SCI Flashcards
SCI demographics M \_\_ F Mean age? Etiology? Distribution of complete vs incomplete para vs tetraplegia?
SCI demographics 17,000 new SCI each year M (80%) >> F (20%) Mean age? 42yo Etiology? MVA (38%), Falls (30%), violence (14%), recreational sports (9%)
66% of all injuries are INCOMPLETE Incomplete tetraplegia = 45% Complete tetraplegia = 14% Incomplete paraplegia = 21% Complete paraplegia = 20%
Impaired __ capacity is the most common cause of death after SCI.
Describe complications in terms of related PT diagnoses
Any interventions that help?
Impaired RESPIRATORY capacity is the most common cause of death after SCI
Reduced ventilation = microatelectasis
Ineffective cough = unable to clear secretions -> PNA and insufficient respiration
Interventions: respiratory muscle training improves VITAL CAPACITY, EXPIRATORY MUSCLE STRENGTH, and RESIDUAL VOLUME - e.g. singing, coughing, and exercising are good interventions to improve respiratory capacity!
Most severe respiratory complications post SCI occur in high-level cervical injuries. Injuries above __ are likely to require endotracheal intubation & mechanical ventilation. May also need ___ nerve stimulation/direct motor point pacing of the __ (muscle)
Describe changes in FEV & FVC relative to age-predicted values in high vs low cervical injuries
Most severe respiratory complications post SCI occur in high-level cervical injuries. Injuries above C5 are likely to require endotracheal intubation & mechanical ventilation. May also need PHRENIC nerve stimulation/direct motor point pacing of the DIAPHRAGM
C3-C5 = FEV 56%, FVC 53% age-predicted values
C6-8 = FEV 65%, FVC 64% age-predicted values
Describe muscles associated with inspiration and spinal nerve innervation
What about exhalation?
Describe muscles associated with inspiration and spinal nerve innervation
- Diaphragm: C3-5
- Accessory mm (SCM/ scalenes C1-8) - these assist w/respiration and may compensate after paralysis of lower musculature!
- Intercostal mm (innervated by intercostal nerves T1-T11) - these increase and decrease rib cage volume, impact deep breathing and coughing
- Abdominal mm (Rectus, transversus abdominus; innervated at T6-L1) - required for an effective cough
Exhalation is usually PASSIVE, except w/coughing, singing, and exercising
Most common infection post SCI? What are the risk factors for this inherent to SCI?
What may decrease risk of this?
UTI
- Urinary retention
- Bladder over distention
- Urine reflux into ureters
- Kidney and bladder stones
- Intermittent catherization
- Assist required for ADLs/lack of independence
Factors to decrease risk of UTIs:
- Independence w/ADLs
- Engaging in weekly exercise
- Good personal hygiene
- Education
Describe neurogenic bladder/urinary management post SCI. How does this change with higher vs lower injuries (UMN vs LMN management)? At what level does it switch?
Neurogenic bladder = lose supraspinal control of bladder due to SCI
Indwelling/foley catheter usually used until medically stable
Injury above t12 = UMN management = REFLEXIVE bladder. Urine fills bladder - nerves signal to contract bladder, it squeezes and empties reflexively - requires a leg bag. Needs intermittent catheterization (~q4 hrs). May still need a leg bag. Bladder augmentation (surgery so bladder can store larger amounts of urine safely) is an option.
In Injuries below T12 (LMN management = AREFLEXIVE bladder). Doesn’t empty based on a reflex; the sensory signal of bladder fullness won’t get back to spinal cord, bladder will overfill/over stretch = bladder accidents.
Requires intermittent catherization vs condom cath. Areflexive bladder. Usually need a leg bag.
Max allowable bladder fillage = 500-600mL. Uses sterile technique in hospital -> clean technique (so they can reuse catheters once clean) at home
Neurogenic bladder complications…
- Leaking
- UTI
- Kidney infection
- LE spasticity
Challenges:
- Men C6-7 level (or lower) may be independent with intermittent catheterization (largely d/t difficult to apply condom cath)
- Women C7 (or lower) may be independent with IC (labia splitter)
Options: intermittent catherization
- Suprapubic catheters
- Bladder augmentation
- Reflex voiding (option for LE injuries/below t12, via essentially “leaking” into leg bag)
Describe how a suprapubic cystostomy works and why this might be a good bladder management option
Suprapubic cystostomy = surgical intervention creating a stoma in the abdomianl wall with a catheter inserted directly into the bladder. Drainage options include free drainage (urine drains freely into bag t/o the day) vs with a catheter valve (drains urine directly into a toilet using a catheter)
This is a secondary option for those who cannot be independent with intermittent catheterization. Very favorable option for individuals with C5-6 level injuries who can’t do intermittent catheterization. Generally good satisfaction rates.
Contributing factors post SCI that makes individuals at high risk for developing skin issues (beyond the obvious)…
- Collagen degradation after SCI
- Decreased peripheral blood flow (low BPs, smoking)
- Immobility and sensory loss
- Muscle atrophy over bony prominences
- Incontinence, moisture
- Dependent mobility = shearing forces
- External pressure > capillary pressure
- Ischemia/necrosis
*Estimated cost to heal 1 pressure sore = >$60k; >%11B spent annually to heal pressure ulcers!
