Studies have shown that nearly all around the world, women have nearly double rates of depression than men although this is not well documented in non-industrialized cultures (Lloyd & Miller, 1997). The National Comorbidity Study reported that 6% of the females vs. 3.8% of males suﬀered from a current depressive episode and that 21.3% of women vs. 12.7% of men had a lifetime experience of a depressive episode (D. G. Blazer, Kessler, McGonagle, & Swartz, 1994). The rates for bipolar disorder are similar however, suggesting this diﬀerence concerns only unipolar depression. A second finding suggests that women with less social support and experiencing social stressors might be at the greatest risk to develop depression. However, there is no significant gender diﬀerence concerning the risk of recurrence, thus suggesting that gender is among the risk factors for initiating depressive symptoms but not among those determining the course and outcome. This higher risk for females is present around the age of 20s until the early 30s and that the rates of first onset before (childhood and adolescence) or after that age (middle age, elderly) are similar for both sexes (Nazroo, Edwards, & Brown, 1997; Philibert, Richards, Lynch, & Winokur, 1997). It seems highly unlikely that there a single, sex-related factor which is responsible for the diﬀerence. Endocrine changes and diﬀerences were being the target of research without convincing results. The role the female reproductive system might play in mental health is still controversial. The fact that the gender diﬀerence is not obvious until puberty, and disappears after menopause, supports the idea that there is something specific connecting the female biology to mood disorders. A more advanced approach suggests that this biology is not a risk factor per se; on the contrary it could be responsible for an increased vulnerability to stressors, thus indirectly leading to depression, especially considering the second fact that women are more likely to experience stressful and even threatening life events and are at a higher risk of early sexual abuse and current spousal abuse (Finkelhor, Hotaling, Lewis, & Smith, 1990; Roesler & McKenzie, 1994). They also might use oral contraceptive use, and often experience mood disorders temporally related to their sexual identity (e.g., premenstrual or postpartum-onset mood disorders). Additionally, almost all societies have designated diﬀerent, unequal roles for women. On the other hand, since no conclusive data are available so far, it is necessary to consider the possibility that men and women share similar rates of depression, but they express depression in diﬀerent ways and the resulting diﬀerent rates is in reality a methodological artifact. In this case, it’s reasonable to suggest that diﬀerent cognitive coping styles between men and women could be responsible for these results and maybe women are more likely to be diagnosed with depression because they seek professional help more often for their depressive symptoms and maybe because they are more sensitive to negative relationships (Phillips & Segal, 1969). It is believed that men might react to emotional distress by trying not to think about it, while women are more likely to ruminate over their problems (Nolen-Hoeksema & Girgus, 1994; Nolen-Hoeksema, Larson, & Grayson, 1999; Nolen-Hoeksema, Stice, Wade, & Bohon, 2007). In this frame, women are more likely to report depressive symptoms due to marital problems than men. This could at least partially be socio-culturally determined, or imposed, since it is reported that the depressed female students who reached out to their friends were met with concerned and nurturing reactions, while in contrasts, the depressed male students who did the same, faced social isolation and often direct rejection, even hostility (Hammen & Peters, 1978; Joiner, Alfano, & Metalsky, 1992). While married, divorced, and separated women were more likely to be depressed than men, widowed men were more likely to be depressed than women and unmarried men and women shared similar rates of depression (Radloﬀ & Rae, 1979). Another possibility is that in men, but not in women, alcohol abuse could mask an underlying depressive disorder an could account for the diﬀerence in the rates. This opinion derives from the observation that alcohol abuse and mood disorders are often inherited in the same family (Triﬄeman, Marmar, Delucchi, & Ronfeldt, 1995). Suicide Today we know that suicide is a complex and