Depression in schizophrenia

Posted on March 27, 2021  in Uncategorized

Depression can occur at any stage of development of schizophrenia: precede the manifestation of attack, complicating early diagnosis, included in a complex structure psychosis attack syndrome appear as relief of psychosis in the step of forming remission
after the first psychotic episode undoubtedly in the pathogenesis of the disease are, in addition to endogenous, and reactive- personal mechanisms. And in this case, active
psychological support of the patient is especially necessary (psychotherapy, psychosocial therapy), whose “targets” are individual personality traits – coping , psychological defense, perfectionism , and self-stigmatization .
The study was conducted on the basis of the department of the first episode of psychosis (PPE) of the Orenburg Regional Clinical Psychiatric Hospital No. 1. We examined 238 patients with schizophrenia with a disease duration of no more than 5 years, having no more than 3 attacks at the stage of recovery from psychosis. Taking into account the presence or absence of postpsychotic depression, patients were divided into PPD groups (presence of depression) – 118 patients and OD (no depression) – 120 patients. Depressive status, objectified, in addition to the clinical method, the Calgary Depression Rating Scale (CDRS) – 6 points or more.
The clinical and psychopathological method is supplemented by the symptomatic questionnaire SCL-90-R, which is filled in by the patient. Patients with a disease duration of more than 5 years, with a history of more than 3 psychotic attacks, with a malignant course of schizophrenia, with somatoneurological pathology, accompanied by severe dysfunction of the affected
system, concomitant alcohol and / or drug addiction were excluded from the study .
To study individual personality traits, the methods of diagnostics of perfectionism by Garanyan- Kholmogorova, coping of SVF and E. Heim , self – stigmatization – SS (Yastrebov et al., 2004), psychological defense – Kellerman-Plutchik were used . The indicators of the Calgary scale of the PPD group (7.63 + 1.59) significantly exceed the data for the OD group (1.73 + 1.67), and a more pronounced subjective experience of distress in patients with depression was also established . In the syndromic profile, according to the SCL-90-R results, the leading in patients with depression are anxiety-depressive disorders with interpersonal sensitivity and obsessive thoughts, primarily in relation to the return of the psychotic state, or in relation to the immediate future after discharge from the clinic. The anxiety-depressive status of patients can be explained by the “reactive” component of experiences, which determines the acquisition of criticality to the past psychosis, along with preserved evaluative resources of the personality at the early stage of schizophrenia. The indices of perfectionism in the PPD group for all the studied factors of the questionnaire significantly exceed those in patients without depression, which reflects the significance of this personality trait for the development of postpsychotic depression. Self-stigmatization is significantly expressed in the PPD group (a general indicator. Among the forms of SS in the PPD group, the leading is socioreversive (40.69 + 21.94), then autopsychic and compensatory. In the OA group, the leading form of SS is also socioreversive , but, unlike the group PPD is followed by, almost in equal severity, compensatory (25.34 + 14.3) and autopsychic forms of SS. These data indicate a greater severity of experiences in relation to the consequences of the disease in patients with PPD. In the structure of psychological defense, the indicators in the group are significantly higher PPD (in descending order of severity) by regression, reactive formations, displacement, replacement, projection In the OA group, the leading in the profile and reliably exceeding in the PPD group, the denial indicator The data on the coping structure are somewhat contradictory . maladaptive coping in the behavioral sphere in the group of patients with depression, which may reflect, on the one hand, the safety ь adaptive behavioral potential, on the other hand, some ambitiousness of the behavioral sphere, defining the “targets” of psychotherapy. On the contrary, in the cognitive and emotional spheres in patients with PPD, the maladaptive orientation of coping is more pronounced . Coping structure is determined by the relationship with the depressive status using self-blame, humility, confusion, submissiveness, suppression of emotions, avoidance tendencies, social encapsulation, mental stuck – maladaptive options, and compensation, substitutionary satisfaction, self-compassion — a relatively adaptive option. At the same time, according to SVF data, in the coping structure of patients with PPD, the need for social support is urgent, the search for alternative self-affirmation is resource coping . The study shows, along with the predominant maladaptive orientation of individual personality traits of patients with postpsychotic depression in the first episode of schizophrenia, in contrast to patients without depression, the presence of an adaptive personal resource in depressed patients, primarily in the coping structure. This indicates the need for active psychotherapeutic support of patients with postpsychotic depression with an emphasis in short-term treatment and rehabilitation programs on cognitive- behavioral methods. The preferential use of cognitive -povedencheskoy therapy at the Division of first psychotic episode Orenburg already shown to be effective as a therapy in the short and in the long catamnesis (up to 10 years).

