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The Modulation of Sensory Input and Motor Output in Autistic Children I
E d w a r d M. O r n i t z 2
The Center for the Health Sciences, University of California, Los Angeles This paper explores the possible pathophysiologic mechanisms which might underlie the unusual motility disturbances which occur in autistic children. These motor behaviors are in some way related to the faulty modulation o f sensory input which is also a significant feature o f the autistic syndrome. Psychologic experiments have revealed that autistic children learn through manipulation and position cues rather than through normal perceptual processes. It is therefore suggested that their spontaneous abnormal motility may be the autistic children's way o f making sense out o f both exogenous and endogenous sensations through kinesthetic (sensorimotor) feedback. Experimental demonstrations o f a deficient oculomotor response to vestibular and visual stimulation parallel clinical observations o f the hypomotility also seen in response to sensory stimulation. Review o f the neurophysiology o f the vestibular system reveals that the vestibular nuclei modulate motor output at the time o f sensory input and sensory input at the time o f motor output. It is suggested that a dysfunction o f the central connections o f the vestibular system with the cerebellum and the brain stem may be responsible for the strange sensonmotor behavior observed in autistic children and may also have implications for understanding the manner in which autistic children learn, since clinical studies point toward a strong motor component to their perceptual processes.
Disordered perceptual processes in autistic children have been n o t e d by many clinicians who have studied this developmental syndrome. The disturbances o f perception in autistic children involve a distortion o f the normal hierarchy o f receptor preferences (Goldfarb, 1956), an impaired ability to use sensory input 1Preprinted by permission from Child Development, Deviations, and Treatment: Proceedings of the First International Kanner Colloquium, October 31-November 2, 1973, University o f North Carolina, Chapel Hill, North Carolina. New York: Plenum Publishing
Corporation, in press.
2 Requests for reprints should be sent to Dr. Edward M. Ornitz, Neuropsychiatric Institute, The Center for the Health Sciences, University of California at Los Angeles, Los Angeles, California 90024. 197
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Anthony. 1961. Stroh & Buick. SYMPTOMS OF INADEQUATE MODULATION OF SENSORY INPUT The inability to adequately modulate sensory input constitutes a striking aspect of autistic symptomatology (Ornitz & Ritvo. They also limit their attention to only one of two stimulus dimensions in a visual discrimination (Hermelin & O'Connor. 1970. the children may ignore new persons or features in their environment and they may walk into objects as if . Frith & Hermelin. 1968a. Goldfarb. auditory. This apparent dominance of visual over auditory stimuli may actually be due to an inability to respond to two or more stimulus modalities in a complex stimulus presentation. e. Visual stimulation itself seems less meaningful to autistic than to nonautistic children in that autistic children show fewer eye movements in response to and spend less time regarding visual displays than do nonautistic children (Hermelin & O'Connor. 1968a. Schopler. Sweeny.198 Ornitz to make discriminations in the absence of feedback from motor responses (Hermelin & O'Connor. Goldfarb. 1958). Autistic children do not show the same preference in the use of the various sensory modalities as do normal children or nonautistic mentally retarded children. Ornitz. and taste) rather than distal receptors (audition and vision. and tactile components (Lovaas. They seem to be dependent on feedback from their own motor responses toward sensory stimuli in order to make sense out of perceptions (Hermelin & O'Connor. 1971). 1969). Both autistic and nonautistic children tend to respond to light in preference to sound. 1970. 1965). 1964). and a faulty modulation of sensory input (Ornitz & Ritvo. While autistic children may have normal or even advanced form perception (Ritvo & Provence. 1956. 1971. whereas this is not possible with autistic children (O'Connor. Sudden sounds which would elicit an impressive startle reaction in normal children may elicit no response whatsoever in some autistic children (Anthony. 1963). Hyporeactivity to auditory stimuli is apparent in the disregard of both verbal commands and loud sounds. but nonautistic children can readily be conditioned to respond preferentially to a sound source. 1949. Sclareibman. Bergman & Escalona. & Rehm. All sensory modalities are affected and the faulty modulation of sensory input may be manifest as either a lack of responsiveness or an exaggerated reaction to sensory stimuli (Goldfarb. 1971). Goldfarb.g. 1970). 1953). 1963). They have been described as preferring to use proximal receptors (touch. Ornitz. 1969. We will return to this theme after reviewing the symptoms of inadequate modulation of both sensory input and motor output. & Lowe.. Visually. Bender. 1966). Autistic children are overselective in responding to only one component of a stimulus complex consisting of. 1971. Both types of abnormal reactivity to sensory stimuli can occur in the same child (Goldfarb. smell. 1970). Bergman & Escalona. 1961. they make poor use of visual discrimination in learning (O'Connor. 1949). 1963. Koegel. 1958. Ottinger. 1947. 1971). 1971. visual. 1965. O'Connor. Lovaas & Schreibman. 1961.
