Alterations in Musculoskeletal

ALTERATIONS IN
MUSCULOSKELETAL
FUNCTION:
TRAUMA, INFECTION, &
DISEASE
P R E P A R E D B Y: B A N D A R A L H U WA M I L
S U P E R V I S E D B Y: H A B I B M E A I B E D
SOFT TISSUE INJURIES
I. INERT SOFT TISSUE INJURIES
a. Ligament Injuries
 A ligament is a dense connective tissue with parallel-fibered
collagenous tissues designed to connect bone to bone. It contributes to
the mechanical stability of the joint, guide motion, and prevent
excessive motion.
 Clinical Manifestations
 Common sites = Anterior cruciate ligament (ACL) & anterior ankle
(talofibular ligament)
 ”Tearing” sensation or “popping” in the knee followed by pain with
weight bearing
 Acute swelling of the knee
 Treatment
 Symptoms relief
 Moderate ligament injury = protection of the ligament
 Severe ligament injury = surgical restoration of ligament
b. Joint Capsule Injuries
 The joint capsule is composed of an inner layer and an outer layer.
 Inner layer = the synovial membrane or synovial lining layer (highly vascularized)
 Outer layer = it is attached to the periosteum of the bones (poorly vascularized but richly innervated by joint nerve receptors)
 Adhesive Capsulitis
 It is the loss of function in the shoulder after even a minor injury, leading to a “frozen shoulder”.
 With an injury to any component of the shoulder complex, inflammation occurs in the joint along with swelling and distention of the
joint capsule.
 Clinical Manifestations
 Loss of movement & increase in pain due to capsular tightness
 Treatment
 Intraarticular corticosteroid injections
 Gentle stretching and physical therapy
 Anti-inflammatory medication
 Prevention
 Avoiding prolonged or excessive immobilization of the shoulder after minor injuries
 Performing early, gentle stretching
c. Internal Joint Derangement
 It may be caused by injury to inert soft tissue structures.
 Common sites
 Meniscal tears at the knee
 Labrum tears at the glenohumeral joint
 Disk tears in the temporomandibular joint
 Acute pain (gradual in onset)
 Joint swelling
 Locking or popping sensation
 Treatment
 Small meniscal tears = anti-inflammatory medication, joint stabilization, and physical therapy
 Other more significant tears = may require surgical repair
d. Injuries to Fasciae & Bursae
1. Fasciae
 When connective tissues of the body are arranged in sheaths that envelop muscles, they are designated fasciae.
 Individual muscles are surrounded by a thin fascia called the perimysium.
 Clinical Manifestations:
 Edema
 Scarring
2. Bursae
 A bursa is located in areas of high friction and is designed to dissipate some of the stress.
 With faulty mechanics of the joint, repetitive movement, or direct trauma, the bursal sac may become inflamed (bursitis) and
painful.
 Common sites of bursitis
 Trochanteric bursa (lateral hip)
 Subacromial bursa (shoulder)
 Pes anserine bursa (medial knee)
 Olecranon bursa (elbow)
e. Injuries to Nerve Roots, or Dura Mater
 Trauma to any soft tissue may lead to adhesive constriction of the nerve, nerve root, or dura mater.
 Irritation or entrapment of a nerve causes pain that radiates along the structures innervated by that nerve.
 Pain
 Altered sensation (numbness and tingling)
 Motor weakness
 Diminished reflexes
 Common sites of intervertebral disk problems
 L3-L4
 L4-L5
 L5-S1
II. CONTRACTILE SOFT TISSUE INJURIES
a. Injury to Tendons
 It occurs along a continuum from a minor strain, in which a few fibers of the tendon are torn, to a complete
tear or rupture.
b. Muscle & Tendon Strains
 As in the case of injury to a tendon, tears in a muscle may range from a minor tear to a complete rupture.
 Most injuries to muscles are due to abnormal or sudden, unexpected muscle contraction.
c. Blunt Trauma
 A soft tissue contusion or crush injury also compromises the contractile structure.
 Any blunt trauma that causes bleeding into the muscle belly may lead to an inability to contract the muscle.
 Common sites
 Proximal muscle groups are most often affected (triceps, quadriceps, and thigh adductor muscles)
 Treatment
 Initial injury = rest, ice, compression, and anti-inflammatory medication.
