NEUROMUSCULAR

Cranial nerves
CN I, II, VIII- pure sensory (128)
CN III, IV, VI. XI, XII- pure motor (112346)
CN V, VII, IX, X- mixed containing both sensory and motor fibers (1975)
Parasympathetic secretomotor fibers are carried in CN III – control of smooth muscles in eye ball
CN VII- control of parotid and lachrymal glands
CN IX- to parotid salivary gland
CN X-heart, lungs and most of digestive system.

LESIONS NERVE INVOLVED

Lesions of nasal cavity, anterior/ inferior Olfactory nerve
cerebrum
Optic pathways, optic nerve, optic chiasma, Visual deficits
optic tract, lateral geniculate body, superior
colliculus and visual cortex
Midbrain CN III , IV
Pontine lesions CN V, VI
Junction of pons and medulla CN VII, VIII
Medulla CN IX, X, XI, XII

Following rhyme can be used to check CN examination

Smell and see
And look around
Pupils large and smaller
Smile, hear
Then say ah…
And see if you can swallow
If you are left in any doubt
Shrug and stick your tongue right out.

Nerves Afferent (sensory) Efferent (motor) Tests

Olfactory Smell - U/L identification of
familiar odors
(Chocolate, p. butter
and coffee)
Optic Sight - Visual acuity, peripheral
Pupillary reflex vision, and pupillary
light reflex.
Oculomotor - Voluntary motor: Upward, downward and
levator of eyelid, medial gaze, reaction to
superior, medial and light.
inferior recti and
inferior oblique
1

muscle of eyeball.
 Autonomic: smooth
muscle of eyeball
Trochlear - Voluntary motor: Extra ocular eye
superior oblique movements, downward
muscle of eyeball and lateral gaze.

Trigeminal Touch, pain skin of Voluntary motor: Corneal reflex,

face, mucous muscles of sensation above ye,
membranes of nose, mastication between eye and mouth,
sinuses, mouth and below mouth to angle of
anterior tongue. jaw, clench teeth, push
down on chin to
separate jaws.
Abducens Voluntary motor: Lateral gaze(eye
lateral rectus muscle abduction)
of eyeball
Facial Taste; anterior 2/3 of Voluntary motor: Facial expressions
tongue facial muscles Close eyes tight, smile
Autonomic : lacrimal, and show teeth, and
submandibular and whistle and puff cheeks
sublingual glands and identify familiar
tastes sweet and sour.
Vestibulocochlear Hearing/ equilibrium Hearing tests and
balance and
coordination tests.
Glossopharyngeal Visceral sensibility Voluntary motor: Gag reflex, ability to
(pharynx, tongue and unimportant muscle swallow and phonation.
tonsils) taste of pharynx.
Autonomic: parotid
gland
Vagus Touch, pain, pharynx, Voluntary motor: Gag reflex, ability to
larynx, trachea, muscles of palate, swallow and speech,
bronchi and lungs. pharynx and larynx. phonation.
Taste: tongue and Autonomic:
epiglottis involuntary muscle
and gland control
Accessory Voluntary motor: Resisted head and
movement of head shoulder shrug.
and shoulders. SCM
and trapezius
muscles
Hypoglossal Voluntary motor: Tongue protrusion if
movement of tongue. injured, tongue deviates
towards injured side and
inspection of tongue for
atrophy.
2
NERVE FUNCTION ASSESSMENT SIGNS AND SYMPTOMS
OF DAMAGE
Olfactory Smell Assess sense of smell Anosmia- inability to detect
smells
Optic Vision Assess visual acuity Blindness, impaired vision.
Pupillary reflexes Central: Snellen eye Visual field deficits
chart Absence of light reflexes on
Peripheral: visual fields shining light in eye.
Test corneal light reflex Ptosis
Assess pupillary size/
shape
Oculomotor Elevates eyelid Assess position of Ptosis(drooping)
Turns eye up, down, in eyelid. Eye deviates down and out
Constricts pupil Test pursuit eye Diplopia with attempted
Accommodate lens movements lateral gaze to C/L side.
Test pupillary light Loss of light and
reflex accommodation
Test accommodation reflexes (I/L eye)
reflex

Trochlear Turns adducted eye down Test pursuit eye Diplopia with attempted
Intorsion of eye movement downward/ adducted gaze.
Adductorparalysis
(I/L eye)

Trigeminal Somatosensation Test sensation: Loss of facial sensations,

Face forehead, cheeks, chin numbness
Cornea Test corneal reflex: Loss of I/L corneal reflex
Anterior tongue Have patient clench Weakness, wasting muscles
Mastication jaw, hold against of mastication. deviation of
resistance jaw when opened to I/L side

Abducens Turns eye out Test pursuit eye Diplopia with attempted
movement lateral gaze to I/L side,
Convergent strabismus.
Abductor paralysis I/L eye

Facial Facial expression Assess motor function; Paralysis I/L facial muscles
Tearing: lacrimal gland Raise eyebrows Inability to close eyes,
Salivary secretion: Show teeth, smile Drooping corner of mouth,
submandibular and Close eyes tightly difficulty with speech
sublingual glands Puff cheeks articulation
Taste from anterior tongue Loss of lacrimation, pain
Somatosensation Test taste: sweet, salty, with blinking
sour, bitter Decreased salivation - dry
mouth

Vestibulocochlear Equilibrium Hearing Assess balance Vertigo, disequilibrium,

Eye head coordination nystagmus,
Assess for nystagmus Gage instability with head
Assess auditory acuity rotations
Weber test-conduction Deafness, impaired hearing,
Rinne test:sensorineural tinnitus.
3
Glossopharyngeal Elevates pharynx
Salivary secretion: parotid
gland
Taste: posterior third of
tongue
Somatosensations;
Posterior tongue
Oropharynx reflexes
Vagus Deglutition , phonation
Cardiac depressor
Broncho constrictor, GI
tract peristalsis,
secretion , taste, visceral
sensations and reflexes
somatosensations
Spinal accessory Deglutition and phonation
Cranial part SCM and trapezius
Spinal part
Hypoglossal Tongue movements
Assess taste: sweet, Dysphagia
salty, sour, bitter Dry mouth
Loss of posterior third of
tongue
Anesthesia of pharynx and
larynx dysphonia
Assess phonation, Dysphonia, hoarseness
articulation Palatal paralysis
Observe movements Cardiac dysrhythmias
Soft palate Respiratory
Swallowing Disturbances (B/L
Test gag reflex vagal dysfunction)
Test pharyngeal Loss of gag reflex
sensation
Assess muscle strength, Muscle weakness
tone and size Inability to shrug I/L
shoulder turn head to
opposite side
Assess strength of Wasting of tongue
tongue movements, Deviation of I/L side on
tongue protrusion protrusion
Difficulty with lingual
sounds dysphagia

Clinically important points:

CN1: clinician should avoid irritant odors that can stimulate trigeminal nerve.
CN 2: visual acuity by Snellen chart
Confrontation test for peripheral field vision.
CN 5: three sensory branches of trigeminal nerve are tested with pinprick close to the midline of
the face, but the skin that is more lateral is overlapped by the nerves of the face.
CN 7: loss or reduced ability to smile and frown is caused by peripheral palsy.
Loss of smile only- supranuclear lesion
CN 8: air conduction: placing tuning fork in front of external auditory meatus
Bone conduction: tuning fork in front of mastoid process (Rinne test)
Conduction deafness (middle ear disease) - reduced bone conduction
Sensorineural deafness- both air and bone conduction Lateralization:

