Neuromuscular Rehabilitation PDF
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This document discusses neuromuscular rehabilitation, specifically focusing on neuroplasticity and its mechanisms. It explores applications in various scenarios, including stroke and blindness, and provides an introduction to clinical decision-making frameworks in neurorehabilitation. The document also includes insights into exercise program design, referral reports, and the biopsychosocial framework.
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Neuromuscular Rehabilitation Neuroplasticity Brain Composed of ~85 billion neurons (functional cells) and ~85 billion glia (supportive cells) Average neuron makes ~ 10 000 synapses — can be excitatory (glutamate) or inhibitory (GABA) Neurons are specialised for controlling motor output, senso...
Neuromuscular Rehabilitation Neuroplasticity Brain Composed of ~85 billion neurons (functional cells) and ~85 billion glia (supportive cells) Average neuron makes ~ 10 000 synapses — can be excitatory (glutamate) or inhibitory (GABA) Neurons are specialised for controlling motor output, sensory processing or connecting regions n Neurons form networks that are responsible for specific functions Neuron structure Soma — cell body where the nucleus sits Inputs from other cells come in via dendrites Signal is propagated down the axon to other neurons Synapses occur in the dendrites — on the spines of the dendritic tree Localisationism Theory of how the brain is organised based on function Front of the brain — motor aspects Back of the brain — sensory aspects Specialised regions for speaking and hearing on the left side of the brain - Broca’s area — speech - Wernicke’s area — speech interpretation Limbic areas — emotions, learning and memory Cerebellum — located at the back of the brain, very important for motor coordination History 1793 — first evidence that the brain can change itself; anatomist Michele Malacarne discovered animals that received motor training had larger cerebellums 1890 — psychologist William James proposed the brain and its function are not fixed 1945 — neuroscientists Justo Gonzalo observed dynamic and adaptive properties after brain injuries 1964 — first scientific evidence of anatomical brain plasticity; Marian Diamond proved rates in an enriched environment had thicker cortices — David Hubel and Torsten Wiesel investigated the effect of long-term closure of one eye on brain activity in corresponding visual region, found that same brain region started processing information from the open eye instead of the shut eye 1984 — Michael Merzenich mapped 5 distinct areas in sensory cortex corresponding to the digits. Digit 3 was removed and 2 months later, stimulation of digit 2 and 4 evoked activity in cortical region where digit 3 mapped (adjacent digits invaded unused region) 1997 — Eleanor Maguire documented changes in hippocampal structure in association with acquiring knowledge of London’s road layout in taxi drivers. Compared to controls, size of hippocampus was the same but posterior hippocampus (involved in spatial navigation) was bigger Definition The ability of the nervous system to respond to intrinsic and extrinsic stimuli by reorganising its structure, function and connections Can occur at molecular, cellular, system and behavioural level Can occur during development (developing brain exhibits a higher degree of plasticity — critical period), in response to the environment, during disease and after therapy Mechanisms Molecular Changes — change in one neuron Change in membrane channels can change excitability Local change in dendritic channels can change synaptic integration Change in channels or length of axon initial segment (axon hillock) can change action potential generation Change in extrasynaptic receptors (on the soma) Examples — change in receptor conformation, altered gene expression effective Cellular Changes — change between two neurons Synaptic plasticity — increases or decreases in the strength of individual synapses Synapse formation or regression — increases or decreases in the number of individual synapses Examples — altered synapses, larger dendritic tree Physiological, Anatomical and Behavioural Changes — change in a network of neurons Creation of new pathways/circuits - unmasking of silent connections - formation of new connections - breaking of old connections Examples — different cortical map, improved motor performance Mechanisms Continued Neuroplasticity is activity-dependent “Neurons that fire together, wire together” Long-term Potentiation (LTP) - strong depolarisation in post-synaptic neuron results in high influx of calcium ions - triggers insertion of AMPA receptors = stronger synapse Long-term Depression (LTD) - Weak depolarisation - low influx of calcium results in removal of AMPA receptors = weaker synapse Neuroplasticity in Development Most of brain growth after birth is in cerebral cortex Growth is mainly from proliferation and elaboration of axons and processes (neurons get bigger, not more forming) - increase in dendritic tree - axons get bigger - neurons become myelinated Critical period — in early years, we develop more neurons than we need, synapses are gradually eliminated in activity-dependent manner Neurogenesis still occurs in hippocampus (memory formation), olfactory bulb (scent interpretation) and cerebellum (motor coordination) in adults It is unknown if and how new neurons integrate into established circuits / degree of neuroplasticity in adults Applications Cerebellar agenesis Rare disorder — born without cerebellum Patients have shown no significant motor dysfunction, minor dysarthria (difficulty speaking) Evidence suggests other parts of the brain absorbed cerebellar function Neurotrophins and Stroke Neurotrophins are very important proteins that influence proliferation neurons (how they survive, function), learning and memory BDNF (brain-derived neurotrophic factor) is involved in neuronal proliferation, survival, synaptic plasticity, learning and memory BDNF is increased in cortex during motor learning Study — BDNF was blocked after a focal ischemia, control group that received rehab showed greatest improvement BDNF likely has a role in motor map reorganisation, learning and memory after a stroke Hemispherectomy In some cases of severe epilepsy, one hemisphere of the brain may be removed or disconnected Extensive reorganisation may occur, such that the remaining ised is responsible for motor and sensory function for both sides of the body Greatest potential is seen for children under the age of 6 Blindness Visual cortex adopts another function — processes tactile information when reading braille Accounts for ‘heightened senses’ when one is no longer in use Maladaptive/Adverse Examples Chronic pain following limb amputation (phantom limb) - 80% of amputees report painful feelings from areas where limbs are no longer present - previous theory — inflamed nerve endings (disproved) - 1990s Vilayanur Ramachandran hypothesised that phantom limb was due to reorganisation of the somatosensory cortex — stroking face resulted in perception of phantom limb being touched - other theories also exist — there is no consensus Onset of epilepsy after cerebral trauma - arises months or years after insult - delayed onset suggests progressive changes in the brain — axonal sprouting and new connections that alter signalling and induce seizures Drug addiction - transition from casual to compulsive and relapse is thought to to be caused by long-lasting neuroadaptations in reward pathways - reward circuits are involuntary activated and executive function circuits are hijacked to support drug seeking behaviour Therapies to promote neuroplasticity Brain stimulation - non-invasive — transcranial magnetic stimulation (TMS) and trasncranial direct current stimulation (TDCS) - invasive — deep brain stimulation Physical Training and Exercise - Constraint-induced movement therapy (forcing patient to use weak limb) results in increased motor map area in subjects 3-9 months after a stroke - Constraint therapy for upper limb has been associated with enlarged motor cortex map Cognitive training Neuropharmalogical interventions Clinical decision and decision making in neurorehabilitation What is clinical decision making? the process of determining the appropriate examination methods to design and customise specific treatment intervention techniques for a consumer process begins when the clinical problem is identified Information gathering and analysis follow a basis upon which the decisions or judgements are made Aka clinical reasoning — implying a procedure/series of cognitive steps involved Process is a continuous, interconnected stream of thought and process What is your role in rehabilitation? develop an exercise intervention plan to maximise consumers outcomes Encourage and motivate the consumer ongoingly Provide opportunities to positively impact the cosumer’s life (and their support systems’) in physical, psychological and social dimensions Biopsychosocial framework ICF framework Exercise Program, Referred Report Writing, & Clinical Decision Making Exercise Program Card Accurate record of exercise program components, completion and efficacy - Document exercises to be completed at a given session - Document whether exercises are being completed at clinic sessions - Highlight the difficulty of existing exercises, provide an indication of the need for progression or regression Allows clients to be supervised by any staff on any given day - Provides a snapshot of client goals and a clear exercise program - Provides details sufficient for a colleague to competently and safely supervise a single session Layout and Expectations Tables are usually best to display all components: - Identifying information, primary/relevant conditions, goals - Exercises (possibly with description or pictures) - Intensity, duration - Progression, regression - Nuances for neuro rehabilitation Sometimes ExRx does not fit through conventional FITT format Single clinic-based exercise session - realistic scope for equipment - deliver your best exercise program for the first session with this program - best = evidence AND goals based, safe and individualised Understood by colleagues (AEPs) - use appropriate standardised abbreviations were relevant - assume understanding for standard exercises (add detail if modified or unusual) Logical layout — ensure the order of the exercises is accurate (top to bottom) Is brief — ~500 words Program cards in home settings and with carer/support person supervision Safety — environment considerations, staff/carer/partner