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Diplegia
Diplegia
Diplegia
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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.[1] Diplegia is the most common cause of disability in children, specifically in children with cerebral palsy.[2] 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.[3] There is also usually some degeneration of the cerebral neurons,[2] as well as problems in the upper motor neuron system.[1] The term diplegia can refer to any bodily area, such as the face, arms, or legs.

Facial diplegia

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Facial diplegia refers to people with paralysis of both sides of their face. Bilateral occurs when the onset of the second side occurs within one month of the onset of the first side.[4] Facial diplegia occurs in 50% of patients with Guillain–Barré syndrome. Facioscapulohumeral muscular dystrophy (FSHD) is the second most common adult-onset muscular dystrophy with facial weakness being a distinct feature of FSHD in over 90% of cases.[5]

Causes

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Facial paralysis is usually caused by traumatic, infectious, neurological, metabolic, toxic, vascular, and idiopathic conditions.[4] While over 50% of the cases of unilateral facial paralysis are caused by idiopathic conditions, less than 20% of bilateral cases are idiopathic. The most common infectious cause of facial diplegia is Lyme disease.[4]

Treatment

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The treatment for facial diplegia depends on the underlying cause. Some causes are usually treatable such as infectious, toxic, and vascular by treating the main problem first. After the underlying problem is cured, the facial paralysis usually will go away.[citation needed]

Diplegia of the arms

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People with diplegia in their arms experience difficulties in reaching, pointing, grasping, releasing, manipulating objects and many other motor functions performed by the hands and arms.[6]

Causes

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There are several ways of getting diplegia in the arms. It is very common for people with cerebral palsy to have diplegia of the arms. Although most people with cerebral palsy have diplegia in their legs, some people have diplegia in their arms. Other ways of getting paralysis of both arms is through a traumatic event or injury.[citation needed]Brachial amyotrophic diplegia, a regional variant of ALS, is a rare motor neuron disease characterized by diplegia in the arms.[7]

Treatment

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There are several different modes of treatment for people with paralysis in their upper limbs. For example, behavioral and environmental treatments may include physiotherapy, occupational therapy, motor learning, strength training, and neurodevelopment treatment. Another treatment may be through the use of splints and casts. Electrophysical agents may be used such as neuromuscular electrical stimulation (NMES). Sometimes pharmacological treatments are necessary such as Botulinum toxin type A. On more severe cases surgery of the upper limbs may be required.[6]

Diplegia in the legs

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Diplegia of the legs consists of paralysis of both legs. There are 3 levels of severity. Mild diplegia means the person can usually walk but might walk a little differently, can usually play and run to a limited extent. Moderate diplegia means the person can usually walk but with a slight bend in the knees. They usually cannot run and have to use the handrails to go up and down steps. People with severe diplegia usually need crutches, a walker, or a wheelchair to be able to get around.[3]

Children with diplegia in the legs have a delayed growth in their leg muscles which causes the muscles to be short. This then causes the joints to become stiff and the range of motion to decrease as the child grows. “For the majority of children with diplegia, growth and development are not a problem. Children with diplegia are eventually able to walk, just normally later; they generally attend regular schools and become independently functioning adults.”[8]

Causes

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The most common cause of diplegia in the legs is cerebral palsy. Paralysis of the legs may also be caused by trauma, injury, or genetics, but this is very rare.[3]

Age of onset

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Usually occurs within 2 periods:[3]

  1. With premature babies
  2. full diagnosis usually between ages 2–5 years

Diplegia is usually not diagnosed before the age of 2 years yet the symptoms and signs of the earlier stages are typical and should enable the diagnosis to be made before the contractures have occurred.[9] Parents suspecting diplegia should take their child to the doctor to potentially get an earlier diagnosis.[citation needed]

Treatment and care

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This is broken up by age categories. Different ages require different forms of treatment which may include: therapy, bracing, walkers, wheelchairs, and surgery. Currently the treatments for children are concentrated primarily on independent walking but instead a more independence-oriented therapeutic approach would be more beneficial.[10] This way the child can still focus on walking but at the same time be taught to do things for themselves while using the best method of walking for them. This could include using a walker or wheelchair to get around and do things easier than focusing all the attention on walking so early. For people requiring surgery, distal hamstring lengthening is the most common operation performed because it reduces knee flexion and improves knee motion.[11]

Birth to 1 year

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“This first year sees the development of many milestones, such as head control, reaching out for a toy, sitting, starting to vocalize sounds, and finger feeding.” [8] Most parents want their children to excel very fast, but there is a wide upper and lower range of development time for premature babies so it's very hard to diagnose cerebral palsy or diplegia this early. The most common symptom of a child with diplegia is stiff lower extremities. This should become apparent by the six month mark which means he or she does not have severe diplegia. During this age if a child is not moving his legs on his own then it is recommended to do some exercise, especially gentle stretching with the child.[8]

1 to 3 years

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“This is the age at which the characteristics of diplegia become more noticeable, mainly because, unlike other children at this age, the child with diplegia is not walking.”[8] By the age of three, it is important for the child to be in a specialized school environment so the child can participate in physical therapy and learn social skills. Parents should not force the child to sit, crawl, or walk a certain way during this age period. Let the child do what's comfortable for them and allow the therapist to correct this problem. If you want to help your child walk more, then push toys are recommended for walking aids. Regular exams should be done to make sure the child's legs are growing normally and he or she is not having any problems with the hip.[8]

