What is central sensitization and how is it treated?
What Is Central Sensitization? Central sensitization, in short, is a hypersensitivity to stimuli from things that are not typically painful. The first evidence of this type of hypersensitivity dates back to 1933. Living with any type of pain, acute or chronic, can interfere with many normal aspects of everyday life.
How does central sensitization affect pain?
Central sensitization decreases pain tolerance and produces lingering pain sensations after an initial injury has healed. Pain signals travel through a path in the spinal cord to the brain. Central sensitization causes this path to enlarge rather than restrict. The nervous system becomes impaired which leads to magnified pain sensations.
What is the difference between acute and central sensitization?
Because central sensitization results from changes in the properties of neurons in the central nervous system, the pain is no longer coupled, as acute nociceptive pain is, to the presence, intensity, or duration of noxious peripheral stimuli.
What is central sensitization in chronic fatigue?
Central sensitization is considered by many experts to be a key mechanism behind fibromyalgia and chronic fatigue syndrome. It helps explain many of the symptoms of these illnesses, including the way the body and brain amplify pain signals. In these conditions, problem stimuli can include: light touch, which becomes painful.
What are the symptoms of central sensitization?
What Are The Symptoms of Central Sensitization Syndrome?Sensitivity to odors, sounds, and lights.Poor short-term memory and concentration.Emotional distress like anxiety and depression.Widespread pain.Poor sleep and fatigue.Abdominal and pelvic pain.Headaches.
What are three conditions of central sensitization?
These include fibromyalgia, tension-type headache, temporomandibular joint disease and irritable bowel syndrome, all of which may have a specific contribution to their phenotype by central sensitization, as detailed above.
Can you cure central sensitization?
Treatments for central sensitization include pharmacological options, exercise therapy, and sleep management, as under the right conditions, central sensitization is manageable and often times reversible.
Is Central Sensitisation the same as fibromyalgia?
Fibromyalgia syndrome (FM), the most common central sensitivity syndrome (CSS) affecting over 5% of the population, is a disorder of chronic widespread pain accompanied by numerous other symptoms that causes significant functional impairment.
What is an example of central sensitization?
Patients who find themselves suffering from forms of central sensitization experience pain from stimuli that should not induce pain. Things as gentle as brushing the back of a hand with a cotton ball can cause extreme, intense pain. Nociceptors are sensory receptors that respond to painful stimuli.
What does sensitization feel like?
Sensitized patients are not only more sensitive to things that hurt, but tend to feel pain to ordinary touch and pressure. Central sensitization occurs through a process called wind-up, leaving the involved part of the nervous system in a state of high reactivity.
Which body systems are mostly affected in sensitization cases?
Central sensitization is responsible for many of the temporal, spatial, and threshold changes in pain sensibility in acute and chronic clinical pain settings and exemplifies the fundamental contribution of the central nervous system to the generation of pain hypersensitivity.
How common is central sensitization syndrome?
Central sensitization syndromes affect millions of Americans, but the exact number is unclear. While people can have overlapping disorders, estimates for some CSS conditions in the United States include: Fibromyalgia: 2% of adults6. Chronic fatigue syndrome: 0.25% to 0.75% of adults7.
How do you desensitize the central nervous system?
Taking deep breaths from your diaphragm can quiet the nervous system. Start with small movements. Focus on movements that you can perform for one or two minutes, and then gradually branch out to different or new ways of moving. Focus on one section of your body.
Is Central Sensitisation a diagnosis?
In both primary care and consultative practices, patients presenting with fibromyalgia (FM) often have other medically unexplained somatic symptoms and are ultimately diagnosed as having central sensitization (CS).
How does a neurologist treat fibromyalgia?
One of the effective methods of neurological treatment of pain syndrome in fibromyalgia is the use of antidepressants, which can reduce the intensity of pain, strengthen sleep and reduce fatigue in patients with fibromyalgia. Muscle relaxants.
Does fibromyalgia destroy nerves?
Researchers at Harvard-affiliated Massachusetts General Hospital found that some sufferers of fibromyalgia have damage to nerve fibers in their skin and other evidence of a disease called small-fiber polyneuropathy.
Which conditions have central sensitization as a feature?
Features of central sensitization have been identified in nearly all chronic pain conditions, and it is considered the primary underlying cause of pain in conditions such as fibromyalgia. Central sensitization is characterized in these conditions by widespread pain and multisite hyperalgesia/allodynia.
What causes central nervous system sensitization?
