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Statistics of SCI
12,000 new cases a year
Ages 16-30 years old with the average age of 43
81% male
Life expectancy is less
causes of TBI
MVA 37%
Falls 29%
Acts of violence 14%
Sports related 9%
Etiology of SCI
31 pairs of spinal nerves
More susceptible due to greatest amount of rotation in these areas:
C1,2,5,6,7
T12
L1,2
Naming levels
Named with the area of the spine first
Then the number of the level of the last spinal nerve root segment that is innervated
C6 = cervical vertebra at the 6th level (wrist extensors present)
two naming levels for the limbs
Tetraplegia (quadriplegia)
Injuries to the cervical area
UE, LE, trunk, and pelvic areas are affected
Paraplegia
Injuries to the thoracic, lumbar, and cauda equina areas
LE, trunk, pelvic areas are affected
American Spinal Injury Association (ASIA) scale
used to classify SCI
neurologic level is defined as the most caudal segment of the cord with intact sensation and muscle movement
Sensory = light touch and pinprick
Motor = lowest key muscle with a manual muscle test of grade Fair (3/5)
Cervical flexion and rotation
Most common
Vertebra displaced over the one below it
Rear-end collision
Cervical hyperflexion
Anterior compression fracture of vertebral body
Wedge-type fracture
Severs the anterior spinal artery causing incomplete anterior cord syndrome
Head-on collision or blow to the back of head
Cervical hyperextension
Rupture of the anterior longitudinal ligament and compresses the intervertebral disc
Spinal cord gets compressed between ligamentum flavum and vertebral body
Central cord injury
Falls where chin strikes a stationary object
Compression
Vertical compressive force and fractures
Vertebral end plate fracture and nucleus pulposus moves into the vertebral body
Bone fragments
Diving accidents
Medical interventions
Immobilization
Bracing (halo, tortoise shell, Philadelphia collars)
Skeletal traction
Surgery (fusion, bone graft, internal fixation devices)
Pharmacologic
Decrease hemorrhage and ischemia
Methylprednisolone (corticosteroid)
Pathologic changes after injury
Hemorrhage into gray matter —> necrosis of axons —> edema in white matter and puts pressure on nerve fiber tracts —> myelin sheath disintegrates —> axons shrink —> scarring
Secondary tissue damage (ischemia, hypoxia, and biochemical changes) continues and can expand the injured area
Close monitoring of level of injury for 24-48 hours because the level of damage may ascend 1-2 levels due to vascular changes
Spinal shock
Immediately after injury due to interruption of pathways between brain and spinal cord
Characterized by:
Flaccidity
Areflexia
Loss of bowel and bladder function
Autonomic deficits (decreased arterial blood pressure, poor temperature regulation below the level of the injury)
Can last from 24 hrs to several weeks
Clinical manifestations of spinal cord injury (SCI)
Motor paralysis/paresis below the level of injury
Sensory loss
Cardiopulmonary dysfunction
Impaired temperature control (autonomic dysfunctions)
Loss of the ability to shiver below the level of injury
Spasticity
Bowel and bladder dysfunction
Sexual dysfunction
Types of lesions
Complete
Incomplete
Complete
Absent sensory and motor function below the level of injury
Usually caused by complete spinal cord transection, spinal cord compression or vascular impairment
Incomplete
Partial preservation of some motor or sensory function (sacral sparing) below the neurologic level and in the lowest sacral segments of S4-5
Perianal sensation and/or have the ability for voluntary contraction of the external anal sphincter indicates an incomplete injury
Clinical findings to confirm diagnosis
Sacral sparing
Abnormal tone or muscle spasticity
Brown-Sequard syndrome
Involves half of the spinal cord
Penetrating injuries (GSW, stab wounds)
Loss of motor function, proprioception and vibration on the same side as injury
Loss of pain and temperature on opposite side of injury
Light touch may or may not be present
