SESSION 6

UZM.FZT. TÜRKÜ ASYA ÇİFTÇİ

 NEUROLOGIC DISORDERS
HUNTINGTON’S CHOREA ESSENTIAL TREMOR TARDIVE DYSKINESIA
• Progressive hereditary condition • Most frequently seen movement
affecting the basal ganglia. disorder that causes progressive • Difficult-to-treat and often
Symptoms: hand shaking during voluntary incurable form of dyskinesia
• Abnormal movements (Chorea), movements. • Motor disorder caused by
• Dementia and psychiatric • No other neurological signs, long-term antipsychotic use.
features (the earliest worsens with fatigue/nervousness. Symptoms: Random movements
PT Focus: Muscle strength, control, of the face and sometimes limbs.
symptoms.)
• Sound drunk (Swallowing and coordination.
speech ) TOURETTE’S SYNDROME
PT Focus: Gait re-education, HEMIBALLISMUS
"Tic Talk Tourette"
balance training
More time to carry out • Rare disorder causing violent,
• Involuntary tics and
everyday tasks exhausting movements.
utterances.
• Caused by basal ganglia
• Caused by a
damage; may remit
combination of genetic
spontaneously.
and environmental
factors.
INFLAMMATORY/INFECTIOUS CNS Medical management:
CONDITIONS • Medications such as an antibiotic for bacterial
meningitis
• Analgesics for pain
Meningitis Inflammation of the meninges (pia, • Anticonvulsants to prevent seizures
arachnoid, dura). • Corticosteroids to decrease inflammation
Increased risk of:
•Infarctions PT Focus: Prevent secondary complications, monitor
•Blood clots: cortical veins may develop a vitals and mobilize as tolerated below the point of
thrombosis fatigue, improve strength mobility once tolerated
•Hydrocephalus: CSF may be blocked secondary to
scar tissue Etiology:
oThis will result in headache = cardinal sign • Aseptic: fungus, virus, parasite
• Can present as acute (hours to days); sub-acute (2 • Can also get with: herpes simplex 2, epstein-
weeks plus); chronic (1 month plus) barr, lupus
• Bacterial: often a medical emergency
• Headache, fever, vomiting, rigidity of the neck • Example: Tuberculosis
• Meningitis = M-E-N-I-N-G
• Meninges affected, Physical test for meningitis
• Elevated fever, • Patient supine, passively flex neck
• Neck stiffness, • Brudzinski’s sign: patient will involuntarily flex
• Increased risk (infarctions, clots), knees and hips to lessen stretch on inflamed
meninges
• Nausea,
• General malaise
 STAGES

Stage 1 Stage 2 Stage 3

Local presentation - Long term neurological

local rash (bulls-eye Infection spreads issues (neuropathy),
rash), erythema, flu through bloodstream arthritis and cognitive
like symptoms deficits

Neurological symptoms
Headache and neck stiffness,
may have Bell’s palsy

PT management: Musculoskeletal
symptoms
•Mimics other diseases like MS, Relieve pain Fatigue and weakness
fibromyalgia, chronic fatigue Prep deconditioned patients for home
syndrome, Guillain-Barre exercises, improve functional strength
•Antibiotics to treat Educate: FITT, pace and plan, exercise Cardiac symptoms:
tachycardia, bradycardia,
without exacerbating symptoms arrythmia, myocarditis
DISEASES AFFECTING THE
NEUROMUSCULAR JUNCTION
Rare, chronic, autoimmune disease. Antibodies block
Myasthenia Gravis Acetylcholine (ACh) receptors at post-synaptic membrane
of neuromuscular junction causing failure of muscle
• Weakness and increased fatigue contraction due to impaired nerve signal
with repeated contraction;
improved with rest. Exercise program:
• oFacial muscles - often first • Strengthening after administration of
shows up in eye muscles acetylcholinesterase inhibitors
• oProgression to generalized • Exercise followed by rest
muscle weakness • Breathing exercises
• oProximal muscles more involved Education:
than distal • Fluctuating nature of symptoms
• Mnemonic: "Myasthenia = MY • Fatigue management
Eyes Got Weak" • Energy conservation techniques
• Pacing and planning
 Slow progression of:
Post-Polio Syndrome • New asymmetrical muscle weakness and
atrophy Strength testing:
• Progressive muscle weakness in • Polio gait: severe atrophy of quads results in • Varies with time of day tested
individuals with a history of polio. inability to keep knee extended at heel and more likely to
strike and patient needs to use hand on demonstrate fatigue and
knee to push knee back to avoid knee
buckling weakness in afternoon.
«P.O.L.I.O.» • Fasciculations (involuntary muscle twitches • Caution with repeated
that are visible under the skin) strength testing - patient will
Progressive • Abnormal levels of fatigue fatigue and results will be
Overuse • Decreased endurance, functional mobility, skewed.
aerobic capacity • Monitor for compensatory
Leg weakness,
Post-polio myalgias (muscle pain): strategies.
Inability to maintain function
• Occurs only in muscles affected by polio
Old (history of polio). • Deep or superficial aching pain
• Typically occurs at night or end of the day PT Focus:
Cause: • General body conditioning
Overuse/biomechanical pain:
• Neural fatigue theory: • Includes injuries to soft tissue as well as (moderate intensity)
• Poliovirus attacks specific brainstem myofascial pain due to overuse • Light to moderate aerobic
and spinal cord neurons (LMNL). • Trigger points, muscle tightness conditioning
• Surviving motor neurons • Degenerative joint disease • Exercise when less fatigued or
compensate by sprouting new nerve • Weakness induced by polio-affected most rested (morning is usually
terminals to affected muscle fibers. muscles, as well as poor body mechanics,
• This initially restores movement, but makes the joints more susceptible to the best)
over time, these overworked motor development of arthritis • Energy conservation,
units fatigue, leading to new • Breathing exercises.
denervation and post-polio Diminished or absent reflexes
• Gait aids
symptoms. Sensory system is not affected
PERIPHERAL NEUROPATHIES
• The most common cause is diabetes.

• Autoimmune disease of unknown cause affecting cranial nerves and peripheral nerves. Acute demyelination. Some cases
Guillain–Barré triggered by viral infection:
Syndrome • Patient experienced the signs and symptoms of an infection in the 3–6 weeks prior to the onset of the neurological
symptoms.
• Symmetrical weakness and paresthesia begin in hands and feet and progress proximally
Presentation: • Rapidly progressive (1 day - 2 weeks to max severity)
• Autonomic system often affected (HR, BP, temperature regulation issues)

• Weeks to years
• Gradual re-myelination with good prognosis (depending on initial severity)
Recovery: • 1/3 of individuals have permanent weakness
o Re-myelination occurs in proximal to distal fashion so distal muscles are slower to recover and have greater potential for
permanent weakness

• Early stages:
o Mechanical ventilation
o Chest physio (secretion removal)
o Breathing exercises (prevent atelectasis)
o Educate patient and family on proper positioning
Treatment:
o Maintain PROM
• Late stages:
o Functional muscle strengthening
o Endurance training
o Gait retraining, gait aids as necessary
 PERIPHERAL NEUROPATHIES Charcot Marie
Tooth Disease

Presentation: Treatment:

Slow Weakness Maintain

Distal to
progressio Weak Diminishe and movement Managem
proximal Atrophy of Foot Loss of Neuropath Orthotics,
n of dorsiflexor d deep sensory Late , muscle ent/educa
disease foot deformitie sensation ic pain Fatigue gait aids
symmetric s (foot tendon loss in stages: strength tion on
progressio intrinsics s in feet issues as needed
muscle drop) reflexes hands and and foot care
n
weakness forearms flexibility
as disease
progresse
s Can see Contractu
proximal re
Pes cavus, muscle
hammer managem
weakness ent
toes leading to
ETIOLOGY postural
(stretching
, resting
issues, splints)
• Hereditary motor and breathing
problems
sensory neuropathology. Moderate
• Extensive demyelination of activity
but
motor and sensory nerves: overexerti
on should
• Especially in feet be
avoided
PERIPHERAL NEUROPATHIES
Bell’s Palsy Causes:
• Peripheral nerve injury: • Idiopathic (unknown) Treatment:
facial nerve (CN VII) • Tumor •Corticosteroids
• Traumatic (e.g. dental work) •Facial muscle exercises
• May be due to viral infection (e.g. latent herpes virus) •Muscle stimulation - poor
• Acute inflammation of facial nerve results in evidence to support that this is
compression of the nerve helpful
• Parotid gland dissection due to malignancy or •Pain management: heat
infection •Protect eye with eye drops
Clinical manifestations: •Recovery can sometimes
• Unilateral facial paralysis occur (partial or full):
CN VII function: • Unable to smile, scrunch forehead, raise • May take days to months
• Muscles of facial eyebrows, puff cheeks
expression • Drooping of corner of mouth
Other causes of facial
• Dampens vibrational • Drooling
weakness:
sound (stapedius • Drooping of corner of eye
Tumor, stroke, meningitis,
muscle of inner ear) • «Crocodile tears”
• Taste (anterior 2/3 diabetes, TBI, sarcoidosis,
• Eyelid won’t close
aspect of tongue) myasthenia gravis, lyme
• Dry eyes
• Tears and salivation disease, guillain-barre
• No taste on anterior 2/3 of tongue
 Question: When might we see a bilateral facial nerve
palsy?

1. Infection: In infections like Lyme disease, the bacteria

can invade the facial nerves directly, causing
inflammation and damage to the nerves on both sides
of the face.
2. Compression: In cases of bilateral acoustic neuromas
or severe trauma, the facial nerves can be compressed
bilaterally. This pressure can disrupt the function of the
nerves, leading to weakness or paralysis on both sides.
LMNL: entire ipsilateral face droops 3. Systemic Conditions: In conditions like diabetes,
UMNL: contralateral face droops but the forehead is chronic hyperglycemia can cause microvascular
spared damage, leading to ischemia and nerve dysfunction on
both sides, potentially resulting in bilateral facial palsy.

4. Inflammation: In conditions like Guillain-Barré Syndrome or sarcoidosis, the body's immune response causes
inflammation of the facial nerves. This inflammation can lead to nerve dysfunction, resulting in muscle weakness on
both sides of the face.
5. Demyelination: In diseases like Guillain-Barré Syndrome and Myastenia Gravis, the immune system attacks the
myelin sheath (the protective covering of nerves), leading to a loss of nerve signal transmission. When this process
affects the facial nerves bilaterally, it results in bilateral facial palsy.
PERIPHERAL NEUROPATHIES
Diabetic Neuropathy
• Peripheral nerve disorder in diabetes that occurs without any other cause for neuropathy

Pathology: Presentation: Treatment:

Chronic metabolic disturbance

affects nerve and Schwann Symmetric Control hyperglycemia
cells. Education on skin care
o Hyperglycemia leads to Distal pattern of sensory loss (amputation is common due to
abnormal micro-circulation diabetic ulcers)
and leads to loss of both Painless paresthesia with
myelinated and unmyelinated minimal motor weakness
axons
PERIPHERAL NEUROPATHIES
Stages:
Complex Regional Pain
Syndrome (CRPS) Stage 1 (0-3 Stage 2 (3-6 Stage 3 (6 months
months): months): plus):
• Formerly known as Reflex Sympathetic
Dystrophy (RSD)
Increased pain and Tight, smooth,
 Chronic pain condition Burning pain glossy, cool, pale
joint stiffness
believed to be the result skin
of dysfunction in central Puffy swelling Stiffness and
Firm edema (feels
or peripheral nervous hard or solid to the contractures
system: touch rather than
o Develops after trauma, Redness soft or pitting) Nail and hair
surgery, UMNL changes

Warmth Cyanosis
Severe osteopenia
Typical features:
•Changes in the color and temp of Joint stiffness Muscle atrophy Treatment:
the skin over the affected limb or •Prevention and early detection -
body part Increased sweating Brittle nails (weak, early AROM and use
prone to cracking, •Pain and edema management
•Intense burning pain, skin splitting, or breaking
sensitivity, sweating, swelling, easily) (desensitization, contrast baths,
Allodynia
stiffness TENS, gentle massage, electrical
Osteopenia on x-ray stimulation)
Positive bone scan •Education
 Signs and
Type Mechanism of Injury Result Recovery
Symptoms

Temporary disruption of Good prognosis (recovery

Pain, minimal or no
nerve conduction without Reversible conduction within minutes to days or
muscle wasting, muscle
Neurapraxia loss of axonal continuity; block; no axonal weeks as
weakness, numbness,
caused by compression or degeneration. swelling/compression
proprioception affected.
mild ischemia. resolves).

Damage to the axon with

intact surrounding
Fair prognosis (axon
connective tissue Pain, muscle wasting,
Axonal degeneration regenerates at a rate of
(endoneurium, complete loss of motor
Axonotmesis distal to the injury approximately 1 mm/day;
perineurium); usually and sensory functions
(Wallerian degeneration). recovery may take
caused by severe below the level of injury.
months).
compression or crush
injuries.

