BOBATH
Bobath’s Philosophy and Physiologic Approach to
Treatment of Hemiplegia
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Aka Neuro-developmental treatment (NDT)
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The Concept considers that motor control is based on a
nervous system working with both hierarchical and parallel
distributive, multi-level processing amongst many systems
and subsystems involving multiple inputs, and with
modulation on a number of levels within this processing. It
sees the potential for plasticity as the basis of
development, learning.
Similar to Brunstromm, Bobath takes advantage of
neuroplasticity
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The Bobath Concept is goal orientated and task specific,
and seeks to alter and construct both the internal
(proprioceptive) and external (exteroceptive) environment

Treatment is an interaction between therapist and patient
where facilitation leads to improved function.
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Movement develops from the interaction of perceptual
(integration of sensory information such as body schema),
action (motor output to muscles) and cognitive systems
(including attention, motivation and emotional aspects of
motor control). Each of these has to be taken into
consideration in the clinical reasoning process.
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This is supported by Mayston (1999) who identifies five
aspects relating to the production of efficient functional
movement in the neurological patient:
1. Motor – postural and task-related activity
2. Sensory – selective attention by the nervous system
to relevant stimuli
3. Cognitive – motivation, judgment, planning and
problem-solving
4. Perceptual – spatial and visual including figureground
5. Biomechanical – complementary neural and
biomechanical aspects of control
Motor Control and Motor Learning
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The Bobath Concept utilizes an understanding of motor
control and motor learning in order to promote the best
possible outcome for each patient.
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Motor control- is defined as the ability to regulate or
direct the mechanisms essential to movement
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Motor learning- is described as a set of processes
associated with practice or experience which leads to
relatively permanent changes in the capability of
producing skilled action
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Mulder and Hostenbach (2001) identified four basic rules
for motor learning:
1. Input (information) is essential.
2. Input must be variable.
3. Input must be meaningful.
4. The site of training must be related to the site of
application
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Motor learning can be divided into three distinct phases
(Halsband & Lange 2006):
1. Initial stage: slow performance under close sensory
guidance, irregular shape of movements, variable
time of performance
2. Intermediate stage: gradual learning of the
sensorimotor map, increase in speed
3. Advanced stage: rapid, atomized, skillful
performance, isochronous movements and whole field
sensory control
The importance of afferent information in the control of
movement
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The control of efficient movement requires the individual
to be tuned into visual, vestibular and somatosensory
information (cutaneous, joint and muscle receptors). All of
these contribute to the development of an internal
representation of body posture which is referred to as the
postural body schema.
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Sensory Networks:
Visual (eyes)
Vestibular (vestibular network):
o VOR – vestibulo-ocular reflex
 Open eyes
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“Window of opportunities”
Pt should be awake during exercise
Ex: ask patient to look at an object, you may
facilitate the movement by touch the head
with your fingertips, then ask patient to keep
looking at the object while you move the
head (or the object) to different directions
o VCR – vestibulo-colic reflex
 Muscle spindles in the neck gives additional
information
 If patient has a kyphotic posture, start
addressing the forward head (chin tucks)
o VSR – vestibulo-spinal reflex
 Contribute to the control of posture
orientation
Somatosensory
The postural body schema consists of:
1. Alignment of body segments to each other and in
relation to the environment;
o Normal body alignment in anatomical position
2. Movement of the body segments in relation to the
base of support;
o Exercises like sit-to-stand where base of support
is decreased
3. Orientation of the body in relation to gravity
(verticality)
o Exercises that challenge their body orientation
like: reaching an object beyond the midline
(diagonal)
Requirements of efficient movement
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Postural control is an essential foundation for movement
with the following being key requirements incorporated
into postural control for functional movement:
1. Balance strategies (single leg stance while reaching
for something or use a wobble board)
2. Patterns of movement [Bobath avoids the use of
associated reactions. These patterns (flexor synergy
and etc.) must be corrected immediately]
3. Speed and accuracy
4. Strength and endurance
Postural control
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It involves the ability to orientate and stabilize the body
within the force of gravity using appropriate balance
mechanisms.
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Bobath therapists analyze posture and movement through
the alignment of key points in relation to each other and
in relation to a given base of support.
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Key points are described as areas of the body from which
movement may most effectively be controlled (Edwards
1996). They are divided into proximal, distal and central
key points.
1. Distal refers to the hands and feet – start controlling
the hands to activate the chain (hands – elbow – SH
– scapula)
2. Proximal to the shoulder girdles, head and pelvis –
control proximally if distal areas are still weak
3. Central to the mid-thoracic region – facilitate the
spine to activate the chain distally (rhomboids –
scapula … hand)
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These areas have a dynamic interrelationship with each
other through active control of body musculature in a
three-dimensional orientation. It is important to recognize
that these key points relate to functional units
Balance strategies
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They are patterns of movement or adaptations in muscles,
resulting from feed-forward and feedback mechanisms
that are influenced by learning, experience and sensory
inputs.
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Preparatory postural adjustments (pAPAs) are
anticipatory balance strategies which prepare the body for
movement – instruct the patient ahead so he/she would
anticipate (before movement)
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Feed-forward postural control/anticipatory
postural adjustments (APAs)- They occur in muscles,
just before or alongside focal movements, in order to
stabilize the body or its segments during the execution of
the movement – pt is already doing the movement
Patterns of movement
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Sequences of selective movement for function. The
strength of appropriate muscle recruitment in functional
patterns is a crucial aspect of motor control and motor
learning. It is also recognized that the ability of muscles to
generate appropriate torque at one joint will be greatly
affected by the torques produced at other joints. Thus,
the production of selective movement in patterns is
dependent on stability at adjacent joints
Muscle strength and endurance

