nuces.org

STRESS AND “PRE-HYPERTENSION”

As you may know, white-coat hypertension is the temporary rise in blood pressure caused by the anxiety of being in a medical setting and interacting with a health professional. The fear and anxiety aroused in this situation stimulate the sympathetic nervous system, which prompts a transient increase in blood pressure. While white-coat hypertension should not be confused with true hypertension, some experts warn that this phenomenon may represent an early stage in the development of true hypertension. Dr. M. A. Weber of the University of California claims that people who experience white-coat hypertension have virtually all of the metabolic and cardiovascular characteristics of hypertension. In comparing these individuals with patients who have been diagnosed as hypertensive, Dr. Weber notes similarities such as heightened norepinephrine and renin activity. He contends that people who are susceptible to white-coat hypertension are more likely to experience anxiety in other situations and are prone to the kind of chronic stress that leads to hypertension.
Among the most significant contributors to psychological stress is our fast-paced lifestyle. If you’re working long hours, eating erratically, and feeling frustrated by heavy traffic and nonstop telephone calls, watch out! This is the land of daily stress that contributes to the development of hypertension or exacerbates the condition if you already have it. Ineffective methods of “coping” with prolonged stress – drinking, smoking, overeating, and other unhealthy habits-may also induce or exacerbate hypertension.
*109/313/5*

STRESS AND “PRE-HYPERTENSION”As you may know, white-coat hypertension is the temporary rise in blood pressure caused by the anxiety of being in a medical setting and interacting with a health professional. The fear and anxiety aroused in this situation stimulate the sympathetic nervous system, which prompts a transient increase in blood pressure. While white-coat hypertension should not be confused with true hypertension, some experts warn that this phenomenon may represent an early stage in the development of true hypertension. Dr. M. A. Weber of the University of California claims that people who experience white-coat hypertension have virtually all of the metabolic and cardiovascular characteristics of hypertension. In comparing these individuals with patients who have been diagnosed as hypertensive, Dr. Weber notes similarities such as heightened norepinephrine and renin activity. He contends that people who are susceptible to white-coat hypertension are more likely to experience anxiety in other situations and are prone to the kind of chronic stress that leads to hypertension.Among the most significant contributors to psychological stress is our fast-paced lifestyle. If you’re working long hours, eating erratically, and feeling frustrated by heavy traffic and nonstop telephone calls, watch out! This is the land of daily stress that contributes to the development of hypertension or exacerbates the condition if you already have it. Ineffective methods of “coping” with prolonged stress – drinking, smoking, overeating, and other unhealthy habits-may also induce or exacerbate hypertension.*109/313/5*

ATHEROSCLEROSIS OF LEG’S ARTERIES

The most common location for atherosclerosis, other than in the heart, is in the arteries that feed the legs. Blood leaving the heart flows into the large aorta, which carries blood to all parts of the body. As the aorta passes down into the abdomen, it divides into two large iliac arteries that supply the pelvis and the legs. When the iliac arteries enter the thighs, their name changes to femoral arteries. The femoral arteries then branch into smaller and smaller vessels that eventually supply the feet and toes. Any of these blood vessels can be affected by atherosclerosis, from the largest (the aorta) to the smallest arteries in the feet.
Arteriosclerosis obliterans is the medical name applied to inadequate blood supply to the legs. The process can also occur in the arms, but does so infrequently. The main symptom that develops in the legs is pain, particularly in the calves, when the person is walking or running. The reason for this is simple. When a person walks or runs, the muscles of his legs are exercising and require more blood flow to supply food and oxygen to the muscles. The heart beats faster and more blood is pumped through the arteries. Just as the heart produces the pain of angina pectoris if it does not get an adequate blood supply during exercise, the leg muscles cause pain if they are getting insufficient blood supply. When the disease process becomes more advanced, the pain in the legs may become constant, occurring even at rest. At this stage, walking is practically impossible.
Another symptom that may be noticed is coldness of the legs and feet, or pain in the legs and feet when they are exposed to cold. For this reason, the afflicted person may keep his feet covered with extra stockings. They may appear very red, or even bluish, when the person is standing or sitting. Another common finding is the disappearance of hair on the feet and toes and slow growth of the toenails.
A mistake is commonly made at this point. Feeling cold in the feet and legs, people frequently wrap their legs with hot water bottles, hot towels or heating pads. The mistake is the application of heat, because the skin and other tissues are easily damaged by outside heat, and it is very easy to “cook” the tissue.
The subject of damaged tissue introduces the next problem. People with inadequate blood supply to the legs do not heal as fast as normal, because the process of healing requires blood flow. If a blister develops on the foot, or if the toe is cut when the nails are trimmed, or if athlete’s foot develops, healing will be considerably delayed. Extra care is therefore necessary to avoid wounding these tissues and to prevent infection.
A stratagem can be followed that will assist healing. The blood flow to the leg is greater when the person is lying down or sitting with his legs up than when he is on his feet or sitting in the usual manner. This is because gravity tends to hold the blood down in the leg and resists its return to the heart. When a person is walking, the muscles of the legs are pumping the blood in the veins back to the heart. The veins of the legs have special one-way valves inside them to facilitate this pumping action. When the leg is elevated, the effect of gravity is cancelled, and the total blood flow to the leg is increased.
If the larger blood vessels (iliac arteries) in the pelvis are affected by atherosclerosis, the person will frequently notice that the pain that he feels when he walks is located in the thighs rather than in the calves. For men, another frequent symptom of blockage in this location is the loss of the ability to have an erection. The process of erection is dependent upon an increased flow of blood into the penis. The artery that supplies this blood is a branch of the iliac vessels.
The ultimate problem that can occur with this condition in the legs is the development of gangrene. This death of tissue caused by inadequate blood flow results in part of the toe or the entire leg turning black. The process usually starts in the toes, and it is frequently immediately preceded by an infection or injury of the tissue in the area. If the blockage is extensive, the gangrene may progress to involve the entire foot or part of the leg. When the disease has progressed to this point, amputation is the only recourse.
*42/309/5*