training, disease-specific safety concerns Home exercise programs (HEPs) are an important adjunct to AEP-supervised exercise sessions - details/images of exercises - options for varied environments and level of supervision Telehealth/Virtual delivery of exercise training Referrer Reports Crucial, often mandatory (MBS, NDIS, Workcover) Optimise healthcare delivery - coordinate care arrangements/cohesion/overlap - consistent messaging between providers - clear lines of accountability and responsibility Improve referrer relationships and grow referrals Professional courtesy Opportunity to communicate ‘what you do’ and results of your interventions Record keeping, reduces risks of treatments provided DO NOT — make it too long, reiterate information they provided you, be unclear/uninformative/unintelligible What do they want? - To know if the referral was effective - To know you have delivered a specialised service beyond their own capability - The effect of your intervention on the primary reason for referral - To know the patient’s status when they see them next Structure Letter head/provider info Date Provider Referee Patient ID Paragraphs/body - needs to provide a logical narrative - greeting + brief recap of referral reason/context + date of consult - table of most important/informative results and how they compare to norms (if appropriate) - plan for exercise program/recommendations — brief goals, potential barriers, expected treatment effects - next contact — set expectation of when you’ll correspond next Sign-off Social Aspects of Disability Disability Act 1992 Definitions of Disability Total or partial loss of the person’s bodily or mental functions Total or partial loss of a part of the body The presence in the body of organisms causing a disease or illness The malfunction, malformation or disfigurement of a part of the person’s body A disorder or malfunction that results in the person learning differently from a person without the disorder or malfunction A disorder, illness or disease that affects a person’s thought processes, perception of reality, emotions or judgement, or that results in disturbed behaviour Includes disability that - presently exists - previously existed nut no longer exist - may exist in the future - is imputed to a person (meaning it is thought or implied that the person has a disability but does not) Types of Disability There are different types (visible and non-visible), and they may vary from: - genetic disorders - illnesses - accidental Physical — affects a person’s mobility or dexterity Intellectual — affects a person’s ability to learn Mental illness — affects a person’s thinking process Sensory — affects a person’s ability to hear or see Neurological — affects the person’s brain and CNS Learning disability Physical disfigurement Immunological — the presence of organisms causing disease in the body Disability in Australia 17.7% of Australians (1/5) - 2-3x more prevalent in Aboriginal peoples and TSI 45% live in or near poverty — often dependent on income support Victims of violence, abuse and exploitation — 3x higher than the general population (much higher/more sustained for women with disabilities) - less likely to be reported, investigated or prosecuted Overrepresentation in the criminal justice system — 3-9x more likely to be part of the incarcerated population Isolated, segregated and vulnerable institutional, inappropriate care Models of Disability Medical Model Disability is perceived as an impairment in a body function or system that is pathological The ultimate goal is to return the system or function to “as normal as possible” Imposes medical/health professionals as “experts” in disability, and people living with disability should rely on their “expert” advice The language used is usually through medical/clinical jargon Moral Model Disability is perceived about the person’s or the family’s deeds, thoughts, karma and character Disability can be perceived as something negative, carrying blame, shame and stigma since a disability can be seen as something evil Disability can be seen as something positive, such as overcoming a tough period or a life-changing event Social Model Disability is perceived as one aspect of someone’s identity, such as gender, ethnicity/race Disability results from an imbalance between extrinsic factors (social and physical) and the disabled person - extrinsic factors create barriers to participation, not the one’s disability The best way to address disability is to change society and extrinsic factors instead of changing people with disabilities What is Disability Impairment A medical condition that leads to disability (eg. Stroke, spinal cord injury) Disability The result of the interaction between people living with impairments and the barriers to participation such as communication, physical, attitudinal, and social environment (eg. Lack of access to buildings, no ramps but several staircases/escalators) Barriers to Participation Attitudinal Barriers Created by people who see only disability when associating with people with disabilities to some extend (seen though discrimination, fear and bullying) People sometimes stereotype those living with disabilities, making assumptions (eg. Poor QoL, unhealthy) Stigma, prejudice and discrimination are common Barriers include low expectations of people living with disabilities and these barriers can lead to all other barriers Communicational Barriers Experienced by people with disabilities, affecting speaking, hearing, reading, writing and understanding and who use different ways to communicate Examples - use of small print - no braille or version for people who use screen readers - videos without captioning - long sentences, too much jargon and use of technical language Physical Barriers Structural obstacles in man-made or natural environments prevent ending or blocking individual’s mobility or access Examples - x-ray equipment that requires people to stand up - absence of a scale that accommodates for a wheelchair - curbs and steps that block a person with a mobility impairment from entering a building or using a sidewalk - lack of ramps or adapted curbs for people using wheelchairs Policy Barriers Lack of awareness or enforcement of existing laws and regulations (differ in different jurisdictions) that require programs and activities to be accessible to people with disabilities Examples - Denying reasonable accomodations to qualifies employees so they can perform essential functions for the job - denying individuals with disabilities access to opportunities in participating in services or opportunities due to physical barriers Programmatic Barriers Limited delivery of a public healthy or healthcare program for people with diverse types of impairments Examples - lack of accessible equipment - insufficient time for examinations and procedures - health provider’s knowledge, attitudes and understanding - inconvenient scheduling - lack of communication Social Barriers Related to the conditions in which people are born, grow, live, learn, work, and age (social determinants of health), contributing to decreased functioning among people with disabilities Examples - Children with disabilities are 4x more likely to experience violence - Adults with disabilities are less likely to have completed high school - People with disabilities are less likely to be employed Transportation Barriers Lack of adequate transportation interfering with a person’s ability to be independent and function in society Examples - unavailability of public transportation adapted for people with disabilities - inconvenient locations and distances to use adapted public transport Falls & Balance: Overview of Assessments Neurological Changes with Aging Sensorimotor changes - loss of motor units as a source of muscle loss - loss of peripheral sensation Cognitive changes — declines in executive function, reaction time and attention Importance of Balance Balance is the ability to maintain the position of the body (its centre of mass) within specific boundaries of space (stability limits) Poor Balance is a significant contributor to falls in people ≥ 65 Balance requires the integration of different sensory information (visual, vestibular, proprioceptive) and the ability to generate appropriate motor responses Vision Important source of information for the control of balance - information about the external environment - feedback about the position and movements of the body Postural saw increases ~ 30% with eyes closed Age affects - visual acuity - contrast sensitivity - depth perception - visual field (peripheral vision) - increased use of spectacles Cataracts 16% of people > 65 Opacity of the lens of the eye, causing clouded vision Usually a result of denaturation of lens proteins Due to Advanced age and diseases such as diabetes Macular Degeneration 9% of people > 65 Thinning of the macular area (centre) of the retina Causes a loss of central vision and inability to see fine details Sensation/Proprioception Balance relies upon combination of cues from the proprioceptive system (awareness of body position in space) Tactile information from hands and feet Input from muscles and joints (angles, muscle spindles/muscle stretch, golgi tendon organs) All sensory receptors deteriorate with age — affected by certain conditions such as T2DM Vestibular sensation Inner ear structures that detect position and motion of the head Important for posture and coordination of head, eye and body movements Reduced sensation with age Some evidence suggests that impaired vestibular function may contribute to falls in older people Age-related neurological changes human brain loses 10% of its weight by age 90 (loss of neurons) - reduced blood flow and metabolism - declining production of neurotransmitters Functional problems depend on region of loss/damage - Degeneration of myelin sheaths, axonal degeneration — reduced nerve conduction velocity (slower responses) Compensatory mechanisms — reorganisation and redistribution of functional networks Reaction Time 25% increase in simple n reaction time from age 20-60 Increased simple reaction time is a strong risk factor for falls in older people Fallers have particularly slower reaction times in more complicated tasks, such as stepping Cognitive changes basic cognitive functions most affected by age are processing speed, attention and memory Balance control requires additional resources — affected by onbe’s information-processing ability when performing two or more tasks simultaneously (distracted) A greater cost of dual tasks in older persons that young, suggests that there is an increase