* BONES AND JOINTS

DISEASES

BY ALBERT MWENYA JR
OSTEOPOROSIS

- Onset is usually between mid-thirties and fifties.

- There is increased porosity, brittleness and rarefaction of bone.
- Thickening and softening of bone resulting in deformities.
- Thereafter, the bones recalcify and become harder. Bones most
commonly affected are the skull, pelvis, femur and tibia.

CLINICAL FEATURES
1. Vary.
2. Pain and aching in the limbs.
3. Muscle tenderness or cramps.
4. Deformities developing e.g. bow legs.
5. Fractures of the femur or tibia following minimal force.
6. OA.
7. Back pain may be present.

PHYSIOTHERAPY
1. To relieve pain and muscle tenderness and keep patient active.
2. Usually patients referred following fractures or OA of the hip/knee
joints.
OSTEOMALACIA

Due to deficiencies of vitamin D and inadequate calcium and phosphate absorption.

Calcium is withdrawn from bone to maintain blood level. Characterized by rarefaction
(i.e. losing density) of bone and thin cortex. Bone bends easily causing pain and
deformities. Pseudo-fractures occur in the ribs and scapula where blood vessels crossing
the bone dissolve it creating “looser’s bone”.

SIGNS AND SYMPTOMS

1. Bone pain.
2. Backache.
3. Muscle weakness.

TREATMENT
Vitamin D and phosphate doses.

COMPLICATIONS
1. Mal-absorption syndromes.
2. Pancreatic disease.
3. Colic disease characterized by diarrhea.
4. Renal failure.
OSTEOMYELITIS

ACUTE OSTEOMYELITIS

- This is an acute or chronic infection of bone usually caused by

“Staphylococcus Aureus”.
- The usual spread is by haemotogenous means or a compound fracture or from
a minor skin abrasion.
- In children the organisms settle in the metaphysis at the growing end of a long
bone. Common in children due to the good blood supply to the growing end
and the rapidly growing cells are susceptible. Also the blood vessels have
been injured and the haematoma is a suitable medium for bacterial growth.
PATHOLOGY
3 stages – suppuration, necrosis and new bone formation.
- Usually occurs in the medullary cavity where there is inflammation and pus
formation.
- This cannot expand, tension increases in the bone and pus is forced through the
Haversian canals to form a sub-periosteal abscess.
- This leads to the underlying bone losing its blood supply as it has pus on either
sides and so a segment of bone dies and separates to form a “sequestrum”.
- The raised periosteum makes new bone called “involucrum”.
- The abscess burst through the periosteum and forms a chronic sinus.
- The disease is chronic when the sequestrum is formed.
SIGNS AND SYMPTOMS
 1. Fever.
2. Malaise.
3. Pain.
4. Swelling may occur.
5. The limb is held still, may feel tender and warm.
6. There may be stiffness of a neighbouring joint.
7. X-rays are normal but may show pathology 3 weeks later when new bone is
laid down.

TREATMENT

1. Rest, splintage and elevation.

2. Antibiotics.
3. Drainage of pus.

PROGNOSIS
May become chronic or return to normal. A chronic condition is treated as an acute one
but sequestrectomy is also performed.

COMPLICATIONS

1. Extension of infection to the adjacent joint leading to pyogenic arthritis.

2. Septicaemia.
3. Arrest of growth with consequent limb shortening due to damage to the
epiphyseal cartilage.
4. Pathological fractures.
BRODIE’S ABSCESS

Form of chronic osteomyelitis found in the tibia over the tibial tubercle. It has no
preceding acute attack. Treated by sequestrectomy.

