GC094 Where Is The Lesion I
"Where Is The Lesion" is a neuroanatomical localization exercise that teaches students to identify the site of a neurological lesion based on clinical signs and symptoms.
Where Is the Lesion I — Comprehensive Exam-Ready Notes
This lecture is the foundational framework for neurological localization — the single most critical skill in clinical neurology. Before you can decide what is wrong (pathological diagnosis), you must first determine where the nervous system is damaged (anatomical diagnosis). The entire lecture builds toward answering:
- Where is the lesion? (Anatomical diagnosis)
- What is the underlying pathology/aetiology? (Pathological diagnosis)
- Is it neurological or functional? (Organic vs. non-organic)
Diagnosis from history alone in many cases (80–90%) [1]
This means your clinical skill in taking a focused neurological history is far more powerful than any scan. The neurological examination confirms the history — it does not replace it.
Why this matters for exams: "Where is the lesion?" questions appear almost every year in the Fourth Summative MCQ and SAQ papers. You will be given a clinical vignette and must identify the anatomical site — hemisphere, brainstem, spinal cord, peripheral nerve, NMJ, or muscle. The 2023 MCQ paper had an entire EMQ section titled "WHERE IS THE LESION WITHIN THE NERVOUS SYSTEM" [3]. The 2024 and 2025 MCQ papers repeated similar stems [4][5]. This lecture gives you the localization framework to answer all of them.
Core Concepts and Mechanisms
Three key questions of neurology:
- Where is the lesion?
- What is the underlying pathology/aetiology?
- Is it neurological or functional? [1]
Why this order? Because anatomy constrains pathology. A 20-year-old with optic neuritis + transverse myelitis = demyelination (multiple sclerosis), but a 70-year-old with sudden hemiplegia = vascular. The where narrows the what. Functional (non-organic) disorders are a diagnosis of exclusion — but certain patterns (e.g., give-way weakness, non-anatomical sensory loss, Hoover's sign) can positively identify them.
History will direct our neurological examination. Examination can confirm history & support diagnosis. [1]
History structure from the lecture:
- C/O (Chief complaint)
- HPI: onset (sudden/gradual), duration, course (progressive/relapsing-remitting/static), recurrence, associated symptoms
- PMH (risk factors — e.g., hypertension, diabetes, AF for stroke)
- Drug & allergy (anticoagulants, neurotoxic drugs)
- Family history (hereditary neuropathies, Huntington's)
- Social (alcohol → cerebellar degeneration, neuropathy; occupation)
- O&G (relevant in women — e.g., pregnancy-related conditions)
- Review of systems
Both open & closed questions. Chronicity & associated features. System-specific questions. Avoid irrelevant information/too much details. Minimum of important 'negatives'. Ideas, concerns, expectations. [1]
Important negatives in neurology = specific symptoms you asked about that were absent. For example, if a patient has leg weakness, you must ask about and document absence of: bladder/bowel disturbance, back pain, sensory level, visual symptoms. These negatives help localize and exclude dangerous diagnoses.
Relative or eyewitness [1] — crucial for seizures, syncope, sudden onset events where the patient may not recall what happened.
This distinction is clinically vital and exam-relevant:
'Hard' physical signs:
- Wasting
- Fasciculations
- Limb reflexes, Babinski's sign
- Nystagmus
- Dysconjugate gaze
- Gag reflex
- Corneal & pupillary reflexes
- Cog-wheel rigidity [1]
'Soft' physical signs:
- Power
- Unsteadiness
- Sensory deficits [1]
Why the distinction? "Hard" signs are objective — they cannot be voluntarily reproduced and are more reliable for localization. Wasting proves denervation. Fasciculations prove anterior horn cell or nerve root disease. An upgoing plantar (Babinski) sign proves UMN pathology. Cog-wheel rigidity proves extrapyramidal disease. These signs carry high diagnostic weight.
