Introduction to Sports Therapy Flashcards
(107 cards)
1
Q
What are the types of athletic tape?
A
Rigid (zinc oxide), elastic adhesive bandage (EAB), kinesiology (K-tape), and under wrap (hypafix).
2
Q
What is rigid tape and what is it’s primary use?
A
It is non-elastic, strong adhesive tape. It’s primary use is joint immobilisation and stabilisation.
3
Q
What is EAB and what is it’s primary use?
A
It is a stretchable, bandage and it’s primary use is to
provide support and compression.
4
Q
What is kinesiology and what is it’s primary use?
A
It is elastic tape that mimics skin elasticity and it’s primary use varies between having proprioceptive and psychological effects.
5
Q
What us under wrap and what is it’s primary use?
A
It is a foam pre-wrap used underneath adhesive tapes. It’s primary use is to protect the skin from irritation caused by adhesive tapes and to provide a base layer for adhesive tapes to stick to.
6
Q
What/how/when rigid tape?
A
Rigid tape is used for support, to reduce excessive ROM, increase movement opportunity and compression.
It supports across joints by increasing the sensory and mechano-receptor stimulation, unloading tissue.
It is used when movement is limited, or for ligament injuries and connective tissue injuries.
7
Q
What/how/when kinesiology tape?
A
It increases movement opportunity and confidence and reduces pain.
It does this because pain causes sensory and mechano-receptor stimulation, increasing psychological effects.
It’s used for pain to increase confidence and proprioception.
8
Q
What is the clinical reasoning process for taping application?
A
What is the affected tissue? What is the mechanism of injury?
Look at joint positioning and direction of tension.
Look for any containdications.
9
Q
What are contraindications?
A
A contraindication refers to a specific situation or condition in which a particular treatment or procedure should not be used because it may be harmful to the patient.
Examples: open wounds, fragile/sensitive/compromised skin, adhesive/tape allergies and circulation issues.
10
Q
How to check if your tape is too tight?
A
Capillary refill: pinch the end of the finger or toe and the colour should come back within 2-3 seconds. >3 seconds is poor refill and blood flow may be restricted. Other signs are pins and needles.
11
Q
How long can you wear tape for?
A
Zinc oxide = >24 hours
K tape = >7 days
12
Q
What happens if failure to check for contraindications?
A
Worsening of condition, patient harm, professional liability, loss of trust.
13
Q
How does cryotherapy work?
A
It reduces blood flow (vasoconstriction), reduces metabolism and inflammation, reduces nerve conduction (analgesia), reduces temperature and muscle spasm.
14
Q
How does cryotherapy reduce blood flow?
A
It decreases tissue temperature, which triggers a sympathetic vasoconstrictive reflex. This reduces blood flow to the injured area.
15
Q
How does cryotherapy reduce metabolism and inflammation?
A
By lowering tissue temperature, cryotherapy decreases the metabolic demands of hypoxic tissues. This helps prevent secondary tissue damage, which can occur when oxygen supply is insufficient during inflammation.
16
Q
How does cryotherapy reduce nerve conduction?
A
Cryotherapy induces a local anesthetic effect by lowering
the activation threshold of nociceptors (pain receptors) and slowing down the nerve
conduction velocity. This cold-induced analgesia helps reduce pain from acute injuries
like ankle sprains.
17
Q
How does cryotherapy reduce temperature and muscle spasm?
A
Cryotherapy inhibits spinal reflex loops, helping to alleviate
muscle spasms that often accompany injuries.
18
Q
How does thermal therapy work?
A
It increases blood flow (vasodilation), increases metabolism and cell activity, reduces nerve conduction (analgesia), and increases temperature and elasticity.
19
Q
How does thermal therapy increase blood flow?
A
Heat increases tissue temperature, causing
blood vessels to dilate, which boosts blood flow to the injured area. This delivers more
oxygen and nutrients to tissues, promoting healing (Malanga et al., 2015).
20
Q
How does thermal therapy increase metabolism and cell activity?
