Magnitude of Neurocognitive Impairment and Severity of Depression in Geriatric Population

Background and Objective: With the increasing life expectancy of the populations and rising prevalence of depressive and neurocognitive disorders, there is a need to address the association between the two in terms of magnitude of the neurocognitive disorders and the severity of depression. The current study addresses this issue and aims to observe the association between the two. Methods: This cross-sectional descriptive study was conducted from September 2014 to March 2015 at the Institute of Psychiatry at Benazir Bhutto Hospital, Rawalpindi, Pakistan where consecutive patients aged ≥ 65 years were screened for depression using Geriatric Depression Scale (GDS). Neurocognitive impairment was assessed using Mini Mental State Examination (MMSE). -square test was used to compute the association between depression severity and neurocognitive deficit. Results: There was approximately equal gender distribution with a mean age of 63.6 ± 9.68 years. Eighty six percent of the study population was found to be suffering from clinical depression while seventy percent had neurocognitive deficit. The severity of depression came out to be directly proportional to the magnitude of the neurocognitive disorder (P = 0.000) with 68.8% of the patients with severe depression having moderate to severe neurocognitive deficit. Conclusions: Depression is associated with significant neurocognitive impairment in elderly in the local population; higher the severity of depression more the magnitude of cognitive impairment.

Neuropsychological Profile of Endogenous Depressions with Overvalued Ideas

Objective: the article presents the results of a study of the neuropsychological profile of cognitive functions in patients with endogenous depression, in the structure of which overvalued formations are revealed. The study of cognitive processes in patients with such disorders will help determine prognostic criteria and contribute to the development of optimal recommendations for personalized therapy of these conditions.The aim of the study was to determine the characteristics of cognitive functioning and its dynamics in patients with endogenous depression with overvalued formations.Patients and methods: using clinical-psychometric, neuropsychological, pathopsychological methods, 45 patients were examined. 26 men (average age 28.7 ± 7.3) and 19 women (average age 34 ± 8.6) had a manifest or repeated depressive state within the framework of an affective disease (F31-34 according to ICD-10) with the phenomenon of overvalued formations. The control group was represented by a similar in number, comparable in terms of sex and age group of patients (45 patients) with a depressive state that forms within the affective phase (F31-34 according to ICD-10), without overvalued formations.Results: in the course of the work, differences were found in the structure of the neurocognitive deficit of endogenous depression with overvalued formations from that of depressions without the phenomenon of overvalued formations. As a result of neuropsychological screening of patients in the group of endogenous depressions with overvalued formations, data were obtained on dysfunction of the anterior sections of the predominantly left hemisphere and related regulatory deficiency. Conclusions: patients with endogenous depressions occurring with a predominance of overvalued formations in the clinical, a neurocognitive deficiency of the regulatory domain is characteristic, which is different from that in depressions without the phenomenon of overvalued formations.

Neurocognitive impairment and evidence-based treatment options in Bipolar disorder

Background The current paper briefly summarizes the literature on the neurocognitive deficit and its treatment in BD patients. Methods The material was chosen on the basis of previous systematic reviews the author has taken part in. Results The data so far suggest that the deficit is qualitatively similar but quantitatively milder in comparison to schizophrenia, it is present already since the first episode, is weakly related to mood symptoms and somewhat stronger to psychotic symptoms, it probably determines much of the disability and treatment is problematic. This deficit is also present during periods of euthymia. The possible adverse effect of psychotropic medication is rather small if any at all and is confounded by the specific clinical symptoms, for which medication is used for their treatment. This is especially true concerning antipsychotics and psychotic symptoms. The origin and the etiopathogenesis of the core neurocognitive impairment remain elusive. The presence of a neurodegenerative and of a neurodevelopmental component has both data in favor and against and they are both the focus of debate. Conclusions Treatment of the neurocognitive deficit and restoration of functioning is problematic. The data are limited and treatment options are few and with a weak overall effect. Pharmacological treatments, ECT and rTMS present some hard data, while the literature is inconclusive concerning psychotherapeutic interventions.

The Ups and Downs of BACE1: Walking a Fine Line between Neurocognitive and Other Psychiatric Symptoms of Alzheimer’s Disease

Although neurocognitive deficit is the best-recognized indicator of Alzheimer’s disease (AD), psychotic and other noncognitive symptoms are the prime cause of institutionalization. BACE1 is the rate-limiting enzyme in the production of Aβ of AD, and one of the promising therapeutic targets in countering cognitive decline and amyloid pathology. Changes in BACE1 activity have also emerged to cause significant noncognitive neuropsychiatric symptoms and impairments of circadian rhythms, as evident from clinical trials and reports in transgenic models. In this study, we consider key characteristics of BACE1 with its contribution to neurocognitive deficit and other psychiatric symptoms of AD. We argue that a growing list of noncognitive mental impairments related to pharmacological modulation of BACE1 might present a major obstacle in clinical translation of emerging therapeutic leads targeting this protease. The adverse effects of BACE1 inhibition on mental health call for a revision of treatment strategies that assume indiscriminate inhibition of this key protease, and stress the need for further mechanistic and translational studies.