The biological basis of depression in schizophrenia

Posted on March 21, 2021  in Uncategorized

From modern positions, depression is considered as an unfavorable factor in the course of schizophrenia. To a large extent, this is determined by an increased risk of suicide and a deterioration in therapeutic sensitivity. But the question of the influence of depression on the course of the schizophrenic process remains open. In studying this problem, a modern approach is relevant, involving the consideration of schizophrenia and affective disorder from the standpoint of brain degeneration. From this point of view, it is of interest to analyze the level of BDNF, which can act as a marker of this process. BDNF promotes the growth and development of immature neurons, improves adult neuron survival and function, and helps maintain synapse connections. Experimental studies have shown the relationship of BDNF with the main transmitters involved in the development of mental pathology.

Studies of neurotrophic factors, in particular BDNF, were of particular interest and led to the formation of the neurotrophic hypothesis of depression. There is now much less research and more conflicting results regarding the relationship between BDNF levels and schizophrenia. Most of the research is focused on studying the relationship of BDNF with ongoing therapy. In the study of psychiatrists from the Institute. V.M. Ankylosing spondylitis included 25 inpatients. All patients met the ICD-10 diagnostic criteria for schizophrenia (F20) and were hospitalized for exacerbated mental illness. The study did not include patients with organic brain disease (severe trauma, history of stroke, etc.), as well as with severe somatic pathology in the acute stage. Patients were examined twice, at admission and after 4-6 weeks of therapy. The survey was comprehensive and included clinical psychopathological, laboratory and psychometric methods. In schizophrenic patients, the Calgary Depression Scale (CDSS) was used to assess depressive symptoms. The BDNF level was measured using the Rand Dsystems EL ISAs test system (R&D systems , USA) based on the enzyme-linked immunosorbent assay (ELISA). Blood sampling to determine the level of cortisol was carried out strictly in the morning. The quantitative determination of the concentration of cortisol in the serum of patients was carried out on an automatic immunochemical analyzer Access-2 (manufactured by Beckman Coulter , USA) using chemiluminescence immunoassay using paramagnetic particles. On the basis of the CDSS scale, two samples were made – 15 patients at the time of the first examination had depressive symptoms in the structure of a schizophrenic attack and 10 patients without signs of depression. The groups were comparable in age. The BDNF level in patients with depressive symptoms is significantly lower than in patients without depression. In turn, the level of cortisol in depressed patients is significantly higher. The obtained data on a significant decrease in the level of BDNF in the serum in the presence of depression in patients with schizophrenia indicates the severity of neurodegenerative processes in this category of patients. This may be due to the neurotoxic effects of cortisol.

Exogenous and endogenous depression

Posted on March 15, 2021  in Uncategorized

Depression is an increasingly commonly diagnosed mental disorder. Suffer from depression are not only adults, but and children (in the past, according to the modern classification of diseases, it is called a depressive disorder or conduct as cyclothymia). And depression really is not just a “bad mood” or a reaction to life difficulties (although it can be provoked by them) – it is a disease that has clearly defined criteria and requires complex treatment.               

Previously, it was believed that a pronounced manifestation of two of the triad of signs was sufficient to define a depressive disorder : 

  1. decreased mood,
  2. motor retardation, 
  3. mental retardation.

The described triad is a classic depressive symptom complex : a depressed person has a persistently low mood background, his movements are slowed down, and mental activity is lower than usual.  