Complete severance of
the nerve, including the
No pain (anesthesia), Poor prognosis without
axon and surrounding Complete loss of nerve
muscle wasting, surgery; even with
connective tissues function; requires
Neurotmesis complete loss of motor surgery, recovery is
(endoneurium, surgical intervention for
and sensory functions variable and may not be
perineurium, and any chance of recovery.
below the level of injury. complete.
epineurium); often caused
by laceration.
Wallerian degeneration: Recovery of peripheral nerves following
• Also known as axonal or anterograde injury:
degeneration. • Distal end of the portion of the nerve fiber proximal
• Process that occurs when a nerve fiber is injured to the lesion sends out sprouts.
but surrounding connective tissue is still intact.
• Sprouts are attracted by growth factors.
• The segment of the axon distal to the injury
degenerates including myelin sheath around it. • Sprouts may eventually reach target tissue allowing
• There is no degeneration of the neurons cell body
for re-innervation.
(as it lies proximal to the injury). • Axon sprout re-growth: 1mm/day:
o Upper extremity 4-6 months (up to 2 years)
o Lower extremity 7-9 months (up to 4 years)

Segmental myelination:
• Focal degeneration of the myelin
sheath with sparing of the axon.
o E.g. Guillain-Barre syndrome
• Re-myelination restores function,
but the nerve conduction velocity can
be slower compared to pre-damage
levels.

Retrograde degeneration:
• The segment of the axon proximal to Regeneration in the CNS:
the injury degenerates (axonal
degeneration spreads backwards). • Compression of any part of the CNS causing
ischemia for greater than 3-5 minutes will result
• There is degeneration of the neurons in death of the nervous tissue.
cell body (as it lies proximal to the
injury). • Regeneration of nerves, as seen in PNS, is not
possible.
VESTIBULAR DISORDERS
Function of vestibular system:
• Gaze stabilization: objects in
visual field stay clear with head Vestibular System
movement. Movement of
otoconia (crystals)
• Postural stabilization: maintain
Semicircular Otolith cause stimulation
balance and equilibrium.
Canals Organs of hair cells
• Spatial awareness: understand
where you are in space
Three Canals Detect acceleration Saccule Utricle
and deceleration
Sense static head
position (relative to
Stimulate vestibulo- Horizontal Anterior Posterior gravity)
ocular reflex (VOR) Detects vertical Detects horizontal
Detect rotational plane motion (e.g. plane motion (e.g.
movements when in an elevator) acceleration in a car

Function: Detects Detects rotation of the head in

the sagittal plane (e.g. nodding)
sagittal plane

rotation of the head

around a vertical axis and rotation in the frontal plane Detects tilting of
(e.g. cartwheeling) Detects tilting of
Movement of fluid that occurs (e.g. pirouette) head
head side to side
during head rotation pushes on forwards/backwards
a structure called the cupula,
which contains hair cells that
transduce the mechanical
movement to electrical signals
 Vertigo Dizziness Oscillopsia Nystagmus Others
Vestibular ocular reflex (VOR):
• Maintain stable vision during A sensation of
head movement by producing being off
balance,
eye movements in the unsteady,
having a
Involuntary,
rapid and
direction opposite to head Subjective discrepancy repeated
movement of
movement. experience
of
between right
and left sides
Blurred
the eyes Change in
hearing,
nystagmus vision due
• Enables us to keep our eyes (room Patient can’t to objects
light-
headednes
focused/fixated on an object spinning work out in vision
Vertical or s, nausea,
around you) jumping/os
while we move around in Occurs
where they
are in space cillating horizontal vomiting,
migraine
space. when you
with torsional
component in
have BPPV peripheral
• Deficient with unilateral and This is not the
same as
vestibular
issues Pure
bilateral vestibular loss. vertigo vertical in
CNS issues
VESTIBULAR CONDITIONS
Benign paroxysmal positional vertigo (BPPV):
• Displacement of otoconia crystals from otolith organs.
• Otoconia displaced most often into posterior semicircular canal.

Presentation:
• Brief transient vertigo when looking up/down, rolling to that side in bed, sitting to supine, bending forward to pick something up
• Due to crystals stimulating hair cells in canal creating the illusion of motion
• Dix-hallpike maneuver to test for BPPV in posterior and anterior canals:
• Head rotated 45 degrees to test ear and neck extended 30 degrees
• Patient lowered from sit to supine maintaining head position and keep for 30 seconds
• Positive test: presence of transient nystagmus
• Supine roll test to test for BPPV in horizontal canal

Contraindications to dix-hallpike:
• Cervical spine instability
• Atlantoaxial subluxation/instability (RA, Down Syndrome)
• Vertebral artery insufficiency
• Prolapsed intervertebral disc with radiculopathy
• Cervical myelopathy
• Previous cervical spine surgeries.

Treatment
• Epley maneuver.
Unilateral Vestibular Loss (UVL):

• Unilateral peripheral vestibular dysfunction.

Causes

• Infection (vestibular neuritis, labyrinthitis), disease (Meniere’s), trauma, surgery (acoustic neuroma).
• Meniere’s disease: disease of the inner ear due to an over accumulation of endolymph

Characterize

• Episodes of vertigo, progressive unilateral deafness, low frequency hearing loss, tinnitus (ringing in the ears), and a sense of
pressure in the ears
• Acoustic neuroma: benign growth forming on the cells of CN VIII

Presentation
• These patients have dizziness and balance issues due to the imbalance between the left and right vestibular systems.

Acute presentation
• Spontaneous nystagmus, reduced VOR gain, vertigo (resolving within a few days), dizziness, oscillopsia, imbalance

Chronic presentation
• Depends on compensation, but can present as dizziness, oscillopsia, imbalance, motion intolerance/sensitivity, and
symptoms worsening with repetitive head movements

Treatment
• Gaze stability exercises, maintain general fitness, education, mobility aids and balance training to reduce falls risk
VESTIBULAR CONDITIONS
Bilateral Vestibular Loss (BVL): Central Vestibular Disorders:

Causes
Causes
• Toxicity, bilateral vestibular infections,
vestibular neuropathy, otosclerosis. • TBI, stroke, brain tumor, MS, congenital
o Gentamicin malformations (e.g. Chiari
o Antibiotic that can have a toxic destructive malformation).
effect on the vestibular system

Presentation:
Red flags

o Very poor balance especially with eyes closed • Direction changing nystagmus, pure
o No sensation of dizziness or vertigo because vertical nystagmus.
there is not a mismatch between the left and • Recovery dependent on cortical
right vestibular systems
reorganization/neuroplasticity.
 Vertigo/Dizzines Other Symptoms Tests Nystagmus
s
• Vertical beating
Benign
Transient +/- Nausea withtorsion
paroxysmal • +’ve dix-hallpike test
positional +/- Vomiting (post/ant canals)
positional
vertigo lasting +/- Imbalance and • Horizontal
vertigo • Negative others
<2mins light-headedness (horizontal
(BPPV)
canal)
• Head thrust test and
dynamic visual
Imbalance
Unilateral Dizziness acuity(DVA)
Oscillopsia
Vestibular Loss worsens with • Symptoms with Acute phase only
+/- Nausea
(UVL) head movement quick head
+/- Poor gaze stabilization
movement, even
when walking
• Imbalance
Oscillopsia
(visual field
Bilateral • +’ve Rhomberg
appear to
Vestibular Loss No vertigo • Worse with eyes No nystagmus
oscillate,
(BVL) closed
move, or
bounce)
• Falls risk ++
• Variable
Variable associated • Red flags:
Central symptoms that can occur Direction
Variable vertigo
Vestibular at rest - unaffected by changing
and dizziness Variable findings
Disorders head position or nystagmus or
movement purevertical
nystagmus

Dynamic visual acuity(DVA) Head thrust test

CRANIAL NERVES
12 pairs of nerves emerging from the brain
(CN I, II) and brainstem (CN III-XII).
• Know their order and their number using
roman numerals (e.g. CN VII = facial nerve).
o Pneumonic: Ooo Ooo Ooo, To Touch And
Feel Very Good Velvet Aaa Hhhh!
• Think about how we can test each nerve.

Know it’s primary function:

o Pneumonic: Some Say Marry Money, But My Brother Says

Big Brains Matter More
▪ The first letter of each words stands for S: sensory M:
motor B: both
• For example: olfactory – contains only sensory as it
controls smell
 CRANIAL NERVES
Cranial Nerve Classification Major Function Damage to Assessment
Nerve will
cause
Have the
patient close
Anosmia: their eyes
I -Olfactory Sensory Smell inability to and identify
detect smells 1-2
identifiable
smells
CRANIAL NERVES
Cranial Nerve Classification Major Function Damage to Nerve Assessment
will cause
Vision (acuity Different types • Have patient read from a
II - Optic Sensory
and field of of vision loss card one eye at atime
vision) depending on • Have the patient cover one eye
where the and stare straight ahead at your
Pupil reactivity damage occurs nose. Have them identify the
along the visual number of fingers you are
pathway from holdingup in each of the four
brain to eye visual field quadrants

See image below

Deficits Lesion Location Description

A Total blindness of Optic nerve Optic nerve injury will result in ipsilateral loss of vision
ipsilateral eye
B Tunnel vision Injury at optic chiasm (e.g. • Loss of temporal vision bilaterally due to the loss of part of
tumor) the visual pathway that crosses at the optic chiasm
Optic chiasm: where • Nasal vision remains = tunnel vision
temporal vision of optic
nerves cross
D Contralateral Optic radiation (pathway • With contralateral homonymous hemianopsia, lose
homonymous within visual cortex) contralateral visual field of both eyes
hemianopsia • The right visual cortex controls the left visual field of both
eyes (and vice versa)
• Left visual field = left temporal vision and right nasal vision
CRANIAL NERVES
Cranial Nerve Classification Major Function Damage to Nerve will cause Assessment

• Extraocular eye • Diplopia (double vision) • Pupillary responses: darken the room
III -Oculomotor Motor
movements • Strabismus (eyes do not and shine a bright light into one of the
(except LR and align properly with each patient’s pupils. Look for constriction in
SO) other when looking at an that eye (directreflex) and the
• Pupil size and object) contralateral eye (consensual)
reactivity • Ptosis: difficulty opening • Accommodation: have the patient stare
eye at your finger as you move it from your
• Convergence • Pupil constrictionissues nose totheirs and look for convergence
and constriction of both pupils
• Eyelid elevation • Eye movement: have the patient cover
one eye and watch your finger as you
move it up,down, diagonally and inward
• Check for ptosis

