Prehospital Neurological Assessment

Introduction

The Framework

Four progressive levels of neurological assessment — from the non-negotiable safety net to a full clinical examination. Each level builds on the last and answers specific diagnostic questions that change what you do.

⚡

The core problem in prehospital neuro: Most crews can perform the tests but cannot interpret findings into a working localisation. This tool teaches both — what to do AND what it means anatomically.

The Four Levels

1
Safety Net Screen
The non-negotiable floor. Detects immediately life-threatening states and reversible causes. Every patient, every call.
2–3 minutes
2
Localisation Screen
Tells you where the lesion is. Cortex, brainstem, or diffuse? UMN or LMN? Anterior or posterior circulation?
5–7 minutes
3
Syndrome Identification
Turns findings into a named syndrome. Wallenberg? BPPV vs posterior stroke? Cerebellar vs sensory ataxia?
10–15 minutes
4
Full Examination
Hospital-equivalent examination. Complete cranial nerve screen, MRC power grading, full sensory modalities, reflexes.
20–30 minutes

Key Principles

🔬

Performing a test and interpreting a test are different skills. Most prehospital training covers technique but not localisation logic. This tool covers both. For every finding you will learn: what it means anatomically, what diagnostic conclusion it supports, and what decision it changes.

🗺

Localisation before diagnosis. The brain is anatomically organised. A lesion in one place produces a predictable pattern of deficits. Once you know the pattern, you know the location — and the location narrows the differential dramatically. Unilateral face + arm/leg = cortex/capsule. Crossed deficits (face one side, body other) = brainstem. Both legs = cord.

⏱

Time vs yield. Level 1 is non-negotiable. Level 2 adds 3–4 minutes and dramatically improves handover quality and clinical thinking. Level 3 is for undifferentiated presentations. Level 4 builds expert knowledge — rarely fully completed on scene.

Anatomy Quick Reference

Lesion Location → Expected Findings

Location	Motor signs	Sensory signs	Other clues
Cortex (MCA)	Contralateral UMN — arm/face > leg	Contralateral hemibody	Dysphasia (dominant), neglect (non-dominant), gaze toward lesion
Internal capsule	Dense equal contralateral hemiplegia — face, arm, leg	Contralateral hemibody	No cortical signs — lacunar pattern
Brainstem	Crossed — ipsilateral face + contralateral body	Crossed or dissociated	Cranial nerve signs, vertigo, diplopia, dysphagia
Cerebellum	Ipsilateral ataxia — no true weakness	None typically	DANIISH signs, nystagmus, HINTS exam critical
Spinal cord	Bilateral UMN below level (may be flaccid acutely — spinal shock)	Sensory level — dermatomal	Bladder/bowel symptoms. Check level with pin prick.
Nerve root	Myotomal weakness	Dermatomal pain + sensory loss	Reflex loss at that root. Radicular pain.
Peripheral nerve	Named nerve territory	Named nerve territory	Wasting, fasciculations (LMN). Context: entrapment, DM, trauma.
Diffuse/metabolic	Symmetrical, generalised	Symmetrical or absent focal	Altered GCS, BM abnormal, no focal signs

Level 1⏱ 2–3 minutes · Every patient

Safety Net Screen

The non-negotiable minimum. Detects immediately life-threatening states and reversible causes. Do this, do it properly, document it completely.

Diagnostic Question This Level Answers

Is this patient safe? Is there a reversible cause I must treat immediately? Do they need urgent transport? What is my baseline to track deterioration?

The Assessments

Blood Glucose (BM)

1
Lateral fingertip — less nerve endings, less discomfort
2
Adequate drop — don't squeeze excessively (dilutes sample)
3
Document the number — not just "normal" or "low"
4
Repeat if doubt, if patient deteriorates, or result doesn't fit

BM Interpretation

BM	State	Action
<2.0	Severe hypoglycaemia	IV 10% dextrose immediately
2.0–3.9 + symptoms	Symptomatic hypoglycaemia	Glucose — IV or oral
4.0–7.8	Normal	No glucose intervention
7.9–11.0	Mildly elevated	Note — worsens stroke/TBI outcomes
>11.0	Significant hyperglycaemia	DKA/HHS screen; ketones
>25.0	Severe	HHS likely. Cautious IV fluids. Urgent.

AVPU → GCS (document as E/V/M)

Eyes (E 1–4): Spontaneous=4, To voice=3, To pain=2, None=1
Verbal (V 1–5): Orientated=5, Confused=4, Words=3, Sounds=2, None=1
Motor (M 1–6): Obeys=6, Localises=5, Withdraws=4, Abnormal flexion=3, Extension=2, None=1
Always document as E/V/M (e.g. E3V4M5=12). Document the trend not just the number.
Decorticate (M3): arms flexed, legs extended — above brainstem
Decerebrate (M2): all extended — brainstem compression. Pre-terminal.

