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Are Joint Contractures in Patients with Alzheimer’s Disease Preventable?

Namirah Jamshed, MD, and Edward L. Schneider, MD

August 2010

Joint contractures impair quality of life and lead to further complications and disability. In severe dementia, many patients are seen in a fetal position. This position causes flexion of the muscles at joints, causing the muscles to undergo shortening, resulting in degenerative tissue changes, and then leading to potential irreversible deformity. The authors discuss the development of joint contractures in Alzheimer’s disease (AD), where it is thought that the natural progression of AD terminates with patients in the fetal position. It has been postulated that this fetal position causes the high incidence of contractures seen in end-stage AD. However, in many situations it is the absence of adequate prevention strategies that produces contractures. (Annals of Long-Term Care: Clinical Care and Aging 2010;18[8]:26-33)
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Joint contractures are well recognized in the geriatric community as a disabling complication of dementia. They impair quality of life and lead to further complications and disability. In severe dementia, patients are commonly seen in a fetal position. The flexion of the muscles at joints causes the muscles to undergo shortening, resulting in degenerative tissue changes, and then leading to potential irreversible deformity. The upper limb is seen in a flexed position with adduction at the shoulder joint and flexion at the elbow, wrist, and fingers. In the lower limb, the hip is usually flexed with inversion of the feet. Earlier intervention with regular passive movements of the affected limbs may prevent contracture development.1 Prevention is thought to be the best medicine for contracture management.

In this article, we will discuss the development of joint contractures in Alzheimer’s disease (AD). It is thought that the natural progression of AD terminates with patients in the fetal position. It has been postulated that this fetal position causes the high incidence of contractures seen in end-stage AD. However, in many situations it is the absence of adequate prevention strategies that produces contractures, resulting in patients assuming the fetal position.

Joint Development and Physiology 

Joints are organs with the function of providing skeletal articulation and allowing movement of the skeletal frame. A joint is stabilized by its capsule, tendons, and ligaments. The ligaments, which are dense connective tissue, provide connection between bones, whereas the tendons connect muscle to bone, which is integral in stabilizing the joint.

Joints first appear at six weeks of gestation. The external mesenchymal tissue forms the joint capsule and tendon, and the internal layer forms the synovial membrane and meniscus. This typically occurs at seven weeks. In a week’s time, cavitation usually occurs, with the end result of an articular cavity.2

Skeletal muscle is comprised of muscle fibers and connective tissue. Each muscle fiber contains thousands of myofibrils, which in turn comprise thick and thin filaments, called myosin and actin, respectively. It is these thick and thin filaments that account for muscle contractions.3 Muscles contain both contractile tissue and connective tissue.4 The contractile component contains filaments that move past each other to cause contraction or lengthening. The connective tissue is what contains the filaments, fibrils, and fibers together. Connective tissue is made up of both collagen and elastic fibers. The collagen provides tensile strength, whereas the elastic fibers are elastic.4 During normal development, muscles grow by adding sarcomeres to the ends of myofibrils. Growth is influenced by rate of bone growth, amount of stretch, presence or absence of hormones, and nutritional status.4 A muscle contains multiple motor units that are involved in contraction of muscle fibers. The function of each skeletal muscle is related to the size of this motor unit.5 Motor units contain innervations and are dependent on stimuli. Muscles have great adaptive potential. However, these could be impaired as part of aging.

Definition of Contractures

Contractures are limitations in the passive range of motion (ROM) at a joint.6 In clinical terms, contractures are a result of muscle shortening to the point that complete ROM at that joint is prevented.7 This is usually due to a restriction of the peri-articular connective tissues, but in more advanced cases also involves tendons, ligaments, muscles, and joint. If not treated, it can lead to bony ankylosis of the joint.2 Contractures can range from minimal reductions in the ROM at a single joint to severe fixed limitations in movement at multiple joints. As a result, they impair physical functioning.8 Often, however, they are preventable.8

Pathophysiology of Contractures 

The pathophysiology of a joint contracture is complex. As mentioned above, a joint contracture not only involves the joint capsule, but also the ligaments, muscles, and tendons present in the joint. Thus, it is not just the joint itself but its surrounding structures that become part of this deformed position.