ATHEROSCLEROSIS OF LEG’S ARTERIESThe most common location for atherosclerosis, other than in the heart, is in the arteries that feed the legs. Blood leaving the heart flows into the large aorta, which carries blood to all parts of the body. As the aorta passes down into the abdomen, it divides into two large iliac arteries that supply the pelvis and the legs. When the iliac arteries enter the thighs, their name changes to femoral arteries. The femoral arteries then branch into smaller and smaller vessels that eventually supply the feet and toes. Any of these blood vessels can be affected by atherosclerosis, from the largest (the aorta) to the smallest arteries in the feet.Arteriosclerosis obliterans is the medical name applied to inadequate blood supply to the legs. The process can also occur in the arms, but does so infrequently. The main symptom that develops in the legs is pain, particularly in the calves, when the person is walking or running. The reason for this is simple. When a person walks or runs, the muscles of his legs are exercising and require more blood flow to supply food and oxygen to the muscles. The heart beats faster and more blood is pumped through the arteries. Just as the heart produces the pain of angina pectoris if it does not get an adequate blood supply during exercise, the leg muscles cause pain if they are getting insufficient blood supply. When the disease process becomes more advanced, the pain in the legs may become constant, occurring even at rest. At this stage, walking is practically impossible.Another symptom that may be noticed is coldness of the legs and feet, or pain in the legs and feet when they are exposed to cold. For this reason, the afflicted person may keep his feet covered with extra stockings. They may appear very red, or even bluish, when the person is standing or sitting. Another common finding is the disappearance of hair on the feet and toes and slow growth of the toenails.A mistake is commonly made at this point. Feeling cold in the feet and legs, people frequently wrap their legs with hot water bottles, hot towels or heating pads. The mistake is the application of heat, because the skin and other tissues are easily damaged by outside heat, and it is very easy to “cook” the tissue.The subject of damaged tissue introduces the next problem. People with inadequate blood supply to the legs do not heal as fast as normal, because the process of healing requires blood flow. If a blister develops on the foot, or if the toe is cut when the nails are trimmed, or if athlete’s foot develops, healing will be considerably delayed. Extra care is therefore necessary to avoid wounding these tissues and to prevent infection.A stratagem can be followed that will assist healing. The blood flow to the leg is greater when the person is lying down or sitting with his legs up than when he is on his feet or sitting in the usual manner. This is because gravity tends to hold the blood down in the leg and resists its return to the heart. When a person is walking, the muscles of the legs are pumping the blood in the veins back to the heart. The veins of the legs have special one-way valves inside them to facilitate this pumping action. When the leg is elevated, the effect of gravity is cancelled, and the total blood flow to the leg is increased.If the larger blood vessels (iliac arteries) in the pelvis are affected by atherosclerosis, the person will frequently notice that the pain that he feels when he walks is located in the thighs rather than in the calves. For men, another frequent symptom of blockage in this location is the loss of the ability to have an erection. The process of erection is dependent upon an increased flow of blood into the penis. The artery that supplies this blood is a branch of the iliac vessels.The ultimate problem that can occur with this condition in the legs is the development of gangrene. This death of tissue caused by inadequate blood flow results in part of the toe or the entire leg turning black. The process usually starts in the toes, and it is frequently immediately preceded by an infection or injury of the tissue in the area. If the blockage is extensive, the gangrene may progress to involve the entire foot or part of the leg. When the disease has progressed to this point, amputation is the only recourse.*42/309/5*

