Development and Autism Part 3
Autism in Infancy: Regulating Social Input in an Atypical System
Several prenatal factors may be at play in developing autism or a system susceptible to autism. Nevertheless, it is not until the infant is born and able to interact with its predominantly social environment that the first symptoms are more easily detected and measured.
Extensive experiments on rodents and non-human primates have investigated brain opioid involvement during mothering and infant-caretaker bonding and attachment. Panksepp et al. (1994) have hypothesized and tested that the opioid system is both important in maintaining maternal motivation and quality of maternal action both by being released and inhibited by oxytocin, respectively. In infant rodents, opioid release seems to suppress social separation distress and gregariousness believed to represent the stress reducing effect of maternal attention to separation or distress calls (Panksepp, Nelson, & Siviy, 1994).
In autism, these researchers have predicted a hyperactive opioid system in affected individuals who thus show no distress signals during social separation and who also exhibit lower levels of social gregariousness. By stimulating dopamine release, this hyperactive opioid system could be linked to the aforementioned dopaminergic hyperactivity documented in autistic brains. Opioid inhibitors, such as oxytocin, have thus been administered in low doses to autistic individuals with the idea that their overly active opioid systems would be suppressed sensitizing them to the social interactions that would both release and inhibit opioid activity (Panksepp et al., 1994).
Interestingly, oxytocin binding sites have been shown to undergo reduction in neonatal rat pups after short phases of social isolation (Nelson & Panksepp, 1998). This animal model may represent the potential deficiency either in autistic individuals after they have isolated themselves or in autistic infants who display an atypical oxytocin response. For these infants, there may be some sort of atypical mechanism that does not respond to the typical social stimuli by either releasing oxytocin or recruiting binding sites (Nelson & Panksepp, 1998).
On the other hand, oxytocin administration in rodents shows a decrease in various typical social-stimulus-seeking behaviors, like contact calling and suckling. While that effect is to be expected in typical individuals, it may be disadvantageous in atypical individuals, as it may negate the need for social stimulation in treated individuals (Nelson & Panksepp, 1998).
Nasal oxytocin administration has been shown to have inconclusive results. While some studies suggest improvements in social recognition and emotion understanding in autistic individuals (Anagnostou et al., 2012; Guastella et al., 2010), others present these results as questionable by administrating more stringent experimental methods (Anagnostou et al., 2012; Dadds et al., 2013). The non-linear relationship between oxytocin administration and social behavior improvements highlights the complex interaction between oxytocin and behavioral outcomes during development.
One common symptom seen both in infants later diagnosed with autism or epilepsy is infantile spasms or early onset seizures (Jeste, 2011; Kanner, 1943). These symptoms represent abnormal connectivity and synaptic plasticity both over short and long neurological ranges (Jeste, 2011). While their specific effects on development remain unclear, there is a correlation between spasms or seizures and neurodevelopmental impairment (Jeste, 2011).
By examining neural connectivity in white matter of high-risk and low-risk infants, a comparative study found significant differences between how white matter changed over time from 6 to 12 to 24 months (Gu, 2012). In the low-risk infants the progression reflected a rapid increase between 6 and 24 months, whereas the high-risk infants showed stunted growth after 6 months. While they started out with greater connectivity, their progression markedly stopped in comparison to the low risk infants (Courchesne, 2004; Gu, 2012). This kind of growth would lead to an overconnectivity in the frontal cortex leaving the rest of the brain underconnected (Courchesne & Pierce, 2005). This overconnectivity paired with the aforementioned potential developmental atypicality in the cerebellum may cause for a disabled ability to integrate sensory and other experiential information.
Aside from neural differences and early seizures, most symptoms are not detectable until later in the first postnatal year. In a prospective study, researchers evaluated 6, 12, 18, 24, and 36-month-old high- and low-risk infants and found interesting differences. While face gazes, reciprocal smiles, and socially directed vocalizations were comparable between the two groups at 6 months, they diverged significantly as the infants grew older (Ozonoff, Iosif, Baguio, Cook, & Hill, 2010). This study suggests that for those individuals tested, autistic behavioral characteristics were not present at birth but emerged once infants grew into their social environments.