Chronic osteomyelitis
 RHEUMATOID ARTHRITIS

DEFINITION: This is a non-supparative, systemic inflammatory disease

characterized by a symmetrical polyarthritis affecting peripheral joints and extra-articular
structures. Usually chronic with exacerbations and remissions.
AETIOLOGY
Affects women more than men usually in the 20 – 55 year age group. The cause is
unknown but is related to a disturbance of the auto-immune system whereby a
rheumatoid factor (RF) is found in the blood serum and synovial fluid of 80% of the
patients.
Some theories as to the cause are:

1. INITIATING FACTOR THEORY: Some initiating factor causes joint

inflammation which does not stop after the acute episode.
2. INFECTIOUS THEORY: e.g. viruses of rubella, herpes zoster or
mycoplasms may be responsible.
3. GENETIC TENDENCY: Relatives of RA patients have a tendency of
developing the diseases than others.
PATHOLOGY
- The synovial membrane is thickened by chronic inflammatory changes.
- Folds are formed in the membrane called “villi”.
- The membrane grows along the joint margins forming a pannus (membrane
produced by exudate overlying synovial cells) from which proteolytic
enzymes are produced which erode the joint cartilage at the joint margins and
NWB areas initially, later spreading to the remaining cartilage and articular
surfaces.
- The erosion of the sub-chondral bone leads to joint subluxation and deformity.
- Excess synovial fluid which contains fibrin leading to joint stiffness and later
fibrous ankylosis.
- The bones become osteoporotic and muscles atrophy.
- There is nodule formation (in areas of pressure, in the heart and lungs) and
inflammation of the tunica intima of arteries and sometimes spleen
enlargement.
- Synovial lining of tendon sheaths in the hands and feet may also be inflamed
and thickened and the contained tendons become soft and may rupture leading
to deformities.
CLINICAL FEATURES

1. Usually the patient is young or middle-aged adult, women more than men.
2. Usually affects peripheral joints – hands, wrist, feet, knees and elbows.
3. Gradual onset with increasing pain and swelling of a joint spreading to other
joints.
4. Pain and stiffness worse after resting.
5. Constitutional disturbances with tiredness and anaemia, fever.
6. Affected joints are swollen and warm with reduced and painful ROM.
7. Characterised by exacerbations and remissions.
8. Deformities: Boutonniere and Swan Neck in the hands. Wrist flexion and
ulnar deviation, knee flexion and valgus deformity, elbow flexion. Shoulders
and hips usually have flexion and adduction deformities. Atlanto-axial joints
subluxation may occur leading to neurological symptoms.
9. Pericarditis in some patients.
10. Pleurisy, pleural effusion and pulmonary fibrosis may occur.
11. Eyes may be inflamed.
COMPLICATIONS
1. Septic arthritis
2. Amyloidosis
 1. Osteoporosis
2. Atlanto-occipital subluxations

INVESTIGATIONS
1. X-rays initially show no changes but later diffuse rarefaction in the joint area.
Eventually there is narrowing of the cartilage space and in severe cases,
localized erosion of the bone ends.
2. ESR is raised during the active phase. RF factor in blood indicates a poor
prognosis.

DIAGNOSIS
Clue to diagnosis is simultaneous involvement of several joints with raised ESR.

COURSE
Tendency for the disease for remission after being active for months or years. Most cases
have permanent joint function impairment. Deformities and severe disability may result
even though the original infection is quiet.
TREATMENT
No cure and management is palliative and aims at achieving maximum functional
capacity. Also depends on the stage and severity of the disease.

1. THE ACUTE STAGE

The patient is in hospital.
AIMS
1. To relieve pain and muscle spasm.
2. To prevent deformity and maintain ROM at unaffected joints.
3. To maintain muscle strength.
4. To prevent respiratory or circulatory complications.

1. Rest on a firm bed with boards under the mattress, no pillows under the knees
and only one pillow for the head at night. During the day a firm back rest
with minimum number of pillows is used to maintain good posture.
Encourage patient to lie flat for 1 hour daily to avoid contractures.
2. Splints worn all the time to prevent deformity and encourage relaxation and
rest.
3. Isometric contractions of the muscles crossing the affected joints as the
inflammation reduces (3-4 contractions twice daily). Assisted active
movements to the unaffected joints and breathing exercises.
4. When patient is allowed up, balancing in high sitting, standing is
practiced and a walking aid is given.
2. THE SUB-ACUTE STAGE
This is a period of reduced activity in the disease but movement can cause a flare-up of
the disease.