Joint contractures can result from changes within the joint and adjacent tissue, with immobility as a result of disease or other extrinsic causes. Joint movement can be limited secondary to pain, paralysis, fibrosis of the capsule, or primary muscle damage. However, a fixed contracture results from lack of joint mobilization, through its full ROM. This causes reduction of resting flexing muscle length and tightness of the capsule and soft tissue, resulting in a fixed joint contracture. The rate of contracture development is determined by limb position, duration of immobilization, and pre-existing pathology. Many joint contractures result from pathologic changes in the joints or muscles. In persons with AD, without intrinsic joint pathology or upper motor neuron (UMN) disease, fixed joint contractures can occur from improper positioning in bed or chair, immobilization, and lack of stretch.9

Risk Factors for Contractures

Any condition that may prevent a joint going through its full ROM can result in contractures.10 Joints must periodically be put through their full ROM to prevent a tightening of the surrounding soft tissues and muscles. Normally, thin layers of loose areolar connective tissue separate tissues, allowing them to glide on one another during normal motion. With immobilization, the loose connective tissue becomes denser, decreasing the gliding property. The process is worsened in superimposed local trauma, hemorrhage, impaired circulation, pre-existing degeneration, or edema.6 In patients with AD, the cause could primarily be immobility, underlying pain, trauma, weakness, or edema.6Any neurological condition that may increase muscle tone or cause muscle weakness can also result in impaired mobility of the joint, resulting in contracture. Patients with lengthy illnesses and chronic conditions are at highest risk of developing contractures, by virtue of immobility.11 Once a contracture is formed, it can become irreversible.

Epidemiology of Contractures

The prevalence of contractures in the nursing home (NH) is between 24% and 75%.12-14 According to the 2005 Online Survey, Certification And Reporting (OSCAR) database, 28.9% of approximately 386,000 NH residents across the United States have contractures.15 It has also been found that the mean length of stay of NH residents with contractures is three times as long as for those without contractures.8,13 Wagner et al8 looked at contractures in frail NH residents; the mean age of their sample was 89 years, and they identified a total of 480 contractures in four medium-sized NHs. Over 60% of the sample had at least one contracture, and 45.4% had two or more contractures. The most common contractures were those affecting the shoulders (44%) and knee (44%). Cognition was significantly lower in patients with contractures. This study reported a higher prevalence of contractures among NH residents than was previously reported in the OSCAR 2005 data.

Selikson et al16 studied the risk factors associated with immobility in a 200-bed skilled nursing facility in a case-comparison, retrospective cohort study. The investigators screened 80 residents, 34 of whom were immobile. These were compared to 12 ambulatory residents. Among the immobilized residents, 70.6% had contractures, and none of the ambulatory residents had contractures. Analysis of the group with the contractures showed that stroke, Parkinson’s disease, and dementia were commonly present in this group.16 Another study done by Resnick17 looked at 59 older people living in a long-term care facility. In this cohort 19 residents had upper-extremity contracture and 15 had lower-extremity contractures. In their stepwise multiple regression model, both upper- and lower-extremity contractures were associated with exercise and functional performance.

Sackley et al18 looked at the prevalence of joint contractures in patients with strokes; however, those with a primary diagnosis of dementia were excluded. Contractures were defined as a 30% or higher restriction when compared with the good side of the body. Mean age was 76 years. Sixty percent of the patients in the study sample had language or cognitive impairment. The investigators assessed status at three, six, and 12 months post-stroke. Out of 122 stroke survivors, 60% had contracture development. The highest percentages of complications unfortunately were seen in patients living in NHs at the time of the 12-month assessment. Other complications included falls, pain, shoulder pain, depression, and pressure sores. The prevalence was higher in the NH residents, likely due to higher impairment and care needs than community-dwelling patients.