4 to 6 years

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“This is the age range at which the child with diplegia makes the most significant physical improvement in motor function.”[8] During this time period the child makes major improvements in motor function. He or she should be in a regular school and focus on cognitive issues not therapy. A child using a walking aid for mobility to move around with the other children is not a bad thing. If a child is not walking yet, then this is usually caused by a problem in balance, muscle coordination, spasticity, or leg alignment. Each of these reasons should be looked into closely so the problem can be addressed and fixed.[8]

7 to 12 years

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“By the time a child reaches this age the rate of physical improvement has leveled off in areas such as balance and coordination, and it's a good idea to refocus the child’s attention away from additional physical improvement and toward intellectual learning.”[8] During this time period a child should lean away from physical therapy and do more outdoor or social exercises such as sports and adaptive P.E. Usually by age 8-10 a child has reached maximum walking ability. This will usually decrease a little when a child hits puberty and gains height and weight because walking becomes harder during this changing period. Any significant problems in walking should be addressed with surgery at this stage.[8]

13 to 18 years

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“During this time period of a child’s development, a major issue is separating from the family.”[8] Parents should learn how to cope with their child growing up and give them more freedom and independence. Teenagers need to make their own decisions and learn from them. One way to do this is for parents to compromise and let the child make smaller decisions so they feel important. Parents should also understand that their child may regress in walking some from increase in height and weight. Going back to therapy during puberty is recommended so the teenager can adjust to the increase in height and weight and not regress as much.[8]

History of the term diplegia

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In 1890 Sachs and Peterson first referenced to the term diplegia, along with the word paraplegia, for their cerebral palsy classification. In 1955 the word diplegia was used in the clinical field to describe a patient whose limbs were affected in a symmetrical way. This included limbs on the same side of the body thus including hemiplegia. Later in 1956 diplegia was presented as a form of bilateral cerebral palsy affecting like parts on either side of the body. In 1965 Milani Comparetti distinguished diplegia from tetraplegia by considering the patient's upper limb's ability to express a sufficient support reaction. Thus diplegia usually refers to just symmetry of one body part or limb, as the legs, or arms. While tetraplegia or quadriplegia refers to paralysis of all 4, both arms and legs.[12]

References

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Revisions and contributorsEdit on WikipediaRead on Wikipedia

Diplegia

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from Grokipedia
Diplegia is a form of bilateral that affects symmetrical parts of the body, most commonly both legs, resulting in , , and impaired mobility. It is distinct from hemiplegia, which involves one side of the body, and can vary in severity from mild weakness to complete loss of function in the affected limbs. While diplegia can arise from various neurological conditions, it is most frequently observed as in , a non-progressive disorder caused by brain damage before, during, or shortly after birth. In , spastic primarily involves and in the lower extremities, with the legs affected more severely than the arms, leading to characteristic abnormalities such as scissoring or toe-walking. Common causes include in premature infants, hypoxic-ischemic , and other perinatal insults that damage the brain's motor areas. Symptoms often emerge in and may include delayed motor milestones, joint contractures, and difficulties with balance, though cognitive function is typically preserved. Beyond , diplegia can result from injuries, strokes, infections, or vascular disorders, potentially leading to additional issues like dysfunction or . Diagnosis involves clinical evaluation, such as MRI to identify lesions, and exclusion of progressive conditions. Treatment is multidisciplinary and cause-specific, focusing on managing through physical and , medications like or injections, orthotic devices, and in select cases, surgical interventions such as selective dorsal rhizotomy. Early intervention can significantly improve quality of life, though diplegia due to irreversible causes such as is not curable and requires lifelong management, while cases from treatable etiologies like infections may resolve with prompt intervention.

Definition and Classification

Definition

Diplegia is a neurological condition characterized by or affecting corresponding parts on both sides of the body, such as both arms, both legs, or both sides of the face. The term derives from the Greek roots "di-" meaning two, and "plegia" from "plēgē" meaning a stroke or blow, referring to bilateral symmetrical impacting like parts bilaterally. The core features of diplegia include non-progressive or progressive or primarily in paired limbs or , typically resulting from lesions in the . This distinguishes it from unilateral conditions like hemiplegia, as diplegia involves symmetrical bilateral involvement, often with greater severity in the lower limbs than the upper in cases associated with cerebral origins. Historically, the term diplegia has been primarily associated with , where it describes forms of bilateral or rigidity, though it applies more broadly to other neurological disorders involving symmetrical motor deficits.
ConditionDescriptionTypical Affected AreasCommon Origin
DiplegiaBilateral symmetrical or affecting corresponding parts.Both s, both s, or both sides of face; legs often more affected.Cerebral ().
HemiplegiaUnilateral or affecting one side of the body.One and one on the same side.Cerebral or .
Paraplegia affecting the lower half of the body.Both s and lower trunk. (thoracic/lumbar).
Quadriplegia affecting all four limbs and the .s, s, trunk, and possibly .High cervical .