Central sensitization involves specific changes to the nervous system. Changes in the dorsal horn of the spinal cord and in the brain occur, particularly at the cellular level, such as at receptor sites. As stated above, it has long been known that strokes and spinal cord injuries can cause central sensitization.
What disorders result in central neuropathic pain?
Central pain syndrome is a neurological condition caused by damage to or dysfunction of the central nervous system (CNS), which includes the brain, brainstem, and spinal cord. This syndrome can be caused by stroke, multiple sclerosis, tumors, epilepsy, brain or spinal cord trauma, or Parkinson's disease.
Which body systems are mostly affected in sensitization cases?
Sensitization is a heightened sensitivity to stimuli that may occur normally in the central or peripheral nervous system, but this condition is also present in many chronic pain conditions. In pathological conditions, sensitization may produce pain stimuli even if no harmful events are occurring.
What is central sensitization?
Central sensitisation is defined as an increased responsiveness of nociceptors in the central nervous system to either normal or sub-threshold afferent input resulting in: Hypersensitivity to stimuli. Responsiveness to non-noxious stimuli.
Which mechanism is used to treat central sensitization?
Central sensitization is characterized by the absence of peripheral sources of nociceptive input, therefore it seems more appropriate to use a treatment with a top-down mechanism, activating descending nociceptive processing together with decreasing descending nociceptive facilitation.
When did Nijs and al. provide guidelines to aid the recognition of central sensitization on musculo?
In 2010 Nijs et al. provided guidelines to aid the recognition of central sensitization on musculoskeletal patients.
What stimuli had to be sustained,intense and repeated?
Found to invoke sensitization the noxious stimuli had to be sustained,intense and repeated.
What is the term used to describe the changes demonstrated in their group's 1983 study as "activity dependent central sensit?
Latremoliere and Woolf describe the changes demonstrated in their group's 1983 study as "activity dependent central sensitization".
What is the role of neural plasticity in cellular changes?
Neural plasticity plays a role in cellular changes with a demonstrable increase in both membrane excitability and synaptic efficacy.
Which pharmacological agents are inappropriate for central sensitization?
Pharmacological agents such as non-steroidal antiinflammatory drugs and coxibs have peripheral effects, and are therefore inappropriate for the treatment of central sensitization in patients with chronic pain.
Why is central sensitization important?
In nearly all chronic pain conditions, physicians and scientists consider central sensitization to be a key source of pain. Comorbidities that affect the nervous system, such as sleep deprivation, fatigue, and poor mood, can exacerbate the central sensitization’s effects, creating a destructive cycle between the conditions ( 5 ).
How Is Central Sensitization Diagnosed?
Conditions that target the nervous system are often difficult to diagnose. Your doctor will conduct a thorough examination, including possibly running several tests, to assess the presence of central sensitization.
What is the difference between neuropathic and nociceptive pain?
Nociceptive pain occurs usually in response to external stimuli, such as thermal, mechanical, or chemical. Neuropathic pain occurs in response to stimulus from an injury or damage to the nervous system itself, as opposed to anything that the nervous system may be connected to ( 6 ).
How do nociceptors respond to pain?
The body senses nociceptive pain through receptors called nociceptors. These sensors only respond to external stimuli. Researchers have found that these nociceptors can become “sensitized” after an injury. Interestingly, nociceptors also interact with immune cells to control inflammation, which may lead to increased pain through what’s called “neuroinflammation.” Injuries or trauma can affect nociceptor function, so that they respond to a stimulus for a prolonged amount of time. This is called hyperalgesic priming, and it occurs in many chronic pain conditions ( 7 ).
What are the two forms of central sensitization?
Central sensitization appears in two forms – allodynia and hyperalgesia.
What is temporal summation?
Temporal Summation. As a potential indicator of central sensitization, your doctor may test your nociceptors for temporal summation, which refers to an increase in the perceived intensity of pain in response to a stimulus of equal physical strength.
Can central sensitization be passed down through generations?
Your doctor will likely ask about your family history with chronic pain conditions. Central sensitization can be passed down through generations. It can also manifest in in neuroimaging scans in the form of gray matter changes in pain processing regions, neurochemical imbalances, and altered resting brain-network connectivity between different regions of the brain ( 8 ). Interestingly, physicians also report altered immune system activity in individuals with central sensitization.
What are the symptoms of central sensitization?
