Profound Cognitive Impairment Research Articles

Long-term predictors of developmental outcome and disease burden in SCN1A-positive Dravet syndrome.

Dravet syndrome is a severe infantile onset developmental and epileptic encephalopathy associated with mutations in the sodium channel alpha 1 subunit gene SCN1A. Prospective data on long-term developmental and clinical outcomes are limited; this study seeks to evaluate the clinical course of Dravet syndrome over a 10-year period and identify predictors of developmental outcome. SCN1A mutation-positive Dravet syndrome patients were prospectively followed up in the UK from 2010 to 2020. Caregivers completed structured questionnaires on clinical features and disease burden; the Epilepsy & Learning Disability Quality of Life Questionnaire, the Adaptive Behavioural Assessment System-3 and the Sleep Disturbance Scale for Children. Sixty-eight of 113 caregivers (60%) returned posted questionnaires. Developmental outcome worsened at follow-up (4.45 [SD 0.65], profound cognitive impairment) compared to baseline (2.9 [SD 1.1], moderate cognitive impairment, P < 0.001), whereas epilepsy severity appeared less severe at 10-year follow-up (P = 0.042). Comorbidities were more apparent at 10-year outcome including an increase in autistic features (77% [48/62] versus 30% [17/57], χ2 = 19.9, P < 0.001), behavioural problems (81% [46/57] versus 38% [23/60], χ2 = 14.1, P < 0.001) and motor/mobility problems (80% [51/64] versus 41% [24/59], χ2 = 16.9, P < 0.001). Subgroup analysis demonstrated a more significant rise in comorbidities in younger compared to older patients. Predictors of worse long-term developmental outcome included poorer baseline language ability (P < 0.001), more severe baseline epilepsy severity (P = 0.003) and a worse SCN1A genetic score (P = 0.027). Sudden unexpected death in epilepsy had not been discussed with a medical professional in 35% (24/68) of participants. Over 90% of caregivers reported a negative impact on their own health and career opportunities. Our study identifies important predictors and potential biomarkers of developmental outcome in Dravet syndrome and emphasizes the significant caregiver burden of illness. The negative impact of epilepsy severity at baseline on long-term developmental outcomes highlights the importance of implementing early and focused therapies whilst the potential impact of newer anti-seizure medications requires further study.

Effectiveness of Polyphenolic Acid Derived from Salvia miltiorrhiza on Injection Combined with Systematic Rehabilitation Nursing for Patients with Ischemic Stroke

Ischemic stroke, a prevalent cerebral circulation disorder, often leads to profound physical and cognitive impairments, necessitating effective rehabilitation strategies. This study encompassed 110 diagnosed ischemic stroke patients treated at our neurology department from August 2019 to December 2021. Patients were randomly allocated into control and observation groups. The former received standard treatment and nursing care, while the latter underwent a combined regimen of salvianolic acids and systematic rehabilitation. Cell culture experiments exhibited heightened cell viability and reduced LDH secretion in the salvianolic acid-treated oxygen-glucose deprivation/reperfusion (OGD/R) injury model. Immunoblotting revealed elevated TGF-β1 protein expression in salvianolic acid-treated cells compared to controls. The observation group demonstrated lower NIHSS scores and improved emotional state relative to the conventional group. Moreover, the observation group exhibited significantly enhanced Barthel Index, cognitive function, and self-efficacy scores (P &lt;0.05). These findings suggest a positive impact of the intervention on these parameters. In ischemic stroke patients, Salvia miltiorrhiza Bunge, a natural herbal remedy rich in salvianolic acids, exerts therapeutic effects through multiple pathways. The amalgamation of Salvia miltiorrhiza polyphenolic acid injection and systematic rehabilitation presents a favorable prospect for enhancing neurological recuperation, self-care capacity, self-efficacy, and patient convalescence. Therefore, Danggui injections hold potential as a clinical intervention for ischemic stroke management.

A Severity Comparison between Italian and Israeli Rett Syndrome Cohorts.

