Dying on dialysis
I've known him
since my first days as a doctor,

and now he wants to quit.
I've been called 
to write the sentence

that says he understands
the meaning of "no."
Seated on the corner of his bed,

I test him with questions
until Eric Clapton comes on the radio 
picking "Lay Down Sally,"

and I drift off, thinking
this is one more riff I'll never master.
Though my white coat touches his gown,

comparing calluses on our fingertips
hardened from playing "Layla,"
and we agree dying is easier

his breathing soft as a gentle strum.
A nurse hangs morphine.
I write my blue notes.

Articles

I've known him since my first days as a doctor,and now he wants to quit.

Lay Down Sally

The headline at Public Citizen's Web site offers a degree of titillation that was once available only from postcards peddled in a parking lot. It proclaims in bold red letters, "20,125 Questionable Doctors." In smaller type, it qualifies this claim with a quick appeal to authority: "Disciplined by State and Federal Governments."

Another headline offers "National CD-Rom Now Available." Scrolling down, a visitor to the site finds the promise of forbidden fruit:

Information in the federal repository of disciplinary actions by state boards and federal agencies -- the National Practitioner Data Bank -- is kept secret from patients and almost all physicians. It is partially in response to this congressionally mandated secrecy that Health Research Group has established our own publicly-available data bank of doctors who have been disciplined."

Public Citizen's Web site is not the only one offering information about physicians today (Table). A broad range of data providers, from individual state licensing boards to private companies, will give -- or sell -- information about medical school, residency, specialty certification and years of practice. 

Forty-one states now post some information on the Internet about disciplinary actions against physicians. In addition, the Federation of State Medical Boards (FSMB) offers a search service (DocInfo) through its Web site. Consumers can obtain disciplinary information from state records through the FSMB for a fee of $9.95, payable over the Internet by credit card.

Despite -- or perhaps because of -- a last-minute change in state law that barred the posting of disciplinary records, the Virginia Board of Medicine Practitioner Information Web site received 16,000 hits in its first 36 hours of operation, according to a health department official quoted in 

. Those records are available on request from the state board of medicine.

"We're projecting 3 million hits this year, which is unbelievable," said Claudette A. Houle, spokesperson for the Massachusetts Board of Registration in Medicine, which was the first state medical licensing agency to post disciplinary files on the Web. She told 

, "We're getting national and international interest."

HealthGrades, a private data service that provides ratings on nursing homes, hospitals and hospices, as well as basic information on physicians, dentists and other providers, gets about 100,000 visitors a month to its site, according to Sarah Loughran, senior vice president of HealthGrades Inc.

Paying customers (employers and online health information providers) can obtain information about physicians, including disciplinary actions by state regulators and Medicare, as well as a profile that includes medical school, specialty board certification and a ranking of the hospital with which a given doctor is affiliated, Loughran told 

. On its public site, HealthGrades provides free basic information about physicians, including driving maps and office hours for each location if the physician works in more than one.

Public Citizen provides no free information on its site. It draws its data on physicians from publicly available records from various state medical boards and uses the site to promote its $400 book (or $20 apiece for regional reports) containing summary information about the 20,125 "questionable" doctors. A CD-ROM version sells for $600. It is based on disciplinary actions taken between 1990 and 1999. According to a press release from Public Citizen on Aug. 8, 2000, "It is likely that [the physicians named in the book] are still practicing." However, Peter Lurie, M.D., M.P.H., co-author of the study Public Citizen conducted that surveyed doctor disciplinary information on state medical board Web sites, admitted in an interview with 

 that the organization has not attempted to verify whether or not all of the doctors are still in practice.

"There is no question that among those 20,000 people there are some who are not in practice. We don't have the ability to go back and one-by-one go through all 20,000," commented Lurie, who is also deputy director of Public Citizen's health research group. Lurie also said the Public Citizen data do not include information on malpractice suits or settlements.

Consumer interest in quality of care issues has spurred greater demand for information about physicians, but leaders of the medical profession have voiced strong concerns about the type of information being provided.

"Even before the state board put up its Web site, we voiced concerns about the information that is being made available about physicians," Sandra Bressler, director of professional standards and quality of care for the California Medical Association (CMA), told 

. "Some years ago, we sued the medical board about the release of information on physicians when they proposed to release pre-accusation notices about investigations they were conducting." The case was eventually settled, with the California regulators agreeing not to publish the information, but Bressler said that new complaints have arisen with the advent of the Web site.

"The California Medical Board's Web site is peculiar. When they file an accusation and then negotiate a settlement, [in which] one condition is that they withdraw the accusation, they still post the word 

 on the Web site in a column called 'Secondary License Status Code.'"

"We have proof that it has jeopardized at least one physician's income," Bressler continued. "A member was accused of gross negligence with respect to an orthopedic procedure. The board said that if he took a competency examination and passed, they'd withdraw the accusation. But they left the word 

 on the Web site. The physician was in the job market at the time, and a friend told him confidentially that he was not going to be hired for one position because of that 'blot' on his record."

Bressler said the CMA is not opposed to releasing information about physicians but believes it needs to be done carefully. "We have always said that it was appropriate to inform the public if a physician was disciplined. While many physicians don't like it, we have agreed that the board can let the public know when they've filed a formal document, such as an accusation, as long as it is clear that the charges are not proven. But if physicians have an accusation on file, many health plans refuse to allow them to take on additional patients. So, it is very significant when all that's out there is an allegation and no proof," Bressler explained.

California's site provides basic information -- e.g., license number, address, medical school, years in practice -- about physicians. In addition, there are 98 "status codes" ranging from "Canceled" and "Deceased" to "Denied," "Probation," "Accusation" and "Accus w/drawn." No explanation is offered as to why the codes were applied; however, consumers can contact the medical board directly for this information.

Of greatest concern to most physicians is whether or not information about malpractice suits and settlements will be posted. Last year, the American Medical Association led the charge against proposals in the U.S. Congress that would have opened the National Practitioner Data Bank, maintained by the U.S. Department of Health and Human Services, to the public -- a move advocated by Public Citizen and some consumer groups and opposed by the health care industry.

The AMA testified before Congress that malpractice settlements often reflected business judgments rather than medical issues. They cited a study that showed that only one malpractice case in five involved questions of negligence, and they also argued that malpractice lawsuits are not a good indicator of quality. The legislation died and the sponsor is no longer in Congress.

Dale L. Austin, interim chief executive officer of the FSMB, told 

 that his organization has no official position on opening the National Practitioner Data Bank to the public, but "we know some of the challenges of extracting the data. The way it was set up in the first place was to provide information on both public actions relative to quality of care, plus malpractice cases, plus hospital actions, and to share that information among hospitals and regulatory agencies. It would be difficult to retrofit that to make it available to the public."

