Chronic Pain (15)
(ĐTĐ) - It is generally a good idea to get more exercise. Most of us can use more activity in our lifestyle. To do this, many of us will use a treadmill. It means we can stay indoors, which is excellent when the weather is bad. It may also be more convenient, since treadmills will often be located in a gym or fitness area at work.
(ĐTĐ) - People who suffer from chronic leg pain are only too aware of how much this problem can interfere with daily activities. Chronic leg pain is the term used to describe a variety of problems that cause an individual discomfort in their legs, and there are a number of different reasons as to why this can happen.
(ĐTĐ) - Shin pain is a fairly common occurrence, particularly for athletes. While there are a number of potential causes of shin pain, one of the most common causes is shin splints. Knowing that shin splints are common, however, is cold comfort to a patient experiencing this pain. So what can one do to prevent shin splints?
(ĐTĐ) - Why is back pain or a knee injury annoying to one person and sheer agony to another? Turns out, an individual's tolerance to pain is as unique as the person, and is shaped by some surprising biological factors, as well as some psychological factors that we can actually try to control.
There are two steps to feeling pain. First is the biological step, for example, the pricking of skin or a headache coming on. These sensations signal the brain that the body is experiencing trouble. The second step is the brain's perception of the pain -- do we shrug off these sensations and continue our activities or do we stop everything and focus on what hurts?
"Pain is both a biochemical and neurological transmission of an unpleasant sensation and an emotional experience," Doris Cope, MD, an anesthesiologist who leads the Pain Medicine Program at the University of Pittsburgh Medical Center, tells WebMD. "Chronic pain actually changes the way the spinal cord, nerves, and brain process unpleasant stimuli causing hypersensitization, but the brain and emotions can moderate or intensify the pain." Past experiences and trauma, Cope says, influence a person's sensitivity to pain.
Managing pain and people's perceptions to their symptoms is a big challenge in a country where more than 76 million people report having pain lasting more than 24 hours, according to the American Pain Foundation. Persistent pain was reported by:
- 30% of adults aged 45 to 64
- 25% of adults aged 20 to 44
- 21% of adults aged 65 and older
More women than men report pain (27.1% compared with 24.4%), although whether women actually tolerate pain better than men remains up for scientific debate.
Pain produces a significant emotional, physical, and economical toll in the U.S. Chronic pain results in health care expenses and lost income and lost productivity estimated to cost $100 billion every year.
Pain may be on the rise in the U.S. because age and excessive weight contribute to pain and discomfort. Americans are living longer into old age, and two-thirds of the population is either overweight or obese.
The most common type of chronic pain in the U.S. is back pain; the most common acute pain being musculoskeletal pain from sports injuries, says Martin Grabois, MD, professor and chair of the department of physical medicine and rehabilitation at Baylor College of Medicine in Houston.
What Drives Your Pain Tolerance?
Pain tolerance is influenced by people's emotions, bodies, and lifestyles. Here are several factors that Grabois says can affect pain tolerance:
-Depression and anxiety can make a person more sensitive to pain.
-Athletes can withstand more pain than people who don't exercise.
-People who smoke or are obese report more pain.
Biological factors -- including genetics, injuries such as spinal cord damage, and chronic diseases such as diabetes that cause nerve damage -- also shape how we interpret pain.
Your Sensitive Side
Some surprising biological factors may also play a role in pain tolerance. For example, recent research shows that one side of your body may experience pain differently than the other side.
A study published in the December 2009 issue of Neuroscience Letters showed that right-handed study participants could tolerate more pain in their right hands than in their left hands. This study also showed that women were more sensitive to pain than men; but women and men were equal in their ability tolerate pain intensity.
A dominant hand -- your right hand, if you're right-handed, for example -- may interpret pain more quickly and accurately than the nondominant hand, which may explain why the dominant side can endure longer. Hand dominance may also be linked to the side of your brain that interprets the pain, the researchers note.
Redheads More Sensitive to Pain?
Another surprising factor is that hair color may reflect pain tolerance. In 2009, researchers reported in the Journal of the American Dental Association showed that redheads were more sensitive to pain and may need more anesthesia for dental procedures.
Why redheads in particular? Redheads, the researchers say, tend to have a mutation in a gene called melanocortin-1 receptor (MC1R), which is what helps make their hair red. MC1R belongs to a group of receptors that include pain receptors in the brain. The researchers suggest that a mutation in this particular gene appears to influence sensitivity to pain.
"We have different receptors for pain in our body, and those receptors respond differently, whether you're taking aspirin or acetaminophen," Stelian Serban, MD, director of acute and chronic inpatient pain service and an assistant professor of anesthesiology at The Mount Sinai Medical Center in New York, tells WebMD.
Getting Better at Handling Pain
A person's biological makeup can affect whether he or she develops resistance to pain medicines, which means a treatment that once worked no longer eases the pain. This can be a "vicious circle" to break, Serban says. "You use more treatment and become more tolerant and you become less active and have more pain."
We can't change our genetic receptors, and not even changing your hair color or which hand you write with can rewire your sensitivity to pain. However, there are coping mechanisms that can influence the brain's perceptions of pain.
Researchers have focused on trying to alter the psychological interpretations of pain by retraining the mind. "You can change the perception [of pain] on the brain," Grabois says. "You haven't changed the perception on the nerves."
Alternative remedies, such as relaxation techniques like biofeedback, teach people how to divert their mind from zeroing in on the pain.
People can empower themselves by learning relaxation techniques, such as breathing practices during natural childbirth, Cope says. When it comes to pain, mind over matter can work. "Meditation, distraction, and a positive attitude are things people can do themselves to lessen pain," she says.
