Sympathetic nervous system (SNS) hyperactivation refers to the sustained stimulation of the sympathetic branch of the nervous system. This branch is the primary driver of the fight or flight response. 

Under normal circumstances when a stressor is detected, sympathetic nerve endings release the majority of the neurotransmitter noradrenaline directly into target tissues. Noradrenaline acts as the chief director in mobilising resources to meet immediate demands. These include redistribution of blood flow toward skeletal muscles to support physical action, to the brain to enhance alertness and processing, and to the heart to increase cardiac output under heightened demand.

This noradrenaline surge is commonly associated with perceived psychological or emotional threats. Yet there are a vast number of non-psychological or emotional triggers that activate the same neural circuits within the brainstem’s autonomic control centers, producing a fight-or-flight response even in the absence of any consciously perceived danger. Examples include:

• Chronic Inflammation 

• Serotoning Deficiency

• Dopamine Deficiency 

• Low blood pressure 

• Iron deficiency 

• Glucose spikes 

• Dehydration

• Chronic Pain

• Endocrine or neurological disorders. 

Noradrenaline in a healthy response is released in brief, pulsed bursts, and rapidly cleared from between nerve cells and bloodstream by reuptake transporters and enzymatic breakdown. This ensures that heightened cardiovascular and cognitive readiness subsides once the stressor resolves. However, in SNS hyperactivation, noradrenaline release is excessive and prolonged, and clearance mechanisms are overwhelmed. As a result, high levels of noradrenaline persist long after the initiating event, sustaining elevated physiological arousal and delaying return to baseline.

This persistent noradrenergic drive manifests in a multitude of ways, some of which include hypervigilance, difficulty relaxing, worry, irritability, impaired emotional regulation, difficulty concentrating, generalised anxiety, muscle tension and disrupted sleep. Over time, this chronic overdrive imposes an allostatic load which increases vulnerability to a multitude of dysregulations. 

In fact, the consequences of SNS Hyperactivity have a causative correlation to 31 of the Physiological and Functional Dysregulations evaluated in our assessment. Accordingly, early prioritisation of modulating this response offers a strategic advantage in addressing all related factors. The supportive measures outlined here should be maintained throughout the entire treatment plan to optimise therapeutic outcomes and facilitate sustained recovery.

[1][2][3][4][5][6]

signs + symptoms

Tongue Twitches or Tremors

Evidence demonstrates that noradrenergic neurotransmission is key in the development of involuntary twitches and tremors, with higher noradrenaline availability correlating positively with tremor severity. [24] This involuntary movement can be detectable in fine motor regions such as the tongue when extended for 10 seconds, which should otherwise remain completely still. 

Busy and Distracted Brain 

Under normal conditions, moderate levels of noradrenaline in the brain’s prefrontal cortex optimise function by fine-tuning communication between nerve cells. However, when noradrenaline levels become excessively high, they overstimulate α-1 adrenoceptors on prefrontal cortex neurons. This triggers nearby support cells to release excess glutamate, a neurotransmitter that excites neurons. 

This excess excitation generates heightened background ‘noise’ that saturates the brain’s main information pathways with random signals. As the noise overwhelms the system, the prefrontal cortex loses precision in controlling thought and behaviour, making it harder to focus and to filter out irrelevant distractions  as if the mind’s ‘spotlight’ keeps drifting off target. [25]
 

Repetitive Thoughts + Behaviours
 

Excessive levels of Noradrenaline disrupt cognitive flexibility by altering the way the prefrontal cortex processes information. Under normal conditions, noradrenaline supports adaptive thinking, however, when noradrenaline concentrations become excessive, overactivation of α1-adrenergic receptors suppresses the neuronal firing patterns required for flexible problem-solving. 

