PT 862 Study Guides PDF

Neural Development and Pathophysiology of CP ★​ Recap of Neural Development ○​ Ectoderm-structure the brain is formed from ○​ Neural crest-PNS ○​ Neural tube-CNS ○​ Notochord-temporary structure ​ Signaling protei...

Neural Development and Pathophysiology of CP ★​ Recap of Neural Development ○​ Ectoderm-structure the brain is formed from ○​ Neural crest-PNS ○​ Neural tube-CNS ○​ Notochord-temporary structure ​ Signaling proteins ​ Differences in brain Prosencephalon (forebrain) Cerebral cortex Telencephalon Subcortical white matter Basal ganglia Basal forebrain nuclei Diencephalon Thalamus Hypothalamus epithalamus Mesencephalon (midbrain) cerebral peduncles Midbrain tectum Midbrain tegmentum Rhombencephalon (hindbrain) Pons Metencephalon cerebellum Myelencephalon medulla Spinal Cord ★​ Mechanisms of Neural Development ○​ Schizencephaly-birth defect w abnormal slits and clefts ion cerebral hemispheres ​ Agenesis of corpus callosum-doesn’t develop connection between hemispheres ○​ Key Steps and Neural Development ​ Patterning-process that decides the fate of neural precursors ​ Motor, sensory, interneurons ○​ Dorsal-sensory (closer to noto) ○​ Ventral-motor ​ Signaling molecules (morphogens) and their concentration gradient-gradient makes exposure to difference chemicals ​ 25 weeks-6 months ​ Neuronal Migration-neurons formed in the center and need to migrate ​ Axonal Migration  ​ Pathway selection-which way to go ​ Target selection-which exit to go ​ Address selection-fine tuning, connect w LMN ​ chemoattractors/repellents-guide cells to the target ○​ Attract-axon to axon ○​ Repel-repel for axon to go another way ​ Synaptogenesis ​ Nature vs nurture ○​ Nature-needed for patterning, migration and synaptic connection ​ Myelination ​ Begins at 28 weeks and at 36 weeks=posterior IC ​ Most of CST by 2→ motor function increases ​ Inferior→superior ​ Posterior→anterior ​ Proximal→distal ​ Sensory then motor ​ Projection fibers before association ​ Leukodystrophy-myelination gone wrong;progressive ○​ Future myelin wont form right either ★​ Role of Environment and Therapy on Neural Development ○​ Example: Development of ocular dominance columns ​ Retinal input connects to lateral geniculate nucleus (thalamus)  ​ LGN connects to visual cortex→cells get stacked together in columns forming stripes ​ normally=distribution but can have issues if all tangled ○​ Patch good eye so give bad eye more input ​ Ocular dominance cell formation severely degraded if deprivation occurred 1-9 wks after birth ○​ Enriched environments-motor, cog, sensory or social ​ Parent-infant interaction ​ Active motor learning ​ Improve motor outcome sin infants at high risk of CP ★​ Development and Pathophysiology of CP ○​ CP-group of permanent disorders of the development of movement and posture, causing activity limitation ​ Non-progressive disturbances that occur in development ​ Classifications: Muscle Tone/Spastic Limb Involvement hypertonia monoplegia hypotonia Diplegia-most common Dystonia-involuntary muscle hemiplegia contraction Ataxia-loss of coordination, triplegia-B/L LE and 1 UE balance Choreoathetosis-writhing quadriplegia movements ​ Associated Comorbidities ​ Developmental disabilities ​ Intellectual disability/autism ​ Epilepsy ​ Vision/hearing impairment ○​ Risk Factors Prenatal Perinatal Postnatal Infection Premature Infection Mom diabetes Birth complications Environmental toxins Abnormal placenta Umbilical cord Trauma Congenital abnormalities abnormalities anoxia Clotting Low birth weight CVA Growth restriction Maternal preeclampsia hypoglycemia/acidosis ○​ Preterm Infant Vulnerability ​ structural/functional immaturity of blood vessels→CVA ○​ RESUME CP PPT Intro to Individuals with Disabilities Education Act ★​ Rehabilitation Act ○​ Section 504 ​ Cannot exclude participation, deny benefits or discriminate ​ Applies to all programs receiving federal funding ★​ IEP vs 504 ○​ IEP-services and accommodations (special ed) ○​ 504-accommodations (food allergies or extra time on tests) ★​ IDEA Sections ○​ Part A: Definitions and Terms ​ Free appropriate education-children entitled to free education ​ Related service-PT, OT, etc ​ Least restrictive environment-most natural (school, home, daycare) ​ Individualized family service plan-EI ​ Individualized education program-school ○​ Part B: 3-21 (school) ​ Specialized instructions/resource study hall ​ Accommodations for standardized test taking ​ PT, OT, SLP ○​ Part C: Birth-3 (EI) ​ Developmental instructions ​ PT, OT, possible SLP ○​ Part D: National Initiatives ​ Grants-personnel, support, assistance Management of the Foot and Ankle ★​ Arthrokinematics ○​ DF-posterior movement of talus + tib anterior translation ​ 10-20 degrees ○​ PF-anterior movement of talus ​ 40-55 degrees ○​ Anterior tibial translation (closed chain) ​ Loading response/gait ​ Sit to stand ​ Stairs ★​ Role in Gait ○​ Initial contact: DF ROM=neutral + DF control/strength ○​ Loading Response/Midstance ​ Functional DF ROM ​ PF strength/control ○​ Terminal Stance ​ DF ROM (for PF stretch for push off) ○​ Pre-Swing  ​ Big toe extension ROM and PF strength ○​ Swing ​ DF ROM and open chain strength and motor control ○​ Energy Conservation ​ Trying to get minimal vertical displacement-inefficient ★​ Balance ○​ Need ankle ROM and strength ○​ Narrow BOS-ankle eversion/inversion ○​ Ex: decrease DF contractions→get pt to lean back and could get it ★​ Sit to Stand ○​ Upright: ​ Requires more torque at knee/ankle ​ Less DF ○​ Lean forward: ​ Greater hip ext torque ​ More energy ​ More DF ROM needed ★​ Stairs ○​ Ascent: ​ DF ROM + PF strength ​ Open chain DF for limb advancement ​ Greater hip and knee angles ○​ Descent: ​ DF ROM and eccentric PF control ​ Greater PF/DF angles ★​ Common Impairments After CNS Injury ○​ Changes in Tone/Reflexes ​ Hypotonic-decreased tone; flexible ​ Excessive pronation-loss of arch in WB ○​ Causes femur and tibia to IR, valgus, hip drop ​ Greater falls risk ​ Spasticity-velocity dependent ​ PF-swing and stance ​ Toe flexors ​ Initial contact→weight acceptance ​ Loss of GRF→BOS issues ​ ROM Deficits ​ DF-functional and open chain ​ Loss of pro/sup ​ Big toe extension ○​ Decrease in DF so PF activate at the wrong time and propel up inside of out ​ Increase vertical displacement ​ Strength/Motor Control Deficits  ​ Isolated vs synergistics ○​ Can be both good and band ○​ More PF strength=better static balance ○​ More DF=better balance ​ Anterior Tibialis-INV ○​ Open chain DF-swing ​ Extensor Digitorum Longus-EVR ○​ Open chain DF-swing ​ Extensor Hallucis-EVR ○​ Open chain DF ​ *all help w ankle strat-controlling posterior displacement ​ Gastroc/Soleus ○​ Closed chain tibia control-loading response ​ Propulsion-pull tibia posterior and knee ext ​ Post Tib ○​ Creates rigid lever for gastroc to work ○​ Controls pronation and creates supination-end of stance ○​ If you cant sup then dont get push off ​ Peroneals ○​ Assist w PF and balance ​ Could get irritated if calves not working and they are compensating ​ Energy System Changes ​ Peak VO2 ○​ Lower thresholds ○​ Decrease in mobility=lower capacity ​ Personal Factors ​ Negative impact on perception ★​ Examination Techniques ○​ Motion ​ DF:open and closed ​ Toe to wall-closed ​ AFO loss-DF,PF and big toe ext ○​ Force ​ MMT and HHD ​ Control vs strength ​ Isolated jt testing ​ Palpation during functional tasks Contributors to Impaired Activity Performance After Chronic Stroke/TBI/CP ★​ Force Effects  ○​ Direct effects-loss of neural tissue secondary to stroke ​ Paresis-partial loss of voluntary activation of motor neurons ​ Plegia-total loss^^ ○​ Indirect-secondary changes ​ Sarcopenia-loss of muscle tissue ★​ Power Effects ○​ Velocity dependent in concentric torque production ○​ Spastic antagonist is not a restraint ○​ Matters w gait→need hip ext ROM for mech advantage for PF power for propulsion ★​ Motion Deficits ○​ Contributors: ​ Weakness ​ Increased tone ​ Immobilization ​ Prior comorbidities ○​ Tissue influence-jt, soft tissue, muscle length, weakness ○​ Altering ROM provides degrees of freedom that could improve performance ★​ Motor Control Deficits ○​ Motor ​ Lack of individual mvmts ​ Fractionated-ability to move one body segment independently of others ○​ Aka abnormal synergies (flexion and ext) ​ Harder task that required more work=greater expression of synergy ​ Changes in tone→see below ​ Motor planning ​ Feedforward-anticipatory control ​ Feedback-important for ongoing and post response correction ​ Anticipatory control-frontoparietal, basal ganglia and cerebellum ​ L hemisphere more specialized for anticipatory control ​ Examples: ○​ Action selection-nonuse of arm, learned comp mvmts ○​ Mvmt specification-poor speed, abnormal muscle activation ​ Reactive control ​ Relies on sensory feedback and error-based reactive mech ​ Response to unexpected perturbation during goal oriented actions ​ Biomechanics-interactive torques ​ Lack of coordination ​ Compensations to accomplish task ​ Trunk play important role in control extremities ​ Altered biomechanics  ○​ Initial posture/initiation ○​ Length-tension relationship for muscle contraction ○​ Sensory perception ​ Somatosensory ​ Anesthesia–partial or complete loss ability to feel ○​ Can interfere w action selection, planning and execution ​ Damage to ascending pathways or cortical areas ○​ Modality-specific-not separate above thalamus ​ Entire limbs impacted ​ Light touch and proprioception ○​ Discriminative-integrated at cortical level ​ Visual ​ perceptual-pusher ○​ Cognitive ​ Attention-focusing, shifting, sustaining ​ Dual task ​ Depression ​ Apraxia ​ Neglect ★​ Mechanisms Contributing to Lack of Fractionation ○​ Paresis→biomech compensations ○​ Recruitment of same side reticulospinal fibers ​ Automatic posture and gait mvmts ​ These fibers innervate multi neurons and cant do individual ​ CST normal does individual mvmts but get taken out w a stroke so the RST steps up but isnt individual ○​ Spasticity? ​ Confusing and unsure ​ Increased tone in antagonist will lead to reciprocal inhibition of agonist and resists volitional mvmt ​ No relationship tho in research ​ Increase tone=abnormal motor control→decreased ability for volitional mvmts=synergies ​ Increased tone at rest=abnormal resting postures that lead to contractures→increase passive noncontractile resistance to mvmt ​ May be true ★​ Energy Systems ○​ Metabolic cost=significant disability ​ Weakness, paresis, gait ​ Deconditioning ​ CAD-limits participation Task-Oriented Examination and Intervention ★​ Approaches to Examination in Neuro Patients  ○​ Disease/Body Structure and Function​ ​ Impairments and diagnosis ​ Function not central-main focus is impairments ○​ Participation and Activity ​ Focus is on function-disease is modulator ★​ Examination and Movement System Diagnosis ○​ Goals ○​ Recovery