Stroke (Cerebrovascular Accident - CVA): An Extensive Overview

A Stroke, or Cerebrovascular Accident (CVA), is a medical emergency that occurs when the
blood supply to part of the brain is interrupted or severely reduced, depriving brain tissue of
oxygen and nutrients. Within minutes, brain cells begin to die. This explains the urgency of
immediate medical attention. "Time is brain" is a widely recognized mantra in stroke care.

1. Definition and Epidemiology

 Definition: A stroke is an acute neurological deficit of vascular origin, affecting specific

brain regions, leading to a sudden loss of brain function due to either ischemia (lack of
blood flow) or hemorrhage (bleeding).
 Epidemiology: Strokes are a leading cause of long-term disability worldwide, and a
significant cause of death. Incidence and prevalence vary by region and demographic,
often increasing with age.

2. Types of Stroke

Strokes are broadly categorized into two main types: Ischemic and Hemorrhagic.

A. Ischemic Stroke (Approx. 87% of all strokes) Occurs when a blood clot blocks or narrows
an artery leading to the brain, cutting off blood flow.

 i. Thrombotic Stroke:
o Mechanism: A blood clot (thrombus) forms in an artery that supplies blood to the
brain, often due to atherosclerosis (hardening and narrowing of arteries). This
process can take hours or days to form, or occur acutely.
o Characteristics: Often occurs in the setting of existing cerebrovascular disease.
Symptoms may fluctuate initially.
 ii. Embolic Stroke:
o Mechanism: A blood clot (embolus) or other debris forms elsewhere in the body
(most commonly the heart, e.g., due to atrial fibrillation, or carotid arteries) and
travels through the bloodstream to the brain, where it lodges in a narrower artery.
o Characteristics: Usually sudden onset, often occurring during activity.
 iii. Lacunar Stroke:
o Mechanism: Occurs when blood flow is blocked to a small vessel in the deep
brain structures (e.g., basal ganglia, thalamus, brainstem). Often associated with
hypertension and diabetes.
o Characteristics: May produce pure motor, pure sensory, ataxic hemiparesis, or
dysarthria-clumsy hand syndrome. Patients often have a good prognosis due to the
small area of brain affected.
 iv. Watershed (Border Zone) Stroke:
o Mechanism: Occurs in areas between the territories of two major cerebral
arteries, which are particularly vulnerable to reductions in global cerebral blood
flow (e.g., due to severe hypotension or cardiac arrest). These areas receive dual
blood supply but are the last to receive blood when pressure drops.
 o Characteristics: Often bilateral, affecting the "distal reaches" of arterial
territories. Can present with symptoms like "man-in-the-barrel" syndrome
(proximal weakness greater than distal).
 v. Cryptogenic Stroke: When the cause of an ischemic stroke cannot be determined.

B. Hemorrhagic Stroke (Approx. 13% of all strokes) Occurs when a blood vessel in the brain
ruptures or leaks, causing bleeding into or around the brain tissue. The blood accumulates,
forming a hematoma that compresses brain tissue and increases intracranial pressure (ICP).

 i. Intracerebral Hemorrhage (ICH):

o Mechanism: Bleeding occurs within the brain tissue, often due to uncontrolled
hypertension, arteriovenous malformations (AVMs), or amyloid angiopathy (in
older adults).
o Characteristics: Often sudden, severe headache, nausea/vomiting, rapid decline
in consciousness.
 ii. Subarachnoid Hemorrhage (SAH):
o Mechanism: Bleeding occurs in the subarachnoid space (the space between the
brain and the meninges), often due to a ruptured aneurysm or AVM.
o Characteristics: "Worst headache of my life" (thunderclap headache), stiff neck,
photosensitivity, loss of consciousness. This is less common but very severe.

C. Transient Ischemic Attack (TIA)

 Often called a "mini-stroke."

 Mechanism: A temporary blockage of blood flow to the brain, causing stroke-like
symptoms that resolve completely within minutes to 24 hours (most often within 1 hour).
 Significance: A strong warning sign of an impending full stroke. Up to 15% of people
who have a TIA will have a stroke within 3 months. Requires urgent investigation and
risk factor management.

