Neuro PT I Midterm Studyguide Neurologic rehabilitation models NDT= more hands on Contemporary Task Approach= Indep learn more from mistakes, modify, etc… Motor Control Theory Movement emerges from interaction of learner, task, environment Movement= a combination of task, environment, individual Motor Control Feedback/Closed loop control Use sensory information Constantly adjust motor response as a result of environment Early skill acquisition or complex movements requiring accuracy Adam’s Closed Loop Theory (1970s) Memory trace/ Perceptual trace Feedforward/ Open Loop control: Motor program (CPGs or GMP) Generates movement without sensory inputs Anticipate Postural set Well-learned, automatic, fast tasks Use sensory input to adjust to unexpected changes Skill Acquistion Goal is to find a NEW movement strategy New task or new strategy for previously learned task Expect: high degree of attention to task Variable performance Heavy reliance on sensory information (FEEDBACK) to adjust motor response Examples of the novice learner Skill Retention Goal is to LEARN the task Permanent change in behavior Develop skill Increase efficiency Increase consistency More automatic Decrease reliance on external feedback Task Oriented Training Manipulation of task and practice variables
Transcript
Neuro PT I Midterm Studyguide
Neurologic rehabilitation modelsNDT= more hands onContemporary Task Approach= Indep learn more from mistakes, modify, etc…Motor Control Theory
Movement emerges from interaction of learner, task, environmentMovement= a combination of task, environment, individual
Motor ControlFeedback/Closed loop control
Use sensory informationConstantly adjust motor response as a result of environmentEarly skill acquisition or complex movements requiring accuracy
Adam’s Closed Loop Theory (1970s)Memory trace/ Perceptual trace
Feedforward/ Open Loop control:Motor program (CPGs or GMP)Generates movement without sensory inputsAnticipatePostural setWell-learned, automatic, fast tasksUse sensory input to adjust to unexpected changes
Skill AcquistionGoal is to find a NEW movement strategy
New task or new strategy for previously learned taskExpect: high degree of attention to task
Variable performanceHeavy reliance on sensory information (FEEDBACK) to adjust motor response
Examples of the novice learnerSkill Retention
Goal is to LEARN the taskPermanent change in behavior
More automaticDecrease reliance on external feedback
Task Oriented TrainingManipulation of task and practice variablesPatient-Centered functional goalsFacilitate motor problem solving by patientConsider patient’s stage of learning
Are they in skill acquisition or are they in skill learning?Practice session
Amount of variation: blocked vs random practiceMotivation: challenge vs successDefine task: speed vs accuracy
Practice motor problem solvingFeedback…
Feedback (info you give the patient)Feedback= ALL sensory information available
Intrinsic/ExtrinsicManual guidance (hands on)
Type of external feedback or form of demonstrationUseful when introducing task or when patient unable to do task safely
Immediate/Continuous vs Terminal/ SummaryBeing stingy with feedback helps with learningConcurrent is detrimental to learningHold your tongue let them try and figure it out
Summary of Task Oriented TreatmentSkill acquisition strategies
Immediate feedback, use of manual guidanceBlocked practice with less variationMotivation important
Skill retention strategiesSummary feedbackRandom practiceHigh variation and challenge
Add components such as counting, talking, etcClinical decision making
Level of evidence:Systematic Reviews, RCTs, Cohort Studies, Case Control studies, Case Series, Case
Reports, Ideas/Editorials/Opinions, Animal Research, In vitro research
Task oriented tx approach: critical component in making the connection with your patient to get the participation component
Disability as DiversityDisability reconsidered: The paradox of PT Medical model vs Social Model
Disability is a form of diversityFocus on improving access, change social policy,, improve social interactions, (vs fixing
impairments)PTs perpetuate negative attitudes?
Helper/helpee relationshipAssume that individuals want to eliminate impairments
Rehab of patients with stroke
Stroke stats:Leading cause of disability, 3rd leading cause of death (5% mortality rate)
Review Blood Circulation in the brainMCA is most common site of CVA (expectations on presentation)Other CVA presentations regarding ACA, PCA
MCA: derived from the internal carotid artery
Supplies a large area of the frontal, parietal, and temporal lobesOcclusion causes dysfunction of the face and upper extremity, language, and speech
ACA: derived from internal carotid arterySupplies the medial portion of the frontal and parietal lobesOcclusion causes dysfunction of the cortical area supplying primarily the lower extremity
PCA: derived from basilar arterySupplies the occipital lobeOcclusion affects vision
Right VS Left StrokeRight:
Left HemiparesisVisual-perceptual deficitsPoor judgement, cognitive, and behavioral issues
Perserveration: repeating of tasksProcessing delays: don’t restate/repeat commands just adds to the delay, allow
time to process and respond to initial requestPathophysiologyIschemci Lesions
Ischemic CascadeIschemic Core- direct damageIschemic penumbra- possible damage
Thrombotic CVAThrombus: atherosclerotic plaques in first major branching of large cerebral arteries. Progressively narrowsUneven progression
Wake-rise fallorthostatic hypotension that causes enough of a decrease in BP that adequate
blood to the brain is not maintained causing strokeThrombus in evolution
Thrombus in evolution: not stable yet, PT shouldn’t be seeing at this stage. Affects of stroke still evolving
Common risk factors: HTN, DM, cardiac/vascular diseaseEmbolic CVA
Thrombus from outside brain (typically from plaque in carotid sinus, internal carotid, heart)Risk factors as Previous PLUS
A-fib, DVT, InfectionLodges in medium sized vessels (MCA, Vertebral, or Basilar branches)Immediate impact: no collateral blood flowSymptoms vary if clot moves
Hemorrhagic CVAAbnormal bleeding in brain
Aneurysm
More global problems than ischemic CVAIschemic injury to area supplied by vesselMechanical injury from blood, edema to distant neurons
Transient Ischemic AttackTIA or RIND (Reversible Ischemic Neurological Disorder )Temporary interruption of brain blood flow, neuro symptoms last <24 hoursEvolving thrombus or small emboliRED FLAG!
