week 3 neuro summary.pdf

3.1 PD: intro PD 1817 by james parkinson: shaking palsy “ characterized by involuntary tremulous motion w lessened muscular power in parts, not in action & even when supported w a propensity to bend trunk forwards & to pass from walking to running pace, the senses and intellects being uninjured” 2nd...

3.1 PD: intro PD 1817 by james parkinson: shaking palsy “ characterized by involuntary tremulous motion w lessened muscular power in parts, not in action & even when supported w a propensity to bend trunk forwards & to pass from walking to running pace, the senses and intellects being uninjured” 2nd most common neurodegenerative disease (alzheimer’s 1st) symptoms: rigidity -bradykinesia micrographs -masked face postural abnormalities resting tremor PD attributed to loss of neurons, decrease in dopamine in substantia nigra & impaired nerve transmission to striatum, impacting fluid mvmnt there lewy body formation (gliosis and scars) -LB is an abnormal deposit of alpha synuclein protein w/in brain (substantia nigra) pathophysiology of PD deficiency of a single neurotransmitter- dopamine degeneration of sub nigra, pars compacts= altered fxn of direct and indirect motor loops lack of dopamine signaling to striatum -diminished ability to inhibit the “go” pathway thru GPi = increased tonic inhibition of thalamus, decreasing excitation of frontal cortex decreased dopamine= less inhibition of striatum to “non go” pathway -decreased inhibition of striatum=increased inhibition of GPe and excitation of subthalamic nucleus to increase tonic inhibition of thalamus = impact is decreased motor activation pedunculopontine nucleus primarily affects reticulospinal tract & lat corticospinal tract reticulospinal tract responsible for postural control and reactions (overactivity of both flexors and extensors leading toward trunk and proximal girdle muscle rigidity) imaging in PD idiopathic PD= changes in sub nigra and pedunculopontine nucleus MRI- look for swallowtail sign normal- area is dark PD- dark area lacking MRI may not be able to capture changes PET: positron emission tomography SPECT: single photon emission computed tomography -investigat extend of activity of dopamine transport w/in a brain red: highly active levels of dopamine transport in midbrain or subcortical gray matter (where dopamine interacts w go or no go pathway in BG) PD: fewer red areas & more green-indicated less uptake of dopamine levodopa: can see it helps in photo pet and spect imaging the best (no real evidence to prove) classification of PD 1. primary PD: idiopathic 2. secondary PD: symptoms due to drugs and toxins parkinsonism symptoms could arise from a diff disorder affecting the CNS and BG including brain injury, HIV, AIDS, and normal pressure hydrocephaly 3. parkinson’s + syndrome: include neurological conditions similar to PD but diff etiology outside of BG not typically responsive to standard tx nor meds 4. other neurodegenerative disorders: AD, spinocerebellar ataxia, inherited dystonia, genetic metabolic abnormalities & picks disease normal pressure hydrocephalus secondary parkinism condition abnormal buildup of CSF in ventricles of brain due to blockage causes ventricular to enlargement, increase ICP &/or urinary continence gait disturbances near normal arm swing WBoS bilateral ER at hips PD and NPH- have a decreased gait velocity, stride length, foot clearance, and flexed trunk posture w impaired postural reflexes both have hypomimia & hypophonia shunt help relieve pressure & allow for improves CSF - known to cause hemorrhage, brain edema, subdural hematomas & infection progressive supranuclear palsy PSP parkinson’s + mvmnt disorder occurs from damage to brain impacts: ocular mvmnt frontal lobe fxn cerebellum -damage to CNS result from neurofibrillary tangles thruout BG, BS, dentate nucleus & frontal lobe atrophy presentation masked face rigidity loss of voluntary ocular motion (vert and horiz eye mvmnts) facial dystopia rare eye blinking classic facial expression: looking surprised pts will be rigid in hyperext lifespan shorter (5-7 yrs after diagnosis) multi-system atrophy MSA parkinson’s + mvmnt disorder widespread neuronal loss (bs), BG & cerebellum w buildup of alpha synuclein protein thru-out brain ^ protein involved w lewy body (in prim PD) MSA results in rapidly progressive multisystem neurodegeneration & impacts autonomic fxn :including BP regulation, B&B control & cardiac dysfxn short lifespan (7-9 years of diagnosis) presentation tremors rigidity postural instability cortico-basal ganglionic degenerartion CBGD parkinson’s + mvmnt disorder degeneration of frontal parietal cortex and BG asymmetric presentation thats dependent on location of parietal lobe atrophy presentation rigidity apraxia aka alien limb syndrome (involuntary but purposeful hand mvmnt pts may have dementia memory impairment visual changes dysphasia lewy body dementia similar to PD have hypomimia rigidity flexed posture tremor short and shuffling gait pattern -linked to buildup of alpha synuclein -impaired ACH and lewy body formation -lewybodies in brainstem PD -lewybodies in cerebral cortex & brainstem same presentation as parkinsonism but also have dementia, psychosis and visual hallucination Robin Williams had it :( diagnosis of PD MDS clinical diagnostic criteria for PD parkinsonism bradykinesia w at least one of resting tremor or rigidity may have postural instability, freezing of gait clinically established PD clinically probable PD: cardinal symptoms like: postural instability, freezing of gait w/o red flags & in absence of other exclusion criteria….idk what this means pts presentation has to be differentiated from 2nd parkinsonism to tremor from: drug exposure essential tremor NPH multiple small vessel disease strokes other conditions to be studies: 1. supranuclear palsy 2. frontal temporal dementia 3. cerebellar ataxia Summary primary parkinsonism is characterized by rigidity, bradykinesia, resting tremor, postural instability, and gait changes other parkinsonism conditions present and progress differently, with limited response to dopamine treatment 3.2 Clincial presentation cardinal symptoms: resting tremor & cogwheel rigidity 2 core motor symptoms 1. rigidity 2. resting tremor cogwheel rigidity: due to hypertonia -ratchet like mvmnt when muscles passively stretched rigidity: also