Please also refer to the Glosssary of DI Terms, also on DiF’s web site.

An adult who urinates more than 50 ml/kg body weight per 2 hours is generally considered to have a higher than normal output. Loosely translated, 50 ml/kg is about 3.5 quarts per day for a 150 Lb adult.

An adult who drinks more than 4 quarts (1 gallon) or approximately 12 glasses (144 oz) of beverages per day would have a higher than normal intake.

Water intoxication is a term used to describe a constellation of symptoms and laboratory abnormalities that result from an accumulation of too much water in the body. Depending on how much and how fast water accumulates, the symptoms can be mild (headache, fatigue, dizziness, loss of appetite) or severe (confusion, coma, seizures). Since these symptoms also occur in other disorders, the diagnosis of water intoxication requires a laboratory test showing that the plasma sodium concentration has been “diluted” be the normal range. Water intoxication occurs whenever water is put into the body (by drinking or intravenous infusion) faster than the kidneys can excrete it (usually because of kidney failure or the act of vasopressin, the antidiuretic hormone). This can occur in a variety of situations. It is common, for example, in patients with dipsogenic DI (a form of DI due to an abnormality in the thirst mechanism) who are treated with dDAVP in the mistaken belief that they have CDI (a form of CDI due to a deficiency of the antidiuretic hormone, vasopressin). The treatment of water intoxication varies depending on the cause and the severity but almost always includes cessation of fluid intake until plasma sodium concentration returns to normal.

By “sodium imbalance” seizures, I assume you mean a low serum sodium concentration. This abnormality is usually referred to as hyponatremia. When it develops in a patient taking dDAVP for CDI, it usually indicates that the DI is due to abnormal thirst, an entity we call dipsogenic DI. Dipsogenic DI occurs in some patents with multiple sclerosis and is often confused with CDI, which is due to a deficiency of the antidiuretic hormone vasopressin and not to a thirst abnormality (although occasionally the two disorders occur together). These two types of DI-dipsogenic and central-can be distinguished with certainty only by measuring antidiuretic hormone during a suitable stimulus such as a fluid deprivation test (although sometimes an MRI of the brain is also helpful). If your son has “pure” dipsogenic DI due to MS, it may or may not improve spontaneously with time or may show ups and downs. In any event, he should not take dDAVP in the usual way to control the DI because it will invariably produce hyponatremia and increase the risk of seizures. If he has combined dipsogenic and CDI, treatments other than dDAVP should be used since they usually provide better control with less hyponatremia. The first and most important issue to settle is which type(s) of DI your son has.

Psychogenic or compulsive polydipsia is a common and well-recognized form of primary polysipsia [also known as dipsogenic DI]. There is no treatment for this form of DI except restricting fluid intake, and that is usually not possible because of patient non-compliance. Unfortunately, I have little to recommend for this patient except that he should not be given dDAVP or any other medication that reduces urine output, since it will produce water intoxication like the episode he has already had.

I have not studied bone density in patients with CDI. Therefore, I can neither confirm nor dispute the report to which you refer. However, I can tell you that none of the patients we have treated (now greater than 150 people) has a history of bone fractures or other signs/symptoms of functionally significant osteoporosis. Therefore, even if the report is correct, the decrease in bone density probably does not significantly increase the risk of symptomatic bone disease in patients with DI. Osteoporosis is relatively common with increasing age in the general population. Therefore, it would be prudent for everyone, including DI patients, to follow the recommended preventive measures and have bone density checked if any of the established risk factors are present.

It sounds as though the hypothalamic cells that regulate appetite and thirst have also been damaged. The only way to control her weight is to put her on a standard, low calorie, weight-reducing diet of the same type used in other forms of obesity. Your doctor or a registered nutritionist should be able to instruct you in the specifics. Her hypernatremia (increased serum sodium) indicates she is not drinking enough water to prevent dehydration because her thirst mechanism is defective. The only way to deal with this problem is to be sure that her dose of dDAVP is always sufficient to prevent breakthrough of her CDI and then teach her how to regulate her fluid intake in accordance with changes in hydration as evidenced by changes in weight, and, when necessary, measurements of her serum sodium. This is a complicated process that requires continual monitoring, support, and advice from a medical doctor on site.

If inadequately treated, CDI may result in incontinence. However, it is more likely due to a separate problem. If the incontinence persists even when the dose of dDAVP is sufficient to normalize urine output, a urologist should be consulted.

