Diagnosis and Treatment of Wrist Injuries:

The wrist joint has multiple axes of movement: flexion-extension and radial ulnar deviation occur at the radiocarpal joints, and pronation-supination occurs at the distal and proximal radioulnar joints. These movements provide mobility for hand function. Injuries to the wrist often occur due to a fall on the outstretched hand. In sportspeople, the most common acute injuries are fractures of the distal radius or scaphoid, or damage to an intercarpal ligament. Intercarpal ligament injuries are becoming more frequently recognized and, if they are not treated appropriately (e.g. including surgical repair where indicated), may result in long-term disability. The anatomy of the wrist and hand is complex and therefore a thorough knowledge of this region is essential to diagnose and treat sports injuries accurately. The bony anatomy consists of a proximal row and a distal row, which are bridged by the scaphoid bone. Normally, the distal carpal row should be stable; thus, a ligamentous injury here can greatly impair the integrity of the wrist. Here a ligamentous injury disrupts important kinematics between the scaphoid, lunate, and triquetrum, resulting in carpal instability with potential weakness and impairment of hand function.

History:

It is essential to determine the mechanism of the injury causing wrist pain.  These injuries are commonly encountered in high-velocity activities such as snowboarding, rollerblading, or falling off a bike. A patient may fracture the hook of hamate while swinging a golf club, tennis racquet or bat and striking a hard object (e.g. the ground). It is very useful to determine the site of the pain; the causes of volar pain are different from those of dorsal wrist pain.

Other important aspects of the history may include:

• Hand dominance
• Occupation (computer related, manual labor, food service industry)
• History of past upper extremity fractures including childhood fractures/injuries
• History of osteoarthritis, rheumatoid arthritis, thyroid dysfunction, diabetes
• Any unusual sounds (e.g. clicks, clunks, snaps, etc.)
• recurrent wrist swelling raises the suspicion of wrist instability
• Musician (number of years playing, hours of practise per week, change in playing, complex piece, etc.)

Examination Involves:

1.    Observation

2.    Active movements

• Flexion/ extension
• Supination/pronation
• Radial/ulnar deviation

3.    Passive movements

• Extension
• Flexion

4.    Palpation

• Distal forearm
• Radial snuffbox
• Base of metacarpals
• Lunate
• Head of ulna
• Radioulnar joint

5.    Special tests

• Watson’s test for scapholunate injury
• Stress of triangular fibrocartilage complex
• Grip- Jamar dynamometer (may be contraindicated if a maximal effort is not permitted, e.g. after tendon repair)
• Dexterity- Moberg pick-up test
• Sensation- Semmes Weinstein monofilament testing
• Nerve entrapment- Tinel’s sign

6.    Standardized rating scales

• Several valid and reliable assessment scales can quantify function of the wrist specifically or the upper extremity after an Injury.

Diagnosis of Wrist Injuries:

• Plain Radiography

If ligament injury is suspected, also obtain a PA view with clenched fist. A straight lateral view of the wrist, with the dorsum of the distal forearm and the hand forming a straight line, permits assessment of the distal radius, the lunate, the scaphoid, and the capitate and may reveal subtle instability. The lateral radiograph of the normal wrist can be. These bones should be aligned with each other and with the base of the third metacarpal. A clenched fist PA view should be taken if scapholunate instability is suspected.

• Special Imaging Studies

The combination of the complex anatomy of the wrist and subtle wrist injuries that can cause substantial morbidity has led to development of specialized wrist imaging techniques. A carpal tunnel view with the wrist in dorsiflexion allows inspection of the hook of hamate and ridge of the trapezium. For suspected mechanical pathology, such as an occult ganglion, an occult fracture, non-union or bone necrosis, several modalities are useful (e.g. ultrasonography, radionuclide bone scan, CT scan or MRI). Ultrasonography is a quick and accessible way to assess soft tissue abnormalities such as tendon injury, synovial thickening, ganglions, and synovial cysts. Bone scans have high sensitivity and low specificity; thus, they can effectively rule out subtle fractures.

Treatment of Wrist Injuries:

Treatments for wrist problems vary greatly. Treatment for wrist injury may include first aid measures. Treatment depends on:

• The position, type, and seriousness of the injury.
• How long ago the injury happened.
• Your age, health problem and actions (such as work, sports, or hobbies).

Symptoms and Treatment of Hand Pain:

Hand and finger injuries finger injuries are extremely common in sport and, although the majority require minimal treatment, some are potentially serious and require immobilization, precise splinting, or even surgery. Finger injuries are often neglected by athletes in the expectation that they will resolve spontaneously. Many present too late for effective treatment. The importance of early assessment and management must be stressed so that long-term deformity and functional impairment can be avoided. Many hand and finger injuries require specific rehabilitation and appropriate protection upon resumption of sport. Joints in this region do not respond well to immobilization, therefore, full immobilization should be minimized.

Mechanism of Injury:

The mechanism of injury is the most important component of the history of acute hand injuries. A direct, severe blow to the fingers may result in a fracture, whereas a blow to the point of the finger may produce an interphalangeal dislocation, joint sprain or long flexor or extensor tendon avulsion. A punching injury often results in a fracture at the base of the first metacarpal or to the neck of one of the other metacarpals usually the fifth. An avulsion of the flexor digitorum profundus tendon, usually to the fourth finger, is suggested by a history of a patient grabbing an opponent’s clothing while attempting a tackle. Associated features such as an audible crack, degree of pain, swelling, bruising, and loss of function should also be noted.

Signs and Symptoms:

Carefully palpate the bones and soft tissues of the hand and fingers, looking for tenderness. The examiner should always be conscious of what structure is being palpated at any particular time. The joints should be examined to determine active and passive range of movement and stability. Stability should be tested both in an anteroposterior direction and with ulnar and radial deviation to assess the collateral ligaments. The cause of any loss of active range of movement should be carefully assessed and not presumed to be due to swelling. Normal range of motion for the second to fifth digits is approximately 80 degree of flexion at the DIP, 100 degree of flexion at the PIP and 90 degree of flexion at the MCP joint. A common injury site that can be overlooked is the volar plate, a thick fibrocartilagenous tissue that reinforces the phalangeal joints on the palmer or volar surface.

