CFB MED04 Central Nervous System
The central nervous system comprises the brain and spinal cord, serving as the primary integration and command center for processing sensory information, coordinating motor output, and governing higher cognitive functions.
Approach to the Central Nervous System — Neurological History, Examination & Lesion Localization
The Big Idea: This CFB lecture by Professor RTF Cheung is the foundational framework for every neurology encounter you will have in clinical practice and exams. It teaches you how to think like a neurologist: take a focused history, perform a systematic neurological examination, and then answer three key questions — Where is the lesion? What is the pathology? Is it neurological or functional? [1]
Why it matters: Roughly 80–90% of neurological diagnoses can be made from the history alone [1]. The examination confirms your hypothesis and localizes the lesion anatomically. This lecture is the skeleton upon which every subsequent neurology GC session (stroke, epilepsy, movement disorders, spinal cord, headache, neuro-ophthalmology) hangs.
Learning Objectives:
- Structure a neurological history systematically.
- Perform a screening and focused neurological examination (higher mental functions → cranial nerves → limbs → gait).
- Distinguish UMN from LMN lesions.
- Apply dermatome and myotome maps to localize the level of lesion.
- Formulate an anatomical diagnosis (brain, spinal cord, root, plexus, peripheral nerve, NMJ, muscle).
High Yield: This lecture directly maps onto the recurrent "Where is the lesion?" extended matching questions (EMQs) and structured answer questions (SAQs) that appear in virtually every Fourth Summative paper. [7][8][9][10][11]
Core Concepts and Mechanisms
"Where is the lesion? What is the underlying pathology? Is it neurological or functional?" — These three questions, derived directly from the lecture, are the backbone of neurological clinical reasoning. [1]
| Question | What It Does | How to Answer It |
|---|---|---|
| Where is the lesion? | Anatomical localization | History (pattern of deficit) + examination (UMN/LMN signs, cranial nerves, sensory level) |
| What is the pathology? | Etiological diagnosis | Temporal profile (acute/subacute/chronic), risk factors, associated features |
| Neurological or functional? | Distinguishes organic from psychogenic | Consistency of signs, positive functional signs (e.g., Hoover's), investigations |
Why these three questions? Neurology is uniquely localizational. Unlike cardiology (where you localize disease to one organ), a lesion anywhere from cortex to muscle can cause "weakness." The combination of history pattern + examination findings lets you triangulate the site.
Central nervous system (CNS) = brain & spinal cord. Peripheral nervous system (PNS) = 12 pairs of cranial nerves & 31 pairs of peripheral nerves. [2]
This distinction matters because:
- CNS lesions → UMN signs (spasticity, hyperreflexia, Babinski)
- PNS lesions → LMN signs (flaccidity, wasting, fasciculations, hyporeflexia)
Slide-by-Slide High-Yield Content
"History will reveal diagnosis & direct our neurological examination. Diagnosis from history alone in many cases (80–90%)." [1]
Structure of the neurological history:
| Component | Key Points | Why It Matters |
|---|---|---|
| Chief complaint (C/O) | In the patient's own words | Frames the differential |
| HPI | Onset (sudden/gradual), duration, course (progressive/relapsing-remitting/static), associated symptoms, risk factors | Temporal profile is the single most powerful localizing/etiological clue |
| PMH | DM, HTN, AF, malignancy, autoimmune disease | Vascular risk factors → stroke; malignancy → metastases/paraneoplastic |
| Drug history | Antipsychotics, metoclopramide → drug-induced parkinsonism; chemotherapy → neuropathy [5] | Always exclude iatrogenic cause |
| Family history | Similar neurological disease, consanguinity | Hereditary neuropathies, Huntington's, spinocerebellar ataxias |
| Social history | Alcohol (neuropathy, cerebellar degeneration), smoking, occupation | Toxic/nutritional causes |
| O&G history | Pregnancy → eclampsia, postpartum, etc. | Specific neurological emergencies |
| Review of systems | Systemic clues (weight loss, joint pain, rash) | May point to systemic disease with neuro manifestations |
Additional information from relatives or eyewitnesses is critical — especially for seizures, syncope, and acute confusional states where the patient cannot give a reliable account [1].
Key Symptoms to Characterize
Always define: (1) Onset — sudden (seconds–minutes) = vascular; subacute (days–weeks) = inflammatory/infective; chronic (months) = degenerative/neoplastic. (2) Duration. (3) Course — monophasic, relapsing-remitting, progressive. (4) Distribution — focal, multifocal, diffuse. (5) Associated symptoms. (6) Risk factors.