Rett syndrome (RTT) is a neurodevelopmental disorder marked by profound cognitive, communication, and motor impairments. Despite identified genotype/phenotype connections, the extent of clinical severity varies even among individuals sharing the same genetic mutation. Diverse sociocultural environments, such as the level of inclusivity of the scholar system, the time spent with family, and the intensity of the rehabilitative intervention provided, might influence their development diversely. This study examines the severity of RTT in people in Italy and Israel, countries with distinct contradictory approaches to caring for those with intricate disabilities, across two age groups. Data from 136 Italian and 59 Israeli girls and women with RTT were assessed and divided into two age categories: above and below 12 years. The RARS, a standardized RTT-specific clinical severity tool, was administered. Despite no differences in age and genetic characteristics, the Italian group showed better scores in the RARS motor and disease-related characteristics areas in both age groups. Moreover, the young Italian participants gathered better total RARS scores and emotional and behavioral characteristics area scores. Furthermore, the young group showed significantly less scoliosis, foot problems, and epilepsy than the older group. These findings endorse the inclusion of girls with RTT in the regular schooling system for a limited daily period, investing in high activity levels within the home and community environments, and suggest continuously providing the person with daily occasions of physical activity and socialization.

Myalgic Encephalomyelitis-Chronic Fatigue Syndrome Common Data Element item content analysis.

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a multisystem chronic disease estimated to affect 836,000-2.5 million individuals in the United States. Persons with ME/CFS have a substantial reduction in their ability to engage in pre-illness levels of activity. Multiple symptoms include profound fatigue, post-exertional malaise, unrefreshing sleep, cognitive impairment, orthostatic intolerance, pain, and other symptoms persisting for more than 6 months. Diagnosis is challenging due to fluctuating and complex symptoms. ME/CFS Common Data Elements (CDEs) were identified in the National Institutes of Health (NIH) National Institute of Neurological Disorders and Stroke (NINDS) Common Data Element Repository. This study reviewed ME/CFS CDEs item content. Inclusion criteria for CDEs (measures recommended for ME/CFS) analysis: 1) assesses symptoms; 2) developed for adults; 3) appropriate for patient reported outcome measure (PROM); 4) does not use visual or pictographic responses. Team members independently reviewed CDEs item content using the World Health Organization International Classification of Functioning, Disability and Health (ICF) framework to link meaningful concepts. 119 ME/CFS CDEs (measures) were reviewed and 38 met inclusion criteria, yielding 944 items linked to 1503 ICF meaningful concepts. Most concepts linked to ICF Body Functions component (b-codes; n = 1107, 73.65%) as follows: Fatiguability (n = 220, 14.64%), Energy Level (n = 166, 11.04%), Sleep Functions (n = 137, 9.12%), Emotional Functions (n = 131, 8.72%) and Pain (n = 120, 7.98%). Activities and Participation concepts (d codes) accounted for a smaller percentage of codes (n = 385, 25.62%). Most d codes were linked to the Mobility category (n = 69, 4.59%) and few items linked to Environmental Factors (e codes; n = 11, 0.73%). Relatively few items assess the impact of ME/CFS symptoms on Activities and Participation. Findings support development of ME/CFS-specific PROMs, including items that assess activity limitations and participation restrictions. Development of psychometrically-sound, symptom-based item banks administered as computerized adaptive tests can provide robust assessments to assist primary care providers in the diagnosis and care of patients with ME/CFS.

Evolution of Cognitive Impairments in Treatment-Resistant Depression: Results from the Longitudinal French Centers of Expertise for Treatment-Resistant Depression (FACE-DR) Cohort.

Previous studies set out profound cognitive impairments in subjects with treatment-resistant depression (TRD). However, little is known about the course of such alterations depending on levels of improvement in those patients followed longitudinally. The main objective of this study was to describe the course of cognitive impairments in responder versus non-responder TRD patients at one-year follow-up. The second aim was to evaluate the predictive aspect of cognitive impairments to treatment resistance in patients suffering from TRD. We included 131 patients from a longitudinal cohort (FACE-DR) of the French Network of Expert TRD Centers. They undertook comprehensive sociodemographic, clinical, global functioning, and neuropsychological testing (TMT, Baddeley task, verbal fluencies, WAIS-4 subtests, D2 and RLRI-16) at baseline (V0) and one-year follow-up (V1). Most patients (n = 83; 63.36%) did not respond (47 women, 49.47 ± 12.64 years old), while one-third of patients responded (n = 48, 30 women, 54.06 ± 12.03 years old). We compared the cognitive performances of participants to average theoretical performances in the general population. In addition, we compared the cognitive performances of patients between V1 and V0 and responder versus non-responder patients at V1. We observed cognitive impairments during the episode and after a therapeutic response. Overall, each of them tended to show an increase in their cognitive scores. Improvement was more prominent in responders at V1 compared to their non-responder counterparts. They experienced a more marked improvement in code, digit span, arithmetic, similarities, and D2 tasks. Patients suffering from TRD have significant cognitive impairments that persist but alleviate after therapeutic response. Cognitive remediation should be proposed after therapeutic response to improve efficiency and increase the daily functioning.