A
The rise in tissue temperature accelerates the metabolic
processes, speeding up the healing of injured tissues by enhancing cellular activity and
repair mechanisms (Malanga et al., 2015).
21
Q
How does thermal therapy reduce nerve conduction?
A
Heat stimulates the activation of thermoreceptors, which helps block pain
signals sent to the brain. This analgesic effect is particularly useful in reducing muscle
and joint pain (Malanga et al., 2015).
22
Q
How does thermal therapy increase temperature and elasticity?
A
Heat therapy helps improve the elasticity of connective
tissues, making it useful for improving flexibility and reducing stiffness, especially in
muscles and joints.
23
Q
How does compression therapy work?
A
It promotes blood flow, reduces swelling and increases joint stability.
24
Q
How does compression therapy promote blood flow?
A
Compression helps veins carry blood back to the heart more
efficiently, reducing pooling of fluids in the extremities.
25
How does compression therapy reduce swelling?
By applying external pressure, it helps to limit fluid buildup (edema)
in tissues.
26
How does compression therapy increase joint stability?
Compression stabilizes soft tissues and reduces the risk of
further injury during the recovery process.
27
What are the contraindications of cryotherapy?
circulatory insufficiency, cold allergy, advanced diabetes, open wounds, DVT and regenerating nerves. Brachy cardia, frost bite cold burn, tissue damage, cold ulcers and infected wounds.
28
What are the contraindications of thermal therapy?
peripheral vascular disease, rheumatoid disease, advanced diabetes, multiple sclerosis, and spinal cord injuries. Burns, pain and increased inflammation.
29
What is the IASP definition of pain?
Pain is an unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage.
30
What are the key components of the IASP definition?
Unpleasant Sensory and Emotional Experience:
Dual nature of pain, involving both physical sensation and emotional impact.
Associated With, or Resembling:
This allows for the inclusion of pain that does not have a clear physical cause but is real and significant to the sufferer.
Actual or Potential Tissue Damage:
This acknowledges that pain serves as a warning signal of harm or potential harm to the body.
Pain is always a personal experience influenced by varying degrees by biological, psychological, and social factors.
Through their life experiences, individuals learn the concept of pain.
A person’s report of an experience as pain should be respected.
Verbal description is only one of several behaviours to express pain;
inability to communicate does not negate the possibility that a human experiences pain.
31
What are the controversies and discussions of pain?
Subjectivity vs Objectivity:
Pain's subjective nature challenges its assessment and management as it relies on personal experience rather than objective measures.
Psychosocial Factors:
The definition's breadth sparks debate over how psychological and social elements influence pain perception and should be incorporated into understanding and treating pain.
Chronic Pain:
The ongoing experience of pain beyond normal healing time complicates the link between pain and tissue damage, raising questions about how chronic pain fits into the definition.
Pain Without Physical Damage:
Recognising pain that lacks a clear physical cause addresses conditions like fibromyalgia but also introduces challenges in clinical recognition and patient stigma.
32
What is nociception?
Nociception is the neural processes of encoding & processing noxious stimuli.
Nociceptors are the specialised sensory receptors responsible for the detection of noxious (unpleasant) stimuli, transforming the stimuli into electrical signals, which are then conducted to the CNS.
In response to the stimuli, nociceptors transduce this information into nerve impulses by releasing a myriad of neurotransmitters such as prostaglandins, bradykinins, substance P & histamine, which all promote an inflammatory response & simultaneously communicate pain signals to the spinal cord.
Nociceptors can be activated by three types of stimulus within the target tissue - thermal (temperature), mechanical (e.g. stretch/strain) & chemical (e.g. pH change as a result of local inflammatory process).
Physiological process by which body tissues are protected from damage.
NB for the "fight or flight response" of the body & protects us from harm in our surrounding environment.
Pain & nociception are different phenomena.
33
What are the nociceptor pathways?
Reflective protective response,
Integrated in spinal cord,
Withdrawal reflex,
Ascending pathway to cerebral cortex ~ Becomes conscious sensation (pain)
34
What organ systems are involved with nociceptors?