Reviewed by Louise Chang, MD - Source WebMD.com
(ĐTĐ) - Most ankle injuries improve quickly, but others become long-term problems. Knowing how to accurately and efficiently make the diagnosis and manage such injuries is an important part of any primary care or orthopaedic practice.
Ankle injuries rank among the most common musculoskeletal complaints, often sending patients to an emergency department or primary care physician's office. Although the most common ankle injuries are sprains that often improve within weeks to months, a subgroup of injuries go on to become long-term problems.
Chronic ankle injuries can be vexing for physicians in that the potential causes are numerous, creating significant difficulty in diagnosis and management. However, by focusing on the anatomical location of the pain and the specific patient complaint, a physician can quickly whittle down the list to a few diagnoses.
In this article, we present a concise overview for evaluation and management of chronic ankle pain. We focus on anatomical considerations, approaches to diagnosis, efficient use of imaging studies, and basic treatment algorithms to provide physicians with a better armamentarium with which to evaluate and treat patients effectively.
Medial and Posteromedial Pain
Posterior Tibial Tendon
Diagnosis: The posterior tibial tendon (PTT) originates from the posterior aspect of the tibia, the fibula, and the interosseous membrane between them. Subsequently, the PTT courses posteromedially around the medial malleolus of the ankle to its insertion on the navicular tuberosity. The tendon has a zone of hypovascularity from 2 to 4 cm proximal to its navicular insertion, which likely contributes to its poor healing potential.
The primary function of the posterior tibialis muscle is to invert the hindfoot during gait; its primary antagonist is the peroneus brevis muscle. With dysfunction of the PTT, the pull of the peroneal tendons is largely unopposed. This leads to attenuation of the medial-sided structures of the foot (eg, spring ligament, deltoid, and midfoot ligaments) and, eventually, to talar plantar flexion, forefoot abduction, calcaneal valgus, collapse of the arch, and Achilles contracture (planovalgus deformity).
Once the heel collapses into valgus, the Achilles lies lateral to the midline, thereby functioning as an evertor and enhancing the deformity.
Patients with early PTT pathology typically complain of medial-sided ankle pain that is exacerbated by activity. Walking up and down stairs often is very difficult. In long-standing cases, lateral pain also develops secondary to subfibular impingement. The majority of cases occur in middle-aged and older persons as a result of chronic degeneration, although many times a history of minor trauma can be elicited. Athletes may experience acute traumatic tears as the result of an acute twisting injury, sometimes in basketball and hockey.
On physical examination, tenderness to palpation may be elicited along the course of the PTT and swelling adjacent to the medial malleolus may be noted. Strength testing of the posterior tibialis may beaccomplished by having the patient invert the foot against resistance from a position of maximal eversion. Usually, there is some collapse of the foot noted on examination, although the degree of collapse is quite variable.
On inspection from behind, patients often exhibit the ‘too many toes’ sign indicative of forefoot abduction relative to the midfoot. In addition, the hindfoot often is in a position of valgus. When asked to perform a single-leg heel rise, patients often are unable to do so (or can only partially do so, and with pain). When they are able to do so, the heel will not invert to the same degree that the other side does. A Silfverskiold test always should be performed to evaluate for gastrocnemius contracture.
Initial imaging studies for the workup of PTT dysfunction should include weight-bearing radiographs of both the foot and ankle. These should be examined for the angle between the talus and the first metatarsal on both the anteroposterior (AP) and lateral views, as well as the degree of talar uncovering on the AP view. In addition, arthritis in the ankle, subtalar, or Chopart joint should be assessed. In cases in which the diagnosis is in question, magnetic resonance imaging (MRI) can be valuable in examining the degree of tendon degeneration and can rule out other pathology.
Dividing PTT pathology into stages of progression helps the physician determine the optimal treatment modality. The pathology may be classified into one of the four following stages:
• 1: The patient presents with pathology that is limited to the PTT, but there is no associated foot deformity.
• 2: Progression to this stage implies the development of a flexible, correctable hindfoot deformity
• 3: The hindfoot deformity has become fixed and is not passively correctable.
• 4: The long-standing hindfoot valgus deformity leads to eccentric loading of the ankle and symptoms secondary to ankle arthritis.
Treatment: A course of nonoperative management typically is indicated initially for all stages of PTT pathology. For stage 1 pathology, immobilization, non-steroidal antiinflammatory drugs (NSAIDs), and orthoses are reasonable options. For stage 2, a hinged ankle brace may be added. For stage 3 and 4 lesions, a rigid orthosis or Arizona brace may be required.
After a 4- to 6-week course of immobilization, physical therapy should be initiated, including ultrasound, iontophoresis, stretching, and gradual strengthening. Overall, between 60% and 90% of patients may be treated effectively with these modalities alone. Corticosteroid injections generally are not indicated because of the risk of rupture or further tendon attenuation.
In patients who remain symptomatic in spite of optimal conservative management, surgical intervention may be warranted. If there is no associated foot deformity, stage 1 lesions may be managed with debridement and tenosynovectomy of the PTT; if any valgus exists, a calcaneal osteotomy to protect the repair should receive strong consideration.
Surgical intervention for stage 2 lesions remains controversial. Some surgeons advocate transfer of the flexor digitorum longus to the navicular as an isolated procedure. However, recent studies have shown that although this procedure may improve pain and function, it does not correct the underlying foot deformity and often does not succeed in the long run. Therefore, most orthopaedists now perform a concomitant calcaneal osteotomy to take tension off the transfer and to correct the hindfoot valgus.
Depending on the degree of the deformity, additional procedures may be indicated to correct the abduction (lateral column lengthening) or forefoot varus (Cotton osteotomies of the medial cuneiform or medial column fusions). A gastrocnemius lengthening also is often necessary for deformity correction.