The two major characteristics of central sensitization involve heightened pain sensitivity ( hyperalgesia) and intensified touch sensations ( allodynia ). The most common symptoms of CS include constant pain, sleep interference and fatigue. Central sensitization symptoms may be mild for years; however, a minor mishap or illness can cause it to flare. Central sensitization can lead to widespread or generalized pain.
What is CS in pain?
It is associated with chronic pain progression due to an increased response to neurons in the central nervous system. Central sensitization decreases pain tolerance and produces lingering pain sensations after an initial injury has healed. Pain signals travel through a path in the spinal cord to the brain. Central sensitization causes this path to enlarge rather than restrict. The nervous system becomes impaired which leads to magnified pain sensations.
What are the symptoms of CS?
The most common symptoms of CS include constant pain, sleep interference and fatigue. Central sensitization symptoms may be mild for years; however, a minor mishap or illness can cause it to flare. Central sensitization can lead to widespread or generalized pain.
What Is Central Sensitization?
Central sensitization, in short, is a hypersensitivity to stimuli from things that are not typically painful. The first evidence of this type of hypersensitivity dates back to 1933. Living with any type of pain, acute or chronic, can interfere with many normal aspects of everyday life.
Central Sensitization and Other Forms of Chronic Pain
Also referred to as allodynia, central sensitization can be associated with other types of chronic pain including:
Central Sensitization Treatments
Because this can affect every individual differently, there is not a one-size-fits-all approach to treatment. At least there shouldn’t be. A multi-faceted approach to treatment is typically considered for patients with allodynia. Tricyclic compound medications also known as TCA’s are often used in cases such as these.
What is Central Sensitization?
When you feel pain, those signals are carried by nerves. Hence, nerves are a key part of your perception of pain. Another key part is your brain that registers the signal. Your sympathetic and other parts of your nervous system spend quite a bit of time regulating your pain and helping you ignore it. For example, we’ve all experienced having something that hurts, but when you’re focusing your attention elsewhere, you don’t notice it. That’s because your body has inhibitory circuitry that can temporarily inhibit the pain signal.
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What if we took all of the brakes off the pain and made the nerves very efficient at carrying pain signals?
What if we took all of the brakes off the pain and made the nerves very efficient at carrying pain signals? That’s called Central Sensitization (CS). Meaning small things cause big pain.
Why is CS a problem?
One of the traditional models for CS is similar to CRPS. This is believed to be a problem with the system that provides the brakes for pain signals. Another possibility is an injury to key nerves or the spinal cord. One of the newer theories for why CS happens is neuroinflammation (2). This is inflammation that impacts nerves which can happen if the patient has high total body inflammation. Also, metabolic syndromes (overweight, high blood pressure, low activity) can cause or make this problem worse.
What is temporal summation?
Temporal summation means that pain signals get added together rather than happening as individual events that each die off. If you look above, a pain stimulus in the form of a blood pressure cuff is used on a leg. In the normal patient, while there is some additive pain effect (building of the height of the VAS pain score) by repeatedly blowing up the cuff, that pales in comparison to what happens in the patient with CS on the bottom. In that case, the pain builds sharply as the number of cycles increases. That’s also called “wind-up”.
How to reduce flare ups of CS?
One of the things you can do to help reduce procedure-related flare-ups of CS is to get fewer pokes. For example, you may want to get it all done at once, but less is more. So if 5 injections were planned for the neck, and 10 for the shoulder, and 5 for the knee for a total of 20 sites, reducing that to 5 injections will often help limit the flare-up.
Is CRPS like CS?
Rarely, this can evolve into Complex Regional Pain Syndrome where even movement or light touch can be painful. CRPS is like CS on steroids.
Why is central sensitization important?
Central sensitization is considered by many experts to be a key mechanism behind fibromyalgia. Central sensitization may also be involved in certain aspects of chronic fatigue syndrome. It helps explain many of the symptoms of these illnesses, including the way the body and brain amplify pain signals.
What is central sensitivity syndrome?
a general increase in symptoms, when the reaction is tied to an illness. Conditions believed to involve central sensitization are classified as central sensitivity syndromes. Along with fibromyalgia and chronic fatigue syndrome, this umbrella term covers: irritable bowel syndrome. migraine.
What is the term for a gradual change in how your body reacts to a particular substance or stimuli?
Sensitization is a gradual change in how your body reacts to a particular substance or stimuli. In the immune system, sensitization results in an allergy. In the central nervous system, the result is called a sensitivity.
How does gradual change work?