HIV: ON LIVING-THE MIND-BODY CONNECTION

Your attitude toward life might in fact be related to your health. A field of research studies the intricate connections between mental state, the brain, and the immune system. The field goes by two impossible names: one is neuroimmunomodulation, the other is psychoneuroimmunology.
Specifically, stress seems to affect the immune system’s ability to respond to infection. Several studies selected people under certain kinds of stresses: people whose spouses had died, people with severe depression, medical students at examination time, people under such extreme physical stresses as marathon running or dieting to the point of malnutrition. Their blood was analyzed for changes in immune response, that is, for changes in certain cells of the immune system: T cells, B cells, and white blood cells called natural killer cells.
Different studies measured immune response differently. In some studies, researchers counted the numbers of T and B cells in the blood. In others, researchers treated people’s T cells with a chemical that stimulates reproduction, then counted the numbers of new T cells. In still others, researchers added natural killer cells to foreign cells, then measured the number of foreign cells not killed.
Regardless of which measure of immune response was studied, most researchers found that people under stress have immune responses that are somewhat lower than the immune systems of people not under stress. In other words, people under stress have fewer of certain immune system cells, or they have cells that reproduce less successfully, or they have cells that respond ineffectively to foreign cells.
The converse is also true: not only do people under stress have lower immune responses, but people with positive attitudes seem to have better immune responses. Some studies, done specifically on people with HIV infection, found that those who describe themselves as vigorous and self-expressive, who have ways of venting their emotions, and who exercise regularly have better immune responses. The level of T cell reproduction and the response of the natural killer cells—the same measures of immune response that had been lower with stressed people—were higher.
Other researchers have suggested theories of how stress might affect immune response. In other words, all these theories suggest how a person’s mental state and the immune system might be linked. When people are under stress, their adrenal glands release hormones called
glucocorticoids (the medications cortisone and prednisone are examples of glucocorticoids). In the immune system, glucocorticoids inhibit the release of chemicals called interferon and interleukin-2, which immune cells use to fight off fungi, bacteria, and viruses. In the bloodstream, glucocorticoids also decrease, temporarily at least, the number of certain T cells called T4 or CD4 cells, the same cells that HIV preferentially infects. And in experiments in the laboratory, another hormone the adrenal gland releases under stress, called adrenaline or epinephrine, seems to suppress reproduction of CD4 cells. In any case, because HIV specifically infects CD4 cells, anything that suppresses CD4 cells might make matters worse for someone trying to combat HIV infection.
It is hard to draw conclusions from any of these studies. The experiments with CD4 cells were done on animals or in laboratory dishes and not on living humans. The studies on humans measured different aspects of the immune system’s response, they did not exclude people who were not eating and sleeping, they measured stress differently, and the stresses themselves were different and of different magnitudes.
Most importantly, many of the changes measured were small, and no one knows whether small changes in immune response are clinically important—that is, whether they actually increase the chances of getting sick. In general, take the research with a grain of salt: this field is only a few years old; it connects psychology, the brain, and the immune system; and all three systems are extraordinarily complex and not yet understood.
In spite of the studies’ inconclusiveness, however, the sense in this new field is that people who are more emotionally stable may be less vulnerable to disease. When sick, they seem to do better, become less severely sick, stay alive longer.
The fact is, to people facing HIV infection, whether the research turns out to be right or wrong is irrelevant. If a positive mental state does affect the immune system, so much the better. If it does not, nothing is lost. A positive outlook makes your life more pleasant. The only trap is the possibility that people who do get sicker might blame themselves for not having worked hard enough. In view of the studies’ inconclusiveness, blaming yourself is both unrealistic and unnecessary.
*248\191\2*

