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Neuromuscular Study guide
Lecture #1 9/4/14
Five Key Elements of Conceptual Framework ( Shumway-Cook and Woolacott):
1. A model of Practice-Guide to Physical therapist Practice
a. Outlines a process for examination and the development of an appropriate plan of care to
address the patient’s problems and goals
2. Disablement/enablement model
a. Nagi model
b. Internation Classification of Functioning, Disability and Health (ICF)
3. Hypothesis-oriented clinical practice- Guides systematic testing of assumptions about the cause
of movement problems
4. Theory of motor control-Guides assumptions about the cause of abnormal movement
5. Evidence based practice-philosophical approach to clinical practice that integrates the best
available research, clinician expertise, and client characteristics
Task Oriented Approach- based on the contemporary theories of motor control and motor learning.
 Advocates examination and treatment of patients at several levels
 Emphasis placed on the patient’s functional performance of task specific activities
 Looks at:
o Functional performance-the task or function performed
o Strategies-how task or function is accomplished
o Examination of impairment-limitations during function or task
Elements of Conceptual Framework for Clinical Practice (In Depth)
1.) Model of practice-Guide to PT Practice
a. Examinationi. Hx
ii. Systems review
1. Neuromuscular
2. Cardio/pulm
3. Integumentary
4. Cognitive
5. Musculoskeletal
iii. Tests and Measures-Outcomes measures
iv. Evaluation
v. Diagnosis
vi. Prognosis and POC-Goals
vii. Intervention
viii. Outcomes
2.) Models of disablement/enablement-describe the impact of disease and injury on human
performance and functioning using common language and terminology.
 Clinicians must understand the path from disease process and injury to limitations in
function and alterations in societal role
o Nagi Model of Disablement
a. Pathology- Interruption in normal cellular processes and efforts of the
organism to regain normal state
b. Impairment-Loss or abnormality at the tissue, organ, and or body system
level
c. Functional limitation-Restriction in the performance of the person
d. Disability- Expression of a physical or mental limitation in social context
***See Page 5/422 in Notepack for Clinical Application***
Margaret Schenkman’s Classification of Impairments
 Direct-are a result of pathology/main cause ex: OA

Indirect-secondary conditions resulting from the primary injury or
disease ex: OA=LOROM, muscle weakness/atrophy, endurance
 Composite-have multiple underlying causes which can result from
both direct and indirect impairments
o Balance is always composite impairment
o International Classification of Functioning, Disability, and Health (ICF)Provides a biophysical view of health states from a biological, personal and
social perspective
e. Body functions and structure- Body functions are the functions of the
body systems; structures are the anatomical parts.
i. Impairments -are problems with body functions or structures
f. Activity-task or action of individual.
i. Activity limitations-difficulties performing these actions or tasks
g. Participation-involvement in a life situation
i. Participation restrictions-Problems performing life situations
***Health conditions and contextual factors (environmental and personal)
affect all three domains. The term disability is used to describe a decrement at
each level or domain.****
3.) Hypothesis-Oriented Clinical Practice-guides systematic testing about the cause of movement
problems. Hypothesis is an educated guess and is based on education, previous hx, and evaluation.
o Hypothesis generated by clinicians reflect the theories a clinician has about the
performance or functional movement and the likely cause of dysfunction
4.) Theories of Motor Control-How a therapist examines and treats a patient is based on underlying
assumptions about the cause of the movement dysfunction. Assumptions are based on best available
evidence or theories as to the cause of the movement dysfunction
o Actions-how we examine and treat patients
o Assumptions- thought processes about why or how our intervention works
o Theory-beliefs about how movement is controlled
5.) Evidence Based Practice-integrating individual clinical expertise with the best available external
clinical evidence from systemic research
Outcome Measures: standardized outcome measures
o Used to assist in the diagnosis and prognosis of patient care in addition to tracking
changes in human performance and health status
o Have reliability and validity, and responsiveness
o Ex: measurement tools, psychometric properties (based on EBP)
o Not a test and measure-ex MMT
***Look at graph on page 8/422***
Lecture #2 9/4/14
What is a Theory? Set of abstract facts, ideas and observations within a specific area of interest. They are
used to explain or predict outcomes given a specific set of circumstances. They generate hypothesis which
are tested through research.
What is a motor control theory? They explain how the brain controls and generates movement.
o Evolution or Motor control Theories
 Helped predict and explain movement dysfunction and have influenced rehab
practice and shaped the way we examine and provide interventions to our
patients with neurological injury
o Reflex theory
o Hierarchical theory
o Systems theory (HOAC)
History of NM PT and Overview of the Theories of Motor Control
o 1940-50 PT’s were treating patients with polio-muscle reeducation and consisted of isolated
muscle strengthening, bracing, ROM, and stretching exercises.
o Strokes, CP, and MS patients were ignored due to epidemic of polio
o 1955 Salk invented Polio vaccine and PT’s turned attention to other NM dysfunctions
o Reflex and Hierarchical theories were used
o Resulted in neurotherapeutic facilitation approaches developed (NDT, PNF, Brunnstrom, sensory
Integration)
o Now systems theory is used and neurotherapeutic facilitations are more task oriented
Reflex Theory (Charles Sherrington)- Proposed that sensory receptors in the skin and muscle elicited
movement
Assumptions:
o Sensation is necessary for movement
o Sensory inputs control motor outputs
o Reflexes are the building blocks of both simple and complex movements
o Complex movement is produced by combining simple reflexes (reflex chaining)
o Close loop control Feedback Mechanism-sensory FB provided during the movement
to monitor and correct motor output
Clinical Implications
o Reflexes were tested to help predict function
o Movement-presence or absence of certain reflexes
o Treatment was aimed at facilitating or inhibiting the effect of various reflexes during
motor tasks
Limitations
o The reflex is not the basic unit of behavior-spontaneous or voluntary movement
o Many coordinated movements can be performed in the absence of sensory input
o It does not explain fast movement such as typing or catching a ball accurately
o Does not explain novel movements
o Reflex chaining does not explain the fact that a single stimuli can result in variable
responses
Hierarchical Theory- Reflexes are modified to adapt to the task via central commands. Reflexes are no
longer considered the only way to produce a movement
Assumptions
o The brain controls all movement
o Organization is “top-down”
o Reflexes are controlled by higher centers and emerge when the brain is damaged.