The key to understanding this is the term gradual change. First, you're exposed, possibly repeatedly. Then, over time, your body becomes more and more irritated by the substance until it rises to a problem level. Now let's put the words back together.
What is the central nervous system?
Central, in this context, refers to the central nervous system, which comprises the brain and nerves of the spinal cord. This system regulates how your body responds to signals from the rest of the body.
What are the reactions to stimuli?
Reactions can include: headache. nausea.
What is central sensitization?
Central sensitization. With the induction of central sensitization in somatosensory pathways with increases in synaptic efficacy and reductions in inhibition , a central amplification occurs enhancing the pain response to noxious stimuli in amplitude, duration and spatial extent, while the strengthening of normally ineffective synapses recruits subliminal inputs such that inputs in low threshold sensory inputs can now activate the pain circuit. The two parallel sensory pathways converge.
What are the consequences of central sensitization?
These include long-term changes in nociceptive withdrawal reflexes [24] and increases in cortical event related potential amplitudes [240]. Magnetic source imaging reveals an increase in the excitability of neurons in the somatosensory cortex evoked by low threshold Aβ stimulation within the capsaicin-induced zone of secondary hyperalgesia [17], while magnetoencephalography detects changes in the patterns of cerebral processing [159] and functional MRI, changes in BOLD signals in the cortex, both during secondary hyperalgesia [16]. Another MRI study found changes in the brainstem that are apparently specific to central sensitization, in addition to the changes in the primary somatosensory cortex that are related to the intensity of pain [153].
What features of the clinical phenotype may be contributed to, or generated exclusively by central sensitization?
What features of the clinical phenotype may be contributed to, or generated exclusively by central sensitization? While the human experimental studies reviewed above indicate that if a patient has dynamic tactile allodynia, secondary punctuate/pressure hyperalgesia, temporal summation and sensory aftereffects, central sensitization may well be involved. Any sensory experience greater in amplitude, duration and spatial extent than that would be expected from a defined peripheral input under normal circumstances, qualifies as potentially reflecting a central amplification due to increased excitation or reduced inhibition. These changes could include a reduction in threshold, exaggerated response to a noxious stimulus, pain after the end of a stimulus, and a spread of sensitivity to normal tissue. However, because we cannot directly measure sensory inflow, and because peripheral changes can contribute to sensory amplification, as with peripheral sensitization, pain hypersensitivity by itself is not enough to make an irrefutable diagnosis of central sensitization. A further complication is that because peripheral input commonly is the trigger of central sensitization, a reduction in pain sensitivity produced by targeting a peripheral trigger with a local anesthetic does not exclude central amplification, but may rather indicate a role of peripheral input in maintaining it [140]. Nevertheless, there are some features of patient’s symptoms which are more likely to indicate central rather than peripheral contribution to pain hypersensitivity. These include pain mediated by low threshold Aβ fibers (determined by nerve block or electrical stimulation), a spread of pain sensitivity to areas with no demonstrable pathology, aftersensations, enhances temporal summation, and the maintenance of pain by low frequency stimuli that normally do not evoke any ongoing pain. To assess how central sensitization may present in patients, we need a detailed phenotyping of different patient cohorts to capture exactly what changes in sensitivity occur, where and when [93; 188; 86; 9; 11; 197; 55]. Ideally this should be combined with objective measures of central activity, such as fMRI, so that clear diagnostic criteria for determining the presence of central sensitization in patients can be established. The utility of diagnostic criteria for the presence of central sensitization would not only be insight into the pathophysiological mechanisms responsible for producing pain, but more so in defining potential treatment strategies. If a particular patient’s pain is primarily the result of abnormal activity in nociceptors, as in patients with primary erythromelalgia [74], the optimal therapy required is likely to be different from a patient whose tactile allodynia and secondary hyperalgesia are entirely maintained by central sensitization due to changes in synaptic efficacy in the spinal cord. This is the rationale for a mechanism-based approach to the diagnosis and treatment of pain [266; 258]. Indeed response to a trial treatment, such as to the NMDA receptor antagonist ketamine, can itself be a potential diagnostic for the presence central sensitization.
Is central sensitization a phenomenon?