We found only one study specifically looking at contractures in persons with AD. This was a case series done by Souren and colleagues13 looking at 161 patients from a university-based dementia research center. More than 75% of the nonambulatory patients developed contractures. In this study, contractures were defined as a 50% or more decrease in ROM at the joint. One hundred fifty-six patients had more than one joint involvement. Contractures correlated with increased disability as well. Data regarding the vulnerable elderly both in the community and NH setting are limited. In addition, many studies have not defined contractures, and where defined, it is not standardized. It is very likely that the prevalence of contractures is much higher than reported in the above studies. Large multicentered studies are needed to accurately report both the prevalence and incidence of contractures in the elderly population.

Role of Aging in Contracture Formation 

Sarcopenia is a well-defined phenomenon in aging. There is an age-related loss in skeletal muscle mass and contractile strength. Age-related atrophy is not reversible. However, studies showing that exercise programs and nutritional intervention can improve or partially reverse this process indicate that some of this loss is more likely related to inactivity or malnutrition than purely age.19 Patients with AD go through the same physiology of aging as do patients who do not have AD. Additionally, in the advanced or severe stages of AD, frailty is associated with impaired function of the musculoskeletal system. First signs of mild impairment in contractile function are seen in the fourth decade of life, with a slowly progressive decline thereafter. In addition to this, other comorbid conditions and chronic diseases complicate longevity, all likely present in persons with AD, in addition to their dementia. Thus, individuals with AD at later stages are exposed not only to the functional decline as a result of the dementia, but also to sarcopenia, frailty, and chronic diseases. All of these can lead to further immobilization and muscle weakness, both of which can result in joint contractures.

Consequences of Contractures
Contractures are frequently used as quality indicators for NHs. The Omnibus Budget Reconciliation Act of 1989 specified that facilities must ensure that residents who enter their facilities without contractures do not experience a reduction in their ROMs without justifiable reasons.20 It is thought that their development can be delayed with exercise programs, massage, and physical therapy.8,21,22 Mollinger et al12 studied knee flexion contractures in the elderly. They looked at 112 NH residents and collected data initially and after a ten-month period. They used the criteria of less than a five-degree knee extension as impaired. In their population they found that only 25% of the elderly had full extension in both knees. The majority of the residents had at least some degree of unilateral knee flexion contracture. Those with severe contractures of greater than 20 degrees were non-ambulatory. These data also showed a significant association between the degree of knee contracture and resistance to passive ROM, cognitive impairment, knee pain, and limited ambulation. They also saw that patients who regressed at the ten-month period were those who had minimal contracture initially and were ambulatory, and showed a decline of ambulation at the ten-month period, along with resistance to passive ROM. This study has implications for a role of physical therapy in patients with both severe contractures and those with minimal contractures who decline in ambulation over time or develop resistance at the joint.

In the older population, the most common causes of contractures are immobility from illness,2 surgery, or neuromuscular diseases such as stroke, Parkinson’s disease, and dementia. Contractures can, in themselves, lead to additional serious conditions in patients with AD. These include pain, circulation problems, pressure sores, wounds, and sometimes even fractures of joints or bones.8,23,24 In patients with stroke, the unopposed spastic contraction of muscle groups commonly leads to contractures. In one study done on complications of stroke, contractures were found in 60% of the patients over the ensuing 12 months.25 This is usually a result of reduced voluntary recruitment of skeletal motor units secondary to paresis, soft-tissue contracture, especially muscle-shortening and joint contracture, and a decreased ability to relax muscles.

A recent randomized, controlled trial in patients with stroke studied the use of routine splint placement to the wrist and hand, for prevention and treatment of contractures. The wrist was splinted in either the neutral or extended wrist position for four weeks. The trial did not show a reduction in wrist contractures after stroke with splinting.26 Other studies on neurological population have shown similar results in regards to splinting and stretching programs. These difficulties in preventing and treating patients with stroke may have influenced clinicians in their approach to contractures in persons with AD. 

