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It is poorly understood why asthma symptoms are often discordant with objective medical tests. Differences in interoception (perception of internal bodily processes) may help explain symptom discordance, which may be further influenced by mood and attention. We explored inter-relationships between interoception, mood and attention in 63 individuals with asthma and 30 controls. Questionnaires, a breathing-related interoception task, two attention tasks, and standard clinical assessments were performed. Questionnaires were analysed using exploratory factor analysis, and linear regression examined relationships between measures. K-means clustering also defined asthma subgroups. Two concordant asthma subgroups (symptoms related appropriately to pathophysiology, normal mood) and one discordant subgroup (moderate symptoms, minor pathophysiology, low mood) were found. In all participants, negative mood correlated with decreased interoceptive ability and faster reaction times in an attention task. Our findings suggest that interpreting bodily sensations relates to mood, and this effect may be heightened in subgroups of individuals with asthma., Biological Psychology, 165, ISSN:0301-0511, ISSN:1873-6246

The attention level of human beings is a very complicated property of the brain. It has demanded a lot of research work which is still being continued to understand how it works on different situations as the human brain shows a mixed level of attention. The attention level is generally derived from the alpha and beta waves processed in the human brain. With the help of an EEG device which is alternatively called as a brain–computer interface (BCI), it can retrieve the data from the human brain. The sole purpose of this study is to find out how the attention level of the human being gets affected when it turns the moods from normal to the stressed. How much variation does the two moods show in terms of attention. It can also be taken into consideration in finding out how much difference is there in the attention levels of boys and girls keeping for both the moods of the human beings. It has been studied how does the age group affect the brains’ attention level when considered a young and an older group of students. It has been collected data from 30 students each of which were girls and boys and of age groups 20 and 22 years. It has been experimented on the data collected and found that with the normal mood the human showed a better level of concentration and attention level than that of the stressed mood. It has been also noticed that the girls irrespective of their moods showed greater value of attention than the boys. The last results showed that the elder group showed a better level of attention than the younger one concluding that with the increase in age, the attention level gets increased.

Attention-deficit/hyperactivity disorder (ADHD) in adults can resemble, and often co-occurs with, bipolar disorder (BD) and borderline personality disorder (BPD). This can lead to mistaken diagnoses and ineffective treatment, resulting in potentially serious adverse consequences. All three conditions can substantially impair well-being and functioning, while BD and BPD are associated with suicidality.To update clinicians on the overlap and differences in the symptomatology of ADHD versus BD and BPD in adults; differential diagnosis of ADHD from BD and BPD in adults; and diagnosis and treatment of adults with comorbid ADHD-BD or ADHD-BPD.We searched four databases, referred to the new Diagnostic and Statistical Manual of Mental Disorders, 5th edition, used other relevant literature, and referred to our own clinical experience.ADHD coexists in ∼20% of adults with BD or BPD. BD is episodic, with periods of normal mood although not necessarily function. In patients with comorbid ADHD-BD, ADHD symptoms are apparent between BD episodes. BPD and ADHD are associated with chronic trait-like symptoms and impairments. Overlapping symptoms of BPD and ADHD include impulsivity and emotional dysregulation. Symptoms of BPD but not ADHD include frantically avoiding real/imagined abandonment, suicidal behavior, self-harm, chronic feelings of emptiness, and stress-related paranoia/severe dissociation. Consensus expert opinion recommends that BD episodes should be treated first in patients with comorbid ADHD, and these patients may need treatment in stages (e.g. mood stabilizer[s], then a stimulant/atomoxetine). Data is scarce and mixed about whether stimulants or atomoxetine exacerbate mania in comorbid ADHD-BD. BPD is primarily treated with psychotherapy. Principles of dialectical behavioral treatment for BPD may successfully treat ADHD in adults, as an adjunct to medication. No fully evidence-based pharmacotherapy exists for core BPD symptoms, although some medications may be effective for individual symptom domains, e.g. impulsivity (shared by ADHD and BPD). In our experience, treatment of ADHD should be considered when treating comorbid personality disorders.It is important to accurately diagnose ADHD, BD, and BPD to ensure correct targeting of treatments and improvements in patient outcomes. However, there is a shortage of data about treatment of adults with ADHD and comorbid BD or BPD.

