Sensory–Amygdala Hyperactivation Loop

🧠 Overview

The “Sensory–Amygdala Hyperactivation Loop” is a state in which the human brain is stuck in a mode of sensory hyper-responsivity, to the point that it becomes a chronic loop between the sensory input system and the amygdala, which is the central hub for processing threat and fear in the limbic system.

Under normal conditions, our brain filters out unnecessary stimuli via the pathway thalamus → cortex → amygdala, allowing us to distinguish whether “this is safe” or “this is dangerous” before we respond. But in this loop state, the direct pathway from the thalamus to the amygdala (the low road) dominates the system, making processing faster and stronger, to the point that it skips the reasoning step.

When any sound, light, or tactile sensation comes in, an over-reactive amygdala automatically interprets it as a threat, sends alarm signals to the autonomic nervous system, and activates the hypothalamus–pituitary–adrenal (HPA) axis to release cortisol and adrenaline.

The result is a racing heart, bodily tension, muscle contraction, and total attentional focus on the “stimulus,” creating the feeling that the external world is attacking from all sides, even if it is only the sound of a fan or the light from a screen.

A brain that has entered this state will increase sensory gain in the sensory cortex, making every sound, every light, and every touch feel much more intense than before. The more input it receives, the more reactive the amygdala becomes → creating a loop of “more fear → more sensitivity → more exhaustion.”

Research on Sensory Over-Responsivity (SOR) and Sensory Processing Sensitivity (SPS) shows that people caught in this loop tend to have heightened co-activation of the amygdala, insula, anterior cingulate cortex, and sensory cortices compared to average, and they display reduced habituation to stimuli—meaning their heightened sensitivity persists even after the trigger is gone.

When this loop is repeated frequently, the brain develops negative neural plasticity—the nervous system learns that “staying on guard = staying safe” and stores this behavior as its default mode, causing the person to exist in a state of chronic hyperarousal.

In the long term, this state can lead to neuro-fatigue (brain exhaustion) and abnormally high emotional hypersensitivity, because the brain never gets a real break from processing sensory input.

Many people in this state don’t realize what’s happening, because it’s not caused by one big dramatic event, but by the accumulation of small stimuli that flood the nervous system every day—notification sounds, screen light, or simply being in crowded places.

Psychologically, this results in fear without a clear reason, irritation without a clear cause, and exhaustion despite not doing anything “heavy,” because so much mental energy is spent processing imagined threats rather than creativity or rest.

The “Sensory–Amygdala Hyperactivation Loop” is therefore not a disease, but a protective mechanism of the brain that has become stuck in alarm mode, unable to reset itself back to a balanced state.

Understanding this loop is crucial, because it explains why some people feel drained so easily in everyday environments, and why sensory sensitivity so often co-occurs with chronic anxiety.

On the positive side, people whose systems are highly sensitive in this way often have above-average abilities in noticing fine details, understanding others’ emotions, and creative thinking—but on the negative side, they are at high risk of sensory burnout if they do not know how to let their nervous system rest properly.

In summary, the “Sensory–Amygdala Hyperactivation Loop” is an emotion–sensory–body loop that keeps the brain in an over-perceptive state, so that fear and fatigue become the underlying tone of daily life—and if left unaddressed, it can ultimately lead to depression, anxiety, or chronic neural exhaustion.

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🧩 Core Symptoms

The Sensory–Amygdala Hyperactivation Loop presents with core symptoms that blend between the sensory input system and the threat–emotion system, producing responses that exceed the brain’s normal balance and crystallize into a chronic pattern embedded in both body and brain.

1. Sensory Symptoms

The central feature is “sensory hyper-responsivity”—the brain is over-sensitive to stimuli, unlike most people whose sensory filtering (thalamic filtering) works normally. In this state, however, the brain turns up the gain on sensory signals across every channel.

People caught in this loop often describe it as, “The world sounds louder, the light feels harsher, or it’s like everything hits me at once and my brain can’t process it.” This reflects abnormal co-activation between the sensory cortices, insula, and amygdala.