Contractures are associated with impaired ambulation,12,13 pain,12 decreased functional status,27,28 and pressure ulcers.25,29,30 This causes increased burden on the caregivers caring for patients with contractures. Increased time can be spent in changing positions and carrying out daily activities, or even transferring patients. Contractures are also associated with institutionalization.25

AD and Contractures

AD accounts for more than one-half of all cases of dementia31 and is estimated to affect five million persons in the United States.13 AD is characterized by slow, progressive cognitive and behavioral deterioration. Mild AD is usually manifested by confusion, disorientation, impairment of judgment, and difficulties with short-term memory. In moderate AD, the symptoms worsen, and impairment in function increases. It is in severe AD where a near vegetative, immobile stage occurs. As the disease progresses, patients progressively have more difficulty walking and become bedridden. Not surprisingly, Souren et al13 found a striking correlation between the degree of functional decline and occurrence of contractures in persons with AD.

While most contractures occur in this final stage of AD, acute conditions in the earlier stages of AD can lead to contractures that have significant effects on the care of these individuals. For example, hip fractures, subsequent hospitalization, and institutionalization can result in contractures at the knee that prevent successful rehabilitation and ambulation. This can result in substantial increases in the long-term care resources needed by these patients.

How Immobilization in AD Leads to Contractures

Immobility has detrimental effects on cardiovascular, respiratory, gastrointestinal, musculoskeletal, urinary, metabolic, and psychosocial effects.32,33 Contractures have also been seen to increase risk of spontaneous fractures in NH residents.34 Immobility is a common denominator in joint contractures,35,36 including those in persons with AD. Even without risk factors such as fractures, arthritis, and neurological damage, immobility causes the joint capsule to undergo changes that can produce a contracture.35 A review done by Farmer and James4 showed that in immobilization, muscle weakness, paralysis, or spasticity can lead to contracture formation in neuromuscular disease. A muscle immobilized in a shortened position leads to reduction in muscle fiber length due to a loss of serial sarcomere. There is also a resultant remodeling of the intramuscular connective tissue leading to increased muscle stiffness.37,38

Thus, immobilization causes changes within the joint, muscle, tendon, and connective tissue. Prolonged immobilization can lead to proliferation of the fibro-fatty connective tissue, which encroaches into the joint space. These initial changes occur within two weeks of immobilization. If immobilization continues, this results in fibrous adhesions and further reduces the mobility of the joint. The two surfaces of the cartilage that are in contact also thin. As this is occurring, immobilized muscle in the shortened position loses sarcomeres. Connective tissue also loses its extensibility. The connective tissue accumulation leads to increased resistance in the muscle to passive stretch. All of these physiological changes as a result of immobilization in turn lead to contracture formation at the joint involved.4

Histological studies of immobilization in animal models have been done to examine joint contractures.39-42 A study done by Evans et al40 showed that even non-rigid immobilization can produce structural changes in joints. After prolonged immobilization, contracture of both the muscles and joints develops and causes restriction in ROM, due to shortening of muscles. In response to immobilization, connective tissue proliferates and limits further motion, and some of these changes are irreversible.39

Trudel et al43 looked at the joint motion limitations after prolonged immobility. They tested 40 rats in which one knee joint was immobilized for up to 32 weeks, and 20 animals were used as controls. In the experimental group, the ROM decreased in the first 16 weeks at an average rate of 3.8 degrees per week, resulting in about 61 degrees of restriction. After that there was a plateau. The loss in ROM was in extension and not in flexion. Their conclusion was that contractures start with immobility and last 16 weeks in these experimental models, and then become chronic.43 This study shows that reduced ROM after immobility in a flexed-knee position resulted from lack of extension at the knee joint. In another study, Trudel and Uhthoff44 looked at the type of restriction in a contracture due to immobility. They again found the development of contractures in all knee joints that were immobilized. They reported that it was the articular structure that was responsible for the limitation in ROM. This indicates the arthrogenic etiology of contractures with immobility.44 Trudel et al45 also found that immobilization caused contrasting patterns of cartilage degeneration at opposed sites as compared with unopposed sites in animal models. Clinically, this implicated that since cartilage has limited potential for self-repair, it is important to focus on prevention and mobilization in patients with joints that are at risk of developing contractures or have developed early contractures.

