What is the aim of core stability?

The aim of core stability training is to learn how to effectively recruit the deep trunk musculature and then to control the position of the lumbar spine during dynamic movements (like a squat).

TVA

Lumbar multifidus

Internal oblique

Pelvic floor

Diaphragm

Medial fibres of QL

The co-contraction of all these babies produces stability via two main mechanisms:

1) Force production via thoracolumbar fascia (TLF) creating tension and stability posteriorly

2) Increasing intra-abdominal pressure (IAP) stabilising the spine

The TLF can provide tensile support to the lumbar spine via deep trunk muscle activity. The TVA and internal oblique both attach to the thoracolumbar fascia which wraps around the spine connecting the deep trunk muscles to it.

When the TVA contracts it creates an increase in tension in the TLF which in turn, transmits a compressive force to the lumbar spine which enhances stability.

The increased tension of the TLF compresses the erector spinae and multifidus muscles, which encourages these to contract and resist spine flexion forces (Lewis et al, 2000)

The IAP mechanism can provide a supportive effect to the lumbar region as the co-contraction of the pelvic floor, diaphragm, TVA and multifidus increase IAP. This results in a tensile force being exerted on the rectus sheath (rectus abdominus) which adds to this effect.

The 'supported bag of air' effect reduces compression and shear forces acting on the spine. Research shows that IAP increases before and during lifting heavy objects e.g. weightlifting.

Vertebro basiliar insufficiency symptoms

Dizziness

Drop attacks

Diplopia

Dysphagia

Dysarthria

Nystagmus

Nausea

Shift of the mediastinum

In a couple of the CRAM case studies for my exam there are reports from a CXR of a shift of the mediastinum to either left or right.

I've now found out what the most common cause for this is, pneumothorax (collection of air in the pleural cavity). However there are different types of pneumothorax and each one causes a shift in a different direction. Here's why...

TENSION PNEUMOTHORAX

Usually occurs as a result of trauma (e.g. a stab wound) and results in an accumulation of air under pressure in the pleural cavity. The wound (or opening) acts as a 'one way valve' allowing air in to the thorax but not out.

In this case the mediastinum would shift AWAY from that area (e.g. if it was a left lung tension pneumothorax the mediastinum would shift to the right). This is due to pressure gradients and the fact that it's encourage to move from an area of high pressure to low pressure.

SPONTANEOUS PNEUMOTHORAX

PSP (primary) refers to those without chronic lung conditions

Secondary refers to those with underlying lung disease

In this case the lung would collapse but there's no 'one way valve' effect letting air in and not out. Therefore the pressure on the side of the collapse is lower than the contralateral side...meaning that the mediastinum shifts TOWARDS the collapsed lung!

Meninges - Membranes surrounding the brain and spinal cord

Dura Mater - Outermost layer

Tough, inflexible and 'leather like'.

Lines the inside of the skull where it's attached to the bones.


Arachnoid mater - Middle layer (separated from the pia mater by the subarachnoid space)

Delicate spider-web like structure

Attached to the inside of the dura

Surrounds the inside of the brain and spinal cord
(aracnoidea encephali & spinalis)


Pia mater - Delicate innermost layer

Thin / mesh like

Closely envelops entire surface of brain

Runs down fissures of the cortex

Supplies brain tissue with blood vessels



Subarachnoid space - Between arachnoid mater and pia mater is the CSF which absorbs and disperses excessive mechanical forces that might otherwise cause serious injury. It's produced by the choroid plexuses in the lateral ventricles and drains into the dural venous sinus into the internal jugular vein.

Slump Test

1) Patient sits with thighs fully supported on plinth / hands clased behind their back

2) Patient is instructed to slump shoulders towards groin

3) Physio applies gentle over pressure to this trunk flexion

4) Patient adds cervical flexion / maintained by therapist

5) Patient performs unilateral knee extension / active dorsiflexion

6) Patient is instructed to extend neck. If cervical extension causes a decrease in symptoms this is a +ve finding indicating ABNORMAL NEURODYNAMICS

TIA

TIA = transient ischaemic attack

Briefl focal loss of function with full recovery occuring in 24hrs

5-10% of people who experience this will go on to have a stroke.