Myalgic Encephalitis/Chronic Fatigue Syndrome: Diagnostic and Therapeutic Approach and Biological Research

Myalgic encephalitis/chronic fatigue syndrome, an intractable disease characterized by profound fatigue, sleep disturbance, cognitive impairment, and orthostatic intolerance, among other features, often occurs after infectious episodes. Patients experience various types of chronic pain; however, post-exertional malaise is the most significant feature, which requires pacing. In this article, I summarize the current diagnostic and therapeutic approaches and describe recent biological research in this domain.

Protocolo diagnóstico y terapéutico de la demencia avanzada en las personas mayores

Dementia is an acquired, chronic, progressive neurodegenerative disease with a terminal phase characterized by profound cognitive impairment with an inability to communicate verbally; functional dependence for basic activities of daily living; and the presence of other common medical problems, including eating problems, infections, and pain. A mean survival of ten years from its diagnosis is estimated. Establishing a prognosis in advanced stages is a challenge due to uncertainty regarding its progress and the onset of complications. Therefore, care and decision-making must be aimed at the patient's needs and care objectives more than the estimated life expectancy, taking into account the patient's and family members’ preferences.

A syndrome of severe intellectual disability, hypotonia, failure to thrive, dysmorphism, and thinning of corpus callosum maps to chromosome 7q21.13-q21.3.

Six individuals of consanguineous Bedouin kindred presented at infancy with an autosomal recessive syndrome of severe global developmental delay, positive pyramidal signs, unique dysmorphism, skeletal abnormalities, and severe failure to thrive with normal birth weights. Patients had a profound intellectual disability and cognitive impairment with almost no acquired developmental milestones by 12 months. Early‐onset axial hypotonia evolved with progressive muscle weakness, reduced muscle tone, and hyporeflexia. Craniofacial dysmorphism consisted of a triangular face with a prominent forehead and midface hypoplasia. Magnetic resonance imaging (MRI) demonstrated thinning of the corpus callosum and paucity of white matter. Genome‐wide linkage analysis identified a single ~4 Mbp disease‐associated locus on chromosome 7q21.13‐q21.3 (LOD score>5). Whole‐exome and genome sequencing identified no nonsynonymous pathogenic biallelic variants in any of the genes within this locus. Following the exclusion of partially resembling syndromes, we now describe a novel autosomal recessive syndrome mapped to a ~4Mbp locus on chromosome 7.

Patients with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) Who Have Already Visited Some Medical Institutions: Diagnosis, Treatment and Research

Myalgic encephalitis/chronic fatigue syndrome (ME/CFS) is an acquired intractable disease characterized by profound fatigue, post-exertional malaise, sleep disturbance, cognitive impairment, and orthostatic intolerance, among other features. The onset often follows an infectious episode. Importantly, the various types of autonomic dysfunctions, pain, and intolerance to various stimuli in ME/CFS patients are intrinsically different from the "fatigue" of healthy individuals. In this short essay, I summarize the current diagnostic and therapeutic strategies for ME/CFS, as well as the progress in the immunological and imaging research on this intractable disease.

Aduhelm, the Newly Approved Medication for Alzheimer Disease: What Epidemiologists Can Learn and What Epidemiology Can Offer.

Alzheimer disease (AD) is a progressive disorder common among older adults and culminating in profound cognitive impairments and high mortality risk. The US Food and Drug Administration (FDA) recently provided accelerated approval for Aduhelm, a medication for AD treatment. Aduhelm (Biogen Inc., Cambridge, Massachusetts) has been described as the first disease-modifying treatment for AD but has not been demonstrated to improve patients' cognitive or functional outcomes. In this commentary, we describe why Aduhelm approval was controversial and aspects of the current evidence of special pertinence to epidemiologists. The FDA decision was based primarily on 2 randomized controlled trials (RCTs), both terminated early, with conflicting findings about the cognitive benefits of Aduhelm. Both RCTs showed important adverse effects of the medication. The FDA cited the documented reduction in brain amyloid, an AD biomarker hypothesized as a surrogate outcome, to justify accelerated approval. Despite lack of racial/ethnic diversity in the RCT participants, concerns about health disparities have been invoked to argue for public funding of this expensive medication. The Centers for Medicare and Medicaid Services recently made a "Coverage with Evidence Development" determination for Aduhelm and similar medications. We end by describing how innovative study designs could accelerate postapproval research and evaluate the proposed surrogate outcomes.

