When facing down a ferocious lion, an oncoming car or maybe just an impending deadline, our bodies trigger a physical stress response that prepares us to either fight or flee the scene. This "fight-or-flight" response is driven by the sympathetic nervous system, a normally harmonized network of brain structures, nerves and hormones that, if thrown off balance, can result in serious complications. The sympathetic nervous system makes up part of the autonomic nervous system, also known as the involuntary nervous system. Without conscious direction, the autonomic nervous system regulates important bodily functions such as heart rate, blood pressure, pupil dilation, body temperature, sweating and digestion, according to a review in the American Journal of Pharmaceutical Education. Research suggests that distinct types of nerve cells , called neurons, control these different physical reactions by directing the action of skeletal muscle, cardiac muscle and gland secretion.
For instance, a person may jump from the path of a falling tree before they fully register that it's toppling toward Persistent sympathetic arousal. During local cooling, CFS patients Change sexual orientation attenuated sympathetic outflow to skin arterioles combined with normalization of Persistent sympathetic arousal temperature [ 35 ]. Important characteristics include elevated plasma levels of epinephrine and a change of set-point in homeostatic control circuits causing, for instance, elevated blood pressure and body temperature [ 20 ]. This response occurs so quickly that people often don't realize it's taken place, according to Harvard Medical School. If not, the arousal may be sustained [ 19 ]. Types of brain disorders Traumatic Brain Injury. Changes in sympathetic nervous activity are evident in the skin, pupils and especially the heart. Medical Sympathetic Storms - Fact Sheet. This, in turn, may counteract homeostasis rather than restoring it, resulting in another vicious circle.
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She was sympathettic a magnetic resonance imaging brain, and an electroencephalography, which were within normal limits. I have since noticed a marked improvement in my PGAD symptoms as well as improved bladder control and bowel function. Psychological Considerations The occurrence of PSAS for a woman is unrelated to demographic concerns such Persistent sympathetic arousal age, socioeconomic level, childhood experiences, marital status, education level or family history. Hidden categories: All articles with unsourced statements Articles with unsourced statements from June Wikipedia articles with NDL identifiers Wikipedia articles with TA98 identifiers. Many health professionals are guilty of dismissing the symptoms, making off-handed comments or telling the patients that its all in their head. A selective internal pudendal arteriogram revealed Puppy lovers inc pelvic AVM. Sympathetic nervous system Schematic illustration showing the sympathetic nervous system with sympathetic cord and target Persistent sympathetic arousal. This secondary vasodilation caused by the primary vasoconstriction is termed functional sympatholysis, the overall effect of which on coronary arteries is dilation. To reach target organs and glands, the axons must Teen hacker long distances in the body, and, to accomplish this, many axons relay their message to a second cell through synaptic transmission. Human Physiology: An Integrated Approach 4 ed. Like sypmathetic Like Loading By Lisa Parris. We are aware of several patients with PSAS based on exposure to certain medication.
- This program was held for those with PSAS and their loved ones.
- Persistent genital arousal disorder PGAD , previously called persistent sexual arousal syndrome ,  is spontaneous, persistent, unwanted and uncontrollable genital arousal in the absence of sexual stimulation or sexual desire ,   and is typically not relieved by orgasm.
- Persistent genital arousal disorder PGAD is a phenomenon, in which afflicted women experience spontaneous genital arousal, unresolved by orgasms and triggered by sexual or nonsexual stimuli, eliciting stress.
When facing down a ferocious lion, an oncoming car or maybe just an impending deadline, our bodies trigger a physical stress response that prepares us to either fight or flee the scene. This "fight-or-flight" response is driven by the sympathetic nervous system, a normally harmonized network of brain structures, nerves and hormones that, if thrown off balance, can result in serious complications.
The sympathetic nervous system makes up part of the autonomic nervous system, also known as the involuntary nervous system. Without conscious direction, the autonomic nervous system regulates important bodily functions such as heart rate, blood pressure, pupil dilation, body temperature, sweating and digestion, according to a review in the American Journal of Pharmaceutical Education.
Research suggests that distinct types of nerve cells , called neurons, control these different physical reactions by directing the action of skeletal muscle, cardiac muscle and gland secretion. The system allows animals to make quick internal adjustments and react without having to think about it.