co-contraction of agnostic and antagonist muscles hypertonia not same as spasticity bc rigidity is not velocity dependent 90% of pts have in extremities, core & trunk m’s & face m’s resting tremor postural or kinetic tremor while resting disappears w volitional mvmnt (diff then intention tremor seen in MS) low frequency 4-6 Hz: fingers, wrist hands, legs, chin, mouth, tongue cardinal symp: hypomimia & micrographia bradykinesia: 3rd of 5 cardinal symptoms -slowness of mvmnt w less fluidity & requires more effort term also used as hypokinesia: loss of dexterity & amplitude of mvmnt brady and hypokinesia include: hypomimia: lack of facial expression micrographia: progressively smaller handwriting hypophonia: lower volume of voice cardinal symptoms: gait & postural instability last two symptoms: gait and postural instability includes: festinating (shuffling gait) postural instability=combined effects of bradykinesia, rigidity causing loss of postural reflexes & righting reactions presents: stooped, flexed posture w shuffling gait & forward propulsion due to ant displacement of COM flexed posture & lack of appropriate motor programs=reduced BOS and perturbations (especially post perturbations) ambulation: smaller & more rapid steps to regain BOS due to poor COG leads to ant falls during gait other symptoms dystonia sialorrhea: excessive salivation dyskinesia blepharospasm: eye twitching inability to keep eyes open dysarthria dysphasia non-motor symptoms decreased attention, planning, language, memory mood disorders >listed over in graph (irritability as well) urinary urgency frequency & incontinence constipation fatigue & sleep disorders pts should be monitored for presence of: hallucinations or delusions lightheadedness or orthostatic hypotension loss of smell, taste, pain vision probs weight loss symptoms specific to etiology or diagnosis of parkinsonism & response to tx disease progression- motor 2 major types 1. disease progression postural instability & gait difficulty PIGD before disease onset or diagnosis of 2. tremor dominant TD pts w these two present w worst motor impairments akinesia non-motor symptoms last 20+ yrs early stage PD early symptoms *she included all the symptoms from earlier again sleep disturbances/disorders so im not adding it again hehe* depression pts w more motor dominant variant present w constipation more unilateral symptoms (more in resting & anxiety action tremors) hypersomnia (decreased sense of smell) can present w slower progression of disease-poor excessive day time sleepiness progression: lead to postural instability & response to dopamine tx research has indicated more than just two falls variants of this condition, categorized based on their motor and non-motor impairments response to dopamine treatment and motor additional symptom responses to levodopa progressive non-motor symptoms progression - not clearly established cognitive impairment looking at progression: look most at motor fatigue components that have direct impact apathy later progression pain variable involvement: B&B changes orthostatic hypotension kinesthia (proprioception) freezing in gait psychosis decline in executive fxn dementia inflexible cognitive & motor programs long term complication due to dopaminergic therapy: motor fluctuations, dyskinesia, & psychosis hoehn and yahr staging categorizing severity of condition stage 1: mild symptoms- don’t interfere w daily activity; unilateral score: 1..5 indicates unilat symptoms w axial/trunk involvement stage 2: symptoms present bilaterally- walking and daily activities can be affected & balance intact score: 2.5 indicated mild bilat disease-ability to maintain balance when pulled backwards stage 3: mild to mod bilat w loss of mvmnt and slownesssome postural instability but pts still physically independent stage 4: severe & limitin- still able to stand but may need walker; no longer independent w daily activities & cant live alone stage 5: wheelchair bound or bed ridden unless aided &. requires continuous care summary parkinson’s disease is characterized by 5 cardinal motor symptoms, but also presents with dysfunction in other symptoms that decrease function, participation, and quality of life 3.3 PD medical management medical management of PD initial way of tx: dopaminergic therapy can indicate etiology of disease; either idiopathic or secondary parkinson’s important: dopamine cant cross BBB -precursor needed before dopamine is administered to BG levodopa (L-DOPA): gold standard tx -given w/in bloodstream and can cross into CNS processes into dopamine & can be facilitated by dopamine agonists monoamine oxidase type B inhibitors (MAOB inhibitors) -provided to minimize breakdown of dop in brain (more availability for BG) together, they increase overall available supply of dop w/in sub nigra to be provided for striatum levodopa (L-DOPA) short half life ~90 mins earlier stages of PD: lasts several hours pts respond well to meds w improved motor symptoms (even if given 2x a day) no significant return/deterioration of symptoms if pt misses occasional dose in early stages oral intake overtime: levodopa carbidopa gel (duodopa) given- more invasive for increased dosage -intra-intestinal booster infusion (in duodenum) via a PEG-J tube- - -level c evidence shown to mitigate side effects of L-dopa usage particularly in those presenting w reduced response to oral intake of L dopa side effects of levodopa early side effects nausea orthostatic hypotension (sudden drops in BP) daytime somnolence progressed SEs progressive loss of neurons duration of clinical benefit gets smallerresulting in wearing off effect (aka “off” mvmnt period) off period- initially improved by increasing frequency or amount of L-dopa doses can lead to side effects due to chronic use, wearing off effects: pounding, performance of repetitive purposeless motor behaviors, drug-induced dyskinesia’s & neuropsychiatric probs side effects start 3-5 yrs after initial tx in ~30 % and progress 50% of pts after 5 yrs https://www.youtube.com/watch?v=4S56JGo826g time is everything “on” vs “off” stage results in pts having 2 faces (clinical presentation) based on timing of meds w respect to when PTs see them “on” state: meds working, minimal motor impairments -may present w: dyskinesia (especially w chronic use) “off” state: meds wearing off, starts to present w