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Structured Approach to Localisation of Stroke
Based on Bradley and Daroff's Neurology in Clinical Practice and Localization in Clinical Neurology, 8e
STEP 1 - THE FUNDAMENTAL FRAMEWORK: TWO CIRCULATIONS
Before anything else, classify every stroke into one of two circulations. This single step halves your differential immediately.
| Anterior (Carotid) Circulation | Posterior (Vertebrobasilar) Circulation |
|---|
| Vessels | ICA, MCA, ACA, anterior choroidal, ophthalmic | Vertebral, basilar, PICA, AICA, SCA, PCA |
| Territory | Frontal, parietal, temporal (most), basal ganglia, internal capsule | Brainstem, cerebellum, occipital, inferior temporal, thalamus |
| Key clues | Language (left), neglect (right), arm > leg weakness, retinal symptoms | Diplopia, dysphagia, dysarthria, ataxia, crossed deficits, vertigo |
STEP 2 - ANATOMICAL LEVEL: WHERE IN THE NEURAXIS?
Work systematically from cortex down. Each level has a signature.
Level 1 - Cerebral Cortex
Signature features:
- Higher cortical functions affected (aphasia, apraxia, agnosia, neglect, hemineglect)
- Cortical sensory loss (astereognosis, agraphesthesia, two-point discrimination impaired)
- Contralateral homonymous visual field defect (if occipital or parietal-occipital involvement)
- Jacksonian march or focal seizures may occur at onset
- No "crossed" deficits (cranial nerve on one side + limb on the other)
- Face + arm > leg weakness (MCA territory) OR leg > arm weakness (ACA territory)
Differentiating cortical from subcortical: Cortical strokes produce cortical signs (aphasia, neglect, agnosia). Pure motor or pure sensory deficits without cortical signs suggest subcortical or lacunar pathology.
Level 2 - Subcortical White Matter / Internal Capsule / Basal Ganglia
Signature features:
- Pure motor hemiparesis (posterior limb of internal capsule): face + arm + leg equally affected
- No cortical signs (no aphasia, no neglect, no visual field defect)
- Lacunar syndromes dominate (see Step 4)
- Homogeneous, equal weakness - the "capsular stroke" pattern
- Striato-capsular infarction (proximal MCA lenticulostriate branches): large area, may have cortical signs if extensive
Level 3 - Brainstem
Signature features - the crossed deficit:
- Ipsilateral cranial nerve palsy + contralateral limb weakness/sensory loss
- This crossing pattern is pathognomonic of brainstem localization
- Specific level determined by which cranial nerve is involved:
- CN III palsy → midbrain
- CN VI or VII palsy → pons
- CN IX, X, XII palsy → medulla
Other brainstem clues: Horner syndrome (any level), internuclear ophthalmoplegia (medial longitudinal fasciculus, pons), "one-and-a-half" syndrome (pons), bilateral limb signs, impaired consciousness with small lesions.
Level 4 - Cerebellum
Signature features:
- Ipsilateral limb ataxia (cerebellar connections are ipsilateral)
- Gait ataxia, truncal ataxia
- Nystagmus (horizontal or direction-changing)
- Dysarthria (scanning speech)
- NO weakness, NO sensory loss (pure cerebellar lesion)
- Vermis lesions: truncal ataxia, gait ataxia
- Hemispheric lesions: ipsilateral limb dysmetria, dysdiadochokinesia
- Beware: large cerebellar infarcts can cause obstructive hydrocephalus and herniation
STEP 3 - VASCULAR TERRITORY SYNDROMES: ANTERIOR CIRCULATION
3A - Middle Cerebral Artery (MCA) - Most Common Stroke Territory
Anatomy: MCA gives lenticulostriate branches (subcortical) and cortical branches (superior and inferior divisions).
