GC148 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.
"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 accurately, plot on an age- and sex-appropriate chart, and compare with previous measurements and parental head size | A single extreme value needs confirmation; crossing centile spaces or a disproportionate head-growth trajectory is usually more informative than one cut-off |
| 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:
- A GCS of 8 or less is coma and an airway emergency, but GCS is not a stand-alone proxy for airway reflexes. Obtain senior anaesthetic/resuscitation help; intubation is indicated for coma, loss of protective reflexes, ventilatory failure, irregular breathing, or safe transfer of a severely head-injured child. [5]
- Abnormal flexion (M3) and abnormal extension (M2) indicate severe brain dysfunction. The traditional “above versus below the red nucleus” rule is an oversimplification at the bedside; describe the response, trend it, and localise using the whole examination and imaging.
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) | Visual behaviour, fields when feasible, pupils (afferent limb), fundus | In infants, observe fixation, following and visually directed reaching; choose age-appropriate optotype or preferential-looking tests. Fundoscopy is important when raised ICP is suspected, but a normal disc does not exclude it. [6] |
| III, IV, VI | Pupillary responses and ocular alignment/movements | Track an interesting target through the full range. A VI palsy may be a false-localising sign of raised ICP, but also has local ocular motor, brainstem and nerve causes. [1] |
| V (Trigeminal) | Facial sensation, muscles of mastication, corneal reflex | Corneal reflex: V1 afferent and VII efferent. The jaw jerk is often absent or slight; a brisk response supports bilateral corticobulbar disease. |
| VII (Facial) | Facial symmetry and movement; taste from anterior two-thirds of tongue when relevant | Observe for asymmetry during crying. Forehead sparing can support a supranuclear pattern, but is not an infallible rule. |
| VIII (Vestibulocochlear) | Hearing and vestibular function | Behavioural response to sound is a screen, not a substitute for age-appropriate audiology. In cooperative children the slide's “Whine and Weber” is a typo: Rinne and Weber. |
| IX (Glossopharyngeal), X (Vagus) | Voice, palate and swallow; taste from posterior one-third when relevant | Observe voice, secretion handling and feeding. The gag reflex is variable, unpleasant and not a useful routine stand-alone screen of safe swallowing. |
| 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
A 6th cranial nerve (abducens) palsy can be a false-localising sign of raised ICP. Its long intracranial course makes it vulnerable to displacement, producing an abduction deficit. Do not assume a pontine lesion—but do not assume raised ICP either; interpret it with headache/vomiting, consciousness, optic discs, other cranial nerves and imaging. [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) | Supports hypotonia, which may be central, peripheral or systemic; it does not localise to LMN by itself |
| Persistent fisting or early hand preference | Concerning when marked, asymmetric or accompanied by abnormal tone/movement; not diagnostic of spasticity alone |
| Asymmetric posture or movement | Localise with tone, reflexes and function; consider central motor disease, peripheral injury, pain and musculoskeletal restriction |
| Paucity of spontaneous movement | Consider weakness, altered consciousness, pain, sedation and systemic illness |
| Muscle bulk | Wasting suggests chronic denervation or myopathy. Calf pseudohypertrophy suggests a muscular dystrophy pattern—classically Duchenne, but not specific to it |
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]
| Slide age | Illustrated task | 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 reaction; a few independent toddler steps | Tests integration of motor, cerebellar, sensory and vestibular systems |
These slide panels are illustrative checkpoints, not pass/fail deadlines. Ask what the child can do across all domains, observe the quality and symmetry of movement, look for loss of previously acquired skills, and use corrected age for a preterm child during early developmental assessment. Milestone checklists support surveillance but are not validated diagnostic screening tests. [9][10]
Postural (Protective) Reactions:
- These are secondary reflexes that emerge as primitive reflexes disappear [4]
- Parachute reaction: with the infant securely supported, the examiner gently lowers/tilts the body toward a surface → arms extend protectively; never simulate a fall or release the child
- Appears around 8–9 months; persists throughout life
- An asymmetric response raises concern for hemiplegia or local upper-limb pain/weakness 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
- Persistent absence or asymmetry outside the expected developmental range warrants fuller motor/developmental assessment
The slide's useful shorthand is that most primitive reflexes integrate in the first 6 months. The categorical statement that all are gone by 1 year is too rigid: reported timing varies with method, gestation and the individual reflex, and an extensor plantar response may remain physiological beyond the first birthday.