"Elicit signs according to history & working diagnosis. Able to interpret findings: normal vs. abnormal; anatomical diagnosis; etiological diagnosis." [1]
The lecture emphasizes two modes:
- Screening examination — quick survey of all systems (appropriate when the history is non-localizing)
- Focused examination — directed by the history to confirm or refute the suspected lesion site
"Higher mental functions: Ability to provide a coherent history; Glasgow Coma Scale (eye, verbal, motor); MMSE; MoCA; Speech & language." [1]
| Test | Components | Clinical Use |
|---|---|---|
| Coherent history | Observe during interview — speech fluency, comprehension, word-finding | Screens for dysphasia, confusion, dementia |
| GCS (3–15) | Eye (4): spontaneous/to speech/to pain/nil; Verbal (5): oriented/confused/inappropriate/incomprehensible/nil; Motor (6): obeys/localizes/withdraws/flexion/extension/nil | Quantifies consciousness; used in trauma, stroke, ICU |
| MMSE (max 30) | Orientation (10), registration (3), attention/serial 7 (5), recall (3), language (8), construction (1) | Screening for cognitive impairment; < 24 suggests dementia |
| MoCA (max 30) | More sensitive for MCI; includes visuospatial, executive, naming, memory, attention, language, abstraction, orientation | Better than MMSE for detecting early/mild cognitive impairment |
| Speech & Language | Fluency, comprehension, repetition, naming → classify as Broca's (non-fluent), Wernicke's (fluent but incomprehensible), global, etc. | Localizes dominant hemisphere lesion |
Why both MMSE and MoCA? MMSE has a ceiling effect — patients with early MCI can score normally. MoCA includes executive function tasks (trail-making, clock drawing) that pick up frontal and subcortical deficits missed by MMSE. The lecture lists both because examiners expect you to know when to use each.
D. Cranial Nerves — Systematic Review
The 12 cranial nerves are listed with their origins: [1]
- CN I & II arise from the cerebrum (forebrain)
- CN III & IV arise from the midbrain
- CN V, VI, VII, VIII arise from the pons
- CN IX, X, XI, XII arise from the medulla
This is clinically essential because the combination of cranial nerve deficits tells you which part of the brainstem is affected.
"Change in smell? Test each side with aromatic, non-irritant materials." [1]
- What to use: Coffee, peppermint, lemon — NOT ammonia (which stimulates trigeminal nociceptors, not olfactory neurons).
- Why non-irritant? Because irritant substances activate CN V, so the patient would respond even with total CN I loss.
- Clinical significance: Anosmia occurs in head trauma (shearing of olfactory filaments at cribriform plate), nasal disease, Parkinson's disease (early feature), and Kallmann syndrome.
"Visual acuity, visual field, direct light reflex, consensual light reflex, accommodation reflex, fundus." [1]
| Test | Method | What It Tests |
|---|---|---|
| Visual acuity | Snellen chart (distance), near reading chart | Afferent visual pathway integrity |
| Visual field | Confrontation (compare with examiner's fields) | Localizes lesion: optic nerve (monocular), chiasm (bitemporal hemianopia), tract/radiation/cortex (homonymous hemianopia) |
| Direct light reflex | Shine light in one eye → that pupil constricts | Afferent (CN II) + efferent (CN III) arc |
| Consensual light reflex | Shine light in one eye → opposite pupil constricts | Same arc but tests bilateral connectivity at pretectal nucleus |
| Relative afferent pupillary defect (RAPD) | Swinging flashlight test → affected pupil dilates when light swings to it | Indicates optic nerve or severe retinal disease on that side |
| Accommodation reflex | Ask patient to look from far to near → pupils constrict, eyes converge | Tests CN III parasympathetic pathway (separate from light reflex) |
| Fundoscopy | Papilloedema, optic atrophy, retinal changes | Raised ICP, MS, glaucoma, hypertensive/diabetic retinopathy |
Why test both direct and consensual? This distinguishes afferent (CN II) from efferent (CN III) lesions. In a CN II lesion: shining light in the affected eye → no direct AND no consensual response, but shining light in the normal eye → both pupils constrict (afferent from the normal eye is intact).
"Abducens (VI) – lateral rectus; Trochlear (IV) – superior oblique; Oculomotor (III) – superior rectus, inferior rectus, medial rectus, inferior oblique, levator palpebrae superioris." [1]
Mnemonic: LR₆SO₄ — the rest are CN III.
| Nerve | Muscle(s) | Action | Palsy Features |
|---|---|---|---|
| CN VI | Lateral rectus | Abduction | Cannot look laterally → diplopia worst on looking to affected side |
| CN IV | Superior oblique | Intorsion + depression (especially in adducted eye) | Head tilt away from affected side; diplopia on looking down and in (e.g., reading, going downstairs) |
| CN III | All the rest + levator palpebrae + parasympathetic to pupil | Elevation, depression, adduction, eyelid opening, pupil constriction | Complete: ptosis, "down and out" eye, fixed dilated pupil. Partial: any combination |
Why does CN III palsy cause a "down and out" eye? With CN III out, only the lateral rectus (CN VI) and superior oblique (CN IV) work. The lateral rectus abducts the eye (pulls it "out"), and the superior oblique intorts and depresses (pulls it "down"). Hence the classic position.