However, from a modern point of view, depression is a much broader concept. In modern classifiers, the criteria for diagnosing depression stand out much more, and they include both psychiatric itself and neurological, therapeutic, psychological symptoms.   

The division into endogenous and exogenous depression, which once existed in domestic practice, is not so popular today , since the definition of endogenous depression is very contradictory. The essence of such a division lies in the name itself: “endogenous” means “internal”, originating “from within”. That is, the development of endogenous depression is based not on external causes (for example, very severe stress), but on some internal ones. Sometimes, this concept can be used to describe a depressive symptom complex , with its inherent decreased mood, tolerance to environmental stimuli, daily mood swings, sleep disorders and early involuntary awakenings, severe inhibition. Sometimes signs of endogenous depression are complaints of bodily malaise: most often these are chest pains that have a completely precise localization. It is in view of the last moment, of the listed symptoms, that people suffering from depressive disorders, most often, first of all, come to general practitioners for help . Is it worth it to say that the prescribed symptomatic treatment in this case does not bring the expected relief at all …                             

Exogenous depression is a disorder caused by circumstances or events in the external environment. Not whether the external stimulus of the disorder could be and not happen. However, sometimes it develops so that, having arisen initially as exogenous, depression receives its further development regardless of external causes, becoming already an endogenous state. And depression, which meets the criteria of endogeneity , develops against the background of external stress factors (after all, few modern people are completely free from stressful experiences and various shocks).            

Thus, exogenous and endogenous depression is an attempt to classify this group of disorders according to their genesis (origin, nature of causes). In addition, according to the classifier, depressions are subdivided according to their severity into mild ( subdepression ), moderate (moderate) and severe.         

One way or another, regardless of the cause that served as the source of the development of depression, at the slightest suspicion of its development , you should seek specialized professional help. It is better if it is a psychiatrist – a specialist who is able to accurately determine the correct diagnosis and, if necessary, prescribe an effective treatment. Remember: depression is a deadly disease. It is she who is the cause of 70% of suicides committed in the world.        

How to get out of depression

Posted on March 9, 2021  in Uncategorized

Depression is one of those disorders that have recently become more common in the practice of psychiatrists around the world.     

The fast pace of life, the lack of a normal alternation of work and rest, psycho-emotional stress and much more are some of the reasons provoking the growth of this disease. This is especially true for residents of large cities.   

In addition, this diagnosis is also “popular” at the present time. This fact causes a large number of speculations among pseudo-healers (representatives of alternative medicine, psychics, etc.), and just people who are ready to give various kinds of recommendations, but are very far from medicine.       

This is a very harmful tendency, since many are captivated by delusions that it is enough to normalize their daily routine, do something that gives pleasure, just relax and sit in silence, as the disease itself will recede.    

K Unfortunately, this is not so.  

Depression is an affective disorder prone to progression, affecting not only the emotional, but also the physical condition of a person. In addition, it is also deadly: about 70 % of people suffering from depression have thought or tried / sometimes successfully / attempted suicide. According to WHO forecasts, by 2030 this particular disease may break records and become the main cause of death in the world, giving way to the prevailing cardiovascular and diseases and oncology today .               

That is why the question of how to get out of depression has the only unequivocally correct answer: see a doctor.   

This disorder is treated by doctors – psychiatrists or psychotherapists. But you need to understand that in domestic medical practice, only a specialist with a higher medical education can be a real psychotherapist. Beware of offers from “just psychotherapists”, people who have completed additional courses in any psychotherapeutic area after receiving any higher education (even psychological) .        

The bottom line is that high-quality treatment of depression often requires a combination of psychotherapeutic assistance with the use of pharmacology (antidepressants), and only a doctor with special knowledge can choose the right drug, its dosage.   

It is also almost impossible to get out of depression on your own (just as it is impossible to get out of tuberculosis on your own , for example, or appendicitis).   

The main signs that should make you pay attention are: 

  • yearning,
  • reduced mood background,
  • despondency,
  • unwillingness to communicate,
  • melancholy,
  • decreased efficiency at work, 
  • anhedonia (inability to enjoy the things that gave him before),  
  • decreased libido (sex drive),
  • indifference, vision of life (present, past and future) in black.  