or flick at their ears or grind their teeth. The children may show both heightened sensitivity to sensory stimuli and heightened awareness of sensory stimuli (Goldfarb. Contrasting starkly to the hyporeactivity to sensory stimuli are markedly exaggerated reactions to the same stimuli. all of which activities induce intense auditory input. 1963. The children may become agitated by the sound of sirens. or injections. 1947. antigravity play.Modulation of Sensory Input and Motor Output 199 they did not see them. They may be distracted by background stimuli of marginal intensity. repetitively rock and sway back and forth. The unusual sensitivity to sensory stimuli is manifest in many ways. Many of the behaviors of autistic children also suggest that they are actively seeking out vestibular and proprioceptive stimulation (Bender. They are often such a predominant part of the syndrome as to merit attention in their own right. or even riding in an elevator. SYMPTOMS OF INADEQUATE MODULATION OF MOTOR OUTPUT The motor behaviors of autistic children do not necessarily provide sensory input. Visually they regard their own writhing hand and finger movements or their more vigorous hand-flapping. the children may not notice painful bumps. There are also brief episodes of intense staring. or the trunk . The repetitive handflapping also provides proprioceptive input. bang. objects placed in the hand may be allowed to fall away as if they had no tactile representation. The children may rub surfaces of furniture or fabric in response to free textural differences. A similar response to tactile stimuli may occur during the first two years of life. The children may show a marked aversion to the vestibular stimulation induced by roughhouse. The deviant motility may involve the hands. or barking dogs and they may cup their hands over their ears in an attempt to shut out both these intense sounds and also mild novel sounds such as the crinkle of paper (Goldfarb. 1949). vacuum cleaners. bruises. To a great extent the strange and bizarre appearance of autistic children is due to their peculiar mannerisms and motility patterns. Bergman & Escalona. Sudden changes in illumination or confrontation with an unexpected object may elicit the same fearful reactions to visual stimuli. 1956). They may rub. cuts. the children are often disturbed by wool blankets or clothing and seem to prefer smooth surfaces. During the first year of life the introduction of the rough-textured table foods may evoke distress. In the tactile modality there may be severe intolerance for certain fabrics. or roll their heads from side to side. The heightened awareness of sensation is often associated with a tendency to seek it out and induce it. Some of the motor behaviors of autistic children seem to provide intense sensory stimulation. and they scrutinize the fine detail of surfaces. They whirl themselves around and around. 1963). the lower extremities. Painful stimuli are often ignored. The children tend to induce sounds by scratching surfaces and putting their ears down close to the surface.
1970). the various behaviors just described may be interrupted by sudden brief episodes of immobility. & Ritvo. 1958). often associated with bizarre posturing of the trunk or extremities. autistic children are not necessarily hyperactive.. stereotyped wiggling of the fingers or the entire hand. Very young autistic children tend to arch the back and hyperextend the neck. Sorosky et al. However. terminated by sudden stops. A history of severe infantile head-banging is often associated with the later development of self-mutilation (Green. maintaining this uncomfortable position for brief periods of time. Some or all of these motility patterns can at times be elicited by rapidly spinning a child's top in front of the patient. Disturbances involving the trunk or entire body include staccato lunging and darting movements. Ornitz. 1965). The deviant motility may appear intermittently or infrequently in some autistic children and may occur continuously in others (Sorosky. Ritvo. Similar flapping movements of the lower extremities may occur. 1968a. & Dietrich. 1971. This type of activity often merges into a repetitive. Sorosky. The children also engage in an unusual amount of body-rocking and swaying. . Ritvo. it is often the only mode of walking and may persist on occasion into adolescence.200 Ornitz and entire body. 1968. but the most striking involvement of the lower extremities is toe-walking (Colbert & Koegler. 1971. 1968. These children are not constantly in motion nor is there necessarily a restless. Some of the most characteristic and striking motor behaviors involve the hands (Ornitz & Ritvo. This may occur transiently during states of excitement or while the child is running in circles. While the mannerisms are often complex and ritualistic and clearly do not have the appearance of either involuntary movements or seizure discharge patterns they are stereotyped. The severity of this aspect of the syndrome varies markedly from one autistic child to another. Ornitz. and do not seem to be entirely voluntary. & LaFranchi. Brown. 1967). Hutt. & Ounsted. In fact. Hurt. The autistic child may hold his hands in front of his eyes and writhe or twist the fingers and palms. often accompanied by headrolling or head-banging. Aug & Ables. In spite of all this gross motor activity. irritable quality to their activity. 1968. EXPLANATORY HYPOTHESES Several different hypotheses have been put forth to explain the relationship between the disturbance of perception and the disturbance of motility observed in autistic children. Brown. This handflapping involves a rapid and untiring alternating flexion and extension of the fingers or hands or an alternating pronation and supination of the forearm. The children also whiff themselves around the longitudinal body axis. strikingly similar in general pattern and form in most autistic children. Ornitz.Ornitz. Lee.
