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Home > JPO > 1993 Vol. 5, Num. 2 > pp. 35-38

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Early Development and Attainment of Normal Mature Gait

Mary Keen, MD

ABSTRACT

This article describes the process of development of normal human locomotion, major neuromotor and musculoskeletal factors that may affect this process, and normal physiological variations.

Introduction

The human body is built for motion. Forty percent of adult body mass is muscle with proportionally more in the lower extremities. Muscles and bones are motors and levers designed to allow movement in many planes. Muscles are necessary not only for propulsion but also for deceleration and shock absorption.

The human body also is designed for efficiency in movement. Because of the unique design of the human body for bipedal locomotion, relaxed standing requires minimal energy, and human beings naturally assume a rate of speed of locomotion that is most efficient for them. Such efficiency requires integration of movement of many joints and muscles. Thus, a large percentage of the human brain is dedicated to gross and fine motor coordination and balance.

Normal gait is cyclic; that is, it involves movements in space that are repeated over and over. For descriptive and analytic purposes, gait has been divided into two phases: the stance phase and swing phase, and the phases have been further divided into specific points. These phases and points are uniformly present in normal gait (see Figure 1 ).

Human locomotion also has idiosyncratic characteristics with unique aspects apparent in every individual. We can identify family and friends by their gaits. However, an individual's gait also varies according to speed, mood, footwear and fatigue.

Human locomotion is also affected by changes in development such as physiological processes affecting neuromotor control, growing and maturing body segments, variable rotation of limbs and joints about an axis of motion, and changes in posture. The attainment of locomotor skills is a complicated process dependent upon an intact neuromotor and musculoskeletal system.

Neuromotor Development

Humans develop all the brain cells they will ever have by 20 weeks of intrauterine life. Interneurons appear and reproduce to interconnect brain cells until about age one. The process of myelination takes several years and is completed in a cephalad to caudal (head to tail) direction. There is much individual variation in the rate of development of neuromotor control.

Early neuromotor maturation is manifested by the suppression of primitive reflexes and the appearance of postural responses (see Figure 2 and Figure 3 ). Abnormalities in either the primitive reflexes or postural responses can reflect a disorder in the central or peripheral nervous system (1).

Primitive reflexes are naturally present in the newborn and infant younger than 6 months. They are never normally obligatory or persistent; rather, infants move in and out of these patterns until the patterns are gradually completely suppressed. Postural responses, on the other hand, gradually appear as the primitive reflexes disappear. Postural responses are under volitional control and are incorporated naturally into movement and locomotion. The evolution of primitive reflexes and postural responses, also occurs proximal to distal (1).

The processes of suppression of the primitive reflexes and integration of postural responses vary greatly. However, persistence of multiple primitive reflexes, failure to develop normal postural responses or asymmetry in the manifestation of either the infantile reflexes or postural responses are signs of abnormal neuromotor development and may indicate neuromotor dysfunction. Causes of persistent infantile reflexes and delayed or absent postural responses are listed in Figure 4 and Figure 5 .

Although deviations from normal may be signs of neuropathology, many children "outgrow" distinctly abnormal neurologic examinations. In the Collaborative Perinatal Project of the National Institute of Neurological and Communicative Disorders and Stroke, more than 37,000 children were examined prospectively and serially by experienced examiners. Fifty-one percent of children with "definite" cerebral palsy and 96 percent of children suspected of having cerebral palsy had normal neuromotor exams at age 7. Therefore, abnormal neuromotor examinations in early childhood may normalize. However, these children are at higher risk for mental retardation.

Effect of Neuromotor Dysfunction on Motor Milestones

Persistence of primitive reflexes will interfere with volitional changes in posture and tone necessary for locomotion. The association of persistent infantile reflexes and delayed ambulation in infants and children with cerebral palsy has been well documented. Postural responses, on the other hand, are critical for maintaining balance in the upright position first in sitting, then in standing and achieving locomotion skills of walking and running.

If primitive reflexes are not suppressed and postural responses do not appear in the normal time range, a child is likely to experience delays in achieving motor milestones (2). Figure 6 lists some basic gross motor milestones and the usual age at which they are attained (1).

A large range of normal variation exists, and a delay in gross motor milestones does not necessarily indicate neuropathology. An examination of 404 late walkers (not taking six steps independently at 18 months) found pathology in only 32 percent (3). Among infants who were small for gestational age or who required admission to the special-care nursery, abnormalities were found in 56 percent. Of these, approximately one-third had cerebral palsy, one-third global delay, and onethird had other neurological or congenital disorders (4).

Musculoskeletal Development

Musculoskeletal development occurs concurrent with neuromotor development (1). During intrauterine growth and development the spinal column assumes a 'c" shape and the limbs a flexed and internally rotated posture. In the first weeks of extrauterine life, this predominant flexor tone relaxes, and an infant assumes a more neutral F posture. The cervical "c" curve flattens for sitting at 6 to 7 months and reverses to a lordosis for standing by 9 to 12 months.

As a result of intrauterine crowding, infants are born with mild joint contractures and curves in long bones that resolve spontaneously after birth. Joints also rotate with growth and development. The rate and extent of these physiological musculoskeletal changes vary considerably in normal children, and during the process of growth and maturation these physiological variations may cause parental concern.

Common Developmental Orthopedic Concerns

Pes planus or flat feet is usually a normal variant. Most children have apparent flat feet until ages 3 to 5 when baby fat diminishes and ligaments tighten. Hypermobile flat feet may require orthopedic shoes or orthoses to prevent overstretching of ligaments (5).