The GDS was developed to address the limited applicability of existing depression scales with older adults1,2. One such problem with scales that were developed and validated with younger populations relates to somatic complaints. Though somatic complaints can be a useful indicator of depression in younger samples, it is common for older adults to report somatic problems that can skew the sensitivity and specificity of a screen where older adults are more likely to have false positive depression scores. As such, the GDS does not include many somatic components in the scale and also consists of questions that are appropriate for the ageing population both in content and format. Initially, 100 questions were selected by researchers and clinicians with geriatric experience and administered to both non-depressed and depressed older adults. Of the original 100 items, the 30 items that correlated most highly with the total score were included in the final scale. The scale was designed so that it could be administered easily in a self-rating format that would not be cumbersome for patients or medical personnel2. Most individuals complete the GDS in under 10 minutes. The GDS has a forced-choice response format where individuals are asked to respond yes or no to each item. However, some patients have problems with the yes/no dichotomy, instead preferring to answer ‘sometimes’ by either writing it in or by circling the space between the yes and no responses, though neither is a scored answer. It can help if explicit instructions are provided to patients to respond to each item in the way that best answers the question. In the initial validation study, the examiner read the items orally and recorded responses for individuals who could not complete the form without assistance. However, later studies found significant differences between mean scores for self-administered and staff-administered modes of presentation, with higher scores reported for self-administered scales3,4. There is no significant difference between scores of a card-based administration and verbal administration of the GDS5. For each of the 30 GDS items, the depressive response garners 1 point for a maximum total of 30 points. Regarding general cutoffs, total scores ranging from 0 to 9 indicate normal mood; scores ranging from 10 to 19 indicate mild depressive symptoms, and scores ranging from 20 to 30 indicate severe depressive symptoms. The measure is free to use and in the public domain. It can be accessed at www.stanford.edu/∼yesavage/GDS.html.

Depressive disorders are commonly occurring psychiatric conditions that tend to run in families. They are heterogeneous and complex, predicted to involve the interplay between multiple genes and nongenetic risk factors, such as stressful life events. Their phenomenology and biological substrates are not clearly distinguished from those of normal mood states on the one hand and frequently comorbid conditions such as the anxiety disorders on the other, further complicating research into their etiology. Preliminary molecular genetic studies performed over the past several decades have implicated only a modest number of specific candidate genes in major depression, thus far offering little insight into its pathophysiological basis. This leaves open the way for a new wave of large-scale, genome-wide association studies that are providing vastly increased amounts of preliminary data for understanding these important conditions.

Nothing is more familiar to people than their moods and emotions. Oddly, however, it is not clear how these two kinds of affective processes are related. Intuitively, it makes sense that emotional reactions are stronger when they are congruent with a preexisting mood, an idea reinforced by contemporary emotion theory. Yet empirically, it is uncertain whether moods actually facilitate emotional reactivity to mood-congruent stimuli. One approach to the question of how moods affect emotions is to study mood-disturbed individuals. This review describes recent experimental studies of emotional reactivity conducted with individuals suffering from major depression. Counter to intuitions, major depression is associated with reduced emotional reactivity to sad contexts. A novel account of emotions in depression is advanced to assimilate these findings. Implications for the study of depression and normal mood variation are considered.