These “released” reflexes are considered primitive and abnormal
o Reflexes are no the only way that a movement is produced
o CNS links together contractions of different muscles to produce movement
patterns (normal synergies)
o One central command is sent out to produce a normal synergy versus
several individual commands
o Normal motor development and postural control depends on the emergences
and disappearance of a progression of reflexes and CNS maturation drives
motor development
Clinical Implications
o Abnormal movements results from a lack of inhibitory control from the brain
o Reflexes were tested to help predict function and to estimate the level of neural
maturation
o Facilitate normal movement patterns with proprioceptive inputs
o Inhibit abnormal tone, movement, and primitive reflexes
o
Recovery follows a predictable sequence, thus patients should be trained through the
developmental sequence
Functional skills will automatically return if you inhibit abnormal movement
o
Limitations
o It does not explain the normal presence of primitive reflexes in neurologically
healthy adults
o Patients are passive recipients dependent on facilitation
o Inhibition of primitive reflexes does not release normal movements
o Unproven carryover to functional tasks
o Does not account for MS and biomechanical changes
Contemporary Systems Theory- integrated theory of motor control that allows for flexibility or motor
patterns that can adapt to the task and environmental constraints.
Assumptions
o Control is distributed across several neural subsystems
o Parallel processing of organized neural networks
o Feed-forward and adaptive –anticipatory mechanisms of movement exist
o Movement arises from the interaction of multiple processes including perceptual,
cognitive, and motor processes
o Goal directed behavior emerges from an interaction between the individual, the task,
and the environment
Clinical Implications
o Practice goal oriented tasks
o Teach motor problem solving
o Practice under variable environments
o Improve the efficiency of compensatory strategies
o Consideration of all systems contributing to movement
Limitations
o Minimizes “hands-on”
o Very cognitive
o Difficult to quantify efficient compensations
o Difficult to provide time consuming practice of skills
Lecture #3 9/8/14
6 Common impairments Following Neurological Injury
o Looks at functional performance and strategies used to accomplish the function
o CNS injury will produce a specific and recognizable impairment
o Look at CN during evaluation
1.) Motor impairment
a. Muscle weakness
b. Abnormalities of muscle tone
c. Coordination problems (non-equilibrium)
d. Involuntary movement
2.) Sensory Impairment (special senses)
a. Somatosensory deficits
b. Visual deficits
c. Vestibular deficits
3.) Perceptual and Cognitive Impairments
a. Perceptual Deficits
i. Agnosia
ii. Neglect
iii. apraxia
b. Cognitive deficits
i. Orientation
ii. Memory
iii. Arousal and level of consciousness
4.) Speech and Language Impairments
a. Aphasia
b. Dysarthria
c. dysphagia
5.) Composite impairments
a. Postural control/balance (equilibrium coordination)
6.) CN impairments
a. LMN lesion=impairment is same side as lesion
1.) Motor Impairment
A.)Muscle Weakness-results from the inability to generate normal levels of muscle force. Can
be mechanical (velocity, force, fiber alignment, x-sectional area, length tension) or neural input
(Firing rate)
i. UMN lesion: involves descending motor pathways (brain to anterior synapse)
and an immediate reduction in neural input on the opposite side of the body
occurs. Symptoms will include hypertonicity, increased reflexes
1. Paralysis: Complete absence of muscle strength and decrease
voluntary recruitment of muscle units
2. Plegia: same as paralysis
3. Paresis: muscle weakness
4. Hemiplegia/hemiparesis: one sided paralysis
5. Paraplegia: L.E. paralysis
6. Tetraplegia : trunk, arms, legs paralysis
ii. LMN lesion: exits SC and goes to the peripheral muscle and causes weakness
along the same side of the body.
Diseases where one would have bilateral weakness
o Parkinsons
o ALS
o Huntingtons
o TBI
o MD
***stroke, MS, and TBI would have unilateral depending on where lesion is***
Why would an individual have more UE weakness than LE weakness?
o Location of UE on the motor cortex homunculus (MCA= UE involvement)
o Outside and top is UE, in longitudinal fissure is LE (ACA=LE involvement)
Clinical Examination of Weakness
o MMT-not optimal
o Dynamometer
o Isokinetic Dynamometer
Abnormal Synergy Pattern- when joint movement cannot be isolated due to an inability
to activate or coordinate muscle contractions. Because the muscles within the mass pattern
are so strongly connected, movement outside the fixed pattern cannot occur. The individual
will move their limb in the same way regardless of the task. i.e stroke patients
B.) Abnormal muscle tone-the resistance felt in the muscle during passive elongation
a. Assessed during slow elongation then quickly
b. Hypotonia-low tone (associated with LMN)
c. Flaccidity-complete lack of resistance (associated with LMN)
*** can occur immediately after UMN lesion involving descending motor tracts
of cerebellum. May be temporary or permanent***
d. Spasticity: Occurs when there is damage to the descending motor systems.
i. Velocity dependent-the faster you passively stretch the muscle, the more
resistance you will feel. Resistance is due: to hyperexcitability of the
stretch reflex leading to an increase in the alpha motor neuron activity of the
same muscle (agonist)
ii. Peaks 1-3 months after UMN lesion and leads to changes in the viscoelastic
properties of the muscle and tendon.
iii. Muscle stiffness component of hypertonia is not velocity dependent
(example of indirect impairment)
e. Rigidity: not velocity dependent
i. May affect both agonist and antagonist muscles
ii. Associated with lesions at Basal ganglia (i.e. Parkinson, Huntingtons)
iii. Poorly understood etiology
C. )Coordination problems- UMN lesions lead to awkward, jerky, inaccurate, slowed, delayed,
and prolonged movement
o Motor cortex, BG, Cerebellum, and dorsal columns contribute to coordination
o Timing
o Delayed reaction time
o Slowed movement execution time
o Problems terminating a movement
o Intra and interlimb coordinationo what happens to the involved limb during movement of that limb
o what happens to contralateral limb during movement of involved limb.
o Accuracy- over and undershooting targets during reaching and pointing
o Scaling force and amplitude-over and undershooting movement force and range of
movement
Clinical Examination of Coordination: cerebellar strokes-decrease movement patterns
D.)Involuntary movements
f. Dystonia: rapid excessive twisting and bizarre repetitive movements caused by axial
and proximal limb muscles; associated with BG lesions
g. Chorea: rapid and jerky limb movements; associated with BG lesions
h. Athetosis: slow twisting snake like movements; associated with CP
i. Tremor: rhythmical oscillating movement of a body part.
i. Resting tremor:occurs when muscles of the involved body part are at rest
and supported against gravity (BG lesions)
1. Will go away with movement
ii. Action tremor: occurs when muscles of involved body part are contracted.