HIV: ON LIVING-THE MIND-BODY CONNECTIONYour attitude toward life might in fact be related to your health. A field of research studies the intricate connections between mental state, the brain, and the immune system. The field goes by two impossible names: one is neuroimmunomodulation, the other is psychoneuroimmunology.     Specifically, stress seems to affect the immune system’s ability to respond to infection. Several studies selected people under certain kinds of stresses: people whose spouses had died, people with severe depression, medical students at examination time, people under such extreme physical stresses as marathon running or dieting to the point of malnutrition. Their blood was analyzed for changes in immune response, that is, for changes in certain cells of the immune system: T cells, B cells, and white blood cells called natural killer cells.     Different studies measured immune response differently. In some studies, researchers counted the numbers of T and B cells in the blood. In others, researchers treated people’s T cells with a chemical that stimulates reproduction, then counted the numbers of new T cells. In still others, researchers added natural killer cells to foreign cells, then measured the number of foreign cells not killed.     Regardless of which measure of immune response was studied, most researchers found that people under stress have immune responses that are somewhat lower than the immune systems of people not under stress. In other words, people under stress have fewer of certain immune system cells, or they have cells that reproduce less successfully, or they have cells that respond ineffectively to foreign cells.     The converse is also true: not only do people under stress have lower immune responses, but people with positive attitudes seem to have better immune responses. Some studies, done specifically on people with HIV infection, found that those who describe themselves as vigorous and self-expressive, who have ways of venting their emotions, and who exercise regularly have better immune responses. The level of T cell reproduction and the response of the natural killer cells—the same measures of immune response that had been lower with stressed people—were higher.     Other researchers have suggested theories of how stress might affect immune response. In other words, all these theories suggest how a person’s mental state and the immune system might be linked. When people are under stress, their adrenal glands release hormones called glucocorticoids (the medications cortisone and prednisone are examples of glucocorticoids). In the immune system, glucocorticoids inhibit the release of chemicals called interferon and interleukin-2, which immune cells use to fight off fungi, bacteria, and viruses. In the bloodstream, glucocorticoids also decrease, temporarily at least, the number of certain T cells called T4 or CD4 cells, the same cells that HIV preferentially infects. And in experiments in the laboratory, another hormone the adrenal gland releases under stress, called adrenaline or epinephrine, seems to suppress reproduction of CD4 cells. In any case, because HIV specifically infects CD4 cells, anything that suppresses CD4 cells might make matters worse for someone trying to combat HIV infection.     It is hard to draw conclusions from any of these studies. The experiments with CD4 cells were done on animals or in laboratory dishes and not on living humans. The studies on humans measured different aspects of the immune system’s response, they did not exclude people who were not eating and sleeping, they measured stress differently, and the stresses themselves were different and of different magnitudes.     Most importantly, many of the changes measured were small, and no one knows whether small changes in immune response are clinically important—that is, whether they actually increase the chances of getting sick. In general, take the research with a grain of salt: this field is only a few years old; it connects psychology, the brain, and the immune system; and all three systems are extraordinarily complex and not yet understood.     In spite of the studies’ inconclusiveness, however, the sense in this new field is that people who are more emotionally stable may be less vulnerable to disease. When sick, they seem to do better, become less severely sick, stay alive longer.     The fact is, to people facing HIV infection, whether the research turns out to be right or wrong is irrelevant. If a positive mental state does affect the immune system, so much the better. If it does not, nothing is lost. A positive outlook makes your life more pleasant. The only trap is the possibility that people who do get sicker might blame themselves for not having worked hard enough. In view of the studies’ inconclusiveness, blaming yourself is both unrealistic and unnecessary.*248\191\2*

BOTULINUM TOXIN: DIAGNOSIS, TREATMENT AND POSTEXPOSURE PROPHYLAXIS

Diagnosis
The diagnosis of botulism requires recognition of the key clinical features. Clinical samples used for naturally occurring disease include direct detection of botulinum toxin and identification of C. botulinum by culture of serum (>30 ml of blood in a red-top tube), stool, gastric aspirate, vomitus, and suspected food. In a bioterrorism aerosol release, serology would be the primary method of diagnosis. Toxins produced by cultured isolates are confirmed by a mouse bioassay.
Treatment and postexposure prophylaxis
Treatment consists of supportive care and passive immunization with a trivalent equine antitoxin. Supportive care may include enteral nutrition, ventilatory support, and treatment of secondary infections. The reverse Trendelenburg position is recommended for non-ventilated patients to prevent aspiration of secretions. Administration of the trivalent (containing types A, B, and E) equine antitoxin, available only through the CDC, should occur immediately after a clinical diagnosis is made and should not await laboratory confirmation. This can minimize subsequent nerve damage and reduce the severity of disease but does not reverse existent paralysis. The dose of licensed botulinum antitoxin is a single 10 ml vial per patient, diluted 1:10 in a 0.9% saline solution, and administered by slow intravenous infusion. Since hypersensitivity reactions are common with the antitoxin, skin testing is usually performed as a screening tool. If hypersensitivity is identified, patients can be desensitized before additional antitoxin is given.
It is unclear how best to care for patients who may have been exposed to botulinum toxin but who are not yet ill. The use of the trivalent equine antitoxin is limited by it scarcity and risk of hypersensitivity. An investigational pentavalent (ABCDE) botulinum toxoid is used by CDC laboratory workers at high risk and by the military for protection of troops against attack. A recombinant vaccine is also in development.
Infection Control
Since person-to-person spread of botulism does not occur, no isolation is necessary. Physicians should use standard precautions when caring for patients with botulism.
*214/348/5*