typical motor impairments severe cases: quickly switch from mobile to complete immobility ^^ this is why its super important to be aware of their med times and treat them during different time periods to provide them w strategies to help them cope negative prognostic indicators neg prog indicators in PD male gender old age presence of dementia cognitive deficits depression psychosis poor response to L-dopa indicating a non-prim PD increased severity of bradykinesia rigidity postural instability gait difficulty -risk of mortality increases by a factor of 2.2 in PD compared to general pop -mean survival ~20 yrs after initial diagnosis (prim PD) Summary primary parkinsonism can be treated with levodopa timing is essential to individualize patient rehabilitation timing: important to teach pt how move in “on” period and “off period” 🌹 3.4 surgical management ablative surgery destruction (removal) of brain tissue to ablate disease symptoms has irreversible effects purpose: disrupt abnormal signaling to thalamus research says it can improve tremor, bradykinesia, rigidity, gait disturbances, balance & Ldopa induced dyskinesias high rates of complications (more bilat cases), especially considering advances made in deep brain stimulation benefits lack of implantable hardware-could house failure or infection few surgeries required typical procedures thalamotimy- targeting thalamus pallidotomy- targeting GP subthalamotomy- targeting subthalamus deep brain stimulation proven to be effective in improving impairments surgery involves implanting electrodes into diff locations of brain stimulation program can be adjusted by med team during and after procedure to determine pts best response to various stimulation parameters where? research supports DBS in: subthalamic nucleus GPi -to counter motor fluctuations & dyskinesia unilateral pallidotomy: effective at reducing CL dyskinesia bilat subthalamic nucleus: recommended to reduce dependence on dopaminergic meds bilat GPi: recommended to reduce hyskinesias if pt is likely to remain on dopaminergic meds after surgery stimulation of GPi for pts w limited cognitive reserve, assessed by processing speed or working memory, or presence of depression who gets the ? ideal candidate for DBS: pts w short med on-off fluctuations ~2-3 hrs & may result in significant uncontrolled dyskinesias or tremors “on” period: good responsiveness to L-dopa tx, minimal gait difficulties, postural instability and speech probs -no to minimal changed in cognitive, psychiatric & behavioral status (typically dx over 5 yrs) no need to do early since theres no evidence of neuroprotective or disease modying effects parkinsonism + syndrome shown to NOT benefit from DBS impact of DBS benefits increased “on” periods decreased resting tremor decreased rigidity decreased bradykinesia decreased dyskinesia Watch Parkinson's Disease Before and After Deep Brain Stimulation https://www.youtube.com/watch? v=vjgzso2iWzM some evidence of improved sleep and pain -causes verbal disruption in fluency -variable impact on mood -decreased cognition w possible dementia w/in 6 months, w changes in mood and behavior post-DBS ^why they say to target GPi DBS ineffective at managing gait & balance impairements that are NOT responsive to meds and can cause potential changes to speech and swallowing summary Deep brain stimulation can be an effective treatment for PD motor symptoms DBS Three Years After Surgery https://www.youtube.com/watch? v=17ch1guvoLA 3.5 PD rehab assessment PD EDGE taskforce APTAs^-recommend these -OCM vary per setting (acute vs in-pt vs out-pt) MDS-UPDRS -taskforce includes: mini BESTest 6 min walk test montreal cognitive assessment 10 meter walk test PDQ-8/PDQ-39 berg ANPT core set of outcomes fxnal gait assessment activity specific balance confidence scale 5x sit to stand parkinsons disease questionnaire (PDQ-39) measures frequency of complications due to pts condition self-report survey subjective 39 q’s separated by 8 dimensions determines impact of PD on their QoL and QoF PDQ-8 shorter 8 version w 1 item per domain self-report pts rate frequency of times they encountered following in the past month designed to understand impact of dimension on pts fxn and well being MDS-unified PD rating scale (UPDRS) mini BESTest 14 item measure assess performance on sit to stand rating scale consisting of 4 sections heel raise 1. standing on 1 leg compensatory stepping evalv of non motor impairments -meditation, mood, behavior (forward, lat & backward 2. self evaluation of ADLs -speech, swallowing, handwriting, 3. motor skills/impairments standing on foams surface w eyes opened and closed dressing, hygiene etc balance on an incline w eyes closed 4. pharmaceutical complications -score out of 176 points (higher changes in gait speed score: higher disease severity) walking w head turns see more in research & NOT pivots clinical settings stepping over obstacles better captures: bradykinesia, dual timed up & go ^pt asked to perform time tremor, & rigidity to help determine classification of TD or up and go while counting or postural instability gait difficulty manually manipulating an variant of PD object -mini BESTest is 28 points w lowest score taken from each leg rehabilitation management cut off scored in PD -per PD EDGE task force recommendation 1. tug>12s= fall risk in PD assessment end goal is to facilitate a. cognitive TUG: serial count backwards of 3 from improved activity level & 50 during tug participation w/in their b. manual tug: carrying a cup of water during tug 2. 5x sit to stand: >16 secs= increased fall risk society 3. gait velocity: 0.88 m/s indicated community 4. measures we pick must serve toward long-term ambulation goal of pts mini-BESTest < 20/28 falls at 6 months in PD w 86% individualized increased sensitivity & 78% specificity community activity and 360 turn test help differentiate bw main subtypes of PD of TD or PIGD participation required counting # of steps it takes to do 360 turn PIGD >7 steps. 83.1% sensitivity or >10 steps 83.8% specificity PIGD > 3.67s 81.5% sensitivity or > 5.01. 