The extensor tendons of the hand are often divided into six compartments. At the wrist on the dorsal side of the hand, the tendons are encased in synovial sheaths as they pass under the extensor retinaculum. When palpating in the most radial of the distal end of the radius. The extensor pollicis longus angles sharply around the bony prominence and can damage or even rupture the tendon after a serious wrist fracture. The anatomical snuffbox is composed of the extensor pollicis longus and brevis and abductor pollicis longus. The floor of the snuffbox is the carpometacarpal joint of the thumb. Clinically this is a significant region for several reasons. Tenderness may suggest scaphoid fracture. The deep branch of the radial arterial passes through as well as the superficial branch of the radial nerve; consequently, if a cast or splint is applied too tightly, it can lead to numbness in the thumb.

Examination Involves:

1. Observation and sensation testing as per the wrist. Special note should be made of the hand arches and any deformities at the proximal or distal interphalangeal joints.

• Hand at rest
• Hand with clenched fist

2.  Active movements-fingers (all Joints)

• Flexion
• Extension
• Abduction
• Adduction

3.  Active movements-thumb

• Flexion
• Extension
• Palmar abduction
• Palmar adduction
• Opposition

4.  Resisted movements (tendons)

• Flexor digitorum profundus
• Flexor digitorum superficialis
• Extensor tendon

5. Special test

• Ulnar collateral ligament of the first MCP joint
• IP joint collateral ligaments

Diagnosis of Hand Injuries:

Routine radiographs of the hand include the PA, oblique and lateral views. All traumatic finger injuries should be X-rayed. Ideally, ‘dislocations’ need to be radiographed before reduction to exclude fracture and after reduction to confirm relocation. Even when pre-reduction radiographs are not performed because reduction has occurred on the field, post-reduction films should be obtained after the game. Care should be taken with lateral views to isolate the affected finger to avoid bony overlap. The use of more sophisticated investigation techniques is usually not required.

Treatment of Hand Injuries:

• The functional hand requires mobility, stability, sensitivity, and freedom from pain. It may be necessary to obtain stability by surgical methods.
• However, conservative rehabilitation is essential to regain mobility and long-term freedom from pain, Treatment and rehabilitation of hand injuries is complex.
• As the hand is unforgiving of mismanagement, practitioners who do not see hand injuries regularly should ideally refer patients to an experienced hand therapist, or at least obtain advice while managing the patient.
• Inflammation and swelling are obvious in the hand and fingers.
• During the inflammatory phase, the therapist must aim to reduce edema and monitor progress by signs of redness, heat and increased pain.
• During the regenerative phase (characterized by proliferation of scar tissue), the therapist can use supportive splints and active exercises to maintain range of motion.
• During remodeling, it is appropriate to use dynamic and serial splints, and active and active assisted exercises, in addition to heat, stretching and electrotherapeutic modalities.

Causes And Treatment of Rotator Cuff Tendinopathy:

Rotator cuff tendinopathy is a common cause of shoulder pain and impingement in athletes. In this condition, the rotator cuff tendons become swollen and hyper cellular, the collagen matrix is disorganized and the tendon weaker. Studies in running rats and in human swimmers suggest the major determinant of the onset of tendinopathy is the volume (e.g. distance swum, time running) of work. Apoptosis (programmed cell death) and associated pathways are increased in overuse tendinopathy and may play a role in the pathogenesis of tendinopathy.

Clinical Features

The athlete with rotator cuff tendinopathy complains of pain with overhead activity such as throwing, swimming and overhead shots in racquet sports. Activities undertaken at less than 90 degree of abduction are usually pain-free. There may also be a history of associated symptoms of instability, such as recurrent subluxation or episodes of dead arm.

On examination, there may be tenderness over the supraspinatus tendon proximal to or at its insertion into the greater tuberosity of the humerus. Active movement may reveal a painful arc on abduction between approximately 70 degree and 120 degree. Internal rotation is commonly reduced. The most accurate method to clinically assess rotator cuff strength is to measure developed resistance when the scapula is stabilized in a retracted position.

For the athlete with rotator cuff tendinopathy, symptoms can be reproduced with impingement tests, as well as pain at the extremes of passive flexion. Pain will also occur with resisted contraction of the supraspinatus, which is best performed with resisted upward movement with the shoulder joint in 90 degree of abduction, 30 degree of horizontal flexion and internal rotation .The investigation of choice in rotator cuff tendinopathy is MRI. These examinations may also demonstrate the presence of a partial tear of the rotator cuff.

Treatment of Rotator Cuff Tendinopathy

The treatment of rotator cuff tendinopathy should be considered in two parts.

• The first part is to treat the tendinopathy itself. The patient should avoid the aggravating activity and apply ice locally.
• There is no level 2 evidence to support NSAIDs, ultrasound interferential stimulation, laser, magnetic field therapy or local massage.
• There is level 2 evidence to support nitric oxide donor therapy (glyceryl trinitrate [GTN] patches applied locally at 1.25 mg/day) and for a single corticosteroid injection.
• Glyceryl trinitrate patches come in varying doses: a 0.5 mg patch should outcomes occurred at three to six months, so patients need to have this explained.
• A corticosteroid injection into the subacromial space may reduce the athlete’s symptoms sufficiently to allow commencement of an appropriate rehabilitation program.
• It has been reported that the second part of the treatment of rotator cuff tendinopathy should be the correction of associated abnormalities.
• These include glenohumeral instability, muscle weakness or in coordination, soft tissue tightness, impaired scapulohumeral rhythm and training errors.
• Impaired scapulohumeral rhythm may predispose to rotator cuff tendinopathy and must be assessed and treated.
• The treatment of scapulohumeral rhythm abnormalities is considered.
• Decreased rotator cuff strength or an imbalance between the internal and external rotators of the shoulder also predisposes to the development of rotator cuff tendinopathy.
• Treatment involves strengthening of the external rotators as they are usually relatively weak compared with the internal rotators.
• An exercise program to strengthen the rotator cuff muscles is described.
• Posterior capsular tightness is commonly associated with decreased internal rotation and reduced rotator cuff strength.
• Stretching of the posterior capsule is helpful. Instability is a common cause of rotator cuff tendinopathy and must be considered in any patient who presents with symptoms typical of rotator cuff tendon problems.
• If the presence of instability is not recognized, rotator cuff tendinopathy is likely to recur upon return to sport.
• While it is possible that correction of any of these disorders may improve tendinopathy, there is no level 2 evidence to support any particular rehabilitation strategy or regimen for managing supraspinatus tendinopathy.
• This provides fertile ground for novel clinical research trials.
• Tightness and focal muscle thickening of the rotator cuff muscle hems may also predispose to the development of rotator cuff tendinopathy.
• These changes reduce the ability of the musculotendinous complex to elongate and absorb shock. They may also alter biomechanics by reducing the full range of motion and impairing scapular control.
• These soft tissue abnormalities should be corrected. Abnormalities along the kinetic chain must be identified and corrected.
• Technique faults, for example, in throwing or swimming, should be corrected with the aid of a coach. Training errors need to be corrected.
• Overuse should be avoided.