BOTULINUM TOXIN: DIAGNOSIS, TREATMENT AND POSTEXPOSURE PROPHYLAXIS DiagnosisThe diagnosis of botulism requires recognition of the key clinical features. Clinical samples used for naturally occurring disease include direct detection of botulinum toxin and identification of C. botulinum by culture of serum (>30 ml of blood in a red-top tube), stool, gastric aspirate, vomitus, and suspected food. In a bioterrorism aerosol release, serology would be the primary method of diagnosis. Toxins produced by cultured isolates are confirmed by a mouse bioassay.
Treatment and postexposure prophylaxisTreatment consists of supportive care and passive immunization with a trivalent equine antitoxin. Supportive care may include enteral nutrition, ventilatory support, and treatment of secondary infections. The reverse Trendelenburg position is recommended for non-ventilated patients to prevent aspiration of secretions. Administration of the trivalent (containing types A, B, and E) equine antitoxin, available only through the CDC, should occur immediately after a clinical diagnosis is made and should not await laboratory confirmation. This can minimize subsequent nerve damage and reduce the severity of disease but does not reverse existent paralysis. The dose of licensed botulinum antitoxin is a single 10 ml vial per patient, diluted 1:10 in a 0.9% saline solution, and administered by slow intravenous infusion. Since hypersensitivity reactions are common with the antitoxin, skin testing is usually performed as a screening tool. If hypersensitivity is identified, patients can be desensitized before additional antitoxin is given.It is unclear how best to care for patients who may have been exposed to botulinum toxin but who are not yet ill. The use of the trivalent equine antitoxin is limited by it scarcity and risk of hypersensitivity. An investigational pentavalent (ABCDE) botulinum toxoid is used by CDC laboratory workers at high risk and by the military for protection of troops against attack. A recombinant vaccine is also in development.
Infection ControlSince person-to-person spread of botulism does not occur, no isolation is necessary. Physicians should use standard precautions when caring for patients with botulism.*214/348/5*

TREATMENT OF LYME DISEASE: EARLY, LATE AND CHRONIC LYME DISEASE

Early Lyme Disease with Acute Neurologic Involvement
Acute neurologic involvement includes aseptic meningitis or radiculopathy. Parenteral therapy with ceftriaxone, penicillin G, or cefotaxime is recommended for both children and adults. Oral or parenteral doxycycline can be used for patients over 8 years of age with intolerance of penicillins or cephalosporins.
Lumbar puncture may be reserved for patients with severe headache, nuchal rigidity, or other signs and symptoms of central nervous system involvement. If cerebrospinal fluid study findings are normal, an oral regimen is preferred. In cases of cranial nerve palsy, an oral regimen may be used to prevent further sequelae.
Late Disease
Arthritis without neurologic disease can be treated with a 28-day course of oral amoxicillin or doxycycline. However, some patients go on to develop signs of neuroborreliosis after treatment with an oral regimen, necessitating parenteral antibiotics anyway. Treatment of arthritis with neurologic involvement is the same as treatment of early Lyme disease with central nervous system involvement and includes parenteral ceftriaxone, penicillin G, or cefotaxime.
Recurrent or persistent arthritis can be treated with oral or parenteral therapy. It is important to wait for months between courses of treatment given the slow resolution of inflammation. If arthritis persists or recurs after two courses of oral therapy or one course of parenteral therapy, symptomatic treatment with non-steroidal anti-inflammatory drugs may be effective. No further antibiotic therapy is recommended.
Chronic Lyme Disease
Despite appropriate treatment, some patients experience persistent fatigue, myalgias, arthralgias, neurocognitive dysfunction, and other subjective symptoms similar to those reported in cases of fibromyalgia or chronic fatigue syndrome. There is still debate over whether chronic Lyme disease represents a separate disease entity. Some experts believe that Lyme disease may trigger the onset of fibromyalgia. In a study by Kalish et al, chronic subjective symptoms were reported to occur more commonly in patients who presented with early dissemination to the nervous system, especially if antibiotic therapy was delayed. In contrast, a recent longitudinal cohort study reports that symptoms consistent with chronic Lyme disease were just as common in age-matched, uninfected control subjects. Prolonged or repeated courses of antibiotics have no demonstrated efficacy in these patients and should be avoided.
*165/348/5*