multicausal behavior and demands a com-plex and sophisticated approach. Statistics point to a substantial decline of suicide rates throughout Europe, the US and Canada during the past two decades, and the major reason for that seems to be the better recognition of major depression as well as availability of treatment (Akiskal, Benazzi, Perugi, & Rihmer, 2005; Cipriani, Pretty, Hawton, & Geddes, 2005; Isometsa, Henriksson et al. 1994; Z Rihmer, Belso, & Kiss, 2002; Z. Rihmer & Akiskal, 2006). The understanding and preventing of suicide is one of the most challenging tasks for psychiatry today. It has been confirmed by several psychological autopsy studies that the majority of suicidal victims were suﬀering from a mood disorder, usually untreated major depression, with frequent comorbidity of anxiety and substance-use disorders (Badawi, Eaton, Myllyluoma, Weimer, & Gallo, 1999; Barraclough, Bunch, Nelson, & Sainsbury, 1974; Henriksson et al. 1993; Monkman, 1987; Rihmer et al. 2002; Rihmer, 2007). Around 60-80% of all suicide victims are suﬀering from depression while on the other hand, an estimated 15% of patients with severe major depression eventually die from suicide. The rate of attempted to completed suicide, is about 5 to 1 in patients with any mood disorder (Tondo, Isacsson, & Baldessarini, 2003). Although many risk factors have been identified, most of them are not clinically useful. An important and useful risk factor is the presence of a depressive mixed state (3 or more simultaneously co-occurring hypomanic symptoms in patients with “unipolar depression”). This clinical picture overlaps to a great extent with agitated depression. Depressive mixed state as well as agitation substantially increase the risk of both attempted and committed suicide (Akiskal, Benazzi et al. 2005; Balazs et al. 2006; Isometsa, Henriksson et al. 1994; Rihmer & Akiskal, 2006; Rihmer, 2007). Other risk factors include family history of suicide, higher number of prior depressive episodes, comorbid anxiety, personality disorders and alcohol dependence, as well as sociodemographic and psycho-social factors such as younger age, being divorced or widowed, and experiencing adverse life-situations which are associated with increased suicidal ideation and higher prevalence of attempts (Balazs et al. 2006; Bernal et al. 2006; Henriksson et al. 1993; Rihmer et al. 2002; Z. Rihmer & Akiskal, 2006; Z. Rihmer, 2007). Although biological research has so far identified several biological correlates of suicide today there is no biological marker found yet to distinguish explicitly between suicidal and non suicidal depressives (Nordstrom et al. 1994; Samuelsson, Jokinen, Nordstrom, & Nordstrom, 2006). An impressive fact is that in spite of frequent medical contact before committing suicide, only a small minority of victims had received appropriate treatment. This is particularly a problem in primary care, where most patients seek help (Henriksson et al. 1993; Isometsa, Aro, Henriksson, Heikkinen, & Lonnqvist, 1994; Luoma, Martin, & Pearson, 2002; Z. Rihmer, Barsi, Arato, & Demeter, 1990; Rihmer et al. 2002). Thus not only early identification of suicidal behavior is possible but also early intervention is possible and could make a diﬀerence. The patient should be put on a plan of regular psychiatric visits on an interval ranging from once to twice weekly. Latter visits could be planned on a month interval or even less frequently. The main factors determining frequency include the clinical picture, social and family support, history of adherence, insight into the illness and the risk and medication adverse eﬀects. The therapist should have in mind that antidepressive agents are the only formally approved treatment for major depression (Akiskal, Benazzi et al. 2005; Z. Rihmer & Akiskal, 2006; Yerevanian, Koek, Feusner, Hwang, & Mintz, 2004) and there are no data supporting the eﬀectiveness of any other approach (Fountoulakis, Gonda, Siamouli, & Rihmer, 2008). Also a marked anti-suicidal eﬀect has been also reported with long-term lithium therapy in bipolar (manic-depressive) patients (J. Angst, Angst, Gerber-Werder, & Gamma, 2005; Cipriani et al. 2005; Rihmer & Akiskal, 2006). Recently, the U.S. Food and Drug Administration issued a warning concerning the use of antidepressants in children and adolescents and possibly in all age groups because of possible induction of suicidality (thinking and behavior but not completed suicide) by antidepressants in juvenile depressives (FDA, 