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These results showed that genetic – not adoptive – relationships mediated the familial prevalence of bipolar disorder prostate oncology zanesville order 250mg eulexin visa. They matched the ill and control adoptees on demographic features of the adopting parents androgen hormone pdf eulexin 250 mg free shipping. Among relatives of ill adoptees the risk to prostate cancer incontinence 250 mg eulexin for sale biological relatives was greater than the risk to prostate cancer 5k harrisburg pa purchase eulexin discount adoptive relatives. Notably, the biologi cal relatives of ill adoptees were six times more likely than the adoptive relatives to have completed suicide. The biological relatives had three times the rate of major depression and alcoholism compared with the adoptive relatives of ill adoptees. In theory, such analyses can provide strong evidence for one mode of transmission over others. Unfortunately, mathematical analyses of mood disorder pedigrees have not been able to consistently support a mode of genetic transmission for bipolar disorder. Reviews of segregation analysis studies find no strong support for either single-gene or polygenic transmission, even when such factors as gender and polarity are taken into account in the analyses (Faraone et al. To date several regions of the genome have been implicated but, because these Genetic epidemiology of bipolar disorder 235 findings have not been consistently replicated, they remain suggestive, not definitive. Using these genetic markers, linkage between bipolar disorder and colour blindness was suggested over two decades ago, but these early results were not easily replicated. Gershon and colleagues (1979) reported results from an international collaborative study of X-linkage under the auspices of the World Health Organization, this collaboration examined 16 pedigrees that had been ascer tained through bipolar patients in the United States, Belgium, Switzerland and Denmark. The overall evidence for linkage was equivocal, but separate analyses of subsamples strongly suggested the presence of significant heterogeneity. All of these provide X-chromosome markers close to the locus for colour blindness. The original report was very compelling and, although some limited support for the finding was reported, most subsequent reports were not consistent with linkage to this region. Nine of 16 studies found a significant increase in blood type O; one reported a significant decrease of blood type O among mood-disordered patients. Two studies found a significant increase in blood type B and one study found a signifi cant increase in blood type A (Tsuang and Faraone 1990). Faraone these studies is the fairly strong suggestion that blood type O is found with greater frequency among patients with bipolar disorder in comparison to individuals from the general population (Lavori et al. In contrast, based on results of a non-parametric affected sib-pair analysis, Berrettini et al. Subsequent studies (reviewed by Van Broeckhoven and Verheyen 1999) provide additional evidence for linkage but implicate a broad region includ ing 18p11-23, which is essentially all of the long arm of chromosome 18. A review of subsequent studies shows that, despite some negative reports, there is now mounting evidence for a bipolar disorder susceptibility locus in this region (Curtis 1999). The possibility that schizophrenia and bipolar disorder may share one or more susceptibility genes has intrigued researchers for many years. For example, Crow suggested that schizophrenia, schizoaffective disorder and affective illness exist along a continuum of psychosis that crosses diagnostic boundaries (Crow 1987). Although he accepted the view of prototypical entities corresponding to schizophrenia and affective illness, he rejected the idea that they had distinct aetiologies. Rather, he suggested that individual disease entities did not actually exist; instead, natural variation along one or more dimensions produced the prototypical disorders. He postulated that a common genetic deficit, located in the pseudoautosomal region of the sex chromosomes, was shared by psychotic disorders, and he hypothe sized that genes related to psychosis were responsible for cerebral domi nance and the localization of language (Crow 1990, 1991). Although support for the pseudoautosomal hypothesis is weak, and a psychosis gene shared by all psychotic disorders has yet to be discovered (Asherson et al. But they did find suggestive evidence in one large pedigree that this region was linked to both schizophrenia and bipolar disorder. Their strongest evidence for linkage derived from an analysis using a broad phenotypic definition that included