WEIGHT LOSS: CONTROLLED, NOT CURED

Before you start on your own personal weight-loss program, using my guidelines, you must accept one fact: Your weight problem is permanent. I’ve said it before, but I need to say it again so you don’t make the mistake of taking on this project as a “summer diet” or a “three-month plan” or to diet just until you get your weight down to where you want it. To really succeed in weight management over the long term, you will never again be able to look at food as casually as you have until this point. Now you must view yourself just as though you were an alcoholic.
Before an alcoholic can recover, he must acknowledge: “I am an alcoholic.” He has to recognize the fact that he will remain an alcoholic throughout his lifetime, even if he never touches another drop of alcohol. He is permanently alcoholic.
You are permanently overweight. Remember that, because if you follow my program for a few months, drop your excess weight, and resume your old eating patterns, you will regain every pound of fat you lost, plus several more. You’ve seen why this happened in the past, and it will happen again. Your old weight will return with a vengeance, and you’ll feel just as bad as you did before. You can NEVER resume your old way of eating without suffering the consequences. In a very tangible sense, you have a physical disability that you cannot cure; you can only control it. You have a permanent weight problem!
In those two words, “control it,” you can literally set yourself free, because even though you can’t cure your obesity, you need never be fat again! Some of you are going to find it difficult to set aside some foods you love dearly in exchange for foods that don’t offer as much sensuous gratification. But stay with me, because I offer you the tools to permanently change how much you weigh, even if I can’t “cure” your weight problem. I offer you the tools to reshape the health of your body!
Throughout this book I have stressed the principle of dietary balance. I’m not advocating some faddish, off-the-wall diet plan that sets you up for failure at the end of the program. I’m teaching you the secret of permanent weight control, which is the balance of dietary proteins, fats, and carbohydrates at every meal, every time you put food in your mouth. I want dietary balance to become second nature to you so that whenever and wherever you eat, you’ll automatically put these principles to work for you.
*54\319\2*

DIFFICULTY FALLING OR STAYING ASLEEP: THE DISORDERS OF INITIATING AND MAINTAINING SLEEP (DIMS)

Generally, DIMS includes those conditions responsible for creating disturbed or insufficient sleep. These disorders are distinct from those that cause excessive daytime sleepiness or disrupt the normal circadian cycle of sleeping and waking. As we will see, however, their symptoms and their effects on health and performance may be much the same.
The DIMS category accounts for approximately 30 percent of all cases of sleep disturbance. DIMS consists of four major groups:
* Disorders caused by a conditioned response or negative expectations about sleep
* Disorders caused by medical, environmental, psychiatric, or alcohol or drug problems
* Disorders caused by breathing or muscular irregularities
* Disorders arising from true organic insomnia (a very rare condition)
DIMS takes many forms: difficulty falling asleep initially, frequent wakenings, trouble returning to sleep once aroused, waking too early in the morning. The pattern of the disturbance is crucial in diagnosis, because it can help to differentiate DIMS from other categories of disorder. For example, disturbances caused by patients’ emotional or environmental situations tend to prevent them from crossing the threshold of sleep. In contrast, victims of endogenous depression are subject to awakenings that occur in the early hours of the morning.
*106\226\8*

DIFFICULTY FALLING OR STAYING ASLEEP: THE DISORDERS OF INITIATING AND MAINTAINING SLEEP (DIMS)Generally, DIMS includes those conditions responsible for creating disturbed or insufficient sleep. These disorders are distinct from those that cause excessive daytime sleepiness or disrupt the normal circadian cycle of sleeping and waking. As we will see, however, their symptoms and their effects on health and performance may be much the same.The DIMS category accounts for approximately 30 percent of all cases of sleep disturbance. DIMS consists of four major groups:* Disorders caused by a conditioned response or negative expectations about sleep* Disorders caused by medical, environmental, psychiatric, or alcohol or drug problems* Disorders caused by breathing or muscular irregularities* Disorders arising from true organic insomnia (a very rare condition)DIMS takes many forms: difficulty falling asleep initially, frequent wakenings, trouble returning to sleep once aroused, waking too early in the morning. The pattern of the disturbance is crucial in diagnosis, because it can help to differentiate DIMS from other categories of disorder. For example, disturbances caused by patients’ emotional or environmental situations tend to prevent them from crossing the threshold of sleep. In contrast, victims of endogenous depression are subject to awakenings that occur in the early hours of the morning.*106\226\8*