2009). A similar warning is in place now concerning anticonvulsants. However, the impact of this warning might be robustly negative. The warnings are based on data from RCTs but there is doubt whether the design of these studies permit these conclusions. A recent study reports that after the warning, (between 2003 and 2005) the SSRIs prescriptions for children and adolescents in the US and the Netherlands decreased by about 22% but simultaneously there was a 49% youth suicide rate increase in the Netherlands (between 2003 and 2005) and a 14% in the US (between 2003 and 2004) (Gibbons et al. 2007). It is highly possible the "natural" population of mood disorders patients does not respond to treatment this way. On the contrary it seems that proper and "aggressive" treatment of mental disorders and especially of major depression aiming at achieving full remission should always be the target and determines to a large extent whether suicidal behavior is expressed or not (Angst et al. 2005; Moller, 2006; Sondergard, Lopez, Andersen, & Kessing, 2007; Tiihonen et al. 2006). However, a caveat is that the most dangerous period for suicide in a patient is immediately after treatment has commenced, as antidepressants may reduce the symptoms of depression such as psychomotor retardation or lack of motivation before mood starts to improve. Although this appears to be a paradox, studies indicate the suicidal ideation is a relatively common component of the initial phases of improvement even with psychotherapy (Moller, 1992). Substance Use Comorbidity Substance use and abuse is an old problem which recently gained significant importance. A large variety of diﬀerent substances could be related with use or abuse and consequently with substance-induced mood disorders (Schuckit et al. 1997; Winokur et al. 1998). They include various medications (e.g., anesthetics, anticholinergics, antidepressants, anticonvulsants, antibiotics, antihypertensives, corticosteroids, antiparkinson agents, chemotherapeutic agents, nonsteroidal anti-inflammatory drugs, and disulfiram), toxic agents (heavy metals, industrial solvents, household cleaning agents), or substances used routinely for recreational purposes (e.g., caﬀeine, nicotine). Almost all the substances are preferred because of their subjective eﬀects which concern mainly the mood. Others are used for their calming or "therapeutic-like" eﬀect (as self-treatment, e.g., alcohol, sedatives) while others for their stimulating, euphoric and augmenting eﬀect (e.g., stimulants). Substance use and abuse could happen in the frame of a pre-existing mood disorder or the use itself can be the cause of the disorder (because of the direct physiological eﬀects, toxicosis, withdrawal or dependence). When the mood disorder is primary and pre-exists, substance use complicates both the clinical manifestations and the treatment, and might lead to poor prognosis. This is especially often during teenage and early adult years, and relates mainly to cyclothymia and probably represents attempts of self-medication for the mood liability. During the withdrawal period many substances including alcohol, opioids, and sedatives might induce persistent mood disturbance, insomnia and cognitive disorder leading to relapse of the abuse. These symptoms need to be distinguished from those of primary mental disorders, and this is often very diﬃcult. The critical factor is the clinician's judgment that the mood disorder is caused by the substance or not. A double diagnosis is usually the only reasonable solution. However, the "self-medication" scenario with mood disorder being primary, or even the double diagnosis are unfortunately not the diagnostic priority of many therapists (especially in therapeutic communities) and consequently, the missing of the diagnosis of mood disorder deprives the patient from proper and eﬀective treatment. Alcohol use and abuse is very frequent especially for mood and anxiety patients. On the other hand, heavy alcohol consumption over a period of days results in a depressive state, which even when it is severe, it largely improves within days to weeks of abstinence. After several weeks, most alcoholic patients manifest residual low mood or mood swings resembling a cyclothymic or dysthymic disorder but they also tend to diminish and disappear with time. The presence of the dysthymic symptoms usually indicates the normal course of a withdrawal syndrome and not an independent mood disorder. Nicotine use and abuse is also very