Except LR and SO
• The oculomotor nerve does not control the
Lateral Rectus (LR) and Superior Oblique
(SO) muscles.
• The Lateral Rectus muscle, which moves
the eye outward (abduction), is controlled
by the Abducens nerve (Cranial Nerve VI).
• The Superior Oblique muscle, which
moves the eye downward and inward
(depression and intorsion), is controlled by
the Trochlear nerve (Cranial Nerve IV).
CRANIAL NERVES
Cranial Nerve Classification Major Function Damage to Nerve will Assessment
cause
Extraocular eye Difficulty looking down Have the patient look
IV -Trochlear Motor
movement: Superior and inwards towards the tip of their
oblique (turning eyes e.g. “can’t see feet” nose
downward while looking
inward)
CRANIAL NERVES
Cranial Nerve Classification Major Function Damage to Nerve will Assessment
cause
• Motor: have the
V -Trigeminal Both • Chewing
• Altered sensation patient open their
• Sensation - pain,
including dysesthesia, mouth and hold their
3 branches:(V1, V2, V3) touch, temperature
paresthesia or jaw as you apply a
to face, neck, sinuses
allodynia medial force on both
and meninges
• Jaw dysfunction sides
• Sensory: have the
patient close their
eyes andlightly touch
the face with a tissue
• 1) on the forehead
• 2) on the cheek and
• 3) base of jaw
CRANIAL NERVES
Cranial Nerve Classification Major Function Damage to Nerve will Assessment
cause
Extraocular eye Eyes cannot abductand
VI -Abducens Motor Have the patient look side
movements: Lateral drift medially to side
rectus (turning eyes
laterally)
CRANIAL NERVES
Cranial Nerve Classification Major Function Damage to Nerve Assessment
will cause
• Have the patient
VII - Facial Both • Facial expression • Droopy mouth • 1) raise the
• Taste (anterior2/3
eyebrows
of tongue) • Difficulty speaking • 2)strongly
• Eyelid and lipclosure
• Difficulty with facial shut the
expression (e.g. eyes
cannot raise • Have the patient
forehead) • 1) smile
• Inability to close • 2) grimace
eyes
• 3) puff
cheeks
• Have sugar and salt
ready and have the
patient identify
which is which by
placing it on the front
of the tongue
CRANIAL NERVES
Cranial Nerve Classification Major Function Damage to Nerve Assessment
will cause
• Have the patient
VIII - Sensory • Hearing • Deafness
close their eyes and
Vestibulocochlear • Balance problems identify when they
• Equilibrium Gaze • Vertigo can hear a subtle
sound, such as
stability • Nystagmus rubbing your fingers
together
• Equilibrium tested in
subsequent testing
if hearing seems
impaired
CRANIAL NERVES
Cranial Nerve Classification Major Function Damage to Nerve Assessment
will cause
IX -Glossopharyngeal Both • Loss of bitter and • Touch back of
• Gag reflex sour taste throat with
• Impaired sterile tongue
• Swallowing swallowing depressor
• Phonation (voice • Speech • Have the patient
quality) impediments swallow
• Taste: post 1/3 of tongue
CRANIAL NERVES
Cranial Nerve Classification Major Function Damage to Nerve Assessment
will cause
• Assess gag and
• Gag reflex swallowing as
• Swallowing above
• Impaired
• Speech (muscles of • Have the patient
swallowing
X - Vagus Both larynx) recite a phrase
• Speech
• Parasympathetic such as “lips,
impediments
control of heart, lung teeth, tip of the
• Organ dysfunction
and digestive tract tongue” to assess
phonation
CRANIAL NERVES
Cranial Nerve Classification Major Function Damage to Nerve Assessment
will cause
• Trapezius: have
patient shrug the
shoulders
• SCM: have patient
• Inability to shrug
side flex
ipsilateral shoulder
• Shoulder movement (via ipsilaterally and
(trapezius)
trapezius) rotate their head
XI - SpinalAccessory Motor
• Head side flexionand contralaterally
rotation (via SCM muscle) • Inability to turn head
to opposite side • E.g.: left SCM is
(SCM) tested by asking
patient to side flex to
the left and rotate to
the right
CRANIAL NERVES
Cranial Nerve Classification Major Function Damage to Nerve Assessment
will cause
• Have the patient
repeat a phrase
• Dysarthria • Have patient stick
XII -Hypoglossal Motor Muscles of the tongue • Deviation of tongue out their tongue and
towards weak side moveit from side to
side
 E before R
B before W

Receptive Aphasia
Graphesthesia Rigidity
• Ability to recognize written symbols traced on the skin. •Constant resistance to passive movement, not varying with
•Can speak but cannot understand verbal commands.
speed; no abnormal postures.
Expressive Aphasia Hyperpathia Dystonia
•Understands speech but cannot speak. • Increased sensitivity to pain, where everything feels •Involuntary muscle contractions causing twisting movements
sharp. or abnormal postures.
Anosognosia
•Lack of awareness or denial of neurological deficits,
Neuropathy Athetosis
especially paralysis. • Disease affecting nerves, leading to motor, sensory, and •Slow, writhing movements primarily in distal extremities, due
autonomic changes. to basal ganglia damage.
Astereognosis
Chorea
•Inability to recognize objects by touch without sensory Diaschisis
loss. •Quick, jerky, random movements, often affecting proximal
• Loss of function in brain areas connected to but distant limbs.
Tone from a damaged site.
•Muscle readiness state, balancing support against Ataxia
gravity and smooth joint movement. Myelopathy •Poor muscle coordination, often due to cerebellar lesions.
Hypertonia • Disease or damage to the spinal cord.
Dysdiadochokinesia
•Excessively stiff muscles due to increased readiness,
often from motor cortex involvement. Fasciculation •Difficulty performing rapid alternating movements.

Hypotonia • Visible twitching of muscle fibers, typically in a single Dysmetria

motor unit, associated with lower motor neuron
•Reduced muscle tone, leading to weak voluntary lesions. •Inaccurate reaching of targets, overshooting or
muscle force. undershooting.
Spasticity Fibrillation Proprioception
•Increased stretch reflexes and exaggerated tendon • Abnormal, involuntary muscle contractions seen only •Awareness of body position in space.
jerks; a sign of upper motor neuron syndrome. on EMG, indicating dying neurons.
 •Bone

ARTHRITIS Sources of pain in

osteoarthritis:
•Soft tissue
•Inflammation
•Muscle spasm

OSTEOARTHRITIS Hallmark signs: •Joint stiffness, especially in the morning

•Loss of range of motion in capsular pattern

•Pain after prolonged immobility
Pain with movement
RISK FACTORS •Pain on joint line with palpation
Abnormal enzyme release and biomechanical
•Joint enlargement
forces damage articular cartilage.
• Increased age •Have you had pain most days in last month?
• Sex (W>M) 4 subjective •Have you had pain over the last year?
questions to
• Genetics diagnose OA: •Is your pain worse with activity?
•Is your pain relieved with rest?
Cartilage loss causes bones to rub together, • Obesity
leading to: • Physical inactivity
•Pain • Injury Knee: most common 3 signs indicative of OA
•Swelling
•Increased bone turnover
• Joint stress (e.g. joint: of the knee:
•Osteophyte formation occupation, kneeling,
• More common in people with a • Flexion contracture
squatting, stair climbing)
varus knee alignment • Antalgic gait
• Crepitus often present • Swipe test or patellar tap
Damage occurs due to: Diagnosed by x-ray
•Abnormal stress on normal cartilage
finding: 4 main features:
•Normal stress on abnormal cartilage
• Joint space narrowing Loose bodies: free floating Treatment: joint traction, open
• Osteophytes piece of bone or cartilage. kinetic chain exercises,
• Subchondral cysts Often a result of OA or chip isometrics through range
Both scenarios result in localized fracture. •Avoid closed pack position for exercises
• Subchondral sclerosis (closed kinetic chain exercises)
increased loading and progressive (increased bone • Typical symptoms: locking or •Example of open kinetic chain exercise:
micro-injury. density) catching knee extension with weight on ankle at
edge of bed
 OSTEOARTHRITIS Scaphoid bone is
more tended to be
COMMON AREAS
avascular necrosis Treatment:
after fracture
•Treatment often progresses from conservative management (PT) to
surgical intervention (e.g. joint replacement)
Hip: Uncommon •Exercise (strengthen/stretch muscles around OA joint)
Knee Spine: Hand: Foot:
common: joints: •Improve proprioception, agility and balance
•Activity modification (e.g. decreased weight bearing activities like
swimming or cycling)
Osteophyte Shoulder, •Bracing or use of walking aids
Walk with PIP First
s in facet elbow, Wrist •Weight loss
Trendelenb osteophytes = metatarsal
joints of wrist and •Acetaminophen
urg Bouchard’s joint
lumbar ankle
node
spine can Unable to move
cause Can occur the limb
stenosis Osteophytes if scaphoid
Groin pain

Red Flags with Arthritis

DIP can form at fracture or
osteophytes this joint avascular Intense joint pain
= causing necrosis
Heberden’s hallux valgus
node and rigidus, Joint swelling
Osteophytes may have
bunions
Signs of septic arthritis: Joint redness

Flexion CMC joints

deformities Low fever
and
decreased
internal B before H Chills may occur
rotation
B more proximal than H Possible
tachycardia
OSTEOARTHRITIS
Inflammatory Non-Inflammatory
Feature Condition Condition Back pain comparison
Pain (worse when?) Yes – worse in the AM Yes – worse after used Inflammatory Mechanical
Features Back Pain Back Pain
Swelling Moderate to severe Mild Usually, prolonged >60
Morning stiffness Minor <40 minutes
minutes
Redness Sometimes Absent Late in the day after
Max pain/stiffness Early morning activity/use
Warmth Sometimes Absent Exercise/activity Improves symptoms Worsens symptoms

Morning stiffness > 1 hour Less than 30 min Duration Chronic Acute/chronic

Sometimes (e.g. fever, Age of onset 12-40 years 20-65 years

Systemic features Absent
fatigue)
Sacroiliitis, Osteophytes, disc
Uncommon (will have Radiographs
Increase in ESR Frequent syndesmophytes, spinal spaces, narrowing,
normal test)
ankylosis malalignment
Examples: RA OA

Erythrocyte sedimentation rate (ESR)

RHEUMATOID ARTHRITIS Presentation:
Symmetrical pattern
Leads to: • Pain
• Fatigue
• Synovitis is the main feature. •Immobility and consolidation of a • Stiffness (decreased ROM)
• Synovium becomes swollen and cells proliferate joint.
into a dense cellular membrane (pannus) which • Swelling
•Bones can become osteopenic.
spreads over articular cartilage and erodes the •Ligaments and tendons become
• Joint deformity
underlying cartilage and bone. damaged or ruptured. • Muscle atrophy.
• Over time the pannus may extend to the opposite •Surrounding muscles deteriorate
articular surface creating: leaving joint unstable and prone to
o 1) fibrous scar tissue 2) adhesions 3) bony deformity Diagnostic criteria for RA (need 4 of 7) for at
ankylosing (union of bones of a joint) least 6 weeks:
Autoimmune disease: 1.Morning stiffness greater than 1 hour
2.Arthritis of 3 or more joints
3.Arthritis of hand joints
• Wrist, MCP or PIP joints
4.Symmetric arthritis
RISK FACTORS 5.Rheumatoid nodules
• Sex: Women are 2-3 times more likely to develop RA. 6.Radiographic changes
• Pregnancy: Can trigger RA due to body changes. • Including erosions or periarticular osteopenia in hands and/or
wrist joints
• Age: Commonly starts between 40-60 years.
7.Serum rheumatoid factor
• Family History: Higher risk if a relative has RA. • Antibodies produced by immune system that attack healthy
• Smoking: Increases RA risk and severity. cells - associated with autoimmune diseases
• Environmental Exposures: Asbestos or silica might
raise RA risk. Abnormal antibody HLA-DR4 in 80% of
people with RA.
RHEUMATOID ARTHRITIS Deformities:
Swan neck Boutonniere
Hallux valgus MTP subluxation Claw toe Hammer toe Mallet toe Ulnar drift
deformity deformity

Synovitis,
MTP and PIP Flexion of DIP, MCP synovitis Flexion of MCP (not Zig zag deformity -
1st MTP synovitis displacement of the MTP synovitis
flexors
synovitis affects longest toe. leads to MCP always) MCP
subluxation causes
re-positioning of
tendons and pull of
Ligament laxity and Unopposed Usually involves phalanges towards Hyperextension of Hyperextension
extensors pull the MTP extension ulnar side of hand.
erosion 2nd toe PIP (not always)
proximal phalanx
into hyperextension

Subluxation --> Flexion of PIP and

Metatarsal head PIP and DIP flexion Flexion of DIP. Flexion of PIP
dislocation hyperextension of
prolapses and get
dislocated and DIP (similar to
cause lateral drift of boutonniere).
toes. Sign =
Valgus (lateral) callouses.
deviation of great Often all toes Hyperextension of
toe and varus except big toe. DIP.
(medial) deviation of
the first metatarsal.
RHEUMATOID ARTHRITIS Surgery: 4 R’s Commonly affected
joints in RA:
Remove (MTP
Atlanto-axial joint (especially
resection) -
transverse ligament):
Contraindications for joint surface
and small •Test used to assess the integrity
Management individuals with rheumatoid amount of of the transverse ligament: sharp
bone removed purser
• Medications (DMARDs, NSAIDs, arthritis (RA): to decrease
pain TMJ
Tylenol, cortisone): • Gentle stretching (during acute stages)
• Disease-modifying antirheumatic • Vigorous stretching (during chronic and Re-align
acute stages) (tendon Shoulder
drugs (DMARDs) can slow the rupture)
progression of disease process and • Gentle mobilizations (during acute •Humeral head
can save joints and other tissue from stages) moves superiorly
Rest
permanent damage and dysfunction. • Manipulative techniques (during (arthrodesis) -
chronic and acute stages) joint fusion AC joint