The need to integrate specific strength training as part of
gaining efficient movement
is seen by Bobath therapists as a key element of
regaining efficient functional movement. It is now
recognized that weakness is an important factor
limiting the recovery of motor performance following
brain damage.
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Loads can be given:
Directly by the therapist and/or carer;
By the therapist using the environment and effects of
gravity;
By the use of the patients own body weight
Speed and accuracy

Altering the speed of an activity can be a useful
adaptation within therapy that can be used as an aspect
of progression to assist creating more adaptable flexible
movement
Assessment of Hemiplegia patient

The Bobath Concept seeks to explore the full potential for
improvement within the patient’s movement control as a
basis for enhanced function.

It is recognized that the nature of the patient’s current
movement strategies may have a positive or a negative
impact upon the fulfillment of optimal functional potential.
This involves the quality of movement as well as the
quantity.
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Assessment and treatment are integrated with a
continuous interaction between the two. This demands
responsiveness on the part of the therapist and clinical
reasoning ‘in action’ in order to determine critical
movement interferences and evaluate them further.
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The assessment process is systematic but flexible as it
does not follow the same sequence for each patient. The
starting point for assessment will vary as will the
progression, with both being determined in response to
the individual’s clinical presentation.
Moving Between Sitting and Standing
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STS has been identified as an important prerequisite for
achieving independent upright mobility and an important
factor in independent living
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Phases of sit to stand
1. flexion momentum (forward lean)
2. momentum transfer (weight shifting)
3. extension (propulsion or push up)
4. stabilization (able to stand in static)
Sit to walk
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STW is a complex transitional task challenging both
locomotor and postural control.
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BIPEDAL LOCOMOTION
Importance is placed on accessing pattern-generated
activity to facilitate efficient walking and automaticity
Recovery of Upper Limb Function
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One of the biggest challenges for many patients is
regaining functional use of their upper limbs. Often, upper
limb recovery is sacrificed in order to concentrate on
mobility and transfers. The Bobath Concept focuses on the
interrelationship of all areas of the body to optimize
overall function in lower and upper limb recovery
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Contactual hand-orientating response
A frictional contact of the hand to a surface that
allows for the hand to begin its functional roles
Ex: prone on hands, wall push-ups, sitting upright w/
handle bar or walker Infront to keep balance
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Midline orientation
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Light touch contact as a balance aid
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Limb support and limb loading
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Postural stabilization for selective wrist, elbow and
shoulder movement of the same limb;
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Contralateral upper limb across midline tasks.
Positioning and seating for recovery
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The goal of good seating and positioning is to provide
adequate postural support to enable appropriate
alignment and stability of the trunk and limbs, therefore
reducing the fear of falling and need for compensatory
fixation appropriate to that postural set. This will give the
patient the foundation BOS on which to move actively and
appropriately within their chair and wider environment.
Seating and positioning may require the use of external
scaffolding specifically to support hypotonic areas using
towels and pillows
Techniques of treatment