The cortical areas involved in processing of emotional prosody (EP), such as joy or sadness, have been reported to be localized in the right basal ganglia, frontal lobes or bilateral temporal lobes in recent fMRI studies. Moreover, event-related brain potentials have not been shown to have ERP components with latencies associated with EP recognition, namely N1, P2 and P3. So, we investigated a processing of EP using magnetoencephalography (MEG), which has a high time and space resolution. In the test session, an emotional voice (expressing joy, sadness or normal mood, and calling a name consisting of 5 moras) was presented, followed by a 900 ms interstimulus interval and then an emotional face (the same emotion as the voice) was displayed for 1000 ms. The subjects were requested to judge whether or not the emotional features of the voice and face were identical. In the control session, the emotional voices were presented while the subjects carried out visual working memory (n-back) tasks between two sessions, and significant differences in the cortical activities associated with processing of EP were observed during the latencies in different periods after the onset of stimuli in both hemispheres.

Depression occurs twice as often in patients with diabetes and is associated with reduced compliance with exercise, diet, and medications. It is also associated with hyperglycemia and increased diabetic complications. Despite evidence that successful treatment is associated with improved glycemic control, many cases of depression are left untreated. Objectives. (1) Evaluate a combination screening strategy in an outpatient population; and (2) explore the association between glycemic control and depressive symptomatology. Methods. Ninety-two patients completed the Patient Health Questionnaire (PHQ-2). Patients with a PHQ-2 score ≥ 1 completed the 16-item Quick Inventory of Depressive Symptomatology (QIDS-SR16). Using the QIDS-SR16, a score of ≤5 corresponded to normal mood, with scores above 5 corresponding to increasing severity of depressive symptoms. Glycemic control was assessed by glycosylated hemoglobin (HbA1c). Results. Using a PHQ-2 cut-off score of ≥3, 37% of the sample screened positive for major depressive disorder (MDD), with an additional 27% reporting sub-threshold symptoms. The depressed group reported significantly more difficulty with reduced interests, insomnia, concentration, self-criticism, energy/fatigue and depressed mood. In terms of glycemic control, there was a marginally significant effect for race and HbA1c. Conclusion. The combined PHQ-2 and QIDS-SR16 can facilitate prompt detection of MDD and provide a means of monitoring specific symptoms and progress once treatment commences.

Objective. As polypharmacy is routinely used for the treatment of bipolar disorder, the relation between the daily number of psychotropic medications and self-reported mood was investigated. Method. Eighty patients (35 men and 45 women) with a diagnosis of bipolar disorder I or II, recruited from academic centres, entered their mood, sleep, and psychotropic medications for 3 months into ChronoRecord software. A total of 8662 days of data was received (mean 114.7 days/per patient). Results. Seventy-nine patients took a mean of 3.8 medications daily (SD 1.7; range 1-9); one took none. Of these patients, 73 (92.4%) took mood stabilizers, 47 (58.8%) took antidepressants, 31 (38.8%) took antipsychotics, 34 (42.5%) took benzodiazepines and 17 (21.1%) took thyroid hormones. Patients reporting normal mood more frequently took fewer medications; the Pearson correlation coefficient between the number of medications and the percent of days normal was -0.481 (P 0.001). Grouping by number of medications, ANOVA analysis showed those taking fewer medications reported normal mood more frequently (P0.001). Conclusion. Combination treatment regimens are routinely prescribed for bipolar disorder. Patients reporting normal mood more frequently took a fewer number of daily medications. Studies are needed to better identify those patients who would benefit from polypharmacy and to optimise the combinations of medications for patients with refractory disorder.

Two studies examined the relationship between memory recall and subjective probability judgement in an attempt to understand the mechanisms involved in depressive future thinking. In study 1, the relationship between general impression memory (GIM) latencies and subjective probability, and the relationship between specific event memory (SEM) latencies and subjective probability, were examined in normal mood individuals. Results demonstrated that GIM latencies were correlated with subjective probability. That is, participants who were faster to say they had experienced events in the past also thought themselves more likely to experience similar events in the future. In contrast, SEMs were not significantly correlated with subjective probability judgements. Study 2 tested the prediction that the same mechanism is operative in depression, but in this instance it is differential accessibility of negative memories which biases judgements for future events. As predicted, depressed patients, relative to controls, recalled more negative events and rated negative events as more likely to happen to them in the future. However, subjective probability judgements were not associated with the recall of either GIMs or SEMs in depressed patients, but GIMs were correlated with subjective probability judgements in the control participants. Copyright © 2000 John Wiley & Sons, Ltd.