CONTRAINDICATIONS TO THE USE OF ANTIHISTAMINES

The term contraindication refers to any situation or circumstance in which the use of a medication would be inadvisable. For most antihistamines, these cases would include the following:
- Hypersensitivity (allergy) to the medication
- Newborn and premature infants
- Nursing mothers
- Narrow-angle glaucoma
- Certain types of peptic ulcers
- Prostatic hypertrophy
- Acute asthma attacks
- Bladder neck obstruction
- Obstruction of the stomach
- Any patient taking monoamine oxidase inhibitor medications (Eutonyl, Nardil, Parnate, etc.)
- For class VII antihistamines (like Phenergan):
Do not give to a comatose patient.
Do not take in conjunction with barbiturates, general anesthesia, tranquilizers, alcohol, narcotics, or narcotic analgesics.
Do not take if you have had a prior adverse reaction to a class VII antihistamine.
Do not give to acutely ill or dehydrated children.
- For Seldane and Hismanal:
Do not take with the antifungal agents ketoconazole (Nizoral) or itraconazole (Sporanox); with the antibiotics azithromycin (Zithromax), clarithromycin (Biaxin), erythromycin (any product), or troleandomycin (TOA).
Do not take if you have liver disease or abuse alcohol. Let your physician know if you have a heart problem.
Do not take more than the dose recommended by your physician.
Warning!
Some medications are not compatible for a variety of reasons.You should always consult your doctor or pharmacist before taking any medication and this is also true if you want to take more than one medication at a time. You should also alert your physician if you notice any unusual side effects while on any medication.
*43/322/5*

CONTRAINDICATIONS TO THE USE OF ANTIHISTAMINESThe term contraindication refers to any situation or circumstance in which the use of a medication would be inadvisable. For most antihistamines, these cases would include the following:- Hypersensitivity (allergy) to the medication- Newborn and premature infants- Nursing mothers- Narrow-angle glaucoma- Certain types of peptic ulcers- Prostatic hypertrophy- Acute asthma attacks- Bladder neck obstruction- Obstruction of the stomach- Any patient taking monoamine oxidase inhibitor medications (Eutonyl, Nardil, Parnate, etc.)- For class VII antihistamines (like Phenergan):      Do not give to a comatose patient.Do not take in conjunction with barbiturates, general anesthesia, tranquilizers, alcohol, narcotics, or narcotic analgesics.      Do not take if you have had a prior adverse reaction to a class VII antihistamine.      Do not give to acutely ill or dehydrated children.- For Seldane and Hismanal:Do not take with the antifungal agents ketoconazole (Nizoral) or itraconazole (Sporanox); with the antibiotics azithromycin (Zithromax), clarithromycin (Biaxin), erythromycin (any product), or troleandomycin (TOA). Do not take if you have liver disease or abuse alcohol. Let your physician know if you have a heart problem. Do not take more than the dose recommended by your physician.
Warning!Some medications are not compatible for a variety of reasons.You should always consult your doctor or pharmacist before taking any medication and this is also true if you want to take more than one medication at a time. You should also alert your physician if you notice any unusual side effects while on any medication.*43/322/5*

TAKING COMMAND OF DIABETES: HOW DO I FIND OUT WHAT MY BLOOD GLUCOSE IS?