Replace Elbow:
(arthroplasty) -
joint •Loss of extension:
Acute Stage Treatment: Chronic: no disease flare up replacement e.g. flexion deformity
•Disease flare up o Capitalize on decreased pain and
•Protect: use resting splints, brace joints during Wrist joint
increased energy
ADLs, adaptive tools to reduce joint strain
during ADLs o ROM - full and pain free
MCP and
•No stretching, as it may stretch the synovial o Increase cardiovascular activity - PIP joints
membrane and cause irreversible damage aquatics is a great suggestion
•Energy conservation – decrease exercise o Strength and endurance activities - pain Knee
•Gentle ROM - pain free free: lighter weights, high reps •Baker’s cyst, flexion
•No lifting heavy weights or doing activities that o Continue joint protection strategies deformity, quadriceps
stress joints wasting
o Use splints/braces while exercising
•Ice to reduce inflammation
•Heat only applied briefly in morning to reduce o Ice after activity to reduce inflammation Ankle joint
morning stiffness o Heat before activity if needed for
•Hydrotherapy stiffness
MTP’s
 JOINT COUNT ASSESSMENT
Evaluate disease activity in
patients with rheumatoid arthritis Swelling Test (Effusion Test): Tenderness Test: OverPressure Test (Stress Pain
1. Assess One Joint at a Time Test):
•Technique: Use techniques like the two- •Technique: Apply pressure over the
2. Progressively More thumb or four-finger method to feel for fluid joint line until the nail bed blanches •Technique: Gently apply pressure
Aggressive Tests shifts in the joint, indicating swelling. (turns white). when the joint is at the limit of its
•Purpose: Detects joint effusion (fluid build- •Purpose: Checks for pain provocation, passive range of motion.
3. STOP on Positive Findings up), which is a sign of inflammation. which indicates joint tenderness, a •Purpose: Tests for pain caused by
common feature in RA. stretching the joint capsule, further
indicating inflammation.
Forefinger palpate
Ask patient to actively
anterior to external Index + middle finger over
TMJ open and close mouth as
auditory meatus, patient joint with mouth closed
wide as possible
opens mouth
Thumb placement lateral
Sternoclavicular 2 thumb technique
to top of sternum

AROM: shoulder
Forefinger presses over
Acromioclavicular horizontal adduction or
AC joint
shrug
2 thumb technique over para-
olecranon grooves with elbow Para-olecranon groove
flexed to 90 degrees or Bulge
Elbow sign over radial head (elbow
with elbow flexed 45 PROM extension/flexion
moved from 45 degrees degrees
flexion to full extension)
JOINT COUNT ASSESSMENT
SWELLING OVERPRESSURE
JOINT • AKA Effusion Test
TENDERNESS • AKA Stress Pain Test

2 thumb technique on
Thumb placement over
Wrist dorsum of radial or PROM extension/flexion
dorsum of neutral wrist
ulnar side of wrist

Thumb placement over

1st CMC PROM extension/flexion
joint

Thumb placement over

MCP 2 thumb technique PROM extension
joint

Palpate over
PIP 4 finger technique medial/lateral joint with PROM extension/flexion
thumb and index finger

Palpate over
DIP 4 finger technique medial/lateral joint with PROM extension/flexion
thumb and index finger
PROM shoulder abduction
Assess for fullness over
to 60 degrees with
Glenohumeral anterior shoulder OR external/internal rotation
over bicipital tendon (in supine)
 SWELLING OVERPRESSURE
JOINT • AKA Effusion Test
TENDERNESS • AKA Stress Pain Test

PROM hip flex to 90 degrees

Hip with external/internal
rotation (in supine)

Thumb placement over

Bulge sign medial to
Knee joint line with knee PROM flexion/extension
patella
flexed 60 degrees
2 thumb technique on either
Thumb placement over Passive dorsiflexion with
Ankle (talocrural) side of tibialis anterior and
extensor hallucis tendon joint line knee in flexion

Passive inversion/eversion of
Subtalar calcaneum over talus with
ankle in dorsiflex

Passive Inversion/eversion of
Midtarsal midfoot with ankle in
dorsiflex

Palpate joint in slight Passive traction and

MTP
flexion flexion

Palpate over
Foot IP medial/lateral joint with PROM into flexion
thumb and index finger
 Collateral Ligament Test Central Slip Tenodesis Test

RHEUMATIC HAND EXAM

• Purpose: Evaluates
the integrity of the
central slip of the
extensor tendon.
• How: Observe PIP
•Purpose: Tests the integrity extension when the
of collateral ligaments at wrist and MCP are
Bunnel Littler Test Test for Subluxation of the MCP joint. flexed.
Extensor Digitorum •How: Apply lateral • Finding: Failure of
pressure to the proximal the PIP to extend
•Purpose: Assesses •Purpose: Detects ulnar suggests a central
tightness of the intrinsic phalanx with the MCP
subluxation of extensor flexed to 90 degrees. slip tear.
hand muscles. tendons.
•How: Compare PIP flexion •Finding: Excessive laxity
•How: Observe tendon suggests a positive test for
with the MCP joint in movement during resisted
extension versus flexion. ligament injury.
finger extension and when
•Finding: Increased PIP making a fist.
flexion with MCP flexion •Finding: Ulnar drift of the
indicates intrinsic muscle extensor tendons over the Grind Test
tightness; limited PIP knuckles indicates a
flexion in both positions positive test.
suggests capsular
tightness. Purpose: Also
assesses arthritis at
the CMC joint.
How: Compress the
Piano Key Test Crank Test 1st metacarpal into the
carpal bones and apply
a rotational force.
•Purpose: Assesses Purpose: Evaluates for Finding: Crepitus and
distal radioulnar joint arthritis at the CMC pain confirm a positive
(DRUJ) instability. (carpometacarpal) joint. test for arthritis.
•How: Push the ulna How: Compress the 1st
volarly (forward) like metacarpal into the
pressing a piano key. carpal bones and add a
•Finding: Excessive perpendicular stress.
motion or pain Finding: Crepitus and
indicates instability. pain suggest arthritis.
SPONDYLOARTHRITIS
Common
features: Inflammation of the spine (spondylitis,
sacroiliitis)
Umbrella term for a group of
inflammatory diseases
Synovitis, typically unilateral (affecting
peripheral joints)

Enthesitis
Most common
Other conditions include:
spondyloarthritis
psoriatic arthritis,
is ankylosing Extra-articular features, such as
enteropathic spondylitis,
spondylitis involvement of eyes (uveitis), skin,
reactive arthritis and
certain forms of juvenile genitourinary tract
idiopathic arthritis (e.g.,
psoriatic and enthesitis-
related JIA). No rheumatoid factor (seronegative)

Can be hereditary: HLA-B27 (genetic

marker)
ANKYLOSING SPONDYLITIS
Bamboo spine, marie-strumpell disease
Clinical criteria of AS:
• Low back pain and stiffness
for more than 3 months that
improves with exercise but is
not relieved with rest.

Medications:
NSAIDS, corticosteroids, DMARDs, biologics.
Physiotherapy goals:
Reduce stiffness and increase ROM:
• Increase trunk flexibility and joint mobility with exercise,
stretching, heat and postural education
Increase endurance and muscle strength
Increase respiratory function through cardiovascular exercise and
deep breathing exercises
• High impact cardio (e.g. running) is not advised
Control/decrease inflammation
Pain management
ANKYLOSING SPONDYLITIS
Hallmark sign Low back pain
• Sacroiliitis - deep, dull • Inflammation in the Synovitis (affecting Inflammatory of the eye
pain in buttocks due to spine (spondylitis and peripheral joints) typically (iritis/uveitis and Enthesitis.
inflamed SI joint. sacroiliitis) unilateral. conjunctivitis).

Syndesmophytes Disease of young adults

• Bony growth within • Onset before 40.
ligaments on either side No rheumatoid factor Can be hereditary HLA-
Males more than females.
of a joint which can (seronegative). B27 (genetic marker).
cause fusion/rigidity.

Other signs Postural deformities –

thoracic kyphosis,
• Inflammation of bowels, decreased lumbar
Stiffness/fusing of the Decreased strength due Fatigue due to disease lungs, heart (cardiac
spine by inflammation. to disuse. process. lordosis, head forward
involvement). posture:
oLimitation of motion of
spine (due to pain, tissue
contractures, muscle
Limitation of chest expansion causing restrictive guarding, fusing)
breathing pattern:
oReduced forced vital capacity
oReduced or normal FEV1
oFEV1/FVC ratio will be normal or possibly high on
pulmonary function testing
ANKYLOSING SPONDYLITIS
POSTURAL ASSESSMENT
Tragus to Wall: Lateral Trunk Flexion: Modified Schober’s:
• How: Stand with heels, • How: Mark 10 cm above
• How: Stand against a
buttocks, and S2 on the lower back.
wall, measure the
shoulders against the Measure the increase in
distance from the
wall. Measure the distance as the patient
middle finger to the
distance from the bends forward.
floor during side
tragus (ear) to the wall. • Finding: Limited
bending.
• Finding: Increased increase suggests
• Finding: Reduced range
distance indicates reduced lumbar
indicates stiffness.
forward head posture. flexibility.

Smythe Test: Trunk Rotation: Chest Expansion:

• How: Mark three 10 cm
• How: Measure the • How: Measure chest
segments above S2 on
distance from the circumference at the
the back. Measure the
xiphisternum to PSIS as xiphisternum during full
change in length as the
the patient rotates to inhalation and
patient extends their
each side. exhalation.
trunk while prone.
• Finding: Reduced • Finding: Reduced
• Finding: Limited
rotation suggests spinal expansion indicates
extension indicates
stiffness. restrictive breathing.
stiffness.

Cervical Mobility:
• How: Measure flexion,
extension, rotation, and
lateral flexion of the
neck with a tape
measure or goniometer.
• Finding: Decreased
range of motion
suggests cervical
stiffness.
OTHER TYPES OF SA
Psoriatic arthritis Enteropathic spondylitis Reactive arthritis

Medications used:
• Acetaminophen, NSAIDs
• DMARDs, biological response
modifiers
• Corticosteroids

Physiotherapy
• Associated with psoriasis Associated with Inflammatory Bowel treatment:
• Occurs equally in males and Disease (IBD): Linked to conditions like • Painful form of inflammatory
females Crohn’s disease and ulcerative colitis. arthritis • Joint protections strategies
• Usually appears in people between • Most often short lasting but can, on • Maintain optimal joint
Theory: Chronic inflammation in the
30-50 years old but can begin in intestines may allow bacteria to enter the occasion, become chronic mechanics and posture
childhood bloodstream, causing joint inflammation. • Occurs in reaction to an infection • Cardiovascular endurance
• Chronic, erosive, inflammation Affected Joints: Often impacts peripheral by certain bacteria in bowel or GI
most commonly found in digits, joints, spine, and sacroiliac (SI) joints. tract
large joints of axial skeleton, back Symptoms: Includes abdominal pain, • Hot, swollen joints often affecting
and SI joints bloody diarrhea, joint pain, and knees, ankles
• Dactylitis: sausage like fingers due inflammation. • Persistent low back pain which
to swelling Disease Course: Symptoms often subside tends to be worse at night or in the
• Enthesitis: usually in heels and after six weeks but can recur; in some morning
back cases, arthritis may become chronic and
destructive.
JUVENILE IDIOPATHIC ARTHRITIS
Joint pain (worse in
the morning or after
Autoimmune disease prolonged positioning)
Periods of remission
where symptoms
improve and flare-ups Joint stiffness
The most common type of arthritis in children and where their symptoms
teenagers (16 years and younger). are worse.

Unlike adult rheumatoid arthritis, which is ongoing

(chronic) and lasts a lifetime, many children will
achieve remission and “outgrow” JIA. Abnormal erythrocyte
The most common areas affected by pain and inflammation sedimentation rate
are knees, ankles, elbows, wrists, and hands. (ESR)
•Note: Rheumatoid Warm swollen joints
factor is present in COMMON FEATURES
only a small % of
individuals with JIA
Not clear why children develop JIA.

Additional signs
Combination of genetics and environmental/external (depending on
triggers. severity):
Genetic marker HLA DR4 oMuscle atrophy
oGeneralized Swollen lymph nodes
Eyes issues (uveitis)
deconditioning (in systemic JIA)
oLoss of ROM and
Girls > boys. soft tissue
contractures
oJoint deformities
Gait abnormalities
High fever (in
Fatigue and malaise
systemic JIA)
 JUVENILE
IDIOPATHIC
ARTHRITIS

Systemic arthritis Enthesitis-related Undifferentiated

Oligoarthritis Polyarthritis Psoriatic arthritis
(Still’s disease) arthritis arthritis

Arthritis as well as Inflammation of

Affects 5 or more joints JIA that does not fit into
Most common subtype systemic symptoms tendons and
– may affect medium Arthritis+ psoriasis any of the other
of JIA such as fever (that can ligaments attach to
and/or small joints categories listed above
last for several weeks), bones
but there is
skin rash, and inflammation in 1 or
inflammation of the more joints
Affects 4 or fewer joints internal organs May affect 1 or more
Can present as
– typically medium and seronegative (negative joints – often affecting
Spine, hips, and knees
larger joints such as rheumatoid factor) or wrists, fingers, knees,
knees, ankles and seropositive (positive ankles or toes
elbows Least common type
rheumatoid factor)

Pediatric : peripheral
Only subtype of JIA that
Adult: axial
affects males>females
involvement

Genetic marker HLA

May or may not carry
B27 (as seen in the
genetic marker HLA
spondyloarthritis
B27
group)
 JIA
General treatment:
• There is no cure for JIA.
• Some children will have complete remission (little or no disease
Diagnosis: activity/symptoms)
• There is no single test to confirm the disease. • Early treatment is critical to get the disease under control and
• Signs and symptoms must be present for 6 weeks to prevent joint damage.
make a diagnosis. • A combination of medication, lifestyle habits and therapy is the best
• Child must be under the age of 16 for JIA diagnosis approach for JIA.
• Medications include: NSAIDs, corticosteroids, DMARDS, biologics
PHYSIOTHERAPY GOALS
• Encourage normal activities when not in a flare; avoid joint-
Reduce pain and stiffness, keep Activity Modification
Physiotherapy stressing activities during flare-ups.
the child participating in as
normal a lifestyle as possible Pacing • Balance activities with rest during active disease phases.