The culprit responsible for contractures in AD is immobilization, which results in a lack of passive or active movement of the joints. The person with AD, as with many elderly hospitalized patients, tends to position him/herself in a flexed position: neck flexed, shoulders internally rotated, thorax flexed, arms flexed, forearms supinated, fingers flexed, hips/knees flexed, and ankles plantar flexed. Joint immobilization often results in the muscle crossing the joint in a shortened position. This leads to decreased neural stimulation because of the decreased tonic muscle stretch. This in turn produces muscle contracture.46 Loss of normal weight-bearing or counter-resistance activity from disuse or immobilization stimulates a catabolic state within the musculoskeletal system. This causes a loss of muscle mass and reduction in bone mineralization. The bed rest or immobilization, along with the sarcopenia of aging, also contributes to the loss of skeletal mass.

Studies in patients with paresis have shown that muscle atrophy, loss of sarcomeres, accumulation of intramuscular connective tissue, increased fat content, and degenerative changes at the myotendinous junction result in the initiation of muscle contracture formation within the first six hours of immobilization.46 After six weeks, the remodeling of muscle with dense connective tissue limits ROM. Studies in humans have shown that a few weeks of immobilization lead to a significant loss of force output detected by electromyogram during maximal voluntary contraction.46 Even in patients without AD, bed rest for a few weeks substantially reduces maximal voluntary strength.

Any decline in a level of activity of a part of human body, such as limb restraints, can lead to reduced physiological demands on the patient’s muscle.46 It has been shown that there is daily loss of muscle strength with bed rest. The loss is faster in the lower extremities. An elderly patient can lose as much as approximately 1 kg of muscle from a lower extremity with ten days of bed rest.47,48 It would be more efficient to prevent the loss of muscle mass from bed rest than to try correcting it. We postulate that unlike patients with stroke, where contracture is a result of both immobilization and central disease, patients with AD but without stroke suffer from contractures mainly as a result of immobilization and disuse.

Immobilization also causes an imbalance between collagen synthesis and degradation, leading to shortening of connective tissue around the joints resulting in contracture formation and loss of ROM.6,49,50 A muscle that has been immobilized in a contracted position (non-neutral) will show evidence of remodeling of loose connective tissue into dense connective tissue.49,51 Most of the contractures in persons with dementia are either of the soft-tissue type involving skin, subcutaneous tissue, tendons, and ligaments, or myogenic, where a muscle has been left in a non-neutral position. Both of these result in joint contractures with loss of ROM.49 For example, being bedridden results in frequent hip flexion contractures. Walking is the only true activity that causes full hip extension, and, therefore, inability to walk could result in hip flexion contractures.52 Animal studies indicate that proliferation of connective tissues occurs within the joint capsule in the immobilized joint. This causes development of adhesions12 and provides yet another mechanism for contractures as the result of immobility.

Another common occurrence in patients with AD is limb apraxia, specifically ideomotor apraxia (IMA). This type of apraxia has functional consequences. IMA is associated with cognitive impairment in declarative knowledge of the action appropriate to a particular object, impairment in problem solving, deficits in motor planning, and difficulty in learning new gestures. Further studies are needed to study the impact of IMA in patients with AD. However, it can be postulated that unrecognized IMA in persons with AD in the community or in the NH could lead to a functional decline, disuse, and, eventually, immobility and possible resulting contractures.53,54

Special Consideration
Knee flexion contractures are one of the most prevalent types of contractures.14 The knee is one of the largest and most complicated joints of the body.55 Not only does it allow rotation about a vertical axis, it also allows flexion and extension. Knee contractures could be arthrogenic, hypertonic, paralytic, congenital, myositic, or postural. Persons with AD may have a primary joint pathology at the root of the immobility in a flexed position, leading to the knee joint contracture. Pain or mobility limitation due to joint pathology results in the patient placing his knee in a slightly flexed position to maximize comfort. This flexed (shortened) position enhances the formation of the contractures.55 However, an underlying knee joint pathology is not necessary in order to have knee joint contractures. Another possible etiology is postural. Flexion contractures of the hip and lack of gastrocnemius function can result in this type of contracture.55 In addition, positioning in chairs or in beds with knees flexed can cause a contracture at the knee joint as well.