May be equally useful and successful in other patients,
who show similar difficulties and needs. The techniques
employed depend on the stage of recovery the patient has
reached, or at which the process of recovery has become
arrested. These stages may be defined as:
1. Initial flaccid stage.
2. Stage of spasticity.
3. Stage of relative recovery
CEREBRAL PALSY
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The term cerebral palsy (CP) (originally “cerebral paresis”)
was first used in 1843 by English orthopedic surgeon
William Little in a series of lectures entitled “Deformities
of the Human Frame.” As a result, CP was known for
many years as “Little’s disease” or “Infantile Cerebral
Paralysis.”
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A collection of syndromes of diverse etiology, pathology,
and clinical manifestations caused by non-progressive
lesions of an immature brain, which leads to
neuromuscular and other symptoms of cerebral
dysfunction
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Lesion affects the immature brain and interferes with the
maturation of the CNS
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The brain damage results in disorganized and delayed
development of the neurological mechanisms of postural
control, balance, and movement
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Individuals have specific impairments such as
hypertonicity or hypotonicity with weakness, abnormal
patterns of muscle activation including excessive cocontractions. There are absent or poor isolated
movements (poor selective motor control), abnormal
postures and problems with manipulation.
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Besides neuromuscular impairments, the motor
dysfunction has musculoskeletal problems. There are
biomechanical difficulties resulting from both the
neuromuscular dysfunction and musculoskeletal problems,
which add to this complex picture.
Epidemiology
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0.5 to 1.5/1000 live births
Other references:
1 to 2.3/1000 live births
4-5/1000 live births
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This the most common childhood disability
Etiology
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Damage to the Central Nervous System
Prenatal
Perinatal
Postnatal
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According to Braddom, gestational age less tan 32 weeks
is one o the most powerful predictors of CP
There is damage to the germinal matrix zone in the
periventricular region of the premature fetus (24 to
28 weeks of gestational age) caused b ischemic
damage associated with hypoperfusion of the area
Prenatal (Fertilization to 38-42 weeks)
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Prematurity (<37 weeks)
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Rh incompatibility
Erythroblastosis fetalis
o RBC is being attacked resulting to anemic baby
(blue baby)
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Maternal infectious diseases (ToRCHS)
Toxoplasmosis (feces from cat)
Rubella (German measles)
Cytomegalovirus
Herpes simplex (chicken pox)
Syphilis
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Eclampsia
Htn + convulsion
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Irradiation (X-ray exposure on the lower abdominal area)
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Metabolic disturbances during pregnancy (DM)
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Drugs
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Alcohol
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Placental dysfunction
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Genetic predisposition (familial athetosis, familial spastic
paraplegia, familial rigidities, atonic diplegias, et.)
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Abdominal trauma during pregnancy
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Small-for-gestational age
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Intrauterine growth retardation
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Fetal deprivation and fetal malnutrition
Decrease in folic acid intake
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Multiple births, twin pregnancies, predisposition to
miscarriage
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Kernicterus – due to improperly treated hyperbilirubinemia
(damage to basal ganglia):
Triad:
1. High frequency hearing loss (deafness)
2. Loss of upward gaze (Parinaud’s syndrome)
3. Athetosis (choreoathetosis)
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Congenital malformations
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Socioeconomic factors
Late/inadequate prenatal care
Perinatal (Birth to 4 weeks/ 1 month)
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Birth injury/trauma
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Sick neonates – systemic complications (pulmonary and
circulatory function) lead to brain hypoxia
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Fetal asphyxia (either mechanical respiratory obstruction
such as cord coil or injudicious use of analgesics and
anesthetics)
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Abnormal birth process
Placenta previa
Prolonged labor (more than 18 hours for primiparous
(first child) and 12 hours for multiparous (multiple
children) mother)
Breech delivery
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Neonatal cardiorespiratory distress
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Prematurity
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Eclampsia during delivery
Postnatal (4 weeks/ 1 month to 2-6 years)
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Traumatic injuries (head trauma)
If a child under 6 years acquires TBI, it is already
under the cluster of CP
Vascular accidents (Arteriovenous malformation)
Encephalopathies
Toxic factors
Cerebral anoxia (carbon monoxide poisoning or highaltitude anoxia)
Brain tumors (also brain cysts and hydrocephalus)
Infections
Meningitis
Encephalitis
Severe respiratory condition
Measles
Polio
Brain abscess
CLASSIFICATIONS
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Based on etiology
Congenital
Acquired
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Topographic classification
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Physiologic/Clinical classification
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Based on severity
Mild – able to amb, use arms, speaks well enough,
does not need special care
Moderate – is not able to amb well, not able to selfhelp well
Severe – total involvement, pt is incapacitated, bed
ridden or restricted to wheelchair