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) | Gently turn the infant's head to one side | Extension on the face side with relative flexion on the occiput side ("fencing posture") | Around 4–6 months | Marked obligatory, asymmetric or persistent response is more concerning than a single age boundary |
| Palmar grasp | Place finger in infant's palm | Flexion of fingers / makes fist | 4 months | Must disappear for voluntary grasp to develop |
| Moro | In a securely supported infant, a trained examiner produces a small, controlled head–trunk extension/startle; never allow an unsupported head drop | Symmetrical arm abduction/extension followed by adduction/flexion, often with crying | 4–6 months | Asymmetry suggests brachial plexus injury, hemiplegia, pain 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 response — extensor | Stroke the lateral sole then across the forefoot | Great toe extends, often with toe fanning | May be physiological through infancy and into the second year | Interpret against age, symmetry and the rest of the corticospinal examination; it is not an isolated diagnosis of UMN disease |
High Yield: Primitive Reflex Key Rules
- Most primitive reflexes integrate in the first 6 months, but use the expected range for the specific reflex, not the slide's absolute “all by 1 year” rule.
- Persistence, obligatory expression or asymmetry beyond the expected range raises concern for impaired motor-system maturation (including cerebral palsy); it is not diagnostic alone.
- Absence or marked depression in a neonate may reflect prematurity, behavioural state, medication, systemic/CNS illness or motor-pathway dysfunction.
- Asymmetry of Moro reflex → brachial plexus injury (Erb's palsy), clavicle fracture, hemiplegia
- Examine reflexes with the infant awake and settled, and repeat an unexpected result.
- An extensor plantar response can be physiological in an infant; age, symmetry and associated signs determine its meaning.
Why do primitive reflexes change? They arise from distributed brainstem, spinal and subcortical motor networks. With maturation, descending control, postural control and voluntary movement increasingly suppress or incorporate them. “The pyramidal tract is not yet myelinated” is therefore an incomplete single-cause explanation.
| Age | Assessment | Method |
|---|---|---|
| Neonate | Response to touch | Observe withdrawal, facial grimace, crying to tactile stimuli |
| Infant/Young child | Response to touch and asymmetry of response | Observe during play; use a noxious stimulus only when clinically necessary (for example, consciousness assessment), not as a routine game |
| 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).
The slide gives a useful pattern-recognition table, but it merges true LMN lesions with muscle disease. Localise to UMN versus the broader motor unit (anterior horn cell, root, peripheral nerve, neuromuscular junction or muscle), then refine.
| Feature | Upper Motor Neuron (UMN) | LMN pattern (compare motor-unit mimics) |
|---|---|---|
| Muscle wasting | Usually less prominent, except with chronic disuse | May be prominent in denervation; variable in NMJ and myopathy |
| Muscle tone | Classically increased (spasticity), but an acute UMN lesion may initially be flaccid | Usually decreased or normal |
| Muscle power | Weakness | Weakness |
| Deep tendon reflexes | Hyperreflexia | Hyporeflexia / Areflexia |
| Clonus | Sustained clonus supports a corticospinal pattern | Not a feature of isolated motor-unit disease |
| Plantar response | Extensor after the physiological infant period supports corticospinal dysfunction | Usually flexor in an older child |
| Examples | Cerebral palsy, stroke, focal brain lesion, spinal cord lesion | SMA (anterior horn cell), neuropathy; muscular dystrophy/myopathy produce a myopathic—not anatomically LMN—pattern |
Exam Discriminator: UMN vs LMN
The mnemonic UMN = tone/reflexes/plantar response UP is useful after infancy, but it has exceptions: acute UMN injury can be flaccid, hypotonia may precede spasticity in cerebral palsy, and an infant's extensor plantar response can be normal. “LMN” should not be used as a synonym for all neuromuscular disease. [1]
Why does a chronic UMN lesion cause hypertonia and hyperreflexia? Loss and reorganisation of descending control alters spinal reflex excitability, producing velocity-dependent spasticity, hyperreflexia and an extensor plantar response in a mature nervous system. It is more complex than loss of one purely inhibitory tract.
Why does LMN disease cause hypotonia and wasting? The lower motor neuron is the final neural pathway to muscle. Denervation causes weakness and neurogenic wasting; tone and reflexes fall when the reflex arc is interrupted. By contrast, primary myopathy often gives proximal weakness with preserved sensation and reflexes until weakness is advanced.