Pupil-involving vs. pupil-sparing CN III palsy:
- Pupil-involving (dilated, fixed) → posterior communicating artery aneurysm compresses parasympathetic fibers running on the outside of CN III → surgical emergency
- Pupil-sparing → microvascular ischemia (DM, HTN) affects the core of the nerve, sparing superficial parasympathetic fibers
Exam Trap: Horner's Syndrome vs CN III Palsy
Both can cause ptosis! Horner's = partial ptosis + miosis (small pupil) + anhidrosis. CN III = complete ptosis + mydriasis (large pupil) + "down and out" eye. The pupil size is the discriminator. Past paper 2022 Q3 tested this directly: "Partial ptosis of left eye with small left pupil" = Horner's syndrome. [7]
"Muscles of mastication; Sensory – 3 divisions; Jaw jerk; Corneal reflex (Afferent – ophthalmic division V1; Efferent – Facial nerve VII)." [1]
Three sensory divisions:
- V1 (Ophthalmic): Forehead, upper eyelid, cornea, bridge of nose
- V2 (Maxillary): Cheek, upper lip, upper teeth, nasal cavity
- V3 (Mandibular): Lower face, chin, lower teeth, anterior 2/3 tongue (sensation, not taste), muscles of mastication (motor)
Jaw jerk: Patient opens mouth slightly, tap on chin → jaw closes. Brisk jaw jerk = UMN lesion above the pons (bilateral). This is important because if you find a patient with bilateral UMN limb signs AND a brisk jaw jerk, the lesion must be above the level of the trigeminal motor nucleus in the pons (e.g., bilateral hemisphere disease, pseudobulbar palsy).
Corneal reflex: Touch cornea with wisp of cotton → bilateral blink. Afferent = V1 (ophthalmic), Efferent = VII (facial) bilaterally. Tests both nerves and pontine connections.
"Muscles of facial expression; Frowning (upper face), Blowing cheek (lower face); Taste of anterior 2/3 of tongue; Salivary secretion; UMN vs LMN weakness." [1]
| Feature | UMN (Supranuclear) Lesion | LMN (Nuclear/Infranuclear) Lesion |
|---|---|---|
| Forehead | Spared (can raise eyebrows, wrinkle forehead) | Affected (cannot raise eyebrow on affected side) |
| Lower face | Weak (cannot show teeth, blow cheek) | Weak |
| Side of weakness | Contralateral to lesion | Ipsilateral to lesion |
| Common cause | Stroke (contralateral hemisphere) | Bell's palsy, CPA tumour, parotid tumour |
| Taste | Usually normal | May be lost (anterior 2/3) if lesion proximal to chorda tympani |
Why is the forehead spared in UMN lesions? The upper face (frontalis muscle) receives bilateral corticobulbar innervation — both hemispheres send fibers to both facial nuclei for the upper face. So a unilateral UMN lesion still leaves the contralateral hemisphere's input intact for the upper face. The lower face, however, only receives contralateral corticobulbar input, so a unilateral UMN lesion causes contralateral lower face weakness.
This UMN vs. LMN facial weakness distinction is tested extremely frequently. The 2025 SAQ Q1 presents a patient with facial asymmetry and then contralateral limb weakness, requiring you to determine whether the facial weakness is UMN or LMN and localize accordingly. [11]
"Conductive deafness: sound not transmitted to the cochlear (e.g., ear wax, middle ear damage). Sensorineural deafness: sound transmitted to cochlear but sensation reduced (e.g., VIII nerve injury, tumour)." [1]
| Test | Method | Conductive Loss | Sensorineural Loss |
|---|---|---|---|
| Weber | Tuning fork (512 Hz) on vertex | Lateralizes to the affected ear | Lateralizes to the normal ear |
| Rinne | Tuning fork on mastoid vs. next to ear | Bone > Air (Rinne negative) | Air > Bone (Rinne positive) — but both are diminished |
Why does Weber lateralize to the affected ear in conductive loss? Because conductive loss blocks ambient noise on that side, making the bone-conducted sound from the tuning fork relatively louder on the affected side (like putting an earplug in).
Why does Weber lateralize to the normal ear in sensorineural loss? The cochlear or nerve on the affected side cannot process the signal properly, so it is perceived as louder on the unaffected side.
Note on Tuning Fork Frequency
The lecture specifies 128 Hz for vibration testing (sensory examination) but clinical practice uses 512 Hz for hearing tests (Rinne/Weber). Don't confuse them — 128 Hz tests dorsal column (vibration sense) while 512 Hz tests hearing.