Types

Diplegia is classified anatomically according to the primary regions of bilateral motor impairment. Facial diplegia involves symmetric of both sides of the face due to bilateral cranial VII dysfunction. Upper limb diplegia, a rarer form, affects both arms and shoulders symmetrically, often with preserved lower limb function. Lower limb diplegia, the most common anatomical variant, primarily impacts both legs, with potential mild involvement. Clinically, diplegic conditions are further subdivided based on and movement characteristics. , marked by and increased resistance to passive movement, represents the predominant subtype, especially in pediatric where it constitutes 30-40% of cases. Flaccid diplegia is characterized by and diminished , occurring infrequently and often linked to early infantile cerebro-cerebellar involvement. features impaired coordination and balance with bilateral limb , typically as a mixed in . As a motor pattern, diplegia frequently manifests as a subtype of , with severity graded via the (GMFCS), which delineates five levels from I (independent ambulation with minor limitations) to V (severe restrictions requiring full assistance or wheeled mobility). It may also arise from isolated neurological insults, such as bilateral post-stroke affecting the lower extremities. Typing of diplegia relies on clinical assessment emphasizing bilateral , degree of impairment, and specific features like scissoring in lower limb variants, where adductor causes the legs to cross midline during locomotion.

Epidemiology

Prevalence and Incidence

Diplegia, most commonly manifesting as spastic diplegic (CP), affects a subset of individuals with CP, which has a global birth prevalence of approximately 1.5 to 2.5 per 1,000 live births. Within spastic CP—the predominant subtype accounting for 70% to 80% of all CP cases—diplegia represents 20% to 30% of instances, primarily involving bilateral lower limb impairment with milder or no involvement.00686-5/fulltext) This form is notably more prevalent among preterm infants, comprising up to 50% of CP cases in very low-birth-weight groups, where overall CP rates can reach 8% to 11% among survivors. Incidence rates for diplegic CP are closely tied to perinatal events, with annual new cases reflecting birth-related risks. Regionally, varies significantly: high-income countries report rates of about 1.5 to 2 per 1,000 live births, compared to 2 to 4 per 1,000 in low- and middle-income countries, where birth complications contribute to higher burdens. These disparities underscore the influence of access to neonatal care on occurrence. Since the 2000s, incidence trends for CP, including diplegic forms, have shown a decline in high-income settings—dropping by up to 40% from 2.1 to 1.6 per 1,000 live births—attributable to advances in neonatal intensive care and perinatal management.00686-5/fulltext) However, rates for genetic etiologies, which account for up to 30% of cases, remain stable.00686-5/fulltext) Recent data from the CDC and WHO through 2025 confirm this stabilization in overall figures, with U.S. at approximately 2.9 per 1,000 children. Among diplegic presentations, lower limb involvement predominates in about 80% of cases, reflecting the typical periventricular damage in CP. Facial diplegia is rare, occurring in less than 5% of neurological diplegic conditions overall, with an incidence of approximately 1 per 5 million population; it is often linked to non-CP causes like Guillain-Barré syndrome (incidence 1–2 per 100,000 person-years). diplegia is even less common, as isolated bilateral upper extremity paralysis seldom arises without broader involvement.

Risk Factors

Diplegia, a subtype of characterized by bilateral motor impairment predominantly affecting the lower limbs, is associated with a range of modifiable and non-modifiable risk factors that span prenatal, perinatal, and postnatal periods. Prenatal risks include maternal infections such as and (CMV), which can disrupt fetal brain development, as well as multiple pregnancies and placental abnormalities like abruption or insufficiency that compromise fetal oxygenation. Exposure to toxins during pregnancy, including alcohol and , further elevates the risk by interfering with neurodevelopment. In term-born cases of , pregnancy complications ( [OR] 4.73, 95% CI 1.91-10.56), maternal diseases (OR 2.52, 95% CI 1.57-3.93), and maternal substance use (OR 3.11, 95% CI 2.10-4.55) have been identified as significant contributors. Perinatal risks are particularly prominent, with prematurity ( <37 weeks) and (<2500 g) increasing the likelihood of diplegia by 10- to 50-fold, depending on severity, due to vulnerability to brain injuries like . , emergency cesarean sections, and in preterm infants are additional key factors, with cesarean delivery showing an OR of 2.35 (95% CI 1.62-3.40) and perinatal adversity an OR of 2.91 (95% CI 1.94-4.50) in term-born . Perinatal infections also contribute, with an OR of 2.72 (95% CI 1.32-5.10). Postnatal risks encompass infections like , head trauma, and hyperbilirubinemia leading to kernicterus, which can cause bilirubin-induced neurological damage and subsequent motor deficits. Genetic factors play a role in a subset of cases, with rare mutations in genes such as CTNNB1, NT5C2, and AP4M1 linked to phenotypes, often through disruptions in development or . Family history of neurological disorders may indicate inherited predispositions, though most genetic contributions to diplegia are sporadic. Socioeconomic influences, including limited access to , are associated with higher odds of diplegia, with low conferring an OR of 1.49 (95% CI 1.16-1.91) compared to high status, potentially exacerbating other risks like prematurity.

Causes and Pathophysiology

General Etiologies

Diplegia primarily stems from neurological origins, which may involve or lesions caused by hypoxia-ischemia, disrupting oxygen supply to neural tissue, particularly in premature infants. Vascular events, such as ischemic or hemorrhagic strokes, represent another key cause, occurring in both pediatric and adult populations and leading to bilateral motor deficits through damage to motor pathways. Infections, including from viral or bacterial sources, can induce inflammatory damage resulting in diplegic symptoms. Developmental disorders form a major category of etiologies, with —often —frequently arising from , a injury common in preterm births that affects corticospinal tracts. Genetic syndromes also play a role, as seen in conditions like or , where mutations lead to muscle weakness, , and potential CNS or spinal involvement mimicking diplegic patterns. Acquired conditions contribute through diverse mechanisms, including trauma such as birth injuries or injuries that cause direct neural damage, metabolic disorders like mitochondrial diseases impairing energy production in neural cells, demyelinating diseases such as , tumors compressing motor pathways, and toxins exemplified by , which induces and motor impairments. Among pediatric cases, approximately 80-90% of diplegia etiologies trace to prenatal or perinatal factors, while 10-20% are postnatal; in contrast, adult-onset diplegia is rarer and commonly linked to , , , or vascular events. The condition's development often exhibits a multifactorial nature, where genetic predispositions interact with environmental triggers to precipitate neural injury.