Stage ○​ Current Status ○​ What can they do? ★​ Movement System Diagnosis for Gait After Stroe ○​ Weight acceptance ​ Driver: DF control (avoid foot slap) ○​ Stance ​ Driver: knee flexion, hip ext control, abductors, knee exts and eccentric PF ○​ Propulsion ​ Drivers: hip ext, eccentric PF control, PF power ○​ Limb Advancement ​ Drivers: hip flexors, knee flexors and DF Atypical Development ★​ Review of Typical Development ○​ Developmental Domains ​ Sensory ​ Cog ​ Motor ​ Communication ★​ Gestational Age ○​ Full term=37-42 weeks ○​ preterm= less than 37 ★​ Screening ○​ Checklist ​ Ages and Stages ​ Comm ​ Gross motor ​ Fine motor ​ Problem solving ​ social ○​ Milestones ○​ Validated Measures of Global Development ​ ADOS  Pediatric Standardized Assessments ★​ Test Properties ○​ Validity-testing what you think you’re testing ○​ Reliability-internal and external ○​ Sensitivity-screening and don’t want to miss anyone ○​ Specificity-important w expensive/higher risk interventions ○​ Norm-Referenced ​ Look at performance relative to certain population ​ Compare to normative distribution ○​ Percentile, age equivalents ​ Administered in standard manner ○​ Criterion-Referenced ​ Examine performance relative to established criteria ​ Change over time w the individual ★​ Test Selection, Administration and Scoring ○​ Considerations ​ Age, setting, behavior/functional abilities ​ Purpose of testing ​ diagnosis/PMH ​ setting/materials ★​ Standardized Tests by Age (all activity) AIMS PDMS-2 BOT-2 GMFM CAPE Identify gross motor delay Identify gross and fine Identify motor Motor performance Assess Norm motor delay impairment for CP participation reference/observational Norm references Norm-referenced Criterion 6-21 y/o Birth-18 months Birth-6 years 4-21 y/o referenced Self report or Prone, supine, sitting Complete w/in 5 days of Fine Manual Control Lying and Rolling interview standing→ need to score all starting 4 cat Gross: -​ Precision and Crawling/Kneeling Can complete across a week -​ (0-11) integration Standing Naked or diaper -​ Stationary Manual Coordination Walk/Run/Jump No min or max # of trials -​ Locomotion -​ UE dexterity Can be placed in Observer or not observed -​ Object manip (12 Body Coordination starting position Don’t have to start at lowest months+) -​ B/L No shoes in window-but need a pt for it Fine: -​ balance Max 3 trials Scoring: age and score for -​ Grasping Strength/Agility Scoring: 0-3 percentile -​ Visual-motor -​ running/speed Raw score/% integration Stick w 1-2 trials Scoring: 0-2 percentiles  *comes w booklet Adult Assessment and Treatment ★​ Accelerated Skill Acquisition Program (ASAP) ○​ Combo of task specific and skill based training-pt centered ○​ Capacity Building ​ exercise/science physiology ​ Improve motion, force and energy ​ Motion provides degrees of freedom ○​ Skill Learning ​ Neural plasticity and behavior ​ Improve motor control ○​ Motivation ​ Social-cog ​ personal/environmental factor ★​ Interventions to Alter Motion ○​ Hypomobility-secondary to immobilization, weakness, increased tone ​ Depends on underlying abnormality ​ Manuals, stretching, progressive splinting ○​ Hypermobility-secondary to weakness, reduced tone ​ Depends on functional activities and safety ​ Splinting for protection ★​ Augmenting Force ○​ Direct training ○​ Functional strengthening ○​ Baseline paretic knee power was associated w changes in locomotion ○​ CPGs recommend strength training but they dont talk about power even tho we know power is crucial ★​ Improving Motor Control ○​ Requires practice ○​ Considerations:  ​ Priming-exposure to one stimulus influences