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227 Cards in this Set
- Front
- Back
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Neurological Classification of SCI
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Sensory Eval- tested by 28 dermatomes
-0=absent -1=impaired -2=normal -tested on both sides! Motor eval-tested by myotomes -tested on 5 point scale (N=5) -tested on both sides FIM |
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ASIA muscles and levels
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C1-4: sensory only
C5: biceps/brachialis C6: extensor carpi radialis L&B 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 hallicus longus S1: gastroc/soleus S2: sensory level |
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Do level of fracture and level of neurological injury correspond?
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NO!!
ASIA levels are neurological levels of function. Doctors name level of injury |
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Naming SCI
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-designate R vs L IF the function is different
-designate sensory vs motor IF the function is different SCI named by last NORMAL level of function |
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Quadriplegia/Tetraplegia
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-impairment or loss of motor and/or sensory function in the upper and lower extremities, trunk, and pelvic organs.
-result of a legion in the cervical cord |
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Paraplegia
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-impairment or loss of motor and/or sensory fxn due to damage in thoracic, lumbar, or sacral segments.
-function may be impaired in the trunk and/or lower extremities |
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Complete lesions
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total absence of sensory and motor function in the LOWEST SACRAL LEVELS (S4-5).
-tested by inserting a finger into the rectum. If pt feels, sensation is intact. -if pt can squeeze anal sphincter, motor is intact *ask if pt can stop urination or bm. Can they feel where they sit? |
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Causes of complete injury
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-complete severing of the cord
-transection of the cord -vascular impairment to the cord *professionals should only dx complete vs incomplete 48 hrs to 1 wk after injury when person has recovered from "spinal shock" |
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Spinal Shock
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4 phases. Body is still recovering.
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Spinal shock phase 1
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-complete loss or weakening of all reflexes below level of injury
-lasts 24-48 hrs -SC loses descending facilitation -neurons in reflex arcs lost input from brain. Less responsive to stimuli *no motor response no matter what you do at this stage |
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Spinal Shock phase 2
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-occurs over 2-3 days
-some return of some reflexes -first reflexes to reappear are polysynaptic -monosynaptic reflexes don't appear yet |
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Phases 3 and 4 of spinal shock
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-phase 3: 1-4 weeks
-Phase 4: 1-12 months -hyperreflexia -phase 3 due to axon-supported synapse growth -phase 4 spasticity due to soma-supported synapse growth |
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Interruption of the spinal cord
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Below injury= still has blood supply.
-sensory input can cause motor output or spasticity because brain is not there to mediate it. Bottom of cord is fine but just uncontrolled by the brain. (no input to or from the brain) |
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Nerve roots and SCI
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-nerve roots are often damaged as they exit the foramen
-frequently happens at the site of the lesion -function of mm innervated by those nn can be expected to return 6 mos after injury. *don't be fooled into thinking complete injury |
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How fast do nerve roots regenerate?
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i inch/month
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what is the prognosis for recovery for people with complete spinal cord injury?
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at this point in time, there is no prognosis for recovery for people with complete spinal cord lesions
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Zone of Partial Preservations
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-used only with complete injuries
-refers to partial preservation of motor or sensory function below the neurological level of injury |
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def of Incomplete Lesions
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-one in which there is partial preservation of sensory and/or motor function below the neurological level and in the LOWEST SACRAL SEGMENT
-incomplete lesions indicate that some viable neural white matter tracts are crossing the area injured and innervating more distal segments -damage from original injury frequently precedes secondary damage to the spinal cord |
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When is secondary damage usually complete?
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within 24-72 hours post trauma
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When is the drug for incomplete lesions effective?
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within 8 hours
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Types of incomplete lesions
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1. central cord syndrome
2. Anterior cord syndrome 3. Brown Sequard syndrome 4. Conus medularis lesions 5. cauda equina lesions |
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Central cord syndrome
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*most common incomplete SC lesion
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possible causes of central cord syndrome
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-anterior and/or posterior cord compression
-acute hyperextension injury -chronic or congenital conditions causing progressive stenosis -spondylosis -osteophytes -damage from microvascular compromise of center of cord |
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What happens in central cord syndrome
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-central gray matter is compromised first
-central white matter also compromised -any hemorrhage or edema begin in the center of the cord and spread to periphery *resolution occurs in opposite manner |
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Spinal cord breakdown
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Anterior- pain, temp
Lateral- motor Posterior- touch, pressure, pain *since damage happens inward out, cervical tracts most likely to be damaged, sacral tracts most likely spared |
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damage to grey horn in central cord syndrome
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if grey horn is damaged, it will never come back. No chance of recovery b/c it's not an axon. It's the cell body of the peripheral nerve
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Result of central cord syndrome
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-sacral tracts are least affected in all but dorsal columns
-followed by lumbar, thoracic, and lastly cervical |
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Clinical picture of central cord syndrome
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-bilateral flaccid paralysis and sensation loss due to loss of grey matter AT level of injury
-spastic paralysis BELOW the level of injury in the order previously listed -clients can regain motor function and sensation and will do so first in sacral, then lumbar, then thoracic, then cervical **progress may stop at any time |
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Prognosis for central cord syndrome
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77% regain ambulation
53% regain bowel, bladder, sex 42% regain hand function |
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Anterior cord syndrome
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extremely poor prognosis for return of motor function!!
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Cause of anterior cord syndrome
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-flexion injuries
-bone or cartilage compromises integrity of anterior spinal artery -frequently caused by teardrop or "burst" fractures of vertebral body *hyperflexion *common in older adults d/t osteoporosis, osteopenia |
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What happens in anterior cord syndrome?
