Autonomic hyperactivity represents a pervasive physiological state characterized by excessive, sustained, or dysregulated activation of the vegetative neural networks that govern involuntary bodily functions. Far from being a mere temporary surge in stress hormones, this pathophysiological condition disrupts cardiovascular stability, metabolic equilibrium, and neurocognitive performance across diverse medical and psychiatric populations. Understanding the complex mechanisms underlying sustained autonomic overdrive is therefore essential for clinicians and researchers seeking to decipher the bidirectional pathways linking psychological trauma, neurological injury, and systemic illness.
Autonomic Hyperactivity
1. Concise Definition
Autonomic hyperactivity is a pathophysiological state defined by excessive, uncalibrated, or prolonged stimulation of the autonomic nervous system, predominantly manifested as persistent or episodic sympathetic predominance over parasympathetic inhibitory control. This state causes exaggerated vegetative responses—such as tachycardia, hypertension, diaphoresis, hyperthermia, tachypnea, and pupillary dilation—disproportionate to external environmental demands or physiological necessity.
In clinical medicine and neuropsychiatry, autonomic hyperactivity encompasses both chronic neurobiological baseline elevations (as observed in generalized anxiety disorder, post-traumatic stress disorder, and panic disorder) and acute, life-threatening paroxysmal crises. These severe surges occur in conditions such as severe traumatic brain injury, substance withdrawal, pheochromocytoma, and autonomic dysreflexia following spinal cord injury. Rather than serving as an adaptive survival mechanism, chronic or pathological autonomic hyperactivity impairs homeostatic set points, accelerating end-organ damage and degrading somatic resilience.
2. Etymology & Linguistic Origin
The term autonomic originates from the Ancient Greek roots autos (αὐτός), meaning "self," and nomos (νόμος), meaning "law" or "custom," literally translating to "self-governing" or "independent." British physiologist John Newport Langley popularized the term "autonomic nervous system" at the turn of the twentieth century (circa 1898–1903) to delineate the peripheral ganglionated network that regulates visceral organs independently of conscious, voluntary volitional control.
The constituent hyperactivity is formed from the Greek preposition and prefix hyper (ὑπέρ), denoting "over," "above," "beyond," or "excessive," combined with the Post-Classical Latin activitas, which stems from agere, meaning "to do," "to drive," or "to set in motion." When synthesized in early-to-mid 20th-century pathophysiological texts, "autonomic hyperactivity" came to characterize an aberrant state wherein involuntary visceral driving mechanisms break free from counter-regulatory homeostatic restraints, exerting continuous, unregulated force upon vascular, glandular, and visceral targets.
3. Pronunciation & Grammatical Form
Pronunciation: /ˌɔːtəˈnɒmɪk ˌhaɪpərækˈtɪvɪti/ (Received Pronunciation), /ˌɔːtəˈnɑːmɪk ˌhaɪpərækˈtɪvəti/ (General American).
Grammatical Form: Compound noun phrase, non-count (uncountable). The adjectival form is autonomically hyperactive (e.g., "the patient presented in an autonomically hyperactive state"). In neurotrauma and neurological intensive care, it frequently appears as an operationalized modifier within diagnostic terms, such as paroxysmal autonomic hyperactivity or sympathetic autonomic hyperreactivity.
4. Detailed Conceptual Explanation
To fully grasp autonomic hyperactivity, one must examine the functional architecture of the visceral motor system. Under resting physiological circumstances, internal bodily homeostasis relies on dynamic, reciprocal antagonism and complementary coordination between two primary branches: the sympathetic nervous system (SNS), which mobilizes resources for energy expenditure, and the parasympathetic nervous system (PNS), mediated largely via the vagus nerve (Cranial Nerve X), which governs vegetative conservation, digestion, repair, and cardiac slowing. A third subdivision, the enteric nervous system, coordinates gastrointestinal functions under the modulatory influence of these primary branches.
Autonomic hyperactivity arises when this finely balanced homeostatic equilibrium breaks down. The condition is characterized primarily by persistent sympathetic hyperexcitability, accompanied by a failure of parasympathetic braking mechanisms (vagal withdrawal) or, less commonly, severe concurrent parasympathetic discharges. At the cellular and neurochemical level, autonomic hyperactivity involves sustained activation of preganglionic autonomic neurons located within the intermediolateral cell column of the thoracolumbar spinal cord. These neurons release acetylcholine onto postganglionic sympathetic fibers, triggering widespread peripheral release of norepinephrine across vascular beds and stimulating chromaffin cells of the adrenal medulla to release epinephrine directly into systemic circulation.