"Soft" signs are subjective — they depend on patient effort/cooperation. Power testing can be affected by pain, poor effort, or functional overlay. Sensory deficits are entirely patient-reported. That doesn't mean they're useless, but you should never base your localization on one isolated soft sign that contradicts the rest of the picture.
Do not rely on just one isolated symptom or sign, especially if it goes against the rest of history or examination findings. [1]
Exam Trap
A common mistake is to over-interpret an isolated soft sign. If a patient has an upgoing plantar (hard sign) but reports normal sensation (soft sign), trust the Babinski. If a patient reports numbness in a non-anatomical distribution with normal reflexes and no wasting, consider functional disorder.
Neuroanatomy: The Localization Framework
Central nervous system = brain & spinal cord Peripheral nervous system = 12 pairs of cranial nerves & 31 pairs of peripheral nerves [1]
Levels of the nervous system:
- Brain: Cerebral hemispheres (left, right), Brain stem (midbrain, pons, medulla), Cerebellum
- Spinal cord & spinal roots
- Cervical, brachial, lumbar, sacral, coccygeal plexuses
- Cranial & peripheral nerves (motor, sensory, mixed)
- Neuromuscular junctions
- Muscles [1]
This hierarchy is the localization ladder. Every neurological presentation must be placed at one of these levels. The clinical features are different at each level, which is the entire point of this lecture.
Hemispheres: cortex, white matter, deep nuclei, ventricles Brain stem: mid-brain, pons, medulla Cerebellum 2% of body weight; 15% of cardiac output; 20% of oxygen intake [1]
Why does the brain get 15% of cardiac output despite being only 2% of body weight? Because neurons have extremely high metabolic demands — they depend almost entirely on aerobic glucose metabolism. This is why the brain is so vulnerable to ischaemia (stroke within minutes of blood flow interruption) and hypoglycaemia.
Most highly developed part. Most recent structure in evolution. Six distinct layers: I to VI. Sensing & interpreting inputs from various sources. Cognitive functions. Motor control & execution. Lobes with specific functions. [1]
Neurone cell bodies. Cortex folded into bulges (gyri) with deep furrows or fissures (sulci). Deep nuclei (basal ganglia & thalami). Information processing. [1]
The cortex has 6 histological layers. Layer IV receives sensory input (thickest in primary sensory cortex). Layer V contains the large pyramidal neurons that project to the spinal cord (thickest in primary motor cortex). This laminar organization is why cortical lesions produce specific functional deficits depending on location.
Subcallosal area, cingulate gyrus, parahippocampus, uncus, hippocampal formation, nucleus accumbens, hypothalamus, mammillary bodies, amygdala Behavioural & emotional responses, especially needed for survival (feeding, reproduction, caring for our young, & fight or flight responses) [1]
Clinically relevant: temporal lobe epilepsy often involves limbic structures → emotional auras, déjà vu, automatisms. Herpes simplex encephalitis targets temporal lobes/limbic structures → personality change, memory loss, seizures.
Lobe Functions & Localization of Cortical Lesions
This is the highest-yield section for exams. You must be able to map symptoms to lobes.