Pathophysiological Mechanisms

Diplegia primarily arises from damage to the upper motor neurons, particularly involving the bilateral corticospinal tracts, which disrupts descending motor signals from the to the , leading to and predominantly in the lower limbs. This bilateral involvement often results in symmetric due to lesions in watershed areas, such as the periventricular , where reduced cerebral blood flow or ischemia preferentially affects these vulnerable border zones between major arterial territories. In premature infants, the immature in these regions are highly susceptible to hypoxic-ischemic injury, culminating in (PVL), a key pathological substrate that selectively damages fibers of the corticospinal tracts en route to the lower extremities. In adults, diplegic symptoms can stem from lesions in the or , where bilateral infarcts or hemorrhages interrupt motor pathways, often triggered by vascular events like strokes in these deep structures. For instance, symmetric involvement may impair the integration of motor control signals, while lesions can directly affect the descending , producing a diplegic pattern through axonal degeneration and . Acute events in both populations frequently involve , where excessive glutamate release during ischemia triggers calcium influx and neuronal death, compounded by inflammation from microglial activation and cytokine release that exacerbates damage. Early-onset damage, as in congenital cases, engages mechanisms that can lead to maladaptive rewiring, where surviving neural circuits form aberrant connections, potentially amplifying through hyperexcitable pathways in the sensorimotor cortex. This rewiring is influenced by the timing of injury, with periventricular disruptions in infancy altering thalamocortical projections and promoting compensatory but inefficient bilateral activation patterns. Diplegic conditions manifest as either static or progressive based on the underlying pathology; static forms, such as those in , involve non-worsening lesions like fixed scars that halt progression after the initial insult. In contrast, progressive variants occur in degenerative diseases, including certain (ALS) subtypes like brachial or leg amyotrophic diplegia, where ongoing degeneration in the corticospinal tracts leads to gradual symmetric weakness through and failure. A textual representation of the core mechanism illustrates bilateral pyramidal tract disruption: motor signals from the descend via the and , converging in the periventricular region; symmetric injury here severs fibers to the spinal segments, resulting in equivalent of both lower limbs while sparing upper body innervation due to more rostral tract preservation.

Diagnosis

Clinical Evaluation

The clinical evaluation of diplegia begins with a thorough to determine the onset, progression, and potential etiologies. Onset is typically assessed as congenital, evident in infancy through delayed motor milestones, or acquired later due to events like trauma or ; in cerebral palsy-related diplegia, symptoms manifest before age 2 years and remain non-progressive. Perinatal events are scrutinized, including , , Apgar scores, and complications such as prematurity or neonatal infections, which are common risk factors for . Family history is essential to identify hereditary conditions like , while the progression rate helps distinguish static lesions (e.g., ) from progressive neurodegenerative disorders. Physical examination focuses on neurological and musculoskeletal findings to confirm bilateral involvement, particularly in the lower limbs. is evaluated using the Modified Ashworth Scale, which grades from 0 (no increase in tone) to 4 (affected part rigid), often revealing increased extensor tone in the legs. Reflexes are tested for and , with persistent like the Babinski sign indicating dysfunction. Motor strength is graded via the Medical Research Council () scale, ranging from 0 (no contraction) to 5 (normal power), typically showing weakness in hip flexors and ankle dorsiflexors in lower limb diplegia. For lower limb involvement, observes patterns such as scissoring (adducted thighs) or toe-walking due to equinus . Associated signs are assessed to gauge overall impact and comorbidities. Sensory deficits, though less common in pure motor diplegia, may include visual impairments like in up to 50% of cases or in 10-20%. Cognitive involvement affects about 50% of patients with overall but is typically preserved or milder in spastic diplegia, manifesting as or speech delays in more severe cases. Orthopedic deformities, such as joint contractures from chronic or hip in 30% of cases, are noted through inspection and range-of-motion testing. Functional scales provide a standardized assessment of impairment severity, particularly in cerebral palsy-related diplegia. The (GMFCS) categorizes patients into five levels based on self-initiated movement, with levels I-II indicating independent walking (common in mild diplegia) and levels III-V requiring assistive devices or use; it is reliable for prognostic planning across ages. Delays in developmental milestones, such as sitting by 6 months or walking by 18 months, are documented to quantify motor progression. Differential diagnosis involves ruling out conditions with similar bilateral , such as hemiplegia (unilateral involvement), (progressive with relapses), or lesions causing without signs above the lesion. A careful and exam help exclude these by confirming symmetric lower limb predominance and static course in true diplegia.

