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142 Cards in this Set
- Front
- Back
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severe blow to the head that not only causes damage under the site of impact but also on the opposite side
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coup/counter coup
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due to acc/decc injury. damage occurs at the poles and the undersurface of the temporal and frontal lobes. may be in form or contusion and or laceration with no abnormal neurological signs until 2-3 days later due to what is known as the mass effect(edema causing brain to shift)
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polar brain damage
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localized to the airea of the brain that is under the site of impact on the skull. damage can be in the form of contusion, laceration, or both.
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local brain damage
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widespread bd results from stretching and tearing of nerve fibers. when brain mass shifts and tears, billions of thread-like nerve connections and pulled and stretched. with this type of injury, pt is usually comatose.
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diffuse brain damage
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pathological reflex that occurs in lesions above T-6. can be hazardous. a noxious stimulus can produce clinical syndrome. after stimulus, a mass reflex at spinal cord level will elevate blood pressure. due to lesion, there is no vasomotor respose to lower BP. death can occur if not tx immeadiately. the noxious stimuli can include pressure anal/genital area, bowel/bladder distension, abdomnial distension, mechanical stretch, and long sitting. symptoms: bradycardia, HA, profuse sweating, increased spasticity, blotchy appearance. Intervention: check the drainage system, if patient is lying, bring to sitting, and check patient's body for any irritating stimuli. If stimulus cannot be relieved, medical/nursing is required.
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autonomic dysreflexia-hyperreflexia
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brain damage from some external inflicted trauma to the head that results in significant impairement to the individual's physical, psychosocail, and or cognitive functional abilities.
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traumatic brain injury
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result of direact unilateral trauma to the cortex but can also result from secondary injuries. very similar to pt with CVA but the pt is more complicated due to associated cognitive deficits.
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hemiparesis
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hemisection of the spinal cord(damage to one side) usually caused by stab wounds. symptoms are assymetrical. loss of sensation and priorecption on ipsilateral side with loss of pain and temperature on contralateral side several layers below the injury.
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brown sequard syndrome
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due to flexion injuries in cervical region. there is loss of motor function, pain and temp below the level of the lesion
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anterior cord syndrome
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hyperext injuries to cervical region. ue will be more involved than le. there will be a varying degree of sensory and motor impairment with complete preservation of sacral tracts, normal sexual, bowel and bladder function
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central cord syndrome
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perservation of motor function, pain and light touch. there will be a loss of proprioception and two point discrimination.
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posterior cord syndrome
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incomplete lesion. there is perianal sensation, rectal sphincter contraction, and cutaneous sensation in saddle ara. it is the first sign that a cervical lesion is incomplete
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sacral sparing
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lesions are peripheral nerve injuries. they have potential to regenerate but full recovery is not common
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cauda equina injury
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preservation or return of function of nerve roots at or near the level of lesion
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root escape
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no sensory or motor function below the level of the lesion. this is due to a complete transaction, severe conpression, or vascular impairement of the spinal cord.
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complete SCI
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some preservation of sensory or motor function below the level of the injury. this is due to contusions produced by pressure on the cord from fractures, soft tissue, swelling within the spinal canal. the clinical picture is unpredictable.
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imcomplete SCI
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blood clot within the vessel. the contributing factor is the loss of normal pumping mechanism provided by contraction of LE musculature. the clinical features are localized swelling, erythema, and heat. these symptoms are very similar to ectopic bone formation, but differenated by doppler studies. managment is prevention, prophylactic anticogaulant therapy, turning program, PROM, elastic support stockings, and positioning of legs to promote venous return
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DVT with SCI
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signs/symptoms of brain injury (5)
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neurological deficits
(paralysis, tone changes, reflex changes, and behavorial changes) |
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recovery stages from CVA concerning tone
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flaccidity to spasticity to normal
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syngery patterns:
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flexion and extension
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reflexes
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initially areflexia, then hyperrelfexia, positive babinski, tponic reflex pattern can be present, STNR, ATNR.
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recovery of CVA time
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recovery is fastest in the first few weeks after onset, with most measurable neurolocial revovery (90%) within the first 3 months. pt. may continue having functional gains 6 months to a year after insult. the rate of improvement depends on the amount of damage sustained.
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procedures for CVA positioning
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usu. performed 1st.