It often happens that being in a depressed state, the person himself is unable to see a doctor. And here his relatives and close people must certainly help him: to persuade, to invite a specialist at home, to start a course of treatment with all his might.     

In the event that there are / even once / statements about the death , or attempts (preparation) for this – inpatient medical care must be provided immediately!       

There are situations when the salvation of our family and friends depends on an attentive attitude to their condition. Depression is where procrastination can really cost your life. At the same time, this disease is quite treatable, you can get out of depression, you just need to be in time.       

Chronic fatigue and depression

Posted on March 3, 2021  in Uncategorized

At the present time, when the pace of life, especially in big cities, is that there is practically no possibility to stop and make a break, doctors are increasingly faced with the phenomenon of the so-called chronic fatigue.     

Its main symptom, which in turn is one of the signs of depression, is a feeling of loss of energy and high fatigue. But, unlike depression, which is included in the group of affective disorders, it is affect (that is, emotions) that suffer less in chronic fatigue syndrome. On foreground muscle weakness, constantly feel tired, not passing without even looking at the long sleep and rest.                   

Chronic fatigue syndrome, in contrast to depressive disorders, was described for the first time relatively recently. He is diagnosed in mainly from residents of large cities.     

In domestic medical practice, CFS was described for the first time in 1991 , at the same time the researchers identified several groups of the population, especially susceptible to this condition. These include the liquidators of the Chernobyl accident and the residents of contaminated areas, patients after surgery (most often – cancer after chemo – and radiation therapy), people with chronic inflammatory diseases. And the last category includes people with high material wealth, more often they are businessmen forced to work a lot, in whose life there are a lot of emotional stress and little physical activity.             

In world practice, viral infections (herpes simplex, Epstein-Bar), immune disorders are considered hypothetical reasons for the development of chronic fatigue syndrome, and some experts tend to believe that this is one of the forms of depression with an atypical course.      

Both diagnosis and treatment of CFS are very difficult. So, first of all, during the examination, you will need to differentiate it from other diseases with similar symptoms. A treatment called the most diverse, since it does not to completely clear the causes of this condition. In mainly high-calorie diet is recommended, orderly daily routine to always to sleep hygiene, vitamins and restorative physio -Procedures. In general, the treatment of this ailment most often comes from work with the most pronounced symptoms. Such symptomatic treatment is able to “extinguish” the most alarming and difficult manifestations, but, unfortunately, it is not able to work with the cause.                  

Thus, the question of the relationship between CFS and depression remains unclear . Some sources note that depression can often accompany this phenomenon, and therefore consider it necessary to use antidepressants. However, there is still no conclusive evidence of the effectiveness of antidepressant use in suspected CFS.        

In any case, remember that normally a healthy person needs 6 to 8 hours of sleep per day to fully recuperate. And after even a short vacation, we should feel refreshed. If this is not the case, if you constantly feel tired for a long time , consult a doctor.               

Stress and depression

Certain adrenal hormones are released in response to stress. They reduce the proliferation of dentate gyrus progenitor cells in the adult hippocaptus . Many corticosteroids reduce the formation of granular nerve cells by inhibiting stem cell division.

NMDA receptors are involved in the realization of the effects of corticosteroids, their blockade prevents the negative effects of corticosteroids. Any violation of neurogenesis develops depression. The hippocampus and prefrontal area may atrophy in depressed patients. When treated with fluoxetine, an antidepressant, the content of new cells in the dentate gyrus increases, and inhibition of serotonin synthesis leads to a decrease in the processes of neurogenesis in the hippocampus .

The microstructure of the hippocampus changes with irradiation, which also leads to an increase in the functioning of microglia and changes in vascularization .

TMS and antipsychotics in the treatment of depression

In the treatment of depression , intermittent transcranial theta stimulation is used for one to three minutes as an additional method of treatment in patients with this disease.  