There are no nociceptors found in the CNS.
Specific sensory modalities leading to nociception differ depending on the type of tissue:
In skin, noxious stimuli are commonly thermal, mechanical (e.g., a cut), & chemical (e.g., exogenous allergens).
In the joints, noxious stimuli commonly derive from mechanical stress (e.g., excessive joint torque) & chemical inflammation.
In the muscles, strenuous mechanical exertion (e.g., blunt force, over-stretching) & chemical modalities are most common.
35
What are nociceptors on a cellular level?
Widespread in skin, joints, viscera, bone, & muscle.
The damaged tissue releases & produces numerous factors which in turn activate nerve endings.
Modulated by local chemicals – mediate inflammatory response.
The two major classes of nociceptors include:
medium diameter myelinated Aδ (delta) afferents which convey an acute, well-localised fast pain,
and small diameter unmyelinated “C” fibres that convey a poorly localised, slow pain.
36
What are the mechanisms of pain?
Transmission of Pain Signals
Nociceptors are activated.
Transmit pain signals through afferent nerve fibres.
Spinal cord brain via spinothalamic tract
Processed in thalamus, somatosensory cortex, & frontal cortex.
Communication pathway for pain signals.
Pain Perception
Brain interprets the signals, leading to the conscious experience of pain.
Emotional and cognitive factors influence perception.
37
What is clinical significance of acute pain?
Short-lived response to injury, trauma, surgery, or illness.
It can last from a few seconds to a few weeks/months & usually resolves once the cause is treated.
Can include numbness, tingling, sharp, throbbing, or stabbing sensations.
Examples of acute pain: Postoperative pain, burns, acute musculoskeletal pain (e.g., strains, sprains, fractures).
38
What is the clinical significance of chronic pain?
Chronic pain persists for longer than six months & may not be localised to one specific area of the body.
It often affects psychological, social, & behavioural aspects of daily functioning.
Can result from chronic diseases, injury, inflammation, or have an unknown cause.
Common causes include osteoarthritis, spinal conditions, fibromyalgia, & peripheral neuropathy.
Chronic pain can become more centralised, leading to a decreased pain threshold & increased pain severity.
39
What is pain modulation?
The ability to influence & change the pain signals.
This may be by inhibiting transmission pathway of pain or by altering the emotional response to pain.
It explains: (1) Why individuals respond to the same stimulus differently. (2) The mechanism of action when using clinical analgesia.
Mainly in the CNS, however several peripheral inputs such as transcutaneous electrical nerve stimulation (TENS) or ‘rubbing it better’ can be involved.
Endorphins:
The body can modulate pain through the release of natural painkillers known as endorphins.
These are produced in the brain & can temporarily reduce pain sensation by binding to opioid receptors.
Gate Control Theory:
Suggests that non-painful input closes the "gates" to painful input, which prevents pain sensation from traveling to the CNS.
40
What is the gate control theory?
The 'gate' is the mechanism where pain signals can be let through or restricted. The gate can either be 'open' or the gate can be 'closed':
If the gate is open, pain signals can pass through and will be sent to the brain to perceive the pain.
If the gate is closed, pain signals will be restricted from travelling up to the brain, and the sensation of pain won't be perceived.
Activation of A-β fibres - facilitate the gate control mechanism - will inhibit the input from the noxious A-δ & C fibres.
If someone experiences a painful (noxious) stimulus, the application of a non-noxious (soothing or light rubbing) stimulus can help activate the gate control mechanism & reduce the pain.
41
What is the clinical significance of TENS?
Activates the pain gate mechanism to inhibit pain signals going up to the brain, thus reducing the sensation of pain.
TENS activates non-noxious afferent fibres, which in turn activates the 'pain-inhibiting' interneurons in the spinal cord, thus reducing perceived pain as an output.
This is because TENS can activate A-β fibres, which helps facilitate the gate control mechanism. The activation of the A-β fibres will inhibit the input from the noxious A-δ and C fibres.
42
What is the clinical significance of massage?