3. Pathophysiology

 Ischemic Stroke:
o Core Ischemia: Area where blood flow is critically low, leading to rapid
neuronal death.
o Ischemic Penumbra: Area surrounding the core, with reduced but not absent
blood flow. Neurons in this region are dysfunctional but still viable for several
hours. This is the target for acute medical interventions (e.g., thrombolysis) to
salvage brain tissue.
o Ischemic Cascade: Complex series of biochemical events (e.g., excitotoxicity
from glutamate release, inflammation, oxidative stress, blood-brain barrier
disruption) that occur after ischemia, leading to further neuronal damage.
 Hemorrhagic Stroke:
o Hematoma Formation: The bleeding forms a clot (hematoma) that occupies
space, compressing adjacent brain tissue, leading to focal neurological deficits.
 o Increased Intracranial Pressure (ICP): The mass effect of the hematoma and
associated edema increases pressure within the rigid skull, reducing cerebral
perfusion pressure and potentially leading to herniation (life-threatening brain
displacement).
o Blood Toxicity: Blood itself can be toxic to brain tissue.

4. Risk Factors

A. Modifiable Risk Factors (Can be changed/managed):

 Hypertension (High Blood Pressure): The single most important modifiable risk factor.
 Atrial Fibrillation (Afib): Major source of cardiac emboli.
 Diabetes Mellitus: Damages blood vessels.
 High Cholesterol (Dyslipidemia): Contributes to atherosclerosis.
 Smoking (Cigarette, Vaping): Damages blood vessels, increases clot formation.
 Obesity: Increases risk of hypertension, diabetes, heart disease.
 Physical Inactivity: Contributes to obesity, hypertension.
 Poor Diet: High in saturated fats, sodium, sugar.
 Excessive Alcohol Consumption.
 Illicit Drug Use (e.g., cocaine, amphetamines).
 Obstructive Sleep Apnea.
 Certain Heart Conditions (e.g., congestive heart failure, valvular disease).

B. Non-Modifiable Risk Factors (Cannot be changed):

 Age: Risk increases significantly with age.

 Gender: Slightly higher risk for men at younger ages, but higher for women at older
ages.
 Race/Ethnicity: Higher risk in certain populations (e.g., African Americans, some
Hispanic groups).
 Family History of Stroke/TIA.
 Prior Stroke/TIA: Significantly increases risk of future events.

5. Signs and Symptoms (Clinical Presentation)

Stroke symptoms appear suddenly and depend on the location and extent of brain damage. A
common mnemonic for recognizing stroke is F.A.S.T.:

 Face drooping: Does one side of the face droop or is it numb? Ask the person to smile.
 Arm weakness: Is one arm weak or numb? Ask the person to raise both arms. Does one
arm drift downward?
 Speech difficulty: Is speech slurred, or is the person unable to speak or hard to
understand? Ask the person to repeat a simple sentence.
 Time to call emergency services: If anyone shows these symptoms, even if the symptoms
go away, call immediately.
Specific Clinical Syndromes (depending on artery affected):

 Middle Cerebral Artery (MCA) Syndrome (Most common): Contralateral

hemiparesis (face and arm > leg), contralateral hemisensory loss, homonymous
hemianopsia (loss of vision in the same half of both visual fields).
o Dominant Hemisphere (usually left): Aphasia (Broca's - expressive, Wernicke's
- receptive, or global).
o Non-dominant Hemisphere (usually right): Neglect (spatial, body schema),
anosognosia (unawareness of deficits), visual-spatial deficits, apraxia (motor
planning deficits).
 Anterior Cerebral Artery (ACA) Syndrome: Contralateral hemiparesis (leg > arm),
contralateral hemisensory loss (leg > arm), urinary incontinence, abulia (lack of
motivation), primitive reflexes.
 Posterior Cerebral Artery (PCA) Syndrome:
o Occipital Lobe: Contralateral homonymous hemianopsia, cortical blindness.
o Thalamic/Deep Structures: Contralateral sensory loss, thalamic pain syndrome.
o Brainstem Syndromes: Ipsilateral cranial nerve deficits, contralateral
motor/sensory deficits ("crossed signs"), vertigo, nystagmus, dysphagia,
dysarthria, altered consciousness. (e.g., Wallenberg's Syndrome from PICA
involvement).
 Cerebellar Stroke: Ataxia (truncal or appendicular), dysarthria, nystagmus, vertigo,
headache, nausea/vomiting.