 Later injury = surgical removal of heterotopic calcification
II. CONTRACTILE SOFT TISSUE INJURIES
d. Compartment Syndrome
 It is due to trauma to soft tissue caused by the unyielding
structure of inert tissue.
 Causes
 Decreased compartment size
 Increased compartment content
 Externally applied pressure
 With an injury, edema causes an increase in pressure within the
compartment.
 Muscle and nerves become ischemic, with resultant
excruciating pain and tissue damage.
BONE INJURIES & INFECTIONS
I. BONE & JOINT TRAUMA
a. Fracture
 It is a break in the continuity of a bone, an epiphyseal plate, or a cartilaginous joint
surface.
 Trauma generating enough energy to fracture a bone also produces force sufficient to
traumatize adjacent soft tissue.
 Types of Fractures
 Transverse Fractures
 Spiral Fractures
 Longitudinal Fractures
 Oblique Fractures
 Impacted Fractures
 Comminuted Fractures
 Greenstick Fractures
 Stress Fractures
 Avulsion Fractures
 Compression Fractures
 Complete & Incomplete Fractures
a. Fracture
 Diagnosis
 History & physical examination
 Radiographs of the skeletal area
 Computed tomography (CT) or magnetic resonance imaging (MRI) = for occult fractures or nondisplaced fractures in areas
not easily seen on plain films (such as the scaphoid of the wrist or the femoral neck)
 Treatment
 Initial management of a simple fracture = icing, elevating, and immobilizing the affected limb
 Simple nondisplaced fractures = hard cast
 Soft tissue damage injury = splinting
 Functional bracing = to allow joint movement while still securing the bone
 Intraarticular fractures = surgical fixation
 Fractures with severely displaced bone = surgical reduction and fixation (internal & external fixation)
 Bone grafting = to bridge wider gaps in a displaced fracture or electrical bone stimulation
 Open fractures = antibiotic prophylaxis, tetanus prophylaxis, pain medication, and eventual rehabilitation of the soft tissue
structures surrounding the fracture
a. Fracture
 Complications
 Delayed healing
 Osteonecrosis
 Osteomyelitis
 Compartment Syndrome
 Fat emboli Syndrome
 Deep Venous Thrombosis & Pulmonary Embolism
 Neurovascular Injury
b. Dislocations & Subluxations

 Dislocation - It is a displacement of a bone from its normal position to the extent that articulating surfaces completely lose contact.
 Subluxation - It is a displacement of a bone from its normal joint position to the extent that articulating surfaces partially lose
contact.
 Common sites = small joints of the fingers, the patella, and the shoulder.
 Clinical Manifestations = pain, alteration in the normal contour of the joint, change in extremity length, and loss of normal
mobility.
 Treatment = consideration of local soft tissue trauma and healing
II. INFECTIONS OF THE BONE
a. Osteomyelitis
 It is a severe pyogenic infection of a bone and local tissue that requires urgent treatment.
 Organisms may reach a bone by one of three routes:
1. via the bloodstream (hematogenous osteomyelitis)
2. from adjacent soft tissue (contiguous focus)
3. by direct introduction of the organism into the bone
 Etiology and Pathogenesis
 Hematogenous osteomyelitis is the most common type of osteomyelitis.
 It occurs most often in children younger than 16 years (mean age of 6 years old) and elderly adults, intravenous (IV)
drug users, and patients with indwelling central lines.
 The long bones, which are rich in red marrow, are most commonly affected (for children & infants).
 The infection usually begins acutely in the metaphyseal region of the bone.
 Bloodborne bacteria reach the marrow space via the nutrient artery, or after blunt trauma, a hematoma develops;
thus a pathway for the organism to reach the bone is present.
a. Osteomyelitis
 High fever & pain at the site of bone involvement (for children)
 Muscle spasms, redness, and swelling are common
 Refuse to move the limb (for children)
 Fever, malaise, anorexia, night sweats, and weight loss (for adults)
 Pain at rest is common
 Diagnosis
 Radiographic signs of bone destruction
 Causative Organism
 Staphylococcus aureus followed by Streptococcus pneumoniae
 Haemophilus influenzae can also be a cause (for 2-3 years old)
 Treatment
 4 to 6 weeks of parenteral antibiotic therapy
 A shorter period of parenteral therapy followed by oral antibiotics can be effective if the infection is under control
 Debridement & antibiotic therapy - if with abscess or extensive necrosis) followed by packing, bone grafts, muscle pedicles, or skin grafts
 Amputation – if antibiotic therapy is unsuccessful
b. Tuberculosis
 Bone and joint tuberculosis (TB) is an extrapulmonary form of TB that
occurs after lymphohematogenous or sometimes contiguous spread from
a primary lung lesion.