CDI does not cause infantile genitals. However, some of the diseases that cause CDI in childhood can interfere with normal sexual development.

As far as we know, CDI does not accelerate the aging process.

MRI of the brain is useful for determining the type of DI and may also reveal the cause if the DI is either central or dipsogenic DI. If the initial MRI does not show the cause of CDI or dipsogenic DI, a repeat MRI in 6 to 12 months is a good idea. After that, additional repeats rarely provide any more information of any clinical value.

The only connection between your DI and multiple orthopedic problems that I can imagine is if they both are the result of some kind of athletic or other trauma that also involves your head. Unless you have some of the other stigmata of Cushings syndrome, I doubt that additional measurements of coritsol would be worthwhile.

There are many different causes for each of the four main types of DI. CDI is usually idiopathic (no known cause), but can also result from a variety of known disorders such as tumors, head trauma, and granulomas that involve the pituitary and hypothalamus.

CDI does not affect any body system except urine production by the kidney. When other systems are affected, it is due to the underlying disease that also caused the CDI.

Once the posterior pituitary is damaged or destroyed, it will never recover. It will always be necessary to take dDAVP or some other antidiuretic drug to control urine output. Damage to one of the hormones from the anterior pituitary sometimes recovers after a while, but it depends on how severe the damage is. Taking replacement hormones will not cause other diseases, provided the doses are correct. If CDI is not controlled with medication, the high urine output occasionally causes the bladder to enlarge, but rarely damages the kidney.

There are other drugs to treat DI, but to my knowledge there are no natural cures.

The combination of a thirst abnormality with CDI is particularly difficult to manage. If she really has both abnormalities, the treatment plan is more involved and should be designed and monitored by a specialist.

I would suggest that you carry a card in your wallet indicating in English that you have CDI. If you become dehydrated and cannot communicate with the Swedish doctors, they will probably know what to do when they see the card. If not, they will at least know who to contact for instructions.

To my knowledge, there is no proven connection between DI and hypersalivation. However, they could be related, because dry mouth is common with dehydrated people with DI (when vasopressin is increased), and there is some evidence that vasopressin reduces water loss from other tissues besides the kidneys. Thus a deficiency of vasopressin could result in increased formation of saliva as well as perspiration. I know of no association between DI and night terrors.

Apart from the unnecessary expense, you do not need to worry about giving him too much dDVAP. Even higher doses of the drug should not result in water intoxication provided his thirst mechanism is normal and he learns to drink only when he is thirsty. Both of these conditions are probably being met if all measurements of his serum sodium have been normal. If you go to a higher dose of dDAVP, I would continue to check his serum sodium weekly for a month and, if they are all normal, repeat them only if he develops symptoms of water intoxication.

The best way and probably the only way to tell for certain if you have taken on too much fluid is to measure your plasma sodium. This needs to be done while you are having symptoms and before the effect of the last dose of dDAVP has worn off. If these measurements confirm that you are taking on too much fluid, it is important to determine why. If you are drinking excessive amounts for reasons other than thirst (e.g., habit), all you need to do is ‘break’ this habit and remember to drink only when your are truly thirsty. If this does not eliminate the problem, you may have a disorder in your thirst mechanism.

CDI results in growth retardation only if it severe and untreated or if it is associated with deficiencies of growth hormone or other anterior pituitary hormones. Since neither condition is present in your son, I would expect him to show “catch up” growth now that he has finished his chemotherapy. Eventually, he will probably reach the same size as if he did not have DI.

It is unlikely that your weight gain or the ‘water pockets’ observed by your surgeon are the results of your DI or the dDAVP used to treat it. Treatment with dDAVP sometimes results in excessive water retention, but when it does it is associated with a low serum sodium or other signs and symptoms of water intoxication. If you are concerned about this possibility, have your doctor check your serum sodium level.

The amount of fluid intake needed to adequately hydrate an infant (or anyone, for that matter) cannot be specified exactly because it will vary markedly depending on factors such as the rate of urine output, loss from the gastrointestinal tract (i.e., vomiting or diarrhea), and normal evaporation of water from skin and lungs. The latter also varies markedly depending on temperature and activity. Generally speaking, if urine output is 50 cubic centimeters (cc) per kilogram body weight (kg) per day and gastrointestinal losses are nil, total fluid intake (including food) will need to be about 1.5 times as much or 75 cc/kg/d. However, as noted above, this can vary markedly depending on the situation. The good news is that it is not necessary to worry about fluid intake if the patient is conscious and can drink normally because the thirst mechanism will ensure that it is appropriate, no matter how much fluid output may vary. If the patient is unconscious or lacks a normal thirst mechanism, it is necessary to externally regulate fluid intake but this should always be done with the help of an expert in water metabolism and the effectiveness of the regulation should always be monitored closely by frequent measures of body weight and plasma sodium concentration.