• Use ice, TENS, massage and relaxation techniques during flare-

Pain Management ups; apply heat during non-active phases,distraction (listening to
Non-active disease music)
Flare-up
Young population - active with state
peers. Modify activities of daily • Light functional exercises during non-active phases; isometrics
living and recreational activities Strengthening
during flare-ups.
during a flare-up and promote
physical activity and exercise Focus on activity
Focus on strengthening, • Gentle active ROM during flare-ups; stretching when symptoms
during periods of remission. modification, joint ROM/Stretching
flexibility, learning how are mild.
protection,
to manage symptoms if
pain/inflammation relief
and gentle ROM.
a flare occurs. Low-Impact Cardio • Use activities like swimming or biking, especially during flare-ups.

Biopsychosocial • Recommend braces, splints such as a gait aid if the patient has
Equipment
approach painful arthritis

• Work with other healthcare providers for comprehensive

Interdisciplinary Care
management.
 OUTCOME MEASURES FOR ARTHRITIS
Knee Injury & Osteoarthritis
Health Assessment Outcome Score (KOOS) /
EuroQoL - 5D (EQ-5D) MACTAR
Questionnaire (HAQ) Hip Injury & Osteoarthritis
Outcome Score (HOOS)

Measures: Generic health status

Measures: Disability specific to RA
Measures: Difficulty in performing across five dimensions: mobility, self- Measures: Changes in symptoms,
(Rheumatoid Arthritis) patients by
ADLs (Activities of Daily Living) over care, usual activities, function, and quality of life, focusing
having them select activities to
the past week. pain/discomfort, and on knee or hip issues.
evaluate.
anxiety/depression.

Scoring: Includes 5 subscales: pain,

Scoring: Lower scores indicate less Scoring: Uses an ordinal scale (0-3 or Scoring: Short questionnaire focused other symptoms, function in ADLs,
physical disability. 0-5) to evaluate overall health status. on 5 activities chosen by the patient. function in sports/recreation, and
knee/hip-related quality of life.

Population: Can be used broadly Population: Tailored for individuals Population: Primarily used for
Population: Useful for assessing
across different patient groups, with RA to assess their specific patients with knee or hip
disease activity in arthritis patients.
including those with arthritis. functional limitations. osteoarthritis

VAS, SF-36, LEFS, DASH, Time Chair Sit to Stand Test, TUG, 6MWT.
 Increased serum uric acid
(hyperuricemia). Uric acid
forms stones called tophi
formations which become
deposited into joints, synovium,
cartilage, tendons causing pain
and inflammation.

Physiotherapy goals:
• Rest, injury prevention
education, restore Most common areas:
normal flexibility and
function • Knee and great toe of foot
• As inflammation PSEUDOGOUT
subsides, add strength
and functional exercises Similar to gout.
• Do not exercise a red,
hot, swollen joint – Painful, swollen joints
instead focus your Different type of crystals (calcium
efforts on pain reduction
pyrophosphate crystals)
No tophi formation
Medications:
• NSAIDS, cox2-inhibitors,
corticosteroids,
adrenocorticotropic
hormone (ACTH)
BONE CONDITIONS
OSTEOPOROSIS AND OSTEOPENIA
Depleted bone mineral density (BMD) Normal = Severe
• Women 10x more than men, especially post within -1 Osteopenia = Osteoporosis osteoporosis
menopause. standard -1 to -2.5 sd = -2.5 sd and = same BMD
deviation for BMD below as
• 26% of adult bone is accrued during 2 years in BMD osteoporosis
puberty.

•+ 1 or more fragility
fracture:
•Fragility fracture:
RISK FACTORS Common fracture areas: pathological fracture
resulting from a fall
• Age (50+) from standing height
Thoracic spine or less
• Gender (F>M)
• Inactivity Lumbar spine
• Menopause Femoral neck
• Hereditary factors,
• Nutrition (low calcium, low Proximal humerus
vitamin D, fatty food, caffeine), Proximal tibia
smoking, long term steroid
use, alcohol use Pelvis
Distal radius
OSTEOPOROSIS AND OSTEOPENIA
PT GOALS FOR OP
ROM/improvin
Reduce falls Promote Educate to g joint
Conserve bone Improve
risk through extended avoid flexion mobility/flexibi
mass balance
education posture exercises lity – e.g. yoga
and tai chi
Wear well- High
fitting intensity Promote extended posture and avoid
Anterior
shoes exercise
compressiv flexion exercises, especially with
e forces to o Weight
Avoid rugs twisting.
the bearing or
and sloppy WHY?
vertebra loaded
slippers
through strengthe Anterior compressive forces to the
Have good flexion ning vertebrae through flexion should be
lighting on (especially exercises
with avoided as they place a high
stairs (e.g. compressive load on the vertebral
nightlight) twisting),
place a bodies.
high Safe spinal movements include weight-
Wear
compressiv
eyeglasses bearing or loaded strengthening
e load on
when
the exercises and range-of-motion
ambulating
vertebral exercises, such as yoga and tai chi, to
(if
bodies and
applicable)
should
improve joint mobility and flexibility
therefore
Use gait be avoided
aids as
needed
BONE CONDITIONS
PATHOLOGICAL FRACTURES
Bone Infections (Osteomyelitis)

Broken bone caused by

disease leading to weakness Inflammation Can occur with
response in sepsis, open Children and
of the bone. bone, caused trauma, immunosuppre
M> F
by infection - infected ssed at highest
• Most commonly due to usually due to surgical risk.
staph infection: implant.
osteoporosis, but may also
be due to other pathologies
such as:
o Cancer (benign bone
tumors, secondary
malignant bone tumors Treatment
and primary malignant
bone tumors) Antibiotics, surgery

o Infection

• Osteitis
o Bone cyst Red flags:
• Inherited bone disorders Non-mechanical pain: Systemic features:
• Pain at night • Fever, redness, heat, swelling,
• Pain at rest feeling of malaise
BONE DISORDERS

Osteomalacia Paget’s Osteogenesis Osteopetrosis

• Softening of the bones due • Caused by the excessive imperfecta • Very rare, inherited
to impaired bone breakdown and formation • Brittle bone disease deficiency in carbonic
metabolism, of bone, followed by anhydrase
• Genetic disorder -
• primarily caused by disorganized bone • Osteoclast dysfunction –
autosomal dominant trait
inadequate phosphate, remodeling. do not get bone breakdown
• Involves defective
calcium, or vitamin D • This causes affected bone • Despite excess bone, this
development of connective
levels, or calcium to weaken, resulting in patient population has
tissue (lack of type 1
resorption. Known as pain, misshapen bones, brittle bones and an
collagen) causing
"Rickets" in children. fractures and arthritis in the increased risk of fracture
abnormally brittle/fragile
joints near the affected
bones that are easily
bones
fractured
• The pelvis, femur, and
• Varies in severity (mild to
lower lumbar vertebrae are
severe)
the most commonly
affected bones
• Viral and genetic causes
PAIN SYNDROMES
Signals from
damage or injury
What is pain? A delta fiber: high threshold,
sharp prickling, localized, fast
are picked up by
sensory receptors
adapting; medications work in nerve endings.
well
Chronic pain
Pain is felt as a result of the •Pain that persists
brain's response to electrical The nerves then
(neural) and chemical
past the normal 2 types of nerve fibers conduct
at different speeds which transmit the signal
(hormonal) changes in the time of healing (e.g. explains why we initially feel a via the nerves to
body as a result of damage. 6 months after an
sharp localized pain when
injured but this turns into a dull
MECHANISM spinal cord and
brain.
injury).
diffuse pain. OF PAIN

C fiber: low threshold,

Pain can be managed in the unmyelinated, dull, aching,
short-term using analgesics, diffuse, slow adapting and
persistent; medications do Signal travels to
but long-term use can be brain via lateral
detrimental to the patient's not work well
Pain relief spinothalamic tract.
health.
• Side effects of the long use of
analgesics may affect liver, kidney or
stomach
PAIN SYNDROMES
Visceral Referred Pain
Persistent or relapsing
Heart Kidney Diagnosis: by fatigue for at least 6
• Chest and upper arm • Lumbar spine (ipsilateral exclusion; months, not resolved with
(typical), back, neck, jaw flank) or upper abdomen. bed rest, reduces daily
or stomach (atypical).
activity by at least 50%.

Chronic Fatigue Syndrome

Typically occurs after viral
Kidney stones Urinary bladder Cause is infection but may be linked
• Acute flank pain radiating • Subpubic or unknown. to hormones, immune
to groin/perineal area. thoracolumbar region. system issues.

Analgesics, anti-
Diaphragm Gallbladder
Medical inflammatories, NSAIDS,
• C4 dermatome region. • Posterior thorax. treatment nutrition, psychological
support.

Build up exercise tolerance,

Physiotherapy check O2 levels.
Appendix
• Right lower quadrant.
treatment
FIBROMYALGIA
Chronic pain syndrome affecting muscle and soft tissue
(non-articular rheumatism).
• Etiology: unknown.
Signs and symptoms:
• Headaches, sensitivity to stimuli, fatigue, myalgia (muscle
pain), generalized aching, sleep disturbances.
• Anxiety and depression are common; more common in
women.

• 18 tender points (9 pairs)

• Tenderness when 11 of 18 tender points are pressed:
• Occiput (suboccipital insertions)
• Low cervical (anterior aspects of intertransverse spaces
at C5-C7)
• Trapezius (mid-point of upper border)
• Supraspinatus (at origin)
• Second rib (lateral to 2nd costochondral junction)
• Lateral epicondyle
• Gluteal (upper outer quadrant of buttocks)
• Greater trochanter
• Knee (at medial fat pad proximal to joint line)
FIBROMYALGIA
o Focus on endurance of conditioning types of exercises
o Recommended amount of exercise for adults should follow the
Canadian Physical Activity Guidelines of 150 minutes per week of
Physical activity moderate to vigorous exercise
should be the ▪ Most patients with fibromyalgia are unable to initiate a program at
cornerstone of this intensity
treatment o Start with as little as 2-3 minutes of low intensity exercise (walking,
cycling, aquatic exercises)
o Education around anything is better than nothing and progress will Refer to physician for:
be slow
• Anti-inflammatories
o Pacing and prioritizing activities
o Balancing rest and activity
• Muscle relaxants
o Listening to body
Healthy lifestyle
habits and coping o Avoiding flare ups and aggravating factors
• Pain medications
skills o Energy conservation techniques
o Sleep hygiene
• Psychological support
o Stress management and relaxation techniques
• Nutrition
o Focus on strategies that can be used as part of active self-
management
▪ Heat and ice
Pain management
▪ Tens – trial in clinic to assess benefit of purchasing a home unit
▪ Massage – patients can be instructed in self massage techniques
to help relieve pain in localized areas (myofascial trigger points)
OBESITY
• Body mass index (BMI) = weight (kg)/height (m2). Measures the

>
ratio of waist
• Abdominal obesity = independent predictor of circumferenc
morbidity and mortality e to hip
circumferenc
e.
Healthy Overweight Obese Morbidly
obese
• 18.5-24.9 • 25-29.9 • 30-39.9
• >40

Waist-
WOMEN MEN
to-hip
Normal weight/low 0.80 or lower 0.95 or lower People who carry more
health risk weight around their
midsection (an apple-
ratio Determines
shaped body) are at how much fat
Overweight/moderate 0.81 – 0.84 0.96 – 0.99 higher risk for heart
is stored on
disease, type 2 diabetes,
health risk and premature death the waist,
than those who carry hips, and
Obese/high health risk 0.85 or higher 1.0 or higher more of their weight in buttocks.
their hips and thighs (a
pear-shaped body).

Skin caliper test: From where?

