‘I want a health check,’ she commanded, forceful and unsmiling. Doctors and nurses are not used to being ordered about in this way; it is easy for hackles to rise and defences to spring up. The doctor felt attacked and was tempted to retaliate, to point out that this was family planning, not a well woman clinic, for example. Instead, she inwardly observed this difficult atmosphere, and wondered what was behind it. ‘We haven’t seen you for some time,’ she commented. Mrs A. shrugged, but remained silent. ‘Are you still on the Pill?’ ‘No,’ another shrug, then defiantly, ‘We use a sheath.’ The tension level in the room rose. ‘Look, I’ve come for a health check – that’s all!’ The doctor thought to herself, ‘Contraception produces tension, but is not to be discussed.’ She changed tack. ‘Of course we will examine you. Have you been having any problems?’ Immediately, the reply shot back, ‘No.’ Another glare at the watch. The doctor sat back and waited, refusing to be bounced into this checkup, realizing that, so far, she had been doing the work here. Now she let the patient decide how to continue.

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Because the structure of your mouth and jawbone changes as you age, if you wear a partial or full denture, you should expect the fit of the denture to change as well. In fact, because of the loss of teeth, the jawbone, which supports the dental appliance, will shrink even more quickly than if your own teeth were intact.

Your lower jawbone is especially at risk if you wear a full or partial lower denture, since the base plate of the denture places an abnormal amount of stress on the natural gums and underlying bone. This can cause the jaw to deteriorate even more. As the bone changes, you’ll probably find that you have to change the dentures to fit better. Fortunately, new technology is making possible dentures that fit better and adjust to changes in pressure. They’re also better able to absorb the shock of chewing and biting down, thus redirecting some of the stress away from the gums.

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As with any viral infection, the most severe period is the initial flare-up. When your physician determines that your rash is Ramsay Hunt syndrome, he will treat it with corticosteroidal preparations in either oral or topical form. But because the virus hides in the nerves of the spine for many years, it may cause permanent nerve damage when it surfaces after being dormant for decades. Though this is rare, you should see a neurologist at the first sign of a flare-up.

Special Mention for the Elderly

When an elderly person is affected with Ramsay Hunt syndrome, an extremely painful condition called postherpetic neuralgia can sometimes occur. Men and women 60 years and older are prone to postherpetic neuralgia because of their naturally lower immune systems. Postherpetic neuralgia is signified by facial paralysis, constant headache, and severe pain where the rash initially occurred.

Medications such as Zovirax and pain medications will help lessen the outbreak. If pain persists, a medication such as Zostrix can be very helpful in alleviating it.

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For most of us, a certain amount of deterioration in our vision is almost inevitable as we grow older. I find I can no longer work on models with small parts, as I have trouble focusing my eyes. I refuse to give in, however, which runs counter to the advice that my own ophthalmologist has given me. I will not wear reading glasses or bifocals, mostly for reasons of vanity. Instead, I wear contacts. The lens in one eye is for distance, while the other lens helps me to do close-up work.

I’ve found that what is almost universal among midlife adults and older is the gradual appearance of a kind of farsightedness called presbyopia, in which you will find it increasingly necessary to hold a book or newspaper farther away from you in order to see clearly. Whether you’ve traditionally been nearsighted or farsighted in the past doesn’t matter. And if you’ve always been envious of a friend who’s enjoyed 20/20 vision most of his life, relax, because there is such a thing as divine retribution—even people blessed with perfect vision are affected by presbyopia to some degree.

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Flashing lights are pretty when they’re part of a Christmas or Fourth of July display, but when they regularly occur as part of the early stages of a migraine headache, they quickly lose their luster.

Migraines have the reputation of being able to totally disable a person, and for good reason. If you’ve ever experienced a migraine, also known as a vascular headache, you know that the pain in your head can be so intense that you’re physically unable to do more than lie in bed in a darkened room and wait for the pain to subside.

Before a migraine hits fully, the flashing lights appear because the constricted arteries reduce the flow of blood to the part of the brain that controls your vision. In addition to the flashing lights, you may experience blind spots, vertigo, and nausea. These are all signs that a migraine is imminent.