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-ant spinal artery vascularizes the entire ant 2/3 of SC
-post spinal arteries only vascularize dorsal columns-which carry conscious proprioception, stereognosis, deep pressure, etc. *remains intact **pic in ppt 15 |
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Clinical picture for ant cord syndrome
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-bilateral flaccid paralysis and sensation loss d/t loss of grey matter AT level of injury
-spastic paralysis BELOW level of injury with voluntary motor and (pain and temp) sensory loss -post column function remains intact on both sides ***prognosis extremely poor for any motor return; bowel, bladder, or sex |
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cause of Brown Sequard syndrome
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-stab, gunshot wound, penetrating injury
-unilateral facet lock injuries -burst fractures at lateral body of the vertebrae *usually not a natural injury |
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What happens in brown sequard syndrome?
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one half of SC is damaged (very seldom exactly half)
-post dorsal columns travel up SC to brain. Paths cross in brainstem (pons area) -lat and ant spinothalamic tracts carry sensory (pain, temp) info up from body to brain. cross immediately -motor (corticospinal) from brain to body. Cross in midbrain |
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Clinical picture for brown sequard syndrome
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-ipsilateral flaccid paralysis and sensation loss due to loss of grey matter AT level of lesion
-BELOW level of lesion 1. white matter damage leads to ipsilateral loss of motor and post column function (deep pressure). Spastic paralysis 2. white matter damage also leads to CONTRALATERAL loss of pain, temp several levels below level of injury **LE will have pain, temp on one side. touch on the other. One of the best injuries to have |
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clinical picture for brown sequard syndrome
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-prognosis is very good
-nearly all patients are able to walk, although some with orthotics on one leg and with a cane 80% regain hand function 100% regain bladder function 80% regain bowel function |
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Conus medularis lesions
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T10-T12
*most lower T lesions lead to flaccid paralysis of legs because blood and swelling pools in bottom of SC causing anterior horn damage |
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Cause of conus medularis lesions
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injury to bottom of spinal cord and lumbar nerve roots
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What happens in conus medularis lesions
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results in flaccidity and lack of return of bowel, bladder, or sexual function
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Prognosis of conus medularis lesions
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if bottom of cord is damaged, there will be no return of function
**poorest prognosis for future return...even with advances in medical care |
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Clinical picture for Cauda equina lesions
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-injuries at L1 or below
-damage occurs to cauda equina, NOT SC -because they injure peripheral nerves, flaccid paralysis with NO SPASTICITY -severe pain, parasthesia, burning, tingling |
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Prognosis for cauda equina lesions
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*EXCELLENT! peripheral injuries regenerate!
-pain can be a limiting factor to return of strength and function -avg clients will NOT regain calf and foot intrinsic strength. may require orthotics |
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ASIA impairment scale
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A= complete. no sensory or motor function is preserved in sacral segments S4-5.
B=Incomplete. Sensory but not motor function is preserved below neurological level and includes sacral segments S4-5. C=Incomplete. Motor function preserved below the neurological level and more than half of key mm below neurological level have a mm grade less than 3 D= Incomplete. Motor function preserved below neurological level, and at least half of key mm below neurological level have a mm grade of 3 or more E= normal |
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Administering ASIA
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touch once. Don't rub! Rubbing elicits more of a response because of stimulation.
Light touch=culmination of ant spinothalamic and dorsal column tract-won't feel unless both are intact. |
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C1-3 Quadriplegia
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-head and neck extensors
-sternocleidomastoid (C2,3) |
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breathing at C1-3
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-need a vent, respirator, or phrenic nerve stimulator b/c diaphragm is innervated at C3,4.5
-max assist with resp hygiene including cough, deep breathing -monitor closely for upper resp illness -abdominal binders may assist with forced voice production -suctioning required for those ventilator dependent |
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functioning at C1-3
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-completely dependent for all care (bed mob, transfers, feeding and eating, driving, hygiene)
-power chair with tilt, recline, and power elevating legs -adapted van -lifts in home essential for easier care -power chairs need vent trays and vent transport |
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Pressure relief at C1-3
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-use tilt, recline
-ROHO required -ROM-pay special attention to: hamstrings heelcords elbows wrist shoulders **keep joints stretched. Contractures make it hard to be functional. Special attention to 2 joint muscles *hoyer lifts not good for showering. Can't go under tubs |
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C4 Quadriplegia
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trapezius C3-4
Diaphragm C3,4,5 *ability to shrug, depress shoulders |
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Breathing at C4
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-still need max A for resp hygiene including cough, deep breathing
-clients require very close monitoring with upper resp illness -abdominal binders helpful with voice production |
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wheelchairs and function at C4
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exactly like C3 except no vent/resp/suction
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C5 quadriplegia
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deltoid
biceps C5,6 teres minor supraspinatus infraspinatus *added shoulder flexion, extension, abduction. Can do some elbow mvmt due to biceps. *can make it through day pretty independently after help getting ready. Can use biceps, ant delt to feed after someone assists with wrist cuff. Camelback for drinks. Cath. |
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what are the biggest concerns at C5?
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breathing, resp control, and resp toilet
-pneumonia and pulmonary embolism are largest causes of death at this and previous levels *no ability to cough |
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C5 presentation
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-first level with elbow flexion!!