Complete MCA Occlusion (main stem):
- Contralateral hemiplegia (face + arm > leg)
- Contralateral hemisensory loss
- Contralateral homonymous hemianopia
- Left MCA: Broca's aphasia (superior division) or Wernicke's aphasia (inferior division) or global aphasia (complete occlusion)
- Right MCA: Hemispatial neglect, hemi-inattention, constructional apraxia, anosognosia (denial of deficit)
- Gaze deviation toward the lesion (frontal eye field involvement)
- Dysarthria
Superior Division MCA:
- Broca's aphasia (left hemisphere): non-fluent, effortful speech, preserved comprehension
- Contralateral face + arm weakness > leg
- No homonymous hemianopia
Inferior Division MCA:
- Wernicke's aphasia (left): fluent, paraphasic, impaired comprehension
- Contralateral superior homonymous quadrantanopia ("pie in the sky")
- Contralateral neglect (right hemisphere)
MCA Lenticulostriate (Subcortical):
- Contralateral hemiparesis with little sensory involvement
- Pure motor stroke (one cause) - see lacunar section
- Striatocapsular infarction: hemiplegia, hypesthesia, visual field defect, transient aphasia
3B - Anterior Cerebral Artery (ACA)
Territory: Medial surface of the frontal and parietal lobes, anterior corpus callosum, anterior internal capsule.
Syndrome:
- Contralateral leg > arm weakness (homunculus: leg is on the medial surface)
- Contralateral leg > arm sensory loss
- Gait apraxia, urinary incontinence (frontal lobe)
- Bilateral ACA occlusion (rare): Akinetic mutism - patient lies with eyes open, follows visual stimuli but is mute and akinetic; caused by bilateral cingulate gyrus infarction
- Transcortical motor aphasia (left ACA): non-fluent speech, preserved repetition (unlike Broca's)
- Grasp reflex, snout reflex (frontal release signs)
- Callosal disconnection syndrome (anterior corpus callosum): left hand apraxia, alien hand syndrome
3C - Anterior Choroidal Artery
Arises from the ICA just distal to the posterior communicating artery.
Classic triad (incomplete in most cases):
- Contralateral hemiplegia (posterior limb, internal capsule)
- Contralateral hemisensory loss (thalamus, posterior limb)
- Contralateral homonymous hemianopia (lateral geniculate body, optic tract, retrolenticular internal capsule)
3D - Internal Carotid Artery (ICA)
Occlusion findings depend on collateral flow:
- If good collaterals: may be silent
- If poor collaterals: MCA + ACA territory infarction (massive hemispheric stroke)
- Ipsilateral monocular visual loss (amaurosis fugax or permanent): ophthalmic artery involvement - this is a hallmark of ICA disease
- Contralateral hemiplegia, hemisensory loss
- Ipsilateral Horner syndrome (sympathetic fibers travel with ICA)
STEP 4 - LACUNAR SYNDROMES (Small Vessel / Penetrating Artery Occlusion)
Lacunar infarcts are small (< 15 mm), deep, caused by lipohyalinosis or microatheroma of penetrating arteries. Five classic syndromes:
| Syndrome | Location | Features |
|---|
| Pure Motor Hemiplegia | Posterior limb internal capsule OR pons OR corona radiata | Face + arm + leg equal weakness, NO sensory, NO cortical signs - most common lacunar syndrome |
| Pure Sensory Stroke | Thalamus (ventral posterolateral nucleus) | Contralateral hemisensory loss all modalities, NO motor deficit; described by C.M. Fisher |
| Sensorimotor Stroke | Posterior limb internal capsule + thalamus, or thalamocapsular | Motor + sensory, no cortical signs |
| Ataxic Hemiparesis | Pons OR posterior limb internal capsule OR corona radiata | Ipsilateral cerebellar ataxia + contralateral hemiparesis, leg > arm; "homolateral ataxia and crural paresis" |
| Dysarthria-Clumsy Hand | Pons OR internal capsule genu | Dysarthria + facial weakness + contralateral hand clumsiness/weakness |
Key principle: Lacunar syndromes have NO aphasia, NO visual field defect, NO cognitive change, NO hemineglect - absence of cortical signs with pure motor or sensory deficit points strongly to lacune.
STEP 5 - POSTERIOR CIRCULATION SYNDROMES
5A - Posterior Cerebral Artery (PCA)
Territory: Occipital cortex, inferior temporal lobe, thalamus (penetrating branches), midbrain.