TREATMENT OF LYME DISEASE: EARLY, LATE AND CHRONIC LYME DISEASEEarly Lyme Disease with Acute Neurologic InvolvementAcute neurologic involvement includes aseptic meningitis or radiculopathy. Parenteral therapy with ceftriaxone, penicillin G, or cefotaxime is recommended for both children and adults. Oral or parenteral doxycycline can be used for patients over 8 years of age with intolerance of penicillins or cephalosporins.Lumbar puncture may be reserved for patients with severe headache, nuchal rigidity, or other signs and symptoms of central nervous system involvement. If cerebrospinal fluid study findings are normal, an oral regimen is preferred. In cases of cranial nerve palsy, an oral regimen may be used to prevent further sequelae.
Late DiseaseArthritis without neurologic disease can be treated with a 28-day course of oral amoxicillin or doxycycline. However, some patients go on to develop signs of neuroborreliosis after treatment with an oral regimen, necessitating parenteral antibiotics anyway. Treatment of arthritis with neurologic involvement is the same as treatment of early Lyme disease with central nervous system involvement and includes parenteral ceftriaxone, penicillin G, or cefotaxime.Recurrent or persistent arthritis can be treated with oral or parenteral therapy. It is important to wait for months between courses of treatment given the slow resolution of inflammation. If arthritis persists or recurs after two courses of oral therapy or one course of parenteral therapy, symptomatic treatment with non-steroidal anti-inflammatory drugs may be effective. No further antibiotic therapy is recommended.
Chronic Lyme DiseaseDespite appropriate treatment, some patients experience persistent fatigue, myalgias, arthralgias, neurocognitive dysfunction, and other subjective symptoms similar to those reported in cases of fibromyalgia or chronic fatigue syndrome. There is still debate over whether chronic Lyme disease represents a separate disease entity. Some experts believe that Lyme disease may trigger the onset of fibromyalgia. In a study by Kalish et al, chronic subjective symptoms were reported to occur more commonly in patients who presented with early dissemination to the nervous system, especially if antibiotic therapy was delayed. In contrast, a recent longitudinal cohort study reports that symptoms consistent with chronic Lyme disease were just as common in age-matched, uninfected control subjects. Prolonged or repeated courses of antibiotics have no demonstrated efficacy in these patients and should be avoided.*165/348/5*

THE OTHER SIDE OF SLEEP: THE DREAM DEBATE

Today, with the increased attention paid to sleep by the medical community, the debate over the function of dreams continues apace. As in any good debate, there are opposing schools of thought, each armed with volumes of data to prove its points. One camp, comprised mainly of psychiatrists and psychologists, stands committed to the belief, inherited from Freud, that dreams serve a largely psychological function by revealing our hidden natures. Another camp, made up largely of investigators from such hard-science disciplines as biology and neurology, believes dreams are merely electrical and chemical phenomena, no more meaningful than the random swirling patterns of light and color you see when you press firmly on your closed eyelids. Somewhere in the middle is another faction, which adopts the view that a certain neurological randomness may indeed trigger the process of dreaming, but that the images and sensations evoked may be tied together in such a way as to hold some psychological meaning for the dreamer.
One reason for the existence of such divergent views stems from the fact that some of Freud’s work has been largely discredited since its initial publication. For example, Freud declared that the dreams of neurotic people do not differ in any significant way from those of normal people. Subsequent research has determined that the dreams of the mentally disturbed do reflect the underlying condition: anxious people dream about their anxieties; phobic people dream about their phobias. The dreams of people suffering from depression focus on themes of violence or the failure to repair damage of some kind, while the dreams of schizophrenics are filled with images of catastrophe and devastation in remote places. The notion that REM sleep deprivation provides therapeutic benefits in the treatment of depression tends to undermine Freud’s theory that dreaming serves as an essential psychological safety valve.
*286\226\8*

THE OTHER SIDE OF SLEEP: THE DREAM DEBATEToday, with the increased attention paid to sleep by the medical community, the debate over the function of dreams continues apace. As in any good debate, there are opposing schools of thought, each armed with volumes of data to prove its points. One camp, comprised mainly of psychiatrists and psychologists, stands committed to the belief, inherited from Freud, that dreams serve a largely psychological function by revealing our hidden natures. Another camp, made up largely of investigators from such hard-science disciplines as biology and neurology, believes dreams are merely electrical and chemical phenomena, no more meaningful than the random swirling patterns of light and color you see when you press firmly on your closed eyelids. Somewhere in the middle is another faction, which adopts the view that a certain neurological randomness may indeed trigger the process of dreaming, but that the images and sensations evoked may be tied together in such a way as to hold some psychological meaning for the dreamer.One reason for the existence of such divergent views stems from the fact that some of Freud’s work has been largely discredited since its initial publication. For example, Freud declared that the dreams of neurotic people do not differ in any significant way from those of normal people. Subsequent research has determined that the dreams of the mentally disturbed do reflect the underlying condition: anxious people dream about their anxieties; phobic people dream about their phobias. The dreams of people suffering from depression focus on themes of violence or the failure to repair damage of some kind, while the dreams of schizophrenics are filled with images of catastrophe and devastation in remote places. The notion that REM sleep deprivation provides therapeutic benefits in the treatment of depression tends to undermine Freud’s theory that dreaming serves as an essential psychological safety valve.*286\226\8*