Cerebral cortex & ascending reticular activating system: consciousness & attention [1]
| Lobe | Functions | Lesion Signs |
|---|---|---|
| Frontal | Problem-solving, self-motivation, planning, mental tracking, abstract thinking, general motor control, language expression [1] | Expressive aphasia, impaired executive functions, disinhibition, emotional lability [1]; contralateral UMN weakness (motor strip); abulia (medial frontal); grasp reflex (primitive reflex release) |
| Temporal | Auditory information, language reception, encoding of memory, affect/emotions [1] | Amnesia, aggression, receptive aphasia, upper quadrantic visual field defect, temporal lobe epilepsy [1] |
| Parietal | Perception & integration of sensory data (stereognosis, graphesthesia, attention & recognition to simultaneous stimuli), space orientation, complex movement, recognition of self & the world [1] | Agnosia (tactile, visual), acalculia, hemineglect (non-dominant), lower quadrantic visual field defect [1] |
| Occipital | Vision & related information [1] | Contralateral hemianopia with macular sparing, visual hallucination [1] |
| Limbic | Memory & emotion [1] | Amnesia (hippocampal), personality change |
| Global/Diffuse | Multiple areas | Disorientation & reduced consciousness, low intelligence [1] |
High Yield — Visual Field Defects by Lobe
- Upper quadrantic visual field defect → temporal lobe (Meyer's loop = inferior optic radiation passes through temporal lobe; "pie in the sky")
- Lower quadrantic visual field defect → parietal lobe (superior optic radiation; "pie on the floor")
- Contralateral hemianopia with macular sparing → occipital lobe (dual blood supply to macular cortex from MCA and PCA protects macular vision even when PCA territory is infarcted) [1]
Apraxia: inability to perform a skilled motor activity despite intact strength, sensation, attention, memory & drive, with no other movement disorders → left inferior parietal lobule, frontal lobes (especially premotor cortex, supplementary motor area), or corpus callosum [1]
Why is this important? Apraxia localizes to specific cortical areas. It is NOT weakness — the patient has full power but cannot execute learned movements (e.g., cannot mime brushing teeth despite understanding the request). This distinguishes cortical lesions from pyramidal tract lesions.
Dominant hemisphere for language: left in 99% Rt-handed, 50% Lt-handed Non-dominant hemisphere for spatial awareness & visual processing [1]
Exam implication: If a question says "right-handed patient with dysphasia," the lesion is in the left hemisphere. If a left-handed patient has hemineglect, the lesion could be in either hemisphere but is more likely in the right (non-dominant for spatial awareness).
Exam Trap — Non-dominant Hemisphere
Non-dominant (usually right) parietal lesions cause hemineglect — the patient ignores the left side of space. This can be mistaken for left hemiplegia or visual field defect. Look for: inability to draw the left side of a clock face, failure to notice stimuli on the left during double simultaneous stimulation, dressing apraxia.
Pyramidal system: voluntary control of movement Extrapyramidal system: involuntary control of movement & coordination Cerebellar system: balance, coordination Autonomic system: HR, BP, respiration, GI, sweating, pupils, urination, sexual Spinothalamic system: crude touch, pain, temp Dorsal column system: fine touch, JPS, vibration [1]
Detailed System Breakdown
| System | Anatomy | Clinical Features When Lesioned |
|---|---|---|
| Pyramidal | Corticospinal tract & corticobulbar tracts; direct control of motor neurons in brainstem cranial motor nuclei & spinal anterior horn [1] | Weakness pattern, spasticity [1]; UMN signs: increased tone, hyperreflexia, upgoing plantar, clonus; pyramidal pattern weakness (upper limb extensors > flexors; lower limb flexors > extensors) |
| Extrapyramidal | Caudate nucleus, putamen, globus pallidus, substantia nigra; modulation & indirect control of motor neurons [1] | Bradykinesia, stiffness, tremor, abnormal movements, abnormal posturing [1]; e.g., Parkinson's (hypokinetic), Huntington's chorea (hyperkinetic) |
