CVA/Stroke Physiotherapy: Week Three

• These notes cover physiotherapy for neurological conditions, specifically cerebrovascular accident (CVA) or stroke.
• These notes are from Week Three of lectures, dated 10-02-2025.

Hemiplegic Stroke

• Hemiplegic stroke refers to clinical presentation

Clinical Manifestations

• Motor impairments
• Sensory impairments
• Speech, language, and swallowing problems
• Cognitive impairments
• Altered emotional status
• Perceptual dysfunction
• Visual changes
• Bladder, bowel, and sexual dysfunctions are not typically a problem in most patients

Motor Symptoms

• Hemi-paralysis or paresis involves weakness or paralysis on one side of the body.
• 80-90% of CVA patients experience paresis, which significantly impairs motor function, limits activity, and causes disability.
• Patients often struggle to generate the force needed to initiate and control movement, which also affects muscle tone and gait.
• The degree of primary weakness depends on the brain injury's location and size. Weakness ranges from complete inability to contract muscles (hemiplegia) to partial weakness (hemiparesis).
• Distal muscles are generally more affected than proximal muscles due to greater corticospinal system facilitation.
• Anti-gravity muscles are weaker than pro-gravity muscles.
• In the upper extremity (UE), extensors are weaker than flexors, leading to spasticity in flexors and weakness in extensors.
• In the lower extremity (LE), flexors are weaker than extensors.

Pyramidal Tracts

• The pyramidal tracts consist of the corticospinal and corticonuclear tracts.
• The corticospinal tract (CST) carries movement-related information from the cerebral cortex to the spinal cord.
• The corticonuclear (corticobulbar) tract controls voluntary movement of facial muscles.
• Pyramidal tracts are part of the descending spinal tract system originating from the cortex or brainstem.
• The corticospinal tract is essential for voluntary skilled movements, such as precise movements of the fingers and toes.
• The corticospinal tract comprises two separate tracts within the spinal cord: the lateral and anterior corticospinal tracts.

The Corticospinal Tract (Details)

• This originates in several cortical areas, including the primary motor cortex (50%) and premotor areas.
• Axons travel via large fiber bundles called the cerebral peduncles into the brainstem.
• The tract continues into the medulla, forming two large collections of axons known as the pyramids.
• Approximately 90% of the corticospinal tract fibers decussate at the base of the pyramids, crossing to the opposite side of the brainstem in a bundle called the pyramidal decussation.
• These decussated fibers form the lateral corticospinal tract, which enters the spinal cord and controls movement on the body's contralateral side.
• The other 10% of fibers don't decussate and continue down the ipsilateral spinal cord as the anterior (or ventral) corticospinal tract.
• Most axons of the anterior corticospinal tract will decussate in the spinal cord just before synapsing with lower motor neurons, while the rest remain uncrossed.
• Lateral corticospinal tract primarily controls muscles in the limbs.
• Anterior corticospinal tract is involved with movement of the muscles of the trunk, neck, and shoulders.

Muscle Tone Disturbances

• Tone is defined as the resistance of muscle to passive elongation or stretch and represents a state of slight residual contraction in normally innervated, resting muscles.
• Tonal abnormalities are categorized as hypertonia (increased tone/spasticity) or hypotonia (decreased tone/flaccidity), which depend on speed.
• In stroke patients, flaccidity (hypotonicity) usually starts due to cerebral shock and lasts a few days/weeks.
• Tone gradually returns, progressing to spasticity (hypertonia) in 90% of patients.
• Spasticity affects antigravity muscles more than pro-gravity muscles.
• Spasticity may decline completely in some patients, promoting smooth, coordinated joint movement.

Pathophysiology of Spasticity

• Spasticity is a motor disorder characterized by a velocity-dependent increase in resistance during passive stretch.
• The underlying mechanism involves a hyperexcitable stretch reflex that is poorly understood.
• It arises from injury to descending motor pathways, producing disinhibition of spinal reflexes, resulting in hyperactive tonic stretch reflexes or failure of reciprocal inhibition.
• Spasticity results in hyperexcitability of muscle spindles (spasticity) and alpha motor neurons (hyperreflexia).
• In normal conditions, two systems work together to control muscle movement: -The Corticospinal Tract helps with voluntary muscle control -The Dorsoreticulospinal Tract helps relax muscles and control reflexes.
• In normal cases, both systems (Corticospinal Tract and Dorsoreticulospinal Tract are in dynamic balance, so the inhibition to the spinal cord is adjustable.
• After stroke, this balance is disrupted with the brain losing its ability to control relaxation (disinhibition). This leads to overactive muscles resulting in spasticity.