Conduction deafness -vibration is heard more on affected side

Sensorineural deafness- vibration is heard more on normal side.
4
DIFFERENTIATE BETWEEN UMN AND LMN

UMN lesion LMN lesion

Location of lesion Central nervous system
Structures involved Cortex, brainstem,
corticospinal tracts, spinal
cord.
Disorders Stroke, TBI, SCI
Tone Increased- hypertonia
Velocity- dependent
Reflexes Increased hyperreflexia,
clonus
Exaggerated cutaneous and
autonomic reflexes, Babinski
response
Involuntary movements Muscle spasms, flexor or
extensor
Strength Stroke: weakness or paralysis
on one side of the body
Corticospinal lesions: C/L if
above decussating in medulla,
I/L if below.
Spinal cord lesions: B. loss
below level of lesion
Peripheral nervous system
SC: anterior horn cell, spinal
roots, peripheral nerves.
CN: cranial nerves.
Polio, GBS, PNI, peripheral
neuropathy, radiculopathy
Deceased or absent:
hypotonia, flaccidity
No velocity dependent
Decreased or absent:
hyporeflexia
Cutaneous reflexes decreased
or absent
With denervation;
fasciculation
Limited distribution :
segmental or focal pattern
Root innervated pattern

Muscle Belk Variable, disuse atrophy Neurogenic atrophy rapid,

Voluntary movements
Impaired or absent,
dyssynergic patterns,
obligatory synergies.
CP, ALS, CVA, birth
injuries, multiple sclerosis,
Huntington’s chorea, TBI,
psedobulbar palsy, brain
tumors, hydrocephalus
focal severe wasting
Weak or absent if nerve
interrupted.
Tumor involving spinal cord,
trauma, progressive muscular
atrophy, infection, bell’s
palsy, carpal tunnel
syndrome, muscular
dystrophy, spinal muscular
atrophy.

REFLEX TESTING

Reflex Site of stimulus Normal response Pertinent CNS

segment
Jaw Mandible Mouth closes CN V
Biceps Biceps tendon Biceps contraction C5-C6
Brachioradialis Brachioradialis tendon or Flexion of elbow or C5-C6
just distant to pronation of forearm
musculotendinous
junction
Triceps Distal triceps tendon Elbow extension C7-C8
above olecranon process
Patella Patellar tendon Leg extension L3-L4
Medial hamstrings Semimembranosus tendon Knee flexion L5,S1
5
Lateral hamstrings Biceps femoris tendon Knee flexion S1-S2
Tibialis posterior Tibialis posterior tendon Plantar flexion of L4-L5
behind medial malleolus foot with inversion
Achilles Achilles tendon Plantar flexion of S1-S2
foot

SUPERFICIAL REFLEXES

Reflex Site of stimulus Normal response Pertinent CNS

segment
Plantar With large pin, stroke up Slow flexion (PF) L5-S1
the lateral side of foot, of great toe, and
moving from the heel to sometimes the other
toe.
base of little toe and then Abnormal
across the ball of foot. response: positive
Babinski- extension
of great toe with
fanning of four
toes(UMN)
Corneal blink reflex Ask patient to look up and Both eyes will Trigeminal and
away from you, stroke the blink with contact facial nerves
cornea with use of cotton. to one eye
Abdominal Patient in supine, make Localized T7-12
quick light stroke with a contraction under
large pin over the skin of the stimulus,
causing the
the abdominals from the umbilicus to move
periphery to the umbilicus. toward the quadrant
Test each abdominal stimulated.
quadrant separately
Gag reflex Therapist lightly stimulates Gag will occur post Glossopharyngeal
each side of the back of stimulation, may be and vagus nerves
throat absent in normal
population
Cremastric reflex Scratch the skin of upper Brisk and brief L1-L2
medial thigh elevation of testicle
on I/L side

GRADING SCALE FOR REFLEXES

GRADE EVALUATION RESPONSE CHARACTERISTICS

0 Absent No visible or palpable muscle contraction with reinforcement.

1+ Hyporeflexia Slight or sluggish muscle contraction with little or no joint

movement. Reinforcement may be required to elicit a reflex
response
2+ Normal Slight muscle contraction with slight joint movement
3+ Hyperreflexia Clearly visible, brisk muscle contraction with moderate joint
movement.
4+ Abnormal Strong muscle contraction with one to three beats of clonus.
Reflex spread to C/L side may be noted.
5+ Abnormal Strong muscle contraction with sustained clonus. Reflex spread
to C/L side may be noted.
6
 DEVELOPMENTAL REFLEXES

PRIMITIVE/SPINAL STIMULUS RESPONSE

REFLEXES
Flexor withdrawal Supine/ sitting Toe extends, foot DF, entire leg
Noxious stimulus to sole of foot flexes uncontrollably
O-28 wks gestation
I-1-2 months
Crossed extension Supine-extremity in extended Opposite LE flexes, adducts and
position. Noxious stimulus to ball of then extends
foot. O-28 wks gestation
I-1-2 months
Traction Grasp forearm and pull up from Grasp and total flexion of UE.
supine to sitting position 0-28 wks gestation
I- 2-5 months
Moro Sudden change in position of head in Extension, abduction of UE,
relation to trunk. Drop patient hand opening crying followed
backward from sitting position by flexion, adduction of arms
across chest.
O- 28 wks gestation
I- 5-6 months
Startle Sudden loud or harsh noise Sudden extension or abduction
of arm across chest.
O-birth
I-persists
Grasp Maintained pressure to palm of hand Flexion of fingers or toes.
(palmar grasp) and ball of foot Palmar: O-birth I-4-6
(plantar) months.
Plantar
O-28 wks gestation
I-9 months

Tonic/brainstem reflexes stimulus response

ATNR Rotation of head to one side Flexion of skull limbs and
extension of jaw limbs.
‘’Fencing posture’’.
O-birth
I-4-6 months
STNR Flexion or extension of head Head flexion: flexion of arms
and ext of legs
Head ext: ext of arms and fle
of legs
O-4-6 months
I-8-12 months
TLR or STLR Prone or supine position Prone- increased flexor tone,
flexion of all limbs
Supine: increased extensor
tone. Ext of all limbs.
0-birth
I-6 months
Positive supporting Contact to ball of foot in upright Rigid ext of LE
standing position O-birth
I-6 months
7
Associated reactions
Midbrain/cortical reflexes
Neck righting action on
body(NOB)
Body righting acting on
body(BOB)
Labyrinthine head righting
Optical righting
Body righting acting on head
Protective extension
Equilibrium reactions(tilting)
Equilibrium reactions
(postural fixation)
Resisted voluntary movements in any Involuntary movements in
part of the body resting extremity.
O-3 months
I-8-9 yrs.
Stimulus Response
Supine. Body rotates as a whole to
Passively turn head to one side align with the head.
O- 4-6 months
I-5 yrs.
Supine. Body segment not rotated to
Passively rotate upper or lower trunk align the body segments.
O- 4-6 months
I-5 yrs.
Occlude vision, alter body position by Head orients to vertical
tipping body in all directions. position with mouth
horizontal.
O- birth to 2 months
I- persists
Alter body position by tipping body in Head orients to vertical
all directions. position with mouth
horizontal.
O- birth to 2 months
I- persists
Place in prone or supine position Head orients to vertical
position with mouth
horizontal.
O- birth to 2 months
I- 5 yrs.
Displace COG outside BOS Arms/legs extend and abduct
to protect body from falling.
O- arms,4-6 months, legs 6-9
months
I-persists
Displace COG by tilting r moving the Curvature of trunk toward the
support surface upper side along with ext and
abd of extremities of that side,
protective extension on the
opp side.
O-prone-6 months, supine 7-8
month, sitting 7-8 months,
quadruped- 9-12 months
standing 12-21
months
I- persists.
Apply a displacing force to the body, Curvature of trunk toward the
altering the COG in its relation to BOS, external force with ext and
can also be observed during voluntary abd of extremities of that side
activity. to which the force is applied.
O-prone-6 months,
supine 7-8 month,
sitting 7-8 months,
quadruped- 9-12 months
standing 12-21 months
I- persists.
8
 PATHOLOGICAL REFLEXES