The downstream consequences of this neurohumoral cascade are systemic and profound. Alpha-1 adrenergic receptor stimulation prompts peripheral vasoconstriction, increasing systemic vascular resistance and raising mean arterial pressure. Concurrently, beta-1 adrenergic activation on cardiomyocytes accelerates the rate of sinoatrial node depolarization and enhances myocardial contractility, resulting in sinus tachycardia, elevated stroke volume, and heightened myocardial oxygen demand. Cutaneous eccrine sweat glands, innervated by sympathetic cholinergic fibers, undergo massive stimulation, producing profuse diaphoresis. In metabolic tissue, circulating catecholamines stimulate hepatic glycogenolysis and adipose lipolysis, inducing acute hyperglycemia and catabolic muscle wasting.
Central nervous system circuits regulate these peripheral dynamics through the central autonomic network (CAN). This network is an integrated forebrain-brainstem hierarchy comprising the insular cortex, anterior cingulate cortex, central nucleus of the amygdala, paraventricular and lateral hypothalamic nuclei, periaqueductal gray, locus coeruleus, nucleus tractus solitarii (NTS), and rostral ventrolateral medulla (RVLM). Under normal conditions, cortical and subcortical structures exert inhibitory tone over lower autonomic nuclei. When neurological damage disrupts descending corticobulbar pathways, or when intense psychological distress disinhibits subcortical limbic centers, the RVLM drives unchecked, basal sympathetic firing, cementing the clinical state of autonomic hyperactivity.
5. Historical Development
The scientific conceptualization of autonomic regulation evolved through several paradigm shifts across physiology, neurology, and psychiatry:
In the mid-19th century, French physiologist Claude Bernard formulated the concept of the milieu intérieur (internal environment), positing that complex organisms survive only by maintaining physiological stability against shifting external surroundings. Bernard’s classic experiments on vasomotor nerves demonstrated that blood vessels receive constant neural tone capable of dynamic dilation and constriction. Building directly upon this work, Walter Bradford Cannon in the 1910s and 1920s coined the term homeostasis and characterized the sympathoadrenal system’s role in the fight-or-flight response. Cannon demonstrated that acute emotional and physical threats trigger a coordinated sympathetic discharge aimed at survival.
In the mid-20th century, Hans Selye extended Cannon’s ideas by outlining the General Adaptation Syndrome. Selye postulated that while the initial "alarm reaction" involves acute autonomic activation, chronic overactivation during prolonged stress leads to a "stage of exhaustion," producing structural pathology in the adrenal glands, cardiovascular tissues, and immune organs. Concurrently, Wilder Penfield in 1929 published his seminal description of "diencephalic autonomic epilepsy," documenting paroxysmal episodes of profuse sweating, flushing, pupillary dilation, and profound hypertension in patients with third-ventricle tumors. Penfield’s observations established that specific intracranial structural lesions could release the lower autonomic centers from normal central inhibition.
Throughout the late 20th and early 21st centuries, intensive care medicine identified comparable hyperadrenergic syndromes in patients surviving severe brain insults. Initially described under a confusing array of names—including dysautonomia, autonomic storming, sympathetic storm, and hyperpyrexia with dystonia—the syndrome was formally unified in 2014 by an international consensus group under the standardized diagnostic nomenclature of paroxysmal sympathetic hyperactivity (PSH). In parallel, modern cognitive neuroscience and psychophysiology established that milder, chronic autonomic hyperactivity forms the physiological core of internalizing psychiatric disorders.
6. Theoretical Foundations
Several theoretical frameworks explain how and why autonomic hyperactivity develops and persists across clinical contexts:
The Neurovisceral Integration Model: Developed by Julian F. Thayer and colleagues, this model conceptualizes heart rate variability (HRV) and autonomic flexibility as an index of central-peripheral neural integration. The model proposes that the prefrontal cortex normally exerts tonic, top-down inhibitory control over subcortical structures such as the amygdala. Under conditions of prefrontal hypoactivation—caused by chronic psychological stress, structural brain injury, or neurodegeneration—the amygdala and downstream medullary sympathetic generators escape inhibition. This leads to a persistent drop in vagally mediated parasympathetic tone and an unchecked rise in sympathetic dominance, presenting clinically as chronic autonomic hyperactivity, emotional rigidity, and impaired cognitive control.