schizophrenia, bipolar disorder, schizoaffective dis order and major depression. This chromosomal region has also been impli cated in studies of bipolar disorder (Berrettini et al. Although these studies suggest that schizophrenia and bipolar disorder may share susceptibility genes, that conclusion must remain tentative until the apparent connection between the two disorders is confirmed and repli cated in large samples. The concordance rate for mood disorder among monozygotic twins is approximately three times the rate observed among dizygotic twins. This strongly suggests that genes play a crucial role in the familial transmission of these disorders. Since concordance is not perfect, non-familial environmental factors must play a role in the aetiology of bipolar disorder. Nevertheless, both twin and adop tion studies suggest that the familial transmission of these disorders has a primarily genetic source. However, since the adoption study literature contains some conflicting reports, we need more adoption studies to provide convergent support for these assertions. The genetic relationship between major depression and bipolar disorder is poorly understood. Further research into this area must distinguish recurrent depressed cases that are not likely to have a subsequent manic episode from non-recurrent cases that may be bipolar. It is probably true that cases of major depression within families that manifest bipolar disorder are genetic variants of bipolar disorder. Faraone difference between the two forms of mood disorder is that relatives of bipolar patients have a greater prevalence of both depression and bipolar disorders than relatives of depressed patients. Thus, it is likely that bipolar disorder has a greater familial component than does major depression, which appears to be more affected by non-familial, environmental factors. Although molecular genetic studies have identified several regions of interest, they have not yet found the genes that underlie the inheritance of bipolar disorder. There have been many attempts to explain this situation as due to the clinical and epidemiological features of psychiatric disorders that point to complex inheritance – as opposed to single-gene inheritance (Gershon and Cloninger 1994). Furthermore, assortative mating, genetic heterogeneity, sporadic cases, misclassification, and low penetrance may further compli cate the picture. Moreover, future work needs to examine the spectrum of subclinical conditions that may share genetic causes with bipolar disorder. These could be milder mood disorders such as dysthymia and cyclothymia or aberrations in brain structure or function as measured by neuropsychological tests, psychophysiological paradigms, neurochemical assays or neuroimaging assessments. These subclinical syndromes and neurobiological markers may have an underlying genetic architecture that is simpler than that for bipolar disorder. If so, then molecular genetic studies of such phenotypes might facilitate the detection of genes relevant to bipolar disorder. Genetic epidemiology of bipolar disorder 239 Asherson P, Parfitt E, Sargeant M, Tidmarsh S et al. No evidence for a pseudoautoso mal locus for schizophrenia linkage analysis of multiply affected families. Two syndromes of schizophrenia as one pole of the continuum of psychosis: a concept of the nature of the pathogen and its genomic locus. An examination of linkage of schizophrenia and schizoaffective disorder to the pseudoautosomal region (Xp22. Pseudoautosomal region in schizophrenia: linkage analysis of seven loci by sib-pair and lod-score methods. Transmitted factors in the morbid risk of affective disorders: a controlled study. Color blindness not closely linked to bipolar illness: report of a new pedigree series. Re-evaluation of the linkage relationship between chromosome 11p loci and the gene for bipolar affective disorder in the old order Amish. Morbidity risks of schizophrenia and affective disorders among first-degree relatives of patients with schizophrenia, mania, depression and surgical conditions. Original article: Pseudoautosomal locus for schizophrenia excluded in 12 pedigrees. However, this seems only partly justified because a number of factors make the identifica tion of disease genes particularly difficult for severe psychiatric disorders. Oligo or poly genic inheritance with interaction between loci and other genetic mecha nisms, such as imprinting or repeat expansion at some of the loci, are possibly involved. To this could be added the reluctance of some patients and relatives to participate in research investigations, and the possible denial of psychiatric symptoms at interviews. Angst (eds), Bipolar Disorders: 100 years after manic-depressive insanity, 243–280.