STROKE

A stroke is also known as a CEREBROVASCULAR ACCIDENT (CVA)


It usually results in HEMIPLEGIA (paralysis to one side of the body) which is contralateral to the side of the brain in which the lesion occurs e.g. stroke on L = hemiplegia on the R

An interruption of blood flow to the brain leaves the patient with a focal loss of function of varying severity.

Motor deficit is the the most common but other neurological deficits can include:

• Visual
• Perceptual
• Sensory
• Communication
• Swallowing

84% of strokes are ISCHAEMIC in origin

• Cerebral thrombosis (mainly affects older population with Hx of high cholesterol)

When a thrombus (blood clot) develops in a cerebral artery (usually one affected by atherosclerosis)

• Emobolic (mainly affects those with heart disease/previous heart surgery)

When a clot forms elsewhere in the body and becomes lodged in a cerebral artery

16% of strokes are HAEMORRHAGIC in origin

Major Risk Factors:

• Hypertension
• Raised cholesterol
• Cardiac disease
• Diabetes
• Smoking
• Atherosclerosis

Minor Risk Factors:

• Obesity (too much Maccie Dees!)
• Physical inactivity (being a lard arse!)
• Contraceptive pill (use a condom!)
• Excessive alcohol consumption ('boozing'!)

http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/neurology/ischemic-stroke/

ISCHAE

Finding the culprit

Yesterday's physio session at Ox city after the game revealed a new lesson after discussion with Leigh.

Player comes in complaining of tightness in anterior proximal thigh.

Q. Which muscle is it?

Process: Think what's likely to be tight in footballers? Running. What muscles originate from that area?

A. Narrowed it down to rec fem and sartorius. You had to palpate deep but resisted isometric strength test for sartorius came out on top. Resisted hip flexion did not.

The process of elimination!

I was helping out at Ox city footy club again earlier this week and we came across an acute adductor strain. When trying to diagnose which adductor muscle it was I was given a handy tip by Leigh:

"it's easier to cross off all the one's it's not than try to immediately pick which one it is"

Turned out to be adductor magnus after I'd originally guessed gracilis. When I thought about it, you could quickly cross off pectineus and brevis because they're only one joint muscles and much higher up than where the patient was complaining. Longus potentially but the magnus 2 heads:

Oblique head
ORIGIN: inferior ramus of pubis & ischial ramus
INSERTION: gluteal tuberosity, linea aspera, proximal supracondylar line of femur

Vertical head (hamstring head)
ORIGIN: ischial tuberosity
INSERTION: adductor tubercle

Remember that anatomically speaking the oblique head FLEXES & ADDUCTS the thigh @ hip
(much like pectineus) and the vertical head EXTENDS thigh at hip (like a hamstring!)

The important thing to remember though is that these muscles work differently in function, but that's for another day.

Bronchiectasis

Classed as an obstructive lung disease in which there's localised irrevisble dilation of the bronchial tree.

Involved bronchi DIE! ... By which I mean the bronchi are:

DILATED
INFLAMMED
EASILY COLLAPSIBLE

This results in:

• Airway obstruction
• Impaired clearance of secretions

http://www.youtube.com/watch?v=zMKaJEgmTT4

Causes:
Necrotizing (flesh eating) bacterial infection

S&S:
Look for frequent GREEN/YELLOW SPUTUM
Smell for bad breath
Productive cough

Frozen Shoulder aka Adhesive Capsulitis

Mr. Francis Lam is an upper limb surgeon and shoulder consultant, he gives some really great explanations on frozen shoulder in a simple easy to understand way.

Q. What is frozen shoulder?
A. Essentially a chronic fibrosing condition in which fibroblast cells become overactive and lay down abnormally thick layers of collagen causing marked thickening of the shoulder joint capsule. The capsular lining of the joint subsequently contracts and leads to shoulder joint stiffness and pain.

