Spastic diplegia

Spastic diplegia
Spastic diplegia
Other names	Little's disease
Specialty	Neurology

Last updated January 24, 2025

Spastic diplegia is a form of cerebral palsy (CP) that primarily affects the legs, with possible considerable asymmetry between the two sides. It is a chronic neuromuscular condition of hypertonia and spasticity in the muscles of the lower extremities of the human body, manifested as an especially high and constant "tightness" or "stiffness",^[1]^[2] usually in the legs, hips and pelvis.^[3]

Presentation

Individuals with spastic diplegia are often very tight and stiff and must work very hard to successfully resist and "push through" the extra tightness they experience. Other than this, these individuals are almost always normal in every significant clinical sense. When they are younger, spastic diplegic individuals typically undergo gait analysis so that their clinicians can determine the best assistive devices for them, if any are necessary, such as a walker or crutches. The main difference between spastic diplegia and a normal gait pattern is its signature "scissor gait" - a style that some non-disabled people might tend to confuse with the effects of drunkenness, multiple sclerosis, or another nerve disease. The degree of spasticity in spastic diplegia (and, for that matter, other types of spastic CP) varies widely from person to person. No two people with spastic diplegia are exactly alike. Balance problems and/or stiffness in gait can range from barely noticeable all the way to misalignments so pronounced that the person needs crutches (typically forearm crutches) or a walking stick to assist in ambulation.

Less often, spasticity is severe enough to compel the person to use a wheelchair. In general, however, lower-extremity spasticity in spastic diplegia is rarely so great as to totally prevent ambulation–most people with the condition can walk and can do so with at least a basic amount of overall stability.^{[ citation needed ]} Regardless, from case to case, steeply varying degrees of imbalance, potential tripping over uneven terrain while walking, or needing to hold on to various surfaces or walls in certain circumstances to keep upright, are typically ever-present potential issues and are much more common occurrences amongst those with spastic diplegia than among those with a normal or near-normal gait pattern.

Among some of the people with spastic diplegia who choose to be ambulatory on either an exclusive or predominant basis, one of the seemingly common lifestyle choices is for the person to ambulate within his or her home without an assistive device, and then to use the assistive device, if any, once outdoors. Others may use no assistive device in any indoor situation at all, while always using one when outdoors. Above the hips, persons with spastic diplegia typically retain normal or near-normal muscle tone and range of motion, though some lesser spasticity may also affect the upper body, such as the trunk and arms, depending on the severity of the condition in the individual (the spasticity condition affecting the whole body equally, rather than just the legs, is spastic quadriplegia, a slightly different classification). In addition, because leg tightness often leads to instability in ambulation, extra muscle tension usually develops in the shoulders, chest, and arms due to compensatory stabilization movements, regardless of the fact that the upper body itself is not directly affected by the condition.^[8]

Social implications

Although the term "spastic" technically describes the attribute of spasticity in spastic cerebral palsy and was originally an acceptable and common term to use in both self-description and in description by others, it has since gained more notoriety as a pejorative, in particular when used in pop culture to insult non-disabled people when they seem overly anxious or unskilled in sports (see also the article Spastic (word)). In 1952, a UK charitable organization with a membership mainly of those with spastic CP was formed; this organization called itself The Spastics Society. However, the charity changed its name to Scope in 1994 due to the term spastics having become enough of a pejorative to warrant the name change.^[9]^[10]

Spastic diplegia's social implications tend to vary with the intensity of the individual’s condition. If its effects are severely disabling, social elements can also suffer. Workplace environments can also be limited, since most labor-intensive work requires basic physical agility that spastic diplegics may not possess. However, the degree of variability among individuals with spastic diplegia means that no greater or lesser degree of stigma or real-world limitation is standard. Lesser effects usually mean fewer physical limitations, better-quality exercise, and more real-world flexibility, but the person is still seen as different from the norm. How such a person chooses to react to outside opinion is of paramount importance when social factors are considered.^{[ citation needed ]}