1. enhance pts awareness of hemiplegic side pt may spend alot of time in bed initially, you must position to prevent 1. contractures 2. pressure ulcers 3. tone dependent 4. and reflex dependent postures upright posture is assumed ASAP |
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positions to avoid with CVA (8)
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sidebend of head/trunk toward affected side with head rotation toward unaffected side
depression/retraction of scapula IR/adduction of UE elbow flexion/forearm pronantion wrist/finger flexion retraction/elevation of hip with knee/hip extension hip adduction ankle plantarflexion |
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positions to promote with CVA (3)
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supine
sitting sidelying |
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bodily functions (automatic) ie: respiration; swallowing; temp control; alertness; coordination
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brain stem
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emotions (anger, love, sadness, happiness)
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limbic system
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ability to register new imformation and later retrive it; time; distance; perception; areas of speech, communication
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temporal lobes
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motor/sensory interpretation
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parietal lobes
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visual processing and interpreting
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occipital lobes
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thinking skills, executive functions, ability to plan, initiate, carry out, monitor, and correct ones own behavior; problem solving skills (21)
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frontal lobes
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CVA recovery and strength goes:
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proximal to distal
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CVA begin with
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approximation and weight bearing
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Indications for shoulder slings
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subluxation greater than one inch.
during positon changes, must not pull on affected UE or let it be unsupported(may use hemi sling, but may create abnormal positionng of UE as well develop contractures, must support upper arm without IR and flexed arm) must control subluxation. contraindicated with spasticity |
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MMT Grades
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1. Trace
2. Poor 3. Fair 4. Good 5. Normal |
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motor control learning techniques
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need to be functionally oriented. Isometric contractions increase recruitment of motor neurons. there are a variety of methods for motor retraining. there is no optimal treatment for stroke patients. no one method has been proven to be more beneficial than the other. need to take an eclectic approach, selecting procedures from the different approaches that have the greatest chance of success
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motor control learning techniques (4)
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1. brunnstorm
2. neurodevelopment treatment 3. proprioceptive neuromuscular facilitation 4. motor relarning progreammed for stroke |
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uses synergy patterns in early recovery for the pt who is unable to move at all. after voluntary movement is acheived, synergistic patterns are then modified to selective patterns.
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brunnstrom (MC learning tech)
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use of reflex inhibiting patterns to promote normal selective movement during functional activity
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neurodevelopment treatment; bobath approach
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use to promote coordinated movement
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PNF
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Tone reducton activities for CVA(8)
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-positioning out of reflex dependent postures
avoid excess effore or heavy resistance rhythmic rotation of limbs out of spastic pattern postures in SL, sitting or hook lying are used PNF patterns stimulating the weak antagonist through tapping, vibraiton WB activties (UE, kneeling, quadruped) use of cold(decrease conduction velocity) |
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neurological deficits with TBI(4)
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paralysis
tone changes reflex changes behavorial changes |
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TBI low level management
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level I-III
decreased level of responsivness (90%) Goals-prevent contractures, skin breakdown, and increase pt level of interaction with environment tx: ROM is decreased due to decreased consciousness, prolonged bed rest, spasticity, and lack of voluntary movement. tx might include oral meds, nerve/motor blocks, serial casting and positoning. sometimes manipulation under anesthesia. PROM should be aggressive caution with stretching secondary to low LOC when ranging shoulder, place pt. in SL positon to allow scapular movement. Rotation is effective with decreasing spasticity. |
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used for arousal and to elicit movement. effective when administerd for short treatment sessions and should be presented in an orderly fashipn to prevent overstimulation.
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sensory stimulation (part of low level management)
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time delay between stimulus and response
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latency
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how many times out of given number of stumulus presentations does the pt respond the same
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consistency
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response should be appropriate to stimulation
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intensity
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brief forms of stimuli should result in brief forms of response
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duration
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use normal conversation, identify yourself, explain what is to be done, constant background noise is detrimental
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auditory
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use objects that are familar family pics, note visual alertness and visual tracking
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visual
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place scents under pt nose for 10-15 secs
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olfactory
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done during most functional activties, can use pt's own hands
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tactile
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rolling, rocking
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vestibular
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mid level managment TBI
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level IV: pt is usu confused; agitated; therefore pt requires structured enviorment, activites need to be familar and liked by the pt.