| Cerebellar | Cerebellum (vermis + hemispheres) | Coordination & rhythm of movements; unsteadiness, clumsiness, vertigo, shaky vision, scanning speech; truncal ataxia (vermis) [1] |
| Autonomic | Hypothalamus, brainstem, intermediolateral column, sympathetic/parasympathetic outflow | Orthostatic hypotension, sexual dysfunction, decreased ability to sweat, supine hypertension, changes in gastrointestinal & urinary habits [1] |
| Spinothalamic | Lateral spinothalamic tract (crosses 1–2 levels above entry) | Crude touch, pain, temperature [1]; contralateral loss below lesion |
| Dorsal column | Fasciculus gracilis/cuneatus (ipsilateral, crosses in medulla) | Fine touch, JPS, vibration [1]; ipsilateral loss below lesion (if spinal cord) |
Why the Distinction Between Spinothalamic and Dorsal Column Matters
These two sensory pathways travel in different parts of the spinal cord and cross at different levels. This is why partial cord lesions produce dissociated sensory loss:
- Brown-Séquard (hemisection): ipsilateral dorsal column loss + contralateral spinothalamic loss below lesion
- Anterior spinal artery syndrome: bilateral spinothalamic loss with preserved dorsal columns
- Syringomyelia: bilateral spinothalamic loss at the level of the syrinx ("cape-like" / suspended) with preserved dorsal columns [6]
This master table synthesizes the lecture content with supporting senior notes for exam use [1][2][6]:
| Level | Motor | Sensory | Reflexes | Other Key Features |
|---|---|---|---|---|
| Cerebral hemisphere | Contralateral UMN weakness | Contralateral cortical sensory loss | Hyperreflexia, upgoing plantar | Higher mental function deficits (aphasia, neglect, apraxia); seizures |
| Basal ganglia | Bradykinesia, rigidity | Usually spared | Normal or mildly increased | Tremor, chorea, dystonia, abnormal movements |
| Cerebellum | Ipsilateral incoordination (NOT weakness) | Usually spared | Pendular reflexes, hypotonia | Ataxia (truncal if vermis, limb if hemisphere), nystagmus, scanning dysarthria, intention tremor |
| Brainstem | Crossed deficits: ipsilateral CN palsy + contralateral UMN limb signs | Crossed sensory deficits possible | Variable | CN palsies, vertigo, diplopia, dysphagia, dysarthria, Horner's syndrome |
| Spinal cord | UMN below level, LMN at level | Sensory level; pattern depends on tract involved | Hyperreflexia below, absent at level | Sphincter disturbance; Brown-Séquard, anterior cord, central cord syndromes |
| Spinal root | Segmental LMN (myotomal) | Dermatomal | Reduced/absent at that segment | Pain (often radicular); no sphincter involvement unless cauda equina |
| Plexus | Multi-segmental LMN | Multi-dermatomal | Reduced | Pain common; multiple nerve territories affected |
| Peripheral nerve | LMN (specific nerve territory) | Specific nerve territory | Reduced/absent | Glove-and-stocking if diffuse; mononeuropathy if single nerve |
| NMJ | Fatigable weakness WITHOUT wasting | None | Normal | Fluctuating pattern; diplopia, ptosis, bulbar symptoms; NO sensory involvement |
| Muscle | Proximal weakness with wasting/pseudohypertrophy | None | Normal or reduced | Muscle pain; elevated CK; NO sensory involvement |
Key Discriminators for Exam Questions
Use these rules to rapidly localize:
- Aphasia/neglect/seizures → Hemisphere (cortical)
- Crossed cranial nerve + limb signs → Brainstem
- Sensory level + sphincter disturbance → Spinal cord
- Fatigable weakness, no wasting, no sensory loss → NMJ
- Proximal weakness, no sensory loss, raised CK → Muscle
- Glove-and-stocking sensory loss → Peripheral nerves
- Involuntary movements without weakness → Basal ganglia
- Ataxia + scanning speech + nystagmus without weakness → Cerebellum
Ability to provide a coherent history. Speech & language. Glasgow Coma Scale (eye, verbal, motor). [1]
Mini-Mental State Examination (MMSE): orientation to time & place, immediate & short-term recall, serial 7, repetition, naming of 2 objects, 3-step command, read & obey command, writing a sentence, copying of a drawing [1]