comparison of the clinical syndrome of childhood autism with that resulting from maternal deprivation has shown that the two conditions are diagnostically distinct and that childhood autism does not result from earlier sensory deprivation (Omitz. Although the motor behaviors appear to provide sensory input..Modulation of Sensory Input and Motor Output 201 Physiologic Overarousal A plausible explanation of the apparent tendency toward a specific and peculiar type of motor discharge which seems to provide and at times to be triggered by sensory input is that autistic children are in a chronic state of physiologic overarousal. a quantitative study of the amount of hand-flapping showed that it was not reduced when autistic children attended to a spinning object. demonstrated that the motor output persisted through long periods of reduced sensory input (Sorosky et al. electroencephalographic studies have not consistently supported the notion that autistic children are in a chronic state of hyperarousal. 1969. 1973).. 1965) were not confirmed in two other studies (Creak & Pampiglione. 1971. Furthermore. suggesting that they are in a more aroused state and therefore more ready to respond to increased stimulation.. 1970. 1957) infants and results in severe sensory deprivation during rite critical early months of life.. However. Hermelin & O'Connor. Ornitz. Hutt et al.. (1965) found that autistic children show more frequent gesturing in more complex environments. Hermelin & O'Connor. However. 1971. perhaps due to a neurophysiologic dysfunction which results in a tendency to gate out too much sensory input. 1973). hand-flapping. This fmding suggested that the . e. Hutt et al. 1968) when stimulus conditions were controlled.g. Two reports of unusuaUy low voltage EEGs suggestive ofhyperarousal (Kolvin et al. 1949. Maternal deprivation is a condition which may occur in institutionally reared (Provence & Lipton. investigations that focused on those motor behaviors that are very specific to the autistic syndrome. it seems natural to assume that autistic children have been in or are in a state of sensory deprivation for which they are trying to compensate by self-generated input. It still remains possible that autistic children are in a functional state of sensory deprivation. 1968) and did not increase significantly in the presence of increasing environmental complexity (Omitz et al. 1970). This seems unlikely since clinical observation shows that the children react as if they are receiving too much sensory input as often as too little (Goldfarb. Insufficient Sensory Stimulation Since many of the autistic motor behaviors seem to provide sensory input (see above). 1962) or home-reared (Coleman & Provence. Bergman & Escalona. The evidence indicates that excessive motor activity by the autistic child is not necessarily caused by a chxonic state of physiologic over-arousal. 1963.
the possibility remains open that autistic motor behaviors may provide sensory input. 1970). Disordered Sensorimotor Integration Two convergent lines of investigation. In the same experiment. Inadequate Modulation of Sensory lnput Closely related to the notion that autistic children may excessively gate out sensory input is the more general concept of the breakdown or failure to develop of the neurophysiologic mechanisms that regulate the level of sensory bombardment (Omitz. This concept of childhood autism as a disorder of sensorimotor integration (Ornitz. 1969). particularly sudden or intense auditory stimuli and visual stimulation with spinning objects. It has been presented in terms of a defective stimulus barrier or filtering function (Anthony. 1973. In young autistic children it is at times observed that certain types of sensory input. restriction of visual input caused one autistic child to modify his hand-flapping by brushing his fingers against his body with each hand movement. 1968a. apparently substituting tactile input for the reduced visual input. Omitz. 1971). Anthony. This failure to take into account the possible interaction of the modulation of sensory input and the strange motor output was a consequence of not paying sufficient attention to certain interesting behavioral sequences which can be observed clinically. At other times such stimuli will cause transient catatonic-like arrests of motion. 1969. 1968b). often with unusual posturing. 1949) or as a basic state of perceptual inconstancy related to an imbalance between neurophysiologic excitation and inhibition (Ornitz & Ritvo. however. 1963. Bergman & Escalona. The concept of failure of regulation of both sensory input and motor output due to a dysfunction of a common neurophysiologic mechanism has been elaborated in terms of the effect of sensory input on motor output and of motor output on sensory input (Ornitz. 1968a. 1971). 1970). one clinical and neurophysiologic (Ornitz. will induce excitatory motor behavior such as stereotyped repetitive flapping or oscillating of the extremities. Those who have accepted these notions have either ignored the strange motility of autistic children or have treated the motility disturbance as an independent consequence of the postdated uncoupling of excitatory and inhibitory mechanisms (Ornitz & Ritvo. 1958. These behavior sequences are similar in form to the subjective experience of adult schizophrenics and have been discussed in relation to a postulated control of bQth sensory input and motor output by central vestibular mechanisms (Ornitz. . Thus. 1970.. In this concept the fact that autistic children both underreact and overreact to sensory stimuli (Goldfarb. 1949. Bergman & Escalona. the other psychologic (Hermelin & O'Connor. 1958) is taken into account.202 Ornitz hand-flapping was not compensating for lack of sufficient sensory input (Omitz et al. 1971) will now be developed in relation to two types of experimental investigation. 1968b).