In stage 3, fixed deformities have developed that cannot be corrected with soft tissue transfers and osteotomies alone. Therefore, arthrodesis is undertaken to restore a plantigrade foot with the ankle in normal anatomical alignment. A subtalar arthrodesis, double arthrodesis, or triple arthrodesis may be required, depending on the degree of involvement. Most of the fixed deformities also require a gastrocnemius-lengthening procedure. In stage 4 deformities, a deltoid ligament reconstruction, ankle replacement or, in severe cases, pantalar fusion may be necessary.
Flexor Hallucis Longus Tendinitis
Diagnosis: The flexor hallucis longus (FHL) originates on the distal twothirds of the posterior fibula as well as on the interosseous membrane. It courses through the fibro-osseous tunnel posterior to the medial malleolus and inserts at the base of the distal phalanx of the great toes. The tendon is particularly vulnerable to irritation and inflammation within the fibro-osseous tunnel.
Injury to the FHL is common in ballet dancers, gymnasts, runners, and other athletes whose sports activity requires extreme plantar flexion of the ankle with repetitive push-off. Patients usually complain of posteromedial ankle pain; they may have a sense of triggering or crepitus.
On physical examination, patients often have pain and swelling posterior to the medial malleolus. In addition, pain may be elicited with active flexion of the great toe against resistance. 4 Passive extension of the great toe often is limited with the foot in neutral; this subsequently resolves with the ankle placed in maximal plantar flexion (Thompson test).
Initial evaluation should include plain radiographs, looking specifically for the presence of an os trigonum (nonunited ossicle at the posterolateral talus) or a fracture. MRI can be very helpful and may show fluid around the tendon or degeneration within the tendon.
Treatment: Initial non-operative management of FHL tendinitis includes rest, immobilization, NSAIDs, and physical therapy. Longitudinal arch supports and hard-soled shoes also may help.
Corticosteroid injections may be helpful, especially in cases in which there is concomitant posterior ankle impingement. We often have injections done under ultrasonographic guidance because of the proximity of the neurovascular bundle and to avoid an intratendinous injection.
In patients who do not respond to a full course of conservative management, surgical debridement of the FHL tendon and release of the flexor retinaculum that is causing constriction may be required. If an os trigonum is present, it often is removed at the same time.
Tarsal Tunnel Syndrome
Diagnosis: The tarsal tunnel is the fibro-osseous tunnel that originates in the posterolateral leg and extends posterior to the medial malleolus. The roof of the tunnel is the flexor retinaculum, its anterior border is the medial malleolus, and the lateral border is the posterior process of the talus and the calcaneus. The tarsal tunnel contains the PTT, the flexor digitorum longus tendon, the FHL tendon, the posterior tibial artery and vein, and the tibial nerve. The tibial nerve gives rise to three terminal branches: the medial and lateral plantar nerves and the medial calcaneal nerve. Although the branching pattern is variable, usually branching occurs within the tarsal tunnel.
‘Tarsal tunnel syndrome’ is the clinical term for compression of the tibial nerve within the tunnel. Causes of compression include a history of trauma (eg, nonunion of sustentaculum tali fracture); valgus heel positioning; space-occupying lesions, including varicosities, lipomas, ganglion cysts, nerve sheath tumours, and accessory slips of muscle; and synovitis. Patients usually complain of a sense of burning pain and numbness on the plantar aspect of the foot. 5 The pain may radiate proximally along the course of the tibial nerve.
On physical examination, a positive Tinel sign (reproduction of the symptoms with percussion over the tarsal tunnel) may indicate tarsal tunnel syndrome. Positioning of the ankle in dorsiflexion and eversion minimizes the space available in the tarsal tunnel and may exacerbate symptoms, much as the Phalen test does for carpal tunnel syndrome in the hand. The posteromedial ankle should be inspected for any signs of varicose veins or masses. The physician should examine the lumbar spine to rule out radiculopathy and evaluate the patient's overall health status for other clinical entities (eg, diabetes mellitus and alcoholism) because they may be associated with similar symptoms that cause generalized neuropathy.
The diagnosis may be confirmed with nerve conduction and electromyographic studies; the results of the sensory nerve conduction velocity test are positive in 80% to 90% of cases. These studies also may help localize the site of compression. Before surgery, MRI often helps the physician evaluate for potential space-occupying lesions.
Treatment: In cases in which there is no identifiable space-occupying lesion, conservative measures should be undertaken (eg, NSAIDs, physical therapy, orthoses, and perhaps brief immobilization). Patients with a positive Tinel sign and positive electromyographic results for whom non-operative management is unsuccessful may benefit from surgical intervention, which may include an extensive release of the flexor retinaculum, as well as excision of any space-occupying lesion.
The best outcomes usually are seen in patients with a positive Tinel sign and with compression caused by space-occupying lesions. Potential complications include wound infection, dehiscence, haematoma formation, complex regional pain syndrome, and a lack of pain relief. The overall success rate is described as 50% to 90%, highlighting the importance of judicious patient selection.
Posterior Ankle Impingement
Diagnosis: The posterior process of the talus projects posteriorly from the articular surface of the ankle (talar dome). It has two distinct projections, posteromedial and posterolateral. The latter is an accessory ossification centre of the talus; in 7% to 14% of the population, it may remain unfused as an os trigonum and it may be confused as a sesamoid bone. Other patients have an enlarged posterolateral tubercle that is fused, known as a Stieda process.
Posterior ankle impingement is not a single clinical entity; it may result when any posterior anatomical structure impinges and causes pain with maximal plantar flexion of the ankle. Potential anatomical causes include an os trigonum (with or without fracture), soft tissue impingement (synovium or capsule), a prominent posterior calcaneal process, and intra-articular ankle pathology (posterior osteochondral or occult fracture). In addition, posterior ankle impingement often is associated with concomitant FHL tendinitis.