In 1882 Kahlbaum published a work on cyclothymia androgen hormone overdose cheap eulexin express, that is the milder forms of the illness man health 1st cheap eulexin 250 mg without a prescription. Kraepelin presented mens health no gym workout buy eulexin 250mg free shipping, in the sixth edition (1899) of his handbook prostate cancer juicing discount 250mg eulexin fast delivery, the manic-depressive entity. Here he calls it manic-depressive insanity, and includes on the one hand the so-called periodic and circular insanity and on the other simple mania, usually kept distinct from it. It was Karl Kleist (1953) in his monograph "The classification of neuropsychological diseases", and his pupil Karl Leonhard (1957) in the book Endogenous Psychoses (1957), who distinguished simple unipolar forms from bipolar forms and cycloid forms corresponding to mixed states. Subsequently Angst (1966) and Ferris (1966) clearly divided manic-depressive illness into monopolar and bipolar forms on the basis of hereditary data. Today there is a great deal of discussion about the actual rate of occurrence of unipolar forms. While formerly they were believed to be prevalent, debate has now developed to the point at which their very existence is being questioned. In our sample (Koukopoulos 1997) of 1257 affective patients, 80% were bipolars including soft bipolar cases. It should be emphasized that the Centro Lucio Bini is a facility for mood disorders, and the affective patients who attended suffer from more severe forms. We feel it is useful to recall that, while for unipolars it is possible to have just one or only a few episodes during a lifetime, this is virtually impossible for bipolars. As we said before, manic-depressive illness is probably a disturbance of normal physiological cycles, which are in turn influenced by the environment and the seasons. We can observe it in the form of multi-year cycles, hard to understand; annual cycles with excitation in summer and depression in winter; 6-month cycles that already represent rapid cycling; seasonal cycles, closely linked to climate or environmental Cyclicity and manic-depressive illness 319 changes; monthly cycles, very frequent in women and linked to the men strual cycle; and 48-hour or circadian cycles with mood swings between the morning and the evening. Finally, we have ultradian cycles with swift changes in mood, even in the space of a few minutes, particularly frequent in the elderly, perhaps because of the impaired regulatory capacity of their central nervous systems. In order to better understand the intimate relationship between the two opposing phases of the manic-depressive cycle, it may be useful to introduce the concept of energy and the underlying biological processes that create and regulate it. Undoubtedly there is in mania an increased energy level with hyperactivity and decreased need for sleep. Periods of nervous excite ment certainly consume great amounts of energy and may exhaust the biological processes that create it. A genetic flaw may prevent the prompt recovery of this energy and give rise to a long-lasting depressive period. This is probably the concept that Willis and Ficino expressed by compar ing mania to a burning fire and melancholia to its soot or smoke. A confirmation of the primacy of mania in the cycle is the fact that all prophylactic treat ments against manic and depressive recurrences or episodes, such as lith ium, anticonvulsants and neuroleptics, are fundamentally antimanic agents which, by preventing or suppressing mania, also prevent depression. This explains the better response to prophylaxis of those cases that start with mania (Faedda et al. Further evidence of the primary role of mania in the manic-depressive cycle comprises relapses after the interruption of lithium maintenance ther apy (Faedda et al. Relapses that occur during the first few months are phases of excitation and not depression. Depressions occur later and follow the manic relapse or the natural course of the disesase. Girardi On the other hand, antimanic treatments, especially neuroleptics, deepen and prolong depression that follows mania. If the cycle starts with a depression, and we treat it with antidepressants, a rebound into mania may occur. As we shall discuss later, these patients are mainly of hyperthymic and cyclothymic temperament, i. Antidepressants probably activate the biological processes that tend to raise energy levels. It is conceivable that in genetically predis posed persons the energy levels may overshoot. Cardiovascular regulation, for instance, is a good example of this complex function. In particular the central nervous system spontaneously tends to push depressed mood back up towards euthymia, and to level off excite