Clinical practice guidelines on the assessment and management of cognitive impairment in major depressive disorder

Indian Journal of Psychiatry, Год журнала: 2025, Номер 67(1), С. 98 - 105

Опубликована: Янв. 1, 2025

INTRODUCTION Epidemiology Cognitive deficit is a trivialized symptom of most prevalent psychiatric condition called major depressive disorder (MDD).[1] With staggering global prevalence approximately 350 million, MDD contributes to significant loss in quality life and increased economic burden.[2] One or more cognitive faculties patients are adversely affected tend persist despite the remission episode [Figure 1].[3]Figure 1: Concise framework assessment management Cognition Subjects with Major Depressive DisorderUpon resolution episode, individual may show experience considerable improvement measures. but there still residual symptoms that continue exist. [Table 1].[4] The one has been reported be standard deviations below normative value, 25–50% subjects MDD.[4]Table domains disorderCognitive disorder: an epiphenomenon endophenotype Recent research suggests impairment depression accurately conceptualized as rather than merely epiphenomenon. As endophenotype, represent heritable trait increases vulnerability persists even during periods remission.[5] presence this create "double hit" effect, where underlying interacts neurotoxic effects episodes, potentially accelerating neurodegeneration increasing risk developing conditions such mild (MCI) dementia. This interplay between deficits vicious cycle, each exacerbating other over time, ultimately leading profound persistent neurocognitive impairments.[6] Aside from continuum, lies pseudodementia. reversible dementia-like phenomenon appears mood-cognition medius. Table 2 gives concise comparison phenotypes associated different conditions. mood cognition further gets complicated when iatrogenic factor takes wheel. mechanisms how psychotropics lead deterioration have presented 3.[7]Table 2: Comparison disorders lying on spectrumTable 3: Mechanisms psychotropic induced impairmentDissecting mdd phenotypic definition DSM5 (Diagnostic Statistical Manual 5) typology for includes discrete clinical as: melancholia, anxious distress, atypicality, psychotic features mixed features, those peripartum onset. Williams et al. 2013, took neural circuitry-based approach define biotypes 4].[13]Table 4: Different Biotypes Depression based circuitryAgainst prevailing belief, problems would automatically improve got better, mediation models improvements control directly influence reduction enhancement after treatment.[4] Course across various Previously we discussed involvement several 1] MDD. However, heterogeneity functioning points course independent treatment[14]Table 5 summarizes longitudinal change domains.Table 5: temporal evolution MDDNeurobiological underpinnings multisystem aberrancy starting at level genetic architecture evolving into myriad cascades. Various chronic proinflammatory neuroimmune axis alterations, advent any stressor, translate changes neurochemistry brain connectivity. leads shift "rational brain" towards "emotional/sensory brain." processing negative stimuli.[17] Predictors outcome line evidence regarding outcomes limited often mixed. While plethora studies incredible, duration investigating demographic age-related variables was short. 6 findings respective reviews predictors.[18,19]Table 6: good poor MDDThe existing qualitative patient-related measures held priority by large number mental healthcare professionals.[20] guideline aims provide evidence-based recommendations individuals disorders. OBJECTIVES To standardize disorder. once they achieve remission. outline strategies persisting achieved enhance awareness understanding among end users i.e., Psychiatrists health professionals. SCOPE intended use psychiatrists, psychologists, professionals involved care ASSESSMENT OF COGNITIVE IMPAIRMENT General evaluation 1]:Any setting undergoes preliminary which screens them psychopathology, its severity. presentation should fulfill ICD 10 DSM criteria, required reach diagnosis Neither these classifications mentions dysfunction phenotype. These guidelines used conjunction Clinical Practice Guidelines issued Indian Psychiatry Society general elderly population.[21,22]Evaluation features: A baseline entails ruling out illnesses. itself not primary pathology. Hence while it relevant exclusive same, empirical cognizant might predictive prognostic marker treatment functioning. widely scales HAM-D 21 MADRS items assessing symptomatology. insufficient information. Several screening tools validated indian population listed 7]. For comprehensive evaluation, prominent institutional bodies constructed application 8].Table 7: Screening cognitionTable 8: tests standardized populationCommon neuropsychological tests: Trail-making test Digit span Controlled oral word association Token Test Stroop Rey Complex figure Wisconsin Card Symbol digit modalities symbol substitution test: California Verbal Learning Test/Ray auditory Clock drawing Weschler Adult Intelligence Scale 4th edition (WAIS-IV) adaptation Other Not India yet Perceived Deficits Questionnaire-Depression (PDQ-D) 20: subjective 4 cognition, namely: attention/concentration, retrospective memory, prospective planning/organization.[3] Online computerized tests[3]: THINC-it® resource CANTAB: Cambridge Neuropsychological Automated Battery (CANTAB) computer-based system. MANAGEMENT There no way addressing challenges impairments In cognizance studied. 