MMSE: > 27 = normal and < 24 = dementia [1]
| MMSE Domain | Maximum Score | What It Tests |
|---|---|---|
| Orientation (time) | 5 | Year, season, month, date, day |
| Orientation (place) | 5 | Country, town, district, hospital, floor |
| Registration | 3 | Immediate recall of 3 objects |
| Attention & calculation | 5 | Serial 7 subtraction from 100 |
| Recall | 3 | Delayed recall of 3 objects |
| Language — Naming | 2 | Name pencil and watch |
| Language — Repetition | 1 | "No ifs, ands, or buts" |
| Language — 3-stage command | 3 | Follow a 3-stage command |
| Language — Reading | 1 | Read and obey written command |
| Language — Writing | 1 | Write a complete sentence |
| Copy | 1 | Intersecting pentagons |
| Total | 30 |
Montreal Cognitive Assessment (MoCA) — mentioned as alternative; more sensitive for mild cognitive impairment [1]
GCS (Glasgow Coma Scale): Eye (4) + Verbal (5) + Motor (6) = max 15. This is tested heavily in past papers, especially in the context of ICH:
| Component | Score |
|---|---|
| Eye: Spontaneous/To voice/To pain/None | 4/3/2/1 |
| Verbal: Oriented/Confused/Inappropriate/Incomprehensible/None | 5/4/3/2/1 |
| Motor: Obeys/Localizes/Withdraws/Abnormal flexion/Extension/None | 6/5/4/3/2/1 |
General examination (stay focused). Neurological examination (screening vs. focused). Examinations of other systems. [1]
Screening examination = a quick run-through of all neurological systems when the history is non-localizing. Includes: higher mental function, cranial nerves I–XII, motor (tone, power, reflexes, plantars), sensory (light touch, pinprick, vibration, proprioception in hands and feet), coordination, gait.
Focused examination = targeted testing based on the history. If history suggests brainstem stroke, focus on cranial nerves, crossed signs, cerebellar signs. If history suggests peripheral neuropathy, focus on distal sensory testing, ankle reflexes.
Interpretation: normal vs. abnormal; anatomical & aetiological diagnosis [1]
Elicit signs (according to history & working diagnosis); new vs. pre-existing [1]
"New vs. pre-existing" — always check old notes. A patient with pre-existing hemiplegia from an old stroke may present with a new problem; don't attribute all findings to the acute event.
Applying the Framework: Past Paper Worked Examples
| Question | Vignette | Key Discriminator | Answer |
|---|---|---|---|
| Q9 | Difficulty climbing stairs + combing hair, no sensory symptoms, no difficulty with fine motor | Proximal weakness, no sensory involvement → Muscle | H. Muscles |
| Q10 | Sudden involuntary movements on left side, no weakness/numbness | Involuntary movements without weakness → Basal ganglia | A. Basal ganglia |
| Q11 | LL weakness, spasticity, bilateral Babinski, no UL symptoms | Bilateral UMN signs in LL only → lesion between cervical enlargement and conus → Thoracic spinal cord | J. Thoracic spinal cord |
| Q12 | Sudden right hemiplegia + global dysphasia | Dysphasia = dominant hemisphere cortical sign → Cerebral cortex dominant hemisphere | E. Cerebral cortex in dominant hemisphere |
| Q13 | Clumsiness, unsteady gait, slurred speech, no stiffness | Ataxia + dysarthria without spasticity → Cerebellum | D. Cerebellum |
"Right facial weakness + right facial numbness + dysarthria + grade 4 left limb power. Normal right limb power."
Analysis: Ipsilateral (right) CN involvement + contralateral (left) limb UMN weakness = crossed signs → Brainstem (Answer: A)
"Normal cranial nerves, grade 5 power, reduced reflexes, downgoing plantars, glove-and-stocking reduced touch/pain, normal JPS."
Analysis: Reduced reflexes (LMN), glove-and-stocking sensory loss, no UMN signs → Peripheral nervous system (Answer: C)
"Left facial weakness + dysarthria + grade 4 left limb power + reduced left limb touch."
Analysis: Same-side face and limb involvement → ipsilateral face + ipsilateral limb → Cerebral hemisphere (contralateral to the deficit side). This is NOT brainstem because in brainstem lesions, the face and limb would be on OPPOSITE sides (crossed signs). Answer: B. Cerebral hemisphere.