the response to another succeeding stim ​ Practice variables-principles!! ​ Task specific ​ intensity/complexity ○​ HR, RPE ○​ Optimal challenge=important (cog and physical) ○​ Higher intensity improves ​ Task performance and learning ​ Energy cost-more efficient ​ Real world activity ○​ Complexity-might be better to challenge more than go from simple to complex ​ dose ​ biomechanics/alignment ​ Altered to challenge to ease ​ Environment ​ Orthoses ​ Does not need to be perfect but optimal ​ Classifications of Skills​ ​ Discrete-distinct start and finish (kicking, throwing) ​ Serial-series of discrete performed in defined order ○​ Transfer, sit to stand ​ Continuous-no distinct beginning or ending (walking, running) ★​ Engaging in Sensory-Perceptual System in Skill Learning ○​ Somatosensory, visual and vestibular ○​ Sensory ​ Sensing environment and task constraints ​ Feedback induced corrections ○​ Movement Correction ​ You’re helping to minimize error and help the pt through movement ​ Making it normal ○​ Error Augmentation ​ Split-belt treadmill ​ Start them off wrong so their body detects error and then tries to normalize it Adult CVA Assessment and Treatment Part 2 ★​ Critical Elements of Gait ○​ Upright trunk ○​ Dynamic balance and static stability ○​ Swing limb advancement ○​ Propulsion  ○​ Adaptability ○​ Metabolic energy efficiency-smooth and shock absorption ★​ Gait After CVA ○​ Slow speed ○​ Asymmetrical-arm swing and step to/shortened step length ○​ Poor stability-falls ○​ Increased energy expenditure ○​ Stance ​ inconsistent/poor heel strike-impaired foot position ​ Lack of knee flexion during loading response ​ Too early or remains ​ Lack of hip ext from mid/late stance ​ Trunk flexed/rotated ○​ Swing ​ Poor clearance of hemiparetic limb ​ Lack of hip ext at initial swing ​ Lack of hip flexion through mid and late swing ​ Lack of knee flexion at initial and mid swing ​ Ack of push off and heel rise ★​ Gait Speed ○​ Indicator of functional and prognosis;community walking ○​ Uses multiple systems ★​ Neuroplasticity ○​ Error-devices, feedback, marching, arm swing, obstacle course ★​ Principles of Plasticity ○​ Use it or lose it ○​ Use it and improve it ○​ Specificity-do the things to improve the thing ​ Treadmill, robots ○​ Repetition matters ○​ Intensity matters ​ Prioritize stepping strategies ​ Higher intensities w orthoses could facilitate gains ○​ Time matters ○​ Salience matters-must have sufficient importance to pt ○​ Age matters ○​ Transference-plasticity in response to one training experience can enhance acquisition of similar behavior ​ Early walking promotes recovery of walking and non-walking tasks ○​ Interference ★​ HIIT ○​ Short interval-short, high intensity bursts ​ 15-30 seconds ​ 1:1 burst to recovery time ratio  ​ Maximizes time spent in high O2 consumption ○​ Long interval-long, high intensity bursts ​ 3-4 minutes ​ 1:1 or 4:3 ​ Emphasizes high neuromuscular intensity ○​ Low volume-short, high intensity bursts ​ 15-30 seconds ​ 1:4 or 1:12 ​ Maximizes time in high % VO2 peak Beyond the Motor System ★​ Praxis ○​ Conception and planning of new action in response to environmental demand ○​ Requires integration of motor, sensory, perception, cog and cultural context ○​ Involved in all complex/sequential behaviors ​ UE: cooking, using tools, eating, dressing ​ Show me how you would use this tool ​ LE: walking ○​ Left Angular and Supramarginal Gyrus ​ Neural node in praxis network ​ Integrates visual, somatosensory and audio ​ Extrinsic→intrinsic ○​ Left Hemisphere specialized for praxis ​ B/L deficits bc connection crosses to the other side