Fat greater than 1 inch is excess Right side of
the Umblicus
Health risks associated
with obesity: BARIATRICS
Increases risk of cardiovascular disease and stroke

Increases risk of cardiovascular disease and stroke

Treatment:
• Lifestyle modifications Individual with BMI > 40:
Hypertension Causes: (diet, exercise, stress),
behavior therapy,
• Multi-factorial: pharmacology, surgery.
Hyperlipidemia
excess calorie intake,
• Exercise program:
psychological/enviro
Type 2 diabetes nmental factors, • Moderate intensity 40- Equipment needed:
genetic factors, 60%, 5-7days/week, 45- bariatric bed, lifts/slings,
endocrine and 60mins, circuits or commode, bedside
Gallbladder disease
metabolic disorders. aquatics chair.
• Cautious of
Menstrual irregularity hyperthermia and risk of
orthopedic injury
Infertility • Ensure patient is well Check skin for pressure
hydrated, wearing sores, skin folds, areas
breathable clothing, has of increased moisture
Cancer
appropriate footwear (excessive sweating is
common).
Osteoarthritis • Pick activities that they
enjoy to ensure
continued participation
Breathing problems (e.g. sleep apnea)
 URINARY
INCONTENCE

2. Urgency/Overactive
1. Stress Incontinence: 3. Functional Incontinence: 4. Overflow Incontinence:
Bladder:

Cause: Leakage due to Cause: Sudden, involuntary

Cause: Mental or physical
weakened pelvic floor muscles, bladder contractions leading to Cause: Inability to fully empty
conditions that prevent timely
often influenced by pregnancy a strong urge to urinate and the bladder, leading to leakage.
bathroom access.
or obesity. difficulty delaying voiding.

Triggers: Activities that

Related Factors: Muscle
increase abdominal pressure,
Characteristics: Usually weakness, nerve damage (e.g.,
such as coughing, sneezing,
results in small amounts of from MS or diabetes), or
laughing, lifting, or jogging,
urine loss. blockage (e.g., constipation,
which surpass the bladder’s
enlarged prostate).
closure mechanism.

Characteristics: Frequent
Exacerbated By: Caffeine, leakage without urge and
Common Surgery Related:
carbonated drinks, and inability to urinate normal
Prostatectomy in males.
alcohol. volumes, with the bladder
remaining full.
 HERNIA

Sports Hernia
Direct Hernia: Indirect Hernia:
(Athletic Pubalgia):

Location Symptoms Location: Symptoms: Location Symptoms

Above the inguinal Protrudes through Pain during Soft tissue injury in
ligament, through Painless the deep inguinal straining, swelling the groin/lower Deep groin pain
the inguinal ring. ring, can descend increases with abdomen.
into the scrotum or pressure (e.g.,
labia. coughing), reduces
when lying down.
Radiates to the
Round swelling near
thigh or lower
the pubis.
abdomen.
Seen in all ages,
often congenital.
Pain worsens with activities
Reduces when lying like running, twisting,
down. kicking, and improves with
rest.

Accounts for 2/3 of

hernias, more Common in
common in older athletes.
adults.
PREGNANCY AND POSTPARTUM CONDITIONS
Exercise During Pregnancy
Physical and Cardiovascular
Postural Changes Changes Contraindications Precautions
Hemodynamically significant heart
Placenta Previa
disease Severe anemia •Placenta is in a position below the
Heart rate usually fetus:
Normal weight gain 20-30lbs. increases 10-20 beats Unevaluated maternal cardiac
per minute by full term. Restrictive lung disease •Continue with pelvic floor and
dysrhythmia breathing exercises.
•Do not do abdominal exercises.
Cardiac output Incompetent cervix Chronic bronchitis
Increased cervical and lumbar
increases 30-60% in
lordosis (anterior pelvic tilt). pregnancy. Multiple gestation with risk of preterm Poorly controlled type 1
labor diabetes mellitus

Increased thoracic kyphosis, Persistent 2nd or 3rd trimester Extreme morbid obesity
scapular protraction. bleeding
Placenta previa after 26 weeks of Extreme underweight
Center of gravity shifts upwards and gestation
forwards due to the enlargement of the History of extremely sedentary
Preeclampsia/pregnancy induced
uterus and breasts. lifestyle
hypertension
Intrauterine growth restriction
Weight shifts towards the heels Ruptured membranes in current pregnancy
to bring the center of gravity to a
more posterior position. Poorly controlled hypertension
Exercise guidelines:
Orthopedic limitation
Genu recurvatum.
• Safe level of exertion during exercise = 60-70% of HR Preeclampsia
max. Poorly controlled seizure •Acute hypertension after 24wks
disorder gestation:
• Maternal HR should not exceed 140 bpm.
•Evaluate patient for signs and
Increased foot pronation. • HR should be measured at time of peak activity. Poorly controlled symptoms: hypertension, edema,
• Avoid deep flexion and extension of joints. hyperthyroidism headache, visual disturb,
hyperreflexia.
• Duration of exercise should be influenced by RPE. Heavy smoker
Ligament laxity due to hormone Relaxin: • Avoid planks or crunches/sit ups to avoid increased
•Can result in hypermobile SI joint and pain pressure to diastasis (abdominal separation).
History of precipitous labor
 On the exhale On the inhale
PREGNANCY AND POSTPARTUM •Diaphragm moves
back up, while our
•Diaphragm moves
down as we and at
CONDITIONS Positioning Explain reverse
kegel and
pelvic floor comes
back up with a
the same time our
pelvic floor
kegels using gentle muscles should
contraction. lengthen (if our
layman’s terms •This is where we breath is deep
Sleeping: Supine: Treatment would do our enough).
“kegel”. •This is our
“reverse kegel”.
Switch to Avoid lying
Left side- the right flat on back High fowlers Side-lying or
as the Focus your breath through
lying side as supine your diaphragm and ribs.
needed. weight of
the pregnant oInto abdomen, sides and
belly can back.
Lying flat oGently place your hands on
To improve circulation to compress
can ribs to facilitate the
fetus (decreased the vena
compress Avoid prone Remember to movement through breath.
pressure on vena cava) cava.
vena cava. positioning. lengthen after each Allow your breath to
and take pressure off contraction in order go all the way down
maternal liver. to avoid to your pelvic floor.
If the overtightening. For cueing your
mother patients
A pillow between the experiences
knees to support the SI dizziness or Exhale: gentle
joint and spinal pain, move contraction and lift Inhale through nose,
alignment. into left of the pelvic floor
side-lying. out through mouth.
"close flower or
jellyfish and lift". Inhale: lengthen/relax
Perform daily, 3 sets of 10 or 2 sets - avoid your pelvic floor -
A pillow underneath the doing more than 30 kegels per day. "blossom flower" or
belly can be used for Think quality over quantity “open jelly fish”.
further support.
 CESEREAN SECTION
o Deep diaphragmatic breathing exercises
o No lifting or pushing (e.g. lifting car seat or pushing Exercises: o Kegel and reverse kegel
stroller) > 10-15lbs for 6 weeks
o Limit stairs as much as possible
o No core exercises (except PF/TA) for 6 weeks Avoid slouching
o
o Log roll into and out of bed – no crunching for 6 ▪ It is important to keep range of motion through the abdomen
Precautions: weeks as the incision heals inside and out
Posture: o Encourage standing and walking upright
o Position in a straight position when laying
o Bring baby to breast (not breast to baby) when breastfeeding
o <20 minute walks for the first 2 weeks.
Recommend the patient to stay indoors and
relative rest. o TENS for incision pain
o 20-30 minute walks for weeks 2 through 4. Early scar o Watch for signs of infection, including pain, redness, swelling,
Recommend walking on flat surfaces and avoid care: bleeding, discharge and heat
pushing a heavy stroller.
Ambulation: o 45 minute walks after 4 weeks if mother is
oApply light pressure to scar during transitional movements
symptom free. Recommend introducing small
inclines and increase as tolerated. (e.g. in and out of bed, chair)
Splinting
o Splint scar when having a bowel movement, coughing or
for
sneezing
movemen
▪ Try to avoid straining
t:
 DIASTASIS RECTI How to test for
diastasis recti:
ABDOMINIS (DRA)
• Complication where there is a separation of the With 1-2 fingers beside each
rectus abdominis muscle at the linea alba. other, place your finger(s)
perpendicular to spine at 3
• DRA is a normal finding during pregnancy and different locations along the
early postpartum. midline of the rectus abdominus: Education Exercise (focus on
• DRA should resolve postpartum. • Level of umbilicus oDo not perform sit-ups, avoiding doming,
• ½ way between umbilicus and straight leg raise or any bulging or widening of
• Prognosis depends on several factors such as xiphoid process core activity that can linea alba):
width, body size, fitness, movement mechanics. • ½ way between umbilicus and cause doming, bulging or
increase discomfort o Address movement
pubic symphysis patterns (e.g. supine
oExternal supports:
kinesiotape/abdominal to sit and squat)
binder o Core exercises:
oExhale on exertion to transverse abdominis
Can result in back May see abdominal Recovery 2-6 months
avoid valsalva, which (belly button to spine),
pain. bulge/doming. or longer. Ask patient to bring their head and increases intra- multifidus
shoulders up off the bed/plinth abdominal pressure (e.g. o Kegel and reverse
and assess the spacing at each of getting in and out of bed,
the above levels kegel
lifting, exercise)
o Deep breathing
Men and woman who have not This population requires oPosture/body mechanics
had a pregnancy may also activity modification to ensure exercises to
experience a DRA due to increase they do not have doming in the strengthen diaphragm
intra-abdominal pressure (e.g. in weaker areas of the midline of
weightlifters) the abdominal muscles.
Palpate for a separation of rectus
abdominis/widening of linea alba
• >2.5cm or 2 fingers width is
significant
Common Pre/Post Pregnancy Conditions
Pelvic floor disorders

WHY? TYPES CAUSES MANAGEMENT

Genetic
Pregnan s-
Respirat
Can cy, pelvic
Due to ory Surgical
lead to labour organ
stretchi problem removal Kegel Postural Refer to
partial Uterine and Pelvic prolaps
ng of Cystoce Rectoce s with a Constip of and re- pelvic
or total prolaps childbirt Obesity organ e–
pelvic le le chronic, ation uterus reverse educati health
organ e h (most cancer connect
floor long (hystere kegel on PT
prolaps commo ive
muscles term ctomy)
e n tissues
cough
causes) may be
weaker
in some
women
Herniati Avoid
on of straining
Lowerin rectum with any
Practice
g of into activitie
Bulge of kegels in
bladder vagina s,
uterus supine,
into through includin
into sitting
vagina/t weakeni g lifting,
vagina and
owards ng of bowel
standing
opening posterio moveme
r vaginal nts and
wall voiding
Common Pre/Post Pregnancy Conditions
Hang off ligaments Post pelvic pain,
(lumbar lordosis,
thoracic kyphosis,
head forward Buttock pain
posture) COMMON
Postural FEATURES
May radiate to leg
Muscle imbalance

COMMON Pain with sit, walk, stand

FEATURES Asymmetry

Gaenslen’s test
Waddling,
Gait shuffling, dragging
a limb SI JOINT Pelvic compression and
Postural Low Back SPECIAL TESTS
DYSFUNCTION distraction
Pain/ Pelvic Girdle Education: balance activity with
Pain rest
Sacral thrust
Improve body
mechanics/posture TA and multifidus strengthening

Address movement patterns

MANAGEMENT
(e.g. squatting, lifting) External stabilization (SI belt)

Exercises for stabilization and MANAGEMENT

symmetry Educate on no single leg weight
bearing

Muscle techniques Massage

Joint protection strategies
 Urinary
Common Pre/Post Pregnancy Conditions incontinence
SIJ/low back/hip/pubic
VARICOSE bone pain
CARPAL TUNNEL / DE
QUERVAIN’S VEINS
Painful sex

COMMON SHORTENED- Weak pelvic floor

MANAGEMENT
FEATURES TIGHT CAN
CAUSES MANAGEMENT
LEAD TO Constipation
Compression
Heaviness
stockings Increased frequency of voiding
Temporary See session
because of fluid 2
retention/hormone Circulatory Increased urge to pee
changes Dull pain exercises (e.g.
ankle pumps) Waking up to pee (nocturia)

Poor lifting Posture/positioning Feeling of heaviness or pelvic

Ache in legs with
technique (lifting (limit cross legs, pressure (pelvic organ prolapse)
standing/walking
baby with elevation)
repetitive radial Unable to hold in gas
Abnormal blood glucose WEAK CAN
deviation strains
readings in pregnancy LEAD TO
EPB and APL) Stress and urge incontinence
COMMON FEATURES If undetected, can be severe HYPERTONIC /
for baby and mom WEAK PELVIC
Low back/hip/SIJ pain Deep inhale into
GESTATIONAL FLOOR MUSCLES abdomen while
DIABETES Compression stockings visualizing the
Shortened and tight: pelvic floor
reverse kegel opening up like
Circulatory exercises (e.g. a flower
MANAGEMENT
ankle pumps) MANAGEMENT “blossoming
flower”
Posture/positioning (limit
cross legs, elevation) Weak Kegel
PEDIATRICS
ROOTING REFLEX MORO REFLEX SUCKING REFLEX PLANTAR GRASP REFLEX STEPPING REFLEX

