Brain Protection in Schizophrenia, Mood and Cognitive Disorders

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Experts agree that once cognitive decline is accelerated and properly identify, it is advisable a prompt intervention [ 2 ]. During periods of nutritional deficiency of omega-3 fatty acids, DHA is retained to depletion from the phospholipids of neurons through two possible mechanisms: a DHA released from membrane phospholipids is rapidly reacylated to specific phospholipids. Mood disorders, such as depression, schizophrenia, and post-partum depression, have also been associated with modification of DHA metabolism.

This transitory and still reversible stage is usually termed mild cognitive impairment [ 47 ]. However, once it is clinically diagnosed there is little prospect of improving the prognosis. The pathology is characterized by the formation of amyloid plaques, neurofibrillary tangles, and dystrophic neuritis. With aging, neural membrane fluidity is compromised due to the increased presence of cholesterol, and reduced activity of glial desaturase enzymes and blockages to phospholipids pathways of transduction signals and oxidative stress, all of which are inversely associated with omega-3 polyunsaturated fatty acids [ 49 ].

In cognitive test animals expressing high levels of a mutant amyloid precursor protein, showed low levels of DHA in brain phospholipids. DHA provided by supplementation e. Depression is characterized by high levels of depressed or low mood, a lost in interest or pleasure in nearly all activities, changes in appetite, weight, sleep or activity, decreased energy, difficulties in thinking, concentration or making decisions, feeling or worthlessness or guilt, and recurrent thoughts of death or suicidal ideation, plans or attempts.

Brain Protection in Schizophrenia, Mood and Cognitive Disorders

Depression and major depressive disorder are serious affective illness with a high lifetime prevalence rate that particularly involves neurotransmission processes, especially serotonin receptors and membrane transporters [ 59 ]. The World Health Organization estimates that depressive disorder will become the second leading cause of disability worldwide by , second to ischemic heart disease, and will be the leading cause in developing regions [ 60 ].

The etiology of the illness is multifactorial and is influenced by genetic, environmental and nutritional factors. Epidemiologic, neurobiologic, and clinical studies suggest that a relative deficiency in omega-3 polyunsaturated fatty acids contributes to depression. Support for a nutritional contribution to the disease derives from studies that report an inverse correlation between the level of omega-3 fatty acids as measured either in red blood cells phospholipids or adipose tissue, and symptoms of depression.

Numerous studies carry-out over the last few years are involving omega-3 long-chain fatty acid supplementation with the reduction of any of the symptoms of different forms of depression, including bipolar disorders, postpartum depression included forward , agoraphobia, and anorexia nervosa. According to meta-analysis realized by Lin and Su [ 62 ], it is concluded that DHA supplementation may reduce the symptoms of depression.

Depression and coronary artery disease often occurs in the same individuals who frequently have low plasma levels of DHA and high levels of AA.

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Omega-3 supplementation shows as effective for the treatment of these disorders. Reducing omega-6 polyunsaturated fatty acid intake as well as increasing omega-3 polyunsaturated fatty acids, specifically DHA, for a more balanced ratio may be beneficial [ 63 ]. However, the mechanism by which DHA may reduce depression is still unclear, and more research is needed.

As discussed, increasing the nutritional level of omega-3 fatty acids may modify the activity of integral membranes proteins receptors, ion channels, molecular pumps, etc. However, there is no consensus about the positive effect of omega-3 fatty acids in depression which is accompanied with other comorbid.

Depression during pregnancy and postpartum depression have negative impact on the development and health of the newborn. Maternal stress in humans is associated with fetal hypoxia, reduced gestational age, and low birth weight. Evans et al. A cross-national analysis of seafood consumption, and the DHA content of breast milk, demonstrated an inverse correlation with the prevalence of pregnancy and postpartum depression.

The prevalence varied from 0. Such transfer to the baby through the placenta and, subsequently through breast milk poses a risk to women to significant depletion of omega-3 fatty acids during lactation, contributing to the perinatal risk of depression. A review by Parker et al. Women and their physicians prefer options to standard antidepressant medication during pregnancy and postpartum. DHA supplementation during these periods may be a plausible alternative.

