Autism and Social Anxiety Disorder
The Human Brain
The human brain is the organ that is the control center for the central nervous system. It determines how we interact and interpret the stimuli received from the environment. The brain is divided into the cerebrum, the cerebellum the diencephalon and the brainstem.
It is the frontal lobe of the cerebrum that controls the following specific functions:
Movement, coordination, cognitive functions, sense of smell and eye movement are controlled by the frontal lobe.
Neurodevelopment disorders refer to a group of biological brain disorders that are genetic or acquired. These disorders refer to any arrest of growth and development of the central nervous system or brain. This can later be manifested by deficiencies in emotion, memory, self-control and learning ability.
Some of the Neuropsychiatric disorders are:
1. Autism spectrum disorder
3. Cognitive dysfunction/Mental retardation
4. Cerebral palsy, motor dysfunction
5. Attention Deficit disorders, behavioral problems
Neurocircuitry of Emotions
There is growing interest in the neurocircuitry of emotions. In research done by P Kirsch et al they sought to establish that oxytocin modulates neural circuitry for social cognition and fear in humans. Experiment done on animal subjects identified the neuropeptide oxytocin as a key mediator of complex social and emotional behaviors within specific animal groups. Some of these behaviors include social recognition, attachment and even aggression. In fact oxytocin has been described by some animal scientist as the “survival hormone” as it reduces anxiety and impacts on fear conditioning and extinction.
There have not been as many experiments done on human subjects but of those done to date the amygdala has been shown to be a central component of the neurocircuitry of fear and social cognition which are linked to trust. This is where the oxytocin receptors are located. The human amygdala function is strongly modulated by oxytocin. Functional magnetic resonance imaging has been used on 15 healthy males to image amygdala activation by fear-inducing visual stimuli after double-blind crossover intranasal application of placebo or oxytocin. Oxytocin potently reduced activation of the amygdala and reduced coupling of the amygdala to brainstem regions implicated in autonomic and behavioral manifestations of fear when compared with the placebo. Results indicate a neural mechanism for the effects of oxytocin in social cognition in the human brain and provide a methodology and rationale for exploring therapeutic strategies in disorders in which abnormal amygdala function has been implicated, such as social phobia or autism.
Oxytocin is a neuropeptide that plays a key role in social attachment and affiliation in non-human mammals; it causes a substantial increase in trust among humans, thereby greatly increasing the benefits from social interactions. We also show that the effect of oxytocin on trust is not due to a general increase in the readiness to bear risks. On the contrary, oxytocin specifically affects an individual’s willingness to accept social risks arising through interpersonal interactions. These results concur with animal research suggesting an essential role for oxytocin as a biological basis of prosocial approach behaviour.
In the 2004 Annual Review of Neurosciences researchers Intel and Fernald demonstrated that oxytocin and vasopressin are key effectors of social behavior. This behavioral study corroborated well with the research done by Kosfeld et al. They showed the correlation between the oxytocin effects in humans and selective increase in trust after the hormone was administered. Since this suggested involvement of the amygdala, this is linked to trust (Winston, J. S., et al. (2002). Nat. Neurosci., 5: 277-283) – presumably because of its role in danger monitoring – and highly expresses oxytocin receptors (Huber, D., et al. (2005). Science, 308: 245-248), we studied amygdala circuitry after double-blind crossover intranasal application of placebo or oxytocin (Kirsch, P., et al. (2005). J. Neurosci., 25: 11489-11493). Oxytocin potently reduced amygdala activation and decreased coupling to brainstem regions implicated in autonomic and behavioral manifestations of fear, indicating a neural mechanism for the effects of oxytocin in social cognition in humans and providing a potential therapeutic approach to social anxiety currently being tested in social phobia and autism. Furthermore, these data suggested a translational genetic approach. Preliminary findings (data not presented) from our laboratory using imaging genetics indeed implicate genetic variants for both AVPR1A, encoding the primary receptor of vasopressin in brain, and the oxytocin receptor, OXTR, in amygdala regulation and activation. Taken together, our results indicate neural mechanisms for human social behaviour mediating genetic risk for autism through an impact on amygdala signaling and provide a rationale for exploring therapeutic strategies aimed at abnormal amygdala function in this disorder and in social dysfunction in general.
The Role of the Amygdala and Human Behavior
Researcher Sobota et al have studied the effects of both oxytocin and dopamine on human behavior. Oxytocin reduces amygdala activity, increases social interactions, and reduces anxiety-like behavior irrespective of NMDAR antagonism.
