Unit 4 Knowledge Check 1

Table of Contents
DEVELOPMENT
• Developmental Milestones ✓
• Typical Development ✓
• Atypical Development ✓
PATHOLOGIES
• Stroke ✓
• Speech and Language Disorders ✓
• Acquired Brain Injury ✓
• Cerebral Palsy ✓
NEUROSCIENCE
• Introduction to Neuroscience ✓
• Theories of Motor Control ✓
• Somatosensory Peripheral ✓
• Somatosensory Central ✓
• Cognition and Perception ✓
• Peripheral Motor System ✓
• Central Motor System ✓
MOTOR MOVEMENT
• Synergies and The Stages of Motor Recovery and Atypical Movement ✓
CLINICAL ASSESSMENT TOOLS
• Clinical Outcome Variables Scale (COVS)
• Chedoke McMaster Stroke Assessment (CMSA)
Developmental Milestones
• Human development: understanding constancy and change throughout the lifespan
o Lifespan development: human development that occurs from conception to death (module – consider birth to
death)
• Several theoretical models for human development that are out of scope – complex
o Continuous – gradually enhancing the same skills that were already there
o Discontinuous – gaps where people learn new/different ways of responding
o One course of development vs. non-universal development
o Biological vs. environmental factors vs. both are the main determinants
▪ The principles of lifespan development remain consistent
• Lifespan principles of development – development is:
o Life-long
▪ Babies are model for how we learn and move but it doesn’t stop at childhood
▪ Develop from conception to death – there is no one period that is more important
▪ Events in each period can have crucial effects on the future
o Multidirectional
▪ Gains and losses throughout lifespan e.g. young person gains height but loses flexibility
▪ Can gain new skills in one area to compensate for another
o Multidimensional
▪ Affected by biological, psychological, social factors
o Plastic
▪ Varies by individual – aging isn’t an eventual decline but continued improvement in potential occurs
o Influenced by multiple interacting forces
▪ Normative – affect large groups of people in similar ways
▪ Age-graded e.g. puberty reached between ages 12-14
• Biology and social customs can impact this (e.g. social – marriage timing)
▪ History-graded e.g. war, famine, introduction of technology
▪ Non-normative influences – irregular and happen to one or a few people, not predictable
• Domains of development – overlaps present
o Understand typical developments in all domains to get overall impression of developmental status
o E.g. crawling (physical) affects learning about toy in corner (cognitive) affects showing toy to sister (social)
o Physical: biological changes that occur in the physical body and brain
o Social-emotional: changes in the way we relate to other individuals, express and comprehend emotions
o Cognitive: changes in the way one thinks, reasons, understands
o Language: changes in the way we communicate
• Major periods of development (8)
o Prenatal [conception to birth]: one-celled organism becomes a human
o Infancy and toddlerhood [birth-2]: dramatic changes in body, brain, motor, intellectual, perceptual skills
o Early childhood [2-6]: play is integral to development
▪ Motor, intellectual, perceptual skills refined
▪ Peer relationships
o Middle childhood [6-11]: school years advances in thinking, basic literacy, peer-relationship, morality, sense of self
o Adolescence [11-18]: onset of puberty
▪ Autonomy from family
▪ Goal setting for future
o Early adulthood [18-40]: leave home; education; work; partnerships; children
o Middle adulthood [40-65]: height of career; help children establish independence; aware of mortality
o Late adulthood [65-death]: retirement; loss of loved ones; reflect on meaning of their lives
o Early development: increase in performance e.g. faster processing speed, faster reaction time
 o Late development: varied patterns of change in stability e.g. overall reduction in performance/tasks that depend
on speed
• Principles of neuromotor development
1. Proceeds from the head downwards
2. Proceeds from the centre of the body outwards
3. Depends on maturation and learning
4. Simple to more complex
5. Growth and development are a continuous process of change
6. Proceeds from general to specific
7. Individual rates of growth and development
▪ Growth and change are dynamic, affected by many factors
▪ Intrinsically determined neurodevelopmental & physical growth take place in sequential/predictable
pattern in early years – developmental milestones
▪ Primary aging: biological mechanisms responsible for age-related changes e.g. sensory systems become
less acute with age
o Predictable changes in physiological systems & physical appearance that occur with aging e.g. teenagers undergo
puberty
o Most extraordinary feature of aging is how each person’s development is unique
▪ Due to secondary aging factors e.g. stress – environmental factors like stress affect primary aging
▪ Individual biological characteristics & circumstances make each person’s development universal and
unique at the same time
▪ Many developmental outcomes are possible, some more likely than others or can be made more likely,
some outcomes might not be possible – monitor through milestones
▪ Understand typical development to recognize atypical development
• Principles of motor learning
o Children/adults build upon skills that they already have a firm grasp of in their repertoire
o Children/adults learn motor movements through interactions with other people
o Frequent practice is critical to success
o Children/adults learn what they are motivated to master
o Objects, in addition to people, help with learning
o Safe environments facilitate motor learning
o Motor skills become ingrained when they are learned in the context of learning other domains
▪ E.g. Jayden – has to go up/down the stairs frequently in class; initially slow to do it but with practice is
now quicker → principles 1, 3, 4, 6, 7
• Physiotherapists should provide principled care, not prescriptive care
• Motor development: the continuous process of change in movement, as well as the interacting constraints (or factors) in
the individual, environment, and task that drive these changes
o Motor performance increase from childhood to young adulthood, decrease from YA to old age; mirrors cognitive
research
• Gross motor development: skills that use large body mvmts (roll, crawl, sit, stand, walk, jump, throw, kick, transfer)
o Goal: independent volitional movement
o Must be able to move from one place to another (locomotion), to do so without falling over (stability), use the
hands to explore/manipulate/learn (good object manipulation skills)
o Depends on integration of MSK + sensory + motor + cardiorespiratory systems
o Depends on maturation of nervous system & interpretation of feedback for skill modification
o Babies have primitive reflexes (to prepare for acquisition of a specific skill) that need to disappear to move
voluntarily
▪ E.g. positive support reflex – prepares infant for standing
▪ Postural reactions, righting reactions, protective reactions begin to develop after birth
▪ Postural & righting reactions: establish normal head and body relationship in space, protect from falls
 o 9 months: equilibrium responses begin to develop, refined into 2nd year to allow for stability while babies are on
their feet
o Ages 2-6: rapid skill acquisition – by age 6, kids have fundamental mvmt skills required to master envt
o Ages 6-10: gradual skill refinement (can go into adulthood)
o Gradual decrease in performance into adulthood
• Fine motor development: use of upper extremities to manipulate the envt for ADLs, work, play
o Depends on gross motor development, cognition, and visuo-perceptual skills
o Hands initially used to support/explore environment (even in supine)
▪ Can later be used to manipulate movements in standing/sitting
o Primitive reflexes initially dominant (e.g. grasp reflex) – over time, infants learn to grasp objects of different
shapes/sizes, release objects, reach for object → develop intrinsic muscles of hand (esp. thumb + index)
o Age 2 – manipulate objects with some mastery → fine motor dev. closely associated with cognitive dev. (infant
able to appreciate what they want and how they can get it)
o Skill progresses from general responses to stimuli (primitive reflexes) to purposeful actions that are refined
• Developmental milestones:
o https://www.who.int/toolkits/child-growth-standards/standards/motor-development-milestones

o
o Milestones: stages of gross motor development that represent progress towards achieving the goals of upright
mobility and object manipulation
o Wide range of times for when typically developing children achieve milestones
• Sequence of motor achievement
o https://cdn.who.int/media/docs/default-source/child-growth/child-growth-standards/indicators/motor-
development-milestones/who-motor-development-study-windows-of-achievement-for-six-gross-motor-
development-milestones.pdf?sfvrsn=3425c1dc_0 → page 6
 o
▪ Milestone order can vary but must always stand alone before walking alone
o Developmental charts show motor development being a smooth upward progression, but it is usually not a smooth
trajectory → detours and steps backwards are common
▪ Child can take unique developmental pathway to achieve each milestone
o Motor milestones develop in overlapping sequences with spurts forward and regressions
o Practicing harder task can help with mastery of easier task e.g. standing alone may help w/ walking with assistance
o Motor skills don’t develop in isolation – multiple domains of development are at play
o Babies are the model for how to move → what they practice regularly (roll, sit, pull to stand, cruise, walk, throw,
kick) are building blocks to movement
▪ E.g. rolling of child = getting out of bed for adult
o All building blocks of movement are achieved by age 6, refined by age 10, continue to be refined into adulthood

VIDEOS – MOTOR MILESTONES (BIRTH TO 12 MONTHS)

https://pathways.org/watch/0-3-month-baby-motor-milestones-to-look-for/ (0-3 Months)

• While lying on stomach, pushes up on arms

• While lying on stomach, lifts and holds head up
• Able to move fists from closed to open
• Able to bring hands to mouth
• Moves legs and arms off surface when excited
https://pathways.org/watch/4-6-month-baby-motor-milestones-to-look-for/ (4-6 Months)

• Uses hands to support self while sitting

• Rolls from back to stomach and stomach to back
• While standing with support, accepts entire weight with legs
• Reaches for toys while on stomach
• While lying on back, reaches both hands to play with feet
• While lying on back, transfers a toy form one hand to the other
https://pathways.org/watch/7-to-9-month-baby-motor-milestones-to-look-for-2/ (7-9 Months)

• Sits without support

• Sits and reaches for toys without falling
• Moves from stomach or back into sitting
• Starts to move with alternate arm and leg movement e.g. creeping, crawling
• Picks up head and pushes through elbows during tummy time
• Turns head to visually track objects while sitting
• Picks up small objects with thumbs and fingers
• Shows more control while rolling and sitting
 • In simple play, imitates others
https://pathways.org/watch/10-12-month-motor-milestones-look/ (10-12 Months)

• Releases objects into a container with a large opening

• Takes several independent steps
• Moves in and out of various positions to explore environment and get desired toys
• Stands alone
• Pulls to stand and cruises along furniture
• Uses thumb and pointer finger to pick up tiny objects
• Maintains balance in sitting when throwing objects
• Claps hands

VIDEO – INFANT DEVELOPMENTAL MILESTONES (0-5 YEARS)

https://www.youtube.com/watch?v=i0fnBTUuRIA

• Major age groups: 1 month, 6 months, 9 months, 12 months, 24 months, 3 years, 4 years
• 1 month:
o Lift head (in prone)
o Track eyes
o Coo
o Recognize parents
• 6 months:
o Sit up
o Raking grasp (use a hand to move an object)
o Babbles
o Stranger anxiety
• 9 months:
o Walk with assistance
o 3-finger grasp
o Mama/Dada (may or may not be able to say it)
o Wave bye-bye/pat a cake
• 12 months:
o Walk (gross motor skill)
o 2-finger pincer grasp to pick up objects (fine motor skill)
o Mama/Dada (language)
o Imitate parent (social cognitive)
o The 1-year-old who cannot walk is not necessarily delayed; the 1-year-old who can only sit up is delayed
• 2 years:
o 2 steps
o 2-word phrases
o 2 step commands
o 6 blocks (stacking)
• 3 years:
o Tricycle
o 3-word sentences
o Brush teeth
o Draw circle (could also be more complex) – drawing a person = 3 parts (face, eyes, mouth)
• 4 years:
o Hop “4”
o Copy a cross (+)
o Play with kids; can draw 4 parts (+ nose)
 • Typically developing adolescents and adults will use building blocks of movement that were developed/refined in childhood
to function
• Determining the age of an infant:
o Gestational age: the number of weeks a baby has been in the uterus – normal pregnancy ranges from 38-42 weeks
▪ Infants born before 37 weeks are premature
▪ Estimated date of delivery: add 280 days (40 weeks) to first day of last menstrual period
o Chronological age: age of baby since birth
o Corrected age: applied to premature babies – actual age in weeks minus weeks preterm
▪ E.g. born at 32 weeks (8 weeks early) with a chronological age of 8 months has a corrected age of 6
months – expect them to function at the level of a 6-month-old
o Functional age: a measure other than chronological age can better reflect one’s position in aging process
▪ Age is treated as primary predictor of landmark motor behaviours
▪ Instead, experience may be a stronger predictor
• e.g. Shane is 2 years old, can roll from back to front and front to back, sit independently, pull to stand, walk; cannot jump on
two feet → functional age: slightly below 2-year-old, in line with a 1-year-old
• e.g. Sasha is an atypically developing teenager, can crawl but has never been able to stand alone or walk independently
o Functional age: 7-9 months (module – 9 months)
o Skills to crawl: reaching, pushing up on arms, alternating legs/arms, push thru elbows, head up, rolling, sitting
o Skills that are emerging: standing with support, walking with assistance
o Skills that are absent: taking independent steps (walk alone), standing alone
o Can this apply to a senior who feels safer crawling in their apartment compared to walking?
• e.g. Anu in middle adulthood with a hip replacement who cannot walk down the stairs with alternating steps but can walk
down leading with the same leg on every step (step-two pattern)
o Functional age: <4 years (a 4-year-old walks down the stairs with alternating steps)
o Skills mastered: stand on one leg
o Skills that are emerging: verbal or tactile cues to alternate steps
o Skills that are absent: cannot balance well on other leg (need exposure/opportunity to do so)
▪ There may be other reasons for gait: pain, acuity of surgery, environment (railing), exercise tolerance,
ROM, strength/MMT, doctor orders
▪ Note the building blocks to the movement to help the patient work up to the movement

VIDEO 1 – PULL TO STAND [older woman on first floor near stairs that are going up]
• Identify motor skills by name – sitting on floor, use hands to push up with help of furniture, pulls to stand
• What do you see, think, wonder?
• Hypothesize functional age based on motor skills and provide examples that justify this hypothesis – 10-12 months
• What skills have been mastered? Are they good? Is this something to maintain? – standing, pulling to stand
• What skills are emerging? (This is something to work on) – standing alone
• What skills have not been initiated (This is something we may need to expose client to) – standing unassisted

VIDEO 2 – PULL TO STAND [infant in crib]

• Identify motor skills by name – rolling over (back to stomach), use furniture to stand, lifting head
• What do you see, think, wonder?
• Hypothesize functional age based on motor skills and provide examples that justify this hypothesis – 4-6 months
• What skills have been mastered? Are they good? Is this something to maintain? – pull to stand, rolling over
• What skills are emerging? (This is something to work on) – standing unassisted
• What skills have not been initiated (This is something we may need to expose client to) – standing unassisted
Typical vs. atypical: https://pathways.org/watch/6-month-old-typical-atypical-motor-development-side-side-comparison/ [horiz.
table]