Massage therapy also makes use of the gate control theory to reduce and inhibit pain, with the same reasoning of activating large diameter A-β nerve fibres.
43
What is motor control?
Motor control is a combination of muscle activation and movement. It is both conscious and subconscious. In response to pain and injury, it reduces tissue stress and leverages.
44
How to measure movement?
Visual:
highly subjective and based on "norms" but it is quick.
Movement screen:
monitors progress and objective but not predictive.
Video analysis:
requires skills and it is time consuming but has minimal cost and is highly objective.
45
What is flexibility?
The range or extent of motion possible in a given joint or joints.
46
47
Why is flexibility reduced?
Scar tissue:
means it is more pliable.
Pain signals:
neurological inhibition and avoidance.
Swelling:
increased pain and reduced joint space.
48
What is the difference between flexibility and motor control?
Flexibility is available ROM at joints and motor control is coordinated movement through ROM.
49
Why do we measure flexibility?
To track normal tissue function, to guide exercise selection and to return to sporting movement.
50
How to measure flexibility?
Manually with goniometer/inclinometer, digitally with goniometer/inclinometer or via phone application.
51
What is the definition of muscle strength?
The ability of a given muscle or group of
muscles to generate force under specific
conditions.
52
Why do we lose strength?
If there is disrupted muscle activation, inhibition: pain reduces muscle activation, muscle fibre damage decreases contractile strength, atrophy: immobilisation reduces muscle size, inflammation: cytokines degrade muscle.
53
What is proprioception?
Afferent information, including joint position sense, kinesthesia and sensation to resistance.
Joint position sense:
The ability to recognise the
orientation and location of the joint.
Kinesthesia:
The ability to appreciate and
recognise joint movement.
Sensation of resistance:
The ability to appreciate and recognise force generated within a joint.
Neuromuscular control:
Appropriate efferent responses to afferent proprioceptive input.
54
Why is proprioception reduced?
Sensory disruptions: mechanoreceptors that detect joint position.
Reduced neuromuscular feedback:
decreased flow of neuromuscular signals.
Impact of immobilisation:
reduced movement means reduced feedback.
55
Why do we measure proprioception?
Normal receptor function, enhanced movement accuracy and faster reaction to danger.
56
What is ballistic jumping?
Increased force and rate of force.
57
What is plyometric jumping?
stretch shortening cycle.
58
What is limb symmetry index (LSI)?
Limb Symmetry Index (LSI) is a ratio used in rehabilitation to compare the performance of an
affected limb to its unaffected counterpart.
𝑈𝑛𝑎𝑓𝑓𝑒𝑐𝑡𝑒𝑑 𝐿𝑖𝑚𝑏÷𝐴𝑓𝑓𝑒𝑐𝑡𝑒𝑑 𝐿𝑖𝑚𝑏×100
* Ease of calculation
* Cost-effectiveness
* Flexibility
* Monitored over time
Normative LSI
90% = Return to Play
59
Pros of LSI?
Benchmarks, often 90%+, for safe return to sports (Sato et al., 2021).
Easy-to-interpret measures for tracking rehab progress (Wellsandt et al., 2017).
Versatile across functional tests (Gokeler et al., 2017).
Ensures consistent evaluation standards in clinical practice
60
Cons of LSI?
May overestimate recovery if both limbs are impaired post-injury (Wellsandt et al.,
2017).
Focuses on symmetry rather than absolute functional capacity, potentially missing deficits like fatigue effects (Sato
et al., 2021)
61
What are the healing phases?
Bleeding and inflammation phase:
▪ Acute response
▪ Prepare wound
▪ Hours to days
Proliferation and Remodeling phase:
▪ Reconstruction phase – rebuilding new tissue
▪ Days to weeks, months to years
Timeline considerations:
▪ Cross-over of phases
▪ Severity
▪ Tissue type
▪ Complications (i.e., infection)
▪ Implications for rehabilitation
62
What is the bleeding phase: clot formation?
1. opening in vessel wall
2. vasoconstriction
3. platelet adhesions
4. platelet aggregation
5. fibrin formation
6. coagulation
63
What is the inflammatory phase?