Over the past ten years or so, several companies have developed blood glucose measuring systems. They all rely on a drop of blood from a finger or ear lobe. There are two main methods. In the older, most widely used strip systems, the drop of blood is placed on a pad containing a chemical, glucose oxidise, and dyes. As the glucose in the blood reacts with the glucose oxidise the pigment in the dyes is released causing a colour change on the pad. This colour change can then be read by eye or by placing the strip into a reflectance meter which uses light reflected off the colour to produce a number – the blood glucose concentration. In order to read the colour the blood must be washed (Dextrostix – now rarely used), wiped (BM strips or Chemstrips bG) or blotted (Glucostix) away so that the colour is revealed. The timing is critical – if the blood is left on the pad for too short or too long a time the reading will be inaccurate. Also, if the blood is not removed properly, residual blood may confuse the reading, or the pad may be damaged. If used properly these techniques are very accurate. If you are colour blind, you must use a meter. People with diabetic eye damage may have poor colour vision and should also use a meter. Commonly used meters are Reflolux II and Glucometer II. Hypoguard is another system. All these methods take at least one minute and usually two.
The other system uses a biosensor. The test strip with its test pad is first inserted into the sensor – the smallest are pen-sized or credit card sized. The drop of blood is placed on the pad which is divided into an active pad coated with glucose oxidase and a reference pad. As the glucose in the blood reacts with the glucose oxidase in the active pad, tiny electrical differences occur between this and the reference pad. These are conducted into the biosensor and converted to a number -the blood glucose concentration. This takes 30 seconds. The most commonly used biosensor is Exactech. This system is as accurate as the laboratory, provided the user follows the instructions exactly. A disadvantage is that you cannot check a colour change by eye to make sure that the reading is about right. Advantages are that the blood does not need to be removed and it is quicker.
At present, in the UK, all blood testing strips are available on prescription from general practitioners but meters must be bought. It is wise to look at several systems before paying 40 pounds or more for a meter or biosensor. Consider ease of operation for you, portability, robustness, battery needs, the availability of help from the company and local support.  Never buy the first meter you see – for example at a demonstration at a local diabetes group meeting. Never let someone else choose for you.
*4/102/5*

TAKING COMMAND OF DIABETES: HOW DO I FIND OUT WHAT MY BLOOD GLUCOSE IS?
Over the past ten years or so, several companies have developed blood glucose measuring systems. They all rely on a drop of blood from a finger or ear lobe. There are two main methods. In the older, most widely used strip systems, the drop of blood is placed on a pad containing a chemical, glucose oxidise, and dyes. As the glucose in the blood reacts with the glucose oxidise the pigment in the dyes is released causing a colour change on the pad. This colour change can then be read by eye or by placing the strip into a reflectance meter which uses light reflected off the colour to produce a number – the blood glucose concentration. In order to read the colour the blood must be washed (Dextrostix – now rarely used), wiped (BM strips or Chemstrips bG) or blotted (Glucostix) away so that the colour is revealed. The timing is critical – if the blood is left on the pad for too short or too long a time the reading will be inaccurate. Also, if the blood is not removed properly, residual blood may confuse the reading, or the pad may be damaged. If used properly these techniques are very accurate. If you are colour blind, you must use a meter. People with diabetic eye damage may have poor colour vision and should also use a meter. Commonly used meters are Reflolux II and Glucometer II. Hypoguard is another system. All these methods take at least one minute and usually two.The other system uses a biosensor. The test strip with its test pad is first inserted into the sensor – the smallest are pen-sized or credit card sized. The drop of blood is placed on the pad which is divided into an active pad coated with glucose oxidase and a reference pad. As the glucose in the blood reacts with the glucose oxidase in the active pad, tiny electrical differences occur between this and the reference pad. These are conducted into the biosensor and converted to a number -the blood glucose concentration. This takes 30 seconds. The most commonly used biosensor is Exactech. This system is as accurate as the laboratory, provided the user follows the instructions exactly. A disadvantage is that you cannot check a colour change by eye to make sure that the reading is about right. Advantages are that the blood does not need to be removed and it is quicker.At present, in the UK, all blood testing strips are available on prescription from general practitioners but meters must be bought. It is wise to look at several systems before paying 40 pounds or more for a meter or biosensor. Consider ease of operation for you, portability, robustness, battery needs, the availability of help from the company and local support.  Never buy the first meter you see – for example at a demonstration at a local diabetes group meeting. Never let someone else choose for you.
*4/102/5*

SIX WAYS TO HELP HYPERTENSION

If your doctor has diagnosed hypertension, then co-operate with him in controlling this ailment. The American Heart Association offers six helpful suggestions:
1.   Try not to worry. Worry, nervous tension and emotional storms all help push up blood pressure.
2.   Keep your weight normal. Overweight is a health hazard.
3.   Follow your doctor’s advice on the use of tobacco and alcohol. Smoking raises blood pressure in some people. Alcohol does not raise blood pressure; a moderate amount may even reduce it by releasing nervous tension. But some people react poorly to alcohol. Always follow your doctor’s specific advice for you.
4.   Get plenty of sleep. Take a short nap or two during the day if you can arrange it. Blood pressure is lowest during sleep and rises during waking hours.
5.   Choose sports that are not competitive. Exercise is good for you, but avoid overexertion at any time.
6.   Rest before you are tired. You’ll find that you can do more in the long run.
*7/151/5*