was associated with induced movement of the child's leg. In the process of confirming the dominant use of "proximal" receptors such as touch over "distal" receptors such as sound (Goldfarb.. the apparent dominance of the tactile sense may have actually been due to a kinesthetic stimulus. The autistic children discriminated not according to. involving motor feedback. 1966)." a tendency that is also seen in very young normal children and therefore represents.Modulation of Sensory Input and Motor Output 203 1970). they noted that a tactile stimulus.e. This was confirmed in a subsequent experiment in which it was found that autistic children were able to make discriminations on the basis o f the position of a sound and light stimulus which determined the child's motor response to reach the reward rather than on the intensity-modality combination of the stimulus complex. Since the position discrimination involved the learning of a motor habit. sensory feedback from the child's own motor response.g.. a developmental delay. e. In the task-oriented experiments. e... Thus autistic children "seem to rely more on perceptual activity than on perceptual analysis. This notion follows from clinical observations which parallel the careful experimental work of Hermelin & O'Connor. a light tug on a string around the child's ankle. have pointed toward a disturbance of sensorimotor integration in autistic children. an upward versus a straight-ahead reach. I will first consider the careful psychological experiments of Hermelin & O'Connor (1970). 1970) help us to understand the significance of their strange motility patterns. reaching in the same direction. In a final series of experiments Hermelin & O'Connor (1970) and Frith and Hermelin (1969)used both a tracking and a card-arrangement task to show that autistic children learned through cues that were primarily manipulative. Schopler. i. i. HOW DOES THE AUTISTIC CHILD MAKE SENSE OUT OF SENSATION? Can the impaired ability of autistic children to use sensory input to make perceptual discriminations in the absence of feedback from their own motor responses (Hermelin & O'Connor. and benefited little from additional visual information. the .g. visual cues.e. 1956. In a related experiment it was shown that both older autistic children (6 to 15 years old) and younger normal children (3 to 5 years old) learned to make a position discrimination more readily than a visual discrimination. 1952) and in experimental sleep studies (Ornitz. Thus. e. i. 1973). 1965. Thus the "maturational lag" which has been observed both clinically (Bender & Freedman. but to their own hand movements.g.e. 1972) of autistic children is also manifest in the need of the immature organism to receive feedback from self-generated motor responses in order to learn. hand-flapping? I have suggested that the bizarre and repetitive motor output may actually be a compensatory activity which helps the autistic child to make sense out of sensation (Ornitz... in part. this result indicated that the defect in responding to sensory cues and the need for kinesthetic feedback from motor responses in the older autistic children represented a developmental disturbance.
and loss of balance which would otherwise occur. Mason. or rubbing objects. twirling. 1974a. through kinesthetic (sensorimotor) feedback in lieu of normal perceptual processes? OBSERVATIONS OF MOTOR INHIBITION IN RESPONSE TO SENSORY STIMULATION Indirect support for this clinical inference comes from clinical neurophysiologic studies of sensorimotor dysfunction in autistic children. 1958.204 Ornitz autistic children utilized either manipulation or positioning of their extremities to make discriminations. Analogous to the experimental learning situations. could autistic children in their spontaneous "play" be getting the sense of objects in their environment. Furthermore. In their spontaneous activity autistic children are continuaUy spirting. 1968). writhe. 1969). Experimental Findings In the alert normal subject the oculomotor response (nystagmus) to vestibular stimulation of the horizontal semicircular canals (provided by acceleration in a rotating chair) is consistently suppressed when optic fixation is permitted (Wendt. including their own bodies and their parts. Studies of nystagmus in figure skaters (Collins. 1969) strongly suggest that the suppression of vestibularly induced nystagmus by optic fixation is an adaptive response which serves to prevent the disorientation. 1974b) have also shown that vestibular nystagmus is more severely suppressed by autistic children than by normal children not only when ocular ftxation is permitted but also when the retina is stimulated by light while fixation is precluded. 1951. Brown. Brown. Three studies of vestibular nystagmus in autistic children have shown that when visual fixation is permitted. the suppression of nystagmus is significantly greater in autistic children than in age-matched normal children (Pollack & Krieger. Recently completed studies in our laboratory (Omitz. Collins. This suggests that the modulation of the oculomotor output not only facilitates the stability of the peripheral vision but also in some way influences the processing of intense sensory input from the vestibular system so as to modify and improve the entire organismic response. wiggle. Ritvo. tapping. or oscillate their extremities while regarding them intently. In these studies the response of the oculomotor system to sensory stimulation during both wakefulness and sleep is presented as a possible model of more general sensorimotor function. 1959. Omitz. flicking. Eviatar. 1966) and baUet dancers (Dix & Hood. Colbert. Therefore excessive damping of the oculomotor response to vestibular stimulation in alert autistic children is dependent on at least two mechanisms. staggering. they repetitively flap. & Mason. one that is oculomotor and does utilize . Koegler. & Putnam. & Markham. Markham.