One explanation for this developmental change in propensity to engage socially may have to do with the atypical development of an infant’s dopaminergic system, specifically in the nucleus accumbens septi (NAS). This system is thought to regulate approach/withdrawal behaviors via positive and negative reinforcement (Ikemoto & Panksepp, 1999). By approaching a desired stimulus, the organism receives positive reinforcement, and by withdrawing from or avoiding an aversive stimulus, the organism experiences negative reinforcement. This system is thus thought to be highly active during appetitive activities, including feeding (Ikemoto & Panksepp, 1999).
As mentioned before, researchers have found evidence for a hyperactive dopamine circuitry in autistic individuals (Previc, 2007). This hyperactivity may be linked to the overconnectivity occurring in the frontal lobe, specifically the prefrontal cortex, followed by stunted specializations of neural connections throughout the rest of the brain. These connections may disable the ability to execute and functionalize the approach/withdrawal system effectively, which in turn may lead to a disoriented and confused infant unable to integrate and synthesize information. It is conceivable that the first instances of such a disrupted appetitive system are displayed in the common difficulties experienced by caretakers trying to feed their atypically developing infants (Ledford & Gast, 2006).
Another manner in which an atypical dopaminergic system may manifest in early infancy is via the exact ways in which approach/withdrawal behaviors are displayed. The NAS dopaminergic system is thought to facilitate flexible approach responses in the presence of various salient environmental stimuli (Ikemoto & Panksepp, 1999). The NAS dopaminergic system also plays an important role in learning as it facilitates the integration of several modality sensations when encountering these various environmental stimuli. Approach responses can occur either flexibly by modulating incentive motivation processes, or fixedly, by forming habits or habitual responses (Ikemoto & Panksepp, 1999). Autistic individuals seem to show difficulties differentiating between flexible responses and habit formations. Specifically, they seem to default to forming stereotyped habits and thus respond more rigidly. To the autistic infant, this tendency may facilitate a more easily interpreted situation in which the possible outcomes become limited and thus more predictable.
Another explanation for the developmental change discovered by Ozonoff et al. (2010) could have to do with the way in which infants structure their social environment and stimuli by smiling. Infant smiles have been shown to be highly important during infant socioemotional development but also for caretaker perception. A study examining how smiling develops over the course of infancy from 6 to 30 months shows correlations between the amount of smiling at 6 months and the amount of anticipatory socially-oriented smiling during joint attention at 8 and 10 months. This in turn is correlated with caretaker social expressivity assessments at 30 months (Parlade et al., 2009).
While an infant's smile can be elicited by many different instances, social or physical, it reliably elicits a dopaminergic reaction in its mother (Strathearn, Li, Fonagy, & Montague, 2008). As mentioned before, dopaminergic pathways in social organisms are oftentimes correlated with approach behaviors, so the infant's smile inadvertently causes its mother to approach the infant either physically, verbally or in some other social way, often in combination with a reciprocated smile. Since 6-month old high- and low-risk infants smiled and gazed comparably, and high-risk infants showed a decline sometime between 7 and 12 months, it is conceivable that these infants are compensating or regulating something in their social environment that may be aversive to them.
While non-emotional facial expressions are encoded locally by parvocellular pathways in the visual system where each facial muscle is examined in isolation (Tardif, Lainé, Rodriguez, & Gepner, 2006), emotional facial expressions are encoded globally using magnocellular pathways in the visual system. Even though 6-month old high- and low-risk infants show no behavioral differences, and while their parvocellular pathways react similarly, their magnocelluar pathways demonstrate measurable differences. The magnocellular pathways in 6-month old high-risk infants respond to emotional facial expression twice the amount measured in low-risk infants' magnocellular responses (McCleery, Allman, Carver, & Dobkins, 2007).
High-risk infants may thus have highly sensitive magnocellular pathways, possibly representative of a generally more highly sensitive perceptual system. Given that their opioid and dopaminergic systems may be more active on a baseline level, these infants may simply be operating at a lower threshold for stimulation than typically developing infants (Makkonen, Riikonen, Kokki, Airaksinen, & Kuikka, 2008; Previc, 2007). This may explain the symptom of being overwhelmed more easily by multi-sensory stimuli and being prone to withdraw from social situations that involve vocalizations, facial expression and physical stimuli (Clancy & McBride, 2005; Davidson, 2008). Interestingly, while this sensitivity is present neurologically in high-risk infants at 6 months it often does not seem to cause the child to act differently until later.