Good prognosis (for many, independent with ADLs and continent of bowel and bladder is possible)
Anterior cord syndrome
Flexion injury to cervical spine with a fracture- dislocation of vertebrae
Damage to the anterior spinal cord or the anterior spinal artery
Loss of motor, pain and temperature bilaterally below the level of injury
Intact proprioception and vibration below the injury
Limited prognosis due to motor function loss
Central cord syndrome
Most common
Progressive stenosis (conflicts w/other sources) or compression due to hyperextension injuries
UE more affected
Damage to 3 different motor and sensory tracts (spinothalamic, corticospinal, and dorsal column)
Sensory varies
Intact bowel, bladder, and sexual functions if these areas are spared
Possibly: ambulation and independent ADLs depending on UE
Dorsal column syndrome (aka Posterior cord syndrome)
Rare
Damage to posterior spinal artery due to a tumor or vascular infarct
Loss of proprioception and vibration bilaterally
Intact motor and pain/temperature sensation
Conus medullaris syndrome
Injuries to the lumbar nerve root and sacral cord within the spinal canal
Upper and lower motor neuron injuries
Back pain
Flaccid paralysis
Areflexic bowel and bladder function
Cauda equine syndrome
Direct trauma from a fracture-dislocation below the L1 vertebrae
LMN symptoms: Flaccidity, areflexia, and loss of bowel and bladder function
Regeneration of peripheral nerve roots is possible but depends on initial damage
Complications following SCI
Pressure ulcers
Autonomic dysreflexia
Postural hypotension
Pain
Contractures
Heterotopic ossification (HO)
Deep vein thrombosis (DVT)
Osteoporosis
Respiratory compromise
Bladder and bowel dysfunction
Spasticity
Male/Female Sexual Dysfunction
Orgasm is controlled at the S3-5 level
Two types of erections:
Reflexive erection from external stimulation; often preserved w/injuries above T10
Psychogenic erections through cognitive imaging; typically lost in complete injuries above T10
Sexual dysfunction for men
Limited erections
Reflexive erections occur at levels S2-4
Most men are able to ha a reflex erection unless the S2-4 pathway is damaged
Psychogenic erections occur at levels T10-L2 when the brain sends messages of arousal
Men with incomplete injuries at a lower level are more likely to have psychogenic erections than men with high level incomplete injuries
Men with complete injuries are less likely to have psychogenic erections
Limited ejaculations
Inc ability to ejaculate if an incomplete level injury than complete
Rarely can a complete injury ejaculate
Limited ability to sire children at any level of injury due to limited ejaculation and slower sperm mobility
Treatment
Medications (Viagra, Cialis), topical agents, and mechanical devices
Sexual dysfunction for women
No physiological change after paralysis that would prevent sex but may need to add lubrication and asst with positioning
Women still have menstruation and so can get pregnant
May not feel labor and there’s inc risk of autonomic dysreflexia during labor
C1-C2
Facial mm, partial SCM, capital mm
Ventilator dependent
Full time attendant
C3
SCM, partial diaphragm, upper Traps
Portable mechanical ventilation
Totally dependent
Full time attendants
Sip and puff or chin controlled WC
C4
Diaphragm so may not have to be on a ventilator
Partial deltoid, SCM, upper traps
Needs neck ROM
Power wheelchair with chin control or mouth stick
Full time attendants
Dependent for ADL, bed mob, and transfers
C5
Deltoid, biceps, rhomboids, elbow flex
Limited functional ability-usually can feed themselves w/a lot of effort
Power wheelchair with hand control
Possibly manual wheelchair with rim projections (high energy expenditure)
Attendant needed: Dependent with bathing and dressing; possibly independent w/some grooming w/adaptive equipment and set up
Needs assist with bed mobility, transfers, and clearing secretions
Pressure relief
Possibly able to drive a van with adaptive hand controls
C6
Pectoralis major, teres major, wrist extensors