-elbow ext is NOT present, contractures occur easily -post portion of rot cuff is innervated -shoulder ext rot stronger than int rot *elbow contractures prevent ability to throw arms back to prop **weak vs strong |
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Weak C5 quadriplegia vs Strong C5 quadriplegia
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Weak-has biceps and shoulder mm of fair or less
Strong- biceps/deltoid F+ or better, shoulder mm present are strong |
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Function at C5
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1. Wheelchairs
-most use power to conserve energy -energy cost of manual chair is unreasonable. Can use quad knobs for short distances. -Usually can use hand to drive when resting on a U joystick -wrist ext splint can help hold wrist in neutral -ROHO -usually dependent for mgmt of legrest, armrest, brakes -universal cuff as part of wrist splint |
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Mobility at C5
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Bed mob- totally dependent, instruct others on care
Transfers-usually dep, can begin to assist with sliding board -usually have hydraulic lift..medicaid will help with -pressure relief 15/15 with good cushion. Use biceps -turn every 2 hours in bed. waterbed best. -can brush teeth, wash face. Max A shaving, brushing. feeding, bowel, bladder dep. Can do some UE dressing |
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ROM for C5
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pay special attention to...
-hamstrings -heelcords -elbows-flexion, no ext -wrists- need splint for stability -shoulders- need hyper ROM for stability *prone on elbows is a good position to stretch mm that get tight from sitting |
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C6 quadriplegia
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tenodesis grip
-subscapularis -ext carpi radialis longus (tenodesis) -serratus anterior *select few can become indep with wc and bed mobility but takes all of their energy *all elbow flexors in at this level |
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Tenodesis grip
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-starts at C6
-only works if you have allowed flexors to become tight!! -can stretch flexors but only with wrist flexed! (long flexors are the important ones) |
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C6 take home points
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-full innervation of rotator cuff
-full scapular stability and strength -strong int rot, adduction, ext of GH joint-makes a huge difference in transfers -full elbow flexion -no elbow extension -first level with any wrist function (ext) which allows tenodesis grip -rare but possible total independence *often accompanied by TBI |
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C6 Function
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Breathing- as before. no thoracic mm
-possibility of manual wc. MUST be ultralight. Pull-to mobility -many have power wc. tilt, recline, power legrests. -regular joystick is usually okay. -ROHO *medicare codes for power wc at this level *work on ways to clear airways |
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Bed mobility and transfers at C6
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Bed mob- can be ind in sitting, rolling, and wc pushups
-sitting balance in non-supported position is fair -VERY FEW can transfer without assistance -nearly all need help getting off floor *important to let back mm get tight. Hang on back ligaments to sit-no trunk control. Hamstrings at 110 to long sit. |
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Pressure relief at C6
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independent with side to side method, or leaning forward using push bar on back of wc for stability
-many use tricep substitution push-up for pressure relief -tilt and recline in power wc |
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ROM in C6 quadriplegia
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Selective hypermobility:
-hamstrings-need 110 deg to prevent stretching lower back -heelcords- feet stay on footrest -elbows-people have flexion, not ext so flexion contractures are common -shoulders Selective hypomobility: -allow long fingers to become tight for tenodesis grip -allow back extensors to become tight for passive sitting control |
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C6 ADL/IADL
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dependent for feeding, grooming, bathing, bowel, bladder
-can assist with UE dressing -max a for shaving, brushing teeth -can feed with mobile arm |
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C7 quadriplegia
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**fully independent at this level except elderly, obese, not fit
-triceps -flexor carpi radialis -extensor digitorum *have radial wrist mm but not ulnar. extend wrist and mp joints only -all shoulder prime movers innervated -full elbow extension -full wrist extension -no wrist flexion **still use tenodesis grip *breathing as before. no fxn in thoracic mm *can consistently use manual wc. MUST be ultralight -ROHO |
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bed mobility and transfers at C7
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-independent in all bed mob
-indep for transfers -very few can do floor transfers |
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pressure relief at C7
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indep using push-up method on wc armrests or wheels
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C7 ROM
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selective hypermobility:
-hamstrings -heelcords -wrists -shoulders Selective hypomobility: -tight long finger flexors for tenodesis grip -tight back extensors |
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ADL/IADL at C7
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-indep with self-care, feeding, eating and hygiene.
-may need assist for bowel, bladder care -most need adaptations to hold and manipulate objects, use loops, etc |
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C8 Quadriplegia
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flexor digitorum prof and superficialis
extensor carpi ulnaris flexor carpi ulnaris -can flex fingers now. grip still weak (no interossei) -can't extend fingers. **pillars for transfer |
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breathing at C8
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as before...no thoracic mm
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mobility and transfers at C8
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-indep for manual wc (must be ultralight)
-Roho -indep in bed mobility -indep for transfers without sliding board -most can do floor transfers |
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ROM at C8
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selective hypermobility:
-hamstrings -heelcords -wrists -shoulders Selective hypomobility: -tight long finger flexors for tenodesis -tight back extensors for sitting |
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ADL/IADL at C8
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-independent with all self-care, feeding, eating, hygiene
-indep with bowel, bladder care -most indep without equipment for self-care |
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T1 Quadriplegia
T2-6 Paraplegia |
dorsal and palmar interossei (T1)
lumbricales *have hand function and progressive trunk function (as levels progress) |
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Breathing at T1-T6
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as before BUT better and better as it gets lower. Resp toilet NOT complete until abs fully innervated
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Mobility at T1-T6
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-wc management, bed mob, transfers, ADLs completely independent
-MUST have ultralight chair Roho -can do floor transfers -wc pushup for pressure relief |
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T1-T6 ROM
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selective hypermobility:
-hamstrings -heelcords -wrists -shoulders Selective hypomobility: tight back extensors until trunk is strong |
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Testing ab innervation
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have pt lift shirt and see if belly button moves up when they tighten abs. Belly button is T10
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Energy cost of walking with orthotics
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double energy of walking. Same with wc
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Precautions for walking
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-health circulatory system-huge energy demand