in the cognitive resources required for postural control with age Definition of a fall WHO 2007 — an event which results in a person coming to rest inadvertently on the ground floor or other lower level Prevention falls network Europe 2007 — an unexpected event in which the participants comes to rest on the ground floor or lower level Kellogg International working group on the prevention of falls in the elderly 1987 — unintentionally coming to the ground or some lower level and other than as a consequence of sustaining a violent blow, loss of consciousness, sudden onset of paralysis in stroke or an epileptic seizure Causes of falls 85% balance-related falls 15% unexplained falls (blackout, dizziness, faint) Incidence of falls 1/3 community dwelling >65 years per year — 10-20% multiple fallers 1/2 people living in residential ages care facilities per year ‘Greying of the population’ — 1/4 Australians will be over 65 by 2051 Falls in clinical groups Incidence rate of falls increases to double that of healthy older people - cognitive impairment - parkinson’s disease - multiple sclerosis - stroke Otehr groups at risk of— visual impairment, peripheral neuropathy (diabetic, chemo-induced) Personal Costs Morbidity and mortality - leading cause of hospitalisation (4%) in older people - leading cause of injury-related death in older adults Loss of independence - institutionalisation - loss of functional mobility, reduced physical activity - loss of confidence Screening vs Assessments Screening Identification of people at risk Increased surveillance Referral for further assessment and intervention Assessment Identification of risk factors amenable to treatments/correction Tailoring of intervention strategies Consideration for instrument selection Reliability — measured consistently each time Validity — measures what it is supposed to measure feasibility — appropriate for population and setting Diagnostic accuracy - sensitivity — how well a test correctly identifies the cases in a population with the condition - specificity — how well a test correctly identifies the cases without the condition Different setting Community Residential Hostel Nursing home Hospital ward Emergency department (ED) Screening tools 2 or more falls in past year (red flag) Mobility/funcitonal tests Standing Balance Tandem Stance — check for excessive swaying or falling One-leg stand — maintained for 10s Sit to stand Time to stand up and sit down 5x from a seated position Complete in < 12s Step Tests strength, balance and coordination Hill step test (one leg at a time) — average 16 steps in 15 seconds Alternate step test (alternate legs each step) — complete in < 10 s Composite measure of balance, strength and processing speed/inhibition Predictive of falls in older people Used as an outcome measure of exercise interventions Walking tests 6m walk test - associated with survival in older people - when performed with concurrent cognitive task, non better than single task to predict falls 6 min walk test — frail/mobility impaired can do 2min version Timed up and go (TUG) stand up, walk 3m, turn, turn, walk back and sit down Useful to assess functional mobility For falls prediction — better in frail, low functioning older people Berg Balance Scale 14 items scored out of 56 (0-4 for each item) Designed for frail older people — has ceiling effect in healthy elderly Has reasonable validity as a screen for falls Most useful in identifying functional limitations for in forming exercise intervention streategies Results - 41-56: low fall risk - 21-40: medium fall risk - 0-20: high fall risk Other balance screening tests FROP-Com Tinetti Performance Oriented Mobility Assessment Short Physical Performance Battery - 5xSTS - Standing with feet together, in semi0tandem and in full tandem for 10s - 4m walk time QuickScreen Clinical Falls Risk Assessment A validated and reliable set of measures used to predict the probability of future multiple falls and identify risk factors Includes - 5xSTS -alternate step test - low contrast visual acuity test - near tandem stand test - tactile sensitivity - questionnaire 72% accuracy in predicting risk Proven feasibility for use with older community dwellers by a variety of health professionals Results guide interventions Quick and easy to use, minimal equipment, low cost Physiological Profile Assessment (PFA) Physiological, rather than disease-oriented Involves direct assessment of sensorimotor abilities Assumes that disease processes will be manifested in impaired performance in one or more tests - cataracts — poor vision - neuropathy— poor sensation - prior-polio — weakness - stroke — weakness, poor coordination, instability predicting outcomes — falls, fall-related injuries, disability, need for institutional care Evaluating interventions Gait Assessments Walking speed Step length Cadence (step rate) Step time variability Rhythm or smoothness Symmetry Stability indices Kinematics Kinetics Complementary assessment Cognitive function — executive function and attention - Montreal cognitive assessment - trail making test — executive function Fear of falling — falls efficacy scale-Internationals (FES-I) Environmental conditions — HOME FAST Medications Medical Conditions Hydrotherapy What is Hydrotherapy Therapeutic and exercise activities generally carried out in heated pools Focussing on pool-based exercise other than swimming, conducted in a class or individual format, for managing or preventing chronic disease Mechanics Drag in the water is velocity dependent so move limbs more vigorously (faster) to increase resistance to movement Buoyancy provides support for body weight and reduce loading on the weight bearing joints The extend of the load-reducing effects if water immersion vary worth the extent of immersion (and speed of movement) Support from the water has particular appears in neuromuscular rehabilitation for people who have some difficulties with balance and who have low strength to be able to stand independently Physiological effects of water immersion Cardiovascular function Hydrostatic pressure shifts blood volume towards the head (cephaladshift) resulting in (note: does not alter the usual CV adaptations to chronic aerobic exercise) increased venous return increased stroke volume increased cardiac output decreased heart rate Respiratory function Immersion to the neck is shown to: decreased forced vital capacity Decrease expiratory reserve volume Decrease total lung capacity (~5.6%) Decrease functional residual capacity (~2.9%) Renal function Increase diuresis (urine excretion) Increase natriuresis (Na+ excretion) Increase Kaliuresis (K+ excretion) recommend water temperatures Varies depending on exercise type and intensity Specific conditions may call for specific temperatures to support condition and symptom management Related considerations - air temp - increased exercise intensity - in/out of pool - clothing Benefits Pain relief Allows people to complete movements that their disability/pain my prevent Reduced stress on joints — arthritis management, low impact exercise Improved mental health, relaxation Enjoyable Buoyancy offloads the force of gravity on immersed joints Drag allows for resistance with movement only Hydrostatic pressure - dissipation of oedema - gradual increase in joint ROM - combats spasticity Thermodynamics - decreased muscle pain - increased vasodilation/blood circulation - decreased HR Considerations Risks and benefits of the modality for people with CVD or respiratory diseases People with COPD or stable heart failure can benefit from hydrotherapy with few or nil adverse events reported Along with having OA, people with neuromuscular conditions may present with a range of comorbidities Water and land-based exercise generally deliver similar benefits Practical considerations Pool accessibility Chairlift, steps, ladders, rails, ramps Flotation support Hydration Swimming attire Hearing and vision impairment Time Contraindications Relative Absolute fear of water/ inability to swim Acute illness (eg. Fever) Gastrointestinal and/or genito-urinary tract issues Open wounds (without dressing) Cognitive impairment Severe kidney disease Compromised immune system Uncontrolled seizures Conditions such as diabetes or seizure disorders Unstable angina SCI related autonomic dysreflexia Uncontrolled diabetes Medications (with cardio/respiratory effects) Urinary/faecal incontinence Heat/chemical sensitivity Presence of nasogastric tibe Ear infections DVT without anticoagulation therapy or filter Sensory impairment/loss Exercise Monitoring in Hydrotherapy Individual supervision and manual resistance/support — how many clinicians needed? Objective monitoring — waterproof HR monitor Subjective monitoring — RPE, dyspnoea scale Exercuse FITT — sets, reps, speed, equipment Muscle strength grading and gauging intensity Land Water 1. Evidence of slight contraction, no joint movement 1. Contraction with buoyancy assisting 2. Complete ROM with gravity eliminated 2. Contraction with buoyancy eliminated 3. Complete ROM against gravity 3. Contraction against buoyancy 4. Complete ROM against gravity with some resistance 4. Contraction against buoyancy at speed 5. Complete ROM against Gravity with full resistance 5. Contraction against buoyancy + some resistance 6. Contraction against buoyancy + more resistance + speed Water positioning with floatation belt Orienting the body away from the vertical towards the horizontal will reduce the resistance to translational movement forward through the after Exercise Programming Standard session — 30-45min Group session or individual session (or combination) Basic principles of programming apply Supervised vs independent prescription Patients generally able to do more sets/reps in water than on lad (eg. X40 or 2x20) Intensity if exercise is difficult to gauge as it is dependent on individual patient and equipment being used Hydrotherapy equipment Railing Aquatic treadmill Aquatic bike Ankle cuffs Aqua dumbbells Weight plates Noodle Floatation belt Water fan Hydrotherapy Exercises Lower limb walking (forwards, backwards, sideways) Hip ROM (flexion, extension, adduction, thigh circles) Knee ROM (lunges on a step, hamstring curl, leg extension) Squats against a rail Upper limb Shoulder ROM (flexion, extension, abduction, adduction) Shoulder press-down Wall push-off against rails Punching (jab, cross, hook, uppercut) Trunk Standing crunches Rotational crunches Trunk rotations Evidence for hydrotherapy in neuromuscular rehabilitation Aquatic exercise had similar effect on balance compared to control Aquatic exercise resulted in greater QoL scores than land-based