89.2% specificity researchers proposed these cutoffs would be beneficial in identifying pts w postural instability or gait difficult dominant subtype who may have high risk for cognitive impairment & less response to DBS 3 meter backwards walk test developed by carter v et al in 2019 assessment of time it takes for pt to walk 3 meters backwards 2020 researcher showed 3 MWBT had the highest overall accuracy for dxing fallers in pts w PD ^compared to TUG, TUG cognitive, 10 MWT, or 5x sit to stand group proposed cutoff score of 4.2 secs- reportedly has a 71% SN rate and 64% SP rehab management: PD specific assessment medication timing balance righting reactions we should assess and treat pt in both “on” and “off” periods pt walking in a crowded place… treat during “on” period useful to observe any side effects due to medication to gain an understanding of challenges thru-out the day useful to observe response to retropulsion pull-release test to assess their ability to perform correct balance riding reaction - bc of high likelihood of postural instability ^done separately or part of mini-BESTest summary outcome measures specific to PD may be useful in investigating PDspecific impairments and limitations not common to other populations MDS-UPDRS Parkinson’s Disease Questionnaire Mini BESTest 3.6 Rehab Management for PD Duties PT- Fxn and balance OT- ADL SLP- cognition, communication, swallowing PT- we as PTs focus fxn, through cueing to improve motor function minimize rigidity, reduce mitigate balance impairments, improve gait, mobility issues, fatigue management Aerobic activity- 150 min per week Results in improved motor action, balance and gait , increase in brain neurotrophic factor levels, strength, physical functioning, sleep, QOL, But not falls Safely exercise as balance improves overtime KNOW THIS 3.7 Rehab Strategies for PD Objectives- address freezing design evidence supported group exercise program for PD Goals: mitigate decline or reinstate movement Address rigidity, bradykinesia. This prevents patients from retropulsion which prevents them from forward flexing, which helps them flex forward for getting up and sit to stand movements Teach strategies supine to sidelying sidelying to sitting vise versa Training Speed, Strength, Amplitude of movement can impact disease progression Retropulsion and balance righting are priorities for PD patients GAIT TRAINING Issues: low velocity Stride clearance festination continued forward leaning fall risk Freezing (difficulty in initiating gait) trembling, shuffling, akinesia Freezing happens when something comes in the way of the usual pattern from the individual obstacles, avoiding something, turning, narrows spaces Types of freezing turning hesitation state hesitation reaching tight quarter open space hesitation Some Strategies for overcoming freezing Marching Intentional Heel strike Stepping over transverse lines Taichi Qigong Increase QOL lower anxiety motor symptoms alleviation lower risk of falls Power Moves PWR targets bradykinesa, rigidity, automaticity, coordinatiohn’ high amplitude movements, effort, attention 3.8 Rehab PD, Cueing Objectives: Cueing LSVT LOUD and LSVT BIG And evidence Primary PD- related to lack of dopamine in substantia nigra, leading toward inability of activation of the thalamus in the primary motor cortex Pre motor area- controls trunk and girdle muscles. Coordination for anticipatory movements Supplementary motor area- facilitates movement initiation planning and coordinating sequential movements Lateral premotor area- selects and initiates motor plans based on external cues lighting, sounds, tactile cues, THIS REGION is less impacted by basal ganglia func. SO this is a opening for PD rehab External cues BYPASS basal ganglia, and engage the INTACT lateral premotor cortex. Auditory cues- cadence velocity and stride length Visual cues- stride length only External cue equipment canes with lights shoe lasers tapes metronome music verbal cues CUE STIM DEVICE- provides tactile electrical stim at the waist to thigh to prevent freezing Q1 device- visual or tactile LSVT Global- Lee Silverman Voice Therapy global intervention intense treatment set protocol to challenge the impaired system and deliver activity dependent neuroplasticity Addresses brady and hypokinesia along with deficit in kinesthetic awareness LOUD and BIG programs Loud- speech , being loud makes patients open mouth, changes breath, articulation in speech changes posture Big- movement - increase drive and amplitude of output. lack of awareness of their smaller movements causes more neurodegeneration 4 week intense protocol for self awareness recalibrate perception of their movement LSVT Big evidence- more effective than home exercise, nordic walking, or shortened tests like the timed up and go and 10 meter walk test. Proven to alter physiology to improve proprioceptive recalibrationImproves amplitude of movement, regain normal movement from brady and hypokinesia 3.9 PD: Rehab Management: PWR! PWR!Moves (nadia thinks this is the coolest thing ever) AKA: Parkinson’s Wellness Recovery importance of exercise at high intensity beyond self selected efforts to enhance neuro plasticity goal: improve amplitude of activities by curing pt how to make big mvmts founded by Dr. Becky Farley PT exercise!!! neural plasticity designed from LSVT BIG principles of LSVT - lee silverman voice treatment protocol - 16 treatments (4x60 min per week for 4 weeks) education pt on mvmts and why big max effort & increase intensity until fatigue calibration: calibrate intrinsically how much effort - must follow EXACTLY - must be certified - Targets 4 impairments rigidity bradykinesia postural instability cognitive/attention - - if not certified call mvmts “large amplitude mvmts” ~ LSVT vs PWR! sitting/standing mainly bradykinesia STRICT - anyone can do it no specific exercises/no order sitting, standing, quadruped, prone, supine focuses on all impairments of PD - bradykinesia - postural instability - cognitive/attention disorders Referring to exercises above implemented w/ all levels of disease but tailored to pt 1:1 ratio or group settings perform 4 repetitive whole body exercises in any of 5 positions Power Up: anti grav extension counteracts rigidity improve postural stab or prevent it Power Twist: axial mob reduce rigidity when practiced w/ rhythm Power Rock: weight shifting decrease effects of freezing to improve balance move more efficiently Power Step: transition efficient mvmt during fxnal activities Prepare: improve axial mob, strength, flexibility & posture start big & slow using sustained effort for large amplitude