-healthy legs: no DVT, minimal swelling, ulcers -healthy skin: no pressure sores -bony skeleton intact: osteoporosis prevalent if walking after one year |
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Requirements for walking
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-normal ROM in legs:
110 deg hamstring length 10 deg of dorsiflexion -UE strength and endurance able to propel a mile in wc without rest |
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Walking at C8 or higher
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not feasible
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T1-9
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-may be able to walk for exercise only, ambulation not realistic
-will need hip, knee, ankle and foot orthoses -need parallel bars, forearm crutches, or walker -will probably only mange swing-to gait |
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T10-12
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-better potential, trunk fully innervated
-huge energy cost, household ambulation -knee, ankle, and foot orthoses -need forearm crutches or walker -most can use swing through gait pattern |
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L1-3
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-potential continues to improve
-huge energy cost, some limited community gait -knee, ankle, foot orthoses -need forearm crutches -most use 4 pt gait pattern -full hip extension allows to hang on ligaments |
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L4-5
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-very strong hip flexors and full quadriceps
-still have huge energy cost -need AFOs to control foot drop -no or weak gluts, hang on ligaments -use post lateral trunk lean -need forearm crutches, auxillary crutches, or 2 canes -2 to 4 pt gait pattern |
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S1-3
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able to achieve full community gait
-until no AE, energy is still double *still need wc for distances -need AFOs until plantar flexors innervated ***AFOs no longer needed -hang on ligaments until normal gluts -need one or 2 canes -use 2 or 3 pt gait pattern |
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high level wheelchair skills
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wheelies
rough, uneven terrain curbs stairs falling ramps |
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Community re-entry performance areas (SCI)
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home and community access
self-care need for caretakers leisure transportation/functional mob school/work wellness/aging/support groups |
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Our role in home and community access
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-home eval; AT availability
-ADA, self advocacy -negotiate ramps, curbs, stairs -community bathroom transfers -educate about accommodations at stadiums, concert halls, etc -travel |
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Our role in self-care
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dressing and undressing (buying clothes)
toileting eating storage for items (backpack, fanny pack) |
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Our role in leisure
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-adaptation to previous leisure interests
-intro to new interests -transportation and financial access to leisure -wheelchair sports |
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Our role in transportation/functional mobility
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-adaptive driving
-van or sedan -full size van or not -drive from chair or not |
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Our role in school work
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-assess previous roles and interests
-perform environmental modification or activity adaptation for role resumption -explore new ideas/interests -know resources -make appropriate referrals |
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Wellness/Aging in SCI (special considerations)
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osteoporosis and arthritis
kidney disease heart disease bowel disease pressure sores respiratory disease musculoskeletal pain |
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Cerebellum
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-cerebellum can be damaged by brain injury, CVA, MS, and alcoholism
-cerebellum has large role in motor learning, motor control, and in connecting regions of brain and SC -cerebellum coordinates mvmt, planning, motor activity, learning and remembering physical skills, cognition -cerebellum plays a role in posture, walking, eating, tracking |
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Ataxia
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problem with cerebellum
movements appear difficult and clumsy |
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Damage to cerebellum affects motor control on what side of the body?
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ipsilateral
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Definition of ataxia
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-incoordination or clumsiness of movement that is not the result of muscle weakness
-can affect gait, upper and lower extremities, speech, eye movement |
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Other causes of cerebellar ataxia
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-damage to cerebellar input and output structures (thalamus, vestibular nucleus, and sensory neuropathy)
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Medial and intermediate zones of anterior lobe
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-appear to control equilibrium
-preferentially involved in gait and stance -people with lesions here have difficulty with standing still, walking, and higher level gait |
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Lateral cerebellar structures
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-control of multijointed limb movements especially reaching and pinching
-also controls movement to visual targets -people with lesions here have difficulty with ADLs |
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Flocculonodular lobe
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-oldest lobe in the cerebellum
-highly connected with vestibular system -lesions ALSO cause balance and equilibrium issues -oculomotor disturbances -most severe mobility disruptions |
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What might you observe in a client with ataxia during an assessment?
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1. balance and equilibrium problems
-postural sway -delayed equilibrium reactions -lack of response to environmental cues -loss of motor learning about gait 2. muscle tone changes -hypotonicity -can correct with attention to task at hand -distal movements almost impossible, can move if proximal supported 3. Dysmetria -deficit in reaching a target -sudden release of force (MMT) can lead to extreme mvmt -mvmt from shoulder separated from elbow -grip strength not appropriate for task 4. Movement decomposition -inter joint movements disconnected -dysdiadochinesia-can't perform rapid alternating movements -Adiadochokinesia- can't make rapid alternating mvmts and seem to reflect abnormal agonist-antagonist control 5. Tremor -attention tremor -postural tremors can also occur. unable to hold posture against resistance 6. Eye movements -nystagmus, inability to track -test by asking client to track object and fixate while turning head 7. Dysarthria |
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Most important test for ataxia
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Funtional testing
-bed mob, posture -ability to move supine to sit -maintain sitting posture -sit to stand -maintain standing posture -ambulation -dress, groom, eat, toilet |
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Other clinical tests for ataxia
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Postural sway
-in quiet standing, eyes closed, feet together Gait analysis Reaching analysis Sensory testing Strength testing Endurance testing |
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Cerebellar clinical testing
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-finger to nose test
-make sure finger to nose test requires movement at more than one joint. Move more normally when they limit mvmt to one joint |
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Intervention for ataxia
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-synthesize result of assessment and physical finding
-what systems are involved? -what systems are intact? -info will assist in determining intervention strategy -sensation -vision -strength -tone -what cerebellar interference is present? -can u modify task or environment |
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Things that help with ataxia
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-compensation!
