Neurological Localisation
Start with the distribution. Find the sign that separates the two plausible sites, then examine for it. A defensible broad localisation is more useful than a confident eponym that does not fit.
Anatomical figures sit beside the relevant patterns. Use Enlarge ↗ for labels, then + to zoom. The pictures are embedded for offline use; credits and clinical caveats sit below each one.
Act while you localise
Sudden focal deficit: glucose, last known well, stroke escalation and urgent brain / vascular imaging through the local pathway. Record a baseline NIHSS and the disabling deficit; a low score, isolated hand weakness or a normal early CT does not exclude stroke. New diplopia, dysphagia, severe imbalance or bilateral signs can be posterior circulation disease.
New bladder / perineal change with leg symptoms; a sensory level; rapidly progressive weakness: urgent senior assessment for cord / cauda equina pathology and emergency MRI as indicated. Bulbar or respiratory weakness, falling consciousness, or a new third-nerve palsy: immediate escalation.
[1] [2] [3] [7] [27] [45] [46]1First pass: where in the nervous system?
Establish onset and progression, then map face, arm, leg and trunk. Compare both sides. Language, visual fields, eye movements, reflexes and the plantar response often change the localisation.
| Feature | UMN pattern | LMN pattern |
|---|---|---|
| Tone / reflexes | Spasticity, brisk reflexes, clonus; extensor plantar | Reduced tone / reflexes in the affected arc; wasting and fasciculations may develop |
| Distribution | Pyramidal pattern; loss of fine movement; may include face | Root, nerve or anterior-horn pattern; compare muscles individually |
| Important exception | Acute stroke / cord injury can be flaccid and hyporeflexic. | Normal reflexes do not exclude mild neuropathy; reflex loss alone does not identify the cause. |
UMN = upper motor neurone; LMN = lower motor neurone; NMJ = neuromuscular junction. Ipsilateral = same side as the lesion; contralateral = opposite side. Roman numerals denote cranial nerves.
2Stroke territories and subcortical patterns
All deficits below are relative to the lesion side. Vascular territories overlap; the examination suggests a territory, while CTA/MRA and brain imaging establish the vascular lesion.
Arterial territories: lateral surface
ACA: medial leg area is mostly hidden here. MCA: lateral face / arm and language or attention networks. PCA: occipital visual cortex. The coloured territories are approximate.
Frank Gaillard, based on Patrick J. Lynch. Original / source. CC BY-SA 3.0. Resized / rendered for display; anatomical content unchanged.
Arterial territories: medial surface
Medial frontal / parietal cortex → leg-predominant ACA pattern. Posterior medial occipital cortex → PCA visual pattern. Surface maps do not show the deep perforator territories.
Fred the Oyster, after Frank Gaillard and Patrick J. Lynch. Original / source. CC BY-SA 3.0. Resized / rendered for display; anatomical content unchanged.
| Likely site / territory | Pattern that points there | Useful discriminator / trap |
|---|---|---|
| MCA, superior division Lateral frontal | Contralateral face / arm weakness > leg; dominant side: effortful, non-fluent aphasia. | Test comprehension and repetition. Destructive frontal eye-field lesion often causes gaze towards the lesion. |
| MCA, inferior division Temporoparietal | Dominant: fluent but impaired comprehension; non-dominant: neglect. Contralateral field deficit; weakness may be slight. | Do not confuse fluent aphasia with confusion. Neglect is an attentional deficit, not simply a visual-field cut. |
| Proximal MCA / ICA | Combined motor, sensory, gaze, field and language / attention abnormalities. | Severe cortical syndrome suggests a large territory; the exact occlusion requires vascular imaging. |
| ACA Medial frontal / parietal | Contralateral leg-predominant weakness / sensory loss; abulia, impaired initiation; sometimes incontinence. | Marked arm–face involvement suggests extension or another site. Bilateral lesions may cause akinetic mutism. |
| PCA Occipital / medial temporal | Contralateral homonymous field loss; memory disturbance if medial temporal involved. | Dominant occipital + splenial lesion: alexia without agraphia. Thalamic / midbrain involvement adds other signs. |
| Internal capsule / corona radiata | Contralateral motor ± sensory deficit; often dense face–arm–leg weakness without obvious cortical signs. | Motor fibres are compact. A small lesion can produce substantial weakness. |
| Anterior choroidal | Contralateral weakness, sensory loss and homonymous field loss; the full combination is often incomplete. | Internal-capsule and visual-pathway involvement; hemiparesis may dominate. |
| Thalamus | Contralateral face–body sensory loss; sometimes ataxia, altered alertness, language / attention change. | Pain may develop later. Bilateral paramedian injury can cause somnolence, amnesia and vertical gaze disturbance. |
| Watershed | Border-zone injury: proximal limb weakness, language or higher-function deficits depending on distribution. | Bilateral ACA–MCA injury can produce disproportionate shoulder / arm weakness. Hypoperfusion and embolism can contribute. |
| Vertebrobasilar / cerebellar | Diplopia, dysarthria, dysphagia, vertigo / ataxia; crossed signs, bilateral weakness or impaired consciousness. | Posterior stroke can be disabling with few NIHSS points. See brainstem and ataxia. |
Lacunar clinical patterns
- Pure motorCapsule / corona radiata / ventral pons.