• 6 months, supine
o Presented a toy
▪ T: reaches, grasps, transfers, explores toy in well-coordinated motion
▪ AT: visually interested, unable to reach/grasp/play in this position
o Extremities
▪ T: can symmetrically lift UE & LE against gravity, bring hands to feet
▪ AT: rarely demonstrates antigravity movement even with assistance; briefly holds knee towards chest
o Body
▪ T: increased antigravity control of trunk muscles
▪ AT: improved ability to hold head and trunk in midline, little abdominal activity
• 6 months, side-lying
o Transition
▪ T: visually follows and reaches, then rolls indep. by initiating movement with LE
▪ AT: visually engages w/ toy, arms rest in passive wide abduction, shoulder extension prevents roll
o Movement
▪ T: choses not to stay in side-lying, too interested in playing
▪ AT: unbalanced neck, shoulder, back extension prevents forward movement of head and arm to assist
rolling to the side
• 6 months, prone
o Head and arms (AT – shoulder retraction)
▪ T: able to be on extended arms, supporting weight while turning head to follow toy
▪ AT: elbows behind shoulders make it difficult to use upper extremities to assist in head and trunk lifting
o Upper extremities
▪ T: emerging UE control in weight shifting for reaching, grasping, playing
▪ AT: decr. UE stability, preventing weight shifts towards pelvis needed for freedom of UE
o Lower extremities
▪ T: pivoting is seen; incr. extension down to lumbar spine and LE
▪ AT: LE kicking but doesn’t possess stability required for UE play
o Play
▪ T: varied schemes of banging, turning, mouthing, transferring; palmar grasp w/ incr. digital participation
▪ AT: challenged when prone; inadequate stability, cannot use vision or hands to explore envt
• 6 months, pull to sit
o Head
▪ T: actively flex neck forward and lift head from support surface to assist in maneuver
▪ AT: minimally able to assist in maneuver, head lag (tilts back) until upright, holds head briefly in midline
o Upper extremities
▪ T: uses UE & abdominals to assist, good symmetry throughout
▪ AT: 6-month-old should be able to assist with UE pulling but this is absent
• 6 months, sitting
o Head
▪ T: stable head and trunk with strong extension through the thoracic spine
▪ AT: struggles to maintain head upright and in midline even when supported
o Stability
▪ T: reaches with one arm at a time, wide base of support gives greater stability in LE
▪ AT: poor trunk extension, doesn’t have solid balance of trunk flexor/extensor muscles to stabilise self
o Reaching
▪ T: can lean forward, reach, and right trunk over pelvis to attain upright sitting
▪ AT: need support high on chest for stability, UE down to sides, no reaching observed
• 6 months, horizontal suspension (dangle)
o Extension
▪ T: full sustained extension in neck and upper thoracic spine down through he hips and legs
▪ AT: only briefly able to lift head symmetrically in midline and extend through upper thoracic spine & hips
• 6 months, protective extension (dangle but tilted forward)
o Tilting forward
▪ T: protective extension is easily and quickly elicited, brings arms forwards (try to place hands on floor)
▪ AT: doesn’t bring UE forward to the surface to protect self
o Upper extremity response
▪ T: props immediately on one UE and actively reaches for toy in front with the other UE
▪ AT: decreased antigravity neck and trunk strength makes it hard to sustain head and trunk extension
needed for arms to come forward
• 6 months, standing
o Head
▪ T: head is free to turn and look around
▪ AT: head and trunk control are still a challenge, lacks necessary antigravity control (floppy neck)
o Alignment
▪ T: hips slightly flexed and a bit behind shoulders; uses UE to assist, strong upper thoracic extension
▪ AT: cannot align head, trunk, hips, knees, and feet in the vertical
o Weight-bearing
▪ T: demonstrates sustained weight-bearing on extended LE
▪ AT: does not initiate or sustain weight-bearing, makes it impossible to develop control in standing
• Alberta Infant Motor Scale (AIMS): scored standard test measure
o Assessment type: observation
o What: assess gross motor development from birth to independent walking
o Age range: 40 weeks conception to 18 months of age, most sensitive on infants between 4-12 months
o References: age-related norms of 2200 infants in Alberta, Canada
o Psychometrics: highly applicable and excellent reliability and validity
▪ Test-retest & inter-rater reliability set at 0.99, concurrent validity defined as 0.87 w/ PDSM, 0.98 w/ BSID
▪ https://www.physio-pedia.com/Alberta_Infant_Motor_Scale_(AIMS)
o Test positions: prone (21 items), supine (9 items), sitting (12 items), standing (16 items) – 58 items in total
o Points for observed skill and points for not observed skill: 1 point if every element of an item has been
accomplished (last and most mature items identified in each position constituting the developmental window;
score each item in the window as observed or not observed)
o Recommended cut-offs for 4 months and 8 months: 10th percentile at 4 months, 5th percentile at 8 months
• AIMS: sample scoring of prone domain

o
o Focus on middle 4 figures – infant’s motor window
o Identify least mature observed item in prone position (2nd figure from left)
o Identify most mature observed item in prone position (2nd last figure from right)
▪ The items between them are the infant’s motor window - score each item in the window as observed or
not observed e.g. in the video, 3/4 positions are observed
▪ Credit 1 point to each item observed and 1 point to each item below the least mature observed item
(assume infant can do all the items below the LMOI) e.g. there is only 1 item shown here but in reality
there are 14 items
o Sum of points – total of points in window + points below least mature level (e.g. 3 + 14 here = score of 17)
 • Functional Independence Measure (FIM): scored standard test measure – motor and cognition subscales
o Assessment type: clinician-reported scale
o What: measure disability for variety of populations (stroke, TBI, SCI, cancer)
o When: assess at start of rehab care and end
o Age range: 7 years and above; another site states 18+
o Referencing: hospitals in the USA, patients with stroke/SCI/brain trauma/four other diagnoses assessed
o Psychometrics: inter-rater reliability between 0.86-0.88, strong construct validity with Barthel Index
o Six areas tested: self-care, sphincter control, transfers, locomotion, communication, social cognition
o Points for skill performed independently: scored on 7-point Likert scale (1 – total assistance in all areas, 7 – total
independence in all areas)
o Points for skill requiring two helpers to assist: between 1 to 5 (1-2: complete dep., 3-5: modified dependence)
▪ 1 – total assistance or not testable (subject <25%)
▪ 2 – maximal assistance (25% or more)
▪ 3 – moderate assistance (50% or more)
▪ 4 – minimal assistance (75% or more)
▪ 5 – supervision (100%)
▪ 6 – modified independence (device)
▪ 7 – complete independence (timely, safety)

Typical Development
• Infants born with 100 billion neurons; the infant brain is only ~1/3rd the size of an adult brain
• Plasticity is greatest in the developing brain
o Dendritic branching of neurons/synapses increases with stimulation and experience
o Synapses are strengthened through repeated experiences
o When pathway isn’t used – eliminated based on “use it or lose it”
o Selective pruning or cell death
• Nature vs. nurture: infant development shows experiential shaping of genetic potential
o Accelerated growth of brain structure during infancy depends on experience & quality of experience
o Early experiences with social/physical environment are critical to brain tissue maturation
• Sensory motor development: sensory system processes and integrates sensory input to assess position of body in space
(proprioception, tactile, vestibular, visual input)
o Babies repeat movements to create awareness of sensation of movements
o Reflexes: involuntary stereotypic motor responses to specific positional/movement stimuli; mediated at sub-
cortical level → can start at 15 weeks gestation
• Primitive reflexes: earliest experiences w/ mvmt, needed for protection/survival – suppressed in the first 6 months
o Allows emergence of more mature postural control mechanisms, mobility, functional limb control
• Biomechanical principles:
o Planes of movement: dynamic extension before flexion (sagittal plane)
▪ Flexion and extension combined allows for lateral flexion (frontal plane)
▪ Refinement of control and coordination leads to rotation (transverse plane)
o ROM/muscle activation: muscles tissue must elongate before it can efficiently activate and contract
o Variety and variability in motor & cognitive development
• Variations in skill acquisition are present
o Skills don’t magically appear at designated times; continuum of motor development and core stability
o E.g. 4-point kneeling to sitting – first 10% learn at 5 months, last 10% learn at 9-10 months
• Ease of movement allows child to concentrate on task at hand instead of their balance/safety
• Patter of scapular adduction/elevation to reinforce spinal extension and provide postural stability in the trunk
o 2 months: prone and sitting
o 4-6 months: sitting
 o 11 months: standing (revert to immature pattern)
o 12 months: walking
• Overlapping sequences of spurts and regressions (immature patterns in more mature skills) driven by experience
• Postural stability – allows child to concentrate on task instead of balance/safety
• Further development: age 2-6 = rapid skill acquisition, age 6-10 = motor skill refinement
o Critical periods for skill modification through reptition

0-3 MONTHS
• Born in physiological flexion (shortening of soft tissue and contractures) → dynamic flexion
• NEWBORN:
o Prone: flexion predominates, provides midline alignment and organization for basic functions (sleeping, feeding)
o Supine: flexion predominates with unilateral activation of neck flexors; high compact chest (horizontal ribs) & belly
breathing
o Sitting: full head lag when going from lie to sit; fold forward when put in sitting unsupported
o Standing: change in tone, can take reciprocal steps and be in weight-bearing position
• 2 MONTHS:
o Prone: flatter pelvis, arms move away from body with elbows behind shoulders; can take some weight through
hands and forearms; lifts head briefly with head and neck extension
o Functional movement requires a stable point in the body off which to initiate the movement
o Supine: asymmetry prevails, can rotate head towards midline and hold briefly; rely on eye focus
▪ Asymmetric tonic reflex & fencing reflex: turn to extended arm, opposite arm is flexed
▪ Can see hand, develop visual field
o Sitting: head held upright briefly when supported; compensate with scapular elevation/adduction to reinforce
thoracic extension
o Standing: astasia-abasia phase; flexor tone decreased, primary standing reflex receding (knees bend in standing)

4-6 MONTHS
• 4 MONTHS:
o Prone: greater extensor activity, experiment with lateral weight shift; anterior pelvic tilt; balance neck flexors and
pectoral muscles
o Standing: take full weight, hips may be slightly behind the shoulders
• 4-5 MONTHS:
o Supine: can reach to grab knees; hip and knee flexion to middle; limited frontal plane control so may roll to side
▪ Core muscles recruited with hip flexion, chin tucked, shoulder flexion
o Sitting: head up in midline; scapular elevation and retraction; hips flexed and externally rotated; prop w/ arms
(maintained briefly) – cannot control side-to-side shifting
• 6 MONTHS:
o Prone: increased shoulder stability and dissociation of extremities; lateral head and trunk righting with weight
shifts
o Sitting: perpendicular pelvis with coordination of abs/hips/lumbar extensors; arms free to play
o Standing: legs gradually abduct in standing, increased control; experiment with bousing, increased vestibular and
proprioceptive input

7-9 [6-9] MONTHS

• 6-8 MONTHS:
o Supine: combine trunk flexion and extension for successful rolling side-to-side; flex and extend hip to help with roll
• 8 MONTHS:
o Transition from sitting: to prone and to four-point
o Early crawling: reciprocal arm/leg movements, increased trunk side flexion reduces the required excursion of
shoulders and hips; weight shifting
o Pull to stand with UE; more mature – use half-kneel position
 o Standing: wide base of support, hip flexion

10-12 MONTHS
• 10 MONTHS:
o Cruises with rotation – being to weight shift in standing, balance improves, use support surfaces
o Can criss-cross legs, stable sitting while playing, crawling, 4 point to sitting
o Stoop to reach: graded hip/knee/ankle muscle control (incl. stability of lumbar spine and pelvis)
• 11 MONTHS:
o Stands alone: lets go of support during play, use toe grasp to gain stability
o Coming to stand with or without support (eccentric squats)
o Controlled lowering: wide base of support, lower centre of gravity using flexion to stabilise
o First steps: high guard, “waddling” gait with little trunk rotation and reduced hip excursion; exaggerated lateral
weight shift → scapular elevation/adduction reinforces spinal extension and postural stability
• 12 MONTHS:
o Increased graded muscle control, active feet and toes to gain stability, ongoing refinement
o Walking with ease; varus to valgus, arms abducted to help with balance and will raise arms higher to stabilise when
moving faster
o Experimentation: play and explore, challenges to help with motor skills

Atypical Development
• Development may start the same but missing components cause baby to compensate to function – these compensations
can become pathological if never modified by development of more advanced typical movements
• Motor development: postural control is at the centre
o Impacts MSK system, motor system, sensory system
o Other influencing factors: cognition, attachment, social factors, environment
• Environment/social: ability to explore is important as are social interactions
• Attachment: emotional bond gives sense of security
o Mother-infant face to face interaction activates right orbitofrontal cortex
o Impacts infant arousal and regulation
o Promote development and maintenance of synaptic connections in the right brain
o Attachment disorder: impairs brain organization
• Cognition: promotes inquisitiveness and desire to explore and play
o Allows problem solving (motor and non-motor)
o Helps w/ retention of learned material
• Issues:
o Cerebral palsy: group of disorders of development of movement/posture, causing activity limitation
▪ Non-progressive disturbances in developing fetal or infant brain
▪ Disturbances: sensation, perception, cognition, communication, perception, behaviour, seizure disorders
o Genetic/metabolic: >6000 known chromosomal and metabolic disorders, along with unknown disorders
▪ Chromosomal: deletion, duplication, relocation
▪ Metabolic: block of essential pathway in metabolism
o Neuromuscular disorders: genetic or congenital disorders affecting nerves and muscles
▪ Many dystrophies/myopathies are progressive, some with poor prognosis
▪ Advances in genetic therapies
o Sensory processing disorders: neurological pathologies; incr. diagnoses of ADS & sensory processing disorders
o Other: attachment issues, environment, prolonged illness
• Movement dysfunction:
o Lesion in CNS/pathology → paucity of movement/decreased movement quality, tone changes, strength changes,
sensory dysfunction
 o Limited abilities to:
▪ Activate antigravity flexion/extension against gravity
▪ Grade motor output
▪ Perform components of or multiple movement patterns
▪ Generate multiple movement patterns
▪ Activate postural adjustments
▪ Plan/execute a motor sequence (motor planning)
o Quality of movement: poor quality or paucity of movement; patterns may be abnormal or inefficient
▪ Hampers the ability to execute ongoing adjustments to deal with changing envt
▪ Interferes with acquisition of new/advanced skills – can alter joint alignment and lead to adaptations
• Muscle tone: resistance to passive motion in the muscle while in a resting state
o Relative to intrinsic properties of the muscle tissue and neural activity producing muscle contraction
o Hypertonia: CNS injury, weakening of postural muscles (floppy, low tone trunk) → compensate with postures to
stabilise, develop high tone extremities
▪ Movement system muscles compensate for lack of postural muscles; used to fix instead of for movement
o Spasticity: hypertonia with a sign of resistance (either 1 or 2)
▪ 1 – resistance to externally imposed mvmt w/ incr. speed of stretch, varies w/ direction of mvmt
▪ 2 – resistance to externally imposed mvmt, rises rapidly above a threshold speed or joint angle
o Hyperactive response to stretch: overactivity of gamma loop at alpha motor neuron
o Hypotonia: look up via hyperextension, like 1-2-month-old child
• Dyskinesias: dystonia, athetosis, ataxia, mixed
• Muscle strength: recruitment of phasic muscles (multi-joint, used for quick bursts of activity) for postural work
o Ability to generate muscle force decreases
o Tighter hypertonic muscles become weak, system loses flexibility
• MSK alignment: ability to hold stable posture det. by alignment of body segments
o Alignment determines which muscles will fire, with how much force
o Ideal alignment allows stable posture using least amount of energy
• Sensory dysfunction: primary sensory deficits e.g. vision, hearing
o Tactile, vestibular, proprioceptive senses are essential for motor planning and problem solving
o Sensory processing pathology – difficulties activating balanced flexion and extension against gravity
• Impairments and compensations:
o Primary impairments: characters that are present/positive or absent/negative as a direct result of CNS
pathophysiology
▪ Spasticity/hyperreflexia
▪ Sensory changes
▪ Altered muscle activation
▪ Changes in muscle and postural tone
▪ Insufficient force generation
▪ Impaired motor execution and coordination
▪ Impaired postural control
o Secondary impairments not a direct result of CNS pathophysiology; can be due to child compensating for primary
impairment to function, can be influenced by therapeutic intervention
▪ Overuse/underuse of muscles/change sin muscle strength
▪ Changes in joint alignment and mobility/ROM
▪ Skeletal/orthopedic impairments
▪ Sensory processing impairments
▪ Poverty of movement
▪ Pain, decreased endurance
• Compensating/”fixing patterns”: without adequate activation of postural muscles, child uses compensations to hold self up
against gravity
o Compensations become stronger and interfere with mobility
 o Overuse of compensations lead to feedforward use – impacts alignment
o Early interventions and treatment before habit patterns (feedforward) develop
• Atypical head/neck: decreased symmetrical activation of neck flexor and extensor muscles (can’t bring head to midline or
tuck chin in supine/prone)
o Might use strong asymmetrical neck extension to initiate movement in all positions
• Atypical shoulder/UE: no scapular stability
o Prevents development of independent, dissociated humeral movements and prevents forearm weight bearing and
extended arm weight bearing
• Atypical pelvis and LE: anterior pelvic tilt (seen in low tone) and posterior pelvic tilt (seen in high tone)
o Ant: supine/prone – with hip flexion, abduction, and external rotation; could move into posterior pelvic tilt in
sitting
o Post: strong unbalanced extension of head/neck with scapular adduction followed by strong hip, knee, ankle
extension
▪ LE extension not balanced by flexion so no kicking, dissociated movements
• Compensations
o Head/neck: lateral flexion, some extension; asymmetrical neck reflex
o Shoulder/UE: shoulder elevation, tripod position (prop arms up to stabilise)
▪ Maintain extension for body
o Trunk/LE: high ribcage, hip abduction in sitting for wide base of support; lack of abdominal muscle use
▪ Windswept posture
▪ Anterior pelvic tilt in low muscle tone
▪ Pelvis: W-sit pattern or ring sitting for wide base of support
▪ Collapse into hip/knee flexion and touch knees together to stabilise against gravity, wide support base
• Functional limitations: address functional limitation & participation restriction; movement is driven by a functional goal
• *Early intervention and treatment are key to reducing the secondary impairments!