so they can learn counteracts festinating gait Activate: increase intensity, effort & speed to decrease bradykinesia Flows: power up, power rock, power twist, power step mvmts improves coordination & cognitive retraining of mvmts w/in sequence like in every day life Boosts: incorporates vision & breathing improves volume of voice, speech promotes CV wellness video examples PWRMoves intensity repetition large amp 4 moves 4 methods pt does some tactile cues but a lot of verbal cues Summary huge mvmts to fix gait 3.10 SCI introduction Spinal Cord Injury damage to the spinal cord due to trauma or non traumatic etiology - tumor, stroke, inflammation damage to sc, nerves at end of spinal canal that can result in altered strength, sensation, other fins afferent n signaling from periphery altered to cns - affects pain, touch, proprioception, mvmt efferent n signaling from brain to periphery can be altered - motor control, strength, cooordination categorized as - paraplegia (both LL deficit) - tetraplegia (all 4 sensory/motor deficit) - hemiplegia (common w/ stroke, only half) Myotomes & Dermatomal loss w/ SCI examine spinal segments classify type/extent of SCI then determine fxnal prognosis Dermatome 30 on each side (C2-S5) C1 no sensory n so not dermatome standardize testing for specific points for validity/reliability anterior & lat spinothalamic tract pain temp crude touch decussates 2-3 spinal levels above point of entry - varied presentations lateral reticulospinal react posture balance trunk prox muscle control ventral & dorsal spinocerebellar tracts proprioception for trunk/LE lateral corticospinal tract largest king of voluntary motion (limbs) ipsi muscles decussates @ midbrain fasiculus gracilis posterior sc LE fasiculus cuneatus UE proprioception deep/discriminative touch visceral pain decussates @ midbrain Vertebrae info 7 cervical - 8 nerve roots 12 thoracic - 12 n. roots 5 lumbar - 5 n. roots 5 sacral - 5 n. roots c1-c7 exit above c8- exit below c7 or above t1 c8 below - all below spinal vertebrae Level of injury determines if UMN/LMN & autonomic nervous system integrity Parasympathetic system - BS & sacral segments of SC Sympathetic system - thoracic/lumbar segments L1-L2/3 SC Injury parasympathetic less impaired bc most control in midbrain/heart innervation coming from vagus n altered b&b fxn bc parasympathetic division disconnect anterior cord syndrome damage to anterolateral system, medial corticospinal tract, vestibulospinal tract significant injury: medial & lateral motor groups & spinocerebellar tractsimpacted - preserves DCML - UE/LE Discriminate touch intact central cord syndrome cervical spine motor impairments in UE mainly sensory minimally impacted flexor muscles impacted bc central reticulospinal tract, med UE fxn in SC affected Brown-Sequard Syndrome hemisection of SC loss of IPSI motor control & proprioception below lesion loss of CL pain & temp few levels below lesion this is bc anterior lat system decussates 2-3 levels above spinal level Conus medullaris syndrome LE weakness, reflexiva, sacral weakness, sensory impairments problems w/ sexual, bladder/bowel dysfxn Cauda Equina syndrome injury to lumbar & sacral roots only LMN arreflex is, flaccid paralysis, sensory loss beyond time for spinal shock impaired sexual & B&B fxn Healthcare Trends Trends in SCI increased prevalence of falls increasing care of burden & healthcare costs pt spending longer time in rehab hospitals decreased amt of acute care stays -> decreased QOL Expectancy w/ SCI 15-30 yrs less of life expectancy higher risk of developing secondary health comorbidities as PT: improve mob right after accident & minimize development of secondary health complications Summary knowledge of fxn & location of neuranatomical structures in SC key to understand impairments Rehab for improved & sustained mvmt 3.11 SCI Emergent Medical Management 1. DO THIS!! ensure medical stability (resuscitation) 2. adequate blood perfusion to SC - Systolic BP 90-100 - HR 60-100 BPM 3. decreasing inflammation to the region pt normally immediately intubated/ventilated - cervical bc innervation to diaphragm medical tx bc damage to chest wall, orthopedic surgeries may need vasopressors/aggressive fluid resuscitation pt presentation bc of neurogenic shock Imaging bradyarrhythmia C5 damage MVA vasodilation multi level impingement low BP (B) hypoperfusion to C5-C6 goal: minimize neuronal death & see if penumbra can regain blood supply Mathylpredinosolone (synthetic glucocorticoid) reduce inflammation enhances blood flow risk of hyperglycemia & pneumonia prevents decline in white matter & ion disruption reduces secondary injury to SC *varying results* Results improve neurological recovery & fxn one year post SCI - if initiated within 8 hours no long term motor or neurological status improvement increases risk of hyperglycemia & pneumonia Referring to graphs above! modest systemic hypothermia 31-34 degrees sparing of motor neurons around level of injury higher ambulatory fxn in comparison to normal temp done on RATS Kevin Everett - Modest systemic hypothermia immediately received tx use endovascular cooling catheters to cool SC maintain cold w/ cooling blankets/ice baths results - high LOF precautions - control bradycardia during tx best treat alignment/stab of vertebral column prevent further neurological damage Conservative measures post fractures traction (closed reduction/realignment) stabilization (immobilization/orthosis) - more stable fractures/multi level fractures in combo w/ surgery Unstable fractures, ones that cant be realigned, reduced, gross malalignment, ongoing SC compression, deteriorating neurological status do surgery to decompress SC, fuse/fixate fracture for stability/correct deformities use screws/plates for bone healing and reduce immobilization/external device retraction Impact - decrease hospital stay, earlier mob/participation in rehab External stabilizers instead of surgery or w/ it thoracic-lumbar-sacral orthosis (TLSO) stabilize parts of thoracic/lumbar spine effectiveness all depends on pt adherence halo traction device or vest addition most effective in philly collar most common restricts flexion/ext in mid/lower c-spine preventing motion in cerv spine con: heavy, cumbersome, restrictive of fxnal mvmt/sitting Summary initial med goal for structural stab & adequate blood supply to SC