What all signs can I demonstrate in a patient with stroke

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In a patient with stroke, demonstrate a focused neurological examination, comparing both sides and documenting the affected side. Do not delay emergency stroke care to complete a lengthy examination.

1. Higher mental functions

  • Level of consciousness: alert, drowsy, stupor, coma
  • Orientation and attention
  • Speech and language:
    • Aphasia: impaired naming, comprehension, repetition, reading/writing, usually dominant hemisphere stroke
    • Dysarthria: slurred articulation with intact language
  • Neglect/inattention: ask the patient to identify stimuli on both sides or draw/copy a figure
  • Memory may be impaired

2. Cranial nerve signs

  • Gaze deviation toward the side of a large hemispheric lesion
  • Visual-field defect, especially contralateral homonymous hemianopia
  • Pupils and ocular movements: diplopia, internuclear ophthalmoplegia, gaze palsy, nystagmus may suggest posterior-circulation/brainstem stroke
  • Upper motor neuron facial weakness: contralateral lower facial droop with forehead sparing
  • Dysphagia, dysphonia, reduced palatal movement, weak cough, tongue deviation: especially brainstem stroke
  • Test swallowing only when it is safe and according to local protocol. Keep the patient nil by mouth if dysphagia is suspected.

3. Motor examination

Look for:
  • Contralateral hemiparesis or hemiplegia
  • Weakness of face, arm, and/or leg. Arm more than leg can suggest MCA territory; leg more than arm can suggest ACA territory.
  • Pronator drift: arms outstretched, palms upward, eyes closed; the weak arm pronates and drifts down.
  • Reduced fine finger movements
  • Tone:
    • early acute stroke may cause flaccidity
    • later, increased tone and spasticity
  • Abnormal posture or contractures in established stroke

4. Reflexes and plantar response

  • Brisk deep-tendon reflexes on the affected side, commonly later in the course
  • Extensor plantar response (Babinski sign) on the affected side
  • Clonus may be present in spastic hemiparesis
  • In very acute severe stroke, reflexes may initially be reduced rather than brisk.

5. Sensory examination

Test and compare sides:
  • Light touch and pinprick
  • Temperature if needed
  • Vibration and joint position sense
  • Contralateral hemisensory loss or sensory neglect
  • Cortical sensory deficits: astereognosis, agraphesthesia, impaired two-point discrimination, if the patient can cooperate

6. Coordination and cerebellar signs

  • Finger-nose and heel-knee-shin tests
  • Dysmetria, intention tremor, dysdiadochokinesia
  • Truncal or gait ataxia, nystagmus, dysarthria
    These may point to cerebellar or posterior-circulation stroke. Do not force a patient with acute weakness or imbalance to walk.

7. Gait, stance, and balance

If safe and supervised:
  • Hemiplegic/spastic gait: circumduction of the affected leg, reduced arm swing
  • Broad-based ataxic gait
  • Romberg test only if the patient can stand safely

8. Other bedside signs

  • Check for headache, vomiting, seizures, neck stiffness, and reduced consciousness, which may occur with intracranial hemorrhage or raised intracranial pressure.
  • Examine pulse/rhythm for atrial fibrillation, blood pressure, carotid bruit, and cardiovascular status. A carotid bruit is not required for stroke and absence does not exclude carotid disease.

Quick exam presentation

You can say:
“This patient has a focal neurological deficit characterized by [right/left] UMN facial weakness, [right/left] hemiparesis with pronator drift, increased tone/hyperreflexia and an extensor plantar response, with/without hemisensory loss, aphasia, visual-field defect, neglect, or cerebellar signs. These findings are consistent with a [hemispheric/brainstem/cerebellar] stroke syndrome.”
For an acute bedside screen, remember BE-FAST: Balance, Eyes, Face, Arm, Speech, Time. Formal severity assessment is commonly recorded with the 11-domain NIH Stroke Scale, which includes consciousness, gaze, visual fields, facial movement, motor function, ataxia, sensation, language, dysarthria, and neglect.

Give me a step-by-step neurological exam for stroke

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NIH Stroke Scale official assessment instructions neurological examination stroke

Step-by-step neurological examination in suspected stroke

First: activate the stroke pathway, note the time last known well, check ABC, vital signs, oxygen saturation, and bedside blood glucose. Do not delay urgent brain imaging or reperfusion treatment for a long examination.
Use a brief examination first, then expand once the patient is stable. Compare right and left throughout.