-little to no neuroplasticity -lesions tend to worsen over time -assistive device -splints and orthotics -bracing if possible -power mobility -modify the household -change tasks and make ADL easier |
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Specific intervention for ataxia
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-change movement patterns: splinting or casting to reduce number of joints pt needs to control, reduce speed of mvmt
-strength and endurance training -if sensation NOT involved, teach to compensate with vision or proprioception |
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Top ten complications for people with spinal cord injury
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10. respiratory complications
9. skin problems 8. orthostatic hypotension 7. deep vein thrombosis 6. thermoregulation 5. spasticity 4. urinary tract infections 3. heterotropic ossifications 2. GI complications 1. Autonomic dysreflexia |
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respiratory complications in SCI
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-inspiratory mm paralysis
diaphragm (C3 and above) external intercostals T1-T12 expiratory mm paralysis abs innervated through T12 internal intercostals through T12 important for forceful expiration and coughing *pulmonary complications primary cause of death |
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Respiratory complication management
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-upright position as soon as possible
-re-train breathing patterns -alternate methods of coughing -encourage deep breathing C5-C8 vital capacity 30% of normal **paradoxical breathing |
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orthostatic hypotension
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-combined frequently with LE edema, blood pooling/venous stasis
-patients feel dizzy |
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managing orthostatic hypotension
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-over time cv system reestablishes enough vasomotor tone to allow resumption of normal upright positions
-initially, gradual resumption of upright helps -abdominal binders and long hose to prevent blood pooling -ephedrine may assist to increase BP, as do low dose diuretics |
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Deep vein thrombosis
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notable swelling
tx is bedrest with no passive or active ROM, meds pulmonary embolism in 5-15% of people with DVT |
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thermoregulation
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controlled by ANS
-interrupted in SCI -no temp control below level of lesion -inability to shiver or sweat |
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Urinary tract infections
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affect 80% of people in acute phase
-to cath or not? |
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Heterotropic ossification
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signs: decreased ROM, swelling, heat, redness, fever
-most frequent in mid thoracic or cervical lesions -hips, knees, shoulders and elbows involved in that order |
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GI complications
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treat with fiber and routine, suppositories
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autonomic dysreflexia
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-sympathetic nervous system overreacts to a stimuli. Parasympathetic system can't respond, so BP rises
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causes of autonomic dysreflexia
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-distended bladder or bladder infections
-bowel implications or other problems -decubitis ulcers -ingrown toenails -stretching hamstrings..stimulation of genitals -exposure to high temp |
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signs and symptoms of autonomic dysreflexia
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*sudden severe headache
-hypertension -chills without fever -sweating above lesion -decreased heart rate |
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Treating autonomic dysreflexia
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**medical emergency
-immediately elevate head-move to sitting (causes hypotension, drop in bp) -check for causes and alleviate if possible |
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What 3 things do we assess for autonomic function, according to ASIA?
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1. general autonomic function
2. lower urinary tract, bowel and sexual function 3. urodynamic evaluation |
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general autonomic function
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patients with SCI do not always retain accurate autonomic control of the heart. In this section, note problems with autonomic control of
1. bradycardia 2. tachycardia 3. other problems And of BP by noting 1. resting systolic bp below 90 2. orthostatic hypotension 3. autonomic dysreflexia-patients above T6 |
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hyperhydrosis
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non-physiologic sweating above or below lesion that occurs in response to noxious or non-noxious stimuli
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hyper and hypothermia
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above 101.3 F or below 95.0 F
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General autonomic and somatic control of bronchopulmonary system
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Therapists note "normal" or
1. inability to voluntarily breathe 2. impaired voluntary breathing 3. voluntary respiration impaired, no vent *resp usually impaired until T12 |
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Types of bladders
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1. Areflexive- occurs when sacral reflex arc dysrupted- urinary retention- renal failure
-manage through catheters 2, Reflexive- intact reflex arc-lack of connection to cortex -bladder empties reflexively with sufficient stretch, can trigger, may need to cath or learn to hold between voidings |
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Bowel control
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assess patient's ability to:
-sense need for bm -prevent stool leakage -voluntary sphincter contraction |
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Reflexive bowel
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if S2-4 have intact reflex arch, bowel functions reflexively. Anal sphincter remains taut and relaxes reflexively when rectum is distended.
*patients can get into bowel routine with suppository, anal stim |
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Areflexive bowel
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defecation reflex remains intact, but stronger parasympathetic defecation reflex is lost so bowel will not empty reflexively
-can lead to impaction *routine suppositories, anal stim, massage can help |
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Assessment of sexual function
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note if patient is capable of:
1. genital arousal, phychogenic or reflex 2. orgasm 3. ejaculation 4. sensation of menses |
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Guide to planning exercise/activity for arm function
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-level of injury
-orthopedic eval of capsular structures, mm tension, nerve tension, pain levels, sensation, ADL needs -previous history: changes in joint or rot cuff |
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Complications with arm function
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-bilateral shoulder pain
-risk factors: >50 dec PROM not initiating ROM within 2 weeks -very serious complication given dependence on UE for ADL, transfers |
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Etiology of shoulder pain
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-weakness of shoulder girdle mm, especially that which occurs with c6 and higher:
contributes to mm shortening, capsular tightening, mm imbalance -neuritic pain from nerve root injury or radicular pain with parasthesias, phantom sensations OR reflex sympathetic dystrophy -referred pain to shoulder from neck or trap -direct trauma during initial accident -indirect trauma (poor positioning, rolling methods) -pre-existing shoulder dysfunction -psychological issues related to control, secondary gain, manipulation |
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Other UE complications after SCI
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-overuse injuries
-lateralization of the thumbs secondary to wheelchair propulsion; can affect the strength of opposed pinch -general loss of joint motion, atrophy, contractures |
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Promoting optimal conditions for UE maintenance and control
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-positioning
-educate re overuse and train for management |
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Smart mm strengthening after SCI
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-gravity assisted--gravity eliminated--against gravity--resistance training
-isometric--eccentric--concentric -adapt exercise for loss of hand control -use neuromuscular re-education principles (e-stim) |
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Basics for UE after SCI
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-UE control enhanced by proximal stability, therefore, we must address head and trunk control control when looking at UE return
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What do we need for effective tenodesis?