Reflex Stimulus Positive response Pathology

Babinski Stroking of lateral Ext of big toe and Pyramidal tract lesion
aspect of foot. fanning of other toes, Organic hemiplegia
common in newborns
Chaddock Stroking of lateral Ext of big toe and Pyramidal tract lesion
aspect of foot beneath fanning of other toes,
the lateral malleolus. common in newborns
Oppenheim Stroking of Ext of big toe and Pyramidal tract lesion
anteromedial tibial fanning of other toes,
surface common in newborns
Gordon Squeezing of calf Ext of big toe and Pyramidal tract lesion
muscles firmly fanning of other toes,
common in newborns
Brudzinski Passive flexion of one Similar movement Meningitis
LL occurs in oppose limb
Hoffmann Flicking of terminal Reflex flexion of distal Increased irritability of
phalanx of index, phalanx of thumb and sensory nerves in tetany,
middle, ring finger distal phalanx of index Pyramidal tract lesion
or middle finger
Lhermitte Neck flexion Electric shock like Abnormalities(demyelination)
sensation that radiates in posterior part of cervical
down spinal column spinal cord
into upper or lower
limbs

JENDRASSIK MANEUVER:
Used during testing to enhance a muscle reflex that is difficult to elicit
For UE reflexes, patient is asked to cross the ankles and then to isometrically attempt to abduct
the legs.
For LE reflexes, patient is asked to interlock the fingers and then to isometrically attempt to pull
the elbows apart.
CLASSIFICATION OF SENSORY SYSTEM

Sensory receptors
Spinal pathway mediating information to higher centers.
Receptors

Superficial Receive stimulus from external Perception of pain, temperature, light

sensation/ environment through skin and
exteroceptors subcutaneous tissue
Deep sensation/ Receive stimulus from muscles,
proprioceptors tendons and fascia.
Combined Requires information from
cortical sensation exteroceptive, proprioceptive and
cortical sensory association areas.
touch and pressure.
Responsible for position sense and
awareness of joints at rest, movement
awareness(kinesthesia) and vibration
Stereognosis, 2 point discrimination,
barognosis, graphesthesia, tactile
localization, recognition of texture
and double simultaneous stimulation
9
CLASSIFICATION OF SENSORY RECEPTORS

Mechanoreceptors Cutaneous sensory receptors

Free nerve endings
Hair follicle endings
Markel’s disks
Ruffini endings
Krause’s end bulbs
Meissner’s corpuscles
Pacinian corpuscles
Deep sensory receptors a. Muscle Receptors
Muscle spindles
Golgi tendon organs
Free nerve endings
Pacinian corpuscles
b. Joint Receptors
Golgi nerve endings
Free nerve endings
Ruffini endings
Paciniform endings
Thermo receptors a. Cold - cold receptors
b. Warmth - warmth receptors
Nociceptors a. Pain
Free nerve endings
Extremes of stimuli
Electromagnetic receptors a. Vision
Rods
Cones
Chemoreceptors a. Taste
Receptors of taste buds
b. Smell
Receptors of olfactory nerves in olfactory epithelium
c. Arterial oxygen
Receptors of aortic and carotid bodies
d. Osmolality
Probably neurons of supraoptic nuclei
e. Blood co2
Receptors in or on surface of medulla and in aortic and
carotid bodies.
f. Blood glucose, amino acids, fatty acids
Receptors in hypothalamus.

Transmission of sensory signals

Sensory signals are then carried to higher centers via ascending pathways from one of two
systems:

ANTEROLATERAL SPINOTHALAMIC SYSTEM:

3 major tracts of spinothalamic system:

Anterior spinothalamic tract- carries the sensation of crudely localized touch and pressure.
Lateral spinothalamic- carries pain and temperature

Spinoreticular tract- involved with diffuse pain sensations.

10
System Type of sensation Afferent fibers Origin Termination
Spinothalamic Non discriminative Small, slowly Skin From dorsal roots (horn) cross in
(Pain, temperature), conducting spinal cord, second order neurons
crude localization project to lower brain stem and
thalamus.
Lemniscal Discriminative Large, rapidly Skin, From dorsal column nuclei,
(stereognosis, 2 point conducting joints, second order neurons project to
discrimination), tendons C/L thalamus cross in medulla),
precise localization third order neurons project to
sensory cortex.

CVA
CLINICAL MANIFESTATIONS OF ACA SYNDROME

Signs & symptoms Structures involved

Paresis of opposite leg and to lesser extent of Primary motor area, medial aspect of cortex,
arm internal capsule
Mental impairment – perseveration, confusion Localization unknown
and amnesia
Sensory impairments primarily in LE. Primary sensory area, medial cortex
Urinary incontinence Posteromedial aspect of superior frontal gyrus
Problems with imitation, bimanual tasks, Corpus callosum
apraxia
Abulia (akinetic mutism), slowness, delay, Uncertain localization
lack of spontaneity, motor inaction

CLINICAL MANIFESTATIONS OF MCA SYNDROME

Signs & symptoms Structures involved

Paresis of C/L arm, face and leg ( leg is least Primary motor cortex and internal capsule
involved)
Sensory impairment over C/L arm, face and Primary motor cortex and internal capsule
leg – pain, temperature, touch, vibration,
position, 2 point discrimination, stereo gnosis

Motor speech disorder- expressive aphasia,
telegraphic halting speech
Wernicke’s or receptive aphasia
Perceptual problems such as unilateral
neglect, apraxia, depth perception problem,
spatial relation difficulties
Homonymous hemianopia
Loss of conjugate gaze to opposite side
Ataxia of C/L limb.
Broca’s cortical area in dominant hemisphere
Wernicke’s cortical area in dominant
hemisphere
Parietal sensory association area
Optic radiation in internal capsule
Frontal eye fields or their descending tracts
Parietal lobe.
11
CLINICAL MANIFESTATIONS OF PCA SYNDROME

Signs & symptoms Structures involved

Peripheral territory
C/L Homonymous hemianopia Primary visual cortex or optic radiation
Prosopagnosia-difficulty in naming people on Visual association areas
sight
Dyslexia without agraphia (difficulty Dominant calcarine lesion and posterior part
writing), color naming (anomia), of corpus callosum
color discrimination problems
Motor defect Lesion of inferomedial portions of temporal
lobe bilaterally or on dominant side only
Topographical disorientation Nondominant primary visual area, usually
bilaterally
Central territory
Thalamic syndrome: sensory impairments, Ventral posterolateral nucleus of thalamus
spontaneous pain, dysthesias
Involuntary movements, choreathetosis, Sub thalamic nucleus or its pallidal
intention tremor, hemiballismus connections
C/L hemiplegia Cerebral peduncle - midbrain
Weber’s syndrome: oculomotor nerve palsy Third nerve and Cerebral peduncle- midbrain
and C/L hemiplegia
Paresis of vertical eye movements, slight Supranuclear fibers to third nerve
miosis and ptosis and sluggish pupillary light
response

