Chronic pain

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Chronic_pain 

 

Chronic Pain
Other names	Burning pain, dull pain, throbbing pain
Heavy and irregular sports, in a long term, can be the basis of joint or bone injuries and as a result chronic pain.
Specialty	Specialist in pain, neurology and psychology
Symptoms	Pain lasts longer than the expected period of recovery.
Usual onset	All age groups
Duration	From three months to several years
Causes	high blood sugar, cancer, genetic disorder in neural differentiation, tissue damage, neurological disorder and viral diseases
Risk factors	diabetes, cancer and heart diseases
Diagnostic method	Based on medical history, clinical examination, questionnaire and neuroimaging
Differential diagnosis	gastric ulcer, bone fracture, hernia and neoplasia of the spinal cord
Medication	Non-opioid: ibuprofen, acetaminophen, naproxen, NSAIDs and olanzapine Opioid: morphine, codeine, endorphins and buprenorphine
Frequency	8% to 55.2% in different countries

Chronic pain or chronic pain syndrome is a type of pain that is also known by other titles such as gradual burning pain, electrical pain, throbbing pain, and nauseating pain. This type of pain is sometimes confused with acute pain and can last from three months to several years; Various diagnostic manuals such as DSM-5 and ICD-11 have proposed several definitions of chronic pain, but the accepted definition is that it is "pain that lasts longer than the expected period of recovery."

Creating a pain mechanism prevents possible damage to the body, but chronic pain is a pain without biological value (doesn't have a positive effect). This pain has different divisions; Cancer, post-traumatic or surgery, musculoskeletal and visceral are the most important of these divisions. Various factors cause the formation of chronic pain, which can be neurogenic (gene-dependent), nociceptive, neuropathic, psychological or unknown. Some diseases such as diabetes (high blood sugar), shingles (some viral diseases), phantom limb pain, hypertension and stroke also play a role in the formation of chronic pain. The most common types of chronic pain are back pain, severe headache, migraine, and facial pain.

Chronic pain can cause very severe psychological and physical effects that sometimes continue until the end of life. Analysis of the grey matter (damage to brain neurons), insomnia and sleep deprivation, metabolic problems, chronic stress, obesity and heart attack are examples of physical disorder; And depression, cognitive disorders, perceived injustice (PI) and neurosis are examples of mental disorder.

A wide range of treatments are performed for this disease; Drug therapy (types of opioid and non-opioid drugs), cognitive behavioral therapy and physical therapy are the most significant of them. Medicines are usually associated with side effects and are prescribed when the effects of pain become severe. Medicines such as aspirin and ibuprofen are used for milder pain and morphine and codeine for severe pain. Other treatment methods, such as behavioral therapy and physiotherapy, are often used as a supplement along with drugs due to their low effectiveness. There is currently no definitive cure for any of these methods, and research continues into a wide variety of new management and therapeutic interventions, such as nerve block and radiation therapy.

Chronic pain is considered a kind of disease, this type of pain has affected the people of the world more than diabetes, cancer and heart diseases. During several epidemiological studies conducted in different countries, wide differences in the prevalence rate of chronic pain have been reported from 8% to 55.2% in countries; For example, studies evaluate the incidence in Iran and Canada between 10% and 20% and in the United States between 30% and 40%. The results show that an average of 8% to 11.2% of people in different countries have severe chronic pain, and its epidemic is higher in industrialized countries than in other countries. According to the estimates of the American Medical Association, the costs related to this disease in this country are about 560 to 635 billion dollars.

Classification

Main article: Pain § Classification

The International Association for the Study of Pain (IASP) defines chronic pain as a general pain without biological value that sometimes continues even after the healing of the affected area; A type of pain that cannot be classified as acute pain and lasts longer than expected to heal, or typically, pain that has been experienced on most days or daily for the past six months, is considered chronic pain. According to the DSM-5 index, a complication is "chronic" when the resulting complication (pain, disorder, and illness) lasts for a period of more than six months (this type of classification does not have any prerequisites such as physical or mental injury). The classification of chronic pain is not only limited to pains that arise in the presence of real tissue damage (secondary pains resulting from a primary event); The title "nociplastic pain" or primary pain is related to the pains that occur in the absence of a health-threatening factor, such as disease or damage to the body's somatosensory system, and as a result of permanent nerve stimulation.

The International Statistical Classification of Diseases, in its 11th edition (ICD-11), proposed a seven-category classification for chronic pain:

1. Primary chronic pain: Defined by 3 months of continuous pain in one or more areas of the body, the origin of which is not understood.
2. Chronic cancer pain: pain in one of the body's organs caused by cancer damage (in internal organs, bone or skeletal muscular) is formed.
3. Chronic pain post-traumatic or surgery: Pain that occurs 3 months after an injury or surgery, without taking into account infectious conditions and the severity of tissue damage; Also, the person's past pain is not important in this classification.
4. Chronic neuropathic pain: pain caused by damage to the somatosensory nervous system.
5. Chronic headache and orofacial pain: pain that originates in the head or face, and occurs for 50% or more days over a 3 months period.
6. Chronic visceral pain: pain originating in an internal organ.
7. Chronic musculoskeletal pain: pain originating in the bones, muscles, joints or connective tissue.

Also, the World Health Organization (WHO) states that optional criteria or codes can be used in the classification of chronic pain for each of the seven categories of chronic pain (for example, "diabetic neuropathic" pain).

Another classification for chronic pain is "nociceptive" (caused by inflamed or damaged tissue that activates special pain sensors called nociceptors) and "neuropathic" (caused by damage or malfunction of the nervous system). The type of "nociceptive" itself is divided into two parts: "superficial" and "deep"; also, deep pains are divided into two parts: "deep physical" and "deep visceral" pain. "neuropathic" pains are also divided into "peripheral" (source The peripheral nervous system) and "central" (Central nervous system from the brain or spinal cord) are divided. Peripheral neuropathic pain is often described as "burning", "tingling", "electrical", "stabbing", or "pins and needles".

"Superficial pain" is the result of the activation of pain receptors in the skin or superficial tissues; "Deep somatic pain" is caused by stimulation of pain receptors in ligaments, tendons, bones, blood vessels, fascia, and muscles. (this type of pain is constant but weak) and "deep visceral pain" is pain that originates from one of the body's organs. Deep pain is often very difficult to localize and occurs in multiple areas of the body when injured or inflamed. In the "deep visceral" type, the feeling of pain exists in a place far from the injury, for this reason it is also called vague pain.