Key features for preventing pressure ulcers…
- Weight shifts q20-30 min
- Regular turns and proper positioning in bed (initially q2-4 hrs, increasing turn times up to 6 hours max as tolerated, monitoring skin) - in supine, keep HOB <15-30 deg to minimize shearing
- Skin checks at least 2x/day
- Good hygiene, keep skin dry
- Proper positioning in w/c, pressure mapping
- Safe transfers (watch that pt isn’t hitting their buttocks
- Shoe tolerance ( need shoes that are 1-1.5 sizes bigger than usual to account for usual LE edema post SCI)
- Pressure reducing DME (cushions and mattresses)
- Good nutrition and adequate fluids
- Decreased prevalence of pressure ulcers in indiduals who:
- maintain normal weight
- return to work/family roles
- no previous hx tobacco use, suicidal behaviors, incarcerations, EtOH/drug abuse
Weight shifting options in SCI for pressure relief
Power: power tilt or power tilt + recline (harder to justify this to insurance; sometimes arguing that it decreases caregiver burden, assists with ADLs/dressing, and can aide individual with doing intermittent catheterization in chair can help w/insurance payout)
Manual:
- Can shift laterally or forward
- Can do chair push up/depression - need triceps! Good for injuries to C7 and below
- Need to weight shift EACH ischial tuberosities for 60 SECONDS (60 sec for each ischial tub, or in a position that you can do both at once!!) every 20-30 MINUTES. Goal is to restore blood flow to that area!
DVT risk in SCI - contributing factors?
- Common in acute phase of SCI
Incidence is 4.5% leading to 3.5% mortality in first 3 months post SCI.
More common in M>F, motor complete, incr weight, longer LOS, pelvic.LE fracture and delayed admission to SCI specialty center
Contributing factors: - Peripheral vasodilation/reduced LE muscle pump
- immobility -> venous stasis
- trauma
- hypercoaguability
Incidence of DVT & PE in SCI (~9% DVT; ~2% PE) is similar to that of trauma (~11.8% DVT; 0.9 PE) patients. IVC filter placed prophylactically in:
- SCI + long bone fx (37% get DVTs!!)
- DVT despite prophylactic anticoag
- If anticoag is contraindicated
- IVC filter placement may actually contribute to increased risk of DVT! So use them only w/particular populations above (esp long bone fx + SCI)
GI complications after SCI
~27% of chronic SCI had significant GI complications:
- Abdominal pain
- 20% difficulty with evacuation
- 74% hemorrhoids (=swollen anal veins; d/t bowel programs)
- 73% abdominal distention
- 43% autonomic hyperreflexia / dysreflexia
- 23% needed at least 1 hospital admission d/t GI complication
Neurogenic Bowel in SCI - damage to the CNS prevents supraspinal control of bowel regulation, determined by the presence of absence of the ___ reflex (BCR). This refers to the contraction of the ___ in response to ___ stimulation. Presence of this reflex = [UMN/LMN] pattern, vs absence of this reflex = [UMN/LMN] pattern. What innervates this reflex?
Neurogenic Bowel in SCI - damage to the CNS prevents supraspinal control of bowel regulation, determined by the presence of absence of the BULBOCAVERNOSUS reflex (BCR). This refers to the contraction of the ANAL SPHINCTER in response to GENITAL STIMULATION. Presence of this reflex = UMN pattern, vs absence of this reflex = LMN pattern (AREFLEXIVE BOWEL). Reflex is innervated by the PUDENDAL NERVE (S2-S4)
Complications of neurogenic bowel
- Bowel accidents
- (“involuntaries”)
Constipation - Impaction
- Diarrhea
- Rectal bleeding
Describe bowel management programs for UMN (lesion above __) pattern.
UMN: Lesion at or above T12
- +BCR
- Good sphincter tone
- Reflexive bowel
- Daily (or every other day) bowel program
- Bristol Stool Scale: Type 5
- Management: digital stimulation (dil stick or finger in rectum to activate reflex), suppository
Describe bowel management programs for LMN (lesion below __) pattern
LMN: Lesion below T12 (L1 & lower) - rectum fills with stool, pushes on sensory nerves, but that signal can’t get back to spinal cord to cause that reflective activity d/t injury, so anal sphincter stays open and loose
- -BCR (so DON’T rely on this reflex for bowel mgmt program!)
- Lacks sphincter tone
- FLACCID bowel
- BID bowel program (aim for 30-60 mins after eating)
- Bristol Stool Scale: Type 2-3
- Management: timing, fiber (needs 25-35g fiber daily to create bulky stool), fluids (gastrocolic reflex); manual evacuation; valsalva maneuver
Role of colestomy vs sacral nerve stimulation in SCI bowel management?
Long story short, traditional bowel programs take a LOT of time during the day!! These can help from a time perspective, but aren’t common largely because they’re invasive.
Historically colestomy is used only as a last resort if bowel complications persist; only 2.4% of SCI pts have a colostomy, but it significantly improves QOL, reduces time spent on bowel care (2hrs vs 12 mins!), reduces # hospitalizations i/s/o chronic bowel dysfunction, increases independence with bowel routine, easier to manage!
Sacral nerve stimulation: anterior sacral nerve root stimulatory implanted at level of cauda equina. Increases frequency fo left colon defication, perianal sensitivity, and deliberate retention. Decreases time for bowel regimen and amount of fecal incontinence, but it can be costly and invasive.
Autonomic dysreflexia occurs in SCI due to loss of supraspinal regulation of the autonomic function of ___. High risk for SCIs above ___ level.
Triggered by noxious stim below the level of injury such as ….
Results in an exaggerated [ sympathetic / parasympathetic ] response, which in turn triggers the __ receptors in the aortic arch, resulting in a [ sympathetic / parasympathetic ] response.
Symptoms?
Autonomic dysreflexia occurs in SCI due to loss of supraspinal regulation of the autonomic function of BLOOD PRESSURE. High risk for SCIs above T6 level.
Triggered by noxious stim below the level of injury such as ….