SummaryMood disorders are characterized by manic and depressive episodes alternating with normal mood. While social function is heavily impaired during episodes of illness, there are conflicting opinions about inter-episode function. The present paper focuses on self-esteem and social adjustment in remitted mood disorders patients.Patients with mood disorders (99 bipolar and 86 major depressive subjects, in remission) were compared with a group of 100 control subjects. The self-esteem scale (SES) and the social adjustment scale (SAS) were used to measure self-esteem and social adjustment, respectively, in both groups of subjects.Patients with mood disorder exhibited worse social adjustment and lower self-esteem than control subjects.These results strongly confirm previous observations of poor inter-episode function in patients with mood disorder.

Background There are several indications that malfunctions of the circadian clock contribute to depression. To search for particular circadian gene polymorphisms associated with depression, diverse polymorphisms were genotyped in two samples covering a range of depressed volunteers and participants with normal mood. Methods Depression mood self-ratings and DNA were collected independently from a sample of patients presenting to a sleep disorders center (1086 of European origin) and from a separate sample consisting of 399 participants claiming delayed sleep phase symptoms and 406 partly-matched controls. A custom Illumina Golden Gate array of 768 selected single nucleotide polymorphisms (SNPs) was assayed in both samples, supplemented by additional SNPlex and Taqman assays, including assay of 41 ancestry-associated markers (AIMs) to control stratification. Results In the Sleep Clinic sample, these assays yielded Bonferroni-significant association with depressed mood in three linked SNPs of the gene FMR1: rs25702 (nominal P=1.77E-05), rs25714 (P=1.83E-05), and rs28900 (P=5.24E-05). This FMR1 association was supported by 8 SNPs with nominal significance and a nominally-significant gene-wise set test. There was no association of depressed mood with FMR1 in the delayed sleep phase case–control sample or in downloaded GWAS data from the GenRED 2 sample contrasting an early-onset recurrent depression sample with controls. No replication was located in other GWAS studies of depression. Our data did weakly replicate a previously-reported association of depression with PPARGC1B rs7732671 (P=0.0235). Suggestive associations not meeting strict criteria for multiple testing and replication were found with GSK3B, NPAS2, RORA, PER3, CRY1, MTNR1A and NR1D1. Notably, 16 SNPs nominally associated with depressed mood (14 in GSK3B) were also nominally associated with delayed sleep phase syndrome (P=3E10-6). Conclusions Considering the inconsistencies between samples and the likelihood that the significant three FMR1 SNPs might be linked to complex polymorphisms more functionally related to depression, large gene resequencing studies may be needed to clarify the import for depression of these circadian genes.

Effects of enacted maternal withdrawal and depression were observed in a sample of 18-36-month-old children during counterbalanced brief (10-min) episodes of simulated depression and normal affect. As predicted, when mothers enacted withdrawal and depressed affect by becoming less positive, expressive, involved, talkative, and responsive, toddlers physically withdrew from them, made more negative physical bids for attention, and became more unfocused and generally negative. Children accepted their unresponsive mothers' infrequent interaction bids, but did not attempt to comfort them when they appeared depressed. In mothers' normal mood episodes, children were more positive, were never unfocused, and played closer to their mothers. As expected, toddlers reacted negatively to transitory maternal withdrawal and depressed affect, displaying their distress in a developmentally appropriate manner.

Publisher Summary This chapter reveals that depression in children and adolescents has often been overlooked or minimized as normal mood swings that accompany developmental changes. In fact, until the past few decades, the spectrum of depressive disorders was not considered applicable to the pediatric population. Depression in children is no longer being dismissed, and researchers and clinicians now recognize it as a substantial problem affecting peer relationships, home life, academics, and physical well-being. Recognizing depression in children is complicated by several factors. Self-reports usually are not obtainable with infants and toddlers. Since most young children are not able to adequately verbalize what they are feeling, clinicians and researchers must rely on information gathered from parents, teachers, and other significant adults in the child's life. Although teenagers are usually able to express their feelings, they may resist doing so and view depression as a sign of weakness. In addition, depressive symptoms may be masked by co-occurring conditions.