To our knowledge, DI does not result in loss of any vitamins or need for more vitamin supplementation than normal. If your fatigue is caused by your DI it may be because it interferes with your sleep at night. Depression can also cause fatigue and weakness. Dryness of the skin, especially on the palms and soles of feet, can be due to many things. Usually DI is not one of the causes although some patients do report such dryness that improves when their DI is controlled. Therefore, there could be a connection.

DI can be present at birth. When it is, it is almost always a genetic version of NDI, although there are genetic forms of CDI.

DI is thought to be uncommon, but we really do not know the incidence or prevalence of DI in the population. It may be more common than we think because it is often goes unrecognized or undiagnosed.

No one knows the number of patients with DI in the United States or any other population. The number with enuresis has been estimated and shown to vary with age (from 25% of children at 5 years of age to 1% in adolescents and adults), but it is not known how many of those have DI. From various sources, it is estimated that the number of DI patients in the United States range between 40,000 to 80,000, but that calculation involves a lot of assumptions and could be way off.

Question # 0009 FAQ, # 0331 EWv3n2 Keywords: diagnosis, diagnostic tests, treatment

DI is rarely episodic. Without treatment, the amount of urine passed each day is usually fairly constant, although it may be reduced from time to time by heavy smoking, or mild dehydration caused, for example, by physical exertion on a hot day. Dehydration so severe as to require intravenous fluids is also very rare in DI unless the thirst mechanism is also defective, or the patient is unable to obtain water to drink until thirst ceases. That is sufficient to prevent dehydration. If thirst does not occur in the presence of dehydration, something else is wrong, probably with the thirst mechanism. Going without water and food for 20 hours or more sometimes makes a patient with primary polydipsia feel better, but it invariably makes a patient with CDI or NDI feel much worse. However, primary polydipsia should not result in dehydration. DI should be treated if it results in intermittent dehydration or other troublesome symptoms such as thirst, getting up at night to urinate, etc. However, the type of treatment depends on which type of DI it is (central or nephrogenic).

There is no proven connection between DI and hypersalivation. However, they could be related because dry mouth is common in dehydrated normal people (when vasopressin is increased) and there is some evidence that vasopressin reduces water loss from other tissues besides the kidneys. Thus, a deficiency of vasopressin could result in increased formation of saliva as well as perspiration.

The association of your DI with intolerance to altitude is interesting because I have never heard of it before. I also cannot easily explain it. Perhaps it is a coincidence.

There is no need for extra fluid during or after surgery if dDAVP is administered to prevent excessive water loss by the kidneys. In fact, extra fluid would be hazardous in this situation since the dDAVP would prevent normal excretion of the excess water. If dDAVP is not given during and after the surgery, extra fluid should be give to compensate for the loss. The amount that is required depends on the rate of urine output. It can be determined by keeping track of urine output and also the plasma sodium concentration.

Anything, such as suction, that increases fluid loss should be counteracted by equal increases in fluid intake.

Empty sella syndrome refers to a condition in which the pituitary gland appears to be flattened within the sella turcica. The sella turcica is a bony pocket in the skull that holds the pituitary where it hangs down from the brain. Normally, it is completely filled by the pituitary gland. In empty sella, most of the space is taken up by the fluid that bathes the brain (called cerebrospinal fluid or CSF). Usually, empty sella is of no consequence because it occurs in a relatively large number of otherwise healthy people and does not result in any significant abnormality in pituitary function. Occasionally, however, it is associated with hormone abnormalities or other symptoms such as frequent headaches or visual disturbances. The cause of empty sella is unknown and probably varied. In some cases, it may reflect an earlier compression by a pituitary tumor that has since shrunken or disappeared altogether.

Hyperemesis gravidarum (excessive morning sickness) during pregnancy is not known to affect the thirst mechanism but it may lead to severe dehydration if the woman has untreated DI.

Microadenomas do not cause CDI. However, infiltrative diseases of the pituitary, which can mimic micros on MRI, can. Given your symptoms, you should have tests to determine whether you do, indeed, have CDI.