We don’t know exactly what causes a migraine headache. However, at a migraine’s worst, the carotid and vertebral arteries in the brain, which supply it with blood, first narrow and then swell up, sometimes to twice their normal size. This decreases the amount of blood supplied to your brain. The combination of the swollen arteries and the reduced blood supply is the reason for the crushing pain that can totally incapacitate you. Most migraines last from a few hours to several days. After the pain subsides, you’ll probably feel groggy and lethargic for a while.

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If you think you have temporal arteritis, you should see your doctor immediately, especially if you have experienced sudden blindness. He will conduct a blood test that includes a test for the erythrocyte sedimentation rate, or ESR, which will check how quickly red blood cells settle in the bottom of a test tube. A high ESR is an indication of an inflamed artery, as in temporal arteritis. Your doctor may also perform a biopsy of the temporal artery in order to make a positive diagnosis.

If you do have temporal arteritis, you will need to treat it with a regimen of corticosteroid medication such as prednisone on a long-term basis, possibly for months. This will help reduce the swollen artery to its normal size. In order to prevent future problems, however, you will need to continue taking the medication for a year or more; regular blood tests that monitor the ESR in addition to your symptoms will help your doctor to guide your treatment.

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Can finasteride help prevent malignant growth in the prostate? In other words, can it stop prostate cancer from forming? The National Cancer Institute has launched a multimillion-dollar study to find this out. For seven years, this massive project will follow 18,000 men, aged 55 and older, who are otherwise healthy (men with any prostate ailment, benign or otherwise, are not eligible). All of-the men will take daily pills; half of them will get finasteride, the rest will get a placebo. All of the men will have regular physical exams, including a digital rectal exam and PSA test, during the study period. And, at the end of the study, all of the men will have a prostate biopsy. The study is double-blind—neither the men participating in the study nor the physicians treating them will know who’s getting the finasteride until it’s over.

Why do scientists think a BPH drug can have an effect on prostate cancer? One reason is that finasteride lowers a man’s levels of PSA, an enzyme made by the prostate used as an indicator for prostate cancer. Another assumption is tied to the fact that finasteride works by interrupting a hormonal process (it blocks an enzyme called 5-alpha-reductase, which changes the male hormone testosterone into a substance called DHT—the active form of male hormone within the prostate). Prostate cancer is intrinsically linked to hormonal activity. So maybe, some scientists speculate, by thwarting the prostate’s normal hormonal pattern, prostate cancer can be stopped before it ever has a chance to begin.

However, other scientists doubt that finasteride will have any effect in preventing prostate cancer. First, there’s no evidence that DHT is the hormone responsible for the growth of prostate cancer. In fact, the levels of 5-alpha reductase activity are actually lower in prostate cancer than in normal tissue. Also, there’s no supporting evidence from laboratory experiments to suggest that finasteride will work; in one animal tumor model, in fact, finasteride has no effect at all. And finally, finasteride’s effect in men who already have prostate cancer is marginal at best—which makes it unlikely that it will have any effect in preventing the disease.

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The first option is called “watchful waiting,” and it doesn’t mean “do nothing.” It means “wait and see.” The course of BPH is often hard to predict; your symptoms could improve, get worse, or stay the same. Beyond watchful waiting, broadly speaking, there are two paths—surgical and medical. (See table 10.1, page 257.) The choice depends on the severity of your symptoms. If you have one or more of the conditions mentioned above that require treatment, your best option is surgery. But if your symptoms are moderate—that is, not severe enough to require surgery—a trial of medical therapy makes sense.

Watchful Waiting

This is the most conservative approach to BPH, and for most men with mild symptoms, it’s the best. Remember, just having an enlarged prostate does not mean you need treatment. It’s only when the symptoms of enlargement become bothersome, or if your urinary function is seriously affected, that you should consider treatment. So, many doctors begin with what’s called a “watch-and-wait” approach to the problem. They keep a close eye on your condition, with checkups once or more a year to make sure you’re not developing any complications. Sometimes the symptoms of BPH get better on their own. If they don’t, then you and your doctor will move on to the next step—deciding what treatment’s best for you.

