Written Exam Musc Notes PDF

1. 2. 3. 4. 5. **Overview** **Common disorders in the hip, groin, and pelvic region** - Bony - Bony stress injuries (spectrum): pubic bone, femoral neck, femoral shaft - Musculotendinous - Tendinopath...

1. 2. 3. 4. 5. **Overview** **Common disorders in the hip, groin, and pelvic region** - Bony - Bony stress injuries (spectrum): pubic bone, femoral neck, femoral shaft - Musculotendinous - Tendinopathies (+/-) related bursitis): adductor conjoined tendon, gluteal tendinopathy, proximal hamstring, inguinal insertion, iliopsoas - Muscle strain injuries: hamstring strain injury, rectus femoris, adductor. - Articular (focus point in this topic) - Hip joint. - Pubic symphysis - SIJ - Spondylogenic - Neural - Obturator nerve related pain - Sciatic nerve related pain - Femoral nerve related pain - Other neural structures e.g. lateral femoral cutaneous **Common hip joint disorders** The paediatric hip joint. - Development hip dysplasia. - Transient synovitis - Femoral head osteonecrosis (Perthes) - Slipped capital/ upper femoral epiphysis. Hip joint disorders in the active adult (adolescence) MAIN FOCUS - FAIS - Hip joint strain and other soft tissue injuries (commonly labral) - PTOA - Early onset hip OA e.g. 2 degrees to hip dysplasia Hip joint disorders in the older adult. - Metabolically driven OA - Biomechanically driven OA (e.g. previous FAIS and/ or trauma) Need to consider past history of the patient's hip issues. Focusing on ages 10-45+ and focus is on the active adults. **Preventative care** - Early intervention and management strategies can help optimise health and function, delaying or preventing the need for expensive surgeries such as total hip replacements. - Physiotherapists play a crucial role in keeping patients independent, functional, and reducing the burden on healthcare systems. **Pathogenesis of hip osteoarthritis** **OA: metabolically driven or biomechanically driven?** - Metabolically driven OA (SCI) - Systemic chronic inflammation caused by poor lifestyle habits such as obesity and diabetes. - Affects multiple joints, particularly weight- bearing joints. - Biomechanically driven OA - Sports with large range of movement demands. - Certain sports like hockey and soccer can lead to premature hip OA, even without extreme range of motion. - FAIS as a risk factor for premature hip OA. **Systemic chronic inflammation** - Chronis and sustained elevation of key inflammatory makers e.g. C- reaction protein (CRP), TNF-a - Minor but SUSTAINED elevation of C- RP - Sub- clinical: classical signs of inflammation are not overtly evident. - Clinical consequences take time to be become evident (between months to years) Triggers of systemic chronic inflammation → Systemic chronic inflammation → Clinical consequences of SCI **Over time:** **Triggers of SCI → Systemic chronic inflammation → Chronic inflammation in local tissues (e.g. synovitis) → Clinical features of OA** [Inflammaging] - Age related increase in levels of pro- inflammatory markers in blood and tissues. - Systemic, chronic and (initially) asymptomatic. - Different types of stress can induce inflammaging to occur earlier and at an accelerated rate. **Physical activity paradox** - Recreational physical activity has a protective effect against chronic disease, while occupational physical activity does not offer the same benefits. - Occupational physical activity is associated with an increased risk of cardiovascular disease. - Low levels of leisure time and physical activity and higher occupational physical activity are associated with increased C-RP levels. **Metabolically/ biomechanically driven OA** Overweight or obese +/- other allostatic overload and lifestyle factors act as trigger/ catalysts for → SCI leading to → chondral- senescence → low grade inflammation → early and accelerated age-related tissue changes in muscle joint tissue (cub- chondral bone plane, synovium etc) → clinical symptoms and signs of OA. **Summary: pathogenesis of hip joint osteoarthritis** - Systemic chronic inflammation can trigger local tissue changes in the hip joint (particularly in synovium and sub- chondral bone plate). - Leads to development of age- related tissue changes, which manifest earlier in individuals exposed to chronic inflammatory triggers. - Obesity, stress, and lack of recreational physical activity can exacerbate the inflammaging process and increase risk of developing OA. Management: improve metabolic health to reduce chronic inflammation and prevent further joint deterioration. **Clinical examination of the hip joint** **Subjective clinical features (hip joint arthropathy e.g. OA)** - Primary complaint = loading, motion- and/or position related pain in the anterior hip or groin - Aggravating factors - Pain with axial loading/weight-bearing: standing, walking, running, steps. - Pain with movement: pain when moving the hip toward end range, particularly flexion. - Pain with sitting (prolonged or otherwise) e.g. low chairs if hip F ROM is limited. History of presenting complaint - Insidious onset, may be episodic and gradual progression. - Acute events of changes in loading may precede episodic symptoms. Past history - Ask about any past childhood hip issues (e.g., developmental dysplasia, FAIS) and history of trauma (e.g., sprains, fractures). - Consider post-traumatic OA, particularly if there\'s a history of FAIS. Age - Middle-aged (45- 50+) patients commonly present with hip OA. - However, younger, active populations may also develop hip joint issues, often related to FAIS or other biomechanical factors. **Patient reported outcomes for hip pain disorders.** - iHOT: useful for assessing the impact of hip problems on quality of life across four domains (symptoms, ADLs, sports/recreation, and emotional well-being). - WOMAC Index: used to measure disability and severity in hip and knee OA, with higher scores indicating mild to severe impact. **Secondary/ associated symptoms: Painful mechanical Sx and/or mechanical Sx that have recently developed alongside pain are of interest.** - Symptom location: hip joint pain can refer to multiple areas, including the lateral hip, groin, buttock, thigh, knee, or even the shin. - Mechanical symptoms: clicking, clunking, or locking of the hip joint may be reported, especially if new, changed, or associated with pain. - Loss of mobility: difficulty with activities such as crossing legs or putting on shoes may suggest hip joint involvement. - Joint stiffness/ pain after rest: especially morning or post- rest. The child or adolescent that presents with thigh, knee, or leg pain -- ALWAYS screen the hip. **Hip joint pain e.g. FAIS -- commonly functionality.** - When symptomatic, sitting is a common functional test. - Often overlooked. - Subjectively and objectively look for the "FAI/hip slouch". - Posterior pelvic tilt + hip ER/abduction - Use SMP's to assess relevance. Subjective Clue (C sign): patients describe deep anterior hip or groin pain by cupping the area between their thumb and fingers in a \"C\" shape. **Objective clinical features** Observation and function. - During function, hip may be held in open-pack position of the hip (especially where acutely symptomatic and/or advanced) - What is this? - Why would this be? Hip ROM -- will reflect the fact that OA is an articular disorder. - Roughly equal loss of AROM and PROM - ROM loss in a capsular pattern (if advanced): capsular pattern restriction (loss of flexion, abduction, and internal rotation) is typical in hip OA. - Altered end-feel. - Impingement signs at ERO - Early, subtle losses of ROM should be looked for and not ignored. Key diagnostic/provocation tests - Pain w/ hip joint impingement tests - FADDIR - FABE Resisted tests? - Likely to be negative (unless concurrent musculotendinous issue) Muscle length tests? - Of limited value - Why? Palpation? - Of limited value - Why? Early warning sign of incipient hip joint issues = loss of hip rotation (IR especially) **Hip objective tests: Femoro- acetabular impingement tests.** Clinical signs (P/E) - Dx of hip arthropathy (e.g., FAIS, hip OA) does not depend on any single clinical sign. - Uniplanar ROM and combined movement tests may provide key clues. - Combined movement/provocation/impingement tests? - FADDIR - FABER - Hip impingement tests must reproduce patient's familiar pain. - Impingement signs on testing are common in most hip. - Clinically we are looking for reproduction of "the" pain and/or symptoms and ROM signs that differ from the unaffected hip. **FADER test (Flexion, Adduction, Internal Rotation)** Checks for anterosuperior impingement, which may provoke pain. **FABER test (Flexion, Abduction, External Rotation)** Assesses for posterior hip impingement and may stretch the anterior hip. **Differential Diagnosis: Hip vs. Lumbar Spine** Signs pointing to the hip joint: - Groin pain/ anterior hip pain. - Loss of internal rotation in affected hip. - Walking with limp. Lumbar spine clearance: - Performing repeated lumbar extension and ipsilateral side flexion/rotation tests. - Repeated lumbar ROM, negative combined extension and rotation, negative slump test, negative thigh thrust. **Symptom Modification Procedures (SMPs):** Alter foot progression walking angle. - Provocative when internally rotated can suggest hip joint -- patient will dislike symptom provocation. - Provocative in externally rotated can suggest hip dysplasia, unstable hip -- patient will dislike symptom provocation. - Can also alter stride length and question the effect upon symptoms. - Changing the foot progression angle (e.g., increasing or decreasing hip internal or external rotation during walking) can help provoke or ease symptoms, indicating hip joint involvement. **Step-Back Lunge = \"Functional Thomas Test\"** Purpose: equivalent to the Functional Thomas test, the step-back lunge assesses dynamic hip extension and helps determine the source of motion limitations. - Assessment focus: observe from the side-on position to assess where the motion is being sourced. - Hip: Is hip extension coming from the trail leg hip? - Lumbo-pelvic region: Is the patient sourcing movement from the lumbar or pelvic region instead of the hip? - Forward trunk lean: Indicates that the trail leg lacks hip extension, and the patient compensates by flexing the front hip. - Key Observations: - Is the limitation in the hip? - Is the limitation in the lumbo-pelvic region? **Lumbar Active Range of Motion (AROM) Symptom Modification Procedures (SMPs)** Purpose: symptom modification procedures are used to differentiate between hip and lumbar spine as the source of symptoms. - For Symptoms with Lumbar Flexion AROM: - Add hip flexion (foot on step): - If symptoms increase or occur earlier, suggests the hip as the source. - If symptoms remain the same (ISQ - In Status Quo), suggests lumbar spine as the source. - Add hip internal rotation (IR) or external rotation (ER): - Modifying hip rotation may influence symptom onset and help determine the involvement of the hip joint. - For Symptoms with Lumbar Extension AROM: - Add hip flexion (foot on low step): - If symptoms ease or occur earlier, suggests the hip as the source. - If symptoms remain the same (ISQ), suggests lumbar spine involvement. - Add hip extension: Exploring hip extension during lumbar AROM helps clarify the relationship between lumbar and hip mobility and symptoms. **Role of hip imaging?