- Pure sensoryOften thalamus; other sensory pathways possible.
- SensorimotorThalamocapsular or adjacent pathways.
- Ataxic / clumsyAtaxic hemiparesis or dysarthria–clumsy hand: pons or subcortical pathways.
Do not infer mechanism from the syndrome
- No cortical signsSupports a subcortical pattern; does not prove small-vessel disease.
- Sudden hand palsyA hand-area cortical infarct can resemble radial, median or ulnar palsy.
- ImagingA normal early non-contrast CT does not exclude ischaemia, particularly in the posterior fossa.
ANZ stroke guidance: function changes eligibility
- DisablingAphasia, hemianopia or substantial hand dysfunction can be disabling despite a low NIHSS. Document the real functional impact and assess for reperfusion; do not impose an arbitrary score cutoff.
- ImprovingIf a disabling deficit remains, improvement alone does not remove IVT eligibility. Low clinical severity must not be the sole reason to omit CTA.
- TreatmentSee the acute stroke guide for the current IVT / EVT pathways; the anatomical pattern cannot establish treatment eligibility by itself.
ANZ stroke guidance: transient or worsening signs
- Ongoing / fluctuatingManage as stroke. Fully resolved focal symptoms still need urgent TIA assessment; ABCD2 alone must not determine urgency.
- DeteriorationRepeat the examination, glucose and physiology; escalate and obtain urgent repeat brain imaging when indicated. Do not wait for the routine 24h scan.
- SwallowAll acute strokes need a validated swallow screen by trained staff within 4h and before oral food, fluid or medicines. Failed screen or deterioration → speech pathology; bedside bulbar signs cannot establish swallow safety.
3Language, vision and cortical clues
Describe the language deficit before naming the aphasia. Test spontaneous speech, naming, a command that cannot be guessed, repetition, reading and writing. Check hearing, attention and premorbid language.
| Speech / language pattern | Typical localisation | Bedside distinction |
|---|---|---|
| Non-fluent; comprehension relatively better; poor repetition | Dominant frontal / perisylvian network; Broca pattern | Short, effortful phrases; complex grammar may still be difficult. |
| Fluent; poor comprehension and repetition | Dominant posterior perisylvian network; Wernicke pattern | Normal rhythm does not imply meaningful language. |
| Fluent; comprehension relatively preserved; repetition disproportionately poor | Dominant dorsal language network; conduction pattern | Use a short phrase, then a longer sentence. |
| Markedly reduced output and comprehension | Extensive dominant language-network injury; global pattern | Exclude reduced arousal or severe hearing / attention impairment. |
| Repetition relatively preserved despite other language deficits | Transcortical pattern; frontal or posterior network disconnection | Describe the profile; repetition alone does not identify one artery. |
| Slurred articulation with intact naming / comprehension | Dysarthria; cortical, subcortical, brainstem, cerebellar or neuromuscular | Dysarthria alone is a poor anatomical localiser. |
Field loss at a glance
Read these as the patient’s visual world, not a face-on eye examination. Homonymous loss affects the same side of space in both eyes. Test each eye separately; acuity and attention still matter.
