Osteoporosis is a major public health threat that affects more than half of persons older than 50 years. The most common bone disease in humans, osteoporosis is associated with pain, disability, and increased risk of mortality.
The primary reference that clinicians use in managing osteoporosis is the National Osteoporosis Foundation’s (NOF) Clinician’s Guide to Prevention and Treatment of Osteoporosis, published in 1999 and updated in 2003. The guidelines in this publication represented the standard of care but did not adequately address some populations that may be affected by osteoporosis. For example, little guidance was offered on how to treat men with osteoporosis or how to approach the variations associated with ethnicity.
Many clinicians welcomed the comprehensive revised NOF guidelines released in February 2008, appreciating the new practice parameters that addressed previous areas of concern not mentioned in the 2003 document. The NOF guidelines were complemented by release of the World Health Organization’s (WHO) fracture risk assessment tool (FRAX), which helped physicians and patients gain a better understanding of a specific patient’s 10-year absolute risk of an osteoporosis-related fragility fracture. The primary goal of treatment is to reduce the incidence and the morbidity and mortality associated with osteoporosis-related fragility fractures. Treatment often includes lifestyle modifications, such as performance of weight-bearing exercises. A number of pharmacological therapies are currently available, although gaining patients’ adherence to therapy remains a challenge. Several new agents are under investigation.
This 2-part article provides an overview of osteoporosis diagnosis and management. In this first part, we interpret and summarize recent publications in this field; pool the data that are of greatest relevance to primary care physicians, including the epidemiology; review technologies available for diagnosis; and help decipher whom to test and to treat. The second part, to appear in a later issue of this journal, will discuss the current therapies for osteoporosis, their adverse effects, and reasonable approaches to monitoring.
Osteoporosis is a threat to an estimated 44 million Americans. Ten million Americans are thought to already have the disorder and an estimated 34 million more to have low bone mass.1
Significant risk has been reported in all ethnicities. An estimated 20% of white and Asian women older than 50 years are thought to have osteoporosis; in a similar age-group, 5% of African American women and 10% of Hispanic women are thought to have the disease.
Osteoporosis risk is increasing most rapidly among Hispanic women.1 Some studies have shown that they consume less calcium than the recommended dietary allowance in all age-groups. Also, Hispanic women are twice as likely as white women to have diabetes mellitus, which may increase their risk of osteoporosis.2 Although osteoporosis is largely thought of as a disease that affects women, its prevalence is 7% in white men, 5% in African American men, and 3% in Hispanic men.3
Research into the diagnosis and management of osteoporosis continues to expand; the disease is projected to affect an even larger portion of the US population over the next 15 years as the average age increases. The economic burden is estimated to rise to more than $17 billion annually in the United States alone.4 By 2025, the costs of osteoporotic-related fractures are expected to rise to about $25 billion.1 The economic consequence is proposed to increase by about 50%.
A dramatic reality is that 1 of 2 women and 1 of 4 men 50 years and older probably will have an osteoporosis-related fracture in their lifetime. Therefore, clinicians should be well aware of osteoporosis and have a good understanding of its diagnosis and appropriate management.
The NOF defines osteoporosis as a disease characterized by low bone mass and structural deterioration of bone tissue that lead to bone fragility and an increased susceptibility to fractures (especially of the hip, spine, and wrist, although any bone can be affected).1 The WHO defines osteoporosis as a systemic skeletal disease characterized by low bone mass and microarchitectural deterioration of bone tissue, with a consequent increase in bone fragility and susceptibility to fractures.5
The WHO further defines osteoporosis through radiographic parameters obtained from dual-energy x-ray absorptiometry (DXA) on the basis of its 1994 classification (Table 1).5 T-score refers to the standard deviation between a patient’s bone mineral density (BMD) and that of a young adult in the reference population. The Z-score is a comparison of the patient’s BMD with an age-matched population.5
Osteopenia is now generally accepted as being synonymous with low bone mass. Note that patients with low bone mass are not necessarily at high risk for fracture.6
A diagnosis of osteoporosis may be made clinically by the occurrence of fragility fractures. In their absence, however, the gold standard test for low BMD and osteoporosis is DXA. A fragility fracture is defined as a pathological fracture that occurs as a result of a fall from a standing height or lower. Fractures in this context suggest weakness of the bony skeleton.