SYNERGY PATTERNS OF EXTREMITIES

Flexion synergy Extension synergy

Upper extremity Scapular retraction/ elevation
or hyperextension
Shoulder abduction, ER
Elbow flexion
Forearm supination
Wrist and finger flexion
Lower extremity Hip flexion, abduction and
ER
Knee flexion
Ankle dorsiflexion
Toe dorsiflexion
Scapular protraction
Shoulder adduction, IR
Elbow extension
Forearm pronation
Wrist and finger flexion
Hip extension, adduction and
IR
Knee extension
Ankle PF, inversion
Toe PF

MODIFIED ASH WORTH SCALE FOR GRADING SPASTICITY

Grade Description
0 No increase in muscle tone
1 Light increase in muscle tone, manifested by a catch and release or by minimal
resistance at the end of ROM when the affected part moved in flexion or extension
1+ Slight increase in muscle tone manifested by a catch followed by minimal resistance
throughout the remainder
2 More marked increase in muscle tone through most of ROM , but affected part
moved easily
3 Considerable increase in muscle tone, passive movement difficult
12

4 Affected part rigid in flexion or extension

TBI
Direct impairments associated with TBI

Impaired cognition Memory deficits

Attention span deficits
Problem solving/reasoning deficit
Impaired safety awareness
Impaired insight
Impaired executive functioning

Impaired communication Expressive aphasia

Neuromuscular impairments Motor control deficits

Impaired strength
Impaired coordination
Ataxia
Impaired balance
Indirect impairments Decreased PROM
Decreased endurance
Functional limitations Supervised ambulation in home, minimal
assistance /contact guard ambulation in an
open environment with devices and orthoses
Contact guard on stairs with rail and orthoses
Moderate assistance with floor to stand
transfers
Glascow coma scale
Activity Score
EYE OPENING
Spontaneous 4
To speech 3
To pain 2
No response 1
BEST MOTOR RESPONSE
Follows motor commands 6
Localizes 5
Withdraws 4
Abnormal flexion 3
Extensor response 2
No response 1
VERBAL RESPONSE
Oriented 5
Confused conversation 4
Inappropriate words 3
Incomprehensible sounds 2
No response 1

Score less than 8= coma or severe brain injury

9-12= moderate brain injury
13-15= severe brain injury
13
RANCHOS LOS AMIGOS LEVELS OF COGNITIVE
FUNCTIONING

I no response Deep sleep. Unresponsive to any stimulus

II generalized response
III localized response
IV confused-agitated
V confused inappropriate
VI confused appropriate
VII automatic appropriate
VIII purposeful appropriate
Inconsistently and nonpurposefully to stimuli in non-specific
manner
Responses ae limited and same
Responses may be gross body movements, physiological
changes/vocalization
Reacts specifically but inconsistently to stimuli
Responses- related to type of stimulus presented.
May follow simple commands such as closing eyes or
squeezing hand
Heightened state of activity. Behavior is bizarre and
nonpurposeful relative to immediate environment.
Verbalizations frequently are incoherent or inappropriate to
environment. Patient lacks short and term recall.
Able to respond to simple commands fairly consistently.
Responses- non purposeful, random or fragmented
Memory- severely impaired
May perform previously learned tasks
Goal directed behavior
Follows simple directions consistently and shows carryover
for relearned tasks such as self-care.
Past memory shows more depth and detail than recent
memory.
Appropriate and oriented within hospital and home settings.
Goes through daily routine but robot like.
Structure is able to initiate social or recreational activities,
judgement remains impaired
Able to recall and integrate past and recent events
Aware of responses to environment. Decreased ability
relative to premorbid abilities, abstract reasoning.

NEUROLOGICAL CONDITIONS

Disease Description Etiology Signs& symptoms

Alzheimer’s disease Deterioration and Unknown, low levels Difficulty in new
irreversible damage of neuro transmitters, learning, changes in
within cerebral cortex genetic inheritance, memory and
and subcortical areas autoimmune disease, concentration.
of brain virus Progression includes
loss of orientation,
word finding
difficulties, poor
judgement, rigidity,
bradykinesia,
shuffling gait, and
impaired ability to
perform self-care
skills.
14
ALS Chronic degenerative Genetic inheritance, LMN- asymmetric
disease produces both virus, metabolic muscle weakness,
UMN & LMN. disturbances, toxicity fasciculation’s,
cramping, atrophy
of lead and aluminum within hands,
weakness goes from
distal to proximal.
UMN-
incoordination,
spasticity, clonus,
positive Babinski
reflex, fatigue, motor
impairment, motor
paralysis
Bell’s palsy Temporary U/L Viral infection, Drooping of
paralysis herpes simplex/zoster eyelid/mouth,
Trauma with virus dryness of eyes,
demyelination and inability to
axonal degeneration close eyelid due to
of facial nerve weakness
Epilepsy Chronic, temporary Idiopathic, genetic Loss of awareness
dysfunction of brain influence, head and disturbances of
results in seizure trauma, dementia, movement, sensation,
activity CVA, cerebral palsy, mod or mental
down syndrome and function
autism
GBS Temporary Unknown, auto Distal to proximal
inflammation and immune response to Motor weakness,
demyelination of previous infection, sensory impairment,
peripheral nerves influenza, respiratory paralysis.
myelin’s heaths result immunization or level of disability
sin axonal surgery peaks in 2 to 4 weeks
degeneration.
Huntington’s disease Degeneration & Autosomal dominant Movement disorder,
atrophy of basal trait with defect involuntary choretic
ganglia and cerebral linked to movements,
chromosome 4 and to grimacing, protrusion
cortex of brain
gene identified as of tongue, ataxia and
IT15 chorea athetoid
movements.
Multiple sclerosis Demyelination in Genetics, viral Visual problems,
myelin sheath, infection paresthesias, sensory
Decrease in nerve changes, clumsiness,
impulse transmission weakness, ataxia,
balance dysfunction
and fatigue.
15
SPINAL CORD INJURY

Lesion
Complete cord lesion: UMN
Central cord lesion :UMN
Brown sequard syndrome :UMN
Anterior cord syndrome : UMN
Posterior cord syndrome: UMN
Cauda equine syndrome
Characteristic
Complete B. loss of all sensory modalities
B. loss of motor function with spastic
paralysis below the level of lesion
Loss of bladder and bowel functions with
spastic bladder and bowel
Cavitation of central cord in cervical section
Loss of spino thalamic tracts with B. loss of
pain and temperature
Loss of ventral horn with B. loss of motor
function: primarily upper extremities
Hemisection of spinal cord
I/L loss of dorsal columns with loss of
tactile discrimination, pressure, vibration and
proprioception
I/L loss of corticospinal tracts with loss of
motor function and spastic paralysis below
level of lesion
C/L loss of spinothalamic tact with los of pain
and temperature below level of lesion
@ lesion level, B. loss of pain an temperature
Loss of anterior cord
Loss of lateral cortico spinal tracts with B.
loss of motor function , spastic paralysis
below level of lesion
Loss of spinothalamic tracts with B. loss of
pain and temperature
Perseveration of dorsal columns -
proprioception, kinesthesia, vibratory sense.
Loss of dorsal columns bilaterally
B. loss of proprioception, vibration, pressure
and epicritc sensations
Perseveration of motor function, pain and
light touch
Loss of long nerve roots at below L1
Variable nerve root damage, incomplete
lesions common
Flaccid paralysis with no spinal reflex activity
Flaccid paralysis bladder and bowel Potential
for nerve regeneration, slows and stops after
about 1 year