ClinicalReference schematic. Anatomy: [8] [10] [11]. Simplified for bedside lookup.
Visual field → pathway
| Finding | Likely site | Check / caveat |
|---|---|---|
| Monocular visual loss | Retina / optic nerve, anterior to chiasm | Acuity, colour, pupils / RAPD, fundus. Sudden retinal ischaemia needs urgent assessment. |
| Bitemporal field loss | Optic chiasm | Test each eye separately; consider sellar / suprasellar disease. |
| Homonymous field loss | Contralateral retrochiasmal pathway | Same side of visual space in both eyes. A right field loss localises to the left pathway. |
| Superior homonymous quadrant | Often contralateral temporal optic radiation (Meyer loop) | Quadrant patterns are suggestive, not perfectly specific. |
| Inferior homonymous quadrant | Often contralateral parietal optic radiation | Look for neglect, sensory extinction and other parietal signs. |
| Congruous homonymous hemianopia | Often contralateral occipital cortex; other retrochiasmal sites possible | Macular sparing supports but does not prove an occipital site. |
Useful cortical signs
Neglect / extinction: commonly non-dominant, usually right, attention network. Astereognosis / agraphesthesia: contralateral parietal association cortex only if primary sensation, attention and comprehension are adequate. Apraxia: impaired learned action despite sufficient strength and comprehension, often dominant parietofrontal network.
ANZ assessment check: assess acuity with the patient’s glasses, fields and ocular alignment / movements. Screen communication; arrange formal specialist assessment when impaired. Suspected neglect warrants assessment with validated tools, even if a brief bedside screen seems reassuring. A language or field deficit is a rehabilitation and safety issue as well as a localising sign.
4Brainstem: level, side, neighbouring tract
Cranial-nerve levels and crossed findings
Use the cranial-nerve sign to suggest a level, then check the nearby motor / sensory pathways. This is a level map: nuclei, fascicles and vascular supply are more complex than the boxes.
ClinicalReference schematic. Anatomy: [12] [13]. Simplified for bedside lookup.
Find the level, then the tract
- MidbrainIII / IV; vertical eye-movement pathways.
- PonsV–VIII; horizontal gaze / facial pathways.
- MedullaIX, X, XII patterns; XI has substantial spinal origin.
- Crossed signsIpsilateral cranial-nerve finding + contralateral limb deficit is a strong clue, not a requirement.
Why the sides differ
- MotorCorticospinal fibres cross in caudal medulla: most brainstem lesions weaken the opposite limbs.
- Body sensationPain / temperature has already crossed in cord; vibration / position crosses in medulla.
- Face / balanceSpinal trigeminal and cerebellar connections often give ipsilateral findings.
- Rule of 4A memory aid. It does not guarantee the whole syndrome or exact artery.
| Site / familiar name | Characteristic combination | What separates it |
|---|---|---|
| Lateral medulla Wallenberg; vertebral / PICA territory | Ipsilateral facial pain–temperature loss, ataxia / Horner; contralateral body pain–temperature loss; vertigo, dysphagia, hoarse voice. | Nucleus ambiguus involvement gives swallowing / voice signs. Limb power may be preserved. Not every case has every feature. |
| Medial medulla | Ipsilateral XII weakness + contralateral limb weakness and vibration / joint-position loss. | Tongue may deviate towards the lesion on protrusion. Facial movement often spared. |
| Lateral caudal pons AICA territory | Ipsilateral whole-face weakness, vestibular / auditory symptoms and ataxia; crossed pain–temperature findings may occur. | New hearing loss with continuous vertigo can be vascular. An abnormal head impulse does not rule out AICA stroke. |
| Medial / dorsal pons | Ipsilateral VI fascicular palsy or horizontal gaze palsy; contralateral weakness if corticospinal tract involved. | VI nerve / fascicle: one eye cannot abduct. VI nucleus: both eyes cannot gaze towards that side. |
| Ventral midbrain Weber pattern | Ipsilateral III palsy + contralateral hemiparesis. | Additional ataxia / tremor suggests tegmental structures; do not force an eponym. |
| Basilar territory | May present with hemiparesis, rather than tetraparesis. More extensive injury can give bilateral long-tract / cranial-nerve signs or impaired consciousness. | Do not require bilateral signs before vascular imaging. Extensive ventral pontine injury can produce locked-in syndrome: quadriplegia / anarthria, awareness and often vertical gaze / blinking preserved; seek communication. |
A cranial-nerve palsy can arise in the nucleus, fascicle, subarachnoid space, skull base, orbit or peripheral nerve. A brainstem localisation becomes stronger when neighbouring pathways are also affected.