But information about malpractice cases remains at the crux of many people's concerns about posting data on public Web sites. In Massachusetts, the legislature worked with the medical establishment to create a rule that would be fair to doctors while providing guidance for consumers.

"In 1996, toward the end of the legislative session, we were told that the legislature was going to pass a profiling bill," recalled Francis X. Rockett, M.D., president of the Massachusetts Medical Society, in an interview with 

. "So, we began to work with the people involved to introduce a bill that allowed this information to appear on the Web site, but it was very careful that it didn't record every time a physician was sued. It allows them to post information about suits, but only closed cases. There can be no statement as to how much money a suit was settled for, if there was a settlement. They can only say that the settlement was average, above average or below average."

In addition, a disclaimer accompanies the information noting the number and frequency of lawsuits against other physicians in this specialty.

"When this first was proposed, the rank and file members initially were very opposed to it," Rockett continued. "They called it an invasion of their privacy and complained that we were the only group of professionals having this done to them and that the state should do the same sort of thing for lawyers. I think the rancor and the fuming and fussing have subsided. We've found out that most people who use the site are looking for what insurance plans a physician [accepts]."

The Massachusetts Web site often is cited as a model for the rest of the country, but it offers some protections for physicians that are not always found in other sites. According to Board of Registration's Houle, information about a physician is removed from the Web site after 10 years. "It's still archived and available, if anyone wants it," she said.

The FSMB appointed a Special Committee on Physician Profiling before developing its Web site. Earlier this year, a special committee of the FSMB issued its report and guidelines for medical information sites (

Journal of Medical Licensure and Discipline

 2001;87[2]:53-68), which includes the following recommendations:

1.	The number of medical malpractice court judgments and arbitration awards against the physician within the last 10 years. This is a numeric field showing the total number of such actions in the designated time period.

2.	The number of malpractice settlements when that number is equal to or exceeds three in the past 10 years. This is a numeric field. The field will be blank or contain a number greater than two.

3.	Dollar amounts of awards, judgments and settlements should not be included for malpractice suits.

In addition, the committee urged that a disclaimer be added to the information explaining that malpractice judgments and settlements do not reflect quality of care.

Providing information on public Web sites is not cheap. Rockett said Massachusetts is contemplating an increase in licensing fees. "We suggested if they just spent their time and effort and money on things the board should be doing, like tracking down some of the reports and weeding out some of the physicians who should not be in practice, the money would be better spent."  

Whether for free or for a fee, many states are now offering public Internet access to information regarding physicians. Much of this information is benign -- specialty certification, years of practice, medical school and so on. However, some Web sites are including more controversial information such as malpractice suits and settlements. Is this going too far?

Revealing Medical Licensure and Discipline Information on the Web

(The following are case studies discussing the impact of proper evaluation of comorbid psychiatric illness and medical disorders. To read more case studies and find out how to effectively recognize and treat patients with these disorders, please see the January 2002 issue of 

 A 52-year-old Asian American gentleman was admitted to the inpatient psychiatry service to "dry out" following a drinking binge. At morning report, the addiction treatment team reported that the patient claimed, "belly discomfort during the night with no relief from antacids." 

. Exquisite right upper quadrant stomach tenderness was noted at bedside exam. 

. Stomach X-rays (films) were performed prior to the hospitalization on the inpatient psychiatry service. The radiologist stated that the calcification visible in the right upper quadrant belly film was "a pill."

. The chief of surgery was consulted for a second opinion, and he diagnosed a gallstone rather than a pill. Upon bedside examination, he diagnosed acute cholecystitis and ordered immediate intravenous antibiotics, intravenous fluids and cholecystectomy. The patient said he appreciated the timely and definitive diagnostics, treatment and care. He added, "Doctor, I was told I had a sick gallbladder with a gallstone years ago. I was advised then to have my gallstone and my gallbladder taken out surgically, but I did not get it done." When asked why his previously recommended gallbladder surgery had not been performed, the patient answered, "Different reasons, Doctor. First my doctor died; then my car died; then my dog died; then I lost my insurance; then I just lost my nerve, and I was afraid to have the surgery. Doctor, I guess the major reason was that I just could not stop drinking long enough, and I could not ever dry out long enough to have my gallbladder taken out." Twelve-step work with sponsorship was recommended, and the recommendation documented, for him to develop and use his Tools of Recovery. 

. When a step-by-step review was initiated to ascertain how our patient with an acutely inflamed gallbladder came to be hospitalized on our detoxification unit, we learned that the findings of the patient's medical physical examination were initially unimpressive; that is, his stomach was soft, with no guarding, tenderness or rebound tenderness. However, as his blood alcohol level dropped and he became more alert, the findings from his medical physical examination changed. The core issue would appear to be that the willingness to provide repeated medical physical examinations at the bedside leads to the correct diagnosis, and thus reasonably timely treatment and care of the underlying and previously ignored medical issues.

. An 85-year-old white gentleman was admitted to the inpatient psychiatry service to "dry out" following a drinking binge. At morning report, the addiction treatment team said that the patient was "sleeping it off." 

. At the bedside, I observed the patient to have a pulse of 120 beats per minute, a respiratory rate of 40 breaths per minute, and to be in a semi-coma, from which he could not be awakened. 

. The medical intensive care team was called. With correction of his fluid and electrolyte imbalance and stabilization of his pulmonary status, the patient woke from his semi-coma and was returned to our inpatient psychiatry unit, where he remained comfortable and stable until our social work service could provide comfortable alcohol-free housing for him. He verbalized his appreciation of our timely diagnostics, treatment and care and also for our human services liaison. Twelve-step work with sponsorship was recommended and documented for him to develop and use his Tools of Recovery. 

. In a review of how this patient came to be hospitalized on our detoxification unit, it became apparent that his first medical physical examination was performed on the morning after he arrived on our detoxification unit. Records documented previous detoxification unit hospitalizations; at this repeat hospitalization the patient appeared in a reasonable disposition. The only glitch was that in the middle of the night the patient was minimally examined, if at all; and, in the absence of a complete medical physical examination, was simply labeled as a patient who was "sleeping it off." Once the pulse rate, respiration rate and level of consciousness were determined on the detoxification unit, then an accurate diagnosis of semi-coma became much more clear. It is probably a good and reasonable diagnostic rule-of-thumb that the majority of hospital inpatients, whether chemically dependent or not, need a thorough medical, physical examination by their health care providers on morning rounds.