Cortical PCA (P2 segment onwards):
- Contralateral homonymous hemianopia - the signature finding; macular sparing common (macular cortex has MCA collaterals)
- Left PCA: Alexia without agraphia (patient cannot read but can write - disconnection of visual cortex from language areas), anomic aphasia, visual agnosia
- Right PCA: Prosopagnosia (failure to recognize faces), topographical disorientation
- Bilateral PCA occlusion: Cortical blindness - patient is blind but denies it (Anton syndrome = cortical blindness + anosognosia); Balint syndrome (bilateral parieto-occipital) = optic ataxia + ocular apraxia + simultanagnosia
Penetrating PCA (thalamo-perforating branches):
- Aphasia (left pulvinar involvement)
- Global amnesia (bilateral hippocampal-parahippocampal)
- Akinetic mutism
- Dejerine-Roussy syndrome (thalamic pain syndrome): Contralateral sensory loss all modalities + severe contralateral dysesthesias/thalamic pain + vasomotor changes + transient hemiparesis + choreoathetoid movements; caused by thalamogeniculate branch occlusion
T2-weighted MRI: posterolateral medullary infarct + small cerebellar infarct in PICA territory (Bradley and Daroff's Neurology)
5B - Thalamic Infarction Syndromes
The thalamus receives blood from 4 vascular regions:
| Territory | Vessel | Syndrome |
|---|
| Posterolateral | Thalamogeniculate (P2 segment PCA) | Pure sensory stroke, sensorimotor stroke, Dejerine-Roussy syndrome |
| Anterior | Polar/tuberothalamic artery (posterior communicating) | Amnesia, confusion, personality change, aphasia (left), neglect (right) |
| Paramedian | Thalamo-perforating artery (P1 segment PCA) | Profound amnesia, vertical gaze palsy, somnolence; Bilateral = artery of Percheron occlusion: bilateral paramedian thalamic infarction with coma |
| Dorsal (pulvinar) | Posterior choroidal arteries | Language disturbance (left), neglect (right), visual field defects |
Artery of Percheron: A single thalamoperforating artery arising from the P1 segment supplying both paramedian thalami. Occlusion causes bilateral thalamic infarction with coma or hypersomnolence, profound amnesia, and vertical gaze palsy - all without motor signs.
5C - Vertebrobasilar Territory - Brainstem Syndromes
The "Crossed Deficit" Rule:
Ipsilateral CN palsy + contralateral hemiplegia/hemisensory loss = brainstem lesion, level determined by CN involved.
MIDBRAIN (CN III, IV)
Weber Syndrome (ventral midbrain - cerebral peduncle):
- Ipsilateral CN III palsy (ptosis, dilated pupil, "down and out" eye)
- Contralateral hemiplegia
Benedikt Syndrome (tegmentum midbrain - red nucleus):
- Ipsilateral CN III palsy
- Contralateral tremor, ataxia, choreoathetosis (red nucleus involvement)
Parinaud Syndrome (dorsal midbrain - superior colliculus, pretectal area):
- Upgaze palsy (vertical gaze paresis)
- Convergence-retraction nystagmus on attempted upgaze
- Light-near dissociation of pupils
- Often from posterior thalamo-midbrain perforator or posterior circulation stroke
Claude Syndrome (combination of Benedikt + superior cerebellar peduncle):
- CN III palsy + contralateral cerebellar ataxia
PONS (CN V, VI, VII)
Millard-Gubler Syndrome (ventral pons):
- Ipsilateral CN VI palsy (lateral gaze palsy, diplopia)
- Ipsilateral CN VII palsy (lower motor neuron facial weakness)
- Contralateral hemiplegia
Foville Syndrome (tegmental pons, PPRF + CN VI nucleus):
- Ipsilateral horizontal gaze palsy (eyes deviate away from lesion - in cortical stroke eyes deviate toward lesion)
- Ipsilateral CN VII palsy
- Contralateral hemiplegia
- Key diagnostic point: In pontine strokes, gaze deviation is away from the lesion (PPRF destroyed); in cortical/hemispheric strokes, gaze deviation is toward the lesion (FEF pushes eyes to the opposite side)
One-and-a-Half Syndrome (paramedian pons - PPRF + MLF):
- Ipsilateral gaze palsy (PPRF/CN VI nucleus lesion)
- Ipsilateral internuclear ophthalmoplegia (MLF lesion)
- Net result: only the contralateral eye can abduct; all other horizontal movements are lost
Locked-In Syndrome (bilateral ventral pons - bilateral corticospinal and corticobulbar tracts):
- Complete quadriplegia and anarthria
- Preserved consciousness, preserved vertical eye movements (RIMLF spared)
- Patient communicates only by blinking or vertical eye movements
MEDULLA (CN IX, X, XI, XII)
Lateral Medullary Syndrome (Wallenberg Syndrome) - PICA or vertebral artery occlusion:
This is the most clinically important posterior circulation syndrome. Caused by occlusion of the PICA or vertebral artery, producing an infarct in the posterolateral medulla.