DI usually does not change much with age but sometimes it gets better. Rarely, it stops altogether.

DI was differentiated from diabetes mellitus (sugar diabetes) in 1787 and the genetic form of DI was discovered in 1841. Your great grandmother probably did not have the genetic form of DI and even if she did, you almost certainly did not inherit it because, if you did, you would have symptoms of DI by now. A treatment for DI was not discovered until 1913 and it was not widely used until many years later. Therefore, it is unlikely that your great grandmother ever received any treatment.

Question # 0753 EWv7n3 Keywords: prevalence, incidence

No one knows for sure how many people have DI because no systematic records of the disease are maintained.

Question # 0754 EWv7n3 Keywords: narcolepsy

Vasopressin is made and stored in the same large neurons of the posterior pituitary. The pituitary stalk through which these neurons pass on their way from the hypothalamus can be severed by trauma, surgery, or disease but when it is severed the neurons die. I know of no relation between DI and narcolepsy.

The bracelet should say that you have central diabetes insipidus (without using abbreviations) and are taking dDAVP. If you lose consciousness, you should be taken to a hospital immediately for monitoring and management of your water balance.

When CDI (the type that is associated with absence of the pituitary bright spot and is treated with dDAVP nasal spray) begins in infancy or early childhood, it is often genetic. If so, one parent or other relative may or may not have CDI also. In any case a genetic analysis should be performed on the child unless, of course, some other cause such as a congenital malformation of the brain or a tumor has already been identified. CDI itself should not effect the child’s prognosis, but the disease that causes it may, depending on what it is.

Patients with DI can have headaches just like any other person. However, they can also occur for any of several special reasons related to the DI. If you have CDI as a result of a brain tumor, pressure from a tumor or other disease affecting the part of the brain that normally makes antidiuretic hormone (vasopressin) could cause your headaches.

Many patients with CDI take dDAVP instead of chlorpropamide because their doctors do not know how effective the latter can be. As you know, chlorpropamide can also lower blood sugar. Usually this does not have any consequences except for a slight increase in appetite, sometimes weight gain, and occasionally irritability. However, the low blood sugar can be more severe if the patient goes on a strict diet or engages in heavy physical exercise. The drug should not be taken during pregnancy since we do not know if it affects the fetus. As far as we know, the chlorpropamide has no significant long-term side effects, and it is a good deal less expensive than dDAVP I would recommend it to patients who do not respond well or cannot afford dDAVP.

You have asked three excellent and very important questions: It is very, unlikely that her angry mood or other personality changes caused her DI. It is much more likely that these personality changes and some of the other symptoms you mention (low blood pressure and dizziness) are due to another disorder (secondary adrenal insufficiency) that often results from the same disease that causes CDI. If dDAVP completely corrected her DI without producing water intoxication or other problems, she almost certainly has CDI and does not need the hormone measured to confirm the diagnosis. Unfortunately, CDI can be controlled but not cured. There are several reasons why she may have been able to reduce her dose of dDAVP, but one of them is she has also developed adrenal insufficiency (as noted above) or hypothyroidism, which can also accompany CDI in some patients. Both of these other diseases are quite dangerous but can be treated easily if she has them. She should be tested for adrenal insufficiency and hypothyroidism and started on treatment as soon as possible if they are present. She should also have an MRI of the brain looking for the cause of the pituitary damage that could be responsible for all of these conditions.

* What research is being done on this?

If your son has CDI due to a severance of his pituitary stalk, it is unlikely the neurons will regrow. He will probably have DI for the rest of his fife. If it does get better, it is not necessarily a good sign because it usually indicates the development of another problem (such as adrenal insufficiency), which “masks” the DI but carries other risks that must be attended to. When DI starts during childhood and is not associated with any overt disease in the pituitary hypothalamic area (i.e., the MRI is normal except for absence of the posterior pituitary bright spot), the possibility, of a genetic cause should be considered, even if there is a history of head trauma. Check with relatives, especially on his mother’s side of the family, to see if any of them have signs of CDI.

I have no experience with behavioral therapy for dipsogenic DI, but am dubious that it would accomplish much, at least in a child so young. I also have some concerns about the diagnosis and would advise careful review of the test results to be sure that partial CDI has been thoroughly excluded. The development of hyponatremia during dDAVP therapy essentially rules out NDI and is in favor of some form of primary polydipsia. However, it does not prove the latter diagnosis in infants or young children, because their diet contains more water.