Clinical Features, Causes And Treatment of Ankle Pain:

Lateral ankle pain is generally associated with a biomechanical abnormality. The two most common causes are peroneal tendinopathy and sinus tarsi syndrome.

Examination

Examination is as for the patient with acute ankle injury with particular attention to testing resisted eversion of the peroneal tendons and careful palpation for tenderness and crepitus.

Peroneal Tendinopathy

The most common overuse injury causing lateral ankle pain is peroneal tendinopathy. The peroneus longus and peroneus brevis tendons cross the ankle joint within a fibro-osseous tunnel, posterior to the lateral malleolus. The peroneus brevis tendon inserts into the tuberosity on the lateral aspect of the base of the fifth metatarsal. The peroneus longus tendon passes under the plantar surface of the foot to insert into the lateral side of the base of the first metatarsal and medial cuneiform. The peroneal tendons share a common tendon sheath proximal to the distal tip of the fibula, after which they have their own tendon sheaths. The peroneal muscles serve as ankle dorsi flexors in addition to being the primary evertors of the ankle.

Causes

Peroneal Tendinopathy may either as a result of an acute ankle inversion injury or secondary to an overuse injury. Soft footwear may predispose to the development of peroneal tendinopathy. Common causes of an overuse injury include:

• Excessive eversion of the foot such as occurs when running on slopes or cambered surfaces.
• Excessive pronation of the foot.
• Secondary to tight ankle plantar flexors (most commonly soleus) resulting in excessive load on the lateral muscles.
• Excessive action of the peroneal (e.g. dancing, basketball, volleyball).

An inflammatory arthropathy may also result in the development of a peroneal tenosynovitis and subsequent peroneal tendinopathy. It has been suggested that peroneal tendinopathy may be due to the excessive pulley action of, and abrupt change in direction of, the peroneal tendons at the lateral malleolus.

There are three main sites of peroneal tendinopathy:

• Posterior to the lateral malleolus
• At the peroneal trochlea
• At the plantar surface of the cuboids.

Clinical Features

The athlete commonly presents with:

• Lateral ankle or heel pain and swelling which is aggravated by activity and relieved by rest.
• Local tenderness over the peroneal tendons on examination sometimes associated with swelling and crepitus (a true paratenonitis).
• Painful passive inversion and resisted eversion, although in some cases eccentric contraction may be required to reproduce the pain.
• Possible associated calf muscle tightness.
• Excessive subtalar pronation or stiffness of the subtalar or midtarsal joints that is demonstrated on biomechanical examination.

Investigations

MRI is the recommended investigation and shows characteristic features of tendinopathy-increased signal and tendon thickening.13 If MRI is unavailable, an ultrasound may be performed. If an underlying inflammatory arthropathy is suspected, obtain blood tests to assess for rheumatologic and inflammatory markers.

Treatment

• Treatment initially involves settling the pain with rest from aggravating activities, analgesic medication if needed and soft tissue therapy and physical therapy.
• Stretching in conjunction with mobilization of the subtalar and Midtarsal joints may be helpful.
• Footwear should be assessed and the use of lateral heel wedges or orthoses may be required to correct biomechanical abnormalities.
• Strengthening exercises should include resisted eversion (e.g. rubber tubing, rotagym), especially in plantar flexion as this position maximally engages the peroneal muscles.

In severe cases, surgery may be required, which may involve a synovectomy, tendon debridement or repair.

Exercise of Type 1 Diabetes and Type 2 Diabetes Disease: 

Firstly, the adjustments the athlete with diabetes might make if he or she wishes to exercise and, secondly, what the risks and benefits are, both in the short term and long term, of exercise to the patient with diabetes.

There are many examples of athletes with diabetes who have been extremely successful. British rower Steven Redgrave developed diabetes at the age of 35 having won gold medals at each of the previous four Olympic Games. Following his diagnosis he was able to continue training and competing and won a fifth consecutive gold medal in the Sydney Olympics Games 2000.

There are two distinct types of diabetes mellitus:

1. Insulin-Dependent (Type 1)
2. Non-Insulin-Dependent (Type 2)

Type 1 Diabetes

Type 1 Diabetes(Insulin-Dependent Diabetes Mellitus, IDDM), previously known as juvenile-onset diabetes, is thought to be an inherited autoimmune disease in which antibodies are produced against the beta cells of the pancreas. This ultimately results in the absence of endogenous insulin production, which is the characteristic feature of type 1 diabetes. The incidence of type 1 diabetes varies throughout the world but represents approximately 10-15% of diabetic cases in the western world. The onset commonly occurs in childhood and adolescence but can become symptomatic at any age. Insulin administration is essential to prevent ketosis, coma and death. The aims of treatment are tight control of blood glucose levels and prevention of micro vascular and macro vascular complications.

Type 2 Diabetes

Type 2 Diabetes (Non-Insulin-Dependent Diabetes Mellitus, NIDDM), previously know maturity-onset or adult-onset diabetes, is a disease as the former names suggest, of later onset ,linked to both genetic and lifestyle factors. It is characterized by diminished insulin secretion relative to serum glucose levels in conjunction with peripheral insulin resistance, both of which result in chronic hyperglycemia. Approximately 90% of individuals with diabetes have type 2 diabetes and it is thought to affect 3-7% of people in Western countries. The prevalence of type 2 diabetes increases with age. The pathogenesis of type 2 diabetes remains unknown but it is believed to be a heterogeneous disorder with a strong genetic factor. Approximately 80% of individuals with 2 diabetes are obese.