RHEUMATOID ARTHRITIS (RA) AND HEALTH INSURANCE: PRIVATE HEALTH INSURANCE

If you are working and your employer provides health insurance benefits, you may not have the option of selecting a specific form of insurance or a specific insurance carrier. (Note: If you are insured through a group plan at work and then lose your job or begin to consider another job, do not drop your health insurance.)
If you do have a choice when it comes to health insurance, we recommend that you examine carefully several types of policies and look into several insurance carriers before making a decision. Choosing wisely is especially important because it is sometimes difficult to make changes in insurance coverage if your health deteriorates in any way.
Selecting the best form of health insurance involves choosing among many variables. Asking the following key questions may help you choose wisely.
For standard policies:
• Is there a deductible? (And can you afford to pay that deductible each year?)
• Are there large co-payments? (If so, do lower premiums offset that expense?)
• What percentage of expenses are you responsible for after the deductible has been met? (Would you prefer to pay higher premiums in exchange for paying a lower percentage of a covered expense?)
•   Is there a “cap” on the amount you have to pay, if a percentage payment applies? (For your protection, there should be.)
For a health maintenance organization (HMO) or prepaid medical insurance:
•   Is your choice of physicians limited? If so, are there a rheumatologist and an orthopedic surgeon experienced in joint surgery on the preferred provider staff? (If the services of these specialists aren’t provided, can you get the HMO or preferred insurance carrier to agree to pay for the services of such specialists if needed?)
• Are you permitted to use only specific hospitals and specific physical therapy services? (If so, find out – by asking your present doctor if necessary – whether the permitted service providers have a good reputation for treatment of RA.)
• Do the primary care doctors in the HMO readily refer their patients for specialty consultation? (They ought to.)
For all insurance:
• Does your policy cover physical therapy, occupational therapy, and the services of a podiatrist? (If not, you’ll probably want to choose a different policy.)
• Is there a prescription policy? (We recommend that you enroll in an insurance plan that pays most of the cost of prescription drugs because arthritis medications can be extremely costly.)
• Will your policy cover durable medical hardware such as splints, braces, orthotics, walking aids? (If there is an additional premium for this coverage, you’ll have to decide whether you would prefer to pay the cost of these aids out of pocket as necessary or whether it is better for you to pay the additional premium on a regular basis.)
Is there a preexisting illness clause that may limit payment for costs related to your RA? (If so, the wiser choice, if it is available, might be to pay a higher premium and obtain coverage for the preexisting condition.)
It is critical for you to examine your insurance options if your employment status is about to change. Be very careful: because you have RA, you may run into difficulties in getting another insurance carrier to cover you. The Cobra law states that you must be allowed to convert your current insurance into an individual policy that is guaranteed at the group premium rate for a given time period. However, before you discontinue your coverage under your former employer’s group plan – or before you allow your former employer to discontinue your coverage – be sure to review your new policy and be certain that it has gone into effect. You will have to pay the premium for this new insurance, of course.
While you are covered under the Cobra law, explore other options: can you obtain coverage under your spouse’s policy, for example, or can you get group insurance through a new job or a professional society? Take every possible precaution to prevent a lapse in coverage. Our experience tells us that insurance carriers are often most reluctant to provide comprehensive coverage to people with chronic medical problems. This is why we emphasize the importance of holding onto one health insurance policy until another one has gone into effect.
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RHEUMATOID ARTHRITIS (RA) AND HEALTH INSURANCE: PRIVATE HEALTH INSURANCEIf you are working and your employer provides health insurance benefits, you may not have the option of selecting a specific form of insurance or a specific insurance carrier. (Note: If you are insured through a group plan at work and then lose your job or begin to consider another job, do not drop your health insurance.)If you do have a choice when it comes to health insurance, we recommend that you examine carefully several types of policies and look into several insurance carriers before making a decision. Choosing wisely is especially important because it is sometimes difficult to make changes in insurance coverage if your health deteriorates in any way.Selecting the best form of health insurance involves choosing among many variables. Asking the following key questions may help you choose wisely.For standard policies:• Is there a deductible? (And can you afford to pay that deductible each year?)• Are there large co-payments? (If so, do lower premiums offset that expense?)• What percentage of expenses are you responsible for after the deductible has been met? (Would you prefer to pay higher premiums in exchange for paying a lower percentage of a covered expense?)•   Is there a “cap” on the amount you have to pay, if a percentage payment applies? (For your protection, there should be.)For a health maintenance organization (HMO) or prepaid medical insurance:•   Is your choice of physicians limited? If so, are there a rheumatologist and an orthopedic surgeon experienced in joint surgery on the preferred provider staff? (If the services of these specialists aren’t provided, can you get the HMO or preferred insurance carrier to agree to pay for the services of such specialists if needed?)• Are you permitted to use only specific hospitals and specific physical therapy services? (If so, find out – by asking your present doctor if necessary – whether the permitted service providers have a good reputation for treatment of RA.)• Do the primary care doctors in the HMO readily refer their patients for specialty consultation? (They ought to.)For all insurance:• Does your policy cover physical therapy, occupational therapy, and the services of a podiatrist? (If not, you’ll probably want to choose a different policy.)• Is there a prescription policy? (We recommend that you enroll in an insurance plan that pays most of the cost of prescription drugs because arthritis medications can be extremely costly.)• Will your policy cover durable medical hardware such as splints, braces, orthotics, walking aids? (If there is an additional premium for this coverage, you’ll have to decide whether you would prefer to pay the cost of these aids out of pocket as necessary or whether it is better for you to pay the additional premium on a regular basis.)Is there a preexisting illness clause that may limit payment for costs related to your RA? (If so, the wiser choice, if it is available, might be to pay a higher premium and obtain coverage for the preexisting condition.)It is critical for you to examine your insurance options if your employment status is about to change. Be very careful: because you have RA, you may run into difficulties in getting another insurance carrier to cover you. The Cobra law states that you must be allowed to convert your current insurance into an individual policy that is guaranteed at the group premium rate for a given time period. However, before you discontinue your coverage under your former employer’s group plan – or before you allow your former employer to discontinue your coverage – be sure to review your new policy and be certain that it has gone into effect. You will have to pay the premium for this new insurance, of course.While you are covered under the Cobra law, explore other options: can you obtain coverage under your spouse’s policy, for example, or can you get group insurance through a new job or a professional society? Take every possible precaution to prevent a lapse in coverage. Our experience tells us that insurance carriers are often most reluctant to provide comprehensive coverage to people with chronic medical problems. This is why we emphasize the importance of holding onto one health insurance policy until another one has gone into effect.*119/209/5*