However, bone strength reflects not only BMD—the amount of calcium hydroxyapatite per square centimeter of bone—but also integration of bone density with bone quality (the architecture, turnover, damage accumulation [eg, microfractures], and mineralization of bone).7 Despite widespread use of DXA for measurement of BMD, currently there is no simplistic way to measure bone quality that also can affect overall bone strength.
Clinical experience has highlighted a number of risk factors related to the development of osteoporosis and fragility fractures (Table 2). Some are modifiable, but others, such as genetic and ethnic predisposition, are beyond the control of the patient and clinician.
Fluctuating hormone levels in both men and women are known risk factors. Low estrogen levels in women (menopause and amenorrhea) and low levels of testosterone in men are both implicated. There is an increased risk with older age, a history of previous fracture, and a family history of osteoporosis or family history of previous fracture. Other reported variables that influence osteoporosis development include low body mass index; inactivity; cigarette smoking; excessive alcohol(Drug information on alcohol) intake (defined as 3 or more drinks per day); and a diet low in calcium and vitamin D but high in protein, sodium, and caffeine(Drug information on caffeine).
The use of a number of medications has been associated with an increased risk of osteoporosis. Systemic corticosteroids, heparin(Drug information on heparin), levothyroxine replacement therapy, and anticonvulsant therapy are among the most common.1 Diseases that may result in an increased risk of secondary osteoporosis include endocrinopathies, malabsorptive GI conditions, congestive heart failure, blood dyscrasia, osteogenesis imperfecta, amyloidosis, and inflammatory arthropathies.1 Read The Full Report
Osteoporosis is a major public health threat that affects more than half of persons older than 50 years. The most common bone disease in humans, osteoporosis is associated with pain, disability, and increased risk of mortality.
The primary reference that clinicians use in managing osteoporosis is the National Osteoporosis Foundation’s (NOF) Clinician’s Guide to Prevention and Treatment of Osteoporosis, published in 1999 and updated in 2003. The guidelines in this publication represented the standard of care but did not adequately address some populations that may be affected by osteoporosis. For example, little guidance was offered on how to treat men with osteoporosis or how to approach the variations associated with ethnicity.
Many clinicians welcomed the comprehensive revised NOF guidelines released in February 2008, appreciating the new practice parameters that addressed previous areas of concern not mentioned in the 2003 document. The NOF guidelines were complemented by release of the World Health Organization’s (WHO) fracture risk assessment tool (FRAX), which helped physicians and patients gain a better understanding of a specific patient’s 10-year absolute risk of an osteoporosis-related fragility fracture. The primary goal of treatment is to reduce the incidence and the morbidity and mortality associated with osteoporosis-related fragility fractures. Treatment often includes lifestyle modifications, such as performance of weight-bearing exercises. A number of pharmacological therapies are currently available, although gaining patients’ adherence to therapy remains a challenge. Several new agents are under investigation.
This 2-part article provides an overview of osteoporosis diagnosis and management. In this first part, we interpret and summarize recent publications in this field; pool the data that are of greatest relevance to primary care physicians, including the epidemiology; review technologies available for diagnosis; and help decipher whom to test and to treat. The second part, to appear in a later issue of this journal, will discuss the current therapies for osteoporosis, their adverse effects, and reasonable approaches to monitoring.
Osteoporosis is a threat to an estimated 44 million Americans. Ten million Americans are thought to already have the disorder and an estimated 34 million more to have low bone mass.1
Significant risk has been reported in all ethnicities. An estimated 20% of white and Asian women older than 50 years are thought to have osteoporosis; in a similar age-group, 5% of African American women and 10% of Hispanic women are thought to have the disease.
