Muscle contracture

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Muscle contractures in terminal neurological condition Muscle contractures of young man.jpg
Muscle contractures in terminal neurological condition

Muscle contractures can occur for many reasons, such as paralysis, muscular atrophy, and forms of muscular dystrophy. Fundamentally, the muscle and its tendons shorten, resulting in reduced flexibility.

Contents

Various interventions can slow, stop, or even reverse muscle contractures, ranging from physical therapy to surgery.

Cause

Immobilization

Joints are usually immobilized in a shortened position resulting in changes within the joint connective tissue, and the length of the muscle and associated tendon. Prolonged immobilization facilitates tissue proliferation which impinges on the joint space. [1] Maintaining a shortened position for a prolonged period of time leads to: fibrous adhesion formation, loss of sarcomeres, and a loss of tissue extensibility. [1]

For example, after a fracture when immobilization is done by casting the limb in plaster of paris, the muscle length shortens because the muscle is not used for a large span of time.

Toe walking in an autistic individual Toe Walking in Autism 1.jpg
Toe walking in an autistic individual

A common cause for having the ankle lose its flexibility in this manner is from having sheets tucked in at the foot of the bed when sleeping. The weight of the sheets keep the feet plantarflexed all night. By not tucking the sheets in at the foot of the bed, or by sleeping with the feet hanging off the bed when in the prone position, is part of correcting this imbalance.

Due to sensory issues, some autism spectrum disorder children prefer to toe walk instead of their feet making full contact with the ground. Chronic toe walking leads to muscle contracture due to the lack of calf muscles being adequately stretched. Once the muscle contracture has developed, the voluntary toe walking then becomes involuntary. [2]

Spasticity

If spasticity is left untreated, contractures can occur. A loss of muscle tone inhibition (hypertonia) causes a muscle to become hyperactive resulting in constant contraction, which reduces an individual’s control of the affected area. The joint will remain in a flexed state producing similar effects as listed in immobilization.

Muscle imbalance

A muscle imbalance between an agonist and antagonist muscle can occur due to a neurological disorder, spinal cord injury, myopathy, and our lifestyle/postural habits. [1] [3] One muscle may be normal while the other is atrophic or hypertrophic; alternately, one muscle may be hypertrophic while the other is atrophic. [3] A decrease in muscle tone leads to continuous disuse and eventually muscular atrophy. The constant contraction of the agonist muscle with minimal resistance can result in a contracture. Selective muscle hypertrophy may exacerbate contractures and postural instability. [3]

For example, in the case of partial paralysis (i.e. poliomyelitis) the loss of strength and muscle control tend to be greater in some muscles than in others, leading to an imbalance between the various muscle groups around specific joints. Case in point: when the muscles which dorsiflex (flex the foot upward) are less functional than the muscles which plantarflex (flex the foot downward) a contracture occurs, giving the foot a progressively downward angle and loss of flexibility.

Low ATP reservoir in the muscle

In the metabolic myopathies of GSD-V (McArdle disease) and GSD-VII (Tarui disease), temporary muscle contractures develop in response to impending muscle damage associated with the ATP (energy) deficiency. [4] The muscle contracts and fails to relax again, becoming hard or stiff, the muscle may swell up, and although temporary, it is longer lasting and generally more painful than muscle cramps. [4] [5] These contractures are different from cramps, because they are not elicited by the nerve, but by intrinsic mechanisms in the muscle itself and are silent on electromyography. [4] This type of transient contracture has also been called pseudomyotonia. [6] [7]

In GSD-V and GSD-VII, a cramp or contracture is managed by cessation of the causal activity until pain resolves; however, repeated episodes can accumulate muscle damage (see below under fibrosis). [4] Unlike stretching of muscle cramps, stretching of a muscle in contracture should be avoided as it may cause further muscle damage by tearing muscle fibres (i.e. resist uncurling the fingers of a "clawed" hand). [4] [5]

Congenital myopathies

Some congenital myopathies, such as Bethlem myopathy and Ullrich congenital muscular dystrophy, cause muscle contractures to develop. [8] In these two myopathies, mutations in collagen VI and XII genes result in deficient or dysfunctional microfibrillar collagen in the extracellular matrix of muscle and other connective tissues. [8] [9] The potential effects on muscle include progressive dystrophic changes, fibrosis and evidence for increased apoptosis. In Bethlem myopathy 1, contractures presenting in infancy may resolve by age 2 years, but reoccur as the disease progresses, typically by late of the first decade or early teens. [8]