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-shortening of FDP/FDS
-shortening of FPL for thumb approximation to fingers -avoid excessive stiffness in MPs and IPs of fingers -encourage stiffness in IP of thumb for greater stability of pinch |
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When to decide to preserve tenodesis
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-decision only as good as medical tests given
-many times we are told someone has had a complete injury and they have function -preserve for one year to be sure you don't miss residual function -at ou, preserve in all c4 and above |
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Tenodesis Rehabilitation
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-no difference between biofeedback, e-stim, or combination with regular functional training
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UE intervention for C1-3
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Goals:
1. limited head control 2. prevent pain Interventions: -headwand and mouthstick -teach competent and thorough PROM to client ASAP |
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C1-3 splints
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-prevent hand contractures to minimize pain
-worn at night |
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C4 UE intervention
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Intervention goals:
1. maximal head control 2. limited scapular control 3. prevent UE pain/hand contractures Interventions: -mouthstick activities -swedish sling -Facilitate: strengthen upper, middle, lower trap function and PROM; if complete-tenodesis is not an issue -prevent shortening of trap; resting pan splint in wc armrest |
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C4 Hand splints
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-prevent hand contractures
-worn at night |
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Intervention for C5 UE
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Intervention goals:
1. limited trunk stability 2. limited, assisted arm placement 3. preserve tenodesis hand function Interventions: -control with short, long, cross leg sitting -PNF patterns, any challenging activity to inc strength -teach competence using both arms to hook on back of wc or using a loop on wc to inc trunk mobility |
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C5 shoulder intervention: Goal of limited arm control
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-strengths: ext rot of shoulder, some flex, abd; elbow flex and sup of forearm
-challenges: IR<ER Interventions: -progressive exercise -PNF -theraband -functional activity -balanced forearm orthoses -positioning to prevent elongation; hand mitts & wrist support to exercise |
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C5 elbow/wrist/hand
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-goals to preserve tenodesis
-strengths: elbow flex and sup -challenges: no hand function Interventions include: -weight bearing with wrist ext, finger flex -all ROM through tenodesis fxn -electrically-powered tenodesis splints; radical wrist and thumb spica to maintain web space -elbow ext splints -progressive exercise |
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C5 hand splint
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-wrist is supported in extension- no true tenodesis unless splint is electric
-cuff made for utensils |
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C6 Intervention for UE
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Intervention goals:
1. limited trunk stability 2. unassisted, limited arm placement 3. tenodesis hand function Interventions: -same as C5 -progress to stability with all -greater use of UE inc ability to stabilize trunk during ADL -goal is unassisted, limited arm placement -progressive ex, wrist and hand supports as needed -accurate arm placement for function with attn to trunk control -goal is to use tenodesis for hand fxn |
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C6 hand splint
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-strengthen wrist ext so that tenodesis can be used
-thumb spica splint gives some stability for pinch -if wrist too weak, need to include in splint like C5 -quad cuff for phone use, electric razor, etc |
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C7 UE goals
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Intervention goals:
1. fair trunk stability 2. full arm placement 3. tenodesis hand function Interventions: progressive trunk activities as seen in C5-6 goal is full arm placement: -practice arm placement accuracy goal is tenodesis hand fxn, more thumb: -progressive activity -hand splint |
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C7 hand splint
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-will generally only use for training as may be able to use evolving strength in thumb w/out support
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C8 injury UE goals
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Intervention goals:
1. trunk stability 2. limited natural hand function Interventions: -advancing PNF patterns -advanced occupational sitting tasks -bilateral UE tasks from wc level Goal for limited, natural hand function |
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T1 goals for UE
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Intervention goal:
1. normal hand function Strengths: limbricales, opponens, interossei Challenges: above are weak Interventions: progressive activity, exercise |
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Dealing with UE complications
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-know your etiology
-treat orthopedic conditions on impairment level -analyze activity and modify mvmt to prevent further pain/injury -educate on life-long process for care of the UEs |
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Guillian-Barre Syndrome
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demyelinating inflammatory polyradiculoneuropathy
-affects nerve roots -affects PERIPHERAL nerves -leads to motor neuropathy and flaccid paralysis *destroys myelin sheath. If doesn't recover, nerve may become affected and die causing permanent damage and disability |
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How does Guillian Barre progress?