"Soft palate, pharynx, ear canal; mainly sensory; salivation; taste & sensations of posterior third of tongue; position & movements of soft palate & uvula; gag reflex." [1]
CN IX is primarily sensory. It provides:
- Taste from the posterior 1/3 of the tongue (compare: CN VII = anterior 2/3)
- General sensation from posterior 1/3 of tongue, pharynx, middle ear
- Afferent limb of the gag reflex (touch posterior pharyngeal wall → CN IX carries signal to medulla)
- Minor motor to stylopharyngeus (one muscle!)
"Pharynx, larynx, viscera; somatic, autonomic, motor, sensory; gag reflex (afferent IX; efferent X)." [1]
- Gag reflex: Afferent = CN IX, Efferent = CN X. Touch pharynx (IX senses it) → soft palate elevates and pharynx constricts (X mediates this motor response).
- Unilateral CN X lesion → soft palate deviates to the normal (unaffected) side when saying "ahh" (the normal side pulls the palate up; the paralyzed side sags).
- Recurrent laryngeal nerve (branch of X) → hoarseness if damaged (e.g., by thyroid surgery, lung cancer, aortic aneurysm).
"Sternocleidomastoid muscle – rotate head to the opposite side; Trapezius muscle – shrug shoulders against resistance." [1]
Clinical trap: The SCM turns the head to the opposite side. So if the right CN XI is damaged, the patient cannot turn the head to the left (weakness of right SCM). This is counterintuitive — the lesion is ipsilateral to the weak SCM but contralateral to the direction of head-turning.
"Motor to intrinsic & extrinsic tongue muscle; atrophy, fibrillation, deviate on protrusion; tongue movements; power." [1]
- LMN lesion → tongue deviates toward the side of the lesion on protrusion (the weak side cannot push the tongue away from itself). Also see ipsilateral atrophy and fasciculations.
- UMN lesion → tongue deviates away from the side of the lesion (contralateral tongue weakness = tongue deviates to the weak side, which is contralateral to the brain lesion).
E. Limb Examination — Arms
Motor Examination of Arms
"Check muscle bulk (if wasting: chart the distribution); inspect for fasciculation or tremor; note any abnormal posture or movements; test muscle tone over elbow & wrist joints: normal, low or high (rigidity or spasticity)." [1]
Sequence: Inspection → Tone → Power → Reflexes → Coordination
| Type | Feel | Lesion |
|---|---|---|
| Hypotonia | Floppy, increased range of passive movement | LMN, cerebellar, acute UMN (spinal shock) |
| Spasticity ("clasp-knife") | Velocity-dependent; initial resistance then gives way | UMN (pyramidal) |
| Rigidity ("lead-pipe") | Constant resistance throughout range of movement | Extrapyramidal (basal ganglia) |
| Cogwheel rigidity | Lead-pipe + superimposed tremor (ratchety feel) | Parkinsonism |
Why is spasticity "velocity-dependent"? Spasticity is due to loss of upper motor neuron inhibition on stretch reflexes. The faster you passively stretch the muscle, the stronger the reflex contraction. This is why a slow passive movement may feel almost normal but a quick one meets strong resistance.
Pronator drift: if present → mild weakness, ataxia, or loss of position sensation. [1]
This is a sensitive screening test. Ask the patient to hold both arms out, palms up, eyes closed. In UMN weakness, the affected arm slowly pronates and drifts downward. In cerebellar disease, the arm drifts upward. In proprioceptive loss, the fingers "wander" randomly. [4]
| Grade | Definition |
|---|---|
| 0 | No contraction |
| 1 | Flicker of contraction |
| 2 | Movement with gravity eliminated |
| 3 | Movement against gravity but not resistance |
| 4 | Movement against resistance but less than normal |
| 5 | Normal power |
The lecture lists these myotome-muscle-nerve associations explicitly [1]:
| Joint Action | Myotome | Muscle | Nerve |
|---|---|---|---|
| Shoulder abduction | C5–6 | Deltoid | Axillary |
| Elbow flexion | C5–6 | Biceps | Musculocutaneous |
| Elbow extension | C7–8 | Triceps | Radial |
| Wrist/finger extension | C6–8 | Extensor carpi radialis longus, extensor carpi ulnaris, long finger extensors | Radial |
| Hand grip | C8–T1 | Long finger flexors | Median/Ulnar |
| Finger abduction | T1 | Dorsal interossei | Ulnar |
| Finger adduction | T1 | Palmar interossei | Ulnar |
| Thumb abduction | T1 | Abductor pollicis brevis | Median |
| Thumb opposition | T1 | Opponens pollicis | Median |
Ulnar vs. Median Hand Intrinsics
Ulnar nerve = all interossei (finger abduction/adduction) + medial two lumbricals. Median nerve = thenar eminence (abductor pollicis brevis, opponens pollicis, flexor pollicis brevis) + lateral two lumbricals. The mnemonic "LOAF" (Lateral two Lumbricals, Opponens pollicis, Abductor pollicis brevis, Flexor pollicis brevis) = median nerve innervated hand muscles.