Mechanism

Spastic diplegia is a particular type of brain damage that inhibits the proper development of upper motor neuron function, impacting the motor cortex, the basal ganglia and the corticospinal tract. Nerve receptors in the spine leading to affected muscles become unable to properly absorb gamma amino butyric acid (GABA), the amino acid that regulates muscle tone in humans. Without GABA absorption to those particular nerve rootlets (usually centered, in this case, around the sectors L1-S1 and L2-S2), affected nerves (here, the ones controlling the legs) perpetually fire the message for their corresponding muscles to permanently, rigidly contract, and the muscles become permanently hypertonic (spastic).^{[ citation needed ]}

The abnormally high muscle tone that results creates lifelong difficulty with all voluntary and passive movement in the legs, and in general creates stress over time, depending on the severity of the condition in the individual, the constant spasticity ultimately produces pain, muscle/joint breakdown including tendinitis and arthritis, premature physical exhaustion (i.e., becoming physically exhausted even when you internally know that you have more energy than you are able to use), contractures, spasms, and progressively worse deformities/mis-alignments of bone structure around areas of the tightened musculature as the person's years progress. Severe arthritis, tendinitis, and similar breakdown can start as early as the spastic diplegic person's mid-20s (as a comparison, typical people with normal muscle tone are not at risk of arthritis, tendinitis, and similar breakdown until well into their 50s or 60s, if even then).^{[ citation needed ]}

No type of CP is officially a progressive condition, and indeed spastic diplegia does not clinically "get worse" given the nerves, damaged permanently at birth, neither recover nor degrade. This aspect is clinically significant, because other neuromuscular conditions with similar surface characteristics in their presentations, like most forms of multiple sclerosis, indeed do degrade the body over time and do involve actual progressive worsening of the condition, including the spasticity often seen in MS. However, spastic diplegia is indeed a chronic condition; the symptoms themselves cause compounded effects on the body that are typically just as stressful on the human body as a progressive condition is. Despite this reality and the fact that muscle tightness is the symptom of spastic diplegia and not the cause, symptoms rather than cause are typically seen as the primary area of focus for treatment, especially surgical treatment, except when a selective dorsal rhizotomy is brought into consideration, or when an oral baclofen regimen is attempted.^{[ citation needed ]}

Unlike any other condition that may present with similar effects, spastic diplegia is entirely congenital in origin - that is, it is almost always acquired shortly before or during a baby's birth process. Things like exposure to toxins, traumatic brain injury, encephalitis, meningitis, drowning, or suffocation do not tend to lead to spastic diplegia in particular or even cerebral palsy generally. Overall, the most common cause of spastic diplegia is Periventricular leukomalacia, more commonly known as neonatal asphyxia or infant hypoxia—a sudden in-womb shortage of oxygen-delivery through the umbilical cord. This sudden lack of oxygen is also almost always combined with premature birth, a phenomenon that, even by itself, would inherently risk the infant developing some type of CP. On the other hand, the presence of certain maternal infections during pregnancy such as congenital rubella syndrome can also lead to spastic diplegia, since such infections can have similar end results to infant hypoxia.^{[ citation needed ]}

Treatment

As a matter of everyday maintenance, muscle stretching, range of motion exercises, yoga, contact improvisation, modern dance, resistance training, and other physical activity regimens are often utilized by those with spastic CP to help prevent contractures and reduce the severity of symptoms.^{[ citation needed ]}

