CHAPTER 41

Postural and Righting Reflexes

The postural and righting reflexes are a complex group of reactions that are relevant primarily in pediatric neurology. Posture is largely reflex in origin, with involuntary muscle contraction creating the necessary tone, especially in the antigravity muscles, to maintain the erect posture and normal position. The vestibular nuclei, especially the lateral, are particularly important for maintaining contraction in the antigravity muscles. Standing may be thought of as a postural reflex, and any interference with the mechanisms mediating postural reflexes may interfere with the act of normal standing. The postural and righting reflexes are difficult to study. Much of our knowledge comes from experimental neurology, but the clinical applicability is limited because of the differences in neurophysiology between the upright biped and the experimental quadruped.

Maintaining the orientation of the head to the body and of the head and body in space are basic functions. The complex reflex mechanisms of standing and righting involve the vestibular system, principally the utricle; proprioceptive impulses from muscles, tendons, and joints; exteroceptive impulses from the body surface; and visual stimuli. Righting reactions involve at least five separate types of reflexes: (a) labyrinthine righting reflexes acting on the neck muscles, (b) neck righting reflexes acting upon the body, (c) body righting reflexes acting upon the head, (d) body righting reflexes acting upon the body, and (e) visual righting reflexes acting upon the head and body. Vestibular input arises from otoliths of the utricles, and to a lesser extent the saccules; these organs respond to changes in head position that then influences body tone. The proprioceptive stimuli involved in neck righting reflexes originate in the muscles, tendons, and other deep structures of the neck and are mediated through the upper two or three cervical nerves and segments, and possibly through the spinal accessory nerve. They act principally on the head, but through the head act on the body as a whole. Afferents subserving body righting reflexes are analogous and arise from tissues in the trunk and extremities. The visual righting reflexes are mediated by the midbrain and the vestibular centers. When the eyes turn toward an object, the head and body follow. Although vision plays a role in posture, lack of vision does not impair postural or righting reflexes if the other mechanisms are intact. Conversely, loss of proprioception, as in posterior column disease, can be compensated for in part by visual input.

Abnormalities of the postural and righting reflexes are clinically relevant in pediatric patients; in certain adult patients, particularly those with extrapyramidal disorders, disturbances of gait and balance, and vestibular disorders; and in the aged. Loss of postural reflexes is an important feature of Parkinson’s disease, and similar impairment is likely related to the tendency of the elderly to fall.

Postural and Righting Reflexes in Infancy and Childhood

Myelination of the nervous system begins during the second trimester and continues for a long period of time, well after birth and perhaps into adolescence. The most rapid phase of myelination occurs during the first 6 months after birth. Different systems myelinate at different times, and the order of myelination is related to the appearance and disappearance of the postural and righting reflexes seen in pediatric patients. Demonstration of these reflexes helps to establish gestational age and assess the function of the immature nervous system.

Reflexes that are usually demonstrable in the normal neonate include the Moro, tonic neck reflex, rooting and sucking, grasp, placing, stepping, and trunk incurvation.

The Moro Reflex

This is the body startle reflex. A sudden stimulus, such as a loud noise or quick movement, directed toward the body causes abduction and extension of all four extremities, extension of the spine, and extension and fanning of the digits, followed by flexion and adduction of the extremities. The reflex is prominent during the first 3 months of life, and then the response gradually disappears, probably with the development of myelination. Children with motor deficits of cerebral origin may show the reflex in a fully developed form for years; the response may be unilateral if only one side is affected.

Landau Reflex

This is present in normal infants during the first 1 to 2 years of life. If an infant is held prone in the examiner’s hand with the body parallel with the floor, there is extension of the head and spine so that the body forms an arc with the convexity downward. With the body in this position, passive flexion of the head causes flexion of the vertebral column, arms, and legs, and the body forms an arc with the convexity upward. If the child is placed supine, there is flexion of the neck, spine, arms, and legs. This posture is probably a combination of otolith and tonic neck reflexes.

Tonic Neck Reflexes

Passively turning the head toward one shoulder causes increased extensor tonus on that side and increased flexor tonus on the opposite side (Figure 41.1). The arm on the side toward which the head is turned goes into extension while the opposite arm flexes. The posture has been likened to that of a fencing thrust. If the head and neck are flexed, the arms flex and the legs extend. If the head and neck are extended, the arms extend and the legs flex. Reflexes of this type are often found in an incomplete form in normal infants but disappear by the age of 4 to 6 months. In later life, they may be demonstrable in patients who have “high” decerebration, or decortication, because of disease involving the upper brainstem or thalamodiencephalic level. The patient lies with the arms semiflexed over the chest and the legs in extension, but turning, flexion, or extension of the head causes the responses just described. These reflexes may contribute to the associated movements found in spastic hemiplegia and cerebral diplegia.