Diagnostic Tests

Diagnosis of diplegia relies on a combination of , electrophysiological studies, laboratory investigations, and advanced imaging techniques to confirm the condition and elucidate underlying etiologies, particularly in the context of or other disorders. is fundamental, with (MRI) serving as the preferred modality due to its superior ability to visualize lesions and periventricular damage, which are common in . Computed tomography (CT) scans are utilized primarily for detecting acute hemorrhage or calcifications in emergent settings, offering rapid assessment when MRI is unavailable. In infants, cranial provides a non-invasive initial evaluation, particularly for identifying through the open . Electrophysiological tests help differentiate central from peripheral causes of diplegia. (EMG) and nerve conduction studies (NCS) assess muscle and nerve function, revealing normal findings in central diplegia while identifying peripheral neuropathies or entrapments that may mimic or complicate the presentation. If clinical features suggest co-occurring seizures, an electroencephalogram (EEG) is indicated to evaluate epileptiform activity, which occurs in approximately 30-50% of cases. Laboratory evaluations target potential genetic, metabolic, and infectious contributors. Genetic panels, such as those screening for (e.g., mutations in SPG genes), are recommended when family history or progressive features suggest an inherited etiology. Metabolic screens, including assays for , organic acids, and acylcarnitines, help identify that can present with diplegic symptoms mimicking . Serologic testing for congenital infections, such as (CMV) IgM and IgG, is essential given CMV's role as a leading infectious cause of cerebral palsy-related diplegia. Advanced imaging modalities provide deeper insights into neural integrity. Diffusion tensor imaging (DTI), an extension of MRI, quantifies tract integrity, demonstrating reduced in corticospinal tracts of children with diplegic . Functional MRI (fMRI) maps activation, revealing altered connectivity in sensorimotor networks that correlates with motor impairment severity in . Interpretation of these tests emphasizes patterns consistent with diplegia, such as bilateral symmetric periventricular lesions on MRI, which confirm central involvement. MRI demonstrates high sensitivity, detecting abnormalities in approximately 86-89% of cases including diplegic subtypes, guiding etiological classification and prognosis.

Facial Diplegia

Facial diplegia, also known as bilateral , is a rare neurological condition characterized by weakness or affecting the muscles on both sides of the face, typically involving the (cranial nerve VII). It differs from unilateral facial palsy, such as , and requires prompt evaluation due to its association with potentially serious underlying conditions.

Causes

Facial diplegia arises from various etiologies, often involving peripheral nerve damage or disorders. The most common infectious cause is , caused by , particularly in endemic areas, where bilateral facial palsy occurs in up to 25% of cases. Guillain-Barré syndrome (GBS), an acute autoimmune often post-infectious, frequently presents with facial diplegia in 30-50% of cases, sometimes as an isolated feature or with limb paresthesias. Other infectious causes include , , reactivation, and . Non-infectious etiologies encompass autoimmune conditions like (neurosarcoidosis) and systemic , malignancies such as or tumors compressing the facial nerves, and idiopathic cases resembling bilateral , though the latter is rare (less than 1% of instances). Trauma, including skull fractures, and congenital disorders like can also lead to facial diplegia. In a of 170 cases as of 2023, infectious causes accounted for approximately 50%, with GBS and predominant.

Symptoms and Presentation

Facial diplegia typically presents with acute or subacute bilateral facial muscle weakness, which may be symmetric or slightly asymmetric, developing over hours to days. Core symptoms include drooping of the eyelids and mouth corners, inability to close the eyes fully (), impaired smiling or frowning, and difficulty with facial expressions, leading to a mask-like appearance. Patients often experience challenges with speaking (), eating, and drinking due to weak lip closure, increasing risks of aspiration or . Eye-related complications are prominent, such as dry eyes from reduced and tear production, potentially causing corneal abrasions or ulcers if unprotected. Associated features depend on the : in GBS, paresthesias or mild limb weakness may occur; in , or ; systemic symptoms like fever in infections. Onset is often simultaneous or within 30 days, with incidence estimated at 0.2-2% of all facial palsies. Severity varies, but isolated facial involvement is more common in idiopathic or early infectious cases, while progressive involvement suggests GBS or .

Treatment

Treatment of facial diplegia is etiology-specific and multidisciplinary, involving neurologists, ophthalmologists, and physical therapists to address the underlying cause and prevent complications. For , antibiotics such as (100 mg twice daily for 14-21 days) or intravenous for severe cases are standard. In GBS-associated facial diplegia, disease-modifying therapies include intravenous immunoglobulin (IVIG) at 0.4 g/kg/day for 5 days or (plasma exchange) initiated within 2 weeks of onset to improve recovery rates. Supportive care is essential regardless of cause: and eye patching during sleep protect against corneal damage; facial , including and exercises, helps maintain and prevent contractures. Corticosteroids like (1 mg/kg/day for 5-7 days) may be used in idiopathic or inflammatory cases, though evidence is stronger for unilateral . Surgical interventions, such as for severe eye exposure or nerve decompression, are reserved for refractory cases. Prognosis is generally favorable, with complete recovery in over 60% of cases as of 2023 data, particularly when treated early; however, residual weakness or synkinesis may persist in 20-30%, depending on etiology and timeliness of intervention.