** - Hip joint arthropathies (e.g., OA) are fundamentally a clinical diagnosis. - Augmented (confirmed) by imaging. - NOT the other way around. OA is very much a spectrum of pathology - both structurally AND functionally. Often a poor correlation between severity of imaging and function **Lateral hip pain** **Common sources of lateral hip pain** - Articular: hip joint arthropathy - Musculotendinous: GTPS/ GT (MAIN FOCUS) - Spondylogenic: somatic referred symptoms from lumbar spine - Bony: proximal femur BSI's - Neural: radicular pain **Greater trochanteric pain syndrome/Gluteal tendinopathy** - Key clinical sign: lateral hip (thigh) pain - Dominant pathology: tendinopathy of gluteal tendon, particularly gluteus medius. Anterior fibres of gluteal medius usually involved. - Trochanteric bursitis may be concurrent but rarely dominant. - Biochemically driven and/ or biomechanically driven? Need to answer this questions. Hip OA and gluteal tendinopathy commonly intersect -- common drivers and triggers. **Who develops GTPS/ GT?** **Athletic adult engaged in stretch shortening cycle activities (F \> M)** - Aggravating activities: running. - Loading profile: recent change in mechanical loading (+/- inadequate recovery) - Functional envelope: large, threshold for triggering symptoms if relatively high. Background levels of conditioning high. - Heightened sensitivity to load: inadequate recovery. - Load exceeds capacity. *[Envelope of Function Concept]* - Represents an individual's physical capacity to cope with daily activities or exercise. - Impact on Injury: - If activity exceeds the envelope of function, there is a higher risk of injury. - Physically active individuals: Usually have a higher envelope of function, but overloading can occur with sudden increases in intensity or frequency. - Sedentary or metabolically driven cases: These individuals have a much smaller envelope of function and can be sensitive to even minor increases in activity (e.g., walking or climbing stairs). **Metabolically driven.** - Heightened tendon sensitivity to load due to: - Decrease in female hormones leads to alteration in tendon mechanical properties (peri- or post-menopausal woman who has recently experienced some unaccustomed loading). - +/- other co- morbidities - Loading profile: recent unaccustomed loading - Load exceeds capacity where functional envelope is small, threshold for triggering symptoms Is low. Background levels of conditioning very low. - Sites: often multi-site (gluteal tendon, Achilles tendon, plantar fascia etc. **Biomechanical drivers of gluteal tendinopathy** - Impaired adductor mechanism/ lateral hip weakness - Can lead to compressive loading of the hip adductors. - Both causative and symptomatic. - Cumulative repetitive loading of the gluteus medius during running or walking. - Especially where frontal plan hip control is sub- optimal = mechanical + compression loading. - Older (40- 60) and usually sedentary women - Mechanically driven younger/ active cases (weakness) - Acute trauma e.g. fall onto lateral hip region can also be a trigger. Poor frontal and transverse plan motor control -- both as a causative source of pain and consequence - Poor control of the frontal plane (side-to-side movement) can lead to excessive load on the lateral hip and compress the gluteal tendons. - Dynamic valgus (inward collapse of the hip) during single-leg stance increases this load -- compression within tendon and loading at length. Compensation due to abductor weakness or pain, leading to altered gait mechanics → frontal plane control is suboptimal. **Key clinical features of gluteal tendinopathy** Tenderness on palpation over the greater trochanter, especially at the proximal attachment of the gluteus medius. Reproduction of pain during muscle contraction, especially under load or at length. [Subjective] - Age: - Metabolically driven: 40-60 - Biomechanically driven: active adult (any age) - Gender: female \> male - Pain experience: lateral hip pain (warm up effect possible) - History: variable - Recent increase/ change in loading - Local trauma (direct impact from a fall) - Aggravating activities: single-limb WB activities - Younger, active - Stair climbing, running, walking. - Sedentary - Walking - Hip posture/position -- compression. - Crossing legs, sleeping on affected side, hip "hang" - If tissues very sensitized Hip hang: A postural compensation where the pelvis drops during stance, increasing strain on the gluteal tendons (can drive and/ or add to tendon sensitisation). Sitting postures: Crossed leg sitting or other positions that increase tendon compression. Place the hip in adduction and may increase compression over the bony 'cam' of the GTr. Both create the lengthening and loading at length (internal compression within tendon) thus important to talk with patient to manage these in the short term. **Screening and patient reported outcomes.** VISA-G (Victorian Institute of Sport Assessment - Gluteal) - Purpose: assesses disability and functional impairment due to gluteal tendinopathy. measures quality of life, pain, and function. - Scoring: total score out of 100. 100 = No disability, 0 = Maximum disability. **Physical Assessment for Gluteal Tendinopathy** - Palpation: Tenderness on palpation over the greater trochanter. - Resisted Abduction Tests: Testing the strength and pain response of the abductors, particularly in positions of lengthened tendons. - Trendelenburg Test: Positive if pain or pelvic drop occurs during single-leg stance test. - Hip Lag Sign: Indicates abductor dysfunction if the leg drops by more than 10 cm in an isometric hold. - Resisted FADER/FABER Tests: Assess for pain and impingement in the lateral hip.  **Lateral Hip Pain vs. Other Conditions:** - Hip Joint OA: Difficulty with activities like taking off shoes and socks, tender greater trochanter, positive FABER test. - Lumbar Spine or Radicular Pain: Differentiate using lumbar spine assessments. - Other Causes: Potential hip joint or lumbar spine involvement should be ruled out. **Activity-related hip and groin pain rehabilitation -- key objectives** 1. "Calm the farm" (if pain-dominant): Modify load and reduce aggravating activities (caveats around de-loading) 2. Address specific impairments of function and build capacity: Individualised rehabilitation. Generalised capacity building (S&C + aerobic capacity) 3. Build/re-build generalised load tolerance: Address linear running mechanics. Build sub-maximal running capacity. 4. Re-build sports-specific load tolerance: Multi-directional running and sprinting drills. **Pathogenesis of FAIS** **Femoro- acetabular impingement syndrome** **Definition:** Motion-related disorder of the hip joint involving premature and symptomatic contact between the acetabulum and proximal femur. [Hip joint disorders in the active adults.] - FAIS, soft tissue injuries and chondral and osteochondral lesions commonly co- exist → e.g. FAIS as a catalyst for hip joint soft tissue and/ or articular surface injury. **Causes**: Alterations in proximal femur morphology, leading to premature end-range contact. - Common in athletes due to high range of movement demands. - Primary Cam Deformity (PCD): Convexity of femoral head-neck junction instead of normal concave shape (additional bony growth leads to an earlier than scheduled contact between acetabulum and proximal femur) - Radiological Feature: Pistol grip deformity visible on x-ray. Having a cam deformity does not guarantee problems within the hip joint. [Mechanism of PCD development] - Repetitive bone opposition at the antero- superior aspect of the head- neck junction. ++ bending forces at this site. - Sports activity alters the shape of the growth plate. **Mechanism:** Growth plate exposed to bending and torsional forces, especially in sports involving running, jumping, twisting. Growth plate bends → bone starts to get laid down at right angles to that shear force → bulge/ pistol grip shape (convex) **When does it develop:** PCD requires an open growth plate to develop → therefore developing during adolescent period before skeletally mature. **Risk factors.** - Higher training frequency when your skeleton is still growing: a critical period is before skeletal maturity, where the growth plates are still open and vulnerable to stress. - Regular participation in sports with high training loads (e.g., running, jumping, twisting) during adolescence increases risk. - Training \>4 times per week by age 12 significantly increases the risk of developing cam deformities. - Younger the starting age the greater the risk of developing PCD. **Screening questions** - Childhood and adolescent training/ loading history - Especially 8-15 yrs. - Types of sports - Training frequency/ week - Session duration - Any hip issues in childhood **Clinical features of FAIS -- similar to OA (more subtle than OA)** **Symptoms** - Primary symptom of FAIS is motion and/ or position related pain in the hip or the groin (pain may also be felt in the buttock, back or thigh) - Mechanical symptoms such as clicking, catching, locking and/ or stiffness, restricted range of motion or giving way. (Painful click that has recently developed). - Aggravating factors - Activities that require repeated, loaded, and large ranges of hip flexion and/ or internal rotation and/ or adduction - Combined running- kicking sports. - Running in deep flexion e.g. hockey, AFL, rugby - Deep squat/ lunge patterns - Sitting especially in low chairs **Signs** - Does not depend on any single clinical sign. - Hip impingement tests usually reproduce patient's typical pain (FADDIR, FABER) - Limited range in hip motion, typically restricted IR in flexion - Reduced total hip rotation (\ - Use video analysis to assess how athletes move during high demand tasks. **Management of hip joint and gluteal tendinopathy disorders** **Management for hip osteoarthritis** **Two key principles** 1. Initial assessment should use a biopsychosocial approach and consider physical and psychological status, ADL's, participation (including work), social determinants and environmental factors. 