Emotional Response Inhibition: A Shared Neurocognitive Deficit in Eating Disorder Symptoms and Nonsuicidal Self-Injury

Eating disorder (ED) symptoms often co-occur with non-suicidal self-injury (NSSI). This comorbidity is consistent with evidence that trait negative urgency increases risk for both of these phenomena. We previously found that impaired late-stage negative emotional response inhibition (i.e., negative emotional action termination or NEAT) might represent a neurocognitive mechanism for heightened negative urgency among people with NSSI history. The current study evaluated whether relations between negative urgency and ED symptoms similarly reflect deficits in this neurocognitive process. A total of 105 community adults completed an assessment of ED symptoms, negative urgency, and an emotional response inhibition task. Results indicated that, contrary to predictions, negative urgency and NEAT contributed independent variance to the prediction of ED symptoms, while controlling for demographic covariates and NSSI history. Worse NEAT was also uniquely associated with restrictive eating, after accounting for negative urgency. Our findings suggest that difficulty inhibiting ongoing motor responses triggered by negative emotional reactions (i.e., NEAT) may be a shared neurocognitive characteristic of ED symptoms and NSSI. However, negative urgency and NEAT dysfunction capture separate variance in the prediction of ED-related cognitions and behaviors, distinct from the pattern of results we previously observed in NSSI.

BRAIN AND EYE AS POTENTIAL TARGETS FOR IONIZING RADIATION IMPACT. Part І. THE CONSEQUENCES OF IRRADIATION OF THE PARTICIPANTS OF THE LIQUIDATION OF THE CHORNOBYL ACCIDENT

Background.Exposure to ionizing radiation could affect the brain and eyes leading to cognitive and vision impairment, behavior disorders and performance decrement during professional irradiation at medical radiology, including interventional radiological procedures, long-term space flights, and radiation accidents. Objective. The objective was to analyze the current experimental, epidemiological, and clinical data on the radiation cerebro-ophthalmic effects. Materials and methods. In our analytical review peer-reviewed publications via the bibliographic and scientometric bases PubMed / MEDLINE, Scopus, Web of Science, and selected papers from the library catalog of NRCRM – the leading institution in the field of studying the medical effects of ionizing radiation – were used. Results. The probable radiation-induced cerebro-ophthalmic effects in human adults comprise radiation cataracts, radiation glaucoma, radiation-induced optic neuropathy, retinopathies, angiopathies as well as specific neurocognitive deficit in the various neuropsychiatric pathology including cerebrovascular pathology and neurodegenerative diseases. Specific attention is paid to the likely stochastic nature of many of those effects. Those prenatally and in childhood exposed are a particular target group with a higher risk for possible radiation effects and neurodegenerative diseases. Conclusions. The experimental, clinical, epidemiological, anatomical and pathophysiological rationale for visual system and central nervous system (CNS) radiosensitivity is given. The necessity for further international studies with adequate dosimetric support and the follow-up medical and biophysical monitoring of high radiation risk cohorts is justified. The first part of the study currently being published presents the results of the study of the effects of irradiation in the participants of emergency works at the Chornobyl Nuclear Power Plant (ChNPP). Key words: ionizing radiation, cerebroophthalmic effects, neurocognitive deficit, radiation accident, radiation cataracts, macular degeneration.

Processing Speed as an Endophenotypic Marker of Paranoid Schizophrenia

Summary Schizophrenia is associated with basic neurocognitive deficit- ineffective space-time information assessment, leading to ineffective judgment and planning of behaviour. Our study aimed to examine and compare the psychomotor speed and number of errors in patients with paranoid schizophrenia (PS), first-degree relatives (FDR) and healthy controls (HC). One-hundred-eight patients with PS, 58 with FDR and 60 HCs were examined via Trail Making Tests (TMT) A and B. The influence of other additional factors as The Positive and Negative Syndrome Scale (PANSS), demographics and education were additionally assessed for PS. Statistical analysis was done using Excel 2010, Statgraphics 5.0+ and SPSS 20. All results were interpreted at 95% confidential level. PS showed most unsatisfactory performances on TMT A and B, as compared to others (p=0.0001). However, FDR differed from HC only in TMTB performance (p=0.0241). The most significant impact in PS group included ageing, education, PANSS and negative syndromes, and syndromes of disorganization. PS showed a significant decline of psychomotor speed and executive functioning, although FDR had average results in TMTB, compared to PS and HC. The above results determined both detentions as endophenotype markers for PS. Additional risk factors for decline include ageing, low education and high PANSS results.