Muscle contracture

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A finger contracture caused by Dupuytren's contracture. Dupuytren's contracture.jpg
A finger contracture caused by Dupuytren's contracture.

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

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

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.

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 autistic people 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] If someone has a disability that causes spasticity (such as cerebral palsy), they may walk on their toes involuntarily.

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 muscular dystrophies

Some congenital muscular dystrophies, such as Bethlem myopathy, Ullrich congenital muscular dystrophy, Merosin-deficient congenital muscular dystrophy (MDC1A) or LAMA2-related CMD, rigid spine syndrome and LMNA-related congenital muscular dystrophy cause muscle contractures to develop. [8] [9] In Bethlem myopathy and Ullrich congenital muscular dystrophy, 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] [10] 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]

Congenital myopathies

Congenital myopathy such as, core myopathies, nemaline myopathies and centronuclear myopathies and so forth can result in muscle contractures of the extremities and spine. [11]

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. [12]

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. [13] [14] [15]

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. [15] [16] [17] [18]

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. [19] 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. [20]

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. [21] Shortening of the surgically lengthened muscle can re-occur.

Related Research Articles

<span class="mw-page-title-main">Muscular dystrophy</span> Diseases in which skeletal muscle breaks down over time

Muscular dystrophies (MD) are a genetically and clinically heterogeneous group of rare neuromuscular diseases that cause progressive weakness and breakdown of skeletal muscles over time. The disorders differ as to which muscles are primarily affected, the degree of weakness, how fast they worsen, and when symptoms begin. Some types are also associated with problems in other organs.

<span class="mw-page-title-main">Glycogen storage disease</span> Medical condition

A glycogen storage disease is a metabolic disorder caused by a deficiency of an enzyme or transport protein affecting glycogen synthesis, glycogen breakdown, or glucose breakdown, typically in muscles and/or liver cells.

<span class="mw-page-title-main">Torticollis</span> Abnormal, asymmetrical head or neck position

Torticollis, also known as wry neck, is a 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 Latin tortus 'twisted' and collum 'neck'.

<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'.

Hypotonia is a state of low muscle tone, often involving reduced muscle strength. Hypotonia is not a specific medical disorder, but a potential manifestation of many different diseases and disorders that affect motor nerve control by the brain or muscle strength. Hypotonia is a lack of resistance to passive movement, whereas muscle weakness results in impaired active movement. Central hypotonia originates from the central nervous system, while peripheral hypotonia is related to problems within the spinal cord, peripheral nerves and/or skeletal muscles. Severe hypotonia in infancy is commonly known as floppy baby syndrome. Recognizing hypotonia, even in early infancy, is usually relatively straightforward, but diagnosing the underlying cause can be difficult and often unsuccessful. The long-term effects of hypotonia on a child's development and later life depend primarily on the severity of the muscle weakness and the nature of the cause. Some disorders have a specific treatment but the principal treatment for most hypotonia of idiopathic or neurologic cause is physical therapy and/or occupational therapy for remediation.

<span class="mw-page-title-main">Muscle biopsy</span> Medical exam

In medicine, a muscle biopsy is a procedure in which a piece of muscle tissue is removed from an organism and examined microscopically. A muscle biopsy can lead to the discovery of problems with the nervous system, connective tissue, vascular system, or musculoskeletal system.

In medicine, myopathy is a disease of the muscle in which the muscle fibers do not function properly. Myopathy means muscle disease. This meaning implies that the primary defect is within the muscle, as opposed to the nerves or elsewhere.

<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">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.

<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 limb-girdle 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 humans

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">Muscle–eye–brain disease</span> Medical condition

Muscle–eye–brain (MEB) disease, also known as muscular dystrophy-dystroglycanopathy congenital with brain and eye anomalies A3 (MDDGA3), is a kind of rare congenital muscular dystrophy (CMD), largely characterized by hypotonia at birth. Patients have muscular dystrophy, central nervous system abnormalities and ocular abnormalities. The condition is degenerative.

<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.

<span class="mw-page-title-main">LAMA2 related congenital muscular dystrophy</span> Medical condition neuromuscular disorders

LAMA2 muscular dystrophy (LAMA2-MD) is a genetically determined muscle disease caused by pathogenic mutations in the LAMA2 gene. It is a subtype of a larger group of genetic muscle diseases known collectively as congenital muscular dystrophies. The clinical presentation of LAMA2-MD varies according to the age at presentation. The severe forms present at birth and are known as early onset LAMA2 congenital muscular dystrophy type 1A or MDC1A. The mild forms are known as late onset LAMA2 muscular dystrophy or late onset LAMA2-MD. The nomenclature LGMDR23 can be used interchangeably with late onset LAMA2-MD.

References

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  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.
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  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.
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  9. ↑ El-Sobky, Tamer A.; Abdulhady, Hala; Mahmoud, Shady; Amen, John (31 January 2024). "Orthopedic manifestations of congenital muscular dystrophy subtypes in children: Emerging signatures need consolidation: a scoping review". Journal of Musculoskeletal Surgery and Research. 8: 11–23. doi:10.25259/JMSR_229_2023.
  10. ↑ 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.
  11. ↑ Claeys, KG (March 2020). "Congenital myopathies: an update". Developmental Medicine and Child Neurology. 62 (3): 297–302. doi:10.1111/dmcn.14365. PMID   31578728.
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  17. ↑ Bugden, Krista (2018-11-30). "Muscle Adhesions: What Are They & How Do I Treat Them? | Sidekick Blog". blog.sidekicktool.com. Retrieved 2023-05-07.
  18. ↑ 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. 20 (2): 79–85. doi:10.1160/vcot-06-01-0007. ISSN   0932-0814. PMID   17546206. S2CID   4026694.
  19. ↑ 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
  20. ↑ 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.
  21. ↑ 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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