The Crossed vs. Uncrossed Rule
This is the #1 discriminator between hemisphere and brainstem:
- Same side face + limb weakness → Hemisphere (contralateral to the lesion; corticospinal fibers haven't crossed yet, and corticobulbar + corticospinal travel together)
- Opposite side face to limb weakness → Brainstem (CN nucleus is ipsilateral to lesion, corticospinal tract is about to cross or has crossed)
Be precise: in brainstem, CN palsy is LMN type (ipsilateral to lesion), limb signs are UMN type (contralateral to lesion). In hemisphere, both face and limb have UMN-pattern weakness contralateral to lesion.
"42-year-old: Day 1 — right facial asymmetry, can't close right eye, mouth deviates left. Day 2 — can't lift left arm, left hand weak, can't walk due to left leg weakness, slurred speech, chokes on water."
(a) Neurological deficits:
- Right LMN facial nerve palsy (inability to close eye = forehead involved → LMN)
- Left upper limb weakness (UMN type)
- Left lower limb weakness (UMN type)
- Dysarthria (slurred speech)
- Dysphagia (choking on water)
(b) Site of lesion: Right facial LMN palsy + left hemiparesis = crossed signs → Right-sided brainstem (specifically pons, where CN VII nucleus is located).
(c) Reflexes and plantars:
- Left upper and lower limb reflexes: hyperreflexic (UMN lesion)
- Left plantar response: upgoing (Babinski positive)
- Right upper and lower limb reflexes: normal
- Right plantar response: downgoing (normal)
Specific Localization Syndromes Worth Knowing
| Syndrome | Level | Artery | Ipsilateral | Contralateral |
|---|---|---|---|---|
| Weber | Midbrain | PCA penetrators | CN III palsy | Hemiplegia |
| Wallenberg | Lateral medulla | PICA / vertebral | CN V sensory loss, CN IX/X palsy, Horner's, cerebellar ataxia | Spinothalamic loss (trunk/limbs) [9] |
| Medial medullary | Medial medulla | Anterior spinal artery | CN XII palsy | Hemiplegia, dorsal column loss |
| Syndrome | Pathology | Motor | Sensory |
|---|---|---|---|
| Brown-Séquard | Hemisection | Ipsilateral UMN weakness below | Ipsilateral dorsal column loss + contralateral spinothalamic loss |
| Anterior cord | Anterior spinal artery occlusion | Bilateral motor paralysis below | Bilateral pain/temp loss; preserved JPS/vibration |
| Central cord | Syringomyelia / hyperextension injury | Arms > legs weakness | "Cape-like" bilateral pain/temp loss at level; preserved dorsal columns |
| Cauda equina | Below L1-L2 | Bilateral LMN (flaccid) | Saddle anaesthesia; bladder/bowel dysfunction |
Exam Intelligence
- EMQ / MCQ: Given clinical features → select the anatomical level
- SAQ: "Where is the site of the lesion?" — must state side AND level (e.g., "right pontine brainstem")
- SAQ: "What are the expected reflexes?" — must know UMN vs. LMN patterns
- GCS calculation from clinical description
- Visual field defect → lobe localization
| Trap | How to Avoid |
|---|---|
| Confusing hemisphere with brainstem | Check if face and limb are on SAME side (hemisphere) or OPPOSITE sides (brainstem) |
| Confusing UMN with LMN facial weakness | UMN = forehead spared (bilateral innervation); LMN = entire face including forehead |
| Assuming all weakness = pyramidal | Extrapyramidal = bradykinesia without true weakness; NMJ = fatigable weakness; muscle = proximal weakness |
| Forgetting NMJ has NO sensory loss | If sensory symptoms present → NOT NMJ |
| Confusing cerebellar with sensory ataxia | Cerebellar: nystagmus, intention tremor, dysarthria, NO Romberg; Sensory: positive Romberg, loss of proprioception |
| Mixing up upper vs. lower quadrantic defects | Upper quadrant = temporal (Meyer's loop); Lower quadrant = parietal (superior radiation) |
- Always state side of lesion (e.g., "left cerebral hemisphere" not just "hemisphere")
- For brainstem: specify level if possible (midbrain/pons/medulla)
- For spinal cord: specify the segment level
- Use the phrase "UMN pattern weakness" or "LMN pattern weakness" — examiners look for this terminology
- For GCS: break down into E + V + M components to show working
-
A 60-year-old man presents with sudden right arm and leg weakness with expressive aphasia. Where is the lesion? → Left cerebral hemisphere (frontal lobe/MCA territory). Aphasia in a right-handed patient = dominant (left) hemisphere.