Will go away at rest.
1. Postural tremor: holding body part in a posture against gravity
2. Intention tremor- occurs during voluntary movements such as
reaching a target (cerebellar lesions)
Clinical examination of involuntary Movement
 What makes it worse/better
 Trial and error
 Fxn and ADLS
 Neurologist consultation/referral
2.) Sensory Impairments- type of sensory impairment and the location of the deficit will depend on the
lesion location.
 Lesions to peripheral nerves cause sensory impairment that follows the distribution of the nerve
and dermatome
 Lesions in the brain are often more complex and cause more diffuse impairment contralateral to
the lesion (sensory homunculus)
a. Somatosensory deficits
i. Spinothalamic system (protective sensations)
1. Pain
2. Temperature
3. Crude touch and pressure
ii. DCML (Discriminative Sensations)
1.) Vibration
2.) Proprioception
3.) Discriminative light touch
4.) Combined cortical sensations: barognosis, sterorognosis, graphesthesia, tactile
locations, texture recognition, 2 point discrimination (Pull upon both systems)
b. Visual Deficits- outside of out area of expertise but necessary to understand and recognize
impairments due to balance and location of lesion in the brain
i. Blurred Vision
ii. Diplopia-double vision
iii. Strabismus-lazy eye
iv. Nystagmus-rapid rhythmic involuntary movement-can be normal or pathological
v. Homonymous Hemanopsia- partial blindness, loss of visual field of both eyes on same
side ex: right sided stroke loses left visual field in both eyes
vi. Occipital blindness-cant perceive images
Clinical Examination of Visual Deficits: CN II, III, IV, VI
c.
Vestibular deficits (CN VIII)- semi-circular canals of the vestibular system provide important
afferent information to the brain. Damage to the vestibular structures that lye within the CNS can
lead to problems with gaze stabilization, posture, and balance control.
3.) Perceptual and Cognitive Impairments
 Perceptual Deficits- processing of sensation into meaningful information about the body and
surrounding environment. Intact sensation is necessary for perception
o Agnosia- R sided damage common-cant process incoming information
o Unilateral neglet (body scheme agnosia)-R sided damage common-lack of perception
of L side in environment
o Apraxia: WNL sensory and motor, but can’t execute normal tasks
Clinical Examination of Perception: rely on OT and Neuropsychologist. PT’s are limited
Finishing of Lecture #3 9/11/14
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Cognitive Deficits-ability to sort, retrieve, and manipulative information (learning), slower
prognosis
Orientation-an understanding of person place and time. Orientation to person is usually the last
thing to be lost and orientation to time is usually the first thing to be lost in a brain injury.
Clinical Examination of orientation: Its happening during HX
Memory- ability to store and retrieve information and past experiences
o Complex and involves many areas of the brain
o Lesions: memory impairments are common and can interfere with learning
o Severe memory problems will be hard to rehab because they wont be able to remember
anything
o Short term memory: within minutes or hours. Ex what did you have for bfast
o Immediate recall: within seconds
o Long term memory: years ago something that is ingrained in their head ex:bday
Arousal and level of consciousness-allows an individual to respond to stimuli in the
environment. Level of alertness
o Normal----lethargy---Obtunded---Stupor----Coma
Clinical Examination of Arousal and Level of Consciousness- Glascow Coma Scale
***PT’s form more of a screen and rely heavily on other specialists to help with these impairments
following neurological injury***
#4 Speech and Language Impairments

Aphasia-language disorder associated with left sided brain lesions. It does not affect
muscles that control speech
o Expressive aphasia: (Broca’s aphasia)-has word finding issues and can’t get it
out (close to motor cortex where muscles for speech are located)
o Receptive aphasia: (Wernicke’s aphasia)-can’t comprehend auditory stimulus
due to impairment
o Global aphasia: have both
 Dysarthria- Speech disorder “slurred speech” that may occur after UMN lesion when
there is damage to the motor speech system (right or left sided lesions)
o Weakness and lack of coordination of the speech and respiratory muscles will
lead to articulation, pitch and volume problems
o Common in CP, TBI, stroke, MS, Parkinson’s, ALS
 Dysphagia- impaired swallowing ability
o occurs in 30-40% of individuals with stroke (NEED SLP!)
o life threatening because they can choke, it can go to lungs and cause pneumonia
(need patient positioning)
#5 Composite impairments – more than one impairment from more than one system (indirect or direct)
 Postural control/balance- ability to maintain ones center of mass within the base of
support when your body is at rest or in motion
 Reactive postural control-feedback system during and after LOB
 Anticipatory Postural control-feedforward system ex: walking downstairs and
brain knows how far to go down
 Maintaining balance requires complex interaction of:
1.) Sensory system (somatosensation, vestibular, and visual input)
2.) CNS (integration of information)
3.) Motor system (executes the postural adjustments)
#6 CN Impairments – 12 CN that exit the brain in the pons and the medulla of the BS. Damage to CN and
their nuclei are considered and LMN lesion and will result in ipsilateral to the lesion
CN1- Olfactory
CN2-Optic
CN3-oculomotor
CN4-Trochlear
CN5- Trigeminal
CN6-Abducens
CN7-Facial
CN8- Vestibulocochlear
CN9-glossopharyngeal
CN10-vagus
CN11- spinal accessory
CN12- hypoglossal
Indirect or Secondary Impairments and Pathology (comorbidities)
Atrophy
Jt contractures
Ulcers
Fractures
Lecture #4-Introduction of Common Upper Motor Neuron Disorders
I. Stroke (Cerebral Vascular Accident)
 Epidemiology
o 4th leading cause of death in the US
o leading cause of long term disability in the US and is the largest diagnostic group
admitted to in-patient rehabilitation
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o there are 795,000 new strokes per year in the US (185,000 recurrent)
o the incidence of stroke is expected to rise related to the aging population
o there are 5.5 million individuals in the US living with the effects of stroke
o women account for 40% new strokes each year but 62% of all deaths
Etiology- two types
1. Ischemic Stroke (occlusive)- 80% of all strokes and higher survival rate
a. Cerebral Thrombus- formation of blood clot (usually due to atherosclerosis)
within the cerebral arteries that blocks distal blood flow to the brain causing cell
death and injury due to lack of O2 and Glucose.