Use as motivation to encourage lifestyle changes Emergency Room
Neuro exam on admissions to hospitalPerformed by acute care physician, nursing staff, perhaps rehab consultantsPURPOSE:
Dx or r/o CVADetermine etiology and pathology of CVAAssess comorbities
Initial DXHistory of events: timing importantPMH/Risk FactorsDx Tests
Confirm CVADetermine cause, location, extentEvaluate complicationsAssess risk of recurrent CVA
DX TestsCT of brain shows bleed, doesn’t show ischemiaMRI doesn’t really affect course of treatment
Acute Care PrioritiesControl life-threatening problems and prevent recurrent stroke
PT screening for Rehab ServicesIdentify patients that may benefitIdentify problems that need treatment: IMPAIRMENTS/FUNCTIONAL LIMITATIONSDetermine appropriate setting for rehab after discharge from acute care
Inpatient RehabilitationRehab Hospital
Rehab unit of hospital or rehab center3-6 hours of therapy per dayMedically stable with functional disability and adequate endurance. Cognition intact
Sub-Acute CareSkilled Nursing FacilityVariable amount of therapyMore serious disability, less endurance. Cognition intact
Long-Term CareNursing home2-3 days/weekNeed for long term 24 hour care because of cognition, comorbidities, lack of home
supportInpatient Rehab
Physiatrist/NeurologistPT, OT, SLP, Dietician, Social Worker, Neuropsychologist, Case Manager, Rec. Therapist
Home Care RehabilitationProvided by home health agencies
Patients who live at home but are functionally homeboundMay be a simple “check out” for safety/functionRehab services can be provided if necessary, typically 2-3 times per week for 30-45minutes each session
Limited equipment, focus is on functional training in relevant settingOutpatient Rehabilitation
Outpatient therapy office or outpatient dept of hospitalPT most common, OT/Speech also availablepatients who live at home and are mobile in communityTypically 2-3 times per week for 30-45 minute sessions may include strength orendurance training
What defines TBI?TBI is a sudden trauma that causes injury to the brainClosed (non-missile; dura mater intact) vs Open (penetrating injury)Focal vs DiffuseSaid to be a violent storm of noises with the inability to filter things out
Primary Damage post-TBICoup injury (at the site)
Forceful blow to resting, moveable headMaximum injury is at the point of cranial impactContusion with/without skull fracture
Contracoup (opposite side)Moving headInjury is opposite of impactFrontal and temporal lobes
Coup/Contracoup Injury Whiplash injuryCar accidents, football playerMultiple areas of the brain injured
Temporal, frontal, occipitalCerebral Spinal Fluid
Shock absorber, dissipates forcesForces on the brain tissue
Diffuse Axonal Injury (Big cause of coma or vegetative state)Brain Swelling
Craniotomy if swelling is severeCerebral edemaIncreased ICP (12mmHg normal)SeizureHypoxic Ischemic injury
Anoxia: no O2 for a period of timeHypotension
Difficulty regulating pressureHOB at 30˚ so pressure doesn’t increaseHematoma
Epidural Hematoma: Skull and duraSubdural Hematoma: between dura and arachnoidIntracerebral Hematoma
Important ConsiderationsBalance vs VisionCognition vs Hearing loss/changes
Structures are vulnerableInjuries to any of these regions/structures can be catastrophicNeed to be protectedRegeneration of tissue limited within specific structuresRecognizing what’s injured, its affect, and preventing secondary injury
CausesMVC #1 causeViolence (GSW) ~20%, 91% of firearm related brain injuries result in death (2/3 suicidal intent)WarFalls, 11% of falls are fatal in elderly (75 and older)Sports Injury (~3%) in 2003-2009
Concussion ~75% of TBIPedestrian cyclist accidentsDrug Overdose/PoisoningDrowningCarelessness
Types of Brain InjuryConcussion
Experience one of the followingPhysical (headache, dizziness, nausea, sleep problems/fatigueCognitive (decreased attention span, concentration, and short term memory loss)Behavioral (irritability, emotional labiality, depression/anxiety)
Grading ScaleGrade 1: (mild)
No loss of consciousnessPost-traumatic amnesiaPost-concussionSigns or symptoms lasting less than 30 min
Grade 2: (moderate)Loss of consciousness lasting less than 1 minutePost-traumatic amnesiaPost-concussion
Signs or symptoms lasting longer than 30 min but less than 24hrsGrade 3: (severe)
Loss of consciousness lasting more than 1 minutePost-traumatic amnesia lasting longer than 24hrsPost-concussion signs/symptoms lasting longer than 7 days
Grade1:Most frequent, but most difficult to recognize and judge the severity>50% of all concussionsOften described as “bell rung” or “dinged”Tx: Remove player and observe for symptoms for 15-30 minutes
Return only if NO symptoms at rest or with exertionGrade 2:
Remove from play, refer to neurologist for examinationGrade 3:
Remove from play and transport via ambulance to hospitalConsider possibility of C-spine injury during LOCMUST consider intracranial hemorrhage
Leading cause of death due to head/neck injuryHematoma
Epidural hematomaOccurs with fracture/arterial insultRapid progression of negative symptoms
Subdural hematomaSurgical emergency
Intracranial hematomaMost common fatal athletic injuryRapid progressing, torn artery
Subarachnoid HematomaBruise
Second Impact SyndromeOccurs due to loss of autoregulation of blood supply to the brainHappens more easily after initial concussive eventPresents with rapid deterioration of status, collapse and can be fatalDo not allow athletes to be returned to play too early and be placed at risk
Second Impact Syndrome PathophysiologyInitial concussion impairs normal brain function
Brain vulnerable during this timeSecond impact unleashes series of metabolic eventsLoss of autoregulation of brain’s blood vesselsCongestion, vasodilation, and large increase in blood flowLarge increases in ICP
Long-Term ConsequencesNeurodegenerative changes- due to loss of autoregulation of blood supplyMild cognitive impairmentAlzheimer’s diseaseChronic Traumatic Encephalopathy (CTE)
Dependent on extent of injury, and neural plasticityNeurons in uninjured areas can take over (regenerative sprouts/collateral sprouts)Brain is always reorganizing to store new information
Glasgow ComaEye opening: 4= Spontaneous 3=to voice 2= to pain 1= noneVerbal: 5=normal 4= Disoriented conversation 3=words; not coherent 2=no words; only soundsMotor: 6=normal 5= localizes to pain= 4=withdraw to pain 3=decorticate 2=decerebrate 1=none