 Etiology & Pathogenesis
 It is estimated to occur in about 1% to 5% of patients with pulmonary TB
worldwide.
 As the incidence of TB increases in the United States, one can expect to see
more cases of skeletal TB.
 M. tuberculosis spreads hematogenously from the lungs or lymphatic
drainage to bone. The bacterium may lie dormant for a long time before it is
detected.
 History
 Pulmonary TB, drug abuse, crowded and poor living conditions, diseases that
depress the immune system, and immigration to the United States after 1991.
 Causative Organism
 Mycobacterium tuberculosis (transmitted via the airborne route)
b. Tuberculosis
 Local pain
 Low-grade fever
 Neurologic symptoms (weakness of lower extremities)
 Common Sites
 Vertebral Column (lower thoracic and lumbar spine called “Pott disease”)
 Weight-bearing joints (hips, knees, and ankles)
 Diagnosis
 Culture of a tissue biopsy
 X-ray - the appearance is of a lytic lesion in the bone without local sclerotic (new bone formation) reaction
 CT or MRI - infection spreads to adjacent disks, and paraspinal fluid may accumulate as a “cold abscess”
 Risk Factors
 Those at extremes of age or individuals who are immunosuppressed or undernourished.
 Treatments
 Long-term combination antibiotic therapy (isoniazid, rifampin, pyrazinamide, ethambutol, and others are used in combinations for at least 6
to 9 months)
 Surgical intervention = for spinal TB with severe deformities or neurologic deficits
ALTERATIONS IN BONE STRUCTURE & MASS
I. BONE STRUCTURE DISORDERS
a. Scoliosis
 It is a lateral curvature of the spine from the normal vertical line by 10 degrees or more that results in an S-
or a C-shaped spinal column with vertebral rotation.
 It can be a consequence of numerous congenital, connective tissue, and neuromuscular disorders.
 The majority of scoliosis cases are classified as idiopathic with a prevalence in the general U.S. population of about
2% to 4% with equal rates in men and women.
 The frequency is greater in children of women with scoliosis.
 Uneven shoulders or hips
 Shoulder or scapular prominence
 Rib or chest hump when bending over
 a C- or S-shaped spine.
I. BONE STRUCTURE DISORDERS
a. Scoliosis
 Diagnosis
 Radiographic examination – to determine the degree of curvature
 Scoliometer - to assess the angle of trunk rotation when the patient
is bent in a forward flexion position.
 Treatment
 Nonsurgical measures - primarily braces and exercises
 Surgical intervention - includes spinal realignment, fusion, and
bracing with internal appliances (requires prolonged body
immobilization postoperatively)
 Conditioning exercises to strengthen muscles and correct posture
are used to treat nonstructural, or postural, scoliosis.
II. METABOLIC BONE DISEASES
a. Osteoporosis
 The World Health Organization (WHO) defines osteoporosis as bone mineral density (BMD) greater than or equal
to 2.5 standard deviations below the mean peak BMD of young normal women (a T score less than −2.5).
 Etiology & Pathogenesis
 It is the most common metabolic bone disease, affecting an estimated more than 10 million people over 50 years of age in
the United States.
 Osteoporotic fractures are associated with increased mortality, with an estimated 740,000 deaths per year worldwide as a
result of hip fractures.
 Osteoporosis occurs when the rate of bone resorption is greater than that of bone formation, osteoblastic and osteoclastic
balance is disrupted, and the levels of mineral and protein matrix components are decreased.
 The number of trabeculae is decreased, and the width and mass of bone are reduced, which leads to fragile bone and thus
fractures.
a. Osteoporosis
 Colles fracture of the wrist, femoral or hip fractures, or vertebral
compression fractures (patient with a long-standing disease).
 Kyphosis of the thoracic spine (dowager’s hump)
 Shortened stature, muscle wasting or spasms of back muscles, and
difficulty bending over
 May complain of impaired breathing and poor dentition.
 Diagnosis
 Screening bone density measurement is also generally accomplished
using DXA (assessing BMD of the hip, spine, and distal radius).