Osteoporosis risk is increasing most rapidly among Hispanic women.1 Some studies have shown that they consume less calcium than the recommended dietary allowance in all age-groups. Also, Hispanic women are twice as likely as white women to have diabetes mellitus, which may increase their risk of osteoporosis.2 Although osteoporosis is largely thought of as a disease that affects women, its prevalence is 7% in white men, 5% in African American men, and 3% in Hispanic men.3
Research into the diagnosis and management of osteoporosis continues to expand; the disease is projected to affect an even larger portion of the US population over the next 15 years as the average age increases. The economic burden is estimated to rise to more than $17 billion annually in the United States alone.4 By 2025, the costs of osteoporotic-related fractures are expected to rise to about $25 billion.1 The economic consequence is proposed to increase by about 50%.
A dramatic reality is that 1 of 2 women and 1 of 4 men 50 years and older probably will have an osteoporosis-related fracture in their lifetime. Therefore, clinicians should be well aware of osteoporosis and have a good understanding of its diagnosis and appropriate management.
The NOF defines osteoporosis as a disease characterized by low bone mass and structural deterioration of bone tissue that lead to bone fragility and an increased susceptibility to fractures (especially of the hip, spine, and wrist, although any bone can be affected).1 The WHO defines osteoporosis as a systemic skeletal disease characterized by low bone mass and microarchitectural deterioration of bone tissue, with a consequent increase in bone fragility and susceptibility to fractures.5
The WHO further defines osteoporosis through radiographic parameters obtained from dual-energy x-ray absorptiometry (DXA) on the basis of its 1994 classification (Table 1).5 T-score refers to the standard deviation between a patient’s bone mineral density (BMD) and that of a young adult in the reference population. The Z-score is a comparison of the patient’s BMD with an age-matched population.5
Osteopenia is now generally accepted as being synonymous with low bone mass. Note that patients with low bone mass are not necessarily at high risk for fracture.6
A diagnosis of osteoporosis may be made clinically by the occurrence of fragility fractures. In their absence, however, the gold standard test for low BMD and osteoporosis is DXA. A fragility fracture is defined as a pathological fracture that occurs as a result of a fall from a standing height or lower. Fractures in this context suggest weakness of the bony skeleton.
However, bone strength reflects not only BMD—the amount of calcium hydroxyapatite per square centimeter of bone—but also integration of bone density with bone quality (the architecture, turnover, damage accumulation [eg, microfractures], and mineralization of bone).7 Despite widespread use of DXA for measurement of BMD, currently there is no simplistic way to measure bone quality that also can affect overall bone strength.
Clinical experience has highlighted a number of risk factors related to the development of osteoporosis and fragility fractures (Table 2). Some are modifiable, but others, such as genetic and ethnic predisposition, are beyond the control of the patient and clinician.
Fluctuating hormone levels in both men and women are known risk factors. Low estrogen levels in women (menopause and amenorrhea) and low levels of testosterone in men are both implicated. There is an increased risk with older age, a history of previous fracture, and a family history of osteoporosis or family history of previous fracture. Other reported variables that influence osteoporosis development include low body mass index; inactivity; cigarette smoking; excessive alcohol(Drug information on alcohol) intake (defined as 3 or more drinks per day); and a diet low in calcium and vitamin D but high in protein, sodium, and caffeine(Drug information on caffeine).
The use of a number of medications has been associated with an increased risk of osteoporosis. Systemic corticosteroids, heparin(Drug information on heparin), levothyroxine replacement therapy, and anticonvulsant therapy are among the most common.1 Diseases that may result in an increased risk of secondary osteoporosis include endocrinopathies, malabsorptive GI conditions, congestive heart failure, blood dyscrasia, osteogenesis imperfecta, amyloidosis, and inflammatory arthropathies.1 Read The Full Report
“Doctor, I’m so relieved to see you,” the patient said. “The nurse practitioner told me I have osteoarthritis (OA) all over. I hurt terribly. I tried Tylenol and Advil, but they didn’t help. Some of my friends with similar problems have told me they had newer treatments, like Lyrica, Neurontin, Cymbalta, Ultram, and Savella, as well as herbal medications, ginger, massage, fish oils, yoga, electromagnetic field therapy, spas, glucosamine(Drug information on glucosamine), chrondroitin, acupuncture, tidal irrigation, marijuana, patches, ointments, Duragesic, joint injections, and operations—after they had extensive MRI and other testing—and swear by the results. I’m confused and don’t know what to do. Please help! I’m so desperate!”