Ischemia

Following trauma (such as fractures, crush injuries, burns and arterial injuries), ischemia (restriction of blood flow) leads to the death of muscle tissue (necrosis) and can cause contracture, such as Volkmann's contracture. [10]

Adhesions and fibrosis

Adhesions bind two separate tissues or organs together with fibrotic scar tissue, joining muscle fibres to facia, ligaments, or joints. Fibrosis occurs within the same organ, the fibrotic scar tissue within skeletal muscle known as myofibrosis, limits muscle contractibility and stiffens muscles. [11] [12] [13]

Muscle injury (such as a large burn or surgery) can cause muscle contractures as internal scar tissue (adhesions and fibrosis) develops. Repetitive muscle injuries (e.g. sports injuries, major muscle strains) and micro-injuries (e.g. overuse injuries, minor muscle strains) can also cause this. Adhesions and fibrosis are made of dense fibrous tissue, which are strong and supportive, helping to prevent the injury or micro-injury from reoccurring. However, the fibrotic scar tissue causes the muscle tissue to become stuck together which restricts movement, causing pain, weakness, and limited joint mobility. [13] [14] [15] [16]

Treatment

Passive stretching

Typically performed by physical therapists, passive stretching is a more beneficial preventative measure and tool to maintain available range of motion (ROM) rather than used as a treatment. [17] It is very important to continually move the limb throughout its full range at a specific velocity but a passive stretch can’t be maintained for the period of time required for optimal benefit.

A 2017 Cochrane review found that stretching does not provide any short-term pain relief. [18]

Splinting

A contracture corrective device (CCD) is a dynamic splint that provides a continuous stretch with a continuous force and operates based on the principles of creep. [1] It is the most advantageous splint but more research is required. Splints are used in long term treatments and must be removed in order to stretch the antagonist muscle to maintain range of motion (passive stretching).

Electrical stimulation

Electrical stimulation improves passive range of motion but only temporarily. [1] Once the treatment is withdrawn, all benefits are reduced. It can play a critical role in muscle atrophy prevention.

Surgery

Surgery is a solution to muscle shortening but other complications may arise. Following muscle lengthening surgery, force production and ROM is usually reduced due to the shift in sarcomere locations between a muscle's maximal and minimal length. [1] In adjunct with surgery, refractory muscle contracture can also be treated with Botulinum toxins A and B; however, the effectiveness of the toxin is slowly lost over time, and most patients need a single treatment to correct muscle contracture over the first few weeks after surgery. [19] Shortening of the surgically lengthened muscle can re-occur.

Related Research Articles

<span class="mw-page-title-main">Scar</span> Area of fibrous tissue that replaces normal skin after an injury

A scar is an area of fibrous tissue that replaces normal skin after an injury. Scars result from the biological process of wound repair in the skin, as well as in other organs, and tissues of the body. Thus, scarring is a natural part of the healing process. With the exception of very minor lesions, every wound results in some degree of scarring. An exception to this are animals with complete regeneration, which regrow tissue without scar formation.

<span class="mw-page-title-main">Rotator cuff</span> Group of muscles

The rotator cuff is a group of muscles and their tendons that act to stabilize the human shoulder and allow for its extensive range of motion. Of the seven scapulohumeral muscles, four make up the rotator cuff. The four muscles are:

<span class="mw-page-title-main">Torticollis</span> Medical condition

Torticollis, also known as wry neck, is an extremely painful, dystonic condition defined by an abnormal, asymmetrical head or neck position, which may be due to a variety of causes. The term torticollis is derived from the Latin words tortus, meaning "twisted", and collum, meaning "neck".

<span class="mw-page-title-main">Sprain</span> Damage to one or more ligaments in a joint

A sprain is a soft tissue injury of the ligaments within a joint, often caused by a sudden movement abruptly forcing the joint to exceed its functional range of motion. Ligaments are tough, inelastic fibers made of collagen that connect two or more bones to form a joint and are important for joint stability and proprioception, which is the body's sense of limb position and movement. Sprains may be mild, moderate, or severe, with the latter two classes involving some degree of tearing of the ligament. Sprains can occur at any joint but most commonly occur in the ankle, knee, or wrist. An equivalent injury to a muscle or tendon is known as a strain.

<span class="mw-page-title-main">Fibrosis</span> Excess connective tissue in healing

Fibrosis, also known as fibrotic scarring, is a pathological wound healing in which connective tissue replaces normal parenchymal tissue to the extent that it goes unchecked, leading to considerable tissue remodelling and the formation of permanent scar tissue.