ment. Our antimanic and antidepressant treatments certainly interfere with this process, and this explains at least part of the increase in circular cases and cyclicity in general, in recent years. For he may easily drive the patient to extreme depression by treating temporary fits of rage, or, alternatively, he may overexcite the patient whose prevailing mood is melancholic". Carus (1846) said that "the nervous system decidedly partakes in the periodicity of the external world". Jamison (1999) states: "We are, with the rest of life, periodic creatures, beholden for our rhythms to the rotations of the earth around the sun and the moon around the earth. Like other mammals, our patterns of eating, sleeping, and other physical activities sway with the seasons, varying in accordance with changes in day length and temperature. In the Hippocratic writings one reads observations such as the following: "But if the weather [in autumn] be northerly and Cyclicity and manic-depressive illness 321 dry it is very harmful to the bilious and some of them become ill with melancholia", or "such diseases as increase in the winter ought to cease in the summer and such as increase in the summer ought to cease in the winter" (Hippocrates 1967b). Pinel (1809) states that "manic attacks begin immediately after the summer solstice, continue with more or less violence through the heat of summer, and commonly terminate towards the decline of autumn". It is significant that Griesinger (1845), after naming as Cyclus the alternation of mania and melancholia, goes on to say: "Other observers and ourselves have seen cases where at a particular season a profound melancholia supervenes and this in spring passes into mania, which again in autumn gradually sinks into melancholia". Emil Kraepelin (1913) describes cases with seasonal patterns and Johannes Lange (1928) compares winter depression with hibernation. In the course of the 20th century, however, these views have been neglected and almost fallen into oblivion. Wehr (1989a) gives a series of reasons for this, including "the cultural shift from a cyclic to a linear perception of time, so that psychiatrists and patients may be more likely to perceive affective recurrences as a succession of separate events than as a seasonal cycle of events". Norman Rosenthal (1993) agrees with the importance of this perception of time as linear or historical rather than cyclic. New interest in the cyclicity of seasonal affective disorders has emerged, especially thanks to the work of Wehr, F. In this development, lithium treatment and studies on the longitudinal course of the disease played a major role in highlighting its relation to the seasons, although continuous lithium treatment often changes the seasonal pattern of the cycles (Koukopoulos et al. Given the importance of the seasons on the incidence of mania and depression, it appears correct to assume that light and heat may trigger and induce a seasonal pattern in the course of the disease. Certainly the relationship between affective illness and the seasons is more profound than a mere modulation of its course. The prevalence of seasonal patterns among patients who attended special ized clinics was found to be 16% by Thase (1988), 29% by Monplaisir (1990), 38% by Garvey et al. This season has the highest peak of suicides while in autumn–winter there is another, smaller peak. One explanation for this may be that winter depressions are generally retarded while spring–summer ones are anxious or agitated, often true mixed depressions. Agitation is certainly a major risk factor for suicide (Koukopoulos and Koukopoulos 1999). In more recent studies other authors have found that the onset occurs earlier in life, especially for bipolar disorder, and this could be explained by the increasing use of substances by young people, and by their change of lifestyle, such as going to sleep much later than earlier generations. The earlier onset of bipolar cases is an important fact and the depression that occurs at a young age is very likely to develop into bipolar disorder. Angst states: "It is obvious that many bipolar cases start in preadolescence or adolescence. Relapsing again and again, the amplitudes get higher and higher until the threshold of a clear disorder is reached. It is important to diagnose such cases as early as possible in order to put them on a long-term prophylaxis and to avoid a disastrous development of personality and social adjust ment, frequently observed in adolescents. About 47% of unipolar depressives suffer only one to three episodes while 95% of bipolar patients suffer more than four episodes. It may be that the unipolars with higher frequency whom one often encounters in clinical practice are probably pseudo-unipolars; that is they also have undetected periods of sub-threshold hypomania. Indeed, real unipolars have very long intervals of several years and it is doubtful whether they should undergo long-lasting prophylactic treatment. Cyclicity and manic-depressive illness 323 Marneros (1999) also found that the annual frequency of episodes of unipolars is 0. The authors of this chapter found, in a sample of 1257 affective patients, the frequency of episodes per year to be: 0.