SIX WAYS TO HELP HYPERTENSION
If your doctor has diagnosed hypertension, then co-operate with him in controlling this ailment. The American Heart Association offers six helpful suggestions:1.   Try not to worry. Worry, nervous tension and emotional storms all help push up blood pressure.2.   Keep your weight normal. Overweight is a health hazard.3.   Follow your doctor’s advice on the use of tobacco and alcohol. Smoking raises blood pressure in some people. Alcohol does not raise blood pressure; a moderate amount may even reduce it by releasing nervous tension. But some people react poorly to alcohol. Always follow your doctor’s specific advice for you.4.   Get plenty of sleep. Take a short nap or two during the day if you can arrange it. Blood pressure is lowest during sleep and rises during waking hours.5.   Choose sports that are not competitive. Exercise is good for you, but avoid overexertion at any time.6.   Rest before you are tired. You’ll find that you can do more in the long run.
*7/151/5*

GYNECOLOGICAL CANCER GUIDE: VAGINA, FALLOPIAN TUBES AND PLACENTA

Vagina
The vagina is a tube that extends from the vulva to the cervix. It is lined by the same tissue as the cervix and is responsible for lubrication during sexual intercourse. Causes of vaginal cancer are very similar to those of cancer of the cervix, with squamous cancers being by far the most common sort, although secondary spread from cancers of the cervix and endometrium are not uncommon.
If vaginal cancer is left untreated, then it can lead to bleeding, vaginal discharge and pain. Eventually the bladder and rectum can be involved, leading to leakage of urine and faeces. In later stages the cancer can spread outside of the pelvis to the lungs, liver and bone.
Fallopian tubes
The fallopian tubes are a pair of slender tubes arising from the corner of the top of the uterus and extending across either side of the pelvis to the ovary. The fallopian tubes are responsible for transporting the sperm and egg to the uterus. They also provide valuable nutrients as the fertilized egg moves along the tube towards the cavity of the uterus where it will ultimately implant and grow to form an embryo.
Fallopian tube cancers are very rare. They very much act like cancers of the ovary, both in the way that they present and in the way that they respond to treatment.
If left untreated, fallopian tube cancers can spread to other areas within the pelvis and abdominal cavity.
Placenta
The placenta – or afterbirth – has a number of functions, but is primarily there to provide nutrients and a hormonal background for the pregnancy. It also removes waste products from the fetus. It is attached to the wall of the uterus and in turn to the baby by the umbilical cord.
Cancers of the placenta are more common in women who become pregnant over the age of 40, in women who have had multiple previous pregnancies, and in women from South-east Asia.
When a tumour arises in the placenta, it may be benign – the ‘hydatidiform mole’ – or malignant – the ‘choriocarcinoma’. Malignant change in hydatidiform moles can occur in 10-15% of cases.
These cancers often present as bleeding during or following pregnancy and if left untreated then very heavy blood loss can be a major problem. The cancer can often spread to the lungs, liver and brain if left untreated.
*6/144/5*

GYNECOLOGICAL CANCER GUIDE: VAGINA, FALLOPIAN TUBES AND PLACENTAVagina The vagina is a tube that extends from the vulva to the cervix. It is lined by the same tissue as the cervix and is responsible for lubrication during sexual intercourse. Causes of vaginal cancer are very similar to those of cancer of the cervix, with squamous cancers being by far the most common sort, although secondary spread from cancers of the cervix and endometrium are not uncommon.If vaginal cancer is left untreated, then it can lead to bleeding, vaginal discharge and pain. Eventually the bladder and rectum can be involved, leading to leakage of urine and faeces. In later stages the cancer can spread outside of the pelvis to the lungs, liver and bone.
Fallopian tubesThe fallopian tubes are a pair of slender tubes arising from the corner of the top of the uterus and extending across either side of the pelvis to the ovary. The fallopian tubes are responsible for transporting the sperm and egg to the uterus. They also provide valuable nutrients as the fertilized egg moves along the tube towards the cavity of the uterus where it will ultimately implant and grow to form an embryo.Fallopian tube cancers are very rare. They very much act like cancers of the ovary, both in the way that they present and in the way that they respond to treatment.If left untreated, fallopian tube cancers can spread to other areas within the pelvis and abdominal cavity.
PlacentaThe placenta – or afterbirth – has a number of functions, but is primarily there to provide nutrients and a hormonal background for the pregnancy. It also removes waste products from the fetus. It is attached to the wall of the uterus and in turn to the baby by the umbilical cord.Cancers of the placenta are more common in women who become pregnant over the age of 40, in women who have had multiple previous pregnancies, and in women from South-east Asia.When a tumour arises in the placenta, it may be benign – the ‘hydatidiform mole’ – or malignant – the ‘choriocarcinoma’. Malignant change in hydatidiform moles can occur in 10-15% of cases.These cancers often present as bleeding during or following pregnancy and if left untreated then very heavy blood loss can be a major problem. The cancer can often spread to the lungs, liver and brain if left untreated.*6/144/5*