2].Figure Modalities crucial elements influencing outcomesA. Stand-alone adjunctive pharmacotherapy AntidepressantsThere randomized controlled trials (RCTs) NMAs comparing effect wide range antidepressants 9. Only Shilyansky 2016[24] Prado 2018[23], meta-analyses study focused conventional antidepressants. rest included multimodal agent Vortioxetine. three studies, Vortioxetine consistently outperformed common terms benefits.[26–29]Table 9: NMA (Network Meta Analyses) describing outcomes.Adjunctive atypical antipsychoticsThere only showed beneficial results executive continuous attention cognition. favoring addition aripiprazole antidepressants.[30] likely indirect stabilizing mood.[31]Non-conventional Drug therapies Ketamine/Eketamine modulates glutamate neurotransmission, can rapid antidepressant procognitive effects.[14–16] Concerns raised long-term modulator MDD.[32] Cholinesterase inhibitors, donepezil galantamine, shown their inhibitors found ameliorate subsyndromal dementia behavioral symptoms. function older adults inconsistent[33,34] Eugeroics: agents promote wakefulness modulating dopamine neurotransmitters. Few modafinil armodafinil depression, reduce fatigue, cognition.[34,35] Memantine, NMDAR antagonist, well established. RCT assessed efficacy adjunct memantine old delayed recall group.[23] Psychological treatments Remediation Therapy (CRT) intervention designed Components: Computerized Exercises: Patients engage structured tasks challenge processes. Strategy Training: Participants learn compensatory manage difficulties. Group Sessions: CRT involves group-based training foster social interaction support. tailored person's specific needs. It combined (e.g., psychotherapy, pharmacotherapy) treatment.[36] behavior (CBT):In meta-analysis Cristea (2015), CBT robust medium improving dysfunctional thinking depression. Its ability restructuring activation available evidence. were differences thoughts. More needed fully understand differential psychotherapies depression.[37,38]Other Psychotherapies: less extensive data psychological outcomes. Neurostimulation Transcranial Magnetic Stimulation (TMS): Individual report however montage used, stimulation intensity, pulse pattern.[39,40] practice therapeutic response rTMS neuropsychiatric mention supporting role relative outcome.[41] systematic review 58 faculties.[42] direct current (tDCS): Anodal tDCS usually applied left dorsolateral prefrontal cortex (DLPFC). Direct Current (tDCS) promising case-control conducted depressed patients. ELECT-TDCS, SELECT-TDCS, DepressionDC trial did corroborate findings.[43] Electroconvulsive (ECT): therapy (ECT) acute, short-term, functions speed, function, attention.[44] Studies suggest ECT achieving memory verbal recall.[45] important note vary factors age, premorbid intellectual gender, anesthetic technique used.[46] Therefore, alternate neurostimulation method recommended better outcomes[47] Vagus Nerve (VNS) Figure 3 illustrates bottom-up mechanism vagus-mediated enhancement. Through preclinical study, vagus nerve efficacious paired learning consolidation phase task.Figure Mechanism enhancementThere also superior transcutaneous Cervical VNS auricular VNS. Two open demonstrated diagnosed treatment-resistant depression.[48,49] within month, gradual improvement. sustained 12 months[48] Complementary Alternative medical (CAMTs): defined "a group diverse systems, practices, products generally considered part medicine." Mind–Body MedicineMindfulness-based stress (MBSR) mindfulness-based (MBCT) body at-least domain least symptomatology.[50] methodology inspecting uniform. Additionally, requires properly trained instructors administer treatment.Aerobic ExerciseA overall use. concluded optimal exercise parameters moderate-to-vigorous times per week, session 60 minutes, weeks less, complementary effective works especially medication inpatient settings.[51]Natural ProbioticsA 2019 performance psychobiotic Lactobacillus Plantarum 299v (LP299v) aligned decrease serum kynurenine levels.[52] improved episodic high doses probiotics.[53]Nootropics: Recombinant erythropoietin (EPO): double-blind, randomized, placebo-controlled, recombinant mood-independent manner.[27] potential novel nootropics: nootropics limited. Well-designed, large-scale RCTs investigate safety. describe benefits.[54] Minocycline Insulin Antidiabetic Agents Thiazolidinediones). S-Adenosyl Methionine (SAMe) Omega-3 Polyunsaturated Fatty Acids N-acetylcysteine (NAC) Curcumin Statins Coenzyme Q10 Gingko biloba extract EGb761.[55] rehabilitation: MDD, flexibility performing goal-directed activity. rehabilitation employs repetitive like working causing disrupted circuitry.[56] 2016 moderate size attention, Memory. two types: Strategy-based training: Personalising target faculty, example, inductive reasoning.[57] Process-based programmed entrain participant hierarchy cumulatively process. speed attentional breadth Task-switching training.[57] tasks: commonly Paced Auditory Serial Addition (PASAT), skills measuring PASAT abilities, Sommer al., metacognitive skills, maladaptive thought patterns (i.e., rumination), Moreover, Computer-based, arithmetic exercises, focus sequencing, intelligence quotient (IQ), increase psychosocial functioning, hippocampal frontotemporal MDD.[56] CONCLUSION much previously thought. observed both symptomatic recovery phases multidomain some being vulnerable others. Early detection watchful prompt all Based resources needs patient tailor-made include repeated detailed assessment. pharmacotherapy, alternative lifestyle management, neuromodulation combination resources. Financial support sponsorship Nil. Conflicts interest conflicts interest.

