Orthopedics - Oleksa A.P. 2006

Neurogenic Deformities of the Musculoskeletal System
Infantile Cerebral Spastic Paralysis (Cerebral Palsy)

The condition was first described by Little (1862) and termed cerebral palsy by Freud (1897).

Spastic cerebral palsy is a complex disorder accounting for 0.8–1.0% of all pediatric musculoskeletal pathologies. While the incidence rates vary across different countries, Faubel (1959) notes that they range between 0.1% and 0.2% in the Americas and Europe.

With advancements in intensive care, the number of surviving patients has increased, as modern medicine now saves newborns who previously would not have survived.

The Etiology of cerebral palsy is multifactorial and can be classified into three main groups: 1) congenital — resulting from fetal Brain malformations caused by maternal toxemia during Pregnancy, infectious diseases (such as tuberculosis, Syphilis, or typhus), Toxoplasmosis, physical or psychological trauma, and X-ray or ionizing radiation; 2) perinatal — resulting from obstetric interventions (forceps, vacuum extraction, etc.), fetopelvic disproportion, and asphyxia (due to impaired placental Circulation or premature placental abruption); 3) postnatal — mechanical trauma (brain contusion, Hemorrhage), meningitis, encephalitis, spasmophilia, and other conditions.

Combinations of different etiological factors are also observed. For instance, difficult labor may simultaneously result in asphyxia and intracranial hemorrhage.

The primary pathogenetic mechanism of cerebral palsy involves impaired Cerebral Cortex activity, and occasionally its subcortical structures, resulting from the aforementioned causes. This leads to secondary functional alterations in nerve pathways, peripheral nerves, and their endings, ultimately causing musculoskeletal dysfunction.

Thus, these neuromuscular disorders arise not only from localized micro- and macrostructural brain changes but also from functional impairments across the entire Central Nervous system, specifically an imbalance between Excitation and Inhibition where excitatory processes predominate, clinically manifesting as spastic paralysis.

The literature contains extensive data regarding The Nature of anatomical changes in both neural and muscular Tissues. As early as 1905, Muritz described brain damage manifesting as softening, scarring, and sclerosis. In cases of atrophy and sclerosis, both white and Gray matter are thinned, the brain tissue is dense, and cysts of varying sizes may be present (Towbin, 1955). Post-mortem examinations of deceased neonates revealed hemorrhages and cerebral vessel thrombosis. Cerebral hypoplasia as a cause of spastic paralysis was noted by Little as early as 1862, as well as by Josephy (1947) and Towbin (1955).

In addition to neuropathological brain changes, children with cerebral palsy develop secondary structural alterations in the neuromuscular system (Mezhenina, 1960; Bogdanov & Mezhenina, 1966). The severity of these changes correlates directly with the degree of paralysis.

In mild Muscle spasticity, pathomorphological changes are restricted to isolated muscle fibers, presenting as patchy atrophy. Areas of normal Structure and regions with homogenized, featureless sarcoplasm can be observed within the same single fiber.

In moderate and severe spasticity, dystrophic changes are detected not only in Muscles but also in nerve fibers and their endings. These changes manifest as uneven silver impregnation, fragmentation, and focal thickenings. Vascular findings include endothelial multilayering and luminal narrowing.

In patients presenting with contractures, deformities, and significant motor impairment, extensive dystrophic changes are invariably found throughout numerous contracted muscle fibers.

Biochemical analyses reveal a reduced content of easily hydrolyzable adenosine triphosphate (ATP) phosphorus and total protein, alongside an elevated Collagen level. These parameters correlate with the extent of muscular dystrophy. The more pronounced the biochemical depletion of the muscles, the more severe the dystrophic changes and, consequently, the Clinical presentation. A reduction in the bioelectrical activity of muscles has also been observed.