in individuals with cerebral palsy Significant improvements in pain perception, vitality, metal health and QoL in indiviudals with fibromyalgia Also beneficial in hemiplegia, MS, Parkinson’s Aquatic exercise has effects that are at least as good as those of land-based exercise Technology in Neurorehabilitation Context Difficult — chronic, neurodegeneration Adherence Lack of enjoyment Contextual (up to date) Motivation Engagement Interventions Assessments Interventions Virtual Reality Computer-based technology that exposes consumers to a multisensory stimulated environment and receives real-time feedback on performance Interactive exergames provide consumers with activities relevant to ADL and real-life scenarios Head-mounted vs Immersion — depends on clients clinical presentation Cerebral Palsy VR is effective to improve: - arm function - postural control - balance - ambulation - gross motor function Traumatic Brain Injury (TBI) VR promotes a positive impact on balance and flexibility in children VR is effective in enhancing motor skills in adults VS is effective in comparison to other modalities in improving balance and mobilty Multiple sclerosis (MS) When examining traditional therapies, VR improves balance VR has a short-term benefit in improving balance and fear of falling Comparison to conventional therapy — VR improves fatigue, physical and cognitive function Parkinson’s Disease (PD) VR has a short-term effect on gait (step/stride length) Compared to passive control, VR improves gait speed, step/stride length, balance, ADL and postural control As effective as other treatments on motor function, step/stride length, balance and QoL Stroke In comparison to conventional therapy, VR improves: - upper limb function - physical performance - muscle strength - gait - balance Alzheimer’s Disease VR improves - balance - cognition - memory - executive function Spinal Cord Injury (SCI) Positive effects on aerobic function, balance (sitting and standing), pain and motor function In combination with Robot Assisted Training (RAT), VR improves upper limb function and muscle length Exergames Technology-driven exercises requiring consumers to be physically active to play the game Contains principles of video gaming (eg. Motivation, reward, progression) Not enough high-level evidence (yet) Robot-Assisted Training (RAT) Modality in which a consumer uses the RAT to support their body weight (for gait training) Helps consumers with functional movements to support their functionality Resistance and % of body weight can be manipulated as progression Cerebral Palsy In comparison to conventional therapy, RAT improves - lower limb function - balance - walking endurance - gait speed - walking, running and jumping ability Stroke Combination of conventional therapy with RAT leads to gait improvement Combined with electrical stimulation — leads to more gait improvement compared to alone Better than no treatment for upper limb function and ADL ability SCI RAT results in improvements in: - spasticity - pain perception - proprioception - gait - sitting posture - overall mobility Telerehabilitation The use of medical/health information to provide rehabilitation to people in different locations Multiple Sclerosis Telerehabilitation is effective in - reducing motor disability - Improving gait - Improving balance SCI Telerehabilitation improves - QoL - Functional ability = Motor impairment TBI Telehrehabilitation improves - global functioning - depression - symptom management PD In comparison to standard treatments — improves QoL and adherence to treatment Maintains and improves — gait, balance and QoL Stroke In comparison to standard treatments, Telerehabilitation improves: - motor function - ADL - Independence Improves balance and functional mobility Assessments Motion Capture Systems — Kinematic analysis of movement 2D and 3D Gait mat systems — pressure sensors embedded, easily measures gait parameters Wearable devices — has sensors measuring acceleration, can also monitor HR, SpO2, etc Exergames — technology driven assessments requiring consumers to be physically active to play the game Telerehabilitation — Telehealth is the use of medical information that is exchanged from one sit to another through electronic communication to improve a consumer’s health Considerations FITT principles Different stages of diseases and conditions Reliability and validity of outcomes For outcomes there is still a lack of information — more studies are needed Falls Prevention Definition of Falls Unexpected events which resulted in the participant in intentionally coming to the ground floor or other lower level ~1/3 older adults fall at least once each year 45-70% of people with neurological disorders fall at least once each year Falls represent - 14% of hospital admissions - cost over $1 billion AUD - represent over 60% of direct costs of all unintentional injuries Consequences of falling Diverse injuries, including fractures Hospital admissions (and possible complications) Psychological and mental health issues — fear of falling, anxiety, etc, Become more dependent Increase in functional inability (leads to the need to live in residential care) Death (1% of cases) Key facts Falls are the second leading cause of unintentional injury deaths worldwide Each year ~ 684 000 individuals die from falls globally of which over 80% are low and middle-income countries Adults > 60 suffer greatest number of fatal falls 37.3 million falls that are severe enough to require medical attention occur annually Prevention strategies should emphasise education, training, creating safer environments, prioritising fall-related research and establishing effective policies to reduce risk Mechanisms of falls Intrinsic mechanisms Biological muscle weakness Balance problems Gait problems Poor vision Limited mobility Cognitive impairment Functional limitations Postural hypotension Behavioural Anxiety Depression Cognitive decline Attentional deficits Fear and concern of falling Loneliness Social isolation Extrinsic mechanisms — environment unstable surfaces Slippery surfaces Narrow pathways Low contrast areas Cluttered areas Pets Others Disease-related (eg. PD, MS) Urinary incontinence Auditory issues Orthostatic hypotension Dizziness Polypharmacy Extra dosage of vitamin D intake Use of psychotropics Sleep disorders Types of Falls How they happen balance-related (slips, trips, sudden loss of balance) Disease-related (freezing of gait in people with PD) Unexplained falls (syncope, vertigo) Where they happen At home (or known location) — due to limited space to move around or excessive confidence regarding that place Away from home (or new environment) — more likely to fall due to not noticing threats (eg. Uneven pathway) How to Assess falls risk Many different tools — choose based on reliability, validity and minimal clinically important difference Particular tool may be effective in one case but not another (PD vs stroke) Particular tool may be effective in early stages of people living with a disease but not in later stages Reliable and valid tools for healthy older adults — work in person and remotely - Berg Balance Scale - TUG - Dynamic Gait Index - Functional Gait Assessment Falls Risk Assessment Tool (FRAT) YES to three or more of the following = high risk of falling - Have you had a fall in the last year? - Do you have PD or history of stroke? - Do you feel you have balance problems? - Can you stand up from a chair without using your arms for support? - Are you limiting what you do due to fear of falling? What really works Highest level evidence given by meta-analyses of Randomised Control Trials - best evidence involves multiple RCTs and/or systematic reviews with little inconsistency Outcome measures - standing balance (time) - One-legged stance (time) - 5xSTS (time) - 4m walk (time) - fear of falling (score) Feasibility — class attendance, enjoyment, adverse events What works in the community High-level balance exercise in group or home setting (functional balance exercises, Otago, Tai Chi) Voluntary and reactive step training Multicomponent and multifactorial interventions in higher-risk populations Occupational therapy interventions (home safety modifications in association with transfer training and education) in high-risk populations Podiatry intervention in people with disabling foot pain Pharmacist-led education and GP medication review Withdrawal of psychoactive medications Expedited first eye cataract surgery Restriction of multifocal glasses use in older people who take part in regular outdoor activities What works in hospitals Intensive interventions in sub-acute hospitals What works in residential care Vitamin D supplementation (excluding mega-doses) Multicomponent and multi-factorial interventions Medication review Physiotherapy exercises New Overall Evidence for Falls Prevention Cerebral Palsy What is Cerebral Palsy A physical disability that affects movement and posture Every week in Aus, 11 babies are born with CP No known cure ~34 000 people living with CP in Australia (1/700 babies diagnosed) Not a disease but an umbrella term that refers to a group of disorders affecting a person’s ability to move Most common motor/physical disability in childhood > 2/3 of congenital brain injury causing cerebral palsy occur in the 3rd trimester of pregnancy, although the cause remains unknown 17 million people worldwide Congenital CP — 90% of cases occur before birth or during delivery Acquired cerebral palsy — occurs up to 28 days after birth Believed to be caused by an injury to the developing brain — stroke is the most common cause of acquired CP Risk factors Low birth weight Premature birth Multiple births Infection during pregnancy Asphyxia Infertility treatments Delivery complications and head trauma Genetics Blood clotting problems (thrombophilia) Types of Cerebral Palsy Spastic CP — increased stiff muscle tone, makes their movement challenging or awkward (most common) - spastic diplegia/diparesis — affects legs more than arms - spastic hemiplegia(hemiparesis if not paralysed) — affects one side of the body - spastic quadriplegia/quadriparesis — affects all limbs and trunk (most severe) Dyskinesia CP — may have trouble moving hands, arms, legs or feet (makes walking and sitting difficult) Ataxic CP — has trouble with coordination and balance Mixed CP — symptoms of several other forms Diagnosis Usually between 12 and 24 months of age Comprehensive birth history, MRI and physical examination Tools like General Movement Assessment (GMA) can assist with early detection Manual ability Classification system (MACS) — 5 item scale of ability to manipulate