The sympathetic nervous system directs the body's rapid involuntary response to dangerous or stressful situations. A flash flood of hormones boosts the body's alertness and heart rate, sending extra blood to the muscles. Breathing quickens, delivering fresh oxygen to the brain, and an infusion of glucose is shot into the bloodstream for a quick energy boost.
This response occurs so quickly that people often don't realize it's taken place, according to Harvard Medical School. For instance, a person may jump from the path of a falling tree before they fully register that it's toppling toward them. The sympathetic nervous system doesn't destress the body once the tree is felled or the danger has passed. Another component of the autonomic nervous system, the parasympathetic nervous system, works to calm the body down, according to the Clinical Anatomy of the Cranial Nerves , published in by Academic Press.
To counter the fight-or-flight response , this system encourages the body to "rest and digest. The sympathetic and parasympathetic nervous systems work together to maintain this baseline and normal body function. Structures in the brain , spinal cord and peripheral nervous system support the function of the sympathetic nervous system, according to a review in the journal BJA Education.
Receptors in internal organs of the chest and abdomen collect information from the body and send it up to the brain through the spinal cord and cranial nerves. The hypothalamus, a brain structure important for regulating homeostasis, receives signals from the body and tunes the activity of the autonomic nervous system in response.
This brain structure also gathers information from areas higher in the brain, such as the amygdala, according to a review in the journal Biological Psychiatry. Often called the emotional brain, the amygdala pings the hypothalamus in times of stress. The hypothalamus then relays the alert to the sympathetic nervous system and the signal continues on to the adrenal glands , which then produce epinephrine, better known as adrenaline. This hormone triggers the profuse sweating, rapid heartbeat and short breaths we associate with stress.
If the danger persists, the hypothalamus sends a new message through the nerve system grapevine, instructing the adrenal glands to produce the hormone cortisol to keep the stress response rolling. Outgoing commands from the sympathetic nervous system exit the spinal cord in the thoracolumbar region, or the mid to lower spine. Sympathetic neurons exit the spinal cord and extend in two columns on either side of it.
These neurons then tag a second set of nerve cells into the relay, signaling them with help from the chemical messenger acetylcholine. Having picked up the baton, the second set of neurons extends to smooth muscles that execute involuntary muscle movements, cardiac muscles and glands across the body.
Often, the parasympathetic nervous system communicates with the same organs as the sympathetic nervous system to keep the activity of those organs in check. The sympathetic and parasympathetic nervous systems rest on either side of a wobbling scale; each system remains active in the body and helps counteract the actions of the other. If the opposing forces are mostly balanced, the body achieves homeostasis and operations chug along as usual.
But diseases can disrupt the balance. The sympathetic nervous system becomes overactive in a number of diseases, according to a review in the journal Autonomic Neuroscience. These include cardiovascular diseases like ischemic heart disease, chronic heart failure and hypertension. A boost of sympathetic signaling raises the blood pressure and enhances tone in smooth muscles, which may cause hypertension.
Beyond cardiovascular ailments, sympathetic dysfunction has been associated with kidney disease, type II diabetes, obesity , metabolic syndrome and even Parkinson's disease.
Changes in sympathetic nervous activity are evident in the skin, pupils and especially the heart. Parkinson's damages the sympathetic neurons that help maintain levels of epinephrine and norepinephrine in the body — chemicals that tell the heart when to pump harder, such as when you move to stand up or exercise. Damage to these neurons can result in a lack of blood flow in patients with Parkinson's, so they often feel lightheaded upon standing, which dramatically increases their risk of falls.
Sympathetic dysfunction also underlies mental health conditions such as anxiety, depression and chronic stress, an article in Forbes reported. In short bursts, the body's physical stress response can be useful and grant an energizing boost of mental focus. If prolonged, however, the stress signals whizzing through the body wreak havoc. Besides maintaining a mental feeling of constant stress, the extra epinephrine and cortisol damage blood vessels, increase blood pressure and promote a buildup of fat.
So, while the fight-or-flight response serves a purpose, you don't want it switched on all the time. Live Science. This child's sympathetic nervous system is probably kicking in right about now.
Submucous plexus Myenteric plexus. This response is also known as sympatho-adrenal response of the body, as the preganglionic sympathetic fibers that end in the adrenal medulla but also all other sympathetic fibers secrete acetylcholine, which activates the great secretion of adrenaline epinephrine and to a lesser extent noradrenaline norepinephrine from it. I could not concentrate or sleep or function properly. Thompson M. The ganglia include not just the sympathetic trunks but also the cervical ganglia superior , middle and inferior , which send sympathetic nerve fibers to the head and thorax organs, and the celiac and mesenteric ganglia , which send sympathetic fibers to the gut.