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 | Progressive or persistent headache, especially with vomiting, altered behaviour, focal signs or worse pain with cough/strain, is concerning; “morning headache” is neither required nor specific |
| Nausea and vomiting | Due to pressure on the area postrema (vomiting centre) in the floor of the 4th ventricle. May be projectile |
| Impaired consciousness | A falling conscious level is an emergency. The slide's Cushing graphic encodes hypertension, bradycardia and abnormal/irregular respiration; this is a late, ominous physiological response, not a screening triad |
| Papilloedema | Transmitted pressure along the optic nerve sheath impedes axoplasmic transport → optic-disc swelling. It takes time to develop, may be absent despite raised ICP, and its absence must never falsely reassure in an acutely deteriorating child |
| 6th CN palsy | False localising sign — long intracranial course makes it vulnerable to stretching when ICP rises |
| Bulging anterior fontanelle | An open fontanelle allows this sign to be seen in infants. Assess when the child is calm and upright because crying and recumbency can transiently make it full; a persistently tense/bulging fontanelle with illness or neurological signs is urgent |
| Sunsetting eyes | An important infant sign: downward-deviated eyes with sclera visible above the iris, classically associated with hydrocephalus affecting upgaze pathways |
High Yield: Raised ICP Signs Specific to Young Babies
A persistently bulging fontanelle, sunsetting eyes and accelerating head growth are infant clues to hydrocephalus/raised ICP. Their absence does not exclude raised ICP, and papilloedema may also be absent. Compare serial OFC measurements and assess alertness, feeding, vomiting, eye movements and neurological asymmetry. [1][7]
Do not turn the slide into a universal pressure cut-off. The Brain Trauma Foundation's suggestion to treat monitored ICP to below 20 mmHg applies to children with severe traumatic brain injury; it is not a diagnostic threshold for every infant or child with possible raised ICP. [11]
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 | The montage is a trisomy 21 phenotype exercise | Recognise the pattern—upslanting palpebral fissures/epicanthic folds, flat facial profile, single transverse palmar crease, fifth-finger clinodactyly and a wide first–second toe gap—without claiming that any one feature is diagnostic. Confirm the clinical suspicion genetically. |
| Case 2: Abnormal posture and movement | The still frame shows striking asymmetric patterned limb posture | First describe exactly what is seen; in the live sequence decide whether the posture is fixed or intermittent, whether tone is velocity-dependent or dystonic, and whether voluntary movement, reflexes and gait support spasticity, dystonia, weakness or an orthopaedic limitation. A still image alone cannot establish cerebral palsy or a movement-disorder subtype. |
| Case 3: Abnormal gait | The slide is a still from a video, so the abnormality itself is not recoverable from the PDF | Watch from front, side and behind; record base, stride, symmetry, arm swing, heel strike/toe walking, foot clearance and turning, then add tandem, heel and toe walking, running and rising from the floor when safe. Do not guess the gait label from one frame. |
| Case 4: "What is the positive sign?" | The child is filmed on the floor, consistent with a rise-from-floor manoeuvre | If the child pushes on the floor or “climbs” up the thighs, name Gowers' manoeuvre and interpret it as proximal lower-limb/hip-girdle weakness. The still frame itself is not the positive sign—the dynamic rise is. |
OSCE Tip: Gowers' Sign
Gowers' manoeuvre — the child uses the hands on the floor, knees or thighs to compensate while rising. It indicates proximal lower-limb weakness but is not specific to Duchenne muscular dystrophy; also consider other dystrophies, inflammatory/metabolic myopathy, SMA and severe deconditioning. Describe the movement before naming a cause. [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 development is a neurological marker, but the lecture's 3-, 6- and 12-month photographs illustrate examination techniques rather than universal diagnostic deadlines. Record the child's trajectory, movement quality and symmetry; ask about regression; correct for prematurity in early childhood; and use a validated screening tool when surveillance raises concern. [9][10]
- 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)
- A true LMN pattern → anterior horn cell, root or peripheral nerve. NMJ and muscle disorders are separate motor-unit localisations that can mimic parts of the flaccid/weak pattern.
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
Active Recall - Lecture Notes
High Yield Summary
- Observe first: interaction, alertness, posture, spontaneous movement, face/eyes, play and gait often reveal more than forced formal testing.
- Keep the six-domain structure: general inspection, consciousness, cranial nerves, motor, sensory and cerebellar/gait examination.
- Adapt to development: use toys, parent-held positioning and functional tasks; interpret milestones as a trajectory and use corrected age after preterm birth.
- Primitive reflexes are patterns, not binary deadlines: timing varies. Persistent, obligatory or asymmetric responses plus abnormal movement/development are concerning.
- Localise carefully: separate corticospinal signs from anterior-horn/root/nerve disease, NMJ dysfunction and myopathy; the slide's “LMN” column groups several distinct sites.
- Raised ICP red flags: falling consciousness, persistent vomiting/headache, papilloedema or VI palsy; in infants also accelerating OFC, persistent tense fontanelle and sunsetting eyes. Cushing physiology is late.
- Read the image cases: the dysmorphism montage depicts a trisomy 21 pattern; the posture, gait and Gowers cases require dynamic description before diagnosis.
[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] NICE. Head injury: assessment and early management (NG232) — coma, airway and transfer recommendations. https://www.nice.org.uk/guidance/ng232/chapter/recommendations [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) [9] CDC. Developmental Milestones / Learn the Signs. Act Early — surveillance checklists are not diagnostic screening tools. https://www.cdc.gov/milestones [10] American Academy of Pediatrics. Primary Care Framework to Monitor Preterm Infants for Neurodevelopmental Outcomes in Early Childhood. Pediatrics. 2023. https://doi.org/10.1542/peds.2023-062511 [11] Brain Trauma Foundation. Guidelines for the Management of Pediatric Severe TBI, 3rd Edition — monitored ICP target in severe TBI. https://braintrauma.org/coma/guidelines/pediatric
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