5Eyes and cranial nerves: the useful distinctions
Worked eye-movement pattern: left INO
Name INO by the side of the failed adduction. Here that is the left MLF. A III palsy or myasthenia can mimic part of the pattern; use the rest of the examination.
ClinicalReference schematic. Anatomy: [13] [14] [15]. Simplified for bedside lookup.
| Eye-movement finding | Localisation | Confirm / trap |
|---|---|---|
| III palsy: ptosis; impaired adduction, elevation / depression; often down-and-out eye | Ipsilateral III nerve / fascicle; nuclear lesions may be more complex | New acquired III palsy needs urgent assessment / imaging for compression. Pupil sparing does not safely exclude aneurysm. |
| IV palsy: vertical / torsional diplopia, worse looking down in adduction | Superior oblique pathway; usually ipsilateral peripheral IV | Look for hypertropia and compensatory head tilt. Skew deviation and myasthenia can mimic it. |
| VI palsy: one eye fails to abduct | Ipsilateral VI nerve / fascicle | VI palsy can be a false-localising sign of raised intracranial pressure. |
| INO: impaired adduction; abducting nystagmus in other eye | MLF on the side of the adduction deficit | Left eye fails to adduct on right gaze → left MLF. Convergence is often preserved; its loss does not exclude INO. |
| One-and-a-half: ipsilateral horizontal gaze palsy + INO | Ipsilateral pontine horizontal gaze centre / VI nucleus and MLF | Only the contralateral eye can abduct horizontally. Facial weakness may coexist. |
| Conjugate horizontal gaze palsy | Ipsilateral pontine gaze circuitry, or contralateral cerebral control | Destructive frontal lesion: eyes often towards lesion. Destructive pontine lesion: gaze often away from lesion. Seizures can reverse the cortical pattern. |
| Vertical gaze palsy | Rostral midbrain / associated thalamomesencephalic pathways | Look for impaired convergence, pupil abnormalities or impaired alertness. |
| Ptosis + miosis, anisocoria greater in dark | Ipsilateral sympathetic pathway: Horner syndrome | Central, preganglionic or postganglionic. Acute painful Horner → urgently assess for carotid dissection. |
Face, palate and tongue
- FaceContralateral lower-face weakness with relative forehead sparing → supranuclear. Ipsilateral upper + lower face → VII nucleus / fascicle / nerve.
- Forehead trapForehead involvement alone does not exclude stroke; a pontine VII lesion gives an LMN facial pattern.
- Palate / voiceUnilateral X weakness: palate weak ipsilaterally, uvula often pulled away. Assess voice, cough and swallow; gag alone is unreliable.
- TongueLMN XII: deviation towards weak side, possible wasting / fasciculation. UMN tongue weakness is often less striking; isolated direction is insufficient.
Multiple cranial nerves: think along the course
- Cavernous sinusIII / IV / VI ± V1 / V2 ± sympathetic fibres; optic nerve usually spared.
- Orbital apexOphthalmoplegia plus optic neuropathy / RAPD; often V1 involved.
- CPAVIII hearing / vestibular signs ± VII / V; may add cerebellar signs.
- Bulbar patternLMN IX / X / XII: weakness, wasting, nasal / breathy speech. Bilateral corticobulbar: brisk jaw jerk, spastic dysarthria ± emotional lability.