Clinical Symptoms. Neurological symptoms vary depending on the localization of the central nervous system lesion. Manifestations include monoparesis of an upper or lower extremity, hemiparesis (affecting both an upper and a lower extremity on the same side), paraparesis (affecting both upper or both lower extremities), and tetraparesis (affecting all four extremities, Fig. 380). Additionally, cranial nerve involvement may occur (strabismus, impaired Vision and visual Reflexes, Hearing loss), along with bulbar symptoms (speech and swallowing disorders) and cognitive impairments (approximately 40% of affected children have intellectual disability, and about 13% suffer from profound mental retardation and are untreatable).

Lesions of the central nervous system and Neural Pathways lead to organic and functional musculoskeletal disorders, which can be clinically categorized as mild, moderate, or severe.

The disease manifests as hyperactive tendon reflexes, the appearance of pathological reflexes, elevated muscle tone and spasm, muscle atrophy and weakness, flexion-adduction contractures, and limb deformities, all of which impair standing, walking, and motor coordination.

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Fig. 380. Spastic tetraparesis.

Orthopedic symptoms, particularly in severe cerebral palsy, are so characteristic that Diagnosis is generally straightforward. In upper limb spastic monoparesis, the shoulder is adducted, the forearm is flexed at the elbow and pronated, and the wrist and fingers are maximally flexed into a fist, severely limiting limb function. In lower limb monoparesis, the thigh is flexed and adducted, while the lower leg and FOOT are flexed (equinus foot).

Limb growth retardation and knee flexion contracture lead to both anatomical and functional limb shortening, resulting in a spastic limp. Hemiparesis presents with Clinical Features similar to those of upper or lower monoparesis: an irregular gait, postural instability, restricted movement due to muscle spasm, pronounced muscle atrophy compared to the healthy side of the body, and pelvic tilt and Asymmetry. Intelligence is preserved in the majority of cases, though patients often suffer from dysarthria and, frequently (10-15%), seizures.

Spastic diplegia (paraparesis) of the lower extremities presents with a characteristic posture. Both thighs are flexed at the hips, adducted, and internally rotated, with the knees pressed against each other or Crossing Over. The lower LEGS AND FEET are flexed, resulting in equinovarus or equinovalgus deformities. The gait is spastic, jerky, with alternating knee-crossing. Patients may be able to walk using crutches.

Tetraparesis is characterized by the aforementioned upper and lower extremity postures. Severe muscle spasticity leads to persistent contractures and subluxations in the JOINTS OF THE upper and, particularly, lower extremities. Due to discordant deformities, patients are unable to walk and remain bedridden with the HEAD flexed or retracted. Tonic reflexes may persist for a very long time, sometimes throughout life. The vast majority of patients exhibit mental disorders, dysarthria, seizures, etc.

Based on the severity of clinical manifestations in cerebral palsy, Bogdanov and Mezhenina (1968) distinguish three degrees of the disorder: mild, moderate, and pronounced.

In mild cases, children are able to walk independently and care for themselves. Their intelligence is unimpaired, allowing them to perform normally in school and acquire occupational skills.

In moderate paresis, patients require crutches or assistance from others to move around, and self-care is severely restricted. They are unable to dress or undress independently and require constant assistance. These children may experience intellectual, speech, visual, auditory, and other impairments. They are unable to attend mainstream schools and have difficulty adapting to physical labor.

Children with severe spastic paresis are unable to move even with assistance and are completely dependent in daily self-care. Most of them present with severely impaired intellect, alongside Disorders of the psyche, speech, vision, hearing, and memory.

As noted above, while severe forms of spastic paralysis present no diagnostic challenges, diagnosing the condition during a child's first weeks and months of life can be quite difficult, as symptoms are often mild initially. Conversely, muscle hypotonia may sometimes be observed immediately after birth, which later transitions into spasticity, with definitive signs of cerebral palsy appearing only after the child reaches one year of age.

Early diagnosis is crucial to initiate timely Treatment and prevent contractures and orthopedic deformities.