MAKING THE DIAGNOSIS FOR RHEUMATOID ARTHRITIS: CLINICAL EVALUATION

Making a diagnosis of rheumatoid arthritis is not easy. As with all other diseases, there are many ways that your disease might manifest itself. In addition, the first complaints might be very general and vague. The doctor initially tries to develop a differential diagnosis-one made by comparing and contrasting the symptoms of different disorders. Once the doctor suspects rheumatoid arthritis, he or she will look for the typical signs and symptoms of the disease. When enough of these signs are present, the doctor may order a few laboratory tests to confirm his or her diagnosis of RA.
Unfortunately, there is no one specific test for rheumatoid arthritis, but the presence of certain findings on more than one test can confirm a positive diagnosis.
What are the clinical signs of rheumatoid arthritis?
There are many clinical signs of RA. Chief among them is what doctors call arthralgia or, “joint pain.” As the disease progresses, the arthralgia worsens and eventually becomes arthritis, or inflammation of the joint, which makes movement very difficult. Morning stiffness exacerbates this problem.
Are there criteria for a diagnosis of RA?
Yes, there are seven criteria a doctor looks for when establishing a diagnosis of RA. At least four of the following seven criteria must be present in order to make the diagnosis. If any of the first four are present, they must have been present for at least six weeks.
1.  Stiffness in the morning that usually lasts for longer than an hour and gradually improves over the course of the day.
2.  Inflammation, pain, and swelling of three or more joints at the same time.
3.  Pain and inflammation of the hand joints (wrist, knuckle, and/or those in the middle finger).
4.  Arthritis on both sides of the body at the same time (symmetry). This does not have to be the case with arthritis in the hands, where some of the smaller joints might not be affected in both hands.
5.  Nodules over the bony parts of the joints or next to them.
6.  Presence of the antibody called rheumatoid factor in the blood.
7.  Evidence of bone erosions or early bleaching of bone on X-ray.
*22/141/5*

MAKING THE DIAGNOSIS FOR RHEUMATOID ARTHRITIS: CLINICAL EVALUATIONMaking a diagnosis of rheumatoid arthritis is not easy. As with all other diseases, there are many ways that your disease might manifest itself. In addition, the first complaints might be very general and vague. The doctor initially tries to develop a differential diagnosis-one made by comparing and contrasting the symptoms of different disorders. Once the doctor suspects rheumatoid arthritis, he or she will look for the typical signs and symptoms of the disease. When enough of these signs are present, the doctor may order a few laboratory tests to confirm his or her diagnosis of RA.Unfortunately, there is no one specific test for rheumatoid arthritis, but the presence of certain findings on more than one test can confirm a positive diagnosis.
What are the clinical signs of rheumatoid arthritis?There are many clinical signs of RA. Chief among them is what doctors call arthralgia or, “joint pain.” As the disease progresses, the arthralgia worsens and eventually becomes arthritis, or inflammation of the joint, which makes movement very difficult. Morning stiffness exacerbates this problem.
Are there criteria for a diagnosis of RA?Yes, there are seven criteria a doctor looks for when establishing a diagnosis of RA. At least four of the following seven criteria must be present in order to make the diagnosis. If any of the first four are present, they must have been present for at least six weeks.1.  Stiffness in the morning that usually lasts for longer than an hour and gradually improves over the course of the day.2.  Inflammation, pain, and swelling of three or more joints at the same time.3.  Pain and inflammation of the hand joints (wrist, knuckle, and/or those in the middle finger).4.  Arthritis on both sides of the body at the same time (symmetry). This does not have to be the case with arthritis in the hands, where some of the smaller joints might not be affected in both hands.5.  Nodules over the bony parts of the joints or next to them.6.  Presence of the antibody called rheumatoid factor in the blood.7.  Evidence of bone erosions or early bleaching of bone on X-ray.*22/141/5*