Key examples include:

• Being highly sensitive to voices, machinery noise, traffic sounds, typing on a typewriter, or even the sound of someone chewing.
• Feeling pain in the ears or intense irritation when hearing high-frequency sounds (e.g., whistles, electronic whine).
• Fluorescent lighting, smartphone screens, or bright lights in malls cause headaches or dizziness.
• Aversion to certain textures, such as silk, wool, or clothing labels at the back of the neck.
• Bodily discomfort even from light touches, like someone brushing past or minor loud sounds.

These experiences lead to what is called “sensory flooding”—the brain is bombarded with more sensory data than its processing capacity (processing overload), causing dizziness, mental numbness, or a strong urge to escape from that environment immediately.

At the brain level, this group tends to show hyperactivation in the auditory/visual cortex and the amygdala when exposed to stimuli. Even non-threatening stimuli, like the sound of an air conditioner or fluorescent lighting, can trigger the alarm system as if it were an explosion.

2. Emotional State

The emotional system of people in this loop operates on a foundation of “false alarms”—an over-reactive amygdala sends out danger signals every time it encounters stimuli previously associated with discomfort or fear.

Common emotional manifestations include:

• Severe anxiety when hearing sounds that once caused intense fear, such as arguments, car crashes, or slamming doors.
• Feeling “as if being attacked” even when the situation is objectively safe.
• Dramatic emotional shifts in response to minor stimuli—calm → stressed → angry → exhausted within seconds.
• After a trigger, the emotional reaction lingers for hours or even days, long after the stimulus has disappeared.

Internally, the brain is in a hyperarousal state—the body remains stuck in fight-or-flight mode almost all the time, so it cannot properly re-enter the rest-and-digest state.

Over time, this constant sense of being “on guard” becomes covert stress, which leads to easy exhaustion, brain fog, and insomnia, because the sympathetic nervous system is working overtime day and night.

Brain imaging studies (fMRI) show that when the amygdala is repeatedly activated:

• The brain develops increased functional connectivity between the amygdala, insula, and ACC,
• And reduced inhibition from the prefrontal cortex (especially vmPFC and dlPFC).

The result is that the “fear–anxiety–irritability” loop gets used so often that it becomes a fixed pattern.

People in this loop therefore often say, “I don’t know why my emotions spike so easily—my brain feels like it has no room to breathe.” That’s because the upper emotional filter (frontal inhibition) is being suppressed by an amygdala stuck in threat mode.

3. Behavioral Responses

Behavioral symptoms are the outer expression of a brain trying to protect itself.

Many people gradually develop avoidance patterns, such as:

• Avoiding malls, restaurants, or meetings that are noisy.
• Wearing noise-cancelling headphones almost all the time, even at home, to avoid disruptive sounds.
• Wearing sunglasses indoors, or arranging their room to be darker than usual.
• When avoidance is impossible, they may experience meltdowns (emotional outbursts) or shutdowns (going silent, motionless, withdrawn).
• Some may snap at close others unintentionally because accumulated stress is so high that the brain can no longer regulate its responses.

Avoidance is a short-term survival strategy, but in the long run it reinforces the brain’s belief that “stimuli = danger”, making the loop even stronger.

4. Cognitive Symptoms

The brain in this state operates in hypervigilance mode—like a radar spinning constantly to scan for threats, leading to:

• Overthinking and constant, often unconscious threat assessment of the environment.
• Inability to sustain focus on one thing for long.
• Rapid mental fatigue and a sense of “brain fog” after spending time in highly stimulating places like malls or noisy workplaces.
• A tendency to interpret stimuli negatively—for example, a ringing phone = bad news, a door slam = someone is angry.
• Reduced capacity for abstract thinking during periods when the emotional system dominates.

This is the phenomenon of “cognitive hijacking”—the limbic system (emotion circuitry) seizes control from the frontal lobes (reasoning), making it feel as if mental processing power has been taken over.

5. Somatic / Autonomic Symptoms

Because the amygdala has direct connections with the hypothalamus and the autonomic nervous system, whenever this loop is triggered, the body reacts immediately, for example:

• Rapid heartbeat, sweating, cold hands, shallow or rapid breathing.
• Headaches or migraines triggered by light and sound.
• Chest tightness, a lump in the throat, or dizziness without any clear medical cause.
• Fatigue and lack of energy even after waking up, because the body spent the night in “threat mode.”

In some cases, a “somatic loop” develops, where bodily sensations trigger the amygdala in return—for example, racing heart → the brain interprets it as danger → anxiety increases → the heart beats even faster—forming a loop within a loop.