1. General observation

From the end of the bed, note:
  • Conscious level, distress, vomiting, seizure activity
  • Facial asymmetry
  • Spontaneous movement or non-movement of one side
  • Speech clarity and ability to engage
  • Head or eye deviation
  • Posture, tone, involuntary movement
  • Any trauma, rash, anticoagulant alert bracelet, or medical devices
State: “The patient is alert/drowsy, has a left/right facial asymmetry and reduced spontaneous movement of the left/right side.”

2. Consciousness and cognition

Assess:
  • Alertness: awake? needs voice or painful stimulus?
  • Orientation: name, age/date, place
  • Attention: ask them to follow a simple command, such as “close your eyes and open them”
  • Observe for confusion, agitation, or reduced awareness
A reduced level of consciousness can occur with a large hemispheric stroke, brainstem stroke, or intracranial hemorrhage.

3. Speech, language, and neglect

While speaking to the patient, determine whether the problem is:
  • Dysarthria: slurred speech due to weak/incoordinated articulation. Language content and comprehension are relatively intact.
  • Aphasia/dysphasia: language impairment, usually from the dominant hemisphere.
    • Ask: “What is your name?” and “Where are you?”
    • Ask them to name familiar objects, e.g. pen, watch.
    • Give commands: “Show me two fingers,” then “Touch your left ear with your right hand.”
    • Ask them to repeat: “No ifs, ands, or buts.”
  • Neglect/inattention: stimulate or show fingers on both sides simultaneously. Extinction of one side suggests neglect, classically with a nondominant parietal stroke.

4. Cranial nerves

Pupils

  • Inspect size, equality, and response to light.
  • Marked anisocoria or an abnormal pupil may point to a third-nerve problem or herniation, not simply an uncomplicated hemispheric stroke.

Visual fields

  • Ask the patient to look at your nose.
  • Present moving fingers in each quadrant and ask which side they see.
  • Look for a homonymous hemianopia, meaning loss of the same side of the visual field in both eyes.

Eye position and movements

  • Observe for resting eye deviation.
  • Ask the patient to follow your finger horizontally and vertically.
  • Look for gaze palsy, nystagmus, diplopia, or internuclear ophthalmoplegia.
  • A large hemispheric stroke may cause gaze deviation toward the side of the lesion.

Facial movement

  • Inspect the face at rest.
  • Ask the patient to raise eyebrows, close eyes tightly, show teeth, and puff cheeks.
  • UMN facial weakness: contralateral lower facial weakness with forehead sparing.
  • Check for dysarthria while they speak.

Palate, tongue, and bulbar function

  • Listen for hoarse or wet voice.
  • Ask the patient to say “ah” and look for palatal asymmetry.
  • Ask them to protrude the tongue and note deviation.
  • Ask about choking, coughing with fluids, or swallowing difficulty.
  • Do not give food or water until a validated swallow screen is passed.

5. Motor examination

Inspect

  • Compare bulk, posture, and involuntary movements.
  • Look for flaccidity or spastic posture.

Pronator drift

A sensitive quick test for mild pyramidal weakness:
  1. Ask the patient to stretch both arms forward at shoulder level.
  2. Palms face upward.
  3. Ask them to close their eyes for 10 seconds.
  4. Observe for downward drift and pronation of one arm.

Tone

Passively move both arms and legs:
  • Shoulder, elbow, wrist
  • Hip, knee, ankle
Look for:
  • Reduced tone/flaccidity in very acute stroke
  • Spasticity/increased tone in established UMN weakness

Power

Grade strength from 0 to 5 and compare sides.
Upper limbs
  • Shoulder abduction
  • Elbow flexion and extension
  • Wrist extension
  • Finger abduction
  • Grip strength
Lower limbs
  • Hip flexion
  • Knee extension and flexion
  • Ankle dorsiflexion and plantarflexion
Document the pattern:
  • Face and arm more affected than leg: often MCA territory
  • Leg more affected than arm: often ACA territory
  • Pure motor weakness without cortical signs can occur in a lacunar stroke

6. Reflexes

Test and compare:
  • Biceps
  • Triceps
  • Supinator
  • Knee jerk
  • Ankle jerk
Then test plantar response:
  • Stroke the lateral sole from heel to little toe, then across the forefoot.
  • Extensor plantar response (Babinski sign) supports an UMN lesion.
Note: in the hyperacute phase, the affected side may initially be hypotonic with reduced reflexes. Hyperreflexia and spasticity can develop later.