[12] [13] [14] [15] [16] [17] [18] [40] [42] ↑ Back to lookup
6Ataxia and the acutely dizzy patient
| Ataxia pattern | Findings to seek | Likely system |
|---|---|---|
| Cerebellar | Dysmetria / decomposition, dysdiadochokinesia, cerebellar dysarthria or ocular signs; remains abnormal with eyes open | Limb findings usually ipsilateral hemisphere / connections; gait and truncal instability may indicate vermis or wider disease. |
| Sensory | Impaired joint position / vibration; pseudoathetosis; much worse with eyes closed | Large-fibre peripheral sensory pathway or dorsal columns. Check reflexes and a sensory level. |
| Vestibular | Vertigo, nausea, nystagmus, lateropulsion; limb coordination may be preserved | Peripheral labyrinth / vestibular nerve or central vestibular pathways. Use timing, triggers and examination together. |
Cerebellar arterial clues
PICA (posterior inferior cerebellar): inferior cerebellum; vertigo, gait / truncal instability ± lateral medullary signs. AICA (anterior inferior): cerebellar / lateral pontine pattern; auditory and facial findings help. SCA (superior): limb / gait ataxia and dysarthria. Territory patterns overlap; none of these signs determines the artery by itself.
HINTS: only in the right setting
- WhoAcute continuous vestibular syndrome with nystagmus, examined by someone trained in HINTS. Not a general dizziness screen or a test for brief positional episodes.
- Central cluesNormal head impulse, direction-changing gaze-evoked nystagmus, or skew deviation; any central / equivocal result requires further assessment.
- Hearing / gaitCheck new unilateral hearing loss and ability to sit / stand / walk safely. Severe gait / truncal instability is concerning.
- ActionFocal neurological signs or a convincing stroke syndrome → stroke assessment directly. Do not wait to complete HINTS.
Two traps worth remembering
- RombergA marked deterioration on eye closure supports sensory / vestibular dependence. It does not establish a cerebellar lesion.
- Negative imagingEarly MRI can miss posterior circulation infarction. Persistent clinical concern needs senior review and an imaging plan.
- Not just vertigoDiplopia, dysphagia, crossed sensory loss or new severe imbalance should prompt a central explanation.
7Spinal cord, conus and cauda equina
A sensory level and face-sparing long-tract signs favour cord disease. Check upper limbs even when the complaint is in the legs. The skin sensory level may lie below the structural lesion; cord segment and vertebral level are different.
Crossings explain which side is affected
Left hemicord pattern: left weakness + left position / vibration loss, with right pain / temperature loss below. The sensory level may lag the lesion by several segments; complete textbook patterns are uncommon.
ClinicalReference schematic. Anatomy: [22] [23] [24]. Simplified for bedside lookup.
Spinal cord: where the tracts sit
Posterior is at the top. Find the dorsal columns, lateral corticospinal tract and anterolateral system. This is a teaching cross-section, not a patient MRI or a precise segment-specific boundary map.
Polarlys and Mikael Häggström; English translation by Selket. Original / source. CC BY-SA 3.0. Resized / rendered for display; anatomical content unchanged.
Corticospinal
- CrossingCaudal medulla.
- Cord lesionIpsilateral UMN weakness below lesion; LMN findings at affected segment.
Dorsal columns
- CarriesVibration, position, discriminative touch.
- CrossingMedulla → cord lesion causes ipsilateral loss below lesion.
Spinothalamic
- CarriesPain / temperature.
- CrossingIn cord, near entry → contralateral loss, often starting a few segments below.