 Laboratory tests = normal levels of urinary and serum calcium,
phosphorus, and alkaline phosphatase but elevated serum osteocalcin
levels
 Cross-linked telopeptides & type I procollagen propeptides
 Radiographic and CT findings - show diffuse radiolucency of bones,
sparse transverse trabeculae, indistinct articular cortices, wedge-
shaped thoracic vertebrae, biconcave lumbar vertebral bodies, and
a. Osteoporosis
 Treatment
 Moderate, regular exercise (walking or riding a stationary bicycle)
 Physical therapy exercises for individuals who are immobilized or paralyzed
 Calcium supplementation (1000 to 1500 mg daily)—prefer calcium citrate, which does not depend on an acidic environment
in the gut for absorption.
 Vitamin D3 (400 to 1000 IU daily), in a deficient state (2000 to 4000 IU daily) appears to be safe
 Antiresorptive agents = bisphosphonates (alendronate, risedronate, ibandronate, and zoledronate)
 Other agents = teriparatide, a recombinant human parathyroid hormone, which is the only true anabolic agent
 Parathyroid hormone (daily subcutaneous administration)
 Denosumab is a monoclonal antibody that inhibits the receptor activator of nuclear factor κB ligand (RANKL)
 Other Causes
 Prolonged bed rest
 Stress of exercise
 Impaired collagen formation such as scurvy (severe vitamin C deficiency), protein deficiency, or Cushing syndrome
b. Rickets & Osteomalacia
 These are characterized by deficits in mineralization of newly formed bone matrix either in the
growing skeleton (rickets) or in the mature skeleton (osteomalacia) with resulting soft osteopenic
bone.
 A deficiency of vitamin D prevents the maintenance of normal levels of calcium and phosphorus.
 Kyphosis, genu valgum (“knock knee”), and genu varum (“bowleg”) are common deformities as well as
growth retardation.
 Delayed eruption of the teeth
 Enlargement of costochondral junctions
 Decreased muscle tone
 Patients may complain of bone pain and muscle weakness
 X-ray result = bowing of bones and “pseudofractures.”
 Treatment
 Adequate intake of vitamin D supplementation (especially vitamin D3)
 Adequate intake of calcium and phosphate is also indicated by dietary adjustments or supplements
c. Paget Disease (Osteitis Deformans)
 It is a slowly progressive metabolic bone disease characterized by an initial phase of
excessive bone resorption, mediated by osteoclasts, followed by excessive bone formation.
 The specific cause of Paget disease is unknown, but a genetic component is suggested.
 It is prevalent in parts of northern Europe but rare in Africa or Asia.
 In the United States, abnormal pelvis films affected by Paget disease were found in about 2% of
individuals 55 to 74 years old.
 Residents of northeastern states and Caucasian individuals were more frequently affected.
 Severe or persistent bone pain
 Fatigue
 Joint stiffness
 Initial stage – affected bones soften and tend to bend
 Disease progression - irregular subperiosteal bone formation occurs and causes bone to become
thick and hard
 Thickening of cranial bones result in vertigo, blindness, deafness, headaches, and facial
paralysis
c. Paget Disease (Osteitis Deformans)
 Common sites
 Sacrum and spine (50%)
 Femur (46%)
 Skull (28%)
 Pelvis (22%)
 Complications
 Hypertension
 Arthritis
 Calcific periarthritis
 Pain
 Treatment
 Calcitonin or bisphosphonates (such as alendronate, risedronate, or pamidronate, among others) = to decrease bone
resorption, stabilize the fragile bone lesions, and reduce pain and the risk of fractures.
III. BONE TUMORS
a. Benign Tumors
 Osteochondroma
 Etiology, pathogenesis, and clinical manifestations
 It is a common cartilage-forming benign tumor that is most often asymptomatic and
may not be discovered until adulthood.
 It can be hereditary and is often found unintentionally.
 The lesion arises from a growth plate defect that can become pedunculated or sessile.
 Pressure on surrounding soft tissue may cause pain.
 These tumors are usually located on the metaphyses of long bones such as the
proximal end of the tibia and the distal part of the femur, the shoulder, and the pelvis.
 Chondroma
 It is a cartilage-forming tumor in a bone that can be located in the medullary cavity or in the
subperiosteal layers of bone. It is believed to arise from remnants of epiphyseal cartilage.
 It develops most often in the small bones of the hands and feet but can be found in other
areas.
 Tumor growth may erode the cortex of bone and expand the contour.