Pattern of Spasticity

• In the upper extremity
  • Scapular retractors
  • Shoulder adductors, depressors, and internal rotators
  • Elbow flexors
  • Forearm pronators
  • Wrist and finger flexors
• In the lower extremity
  • Pelvic retractors
  • Hip adductors and internal rotators
  • Knee extensors
  • Ankle plantarflexors and invertors
  • Toe flexors
• Spasticity in the neck and trunk may cause increased lateral flexion to the hemiplegic side.

Abnormal Reflexes

• A reflex is an involuntary, predictable, and specific response to a stimulus that depends on an intact reflex arc. Reflexes are altered and vary according to the stage of recovery.
• Initially after a stroke, hyporeflexia and flaccidity will occur. When spasticity emerges, hyperreflexia will be seen.
• Deep reflexes are lost during the stage of neural shock, followed by hyperreflexia.
• Superficial reflexes are lost, such as the abdominal reflex.
• Pathological reflexes include primitive and tonic reflexes, often present during infancy.

Pathological Primitive Reflexes:

• Grip reflex: Normally starts at birth and disappears by 3 months.
• Symmetric Tonic Neck Reflex (STNR):
  • Neck flexion causes arm flexion & leg extension.
  • Neck extension causes opposite effects.
• Asymmetric Tonic Neck Reflex (ATNR):
  • Head rotation to the left: extension of left arm and leg, flexion of the right arm and leg.
  • Head rotation to the right leads to the reverse pattern.
• Positive Babinski sign.

Synergy Patterns

• These are stereotyped, primitive movement patterns associated with spasticity.
• A patient can't perform an isolated movement of a limb segment without producing movements in the remainder of the limb (obligatory Synergies).
• Efforts to flex the elbow may result in shoulder flexion, abduction, and external rotation.
• A patient is severely limited in adapting movements to varying task or environmental demands.
• Two abnormal movement combinations exist for upper and lower limbs: flexor synergy and extension synergy.
• These synergies are considered the only way for the hemiplegic patient to move their upper and lower limbs.

Obligatory Synergy Patterns Following Stroke

• Flexion synergy components in the upper extremity
  • Scapular retraction/elevation or hyperextension
  • Shoulder abduction, external rotation
  • Elbow flexion*
  • Forearm supination
  • Wrist and finger Flexion
• Flexion synergy components in the lower extremity
  • Hip flexion,* abduction, external rotation
  • Knee flexion
  • Ankle dorsiflexion, inversion
  • Toe dorsiflexion
• Extension synergy components in the upper extremity
  • Scapular protraction
  • Shoulder adduction,* internal rotation
  • Elbow extension
  • Forearm pronation*
  • Wrist and finger flexion
• Extension synergy components in the lower extremity
  • Hip extension, adduction,* internal rotation
  • Knee extension*
  • Ankle plantarflexion,* inversion
  • Toe plantarflexion
• Muscles that are generally difficult to activate when the patient is exhibiting these patterns are:
  • Latissimus dorsi
  • Teres minor
  • Serratus anterior
  • Finger extension
  • Ankle evertors

Stages of Motor Recovery

• An overall pattern of motor recovery exists but individual recovery is highly variable.
• Some patients experience mild involvement with early full recovery. Others demonstrate severe involvement with incomplete recovery.

Sequential Motor Recovery Stages Following Stroke

• Stage 1: Recovery from hemiplegia occurs in a stereotyped sequence of events that begins with a period of flaccidity immediately following the acute episode. No movement of the limbs can be elicited.
• Stage 2: As recovery begins, the basic limb synergies or some of their components may appear as associated reactions, or minimal voluntary movement responses may be present. At this time, spasticity begins to develop.
• Stage 3: The patient gains voluntary control of movement synergies, although the full range of all synergy components does not necessarily develop. Spasticity has further increased and may become severe.
• Stage 4: Some movement combinations that do not follow the paths of either synergy are mastered; first with difficulty, then with more ease, and spasticity begins to decline.
• Stage 5: If progress continues, more difficult movement combinations are learned as the basic limb synergies lose their dominance over motor acts.
• Stage 6: With the disappearance of spasticity, individual joint movements become possible and coordination approaches normal. From here on, as the last recovery step, normal motor function is restored, but this last stage is not achieved by all, for the recovery process can plateau at any stage.

Sensation Impairment

• Sensation is usually impaired but not lost depending on the site and size of the lesion.
• Crossed symptoms indicating a brain stem lesion: Ipsilateral facial impairment with contralateral trunk and limb involvement.
• Patients may complain of abnormal sensations such as numbness, dysesthesia, or hyperesthesia.
• Specific localized areas of dysfunction are common with cortical lesions. Diffuse involvement throughout one side of the body suggests deeper lesions involving the thalamus and adjacent structures.