Clinical.the hypomotility of autistic children. Since it is known that there is an enhanced activity of the visual system (increased neuronal discharge in the occipital cortex and the lateral geniculate nuclei) synchronous with the eye-movement bursts (Bizzi. the deficient vestibularly initiated oculomotor responses in the presence of visual sensory input are more closely related to another aspect of the clinical s y n d r o m e . The present findings are more compatible with the hypothesis that in the presence of visual stimulation (either light or a fixation point) the excessive damping of the response to vestibular input reflects a basic neurophysiologic dysfunction. Observations Before indulging in speculations as to which neural pathways might be involved. it now seems less likely that the greater suppression of vestibular nystagmus in the presence of ocular fLxation in autistic children represents a learned response. Quantitative measures of the duration and organization of the rapid-eye-movement bursts significantly increased during the course of the night in the normal children in response to the vestibular stimulation and showed no response during the course of the night in the autistic children. 1973a. this relatively deficient oculomotor response to vestibular stimulation during REM sleep at the time of endogenous oculosensory stimulation may tentatively be attributed to defects in the same pathways which are involved in the deficient vestibular nystagmus response in the presence of visual input in the waking state. Instead. Furthermore. 1969). Forsythe. 1973b). and another that is oculosensory and does not utilize ocular fLxation. In these experiments a very mild sinusoidal oscillation was applied to a special bed in which the children slept throughout the night. it is necessary to return briefly to clinical observations of autistic children in order to document the suggestion that the deficient oculomotor response to combined vestibular and visual sensory stimulation is a model of a more general sensorimotor dysfunction. Autistic children probably are not reacting to the vestibular stimulus by fixating in the sense that this reaction occurs in figure skaters (Collins. Thus the suppression of postrotatory nystagmus in autistic children does not depend only on the occurrence of ocular fLxation. 1966b). However.Modulation of Sensory Input and Motor Output 205 ocular fLxation. 1966) and ballet dancers (Dix & Hood. A similar phenomenon has been demonstrated in a small group of sleeping autistic children who showed a damping of the phasic ocular activity of REM sleep in response to vestibular stimulation (Ornitz. a more pervasive interaction of the visual system and the vestibular system is involved. These children fre- . Attention has already been directed to the hypermotflity of autistic children in connection with the suggestion that they are comprehending their environment through sensorimotor feedback (see above). & de la Pc?m. The induced changes can be interpreted as manifestations of a specific effect on the phasic ocular activity of REM sleep since no changes in the percent of REM sleep time or the nocturnal sleep cycle occurred.
auditory. 1974b). Thus under conditions of no visual input the time course of the response o f an autistic child to vestibular input is also less predictable from trial to trial than is the response of a normal child.the combination of hyperreactive and hyporeactive motor responses to sensory s t i m u l a t i o n . that the central connections of the vestibular system play a significant role in the mutual regulation of sensory input and motor output in normal development. There is evidence. 1968b). In the context of both the clinical and experimental data under consideration. Both inhibited and exaggerated motor responses to sensory stimuli are typical of autistic children.also has a parallel in the oculomotor response to vestibular stimulation. Minimal motor and emotional responses are characteristic symptoms o f autism. SENSORIMOTOR INCONSTANCY Autistic children show both inhibited and facilitated motor responses to sensory stimuli. or painful stimuli. the variation of responses of the same subject is greater in autistic than in normal children.206 Omitz quently respond to visual. 1959). Recently we have obtained a similar result for the nystagmus response to an abrupt braking deceleration (Ornitz et al. Greater within-subject trial-to-trial variability of the nystagrnus duration in response to caloric vestibular stimulation has been demonstrated in autistic than in normal children under conditions of visual input (Colbert et al. this aspect of autistic behavior is better described as a state of sensorimotor inconstancy. This unpredictability or inconstancy of behavior in response to stimulation had earlier been referred to as a state of perceptual inconstancy in autistic children (Ornitz & Ritvo.. or general lack of emotional reaction. we fred that this facet of the clinical material .. a reduced motor response to sensory stimulation is a significant aspect of autistic symptomatology: Autistic children often "under-react" to visual. catatonic arrests of motion. Returning to the experimental data. In general. In darkness the slope of nystagmus frequency as a function of postrotatory time is significantly more variable in autistic children than in normal children. auditory. This role will now be discussed as a background . THE IMPORTANCE OF THE CENTRAL CONNECTIONS OF THE VESTIBULAR SYSTEM In the preceding discussion the deviant oculomotor responses to vestibulosensory stimulation have been used as an experimental model for the more generalized sensorimotor dysfunction observed clinically in autistic children. or painful stimuli with a hypoactive startle response. 1968a. in nystagmus studies conducted both with visual input and in darkness. however. Thus it is not surprising that.