frequent usually in the form of cigarette smoking and withdrawal is manifested by changes in mood, anxiety and weight gain (average is 2 to 3 kg) which can persist even for months. Amphetamine, cocaine, opioid, hallucinogen or inhalant - induced mood disorder can occur during intoxication or withdrawal. In general, for all this substances, intoxication is associated with manic or mixed mood features, whereas withdrawal is associated with depressive mood features. An induced mood disorder by any of them usually remits within a week or two (several weeks for opioids), except from panic episodes that develop during cocaine use which could persist for many months following cessation (Krystal, Price, Opsahl, Ricaurte, & Heninger, 1992; Weddington et al. 1990). An important outcome is suicide which is not an uncommon complication. Pediatric Although the core features of mood disorders are essentially the same across the life span, traditionally children and the elderly are considered somewhat separately because of the special features their phase of life includes and the way these features might influence the overall manifestation of mental disorders and their treatment. Additionally, an early age of onset of any disorder puts forward the question whether this determines a more severe and chronic disease and also poor response to treatment. It seems that the developmental phase might influence the expression of certain mood symptoms and that’s why e.g., pervasive anhedonia or significant psychomotor retardation are rare among depressive children and auditory hallucinations and somatic complaints are seen more often in prepubertal children. The incidence of mood disorders among children and adolescents is reported to increase during the last few decades. These reports are rather consistence and they also suggest there is a decrease of the age of onset of mood disorders. The general picture suggests that the prevalence of depression is around 0.3% for pre-school children, 0.4–3% for school aged children and 0.4–6.4% for adolescents; the prevalence of bipolar disorder is 0.2–0.4% in children and 1% in adolescents. Research suggests that 40-70% of children and adolescents with a mood disorder have also at least one comorbid psychiatric disorder. The risk factors as well as the etiopathogenesis for this age group are uncertain. Concerning suicide and related behavior, the attempted suicide is 1% in children and 1.7–5.9% in adolescents, while the completed suicide rate ranges from nearly zero in children below the age of 10, to a peak of above 18/100,000 in boys 15-19 years old. The data suggest that among 15-19 year-olds, the suicide rates have quadrupled over the last four decades, and the reason for this is not known. Unfortunately, suicide is currently the fourth leading cause of death in children aged 10-15 years and the third leading cause of death among adolescents and young adults aged 15-25 years. The suicidal method is the most significant factor which determines whether the attempt will result in death. The great majority of attempts among children and adolescents have little lethal potential partially because of restricted access to lethal material and inadequate cognitive potential to plan a successful attempt. What is unique in this age group is suicide imitation and contagion. This means that the suicidal behavior increases in adolescents following exposure to well-publicized news stories of suicide or a film involving a teen suicide, but this seems to concern vulnerable individuals and not the age group as a whole (Brent et al. 1993; Cheng, Hawton, Lee, & Chen, 2007; Gould & Shaﬀer, 1986). The etiopathogenesis of mood disorders in children and adolescents is not well understood. It is an age group which combines developmental vulnerability and high potency for neuro-plastisity and compensation for any insults. It is generally believed that genetic factors play a significant role; however there are vague data in support of this and no clear conclusions can be made. Non-shared environmental factors might also play an important role (Pike & Plomin, 1996). At the cognitive level, the theoretical approach suggests the presence of cognitive distortions similar to those seen in adults but again data are inconsistent and scarce. Traditionally there has been significant interest on the family interactions and their rela-tionship to the development of depression, but the conditions are usually complicated and diﬃcult to interpret. The most diﬃcult