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🧠 Diagnostic Criteria 

Important note:
This condition does not yet exist as a formal diagnosis in DSM-5 or ICD-11. The idea is used to describe the mechanisms of a “sensory–emotion dysregulation loop.”
It is therefore a conceptual clinical framework that helps us understand the pattern and recognize the cluster of symptoms in each individual.

A. Chronic Sensory Hyper-Responsivity

People caught in this loop show hyper-responsive reactions to stimuli in at least two sensory modalities, such as sound + light, or touch + smell. Key features include:

• Over-reactive responses to stimuli that most people do not perceive as problematic.
• Symptoms persisting for at least 6 months.
• A tendency to experience sensory overload in highly stimulating environments such as malls, schools, or offices.

This reflects an imbalance in sensory gating at the level of the thalamus and amygdala, which normally filter out irrelevant input before passing it on to higher brain regions.

B. Association with Fear/Anxiety or a Sense of Threat

Sensory sensitivity in this condition is not just annoyance; it is tightly linked with fear.

• Every time a stimulus appears, the brain responds as if a genuine emergency were happening.
• There is a rapid surge of adrenaline and cortisol.
• Some individuals even experience panic attacks or flashbacks if the stimulus is tied to a past adverse event.
• There is a chronic feeling that “my brain is constantly over-warning me.”

The resulting emotion is therefore not just ordinary anxiety, but sensory-induced fear, arising from a direct linkage between perception and the amygdala.

C. Patterns of Avoidance or Ritualized Environmental Control

People in this state develop behaviors to control stimuli so they can feel safe, such as:

• Avoiding loud or brightly lit places.
• Always carrying headphones, or checking sound levels before entering a room.
• Having small rituals—like turning on a fan at a low setting to mask other sounds.
• Checking lights/temperature/smells in the room every night before bed.

These behaviors calm the brain in the short term but, over time, reinforce the belief that “stimuli = danger”, causing the amygdala to become even more reactive.

D. Impact on Daily Functioning

This condition deeply affects quality of life, for example:

• Decreased concentration, difficulty working in offices or studying in classrooms.
• Avoidance of social activities, leading to isolation.
• Persistent fatigue, mental exhaustion, and poor sleep because the nervous system never truly switches off.
• Strained relationships, as others may perceive the person as “easily annoyed” or “emotionally unstable.”

These accumulated psychological impacts can develop into depression, low self-worth, or full-blown neuro-burnout.

E. Differential Diagnosis and Comorbidity

It is important to distinguish this pattern from similar conditions, such as:

• Psychosis or mania, where perception itself is distorted.
• Substance intoxication, e.g., excess caffeine or stimulant drugs.
• Acute neurological conditions, such as migraine aura or epilepsy.

However, this pattern often co-occurs (is comorbid) with other disorders, such as:

• ASD (Autism Spectrum Disorder): pronounced sensory over-responsivity and amygdala hyperconnectivity.
• ADHD: sensory gating deficits and hypervigilance due to dopamine imbalance.
• Anxiety Disorders / PTSD: threat system circuits are repeatedly activated.
• Migraine: the nervous system is hypersensitive to light and sound due to cortical spreading depression.

Conceptual Summary of the Criteria

To simplify, this condition can be recognized by four key patterns:

1️⃣ The brain is hypersensitive to at least two sensory channels (sound, light, touch).
2️⃣ The responses are tied to fear or stress.
3️⃣ There are avoidance behaviors or rituals to modify the environment.
4️⃣ Symptoms significantly affect quality of life or relationships.

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🔍 Mechanistic Summary

The “Sensory–Amygdala Hyperactivation Loop”
= a brain calibrated to “detect danger before thinking.”

Because the sensory system constantly fires signals into the amygdala, the loop of “feel → fear → react → become even more sensitive” becomes a pattern the brain adopts as its new normal.