Type 2 diabetes is characterized by three major metabolic abnormalities:

• Impairment in pancreatic beta cells insulin secretion in response to a glucose stimulus.
• Reduced sensitivity to the action of insulin in major organ systems such as muscle, liver and adipose tissue.
• Excessive hepatic glucose production in the basal state.

Exercise and Diabetes:

The sports physician should be encouraged to work closely with the endocrinologist when considering exercise prescription for a diabetic patient. The target of an adult should be to achieve at least 30 minutes of continuous moderate activity, equivalent to brisk walking five or six days a week, with the flexibility of shorter bouts of more intense activity being considered important. This is provided that cardiovascular and hypertensive problems are taken into account. Heart rate may be an unreliable indicator of exertion because of autonomic neuropathy, and the rating of perceived exertion scales may be more useful.

Although exercise in conjunction with a proper diet and medications is the cornerstone in the treatment of diabetes, special care must be taken in those taking insulin. Both insulin and exercise independently facilitate glucose transport across the mitochondrial membrane by promoting GLUT4 transporter proteins from intracellular vesicles. The action of insulin and exercise is also cumulative. As such, an exercising type 1 diabetic will have lowered insulin requirements, and may notice up to a 30% reduction in insulin requirements with exercise. Importantly, in the person with type 1 diabetes, glycemic control may not be improved with regular exercise if changes in the individuals diet and insulin dosage do not appropriately match exercise requirements. In the absence of exercise, even for a few days, the increased insulin sensitivity begins to decline.

All patients with diabetes should carry an identification card or bracelet identifying them as having diabetes. They should be educated to be alert to the early signs of hypoglycemia for at least 6-12 hours after exercise. It is essential that they carry glucose tablets or an alternative source of glucose with them at all times. Dehydration during exercise should be prevented by adequate fluid consumption. It is also recommended that the diabetic athlete exercise with somebody else, if possible, in case of adverse reactions.

Benefits of Exercise:

• The benefits of exercise in type 1 diabetics include improved insulin sensitivity, improved blood lipid profiles, decreased heart rate and blood pressure at rest, decreased body weight and possible decreased risk of coronary heart disease.
• It does not appear that exercise improves glycemic control; however, insulin requirements may be decreased slightly.
• While exercise may not improve glucose control, the benefits of exercise in those with diabetes occur mainly through reducing the risk factors for cardiovascular disease.
• People with type 1 diabetes typically live longer if they participate in regular physical activity as a part of their lifestyle.
• It is well recognized that exercise reduces the risk of developing type 2 diabetes. There are also considerable benefits for those with type 2 diabetes.
• A program of regular physical activity can reverse many of the defects in metabolism of both fat and glucose that occur in people with type 2 diabetes.

As noted above, Hb is used as an index of long term blood glucose control. The lower the value, the better.  Hb is reduced by chronic exercise in people with type 2 diabetes. The evidence for improvement of Hb with exercise in type I diabetes is not as convincing.

Exercise and Type 1 Diabetes

Control of blood glucose is achieved in a patient with type 1 diabetes through a balance in the carbohydrate intake, exercise level and insulin dosage. The meal plan and insulin dosage should be adjusted according to the patient’s response to exercise. Unfortunately a degree of trial and error is necessary for type 1 diabetics taking up new activities. Frequent self-monitoring should occur, at least until a balance is achieved among diet, exercise and insulin parameters. Those with blood glucose levels less than 5.5 mmol/L (100 mg/dL) require a pre-exercise carbohydrate snack (e.g. sports drink, juice, glucose tablet, fruit).

• Exercise of 20-30 minutes at less than 70% VO (e.g. walking, golf, table tennis) requires a rapidly absorbable carbohydrate (15 g fruit exchange or 60 calories) before exercise but needs minimal insulin dosing adjustments.
• More vigorous activity of less than I hour (e.g. jogging, swimming, cycling, skiing, tennis) often requires a 25% reduction in pre-exercise insulin and 15-30 g of rapidly absorbed carbohydrate exchange before and every 30 minutes after the onset of activity.
• If early morning activity is to be performed the basal insulin from the evening dose of intermediate-acting insulin may need to be reduced by 20-50%, with checking of the morning blood glucose level.
• The morning regular-acting insulin dose may also need to be reduced by 30-50% before breakfast, or even omitted if exercise is performed before food.
• Depending on the intensity and duration of the initial activity and likelihood of further activity, a reduction of 30-50% may be needed with each subsequent meal.
• After exercise hyperglycemia will occur, but insulin should still be decreased by 25-50% (because insulin sensitivity is increased for 12-15 hours after activity has ceased).
• Consuming carbohydrates within 30 minutes after exhaustive, glycogen-depleting exercise allows for more efficient restoration of muscle glycogen.
• This will also help prevent post-exercise, late-onset hypoglycemia, which can occur up to 24 hours following such exercise.
• If exercise is unexpected, then insulin adjustment may be impossible. Instead, supplementation with 20-30 g of carbohydrate, at the onset of exercise and every 30 minutes thereafter, may prevent hypoglycemia.
• In elite athletes and with intense bouts of exercise, reductions in insulin dosage may be even higher than those listed above.
• During periods of inactivity (e.g. holidays, recovery from injury), increased insulin requirements are to be expected.

Exercise and Type 2 Diabetes

• Those patients with type 2 diabetes who are managed with diet therapy alone do not usually need to make any adjustments for exercise.
• Patients taking oral hypoglycemic drugs may need to halve their doses on days of prolonged exercise or withhold them altogether, depending on their blood glucose levels.
• They are also advised to carry some glucose with them and to be able to recognize the symptoms of hypoglycemia.
• Hypoglycemia is a particular risk in those people with diabetes taking sulfonylureas due to their long half lives and increased endogenous insulin production.
• Biguanides provide less of a problem as they do not increase insulin production.