goals: maintain improve ROM, prevent deconditioning, and prevent agitated outburst, need to redirect pt, first to therapist then back to activity, need quiet enviroment. confused-same person needs to be seen every day-establish routine expect no carryover-do not teach new skills, use charts to help progress assume calm behavior be prepared with numerous activities-pt short att sp an and decreased concentration offer options pt will not see other points of views-egoconcentricity |
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levels V and VI (mid)
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pt is still confused; not agitated, a formal PT evaluation can be performed
Goals: increase/maintain ROM increase endurance, and treat any focal motor deficits maintain structure-needed for pt to perform optimally emphasize safety keep insutructions to a minimum speak slowly and allow time to process info use physical props to improve compliance-timeer, charts and graphs to document progress |
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High level (VII VIII)
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pts usually discharged from inpatient facilities. pt should be weaned from weaned. when a pt can control their behavior, controlled environemnt is lessened. need to maintain performance while decreasing structure and supervision. still may need some external memory aids. assist pt in intergrating the cognitive, physical and meotional skills needed to function in real world. physical fitness is imprtant and pt should be able to continue at home. overall goal is for pt to function optimally in society.
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difficulty with initiation and performing sequences of movement
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left CVA
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demonstates motor impersistence
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right CVA
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spech and language disorders
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occur when left hemisphere is affected. aphasia.
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MOTOR relarning program for stroke(4)
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1. analysis of task
2. practice missing component 3. practice task 4. transfer of training |
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types of deficits with TBI (5)
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1. residual deficits(decresased LOC)
2. Cognitive deficits 3. Communication 4. Behavioral 5. sensimotor deficits |
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residual deficits (3)
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low LOC
1. coma 2. persistent veg. state 3. PT amnesia |
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not obeying commands; not uttering words, and not opening eyes, usu last only a few weeks at most
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coma
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continuing LOC, pt will have responses (eye opening, visual tracking, but not speak or produce type of behavior that is purposeful or psychologically meaningful
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persistent vegetivtie state
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time when pt is again able to remember ongoing events, no carryover of info from hour to hour or day to day during tx, implications are obvious for functinal training
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PT amnesia
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deficits will range from selective attention to problem understanding a task, to prob with planning strategies for solution. great impact on tx if pt has attention deficit
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cognitive deficits
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pts can have receptive and expressive communication disorders and should be evaluated by a speech/language pathologist.
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communication deficits
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most enduring and socially disabling of TBI. include apathy, aggression, low frustation tolerance, depression, sexually disinhibiting. psychologist plays important role in determining programs
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behavioral deficits
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pt will evaluate, assess deficts/strenghts, and set app short and long term goals and develop tx plan
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sensimotor deficits
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generalized weakness and loss of flexibility due to immobilty.
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general deconditioning
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indicated involement of trunk and all four extrememties, result from bilateral brain damage, movement may be dominated by reflex activity.
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bilateral hemiparesis
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all TBI will have some loss of this
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balane deficits
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damage to cerebellum and basal ganglia. can be unilateral or bilateral. pt will have problesm with smooth execution of movement. intention tremors may be present.
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ataxia and incoordination
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pt may have other injuries (fractures, peripheral neruve damage, SCI)
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associated injuries
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sensimotor deficits (6)
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1 general decondtioning
2. hemiparesis 3. bilateral hemiparesis 4. balance deficits 5. ataxia and incoordination 6. associated injuries |
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steps of gait training with TBI
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-focus on controlling selective movements of gait with appropriate timing (lower trunk rotation practiced in SL, then kneeling, plantigrage, then standing and walking.)
-advanced gait- practicing forwards, backwards, sideways, and braiding |
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types of SCI stabilization techniques(4)
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tongs
turning frames/beds halo devices thoracic lumbar injuries(spinal orthotics) |
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inserted on outer area of skull; traction is accomplished by attachement of a rope to skull fixation and weights at other end. temporary mode of skeletal traction or for uncomplicated low cervical injuries.
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tongs
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turning frames/beds
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1. stryker frame
2. roto rest kinetic |
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allow positioning chages while maintaining automatic alignment of the spine, but only allows turning supine to prone positon. does not interrupt cervical traction
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stryker frame
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tx table is electronially operated bed that provides continuous side to side rotation along longitutional axis. advantage is maintaing spinal alignment with the decrease effects of bed rest; improve pulmonary/kidney function; and prevent pressure ulcers.