Stroke
BACKGROUND
• Stroke: cerebrovascular accident (CVA); sudden death of brain cells due to lack of oxygen
o Ischemic stroke: blockage of blood flow
o Hemorrhagic stroke: rupture of artery to the brain

o
• Epidemiology and statistics
o Incidence: ~50 000 strokes in Canada each year (1 stroke every 10 minutes)
▪ 25% of those who had a stroke are <65
▪ Men have higher occurrence and rate of first stroke over time, occurrence increases with age for women
o Impact: 3rd leading cause of death and 10th largest contributor to disability-adjusted life years
▪ Over 14 000 Canadians die from stroke each year
▪ ~741 800 Canadians >20 years are living with the effects of a stroke
 o Costs: cost the CDN economy $3.6 billion a year in physician services, hospital costs, lost wages, decreased
productivity
▪ The number of CDNs living with stroke with almost double in the next 20 years
• Risk factors:
o Non-modifiable: age, gender
o Modifiable: hypertension, hypercholesterolemia, diabetes, cardiac disease (e.g. atrial fibrillation and cardiac valve
abnormalities), physical inactivity, unhealthy weight and obesity, smoking, excessive alcohol and drug abuse,
stress, unhealthy diet
• Stroke signs: FAST (Face, Arms, Speech, Time)
o F – is face drooping?
o A – can both arms be raised?
o S – is speech slurred or jumbled?
o T – call 911 right away
• Transient ischemic attack (TIA): episode of temporary and focal cerebral dysfunction of vascular origin
o Variable in duration, commonly lasts from 2-15 minutes but can occasionally last as long as a day (24 hours), which
leaves no persistent neurological deficit
o Not a stroke – but it is a medical emergency and a warning sign for a higher risk for stroke
• Ischemic stroke: ~80%
o Thrombotic: caused by blood clot/thrombus that develops in the arteries supplying blood to brain
▪ Large vessel; small vessel = lacunar stroke
o Embolic: caused by blood clot or another solid mass forming from another part of the body and travelling to brain
• Hemorrhagic stroke: ~20%
o Intracerebral hemorrhage: caused by rupture of weak blood vessel in the brain, causing bleeding in brain tissue
o Subarachnoid hemorrhage: caused by ruptured aneurysm of arteriovenous malformation resulting in subarachnoid
space bleeding
• Comparison: imaging is required to differentiate between IS & HS
Characteristic Ischemic Stroke Hemorrhagic Stroke
Hypertension Often present Usually present
Preceding TIA Occasionally No
Onset Usually at night, not activity induced Activity induced
Clinical Course Stepwise or static Severe at onset, progressive
CT Scan Normal or subtle Blood visible
Mortality Rate at 30 Days ~10% ~35%

CLINICAL MANIFESTATIONS AND LOCATION

• Clinical presentation & impairments are related to area(s) of brain affected
o Consider neuroanatomy, vascular supply roles of the regions in the brain to understand clinical presentation
• Vascular territories:
 Anterior cerebral artery (ACA)
supplies frontal and parietal
lobes

o
Middle cerebral artery (MCA)
supplies lateral aspects of
frontal, parietal, temporal lobes

o
• Hemispheres:

o
o Left: right hand control, spoken language, mathematical skills, written language, scientific skills, logical reasoning
o Right: left hand control, music awareness, three-dimensional forms, art awareness, insight, imagination
• Brain regions and functions:

o
o Frontal lobe:
▪ Premotor cortex: motor patterns
▪ Prefrontal area: concentration, judgement, inhibition, personality
▪ Broca’s area: language production
 o Parietal lobe:
▪ Processing sensory input, sensory discrimination, body orientation
o Temporal lobe:
▪ Auditory reception, receptive speech, memory
▪ Wernicke’s area: language comprehension
o Occipital lobe:
▪ Visual reception, visual interpretation
o Brainstem:
▪ Breathing, digestion, heart control, alertness
o Cerebellum:
▪ Coordination and control of voluntary movement
• Homunculus: schematic representation of region and extent of primary motor and somatosensory cortex supplying
different parts of the body
o Each hemisphere received info from the opposite side of the body
o Motor map in precentral gyrus (anterior); sensory map in postcentral gyrus (posterior)

Primary
Primary somatosensory
motor cortex cortex

MEDICAL MANAGEMENT
• Stroke is a medical emergency – brain tissue is irreplaceable, every minute during a stroke matter
o Initial medical management depends on type, severity, time post-stroke
o Assessment for accurate and rapid diagnosis: assessment of deficits, vitals, bloodwork, neurovascular imaging
(CT/MRI), cardiovascular investigations
• Ischemic stroke management: restore blood flow to the penumbra
o Penumbra: area of mild to moderately ischemic tissue lying between normally perfused tissue and area with
infarction; may remain viable for several hours
o Pharmacological mgmt:
▪ Tissue plasminogen activator (tPA)
• Can stop ischemic stroke by breaking up a clot
• Standard of care with specific inclusion criteria → must be provided within 4.5 hours of onset of
stroke Sx
• Risk of intracerebral hemorrhage
▪ Antiplatelet agent (e.g. Aspirin)
• Reduces the risk of recurrent ischemic strokes
 o Surgical mgmt: endovascular techniques including removal of blood clot via stents; tPA is standard of care
• Hemorrhagic stroke management:
o Pharmacological mgmt: antihypertensive medications to stabilise and/or lower BP
o Surgical mgmt: endovascular coiling or surgical clipping to treat aneurysm; evacuation of hemorrhage/hematoma
• Prevent secondary complications:
o DVT and/or pulmonary embolism: DVT prophylaxis, early ambulation, anti-embolism stockings
o Aspiration pneumonia: nutrition and dysphagia assessment
o Urinary tract infections: avoid indwelling catheter
o Cardiac complications (cardiac arrest, congestive heart failure: cardiovascular investigations

STROKE RECOVERY AND PREVENTION

• After neurological injury (incl. stroke), recovery is based on spontaneous recovery and neuroplasticity
o Spontaneous recovery: due to repair occurring immediately following the injury which restores the function of
neural tissue
o Neuroplasticity: the brain’s ability to reorganize itself by forming new neural connections throughout life
▪ Allows brain neurons to compensate for injury/disease, adjust their activities in response to new
situations or envt changes
▪ Life-long evolving process of use-dependent cortical re-organization
• Time course:

o
• Factors influencing stroke recovery:
o Physical: type and severity of stroke, age, health
o Emotional: mood, motivation
o Social: support of friends and family
o Therapeutic: availability of rehab services, early start to rehab
• Canadian Stroke Best Practices Recommendations (CSBPR): up-to-date evidence-based guidelines for prevention and mgmt
of stroke, promote optimate recovery and reintegration for those who experienced stroke (patients, family, caregivers)
 o

Transitions of Care
Emergency
Prevention of Medical Services - Acute Stroke Community
Public Awareness Rehabilitation
Stroke Acute Management Reintegration
Management
•
Telestroke

o Transitions of care: coordinated and seamless system to provide patient, family, and caregiver-centred care across
all transitions
▪ Educating and supporting persons with stroke, families, caregivers
▪ Interprofessional care planning and communication
▪ Identification of resources, training, and access to services
o Telestroke: services to support timely access and expertise in management of patients with strokes, families, and
caregivers across the continuum of care
o Public awareness: coordinated and organized approach to public awareness
▪ Recognize that stroke is a medical emergency
▪ Education on signs of stroke
▪ Education and public awareness to promote “FAST” and respond immediately by calling 911
o Prevention of stroke: coordinated and organized approach to enhance:
▪ Primary prevention: health promotion and lifestyle and risk factor management
▪ Secondary prevention: reduce recurrence of vascular events, includes assessment and risk management
in all stages of stroke care
o EMS – acute management: coordinated and organized approach to guide assessment, diagnosis and management
in the first hours following a stroke – recognize and mobilize
o Acute stroke management: coordinated and seamless system of care for timely access to diagnostics and
interventions to optimize recovery and patient outcome
▪ Stroke units with interprofessional teams
▪ Early access to rehab assessment and initiation of therapy
o Rehabilitation: progressive, dynamic, goal-oriented process aimed at enabling a person with impairment to reach
their optimal physical, cognitive, emotion, communicative and functional care
o Community reintegration: patients/families should be provided with information, support and access to services
throughout transitions to the community to optimize the return to life roles and activities
• Interprofessional team – comprehensive vision for prevention/management of stroke
o Client, caregiver, physician, OT, SLP, social worker, dietician, nurse, recreational therapist, psychologist, PTs
• Stroke prevention (including recurrent strokes)
o Medical management of risk factors: anticoagulants, blood pressure meds
o Education: risk factors, FAST
o Lifestyle modifications: exercise, diets
• Rehabilitation and recovery: aim at facilitating achievement of optimal functional and participation goals identified by
stroke patient
o Interventions occur across continuum of stroke, in various settings, for varied length of service
 o Use www.strokebestpractices.ca/recommendations/stroke-rehabilitation (e.g. management of the UE following
stroke; ROM and spasticity in the shoulder, arm and hand; management of shoulder pain & CPRPRS; balance and
mobility; rehabilitation of visual and perceptual deficits; etc.)
STROKE SUMMARY SHEET
WHAT IS A STROKE?
• Cerebrovascular accident
(CVA)
• Sudden death of brain
cells due to lack of oxygen
• Ischemic stroke – blockage
of blood flow
• Hemorrhagic stroke –
rupture of artery to brain
RISK FACTORS
Non-modifiable:
• Age
• Gender
Modifiable:
• Hypertension, hypercholesterolemia, diabetes, cardiac disease (e.g. atrial fibrillation & cardiac valve abnormalities),
physical inactivity, unhealthy weight, obesity, smoking, excessive alcohol and drug abuse, stress, unhealthy diet
SIGNS OF A STROKE
• F – face – drooping
• A – arms – can both arms
be raised?
• S – speech –
slurred/jumbled
• T – time – call 911 ASAP
PT TREATMENT OF STROKE
• Inpatient – receive rehab
as early as possible,
individualized rehab plans
• Early mobilisation
reasonable if acute stroke
but early prolonged
mobilisation is not
recommended
• 3 hours/day of direct task-
specific therapy
PT ASSESSMENT OF STROKE
• Assess to determine
severity of stroke and
early rehab needs
• Spasticity, ROM, shoulder
pain and complex regional
pain syndrome, balance
and mobility, LE spasticity,
falls
prevention/management,
dysphasia and
malnutrition,
TYPES OF STROKES
• Ischemic: 80%
o Thrombotic: caused by blood clot/thrombus that develops in the arteries
supplying blood to the brain, a large vessel; small vessel blockage – lacunar
stroke
o Embolic: caused by blood clot or another solid mass forming from another
body part and travelling to the brain
• Hemorrhagic: 20%
o Intracerebral hemorrhage: rupture of weak vessel in brain, cause bleeding in
brain tissue
o Subarachnoid hemorrhage: rupture aneurysm of arterio-venous
malformation resulting in subarachnoid space bleeding
MEDICAL MANAGEMENT STROKE RECOVERY
Ischemic stroke: • Spontaneous recovery: due to
• Pharmacological: restore blood flow repair occurring immediately
to penumbra (area of moderately following injury which restores
ischemic tissue); tPA to break up cloth function of neural tissue
within 4.5 hours of stroke symptoms • Neuroplasticity: brain can
onset (risk of intracerebral reorganize to form new neural
hemorrhage) → anti-platelet agent connections; lifelong evolving
(e.g. Aspirin) to reduce risk of process of use-dependent
recurrent ischemic strokes cortical re-organization
• Surgical: endovascular techniques • Most recovery in first 3-4
including removal of blood clot via months (90-120 days)
stents; however, tPA is standard of o Start tot reach limit by 90
care days, minimal
Hemorrhagic stroke: improvements after
• Pharmacological: antihypertensives to • Factors influencing stroke
stabilise and/or lower blood pressure recovery:
• Surgical: endovascular coiling or o Physical
surgical clipping to treat aneurysm; o Emotional
evacuation of hemorrhage/hematoma o Social
o Therapeutic
• Frontal
o Premotor cortex: motor patterns
o Prefrontal area: concentration, judgement, inhibition, personality
 vision/perception, central
pain, language and
communication
o Broca’s area: language production
• Temporal: auditory reception, receptive speech, memory
o Wernicke’s area: language comprehension
• Parietal: processing sensory input, sensory discrimination, body orientation
• Occipital: visual reception and interpretation
• Cerebellum: coordination and control of voluntary movement
• Brainstem: breathing, digestion, heart control, alertness

Speech and Language Disorders

• Communication: talking, listening, reading, writing, emailing, texting, gesturing, sign language, using eye contact and
body language
o Exchange of information (incl. giving and receiving information; verbally and non-verbally)
• Language: mental process which makes speech sounds or written configurations become meaningful words
(understanding, thinking, talking, reading, writing)
• Speech: mechanical production and molding of human sound into words using muscles of chest, mouth, throat
• Aphasia: condition; loss/decrease in language abilities due to brain injury – usually after a stroke, sudden focal
damage to language areas of the brain (frontotemporal or parietal areas) on left side (no cure)
o Can affect one or more of: understanding, talking, writing/email, reading
o Can have aphasia in more than one language; usually language learned later in life more affected
o Fluent/receptive aphasia: damage to posterior brain; speech sounds fluent but often lacks meaning
o Non-fluent/expressive aphasia: damage to anterior brain; speech sounds effortful but usually has meaning
• Fluent aphasia:
o (1) Wernicke’s aphasia (receptive aphasia): more severe; comprehension is impaired
▪ Talking sounds fluent but often lacks meaning
▪ Awareness of language difficulty often impaired
o (2) Anomic aphasia: less severe; comprehension relatively spared
▪ Talking and writing contain mild word-finding errors (paraphasia)
• Non-fluent aphasia:
o (1) Broca’s aphasia (expressive aphasia): comprehension is relative strength, may have some difficulty
▪ Talking and writing are limited – conversation and writing are effortful and telegraphic (concise)
o (2) Global aphasia (expressive and receptive aphasia): most severe type of aphasia
▪ All areas of communication are significantly affected (talking, reading, writing, understanding)
▪ Large stroke or several areas of brain are affected by stroke
• Aphasia management:
o Augmentative and alternative communication (AAC): computers or picture/word-based books
o Tech features for accessibility (iPhone, iPad)
o Community groups (e.g. Aphasia Institute)
• Speech components: respiration, phonation, articulation, resonance, prosody
• Dysarthria: speech disorder characterized by weakness and/or incoordination of speech muscles – speech is
slurred/hard to understand
o (1) Flaccid dysarthria: unilateral or bilateral damage to brain
 ▪ Slurred, slow and hyper-nasal speech sounds
o (2) Spastic dysarthria: bilateral damage to brain
▪ Slow, slurred, monotone speech with strained/harsh voice quality
o (3) Ataxic dysarthria: damage to cerebellum
▪ Slow, slurred, monotone speech with irregular breakdown of sounds
o (4) Hypokinetic dysarthria: multiple/bilateral strokes affecting basal ganglia
▪ Speech rate is too fast, stuttering present, voice is quiet, speech is monotone
• Dysarthria treatment:
o Speech therapy
o Patient/family and team education, including strategies
o Patient/family counselling
o Modify environment e.g. reduce background noise, be face-to-face, clear masks
• Apraxia: damage to left frontal area; can co-occur with aphasia
o Difficulty planning/coordinating speech muscles – voluntary muscle movement affected
o Groping movements to say words
o Errors in pronunciation – may need to repeat a word several times to come out clearly
o Speech sounds effortful, like stuttering
o Patient tends to be aware of speech difficulty, may become frustrated
• Apraxia management: speech therapy (visual & physical prompts, modelling); computer assisted therapy programs;
patient/family education and counselling
• Cognitive-communication disorders: right hemisphere damage (contributes to cognitive skills underlying language
processing and communication) – may affect social interaction (e.g. off-topic, socially inappropriate, verbose)
• Pragmatic disorders: difficulties with social aspects of communication (eye contact, topic initiation, facial expression)

Acquired Brain Injury

Terminology:
• Acquired brain injury = damage that happens after birth, does not include brain damage associated with a
neurodegenerative disorder
• Traumatic brain injury = brain damage caused by an external force
• Non-traumatic brain injury = brain damage caused by internal (e.g., tumor) or external (e.g., poisoning) source, but not by
force

Epidemiology:
• 50,000 Canadians/year
• Leading cause of death and disability of young Canadians (i.e. <40 years old)
• Twice as many young males as young females, incidence equal in elderly
• 30% sustained by children & youth
• Older adults also at high risk
• >50% of Toronto’s homeless population has TBI, with 1st TBI occurring before homelessness in 70%
• High-risk groups:
o Males aged 15-24 years
o Substance abusers
o Young children (0-4 years of age)
o Older adults (i.e. >75 years)
o Those who have a history of brain injury
• US data on long-term consequences of TBI:
o 4/10 are unemployed 1-year post-injury
o 1/3 have difficulty with social integration
o 1/4 of those with moderate to severe injuries require assistance with ADLs
 o 40% report poor physical & mental health

Etiology:
[1] Causes of traumatic brain injury:
• Falls
• MVA/Traffic accidents
• Struck by something
• Assaults
• Sports/recreation
• External forces cause brain to make contact with object (skull or penetrating object)
o Cause contusions, lacerations & intracerebral hematomas
o Usually focal injuries, common areas: anterior temporal poles, frontal poles, lateral & inferior temporal cortices,
orbital frontal cortices
• Rapid acceleration/deceleration forces
o Cause shear, tensile, & compressive forces leading to diffuse axonal injury (DAI), tissue tearing, intracerebral
hemorrhage
o DAI is main mechanism of injury in those with moderate to severe TBI
o Despite the name, DAI usually occurs in focal areas
o Disrupts neurofilaments in axon causing Wallerian-type axonal degeneration
o Mechanisms are microscopic, so initially few or no signs on CT or MRI
• Blast waves from an explosion
[2] Causes of nontraumatic brain injury
• Numerous causes
• E.g., hypoxic brain injury, brain tumor, airway obstruction, stroke, infectious disease, toxic exposure, illegal drug use…