2. Care of people with hip or knee OA should be based on shared decision-making considering the needs, preferences, circumstances, and capabilities of the individual. [8 best practice guidelines] - Individualised, multicomponent management plan - Information, education, and self- management - Exercise with adequate tailoring of dosage and progression. - Mode of exercise delivery should be selected according to local availability and patient preferences. - Maintenance of healthy weight and weight loss - Offer adjuncts where indicated (footwear, gait aids and assistive devices) - Work- related advice. - Behaviour changes techniques to improve lifestyle. **Hip OA and proximal hip tendon problems commonly intersect.** **Key objectives of clinical examination** - Diagnostic clarity achieved: identified what is hurting and where in the body. Features of concern identified. - Primary drivers identified: identified why it is hurting (sign posts for management). Short term management to calm things down, reduce symptoms and pain → then use rehab program to build and re- build confidence. - KPI based programs, not time based. - Give patient autonomy to be in charge of her program. - Behaviour change - Goals that have included shared decision making. [When is the patient ready for rehabilitation?] - No longer pain dominant. - Initially activity modifications successfully implemented: symptom monitoring model. - Collaborative KPI based management plan established and explained. - Training history mapped: gym and strength and conditioning experiences especially (entry point for rehab) [Pain dominant] - Symptoms are in the red zone. - Irritability is high. - Significant levels of disability - Morning stiffness → patient not ready to begin rehab program, pain needs to subside first. **Both neuromuscular exercises and progressive resistance training both equally effective.** **Management and patient care in gluteal tendon cases** Compelling evidence that exercise should be the first line of treatment, alongside load management in the short term. Calm the farm in GT = load management + limiting aggravating activities and postures - Modify aggravating factors that put tension on the tendon → simple but powerful changes. [Positions that can be managed] - Positions that place the hip in adduction and may increase compression over the bony cam deformity of the greater trochanter. - Common positions that can be adding that kind of stretching and loading at length → creating compression by wrapping the tendon insertion around the greater trochanter → sensitising the tendon when it is already sore. **Broad overview of gluteal tendinopathy management plan (3-6 months prognosis)** 1. Diagnostic clarity - Differential diagnosis: spondyloarthropathies, hormonal, metabolic, rupture, tears etc. - Screening for background medical conditions and contributors. 2. Primary management - Education and advice. - Load management and graded return to aggravating activities. - Rehab: address local muscle issues (e.g. glute medius) and kinetic chain (neuromuscular) - Multidisciplinary care: exercise physiology, dietetics (weight management), psychology. 3. Adjunct therapies - Manual therapy and soft tissue work - SWT: shock wave therapy. - Orthoses - Avoid corticosteroids. 4. Recovery - Return to sport. - Return to play. - Return to work. - Monitor progress via VISA- G + functional measures. **Broad overview of osteoarthritis management plan (3-6 months prognosis)** 1. Diagnostic clarity - Differential diagnosis: spondyloarthropathies, metabolic factors - Screening for background medical conditions and contributors. 2. Primary management - Education and advice. - Load management and graded return to aggravating activities. - Rehab: address local muscle issues (e.g. glute medius) and kinetic chain (neuromuscular) - Multidisciplinary care: exercise physiology, dietetics (weight management), psychology. 3. Adjunct therapies - Manual therapy (improve mobility of hip joint) - Taping - Orthoses - Avoid corticosteroids. 4. Recovery - Return to sport. - Return to play. - Return to work. - Monitor progress via WOMAC, iHOT and functional measures. [Overall] - Educate and load management of aggravating activities in the short term. - Load management: graded, KPI based return to full activity. - Load management includes positioning and postures to limit/ avoid in the short term. - In an athlete, prevent detraining. - Address biomechanical deficits: frontal and transverse plan hip especially. - Address capacity deficits: local and whole kinetic chain (hip abductors and external rotators especially) - Address extrinsic training load errors. - Monitor progress via PRO's and FOM's - Referral may be required e.g. sport and exercise physiotherapist. Strengthening and tendon loading programs - Exercise selections. - Entry point parameters - Programming and progression 1. Describe the anatomy of the spinal motion segment and how these changes as part of the normal aging process versus the pathology and clinical features of serious or specific conditions.  2. Demonstrate assessment of a person with spinal pain and related limb symptoms, to clinically diagnose serious or specific spinal pathologies.  3. Demonstrate knowledge of indications for investigations and onwards referral for suspected serious or specific spinal pathology  4. Synthesise current evidence with assessment findings to plan high value person centred care in people with specific spinal disorders.  5. Demonstrate the implementation of high value person centred care for people with specific spinal pathology and understand the potential need for co-care with other health professionals.  **Anatomy and pathology of the lumbar region** **Radiculopathy -** Neurological condition caused by compression or irritation of spinal nerve roots. - Symptoms: - Motor deficits and sensory deficits - Pain - May include changes in gait or posture due to muscle weakness. **Radicular pain -** Pain radiating along the path of a specific spinal nerve root due to inflammation or irritation. - Symptoms: - Pain: Sharp, shooting, or burning pain following a dermatomal pattern. - May have accompanying tingling or numbness but without significant motor or sensory deficits. **Intervertebral discs** - ***Function of disc* --** allow movement in the lumbar spine, binding two vertebrae together and absorbing compression forces. [Disc Composition] - Annulus Fibrosis: The outer structure of the disc. - Nucleus Pulposus: The inner, gel-like core of the disc. - Disc sits relatively low to the intervertebral foramen (intervertebral foramen -- whole between vertebra through which spinal nerves comes out) Intervertebral foramen: Within IVF sits the spinal nerve and the dorsal root ganglion. At this point, as the nerve passes through the IVF it is a mixed nerve (both sensory and motor). **Age related changes** - Age related changes occur in the lumbar spine very early (second decade onwards) - → therefore, age related changes are a much more appropriate term to describe changes compared to degeneration. - By age 50, prevalence of disc aging is very high. **Classification of annular tears/ fissures** Can get tears within annular fibrosis (different types - peripheral, circumferential, radiating/ radial) **Disc herniation.**  - Broad-based disc bulge: the disc bulges in a broader direction, changing its shape. - Disc protrusion: a more obvious bulge in one particular direction, with a broader base than the distal end of the protrusion. - Disc extrusion: the nucleus pulposus pushes further outward through the annulus. - Disc sequestration: a portion of the disc becomes detached from the main body of the disc. [Location of disc herniation is important and is broken down into different zones:] - Posterolateral are more common. - Foraminal disc herniations reduce size of foramen as well. - Extra- foraminal much wider but less common. **Increased loading posteriorly in the presence of disc aging leads to facet joint arthropathy** With changes in the disc over time → knock on effect on the spines ability to influence compressive forces passing through it with a relative shift of the compressive forces to the posterior elements of the spine (facet joints) → facet joint arthropathy. [Left side of diagram] - Patent IVF where nerve root is not being compressed by nerve root or the disc. [Right side of diagram] - Degenerative changes in both the facet joint and within the disc. - IVF has a reduced lumen and thus compressive forces to be placed upon the spinal nerve as it passes through the IVF. **Dermatomes** - A unilateral area of skin supplied by a single spinal nerve. Impact of compression of a nerve as it passes through the IVF can lead to potential pain and/ or motor and sensory changes. - Pain and motor/ sensory changes will relate to the dermatome of the spinal nerve. **Myotomes** - A myotome is a unilateral mass of muscles supplied by a single spinal nerve. Important to consider motor changes that are potential through compression of the spinal nerve in the IVF → lead to myotome weakness. **Nerve pathways** -- consider these in relation to neural tissue provocation testing. Sciatic Nerve - Arises from the L4 to S3 spinal nerves. - Passes through the greater sciatic foramen, near the piriformis muscle, and then splits into the common peroneal (fibular) and tibial nerves about two-thirds down the thigh. - Tibial Nerve: Passes through the tarsal tunnel, behind the medial malleolus, and splits into the medial and lateral plantar nerves. - Common Peroneal Nerve: Passes around the fibular neck and splits into the deep and superficial peroneal nerves. Femoral Nerve - L2 to L4 spinal nerves. - Passes under the inguinal ligament alongside the vein and artery, then branches into the saphenous nerve, which runs down to the ankle. **Palpation of lower limb pulses** - Dorsalis Pedis Pulse: Located between the extensor hallucis and extensor digitorum longus muscles. - Posterior Tibial Pulse: Found posterior to the medial malleolus. **Low back related leg pain** **Three different presentations:** - Radiculopathy - Radicular pain - Central lumbar spinal stenosis **Radiculopathy:** lesion or disease of a **nerve root** or dorsal root ganglia. Associated with a conduction slowing or blocking of that spinal nerve root (mixed -- both sensory and motor). - Motor, reflex, and sensory reduction/ loss. - More common in lumbar spine and cervical spine. - Most often caused by compression of the spinal nerve as it passes through the IVF (facet joint degenerative changes and disc related changes). **Radicular (nerve root) pain:** pain associated with inflammation, ischemia, or mechanical deformation of dorsal roots or dorsal root ganglia. - Pain that stems from a particular nerve root - Pathology - inflammatory/ ischemic, may not have a neuropathic component to it. - Relates to a dermatomal presentation and the presence of neuropathic pain descriptions (burning, numbness). - Can be with or without radiculopathy - grey area (can just have pain without sensory/ motor deficits. *Don't use neuropathic pain descriptors → most likely to be radicular pain.