Treatment of patients with OA pain can be challenging but is rewarding, because they can be helped, sometimes dramatically. By using a principle- and evidence-based approach, physicians can improve patients’ function and comfort and reduce their pain and disability. Their lives are restored, at least in part, and that is enormously satisfying.
By clinical definition, OA includes painful symptoms. Therefore, all approaches to management—from the simplest to the most aggressive—are designed to benefit patients. Used properly, they are inextricably linked and are part of an effective therapeutic regimen.
This principle- and evidence-based approach has been effective for most patients, providing comfort, reducing disability, and improving quality of life. The occasional patients who do not respond reasonably well to such a comprehensive therapeutic regimen may benefit from referral to more expert consultants. In this article, we describe the principles of caring for patients with painful OA. We discuss approaches to patients with “pain all over” and approaches to pain management in specific joints.
Principles of managing OA
PRINCIPLES OF CARE
• Confirm the diagnosis. Do not miss calcium pyrophosphate dihydrate crystal deposition disease, inflammatory arthritis, erosive/inflammatory OA, polymyalgia rheumatica (PMR), fibromyalgia syndrome (FMS) (alone or superimposed), associated depression, neurological or vascular disease, endocrinological disease (thyroid or parathyroid), chronic pain syndromes (eg, complex regional pain syndrome), tendinitis/bursitis (do not confuse epicondylitis with elbow disease, de Quervain tenosynovitis with wrist arthritis, anserine bursitis with knee arthritis, or trochanteric bursitis with hip disease), ochronosis, or hemochromatosis. When in doubt, obtain expert consultation.
• Seek preventable or reversible underlying or primary disease.
The basic principles for managing osteoarthritis (OA) pain include identifying the disease site or sites. Disease may be “generalized” but often is localized to specific joints. As in other joints, local heat, physical measures, and topical therapies may be beneficial for knee OA.
• Identify the site or sites of OA. Disease may be “generalized” but often is localized to specific joints, such as the distal interphalangeal (DIP), first metacarpophalangeal (MCP), first carpometacarpophalangeal (CMC), axial skeleton, hip, knee (Figure), and first metatarsophalangeal (MTP) joints.
• Use reasonable clinical judgment in assessing patients. Experienced clinicians usually recognize OA readily without obtaining extensive diagnostic studies. Plain x-ray films usually are sufficient to identify anatomical abnormalities. Serological studies usually are not necessary, and they may simply introduce confusion—rheumatoid arthritis, systemic lupus erythematosus, and other rheumatologic disorders may be excluded with a thoughtful, thorough, informed clinical evaluation without laboratory testing.
• Begin therapy with patient education, explanation, discussion of prognosis, and nonpharmacological modalities. Many patients feel relieved to learn that their disease is not necessarily rapidly progressive or destructive. Patients can benefit from various nonpharmacological strategies. Because obesity is a risk factor for the development and progression of OA, patients should be counseled on weight loss. Exercise programs should be tailored to individual patients.
Attention to footwear, gait, and ambulation may result in symptomatic improvement. Patients should be educated about the proper use of walking aids because they may help reduce hip and knee OA pain.
Useful adjuncts to management include help with activities of daily living, activity modification, quadriceps strengthening exercises, patellar taping, and formal programs of occupational and physical therapy. Some patients cope better and some symptoms may be minimized with cognitive-behavioral therapy or formal counseling.
• Pharmacological therapy, if needed, begins with acetaminophen (up to 4 g/d). NSAIDs also are beneficial but should be used at the lowest effective dose. The advantage of acetaminophen over NSAIDs is its safety profile. Because NSAIDs have been associated with GI and renal adverse effects, they should be used with caution in patients who have underlying cardiovascular, renal, or GI disease. The response to a specific NSAID differs from one patient to another.