≤8 = consider airway intervention
3=minimum · 15=normal · GCS 15 does NOT exclude serious pathology

Pupil Assessment — PERLA

1
Dim lighting if possible
2
Size in mm both sides (2mm=pinpoint, 4mm=mid, 7mm=dilated)
3
Shape — round or irregular?
4
Equality — same size? Anisocoria <1mm often physiological
5
Direct reflex: light in → that pupil constricts
6
Consensual reflex: light in one eye → BOTH constrict

Finding	Think
Unilateral fixed dilated	CN III compression — PComm aneurysm / uncal herniation. EMERGENCY.
Bilateral fixed dilated	Brainstem death, anoxia, atropine/sympathomimetics
Bilateral pinpoint	Opioids (+ ↓RR), pontine haemorrhage, OP poisoning, clonidine
Unilateral partial miosis + ptosis	Horner's — sympathetic chain. Carotid dissection?
Pupil-sparing CN III palsy	Diabetic mononeuropathy (needs imaging)

FAST / BE-FAST Screen

B
Balance: sudden loss of balance, unsteadiness, ataxia — catches posterior circulation
E
Eyes: visual loss, diplopia, gaze deviation — catches posterior circulation
F
Face: "Show teeth / smile." Nasolabial fold flattening. Note: does forehead move equally? (key at Level 2)
A
Arms: "Hold arms out, palms up, eyes closed." Watch for drift + pronation over 10 seconds.
S
Speech: "Say British Constitution." Articulation wrong = dysarthria. Words themselves wrong = dysphasia. Critical distinction.
T
Time: Exact onset or last known well. Critical for thrombolysis (4.5h) / thrombectomy window.

Vital Signs in Neurological Context

RR <12 + reduced GCS: respiratory depression — opioids, brainstem. Cheyne-Stokes = deep cerebral/brainstem lesion.
SpO₂: target 94–98%. Hypoxia worsens ALL neurological injury. Hyperoxia worsens stroke/post-arrest.
Cushing's triad: Hypertension + Bradycardia + Irregular respirations = raised ICP, imminent herniation.
Temp: fever worsens neurological secondary injury. ≥41°C = active cooling in neuro patients.
BP: both arms documented. Note which arm used for ongoing monitoring.

⚠

Cushing's triad is a late pre-terminal sign. Head 30° up, minimise stimulation, expedite immediately.

Level 1 — Finding → Decision

What Each Finding Changes

BM <4.0 + symptoms

Treat hypoglycaemia first. Reassess neuro signs after — may resolve (stroke mimic).

TREAT FIRST

GCS ≤8

Airway management consideration. Position, suction, consider OPA/NPA. Reassess continuously.

AIRWAY

Unilateral fixed dilated pupil

CN III compression until proved otherwise. Herniation or PComm aneurysm.

EXPEDITE

FAST positive

Stroke pre-alert. Note last known well precisely. Direct to HASU if in window.

PRE-ALERT

Cushing's triad

Raised ICP — head 30° up, avoid hypoxia, minimise stimulation.

CRITICAL

GCS 15, BM normal, FAST negative

Proceed to Level 2. Time allows deeper assessment.

GO TO L2

Level 2⏱ 5–7 minutes · Any neuro presentation

Localisation Screen

Tells you WHERE the lesion is. This is the interpretive gap where most prehospital assessment stops. Each test here answers an anatomical question — cortex, brainstem, or diffuse? UMN or LMN?

Diagnostic Question This Level Answers

Where is the lesion? Is the pattern consistent with a cortical stroke, brainstem lesion, diffuse metabolic process, or spinal cord problem? Does my working diagnosis match the anatomical findings?

The Localisation Tests

1 — Pronator Drift (most sensitive early UMN sign)

TECHNIQUE

1
Arms outstretched in front, palms UP (supinated), fingers spread
2
Eyes closed — removes visual compensation
3
Hold 10–15 seconds. Watch carefully.
4
Optional: tap each arm gently downward and observe recovery speed

INTERPRETATION

Normal: arms stay level, palms up, no drift
Positive: arm drifts DOWN AND pronates (palm rotates inward). Contralateral UMN lesion.
Why it works: pyramidal weakness affects extensors and supinators more — gravity plus lost anti-gravity control = drift. Supination requires active corticospinal effort.
Clinical importance: often positive BEFORE you detect weakness on formal power testing. Most sensitive prehospital UMN sign.
Cerebellar: arm may drift UPWARD — opposite of UMN

2 — Facial Assessment: The Critical UMN vs LMN Distinction

TECHNIQUE — IN ORDER

1
"Raise your eyebrows" — watch forehead wrinkling both sides
2
"Close your eyes tight" — try to force them open. Equal resistance?
3
"Show me your teeth / big smile" — compare nasolabial folds
4
"Puff your cheeks out" — symmetry?

⚠

UMN facial palsy (stroke): FOREHEAD SPARED. Lower face weak on side contralateral to lesion. Forehead wrinkles bilaterally. The forehead has bilateral cortical representation — the ipsilateral hemisphere takes over.

⚡

LMN facial palsy (Bell's, Ramsay Hunt, parotid): COMPLETE ipsilateral hemiface — forehead INVOLVED. Cannot wrinkle forehead on affected side. Cannot fully close eye. Forehead = always the differentiator.

3 — Eye Deviation and Gaze Preference

1
Resting eye position — both eyes looking same direction?
2
"Follow my finger" — horizontal H-pattern. Note restriction, nystagmus.
3
In unconscious patient: passive head turn (doll's eyes) — eyes should counter-rotate if brainstem intact

Why it works — the anatomy

Each frontal lobe drives gaze to the opposite side. The pontine gaze centre (PPRF) drives gaze to the same side. Balanced = midline. Damage one and the other wins.