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Subtypes or Specifiers

For writing and psychoeducational purposes, the pattern can be conceptually divided into specifiers:

1. Threat-Dominant Type

• The focus is on “fear” and “threat.”
• Small sounds become signals that “something bad is going to happen.”
• Closely resembles the anxiety / PTSD spectrum, with very high hypervigilance.
• Corresponds to findings that the amygdala and fear circuits are overactive in anxiety disorders and post-traumatic stress disorders (PTSD). PMC+1

2. Irritability-Dominant Type

• The core emotion is “irritation–anger” rather than fear.
• Loud sounds/stimuli = feeling “invaded” or “having personal space violated.”
• Often expressed as snapping, lashing out, or emotional outbursts in highly stimulating environments.
• May be linked to deficits in emotion regulation.

3. Social-Cue Hyperactivation Type

• Highly sensitive to social stimuli such as conversations, laughter, eye contact, facial expressions.
• The amygdala shows heightened activation when viewing others’ faces or emotions—similar to what is seen in SPS and partially in ASD. PMC+1
• Tends to interpret others’ facial expressions/tone of voice negatively → feeling judged or disliked → entering a social loop of avoidance and anxiety.

4. Interoceptive Hyperactivation Type

• Hypersensitive to internal bodily sensations, such as a racing heart, sweating, or chest tightness.
• The amygdala has learned that bodily sensations = danger → leading to panic or health anxiety.
• Similar to patterns in panic disorder, where internal signals are catastrophically misinterpreted.

5. Mixed / Trauma-Linked Type

• Contains a mixture of fear, irritation, and dissociation.
• Often associated with a history of trauma or abuse in loud/chaotic environments.
• Certain stimuli act as “trauma cues” → sending intense input into the amygdala–hippocampus loop. PMC+1

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🧠 Brain & Neurobiology

1. Sensory Pathways to the Amygdala

The brain systems involved in the Sensory–Amygdala Hyperactivation Loop function like two expressways connecting the external world directly to inner emotion.

When a stimulus (sound, light, smell, touch) arrives, the signal passes through the thalamus, the central relay hub for sensory information (with the exception of smell, which can project directly to the amygdala without passing through the thalamus). From there, the thalamus sends information to the amygdala via two main routes:

Low Road (Thalamus → Amygdala):

• Short, fast, and crude.
• An automatic alarm system that lets us react before we think. For example, when we see a dark shape, this system triggers a startle response before the rational part of the brain evaluates whether it’s a person or just a lamppost.
• In people with hyperactivation, this “low road” is overly active and bypasses filtering, so even minor stimuli are interpreted as dangerous.

High Road (Thalamus → Sensory Cortex → Association Cortex → Amygdala):

• Slower but more accurate.
• Involves context evaluation—Where is this light coming from? Is this sound actually safe?
• In a healthy brain, the high road double-checks signals from the low road before a final decision. But when the system is exhausted or overused, the high road gets “switched off”—as if the brain cuts out the reasoning step and leaves only raw emotional reactions.

When the amygdala is repeatedly activated by stimuli without sufficient rest, the system undergoes neural sensitization—fear circuits within the amygdala become stronger (synaptic potentiation) while inhibitory control from the prefrontal cortex weakens (top-down inhibition failure).
The result is a brain that responds too quickly and is hard to stop—like an alarm that keeps ringing even when there is no smoke.

2. Relationship Between the Sensory Cortices and Amygdala

Research on Sensory Over-Responsivity (SOR) shows that brains of highly sensitive individuals often exhibit strong co-activation of the sensory cortices, insula, anterior cingulate cortex (ACC), and amygdala.

This co-activation has three key characteristics:

• Increased Sensory Gain: the brain amplifies sensory signals so that mild stimuli become intense.
• Reduced Habituation: the brain does not “get used to” stimuli even with repetition—for instance, the hum of an air conditioner remains loud every time.
• Emotional Amplification: the amygdala repeatedly tags those stimuli with fear/irritation every time they are perceived.

When this occurs over and over, the brain forms emotional memory traces in the hippocampus, binding specific stimuli to fear. The response then becomes automatic, requiring no conscious reasoning.

In fMRI scans, we see clear activation in the amygdala, insula, hippocampus, primary auditory/visual cortex, and prefrontal areas—the same pattern observed in anxiety, ASD, and high sensitivity traits.

3. Limbic System and the Threat System

The limbic system is the hub of emotion, memory, and threat perception. It includes the amygdala, hippocampus, hypothalamus, cingulate gyrus, and parts of the orbitofrontal cortex.