Major clinical treatments for spastic diplegia are:^{[ citation needed ]}

Baclofen (and its derivatives), a gamma amino butyric acid (GABA) substitute in oral (pill-based) or intrathecal form. Baclofen is essentially chemically identical to the GABA that the damaged, over-firing nerves cannot absorb, except that it has an extra chemical 'marker' on it that makes the damaged nerves 'think' it is a different compound, and thus those nerves will absorb it. Baclofen is noted for being the sole medication available for GABA-deficiency-based spasticity which acts on the actual cause of the spasticity rather than simply reducing symptomatology as muscle relaxants and painkillers do. The intrathecal solution is a liquid injected into the spinal fluid for trial, and if successful in reducing spasticity, thereafter administered via an intrathecal pump, which has variously been proven potentially very dangerous on one or another level with long-term use (see article), including sudden and potentially lethal baclofen overdose, whereas the oral route, which comes in 10- or 20-milligram tablets and the dosage of which can be gently titrated either upward or downward, as well as safely ceased entirely, has not.
Antispasmodic muscle relaxant chemicals such as tizanidine and botulinum toxin (Botox), injected directly into the spastic muscles; Botox wears off every three months.
Phenol and similar chemical 'nerve deadeners', injected selectively into the over-firing nerves in the legs on the muscle end to reduce spasticity in their corresponding muscles by preventing the spasticity signals from reaching the legs; Phenol wears off every six months.
Orthopedic surgery to release the spastic muscles from their hypertonic state, a usually temporary result because the spasticity source is the nerves, not the muscles; spasticity can fully reassert itself as little as one-year post-surgery.
Selective dorsal rhizotomy, a neurosurgery directly targeting and eliminating ("cutting" or "lesioning") the over-firing nerve rootlets and leaving the properly firing ones intact, thereby permanently eliminating the spasticity but compelling the person to spend months re-strengthening muscles that will have been severely weakened by the loss of the spasticity, due to the fact of those muscles not really having had actual strength to begin with.

Prognosis

Unusually, cerebral palsy, including spastic cerebral palsy, is notable for a glaring overall research deficiency - the fact that it is one of the very few major groups of conditions on the planet in human beings for which medical science has not yet (as of 2011) collected wide-ranging empirical data on the development and experiences of young adults, the middle aged and older adults. An especially puzzling aspect of this lies in the fact that cerebral palsy as defined by modern science was first 'discovered' and specifically addressed well over 100 years ago and that it would therefore be reasonable to expect by now that at least some empirical data on the adult populations with these conditions would have long since been collected, especially over the second half of the 20th century when existing treatment technologies rapidly improved and new ones came into being. The vast majority of empirical data on the various forms of cerebral palsy is concerned near-exclusively with children (birth to about 10 years of age) and sometimes pre-teens and early teens (11-13). Some doctors attempt to provide their own personal justifications for keeping their CP specialties purely pediatric, but there is no objectively apparent set of reasons backed by any scientific consensus as to why medical science has made a point of researching adult cases of multiple sclerosis, muscular dystrophy and the various forms of cancer in young and older adults, but has failed to do so with CP. There are a few orthopaedic surgeons and neurosurgeons who claim to be gathering pace with various studies as of the past few years, ^{[ citation needed ]} but these claims do not yet seem to have been matched by real-world actualization in terms of easily accessible and objectively verifiable resources available to the general public on the internet and in-person, where many, including medical-science researchers and doctors themselves, would more than likely agree such resources would ideally belong.

Prevalence

In the industrialized world, the incidence of overall cerebral palsy, which includes but is not limited to spastic diplegia, is about 2 per 1000 live births. Thus far, there is no known study recording the incidence of CP in the overall non-industrialized world. Therefore, it is safe to assume that not all spastic CP individuals are known to science and medicine, especially in areas of the world where healthcare systems are less advanced. Many such individuals may simply live out their lives in their local communities without any medical or orthopedic oversight at all, or with extremely minimal such treatment, so that they are never able to be incorporated into any empirical data that orthopedic surgeons or neurosurgeons might seek to collect. It is shocking to note that - as with people with physical disability overall - some may even find themselves in situations of institutionalization, and thus barely see the outside world at all.

From what is known, the incidence of spastic diplegia is higher in males than in females; the Surveillance of Cerebral Palsy in Europe (SCPE), for example, reports a M:F ratio of 1.33:1. Variances in reported rates of incidence across different geographical areas in industrialized countries are thought to be caused primarily by discrepancies in the criteria used for inclusion and exclusion.