Patient evaluation should focus on cranial nerve innervation, muscle strength and tone, the range of motion in limb joints and their coordination, as well as the presence of pathological reflexes and hyperactive deep tendon reflexes. Due to impaired balance between inhibitory and excitatory processes, any limb movement lacks the normal alternation of these phases, as children with cerebral palsy exhibit a reduced speed of motor reaction. They also show a diminished range of joint motion, reduced muscle strength and endurance, and impaired motor coordination.

Treatment. Management of children with cerebral palsy must begin at an early age to prevent The Development of contractures and functionally disadvantageous limb positions.

The scope and Methods of treatment are selected based on the child's age, the severity of central nervous system involvement, clinical manifestations, and the findings of supplementary diagnostic examinations.

To alleviate the patient's condition, measures are taken to improve the function of the spastic limb, while patients with severe para- or tetraparesis undergo a comprehensive regimen of conservative and Surgical treatment.

Administering required treatments can be challenging in children with intellectual disabilities of varying severity, whereas patients with idiocy (13% according to E.P. Mezhenina, 1958) do not receive treatment.

It should be noted that as therapeutic interventions improve children's functional capabilities, their cognitive development also advances, because the child becomes ambulatory (even with the aid of crutches), more active, and shows greater interest in everyday life.

Kinesiotherapy plays a vital role in the development of postural reflexes. It serves as a core component of comprehensive rehabilitation, capable of improving musculoskeletal function. Therapeutic Exercises should be performed consistently from the moment the diagnosis is established—both in clinical settings and at home by parents, who must be properly trained. The Nature of the exercises depends on the child's age. Ongoing training of patients in independent, goal-directed therapeutic physical culture enhances their motor activity and coordination.

To reduce hypereflexia and excessive reflex excitability, exercises involving changing body positions are utilized, such as supine exercises, rolling from side to side, and rising from a sitting position. To increase muscle strength, exercises with resistance and pulley weight systems are performed, carefully dosing the load for specific muscle groups and regulating the movement rhythm.

To decrease heightened reflex excitability, simple, light exercises are prescribed, with the volume increased gradually. This is particularly important for children with pronounced muscle spasticity who exhibit slowed motor responses and reduced muscle strength.

To improve motor coordination, exercises involving sticks and balls, stacking cubes, manipulating matches, and touching the Nose or ear are prescribed. Session durations are gradually increased to 30–40 minutes. Because physical exertion quickly induces fatigue in these children due to excessive effort and strain, relaxation exercises should be incorporated to support cortical inhibitory-excitatory balance and enhance reciprocal innervation.

The Use of plaster splints is essential, particularly overnight, to maintain the limbs in a corrected position.

Therapeutic exercises are most effectively performed following physical and balneological Procedures that facilitate their execution. Warm saline baths, paraffin-ozokerite Applications, pelotherapy (mud therapy), and diathermy are most commonly employed.

Because cerebral palsy is characterized by the dominance of hypertonic flexor and adductor muscles while their antagonists remain relaxed, It is important to balance their interaction through both physical exercises and light massage of the relaxed muscle groups. Orthopedic footwear is prescribed to ensure proper foot alignment.

A.V. Dyudin, I.I. Talko, and V.S. Shargorodsky (1987) utilized non-thermal millimeter-wave electromagnetic radiation in their practice. They reported that immediately following the Procedure, patients experienced Skin hyperemia, generalized muscle relaxation, and a reduction in spasticity, followed by improved motor coordination and physical activity.

Pharmacotherapy is an essential component of comprehensive patient care. To relieve muscle spasms and enhance regenerative processes within the central nervous system, medications such as diplacin, tropacin, dibazol, galantamine, or dynesine are prescribed. Tropacin is particularly effective because it reduces muscle spasms without producing side effects and can be administered per os to children.

Tropacin is taken one hour before meals, once or twice daily, depending on the severity of spasms.

The dosage is calculated per kilogram of body weight and, according to F.R. Bogdanov and E.P. Mezhenina, increases as the patient grows older.