Q. What are the features of frozen shoulder?
A.

• Slow onset of pain felt near insertion of deltoid
• Trouble sleeping on affected side
• Restriction in both active and passive elevation & external rotation

Q. What's the difference between primary and secondary frozen shoulder?

http://www.shoulderspecialist.org/Frozen_Shoulder.html

See also Bowen technique

ABG's Normal Values

Interpreting ABG's is an important especially if working in a respiratory setting, but to recognise abnormalities you need to know the normal values of blood gases.

pH - 7.35 - 7.45

pCO2 - 4.7 - 6.0 kPa (35-45 mmHg)

pO2 - 11 - 14 kPa (80-100 mmHg)

HCO3 (bicarbs) - 22 - 26 mmol/l

BE (metabolites) - +2 - -2

BELIEF

I'd like to share something that isn't strictly physio related, but in this context involves it.

"Hello it's Thursday the 19th, it's the day after the viva exam and was there any point in worrying? Not at all."

Were my first words that I said on a recording of myself made about a week before my PAM 2 viva exam. I go on to speak about how I was comfortable and settled in very quickly, had an answering for every question, was able to elaborate on every question and that it went better than I thought it would and I had expected it to go well. Also that movement analysis was easy and was just a case of looking and working it out.

I had realised and taken action on the insight about BELIEF and visualisation. The more vivid, the more real, the more tangible you can make it the more likely it will become your reality.
I was constantly thinking and visualising myself doing well, not just well but great! Thoughts enterred my head during this with comments such as "come on, that's not realistic", "you can't really think that, it doesn't happen". But I just suspended those thoughts and accepted that it's just conditioned thinking and not a part of me. Like Tony Robbins advised, I dared to be powerful beyond measure. Or to put it more accurately, beyond expectation. My own expectation to be precise.

If you want to do something that nobody's ever done, that you've never done and/or that you think you can't do. DON'T EVER PUT A LIMIT ON YOUR DREAMS! That is your power! No one can tell you not to dream big, no one can stop you and for every person that says "it's just not realistic" (including yourself) shut them the fuck up! Like Will Smith said, "it's not realistic that somebody could walk into a room flick a switch and light would appear, that's not realistic". Thomas Edison didn't think so. "It's not realistic that someone can mould metal into an object and design it so that it can fly across oceans, that's unrealistic". Fortunately the Wright brothers and others didn't agree with that. Every great moment, every achievement that's wowed and surprised the world and made history has occured as a result of somebody saying "NO!" to thinking realistically and "YES!" to daring to dream, visualise and act upon creating something never done before, something incredible in their eyes.

Reality matched my voice recording to the letter by the way. To the absolute letter and I now have even more belief that the level we vibrate at, that energy you feel when you think of an idea or something you want to do that gets you so excited is sending out a signal to the universe that then conspires to assist you in making that a reality. If this sounds stupid to you, I don't care because it's worked for me on many occasions now and it seems like the more in tune I get with it, the better the results.

My advice to you is this. If you want to do something, be something, reach your goals and dreams start living them in your mind. Really living and experiencing them! If you get a thought that tells you to pull the reigns back because you're getting a bit to ambitious dream even bigger! Great moment are created when beyond achieve things beyond their own expectations of themselves. So work your imagination and stretch it as far as it will go and with action you'll go far :)

Colle's Fracture

Fracture of the distal radius in the forearm with posterior displacement of the wrist

Clincally reffered to as 'dinner fork deformity' due to the resultant shape of the forearm

Usually caused by falling onto outstretched hands (falling on flexed wrists would cause a Smith's fracture)

Common fracture in people with osteoporosis

Enthesopathy

Refers to a disorder which affects the the point at which a ligament or tendon attaches to the bone!

Radiculopathy ?

A radioculopathy is a condition due to a compressed nerve in the spine that can cause: pain, numbness, tingling or weakness along the course of the nerve.

Radiculopathy can occur in any part of the spine but is usually most common in the lumbar and cervical regions.

Occurs due to nerve root compression and results in dermatomal loss of sensation, myotomal loss of motor recruitment and disturbance of spinal reflexes

ULTT2B

For radial nerve (that can also mimic the symptoms of tennis elbow)

You do this one facing the feet!

• Shoulder Depression
• wrist flexion and pronation
• elbow extension
• shoulder medial rotation
• then abduction (LAST!)