Pathogenesis:
• Categorization of brain tissue damage:
• [1] Primary injury
o Results from direct trauma to brain tissue
• [2] Secondary injury
o Results from biochemical, cellular & molecular events that occur over time (hours & days)
o Events include glutamate neurotoxicity, free radical damage, inflammatory processes → all lead to cell death
o Events may be part of initial injury, or related to hypoxia, edema or ↑ intracranial pressure
o Normal intracranial pressure is 5-20 cm H2O, brain herniation will result if it is increased significantly
• Head trauma can be classified as open or closed:
o Open head injury: bullets wounds, etc.; penetration of skull; typically focal damage
o Closed head injury: falls, MVA, etc.; skull & dura remain intact; focal & diffuse damage
• Common closed head injuries:
o Concussion
o Intracranial hematoma: Often occurs with a fracture. A blood vessel is disrupted and blood pools in the subdural
space (subdural hematoma) or between the dura and the skull (epidural hematoma). Causes ↑ pressure on the
brain and requires immediate medical attention (e.g., surgery).
o Cerebral contusion: Bruising of the brain. Coup and contre-coup injuries.
o Diffuse axonal injury: Described above. Common in MVA.
Diagnosis:
• TBI is classified as mild, moderate or severe using the Glasgow Coma Scale (GCS)
• GCS consists of 3 scores (verbal, motor, eye opening) that are summed to give a total score between 3 and 15
• Highest responses recorded
• Interrater reliability adequate for motor and eye, poor for verbal
• Adequate construct validity
 • Best practice guidelines recommend that clinicians attempt to increase arousal level prior to performing evaluations of level
of consciousness whenever reduced arousal is observed/suspected

Glasgow Coma Scale

Activity Score
Eye Opening
Spontaneous 4
To speech 3
To pain 2
No response 1
Best Motor Response
Follows motor commands 6
Localizes 5
Withdraws 4
Abnormal flexion 3
Extensor response 2
No response 1
Verbal Response
Oriented 5
Confused conversation 4
Inappropriate words 3
Incomprehensible sounds 2
No response 1

Distinction between mild, moderate & severe TBI

Mild Moderate Severe
GCS score 13 – 15 9 - 12 <9
Loss of consciousness 0-30 min >30 min and <24 hr >24hr
Altered consciousness Brief >24hr >24hr
Post-traumatic amnesia 0-1 day >1 and <7 days >7 days
Neuroimaging Normal Normal or abnormal Normal or abnormal

Prognosis
Predictors of poor outcome:
• Low initial GCS score
• Lower education level
• Very young age (<7 years) and older age (>40 years)
• Longer periods of post-traumatic amnesia

Clinical Presentation
**The cognitive & neurobehavioral impairments are often the most disabling.

Common Primary Impairments of ABI:

1. Neuromuscular
• Paresis
• Abnormal tone
• Impaired motor function
• Impaired postural control
• Abnormal involuntary movements are less common, e.g., tremor, chorea, dystonia

2. Cognitive
• Decreased arousal level
o E.g., coma, vegetative state, minimally conscious state are altered arousal levels that may be seen after severe ABI
o Coma = often seen immediately after a severe injury; arousal system not functioning; no sleep/wake cycles;
ventilator-dependent; no cognitive, communicative, auditory or visual function; abnormal postural & motor
reflexes; not a permanent state, individuals will go from a coma into a vegetative or minimally conscious state or
become brain dead or make a full recovery
 o Vegetative state = brainstem & higher brain centres are not integrated; brainstem able to control basic cardiac &
respiratory functions; individual weaned off ventilator; sleep/wake cycles present; individuals may startle or orient
to visual & auditory stimuli; no awareness of surroundings; no meaningful cognitive or communicative function;
withdraw response to noxious stimulus; non-purposeful movements
o Minimally conscious state = minimal awareness of self and/or environment; some purposeful behavior that is
inconsistent; localizes to noxious stimuli; shows visual fixation & visual pursuit; localizes to sound location
o Inattention
• Reduced ability to concentrate
• Impaired memory
• Impaired learning
• Impaired executive functions (i.e., planning, cognitive flexibility, initiation, response inhibition, serial ordering &
sequencing)

3. Neurobehavioral
• Agitation/Aggression
• Disinhibition
• Apathy
• Emotional lability
• Mental inflexibility
• Impulsivity
• Irritability

4. Communication
• Deficits related to cognitive impairment, not aphasic
• Disorganized verbal & written communication, difficulty with word retrieval, socially inappropriate language
• Communicating becomes a greater challenge in distracting environments
• Impaired ability to read social cues
• These communication impairments impact quality of life, social interactions and employability.

5. Swallowing
• Dysphagia

6. Dysautonomia
• Paroxysmal sympathetic hyperactivity = ↑ sympathetic nervous system activity in response to trauma; this response is
normal, however, after ABI this response is excessive or overactive
• ↑ sympathetic → ↑ heart rate, ↑ respiration rate, ↑ blood pressure, diaphoresis, hyperthermia

7. Abnormal tone
• Spasticity – presentation variable, e.g., may affect whole body or individual muscle groups
• Decorticate or decerebrate rigidity/posturing

(A) Decorticate posturing (top figure)

• UE flexed, LE extended
• Damage to cerebrum, internal capsule and/or thalamus
• May also indicate damage to midbrain
 • Involves disinhibition of red nucleus causing facilitation of the rubrospinal tract (since rubrospinal tract activates motor
neurons in cervical spinal cord supplying flexor muscles, upper extremities are flexed)
• Disrupts lateral corticospinal tract, which activates motor neurons in lower spinal cord that supply flexor muscles (i.e. result
is lower limbs are extended)

(B) Decerebrate posturing (bottom figure)

• UE & LE extended, head may be arched back
• Damage to brainstem, specifically below the level of the red nucleus (i.e. no facilitation of rubrospinal tract)
• Generally indicates a worse prognosis compared with decorticate posturing

Common Secondary Impairments of ABI:

• DVT
• Heterotopic ossification
• Pressure injury
• Pneumonia
• Chronic pain – headache is especially common
• Contractures
• ↓ endurance
• Muscle atrophy

Early Medical Management

• At the scene of the incident, goals are to stabilize respiratory & cardiovascular systems and maintain adequate flow of
blood & oxygen to brain
• In ER, goals are to minimize secondary brain injury by optimizing blood flow & oxygenation, stabilize vital signs, address
non-neurological injuries (e.g., fractures)
• Extracranial injuries, such as fractures, are present in 35% of individuals with TBI
• To prevent or treat increased intracranial pressure: head elevated 30o, hypothermia, surgical decompression, barbiturates
• Surgery may be indicated in cases of large intracranial hematomas or mass lesions
• Adults aged 16-65 years who are 4-16 weeks post-TBI can be given amantadine, which has been shown to accelerate
functional recovery in early stages post-injury (best practice guideline #2 in self-study questions)
• Manage associated conditions (e.g., post-injury epilepsy)

PT Management of ABI: Early Stage of Brain Injury

• ABI requires lengthy rehab process that extends across care settings

*Before PT Assessment:
• Check for precautions & contraindications
o E.g., weight-bearing or ROM restrictions due to MSK complications or wounds
• Review medical record carefully
• Medical status likely fluctuating → check with primary nurse before beginning

Relevant ABI-specific outcome measures appropriate for the Early Stage:

1. Disability Rating Scale (DRS) – to measure disability
2. Rancho Los Amigos Levels of Cognitive Functioning (LOCF) – to measure cognition

Disability Rating Scale (DRS)

• Documents recovery from “coma to community”
• 3 ICF domains
• 8 areas of functioning in 4 dimensions:
o Consciousness (eye opening, communication ability, motor response)
o Cognitive ability (feeding, toileting, grooming)
o Dependence on others for function
o Employability
• Score ranges from 0 (no disability) to 29 (extreme vegetative state)
• Psychometric Properties:
o High test-retest, inter-rater and intra-rater reliability
o DRS scores correlate with scores on the FIM (i.e., convergent validity)
 o Predictive of return to work, long term functional outcome, independent living status (i.e., predictive validity)
• Item Example:

Rancho Los Amigos Levels of Cognitive Functioning

• Ordinal rating scale with 8 levels (see below)
• Psychometric Properties:
o Test-retest reliability adequate
o Inter-rater reliability adequate to excellent
o Predicts those who will return to work with good accuracy (i.e., predictive validity)

Level I – No Response
Level II – Generalized Response
Level III – Localized Response
Level IV – Confused, Agitated Response
Level V – Confused, Inappropriate, Non-agitated Response
Level VI – Confused, Appropriate Response
Level VII – Automatic, Appropriate Response
Level VIII – Purposeful, Appropriate Response

PT Management of ABI: Rehabilitation

PT Assessment in Rehabilitation
• Cognitive & behavioral impairments can be barriers
o E.g., disorientation, physical aggression, confusion, memory deficits, ↓ attention span
• May be difficult to use standardized approaches that require client cooperation
o E.g., MMT
• PT often relies more on observation skills
o E.g., Gauge strength based on ability to complete functional task
• Assess movement in a variety of environments
o Client may perform well in quiet room with no distractions, but may perform poorly in ‘real-world’ environment

*Consider how cognitive impairments may impair ability to re-learn motor tasks
• Include sufficient rest periods during PT sessions to reduce fatigue (physical & mental)
• Video self-modeling is beneficial in some cases (i.e., client watches him/herself performing a task or behavior & identifies
areas of improvement)
• Explicit or augmented feedback is helpful during early learning stage, but do not overwhelm client with information
• Begin with familiar tasks that client can accomplish rather than more challenging tasks that require new learning

Relevant ABI-specific outcome measures appropriate for the Rehab Stage

The Community Balance & Mobility Scale
• Assesses high-level balance & mobility
o No gait aids permitted
• Involves multi-tasking, sequence of movements, complex motor skills
• Psychometric Properties:
o Population tested: TBI in acute care, inpatient & outpatient rehab
o Content & construct validity established
o High interrater, intra-rater & test-retest reliability
Timed Walking Tests
• 10-meter Walk Test (10mWT) and the 6-minute Walk Test are valid & reliable in the ABI population

Cerebral Palsy
OVERVIEW
Cerebral Palsy:
• CP: group of permanent disorders of the development of movement and posture causing activity limitation that are
attributed to non progressive disturbances that occur in the develop fetal or infant brain.
o Motor disorders of CP are accompanied by disturbances of:
▪ Sensation
▪ Perception
▪ Cognition
▪ Communication
▪ Behaviour
▪ Epilepsy
▪ MSK problems
Diagnosis:
• No test that demonstrations the existence/ absence of CP
• Based on clinical presentation and medical history
• Imaging studies will help to confirm diagnosis (MRI, CT, US) but may not be etiologically specific
• Diagnosis is made before age 2 usually
Prevalence:
• Most common motor disability in children
• 1.4/1000 live births (declining)
• 94% occurred during prenatal or perinatal (within 28 days of birth) stage
• Of the 6% who acquired CP after 28 days, main cause is CVA
• Slightly more common in boys (57%)
Etiology/Causes:
• Single severe risk factor can be enough to cause CP, more often multiple concurrent risk factors precede CP:
o Prematurity
▪ Percentage of children born at <37 weeks
• Children with CP – 43%, general pop – 7%
o Low birth weight – LBW
▪ Percentage of children born <2500h
• Children with CP – 43%, general population – 6%
o Prematurity/LBW - common leads to spastic diplegia, commonly see white matter disorder
▪ Increased risk of prematurity/LBW due to:
• Intrauterine infection of inflammation
• Previous preterm birth
• Maternal vascular disease
• Multiple gestation
o Multiple gestation
▪ Risk of CP increases with multiple gestations – 4x greater risk in twins and 18x greater risk in triplets
▪ 11% of children with CP were twins; 1% were higher order multiples
▪ Associated with increased risk of prematurity
▪ Also related to death of one infant:
• Monozygotic twins/triplets at greatest risk as they might have conjoined circulation in the
placenta
• After one twin/triplet dies, vascular collapse may occur in the survivor,
o Cerebrovascular accident (CVA)
 o Others
▪ Prenatal/perinatal:
• Infection
• Ischemic stroke
▪ Postnatal:
• CVA – most common
• Acquired/traumatic brain injury
• Infection (i.e meningitis)
• Seizures
• Previously believed that birth asphyxia was primary cause of CP
• In many areas, incidence of birth asphyxia has decreased (secondary to medical advancement) but incidence of CP has not
changed much
• Birth asphyxia is responsible for ~6% of CP cases

TYPES OF CP
Hypertonia:
• Abnormally increased resistance to externally imposed movement about a joint
• Consists of
o Spasticity – resistance to externally imposed movement increases with increasing speed of stretch and varies with
the direction of joint movement and/or resistance to externally imposed movement rises above a threshold speed
or joint angle
o Dystonia – movement disorder in which involuntary sustained or intermittent muscle contractions cause twisting
and repetitive movements, abnormal postures, or both
o Rigidity (uncommon in children with CP) - velocity independent bidirectional resistance to externally imposed
movement

Spastic: 85%
• Unilateral/hemiplegia: 40% of spastic
o Spasticity noted on arm and leg of same side
o Typically bc of focal or multifocal pathology and not generalized hypoxia/ischemia
o Leading cause is perinatal stroke (MCA infarct) and congenital malformations
o Affects grey matter – seizures may be present
o Most children walk independently but gross motor milestones are delayed and have difficulty with high lvl balance
skills
• Bilateral/diplegia: 36% of spastic
o Affects legs>arms
o In pre-term infants, predominant spastic distribution
o Periventricular leukomalacia (PVL) damage to the white matter beside the ventricles – often found on head
ultrasound
o Legs more often affected by PVL bc leg fibres of the corticospinal tract run closest to the ventricles
o Most children walk independently or with the use of a gait aid but gross motor milestones are delayed
• Bilateral/quadriplegia: 24% of spastic
o Spasticity significant in all 4 limbs
o Caused by any pathology resulting in global damage to brain
o Often due to alterations to blood flow to the subcortex and cortex, affecting diffuse areas of the brain bilaterally
o Often associated with other medical problems; visual, auditory, seizures, cognitive, digestive
o Majority of children are non-ambulatory

Dyskinetic: 7% (varying tone)

• Dystonia
 o Triggered by voluntary movements
o MRI often indicates involvement of the thalamus, caudate nucleus, and or putamen
o Often demonstrates significant limitations in GM function
o High metabolic demand
o Cognition may not be affected
• Choreoathetosis
o Slow, continuous, involuntary writhing movement that prevents maintenance of a stable posture
o GM function limitations are often significant
o Cognition is typically not affected

Ataxic: 4%
• Characterized by intention tremor and poor coordination of movement
• Typically, due to infarct to the cerebellum
• Most children walk without gait aid but have difficulty with balance, endurance, and high-level GM skills
• Cognition typically not affected

Mixed: (presents with both spastic and dyskinetic features)

• Combination of dyskinetic and spastic features
• Often affects entire body, all 4 limbs
• Secondary to diffuse injury to the motor cortex and basal ganglia
• GM function varies, dependent upon the severity of the impairments

GROSS MOTOR FUNCTION CLASSIFICATION SYSTEM

• Severity of CP: used to be described based on topographical distribution of physical involvement
o Did not indicate severity level – mild/moderate/severe was too subjective
• Classify based on child’s usual functional abilities at home, school, community – considers need for assistive tech
o Ordinal scale with no intent that distance between levels is equal or that there is equal distribution
• Gross Motor Function Classification System (GMFCS): five levels, describes gross motor abilities of children/youth
o Separate descriptions for 5 age ranges (0-2, 2-4, 4-6, 6-12, 12-18)
o Classic description: related to functional ability in 6-12 age group – original version created for 0-12 years but scale
recently expanded to include 12-18
o The scale is stable after the age of 4 (GMFCS I – 35%; II – 24%; III – 12%, IV – 13%, V – 15%)
• GMFCS I: walks w/o restrictions; limitations in more advanced gross motor skills
• GMFCS II: walks without assistive devices; limitations in walking outdoors and in the community
• GMFCS III: walks with assistive mobility devices; limitations in walking outdoors and in the community
• GMFCS IV: self-mobility with limitations; children are transported or use power mobility outdoors and in community
• GMFCS V: self-mobility is severely limited even with assistive tech
• YouTube video: GMFCS – classification system to describe level of functioning
o Can help parents to better understand where child is (using description/pictures)
o Level 5: full time wheelchair users, need a lot of help with posture and body control
o Level 4: wheelchair user, can use independently (power wheelchair or manual chair)
o Level 3: some ability to walk (with support); are wheelchair users for longer distances
o Level 2: some awkwardness but can walk on feet with cane or walker
o Level 1: walk independently but may have visible differences in walking
o GMFCS level is not associated with their QOL!
o For level 4 & 5 – give kids therapy as mobility is important for development in mobility, language, social
• Other classification systems:
o Manual ability classification system (MACS) – classify upper extremity function
o Communication function classification system (CFCS) – classify communication preference
PROGNOSIS, IMPAIRMENTS, & CLINICAL PRESENTATION
Prognosis for Gross Motor Function in CP:
• Gross motor function measures (GMFM) scores decrease as GMFCS level increases
• Max GMFM score is reached at an earlier age as GMFCS level increases
• Aids in treatment planning (remediation vs compensation), resource allocation and realistic goal setting
• Caveats: does not consider activity endurance
o Does not consider quality of movements
o Only reflects GM function, not overall development
o Often GM function decreases in teen years