NEURO MUSCULAR SYSTEM

Medical procedures/testing for neurological dysfunction

Procedure/test Rationale
Cerebral angiography Invasive, shows narrowing of artery inside brain.
Used: CVA, brain tumor, aneurysm, vascular malformation Catheter-
threaded into an artery within neck and contrast dye is released into
blood stream, series of X rays are then taken.
CT Noninvasive, cross sectional area of brain with 2 dimensional views of
bones, tissues and organs.
Used: vascular malformations, tumors, cysts, herniated disks,
16

hemorrhage, epilepsy, spinal stenosis, head injury.

 Discography Invasive, evaluate integrity and pathology of spinal disk. Contrast dye
with CT used for better assessment.
EEG Noninvasive, records electrical activity of brain using multiple
electrodes attached to skull.
Used: seizure disorder, brain death and tumors, brain damage,
inflammation, alcoholism and degenerative disorders.
EMG Invasive, to assess nerve and muscle dysfunction or spinal cord
disease. Records electrical activity of brain or spinal cord to the
peripheral root tested.
Used: muscle pathology, nerve pathology, spinal cord disease,
denervated muscle and LMN injury.
Evoked potentials Noninvasive, 2 sets of electrodes used to record time it takes an
impulse to travel into brain.
Used: multiple sclerosis, brain tumor, acoustic neuroma and SCI.
MRI Noninvasive, detailed images including tissues, organs, bones and
nerves.
Used: tumors of brain or spinal cord, multiple sclerosis and head
trauma.
Myelography Invasive, using contrast dye and contrast imaging, High risk of
headache after procedure.
Used: abnormalities around subarachnoid space, spinal nerve injury,
herniated disks, fractures, back or leg pathology and spinal tumors.
NCV Noninvasive, stimulation of peripheral nerve to determine nerve
action potentials and nerve’s ability to send a signal.
Used: peripheral neuropathies, carpal tunnel syndrome, demyelination
pathology, peripheral nerve compression.
PET Brain scan, provides 2 or 3 dimensional pictures of brain activity.
Used: cerebral circulatory pathology, metabolism dysfunction, tumors,
blood flow, brain changes following injury or drug abuse.
Spinal lumbar Invasive, inserts needle through lumbar puncture below the level of
puncture L1-L2 for cerebral spinal fluid sample.
Used: hemorrhage, inflammation, infection, meningitis and tumor.

PHARMACOLOGY IN NERVOUS SYSTEM MANAGEMENT

Action Indications Side effects PT implications Examples

Antiepileptic Reduce or Seizure Ataxia, skin issues, Knowledge Seconal,
eliminate activity behavioral changes, GI about seizure is klonopin,
seizure distress, headache, necessary. Depakote,
Patients will Dilantin,
activity in blurred vision, weight tegretol.
brain. gain. show greater Celontin,
Inhibit the sensitivity to Neurontin.
firing of environmental
cerebral stimuli like
neurons light or noise
within CNS. level.
Antispasticity Promotes Increased Drowsiness, confusion, Once spasticity Lioresal,
relaxation in tone, SCI, headache, dizziness, is reduced, valium,
spastic CVA, generalized muscle therapist should dantrium,
multiple
muscle. weakness, tolerance , focus on zanaflex.
sclerosis
Agents bind dependence therapeutic
selectively handling
within CNS or techniques,
within skeletal facilitation and
17

muscle cells strengthening to

 to reduce promote overall
spasticity. mobility.

Cholinergic Direct Glaucoma, GI distress, impaired PT may see Direct:

stimulant dementia, visual accommodation, decrease in duvoid,
agents mimic myasthenia bronchoconstriction, heart rate and pilocar
acetylcholine gravis. bradycardia, flushing. dizziness, Indirect:
and bind should aware of Aricept,
directly to sympathetic and tensilon.
cholinergic parasympathetic
receptor to side effects to
activate and notify
create a physician.
response at
cellular level.
Dopamine Agents are Parkinson’s Arrhythmias(levodopa), Maximal Sinemet or
replacement able to cross disease GI distress, orthostatic benefit- one madopar,
BBB through hypotension, mood and hour after symmetral
administration
active behavioral changes,
of levodopa.
transport and tolerance Monitor patient
transform to BP for
dopamine orthostatic
within brain. hypotension.
Muscle Promote Muscle Sedation, drowsiness, Maximize the Valium,
relaxant relaxation in spasm dizziness, nausea, potential for flexeril and
agents muscles that vomiting, headache, relaxation paraflex.
typically tolerance and through
present with dependence. therapeutic
spasm, modalities
continuous, during
tonic treatment.
contraction. Retaining Prevention of
Stretching, posture injury through

NEUROLOGICAL CONDITIONS

Alzheimer’s disease Progressive neuro degenerative disorder that results in deterioration.

Increases with age, higher incidence in women
Dementia, change in higher cortical functions- key features.
Amyotrophic lateral Chronic degenerative disease produces both UMN & LMN symptoms.
sclerosis Seen in 40-70 years of age and higher incidence in men.
LMN- muscle weakness, atrophy
UMN- incoordination , spasticity
Bell’s palsy U/L facial paralysis due to degeneration of facial nerve.
Age: 15 to 45 years of age.
Sooner the treatment given, better the outcome.
Carpal tunnel Peripheral nerve pathology, LMN.
syndrome Sensory and motor disturbances in median nerve root distribution.
Night pain, pain radiating to shoulder, neck.
Cerebellar disorders congenital- early life and non-progressive
Hereditary- autosomal recessive or autosomal dominant.
Gait steadiness will start early followed by UE ataxia, dysarthria and
paresis.
Spino cerebellar ataxias: main autosomal dominant ataxias.
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Acquires ataxias: non hereditary neurodegenerative systemic disorders.

Diabetic neuropathy Symmetric polyneuropathy and autonomic neuropathy.
Distal symmetric involvement in feet, involves sensory, motor and
autonomic systems.
‘Stocking glove’ appearance.
Epilepsy Symptom of interrupted brain functioning.
GBS Temporary inflammation in peripheral nerves resulting in axonal
degeneration.
Peak in young adults, 5th to 8th decades.
Symptoms starts from distal and progress to UE and head.
Level of disability- peaks- within 2 to 4 weeks after onset.
Huntington’s chorea Degeneration and atrophy of basal ganglia.
35-55 years of age is common.
Involuntary movements predominates.
Multiple sclerosis Seen in 20-35 years of age.
Frequency & intensity of exacerbations and remissions shows disease
progress.
Myasthenia gravis Neuromuscular junction pathology.
Cardinal signs: extreme fatigue and muscle weakness within minutes to
extended time. Ptosis and diplopia- exist in half patients.
Parkinson’s disease Majority- 50 to 79 years of age, 10% diagnosed before 40 years.
Resting tremor-pin rolling tremor- cardinal symptom.
Cog wheel or lead pipe rigidity, festinating gait.
Post-polio syndrome Focal and asymmetrical motor impairments.
Previous diagnosis of polio is essential to diagnose PPS. Slow
and progressive weakness.