III. BONE TUMORS
a. Benign Tumors
 Osteoid Osteoma
 It accounts for approximately 10% to 13% of symptomatic benign lesions.
 The patient often complains of persistent, dull pain, which is often worse at night and
alleviated by aspirin or other nonsteroidal anti-inflammatory drugs.
 Radiographs show the lesion enclosed in a sclerotic shell.
 This tumor usually occurs in persons in their 20s.
 Giant Cell Tumor (Osteoclastoma)
 It is a benign but aggressive with richly vascularized tissue consisting of plump
spindle-shaped cells and numerous giant cells.
 These lesions account for about 5% to 10% of all primary bone tumors.
 It commonly occur during the third decade of life and are slightly more common in
females.
 Pain is the initial complaint.
III. BONE TUMORS
b. Malignant Bone Tumors
 Osteosarcoma
 Etiology and Pathogenesis
 It is an extremely malignant bone-forming tumor, is the most common primary
malignant bone tumor, and accounts for 20% of all primary malignant bone cancers.
 The majority of patients are adolescents and young adults 20 to 30 years of age,
although cases can be seen in adults 60 to 70 years old.
 It develops in the metaphyseal region of long bones and is characterized by the
formation of bone or osteoid by tumor cells.
 Destruction of the cortex of the metaphyseal region predisposes it to pathologic fracture.
 Metastasis in the lungs can be noted early in disease development
 Limb pain
 Compromised joint function
 Treatment
 Although radical amputation was the only treatment previously employed, conservative
surgery and chemotherapy are currently providing positive results
III. BONE TUMORS
 Chondrosarcoma
 Pathogenesis
 It is a malignant cartilage-forming tumor most often diagnosed in
adults 30 to 60 years old with a higher predominance in women.
 These tumors usually develop slowly and have higher cellularity
and greater pleomorphism than a chondroma.
 Evidence of malignant transformation may include pain, an irregular
border, or an increase in the proximal end of long bones after patient
growth is complete.
 Pain is not usually a prominent clinical symptom initially
 Lung metastasis
 Chondrosarcomas tend to develop in the pelvic and shoulder girdles,
as well as the ribs and the proximal ends of long bones such as the
femur
III. BONE TUMORS
 Ewing Sarcoma
 Pathogenesis
 It is the third most common primary sarcoma of bone and is characterized as
a rapidly growing, malignant, round-cell tumor.
 This tumor most often develops in the bones of children and young adults
between the ages of 5 and 25 years with higher frequency in males than
females.
 Ewing tumor is composed of densely packed small cells with round nuclei.
 It arises in the medullary canal of the bone and perforates the cortex of the
shaft, producing a painful soft tissue mass overlying the involved bone.
 Clinical Manifestations & Treatment
 Patients often appear systemically ill and may develop fever, anemia,
leukocytosis, and an increased sedimentation rate
 Treatment
 Local resection and chemotherapy of an isolated lesion can have a 5-year
survival approaching 70%.
III. BONE TUMORS
 Multiple Myeloma
 Etiology and Pathogenesis
 It is a slowly growing bone marrow malignancy with the neoplastic proliferation of a single clone
of plasma cells.
 The annual incidence is approximately 4 per 100,000 and represents about 1% of all malignant
cancers.
 It is usually a disease of elderly adults.
 Clinical Manifestations and Treatment
 Radiographs - evidence of bone destruction by a lytic, or bone destroying, process, and bone
marrow involvement can be seen.
 Homogeneous immunoglobulin is also present in urine or serum.
 Bone pain is the most common symptom, particularly in the chest and back
 Patients experience hypercalcemia and pathologic fractures where the bone has been destroyed.
 This disease can also cause kidney dysfunction, lung or pleural involvement, and neurologic
symptoms attributable to nerve compression.
 Treatment
 Aggressive combination chemotherapy, although at times local radiation or the use of
bisphosphonates may be useful for refractory bone pain.
 Chemotherapy can induce temporary remission in 50% to 70% of cases, but survival longer than 2
to 3 years is less than 10%.
DISEASE OF SKELETAL MUSCLE
I. IDIOPATHIC INFLAMMATORY MYOPATHY
a. Polymyositis and Dermatomyositis
 These are idiopathic inflammatory myopathies.
 There is focal or extensive degeneration of muscle fibers attributable to inflammatory infiltrates of
lymphocytes, macrophages, and other inflammatory cells.