Superficial Sensation includes

• Pain Perception
• Temperature Awareness
• Touch Awareness
• Deep Sensation includes
  • Kinesthesia Awareness/proprioception
  • Vibration Perception
• Combined Cortical Sensation includes
  • Stereognosis Perception
  • Tactile Localization
  • Two-Point Discrimination
  • Double Simultaneous Stimulation
  • Graphesthesia
  • Recognition of Texture
  • Barognosis

Definition of Some Sensations

• Kinesthesia Awareness includes awareness of movement. The Therapist passively moves a joint through a relatively small range of motion, and the patient is asked to describe the direction of movement. The patient can also respond by simultaneously duplicating the movement with the opposite extremity.
• Proprioception Awareness includes a position sense and awareness of the joint at rest. The joint is moved through a range of motion and held in a static position by the therapist. The patient is asked to describe the position verbally or on another limb.
• Vibration Perception is tested by placing the base of the vibrating tuning fork on the bony prominence, such as the sternum, elbow, or ankle. A 128Hz tuning fork is generally used. If impaired, the patient will be unable to distinguish between vibrating and nonvibrating stimuli.
• Two points applied simultaneously to the skin are discriminated to determine sensation. Tips applied to the skin simultaneously with the tip spread apart as stimulus. Gradually move them together until perceived as one. The small est distance at perception is measured for two points.
• Double Simultaneous Stimulation (DSS) examines a simultaneous touch stimulus on opposite sides of the body. It occurs proximally and distally on a single extremity or proximally and distally on one side of the body.
• Graphesthesia: the skill to identify traced figures where the designs on the skin examined using a fingertip or pencil eraser.
• Recognition of Texture: The examined ability differentiates among various textures like cotton, wool, or silk.
• Barognosis is assessed by determining the recognition of weight using different weights.

Neural Pathways

• Dorsal column medial lemniscus tract is for discriminative sensation whereas anterolateral spinothalamic tract is for pain, temperature and coarse touch.
• Discriminative sensation includes; stereognosis Perception, tactile Localization, two-Point Discrimination, double Simultaneous Stimulation, graphesthesia, Recognition of Texture, barognosis, Kinesthesia and Awareness/proprioception- as well as Vibration Perception.
• Transmits afferent fibers of large diameter,is myelinated and rapidly conducting.
• Activated by mechanoreceptors, thermoreceptors, and nociceptors. Composed of afferent fibers that are small diameters and slowly conducting.

Gait and Locomotion

• Gait is altered following stroke due to a number of factors.
• Gait examination includes observational gait analysis (OGA).
• The therapist examines the movements occurring at the ankle, foot, knee, hip, pelvis, and trunk, which is kinematic gait analysis.
• Gait is observed from different planes of motion and deviations.
• Digital video recording of the patient's gait improves identification of gait deviations.
• Quantitative measures of distance and time, cadence, velocity, and stride times are obtained using measured walkways and a stopwatch.
• Kinetic gait analysis examines the forces involved with the production of movement during walking and requires sophisticated instrumentation, such as force plates.

Common Gait Deviations Following Stroke - Stance Phase

• Trunk/pelvis unawareness of affected side shows poor proprioception and forward trunk.
  • Weak hip extension and flexion contracture
• Hip displays poor hip position in adduction or flexion. This means poor proprioception. A Trendelenburg limp shows weak abductors. Scissoring displays spastic adductors.
• Knee displays flexion during forward progression.
  • Flexion contracture can be seen from weak hip and knee extensors, and poor proprioception. Ankle displays weak extension past neutral, as well as extension pattern or in selective motion of these parts.
  • Plantarflexion during forward progression:
  • Plantarflexion contracture past 90° can display impaired proprioception, severe spasticity in quadriceps and weak knee extensors.
• Compensatory knee hyper extension
• Ankle displays Equinus gait where there isnt heel touch, which is spasticity/contractures of gastrocnemius soleus.
  • Varus foot is hyperactivity of the anterior tibialis, post tibialis, toe flexors, and soleus
• Unequal step lengths can be caused by spastic toe extensors or flexors
• Lack of dorsiflexion range 10 deg is needed.