Independent with rolling, feeding, UE dressing but needs assist with other care
Propel a manual wheelchair with rim projections
Possibly independent sliding board transfers, feeding w/adaptive equip, independent UE dressing but needs asst for LE
Able to wt shift independently
Will need an attendant at times
Possibly able to drive with adaptive hand controls
Possibly have employment outside the home
C7
Triceps
Possibly living independently
Independent in self-care and UE/LE dressing
Independent w/pressure relief, transfers with sliding board then sit pivot, self-ROM LE, wc mob but may need asst w/ramps and uneven ground
Limited use of an attendant
Driving a regular vehicle with adapted hand controls
C8
Finger flex
Living independently
Asst w/floor transfers
Wheelies in a wheelchair
T1-T8
Intercostals (upper half), Pect major, hand intrinsics, finger abd
Improved but still limited trunk control
Productive coughing
Independent with all transfers but may need min asst w/floor transfers
Independent with manual wheelchair on all surfaces
Limited standing and therapeutic ambulation in parallel bars with much assist and bracing (T6-8)
T9-11
Abdominals
Independent manual wc mob
Therapeutic ambulation at home with braces and assistive devices
T12-L2
Quadratus lumborum, hip flex, knee ext, ankle dorsiflex, great toe ext
Independent household ambulation with KAFO (orthoses)
WC for community mob
L3-5
Iliopsoas, rectus, quads, hamstrings
Independent household and community ambulation w/AFO and canes (L4-5)
S1-2
Plantar flexors, glut max, anal sphincter
Ambulation w/articulated AFO
Physical therapy intervention: acute careaverage stay and goals
Average stay is 11 days
Goals:
prevent contractures
increase muscle and respiratory function
acclimate to upright position
prevent secondary complications
pain management
pt/family education
*PT treat patient initially then co-treat with PTA until patient is more stable
PT acute care spinal cord levels
C1-4- Allows patient to be off of ventilator for short periods, Lateral expansion
C4-T1- Increase diaphragm and accessory muscle strength due to diaphragmatic breathing pattern, Breathing exercises, Glossopharyngeal breathing
T1-12- Deep breathing with manual resistance, Incentive spirometry, Chest wall stretching, Postural drainage, percussion, and vibration, Cough techniques
ROM- tenodesis grip, PROM
Strengthening- Bilateral UE exercise are beneficial
Key UE exercise for tetraplegics: anterior deltoids, shoulder extension, and biceps
Key ex for paraplegics: shoulder depressors, triceps, and latissimus dorsi
Acclimation to upright
PT intervention: inpatient rehabilitation average stay and goals
Average stay is 36 days
Goals:
Increase strength in key muscle groups
Independence with skin inspections
Increase PROM
Increase vital capacity
Increase tolerance to upright position
Increase independent bed mobility, transfers, wheelchair mobility, and exercises
Independence with driving a motor vehicle if possible
Continue with patient/family education
inpatient rehab Early treatment interventions
Mat activities- rolling, strengthening, stretching
Prone
Prone on elbows
Prone to supine
Supine on elbows
Long sitting
Transfer for inpatient rehab
Preparation phase
Two-person lift
Sit-pivot transfer
Modified stand-pivot transfer
Airlift (para transfer)
Sliding board transfers
Prone on elbows transfer
Rolling out of the wheelchair
Lateral push-up transfer
Intermediate treatment interventions
Mat activities
Rolling, supine to prone, supine to long sitting, prone to supine
Independent self range of motion
Long sitting (trunk to leg or leg to trunk), p. 432
Gluteus maximus, p. 433
Hip flexors
Hip abd, add, IR, ER, p. 433
Ankle plantar flexors, p.434
Advanced mat activities
Sitting swing-through
Hip swayer
Trunk twisting and raising
Prone push-ups
Forward reaching
Creeping
Tall kneeling
advanced wheelchair skills
Must readjust sitting balance to do certain activities
Wheelies
Ascending/descending ramps, p.439