Exercise and the Complications of Diabetes:

Exercise is often neglected when the secondary complications of diabetes occur. Some unique concerns for the patient with diabetes that warrant close scrutiny include autonomic and peripheral neuropathy, retinopathy and nephropathy. Poor glucose control appears to be associated with an increased occurrence of neuropathy.

• Abnormal autonomic function is common among those with diabetes of long duration.
• The risks of exercise when autonomic neuropathy is present include hypoglycemia, abnormal heart rate and blood pressure responses (e.g. postural drop), impaired sympathetic and parasympathetic nervous system activity and abnormal thermoregulation.
• Patients with autonomic neuropathy are at high risk of developing complications during exercise. Sudden death and myocardial infarction have been attributed to autonomic neuropathy and diabetes. High-intensity activity should be avoided, as should rapid changes in body position and extremes in temperature. Water activities and stationary cycling are recommended.
• Peripheral neuropathy (typically manifested as loss of sensation and of two point discrimination) usually begins symmetrically in the lower and upper extremities and progresses proximally.
• Podiatric review should occur on a regular basis, and correct footwear can prevent the onset of foot ulcers.
• Regular close inspection of the feet and use of proper footwear are important and the patient should avoid exercise that may cause trauma to the feet.
• Feet and toes should be kept dry and clean and dry socks should also be used.
• Non-weight-bearing activities, such as swimming, cycling and arm exercises, are recommended in those with insensitive feet.
• Activities that improve balance are appropriate choices.
• Diabetics with proliferative retinopathy should avoid exercise that increases systolic blood pressures to 170 mmHg and prolonged Valsalva-like activities.
• Exercise that increases blood pressure may worsen retinopathy.
• Exercise that results in a large increase in systolic pressure (such as weightlifting) can cause retinal hemorrhage.
• Exercise for these patients could include stationary cycling, walking and swimming. If possible, blood pressure should be monitored during the exercise program.
• Exercise is contraindicated if the individual has had recent photocoagulation treatment or surgery.
• These include lifting heavy weights and high-intensity aerobic activities. Activities that are weight-bearing yet low impact are preferable.
• It is important to wear well-cushioned shoes. Renal patients should be fully evaluated before commencing an exercise program. Fluid replacement is extremely important in these patients. Specific training programs for patients undergoing hemodialysis are advised.

Symptoms and Causes of Chronic Fatigue Syndrome: 

Chronic Fatigue Syndrome (CFS) is a controversial condition, the existence of which is hotly debated within the medical profession. The term itself was first used in 1988 but the syndrome has existed for much longer. It has previously been known as neurasthenia and myalgic encephalomyelitis (ME). The term CFS has been adopted to define a sufficiently homogeneous group of patients to allow research into etiology, pathogenesis, natural history and management. As the word syndrome suggests, CFS is not recognized as a distinct disease process.

Definition

A number of definitions of CFS have been proposed. All include the concept of fatigue that interferes with activities of daily living and is of at least six months duration. The Center for Disease Control (CDC) in Atlanta has defined CFS as the presence of:

1. Clinically evaluated, unexplained, persistent or relapsing fatigue that is of new or definite onset; is not the result of ongoing exertion; is not alleviated by rest; and results in a substantial reduction of previous levels of occupational, educational, social or personal activities.
2. Four or more of the following symptoms that persist or recur during six or more consecutive months of illness and that do not predate the fatigue:

• Self-reported impairment in short-term memory or concentration
• Sore throat
• Tender cervical or axillary nodes
• Muscle pain
• Multi -joint pain without redness or swelling
• Headaches of a new pattern or severity
• Un-refreshing sleep
• Post-Exertional malaise of at least 24 hours

Symptoms

The most prominent symptom of CFS is usually overwhelming fatigue, especially after exercise.

• Other common symptoms include headaches, sore throat, enlarged lymph nodes, muscles pain especially after exercise, un-refreshing sleep, chest and abdominal pains.
• The diagnosis of CFS is difficult to confirm in the absence of any definitive sign or test.
• It is often a diagnosis of exclusion.
• The other problem with the diagnosis of CFS is that there are a number of conditions whose symptoms overlap with those of CFS.
• The two most significant are fibromyalgia and depression.
• The major presenting symptom in fibromyalgia is usually widespread muscle and joint pain but fatigue is nearly always present.
• Fibromyalgia is characterized by the presence of multiple tender points in the muscles.
• Trigger points are also frequently seen in patients with CFS and form an important part of the treatment.
• Fatigue is often the primary presenting symptom in patients with depression and many of the symptoms described in CFS are found in depressive patients.

Management

Management of the patient with CFS (or fibromyalgia and depression) is a considerable challenge for the practitioner. The natural history of CFS is of a very gradual improvement over a period of months and sometimes years.

• Treatment should be oriented towards psychological support and symptom relief.
• It is essential that the treating practitioner acknowledges that the patient has a real problem and is prepared to give the patient a diagnosis.
• It is important to give the patient plenty of time and both the patient and those close to her (or him) will have many questions.
• We recommend seeing the patient at least weekly in the initial treatment phase and later on a less frequent but still regular basis.
• Exercise is the cornerstone of treatment of chronic fatigue.
• This may seem strange when one considers that post-exercise fatigue and muscle pain are two of the most significant features of the disease but a slow, graduated increase in activity is an essential part of management.
• The exercise program may have to commence at a ‘ridiculously’ low level considering the history of some athletes.
• But it should commence at a level that the patient can achieve comfortably with minimal or no adverse effects in the 24-48 hours post-exercise.
• The increase in activity should be very gradual and if adverse symptoms develop, the patient should return to the previous level of activity and build up even more slowly.
• In a six-month randomized blinded prospective trial in individuals with CFS, it was found that a graded exercise program significantly improved both health perceptions and the sense of fatigue whereas the use of an antidepressant (fluoxetine) improved depression only.
• Another study of 66 patients with CFS also demonstrated a positive effect with graded aerobic exercise.
• Many drug treatments have been advocated but with little evidence of their efficacy.
• Simple analgesics may be helpful and we recommend the use of a tri- cyclic antidepressant (e.g. amitryptiline 10-25 mg) in a single nocte dose.
• This drug seems to improve sleep quality and patients will usually wake up more refreshed as a result.
• Many nutritional supplements have also been advocated but again there is no evidence of their efficacy we have found the treatment of muscle trigger points with dry needling to be helpful in reducing muscle pains and headaches in a number of patients with CFS.