AIMS
1. To prevent further exacerbations.
2. To correct deformity.
1. Cold therapy to reduce pain and swelling in joints.
2. Wax for the hands.
3. SWD/hot packs/IR for residual pain.
4. A home programme consisting of mobilizing and strengthening exercises to
be done fives times daily.

3. THE CHRONIC STAGE

AIMS
1. To prevent joint contractures.
2. To improve joint range.
3. To improve muscle power.
4. Correct posture.
5. Retrain function.

1. Exercises to maintain joint range and muscle power. Heat to reduce pain.
2. Posture correction.
3. Splints to maintain optimum position and aids for eating, dressing, mobility
aids.

SURGERY

1. SYNOVECTOMY: Removal of synovial membrane to reduce pain and

swelling and may arrest the disease.
 1. OSTEOTOMY: Division of bone near a joint to realign the bone and alter
the weight distribution.
2. ARTHROPLASTY: Joint replacement.
3. TENDON REPAIR: Where extensor tendons of the fingers have ruptured.
4. ARTHRODESIS: Fixing of a joint permanently to relieve pain and improve
function.

DRUGS
1. Analgesics
2. NSAID’s
3. Gold
4. Corticosteriods
 TUBERCULOUS ARTHRITIS

CAUSE
Infection of joint by tubercle bacilli and is commonly contracted from another
person with open pulmonary TB. Large joints are mainly affected such as hips,
knees, ankles, elbows, vertebral joints in the thoracic and lumbar spine.

PATHOLOGY
 The organisms reach the joint via the blood stream from a primary focus
elsewhere.
 Synovial membrane is thickened by the tuberculous inflammatory reaction.
 If the disease is not stopped, the articular cartilage is destroyed and the
bone is eroded.
 Sometimes the infection begins in the adjacent bone to a joint and then
extends into the joint by direct continuity.
 An abscess is formed and this moves to the skin surface and may rupture
giving rise to a chronic tuberculous sinus. This is a “cold” abscess.
 If healing occurs before the cartilage and bone have been damaged, joint
function is restored to nearly normal otherwise permanent impairment or
even complete loss of function result.

CLINICAL FEATURES
1. Children and young adults commonly affected.
2. Pain.
3. Swelling.
4. Impaired function.
5. General ill health.
6. Reduced joint range.
7. Muscle wasting over the affected joint.
8. An abscess or sinus is often apparent.
9. A tuberculous lesion in some other part of the body.
INVESTIGATIONS
1. Raised ESR.
2. Positive Mantoux test.

COMPLICATIONS
1. Sinus formation.
2. Secondary infection through a sinus track.
3. Spread of disease.

TREATMENT
1. Anti-tuberculous drugs e.g. rifampicin, isoniazid, streptomycin,
pyrazinamide in a combination for 6-9 months.
2. Rest in a POP or splint in the early stages to relieve pain and allow
healing. Splintage should continue for 2-4 months.
3. Aspiration of the abscess.
4. Physiotherapy when the disease is quiescent and on doctor’s consent.
Isometric contractions given in POP/splint. Later only active exercises
– passive movements are contra-indicated.
5. If the disease progresses, fusion may be necessary.
TUBERCULOSIS OF THE THORACIC OR LUMBAR SPINE (POTT’S
DISEASE)
Most commonest forms of skeletal TB.
PATHOLOGY
 Infection begins in the anterior margin of a vertebral body near the intervertebral
disc, which is usually involved.
 Usually there is complete destruction of one intervertebral disc with partial
destruction of the 2 adjacent vertebrae – mostly anteriorly.
 Anterior collapse of the affected vertebrae leads to an angular kyphosis –
“Gibbus”.
 Abscess formation is usual.
 An abscess or mass of granulation tissue may compress the spinal cord (or spinal
nerve) leading to weakness an numbness in the lower limbs i.e. paraplegia.
CLINICAL FEATURES
1. Commonest in young adults.
2. Pain in the back and stiffness.
3. Visible deformity of the back.
4. Localised swelling (abscess).
5. Weakness of legs or visceral dysfunction.
6. Ill-looking with tenderness over the affected vertebrae.
7. Restriction in spinal movements and muscles go into spasm if movement is
attempted.
COMPLICATIONS
1. A chronic discharging sinus.
2. TB of other organs.
3. Spinal cord interference leading to weakness or paralysis in the lower limbs.