MANAGEMENT OF CHRONIC HEPATITIS С: HISTORY AND FEATURES

Hepatocellular Carcinoma
Like infection with hepatitis В virus, chronic HCV infection is associated with an increased risk of hepatocellular carcinoma. Hepatocellular carcinoma occurs primarily in the setting of HCV-induced cirrhosis and rarely in patients with chronic HCV infection who do not have cirrhosis. Once cirrhosis is established, the risk of hepatocellular carcinoma is 2% to 5% per year. The risk for development of hepatocellular carcinoma is increased in patients who have chronic hepatitis В or consume alcohol.
Extrahepatic Manifestations
In addition to hepatic disease, there are important extrahepatic manifestations of HCV infection. These are primarily associated with autoimmune or lymphoproliferative states. HCV is the main cause of essential mixed cryoglobulinemia (type II cryoglobulinemia), with up to 90% of affected individuals having HCV viremia. Cryoglobulins can be found in up to half of patients with HCV infection, although only 10% to 15% have symptomatic disease (primarily weakness, arthralgias, and purpura). Membranoproliferative glomerulonephritis and porphyria cutanea tarda are also common extrahepatic manifestations. A higher incidence of non-Hodgkin’s lymphoma has been observed in association with HCV infection. Other extrahepatic conditions, including Sjogren’s syndrome, autoimmune thyroiditis, lichen planus, and Mooren’s corneal ulcers, have been reported in patients with HCV infection, but no definitive associations have been established.
*81/348/5*

MANAGEMENT OF CHRONIC HEPATITIS С: HISTORY AND FEATURESHepatocellular CarcinomaLike infection with hepatitis В virus, chronic HCV infection is associated with an increased risk of hepatocellular carcinoma. Hepatocellular carcinoma occurs primarily in the setting of HCV-induced cirrhosis and rarely in patients with chronic HCV infection who do not have cirrhosis. Once cirrhosis is established, the risk of hepatocellular carcinoma is 2% to 5% per year. The risk for development of hepatocellular carcinoma is increased in patients who have chronic hepatitis В or consume alcohol.
Extrahepatic ManifestationsIn addition to hepatic disease, there are important extrahepatic manifestations of HCV infection. These are primarily associated with autoimmune or lymphoproliferative states. HCV is the main cause of essential mixed cryoglobulinemia (type II cryoglobulinemia), with up to 90% of affected individuals having HCV viremia. Cryoglobulins can be found in up to half of patients with HCV infection, although only 10% to 15% have symptomatic disease (primarily weakness, arthralgias, and purpura). Membranoproliferative glomerulonephritis and porphyria cutanea tarda are also common extrahepatic manifestations. A higher incidence of non-Hodgkin’s lymphoma has been observed in association with HCV infection. Other extrahepatic conditions, including Sjogren’s syndrome, autoimmune thyroiditis, lichen planus, and Mooren’s corneal ulcers, have been reported in patients with HCV infection, but no definitive associations have been established.*81/348/5*