For children aged 3 to 5 years, the dose ranges from 0.002 to 0.004 per kg of body weight; for ages 5–9, 0.004–0.007; for ages 10–12, 0.007–0.008; for ages 13–18, 0.008–0.01; and for adults, 0.01–0.016.

The course of treatment should last for at least one month. Proserine serves as the antidote for tropacin.

Galantamine exhibits anticholinesterase properties. By facilitating neural impulse transmission across nerve Cell synapses, throughout the neuron, and at neuromuscular junctions, galantamine Supports the function of previously dormant neural systems and enhances the patient's motor capabilities.

Galantamine (0.25% solution) is administered intramuscularly, up to 20 injections per treatment course.

Dynesine (diparcol) is a quite effective therapeutic agent: it is administered per os, starting with an initial dose of 0.15–0.5 g taken 3 to 5 times daily, gradually increasing to 1.0–1.5 g, calculated at 0.0001–0.0002 g per kg of body weight, three times a day, one hour before meals.

The treatment is administered in two-month courses with equal intervals between them. In the event of complications (drowsiness, dizziness, adynamia, rash, or joint pain), the drug should be discontinued.

In addition, there are A number of similarly acting medications manufactured by foreign companies.

Comprehensive conservative treatment, especially when initiated in a timely manner, yields encouraging results and, when combined with surgery (if indicated), significantly enhances the functional capabilities of patients.

Indications for surgery include: insufficiently effective conservative treatment accompanied by pronounced muscle spasms during movement and walking that exacerbate reflex contractures; the development of persistent contractures resulting from spasms and pathological Changes in the capsular-Ligamentous apparatus of the joints, which impair the patient's statics, walking, or upper extremity function.

Despite the considerable number of proposed surgical techniques, only a few remain useful from a practical standpoint. The choice of surgical method should be based on a clinical Assessment of the patient's general condition and age, the degree of intellectual impairment and muscle spasticity, as well as the nature of the contractures and orthopedic deformities.

Before surgery, parents should be informed about the multi-stage nature of the interventions, which may involve nerves, tendons, muscles, and occasionally bones. The sequence of the procedures is crucial. In some cases, contractures can be resolved through surgically straightforward interventions that are well tolerated by the patient. For example, in flexion-adduction contractures of the hip joint, tenomyotomy of the thigh adductors and resection of the Branches of the obturator nerve (n.obturatorius) are performed.

Surgical technique. The procedure is performed under general anesthesia. First, resection of the branches of the obturator nerve must be carried out, followed by tenomyotomy of the thigh adductors.

The surgical approach to the obturator nerve may be extrapelvic or, somewhat more complex, intrapelvic.

The extrapelvic approach is advantageous because tenomyotomy of the thigh adductors can be performed through the same incision after the nerve branches are divided. A linear incision of the skin, subcutaneous tissue, and fascia, approximately 10 cm in length, is made starting from the pubic bone and extending downwards along the PROJECTION OF THE adductor longus muscle of the thigh. After separating this muscle from the adductor brevis, the anterior branch of the obturator nerve is identified lying upon it. This nerve branch is transected, and a portion of the peripheral segment is excised. The adductor brevis is then retracted to locate and resect the posterior branch of the nerve. The procedure must be performed with caution to avoid damaging adjacent Blood Vessels, particularly the obturator artery (a.obturatoria). Subsequently, the leg is abducted to put tension on the adductor muscles, and the tendons of the adductor longus and adductor brevis (and, if necessary, the adductor magnus) are successively transected. The wound is closed, and a hip spica cast is applied, extending down the healthy leg with a spreader bar to maintain the legs in an abducted position.

The technique of obturator nerve resection via an extraperitoneal intrapelvic approach is technically more complex and traumatic, carrying a risk of injury to the blood vessels adjacent to the nerve; therefore, it is not described here and is not recommended for general practice among orthopedic surgeons.

One month after surgery, the plaster cast is removed, mobilization of the hip joint is initiated, and the patient is allowed to walk, using crutches if necessary.