The Gross Motor Classification System for children aged 6
to 12 years
GMFCS I
GMFCS
II
GMFCS
III
GMFCS
IV
GMFCS V
Children walk indoors and outdoors and climb
stairs without limitation
Walk indoors and outdoors and climb stairs
holding onto a railing but experience
limitations walking on uneven surfaces and
inclines
Walk indoors or outdoors on a level surface
with an assistive mobility device. Children may
climb stairs with a railing or propel a manual
wheelchair
May walk short distances with a device, but
rely more on wheeled mobility at home and in
the community
Have no means of independent mobility
Topographic Classification
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Monoplegia – one extremity
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Tetraplegia (quadriplegia) – involvement of all limbs
and body. Arms are equally or more affected than the
legs. Many are asymmetrical (one side more affected)
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Diplegia – involvement of limbs, with arms much less
affected than legs. Asymmetry may be present
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Hemiplegia – unilateral involvement of the upper and
lower extremities
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Triplegia – is uncommon and involves three limbs. This
may be a combination of diplegia and hemiplegia
Physiologic/Clinical Classification
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Spastic cerebral palsy (50 to 60% - most common)
hypertonus; the velocity-dependent hyperactive
stretch reflex is the most physiological definition of
spasticity
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Non-spastic: Athetoid (dyskinetic, dystonic)
cerebral palsy
(25 to 30%)
These are bizarre, purposelessness movements which
may be uncontrollable. The involuntary movements
may be slow or fast; they may be writhing, jerky,
tremor, swiping or rotary patterns or they may be
unpatterned
Indicating a lesion in the basal ganglia
Ataxic (5%)
Movements are characterized by clumsiness,
imprecision, or instability
Indicating a lesion involving the cerebellum or cranial
nerve 8
Mixed
Mixed athetosis and spasticity
Spastic athetoid – most common
Hypotonia - floppiness
Spastic Cerebral Palsy
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Lesion in the pyramidal tract; affects Brodmann area 6
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Hemiplegia
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Diplegia (most common)
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Quadriplegia
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Common manifestations:
Hyperreflexia
Persistence of neonatal reflexes
Sustained ankle clonus
Babinski sign
Hypertonic
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2.
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3.
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Spastic Hemiplegia
Affected one side of the body (pts vary UE> or <LE; but
often UE) often distal but sometimes also proximal
The anatomical and neuroradiological correlate is mostly
represented by isolated porencephalic cysts, lesions of the
internal capsule, or even periventricular lesions, also
bilateral or by more diffuse damage of the cerebral
hemisphere
Muscle spasticity on the affected side decreases muscle
and bone growth (affected limb is smaller), resulting in
decreased range of motion (ROM)
Often present with:
Contractures and limb-length discrepancies on the
involved side
Affected side: shoulder protraction, elbow flexion,
wrist flexion and ulnar deviation, pelvic retraction, hip
internal rotation and flexion, knee flexion, and
forefoot contact only due to plantarflexed foot
May have homonymous hemianopsia and astereognosia
May have moderate intelligence impairment or can be
normal
Emotional disorders such as hyperactivity (10%)
Present associated reactions
Brain asymmetry (midline towards normal side – lean
towards sound side)
Spastic Diplegia
High incidence of periventricular leukomalacia
Primarily affects bilateral Les, resulting in issues with gait,
balance, and coordination
In standing, children with diplegia often present with an
increased lumbar spine lordosis, anterior pelvic tilt,
bilateral hip internal rotation, bilateral knee flexion,
intoeing, and equinovalgus foot position
In motion, poor pelvic dissociation, toe walking or
scissoring gait
May preset with bunny hopping and combat crawl
Normal or near normal intelligence but may have some
social and emotional difficulties
Strabismus or visual deficits
Children with diplegia often require assistive devices such
as a posterior walker or lofstrand crutches
A scooter or wheelchair may be necessary for longdistance mobility due to decreased endurance
Spastic Quadriplegia
Most severe; poorest prognosis
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Volitional muscle control of all four extremities is severely
impaired, often accompanied by neck and trunk
involvement
Characterized by seizure, mental retardation and
strabismus
(+) Straphanger sign (shoulder abd with flexed elbow and
fingers)
Severe – extensive lesions affecting the basal ganglia or
occipital area often lead to visual impairments and
seizures; unable to speak (cognitively impaired); non amb
Moderate (may be non-ambulatory) and Mild
(ambulatory) – able to express level of understanding
and critical thinking
Cognition can vary from normal to severely impaired and
is unique to each child with quadriplegia
Athetoid (dyskinetic, dystonic cerebral palsy)
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Characterized by abnormal and involuntary movements
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Affects subcortical structures and basal ganglia
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With high intelligence, happy disposition and extroverted
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(+) hand spooning (extension of fingers)
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May present with normal reflexes
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Fluctuating tone
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Extrapyramidal system dysfunction (prevalent location in
the caudate and putamen)
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Poor midline orientation
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Poor grasp and release (hand function)
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Rapid movements
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2.
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Dyskinetic
Common abnormalities found in imaging include deep
gray matter lesions and to a lesser extent, periventricular
white matter lesions
The muscles switch between stiffness and floppiness,
causing random, uncontrolled body movements or spasms
Tone regulation alterations:
During rest: normal muscle tone
When stimulated: increase muscle tone
Dystonic
Dystonia is a slow motion with a torsional element that
may involve one limb or the entire body and in which the
pattern itself may change over time
Result from an extrapyramidal system dysfunction
(thought to be in the basal nuclei) – responsible for
inhibition of movement
Tone regulation alterations
During rest: decrease muscle tone
When stimulated: increase muscle tone
Rapid and non-coordinated involuntary hyperkinetic
syndromes (especially in face and mouth)
Impaired voice emission (very fast and incomprehensible
speech)
Cognitive development is seldom impaired
Ataxic
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Primary incoordination due to the disturbance of
kinesthetic or balance sense
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Affectation of cerebellum and cranial nerve 8
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(+) Romberg sign
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Hypotonic with normal or decreased DTRs
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With equilibrium dyssynergias and nystagmus