Body’s reaction to injury or an irritant.
A defensive response that:
▪ a. Attempts to remove the irritant, debris and
dead cells (phagocytosis)
▪ b. Prepare the area for repair prior to the
proliferation and remodelling phase
64
What is the inflammation phase: vascular response?
1. normal capillaries
2. vasodilation
3. white blood cell migration
A. blood plasma "leaks" into surrounding tissue = swelling
B. increase surface are of dilated capillaries = redness C. increase surface area of dilated capillaries = heat.
65
What is the cellular response?
1. injured tissue
2. bleeding and clot formation
3. debris present
4. neutrophil formation
5. neutrophils dies off and monocyte's continue process
6. monocytes mature into macrophages
66
What is the proliferation phase?
Proliferation Phase: Migration, proliferation, and
activity of fibroblasts & endothelial cells.
Collagen Formation: Structural support via collagen laid down by fibroblasts.
Angiogenesis: New blood vessel formation for nutrient supply.
Wound Contraction: Myofibroblasts initiate
contraction, reducing wound size.
67
What is the remodelling phase?
Remodelling Phase: Collagen fibre
orientation and reabsorption of Type III
collagen.
Collagen Replacement: Transition to Type I collagen.
Scar Tissue Structure: Resembles parent tissue for enhanced quality and
function.
1. cells and capillaries disappear
2. type III collagen is reabsorbed and replaced with type I
3. orientation or collagen becomes organised
68
What are the factors affecting healing?
Local factors:
▪ Oxygenation: Oxygen required for proliferation phase
▪ Infection: Bacteria prolongs and interfere with the healing process
▪ Foreign bodies: Prolongs the inflammatory session in order to prepare the area.
Systemic factors:
▪ Age: Delay in initial wound healing response
▪ Drugs: NSAID’s reduce collagen synthesis secondary to reduced fibroblasts
▪ Macro-nutrition: Carbohydrates provide energy for the wound-healing
process. Protein important for capillary formation and fibroblast proliferation
▪ Micro-nutrition: Vitamin C deficiency results in failure in collagen synthesis
and cross-linking
▪ Immune system dysfunction: Impairs inflammation phase through reduced
phagocytosis.
69
What are the goals and strategies for the inflammatory phase?
Prevention of new tissue disruption and prolonged inflammation with the use of relative rest and
passive modalities
Minimal active exercise for the injured area
Maintenance of function of the cardiorespiratory and surrounding neuromusculoskeletal systems.
70
What are the goals and strategies for proliferation phase?
Prevent excessive muscle atrophy and joint deterioration of the injured area.
Maintenance/Development of function of the cardiorespiratory and surrounding
neuromusculoskeletal systems.
Possible exercise options:
* Flexibility
* Balance and proprioceptive training
* Submaximal strengthening exercises: isometric, isokinetic and isotonic.
71
What are the goals and strategies for the remodelling phase?
Optimisation of tissue function.
Specific exercises to prepare for sport participation.
Progressive loading of the cardiorespiratory and neuromusculoskeletal systems as required.
72
What is myofibril?
Myofibril made up of sacromeres in series.
❑Sarcomeres are comprised of two
proteins that form the contractile elements: Actin
and Myosin
❑Muscle contraction occurs through binding
of these proteins (Sliding filament theory).
73
What are satellite cells?
❑Skeletal muscle stem cells
❑Located between plasma membrane of myofibers and basal lamina
❑Remain in a quiescent state – need to be
activated
❑As part of healing process for muscle, satellite
cells are activated and proliferate
❑Generate myoblasts to support healing of
damaged tissue
74
What are the common mechanisms for muscle strains?
Eccentric action in lengthened position at high velocity. Muscle taken beyond its absolute ROM = overstretching.
75
What are partial tears - mild vs moderate?
Type 3A = tear with a maximum diameter of < muscle fascicle.
Type 3B = tear with a diameter of > muscle fascicle and damage to
perimysium.