7. Sensory examination

Ask the patient to close their eyes and compare both sides.
Test:
  • Light touch over face, arm, trunk, and leg
  • Pinprick if needed
  • Vibration at distal bony points, if time allows
  • Joint position at the great toe or finger, if needed
Look for:
  • Contralateral hemisensory loss
  • Sensory extinction on double simultaneous stimulation
  • A sensory level, which suggests a spinal rather than cerebral lesion

8. Coordination and cerebellar testing

Only interpret these if power is adequate.
  • Finger-nose-finger: dysmetria, intention tremor
  • Heel-knee-shin
  • Rapid alternating movements: dysdiadochokinesia
  • Look for nystagmus and scanning dysarthria
Cerebellar stroke may present with prominent ataxia, vertigo, vomiting, nystagmus, or inability to sit or stand unaided, sometimes with little limb weakness.

9. Gait and balance

Perform only if safe and assisted.
  • Observe sitting balance first.
  • Assess ability to stand and walk with assistance.
  • Look for hemiplegic gait, circumduction, reduced arm swing, or broad-based ataxic gait.
  • Avoid making an acutely weak, dizzy, or unstable patient walk.

10. Screen for a stroke mimic and examine relevant systems

  • Bedside capillary glucose immediately
  • Temperature
  • Blood pressure and oxygen saturation
  • Pulse rate and rhythm, especially atrial fibrillation
  • Cardiac examination for murmurs
  • Carotid bruits if appropriate, but do not press or repeatedly manipulate the carotids
  • Consider seizure, migraine, hypoglycemia, infection, drug toxicity, and functional neurological disorder as possible mimics

Quick acute-stroke sequence: NIHSS domains

For a formal standardized assessment, use the NIH Stroke Scale, which examines:
  1. Level of consciousness
  2. LOC questions
  3. LOC commands
  4. Best gaze
  5. Visual fields
  6. Facial palsy
  7. Left arm motor function
  8. Right arm motor function
  9. Left leg motor function
  10. Right leg motor function
  11. Limb ataxia
  12. Sensory loss
  13. Best language
  14. Dysarthria
  15. Extinction/inattention

Example of a concise examination summary

“The patient is alert but has expressive aphasia. There is right lower facial weakness with forehead sparing, right pronator drift, reduced power in the right arm and leg, brisk right-sided reflexes, and an extensor right plantar response. There is reduced right-sided sensation and a right homonymous hemianopia. This is a left hemispheric cortical stroke syndrome, likely in the left MCA territory.”
The formal NIHSS should be performed by clinicians trained in its standardized method.

Now how do I localise stroke

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Clinical localisation of stroke

Localise in this order:
  1. Is it cortical, subcortical, brainstem, or cerebellar?
  2. Which side is involved?
  3. Which vascular territory fits: MCA, ACA, PCA, vertebrobasilar, or lacunar?
  4. Confirm with urgent CT/CTA and often MRI. Clinical localisation guides urgency but does not replace imaging.

1. First decide: anterior or posterior circulation?

Anterior circulation: carotid, ACA, MCA

Suggestive features:
  • Contralateral face/arm/leg weakness or sensory loss
  • Aphasia
  • Neglect
  • Gaze deviation
  • Homonymous visual-field loss
  • Cortical sensory signs

Posterior circulation: vertebral, basilar, PCA, cerebellar arteries

Suggestive features:
  • Vertigo, vomiting, severe imbalance
  • Diplopia, nystagmus, dysarthria, dysphagia
  • Cranial nerve signs
  • Ataxia
  • Reduced consciousness
  • “Crossed” signs: ipsilateral cranial nerve deficit with contralateral limb weakness or sensory loss
A useful rule: cortical signs suggest a hemispheric stroke; crossed cranial nerve and body signs suggest a brainstem stroke. This pattern is described in Bradley and Daroff's Neurology in Clinical Practice under brainstem ischemic stroke syndromes.

2. Decide the side

Hemispheric lesions

The cerebral hemisphere usually produces opposite-sided motor and sensory deficits.
  • Right face/arm/leg weakness → usually left hemisphere
  • Left face/arm/leg weakness → usually right hemisphere
Then use cortical signs:
  • Aphasia → dominant hemisphere, usually left MCA
  • Left-sided neglect → usually right, nondominant parietal MCA
  • Right homonymous hemianopia → left retrochiasmal visual pathway, commonly left PCA or posterior MCA
  • Left homonymous hemianopia → right PCA or posterior MCA

Brainstem lesions

Think same-side face, opposite-side body:
  • Left facial palsy or left palate weakness + right hemiparesis → left brainstem
  • This is called a crossed neurological deficit.