Allostatic Load Theory: Formulated by Bruce McEwen and Eliot Stellar, this model distinguishes between allostasis (the active process by which the body maintains stability through physiological change) and allostatic load (the cumulative wear and tear inflicted on tissues by sustained allostatic responses). When physiological stress responses are triggered repeatedly, fail to shut off following stressor cessation, or lack adequate counter-regulatory damping, an individual enters severe allostatic overload. In this framework, chronic autonomic hyperactivity is an allostatic state where sustained sympathetic outflow and elevated catecholaminergic exposure directly cause endothelial injury, atherosclerotic plaque destabilization, insulin resistance, and systemic low-grade inflammation.
The Polyvagal Theory: Advanced by Stephen Porges, this evolutionary model posits a phylogenetic hierarchy in the vertebrate autonomic nervous system comprising three circuits: the ancient unmyelinated dorsal vagal system (responsible for metabolic conservation and passive immobilization), the sympathetic nervous system (governing active mobilization and defense), and the evolutionarily newer, myelinated ventral vagal system (mediating social engagement and visceral calm). In Porges’s framework, autonomic hyperactivity reflects the loss or functional suppression of the ventral vagal "smart brake." Without adequate myelinated vagal inhibition on the cardiac pacemaker, primitive defensive sympathetic circuits dominate visceral signaling, locking the organism into defensive vigilance.
7. Key Components, Types & Dimensions
Autonomic hyperactivity can be systematically deconstructed across physiological domains, temporal profiles, and clinical subtypes:
- Cardiovascular Components: Resting sinus tachycardia, labile or refractory arterial hypertension, elevated pulse pressure, reduced baroreflex sensitivity, and marked suppression of parasympathetic indices on continuous electrocardiography.
- Thermoregulatory & Sudomotor Components: Profuse episodic or continuous diaphoresis (sweating), cutaneous vasomotor instability (alternating flushing and pallor), piloerection ("goosebumps"), and central neurogenic hyperthermia resistant to standard antipyretic medications.
- Respiratory Components: Tachypnea, hyperpnea, neurogenic pulmonary edema, and irregular respiratory rhythms secondary to brainstem autonomic overdrive.
- Neuro-Ophthalmologic & Neuromuscular Components: Bilateral pupillary dilation (mydriasis), severe motor agitation, dystonic posturing, muscular rigidity, and dramatic shivering-like clonus triggered by light sensory stimulation.
- Paroxysmal Sympathetic Hyperactivity (PSH): An acute, high-intensity subtype occurring after severe structural neurological injuries (e.g., traumatic brain injury, anoxic-ischemic encephalopathy, or stroke). It is characterized by episodic "sympathetic storms" marked by hypertension, tachycardia, hyperthermia, tachypnea, diaphoresis, and dystonic decerebrate or decorticate posturing.
- Chronic Psychogenic Autonomic Hyperactivity: A low-to-moderate-intensity, persistent baseline condition seen in post-traumatic stress disorder, generalized anxiety, and panic disorder. It manifests as somatic palpitations, chronic muscular tension, gastrointestinal hypermotility, sleep architectural fragmentation, and reduced heart rate variability.
- Pharmacological & Toxicological Hyperactivity: Sympathomimetic surges precipitated by drug intoxication (e.g., cocaine, amphetamines, synthetic cathinones) or sudden withdrawal from central nervous system depressants (e.g., alcohol delirium tremens, benzodiazepine withdrawal, severe opioid withdrawal).
- Endocrine & Reflexive Hyperactivity: Peripheral catecholaminergic surges driven by functional neuroendocrine tumors (e.g., pheochromocytoma, paraganglioma) or reflex spinal arches detached from supraspinal control (e.g., autonomic dysreflexia in spinal cord injuries at or above T6).