"Biceps jerk, supinator jerk for C5–6; Triceps jerk for C7–8; Finger jerk for C8–T1; Hoffmann sign for C8–T1 hyperreflexia." [1]
Hoffmann sign: Flick the nail of the middle finger → involuntary flexion of the thumb and/or index finger. This is an upper limb equivalent of the Babinski sign — it suggests UMN lesion (corticospinal tract dysfunction) affecting the upper limb.
"Finger-nose test; rapid alternating movements." [1]
- Finger-nose test: Intention tremor (oscillation that worsens as finger approaches the target) = cerebellar disease. Past-pointing = cerebellar hemisphere lesion (past-points to the side of the lesion).
- Rapid alternating movements (dysdiadochokinesia): Inability to perform rapid pronation/supination = cerebellar dysfunction.
"Broken wooden stick for pin prick (Pain); Cotton wool for light touch; Thumb movement for joint position sensation; Tuning fork (128 Hz) for vibration; As a minimum, screen one modality for Spinothalamic & Dorsal column sensations." [1]
| Pathway | Modalities | Fiber Type | Crosses At |
|---|---|---|---|
| Spinothalamic tract | Pain (pin prick), temperature, crude touch | Small fibers (Aδ, C) | Crosses at segmental level (within 1–2 segments of entry) |
| Dorsal columns (DCML) | Vibration, proprioception (joint position sense), fine/discriminative touch | Large fibers (Aβ) | Crosses at medulla (nucleus gracilis/cuneatus → medial lemniscus) |
Why screen at least one modality from each system? Because certain lesions selectively affect one pathway (e.g., syringomyelia → central cord lesion → disrupts crossing spinothalamic fibers → "dissociated sensory loss" with loss of pain/temperature but preserved vibration/proprioception). If you only check one system, you'll miss the dissociation.
"C5–T1 for arm (C6 – thumb; C7 – middle finger; C8 – little finger); C4 & T2 contiguous over sternal angle." [1]
| Dermatome | Landmark |
|---|---|
| C5 | Lateral arm (deltoid area) |
| C6 | Thumb and lateral forearm |
| C7 | Middle finger |
| C8 | Little finger and medial forearm |
| T1 | Medial arm (above elbow) |
| T2 | Medial upper arm/axilla |
Why are C4 and T2 contiguous at the sternal angle? Because C5–T1 are "drawn down" into the upper limb during embryological development. So dermatomes jump from C4 (neck/upper chest) directly to T2 (upper anterior chest wall) on the trunk.
F. Limb Examination — Legs
Motor Examination of Legs
"Check muscle bulk; inspect for fasciculation or tremor; note any abnormal posture or movements; test muscle tone over hip, knee & ankle joints." [1]
| Joint Action | Myotome | Muscle | Nerve |
|---|---|---|---|
| Hip flexion | L2–3 | Iliopsoas | Nerve to iliopsoas (femoral branches) |
| Hip extension | L4–5, S1 | Glutei | Gluteal nerves |
| Hip adduction | L3–4 | Hip adductors | Obturator |
| Hip abduction | L5, S1 | Gluteus medius, tensor fascia lata | Gluteal nerve |
| Knee extension | L3–4 | Quadriceps femoris | Femoral |
| Knee flexion | L5, S1 | Hamstrings | Sciatic |
| Ankle dorsiflexion | L4–5 | Toe extensors (tibialis anterior, extensor hallucis longus) | Peroneal (deep) |
| Ankle plantar flexion | S1–2 | Toe flexors (gastrocnemius, soleus) | Tibial (popliteal) |
High-Yield Root Values
Remember: L3-4 = knee jerk, L5 = ankle dorsiflexion (foot drop if lost), S1-2 = ankle jerk + plantar flexion. These are tested constantly in OSCE and written exams.
"Knee jerk for L3–4; Ankle jerk for S1–2; Plantar response down-going; Upgoing plantar response = Babinski sign for Upper Motor Neurone Lesion." [1]
Why does the Babinski sign occur? Normally, the corticospinal tract inhibits the primitive toe-extension reflex. When the corticospinal tract is damaged (UMN lesion), this inhibition is released, so stroking the sole causes the big toe to extend (dorsiflex) and the other toes to fan out.
Babinski sign is the cardinal sign of UMN lesion. It is more reliable than hyperreflexia or spasticity because those can be affected by examiner technique, patient anxiety, etc.