PEDIATRIC PATHOLOGY

Arthrogryposis Non progressive, occurs in 1st trimester in utero.

multiplex congenita Genetic inheritance in autosomal dominant trait.
Cylinder like extremities, dislocation of joints.
Cerebral palsy Non progressive, acquires in birth or in utero.
Impaired modulation of movement, presence of abnormal reflexes
and impaired mobility.
Down syndrome Genetic abnormality, extra 21st chromosome, trisomy 21.
Advanced maternal age increases risk.
Duchenne muscular Progressive disorder, absence of gene produce the muscle proteins
dystrophy dystrophin and nebulin.
Seen prior to age 25.
Child mother – carrier, male offspring will inherit disease
Manifest 2 -5 years of age, proximal muscle weakness, Gower’s
sign
Prader Willi syndrome Partial deletion of chromosome 15.
Small hands, feet and sex organs, almond shaped eyes,
coordination impairments and mental retardation.
Spina bifida Insufficient closure of neural tube by 28th day of gestation.
Low thoracic, lumbar, sacral regions and affects CNS, MS US.
Spina bifida occulta: non fusion of spinous processes of vertebra.
Spina bifida cystica: cyst like protrusion through non fused
vertebra.
Spinal muscular Progressive degeneration of AHC.
atrophy. Acute: occurs between birth and 2 months of ag.
Chronic: six months to 1 year and has slower progression that
acute.
Juvenile: 4-17 years of age.
19

Charcot Marie- Hereditary disorder of peroneal and distal leg muscles.

toothdisease Foot drop and stork leg deformity.
Legg-calve-perthes Idiopathic aseptic necrosis of femoral capital epiphysis Boys,
disease between 5 to 10 years of age..

NEUROMUSCULAR INTERVENTIONS

Vestibular rehabilitation

Indications Anatomic goals Therapeutic goals

Vestibular Vestibular or central Vestibular retraining Improve balance,
rehabilitation balance disorders. utilize compensation, trunk stability.
adaptation and Increase ROM &
strength in order to
plasticity to increase
improve MS balance
brain’s sensitivity, responses and
restore symmetry. strategies.
Improve vestibule Decrease the rate and
ocular control and risk of falls.
increase motor Minimize dizziness.
control and
movement.

Guidelines for vestibule ocular retraining therapeutic guidelines

VOR 7 VSR stimulation exercises. Use of practice, feedback ad repetition to

Oculomotor exercises
Balance and gait exercises
Combination exercises (obstacles)
Habituation training exercises
Individualize each program based on patient’s
specific impairments
improve skills.
Use of gravity, varying surface conditions,
visual conditions and environmental cues
should be included in therapeutic planning
COG must be controlled in each stage.
Strategy (hip, ankle, stepping, and suspense)
training should be implemented during
treatment so that strategies become automatic
responses.
Force plate systems, EMG biofeedback,
Optokinetic visual stimulation ad videography
technical systems that can provide feedback
to motor learning during vestibular
rehabilitation.
Foam, mirrors, rocker boards, BAPS board,
Swiss balls, Foam rollers, trampolines and
wedges are lower tech treatments tools that
are successfully used for vestibular rehab.

Treatment for aphasia

PT role PT should alter the traditional methods to enhance communication and
provide a safe and comfortable environment for patient.
Considerations Cueing- avoid verbal input, use tactile and visual cues.
One person should talk to patient at a time.
Extra noises and multiple voices will confuse the patient.
Use concise sentences and yes/ no questioning for easy understanding.
Give adequate time to process and respond before progressing with
treatment.
Allow for ample time for communication during treatment.
20

If communication is rushed that will decrease the effectiveness of treatment.

Patient may also become frustrated with feeling pressure to respond.
 Attempt to allow the patient to perform an activity or segment of therapy
without repetitive feedback.

Seizure treatment guidelines

Considerations while attempting 1. Stay calm and prevent injury.

to manage patient with seizure.
2. Remove all objects around person to prevent harm
3. Maintain awareness of length of time of seizure.
4. Ensure that person is as comfortable as possible
5. Do not allow other people near the person in an effort
to keep the individual isolated.
6. Consider PT safety and do not hold person down, no
need for restraint if the person is thrashing during the
seizure.
7. Avoid placing anything into person’s mouth
8. Avoid providing any water, food or medicine until the
person is fully alert.
9. After the seizure is over, Place patient in left side
lying to avoid choking in case the person vomits.
10. Patient should remain in position until they are fully
alert.
11. PT should be aware of at risk for seizure activity in
order to avoid unnecessary safety risks.
12. Call 911 if seizure lasts longer than 5 minutes.

MYASTHENIA GRAVIS

Facts associated with myasthenia gravis

Encompasses mild to severe symptoms and can fluctuate in severity from hour to
hour.
Proximal muscle groups > distal muscle groups
Speech, swallowing and chewing difficulty-weakness of pharyngeal muscles and
muscles of mastication.
Cranial nerve involvement- eyelid weakness, diplopia and ptosis
Typified by exacerbations, remissions and atypically crisis which is life
threatening
Remissions are not typically complete or permanent.

PT guidelines
Acquire a baseline for respiratory and
neurological status.
Monitor respiratory function on a regular
basis to ensure that muscles of respiration are
not weakening.
Review proper techniques for positioning
during meals to prevent aspiration.
Instruct and review energy conservation
techniques
Avoid excess heat or cold as it exacerbates
symptoms
Initiate strengthening for patients to mild to
moderate symptoms using moderate to
maximal isometric contraction while avoiding
Observe the signs of myasthenia crisis-
referred as respiratory difficulty, swallowing
issues, labored talking or chewing.
Review signs of toxicity and side effects of
pharmacological intervention.
Educate the patient to plan activity around
periods of increased energy.
Avoid strenuous exercise and stress
Educate regarding osteoporosis for long term
corticosteroid patients
Treatment should always be based on patient
current symptoms, fatigue level and strength
21

muscle fatigue.
MOTOR CONTROL
Study of nature of movement or ability to regulate or direct essential movement.
Motor control theories: reflex theory, hierarchical theory, motor programming theory, task
orienting theory, ecological theory.
Motor learning: study of acquisition or modification of movement.
Goals
Differentiates learning vs performance
Provides guidelines for appropriate use of feedback
Prioritize the impact of practice as it relates to skill and movement.
Focuses on the transfer of learning across tasks and in various environments.
Two initial theories of motor learning
Adam’s closed loop theory Schmidt’s schema theory

Premise of sensory feedback as an ongoing Created as a response to limitation of Adam’s

process for NS to compare current movement closed loop theory.
with stored information on memory of past Construct relies on open loop control
movement. processes and a motor control concept.

High emphasis on concept of practice. Promotes clinical value of feedback and

importance of variation with practice.

