The science of distraction. How “brain filters” explain inattention in ADHD and autism
In this post, I continue our series on how neurocognitive models not only offer a holistic view of the neurodevelopmental conditions we see in our clinical practice, but also provide a powerful lens for interpreting the symptoms we observe.
Crucially, this approach transcends categorical diagnoses by adopting a truly transdiagnostic framework. Dimensional models, such as the Research Domain Criteria (RDoC) aim to identify shared neural and genetic substrates, mapping constructs like “attention” across multiple level of analyses: from the “micro” (genes, molecules, cells) through “macro”, such neural circuits and physiological processes, right up to observable behaviours. A neurocognitive model applies this same philosophy in a more streamlined form, prioritising the macro scale, from brain circuit systems and physiology to cognitive functions and behavioural outcomes.
In cases of inattention, for example, a neurocognitive framework allows us to make sense of our clients’ experiences and to give them clear, meaningful feedback.
Inattentiveness manifests across numerous neurodevelopmental conditions, most notably ADHD and autism (albeit in the latter is not a diagnostic feature), and can present in many different ways. During any diagnostic assessment, it is essential to pinpoint how inattention shows itself, when it occurs and why, and to identify its specific triggers. I will examine those distinctions in greater detail in a future post, as they are crucial for an accurate differential diagnosis or to screen for possible comorbidities. Here, however, I want to focus on one key contributor to inattention that can be explored in a transdiagnostic fashion using a neurocognitive model approach: distractibility.
The Dual Nature of Distractibility: External and Internal Distractions
First, using this model already helps in dissecting the construct into its constituent parts. In fact, cognitive science defines distractibility as a multicomponent entity: (a) an inability to sustain focus because irrelevant stimuli capture attention; (b) a propensity to orient towards or react to non-pertinent information; and (c) a failure of inhibitory control over responses to distractions. Analysing the definition then two common themes emerge: distractibility involves difficulty filtering out environmental inputs and difficulty suppressing internally generated distractions.
External distractors include ambient sounds, movements, touch, or other sensory inputs unrelated to the task. Internal distractors consist of spontaneous thoughts, worries, intrusive memories or daydreaming. In other words, goal-directed activities can be derailed by interference from irrelevant stimuli in the external environment and similarly by thoughts, emotions, and urges from one’s own mind. Distractions can come from without or within, and both can impact attention. In more details external distractions can be any sensory input (visual, auditory, etc.) that pulls attention away. Internal distractions can be thought intrusions (automatic thoughts or images that break one’s focus, repetitive negative thinking (rumination, worry), persistent, hard-to-control thoughts that consume cognitive resources), mind-wandering, spontaneous shifts of attention away from a task toward unrelated inner content, and even mind-blanking which are transient, meta-aware lapses (you know you are not thinking), lasting generally only a few seconds, during which one experiences a subjective absence of any conscious thought content.
Sensory Gating and Executive Filters: Keeping Distraction in Check
Brains possess executive and sensory filters that actively block or dampen those distractors. Executive processes are top-down functions that are modulating signals when they have already reached central components of the CNS, for instance engaging the prefrontal cortex (PFC) and its networks can maintain attention on task-relevant information and suppress distractions. In addition, there are also more peripheral processes, bottom-up, pre-attentive mechanism, meaning they operates at early stages of sensory processing, to filter out redundant or irrelevant inputs before they reach higher cortical areas.
Sensory gating is a prime example: it is a physiological process that suppresses neural responses to repetitive or irrelevant stimuli. One common way to measure it is via auditory sensory-gating test, which uses EEG to record brain waves. In this test you hear two identical clicks through headphones about half a second apart. Electrodes on the scalp pick up the brain’s response to each click, called event-related potentials or ERPs. We focus on the P50 wave, a small positive blip that shows up roughly fifty milliseconds after a click. In people with typical sensory filtering, the P50 response to the second click is much smaller, often half the size, because the brain has already “seen” the sound and filters it out. This reduction, called P50 suppression, shows that the brain is quickly ignoring repetitive, unimportant noises. Gating is thought to prevent “sensory overload” by inhibiting the processing of uninformative inputs.