Other Associated Impairments:

• Intellectual impairment (46%)
• Seizures (32%)
• Visual impairment (34%)
• Hearing impairments (11%)
• Speech impairments (63%)
• Pain – 3 in 4
• Incontinence – 1 in 4
• Sleep disorder – 1 in 4
• Behaviour disorder – 1 in 4
• Decreases saliva control – 1 in 5
• Feeding/GI disorder – 1 in 15
• Sensory deficits

Clinical Presentation:
• Varies
• As illustrated by the GMFCS, gross motor abilities also vary greatly
• Gross motor function limitations are due to a combination of:
o MSK impairments (spasticity, strength, range of motion, skeletal alignment)
o Sensory deficits (visual, proprioception, vestibular)
o Motor coordination impairments

PT PERSPECTIVE
BODY STRUCTURE & FUNCTION
Impairments:
• Hypertonia – spasticity, dystonia (primary)
o Classic muscles affected:
▪ U/E: shoulder adductors/IRs, elbow flexors, forearm pronators, wrist flexors, finger flexors, thumb
adductors/flexors
▪ L/E: hip flexors/adductors, knee flexors, ankle PFs
▪ Commonly affects bi-articular muscles: biceps brachii, gracilis, hamstrings, gastrocs
• Decreased strength (primary and secondary)
o Spastic muscles are weak – primary impairment
▪ Longer sarcomeres
o Can also develop weakness from disuse – secondary impairment
▪ Decreased muscle volume
o Weakness is seen in decreased power generation and decreased endurance
o Antagonist muscles of spastic muscles are also commonly weak (i.e. tib ant, quads, hip extensors, hip abductors)
• Decreased PROM (secondary)
 o Bones lengthen at the growth plates, but the muscles grow through stretch (typically through physical activity)
o Due to spasticity, and limited physical activity, spastic muscles in children with CP don’t lengthen as much as
typically developing children during skeletal growth
o Lack of muscle lengthening during skeletal growth leads to limitations in associated joint mobility
▪ e.g. gastrocs don’t grow in proportion to tibia, leading to progressive loss of ankle PF ROM
o Increased muscle stiffness is also noted in spastic muscles due to:
▪ Changes in ECM
▪ Increased fibrosis
o Muscle stiffness also limits mobility of associated joints
o Classic ROM limitations:
▪ U/E: shoulder abduction, elbow ext, forearm sup, wrist ext, finger ext, thumb abd/ext
▪ L/E: hip ext/abd, knee ext, ankle DF
• Skeletal malalignment (secondary)
o Alterations to posture and alignment due to development or persistence of bone or joint deformities
o Caused by:
▪ Abnormal skeletal development
▪ Increased tone pulling on developing skeleton
▪ Abnormal ground reaction force on developing skeleton
o Common skeletal malalignments:
▪ Joint contractures (intra-articular)
▪ Scoliosis/kyphosis
▪ Hip subluxation/dislocation
▪ Excessive torsion of femur/tibia (e.g. femoral anteversion)
▪ Malalignment of the foot and ankle (pes cavus, hallux valgus)
▪ Leg length discrepancy
• Balance and postural control (primary)
• Decreased motor coordination (primary and secondary)
o Difficulty sequencing muscles to perform task effectively and efficiently
▪ Incorrect muscles are activated, co-contractions present
▪ Difficulty grading muscle activation
• Sensory deficits (primary)
o Decreased proprioception
o Visual impairment
o Vestibular dysfunction (auditory impairment)
• Pain (secondary)
o Spasms (spasticity)
o Muscle soreness/fatigue (strength/alignment)
▪ Quads, calves, hip extensors
o Joint pain (skeletal malalignment)
▪ Low back pain, patellofemoral syndrome, hip dislocation
o Overuse injury (strength/alignment)
▪ Patella tendonitis, rotator cuff tendonitis, lateral epicondylitis
o Pain due to excess pressure on specific area
▪ Feet, knees, spine, any bony prominence

ACTIVITY/FUNCTION
• Limited gross function:
o Head control
o Ability to sit/stand
o Transitional movements (lie to sit, sit to stand, etc.)
 o Ambulation
o High level balance skills
• Abnormal postures
• Abnormal gait

GAIT CLASSIFICATION
• Categorize the most common gait patterns seen with 3D analysis – testing can be done with gait aids and orthoses
o Separate classification systems for diplegic gait and hemiplegic gait
• Spastic diplegic classification: identifies the static position of each lower limb in midstance in sagittal plane
o There can be different classification for each leg
• Spastic hemiplegic classification: identifies static position of hemiplegic limb in midstance in sagittal plane and may
describe the limb position at other phases of gait cycle

PT GOALS
• YouTube – goals of PT
o CP: damage to motor brain in development; weakness and involuntary movement
o Previously, did more hands-on skills (stretching, different positions) – now, focus on functional goals
o What can child do? Challenges? What does the child like to do? – incorporate exercise into daily activities
• YouTube = importance of activity and motor interventions for individuals with CP
• PT goals:
o Maximize present and future gross motor function
o Prevent secondary impairments
o Goals must be consistent with client and family goals
o Optimize quality of life
▪ Function (mobility, independence, ADLs)
▪ Pain
▪ Ease of caregiving for caregivers

MANAGEMENT
• 6 key areas of child development, building on ICF framework
o Function
o Family
o Fitness
o Fun
o Friends
o Future (includes expectations and dreams)
• Approach to childhood disability
o Family centred care – parents are experts in their child; recognize family strengths and individuality; respect
different values and preferences
o Clinicians bring knowledge/expertise to the table with evidence-based practice
• Aim of PTs: maximize quality of life via
o Optimize gross motor function/mobility
o Independence with ADLs
o Participation in leisure, recreational and physical activities
o Optimize ease of caregiving
o Decrease pain
o + manage/minimize secondary complications related to underlying impairments – must know natural history and
prognosis
 • Why treat hypertonia?
o Mobility goals – GMFCS level 1-3: gait stability and efficiency (endurance), standing balance, transitions (pull to
stand); GMFCS level 4: participation in transfers, sitting balance
o Ease of caregiving (dressing, diapering, bathing)
o Pain (muscle spasm)
o Positioning (seating tolerance, standing frame, ease of putting on AFOs/ankle foot orthosis and tolerance)

PT HYPERTONIA OBJECTIVE ASSESSMENT

[1] ASSESSMENT OF MUSCLE TONE
• Hypertonia Assessment Tool (HAT): TYPE OF TONE
o Use to discriminate/classify the type(s) of tone present (spasticity, dystonia, rigidity)
▪ YOU NEED TO KNOW WHAT TYPES OF HYPERTONIA IS PRESENT TO GUIDE YOUR TREATMENT
CONSIDERATIONS
o The HAT has 7 items, and each limb is tested separately
• Assessing SEVERITY AND LOCATION:
o Modified Ashworth Scale (MAS) or the Modified Tardieu to quantify severity of tone
o Modified Ashworth Scale:
▪ Quantifies resistance to passive movement (muscle tone)
▪ 5 defined grades from 0 to 4
o Modified Tardieu Scale:
▪ Measure of severity of spasticity by assessing muscle response to stretch at different velocities
▪ We get info about severity of spasticity and passive ROM
▪ R1: angle of spastic catch with rapid passive movement
▪ R2: angle of passive ROM
▪ The earlier the R1 value, the more significant the spasticity
▪ The difference between R1 and R2 is often called the dynamic window and this is the range where tone is
having most impact on function
[2] ASSESSMENT OF RANGE OF MOTION
• Movements most commonly assessed:
o Hip abduction (assessing tone and ROM through hip adductors)
▪ With the hip and knee flexed targeting adductor longus, magnus and brevis
▪ With the hip and knee extended targeting the gracilis
o Knee popliteal angle (assessing tone and ROM through hamstrings)
o Ankle DF (assessing tone and ROM through the plantarflexors)
▪ With the knee flexed targeting the soleus
▪ With the knee extended targeting the gastrocnemius

[3] GAIT AND MOBILITY

• Observe gait pattern with and w/o AFOs (from front, back, side)
• Observe foot contact throughout gait cycle (at initial contact, midstance, and timing of heel strike)
• Knee position midstance – flexed, extended, hyperextended
• Base of support – watch for adducted femurs, feet approaching or crossing midline
o Think about gait classifications!
o Observe other relevant functional activities (transfers, sitting balance, standing posture)
• Observational gait activity: YouTube – Sam at Gillette

o
o Gait with AFOs – apparent equinus
▪ Initial foot contact: toes first
▪ Foot contact at midstance: still just toes, legs never straighten
▪ Knee position at midstance: flexed
▪ Base of support: narrow – knees closer together than feet
▪ Hips: -
o Barefoot gait – left side has consistent jump knee gait; right side also jump knee gait but some equinus gait
 ▪ Initial foot contact: toes only, part of the area right below the toes (sometimes right foot will be flat)
▪ Foot contact at midstance: heels up, more pronounced when moving faster
▪ Knee position at midstance: flexed
▪ Base of support: narrow
▪ Hips: -
• Gait assessment tools:
o Observational gait scale (OGS): assess gait treatment outcomes in clinical setting, specifically the knee joint and
foot position at mid-stance
o Edinburgh visual gait scale (EVGS)
• HYPERTONIA AX SUMMARY:
o Subjective hx focus on impact of hypertonia on mobility/function, ease of caregiving, pain, positioning
o Info on orthotics, mobility, positioning equipment
o Objective exam: assess tone (HAT determines type of tone, Tardieu or MAS quantifies tone); PROM (R2);
observation of gait; observe other relevant functional mobility skills; alignment, strength, selective motor control
• Hypertonia management: intervention is goal directed to improve QOL (gross motor f(x), pain, ease of caregiving)
o Orthoses (ankle foot orthotics/AFOs)
o Botulinum toxin (BTX)
o Selective dorsal rhizotomy (SDR)
o Intrathecal baclofen (ITB)
o Deep brain stimulation (DBS)
o Oral medications (oral Baclofen, trihexyphenidyl)
o Intervention is goal directed to improve QOL (gross motor function, pain, ease of caregiving

Orthoses:
• Ankle foot orthotics (AFOs) are the most common type of orthotic used in children/youth with CP
• Goals for the use of AFOs with hypertonic gait:
o Improve foot contact for stability (minimize toe contact)
o To improve foot clearance during swing (help prevent tripping)
o Help protect alignment of the foot and ankle
o There are different types of AFOs, 2 of the most common
▪ Rigid – do not allow for any movement at the ankle
▪ Hinged – allow for DF at the ankle (PF remains blocked)
o AFOs also play an important role in maintaining ankle DF ROM

Botulinum Toxin A (neurotoxin)

• Focal hypertonia management (injected into specific muscles)
• Temporary effect
• Antispastic effect appears within 24h to 3 days, max effect at 10 days to a month, noted benefits generally last 3-4 months
• Works at level of neuromuscular junction by inhibiting release of acetylcholine from the motor neuron
• Side-effects – most common is weakness in adjacent muscles caused by diffusion of BTX and less commonly can cause
weakness in more distant muscle groups
• BTX A Indications:
o Objective exam indications:
▪ Early R1 value in the range with a relatively large difference between spastic catch (R1) and PROM (R2)
• This means significant tone is present with an opportunity to increase functional range of motion
if tone is decreased so that R1 occurs later in the range (approaches R2)
▪ No significant fixed contractures:
• Botulinum toxin does NOT treat contractures
▪ Evidence of spastic gait/stance through observation
▪ Adequate underlying strength
 ▪ Good underlying general health (no recent pneumonia, no aspiration with feeding or swallowing
difficulties, no breathing difficulties – think risk for potential of diffusion or BTX toxin muscle groups
responsible for breathing and swallowing functions)

Post BTX Management:

• Possible role for serial casting to improve ROM for mild contractures (most commonly at the ankle)
o Serial casting at the ankle is when a below knee cast is applied for 7-10 days providing a prolonged low load stretch
to the plantar flexors. The cast is removed and often a second cast is applied stretching further with the range that
is gained. There are no weightbearing restrictions, walking and activity is encouraged!
o Use of orthotics (AFOs)
o Functional goal directed PT when gross motor goals identified (PT 1x/week for 6-12 weeks depending on goals)
o Home stretching/strengthening program
o Return to hypertonia clinic for reassessment in 4-6 months time

Selective Dorsal Rhizotomy (SDR)

• Permanent surgical procedure to reduce spasticity – can reduce spasticity in multiple muscle groups
• Surgical procedure:
o Laminectomy to expose nerve roots
o Each sensory nerve root is subdivided into 4-5 rootlets from L1 to S2
o Each rootlet is stimulated to identify the ones contributing the most to spasticity
o A % of these rootlets are cut – by cutting a % of sensory/dorsal nerve rootlets, the excitatory afferent input is
decreased on motor neuron = less motor output
• Selection guideline: most performed with spastic diplegic subtype (can have mild dystonia present, but spasticity must be
dominant)
o Mostly performed in children at GMFCS levels 2 or 3 (1 or 5 can be considered in certain circumstances)
▪ Typically, 4-8 years old
o Adequate underlying strength
o Sufficient motor control (not mass flexor or extensor patterning; look for ability to dissociate movement)
o Ability to participate in therapy post-op
• Goals: LTG are individual to the client but in general
o Improve gait pattern and functional mobility
o Improve gait efficiency (speed/oxygen cost)
o Improve independence with ADLs
o Decrease pain
o Improve gross motor function/ability to walk, greater ease of completing ADLs, improved motor patterns
decreased energy expenditure b/c of reduced spasticity
• Video: knees always bent in walking, slight limp/unsteady movement; after – much smoother, looks normal
• SDR post-op PT: goal-directed, activity/task-based intervention
o Follows principles of motor learning
o Practice new motor patterns with reduced spasticity
o Strengthening – both functional and isolated (as indicated)
• SDR 0-3 months post-op, GMFCS levels 1-3: PT/PTA 5 days/week, OT/OTA 2-3x/week
o Therapy focus – strengthening and postural control, ROM, positioning
o Strengthening focus – proximal muscle groups (hip extensors, flexors, abductors, quads, hamstrings) & trunk
strengthening
o Standing, gait, functional mobility activities gradually introduced, independence with ADLs
o Equipment: AFOs (usually rigid), wheelchair, stander, walker, tricycle
• SDR 3-6 months post-op, GMFCS levels 1-3: PT/PTA 2x/week
o Increased ambulation – treadmill training, gait pattern, endurance
o Continue to reassess use of gait aids as indicated for patterning, stability or endurance
 o Strengthening – continue to work on proximal muscle groups and incorporate ankle PF/DF
o Static and dynamic balance – focus on weight shift, core stability during movement
o Refine skills working on improved dissociation
o Maintaining ROM
• SDR 6-12 months post op, GMFCS levels 1-3: PT 1-2x/week delivered by PT/PTA/group program if appropriate
o Maximize independent mobility within home and community settings (+/- gait aid), endurance, functional goals
specific to individual
o Participation in adapted sport and leisure activities is encouraged
o Focus:
▪ Strengthening – progress LE strengthening
▪ Increased independence and challenging gross motor coordination, higher level balance and agility skills
▪ Community sports – martial arts, sports, dance
▪ Maintain ROM

Intrathecal Baclofen Pump (ITB Pump) Mechanism:

• Precise mechanism of action of baclofen not fully understood
• Works at lvl of spinal cord by inhibiting monosynaptic & polysynaptic reflexes possibly by decr. excitatory NT release
• Pump is surgically implanted under the skin of abdomen and a catheter delivers baclofen directly to the intrathecal space
• Side effects:
o Abrupt discontinuation of intrathecal baclofen result in high fever, altered mental status, increased
spasticity/rigidity and in rare cases rhabdomyolysis
▪ This can be from catheter dislodgement from the intrathecal space, catheter breaks, pump fails
o This means the client needs to live close to a medical facility that can address these emergency situations
o Other considerations:
▪ Pump needs to be refilled periodically, needs to be replaced ~7 yrs (battery life)

Deep Brain Stimulation (DBS):