Contraindications to ultrasound

DOC-P (2's and 3) MINS-U (1's)

D1 - Deficient sensation (will be unaware if unstable cavitation is occuring resulting in burns)
D2 - DVT in treatment area (could become dislodged and cause pulmonary embelism)
O1 - Over spinal cord after recent spinal surgery (unstable cavitation in CSF)
O2 - Over pelvis or abdomen during menstruation or pregnancy
C1 - Compromised circulation (vessels can't deal with excess demand)
C2 - Cancer (irradiated tumours grow larger and heavier)
P1 - Physio untrained
P2 - Peripheral vascular disease (tissues can't cope with excess metabolic demand)
P3 - Previous deep x-ray therapy (radiotherapy)

M - Metal or plastic implants (cause more standing waves)
I - Infection in treatment area
N - No consent
S - S.E.G Skull, eyes, gonads
U - Unknown diagnosis

ULTT1

ULTT1 - all 3 major upper limb nerves are stretched with a median bias

• Stabilise scapula by depressing shoulder
• Abduct shoulder 1st
• Supinate
• Extend wrist and fingers
• Laterally rotate
• Extend elbow

Apply each one fully and check if the patient's alright before progressing to the next movement.

Be aware of your posture and ELITE

Inform the patient of what you're looking for, for them to not adjust their position as it will effect the results of the test and may produce a false positive and to inform you if they feel any pain or parasthesia

No pillows

Make sure patient is positioned properly on plinth so arm doesn't fall into horizontal extension or not enough room for abduction

ANT - Adverse Neural Tension

Also known as AND (adverse neurodynamics) and AMT (adverse mechanical tension) but all basically mean the same thing.

They all describe the process whereby neural tissue is compromised and looses its ability to fully lengthen leading it to be unable to conform to changes in limb and or trunk position.

The 3 mechanisms nerves conform to positions are:

1) Sliding across mechanical interface (bone, muscle, fascia etc)

2) Unwinding of a nerve

3) Becoming stretched and therefore increasing their internal and external tension

In a nutshell, if mechanism 1 and 2 become compromised, mechanism 3 is greatly increased!

• ANT can be used to both diagnositcally test (assess) and treat neural problem

Carpal tunnel syndrome

Carpal tunnel syndrome, or median neuropathy at the wrist, is a condition where the median nerve is compressed at the wrist. This leads to paresthesias (pins & needles) and muscle weakness in the hand. Night symptoms and getting woken up is also something that from your subjective assessment would be ringing bells to test for carpel tunnel syndrome. But what are these "tests" you speak of??

The median nerve sits between flexor digitorum profundus and flexor digitorum superficialis

Phalen's Test

This position reduces the size of the carpal tunnel, so if you did

have it, the symptoms would be aggravated temporarily. A +ve

test would reproduce pain, numbness or tingling.

Tinnel's Test

Uses a tapping movements over the line of the median

nerve over the flexor retinaculum area.

You're looking for setting off the sensations of pin's and needles

Peripheral Vascular disease (PVD)

Peripheral vascular disease or PVD is a broad 'umbrella' term used to describe any disease (or pathology) which involves compromised circulation of the large arteries to the arms or legs due to obstruction.

It can result from:
- atherosclerosis
- embolism
- thrombus formation

Causes either acute or chronic ischemia to arms or legs

Beat frequency

"The beat frequency is the resulting low frequency at the cross over point of 2 medium frequency currents"

E.g. If the current at at electrode A is set at 4100 Hz and 4000 Hz at electrode B'

the beat frequency will be 100 Hz and therefore target Abeta fibres (high frequency, low intensity)

Hyperalgesia & Hyperesthesia

Hyperalgesia = An increased sensitivity to pain, may be caused by damage to nociceptors or peripheral nerves. Hyperalgesia also occurs as part of the evolved response to infection and as part of sickness behaviour

Hyperesthesia = a condition that involves an abnormal increase in sensitive stimuli of the senses (hear,touch,taste etc). Increased touch sensitivity is known as 'tactile hyperesthesia' and increased sound sensitivity is known as 'auditory hyperesthesia'.

Aetiologies leading to GH impingement

Well for starters let's remind ourselves that aetiology is 'the study of the causes'!