| Structure damaged | Feature |
|---|
| Spinothalamic tract | Contralateral loss of pain and temperature (limbs and trunk) |
| Descending trigeminal nucleus | Ipsilateral facial loss of pain and temperature |
| Vestibular nuclei | Vertigo, nausea, vomiting, nystagmus |
| Nucleus ambiguus (CN IX, X) | Ipsilateral palatal palsy, dysarthria, dysphagia, hoarseness |
| Descending sympathetic fibers | Ipsilateral Horner syndrome (ptosis, miosis, anhidrosis) |
| Inferior cerebellar peduncle / cerebellum | Ipsilateral limb and gait ataxia |
| Solitary nucleus / dorsal vagal nucleus | Hiccups |
Classic "crossed sensory deficit": Ipsilateral face loss of pain/temperature + contralateral body loss of pain/temperature (thermoanalgesia). Motor power is characteristically SPARED (corticospinal tracts are in the ventral medulla, not affected in lateral medullary syndrome).
Medial Medullary Syndrome (Dejerine's Anterior Bulbar Syndrome) - ASA or vertebral artery branch:
| Structure | Feature |
|---|
| Corticospinal tract (pyramids) | Contralateral hemiplegia (spares face) |
| Medial lemniscus | Contralateral loss of discriminative touch, vibration, proprioception |
| CN XII (hypoglossal nerve) | Ipsilateral tongue weakness/atrophy (tongue deviates toward lesion) |
5D - Cerebellar Artery Territories
| Artery | Territory | Key Syndrome |
|---|
| PICA (Posterior Inferior Cerebellar Artery) | Posteroinferior cerebellum + lateral medulla | Wallenberg syndrome (lateral medullary); cerebellar infarct causing vertigo, ataxia, possible obstructive hydrocephalus |
| AICA (Anterior Inferior Cerebellar Artery) | Anteroinferior cerebellum + lateral caudal pons | Ipsilateral CN VII + VIII involvement (facial palsy + deafness + tinnitus) + lateral pontine syndrome + ipsilateral Horner; AICA infarct should be suspected when lateral pontine features accompany hearing loss |
| SCA (Superior Cerebellar Artery) | Superior cerebellum + lateral rostral pons | Ipsilateral cerebellar ataxia (severe), ipsilateral Horner, ipsilateral CN IV palsy, contralateral hemisensory loss (spinothalamic), ipsilateral CN V partial deficit; contralateral loss of pain/temperature |
STEP 6 - SPECIAL LOCALIZING CLUES: CLINICAL PEARLS
Visual Field Defects - Localizing Value
| Defect | Localization |
|---|
| Monocular blindness | Retina or optic nerve (ipsilateral) - anterior to chiasm |
| Bitemporal hemianopia | Optic chiasm |
| Contralateral homonymous hemianopia | Optic tract, LGN, optic radiation, occipital cortex |
| Superior quadrantanopia ("pie in sky") | Inferior optic radiation, temporal lobe (Meyer's loop) |
| Inferior quadrantanopia ("pie in floor") | Superior optic radiation, parietal lobe |
| Macular-sparing hemianopia | Occipital cortex (MCA/PCA boundary zone at occipital pole) |
Gaze Deviation Lateralizing Rule
| Gaze deviation | Meaning |
|---|
| Eyes deviate TOWARD the hemiplegia side | Cortical/hemispheric stroke (FEF pushes eyes to the opposite hemisphere's territory, i.e., away from lesion, but patient presents with eyes toward ipsilateral side to lesion) - eyes look "away" from the hemiplegic limbs but "toward" the lesion |
| Eyes deviate AWAY from hemiplegia | Pontine stroke (PPRF destroyed; contralateral PPRF pulls eyes to that side) |
Practical rule: "The eyes look toward a cortical stroke and away from a pontine stroke."