Persistent sympathetic arousal. What is Hyperarousal?
Metrics details. We present an integrative model of disease mechanisms in the Chronic Fatigue Syndrome CFS , unifying empirical findings from different research traditions. Based upon the Cognitive activation theory of stress CATS , we argue that new data on cardiovascular and thermoregulatory regulation indicate a state of permanent arousal responses — sustained arousal — in this condition.
We suggest that sustained arousal can originate from different precipitating factors infections, psychosocial challenges interacting with predisposing factors genetic traits, personality and learned expectancies classical and operant conditioning. Furthermore, sustained arousal may explain documented alterations by establishing vicious circles within immunology Th2 humoral vs Th1 cellular predominance , endocrinology attenuated HPA axis , skeletal muscle function attenuated cortical activation, increased oxidative stress and cognition impaired memory and information processing.
Finally, we propose a causal link between sustained arousal and the experience of fatigue. The model of sustained arousal embraces all main findings concerning CFS disease mechanisms within one theoretical framework. Chronic Fatigue Syndrome CFS is characterized by unexplained and disabling fatigue, accompanied by symptoms such as musculoskeletal pain, impaired memory and concentration, headache and sleep problems [ 1 ]. Research on disease mechanisms has been conducted along several tracks Table 1.
Twin studies indicate a moderate heritability of CFS [ 2 ]. Recent molecular analyses report an association to polymorphisms of genes involved in autonomic and endocrine effector systems [ 3 ]. Personality traits such as perfectionism, conscientiousness and internalization may have an impact [ 4 ], as do illness perceptions such as a poor sense of personal control over symptoms and a strong focus on bodily sensations [ 5 ].
In many patients, firm evidence supports a relation to long-lasting infection caused by different microorganisms, such as Epstein-Barr virus, enteroviruses, and Coxiella burnetii [ 6 , 7 ].
In addition, CFS may be initiated by critical life events or perceived chronic difficulties [ 8 , 9 ]. Regarding perpetuating and associated factors, hemodynamic disturbances characterized by increased sympathetic and attenuated parasympathetic cardiovascular neurotransmission have been documented [ 10 , 11 ].
Immune system alterations Th2 vs Th1 immune response predominance are also reported [ 2 ]. Reduced function of skeletal muscles [ 13 ] might be due to functional changes in cortical motor areas [ 14 ], but could also be caused by changes in muscle metabolism due to increased oxidative stress [ 15 , 16 ]. Finally, cognitive tests have revealed disturbances of memory and speed of information processing [ 17 , 18 ], but overall normal functioning in other cognitive domains.
A coherent and integrative model of CFS disease mechanisms combining these findings is lacking. In this article, we propose such a model, based upon the Cognitive activation theory of stress CATS [ 19 ]. Specifically, we suggest that CFS is caused by sustained arousal. Below, we first present CATS — the stress theory upon which our model is based. Then we outline empirical indications of an association between sustained arousal and CFS.
From this point of departure, we apply CATS to hypothesize the potential mechanisms leading to sustained arousal in CFS, and finally we substantiate our model by discussing sustained arousal consequences in other organ systems in relation to CFS research evidence.
Among various definitions of the term "stress", a common denominator is that stress denotes any condition being a threat to homeostasis in a broad sense [ 20 , 21 ].
Stress occurs whenever there is a discrepancy between what is expected "set value" and what really exists "actual value" ; hence, it always implies comparison of present sensory information with stored brain information [ 19 , 22 ]. This may be a fast and partly automatic process, for instance when exposed to a significant and unexpected change in the environment [ 23 ], or when certain physiologic variables such as blood pressure are perturbated [ 20 ].
Eventually, the comparison may involve complex cognitive evaluations of situations and their potential consequences, which in turn is based on previous experiences in equal or similar situations [ 19 , 24 ]. Stress normally elicits a quite non-specific arousal response , involving the somatic and autonomic nervous system as well as several endocrine axes [ 25 ] Figure 1.