Comparison of bipolar disorder and schizophrenia - Wikipedia

However, more clinical trials are needed to confirm the recommendation of omega-3 fatty acid supplementation to avoid or reduce symptoms of depression [ 3 ]. Schizophrenia is defined by a mixture of characteristics positive and negative signs and symptoms which have been present for a significant proportion of time during a one-month period with indications of the disorder persisting for at least six months.

Positive symptoms reflect an extension or distortion of normal functions, for example, delusions, hallucinations, and disorganized speech or behavior. Negative symptoms reflect a diminution or loss of normal functions, for example, restrictions in the range or intensity of emotional expression, restriction in the fluency or productivity of thought or speech, and restrictions in the initiation of goal-directed behavior [ 66 ].

Schizophrenia is a psychiatric disease that affects The predominant hypothesis regarding the pathophysiology of the disease is dysfunction of the dopaminergic system. However further finding concerning the disease suggests a close relationship with reduced tissue levels of omega-6 and omega-3 fatty acids specially AA and DHA [ 67 ]. While taking the psychiatric examination, the patient remained awake, with hypoprosexia, temporal and spatial disorientation, hypokinesia and upper stereotyped movements.

He showed no response to external stimulation nor to simple verbal commands and sometimes became restless when hearing his name. He was unable to speak complete words, babbled unspecific sounds and did not seem to understand the examiner's questions. A decrease in displays of affectivity and inaccessible memory were also verified. No hallucinatory attitude was observed. An investigation of his prior medical history revealed a Papilliferous Carcinoma of the Thyroid, treated with total resection in His post-surgical control and treatment in an outpatient endocrinological clinic was irregular and the patient abandoned the treatment altogether, at the onset of psychiatric symptoms.

It has been verified family history of schizophrenia on his maternal grandparents. Despite the treatment adopted, cognitive deficits reminded, such as severe dementia syndrome aphasia, alogia, temporal and spatial disorientation and movement disorders. In light of the complexity of the case, he was transferred to a general hospital.

We also look into an extreme case of extensive CC, derived from iatrogenic hypoparathyroidism. The patient's initial clinical manifestations consisted in a delusional-hallucinatory syndrome, with characteristics of paranoid schizophrenia, and he also had a positive family history of mental disorder.

The atypical characteristics of his syndrome were the absence of a premorbid personality and the late onset, in his fifties. The post surgical hypoparathyroidism and the period of time that elapsed until the onset of psychiatric symptoms are compatible with the patient's clinical condition, as well as the laboratory and imaging findings 1, However, it's likely that hypothyroidism contributed to the patient's cognitive-motor neurological condition. Seizures and signs of tetany could be seen in most of the cases described 3,4,6,7 , yet our patient only manifested the latter.

Despite the protective effect of the blood-brain barrier, the sub cortical nuclei are vulnerable to impregnation by minerals such as copper Wilson's disease , iron neurodegeneration associated with pantothenate kinase and calcium 3,4,8. CC occurs in several clinical conditions Table 1 and may commonly be classified as part of three main groups: Idiopathic, Familial and especially calcium and phosphorus metabolic disorders 1. Calcifications are usually located at the basal ganglia, dentate, thalamus and semioval center 1.

In cases of primary hypoparathyroidism, calcifications tend to be diffuse, while in secondary hypoparathyroidism they tend to be more localized 3. Recent histochemical studies have revealed the presence of other chemical elements in these lesions such as copper, zinc, magnesium, aluminum, potassium, iron and calcium. These elements surround the organic matrix and lead to mineralization 3. Special attention should be given to iron, which is found in higher concentrations in these CC regions and apparently increases local dopaminergic neurotransmission 3.

Clinical manifestation seems to vary according to the patient's age at the onset of the calcification process: from 20 and 40 years of age symptoms are predominantly manifested as schizophreniform psychosis, with no neurological signs 3. When the onset occurs after 49 years of age, the psychosis is often accompanied by disorders of movement and dementia 3.

Psychotic symptoms characterized by paranoid delusions, auditory hallucinations sometimes musical , complex visual hallucinations, hiker behavior and catatonic states, were reported within this age range 3,5. The extension of the calcification and the severity of the neuropsychiatric symptoms are directly correlated, even though they bear no relationship to any specific kind of symptomatology 3.