8. Examples & Illustrative Cases
The practical manifestations of autonomic hyperactivity can be illustrated through distinct clinical scenarios:
Case Illustration 1: Acute Neurological Paroxysm (PSH in Neuro-ICU). A 24-year-old male was admitted to the neurointensive care unit following a high-velocity motor vehicle collision that caused severe diffuse axonal injury (Glasgow Coma Scale score of 4). On post-injury day 10, while weaning from mechanical ventilation, the patient developed recurring episodes lasting 45 to 90 minutes. During these episodes, his heart rate surged from 75 to 160 beats per minute, his blood pressure spiked from 120/70 to 195/110 mmHg, his temperature rose to 39.2°C (102.6°F) without infectious etiology, and he exhibited drenching diaphoresis alongside severe extensor posturing of all four extremities. Simple bedside stimuli, such as endotracheal suctioning or changing position, triggered these attacks. Diagnostic workup ruled out sepsis, pulmonary embolism, and intracranial hypertension. The patient was diagnosed with Paroxysmal Sympathetic Hyperactivity using the PSH Assessment Measure (PSH-AM) and successfully stabilized with a multimodal regimen of enteral propranolol, clonidine, and gabapentin.
Case Illustration 2: Chronic Psychophysiological Overdrive (PTSD). A 38-year-old combat veteran presented to an outpatient clinic with intractable insomnia, daily palpitations, pervasive vigilance, and severe startle reactions. Ambulatory psychophysiological monitoring revealed an elevated resting heart rate averaging 92 beats per minute, blunted respiratory sinus arrhythmia, and high resting skin conductance levels that spiked dramatically upon exposure to unexpected acoustic cues. Laboratory evaluations ruled out primary hyperthyroidism and pheochromocytoma. This individual’s persistent autonomic hyperactivity reflected structural and functional alterations within the amygdala-prefrontal circuitry, keeping the sympathetic nervous system continuously mobilized against perceived external threat.
9. Measurement & Assessment
Assessing autonomic hyperactivity requires objective, multimodal evaluations designed to capture central and peripheral autonomic function:
Heart Rate Variability (HRV) Analysis: Resting continuous electrocardiography enables frequency-domain and time-domain HRV measurements. Autonomic hyperactivity typically shows an elevated Low Frequency to High Frequency (LF/HF) power ratio, marked reductions in High-Frequency power (0.15–0.40 Hz, reflecting vagal parasympathetic modulation), and low time-domain variance metrics such as the root mean square of successive differences (RMSSD) and standard deviation of NN intervals (SDNN).
Electrodermal Activity (EDA): Continuous measurement of skin conductance level (SCL) and transient skin conductance responses (SCR) via electrodes on the palmar surface provides a direct index of sympathetic cholinergic stimulation of eccrine sweat glands. Pathological hyperactivity appears as elevated baseline SCL, slow habituation rates, and spontaneous, non-stimulus-locked electrodermal fluctuations.
Biochemical & Biomarker Profiling: Laboratory quantification includes 24-hour urinary fractionated metanephrines and catecholamines (epinephrine, norepinephrine, dopamine) to detect sustained systemic surges, alongside plasma free metanephrines. Serial serum lactate, blood glucose, and creatine kinase levels help quantify systemic catabolism, end-organ hypoperfusion, and muscle breakdown driven by extreme hyperadrenergic episodes.
Standardized Diagnostic Instruments: In neurocritical care, clinicians use the Paroxysmal Sympathetic Hyperactivity Assessment Measure (PSH-AM), developed by Baguley and an international consensus panel. The tool integrates the Clinical Feature Scale (grading the severity of heart rate, respiratory rate, blood pressure, temperature, sweating, and posturing) with the Diagnosis Likelihood Tool (evaluating predisposing etiology, temporal pattern, and response to stimuli) to yield a definitive diagnostic probability score.
10. Applications & Practical Significance
Recognizing and managing autonomic hyperactivity has direct therapeutic and operational relevance across several clinical specialties:
In critical care and neurology, unmanaged autonomic hyperactivity is an independent predictor of poor outcomes, increased intensive care length of stay, and secondary neurological injury. Severe hyperthermia, extreme hypertension, and sustained tachycardia accelerate brain tissue metabolism, worsen cerebral edema, precipitate myocardial ischemia, and cause neurogenic stunned myocardium. Pharmacological strategies aim to suppress excessive sympathetic outflow using centrally acting alpha-2 adrenergic agonists (clonidine, dexmedetomidine), lipophilic non-selective beta-blockers (propranolol), gamma-aminobutyric acid (GABA) agonists, and voltage-gated calcium channel modulators (gabapentin).