If the patient exhibits bilateral hip adduction, the same procedure is performed on the opposite limb one and a half months after the initial surgery. Occasionally, if needed, the tendon of the sartorius muscle (m.sartorius) is transected near the anterior superior iliac spine (spina iliaca ant.sup.) to reduce hip flexion contracture. Postoperative management follows a similar protocol.

Following the orthopedic principle of sequential correction of lower limb joint contractures, once the aforementioned procedure is completed, the flexion contracture of the knee joint must be addressed and the foot corrected from pes aequinus.

Initially, flexion contractures of the knee and ankle joints are managed using serial casting. This approach helps determine the compliance of the triceps surae muscle and serves as preparation for surgery.

To reduce the spasticity of the m.gastrocnemius, a Stoffel procedure is performed, which involves neurectomy of a portion of its innervating branches.

Under anesthesia, tissues in the popliteal fossa are dissected to expose the muscle along with its two tendinous heads attached to the medial surfaces of both femoral condyles. The nerve branches entering the muscle bellies are located within the loose Connective Tissue, transected, and the wound is closed. A long-leg cast (gonitis cast) is applied with the knee fully extended. The surgery can be performed simultaneously on both legs by two surgical teams.

For moderate to severe spastic paralysis, following preliminary serial redression with casts, the Eggers procedure and achilloplasty are performed.

The Eggers procedure can be performed via a single S-shaped incision in the popliteal region or through two linear lateral incisions — one along the projection of the biceps femoris tendon and the other over the tendons of the semimembranosus, semitendinosus, and gracilis muscles (mm. semimembranosus, semitendinosus et gracilis). While isolating the biceps femoris tendon (m. biceps femoris) and detaching it from the apex of the fibular head, care must be taken to avoid injuring the common peroneal nerve (n. peroneus). This tendon is then transferred and fixed subperiosteally to the posterior aspect of the lateral femoral condyle. To ensure secure fixation, the tendon is additionally sutured to the adjacent fibrous tissues, and sometimes the suture is anchored to a U-shaped Kirschner wire staple driven into the bone.

Similarly, the tendons of the aforementioned three muscles are mobilized from the medial side and fixed to the posterior aspect of the medial femoral condyle. The wounds are closed, and a long-leg cast is applied with the knee in full extension.

Procedures for lowering the triceps surae muscle (m. triceps surae) by transecting its tendons at their attachment sites to the femoral condyles are no longer used, as this technique has proven less effective (Bogdanov F.R., Mezhenina E.P., 1968).

To correct foot flexion contracture (with varus or valgus deviation), serial casting with compression-distraction devices (Krasnov A.F., Savin A.M., 1983; Umkhanov Kh.A., 1989; Ustyantsev V.I., Kolomiets A.A., 1991) or classical tendon plastic surgery is performed.

Achilloplasty procedures.

While acknowledging the effectiveness of compression-distraction devices in correcting Foot deformities, their limitations must be noted. These include mechanical overstretching of the foot muscles and ligaments resulting in subsequent functional impairment, as well as incomplete correction of certain Components of the deformity (Danilov A.A., Kramchaninova E.G., Pylypchuk O.R. et al., 2001), which necessitates supplementary surgical interventions (Ukhmanov Kh.A., 1991).

Myotenotomy and muscle transposition make it possible to correct all components of foot deformity in children or to substitute for the function of lost muscles.

As a rule, lengthening of the Achilles tendon is most frequently required in cases of severe morphofunctional changes in the triceps surae muscle.

Surgical technique of achilloplasty. Under anesthesia, an arcuate incision is made laterally to the Achilles tendon in such a way that the scar is not traumatized by footwear. The tendon is incised in a Z-form in the frontal plane, and in the case of an equinovarus foot deformity, in the sagittal plane, so that the distal segment of the tendon remains attached to the lateral region of the calcaneal tuberosity.