Our patient developed belated psychiatric symptoms and had already been diagnosed with dementia, close to the kind of outcomes found in literature on the subject 6, In most patients the prognosis is negative, with permanent cognitive and behavioral damage 6,7,11, Similar case reports have been found for patients with Fahr's disease 6. Treatment of the underlying cause, when possible, can improve neuropsychiatric symptoms, yet rarely stops the progression of CC Clinical intervention in electrolytic disturbances and intoxications is mandatory. The theoretical benefit of using chelating agents deferoxamine, penicillamine has not been proven by clinical studies up to this date 2,4.

The psychotic symptoms may not respond to antipsychotic medication. Lithium carbonate is recommended for refractory patients 1. Mental disorders derived from organic causes are generally reversible, if the appropriate treatment is started early on in the process. Metabolic disturbances linked to calcium and phosphorus are potential causes of severe neuropsychiatric syndromes and permanent cognitive damage.

Excluding organicity is mandatory in any psychiatric diagnosis investigation. The other authors helped with the bibliography, discussions on the theme and final copy-editing. Lishman's Organic Psychiatry. Neurology and clinical medicine. New York: Churchill Livingstone, Mineralization of basal ganglia: implications for neuropsychiatry and neuroimaging. Psychiatry Res. Manyam V. What is and what is not Fahr's disease. Parkisonism Relat Disord. Schizophrenia and familial idiopathic basal ganglia calcification: a case report.

The peak of illness onsets falls in the period of life in which major socioeconomic development takes place. Equal proportions of high-risk individuals and controls, in the mean, are capable of finishing basic school education, but the former frequently drop out of lengthy further education, for example, university. In terms of marriage, patients do not differ from controls at illness onset, but they fall behind their healthy peers during the prodromal phase. This also applies to their occupational career e. Due to their lower age at illness onset, male patients suffer a greater number of and more pronounced social deficits at illness onset compared with women.

Another factor influencing the social course—mediated by therapy adherence and coping behaviour—is the adverse social behaviour exhibited by young men falling ill with schizophrenia: self-neglect, lack of hygiene, lack of interest in finding or keeping a job, and lack of interest in leisure activities and social contacts [ ]. In contrast, women with schizophrenia tend to exhibit socially positive behaviour, for example, over-adaptiveness and conformity [ ]. All these conclusions apply only to the age range studied 12 to 59 years [ ].

The situation is different after 60 years of age when working life comes to an end and certain risk factors and the living conditions change. In countries with well-developed social safety nets, pension systems guarantee the socioeconomic status of the elderly. Long-standing partnerships tend to reduce losses in this domain. A stable matrix of psychological reaction patterns reduces the risk of extremely severe symptoms appearing at illness onset.

As a consequence, the risk of experiencing adverse effects in the socioeconomic and personal domains is also reduced. Although the features of mental disintegration and social deterioration are lacking, late-onset psychoses must be classified as part of the disease construct currently called schizophrenia. Unlike in the prodromal phase, it is the treated rather than the natural course of schizophrenia that can be studied after first admission, because it would be unethical to withhold treatment for research purposes.


Like incidence and prevalence, the results of follow-up studies, too, depend on the underlying diagnosis. The requirement for a diagnosis of schizophrenia according to the DSM-III to -V that functional impairment has persisted for at least six months and positive symptoms for at least four weeks prior to initial assessment yields an excess of poor illness courses.

In contrast, the criteria of the ICD-9 and four weeks of symptoms without an indication of functional impairment lead to a selection of more acute and benign illness courses. This has prognostic implications for course and outcome. In studies proceeding from population-based cohorts of first-episode cases of ICD-9 or schizophrenia, the psychotic symptom dimension, as based on mean scores for males and females, displays neither significant deterioration nor significant amelioration over the medium-term course 5 years or so following the remission of the first episode [ 60 , ].