Other Causes of Tiredness

A number of psychological problems are associated with a feeling of excessive tiredness. The two most common states are anxiety and depression. These problems may be related to the athletes sporting endeavors or, alternatively, may be quite unrelated.

• The presence of eating disorders such as anorexia, nervosa and bulimia should also be considered.
• Hypothyroidism is more common than most realize, occurring in 1% of adults, with subclinical disease in Solo. The condition can affect any organ system.
• Hypothyroidism is characterized by a general slowing of body processes and can present as chronic fatigue, cold intolerance, weight gain and, in women, menorrhagia.
• It is often associated with high cholesterol levels.
• An elevated serum thyroid stimulating hormone level is a sensitive indicator and patients with this condition generally respond well to treatment with levothyroxine.
• Diabetes, neuromuscular disorders and cardiac problems are all associated with excessive tiredness.
• Exercise induced as the major symptom rather than the more typical cough, chest tightness or shortness of breath post exercise.
• A number of medications may cause excessive tiredness.
• These include beta-blockers, antihistamines, diuretics, anticonvulsants, sedatives and muscle relaxants.

Physical Health Benefits of Exercise:

Physical activity benefits all body organs as well as the psyche. The most dramatic benefits have been found in the cardiovascular system. Exercise interventions in older patients with coronary heart disease decreased morbidity, mortality and symptoms, and reduced cardiac re-hospitalizations.

Benefits of Exercise

Numerous mechanisms may contribute to these benefits. Increased demand on the myocardium improves oxygen utilization. Capillaries dilate and multiply to improve the delivery of oxygen and other nutrients to muscles. The myoglobin content of muscle is increased, thus improving the transfer of oxygen from the red blood cells to muscle cells. Inside the cell, the number of mitochondria increases, enhancing aerobic metabolism. There is also an increase in the glycogen storage sites of muscle. Here following are the exercise benefits:

• Exercise tends to lower the resting heart rate and the resultant increased diastolic time allows improved coronary blood flow. Stroke volume increases.
• Exercise also has an effect on blood lipid levels, raising levels of high-density lipoprotein cholesterol, the cardio protective lipid, and lowering levels of low-density lipoprotein cholesterol.
• Exercise lowers blood pressure and reduces obesity. A combination of these two factors, in addition to the reduction in cholesterol, decreases the risk of ischemic heart disease.
• Exercise may also improve exercise tolerance in older people with chronic obstructive pulmonary disease. They will also benefit from the associated benefits of aerobic fitness.
• Exercise may improve blood sugar control in people with diabetes by decreasing insulin resistance, and may reduce the need for medication.
• Resistance training and high-impact activities help maintain bone mass in the elderly.
• An exercise program may also be beneficial for older people with osteoarthritis by improving joint mobility and increasing muscle strength.
• Exercise in the form of strength and balance training has been shown to reduce an older person’s risk of falling.
• Along with the physical benefits of exercise, the older athlete benefits from improved sleep, cognitive function and mood.
• The muscle control and weight loss associated with exercise may lead to improvements in body image and reverse the elderly person’s fear of activity.
• Exercise reduces anxiety in elderly patients, especially in those recovering from illness.
• Exercise can lessen depressive symptoms and perhaps even reduce the risk of developing depression.

Risks of Exercise in the Elderly

The risks associated with a sedentary lifestyle are well known although difficult to quantify objectively and compare with the risks associated with exercise in later years. Underlying co-morbidity is often cited as a reason to preclude exercise despite the overwhelming evidence to support the benefits of exercise in many common and chronic diseases.

From a safety standpoint, clinicians prescribing exercise for older people are concerned that exercise may induce myocardial ischemia and, in turn, precipitate myocardial infarction or sudden death. Gill and colleagues have provided recommendations regarding precautions that can be taken to minimize the risk of serious adverse cardiac events among previously sedentary older persons who do not have symptomatic cardiovascular disease and are interested in starting an exercise program.

Reducing the Risks of Exercise

Before starting an exercise program, all older persons should have a complete history and physical examination performed by a physician. Contraindications to exercise outside of a monitored environment include: myocardial infarction within six months, angina or physical signs and symptoms of congestive heart failure, and a resting systolic blood pressure of 200 mmHg or higher. A functional test of cardiac capacity is to ask the patient to walk 15 m (50 ft) or climb a flight of stairs. A resting ECG/EKG should be reviewed for new Q waves, ST segment depressions or T-wave inversion.

Persons who have features of cardiovascular disease should be referred for appropriate management. If the patient has no overt cardiovascular disease, and no other medical or orthopedic contraindications to exercise, he or she can begin a low-intensity exercise program.

Treatment of Headache:

Cervical or cervicogenic headache is a term used to describe headache caused by abnormalities of the joints, muscles, fascia and neural structures of the cervical region. There are a number of classifications for cervical or cervicogenic headache with differing criteria for physical dysfunction.

Mechanism

The mechanism of production of headache from abnormalities in the cervical region is variable. It may be primarily referred pain caused by irritation of the upper cervical nerve roots. This may be due to damage to the atlantoaxial joint or compression of the nerves as they pass through the muscles. Headache emanating from the lower cervical segments probably originates from irritation of the posterior primary rami, which transmit sensation to the spinal portion of the trigeminocervical nucleus.

Commonly, pain may also be referred to the head from active trigger points. Frontal headaches are associated with trigger points in the suboccipital muscles, while temporal headaches are associated with trigger points in the upper trapezius, splenius capiitis and cervicis, and sternocleidomastoid muscles.

Clinical Features

History

A cervical headache is typically described as a constant, steady, dull ache, often unilateral but sometimes bilateral. The patient describes a pulling or gripping feeling or, alternatively, may describe a tight band around the head. The headache is usually in the suboccipital region and is commonly referred to the frontal, retro-orbital or temporal regions.