- Ingrown toenail
- Full bladder/blocked catheter
- Fecal impaction
- Constipation
Results in an exaggerated SYMPATHETIC response BELOW level of lesion, which in turn triggers the BARORECEPTORS in the aortic arch, resulting in a PARASYMPATHETIC response BELOW level of lesion
Symptoms include:
- Increased BP
- Headache
- Flushing
- Anxiety
Autonomic dysreflexia in SCI results in a sympathetic response [above / below] the level of the lesion with related vaso [constriction/dilation] as a compensatory mechanism. Symptoms include [tachy / brady] cardia and [diaphoresis / goosebumps] above the level of the lesion.
Alternatively, the sympathetic response triggers baroreceptors in the aortic arch to subsequently trigger a parasympathetic response [above / below] the level of the lesion. Symptoms of this include [ diaphoresis / goosebumps] [ above/ below] level of lesion.
Treatment?
Autonomic dysreflexia in SCI results in a sympathetic response ABOVE the level of the lesion with related VASODILATION as a compensatory mechanism. Symptoms include BRADYcardia and DIAPHORESIS above the level of the lesion.
Alternatively, the sympathetic response triggers baroreceptors in the aortic arch to subsequently trigger a parasympathetic response BELOW the level of the lesion. Symptoms of this include GOOSEBUMPS BELOW level of lesion.
Treatment? UPRIGHT POSTURE to manage HTN while finding the NOXIOUS SOURCE - can be life threatening, as BP will continue to increase until noxious source is removed
Heterotrophic Ossification (HO)
- What is it?
- Where does it occur/impact? (structures? location relative to SCI level?)
- Pathophysiology?
- Prevalence post SCI?
- Factors significantly correlated with HO?
- How do we find/diagnose it?
- How to prevent it?
- How to treat it? (meds? surgery? role of ROM?)
Heterotrophic Ossification (HO)
- What: ectopic bone formation in the soft tissue surrounding a joint
- Where: typically CAUDAL to level of injury in SCI, often in hips
- Why? Pathophysiology isn’t well understood, but thought that bone morphogenic proteins act on mesenchymal stem cells causing them to differentiate into osteoblasts i/s/o decreased WB post SCI.
- Prevalence: as high as 53% post SCI, with clinically significant HO ~27% (clin significant = areas w/bone formation that limits ROM & impacts positioning/ mobility)
- Factors correlated w/HO: Motor complete paraplegia, spasticity, and pressure sores
- How to diagnose? ~50% show elevated levels of alkaline phosphatase in the blood (but that’s not a lot) - often picked up by therapist during regular ROM, then refers to imaging/XR to confirm.
Prevention: regular ROM; NSAIDs, when given early, showed greatest efficacy to prevent HO.
Treatment: Continual ROM is important!
- Medication: Etidronate
- Surgical resection (after bone has reached maturity) - ROM exercise may maintain joint ROM in the presence of immature ectopic bone (just don’t be crazy aggressive)
Spasticity post SCI consists of 2 components:
- Hyperexcitable __ reflex
- Hypertonia: soft tissue changes due to limb immobilization leads to increased muscle ___ to passive movement
Spasticity results from both disordered spinal mechanisms and disordered supraspinal mechanisms.
Spinal mechanisms: altered __ activity, imbalance of __ and __, inactive __ cell.
Supraspinal mechanisms: hyperexcitability of __ [afferents / efferents] of the stretch reflex.
Spasticity post SCI consists of 2 components:
- Hyperexcitable STRETCH reflex
- Hypertonia: soft tissue changes due to limb immobilization leads to increased muscle RESISTANCE to passive movement
Spasticity results from both disordered spinal mechanisms and disordered supraspinal mechanisms.
Spinal mechanisms: altered SYNAPTIC activity, imbalance of NEUROTRANSMITTERS and ELECTROLYTES, inactive RENSHAW cell.
Supraspinal mechanisms: hyperexcitability of GAMMA EFFERENTS of the stretch reflex.
Treating spasticity?
- Stretching
- EStim
- Standing
- Vibration
- Anti-spasmodic meds (may decrease reflex activity accentuate paresis in motor incomplete SCI, so consider in the setting of fxn!)
Osteoporosis in SCI
- Why?
- Increases likelihood of __
Osteoporosis in SCI
- Why? Decreased Ca2+ and collagen in bone immediately following SCI (most significant loss in first 1-2 yrs post injury then plateau ~4-5 yrs post injury. Loss is particularly proximal tib & distal femur = WB surfaces) d/t neurogenic osteoporosis
- Increases likelihood of FRACTURES (incidence of fractures increases as a function of time)
Treating osteoporosis in SCI:
Low level evidence but…
- High dose standing + electrical stim shows positive trend for bone health
- FES cycling in chronic SCI is variable, but 1 systematic review = increased 9% bone mineral density after 12 months of cycling. More effective for bone health cycling 5x/week than 3x/week
- Vibration needs more research with standing + vibration, not helpful in sitting
- Bisphosphinates may help too for BMD after SCI
Sympathetic control UE vasculature occurs at __-__ levels
Sympathetic control of LE vasculature occurs at __-__ levels
We see vasodilation [above / below] level of injury d/t impaired [ parasympathetic / sympathetic] response, so you need to monitor for ____.
Management/ treatment of orthostasis includes…
Sympathetic control UE vasculature: T1-T5
Sympathetic control of LE vasculature: T2-T12
Vasodilation BELOW level of injury d/t impaired sympathetic response, so monitor for ORTHOSTATIC HOTN.
Management:
- Compression! (to help maintain BPs and minimize blood pooling in LEs)
- Meds (give 20-30 min before upright mobility)
- Adequate hydration
Sexual health post SCI:
- Innervation of sexual organs comes from __ and __ segments of spinal cord.