Patients usually present with chronic and recurrent posterior ankle pain that worsens with forced plantar flexion and with push off during running. This often is seen in athletes who run and jump suddenly, such as basketball players, and initially may be confused with a routine ankle sprain.
Imaging studies often reveal an os trigonum and may show an occult fracture. A plantar flexion lateral X-ray view is particularly helpful; it may show dynamic impingement. Computed tomographic (CT) scans may be used to rule out occult fractures, and MRI can be very helpful in looking for posterior oedema, bone bruising, and concomitant FHL pathology.
Treatment: Posterior ankle impingement often improves with rest and avoidance of aggravating activities. NSAIDs and brief immobilization help in up to 60% of patients. When conservative management does not alleviate the symptoms, surgery is warranted. The goal is to prevent the anatomical impingement from occurring with maximal plantar flexion. Surgical intervention could include excision of a symptomatic os trigonum, resection of a prominent posterior process of the calcaneus, and debridement of a redundant posterior capsule. If FHL pathology is present, it should be addressed at the same time, generally with a medial approach. More recently, arthroscopy has become a viable option; some studies suggest an earlier return to function in patients who undergo this procedure.
Diagnosis: The most common reason for chronic posterior ankle pain is Achilles tendon pathology. The Achilles tendon is formed from contributions of both the gastrocnemius (originating from the posterior femoral condyles) and soleus muscles. It receives its blood supply from proximal (muscular branches) and distal (calcaneal branches) areas but has a somewhat avascular zone between 2 and 6 cm from its insertion. There are two distinct types of Achilles tendinitis: insertional and non-insertional.
Non-insertional Achilles tendinitis tends to occur 2 to 6 cm proximal to the Achilles insertion of the calcaneal tuberosity. Most cases are thought to result from repetitive microtrauma and overuse; the condition is seen most often in runners. It is associated with increasing age, male sex, and overuse. Patients often describe a recent change in their type or intensity of activities. Symptoms usually are exacerbated with activity and relieved by rest.
Non-insertional Achilles tendinitis may include peritendinitis inflammation of the peritenon without frank tendinosis, tendinosis with significant degeneration of the tendon, or a com-bination of the two. Tenderness often is elicited by gently squeezing the tendon in the affected area, and the tendon often has a visible or palpable thickening in the area.
Insertional Achilles tendinitis occurs directly at the tendon's calcaneal insertion. It also may be associated with retrocalcaneal bursitis. The condition is associated with increasing age, female sex, obesity, and repetitive microtrauma. Tenderness and swelling are isolated to the calcaneal insertion of the tendon and retrocalcaneal bursa. Patients often report that open-backed shoes provide some pain relief.
For both types of Achilles tendinitis, plain radiographs should be obtained. The presence or absence of a Haglund deformity (enlargement of the posterior superior calcaneal process) should be noted. MRI may be very helpful when the diagnosis is in question and generally is very sensitive for both conditions.
Treatment: Initial management of both insertional and non-insertional Achilles tendinitis is aimed at decreasing the painful inflammation. The treatments include NSAIDs, ice, heel lifts, and activity modification. In severe cases, 4 to 6 weeks of immobilization in a walking boot can be helpful. For insertional Achilles tendinitis, footwear modification or gel heel sleeves can help alleviate external pressure on the heel. Corticosteroids are not recommended because of the risk of tendon rupture. Physical therapy and heel-cord stretching may be very helpful, particularly with attention toward eccentric calf stretching. More than 50% of patients attain relief with these modalities.
Recent studies have looked at new therapies for Achilles tendinitis. In one study, low-energy shock wave therapy was more successful than eccentric training for patients with Achilles tendinitis. Several studies also have looked at the effectiveness of platelet-rich plasma (PRP) injections for Achilles tendinitis. To date, the randomized studies looking at PRP injections have shown no increased efficacy with PRP compared with placebo, although studies are ongoing.
In refractory cases, surgery may be performed (for non-insertional Achilles tendinitis, tenolysis of the paratenon, and debridement of the degenerative areas of the tendon). In cases in which significant portions of the Achilles tendon are excised, augmentation with an FHL tendon graft may be warranted.
For insertional Achilles tendinitis, surgery includes debridement and repair of the diseased tendon; resection of the Haglund deformity, if present; excision of the retrocalcaneal bursa; and, if significant tendon degeneration is seen, an FHL transfer. The FHL tendon transfer now can be performed through a single incision with the use of interference screw technology. Satisfactory results are seen in 90% or more of patients who have chronic Achilles tendinitis.
Peroneal Tendon Injuries
Diagnosis: Chronic injuries to the peroneal tendons are a frequent cause of lateral-sided ankle pain. These injuries usually are tendon subluxations or longitudinal tears of the peroneus brevis muscle. The peroneus longus originates on the head and proximal two-thirds of the fibula and courses posterolaterally to the peroneus brevis at the level of the ankle; it inserts at the base of the first metatarsal. The peroneus brevis originates on the distal two-thirds of the fibula and inserts at the base of the fifth metatarsal. At the level of the ankle, the tendons course through a fibro-osseous tunnel posterior to the lateral malleolus, bordered laterally by the superior peroneal retinaculum, which is the chief restraint to peroneal subluxation.
The peroneals are the primary evertors of the foot. Patients with chronic peroneal tendon injuries typically report the insidious onset of lateral ankle pain that is worsened with activity. In the case of tendon subluxation, a painful snapping behind the lateral malleolus often is present.
Physical examination includes palpation of the tendons to identify both pain and swelling. In the case of subluxation, the foot should be passively placed into maximal inversion. Asking the patient to actively evert the foot against resistance while the peroneals are palpated may produce a snapping. Hindfoot alignment should be evaluated, because varus deformities place increased stress on the peroneals and may need to be addressed at the time of surgery.