Neural Circuits and Neurotransmitters in Sensory Gating
Neuroscience has pinpointed several brain regions and neurotransmitter systems underlying sensory gating and distraction control. Key structures include the prefrontal cortex (especially dorsal and ventrolateral PFC), the hippocampus, and early sensory areas for instance, for auditory stimuli, Heschl’s gyrus (primary auditory cortex). The PFC is thought to exerts top down inhibitory influence contributing to suppress responses in sensory cortices when stimuli are deemed irrelevant. The hippocampus and is also implicated in gating, possibly by helping to determine stimulus novelty.
Neurochemically, attention and sensory filtering rely on dopamine and noradrenaline, while cholinergic mechanisms, particularly activation of nicotinic α7 receptors that dampens responses to repeated stimuli, also play a key role in gating. In sum, effective filtering involves a network of PFC–hippocampal circuitry modulated by neurotransmitters like DA, NA, and acetylcholine.
From Sensory Gating to Inattention across ADHD and Autism
When these filters are weak or immature, distractors may intrude, and challenges arise in regulating attention and to inhibit distraction by irrelevant stimuli. In clinical terms, a gating dysregulation means that even subtle stimuli (e.g. a faint sound or a passing thought) can break focus. For example, a page of text may remain unread because attention keeps snapping to a minor noise or gets distracted by constant flux of new thoughts.
Some evidence shows that these neural filters may indeed be altered in ADHD showing that individuals with ADHD have reduced P50 suppression compared to controls. In other words, ADHD may struggle to “tune out” redundant sounds, which in turn may trigger overload. This finding aligns with many clinical reports of hypersensitivity to noise and difficulty concentrating in ADHD. Other ERP components (e.g. N100, P300) are also often attenuated or delayed in ADHD, reflecting broader attention-control dysregulations. Importantly, administering stimulant medication normalized some of these gating measures, linking the electrophysiology to the known pharmacology.
Also, in autism some studies do find sensory gating differences: for instance, individuals with autism can show abnormal oscillatory responses to repeated sounds. However, other studies fail to replicate these results. Notably, several papers have reported that individuals with high functioning autism display reduced P50 amplitude. Thus, while sensory overload is common in autism, classic P50 gating deficits are not as consistently observed as in ADHD. It may be that ASD involves more complex processing issues such as altered connectivity, local over or under connectivity, or atypical sensory integration rather than a single gating dysregulation. As I discussed in a previous post, the presence of different clinical presentations within autism may mean that sensory gating abnormalities appear only in specific subgroups. Hence, further research with more homogeneous samples is required.
Conclusions
From a neurocognitive standpoint, distractibility can be viewed, at least in part, as a dysregulation of the brain’s sensory-gating mechanisms. Generally speaking, internally and externally driven distractions are kept at bay by networks involving the prefrontal cortex, hippocampus and sensory cortices, tuned by neurotransmitters such as dopamine and acetylcholine. In ADHD, and, to a degree, in ASD, these inhibitory mechanisms may be altered, leading to sensory-gating dysregulation that can help, again at least in part, explain distractibility and, in turn, inattention.
For clinicians, this framework connects a symptom (“my patient is so distractible”) into a tangible mechanism. Understanding that, say, weaker gating may underlie our patients’ distractibility gives meaning and may guide treatment (e.g. targeting DA/NE or increase “barriers” to irrelevant stumuli). By “increasing barriers” to irrelevant stimuli, we mean introducing simple strategies that help compensate for weak sensory gating, for instance, modifying the environment to reduce background noise or distractions, or using more complex behavioural techniques such as discrimination training, which teaches patients to focus on relevant information while ignoring competing sensory input.
Ultimately, by highlighting the shared neurocognitive roots of attention problems across conditions, we move toward a precision psychiatry that treats each symptom in context of brain-behaviour biology.
Want to explore further? See:
Kas MJH et al. (2025) Mol Psychiatry • Madsen GF et al. (2015) Autism Res • Martinez S et al. (2024) Front Psychiatry • Michelini G et al. (2024) World Psychiatry • Micoulaud-Franchi JA et al. (2015) Biol Psychol • Patil O, Kaple M (2023) Cureus • Zhang H et al. (2023) PLoS One • Ziegler DA et al. (2018) Sci Rep
Author:
Dr Valentino A. Pironti
Senior Clinical Psychologist | Cognitive Neuroscientist
Specialist in Adult ADHD & Autism
Clinical Director, Cambridge Adult ADHD & ASD Clinic
#ADHD #Autism #Neurodevelopmental #Attention #SensoryGating #Distractibility #ClinicalNeuroscience #Transdiagnostic #Neurocognitive #PrecisionPsychiatry
The science of distraction. How “brain filters” explain inattention in ADHD and autism
In this post, I continue our series on how neurocognitive models not only offer a holistic view of the neurodevelopmental conditions we see in our clinical practice, but also provide a powerful lens for interpreting the symptoms we observe.