Etiology

Chronic pain has many pathophysiological and environmental causes and can occur in cases such as neuropathy of the central nervous system, after cerebral hemorrhage, tissue damage such as extensive burns, inflammation, autoimmune disorders such as rheumatoid arthritis, psychological stress such as headache, migraine or abdominal pain (caused by emotional, psychological or behavioral) and mechanical pain caused by tissue wear and tear such as arthritis. In some cases, chronic pain can be caused by genetic factors which interfere with neuronal differentiation, leading to a permanently lowered threshold for pain.

The pathophysiology of chronic pain remains unclear. Many theories of chronic pain fail to clearly explain why the same pathological conditions do not invariably result in chronic pain. Patients' anatomical predisposition to proximal neural compression (in particular of peripheral nerves) may be the answer to this conundrum. Difficulties in diagnosing proximal neural lesion may account for the theoretical perplexity of chronic pain.

Pathophysiology

Continuous pressure on the spine can destroy the intervertebral disc and cause the sciatic nerve to actively produce pain.

The mechanism of continuous activation and transmission of pain messages, leads the body to an activity to relieve pain (a mechanism to prevent damage in the body), this action causes the release of prostaglandin and increase the sensitivity of that part to stimulation; Prostaglandin secretion causes unbearable and chronic pain. Under persistent activation, the transmission of pain signals to the dorsal horn may produce a pain wind-up phenomenon. This triggers changes that lower the threshold for pain signals to be transmitted. In addition, it may cause non-nociceptive nerve fibers to respond to, generate, and transmit pain signals. Researchers believe that the nerve fibers that cause this type of pain are group C nerve fibers; These fibers are not myelinated (have low transmission speed) and cause long-term pain.

These changes in neural structure can be explained by neuroplasticity. When there is chronic pain, the somatotopic arrangement of the body (the distribution view of nerve cells) is abnormally changed due to continuous stimulation and can cause allodynia or hyperalgesia. In chronic pain, this process is difficult to reverse or stop once established. EEG of people with chronic pain showed that brain activity and synaptic plasticity change as a result of pain, and specifically, the relative activity of beta wave increases and alpha and theta waves decrease.

Inefficient management of dopamine secretion in the brain can act as a common mechanism between chronic pain, insomnia and major depressive disorder and cause its unpleasant side effects. Astrocytes, microglia and satellite glial cells also lose their effective function in chronic pain. Increasing the activity of microglia, changing microglia networks, and increasing the production of chemokines and cytokines by microglia may exacerbate chronic pain. It has also been observed that astrocytes lose their ability to regulate the excitability of neurons and increase the spontaneous activity of neurons in pain circuits.

Management

Main article: Pain management

Pain management is a branch of medicine that uses an interdisciplinary approach. The combined knowledge of various medical professions and allied health professions is used to ease pain and improve the quality of life of those living with pain. The typical pain management team includes medical practitioners (particularly anesthesiologists), rehabilitation psychologists, physiotherapists, occupational therapists, physician assistants, and nurse practitioners. Acute pain usually resolves with the efforts of one practitioner; however, the management of chronic pain frequently requires the coordinated efforts of a treatment team. Complete, longterm remission of many types of chronic pain is rare.

Chronic pain may originate in the body, or in the brain or spinal cord. It is often difficult to treat. Epidemiological studies have found that 8–11.2% of people in various countries have chronic widespread pain. Various non-opioid medicines are initially recommended to treat chronic pain, depending on whether the pain is due to tissue damage or is neuropathic. Psychological treatments including cognitive behavioral therapy and acceptance and commitment therapy may be effective for improving quality of life in those with chronic pain. Some people with chronic pain may benefit from opioid treatment while others can be harmed by it. People with non-cancer pain who have not been helped by non-opioid medicines might be recommended to try opioids if there is no history of substance use disorder and no current mental illness.

Nonopioids

Initially recommended efforts are non-opioid based therapies. Non-opioid treatment of chronic pain with pharmaceutical medicines might include acetaminophen (paracetamol) or NSAIDs.

Various other nonopioid medicines can be used, depending on whether the pain is a result of tissue damage or is neuropathic (pain caused by a damaged or dysfunctional nervous system). There is limited evidence that cancer pain or chronic pain from tissue damage as a result of a conditions (e.g. rheumatoid arthritis) is best treated with opioids. For neuropathic pain other drugs may be more effective than opioids, such as tricyclic antidepressants, serotonin-norepinephrine reuptake inhibitors, and anticonvulsants. Some atypical antipsychotics, such as olanzapine, may also be effective, but the evidence to support this is in very early stages. In women with chronic pain, hormonal medications such as oral contraceptive pills ("the pill") might be helpful. When there is no evidence of a single best fit, doctors may need to look for a treatment that works for the individual person. It is difficult for doctors to predict who will use opioids just for pain management and who will go on to develop an addiction. It is also challenging for doctors to know which patients ask for opioids because they are living with an opioid addiction. Withholding, interrupting or withdrawing opioid treatment in people who benefit from it can cause harm.

Interventional pain management may be appropriate, including techniques such as trigger point injections, neurolytic blocks, and radiotherapy. While there is no high quality evidence to support ultrasound, it has been found to have a small effect on improving function in non-specific chronic low back pain.

Psychological treatments, including cognitive behavioral therapy and acceptance and commitment therapy can be helpful for improving quality of life and reducing pain interference. Brief mindfulness-based treatment approaches have been used, but they are not yet recommended as a first-line treatment. The effectiveness of mindfulness-based pain management (MBPM) has been supported by a range of studies.

Among older adults psychological interventions can help reduce pain and improve self-efficacy for pain management. Psychological treatments have also been shown to be effective in children and teens with chronic headache or mixed chronic pain conditions.

While exercise has been offered as a method to lessen chronic pain and there is some evidence of benefit, this evidence is tentative. For people living with chronic pain, exercise results in few side effects.

Opioids

In those who have not benefited from other measures and have no history of either mental illness or substance use disorder treatment with opioids may be tried. If significant benefit does not occur it is recommended that they be stopped. In those on opioids, stopping or decreasing their use may improve outcomes including pain.