- Injuries above T12 (UMN injury) have a primarily ___ response to genital stimulation, vs injuries below T12 have a ___ response to stimulation.
Females: Menstrual cycle temporarily ceases__-__ months post injury; women can carry a baby to full term and deliver vaginally (~22%), but increased risk for ___.
75% of men post SCI can achieve erection, but testicular atrophy, decreased semen production, and decreased sperm viability impact fertility. May need vibration ejaculation or electroejaculation to collect semen if hoping to become fathers.
Sexual health post SCI:
Thoracolumbar and sacral segments of spinal cord innervate sexual organs. Injuries above T12 (UMN injury) have a primarily reflexogenic response to genital stimulation. Under T12 is psychogenic response to stimulation. Menstrual cycle temporarily ceases then resumes within 5-12 months post injury; women can carry a baby to full term and deliver vaginally (~22%)! Increased risk for autonomic dysreflexia (especially if injury is T6 or higher).
75% of men post SCI can achieve erection, but testicular atrophy, decreased semen production, and decreased sperm viability. May need vibration ejaculation or electroejaculation to collect semen if hoping to become fathers.
Predictors of clinical outcomes in SCI
- For complete SCI:
- For incomplete SCI:
Predictors of clinical outcomes in SCI
- For complete SCI: AGE MATTERS = decreased motor and functional recovery with increased age; increased mortality and worse neuro and functional outcomes
- For incomplete SCI: AGE DOES NOT CORRELATE with motor and functional recovery. SEVERITY of SCI is the most significant predictor of outcome.
Predictors of clinical outcomes in SCI
Predictors of clinical outcomes in SCI
- AGE MATTERS in complete SCI but NOT in incomplete SCI. With complete SCI, increased age = decreased motor and functional recovery, increased mortality and worse neuro and functional outcomes
- SEVERITY of injury is a PRIMARY predictor of recovery. At 72h post injury: 12.8% with complete SCI (AIS A) vs 46% with sensory incomplete (AIS B) vs 84% motor incomplete (AIS C and D) demonstrated recovery.
- Walking Recovery:
- –> LE Motor Score <=20: limited ambulators, slow walking velocities, higher HRs, higher energy expenditure
—>LE Motor Score >= 30: Community ambulators
Predicting walking recovery after SCI by AIS score - % of each expected to recover some walking function?
- AIS A
- AIS B
- AIS C
- AIS D
Predicting walking recovery after SCI by AIS score - % of each expected to recover some walking function?
TIME is a big factor. (The following per Scivoletto 2014)
- AIS A: ~14% recover some walking function (which includes the ~10% of folks who convert to AIS B; 10% convert to AIS C). Of the 80% still AIS A when evaluated after initial 72h post injury, only ~2.5% demonstrate neurologic improvement.
- AIS B: ~33% expect to recover some walking function. If PINPRICK is preserved, may demo better recovery of walking due to possible sparing of motor tracts
- AIS C: ~75% expect to recover some walking function - does not account for using LE bracing and assistive devices
- AIS D: ~100% expected to recover some walking function
Gold standard to classify SCI?
ISNCSCI: International standards for the Neurological Classification of SCI
ASIA Impairment Scale is derived from the ISNCSCI
AIS A
Complete. No sensory or motor function preserved, includign S4-5
AIS B
Incomplete
Sensory function preserved below neurologic level, includes S4-5
AIS C
Incomplete
Motor function preserved below neuro level of injury - More than HALF of key muscles are LESS THAN 3/5
AIS D
Incomplete
Motor function preserved below neuro level of injury. At least HALF of key muscles below neuro level of injury are GREATER THAN or EQUAL TO 3/5
AIS E
Incomplete, sensory and motor fxn return to normal
How do you test the ISNCSCI
Sensation: Tests with eyes closed, 28 dermatomes from C2-S4-5 for R/L sides. Compare to “normal sensation” in a non-injured area (face).
Tests:
Light touch = wisp of cotton
Pin prick/sharp vs dull = pointed vs rounded end of safety pin.
0 = no sensation; 1 = altered sensation = 2 normal
Motor: Key muscle groups from 10 myotomes (5 UE, 5 LEs), test supine. C1-4: (Sensory level) C5: Biceps, brachialis C6: Extensor carpi radialis and brevis C7: Triceps C8: Flexor digitorum profundus, middle finger T1: Abductor digiti minimi T2-L1: (Sensory level) L2: Iliopsoas L3: Quadriceps L4: Tibialis anterior L5: Extensor hallucis longus S1: Gastroc S2-5: (Sensory Level)
Graded: 0 = paralyzed 1: palpable 2: full range gravity eliminated 3 full range against gravity 4: full ROM w/ mod resistance 5: full range takes resistance 5*: Full ROM against gravity, but something else WITHOUT NEUROLOGIC COMPONENT limits function - e.g. if scapular fx or pain, may limit biceps strength NT = not testible d/t immobilization, contracture, amputation, pain. Need to have at least 50% of normal ROM to score, otherwise is NT.
Anorectal exam:
Sensation at S3 and S4-5
Deep anal pressure/sensation (DAP) Y/N (if this is present, they’re not a complete/AIS A!)
Voluntary Anal contraction Y/N
ISNCSI Scoring/terms
Sensory level =
Motor level =
Neurologic level of injury =
Zone of partial preservation =
ISNCSI Scoring/terms
Sensory level = most caudal “intact” (both scores = 2) for both light touch and pinprick at that level and above, for R and L.