* - Inflammatory process adjacent to that nerve - may well still have a dermatomal distribution. *Compression of nerve root -* reduce space of the IVF (lumbar movements - extension and ipsilateral side flexion) *Stretch/ lengthening of nerve feeding into nerve root* - movements that elongate the course of the sciatic nerve (movements - forward bending with straight legs, slump test - straight knee and flexed hip +/- dorsiflexion of the ankle) **Central lumbar spinal stenosis:** a condition in which there is diminished space available for the neural and vascular elements in the lumbar spine secondary to degenerative changes in the spinal canal. - Involves the space that the spinal cord and the cauda equina sit within *→* reduced space for the nerve and vascular elements around that region because of pathological changes such as broad-based disc bulges, facet hypertrophy due to degenerative changes, thickened ligamentum flavum etc. - Space within the region is dynamic. - More compressed in erect postures (standing and walking) - Less compressed in flexed postures *Signs and symptoms* - Neurogenic claudication - Bilateral leg symptoms - Develops slowly. - Leg pain with walking/ standing that is eased by flexion or sitting. - Tends to happen in older age group - degenerative changes. **Cauda equina syndrome** - Vital for early diagnosis → within first 24 hours - Usually due to a large disc bulge, could be due to a tumour in the region. - Effects may be permanent if the compressive material is not removed quickly. Alerting features - Early: - Bilateral alternating radiculopathy +/- leg pain. - Subjective sphincteric problems - Perineal/ saddle sensory change - Established: - Altered bladder and bowel function (urinary retention, faecal incontinence). - Reduced sensation in the saddle region. - Progressive bilateral foot or leg weakness. - Erectile dysfunction.  **Patient interview** - Dermatomal distributions - Neuropathic sensations - Cauda equina signs and symptoms **Physical examination → similar to low back assessment** - Observation - Function tests - Active movements/ repeated movements - Myotomes/ dermatomes/ reflexes - Upper motor neuron tests - Neural tissue provocation tests - Lumbar pain provocation - Perianal sensation → looking at repeated movements, myotomes/ dermatomes, reflexed, UPN tests, neural tissue provocation tests in particular. Repeated movements - *Presentation of pain along entirety of right leg:* Pain gradually becomes more proximal and distal pain starts to disappear → centralisation in action (positive phenomenon) - Presentation of just low back pain and repeated movements lead to pain working its way down the leg → peripheralization in action (negative phenomenon) **Management of radicular pain:** - Potential referral for medication, injections, surgery. **Precautions: radiculopathy** - Rapidly worsening neurological signs and symptoms (especially motor) - Suggests progressive pathology. - Requires medical review and imaging -- urgent GP review. - May require other management e.g. surgery. - Significant neurological deficit e.g. significant weakness like drop foot. - Requires medical review and imaging -- urgent GP review. - Surgery may improve outcomes if addressed early i.e. return of motor function. - Bilateral signs and symptoms and multi- level involvement - Unlikely to be pathology favourably influenced by physio. - Watch for developing CES and safety net the patient. - Requires medical review and imaging -- urgent GP review. - May require other management e.g. surgery. **Is it neuropathic pain?** - Neuropathic pain is caused by a lesion or disease of the somatosensory nervous system. - Knowing whether or not a person has neuropathic pain is essential to guide management strategies. **Neuropathic pain grading system** - Set of 4 criteria - unlikely, possible, probable, or definite neuropathic pain *Criteria 1* - Medical history with a clinical presentation that suggests a relevant neurological lesion or disease. - Temporal developments e.g. diabetic neuropathy (diagnosis of diabetes → tingling, numbness in the feet) - Mechanism of injury may be reported that is indicative of a nerve lesion. - Symptom descriptors that are suggestive of neuropathic pain such as electric shock, shooting, burning, numbness, tingling (presence of several descriptors increases likelihood of neuropathic pain) - Presence of spontaneous pain is indicative of neuropathic pain. - Aggravating (movement that compress the spinal foramen) and alleviating factors (postures that open the foramen) *Criteria 2* - Whether the pain is neuroanatomically plausible - Painful radiculopathies - pain should be dermatomal. Both criteria 1 and 2 are gained from the clinical interview - gain a detailed understanding of patient's symptoms *Criteria 3* - Whether the pain is associated with sensory signs in the same distribution → proved through sensory examination (touch, vibration, prick, thermal sensation) - Myotomal/ reflex deficits (motor signs) - Loss of motor function may increase suspicion of nerve lesion. *Criteria 4* - Requires an objective diagnostic test to confirm → sensory nerve conduction studies, spinal imaging etc. **Other serious/ specific spinal pathologies** **Acute LBP clinical care standard** - Clinical exam - Screen and address psychosocial factors. - Imaging only when indicated. - Provide patient education and advice. - Encourage self-management and physical activity. - Provide physical and/ or psychological care. - Judicious use of pain medicines. - Review and referral. **What are red flags related to MSK disorders?** - Red flags are signs or symptoms that raise the suspicion of serious pathology. - If suspicion is high, usually require medical review. - Red flags are common in non- specific spinal pain. - They don't always mean there is a serious pathology. - An accumulation of red flags increases the likelihood of serious pathology. - Clear and open communication and shared decision making is vital. **Screening for serious and specific pathology** - Neurological → sensory loss (numbness, pins and needles, tingling), reflex change, weakness - Infection → signs the person is unwell - fever, temperature, fatigue. - Fracture → trauma (mechanical injury), age, osteoporosis. - Tumour/ cancer → history of cancer, old age - Inflammatory → has this person got morning pain and stiffness eased by movement - is this a dominant spondylarthritis (longer than 30 minutes - red flag), do anti- inflammatory help? - Visceral → heart/ lung giving chest pain. - Vascular → such as cervical arterial dissection, (5 D's, 3 N's) Common alerting features - Trauma - Age older than 65. - Non- mechanical pain - Pain that wakes you at night - Unrelenting severe pain not eased by positional change or rest. - Worsening/ progressive pain or other symptoms. - Cluster of findings that just generally don't fit or add up. **Fracture** Alerting features - Age older than 65. - Osteoporosis - High energy mechanism - High traumatic vs low energy trauma in weakened/ osteoporotic bone. - Severe pain - History of cancer - Corticosteroid use - related to pathological cause of the fracture. - Prior history of fracture - History of falls - No relieving position. - Between T10- L2 most common. **Infection:** discitis and osteomyelitis Alerting features - Fever - General malaise/ feeling unwell. - Pain that is non- mechanical - Unrelenting pain - High pain at rest - History of IVD, penetrating wound or recent surgery - Immunosuppression **Cancer** Alerting features - General malaise/ feeling unwell. - Pain that is non- mechanical. - Recent unexplained weight loss. - High pain at rest. - Night pain. - Prior history of prostate, breast, lung, thyroid, kidney (around 60% will metastasise in the spine) - Approx. 70% thoracic, 20% lumbar, 10% cervical. - Age over 50. **Visceral** - Kidney stones - Urinary tract infection - Reproductive/ pelvic pain e.g. endometriosis, ovarian cyst Alerting features - Unrelenting - Not changed by positions - Conditions related to the kidney, urinary tract and reproductive system are most likely to provoke pain in lumbar region. - Other viscera also give symptoms in the thoracic and cervical spine regions - worth noting. **Vascular** - Abdominal aortic aneurysm. Alerting features - Pulsatile feeling in abdomen. - Risk factors: smoking, high blood pressure and high cholesterol. - Age older than 65. - Family history. **Safety netting --** important When we have a person with low back pain presenting with symptoms → consider possibility of serious and specific spinal causes - Based upon clinical findings including interview and physical assessment - determine level of concern as to whether there are red flags. - As the level of concern increases → need to determine if onwards referral is appropriate (imaging, blood tests) - High level of concern → emergency referral (e.g. fracture) **Onwards referral:** After assessment of patient with low back pain consider if physiotherapy is indicated and if not, the requirement of medical attention and its urgency. - If not improving over 2-4 weeks or 2-4 sessions (by patient report or outcome measure). - Important to have appropriate outcome measures in place and a baseline assessment to compare to. - Refer onwards: intra- disciplinary, extra- disciplinary, co- management or medical referral.  **Cervical anatomy and pathology** Focus on the mid to the lower cervical spine → where most radiculopathy and radicular pain occurs. **Uncovertebral Joints** Unique Aspect of Cervical Spine: - The uncovertebral joints, which are absent in other regions of the spine, are formed by the uncinate processes. - They play a crucial role in cervical mobility and function. Key Features: - Located on the left and right side of each vertebra from C2/3 downwards. - Influence nerve roots, making them important for radicular pain and radiculopathy. Anatomical Relations: - Uncovertebral joints sit relatively anterior to the nerve root and lateral to the disc. - X-rays show these joints near the lateral aspects of each disc. - In cross-sectional images of the cervical spine, the joint is seen near the nerve root**.** **Disc Fissuring in the Cervical Spine** Cervical vs. Lumbar Discs: - Cervical disc fissuring spreads horizontally from the uncovertebral joint across the disc. - Fissuring begins as early as the late twenties or around the age of 30 and is considered a normal part of aging. **Zygapophysial joint form the articular pillar which you can palpate.** - This is where each of the superior and inferior articular facets contact each other. - Note angulation of different facet joints (point towards the eye) → upper part of cervical spine more horizontal and as we go down towards the thoracic spine the angulation increases. **Neural and vascular structures** - Disc and vertebral body are relatively anterior to the intervertebral foramen. - Uncinate processes which form the uncovertebral joints are also part of this complex. - Posterior is the zygapophysial joints. - The vertebral artery runs through the transverse foramen. - The transverse processes in the cervical spine sit anterior to the nerve root as it passes through the intervertebral foramen. There are eight cervical nerve roots: - C1 - occiput and C1 vertebra - C2 - between C1 and C2 - C8 nerve root - C7 and T1 **Radiographic views** X-ray Interpretation: - Lateral X-rays show vertebral bodies and disc spaces but are less clear for intervertebral foramina. - Oblique X-rays are useful for assessing the size of the intervertebral foramen and potential nerve compression. **Age-related changes and degeneration** Degenerative Changes: - Age-related changes in the cervical spine lead to increased loading on the facet and uncovertebral joints. - Degenerative changes may lead to encroachment on the intervertebral foramen, often due to a disc-osteophyte complex rather than soft disc protrusion, as seen in the lumbar spine. Stenosis: - Degenerative changes, particularly in the lower cervical spine, may cause spinal stenosis due to the disc-osteophyte complex and hypertrophy of the joints. - Most common at C5/6, 6/7 Disc-Osteophyte Complex: - The cervical spine, particularly with age-related changes, may develop a disc-osteophyte complex, which is harder and can encroach upon the intervertebral foramen from both anterior and posterior aspects. - Stenosis can result from these factors, affecting neural structures. Overall: Age related changes in the cervical spine lead to a loss of disc height - Relates to the fissuring and make up of cervical spine. - Leads to greater loading on the zygapophysial and uncovertebral joints because of the weight. - Eventually leads to degenerative changes in these joints too. - With greater age-related changes, you start to see the same thing in the lumbar spine (encroachment on the IVF) → disc osteophyte complex. Compression of a spinal nerve → mixed motor and sensory changes which will relate to myotomes and dermatomes. **Key cervical myotomes:** - C1-C2: Neck flexion/extension. - C3: Lateral neck flexion. - C4: Shoulder elevation. - C5: Shoulder abduction. - C6: Wrist extension and elbow flexion. - C7: Elbow extension. - C8: Finger flexion (extensor pollicis longus). - T1: Finger abduction. **Brachial Plexus and Nerve Testing** Brachial Plexus: - Median nerve originates from C5-T1. - Median nerve pathway: From the brachial plexus to the cubital fossa, through the pronator teres, and into the wrist under the flexor retinaculum within the carpal tunnel. Clinical Testing: - Focus on neural tissue provocation tests, with emphasis on the median nerve\'s function and provocation for clinical assessment. **Cervical myelopathy** Myelopathy definition: any functional disturbance or pathological change in the spinal cord (SC). **Age-related Changes:** - Common degenerative changes include: - Disc-osteophyte complexes: Formed from the disc and uncovertebral joints, located anterior to the spinal canal. - Facet joint hypertrophy: Along with soft tissue changes such as ligamentum flavum thickening, which impacts the spinal canal from the posterior. - These changes reduce the cross-section of the spinal canal, potentially leading to compression of the spinal cord. **Cervical myelopathy** - Develops in only a fraction of people in late- stage spondylosis. Mechanical spinal cord compression does not always cause myelopathy -- spinal cord adapts well to slow compression (similar story with nerve roots). - Cord compression, even in absence of symptoms requires review with a spinal surgeon. **Clinical features** - Neck pain - Weakness UL/ LL - Age \ 50 - Bilateral/ quadrilateral pain/ paraesthesia/ numbness -- non -- dermatomal - Hyperreflexia - Clumsiness in the hands - Gait disturbance. - Balance issues *Verbal cues:* - Do you have any pins and needles, tingling, numbness or strange sensations in your hands or feet? - Have you noticed any weakness or clumsiness in your hands? - Have you had any difficulty with tasks such as doing up bottoms? - Have you noticed any change in your walking such as feeling unsteady, unbalanced, or uncoordinated? **Objective clinical features** - Gait disturbance -- ataxic, spastic, wide- based, unsteady. - Balance and/ or coordination deficits. - Non- dermatomal sensory loss (upper limb and/ or lower limb and/ or torso) - Non- myotomal upper limb and/ or lower limb weakness - Hyper- reflexia (upper limb and/ or lower limb - Increased lower limb muscle tone/ spasticity. - Clonus - Positive Babinski - Hoffman's sign positive - Inverted supinator sign/ test -- tap over distal brachioradialis tendon with reflex hammer (positive = finger flexion). *Screening for CSM using a cluster of clinical tests.* - 5 tests: Babinski's, Hoffmans, inverted supinator sign, gait abnormality, age \> 45 years. - 3 or more out of the 5 tests positive = fairly confident patient does have myelopathy **Management** - Presence of clinical signs and/ or symptoms suggestive of cervical myelopathy requires medical review (and investigation/ imaging) - Refer to GP -- physiotherapy not indicated. - Only requires emergency referral if traumatic/ acute onset e.g. after a fall or head injury. **Care -- specific spinal disorders.** **Cervical radiculopathy** Manual Therapy: Short-term evidence shows that manual therapy can reduce pain and disability in people with cervical radiculopathy. No specific dose or technique is superior. Cervical Traction: Some evidence suggests that cervical traction procedures can reduce pain and improve function in the immediate term. Exercise: Exercise can decrease pain and disability, but again, no dose or technique is superior. Surgery vs. Physiotherapy: Surgery provides short-term improvements in pain compared to physiotherapy, but at the one-year mark, there is no significant difference between the two treatments. **Lumbar radiculopathy** Clinical practice guideline recommendations: - Stay Active: Advice to remain active is supported by evidence. - Manual Therapy and Exercise: Both are weakly recommended for lumbar radiculopathy. - Directional exercises focused on centralization and peripheralization may be superior to motor control exercises. Injection therapy: Not recommended for lumbar radiculopathy. Surgical intervention: Surgery offers better short-term improvements in pain and disability compared to non-surgical treatment, but at one year, the outcomes between surgery and conservative management are similar. **Cervical myelopathy** Mild, Moderate, and Severe Myelopathy: - *Mild Myelopathy:* No significant difference between surgery and conservative treatment after three years. - *Moderate to Severe Myelopathy:* Surgery offers superior outcomes in cases with more severe functional deficits (e.g., motor, sensory, bladder, and bowel dysfunction). Risk Factors: - There is insufficient evidence to suggest that specific activities or minor trauma are risk factors for developing neurological conditions in people with asymptomatic cord compression. **Neurogenic Claudication (Secondary to Spinal Stenosis)** Multimodal Care: - Education: Lifestyle changes, advice. - Exercise: Manual therapy, supported by moderate-quality evidence for symptom improvement. - Specific Antidepressants: May be considered. - Epidural Steroid Injections: Not recommended based on high-quality evidence. Exercise Recommendations: - Weight-supported walking, aquatic exercises, and cycling are particularly helpful for neurogenic claudication. Surgical Decompression: - The Danish Clinical Practice Guidelines recommend surgical decompression as the first line of treatment for lumbar spinal stenosis. - They suggest that supervised exercise may not alleviate neurogenic pain but is beneficial for general health. - Manual therapy and neurogenic pain medication are not recommended due to a lack of beneficial evidence. 1. Describe the biological and psychosocial contributors to complex, non-specific spinal pain. 2. Demonstrate assessment of biological and psychosocial contributors to complex non-specific spinal pain. 3. Use a clinical reasoning structure to reflect on assessment findings to provide a diagnosis and key contributing factors complex non-specific spinal pain. 4. Synthesise current evidence with assessment findings to plan high value person centred care in people with complex non-specific spinal pain. 5. Demonstrate the implementation of high value person centred care for people with complex non-specific spinal pain. **Whiplash associated disorders.