Background For the purposes of our research programme we needed a simple, reliable and validated method for allowing choice of a color in response to a series of questions. On reviewing the literature no such instrument was available and this study aimed to rectify this situation. This was achieved by developing a simple method of presenting a series of colors to people validating it in healthy volunteers and in individuals where color choice might be distorted, namely anxiety and depression. Methods A series of different presentations of four shades of eight colors and grey, as well as black and white were evaluated. 'Mood', 'favourite' and 'drawn to' colors were assessed in 105 healthy, 108 anxious and 110 depressed participants. The positive, neutral or negative attribution of these colors was recorded in a further 204 healthy volunteers. Results The circular presentation of colors was most favoured (Color Wheel). Yellow was the most 'drawn to' color and blue the commonest 'favourite' color in all subjects. Yellow was most often associated with a normal mood and grey with an anxious or depressed mood. Different shades of the same color had completely different positive or negative connotations. Reproducibility was exceptionally high when color choice was recorded in positive, neutral or negative terms. Conclusions The Color Wheel could be used to assess health status, mood or even treatment outcome in a variety of clinical situations. It may also have utility in circumstances where verbal communication may not be optimal, such as with children.

We report a natural experiment that took place in a cardiac intensive care unit (CICU). We had been alerted to the possibility that sunny rooms would be conducive to better outcomes by our findings in the psychiatric unit, and by reports that depressed cardiac patients did less well than those in normal mood. The 628 subjects were patients admitted directly to the CICU with a first attack of myocardial infarction (MI). Outcomes of those treated in sunny rooms and those treated in dull rooms were retrospectively compared for fatal outcomes and for length of stay in the CICU. Patients stayed a shorter time in the sunny rooms, but the significant difference was confined to women (2.3 days in sunny rooms, 3.3 days in dull rooms). Mortality in both sexes was consistently higher in dull rooms (39/335 dull, 21/293 sunny). We conclude that illumination may be relevant to outcome in MI, and that this natural experiment merits replication.

Numerous studies have examined the acute antidepressant effects of prefrontal transcranial magnetic stimulation (TMS). However, there is little information on whether TMS can be used as a maintenance treatment to maintain normal mood once subjects have responded. We describe seven adults with bipolar depression who responded acutely to TMS and were then treated with TMS weekly for up to 1 year. TMS was carried out over the left prefrontal cortex at 110% motor threshold, 5 Hz for 8 s for 40 trains. Three subjects completed 1 full year of weekly TMS with an average Hamilton Rating Scale for Depression of 13 (sd = 5.9) over the year. These data suggest but do not prove that TMS might eventually be used as an adjunctive maintenance treatment for at least some patients with bipolar depression. Much work remains.

Until 1980, manic depressive illness (MDI) was defined as follows: the presence of recurrent severe depressive or manic episodes alternating with periods of normal mood or markedly decreased mood symptoms.[1][1] In that year, the DSM-III rejected this definition of MDI and replaced it with two

A considerable amount of evidence has accumulated indicating a greater rate of depression among females compared to males. In addition, recent investigations have revealed distinct patterns of depressive responding as a function of sex. The present study provided a cross-validational test of findings reported by Funabiki and colleagues. Male and female college students indicated the likelihood that they would engage in 79 behavioral analytically derived behaviors or cognitions if depressed. Stepwise discriminant function analyses were performed to determine maximum separation of male and female responses. This procedure yielded a 55.6% overall variable cross-validation rate. Many of the findings were consistent with Radloff and Rae's theoretical view of sex differences in learned susceptibility to depression. The data also suggest several avenues for future research and support the utility of investigating theories of depression within the context of a continuity between normal mood states and depressive phenomena.