Toe walking. Some children learn to walk with a toe-walking pattern instead of the normal foot flat during stance. Approximately 30 percent have a family history of toe walking, and the condition is more common in boys than girls. Toe walking can be caused by such neurological conditions as cerebral palsy; idiopathic toe walking usually resolves sometime during childhood. Stretching exercises are indicated when shortening of the gastrocsoleus muscle groups occurs. Serial casts and dynamic splints are sometimes used, and surgery is rarely necessary.

Intoeing. Major causes of intoeing include femoral anteversion, internal tibial torsion and problems of the foot, including metatarsus adductus, clubfoot and dynamic intoeing.

Femoral anteversion is a normal anatomic condition. Excessive anteversion is generally due to ligamentous laxity and usually resolves by age 5.

Internal tibial torsion is also a normal anatomic variant that generally corrects spontaneously with growth. Night splints may accelerate correction. Surgery is rarely required.

Metatarsus adductus is the most common congenital foot deformity. Five to 10 percent of cases are associated with dysplasia of the hip. If the foot is not passively correctable (by stretching), serial splinting or casting is necessary. Surgical release is required when rigid metatarsus adductus persists after two years.

Outtoeing, like intoeing, has several causes: external rotation contracture of the hip, which usually resolves spontaneously; femoral retroversion in which the patella faces outward (very rare); and external tibial torsion, which is usually a compensatory mechanism for excessive femoral anteversion.

Bowlegs or genu varus is a physiological condition and corrects spontaneously by age 2. If the bowing is greater than 15 degrees, splinting with a Denis Browne bar may be indicated. Blount's disease or progressive bowing, or bowing beyond age 2, requires splinting and/or surgery to prevent damage to growth plates.

Knock knees or genu valgus is classified as apparent, physiologic or pathologic. Most cases are physiologic and resolve before age 7. Pathologic genu valgus caused by juvenile rheumatoid arthritis or paralysis may require surgery.

Maturation of Gait

It takes several years for a mature gait pattern to evolve. Characteristics of a mature gait pattern include a narrow base of support, smooth movements with minimal oscillations of the center of gravity and reciprocal arm swing.

Most practitioners agree a mature gait is present in normal children by age 5. However, after analyzing 186 normal children, Sutherland concluded a mature gait pattern is well established in most children by age 3 (6). The criteria he used included duration of single-limb stance, walking velocity, cadence, step length and ratio of pelvic span to ankle spread.

Children at age 1 have much higher step frequency (180 steps/minute) than adults. They do not have reciprocal arm swing; arms are held in "high guard." The hip joint remains externally rotated throughout the gait cycle, and the knee remains flexed. The ankle is in plantarflexion at heelstrike, and dorsiflexion during swing phase is diminished. Hip flexion, pelvic tilt and hip abduction are all increased during swing phase. Single-limb stance is reduced, and the base of support is wide.

At 18 months, nearly all children walk with heelstrike and more than 70 percent have reciprocal arm swing. The base of support narrows significantly but remains wider than a mature gait pattern.

Two-year-old children have less pelvic tilt, abduction and external rotation of the hip. Nearly 80 percent have reciprocal arm swing, and knee flexion during stance is more pronounced than in older walkers. Duration of single-limb stance is less than 34 percent, and the base of support remains wide although it has narrowed somewhat.

In 3-year-old children, duration of single-limb stance is about 35 percent. Ninety percent have reciprocal arm swing. The base of support is proportionately similar to adults. Differences from a mature adult gait include a greater knee flexion wave during stance and slightly increased pelvic rotation, hip joint rotation and hip abduction. However, children have achieved an adult pattern of joint angles throughout the gait cycle by this stage.

The gait of a 7-year-old child has the same differences from an adult's gait as a 3-year-old's does-but to a lesser degree. Adult cadence, step length and velocity cannot be achieved until adequate growth occurs. Duration of single-limb stance in a 7-year-old is about 38 percent. (In adults, duration is about 39 percent).

Summary

Human locomotion is a complicated process. The attainment of normal gait in humans is also a complicated process, involving not only physical maturation, but learning. It is not simply the result of inborn reflexes, although re flexes contribute to balance and efficiency. It requires an intact musculoskeletal system as well as an intact neuromotor system.


Mary Keen, MD, is board certified in physical medicine and rehabilitation, orthopedics and pediatrics. She is clinical assistant professor of pediatrics and orthopedics at Loyola University Medical Center, 2160 S. First Ave., Maywood, IL 60153.

References:

  1. Molnar GE. Pediatric rehabilitation, Second edition. Williams & Wilkins, 1992.
  2. Molnar GE. Motor deficit of retarded infants and young children. Arch Phys Med Rehabil September 1974;55:393-8.
  3. Chaplais J DE Z, MacFarlane JA. A re view of 404 late walkers,' Archives of Disease in Childhood. 1984;59:512-6.
  4. Johnson A, Goddard 0, Ashurt H et. al. Is late walking a marker of morbidity? Archives of Disease in Childhood 1990; 65 :486-8.
  5. Renshaw TS. Pediatric orthopedics. W.B. Saunders Co., 1986.
  6. Sutherland DH, Olshen R, Biden EN, Wyatt MP. The development of mature walking. MacKelth Press. Oxford/Philadelphia. 1988.
  7. Sutherland DH, Glshen R, Cooper Woo SLY. The development of mature gait. JBJS 1980;62-A:3:336-53.
  8. Inman VT, Ralston HJ, Todd F. Human walking. Williams & Wilkins, Baltimore London.
  9. Nelson KB, Ellenberg JH. Children who outgrew' cerebral palsy. Pediatrics 198 59:5:529-36.
  10. Molnar GE. Cerebral palsy. Prognosis and how to judge it. Pediatric Annals 1979;8: 10.


 

Home > JPO > 1993 Vol. 5, Num. 2 > pp. 35-38

 

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