Levels of consciousnessAbnormal
Stupor=unresponsive; aroused by strong stimulusComa= unconscious; unaware, unarousable, absent sleep-wake cycleVegetative state=unconscious and unaware but have sleep-wake cycle Persitent vegetative state= don’t recover w/in 30 daysLocked in syndrome= aware and awake but can’t move or communicate
Rancho Los Amigos Scale
PARKINSONSAge of typical onset >65Cardinal characteristics: 1)Resting tremor 2)Bradykinesia 3)Rigidity 4)Postural instability (have to have 2 out of 4 cardinal characteristics to be diagnosed)Other symptoms: micrographia (small writing), masked face, slow ADLs, stooped and shuffling gait with decreased arm swingClinical exam is “gold standard”, can only have definitive diagnosis with autopsy ( to analyze substantia nigra)
ParkinsonismCorticobasal degenerationDementia with Lewy bodies (small microvascular strokes)Multiple system atrophyProgressive supranuclear paulsy: typically more global neurodegeneration in multiple areas of brain, gliosis, accumulation of tau protein (progresses much faster than PD, difficulty moving eyes vertically) Consider response to L-Dopa to determine Parkinsonism vs Parkinson’s
Stages of PD
I/Early=unilateral tremor, rigidityII/Early Middle=Bilateral symptoms, gait deviationsIII/Late Middle=Balance problems, but still indep with ADLs (falls prevalent in this stage)IV/Late=Severely disabled*PTs tend to see pt’s that are in level III or IV (should be getting into an exercise program by Level I or II)
DrugsL-Dopa: replaces dopamine, does NOT change progressive loss, effective for <10 yrsAmantadine: stimulates dopamine These drugs prevent dopamine breakdown, but do NOT replace: COMT inhibitors, MAO-B inhibitors, Anticholinergics
Cognitive Issues11-29% of patients with PD have memory difficulties (may present like Alzheimers)Psychosis: vivid dreams/nightmares, disorientation, hallucinations May have to stop L-Dopa if it becomes too serious
TreatmentWant to bypass basal ganglia and activate SMA (pt can then respond to cues rather than relying on a set motor program), can use tiles on floor, rhythmic auditory stimulation, etc. Make sure to address freezing. Want to also reduce stress b/c this will only exacerbate symptomsLocomotor training in early stages: 1) Baseline data to evaluate progression 2) Teach core strategies for large quick movements 3) Practice gait with variation (longer steps, different cues, concurrent activities) 4) Fall prevention education 5) Lifestyle activities (such as an exercise program, Tai Chi, etc)Locomotor training after L-Dopa: 1)Monitor response to off/on meds 2) Focus on safety (avoid secondary tasks if needed, address freezing, etc)Locomotor training 5-8 years later: 1) Maintain functional movements 2) Optimize postural alignment 3) Focus on postural stability (become very kyphotic, monitor fall risk, footwear recommendations, make gradual turns, consider “on” and “off” cycles)PT for advanced disease: may need assistive device, provide education and support to caregiver, need to address gait dyskinesia, enhance participation in community
HUNTINGTON’S DISEASEInherited and progressive disorder, autosomal dominantExcessive face and trunk movementSymptoms appear at 30 years (death around 15 years from onset)May have dementia, behavioral and emotional disordersNo specific treatment options
OTHER BASAL GANGLIA DISORDERSWilson’s disease: faulty copper metabolism, rare, autosomal recessiveTardive dyskinesia: extraneous facial rhythmic motion, due to psychotropic meds
MULTIPLE SCLEROSISProgressive disorder with periods of exacerbations and remissions (stress can trigger exacerbations)Typical pt presentation: 1) 15-45 years old 2) Women>men 3) Charcot’s Triad (intention tremors, speech, nystagmus)Demyelinating lesions of the CNS (axons spared), UMN diseaseEtiology: Autoimmune, genetics, environment (more prevalent in northern states) may all play a role (all still questionable)Diagnosis: Clinical presentation + lab results (rules out other things); can test using MRI (small and tend to not show up until function already disrupted), CT (can only see big lesions), EMG (slowed nerve conduction velocity), blood tests and CSF (elevated T cell count)Prognosis: mean survival rate=20-25 years after diagnosis; + indicators= <35 and initial onset with 1 symptom; - indicators= >35 and insidious onset with multiple symptoms Most common problems: 1) Fatigue (might need to break up PT session, heat exposure increases fatigue) 2) Visual disturbances 3) Cognitive dysfunction (denial and poor safety awareness) 4) Bowel/bladder dysfunctionManifests within sensory (n/t) and motor systems (spasticity, ataxia, paresis), may also cause problems with dizziness and speech/swallowing
TypesBenign: mild, little or no disabilityExacerbating/remitting: almost full recovery from exacerbationsRemitting/progressive: incomplete recovery from exacerbationsProgressive: very little recovery (steady downward decline)***not mutually exclusive (patients can go back and forth)
Medical managementCorticosteroids decrease inflammation during periods of exacerbationInterferon injections: prevent exacerbation by 30% (make sure women not using this when trying to get pregnant) Anti-spasticity meds Avoid heat exposureDo NOT push pt too hard during an exacerbation Ask pt what they have been told and if they would like more information (figure out what they know about their disease)
ALSProgressive and fatal neuromuscular disease (50% die within 3 years of diagnosis->muscles of breathing and swallowing eventually are affected)Upper AND lower motor neuron disease, voluntary muscle action affected (cognition and sensation not affected)Typical pt presentation: 1) 40-70 years old 2) Men>women
Again, ask pt what they have been told and if they would like more information (figure out what they know about their disease)
TUMORSBenign vs malignant (benign can still interfere with function)Most common signs: 1)Headaches 2) Nausea/vomiting 3) Papilledema (pressure in the pupil)Primary brain tumors: Gliomas (most common, men>women, invasive, rarely metastasizes)Types of gliomas: 1) Astrocytoma (occurs in frontal lobe in adults and cerebellum in children, Grades I-IV) 2) Medulloblastoma (children)Meningiomas: affects women>men, encapsulated and slow growingNeuilemomas: Schwann cells, acoustic neuroma (CN VIII) typically one sided)Pituitary Adenomas***Adjust expectations as disease progresses