problem is that when the family environment is problematic, then, there is a high probability of a genetic vulnerability in the family and sometimes in both parents. However, this does not exclude the possibility the environment to induce a kind of emotional vulnerability in the child by shaping the early experiences. Depressed parents may model negative cognitive styles and poor self-esteem, leading to a deficit of social problem-solving skills and in coping with stressful life events; marital conflict and lack of an adequate family support system especially when a mental illness of the parent(s) of an early onset, is recurrent, and disrupts parental functioning puts the child at a high risk for any mental disorder but especially for a mood disorder. In this frame, it is understandable why family conflict is the most frequent event adolescents report they experienced, before they manifest suicidal behavior. There are several studies suggesting that depressed children and adolescents might experience more stressful life events like interpersonal losses, problems in relationships, parental divorce, bereavement, physical abuse and suicide in the environment (Beautrais, Joyce, & Mulder, 1997; Gould, Shaﬀer, Fisher, & Garfinkel, 1998; Kaplan, Pelcovitz, Salzinger, Mandel, & Weiner, 1997; Williamson, Birmaher, Anderson, al-Shabbout, & Ryan, 1995). The conclusion concerning the etiopathogenesis of mood disorders in children and adolescence is that genetics clearly plays at least a moderate role while both shared and non-shared environmental influences appear to be also important. Clinically depression in this age group presents with the same core features manifested in adults. Some minor diﬀerences suggest the presence of irritable rather than depressed mood and failure to attain expected weight gain instead of weight loss. Among pre-school children often lack of smiling, apathy towards play, lack of involvement in all activities, physical complaints, and physical aggression while among school-aged children, deteriorating school performance, increased irritability, fighting, or argumentativeness and avoidance of peers may signal depression. Exacerbation of anxiety symptoms and school refusal are not uncommon among children who are depressed. Switching from unipolar depression to bipolar disorder is significantly higher in children than it is in adults, and it reaches 32% within a 5 year period. Also, it is reported that in children, mania might present with a chronic instead of an episodic pattern, with mixed and rapid cycling features instead of classic manifestations and high comorbid mental disorders. These suggest that childhood-onset bipolar disorder is a more severe form of the illness, and relatively treatment resistant. The main disorders that should be diﬀerentially diagnosed are attention-deficit/hyperactivity disorder and disruptive behavior disorders (Geller & Luby, 1997). The psychological treatment of children and adolescents with mood disorders are similar to those for adults. On the contrary there is a significant controversy concerning pharmacother-apy. Double-blind studies are missing and it seems that these age groups are particularly vulnerable for the induction of suicidality by antidepressants. Flouxetine, quetiapine and lithium are the better studied agents in terms of eﬃcacy in these age groups (Andrade, Bhakta, & Singh, 2006; Azorin & Findling, 2007; Barzman, DelBello, Adler, Stanford, & Strakowski, 2006; Chang, 2008; DelBello et al. 2006; DelBello, Adler, Whitsel, Stanford, & Strakowski, 2007; Dudley, Hadzi-Pavlovic, Andrews, & Perich, 2008; Jensen, Buitelaar, Pandina, Binder, & Haas, 2007; Marchand, Wirth, & Simon, 2004; Tsapakis, Soldani, Tondo, & Baldessarini, 2008; Usala, Clavenna, Zuddas, & Bonati, 2008). ECT and TMS might be reasonable alternatives if initial therapeutic attempts fail (Morales, Henry, Nobler, Wassermann, & Lisanby, 2005). Geriatric A world wide trend is the increase in both the absolute numbers and percentage in the total population of the elderly. This of course leads to an increase in the numbers of geriatric psychiatric patients and a shift of the focus of health care services. At the same time, geriatric mental patients present with multiple challenges both at the diagnostic as well as the therapeutic level. The prevalence of major depression is estimated to be 2% in the general population over 65 years of age (Blazer, Burchetti, Service, & al, 1991; Reynolds, 1992; Vaillant, Orav, Meyer, McCullough