Cyclooxygenase (COX)-2 inhibitors, such as celecoxib(Drug information on celecoxib), may be preferable for patients who have a history of GI ulcers, are receiving anticoagulation therapy, or have a bleeding diathesis. NSAIDs may be added as clinically indicated for younger patients and perhaps patients who do not have comorbid medical problems, are also taking corticosteroids or anticoagulants, and did not have previous ulcer disease or GI bleeding. To prevent GI adverse effects, a COX-2 selective inhibitor or a nonselective NSAID together with misoprostol(Drug information on misoprostol) or a proton pump inhibitor may be prescribed. We also might prescribe a nonacetylated salicylate (disalicylate, choline magnesium trisalicylate).
For persistently symptomatic joints for which injections are feasible, intra-articular corticosteroids or hyaluronan may be considered. If there is persistent pain, tramadol(Drug information on tramadol) also should be considered. This regimen should provide satisfactory symptomatic relief for most patients with OA. Additional pharmacological treatments include some topical medications (capsaicin cream and diclofenac(Drug information on diclofenac) patch or ointment) that also may be quite useful for specific painful or tender areas.
• Whenever possible, manage monarticular or oligoarticular disease with topical or local therapies or both, avoiding unnecessary systemic medications.
• Other approaches to treatment that have been suggested to provide benefit include acupuncture, pregabalin(Drug information on pregabalin), gabapentin(Drug information on gabapentin), milnacipran, and duloxetine(Drug information on duloxetine). Many clinicians now consider glucosamine and chondroitin to have no important clinical value, but they are generally safe and well-tolerated and some patients do report benefit. In our opinion, there is insufficient evidence to support nonexperimental use of tidal lavage, platelet-rich plasma therapy, or herbal and other complementary and alternative medicines for patients with OA.
• We do not recommend routine or long-term use of narcotic analgesics for managing patients with OA. Although these medications are effective for pain management, they should be used rarely and only in patients who are refractory to other pharmacological treatments. Narcotic analgesics should be prescribed by physicians who are experienced in caring for persons receiving these agents.
• Some surgical procedures for appropriate joints in select patients can result in dramatic benefit.
GENERAL APPROACHES
How to approach patients with “pain all over”? Read Full Article
“Doctor, I’m so relieved to see you,” the patient said. “The nurse practitioner told me I have osteoarthritis (OA) all over. I hurt terribly. I tried Tylenol and Advil, but they didn’t help. Some of my friends with similar problems have told me they had newer treatments, like Lyrica, Neurontin, Cymbalta, Ultram, and Savella, as well as herbal medications, ginger, massage, fish oils, yoga, electromagnetic field therapy, spas, glucosamine(Drug information on glucosamine), chrondroitin, acupuncture, tidal irrigation, marijuana, patches, ointments, Duragesic, joint injections, and operations—after they had extensive MRI and other testing—and swear by the results. I’m confused and don’t know what to do. Please help! I’m so desperate!”
Treatment of patients with OA pain can be challenging but is rewarding, because they can be helped, sometimes dramatically. By using a principle- and evidence-based approach, physicians can improve patients’ function and comfort and reduce their pain and disability. Their lives are restored, at least in part, and that is enormously satisfying.
By clinical definition, OA includes painful symptoms. Therefore, all approaches to management—from the simplest to the most aggressive—are designed to benefit patients. Used properly, they are inextricably linked and are part of an effective therapeutic regimen.
This principle- and evidence-based approach has been effective for most patients, providing comfort, reducing disability, and improving quality of life. The occasional patients who do not respond reasonably well to such a comprehensive therapeutic regimen may benefit from referral to more expert consultants. In this article, we describe the principles of caring for patients with painful OA. We discuss approaches to patients with “pain all over” and approaches to pain management in specific joints.
Principles of managing OA
PRINCIPLES OF CARE
• Confirm the diagnosis. Do not miss calcium pyrophosphate dihydrate crystal deposition disease, inflammatory arthritis, erosive/inflammatory OA, polymyalgia rheumatica (PMR), fibromyalgia syndrome (FMS) (alone or superimposed), associated depression, neurological or vascular disease, endocrinological disease (thyroid or parathyroid), chronic pain syndromes (eg, complex regional pain syndrome), tendinitis/bursitis (do not confuse epicondylitis with elbow disease, de Quervain tenosynovitis with wrist arthritis, anserine bursitis with knee arthritis, or trochanteric bursitis with hip disease), ochronosis, or hemochromatosis. When in doubt, obtain expert consultation.