** When compared to other conditions, individuals with whiplash have more pain, more painful locations, and higher pain intensity than individuals with chronic pain from other causes. **Guidance for management:** - Australian clinical guidelines for health professionals managing people with whiplash associated disorders, 4^th^ edition. - Mywhiplash navigator -- use on placement. - WhipPredict: assessment questionnaire. **Whiplash** - **Definition:** whiplash is an acceleration- deceleration mechanism of energy transfer to the neck. It may result from motor vehicle crashes, the impact may result in bony or soft tissue injuries (whiplash injury), which may in turn lead to a variety of clinical manifestations. **Quebec task force classification of grades of WAD -- need to know.** - Grade 0: no complaint about the neck. No physical signs. - Grade 1: complaint of neck pain, stiffness, or tenderness only. No physical signs. - Grade 2: neck complaint and musculoskeletal signs. Musculoskeletal signs include decreased range of movement and point tenderness. - Grade 3: neck complaint and neurological signs. Neurological signs include decreased or absent tendon reflexes, weakness, and sensory deficits. - Grade 4: neck complaint and fracture or dislocations. *Triage system → looking for red flags/ serious signs.* - Fracture, dislocation. - Radiculopathy - screen for this (grade 3) - Non- specific neck/ back pain (whiplash grade 2) **Day 1 assessment and management** **History:** - Initial disability: a baseline measure (Neck disability index - most common outcome measure) - Other symptoms: dizziness, headache, screening for serious pathologies (cervical arterial dysfunction - screening for these factors) - History of pre- crash health - Factors that would enable you to make a diagnosis for a whiplash grade → looking for serious pathology (fracture) **Physical examination:** - Assess factors to establish diagnosis (WAD grade). - Neurological assessment (WAD 3) - Cervical range of motion (ROM) and palpation (WAD 1-3). **Management** *WAD 1- 3* - Provide guidance-based care (recommended treatments: advice, exercise, medications). - For high pain consider additional neutral treatment recommendation (intermittent immobilisation). - For neuropathic pain, consider additional neutral treatment recommendation (pregabalin or pain medication). *WAD 4* - Manage according to cervical fracture guidelines. **Canadian C- spine rule -- must know.** - To screen for cervical fracture (whiplash grade 4) - Keep a copy easily accessible so can refer to. **Reassessment at day 7** **History** - Need to see if they are progressing or settling or if they are getting worse. - Looking at pain and disability → high pain and high neck disability start to indicate medium to high risk. - Risk assessment predictor like the whip predict or the OREBRO. - Patient's expectations of their recovery → where do you see yourself in a couple months' time? **Physical examination** - Reassess neurological exam. - Palpation and ROM - Reassess a need for immobilisation if prescribed for high pain. **Management** - Low risk: continue treatment, provide low risk advice about their recovery. - Medium/ high risk: continue recommended treatments. Provide medium/ high risk advice regarding recovery and consider referral for physical therapy. - Grade 3 and not recovering -- refer for advanced imaging (MRI). Manage according to cervical radiculopathy recommendations. **Prognostic Risk Factors:** - Strong recommendations: high initial pain, disability, number of painful areas, recovery expectations, and post-traumatic stress symptoms. - Psychological factors: mood, coping strategies, and pain catastrophizing are moderate risk indicators. - Physical assessments: cervical range of motion, pain sensitivity (e.g., cold hyperalgesia). - Non-predictive factors: socio-demographic factors, crash details (e.g., head position during impact), healthcare utilization, and routine imaging (unless clinically indicated). **Week 6** **History:** - Reassess pain (VAS). - Reassess neck disability (NDI). **Physical Examination:** - Reassess ROM and palpation. - For WAD III: Reassess neurological function. **Management** Low Risk: - If recovered: Discontinue treatment. - If recovering: Wean off recommended treatments for self-management by 12 weeks. On average, 3 sessions are required. Medium/High Risk: - *History:* Reassess PTSS (Post-Traumatic Stress Symptoms) and other psychological factors - *Additional physical Examination:* as in Week 3. - *If recovering:* continue treatment as in Week 3. - *If not recovering:* - Refer to psychologist if PTSS is above the threshold on PCL-5 and DASS-21. - Refer to physician if pain remains high for medication review. - Contact insurer and/or general practitioner to facilitate further care. - Refer to a whiplash specialist if not confident in managing physical treatments. - Continue treatment as in Week 3 or follow specialist advice. **Week 12** - **Low Risk:** Discharge. - **Medium/High Risk:** Refer to chronic guideline. **Impact of events scale** - Patient interview - PTSS symptoms **Grade 2 whiplash** - Musculoskeletal signs including decreased range of motion and point tenderness. - Muscle function and morphological changes. - Psychological contributors e.g. PTSS, pain catastrophising. - Pain sensitivity - Pain sensitivity findings can be similar to radiculopathy. - More pronounced in people with PTSS. - Frequent findings of decreased pressure pain thresholds and cold pain thresholds. How would you assess pain sensitivity in whiplash? - Pressure pain thresholds. - Mechanical pain thresholds. - Ice pain test. - Exercise induced hyperalgesia. **Muscle function and morphological changes** - Neck muscles cross sectional area can: - Increase acutely due to inflammation. - Increase due to muscle fat infiltration. - Decrease due to disuse atrophy. **Clinically: loss of strength and fatigue resistance** Changes in muscle fibre type: transition from fatigue resistance type 1 to fatigable type 2 muscle fibres - Muscle atrophy - Fatty infiltration. Clinically: - Reduced isometric strength e.g. head lift and hold (supine or prone). - Reduce activation: cranio- cervical flexors and cranio- cervical extensors, cervical extensors. - Deficits in precision of cranio- cervical flexion in people with neck pain. *Symptoms* - Head feels too heavy for neck. - Find sustained head positions difficult e.g. computer use, cinema, hard to hold head up. - Ease by supporting head e.g. back of chair/ lying down. *Signs* - Weakness on testing. - Symptom modification: changing posture and/ or muscle activation improves symptoms. - Initially better post exercise targeting fatigue resistance. - On ROM, function, or palpation. - Could be worse if overloaded. **Sensori- motor impairments in spinal pain** - Reduced precision in the control of trunk or neck movement. - Joint position error/ re- positioning error. - Greater postural sway vs healthy control. - Impaired laterality or body perception. Assessment of sensori- motor impairments - *Joint position error:* e.g. ability to rotate neck and return to target. Ability to find, maintain and re- position body part. - *Body perception.* - Laterality: ability to recognise left and right limbs/ areas of spine. Recognise app. - E.g. body perception via questionnaires, drawing images, visual imagery. **Assessment for someone with whiplash** - Observations - Functional movement - Active movements - Palpation - Manual assessment → looking at range, quality, symptom reproduction, breathing pattern, symptom modification procedures. Further testing - Isometric muscle test for pain provocation: isolation to movements and muscle groups vs. isolated muscles in spine. - Muscle length tests (caution). - Strength testing - Motor control: low load activation and endurance. Assessment of movement and motor control - Individualised assessments: - What movements or functions is this person struggling with? - What do you observe during movement assessment (functional/ active movements)? - Difficult movement/ where they struggle. - Where person has pain - How intense/ irritable is it? - What is their response to changing movement, posture, or motor control? - Symptom modification: - Repeating movement. - Modifying the movement. - Relaxing, changing position, increasing control. Specific motor control cervical spine *Cranio- cervical flexion assessment* - Deep neck flexors. - Start in crook- lying, folded towel under head. Head in neutral. - Assess breathing pattern and resting tone. - Slow gentle activation: look down, perform gentle chin nod. - Assess quality of movement: muscle contraction. E.g. assess for excessive SCM activation. - Assess endurance (up to 10 secs, 10 reps = normal) - Can use pressure biofeedback unit to assess and treat. *Cervical extensors -- 4 p.t kneeling* - Full flexion to return to neutral. - Look for coordinated movements and re- positioning for accuracy. - Measure reps to fatigue, loss of control. - Monitor symptoms but not main assessment. - Normal response: can perform 10+ well. *Sub- occipital muscles (deep neck extensors) -- 4 pt. kneeling* - Maintain neutral position -- rotate to look at little finger. - Look for coordinated movement and re- positioning accuracy. - Measure reps to fatigue, loss of control. - Monitor symptoms but not main assessment. - Normal response: can perform 10+ well. *Prone scapula holding test.* - Assess prone on plinth. - Assess breathing pattern and resting tone. - Passively position scapula to teach movement. - Ask patient to positional scapula and hold. - Slow gentle activation -- gently draw scapula back. - Assess quality of movement; muscle contraction e.g. assess for excessive lat dorsi or UFT activation. - Assess endurance (up to 10 secs, 10 reps = normal). **Cervical spine disorders - headache** Tension headache, migraine, cervicogenic headaches → overlap between different types of headaches (important to recognise) **Red flags** → Needs to be integrated into clinical exam. 4 main categories - Malignancy - Cauda Equina Syndrome - Fracture - Infection - Cord compression: cervical myelopathy. - Arterial dissection e.g. aortic aneurysm/ cervical arterial dysfunction. - Visceral referred pain/ other neurological e.g. MS. **Cervical arterial dysfunction** - Vascular pathology of the neck which can manifest as neck pain and headache. *Risks* - Trauma → increases suspicion for red flags - Vascular history (high blood pressure) - Current/ past smoker  **Early presenting features of CAD -- need to screen for 5 D's and 3 N's** - Acute onset of moderate to severe unfamiliar headache or neck pain and they are under the age of 55 → referral to ED and send a written report of history and signs and symptoms of concern (e.g. neurological symptoms). **Red flag disorders headache related.