Vaillant, & Roston, 1996), with up to 15% having some kind of other mood disorder (Branconnierm et al. 1983) and 25-40% of patients in the general hospital setting having a sub-threshold depression (Rapp, Parisi, & Walsh, 1988). In residential homes, the accepted value for patients with MDD is approximately 12%, with an additional 30% manifesting a milder form of depressive-like symptomatology (Foster, Cataldo, & Boksay, 1991; Katz, Lesher, Kleban, Jethanandani, & Parmelee, 1989; Katz & Parmelee, 1994; NIH, 1992; Parmelee, Kleban, Lawton, & Katz, 1991; Weyerer, Hafner, Mann, Ames, & Graham, 1995). The recognition of geriatric mood patients (with a late onset mood disorder) is poor and less than 50% of hospitalised patients with depression in general medical practice are referred to a psychiatrist, and less than 20% receive adequate treatment (Shah & De, 1998). The same time, geriatric patients with depression have up to 1.5-3 times higher morbidity (Parmelee, Kalz, & Lawton, 1992), with the lifetime risk of suicide being as high as 15%; almost 10% of them die annually (Murphy, 1994). The ratio of males to females with MDD remains stable across the age spectrum (PW Burvill, Hall, Stampfer, & Emmerson, 1989). Late onset mood patients are less likely to have a positive family history for mood disorders compared to younger patients (Hopkinson, 1964; Mendlewicz, 1976) and are more likely to manifest structural changes of the CNS (Burvill et al. 1989; Jacoby & Levy, 1980; Rabins, Pearlson, Aylward, Kumar, & Dowell, 1991). Neuroimaging studies have reported a variety of morphological disturbances, which clearly diﬀerentiate late-life depression from depression of younger ages (Greenwald et al. 1996; Jakoby, Lewy, & Bird, 1980, 1981; Rabins et al. 1991; Sackheim, Prohonik, Moeller, & al., 1993; Steﬀens & Krishnan, 1998; Uradhyaya, Abou-Saleh, Wilson, Grime, & Critchley, 1990), clearly suggesting an association to an increased severity of subcortical vascular disease and greater impairment of cognitive performance (Salloway et al. 1996). More, major depression is more common and more severe in patients with vascular dementia (Ballard, Bannister, Solis, Oyebode, & Wilcock, 1996). Various studies of depression in the elderly reported that mood is more often irritable than depressive (Monfort, 1995), and also several symptoms like loss of weight, feelings of guilt, suicidal ideation, melancholic features, hypochondriasis as well as associated symptoms of psychosis could be more frequent (Brown, Sweeney, Loutsch, Kocsis, & Frances, 1984; Lader, 1982; Lyness, Conwell, & Nelson, 1992; Musetti, Perugi, Soriani, Rossi, & Cassano, 1989; Nelson, Conwell, Kim, & Mazure, 1989). However, these findings vary across studies. Many of these patients manifest a type of behavior that can be characterized as "passive-aggressive" or "self-aggressive." They refuse to get up from bed, eat, wash themselves, or talk. Also, they often hide important information concerning severe somatic disease and in this way they let it go untreated. Somatic symptoms are diﬃcult to assess and, as a general rule, physicians should avoid assigning this symptomatology to an underlying mental disorder. It is highly likely the patient indeed suﬀers from a true "somatic" disorder even in cases the physician is unable to diagnose it (APA, 1994). On the other hand, it is clear that elderly depressives manifest more somatoform symptomatology, in comparison to younger depressives. In this frame, the concept of Masked Depression (Modai, Bleich, & Gygielman, 1982) used to be popular in the past, but today it is not accepted by either classification system although it is accepted that the onset of health concerns in old age is more likely to be either realistic or to reflect a mood disorder (APA, 1994). Percentages of comorbidity between depression and physical illness vary from 6% to 45% (Kitchell, Barnes, Veith, & al. 1982; Kok, Heeren, Hooijer, & al., 1995). The large discrepancy reflects the diﬃculty in the application of operationalized criteria for the diagnosis of depression in patients with general health problems. Greater overall severity of medical illness, cognitive impairment, physical disability and symptoms of pain or other somatic complaints seem to be a more important predictor of depression than specific medical diagnoses (Williamson & Schulz, 1992). About 38-58% (Alexopoulos, 1991) of the elderly suﬀering from major depression also fulfill criteria for an anxiety disorder while