• Seek preventable or reversible underlying or primary disease.
The basic principles for managing osteoarthritis (OA) pain include identifying the disease site or sites. Disease may be “generalized” but often is localized to specific joints. As in other joints, local heat, physical measures, and topical therapies may be beneficial for knee OA.
• Identify the site or sites of OA. Disease may be “generalized” but often is localized to specific joints, such as the distal interphalangeal (DIP), first metacarpophalangeal (MCP), first carpometacarpophalangeal (CMC), axial skeleton, hip, knee (Figure), and first metatarsophalangeal (MTP) joints.
• Use reasonable clinical judgment in assessing patients. Experienced clinicians usually recognize OA readily without obtaining extensive diagnostic studies. Plain x-ray films usually are sufficient to identify anatomical abnormalities. Serological studies usually are not necessary, and they may simply introduce confusion—rheumatoid arthritis, systemic lupus erythematosus, and other rheumatologic disorders may be excluded with a thoughtful, thorough, informed clinical evaluation without laboratory testing.
• Begin therapy with patient education, explanation, discussion of prognosis, and nonpharmacological modalities. Many patients feel relieved to learn that their disease is not necessarily rapidly progressive or destructive. Patients can benefit from various nonpharmacological strategies. Because obesity is a risk factor for the development and progression of OA, patients should be counseled on weight loss. Exercise programs should be tailored to individual patients.
Attention to footwear, gait, and ambulation may result in symptomatic improvement. Patients should be educated about the proper use of walking aids because they may help reduce hip and knee OA pain.
Useful adjuncts to management include help with activities of daily living, activity modification, quadriceps strengthening exercises, patellar taping, and formal programs of occupational and physical therapy. Some patients cope better and some symptoms may be minimized with cognitive-behavioral therapy or formal counseling.
• Pharmacological therapy, if needed, begins with acetaminophen (up to 4 g/d). NSAIDs also are beneficial but should be used at the lowest effective dose. The advantage of acetaminophen over NSAIDs is its safety profile. Because NSAIDs have been associated with GI and renal adverse effects, they should be used with caution in patients who have underlying cardiovascular, renal, or GI disease. The response to a specific NSAID differs from one patient to another.
Cyclooxygenase (COX)-2 inhibitors, such as celecoxib(Drug information on celecoxib), may be preferable for patients who have a history of GI ulcers, are receiving anticoagulation therapy, or have a bleeding diathesis. NSAIDs may be added as clinically indicated for younger patients and perhaps patients who do not have comorbid medical problems, are also taking corticosteroids or anticoagulants, and did not have previous ulcer disease or GI bleeding. To prevent GI adverse effects, a COX-2 selective inhibitor or a nonselective NSAID together with misoprostol(Drug information on misoprostol) or a proton pump inhibitor may be prescribed. We also might prescribe a nonacetylated salicylate (disalicylate, choline magnesium trisalicylate).
For persistently symptomatic joints for which injections are feasible, intra-articular corticosteroids or hyaluronan may be considered. If there is persistent pain, tramadol(Drug information on tramadol) also should be considered. This regimen should provide satisfactory symptomatic relief for most patients with OA. Additional pharmacological treatments include some topical medications (capsaicin cream and diclofenac(Drug information on diclofenac) patch or ointment) that also may be quite useful for specific painful or tender areas.
• Whenever possible, manage monarticular or oligoarticular disease with topical or local therapies or both, avoiding unnecessary systemic medications.
• Other approaches to treatment that have been suggested to provide benefit include acupuncture, pregabalin(Drug information on pregabalin), gabapentin(Drug information on gabapentin), milnacipran, and duloxetine(Drug information on duloxetine). Many clinicians now consider glucosamine and chondroitin to have no important clinical value, but they are generally safe and well-tolerated and some patients do report benefit. In our opinion, there is insufficient evidence to support nonexperimental use of tidal lavage, platelet-rich plasma therapy, or herbal and other complementary and alternative medicines for patients with OA.