Management Strategies for Contractures

One of the major roles of physical therapy is to maintain or regain ROM where there is dysfunction or deformity as a result of disease. The most popular strategies for management of contractures are “passive ROM.” This refers to any movement at a joint that is “produced by an external source.”56 Most commonly, this is used for mobilizing joints with contractures from any condition. Abnormal or contracted tissue is stretched carefully without disrupting it. There are two major types of passive ROM. One uses slow, strong, repeated forcing to stretch contracted tissue, and the other is done under anesthesia to tear adhesions selectively. However, for prevention purposes it is thought that the physiological consequences of immobilization can be prevented by passive ROM, and thus can prevent complications of immobility, such as contractures.56

Williams37 conducted a study to determine whether short, daily periods of stretching prevent sarcomere loss and the resultant loss of ROM. In mice animal models, he found that periods of stretching as short as 30 minutes daily were sufficient not only to prevent loss of sarcomeres, but actually to cause an increase in the number of sarcomeres in series. Range of joint motion remained normal.

Two randomized, controlled trials have looked at low-load prolonged stretching as an intervention for treating knee flexion contractures. Both studies were done in the NH setting. In one study, the mean passive ROM at the knee increased by 18 degrees for extension 57 The other study found no benefit from this kind of stretching.58 A study by Kaegi et al59 looked at a passive ROM exercise program for treating institutionalized older adults with contractures and found no benefit. The investigators studied 35 patients for six months and observed the amplitude change at the knee and/or elbow during passive ROM exercise. However, they found no significant change in the amplitude over this time.

Harvey et al60 conducted a systematic review of 13 studies that looked at effects of stretching on joint ROM in healthy subjects without functionally significant contractures. Out of the 13, only four were of “moderate” quality, and these suggested that regular stretching increases joint ROM for more than one day after cessation of stretching. However, these findings have not been verified in randomized, controlled trials. In addition, these studies need to be done on patients with functionally significant contractures. The only conclusion relevant to persons with AD from this review is that some benefit of stretching has been found in patients with contractures. Whether this applies to a patient with AD is still unknown.

Some studies looking at preventing and treating contractures with stretching exercises have been done in patients with cerebral palsy and neuromuscular diseases.61,62-64 Recently, Khalili and Hajihassanie65 looked at electrical stimulation in addition to passive stretching in reducing spasticity and contractures in children with cerebral palsy. They conducted a randomized within-participant controlled trial. The intervention was to provide 30 minutes of electrical stimulation of the quadriceps muscles three times per week and passive stretching five times per week. The other leg received only passive stretching. The investigators found that combining electrical stimulation with passive stretching was marginally more effective than stretching alone in these children. Using electrical stimulation with passive stretching can potentially be used in the earliest phase of contracture formation in older people with AD. One of the major contributions of physical therapy to muscular dystrophy is in the prevention and treatment of contractures. Passive stretching is used in patients with muscular dystrophy for management of contractures.7 However, this needs to be maintained on a regular basis. Unfortunately, passive ROM does not strengthen the opposing muscles, and in patients with AD this is especially challenging since they cannot usually participate in active exercise programs or active ROM exercises. Similar to patients with AD, in later stages of neuromuscular disease, patients develop severe knee and hip contractures. This usually occurs when they lose the ability to ambulate independently. Studies in boys with Duchene dystrophy have shown that the lower-extremity contractures can be minimized if they continue to ambulate and stand in long leg braces.66 This implies that in persons with AD, if ambulation can be maintained even with assistance for as long as possible, it would minimize the development of lower-extremity contractures. However, much effort on the part of caregivers and staff in NHs is needed to maintain function, especially ambulation, in patients with severe AD.

Cherr67 has described alternatives to passive stretching in contracture management. If possible, in addition to passive stretching, strengthening the weak opponent muscles wherever possible should be done to enable the joint to move through a full ROM and to prevent recurrence or worsening of the contracture. This can best be evaluated by a physical therapist, and then taught to the caregiver, or in the case of the NH, to the staff. Other alternatives in cases of localized tightness that may be helpful in reducing muscle contractures include vibration to the opposing muscle group, heat, or prolonged icing. These methods work by causing local inhibition of the contracted muscle. Finally, maintaining the joint in a neutral position or encouraging ambulation or movement of any form could prevent further contracture development.