Ascending/descending curbs, p. 440
Powered mobility
Wheelchair cushions
Advanced treatment intervention
Cardiopulmonary training
Circuit training
Aquatic therapy
Pool program
Pool exercises
Floating and swimming
Ambulation training Benefits of standing and walking
Decrease risk of osteoporosis
Decrease risk for bladder and kidney stones
Increase circulation
Increase digestion
Decrease muscle spasms
Decrease fatigue
Guidelines for success with ambulation
Motivation
Patient’s weight and body build
PROM at hips, knees, and ankles
Amount of spasticity
Cardiopulmonary status
Status of the integumentary system
T2-11 injury (chest level)
Therapeutic or Functional Ambulation | Assistance | Equipment | Household or Community Ambulator |
Therapeutic standing or ambulation possible | Can only stand or ambulate in Physical Therapy | Needs physical assistance for sit to stand and gait; needs bracing; standing frame or a tilt table | Unable |
T12-L2 injury (belly button level and down)
Therapeutic or Functional Ambulation | Assistance | Equipment | Household or Community Ambulator |
Limited Functional ambulator | Independent for short distances only due to amount of energy expended | Orthosis and assistive device for ambulation; independent transfers | Household ambulatory only; wheelchair for longer distances outside the home |
L3-5 injury
Therapeutic or Functional Ambulation | Assistance | Equipment | Household or Community Ambulator |
Functional ambulator | Independent | With or without orthosis and assistive device for ambulation; independent transfers | Household and community ambulator |
Orthoses
Knee-ankle-foot orthosis –Scott-Craig
Reciprocating gait orthosis – cable system
ReWalk system – robotic exoskeleton
Preparation for ambulation
Should be independent in mat activities, transfers, and wheelchair mobility on level surfaces
Standing in parallel bars
Once the orthotic is on, begin gait in the parallel bars
What should you work on in the parallel bars?
What is a progression in the parallel bars?
gait progression
Swing to
Jack-knife position if patient loses balance during gait
Sitting
Patient should be ~12” away from the chair prior to sitting since orthosis is locked in extension and patient’s buttocks should be in the center of the chair
Ambulation training
Other gait patterns
Four-point or two-point gait pattern possible with Loftstrand or axcillary crutches
Backing up
Standing from the wheelchair with orthoses, p. 449
Gait training with crutches
Falling
Getting up from the floor, p. 451
Negotiating environmental barriers
Ramps
Curbs
Stairs
Discharge planning
Discharge planning conference
Should be done 1-2 weeks prior to discharge
Procurement of equipment
Wheelchair/bed and cushion
ADL adaptive equipment
Home exercise program
Family teaching
Equipment
Handling patient
Safety, complications, precautions, injury
Community reentry – 35% are employed 20 years after injury
Quality of life
Long-term health-care needs
Parkinson’s Disease(PD)
group of disorders
Most common movement disorder in the US
Pathophysiology
Chronic progressive disorder
Lack of dopamine-producing neurons
Disorder of the substantia nigra located in the basal ganglia
Clinical features of PD
Bradykinesia
Rigidity
Resting tremor
Postural instability
Festinating gait
Bradykinesia
Slow movement affects ADLs
Oral movement
unintelligible speech, soft monotone voice, swallowing difficulties
Akinesia
trouble initiated movement
Rigidity
Not dependent on movement velocity
Lead pipe and cogwheel
Restricted chest wall that affects breathing and phonation
Tremors
Often 1st sign
Resting tremors
“Pill rolling”
Postural Instability for PD
Loss of postural extension
Flexed posture
COG is forward
Loss of extension, rotation, arm swing
Inability to respond to postural disturbances
Increased fall risk
Decrease proprioception
Relies on vision for movement cues
Other features of PD
Masked face
Dysphagia
Festinating gait
Shuffling feet with progressive increase in speed
Freezing episodes