These two case studies are representative of the many reasons why health care providers need to put aside typical stereotypes and tunnel vision and provide our chemically-dependent patients with the same care as our non-chemically dependent patients.

The following are case studies discussing the impact of proper evaluation of comorbid psychiatric illness and medical disorders. To read more case studies and find out how to effectively recognize and treat patients with these disorders, please see the January 2002 issue of Psychiatric Times.

Detox Diagnosis--Keeping Medicine in Psychiatry

On Oct. 4, 2001, California Gov. Gray Davis signed into law a bill that will allow courts to consider the patient's mental health history during commitment hearings. Sponsored by Democrat Assemblywoman Helen Thomson, AB 1424 also prohibits insurers from denying payment based on whether the hospitalization was voluntary or involuntary.

The new law, which went into effect on Jan. 1, 2002, has four basic provisions:

Information from family members, the patient or their representative, and medical records must be considered by the court as evidence of mental health history.


The police may consider information on the patient's mental health history provided by family members when determining probable cause for taking a patient into custody for evaluation and treatment.


Irrelevant information may not be considered as evidence during commitment hearings.


Insurers may not use voluntary or involuntary commitment status as criteria for reimbursement.

In a statement to the press the day after the bill was signed, Thomson said, "AB 1424 will eliminate some of the barriers to family members and at the same time improve the quality and accuracy of information used to determine who needs court-ordered mental health services. It will also end a disincentive to persons suffering from a severe mental illness to seek voluntary mental health inpatient services, which are medically necessary. It's outrageous that insurers were denying coverage for inpatient psychiatric care unless it was involuntary care."

The new law was introduced in response to a series of legislative hearings across the state to help reform the 1967 Lanterman-Petris-Short Act. That act attempted to reduce the number of patients committed to psychiatric facilities--TB 

New Law Allows Consideration of Mental History for Involuntary Hospital Admission

In December 1880, the emerging profession of neurology almost absorbed psychiatry, which had established itself four decades earlier. The final confrontation was the culmination of an extremely bitter three-year battle, and the outcome was very much in doubt as representatives of each side prepared to testify before the New York State Senate Investigative Committee on Asylum Management. One possible outcome would be the recommendation that neurologists be given administrative control of the state asylums and, effectively, of psychiatry. Other states watched New York's battle closely and seemed likely to follow its lead.

The events of 1880 and their antecedents are little-known to contemporary psychiatrists and neurologists. Understanding these events, however, is relevant to the present, since psychiatry and neurology are moving ever closer together. Increasing numbers of psychiatrists are also taking training in neurology. In Bethesda, Md., the administrative offices of the National Institute of Mental Health (NIMH) and the National Institute of Neurological Diseases and Stroke (NINDS) share the same building, and some NIMH and NINDS laboratories share common space. Some professionals believe it is just a matter of time before NIMH and NINDS merge into a National Institute of Brain Research. Psychiatry and neurology may ultimately become a single profession.

Like many professional turf battles, the neurology-psychiatry imbroglio was based on big ideas and even bigger egos. The leader of the fledging neurologists was 48-year-old William Alexander Hammond, M.D., a large man, "pompous and arrogantwith a voice so powerful that [he] could be heard upwind in a hurricane" (Haymaker, 1953). Like most of the emerging neurologists of his time, he acquired his skills treating war injuries during the Civil War. He had become Surgeon General of the Union Army, but in 1864 was charged with "irregularities in granting contracts for hospital supplies" and court-martialed (Werman, 1973). He then established a private practice of neurology in New York City, charged high fees and became very wealthy. He was one of seven founders of the American Neurological Association in 1874 and was appointed to the first professorship of nervous and mental diseases in the nation.

The leader of the more established psychiatrists was 51-year-old John Perdue Gray, M.D., known for his 300-pound girth and said by some to be "autocratic," "powerful and manipulative," and "an enduring hater" (Rosenberg, 1968). In 1844, he was one of the 13 founders of the Association of Medical Superintendents of American Institutions for the Insane (AMSAII), which later became the American Psychiatric Association. He was also superintendent of the Utica State Lunatic Asylum in New York, editor of the 

) and an advisor to government officials, including President Lincoln.

The battle between the psychiatrists and neurologists was for control of the state insane asylums, with the accompanying patronage system of jobs, and the teaching of mental disorders in medical schools. The psychiatrists claimed that they had been running the asylums for more than half a century and were best qualified to do so. The neurologists countered that the psychiatrists were incompetent, failed to do research on psychiatric disorders and focused almost exclusively on the administrative aspects of their jobs. Furthermore, the neurologists believed themselves to be the true experts on all brain disorders, including various forms of neuroses. Neurologist George Beard, M.D., coined the term 

 in 1869, and many neurologists were practicing forms of what today would be called psychotherapy. In short, the neurologists claimed, "the study of insanity should be considered a subdivision of neurology" (Spitzka, 1878a).

Hammond and Gray initially clashed during the 1871 trial of David Montgomery who was accused of killing his wife. Gray testified that Montgomery, who had epilepsy, was insane at the time. Hammond argued that the defendant was "perfectly sane" and that Gray's testimony was a product of his "want of practical experience with epilepsy or insanity" (Echeverria, 1873). Hammond won the case.

The feud continued to simmer until 1878, when neurologist Edward Spitzka, M.D., a close associate of Hammond's, publicly attacked the psychiatrists. The asylum superintendents, said Spitzka (1878b), were selected "on grounds of nepotism and political favor," showed only "apathy and ignorance manifested by [their]dereliction of scientific duty," and were mostly concerned "over the prizes gained by their hogs and strawberries [from the asylum farms] at agricultural fairs." Spitzka also attacked Gray personally, calling him an "indifferent, superficial man, owing his position merely to political buffoonery" and accused him of having "harmoniously confused, if not falsified, the [asylum's] financial statements."

The psychiatrists' reply was delivered two months later at their association meeting by Eugene Grissom, M.D., (1878) an asylum superintendent who had been Gray's medical school classmate and close friend. Dispensing with any pretense of civility, Grissom attacked Hammond as a criminal, an atheist and a "prisoner of the fountain of justice." Grissom focused much of his attack on Hammond's high fees, calling him "a Judas Iscariot to humanity, selling the blood of his children for thirty pieces of silver." Grissom concluded, "Now at last we shudder as we recognize that the false expert is no man at all, but a moral monster, whose baleful eyes glare with delusive light; whose bowels are but bags of gold, to feed which, spider-like, he casts his loathsome arms about a helpless prey." Grissom's presentation was reported to have been "greeted with thunderous applause" (Spitzka, 1878a).