Finding	Lesion
Eyes toward weak side	Cortical/capsular stroke — frontal eye field lost, pontine pulls eyes toward lesion side
Eyes away from weak side	Pontine lesion — PPRF lost, cortex pushes eyes contralateral
Eyes toward seizure, ictal	Irritative focus firing drives gaze away from focus — opposite of destructive
Eyes away from seizure, post-ictal	Exhausted cortex mimics destructive lesion transiently

⚡

Wrong-way deviation — eyes opposite to expected for cortical lesion = large lesion with raised ICP affecting brainstem, or parietal neglect. Reconsider your localisation.

4 — Speech and Language

STEP 1 — Dysarthria vs Aphasia

Dysarthria: words correct, articulation wrong — slurred, nasal, scanning. Motor problem. Language intact.
Aphasia: the words themselves are wrong or absent. Always cortical. Almost always left hemisphere.

STEP 2 — Four-Question Screen (<90 sec)

Ask	Tests	Fail =
"Close your eyes then stick out your tongue"	Comprehension	Wernicke's / receptive
"What is this?" (watch, pen)	Naming	Any aphasia type
"Repeat: no ifs, ands, or buts"	Repetition — arcuate fasciculus	Conduction aphasia if isolated
Spontaneous speech — fluent?	Production — Broca's area	Non-fluent = expressive / Broca's

STEP 3 — Classify

Type	Fluent?	Understands?	Repeats?	Lesion
Broca's	No — effortful	Yes	No	Left frontal — anterior MCA
Wernicke's	Yes — but wrong	No	No	Left temporal — posterior MCA
Conduction	Relatively	Good	Severely impaired	Arcuate fasciculus — parietal
Global	No	No	No	Large left MCA
Nominal	Yes	Yes	Yes	Left temporal/parietal

⚠

Wernicke's aphasia is routinely misdiagnosed as confusion. Patient talks fluently but has understood nothing you said. Consent, pain score, and history are unreliable. Document as aphasia — not confusion.

⚡

Broca's patients understand everything. They are often acutely distressed. Speak directly to them. Do not discuss them as though absent.

5 — Limb Power — Rapid Comparison

Not formal MRC grading — comparative testing to detect asymmetry.

1
"Squeeze both my hands simultaneously" — compare grip
2
"Push your feet down against my hands" — compare plantar flexion
3
"Lift your knees up" — compare hip flexion
4
Proximal > distal weakness = myopathy. Distal > proximal = neuropathy. Pyramidal = extensors weak (arm) / flexors weak (leg).

6 — Plantar Response (Babinski)

1
Blunt object — key or back of pen
2
Stroke firmly from heel along LATERAL sole, curve medially across ball of foot
3
Normal = big toe FLEXES (curls down). Babinski positive = big toe EXTENDS (points up) ± fanning of other toes

⚠

Upgoing plantar = UMN pathology. In acute stroke or acute cord injury, reflexes may be absent initially (spinal shock) — do not be falsely reassured by absent reflexes in acute neurological injury.

7 — Neglect and Cortical Signs

Neglect Testing — Right MCA / Non-Dominant

Neglect is a failure to attend to one side of space. The patient isn't blind or weak in that territory — they simply don't register it. Common after right hemisphere strokes. Easily missed if you only look for weakness.

1
Extinction: Wiggle fingers in both visual fields simultaneously. Patient detects each side alone but ignores one side when both stimulated simultaneously — the affected side "extinguishes."
2
Gaze: Does the patient spontaneously look toward both sides? Persistent ipsilesional gaze without exploring the contralateral side = neglect.
3
Limb awareness: "Are both your arms working?" A patient who denies weakness of a clearly paralysed limb (anosognosia) has right hemisphere parietal damage.
4
Line bisection (if pen available): Draw a line. "Put a mark in the middle." Healthy people bisect accurately. Neglect = mark displaced toward the ipsilesional side.

Neglect Interpretation

⚡

Left-sided neglect is more common and more severe than right-sided neglect — the right hemisphere has a broader attentional role. A right MCA stroke causing left neglect can look deceptively mild on standard FAST because the patient may have relatively preserved motor power but be clinically significantly impaired.

Neglect without weakness = non-dominant parietal cortex (usually right). Stroke, tumour, haemorrhage.
Anosognosia (denial of deficit) = right parietal. Patient insists paralysed arm works fine. Not psychologically motivated — genuine neurological unawareness.
Hemispatial neglect at handover: document explicitly — receiving team needs to know for falls risk, eating, rehabilitation planning.
Extinction without neglect = milder form — each side intact alone but suppressed when competing. Early parietal sign.

Level 2 — Pattern → Localisation

Finding Pattern → Where is the Lesion?

Contralateral face + arm > leg + dysphasia

Left MCA territory cortical stroke. Dominant hemisphere. Pre-alert stroke team.

MCA STROKE

Dense equal face/arm/leg — no cortical signs

Internal capsule lacunar infarct. Small vessel. No dysphasia, no neglect.