When this system is over-activated, it becomes a Threat System Loop cycling between:

• Threat detection by the amygdala.
• Emotional memory encoding by the hippocampus.
• Bodily responses via the hypothalamus (through the autonomic nervous system).

When the Threat System is often triggered—by daily noise, frequent alerts, or repeated stimuli—the brain shifts into Survival Mode more and more easily.
Symptoms include rapid heartbeat, easy sweating, irritability, fatigue, and a brain that refuses to enter the parasympathetic (rest) state.

Many studies compare the amygdala to the “brain’s smoke detector”—overly sensitive to even tiny traces of “smoke.”
When minor stimuli appear, it interprets them as fire and turns on the entire alarm system, leaving the “user” of the brain (us) exhausted without knowing why.

Thus, the Sensory–Amygdala Hyperactivation Loop is essentially this smoke detector “stuck in chronic panic,” triggered by pseudo-smoke from everyday stimuli: notification sounds, lights, screens, or even our own thoughts.

4. Neurochemical Systems Involved

The functions of the amygdala and sensory systems depend on the balance of several neurotransmitters:

• Glutamate: the primary excitatory neurotransmitter. Excess levels drive neural over-arousal and excitotoxicity—often seen in individuals with high sensory sensitivity.
• GABA: the main inhibitory neurotransmitter. If levels are low, the brain cannot effectively dampen sensitivity after stimulation.
• Norepinephrine (NE): increases alertness; chronic stress raises NE, pushing the brain into an ongoing alert state.
• Cortisol: the stress hormone. Frequent release causes hippocampal shrinkage and reduces its ability to regulate and contextualize amygdala activity.
• Serotonin & Dopamine: regulate mood and our ability to “frame” experiences. Deficits heighten the threat system’s reactivity.

5. Neuroplasticity and a Stuck Loop

If this loop occurs repeatedly, the brain undergoes maladaptive plasticity—amygdala pathways strengthen their connections with the insula and ACC, while prefrontal control declines.

This produces the pattern: “slow thinking – fast feeling,” which becomes the brain’s default mode.

Over time, the brain recalibrates its baseline so that the person lives in a state of “innate hyper-alertness,” where even minor stimuli can feel like genuine threats.

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⚡ Causes & Risk Factors

1. Temperament & Genetics

Genetic factors and basic temperament play major roles in nervous system sensitivity.

• Studies on Sensory Processing Sensitivity (SPS) suggest roles for genes related to the serotonin transporter (5-HTTLPR) and dopamine receptor (DRD4), which are linked to brains that are more responsive to stimuli and emotion.
• Individuals with a “Highly Sensitive Personality (HSP)” often show stronger activation of the amygdala and insula when exposed to emotional stimuli such as faces, voices, or smells.
• A family history of ASD, ADHD, anxiety, or mood disorders increases the risk that the sensory gating system will function atypically, partly due to gene variants affecting GABAergic and glutamatergic balance.

Simply put, some brains are “born more sensitive” than others—not because they are broken, but because their nervous systems are designed to perceive more deeply and intensely than average.

2. Developmental & Trauma Factors

Early life experiences strongly shape the calibration of amygdala circuits:

• Growing up in a household full of yelling, loud conflict, or chaos can raise amygdala baseline activation from childhood.
• Childhood adversity—abuse, lack of safety, or emotional neglect—can make the amygdala highly reactive to sound/light/smell.
• Stimulus-linked trauma (e.g., a slamming door paired with terror) is encoded in the hippocampus and linked with the amygdala as “memory-based triggers” that can last a lifetime.

Thus, people who have experienced even seemingly small traumas may react to ordinary stimuli as if the original event were still happening now.

3. Co-occurring Neurodevelopmental Conditions

Multiple neurodevelopmental conditions are prone to abnormal nervous system sensitivity, such as:

• ASD (Autism Spectrum Disorder):
  Frequently involves sensory over-responsivity, amygdala enlargement, and atypical connectivity in the relevancy detection network (amygdala–STG–OFC), which misjudges the importance of stimuli.
• ADHD:
  Issues with sensory gating and distractor filtering mean the brain is flooded with stimuli and quickly exhausted; dopaminergic dysregulation destabilizes emotional responses.
• Learning Disorders / Tic Disorders / DCD:
  Extra mental energy is required to control the body or learn, causing the brain to tire easily and the limbic system to become overactive.