Common Impairments Post-Stroke:

 Motor: Hemiparesis/hemiplegia (weakness/paralysis), spasticity, abnormal synergies,

loss of selective motor control, abnormal muscle tone (flaccidity initially), ataxia,
apraxia.
 Sensory: Hemianesthesia, impaired proprioception, impaired discriminative sensation,
central post-stroke pain.
 Balance & Coordination: Postural instability, impaired equilibrium reactions, increased
fall risk.
 Gait: Hemiplegic gait pattern, decreased speed, asymmetry, increased energy cost.
 Cognitive: Memory deficits, attention deficits, executive dysfunction, unilateral spatial
neglect.
 Perceptual: Visuospatial deficits, anosognosia, apraxia, agnosia (inability to recognize
objects/people).
 Communication: Aphasia (expressive, receptive, global), dysarthria (slurred speech),
dysphonia (voice changes).
 Swallowing (Dysphagia): Risk of aspiration.
 Bladder and Bowel Dysfunction.
 Emotional/Psychological: Depression, anxiety, lability, apathy.
 Visual Deficits: Homonymous hemianopsia, diplopia, visual field cuts.

6. Diagnosis
  Clinical Presentation: Initial assessment by medical professionals using FAST and
neurological examination.
 Imaging:
o CT Scan (Computed Tomography): Primary initial imaging. Rapidly
differentiates between ischemic and hemorrhagic stroke (blood is immediately
visible on CT). Less sensitive for acute ischemic changes in the first few hours.
o MRI (Magnetic Resonance Imaging): More sensitive for detecting acute
ischemic stroke (especially diffusion-weighted imaging - DWI), and better for
identifying smaller lesions or posterior fossa strokes.
o CT Angiography (CTA) / MR Angiography (MRA): Visualize cerebral blood
vessels to identify blockages or aneurysms.
o Cerebral Angiography: Invasive but provides detailed images of blood vessels.
 Lab Tests: Blood glucose, electrolytes, complete blood count, coagulation studies (INR,
PTT).
 Cardiac Evaluation: ECG, echocardiogram (to identify cardiac sources of emboli).

7. Acute Medical Management (Brief Overview)

 Ischemic Stroke:
o Thrombolysis (IV tPA - tissue plasminogen activator): "Clot-busting" drug
administered intravenously within a narrow time window (typically 3-4.5 hours
from symptom onset) to dissolve the clot.
o Mechanical Thrombectomy: Endovascular procedure to physically remove large
clots, typically within 6-24 hours for selected patients with large vessel
occlusions.
o Antiplatelets (e.g., aspirin) / Anticoagulants (e.g., heparin): Prevent further
clot formation.
o Blood Pressure Management: Careful management to optimize cerebral
perfusion.
 Hemorrhagic Stroke:
o Blood Pressure Control: Aggressive management to prevent re-bleeding.
o ICP Management: Medications (e.g., mannitol), ventricular drainage, sometimes
decompressive craniectomy.
o Surgical Intervention: For large hematomas, aneurysm clipping/coiling, AVM
resection.
 General Medical Management: Airway protection, oxygenation, hydration, temperature
control, blood glucose control, seizure management, DVT prophylaxis.

8. Prognosis and Recovery Principles

 Spontaneous Recovery: Some recovery of function occurs naturally, primarily in the

acute phase (first few weeks to months) due to resolution of cerebral edema, absorption
of blood, and some degree of neuronal "stunning" wearing off in the penumbra.
 Neuroplasticity: The brain's remarkable ability to reorganize itself by forming new
neural connections throughout life. This is the biological basis for rehabilitation.
Rehabilitation aims to harness and optimize neuroplasticity.
 o Principles of experience-dependent plasticity: Use it or lose it, Use it and improve
it, Specificity, Repetition matters, Intensity matters, Time matters, Salience
matters, Age matters, Transference, Interference.
 Learned Non-Use: Phenomenon where an individual neglects to use an impaired limb
even if some movement capacity exists, due to repeated failure or compensation with the
stronger limb. Addressed by therapies like Constraint-Induced Movement Therapy
(CIMT).

9. Physiotherapy Management: Comprehensive Rehabilitation

Physiotherapy is crucial in maximizing functional recovery, preventing complications, and

improving quality of life for stroke survivors. It's an ongoing process starting acutely and
continuing into chronic phases.