TREATMENT
 Early onset paresis is treated by anterior decompression and debridement
followed by spinal fusion. About 80% recover within a few weeks.
 Antibiotics.
 Rehabilitation begins after the 8th week of bed rest up to independence.
The general health is improved by a good diet, light graduated exercises
and plenty of fresh air.

PHYSIOTHERAPY
Bed activities may start 8 weeks after onset of bed rest when the surgeon allows the
patient to sit up. Stretching of the limbs, positioning, stabilizations, ADL, transfers, mat-
work and gait training are all encouraged.
CONTRA-INDICATIONS
Since the condition affects the thoracic spine, no passive movements above 90 degrees in
the lower limbs. Not straight leg raise above 90 degrees and no trunk rotation.
NB: Encourage prone lying to counteract flexion deformities.

PROGNOSIS
Depends on the general condition of the patient and severity of the disease.
HAEMOPHILIC ARTHRITIS

There is a deficiency of Factor VIII leading to an inability of the blood to clot. Males are
affected, mother is the carrier.
PATHOLOGY
 Bleeding into joints may lead to haemarthrosis.
 There is joint degeneration following repeated bleeding, the cartilage degenerates
with resultant narrowing of the joint space.
 Bony erosions appear and eventually the joint becomes deformed, unstable and
stiff.
 Usually the knees, elbows and ankles are affected.
 Fibrosis of synovial membrane occurs.
 In between attacks of haemarthrosis, there is moderate thickening of the joint
from synovial fibrosis, movements are slightly reduced and usually a small fixed
deformity e.g. knee flexion.
CLINICAL FEATURES
1. Pain
2. Warmth
3. Swelling
 1. Tenderness
2. Loss of joint range
TREATMENT
Blood transfusion or plasma with Factor VIII.
Arthritis treated by:
1. Rest and splintage.
2. Analgesics.
3. Blood aspiration.
4. Joint replacement surgery.

PHYSIOTHERAPY
1. Movement starts when bleeding stops.
2. Mobilising and strengthening exercises progressing slowly.
3. Hydrotherapy.
GOUT

This is characterized by increased uric acid in plasma and recurrent attacks of acute
synovitis due to sodium urate crystal deposition.

AETIOLOGY
ACUTE
30 –50 years commonly affected, men more than women. There is a family tendency.
Diet, as well as alcohol, influences blood uric acid values.

PATHOLOGY
 The high concentration of blood uric acid causes deposition of urate crystals in
synovial membranes, sheaths, articular cartilage and subcutaneous tissues.
 These crystals are called “Tophi” and cause acute inflammation.
 In joint structures, there is increased synovial fluid production causing synovitis.
 Commonly the first signs appear in the MTP joint of the big toe.

CLINICAL FEATURES
1. History – recurrent synovitis with remission.
2. Joints involved – MTP joint of big toe, ankles, knees, wrists and hands.
 NEUROPATHIC ARTHRITIS

Appreciation of pain and joint position sense is diminished – thus there is no reflex to
protect against injuries and a rapidly progressive degeneration of joints results. The
underlying causes include conditions such as:

1. Tabes Dorsalis
2. Diabetic Neuropathy
3. Cauda Equin lesions
4. Leprosy
5. Peripheral neuritis.

SIGNS AND SYMPTOMS

1. Painless swelling (Charcot joint).
2. Joint instability due to lax ligaments.
3. Signs of the underlying neurological disorder.