"Heel-shin test; Heel-toe gait." [1]
- Heel-shin test: Run the heel of one foot down the shin of the opposite leg. Incoordination (zig-zagging) = ipsilateral cerebellar hemisphere lesion.
- Heel-toe (tandem) gait: Walk heel-to-toe in a straight line. This is extremely sensitive for cerebellar midline (vermis) dysfunction and mild ataxia.
"Broken wooden stick for pin prick; Cotton wool for light touch; Big toe movement for joint position sensation; Tuning fork (128 Hz) for vibration." [1]
Same two-system principle: screen at least one spinothalamic modality AND one dorsal column modality.
"Nipple = T4; xiphisternum = T7; umbilicus = T10; symphysis pubis = L1; L2–S2 for leg; Saddle = S3; perianal = S4/5; No C1 dermatome." [1]
| Dermatome | Landmark |
|---|---|
| T4 | Nipple |
| T7 | Xiphisternum |
| T10 | Umbilicus |
| L1 | Inguinal ligament / symphysis pubis |
| L3 | Knee (medial) |
| L4 | Medial malleolus |
| L5 | Dorsum of foot / great toe (first web-space region) |
| S1 | Lateral foot, heel and plantar/lateral sole |
| S2 | Posterior thigh |
| S3 | Saddle area |
| S4/5 | Perianal |
The Sacral Dermatomes
Never forget to check perianal sensation (S4/5) in suspected spinal cord or cauda equina lesions! Loss of perianal sensation with urinary retention = cauda equina syndrome = surgical emergency. Students commonly omit this in OSCE.
Dermatome maps vary
The lecture graphic prints “L5—sole,” but dermatome boundaries overlap and published maps differ. At the bedside, the more useful anchors are L5 at the dorsum/great toe and S1 at the lateral/plantar foot; interpret a sensory level as a pattern rather than a single dot.
This is perhaps the single most important distinction in clinical neurology and the lecture provides a clean comparison [1]:
UMN signs: Spastic paralysis, little atrophy, hyperactive reflexes, clonus, Babinski's sign. [1] LMN signs: Flaccid paralysis, early-onset atrophy, reduced reflexes, fasciculations & fibrillation. [1]
| Feature | UMN | LMN |
|---|---|---|
| Tone | Increased (spasticity) | Decreased (flaccid) |
| Wasting | Minimal/late (disuse atrophy) | Early and prominent |
| Reflexes | Hyperreflexia | Hyporeflexia/areflexia |
| Clonus | Present | Absent |
| Babinski sign | Upgoing (extensor plantar) | Downgoing (normal) |
| Fasciculations | Absent | Present |
| Pattern of weakness | Pyramidal distribution (UL extensors > flexors; LL flexors > extensors) | Follows specific nerve/root distribution |
Why pyramidal distribution weakness? UMN lesions preferentially affect the antigravity muscles differently in upper vs. lower limbs. In the upper limb, extensors are weaker (so the arm flexes — hence the hemiplegic posture with flexed arm, extended leg). In the lower limb, flexors are weaker (so the leg extends and circumducts during walking).
Why do fasciculations occur only in LMN lesions? When a motor neuron degenerates, its denervated muscle fibers become supersensitive to acetylcholine. Spontaneous depolarization of these fibers causes visible twitching (fasciculations). In UMN lesions, the lower motor neuron is intact, so there is no denervation supersensitivity.