Motor level = lowest key muscle function that is at least a 3, providing that key muscle functions of segments above that level are 5s (intact)
Neurologic level of injury = normal sensory (2s across!) and antigravity muscle function (3), provided there is normal (5) motor function below this
Zone of partial preservation = partial preservation of motor or sensory function for 1-3 segments caudal to then neurological level of lesion (ONLY used with COMPLETE lesions!)
Brown-Sequard Syndrome
Hemicord injury.
Often r/t gunshot or stab wounds
IPSILATERAL loss of Lateral CS tract (motor), and DCML (proprioception, vibration, and 2-pt discrim; cross in medulla)
CONTRALATERAL loss of lateral spinothalamic tract (pain and temp, since it already crossed over!)
Central Cord Syndrome
Damage to central aspect of spinal cord, spares peripheral portions of cord
Common in older adults after EXTENSION injuries of neck, can result from even minor trauma
Results in UE»LE impairment (because neurons innervating UEs lie more medially than those innervating LEs!)
Bowel, bladder, and sexual function remain intact (since these are pretty peripheral/lateral)
Prognosis: likely to experience neurological return and achieve functional recovery in rehab (depends on severity of injury)
Lateral Corticospinal tract
fine motor of extremities
Lateral vestibulospinal tract
Maintains upright balance and posture. Stimulates LE extensor motor neurons, inhibits LE flexor motor neurons
Medial vestibulospinaltract
coordinates head/neck with eye position
Tectospinal tract
mediates neck reflexes related to visual and acoustic stim
Tectospinal tract
Mediates neck reflexes related to visual and acoustic stim
Reticulospinal tract
Locomotion and postural control. Can be inhibatory or excitatory, depending on phase of gait cycle.
Ventral and dorsal spinocerebellar tracts
relay sensory information to Cb via inferior Cb peduncle
Lateral spinothalamic tract
Pain and temp, sends to thalamus
Faciculus cuneatus
Faciculus gracilis
Cunateus = UE info, more lateral Gracilis = LE info, more medial
Both carry info related to 2-pt discrimination, vibration, proprioception
Posterior Cord Syndrome
Dorsal Columns (Gracilis facilis, gracilis cuneatus)
BILATERAL loss of [things the DCML does] = tactile discrimination, vibration, pressure, proprioception
Motor function is PRESERVED, but this sensory loss will negatively impact ambulation/ balance
Anterior spinal artery syndrome
Anterior spinal artery supplies 2/3 of spinal cord, so you lose function in the tracts located anteriorly and laterally in it’s vascular zone
BILATERAL loss of:
- Motor function (lateral CS tract)
- Pain and temp (lateral spinothalamic tract)
- -> Prognosis is poor for ambulation
DCML (light touch, propriocept, vibration) are preserved.
Conus Medullaris Syndrome
- Terminal end of spinal cord
- Contains motor neurons of S4-S5 spinal segments
- > Decreased perianal sensation
- > Diminished achilles reflexes
- > Areflexive bladder and bowel
- > Impaired sexual function
- Damage to sacral cord and lumbar nerve roots within neural canal
- Mixed UMN an dLMN damage can be seen
- Results in LE motor and or sensory loss
Cauda Equina Syndrome
- Bundle of nerve ROOTS extending through vertebral canal below conus medullaris
- Damage occurring at T12/L1 vertebral level and below
- Results in a LMN lesion (areflexive bowel, bladder, and sexual function; denervation atrophy of deafferented mm; flaccid paralysis with no spinal reflex activity present)
- Usually an incomplete lesion (some potential for recovery)
- -> Prognosis follows that for peripheral nerve injuries, and has a greater potential for spontaneous regrowth (1mm/day).
- -> Depends on severity of injury. Quads are often spared, so ambulation potential is GOOD!
UMN Injury (Suprasegmental Control) includes damage to the motor neuron that carries motor information from ___ or subcortical region to
- -> Cranial [ nerves / nerve nuclei]
- -> ____ that synapse with motor cell bodies in the ventral horn (LMNs)
- -> [absent / intact] reflex loops
- -> [ Flaccidity / Hyperreflexia ] at the level of the injury
- -> [ Flaccidity / Hyperreflexia ] below level of injury
- -> Includes SCIs above ___/___ level
UMN Injury (Suprasegmental Control) includes damage to the…
- motor neuron that carries motor information from MOTOR CORTEX or subcortical region to
- -> Cranial nerve NUCLEI
- -> INTERNEURONS that synapse with motor cell bodies in the ventral horn (LMNs)
- -> INTACT reflex loop (sensory nerve, spinal motor neuron, motor, nerve muscle activation)
- -> FLACCIDITY at the level of the injury
- -> HYPERREFLEXIA below level of injury
- -> Includes SCIs above T12/L1 level
LMN (Segmental Control) includes damage to the motor neuron that carries info from motor neuron ___ ___ in the ___ horn to skeletal muscles
- -> Includes cranial [ nerves / nerve nuclei] and ___ ___
- -> Results in [flaccidity / hyperreflexia ]
- -> Includes SCIs at and below __/___
LMN (Segmental Control)
- Motor neuron that carries info from motor neuron CELL BODIES in ANTERIOR horn to skeletal muscles
- -> Includes CRANIAL NERVES and CAUDA EQUINA
- -> Results in FLACCID PARALYSIS
- -> HYPOREFLEXIA
- -> Includes SCIs at and below T12/L1
UMN Injury (loss of ____ control) includes damage to the motor neuron that carries motor information from ___ or subcortical region to
- -> Cranial [ nerves / nerve nuclei]
- -> ____ that synapse with motor cell bodies in the ventral horn (LMNs)
- -> [absent / intact] reflex loops
- -> [ Flaccidity / Hyperreflexia ] at the level of the injury
- -> [ Flaccidity / Hyperreflexia ] below level of injury
- -> Includes SCIs above ___/___ level