Crucially, this approach transcends categorical diagnoses by adopting a truly transdiagnostic framework. Dimensional models, such as the Research Domain Criteria (RDoC) aim to identify shared neural and genetic substrates, mapping constructs like “attention” across multiple level of analyses: from the “micro” (genes, molecules, cells) through “macro”, such neural circuits and physiological processes, right up to observable behaviours. A neurocognitive model applies this same philosophy in a more streamlined form, prioritising the macro scale, from brain circuit systems and physiology to cognitive functions and behavioural outcomes.
In cases of inattention, for example, a neurocognitive framework allows us to make sense of our clients’ experiences and to give them clear, meaningful feedback.
Inattentiveness manifests across numerous neurodevelopmental conditions, most notably ADHD and autism (albeit in the latter is not a diagnostic feature), and can present in many different ways. During any diagnostic assessment, it is essential to pinpoint how inattention shows itself, when it occurs and why, and to identify its specific triggers. I will examine those distinctions in greater detail in a future post, as they are crucial for an accurate differential diagnosis or to screen for possible comorbidities. Here, however, I want to focus on one key contributor to inattention that can be explored in a transdiagnostic fashion using a neurocognitive model approach: distractibility.
The Dual Nature of Distractibility: External and Internal Distractions
First, using this model already helps in dissecting the construct into its constituent parts. In fact, cognitive science defines distractibility as a multicomponent entity: (a) an inability to sustain focus because irrelevant stimuli capture attention; (b) a propensity to orient towards or react to non-pertinent information; and (c) a failure of inhibitory control over responses to distractions. Analysing the definition then two common themes emerge: distractibility involves difficulty filtering out environmental inputs and difficulty suppressing internally generated distractions.
External distractors include ambient sounds, movements, touch, or other sensory inputs unrelated to the task. Internal distractors consist of spontaneous thoughts, worries, intrusive memories or daydreaming. In other words, goal-directed activities can be derailed by interference from irrelevant stimuli in the external environment and similarly by thoughts, emotions, and urges from one’s own mind. Distractions can come from without or within, and both can impact attention. In more details external distractions can be any sensory input (visual, auditory, etc.) that pulls attention away. Internal distractions can be thought intrusions (automatic thoughts or images that break one’s focus, repetitive negative thinking (rumination, worry), persistent, hard-to-control thoughts that consume cognitive resources), mind-wandering, spontaneous shifts of attention away from a task toward unrelated inner content, and even mind-blanking which are transient, meta-aware lapses (you know you are not thinking), lasting generally only a few seconds, during which one experiences a subjective absence of any conscious thought content.
Sensory Gating and Executive Filters: Keeping Distraction in Check
Brains possess executive and sensory filters that actively block or dampen those distractors. Executive processes are top-down functions that are modulating signals when they have already reached central components of the CNS, for instance engaging the prefrontal cortex (PFC) and its networks can maintain attention on task-relevant information and suppress distractions. In addition, there are also more peripheral processes, bottom-up, pre-attentive mechanism, meaning they operates at early stages of sensory processing, to filter out redundant or irrelevant inputs before they reach higher cortical areas.
Sensory gating is a prime example: it is a physiological process that suppresses neural responses to repetitive or irrelevant stimuli. One common way to measure it is via auditory sensory-gating test, which uses EEG to record brain waves. In this test you hear two identical clicks through headphones about half a second apart. Electrodes on the scalp pick up the brain’s response to each click, called event-related potentials or ERPs. We focus on the P50 wave, a small positive blip that shows up roughly fifty milliseconds after a click. In people with typical sensory filtering, the P50 response to the second click is much smaller, often half the size, because the brain has already “seen” the sound and filters it out. This reduction, called P50 suppression, shows that the brain is quickly ignoring repetitive, unimportant noises. Gating is thought to prevent “sensory overload” by inhibiting the processing of uninformative inputs.