Some people with chronic pain benefit from opioid treatment and others do not; some are harmed by the treatment. Possible harms include reduced sex hormone production, hypogonadism, infertility, impaired immune system, falls and fractures in older adults, neonatal abstinence syndrome, heart problems, sleep-disordered breathing, opioid-induced hyperalgesia, physical dependence, addiction, abuse, and overdose.

Alternative medicine

Alternative medicine refers to health practices or products that are used to treat pain or illness that are not necessarily considered a part of conventional medicine. When dealing with chronic pain, these practices generally fall into the following four categories: biological, mind-body, manipulative body, and energy medicine.

Implementing dietary changes, which is considered a biological-based alternative medicine practice, has been shown to help improve symptoms of chronic pain over time. Adding supplements to one's diet is a common dietary change when trying to relieve chronic pain, with some of the most studied supplements being: acetyl-L-carnitine, alpha-lipoic acid, and vitamin E. Vitamin E is perhaps the most studied out of the three, with strong evidence that it helps lower neurotoxicity in those with cancer, multiple sclerosis, and cardiovascular diseases.

Hypnosis, including self-hypnosis, has tentative evidence. Hypnosis, specifically, can offer pain relief for most people and may be a safe alternative to pharmaceutical medication. Evidence does not support hypnosis for chronic pain due to a spinal cord injury.

Preliminary studies have found medical marijuana to be beneficial in treating neuropathic pain, but not other kinds of long term pain. As of 2018, the evidence for its efficacy in treating neuropathic pain or pain associated with rheumatic diseases is not strong for any benefit and further research is needed. For chronic non-cancer pain, a recent study concluded that it is unlikely that cannabinoids are highly effective. However, more rigorous research into cannabis or cannabis-based medicines is needed.

Tai chi has been shown to improve pain, stiffness, and quality of life in chronic conditions such as osteoarthritis, low back pain, and osteoporosis. Acupuncture has also been found to be an effective and safe treatment in reducing pain and improving quality of life in chronic pain including chronic pelvic pain syndrome.

Transcranial magnetic stimulation for reduction of chronic pain is not supported by high quality evidence, and the demonstrated effects are small and short-term.

Spa therapy could potentially improve pain in patients with chronic lower back pain, but more studies are needed to provide stronger evidence of this.

While some studies have investigated the efficacy of St John's Wort or nutmeg for treating neuropathic (nerve) pain, their findings have raised serious concerns about the accuracy of their results.

Kinesio tape has not been shown to be effective in managing chronic non-specific low-back pain.

Myofascial release has been used in some cases of fibromyalgia, chronic low back pain, and tennis elbow but there is not enough evidence to support this as method of treatment.

Epidemiology

Chronic pain varies in different countries affecting anywhere from 8% to 55% of the population. It affects women at a higher rate than men, and chronic pain uses a large amount of healthcare resources around the globe.

A large-scale telephone survey of 15 European countries and Israel found that 19% of respondents over 18 years of age had suffered pain for more than 6 months, including the last month, and more than twice in the last week, with pain intensity of 5 or more for the last episode, on a scale of 1 (no pain) to 10 (worst imaginable). 4839 of these respondents with chronic pain were interviewed in-depth. Sixty-six percent scored their pain intensity at moderate (5–7), and 34% at severe (8–10); 46% had constant pain, 56% intermittent; 49% had suffered pain for 2–15 years; and 21% had been diagnosed with depression due to the pain. Sixty-one percent were unable or less able to work outside the home, 19% had lost a job, and 13% had changed jobs due to their pain. Forty percent had inadequate pain management and less than 2% were seeing a pain management specialist.

In the United States, chronic pain has been estimated to occur in approximately 35% of the population, with approximately 50 million Americans experiencing partial or total disability as a consequence.^[91] According to the Institute of Medicine, there are about 116 million Americans living with chronic pain, which suggests that approximately half of American adults have some chronic pain condition.^[92][93] The Mayday Fund estimate of 70 million Americans with chronic pain is slightly more conservative.^[94] In an internet study, the prevalence of chronic pain in the United States was calculated to be 30.7% of the population: 34.3% for women and 26.7% for men.

In Canada it is estimated that approximately 1 in 5 Canadians live with chronic pain and half of those people have lived with chronic pain for 10 years or longer. Chronic pain in Canada also occurs more and is more severe in women and Canada's Indigenous communities.

Outcomes

Sleep disturbance, and insomnia due to medication and illness symptoms are often experienced by those with chronic pain. These conditions can be difficult to treat due to the high potential of medication interactions, especially when the conditions are treated by different doctors.

Severe chronic pain is associated with increased risk of death over a ten-year period, particularly from heart disease and respiratory disease. Several mechanisms have been proposed for this increase, such as an abnormal stress response in the body's endocrine system. Additionally, chronic stress seems to affect risks to heart and lung (cardiovascular) health by increasing how quickly plaque can build up on artery walls (arteriosclerosis). However, further research is needed to clarify the relationship between severe chronic pain, stress and cardiovascular health.

People with chronic pain tend to have higher rates of depression and although the exact connection between the comorbidities is unclear, a 2017 study on neuroplasticity found that "injury sensory pathways of body pains have been shown to share the same brain regions involved in mood management." Chronic pain can contribute to decreased physical activity due to fear of making the pain worse. Pain intensity, pain control, and resilience to pain can be influenced by different levels and types of social support that a person with chronic pain receives, and are also influenced by the person's socioeconomic status.

Chronic pain of different causes has been characterized as a disease that affects brain structure and function. MRI studies have shown abnormal anatomical and functional connectivity, even during rest involving areas related to the processing of pain. Also, persistent pain has been shown to cause grey matter loss, which is reversible once the pain has resolved.

One approach to predicting a person's experience of chronic pain is the biopsychosocial model, according to which an individual's experience of chronic pain may be affected by a complex mixture of their biology, psychology, and their social environment.

Psychology

Personality

Two of the most frequent personality profiles found in people with chronic pain by the Minnesota Multiphasic Personality Inventory (MMPI) are the conversion V and the neurotic triad. The conversion V personality expresses exaggerated concern over body feelings, develops bodily symptoms in response to stress, and often fails to recognize their own emotional state, including depression. The neurotic triad personality also expresses exaggerated concern over body feelings and develops bodily symptoms in response to stress, but is demanding and complaining.

Some investigators have argued that it is this neuroticism that causes acute pain to turn chronic, but clinical evidence points the other way, to chronic pain causing neuroticism. When long term pain is relieved by therapeutic intervention, scores on the neurotic triad and anxiety fall, often to normal levels. Self-esteem, often low in people with chronic pain, also shows improvement once pain has resolved.