POSTINFECTIOUS ENCEPHALOMYELITIS

Postinfectious encephalomyelitis is an acute inflammatory demyelinating disease of the brain and spinal cord that, as its name implies, occurs after the onset of a viral illness. It has also been called acute disseminated encephalomyelitis, acute demyelinating encephalomyelitis, and post-viral encephalomyelitis. This disorder generally develops after a respiratory tract infection, a viral exanthem (particularly measles or varicella), or an immunization (historically, smallpox immunization with vaccinia virus). It is more common in children than in adults. Worldwide, measles remains the most important cause of postinfectious encephalomyelitis. In the United States, postinfectious encephalomyelitis is most commonly associated with varicella infection and infections of the respiratory tract, especially influenza.
Pathogenesis
Postinfectious encephalomyelitis is likely an autoimmune disease triggered by a viral infection. Investigators have suggested that the viral infection activates peripheral blood lymphocytes to migrate into the central nervous system and react against the myelin of neurons.
Perivascular inflammation and demyelination of brain tissue are prominent pathologic findings.
Clinical Presentation
Many symptoms and signs of postinfectious encephalomyelitis resemble those of acute viral encephalitis. Patients present with abrupt onset of fever, confusion, and multifocal neurologic signs.
There is usually a history of nonspecific respiratory or gastrointestinal illness for about 5 days to 3 weeks prior to the onset of the encephalomyelitis.
Diagnosis
This disorder should be considered if encephalomyelitis occurs days to weeks after an infection or immunization. Examination of the CSF typically demonstrates a mononuclear or lymphocytic pleocytosis, elevated protein level, and normal glucose level, but the results of this analysis are normal in one third of patients. An EEG usually reveals diffuse slowing of brain waves. MRI may show enhancement of multifocal white matter lesions. Abnormalities resemble multiple sclerosis, but the lesions of postinfectious encephalomyelitis are all of the same age, whereas those of multiple sclerosis are of varying age.
Therapy
- Treatment of postinfectious encephalomyelitis is supportive and includes the following:
- Lowering patient’s temperature with antipyretic agents
- Administering adequate fluids
- Treating seizures, if they develop
- Reducing intracranial pressure
- Initiating mechanical ventilation, if necessary
Treatment with high-dose intravenous methylprednisolone has been suggested, but well-controlled clinical trials detailing its benefit have not been performed. Aggressive supportive therapy is needed, because patients with postinfectious encephalomyelitis can make remarkable recoveries after prolonged period of coma.
*26/348/5*

POSTINFECTIOUS ENCEPHALOMYELITISPostinfectious encephalomyelitis is an acute inflammatory demyelinating disease of the brain and spinal cord that, as its name implies, occurs after the onset of a viral illness. It has also been called acute disseminated encephalomyelitis, acute demyelinating encephalomyelitis, and post-viral encephalomyelitis. This disorder generally develops after a respiratory tract infection, a viral exanthem (particularly measles or varicella), or an immunization (historically, smallpox immunization with vaccinia virus). It is more common in children than in adults. Worldwide, measles remains the most important cause of postinfectious encephalomyelitis. In the United States, postinfectious encephalomyelitis is most commonly associated with varicella infection and infections of the respiratory tract, especially influenza.
PathogenesisPostinfectious encephalomyelitis is likely an autoimmune disease triggered by a viral infection. Investigators have suggested that the viral infection activates peripheral blood lymphocytes to migrate into the central nervous system and react against the myelin of neurons.Perivascular inflammation and demyelination of brain tissue are prominent pathologic findings.
Clinical PresentationMany symptoms and signs of postinfectious encephalomyelitis resemble those of acute viral encephalitis. Patients present with abrupt onset of fever, confusion, and multifocal neurologic signs.There is usually a history of nonspecific respiratory or gastrointestinal illness for about 5 days to 3 weeks prior to the onset of the encephalomyelitis.
DiagnosisThis disorder should be considered if encephalomyelitis occurs days to weeks after an infection or immunization. Examination of the CSF typically demonstrates a mononuclear or lymphocytic pleocytosis, elevated protein level, and normal glucose level, but the results of this analysis are normal in one third of patients. An EEG usually reveals diffuse slowing of brain waves. MRI may show enhancement of multifocal white matter lesions. Abnormalities resemble multiple sclerosis, but the lesions of postinfectious encephalomyelitis are all of the same age, whereas those of multiple sclerosis are of varying age.
Therapy- Treatment of postinfectious encephalomyelitis is supportive and includes the following:- Lowering patient’s temperature with antipyretic agents- Administering adequate fluids- Treating seizures, if they develop- Reducing intracranial pressure- Initiating mechanical ventilation, if necessaryTreatment with high-dose intravenous methylprednisolone has been suggested, but well-controlled clinical trials detailing its benefit have not been performed. Aggressive supportive therapy is needed, because patients with postinfectious encephalomyelitis can make remarkable recoveries after prolonged period of coma.*26/348/5*