Upper Limb Diplegia

Causes

Upper limb diplegia, also known as brachial diplegia, refers to bilateral weakness or paralysis primarily affecting the arms and shoulders, often sparing the lower extremities. It most commonly results from central nervous system lesions that symmetrically impair motor pathways to the upper limbs. A key etiology is Man-in-the-Barrel syndrome, caused by bilateral watershed infarcts in the border zones between anterior and middle cerebral artery territories, typically due to systemic hypotension from cardiac arrest, sepsis, or perioperative complications. These infarcts damage corticospinal tracts controlling arm movement while preserving leg function. Other central causes include bilateral cortical or subcortical strokes, traumatic brain injuries, multiple sclerosis plaques in the cervical spinal cord, or tumors compressing motor pathways. Spinal cord etiologies involve lesions at the cervical level, such as central cord syndrome from hyperextension injuries in older adults with spondylosis, leading to greater upper extremity involvement due to vulnerability of hand motor fibers in the central cord. Peripheral causes are less common but include bilateral brachial plexus injuries from trauma (e.g., motorcycle accidents) or inflammatory conditions like acute bilateral brachial neuritis (Parsonage-Turner syndrome). In neuromuscular disorders, conditions like amyotrophic lateral sclerosis (ALS) or inclusion body myositis can present with progressive bilateral upper limb weakness, though these often involve lower limbs over time. Unlike lower limb diplegia, which is frequently linked to perinatal brain injuries in cerebral palsy, upper limb diplegia is rarer in pediatric populations and more often associated with adult-onset vascular or degenerative processes.

Symptoms and Presentation

Upper limb diplegia manifests as symmetric in both arms, ranging from mild to complete flaccid or spastic , depending on the level. Core symptoms include bilateral abduction and flexion , often resulting in a "man-in-the-barrel" appearance where patients can move their legs but have pendulous, non-functional arms. In lesions, develops with increased tone, , and positive Babinski sign, leading to contractures in flexors and internal rotators. Lower motor neuron involvement, as in damage, presents with , , fasciculations, and in a dermatomal pattern. Onset is typically acute in vascular causes like , with sudden inability to lift arms or perform overhead activities, whereas degenerative conditions like show insidious progression over months. Associated features may include from compression, shoulder due to flaccid muscles, or autonomic dysfunction in spinal lesions. Functionally, it impairs such as self-feeding, dressing, and writing, often graded using scales like the Upper Extremity Function Test for severity assessment. In chronic cases, disuse atrophy and secondary joint deformities exacerbate limitations, though cognitive and lower limb functions are usually preserved.

Treatment

Treatment for upper limb diplegia is multidisciplinary, tailored to the underlying cause and aimed at preserving function, managing , and promoting independence. Acute management focuses on addressing reversible etiologies: or mechanical for ischemic strokes within 4.5-24 hours of onset, blood pressure stabilization in watershed infarcts, and surgical decompression for compressive spinal lesions. Pharmacological options include antispastics like or for , and analgesics for . Rehabilitation is central, with emphasizing fine motor retraining, adaptive techniques, and strengthening exercises to improve arm use. incorporates range-of-motion activities to prevent contractures, often using slings or braces for shoulder support. Assistive devices such as powered arm orthoses, reachers, or voice-activated technologies enhance daily function. In severe peripheral cases, nerve transfers or tendon reconstructions may restore some movement, while injections target focal in elbow flexors or wrist pronators. Prognosis varies; recovery is better in vascular causes with early intervention, potentially regaining partial function in 50-70% of cases within 6 months, whereas neurodegenerative etiologies like are progressive and palliative. As of 2025, emerging techniques like show promise for improving upper limb motor control in clinical trials.

Lower Limb Diplegia

Causes

Lower limb diplegia most commonly arises in the context of , where damage to the developing brain's disrupts , particularly affecting the legs more severely than the arms. The predominant etiologies include (PVL), a softening and of near the brain's ventricles, often occurring in premature infants due to immature vascular development and vulnerability to ischemia. PVL is strongly associated with very , which significantly elevates the risk, with odds ratios reported as high as 11.5 for infants under 1,250 grams delivered vaginally compared to those born via cesarean section. Hypoxic-ischemic encephalopathy (HIE), resulting from oxygen deprivation and reduced blood flow during the perinatal period, also frequently leads to by causing periventricular lesions that impair lower extremity function. Beyond cerebral palsy, other causes encompass hereditary spastic diplegia, primarily due to mutations in the SPAST gene (also known as SPG4), which encodes the spastin protein essential for microtubule dynamics in neurons; these autosomal dominant mutations account for up to 45% of familial cases of hereditary spastic paraplegia, manifesting as progressive lower limb spasticity. Spinal cord lesions, such as those from tethered cord syndrome, contribute by anchoring and stretching the caudal spinal cord, leading to lower limb weakness and sensory deficits through chronic ischemia and neural traction. Post-infectious sequelae, including those from poliomyelitis, can result in asymmetric lower limb involvement, though this is less common in modern contexts due to vaccination. The majority (85-90%) of cases, including those with lower limb diplegia, originate from prenatal or perinatal insults, such as vascular disruptions or , while a smaller portion are postnatal, often from infections or trauma. Hereditary spastic paraplegias represent a key genetic subset of non- causes. The spastic form, typical of lesions like those in PVL or HIE, contrasts with rare flaccid diplegia from anterior horn cell damage, as seen in sequelae, where lower motor neurons degenerate leading to and .