| Pattern | Expected findings | Bedside implication / caveat |
|---|---|---|
| Cervical myelopathy | Hand clumsiness ± segmental arm wasting / reduced reflexes, with brisk legs, extensor plantars and gait disturbance | Coexisting radiculopathy / neuropathy can mask reflex changes. No facial signs from an isolated cervical lesion. |
| Thoracic cord | Paraparesis, trunk sensory level and possible sphincter dysfunction; arms spared | A normal upper-limb examination helps distinguish from cervical disease; imaging level cannot be read exactly from skin level. |
| Hemicord / Brown-Séquard | Ipsilateral weakness and position / vibration loss; contralateral pain–temperature loss below lesion | Real lesions are often partial. At-level root / segmental findings may coexist. |
| Anterior cord | Bilateral motor and pain–temperature impairment; relative preservation of vibration / position | Consider infarction or compression in the clinical setting; the pattern does not identify the cause. |
| Central cervical cord / syrinx | Central cord injury: arms often weaker than legs. Syrinx: segmental bilateral pain–temperature loss ± hand LMN signs | These are related anatomical patterns with different clinical settings; do not equate every central cord lesion with a syrinx. |
| Conus medullaris | Saddle sensory and early bladder / bowel / sexual dysfunction; often bilateral; mixed UMN / LMN features possible | Often around L1–L2 vertebral region in adults. Symptoms overlap cauda equina. |
| Cauda equina | Root pain, asymmetric or bilateral flaccid weakness, reduced reflexes, saddle / sphincter disturbance | A root syndrome below the cord. New urinary sensation / voiding change matters before complete retention. Do not wait for every classic sign. |
Possible compression: examination cannot safely exclude it
New perineal or bladder / bowel changes, a sensory level, rapidly worsening weakness, or severe spinal pain with infection / cancer / bleeding risk need urgent escalation and an MRI plan. Normal anal tone or a reassuring bladder measurement alone must not close the diagnosis.
Approximate sensory landmarks: T4 nipple line; T10 umbilicus; L1 groin; S2 posterior thigh; S3–5 saddle / perianal region. Dermatomes overlap. In acute cord injury, spinal shock can initially suppress reflexes and tone.
8Roots, sensory clues and reflexes
These are practical root contributions, not exclusive wiring. Confirm a suspected root using several muscles supplied by different peripheral nerves, sensation and reflexes. A normal single muscle does not exclude radiculopathy.
Dermatomes: a root map
Dermatomes overlap and published maps differ. Use this with the movement / reflex table, not as an exact border test. “Th” means thoracic (T). A dermatome is different from a named peripheral nerve’s cutaneous field.
Ralf Stephan. Original / source. Public domain. Rendered for display; anatomical content unchanged.
| Root | Useful movement / muscle | Sensory clue | Reflex |
|---|---|---|---|
| C5 | Shoulder abduction (deltoid / axillary); elbow flexion (biceps / musculocutaneous, C5–6) | Lateral upper arm | Biceps C5–6 |
| C6 | Wrist extension (radial, C6–7); elbow flexion / brachioradialis | Thumb / lateral forearm | Brachioradialis C5–6, mainly C6 |
| C7 | Elbow extension (triceps / radial); wrist flexion and pronation (median / ulnar contributions) | Middle finger | Triceps C7–8, mainly C7 |
| C8 | Distal finger flexion (median + ulnar); thumb interphalangeal flexion (median / AIN) | Little finger / ulnar hand | No dependable routine reflex |
| T1 | Finger abduction / adduction (interossei / ulnar; C8–T1); compare median-innervated thenar muscles | Medial forearm | No routine reflex |
| L2–3 | Hip flexion (iliopsoas, L1–3); hip adduction (obturator, L2–4) | Anterior thigh / medial knee | Knee L3–4 |
| L3–4 | Knee extension (quadriceps / femoral); L4 also contributes ankle dorsiflexion | Medial knee / medial leg to medial malleolus | Knee L3–4, mainly L4 |
| L5 | Great-toe extension (deep fibular); inversion (tibialis posterior / tibial); hip abduction (superior gluteal) | Dorsum of foot / great toe | No reliable routine reflex; medial hamstring sometimes helpful |
| S1 | Plantarflexion (gastrocnemius–soleus / tibial); eversion (superficial fibular, L5–S1) | Lateral foot / sole | Achilles S1–2, mainly S1 |
Make the movement test discriminating
- Thumb abductionTest APB by lifting the thumb perpendicular to palm: median. Thumb adduction is ulnar.
- Finger extensionTest MCP extension: radial / PIN. IP extension also uses intrinsic muscles.
- InversionPlantarflex slightly and invert to emphasise tibialis posterior. Dorsiflexion–inversion recruits tibialis anterior and can mislead.
- PlantarflexionSingle-leg heel raises, if safe, reveal weakness that a supine push may miss.
Reflexes are comparisons
- AsymmetryA focal change is often more useful than the absolute grade.
- Brisk + LMNA cord lesion may give reduced arm reflexes at the level and brisk leg reflexes below.