Triggered by changing surfaces like doorways or flooring
Fatigue - worsens as the day progresses
Gait
Falls
Cognition
½ have dementia and cognitive changes
Slow thought processes, decreased attention and concentration, depression
Stages of PD
Hoehn and Yahr classification of disability for Parkinson’s
Average person has a life expectancy slightly less than a person without Parkinson’s
Stage 0 to Stage 5
Stage 0 = no signs of disease
Stage 5 = needing a wheelchair or is bedridden unless assisted
Surgical management of PD
Deep brain stimulation (DBS)
Electrodes in the sub-thalamic nucleus with a stimulation box placed under the skin by the clavicle
Pt can turn on/off
Blocks nerve signals that produce symptoms
Physical therapy management of PD
Gait interventions, p. 466
Postural interventions, p. 466-468
Lee Silverman voice treatment (LSVT) BIG
Certification
Motor training principle
Big movement and big stretches with voice commands
Exercise strategy and results, p. 469, Table 13-3
Multiple Sclerosis (MS) Pathophysiology
Demyelination of white matter in the brain and spinal cord
Axon is unprotected and sclerotic plaques form in the brain and spinal cord
Usually ages 20-40 with females being more prevalent
Areas that are usually affected with MS
Optic nerve- Decreased acuity, diplopia, nystagmus,
Periventricular white matter
Corticospinal tract- Weakness in one or both legs
Posterior columns
Sensory disturbances are the 1st sign
“Pins and needles” or “burning/aching”
Cerebellar peduncles
Clumsiness with reaching (overshooting)
Impaired coordination of movement
Poor balance
Ataxia
Clinical features of MS
Fatigue
Most common complaint
Worsens with heat
Cognitive impairment
½ will have some kind of impairment (problem solving, short-term memory, visual-spatial perception)
Autonomic dysfunction
Bowel and bladder problems (urinary frequency, constipation, inadequate emptying)
Disease course
Variable
Exacerbations and remissions
Diagnosis of MS
Based on clinical evidence of multiple lesions in the CNS white matter, distinct time intervals, and age of occurrence (10-50 yrs old)
Cerebrospinal fluid examination
Higher amounts of myelin protein
Magnetic resonance imaging (MRI)
Best way to diagnosis
Medical management of MS
Purpose is to reduce the frequency and severity of the attacks. All are injectables.
Avonex
Betaseron
Copaxone
New medications (IV):
Tysabri
Novantrone
Most common neurologic symptoms of MS
Weakness- Lesions in corticospinal tract or cerebellum, inactivity
Spasticity- UMN damage
Most often spastic plantar flexors, adductors, and quadriceps
Ataxia
Additional concerns
Mood swings
Continuous nystagmus
Vertigo
Clinical presentation of ALS
A progressive neurodegenerative disease that affects nerve cells in the brain and the spinal cord
Usually patients are 40-70 years old
Muscle weakness – cardinal sign
Distal symptoms occur before proximal
Most have asymmetrical muscle weakness in an arm or leg
Early signs: muscle cramps, weakness, atrophy, and fatigue
May lose the ability to speak, eat, move and breathe
Diagnosis based on S&S, EMG, imaging, nerve and muscle biopsies
No involvement of eye muscle or sensory
½ of the patients will have cognitive impairment
Death is usually from respiratory complications as muscles weaken
Medical management of ALS
No cure
Symptom management
There is one FDA-approved drug, riluzole, that slows the progression of ALS in some people
Physical therapy management of ALS
General initial guidelines:
Avoid heavy eccentric exercise
Moderate resistance can increase strength
Needs to rest in between exercises
Pulmonary care at late stages for aspiration and airway clearance
Later on, need support of weak muscles by using orthosis (neck)
Pressure reducing devices
Pathophysiology of GBS
Autoimmune reaction
Schwann cells destroyed in peripheral nervous system but the axons are intact so after 2-3 weeks, the cells begin to proliferate, inflammation dissipates, and remyelination begins
Clinical features of GBS