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-rapidly evolving, symmetrical onset of weakness or flaccid paralysis
-decreased DTR -20-30% become so weak they need resp support -5% die from resp distress or organ failure -50% develop cranial nn weakness primarily in facial nn |
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Sensory problems in GBS
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-hyperesthesias, parasthesias, numbness and dec vibratory or position sense are common
-sensory distribution loss frequently stocking/glove patterns |
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Pain and prognosis in GBS
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-pain is symmetrical aching in larger mm groups
-recovery usually starts 2-4 wks after progression stops -most reach full extent of paralysis by 3 weeks |
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Long term deficits in GBS
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-weakness in ant tib
-weakness in hand and foot intrinsics -weakness in quadriceps -weakness in gluts |
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Medical treatment in GBS
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-watch for resp failure
-watch for aspiration from oral mm weakness or paralysis -plasma exchange demonstrates promise -IV immunoglobin shows promise |
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Therapy for GBS
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-chest PT
-oral-motor eval -Pain (TENS) -ROM/stretching to prevent contractures -positioning with good skin care -splints, casting, positioning devices -tolerance to upright -progressive program of active exercise while monitoring for overuse and fatigue |
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Rule of thumb for exercise in GBS
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exercise will not hasten or improve nerve regeneration, nor will it influence the reinnervation rate during the rehabilitation process
-goal is to keep pt mm in a ready state -avoid mm fatigue *provide rest |
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Progression of exercise with GBS
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-short periods appropriate to the patient's strength
-inc this only if pt improves or if there is no deterioration after 1 week -return to bed rest if a dec in fxn or strength occurs -direct exercise at strengthening for FUNCTION, not for strengthening itself! -limit fatigue for 1 year! |
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Polio/Infantile paralysis
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-means inflammation of gray matter of spinal cord
-destroyed nn cells in anterior horns of SC and brain stem -primary theory of virus transmission is feces -most people experienced as flu like symptoms -most experienced some level of recovery and all encouraged to use mm in superhuman ways |
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Polio recovery
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-surviving motor neurons in brain stem and SC extend new branches called axonal sprouts to reinnervate mm fibers that have lost motor nerve supply
-mm function may be fully or partially regained -new axonal sprouts innervate several times the mm fibers that ordinary neuron would supply |
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Post Polio Syndrome
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-new mm weakness and other symptoms including problems swallowing, breathing, and sleeping occurring at least 15 yrs after initial infection and lasting >1 yr
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Two general presentations of post polio syndrome
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1. flu-like- generalized exhaustion, difficulty with concentration and memory
2. Muscular- decline in mm strength with exertion; lack of endurance |
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What causes post polio syndrome?
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-distal degeneration of overextended motor neurons
-surviving motor units can't sustained increased metabolic demand to contract more often to achieve same force of contraction -new fragile axonal sprouts degenerate -nm junction transmission defects -relative weakness may lead to joint and mm misuse and overuse |
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Intervention for post polio
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-management of weakness
-strengthening exercise -aerobic exercise -stretching to prevent/decrease contractures - avoid specific mm overuse -bracing -weight loss -assistive device -energy conservation |
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Intervention for weakness from post polio
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-inc mm capacity to improve functional capacity
-no proof mm overuse is contraindicated -custom exercise program -must determine individual mm strength -establish level of peak performance--work up from 50% |
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Assistive devices for post polio
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-braces
-canes and crutches -wheelchair -scooters |
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Interventions for pain in post polio
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-modify lifestyle, environment, task
-modalities -strengthening -assistive devices -orthosis -NSAIDs |
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Physchological implications of PPS
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-polio perceived as something in the past
-difficulty adjusting to re-emergence of problems associated with polio -depression |
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what is the largest risk factor for parkinson's?
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increasing age
-avg age of onset is 61 |
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What 2 things are liked with reduced risk of parkinsons
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caffeine
smoking |
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What happens in parkinsons
|
-severe loss of dopamine (neural transmitter) in substantia nigra in the basal ganglia of midbrain
*60-70% loss before the first symptom *dopamine produces smooth and controlled movements |
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Lewey bodies
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-abnormal aggregates of protein that develop inside nerve cells in parkinsons
*identified by autopsy -may be associated with nerve cell death |
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Diagnosing Parkinsons
|
depends on presence of at least 2 of 3 cardinal motor signs:
1. resting tremor 2. rigidity 3. bradykinesia- slowed mvmt *plus postural instability with poor balance |
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Other symptoms of Parkinsons
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constipation
difficulty swallowing choking, coughing, drooling excessive salivation excessive sweating loss of bowel/bladder control loss of intellectual capacity anxiety, depression, isolation scaling, dry skin on face or scalp slow response to questions small cramped handwriting soft, whispery voice |
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what is the definitive test for Parkinsons
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patient's reaction to dopamine. Idiopathic Parkinsons starts on one side of body. Definitive only through autopsy
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Direct or primary impairments of Parkinson's pathology
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Muscle rigidity
-cogwheel rigidity -leadpipe rigidity Hypokinesia -bradykinesia Resting or pill rolling tremor Motor freezing during movement Loss of motor planning ability Visuoperceptive dysfunction Postural instability Micrographia (tiny handwriting) |
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Cardiopulmonary complications in parkinsons
|
-orthostatic hypertension
-cardiac arrythmias -airway dysfunction-aspiration pneumonitis -venous pooling in LE |
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Assessing disease progression in Parkinsons
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Unified Parkinsons Disease Rating Scale
Modified Hoehn and Yahr Scale ADL scales |
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Hoehn and Yahr Disability Index for Parkinsons
|
1- minimal or absent; unilateral if present
2- minimal bilateral or midline involvement. Balance not impaired 3- impaired righting reflexes. Unsteady when turning or sit to stand. Some restriction of activity but can live independently 4- all symptoms present and severe 5- confined to bed or wheelchair |
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At what stage do falls become a major problem?
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Stage 3
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Dopamine replacement for Parkinsons
|
Levadopa and Cabidopa
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Signs of dopamine toxicity
|
-on,off episodes: sudden freezing or fluctuations in motor performance
-dyskinesias -psychiatric toxicity -cardiac arrythmia and orthostatic hypotension |
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Other treatments for Parkinsons
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Surgical interruption of basal ganglia circuits
pallidotomy, thalomotomy deep brain stimulation fetal and stem cell transplant |
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Therapy for Parkinsons
|
Cueing strategies
cognitive movement strategies work on balance physical capacity |
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Cueing strategies for parkinsons
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Auditory: walkman, metronome, counting
Visual: stripes on floor, focus on object Cognitive: mental pic of step length |
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Why do cognitive movement strategies work
|
they substitute for missing automatic pattern...reorganize to cerebellum instead of basal ganglia
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Working in balance for Parkinsons
|
-patients emphasize visual and vestibular feedback
-combine this with leg strengthening |
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Physical capacity and Parkinsons
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ROM
Stretching Functional mobility and ADL training Strength training |
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Most important for exercise with parkinsons
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big gross body movements!!
