Orthopedics - Oleksa A.P. 2006

Pathophysiology of Joints
Developmental Defects and Congenital Skeletal Anomalies
Torticollis

Torticollis (torticollis seu cervix obstipa) is a neck deformity characterized by an abnormal HEAD position, with the head tilted to one side and rotated in the opposite direction.

Torticollis is classified as congenital or acquired. Congregenital torticollis can be either muscular or osseous.

Congenital muscular torticollis is typically caused by unilateral shortening of the sternocleidomastoid Muscle, and less frequently by pathological Changes in the trapezius muscle or the platysma. In terms of frequency, muscular torticollis ranks third among congenital orthopedic deformities, accounting for 0.5–3% of newborns. Such discrepancies in the reported incidence rates in literature are attributed to differences in data collection and analysis methodologies. For instance, Protasevych (1934) notes that torticollis accounts for 0.5% of all orthopedic conditions, whereas maternity hospital and inpatient data from Riga place the figure within the 2–3% range (Biezins, 1968).

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Fig. 75. Lateral radiograph of the Tibia in a 68-year-old patient with Paget's Disease (showing an affected tibia and a normal Fibula).

Congenital muscular torticollis occurs with equal frequency in boys and girls, and can be either left-sided or right-sided (Fig. 76). This also applies to osseous forms of congenital torticollis, which are caused by Developmental anomalies of the cervical vertebrae and their articular processes, the presence of Cervical Ribs, and similar malformations. The osseous form of torticollis is extremely rare.

Several hypothetical theories have been proposed regarding the Etiology of congenital muscular torticollis.

The hereditary nature of torticollis was suggested as early as the late 19th century by Stromeyer, Dieffenbach, and others. Konrad (1927) reported heredity in 3% of cases, while Isigkeit (1931) observed it in 11%. Another widely supported theory attributes the condition to a developmental defect of the sternocleidomastoid muscle, suggesting that torticollis develops when this muscle is underdeveloped and its muscle fibers are replaced by Connective Tissue.

In newborns with torticollis, Kastendieck observed a thinned sternocleidomastoid muscle lacking cross-striations, exhibiting waxy degeneration and a high concentration of fibroblasts. Histological examination reveals connective tissue at various stages of maturation interspersed between atrophied and degenerated muscle fibers.

Fig. 76. Congenital right-sided muscular torticollis: a - rear view, b - front view.

Another widely accepted theory is that of forced abnormal fetal positioning in utero, originally proposed by Petersen in 1884. During fetal development, an abnormally flexed head brings the attachment points of the sternocleidomastoid muscle closer together, shortening the muscle and resulting in torticollis. According to Sippel, this occurs in breech and transverse fetal presentations.

Furthermore, A number of authors (Sippel, 1920; Kastendieck, 1925; Osten-Sacken, 1931, and others) emphasize The Role of increased intrauterine pressure on the fetus in The Development of torticollis. In a forced fetal position, the shoulder exerts pressure on the neck and the sternocleidomastoid muscle, thereby arresting its growth. Pressure caused by umbilical cord entanglement is believed to play a similar role (Sholomyantsev-Tersky, 1952; Studzinsky, 1950).

Volcker, Nove-Josserand, and Viannay attribute the condition to ischemia and muscle scarring resulting from intrauterine pressure, although Sherov and Zatsepin reject this interpretation.

We concur with orthopedic specialists who believe that one of the primary causes of muscular torticollis is Hemorrhage into the sternocleidomastoid muscle or its rupture during birth assistance. By the seventh to tenth day, this hemorrhage can be palpated within the muscle as a spindle-shaped infiltrate located inside its fascial sheath. Over time, and with the help of massage and physical therapy, this dense infiltrate gradually resolves and is replaced by connective tissue. This, in turn, leads to scar contraction, delayed growth, and shortening of the muscle. This theory was proposed long ago by Stromeyer (1833) and subsequently supported by Dieffenbach, Starkov, and other orthopedic surgeons (Exner G., 1958; Max Grob, 1957, and others).

The severity of torticollis varies depending on the extent of the pathological changes within the muscle.

In summary, we conclude that muscular torticollis can be triggered by a variety of detrimental factors that are genetically inherited, affect the fetus during intrauterine development, or occur during delivery. Developmental Anomalies of the cervical spine, inflammatory processes, and similar factors play an extremely minor role in the Pathogenesis of congenital muscular torticollis.

The clinical manifestations of torticollis vary depending on the child's age, but they are generally pronounced and rarely present diagnostic challenges. If any doubt arises, the child should be re-examined in two to three weeks. The older the child, the more distinct the signs of torticollis become.

The primary symptom is tilting of the head toward the shortened muscle and Rotation of the face in the opposite direction. Palpation may occasionally reveal a spindle-shaped induration and thickening of the sternocleidomastoid muscle. When the face is turned toward the affected side, the muscle becomes tight and tense, clearly demonstrating its shortening, and head mobility is restricted. The trapezius muscle is also tense. If left untreated, the deformity progresses as the child grows, leading (in accordance with Wolff's law) to secondary changes: facial and cranial Asymmetry, and curvature of the cervical spine caused by uneven vertebral growth (stunted growth of the compressed vertebrae on the side of the torticollis), which ultimately results in the osseous form of the condition.

Treatment. Early detection of muscular torticollis relies on routine neonatal screenings performed in the maternity hospital by a neonatologist, and at home by a visiting nurse, district pediatrician, or family physician. The infant should be examined carefully and thoroughly using head rotation and comparative palpation of the sternocleidomastoid Muscles. Rotating a newborn's head allows one to feel the tension in this muscle and observe restricted head rotation away from the side of the torticollis. Palpation can reveal a spindle-shaped thickening of the muscle and a dense infiltrate. If torticollis is suspected, the infant should be referred to an orthopedist for dispensary registration and treatment planning.