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Exhibits rebound phenomenon
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Clumsiness, imprecision, instability
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Not smooth, disorganized or jerky
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Unsteady, shaky movements or tremor
Their sense of balance and depth perception is
affected
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Difficulty maintaining balance
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Low postural tone (not excessive)
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Low cognition level than age
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Problems in stability
Nystagmus
Head titubation
Lack of co-activation proximally
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Problems in mobility
Dysmetria (hypometria, hypermetria)
Intention tremor
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Poor grading
Speech problems – monotone, dysarthria
Emotional problems
Classification:
Simple congenital ataxia
o Pure ataxia in CP, non-progressive and genetic
Ataxic diplegia
o Ataxic movements in the UE and trunk; spastic
movement in the LE
Disequilibrium syndrome
o All progressive and non-progressive child
o Genetic/hereditary (poor cognitive)
o No equilibrium reflexes (falls like a timber)
o No saving reaction (no protective reflex)
o Wide based/high guard walking
Hypotonia
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Having reduced muscle tone (floppiness), making any
movements against gravity and sustaining upright
postures such as sitting and standing difficult
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Other reference:
Hypotonia or “flaccid type” is just a phase every CP
child goes through
This is called “transient stage”
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The word floppy can mean:
Decrease in muscle tone (hypotonia)
Decrease in muscle power (weakness)
Ligamentous laxity and increased range of joint
mobility
o (+) heal to ear test
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Types:
Severe – little or no postural control against gravity
Mild – almost normal repertoire of postures against
gravity
Transient stage
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Lack of antigravity activity (necessary full support)
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Lack of alignment (insufficient proximal stability)
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Threshold of stimulation is abnormally high:
Associated reduced state of alertness
Lack of motivation
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Persistence of hypotonia: delayed intellectual development
Associated Problems:
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Visual impairments
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Hearing impairments
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Cognitive impairments
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Epilepsy
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Oromotor impairments
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Psychological impairments
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Nutritional disorders
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Genitourinary disorders
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Bone and mineral density disorders
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Musculoskeletal disorders
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Respiratory disorders
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Gait impairments
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Visual impairments
Common in children with CP (prevalence of 39% to 100%)
Strabismus (esotropia or exotropia)
Retinopathy of prematurity in premature infants – may
cause blindness if left untreated
Cortial visual impairment in hypoxic ischemic
encephalopathy
Homonymous
Hemianopsia in hemiparesis
2.
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Hearing impairments
Rare in CP
Kernicterus was a relatively common cause of
sensorineural deafness in athetoid CP
3.
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Cognitive impairments
Overall frequency of mental retardation, defined as an IQ
sore of 69 or below, is reported to be 50% to 70%
4.
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Epilepsy
The overall occurrence of epilepsy is reported to be
between 15% to 55%
5.
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Oromotor impairments
Associated with more severe CP
Weak suck
Poor coordination of the swallowing mechanism
Tongue thrusting
Toni bite reflex
More cavities due to neglect
May all lead to:
Feeding difficulties
Increased risk for aspiration
Drooling
Speech disorders range from mild articulation disorders to
anarthria, and are most commonly seen in children with
spastic quadriparesis or athetosis
6.
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Psychological impairments
Prevalence of emotional and behavioral problems is 30%
to 80%
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Attention deficit disorder
Passivity
Immaturity
Angler
Sadness
Impulsivity
Emotional lability – rapid changes in mood
Low self-esteem
Anxiety
7.
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Nutritional disorders
Poor oromotor skills, gastroesophageal reflux, and the
inability to self-feed or communicate hunger can all
increase the risk for malnutrition in children with CP
Although malnutrition is a primary concern, children with
CP are also at risk for overfeeding and obesity
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8.
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Genitourinary disorders
Incontinence was the most common complaint, but
frequency, urgency, hesitancy, and urinary retention may
also be present
9.
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Bone and mineral density disorders
Decreased bone mineral density (BMD) and increased risk
of fracture with minimal trauma is common in patients
with moderate to severe CP, especially those who are
non-ambulatory
10. Musculoskeletal disorders
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Foor/ankle
Equinus deformity, due to increased tone or
contractures of the gastrocsoleus complex, is the
most common musculoskeletal deformity in CP
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Knee
Knee flexion contractures are common due to
spasticity in the hamstring muscles and static
positioning in a seated position
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Hip
Acquired hip dysplasia is common in CP and often
leads to progressive subluxation and possible
dislocation
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Spine
Spinal deformities, including kyphosis, lordosis, or
scoliosis, are common in children with CP
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UE:
Shoulder is often positioned in an adducted and
internally rotated position
Spasticity in Biceps, brachioradialis, and the brachialis
frequently result in elbow flexion contractures
Forearm pronation deformities, wrist is flexion,
typically with ulnar deviation, finger deformities are
flexion ad swan neck deformities due to hand intrinsic
muscle spasticity. A thumb in palm deformity is
commonly seen with adduction at the
carpometacarpal joint, which may be associated with
hyperextension of the metacarpophalangeal and
interphalangeal joints
11. Respiratory disorders
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Impaired control of respiratory muscles, ineffective cough,
and aspiration due to an impaired swallow;
gastroesophageal reflux; or seizures all increase the risk
for chronically increased airway secretions
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Increased airway secretions may lead to wheezing,
atelectasis, recurrent aspiration pneumonia, restrictive
lung disease, or bronchiectasis
12. Gait impairments