*dance, bicycle... |
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Criteria for dementia
|
-loss of intellectual abilities severe enough to interfere with function
-memory impairment including recent and remote memory -plus at least one of the following: 1. impaired abstract thinking 2. impaired judgement 3. other disturbance in higher cortical functioning |
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Reversible dementias
|
psychiatric disorders
medication side effects nutritional disorders metabolic disorders obstructive or normal pressure hydrocephalus |
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Irreversible Dementias
|
Alzheimer's
multi-infarct dementia AIDS dementia MS dementia PArkinson's dementia Huntington's dementia Pick's disease |
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What is Alzheimers
|
irreversible, progressive brain disease that slowly destroys memory and thinking skills
-although risk increases with age, in most people symptoms first appear after age 60, AD caused by fatal disease that affects the brain |
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Science of Alzheimers
|
neurons have to communicate, metabolize, and repair themselves. Alzheimer's affects all 3 areas
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What are the hallmarks of Alzheimers
|
plaques and tangles
Plaques-dense deposits of protein around nerve cells Tangles- twisted fibers built up inside nerve cell **protein called tau helps stabilize microtubules. In AD, tau changes. Trying to make meds to keep tau stable |
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Tools used to help diagnose AD
|
-detailed patient history
-information from family and friends -physical exams and lab tests -neurophyschological tests -CT, PET, MRI |
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Preclinical AD
|
*memory loss is the first sign
-signs are first noticed in entorhinal cortex, then proceed to hippocampus -affected regions begin to shrink -changes begin 10-20 yrs before symptoms appear |
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Mild AD
|
-cerebral cortex begins to shrink
-deficits include impaired learning, can't attend to task in complex environment, losing things, word finding -interventions: memory aids, central location for possessions, ask simple questions, avoid correcting errors, respect denial as a coping skill, protect safety |
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Moderate AD
|
-intervention focused on changing the environment and helping caregivers to cope
-confusion and disorientation, safety concerns, difficulty with self care, perseveration, sleep disturbance, angry outburst, agitation -Intervention: repetition, minimal distraction, focus on big picture, change environment for safety, simple instruction, humor, distraction, regular exercise and sleep habits **blocked practice |
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Severe AD
|
-extreme shrinkage in brain. Completely dependent for care. Ultimately results in death
-symptoms include dec recognition of faces, unable to dress, eating problems, incontinence, immobility, skin breakdown -Intervention: use routine, links from past and environmental cues, reassurance and repetition, avoid correcting, avoid rushing, eliminate safety hazards |
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Coping strategies for managing difficult behaviors in AD
|
-stay calm and understanding
-be patient and flexible. Don't argue or try to convince -acknowledge requests and respond to them -try not to take behaviors personally. |
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Other possible treatments for AD
|
-cholesterol lowering drugs
-vitamins and folic acid -anti-inflammatory drugs -substance that prevent formation of beta-amyloid plaques -nerve growth factor to keep neurons healthy |
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Motor Neuron Disease
|
Progressive bulbar palsy (U & LMN)
-life expectancy 6m-3y from diagnosis Progressive/Spinal muscular atrophy -live>5yrs Primary lateral sclerosis (UMN) -may have normal life expectancy ALS (U&LMN) -most common -life expectancy 2-5 yrs from diagnosis |
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ALS
|
-irreversible, progressive disorder of the nervous system
-degeneration of both UMN and LMN -neurons in motor cortex and brainstem and ant horn stop relaying messages to the mm (weakness, atrophy) -loss of all voluntary movement, then death -chest and diaphragm mm become involved and person is no longer able to breathe -respiratory failure leading cause of death |
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Amyotrophy
|
atrophy of the mm fibers as their corresponding anterior horn cells degenerate
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Lateral sclerosis
|
hardening of the anterior and lateral columns of the spinal cord as the motor neurons degenerate and are replaced by fibrous astrocytes (gliosis)
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Disease course of ALS
|
-onset to ventilator dependence or death is 2-4 yrs
-after vent mean life expectency is approx 5 yrs-10 yrs -cognition, occulomotor function, sensation, and bowel and bladder function remain normal -skin integrity -research focused on finding source of neuron degeneration and stopping it |
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Clinical manifestations: Vary from patient to patient
|
LMN:
-asymmetrical weakness -cramping with voluntary mvmt in early morning -fasciculations -ext mm become weaker than flexors UMN: +Babinski +Hoffman's sign -hyperreflexivity |
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Pharmacological management for ALS
|
-baclofen
NSAIDs antioxidant rich foods Rilusole/Rilutek |
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Indicators for therapy
|
-fatigue
-spasticity -functional losses noted when isometric strength declines -progressive weakness of scapulohumeral mm and subluxation -contractures: need for routine stretching -unable to shift weight for pressure relief (seating adaptations with reclining schedule) -Loss of diaphragm: teach use abdominals to help with inspiration |
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Physical Therapy for ALS
|
-slow stretching for spasticity and cramping
-daily ROM taught to caregivers -safe and efficient transfers -initially, assistive devices for walking including AFO -wheelchair -submaximal exercise for those with slow disease progression |
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OT for ALS
|
-energy conservation techniques for patient and caregivers
-assessment and intervention for dysphagia -AE for meaningful activity: universal cuff splint for grip strength balanced forearm orthosis slings, tape for shoulder girdle weakness environmental control units |
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Most important for ALS
|
-understand needs and wants of person
-anticipate progressive nature of disease -problem solve with pt; make recommendations for AT -understand and appreciate impact of environment to help them remain as functional for as long as possible -work with caregiver and other providers |