Treatment should be initiated as early as possible. The mother should place the newborn on its side with the head maintained in a correcting position. During the first weeks and months of life, comprehensive conservative therapy is administered, including:

1) corrective manual redressement of head tilt and rotation to stretch the shortened sternocleidomastoid muscle;

2) massage of the pathologically altered muscle;

3) immobilization of the head in a corrected position using a Schanz collar (Fig. 77) or its modifications (such as Biezins' semi-collar);

4) thermal Procedures (heating pads), UHF therapy, potassium iodide Electrophoresis, and similar treatments.

The administration of ronidase and lidase is ineffective.

Corrective maneuvers should be performed gently and without force, turning the child's head toward the side of the torticollis and tilting it backward. To perform these movements, one hand Supports the child's shoulder and upper chest, while the other slowly turns the head, repeating the motion every 5–10 seconds. Massage of the shortened muscle area is performed both before and after manipulation, or sometimes combined simultaneously with turning the head with one hand and massaging with the other. The duration of these manipulations should be at least 10 minutes.

It is important to explain The Nature of the pathology to the parents and teach them how to perform these corrective maneuvers and massage. They should be warned that if they are unable to perform the manipulations independently, a physical therapy specialist must be consulted.

Fig. 77. Shanz corrective collar for torticollis.

It is advisable to massage all the Muscles of the neck and extremities. Physiotherapy procedures or UHF therapy are prescribed either before or after manual manipulations. It is essential to achieve correction (or even overcorrection) and secure it. In the past, various bandaging techniques, ribbon-secured caps tied to undergarments, and traction devices with pads and straps were used for this purpose. Because manual manipulations must be performed systematically every day, the achieved correction is now most commonly immobilized using a segmented plaster Shanz collar, which is replaced with a new one as correction progresses.

It should be noted that early conservative treatment is the most effective, as the Tissues are pliable and easily amenable to correction. With timely initiated treatment, success is achieved in nearly 80% of patients. However, children must remain under dispensary observation and be re-evaluated every six months. We have observed cases where children recovered, only to experience a recurrence of torticollis several years later.

In all cases where conservative treatment is ineffective or when torticollis recurs, surgical intervention is necessary. If Conservative Methods fail to completely eliminate the deformity, surgery is performed after 1–1.5 years of life, before secondary structural changes develop.

We disagree with certain foreign orthopedists (Altenberg, 1944; Lange, 1951; Spitzy, 1930, and others) who considered it appropriate to operate on infants during the first year of life without spending time on conservative treatment.

Surgical Technique. The child is placed on the operating table with a roll placed under the scapulae, and the head turned to the side. The operation is performed under general anesthesia. Through a supraclavicular Skin incision, division of the platysma myoides, and fascia, the clavicular and sternal heads of the distal tendon of the sternocleidomastoid muscle are exposed. A Kocher probe is sequentially passed beneath each head and they are transected.

Surgery must be performed with great care to avoid injuring the Internal jugular vein, especially when dissecting the fascial Sheath of the muscle to facilitate head repositioning. In all cases, both heads of the tendon must be transected, not just one.

In female patients, to avoid scarring over the clavicle, M. Lange (1951) and others transect the proximal tendon near the mastoid process. Caution is equally required here due to the proximity of the External Jugular Vein, the Accessory nerve (n. accessorius), and the Facial Nerve (n. facialis). Therefore, the muscle should be carefully separated and the tendon transected 1 cm below the apex of the mastoid process.

During the surgery, THE POSITION OF the head is corrected, hemostasis is achieved, and the wound is closed.

Following tenotomy, the corrected head position is immobilized using a plaster thoraco-cranial cast (Fig. 78). This cast is applied while the child is in a sitting position, and it can be difficult to properly maintain the degree of achieved correction as the child emerges from anesthesia. Therefore, Glisson loop traction is applied for 2–3 days postoperatively, followed by the plaster cast. If readjustment is required, the cast is cut around the neck (creating a wedge if necessary), the head tilt is increased, and the cut area is secured with a plaster bandage. If necessary, this correction can be repeated after three to four days.

Similar manipulations can be performed using a Matzen cast; however, in our opinion, this cast is less stable and less convenient when the child is lying down.

While immobilized in the plaster cast, the hematoma at the site of tendon transection undergoes scarring, and the scar tissue consolidates.

The plaster cast is removed after 4–5 weeks, and rehabilitation therapy is initiated. This includes neck muscle massage, corrective physical therapy, thermal procedures, and a corrective collar. Occasionally, corrective spinal traction using a Glisson loop is employed. It is important to teach the child how to maintain proper head posture.

Postoperative conservative treatment is conducted for 2–2.5 months.

Recurrences of torticollis occur only in patients where both tendon heads and scar adhesions were not fully transected, or where adequate hemostasis was not performed.

When discussing the Surgical treatment of torticollis, mention should be made of the plastic lengthening of the sternocleidomastoid muscle once developed by I. Foderl (1903). The Procedure involved separating both heads of the muscle, then detaching the clavicular head near the clavicle and the sternal head near the muscle body. After positioning the head in overcorrection, the ends of the distal tendon heads were sutured together.

Fig. 78. Head immobilization following sternocleidomastoid tenotomy: a — using a Matzen cast, b — using a thoraco-cranial plaster cast after head position correction.

This operation is no longer performed today, much like the procedure proposed by Mikulicz, which involved the resection of a portion of the pathologically altered muscle.

As previously mentioned, if a child is left untreated or if orthopedic recommendations are not followed, bone torticollis, facial asymmetry, and cranial "Scoliosis" develop, which are irreversible and persist for life.