The wires are then levered up and then directed into the proximal intact opposite cortex prostate ultrasound cpt buy eulexin 250 mg online. In addition to prostate cancer guidelines eulexin 250 mg cheap being relatively simple and inexpensive mens health xbox 360 discount eulexin 250 mg without prescription, this tech nique has been shown to prostate oncology ward buy line eulexin be very effective, particularly in elderly patients. Spanning external fixation Ligamentotaxis is used to restore radial length and radial inclination, but it rarely restores palmar tilt. Nonspanning external fixation A nonspanning fixator is one that stabilizes the distal radius fracture by securing pins in the radius alone, proximal to and distal to the fracture site. Volar nonlocked plating the primary indication is a buttress plate for the shear frac ture of the volar Barton. Volar locked plating Chapter 22 Distal Radius 279 Locked volar plating has increased in popularity because this implant has been shown to stabilize distal radius fractures with dorsal comminution. Fragment specific plating Has been advocated for more complex fracture patterns involving several aspects of the radial and ulnar columns. Some authors have advocated fixation for displaced fractures at the base of the ulna styloid. Median nerve dysfunction developing after reduction mandates release of the splint and positioning of the wrist in neutral posi tion; if there is no improvement, exploration and release of the carpal tunnel should be considered. An incomplete lesion in a fracture requiring operative interven tion is a relative indication for carpal tunnel release. Open pin placement is advisable to allow visualization of the superficial ra dial nerve. Degeneration of the tendon, owing to vascular disruption of the tendon sheath as well as mechanical impingement on the callus, results in attrition of tendon integrity. Distal row: the trapezium, trapezoid, capitate, and hamate are connected to one another and to the base of the metacarpals by strong ligaments, making the distal row relatively immobile. The more distal and superficial component is often referred to as the arcuate liga ment or distal V. Space of Poirier: this ligament-free area in the palmar aspect of the capitolunate space is an area of potential weakness. The blood supply to the scaphoid is derived primarily from the radial artery, both dorsally and volarly. The volar scaphoid branches supply the distal 20% to 30% of the scaphoid, whereas branches entering the dorsal ridge supply the proximal 70% to 80%. Circulation of the wrist is ob tained through the radial, ulnar, and anterior interosseous ar teries and the deep palmar arch: 1, palmar radiocarpal arch; 2, palmar branch of anterior interosseous artery; 3, palmar in tercarpal arch; 4, deep palmar arch; and 5, recurrent artery. The radiocarpal articulation acts as a universal joint allowing a small degree of intercarpal motion related to rotation of individ ual carpal bones. Radiocarpal joint motion is primarily flexion and extension of nearly equal proportions (70 degrees), and radial and ulnar deviation of 20 and 40 degrees, respectively. Using the ligament as an axis, it rotates from a volar flexed perpendicular position to a dorsiflexed longitudinal position. With the wrist in radial deviation, the scaphoid flexes; with ulnar deviation, the scaphoid extends. Any flexion moment transmitted across the scaphoid is balanced by an extension moment at the triquetrum. The volar ligaments are placed under ten sion with compression and shear forces applied dorsally, especially when the wrist is extended beyond its physiologic limits. Fractures at the scaphoid waist or proxi mal third depend on fracture union for revascularization (Fig. Provocative tests include the scaphoid shift test: reproduction of pain with dorsal-volar shifting of the scaphoid. The Watson test: painful dorsal scaphoid displacement as the wrist is moved from ulnar to radial deviation with palmar pressure on the tuberosity. If the clinical examination suggests fracture but radiographs are not diagnostic, a trial of immobilization with follow-up radi ographs 1 to 2 weeks after injury may demonstrate the fracture. The volar approach is the least damaging to the vascular supply of