Язык: Английский

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Beurteilung kognitiver Funktionen

Springer eBooks, Год журнала: 2025, Номер unknown, С. 1007 - 1023

Опубликована: Янв. 1, 2025

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Neurostructural changes in schizophrenia and treatment-resistance: a narrative review

Deleted Journal, Год журнала: 2024, Номер 4

Опубликована: Янв. 1, 2024

Abstract Schizophrenia is a complex disorder characterized by multiple neurochemical abnormalities and structural changes in the brain. These may begin before recognizable clinical symptoms appear continue as dynamic process throughout illness. Recent advances imaging techniques have significantly enriched our comprehension of these alterations, particularly focusing on gray white matter irregularities prefrontal, temporal, cingulate cortex alterations. Some suggest treatment resistance to antipsychotic medications, while nonadherence relapses further exacerbate abnormalities. This narrative review aims discuss literature about alterations deficits within brain, which could improve understanding schizophrenia how interpret neurostructural changes.

Язык: Английский

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Effects of mindfulness-based interventions (MBIs) on psychotic symptoms and psychological outcomes in patients with schizophrenia spectrum disorders: A systematic review and meta-analysis

Psychiatry Research, Год журнала: 2024, Номер unknown, С. 116272 - 116272

Опубликована: Ноя. 1, 2024

Язык: Английский

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Beurteilung kognitiver Funktionen

Springer eBooks, Год журнала: 2024, Номер unknown, С. 1 - 17

Опубликована: Янв. 1, 2024

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Blood metabolites, neurocognition and psychiatric disorders: a Mendelian randomization analysis to investigate causal pathways

Translational Psychiatry, Год журнала: 2024, Номер 14(1)

Опубликована: Сен. 16, 2024

Neurocognitive dysfunction is observationally associated with the risk of psychiatric disorders. Blood metabolites, which are readily accessible, may become highly promising biomarkers for brain However, causal role blood metabolites in neurocognitive function, and biological pathways underlying their association disorders remain unclear.

Язык: Английский

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Iowa Gambling Task performance in individuals with schizophrenia: the role of general versus specific cognitive abilities

Frontiers in Psychiatry, Год журнала: 2024, Номер 15

Опубликована: Дек. 10, 2024

Objective We aimed to explore how specific cognitive processes, such as attention and executive functions, account for variance in decision-making measured by Iowa Gambling Task (IGT) performance among individuals with schizophrenia spectrum disorders. Methods Adults ( N = 65, M age 25.4) disorders participating a clinical trial (registered at clinicaltrials.gov NCT03048695) completed the IGT, neuropsychological tests of attention, response inhibition, mental flexibility, working memory, planning, well subtests from Wechsler intelligence estimate IQ. Associations between on tasks, composite score function IGT two ways, one using total net score, decks (C+D) – (A+B) other preference more frequent gains than losses, (B+D) (A+C), were analyzed correlational hierarchical regression analysis controlling estimated IQ psychotic symptoms, Positive Negative Syndrome Scale. Results In analyses, strongest predictor was b 1.43, p <.001). Neither tasks nor functioning significantly contributed explaining beyond symptoms psychosis. However, psychosis did not predict tendency towards selecting different gain-to-loss frequency, whereas poorer predicted pattern A C 8.30, <.05). Discussion The results suggest that both functions contribute performance, but distinct ways. Whereas lower may overall disadvantageous decision-making, risk-aversive style. implication be or will have higher need support interventions targeting decision-making.

Язык: Английский

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