Hip
Increased hip adduction tone can cause scissoring
and difficulty advancing the limb in swing phase
Increased tone in the iliopsoas can lead to increased
hip flexion, resulting in an anterior pelvic tilt and a
crouched gait
Increased femoral anteversion can contribute to intoeing

Knee
Tight hamstrings can inhibit the knee from extending
during stance phase further contributing to a
crouched gait
Spasticity of the rectus femoris may limit knee flexion
during the swing phase, causing a stiff-kneed gait
pattern

Ankle
Spasticity of the plantarflexors can lead to toe
walking, difficulty clearing the foot during swing
phase, or genu recurvatum (due to limited
dorsiflexion in stance phase creating an extension
moment at the knee)
Spasticity of the ankle invertors, most commonly
seem in spastic hemiparesis, can lead to supination of
the foot and weight bearing on the lateral border of
the foot
Weight bearing on the talar head is more common in
spastic diparesis or quadriparesis, and is associated
with an equinovalgus deformity
Malrotation of the leg can interfere with stability
during stance phase and effective push off
Internal rotation is more common with a varus
deformity and external rotation with a valgus
deformity
DIAGNOSIS

Developmental milestones and motor skills
The signs and symptoms of CP may be apparent in
early infancy
Infants presenting with abnormal muscle tone,
atypical posture and movement with persistence of
primitive reflexes may be diagnosed earlier than 2
years of age
Milder cases of CP may not be diagnosed until 4 to 5
years of age

Neuroimaging of the brain can show the location and
type of brain damage
Cranial ultrasound
Computed tomography (CT)
Magnetic resonance imaging (MRI)
PROGNOSIS

Depends on:
Degree of involvement
Level of tone
Classification
TREATMENT FOR CEREBRAL PALSY

Treatment of cerebral palsy is a lifelong process.
Intervention includes ongoing family and caregiver
education, normalization of tone stretching, strengthening,
motor learning and developmental milestones, positioning,
weight bearing activities, and mobility skills. Splinting
assistive devices and specialized seating ma be indicated.

Surgical intervention may be required for orthopedic
management or reduction of spasticity
Teamwork with Family




Planning of interventions should consider the child within
the context of the family
Therapists should be sensitive to the family’s stresses,
dynamics, child-rearing practices, coping mechanisms,
privacy, values, and cultural variations and be flexible in
their approach and programming
Home programs are important for optimal therapy results
because strengthening, extensibility, and motor learning
require more input that can be provided in treatment
sessions
Parents use the guidance and support that the can gain
from home programs to build confidence about how to
help their child
General Treatment

Handling and positioning

Stretching

Partial Body Weight Support Treadmill Training (PBWSTT)

Constraint-Induced Movement Therapy (CIMT)

Electrical Stimulation

Aquatics
General Principles of Good Positioning:
1. Symmetry and alignment should be respected as much as
possible in all positions
2. The child should feel comfortable
3. The positions should be varied and changed at least 2
hours to prevent pressure ulcer
Proper Bed Positioning:
Wheelchair to bed - Keep the child’s body close to you while
keeping the pt’s legs adduted/crossed
Bed to wheelchair –
NEUROREHABILITATION
NEURODEVELOPMENTAL TECHNIQUES

neuromuscular and functional reeducation technique now
includes neuroplasticity as a basis how the brain can
change and reorganize itself and its processes based on
practice and experience

Neuroplasticity - the ability of the brain to change and
repair itself.
Principles of Promoting Function-Induced Recovery
Focus on active
Engage the patient in active practice of
practice of
specific goal-directed activities
motor skills
“Use it or lose
it”
Repetition is
Focus on sufficient repetition to stimulate
important
brain reorganization using high levels of
practice both in-therapy and out-oftherapy and a carefully developed home
exercise program (HEP)
Intensity is
Focus on sufficient intensity of training
important
to stimulate brain reorganization,
carefully balancing the need for rest with
activity
Focus on
Continually challenge the patient’s
modifying motor movement capability with acquisition of
skills “Use it and new skills to ensure continued learning;
shape it to the
progressively modify skills to achieve
patient’s ability” functional outcomes
Enhance
selection of
behaviorally
important
stimuli
Enhance
attention and
feedback
Target goaldirected skills
Timing is
important
Age
I.
II.
III.
Reinforce behaviorally important stimuli
to enhance skill learning; create the best
possible environment for learning
Actively engage the patient in evaluating
goal-achievement and in making
accurate adjustments of motor skills
based on appropriate use of feedback
Select skills that are functionally relevant
and important to the patient; focus on
enhancing patient motivation and
commitment; allow for success, select
activities that are engaging and fun
Select skills that are functionally relevant
and important to the patient; focus on
enhancing patient motivation and
commitment; allow for success, select
activities that are engaging and fun
Plasticity and adaptive brain changes are
strongest in the young; plasticity and
brain changes in older adults may be
slower and less demonstrable
FACILITATION AND REMEDIATION
FACILITATION- Making things easier by guiding,
assisting and supporting (Roods, PNF, Brunnstrom)
REMEDIATION-CURE & CORRECTION (BOBATH)
OLD SCHOOL TECHNIQUES:
A. Doman-Delecato
B. Temple-Fay
C. Deaver
D. Phelps
E. Ayres
DOMAN-DELECATO (Deligado – some patterns are not safe for
the patient)

Aka patterning

Respiratory alkalosis (due to hyperventilation)
carbon dioxide inhalation
o paper bag to inc co2 – the imbalance may cause
“relaxation” or fainting
o has risk for suffocation

hypertonic

colic children -> always crying
sit on pt
hang upside down and whirled around
o decrease ms tone
o relaxation
 patterned with animals
TEMPLE-FAY

Ontogeny recapitulates phylogeny
more of evolutionary process
o ontogeny-normal human development
o phylogeny-animal evolution

Bacteria to fish to amphibians to reptiles to mammals to
four-legged animals to humans

Prone lying to unilat creep/crawl to contralat creep/crawl
to quadruped/all fours to standing ”walking” (ultimate
movement)

Progressive pattern movements
stage 1: prone lying
stage 2: homolateral stage
stage 3: contralateral stage
stage 4: on hands and knees
stage 5: walking pattern
DEAVER