UMN Injury (SUPRASEGMENTAL Control) includes damage to the…
- motor neuron that carries motor information from MOTOR CORTEX or subcortical region to
- -> Cranial nerve NUCLEI
- -> INTERNEURONS that synapse with motor cell bodies in the ventral horn (LMNs)
- -> INTACT reflex loop (even though it isn’t under voluntary control; sensory nerve, spinal motor neuron, motor, nerve muscle activation)
- -> FLACCIDITY at the level of the injury (injury itself damaged motor neuron cell bodies in anterior horn, essentially creating a localized LMN lesion)
- -> HYPERREFLEXIA below level of injury
- -> Includes SCIs above T12/L1 level
LMN (loss of ___ control) includes damage to the motor neuron that carries info from motor neuron ___ ___ in the ___ horn to skeletal muscles
- -> Includes cranial [ nerves / nerve nuclei] and ___ ___
- -> Results in [flaccidity / hyperreflexia ]
- -> Includes SCIs at and below __/___
LMN (Segmental Control)
- Motor neuron that carries info from motor neuron CELL BODIES in ANTERIOR horn to skeletal muscles
- -> Includes CRANIAL NERVES and CAUDA EQUINA
- -> Results in FLACCID PARALYSIS
- -> HYPOREFLEXIA
- -> Includes SCIs at and below T12/L1 (again, because this is where the bundled nerves end at this level)
Locomotor training after motor incomplete SCI (AIS C and D)
AIS C and D
- Significant improvement in walking and balance outcomes - CAN improve walking in both acute and chronic motor incomplete injuries
Insufficient evidence to conclude that any one approach to locomotor training is better than another to improve walking function, BUT recent intensive clinical paradigms seem more effective than older interventions!
Needs a LOT of reps/intensity (goal: 70-85% HRMax -> walking improvements even after a plateau! Faster training = faster walking). Robotics can help to get this, but if pt is ambulatory, no difference btwn robotic assisted vs independent gait training.
(1) Rely on NEUROPLASTICITY: promote recovery of existing paths or promote new paths to carry motor/sensory info to promote recovery. May be unmasking latent connections (d/t change in inhib/excitation), altered synaptic efficacy, shifts in CNS activation patterns (in SCI, shift to Cb playing greater role in movement!), synaptogenesis. Training paradigm is KEY.
(2) Priming: implicit motor learning using a stimulus to prompt a change in behavior, or to facilitate motor learning! Enhanced neural activity just before or during skill-based training may facilitation long term potentiation or depression. 2 mechanisms for priming:
1. Homeostatic plasticity: increased neuronal excitability after LOW synaptic activity, done prior to motor training to induce plasticity.
2. Gaiting: disinhibition of inhibitory cortical circuits. Done CONCURRENTLY with motor training
Vibration (?d/t tonic vibratory reflex) can help to activate
Priming in SCI recovery
Definition?
Ways of doing it?
Types of priming?
Priming: implicit motor learning using a stimulus to prompt a change in behavior, or to facilitate motor learning!
Enhanced neural activity just before or during skill-based training may facilitation long term potentiation or depression.
2 mechanisms for priming:
- Homeostatic plasticity: increased neuronal excitability after LOW synaptic activity, done prior to motor training to induce plasticity.
- Gaiting: disinhibition of inhibitory cortical circuits. Done CONCURRENTLY with motor training
Priming types:
- Stimulation-based
- Sensory-based
- Movement based
- Motor imagery and action-observation-based
- Pharmacology-based
How does vibration help with locomotor training/plasticity post SCI?
Vibration ->
- Decreased spasticity
- Increased walking speed
- Increased muscle performance (Tonic vibratory reflex)
- Increased excitation of spinal circuitry for locomotion (reticulospinal tract)
- Increased frequency and amplitude = greater EMG
Activity recs for SCI in terms of…
- Aerobic training
- Resistance Training
- Locomotor Training
- FES
Activity recs for SCI in terms of…
- Aerobic training: 2-3x/wk, >=20 mins/session, moderate to vigorous intensity
- Resistance Training: 3 x 8-10 reps of each exercise. 1-2 mins between sets.
- Locomotor Training: 3-5x/wk, mod to heavy intensity, 30-45 mins
- FES: 3x/wk, variety of modes
Reactive plasticity in SCI may be more sensitive in the acute vs chronic stages of recovery. Acute SCI showed greater improvements in locomotor fxn, decreased tissue loss to lesion, an dincreased allodynia. Of note, time since SCI was not associated significantly with outcome measures at enrollment but WAS related inversely to level of improvement.
LIMITED recovery expected after 1 yr of injury
Only 1% of patients achieve full neurological recovery after injury!
SCI Outcome measures
Highly rec:
- Handheld myometry
- ASIA
- 10MWT
- 6MWT
- TUG
- Walking index for spinal cord injury (WISCI II) (acute 4, rehab 3)
(NPRS - 3 acute/subacute, 4 outpt, MMT, Berg, SCI Fxn’l Amb inventory, FIM, SCIM III, Needs assessment checklist; World Health Org Quality of Life - BREF [4 Chronic] also recommended)
SCI Recovery Expectations for…
ALL levels of injury
- Upright tolerance 10-12hrs/day
- Utilize appropriate seating system to support posture and maximize function
- Utilize appropriate mobility device(s) to maximize fxn’l independence and mobility
- Maintain intact skin
- Independnetly verbalize all assist needed w/ADLs and mobility
- Pt/caregiver indep w/all aspects of care
- Body habitus is imiportant for all levels of injury
Left Pelvic obliquity = __ side is lower
Left pelvic obliquity = LEFT side is lower (in coronal plane)
*Obliquities are named for the LOW side
Advantages and disadvantages to mid-wheel drive power wheelchair?