There is an important distinction to make between outcome studies and longitudinal studies. Outcome studies compare findings between an initial and a follow-up assessment pre-post comparisons. The illness course between these timepoints has to be reconstructed: the longer the period in question, the higher the risk of misinterpretation. More assessments done over the period covered yield a more realistic picture of the illness course [ ]. In the s, a few European longitudinal studies covering histories of illness of 20 years or more were published Table 1. Although the information provided on the inclusion criteria, histories of illness 20 to 40 years , and the assessment and evaluation methods used was in part incomplete or lacking and these parameters varied a lot across the studies, the simple outcome rates were fairly similar in size, except for the study listed at the bottom of Table 1 [ ].

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These surprisingly favourable results attracted a lot of interest in the USA, especially since they fell in the period when convergence to European diagnostic definitions was under way in the USA [ 72 , 73 , 77 ]. The DOSMeD Study reported higher proportions of acute psychosis showing rapid remissions in developing countries compared with industrialized countries. This transcultural difference has not yet been explained conclusively despite several attempts. Two recent longitudinal studies from a high-income country Germany are worth mentioning: the one assessed first-admission patients with schizophrenia Schneiderian first-rank symptoms in age range 15 to 44 years at nine cross-sections initial; follow-up over a period of Seven cross-sectional assessments were done with half of the sample and only one follow-up assessment was conducted with the rest.

But, as already mentioned, the bulk of social impairment is suffered in the prodromal phase. More female than male patients were married, but their number was lower than that for married healthy controls. Both male and female patients showed a high rate of divorce, but it was almost exclusively female patients that had remarried after illness onset. Large proportions of male patients, but very few women with schizophrenia, were living in residential homes or supervised apartments [ ]. More or less similar results have been reported from the follow-up assessments of samples from the WHO longitudinal studies of schizophrenia, comparable in their methods and designs—done, besides in Mannheim Germany [ — ], in Nottingham UK [ ], and in Groningen NL [ ].

Both the medium and the long-term course of schizophrenia are influenced by age. Illness onset in youth and adolescence is associated with social stagnation rather than social decline, because illness at this early age impedes typical social ascent. Late-onset illness, after a long period of life lived in health, usually permits patients to experience normal social ascent. This is why these patients tend to suffer considerable social decline.

Patients with illness onset at an intermediate age occupy an intermediate position between these two groups [ ]. Modal values for the overall course of schizophrenia that would be valid worldwide are impossible to calculate due to the heterogeneity of sociocultural environments, due to differences in the proportions of acute, rapidly remitting cases and due to the variation in the quality of the studies on the topic.

A finding that has implications for our understanding of schizophrenia is the missing or only modest deterioration in both the symptom-related and social course, as based on mean values, in the period starting some time after the remission of the first episode on average about 2 years , while individual illness courses vary a lot. The way Kraepelin understood the disease concept, that is, as a progressive process leading to increasing deficits, is applicable only to a tiny proportion of cases. Typical of the symptom-related course of schizophrenia are irregular relapse episodes with intervals occurring in between with only few, if any, symptoms present [ , ].

The number of episodes depends on their definition. To ensure comparability of the results, the authors of the ABC Schizophrenia Study [ 60 , , ] right censored history of illness mean Over the period of months, the authors counted a total of psychotic relapse episodes, operationalized by an at least day period of increasing symptoms between two at least 4-week intervals of decreasing symptoms. The fact that the number of episodes varied from 0 to 29 with a mean of three per patient reflects the heterogeneity of the illness course [ , ].

The great variation observed in the illness courses was one of the reasons why attempts have been made to identify simple course types that would be of prognostic relevance in clinical practice. Harding [ ] compared longitudinal studies, two from Switzerland and one from the USA, on the basis of eight course types. The criteria Harding used for defining the course types and estimating the proportions of patients exhibiting them are not precise enough, so the results are not really comparable Figure 3.

For this reason, British authors [ ] limited the number of course types to four and defined them by simple criteria—number of episodes, presence of functional impairment, and persistence of versus increase in symptoms and impairment Figure 4. Simple models like this are more useful in clinical practice. As stated, individual illness courses differ a great deal.

In a small proportion—about equal in size—the disorder has a progressive course sometimes leading to need for residential care. The life-expectancy of patients with schizophrenia is considerably reduced compared with that of general populations [ , ]. The figures vary. A meta-analysis of 37 studies calculated a median standard mortality rate of 2. It means that the risk of dying in the following year is 2. Brown et al. According to Seeman [ ], the life-expectancy of persons with schizophrenia was 61 years compared with 76 years for the general population. Controlling for age, Colton and Manderscheid [ ] found a median of lost years of life varying from 25 to 30 years in several US states, a surprisingly high figure.