30 patients suffering from therapy-resistant chronic pain were divided into three groups according to drive and mood: I. psychomotor inhibition combined with depressive mood, II. agitation and depressive mood, III. agitation combined normal mood. The psychopharmacological treatment of pain showed sufficient results, when the drugs were directed to the target symptoms "agitation", "lack of drive", and "depression". The differentiated administration of activating or sedative antidepressants and neuroleptics caused reduction or absence of pain while the routine administration of neuroleptics (i.e. chlorpromazine) was less effective.

In the whirl of the holiday season, the maintenance of normal mood is no mean task. Demoralization and despair are no paradox, no mystery, no fashionable topic. Nevertheless, they are also not depression, not a disorder, not a disease, but a predictable, genuine human reaction to an annual social ritual. Language: en

Four hundred sixty-nine female and 311 male college students were administered a depression scale, an analogies test, and questions related to expectations and evaluations of performance. As predicted, significant negative correlations were found between subclinical depression and expectations and evaluations of performance. A significant negative correlation between depression and actual performance was apparent for females only. However, this correlation was much weaker than similar correlations previously reported for college student populations. It was concluded that low performance expectations constitute one dimension of subclinical depression. This suggests that Beck's theory of clinical depression, which holds that negative self-perceptions and other cognitions are importantly involved in depression, may be useful in understanding normal mood variation. The findings also suggest that some similarities exist between clinically and subclinically depressed groups in that both groups are reported to hold low performance expectations, but display minimal performance deficits.

Monoamines have been associated with affective disorders following observations with mood elevating and mood depressing drugs. In addition, abnormalities in the metabolism of the biogenic amines have been reported in these illnesses. Experimental studies on animals have further supported the view that both catecholamines and indoleamines are important for the maintenance of normal mood states. The monoamine hypothesis of affective disorders states that severe depression is associated with a relative deficiency of brain monoamines, while clinical improvement follows correction of this deficit. The converse applies to mania and antimanic treatments. The evidence for these assertions is critically examined, and pertinent experimental observations will be discussed. The monoamine hypotheses of Brodie and of Dewhurst are examined to integrate the findings reported, and the biogenic amines will be shown to be only part of a more complex biochemical disturbance involving the hypothalamic-pituitary-adrenocortical system.

The simultaneous recording of spontaneous EDA (mono and diphasic SPR), HR and mood self-rating ( Q -sort of adjectives), on 35 normal subjects, for 5 consecutive weeks has shown that: 1. (1) The emission of diphasic SPR is significantly related to an increase in monophasic EDA (in frequency and in amplitude) and to a lesser degree with HR acceleration; 2. (2) Such a physiological pattern is significantly associated with depressive mood, though independent from anxious mood. These results confirm the importance of morphological aspects of SPR in assessing normal mood states .

Stress is a hypothetical construct which has been extensively studied for the past three decades at different levels of analysis. It is a ubiquitous concept in physiology, psychology and medicine that often eludes precise definition. Hans Selye conceptualized stress as “a nonspecific response to any demand upon the body (usually, but not always, noxious), or anything which causes an alteration of homeostatic processes (1)”. A more modern version of this definition, taken from Burchfield (2) has emphasized the concept of psychological homeostasis or the maintenance of a normal mood state at rest. All emotions then are changes from this state. Indeed, as Dr. John Mason showed so elegantly, without emotional changes accompanying a stressor, the stress response is minimal (3). Thus commonly accepted physiological “stressors” (heat, excercise, hunger) do not elicit a “stress response” when they are presented in a way that eliminates their psychological (emotional) effects (fear, conflict, uncertainty, frustration).

Depression covers a wide range of human, emotional, and clinical states. As a normal mood, depression is ubiquitous in human existence; not to grieve after the loss of a loved one is to make one “less than human.” As a symptom, depression occurs in a wide variety of reactions to stress, medical, and psychiatric conditions. As a clinical state, the various psychiatric syndromes are usually considered along with mania as belonging to the affective disorders.