This shift reduces the influence of goal-directed cortical circuits and strengthens the dominance of more rigid, stimulus response pathways. As a result, the brain becomes locked into a single mode of responding, leading to a pattern of repetitive, inflexible thinking or behaviour that persists even when new information indicates a need for change. [25]

Sensory Hypersensivity 

In the central nervous system, noradrenaline is released predominantly from the brainstem, binding to receptors in the cerebral cortex, thalamus, and limbic system. This drives heightened neuronal excitability, making nerve cells exceptionally responsive to incoming sensory input. In states of SNS hyperactivation, this constant amplification heightens situational awareness but can also lead to hypersensitivity to sensory input such as sound, light and touch. [9][10]

Psychological Dispositions

Elevated noradrenaline levels preferentially activate low-affinity excitatory receptors, particularly α1- and β1-adrenoceptors, in brain regions such as the prefrontal and sensorimotor cortices. This receptor overstimulation contributes to a state of hyperarousal, driving a distinct cluster of cognitive, emotional, and physiological symptoms commonly observed across multiple psychological dispositions, such as:

• Suspiciousness or mistrust

• Racing Thoughts 

• Quick to frustration

• Quick to Impatience

• Exaggerated reactions to sudden stimuli

• Difficulty sitting still, constant movement

• Difficulty modulating stress related emotions

• Hypervigilant to dangers or threats [26]

Iris furrows

In the eye, sympathetic nervous system activation stimulates α₁-adrenergic receptors on the radial muscle of the iris, causing the pupil to dilate so that more light can enter. When noradrenaline levels subside, β₂-adrenergic receptor–mediated relaxation allows the pupil to constrict. Over time, repeated cycles of strong dilation and constriction, such as during chronic stress, can place mechanical strain on the iris stroma. This strain may produce shallow grooves in the iris tissue near its outer edge, known as contraction furrows or ‘stress rings’, which appear as concentric circular lines encircling the pupil. [21]

A study involving 62 participants found that individuals with contraction furrows in the iris tended to have higher scores on the State-Trait Anxiety Inventory (STAI). Statistical analysis revealed a positive and significant relationship between furrow quantity and anxiety levels, suggesting that contraction furrows can serve as a marker towards a predisposition towards SNS Hyperactivation. [29]

Chronic Muscle Hypertonicity

• Neck and shoulder tightness

• Back tightness

• Jaw Clenching + Teeth Grinding

• Tension Headaches

Chronic high levels of noradrenaline encourage persistent muscle hypertonicity, where certain muscles remain in a constant state of increased tension or contraction. This occurs due to noradrenalines amplification of glutamatergic input, which lowers the threshold for motoneurone activation and prolonging excitatory signals. This sustained amplification creates a state of heightened basal muscle activity, where muscles remain partially contracted even at rest.

Clinically, hypertonicity manifests in predictable physical patterns. The neck and shoulders often become tight due, and tension-type headaches can occur, due to constant activation of postural muscles such as the trapezius and cervical extensors. Similarly, persistent activation of the masseter and temporalis muscles drives jaw clenching and teeth grinding. In the back, chronic noradrenergic drive maintains paraspinal muscle contraction, leading to back tightness. [63]

Poor Eating Habits + Food Cravings

Several studies have highlighted the impact of chronic stress on reshaping eating habits by rewiring the brain’s response to food cues and weakening self-regulation. Under persistent stress, the brain’s reward and motivation circuits, including the amygdala, hippocampus, and striatum become more reactive to the exposure of high-calorie, palatable foods, making them appear more appealing and harder to resist. 

At the same time, executive control regions of the prefrontal cortex that normally help regulate impulses and weigh long-term consequences show reduced activity, which diminishes the ability to resist cravings. This combination strengthens habit-driven and emotional eating pathways, leading individuals to reach for sugary or fatty foods more automatically as a form of comfort. [64][65]

Intense Dreams + Disrupted Sleep

When noradrenaline levels remain abnormally high during REM sleep, the prefrontal cortex fails to fully disengage as it normally would. This heightened activity keeps the brain in a state of vigilance, which both fragments sleep and increases the likelihood of awakenings. Dream content is also altered, tending to become more rigid, emotionally intense, and vividly realistic rather than fluid and surreal. The persistent arousal further interferes with the natural “forgetting” mechanisms of REM, causing these dreams to be retained more clearly in memory. [30]