SYPHILIS – CONGENITAL SYPHILIS

The early lesions are similar to those of secondary syphilis with rhinitis, rash, bone involvement, hepatosplenomegaly, meningitis and anaemia.

Late congenital syphilis is comparable to late acquired syphilis. It usually occurs after 2 years of age. Manifestations include Hutchinson’s triad (interstitial keratitis, incisor defects and perceptive deafness), gummas and neurosyphilis. Cardiovascular lesions do not occur in congenital syphilis.
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SYPHILIS – LATENT SYPHILIS; LATE SYPHILIS

Positive serology in a patient without symptoms or signs of disease is referred to as latent syphilis and is the commonest presentation of syphilis in Australia today. Possibly because of the widespread use of antibiotics, the infection often proceeds to the latent stage without a recognised primary or secondary stage. An attempt should be made to determine the duration of latency (by asking about previous syphilis serology at the time of blood transfusion, STD or pregnancy, by identifying the occurrence of a primary lesion etc.) because specific treatments for early and late latent syphilis are different

Tertiary manifestations of syphilis may be ‘benign’ with development of gummas (granulomatous lesions) in almost any organ, or more serious with cardiovascular or central nervous system involvement. Benign gummatous disease is rare but cardiovascular disease and neurosyphilis occasionally occur. Careful management and follow up of patients with early or latent disease is essential to prevent late sequelae.

Late syphilis should be excluded in any patient with aortic incompetence or dilatation of the ascending arch of the aorta. Syphilis should be excluded as the cause of dementia, personality change, multifocal neurological disorders, nerve deafness, pupillary abnormalities, retinal disease or uveitis.
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SYPHILIS – SECONDARY SYPHILIS

Secondary syphilis is generally an immune complex disease presenting in various ways. In many cases symptoms are too mild to be of concern to the patient. The most common feature of the secondary stage of infection is a rash which is present in about 80% of cases. The rash is typically a symmetrical, generalised, coppery-red maculopapular eruption on face, palms and soles and is neither itchy nor tender. It can resemble any skin disease except those characterised by vesicles. Other features may be:

condylomata lata which are broad based, moist warty or papular growths occurring in skin folds or creases;

patchy alopecia;

oral, pharyngeal or vulvovaginal ulcers or ‘mucous patches’ which are round lesions with a greyish-white base edged by a dull red areola which may coalesce to produce a serpiginous ulcer — the ‘snail-track ulcer1; and

lymphadenopathy characterised by firm, enlarged painless nodes typically involving inguinal, suboccipital, posterior cervical, axillary and preauricular groups.
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