Two months later, Grissom's presentation was published in the 

. Hammond promptly sued Gray for libel, both as an editor of the journal and because Gray was widely assumed to have written Grissom's paper. Medical and lay publications widely reported the increasingly personal fight. Because of this interest, the rules of the New York Neurological Society were suspended to permit newspaper reporters to attend the October 1878 meeting, at which Spitzka was scheduled to reply to the Grissom and Gray charges (Blustein, 1979).

In his presentation, Spitzka (1878a) briefly took the high ground, deploring Grissom's "purely personal attack" and "its language exceeding anything which has yet appeared in a professedly medical publication." However, he then attacked the asylum superintendents as "shallow pretenders and ignorant indifferentists," who had led psychiatry to the "slough of despond into which it has sunken in every scientific and administrative respect." Furthermore, according to Spitzka, one prominent superintendent was under official investigation for extravagances and looseness in financial accounts, another was accused of falsifying asylum death certificates to hide patient abuses by the staff, and two others had been dismissed for being repeatedly intoxicated. Simultaneously, Hammond published an open letter in which he defended his high fees and suggested that Grissom himself might possibly be insane.

The neurologists appeared to be winning the battle. 

 reported favorably on Spitzka's call for asylum reform, the Connecticut Medical Society invited Hammond to speak, and the Michigan legislature opened an inquiry into the management of its state asylum. Most significantly, the New York legislature appointed a board to investigate the asylums.

Throughout 1879 and early 1880, the neurologists continued the attack. Since the asylums were increasingly overcrowded, it was not difficult to find areas to criticize. In 1879, the neurologists, together with social workers and laypeople interested in asylum reform, organized a National Association for the Protection of the Insane and the Prevention of Insanity (NAPIPI). This organization provided yet another venue for attacking the psychiatrists. As one neurologist later wrote in the NAPIPI newsletter, the average asylum superintendent was more interested in "the growth of cabbagethan [in] morbid growths within the encephalon" and "the location of turnip or potato patches interest him more than the localization of cerebral lesions" (Ayres, 1884).

Finally, in December 1880, the New York State Senate Investigative Committee held hearings. The hearing room was described as "overflowing with witnesses and interested spectators," including many representatives of the media. Hammond cited his usual litany of shortcomings of the asylum superintendents and drew laughter, according to the

 (The Care of the Insane, 1880), when he proposed that psychiatrists not be permitted to be asylum superintendents and recommended instead that "a lay superintendent [be] appointed to raise turnipsand entertain the friends of visitors." Spitzka, following Hammond, accused the superintendents of committing perjury in their attacks on him. The psychiatrists, predictably, defended their integrity and their record.

The hearings would emerge in historical retrospect as the turning point in attempts by the neurologists to oust the psychiatrists from the asylums. There appear to be at least three reasons for this. First, the legislators and the public in general were growing tired of the bitter and unseemly personal attacks and counterattacks by both groups of professionals. Second, the neurologists criticized the psychiatrists without offering an alternative plan for asylum management. As summarized by Blustein (1981) in an article about this conflict, the neurologists "failed to establish themselves as the sole authorities on the treatment of the insane, and even appeared to be somewhat irresponsible and sensationalist."

The most important reason, however, was probably the fact that the psychiatrists had friends in the legislature. Friends and relatives of state legislators looked to the psychiatrists to get their mentally ill family members admitted to overcrowded hospitals. In addition, the asylum superintendents controlled all the jobs in the asylums and could offer these to the friends of helpful state legislators. The New York State Senate Investigative Committee was thus stacked against the neurologists. As Hammond himself summarized it, the commission "could not have been more favorable to the superintendents if the latter had themselves, as was very likely, selected the names of the appointees" (Blustein, 1981).

After 1880, the neurologists never again mounted a serious threat to the asylum superintendents. Their position was further weakened in 1881 when President James Garfield was shot by Charles Guiteau. At Guiteau's trial, Gray was the chief prosecution witness, and he argued that Guiteau had been perfectly sane when he shot the President. Spitzka, Hammond and other neurologists argued that Guiteau was affected by "reasoning mania" and thus was insane. The vast majority of the public, as well as the jury, sided with Gray. Guiteau was found guilty and was hung on June 30, 1882. On autopsy, evidence was found of what today would be diagnosed as brain syphilis; thus, the neurologists won the battle, but they had lost the war.

Hammond and Spitzka went on to have successful careers as prominent neurologists. Gray, ironically, was himself shot to death by one of his patients two months after he had testified regarding Guiteau's sanity. And Grissom, whom Hammond had suggested might be insane, did indeed become insane from brain syphilis and, in 1902, committed suicide "by firing a pistol into his brain" (Werman, 1973).

 Ayres S (1884), Our asylums and our insane. American Psychological Journal 1:341-347. 
 

 Blustein BE (1979), New York neurologists and the specialization of American medicine. Bull Hist Med 53(2):170-183.
 

 Blustein BE (1981), "A hollow square of psychological science": American neurologists and psychiatrists in conflict. In: Madhouses, Mad-Doctors, and Madmen: The Social History of Psychiatry in the Victorian Era, Scull AT, ed. Philadelphia: University of Pennsylvania Press, pp241-270. 
 

 Care of the insane, The. New York Times. Dec. 8, 1880, p2.
 

 Echeverria MG (1873), Criminal responsibility of epileptics as illustrated by the case of David Montgomery. American Journal of Insanity 29:341-425. 
 

 Grissom E (1878), True and false experts. American Journal of Insanity 35:1-36.
 

 Haymaker W, ed. (1953), The Founders of Neurology: One Hundred and Thirty-Three Biographical Sketches Prepared for the Fourth International Neurological Congress in Paris by Eighty Four Authors. Springfield, Ill.: Charles C. Thomas, p297. 
 

 Rosenberg CE (1968), The Trial of the Assassin Guiteau: Psychiatry and Law in the Guilded Age. Chicago: University of Chicago Press, pp63,73,190. 
 

 Spitzka EC (1878a), Merits and motives of the movement for asylum reform. J Nerv Ment Dis 5:694-714. 
 

 Spitzka EC (1878b), Reform in the scientific study of psychiatry. J Nerv Ment Dis 5:201-228. 
 

 Werman DS (1973), True and false experts: a second look. Am J Psychiatry 130(12):1351-1354.

E. Fuller Torrey, M.D., explores the battle for control of the state asylums in the late 1800s. Using everything from rational arguments to blatant defamation of character, William Hammond's neurologists and John Gray's psychiatrists duked it out in New York as other states watched carefully in pursuit of what might follow.