the vulnerable proximal pole. Postoperative immobilization consists of a short arm thumb spica cast for 6 weeks. Osteonecrosis: this occurs especially with fractures of the proximal pole, owing to the tenuous vascular supply. Lunate the lunate is the fourth most fractured carpal bone after the scaphoid, triquetrum, and trapezium. Displaced or angulated fractures should be treated surgically to allow adequate apposition for formation of vascular anasto moses. This may require further operative intervention for pain relief, including radial shortening, radial wedge osteotomy, ulnar lengthening, or salvage procedures such as proximal row carpectomy, wrist denervation, or arthrodesis. Displaced fractures may require fragment excision, either early, in the case of a severely displaced fragment, or late, in the case of a pisiform fracture that has resulted in painful nonunion. Trapezium Fractures of the trapezium comprise approximately 3% to 5% of all carpal bone fractures. A carpal tunnel view may be necessary for adequate visualization of dorsal ridge fractures. Indications for open reduction and internal fixation include ar ticular involvement of the carpometacarpal articulation, comminuted fractures, and displaced fractures. Trapezoid Because of the shape and position of the trapezoid, fractures are rare. An axial load transmitted through the second metacarpal may lead to dislocation, more often dorsal, with associated capsu lar ligament disruption. The trape zoid, or fracture fragments, may be superimposed over the trapezium or capitate, and the second metacarpal may be proximally displaced. Indications for open reduction and internal fixation include dis placed fractures, especially those involving the carpometacarpal articulation. Capitate Isolated injury to the capitate is uncommon, owing to its relatively protected position. If closed reduction is unattainable, open reduc tion and internal fixation are indicated, usually with Kirschner wires or lag screws, to restore normal anatomy. Osteonecrosis: this is rare but results in functional impairment; it emphasizes the need for accurate diagnosis and stable reduction. Hamate the hamate may be fractured through its distal articular surface, through other articular surfaces, or through its hamulus, or hook. Generally, it occurs at the base of the hook, although avulsion fractures of the tip may occur. Chapter 23 Wrist 297 Clinical evaluation: Patients typically present with pain and tender ness over the hamate. Ulnar and median neuropathy can also be seen, as well as rare injuries to the ulnar artery, which is located in proximity to the hook of the hamate, in Guyon’s canal, along with the ulnar nerve. A frac ture of the hook of the hamate can be visualized on the carpal tunnel or a 20-degree supination oblique view (oblique projec tion of the wrist in radial deviation and semisupination). A hamate fracture should not be confused with an os hamulus proprium, which represents an ossification center that has failed to fuse. Displaced fractures of the body may be amenable to Kirschner wire or screw fixation. Fractures of the hook of the hamate may be treated with excision of the fragment for displaced fragments or in cases of symptomatic nonunion. Ulnar or median neuropathy: this is related to the proximity of the hamate to these nerves and may require surgical exploration and release. Ruptures of the flexor tendons to the small finger: They result from attritional wear at the fracture site. Injury progresses through several stages (Mayfield progression): It usually begins radially through the body of scaphoid (frac ture) or through scapholunate interval (dissociation), although both are possible in the same injury (rare). Swelling is general ized about the wrist with variable dorsal prominence of the entire carpus in cases of dorsal perilunate dislocations. Lateral view (most important view): Carefully look at the outline of the capitate and the lunate. Technique of closed reduction Longitudinal traction is applied for 5 to 10 minutes. Immediate surgery is needed if there are progressive signs of median nerve compromise.