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turning frames/beds
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most frequently used to immobiize cervical fractures. a ring with four steel screws attached to the skull. attatached to body jacket/vest by four vertical steel posts. advantage: reduced effects of prolonged bed rest; permits earlier progression to upright activites, earlier involvement of rehab, decreased LOS in hospital. devices are kept in place until xrays reveal stabillity (12 wks) after removal, othosis is applied 4-6 weeks until unrestricted movment is allowed. these include SOMI, philly collar, and custom made orthosis.
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Halo
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immobilized with bed rest or by application of body cast/jacket. use of turning frame/bed pt. is rolled with log roll technique. spinal orthotics allow earlier mobility activities and earlier rehab program
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thoracic lumbar injuries
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damage sustained to brain at time of injury (4)
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primary brain damage- local BD,
coup/countercoup, polar BD, diffuse BD |
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damage that occurs later. (7)
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secondary BD. -hypoxic ischemic injury, intracranial hematomas, cerebral edema, imbalance of CSF, intracraninal infection, seizures, and surgery
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infarction that occurs in a particualr area inthe brain due to compromise of circulation secondary to shifting brain structures.
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hypoxic ischemic injury
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extended bleeding can be life threatening. pt. talk and die. pt who is lucid for a period of time after initial injury but who later laspes into coma and dies. due to compression of brain by hematoma. hematoma classified by site (epiduaral, subdural, intracerebral) and by time after injury that they develop: acute (3 days) subacute or chronic (greater than 2-3 weeks.
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intracranial hematomas
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swelling of damaged brain tissue that can increase intracraninal pressure. increaesed ICP can result in a herination of the brain.
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cerebral edema
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causes hydrocephalus than can increase ICP
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imbalance of CSF
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can occur at any time from immedatiely after the injury to one or more years after injury
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seizures
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primary cause of TBI with pediatrics
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falls, motor vehicle accidents, GSW, abuse/assault, sports, recreational activties.
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why teach bridinging?
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important for bedpan use
reduction of pressure on buttocks promote knee flexion with hip extension (break syngery) |
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occurs immeadiately after SCI where there is complete loss of reflex activity (areflexia) sensation below the level of injury. though to be due to abrupt withdrawal of connections bewtwen the SC and brain. can last several hours to several weeks but usually subsides within 24 hours. resolution is distal to proximal. begins at sacral to lumbar to thoracic to cervical. bulbocavernous reflex is first indicator that its resolving
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spinal shock
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there will be complete/partial loss of sensation adn muscle function below the lesion level
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motor and sensory deficits.
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pathological reflex that occurs in lesions above t-6
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autonomic dysreflexxia (hyperflexia)
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decrease of BP when pt is moved from horiontal to a vertical positon. due to bed rest and lost of vasocons. control. enhaced by lack of muscle tone, venous pooling. tx should include gradual slow progression to vertcial positon (elevation of head of bed, reclining wc, compressive stocking/abdomial binders) vital signs should be monitored.
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postual hypotension
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automonic dysfunction results in a loss of internal thermoregulatory response. there will be diaphoresis above level of lesion because of inabiluty to sweat below lesion. unable to shiver
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impaired temp control
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result of interruption of intact reflex from CNS control. characterzied by hypertoncity, hyperactive stretch reflexes, and clonus. occurs below level of lesion. spasticity is increased by postional changes, cuataneous stimuli, environmental temp, tight clothing, bladder/kidney and emotional stress. pt with minimal to mod involvement may learn to trigger spasticity at certain times to assist with functional activities. severe spasticity can be controlled somewhat with drugs, peripheral nerve blocks, intrathecal injections, rhizotomy (nerve roots) or myelotomy (nerve fibers)
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spasticity
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urinary bladded is flaccid during spinal shock; bladder reflexes are absent. after ss, one or two types of bladder dysfunction will develop. bladder contracts and reflexly empties in response to certain filling pressure. reflex is intact. when lesion is at the conus medullaris/cauda equina, an automomous nonreflex neurogenic bladder will devlop. reflex arc is not intact. bladder can only be emptied by increasing intraabdomial pressure using valsuva maneuver or by crede maneuver (compressing lower abdomen(
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bladder dysfunction
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2 types of this will develp after SS. reflex bowel is a lesion above conus medullaris. requires use of suppositoires and digital stimulation to initate defaction. autonomous or nonreflex bowel results froma lesion of conus medullaris or cauda equina. relies on straining with available musculature and manual evacatiation technuques.