Cerebellar lesions

Cerebellar signs are generally ipsilateral:
  • Left limb dysmetria, left-sided falling, left ataxia → left cerebellar hemisphere

3. Localise by vascular territory

TerritoryKey clinical patternUseful localisation clue
MCAContralateral face and arm weakness/sensory loss more than leg; gaze preference; contralateral homonymous hemianopiaAphasia if dominant side, neglect if nondominant side
ACAContralateral leg weakness/sensory loss more than arm or face; gait difficultyAbulia, apathy, urinary incontinence, grasp reflex may occur
PCAContralateral homonymous hemianopia, often with macular sparingMemory problems or thalamic sensory symptoms; dominant occipital lesion may cause alexia without agraphia
Internal carotid arteryLarge MCA syndrome, sometimes combined MCA plus ACA deficitsSevere deficit with cortical signs; possible monocular visual loss before or with stroke
Lacunar infarctPure motor, pure sensory, sensorimotor, ataxic hemiparesis, dysarthria-clumsy handNo cortical signs: no aphasia, neglect, gaze deviation, or visual-field defect
Brainstem/vertebrobasilarCranial nerve deficits, crossed signs, diplopia, dysarthria, dysphagia, bilateral signs“Face one side, body other side”
Cerebellar infarctAcute severe vertigo, vomiting, nystagmus, dysmetria, truncal/gait ataxiaOften little or no weakness; inability to sit or walk is a major warning sign
The classic MCA, ACA, and PCA territory syndromes remain a core part of acute stroke assessment, as described in Neuroanatomy Through Clinical Cases, “Clinical Syndromes of the Three Cerebral Arteries.”

4. High-yield patterns to memorise

MCA stroke

Face and arm > leg
  • Contralateral lower facial weakness
  • Contralateral arm weakness and sensory loss
  • Contralateral homonymous hemianopia
  • Eyes may deviate toward the lesion
  • Dominant hemisphere: aphasia
  • Nondominant hemisphere: neglect
Example: right facial droop + right arm more than leg weakness + expressive aphasia
left MCA stroke

ACA stroke

Leg > arm
  • Contralateral leg-predominant weakness and sensory loss
  • Difficulty initiating walking
  • Abulia/apathy, reduced spontaneous speech
  • Urinary urgency or incontinence in larger bilateral/medial frontal lesions
Example: isolated marked right leg weakness with relatively preserved face and arm
left ACA stroke

PCA stroke

Visual field > motor deficit
  • Contralateral homonymous hemianopia
  • May have visual neglect or visual hallucinations
  • Dominant occipital plus splenial involvement: alexia without agraphia
  • Thalamic involvement: contralateral sensory loss or pain
Example: sudden left homonymous hemianopia without major limb weakness
right PCA stroke

Lacunar stroke

Pure motor or pure sensory syndrome without cortical dysfunction
Common sites:
  • Posterior limb of internal capsule
  • Corona radiata
  • Thalamus
  • Pons
Patterns:
  • Pure motor hemiparesis
  • Pure sensory stroke
  • Sensorimotor stroke
  • Ataxic hemiparesis
  • Dysarthria-clumsy hand syndrome
Example: left face, arm, and leg weakness with dysarthria but no aphasia, neglect, visual-field defect, or gaze palsy
→ likely right internal-capsule or pontine lacunar stroke
Textbook sources note that pure motor hemiparesis commonly reflects a lacunar lesion of the contralateral internal capsule or pons.

5. Brainstem localisation: practical approach

Think of three components:
  1. Cranial nerve signs: diplopia, facial weakness, impaired facial sensation, dysphagia, dysphonia, tongue weakness
  2. Long-tract signs: contralateral weakness, sensory loss, hyperreflexia, Babinski response
  3. Cerebellar signs: ipsilateral limb ataxia, nystagmus, vertigo

Rule

Cranial nerve deficit on one side + weakness/sensory loss on the opposite side = brainstem stroke until proven otherwise.
Examples:
  • Ipsilateral facial weakness + contralateral hemiparesis → pontine lesion
  • Ipsilateral palate weakness/hoarseness + contralateral body pain-temperature loss, with ipsilateral facial pain-temperature loss and ataxia → lateral medullary pattern
  • Diplopia, dysarthria, quadriparesis, or reduced consciousness → consider basilar artery occlusion urgently

6. Cerebellar stroke

Suspect it in abrupt:
  • Severe vertigo and vomiting
  • Gait or truncal ataxia
  • Ipsilateral dysmetria
  • Nystagmus
  • Dysarthria
  • Inability to sit unsupported or walk
Do not dismiss severe acute vertigo as peripheral vertigo when there are neurological features. Cerebellar infarction can deteriorate because of edema and obstructive hydrocephalus. A posterior-circulation review notes that gait ataxia is frequent with brainstem/cerebellar posterior-circulation stroke and may be severe.