Risks. Like any other treatment option, watchful waiting is also something of a gamble—low-risk, but a gamble all the same. A few men in programs of watchful waiting develop acute urinary retention, the inability to urinate. A few develop urinary tract infections; some see blood in their urine; some go on to develop kidney or bladder damage without any noticeable change in their symptoms (this is called silent prostatism). But such complications from watchful waiting are rare indeed. You can lower the odds even further by limiting your fluid intake before bedtime and by refraining from taking certain over-the-counter medications, such as decongestants, which can make your BPH symptoms worse.

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Hormone therapy works in almost every man; it prolongs life and eases many symptoms of advanced prostate cancer. In some men, its effects last for years. Why doesn’t it cure the disease? Because prostate cancer is “heterogeneous”—it’s a bunch of different cells mixed up together. Some of these cells respond to hormones; some of them don’t. This means that a hormone treatment which targets one kind of cell, the kind that responds to hormones, has absolutely no effect on the hormone-insensitive cells all around it. They keep right on growing, unfazed. Ultimately, if a man lives long enough, these cells eventually overtake the hormone-sensitive cells. And right now, we don’t have any way to stop them.

This fact has two important implications for patients: One, there’s no evidence that starting hormone therapy early in the course of prostate cancer is any more effective in prolonging survival than starting treatment if and when a patient needs it—when a man has bone pain from the cancer, for instance. Again, the cells that ultimately prove fatal are the hormone-insensitive cells—and to these cells, whether hormone therapy comes earlier or later does not matter one bit. Two, there is no good evidence that other forms of hormone manipulation—total androgen ablation, for instance— provide much benefit after hormone therapy has stopped working.

If hormones lose their effect on the tumor, there are several other options for treatment of the disease and specific symptoms, including new chemotherapy drugs, “spot” radiation to painful sites of metastases (chunks of cancer that have broken off from the main tumor and established themselves in new locations, such as the bone), a radioactive substance called strontium-89, which is specially tailored to treat bone pain, and a whole host of powerful pain medications, their is no reason for any man with prostate cancer to live in excruciating pain. Aggressive pain management is not only beneficial—it’s been shown that men who aren’t in terrible pain live longer—it’s your right as a patient. Help is available; take it.

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Surgical removal of a man’s testicles (also called an orchiectomy) is the easiest and least expensive way to control testosterone. As surgical procedures go, it’s simple. The operation can be performed under spinal anesthesia or, if the patient is not strong enough to tolerate this, even a local anesthetic. This is what happens: A surgeon makes a small incision in the scrotum, and brings out each testicle individually through this opening. Then the surgeon cuts the vas deferens and blood vessels that supply each testicle, and the testicles are removed. Some surgeons perform what’s called “subcapsular orchiectomy.” In this operation, the surgeon opens the lining to the testicles and empties the contents of each testicle. The lining is closed again, and this empty shell is placed back inside the scrotum—so nothing looks different; in other words, no one can tell from outward appearance that there’s nothing inside the scrotum. The basic differences here are cosmetic—and therefore psychological—and for some men, this makes the thought of castration easier to accept. However, some surgeons don’t like to perform this operation because they worry that some testosterone-producing cells may be left behind.

After surgery, patients usually can go home from the hospital the same day—or, at the very latest, the next day. The only major complication to worry about with surgical castration is bleeding. However, this shouldn’t be a problem if the surgeon makes a point of checking that all bleeding is stopped before the scrotum is closed, and that a compression dressing is left in place to control the smaller, harder-to-see blood vessels.

Castration works fast; it reduces the body’s amount of testosterone by 95 percent almost immediately, and permanently. Boom—within about three hours after surgery, testosterone levels begin to plummet to a level called the “castrate range.” This is considered the gold standard, an important point of comparison in monitoring hormone therapy—as certain drugs are judged by their ability to reduce testosterone to this range.

Some doctors used to believe that several months after castration, the body began producing more testosterone at other sites—and that this was the reason prostate cancer continued to grow This is not true. There is no delayed increase in testosterone and anyway, that’s not why prostate tumors keep growing—they continue to spread because of the cancer cells that are not affected by hormone therapy.

What happens to the prostate tumor after castration? It begins to shrink, and men with symptoms of obstruction or pain caused by the cancer begin to feel better right away.

Castration’s advantages are that it’s effective almost immediately and that its results are permanent—there’s no need to take daily medication. And, because it is a “one-shot” treatment, it’s relatively inexpensive.

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