The following conclusions can be made from this survey of the published studies of experimental pain hypersensitivity in human volunteers. Central sensitization is a robust phenomenon, readily induced in human volunteers in response to diverse ways of activating nociceptors (electrical stimulation, capsaicin, mustard oil, acid, heat burn, UV burn, hypertonic saline). Generally this activity-dependent plasticity manifests immediately, but its effects persist for many hours beyond the inducing conditioning stimulus, eventually returning, however, back to baseline, indicating its usual full reversibility. The phenomenon can be elicited by conditioning skin, muscle or visceral organs, and typically presents as dynamic tactile allodynia and punctate hyperalgesia but also enhanced pressure, and in some cases, thermal sensitivity, spreading from the conditioning site to neighboring non stimulated sites, and even to very remote regions. Although there is a homosynaptic (homotopic) aspect to the phenomenon, its major manifestation is heterosynaptic (heterotopic), and for this reason and its reversibility, it is perhaps inaccurate to equate central sensitization with the LTP like phenomena in the cortex that are specifically associated with long term memory. Because central sensitization can be induced in almost all subjects and detected using subjective and objective outcome measures and is sensitive to pharmacological interventions, it is a useful tool for determining the activity of drugs on centrally driven pain hypersensitivity.
Is there a gender difference in pain sensitivity?
Interestingly, while gender has been described as important for differences in nociceptive pain sensitivity, a study on the secondary hyperalgesia induced by heat and capsaicin did not reveal a gender difference [119]. Nevertheless, recent data show that pain sensitivity including secondary hyperalgesia and brush evoked allodynia is heritable, with an estimated 50% genetic contribution to the pain variance [172]. The genetic polymorphisms involved in the differential susceptibility to secondary hyperalgesia have not been comprehensively investigated, although some candidates are beginning to be identified in studies of experimental central sensitization [228]. This is an area that requires major research.
Does central sensitization cause pain?
That central sensitization could cause a spread of pain sensitivity across peripheral nerve territories, the neurological dogma for diagnosing a disease of the central rather than peripheral nervous system, was shown by Max and colleagues using the intradermal capsaicin model in volunteers together with radial or ulnar nerve blocks to clearly identify individual nerve territory [192]. Complementing this, a study comparing skin hyperaemia induced by a skin burn injury found that the skin blood flow changes induced by the injury had disappeared by the time secondary mechanical hyperalgesia peaked, and the two were not correlated in time or space, supporting the conclusion that peripheral mechanisms do not contribute to secondary hyperalgesia [198]. Even more dramatic perhaps, was the relatively recent demonstration that intradermal capsaicin induces contralateral hyperalgesia and allodynia that is delayed in its manifestation and reduced in extent compared to the ipsilateral secondary hyperalgesia, but present in a majority of subjects [206], a form perhaps of “tertiary hyperalgesia” that cannot be peripheral in origin. What pain sensitivity we feel then, can be determined by the state of excitability of neurons in the CNS.
Which system is mediated by the strong synaptic inputs between the particular sensory inputs and pathways?
Normal sensation. The somatosensory system is organized such that the highly specialized primary sensory neurons that encode low intensity stimuli only activate those central pathways that lead to innocuous sensations, while high intensity stimuli that activate nociceptors only activate the central pathways that lead to pain and the two parallel pathways do not functionally intersect. This is mediated by the strong synaptic inputs between the particular sensory inputs and pathways and inhibitory neurons that focus activity to these dedicated circuits.
What is CSS treatment?
The different individual symptoms and mechanisms of each CSS require a customized treatment approach, but in general, most CSS tend to respond to some of the same types of treatment, especially antidepressants (which help correct neurotransmitter dysregulation), exercise, and cognitive-behavioral therapy (CBT). 4
What is the pain of CSS?
The pain of CSS comes from a couple of different abnormal pain types: hyperalgesia and allodynia. Hyperalgesia takes normal pain from things that everyone considers painful (a broken limb, an infected tooth, etc.) and makes it worse. It's often referred to as "turning up the volume" of pain.
What are the conditions that are part of CSS?
It may also involve certain foods or chemicals. Especially in FMS, the body is sensitized to anything unpleasant, i.e., cold, heat, a tickle or an itch. Aside from FMS and ME/CFS, the following conditions have been proposed to be part of the CSS family: 2 . Chronic pelvic pain, including vulvodynia.
What is CSS in medical terms?
An illness described as a CSS involves something called central sensitization. "Central" means the central nervous system, which is made up of your brain and spinal cord. "Sensitization" is the end result of something that has made you sensitive.
Is CSS a physical reaction?
In fact, while the sensitivities of a CSS aren't exactly allergies, they do involve an inappropriate physical reaction. In CSS, we become sensitive to things that are processed by the central nervous system, which can include bright lights, loud noises, strong smells, rough textures, and pressure on the body.