objects Communication Function Classification System (CFCS) Eating and Drinking Ability Classification System (EDACS) General Motor Function Classification System (GMFCS) Categorises gross motor function GMFCS levels I - V Involves — walking, sitting and assistive technology use Has not been validated in adults Treatments and Therapies Early diagnosis is imperative Medications - Anticholinergics — block neurotransmitters - Benzodiazepines — treat seizures, anxiety and insomnia - Antidepressants — ease symptoms of depression - Anti-inflammatories — reduce pain and inflammation - Baclofen — relaxes muscles - Botox — treated spasticity - Anticonvulsants — suppress neurons that lead to seizures Physical therapy Occupational therapy Speech therapy Alternative therapy — music, acupuncture, aquatic, etc. Surgery for muscle immobility Other impairments CP primarily affects movement and balance, however: Sensory problems Vision impairments Cognitive deficits Behaviour and emotion Pain Mood Fatigue Comorbidities Obesity CVD Metabolic Syndromes Poor mental health Assessment and Treatment Chronic Fatigue Syndrome Definition CFS (aka myalgic encephalomyelitis) is a complex multi system condition characterised by medically-unexplained, prolonged, disabling fatigue lasting at least 6 months Fatigue may describe a diverse range of clinical phenomena including: - muscle weakness (eg. Myopathy, polymyositis) - neuromuscular fatiguability (eg. Myasthenia gravis) - central fatigue (eg. MS) - anhedonia (eg. Major depression) - somnolence (eg. Sleep apnoea, narcolepsy) - Dyspnoea (eg. Airflow limitation, cardiac failure, anaemia) - Inflammation or infection (eg. Systemic lupus erthematosus, influenza) Fatigue from CFS differs from the above as it is not relived by sleep and they can generate muscle strengthen and endurance Physical activity can result in post-exertions malaise that can take hours or days to recover from Along with physical fatigue, most people with CFS experience mental fatigue, typically following neuropsychological tasks Diagnosis No consensus agreement amongst medical professionals as to how CFS may be definitely diagnosed Typically diagnosed through: - clinical history - examination - investigation - specialise referral Symptoms — fatigue needs to be new in onset and lasting for at least 6 months, significant reduction in ADLs, ability to work etc. - impaired short term memory - sore throat - tender cervical or axillary lymph nodes - muscle pain - multi-joint pain without arthritis - headaches of anew type, pattern or severity - unrefreshing sleep - post-exertional malaise lasting > 24hrs Pathophysiology Pathophysiology of CFS is unclear, several proposed hypotheses including: Unique pattern of infection with recognised or novel pathogen Altered CNS functioning following abdominal immune response against a common antigen Neuroendocrine disturbance Neuropsychiatric disorder with clinical/neurobioloigcal aspects linking to depressive disorders Psychologically determined response to infection in “vulnerable” individuals Epidemiology Prevalent condition — affecting ~ 1/100 patients attending primary care 0.2-0.7% of the population Risk Factors Infections Psychological distress Genetic makeup Environmental influences Gender-environmental interactions Signs and Symptoms Management and Treatment Post-exertional exacerbations — important consideration when introducing exercise (both physical and cognitive) Fatigue types - boom-bust cycle — periods of low energy following periods of high energy can lead to avoidance and reconditioning - optimal activity zone — the zone at which an individual can complete the same exertions daily without incurring additional fatigue (stabilise before increasing, minimum 2 weeks) PACE Trial — improvement in fatigue and physical function for individuals who underwent graded physical therapy Initial Assessment/interview and monitoring — multidisciplinary management at UNSW lifestyle clinic - comprehensive interview - onset of symptoms and time to diagnosis - sleep-wake cycle - physical activity vs cognitive activity - work/study status - home status - support resources - leisure/recreation: pre- and post-diagnosis - walking tolerance - symptom limited functional capacity - activity diary — 1-2 weeks - step count diary Activity Pacing Integrated approach; physical and cognitive Overall aim to stabilise activity patterns Involves limiting activity to symptom threshold limits ‘True rests’ and detailed scheduling Micro- (pacing of individual activity) and macro-pacing (pacing of activities throughout the day) Graded Actvity Graded activity / Exercise ≠ Conventional exercise Symptom Limited — post-exertional exacerbation in symptoms Increase by 10-20% every 1-2 weeks — focus is on controlling symptoms Compensate activity during symptom aggravation Psychological and Social Support Belief that should be challenged through cognitive behavioural therapy: more sleep will alleviate fatigue Avoiding activity is preferable Ignoring symptoms and simply pushing beyond activity thresholds will overcome the illness Pharmacotherapy Orthostatic intolerance — fludrocortisone, low-dose beta blockers, alpha-adrenergic agonists, pyridostigmine, desmopressin, ivabradine intravenous saline Sleep issues — Trazodone, low-dose tricyclic antidepressants, mirtazapine, antiepileptics, clonazepam, cyclobenzaprine, zolpidem, etc Cognitive dysfunction and fatigue — Methylphenidate, modafinil, armodafinil, amantadine, caffeine Immune dysfunction — intravenous immunoglobulin, subcutaneous gamma globulin, ion sine pranobex, hydroxychloroquine Pain — Low-dose naltrexone, SSRIs, muscle relaxants, medical marijuana, etc GI issues — drirfaximin, oral vancomycin, metronidazole Traumatic Brain Injury (TBI) Demographics Incidence of TBI peaks in 15-35 years age group By gender — 3.4:1 male to female (largely thought to be related to risk-taking behaviour among young males) 2/3 mod-severe TBI cause by multi-vehicle accidents ~50% of the adult and paediatric NSW BIRP populations have 1 or more challenging behaviours following TBI Mental health, drug and ETOH are common-comorbidities both pre- and post-TBI Employment rates post TBI average 29% and there is a marked and consistent post injury shift from full-time to part-time employment Pathophysiology Primary injury — initial application of force to the skill that disrupts white/grey matter and blood vessels in the brain Secondary Injury — events occuring following the primary injury that cause further injury: edema, build-up of neurotoxins - intracranial haemorrhage (bleeding inside the skull) - brain swelling - increased intracranial pressure (pressure inside the skull) - brain damage associated with lack of oxygen - infection inside the skull, common with penetrating trauma,a - chemical changes leading to cell death - increased fluid inside the skull (hydrocephalus) Location and severity of injury dictates function changes in TBI - frontal love — speech problems, inattentiveness - parietal lobe — sensory deficits Severity graded on degree of neurological deficit resulting from injury (not severity of injury per se) Glasgow Coma Scale (GCS) - < 8 — severe - 9-12 — moderate - 13-15 — mild Duration of post-traumatic amnesia — period of time the brain is unable to lay day-to-day memory (best indicator of function and cognitive deficits after TBI) 10-15% of mild TBI survivors have persisting symptoms and impairments Clinical Presentation Seizures (penetrating TBIs) — require medications (side effects), lifestyle implications - early seizures (within the first few weeks of injury) - later seizures (within 2 years) Hypertonia and Spasticity (brainstem/cerebellum or midbrain TBIs) - High muscle tone/muscle stretch reflex - Spasticity — velocity depended increase in resistance when a joint is passively moved through ROM - Often prevents/interferes with ADLs - Medications - measurement of spasticity - Poor muscle co-ordination/co-contraction - Spastic dystonia - Contractures Hypotonia (cerebellum) - less common than spasticity - low muscle tone Heterotopic ossification - ectopic growth of bony tissue in tissue planes around major joints — surgery/pharmacological intervention n Balance Disroders - high prevalence - diverse presentation and root cause Muskuloskeletal Injuries - MSK injuries associated with cause of TBI (MVA or fall) - Need to be treated alongside TBI Neurocognitive function, sensory funciton, speech and communication - psychiatric disturbance (depression, anxiety, mood disorders) — extremely common - sensory changes — heightened sensitivity, difficult filtering sensory input, sensory loss - cognitive problems - memory impairment, difficulty with new learning, attention and concentration, reduced speed and flexibility of thought processing, impaired problem-solving - problems in planning, organising and making decisions - language problems — dysphasia, problems finding words, impaired reading and writing skills - impaired judgement and safety awareness - Personality/behaviour changes (includes psychiatric disorders: anxiety, depression, PTSD, etc) - impaired social and coping skills, reduced self esteem, altered emotional control (poor frustration tolerance, anger management, denial and self-centeredness) - reduced insight, disinhibition, impulsivity, apathy, a motivational states - other: sleep disturbances, chronic pain, headaches, etc Psychological Complications Common lifestyle consequences Unemployment and financial hardship Inadequate academic achievement Lack of transportation alternatives Inadequate recreational opportunities Difficulty maintaining interpersonal relationships, marital breakdown Loss of pre-injury roles — loss of independence AEPs need to be aware of changes and refer when appropriate Rehabilitation for people with TBIs Rehabilitation is effectively using an interdisciplinary approach — multidisciplinary, patient-centred Focus is on issues such as retraining in ADLs, pain management, cognitive and behavioural therapies, and pharmacological management Social burden of TBI is significant — family and carers need education, support and counselling Goals Reduce impairement and pathology — spasticity, hypotonia, balance, cognitive Improve activity/participations — capacity to carry out ADLs - task specific skills - functional capacity Factors that influence recovery Severity of injury Age at TBI Time between injury and rehab commencement Duration and intensity of rehab intervention Support system — family care, QoC, community resources Exercise and TBIs People in recovery from mod-severe TBIs can, with minimal guidance, perform