Plain radiographs should be obtained to evaluate for occult fracture, osteochondral lesions, and arthritis that can mimic lateral ankle pain. MRI is the gold standard for imaging of peroneal tendon injuries; increased signal is seen on T2-weighted images.
Treatment: Medical management of chronic peroneal tendon pathology includes immobilization, NSAIDs, and footwear modification. A lateral heel wedge can unload the peroneal tendons and provide symptomatic relief in patients with a correctable varus deformity.
Refractory cases of peroneal tendon pathology may require surgical intervention tailored to the specific pathology. In the case of tenosynovitis, the inflamed tissue simply is debrided. Tears of the peroneus brevis may be repaired primarily with tubularization of the tendon or, if less than one-third of the tendon remains, a tenodesis may be performed. In the case of chronic tendon subluxation, the multiple procedures that have been described to address the pathology include repair or reconstruction of the superior peroneal retinaculum, rerouting of the peroneal tendons, and bony procedures (eg, bone block and deepening of the fibular groove).
Chronic Ankle Sprains
Diagnosis: Inversion injuries to the lateral ankle ligaments rank among the most common injuries sustained in sports activities; in the United States, more than 25,000 such injuries occur every day. Chronic ankle symptoms develop in about 20% to 40% of patients; higher-grade acute sprains portend a worse outcome.
The fibular collateral ligament complex is made up of three distinct anatomical structures: the anterior talofibular ligament, calcaneofibular ligament, and posterior talofibular ligament. Patients usually relate a history of a previous acute injury with subsequent persistent ankle pain often localized to the anterolateral aspect of the ankle. This pain often is accompanied by a sense of instability, a history of recurrent sprains, the inability to participate in sports, and difficulty in walking on uneven ground.
Chronic ankle instability often is broken down into mechanical or functional. Mechanical instability implies ankle mobility beyond the normal range of motion, including more than 10 mm of motion on anterior drawer testing (or a 3-mm difference compared with the contralateral side) or a talar tilt of greater than 9° (or a 3° difference compared with the contralateral side). Functional instability is a subjective sensation of the ankle ‘giving way’ during activities of daily living; it may be accompanied by mechanical instability.
Concomitant ankle pathology should be evaluated in patients who present with persistent pain between episodes of ankle sprains, because chronic instability in and of itself often is painless. Such pathology might include peroneal tendon dysfunction, syndesmotic injuries, complex regional pain syndrome, sinus tarsi syndrome, osteochondral lesions of the talus, loose bodies, synovitis, and ankle arthritis.
The physical examination should focus on assessing for mechanical ankle stability and looking for associated pathology. Mechanical stability is tested with the anterior drawer test and assessment of talar tilt. Comparing with the contralateral side is imperative because patients have varying degrees of inherent laxity. The overall positioning of the hindfoot also is important to consider—varus malalignment predisposes to recurrent inversion injuries.
Standard three-view radiographs of the ankle should be obtained to rule out bony abnormalities and concomitant arthritic changes. Stress radiographs, including an anterior drawer stress X-ray and a talar tilt view, also may be very helpful. MRI is warranted to evaluate for associated injuries to the peroneal tendons or osteochondral lesions in some cases and in most patients who will undergo surgery.
Treatment: Conservative management of chronic ankle instability includes physical therapy that focuses on strengthening, proprioception, and peroneal strengthening. Orthotic devices include small lateral heel wedges and ankle braces that reduce talar tilt during exercise. A common cause of persistent pain after an acute ankle sprain is inadequate rehabilitation; such cases should be managed with rest and therapy.
Chronic ankle sprains with mechanical instability that do not improve with maximal conservative management may require surgical reconstruction of the lateral ankle ligaments. More than 80 procedures have been described for the management of chronic ankle instability. These can be divided into anatomical reconstructions, in which the injured ligament is repaired secondarily with or without augmentation, and nonanatomical reconstructions, in which the peroneal tendons, plantaris, or a free tendon graft is used to re-create the stability of the lateral ligamentous structures.
Most patients can be treated effectively with an anatomical repair. Patients with severe instability or generalized ligamentous laxity and those with recurrent ankle instability may benefit from a non-anatomical repair.
Diagnosis: Occult fractures about the foot and ankle are common sources of persistent pain after a traumatic injury. The keys to diagnosis are a high index of suspicion and a very careful physical examination. Occult fractures may occur anywhere about the foot or ankle. In cases in which pain is out of proportion to the injury or when pain lingers beyond what would be expected in spite of appropriate immobilization, further workup is warranted.
CT scans pick up most clinically relevant fractures and provide valuable information about fragment size and displacement. MRI is very effective at picking up occult fractures as well and shows significant bony contusions, which also are a source of lingering pain. Two specific occult fractures bear special mention because they often are missed in the emergency setting: the lateral process of the talus fracture and the anterior process of the calcaneus fracture.
Anterior process of the calcaneus fractures occur with inversion of a plantar flexed ankle; they essentially are an avulsion fracture of the bifurcate ligament. Maximal tenderness is encountered anterior and inferior to the anterior talofibular ligament, adjacent to the calcaneocuboid joint, unlike with a standard sprain, which is maximally tender over the ligaments themselves.
Detailed knowledge of the anatomy is imperative in making the diagnosis. These fractures often are not well visualized on standard radiographic views. An oblique X-ray film of the foot that projects the anterior process away from the talar neck allows for the best visualization. In cases in which there is any question, fine-cut CT scans or MRI scans may be used to confirm the diagnosis.
Lateral process of the talus fractures, also known as snowboarder fractures, occur most frequently with a fall or a motor vehicle accident. The area of maximal pain is elicited just anterior and inferior to the lateral malleolus. Most fractures may be seen on standard three-view radiographs of the ankle, but small fragments may not be visualized, especially if the film quality is suboptimal.