There is no nutritional therapy that is known to help CDI, although a low-sodium diet (30-50 mg sodium/day for children; 500-600 mg sodium/day for adults) will reduce the volume of urine produced. There is no known cure for CDI, and it sometimes goes away, but only in a few patients when they get older (over 40 years).

It would be a good idea to have a medical alert bracelet or card so that any doctor who treats you for an emergency will know that you require special treatment for the DI. For information about obtaining Medic Alert cards, bracelets, or necklaces, contact Medic Alert (a nonprofit organization), 2323 Colorado Ave., Turlock, CA 95382; 800-432-5378; www.medicalert.org. If you have NDI, medical alert cards are also available, free, from the Nephrogenic Diabetes Insipidus Foundation by registering at its Web site, www.ndif.org.

CDI (the type treated with dDAVP) can go from partial to full particularly in patients with the inherited (genetic) form. You are in the correct age group to have the inherited form and may want to have a genetic analysis performed even if you do not know of any other family members who also have the disorder.

* I have constant leg cramps. Is that caused by dehydration?

Legs cramps are probably not a sign of dehydration. They are more likely due to over-hydration, which is also a cause of low serum sodium. Again, therefore, I would suggest that your serum sodium (and potassium) be measured while you are having the leg cramps.

Once established for as long as 13 months, CDI rarely goes away unless other problems develop. One such problem is adrenal insufficiency. It can also result from damage to the pituitary, can cause episodes of nausea and vomiting, and can mask the signs of DI. If you have not already been evaluated and treated for adrenal insufficiency, the possibility should be investigated by your doctor as soon as possible, because it is a serious, even life-threatening condition. The other problem that can make it appear that the DI has stopped is damage to the thirst mechanism with hypernatremic dehydration. Your doctor can check for this by measuring your serum sodium.

If your baby has CDI, he will probably need treatment for the rest of his life. Sometimes these kinds of DI remit, get better, or stop around the age of 40 to 50 years, but that occurs in only about 10% to 20% of patients. The answers to your other questions depend on the cause of his CDI. If it is genetic, he will not have any other abnormalities. However, if it is due to a congenital malformation or another form of more general brain injury, he may have defects in other pituitary or brain functions. It would be important to ask the doctors who took care of him if they know the cause of his CDI, or if not, whether there are any other members of his biologic family who have signs or symptoms of DI.

It is possible that you have some type of DI, since it is known to be a complication of anorexia/bulimia syndrome. Usually it gradually improves after the anorexia/ bulimia stops and weight returns to normal. However, that is not always the case. The easiest way to tell if you have some type of DI is to collect a 24-hour urine sample and measure it for volume, osmolality, and creatinine. If It Is consistent with DI (high volume, low osmolality, and normal creatinine), your endocrinologist will have to do some additional tests to determine which type of DI you have. In your case, the tests may be particularly difficult to interpret and may require the intervention of a specialist. Until these questions are answered, the only thing you should do is drink as much as you need to satisfy your thirst. You should not start any antidiuretic therapy unless and until DI has been diagnosed.

It is relatively common for CDI to start for no apparent reason. In fact, such “idiopathic” forms happen about 50% of the time. When idiopathic CDI begins in childhood, there is an increased chance that it is genetic. When it is genetic, one parent (and possibly other relatives) usually has DI also. However, that is not always the case, and if you want to find out for sure (because of concern about passing DI on to your children) you can have an analysis of your vasopressin-neurophysin gene.

There is no urine osmolality value that is normal for all circumstances. It depends on a variety of factors, such as fluid intake and state of hydration, and varies widely throughout the day. Generally, however, it should be in the range 300 to 900 mosmoles/kg if the child is eating and drinking normally and is not dehydrated or overhydrated (due, for example, to IV fluids). However, a physician who understands water physiology and the exact condition of the child when the sample was collected could give a more definitive answer.

Your daughter may have a growth hormone deficiency in addition to CDI. This can result from a variety of congenital malformations or acquired diseases of the pituitary hypothalamus that are often evident on MRI of the brain. An MRI should be done if it has not been already. She also should have tests of growth hormone and other pituitary hormones.