b. Embolism- “traveling blood clot” that forms elsewhere (usually heart) and
eventually gets lodged in a vessel and blocks distal bloof flow to the brain
causing cell death and injury due to a lack of O2 and glucose
i. related to Heart disease
c. atherosclerosis-hardening of the BV wall accompanied by plaque deposits.
Plaques consist of fatty substances, calcium, cellular waste, and cholesterol
i. plaque builds up and then ruptures
ii. the body attempts to repair the rupture via platelet adhesion and blood
clot formation and this clot can block blood flow causing an ischemic
stroke or embolism
2. Hemorrhagic Stroke (abnormal bleeding)- accounts for 20% of all strokes and is
ssociate with higher mortality and ischemic stroke. IT is due to bleeding due to a
ruptured BV, most often due to an aneurysm or trauma. Blood leaks into or around the
brain and loose blood is an irritant to the nervous tissue and leads to neural death. There
is also ischmia distal to the ruptured vessel causing further injury
a. Intracerebral hemorrhage- bleeding that occurs from smaller ruptured arteries
that penetrate the brain (the most deadly and limiting)
b. Subarachnoid hemorrhage-bleeding that occurs from a larger BV that travels
in the subarachnoid space
i. due to a berry aneurysm (congenital)
Pathophysiology
o Complete occlusion of blood flow leads to a core area of neuronal cell death
o Around the core is the ischemic prenumbra-the neurons are lethargic but remain viable
o Cascade of events:
 Ischemia causes neurons to release excessive glutamate
 Altered ca ion channels causes an influx of Ca into the neurons
 High levels of intracellular CA activates a series of destructive Ca sensitive
sensitive enzymes
 Activation of these destructive enzymes causes further neuronal cell death and
damage into the prenumbra area
 Damage neurons stimulate brain edema which begins minutes of stroke onset,
peaks around 3-4 days and disappears within 3 weeks (secondary brain damage)
Risk Factors
o TIA- temporary interruption of BF, which last a few minutes to a few hours but no more
than 24 hours. Causes no permanent neurological dysfunction
o Modifiable
 Hypertension, smoking, DM, CAD, PAD, Atrial fib, Hypercholesterolemia,
obesity, inactivity, diet
 unhealthy triad=hypertension, DM, hypercholesterolemia
o Non-modifiable
 Age, gender, family history, race, previous stroke
Medical management
o Diagnosis- CT, MRI
o Pharmacological Neuroprotectives-glutamate antagonists, Ca antagonists
 To minimize ischemic prenumbra

Thrombolytics- tissue Plasminogen-Activase (t-PA)-optimal 3 hour window
from onset of symptoms
 Cannot be used for hemorrhagic stroke
o Surgical- clot evacuation and remove blood
o Preventative Medical management of stroke
 Pharmacological-anti-coagulants
 Surgical- carotid endarterectomy, balloon angioplasty with stent placement,
surgical aneurysm clipping
 Vascular Stroke Syndromes
o Anterior Cerebral Artery- supplies the medial aspect of the frontal and parietal lobes
and the anterior limb of the internal capsule, caudate nucleus, putamen, corpus callosum
 Problems: contralateral hemiparesis/plegia and sensory loss with mostly LE
involvement, mental confusion
o Middle Cerebral Artery- supplies the lateral aspect of the frontal, temporal, parietal,
and occipital lobes, the head of the caudate nucleus, putamen, external capsule,
claustrum, and anterior internal capsule.
 Problems: contralateral hemiparesis/plegia and sensory loss with mostly UE
involvement, homonymous hemianopsia, or other visual and spatial perceptual
deficits, possible coma, aphasia (if dominant side)
 Most common
o Posterior Cerebral Artery-supplies the medial aspect of the occipital lobe and medial
and inferior aspect of the temporal lobe, corpus callosum, posterior diencephalon,
thalamus, midbrain
 Problems: homonymous hemianopsia, or other visual deficits
o Vertebrobasilar Artery- supplies the medulla, pons, midbrain, cerebellum, and
laybrinths
 Problems: cell death, ipsilesional atazia, coordination impairments, coma,
diplopia, tetraplegia, and bulbar paralysis
 Locked in syndrome-occurs with basilar artery occlusion and bilateral
infarction of the ventral pons
 Characteristics of Left and Right sided brain damage post stroke
o Right sided brain damage/Left sided hemiplegia
 Unilateral left sided neglect (perceptual impairment)
 Agnosia (perceptual impairment)
 Quick and impulsive behavior
 Poor judgement
 Unaware of deficits
 Emotional lability
o Left sided brain damage/ Right sided hemiplegia
 Aphasia
 Apraxia
 Slow, cautious and hesitant behavior
 Aware of deficits
 Depressed and negative attitude
II. Multiple Sclerosis
 Epidemiology
o 400,000 individuals living with the effects of MS in the US
o 10,500 new cases diagnosed per year in the US
o 2-3x more common in women than men
o symptoms occur between 15-50
o more common in caucasions
o 40 degree latitude (away from equator)
 Etiology-chronic demyelinating disease of CNS (affects brain and SC)
o Autoimmune-theorized that a viral infection triggers the immune response or genetic
predisposition
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Pathophysiology- a viral infection stimulates an immune response (Tcells, B cells, and
macrophages which mistakenly attacks the bodies myelin-producing cells of the CNS
o Demyelination slows nerve conduction and causes nerves to fatigue quickly
o When demyelination is severe, conduction is blocked
o Inflammatory response occurs which further impairs nerve conduction
o Inflammation subsides and the surviving oligodendrocytes re-myelinate the nerves
restoring nerve conduction (remission)
o The disease with progress and relapse causing the oligodendrocytes to be wiped out and
demyelinated areas are replaces with fibrous astrocytes (supporting cells) called CNS
plaques which are permanent
o Generally attack the white matter tracts in the brain-optic pathway, corticospinal tracts,
DC of the SC and cerebellar peduncles
o 4 main clinical subgroups
1. relapsing-remitting MS- relapses are followed by remission with either
full or partial recovery. There is no disease of progression during remission
2. Secondary-Progressive MS- initial relapsing-remitting course followed by
progression and irreversible decline
3. Primary-Progressive MS- disease progression and steady functional
decline from onset; associate with later onset
4. Progressive-Relapsing MS- steady deterioration in disease from onset, but
with occasional acute attacks
 Medical management
o Diagnosis for relapse-remitting- two or more attacks lasting greater than 24 hours and
separate by more than a month
o Diagnosis for progressive- when there is impairment lasting greater than 6 months
o Lumbar puncture- CSF will reveal elevated levels of myeling proteins
o MRI and CT- reveal acute lesions and chronic plaque formations
o Pharmocological-immunosuppressant/anti-inflammatory drugs, corticosteroids,
methotrexate
o Long term use of immunomodulating drugs (reduces frequency of attacks): interferons
III. Parkinson’s Disease
 Epidemiology
o Affects more than 2% of the population over 65 y.o with dramatic increase in incidence
with age
o 10 new cases per 100,000 under 50 and 300 new cases per 100,000 ages 80-99 years
o the incidence of PD is expected to rise related to the aging population
o mean age of onset is 50-60 years of age
o 10% of all cases develop before the age of 40 years (young-onset PD)
 Etiology
o Chronic progressive neurodegenerative disease which is idiopathic in 80% of the cases.