When such discrepancies are taken into account in comparing two or more registers of patients with cerebral palsy and also the extent to which children with mild cerebral palsy are included, the incidence rates still converge toward the average rate of 2:1000.

In the United States, approximately 10,000 infants and babies are born with CP each year, and 1200–1500 are diagnosed at preschool age when symptoms become more obvious. Those with extremely mild spastic CP may not even be aware of their condition until much later in life: Internet chat forums have recorded men and women as old as 30 who were diagnosed only recently with their spastic CP.

Overall, advances in care of pregnant mothers and their babies have not resulted in a noticeable decrease in CP; in fact, because medical advances in areas related to the care of premature babies have resulted in a greater survival rate in recent years, it is actually more likely for infants with cerebral palsy to be born into the world now than it would have been in the past. Only the introduction of quality medical care to locations with less-than-adequate medical care has shown any decreases in the incidences^{[ spelling? ]} of CP; the rest either have shown no change or have actually shown an increase. The incidence of CP increases with premature or very low-weight babies regardless of the quality of care.

Related Research Articles

Cerebral palsy (CP) is a group of movement disorders that appear in early childhood. Signs and symptoms vary among people and over time, but include poor coordination, stiff muscles, weak muscles, and tremors. There may be problems with sensation, vision, hearing, and speech. Often, babies with cerebral palsy do not roll over, sit, crawl or walk as early as other children. Other symptoms may include seizures and problems with thinking or reasoning. While symptoms may get more noticeable over the first years of life, underlying problems do not worsen over time.

Spasticity is a feature of altered skeletal muscle performance with a combination of paralysis, increased tendon reflex activity, and hypertonia. It is also colloquially referred to as an unusual "tightness", stiffness, or "pull" of muscles.

Hereditary spastic paraplegia (HSP) is a group of inherited diseases whose main feature is a progressive gait disorder. The disease presents with progressive stiffness (spasticity) and contraction in the lower limbs. HSP is also known as hereditary spastic paraparesis, familial spastic paraplegia, French settlement disease, Strumpell disease, or Strumpell-Lorrain disease. The symptoms are a result of dysfunction of long axons in the spinal cord. The affected cells are the primary motor neurons; therefore, the disease is an upper motor neuron disease. HSP is not a form of cerebral palsy even though it physically may appear and behave much the same as spastic diplegia. The origin of HSP is different from cerebral palsy. Despite this, some of the same anti-spasticity medications used in spastic cerebral palsy are sometimes used to treat HSP symptoms.

Functional electrical stimulation (FES) is a technique that uses low-energy electrical pulses to artificially generate body movements in individuals who have been paralyzed due to injury to the central nervous system. More specifically, FES can be used to generate muscle contraction in otherwise paralyzed limbs to produce functions such as grasping, walking, bladder voiding and standing. This technology was originally used to develop neuroprostheses that were implemented to permanently substitute impaired functions in individuals with spinal cord injury (SCI), head injury, stroke and other neurological disorders. In other words, a person would use the device each time he or she wanted to generate a desired function. FES is sometimes also referred to as neuromuscular electrical stimulation (NMES).

Baclofen, sold under the brand name Lioresal among others, is a medication used to treat muscle spasticity, such as from a spinal cord injury or multiple sclerosis. It may also be used for hiccups and muscle spasms near the end of life, and off-label to treat alcohol use disorder or opioid withdrawal symptoms. It is taken orally or by intrathecal pump. It is sometimes used transdermally in combination with gabapentin and clonidine prepared at a compounding pharmacy. It is believed to work by decreasing levels of certain neurotransmitters.

Pachygyria is a congenital malformation of the cerebral hemisphere. It results in unusually thick convolutions of the cerebral cortex. Typically, children have developmental delay and seizures, the onset and severity depending on the severity of the cortical malformation. Infantile spasms are common in affected children, as is intractable epilepsy.