LACUNAR

Ipsilateral face + contralateral arm/leg

CROSSED DEFICIT = brainstem until proved otherwise. Add Level 3 cranial nerve screen.

BRAINSTEM

Both legs weak, no arms, no CN signs

Spinal cord or bilateral cortex (rare). Check sensory level. Ask re: bladder/bowel.

CORD?

Symmetric, no focal signs, fluctuating GCS

Metabolic/toxic/diffuse encephalopathy. No lateralising lesion. Check BM again.

METABOLIC

LMN face (forehead involved) + no limb signs

Peripheral CN VII palsy. Bell's palsy or Ramsay Hunt most likely. Isolated.

BELL'S

Level 3⏱ 10–15 minutes · Undifferentiated neuro

Syndrome Identification

Turns a collection of findings into a named clinical syndrome. Level 2 tells you where — Level 3 tells you what. Requires knowledge of cranial nerve function, cerebellar signs, and vestibular testing.

Diagnostic Question This Level Answers

Which named syndrome does this presentation fit? Is this vertigo BPPV or posterior stroke? Is this Bell's palsy or Ramsay Hunt? Is the ataxia cerebellar or sensory? What cranial nerve is involved and what does that tell me anatomically?

Abbreviated Cranial Nerve Screen — Priority Order

⚡

Prehospital priority order: II → III/IV/VI → V → VII → VIII → IX/X → XII. Focus on the ones that change your diagnosis and pre-alert decision. I and XI are rarely time-critical on scene.

CN II — Optic | Vision and Pupil Afferent Pathway

1
Acuity: "Can you read this text?" / count fingers / hand movements. Each eye separately.
2
Fields: Confront — wiggle fingers in 4 quadrants of each eye. "Can you see my finger?"
3
RAPD test: swing bright torch side to side 2–3 seconds each eye. Watch for dilation on the affected side (Marcus Gunn pupil).

Field Defect	Localisation
Monocular loss	Eye or optic nerve — amaurosis fugax, optic neuritis (MS)
Bitemporal hemianopia	Optic chiasm — pituitary tumour
Homonymous hemianopia	Post-chiasm contralateral — posterior stroke, occipital
RAPD positive	Ipsilateral optic nerve disease — MS, ischaemic optic neuropathy

CN III / IV / VI — Eye Movements and Nystagmus

H-pattern tracking: follow finger in large H. Note restriction, ask about diplopia in each position.
CN III (oculomotor): eye "down and out" + ptosis + dilated pupil. Surgical (pupil dilated) = aneurysm. Medical (pupil spared) = diabetic.
CN IV (trochlear): diplopia worst looking down-inward (descending stairs). Head tilts to compensate. Most common cause: head trauma.
CN VI (abducens): cannot abduct — failure to look laterally. Convergent squint. Horizontal diplopia worst toward weak side. False localising sign in raised ICP.
INO (internuclear ophthalmoplegia): on lateral gaze, the adducting eye (moving medially) is slow or stops. Nystagmus in abducting eye. MLF lesion = MS or brainstem stroke.

NYSTAGMUS — PERIPHERAL vs CENTRAL

Feature	Peripheral	Central
Direction	Horizontal/rotatory, unidirectional	Any — may change with gaze direction
Vertical	Never purely vertical	Can be purely vertical
Fixation	Suppressed by fixation	Not suppressed
Fatigability	Fatigues with repetition	Non-fatigable

⚠

Purely vertical nystagmus is always central. Direction-changing nystagmus is always central. Either finding = posterior fossa until proved otherwise.

CN V — Trigeminal | Facial Sensation + Jaw

1
Sensation: Light touch to forehead (V1), cheek (V2), chin (V3) both sides. "Same on both sides?"
2
Corneal reflex: from side, touch cornea (not sclera) with cotton wisp. Both eyes should blink. Afferent CN V, efferent CN VII.
3
Motor: "Clench jaw" — feel masseter. "Open mouth" — jaw deviates toward weak pterygoid.

⚡

Absent direct AND consensual blink when touching cornea = CN V afferent lesion. Absent direct blink only (but consensual preserved) = CN VII efferent lesion on that side. The distinction matters.

CN IX / X — Swallow, Palate, Voice

1
Listen to voice — hoarse (X/vocal cord), nasal (palatal incompetence), slurred (VII/XII/cerebellar)
2
"Open wide and say aah" — uvula rises midline. Deviation = away from CN X lesion
3
Watch for pooling secretions, drooling, spontaneous coughing — signs of impaired swallow
4
Gag reflex if indicated. Absent gag = up to 20% of normal adults — context matters.

Bovine cough = weak breathy cough — vocal cord palsy CN X. Consider Pancoast tumour, aortic aneurysm.
Any IX/X lesion = compromised airway protection. Plan accordingly.