7. A simple bedside localisation algorithm

A. Is there aphasia, neglect, a field defect, or gaze deviation?
Cortical hemispheric stroke, commonly MCA.
B. Is weakness mainly face and arm?
MCA.
C. Is weakness mainly leg?
ACA.
D. Is there isolated homonymous hemianopia?
PCA.
E. Is there pure motor/pure sensory deficit without cortical signs?
Lacunar internal capsule, thalamus, corona radiata, or pons.
F. Are there cranial nerve signs plus contralateral body findings?
Brainstem/posterior circulation.
G. Is there acute severe ataxia, vertigo, vomiting, or inability to stand?
Cerebellar/posterior circulation.

Exam-style summary format

“The patient has a left hemispheric cortical syndrome, with right lower facial weakness, right arm-predominant hemiparesis, right hemisensory loss, expressive aphasia, and right homonymous hemianopia. This localises to the left MCA territory.”
Or:
“The patient has a posterior-circulation syndrome with left facial weakness and impaired palatal movement, right-sided body weakness, dysarthria, and ataxia. The crossed signs localise to the left brainstem.”
Do not use clinical localisation to decide whether a stroke is ischemic or hemorrhagic. Both can produce similar focal syndromes, so urgent neuroimaging is required.

Make me understand more . Bcz I can't memorize the symptoms . Give me the reasoning.

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Don’t memorize a list of symptoms. Build the symptoms from a map.

The core idea

A stroke causes symptoms because an artery stops supplying a particular piece of brain.
So ask:
What brain function is lost, where is that function located, and which artery supplies that location?
There are four major maps to understand:
  1. Each hemisphere controls the opposite side of the body
  2. The motor/sensory body map has leg on the inner surface, face and arm on the outer surface
  3. The left hemisphere is usually language dominant
  4. The back of the brain is mainly vision and balance/coordination
Once those make sense, ACA, MCA, PCA, brainstem, and cerebellar syndromes become logical.

1. Why are stroke deficits on the opposite side?

Motor commands begin in the cerebral cortex and descend in the corticospinal tract.
Most fibers cross in the lower medulla, called the pyramidal decussation.
So:
  • Left cerebral hemisphere controls the right face, arm, and leg.
  • Right cerebral hemisphere controls the left face, arm, and leg.
Therefore:
Right hemiplegia usually means a left cerebral hemispheric stroke.
The same broadly applies to cortical sensation and vision: damage above the brainstem usually produces a contralateral deficit.

2. The homunculus: why MCA is face-arm and ACA is leg

Imagine the brain's motor strip as a person lying upside down along the edge of the cortex:
Inner (medial) surface                 Outer (lateral) surface

        LEG / FOOT  |  TRUNK  |  ARM / HAND / FACE
Now place the arteries on this brain surface:
          ACA
   supplies the INNER surface
      ↓
      LEG and FOOT area


          MCA
   supplies the OUTER surface
      ↓
      FACE, ARM and HAND area
This is the main reason for the patterns.
  • ACA infarct damages the medial leg area.
    • Therefore: opposite leg weakness and sensory loss more than arm
  • MCA infarct damages the lateral face-arm area.
    • Therefore: opposite face and arm weakness/sensory loss more than leg
This relationship is supported by the clinical anatomy: MCA occlusions characteristically affect the contralateral face and arm more than the leg, whereas ACA infarction produces leg-predominant deficits. Cortical homunculus explanation

Easy memory image

Think of the brain as two vertical walls facing one another.
  • The legs are on the inside, near the midline, so ACA supplies them.
  • The face and arms are on the outside, so MCA supplies them.
ACA = Along the midline = leg
MCA = Most of the side surface = face and arm

3. Why do MCA strokes cause aphasia or neglect?

The MCA supplies not only the motor strip. It also supplies much of the lateral frontal, parietal, and temporal cortex.
Those regions handle higher cortical functions.

Left MCA: language

For most people, especially right-handed people, the left hemisphere is dominant for language.
So a left MCA stroke can damage:
  • Frontal language output area: speech becomes nonfluent or effortful
  • Temporal language comprehension area: speech may be fluent but meaningless, with poor comprehension
  • Larger lesion: both affected, causing global aphasia
Thus:
Right weakness + aphasia = left MCA until proven otherwise.
Aphasia is a language problem, not merely slurred speech. The patient may be unable to name, understand, repeat, read, or write properly.