Bed positioning is another technique that has been used in the management of contractures. A study looked at bed positioning for treatment of patients with knee contractures.25 The study involved 16 patients with cognitive and functional impairment in a chronic care hospital. The patients’ knees were stretched into extension, and then secured and maintained in this position for 40 minutes four times per week. Patients were randomly assigned to two groups. One group received treatment for eight weeks and then no intervention, and the other group was treated in reverse order. Twelve participants completed the study, and there was no improvement in the knee ROM at the end of the study. The negative results of this could be attributed to the long-standing contractures and the severity of them. However, once a contracture has developed, providing stretch and position has not shown to be of benefit.

The key to contracture management is prevention. Another key to successful prevention is physical therapy provided by well-trained therapists.51 Contractures can be prevented by trained professionals administering ROM exercises.4,56 Both active and passive ROM exercises can deter immobilization “atrophy.”57 Immobilization atrophy may result in both structural and functional muscle atrophy. The former is accompanied by loss of muscle mass, and the latter may have only impaired force-generating capacity without any muscle loss.68 Properly performed, ROM exercises may prevent contractures by moving the joint through its fullest range of stretch and movement.16 

There have been recent developments in orthotic devices to treat contractures. Orthoses can be used as possible treatments in addition to physical therapy, proper positioning, and contracture prevention and treatment. Orthoses work through continuous stretching.6 In addition, studies done on patients with stroke and immobilized limbs were able to show some reduction in wrist flexion and muscle atrophy with functional electrical stimulation.70,71

Performing ROM exercises in persons with AD may be challenging in some patients. It is important to allow time to try to explain as best as possible the purpose of these exercises to caregivers and relatives. Photographs of contractures may be necessary to demonstrate the importance of these exercises. Conducting ROM exercises in conjunction with massage of muscle groups may make cooperation easier. It may be helpful to have diagrams or other visual aids to ensure that all major joints are moved. There may also need to be a checklist to ensure this. As an adjunct to ROM exercises, maintaining the joint at a position where the muscle is not contracted may help prevent contracture development.49

Concluding Thoughts

Persons with AD commonly develop contractures. It affects the quality of their life and their interaction with relatives and friends. Persons with dementia have one of the highest rates of elder abuse,63 and contractures may be one of the indications that elder abuse by neglect is occurring. Since contractures, once they occur, are difficult—if not impossible—to correct, the focus needs to be on prevention of contractures before they occur. In individuals with dementia, development of contractures can lead to problems with hygiene, cause discomfort, and lead to the development of skin conditions that make nursing care more difficult. Successful prevention of contractures will ensure a higher quality of life for the patient, improve the quality of nursing care provided, and decrease the medical complications that can result from contractures. At this time, there is no evidence that AD pathology itself causes contractures, but it certainly increases the risk of developing them. There are also no randomized, controlled trials studying the benefits of passive ROM exercises in patients with AD who have contractures. The evidence on benefits of stretching exercises comes from prevention and treatment in neuromuscular disease. Other limiting factors in persons with AD is caregiver burden in those caring for persons with severe dementia, leading to disuse and passive neglect, and thus leading to contracture formation. Until high-quality studies are done, it appears that passive ROM exercises have shown some benefit in the management of contractures. We strongly urge healthcare professionals to energetically apply their skills to prevent contractures in their patients.

Dr. Jamshed is Assistant Professor of Clinical Medicine, Department of Internal Medicine, and at Washington Hospital Center, Georgetown University School of Medicine, Washington, DC; and Dr. Schneider is Professor, Leonard Davis School of Gerontology, and Professor of Internal Medicine, Keck School of Medicine, University of Southern California, Los Angeles.

Acknowledgment
Dr. Jamshed is supported by grant #HRSA-07-GACA. The authors report no relevant financial relationships.

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