Important characteristics include elevated plasma levels of epinephrine and a change of set-point in homeostatic control circuits causing, for instance, elevated blood pressure and body temperature [ 20 ]. The overall purpose of the arousal response is to restore homeostasis by counteracting the initial discrepancy between expectations and reality. The arousal response is gradually turned off when successful "coping".
If not, the arousal may be sustained [ 19 ]. A threat to homeostasis elicits an arousal response, characterized by nervous and endocrine adjustments aiming at regaining homeostatic stability 1.
This compensatory mechanism is mutually connected to cognitive processes; in addition, it is influenced by personality, genetic traits and sensitization 2. If successful, i. Although quite uniform in gross, the details and dynamics of the arousal response vary among individuals. Genetic variability has some impact [ 20 ], but cognitive processes, evaluating the relationships between stimulus and expectancy, may be more important to explain individual variation [ 22 ].
The theoretical basis of CATS is the cognitive reformulations of learning theory [ 24 , 26 ], where classical conditioning is regarded as acquisition of expectancies of the outcomes of stimuli stimulus expectancies , and instrumental or operant conditioning as the acquisition of expectancies of the results of available responses response outcome expectancies.
Arousal response intensity increases if the stimulus expectancy has high affective value or if the response outcome expectancy is inadequate. Furthermore, experimental studies have demonstrated that arousal response can be modified by sensitization , the enhanced response to repeated stimulation [ 27 ]. This phenomenon has been described in detail on the cellular level [ 28 ], and is also considered important for disease development [ 29 , 30 ].
Thus, sensitization has been suggested as an important underlying mechanism in fibromyalgia [ 31 ], irritable bowel and functional dyspepsia [ 32 ], chemical intolerance, and somatization [ 30 ].
The arousal response is primarily adaptive and health-promoting. However, alterations of the response dynamics — in particular a state of maintenance, in CATS denoted sustained arousal — may contribute to disease [ 19 , 21 ].
The first author investigated cardiovascular and thermoregulatory homeostasis in adolescent CFS patients and healthy controls.
During supine rest, CFS patients had increased sympathetic nerve activity to the heart, the skeletal muscle arterioles and the adrenals; the latter causing increased plasma levels of epinephrine.
There was also evidence of increased arterial blood pressure and body temperature [ 33 — 35 ]. During orthostatic challenge, CFS patients demonstrated enhanced sympathetic nerve activity to the heart and the skeletal muscle arterioles, as well as increased arterial blood pressure [ 33 — 37 ]. However, when orthostatic challenge was combined with isometric exercise, CFS patients presented attenuated sympathetic cardiovascular outflow and a smaller increase in the arterial blood pressure [ 34 ].
During local cooling, CFS patients had attenuated sympathetic outflow to skin arterioles combined with normalization of body temperature [ 35 ]. Finally, CFS patients presented symptoms suggesting enhanced sympathetic nerve activity to the sweat glands, the skeletal muscles and the skin vessels [ 34 , 35 ].
Similar findings have previously been reported in other studies [ 10 , 11 ], and hypovolemia and deconditioning have been suggested as possible underlying mechanism. Yet, neither of these mechanisms can fully explain the results: Moderate hypovolemia usually does not cause altered blood pressure and body temperature [ 38 ], and deconditioning leads to attenuated sympathetic cardiovascular responses during orthostatic challenge [ 39 ].
Rather, the results suggest alterations of CNS autonomic control, corresponding with neuroimaging studies indicating functional alterations in relevant brain stem areas [ 40 ]. More specifically, the response patterns might all be explained by abnormalities in homeostatic set-point adjustments of blood pressure and body temperature [ 41 ]. For instance, abnormal increase in arterial blood pressure set-point during orthostatic challenge might enhance sympathetic nerve activity to the heart and the skeletal muscle arterioles, causing increased heart rate and total peripheral resistance and bringing the observed blood pressure value to a higher level.
According to stress theory, set-point changes of homeostatic control circuits are hallmarks of the arousal response, as is increased level of epinephrine [ 20 ], demonstrated in CFS patients by Wyller [ 35 ] and others [ 42 ]. Furthermore, Wyller and co-workers' results comply neatly with human and animal studies directly addressing cardiovascular and thermoregulatory alterations during arousal [ 43 , 44 ]. Thus, CFS patients seem to present an arousal response-physiology which is, however, inappropriate, being present both at rest and during maneuvers which are normally not distressing.