to minimize secondary damage 3.12 SCI Medical Management Medical Concerns - Respiratory Status - Spinal Shock - Autonomic Dysfunction & Dysreflexia - Blood Clots - Pressure Ulcers Respiratory Status - Cardiovascular & aerobic capacity are of immediate concern for complications following trauma - Leading cause of mortality in 1st year after injury - Will present w/ difficulty clearing of secretions, atelectasis, & hypoventilation - Important to monitor & provide multidisciplinary interventions - Innervations w/ respiratory status - Inspiration - Diaphragm (C3-C5) - Accessory Muscles (C2-C7) - Sternocleidomastoid, Scaleni, Upper Trap - External Intercostals (T1-T11) - Expiration - Internal Intercostals (T1-T11) - Abdominals (T6-T12) - Both forced expiration - Impaired muscle strength to any or all will impact respiration - Initial Assessment - Test overall vital capacity, & ability to clear secretions - Test forced vital capacity or forced expiratory volume to provide objective numbers for a baseline Spinal Shock - It is the temporary loss or depression of all or most spinal reflex activity below level of injury - Attributed to loss of sympathetic nerve activation - Occurs in almost every person w/ SCI, can contribute to hypotension - Present w/ flaccid paralysis for days-weeks, regardless of level of injury - Can be prolonged by infection - EX. UTI, wound - Resolves from weeks 1-4 after injury - Will note muscle spasms or unintended movement below injury - Movements reflexive & unintentional, educate on hypotonicity or spasticity - Do not prematurely attribute movement to return of voluntary motor control Autonomic Dysfunction - Neurogenic shock due to altered autonomic system function - Person w/ new SCI, connection b/w parasympathetic/sympathetic is disrupted - Extent of disruption depends on level - Injuries below T1-T3 - Partial sympathetic innervation to heart - Injuries above T9 - Impaired adrenal response to exercise - Full response to increased HR, blood pressure, & ventilation is blunted due to disconnect - For SCI injuries - Parasympathetic system less impaired due to it being housed in midbrain - Altered balance leads to neurogenic shock - Combo of hypotension, bradyarrthymia, temp. dysregulation - Body can adapt to imbalance over time - Initially will lead to medical instability Comparing Neurogenic & Spinal Shock -Spinal Shock - Due to loss of muscle tone & sensation - Temporal w/ variable impact on other systems - Neurogenic Shock - Due to loss of sympathetic system activation - Not temporary, impairments can be less impactful over time - Both can lead to distal weakness & decreased sensation - Can present w/ both shock simultaneously Autonomic Dysfunction - Lack of sympathetic system activation can lead to more than just neurogenic shock - Cardiac Function - Lower resting HR, loss of tone in peripheral vasculature - Could lead to bradycardia, bradyarrhmia, hypotension, orthostatic hypotension - As shock resolves, spinal sympathetic reflexes return but lack regulation or control of any input form above injury - Imbalance remains, can lead to chronic issues of extra size intolerance, exercise induced hypotension, reduced resting stroke volume, venous return, cardiac output - Long term impact on body’s ability to maintain blood pressure - Loss of sympathetic outflow, dilation of peripheral vasculature - Causes hypotension - Orthostatic Hypotension - Result of peripheral vasodilation & bradycardia - Reduced venous return, lack of muscle pump in legs, reflexive blood distribution - Leads to increase risk of blood clots & emboli - Chronic imbalance b/w 2 systems alter cerebral vascular control - Brain can learn to adapt over time - In respiratory system - Loss of sympathetic input leads to impaired bronchi dilation - Contributes to excessive mucus production & lower secretion clearance - Early, presents increased bradycardia & cardiac arrest during tracheal suction - Due to stimulation of vagus or parasympathetic output - Can result in impaired thermoregulation - People w/ SCI - Increase in temperature leads to loss of control of peripheral vasodilation - Bladder initially hypotonic or flaccid several months after injury - Creates reflexive bladder w/ UMN, atonic bladder in LMN - Reflexive - Leads to urinary incontinence due to uncontrolled, ineffective voiding - Also inability to empty bladder due to coordination b/w detrusor & sphincter - Atonic - Leads to urinary retention & incontinence due to leakage - Increases risk of developing UTI - Bowels - Paralyzed isles leads to bowel incontinence & constipation - Result in impaired sexual function, significant concern after walking - Spinal Cord Arousal Pathways - Housed in 2 locations - Psychogenic Pathway (T11-L2) - Reflex Pathway (S2-S4) - For enjoyable sex life, may have to rely on reflexive pathway Autonomic Dysreflexia - Stems from excessive uncontrolled sympathetic output that’s unregulated by parasympathetic system - Usually affects people w/ injuries above T6 - Key Signs & Symptoms - Severe headache - Sudden increase in blood pressure of 20-40 mm above baseline - Diaphoresis above injury - Flushing of skin due to vasodilation above injury - Goosebumps below - Blurred Vision - Nasal congestion - Condition can be fairly silent w/ unnoticed but dangerous rise in blood pressure - Usually caused by noxious stimuli - Could be bowel or bladder distention, UTI, ingrown toenail, tight clothing, pressure ulcer - Process Autonomic Dysreflexia - Taking Action - Patient must immediately sit upright & lower legs to decrease cerebral vascular blood pressure - Identify & remove any noxious stimulus - Possibly urinary or bowel related - Loosen clothing or restrictive devices - If not found or cannot be removed, use of antihypertensive meds if above 150 systolic persistently - Continue monitoring blood pressure every 1-2 minutes stabilized or in ER Blood Clots - Monitor patient for signs & symptoms of DVT - Patient will likely not feel pain or complain of any in that region - Typically placed on low molecular weight heparin within 72 hours of SCI - Usually continue on this for 12 weeks Pressure Ulcers - Significant concern throughout recovery process - Development is related to prolonged position due to team achieving medical stability - Acute Care Phase - Positioning key for managing skincare - Typical to change