- HoffmannSupports a pyramidal pattern in context; isolated positivity is not diagnostic of myelopathy.
- Pain / effortRecord limitations; joint disease and pain can distort apparent myotomes.
9Named nerves and plexus patterns
Upper limb: named-nerve sensory territories
Compare with the root map above. The medial forearm is supplied by the medial antebrachial cutaneous nerve, so sensory loss there needs an explanation beyond an isolated ulnar lesion. Historical drawing; boundaries and root labels are approximate.
Gray’s Anatomy, Henry Vandyke Carter / Henry Gray; vectorised by Fred the Oyster, corrected by Mikael Häggström. Original / source. Public domain. Rendered for display; anatomical content unchanged.
Upper limb
| Nerve / site | Motor pattern | Sensory / distinguishing clue |
|---|---|---|
| Axillary | Deltoid weakness: shoulder abduction; teres minor may affect external rotation | Lateral shoulder patch. Compare biceps / supraspinatus to assess C5 / upper trunk. |
| Suprascapular | Supraspinatus / infraspinatus: initiation of abduction / external rotation | No cutaneous loss; spinoglenoid lesion may spare supraspinatus. |
| Long thoracic | Serratus anterior weakness; medial scapular winging, accentuated by wall push | Pure motor. Trapezius weakness / shoulder droop suggests accessory nerve instead. |
| Radial, upper arm / spiral groove | Wrist + finger / thumb extension weakness; triceps usually spared at spiral groove | Dorsal first web-space loss may occur. A more proximal lesion can affect triceps. |
| Posterior interosseous (PIN) | Finger / thumb extension weakness; wrist extension often retained with radial deviation | No cutaneous sensory loss. Extensor carpi radialis longus is supplied proximally. |
| Median at carpal tunnel | APB / opposition weakness in advanced disease | Lateral 3½ digits; thenar eminence sensation usually spared (palmar cutaneous branch bypasses tunnel). |
| Anterior interosseous (AIN) | Weak thumb IP and index DIP flexion → abnormal tip-to-tip “OK” pinch | Pure motor; no cutaneous loss. Tendon injury can mimic this. |
| Ulnar, elbow versus wrist | Interossei / ADM / adductor pollicis weakness; finger abduction and key pinch affected | Little finger / ulnar half ring finger. Dorsal ulnar hand loss supports lesion proximal to Guyon canal. Forearm ulnar muscles may be spared even at elbow. |
Lower limb: where to test sensation
The first dorsal web space helps assess deep fibular sensation; the sole tests tibial branches. Sensory overlap limits any single point. For foot drop, add inversion and hip abduction to distinguish common fibular from L5 patterns.
ClinicalReference schematic. Anatomy: [34] [35] [36]. Simplified for bedside lookup.
Lower limb
| Nerve / site | Motor pattern | Sensory / distinguishing clue |
|---|---|---|
| Common fibular at fibular neck | Weak dorsiflexion, toe extension and eversion; inversion relatively preserved | Anterolateral lower leg / dorsum foot; sole spared. Deep branch: first dorsal web space. |
| Tibial, proximal | Weak plantarflexion, toe flexion and tibialis-posterior inversion; reduced Achilles may occur | Sole sensory loss. Tarsal tunnel is distal and should spare calf power / Achilles. |
| Sciatic | Fibular division often worse: foot drop ± tibial weakness; hamstrings may be affected | Much of foot / lateral leg; medial leg (saphenous) relatively spared. Hip abduction suggests a site above isolated sciatic nerve. |
| Femoral | Knee extension weakness; reduced knee reflex; hip flexion may be affected depending on level | Anterior thigh / medial leg. Preserved adduction favours femoral over L2–4 root / lumbar plexus, but is not absolute. |
| Obturator | Hip adduction weakness | Small / variable medial-thigh sensory patch; compare quadriceps for plexus / root involvement. |
| Lateral femoral cutaneous | No motor deficit or reflex change | Anterolateral thigh sensory symptoms only: meralgia paraesthetica. Weakness requires another explanation. |
Upper brachial plexus
- C5–6 trunkWeak shoulder abduction / external rotation and elbow flexion across several nerves.
- DistinctionLateral arm / forearm sensory change. Root disease may add paraspinal or root-branch muscle abnormalities.