Digestive Disorders 

Noradrenaline suppresses gastrointestinal activity by inhibiting the release of acetylcholine, the principal excitatory neurotransmitter responsible for stimulating intestinal muscle contraction and promoting digestive secretions. As a result, digestive movement slows and the output of digestive enzymes and gastric acid decreases. These are mechanisms designed to conserve energy during acute stress but chronic SNS activation impairs overall digestive function and over time, this contributes to a wide spectrum of functional gastrointestinal disturbances and disorders including, 

• Functional dyspepsia - Upper abdominal discomfort and bloating

• Intestinal Hypomobility - Sluggish Bowels

• Reflux - Heartburn

• Small intestinal bacterial overgrowth (SIBO) - Bloating

• Enzymatic Maldigestion [13]

Elevated Cortisol [ Hypercortisolism ] 

Noradrenaline stimulates the hypothalamic–pituitary–adrenal (HPA) axis indirectly by acting on α₁-adrenergic receptors in the hypothalamus. This triggers the release of CRH and ACTH, which then stimulates the adrenals to release cortisol, which supports the stress response. [12]

Insulin Resistance [ Impaired Glucose Tolerance ] 

• Energy Fluctuations

• Sugar Cravings

• Frequent Urination 

Noradrenaline binding to α2-adrenergic receptors on pancreatic β-cells inhibits voltage-gated calcium influx, which directly suppresses insulin secretion. This is an adaptive response during acute stress, ensuring glucose remains available to the brain and working skeletal muscles. However, when sympathetic activity and noradrenaline release remain chronically elevated, persistent inhibition of insulin secretion combined with increased liver glucose output contributes to impaired glucose tolerance and in a sequence of downstream events, it drives the development of insulin resistance - impaired glucose metabolism. [11][16] Therefore, long-term SNS Hyper-activation and the development of Insulin Resistance can manifest as symptoms of energy fluctuations, sugar cravings and frequent urination.

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Headaches + Migraines

When the sympathetic nervous system becomes overactive for long periods, it can disrupt the way pressure-sensing receptors and blood vessels in the brain normally work. This disruption makes the nerves and blood vessels more sensitive, partly because of changes in calcium levels inside the cells and increased release of CGRP, a neuropeptide heavily involved in sensations of pain and the widening of blood vessels. 

When these changes are mild, they usually cause general headaches, such as pressure, tightness, or tension-type pain. But when the same pathway becomes more intense, with higher CGRP release and stronger nerve overactivity, it can lead to a full migraine. In this way, the same stress-driven neurovascular process can cause both everyday headaches and more severe migraine attacks, depending on how strongly the system is activated. [17]

High Blood Pressure or Blood Pressure Spikes

• Head pressure or Headache

• Flushing - face, neck, or ears to feel hot

• Short of Sustained Rapid Heartbeat

• Chest Tightness

Noradrenaline raises blood pressure primarily through activation of receptors on vascular muscle. This receptor stimulation triggers a signalling cascade, increasing intracellular calcium and causing vasoconstriction of arterioles. The resulting increase in vascular resistance elevates blood pressure. The effect is rapid and sustained as long as noradrenaline levels remain high.[7][8][16]

Irregular Heart Rhythms 

When the sympathetic nervous system (SNS) stays activated for too long, it becomes a major source of stress on the heart. Constantly high noradrenaline levels keep stimulating the heart’s β₁-adrenergic receptors, and over time this pushes the heart into maladaptive changes, such as left ventricular enlargement and dilation, which weaken how the heart pumps. [27]

In addition, long-term SNS activation promotes myocardial fibrosis, oxidative damage, and even cardiomyocyte (heart cell) loss. These structural and cellular changes make the heart’s electrical system unstable, increasing the likelihood of developing irregular heart rhythms. [28]