STAGES OF MOTOR LEARNING AND TRAINING STRATEGIES

Cognitive stage Training strategies

‘What to do’ decision
Learner develops an
understanding of task.
Cognitive mapping assesses
abilities, task demands, identifies
stimuli, contacts memory, selects
response, perform initial
approximation of task, structures
motor program, and modifies
initial responses.
Highlight purpose of task in functionally relevant terms
Demonstrates ideal performance of task to establish a
reference of correctness
Have patient verbalizes task component and requirements
Point out similarities to other learned tasks.
Direct attention to critical task elements
Select appropriate feedback
Emphasize intact sensory systems, intrinsic feedback
systems.
Carefully pair extrinsic feedback with intrinsic feedback.
High dependence on vision: have patient watch
movement.
Knowledge of performance: focus on errors as they
become consistent, do not cue on large number of random
errors.
Knowledge of results: focus on success of movement
outcome.
Ask learner to evaluate performance, outcomes identify
problems, solutions.
22

Use reinforcements for correct performance, continuing

motivation.

Associated stage
Learner practices movements,
refines motor program, spatial
and temporal organization,
decreased errors, and extraneous
movements.
Dependence on visual feedback
decreases, increases for use of
proprioceptive feedback,
cognitive monitoring decreases.
‘How to do’ decision
Organize feedback schedule
Feedback after every trial improves performance during
early learning.
Variable feedbacks (summed, fading, bandwidth designs)
increases depth of cognitive processing, improves
retention may decrease performance initially.
Organize initial practice
Stress controlled movement to minimize errors.
Provide adequate rest periods (distributed practice) if task
is complex, long o energy costly or if learner fatigues
easily, has short attention or poor concentration.
Use manual guidance to assist as appropriate.
Break complex tasks down into component parts, teach
both parts and integrated whole.
Utilize bilateral transfer as appropriate.
Use blocked/ repeated practice of some task to improve
performance.
Use variable practice (serial or random practice order) of
related skills to increase depth of cognitive processing and
retention, may decrease performance initially.
Use mental practice to improve performance and learning,
reduce anxiety.
Assess, modify arousal levels as appropriate
High or low arousal impairs performance and learning.
Avoid stressors, mental fatigue.
Structure environment
Reduce extraneous environmental stimuli, distractors to
ensure attention, concentration
Emphasize closed skills initially gradually progressing to
open skills.
Training strategies
Select appropriate feedback
Continue to provide KP, intervene when errors become
consistent.
Emphasize proprioceptive feedback, feel of movement to
assist in establishing an internal reference of correctness.
Continue to provide KP, stress relevance of functional
outcomes.
Assist learner to improve self-evaluation, decision making
skills.
Facilitation techniques, guided movements may be
counterproductive during this stage of learning.
Organize feedback schedule
Continue to provide feedback for continuing motivation,
encourage patients to self-access achievements.
Avoid excessive augmented feedback.
Focus on use of variable feedback (summed, fading,
bandwidth) designs to improve retention.
Organize practice
Encourage consistency of performance.
Focus on variable practice order (serial or random) of
related skills to improve retention.
Structure environment
Progress toward open, changing environment.
Prepare the learner for home, community and work
environments.
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Autonomous stage
‘How to succeed’ decision
Learner practices movements,
continues to refine motor
responses, spatial and temporary
highly organized, movements are
largely error free, minimal level
of cognitive monitoring.
Training strategies
Assess need for conscious attention, automaticity of
movements.
Select appropriate feedback
Learner demonstrates appropriate self-evaluation,
decision making skills. Provide occasional feedback (KP,
KR) when errors evident.
Organize practice
Stress consistency of performance in variable
environments, variations of tasks (open skills).
High levels of practice (massed practice) are appropriate.
Structure environment
Vary environments to challenge learner.
Ready the learner for home, community, and work
environments.
Focus on competitive aspects of skills as appropriate.
Wheel chair sports.

General concepts of motor learning to be considered when evaluation, developing a plan of care,
and treating patients.

Motor learning intervention constructs

Models of motor control vary based on
interpretation of brain function
Intervention is designed at the level of
impairment
Sensory, motor and cognitive strategies
should be used to acquire postural control.
Belief that sensory, motor and perceptual
input contribute to motor control.
Type and amount of feedbacm9visual, verbal,
tactile) should be determined for each
individual patient.
Intervention should create multiple ways to
solve a movement disorder
Environmental factors must be considered
with intervention, planning and
implementation.
Examination determines the degree of
impairment
Essential for a patient to relearn how to
perform a functional task in order to
maximize recovery and independence.
Focus is both on recovery and compensatory
techniques.
Movement is based around a behavioral goal
Emphasis on postural control, alignment and
sequencing of movements is essential.
Belief that performance is observed, act of
learning is not.

Motor relearning approach

Carr and shepherd targets normal movement and how it is relearned after neurological insult.

Factors that are involved in learning also involved in relearning and which includes
Identification of goal Inhibition of any unnecessary activity to the
effects of gravity and balance
Proper body alignment Proper motivation
Feedback Knowledge of results
Incorporate internal or mental practice as well
as external or physical practice
24
4 steps in motor relearning programme
Step 1: Analysis of task
Step 2: Practice of missing components Explanation- identification of goal
Step 3: Practice of task
Step 4: Transference of training
Observation
Comparison
Analysis
Instruction
Practice + verbal and visual feedback + manual
guidance
Explanation-identification of goal
Instruction
Practice+ verbal and visual feedback +manual
guidance Reevaluation
Encourage flexibility
Opportunity to practice in context
Consistency of practice
Organization of self-monitored practice
Structures learning environment
Involvement of relatives and staffs

Motor relearning intervention constructs

Utilize various techniques from other
treatment approaches
Belief that treatment cannot be routine or
based on diagnosis, must be individual to
the patient.
Developmental sequence may not be
necessary in treatment when treating adults.
Practice may include breaking the task into
discrete components, followed by task as a
whole.
Intrinsic and extrinsic /augmented feedback
are important during treatment.
Use of Bobath techniques for handling,
facilitation, inhibitive casting, use of
therapeutic ball.
Use of Rood’s technique of application of
ice, brushing, tapping for facilitation.
Biofeedback should be utilized for
decreasing hyper tonicity with movement or
for targeting facilitation of a muscle group.
Self-correction and self-awareness should
be incorporated into treatment through the
use of mirror, verbal feedback and
biofeedback.

Bobath (NDT)
Concept recognizes the interference of normal function within the brain caused by CNS
dysfunction leads to slowing down or cessation of motor development and the inhibition of
righting reactions, equilibrium reactions and automatic movements.
Patient should learn to control movement through activities that promote normal movement
patterns that integrate function.
Postural control can be learned and modified through experience.
Postural control uses both feedback and feed forward mechanisms for execution of tasks.
Postural control is initiated from a patient’s BOS.
Postural control is requires for skill development.
Postural control develops by assuming progressive positions in which there is an increase in
distance between the COG and BOS, BOS should also decrease.
25
NDT intervention constructs
Inhibition of abnormal patterns of
movement with simultaneous facilitation of
normal patterns.
Avoid utilization of abnormal reflexes or
associated reactions during treatment.
Achieve a balance between muscle groups
during therapeutic interventions
Emphasize the use of rotation during
treatment activities.
Treatment should be active and dynamic,
incorporating function.
Belief that compensation techniques are
unnecessary and should be avoided.
Alteration of abnormal tone and influencing
isolated active movement.
Utilize manual contact and handling
through key points of control for
facilitation and inhibition.
Utilize the developmental sequence,
dynamic RIP and functional activities with
varying levels of difficulty during
therapeutic intervention.
Provide the patient with sensation of
normal movement by inhibiting abnormal
postural reflex activity.
Provide orientation to midline control by
moving in and out of midline with dynamic
activity.