vigorous community-based exercise Independent exercise (once oriented) is appropriate Aerobic exercise result in significant improvement in exercise capacity but do not extend to change in function or psychological state - more vigorous intensity may have better effect on ambulatory status Circuit training — improvements in oxidative capacity and abdominal muscular endurance, not beneficial in improving oxygen cost of walking (walking efficiency) - specific functional training is more beneficial - improvements in CV fitness required 6+ weeks off circuit training Bodyweight supported treadmill has potential to favourably change cardiorespiratory capacity after TBI Lack of evidence surrounding PRT and 1RM — seen to improve sit-to-stand, maximal gait and speed, muscle speed Exercise is beneficial in reducing depressive symptoms Mobility training — improvements in walking speed, mobility and balance post-intervention Exercise shown to improve cognitive impairment following TBI Exercise Goals Increase PALs Consistency/habit forming is more important that mode/intensity, etc People with TBI of minor severity — follow same PA guidelines as healthy adults (150min per week of MICT/75min vigorous 2*PRT) People with TBI of moderate+ severity — Taylor exercise to: - type and severity of impairment - personal interests - support levels Exercise prescription to meet personalised functional outcomes (eg. Step over a curb with confidence) Exercise Considerations Risk of another TBI (falls risk, lack of spatial awareness, etc) Likely working within a rehab team — ensure knowledge of medical, mobility, communication, behavioural and cognitive needs Patience and Adaptive communication methods may be needed — attentional and understanding instructions may be impaired Hypotonia/Spasticity — use wrist wraps, Velcro fasteners to facilitate use of exercise equipment when hand function is impaired Altered joint junction and form — affected side may have reduced ROM, strength, tone Reduced fitness, strength and mobility — compounded by sedentary lifestyle - concomitant disease - higher CVA risk for TBI - early onset fatigue (prior to reaching exercise max) - effect of fatigue on the rest of the client’s day Rehab environment — distractions family/carer involvement Working with neurologists and medico specialists Medications Anti-anxiety/anti-depressant medication to lesson feelings of nervousness and dear May cause fatigue and many require longer cooldown post exercise Anticoagulants to prevent bloos clots and improve blood flow — may increase likelihood of bruising Anticonvulsants to prevent seizures Diuretics to help remove fluid that can increase pressure inside the brain Muscle relaxants to reduce muscle spasms and to relax constricted muscles — may cause bradycardia, hypotension, weakness Stimulants to increase alertness and attention CONTRAINDICATIONS Exercise Pre-screening Assessment Sensory deficits CVD Physiological factor Function Outcome measures 60s STS TUG Berg Balance Scale 5xSTS Measuring CRF and aerobic capacity Mode suited to individuals capability — balance considerations, sensorimotor impairments (spasticity) Focus on large muscle groups Testing protocol modify existing tests if needed — reduce power/speed increases between sets Submax testing protocols may be more appropriate RPE may not be valid - use objective measurements - TBI usually does not impair acute CVD/respiratory response to exercise Field tests maybe more appropriate than lab based testing — 6MWT vs gas exchange Measuring strength and anthropometry Mode Machines vs free weights Bodyweight tests Hand grip dynamometers Considerations during testing Spasticity Bilateral deficits Joint morphology Motivation Cognition deficits Anthropometry BMI Waist circumference HAR Weight DXA/skin folds Exercise Prescription for TBI Circuit Training resistance exercise to enhance muscle at strength and endurance of the major muscle groups Balance training — separate sessions may also be useful Shorter duration of 20mins at the aerobic station may be used to avoid undue fatigue and increase compliance Duration — 50mins WU/CD inclusive Strength training consider 1RM as correct form not if weight was removed Potential to use rests between sets for other exercises training Balance incorporate into circuit training Task/deficit specific Progress overtime Spinal Chord Injury (SCI) What is a SCI? lesion or damage to the spinal column that disrupts neural flow from the brain to the body and vice versa Can result from a number of mechanisms - intrinsic — tumour, cyst, prominent disk herniation, stenosis of spinal column etc. - extrinsic — car accident, crush injury, hyperflexion, hyperextention, etc. Damage to the neural elements of the spinal canal, often resulting in permanent impairments in motor, sensory or autonomic nervous system function Injury severity is dependent on the segmental level and completeness of injury — spinal cord does not need to be completely severed for dysfunction to occur Profound consequences for functioning and disability affecting body systems, physical activity and participation Associated with reduced health related outcomes — increased in morbidity and mortality Anatomy Segmental organisation— each segment of the spinal cord is connected to a specific region of the periphery by axons travelling through a pair of spinal nerves In the cervical region, spinal nerves are found above the corresponding vertebrae (except the c* spinal nerve) Remaining spinal nerves lie below the corresponding vertebrae Each spinal nerve innovates a myotome, dermatome and peripheral nerve field - Myotome — the muscles innervated by axons from a single spinal segment - Dermatome — area of skin innervated by the axon from a single segment - Peripheral nerve field — muscle or areas of skin innervated by axon from an individual peripheral nerve Myotomes Upper limbs C5 — deltoid C6 — wrist extensors C7 — elbow extensors C8 — long finger flexors T1 — small hand muscles Lower limbs L2 — hip flexors L3,4 — knee extensors L4,5-S1 — Knee flexion L5 — ankle dorsiflexion S1 — ankle plantar flexion Classifications of SCIs Tetraplegia — injury to spinal cord in the cervical region, loss of muscle in all four extremities - central cord injury where only arms are affected are still considered tetraplegia as it occurs in cervical region Paraplegia — injury to spinal cord in thoracic, lumbo and/or sacral segments, symptoms and strength loss presenting in the lower limbs only Complete No voluntary motor or contraction-sensory function below injury site absence of motor functions in lower sacral segments (S3 for sphincter management not in tact) Often complete SCI presentations don’t see spontaneous recovery significant impactful trauma — results in severe compression and/or inflammation Incomplete preservation of some sensory or motor function below the level of injury S3 still in tact see some significant a gain in a neuroplasticity response or return to function following an STI Anterior cord syndrome — usually caused by cervical flexion complete motor fucntion loss bilaterally Complete loss of crude touch, pain and temperature sensation bilaterally Fine touch and perception sense are preserved Central cord syndrome — usually caused by hyperextension and compressive injuries that cause central cord swelling Impairment of fucntion is more affected in the upper extremities Varying degrees of sensory loss — less severe than motor deficits High percentage of patients will attain ambulatory function, bowel/bladder control, and hand function Posterior cord syndrome — caused by compression from tumour or infarction of the posterior spinal artery Rare Touch and proprioception are lost below site of injury Complete motor function, crude touch, pain and temperature senses are preserved Brown-Sequard’s Syndrome / Hemicord Lesion — caused by hemisection of the spinal cord by gunshot or stab wound Ipsilateral paralysis and loss of fine touch and Proprioception Contralateral loss of crude touch, pain and temperature sense Aetiology and Epidemiology Worldwide 2:1 ratio of non traumatic cases of SCI 350 new cases per year in Australia males: females — 4:1 Age < 30 years (15-25 years old) - ~80% from traumatic causes - 50-75% motor vehicle accidents - falls, sports, water based activities, work-related, falling objects - ~20% from non-traumatic causes — secondary to such conditions as vascular disease, infection diseases, disc herniation, etc Pathophysiology 4-5 days — high death rate from respiratory failure, breathing is entirely reliant on diaphragm Early recovery phase — after 3 months can focus on physical presentation of individuals Flattening of recovery phase — 9 months Importance of early intervention — admission < 24hrs post-injury have less prevalence of complications in every metric - ‘golden window’ — rate of improvement is fastest in the first 6-9 months post-injury (focus on neuroplastic/functional change ASAP is imperative) American Spinal Injury Association Classification of SCI most commonly used Sensory and Motor classification A - Complete B - Sensory incomplete C - Motor incomplete (more than half the muscles below injury level have strength 3/5) E - normal Response to exercise Persons with low level lesions (paraplegia) may have near normal CV responses to exercise - Major limitations: smaller muscle mass used for exercise (arms) resulting in lower peak VO2, lower peak power output and cardiac output (50% of predicted value) Persons with higher lesions (tetraplegia) have higher proportion of the active muscle group that is paralysed and ANS sympathetic control may be impaired - peak exercise capacity values may be 33-50% of estimated - MHR may not exceed 120bpm - strenuous exercise may not be tolerated The higher the lesion, the lower the CV capacity and more limited the VO2 & Exercise Prescription in SCI Neurological Changes Complications Autonomic Dysreflexia — considered a medical emergency and must be recognised immediately - if left untreated can cause: seizures, retinal haemorrhage, pulmonary edema, renal insufficient, MI, stroke, death - management: sit client upright, loosen tight clothing, find source of instigating cause - monitor BP every 2-3 mins and seek medical attention Pressure injury / skin integrity Hypotension Bone mineral density Deep vein thrombosis — a blood clot in the legs primarily related to physical inactivity and immobility - may lead to pulmonary embolism that can be fatal - symptoms: local swelling, redness, heat Pressure sores Osteoporosis Diminished pulmonary function Blunted CVD responses and diminished exercise capacity - SCI is