A. Initial Assessment (Acute & Sub-Acute Phases):

 Subjective History: Onset, type of stroke, medical history, medications, previous

functional status, goals.
 Objective Examination:
o Neurological Screen: Cranial nerves, reflexes, sensation (light touch,
proprioception, pain, temperature, stereognosis), coordination (finger-nose, heel-
shin), muscle tone (Modified Ashworth Scale).
o Motor Function:
 Strength: MMT (manual muscle testing) for selective movements, or
observation for synergistic patterns.
 Voluntary Movement Control: Fugl-Meyer Assessment (FMA) for
motor recovery stage.
 Synergies: Identification of flexor/extensor synergies.
o Balance: Static (sitting, standing) and dynamic (reaching, stepping). Outcome
measures like Berg Balance Scale, Mini-BESTest, Tinetti Performance Oriented
Mobility Assessment (POMA).
o Gait: Observational gait analysis (symmetry, cadence, step length, clearance),
specific tests (10-meter walk test, 6-minute walk test, TUG).
o Functional Mobility: Bed mobility, transfers (sit-to-stand, commode),
wheelchair skills. Functional Independence Measure (FIM) or Modified Barthel
Index (MBI).
o Posture and Alignment: In sitting and standing.
o Cognitive/Perceptual Screen: For safety and ability to follow commands (e.g.,
MOCA, neglect screen).
o Cardiopulmonary Status: Vital signs, endurance.
o Integumentary Integrity: Skin checks, especially over bony prominences.
o Pain Assessment: Including central post-stroke pain, shoulder pain.
o Environmental Assessment: Home assessment for discharge planning.

B. Impairment-Based Interventions: The focus is on restoring normal movement patterns and

functional abilities by addressing underlying impairments and promoting neuroplasticity.
 i. Motor Control and Strength Training:
o Task-Specific Training: Highly emphasized. Practicing real-life tasks (e.g.,
reaching for a cup, stepping over obstacles) with high repetition and intensity.
o Strengthening Exercises: Progressive resistive exercises for weak muscles, often
incorporated into functional tasks.
o Constraint-Induced Movement Therapy (CIMT): For patients with mild to
moderate upper limb paresis; involves restraining the less affected limb to force
use of the more affected limb.
o Functional Electrical Stimulation (FES): Application of electrical currents to
paretic muscles to facilitate movement (e.g., for foot drop, grasping).
o Body-Weight Supported Treadmill Training (BWSTT): To facilitate stepping
and normalize gait patterns.
o Robotics: For high-intensity, repetitive training of upper and lower limbs.
o Biofeedback: To help patients gain awareness and control of muscle activity.
o Neuromuscular Facilitation Techniques (e.g., PNF - Proprioceptive
Neuromuscular Facilitation): To improve movement quality and motor control
by stimulating proprioceptors.
o Neurodevelopmental Treatment (NDT/Bobath Concept): While traditionally
focused on inhibiting abnormal tone and facilitating normal movement, modern
NDT incorporates task-specific, goal-oriented training grounded in motor learning
principles.
 ii. Spasticity Management:
o Stretching: Prolonged, low-load stretching to maintain range of motion and
reduce contracture risk.
o Positioning: Proper bed and seating positioning.
o Modalities: Cold packs, heat (caution), therapeutic massage.
o Serial Casting/Splinting: To maintain joint range and reduce spasticity.
o Therapeutic Exercise: Active movement through full range to reduce tone.
o Addressing Triggers: Avoiding noxious stimuli, managing pain.
o Collaboration: With physicians for pharmacological (e.g., Botox, oral anti-
spasticity meds) or surgical interventions (e.g., baclofen pump, selective dorsal
rhizotomy).
 iii. Balance and Coordination Training:
o Static Balance: Progressing from stable to unstable surfaces, eyes open/closed.
o Dynamic Balance: Weight shifting, reaching, trunk rotation, stepping strategies.
o Perturbation Training: Practicing reactions to unexpected pushes or pulls.
o Dual-Task Training: Performing motor and cognitive tasks simultaneously to
mimic real-life challenges.
o Vestibular Rehabilitation: If vestibular deficits are identified.
 iv. Gait Training:
o Pre-gait Activities: Bridging, quadruped, kneeling, sit-to-stand.
o Overground Walking: Progression of distance, speed, varying surfaces.
o Orthotics: Ankle-Foot Orthoses (AFOs) for foot drop, knee-ankle-foot orthoses
(KAFOs) for more extensive weakness.
o Assistive Devices: Canes, walkers, crutches – appropriate selection and training
for safe use.
 o Treadmill Training: With or without body-weight support.
 v. Sensory Re-education:
o Sensory discrimination exercises (texture, temperature, localization).
o Mirror therapy (for neglect or motor recovery).
 vi. Managing Secondary Complications:
o Pressure Injury Prevention: Regular repositioning, pressure-relieving devices,
skin inspection.
o Deep Vein Thrombosis (DVT) Prevention: Early mobilization, ankle pumps,
compression stockings.
o Contracture Prevention: Range of motion exercises, stretching, proper
positioning.
o Shoulder Pain/Subluxation Management: Proper handling, slings (judiciously),
strengthening, education.
o Dysphagia: Referral to Speech and Language Pathologist (SLP) for swallowing
assessment and intervention, positioning for feeding.
o Respiratory Management: Deep breathing exercises, coughing techniques.