<span class="mw-page-title-main">Arthrogryposis</span> Medical condition

Arthrogryposis (AMC) describes congenital joint contracture in two or more areas of the body. It derives its name from Greek, literally meaning 'curving of joints'.

A connective tissue disease (collagenosis) is any disease that has the connective tissues of the body as a target of pathology. Connective tissue is any type of biological tissue with an extensive extracellular matrix that supports, binds together, and protects organs. These tissues form a framework, or matrix, for the body, and are composed of two major structural protein molecules: collagen and elastin. There are many different types of collagen protein in each of the body's tissues. Elastin has the capability of stretching and returning to its original length—like a spring or rubber band. Elastin is the major component of ligaments and skin. In patients with connective tissue disease, it is common for collagen and elastin to become injured by inflammation (ICT). Many connective tissue diseases feature abnormal immune system activity with inflammation in tissues as a result of an immune system that is directed against one's own body tissues (autoimmunity).

<span class="mw-page-title-main">Congenital muscular dystrophy</span> Medical condition

Congenital muscular dystrophies are autosomal recessively-inherited muscle diseases. They are a group of heterogeneous disorders characterized by muscle weakness which is present at birth and the different changes on muscle biopsy that ranges from myopathic to overtly dystrophic due to the age at which the biopsy takes place.

<span class="mw-page-title-main">Muscle atrophy</span> Medical condition

Muscle atrophy is the loss of skeletal muscle mass. It can be caused by immobility, aging, malnutrition, medications, or a wide range of injuries or diseases that impact the musculoskeletal or nervous system. Muscle atrophy leads to muscle weakness and causes disability.

<span class="mw-page-title-main">Emery–Dreifuss muscular dystrophy</span> Medical condition

Emery–Dreifuss muscular dystrophy (EDMD) is a type of muscular dystrophy, a group of heritable diseases that cause progressive impairment of muscles. EDMD affects muscles used for movement, causing atrophy, weakness and contractures. It almost always affects the heart, causing abnormal rhythms, heart failure, or sudden cardiac death. It is rare, affecting 0.39 per 100,000 people. It is named after Alan Eglin H. Emery and Fritz E. Dreifuss.

<span class="mw-page-title-main">Contracture</span> Permanent shortening of a muscle or joint

In pathology, a contracture is a shortening of muscles, tendons, skin, and nearby soft tissues that causes the joints to shorten and become very stiff, preventing normal movement. A contracture is usually permanent, but less commonly can be temporary, or resolve over time but reoccur later in life.

Arthrofibrosis has been described in most joints like knee, hip, ankle, foot joints, shoulder, elbow, wrist, hand joints as well as spinal vertebrae. It can occur after injury or surgery or may arise without an obvious cause. There is excessive scar tissue formation within the joint and/or surrounding soft tissues leading to painful restriction of joint motion that persists despite physical therapy and rehabilitation. The scar tissue may be located inside the knee joint or may involve the soft tissue structures around the knee joint, or both locations.

<span class="mw-page-title-main">Bethlem myopathy</span> Medical condition

Bethlem myopathy is predominantly an autosomal dominant myopathy, classified as a congenital form of muscular dystrophy. There are two types of Bethlem myopathy, based on which type of collagen is affected.

<span class="mw-page-title-main">Collagen, type VI, alpha 3</span> Mammalian protein found in Homo sapiens

Collagen alpha-3(VI) chain is a protein that in humans is encoded by the COL6A3 gene. This protein is an alpha chain of type VI collagen that aids in microfibril formation. As part of type VI collagen, this protein has been implicated in Bethlem myopathy, Ullrich congenital muscular dystrophy (UCMD), and other diseases related to muscle and connective tissue.

<span class="mw-page-title-main">Ullrich congenital muscular dystrophy</span> Medical condition

Ullrich congenital muscular dystrophy (UCMD) is a form of congenital muscular dystrophy. There are two forms: UCMD1 and UCMD2.

Collagen VI (ColVI) is a type of collagen primarily associated with the extracellular matrix of skeletal muscle. ColVI maintains regularity in muscle function and stabilizes the cell membrane. It is synthesized by a complex, multistep pathway that leads to the formation of a unique network of linked microfilaments located in the extracellular matrix (ECM). ColVI plays a vital role in numerous cell types, including chondrocytes, neurons, myocytes, fibroblasts, and cardiomyocytes. ColVI molecules are made up of three alpha chains: α1(VI), α2(VI), and α3(VI). It is encoded by 6 genes: COL6A1, COL6A2, COL6A3, COL6A4, COL6A5, and COL6A6. The chain lengths of α1(VI) and α2(VI) are about 1,000 amino acids. The chain length of α3(VI) is roughly a third larger than those of α1(VI) and α2(VI), and it consists of several spliced variants within the range of 2,500 to 3,100 amino acids.

