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)
- Could this be a functional neurological presentation?
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 plus transverse myelitis raises demyelination in the differential, while sudden hemiplegia in an older adult raises a vascular cause; neither pattern alone establishes the final diagnosis. The where narrows the what.
Current practice — functional neurological disorder
Functional neurological disorder (FND) is not simply a diagnosis of exclusion. Diagnose it from positive, internally inconsistent or incongruent features demonstrated on examination (for example, Hoover's sign or tremor entrainment), while still investigating plausible comorbidity. Symptoms are real and can coexist with another neurological disease [11]. “Non-organic” is therefore best treated as lecture-era wording rather than a synonym for fabricated symptoms.
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]
The slide also ends with reflecting experience and knowledge: periodically summarize the story back to the patient, check that your interpretation is correct, and use each answer to refine the next question and the examination rather than merely transcribing events.
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]
How to use the distinction: the lecture's “hard/soft” labels describe relative objectivity, not proof. Wasting, fasciculations, reflex asymmetry, an extensor plantar response and ocular-motor abnormalities often carry high localizing weight, but each still requires technique and context. Fasciculations can be benign; wasting is not specific to denervation; plantar responses can be equivocal; and cogwheeling can be mimicked by voluntary opposition or coexisting tremor.
Power, gait and sensory testing are more dependent on effort, comprehension, pain and examiner technique, but they remain essential. Repeat unexpected findings, compare sides, look for a coherent anatomical pattern and reconcile the examination with the history rather than automatically discarding a “soft” sign.
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 any isolated sign. An extensor plantar response supports corticospinal dysfunction but should be elicited correctly and interpreted with the rest of the examination. A non-dermatomal sensory complaint alone does not diagnose FND; look for positive inconsistency/incongruence and consider organic and functional comorbidity.
Neuroanatomy: The Localization Framework
Central nervous system = brain & spinal cord Peripheral nervous system = 12 pairs of cranial nerves & 31 pairs of peripheral nerves [1]
Anatomy correction: the slide means 31 pairs of spinal nerves, not 31 pairs of peripheral nerves. Distal named peripheral nerves are far more numerous and arise through roots and plexuses; that root → plexus → named nerve sequence is central to localization.
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.
Slide 14 places primary cortices beside association cortices. Read the lateral surface from anterior to posterior:
- Prefrontal cortex supports executive and behavioural control; the premotor/supplementary motor network plans learned movements.
- Primary motor cortex lies in the precentral gyrus, immediately anterior to the central sulcus; primary somatosensory cortex lies in the postcentral gyrus immediately posterior to it.
- Posterior parietal somatosensory association cortex integrates modalities for stereognosis, graphesthesia and spatial attention.
- Primary auditory cortex is in the superior temporal region, with surrounding auditory/language association cortex; primary visual cortex is occipital, with surrounding visual association cortex.
- The labelled Broca and Wernicke regions are useful bedside shorthand, but real language function is a distributed, connected network. Lesion size and disconnection therefore affect the aphasia phenotype.
The adjacent motor homunculus explains the somatotopic pattern of weakness:
| Motor cortex surface | Predominant representation | Localization consequence |
|---|---|---|
| Medial/paracentral lobule | Foot and leg | Medial frontal/ACA-territory lesion → contralateral leg-predominant weakness |
| Superior lateral convexity | Trunk, shoulder, arm and hand | Lateral hemisphere/MCA lesion → contralateral arm-predominant weakness |
| Inferolateral convexity | Face, lips, tongue and pharynx | Inferolateral motor cortex lesion → contralateral central facial/bulbar-pattern deficit |
The drawing is intentionally distorted: cortical area reflects fineness and complexity of motor control, not the physical size or strength of the body part. The sensory homunculus follows a broadly similar medial-leg to lateral-face ordering on the postcentral gyrus.
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 | Bilateral cortex and/or arousal networks | Disorientation, impaired attention and global cognitive dysfunction; reduced consciousness particularly implicates diffuse hemispheric dysfunction or the ascending arousal system |
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 homonymous hemianopia, sometimes with macular sparing → occipital lobe. Macular sparing is a useful clue, not a requirement; the traditional explanation invokes collateral/dual supply to the occipital pole, but an occipital lesion may also involve macular vision.