•Stimulus: Touch side of their •Stimulus: Roof of mouth is •Stimulus: Pressure to base of •Stimulus: Supported upright
•Stimulus: Head dropping into
cheek touched toes position with soles of feet on
extension suddenly for a few inches
•Response: Turning of head to •Response: Initiate sucking •Response: Toe flexion a firm surface
(child feels like they are falling)
side of stimulus with mouth •28 weeks of gestation to 5 •0-4 months •Response: Reciprocal
•Response: The child will open their
open months flexion/extension of legs
arms (abduction) then bring them
•28 weeks of gestation to 3 (stepping motions)
back to their chest (horizontal
months adduction); cry •38 weeks of gestation to 2
months
•28 weeks of gestation to 5 months
Developmental reflexes

• Automatic responses from the

central nervous system.
• They help develop motor and
cognitive skills.
• Present in infants but absent in TONIC LABRINTHINE REFLEX
(TLR) SYMMETRICAL TONIC NECK BABINSKI REFLEX
healthy adults. REFLEX (STNR)
ASYMMETRICAL TONIC •Stimulus: Head position •Stimulus: Stroking lateral
• Reflexes are inhibited as the •Stimulus: Head position, neck
NECK REFLEX (ATNR) (extension in supine; flexion in aspect of the sole of the
cortex matures. prone) flexion or extension foot
•Stimulus: Head position, •Response: When head is in
• Non-integrated reflexes affect turned to one side •Response: In supine position, the •Response: Fanning of
flexion, arms are flexed and
movement smoothness. •Response: Arm and leg on
body and extremities are held in toes and extension of
extension legs are extended great toe (normal
• Reflexes can return after CNS face side extend, arm and •When head is in extension, response in babies)
leg on scalp side flex •In the prone position, body and
injury, impacting movement and extremities are held in flexion arms are extended and legs are •1-2 years
posture. •0-6 months flexed
•0-6 months
•6-9 months
PEDIATRICS
REACTION GOAL EXAMPLE

Postural Control To create

Hold baby
efficient
diagonal and
• The control of the body’s Righting alignment of
they will right
reactions body parts
position in space in order Head, neck, and
their head to the
to obtain stability and vertical
body righting
orientation.
• Development of
Postural
postural control: changes to Initiate ankle
o Early reflexes Equilibrium maintain strategy for
o Development of reactions alignment Ankle, small
postural reactions hip and stepping perturbations
strategies
o Refinement of
postural control and
Automatic
balance reactions response to
throughout childhood protect oneself If you push them,
Protective from a fall using they will put out
reactions the arms their arms for
•Develop sequentially: protection
•Forward
•Sideways
•Backwards
Hypotonia Hypertonia
Often seen in children with delayed motor
development, Down Syndrome, CP. May co-exist
with weakness. Often exists in trunk despite higher
tone limbs (e.g. Cerebral Palsy).

May be caused by spasticity,

Challenges: rigidity, dystonia or a combination.
o Decreased joint stability and co-contraction
o Difficulty grading movements
o Decreased proximal stability results in
decreased distal stability Challenges:
o Difficulty initiating movement
o Often uses excessive co-contraction
o Difficulty controlling movement due to
Features: issues with grading
o Muscles appear floppy/soft o Movement often limited to stereotypical
o Use of wide base of support for stability synergies (e.g. extension of lower limbs)
o Tendency to lean against things for support o General muscle and joint stiffness;
o Tendency to lock joints (e.g. hyperextension of
contractures
knees in standing) o Disuse atrophy
o Extreme ranges of movement
o Lower levels of activity
o Delayed gross motor skills
Features:
• Poor sitting posture: o Stiff looking extremities
oPosterior pelvic tilt, kyphotic posture, forward head o Decreased selective movement
posture, decreased trunk rotation, wide base of support
• Poor standing posture:
oKnee hyperextension, hip abduction and external
rotation, foot pronation, wide base of support
 MOTOR MILESTONES
Develop ability to control head in Pelvis and legs stabilize in prone Can roll from prone to supine Have control of arms and upper Key development: ease of
0-3 months

4-5 months

5 months

6-7 months

8-9 months
all positions (e.g. able to turn head and prop up on extended elbows Demonstrates head control in trunk movement
to follow toy in supine) Feet to hands and mouth in supported sitting Able to reach for an object utilizing Can get into 4-point position from
++ random kicking in supine supine only one hand prone Can pivot in sitting
Head right and reflex stepping Good head control in supported Can roll from supine to prone Demonstrate rocking in 4 point
(when held in standing) sitting Independent getting into sitting which is the precursor to crawling
Pelvis and legs must be a stable Can weight bear if supported in Can sit independently - key Can develop ability to crawl
base of support for prone standing milestone: should be able to sit forwards on hands and knees
propping Able to follow objects (180 unsupported by 7 months Sitting: Can pull to stand at furniture
Requires full support in sitting degrees) with eyes, laughing uses hands for play and Able to stand at furniture, stand
exploration alone, cruise sideways
Standing with support with good Can lower into sitting from
alignment supported standing
Able to bounce in standing (this
promotes mobility and walking)
May start commando (belly)
crawling
 MOTOR MILESTONES
Have control of lower No longer stays in prone Independent standing Can squat and transition Walk on tiptoes Jump with Becoming functionally
At 9 months4

10-11 months

12-15 months

16-24 months

2-2.5 years

3-5 years
trunk and pelvis and supine Can walk independently back up to standing 2 feet independent
Able to transfer objects Can stand hands free for 12 months – holds a cup Walks up/down the stairs Stands on one foot Climb stairs 1 foot/step
from one hand to another a few seconds by handle while drinking with handheld Controlled kick of a ball Walk a straight line with
(fine motor behaviour) Can crawl up stairs Throws a ball with whole Propel/steer push toys Throw and catch a large heel touching toe
Bear walks (hands and body movement (not ball Controlled faster running
feet) dissociated) Running and with controlled stop and
Can walk with hands held Walks backwards and ascend/descend stairs jump/hop on 1 foot
Develops pincer grasp sideways a few steps slowly Rides tricycle Ride a bike
•Initiates kicking a ball Throwing to targets
Somersaults
Dress and eat
independently
GRASP DEVELOPMENT
PALMAR GRASP RAKING GRASP RADIAL DIGITAL PINCER GRASP
• 5-6 months • 7-8 months GRASP (3 Fingers) o 10-12 months
o Use entire hand to o Use finger flexion like o 8-9 months o Pick up objects
grasp objects a rake to pull objects o Pick up objects with between tip of thumb
into palm thumb, index and and index finger
middle fingers (requires significant
(increased precision) coordination and
precision)
APGAR ASSESSMENT
System used to perform an evaluation of an

Based on a rating of five factors

that reflect the
Administered at 1
and 5 minutes after
infant’s birth:
Low score is
physical infant’s ability to correlated with oScore of each
condition. adjust to extra- developmental assessed item
uterine life. delay. range from 0-2
oTypical score = 7-
10
•Score of less than
4 is indicative of
respiratory
distress
PEDIATRIC CARDIORESPIRATORY
Newborns 3-6 Months Old 6-12 Months Old Children

•Increased compliance of chest wall, • Slight increase in TV, so RR • Most significant change in • As child gets older: HR and
paradoxical movement of upper
chest/sternum. goes down a bit. chest development is due to RR slowly decrease and BP
oChest wall compliance decreases • Respiratory rate = 30-60. increases in mobility. slowly increases.
with age with ossification of rib cage • Airways size increase 3-fold, • 1-5 year old respiratory rate =
and increased intercostal muscle tone lung volume increase 4-fold, 20-30.
•Shape of lungs on chest x-ray are
triangular and ribs more horizontal/flat accessory muscles develop. • ~12 year old respiratory rate =
(in comparison to rectangle in adults). • Respiratory rate = 24-30. 12-20.
oNormal shape by around 10 years old • Normal BP for 2 year old = 85
•Preferentially ventilate the upper most
lungs.
SBP, 60 DBP.
•Immature alveoli structure and
function = increased susceptibility to
collapse, lungs less compliant.
•Narrow airways (easy to clog).
Possible respiratory issues in children
•Diaphragmatic nose breather. with neuromuscular disorders:
•Lack of accessory muscles for
ventilation. • Ineffective cough
•Respiratory rate = ~60; increase in RR
indicates challenge with breathing (TV • Poor chest structure
will not change in infants).
• Inability to take deep breaths
• Early fatigue
• Hypoventilation

• Increased work of breathing

• Increased risk of aspiration
PEDIATRIC CONDITIONS
RESPIRATORY/ DIGESTIVE
BRONCHIOLITIS BRONCOPULMONARY DYSPLASIA

Chronic lung disease in

Lower respiratory tract newborns, be can mild,
moderate or severe.
More common in premature
babies with low birth weight
Physical findings: cyanosis,
hypoxemia, hypercapnia,
infection Abnormal development of
the lungs (bronchioles and
or who required mechanical
ventilation.
delayed growth and
development.
alveoli).

Usually caused by respiratory syncytial virus

(RSV) - highly contagious.
On auscultation: crackles, Abnormal chest x-ray:
Frequent lower respiratory
wheezing and decreased hyperinflation, low
Causes inflammation and mucus tract infections.
breath sounds. diaphragm, atelectasis.
congestion in small airways (bronchioles).

V/Q mismatch causes hypoxia (decreased

O2) and hypercapnia (increased CO2).
PT can help with secretion
clearance.
PEDIATRIC CONDITIONS
RESPIRATORY/ DIGESTIVE BONE CONDITIONS

HIRSCHPRUNG’S DISEASE OSTEOCHONDROSIS

Characterized by
Constipation in an infant caused by absent ganglion cells in Family of orthopedic
interruption of blood
large intestine (functional obstruction). joint diseases in
supply to the
children and
epiphyseal growth
adolescence.
plates.
Absence of ganglion cells causes the muscles in the bowels to
lose their ability to move stool through the intestines

OSTEOCHONDROSIS
Will fail to pass first stool (meconium) within first 48 hours after
birth.

Articular (e.g. legg- Physeal

Will also have abdominal distention. calve-perthes, (scheuermann's Non-articular (e.g.
osteochondritis disease/juvenile osgood- schlatter).
dissecans) kyphosis
Treatment: surgery (resection).
PEDIATRIC CONDITIONS
BONE CONDITIONS
ETIOLOGY/ PRESENTATIO
CONDITION AGE TESTS TREATMENT
CAUSES N
Decrease loading of the
knee by the quadriceps
muscle/tendon
Inlammation of the
patellar ligament and Mild and Painful resisted
tibial tuberosity intermittent knee knee extension Control knee loading
Young
OS-GOOD pain on the activities (limit squats
adolescence (9-
SCHLATTER anterior surface and jumping)
16) M>F Overuse (sports,
running, jumping, of the proximal When stressing
squatting) tibia especially quadriceps Hamstring and
during activity quadriceps ROM and
strengthening
X-ray findings
Bracing/taping (e.g.
patellar strap)

Pain management
PEDIATRIC CONDITIONS
BONE CONDITIONS
AGE ETIOLOGY CAUSES PRESENTATION TESTS TREATMENT
OSTEO Disruption of blood
Children and supply causing Painful
Unknown X-ray or MRI May need surgery to
CHONDROITIS adolescence (10- subchondral necrosis
DISSECANS 20) highly active remove fragments
of bone Swollen joint
Possible factors which increases
Results in include: with activity
cracking/loosening of trauma/abnormal Pain management
the bone and bone stress Joint may
cartilage lock/catch
Activity modification
The bone and
Sensation of
cartilage can pull
“giving away”
away and float within Strengthening and
the joint Decreased joint stretching exercises
ROM
Most commonly
affected joints are:
knee, elbow and ankle

Mild and intermittent

knee pain on the
anterior surface of the
proximal tibia
especially during
activity
 LEG-CALVE-
PERTHES

4-8 years 2-15 years

old old AGE
Avascular Leads to Increased
necrosis of abnormal
femoral head shape of the
risk of hip ETIOLOGY
OA
due to femoral
inadequate head and
blood supply secondary Endocrine
to head and changes to
Unkno
wn
Genetics Trauma dysfunctio
Inflam
mation
Nutritio
n
CAUSES
neck of shape of n
femur from acetabulum Pain Decreased Usually PRESENTATION
the artery in Limp
exacerbated by ROM into unilateral
the middle of Mild hip,
hip/leg internal
the round knee or
movement and rotation/abd
ligament groin pain
activities such uction Diagnosed
with hip X-ray
TESTS
as running,
walking,
jumping Limit Minimize
mechanic femoral
Decrea Maintain Positio Stretch al
TREATMENT se pain hip ROM ning ing stressors
head
deformit
on joint y to
(e.g. decrease
encourage risk of
swimming OA
)
OTHER PEDIATRIC HIP CONDITIONS
CONDITION AGE ETIOLOGY PRESENTATION TESTS TREATMENT

Hip, groin, medial Almost all children

Most common Slippage of the overlying require surgery
adolescent hip thigh and/or knee
SLIPPED epiphysis on the growth pain
CAPITAL condition plate of the femur
FEMORAL Epiphysis is
10- 16 years Hip joint heals Pain increases with screwed into place
EPIPHYSIS
old abnormally activity X-ray findings
Stable slips = partial weight
bearing to tolerance for 6
If untreated will lead Acute or insidious
weeks post-surgery
to severe hip OA onset of a limp
Unstable slips = feather
weight bearing for 6 weeks
post-surgery
Decreased hip ROM
OTHER PEDIATRIC HIP CONDITIONS
CONDITION AGE ETIOLOGY PRESENTATION TESTS TREATMENT

Asymmetry of the Good prognosis

gluteal or thigh skin Barlow (subluxes
folds the hip) Surgery or Pavlik
harness (hips
Decreased positioned into
abduction on the Ortolani tests abduction) - worn
affected side (relocates the hip) 24 hours per day
DEVELOPMENTAL Present at birth, or Abnormal growth of and re-evaluated
DYSPLASIA OF THE later if walking is the hip = shallow with ultrasound
HIP delayed acetabulum Standing or walking
with external every 2-3 weeks
rotation

Leg length
discrepancy
(shorter on affected
side)
OTHER PEDIATRIC HIP CONDITIONS
SALTER HARRIS FRACTURES
Physiotherapy
treatment:
I – S = Slip (separated II – A = Above Restore ROM and
or straight across) o The fracture lies above the strength once
o Fracture of the cartilage of growth plate, or away from fracture has
the joint
• A fracture that the growth plate healed.
involves the
growth plate of a III – L = Lower IV – TE = Through Approximately
bone. o The fracture is below the Everything 85% of growth
plate fractures
• There are 9 types growth plate in the
epiphysis
o The fracture is through the
heal without any
metaphysis, growth plate
- 5 common. and epiphysis long-term deficits.