C. Functional Training:

 Activities of Daily Living (ADLs): Training for dressing, bathing, grooming, feeding.
 Instrumental ADLs (IADLs): Cooking, cleaning, managing finances, driving (referral
for assessment).
 Transfers: Bed to chair, chair to commode, car transfers.
 Wheelchair Mobility: If required, proper fitting, propulsion, and safety training.

D. Discharge Planning and Community Reintegration:

 Home Exercise Program (HEP): Tailored to individual needs and goals, progressing
over time.
 Equipment Prescription: Assistive devices, home modifications (ramps, grab bars).
 Patient and Family Education: On stroke recovery, safe transfers, managing
impairments, fall prevention, risk factor modification.
 Referrals: To other healthcare professionals (OT, SLP, dietitian, social worker,
neuropsychologist), community support groups, outpatient rehabilitation.
 Long-term Follow-up: Ensuring continued support and addressing evolving needs.

10. Common Physiotherapy-Relevant Complications Post-Stroke

 Shoulder Pain and Subluxation: Very common, due to flaccidity, poor handling, or
spasticity. Requires careful management to prevent adhesive capsulitis.
 Foot Drop: Weakness of ankle dorsiflexors leading to difficulty clearing the foot during
swing phase; managed with AFOs or FES.
 Pusher Syndrome: Patients actively push away from the unaffected side, disrupting
balance and increasing fall risk. Requires specific retraining strategies.
 Central Post-Stroke Pain (CPSP): Chronic neuropathic pain that results from damage
to the central nervous system. Challenging to treat.
  Fatigue: A debilitating and common symptom that can significantly impact participation
in rehabilitation and daily activities.
 Depression and Anxiety: Common psychological sequelae that can affect motivation
and recovery.
 Deep Vein Thrombosis (DVT) / Pulmonary Embolism (PE): Risk due to immobility.
 Pressure Injuries: Due to prolonged immobility and sensory loss.
 Heterotopic Ossification: Abnormal bone formation in soft tissues around joints (rare
but severe).

This extensive overview provides a strong foundation for understanding stroke from a
physiotherapy perspective, covering its medical aspects, the resulting impairments, and the core
strategies for rehabilitation. Remember to integrate your knowledge of neuroanatomy and
neurophysiology to understand why specific deficits occur and how interventions promote
recovery.

vMiddle Cerebral Artery (MCA) Syndrome - The Most Common Blockage

Imagine the MCA is like the main highway supplying power to a large chunk of the city
responsible for movement, sensation, and speech (for most people, the left side) or spatial
awareness (usually the right side).

 Contralateral hemiparesis (face and arm > leg): This means weakness or paralysis on the
opposite side of the body from where the stroke happened. The face and arm are
usually more affected than the leg because the MCA supplies the part of the brain
controlling those areas more directly. Think of it like the blockage hitting the "arm and
face" part of the highway harder.

 Contralateral hemisensory loss: Loss of sensation (like touch, pain, temperature) on the
same side of the weakness. The same highway also carries information about how things
feel on that side.

 Homonymous hemianopsia: Loss of vision in the same half of the visual field in both
eyes. Imagine if the left side of the brain is affected, you might only see things on your
right side. The MCA supplies part of the visual pathway.

 Dominant Hemisphere (usually left): Aphasia: This is trouble with language.

o Broca's (expressive): Difficulty getting words out, like you know what you want to
say but can't form the sentences properly. Think of it like the "speaking factory"
is damaged.
 o Wernicke's (receptive): Difficulty understanding language. People might speak
fluently, but what they say doesn't make sense, and they don't understand what
others are saying. Think of the "understanding factory" being offline.

o Global: A mix of both, where the person has significant difficulty both speaking
and understanding.

 Non-dominant Hemisphere (usually right): Neglect: This is like ignoring one side of the
world.

o Spatial: Might not be aware of things on their left side (if the right brain is
affected). They might not eat food on the left side of their plate or bump into
things on that side.

o Body schema: Not being aware of their left side of their body, maybe even
forgetting they have a left arm or leg.

o Anosognosia: Not being aware that they have any problems at all. They might
deny their arm is weak even when you show them.

o Visual-spatial deficits: Difficulty with tasks that involve judging distances,

understanding maps, or drawing.

o Apraxia: Difficulty with planning and carrying out movements, even though they
have the strength. For example, they might struggle to put on a shirt even though
their arm isn't paralyzed.