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 [1] Non-dominant hemisphere for spatial awareness & visual processing [1]
Interpret the percentage as lecture-era shorthand, not a rule. In a direct study of 326 healthy people, right-hemisphere language dominance increased from 4% in strong right-handers to 27% in strong left-handers; most strong left-handers therefore still had left-hemisphere language dominance [12]. For a typical examination vignette, aphasia still points to the dominant hemisphere (usually left), but handedness alone cannot establish dominance in an individual—especially before epilepsy/neurosurgical procedures.
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]
“Extrapyramidal” is retained here because it appears in the lecture and examinations. It is a descriptive historical umbrella, not one discrete tract: basal-ganglia–thalamocortical circuits select and scale movement, while multiple brainstem pathways also influence posture and tone.
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]
Current interpretation — a screen is not a diagnosis
The slide's fixed labels (“> 27 normal”, “< 24 dementia”) are not safe as stand-alone diagnostic rules. MMSE performance is influenced by age, education, language/culture, sensory impairment, delirium and testing conditions. A low score supports further evaluation but does not by itself diagnose dementia; a normal score does not rule dementia out. Interpret a locally validated instrument alongside change from baseline, functional impact, informant history, examination and evaluation for reversible contributors. NICE explicitly advises not ruling out dementia solely because a cognitive-instrument score is normal [10], and the US National Institute on Aging likewise states that cognitive-test results alone are insufficient for diagnosis [13].
| 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]
Reading the MoCA Visual
Slide 22 shows English MoCA v8.1 beside the Hong Kong MoCA, making two important points:
- Both are 30-point multidomain screens covering visuospatial/executive tasks, naming, memory, attention, language, abstraction, delayed recall and orientation. The original validation study found MoCA more sensitive than MMSE for mild cognitive impairment in its study population [14].
- A translated form is not automatically interchangeable with the source form. Use a version validated for the patient's language and cultural context, record the exact version, and interpret against appropriate norms. Limited literacy, aphasia, impaired vision/hearing or motor disability may invalidate particular items.
MoCA is still a screen, not an anatomical localization test or a dementia diagnosis. The pattern of errors can guide a fuller cognitive and neurological assessment, but the total score must be integrated with function and clinical context [13].
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.
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 ataxia is evident with eyes open and remains when they close; sensory ataxia worsens markedly when visual input is removed (positive Romberg) and accompanies impaired proprioception. “No Romberg in cerebellar disease” is misleading. |
| 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
High Yield Summary
-
The "Where is the Lesion?" framework is the foundation of neurological diagnosis.
-
Start with a focused history, then test whether multiple examination findings form one coherent anatomical pattern; no single “hard” or “soft” sign is proof.
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Move down the localization ladder: hemisphere → basal ganglia → cerebellum → brainstem → spinal cord → root → plexus → peripheral nerve → NMJ → muscle.
-
Hemisphere: contralateral UMN deficit plus cortical features such as aphasia, neglect, visual-field loss, apraxia or seizures. The motor homunculus explains leg-medial, arm-lateral and face-inferolateral somatotopy.
-
Brainstem: an ipsilateral cranial-nerve deficit with contralateral long-tract signs is a high-yield crossed pattern.
-
Spinal cord: seek a sensory level, UMN signs below the lesion and sphincter/autonomic involvement.
-
Peripheral nerve: expect LMN signs and sensory loss in a named-nerve or length-dependent pattern; NMJ and muscle do not produce primary sensory loss.
-
Aphasia points to the language-dominant hemisphere (usually left), but handedness does not determine dominance with certainty.
-
Temporal optic-radiation lesions tend to cause contralateral superior quadrantanopia; parietal lesions inferior quadrantanopia; occipital lesions homonymous hemianopia, sometimes with macular sparing.
-
MMSE and MoCA are screening instruments. Neither a threshold nor a total score alone diagnoses or excludes dementia.
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) [10] NICE. Dementia: assessment, management and support — recommendations (sections 1.2.1–1.2.11; accessed 10 August 2026). [11] NHS Scotland Right Decisions. Functional neurological disorder pathway (positive diagnostic criteria and comorbidity; accessed 10 August 2026). [12] Knecht S, et al. Handedness and hemispheric language dominance in healthy humans. Brain. 2000;123:2512–2518. doi:10.1093/brain/123.12.2512. [13] US National Institute on Aging. Assessing cognitive impairment in older patients (accessed 10 August 2026). [14] Nasreddine ZS, et al. The Montreal Cognitive Assessment, MoCA: a brief screening tool for mild cognitive impairment. J Am Geriatr Soc. 2005;53:695–699. doi:10.1111/j.1532-5415.2005.53221.x.
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