Treatment: Management of anterior process of the calcaneus fractures varies with the fracture size. Most fractures can be managed nonoperatively at first, with casting or placement of a fracture boot, followed by progressive weight bearing after 4 to 6 weeks. Small fracture fragments that remain symptomatic after several months may be managed with surgical excision. Larger fractures (greater than 1 cm with displacement of greater than 2 mm) are best managed with open reduction and internal fixation. For lateral process of the talus fractures, small fragments with minimal displacement are managed non-operatively; larger fragments are managed with surgery (surgical excision or fixation, depending on the size and the degree of comminution).
Osteochondral Lesions of the Talus
Diagnosis: The ankle is subjected to more weight-bearing force per unit area than any other joint. Osteochondral lesions of the talus may result in chronic, intra-articular ankle pain. Lesions of the medial talar dome are responsible for about 60% of talar osteochondral lesions, usually are larger than lateral lesions, and are posttraumatic in about 60% to 80% of cases. Lateral talar dome osteochondral lesions are slightly less common; they account for about 40% of lesions, although essentially all of them are posttraumatic.
Persistent ankle pain in the absence of obvious prior trauma or lack of improvement of an acute injury over time should raise suspicion of a talar osteochondral lesion. Patients often complain of vague pain about the ankle. They may complain of mechanical symptoms with the presence of a loose body within the ankle joint.
Plain radiographs should be obtained; they often show irregularities of the talar dome and may show a loose body. The importance of MRI in the evaluation of possible osteochondral lesions cannot be overstated. MRI highlights the size of the lesion, shows the extent of underlying bony oedema, and may be used to evaluate the surrounding tissue for concomitant injuries. In addition, MRI may pick up purely cartilaginous or non-displaced lesions that might be missed with plain radiographs.
Treatment: Non-surgical management, which includes immobilization initially in a cast and non–weight bearing to allow the lesion to heal, generally is more effective in acute injuries and in younger patients. This treatment can be expected to result in a successful outcome in about 50% of cases.
The choice of a surgical approach to management varies with the size and chronicity of the lesion. Surgery at first generally consists of arthroscopic debridement and microfracture. In cases in which there is an intact cartilage cap, retrograde drilling may be entertained. Other techniques include osteochondral autograft, osteochondral allografts, autologous chondrocyte implantation, and newer natural tissue grafts. The specific indications and details of these procedures are beyond the scope of this article.
Diagnosis: Although the ankle has the thinnest and most uniform cartilage of any major weight-bearing joint, it is subjected to strong forces with ambulation. Even so, the incidence of symptomatic arthritis in the ankle is markedly lower than that in the hip or knee.
In most cases, ankle arthritis is posttraumatic; it may occur after ankle, talus, or pilon fractures (intraarticular fractures of the distal tibia) or severe ligamentous injuries. Of note, the radiographic changes of arthritis usually are seen within 2 years of the injury.
The most common presenting symptom is anterior ankle pain. Such pain often is described as worsening with uphill ambulation and improving somewhat with walking down an incline. Plain radiographs usually are the only imaging modality needed; joint-space narrowing, subchondral sclerosis, osteophyte formation, and subchondral cysts all are seen frequently. MRI may be helpful when osteochondral lesions or osteonecrosis of the talus is suspected.
Treatment: Conservative management approaches include systemic NSAIDs, intra-articular injections (both diagnostic and therapeutic), footwear modification (eg, solid ankle cushion heel or rocker bottom sole), and bracing. Some groups advocate the use of intra-articular hyaluronic acid injections, although to date there are no randomized prospective trials to support their efficacy. In cases of ankle arthritis that are refractory to conservative therapies, several surgical options may be considered.
Historically, ankle fusion has been the gold standard for debilitating ankle arthritis. More recently, total ankle replacement has seen a resurgence in popularity. Good candidates for ankle replacement include older patients with minimal deformity and instability. Early to mid-term results are encouraging, but long-term data with the newer total ankle prostheses are still pending.
(ĐTĐ) - Pain is purely subjective, difficult to define, and often hard to characterize or interpret. It is currently defined as an unpleasant sensory and emotional response to a stimulus associated with actual or potential tissue damage or described in terms of such damage (3–5).
However, pain has never been shown to be a simple function of the amount of physical injury; it is extensively influenced by anxiety, depression, expectation, and other psychological and physiological variables. It is a multifaceted experience, an interweaving of the physical characteristics of the stimulus with the individual’s motivational, affective, and cognitive functions. The pain experience is in part behavior based on an interpretation of the event, influenced by present and past experiences.
Acute pain is a biologic symptom of an apparent nociceptive stimulus, such as tissue damage that is due to disease or trauma that persists only as long as the tissue pathology itself persists. The pain may be highly localized or may radiate. Acute somatic pain may be well localized, aching, and sharp, whereas acute visceral pain may be burning, cramping, and radiating. It is usually associated with upregulated sympathetic activity, tachycardia, hypertension, tachypnea, increased metabolic rate, and hypercoagulability. Acute pain is generally self-limiting, and as the nociceptive stimulus lessens, the pain decreases. Acute pain usually lasts a few days to a few weeks (4). If it is not effectively treated, it may progress to a chronic form.