• We do not recommend routine or long-term use of narcotic analgesics for managing patients with OA. Although these medications are effective for pain management, they should be used rarely and only in patients who are refractory to other pharmacological treatments. Narcotic analgesics should be prescribed by physicians who are experienced in caring for persons receiving these agents.
• Some surgical procedures for appropriate joints in select patients can result in dramatic benefit.
GENERAL APPROACHES
How to approach patients with “pain all over”? Read Full Article
Post-traumatic stress disorder is a particularly painful disorder that is best seen as a problem owned by someone who has witnessed, experienced, or heard about a trauma. The concept of death is intrinsically involved in PTSD. In order to qualify for this diagnosis the person needed to have feared for her life or believed his life or the life of another was being threatened.
There is considerable information out there on PTSD and this is a good thing. It is my belief that PTSD is much more common than previously thought. We know about combat PTSD and other types of PTSD created by rape, sexual abuse of children and survivors of genocide or other human-made atrocities. Nature can create a situation where death is central to the equation through hurricanes, tornadoes, monsoons, earthquakes, wild fires and blizzards. When traumas originate from human beings it is a different scenario for many reasons.
When human beings harm human beings it sets into motion a problem with human relationships that will last a lifetime for the person who was harmed. Of course, it depends on the severity of the trauma, the age of the person who was harmed, and the re-occurence of trauma afterwards. It also depends on whether help was available and utilized by the person who experienced the trauma.
We want to talk here about the phenomenon of trauma occurring over and over again. This is known as repetition compulsion or returning to the scene of the crime. I believe all traumas are crime scenes. Crime scenes are terrible places that involved terrible events.
Sigmund Freud was the first person to describe what would come to be known as repetition compulsion. He noticed that some people seemed to place themselves in positions of potential harm. These people had a history of surviving trauma and then seemed to thrust themselves into harms way time and again. He referred to this tendency as the “death wish or death instinct.”
If trauma is not resolved our unconscious minds will place us at the crime scene or one that closely resembles it. This is not because people are masochistic and want to be harmed again. It is because the person who was harmed is looking for a different outcome than the one that happened in the first place. Sometimes people feel, if given another chance, it will turn out differently.
It seldom turns out differently until the person who experienced the trauma has come to terms with the trauma and the numerous ways the trauma infiltrates every aspect of their life. This takes time, this takes counseling, and this takes trying to create a consciously working awareness of what is safe and what is unsafe. It is the Safe versus UnSafe part that became altered or damaged when the trauma took place initially. Things became confused.
People who have PTSD often have difficulty discerning between safe and unsafe. They return to old crime scenes looking for a different outcome. The same outcome is typically waiting.
How do you change repetition compulsion as it applies to PTSD and trauma?
Identify your trauma. What, when, who and how are all very important.
Detail The Crime Scene and Perpetrator: Make a list of what, when, who, and how in as much detail as possible. Include: Time of day, season of the year, do a physical description of the person including facial and physical features and any identifying marks. Imagine you are working for CSI: Your Town and do a forensic evaluation of the crime scene.
List of Triggers: from your crime scene list as many triggers as you can. Remember that a trigger is something that activates a memory and emotional response; a trigger is not the cause of the emotional response. It is simply a trigger to old memories. Triggers can be a tone of voice, a mannerism, certain words, or anything that starts a landslide to a feeling of being powerless or trapped.
Memory Game: When you have an emotional flashback or feel compulsively inclined to act in a way that would potentially place you in danger STOP. You have to do the memory game first.
The memory game involves matching what you are about to do, triggers and the past trauma. An example would be: You had an argument with a friend. You want to go drink. You know your wife doesn’t want you to drink. You decide to make up an excuse about needing to go somewhere. You are planning to go buy alcohol to numb your feelings. You also want to confront your friend. You know that Carl works at the liquor store and he reminds you of Joe who sexually abused you when you were 12. Wow, this is going to end up with a repetition compulsion or putting yourself in a situation to be harmed somehow again.
This is just a short list of things to keep in mind when looking at PTSD and repetition compulsion. Read More…