Age of Onset and Symptoms

Lower limb diplegia, most commonly manifesting as in the context of , typically presents with a congenital onset, with the majority (85-90%) of cases from birth or early infancy due to perinatal brain injury such as . In many instances, the condition becomes evident through delayed achievement of developmental milestones, such as missing crawling or standing by 6-12 months of age, reflecting an initial phase of that progresses to as the child grows. Rare adult-onset forms may arise from acquired insults like , leading to bilateral lower extremity weakness and without the developmental history typical of pediatric cases. During infancy, early symptoms often include generalized , which evolves into spastic , particularly in the legs, resulting in delayed motor skills like poor head control, rolling, or supported sitting. As the child reaches toddlerhood and , characteristic abnormalities emerge, such as scissoring (inward crossing of the legs during walking), toe-walking due to persistent equinus , and potential knee hyperextension, all of which increase the risk of orthopedic complications like hip subluxation or . Equinus foot , the most prevalent associated orthopedic issue, affects up to 80% of individuals with , often compounded by from muscle overuse and joint stress. Severity varies significantly, classified using the (GMFCS), where levels I-III indicate milder involvement allowing independent ambulation, often with assistive devices, while levels IV-V denote more profound impairment necessitating use for mobility. Associated non-motor symptoms may include bladder dysfunction in about 30% of cases, manifesting as incontinence or urgency due to neurogenic lower urinary tract involvement. These progressive manifestations underscore the developmental trajectory of lower limb diplegia, emphasizing early monitoring of motor milestones to guide supportive care.

Treatment

The treatment of lower limb diplegia, commonly associated with , employs a multidisciplinary approach involving , orthotists, pharmacologists, and orthopedic surgeons to optimize mobility, reduce , and prevent deformities. forms the cornerstone, incorporating stretching exercises to maintain joint and strengthening activities to support and stability. Orthotic devices, such as ankle-foot orthoses (AFOs), provide essential ankle support to correct and improve efficiency by reducing energy expenditure during ambulation. Serial casting is utilized for managing contractures, particularly in the ankles and knees, through progressive applications that gradually elongate shortened muscles over weeks. Pharmacological interventions target to facilitate therapy adherence and functional gains. Botulinum toxin injections, administered every 3-6 months into key lower limb muscles like the gastrocnemius and hamstrings, temporarily weaken overactive fibers, thereby enhancing stretch tolerance and orthotic tolerance. Oral serves as a systemic option to modulate spasticity via GABA-B receptor agonism, while intrathecal delivered through an implanted pump offers more precise dosing for severe cases, minimizing systemic side effects and improving lower limb tone control. Surgical management addresses persistent deformities and contractures unresponsive to conservative measures. Soft tissue releases, including lengthening of the hamstrings and , correct equinus and crouch patterns, often combined with tendon transfers to balance muscle forces. Osteotomies are performed for hip to realign the and prevent progression to , particularly in children. Multilevel , involving concurrent procedures at the hips, knees, and ankles, is undertaken to achieve comprehensive correction in a single event, reducing recovery periods. Age-adapted strategies ensure interventions align with developmental stages. From birth to 1 year, emphasis is placed on proper positioning and early intervention to promote motor milestones and prevent early contractures. Between ages 1-3 years, gait training with assistive devices fosters independent walking, while 4-6 years focuses on school integration aids like adaptive to support participation in activities. For 7-12 years, integrates with ongoing to address growing pains from , and 13-18 years involves transition planning to adult care, including vocational for long-term independence. Emerging therapies, such as transplantation, are under investigation as of 2025, with clinical trials demonstrating safety and improvements in gross motor function in some children with , though high-quality randomized controlled trials remain limited. For example, a 2025 study on blood reported benefits in motor function associated with higher doses.

Prognosis

General Outcomes

Diplegia encompasses various forms, including spastic diplegic (CP) and acute variants like facial diplegia in Guillain-Barré syndrome (GBS), with long-term outcomes varying by etiology but generally favoring functional independence in milder cases. In spastic diplegic CP, children classified at (GMFCS) levels I-II can walk independently or with limitations, and approximately 50-80% of individuals with CP overall achieve some form of ambulation. For facial diplegia as a GBS variant, recovery rates are high, with about 80% of GBS patients achieving independent walking at 6 months and most experiencing substantial improvement in facial symptoms following . For diplegia resulting from spinal cord injuries or strokes, prognosis depends on injury severity and rehabilitation timing, with 40-60% achieving partial functional recovery in the lower limbs, often requiring assistive devices for mobility. Lifespan in diplegic CP is typically normal for mild cases, with over 80% of individuals surviving beyond age 58, comparable to the general population, though severe overlaps with quadriplegia reduce expectancy due to comorbidities like respiratory issues. Complications such as affect approximately 10-30% of those with diplegic CP, potentially impacting mobility and requiring surgical intervention in progressive curves exceeding 40 degrees. remains high with early intervention, including , which enhances motor function and ; employment rates for adults with mild CP, including diplegic forms, range from 30-45% in some studies, higher than overall CP rates of around 20-30% and among those with preserved ambulation and lower pain levels. Common trajectories differ by lesion type: static encephalopathies like CP show functional improvements over time through targeted therapies such as neurodevelopmental treatment, leading to gains in balance and in 70-80% of cases. In contrast, progressive genetic forms, such as or argininemia-related diplegia, often worsen over decades, with increasing and dependency despite interventions. Longitudinal studies, including a 13-year prospective cohort of 151 adults with CP (many diplegic), indicate that 65% maintain community living with varying participation levels, though difficulties in housing and relationships rise in the mid-20s. A 20-year Norwegian registry follow-up further supports these patterns, emphasizing sustained for optimized outcomes across forms of diplegia.