• Neurological procedure to treat dystonia
• A stimulator is placed in the chest (subclavicular region) and connected to electrodes in the brain via extension leads/wire
(like the function of a cardiac pacemaker)
• Mechanism of action is by neuromodulation - stimulating or inhibiting – cellular functions in the brain: cell-cell signalling
and communication
• DBS changes the ability of the stimulated areas of the brain to fire – this impacts other parts of the brain the stimulated
areas communicated with, and ultimately alters patterns of brain activity and associated movement
• Can see some response immediately related to the change in brain activity that occurs bc of stimulation – often takes weeks
to months to see full benefits from stimulation related to the effects of neural plasticity in the presence of
neuromodulation
• Side effects:
o Risk of infection is the biggest adverse side-effect
o Hardware complications
o Other considerations:
▪ Need for adjustments to stimulator settings based on response and due to the longer-term effects of
neuromodulation (brain plasticity)
▪ Battery replacement of stimulator required

ITB & DBS Indication/Goals:

• Goals:
o Decrease pain
o Improve ease tolerance of seating/wheelchair
 o Improve quality of sleep (decreased waking and need to reposition related to discomfort)
o Improve ease of caregiving (dressing, diapering, bathing, lift transfers)
o Not functional mobility goals
• Indications:
o Severe generalized hypertonia
▪ ITB pump spasticity and/or dystonia
▪ DBS dystonia
▪ Generally, GMFCS level V (dependent for mobility and ADLs)
▪ Rely heavily on subjective history from caregiver

ORTHOPAEDIC CONDITIONS
• Secondary impairment
o Soft tissue tightness/joint contractures/skeletal malalignments develop which significantly limits QOL
o Decreased function (gross motor, mobility, fine motor, ADLs)
o Pain
o Difficulty for caregivers to manage client’s care (diapering, dressing)
• Common conditions:
o Equinus contraction – most common ortho condition in CP
o Knee flexion contracture
o Hip flexion contracture
o Hip adduction contracture
o Patella alta
o Femoral anteversion
o Excessive tibial torsion
o Foot deformity
o Leg length discrepancy
o Hip displacement
o Scoliosis
• Single event multi-level surgery (SEMLS): single surgery to address multiple issues (orthopedic) at the same time
o Avoids undergoing multiple procedures; key is to time procedure to minimize additional surgery
o Try to delay if possible since risk of orthopedic abnormalities after surgery is greater when increase amounts of
skeletal growth remains
o Soft tissue release, osteotomies, and/or tendon transfers
• Soft tissue procedures:
o Increase ROM
▪ Tendon lengthening
▪ Intramuscular lengthening
▪ Tenotomies
▪ Common muscles: hip flexors, hamstrings, hip adductors, ankle plantarflexors
o Reduce muscle imbalance
▪ Tendon transfers
▪ Common muscles: rectus femoris, tibialis posterior
Osteotomy:
• Improve bone alignment
• Proximal femoral varus derotation osteotomy
• Tibial derotation osteotomies
• Distal femoral extension osteotomies
• Foot surgery, spine fusion
Goals of Surgery:
• Improve muscle length/skeletal alignment, improve joint ROM
• Improve posture/alignment/gait, ease caregiving ease positioning
• Improve muscle length/skeletal alignment
• Improve joint ROM, improve function, decrease pain
• Improve posture/alignment/gait
• Ease caregiving, ease positioning

Post-OP Management:
• Maintain ROM – stretches and positioning
• Strengthening, balance, coordination
• Gait re-education
• Equipment: walkers, standers, orthoses, wheelchairs
• 3-9 months to return to pre-op functional status

Key Points
• Treatment is goal-directed (think of 6Fs)
o Use natural history and prognosis knowledge when developing management plan
• Use AFOs:
o Optimize foot contact (stability), foot clearance, knee extension during gait and bipedal activities
o Maintain ankle DF for ROM
• If significant limitations in ROM/skeletal malalignment tis present, consider orthopedic surgery
• Use HAT to determine what types of hypertonia are present
• Modified Tardieu to quantify tone and PROM

Botulinum Toxin (Temporary) SDR (Permanent) ITB and DBS (Reversible)

Problem is fairly focal
Spasticity or dystonia
GMFCS 1-5
Large difference (dynamic window)
between R1/R2; no significant
contractures, breathing/feeding issues
Goals – improve mobility, caregiving,
decrease pain
Therapy post-Botox if functional goal
identified
Spastic diplegia affecting multiple muscle Significant generalized hypertonia (DBS –
groups in LE dystonia ITB spasticity &/or dystonia)
GMFCS II/III (some I & IV) Generally, GMFCS level V
Large difference R1/R2
No significant contractures, underlying
strength is good and motor control
GMFCS 1-3: functional mobility goals and Goals related to comfort and ease of
decreased pain caregiving
GMFCS 4: caregiving, pain, potentially
increased sitting balance
Intensive PT post-op Generally, no role for active therapy

Introduction to Neuroscience
• Anatomical terms: locate structures in relation to anatomical axes or other structures
Term Definition
Anterior In front of, toward the face
Posterior Behind, toward the back
Superior Above, toward the head
Inferior Below, toward the feet
Medial Toward the middle
Lateral Toward the edge/outside
Dorsal Toward the top of the brain or back
Ventral Toward the bottom of the brain or front
 Rostral Toward the front of the brain or top
Caudal Toward the back of the brain or bottom
• Directional terms: rostral = top of body, front of brain; caudal = bottom of body, back of brain

o
• Anatomical planes: sagittal, horizontal, coronal/frontal

o
o Sagittal: divides left and right (e.g. hot dog bun)
o Horizontal: cuts at right angle to long axis of the structure (e.g. cutting a bagel)
o Coronal (frontal): divides front and back (e.g. slicing bread)
• Human brain: 1.5kg (2% of body weight), with 86 billion neurons and 100-500 trillion synapses → equivalent to the number
of stars in the Milky Way
• Neuron: cell of the nervous system (basic building block)

SOMA

o
o Dendrites: input site, connect with other neurons to feed information into the cell
o Axon: output site, sends information to other neurons
o Can be myelinated or unmyelinated
o Myelin: insulation, high fat content which makes it appear white
• White matter: axons – projections of neurons, convey info away from cell body; myelin – insulating layer around axons
o Function: send signals (actional potentials) & convey information
o If neurons are bundled/grouped together: tract, lemniscus, fasciculus, column, peduncle, capsule
 • Grey matter: neuron cell bodies
o Function: integration
o If neurons are grouped together: ganglion (sing.)/ganglia (pl.), nucleus (sing.)/nuclei (pl.)
o Nucleus/nuclei for the CNS (brain & spinal cord), ganglion/ganglia for the PNS
o Dendrites that come off cell bodies, convey and integrate the info
• Divisions of nervous system: peripheral NS and central NS

PERIPHERAL NERVOUS SYSTEM

• Structures outside the brain and spinal cord that aren’t encased in bone
• Somatic NS: controls muscles, relays sensory info – voluntary mvmt, reaches consciousness (sensation)
• Autonomic NS: involuntary bodily function (e.g. regulate heart rate, glands, organs)
o Contents: cranial nerves, spinal nerves, peripheral nerves, neuromuscular junction
• Function: transmit info between brain and body
o Afferent: peripheral to central
o Efferent: central to peripheral

CENTRAL NERVOUS SYSTEM

• Spinal cord, brain (cerebrum, cerebellum, brainstem) – three regions (spinal cord, brainstem & cerebellum, cerebrum)
o Spinal cord: contained in vertebral column; foramen magnum to L1
o Brainstem & cerebellum:
▪ Brainstem (hindbrain) – cylinder shape, wider at top
▪ Cerebellum – 2 hemispheres connected to posterior brainstem
o Cerebrum: two cerebral hemispheres + diencephalon = forebrain
• [1] Spinal cord: adult SC is shorter than vertebral column (C1-L1)
o The nerves that come out lower than L1 are the cauda equina, innervating the lower extremities
o SC level ≠ vertebral level below C2; labelling is similar to vertebra (cervical, thoracic, lumbar, sacral)
▪ First nerve exits above C1 vertebra, second nerve exits below C1 vertebra
▪ The level of SCI = level of the orthopedic (vertebra) injury OR the level of the nerve (spinal cord)
o Functions: convey somatosensory and autonomic info to brain; convey signals from brain to control movement
and autonomic function

o
• [2] Brainstem
o Structure: cylinder shape, wider at the top
o Midbrain (closest to brain), pons, medulla (closest to spinal cord)
o Functions: equilibrium (vertical position, postural control), cardiovascular activity (heart rate, vasal tone,
vasodilation), respiration, eye movements
▪ Functions are not consciously controlled

o
• [2] Cerebellum
o Structure: 2 hemispheres connected to the brainstem posteriorly by peduncles
o Peduncles: axons that are bundled together, two stalks attaching cerebrum to brainstem
o Function: motor coordination and motor learning

o
• [3] Cerebrum
o Forebrain – divided into diencephalon (interior) and 2 cerebral hemispheres (exterior, covers diencephalon)

o
• [3] Diencephalon
o Structures: thalamus, hypothalamus, epithalamus, subthalamus (lateral to the section)
o Functions: consciousness, arousal, homeostasis, endocrine function
 o
• [3] Hemispheres
o Surface – grey matter
▪ Gyrus/gyri: rounded elevations
▪ Sulcus/sulci: grooves
o Many functions
o Deeper surface – white matter (axon bundles); defined as tracts or capsule
▪ Connect different areas of brain

▪
o 6 lobes: frontal, parietal, temporal, occipital, limbic, insular

MENINGES
• 3 layers of connective tissue [PAD deep to superficial, from internal/brain to external/skull]
o Dura mater – tough membrane, next to skull
o Arachnoid mater – delicate web-like membrane
o Subarachnoid space – cerebrospinal fluid
o Pia mater – delicate membrane, stuck to brain surface and spinal cord

•
• Function: protection (shock absorber and anchor), support system (for blood vessels, nerves coming out of spine, CSF)
CEREBROSPINAL FLUID (CSF) & VENTRICLES
• Functions:
o Protection: CNS is floating in CSF to provide buoyancy and shock absorption
o Nourishment: provides elements of nutrients
o Waste removal: dead cells, remove things that must be cleared away, by-products of neural activity
• Components: 4 ventricles, CSF, choroid plexus
o Ventricles: cavities inside the brain
o CSF: clear fluid that is a modified filtrate of plasma; secreted by choroid plexus
o Choroid plexus: secretory tissue found inside each ventricle
• Ventricles: 2 lateral ventricles (numbered 1 and 2); third ventricle; fourth ventricle

o
Name Location
Lateral (2) ventricles Cerebral hemispheres
Interventricular foramen
Third ventricle Diencephalon
Cerebral aqueduct
Fourth ventricle Posterior to medulla and pons; anterior to cerebellum
Pass into subarachnoid space
o Flow: choroid plexus → LV → interventricular foramen → 3rd → cerebral aqueduct → 4th → pass into
subarachnoid space

Theories of Motor Control

• Motor control: ability to regulate or direct the mechanisms essential to movement; how the CNS produces purposeful,
coordinated movements in its interaction with the rest of the body and the environment
o Reason to learn theories: conceptual framework on how movement occurs and framework for clinical practice
• Motor redundancy/abundance: repetition without repetition; multiple ways to execute a specific movement and achieve
equivalent outcomes
o E.g. motor task of reaching to and grasping a cup – multiple joints and muscles used, multiple trajectories and grips
• Feedforward control: signal from source to load in external environment
Past experiences
Sensory input Motor Centre Motor Output
Anticipation

Motor
Command
o
o Source can also include executive function e.g. anticipation, motivation
o Sends signal for impetus to move → motor centre creates motor command → send down spinal cord out to
peripheral system to neuromuscular junction for motor output
o From top to bottom
• Feedback control: new information generated by sensory system provides status about system and whether goal was
achieved

Information about
Motor Centre Motor Output
system status

Motor
Command

feedback
o
o New information generated by sensory system provides status about system (body position in space) and whether
goal was achieved (if movement occurred as expected; if it wasn’t achieved then info about whether there were
errors)
▪ Info sent back to motor centre as feedback – subsequent commands can be adjusted depending on
whether goal was achieved
o NOTE: most movement involves both feedforward and feedback control; no one model can fully explain all the
complex movement and behaviours that are observed (concept of false dichotomy)
• Gentile’s taxonomy of tasks: 2 general characteristics of all skills are: [1] environmental context & [2] function of the action
o Acts as a guide/framework for:
▪ Understanding how skills are distinct and/or related to other skills + how they build to advanced skills
▪ Understanding the demands placed on person to perform the skill (what is hard or easy, how to modify
the task for people to be successful) → can match up to current functional status
▪ Assess movement problems
▪ Progress exercises (e.g. poor balance control – start with standing without control; can progress by adding
object manipulation while standing OR change environment to make it unpredictable)
o Can have either body stability (not moving through space) or body transport (moving through space)
o Taxonomy: classification system that is organized according to relationships among the component characteristics
of what is being classified
 • Understand how movements are
related to each other and build up to
more advanced skills
• Know the demands placed on person
to perform a skill (which tasks are
hard, easy, how to modify for people
to be successful)
• Also know how to progress an exercise
(e.g. add object manipulation)