Aetiologies for glenohumeral impingement can be divided into primary (direct cause) or secondary (indirect cause)

Primary

• Subacromial bursal thickening
• Increased subacromial loading
• Trauma (direct macrotrauma/repetetive microtrauma)
• Excessive overhead activity (too much waving to someone)
• Acromioclavicular arthrosis (osteophytes)

Secondary

• GH laxity/instability (note: laxity may be normal for some people)
• Muscle imbalance
• Scapula dyskinesia (difficulty or distortion in performing voluntary movements)
• Glenoid labrum lesions (joint will be less stable if the socket depth is decreased)

Arthroscopy?

A minimally invasive surgery used to either examine and/or treat the damage the interior of a joint, performed using an arthroscope.

Arthroscopic procedures can be used to evaluate or to treat many orthopaedic conditions such as: floating cartilage, torn surface cartilage, ACL reconstruction, trimming damaged cartilage.

'RESPIM' a sure fire way to stimulate Abeta fibres ;)

'R' is for

Rub

'E' is for ...

Exercise (high intensity cardiovascular exercise/that stimulates proprioceptors)

'S' is for

Sweeping...synovial sweeping that is

'P' is for Passive movements / accessory

movements

'I' is for

Interferential treatment














'M' is for


Massage

Pseudo & True Winging which causes which?

PSEUDO WINGING = Tight pec minor / weak LF traps

TRUE WINGING = Weak serratus anterior

"Oh and thanks Colonel Sanders...too bad most of it's pigeons with aids"

Grimsby's 3 stage program - instability rehab

Stage 1 - low speed, high reps, minimum resistance, beginning and middle range

- to increase muscle endurance and circulation whilst avoiding overexertion

Stage 2 - increasing resistance, add in isometrics in inner ranges

- designed to increase strength and sensitivity to stretch

Stage 3 - Continue to increase resistance (usually 80% 1RM) and add isometrics through a full but not maximal range

Barkark or Bankart lesion?

An injury of the anterior glenoid labrum due to repeated anterior shoulder dislocation.

It's an indication for surgery and often accompanied by a Hill-Sachs lesion, damage to the posterior humeral head

Tennis elbow

A condition characterized by pain and tenderness on the outside of the elbow and in the back of the forearm. Its medical name is lateral epicondylitis.

Tennis elbow is caused by inflammation of the tendon that attaches the extensor muscles (in this case the muscles that straighten the fingers and wrist) to the humerus. The condition results from overuse of these muscles, causing constant tugging of the tendon at its point of attachment to the humerus.

Causes

Tennis elbow may be caused by playing tennis or other raquet sports with a faulty grip, but more commonly due to other activities such as gardening, manual labour (screwdriving).

Treatment

- Ultrasound

- RICE

- NSAIDS

- corticosteroid injection

- surgery to release the tendon

If it keeps recurring it's wise to take a break for a couple of weeks from raquet sports to see if that's definately what's causing it and then if it is seek professional advice is playing technique and equipment.

Tenosynovitis

Inflammation of the thin inner lining of the sheath that surrounds a tendon. Tenosynovitis is usually caused by excessive friction due to overuse; it is often brought on by working in an awkward position to do a job that involves repetitive movements. A reare cause is bacterial infection. Tendons in the hand and wrist are most commonly affected.

Symptoms

- Pain

- Tenderness

- Swelling over the tendon

- Occasionally crepitus

- Persistent recurrent tenosynovitis may lead to restricted movement as a result of the formation of adhesions (fibrous bands) between the tendon and its sheath.

Treatment

If infection is the cause, antibiotic drugs. Otherwise, treatment is usually NSAIDS, corticosteroid drug injection around the tendon. The hand and wrist may need to be immobilised in a splint for a few weeks. If the condition does not improve, surgery may be required to release adhesions.

Contraindications to massage

1. Open wounds

2. Muscle ruptures

(In the acute stage these may still be bleeding. Massage will increase bleeding and tissue damage at this stage and prolong recovery. After the initial 0-72 hrs of acute phase massage may be possible but depends on extent of injury)

3. Tendon ruptures

(Complete ruptures will require surgery not massage. The above also applies)

4. Contusions

(These are impact injuries within the muscle - intramuscular - Massage to a contusion may cause further damage and possibly bone growth within the muscle aka myositis ossificans)

5. Burns, chillblains and broken bones

6. RA and gout

(These are active inflammatory conditions, so massage may cause further inflammation)

7. Bursitis

8. Myositis Ossificans

9. Infections of skin and soft tissue

(Bacterial, viral, fungal infections can be spread to other areas of the body)

10. DVT (thrombosis)

(If dislodged can lead to pulmonary embelism, heart attack, stroke)

11. Artificial blood vessels

(Implanted through surgery should be avoided)

12. Bleeding disorders such as heamophillia

(May cause tissue damage and further bleeding)

13. Tumors

14. Anything else you're not sure of!

Shoulder Impingement

Impingement in the shoulder is a pathology that occurs when a structure (inert or contractile) becomes trapped between the acromion and the humeral head).