 Possible triggers of this immune-mediated inflammation include viruses, bacteria, parasitic organisms,
neoplasms, drugs, vaccinations, and stress.
 Proximal limb and neck weakness and associated muscle stiffness
 Muscle pain is often mild
 Hip and leg weakness and difficulty with climbing stairs and rising from a chair
 Weakness in the arms (progression of the disease)
 Anterior neck weakness makes lifting the head from the pillow very difficult
 Inflamed, injured skeletal muscle leaks several enzymes (creatine kinase, aldolase, aspartate aminotransferase)
into the bloodstream and is found at high levels on laboratory testing
I. IDIOPATHIC INFLAMMATORY MYOPATHY
a. Polymyositis and Dermatomyositis
 Diagnosis
 Electromyography
 Presence of inflammatory changes and muscle edema on MRI
 Diagnosis is confirmed on skeletal muscle biopsy of involved areas
 Treatment
 Initial therapy - corticosteroids
 Immunosuppressive agents (methotrexate, azathioprine, or mycophenolate mofetil)
 Physical therapy is also important and should include passive range-of-motion activities, followed by assisted and
then active strengthening exercises
II. MUSCULAR DYSTROPHY
a. Duchenne Muscular Dystrophy
 It is the most common and most severe form of muscular dystrophy is inherited as an X-linked trait and therefore afflicts only males.
 The incidence is 1 in 5000 male births.
 Because of a genetic mutation, muscle cells are deficient in the protein dystrophin, a deficiency that weakens the cell membrane and
allows extracellular fluid to leak into the cell.
 The disease begins at birth and is usually apparent by the age of 2 to 5 years, with initial involvement of the pelvic girdle and
progression to the shoulder girdle.
 Enlarged calf muscles
 Some muscles, such as those in the hands, face, jaw, pharynx, larynx, and eyes, are spared to the end.
 Survival expectancy is late 20s or early 30s with cardiac failure or pulmonary infection as the usual cause of death
 Treatment
 Appropriate education for the patient and family, preservation of physical function as long as possible, and prevention of
contractures.
 Corticosteroid therapy may be useful to delay loss of muscle strength and prolong independent ambulation
 Medical management of the complications of cardiomyopathy and declining pulmonary function
 Immunosuppressive therapies
b. Becker Muscular Dystrophy
 Etiology, Pathogenesis, and Clinical Manifestations
 It is a milder form of inherited muscle degeneration, somewhat less common than the Duchenne type.
 The genetic mutation leads to the production of a reduced amount of an abnormal dystrophin protein and slower
muscular degeneration.
 Calf hypertrophy is still prominent and often painful with progressive loss of strength and ability to ambulate.
 The mean age of symptom onset is somewhat later (older than 5 years and even into adulthood) with patients requiring a
wheelchair by the age of 30 years.
c. Facioscapulohumeral Muscular Dystrophy

 It is an inherited autosomal dominant trait that affects the muscles of the shoulder girdle and the face.
 It is rare, with an annual incidence of 1 in 15,000.
 The onset of disease can occur at any age, but it usually begins in the second decade.
 Facial muscles are involved early, with later involvement of scapular and upper arm musculature.
 Associated symptoms may include sensorineural hearing loss or retinal vascular abnormalities.
 Both males and females are affected, and with supportive management, most live to a normal age.
d. Myotonic Dystrophies
 These are the second most common inherited muscle disease, and it has an autosomal-dominant pattern of
inheritance.
 Prevalence is about 1 in 8000.
 This leads to progressive muscle weakness and myotonia with delayed muscle relaxation after stimulation.
 Type 1 myotonic muscular dystrophy (MMD1)
 Affects facial muscles, distal limb muscles, and oropharyngeal and extraocular muscles
 Distal limb weakness can develop slowly as well as muscle wasting
 Type 2 form (MMD2)
 The proximal limb muscles are more affected, sparing the face.
 Cardiac conduction defects, cataract formation, endocrine dysfunction, testicular atrophy, hypersomnolence, and sleep apnea
 Treatment
 Supportive along with management of complications
 Antiarrhythmic drug mexiletine functions as a sodium channel blocker and has been shown in limited studies to improve
muscle relaxation
OTHER DISORDERS OF MUSCLE
I. MYASTHENIA GRAVIS
 It is a chronic autoimmune disease affecting the neuromuscular function of voluntary muscles and
characterized by profound muscle weakness and fatigability.