** **Cervicogenic headaches** - Cause: Arising from disorders of the cervical spine (bone, disc, or soft tissue elements). - Usually accompanied by neck pain - Headaches develops after neck pain. - Headache disappears once neck pain subsides. Evidence of causation demonstrated by at least two of the following: - Headache has developed in temporal relation to the onset of the cervical disorder or appearance of the lesion. - Headache has significantly improved or resolved in parallel with improvement in or resolution of the cervical disorder or lesion. - Cervical range of motion is reduced, and headache is made significantly worse by provocative manoeuvres. - Headache is abolished following diagnostic blockade of a cervical structure or is nerve supply. **Subjective diagnostic criteria** - Unilateral pain without side shift: may be unilateral on both sides but doesn't shift sides like migraines. - Starts in the neck or occiput, with possible shoulder or arm pain. - Moderate headache intensity (not stabbing/ lancinating) - Episodic or continuous -- frequency/ duration highly variable. - Associated symptoms (mild nausea, dizziness, photophobia, blurred vision) may occur but are usually intermittent and less severe than in migraines. **Physical diagnostic criteria** - Headache reproduced by neck movement, posture, or palpation. - Restricted neck mobility (AROM) - Pain reproduced with external pressure to upper cervical spine, occiput, or related muscles (accessory palpation) - Changes in muscle contour, texture, or response to stretch or contraction. - Positive anaesthetic block (in research). **Clinical features of cervicogenic headache** Cervical flexion rotation test - Specific to upper cervical spine and cervicogenic headache - Important in differentiating in people who have a cervicogenic headache to those who have a migraine. - Limited ROM (less than 40-45 degrees) or headache reproduction indicates a positive test. People with cervicogenic headache compared to migraine: - Decreased AROM upper cervical flexion and extension. - Higher incidence of painful upper cervical joint dysfunction assessed by manual examination. - Higher incidence of muscle tightness. **Physical examination** *Cervical movement assessment* - NB rotation: (most of rotation comes from C1 and C2) - Upper vs lower differentiation: protraction/ retraction. Combined retraction/ protraction + rotation and/ or side flexion. - Manual examination: palpation, passive movements, pain provocation of spine. - Flexion rotation test. *Cervical motor function/ motor control assessment* - General strength/ deconditioning - Muscle length tests - Motor control impairment - Cervical extensors/ sub- occipital muscles (cranio- cervical extensors). - Cranio- cervical flexors. - Scapular control. **Radiology** Questionable. - May be helpful to exclude pathology. - OA changes may have some significance - highly variable. - No radiological changes specific for CHA. **Possible nociceptive inputs in cervicogenic headache**  When thinking about cervicogenic headache → occiput to C3 and the muscles at these levels **Differential features of cervicogenic headache** - Migraine: Pain often starts in the anterior head, tends to have a pulsatile quality, and is aggravated by exertion. Associated with photophobia, phonophobia, and nausea. - Cervicogenic headache: Pain starts in the neck or occiput, usually triggered by neck movement, posture or pressure to neck or head. Associated symptoms like photophobia are milder and intermittent. - Tension headache: Band-like or bilateral pain, usually mild/moderate in intensity. No pulsating pain and not aggravated by physical activity. Lack of photophobia. **Classification of cervicogenic headaches** MSK framework → broad and widespread understanding - Need to look at functional movements - helpful/ unhelpful. - Looking at whether it's an impairment of control, pain behaviours, deconditioning. - Impairment of control linked with postural loading. Will help guide treatment selection and determining likely prognosis. Based on history, symptom behaviour, physical examination. **Migraine** - Migraine without aura is a clinical syndrome characterised by headache with specific features and associated symptoms. - Migraine with aura is primarily characterised by the transient focal neurological symptoms that usually precede or sometimes accompany the headache. Features: - 5 or more attacks of headache - 4- 72 hours if left untreated. - 1 of the following: nausea, vomiting, photophobia. - 2 of the following: unilaterality, pulsatile quality, moderate- severe, aggravated by exertion. Manual therapy - no change to headache frequency - Role of physio's is to identify and to refer onwards so they can be managed medically. **Tension headache.** - Likely a neurobiological basis. - Sub classifications from episodic (\15 days/ month). - Most significant abnormal finding is increased peri cranial tenderness reproduced by manual palpation - tenderness around the band- like tendon around the head. Has at least two of the following: - Bilateral location - Pressing/ tightening (non- pulsing) quality. - Mild or moderate intensity. - Not aggravated by routine physical activity such as walking or climbing stairs. Management - Avoidance of stress. - Relaxation - Psychotherapy - Rest - Medications **Physiotherapy management of cervicogenic headaches** Need to think about different aspects: - Frequency - Intensity - Duration - Medication intake **Treatment considerations** *Acute episodic* - Focus on treating impairment and clinical signs. - Identification of precipitating factors. - More rapid response to treatment. *Chronic continuous* - Focus on aetiological and perpetuating factors (underlying drivers) - Emphasis self- management and exercise. - Concurrent pharmacological treatment - Slow response to treatment. **Key Treatment Interventions** - Manual Therapy: Mobilization and manipulation techniques. - Exercise Therapy: To improve neck function and muscle control. - Treatment should aim to reduce headache intensity, frequency, duration, and dependence on medication. **Manual Therapy Techniques** - *Sustained Natural Apophyseal Glides (SNAGs):* - Applied pressure over the facet joint of the cervical spine, followed by passive movements to mobilize the joint. - SNAGs are used in both passive and self-treatment techniques (e.g., using a belt for self-SNAG). - *Treatment Framework:* - For patients presenting with cervicogenic headaches, if the cervical spine appears to be the cause or contributor, treatment should be offered. - If musculoskeletal dysfunction is present but not clearly related to the headache, trial treatment and monitor responsiveness. - If no cervical musculoskeletal pattern is present, treatment is not indicated, and referral to other healthcare providers should be made. **Spinal disorders: functional behaviours overview** **Musculoskeletal clinical translation framework** - Integrate how someone's functional behaviours or how they are moving is influenced by their pain features (e.g. mechanical pattern of pain) or the state of their healing, stage of their injury, how they are thinking about their problem or feeling about their problem. When looking at a patient with pain, need to consider all aspects → looking at the patient holistically. **What is non- specific low back pain?** - Pain between the 12th rib and the gluteal fold of musculoskeletal origin with no known pathoanatomical cause. - Cannot attribute a specific or serious cause to the pain. **Functional behaviours** Adaptive (helpful) vs Maladaptive (unhelpful) +-----------------------------------+-----------------------------------+ | Helpful | Unhelpful | +===================================+===================================+ | - Reflects behaviours that | - Reflects behaviours that are | | serve to prevent further | provocative of a disorder. | | tissue damage/ allow tissue | | | healing to occur. | - May reflect the persistence | | | of behaviours in the absence | | - Normalising the behaviour | of or past the time of tissue | | results in increased symptom | healing. | | response. | | | | - Normalising the behaviour | | e.g. splinting of the neck or | results in reduced symptom | | spine in the context of an acute | response. | | spinal injury | | | | e.g. a person with acute neck | | - Relative rest and avoidance | pain of insidious onset, with no | | in the early stage of these | patho- anatomical basis for | | types of disorders is usually | symptoms (pain that may arise | | appropriate | subsequent to a period of high | | | psychological distress). The | | | protective movement and pain | | | behaviours are unlikely to be | | | helpful, rather contributing to | | | the onset and persistence of | | | pain. | +-----------------------------------+-----------------------------------+ - Adaptive - helpful, protective in a useful way e.g. limiting movement during first few days of ankle sprain. Relative rest during the first few days, within pain limits. - Maladaptive - provocative, hold onto the behaviours past the time of tissue healing. Holding of body tension (due to overall stress, patent behaviour learnt early on). Normalising behaviour → leads to reduced symptom response (helpful to change it). **Functional behaviours definitions** ***Impairment of movement (about restricted range of motion)*** - Restricted AROM and PROM in the direction of pain provocation. - E.g. restricted movement bending forwards → limitation of PROM into that direction as well (pattern of functional AROM and PROM supporting one another). *Clinical interview -- impairment of movement* - History: insidious onset, subacute phase post injury, resolving specific disorder. - Aggravating factors: pain provoked moving into the hypomobile direction, pain/ stiffness following periods of rest/ being still. - Eases: movement (often getting up and getting moving, particularly into the direction of stiffness, will assist/ reduce pain). - 24 hour: morning stiffness due to being still overnight. Could improve with movement throughout the day provided not overloading sensitive structures. *Physical exam -- impairment of movement* - Functional test: pain into direction of reported stiffness -- minimal change with SMP. Symptoms may ease with repeated or sustained movements into the direction of pain. - ROM: limited movement actively and passively into painful direction. - Pain provocation: usually painful over sensitised spinal structures. *Care strategies -- impairment of movement.