Chronic pain is a disease process in which the pain is a persistent symptom of an autonomous disorder with neurologic, psychological, and physiologic components. Differing significantly from acute pain, it is defined as pain lasting longer than anticipated (greater than 3 months) within the context of the usual course of an acute disease or injury. The pain may be associated with continued pathology or may persist after recovery from a disease or injury. Due to the complex nature of chronic pain, many other definitions have been proposed. Some include factors such as the persistence of pain despite extraordinary measures in a nonacute setting or pain that is without apparent biological value (6). Operational definitions include aspects such as pain sensation, pain behavior, functional status, emotion, and somatic preoccupation (6). As with acute pain, treatable chronic pain that is due to organic disease is managed by effectively treating the underlying disorder; however, no such identifiable organic disease may be evident. Chronic pain can mimic the qualities of acute pain except that associated signs of autonomic nervous system response may be absent, and the patient may appear exhausted, listless, depressed, and withdrawn. Chronic pain can have exacerbations that are triggered by progression of organic pathology, physiologic stress, or worsening emotional, social, and psychiatric problems. As these problems subside, the pain may improve. Chronic pain may also be highly persistent and reported as severe for years without remission. Proper management of pain requires an understanding of its complexity and knowledge of the nonneurologic factors that determine its individual expression. The treatment of pain with physical modalities is as ancient as the history of humanity, but the use of interdisciplinary rehabilitation techniques has gained acceptance only within the past few decades.
Nearly everyone experiences acute pain. Its incidence approximates the cumulative total of all acute diseases, trauma, and surgical procedures. In studies of the general population, patients have identified the head and lower limbs as the most common sites of acute pain and have identified the back as the most common site of chronic pain (7). Chronic pain is less frequently experienced but is reaching epidemic proportions in the United States. There are more than 36 million individuals with arthritis, 70 million with episodic back pain, 20 million with migraine headaches, and additional millions with pain that is due to gout, myofascial pain syndromes, phantom limb pain, and complex regional pain syndromes (CRPS) (8–11). The pain resulting from cancer afflicts approximately 1 million Americans and 20 million individuals worldwide. Moderate to severe pain occurs in about 40% of patients with intermediate-stage cancer and in 60% to 80% of patients with advanced cancer (12–14). Back pain, as a general condition, episodically affects nearly 75% of the population in most industrialized nations. It is estimated that at least 10% to 15% of the working population of industrialized nations are affected by back pain each year (9,10).
Genetics and Pain
The genetic determinants have been evaluated in humans with clinical pain (47). The variability in pain syndromes has been associated with inherited genetic factors in back pain (48), fibromyalgia (FM) (49), menstrual pain (50), and migraine (51). Family and twin heritability estimates indicate genetic as well as significant environmental factors modulating pain (52,53). Polymorphic pain genes have been associated with congenital insensitivity to pain (54), drug metabolism due to cytochrome P450 (55), familial hemiplegic migraine (52,56), FM (57), and reflex sympathetic dystrophy (58).
Gene therapy and other advances in molecular medicine may offer a means of enhancing antinociceptive receptors ( cannaboid—1 and 2, acetylcholine—m and n, opioid—m and k, adrenergic—a2) or blocking pronociceptive receptors (neurokinin—1-a-amino-3-hydroxy-5-methyl-4-isoazoleproprionate [AMPA], n-methyl-d-aspartate [NMDA]); acting directly on the calcium channels of pain fibers; or acting directly on membrane receptors, protein C-GAMA, or other areas of the central nervous system involved in the transmission of pain (59,60). Definitive applications of gene intervention in pain control remain to be developed.
Resolution of Pain
Acute pain is frequently the result of tissue damage in which the initial pain leads to an increase in anxiety, which magnifies the pain experience. The amount of anxiety generated and possibly the level of pain seem to be more influenced by the setting in which the pain develops rather than personality variables. With the healing process comes a reduction or termination of the anxiety and acute pain perception. When acute pain, which functions as a warning signal, fails to respond to treatment with conventional medical therapies, illness behavior and chronic pain develop. The anxiety characteristic of acute pain is replaced by depression with hopelessness, helplessness, and despair. When pain relief fails, physical activities decrease and suffering and depression increase.
Acute pain usually resolves when the source of nociception is removed or cured and resolves quickly with application of appropriate pharmacologic or regional analgesic therapy. The cause of acute pain can be documented by physical examination findings and diagnostic procedures. When indicated, appropriate operative intervention can be performed on the basis of these findings. A short course of analgesic medication usually controls postoperative pain, and a return to full, painless function can be anticipated in a matter of weeks. Acute pain control requires the administration of an efficacious analgesic dosage. Too little analgesia promotes suffering and anxiety, thus defeating the purpose of prescribing medications. Fear of drug addiction contributes to the underutilization of analgesic medications, and physicians tend to undermedicate in terms of frequency and dosage of pain medications (61,62). By prescribing low oral doses of opioids at infrequent intervals, physicians inadvertently force patients to adopt pain behavior in order to obtain adequate opioid analgesia. Pain behavior is characterized by high verbalization of pain, dependency, and the inability to work. Addiction in the acute pain situation is very rare, approximating less than 0.1% (63,64).
Unfortunately, a significant minority of acute pain patients continues to experience pain, which may progress into a more complex disease entity. Pain, a symptom of physiologic malfunction, now becomes the disease itself. Chronic pain represents a complex interaction of physical, psychological, and social factors in which the pain complaint is a socially acceptable manifestation of the disease. The etiology of chronic pain may be persistent nociceptive input, such as arthritis or terminal cancer; psychological disorders, such an anxiety, depression, and learned behavior; or social factors, such as job loss, divorce, and secondary gain.
The optimal treatment for chronic pain is prevention. Once the disease state of chronic pain commences, reinforcers such as monetary compensation, presence of job-related problems, manipulation of the environment to satisfy unmet needs, and retirement from the competitive world obstruct complete disease resolution. Therapies designed for acute pain are often contraindicated for chronic pain.