Standard dopamine therapies for schizophrenia are not efficacious for negative symptoms of the disease, including asociality. This reduced social behavior may be due to glutamatergic dysfunction within the amygdala, leading to increased fear and social anxiety. Several studies have demonstrated the prosocial effects of oxytocin in schizophrenia patients. Therefore, this study evaluates the effect of sub-chronic oxytocin on EEG activity in amygdala of mice during performance of the three-chamber social choice and open field tests following acute ketamine as a model of glutamatergic dysfunction. Oxytocin did not restore social deficits introduced by ketamine but did significantly increase sociality in comparison to the control group. Ketamine had no effect on time spent in the center during the open field trials, whereas oxytocin increased overall center time across all groups, suggesting a reduction in anxiety. Amygdala activity was consistent across all drug groups during social and nonsocial behavioral trials. However, oxytocin reduced overall amygdala EEG power during the two behavioral tasks. Alternatively, ketamine did not significantly affect EEG power throughout the tasks. Decreased EEG power in the amygdala, as caused by oxytocin, may be related to both reduced anxiety and increased social behaviors. Data suggest that separate prosocial and social anxiety pathways may mediate social preference. (PsycINFO Database Record)
Autism and Anxiety Disorders
The prevalence of autism has been increasing worldwide and the search is on in earnest to examine all possible etiology as well as interventions that could allow children to reach their highest possible neuropsychiatric development potential.
Children with autism are less able to interact with the world as their normal peers. They exhibit deficits in three major functions:
I. Social awareness and interactions
II. Verbal and non-verbal communication
III. Imaginative play demonstrating variable behaviors and interests
The term autism spectrum disorder ASD acknowledges that there is a range of functionality seen in children with autism. At one end of the spectrum some children function at a high level while those at the lower end exhibit the classic deficits.
Social Anxiety Disorder SAD
There is a spectrum of how anxiety can manifest from a fleeting short term mood which is self-limiting to the most severe forms of manifestation which requires medical intervention and perhaps even hospitalization.
Individuals who have a fear of being judged or embarrassed in public have an anxiety disorder called Social Anxiety Disorder (SAD). Individuals suffering from this disorder often tend to avoid being in public and public events.
Autistic persons have a deficit in social awareness and interactions and very often exhibit SAD.
Comorbid Social Anxiety Disorder with Autism Spectrum Disorder
The research done by Maddox and White is significant. They established an important association/co-morbidity between SAD and ASD.
Cognitively unimpaired youth and adults with autism spectrum disorder commonly exhibit social anxiety disorder. In the preliminary study with a small study population of adults with SAD+ ASD(n=28) and adults with only ASD, approximately 50% of the adults with ASD met the criteria for SAD. There were differences between the groups on many characteristics. These findings are signaling that adults with ASD are aware of their deficit with social interactions and therefore experience what is called impairing social anxiety.
Advancements in the Treatment of Autism and SAD
There is still no cure for autism but there are a few drugs, educational & behavioral programs, which have improved the lives of autistic children and adults. Some of these programs are:
1. Cognitive Behavioral Therapy
2. Social Skills Intervention
3. Early Start Denver Model Therapy
4. Sensory Based Therapy
5. Floortime and Pivotal Response Training
• Antipsychotic drugs
• Mood stabilizers
Stem cell therapy
Research is ongoing to evaluate which therapies are effective and result in consistent good outcomes.
– Written by a doctor for Khemcorp
1. Oxytocin reduces amygdala activity, increases social interactions, and reduces anxiety-like behavior irrespective of NMDAR antagonism.
a. Sobota R, Mihara T, Forrest A, Featherstone RE, Siegel SJ.
2. Oxytocin modulates neural circuitry for social cognition and fear in humans.
a. Kirsch P, Esslinger C, Chen Q, Mier D, Lis S, Siddhanti S, Gruppe H, Mattay VS, Gallhofer B, Meyer-Lindenberg A.
3. Oxytocin increases trust in humans, Kosfeld M, Heinrichs M, Zak PJ, Fischbacher U, Fehr E.
4. Impact of prosocial neuropeptides on human brain function, Meyer-Lindenberg
5. Oxytocin modulates neural circuitry for social cognition and fear in humans, Kirsch P, Esslinger C, Chen Q, Mier D, Lis S, Siddhanti S, Gruppe H, Mattay VS, Galhofer B, Meyer-Lindenberg A
6. Oxytocin reduces amygdala activity, increases social interactions, and reduces anxiety-like behavior irrespective of NMDAR antagonism, Sobota R, MiharaT, Forrest A, Featherstone RE, Siegel SJ
7. Effect of intranasal oxytocin administration on psychiatric symptoms: A meta-Analysis of placebo-controlled studies, Hoffmann SG, Fang A, Brager DN
8. What is oxytocin, and what does it do?, Oxytocin as potential psychiatric therapy, Markus MacGill
9. Stanford Study clarifies biology of oxytocin in autism. Published in the Proceeding of the National Academy of Sciences
10. Low levels of Oxytocin linked to Poor Social Skills, published in the proceedings of the National Academy of Sciences
11. Comorbid Social Anxiety Disorder with Autism Spectrum Disorder,Maddox BB1,2, White SW3.