o Disruption of the dopamine systems of the BG lead to the physical impairments
o Environmental toxins, genetic factors, and acceleration of the normal aging process have
all be theorized to cause PD
o Secondary parkinsonism is in 20% of cases and may be due to infection, head trauma,
and drugs (heroin and cocaine)
 Pathophysiology
o BG creates a complete motor circuit by receiving input from the cortex and
communicating back to the cortex via the thalamus
o Important for initiation, planning, production, and control of voluntary movement and
postural adjustments
o Through direct and indirect pathways within the BG, information is integrated and
modulated to either facilitate or inhibit movement
o PD causes a slow degenerationg of the dopamine producing neurons in the substantia
nigra which has neuronal connections with the striatum
o Destruction of this pathway leads to a reduction in the amount of dopamine reaching the
striatum.
o
o
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A loss if dopamine causes overactivity of indirect pathways which inhibits movement
Excessive motor inhibition is manifested clinically as akinesia, bradykinesia, and
postural instability
o Excessive activity of facilitory pathways is anifested as tremor and rigidity
o symptoms do not surface until 30-60% of dopamine producing neurons in SN are
destroyed
o degeneration of the melanin-containing SN neurons produces depigmentation of SN
o as disease progresses, striatal dopamine receptors become damaged and result in
reduction of active binding sites for dopamine causing a worsening impairments and
insensitivity to pharmacological dopamine
Clinical manifestations- 4 cardinal features
1. Tremor
a. Active-only during task
b. Resting- most common and unilateral
2. Rigidity- increase resistance to passive elongation not velocity dependent
a. Leadpipe rigidity
b. Cogwheel rigidity
c. Masked face-no facial expression
3. Bradykinesia- decreased movement
a. Akinesia- no initiate movement, freeze during changes in movement pattern,
and underscale movement
4. Postural instability- inability to activate postural responses which lead to increase in
falls-NEED EDUCATION!!!
a. Retropulsion or pull test-LOB of pt upon the PT pushing or pull them
 Autonomic dysfunction-problems with bowels and bladder function (constipation,
urinary urgency and incontinence, impotence)
 Cognitive impairment-dementia 20-40%
 CV impairment-orthostatic hypotension
 Muscle weakness – direct impairment due to insufficient neural activation
o Extensor muscles appear to be mire affected than flexor muscles which in
addition to rigidity contribute to the well-known “stooped” posture
 Indirect Impairements associated with PD
o Postural deformities-stooped/kyphotic posture-sets them up for uncontrolled
increase in speed
o Musculoskeletal changes-contractures
o Gait disturbances-decrease foot clearance, decrease arm swing, decrease trunk
rotation, decrease stride length
 festinating gait-picking up of speed, turning “on” block
o Dysphagia and drooling
o Dysarthria
o CV impairment
Individuals with idiopathic PD fall into 2 clinical subgroups
1.) postural instability gait disturbed (55%)
a. postural instability and gait disturbances
b. bradykinesia common
c. more debilitating
d. rapid progression
e. impaired cognition common
f. older pt
2.) tremor predominant (45%)
a. less likely to have bradykinesia or postural instability
b. less debilitation
c. slower progression
d. earlier onset

Disease progression - five stages I-V
o Has 40% mortality rate 15 years post diagnosis
o I-unilateral symptoms present
o II-bilateral symptoms or axial involvement present but no postural instability
o III-postural instability present but individual remains physically independent
o IV- all symptoms present and severe, individual needs assistance to walk or stand
o V-individual is wheelchair or bed bound
 Medical Management
a. Diagnosis-2 out of fourcardinal features are present and asymmetrically distributed
i. lab work and scans are normal and r/o other Differential diagnoses
ii. confirmed with a positive response to the medication levodopa
b. Pharmocological management
i. Levodopa-given with carbidopa to inhibit its systemic metabolism. Dopamine
replacement therapy is the most common medication
ii. Sinemet- reduces bradykinesia and rigidity with little effect on tremor and
postural instability
1. End-dose deterioration-a sudden worsening of symptoms when the
medication begins to wear off
2. it loses effectiveness after 5-7 years and fluctuations in motor
performance occurs in 50% of patients as early as 2 years into tx (onoff phenomenon)
3. side effectiveness-nausea, vomiting, orthostatic hypotension sleep
disturbances, involuntary movements (chorea)
IV. Traumatic Brain Injury
 Epidemiology
o 1.7 million individuals sustain TBI each year
o leading causes: falls 28%, MVA 20%, struck by object 19%, Assaults 11%
o causes vary by age: between 5-65 MVA, under 5 and over 65 due to falls
o children 0-4 and adolescents 15-19 years of age are at the highest risk for TBI
o males are about 1.5 times more likely to have a TBI
 Etiology
o Open head injury-skull is fractured
 Compound skull fracture-when scalp is cut and is associated with dural tears
which can increase risk of infection
o Closed head injury- skull remains intact
 Pathophysiology
o Primary brain damage
 Focal brain injuries- occurs at opposite side of impact. Damage may take the
form of a contusion or laceration or both. Lacerations are associated with
hematomas
 Coup-contrcoup-if the blow to the head is hard enough the brain will bounce
and make contact with the skull at a site opposite the local brain damage. Coupfocal injury and contrecoup refers to the injury on the opposite side of the brain
 Polar brain injury- occurs in response to acceleration-decelleration and
rotational forces. The moving body and head suddenly stop with impact but the
brain continues to accelerate until it slams into the skull
 Common in frontal and temporal lobes
 Diffuse axonal injury- occurs in response to acceleration-deceleration and
rotational forces and can occur in conjuction with focal and polar brain injuries.