FIGURE 41.1 In decerebrate rigidity, the arms are adducted and extended at the elbows, with the forearms pronated and the wrists and fingers flexed. The legs are extended at the knees and internally rotated with the feet plantar flexed. The posture may occur spontaneously or in response to external stimuli such as light, noise, or pain. (Reprinted with permission from Bickley LS, Szilagyi P. Bates’ Guide to Physical Examination and History Taking. 8th ed. Philadelphia: Lippincott Williams & Wilkins, 2003.)

The Neck Righting Response

This is a variation of the tonic neck reflex. With the infant supine, its head is turned toward one side. A positive response results in rotation of the shoulder, trunk, and pelvis toward that side, occasionally followed by a turn of the entire body. The response should be approximately equal on each side. The reflex appears at about the time the tonic neck reflexes disappear and can be obtained in nearly all infants by the age of 10 months; it disappears at about the time the child can arise directly without first turning on its abdomen.

The Parachute Response

The parachute response appears at the age of 8 to 9 months and persists. To elicit it, the infant is held prone in the air and then suddenly thrust headfirst toward the examining table or floor. When the response is present, the arms immediately extend and adduct slightly, and the fingers spread as if to attempt to break the fall. Asymmetry of the response indicates unilateral upper-extremity weakness or spasticity. Absence of the response is seen in severe motor disorders. The response does not depend upon vision and may occur in blindfolded children.

The Placing Reaction

With the infant held vertically, touching the dorsum of each foot to the side of the examining table causes placement of the foot on top of the table. The response usually disappears by the end of the first year of life.

Supporting and Stepping Reactions

Holding the infant vertically and allowing its feet to make firm contact with the top of the examining table produces contraction of the lower extremities as if to support the weight. This is usually followed by automatic stepping or walking movements. These responses are usually present at birth and gradually disappear.

Decerebrate and Decorticate Rigidity

Severe lesions of the brainstem often produce increased tone in the extensor, or antigravity, muscles of the limbs and the spine. This phenomenon is known as decerebrate rigidity. In patients with extreme decerebrate rigidity, there is opisthotonos, with all four limbs stiffly extended, the head back, and the jaws clenched. The arms are internally rotated at the shoulders, extended at the elbows, and hyperpronated, with the fingers extended at the metacarpophalangeal joints and flexed at the interphalangeal joints. The legs are extended at the hips and knees while the ankles and toes are plantar flexed (Figure 41.1). The position is an exaggeration or caricature of the normal standing position. The deep tendon reflexes are exaggerated, the tonic neck and labyrinthine reflexes are present, and the righting reflexes abolished.

Decerebrate rigidity may follow severe insults to the brainstem at any level between the superior colliculi or the decussation of the rubrospinal pathway and the rostral portion of the vestibular nuclei. The vestibular nuclei enhance extensor tone, and integrity of the vestibular nuclei is necessary for decerebrate rigidity to occur. These nuclei are intact, but isolated from the midbrain, specifically from the red nuclei and rubrospinal tracts. Activity in the reticular formation is also important, particularly the pontine reticular nuclei and the medial reticulospinal tract, which also facilitates extensor muscle tone. Experimentally, decerebrate rigidity is abolished by section of the vestibulospinal pathways. In patients, when the process extends to involve the medulla, the decerebration disappears. The most common cause of decerebrate rigidity in humans is trauma, and the presence of extensor posturing is a poor prognostic indicator. The incidence of decerebrate rigidity in severe TBI is as high as 40%, and the presence of extensor posturing increases the mortality dramatically. An MRI investigation showed a significant correlation between decerebrate rigidity and the presence of midbrain lesions.

Decorticate rigidity is characterized by flexion of the elbows and wrists with extension of the legs and feet (Figure 41.2). The causative lesion is higher than that causing decerebrate rigidity, preserving the function of the rubrospinal tracts, which enhance flexor tone in the upper extremities.

FIGURE 41.2 In decorticate rigidity, the elbows, wrists, and fingers are flexed with the legs extended and internally rotated. (Reprinted with permission from Bickley LS, Szilagyi P. Bates’ Guide to Physical Examination and History Taking. 8th ed. Philadelphia: Lippincott Williams & Wilkins, 2003.)

The functional significance of the rubrospinal and vestibulospinal tracts can be best appreciated by observing a patient progress from decorticate rigidity to decerebrate rigidity to the flaccidity of brain death. After rostrocaudal deterioration to a certain level, the patient lies with arms flexed and legs extended—decorticate rigidity. This is due to the fact that the rubrospinal pathways are still intact and are enhancing flexor tone to the upper extremities, producing a flexed arm posture with an extended leg posture. With further rostrocaudal deterioration, the rubrospinal tracts cease to function, but the vestibulospinal tracts remain intact, facilitating extensor tone to all four extremities and resulting in an extension posture of both arms and legs. This is decerebrate rigidity. With further rostrocaudal deterioration, the vestibulospinal tracts cease to function and the patient becomes flaccid in all four extremities, an agonal condition.

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