CN VIII — Hearing and Balance

Hearing screen: whisper test each ear separately
Rinne's test: 512Hz fork on mastoid (bone) then in air. Air > bone = normal/SNHL. Bone > air = conductive loss.
Weber's test: fork on forehead midline. Lateralises to conductive loss side OR away from SNHL side.
Vestibular: dizziness, vertigo, nystagmus — see HINTS exam below

CN XII — Tongue Movement

"Stick your tongue out" — note direction of protrusion
Look for wasting, fasciculations (LMN — motor neurone disease)
LMN: tongue deviates TOWARD the lesion (weak side). Wasting on affected side.
UMN: tongue deviates AWAY from lesion. No wasting. Spastic tongue.
Bilateral LMN (no tongue movement at all) = bulbar palsy — MND, bilateral CN XII lesion

Cognitive and Higher Cortical Screen

Bedside Cognitive Assessment — Confusion vs Aphasia vs Delirium vs Dementia

⚡

The prehospital label "confused" is diagnostically almost useless — it describes the observation but not the mechanism. The cognitive screen distinguishes four very different states that look similar but have different causes, urgencies, and destinations.

FIVE-MINUTE STRUCTURED SCREEN

Domain	Test	Why this domain
Orientation	"What is today's date / where are we / who am I?" — person, place, time	First to go in delirium and dementia. Preserved in aphasia.
Attention	"Count backwards from 20" or "Months of the year backwards"	Impaired in delirium. Usually preserved in dementia early on.
Registration	"Remember these three words: apple, table, penny." Test immediately.	Immediate memory — tests registration not recall
Recall	After 3–5 minutes of other tasks: "What were those three words?"	Short-term memory — hippocampus. Fails early in dementia.
Dual task	Ask them to hold arms out and count backwards simultaneously	Frontal lobe executive function — fails in frontal lesions and delirium
Visuospatial	"Draw a clock face showing 10 past 11" (if pen available)	Right parietal + frontal planning. Neglect, dementia, delirium all impair this.

INTERPRETING THE PATTERN

State	Key features	Prehospital implication
Delirium	Acute onset, fluctuating, impaired attention, often agitated or withdrawn. Orientation and attention fail first.	Medical emergency — find the cause. Sepsis, hypoxia, metabolic, drugs, head injury, urinary retention.
Dementia	Chronic, stable or slowly progressive, family/carer usually knows. Recall fails before attention. Relatively coherent.	Baseline — ask carer what is normal. New change on baseline = acute delirium on dementia.
Wernicke's aphasia	Fluent speech, doesn't follow commands, appears confused but orientation cannot be tested because language is broken.	Not confused — aphasic. Left posterior hemisphere. Pre-alert stroke team.
Functional / psychiatric	Inconsistent performance, intact on casual conversation, distress prominent, usually younger.	Diagnosis of exclusion. Never assume functional until structural and metabolic excluded.

⚠

Delirium on dementia is the most common pattern in elderly patients — the underlying dementia makes them more vulnerable. The acute change is the emergency, not the dementia itself. Always ask the carer "is this normal for them?"

✓

The 4AT score — Alertness, AMT4 (age/DOB/place/year), Attention (months backwards), Acute change — is a validated 1-minute delirium screen you can run on any patient. Score ≥4 = probable delirium.

HINTS Exam — Acute Vertigo — Peripheral vs Posterior Stroke

Head Impulse · Nystagmus · Test of Skew

🚨

HINTS has higher sensitivity for posterior circulation stroke than early DWI MRI in the first 24–48 hours. Any single central feature = treat as posterior fossa stroke. Requires training — but knowing the framework is the starting point.

H
Head Impulse: Hold head, patient fixes on your nose. Rapid small rotation 10–15° to one side. Watch for catch-up saccade (corrective eye movement). Saccade present = PERIPHERAL = reassuring. No saccade = CENTRAL = danger.
I
Nystagmus: Direction-changing (changes with gaze direction) OR purely vertical = CENTRAL. Unidirectional horizontal = peripheral.
T
Test of Skew: Cover one eye, quickly uncover. Watch for vertical refixation (skew deviation — one eye higher than other). Present = CENTRAL.

	Peripheral (safe)	Central (stroke)
Head Impulse	Abnormal (catch-up saccade)	Normal — NO saccade = DANGER
Nystagmus	Unidirectional horizontal-torsional	Direction-changing or vertical
Skew	No vertical skew	Vertical skew deviation

⚠

Central pattern on ANY one component overrides the others. One central feature = treat as posterior stroke regardless of the other findings.

Coordination Tests

Finger-Nose · Heel-Shin · Dysdiadochokinesia

1
Finger-nose: Hold your finger ~50cm away. "Touch your nose, then my finger." Move your finger each time. Watch for intention tremor and past-pointing (dysmetria).
2
Heel-shin: Patient supine. "Place heel on opposite knee and slide down the shin to ankle." Watch for deviation off the shin.
3
Dysdiadochokinesia: "Tap the back of your hand on your palm as fast as possible, alternating." Slow, irregular, clumsy = cerebellar.

Cerebellar = DANIISH
Dysdiadochokinesia · Ataxia · Nystagmus · Intention tremor · Impaired finger-nose · Scanning speech · Hypotonia — all IPSILATERAL to lesion

Romberg's Test — Sensory vs Cerebellar Ataxia

1
Feet together, arms at sides. Stand close to catch patient.
2
Observe 30 seconds eyes OPEN
3
Then eyes CLOSED — observe 30 seconds

⚡

Romberg positive = stable eyes open, significantly unsteady eyes closed. Dorsal column / proprioceptive loss — sensory ataxia. Patient uses vision to compensate. Causes: B12 deficiency, MS, peripheral neuropathy, tabes dorsalis.