2 main types: SUB ACROMIAL (supraspinatus tendon or subacromial bursa)

CORACO HUMERAL (long head of biceps or subscapularis tendon)

Tests to determine impingement: 'Empty Can' test, Kinetic medial rotation test (KMRT) to differentiate between impingement and instability.

Impingement can result from a number of factors but it's important to remember to not just concentrate on the area of pain the patient presents but to look at the big picture (i.e. kinetic chain) as the pain may be resulting from dysfunction or imbalance elsewhere. It could be a postural habit, a muscle imbalance, trauma or a combination of other pathologies that have led to the impingement syndrome.

REMEBER! at the initial assessment cast your net wide!

Some things I learnt from PAM1 Summative Assessment

1. Greenstick fractures usually occur in immature bone (i.e. children)


2. Pathological fractures are normally a result of cancer and/or osteoporosis etc


3. When looking for problems with non-contractile elements, you'll get pain on passive, isotonic, active etc just NOT with isometric! Why? Because isometric is straining the soft tissues structures (i.e. muscle) and not stressing the joint!


4. Remember during gait there is a lot of eccentric muscle activity occuring so don't get stuck in the concentric mind frame!

Passive Movements

"Movements produced on a person by an external force (i.e. no voluntary muscle contractions by patient) provided either by a person or a machine (CPM)"

Sub-divided into:

• Physiological passive movements (mobilisations)
• Accessory movements (mobilisations) - Glides,Rolls,Distractions,Compressions,Rotations (cannot be performed actively)
• Passive stretching (mobilisations)
• Adverse Neural Tensioning (ANT)
• Manipulations

Structures Involved:

• INTRA-ARTICULAR: subchondral bone; articular cartilage, synovial fluid, synovial membrane, menisci and fat pads
• PERI-ARTICULAR: joint capsule, supporting ligaments, tendons, muscles, fascia, skin, blood & lymphatic vessels, nerves

Normal Restrictions to Joint ROM:

• Joint capsule
• Ligaments
• Muscles & their tendonous attachements (active/passive insufficiency)
• Bone/cartilage approximation i.e. shape and joint surface (loose packed,closed packed)

Abnormal Restrictions to Joint ROM:

• Increased synovial fluid volume/pressure
• Muscle imbalance
• Mal-tracking
• Trauma
• Abnormal physiological changes in connective tissue due to immobilisation
• Decrease in water in tissue matrix = abnormal points of collagen cross-linking - 'adhesions'
• Atrophy of ligaments
• Tendons degrade
• Muscle contractures
• Nerve tensioning
• Synovial tissue atrophy
• Pain/guarding mechanism (muscle spasm)

Beneficial Physiological Effects:

• Maintains ROM/Increases ROM
• Cartiliage healing/nutrition (hydrokinetic transport)
• Smearing of synovial fluid reducing friction
• Appropriate alignment
• Increases lymphatic drainage/helps reduce oedema

Indications

• Assessment of passive ROM
• Diagnostic testing
• Maintaining joint ROM in a paralysed or unconscious patient
• Reducing joint pain
• Reducing muscle spasm / guarding
• Restoration of range (correction of 'mal-tracking and/or passive stretching)
• Facilitates healing process

Limitations

• CANNOT CHANGE DISEASE PROCESS
• WILL NOT prevent muscle atrophy
• WILL NOT increase strength or endurance

Contractions

• Excessive pain
• Joints adjacent to unstable fractures
• DVT in area
• Infection
• Active inflammatory (R.A)

Range of Motion

• Direction of movement will depend on the desired efffect
• Amplitude of the passive movement can be graded to indicate where in the available range the technique is being performed
• Helpful in matching the induced range of P.M. to the desired mobilising effect depending on the irritiability of the lesioned structure

Maitland Grading Scale

• 1 - SMALL amplitude movement performed at the beginning of range (within resistance free zone)
• 2 - LARGE amplitude movement performed within a resistance free part of the range
• 3 - LARGE amplitude movement performed into resistance or up to the limit of resistance
• 4 - SMALL amplitude movement performed into resistance or up to the limit of resistance
• 5 - High velocity, short amplitude thrust often near or at the limit of abnormal movement, at speed outside of patient's control

Rationale For Proprioceptive Exercises

Is the exercise...