o
• History of motor control theories:
o 1920s: reflex theory
o 1940s: hierarchical theory
o 1960s-present: systems theory
• Reflex theory: reflex is the basic unit of behaviour and are the building blocks for complex behaviour
o Studied reflexes mediate by spinal cord – feedback control
o Reflex chaining: stimulus → response (stimulus) → response (stimulus) [fly → tongue out → tongue in → swallow]
o Disproved: voluntary movement, internally generated movement, motor learning (e.g. learn to play violin),
reacting differently to same stimulus, control component movements, overriding reflex (hold a hot mug)
• Hierarchical theory: nervous system has hierarchical organization; each successively higher level exerts control over the
level below it (brain – highest; brainstem – middle; spinal cord and periphery – lowest)
o Reflex is not the only form of neural control; there are different levels of neural control – feedforward control
o Motor development: appearance and disappearance of reflexes
▪ Initially, only lowest levels are “online” – with development, higher levels become active
o Brain pathology: results in persistence of primitive lower-level reflexes
o Disproved: existence of Babinski reflex, reflex from hand on hot surface, adjusting movement midway, spinal cord
reflexes, central pattern generators (for walking)
• Systems theory: movement is not exclusively controlled by the central or peripheral systems, but motor control is a
distributed process
o Movements are produced by interactions among multiple systems
o Nervous system governs rather than produces/programs movement – CNS takes advantage of motor abundance
o Task + Individual + Environment → Movement
o TASK: Gentile’s taxonomy of tasks; break into components
▪ Discrete (e.g. pick up object) vs. continuous (e.g. run/walk)
 ▪ Stability/base of support (is balance involved?)
▪ Manipulation (involvement of hands; single-handed or both hands)
▪ Attention demands (intense focus or can be distracted)
▪ Variability of task (does it change over time)
▪ Biomechanical demands (range of motion required)
o INDIVIDUAL:
▪ Cognition – executive function, are they aware of any deficits?
▪ Perception – sensory abilities – can they sense and detect/interpret properly?
▪ Action – how is their movement? Is there enough strength? Can they produce it? Do they have endurance
to reliably produce it over time?
o ENVIRONMENT:
▪ Regulatory – shapes movement, interacts with the task (e.g. angle of walking surface, shape of ball)
▪ Non-regulatory – affects performance, interact with individual (e.g. background noise, air temperature)
o Limitation: only tells you what might influence the movement, doesn’t describe how movement is accomplished
• History of therapeutic approaches:
o 1940s-1950s: muscle re-education
o 1950s-present: neurophysiological
o 1980s-present: motor learning/task oriented
• Muscle re-education: developed during polio epidemic, aim to change muscle function
o Strengthen weak muscles, supports & bracing to compensate for impairments
o Advantages: useful in polio, increase strength, focused approach
o Limitations: aimed at degenerative/weakened muscle conditions, not a whole-body approach, ignores CNS training
• Neurophysiological: aim to modify CNS
o Retrain motor control by facilitating/inhibiting movement patterns
o Brunnstrom, Rood, sensory integration, proprioceptive neuromuscular facilitation (PNF), neurodevelopmental
treatment (NDT), Bobath (historical)
o Advantages: can cover range of movements, works for lower cognitive capacity people (e.g. infants) or those with
lower function/independence/motor control (cannot problem solve), takes advantage of reflexes and central
pattern generators, facilitates movement patterns in SCI (neuroplasticity)
o Limitations: forcing disuse could weaken unaffected side, might be overstimulating, commands are not direct so
could be frustrating, passive (doesn’t promote agency); little carryover to functional tasks
• Motor learning/task-oriented: aim to shape observed behaviour, help patient learn various ways to solve task
problem/achieve their goal; the key is changing the environment and task demands
o Assumptions: observed movements in patients with neurological lesion represent behaviour that emerges from
systems remaining; patients learn actively by attempting to solve the problems inherent in a functional task
o E.g. task oriented: constraint induced movement theory (constrain unaffected hand/arm to force affected use)
▪ Forced use and repetitive practice, mostly for stroke patients
o E.g. motor learning: active problem solver, emphasizing biomechanics and behaviour context of movement
▪ Circuit training and functional tasks training (e.g. picking up object from ground on the side while sitting –
initially have forward trunk flexion ∴ move glass higher to isolate lateral side trunk flexion)
o Advantages: more functional, carryover into daily tasks, encourages independence and future problem solving
o Limitations: must learn for each specific task, depends on cognition and independence, could be overwhelming or
frustrating, might not address individual patient issues (if it’s a circuit)
Somatosensory Peripheral
Concepts and Terms
• Stereognosis: ability to perceive form through touch (familiar object)
o CNS reconstructs coherent image form fragmented info conveyed from multiple neurons, sensory receptors in
hand
o Objects stimulate large population of sensory neurons on hand
o No single receptor/single axon will send all relevant info to brain
• Peripheral somatosensation: info from skin and MSK conveyed to spinal cord
o Purpose: investigate world, avoid injuries, move accurately
o Modulate movement resulting form higher centre commands; stimuli for reflexive movement; modulate output of
central pattern generators
o Conscious sensation: info reaches thalamus or cerebral cortex – sensory input is received
o Unconscious: sensory input is used but we aren’t aware of it/no perception (e.g. cerebellum uses sensory input to
modify motor output)
• Types of somatosensation:
o Cutaneous: sensory info from skin (touch – superficial, vibration), temperature
o Proprioception: sensory info from MSK (static joint position sense, kinesthetic sense)
o Nociception: info about tissue damage or potential tissue damage
Sensory Receptors
• Sensory receptors: located at distal ends of peripheral neuron
o Specialized end organ/structure or free nerve endings
o Sensitive to stimuli (e.g. touch, chemicals, temperature)
o Types according to stimulus:
▪ Mechanoreceptors: mechanical deformation of the receptor (touch, pressure stretch, vibration)
▪ Chemoreceptors: exogenous chemicals or substances released by cells
▪ Thermoreceptors: respond to heating or cooling
o Types according to signalling
▪ Tonic: responds the entire time a stimulus is present
▪ Phasic: adapt, stops responding while stimulus is still present (fires at beginning and end)
Primary Afferent/1st Order Neuron
• Primary afferent/1st order neuron: dorsal horn; pseudo-unipolar
o Has central axon (connected to spinal cord; conduct signal from T-junction to spinal cord) and peripheral axon
(connects to sensory receptor/end organ/free nerve ending; conduct signal from receptor to T-junction)
o T junction: between peripheral axon-soma-central axon
o Soma/cell body located outside the spinal cord in the dorsal root ganglion
• Classification of primary afferents – by axon diameter, by tissue they innervate
o MSK afferents (+ AXON DIAMETER -): Ia – Ib – II – III – IV
o Cutaneous afferents (+ AXON DIAMETER -): Aβ (similar size to II) – Aδ (similar size to III) – C (similar size to IV)
o Transmit signals from mechanical: Ia, Ib, II, Aβ
o Transmits signals from mechanical, thermal, chemical stimuli (polymodal): III, IV, Aδ, C
Coding Sensory Information & Peripheral Receptors
• Somatosensory system codes 4 types of info: modality, location, intensity, timing
o Modality: coded by receptor type (each receptor responds to one type of stimulus)
o Location: coded by receptive field (areas of skin from which sensation is perceived or area of skin innervated by
single primary afferent neuron)
o Intensity and timing: coded by signal pattern
o Fingers have smaller receptive fields and more primary afferents – 2-point discrimination is more sensitive
• Peripheral receptors:
o Muscle spindles
 o Golgi tendon organs (GTOs)
o Joint receptors
o Cutaneous receptors
• Muscle spindle:
o Structure: intrafusal fibres; sensory neurons (Ia, II); gamma motor neuron endings
o Detects: absolute muscle length, changes in muscle length
o Function: spinal level – stretch reflex; ascending – regulates muscle length during movement, contributes to sense
of effort
• Golgi tendon organ:
o Structure: spindle shaped receptor at muscle-tendon junction; Ib sensory fibre
o Detects: muscle tension
o Functional: spinal level – inverse stretch reflex autogenic inhibition [if stretched, causes it to relax]
o Ascending: modulate muscle output in response to fatigue
• Joint receptor:
o Different types within joint capsule and ligaments
o Detects: deformation of structures in which they are embedded
o Function (debate): minor influence on perceived joint angle (especially during rapid movements)
• Cutaneous receptor:
o Structure: different types of receptors within layers of skin
o Detects: pressure, vibration, temp, tissue damage
o Function spinal level – placing reaction and withdrawal reflex movements
o Ascending = info about body position for orientation within environment
• Somatosensory pathway
Neuron From To
First order Sensory receptor Brainstem
Second order Brainstem Thalamus
Third order Thalamus Cerebral cortex
• Pathway:
o 1st order neuron/primary afferent enters through dorsal root into the dorsal horn of the spinal cord
o White matter is more exterior, grey matter more interior in spinal cord

Somatosensory Central
• Peripheral somatosensory system: info coded by receptors; info relayed to spinal cord/brain stem
• Central somatosensory system: how CNS processes this info
• Distinctions:
o Sensory info: impulses/action potentials; generated from original stimulus
o Sensation: awareness of sensory stimulus
o Perception: interpretation of sensory information; takes a meaningful form
• 3 neuron pathway – only counting projecting neurons (interneurons are along the pathway)
 o Some pathways named for origin & termination of the tract in which 2nd order neuron is located
• 3 types of pathways bringing somatosensory info to the brain:
o Conscious relay pathways
▪ Highly detailed – location, size, intensity
▪ Somatotopically arrange
▪ Light touch, proprioceptive, nociceptive, temperature
▪ Leads to conscious perception – sent to somatosensory cortex
o Nonconscious relay pathways
▪ Highly detailed
▪ Somatotopically arranged
▪ Proprioceptive information
▪ Non consciously aware of information – sent to cerebellum
o Divergent pathways
▪ Less detailed (e.g. dull aching pain)
▪ Info sent to brainstem and areas of the cerebrum
▪ Used in both conscious and nonconscious processes

Dorsal Column Medial Lemniscus Pathway

Type of Pathway Conscious relay
Information Carried Light touch, vibration, discriminative touch, proprioception
Role of Information Fine motor control, smooth/coordination of movement, stereognosis
1st Order Neuron Sensory receptor → medulla (brainstem) • FG – more medial neurons
Ascends in ipsilateral dorsal column of spinal cord • FC – more lateral neurons
Fasciculus gracilis – axons from lower body (T6 & below) • Terminate in medulla in
Fasciculus cuneatus – axons from upper body corresponding nuclei
• Pseudounipolar neuron,
enters cord through dorsal
horn
2nd Order Neuron Medulla/brainstem → thalamus (ventral posterolateral nucleus VPL) • Crosses midline
Cell body in medulla = nucleus gracilis & nucleus cuneatus
Axon crosses over to contralateral side
Ascends in medial lemniscus tract
3rd Order Neuron Thalamus → primary somatosensory cortex • Originates in VPL of thalamus
Originate in ventral posterolateral nucleus of the thalamus • Terminates in somatosensory
Ascends as part of internal capsule cortex
• Axons are part of internal
capsule

Spinothalamic Tract
Type of pathway Conscious relay
Information carried Nociception, temperature, crude touch
Role of information Fast nociception, localize site of noxious stimuli
st
1 order neuron Free nerve ending → dorsal horn (Aδ fiber)
Synapses in dorsal horn
2nd order neuron Spinal cord → thalamus
Cell body in dorsal horn of spinal cord
Axon crosses over to contralateral side
Ascends in anterolateral column (spinothalamic tract)
3rd order neuron Thalamus → primary somatosensory cortex
Originate in ventral posterolateral nucleus of the thalamus
Ascends as part of internal capsule
Other Somatosensory Pathways (Spinomesencephalic, Spinoreticular, Spinolimbic)
Type of Pathway Divergent
Information carried Nociception, not well-localized
Role of information Slow nociception elicits affective, withdrawal, autonomic response (e.g. direct head towards
noxious stimuli, move body away, pale, nauseous, distressed)
1st order neuron Free nerve ending → dorsal horn (unmyelinated C fibers)
Synapses on interneurons
Ascending projection neurons Project to wide distribution of areas related to areas that modulate nociception, attention,
sleep, emotion, cognition

Thalamus
Structure Egg-shaped, bilateral structure
Input Info from basal ganglia, cerebellum, all sensory systems
Function Selective filter for cortex
Processes information and relays it to appropriate cortical areas
• Collection of nuclei
• Y-shaped sheet of white matter
• 3 groups of nuclei
o Anterior
o Medial
o Lateral
▪ Ventral
▪ Dorsal

Primary Somatosensory Cortex

• Primary somatosensory cortex (S1) – posterior to central sulcus, Brodmann areas 3, 1, 2

o
 o Marks beginning of conscious awareness
• S1 inputs and function
Input From thalamus via DCML & STT
Information Tactile, proprioception
Nociception & temperature (more widespread)
Function Identifies stimuli location, size, shape, texture
Perception
Example – pick up pen Determines it is smooth, cylindrical, small
• S1 somatotopic organization – map represents innervation density of skin
o Not total surface area of skin

o
• S1 structure/organization:
o 4 cytoarchitectural areas
▪ Area 3a
▪ Area 3b
▪ Area 1
▪ Area 2

o
o Extensively interconnected – serial and parallel processing of sensory information

Coding In Somatosensory Cortex

• Sensory information becomes increasingly abstract:
o As information flows towards higher-order cortical areas
o Specific combinations of stimuli or patterns are needed to get cortical neurons to fire
o Areas 1 and 2 fire with more abstract features than just for example location of a tactile stimulus
• Feature detecting neurons:
o Represent more complex processing
o Examples:
▪ Orientation sensitive
▪ Direction sensitive
Orientation sensitive neuron:

• Stimulus = edge of object pressed on palm at different orientations

Direction sensitive neuron:

• Stimulus = move an object across the palm in different directions (A-F)

Population Coding in S1

• Cortex contains many subnetworks/populations

• neurons in subnetworks are more likely to have same feature preference
• Grey neurons – interneurons (inhibitory)
• Sensory stimulus causes complex patterns of activity in neural populations
• The firing pattern of different populations/subnetworks that encodes a sensory event/scene

Secondary Somatosensory Cortex

• Tucked in the lateral sulcus – secondary somatosensory cortex (SII)

o
• SII inputs and function
 Input S1 & thalamus
Information Tactile, proprioception
Function Exact functions still poorly understood
Contribute to analysis of somatosensory input
Integrates tactile & proprioceptive info when manipulating object (+ past memories)
Stereognosis
Example – pick up pen Identifies the object as a pen

Cognition and Perception

• Cognitive and perceptual systems are inter-related and complex

o
o Awareness and emotions can support or impede cognitive function at any pyramid level
• Visual foundations:
o Acuity: sharpness of vision
o Contrast sensitivity: distinguish between finer increments of lightness and darkness/foreground and background
o Field deficits: homonymous hemianopsia
o Oculomotor control: diplopia, visual/ocular pursuit
• Auditory foundations:
o Presbycusis: hearing loss with age
o Recommendations: speak closer, face the listener, eliminate background noise, ensure aids are available and
working, use facial expression/body language/gestures, ask for confirmation/repeat back
• Attention:
o Sustained: vigilance and working memory
▪ Vigilance: maintenance of attention over time during continuous activity
▪ Working memory: actively holding and manipulating material
o Selective: freedom from distractibility
o Alternative: capacity for flexibility; shift between tasks
o Divided: ability to respond to 2 tasks simultaneously
• Visual inattention
o Unilateral neglect/hemi-neglect/hemi-inattention: inability to perceive, report, and orient to sensory events
towards one side of space – contralateral to side of the lesion, with or without a primary sensory deficit
o Strategies: anchors, fingers/object guides, head/eye turns, lighthouse (combo of first 3 strategies)
o Left homonymous hemianopsia: left field of view is blocked (greyed out)
o Left inattention: not focussing on left side (left field of view is blurry)
• Information processing: input → working memory (7 +/-2 items) → long-term memory (save) → output
o Slower processing speed: repeat/practice, priming, provide time for prolonged processing, environmental cues,
concise instructions, info in small chunks, ask client to repeat back instructions
• Memory & learning – time-wise:
o Immediate/sensory register: lasts milliseconds to seconds (iconic, echoic)
 o Short-term/working: limited capacity (7 +/- 2 items), lasts seconds to minutes to allow for manipulation/immediate
use
o Long-term:
▪ Delayed – events in previous few minutes
▪ Recent – events previous hours/days/weeks
▪ Remote – events several years ago
• Memory & learning – information types:
o Prospective: things to be remembered in the future
o Semantic: for facts
o Episodic: events, autobiography (sensory and emotional)
o Procedural: skills and procedures (most often intact)
• Memory & learning – consciousness during learning:
o Implicit
o Explicit
• Memory & learning – modalities:
o Visuospatial: pictorial, graphic
o Verbal: written, spoken
• Encoding, storage, retrieval: 3 stages involved in remembering
o Encoding: get information into memory
o Storage: keep information in memory
o Retrieval: extract information when needed
o Memory strategies: rote rehearsal, chunking, mnemonics, recall and recognition, priming, spaced retrieval, etc.
• Executive function: ultimate goal of creating plans and attaining goals (attention, consolidation)
o Basic:
▪ Attentional control (choose what to focus on and what to ignore)
▪ Cognitive inhibition (tune out irrelevant info)
▪ Response inhibition (inhibit inappropriate response)
▪ Working memory
▪ Cognitive flexibility (switching)
o Higher order: planning, organization, reasoning, problem solving, fluid intelligence
• Integrative approach to rehab – restorative/bottom-up intervention:
o Target basic cognitive skills/functions (arousal processes, attention, info processing)
o Directly engage fundamental skills through repeated drills or graded exercises
o Train brain to encode and process increasingly complex stimuli, more accurately and quickly via intensive
procedural training
o Poor generalization to untrained tasks and poor application to daily life
• Integrative approach to rehab – adaptive/compensatory/top-down intervention:
o Address deficits in higher-order “executive” functions through instruction and systematic practice of principles,
strategies or rules that can be generalized across a variety of situations
o Individuals are trained to consciously use internal verbalization of strategies and self-monitoring procedures across
a variety of situations
o Compensatory strategies include employing external prosthesis (e.g. memory notebook, calendar)
• Executive dysfunction
o Add structure to task
o Simplify task
o Follow routine
o Redirect
o Co-create checklists and plans
o Use metacognitive strategies (goal management training, co-op)
o Engage family members if possible
• Memory problems
 o Adapt environment
o Use external memory aides
o Follow routine
o Combine several strategies for “memory system”
o Use methods for encoding more efficiently, storing more efficiently, recalling more efficiently
o Implement errorless learning techniques
• Attentional deficits
o Minimize distractions in envt (visual, auditory)
o Cue and allow time to scan visual envt
o Simplify written instructions (e.g. 1-2 exercises/page, large/simple font, highlight or bold)
o Provide info in small chunks
o Ask to repeat back in own words

Peripheral Motor System

Muscle Structure
• Characteristics of Skeletal Muscle:
o Excitable: you can send an action potential to it and trigger it to cause it to contract
o Contractable
o Extensile: you can stretch a muscle out
o Elastic: if you stretch a muscle, it can go back to its original length

• Myofibrils are arranged in a stripped/striated pattern

o Parallel to long axis of muscle
• Pattern forms sarcomeres
o Functional unit
o Contractile
• Sarcomere:
o Comprised of 2 types of protein:
▪ Contractile
• Myosin (thick)
• Actin (thin)
• Tropomyosin, troponin
▪ Structural
• Z line - MOVES
• M line – STAYS PUT
• Titin
• Skeletal Muscle Structure:
o Membrane of the muscle fiber
o Projections into the muscle = T tubule (t=transverse)
 o Storage sacs (store Ca2+ ions) = sarcoplasmic reticulum

Muscle Contraction
• Sliding filament theory
o When calcium ions are present (Ca2+), actin slides relative to myosin
o Sarcomere shortens
o Action potential from motor neuron → release of Ca2+ from sarcoplasmic reticulum → Ca2+ binds to troponin and
slides tropomyosin back → binding site on actin is exposed → myosin binds to actin and pulls it along