Manic-depres sive (bipolar) disorder: the course in light of a prospective ten-year follow-up of 131 patients prostate cancer in females cheap eulexin 250 mg on-line. Unfortunately mens health 7 day workout plan discount eulexin 250 mg on-line, according to prostate cancer institute discount 250mg eulexin projections from the Global Burden of Disease report (Jenkins 1997) mens health ebook the six-pack secret proven 250 mg eulexin, the global burden of bipolar disorder and other major psychiatric disorders (schizophrenia, major depression, alcohol abuse and dependence, and obsessive–compulsive disorder) will increase by 10. A number of factors contribute to the enormous costs of disability from bipolar disorder. First, bipolar disorder is common and, with an average early age of onset, is frequently a lifelong illness (Weissman et al. For example, estimates from the Cross-National Collaborative Group epidemio logical study indicated that the lifetime prevalence of bipolar disorder ranged from 0. The results of this study also replicated previous findings of an early age of onset of the illness. In addition to being common, bipolar disorder is a recurrent illness; 80–90% of patients with an index manic episode will have subsequent affective episodes (Goodwin and Jamison 1990, Winokur et al. Untreated, the natural course of the illness is towards more frequent epi sodes with shorter intervals of mental health (Goodwin and Jamison 1990). Angst (eds), Bipolar Disorders: 100 years after manic-depressive insanity, 437–448. A third factor contributing to high rates of disability is the lag of functional recovery from an affective episode behind symptomatic recovery. Many weeks and months may separate remission of symptoms and recovery of premorbid functional status (Dion et al. In fact, many patients do not reach full functional recovery and recurrent affective episodes may lead to progressive deterioration in func tioning between episodes (Coryell et al. Thus, disability from bipolar disorder is not simply limited to discrete affective episodes. For example, recent studies provided data regarding the impact of bipolar disorder on voca tional functioning (Kessler and Frank 1997) and marital stability (Kessler et al. Clearly, by these estimates, the personal, social and economic costs of bipolar disorder are staggering. However, economic cost estimates at least provide a means of quantifying the impact of this illness and a means of demonstrating the benefits of effective treatment. In general, costs, in cost-of-illness studies, have typically been defined as core costs resulting directly from the illness and other related costs, including non-health costs of the illness (Rice 1994). Within the core and related cost categories there are direct costs (requiring expenditure of payments) and indirect costs (lost resources) (Rice 1994). Examples of direct costs include funds spent for hospital and nursing-home stays, physician and other professional services, medicines and equipment. In the first study to examine the economic cost of bipolar disorder, Greenberg et al. In their analysis, patients with bipolar disorder in treatment were estimated to have lost approximately 152 million cumulative days from work, and untreated patients an additional 137 million days in 1990. Morbidity costs based on diminished productivity from affective symptoms from bipolar disorder or major depression were $6. For patients with bipolar disorder specifically, impairment was highest in individuals aged 18–24 years. Morbidity costs (in 1985 dollars) were estimated at $137 million for people with bipolar disorder, 18–24 years old; $802 million 25–34 years old; $206 million 36–54 years old; and $18 million 55–64 years old. The authors concluded that "substantial potential cost savings to society could be gained by timely and appropriate treatment interventions to patients suffering from affective disorders" (p. Of the $45 billion total, $7 billion was expended on core costs which included the direct costs of inpatient and outpatient care and other related costs (see Table 1). Indirect costs of $38 billion were substantial, the greatest component of which was lost productivity of wage-earners and homemakers, together totalling $20 billion (Table 1). Thus, the overall cost of treatment of bipolar disorder is only a small portion of its total economic cost and is greatly outweighed by the morbidity and mortality costs of the illness itself. The results of a Cox regression analysis of time to rehospitalization revealed that older patients and those with a predomi nance of manic symptoms at index episode had a significantly greater probability of not being rehospitalized during the follow-up period. In contrast, the presence of neurovegetative symptoms of depression and a greater number of previous hospitalizations predicted rehospitalization. Overall, 44% of patients required rehospitalization over the subsequent 15 months after discharge. In this study it was unclear whether neurovegetative symptoms were associated diagnostically with bipolar depression, mixed mania or both. Since inpatient care contributes a substantial component to the cost of treatment of bipolar disorder, the predictive value of these factors Costs of treatment of bipolar disorder 441 is potentially economically as well as clinically significant. Estimated (1990) treatment