Brunnstorm approach
Movement therapy in hemiplegia, Based on hierarchical theory.
This approach created the term synergy and initially encouraged the use of synergy patterns
during rehabilitation.
Synergies- primitive patterns that occur at spinal cord level as a result of hierarchical
organization of CNS.
Brunnstorm developed seven stages of recovery which are used for evaluation and
documentation of patient progress.

Stages Description
Stage 1 No volitional movement initiated
Stage 2 Appearance of basic limb synergies. The beginning of spasticity
Stage 3 Synergies are performed voluntarily; spasticity increases.
Stage 4 Spasticity begins to decrease. Movement patterns are not dictated solely by
limb synergies.
Stage 5 A further decrease in spasticity is noted with independence from limb
synergy patterns.
Stage 6 Isolated joint movements are performed with coordination.
Stage 7 Normal motor function is restored.

Movement therapy in hemiplegia intervention

Evaluation of strength focuses on patterns of Sensory examination is required to assist with
movement rather than straight plane motion at treating motor deficits.
a joint.
Initially limb synergies are encouraged as a Encourage overflow to recruit active
necessary milestone for recovery. movement of the weak side.
Repetition of task and positive reinforcement A patient will follow the stages of recovery,
should be emphasized during treatment but may experience a plateau at any point so
activities. that full recovery may not be achieved.
26
Movement combinations that deviate from the Treatment should incorporate only tasks that
basic limb synergies should be introduced in the patient can master or almost master.
stage 4 of recovery.

Proprioceptive neuromuscular facilitation

PNF – using the hierarchical model.

Goal of treatment: establish gross motor patterns within CNS. Based on premise that stronger
parts of the body are utilized to stimulate and strengthen the weaker parts.
Normal movement and posture is based on a balance between control of antagonist and agonist
muscle groups.
Development will follow the normal sequence through a component of motor learning.
PNF: utilize methods that promote or hasten the response of neuromuscular mechanism through
stimulation of proprioceptors.
Movement pattern follows diagonals or spirals that each possess a flexion, extension and rotatory
component and are directed toward or away from midline.

PNF intervention strategies

Patient learns diagonal pattern of movement.
Verbal commands must be short and concise.
Resistance given during the movement
pattern is greater if the objective is stability,
less if the objective is mobility.
Treatment objectives will dictate the use of
techniques through either full movement or at
a points within the range.
PNF techniques are implemented to progress
a patient through the stages of motor control.
Techniques should be utilized that increase
strength or improve relaxation by enhancing
overflow from the stronger to weaker
muscles.
Techniques must have accurate timing,
specific commands and correct hand
placement.
Repetition of task or activity is important in
motor learning.
Techniques should utilize isometric and
isotonic muscle contractions.
Developmental sequence is used in
conjunction with PNF techniques in order to
increase the balance between agonists and
antagonist.
Functional patterns of movement ae used to
increase control.

PNF Diagonal Pattern- UE responses

D1 Flexion D1 extension D2 flexion D2 extension

pattern pattern pattern pattern
Scapula Elevation Depression Elevation Depression
abduction adduction adduction abduction
upward rotation downward upward rotation downward
rotation rotation
Shoulder Flexion Extension Flexion Extension
adduction lateral abduction abduction lateral adduction
rotation medial rotation rotation medial rotation
Elbow Flexion or Flexion or Flexion or Flexion or
extension extension extension extension
27

Radio ulnar Supination Pronation Supination Pronation

Wrist Flexion radial Extension ulnar Extension radial Flexion
deviation deviation deviation Ulnar deviation
Thumb Adduction Abduction Extension Opposition

PNF Diagonal patterns - LE responses

D1 Flexion D1 extension D2 flexion D2 extension

pattern pattern pattern pattern
Pelvis Protraction Retraction Elevation Depression
Hip Flexion Extension Flexion Extension
adduction lateral abduction abduction adduction lateral
rotation medial rotation medial rotation rotation
Knee Flexion or Flexion or Flexion or Flexion or
extension extension extension extension
Ankle & toes Dorsiflexion Plantar flexion Dorsiflexion Plantar flexion
inversion eversion eversion inversion

PNF therapeutic exercises

Technique Mobility Stability Controlled Skill Strength
mobility
Increased Initiate Distal Proximal
ROM movement functional dynamic
movement stability
Agonistic * *
reversals
Alternating * *
isometrics
Contract
relax *
Hold relax *
Hold relax *
active
movement
Joint * *
distraction
Normal *
timing
Repeated * *
contraction
Resisted * *
progression
Rhythmic *
initiation
Rhythmic * *
rotation
Rhythmic * *
stabilization
Slow * * *
reversal
slow reversal * * *
hold
28

Timing for *
emphasis
Rood approach
Rood believed that all motor output was the result of both past and present sensory input.
Treatment is based on sensorimotor learning.
Used a developmental sequence which was seen as “key patterns” in the enhancement of motor
control.
Goal of approach: obtain homeostasis in motor output and to activate muscles to perform task
independent of a stimulus.
Exercise is seen as treatment technique only if response is correct and it provides sensory
feedback that enhances the motor learning of the response. Once the response is obtained,
stimulus should be withdrawn.
Sensory stimulation techniques

Facilitation Inhibition
Approximation Deep pressure
Joint compression Prolonged stretch
Icing Warmth
Light touch Prolonged cold
Quick stretch
Resistance
Tapping
Traction

Rood’s intervention constructs

Utilization of sensory stimulation to achieve
motor output during treatment
Movement is considered autonomic and
noncognitive
Homeostasis of all systems is essential.
Techniques such as neutral warmth,
maintaining pressure and slow rhythmical
stroking can be used to calm a patient
Tactile stimulation is used to facilitate normal
movement
Environment can influence the effects of
therapeutic intervention
Exercise must provide proper sensory
feedback in order to be therapeutic.
Belief in techniques used to stimulate the
proprioceptive, exteroceptive and vestibular
channels of CNS.

(see table for SCI functional outcomes)

Spinal cord injury intervention constructs

Positioning Wheel chair mobility

Prevention of pressure ulcers Balance and COG retraining
Pressure relief techniques and equipment Motor function retraining
Range of motion Mobility training including floor transfers if
appropriate
Family/caregiver teaching Pain management
Bowel and bladder programming Use of FES, biofeedback, TENS if
appropriate
Respiratory training /airway clearance Self-care skills
Assisted cough and secretion clearance
Breathing exercises
Abdominal binders
Mechanical ventilation
Glossopharyngeal breathing
29
Wheel chair, cushion and orthotic Gait training (T9 or lower)
prescriptions

TBI intervention guidelines

Emphasis on motivation Avoid overstimulation during therapy

Promote independence
Therapy should be goal oriented, functional
ad recreational
Focus on orientation
Focus on behavior modification strategies
Repetition is typically useful
Educate patient in compensatory strategy for
success
A calm voice and simple commands are
desirable when interacting with patient
Perform activities that are both enjoyable and
familiar to patient
Family support and education can enhance
and assist the rehabilitation process
Allow patient to choose activities on occasion
Flexibility in treatment is needed on basis of
patient’s immediate needs and state of mind.
Structure is essential depending on the level
of patient

Interventions of TBI

Cognitive and orientation training Range of motion

Therapeutic exercise Motor function training
Positioning Wheel chair and adaptive equipment
prescription
Sensory integration Splinting and serial casting
Balance and vestibular training Mobility training

30