CEREBELLAR DISORDERSCerebellum compares planned movement to actual movement Ipsilateral symptomsInherited/Idiopathic cerebellar degeneration: group of disorders (progressive degeneration)Friederich’s Ataxia: adolescent disorder with children going through growth spurt (onset 8-15 years)Acute Alcoholism Chronic Alcoholism: Nutritional deficiency of vitamin B1, Wernicke-Korsakoff syndrome (all characteristics of cerebellar problem along with a cognitive component) Cerebellar CVA (unilateral symptoms) or tumor (unilateral or bilateral symptoms)OTHER NEUROMUSCULAR DISORDERSPOLIO: virus infected alpha motor neuron cell body, remaining motor neurons re-innervatedPOST-POLIO SYNDROME: surviving motor neurons work extra hard and eventually give out, avoid exercise (energy conservation is essential)PERIPHERAL NERVE DISORDERS: 1) Axonal neuropathy (DM, toxins, drugs) 2)Demyelinating neuropathy (Guillian Barre and CIDP); CIDP continues to progress which is unlike AIDP/Guillian Barre; Guillian Barre is ascending motor neuropathy which may be triggered following virusMYASTHENIA GRAVIS: affects neuromuscular junctionLAMBERT EATON MYASTHENIC SYNDROME: affects neuromuscular junction, associated with cancer malignancyMYOPATHIES: 1) Muscular dystrophies (inherited and idiopathic, Duchenne’s-lacks dystrophin protein) 2) Metabolic muscle disease (inherited) 3) Inflammatory myopathies (acquired)
CNS INFECTIONSTypes: 1) Brain abscess: (cavity filled with purulent exudate) 2) Meningitis (bacterial infection of CSF in subarachnoid space 3) Encephalitis (viral/HIV)
TRANSVERSE MYELITIS: inflammation of spinal cord (white and gray matter), acute onset of paraplegia, sensory loss, and bladder incontinence, stable->not progressive (1/3 with minimal deficits, 1/3 ambulatory with difficulty, 1/3 complete paralysis)
OTHER DISORDERSCONVERSION DISORDER: present with specific symptoms based on their mental stateWEST NILE VIRUS: due to mosquitoes, damage to anterior horn of the spinal cord, currently no tx availableLYMES DISEASE: caused by ticks Stage 1: Rash around tick bite 8-9 days later
Flu symptomsStage 2: Cardiac and neurologic complications several months later
Headache, neck stiffness, cranial nerve palsiesStage 3: Chronic arthritis 1 year later in large joints of the body
May have memory, cognitive dysfunction***Nervous system complications in 10-15%
SPINAL CORD INJURYMechanism of injury: Traumatic (MVA, fall, sports injury, etc) vs atraumatic (infection, MS, AV malformation, etc)**The cord does not need to sever to have complete injury (even bruising can result in complete paralysis)Higher risk for SCI if: 1) African American 2) Male 3) age 16-30 Quadriplegic=tetraCritical information to obtain during PT eval: method of injury, co-morbidities, PMH, precautions (pre and post surgical), level of injury, ASIA level
StabilizationORIF=open reduction internal fixation->can be combined with bracing: 1) Halo traction (more for high cervical injuries and those with no signs of neurological
damage->may be more of ligamentous injury) 2) Cervical collar (Aspen, Miami J, Philadelphia->most uncomfortable and least form
fitting ) 3) CTLSO (can’t separate cervical from thoracic-may be seen with injury at C7 or T1)4) TLSO**Bracing is physician dependent
Spine Precautions (Based on KU Hospital-precautions will vary by facility)Cervical: If spine is unstable-> pt is on bed rest, If spine is pending clearance but has no fx/dislocation is identified->pt can move with use of a collar, If pt is post fixation->may be up with use of a collar (collar is typical but physician dependent)Thoracic/Lumbar: Do NOT elevate head of bed, bed rest, limit extremity movement to avoid spine movement, place pt in reverse trendelenberg to prevent aspiration, log roll with assist x2
Determining Level of InjuryLevel of injury is determined by last intact muscle group of at least 3/5 rather than by level of spinal fractureFor thoracic injuries, it is determined by sensory levelC1-C4=diaphragm and sensoryC5=BicepsC6=Wrist extensionC7=TricepsC8=Finger FlexorsT1=Small finger abductorsT2-L1=Sensory levelL2=Hip flexorsL3=Knee extensorsL4=Ankle dorsiflexorsS1=Ankle plantarflexorsS2-S5=Sensory level and sphincter tone
ASIA LevelsA: Complete: no motor or sensory function is preserved in the sacral segments S4-S5B: Incomplete: sensory but not motor function is preserved below the neurological level. Sacral segments S4-5 are intact C: Incomplete: motor function is preserved below the neurological level and more than have of key muscles have a muscle grade less than 3D: Incomplete: motor function is preserved below the neurological level and at least half of key muscles have a muscle grade of 3 or moreE: Motor and sensory function is normal**May be typical for ASIA C to go to D as they recover and ASIA A to go to B **Incomplete tetraplegia is most common
Types of Incomplete LesionsAnterior cord syndrome (sparing of dorsal columns): preservation of light touch, proprioception, and deep pressure; absences of pain and motor functionCentral cord syndrome (sacral sensory sparing): UE weakness >LE; due in part to corticospinal and spinothalamic tracts of LE being spared bc of lateral positioning in spinal cord (typically seen with hyperextension injury->generally favorable prognosis) Brown sequard syndrome: hemi-section of cord, ipsilateral paralysis and loss of proprioception; contralateral loss of pain and temperatures (not common with trauma, more likely to see due to tumor)Posterior cord syndrome: preservation of temperature, pain, and touch with varying degrees of motor preservationCauda Equina: LMN injury resulting in flaccidity (tend to have bowel/bladder problems)**The most important prognostic variable relating to neurologic recovery is completeness of the lesion
Treatment
