity), and the Babinski reflex (which is normally suppressed in mature individuals) re-emerges.
Why does LMN cause hypotonia and wasting? The lower motor neuron is the "final common pathway" to the muscle. If it is damaged, the muscle receives no neural input → it wastes (denervation atrophy), tone drops (no tonic neural input), and reflexes are absent (the reflex arc is broken).
Symptoms and Signs of Raised ICP: Headache, Nausea and vomiting, Impaired conscious level, Papilloedema, 6th cranial nerve palsy (false localising sign), Bulging anterior fontanelle (young baby), Sunsetting eyes (young baby) [1]
| Feature | Explanation |
|---|---|
| Headache | Worse in morning (lying down increases venous return → ICP rises); worsened by coughing/straining |
| Nausea and vomiting | Due to pressure on the area postrema (vomiting centre) in the floor of the 4th ventricle. May be projectile |
| Impaired consciousness | Diffuse cortical dysfunction from compression; Cushing's triad (hypertension, bradycardia, irregular respiration) is a late, ominous sign |
| Papilloedema | Transmitted pressure along the optic nerve sheath → impedes axoplasmic transport and venous drainage from the retina → disc swelling. Takes hours-days to develop; NOT present in acute trauma |
| 6th CN palsy | False localising sign — long intracranial course makes it vulnerable to stretching when ICP rises |
| Bulging anterior fontanelle | Unique to infants — fontanelle is still open and acts as a pressure release valve. A tense, bulging fontanelle is an emergency sign |
| Sunsetting eyes | Unique to infants — downward deviation of eyes with sclera visible above the iris. Due to pressure on the tectum of the midbrain (upgaze centre) |
High Yield: Raised ICP Signs Specific to Young Babies
Bulging anterior fontanelle and sunsetting eyes are signs of raised ICP unique to young babies (i.e., before fontanelle closure). In older children, the skull is fused, so ICP rises more rapidly and presents with headache, vomiting, and papilloedema instead. Also remember: infants' skulls can expand (sutures are not fused), which provides some compliance — so ICP may rise more slowly, and signs can be subtle initially. Rapidly increasing head circumference crossing centiles should prompt urgent evaluation. [1][7]
Normal ICP values (from senior notes for reference):
- Adults: 10–15 mmHg
- Young children: 3–7 mmHg
- Infants: 1.5–6 mmHg
- Intracranial hypertension: ≥ 20 mmHg [7]
The lecture ends with four clinical cases shown via photos/videos. These represent the types of cases you may see in OSCE stations: [1]
| Case | Topic | What to Look For |
|---|---|---|
| Case 1: Dysmorphism | Genetic disorders and dysmorphic conditions | Facial features (epicanthic folds, flat nasal bridge, micrognathia, low-set ears), hand anomalies (single palmar crease, clinodactyly), syndromic patterns |
| Case 2: Abnormal postures and movement | Movement disorders, cerebral palsy, dystonia | Resting posture abnormalities, involuntary movements (choreiform, dystonic, athetoid), stereotypies |
| Case 3: Abnormal gait | Gait analysis | Hemiplegic gait (circumduction), diplegic gait (scissoring), ataxic gait (wide-based), Trendelenburg gait (hip abductor weakness), toe-walking (spasticity or habit) |
| Case 4: "What is the positive sign?" | Identifying specific clinical signs | Could be Gowers' sign (Duchenne), Babinski sign, Romberg sign, or any physical sign demonstrated in a video |
OSCE Tip: Gowers' Sign
Gowers' sign — child rises from the floor by "climbing up their own legs" (hands pushing on thighs). This indicates proximal muscle weakness, classically seen in Duchenne muscular dystrophy (X-linked, progressive, pseudohypertrophy of calves, CK massively elevated). If you see this on an OSCE video, mention Duchenne first. [4]
| Domain | Neonate | Infant | Younger Child | Older Child |
|---|---|---|---|---|
| General | OFC, head shape, fontanelle, dysmorphism, skin, genitalia | Same + face, hands, feet, spine | Same | + Heart, abdomen |
| Consciousness | Alertness, responsiveness | Alertness, responsiveness | Alertness, behaviour, understanding | GCS, orientation, MMSE |
| Cranial Nerves | Facial symmetry, eye opening, ptosis | + visual follow, bulbar sounds, feeding | + simple words | Full adult CN exam |
| Motor | Resting posture, active movement, tone, DTR, primitive reflexes | + muscle bulk, postural reactions, gross & fine motor milestones | + no primitive reflexes; milestones | + formal muscle power (MRC) |
| Sensory | Response to touch | Response to touch | Response to touch ± light touch/pain | Full adult sensory exam |
| Cerebellar | Nystagmus | Coordination, tremor, nystagmus | Same | Finger-nose, heel-shin, RAM, Romberg, gait |
8. Integration With Related Material
Motor milestones ARE neurological markers. Failure to meet milestones is often the first sign of neurological disease. Key milestones to remember:
- Head control: 3 months
- Sitting unsupported: 6 months
- Walking: 12 months
- Running: 18–24 months
- Most common neurological disorder of infants/children (2–5% of all children)
- Simple vs complex febrile seizures — know the distinction [8]
- Neurological exam is essential to exclude CNS infection (meningitis signs: bulging fontanelle, neck rigidity)
The purpose of the neurological examination is localisation. Once you find UMN or LMN signs, you apply the lesion localisation framework:
- UMN signs → lesion is above the anterior horn cell (brain, brainstem, spinal cord above the relevant level)
- LMN signs → lesion is at or below the anterior horn cell (anterior horn cell, nerve root, peripheral nerve, NMJ, or muscle)
When examining a child for "seizures," remember the differential:
- Neonates: jitteriness, hyperekplexia, benign neonatal sleep myoclonus
- Infants: breath-holding spells (cyanotic and pallid)
- Children: syncope, migraine, staring spells
9. Likely Exam Questions
Q1: "List the primitive reflexes in a neonate and the age at which each disappears." → Markscheme: Stepping (2m), Rooting (4m), ATNR (4m), Palmar grasp (4m), Moro (4–6m), Galant (4–8m), Plantar extensor (up to 1 year). State that most gone by 6 months, ALL gone by 1 year.