<span class="mw-page-title-main">Dynasplint Systems</span>

Dynasplint Systems, Incorporated (DSI) is a company that designs, manufactures and sells dynamic splints that are used for range of motion rehabilitation. The corporate headquarters are located in Severna Park, Maryland and it is considered a major employer in Anne Arundel County. Products are Made in the US in Stevensville, Maryland. There is a national sales force throughout the US as well as a presence in Canada and Europe.

Congenital distal spinal muscular atrophy (cDSMA), also known as distal hereditary motor neuropathytype VIII (dHMN8), is a hereditary medical condition characterized by muscle wasting (atrophy), particularly of distal muscles in legs and hands, and by early-onset contractures of the hip, knee, and ankle. Affected individuals often have shorter lower limbs relative to the trunk and upper limbs. The condition is a result of a loss of anterior horn cells localized to lumbar and cervical regions of the spinal cord early in infancy, which in turn is caused by a mutation of the TRPV4 gene. The disorder is inherited in an autosomal dominant manner. Arm muscle and function, as well as cardiac and respiratory functions are typically well preserved.

<span class="mw-page-title-main">Pseudohypertrophy</span> False enlargement of muscle due to infiltration of fat or other tissue

Pseudohypertrophy, or false enlargement, is an increase in the size of an organ due to infiltration of a tissue not normally found in that organ. It is commonly applied to enlargement of a muscle due to infiltration of fat or connective tissue, famously in Duchenne muscular dystrophy. This is in contrast with typical muscle hypertrophy, in which the muscle tissue itself increases in size. Because pseudohypertrophy is not a result of increased muscle tissue, the muscles look bigger but are actually atrophied and thus weaker. Pseudohypertrophy is typically the result of a disease, which can be a disease of muscle or a disease of the nerve supplying the muscle.