Influencing Factors

Several factors influence the prognosis of diplegia, particularly in the context of (CP), by modulating motor function, independence, and over time. These include clinical, demographic, and environmental variables that can either enhance or hinder recovery and functional gains. Personalized predictions often rely on assessing these elements early to guide interventions and expectations. Positive influencing factors include early and , which can significantly improve motor outcomes. For instance, intensive early motor interventions, such as goal-directed initiated before 12 months, have been shown to enhance gross motor function in infants with CP, with some programs leading to superior gains in ambulant children compared to standard care. Mild severity, as classified by (GMFCS) level I, is associated with better functional outcomes, including higher gait efficiency and independence in daily activities. The absence of comorbidities further supports favorable prognosis, as isolated diplegia without additional neurological impairments allows for more targeted rehabilitation and reduced complication risks. Negative influencing factors encompass perinatal and social elements that exacerbate severity. Prematurity is a key risk, increasing the likelihood of persistent motor deficits and CP subtypes like due to associated brain injuries. Co-occurring , present in approximately 40% of children with CP, worsens overall prognosis by limiting adaptive skills and engagement. Delayed intervention beyond the critical early developmental window correlates with poorer motor trajectories and increased dependency. Socioeconomic barriers, such as low neighborhood status, are linked to greater CP severity, including higher GMFCS levels and reduced access to specialized care. Form-specific considerations also play a role. In lower limb diplegia, involvement, such as displacement, significantly worsens mobility by promoting contractures and abnormalities, often requiring surgical correction for preservation of function. Early initiation of can improve outcomes in rare cases of upper or facial diplegia in CP by minimizing , though such variants depend on the underlying . Long-term prognosis is bolstered by consistent adherence to rehabilitation, which helps prevent secondary issues like contractures through sustained and strengthening; studies indicate that regular home exercise programs reduce the incidence of limitations and support ongoing mobility gains. Access to , when indicated, further improves outcomes by addressing deformities early. Predictive tools like the Hammersmith Infant Neurological Examination (HINE) aid in forecasting outcomes, with lower scores in infancy strongly correlating with later CP diagnosis and motor impairments, enabling earlier risk stratification.

History

Origin of the Term

The term "diplegia" derives from the Greek roots di- meaning "two" or "double" and -plēgía from plḗgē meaning "" or "blow," referring to affecting corresponding parts on both sides of the body. It entered medical lexicon as a borrowing from New Latin in the , with the earliest documented use appearing in English-language texts around 1883. English surgeon William John Little provided early descriptions of the condition in the mid-19th century, though he did not initially employ the term "diplegia." In his 1853 publication On the Nature and Treatment of the Deformities of the Human Frame, Little detailed congenital deformities associated with and of the lower limbs, attributing them to perinatal insults such as difficult labor or , and later termed this "congenital spastic paralysis" or "Little's disease" in works from the 1860s. The term "diplegia" itself first appeared in the context of classification in medical literature in 1890, when neurologists and Frederick Peterson used it to classify bilateral spastic forms of in their analysis of 140 cases, distinguishing it from unilateral hemiplegia and total . further adopted and elaborated on "diplegia" in his 1893 article Zur Kenntniss der cerebralen Diplegien des Kindesalters (im Anschluss an die Little'sche Lähmung), applying it specifically to bilateral cerebral palsies with predominant lower limb involvement and emphasizing the poor correlation between clinical symptoms and brain lesions. In 19th-century , "diplegia" was initially contextualized to differentiate cerebral-origin bilateral from spinal , which affects only the lower body due to cord injury, as highlighted in early classifications like those of Sachs and Peterson. By the , debates emerged regarding the term's ambiguity, particularly its overlap with quadriplegia in describing upper and lower limb involvement; a 2003 analysis argued for its abandonment to avoid confusion in subtypes, while a 2010 response countered that retaining "diplegia" and "quadriplegia" aids precise clinical communication.

Key Historical Developments

In the late , advanced the understanding of cerebral diplegia by classifying it within as a form of bilateral motor impairment originating from brain lesions, emphasizing prenatal and perinatal factors over purely birth-related trauma. This classification, detailed in his 1897 work Die infantile Cerebrallähmung, shifted focus toward neurological etiology and remains foundational. During the 1940s, orthopedic surgeon Winthrop Phelps pioneered surgical interventions for , introducing techniques like tendon lengthening and muscle releases to improve mobility and reduce contractures in affected children. His work, including long-term outcome studies on orthopedic procedures, established multidisciplinary management combining surgery, bracing, and therapy as standard for spastic forms. By 1997, the (GMFCS) was introduced to standardize assessment of motor impairment severity in , including diplegic subtypes, facilitating better research and prognosis. The 1980s brought (MRI) as a key tool for identifying diplegia's underlying brain lesions, such as , enabling precise etiological diagnosis beyond earlier imaging limitations. In the 1990s, intrathecal pumps emerged for managing severe in diplegic , with early trials demonstrating reduced tone and improved function via targeted delivery. The incorporated , encompassing diplegia, into in 1992, standardizing global coding and epidemiological tracking. therapies gained traction in the 2010s, with clinical trials exploring mesenchymal stem cells for in , including diplegic cases; as of 2025, ongoing phase III trials, such as Duke University's study using allogeneic unrelated , report safety and modest motor gains. Debates on terminology intensified in 2010, with publications arguing for phasing out "diplegia" and "quadriplegia" in favor of GMFCS-based descriptions to reduce ambiguity in clinical communication. Key figures include William John Little, whose 19th-century descriptions of —known as "Little's disease"—laid early groundwork for recognition, and modern epidemiologist Karen Østergaard, whose work on registries in has informed prevalence studies and long-term outcomes.

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