It has been suggested that catastrophizing might play a role in the experience of pain. Pain catastrophizing is the tendency to describe a pain experience in more exaggerated terms than the average person, to think a great deal more about the pain when it occurs, or to feel more helpless about the experience. People who score highly on measures of catastrophization are likely to rate a pain experience as more intense than those who score low on such measures. It is often reasoned that the tendency to catastrophize causes the person to experience the pain as more intense. One suggestion is that catastrophizing influences pain perception through altering attention and anticipation, and heightening emotional responses to pain. However, at least some aspects of catastrophization may be the product of an intense pain experience, rather than its cause. That is, the more intense the pain feels to the person, the more likely they are to have thoughts about it that fit the definition of catastrophization.

Comorbidity with trauma

Individuals with post-traumatic stress disorder (PTSD) have a high comorbidity with chronic pain. Patients with both PTSD and chronic pain report higher severity of pain than those who do not have a PTSD comorbidity.

Comorbidity with depression

People with chronic pain may also have symptoms of depression. In 2017, the British Medical Association found that 49% of people with chronic pain had depression.

Effect on cognition

Chronic pain's impact on cognition is an under-researched area, but several tentative conclusions have been published. Most people with chronic pain complain of cognitive impairment, such as forgetfulness, difficulty with attention, and difficulty completing tasks. Objective testing has found that people in chronic pain tend to experience impairment in attention, memory, mental flexibility, verbal ability, speed of response in a cognitive task, and speed in executing structured tasks. A review of studies in 2018 reports a relationship between people in chronic pain and abnormal results in test of memory, attention, and processing speed.

Prognosis

Chronic pain leads to a significant decrease in quality of life, decreased productivity, decreased wages, worsening of other chronic diseases, and mental disorders such as depression, anxiety, and substance use disorder. Many drugs that are often used to treat chronic pain have risks and potential side effects and possible complications associated with their use, and the constant use of opioids is associated with decreased life expectancy and increased mortality of patients. Acetaminophen, a standard drug treatment for chronic pain, can cause hepatotoxicity when taken in excess of four grams per day. In addition, therapeutic doses for patients with chronic liver diseases may also cause hepatotoxicity. Long-term risks and side effects of opioids include constipation, drug tolerance or dependence, nausea, indigestion, arrhythmia (QT prolongation of electrocardiography in methadone treatment), and endocrine gland that can lead to amenorrhea, impotence, gynecomastia, and decreased become energy. Also there is a risk of opioid overdose depending on the dose taken by the patient.

Current treatments for chronic pain can reduce pain by 30%. This reduction in pain can significantly improve patients' performance and quality of life. However, the general and long-term prognosis of chronic pain shows decreased function and quality of life. Also, this disease causes many complications and increases the possibility of death of patients and suffering from other chronic diseases and obesity. Similarly, patients with chronic pain who require opioids often develop drug tolerance over time, and this increase in the amount of the dose taken to be effective increases the risk of side effects and death.

Mental disorders can amplify pain signals and make symptoms more severe. In addition, comorbid psychiatric disorders, such as major depressive disorder, can significantly delay the diagnosis of pain disorders. Major depressive disorder and generalized anxiety disorder are the most common comorbidities associated with chronic pain. Patients with underlying pain and comorbid mental disorders receive twice as much medication from doctors annually as compared to patients who do not have such co-morbidities. Studies have shown that when coexisting diseases exist along with chronic pain, the treatment and improvement of one of these disorders can be effective in the improvement of the other. Patients with chronic pain are at higher risk for suicide and suicidal thoughts. Research has shown approximately 20% of people with suicidal thoughts and between 5 and 14% of patients with chronic pain who commit suicide. Of patients who attempted suicide, 53.6% died of gunshot wounds and 16.2% died of opioid overdose. A multimodal treatment approach is important for better pain control and outcomes, as well as minimizing the need for high-risk treatments such as opioid medications. Managing comorbid depression and anxiety is critical in reducing chronic pain. Also, patients with chronic pain should be carefully monitored for severe depression and any suicidal thoughts and plans. Periodic referral of the patient to the doctor for physical examination and to check the effectiveness of treatment 2 is necessary, and the rapid and correct treatment and management of chronic pain can prevent the occurrence of potential negative consequences on the patient's life and increase in healthcare costs.

Social and personal impacts

Social support

Social support has important consequences for individuals with chronic pain. In particular, pain intensity, pain control, and resiliency to pain have been implicated as outcomes influenced by different levels and types of social support. Much of this research has focused on emotional, instrumental, tangible and informational social support. People with persistent pain conditions tend to rely on their social support as a coping mechanism and therefore have better outcomes when they are a part of larger more supportive social networks. Across a majority of studies investigated, there was a direct significant association between social activities or social support and pain. Higher levels of pain were associated with a decrease in social activities, lower levels of social support, and reduced social functioning.

Racial disparities

Evidence exists for unconscious biases and negative stereotyping against racial minorities requesting pain treatment, although clinical decision making was not affected, according to one 2017 review. Minorities may be denied diagnoses for pain and pain medications, and are more likely to go through substance abuse assessment, and are less likely to transfer for pain specialist referral. A 2010 University of Michigan Health study found that black patients in pain clinics received 50% of the amount of drugs that patients who were white received. Preliminary research showed that health providers might have less empathy for black patients and underestimated their pain levels, resulting in treatment delays. Minorities may experience a language barrier, limiting the high level of engagement between the person with pain and health providers for treatment.

Perceptions of injustice

Similar to the damaging effects seen with catastrophizing, perceived injustice is thought to contribute to the severity and duration of chronic pain. Pain-related injustice perception has been conceptualized as a cognitive appraisal reflecting the severity and irreparability of pain- or injury-related loss (e.g., "I just want my life back"), and externalizing blame and unfairness ("I am suffering because of someone else's negligence."). It has been suggested that understanding problems with top down processing/cognitive appraisals can be used to better understand and treat this problem.

Chronic pain and COVID-19

COVID-19 has disrupted the lives of many, leading to major physical, psychological and socioeconomic impacts in the general population. Social distancing practices defining the response to the pandemic alter familiar patterns of social interaction, creating the conditions for what some psychologists are describing as a period of collective grief. Individuals with chronic pain tend to embody an ambiguous status, at times expressing that their type of suffering places them between and outside of conventional medicine. With a large proportion of the global population enduring prolonged periods of social isolation and distress, one study found that people with chronic pain from COVID-19 experienced more empathy towards their suffering during the pandemic.