Neural Circuits and Neurotransmitters in Sensory Gating
Neuroscience has pinpointed several brain regions and neurotransmitter systems underlying sensory gating and distraction control. Key structures include the prefrontal cortex (especially dorsal and ventrolateral PFC), the hippocampus, and early sensory areas for instance, for auditory stimuli, Heschl’s gyrus (primary auditory cortex). The PFC is thought to exerts top down inhibitory influence contributing to suppress responses in sensory cortices when stimuli are deemed irrelevant. The hippocampus and is also implicated in gating, possibly by helping to determine stimulus novelty.
Neurochemically, attention and sensory filtering rely on dopamine and noradrenaline, while cholinergic mechanisms, particularly activation of nicotinic α7 receptors that dampens responses to repeated stimuli, also play a key role in gating. In sum, effective filtering involves a network of PFC–hippocampal circuitry modulated by neurotransmitters like DA, NA, and acetylcholine.
From Sensory Gating to Inattention across ADHD and Autism
When these filters are weak or immature, distractors may intrude, and challenges arise in regulating attention and to inhibit distraction by irrelevant stimuli. In clinical terms, a gating dysregulation means that even subtle stimuli (e.g. a faint sound or a passing thought) can break focus. For example, a page of text may remain unread because attention keeps snapping to a minor noise or gets distracted by constant flux of new thoughts.
Some evidence shows that these neural filters may indeed be altered in ADHD showing that individuals with ADHD have reduced P50 suppression compared to controls. In other words, ADHD may struggle to “tune out” redundant sounds, which in turn may trigger overload. This finding aligns with many clinical reports of hypersensitivity to noise and difficulty concentrating in ADHD. Other ERP components (e.g. N100, P300) are also often attenuated or delayed in ADHD, reflecting broader attention-control dysregulations. Importantly, administering stimulant medication normalized some of these gating measures, linking the electrophysiology to the known pharmacology.
Also, in autism some studies do find sensory gating differences: for instance, individuals with autism can show abnormal oscillatory responses to repeated sounds. However, other studies fail to replicate these results. Notably, several papers have reported that individuals with high functioning autism display reduced P50 amplitude. Thus, while sensory overload is common in autism, classic P50 gating deficits are not as consistently observed as in ADHD. It may be that ASD involves more complex processing issues such as altered connectivity, local over or under connectivity, or atypical sensory integration rather than a single gating dysregulation. As I discussed in a previous post, the presence of different clinical presentations within autism may mean that sensory gating abnormalities appear only in specific subgroups. Hence, further research with more homogeneous samples is required.
Conclusions
From a neurocognitive standpoint, distractibility can be viewed, at least in part, as a dysregulation of the brain’s sensory-gating mechanisms. Generally speaking, internally and externally driven distractions are kept at bay by networks involving the prefrontal cortex, hippocampus and sensory cortices, tuned by neurotransmitters such as dopamine and acetylcholine. In ADHD, and, to a degree, in ASD, these inhibitory mechanisms may be altered, leading to sensory-gating dysregulation that can help, again at least in part, explain distractibility and, in turn, inattention.
For clinicians, this framework connects a symptom (“my patient is so distractible”) into a tangible mechanism. Understanding that, say, weaker gating may underlie our patients’ distractibility gives meaning and may guide treatment (e.g. targeting DA/NE or increase “barriers” to irrelevant stumuli). By “increasing barriers” to irrelevant stimuli, we mean introducing simple strategies that help compensate for weak sensory gating, for instance, modifying the environment to reduce background noise or distractions, or using more complex behavioural techniques such as discrimination training, which teaches patients to focus on relevant information while ignoring competing sensory input.
Ultimately, by highlighting the shared neurocognitive roots of attention problems across conditions, we move toward a precision psychiatry that treats each symptom in context of brain-behaviour biology.
Want to explore further? See:
Kas MJH et al. (2025) Mol Psychiatry • Madsen GF et al. (2015) Autism Res • Martinez S et al. (2024) Front Psychiatry • Michelini G et al. (2024) World Psychiatry • Micoulaud-Franchi JA et al. (2015) Biol Psychol • Patil O, Kaple M (2023) Cureus • Zhang H et al. (2023) PLoS One • Ziegler DA et al. (2018) Sci Rep
Author:
Dr Valentino A. Pironti
Senior Clinical Psychologist | Cognitive Neuroscientist
Specialist in Adult ADHD & Autism
Clinical Director, Cambridge Adult ADHD & ASD Clinic
#ADHD #Autism #Neurodevelopmental #Attention #SensoryGating #Distractibility #ClinicalNeuroscience #Transdiagnostic #Neurocognitive #PrecisionPsychiatry
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