A direct comparison of age at death for persons with schizophrenia on data from the national psychiatric case register in Denmark and for the Danish general population revealed considerable differences [ ]. Men with schizophrenia had a mean of An excess mortality risk for patients with schizophrenia can, thus, be regarded as established. Schizophrenia as such is not a deadly disease. Nowadays, when the risk of death can be successfully warded off by timely recognition and appropriate treatment, it is nearly exclusively from countries with inadequate health care systems that fatal outcomes of pernicious catatonia are reported [ , ].

As long as patients with schizophrenia used to be hospitalized under poor hygienic conditions over extended periods of time, infectious diseases, tuberculosis in particular, were the main cause of premature death [ — ]. Today, long hospital stays are an exception in industrialized countries and, if necessary, they take place under adequate hygienic conditions. In addition, most infectious diseases can nowadays be cured. Contributing to the excess risk of death in schizophrenia used to be suicide and other unnatural causes accidents, etc.

Recent reports are consistent in indicating that cardiovascular disorders have overtaken the other causes of extra deaths in schizophrenia [ , , , — ]. According to Laursen et al. In a review of the topic, Leucht et al. Since this spectrum of causes of death was, more or less, similar to that of the general population, it was only natural to see whether the same risk factors showed excess frequencies in schizophrenia, too, and indeed, the rates for nearly all relevant risk factors were found to be elevated [ , ]. Responsible for these elevated prevalences were, in part, an unhealthy way of life and lack of prevention, in part also addiction [ , ].

Obesity plays a key role as a risk factor for cardiovascular disease [ — ]: it is up to twice as frequent in patients with schizophrenia as in the general population [ — ]. Obesity and weight gain increase the risk for hypertension, elevated blood fat levels, and type-2 diabetes. These metabolic risks can also be associated with neuroleptic medications, which is a severe problem. Various neuroleptics, especially the new ones, have adverse metabolic effects in different degrees, so research results in this field urgently need to be translated into preventive action.

The elevated risk of suicide in patients with schizophrenia is associated with the same demographic risk factors as in the general population: male sex, social isolation, being single, and recent loss [ ]. They are compounded by illness-related factors, depressive mood in particular in the early course of the disorder [ , — ], and preserved insight [ — ], which, on the other hand, is an indicator of good outcome.

Recently, the question was raised again whether the disease construct of schizophrenia should be continued to be defined categorically or better broken down to dimensions. A dimensional understanding of the disease process was intensively debated during the preliminary consultations for the 5th edition of the DSM [ , — ]. However, it was finally decided not to adopt the dimensional approach in the interest of a more than year history of the disease concept, its worldwide use, and the role it plays in clinical practice.

For research purposes, however, dimensional models are preferred. The negative dimension turned out to be the most stable one and fairly independent of the other symptom dimensions. In the ABC long-term follow-up study, the authors defined four clinical symptom dimensions phenomenologically: a psychotic, negative, depressive, and manic dimension. Since many of the symptoms belonged to multiple dimensions, the four most prevalent symptoms with the least overlap with the other dimensions were chosen on each dimension as constituting a core dimension.

As the figure illustrates, the rates for depressive, positive, and manic symptoms exhibit plateau-like trajectories after 1 to 2 years following first admission without any change in their frequencies relative to each other. The pronounced decrease in symptoms on all three symptom dimensions after the first psychotic episode is accounted for by treatment effects and spontaneous remissions, but it is partially also attributable to an artefact: because first psychotic episode was used as the inclusion criterion, the patients studied all had maximum symptom scores at entry in the study.

Afterwards, they showed the usual sequence of episodes and intervals. The trajectories depicted only confirm what the medium-term course had already indicated, namely, that, under the study conditions described, the core dimensions of schizophrenia show no clear-cut trend of either improvement or deterioration after the remission of the first psychotic episode 1 to 2 years after first admission.