Hypertonia is a term sometimes used synonymously with spasticity and rigidity in the literature surrounding damage to the central nervous system, namely upper motor neuron lesions. Impaired ability of damaged motor neurons to regulate descending pathways gives rise to disordered spinal reflexes, increased excitability of muscle spindles, and decreased synaptic inhibition. These consequences result in abnormally increased muscle tone of symptomatic muscles. Some authors suggest that the current definition for spasticity, the velocity-dependent over-activity of the stretch reflex, is not sufficient as it fails to take into account patients exhibiting increased muscle tone in the absence of stretch reflex over-activity. They instead suggest that "reversible hypertonia" is more appropriate and represents a treatable condition that is responsive to various therapy modalities like drug or physical therapy.

Primary lateral sclerosis (PLS) is a very rare neuromuscular disease characterized by progressive muscle weakness in the voluntary muscles. PLS belongs to a group of disorders known as motor neuron diseases. Motor neuron diseases develop when the nerve cells that control voluntary muscle movement degenerate and die, causing weakness in the muscles they control.

Foot drop is a gait abnormality in which the dropping of the forefoot happens out of weakness, irritation or damage to the deep fibular nerve, including the sciatic nerve, or paralysis of the muscles in the anterior portion of the lower leg. It is usually a symptom of a greater problem, not a disease in itself. Foot drop is characterized by inability or impaired ability to raise the toes or raise the foot from the ankle (dorsiflexion). Foot drop may be temporary or permanent, depending on the extent of muscle weakness or paralysis and it can occur in one or both feet. In walking, the raised leg is slightly bent at the knee to prevent the foot from dragging along the ground.

An intrathecal pump is a medical device used to deliver medications directly into the space between the spinal cord and the protective sheath surrounding the spinal cord. Medications such as baclofen, bupivacaine, clonidine, morphine, hydromorphone, fentanyl or ziconotide may be delivered in this manner to minimize the side effects often associated with the higher doses used in oral or intravenous delivery of these drugs.

Diplegia, when used singularly, refers to paralysis affecting symmetrical parts of the body. This is different from hemiplegia which refers to spasticity restricted to one side of the body, paraplegia which refers to paralysis restricted to the legs and hip, and quadriplegia which requires the involvement of all four limbs but not necessarily symmetrical. Diplegia is the most common cause of crippling in children, specifically in children with cerebral palsy. Other causes may be due to injury of the spinal cord. There is no set course of progression for people with diplegia. Symptoms may get worse but the neurological part does not change. The primary parts of the brain that are affected by diplegia are the ventricles, fluid filled compartments in the brain, and the wiring from the center of the brain to the cerebral cortex. There is also usually some degeneration of the cerebral neurons, as well as problems in the upper motor neuron system. The term diplegia can refer to any bodily area, such as the face, arms, or legs.

A selective dorsal rhizotomy (SDR), also known as a rhizotomy, dorsal rhizotomy, or a selective posterior rhizotomy, is a neurosurgical procedure that selectively cuts problematic nerve roots in the spinal cord. This procedure has been well-established in the literature as a surgical intervention and is used to relieve negative symptoms of neuromuscular conditions such as spastic diplegia and other forms of spastic cerebral palsy. The specific sensory nerves inducing spasticity are identified using electromyographic (EMG) stimulation and graded on a scale of 1 (mild) to 4. Abnormal nerve responses are isolated and cut, thereby reducing symptoms of spasticity.

Spastic quadriplegia, also known as spastic tetraplegia, is a subset of spastic cerebral palsy that affects all four limbs.

Scissor gait is a form of gait abnormality primarily associated with spastic cerebral palsy. That condition and others like it are associated with an upper motor neuron lesion.

Spastic gait is a form of gait abnormality. It is caused by lesions in the corticospinal tract.