Lower Motor Neuron

• Directly innervates skeletal muscle fibers
• Cell bodies in ventral/anterior horn of spinal cord
• Axon exists cord via ventral nerve root

o
• Ventral horn:
o Motor pools: cluster of cell bodies of neurons that innervate a single muscle
o Medial pools: axial & proximal muscles
o Lateral pools: distal muscles
o Anterior pools: extensors
 o Posterior pools: flexors

o
Alpha motor neuron Gamma motor neuron
Cell body Ventral horn Ventral horn
Axon exits cord via Ventral nerve root Ventral nerve root
Cell body size Large Medium
Axon Large & myelinated Medium & myelinated
Muscle fibre innervated Extrafusal fibers Intrafusal fibers
• Muscle spindle:
o Structure: intrafusal fibers, sensory neurons (Ia, II), gamma motor neuron endings
o Detects: absolute muscle length, changes in muscle length
o Function:
▪ Spinal level – stretch reflex
▪ Ascending – regulates muscle length during movement, contributes to sense of effort
• Alpha-gamma coactivation: during movements, alpha and gamma motor neurons fire/are active simultaneously
o Maintains stretch sensitivity of the muscle spindle when the extrafusal fibers contract
o NO COACTIVATION: when extrafusal muscles contract → intrafusal muscles become slack
▪ Action potentials are recorded from Ia afferent (from spindle)
o WITH COACTIVATION: ends of intrafusal fibers contract and tension is maintained
▪ Muscle spindle remains sensitive to stretch
▪ This occurs because descending input to alpha motor neuron has collaterals that synapse on gamma
motor neuron
o Gamma MN cell bodies are smaller so require less excitation to reach firing threshold
• Stretch reflex: muscle contraction in response to quick stretch
o Only 1 synapse ∴ quick response
o Muscle stretch (change in muscle length) activates muscle spindles → Ia afferent sends signal to cord → Ia
synapses with alpha motor neuron of that muscle → alpha motor neuron is stimulated to send signals to muscle →
the muscle contracts

Motor Units
• Motor unit = alpha MN and the muscle fiber it innervates
• Alpha MN activated
• ACh released at neuromuscular junction
• All muscle fibers innervated by that MN contract

Motor Unit Classification:

Slow twitch Fast twitch
• MN has smaller axon diameter • MN has larger axon diameter
• Muscles involved in posture and slow contracting muscles • Muscles involved in fast powerful movements
• Activated first (depolarized first and continue to
contribute to faster actions)

Motor Unit Size:

• Vary in number of muscle fibers innervated by single alpha MN
 o Gastrocnemius = 2000 muscle fibers per alpha MN
o Lateral extraocular muscle = 2-3 muscle fibers per alpha MN

Spinal Cord in Motor Function

• Movement occurs from interacting signals in the spinal cord
• Elicits MN firing
• Communication within the cord contributes to the coordination of movement
o Reciprocal inhibition
▪ What is it: inhibition of antagonist muscles during agonist contraction
▪ How is it controlled?
• Agonist muscle contracts
• Muscle spindle sense change in muscle length
• Ia afferent sends signal to spinal cord
• Ia collateral synapses with inhibitory interneuron
• Activated interneuron inhibits alpha MN of antagonist
▪ Used extensively during voluntary motion and when agonist is reflexively activated
o Proprioceptive input (GTO)
▪ What is it: adjusting muscle contraction during movement
▪ How is it controlled?
• GTO senses change in muscle tension
• Ib afferents transmits signal to spinal cord
• Stimulates interneurons
• Interneurons excite/inhibit LMN of synergists and muscles of origin
▪ Note – GTOs do not act in isolation
• Interneurons receive input from other afferents and descending command
o Muscle synergies
▪ What is it: coordinated muscle action
▪ How is it controlled?
• Muscle synergies are calculated from EMG data
• Have been described in frogs, cats, and humans
• Studies have demonstrated synergies in voluntary movements such as walking, cycling, and
upper limb reaching

Relationship: Reflexive and Voluntary Movement

Used to Think
Reflexes occurred in response to particular sensory info
Worked in isolated pathways in the spinal cord
Voluntary movement entirely separate
Current Thought
Sensory stimuli, interneurons and higher centers interact
Produce context dependent movement
e.g. arousal level modifies response to tendon tap
e.g. muscle spindle output modified by sensitivity adjustments from
descending commands

Lower Motor Neuron Signs

• Interrupting alpha motor neuron signals to muscle prevents muscle contraction
• Causes:
o Trauma
o Genetic diseases – spinal muscular atrophy
o Infection (e.g. poliomyelitis)
o Neuropathy (e.g. diabetes)
• Symptoms of lower motor neuron lesion
 Symptom Description
Hyporeflexia Reduced response to stretch reflex
Paresis/paralysis Loss of or decreased ability to generate muscle force
Atrophy Loss of muscle bulk (neurogenic)
Hypotonia/flaccidity Low resistance to passive stretch
Fasciculations Random, spontaneous, brief contractions of single muscle fibres

Central Motor System

Spinal Cord Role in Motor Function:
• Movement occurs from interacting signals in the spinal cord
• Elicits MN firing

Upper Motor Neurons/Motor Tracts:

• Upper motor neurons provide all the motor signals sent to the spinal cord
• Arise in:
o Cerebral cortex
o Brainstem
• Synapse with:
o LMN
o Interneurons
• Spoiler alert: activity adjusted by basal ganglia and cerebellum

Types of Tracts that Control Movement:

Type of tract Muscles controlled What the UMN synapses with Where the UMN synapses in VH
Postural/gross Antigravity muscles, groups of Branches widely Medially
movement limb muscles Synapses with LMN to multiple
muscles
Selective motor Isolated contractions of On LMN that innervate specific Laterally
control individual muscles in limbs muscles
On interneurons
Nonspecific Facilitate all lower motor Contribute to background levels of Throughout
neurons excitation in cord
Facilitate local reflex arcs

Medial UMN/Tracts:
• Descend in the anterior column of the spinal cord
o Reticulospinal tract
Origin Synapse/termination Movements elicited Function
Reticular formation LMN at various levels of Simultaneous contraction Anticipatory movements
spinal cord bilaterally of muscle groups across Muscle synergies
Propriospinal multiple joints
interneurons
• Anticipatory movements: related to balance – activate muscles to stabilize body ahead of voluntary
movement that has the potential to destabilize
• Muscle synergies:
o Activation of a group of muscles to achieve a specific task
o Flexor or extensor synergies of the limb (modified by the lateral corticospinal tract)
o Coordinating trunk with proximal limb muscles during walking
o Medial and lateral vestibulospinal – located in medulla
Origin Synapse/termination Movements elicited Function
 Medial vestibular nuclei Bilateral cervical and
thoracic spinal cord
Lateral vestibular nuclei Ipsilateral flexors and
extensors
o Medial corticospinal
Origin Synapse/termination
Cerebral cortex Ipsilateral, contralateral,
and bilateral LMN
Neck and upper back Coordinate head and eye
muscles movement
Facilitate extensors Maintain posture and
Inhibit flexors balance
Movements elicited Function
Neck, shoulder, trunk Voluntary muscle control
muscles

Non-specific UMN/Tract:
• Tracts descend from brainstem nuclei
• Enhance activity of:
o LMN
o Interneurons
• “emotional motor system”

Lateral UMN/Tract:
• Descends in the lateral column of the spinal cord:
o Lateral corticospinal tract
Origin Synapse/Termination Movements Elicited Function
Motor areas of LMN that innervate single muscle Wrist and hand extension Selective
cortex Interneurons that inhibit muscles Ankle and toe dorsiflexion motor
Selective motor control throughout limbs control
Pathway: Most (80-90%) of CST axons cross to the contralateral side
• Cortex • Medulla, base of the pyramids
• Internal capsule • Descend in lateral corticospinal tract
• Cerebral peduncles 10% of CST axons descend and terminate in ipsilateral cord
• Anterior pons
• Pyramids of medulla
• Lateral spinal cord

Motor Cortices:
 • Primary motor cortex in precentral
• Somatosensory cortex in postcentral area

Somatotopic organization:
• Size of cortical representation dedicated to a body part is proportional to the amount of motor control/precision required

Motor Cortices: Inputs and Outputs

Cortical inputs to M1:
• Somatosensory
• Posterior parietal
• SMA and premotor

Inputs to premotor areas:

 • Posterior parietal
• Prefrontal
• Between the premotor areas

Subcortical inputs to M1 and premotor areas:

1) Cerebellum
2) Basal ganglia

Outputs:
• Premotor areas:
o Directly to M1 (majority)
o Spinal cord:
▪ Some corticospinal tract cells originate in SMA and premotor areas
▪ Some overlap in the innervation of muscles with M1
• Primary motor cortex:
o Corticospinal tract

Motor Cortices – Function: Distinguishing primary and premotor function

• Instructed delay task:
 • 1 auditory cue was to hit panels based off visual stimuli
• Other auditory cue was to hit panels based off pre-learned sequence

M1
Visually triggered task Active little bit before panel
press and after
Internally guided task Active little bit before panel
press and after
Function The motor command to the
muscles, signal/coding to move
Lateral PM
More active before panel press
(a little bit after)
Relatively silent
Create motor plan for
movements in response to an
external cue (in this case a light)
SMA
Relatively silent
More active before panel press
(and a little bit after)
Create motor plan for
movements that generated from
memory (internal cue)

Coding in the Primary Motor Cortex:

How Does M1 Signal Movement?
• Old theory – giant switchboard
o Switch muscles on/off
• Points that disprove:
o Stimulate cortex get a muscle contraction
o But stimulate a different site, can get same muscle contraction
o Stimulation can activate several muscles simultaneously
▪ Corticospinal axons diverge and innervate motor neurons to more than 1 muscle

Coding by M1 Neurons: Direction of Muscle Force

Coding by M1 Neurons:
• Movements are encoded by overall activity profile of a population of M1 neurons
o Direction and amplitude (force) of movement
o Distance and speed (examples not shown)
• M1 neurons do not encode degree of joint displacement
• M1 neurons do not encode movement in 1 to 1 way
• Why is this important?
o Implies parallel neuron populations/networks for carrying out an action sequence

Division of Lateral Premotor Area

Dorsal Ventral
• Planning/influence motor control for learned • Planning/influence motor control of hand movements
association movements for manipulation of objects
• Learned associations between arbitrary cues and • Planning movements guided by visual information
motor response about object properties

Lateral Ventral Premotor Area (LVPM)

 • The same neuron was active in all 3 conditions showing that you are creating a plan to do movement in all 3 situations

Mirror Neurons;
• Neurons that fire both when performing an action and when observing another individual performing that action
• Mirror neurons are a class of neuron that modulate their activity both when an individual executes a specific motor act and
when they observe the same or similar act performed by another individual
• Evidence for existence in humans from fMRI studies
• Mirror neurons:
o Understanding actions of others
o Basis for learning through imitation
o Involved in building motor memories
• Mirror neurons and neurorehab:
o Potential to induce neuroplasticity in the motor cortex by coupling action observation and execution
o Patients watched a video of daily life arm and hand actions for 6 minutes
o Controlled study in stroke (n=8):
▪ Treatment group:
• Video of daily life and hand actions for 6 minutes
• Perform observed action for 6 min with paretic limb
• 90 minutes/day for 18 days
▪ Control group:
• Matched to treatment group except watched videos of geometric shapes
▪ Results:
• Improvement on clinical tests
• Changes in bran activation measured with fMRI
o SMA, ventral premotor cortex, cerebellum, parietal areas
• Significant differences only in experimental group
Summary of Functions:
Premotor area Function/role
Supplementary motor area Preparation of internally guided movements
Bilateral coordination
Lateral premotor areas Preparation of externally guided movements
Map relationship between stimulus and response
Lateral dorsal PM Preparation of movements with learned associations with arbitrary cues
Lateral ventral PM Preparation of movements guided by visual information (i.e. hand movements for
manipulation of objects)
 Cingulate motor area Suggested role in motor selection based on reward evaluation

Impairments Associated With:

Lesion to M1 UMN signs Lesion to Premotor areas
Paresis/weakness Inability to respond to external stimuli
Poor coordination Apraxia
Moving in synergies
Substitution/compensation
Hypertonia/hyperflexion/spasticity

Synergies and The Stages of Motor Recovery and Atypical Movement

• Abnormal synergies: during attempts at active movements
o Movements occur in stereotyped and obligatory mass patterns
o Unable to isolate a movement to 1 muscle group or 1 joint
o 2 synergies for arm and leg: flexor and extensor
▪ Flexion synergy usually dominates in the arm; extension synergy usually dominates in the leg
• Part of impairment inventory in the CMSA (“arm, hand, leg & foot stage of motor recovery”)
• Least to most – motor recovery:
o Flaccid paralysis is present. Active movement cannot be elicited reflexively w/ a facilitative stimulus, or volitionally
o No voluntary movement is present. A facilitative stimulus will elicit the limb synergies reflexively. These limb
synergies consist of stereotypical flexor and extensor movements
o The synergistic movements can be elicited voluntarily but are obligatory. In most cases FS – arm, ES – leg
o Synergy patterns can be reversed if movement takes place in the weaker synergy first (e.g. arm – ext. to flex.)
o Synergy patterns can be reversed even if the movement takes place in the strongest synergy first
o Coordination and patterns of movement are near normal. Abnormal patterns of movement with faulty timing
emerge when rapid or complex actions are requested.
o A “normal” variety of rapid, age-appropriate complex movement patterns are possible with normal timing,
coordination, strength, and endurance
• CMSA stages of motor recovery: 7 stages that are passed through consecutively (none are skipped)
o May stop progress at any stage; not everyone begins at stage 1 depending on stroke severity
• Stages of motor recovery:
1. Flaccid paralysis is present
2. No voluntary movement but movement can be facilitated or occurs as an associated reaction (may also have
minimal voluntary movement in stage 2)
3. Synergistic movements (or components) can be elicited voluntarily.
4. Simple movements are possible outside of the synergy. Synergy patterns can be reversed if movement occurs in
the weaker synergy first.
5. Relative independence from basic synergy. Synergy patterns can be reversed even if the movement occurs in the
stronger synergy first.
6. Coordination and movement are near normal.
7. Normal.
• Upper extremity – synergies (relatively stronger* | opposite of all above®)
o Flexor synergy*
▪ Shoulder girdle – retraction, elevation
▪ Shoulder – abduction®, external rotation®, (hyperextension)
▪ Elbow – flexion*
▪ Forearm – supination
▪ Wrist – flexion
o Extensor synergy
▪ Shoulder – adduction*, internal rotation*
 ▪ Elbow – extension®
▪ Forearm – pronation
▪ Wrist – flexion or extension
o Both synergies
▪ Fingers and thumb – flexion & adduction
• Lower extremity – synergies (relatively stronger*)
o Flexor synergy
▪ Hip – flexion*, abduction, external rotation
▪ Knee – flexion® (up to 90° only)
▪ Ankle – DF, inversion
▪ Big toe – extension
▪ Toes – flexion
o Extensor synergy*
▪ Hip – extension, adduction, internal rotation
▪ Knee – extension*
▪ Ankle – plantarflexion, inversion
▪ Toes – flexion or extension
• Motor recovery progression:
Stages/Synergies Spasticity Paresis
1 – no active Flaccid Less
2 – with stimulation
3 – voluntarily Spasticity increases
4 – increasingly selective Less
5 – can be reversed even if stronger first Spasticity decreases
6 – towards normal Less
7 – normal Normal DECREASING
• Benefits of CMSA:
o Provides framework promoting understanding of movement problems to clients
o Considers positive and negative signs
o Evaluative and discriminative
o Defines conditions under which active movement/strength is tested
o Easily communicates patient’s impairment status
o Can be used to determine appropriate treatment
o Reliable and valid; can provide a prognostic indicator
• Administration: be familiar with scoring, interpretation, reliability, validity
o Manual has detailed instructions for each task
o Patient – dress in comfortable clothing with socks and shoes off
o 45-60 minutes to complete but may not be possible in one session
o Ensure patient comprehension – PT can demonstrate movement or patient can demo on unaffected side
o Movement may be attempted twice, must be performed correctly on at least 1 trial to receive credit
• Scoring rules:
o Separate scoring for arm, leg, hand, foot
o 3 tasks at each stage
o Start test at stage 4 for leg and stage 3 for arm, hand, foot
o Patient’s stage: highest stage at which they can perform 2/3 tasks EXCEPT stage 6 patient must pass 3/3 tasks
o If able to perform 2/3 tasks, test the next stage; if they cannot perform 2/3 tasks, test the lower stage
o Each task can only be attempted twice
o Stage 2: facilitated mvmt at any part of the range (can only allow manual facilitation allowed for a max of 2 ways)
o Stages 3-7: voluntary movement with no facilitation allowed
o Minimize position changes as much as possible; stages 2 & 3 must be done in order presented
o If patient cannot do task exactly as written, do not accept task as achieved (err on scoring patient lower)
Clinical Outcome Variables Scale
• Measure of mobility that has been applied to specific diagnostic groups such as stroke, traumatic brain injury,
amputations, and musculoskeletal injuries in a variety of settings (acute, inpatient/outpatient rehabilitation, and
community settings).
• Items include rolling, lying to sitting, sitting balance, transfers, ambulation, wheelchair mobility, and arm
function.

Chedoke McMaster Stroke Assessment

• 3 tasks per level, must complete 2/3 tasks to pass (except for Stage 6, where you have to pass all 3 tasks)