Effect of chronic pain in the workplace

In the workplace, chronic pain conditions are a significant problem for both the person with the condition and the organization; a problem only expected to increase in many countries due to an aging workforce. In light of this, it may be helpful for organizations to consider the social environment of their workplace, and how it may be working to ease or worsen chronic pain issues for employees. As an example of how the social environment can affect chronic pain, some research has found that high levels of socially prescribed perfectionism (perfectionism induced by external pressure from others, such as a supervisor) can interact with the guilt felt by a person with chronic pain, thereby increasing job tension, and decreasing job satisfaction.

Postural orthostatic tachycardia syndrome

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Postural_orthostatic_tachycardia_syndrome

 

Postural orthostatic tachycardia syndrome
Acrocyanosis in a male Norwegian POTS patient
Specialty	Cardiology, neurology
Symptoms	More often with standing: lightheadedness, trouble thinking, tachycardia, weakness, palpitations, heat intolerance, acrocyanosis
Usual onset	Most common (modal) age of onset is 14 years
Types	Neuropathic POTS, Hyperadrenergic POTS, Secondary POTS.
Causes	Antibodies against the Alpha 1 adrenergic receptor and muscarinic acetylcholine M4 receptor
Risk factors	Family history, Ehlers Danlos Syndrome
Diagnostic method	An increase in heart rate by 30 beats/min with standing
Differential diagnosis	Dehydration, heart problems, adrenal insufficiency, epilepsy, Parkinson's disease, anemia
Treatment	Avoiding factors that bring on symptoms, increasing dietary salt and water, compression stockings, exercise, medications
Medication	Off label Medications: Beta blockers, Ivabradine, midodrine, and fludrocortisone.
Prognosis	c. 90% improve with treatment, 25% of patients unable to work
Frequency	~ 1,000,000 ~ 3,000,000 (US)

Postural orthostatic tachycardia syndrome (POTS) is a condition characterized by an abnormally large increase in heart rate upon sitting up or standing. POTS is a disorder of the autonomic nervous system that can lead the individual to experience a variety of symptoms. Symptoms may include lightheadedness, brain fog, blurred vision, weakness, fatigue, headaches, heart palpitations, exercise intolerance, nausea, diminished concentration, tremulousness (shaking), syncope (fainting), coldness or pain in the extremities, chest pain and shortness of breath. Other conditions associated with POTS include migraine headaches, Ehlers–Danlos syndrome, asthma, autoimmune disease, vasovagal syncope and mast cell activation syndrome. POTS symptoms may be treated with lifestyle changes such as increasing fluid and salt intake, wearing compression stockings, gentler and slow postural changes, avoiding prolonged bedrest, medication, increasing electrolyte intake, and physical therapy.

The causes of POTS are varied. POTS may develop after a viral infection, surgery, trauma, or pregnancy. It has been shown to emerge in previously healthy patients after COVID-19, or in rare cases after COVID-19 vaccination. POTS is more common among people who got infected with SARS-CoV-2 than among those who got vaccinated against COVID-19. Risk factors include a family history of the condition. POTS in adults is characterized by a heart rate increase of 30 beats per minute within ten minutes of standing up, accompanied by other symptoms. This increased heart rate should occur in the absence of orthostatic hypotension (>20 mm Hg drop in systolic blood pressure) to be considered POTS. A spinal fluid leak (called spontaneous intracranial hypotension) may have the same signs and symptoms as POTS and should be excluded. Prolonged bedrest may lead to multiple symptoms, including blood volume loss and postural tachycardia. Other conditions which can cause similar symptoms, such as dehydration, orthostatic hypotension, heart problems, adrenal insufficiency, epilepsy, and Parkinson's disease, must not be present. Treatment may include avoiding factors that bring on symptoms, increasing dietary salt and water, small and frequent meals, avoidance of immobilization, wearing compression stockings, and taking medications. Medications used may include beta blockers, pyridostigmine, midodrine or fludrocortisone. More than 50% of patients whose condition was triggered by a viral infection get better within five years. About 80% of patients have symptomatic improvement with treatment, while 25 percent of patients are so disabled they are unable to work. A retrospective study on patients with adolescent-onset has shown that five years after diagnosis, 19% of patients had a full resolution of symptoms.

It is estimated that 1–3 million people in the United States have POTS. The average age for POTS onset is 20 years, and it occurs about five times more frequently in females than in males.

Signs and symptoms

Person standing and measuring heart rate with a pulse oximeter which shows tachycardia of 108 bpm

In adults, the primary manifestation is an increase in heart rate of more than 30 beats per minute within ten minutes of standing up. The resulting heart rate is typically more than 120 beats per minute. For people between ages 12 and 19, the minimum increase for a POTS diagnosis is 40 beats per minute. POTS is often accompanied by common features of orthostatic intolerance—in which symptoms that develop while upright are relieved by reclining. These orthostatic symptoms include palpitations, light-headedness, chest discomfort, shortness of breath, nausea, weakness or "heaviness" in the lower legs, blurred vision, and cognitive difficulties. Symptoms may be exacerbated with prolonged sitting, prolonged standing, alcohol, heat, exercise, or eating a large meal.

Up to one-third of POTS patients experience fainting for many reasons, including but not limited to standing, physical exertion, or heat exposure. POTS patients may also experience orthostatic headaches. Some POTS patients may develop blood pooling in the extremities, characterized by a reddish-purple color of the legs and/or hands upon standing. 48% of people with POTS report chronic fatigue and 32% report sleep disturbances. Other POTS patients only exhibit the cardinal symptom of orthostatic tachycardia. Additional signs and symptoms are varied, and may include excessive sweating, lack of sweating, heat intolerance, digestive issues such as nausea, indigestion, constipation or diarrhea, post-exertional malaise, coat-hanger pain, brain fog, and syncope or presyncope.

Whereas POTS is primarily characterized by its profound impact on the autonomic and cardiovascular systems, it can lead to substantial functional impairment. This impairment, often manifesting as symptoms such as fatigue, cognitive dysfunction, and sleep disturbances, can significantly diminish the patient's quality of life.