• Weight bearing appropriate?
• Reactive (external stimuli or not and are these varied in weight,size,shape if objects, speed, is the trainer or therapist the stimuli?)
• Goal driven?
• Functional? (e.g. sports specific)
• Base of support (wide, narrow, stable, unstable)
• Visual Stimuli or no visual stimuli (eyes closed or open?)
• Pace (slow or quick? Does it hit the slowly adapting and rapidly adapting proprioceptors?)
• Pertubation/Complexity?
• Multiplane/multiaxial?

Rationale For Strength Exercises

IS THE EXERCISE...

• Weight bearing appropriate? (NWB/PWB/FWB)
• With or against gravity? (e.g. gravity counter balanced or additional resistance - Oxford Scale)
• Functional?
• OVERLOAD (is the target muscle or muscle group being stressed enough to elicit an adaption?)
• SPECIFICITY (SAID - Specific Adaptions to Imposed Demands)
• Single plane or multi-plane? (is the muscle being loaded in all 3 planes?)
• Open or closed chain?
• Ranges? (through full ROM? Inner/Mid/Outer - appropriate to rehab level?)
• Isometric/eccentric/concentric (appropriate to stage of injury?)
• Motivational?
• Fun?
• Fibre recruitment (is it recruiting the fibres required for their function e.g. Type I, Type IIa/IIb slow and fast twitch)
• Intensity (high/med/low?)
• Reps & Sets? (endurance,hypertrophy,strength) avoid atrophy
• Isolated or intergrated? (compound/mutli-joint exercise or isolated muscle?)

Joint Classification (Smart Arse way of describing joints!)

KNEE - Modified bicondylar synovial joint
- 2 degrees freedom of movement (flexion/extension & ext/interal rotation)
- Conjunt rotation (external rotation) occurs during the last 30 degrees of extension to
achieve closed packed position (automatic/accessory movement)
- Adjunct rotation (physiological/voluntary) movement in flexion


ANKLE - Uniaxial hinge type synovial joint
- Between tibia/fibula and trochlea of talus
- Reinforced by fibrous capsule, medial deltoid ligament (4 parts), lateral ligament
(3 parts)
- 1 degree freedom of movement (dorsi/plantar flexion)


HIP - Multi axial ball & socket synovial joint
- Between acetabulum and head of femur
- Acetabular labrum deepens the acetabular cavity creating more stability
- Fibrous joint capsule reinforced by 3 ligaments
- 3 degrees freedom of movement (flexion/extension, ab/adduction, med/lateral rotation)


MTP - Multiaxial condyloid synovial joint
- Surrounded & strengthened by articular capsules and collateral ligaments
- 2 degrees freedom of movement (flexion & extension & ab/adduction)

Acute/inflammatory stage 0-72hrs

1) Damage to local blood vessels (capillaries), bleeding and cell death (trigger inflammation)

2) Local initial vasoconstriction (to limit fluid loss - but results in more cell death due to increased lack of oxygenated blood available at injury site)

3) Release of chemical mediators (histamine/serotonin etc) from dying cells causing VASODILATION or surrounding undamaged vessels, increasing their permeability, which can be seens as REDNESS (erythema) and felt as HEAT (calor) - permeability allows leukocytes to emigrate into site of injury guided by chemotaxis.

4) Damaged nerve endings give rise to pain (dolor), chemical irritation from mediators and increasing pressure from excess fluid and inflammatory exudate in the area (more responsible for pain in the later stages)

5) 'Walling Off' - Local vasodilation is not enought to prevent fluid loss so we get platelets activated by cell death (necrosis) become very sticky and release chemicals to activate the enzyme thrombin which converts fibrinogen (element of blood plasma) into FIBRIN which creates a sticky matrix to trap cellular debris and platelets to form a blood clot (temporary solution to fluid loss)

6) Leukocytes (neutrophils 6-24 hrs / monocytes & lymphocytes 24-48hrs) or white blood cells clear debris that wasn't caught by the sticky matrix and fight off an infection present.