* - Make sense of pain. - Need a plan to restore normal mobility of the spine. - Advice that moving into the direction of pain is not harmful and is in fact beneficial. - Exercises and daily habits that promote movement towards the restricted movement. - Complementary manual therapy with the aim of promoting movement, easing pain, and reducing muscle tension/ guarding. - Spinal mobilisation/ manipulation. - Soft tissue techniques. ***Impairment of control*** - No impairment of movement in the direction of pain provocation, but where pain is associated with aberrant movement control. - Don\'t really see an impairment of movement. - Pain is associated with an aberrant (not quite right - looks unhelpful) movement pattern. *Clinical interview -- impairment of control* - History: more likely persistent or recurrent, persistent following traumatic incident, could become apparent following overload -- either increased sustained load or increased repetitive movement. - Aggravating factors: pain with sustained postures, pain worsens with sustained positioning or repeated movement into provocative direction. - Eases: de- loading (e.g. laying down), movement away from the provocative posture or movement. - 24 hour: - Morning: often feel better in the morning after a period of de- loading. - Day: often worsen throughout the day if continuing to posture or position on provocative ways throughout the day. - Psychosocial: may have maladaptive beliefs, fear or pain/ movement potentially driving the unhelpful control pattern. *Physical exam -- impairment of control* - Functional test: aberrant movement pattern, posture, or muscle activity. When altered via SMP leads to a reduction in symptoms. Will not be lacking movement into the direction of the functional task. - ROM: no limitation to movement into the direction of pain provocation -- may need to reduce muscle guarding/ offload to observe properly. Often have through range or an arch of pain on active movement. - Pain provocation: usually painful over sensitised spinal structures. *Care strategies -- impairment of control.* - Make sense of pain for patient: may need emphasis on de- threatening in some people. - Need a plan to increase postural and movement variability and de- load sensitised structures. - Promote postures and movements that move the patient out of/ away from sustained or habitually sensitising movement patterns. - Specific focus on retraining postures and movements into positions and postures that are not provocative. - May include manual therapy for pain relief or to meet patient expectations (often not needed) Pain behaviours - Overt behavioural responses to pain experience or anticipation of pain e.g. grimacing, holding breath, overt avoidance etc. De- conditioning - A deficit in muscle strength, endurance and/ or physical capacity. **Impairment of control** **Impairment of control** - No impairment of movement in the direction of pain provocation, but where pain is associated with aberrant movement control. - Don\'t really see an impairment of movement. - Pain is associated with an aberrant (not quite right - looks unhelpful) movement pattern. **Loose vs Tight control** **Tight impairment of control** +-----------------------------------+-----------------------------------+ | *Findings in low back pain* | *Findings in neck/ trunk* | +===================================+===================================+ | - Trunk movements performed | - People with chronic neck pain | | more slowly. | walk with a stiffer spine = | | | reduced trunk rotation. | | - Stronger coupling of pelvis | | | and thorax movements. | - Increased activity ion | | | superficial muscles e.g. SCM, | | - Reduced trunk movements | anterior scalene with upper | | during gait and repetitive | limb activities. | | trunk bending. | | | | - Reduced speed and | | - Individuals with high fear of | accelerations during overhead | | pain are more likely to | activities with light weight. | | stiffen their trunk in | | | anticipation of a | - Prolonged co- contraction of | | perturbation. | cervical and thoracic muscles | | | throughout task cycle. | +-----------------------------------+-----------------------------------+ - Movement patterns where trunk movements are slower, pelvis and thorax are strongly coupled, with rigid movement patterns. - Seen in low back pain and neck pain, resulting in a stiffer spine. Advantages - Increases safety margin in movement control. - Useful in early injury stages or activities like lifting or anticipating movement (e.g., sports or lifting). Disadvantages - Increases spinal loading. - Exposed to higher loading e.g. during lifting. - Sustained muscle activation at rest. - Negative effect on spinal structures -- excessive compressive loading. - Muscle fatigue -- discomfort. - Reduced motor variability. - High stiffness can reduce balance. - Extreme: avoidance of movement/ function entirely. **Loose impairment of control** +-----------------------------------+-----------------------------------+ | *Findings in low back pain* | *Findings in neck/ trunk* | +===================================+===================================+ | - Inhibition of trunk muscles | - Reduced neck isometric | | | strength. | | - Higher variability of trunk | | | movements during gait, | - Reduced activation -- cranio- | | reaching and repetitive trunk | cervical flexors | | bending. | | | | - Deficits in precision of | | - Less precision in controlling | cranio- cervical flexors in | | trunk posture or movement. | neck pain. | | | | | - Delays in muscle activation | - Level of neck pain intensity | | and control in response to | associated with dysfunction | | perturbations. | of cranio- cervical flexors. | +-----------------------------------+-----------------------------------+ Advantages - Allows for fast, large amplitude movements. - Allows for movement variability. Disadvantages - Faster and larger amplitude movements. - More variability between repeated movements. - Can lead to large tissue strains and pain. Loss of fatigue resistance - Changes in muscle fibre type from fatigue resistant type 1 fibres to fatigable type 2 fibres. - Muscle atrophy - Fatty infiltration - Well established in deep muscles. **Lumbar spine directional sub- groups** - Flexion pattern: physiological direction of pain provocation is in flexion. - Active extension pattern: physiological direction of pain provocation is in extension. - Passive extension pattern: physiological direction of pain provocation is extension. **Active extension pattern vs flexion pattern** - Due to differences in presentations, they can require quite different management plans.  Active extension pattern -- tight impairment of control - Pain provoked by extension (even into flexion movements) - Postures (sit -- stand -- sustained bend) - Movements (backward bend, forward bend) - Activities (walking, lifting) - Pain eased with relaxed flexion. - Features: - Anterior pelvic rotation/ lumbar extension - Back and abdominal wall co- contraction. - Loss of back extensor flexion relaxation (sitting and forward bending) Flexion pattern -- loose impairment of control - Pain reported with flexion-based activities and postures. - Tendency to hold lumbar spine in relative end range flexion positions. - May have abdominal bracing. - Often with concomitant thoracic extension. - Eased when lumbar spine moved into extension. Understanding movement patterns and how they relate to symptoms is key to identifying impairments of control. Experimenting with symptom modification can offer insights into relevant impairments. **Management of impairment of control with low back pain** **Reflect on clinical care standard.** - Address broader concepts → overall care for low back pain. - Make sense of pain that is specific to that individual → providing a new understanding of pain. - Explain how cognitive, affective and lifestyle factors as well as functional behaviours (whatever might be relevant to the patient) can influence the patient's pain experience. - SMP's to inform making sense of pain → integrate with cognitive effect and lifestyle factors. **Changing motor control** - Identify provocative movements and motor control. - Use SMP's to assess relevance: - Re- train movement pattern. - Build exercise program around this. - Progress and integrate back into function. - Some people will be able to start with re- training in functional positions. - Other will need to start in unloaded or easier positions. - To re- train localised movement. - To enhance muscle recruitment. **Retraining active extension patterns vs flexion patterns.** +-----------------------------------+-----------------------------------+ | *Active extension pattern* | *Flexion pattern* | +===================================+===================================+ | - Relax global bracing → find | - Facilitate anterior pelvic | | positions that the person is | tilt. | | more relaxed in (slumped), | | | cueing to relax muscles, deep | - Flexing a lot through the | | breathing, diaphragmatic | lumbar spine, not flexing at | | breathing to relax abdominal | hip and remaining in | | muscles. | extension in thoracic spine → | | | encourage more flexion at the | | - Facilitate lumbar flexion. | thorax and the hip and try to | | | maintain a more neutral | | - Facilitate posterior pelvic | lumbar spine. | | tilt | | | | - Relax abdominal bracing if | | | present. | | | | | | - Reduce thoracic extension if | | | relevant. | +-----------------------------------+-----------------------------------+ Need to be careful about some of the myths → need to be explicit about this. - Re- train with the idea that there is no single correct posture. - Differences in posture are normal. - Encourage comfortable posture. - Enforce idea that spine is robust. Care for patients with impairment of control **-- exposure with control.** - Exposure with control: must be specific for the patient, not