Smallest turning radius
Maneuverable indoors
BUT it is slower than a rearwheel drive, may fishtail when going downhill
Advantages and disadvantages to rear-wheel drive power wheelchair?
Easy to control on straightaways
Fastest speeds of any power chair options
Can be assisted ove ra curve
BUT also has largest turning radius, not great for indoor mobility d/t this
Advantages and disadvantages to front-wheel drive power wheelchair?
Small turning radius - tightest 90 deg turn which is really helpful for homes with smaller entryways and halls
Can be pulled over a small 2-3” obstacle
Slower maximal speed
Can fishtail at higher speeds
Less intuitive to learn to drive d/t wheel base in front of COM
What are the requirements for someone to qualify for a group 3 wheelchair?
- Writen order from physician stating mobility limitation is due to a NEUROLOGICAL condition
- Face to face mobility exam w/physician, with the note reflecting that the specific reason of the exam was for w/c assessment
- Home assessment (so w/c can actually fit/work in home setting)
- Eval by specialized PT/OT and ATP (supplier)
- Pt needs to require alternate drive control interface (e.g. head control, sip and puff, switch control) AND power tilt/incline OR ventilator
Group 2 w/cs have “captain’s chair” style seating and can go up to 3mph, but aren’t customizable, can’t tilt, etc. vs Group 3 goes a little faster (up to 4.5ish mph!), can get over 2” obstacles, have lots of options to customize, are more of a “rehab” chair
What features must someone need to justify a K0005 ultralightweight w/c to medicare?
- For medicare, pt must be a full time manual w/c user or require custom fitting/adjustment to one or more of the following:
- axle configuration needed for optimal propulsion, shoulders needs to be in line with or just in front of wheel axle
- Wheel camber: wheels angled toward body at the top and out/away at bottom - better for pushing, adds stability BUT wheelchair becomes wider overall, may be tricky in narrow environments
- Seat/back angle: opening this can create more balance/stability, can also accommodate for hip contraction contractures, also seat “dump” (angle from front to back to seat) can help to “lock in” pelvis - seat/back angle cannot be accommodated with K1-K4 options
Lower level chairs are not approp
Manual w/c frame type options
Rigid frames: more exact fit, often pts feel these are more comfy, more efficient, more durable, more lightweight. Have quick release axels to remove wheels to put in car.
- Box frame - boxy, can be difficult to transport
- Cantilever frame - may be a bit easier to load into/out of car given open frame. Better if someone will be an independent driver.
Folding frame - has center cross bar, can fold easily. Have more adjustability, accessories. Have swing away leg rests, make it easier to transition to propelling w/feet if needed. Easier to load into trunk of car.
How to select cushions for w/c?
Air cushion/ROHO
- pressure relieving
- BUT less stable for transfers/posture, more maintenance
Gel
- Pressure relieving, but not as great as air cushions for this
- More stable, lower maintenance
- BUT may be heavy
How to select cushions for w/c?
discuss Air cushion vs gel vs foam vs hybrid/honeycomb
Air cushion/ROHO
- pressure relieving
- BUT less stable for transfers/posture, more maintenance (to check height of air/degree of inflation)
Gel
- Pressure relieving, but not as great as air cushions for this
- More stable, lower maintenance
- BUT may be heavy
Foam
- Pressure relieving, but not as great as air or gel
- Stable for transfers/posture
- May be porous/incontinence issue
- Low maintenence
Hybrid/honeycomb
- Foam + air; gives stability for posture but some air might help w/pressure relief!
- May be a good balance for some!
Pressure mapping can help to select!
C2-3 injury
Functional outcomes:
- Mobility / type of w/c propulsion??
- Level of independence
Big concerns?
Primary points for rehab focus?
C2-3 injury
Functional outcomes:
- POWER w/c, with sip and puff, chin drive, or head array to propel
- INDEP with weight shifts (via power tilt) and indep to direct all care
Big concerns?
RESPIRATORY management! Most respiratory mm need innervation of at least C2-3, with some (e.g diaphragm) extending down through C4 or even C5
Rehab focus?
- Directing care
- Vent weaning (if able)
- Education
- Assistive technology (computer, phone access)
- Recovery of upright mobility when motor incomplete
Spinal level innervations of respiratory mm?
Diaphragm (C3-5) Scalenes (C2-3, CN XI) Upper traps (C3-4, CN XI) Levator Scapulae (C3-5) Facial mm (CNs) SCM (C2-3, CN XI) Traps (C3-4, CN XI)
C4 injury
Functional outcomes:
- Mobility / type of w/c propulsion??
- Level of independence
Big concerns/Muscles impacted?
Primary points for rehab focus?
C4 injury
Functional outcomes:
- POWER w/c, with sip and puff, chin drive, or head array to propel
- INDEP with weight shifts (via power tilt) and indep to direct all care
- Breathing without assist and performing assisted coughing
Big concerns/Muscles impacted? Respiratory function, starting to get a little innervation into UE muscles
- Diaphragm (C3-5)
- Scalenes (C2-3, CN XI)
- Upper traps (C3-4, CN XI)
- Levator Scapulae (C3-5)
- Infraspinatus (C4-6)
- Supraspinatus (C4-6)
- Rhomboids (C4-6)
Primary points for rehab focus?
Rehab focus?
- Directing care
- Vent weaning, respiratory mm training
- Education
- Assistive technology (computer, phone access)
- Recovery of upright mobility when motor incomplete
C5 injury
Functional outcomes:
- Mobility / type of w/c propulsion??
- Level of independence
Big concerns/Muscles impacted?