In clinical psychology and psychiatry, recognizing that panic attacks, PTSD, and generalized anxiety involve biological autonomic hyperactivity helps counteract the stigma that these disorders are purely cognitive or volitional weaknesses. Psychophysiological biofeedback protocols, such as resonance frequency breathing training, teach individuals to restore parasympathetic tone by maximizing heart rate variability. Somatic therapies and interoceptive exposure likewise focus on re-regulating visceral homeostatic signaling.
In occupational and performance medicine, identifying chronic autonomic hyperactivity among first responders, military personnel, and elite athletes helps prevent overtraining syndrome, burnout, and early cardiovascular morbidity. Systematic monitoring of nocturnal autonomic indicators, such as sleeping heart rate and RMSSD, allows coaches and medical teams to detect autonomic exhaustion early and adjust operational loads accordingly.
11. Research & Empirical Evidence
Contemporary empirical research has clarified the neurobiological roots and clinical consequences of autonomic hyperactivity:
Neuroimaging studies utilizing functional Magnetic Resonance Imaging (fMRI) have mapped central autonomic control networks. Seminal investigations by Gianaros, Critchley, and colleagues demonstrated that stressor-evoked blood pressure reactivity and sympathetic activation correspond directly to elevated regional cerebral blood flow within the dorsal anterior cingulate cortex, bilateral anterior insula, and amygdala, alongside functional uncoupling from the ventromedial prefrontal cortex. This pattern confirms that structural or functional disruption of top-down inhibitory pathways directly triggers peripheral autonomic hyperactivity.
In neurotrauma research, Baguley and colleagues established the "Excitatory:Inhibitory Ratio (EIR) Model" to explain paroxysmal sympathetic hyperactivity. Their electrophysiological and neurochemical findings show that midbrain damage disrupts descending inhibitory pathways from the periaqueductal gray and brainstem reticular formation to the spinal cord. Without tonic descending inhibition, spinal sympathetic circuits become hyperexcitable, causing non-noxious peripheral sensory inputs (such as bladder distension or endotracheal movement) to trigger massive, disproportional efferent sympathetic storms.
Epidemiological and longitudinal cohorts, including the Whitehall II study and the Framingham Heart Study, have investigated the systemic health costs of long-term autonomic dysfunction. These studies consistently demonstrate that sustained sympathetic dominance and reduced heart rate variability predict accelerated coronary artery calcification, ventricular arrhythmias, metabolic syndrome, stroke, and all-cause cardiovascular mortality, even after controlling for baseline demographic variables.
12. Cultural & Cross-Cultural Considerations
The interpretation, reporting, and experience of autonomic hyperactivity vary across distinct cultural contexts. In many non-Western populations, psychological distress is expressed primarily through somatic manifestations of autonomic arousal rather than cognitive affective terms—a phenomenon described in transcultural psychiatry as somatization or "bodily distress."
For instance, idioms of distress such as ataques de nervios among Latin American populations, shenjing shuairuo (neurasthenia) in traditional Chinese diagnostic frameworks, or khyâl cap (wind attacks) among Cambodian communities represent culturally shaped experiences grounded in acute autonomic hyperarousal. Patients experiencing these syndromes often report dramatic autonomic symptoms, including intense palpitations, ascending heat, profuse diaphoresis, dizziness, and somatic panic. Rather than viewing these manifestations merely as subjective anxiety, ethnopsychological research highlights how cultural explanatory models shape how visceral autonomic feedback is interpreted, amplified, and integrated into behavioral responses.
Conversely, Western clinical paradigms risk over-medicalizing or fragmenting autonomic symptoms into separate specialty presentations—referring tachycardia to cardiology, diaphoresis to dermatology, and hypermotility to gastroenterology. These differences underscore the importance of cross-cultural competence and systemic physiological thinking when evaluating autonomic hyperactivity across diverse patient populations.
13. Criticisms, Debates & Limitations
Despite clinical and scientific progress, the study of autonomic hyperactivity faces ongoing theoretical and diagnostic challenges:
A persistent debate concerns whether autonomic hyperactivity is a distinct pathophysiological entity or merely a shared downstream epiphenomenon seen across diverse conditions. For decades, heterogeneous terminology—such as dysautonomia, neurostorming, sympathetic storm, and diencephalic seizures—hindered collaborative research and meta-analyses. While the 2014 consensus criteria for Paroxysmal Sympathetic Hyperactivity brought clarity to neurotrauma settings, diagnostic standardization remains inconsistent across psychiatry, rheumatology, and post-viral dysautonomias (such as post-acute COVID-19 sequelae).