Common Gait Deviations Following Stroke - Swing Phase

• Trunk/pelvis displays insufficient pelvic rotation
• Inclination is to the sound side for clearance of extensor muscles
• Hip inadquate - Weak muscles, poor propriocetion, Spastic Quadriceps, abdominal weakness, and hip weakness
• Abnormalities include circumduction, external, Rotation, Adduction, dragging, momentum, trunk issues and uncontrolled swings
• Exaggerated hip flexion is with strong flexor synergy
• Knee shows - inadequte Flexion and extensor, with spastic hamstrings and or sustained total flexor
• weak knee extensors or proocepction
• Ankle and Foot - Presistent entiquous and entinovarus with contature and or spasticity
• weak dorsiflexors, delayed and tows drag.
• Spasticity and equinovarus and dorsi flexors is common

Community Walkers

• Limited walkers rely on all 4 for certain tasks. Unlimited can rely without. Most limited walkers can enter the home independently while least limited use shopping centres and crowded terrain. Community walkers will do all.

Postural Control and Balance

• Disturbance following stroke is common in steadiness, symmetry, and dynamic stability.
• Problems occur with a destabilizing external force with reactive postural control and or self initiated movements from anticipatory.
• Reactive Posture control is recover after unexpected moments.
• Anticipatory is ability to modidy before a situation.

Balance Deficits Post-stroke

• Patients demonstrate asymmetry because the weight shifts to the stronger side in sitting and standing. Delays occur in movement, so synergies are abnormal.
• They display more postural sway in standing and compensate in the hip and knee movements. Pts fall towards their weakness direction.
• Table 15.7 lists common postural alignment deviations with balance issues

Ipsilateral Pushing

• This (pusher syndrome) is an unusual motor behavior of active pushing with the stronger extremities. This is toward the hemiparetic side with a lateral postural imbalance. The end result is a tendency to fall. Occurs in about 10 % of Pts where the posterolateral thalamus is affected. There will be loss of orientation and gravity issues.
• 20 deg tilting with misperception of vertical when in the hemi side. When in chair will fall to the weak side.
• High risks from stance due to falls and LE are not enough. Long recovery times with functional scores decreasing.

Acute Complications and Associated Conditions include

• Neurological, coma, expressive and receptive impairments, dysphasia.

Altered Consciousness

• Decreased coma and arousal happen from extensive brain function with use of Glasgow Scale. Exam if Pt is eye opens and there is verbal/ best response of motor skills.

Disorders of Speech and Language

• If dominant hem is affected, speech and language happens with acquired disorder like Aphasia, formulation loss. The range happens in 30 to 36%.

Fluent Aphasia

• (Wernicke's , Sensory and or Receptive) which flows smoothly from speech preservations and construction of melodic speech. Difficult of language and commands which is an auditory impairments from a lesion of the cortex in the temporal lobe

Non Fluent Aphasia

• Expressive / Motor
• Slow Speech due to limited words with synax issues. The loss production and comprehensions exists.
• Production is labored and compelety lost, comprehensions is fine

Global Aphasia

• Production and comprehensions with lesions from carotid artery. If is severe than they are unable to learn the situation and impede successfulness of out comes.

Dysarthria

• Often reported with a range frequency with nervous system and speech production
• Location Primary motors and sensory
• Results in limited jaw, tonuge movements with speech

Dysphagia

• 51% Pts with stroke are involved with swallow issues.
• Often happen with psedobular / suprabular palsy from the trigemnial VII/ facial VII and hypoglossal XII.
• common impairments is less movement of tongues
• Pt often have posture impairement

Additional Components For Dysphagia

• Pt often have multiple impairments from dehydration.
• Aspiration is one of the biggest concerns leading to death
• A PT role is to improve functions when Pt swallows

Cognitive Dysfunction

• Pt have inpairments in the Prefrontal for memory, alert, orientaiton, attention and executive functions.

Categories

• Are selective, focus, sustained
• Lesions is prefrontal cortex.

Additional Functions

• Confusion, memories, fabrications, retention and understanding
• Lesions is the frontal context for the abilities
• Abilities is decisions, planning and action

Functional Disorders and Attention

• Acute delerium with drugs loss of O2, metabolic imbalance
• Patient cannot attend and will be loss

Altered Emotional Status

• Brain function can produce number of changes leading to depression, euphoria and motivation

Perceptual Dysfunction

• 32 to 41 % Pt visual losses, caused by cortex
• Includes body image, with unilater neglect and discrimination
• Agnosia is the inability to recognized and can cause the Pt to not recognize they have the illness

Visual Impairment details

• "Where"- location of objects in motion
• damage results in neglect and Ataxia.
• "What"identifying objects, and features. Damage results in agnosia.
• Both associated with their related lobes.

Types Of Spatial Neglect

• They will ignore even with motor and have normal coordination

Additional

• Issues with bowl and bladders with 29% Pts.

Cardio Impairment from stroke and pulmonary. low levels from lack of O2

• Stasis from Prolonged Bedrest has DTV risk

Osterosris

• risk and weakness

Prognostic

• good younder, lessor side bad is coma lack of support