From the point of view of exact diagnosis perhaps no psychiatric condition is as unsatisfactory as depression. It can be a symptom or a diagnosis. It is recognized as a normal mood. There is even considerable variation in the diagnostic use of the term. The diagnoses manic-depressive psychosis, involutional depression, reactive depression, neurotic depression, etc., are still widely used, even though they no longer have official standing. To add to the semantic confusion, it must be admitted that the diagnosis of depression in psychiatry is still largely impressionistic and lacks precision. The psychiatrist bases his clinical opinion on a careful evaluation of the history, the complaints, the appearance of the patient, the course under observation or treatment, psychological tests, and intuition. As bad as this state of affairs is, the diagnosis of suicide risk is even worse. Here even educated guessing it notoriously fallible

In Reply.— It was somewhat disappointing to learn that our recent research on the prevalence of psychiatric disorders among cancer patients was not found to be instructive by Dr Schacter; however, on reading his letter, I believe the reasons for this pedagogic failure are rather clear. The fundamental problem seems to reside with the fact that Dr Schacter does not assign the process of diagnosis the same pivotal status in psychiatric disorders that he presumably does in medicine in general. Taking depression as an example, he fails to discriminate between depression as a normal mood state, a symptom, a clinical syndrome, or a disease entity. Although it may be perfectly "appropriate" and understandable to react to the news of a cancer diagnosis with depressed mood, it is another matter to experience a major affective disorder (depression) concomitantly with cancer. This is particularly true since optimal treatments for the two conditions

The title of this work might lead us to expect a comprehensive text on depressive illness, but this is not the author's intent. Edith Jacobson is an outstanding psychoanalytic clinician and theoretician. This book is a collection of her papers on the psychoanalytic conceptualization and treatment of depression, as it appears in normal mood swings and in neurotic and psychotic personalities. Furthermore, the book is not designed to be a comprehensive study of all psychoanalytic views of depression. Rather, it records the struggles of one particularly gifted person to understand depression within the framework of classical Freudian psychoanalytic theory and the ego-psychological studies of Heinz Hartmann. In all of the papers Dr. Jacobson presupposes familiarity with classical psychoanalytic concepts and with the influential work of Hartmann. The book starts with a 40-page paper on the psychoanalytic theory of affects. Some readers may have difficulty following Jacobson's theoretical exposition. For them

ministration Hospital in Tuscaloosa, Alabama, it has been receiving new emphasis, however. It is our philosophy that emotional needs can be met through the consistent use of specific, prescribed attitudes by all those with whom a patient comes in contact. If such a treatment program is to be successful, all members of the hospital team must understand, support, and use the prescribed attitudes. An attitude is the way one feels toward an individual or an experience; it evolves out of one's past xperiences. Since we learn to modify or change our attitudes through the influence of other people, it is obvious that attitudes can change attitudes. This is seen in the hospital when team members, through the use of attitudes, successfully produce changes in the attitudes of patients and co-workers and, thereby, produce changes in behavior. Attitude therapy can perhaps best be understood by examining one's own feelings and responses to others during various normal mood changes. A normal friendly response to a person's approach changes, for example, when one feels blue to "Go away; leave me alone." However, if one is in a cheerful mood, the response probably would be one of acceptance, and interaction would be invited. Since the difference in behavior

Clinical manifestations of disease are in the final analysis the result of altered physiologic or biochemical relations. This is true whether one observes the direct evidence of abnormal function or the compensatory reactions invoked to counteract abnormal forces. The central nervous system is no exception to this principle. And this is no less true whether one deals with disease directly involving the central nervous system or with the effects on it of disease having its origin elsewhere. This report is concerned with secondary effects. Neuropsychiatric complications of underlying disease may vary widely from mild aberrations of normal mood and behavior to sweeping disturbances that dominate the entire clinical picture and may obscure the disease itself. The basis for these reactions depends primarily on the fundamental nature of brain metabolism. The central nervous system has the most exacting metabolic requirements in the body. Unlike other tissues, it is primarily aerobic in