 Rapid movement of the brain within the skull causes widespread
stretching and tearing of the neuronal axons within their myelin sheaths
 If the injury is severe, damage will extend into the brainstem and lead
to coma and abnormal posturing
 Damage is not evident on CT scan


Blast injury- can cause primary and secondary injuries b/c the blast itself causes
transient shock wave causes the brain damage and injury.
 Primary injuries relate to blast overpressure within the brain and of
brain tissue and secondary injuries relate to shrapnel and other objects
that end up embedded in the individual
o Secondary brain damage
 Intracranial hematomas- a rise in intracranial pressure occurs as blood
accumulates and causes shifting and compression of brain structures
 Epidural hematoma-blood accumulates on top of dura (medial
meningeal artery)
 Subdural hematoma- venous blood accumulates beneath the dura
o common in the elderly related to brain shrinkage and
excessive brain movement
 Intracerebral hematomas-intrinsic cerebral arterial blood accumulates
within the brain (most deadly)
 Herniation- if ICP continues to rise, a herniation of brain tissue may occur
 Uncal herniation Central hematoma Tonsillar herniation Hypoxic-ischemia injury- due to a lack of Oxygenate blood to the brain
 Can also occur due to Increased ICP and Cerebral Vasospasm
 Arterial hypoxemia-a systemic injury such as an obstruction of
airway, pneumothorax, pulmonary embolus which leads to a reduction
in the amount of O2 in the blood.
o common in TBI and they deprive the brain of needed O2
(leads to secondary damage that is widespread)
 Arterial hypotension-Systemic blood loss due to bodily injuries may
lead to low BP and brain doesn’t receive enough blood flow and
widespread secondary brain ischemia occurs
 Post-traumatic epilepsy/seizures-occurs immediately after TBI or 1-2 years
later
 Individuals should avoid bright lights and spinning or inversion
activities
 Intra-cranial infections- common with skull fx and ICP catheters
Medical Management
o Restore vital functions and prevent secondary brain damage
o Glascow Coma Scale
o ICP is monitored via a catheter into the brain (normal is 4-15mmHG)
 If goes above 20mmHg notify the nurses or Dr.
 If goes above 30mmHg immediately STOP all therapeutic interventions and
notify someone (40mmHg will impair BF)
 Never invert an individual with elevated ICP
Lecture #5 9/15/14-Disorders of Strength movement synergies, Tone, and Coordination
1.) Strength- have both primary and secondary weakness. Primary is contralateral the lesion and
secondary is from reduced activity levels.
Direct or primary Muscle weakness- an UMN lesion to the motor cortex or corticospinal tracts will
alter neural input to the motor neuron pool contralateral to the lesion. Can lead to:
1.) Reduced motor unit recruitment
2.) Impaired motor unit firing rates and rate coding
3.) Slower contraction and relaxation times
4.) Abnormal co-contraction of agonists and antagonists
Indirect or Secondary Muscle Weakness

Disuse atrophy-Selective atrophy of Type II fibers because they have a larger x-sectional
area
o patient cant move as fast or develop force for tasks
 Viscoelastic Changes- increased muscle stiffness and fiber shortening
Clinical examination of strength (muscle weakness)
 Functional testing- documentation of a person;s ability to perform a functional task such
as bridging, sit-to stand, squatting, transferring, grip strength. Seen mainly during
observation
 Manual muscle testing-most appropriate when patient can isolate movement
 Examination of movement strategies- when isolated movement is not possible,
examination of the individuals’ movement strategies during AROM reveals info
regarding their ability to generate muscle force. A complete description of the movement
strategy against gravity and with gravity eliminated is necessary to describe the
individuals’ active motor control
Abnormal Synergy Patterns-muscles within an abnormal massed pattern that are strongly connected and
cannot be adapted to meet the demands of a changing task or environment.
 Neurologically impaired have only one or two synergies to choose from a
flexion and extension synergy on the affected limb
Brunnstrom abnormal synergy patterns- first person to describe abnormal flexion and extension
patterns for UMN lesions
Flexion Synergy
Extension synergy
Scapular: retraction/elevated
Scapular: Protraction
UE
Shoulder: abd, ER
Shoulder: add, IR
Elbow: extension
Elbow: Flexed
Forearm: supinated
Forearm:Pronation
Wrist: flexed
Wrist: ext (variable)
Fingers:flex
Fingers:flex
Hip: flex. Abd, ER
Hip: Ext, ADD, IR
LE
Knee: flex
Knee: Ext
Ankle: DF, inversion
Ankle: PF, Inversion
Toe: DF
Toe: PF


What joint action is missing from the UE? LE?