Brain fog

One of the most disabling and prevalent symptoms in POTS is "brain fog", a term used by patients to describe the cognitive difficulties they experience. In one survey of 138 POTS patients, brain fog was defined as "forgetful" (91%), "difficulty thinking" (89%), and "difficulty focusing" (88%). Other common descriptions were "difficulty processing what others say" (80%), "confusion" (71%), "getting lost" (64%), and "thoughts moving too quickly" (40%). The same survey described the most common triggers of brain fog to be fatigue (91%), lack of sleep (90%), prolonged standing (87%), and dehydration (86%).

Neuropsychological testing has shown that a POTS patient has reduced attention (Ruff 2&7 speed and WAIS-III digits forward), short-term memory (WAIS-III digits back), cognitive processing speed (Symbol digits modalities test), and executive function (Stroop word color and trails B).

A potential cause for brain fog is a decrease in cerebral blood flow (CBF), especially in upright position.

There may be a loss of neurovascular coupling and reduced functional hyperemia in response to cognitive challenge under orthostatic stress – perhaps related to a loss of autoregulatory buffering of beat-by-beat fluctuations in arterial blood flow.

Causes

The symptoms of POTS can be caused by several distinct pathophysiological mechanisms. These mechanisms are poorly understood, and can overlap, with many patients showing features of multiple POTS types. Many people with POTS exhibit low blood volume (hypovolemia), which can decrease the rate of blood flow to the heart. To compensate for low blood volume, the heart increases its cardiac output by beating faster (reflex tachycardia), leading to the symptoms of presyncope.

In the 30% to 60% of cases classified as hyperadrenergic POTS, norepinephrine levels are elevated on standing, often due to hypovolemia or partial autonomic neuropathy. A smaller minority of people with POTS have (typically very high) standing norepinephrine levels that are elevated even in the absence of hypovolemia and autonomic neuropathy; this is classified as central hyperadrenergic POTS. The high norepinephrine levels contribute to symptoms of tachycardia. Another subtype, neuropathic POTS, is associated with denervation of sympathetic nerves in the lower limbs. In this subtype, it is thought that impaired constriction of the blood vessels causes blood to pool in the veins of the lower limbs. Heart rate increases to compensate for this blood pooling.

In up to 50% of cases, there was an onset of symptoms following a viral illness. It may also be linked to physical trauma, concussion, pregnancy, surgery or psychosocial stress. It is believed that these events could act as a trigger for an autoimmune response that result in POTS. It has been shown to emerge in previously healthy patients after COVID-19 or after COVID-19 vaccination. A 2023 review found that the chances of being diagnosed with POTS within 90 days after mRNA vaccination were 1.33 times higher compared to 90 days before vaccination, still, the results are inconclusive due to a small sample size; only 12 cases of newly diagnosed POTS after mRNA vaccination were reported, all these 12 patients having autoimmune antibodies. However, the risk of POTS-related diagnoses was 5.35 times higher after getting infected with SARS-CoV-2 compared to after mRNA vaccination. Possible mechanisms for COVID-induced POTS are hypovolemia, autoimmunity/inflammation from antibody production against autonomic nerve fibers, and direct toxic effects of COVID-19, or secondary sympathetic nervous system stimulation.

POTS is more common in females than males. POTS also has been linked to patients with a history of autoimmune diseases, Long Covid, irritable bowel syndrome, anemia, hyperthyroidism, fibromyalgia, diabetes, amyloidosis, sarcoidosis, systemic lupus erythematosus, and cancer. Genetics likely plays a role, with one study finding that one in eight POTS patients reported a history of orthostatic intolerance in their family.

Autoimmunity

There is an increasing number of studies indicating that POTS is an autoimmune disease. A high number of patients has elevated levels of autoantibodies against the adrenergic alpha 1 receptor and against the muscarinic acetylcholine M4 receptor.

Elevations of autoantibodies targeting adrenergic α1 receptor has been associated with symptoms severity in patients with POTS.

More recently, autoantibodies against other targets have been identified in small cohorts of POTS patients. Signs of innate immune system activation with elaboration of pro-inflammatory cytokines has also been reported in a cohort of POTS patients.

Secondary POTS

If POTS is caused by another condition, it may be classified as secondary POTS. Chronic diabetes mellitus is one common cause. POTS can also be secondary to gastrointestinal disorders that are associated with low fluid intake due to nausea or fluid loss through diarrhea, leading to hypovolemia. Systemic lupus erythematosus and other autoimmune diseases have also been linked to POTS.

There is a subset of patients who present with both POTS and mast cell activation syndrome (MCAS), and it is not yet clear whether MCAS is a secondary cause of POTS or simply comorbid, however, treating MCAS for these patients can significantly improve POTS symptoms.

POTS can also co-occur in all types of Ehlers–Danlos syndrome (EDS), a hereditary connective tissue disorder marked by loose hypermobile joints prone to subluxations and dislocations, skin that exhibits moderate or greater laxity, easy bruising, and many other symptoms. A trifecta of POTS, EDS, and mast cell activation syndrome (MCAS) is becoming increasingly more common, with a genetic marker common among all three conditions. POTS is also often accompanied by vasovagal syncope, with a 25% overlap being reported. There are some overlaps between POTS and chronic fatigue syndrome, with evidence of POTS in 10–20% of CFS cases. Fatigue and reduced exercise tolerance are prominent symptoms of both conditions, and dysautonomia may underlie both conditions.

POTS can sometimes be a paraneoplastic syndrome associated with cancer.

There are case reports of people developing POTS and other forms of dysautonomia post-COVID. There is no good large-scale empirical evidence yet to prove a connection, so for now the evidence is preliminary.

Diagnosis

Results of a tilt table test positive for POTS

POTS is most commonly diagnosed by a cardiologist (41%), cardiac electrophysiologist (15%), or neurologist (19%). The average number of physicians seen before receiving diagnosis is seven, and the average delay before diagnosis is 4.7 years.

Diagnostic criteria

A POTS diagnosis requires the following characteristics:

• For patients age 20 or older, a sustained increase in heart rate ≥30 bpm within ten minutes of upright posture (tilt table test or standing) from a supine position.
  • For patients age 12–19, heart rate increase must be >40 bpm.
• Associated with frequent symptoms of lightheadedness, palpitations, tremulousness, generalized weakness, blurred vision, or fatigue that are worse with upright posture and that improve with recumbence.
• An absence of orthostatic hypotension (i.e. no sustained systolic blood pressure drop of 20 mmHg or more).
• Chronic symptoms that have lasted for longer than three months.
• In the absence of other disorders, medications, or functional states that are known to predispose to orthostatic tachycardia.