Language as a Lateralizing Tool (Left Hemisphere = Dominant in 90%)
| Aphasia Type | Localization | Key Features |
|---|
| Broca's (expressive) | Left inferior frontal (Broca's area, BA44/45), superior MCA division | Non-fluent, telegraphic, effortful; comprehension intact; patient aware of deficit |
| Wernicke's (receptive) | Left posterior superior temporal (BA 22), inferior MCA division | Fluent, paraphasic, neologisms; comprehension severely impaired; patient unaware |
| Global | Large left hemisphere (Broca + Wernicke areas both) | Non-fluent + poor comprehension + poor repetition |
| Conduction | Left arcuate fasciculus (connects Broca and Wernicke) | Fluent, good comprehension, severely impaired repetition; paraphasic errors |
| Transcortical Motor | Left frontal (ACA territory, anterior to Broca's) | Non-fluent, but repetition preserved (unlike Broca's) |
| Transcortical Sensory | Left parieto-occipital (posterior watershed) | Fluent, poor comprehension, repetition preserved (echolalia) |
| Alexia without agraphia | Left PCA territory (left occipital cortex + splenium of corpus callosum) | Cannot read, can write; disconnects right visual cortex from language areas |
Hemispatial Neglect
- Right hemisphere (usually right parietal or frontoparietal) causes left hemispatial neglect
- Patient ignores left side of space, left side of body
- Line bisection test: bisects to the right of midline
- Much more severe and persistent with right hemispheric strokes than left
Horner Syndrome Localizing Value in Stroke Context
- Central Horner (hypothalamus to ciliospinal center of Budge, C8-T2): Any stroke affecting the lateral hypothalamus, lateral brainstem (especially lateral medullary), or cervical cord
- In posterior circulation stroke: Ipsilateral Horner + ipsilateral ataxia + ipsilateral CN palsy = lateral brainstem involvement
- Horner syndrome without anhidrosis suggests post-ganglionic; with anhidrosis (face and body) suggests pre-ganglionic or central
STEP 7 - CORTICAL vs. SUBCORTICAL vs. BRAINSTEM DIFFERENTIATION TABLE
| Feature | Cortical | Subcortical/Lacunar | Brainstem | Cerebellar |
|---|
| Aphasia | YES (left) | NO | NO (except peduncle lesions) | NO |
| Neglect | YES (right) | NO | NO | NO |
| Visual field defect | YES (hemianopia) | NO (unless thalamocapsular) | YES (rare cortical blindness) | NO |
| Face + arm + leg equal weakness | Rarely | YES (capsular) | YES (with CN palsy) | NO |
| Crossed deficits | NO | NO | YES - hallmark | NO |
| Cerebellar signs | NO | NO | Possible (peduncle) | YES (ipsilateral) |
| Consciousness affected | If large | Rarely | YES if basilar | Late (herniation) |
| Seizures at onset | Possible | Rare | NO | NO |
STEP 8 - THE OCSP (OXFORD/BAMFORD) CLINICAL CLASSIFICATION
A practical bedside classification requiring no imaging:
| Category | Criteria | Vascular Territory |
|---|
| TACI - Total Anterior Circulation Infarct | All 3: motor/sensory deficit + cortical sign + homonymous hemianopia | Complete MCA or ICA territory |
| PACI - Partial Anterior Circulation Infarct | 2 of 3 above, or cortical sign alone | MCA branch territory |
| LACI - Lacunar Infarct | Pure motor, pure sensory, sensorimotor, or ataxic hemiparesis; NO cortical signs | Small perforating artery |
| POCI - Posterior Circulation Infarct | Any of: brainstem, cerebellar, bilateral motor/sensory, crossed deficit, isolated hemianopia | Vertebrobasilar |
Clinical utility: TACI has worst prognosis (60% dead or dependent at 1 year); LACI best (10-15% dead or dependent). OCSP classification predicts functional outcome, etiology, and recurrence risk.