The pt with complete injury will not be able to strengthen or influence recovery of lost motor function; will need to focus on compensations in order to carry out certain functional activitiesTransfers: head moves opposite of bottom; need to lead with bottom rather than head; make sure pt has shoes on; do NOT stretch finger flexors when in wrist extension (they may need this for compensatory movements)Balance: long sit achieved more easily than short sit due to larger base of support (may have difficulty if pt has tight hamstrings)Primary focus in initial stages=prevention of secondary complications, gain tolerance to upright positioning in order to begin rehab, positioning, prevention of DVTs and pneumonia, promotion of GI function
Pressure reliefDependent: reclining (more supine positioning) or tilt in space (seat to back angle stays the same) wheelchair ->In reference to ischial tuberosity: 65 degree backward tilt for actual pressure relief, 35 degrees for minimal drop in pressurePressure ulcer: redness that does not fade within 20 minutesPhysiologic changes to skin include thinning of the epithelial layer, changes to collagen and hyperhidrosis for T8 and aboveMight be a candidate for ambulation if lower level and incomplete (may need KAFOs/AFOs)Teach pt how to fall bc this WILL happen
Wound AssessmentGrade 1: Skin area with erythema of in duration overlying a bony prominence
Grade 2: A superficial ulceration that extends into the dermis
Grade 3: An ulcer that extends into the subcutaneous tissue but not into muscle
Grade 4: Deep ulceration that extends through muscle tissue down to the underlying bony prominence
Grade 5: An extensive ulcer with widespread extension along bursa and into joints or body cavities
WheelchairsConsider: patient’s functional level, ability to perform pressure relief indep, type of terrain, amount of time pt will be in wheelchair, transfer technique, weight of wheelchair, position desired, number of caregivers, accessibility at home and other destinations, patient preferencePower vs manual (C6 and above-power; C7-T1 MAY be able to propel wheelchair, but must weigh energy expenditure costs) Power controls may be head control, sip and puff or joy stick. Paraplegia should be able to manage manual w/c.If new w/c user, rigid frame is more efficient than foldingPros of using a back: better posture and shoulder positioning, Cons: hassle loading into car
Expected Outcome vs VariabilityKnowing the expected outcome and reasons for variability will help with goal setting and treatment planningCARDIOVASCULAR: Higher level of injury will have more difficult time maintaining blood pressure (may require use of ace bandages and abdominal binder for maintaining vascular support)Dysreflexia: If someone has tolerated upright positioning and then has a problem with it all of a sudden, may be a signal of infectionRESPIRATORY: C6-C7 have intact diaphragm, but may have limited intercostal musculature (the lower the level of injury, the better the respiratory function)ROM: May have limitations with ROM due to HO (develops over time), premorbid contractures, arthritis and spasticity; **have to have 90 degrees of hip flexion in order to balance without any abdominalsSTRENGTH: Muscles may be be flaccid initially and become spastic once shock has passed; if LEs stronger than UEs (suspect central cord); if unilateral differences (suspect Brown-sequared); if there is progressing weakness proximal to the spinal cord lesion (big red flag, especially at C level)SENSATION: may have phantom pain below the level of the lesion with absent localization/sensationBOWEL and BLADDER: neurogenic bladder/bowel-bladder/bowel will not empty with voluntary control, hypo reflexive-does not empty (more prone to infection), hyper reflexive-empties too oftenSEXUAL FUNCTION: some may achieve psychogenic or reflex erections (may be due to vagus nerve); infertility common with males due to problems with temperature regulation, women still have potential to get pregnant (should continue birth control if on it previously)
ComplicationsAUTONOMIC DYSREFLEXIA; Single most common cause is a blocked urinary catheter (risk for patients at T6 and higher); get assistance, check catheter, elevate head, look for other sources if catheter is not the culprit. Symptoms: headache, sweating, nasal congestion, sustained penile erection, hyperhydrosis above level of lesion, paresthesias (If the face is red raise the head, if the face is pale raise the tail)POSTURAL HYPOTENSION: lightheadedness, low BP, may yawn or pass out; ace wrap LEs, binder, TED hose, reclining wheelchair, medsHETEROTROPHIC OSSIFICATION: sudden limitation of ROM, may be warm over joint; early detection is important so meds can be started, no aggressive ROMDVT: swollen calf or LE, warm to the touch and may be painful; use SCDs, IVC filter, movement, and may use meds such as heparin, coumadinHYPOTHERMIA/HYPERTHERMIA: body is unable to regulate temperature, very susceptible to external conditions; should provide education on proper clothing and avoiding extreme temperatures
BURNS: may occur from touching hot products such as coffee or or plate due to loss of sensation; be cautious with modalities!!PAIN: often in shoulders along with area of injury; may use modalities for painSPASTICITY: hypertonicity of extremities denervated distal to the lesion; can manage with medications such as baclofen and valiumSYRINGOMYELIA: progression of weakness proximal to the level of injury, especially problematic for cervical injuries; requires surgical management (be alert to change in level of function->decrease in motor function is a sign of new pathology)CONTRACTURES: fixed limitation of ROM over a joint or multiple joints; managed by prevention, ROM, and proper positioning (surgical release is also an option)OSTEOPOROSIS: lack of bone density due to lack of weight bearing over time; managed by weight bearing in a standing frame, be cautious with PROMSPINAL DEFORMITIES: scoliosis, pelvic obliquities, kyphosis; due to poor wheelchair positioning over time (only correction of a fixed deformity is a surgical correction)SHOULDER INJURIES/CARPAL TUNNEL SYNDROME: overuse injuries from wheelchair use which cause pain/weakness in shoulders and wrists; manage by proper positioning in wheelchair and may need power chair vs manual
ADAPTATION SUGGESTIONSRamps: one foot of run for one inch of riseReplace carpet with hardwood floors and remove throw rugsPedestal sink or cut out cabinet in the bathroomFlat surfaces for bathroom sink for easier accessPlace frequently used items on lower shelvesThe clapper or other remote control ideasLoops on the cabinet for easier openingLever door handlesRaise the floor of the kitchen (eliminate the toe boxStackable washer and dryer