The Year Neurology Almost Took Over Psychiatry

The exact therapeutic mechanism of lithium in bipolar disorder (BD) remains unclear, due in part to its many actions on the cells of the central nervous system. The same complexity applies to the interactions between lithium and the thyroid. Lithium is widely known to impair the function of the thyroid through a variety of mechanisms. 

In 1998, Lazarus listed impaired thyroidal uptake of iodine, impaired iodination of tyrosine, altered thyroglobulin structure and impaired release of thyroxine from the thyroid gland as the mechanisms by which lithium induces hypothyroidism. Impaired release of thyroxine is considered the most clinically significant, and this phenomenon has been used to enhance the effectiveness of radioactive iodine when treating thyrotoxicosis (Bogazzi et al., 1999). Lithium has also been used, with reported success, to treat refractory hyperthyroidism (Dickstein et al., 1997).

Elevation of thyrotropin in response to lowered circulating thyroxine is probably the main stimulant for goiter formation, which has been reported with incidences of 3% to 60% in lithium-treated patients; much of this variation is related to varying definitions of 

 and differences in the methods used to measure thyroid size (Lazarus, 1998). 

Thyroxine is secreted as T4 and then metabolized to its active form, T3, by the enzyme 5'deiodinase. Lithium appears to impair the process of deiodination of T4 peripherally (deiodinase I) and within some cells (deiodinase III) (Terao et al., 1995). Eravci et al. (2000) found varying effects of lithium on different isoenzymes of deiodinase and noted that it appeared to enhance the activity of deiodinase II present in rat frontal lobes. This effect may contribute to alterations in cellular responsiveness to thyroxine.

It is widely known that patients receiving lithium therapy commonly develop hypothyroidism. Johnston and Eagles (1999) found hypothyroidism in 10.4% of 718 patients treated with lithium. Women suffered a higher risk of developing hypothyroidism within two years of therapy, compared to the general population of the geographical area studied. Hypothyroidism occurred in 14% of women, significantly more frequently than in men (4.5%), however, both sexes had a significantly increased risk. Women who were 40 to 59 years of age had the highest risk, with an incidence of 20%. 

An even larger number of patients appear to develop subclinical hypothyroidism. Deodhar et al. (1999) reviewed 132 outpatients receiving lithium therapy and found 39% had an elevated thyroid stimulating hormone (TSH), low T4 and normal T3 levels. This fits well with older series documenting elevated TSH and goiter without overt hypothyroidism in similar numbers of patients taking lithium. It remains to be elucidated why some individuals and not others develop clinically significant hypothyroidism, but it seems likely that some other predisposing factor is required.

For instance, in the Deodhar et al. study (1999), a large number of cases were from an area where dietary deficiency of iodine is common; and Kusalic and Engelsmann (1999), prospectively studying a group of patients with BD treated with lithium, found that cases with a family history of thyroid disease had an earlier onset of hypothyroidism than those who did not.

The association between hyperthyroidism and lithium is less widely recognized than that of hypothyroidism. However, Barclay et al. (1994) documented a statistically significant increase in the incidence of hyperthyroidism in lithium-treated patients. The mechanism of this association remains unclear, especially in view of the many ways lithium impairs thyroid function. Enhanced immune stimulation is an unsatisfactory explanation since the bulk of cases were due to toxic multi-nodular goiter, not Graves' disease or other immune conditions (Barclay et al., 1994). Nonetheless, this relationship appears to be both real and relevant.

An increasing body of research supports the hypothesis that lithium alters cellular responsiveness to thyroxine in addition to inducing significant changes in the function of the thyroid gland. The induction of cellular unresponsiveness to thyroxine may account for the apparent efficacy of lithium in treating thyrotoxicosis. My colleagues and I reported two cases in which cessation of lithium appeared to precipitate a thyroid crisis, presumably because the presence of lithium prevented clinical manifestations of thyroid excess (Oakley et al., 2000).

Bolaris et al. (1995) documented altered binding of T3 in the CNS of rats, implying that a state of cellular hypothyroidism developed. Hahn et al. (1999b) studied the effect of lithium on gene expression in response to T3 in different cells. In some cell lines, lithium reduced the transcription of mRNA in response to T3, while other cell lines were unaffected. This effect changed with duration of therapy and was deemed to be time-dependent and cell-line specific. Thus, the effect of lithium to alter cellular responsiveness to thyroxine is not uniform for all cells and may change with duration of lithium therapy.

The same group studied the effect of lithium on the expression of different subtypes of thyroid hormone receptors in rat brains (Hahn et al., 1999a). These studies showed that transcription of messenger RNA induced by thyroxine was actually enhanced by the presence of lithium in some cells and reduced in others, depending on the receptor subtype. As different receptor subtypes are distributed differently throughout the CNS, cellular responsiveness to thyroxine is enhanced by the presence of lithium in some areas of the brain and impaired in others. In this study, gene expression was enhanced by the presence of lithium in the cortex and reduced by its presence in the hypothalamus. 

Overall, the picture is far more complicated than the initial proposal of cellular hypothyroidism induced by lithium, but the effect is likely to be clinically significant. How much this contributes to the therapeutic effect of lithium in treating BD is difficult to estimate, as lithium significantly alters the metabolism and effects of many neurotransmitters. 

Some alterations in thyroid function have been shown to significantly alter lithium excretion. Hyperthyroidism induces a reduction in renal lithium clearance of 10% to 15% (Owada et al., 1993). This is due to enhanced resorption of lithium by the proximal convoluted tubule and occurs despite the increases in renal blood flow and glomerular filtration rate (GFR) that occur in hyperthyroidism. Thus, the development of hyperthyroidism or overzealous use of thyroxine as augmentation for lithium may result in lithium toxicity.

Hypothyroidism has not been reported to alter lithium excretion or result in cases of lithium toxicity. It is conceivable that reduced GFR in hypothyroidism may reduce lithium excretion, but concomitant changes in tubular function may attenuate these changes. In view of the high incidence of hypothyroidism in lithium-treated patients and the lack of any reports of an interaction with lithium, it seems less likely that hypothyroidism precipitates lithium toxicity.

In a recent study of 97 patients with lithium toxicity, a significant association was found between abnormalities of the thyroid axis and the risk of chronic toxicity (Oakley et al., in press). Other factors found to be associated with chronic toxicity were age over 50 years, presence of nephrogenic diabetes insipidus and renal impairment. This study focused on the important contribution of chronic medical conditions, including endocrine disease induced by lithium, to the development of lithium poisoning and toxicity. 