costs for the combined group of patients with schizo phrenia and bipolar disorder were $380/month ($4560/year) compared with $149/month ($1788/year) for pharmacy controls. Not surprisingly, 75% of patients receiving lithium had a diagnosis of bipolar disorder. The admin istration of concurrent psychotropic agents in this group of patients was widespread: 54% received tricyclic antidepressants; 41% antipsychotics; 39% anxiolytics; 18% anticonvulsants; and 14% thyroid medications. The most striking findings of this survey concerned the adherence to lithium mainte nance treatment. The pre dominant pattern of lithium use was of multiple periods of short continuous use rather than few periods of long continuous use. During periods of lithium use, patients had significantly more mental health visits per month but significantly less risk of psychiatric hospitalization compared with periods of non-use. Furthermore, patients with a pattern of interrupted multiple-period short continuous use had a relative risk of emergency psychiatric evaluation and of psychiatric hospitalization of 2. Since the costs of psychiatric hospi talization constitute the major component of treatment costs for bipolar disorder, the economic and clinical impact of lithium non-adherence in this study was likely to be substantial. There are virtually no data regarding the economic impact of specific forms of psychotherapy on bipolar disorder. Three studies estimated the cost savings attributable to the introduction of lithium for patients with bipolar disorder (Reifmann and Wyatt 1980, McCreadie 1989, Peselow and Fieve 1987). They then compared these estimates with similar calculations during a single year (1969) after lithium became available. Finally, these cost savings were then extrapolated over the subse quent decade when lithium was the first-line pharmacological treatment for bipolar disorder. A number of assumptions and exclusions were incorpo rated in the calculations of cost savings from lithium. In total, these assumptions and exclu sions yield a conservative estimate to the cost savings from lithium. In the second study of the potential cost savings from lithium in bipolar disorder, McCreadie (1989) compared the average hospital length-of-stay for patients with bipolar disorder in southwest Scotland before and after the introduction of lithium. The average length-of-stay fell from 25 days/year before lithium to 11 days/year after. Peselow and Fieve (1987) also estimated the cost savings from lithium by examining pre and post-marketing data. For 32 patients with bipolar I disorder followed at their clinic, the number of affective episodes requiring hospitalizations in the 3-year period before lithium was 45, compared with 13 in the 3-year period after. Similarly, affective episodes requiring outpa tient intervention dropped form 72 to 39. By assuming that the average length of stay for an affective episode averaged 20 days (circa early 1970s) at a cost of $250/day, the annual cost savings per patient from lithium was estimated as $1435 (1971 dollars) (Table 2). Five studies have compared cost savings from treatment with different mood-stabilizing medications. This was a naturalistic treatment study; thus, patients received antipsychotics and benzodiazepines in addition to a primary mood-stabilizer. The four mood-stabilizer treatment groups consisted of patients who received lithium, divalproex, carbamazepine, or combined lithium and carbamazepine. All mood-stabilizers were administered using gradual titration to therapeutic serum concentrations. The mean length-of stay for patients treated with divalproex (days) or combined lithium and carbamazepine (12 + 2 days) was approximately 40% shorter compared with patients treated with lithium (days). The potential cost savings from divalproex were $8540/patient and were $6783/patient from the com bination of lithium and carbamazepine, based on reductions in length of 444 P. As anticipated from other data regarding the component costs of treatment of bipolar disorder (Rice and Miller 1995, Wyatt and Henter 1995), the estimates of potential cost savings from dival proex and the combination of lithium and carbamazepine reflect the savings associated with shortened periods of hospitalization which are substantially higher than the costs of medications. Patients (n = 96) with a discharge diagnosis of bipolar disorder, mania were retro spectively divided into four treatment groups: lithium monotherapy, anti convulsant. Patients receiv ing multiple mood-stabilizers had significantly longer mean lengths-of-stay (days) compared with patients receiving lithium (days), an anticonvulsant (days), or no mood-stabilizer (days).
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