Another controversy centers on assessing autonomic balance. The conventional practice of interpreting the LF/HF ratio from power spectral analysis of heart rate variability as an index of pure "sympathovagal balance" has faced significant criticism from neurophysiologists. Research shows that Low-Frequency power is not a simple proxy for sympathetic activity; it reflects a complex mix of sympathetic outflow, parasympathetic modulation, and arterial baroreflex activity. Relying solely on HRV frequency metrics without validating them through direct microneurography (muscle sympathetic nerve activity, MSNA) or catecholamine clearance studies can lead to misleading conclusions about the presence or mechanisms of autonomic hyperactivity.
14. Related Terms & Distinctions
Autonomic hyperactivity overlaps with several related concepts, making precise clinical distinctions essential:
- Dysautonomia: An overarching umbrella term describing any functional abnormality, failure, or dysregulation of the autonomic nervous system. Distinction: Dysautonomia includes both hypofunction (such as pure autonomic failure or orthostatic hypotension) and hyperfunction; autonomic hyperactivity refers specifically to excessive, unchecked autonomic outflow.
- Paroxysmal Sympathetic Hyperactivity (PSH): A specific neurocritical care syndrome characterized by episodic, acute surges of sympathetic tone and motor posturing after severe acquired brain injury. Distinction: PSH is an episodic, life-threatening neurological subtype, whereas autonomic hyperactivity can be chronic, low-grade, psychogenic, or medically induced.
- Autonomic Dysreflexia: A medical emergency occurring in individuals with spinal cord injuries at or above T6, where an uninhibited sympathetic reflex discharge below the level of the lesion triggers severe hypertension, counterbalanced by vagal bradycardia above the injury. Distinction: Autonomic dysreflexia is a spinal-reflex phenomenon driven by local stimuli (e.g., bladder distension), whereas general autonomic hyperactivity can stem from cortical, brainstem, toxicological, or psychological mechanisms.
- Sympathicotonia: An older constitutional term designating a physiological temperament characterized by high resting sympathetic tone. Distinction: Sympathicotonia was historically treated as an individual constitutional variant, whereas autonomic hyperactivity implies pathological, maladaptive, or clinically significant excessive activity.
- Hyperarousal: A psychiatric construct reflecting elevated psychological vigilance, alertness, and cognitive threat sensitivity. Distinction: Hyperarousal is primarily a cognitive and behavioral state that often accompanies, but is physiologically distinct from, systemic autonomic hyperactivity.
15. Summary / Key Takeaways
Autonomic hyperactivity is a widespread, clinically significant state characterized by excessive, sustained, or uncoordinated activation of the visceral nervous system, primarily marked by persistent sympathetic dominance and blunted parasympathetic inhibition. Arising from structural interruptions within descending central inhibitory networks or from chronic psychological stress, the syndrome produces sinus tachycardia, refractory hypertension, neurogenic hyperthermia, drenching diaphoresis, and profound metabolic catabolism. From acute, life-threatening paroxysms in neurointensive care to subtle, chronic wear-and-tear in post-traumatic stress disorder, this pathological state drives sustained allostatic overload, tissue remodeling, and cardiovascular morbidity. Accurate diagnosis demands multimodal assessment—including heart rate variability analysis, electrodermal testing, and validated clinical scoring tools—while effective treatment requires integrated, centrally and peripherally targeted pharmacological interventions alongside autonomic rehabilitation.
References
- Baguley, I. J., Perkes, I. E., Fernandez-Ortega, J. F., Rabinstein, A. A., Dolce, G., & Hendricks, H. T. (2014). Paroxysmal sympathetic hyperactivity after acquired brain injury: Consensus on conceptual definition, nomenclature, and diagnostic criteria of a consensus working group. Neurorehabilitation and Neural Repair, 28(8), 715–720. https://doi.org/10.1177/1545968314528652
- Cannon, W. B. (1929). Bodily changes in pain, hunger, fear and rage: An account of recent researches into the function of emotional excitement (2nd ed.). D. Appleton and Company.
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- McEwen, B. S. (1998). Protective and damaging effects of stress mediators. New England Journal of Medicine, 338(3), 171–179. https://doi.org/10.1056/NEJM199801153380307
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