Cervical headache is usually of gradual onset. The patient often wakes with a headache that may improve during the day. Cervical headaches may be present for days, weeks or even months. There may be a history of acute trauma, such as a whiplash injury sustained in a motor accident, or repetitive trauma associated with work or a sporting activity.

Cervical headache is often associated with neck pain or stiffness and may be aggravated by neck or head movements, such as repetitive jolting when traveling in a car or bus. It is often associated with a feeling of light-headedness, dizziness and tinnitus. Nausea may be present but vomiting is rare. The patient often complains of impaired concentration, an inability to function normally and depression. Poor posture is often associated with a cervical headache. This may be either a contributory factor or an effect of a headache. The abnormal posture typically seen with cervical headache is rounded shoulders, extended neck and protruded chin. This results in tightness of the upper cervical extensor muscles and weakness of the cervical flexor muscles.

Stress is often associated with cervical headache. It may be an important contributory factor to the development of the soft tissue abnormalities causing the headache or may aggravate abnormalities already present. Thus, it is important to elicit sources of stress in the clinical history.

Exercise-Related Causes of Headache

Benign Exertional Headache

Benign exertional headache (BEH) has been reported in association with weightlifting, running and other sporting activities. The IHS criteria include that the headache:

• Is specifically brought on by physical exercise
• Is bilateral, throbbing in nature at onset and may develop migrainous features in those patients susceptible to migraine
• Lasts from 5 minutes to 24 hours
• Is prevented by avoiding excessive exertion
• Is not associated with any systemic or intracranial disorder.

The onset of the headache is with straining and Valsalva maneuvers such as those seen in weightlifting and competitive swimming. The major differential diagnosis is subarachnoid hemorrhage, which needs to be excluded by the appropriate investigations. It has been postulated that exertional headache is due to dilatation of the pain-sensitive venous sinuses at the base of the brain as a result of increased cerebral arterial pressure due to exertion. Studies of weight- lifters have shown that systolic blood pressure may reach levels above 400 mmHg and diastolic pressures above 300 mmHg with maximal lifts.

A similar type of headache is described in relation to sexual activity and has been termed benign sex headache or orgasmic cephalalgia (IHS 4.6). The management of this condition involves either avoiding the precipitating activity or drug treatment, for example, indomethacin (25 mg three times a day). In practise, the headaches tend to recur over weeks to months and then slowly resolve in some cases they may be lifelong.

Treatment

• Treatment of the patient with cervical headache requires correction of the abnormalities of joints, muscles and neural structures found on examination as well as correction of any possible precipitating factors such as postural abnormalities or emotional stress.
• Treatment of cervical intervertebral joint abnormalities involves mobilization or manipulation of the Cl-2 and C2-3 joints.
• Stretching of the cervical extensor muscles and strengthening of the cervical flexor muscles are important.
• Soft tissue therapy to the muscles and the fascia of the cervical region is aimed at releasing generally tight muscles and fascia (commonly the cervical extensors).
• Active trigger points should be treated with spray and stretch techniques or dry needling.
• Cervical muscle retraining has been shown to be beneficial by itself and in combination with manipulative therapy in reducing the incidence of cervicogenic headache.
• This includes retraining of the deep cervical flexors ,extensors and scapular stabilizers.
• Postural retraining is an essential part of treatment. The patient must learn to reduce the amount of cervical extension by retracting the chin.
• Identification and reduction of sources of stress to the patient should be incorporated in the treatment program.

Symptoms And Treatment of Knee Pain :

Anterior knee pain is the most common presenting symptoms in many physiotherapy and sports physician practises.1 It contributes substantially to the 20-40% of family practise consultations that relate to the musculoskeletal system. Two common causes of anterior knee pain in sports people are patellofemoral pain and patellar tendinopathy.

We first outline a practical approach to assessing the  patient  with  anterior knee pain particularly with a view to distinguishing the common conditions; we  then detail their management. These concludes with an outline of other cause of anterior knee pain such as fat pad impingement, which may mimic features of both patellofemoral pain and patellar tendinopathy.

Clinical approach

Distinguishing between patellofemoral pain and patellar tendinopathy as a cause of anterior knee pain can be difficult as their clinical features can be similar. Furthermore, on occasions, the two conditions may both be present.

History

There are a number of important factors to elicit from the history of a sportsperson with the general presentation of anterior knee pain. These include the specific location of the pain, the nature of aggravating activities, the history of the onset and behaviour of the pain and any associated clicking, giving way of swelling.

Although it may be difficult for the patient with anterior knee pain to be specific, the area of pain often gives an important clue as to which structure is contributing to the pain .For example, retropatellar or peripatellar pain suggests that the patellofemoral joint (PFJ) is a likely culprit, lateral pain localized to the lateral femoral epicondyle indicates iliotibial band friction syndrome and inferior patellar pain implicates the patellar tendon or infrapatellar fat pad. The patient presents with bilateral knee pain is more likely to have patellofermoral pain or tendinopathy than an interal derangement of both knees.

The onset of typical patellofemoral pain is often insidious but it may present secondary to an acute traumatic episode (e.g. falling on the knee) or post other knee injury (e.g. meniscal, ligament) or knee surgery. The patient presents with a diffuse ache, which is usually exacerbated by loaded activities, such as stair ambulation or running. Sometimes patellofemoral pain is aggravated by prolonged sitting (movie-goers knee), but sitting tends to aggravate pain of patellar tendinopathy so is not diagnostic of patellofemoral pain. Pain during running that gradually worsens is more likely to be of patellofemoral origin, whereas pain that occurs at the start of activity, settles after warm-up and returns after activity is more likely to be patellar tendinopathy. To clinical differentiation of patellofemoral pain, patellar tendinopathy and fat pad impingement. As these conditions can coexist, accurate diagnosis can be challenging.

A history of recurrent crepitus may suggest patellofemoral pain. A feeling that the patella moves laterally at certain times suggests recurrent patellofemoral instability. An imminent feeling of giving way may be associated with patellar subluxation, patellofemoral pain or meniscal abnormality, although frank, dramatic giving way is usually associated with anterior cruciate ligament instability. Nevertheless, giving way due to muscle inhibition, or due to pain, is not uncommon in anterior knee pain presentations.

