Neurofeedback training for Autistic Spectrum Disorder (ASD)
The first ASD-neurofeedback case study was by Cowan and Markham in 1994. The team performed Neurofeedback training (NFT) on an eight-year-old girl with high-functioning ASD; to suppress the ratio of alpha and theta (4-10 Hz) to beta (16-20 Hz) EEG activity in the parietal and occipital lobes.
The protocol was created after the young girl's QEEG assessment revealed abnormality in the levels of these frequencies at the areas assessed. After 21 sessions, autistic behaviour (e.g., inappropriate giggling and spinning) reduced and sustained attention increased. Her teachers and parents also reported improved socialisation. The results also highlighted improvements in the test of variables of attention (TOVA) for measures of inattention and impulsivity.
More significantly, the two years follow-up found that behaviour and attention scores were maintained and still within the normal range.
Coben 2009 and Kouijzer et al. 2009 supported these promising findings by demonstrating that their ASD-NFT cohorts also maintained positive changes one year later. Furthermore, both studies demonstrated that in some situations, participants made additional gains, e.g., further improvements were found in motor response inhibition and sustained auditory selective attention.
Though more research on neurofeedback’s effects on ASD is required, thus far, there is evidence demonstrating significant improvements, be it in the comorbidities associated with ASD or in ASD-specific symptomology.
The symptoms that accompany autism
Autism is an early-onset neurodevelopmental disorder that occurs before the age of 3. The diagnosis requires a triad of behavioural domains (concerning social development, communication, repetitive behaviour or obsessive interests) to be met. The symptoms that accompany autism comprise: •Issues with social interactions: For example, a lack of eye contact and appropriate facial expressions, difficulties with developing and sustaining peer relationships •Communication: There is often a delay in spoken language and difficulties with initiating and sustaining conversation •Restricted and repetitive behaviour: For example, adhering tightly to routines and rituals and the inability the partake in random activity
Five diagnostic subtypes make up autism spectrum disorder
A rise in autism is reported. Faras et al. reported 6 cases per 1,000 in 2007. However, this figure is suggested to have increased, with 1 in 59 individuals meeting the ASD criteria according to Baio et al. Five diagnostic subtypes make up autism spectrum disorder (ASD). These disorders are characterised by a range of differing abilities and levels of severity: •Autistic disorder: The social presentation can involve rarely responding or using language to communicate, difficulties understanding gestures, limited facial expressions (during communication) and a lack of interest in friends. Whereas restricted, repetitive behaviour and interests can present as rarely engaging in imaginative play, speaking in a repetitive manner, needing to adhere to rituals (e.g., always lining up toys or having problems changing between activities), frequent spinning or flicking of switches and having very narrow or intense interests. Sensory behaviour can manifest as being distressed by everyday sounds or licking and sniffing objects. •Pervasive developmental disorder – not otherwise specified (PDD-nos): PDD-nos is diagnosed when an individual is on the autism spectrum but does not meet the full criteria for the other subtypes, e.g., Autistic disorder. It is characterised by a lack of language and social skills. •Rett syndrome: Rett’s is termed a regressive disorder as it begins with a typical postnatal development period but later deviates to a loss of acquired skills around the ages of 1.5-3 years. The loss includes expressive language, fine motor skills, social interactions and responsiveness. Rett’s is further accompanied by gastrointestinal abnormalities, seizures and global cognitive and motor delays. •Child disintegrative disorder (CDD): CDD is also a regressive disorder but is considered very rare, cases are between 1.1-9.2 per 100,000. Regression in CDD occurs rapidly and can involve high levels of fear and hallucinations in the individual at onset. The loss also comprises adaptive skills such as bowel and bladder control. •Asperger syndrome: Asperger's constitutes high levels of cognitive function, very literal communication, inappropriate social interactions and issues with interpreting implied meaning. However, there are no delays in language and IQ is either average or above.