Symmetrical ascending progressive disorder
Weakness begins distally and progresses proximally
Burning and tingling of toes or hyperesthesia distally
Motor involvement more than sensory
If progresses to diaphragm, mechanical ventilation is needed
½ will have ANS changes (BP and HR)
½ oral-motor involvement (dysarthria and dysphagia)
Myalgia
Throughout the process
DTRs absent due to areflexia (demyelination) of peripheral nerves
Medical management of GBS
Plasmapheresis (PE)
Infusion of IV immunoglobulins
Phases of GBS
Acute phase
Up to 4 wks
Symptoms continue to worsen
Plateau phase
Up to 4 wks
Stabilzation of symptoms
Recovery phase
From a few months to a couple of years
Improvement
80% recover in a year but may still have some deficits
Physical therapy management of GBS
Acute phase
Usually in ICU on a ventilator
Treat symptoms as they occur
Plateau phase
Upright positions (slowly)
Gradually increase ROM and movements as tolerated
Recovery phase
Muscle strength returns in reverse order (descending)
Tilt table—>standing—>transfers—>gait training
Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP)
is a slowly developing autoimmune disorder of the peripheral nervous system in which the body's immune system attacks the myelin sheath
Unknown etiology
It’s most common in older adults, and more in men than women.
No specific test to determine diagnosis but weakness must be present for at least 2 months
There are periods of remission and relapse
Common symptoms are gradual weakness or sensation changes in the arms or legs
Symmetrical motor and sensory involvement
Stocking glove distribution of numbness and tingling
Hypo or areflexia
Postural tremor of the hands
Papilledema, vision loss
Facial weakness
CIDP vs GBS
CIDP
Nerve involvement
Weakness
Numbness
Not linked to illness
Tends to be a long-term recovery
Chronic
GBS
Nerve involvement
Weakness
Numbness
Begins after an illness
Most recover fairly quickly
Acute
May develop into CIDP if it reoccurs
Medical Management of CIDP
Corticosteroids
Plasmaphoresis
Intravenous immunoglobin (IVIG)
Physical Therapy Management of CIDP
ROM
Balance
Aerobic conditioning
Strengthening
Gait training
Avoid overexertion
Post-Polio Syndrome (PPS) Etiology
Most believe that it is caused by increased metabolic demand made on the body by giant motor units that were formed during the recovery process from the original viral infections
Clinical features of Post-Polio Syndrome
Fatigue
New weakness- Hallmark sign
Asymmetrical proximal weakness and progressive
Pain
Cold intolerance
Decreased function
Medical management of Post-Polio Syndrome
No specific medication
Healthy diet
Sleep apnea treatment
Increase activity
Staying warm
Good pulmonary ventilation
Physical therapy management of Post-Polio Syndrome
Exercise
General guidelines: avoid overuse and disuse, modify activity level to decrease pain, monitor vitals
Customize exercise programs with rests periods
Stretching – caution due to joint instability
Pain management- Cramping, musculoskeletal, and biomechanical
Lifestyle modification- Must change and slow down
Energy conservation- Helps to manage fatigue
TBI
“an alteration in brain function…caused by an external force”
Effects of TBI
Impaired cognition
Deficits in movement and sensation
Impaired behavior and emotional responses
Financial
2.2 million Americans treated each year
80K - significant loss of function
52K – die
Acute care and rehab = $10 billion yearly
Ave lifetime expense with caregiving = $1.8 million
Causes of TBI
Falls = 41%
Unknown/other = 19%
Struck by an object = 16%
MVA = 14%
Assaults = 11%
Trivia
More prevalent in men
Ages: (CDC, 2014)
1-2 years old
15-24 years old
Over 75 years old
Classification of brain injuries
Open and closed injuries
Subtypes of brain injuries
Concussion
Contusion
Hematomas
Open
Penetrating types of wounds
GSW, Knife, sharp objects
Skull fracture or displaced
Damage to meninges-inc risk of infection
Closed
Subtypes
Impact to head but no open wound, fracture or displacement
Brain tissue damage