Examination

Initially, the primary aim of the clinical assessment to determine the most likely cause of the patient’s since location of tenderness and aggravating factors are integral to the differential diagnosis, it is critical to reproduce the patient’s anterior knee pain. This is usually done with either a double- or single-leg squat. A squat done on a decline may make the test more specific to the anterior knee. The clinician should palpate the anterior knee carefully to determine the site of maximal tenderness.

Examination includes:

1. Observation

• standing
• walking
• supine

2. Functional tests

• squats
• step-up/step-down
• jump
• lunge
• double-then single – leg decline squat

3. Paplation

• patella and inferior pole
• medial lateral retinaculum
• patellar tendon
• infrapatellar fat pad
• tibial tubercle
• effusion

4. PFI assessment

static assessment of patella position

• superior
• inferior
• medial
• lateral glide
• dynamic assessment of patella position
• assessment of vasti function

5. Flexibility

• lateral soft tissue structures
• quadriceps
• hamstring
• iliotibial band
• gastrocnemius

Investigations

Imaging may be used to confirm a clinical impression obtained from the history and examination. Structural imaging includes conventional radiography, ultrasound, CT and MRI. Occasionally, radionuclide bone scan is indicated to evaluate the metabolic status of the knee (e.g. after trauma, in suspected stress fracture).

The majority of patients with patellofemoral pain syndrome will require either no imaging, or plain radiography consisting of a standard AP view, a true lateral view with the knee in 300 of flexion, and an axial view through the knee in 300 of flexion. Plain radiography can detect bipartite patella and osteoarthritis, provide evidence of an increased likelihood of Sinding-Larsen-Johansson lesions as well as rule out potentially serious complications such as tumor or infection .Although CT and three dimensional CT have been used to assess the PFI ,MRI is gaining increasing popularity as an investigations of patellofermoral pain, and the unstable patella because of its capacity to image the patellar articular cartilage.

Treatment

Treatment of patellar tendinopathy requires patience and a multifaceted approach, which is outlined. It is essential that the practitioner and patience recognize that tendinopathy that has been present for months may require a considerable period of treatment associated with rehabilitation before symptoms disappear. Conservative management of patellar tendinopathy requires appropriate strengthening exercises, load reduction, correcting biomechanical errors, and soft tissue therapy. An innovation has been the use of sclerotherapy of neovessels with polidocanol.

Surgery is indicated after a considered and lengthy conservative program has failed. This section outlines the physical therapy approach of correction of biomechanics that might be contributing to excessive load on the tendon, targeted exercise therapy and soft tissue treatment before outhning medical treatments including medication, sclerotherapy and surgery.

How you get relief from Stress Fracture of the Tibia?

Symptoms:

Stress fractures are more commonly a cause of shin pain in athletes in impact, running and jumping sports. Overall limb and foot alignment as well as limb length discrepancy may also play a role. The incidence of stress fractures is increased by playing on more rigid, unforgiving surfaces.

Approximately 90% of tibial stress fractures will affect the postero-medial aspect of the tibia, with the middle third and junction between the middle and distal thirds being most common. Proximal metaphyseal stress fractures may be related to more time loss from sports as they do not respond as well to functional bracing, which allows earlier return to play.

Stress fractures on the anterior edge of the tibia, the tension side of the bone, are more resistant to treatment and have a propensity to develop a non-union when compared to the risk of posteromedial stress fractures. A simple memory tool for the problematic anterior tibial stress fracture is anterior is awful.

A classic case presentation for a routine postero-medial stress fracture is as follows:

• Gradual onset of leg pain aggravated by exercise.
• Pain may occur with walking, at rest or even at night.
• Examination-localized tenderness over the tibia.
• Biomechanical examination may show a rigid, cavus foot incapable of absorbing load, an excessively pronating foot causing excessive muscle fatigue or a leg length discrepancy.
• Tenderness to palpation along the medial border with obvious tenderness. A stress fracture of the posterior cortex produces symptoms of calf pain.
• Bone scan and MRI appearances of a stress fracture of the tibia. MRI scan is of particular value as the extent of edema and cortical involvement has been directly correlated with the expected return to sport.
• A CT scan may also demonstrate a stress fracture.

Treatment:

Prior to initiating treatment or during the treatment plan, it is important to identify which factors precipitated the stress fracture. The most common cause is an acute change in training habits, such as a significant increase in distance over a short period of time, beginning double practice days after lying off training for a season, or a change to a more rigid playing surface. Shoe wear, biomechanics and repetitive impact sports such as running and gymnastics have also been implicated. The athletes coach can play a key role in modifying training patterns to reduce the risk of these injuries. In women, reduced bone density due to hypoestrogenemia secondary to athletic amenorrhea (the female athlete triad) may be a contributing factor. All female athletes with a first-time stress fracture should be screened for the female athlete triad.

The classic treatment plan is as follows:

• Initial period of rest (sometimes requiring a period of non-weight-bearing on crutches for pain relief) until the pain settles.
• The use of a pneumatic brace has been described. Studies have shown a markedly reduced return to activity time with such use compared with average times in two of three studies and compared with a traditional treatment group in the third. In this latter study the brace group returned to full, unrestricted activity in an average of 21 days compared with 77 days in the traditional group. The brace should extend to the knee as the mid-leg version may actually increase the stresses across a mid shaft stress fracture. Once a stress fracture is clinically healed the athlete is advised to use the brace during practise and competition. Clinical healing implies minimal to no palpable pain at the fracture site and minimal to no pain with activities in the brace. Using this plan, there have been no reported cases of progression to complete catastrophic fracture of the tibia.
• If pain persists, continue to rest from sporting activity until the bony tenderness disappears (four to eight weeks).
• Once the patient is pain-free when walking and has no bony tenderness, gradually progress the quality and quantity of the exercise over following month. The athlete should be asked to continue to use a pneumatic brace to complete the current season until an appropriate period (four to eight weeks) of rest can occur.
• Cross training with low impact exercises, including swimming, cycling and deep water running, maintains conditioning and reduces risk of recurrence.
• Pain associated with soft tissue thickening distal to the fracture site can be treated by soft tissue techniques.
• General principles of return to activity following overuse injury should be followed.