TREATMENT
 Treat the underlying disorder.
 Provide support and splintage.
 Advise patient to use the eyes carefully to avoid injury.
SEPTIC ARTHRITIS
This is an acute suppurative arthritis.
CAUSE
Commonly caused by Staphylococcus Aureus, Haemolytic Streptococci and
Pseudomonas. There are three modes of entry into a joint:
1. From a penetrating wound.
2. Via blood stream from an infection elsewhere.
3. Through tissue from an infected wound e.g. pressure sore/osteomyelitis.
PATHOLOGY
 The infection spreads through the joint, the articular cartilage
disintegrates.
 Pus is formed and may burst out of the joint to form abscesses and sinuses.
 Healing is by fibrous tissue formation or bony ankylosis or complete
resolution with normal function.
MAIN CLINICAL FEATURES
1. Throbbing pain making movement difficult.
2. Tenderness.
3. Redness of skin around the joint.
4. Hot peri-articular structures.
5. Swelling.
 1. Knees mostly affected.
2. Loss of joint range due to pain and protective muscle spasm.
3. Fever.

MANAGEMENT
1. Rest in elevation and splintage in the form of a bi-valved POP.
2. Antibiotics.
3. Aspiration of fluid.
4. For the hip or knee, sustained weight traction is used to reduce pain and
spasm.

PHYSIOTHERAPY
1. When the inflammation starts subsiding, isometric contractions are
encouraged.
2. NWB free active or assisted active exercises to move all the affected joints
through full range.
3. Encourage walking with crutches and splint PWB and progress to using sticks
as soon as the pain reduces.
Early mobilization is very important to prevent muscle atrophy and joint stiffness as loss
of function can be very severe
 ANKYLOSING SPONDYLITIS

DEFINITION: This is a sero-negative, progressive inflammatory disease presenting

with pain and stiffness in the spine progressing to bony ankylosis of the sacroiliac and
spinal joints.

AETIOLOGY
AGE: Onset between 15-40 years but can occur at any age.
SEX: Men more affected than women but is pattern is changing.
HEREDITY: 30 times more common in relatives of patients.
CAUSE: Unknown but evidence of inherited tendency.

PATHOLOGY

 The disease beings with synovitis at the sacroiliac joints and progresses up the
spine sometimes affecting the hips or shoulders.
 The articular cartilage, synovium and ligaments show chronic inflammatory
changes and eventually they ossify.
 Bony ridges form at the periphery of the intervertebral joints due to
ossification of the annulus fibrosis and neighboring tissues giving the spine a
“bamboo spine” appearance.
 The condition may progress to bony ankylosis of the SI joints, symphysis
pubis, lumbar, thoracic, cervical spines, costo-vertebral joints and the
manubriosternal junction.
 Changes have exacerbations and remissions.
CLINICAL FEATURES
1. Early symptoms are pain in the lower back and increasing stiffness.
2. Pain starts ascending.
3. Sciatica.
4. Muscle spasm of the lumbar paravertebral muscles and lumbar spine flattening.
5. Limitation of all spinal movements (“Poker back”) – extension is worse.
6. Straight leg raise is limited bilaterally.
7. Symptoms progress up the spine.
8. When the thoracic region is affected, there is reduced chest expansion due to
ankylosis of the costo-vertebral joints. There is reduced vital capacity and
breathing is diaphragmatic.
9. Patient shows a fixed spinal flexion deformity with the head and neck carried
forwards showing a “Question Mark” posture.
10. There is general ill-health, aortic incompetence.

PROGNOSIS

Life long disease. Course is variable, some patients become very stiff, others have some
functional limitation but can lead a full active life.
COMPLICATIONS
1. Fixed flexion spinal deformity.
2. Intercurrent respiratory infections.
3. Iridocyclitis.
4. Fractures of a rigid spine.