While lithium generally impairs thyroid function and has the potential to precipitate hypothyroidism, chronic therapy with this agent appears to increase the risk of thyrotoxicosis as well. In addition to affecting thyroid gland function, lithium alters the bioactivation of secreted thyroxine and alters the responsiveness of cells to thyroxine, enhancing it in some areas of the CNS and impairing it in others. Furthermore, alterations in the thyroid axis can substantially alter the pharmacokinetics of lithium and lead to toxicity. 

Clinicians who prescribe lithium to their patients should be aware of these potential deletenous effects, at least in principle, and should regularly evaluate the thyroid health status of all of their patients receiving lithium.

 Barclay ML, Brownlie BE, Turner JG, Wells JE (1994), Lithium associated thyrotoxicosis: a report of 14 cases, with statistical analysis of incidence. Clin Endocrinol (Oxf) 40(6):759-764. 
 

 Bogazzi F, Bartalena L, Brogioni S et al. (1999), Comparison of radioiodine with radioiodine plus lithium in the treatment of Graves' hyperthyroidism. J Clin Endocrinol Metab 84(2):499-503. 
 

 Bolaris S, Margarity M, Valcana T (1995), Effects of LiCl on triiodothyronine (T3) binding to nuclei from rat cerebral hemispheres. Biol Psychiatry 37(2):106-111.
 

 Deodhar SD, Singh B, Pathak CM et al. (1999), Thyroid functions in lithium-treated psychiatric patients: a cross-sectional study. Biol Trace Elem Res 67(2):151-163. 
 

 Dickstein G, Shechner C, Adawi F et al. (1997), Lithium treatment in amiodarone-induced thyrotoxicosis. Am J Med 102(5):454-458.
 

 Eravci M, Pinna G, Meinhold H, Baumgartner A (2000), Effects of pharmacological and nonpharmalogical treatments on thyroid hormone metabolism and concentrations in rat brain. Endocrinology 141(3):1027-1040.
 

 Hahn CG, Pawlyk AC, Whybrow PC et al. (1999a), Lithium administration affects gene expression of thyroid hormone receptors in rat brain. Life Sci 64(20):1793-1802.
 

 Hahn CG, Pawlyk AC, Whybrow PC, Tejani-Butt SM (1999b), Differential expression of thyroid hormone receptor isoforms by thyroid hormone and lithium in rat GH3 and B103 cells. Biol Psychiatry 45(8):1004-1012.
 

 Johnston AM, Eagles JM (1999), Lithium-associated clinical hypothyroidism. Prevalence and risk factors. Br J Psychiatry 175:336-339 [see comments].
 

 Kusalic M, Engelsmann F (1999), Effect of lithium maintenance therapy on thyroid and parathyroid function. J Psychiatry Neurosci 24(3):227-233. 
 

 Lazarus JH (1998), The effects of lithium therapy on thyroid and thyrotrophin-releasing hormone. Thyroid 8(10):909-913.
 

 Oakley PW, Carter GL, Whyte IM (in press), Lithium toxicity: an iatrogenic problem in susceptible individuals. Aust N Z J Psychiatry. 
 

 Oakley PW, Dawson AH, Whyte IM (2000), Lithium: thyroid effects and altered renal handling. J Toxicol Clin Toxicol 38(3):333-337.
 

 Owada A, Tomita K, Ujiie K et al. (1993), Decreased lithium clearance in patients with hyperthyroidism. Nephron 64(1):37-41.
 

 Terao T, Oga T, Nozaki S et al. (1995), Possible inhibitory effect of lithium on peripheral conversion of thyroxine to triiodothyronine: a prospective study. Int Clin Psychopharmacol 10(2):103-105.

Although incomplete, the link between thyroid function, bipolar affective disorder, and lithium has been acknowledged for many years. This article provides an overview of the relationship and recent literature.

The Complex Interrelationship of Lithium and the Thyroid

EASD: Studies Link Depression and Type 2 Diabetes

Diabetes May Compromise a Mother’s Mental Health

Medical Comorbidities in Late-Life Depression

Patients with diabetes are twice as likely to experience depression as those without diabetes (Anderson et al., 2001). The odds of depression are similar in type 1 and 

 and are significantly higher in women than in men. Moreover, the psychiatric condition presents as major depression or elevated depression symptoms in 11% and 31%, respectively, of adults with diabetes (Anderson et al., 2001). The course of 

 tends to be severe, with recurrences being the norm and not the exception. Following successful treatment, fewer than 10% of patients remain depression-free over the ensuing five years, and afflicted patients tend to suffer about one episode of major depression annually (Lustman et al., 1997c).

The exact cause of depression in patients with diabetes is unknown, but it is likely complex, involving interactions among psychological, physical and genetic factors. Diabetes is a challenging illness, and coping with the disease and its complications (such as loss of vision or sexual capacity) is difficult and may contribute to depression. While the clinical sentiment that depression is merely secondary to diabetes (i.e., "you'd be depressed, too, if you were this sick") is evident in some cases, this hypothesis insufficiently accounts for most cases of depression. The contribution of psychosocial factors to the initial 

 is modest. However, in those with a prior history of depression, these factors significantly affect the risk of depression recurrence. Some cases of depression, particularly in type 1 diabetes, may be organic affective illnesses that reflect cerebrovascular, neurohormonal and neurotransmitter abnormalities caused by the medical illness (MacKenzie and Trulson, 1978; Popkin et al., 1988; Trulson and Himmel, 1985). There is also a greater risk of depression in patients with diabetes who have a family history of depression; this may be indicative of a genetic vulnerability (Lustman et al., 1987).

 of these disorders results from depression and not from diabetes. A number of studies have shown increased insulin resistance in depressed patients without diabetes (Nathan et al., 1981; Wright et al., 1978). Recent prospective population studies that controlled for conventional risk factors (e.g., age, obesity, body mass index) found that depression was associated with a twofold increased risk of type 2 diabetes (Eaton et al., 1996; Kawakami et al., 1999).

No matter what causes the co-occurrence of depression and diabetes, when they are both present, interactions at behavioral and physiologic levels are likely. Glucose dysregulation, depression, substance abuse, smoking, noncompliance, physical activity and weight gain all affect one another, and depression is related to all of the factors listed. There is evidence supporting all of these associations. In both cross-sectional and prospective studies, depression has been associated with poor glycemic control, the principle cause of diabetes complications (Lustman et al., 2000a). The average increase in glycosylated hemoglobin attributable to depression in these studies was approximately 1.0%, a clinically significant elevation (Lustman et al., 2000b). Depression is also associated with other factors related to poor glycemic control, such as physical inactivity, obesity and treatment noncompliance, which are all factors that could contribute to insulin resistance (Farmer et al., 1988; Frederick et al., 1988; Littlefield et al., 1992; Lustman et al., 1992).