Extensive use of bracing

Has evolved to ortho pros

Bed mobility & w/c techniques for ADL
AYRES

Sensory integration – other sensory stimuli may be used,
not only visual

E.g
sidelying to stimulus on side to roll (reflex roll)

Pts with:
visual agnosia, figure ground discrimination
PHELPS

RGR – reach-grasp-release

Focus on cp

Uses modalities
hot – to relax the patient
cold – facilitation/stimulation ex: in the RGR, if patient
cannot release object, ice may be used to stroke the
extensors and stimulate contraction of the muscles
sound
light
mechanical forces – from PT or machines
evolved to hydro & electro
MAJOR INTERVENTIONS
BOBATH

a problem-solving neurodevelopmental approach for
assessment and treatment of individuals with cerebral
palsy and other allied neurological conditions.

named after Berta Bobath, a physiotherapist, and her
husband Karel, a psychiatrist/neurophysiologist

avoids synergies & associated reactions

active and dynamic movements to bad side

key points of control
proximal: shoulder & pelvic girdle, spine
distal:
o UE to wrist thumb, thenar & hypothenar
eminence
o le-knee, ankle, big toe

Reflex Inhibiting Pattern/Posture (RIP)
clasping
o weak thumb above to prevent cortical thumb
o progress: rolling; flex & extend of shoulder
o shoulder EXABER, elbow ext & supination, wrist
and finger extension
o counter acts typical arm posture
o knee flex o counteracts knee ext synergy
 eg. bridging, tall kneeling, quadruped,
hooklying
Stages:
I.
Initial flaccidity
1. Bed: bed mobility-> use foot board, bed
positioning
2. Clasping to rolling (affected first then unaffected)
3. Supine to sit
4. Bridging
5. Sitting
II.
-
III.
-
-
Marked Spasticity
PIP & key pts of control
Tone inhibiting modalities & devices
Bobath sling, AFO (post leaf spring)
Sit to stand
o transfers (bed to chair w/c or mat)
o WT shifting
o bad leg at front at first then progress to bad leg
at back to promote
WB and dec spasticity WT shift lunge (at front to
back) walking no foot board to clonus
Relative recovery
only up to 90%
difficult to recover:
o ankle df
o wrist ext
o thumb opp
home & community amb – compensatory activities
pag nasa bahay na
o quad cane to single tip cane to indep
o ankle dorsiflexor assist
BRUNNSTROM














Signe Brunnstromm
uses assoc reactions
“Opportunistic” “movement therapy”
associated reactions:
reflex tensing of ms and involuntary limb mvts
imitation synkinesis
good copies what the bad cant do (squeeze ball)
Raimste’s phenomena
abd/add resist to abd/add of c/l le
add is easier to elicit
Sterlings phenomenon
Raimiste of UE
add is still easier to elicit
Souques phenomena
elev of UE beyond 90 deg to passive finger extension
used to grasp and release
Marie-foix/ Bechterev
bigtoe ext & toe flex to ankle df, knee and hip flex
Hungtington phenomenon
cough, yawn, sneeze
o increases spasticity
Pusher’s/ Listing phenomenon
at sitting - head rotation to good side and lat flex to
bad
ATNR (Fencer’s/Archer’s)
face side: ext o skull side: flex
STNR
neck flex: UE flex & LE ext
neck ext: UE ext & LE flex
TLR
prone: flex
supine: ext
STAGES:
1. Flaccid
no actions possible
2. Beginning spasticity
min assoc reactions and weak flexor and extensor
synergies
3. Peak spasticity
max assoc reactions
no voluntary control but with voluntary movement
within synergy
4. Declining spasticity/ into-synergy
voluntary control within synergy with minimal
movement outside synergy
5. Further declining spasticity/ out of synergy
voluntary control outside synergy (majority)
6. Isolated joint/motor actions
isolated motions
balance and equilibrium is present & coordination
7. Normal/ full motor control


IV
V
-
Reach forward 90deg
Hand slide at back
Pron & sup at 90deg, elbow flexion
Lat prehension at thumb
(-) sh abd
Reach FWD >90
Abd >90
Pron & sup at elbow ext
Soup number 5
o palmar prehension
o spherical
o cylindrical
o release
Hand correlations:
1. No hand actions
2. Start of mass grasp (min finger flex)
3. Strong mass group + min thumb actions (hook grasp- no
thumb)
4. Lat prehension/ min finger ext + mass grasp (mild) (some
thumb movement possible)
5. Soup no 5
6. All actions of thumb-EXAB (opp can’t be regained)
ROODS

Margareth Rood

Use of sensory motor stimulation

Sensory input = motor output (inc gamma efferent
activity)
Currently Used: 4 Ontogenic Stages

Mobility – OKC

Stability – CKC

Controlled mobility – wtshifting + CKC

Skill – OKC + CKC + wt shifting
8 ONTOGENIC MOTOR PATTERNS
1. Flexor withdrawal
2. Roll over
3. Pivot prone
4. Neck co-contraction
5. Prone on elbows
6. Quadruped
7. Standing
8. Walking
(i-table)