Primary points for rehab focus? What DO they have for movement?
C5 injury
Functional outcomes:
- POWER w/c with hand drive/mobile arms support
- INDEP with weight shifts (via power tilt) and indep to direct all care, still needs assist w/ADLs
Big concerns/Muscles impacted? THey have ELBOW FLEXION, SHOULDER FLEX, and SHOULDER ABDUCTION (though weak)
- Starting to get some but not full proximal UE function (flexors) and scapular stability
- HIGH risk for impingement given poor scapular stability during glenohumeral movement
- Scapular winging d/t limited innervation of serratus anterior (C5-7)
- Watch for development of elbow flexion contractures over time given no antagonist innervation
- Biceps C5-6
- Brachialis C5-6
- Brachioradialis C5-6
- Infraspinatus C4-6
- Deltoid C5-6
- Supraspinatus C4-6
- Pec major C5-T1
- Rhomboids C4-6
- Serratus C5-7
Primary points for rehab focus?
- UE strengthening: provide SCAPULAR STABILITY first, then work on distal mobility. Powder board, skates, air splints (to keep elbows straight), Swedish aid, inclined board, mobile arm support, and theraband all helpful!
- Pt assisting w/ADLs (Feeding, grooming)
- Prop sitting to support ADLs
- Education
- Assistive technology (computer, phone access)
- Driving (likely more OP goal)
- Recovery of upright mobility when motor incomplete
C6 injury
Functional outcomes:
- Mobility / type of w/c propulsion??
- Level of independence
Big concerns/Muscles impacted?
Primary points for rehab focus? What DO they have for movement?
C6 injury
Functional outcomes:
- Starting to think about power (group 2; wouldn’t need tilt or optimum drive control) vs manual w/c - many C6ers go for the middle ground with manual w/c with power assist wheels, but can be heavy. Scapular winging can still bel present at this level, needs stability if manual w/c!
- Independent weight shifts (lateral and forward; can’t do a depression/push up weight shift)
- Limited assistance for transfers and ADLs
Big concerns/Muscles impacted?
- Biceps (C5-6)
- Latissimus dorsi (C6-8)
- Extensor carpi radilais longus (C6-7)
- Pec minor (C6-T1)
- Serratus anterior (C5-7)
- Supinators (C6-7)
Primary points for rehab focus? What DO they have for movement?
We now have some distal stability with some wrist extension activation!! And back extensors from lats.
- TENODESIS GRIP important (passive shortening of finger flexors to use as gripping strategy with active wrist extension; don’t stretch those finger flexors!)
- Bed mobility (chain loops/things to hook and pull on can help initially. Start with legs crossed, then uncrossed as they progress. Momentum can help!)
- Propping and long sitting (need hamstring length: ~110* ROM for function! But DON’T overstretch low back, needed for passive stability). Prop w/elbows locked out via ER. Consider stability vs mobility arm, head/hip relationships.
- Level transfers (slideboard; need BIG anterior weight shift, flexing so chest is almost on legs to offload hips)
- ADLs (bowel program, ICs, showers, dressing - but takes a lot of TIME and is laborious)
- Driving
- Education
- Recovery of upright mobility when motor incomplete
C7 injury
Functional outcomes:
- Mobility / type of w/c propulsion??
- Level of independence
Big concerns/Muscles impacted?
Primary points for rehab focus? What DO they have for movement?
C7 injury
Functional outcomes:
- MANUAL w/c, working on mobility skills (curbs, ramps)
- INDEP mobility (transfers, bed mobility, weight shifts)
- ADLs without assist
- Household ADLs may require assist
Big concerns/Muscles impacted?
- Triceps (C6-8)
- Ext carpi radialis brevis (C7-8) and longus (C6-7)
- Extensor digitorum (C7-8)
- Pecs major and minor (C6-T1)
- Serratus (C5-7)
- Pronator Teres and flexor carpi radilis (C6-7)
- Flexor carpi ulnaris (C7-T1)
- Palmaris longus (C7-C8)
- Finger flexors (FDS and FDP: C8-T1)
- Flexor pollicis longus
Primary points for rehab focus? What DO they have for movement?
Now has full active elbow extension AND wrist flexion!!
- Bed mobility
- Level and unlevel transfers
- Depression transfers, floor transfers
- W/c mobility skills
- ADLs (bowel program, ICs, dressing, showers, home management)
- Driving
- Education
- Upright mobility when motor incomplete
Thoracic and Lumbar injuries
Big concerns/Muscles impacted?
Thoracic and Lumbar injuries
Big concerns/Muscles impacted?
- Hand fully innervated at T1 (intrinsic hand mm)
- Iliopsoas (L1-3)
- Quads (L2-4)
- Hamstring (L4-S3)
- Anterior tib (L4-S1)
- Ext hallicus longus (L4-S1)
- Gluteals (L5-S2)
- Gastroc (S1-2)
LE bracing with lumbar injuries
KAFO
RGO - decreased physiological cost of walking, lets you walk faster compared to using B KAFOs
HIGH energy expenditure, lots of UE force required, can result in shoulder injury
Brace walking needs great hip extension ROM (relying on Y ligaments) shoulder strength & ROM
Walking Index for Spinal Cord Injury (WISCI II)
Description: Quantifies pt’s ability to walk 10 meters post SCI based on:
- Level of assist (#of people needed to walk, how much asst)
- +/- bracing (unilateral vs bilateral long leg brace vs AFOs)
- Type of UE support (parallel bars -> walker -> 2 crutches -> 1 cane/crutches)
(also consider’s pt’s reported comfort level)
Scoring: 0 (unable) - 20 (walking w/out support, bracing, or help)
Less responsive in higher level individuals