Prevention of chronic pain requires identifying contributing factors and resolving them early in the acute stage. Aspects worthy of attention include psychological stress, drug or alcohol abuse, and poor posture or muscle tone, as well as significant psychological and operant pain mechanisms. Physicians should set a reasonable timeframe for the resolution of the acute pain process. Patients should be advised when the pain medication will no longer be needed and that those medications that are no longer effective will not be continued. The patient’s attention should be directed to a gradual return of full activity on a prescribed schedule. Follow-up appointments should be planned at specified intervals so that the patient does not need to justify a visit. Work intolerance and job conflicts should be resolved.
Chronic pain syndrome is a learned behavior pattern reinforced by multiple factors. These behaviors are frequently found in individuals who are depressed, are inactive, and lack the skills or opportunity to compete in the community. These environmental factors promote pain behavior, regardless of the etiology of the pain, thereby distinguishing the patient with chronic pain from the population at large. Patients often develop a new self-image and see themselves as disabled by their pain. This self-perceived disability justifies their inactivity and manipulation of others and attempts to collect compensation. The typical patient often has been unemployed, has low job satisfaction, or has been on sick leave for long periods of time (65–68). Our data indicate that individuals who have been removed from the labor market because of pain for less than 6 months have a 90% chance of returning to full employment; those removed from the labor force because of pain for more than 1 year have less than a 10% chance of return to full employment (66). Individuals with chronic pain syndrome receive gains from their pain behavior; hence, they continue this behavior to maintain those positive reinforcers. Physicians reinforce the pain behaviors by lacking knowledge of this chronic disease process, failing to identify the chronic pain behavior and prolonging prescription of inappropriate medications, inactivity, and work limitations. The physician’s failure to acknowledge and direct the patient toward recovery tends to validate the chronic pain syndrome by providing an undiagnosable and untreatable problem. Family members also frequently reinforce the chronic pain behavior. They allow the individual to become inactive and cater to the patient’s requests and needs over prolonged periods of time. In some instances, patients with chronic pain provide role models for pain or disability behavior for other family members (69,70).
Chronic pain is complex. Research over the past 25 years has shown that pain is influenced by emotional and social factors. These need to be addressed along with the physical causes of pain. Chronic stress is one factor that contributes to chronic pain. The good news is that you can get natural pain relief by making relaxation exercises a part of your pain-management plan.
The Body's Response to Stress
To understand how natural pain relief works, it's important to understand how stress affects your body. Pain and stress have a similar effect on the body: your heart rate and blood pressure rise, breathing becomes fast and shallow, and your muscles tighten.
You can actually feel your body's response when you're faced with a sudden, stressful event, such as fearing that a car is about to hit you. The car misses you and, in time, your system returns to normal. You relax.
With chronic stress, such as worrying about health or finances, feeling stuck in a bad job or marriage, or fearing that something bad will happen, the nervous system keeps the body on alert. This takes a big toll on your body. Levels of stress hormones increase, and muscles remain in a nearly constant state of tension.
Chronic stress hurts.
Here's just one example: Studies that measure site-specific muscle tension in patients with chronic back pain have shown that simply thinking or talking about a stressful event dramatically increases tension in back muscles.
Relaxation Techniques for Natural Pain Relief
Relaxation exercises calm your mind, reduce stress hormones in your blood, relax your muscles, and elevate your sense of well-being. Using them regularly can lead to long-term changes in your body to counteract the harmful effects of stress.
Don't get stressed trying to pick the "right" relaxation technique for natural pain relief. Choose whatever relaxes you: music, prayer, gardening, going for a walk, talking with a friend on the phone. Here are some other techniques you might try:
- Foursquare breathing. Breathe deeply, so that your abdomen expands and contracts like a balloon with each breath. Inhale to a count of four, hold for a count of four, exhale to a count of four, then hold to a count of four. Repeat for ten cycles.
Guided imagery. Breathe slowly and deeply. For example, imagine a tranquil scene in which you feel comfortable, safe, and relaxed. Include colors, sounds, smells, and your feelings. Do five to ten minutes each day.
Self-talk. Change how you think about your pain and yourself. For example, change "Pain prevents me from keeping house the way I used to -- I'm a failure" to "No one will die if the house isn't perfect. I can get a lot done by breaking down tasks into baby steps."
Hypnosis. Hypnotherapists can induce hypnosis and implant suggestions, such as, "You're going to sleep soundly tonight." Audiotape the session so that you can repeat it at home.
Mindfulness meditation. Sit or lie quietly and notice your breathing without controlling it. If pain or thoughts interfere, simply notice them without trying to push them away. Think of them as a cloud passing over; then return to observing your breath. Do this for about 20 minutes.
Medicines can often help control chronic pain. Many different drugs, both prescription and nonprescription, are used to treat chronic pain. All these medicines can cause side effects and should be taken exactly as they are prescribed. In some cases, it may take several weeks before medicines work to reduce pain. To avoid dangerous drug interactions, tell your doctor all the medicines you are taking (including herbal and other complementary medicines).
The cause of chronic pain is not clear. When you have an injury or illness, certain nerves send pain signals to your brain. With chronic pain, these pain signals continue for weeks, months, or even years after you recover. Chronic pain can develop after a major injury or illness, such as a back injury or shingles, or it can develop without a known cause. It is also possible that certain brain chemicals that usually suppress pain may not work properly. The pain may be:
Pains from your skin and muscles are easily localized by the brain because these pains are common. You have experienced general somatic pain since childhood when you have fallen or been hit by a person or an object. Normally, somatic pain gets better in a few days.
In some cases, chronic pain develops after an injury or illness. The pain continues even after you have recovered from the injury or illness. For example, many people who have had a limb amputated report feeling chronic pain in the missing limb (phantom limb pain). Chronic pain can also develop even though you have not had an injury or illness. But the result is often the same-a cycle of sleeplessness, inactivity, irritability, depression, and more pain.