Given depression's effects on glycemic control, it is not surprising that it is linked to the risk of diabetes complications. In a recent meta-analysis, depression was significantly associated with an increased risk for the occurrence of neuropathy, nephropathy, retinopathy and macrovascular disease in adults with diabetes (range of effect sizes (r)=0.17 to 0.32, p<0.05 for all) (de Groot et al., 2001). Prospective studies have found that depression accelerates the presentation of coronary heart disease in women with diabetes (Lloyd et al., 1997).

Depression influences perceptual processes and is thought to make people less tolerant of pain and physical symptoms. For example, neuropathic pain that would normally be only an occasional annoyance may feel constant and overwhelming during an episode of depression and can result in a visit to the doctor. Mood at the time of clinical evaluation is often a stronger predictor of symptoms than the biomedical markers that are presumed to cause these symptoms. In this manner, depression may influence the presentation of physical symptoms.

, the diagnosis of depressive disorder is assigned when five or more criterion symptoms occur, are severe and persist over a period of at least two weeks. Sad mood or a significant loss of interest or pleasure are the essential symptoms for the diagnosis, and one of them must be present along with at least four other criterion symptoms. Symptoms attributable to the medical condition cannot count toward the diagnosis. This rule discourages overdiagnosis of depression, which is important since hypo- and hyperglycemia may produce some of the symptoms of depression (e.g., fatigue, weight loss). Diabetes does not, however, directly produce the two 

 symptoms of depression (sadness and loss of interest or pleasure), thus reducing the likelihood of false-positive depression diagnoses.

Despite substantial evidence of its adverse effects on the presentation and course of diabetes, and new evidence that treatment of depression has therapeutic effects on both mood and diabetes (see treatment section), major depression is recognized and treated in only about one-third of cases (Lustman et al., 1997a). This situation has been blamed on a variety of factors, including the presumption by clinicians that depression is merely a secondary reaction to the medical illness, the view (often shared by patients and family members) that the diagnosis conveys additional burden, and the stigma attached to having a mental illness. Primary care physicians may also lack sufficient training and face financial disincentives to perform psychodiagnostic testing. The fact that the average physician-patient interaction in the United States is currently eight to 12 minutes long (Kathol R, personal communication, May, 1996) also contributes to poor depression recognition. Despite these rather formidable obstacles, simple and effective methods are available to readily identify those patients most likely to benefit from depression treatment. These include simple paper-and-pencil screening instruments, like the 21-item Beck Depression Inventory (BDI), which are self-administered and take under 10 minutes to complete. When used in the physician's office, these tests are accurate and sensitive for the detection of depression.

Patients meeting the criteria for major depressive disorder are the most obvious candidates for treatment. A therapeutic trial may also benefit those patients with persistent depression symptoms that fall short of these criteria but, nevertheless, are associated with sustained impairments in function. Some patients or professionals have a preference for either psychotherapy or antidepressant medication; others may desire a combined approach. Consideration of the individual's symptom picture may provide a basis for treatment selection; the treatment of choice for depression dominated by somatic symptoms might be medication, whereas psychotherapy would be more effective for depression characterized by existential difficulties.

The presence of diabetes and its myriad physical complications can make the selection of depression treatment even more difficult. Conventional tricyclic antidepressants have long been used in primary care and have proved beneficial in regulating sleep. However, the potential for weight gain, anticholinergic side effects, orthostatic hypotension and other adverse cardiovascular side effects can be harmful for patients with diabetes. Furthermore, one study showed that TCAs may worsen glycemic control in patients with diabetes (Lustman et al., 1997b). These researchers found that although nortriptyline (Aventyl, Pamelor) was effective in treating depression, it had an adverse hyperglycemic effect that was unrelated to the medication's effect on weight.

Selective serotonin reuptake inhibitors and other newer antidepressants do not seem to cause hyperglycemia in patients with diabetes. These agents may in fact improve glycemic control, as was demonstrated in a recent trial using fluoxetine (Prozac) (Lustman et al., 2000b). The SSRIs are as effective as TCAs in treating depression but have less problems with weight gain and sedation as side effects. Side effects like sexual dysfunction, gastrointestinal distress and agitation are common and must also be considered, however.

Psychotherapy offers a unique alternative to medication; it has shown to be effective in treating depression, in addition to improving glycemic control, in patients with diabetes (Lustman et al., 1998).

Depression is a prevalent and recurrent condition among patients with either type 1 or type 2 diabetes. This psychiatric disorder complicates the medical disease by promoting poor glycemic control and increasing the risk of diabetes complications. Treatment of depression has significant favorable effects on mood and quality of life, as well as beneficial effects on glycemic control. The presence of diabetes complications or hyperglycemia decreases the likelihood of recovery during depression treatment and increases the probability of recurrence following treatment. Optimal treatment of depression in patients with diabetes may require a comprehensive approach that couples specific depression treatment with focused efforts to improve glycemic control.

Dr. Lustman's research on diabetes and depression was supported in part by grants DK36452 and DK53060 from the National Institutes of Health.

Dr. Lustman is professor of medical psychology in the department of psychiatry at Washington University in St. Louis School of Medicine and is recognized for his research on the interaction of psychiatric illness and diabetes. He serves on the editorial board of Clinical Diabetes and the grant review panel of the American Diabetes Association.

Mr. Anderson is clinical research associate in the department of psychiatry at Washington University in St. Louis School of Medicine.

 Anderson RJ, Freedland KE, Clouse RE, Lustman PJ (2001), The prevalence of comorbid depression in adults with diabetes: a meta-analysis. Diabetes Care 24(6):1069-1078.
 

 de Groot M, Anderson R, Freedland KE et al. (2001), Association of depression and diabetes complications: a meta-analysis. Psychosom Med 63(4):619-630.
 

 Eaton WW, Armenian H, Gallo J et al. (1996), Depression and risk for onset of type II diabetes. A prospective population-based study. Diabetes Care 19(10):1097-1102.
 

 Farmer ME, Locke BZ, Moscicki EK et al. (1988), Physical activity and depressive symptoms: the NHANES I Epidemiologic Follow-Up Study. Am J Epidemiol 128(6):1340-1351.
 

 Frederick T, Frerichs RR, Clark VA (1988), Personal health habits and symptoms of depression at the community level. Prev Med 17(2):173-182.
 