Right MCA: neglect

The right parietal cortex is especially important for awareness of space, particularly the left side.
So a right MCA stroke may cause:
  • Left-sided neglect
  • Failure to attend to the left side of body or room
  • Extinction on double simultaneous stimulation
  • Sometimes denial of deficit
Thus:
Left weakness + left neglect = right MCA.
A useful contrast:
ProblemWhat it means
AphasiaLanguage network damaged, usually left MCA
NeglectAttention-to-space network damaged, usually right MCA
DysarthriaSpeech muscles are weak/incoordinated, can occur in many locations

4. Why does MCA stroke cause visual-field loss?

The visual pathway from each eye does not stay entirely on its own side. After the optic chiasm, information from the left visual field of both eyes travels to the right occipital cortex, and vice versa.
Therefore:
  • Left occipital or posterior temporal/parietal lesion → right homonymous hemianopia
  • Right occipital or posterior temporal/parietal lesion → left homonymous hemianopia
“Homonymous” means the same half of vision is gone from both eyes.
MCA can affect optic radiations passing through the temporal/parietal lobes. A large MCA stroke may therefore cause a contralateral homonymous hemianopia.

5. PCA stroke: why is it mainly visual?

The posterior cerebral artery (PCA) supplies the occipital lobe, where primary visual cortex lies.
So:
PCA = posterior = picture/vision
A PCA infarct commonly produces:
  • Contralateral homonymous hemianopia
  • Often relatively preserved limb strength
  • Possible visual hallucinations or impaired visual recognition
Example:
Sudden inability to see objects on the right side, with normal power and speech
left PCA/left occipital stroke
If the left PCA damages both the left occipital visual cortex and the splenium of the corpus callosum, the patient may write but cannot read, called alexia without agraphia. The reasoning is that visual information cannot reach the dominant language network.

6. Why does ACA stroke cause apathy and incontinence?

ACA supplies the medial frontal lobe.
This region is involved in:
  • Initiation and motivation
  • Voluntary movement, especially of the leg
  • Frontal control of bladder function
Therefore an ACA stroke can give:
Medial frontal cortex damaged
        ↓
Leg area damaged      Frontal initiation impaired     Bladder control impaired
        ↓                     ↓                         ↓
Leg weakness       Abulia/apathy, reduced speech     Urinary incontinence
So remember:
ACA = leg + lack of initiation + loss of bladder control
Not every ACA stroke produces all three, but the pattern is coherent.

7. Why does a lacunar stroke have weakness but no aphasia or neglect?

A lacunar stroke affects a small deep penetrating artery, commonly supplying:
  • Internal capsule
  • Thalamus
  • Pons
  • Corona radiata
Think of the internal capsule as a crowded cable bundle. Motor fibers from the cortex pass very tightly together through it.
A tiny lesion there can interrupt many motor fibers at once:
Cortex
  ↓
Motor fibers converge tightly
  ↓
Internal capsule = small lesion can hit all fibers
  ↓
Contralateral face + arm + leg weakness
But the cortex itself is intact. Therefore there are usually no cortical signs:
  • No aphasia
  • No neglect
  • No gaze deviation
  • No clear visual-field defect
  • No seizure at onset due to cortical irritation
Thus:
Pure motor hemiparesis, with no aphasia/neglect/field defect, suggests a lacunar internal-capsule or pontine stroke.
A common clinical pattern is left face, arm, and leg weakness with dysarthria but no language or visual problem. That points to a right lacunar stroke rather than a large right MCA cortical stroke.

8. Brainstem: why are signs “crossed”?

The brainstem contains two different things close together:
  1. Cranial nerve nuclei/fibers, which usually supply the same side of the face
  2. Long motor and sensory tracts, which affect the opposite side of the body at many brainstem levels
Therefore a brainstem lesion can produce:
Lesion on LEFT side of brainstem

Left cranial nerve signs     +      Right body signs
(face, eye, palate, tongue)         (arm/leg weakness or sensory loss)
That is the famous crossed finding.
Example:
Left facial weakness or left palate weakness + right arm and leg weakness
left brainstem stroke
This is a high-yield rule:
Face and body affected on opposite sides = brainstem.
Brainstem strokes may also cause diplopia, dysphagia, dysarthria, nystagmus, hearing symptoms, altered consciousness, or bilateral weakness because important eye-movement, swallowing, arousal, and motor pathways run through this small area.