Safety SuggestionsCordless/cell phoneSmoke detectorsEncourage pt to call fire depart and inform them there is a person with a disability in the homeAdjust hot water heater to lower temperature
Position modifications / substitutionsHand-held dynamometer
Reliability (ICC) ranged from 0.85 to 0.98 for both hemiparetic and non-paretic Isokinetic dynamometer
Interventions for impairments in muscle performanceNo active movement
0 or 1 on MMT scaleInsufficient alpha motor neuron inputFacilitation techniques:
Utilize stretch reflex pathway for autogenic facilitationTapping, vibration, also light touchBut activating only alpha motor neuron
Modify functional task / environmentTrying to activate alpha and gamma mn
Some Active MovementLack anti-gravity muscle power (2 or 3 on MMT scale)
Possibly only activating alpha mnUse gravity-eliminated positions; can begin PREsFunctional task training / NDT
Modify task requirements to make it easierManual guidance may be required for safety
help learn new task Goal to maximize patient-initiated activity as soon as possible
NDTHierarchical model of motor controlFirst goal of treatment is to normalize tone Use of dev’t sequence to challenge trunk muscles, proximal mm stabilityUse of resistance not advocated secondary to hypertonicityFunctional relevanceManual guidance:
Mvmt should be effortless, if patient compensates then provide assistanceGoal to provide pt with experience of correct mvmt pattern
FES and BiofeedbackAppropriate when “some” active movementAugmented feedbackImportant to withdraw for learningBilateral Training
Weak “intact” upper extremityInvolve both motor cortexesStronger arm models weaker arm
Active Movement but Weak Weakness as a primary or secondary impairment Lack full muscle power (4 on MMT scale)Resistance:
PREs with weightsManual resistance in PNF diagonals
Consider body positionTrunk and extremity muscle powerEndurance
Overload principleRationale for strengthening in neuro population
Functional Task Training “Repetition without Repetition” as an exercise
LE strength difference is a significant individual predictor for gait speed, gait endurance, and functional balance. Cognition significantly predicted only gait speed
Resistance Exercise Training Intensity and number of repsSets and frequencyDuration and SpeedMode of exercise such as static, eccentric , of concentricRange of movement e.g short arc vs. long arcPosition of the patient
Ottawa Panel GuidelinesClinical practice guidelines for therapeutic exercisesAdult patients (>18 years of age) presenting with hemiplegia or hemiparesis following a single clinically identifiable ischemic or hemorrhagic CVAUse of progressive resistance training in lower extremity has clinically important
benefit in patients with post-acute stroke.
Proprioceptive Neuromuscular FacilitationDefinition: methods of promoting the response of the neuromuscular mechanism through
stimulation of the proprioceptorMethods are most useful for: Stretching and Strengthening
Move from passive, active assistive, resistedD1 upper extremity
Wrist and finger flexion, Elbow flexion and supination, shoulder ER and flexionTO: wrist and finger extension, elbow ext and pronation, Shoulder IR and extension
D2 upper extremityWrist and finger flexion, elbow flexion and pronation, shoulder IR and extensionTO: Wrist and finger extension, elbow ext and supination, shoulder ER and flexion
D1 lower extremityHip ext and IR, knee ext, PF and pronationTO: Hip flexion and ER, knee flexion, DF and supination
D2 flexion lower extremityHip flex and IR, knee flex, DF and pronationTO: Hip ext and ER, Knee ext, PF and supination
D2 extension lower extremityHip ext and ER, Knee ext, PF and supination
Good for working on standingTrunk Patterns
Isolate one component of the pattern, Scapula or PelvisPerform in sidelying
Repeated ContractionsInduce contractions with quick stretchDistal muscle groups3-4 stretches applied, then apply resistance when contraction is strongestUse with pattern or functional activitiesUsed as a strengthening technique when little active movement present
Agonist ReversalsResisted concentric then eccentric of same muscle groupUse with pattern or during position changes (rolling)Strengthening technique when poor eccentric control
Alternating IsometricsPatient holds position with isometric resistance of agonists followed by antagonists
Use to hold positions, less useful to use with patternsStrengthening exercise when poor trunk control
Rhythmic StabilizationIsometric resistance in rotational mvmt (similar to AI) Use to hold positions, less useful to use with patternsStrengthening exercise when poor trunk control
Resisted ProgressionResistance applied during gaitShould not disrupt patient’s momentum or coordinationManual resistance or with elastic band/tube
Abnormalities in Voluntary Movement:
Coordination: Involves the ability to carry out any motor task precisely and quickly. Dependent upon the environment and proprioceptive input (whereas strength does not). Multiple joints and mm’s activated at appropriate times to work together. Common to have frontal plane instabilities with incoordination issues.
Role of cerebellum: Input/Output to M1 Corrects mistakes. Cerebellar pathology leads to unique coordination problems without motor weakness
-e.g. Friedrich’s ataxia, acute/chronic alcoholism, stroke/TBI, MS The primary problem w/cerebellar issues = balance/coordination whereas
balance/coordination will be a secondary issue with stroke and others.Definitions:
Ataxia : general term for incoordination. Gait ataxia = uncoordinated gait. Dysmetria : overshoot/undershoot phenomenon. E.g. finger to nose test or putting their toe on
the ‘X’ on the floor. Dydiadochokinesia : rapid alternating mvmts. E.g. supination/pronation or toe tapping. Tremors :
o Resting - Parkinson’s or some people might have neopathic tremors.o Voluntary: Extra mvmts when completing tasks and resulting in incoordination.
Types of coordination Problems: Abnormal synergies means the inability to move a single joint w/o simultaneous mvmt in other
joints. Brunnstrom stages show abnormal synergies. With stroke, UE has higher incidence of flexor synergy over extensor synergy whereas the LE has extensor synergy (more common) > flexor synergy.