✓

Ataxic eyes OPEN = cerebellar. Vision doesn't help cerebellar ataxia. Romberg is negative — equally unsteady regardless of eye state.

Named Syndrome Recognition

Wallenberg Syndrome (Lateral Medullary)

Ipsilateral: face pain/temp loss (V), Horner's, ataxia, dysphagia/hoarse (IX/X). Contralateral: body pain/temp loss (spinothalamic). PICA occlusion. No limb weakness — corticospinal tract spared (medial).

Weber Syndrome (Midbrain)

Ipsilateral CN III palsy (eye down/out, ptosis, dilated pupil). Contralateral hemiplegia (corticospinal). PCA territory infarct.

Foville Syndrome (Pons)

Ipsilateral CN VI (lateral gaze palsy) + CN VII palsy. Contralateral hemiplegia. Eyes deviate AWAY from lesion (opposite of cortical stroke). Pontine perforator.

Horner's Syndrome

Ipsilateral miosis (partial) + ptosis + anhidrosis. Sympathetic chain anywhere from hypothalamus to orbit. Key causes: carotid dissection, Pancoast tumour, lateral medullary stroke, thoracic cord lesion.

Cerebellar Stroke

DANIISH signs ipsilateral. Truncal ataxia — may not sit unsupported. Horizontal nystagmus. HINTS: normal head impulse = danger sign. PICA/AICA/SCA territories.

Cauda Equina Syndrome

Saddle anaesthesia (S3–S5) + bladder/bowel dysfunction + bilateral leg weakness. LMN signs (flaccid, areflexic). Emergency MRI — do not miss in back pain + leg neurology.

Level 4⏱ 20–30 minutes · Complex / learning / time permits

Full Clinical Examination

Hospital-equivalent neurological examination. Rarely fully completed on scene — but knowing it makes every lower level more meaningful and your clinical reasoning sharper. This is the level that builds toward expert practice.

Diagnostic Question This Level Answers

What is the exact motor power by muscle group? What is the precise sensory level? Which nerve root, nerve, or tract is involved? Is this UMN or LMN at each segment? Does the complete picture fit a single anatomical lesion?

Formal Motor Assessment — MRC Power Scale

MRC Scale — Formal Application and Technique

Grade	Description	How to test
0	No contraction at all	Visual and palpation — no flicker
1	Visible/palpable flicker	Watch for muscle belly twitch only
2	Movement, gravity eliminated	Test horizontally — arm slides on surface
3	Against gravity, no resistance	Can lift limb, you can overcome immediately
4−/4/4+	Against resistance — reduced	You can overcome with effort (−/=/+)
5	Normal power	Cannot overcome with full effort

PYRAMIDAL PATTERN OF WEAKNESS

Upper limb: extensors weaker — shoulder abduction, elbow extension, wrist/finger extension.
Lower limb: flexors weaker — hip flexion, knee flexion, ankle dorsiflexion.
This explains the hemiplegic posture: arm flexed, leg extended. The stronger muscle groups dominate.
LMN / myotomal pattern: specific muscle group only — follows nerve root or peripheral nerve territory
Myopathic pattern: proximal > distal, symmetric — difficulty rising from chair, raising arms above head

Key Muscle Testing by Root Level

UPPER LIMB

Root	Muscle	Test
C5	Deltoid	Arm abduction 0–90°
C5/6	Biceps / brachialis	Elbow flexion supinated
C6/7	Wrist extensors (ECRL)	Wrist extension against resistance
C7	Triceps	Elbow extension against resistance
C8	Finger flexors (FDP)	Grip strength
T1	Interossei	Finger abduction/adduction

LOWER LIMB

Root	Muscle	Test
L1/2	Iliopsoas	Hip flexion against resistance
L3/4	Quadriceps	Knee extension — knee jerk L3/4
L4/5	Tibialis anterior	Ankle dorsiflexion "pull toes up"
L5	Extensor hallucis longus	Big toe extension — sentinel muscle for L5
S1	Gastrocnemius	Ankle plantarflexion — ankle jerk S1
S3/4	External sphincter	Anal tone on PR — cauda equina screen

Full Sensory Assessment — Spinal Tract Anatomy

Two Tracts — Two Clinical Tests

DORSAL COLUMN (DCML) — Ipsilateral

Carries: light touch, vibration, proprioception, 2-point discrimination
Crosses: at medulla — contralateral cortical representation
Test vibration: 128Hz fork on bony prominences — great toe MTP joint first, then move proximally until felt
Test proprioception: hold toe at sides, move up or down, eyes closed. "Which way?" Start distal.
Damaged by: B12 deficiency (subacute combined degeneration), MS, dorsal cord compression

SPINOTHALAMIC TRACT — Contralateral

Carries: pain, temperature, crude touch
Crosses: at the cord level it enters — so deficit is contralateral
Test pain: neuro pin or orange stick. "Sharp or blunt?"
Test temperature: cold metal of stethoscope or cold tuning fork
Damaged by: anterior cord syndrome, syringomyelia (central cord — spinothalamic affected first), Brown-Séquard

⚡

Dissociated sensory loss = dorsal column and spinothalamic tracts affected differently. Classic: syringomyelia — pain/temp loss at level (spinothalamic), proprioception/vibration initially intact (dorsal column). Brown-Séquard: ipsilateral DC loss + contralateral spinothalamic loss — hemisection of cord.