Spinal cord lesion produces BOTH:
- At the level of the lesion: LMN signs (damage to anterior horn cells)
- Below the level of the lesion: UMN signs (interruption of descending corticospinal tracts) [3]
"Single vs. multiple vs. diffuse; Localization: Brain (hemisphere, brain stem, cerebellum), Spinal cord, spinal root, plexus, Peripheral nerve, Neuromuscular junction, Muscle." [1]
| Lesion Site | Key Features |
|---|---|
| Cerebral hemisphere | Contralateral hemiplegia + hemianesthesia ± homonymous hemianopia ± dysphasia (if dominant); UMN facial weakness (forehead spared) |
| Internal capsule | Dense contralateral hemiplegia (face + arm + leg equally) — because motor fibers are concentrated |
| Brainstem | Crossed signs: ipsilateral cranial nerve palsy + contralateral hemiplegia; may have vertigo, diplopia, dysarthria, dysphagia |
| Cerebellum | Ipsilateral limb ataxia, dysarthria, nystagmus, intention tremor; NO weakness, NO sensory loss |
| Spinal cord | Motor + sensory level; UMN signs below, LMN signs at level; bladder/bowel dysfunction |
| Spinal root | Dermatomal sensory loss, myotomal weakness, pain in root distribution |
| Plexus | Multinerve, multisegmental pattern (not fitting single nerve or single root) |
| Peripheral nerve | Single nerve territory: motor + sensory in that nerve's distribution |
| NMJ | Fatigable weakness, proximal > distal, NO sensory loss, NO wasting (initially) |
| Muscle | Proximal weakness, NO sensory loss, ± pain/tenderness, ± elevated CK |
The Brainstem Crossed-Signs Rule
Brainstem lesions produce IPSILATERAL cranial nerve palsies + CONTRALATERAL long tract signs (hemiplegia/hemianesthesia). This is because the cranial nerve nuclei are in the brainstem (ipsilateral effect), while the corticospinal and spinothalamic tracts pass through the brainstem before/after crossing. This pattern is pathognomonic for brainstem lesions and is a favorite exam question. [8][9]
Past paper integration:
The 2024 MCQ Q9 presents: "Right facial weakness, right facial numbness, dysarthria, grade 4 left arm and left leg power." This is crossed signs = right CN VII + right CN V involvement (ipsilateral) + left hemiparesis (contralateral) → brainstem lesion. [9]
The 2025 MCQ Q7 presents: "Left facial weakness, dysarthria, grade 4 left limb power, reduced left limb touch sensation." Here everything is on the SAME side (left face + left limbs) → this is NOT crossed → cerebral hemisphere (right hemisphere) lesion. [10]
The 2024 MCQ Q45 presents: "Glove and stocking pattern of reduced touch and pain, reduced tendon reflexes, down-going plantars." → Peripheral nervous system. [9]
Clinical Approach — Integration
- What happened? — Weakness, numbness, headache, seizure, visual loss, speech difficulty, unsteady gait
- When and how did it start? — Sudden (vascular), subacute (inflammatory/infective), chronic (degenerative/neoplastic)
- What is the distribution? — One limb (nerve/root), one side of body (hemisphere/brainstem/cord), bilateral (cord/bilateral hemisphere), proximal (muscle/NMJ), distal (neuropathy)
- What is the course? — Progressive (tumour, degeneration), relapsing-remitting (MS), static (completed stroke)
- Risk factors? — HTN, DM, AF, smoking, family history, immune status
- Associated symptoms? — Headache, seizures, visual change, sphincter dysfunction
- Higher mental functions: Consciousness, cognition, speech
- Cranial nerves: I through XII systematically
- Motor (arms then legs): Inspection → Tone → Power → Reflexes → Coordination
- Sensory (arms then legs): At minimum one spinothalamic modality + one dorsal column modality
- Gait: Normal, spastic (hemiplegic/scissoring), ataxic (wide-based), steppage (foot drop), waddling (proximal weakness), parkinsonian (shuffling, reduced arm swing)
- Special tests: Romberg (proprioception), Lhermitte sign (cervical cord — electric shock down spine on neck flexion)
| Lesion Site | First-Line Investigation |
|---|---|
| Hemisphere | CT/MRI brain |
| Brainstem | MRI brain (CT poor for posterior fossa) |
| Spinal cord | MRI spine |
| Peripheral nerve | Nerve conduction studies (NCS) |
| NMJ | Repetitive nerve stimulation (RNS), anti-AChR antibodies |
| Muscle | CK, EMG, muscle biopsy |
| Meningitis suspected | LP (after CT if raised ICP suspected) [6] |
Exam Intelligence
-
"Where is the lesion?" — Given clinical features, pick from: hemisphere, brainstem, cerebellum, spinal cord, cauda equina, peripheral nerve, NMJ, muscle. This is the #1 most tested stem in CNS [7][8][9][10].
-
UMN vs. LMN — Given signs, classify. Look for the discriminators: Babinski, fasciculations, wasting pattern, reflex changes.
-
Cranial nerve palsy identification — Given a clinical scenario (ptosis, diplopia, facial weakness), identify which CN is affected and whether it's UMN or LMN.
-
Dermatome/myotome identification — "A patient cannot dorsiflex the ankle. What root level?" → L4–5.
-
Brown-Séquard syndrome — Hemitransection of cord → ipsilateral UMN weakness + ipsilateral dorsal column loss + contralateral spinothalamic loss. Tested in 2023 SAQ Q8 [8].