Lower brachial plexus
- C8–T1 trunkIntrinsic hand / finger-flexor weakness across ulnar and median territories.
- DistinctionMedial forearm sensory loss is not explained by an isolated ulnar lesion. Painful lower-trunk + Horner: consider apical / proximal pathology.
Lumbar / sacral plexus
- LumbarFemoral + obturator findings: knee extension and adduction weak.
- SacralSciatic plus gluteal involvement; hip abduction / extension can help.
- PatternOften painful and patchy; root–plexus–nerve overlap needs electrodiagnosis / imaging.
[20] [29] [30] [31] [32] [33] [34] [35] [36] [37] ↑ Back to lookup
10Common look-alikes: the next muscle to test
| Presentation | Compare these sites | Highest-yield extra examination |
|---|---|---|
| Foot drop | Common fibular ↔ L5 root ↔ sciatic / plexus ↔ central | Test inversion and hip abduction. Both can be weak in L5; should be spared in an isolated common fibular lesion. Add plantarflexion / hamstrings for sciatic involvement and plantar responses for central disease. |
| Wrist drop | Radial ↔ C7 ↔ cortical hand area | Test pronation and wrist flexion. Weakness outside radial muscles supports C7. Sensory loss at middle finger supports C7; first dorsal web space supports radial. Sudden onset still warrants a central assessment. |
| Ulnar-looking weak hand | Ulnar ↔ C8/T1 root ↔ lower trunk | Test median APB / thumb IP flexion, medial forearm sensation and dorsal ulnar hand sensation. Weakness across median + ulnar muscles points proximal to an isolated ulnar lesion. |
| Weak quadriceps | Femoral ↔ L3/4 root ↔ lumbar plexus | Test hip adduction (obturator) and ankle dorsiflexion. Knee reflex / medial-leg sensation can be abnormal in either femoral or L4 disease. |
| Bilateral weak legs | Cord ↔ cauda / polyradiculopathy ↔ neuropathy / muscle | Check a trunk level, plantars, perineal / bladder symptoms and arms. Acute cord disease may lack brisk reflexes. New sphincter symptoms require urgent escalation. |
What NCS / EMG can add
Radiculopathy is usually proximal to the dorsal-root ganglion, so distal sensory responses are often preserved; a plexus / peripheral nerve lesion may reduce the relevant sensory responses. Paraspinal denervation supports root involvement but is not sufficient alone. Early or purely sensory radiculopathy can have a normal study. Choose timing and muscle sampling with neurophysiology; do not delay urgent imaging for EMG.
11Present the localisation, then test the explanation
A concise presentation
“There is [distribution] weakness / sensory loss with [two positive localising findings]. This favours [side and anatomical level]. [Alternative site] remains possible because [specific uncertainty]. I would distinguish them by [targeted examination / imaging].”
Worked examples
- HemisphericRight face–arm weakness, impaired naming and right field loss → left hemispheric lesion, likely MCA territory; vascular imaging defines the occlusion.
- BrainstemLeft facial and right body pain–temperature loss, hoarse voice and left ataxia → left lateral medulla; vertebral / PICA territory.
- Foot dropDorsiflexion + eversion weak; plantarflexed inversion and hip abduction preserved → common fibular lesion favoured; confirm sensory pattern and exclude central signs.
When one focal lesion does not fit
- Length-dependentSymmetric distal sensory loss ± distal weakness / ankle areflexia → polyneuropathy pattern.
- MultifocalPainful, asymmetric, non-contiguous nerve deficits → multiple mononeuropathies; consider systemic disease.
- NMJFluctuating fatigable ocular / bulbar weakness, sensation intact; reflexes often preserved in MG, may be reduced in LEMS.
- MuscleUsually proximal weakness with intact sensation; reflexes relatively preserved until weakness is severe. Important distal / asymmetric exceptions exist.
- Motor neuroneProgressive regional UMN + LMN findings without a matching sensory deficit; exclude structural and treatable mimics.
Document what you actually found, including pain, fatigue, attention, language or cooperation limiting the examination. If localisation remains unclear, say which two sites remain plausible and what you need to discriminate them.