Alternative tests to the tilt table test are also used, such as the NASA Lean Test and the adapted Autonomic Profile (aAP) which require less equipment to complete.

Orthostatic intolerance

An increase in heart rate upon moving to an upright posture is known as orthostatic (upright) tachycardia (fast heart rate). It occurs without any coinciding drop in blood pressure, as that would indicate orthostatic hypotension. Certain medications to treat POTS may cause orthostatic hypotension. It is accompanied by other features of orthostatic intolerance—symptoms that develop in an upright position and are relieved by reclining. These orthostatic symptoms include palpitations, light-headedness, chest discomfort, shortness of breath, nausea, weakness or "heaviness" in the lower legs, blurred vision, and cognitive difficulties.

Differential diagnoses

A variety of autonomic tests are employed to exclude autonomic disorders that could underlie symptoms, while endocrine testing is used to exclude hyperthyroidism and rarer endocrine conditions. Electrocardiography is normally performed on all patients to exclude other possible causes of tachycardia. In cases where a particular associated condition or complicating factor are suspected, other non-autonomic tests may be used: echocardiography to exclude mitral valve prolapse, and thermal threshold tests for small-fiber neuropathy.

Testing the cardiovascular response to prolonged head-up tilting, exercise, eating, and heat stress may help determine the best strategy for managing symptoms. POTS has also been divided into several types (see § Causes), which may benefit from distinct treatments. People with neuropathic POTS show a loss of sweating in the feet during sweat tests, as well as impaired norepinephrine release in the leg, but not arm. This is believed to reflect peripheral sympathetic denervation in the lower limbs. People with hyperadrenergic POTS show a marked increase of blood pressure and norepinephrine levels when standing, and are more likely to have from prominent palpitations, anxiety, and tachycardia. People with POTS can be misdiagnosed with inappropriate sinus tachycardia (IST) as they present similarly. One distinguishing feature is those with POTS rarely exhibit >100 bpm while in a supine position, while patients with IST often have a resting heart rate >100 bpm. Additionally patients with POTS display a more pronounced change in heart rate in response to postural change.

Treatment

POTS treatment involves using multiple methods in combination to counteract cardiovascular dysfunction, address symptoms, and simultaneously address any associated disorders. For most patients, water intake should be increased, especially after waking, in order to expand blood volume (reducing hypovolemia). Eight to ten cups of water daily are recommended. Increasing salt intake, by adding salt to food, taking salt tablets, or drinking sports drinks and other electrolyte solutions is an effective way to raise blood pressure by helping the body retain water. Different physicians recommend different amounts of sodium to their patients. Combining these techniques with gradual physical training enhances their effect. In some cases, when increasing oral fluids and salt intake is not enough, intravenous saline or the drug desmopressin is used to help increase fluid retention.

Large meals worsen symptoms for some people. These people may benefit from eating small meals frequently throughout the day instead. Alcohol and food high in carbohydrates can also exacerbate symptoms of orthostatic hypotension. Excessive consumption of caffeine beverages should be avoided, because they can promote urine production (leading to fluid loss) and consequently hypovolemia. Exposure to extreme heat may also aggravate symptoms.

Prolonged physical inactivity can worsen the symptoms of POTS. Techniques that increase a person's capacity for exercise, such as endurance training or graded exercise therapy, can relieve symptoms for some patients. Aerobic exercise performed for 20 minutes a day, three times a week, is sometimes recommended for patients who can tolerate it. Exercise may have the immediate effect of worsening tachycardia, especially after a meal or on a hot day. In these cases, it may be easier to exercise in a semi-reclined position, such as riding a recumbent bicycle, rowing, or swimming.

When changing to an upright posture, finishing a meal, or concluding exercise, a sustained hand grip can briefly raise the blood pressure, possibly reducing symptoms. Compression garments can also be of benefit by constricting blood pressures with external body pressure.

Aggravating factors include exertion (81%), continued standing (80%), heat (79%), and after meals (42%).

Medication

If nonpharmacological methods are ineffective, medication may be necessary. Medications used may include beta blockers, pyridostigmine, midodrine, or fludrocortisone. As of 2013, no medication has been approved by the U.S. Food and Drug Administration to treat POTS, but a variety are used off-label. Their efficacy has not yet been examined in long-term randomized controlled trials.

Fludrocortisone may be used to enhance sodium retention and blood volume, which may be beneficial not only by augmenting sympathetically mediated vasoconstriction, but also because a large subset of POTS patients appear to have low absolute blood volume. However, fludrocortisone may cause hypokalemia.

While people with POTS typically have normal or even elevated arterial blood pressure, the neuropathic form of POTS is presumed to constitute a selective sympathetic venous denervation. In these patients the selective Alpha-1 adrenergic receptor agonist midodrine may increase venous return, enhance stroke volume, and improve symptoms. Midodrine should only be taken during the daylight hours as it may promote supine hypertension.

Sinus node blocker Ivabradine can successfully restrain heart rate in POTS without affecting blood pressure, demonstrated in approximately 60% of people with POTS treated in an open-label trial of ivabradine experienced symptom improvement.

Pyridostigmine has been reported to restrain heart rate and improve chronic symptoms in approximately half of people. However, it may cause GI side effects that limit its use in around 20% of its patient population.

The selective alpha-1 agonist phenylephrine has been used successfully to enhance venous return and stroke volume in some people with POTS. However, this medication may be hampered by poor oral bioavailability.