It is not uncommon to develop CDI after surgery for a pituitary tumor. Usually, however, it starts sooner than 7 weeks and is not associated with a tendency to develop water intoxication (low serum sodium) on dDAVP therapy. These two discrepancies make me wonder if there was some damage to the part of your thirst mechanism, which is located in the hypothalamus just above the pituitary. If so, it could result in abnormal excessive thirst and fluid intake which either mimics CDI or complicates its treatment with dDAVP I would suggest that you begin to strictly follow the rule of drinking only when you are truly thirsty and then try increasing your dose of dDAVP until it completely controls your DI. If this again results in the development of water intoxication (low serum sodium), you should be further evaluated by a specialist to determine the true cause of your DI and design the most appropriate therapy.

In young infants, treating CDI can be very difficult because they must drink more water than adults and the dDAVP treatment prevents them from excreting the excess water. Therefore, they are much more likely to develop water intoxication (hyponatremia) when given doses of dDAVP sufficient to completely prevent DI. I would recommend that you try three things: 1) provide a formula with the smallest amount of solute free water possible, 2) reduce the does of dDAVP until urine output roughly equals the daily intake of formula, and 3) allow the child to drink enough pure water (not juice or milk) to replace her insensible losses (10 to 30 ml/kg body weight depending on temperature and activity).

The principle reason is to reduce the risk of severe dehydration and provide greater freedom to participate in activities in which it is difficult, if not impossible, to drink and urinate frequently.

Some of the symptoms, such as thirst and incontinence, may be due to DI. If so, it is probably CDI and could be managed quite easily with dDAVP. It is also possible, though much less likely, that these symptoms are due to abnormal thirst caused by the tumor or the surgery. If so, dDAVP should not be given since it will induce water intoxication. Therefore, the type of DI, and whether she in fact has DI, should be determined before treatment is started.

Water intoxication is a term used to describe a constellation of symptoms and laboratory abnormalities that result from an accumulation of too much water in the body. Depending on how much and how fast water accumulates, the symptoms can be mild (headache, fatigue, dizziness, loss of appetite) or severe (confusion, coma, seizures). Since these symptoms also occur in other disorders, the diagnosis of water intoxication requires a laboratory test showing that the plasma sodium concentration has been “diluted” be the normal range. Water intoxication occurs whenever water is put into the body (by drinking or intravenous infusion) faster than the kidneys can excrete it (usually because of kidney failure or the act of vasopressin, the antidiuretic hormone). This can occur in a variety of situations. It is common, for example, in patients with dipsogenic DI (a form of DI due to an abnormality in the thirst mechanism) who are treated with dDAVP in the mistaken belief that they have CDI (a form of CDI due to a deficiency of the antidiuretic hormone, vasopressin). The treatment of water intoxication varies depending on the cause and the severity but almost always includes cessation of fluid intake until plasma sodium concentration returns to normal.

No one knows the number of patients with DI in the United States or any other population. The number with enuresis has been estimated and shown to vary with age (from 25% of children at 5 years of age to 1% in adolescents and adults) but it is not known how many of those have DI. From various sources, it is estimated that the number of people with DI in the United States range between 40,000 to 80,000, but that calculation involves a lot of assumptions and could be way off.

Patients with psychogenic polydipsia have severe psychoses such as schizophrenia. Some physicians use the term compulsive polydipsia to describe patients who they believe have primary polydipsia due to neurosis or some other less severe form of mental illness. However, many of these patients also complain of thirst and are no likelier than the rest of us to be suffering from a mental disability. Therefore, I believe they also have a thirst disorder (dipsogenic DI). I do not like or use the term compulsive polydipsia.

The test result that you refer to was probably Somatomedin C (or IGF-1, as it is also called). It is normal and indicates that she does not need growth hormone treatment although it may still increase her growth. Even if the thickening of her pituitary stalk decreases, it is unlikely that her CDI will improve since the neurosecretory cells that normally make vasopressin do not regrow when they are destroyed. However, the reduction in thickening may prevent or improve other abnormalities in anterior pituitary function.

It is known that head trauma sometimes causes CDI or the problems in the pituitary or brain.

Yes, there are other medications that work quite well in CDI. One is Tegretol. Another is chlorpropamide. Both can be taken by mouth and may have side effects but they are usually not serious.

CDI may result in increased loss of water from skin or lungs (so called insensible loss) but it does not manifest as an appreciable increase in perspiration. Moreover, it appears to be controlled completely by dDAVP. If hyperhidrosis (increased perspiration) is present, it is probably due to a separate problem.