TREATMENT OF STRESS BREAKDOWN: BRAIN RESPONSE TO SEDATION CAUSING WITHDRAWAL AGITATION

Sedative drugs include alcohol, chloral hydrate, barbiturates, and the benzodiazepine drugs such as diazepam (Valium), oxazepam (Serepax), nitrazepam (Mogadon), and the increasing number of drugs on the market whose generic names end in ‘azepam’. The effect of any of these drugs is mainly on the cerebral cortex, interfering with the inhibitory cell groups and the mechanisms which trigger the alarm or anxiety response. Some of us like to feel slightly sedated, relieved of our fears by the Dutch courage of alcohol and other sedative drugs.
However, while sedative drugs may make us momentarily feel good, the brain does not happily accept the sedative drug’s slowing-down effect on the brain cells in the cerebral cortex. In response, the reticular activating system reacts to the sedation by sending increased stimulatory impulses to the cerebral cortex.
As the sedation from the last dose of drug wears off, the person begins to experience a hangover, a feeling of touchy hypersensitive agitation, due to the over-stimulation by the reticular activating system. This vague over-stimulation of the brain, as a reaction to the last sedative dose, usually lasts four times as long as the sedation did. After that time, the brain is able to reduce the stimulation and the cells get back to normal function.
Thus, a person feels more anxious after a sedative drug wears off than he would have if he hadn’t taken the drug.
After the sedation wears off the mild agitation from the brain’s response to the drug feels very uncomfortable and the person seeks another dose to relieve the agitation resulting from the previous drug dose. The problem is that this agitation is additive; after taking multiple doses of the drug, the person will experience such a high degree of agitation on ceasing the drug, he or she may become fearful of not being able to relieve the agitation with another dose and drug dependence may result. The risk of sedative dependence is so high where a person is being treated for stress-breakdown symptoms that sedative drugs should only ever be given when the anxiety symptoms themselves have become the major cause for concern. For example, a person who reacted to stress-breakdown symptoms with a phobic avoidance reaction (such as agoraphobia) and became unable to leave the house for fear of experiencing anxiety, might be more disabled from being unable to leave the house from fear of anxiety than by drug dependence.
Sedative drugs, in order to bring the situation under control, might be justified in those circumstances. However, I believe that in the vast majority of cases of anxiety symptoms caused by stress overload, the use of sedative drugs cannot be justified.
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TREATMENT OF STRESS BREAKDOWN: BRAIN RESPONSE TO SEDATION CAUSING WITHDRAWAL AGITATION
Sedative drugs include alcohol, chloral hydrate, barbiturates, and the benzodiazepine drugs such as diazepam (Valium), oxazepam (Serepax), nitrazepam (Mogadon), and the increasing number of drugs on the market whose generic names end in ‘azepam’. The effect of any of these drugs is mainly on the cerebral cortex, interfering with the inhibitory cell groups and the mechanisms which trigger the alarm or anxiety response. Some of us like to feel slightly sedated, relieved of our fears by the Dutch courage of alcohol and other sedative drugs.However, while sedative drugs may make us momentarily feel good, the brain does not happily accept the sedative drug’s slowing-down effect on the brain cells in the cerebral cortex. In response, the reticular activating system reacts to the sedation by sending increased stimulatory impulses to the cerebral cortex.As the sedation from the last dose of drug wears off, the person begins to experience a hangover, a feeling of touchy hypersensitive agitation, due to the over-stimulation by the reticular activating system. This vague over-stimulation of the brain, as a reaction to the last sedative dose, usually lasts four times as long as the sedation did. After that time, the brain is able to reduce the stimulation and the cells get back to normal function.Thus, a person feels more anxious after a sedative drug wears off than he would have if he hadn’t taken the drug.After the sedation wears off the mild agitation from the brain’s response to the drug feels very uncomfortable and the person seeks another dose to relieve the agitation resulting from the previous drug dose. The problem is that this agitation is additive; after taking multiple doses of the drug, the person will experience such a high degree of agitation on ceasing the drug, he or she may become fearful of not being able to relieve the agitation with another dose and drug dependence may result. The risk of sedative dependence is so high where a person is being treated for stress-breakdown symptoms that sedative drugs should only ever be given when the anxiety symptoms themselves have become the major cause for concern. For example, a person who reacted to stress-breakdown symptoms with a phobic avoidance reaction (such as agoraphobia) and became unable to leave the house for fear of experiencing anxiety, might be more disabled from being unable to leave the house from fear of anxiety than by drug dependence.Sedative drugs, in order to bring the situation under control, might be justified in those circumstances. However, I believe that in the vast majority of cases of anxiety symptoms caused by stress overload, the use of sedative drugs cannot be justified.
*48/129/5*

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