o UE: Finger extension
o LE: Foot eversion
Would you expect to see abnormal synergy patterns in an individual with PR? No b/c they
don't have a problem with the corticospinal tract
Associated Reactions-involuntary movement of the involved limb resulting from resisted voluntary
movement of another limb or from reflex stimulation (cough, sneeze, cough)
Testing associated Reactions (uninvolved):
Resist
Expected abnormal synergy Response
Flexion at a joint of the uninvolved UE
Flexion synergy of the involved UE
Extension at a joint of the uninvolved UE
Extension synergy of the involved UE
Flexion at a joint of the uninvolved LE
Extension synergy of the involved LE
Extension at a joint of the uninvolved LE
Flexion synergy of the involved UE
Testing associated Reactions (involved)
Resist
Flexion at a joint of the involved UE
Extension at a joint of the involved LE
Expected abnormal synergy Response
Flexion synergy of the involved LE
Extension synergy of the involved UE
 Raimiste’s Phenomena:
Sequential Motor Recovery Stages Following Stroke Stages of Recovery-as patient
recovers there will be more movements out of synergy that emerge

Stage 1 –Flaccidity; no voluntary or facilitated movement of the limbs (no
associated reactions or reflexes)
 Stage 2- Spasticity begins; involuntary associated reactions and reflexes present
by no voluntary movement occurs
 Stage 3- Spasticity worsens; voluntary movement occurs in synergy
 Stage 4- Spasticity declines;some voluntary movement out of synergy may
occur (some isolated movement possible)
 Stage 5- Spasticity continues to decline; Relative independence form synergistic
movement (mostly isolated movement)
 Stage 6- Spasticity disappears; all isolated joint movements present,
coordination/speed near normal
***Clinical Notes Regarding Brunnstrom Staging***
 Not all individuals with UMN lesions have spasticity
 Recovery can start and stop at any stage depending on the severity of the lesion
 Individuals recover at different rates
 With the same individual, the UE can recover at a different rate than the LE
2.) Tone- the resistance felt in the muscle during passive elongation
 determined by both non-neural and neural factors
 abnormalities of muscle tone occur when there is damage to the descending
motor systems
 Hypotonia-decrease in the resistance or stiffness to passive elongation when compared to the
normal range. Will be felt in both slow and fast passive elongation
o Flaccidity- associated with LMN lesion and limb will feel heavy and limp
 No resistance to passive elongation
 No voluntary movement possible
 No reflex activity
 Hypertonia-incrase in resistance to passive elongation and will feel it during slow and fast
passive elongation
o Muscle Stiffness-not velocity dependent, thus with increasing speed of passive
movement, the resistance felt does not change from that which was felt during slow
passive elongation
 Stiffer towards end range of motion
o Spasticity-resistance felt during fast passive elongation (velocity dependent)
 Pathophysiology of Spasticity-stretch reflex is mediated by the Ia sensory
afferents of the muscle spindle (Ia afferents are sensitive to both fiber length
changes and velocity)
 when a muscle is elongated rapidly the Ia fibers fires and makes
excitatory connection with the alpha motor neuron of the same muscle
cauding it to contract
 inhibitory interneurons cause relaxation of antagonist
 it is normally controlled by descending pathways from the brain but
after a UMN lesion there is a loss of descending input and this a loss of
inhibition of the stretch reflex resulting in hyperactivitiy of the stretch
reflex or spasticity.
o Decorticate-extreme form of hypertonia from damage to the corticospinal tracts as they
descend through the brainstem. UE flexion LE extension
o Decerebrate Posturing- extreme form of hypertonia from damage to the corticospinal
tracts as they descend through the brainstem. UE Extension, LE extension
o Rigidity-felt during slow and passive elongation but not velocity dependent and affects
both the agonist and antagonist.
 due to BG involvement and uniform throughout ROM
 Leadpipe: uniform resistance throughout entire range
 Cogwheel: catching
***SEE CLINICAL EXAMINATION OF TONE IN LAB NOTES PG 56***
3.) Coordination-ability to perform movements with appropriate timing, distance, efficiency, and
muscular tension. Involves the ability to initiate control and terminate movement effectively
2 Main Types:
 Equilibrium Coordination- ability to maintain posture and balance both static and dynamic
in an upright position.
 Non-equilibrium Coordination- ability to perform smooth, accurate and efficient single
limb and interlimb movements. Also includes the ability to hold a static limb position
o Impaired coordination-inability to integrate sensory, motor, and neural processes
which leads to awkward movement
o Related to lesions at the cerebellum, BG, and dorsal columns
Cerebellum-receives sensory information form the vestibular, auditory, and visual systems, as
well as muscle spindles GTO, jt, skin receptors and detects errors and corrects movement
 Same sided lesions
 Inhibitory in nature
 UMN control
 Doesn't control corticospinal tract
 Dysmetria- inability to judge distance and RO movement (nose to finger)
 Dysdiadochokinesia- inability to form rapid alternating movements
 Tremor-active
 Movement Decomposition- dis synergic movement
 Rebound Phenomenon-loss of check reflexes when resistance is applied
Basal Ganglia- influence on movement is indirect and receives infor from the cortex and returns it
via the thalamus.
 Involved in planning, initiating, and executing movement and maintaining
muscle tone, automatic movements, and postural control. Does not receive
peripheral sensory input
 Akinesia-can’t initiate movement
 Bradykinesia-slow movement
 Rigidity- increase resistance to agonist/antagonist
 Tremor-resting/ pill rolling
 Involuntary Movements-chorea, athetosis
Dorsal Columns-proprioception from the periphery to the brain and cerebellum
 Dysmetria
 Slowness of movement related to visual compensation
**Note: Ataxic gait is also associated with DC lesions and would fall under equilibrium
coordination***
Clinical Examination of Coordination (non-equilibrium)
Lecture #6 9/22/14
 Task oriented approach to examination looks at function performance and strategies used to
accomplice the function.
 Based on findings and clinical knowledge, you will begin to hypothesize about the impairments
that care limiting the function
 Why is it essential for PT to understand and recognize cognitive, visual, and perceptual
disorders as well as speech and language disorders? To evaluate and integrate, make
appropriate referrals, see how they affect function (gait, ADL’s, balance), which is what WE do.
 Cognitive and perceptual abilities are linked to one’s ability to learn motor skills. The
rehabilitation process requires the re-learning of motor skills. Patient with these impairments will
be limited in functional tasks
I. Mental Status and Cognitive Impairments
 Conciousness and arousal indicate the degree to which an individual can respond to specific
stimuli
 Cognition is the ability to sort, retrieve, and manipulate info

Higher order cognitive includes capacity to plan, manipulate info, recognize errors and
problem solve
1.) Arousal and level of consciousness
 allows individual to respond to stimuli in the environment (level of alertness)
 Ranges from:
 Normal
 Lethargy: drowsy, slow motor response that is generalized
 Obtunded: difficult to arouse
 Stupor: semi-conscious state
 Coma: no response
2.) Orientation-understanding person, place, time, and situation.