Following the tenotomy, the foot is brought into the correct position. If this cannot be achieved in children aged 12–14 years due to retraction of the posterior capsuloligamentous apparatus, a posterior capsulotomy is performed by incising the capsule along the posterior surface of the ankle joint and near the malleoli. The foot is set into the desired position (hypercorrection), the ends of the tendon are sutured "side-to-side", and the wound is closed. During the tendon incision, it is advisable to preserve the paratenon (tendon sheath) to prevent the tendon from retracting into the dermis-subcutaneous scar.

In moderate retraction of the m. triceps under anesthesia, it is impossible to establish optimal limits for lengthening the Achilles tendon in its spasticity. Therefore, fractional tendon lengthening is currently used, which involves making 8–10 staggered incisions up to 0.5–0.8 cm long over a length of 5–6 cm, penetrating through the entire thickness of the tendon. Then the foot is extended by 60–70° and the tightened tendon bundles are transected. The foot, extended to 70–80°, is immobilized with a plaster boot for 4–5 weeks. Children are allowed to bear weight on the operated leg after the eighth or ninth day (Danilov A.A. et al., 2001).

In functional insufficiency of the peroneal muscles, varus deviation of the foot with adduction of its distal section is added to the equinus deformity. As a result of retraction of the plantar aponeurosis, the abductor hallucis muscle, the flexor hallucis brevis, and the long plantar ligament, aequino-excavato-varus develops.

In pronounced spastic Clubfoot (pes aequino-varus), in addition to achilloplasty, transposition of the tibialis anterior muscle tendon (m. tibialis ant.) to the anterolateral border of the foot (the II or III metatarsal bone) is performed.

The main cause of calcaneal and calcaneovalgus foot deformities is pronounced spasticity of the tibialis anterior muscle and the long extensors of the toes, and sometimes excessive lengthening of the Achilles tendon. Subsequently, due to the pathological Influence of the peroneal muscles and the long toe extensors, the foot pronates and abducts.

In calcaneal and calcaneovalgus foot, one of the pronators is relocated to the medial border of the foot with mandatory anterolateral and posterior capsulotomy.

Following the specified surgeries, short leg plaster casts (boots) are applied in the corrected position of the feet for a period of one month.

Afterward, restorative rehabilitation treatment is carried out, and patients are recommended to use orthopedic footwear. Foot supination (supinators) is required for valgus foot, and foot pronation (pronators) for varus foot.

In infantile spastic cerebral palsy, especially in athetosis in children older than 12–14 years who have developed deformations of the talus and calcaneus during growth, it is sometimes necessary to perform surgery on the Bones and joints of the foot to correct a severe deformity. Such operations include triple arthrodesis and corrective osteotomies (the surgical technique is described on page 450). These surgeries are combined with tendon-muscle plasty.

Upon completion of growth, patients undergo supra-metaphyseal femoral osteotomy for secondary contracture (incomplete knee extension) in the knee joint, which causes functional limb shortening and the onset of pathological changes in the spine.

In persistent flexion-adduction contracture of the hip, an intertrochanteric osteotomy or intertrochanteric transposition of the Femur according to F.R. Bogdanov is performed when the flexion angle is 120° or less, and adduction is 30°. This operation consists of an intertrochanteric osteotomy and relocation of the distal fragment to the posterolateral surface of the greater trochanter, where it is fixed with a metal construct.

Such surgeries normalize limb length, which simultaneously corrects the compensatory curvature of the spine.

More complex to treat are upper extremity deformities in cerebral palsy. As a rule, they manifest as classical shoulder adduction, forearm flexion and pronation, wrist flexion, and thumb adduction. Treatment effectiveness depends on the severity of muscle spasm and secondary changes in the upper extremity.

The difficulty of surgical interventions lies in the diffuseness of muscle involvement and the overlapping of their innervation. Despite this, such children must undergo both conservative treatment, as indicated earlier, and surgical treatment aimed at improving the functional capabilities of the hand, especially the hand itself, as well as eliminating cosmetic defects.