Other sequencing problems include:1) Coactivation across joint. Ex’s = toe walking where DF’s are coming on strongly but
the PF’s are over-powering them OR when someone has genu recurvatum when there is coactivation of the hams/quads simultaneously.
2) Interjoint/trunk coordination – a stable/solid trunk is very important Reaction time (delayed) Slowed mvmt time Difficulty stopping mvmt
Inaccurate force estimation – Happens when you go to pick something up, you need to have the ability to grade their grip strength appropriately for the activity you are performing. If there is a deficit in this, they will be unable to pick up varying cups due to they will be unable to grade their grip strength appropriately.
Brunnstrom Synergy Patterns:Stage 1: no mvmtStage 2: involuntary mvmt (like when they cough/sneeze)Stage 3: abnormal synergy only (locked in that synergy pattern no matter what they do; they are
just stuck)Stage 4: isolate one joint (they can have mvmt at one joint or body part only)Stage 5: isolate two joints (ex: elbow ext with wrist flex or ext)Stage 6: isolate all joints (still not coordinated and can still have slow mvmts or some ataxia)Stage 7: normal mvmt-These are developed for stroke only.-Is useful to progress them through these stages.-Stages 4 through 7 = where you move out of that locked in pattern.
Examination of Coordination: Brunnstrom stages Outcome measures
o Wolf Motor Function Test: for UE’s, has functional components (reaching, grasping), used primarily for research.
o Gait: 10MWT for velocity, 6MWT for enduranceo Nine hole peg test: (more for OT) very standardized
Special Tests (if there is active mvmt):o Finger to nose (can time it and compare R and L) – tests for dysmetria.o Knee to ankle (supine or sitting; can they hit the target or compare side to side; have to
make sure they have adequate strength/ROM for this)o Rapid alternating mvmts – sup/pro; DF/tapping of feet; how long does it take to do 10
taps or how many can they do in 10 seconds – tests for dysdiadochokinesia.Interventions for Coordination:
Functional task training: Modify the task to make it easier or harder. Modify target constraints. Reaching for various cups with different heights/weights or varying amounts of water.
Practice w/varied timing or force demands. LE/Gait: Challenge them in different ways (accuracy vs speed). Can do LE target practice. Important to find out things that motivate them Make a big target and then make it smaller. Can start in sitting and progress to standing then walking, etc. PNF patterns: have both strength and coordination component . Frenkels Exercises “coordination ex’s”: Reciprocal mvmts of hands/feet or tracing
shapes/numbers. These are ways to exercise/practice outside of functional mvmts. The use of weights and the role of strengthening ex’s for coordination is unknown.
o The use of weights can be used to decrease voluntary tremors or decrease incoordination. The weights are used to give proximal (trunk) feedback to decrease tremors or decrease UE/LE (distal) symptoms.
o With strengthening ex’s you want to cover both strengthening and coordination. You need to add a speed + accuracy component into treatment sessions in order to improve coordination.
UE Intervention for Coordination: Manipulation and dexterity:
o Examples include: 1) Finger tapping, 2) Picking up various objects (very small ones, different weights, modifying cups), 3) Drawing/writing, 4) Turning pages, 5) Using phone/keyboard
Motor Control Impairments: Tone/Spasticity
Muscle tone: Definition: resistance offered by mm’s when passively lengthened. Can be either hyper- or hypo- tonic. Range of mm tone is as follows from hypo to hyper tone: Flaccidity, hypotonia, normal,
spasticity, rigidity.Hypotonicity:
Can be an UMN or LMN problem. Examples include: Peripheral nerve damage, Down’s syndrome, cerebellar damage, UE after
CVA (b/c there is no alpha motor neuron or gamma motor neuron activation; no spindle response to high velocity mvmts; the spindle is lax and isn’t taut like spasticity).
Loss of normal alpha-gamma coactivation – slack spindle, no input. Upon examination, the pt will have a relaxed hand posture rather than the normal slighltly
flexed finger/wrist posture (in normal folks).Spasticity:
Encompasses many motor control issues clinically, not useful. Definition: Velocity-dependent hypertonia AND hyperreflexia.
o Examine this by passive motion for hypertone and reflex hammer for hyperreflexia (Need to have both!)
Diagnostic indicator of UMN problem Examples include CVA, PD. Causes can include neural mechanisms, non-neural mechanisms, or both.
o Neural: Alpha motor neurons are more sensitive to input (a small trigger can cause a high motor response). When the neurons are depolarized, they are closer to the firing threshold. This happens b/c there is a net increase in excitatory synaptic inputs and/or net decrease in inhibitory synaptic inputs. This may develop over time as new synapses form. The alpha motor neuron gets extra sensitive. A quick small stretch stretches the spindle and gets facilitation/motor response. The alpha motor neuron is right at that threshold so it doesn’t take much to depolarize. Is velocity-dependent.
o Non-Neural Cause: Immobilization has an effect of changing viscoelastic properties (tendons, ligaments, joint capsule, and contractures). There is an actual change in mm fiber structure (fibrosis, atrophy, or free calcium in motor fibers). Are NOT velocity-dependent.
Treatmento Selective dorsal rhizotomy procedure: revealed weakness after neurosurgery to reduce
spasticity.o Intrathecal baclofen studies.
Examination: Passive mvmt of limbs at varying speeds
o Min, mod, severe tone on Modified Ashworth Scale
o Clasp-knife, cog wheel (release and catch), lead pipe (trying to bend that pipe to get rid of tone)
o Describe specific mm groups and part of range resistance encounteredo No scale for hyptoniao Reflexes
DTR’s/Clonus H-Reflex: indicates sensitivity of alpha motor neuron system. This is a good way
to look at the sensitivity of an alpha motor neuron directly (good for research). This will give an exact/precise measurement of hypertonicity. This is the only way to physiologically measure this. It looks at the amount of depolarization of the alpha motor neuron.
o Self report scaleo Functional performanceo Brunnstrom Synergy Patterns
Other related definitions for tone: Dystonia : Specific motor control disorder (Parkinson’s, Huntington’s) Spasm : Sustained involuntary mm contraction. Decerebrate rigidity : Extension of trunk, all extremities. Is seen in advanced brain cancer or very
bad hemorrhagic stroke. -There is limited clinical relevance Decorticate rigidity: UE flexion, trunk and LE’s in extension. -There is limited clinical relevance
with this.Outcome Measures used for motor recovery in stroke:
Fugl Meyer: Test of Motor Controlo Gold Standard o Takes 20-30 minutes to administero Has sensation, UE, and LE component.o Highly valid/reliable/standardized.o 124 points total (0-35 is severe; 36-55 moderately severe; 56-79 moderate; >80mild)
STREAM (Stroke Rehabilitation Assessment of Movement):o Looks at UE mvmt, LE mvmt, and functional mobility.o 15 minutes to administero Complicated scoring.