EEG patterns trained in ASD brains
Coben et al. 2007 demonstrated that children with autism displayed greater alpha and beta coherence but less interhemispheric and intra-hemispheric asymmetry. Thus, they theorised that normalising connectivity should improve autistic symptoms. The results demonstrated that personalised protocols based on connectivity-guided neurofeedback led to improved connectivity and a 45% reduction in autistic symptoms. These findings have been replicated. For example, Coby and Padolsky 2007 obtained a 40% reduction in autistic symptoms and hypercoherence, followed by an enhancement in neuropsychological functions after 20 sessions. Neurofeedback appears promising in connectivity, as it uses operant conditioning to exercise and strengthen desired network connections and diminish undesired connections.
Low frequency bands: Decrease theta & increase SMR
Low-frequency waves are also targeted in neurofeedback, as attenuated cortical excitability with excessive slow-wave activity (within the frontal regions) and a diminished alpha power band are observed in ASD. Kouijzer et al. carried out several studies in this domain after past research demonstrated that increasing low beta and decreasing theta attenuates ASD symptomology and promotes brain flexibility via; 1. enhancing medial prefrontal brain activation and 2. enhancing the flexibility of the default mode network’s activation, which improves executive functions. The team found that inhibiting theta and increasing beta activation reduced the heightened theta/beta ratio and improved ASD symptomology. What is significant about the improvements is that they were not observed in the age, sex and IQ-matched control group. Additionally, the improvements in executive functioning that occurred immediately after the neurofeedback treatment either persisted or further improved 12 months after training.
Mu rhythm training
As previously mentioned, social deficits in ASD are suggested to involve the human mirror neuron system. In normal conditions, mu power around the sensorimotor cortex is suppressed during the observation, imagination and execution of body movements. Mu suppression is accompanied by the activation of regions linked to the hMNS. In ASD however, it has been observed that mu rhythm is absent during the observation of body movements unless the observed or imitated person is familiar to the individual with ASD. Datko et al. performed 20 hours of mu-rhythm neurofeedback targeting the sensorimotor cortex in children. When assessing the results via fMRI, the ASD group displayed increased activation in brain regions containing the hMNS, e.g., the inferior parietal lobe (IPL). The IPL is involved in sensorimotor integration, perception and performance of goal-directed actions. Thus, increased IPL activation suggests that Neurofeedback treatment enhanced visuomotor integration during imitation. These brain changes were accompanied by behavioural improvements.
Targeting ASD symptoms
40% of individuals with ASD have comorbid anxiety that comprises both typical and autism-related anxiety. Examples of autism-related anxiety are concerns about sensory stimuli, worries concerning change or unpredictable situations and uncommon but specific phobias. Neurofeedback training targets lowering anxiety bu training down overactivation of the limbic system. Please follow the relevant links to read more about it.
Autism's impact on the Brain
Autism is observed to impact several brain regions. Social disruptions in ASD are likely generated by abnormalities in brain networks associated with social cognition, action perception and the human mirror neuron system (hMNS). The hMNS plays a significant role in vicarious learning and the ability to understand the intentions and actions of others via imitation. Whereas issues with executive functioning, e.g., the inability to shift attention and perseveration, are tied to frontal lobe dysfunction. The attention to detail observed in ASD is suggested to be the result of weak central coherence. A weak central coherence results in a preference for focusing on local detail rather than global processing. Magnetic resonance imaging (MRI) is significant in highlighting some of the many ways ASD impacts the brain's structure. MRI findings have shown reduced total grey matter volume and white matter reduction in the cerebellum, the left internal capsule and fornix. In addition to abnormal metabolites in the amygdala-hippocampal region. Another vital neuroimaging tool that provides aid to better understanding ASD is positron emission tomography (PET). PET has been used to identify atypical activation within the fusiform gyrus, insula, parahippocampal gyrus, amygdala, cerebellum and the medial and orbital sites of the frontal lobe. Due to the complexity of ASD, e.g., the vast array of brain regions and mechanisms associated with the pathology, several neurofeedback (NFT) protocols are investigated.