References

  1. 1 2 3 4 5 6 Farmer, S.E; M. James (2001). "Contractures in orthopaedic and neurological conditions: a review of causes and treatment". Disability and Rehabilitation. 23 (13): 549–558. doi:10.1080/09638280010029930. PMID   11451189. S2CID   22732753.
  2. ↑ Valagussa, Giulio; Balatti, Valeria; Trentin, Luca; Piscitelli, Daniele; Yamagata, Momoko; Grossi, Enzo (2020-08-20). "Relationship between tip-toe behavior and soleus - gastrocnemius muscle lengths in individuals with autism spectrum disorders". Journal of Orthopaedics. 21: 444–448. doi:10.1016/j.jor.2020.08.013. ISSN   0972-978X. PMC   7493131 . PMID   32982098.
  3. 1 2 3 Kornegay, Joe N.; Childers, Martin K.; Bogan, Daniel J.; Bogan, Janet R.; Nghiem, Peter; Wang, Jiahui; Fan, Zheng; Howard, James F.; Schatzberg, Scott J.; Dow, Jennifer L.; Grange, Robert W.; Styner, Martin A.; Hoffman, Eric P.; Wagner, Kathryn R. (February 2012). "The Paradox of Muscle Hypertrophy in Muscular Dystrophy". Physical Medicine and Rehabilitation Clinics of North America. 23 (1): 149–xii. doi:10.1016/j.pmr.2011.11.014. ISSN   1047-9651. PMC   5951392 . PMID   22239881.
  4. 1 2 3 4 5 Lucia, Alejandro; Martinuzzi, Andrea; Nogales-Gadea, Gisela; Quinlivan, Ros; Reason, Stacey; International Association for Muscle Glycogen Storage Disease study group (December 2021). "Clinical practice guidelines for glycogen storage disease V & VII (McArdle disease and Tarui disease) from an international study group". Neuromuscular Disorders. 31 (12): 1296–1310. doi: 10.1016/j.nmd.2021.10.006 . ISSN   1873-2364. PMID   34848128. S2CID   240123241.
  5. 1 2 "IAMGSD | Medical emergencies". iamgsd. Retrieved 2023-05-07.
  6. ↑ Bhai, Salman (September 2021). "Neuromuscular Notes: Diagnosing Metabolic Myopathies". Practical Neurology. Retrieved 2023-10-13.
  7. ↑ Chen, Y.; Hagen, M.; Lawandy, M.; Do, J.Y. (2017-03-09). "Congenital and Acquired Myotonia". PM&R KnowledgeNow. Retrieved 2023-10-13.
  8. 1 2 3 Bönnemann, Carsten G. (2011-06-21). "The collagen VI-related myopathies: muscle meets its matrix". Nature Reviews. Neurology. 7 (7): 379–390. doi:10.1038/nrneurol.2011.81. ISSN   1759-4758. PMC   5210181 . PMID   21691338.
  9. ↑ Hicks, Debbie; Farsani, Golara Torabi; Laval, Steven; Collins, James; Sarkozy, Anna; Martoni, Elena; Shah, Ashoke; Zou, Yaqun; Koch, Manuel; Bönnemann, Carsten G.; Roberts, Mark; Lochmüller, Hanns; Bushby, Kate; Straub, Volker (2014-05-01). "Mutations in the collagen XII gene define a new form of extracellular matrix-related myopathy". Human Molecular Genetics. 23 (9): 2353–2363. doi: 10.1093/hmg/ddt637 . ISSN   1460-2083. PMID   24334769.
  10. ↑ Mirza, Taaha M.; Taqi, Muhammad (2023), "Volkmann Contracture", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID   32491686 , retrieved 2023-05-07
  11. ↑ Massage, Walnut Creek (2014-10-02). "Adhesions vs. Fibrosis • Loosen Up Bodywork". Loosen Up Bodywork. Retrieved 2023-05-07.
  12. ↑ Nelson, Fred R. T.; Blauvelt, Carolyn Taliaferro (2015-01-01), Nelson, Fred R. T.; Blauvelt, Carolyn Taliaferro (eds.), "2 - Musculoskeletal Diseases and Related Terms", A Manual of Orthopaedic Terminology (Eighth Edition), Philadelphia: W.B. Saunders, pp. 43–104, ISBN   978-0-323-22158-0 , retrieved 2023-05-07
  13. 1 2 Lieber, Richard L.; Ward, Samuel R. (2013-08-01). "Cellular Mechanisms of Tissue Fibrosis. 4. Structural and functional consequences of skeletal muscle fibrosis". American Journal of Physiology. Cell Physiology. 305 (3): C241–C252. doi:10.1152/ajpcell.00173.2013. ISSN   0363-6143. PMC   3742845 . PMID   23761627.
  14. ↑ Nemoto, F. (January 1980). "[Pathogenesis of quadriceps contracture in children and adolescence (author's transl)]". Nihon Seikeigeka Gakkai Zasshi. 54 (1): 15–31. ISSN   0021-5325. PMID   7381269.
  15. ↑ Bugden, Krista (2018-11-30). "Muscle Adhesions: What Are They & How Do I Treat Them? | Sidekick Blog". blog.sidekicktool.com. Retrieved 2023-05-07.
  16. ↑ Taylor, J.; Tangner, C. H. (2007). "Acquired muscle contractures in the dog and cat. A review of the literature and case report". Veterinary and Comparative Orthopaedics and Traumatology: V.C.O.T. 20 (2): 79–85. doi:10.1160/vcot-06-01-0007. ISSN   0932-0814. PMID   17546206. S2CID   4026694.
  17. ↑ Worland, R., Arredondo, J., Angles, F., Lopez-Jimenez, F., & Jessup, D. (1998). Home continuous passive motion machine versus professional physical therapy following total knee replacement. Journal of Arthroplasty, 784-787, doi : 10.1016/S0883-5403(98)90031-6
  18. ↑ Harvey, Lisa A; Katalinic, Owen M; Herbert, Robert D; Moseley, Anne M; Lannin, Natasha A; Schurr, Karl (2017-01-09). "Stretch for the treatment and prevention of contractures". Cochrane Database of Systematic Reviews. 1 (2): CD007455. doi:10.1002/14651858.cd007455.pub3. ISSN   1465-1858. PMC   6464268 . PMID   28146605.
  19. ↑ Sanchez-Sotelo, Joaquin (2018-01-01), Morrey, Bernard F.; Sanchez-Sotelo, Joaquin; Morrey, Mark E. (eds.), "56 - Elbow Stiffness: Rehabilitation After Surgical Contracture Release", Morrey's the Elbow and its Disorders (Fifth Edition), Philadelphia: Elsevier, pp. 552–556, ISBN   978-0-323-34169-1 , retrieved 2023-05-06
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