an independent risk factor for CVD and stroke Considerations Spasticity / tone Impaired thermoregulation Contracture / changes in ROM Pain Bladder/bowel function Proprioceptive changes Sensory/motor changes Assistive devices What should we focus on? Activity Based Training Traditional Therapy Activity Based Training Activate nervous system above level of lesion Activate nervous system above and below the lesion Low intensity practice High intensity practice Non-patterned movements patterned movements Compensates for loss of function restores lost function uses compensatory Devices Minimises or eliminates compensatory devices Benefits of Locomotor Training Incomplete SCI Complete SCI Increased walking speed Improved trunk trunk control Increased walking independence Improved bone density Increased walking endurance Improved QoL Improved balance Improved bladder/bowel sensation and fucntion Decreased asymmetry of gait Reduction in muscle spasms and neural pain Improved gross motor skills Increased muscle length and joint mobility Improved wellbeing, life satisfaction and perceived health Improved wellbeing, life satisfaction and perceived health Functional Electrical Stimulation Improves strength, resistance to fatigue and contractile properties of the muscle Enhance levels of fitness Improve LL circulation Attenuation of osteopenia, improve bone mass Incomplete injuries — LL mass, isometric strength and endurance Improved body composition — lean mass, fat mass Promote cardiovascular and hempodynamic benefits Prevent muscle atrophy and pressure sores Reduced spasticity and neurogenic pain Have a positive effect on psychosocial factors — self-image and depression Recommendations for Cardiorespiratory Exercise Programming F — 3-5 days/week Consider multiple daily bouts for those with very low functional capacity (peripheral fatigue) I — method of intensity monitoring is controversial HR responses are variable depending on level of injury — in many 30-80% HRR correlates to 50-85% peak VO2 RPE is often used and preferred — 11-14 is best T — follow physical activity guidelines for general population and work up to 60min per session T — adapted or adaptable equipment mat be necessary for appropriate and safe exercised training Recommendations for Resistance Exercise Programming F — 2-3 days/per week (never 2 consecutive days) I — as tolerated T (volume) — Initially, 2x10 as tolerated and progress T — focus on strength/endurance, maintaining muscular balance and reducing repetitive strain around the shoulder Dperessors (infraspinatus, subscapularis, pec major and lats) Scapular stabilisers (traps and rhomboids) Internal and external rotators Dementia Incidence and Prevalence 10 million new cases every year 50 million people worldwide — 152 million projected by 2050 490 000 people with dementia in Australia in 2022 Second leading cause of death in Australia — first leading cause of death for women 6-10% of the population >65 will have dementia, increases to 30% > 85 years Risk Factors Non-modifiable Age CV risk (potentially modifiable) Genetic risk Family history Sex — DLB (dementia with leeway bodies) and VaD (vascular dementia) greater in men, Alzheimer’s greater in women Down syndrome PD/MS Chronic kidney disease Head injury (potentially modifiable) Risk Reduction Stop smoking Stop drinking ETOH Cognitive training Social activity Weight management (mid-life) Manage hypertension Manage diabetes Manage dyslipidaemia (mid-life) Manage depression Hearing loss Diagnosis DSM-5: major neurocognitive disorder Progressive neurodegeneration disorder affecting cognition and as a result ability to function Cognitive decline — complex attention, executive function, learning and memory, language, perceptual-motor or social cognition Cognitive deficits not better explained by another condition (eg. Depression, delirium) Umbrella term — aka Major neurocognitive disorders Limbic-predominant age-related TDP43 encephalopathy (LATE) — relatively new, for people > 80 Alzheimer’s disease Most common Vascular dementia Parkinson’s disease dementia Frontotemporal dementia Mixed aetiology Dementia with Lewy bodies Mild Cognitive Impairment Cognitive decline that is not affecting ability to function 3-5x higher risk of developing dementia ADLs preserved — minor issues with complex ADLs Cognitive complaints Amnestic vs non-amnestic — is memory impaired? Single vs multidomain Disease onset and progression Differs for each person Eventually terminal Alzheimer’s Disease — insidious onset and gradual progression Vascular dementia — step-wise or may appear gradual, usually more rapid than AD Frontotemporal dementia — often younger (50-60), insidious onset and gradual progression Dementia with Lewy bodies — insidious onset and gradual progression Presentation and Pathology Each type of dementia presents with different clinical features - AD — early memory and learning impairment - DLB — fluctuating cognition, reduced attention, hallucinations, REM sleep disorder, autonomic dysfunction Each type of dementia or presents with different brain pathology - AD — neurofibrillary tangles (Tau) and amyloid plaques - FTD — two proteins accumulate (TDP43 and Tau) Mixed pathology is relatively common Physical Impairment/decline ADLs and gait Comorbidities Any comorbidity associated with older age — arthritis, CV, etc Can depend on sub-type On average 4 comorbidities (2 in cognitively healthy people) Behavioural and Psychological Symptoms of Dementia (BPSD) Depression 20% Anxiety 16-35% Apathy 55-90% Agitation/aggression 60% Psychosis 25% - hallucinations - delusions — fixed, false beliefs that are implausible or untrue - misidentification — mistakes people or objects for something else Often a sign of unmet needs Dementia and Falls Pharmacological Management No cure Aimed at slowing cognitive decline and managing symptoms Cholinesterase inhibitors Memantine BPSD — only when non-pharmalogical treatment has failed (SSRIs, antipsychotics etc) Exercise Programming Common communication changes Difficult finding a work Speaking fluently but not making snes e May not be able to understand what you are saying Writing and reading skills may deteriorate May lose the normal social conventions of conversations and interrupt or ignore a speaker, or fail to respond when spoken to May have difficulty expressing emotions Communication Respect, empathy, listen Body language (55%) and tone/pitch (38%) Body position Speak slowly, clearly and without jargon Short sentences — break down instructions Allow processing/response time — be patient Clarify meaning and understanding Minimise competing noise Hearing and vision aids Use personal references Carer engagement work in partnership and acknowledge their expertise Source of information Get to know the person Communicate about the person with dementia’s needs Consider impact of intervention on carer Eduction and support Practical examples Focus on the ionic ideals strength How to help them keep doing what they can do Exercise practical considerations Supervision and safety Focus on strength Tailored (cognitive and physical) and progressive ‘ Instructions and communication Comorbidities Currently level of function and falls risk Achievable, sustainable and enjoyable Environment — consider noise and set-up Group vs individual FITT Person-centred care Centres around the persons’ needs Shared goals based on persons’ values and experiences Past lived experiences Likes/dislikes Cultural and religious beliefs Precipitants to behaviours Specific behaviours are often a result of unmet needs Respect, dignity and compassion Exercise selection evidence-based Purpose — functional, falls prevention, cognitive, etc Setting — community, residential, hospital, etc Cognitive and physical abilities Social and socioeconomic situation Exercise and Physical/functional performance Exercise improves: ADLs Balance Gait performances (speed, step length) Functional/mobility performance Dual task performance Endurance Strength Exercise prescription goal Tailored and progressive Mode — supervised, combination of strength, balance, functional, dual task, aerobic, multimodal Session duration — 60mins (work up to) Session frequency— 2-3x/week Intervention — 3 month minimum Tailor to desired outcome Exercise and fall prevention Moderate certainty evidence exercise can prevent falls - most evidence in community-dwelling - exercise has been used in a Multicomponent intervention in residential aged care — some successful - many trials are underpowered and have methodological limitations Exercise prescription goal - tailored and progressive - mode — supervised strength, balance and functional training - intensity — moderate to high challenge balance - dose — 1-2hrs per week, > 50hrs - intervention duration — 6-12 months - utilised caregiver supervision (community) 23% reduction in rate of falls (29% in community) Sunbeam program Exercise and Cognitive performance Exercise probably improves (and delays decline) in cognitive performance (low certainty) - small to medium effect - some studies do not support - evidence suggests best effect on global cognition and executive function/attention Exercise prescription goal - tailored and progressive - mode — Multicomponent or aerobic or aerobic combined with another modality (resistance, DT): may depend on cognitive domain - intensity — moderate - dose — can aim for 150min/week aerobic, but lower dose interventions also work and potentially have greater effect (≤ 2h/week) >24hrs total - session duration — short, 30-45mins - session frequency — 3x/week, resistance 2-3x/week - intervention duration — >16 weeks aerobic, 50 worldwide 30% of stroke survivors are under 65 65% of stroke survivor suffers a long-term disability 80% of strokes are preventable Risk factors Hypertension Diabetes Hyperlipidemia Heart diseases Personal/family history of Transient ischemia attack (TIA) Age, gender and ethnicity Blood vessel malformations (AVM) or aneurysms in brain Smoking Alcohol Obesity or lack of physical activity Types of Stroke Ischemic 87% Large artery atherosclerosis — narrowing and hardening of blood vessels Cardio-embolism — blood clot forms in the heart and travels to the brain Small Cessel Occlusion — occlusion of small, deep penetrating arteries Other determined etiology — genetic conditions, vasculitis, sickle cell disease, etc Undetermined/mixed etiology Hemorrhage 13% Silent infarct/haemorrhage — without history of related neurological dysfunction despite radiological evidence Hemorrhagic stroke are often associated with excruciating headache and vomiting Less common, more deadly (40% of all stroke