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bowel dysfunction
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respiratory management after SCI
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depends on lesion level. if cord is severed C1-C3, phrenic nerve innervation, spontaneous respiration is impaired or lost. Quadriplegia and high level paraplegia will result in some compromise in respiratory function due to innervation of both primary and seconday respiratory muscles. Secondary prombles that could arise are pneumonia, actelectasis, phenumothorax, and pulmonary emboli.
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secondary problems with SCI (6)
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1. pressure ulcers
2. heteroptoic bone formation 3. contractures 4. dvt 5. pain (traumatic, nerve root, spinal cord dysesthesias, musculoskeletal) |
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in order to ambulate SCI must have:
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adequate strength, postual alignment, ROM, and cardiovasular endurance
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Gait pattern best for L5 SCI
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2 pt or 4 pt gait patterns with hip flexion or hiking are used with lower level lesions
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sexual dysfunction with SCI male
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erectile capacity is greater with UMN lesions and incomplete lesions. Reflexogenic erection is physical stumulation of genitals and requires an intact reflex arc. psychogenic erection occurs through cognitive acticity such as fantasy and is required with LMN. ejauclation is higher with LMN lessions and with incomplete.
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sexual dys. with SCI female
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with UMN, reflex arc is intact. therefore sexual arousal componenets will occur thru reflexogenic stimulation. with LMN, physogenic respsnses will be preserved while reflexive responses will be lost. menstrual cycle will be interrupted temp for 1-3 months. able to coneive but closely supervised due to impatied sensation and inability to bear down.
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mat activites with SCI
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should be sequenced from easiest to most difficult
do not have to master one activity to move on to next help develop imporved strength and functional ROM improves awareness of the new COG, promotes postural stability, and facilitates dynamic balance. |
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Manual contacts over epigastic area pushing inward/upward while pt is coughting.
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levels of coughing.
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electric wc required for
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c4 lesions and above
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no increase in muscle tone
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0 (muscle spasticity grade ashworth scale)
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slight increase in muscle tone, maifested by a catch and relase or by minimal resistance at the end of the ROm when the affected parts is moved in flex or ext
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1 (ashworth)
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slight increase in tone, maiffested by a catch, followed by minimal resistance throughtout the remainder (less than half) of ROM
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1+ (ashworth)
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more marked increase in tone through most ROM, but affected parts easily moved
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2
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considerable increase in muscle tone, passive movement difficult
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3
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affected parts rigid in flexion or extension
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4
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C1, C2, C3
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facial muscles
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C-4
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diaphragm and trapezius
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c5
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deltoid and biceps
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c6
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wrist extensors
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c7
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triceps
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c8-t1
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hands and fingers
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t2-t-8
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chest muscles
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t6-t12
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abs
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l1-s1
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leg muscles
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s1-s2
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hip and foot
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s-3
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bowel and bladder
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.5
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just notice (borg scale)
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2
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weak; light (slight)
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5
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strong; heavy(severe)
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10
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extremely strong(maximal)
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contraindicated LE motions with paraplegia
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SLR past 60
hip flex past 90 |
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pressure relief schedule for SCI
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10-15 seconds for every 10 minute sitting
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strong enough to clear secretions
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functional (1) cough
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adquate to clear upper RI secreations; assiatance is required to clear muscus secondary to infection
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weak functional 2
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unable to produce any cough force
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nonfunctional 3
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speech flows smoothly with a vetiety of grammatical constructions and preserved melody of speech. auditory comprehension is impaired. pt demonstrates trouble conprehending spoken language and in following commands. lesion locared in the audtory associattion cortex in the left lateral temporal lobe
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receptive aphasia
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flow of speech is slow and hesistant, vocab is limited, and syntax is impaired. speech production is labored or lost completely while comprehension is good. liesion is premotor are a of left frontal lobe
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expressive aphasia
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severe. marked impairements of both productionaand comprehension of language. often an indication of extensive brain damamge. severe probs in communication. may limit rehab
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global aphasia
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sequence of activties with brain and SCi patients
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1. prone on elbows
2. quadruped 3. bridging 4. sitting 5. kneeling/half 6. plantigrade 7. standing |
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KAFO
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T9-T12
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AFO
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L3 and below
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RGO
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T2-T8
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