labyrinthine receptors. and motility. Vestibular output influences motility in respect to postural adjustment. Schilder (1933) was one of the first to emphasize that "the vestibular nerve occupies a special position among the senses. Whenever we perceive an object we have already the basic knowledge about our body and about the attitude of our b o d y . . . . It will also be suggested that central vestibular dysfunction may be responsible for much of the general sensorimotor dysfunction observed in autistic children. THE INFLUENCE OF VESTIBULAR INPUT ON SENSORIMOTOR INTEGRATION How might vestibular input influence sensorimotor integration? In addition to the impact of descending volleys from the lateral vestibular nucleus via the vestibulospinal tract to the alpha motoneurones. " Bender (1956) noted that "gravity is the first sensory experience and responded to long before birth. or being lifted by the mother or in anticipation of such contact. the vestibular apparatus with its influence on the muscle tone plays a part in every perception . if the individual is to correctly and consistently receive information through auditory. Its sensations do not form a part of our conscious knowledge of the word . . . . muscle spindles. . It seems reasonable that mechanisms may have evolved to regulate the complex interrelationships between general sensory input. and tactile sensory modalities. visual. Both Von Hoist (1954) and Dijkgraaf (1955) pointed out that all animals must discriminate between externally generated sensory stimuli and those stimuli evoked by movement of the animal itself since the same tactile receptors. . After birth the earliest relationship with the mother in which the child responds is in the setting and adjusting of body tone due to contact with the mother's body. . We may also expect that every change in the vestibular apparatus must have an immediate effect on all our senses . Thus the other senses do have a functional dependence on and interaction with the vestibular sense. In order to receive reliable information about externally generated stimuli." In general. 1968). Cangiano. vestibular input and output. motility is readily effected . then these perceptions must take place in relation to the simultaneous perception of the individual's own position in the space from which these sensory inputs are derived. Central vestibular mechanisms suppress sensory volleys elicited during movements and thus may fulfill this function (Cook. 1955). .Modulation of Sensory Input and Motor Output 207 to our speculations concerning the pathways which may be involved in the deficient nystagmus response in autistic children. self-generated stimuli must be "neutralized in some way within the central nervous system" (Dijkgraff. & Pompeiano. . and retinal receptors are active both when at rest and while in motion.