STEP 9 - INTEGRATING THE APPROACH - BEDSIDE ALGORITHM
SUDDEN FOCAL DEFICIT
↓
1. CORTICAL SIGNS? (aphasia, neglect, visual agnosia, cortical sensory loss)
YES → Cortical involvement → Anterior (MCA/ACA/PCA) or large vessel
NO → Subcortical / brainstem / cerebellum
↓
2. CROSSED DEFICIT? (ipsilateral CN + contralateral limb)
YES → BRAINSTEM (identify CN → level: III=midbrain, VI/VII=pons, IX/X/XII=medulla)
NO → Not brainstem
↓
3. CEREBELLAR SIGNS WITHOUT WEAKNESS?
YES → Cerebellar (identify artery by co-features: PICA=lateral medulla, AICA=hearing, SCA=high ataxia)
NO → Continue
↓
4. PURE MOTOR / PURE SENSORY / ATAXIC HEMIPARESIS?
YES → LACUNAR - no cortical signs confirm
NO → Continue
↓
5. VISUAL FIELD DEFECT?
Hemianopia + language → MCA (left) or PCA (left or right)
Hemianopia alone, macular sparing → PCA
Monocular → Retinal / optic nerve (carotid territory)
↓
6. ARM > LEG WEAKNESS → MCA
LEG > ARM WEAKNESS → ACA
Equal face + arm + leg → Internal capsule / pons
STEP 10 - IMAGING CORRELATION
| Syndrome | Expected Imaging Finding |
|---|
| MCA territory | CT: wedge hypodensity frontal-parietal-temporal; loss of insular ribbon; MRI DWI: bright cortical + subcortical |
| Lacunar | CT: small deep hypodensity (often missed acutely); MRI: small DWI-bright lesion < 15mm in basal ganglia, capsule, pons, thalamus |
| PCA | CT: occipital hypodensity; MRI DWI: occipital, thalamic, and hippocampal involvement |
| Lateral medullary (Wallenberg) | CT: often normal; MRI T2/DWI: posterolateral medullary hyperintensity; may see vertebral/PICA poor flow void |
| Basilar artery occlusion | CT: "dense basilar" sign; CT angiography: cut-off at basilar; MRI: bilateral pontine, thalamic, occipital DWI changes |
| Artery of Percheron | MRI: butterfly-shaped bilateral paramedian thalamic DWI lesion; may see mesencephalic involvement |
SUMMARY MEMORY AID
- MCA (left): Aphasia + contralateral face/arm hemiplegia + hemianopia
- MCA (right): Neglect + anosognosia + contralateral hemiplegia
- ACA: Leg > arm + frontal release signs + akinetic mutism (bilateral)
- PCA: Hemianopia (macular sparing) + alexia without agraphia (left) + thalamic pain
- Lacune: Pure motor / pure sensory / sensorimotor / ataxic hemiparesis - NO cortical signs
- Wallenberg: Crossed sensory (ipsilateral face / contralateral body) + Horner + dysphagia + ataxia + NO motor weakness
- Medial medulla: Contralateral hemiplegia (spares face) + contralateral dorsal column loss + ipsilateral tongue palsy
- Pons (ventral): Locked-in / one-and-a-half / eyes deviate away from lesion
- Midbrain: CN III palsy + contralateral hemiplegia (Weber) or tremor (Benedikt)
- Thalamus (paramedian, bilateral): Artery of Percheron → coma + amnesia + vertical gaze palsy - NO motor deficit
Sources: Bradley and Daroff's Neurology in Clinical Practice; Localization in Clinical Neurology, 8e (Brazis et al.)