Over time, the approach to cerebral palsy management has shifted away from narrow attempts to fix individual physical problems – such as spasticity in a particular limb – to making such treatments part of a larger goal of maximizing the person's independence and community engagement. Much of childhood therapy is aimed at improving gait and walking. Approximately 60% of people with CP are able to walk independently or with aids at adulthood. However, the evidence base for the effectiveness of intervention programs reflecting the philosophy of independence has not yet caught up: effective interventions for body structures and functions have a strong evidence base, but evidence is lacking for effective interventions targeted toward participation, environment, or personal factors. There is also no good evidence to show that an intervention that is effective at the body-specific level will result in an improvement at the activity level, or vice versa. Although such cross-over benefit might happen, not enough high-quality studies have been done to demonstrate it.

Athetoid cerebral palsy, or dyskinetic cerebral palsy, is a type of cerebral palsy primarily associated with damage, like other forms of CP, to the basal ganglia in the form of lesions that occur during brain development due to bilirubin encephalopathy and hypoxic–ischemic brain injury. Unlike spastic or ataxic cerebral palsies, ADCP is characterized by both hypertonia and hypotonia, due to the affected individual's inability to control muscle tone. Clinical diagnosis of ADCP typically occurs within 18 months of birth and is primarily based upon motor function and neuroimaging techniques. While there are no cures for ADCP, some drug therapies as well as speech, occupational therapy, and physical therapy have shown capacity for treating the symptoms.

<span class="mw-page-title-main">Ataxic cerebral palsy</span> Medical condition

Ataxic cerebral palsy is clinically in approximately 5–10% of all cases of cerebral palsy, making it the least frequent form of cerebral palsy diagnosed. Ataxic cerebral palsy is caused by damage to cerebellar structures, differentiating it from the other two forms of cerebral palsy, which are spastic cerebral palsy and dyskinetic cerebral palsy.

Spastic cerebral palsy is the type of cerebral palsy characterized by spasticity or high muscle tone often resulting in stiff, jerky movements. Cases of spastic CP are further classified according to the part or parts of the body that are most affected. Such classifications include spastic diplegia, spastic hemiplegia, spastic quadriplegia, and in cases of single limb involvement, spastic monoplegia.

Spastic hemiplegia is a neuromuscular condition of spasticity that results in the muscles on one side of the body being in a constant state of contraction. It is the "one-sided version" of spastic diplegia. It falls under the mobility impairment umbrella of cerebral palsy. About 20–30% of people with cerebral palsy have spastic hemiplegia. Due to brain or nerve damage, the brain is constantly sending action potentials to the neuromuscular junctions on the affected side of the body. Similar to strokes, damage on the left side of the brain affects the right side of the body and damage on the right side of the brain affects the left side of the body. Other side can be effected for lesser extent. The affected side of the body is rigid, weak and has low functional abilities. In most cases, the upper extremity is much more affected than the lower extremity. This could be due to preference of hand usage during early development. If both arms are affected, the condition is referred to as double hemiplegia. Some patients with spastic hemiplegia only experience minor impairments, where in severe cases one side of the body could be completely paralyzed. The severity of spastic hemiplegia is dependent upon the degree of the brain or nerve damage.