Simplified STREAMTreating abnormal tone:
Need to consider:o Neural mechanisms: high velocity stretch puts a stretch on the spindle that sends signal
to the alpha motor neuron via Ia afferent fiber. The alpha motor neuron is the cause of the tone NOT the spindle. The alpha motor neuron is hypersensitive to a quick stretch b/c it’s at a lower threshold.
o Non-neural mechanisms: Tissue becomes fibrotic. Mm’s/tendons conform to being in that same place = why you feel resistance/stiffness throughout the ROM
o Influence of other systems: Stress, effort, body position, bright lights, and loud noises are all stimulating inputs which increase tone. Relaxing noises or slow rhythmic mvmts will decrease tone.
o Functional relevance.o Need to think: why are we treating tone? How does it relate functionally? You wouldn’t
treat JUST tone.o Tone is in “Body Function/Structure” category of the ICF model.
Surgical tx: o Nerve cut or block (common in ped’s, not so much in adults)
Pharmacological tx:o Baclofen (oral or intrathecal)o Valiumo Bo Tox injection
Treating Hypertonicity: Prolonged Stretch – affects neural and non-neural structures to decrease that sensitivity of the
alpha motor neuron and decrease the tightness of the soft tissues around that joint.o NDT: reflex inhibiting positions (RIP)o Serial casts – series of casts to increase stretch. These are really effective but has side
effects of not being able to weightbear. Disadv is that it will limit other motions and will have the other effects of immobilization
o Air splints – temporary Rhythmical Rotation – stretching with a rotation component to decrease tone (hand/elbow). Weightbearing after you get it extended.
Rationale for treating hypertonicity (GTO/mm spindle explanation): The prolonged stretch activates the GTO’s autogenic inhibition and reciprocal facilitation. Is temporary but may allow functional task practice. Autogenic inhibition:
o GTOspinal cord via dorsal columnaction potentialIb inhibitory interneuronsactivates inhibitory interneuron and causes inhibition of alpha motor neuron
Reciprocal facilitationo Facilatory synapseso Example: Prolonged stretch on the biceps leads to autogenic inhibition (relaxation) of
biceps and reciprocal facilitation of the antagonist (triceps) Basically with a prolonged stretch, there is autogenic inhibition of agonists mm’s which causes
them to relax and reciprocal facilitation of the antagonist mm’s(contraction of antagonist). GTO has stretch sensitive endings at the musculotendinous junction (Ib afferent fibers; no motor
component) GTO acts as a balance to the mm spindle where the mm spindle is facilatory and GTO is
inhibitory.
Function of GTO:o 1) Protective responseo 2) Fatigue
Is very sensitive Has low threshold Even a very small threshold will activate the Ib afferent fibers. Is always active whereas mm spindle is not always active.
2 ways to activate the GTO:o 1) Manual prolonged stretcho 2) Mm contraction which stretches the GTO and causes inhibition.
Another way to inhibit GTO (besides prolonged stretch (is manual pressure on the tendon).NDT Approach:
Requirements for Normal Movemento First you want to normal tone then move on to automatic reactions then to isolated
mvmts.o 1) Normalize Tone
With hypertone pt’s, perform rhythmic rotation, hands on stretching, RIP’s, using GTO as inhibitory input, etc.
With hypotone pt’s, you would want to do things to increase tone which may include fast mvmts, bouncing, bright lights, activate excitatory ANS
o 2) Automatic Reactions A.k.a. balance, trunk, head control Goal is to keep trunk upright and maintain good postural control. Righting reactions = head control Equilibrium reactions = trunk control Protective extension = After you lose your balance, you extend your extremities
as protection. This is why people with hemiparesis tend to fall to their weak side b/c they might lack this automatic reaction.
o 3) Isolated Movement Individualized Key points of control Manual guidance – very hands on approach as compared to the traditional
approach which is very hands off. NDT is focused on doing the task correctly without a synergy pattern; if they
start to exhibit a synergy pattern then you would make the task easier. Advantages of NDT
o The therapist uses a hands on approach and are skilled at providing contact in certain places to increase their function.
o Works on functional tasks; normal mvmts w/o a synergy pattern Disadv’s of NDT:
o Evidence is against NDT vs motor control (functional task practice) in terms of function.
Interventions for Limited PROM/Contractures: Stretching
o Stretching in healthy people can increase PROM (30second hold x15 mins)o Stretching can prevent a contracture in people with stroke w/minimal motor function
(daily positioning x30minutes static stretch)o Stretching does not reduce a contracture if they have already obtained a contracture.
Splintingo Static hand splints have no benefit in preventing contracture following strokeo Dynamic hand orthosis only has case studies to support it and they ‘look promising’o Other dynamic splints – Research is variable
Serial castingo Effective at improving ROM in people with CP and TBIo Disadvantages: Higher risk of adverse events, difficult technique/skill requirements,
impaired function due to being in cast. Joint mobilization
o Small uncontrolled studies have shown increased PROM but no functional change w/use of ankle joint mobilization in people w/stroke.
Heat modalitieso US effective at increasing Rom in healthy subjects.o Limited research on hot packs (increased wrist Rom in subjects w/stroke)o Take precaution with pt’s that have sensory/communication/cognition deficits.
Surgical releaseo Tendon lengthening used in children w/CP (Achilles or hamstring)o Achilles tendon lengthening in people w/diabetic neuropathy to prevent pressure ulcer
formationo Resection of HO (heterotrophic ossification)o Recurrence rates are common
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