7) Histamine causes local vasodilation within hours to introduce new plasma* rich blood for next stage of repair (each phase is laying the ground work for the next)

*Plasma = liquid portion of blood (90% water)

Internal anatomy of muscle fibres

• Sarcomere - The portion of a myofibril between two Z-discs

• Sarcoplasmic reticulum (SR) - Loose network of flattened tubules that surrounds the myofibrils in the muscle cell

• Transverse 'T' tubules - Invaginations of the sarcolemma that allow muscle action potentials (electrical chemical impulses) to pass into the centre of the cells causing depoloraization and release of calcium ions from the SR (run over and around the sarcoplasmic reticulum)

• Terminal Cisternae (lateral sacs) - Expanded regions of the SR, found on both sides of T tubules

• Calcium ions - concentrated in the SR when muscle fibre is at rest (flood out when muscle contracts)

• Triad - A T tubule and two terminal cisternae

General anatomy of muscle fibres

• Sarcolemma - the plasma membrane in muscle fibre

• Muscle fibres are multinucleotide - Being exceptionally wide and long, muscle fibres (0r cells) need many nuclei to regulate the metabolic demands of contractile proteins (e.g. actin and myosin)

• Sarcoplasm - The protein filled cytoplasm of muscle fibres

Tissue Proliferation (fibrous repair) 1-10 days + post injury - Pathophysiology

• Ongoing phagocytosis
• Angiogenesis
• Production of collagen fibres (initially produced in random fashion)
• Absorption of inflammatory exudate

Angiogenesis

FORMATION OF NEW BLOOD VESSELS

Factors influencing the rate of healing in the stages of proliferation and remodelling

• Severity of initial trauma: A severe second degree ligament sprain of the lateral ligament complex of the ankle will have a more prolonged proliferation and remodelling period than a first degree ligament sprain affecting the same structure.

• Early Management: When the necessary foundations have been set in place (e.g. protection, rest of tissues etc) for proliferation and repair can potentially reduce onset of chronic inflammation.

• Tissue Vascularity: e.g. skeletal muscle = highly vascular = more potential for repair than a a ligament = avascular

• Age: Younger people are quicker to heal than older

• Nutrition: e.g. protein deficiency, adequate nutrition that is also related to bloodflow is required for healing to take place

• Medication: Use of NSAIDS and steroidal drugs slow down proliferation and remodelling processes.

• Temperature: Colder it is = slower rate of healing

• Appropriate loading of healing tissue during rehab

EXUDATE - a definition

Material such as fluid, cells, cellular debris

(serous fluid, red blood cells, fibrinogen, tissue debris, white blood cell break down products)

which have escaped blood vessels and been deposited into tissues or on tissue surfaces, usually as a result of inflammation

EXUDATE (in contrast to transudate) characterised by high content of protein, cells or solid material

Intersitial Fluid / Hydrostatic Pressure

Interstitial Fluid

The fluid that bathes and surrounds the cells (intercellular spaces)

Composed of: water, sugar, salt, hormones, co-enzymes, fatty acids, amino acids, neurotransmitters, cellular products

Provides a means of delivering materials to the cells (intercellular communication), and removal of metabolic waste products.

Hydrostatic Pressure

The pressure exerted by fluid (e.g. water) at rest

Increases in direct proportion to the density and depth of the fluid

General physiotherapy aims of early-phase management (Bleeding & Inflammation)

Acute Phases 1 & 2 : Bleeding (0-10hrs) & Inflammation (72hrs)

The aims are:

• To reduce pain


• To limit and reduce inflammatory exudates


• To reduce metabolic demands of tissue


• To protect the newly forming tissue from disruption


• To promote new tissue growth and fibre alignment


• To maintain general levels of cardiovascular and musculoskeletal fitness / activity

'REDUCE, REDUCE, PROTECT, PROMOTE, LIMIT, MAINTAIN'