Facilitatory
Heavy joint approx. – tripod position (patient is
seated with affected UE placed on the back of the
seat, then ask patient to lean backward)
Fast icing/quick icing
o Reciprocal inhibition
Quick monitoring brushing
Pressure on ms belly/ origin
Quick stretch
Vibration
Gravity inversion – to facilitate elbow flexion, prone
whith elbow on the edge of the bed
Osteopressure (joint pounding) – heavy joint approx.
with pounding of the joint

Inhibitory
Light joint approx.
Slow icing to fatigue
o Autogenic inhibition
Slow brushing/stroking
Pressure on tendon/insertion
Slow stretch
Slow rocking/rolling
Rhythmic motion
Neutral warmth
Quadruped
PNF

Kabat & Ross

ADLS
Diagonals 7 spiral
Adjunct: roods
Maximum contraction=maximum effect

PNF devt/ progression
Motion start: prox to distal
Cephalo-caudal

Diagonals
D1 - UE
D2 - UE
D1 - LE
D2 - LE
A.
B.
C.
D.
E.
F.
G.
H.

1.
2.
3.
4.
Overflow & Irradiation
Max contraction of large ms to contraction of small/
weak ms
1 joint to movement of prox & distal joints
Max resist to max contraction
E.g. resist hip flexion to knee flexion + ankle
dorsiflexion
Ankle df to knee flex + hip flex
Timing for emphasis
Fast = concentric
Slow = eccentric
Alternating isometrics
Same side
Promotes mobility of trunk
Used prior to gait
Rhythmic stabilization
Opposite side
Trunk control
AI first before RS
Both used for PD & CVA & is prerequisite to gait
Rhythmic initiation
Passive to active assisted to resistive to active
Used to start movement
For PD, apraxia
Repeated contraction
Strengthening
Starts with quick stretch to activate ms spindle then
agonist contraction to new range & repeat until full
range
Fatigue
Chopping
Starts with D1 flexion to D1 extension
Assisted by: good side
For breaking synergy
For turning supine to prone
*Reverse shop: D1 ext to D1 flex (less functional)
Lifting
Start D2 ext to D2 flex
For overhead actions
For turning prone to supine
*Reverse lift: D2 flex to D2 ext (less functional)
Dual diagonals
B/L symmetrical
a. D1flex- eating, pray
b. D1 ext-push off chair
c. D2 ext-take shirt off, zipper
B/L asymmetrical
a. D1D2 flex-deodorant, violin, wearing shirt
b. D1D2 ext-pulling, mopping
Cross diagonals
a. D1flex & D2 ex-hugging
Reciprocals
b. D1 ext & D2 flex-towel at back

1.
Classifications
Directed to Agonist
Weak ms
Strengthening & initiation
a. Repeated Contraction
b. Rhythmic Initiation
c. Hold Relax Active Motion
o Reciprocal inhibition - when a ms contracts, the
antagonist relaxes
2.
Reversal of Antagonist
2 opposing consecutive/actions
a. Alternating Isometrics/ Rhythmic Stab
b. Quick Reversal
c. Slow Reversal
d. Slow Reversal Hold
3.
Relaxation
a. Hold Relax
o Of Agonist
o AI
o Ison: 30 Sec Hold
b. Contract Relax
o Of Antagonist
c.
d.
o RI
o Isotonic
Rhythmic Rotation
o Segmental Rolling
o Shoulder Girdle Rotate-Pelvic ms Relax
o Pelvic Girdle Rotate-Shoulder ms Relax
Slow Reversal Hold Relax
MOTOR CONTROL & LEARNING
1. Feedback
Internal: pain, stretch, kinesthesia,
proprioception
External: verbal, visual, tactile
2. Practice
Serial (a-b-c-d)
o with rest period: 3-5 min
Random (b-c-d-a)
o for long term memory retention
Blocked (ab-cd)
o decrease rest period: for endurance
TASK RELATED APPROACH

Carr’s & Shepards

Task-related activity
E.g.
o Go up stairs - march in place
o Go down stairs - squats
o Walking & running - bike ergo

Task-related position
Walking- standing
COMPENSATORY TRAINING APPROACH:

CIMT (Constraint Induced Movement Therapy)
Constraining good side to promote movt of bad

BWSTT (Body Weight Supported Treadmill Training)
Pt is forces to walk even though with difficulty so he
wont fall from treadmill
OTHERS

Specific Muscles
Serratus Anterior - push ups with plus
Upper trapz - shoulder shrugs
Middle trapz and rhomboids - prone arm lift
Lower trapz - prone superman lift
Pecs major - bench press
Lats dorsi - lats pull-up/down
Quads - squat
Iliopsoas - sit ups
Rectus femoris - SLR
Hamstring - hamstring curls
TA - dorsiflexion
Gastroc – tiptoes

Spine Exercises
a. McKenzie Extension Exercises
Herniation
Osteoporosis
AS
Post traumatic compresion fx
-
Prone 5 min
Prone on elbows
Prone on hands
Prone on fingers
Cat and camel
Standing hyperextension
b.
William’s Flexion Exercises

Post pelvic tilt
U/L knee to chest
B/L knee to chest
SLR
Wall slides
Slump
Neck & TMJ Exercises
Calliet exercises - rhythmic neck exercises