Collectively, these conditions create brains that “perceive more strongly – inhibit more slowly,” which is the ideal ground for the Sensory–Amygdala Hyperactivation Loop.

4. Chronic Stress & Lifestyle

Modern environments are one of the most powerful accelerators of this loop—we live in a world saturated with notification sounds, screen light, and digital stimuli every second.

When the nervous system constantly receives input without rest, the brain never truly enters parasympathetic recovery mode.

Consequences include:

• The amygdala recalibrates its danger threshold → easier to trigger.
• Cortisol remains chronically elevated → hippocampal shrinkage and reduced ability to distinguish past from present.
• The prefrontal cortex tires easily → diminished emotion regulation and reasoning.

Additional contributing factors:

• Sleep deprivation.
• Continuous use of caffeine or other stimulants.
• Living in large cities with high noise and light pollution.
• Working with multiple screens simultaneously.

All of these create frequent, subtle “micro-stressors” that keep the brain’s threat system permanently switched on.

5. Medical & Biological Factors

Certain physical and biochemical states can directly increase brain sensitivity, such as:

• Migraine: involves vasodilation and cortical spreading depression, heightening sensitivity to light and sound.
• Chronic Pain / Fibromyalgia: show overactivation of the insula and ACC similar to SOR.
• Hormonal Imbalances: e.g., premenstrual phase or thyroid overactivity.
• Post-Concussion Syndrome / Neuroinflammation: micro-inflammation in the brain makes sensory systems more reactive.

All of this leads to faster, stronger responses to stimuli, which—when combined with emotional stress—makes it very easy to fall into the Sensory–Amygdala Hyperactivation Loop.

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🔄 Overall Summary

“A sensitive brain is not weak; it is a protective system tuned to keep us safe—
it’s just that the system has become stuck in alarm mode.”

This condition arises from the combination of:
🧬 Genetics that predispose the brain to sensitivity
🧒 Childhood experiences that teach it to fear
🧠 Neural load from developmental or medical conditions
⚡ A modern environment that constantly stimulates the brain

When all of these stack together, the brain becomes “locked in chronic survival mode” (chronic hyperactivation mode),
which lies at the heart of what we call the Sensory–Amygdala Hyperactivation Loop 🌀

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Treatment & Management

The following are broad frameworks for education or writing, not individualized medical instructions.
Anyone with severe symptoms should consult a psychiatrist, psychologist, or relevant medical professional.

1. Psychoeducation: Naming the Loop

• Simply knowing “This is the Sensory–Amygdala Hyperactivation Loop, not weakness,” greatly reduces self-blame.
• Explaining that the amygdala acts like an over-sensitive smoke detector helps people understand themselves more deeply. briechildress.com+1

2. Sensory Modulation Strategies

From SOR and ASD research, various sensory-based interventions are used to lessen distress from stimuli, for example: MDPI+1

• For sound: earplugs, noise-cancelling headphones, creating a “quiet corner.”
• For light: tinted lenses, reducing fluorescent lighting, using warm lighting.
• For touch: choosing non-irritating fabrics, cutting off labels, avoiding triggering textures.
• Creating a sensory diet: scheduling regular periods of “stimulus rest” throughout the day.

3. Cognitive-Behavioral & Emotion Regulation Therapies

• CBT for anxiety: helps challenge and reframe catastrophic interpretations of stimuli.
• Graded exposure: training the brain to remain with mild stimuli without complete avoidance, building new habituation.
• Emotion regulation training / DBT skills: learning to tolerate distress and ground oneself when triggered.
• Trauma-focused approaches (e.g., EMDR, trauma-focused CBT) when the loop is linked to past traumatic events.

4. Body-Based & Nervous System Regulation

• Slow, deep breathing techniques (e.g., slow breathing, box breathing).
• Stretching, yoga, and gentle movement to reduce physiological arousal.
• Mindfulness that emphasizes “observing stimuli without judgment” (noticing sound/light as sensations rather than danger) has evidence for helping anxiety-related circuits to some degree. mi-psych.com.au+1

5. Medication (By Psychiatrist Only)

When anxiety disorders, depression, or PTSD are present, a physician may consider:

• SSRIs / SNRIs.
• In some cases, medications that reduce sympathetic arousal (e.g., beta-blockers for situational anxiety).