9. Cerebellum: why is there ataxia on the same side?

The cerebellum coordinates movement. Its pathways effectively cross twice before influencing the body, so the final clinical effect is usually ipsilateral.
Thus:
  • Left cerebellar lesion → left limb dysmetria and left-sided falling
  • Right cerebellar lesion → right limb dysmetria and right-sided falling
Cerebellar stroke is not mainly weakness. It is mainly a coordination and balance problem:
  • Sudden severe vertigo
  • Vomiting
  • Nystagmus
  • Dysarthria
  • Limb dysmetria
  • Severe gait/truncal ataxia
  • Falling toward the lesion
Severe sudden inability to sit or walk, even with normal strength, is a posterior-circulation red flag.

The reasoning algorithm at the bedside

When you see a stroke, do not start by trying to recall every named syndrome. Ask these questions.

Question 1: Is there a cortical sign?

Look for:
  • Aphasia
  • Neglect
  • Gaze deviation
  • Homonymous hemianopia
  • Seizure at onset
  • Cortical sensory loss
Yes → likely a cortical hemispheric stroke, often MCA, ACA, or PCA.
No → consider lacunar stroke, brainstem stroke, or cerebellar stroke.

Question 2: Which side of the body is weak?

  • Right body signs → left cerebral hemisphere
  • Left body signs → right cerebral hemisphere

Question 3: Which body part is worst?

  • Face and arm > leg → MCA
  • Leg > arm/face → ACA
  • No clear motor deficit but field defect → PCA
  • Face, arm, leg equally affected, no cortical signs → lacunar/internal capsule

Question 4: Is there a cranial nerve sign on one side and body weakness on the other?

  • Yes → brainstem.

Question 5: Is the major problem balance/coordination rather than power?

  • Yes → cerebellum or posterior circulation.

Build the diagnosis from examples

Example 1

Right facial droop, right arm weakness greater than right leg weakness, cannot name objects, understands poorly.
Reasoning:
  • Right body signs → left hemisphere
  • Face-arm > leg → MCA
  • Aphasia → dominant hemisphere, usually left
Answer: left MCA stroke.

Example 2

Left leg is weak and numb, arm and face are nearly normal. Patient is slow, apathetic, and incontinent.
Reasoning:
  • Left side deficit → right hemisphere
  • Leg > arm → ACA
  • Apathy and incontinence → medial frontal lobe, also ACA territory
Answer: right ACA stroke.

Example 3

Sudden right visual-field loss. Strength, sensation, language, and coordination are normal.
Reasoning:
  • Right visual field is represented in left occipital cortex
  • Occipital cortex is supplied mainly by PCA
Answer: left PCA stroke.

Example 4

Left facial weakness and diplopia with right arm and leg weakness.
Reasoning:
  • Face on left, body on right = crossed signs
  • Crossed signs = brainstem
  • Cranial nerve features support posterior circulation
Answer: left brainstem stroke.

Example 5

Left face, arm, and leg weakness with dysarthria. No aphasia, neglect, gaze palsy, or field defect.
Reasoning:
  • No cortical signs
  • Dense motor deficit can arise where motor fibers are packed together
  • Internal capsule or pons are likely sites
Answer: right lacunar stroke, often internal capsule.

The shortest memory framework

MCA = Mouth, Manual work, Meaning
      Face-arm weakness + aphasia/neglect

ACA = Ankles and Apathy
      Leg weakness + abulia/incontinence

PCA = Pictures
      Visual-field loss

Lacune = Little deep lesion, no cortical signs
      Pure motor or pure sensory syndrome

Brainstem = Crossed face-body signs

Cerebellum = Coordination, same-side ataxia
A final caution: this is clinical localisation, not definitive proof of stroke type. Ischemic stroke and hemorrhage can both cause these focal patterns, and urgent CT/CTA, with MRI when needed, is required for confirmation.

How to check gaze deviation

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NIH Stroke Scale best gaze testing forced deviation stroke official instructions

How to check gaze deviation in a stroke patient

Gaze deviation means both eyes are persistently turned to one side at rest, and the patient cannot easily look to the other side.

Step 1: Observe at rest

Stand at the end of the bed before asking the patient to do anything.
Look for:
  • Are both eyes looking in the same horizontal direction?
  • Is the head also turned that way?
  • Does the patient spontaneously look toward you when you speak from either side?
For example: if both eyes and the head are persistently turned to the left, record:
“There is conjugate left gaze deviation.”
Conjugate means both eyes move together in the same direction.