position every 2-4 hours - Often limited by orthotics or immobilizers - Positioning can be affected by respiratory concerns - Common pressure areas for patients in photo to R 3.13 Spinal Cord Injury Clinical Presentation Objective: motor and sensory impairments with SCI General management Presentation: Variable changes in function and sensation motor control and strength, range of motion deficits, altered muscle tone, impaired cardio and aerobic capacity, and neuropathic pain 30 dermatomes- c2-s5 C1 spinal nerve has no sensory nerve= no dermatome Vertical tractsanterolateral- pain and temp decussates at spinal cord 2-3 levels above point of entry dorsal column medialemniscus tracts- sensory info on discriminate touch and pressure from UE LE - does not decussate or cross over until reaches midbrain Muscle innervation muscles are innervated by multiple spinal levels If c6 is injured, biceps can still be trained because c5 contributes towards bicep activation as well Oral meds baclofen, tizanidine, dantrolene, andiazepam Botox is considered if these oral meds have little to no affect Spasticity- impacts ROM and motor control and strength Presentations adducted Thigh flexed knee extended knee PLantar flexed foot/ankle equinovarus foot striatal toe flexed toe Affects QOL painful at times decreased adls gait issues participation loss chronic pain 3.14 SCI ASIA Assessment ASIA Assessment Form - Has different tests & interpretations needed to capture levels of injury - Used worldwide in clinical & research settings - First developed in 1982 - Revised in 2011, 2019 - Added Zone of Partial Preservation for function below level of injury Motor Testing Anatomy - Includes 10 key muscle groups on each side of the the body - C5 (Elbow Flexors) - C6 (Wrist Extensors) - C7 (Elbow Extensors - C8 (Finger Flexors) - T1 (Finger Abductors) - L2 (Hip Flexors) - L3 (Knee Extensors) - L4 (Dorsiflexors) - L5 (Big Tow Extension) - S2 (Plantar Flexors) Motor Testing - Standardized testing of muscle groups on scale of 0-5 - 0 (Total Paralysis) - 1 (Palpable/Visible Contraction) - 2 (Full ROM, Gravity Eliminated) - 3 (Full ROM, Against Gravity) - 4 (Full ROM, Moderate Resistance) - 5 (Full ROM, Full Resistance) - * (Special Circumstances, NT) - Can’t be tested due to MSK injury or some immobilization - Same as MMT scores - Muscle rating of 3-4 & muscle group immediately below a 5 can indicate intact spinal level - Score of 4 or less, and level immediately above not rated 5, it is considered injured Motor Level - Only testing 5 muscle groups in UE & LE respectively - Injury b/w T2-L1, can not determine motor level by looking at muscle function only - Motor Level is determined by sensory level - Lowest key muscle function that has a grade of at least 3 - Grades above are 5 - Motor level can differ from R & L sides - Motor level is based on upper most intact level b/w the sides Sensory Assessment - Testing for both light touch & pinprick bilaterally at each dermatome - Rated on a 0-2 scale - 0 (Absent) - 1 (Impaired) - 2 (Normal) - * (Special Circumstances) - Inability to access dermatome due to wounds, immobilization, other injuries Sensory Level - Persons designated sensory level is most caudal or lowest intact dermatome for both w/ grade of 2 - Testing begins at C2, go down until segment that scores less than 2 - If none, go to C8 - Can differ from R & L sides - Sensory level based on uppermost intact level b/w 2 sides Complete or Incomplete - Selecting the level does not effectively capture the individuals true function - Complete - Indicates that neither sensory or motor is preserved in sacral segments S4-S5 - Would be looking for the N-O-O-O-O-N on form - Would indicate lack of voluntary anal contraction & deep anal pressure - Lack sensory pinprick/light touch - Incomplete - Denotes the presence of sacral sparing - Either motor or sensory function is present in S4-S5 Zone or Partial Preservation - Used as descriptor for complete or incomplete injuries - Indicates the sensory & motor levels below level of injury that has some degree of innervation/function - Motor - Indicates the most caudal spinal level w/ some degree of motor function - Sensory - Indicates the most caudal spinal level w/ some degree of sensory function ASIA Impairment Scale (AIS) - See table to the below - A (Complete) - B (Sensory Incomplete) - C (Motor Incomplete) - D (Motor Incomplete) - E (Normal) 3.15 SCI Rehab Assessment Body Structure & Impairment Assessment - ASIA Impairment Scale - Manual Muscle Testing or Handheld Myometry - Modified Ashworth Scale - Penn Spasm Frequency Scale - Assesses spasticity Penn Spasm Frequency Scale - Self report measure that asks individual to characterize frequency or triggers of spasm - 0, No Spasm - 1, No spontaneous spasm (elicited by vigorous sensory/motor stimulation) - 2, Occasional spontaneous spasm (easily induced) - 3, 1-10 spontaneous spasms/hour - 4, spontaneous spasms, >10/hour - Added intensity of spasms to improve overall outcome measure, improves inter/intra reliability - 1, Mild - 2, Moderate - 3, Severe Function/Activity Assessment - Functional Mobility - Functional Independence Measure - Spinal Cord Injury Independence - Measure - Balance - BERG Balance Test - Gait - Timed Up and Go - 6-minute walk - 10-meter walk test - Dynamic Gait Index - Functional Gait Assessment - Walking Index for SCI 2 - WC Mobility - Wheelchair Skills Test Functional Mobility: Sitting - Should be initially assessed & treated is sitting tolerance - Indicated by the time spent in chair or in supported/unsupported sitting - Sitting posture/balance also assessed - Test for equilibrium & protective reactions - Modified Functional Reach Tests - Possible for this population SCI Independence Measure - Developed by Catz in 1997, revised in 2007 - Contains 19 items specific to SC pathology - Includes self care, respiration, toileting, mobility - Mode of respiration, ability to move in bed, ability to ambulate, ability to transfer positions Walking Index for Spinal Injury (WISCI) - Rates ability of person w/ SCI to ambulate 10 meters on scale 0-20 - Designed for patients classified as ASIA A or complete injuries below T10 - Or ASIA B,C,D at any level - Takes into account different orthotics, assistive devices, physical assistance - Recommended in use w/ 10 meter walk test Wheelchair Skills Test - Rates 32 specific skills on 0-2 scale - Accounts for patient vs. caregiver ability - Accounts for manual or power wheeled wheelchair -Score of over 80% indicates advance manual wheelchair skills - Average scores of 72.1% in tetraplegia & 82-84% in paraplegia - See picture for tasks & different functional items - Separate wheelchair propulsion tests can assess technique & efficiency - Can focus on bilateral UE or hemi propulsions Participation Assessment - Assessments - World Health Organization Quality of Life - BREF - Self report measure, applicable across different cultures - Uses 26 items in domains of physical & psychological health, social relationships, environment - Spanish score has cutoff of >60, indicates independence w/ ADLs - Sickness Impact Profile - 68 item self report measure - Assesses physical, psychological, social dimensions of QOL - Assess participation, particularly at chronic stage of SCI to understand community reintegration 3.16 SCI Acute Rehab Management MOST IMPORTANT ongoing education of pt/family (from acute to community) - acute: maintaining ROM, signs/symptoms of DVT, b&b routine, skin/wound management main question: prognosis - when walk progressing mobility sitting tolerance/endurance to out of bed activity monitor everything - BP, autonomic dysfxn, respiratory status, fatigue, amt of time gradually increase time/degree of incline to train body to tolerate upright pos pressure garments, abdominal binder for BP longer than 20 min - educate on off loading and skin checks sitting balance most likely dont have core control/cant sense surface only feel head/trunk bc lack sense/motor control in abominal relearn motor control/strength - use remaining sensory cues to maintain balance always challenge/adjust skill - ex: sitting unsupported, fxnal mvmts, stability of surface, equilibrium rxns, anticipatory/rxns, dressing, peri care, catch oneself during loss of balance Respiratory management : improves QOL manages orthostatic hypotension acute: assisted coughing, abdominal binders for core support, positing techniques to challenge breathing, spirometers to increase inhalation, clearance of secretions, diaphragmatic pacing (intramuscular stim to ween off vent) diaphragmatic pacing earlier transition from acute to subacute increase in muscle strength greater recovery of indep breathing that were initially on vent respiratory training start as early as possible to promote lifelong health w aging w/ SCI REVIEW CHART ROM Eriks-Hoagland decreased PROM in shoulder flexion, abd, ER at discharge linked to fxnal limitations in participation 5 years post injury Key goal maintain ROM in all jts educate on self ROM activities to optimize time w/ professionals Tetraplegia Injuries at C6/C7 specific ROM to maintain tenodesis grip HS Rom increased shoulder range into ext/ER in order to increase potential for independence w/sitting balance/transfers - 90-110 degrees of straight leg raise hip/elbow ext maintain at neutral Tenodesis compensatory strategy attain hand grasp w/o active use of wrists/finger flexors key for C5-C6 injuries that don’t have wrist/finger flexion passive tension in extrinsic wrist/finger flexors during wrist ext for grasp use eccentric control of wrist ext for release DONT OVERSTRETCH WRIST/FINGER FLEXORS full ext is contraindicated summary video example of tenodesis! large object - active ext: fingers curl, active flex: fingers extend tenodesis grasp: conc extensors = finger flexion, eccentric wrist extensors = release grasp not as strong initial acute management of SCI improving endurance, preventing pt w/ tetraplegia - lose/decreased ability to grasp/release/manipulate secondary complications tenodesis can be a fxnal savior 3.17 SCI Compensatory Strategies Functional Mobility Training - Must consider 2 aspects of functional training - Aim to restore as much function as possible (Improve neuroplasticity, motor control, strength, sensation) - Plays significant role in recovery in ASIA C or D - Compensatory strategies to improve function - Plays role in ASIA A or B - Can also be used for patients w/ stroke, TBI, Parkinson’s, Vestibular Compromised, etc. - Key Questions - What is underlying impairment? - What’s the prognosis for recovery from neurological perspective? - Can help determine general percentage of compensation vs. recovery that should be used Key Compensatory Movement Strategies - Can be the only way for patients to become independent at certain tasks - Can provide pathways to efficiency by decreasing fatigue, injury, or reliance on other devices - Strategies - Muscle Substitution - Gravity -Key to generating motion that requires little to no assistance - Occurs w/ movements that require little force generation/facilitated by gravity - Tension in Passive Structures - Provides more force than gravity alone - Idea behind Tenodesis grasp (Video in lecture) - UE Flexors.- Tenodesis - Hammys/Lumbar Extensors - Sitting balance - Distal Fixation - Key in ability to stabilize themselves in sitting - Uses trick elbow ext from functional mobility & support - Relies on fixating the hand or foot, using proximal musculature to create movement - Can create significant amount of force compared to gravity or passive tension - Uses counter forces to assist w/ support & stability - Angular Momentum - Highly used & effective in increasing independence w/ function - Uses derivatives of mass, velocity, & moment arm to facilitate rotation once motion has begun - Most evident in rolling, used in transfers & positioning - Increase momentum by altering weight, speed, leverage - Head-Hips Relationship - Involved head position to facilitate movement of trunk or lower limbs in opposite direction - Primarily used during transfers, bed mobility, or ambulation - Can do head down, bum up Functional Training Strategies - Compensatory & training strategies used to increase comfort & confidence - Can train skill - In reverse - Possibly start in sidelying position & roll into supine before training to roll into sidelying - Part-Practice - W/ use of adaptive equipment - Provides patient w/ more knowledge of what movement should feel like & end position desired Important Functional Tasks - Take priority in acute care & tertiary rehab settings - Bed Mobility - Transfers - Wheelchair Mobility - Gait - Mat Mobility for rolling - Prone arm elbows, scooting, lifts