| Trap | Correct Answer |
|---|---|
| "Left facial weakness + left hemiparesis" → brainstem? | No — same side = cerebral hemisphere (right). Brainstem = CROSSED. [10] |
| Horner's syndrome confused with CN III palsy | Horner's = partial ptosis + miosis. CN III = complete ptosis + mydriasis [7] |
| Forgetting that UMN facial weakness spares forehead | Always test forehead (frowning) vs. lower face separately |
| Glove-and-stocking sensory loss with areflexia → cord? | No — this is peripheral neuropathy [9] |
| Proximal weakness without sensory loss → neuropathy? | No — think muscle disease or NMJ [8] |
| Tongue deviates to the left on protrusion → left or right CN XII lesion? | Left CN XII (LMN) — tongue deviates toward the lesion |
For "Where is the lesion?":
- State the specific anatomical level: "Right cerebral hemisphere" not just "brain"
- For brainstem: specify side AND mention crossed signs
- For cord: specify level (cervical/thoracic) and pattern (complete/hemisection/central)
For "Describe the signs":
- Use the UMN/LMN framework
- Always mention tone, power pattern, reflexes, plantar response, sensory modality affected
GC 094 "Where is the lesion I": Directly builds on this CFB lecture — reinforces CNS vs. PNS distinction and provides worked examples of localization. [2]
GC 110 (Paraplegia): Applies the UMN/LMN framework to spinal cord compression and transverse myelitis — extends the concept of "sensory level" and cord syndromes (Brown-Séquard, anterior cord, central cord). [3]
GC 081 (Seizure and loss of consciousness): Requires GCS assessment skills taught in this lecture.
Prof KC Teo's "Introduction to Neurological Investigations": Reinforces that investigations are chosen based on the clinical localization ("Where is it? What is it?") — the history and exam come first, imaging/electrophysiology confirm. [12]
Ryan Ho Neurology Notes: Provide excellent tables for approach to generalized weakness (CNS vs. nerve vs. NMJ vs. muscle) that extend this lecture's anatomical framework. [4]
High Yield Summary
-
Three key questions
- Where is the lesion? What is the pathology? Neurological or functional?
-
History diagnoses 80–90% of neurological cases.
- Always characterize onset, duration, course, distribution, risk factors.
-
Cranial nerve origins
- I–II (cerebrum), III–IV (midbrain), V–VIII (pons), IX–XII (medulla). Know this to localize brainstem lesions.
-
UMN signs:: Spasticity, hyperreflexia, clonus, Babinski, minimal wasting. LMN signs: Flaccidity, early wasting, fasciculations, hyporeflexia. This distinction is tested on EVERY summative paper.
-
Facial nerve UMN vs. LMN
- UMN spares forehead (bilateral innervation); LMN affects entire half of face.
-
Brainstem = crossed signs
- (ipsilateral CN + contralateral long tracts). Same side face + limb weakness = hemisphere, NOT brainstem.
-
Key dermatome landmarks
- T4 nipple, T10 umbilicus, L1 groin, C6 thumb, C7 middle finger, C8 little finger, S4/5 perianal.
-
Sensory exam
- Screen at least one spinothalamic modality (pin prick) + one dorsal column modality (vibration or proprioception).
-
Anatomical diagnosis hierarchy
- Hemisphere → Brainstem → Cerebellum → Spinal cord → Root → Plexus → Peripheral nerve → NMJ → Muscle.
Active Recall - Central Nervous System
[1] Lecture slides: CFB (MED04) Central Nervous System.pdf (all pages) [2] Lecture slides: GC 094. Where is the lesion I.pdf (p9) [3] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (p1112 — Spinal cord lesion localization) [4] Senior notes: Ryan Ho Neurology.pdf (p178 — Approach to generalized weakness; p24 — Neurological examination) [5] Senior notes: Ryan Ho Fundamentals.pdf (p102 — Drug history causing neuropathy; p322 — Sensory loss patterns) [6] Past papers: 2020 Fourth Summative Assessment MCQ paper.pdf (Q34 — LP contraindication with raised ICP) [7] Past papers: 2022 Fourth Summative MCQ.pdf (Q1–5 — Cranial nerve EMQ including Horner syndrome) [8] Past papers: 2023 Fourth Summative MCQ.pdf (Q9–13 — "Where is the lesion" EMQ; 2023 Fourth Summative SAQ.pdf Q8 — Brown-Séquard) [9] Past papers: 2024 Fourth Summative MCQ.pdf (Q9 — brainstem crossed signs; Q45 — peripheral neuropathy) [10] Past papers: 2025 Fourth Summative MCQ.pdf (Q7 — hemisphere lesion; Q36 — IV ceftriaxone for bacterial CNS infection) [11] Past papers: 2025 Fourth Summative SAQ.pdf (Q1 — facial asymmetry + contralateral weakness localization) [12] Medicine lecture slides: Introduction to Neurological Investigations and Emergencies (Prof KC Teo) (p3, p11, p65)
CFB MED06 Cardiovascular (II) Physical Examination
Systematic clinical assessment of the heart and vasculature through inspection, palpation, percussion, and auscultation to evaluate cardiac structure, function, and hemodynamic status.
CFB PAE02 Child Growth And Development
Child growth and development encompasses the progressive physical, cognitive, emotional, and social maturation from infancy through adolescence, assessed through standardized milestones and growth parameters.