Studies of single neurons also demonstrate the convergence of vestibular responses with responses in other sensory modalities throughout the cortex and in the lateral geniculate nucleus (Kornhuber & da Fonseca.. 1968). and (2) reduction of flash evoked responses in the lateral geniculate and in the visua 1 cortex (Bizzi. As the medial longitudinal fasciculus carries fibers of the medial vestibular nucleus to motoneurons. Slow wave potentials in this same area have also been evoked by somatosensory. It has also been suggested that since natural labyrinthine stimulation induces eye movement. suggesting presynaptic inhibition of visual input (Marchiafava & Pompeiano. & Satoh. & Pompeiano. the vestibular system actively inhibits segmental afferent input to these motoneurons. thereby preventing "instabilities. 1967). The same presynaptic inhibition occurring during the rapid eye movements of REM sleep has been demonstrated by: (1) augmentation of the optic tract antidromic response and reduction of the optic tract orthodromic response to electrical stimulation of the lateral geniculate and the optic tract. low-intensity stimulation of the vestibular nerve results in ascending activity. vestibulafly induced inhibition of visual input at the lateral geniculate level might control the strong retinal . 1966). The pathway for this vestibularly induced inhibition of visual input is through the medial and descending vestibular nuclei which activate the spontaneous neuronal activity of the lateral geniculate nucleus during the eye movement bursts of REM sleep (Morrison & Pompeiano. Stimulation of the eighth cranial nerve augments the antidromic response in the optic tract to lateral geniculate stimulation. Also. 1968). 1964). and sensorimotor integration. 1967). motility. since muscle afferents project to sensory cortex (Gardner & Morin.208 Orni~ through excitation of fusimotor neurons by stimulation of vestibular components of the eighth cranial nerve (Diete-Spiff. responses to eighth cranial nerve stimulation recorded in the medial longitudinal fasciculus are depressed during phasic excitation accompanying the eye-movement bursts of REM sleep and during orienting reactions to arousing stimuli (Lenzi. a depression of the influence of vestibular input on motor output occurs just at the time of internally generated excitation during both REM sleep and extemaUy induced excitation during waking. Pompeiano. Carli. visual. 1953). which might occur when somatic sensory volleys elicited during movements are fed back into the spinal cord and interact with the discharging motoneurons" (Cook et al. At the same time that spinal motoneurons are excited by stimulation of the vestibular components of the eighth cranial nerve. In addition to these descending effects upon the modulation of sensation. 1966). 1966a).. and auditory stimulation. evoking slow wave potentials from the orbital surface of the feline cerebral cortex (Megirian & Manning. while electrical stimulation of this area affects spinal motoneuron excitability.. 1960). Information from the contracting spindles may be fed back into the central nervous system and possibly partake in the adjustment of sensory perception (Eldred.
1973). THE INFLUENCE OF THE CENTRAL NERVOUS SYSTEM ON THE VESTIBULAR SYSTEM Thus vestibular input seems to interact with and may modulate both other forms of afferent input and motor excitability at spinal.. The vestibular nuclei affect sensorimotor integration at spinal. and (2) a reduced oculomotor response (rapid eye movement bursts) to vestibular stimulation in the presence of endogenous visual stimulation in the sleeping autistic child. Since the experimental data have been in the direction of a reduced nystagmus in response to vestibular stimulation of autistic children. and cortical levels (see above) so do these regions both facilitate and inhibit the vestibular system (Markham. 1974a. these regions both facilitate and restrain the vestibular system. At the cortical level experimental ablations of either occipital lobes or frontal lobe areas 4 and 6 enhanced . midbrain. the basal experimental conditions facilitated the production of nystagmus in both the normal and autistic children (see Tjemstr6m. thereby completing a feedback loop with broad implications for sensorimotor control. 1965). Since all subjects were studied with eyes open in a nonsleepy state of relaxed attention. 1966). midbrain. Thus our attention must now turn to consideration of those central nervous system mechanisms which can influence the vestibular system and thus modify its effect on sensorimotor interactions. and cortical levels. Several possible pathways could be involved in this type of excessive inhibition. Only the experimental variables. 1974b). inhibited the nystagmus. The final common pathway of this descending control over the vestibular nuclei may be an efferent vestibular system which modifies the impact of vestibular stimuli at the level of the peripheral receptors (Sala. the continuing discussion will focus on those neural pathways which inhibit the response of the vestibular system. and both forms of visual stimulation induced a significantly greater degree of inhibition in the autistic children (Ornitz et al. A central dysfunction of this vestibular control of sensory input-motor output interaction could explain much of the sensorimotor dysfunction observed clinically in autistic children.Modulation of Sensory Input and Motor Output 209 barrage accompanying postrotational nystagmus elicited in fight (Marchiafava & Pompeiano. completing a feedback loop vital to sensorimotor control. 1972). Just as the vestibular nuclei effect sensorimotor integration at spinal. The experimental observations relevant to vestibular dysfunction have demonstrated: (1) a reduced oculomotor response (nystagmus) to vestibular stimulation in the presence of exogenous visual input in the waking autistic child. and cortical levels. subcortical. oculomotor (visual fLxation) and oculosensory (diffuse light) stimulation. At the same time.