We propose these findings to be interpreted as indications of sustained arousal in CFS patients. The mechanism leading to sustained arousal in CFS might be hypothesized from stress theory Figure 2. Infections, which commonly trigger CFS, generally elicit a normal arousal response [ 45 ]. Comparable arousal responses can also be elicited by critical life events and perceived chronic difficulties [ 20 ], which have been associated with CFS outbreak Table 1.
Thus, a common characteristic of CFS precipitating factors seem to be their long-lasting character, which — according to CATS — may cause a comparably prolonged arousal response [ 19 ].
Proposed model of the origin of sustained arousal in Chronic fatigue syndrome. Certain threats to homeostasis, such as long-lasting infections and psychosocial challenges, may elicit a prolonged arousal response, which does not, however, solve the initial problem 1. The mutual relation to cognitive processes results in negative stimulus and response outcome expectancies, creating a vicious circle 2.
Certain genetic traits and aspects of personality may reinforce the arousal response further. This situation causes homeostatic instability in itself, establishing another vicious circle 3. In addition, the arousal response may eventually become associated with neutral events, such as moderate physical activity, through the process of classical conditioning 4. We propose that these mechanisms altogether elicit a state of sustained arousal 5. However, this arousal response might be insufficient in solving the initial problem.
An attempt of compensation would be to generate a stronger one. As there is no apparent solution to the individual, such attempts might be perceived as inadequate, resulting in negative stimulus and response outcome expectancy. Thus, a vicious circle is established, as the evaluation of the arousal response depends upon expectancies: negative expectations reinforce the arousal response [ 19 ].
This inappropriate learning process can be strengthened by attentiveness, corresponding with reports of increased focus on bodily sensations in CFS [ 5 ].
Increased worry about coping abilities is also suggested to be a risk factor [ 29 ], complying with personality traits that might be associated with CFS [ 4 ]. Finally, genetic factors might have important impact [ 19 ], and recent evidence indicates that certain polymorphisms in autonomic and endocrine effector systems are associated with CFS [ 3 ].
Therefore, when certain prerequisites are met, the arousal response might be strongly and paradoxically reinforced. This, in turn, may counteract homeostasis rather than restoring it, resulting in another vicious circle. Similar phenomena are demonstrated in hyperventilation, where an unpleasant experience triggers a mutual amplifying cascade of arousal response and unstable respiratory homeostasis, resulting in grossly abnormal blood gas levels [ 46 ]. A parallel would be that CFS patients maintain arousal in their pursuits to gain control over their own arousal response.
When the initial triggering factor subsides, classical conditioning may lead to associations between the arousal response and common neutral stimuli [ 47 ], like moderate physical activity. Therefore, inappropriate arousal may be precipitated in numerous situations. Sustained arousal might have detrimental effects, as evident from stress research experiments Figure 3.
Such consequences correspond well with empirical findings in CFS patients Table 1. The hemodynamic alterations have been presented above. Below, we shall substantiate our model discussing sustained arousal consequences in other organ systems in relation to CFS research evidence. Proposed model on the consequences of sustained arousal in CFS. Sustained arousal may cause alterations of immunity, skeletal muscle, cognitions, endocrine function and hemodynamics.
Some of these alterations may in turn establish vicious circles due to altered cytokine pattern, oxidative tissue damage and insufficient coping.
Finally, sustained arousal might be directly responsible for the experience of fatigue in these patients. A broad range of distressing events, including psychosocial challenges, have an impact on the immune system, such as attenuated cellular immunity and a tendency towards reactivation of latent virus infections [ 48 ]. Some of these effects might be attributed to increased sympathetic nerve activity and heightened levels of catecholamines, which in general promote a shift towards Th2 immune responses at the cost of Th1 immune responses [ 49 ], complying with findings among CFS patients [ 2 ].
Thus, immune dysfunction in CFS may be regarded an epiphenomenon rather than a causal factor [ 50 ]. Furthermore, the findings of increased activity of intracellular microorganisms in CFS patients, most convincingly reported for enteroviruses [ 7 ], are explained by reactivation of latent infections due to immunological alterations [ 51 ]. Although not a primary abnormality according to the sustained arousal model, immune dysfunction in CFS may contribute to vicious circles. For instance, catecholamines stimulate CNS secretion of the Th2-cytokine IL-6 [ 49 ], which in turn influences centers involved in arousal responses [ 52 ].