Obviously, if mobility of the hand and fingers is completely absent during a contracture, it recovers with difficulty or does not recover at all after surgery. In cases where even minor finger movements are preserved, they improve after treatment, and compensatory adaptations develop.

For this purpose, muscle-tendon transfer surgeries are most frequently used. F.R. Bogdanov and Ye.P. Mezhenina indicate that in all cases they achieved a positive result after transplanting one flexor tendon of the wrist to the wrist extensor, and the other to the finger extensor. Thus, the hand assumes a position of functionally advantageous extension, and extension in the metacarpophalangeal joints improves. However, the fingers remain flexed because their extension is carried out mainly by the interosseous and lumbrical muscles.

Improvement of hand Functions is also achieved by the Steindler-Grip operation, which consists of transferring the tendon of the flexor carpi ulnaris to the radial wrist extensor. This operation has an advantage over Bogdanov's previous procedure because it does not create significant ulnar deviation of the hand and even slightly reduces pronounced hand pronation.

Thumb adduction is eliminated by transecting the adductor pollicis muscle and blunt detachment of the interosseous muscle from the first metacarpal bone. The tendon of the abductor pollicis longus is transferred to the tendon of the extensor pollicis longus to enhance its function.

K. Biesalski and R. Meyer transplanted the tendon of the second digit to the tendon of the thumb extensor.

In the case of thumb subluxation, which may occur either before or after surgery, arthrodesis of the metacarpophalangeal joint is performed, Setting the thumb in a functionally advantageous position. The hand and thumb are immobilized with a plaster cast for 3–4 weeks.

Pronation contracture of the forearm is eliminated by A.N. Tivv's operation (1920). It consists of detaching the pronator teres and flexor carpi radialis from the radius throughout their entire attachment. Afterwards, the pronator teres is sutured to the flexor carpi radialis tendon, passed through the interosseous membrane to the dorsal surface of the forearm, and fixed in a drilled hole in the radius.

Thus, these muscles perform the function of forearm supinators. If necessary, the operation can be supplemented by detaching the insertion site of the pronator quadratus. Following surgery, a plaster cast is applied up to the upper third of the arm with the forearm in complete supination. After a month, the cast is removed and rehabilitation treatment is carried out.

If Tivv's forearm operation does not yield the desired result, derotational osteotomy of the radius and ulna can be applied, fixing them with metal constructs.

When fixing with rods, the forearm is additionally immobilized with a plaster cast in a functionally advantageous position until the fragments unite. The most stable fixation is achieved using plates, in which case a plaster cast may not be used. This facilitates the Implementation of rehabilitation treatment.

An important role in the comprehensive treatment of patients with infantile cerebral palsy is played by the Organization and provision of orthopedic appliances, orthoses, and footwear. In cases of severe lower limb impairment, following conservative treatment and lower limb surgeries, a significant number of children require prosthetic support. To prevent flexion contractures in the presence of pronounced muscle spasticity, locking orthoses for the Hip and knee joints are prescribed, whereas non-locking orthoses are used for moderate spasticity. Shenk non-locking braces ensure the correct positioning of the lower limbs while allowing flexion and extension in the joints. It is crucial to provide children with orthopedic footwear that corrects foot alignment and facilitates as well as improves gait.

When choosing a treatment method for children with cerebral palsy, their mental status and the degree of cognitive impairment must be taken into account in all cases.

An individualized approach to comprehensive treatment yields good outcomes in the majority of children. Even in severe cases of musculoskeletal disorders, children are able to move around, care for themselves, and even perform appropriate physical labor following treatment. If they have attended kindergarten and gone to school, their intellectual development and behavior do not differ significantly from those of their peers.

All children with spastic cerebral palsy must be registered for clinical follow-up, undergo prolonged treatment, and remain under the constant supervision of a neurologist and an orthopedist, with consultations from a speech therapist and psychotherapist as needed.