Complete Reflex Assessment

Reflexes — Grading, Technique, and Significance

Reflex	Root	Technique
Biceps	C5–C6	Finger on tendon, tap finger
Supinator	C5–C6	Tap radial styloid
Triceps	C6–C7	Direct tap on triceps tendon
Knee (patellar)	L3–L4	Leg relaxed, tap below patella
Ankle (Achilles)	S1–S2	Foot dorsiflexed, tap Achilles
Plantar	L5–S1	Lateral sole stroke — toe direction?

GRADING AND MEANING

0 Absent: LMN, peripheral neuropathy. Always reinforce with Jendrassik (interlock fingers, pull apart during testing).
+ Reduced: LMN or peripheral neuropathy
++ Normal
+++ Brisk: UMN, anxiety, hyperthyroid
++++ Clonus: ≥5 beats pathological — UMN. Cervical myelopathy, cord lesion.
Hoffman's sign: flick middle fingernail downward — thumb and index flex = UMN upper limb (upper equivalent of Babinski). Cervical myelopathy.
Inverted reflex: tapping biceps → finger flexion (not elbow) = C5/6 cord lesion. LMN at level + UMN below simultaneously.

UMN vs LMN — Complete Reference

Upper vs Lower Motor Neurone — Every Feature

Feature	UMN — Central	LMN — Peripheral
Tone	Increased — spasticity (velocity-dependent, clasp-knife). Extrapyramidal = rigidity (lead pipe or cogwheel).	Decreased — flaccid
Power	Reduced — pyramidal distribution (extensors UL, flexors LL weakest)	Reduced — myotomal or named nerve territory
Reflexes	Brisk / hyperreflexic. Clonus may be present.	Diminished or absent. Cannot be reinforced.
Babinski	Extensor (upgoing) — PATHOLOGICAL	Flexor (normal downgoing)
Wasting	Late, mild — disuse only	Early, marked — denervation atrophy
Fasciculations	Absent	Present — spontaneous muscle fibre contractions visible through skin
Acute phase	May be FLACCID/AREFLEXIC initially — spinal shock. Evolves to spasticity over days/weeks.	Always flaccid/areflexic from onset
Lesion location	Brain, brainstem, spinal cord (above anterior horn cell)	Anterior horn cell, nerve root, plexus, peripheral nerve, NMJ, muscle

⚠

Spinal shock: Acute cord injury presents with FLACCID tone, AREFLEXIA, and autonomic failure below the level — mimicking LMN. This resolves over hours–weeks, evolving into expected UMN signs. Do not interpret acute flaccid areflexia in a cord injury patient as evidence of an LMN lesion.

Gait Patterns — Recognition and Anatomical Basis

Gait Analysis — Complete Reference

Gait	Description	Anatomical basis	Causes
Hemiplegic	Stiff extended leg swings in arc (circumduction). Arm flexed/adducted.	Unilateral UMN — internal capsule / motor cortex	Stroke, TBI
Scissor	Both legs stiff, adducted, cross midline	Bilateral UMN	Cerebral palsy, bilateral cord lesion
Steppage	High knee lift to clear foot — foot slap on landing	Foot drop — common peroneal nerve / L4/5	L4/5 disc, common peroneal palsy (fibular head), stroke (mild)
Cerebellar ataxic	Wide-based, unsteady, falls toward lesion side. Eyes open or closed — equally bad.	Ipsilateral cerebellum	Cerebellar stroke, MS, alcohol, tumour
Sensory ataxic	Wide-based, stamps feet, dramatically worse eyes closed (Romberg positive)	Dorsal column proprioceptive loss	B12 deficiency, MS, tabes dorsalis, large fibre peripheral neuropathy
Parkinsonian / festinating	Stooped, small shuffling steps, accelerates forward, reduced arm swing, en-bloc turning	Basal ganglia — nigrostriatal dopaminergic pathway	Parkinson's disease, drug-induced (metoclopramide, haloperidol, prochlorperazine)
Waddling / Trendelenburg	Hip drops on contralateral side with each step — lateral shift of trunk	Proximal muscle weakness / hip girdle	Myopathy, muscular dystrophy, bilateral hip OA
Apraxic	Feet barely leave floor — "walking on ice". Normal power on formal testing when lying. Normal tone.	Frontal lobe — motor planning disconnection	Normal pressure hydrocephalus, vascular dementia, frontal tumour
Antalgic	Short stance phase on one side — minimises weight through painful limb	Pain — not neurological	Hip/knee pathology, fracture

Reference

Localisation Logic

The interpretive framework — how to take your findings and reason toward the anatomical location of the lesion. This is the skill that separates systematic assessment from genuine clinical pattern recognition.

The Five-Step Localisation Process

1️⃣

Unilateral or bilateral? Unilateral findings = structural lesion (stroke, tumour, haemorrhage, demyelination). Bilateral symmetrical = metabolic/toxic (hypoglycaemia, uraemia, drugs, septic encephalopathy, alcohol) or bilateral structural (cord, bilateral cortical very rare).