And the same was true for the overall symptomatology [ 60 , , ]. To find out whether there are factors at work on the individual level that influence the seemingly uniform, but interindividually heterogeneous illness course the investigators in the ABC Schizophrenia study ascertained the individual durations of all symptom exacerbations on the psychosis and the depression dimension over the month period—instead of just counting the number of relapse episodes operationally limited in their duration [ 60 , , , , , ]. The manic dimension could not be included because of low values.

The median duration of symptom exacerbations was five months mean: 20 months on the depression dimension and two months mean: 6. Negative symptomatology, not yet broken down to dimensions, was assessed on the basis of a sum score of 19 IRAOS items. After the remission of the first episode the prevalence of negative symptoms decreased markedly, showing a plateau-like course after five years of initial assessment in male patients and after three years in female patients.

An explanation for this unexpected finding has not yet been found. In the past, persons who fell ill with schizophrenia and sought help at mental-health services used to be—and still are today—subject to social isolation in many countries. In part, they are also discriminated against in the family, at workplace, and in public [ — ]. The consequences are an increased psychological strain on the patients and their families, reduced help-seeking and shortcomings in mental-health care and therapy. By , people had become more open-minded towards individuals suffering from these disorders, knowledge on mental disorders had increased, and mental health care had considerably improved.

Although more people than 20 years earlier regarded schizophrenia as a biological disorder and willingness to seek help at mental health services, if need be, had considerably increased, individual attitudes towards persons with schizophrenia had even worsened. An investigation of attitudes in the aftermath of an antistigma and antidiscrimination campaign in New Zealand yielded a similar result [ ].

The diagnosis of schizophrenia and the underlying disease concept have recently been subject of debate, and not for the first time. Today, it can be considered established that there is a continuum ranging from the spectrum of schizophrenia symptoms to related syndromes, affective psychosis in particular, to mild schizophrenia-like disorders and normality. The continuity also seems to be reflected on the neurobiological and genetic level. This multilevel picture of a continuum is better compatible with a dimensional than a categorical disease model.

However, bidding farewell to the categorical diagnosis of schizophrenia would have far-reaching consequences, so it has been deferred for the time being. Approaching an answer to the question of what schizophrenia is, we must start by accepting the fact that, contrary to a widespread belief, it is not just a disorder of the young, but can strike at any age.

Age at onset, severity of illness, some of the symptoms, and the social consequences involved are influenced by genetic factors, environmental risk factors, hormones oestrogen secretion , and sociocultural factors, depending on age. As a consequence, symptoms, illness course, and social outcome vary a great deal between the sexes and between young, medium, and old age. Men fall ill with schizophrenia more frequently and more severely in the first half of life, women more frequently and more severely in the second.

In spite of this, mild late- and very-late-onset psychoses should be classified as representing the disease process currently called schizophrenia. When this is done, the sex difference in schizophrenia incidence disappears almost completely over the entire age range. Among the most important recent re discoveries are the findings on the precursors and the prodromal phase of psychosis and the underlying psychopathological, neurophysiological, and functional-morphological associations. The discovery that oestrogen secretion, probably by reducing the sensitivity of D 2 receptors, is capable of postponing psychosis onset and reducing symptom severity has opened up new avenues of therapy.

Although their efficacy has already been confirmed, they are not yet in widespread use because of the risk of unwanted side-effects. Based on the ICD-9 or diagnosis with emphasis on the psychotic symptomatology, the schizophrenia syndrome seems to be encountered and to be fairly evenly distributed in all cultures and ethnicities. In that multisite study conducted with fairly similar designs and culture-independent assessment techniques, annual incidence rates for ICD-9 schizophrenia were calculated for populations aged 15 to 54 years in ten countries—four centres in three developing countries and six in industrialized countries.

A restrictively defined, precise diagnostic definition produced annual incidence rates showing fairly little variation, while the incidence based on a broader, less precise diagnostic definition varied more markedly across the centres. None of the later transnational and transcultural studies have provided more reliable incidence data, although, strictly speaking, in the WHO study, too, the number of countries adequately researched was too small. The course of schizophrenia is characterized by irregularly alternating episodes of exacerbation and remission of psychotic, partly also of depressive symptoms. If all exacerbations on the positive, negative, and depressive symptom dimensions are counted irrespective of their duration, differences will emerge in their frequency, with the exacerbations on the positive dimension showing the highest frequency and the shortest duration and those on the depression dimension a considerably lower frequency and longer duration.