many authors have suggested that the presence of anxiety in the elderly should be considered as a sign of depression, even in cases, which lack true depressive symptomatology (Collins, Katona, & Orrell, 1994). In elderly individuals there is an increased possibility of the co-existence of depression and dementia, or some other type of "organic" decline of cognitive disorder. The syndrome of "pseudodementia" has also been described (Kiloh, 1961). This term refers to the manifestation of dementia symptomatology, which in fact is due to depression and disappears after antidepressant therapy. It is also described the emergence of late onset bipolarity in the frame of an ongoing dementing pathology (Akiskal & Pinto, 1999; Akiskal & Benazzi, 2005; Ng et al. 2007) Suicide constitutes an important health problem for the elderly. Elderly men are at a higher risk for completing suicide than elderly women. The co-existence of a serious somatic disease, like renal failure or cancer, represents a major risk factor for a well-planned suicide attempt (Heikkinen & Lonnqvist, 1995). Other risk factors include loneliness and social isolation, usually as a consequence of bereavement. The failure to follow medical advice in serious general medical conditions could be considered to be a form of "passive suicide." On the other hand, "rational" suicide plans are not common even in severely ill patients. There is a possibility of acute-onset suicidal plans (after an acute incidence concerning general health e.g., stroke or heart attack) (Kishi, Robinson, & Kosier, 1996). The pharmacotherapy of late-onset mood disorder includes the cautious use of antidepressants including amitriptyline, imipramine, nortriptyline and all the SSRIs which are most widely prescribed antidepressants among the geriatric population, because of their favorable side-eﬀect profile, relative safety in overdose, ease of use and smaller dosage adjustment makes them first-line choices. Also venlafaxine, mirtazapine, and bupropion could be useful. For bipolar cases, lithium and anticonvulsants are useful although they are not well studied in elderly patients (Fountoulakis et al. 2003). It is mostly used in cases of refractory depression for the augmentation of antidepressant therapy. Antipsychotics, especially second generation ones could be used although there is a warning for a higher mortality because of their use in the elderly. ECT is another option with many studies reporting better outcomes in older than in younger patients. However, by far the most troubling side eﬀect of ECT, especially in the elderly, is cognitive impairment. Psychotherapy is also an option (Gerson, Belin, Kaufman, Mintz, & Jarvik, 1999; Gum & Arean, 2004). The presence and severity of medical illnesses, physical disability, cognitive impairment and psychomotor retardation make psychotherapeutic intervention diﬃcult and aﬀect its eﬃcacy and success. The form of psychotherapy should be adjusted to the patient’s personality, behavior patterns as well as his/her cultural and educational level. Behavioral therapy, cognitive-behavioral therapy and problem-solving therapy have been extensively studied for their eﬀectiveness in the treatment of depression in elderly. Fewer studies have been carried out for the eﬃcacy of interpersonal psychotherapy. Non-standardized psychotherapies such as, psychodynamic psychotherapy and reminiscence therapy, are also proposed as appropriate treatments for geriatric depression. The combination of pharmacological and psychological treatments is associated with higher improvement rates than pharmacotherapy alone and considered more eﬀective than either treatment alone in preventing recurrence of depression (Bartels et al. 2002). In long-term therapies, the addition of psychotherapy promotes adherence to treatment (Pampallona, Bollini, Tibaldi, Kupelnick, & Munizza, 2004). Eventually however, most studies support the opinion that geriatric depression carries a poorer prognosis than depression in younger patients. However, many authors attribute this, to factors like failure to make an early diagnosis and improper or insuﬃcient treatment. For patients with geriatric depression, the prognosis is more dependent on physical handicap or illness and lack of social support, however further research on this issue is needed. Thus, the eﬀective prevention of late-life depression requires attention to maintaining the community infrastructure and support.
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