 Kawakami N, Takatsuka N, Shimizu H, Ishibashi H (1999), Depressive symptoms and occurrence of type 2 diabetes among Japanese men. Diabetes Care 22(7):1071-1076.
 

 Littlefield CH, Craven JL, Rodin GM et al. (1992), Relationship of self-efficacy and binging to adherence to diabetes regimen among adolescents. Diabetes Care 15(1):90-94.
 

 Lloyd CE, Wilson RR, Forrest K (1997), Prior depressive symptoms and the onset of coronary heart disease. Diabetes Care 46(1):13A.
 

 Lustman PJ, Anderson RJ, Freedland KE et al. (2000a), Depression and poor glycemic control: a meta-analytic review of the literature. Diabetes Care 23(7):934-942.
 

 Lustman PJ, Clouse RE, Carney RM, Griffith LS (1987), Characteristics of depression in adults with diabetes. Proceedings from NIMH conference on mental disorders in general health care settings. Seattle.
 

 Lustman PJ, Freedland KE, Griffith LS, Clouse RE (2000b), Fluoxetine for depression in diabetes: a randomized, double-blind, placebo-controlled trial. Diabetes Care 23(5):618-623.
 

 Lustman PJ, Griffith LS, Clouse RE (1997a), Depression in adults with diabetes. Semin Clin Neuropsychiatry 2(1):15-23.
 

 Lustman PJ, Griffith LS, Clouse RE et al. (1997b), Effects of nortriptyline on depression and glycemic control in diabetes: results of a double-blind, placebo-controlled trial. Psychosom Med 59:241-250.
 

 Lustman PJ, Griffith LS, Freedland KE, Clouse RE (1997c), The course of major depression in diabetes. Gen Hosp Psychiatry 19(2):138-143.
 

 Lustman PJ, Griffith LS, Freedland KE et al. (1998), Cognitive behavior therapy for depression in type 2 diabetes mellitus: a randomized, controlled trial. Ann Intern Med 129(8):613-621.
 

 Lustman PJ, Griffith LS, Gavard JA, Clouse RE (1992), Depression in adults with diabetes. Diabetes Care 15(11):1631-1639 [see comment].
 

 MacKenzie RG, Trulson ME (1978), Effects of insulin and streptozotocin-induced diabetes on brain tryptophan and serotonin metabolism in rats. J Neurochem 30(1):205-211.
 

 Nathan RS, Sachar EJ, Asnis GM et al. (1981), Relative insulin insensitivity and cortisol secretion in depressed patients. Psychiatry Res 4(3):291-300.
 

 Popkin MK, Callies AL, Lentz RD et al. (1988), Prevalence of major depression, simple phobia, and other psychiatric disorders in patients with long-standing type I diabetes mellitus. Arch Gen Psychiatry 45(1):64-68.
 

 Trulson ME, Himmel CD (1985), Effects of insulin and streptozotocin-induced diabetes on brain norepinephrine metabolism in rats. J Neurochem 44(6):1873-1876.
 

 Wright JH, Jacisin JJ, Radin NS, Bell RA (1978), Glucose metabolism in unipolar depression. Br J Psychiatry 132:386-393.

Diabetes doubles the likelihood of comorbid depression, which impairs functioning and quality of life. This mood disorder has a unique importance in diabetes because of its associations with treatment noncompliance, insulin resistance, hyperglycemia and an increased risk for diabetes complications.

Depression in Adults With Diabetes

Nemo Psychologus Nisi Physiologus  -- Johannes Mueller

Recognition of the relationship between psyche and soma dates back to antiquity and is captured in written records and historical accounts. Galen, in the first century CE, was reported to have written that the condition of intermittent obstruction of breathing (now called asthma) was secondary to secretions dripping into the lung from the brain. This was arguably among the earliest accounts of the important link between mind and body in medical illness. Indeed, asthma is considered by many to be the prototype of psychosomatic illness. Maimonides, circa 1190 CE, wrote in his 

When in mental anguish, fear, mourning or distress...his agitation affects the respiratory organs and he can not exercise them at will...The cure of such conditions lies not in food recipes, neither in drugs alone, nor in regular medical advice...psychological methods are a greater help.

Current literature documents negative effects of stress and emotion on asthma. However, there is controversy as to whether emotions and stress adversely influence asthma directly or by exacerbating poor treatment adherence. The purpose of this article is to elaborate pathways of connection between psyche and soma in asthma, placing emphasis on empirical support and rationale for psychophysiologic mechanisms underlying the impact of stress and emotions on asthma. 

The National Heart, Lung, and Blood Institute (NHLBI) defines asthma as a chronic inflammatory disorder of the airways, in which bronchial hyper-reactivity causes recurrent episodes of wheezing, breathlessness, chest tightness and cough associated with airflow obstruction that is reversible (NHLBI, 1997). The pathogenesis underlying asthma is best understood as a genetically predetermined vulnerability of the airway to a complex set of interactions involving inflammatory mediators (cytokines and chemokines), effector cells (e.g., eosinophils, T cells) and the (autonomic) nervous system (Middleton et al., 1998). Pharmacologic treatment of asthma is directed both at anti-inflammatory (immune/allergic) and bronchodilator (neural) pathways.

Many diverse stimuli can trigger asthma symptoms including allergens, infections, exercise, cold air and emotions. More than one stimulus may trigger an asthma attack, and it is often difficult to identify with certainty the specific stimuli that triggered symptoms (NHLBI, 1997). An individual's susceptibility to asthma triggers may change in the course of maturation or in response to life circumstances. 

Asthma is known to have a strong genetic predisposition. Children with one asthmatic parent have approximately a 20% chance of developing the disease, while those with two asthmatic parents have nearly a 50% risk. Risk factors for the phenotypic expression of asthma in children with genetic loading include early exposure to viral infections, highly allergenic substances and emotional stress in the family (Mrazek et al., 1991). 

Asthma is one of the most common chronic diseases of childhood, affecting 4.8 million children in the United States (NHLBI, 1997). Among children with chronic medical conditions, asthma is the most common cause for hospitalization and school absence (Newacheck and Halfon, 2000). Asthma is more prevalent in adolescent males than females and in African American children than Caucasians. Asthma prevalence, morbidity and mortality have been increasing over the past two decades, despite new effective medical regimens (Weitzman et al., 1992). 

The reasons for these increases are unclear. However, increased exposure to emotional stress in the environment must be considered among other causes (Wright and Steinbach, 2001). 

Asthma is a serious health condition that can be exacerbated by emotional triggers. Furthermore, depression in these patients can affect treatment compliance, thus worsening prognosis. What role does psychiatry play in treating these patients?

Psychiatric Times Vol 19 No 1