TREATMENT
1. NSAID’s
2. Analgesics

PHYSIOTHERAPY
This is the mainstay of treatment.

a) DURING EXACERBATIONS

AIMS
1. To relieve pain
2. To mobilize affected joints
3. To minimize deformity
4. To regain fitness

1. Pain relief by IR/hot packs.

2. Hydrotherapy or active exercises are used to mobilize, strengthen and
retain fitness and breathing exercises.
3. Encourage swimming.
b) AFTER AN EXACERBATION

AIMS
1. To maintain spinal and peripheral joint mobility
2. To teach posture awareness
3. To improve and maintain fitness
4. To provide motivation and encouragement
5. To maintain costo-vertebral joint mobility and vital capacity

Patient has to do exercises daily, moving the spine in full range in every direction and
working the spinal extensor muscles in inner range. May attend a class weekly.
Encourage walking three times a week.

ADVICE
1. Avoid contact sports.
2. Exercise daily.
3. Encourage prone lying on a firm bed and use of one pillow only.
4. Teach correct lifting techniques.
During prolonged sitting, advise the patient to do spinal extension every half hour
MONITORING
Measurements are taken at:

a) 2nd costal cartilage

b) Xiphii sternum
c) 10th rib
d) Check the distance between the wall and occiput – “Wall Test”.

Arrange treatment so that periods of intensive physiotherapy of 2-3 weeks duration occur
at 6 month intervals.

SURGERY
A posterior spinal osteotomy for correction of the spinal deformity.
OSTEOARTHRITIS

This is a degenerative wear and tear process occurring in joints that are impaired by
congenital defect, vascular insufficiency or previous disease or injury. It is associated
with exacerbations of acute inflammation.

DEFINITION: A chronic degenerative disease of joints with exacerbations of acute

inflammation.

CLASSIFICATION
2 types:
1. PRIMARY: No cause is obvious.
2. SECONDARY: When it follows conditions such as fractures of joint surfaces,
dislocations, occupational, infection e.g. TB joint, deformity, obesity, haemophilia.
CAUSE
Not known but predisposing factors include:
1. Heredity
2. Poor posture
3. Age
4. Defective lubricating mechanism and uneven nutrition of the articular
cartilage
5. All the causes of secondary OA
6. Metabolic disorders e.g. acromegaly

PATHOLOGY
 The articular cartilage is worn away at the point of maximum pressure.
 The underlying bone is exposed which becomes hard and glossy
“Eburnation”.
 The bone at the joint margins hypertrophies to form a ring of projecting spurs
called “Osteophytes”.
 These may free themselves into the joint creating “Loose Bodies”.
 Due to the recurrent strains the capsule and synovial membrane thicken and
firbrosis occurs.

CLINICAL FEATURES
1. Pain – 3 types – on weight bearing, during and after exercise and at night
especially after an active day
2. Muscle spasm
3. Stiffness following inactivity that reduces with activity
 1. Loss of joint movement
2. Muscle wasting and weakness
3. Joint enlargement due to chronic oedema of the capsule and synovial
membrane and muscle wasting makes the joint look larger
4. Deformity
5. Crepitus
6. Loss of function
7. X-rays show narrowing of joint space, sclerosis, osteophytes and altered shape
of bone ends

MANAGEMENT

PHYSIOTHERAPY

AIMS
1. To relieve pain
2. To strengthen muscles
3. To mobilize joints
4. To improve coordination
5. To minimize deformity
6. To reduce postural stress
7. To give a home programme
1. Relieve pain by heat or ice for the acute stage. Muscle spasms may be
reduced by massage, relaxation.
2. Strengthen muscles by strengthening exercises.
3. Mobilise joints by free active exercises. If swelling is reducing movement
this must be removed. Use a stick to relieve weight.
4. Use Frenkel’s exercises to improve coordination, wobble board to re-educate
proprioception, gait training.
5. Minimise deformity by exercises and maintaining good posture.
6. Reduce postural stress by training posture.
7. Advice:
a) Walking within limits of pain everyday.
b) Rest frequently.
c) Reduce weight.
d) Rest in prone lying.
e) Avoid putting strain on joints.
8. Home programme to be done daily.