 Orientation to person is the last thing to be lost and orientation to time is the first thing to
be lost
3.) Attention-ability to select and attend to specific stimuli while ignoring or suppressing other stim
a. Sustained attention: reading a page in a book
b. Selective attention: trying to do a task in a busy environment
c. Alternating attention: alternating attention onto different tasks (FB and studying)
d. Divided attention: multiple stimuli are happening
 To help attention impairments: dim lights, take away stimulus
4.) Memory-the ability to store and retrieve information for recall at a later time
 Common following TBI and interfere with learning
 Immediate recall- few seconds (three words)
 Short-term memory- minutes to hours (what did you have for bfast?)
 Long term memory- remote (presidents)
 How would you screen for memory impairments? During Hx
5.) Executive functions-enable person to be independent in initiating, maintaining, and effective in
self monitoring of activities for achieving self-identified goals.
 will work with a team of health professionals in determining if a patient will be
able to return home safely and independently Include:
 Volition- the capacity to determine what one needs and wants to do
 Planning- including weighing alternative and decision making
 Purposive action- productivity and self-regulation
 Effective performance- quality control and self correction of behaviors
II. Visual Deficits
 Common visual impairments
o Homonymus Hemianopsia( lesions 5-7): visual field deficit associated with CVA
that reduces part or all of the contra-lesional visual field.
 Commonly seen in right hemispheric stroke and often correlated with visual
neglect
 Named after the visual field that is lost
 Treatment is by scanning training to facilitate compensation
o Diplopia-double vision, can be result of a decrease in oculomotor control or ROM. (
common in MS or CVA)
o Strabismus-lazy eye that lead to depth perception
o Nystagmus- involuntary, cyclic movement of the eye common in vestibular
disorders
o Clinical examination of visual deficits-visual acuity, depth perception, visual
fields, oculomotor control
 Eye movement
 Visual fixation- maintaining focus on an object when it is brought near or moved further
away
 Ocular pursuits-smooth pursuits
 Sacaades- sequenced rapid eye movements. Eyes move rapidly to localize on specific
stimuli, such as during reading

Vestibular ocular-reflex-connects vestibular afferents sending information regarding
head movement and velocity to the extra-ocular muscles of the eye thus allowing visual
focus to remain on objects even when the head is moving or turning rapidly
III. Perceptual Deficits- perception is the processing of sensation into meaningful information about
the body and the surrounding environment
 Body scheme/Body image disorders
o Body image- is a visual and mental image of ones body including feelings in relation
to health and disease
o Body scheme- is the awareness of the spatial relations among the parts of the body
and the relationship of the body to the environment
o Unilateral neglect-failure to report, respond, or orient to stimuli on the contralateral
side of brain lesion.
 Persons will ignore one half of the body (body neglect) or hemisphere
(spatial neglect) and they may ignore auditory visual, or tactile stimuli on
the contralesional side even through sensory ability is intact.
 Attentional bias towards the ipsilateral side
 Common in right damage b/c responsible for attention to right and left sides
 Also be due to focusing on the ipsilateral lesion
o Phenomenon of extinction (less severe): can attend to stimuli when it is isolated to
one side but when simultaneous stimuli is presented the person with neglect will only
reposnd to stimuli on the ipsilesional side (extinguishing the contralesional stimuli)
o Clinical examination to assess for unilateral neglect- line bisections, drawing
tasks, behavioral inattention test
o Anosognosia: severe form a neglect and safety is a concern
o R-L discrimination-inability to identify the right and left sides of ones own body or
that of another. Disorder of spatial orientation. A selective incapacity to distinguish
between the right and left symmetrical parts of the body (parietal lobe dysfunction)
 Examination: asking patient to point to right or left body parts
 Spatial Relations Disorders- have difficulties in perceiving relationships btwn the self and 2
or more objects (make sure to rule out vision!!!)
o Figure-ground discrimination-inability to visually distinguish an object from the
background from which it is embedded. Consider trying to locate objects on a busy
surface (bed spread with busy patterned fabric)
 Ayres Figure Ground Test- standardized assessment that asks a patient to
identify objects embedded in a picture
o Spatial relations deficit- inability to perceive the relationship of one object in
relation to another object or to oneself (i.e. setting the table)
 Agnosias-inability to recognize or understand incoming information despite intact sensory
ability (vision, audition, touch, taste, recognition to familiar objects such as color, cound,
faces)
o Visual agnosia
 Visual object agnosia-failure to recognize visually presented objects
despite normal vision
 Simultagnosia- inability to perceive more than one thing at a time in order
to perceive a stimulus as a whole. Patient precieves one part at a time
 Prosopagnosia- cant recognize person
o Auditory agnosia-cant recognize non speech sounds
o Tactile agnosia (astereognosis)- cant recognize object by touching it
 Apraxia- impairment in the performance of a purposeful movement not a result of a motor,
sensory, or intellectual deficit
o Occurs with aphasia due to lesion in dominant hemisphere and difficult to
distinguish
o Ideomotor apraxia-understand what to do but cant do it.
o Ideational apraxia-lost the idea of what to do and will use the object incorrectly
IV. Speech and Language Impairments




Aphasia-comminucation or language disorder (left sided brain lesions)
o can be fluent (speech output is produced at a normal rate with preserved flow and
melody) and non fluent (speech is hesitant, awkward, and interrupted and produced
with effort)
o does not affect the muscles controlling speech
o Expressive aphasia
o Receptive aphasia
o Global aphasia-both
Dysarthria-speech (not language disorder) “slurred speech”
o occurs with UMN lesion when there is damage to the motor system controlling the
muscles and movements associate with speech production (right or left sided)
Dysphagia- impaired swallowing (30-40% of individuals with stroke and PD, MS, CP)
o Needs SLP
Clinical Examination of speech and language- work with SLP
o We can address posture to prevent pneumonia