2. Anterior Cerebral Artery (ACA) Syndrome - The Leg Highway

Think of the ACA as the road that mainly supplies power to the part of the brain that controls
your legs and some aspects of personality and decision-making.

 Contralateral hemiparesis (leg > arm): Weakness or paralysis on the opposite side of the
body, but this time the leg is more affected than the arm.

 Contralateral hemisensory loss (leg > arm): Loss of sensation on the opposite side,
mainly affecting the leg.

 Urinary incontinence: Loss of bladder control. The ACA can affect the brain regions that
help regulate this.

 Abulia (lack of motivation): Difficulty initiating actions or speech. They might seem
apathetic or unmotivated.

 Primitive reflexes: Reappearance of reflexes that are normally present in babies but
disappear as the brain matures (like the grasp reflex).
3. Posterior Cerebral Artery (PCA) Syndrome - The Vision and Deep Thinking Road

The PCA mainly supplies the back of the brain, which is crucial for vision, and also deeper
structures involved in sensation and pain.

 Occipital Lobe: This is the vision center.

o Contralateral homonymous hemianopsia: Similar to MCA, loss of vision in the

same half of the visual field in both eyes, but often without the other MCA
symptoms.

o Cortical blindness: Complete loss of vision due to damage in the brain's visual
cortex, even though the eyes themselves might be fine. Sometimes people with
cortical blindness might not even realize they are blind (Anton's syndrome).

 Thalamic/Deep Structures: The thalamus is a relay center for sensory information.

o Contralateral sensory loss: Loss of sensation on the opposite side of the body.

o Thalamic pain syndrome: Severe, often chronic pain on the opposite side of the
body.

4. Brainstem Syndromes - The Central Control Hub

The brainstem is like the main control center connecting the brain to the spinal cord. It controls
many basic life functions and houses the cranial nerves (nerves that come directly from the
brain to control face, eyes, swallowing, etc.). Strokes here can be complex.

 Ipsilateral cranial nerve deficits: Problems with the cranial nerves on the same side as
the stroke (e.g., facial weakness on the left if the stroke is on the left brainstem).

 Contralateral motor/sensory deficits ("crossed signs"): Weakness or sensory loss on the

opposite side of the body from the stroke. This "crossing over" of nerve pathways
happens in the brainstem.

 Vertigo, nystagmus: Dizziness and involuntary eye movements due to involvement of

balance centers.

 Dysphagia, dysarthria: Difficulty swallowing and speaking due to cranial nerve

involvement.

 Altered consciousness: Changes in alertness or even coma if the stroke is severe.

 (e.g., Wallenberg's Syndrome from PICA involvement): A specific example where

blockage of the Posterior Inferior Cerebellar Artery (PICA) leads to a particular set of
symptoms including:
 o Ipsilateral (same side): Loss of pain and temperature sensation in the face,
hoarseness and difficulty swallowing (dysphagia), Horner's syndrome (droopy
eyelid, constricted pupil, decreased sweating).

o Contralateral (opposite side): Loss of pain and temperature sensation in the

body.

o Vertigo and ataxia (poor coordination).

5. Cerebellar Stroke - The Coordination Center

The cerebellum is like the brain's coordinator, responsible for balance and fine-tuned
movements.

 Ataxia: Lack of coordination.

o Truncal: Difficulty with balance while sitting or standing.

o Appendicular: Difficulty coordinating movements of the arms and legs (e.g.,

clumsy movements, difficulty with tasks like touching your nose).

 Dysarthria: Difficulty speaking clearly due to lack of coordination of speech muscles.

 Nystagmus: Involuntary, rapid eye movements.

 Vertigo: Sensation of spinning.

 Headache, nausea/vomiting: These can be common with cerebellar strokes.

Key Takeaways for Remembering:

 Contralateral: Generally, a stroke in one side of the brain will affect the opposite side of
the body for motor and sensory functions.

 Dominant vs. Non-dominant: For language, the left side is usually dominant. For spatial
awareness, the right side often is.

 Brainstem: Think of "crossed signs" - problems on one side of the face and the opposite
side of the body. Also, cranial nerve issues are a big clue for brainstem involvement.

 Cerebellum: Think "coordination" - problems with balance and smooth movements.