2️⃣

Are there cranial nerve signs? If yes — are CN signs on the SAME side as limb weakness (= above brainstem, cortex/capsule, both contralateral) OR OPPOSITE side (= CROSSED DEFICIT = brainstem until proved otherwise — ipsilateral CN + contralateral limb)?

3️⃣

UMN or LMN signs? Brisk reflexes + Babinski + spasticity = UMN (above anterior horn cell). Absent/reduced reflexes + flaccidity + wasting + fasciculations = LMN (at or below anterior horn cell). Mixed at one level = cord lesion at that level affecting both.

4️⃣

Which limbs are involved? All four = cord above C4 or diffuse. One side face/arm/leg = hemiplegia (cortex/capsule/brainstem/cervical cord). Both legs only = paraplegia (thoracic/lumbar cord or bilateral parasagittal cortex). One arm + same leg + same face = corticospinal anywhere.

5️⃣

Sensory pattern? Hemibody = thalamus/cortex/internal capsule. Dermatomal band = nerve root. Glove and stocking = peripheral neuropathy length-dependent. Clear sensory level = cord. Dissociated (one tract affected, other preserved) = cord lesion — syrinx or Brown-Séquard.

Clinical Pattern → Lesion Site

Finding Pattern → Localisation → Classic Cause

Pattern	Lesion	Think first
Contralateral hemiplegia + dysphasia + gaze toward lesion	Left MCA cortex (dominant)	Ischaemic stroke — pre-alert HASU
Dense equal face/arm/leg hemiplegia — no cortical signs	Internal capsule (lacunar)	Small vessel disease — hypertension
Ipsilateral CN III palsy + contralateral hemiplegia	Midbrain — Weber syndrome	PCA territory infarct
Ipsilateral CN VI/VII + contralateral hemiplegia + eyes deviate away from weak side	Pons — Foville syndrome	Basilar perforator infarct
Ipsilateral face pain/temp loss + Horner's + ataxia + dysphagia + contralateral body pain/temp loss	Lateral medulla — Wallenberg	PICA occlusion
Bilateral leg weakness + sensory level + bladder symptoms	Spinal cord — find the level	Cord compression, MS, trauma
Dermatomal pain + myotomal weakness + reflex loss at one level	Nerve root — radiculopathy	Disc prolapse, foraminal stenosis
Ipsilateral ataxia, no weakness, DANIISH signs	Ipsilateral cerebellum	PICA/AICA/SCA stroke, MS, alcohol
Symmetric distal weakness and sensory loss — glove and stocking	Peripheral nerves — length-dependent	Diabetic neuropathy, alcohol, B12
Fluctuating GCS, symmetric, no focal signs, BM abnormal	Diffuse/metabolic — no structural lesion	Hypoglycaemia, septic encephalopathy, drugs
Saddle anaesthesia + bilateral leg LMN + bladder/bowel	Cauda equina (conus/roots S1–S5)	Disc prolapse, tumour — MRI emergency

Speed of Onset → Aetiology

Temporal Pattern Narrows the Differential

Onset	Pattern	Think first
Seconds — maximal at onset	Sudden, no warning	Vascular — ischaemic stroke, haemorrhagic stroke, SAH (thunderclap headache)
Minutes	Rapid progression from onset	Stroke (progressing), seizure, Todd's paresis, hypoglycaemia
Hours	Gradual build over hours	Expanding haematoma (extradural, SDH), encephalitis, ascending GBS
Days	Progressive, subacute	Tumour with oedema, ADEM, subacute SDH, inflammatory
Weeks to months	Slowly progressive	Tumour, chronic SDH, degenerative (MND, Parkinson's, MS progressive)
Relapsing-remitting	Episodes with recovery between	MS, TIA (no recovery = stroke), migraine with aura, epilepsy, channelopathy

Self-Test

Knowledge Check

Seven clinical scenarios across all levels. Select an answer to get immediate feedback with the clinical reasoning explained in full.

Clinical Scenarios

Tap an answer to reveal the explanation. Correct answer highlighted in green if you get it wrong.

Q1 — 68-year-old, sudden onset right arm and face weakness. Cannot get words out despite appearing to understand you. BM 7.2. Where is the lesion most likely?

Q2 — You test pronator drift. The left arm drifts down and pronates. Which side has the UMN lesion?

Q3 — Patient has right-sided face weakness including the forehead, with right eye unable to fully close. The rest of the neuro exam is normal. What does this indicate?

Q4 — 55-year-old, sudden severe vertigo, vomiting, cannot walk. HINTS exam: normal head impulse (no corrective saccade), direction-changing nystagmus, no skew deviation. What is the most likely diagnosis?

Q5 — Patient unconscious, bilateral pinpoint pupils, respiratory rate 8. You consider naloxone. What sign most usefully differentiates opioid toxidrome from pontine haemorrhage on scene?

Q6 — Patient presents with: ipsilateral right face pain/temperature loss, right Horner's syndrome, right limb ataxia, dysphagia and hoarse voice — AND contralateral left body pain/temperature loss. No limb weakness. Where is the lesion?

Q7 — Patient involved in RTC, suspected T6 spinal cord injury. On assessment you find flaccid tone and absent reflexes in both legs. What is the correct interpretation?