 Its peak onset in females occurs at 20 to 30 years of age.
 Women are affected more often than men, with a prevalence of 15 per 100,000.
 The acetylcholine receptor antibodies are produced that destroy or block acetylcholine receptors of
the muscle end-plate of the neuromuscular junction.
 Painless muscle weakness begins with ocular and cranial muscles, and then proximal limb muscles can
be involved
 During times of emotional stress, respiratory muscles may be involved.
 A sudden increase in blood pressure and pulse rate
 Other symptoms = cyanosis from hypoxia, absent cough and gag reflexes, restlessness, increased
secretions and lacrimation, diaphoresis, decreased urine output, bowel and bladder incontinence,
dysarthria, and respiratory distress.
 Treatment
 Anticholinesterase inhibitors (pyridostigmine bromide, neostigmine) may be used to inhibit the
breakdown of acetylcholine in the neuromuscular synapse.
 Corticosteroids, IV immunoglobulin, plasmapheresis, and immunosuppressive agents may be used to
regulate the immune system.
 Mechanical ventilation = for respiratory muscle fatigue
 Thymectomy = is often recommended when patients fail to respond well to medications
II. CHRONIC MUSCLE PAIN
a. Fibromyalgia Syndrome
 The cause of fibromyalgia syndrome (FMS) is unknown.
 No laboratory abnormalities have been found, muscle biopsy findings are nonspecific, and patients are usually normal on
psychological testing.
 The condition is not an inflammatory process but rather a “pain syndrome,” that changes in the central nervous system may
lead to the amplification of pain fiber impulses, a theory called central sensitization.
 It is characterized by chronic pain in muscles and surrounding structures often of months’ or years’ duration.
 It is characterized by a strong female preponderance, with an estimated prevalence in the United States of more than 45% of
the general population.
 Widespread musculoskeletal pain, stiffness, and fatigability
 Joint pain and swelling may be perceived by the patient, but the swelling, if present, is usually soft tissue “puffiness” and not
a true inflammatory process.
 Muscle pain and weakness are expressed without objective demonstration.
 Sleep disturbances
 No diagnostic laboratory or radiographic findings.
II. CHRONIC MUSCLE PAIN
a. Fibromyalgia Syndrome
 Treatment
 Treatment focuses on maintaining functionality and reducing symptoms.
 Patient education is important and may be associated with improved outcomes and better prognosis.
 An exercise regimen is essential and should include regular stretching; improvement in physical conditioning via low-
impact aerobic exercise (biking, swimming, walking); and measures of pacing, muscle protection, and relaxation.
 Counseling for stress and psychological factor.
 Blinded, randomized, placebo-controlled studies of amitriptyline, cyclobenzaprine, zolpidem, and alprazolam
administered at bedtime have indicated that all are effective FMS therapy.
 The selective serotonin reuptake inhibitors (fluoxetine, sertraline, and citalopram)
 Pregabalin (an anticonvulsant agent) has been shown to be effective in reducing pain
 Additional medications = venlafaxine, duloxetine, milnacipran (serotonin-norepinephrine reuptake inhibitors), and
tramadol (an opioid-like analgesic)
 Moclobemide and pirlindole are monoamine oxidase inhibitors.
EVALUATION
 A solid working knowledge of the anatomy, physiology, and biomechanics of movement is extremely important when
dealing with any type of alteration in the musculoskeletal system.
 With a grasp of the mechanics involved in function, the clinician is able to approach each aberration with an awareness of
the time requirements for healing, stress tolerances, and expected management outcomes.
 The injuries and diseases discussed in this chapter are a small representation of the many dysfunctions that may afflict the
musculoskeletal system.
 An ability to determine the specific type of tissue involved (contractile or inert) allows the clinician to be cognizant of
activities that would aggravate trauma, types of injury that require supportive devices, and injuries that respond to medical
intervention.
 An awareness of the tissue response to healing enhances the clinician’s evaluative skills and provides a signal regarding
when intervention has achieved the expected results within an appropriate timeframe.
 It is the responsibility of the practitioner to become knowledgeable about the variety of dysfunctions that occur.
 This knowledge base must continue to expand as technological advancements provide increasingly complex levels of
information and new diagnostic tools become available.

Alterations in Musculoskeletal

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Alterations in Musculoskeletal

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ALTERATIONS IN

b. Dislocations & Subluxations

c. Facioscapulohumeral Muscular Dystrophy

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