Step 2: Test voluntary horizontal gaze

Ask:
“Keep your head still and follow my finger with your eyes.”
Hold your finger about 30 to 50 cm from the patient and move it slowly:
  1. To the right
  2. Back to midline
  3. To the left
  4. Back to midline
Test horizontal movements first, because this is what the NIH Stroke Scale uses for “best gaze.”
Look for:
  • Can both eyes move fully to both sides?
  • Is movement reduced to one side?
  • Does one eye fail to abduct or adduct?
  • Can the eyes return to the midline?
  • Is there double vision or nystagmus?

Step 3: Distinguish partial gaze palsy from forced deviation

Normal gaze

  • Both eyes move fully right and left.
  • No sustained deviation at rest.

Partial gaze palsy

  • Eyes can look toward the affected side, but movement in the other direction is limited.
  • Or the patient has a mild resting deviation but can overcome it when asked.
Example:
The patient’s eyes rest slightly leftward but can voluntarily look right.
This is a partial gaze palsy.

Forced gaze deviation

  • Both eyes are held toward one side.
  • The patient cannot voluntarily bring them to the midline or move them to the opposite side.
  • Usually associated with a large hemispheric stroke.
Example:
Both eyes are forced to the left and cannot look right.
This is forced left gaze deviation.
The NIHSS categorises gaze as normal, partial gaze palsy, or forced deviation/total gaze paresis. The official NIH Stroke Scale instructions specify that only horizontal eye movements are tested for this item.

How to localise it

Cortical hemispheric stroke: eyes look toward the lesion

The frontal eye field normally drives the eyes to the opposite side.
Left frontal eye field pushes eyes to the RIGHT
Right frontal eye field pushes eyes to the LEFT
If the left frontal eye field is damaged by a left MCA stroke, it can no longer push the eyes right. The intact right frontal eye field pushes unopposed to the left.
Therefore:
Left MCA/frontal eye field stroke
        ↓
Eyes deviate LEFT, toward the lesion
        ↓
Body weakness is RIGHT, opposite the lesion

High-yield rule

In an acute hemispheric stroke, eyes look toward the lesion and away from the weak side.
Examples:
FindingsLocalisation
Eyes deviate left + right hemiparesisLeft hemispheric, often left MCA stroke
Eyes deviate right + left hemiparesisRight hemispheric, often right MCA stroke
Acute hemispheric lesions may cause a transient gaze deviation toward the lesion because of impaired gaze toward the hemiplegic side. Bradley and Daroff's Neurology in Clinical Practice, “Cortex.”

Seizure: eyes often look away from the seizure focus

This is the opposite pattern.
A seizure activates the frontal eye field rather than destroying it:
Left frontal seizure
        ↓
Excess activation pushes eyes RIGHT
So:
Stroke: eyes look toward the lesion.
Seizure: eyes often look away from the focus.
This is a clue only. It is not definitive, especially after a seizure or in prolonged focal seizures.

What about brainstem gaze palsy?

A pontine lesion can prevent gaze toward the side of the lesion.
Example:
Left pontine gaze center lesion
        ↓
Cannot look LEFT
        ↓
Eyes may rest deviated RIGHT
So the patient may have:
  • Inability to look left
  • Eyes deviated right, which is away from a left pontine lesion
  • Often other brainstem signs: diplopia, facial weakness, dysarthria, dysphagia, or crossed motor/sensory deficits
This is why you should not use gaze deviation alone. Combine it with limb weakness and cranial nerve examination.

If the patient cannot cooperate

For a reduced-consciousness patient, trained clinicians may assess reflex eye movements using the oculocephalic maneuver:
  1. Hold the eyelids open.
  2. Gently rotate the head horizontally.
  3. In an intact brainstem, the eyes move in the direction opposite to head rotation, like doll’s eyes.
Do not perform this if cervical-spine injury is possible or the neck has not been cleared.
In NIHSS assessment, a forced deviation that cannot be overcome by voluntary or reflexive movement is scored more severely than a partial gaze palsy.

How to document it

Use one of these:
  • “Extraocular movements are full. No gaze deviation.”
  • “There is a partial left gaze palsy. The patient has reduced ability to look left but can cross the midline.”
  • “There is conjugate forced left gaze deviation. The patient cannot voluntarily move the eyes to the right.”
  • “Left gaze deviation with right hemiparesis suggests a left hemispheric, likely left MCA, stroke.”

One-line memory aid

Cortex stroke: eyes look at the lesion.
Weak body: opposite the lesion.
Pons lesion: eyes may look away from the lesion.
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