Pharmacologic treatments for postural tachycardia syndrome

POTS subtypes	Therapeutic action	Goal	Drug(s)
Neuropathic POTS	Alpha-1 adrenergic receptor agonist	Constrict the peripheral blood vessels aiding venous return.	Midodrine
	Splanchnic–mesenteric vasoconstriction	Splanchnic vasoconstriction	Octreotide
Hypovolemic POTS	Synthetic mineralocorticoid	Forces the body to retain salt. Increase blood volume	Fludrocortisone (Florinef)
	Vasopressin receptor agonist	Helps retain water, Increase blood volume	Desmopressin (DDAVP)
Hyperadrenergic POTS	Beta-blockers (non-selective)	Decrease sympathetic tone and heart rate.	Propranolol (Inderal)
	Beta-blockers (selective)		Metoprolol (Toprol), Bisoprolol
	Selective sinus node blockade	Directly reducing tachycardia.	Ivabradine
	Alpha-2 adrenergic receptor agonist	Decreases blood pressure and sympathetic nerve traffic.	Clonidine, Methyldopa
	Anticholinesterase inhibitors	Splanchnic vasoconstriction. Increase blood pressure.	Pyridostigmine
Other (refractory POTS)	Psychostimulant	Improve cognitive symptoms (brain fog)	Modafinil
	Central nervous system stimulant	Tighten blood vessels. Increases alertness and improves brain fog.	Methylphenidate (Ritalin, Concerta)
	Direct and indirect α1-adrenoreceptor agonist.	Increased blood flows	Ephedrine and Pseudoephedrine
	Norepinephrine precursor	Improve blood vessel contraction	Droxidopa (Northera)
	Alpha-2 adrenergic antagonist	Increase blood pressure	Yohimbine

Prognosis

POTS has a favorable prognosis when managed appropriately. Symptoms improve within five years of diagnosis for many patients, and 60% return to their original level of functioning. Approximately 90% of people with POTS respond to a combination of pharmacological and physical treatments. Those who develop POTS in their early to mid teens will likely respond well to a combination of physical methods as well as pharmacotherapy. Outcomes are more guarded for adults newly diagnosed with POTS. Some people do not recover, and a few even worsen with time. The hyperadrenergic type of POTS typically requires continuous therapy. If POTS is caused by another condition, outcomes depend on the prognosis of the underlying disorder.

Epidemiology

The prevalence of POTS is unknown. One study estimated a minimal rate of 170 POTS cases per 100,000 individuals, but the true prevalence is likely higher due to underdiagnosis. Another study estimated that there are at least 500,000 cases in the United States. POTS is more common in women than men, with a female-to-male ratio of 4:1. Most people with POTS are aged between 20 and 40, with an average onset of 21. Diagnoses of POTS beyond age 40 are rare, perhaps because symptoms improve with age.

As recently stated, up to one-third of POTS patients also present with Vasovagal Syncope (VVS).  This ratio is probably higher if pre-Syncope patients, patients that report the symptoms of Syncope without overt fainting, were included.  Given the difficulty with current autonomic measurements in quantitatively isolating and differentiating Parasympathetic (Vagal) activity from Sympathetic activity without assumption or approximation, the current direction of research and clinical assessment is understandable:  perpetuating uncertainty regarding underlying cause, prescribing beta-blockers and proper daily hydration as the only therapy, not addressing the orthostatic dysfunction as the underlying cause, and recommending acceptance and associated lifestyle changes to cope. 

Direct measures of Parasympathetic (Vagal) activity obviates the uncertainty and lack of true relief of POTS as well as VVS.  For example, the hypothesis that POTS is an auto-immune disorder may be an indication that a significant number of POTS cases are indeed co-morbid with VVS.  Remember the Parasympathetic Nervous System is the memory for, and controls and coordinates, the immune system.  If Parasympathetic (Vagal) over-, or prolonged-, activation is chronic then portions of the immune system may remain active beyond the limits of the infection.  Given that portions of the immune system are not of self, these portions remain active and continue to “feed.”  Once the only source of “feed” is self, the immune system begins to attack the host.  This is the definition of autoimmune.  This is a counter-hypothesis that may provide a simpler explanation with a more immediate plan for therapy and relief.  For it may be that relieving the Vagal over-activation, will retires the self-attacking portion of the immune system, thereby relieving the autoimmunity.

Another example may be “Hyperadrenergic POTS.”  A counter hypothesis and perhaps a simpler explanation that leads to more direct therapy and improved outcomes is again the fact that POTS and VVS may be co-morbid.  It is well known that Parasympathetic (Vagal) over-activation may cause secondary Sympathetic over-activation.  Without direct Parasympathetic (Vagal) measures, the resulting assumption is that the secondary Sympathetic over-activation (the definition of “hyperadrenergic”) is actually the primary autonomic dysfunction.  Simply treating the (secondary) Sympathetic over-activation may be just treating a symptom in these cases, which may work for a while but then the body compensates and more medication is needed or the patient become unresponsive and the permanent degraded lifestyles are considered the only option.  Again, this is unfortunate.  Given that cases of POTS with VVS involves different portions of the nervous system (Parasympathetic and Sympathetic), and that both branches may be treated simultaneously, albeit differently, true relief of both conditions, as needed, is quite possible, and the cases of these newer hypothesized causes may be relieved with current, less expensive, and shorter-term therapy modalities.

Co-morbidities

Conditions that are commonly reported with POTS include:

• Migraine headaches (40%)
• Ehlers–Danlos syndrome (18–25%)
• Asthma (20%)
• Autoimmune disease (16%)
• Vasovagal syncope (13%)
• Mast cell activation disorder (9%)

History

In 1871, physician Jacob Mendes Da Costa described a condition that resembled the modern concept of POTS. He named it irritable heart syndrome. Cardiologist Thomas Lewis expanded on the description, coining the term soldier's heart because it was often found among military personnel. The condition came to be known as Da Costa's syndrome, which is now recognized as several distinct disorders, including POTS. Postural tachycardia syndrome was coined in 1982 in a description of a patient who had postural tachycardia, but not orthostatic hypotension. Ronald Schondorf and Phillip A. Low of the Mayo Clinic first used the name postural orthostatic tachycardia syndrome, POTS, in 1993.

Notable cases

British politician Nicola Blackwood revealed in March 2015 that she had been diagnosed with Ehlers–Danlos syndrome in 2013 and that she had later been diagnosed with POTS. She was appointed Parliamentary Under-Secretary of State for Life Science by Prime Minister Theresa May in 2019 and given a life peerage that enabled her to take a seat in Parliament. As a junior minister, it is her responsibility to answer questions in parliament on the subjects of Health and departmental business. When answering these questions, it is customary for ministers to sit when listening to the question and then to rise to give an answer from the despatch box, thus standing up and sitting down numerous times in quick succession throughout a series of questions. On 17 June 2019, she fainted during one of these questioning sessions after standing up from a sitting position four times in the space of twelve minutes, and it was suggested that her POTS was a factor in her fainting. Asked about the incident, she stated: "I was frustrated and embarrassed my body gave up on me at work ... But I am grateful it gives me a chance to shine a light on a condition many others are also living with."