-
A patient has left CN III palsy with right hemiplegia. Name the syndrome and level. → Weber syndrome, left midbrain.
-
A 70-year-old has bilateral lower limb spasticity, bilateral upgoing plantars, and a sensory level at T6. No upper limb signs. Where is the lesion? → Thoracic spinal cord (at or above T6).
-
A 30-year-old has proximal weakness in arms and legs, cannot climb stairs or comb hair, no sensory symptoms, normal reflexes. Where is the lesion? → Muscle (myopathy).
-
A 50-year-old has fatigable ptosis and diplopia, worse at end of day, no sensory symptoms. Where is the lesion? → Neuromuscular junction (myasthenia gravis).
-
Distinguish between cerebellar ataxia and sensory ataxia. → Cerebellar: nystagmus, intention tremor, dysarthria, negative Romberg; Sensory: positive Romberg, loss of proprioception, no nystagmus.
High Yield Summary
The "Where is the Lesion?" framework is the foundation of neurological diagnosis.
- History gives you the diagnosis 80–90% of the time. Examination confirms.
- Hard signs (wasting, fasciculations, reflexes, Babinski, nystagmus, pupillary reflexes) are more reliable than soft signs (power, sensation).
- The localization ladder: Hemisphere → Basal ganglia → Cerebellum → Brainstem → Spinal cord → Root → Plexus → Peripheral nerve → NMJ → Muscle.
- Hemisphere: contralateral UMN + cortical signs (aphasia, neglect, seizures). Face and limb on SAME side.
- Brainstem: CROSSED signs (ipsilateral CN palsy + contralateral limb UMN). This is the #1 discriminator from hemisphere.
- Spinal cord: sensory level, UMN below, sphincter disturbance.
- Peripheral nerve: LMN, glove-and-stocking, reduced reflexes.
- NMJ: fatigable weakness, NO sensory loss, NO wasting.
- Muscle: proximal weakness, NO sensory loss.
- Dominant hemisphere (left in 99% right-handed) = language. Non-dominant = spatial awareness.
- Visual field defects: upper quadrantanopia = temporal lobe; lower quadrantanopia = parietal lobe; hemianopia with macular sparing = occipital lobe.
- MMSE: > 27 normal, < 24 dementia. Know the domains and scoring.
Active Recall - Where Is the Lesion I
[1] Lecture slides: GC 094. Where is the lesion I.pdf [2] Senior notes: Ryan Ho Neurology.pdf (Section 1.3 — Where and What is the Lesion) [3] Past papers: 2023 Fourth Summative MCQ.pdf (Q9–Q13, "Where is the Lesion" EMQ) [4] Past papers: 2024 Fourth Summative MCQ.pdf (Q9, Q45) [5] Past papers: 2025 Fourth Summative MCQ.pdf (Q7); 2025 Fourth Summative SAQ.pdf (Q1) [6] Senior notes: Ryan Ho Fundamentals.pdf (p322 — Spinal cord lesions, peripheral nerve lesions) [7] Past papers: 2018 Fourth Summative SAQ.pdf (Q8 — GCS calculation, basal ganglion haemorrhage) [8] Past papers: 2019 Fourth Summative SAQ.pdf (Q8 — GCS calculation, basal ganglion haemorrhage) [9] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (p1110 — Wallenberg syndrome)
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