SURGERY
Arthrodesis, arthroplasty to relieve pain and osteotomy to shift the weight-bearing
zone.

PROGNOSIS
No cure but function can be maintained.
 CERVICAL SPONDYLOSIS
DEFINITION: This is a condition in which there are degenerative changes in the
intervertebral joints between the bodies and the discs.
AETIOLOGY
AGE; From 30 years onwards, common around 45 years.
SEX: Women are affected more than men.
PREDISPOSING FACTORS
1. Poor posture
2. Occupational stress e.g. computer workers
3. Body type
Commonly affects C4-T1 (other areas in the spine are L2-L4 and T4, T5, T6)
4. Injury.
PATHOLOGY
 Degenerative changes affect the central intervertebral joints and later
the posterior intervertebral joints (facet joints).
 In the central joints there is narrowing of the disc and bone reaction at the
joint margins leads to osteophyte formation.
 In the facet joints, there is degeneration of the articular cartilage and
osteophyte formation (spurs) at the joint margins.
 Osteophytes reduce the intervertebral foramina leading to nerve compression.
Disc degeneration is part of the ageing process
CLINICAL FEATURES
1. Headaches due to upper cervical pathology
2. Neck ache, shoulder girdle, shoulder and arm pain
3. Neck postural muscle weakness
4. Slight weakness in muscles supplied by the compressed nerve roots
5. Nerve root irritation manifests as a radiating pain along the course of the
affected nerve/s, sometimes reaching the fingers. May be accompanied by
burning and tingling sensations.
6. Muscle spasm of the trapezius
7. Neck movements are limited
8. Tendon reflexes may be absent/reduced
9. X-rays show lipping of the vertebral bodies, osteophytes and reduced
intervertebral disc space

TREATMENT

AIMS
1. To relieve pain
2. To mobilize the joints
3. To strengthen muscles
4. To correct posture
5. To teach home exercises and give advice
TREATMENT

1. Heat and massage to relieve pain, muscle spasm. Local relaxation is taught.
2. General exercises for the neck and shoulder girdle.
3. Posture correction to relieve pain.
4. Collar support during acute pain. This should be removed when resting when
pain starts reducing for gradually increasing periods.
5. If there is nerve root pressure, traction is applied.
6. Advice: Use only one pillow in supine lying. Ergonomic advice. Every half
hour stretch the neck and move it in full range especially when sitting or
writing.
7. Home exercises.
FROZEN SHOULDER

DEFINITION: This is also known as Adhesive Capsulitis and is an inflammation of the

capsule and synovial membrane leading to adhesion formation.

AETIOLOGY
AGE: Affects over 40 years. Females affected between 45-55 years, males 50-60 years.
CAUSE: Unknown but may be due to:
a) Trauma: “Wrench” or fall on to the shoulder, dislocation, fracture of
the surgical neck of humerus
b) Secondary to: cervical spondylosis, CVA, coronary thrombosis

PATHOLOGY
 Inflammatory changes occur in the capsule and synovial membrane.
 Adhesions form in the exudates.
 The inflammatory changes may spread to other periarticular structures.
 The changes are reversible and the joint is eventually restored to normal.

CLINICAL FEATURES
1. Pain radiating in the arm of gradual and spontaneous onset – worse at night.
2. All movements are limited.
3. Muscle spasm.
4. Functional loss.
5. X-rays are normal.
PHYSIOTHERAPY
AIMS
1. To mobilize the joint
2. To relieve pain
3. To strengthen muscles
4. To correct posture
5. To teach home exercises

TREATMENT
1. Heat or cold.
2. Massage.
3. Exercises
4. Advice: no passive movements or force, no heavy weight lifting.
5. Posture correction and relaxation training.
THE END.
JAR GUIDE.

PROVERBS 16:16

“ WISDOM IS BETTER THAN MONEY”.

~DONE BY ALBERT MWENYA JR~