The goal is to lower the baseline arousal of the amygdala–limbic loop so the nervous system can handle stimuli more effectively, not to “erase feelings.”

6. Environmental & Life Design

• Designing life layouts with “low-stim zones”: quiet rooms, notification-free periods, offline windows.
• Scheduling demanding work during times of low sensory load (early morning / late night, depending on the person).
• Limiting caffeine, alcohol, and other stimulants that speed up heart rate.
• Building nervous system recovery routines: sufficient sleep, screen breaks, slow walks in calm places.

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Notes

• The “Sensory–Amygdala Hyperactivation Loop” is a model for explanation, not an official medical diagnosis.
• This cluster of symptoms overlaps with many conditions: SOR, ASD, ADHD, anxiety disorders, PTSD, migraine, etc.

• People with high sensory sensitivity do not only have negatives—SPS research shows they often possess above-average capacities in:

• Detail perception
• Depth of emotional processing
• Empathy and creativity PMC+1
• However, if this loop makes life unmanageable or leads to suicidal or self-harm thoughts, professional help is urgently needed.
• This model is highly suitable for use on neuroscience + psychoeducation platforms (like Nerdyssey) to help people understand that “the brain is not broken—it's just calibrated into an excessively high alarm mode.”

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📚 Reference

Green, S. A., Ben-Sasson, A., Soto, T. W., & Carter, A. S. (2012). Anxiety and sensory over-responsivity in toddlers with autism spectrum disorders: bidirectional effects across time. Journal of Autism and Developmental Disorders, 42(6), 1112–1119.

Green, S. A., Hernandez, L., Tottenham, N., Krasileva, K., Bookheimer, S. Y., & Dapretto, M. (2015). Neurobiology of sensory overresponsivity in youth with autism spectrum disorders. JAMA Psychiatry, 72(8), 778–786.

Lane, S. J., Reynolds, S., & Thacker, L. (2010). Sensory over-responsivity and ADHD: differentiating using electrodermal responses, cortisol, and anxiety. Frontiers in Integrative Neuroscience, 4(8), 1–12.

Acevedo, B. P., Aron, E. N., Aron, A., Sangster, M. D., Collins, N., & Brown, L. L. (2014). The highly sensitive brain: An fMRI study of sensory processing sensitivity and response to others’ emotions. Brain and Behavior, 4(4), 580–594.

Rundcrantz Zubcevic, C., et al. (2023). The Neural Correlates of Sensory Processing Sensitivity. Frontiers in Psychology, 14, 111–128.

Maren, S., & Quirk, G. J. (2004). Neuronal signalling of fear memory. Nature Reviews Neuroscience, 5(11), 844–852.

Fast, C. D., & McGann, J. P. (2017). Amygdalar Gating of Early Sensory Processing through Interactions with Locus Coeruleus. Neuron, 93(6), 1530–1545.

Roozendaal, B., & McEwen, B. S. (2009). Amygdala activity, fear, and anxiety: modulation by stress. Biological Psychiatry, 67(12), 1121–1128.

Cummings, K. K., et al. (2021). Shared and distinct biological mechanisms for anxiety and sensory over-responsivity: a review. Neuroscience & Biobehavioral Reviews, 129, 57–68.

Dalton, K. M., Nacewicz, B. M., Alexander, A. L., & Davidson, R. J. (2007). Gaze-fixation, amygdala activation, and face processing in autism. Nature Neuroscience, 10(4), 519–526.

Ben-Sasson, A., et al. (2009). The prevalence of sensory over-responsivity among elementary school children and its relationship to anxiety symptoms. Journal of Abnormal Child Psychology, 37(5), 705–716.

Liss, M., Mailloux, J., & Erchull, M. J. (2008). The relationships between sensory processing sensitivity, alexithymia, autism, depression, and anxiety. Personality and Individual Differences, 45(3), 255–259.

Cleveland Clinic. (2023). Amygdala Function & Disorders. Retrieved from my.clevelandclinic.org.

National Institute of Mental Health (NIMH). (2022). Brain Basics: The Amygdala and Emotional Processing.

StatPearls Publishing. (2024). Anatomy, Head and Neck, Amygdala. In StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing.

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