References

↑ "Spastic diplegia cerebral palsy". Genetic and Rare Diseases Information Center (GARD) – an NCATS Program. U.S. National Institutes of Health. Retrieved 15 July 2021.
↑ "Spastic diplegia". MedGen. National Center for Biotechnology Information (NCBI), U.S. National Institutes of Health. Concept ID: C0023882. Retrieved 15 July 2021.
↑ Brandenburg JE, Fogarty MJ, Sieck GC (May 2019). "A Critical Evaluation of Current Concepts in Cerebral Palsy". Physiology. 34 (3): 216–229. doi:10.1152/physiol.00054.2018. PMC 7938766 . PMID 30968751.
↑ Whittle MW (2007). Gait assessment in cerebral palsy (4th ed.). Elsevier - Health Sciences Division. pp. 195–218. ISBN 9780750688833.
↑ Nourizadeh M, Shadgan B, Abbasidezfouli S, Juricic M, Mulpuri K (July 2024). "Methods of muscle spasticity assessment in children with cerebral palsy: a scoping review". Journal of Orthopaedic Surgery and Research. 19 (1): 401. doi: 10.1186/s13018-024-04894-7 . PMC 11238363 . PMID 38992701.
↑ Emara HA, Al-Johany AH, Khaled OA, Al-Shenqiti AM, Ali AR, Aljohani MM, et al. (2024-01-30). "Effect of the Dynamic Orthotic Garment on Postural Control, and Endurance in Children with Spastic Diplegic Cerebral Palsy: A Randomized Controlled Trial". Journal of Multidisciplinary Healthcare. 17: 419–428. doi: 10.2147/JMDH.S438474 . PMC 10838099 . PMID 38314010.
↑ Shamsoddini A, Amirsalari S, Hollisaz MT, Rahimnia A, Khatibi-Aghda A (August 2014). "Management of spasticity in children with cerebral palsy". Iranian Journal of Pediatrics. 24 (4): 345–351. PMC 4339555 . PMID 25755853.
↑ Whittle M (2007). "Chapter 6 - Gait assessment in cerebral palsy". Gait analysis: an introduction (4th ed.). Edinburgh: Butterworth-Heinemann. pp. 195–218. doi:10.1016/B978-075068883-3.50011-8. ISBN 978-0-7506-8883-3 . Retrieved 15 July 2021.
↑ "Formerly known as the Spastics Society: The importance of charity names". BBC. March 31, 2014. Retrieved December 12, 2024.
↑ Burden S. "The Spastics Society/ Scope name change campaign". WARC. Retrieved December 12, 2024.

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[1] "Spastic diplegia cerebral palsy". Genetic and Rare Diseases Information Center (GARD) – an NCATS Program. U.S. National Institutes of Health. Retrieved 15 July 2021.

[2] "Spastic diplegia". MedGen. National Center for Biotechnology Information (NCBI), U.S. National Institutes of Health. Concept ID: C0023882. Retrieved 15 July 2021.

[3] Brandenburg JE, Fogarty MJ, Sieck GC (May 2019). "A Critical Evaluation of Current Concepts in Cerebral Palsy". Physiology. 34 (3): 216–229. doi:10.1152/physiol.00054.2018. PMC 7938766 . PMID 30968751.

[4] Whittle MW (2007). Gait assessment in cerebral palsy (4th ed.). Elsevier - Health Sciences Division. pp. 195–218. ISBN 9780750688833.

[5] Nourizadeh M, Shadgan B, Abbasidezfouli S, Juricic M, Mulpuri K (July 2024). "Methods of muscle spasticity assessment in children with cerebral palsy: a scoping review". Journal of Orthopaedic Surgery and Research. 19 (1): 401. doi: 10.1186/s13018-024-04894-7 . PMC 11238363 . PMID 38992701.

[6] Emara HA, Al-Johany AH, Khaled OA, Al-Shenqiti AM, Ali AR, Aljohani MM, et al. (2024-01-30). "Effect of the Dynamic Orthotic Garment on Postural Control, and Endurance in Children with Spastic Diplegic Cerebral Palsy: A Randomized Controlled Trial". Journal of Multidisciplinary Healthcare. 17: 419–428. doi: 10.2147/JMDH.S438474 . PMC 10838099 . PMID 38314010.

[7] Shamsoddini A, Amirsalari S, Hollisaz MT, Rahimnia A, Khatibi-Aghda A (August 2014). "Management of spasticity in children with cerebral palsy". Iranian Journal of Pediatrics. 24 (4): 345–351. PMC 4339555 . PMID 25755853.

[8] Whittle M (2007). "Chapter 6 - Gait assessment in cerebral palsy". Gait analysis: an introduction (4th ed.). Edinburgh: Butterworth-Heinemann. pp. 195–218. doi:10.1016/B978-075068883-3.50011-8. ISBN 978-0-7506-8883-3 . Retrieved 15 July 2021.

[9] "Formerly known as the Spastics Society: The importance of charity names". BBC. March 31, 2014. Retrieved December 12, 2024.

[10] Burden S. "The Spastics Society/ Scope name change campaign". WARC. Retrieved December 12, 2024.

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