Challenging to differentiate Type 3A and 3B. Present similarly clinically. In some instances, MRI and US
may not be sensitive enough.
76
What are diagnostic tools?
MRI can provide an indication of :
Exact location of injury
Size of disruption
Length and size of muscle oedema
MRI may be more sensitive than ultrasound for identifying injuries in the deep portion of the hamstrings.
Ultrasound is an option in the clinic – affordable, convenient, portable and accurate.
77
What is the role of tendons?
Muscle to bone to produce movement.
Very strong structures withstand high forces.
Achilles 6-8 x body mass during running.
78
What is tendinitis?
* Tendinitis suggests inflammation
* Inflammation of the tendon resulting form microtears
* Occur when the musculotendinous unit
is acutely overloaded with a tensile force that is too sudden/heavy
79
What is tendinosis?
* Tendinosis suggests degeneration
* Degeneration of the tendon’s collagen in
response to chronic overuse
* When overuse is continued without
providing the tendon time to heal and rest
80
What is tendinopathy?
▪ Tendinopathy is an umbrella term that
indicates a non-rupture injury to the tendon,
which is exacerbated by mechanical loading
▪ Research suggests that both inflammation and degeneration play a role in the development tendon pathology
▪ Tendinopathy the term which should be used
as therapist cannot see what is going on at a
cellular level
81
What is the tendinopathy failed healing process?
1. Loss of parallel orientation of collagen
fibres - irregular
2. Decrease in collagen fibre diameter and density
3. Increase type III collagen fibres
4. Increased vascularity with blood
vessels randomly orientated
5. Degeneration and haphazard proliferation of tenocytes
82
What is the tendon response to load?
Reactive tendinopathy: tendocytes become activated and can proliferate – can cause short-term thickening
of the portion of the tendon.
Tendon dysrepair: collagen separates and becomes
disorganised, allowing for ingrowth of nerves and
vessels – swollen tendon present on MRI.
Degenerative tendinopathy: cell death has occurred,
collagen fibres are disorganised with increased number of type III fibres
83
What are ligaments?
▪ Ligament = ligare meaning “to bind”
▪ Anatomically distinct, inserting into specific areas on bones
▪ Tensioned with movement – prevent end ROM
▪ Functional subunits: components tighten or loosen relative to joint position - e.g. ACL
84
What are ligaments normal structure?
▪ Tend to be white bands of connective tissue running from bone-to-bone
▪ Composed of parallel fibres of collagen – similar to tendons
▪ Not richly endowed with blood vessels or nerves, but does have a supply
▪ Implications:
1. Bleeds upon damage
2. Slower healing
3. Provide proprioceptive and nociceptive information
85
What is ligament microstructure?
▪ Water comprises majority of ligament - predominantly due to Glycosaminoglycan (GAG) content
▪ GAG are water-binding, which provides two main functions:
1. Forms a lubricant between collagen fibres
2. Maintains a distance between collagen fibres
▪ Immobilisation results in a significant reduction in GAGs (and therefore water)
▪ Collagen fibre distance decreases and friction is created between fibres
▪ Immobilisation = Arthrofibrosis = joint stiffness
86
What are ligaments functional role?
Functions are:
To guide joint movement so to maintain joint stability.
Provide sensory information.
... therefore, ligament damage results in:
1. Instability
2. Distorted sensory information
87
What are mechanoreceptors?
Specialised nerve endings that are transducers for converting mechanical stimuli to action potentials for transmission to the CNS.
88
What are the types of injuries to ligaments?
Three types of traumatic injury:
1. Mid-substance tears - transverse or oblique
2. Avulsion of ligament from bony interface - just ligament torn away
3. Avulsion fracture - bone and ligament torn away.
89
What is bone?
▪ Bone is a specialised connective tissue that serves as a structural tissue and an organ system.
▪ Considerable contribution to overall body mass – 15%
▪ Comprised of fibrous connective tissue and mineral salts - blend of elasticity and rigidity
90
What is the function of bones?