Q2: "A 3-month-old infant is brought in with poor feeding and decreased movement. On examination, the baby is hypotonic with absent deep tendon reflexes. Differentiate between UMN and LMN signs." → Markscheme: Table of UMN vs LMN (tone, reflexes, wasting, clonus, Babinski). This baby has LMN signs. Differential includes SMA, congenital myopathy, peripheral neuropathy.
Q3: "List signs of raised intracranial pressure in a 4-month-old infant." → Markscheme: Bulging anterior fontanelle, sunsetting eyes, irritability, poor feeding, vomiting, increasing head circumference, impaired consciousness, 6th nerve palsy.
Q4: "What parameters obtained during physical examination could be used as an indicator of the general well-being of a child?" (Past paper Q — appeared in 2016 and 2018 SAQs [2][3]) → Markscheme: Growth parameters (weight, height/length, OFC), vital signs (HR, RR, BP, temperature, SpO2), hydration status, nutritional status, skin colour/perfusion, level of alertness/activity, developmental milestones, presence/absence of dysmorphic features.
Q5: "In the paediatric neurological examination, how do you assess motor function in an infant?" → Markscheme: Observe resting posture, spontaneous active movement, muscle bulk. Examine tone (passive movement, ventral/vertical suspension), DTRs, primitive reflexes (list with ages), postural reactions (parachute), and motor milestones (gross and fine).
- "Demonstrate examination of primitive reflexes" — show Moro, palmar grasp, stepping, ATNR, rooting on a doll/simulated infant
- "This child has been referred for developmental delay. Perform a focused neurological examination." — structured approach through all six components
- "Interpret this examination video" — identify Gowers' sign, hemiplegic gait, dystonic posturing, nystagmus
| Year | Question | Relevant Content |
|---|---|---|
| 2016 SAQ Q10 | "Parameters for general well-being of a child" | OFC, growth, vitals, alertness, skin, milestones [2] |
| 2018 SAQ Q2 | Same question repeated | Same markscheme [3] |
| Various MCQs | UMN vs LMN differentiation | Lecture slide table [1] |
| Various MCQs | Primitive reflexes and disappearance age | Lecture slide table [1] |
| OSCE stations | Neurological examination of infant | Full structured approach from this lecture [1] |
Active Recall - Lecture Notes
High Yield Summary
Core principles: (1) Paediatric neuro exam = observe first, then examine. (2) Six components: general inspection, consciousness, cranial nerves, motor, sensory, cerebellar. (3) Primitive reflexes: most gone by 6 months, ALL by 1 year — persistence = UMN pathology. (4) UMN = tone UP, reflexes UP, Babinski UP; LMN = tone LOW, reflexes LOW, wasting prominent. (5) Raised ICP in infants: bulging fontanelle, sunsetting eyes, increasing OFC — CN VI palsy is a false localising sign. (6) Always check OFC and plot on centile chart. (7) Modified paediatric GCS: verbal scale differs for children ≤ 4 years. (8) Motor milestones are neurological markers: 3 months = head control, 6 months = sitting/propping, 12 months = walking/parachute. (9) Neurocutaneous syndromes: skin findings = brain pathology (café-au-lait → NF1, ash-leaf → TS, port-wine → Sturge-Weber). (10) Past paper favourite: "parameters for general well-being of a child" — know growth, vitals, hydration, alertness, milestones, dysmorphism.
[1] Lecture slides: GC 148. Neurological examination in neonates, infants, and young children, including those with neurological diseases.pdf (all pages) [2] Past papers: 2016 Fourth Summative SAQ.pdf (Question 10) [3] Past papers: 2018 Fourth Summative SAQ.pdf (Question 2) [4] Senior notes: Adrian Lui Pediatrics Notes.pdf (p105, Chapter 4 — Neurology) [5] Senior notes: Maksim Surgery Notes.pdf (p352-353, TBI and GCS) [6] Senior notes: Ryan Ho Opthalmology.pdf (p108-109, Paediatric Ophthalmology) [7] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (p1117, Increased ICP) [8] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai).pdf (p477-487, Non-epileptic paroxysmal disorders, Febrile seizures)
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