Some studies have shown that blocking the dopamine D2 receptor alters the therapeutic effect of intermittent theta stimulation.  

An analysis of the case histories of 105 patients with depression, resistant to drug treatment, showed that dorsolateral prefrontal intermittent theta stimulation had a positive result with additional intake of drugs from the antipsychotic group.

Causes of depression

Previously, scientists and doctors believed that neurotransmitters – monoamines, in particular serotonin, dopamine, norepinephrine – play a role in the genesis of depression . This hypothesis arose under the influence of the results of research on antidepressants, but today two more mediators deserve attention – glutamate , which regulates excitation processes, and gamma- aminobutyric acid (GABA), the main mediator of inhibition.

This is supported by evaluations of the effects of ketamine, amantadine , lamotrigine, and anticonvulsants on the severity of depression. These drugs act on the NMDA (N – methyl – D – aspartate ) glutamate receptors. 

The factors that provoke stress play an important role in the development of depression, especially the stress factor is important in the first episode of depression. A person’s predisposition to the effects of stress factors depends on disorders in the regulation of the hypothalamic-pituitary-adrenal system.

Some researchers have found elevated levels of the adrenal hormone cortisol in a large number of depressed patients who have not yet received drug therapy. Moreover, the level of cortisol did not decrease after the administration of dexamethasone. This effect formed the basis for the creation of the dexamethasone test, which was introduced into clinical practice. It detects endogenous depression.

Disturbances in the regulation of the hypothalamic-pituitary-adrenal system occur primarily at the level of secretion of corticotropin- releasing hormone (CRH), which promotes the secretion of adrenocorticotropic hormone (ACTH). A decrease in the level of CRH secretion in patients with high CRH values ​​reduces the production of ACTH by the pituitary gland and subsequently cortisol. A decrease in CRH secretion occurs in response to the introduction of synthetic CRH.

The remissions that occur after episodes of depression can be traced by the dexamethasone test. 

Adults who have suffered severe psychological trauma in childhood are vulnerable to stress, which means to the development of depression, since they have impaired regulation of the hypothalamic-pituitary-adrenal system. Such patients have a tendency to be hyperactive, especially during critical periods of brain development, and a predisposition to depression throughout life, especially in the presence of stress. Numerous changes in the hypothalamic-pituitary-adrenal system, leads to an increase in the secretion of glucorticoids , which leads to structural and functional changes in the limbic system in patients with depression. Antidepressant therapy leads to a decrease in the proliferation of cells in the limbic system of the brain. The modern approach to the genesis of depression does not exclude the role of neuroplasticity in the development of depression. The role of hereditary factors in the development of depression was also noted. 

Medicines that provoke the appearance of depression

Drugs that can cause depression include:

  • oral contraceptives;
  • antimicrobial drugs (ampicillin, evaferents , azithromycin, streptomycin, tetracycline ); 
  • anticonvulsants ( leviracetam, vigabatrin, topiramate );
  • immunomodulators (alpha interferon, steroids, cyclosporine );
  • antihypertensive drugs (beta-blockers, methyldopa , reserpine, flunarizine );
  • psychotropic drugs ( levodopa , metaclopramide , amantadine , sedative hypnotics, phenothiazine , disulfiram );
  • medicines used in oncology ( vinblastine vincristine );
  • barbiturates;
  • antihistamines;
  • psychoactive substances (amphetamine, cocaine).

Focused Ultrasound Treatment for Depression

Ultrasound examination is not only a diagnostic method for imaging human organs and systems. It can be used as a method of focused treatment of mood disorders. The use of ultrasound as a therapeutic agent depends on the frequency parameters and the type of equipment. In addition, ultrasound facilitates the delivery of a drug across the blood- brain barrier to specific brain structures. 

Thus, ultrasound can be one of the means of neurostimulation .

The use of low-intensity and low-frequency ultrasound as a stimulator of neural networks ultimately leads to the activation of neurons through the influence on the sodium- calcium channels of the cell membrane. ( Tyler with et al , 2008).  

Other possibilities and ways of achieving a similar effect in a non-invasive way remain problematic.