Negative symptom exacerbations, not yet analysed as a dimension, are even less frequent and of a longer duration than the depressive ones. But negative symptoms, too, show an episodic course over time despite stable mean values. The construct of a disease entity, the way the early Kraepelin understood dementia praecox or schizophrenia, has become untenable, no matter which way we look at it, and the Kraepelinian dichotomy of affective and schizophrenic psychosis is now questionable. Schizophrenia is very unlikely to have a uniform aetiology. It rather represents the expression of recurring functional vulnerability of various neural networks in the human brain caused by different types of neurobiological disorder.

It is the resulting neural dysfunction that brings forth the exacerbations described and their combinations, thus, leading to schizophrenia, which, hence, is nothing else than the final common pathway of various influences. Quite frequently neuroreparative mechanisms seem to be capable of bringing that dysfunction to remission, partly or completely. In sum, we still do not really know what schizophrenia is, but at least we have a better idea of what it is not. And it is uncertain whether we will ever know its real cause, because single causation does not exist and, given the diversity of the aetiological factors involved, it is difficult to single out those ultimately responsible for it.

The author wishes to thank Professor Marcella Rietschel, head of the Department of Genetic Epidemiology in Psychiatry, Central Institute of Mental Health, for the intensive discussions and her active support in writing the Genetics chapter. The author also thanks his research assistant Auli Komulainen-Tremmel for her help in preparing the various drafts of the paper and for compiling the References section. Advances in Psychiatry. Table of Contents. Journal Menu. Abstract After over years of research without clarifying the aetiology of schizophrenia, a look at the current state of knowledge in epidemiology, genetics, precursors, psychopathology, and outcome seems worthwhile.

Introduction For more than a century, there has been research into the question of what schizophrenia really is. Epidemiology 3. General Epidemiology Schizophrenic psychosis, characterized by positive symptoms such as hallucinations, delusions, and thought disorders, is encountered in all ethnic groups, cultures, political systems, and socioeconomic classes at frequencies that show only moderate variation when based on a sufficiently reliable and culture-independent diagnosis e.

Figure 1: Annual incidence of schizophrenia per population aged 15—54 both sexes for the broad and restrictive definitions. Source: [ 46 ]. Besides the amygdala, there are other neuropathological areas of degeneration as well; the overall brain volume can also be measured. Research shows that the overall brain volume is not statistically significantly different between patients with bipolar disorder and patients with schizophrenia, except when making comparisons in the intracranial volume.

Due to low rates of full remission for either disorder, with poorly understood and under-researched mechanisms of change, most treatments are designed to control symptoms and make them more tolerable. Treatments for the diseases include medication , psychotherapy , and others. Mood-stabilizers, such as lithium , are the primary medication treatment bipolar disorder. Psychotherapy is a treatment both types of disorder patients use. They guide the patients in their thoughts, and use communication or behavioral work as a means of healing.

Families of the affected also benefit from this treatment, as they can sit on sessions and talk to the therapist as well. Rehabilitation is one of several psychosocial treatments for schizophrenia. It involves social and job-skills training to improve an individual's ability to function in society. From Wikipedia, the free encyclopedia.

Frontiers in Psychiatry.

What is Mild Cognitive Impairment? (Symptoms, Causes, Treatment, Prevention)

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Mitochondrial complex I activity and oxidative damage to mitochondrial proteins in the prefrontal cortex of patients with bipolar disorder. Arch Gen Psychiatry. Elevated cerebrospinal fluid lactate concentrations in patients with bipolar disorder and schizophrenia: implications for the mitochondrial dysfunction hypothesis. Biol Psychiatry. Differences in lymphocyte electron transport gene expression levels between subjects with bipolar disorder and normal controls in response to glucose deprivation stress.

Lithium-induced enhancement of mitochondrial oxidative phosphorylation in human brain tissue. Decrease in creatine kinase messenger RNA expression in the hippocampus and dorsolateral prefrontal cortex in bipolar disorder.

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