death) but have better long term prognosis Partial Anterior Circulation Syndrome Total anterior Circulation syndrome Clinical features Clinical features higher cortical dysfunction only (dysphasia, visuospatial neglect) higher cortical dysfunction only (dysphasia, visuospatial neglect) OR AND any two: sensorimotor hemiparesis - higher cortical dysfunction AND - sensorimotor hemiparesis homonymous hemianopia - homonymous hemianopia Location Location Usually middle cerebral artery or internal carotid artery Usually anterior cerebral artery, middle cerebral artery or their branches Affects both cortical and subcortical regions Mainly affects the cortical region Lacunar Syndrome Clinical features Pure motor impairments Pure sensory impairments Limited sensorimotor stroke Ataxic hemiparesis Dysarthria Location Small deep penetrating artery Affects the subcortical regions Transient Ischemic Attack (TIA) A transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia without acute infarction (< 24hrs) Short episode of ischemic stroke that recovers spontaneously Different in quantity but not quality Signs and Symptoms Clinical presentation depends on: Type Anatomical location Size of lesion Rapidity of occlusion Age Assessing acute stroke-related impairment Primary impairments in acute stroke Motor Communication Weakness Dysphasia (reduced ability to communicate using language) Hypertonia (increased resistance to passive stretch) Dysarthria (reduced ability to produce clear speech) Hypotonia (decreased resistance to passive stretch) Ataxia Cognitive Dexterity Attention Paresis Memory Hemiparesis Processing Hemiplegia Behavioural Sensory Agitated Pain Alertness Tactile Temperature Visual Vestibular Secondary Imparments in acute stroke Musculoskeletal Swelling Pain contracture Shoulder subluxation (later) Cardiorespiratory Deconditioning Emotion Anxiety Depression Functional limitations in acute stroke Mobility Rolling over Lying too sitting Sitting to standing Walking Postural control Independent sitting Independent standing Object manipulations Reaching for objects Holding objects Feeding Dysphagia Swallowing disorder Interventions for Stroke Survivors Training principles Individualised, functional and relevant to the patient Task-specific Fragmentation (movement decomposition) Progression Repetition with variation Real-time feedback Aerobic Exercise All patients following stroke/TIA should be considered for possible aerobic intervention Symptom-limited or submax exercise stress test should be a part of pre-participation screening with ECG monitoring and direct access to physician support and an external defibrillator Timeframe — 8 weeks Frequency — 3+ days/week Duration — 20+ minutes, progress Monitoring — frequent HR, periodic BP and RPE Usual Timeframe Very acute stage — hospital/stroke unit Rehabilitation needs to be assessed within 24-48hrs of admission Blood pressure target - ischemic stroke < 185/110 - intracerebral haemorrhage (ICH) ~140 — attention to intracranial pressure in large ICH Within 24hrs — abound intensive out-of-bed activities 24-48hrs commence short session of out-of-bed activity Undertake appropriate and regular physical activities with reference to guidelines Why is early intervention important Immobility is a primary cause of neurological intensive care unit complications Reduce pressure ulcers, infections, length of hospital stay, anxiety, mechanical ventilation duration and mortality Improve QoL, motor function, walking and ADLs Lower the cost of care by 15-30% Timing for out of bed activities mobilisation within the first 24hrs have negative impacts - higher risk of moderate-severe disability - higher mortality - similar immobility-related complications - similar mobility recovery Implication - out of bed exercise in the first 24hrs post stroke provides no additional functional benefit - Intensive mobilisation in the first 24hrs of stroke onset leads to adverse long-term outcomes and is NOT recommended Day 1-3 — gradual mobilisation Stroke patients should commence out-of-bed activity with 3 days of stroke onset — more than once per day, 200 000 of the Aus population 2/3 diagnosed are men 18% of people with PD are ≥ 65, 10% are diagnosed < 45 years Globally, number of people with PD will double by 2040, reaching 17.5M — increased longevity, industrial by-products, reduction in smoking What is Parkinson’s Neurodegenerative and progressive disorder Death and depletion of dopaminergic neurons in substantia nigra pars compacta Heterogeneous Progressive Motor symptoms/complications and non-motor symptoms Signs and Symptoms Motor Symptoms Non-motor Symptoms Bradykinesia Anxiety Resting tremor Depression Rigidity Cognitive impairment Postural instability Sleep disorders Gait disorders Apathy Autonomic dysfunction Hoehn and Yahr Stages 1. Unilateral motor impairment 2. Bilateral motor and axial impairment 3. Bilateral disease with impaired postural control 4. Moderate/severe disease — might still walk or stand unassisted 5. Wheelchair bound or bedridden Presence of Impairments with PD progression More common presence of cognitive impairment Freezing of gait Falls Physical dependence Weakness Issues associated with ageing become exacerbated Main Medications for Parkinson’s Symptomatic treatment — not disease modifying Dopamine replacements and agonists COMT inhibitors Anticholinergics — for tremors mostly MAO type B inhibitors — prolong dopamine effect Too much PD medication can cause dyskinesia — amantadine helps with severe dyskinesias Role of an EP Examine client Plan and deliver an exercise program to attenuate PD symptoms To plan and deliver an exercise program to tackle comorbidities Be part of a multidisciplinary team Recommended Parkinson’s assessments PIGD score — postural gait and stability Berg Balance scale — static balance Mini-BESTest — gait stability and posture Dynamic gait index — balance during walking Functional gait assessment — balance during walking ABC scale — balance confidence Falls Efficacy Scale — fear of falling Freezing of gait questionnaires — freezing of faith SAFFE-m — anti city avoidance because of fear of falling MDS-Unified Parkinson’s Disease Rating Scale (MDS-UPDRS) - part I — non-motor experiences of daily living - Part II— motor experiences of daily living - Part III — motor examination - Part IV — motor complications Exercise for Parkinson’s Disease Motor Examination Quality of Life Virtual Reality Freezing of Gait (FoG) One of the most disabling PD symptoms Occurrence increases with disease progression (usually Hoehn and Yahr ≥3) Fog usually occurs during turning, gait initiation and narrow pathways Severe FoG can happen during normal walking Increases risk of falling substantially 155x more likely to fall due to FoG over balance-related issues Types of Visual Cueing Stripes typed on the floor/cones Laser shoes/belt Holographic cueing Floor pattern Falls Prevention 45-68% of people with PD fall in each year 50-86% of people with PD fall multiple times a year Increase in occurrence with disease progression (Hoehn and Yahr ≥3) People with PD PIGD are more likely to fall due to: - FoG -Balance-related circumstances (trips, slips, etc) - At home Exercise at higher disease severity may be harmful Cognitive Impairments Impaired visual-spatial processing Poor attentional processing Poor short-term memory Executive dysfunction Deficient information processing Difficulties with dual-tasking Reduced cortical activity during inhibitory complex stepping tasks may reflect a ‘slow-down’ phenomenon in PD — fro to-striatal circuit damage Training groups Locomotor — maintenance in cognitive levels Delay in the progressive course of PD on non-motor symptoms Multi-modal — reduced physical stress Cognitive — maintenance in cognitive levels Exercise Considerations Higher disease severity (increased falls risk) Dyskinesia Tremor Not in ‘off’ stage Cognitive e impairment Fog Orthostatic hypotension Comorbidities Multiple Sclerosis Definition Chronic neurodegenerative disease affecting CNS Demyelination — destruction of myelin insulation covering nerve fibre, disruption of transmission of information in CNS Cortical lesions and deep grey matter lesions — decrease in grey matter (volume loss) closely associated with physical and cognitive changes Progressive and unpredictable Exact cause remains unknown No cure Prevalence ~ 26 000 — F;M = 3:1 103 700 people in 2017 in Aus 50 new cases/week in Aus High prevalence further from the equator (TAS has double the cases of QLD) Development of MS Worsening factors: Infectious Agents lack of sleep, & Genetic Predisposition L infections, Environmental factors & Abnormal immunological response & MS depression, smoking Other risk factors: gender, family history, smoking Diagnosis Type of MS Active — experiencing relapses of neurological symptoms: new or enlarging lesions visible on MRI Inactive/stable — No apparently relapse or progression noted Worsening — experiencing an increase in neurological dysfunction or disability as a result of either relapses or progression Relapse forms Clinically Isolated Syndroms Relapse-remitting MS Progressive forms Primary progressive Secondary progressive Current Disease Modyfying Therapies (DMTs) Infusion Oral Tablets Injections Autologous Hematopoietic Stem Cell Transplant (AHSCT or HSCT) Intensive form of treatment Steps 1. Release bone marrow from stem cells 2. Collecting AHSC 3. Freezing 4. Chemotherapy 5. Return AHSC back by infusion promising, aggressive treatment for MS High risks Disease Steps in MS 0. Normal 1. Mild Disability (visibly abnormal gait) 2. Moderate disability (visibly abnormal gait) 3. Early cane (25feet/7.6m without cane) 4. Bilateral support (25feet/7.6m) 5. Wheelchair (may be few steps) U. Unclassifiable MS vs healthy controls Decreased muscle strength, muscle fibres/muscle mass Decreased cardiorespiratory fitness Decreased risk of CVD Increased depression/fatigue Decreased physical activity level Decreased functional capacity/walking Decreased balance Decreased QoL Decreased employment Increased cognitive impairment Increased falls Symptoms of MS Numbness/tingling Walking difficult Vision problems Fatigue Cognitive dysfunction Depression Dizziness Pain Bladder/bowel. dysfunction Muscle spasms Weakness Exercise for MS Resistance and aerobic training exercises are effective in alleviating some characteristic signs and symptoms of Should be supplemented by balance exercises to prevent falls Should be delivered and prescribed by qualified exercise professionals Recognise and accomodate for complications such as fatigue and heat sensitivity Clinical features of impaire