V – R = Rammed Most common

(crushed) complication is a
o The growth plate has been leg length
crushed discrepancy
OTHER PEDIATRIC HIP CONDITIONS
DOWN SYNDROME
Hypotonia

Also known as Trisomy 21:

Genetic disorder caused by the Flattened
facial profile
presence of part or all of a third copy with tongue Hypermobile
too large for
of chromosome 21. mouth
Features:

Hallmark Ligament laxity: Physical

Intellectual
feature: oCheck transverse ligament, laxity can lead
to atlantoaxial instability and spinal cord
challenges
growth
delays
impingement
oSigns of atlantoaxial instability
oNeck pain, cervical ROM changes and
neurological manifestations such as:
oChanges in coordination and balance,
sensory changes, bladder changes, UMNL
signs (e.g. spasticity, hyperreflexia,
clonus)
CEREBRAL PALSY
Results in a variety of impairments:
• Movement disorders
• Altered muscle tone
• Decreased functional independence
Non progressive lesion of the brain the occurs before the age of 2 • Hearing and speech problems
• Hydrocephalus
• Microcephaly
CAUSES
• Scoliosis
Older • Joint contractures
mother • Hip dislocation
Low birth • Cognitive impairments
Any prenatal, perinatal or postnatal weight/s
condition that results in anoxia, • Seizures
Anoxia mall for • Gastrointestinal, nutritional and oral
hemorrhage or brain damage.
gestation motor issues
Periventricular leukomalacia: most al age
common ischemic brain injury in
premature babies:

Is a form of brain injury

Classified by area of deficit:
It is characterized by damage to the
white matter near the lateral
Low
apgar
RISK Invitro
fertilization
ventricles score FACTORS (IVF) Monoplegia: single limb affected
It is most often due to hypoxia and
most commonly affects premature Diplegia: both lower limbs affected
babies
(upper extremities usually not as
Most commonly presents with spastic extensive as legs)
diplegia
Abnormal
placenta Triplegia: three limbs affected
Prematurity
attachme
nt Quadriplegia: all 4 limbs affected
Blood
type
incompa Hemiplegia: both upper and lower limb
tibility on one side of body affected
CEREBRAL PALSY Types of cerebral
palsy:

Spastic: Ataxic: Athetoid: Dystonic: Hypotonic:

Caused by lesions to motor cortex Caused by cerebellar Caused by damage to Caused by damage to basal Lack of muscle
or projections from motor cortex. damage. basal ganglia. ganglia. tone, weakness.

Spasticity present - velocity Uncontrolled writhing Long sustained involuntary

dependent resistance to muscle Coordination problems. movements of extremities movements and postures
stretch. and peri-oral muscles. (whole body movements).

Abnormal rate, range, Fluctuating muscle tone

Tend to lock joints at end
Increased muscle tone. force, duration of (both hyper and
range.
movements. hypotonia).

Difficulty with rapid

Slow, twisting, wide Middle range control is
Decreased ROM and contractures. movement, gait, fine
amplitude movements. difficult.
motor and balance.

Movements often limited to

Changing of mouth
synergies (primitive movement Full ROM is usually present.
positions.
patterns).

Lack of co-contraction of
Trouble with starting/stopping a
muscles leads to postural
movement.
instability.

May walk with scissors gait pattern

due to high tone adductors.
CEREBRAL PALSY Physiotherapy treatment:

General treatment principles

Use play to ensure Promote social Engage the child Mobility Prevent
Maximize Parent Education:
compliance and fun. integration and with activities like Improvement: Deformity/Maintain
participation in
involve the family. equine and aqua ROM:
ADLs with adaptive
therapy. aids and Teach functional
encourage Set realistic goals movements Use braces,
independence, (rolling, sit to splints,
Equine Therapy: Aqua Therapy: even if tasks take stand)
longer. Support home
exercises. Manage spasticity
Improves pelvic Reduces Strengthen with stretching and
weight shift contracture muscles, exercises.
especially the
core.
Ensure hip health
Movement Strengthens
to prevent
sensation muscles Use gait aids subluxation.
(walkers, crutches)
and focus on gait
Head/trunk control Enhances fitness training.

Self-esteem Improves walking.

Emotions.
CEREBRAL PALSY
Commonly Used Braces
Bracing in CP: Hip subluxation in CP:
• Spasticity of adductor longus and iliopsoas can
Goals of bracing cause hip dislocation.
•Increase function
Ankle foot Knee ankle foot • Non-ambulatory child is most at risk.

orthoses orthoses • First indication is inability to abduct hip through

•Prevent deformity
full range (~45 degrees).
•Keep joint in a functional position
• Treatment:
•Stabilize the trunk and extremities
o Seating (pummel between legs)
•Facilitate selective motor control Supra-malleolar
•Decrease spasticity
orthoses Hand splints o Adductor stretching
•Protect extremity from injury in the o Medications to manage adductor spasticity:
postoperative phase ▪ Botox
▪ Baclofen pump
o Surgery (tendon release, osteotomy)
Spinal braces
Functions of spinal braces
Slow progression of spinal deformity
Delay surgery Functions of the AFO
Common outcome measures used in CP:
Allow skeletal growth Stance phase → stable base of
•Gross Motor Function Measure (GMFM)
Assist sitting balance support •Gross Motor Function Classification System (GMFCS)
Protect surgical site from excessive Swing phase → prevent drop foot
loading post surgery At night → prevent
SPINA BIFIDA
• Neural tube defect resulting in vertebral and/or spinal Types:
cord malformation.
• Risks: link between decreased maternal folic acid,
infection, exposure to teratogens (alcohol).

Spina bifida occulta:

Spina bifida cystica:
no spinal cord
visible or open
involvement, may be
lesion:
indicated by hair tuft.

Results in: Secondary features:

Meningocele: cyst
• Flaccid paralysis • Skin breakdown/ulcers due to includes
Muscle wasting lack of sensation
•
• Muscle weakness • Osteoporosis cerebrospinal fluid
• Decreased/absent reflexes • Delayed development if unable (CSF); cord intact.
• Bowel and bladder incontinence to explore the environment
• Hydrocephalus • Soft tissue contractures
• Meningitis • Higher risk of latex allergy
• Foot deformities Myelomeningocele:
o Talipes equinovarus (club foot)
– see below
cyst includes CSF
▪ Especially with L4-5 level and herniated cord
• Decrease/absent sensation tissue; cord damage
 HYDROCEPHALUS

60% of children with TALIPES EQUINOVARUS (CLUBFOOT)

A condition in which there
myelomeningocele
is an abnormal
develop hydrocephalus
accumulation of CSF
after surgical closure of
within the brain: Clubfoot is a complex congenital foot deformity involving the bones of
their lesion
the hindfoot, midfoot and forefoot.

oThe hindfoot is in a varus and plantarflexed (equinus) position and the midfoot and
Early warning signs of forefoot are adducted and inwardly rotated
oThe affected foot is shorter, and the calf circumference is less than a normal unaffected
hydrocephalus include 80 - 90% of children who foot
irritability, changes in acquire hydrocephalus will
sleep patterns and require a cerebrospinal The condition is present at birth and may involve one or both feet and
changes in appetite and fluid shunt can range from mild to severe.
weight
oIf left untreated, or not managed properly, clubfoot can lead to major issues with
ambulation and impairments in activities of daily living as well as pain and arthritis.
Signs of a blocked shunt: While most causes of clubfoot are unknown (idiopathic), it can be
▪Vomiting, fever, irritability, associated with other conditions such as Spina Bifida and
headache, head enlargement, Arthrogryposis.
bulging eyes
▪Can be life threatening - refer to oMales are twice as likely to develop clubfoot as females
emergency immediately

Treatment options include serial casting, bracing and/or surgery.

 FUNCTIONAL OUTCOMES

• Mostly
T12 wheelchair

L1
• Household/therapeutic ambulation
with reciprocating gait orthotic
(RGO) and forearm crutches or
Physiotherapy
walker; wheelchair for distance

• KAFO's (L2) or AFO (L3) with

treatment:
L2-L3 crutches or walker; wheelchair Positioning - including prone position to
for distances prevent hip flexion contractures

• AFO's with crutch or cane for Strengthen weak muscles

balance; potential for
L4
community ambulation; may Teach transfers
need wheelchair in adulthood
Equipment needs (standing frames,
• AFO’s, may need orthotics, walkers)
L5-S1 crutch/cane for balance;
community ambulation Standing and ambulation

• Ambulation Balance training

S2-3-4
without aid
Education about sensory issues and skin
health
 MUSCULAR DYSTROPHY Presentation:
•Proximal muscle weakness (pelvic girdle, shoulder girdle) and progresses to
distal muscles
A group of inherited diseases that are characterized by
weakness and wasting away of muscle tissue. There are •Symmetrical muscle wasting
many sub-types with Duchenne’s being the most common. •Waddling gait
•Toe walking
•Lordosis (anterior pelvic tilt) and scoliosis
Duchenne muscular dystrophy (DMD) •Frequent falls
•Difficulty standing up and climbing stairs
Mutation of a single gene on the X •Lower IQ
Key features:

chromosome and failure to produce •On pulmonary function test:

dystrophin protein. oFunctional residual capacity should be normal
Dystrophin: oTLC, vital capacity and FEV1 will be decreased due to weakened respiratory
o Necessary for muscles to function muscles
properly
o Provides structural integrity to muscles o Slow the development of contractures with stretching
by linking sarcolemma to actin and bracing
o Disruption of dystrophin gene leads to o Slow the onset of muscle weakness with functional
muscle weakness strengthening
o Muscle cells are replaced by fat and ▪ No aggressive high impact, strenuous exercises
connective tissue, leading to progressive o Maximize independence with mobility for as long as
muscle wasting
Creatine kinase levels are high (necrotic PT possible using aids once necessary –
• orthoses, walkers and wheelchairs

Goals:
muscle). o Slow deconditioning by implementing aerobic exercise
• Normally diagnosed by 5, death by programs (e.g. low impact exercises such as swimming)
around 20. o Minimize pain
o Prevent or minimized skin breakdown
KEYS SIGNS

Gower’s sign: Calf pseudohypertrophy o Slow cardiorespiratory compromise and prevent/reduce

oUses hands on legs to stand oEnlargement of calf muscles chest infections
up due to weak gluteal - creates appearance of o Educate the patients and family members about the
muscles strong calf muscles disease to maximize adherence to PT program
oDue to fat and connective
tissue accumulation
 ORTHOTICS TYPES

• Purpose
• Serve to support, align,
prevent or correct Custom or off the shelf
deformities of a body part, or (OTS)
Shoe inserts Heel cups
to improve the function of
movable parts of the body.
• Maintain or increase joint
ROM
• Protect or stabilize a joint
• Promote joint alignment
• Promote improved function
Supra-malleolar orthotic Ankle-foot orthosis (AFO) - Knee-ankle-foot orthosis
(SMO) hinged or un-hinged (KAFO)

Hip-knee-ankle-foot Reciprocating gait orthosis

orthosis (HKAFO) (RGO)