Smiling may be one of the first ways in which all infants, but especially those with atypical perceptual systems, learn to regulate social stimuli, and thus could be viewed as a social approach/withdrawal regulator. Smiling and its absence are so highly salient to any caretaker that they can actively control caretaker behavior during infant-caretaker interactions. Additionally, the autistic infant’s tendencies to behave socially inappropriately by using atypical vocalizations, non-social gazes, or by not reciprocating smiles may in fact be a regulatory mechanisms with which to withdraw from its overwhelming environment (Clancy & McBride, 2005).
Smiling has also been shown to be highly effective and important in developing the ability for joint attention. In typical development, instances permissive of joint attention emerge during the first year of life. In that infants are usually accompanied by caretakers who display varying degrees of attentiveness, infant actions often elicit caretaker actions as well. The caretaker, by paying close attention to the infant’s actions, creates first instances of joint attention. Additionally, as the caretaker follows the infant’s actions by following the infant’s gaze, attention, and activities, they are more likely to share the affective results of such actions creating instances of reciprocated smiling.
Infants as young as 8 months have been shown to demonstrate anticipatory smiles as voluntary social signals when interacting with their caretakers (S. S. Jones & Hong, 2001). A study examining the onset of voluntary communication was conducted by looking into how understanding means-end relationships between actions and actor allowed subjects to form anticipatory smiles while also gesturing and vocalizing intentionally (S. S. Jones & Hong, 2001). Naturally, these anticipatory smiles are reinforcing to caretakers and encourage them to continue their interactions. It is presumed that those interactions lacking anticipatory smiles may also stunt the maintenance of joint attention instances.
In typically developing infants, joint attention is scaffolded by extensive and rewarding dyadic interactions between caretaker and infant during the first couple months (Wetherby, 2006). During the first year, the infant begins to understand that it can use its ability to control caretaker behavior to achieve certain goals. As the infant becomes more advanced in its abilities these dyadic interactions become triadic as other objects, events or social entities are incorporated into the interactions (Vygotsky, 1978). By drawing attention either to itself, to the object or event of interest, the infant can create its first moments of initiated joint attention. Additionally, the infant will become more interested in what the caretaker does as these activities usually have rewarding outcomes for the infant. The caretaker, being a social representative of positive events – nutrition and warmth – begins to use their capability to direct the infant’s attention by interacting with engaging objects in the environment, such as toys. Should the infant follow these directions, it displays first instances of response joint attention.
In typically developing individuals, instances of joint attention are emotionally and cognitively facilitative both when responding to others’ bids and when initiating them. In both cases, the unity of social attention can be rewarding as this allows for shared affective behavior such as smiles, laughs, coos and caretaker vocalizations. In response joint attention, the child experienced initial pairings between the physical environment (i.e., objects) and social communication (i.e., words and labels). These pairings permit a whole new level of predictability between engaging the environment and eliciting action from those surrounding the infant. In initiated joint attention, predictability again plays a rewarding role, in that individuals learn their social and environmental agency when directing others’ attention.
Interestingly, researchers and caretakers have noticed a lack of joint attention, specifically infant-initiated joint attention involving a shared affect for the event (Schertz & Odom, 2004). While typically developing infants show instances of joint attention as early as 9 months with a solidification of the social ability at around 18 months, infants later diagnosed with autism either do not engage in these instances at all or begin to at around 9 months but do not progress in their joint attention procedures (Schertz & Odom, 2004).
Typically, at around 6 months of age, infants develop an increasing ability to grasp, reach for and shift objects, and start to direct a lot of their attention toward surrounding toys and other objects, which usually elicits caretaker narration, labeling, and acts of assistance (Schertz & Odom, 2004). These interactions are paramount to teaching the infant about communicative contingencies, lingual information and the idea that two social entities can pay attention to and share an affect about the same thing (Schertz & Robb, 2006). Many of the necessary infant activities, however, involve certain levels of motoric competence. While impeding motoric deficiencies in autism are not commonly documented earlier than 24 months (Ozonoff et al., 2007), some individual cases at as early as 6 months have demonstrated motor atypicalities such as abnormal repetition or lack of social orienting (Ozonoff et al., 2008; Zwaigenbaum et al., 2005). For atypically developing infants, these motor deficiencies may stunt their ability to initiate the valuable infant-initiated instances of joint attention (Bruckner & Yoder, 2007).
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