Precht. the later observation suggests that an excitatory effect may be associated with the manifest inhibition of the vestibulo-ocular reflex arc. (1961) were able to consistently inhibit vestibular nystagmus by stimulating the brain stem reticular core. Another midbrain inhibitory circuit may take its origin in supranuclear oculomotor centers. 1953). & Wist. indicating a release from cortical inhibition (Wycis & Spiegel. 1972) can be inferred from the enhancement of postrotational nystagmus following lesions of the LGN (Spiegel & Scala. Observation of frequency modulation in the vestibular nerve in relation to vestibularly induced eye movements demonstrated the possible existence of vestibular afferent modulation by oculomotor impulses mediated by efferent fibers (Dichgans. 1972). & Shimazu. 1961) while stimulation of the interstitial nucleus of Cajal inhibits type-I vestibular cells of the horizontal semicircular canals (Markham. Tonic retinal inhibition of the vestibulo-ocular reflex arc by retinal stimulation (Markham. 1946). lightevoked discharges from the LGN may be enhanced or depressed by labyrinthine stimulation (Papaioannou. Scheibel et al. 1969). 1972). LGN. 1973). a complex brain stem circuitry may involve the mutual regulation of visuosensory input (retina. 1972). Precht. Markham. 1961). 1970). These impulses may also be the source of monophasic wave activity in the lateral geniculate nuclei (LGN). although they point out that the suppression of nystagmus amplitude was associated with a very great increase in nystagmus frequency. 1945) or the superior quadrigeminal bodies (Spiegel & Scala. 1972) and the semicircular canals (Baker.. Alterations in the DC resting potential of one labyrinth after electrical stimulation of the reticular substance or caloric stimulation of the other labyrinth in precollicularly decerebrated and decerebellated preparations suggested a bulbopontine reticular origin of the efferent vestibular system (Sala. Finally. Also stimulation of cortifugal fibers in the cerebral peduncles and internal capsule inhibited vestibular nystagmus (Scheibel. Thus.210 Orni~ nystagmus to the side of the lesion. Schmidt. & Llinfis. Cerebellar inhibition of vestibular nystagmus is particularly relevant to the experimental Finding of increased suppression of nystagmus during visual fixation in autistic children. 1966). & Koegler. since monophasic waves recorded in both LGN and visual cortex are preceded by monophasic waves in the oculomotor nuclei (Costin & Hafemann. Several studies have suggested that the efferent vestibular system may receive impulses directly from brain-stem regions. This system has inhibitory components which are probably located in part within and between the vestibular nuclei and work through a cholinergic mechanism (Pompeiano. The cerebellum has also been implicated in inhibitory control over vestibular afferents from both the otolith system (Llings & Precht. since stimulation of the cerebellar roof nuclei induce centering of the eyes and complete inhibition of nystagmus in the cat (Wolfe. superior col- . Markham (1972) has discussed the complex pathways by which two specific midbrain centers may inhibit the vestibulo-oculomotor arc: the mechanism by which the nucleus of Darkschewitsch inhibits vestibularly induced eye movements is unclear (Scheibel et al. 1965).
Psychologic experiments have revealed that autistic children learn through manipulation and position cues rather than through normal perceptual processes. there is reason to suspect that a dysfunction of the central vestibular system might be fundamental to this facet of the autistic syndrome. vestibular nuclei). Clinical neurophysiologic studies of the oculomotor response to vestibulosensory stimulation in the presence of visuosensory stimulation have demonstrated that there is a significantly greater inhibition of postrotatory nystagmus in autistic children than there is in normal children. the flapping and oscillating of their extremities. These experimental demonstrations of a deficient oculomotor response to vestibular or vestibularand-visual stimulation parallel clinical observations of the hypomotility also seen in response to sensory stimulation. oculomotor output (oculomotor nuclei. 1974b). the experimental findings of depressed oculomotor response to vestibular stimulation in the presence of either visual fixation or visuosensory stimulation are more compatible with a dysfunction of cerebellar or brain-stem .. While cortical centers may inhibit vestibular function. through kinesthetic (sensorimotor) feedback. which is also a significant feature of the autistic syndrome because the children frequently show underreactive or overreactive motor responses to sensory stimuli. While the oculomotor responses to vestibulosensory stimulation serve as an experimental model for the more generalized sensorimotor dysfunction observed in autistic children. and vestibular input (labyrinth. including their own bodies and their parts. During sleep the vestibularly mediated phasic eye movement bursts of REM sleep are also diminished in autistic children in response to vestibular stimulation. and the whirling and rocking of their bodies may be the autistic children's way of making sense out of the sensations in their environment. vestibular nuclei). Review of the neurophysiology of the vestibular system reveals that the vestibular nuclei either directly modulate or transmit modulating influences over motor output at the time of sensory input and over sensory input at the time of motor output. This dysfunction of the modulation of motor output is in some way related to the faulty modulation of sensory input.Modulation of Sensory Input and Motor Output 211 liculus). The strange motility patterns of autistic children are characterized by both hypomotility and hypermotility and cannot readily be explained by either postulated states of overarousal or insufficient sensory stimulation. 1974a. Dysfunction of such a system could be the neurophysiologic basis of the excessive inhibition of postrotatory nystagmus in autistic children which was found in the presence of retinal stimulation (Ornitz et al. It is therefore suggested that the spontaneous spinning and flicking of objects. SUMMARY A N D CONCLUSIONS This paper explores the possible pathophysiologic mechanisms which might underlie the unusual motility disturbances which occur in autistic children.
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