1. Support
2. Protection
3. With muscles they provide movement
4. Mineral storage (calcium)
5. Production of blood cells
6. Triglyceride storage
7. Hormonal production (Osteocalcin – regulates bone formation)
91
What is mechanical loading?
Loading of bone is predictable:
* Compressional forces = shortening of bone
* Tensile forces = elongation of bone
* Bending forces = bowing of bone
92
What is failure point?
When a force is applied to a bone, the point of the bone under the highest stress will fail first.
93
What are fracture patterns?
▪ Fracture pattern depends on the type of injury – loading patterns
▪ Lower energy injuries = simple fractures = transverse, spiral or oblique
▪ Higher energy injury = more severe (e.g., car accident) = comminuted
▪ More common in children due to buckling of immature bone = greenstick and torus.
94
What are stress fractures?
* Bone requires mechanical loading for mineral mass and
strength
* Repetitive loading cycles however that do not allow for
recovery may lead to bone failure
* Metabolic imbalance between osteoblasts and osteoclasts
activity:- ↑Osteoclastic resorption- ↓Osteoblastic bone synthesis
* Continuum of failure:
* Stress reaction – pathophysiological response
* Stress fracture – structural failure of bone tissue
95
Risk factors for stress fractures?
Type of exercise:
* Increased risk for running, track and field sports, basketball, gymnastics, and dance
* Harder training surface
* Footwear (there is only weak evidence that shoes play any role)Pegrum et al., 2012
Training regimen:
* Large spikes in training volume (e.g. mileage)
* Large spikes in training intensity (e.g. speed)
* Inadequate recovery/rest periods and training with fatigued muscles
96
What does healing look like?
Step 1: Injury Occurs
* Cartilage matrix disruption; limited
chondrocyte damage.
Step 2: Inflammation
* Minimal inflammatory response due to avascularity.
Step 3: Chondrocyte Activation
* Chondrocytes near the injury attempt minimal repair; low cell division.
Step 4: Fibrocartilage Formation
* In full-thickness injuries, progenitor cells from bone marrow form fibrocartilage.
Step 5: Poor Remodelling
* Fibrocartilage remains; limited structural integration; weaker tissue forms.
97
Why is healing limited?
Cartilage is avascular, so no natural bleeding; techniques like
microfracture induce controlled bleeding to recruit cells for repair.
Minimal inflammation occurs, limiting natural repair signals and
increasing susceptibility to degeneration.
Mesenchymal stem cells (MSCs) proliferate and form
fibrocartilage rather than durable hyaline cartilage; tissue engineering aims to support better cartilage formation.
Fibrocartilage deteriorates under stress; stem cells, scaffolds, and gene therapy target improved integration and longevity.
98
What are the types of meniscus tear?
Outer One-Third (Vascular
Zone):
* Higher healing rates due to good blood
supply.
Central One-Third (Avascular
Zone):
* Lower healing rates; limited healing
potential.
99
What is a massage?
It is a scientific manipulation of soft tissue. Swedish techniques involving hands producing mechanical pressure. Focus on holistic therapeutic goals.
100
What are the effects of massage?
It helps reduce pain, soreness, physiological and psychological.
101
What are the limitations of a massage?
Cannot directly improve physical performance.
102
How does massage work?
There are various skin receptors: merkel discs (light touch), pacinian corpuscles (deep pressure), and meissner's corpuscles (rapid touch). Nerve types and their roles.
103
What is muscle tone?
A state of continuous passive partial contraction. Combination of muscle spindles and central nervous system. Massage stimulates the CNS reducing muscle tone.
104
What is the lymphatic system?
transports larger molecules capillaries can't (infections etc). Pumps proximal to distal. Basis for massaging proximal to distal.
105
What are the key points in massage?
Mechanical pressure from massage stimulates the skin. Skin receptors, muscle spindles and vessels respond to this stimulus.
106
What is the role of the nervous system?
Reflex, involuntary actions in response to stimuli (touch). Autonomic nervous system (ANS) has sympathetic nervous system (active, fight-or-flight), and parasympathetic nervous system (rest-and-digest). Massage = input. Dampen overactive signals via the CNS.
107