"Communicating Lily's Pain": A reflective narrative commentary about co-creating a resource to provoke thinking and change about assessing and managing the pain of children with profound cognitive impairment.

This paper draws together about 20 years of research work and discovery and the development of a resource about pain assessment and management in children with profound cognitive impairment. The animation tells the story of an imagined child called Lily and the skills her mother uses and the challenges that her mother faces in assessing and managing Lily's pain. The animation is built on stories drawn from qualitative research findings, conversations while in clinical practice and with members of the general public, parent advisers and other sources. Most of the “evidence” came from stories shared by parents and healthcare professionals. This paper draws on some elements of socio‐narratology and is predicated on the basis that stories are important and they can act on and with us. By using an animation to tell Lily's story, the intention was to communicate research findings to a wider and more diverse audience than the typical readership of an academic journal. The intention was to act in and on people's consciousness about children's pain and to strengthen relationships and create bonds between clinicians, parents, and children in pain to make their dialog more social, connected, and meaningful. All three of us—the researcher, the writer, and the animator—have been marked and “re‐shaped” by our work related to creating Lily; we have learned more about children like Lily and their mothers, and we have learned more about ourselves and our humanity. This animation is still a story in progress, a story ‘in the wild’, a story (and a resource) we would like you to re‐tell and share. The story of Lily's pain aimed to change the lives of parents and children and professionals. Our hope is that you can be part of that change.

The “Recreated Experiences” Approach: Exploring the Experiences of Persons Previously Excluded in Research

Individuals with profound motor, communication, and/or cognitive impairments may face difficulties describing subjective or experiential information through (i) speech, (ii) writing using a pencil and paper, and (iii) typing using a standard computer keyboard. Although patient-reported outcome measures and patient-reported experience measures can capture information about this group through proxy-report, we cannot solely rely on the responses of a single proxy for experiential information. Research methods to understand the experiences of individuals with profound motor, communication and cognitive impairments are not well defined in the literature. Purpose: To provide guidance to disability researchers on how to explore the subjective and personal experiences, of individuals with profound, motor, communication, and/or cognitive impairments. Three axes are proposed as important to the structure of the “recreated experiences” method: (i) informants, (ii) data collection methods, and (iii) analyses and reflexivity. Different types of information can be gained by involving different informant groups in research about the central person’s experience. Primary guardians can provide information about interpreting central persons’ indicators of expression and broad assessments of their personal life. Other adults can provide insight relative to the central person’s capacities outside of the primary guardian-central person dyad. Peers can provide insight about personal characteristics (i.e., personality traits). Utilizing different data collection methods can foster manifest and latent content to emerge. Analyses and reflexivity which involve diverse perspectives are essential to ensure findings are grounded in lived experience and professional lenses. The method highlights the importance of furthering research to understand the experiences of individuals who cannot traditionally self-express, which may influence possibilities for enhancing care, participation opportunities, and overall well-being.

A Two‐Clone approach to study signaling interactions among neuronal cells in a pre‐clinical Alzheimer’s Disease model

AbstractBackgroundAlzheimer’s disease (AD) is a debilitating neurodegenerative disorder with no cure and few treatments. AD causes profound cognitive deficits and memory impairments. Accumulation of the peptide amyloid beta plaque is one of the characteristics of the disease. To understand the progression of Alzheimer’s disease, studies often rely on ectopic expression of amyloid‐beta 42 (Aβ42) throughout an entire tissue. Uniform ectopic expression of Aβ42 may obscure cell‐cell interactions that contribute to the progression of the disease.MethodWe developed a two‐clone system to study the signaling cross talk between GFP‐labeled clones of Aβ42‐expressing neurons and wild‐type neurons simultaneously generated from the same progenitor cell by a single recombination event.ResultSurprisingly, wild‐type clones are reduced in size as compared with Aβ42‐producing clones. We found that wildtype cells are eliminated by the induction of cell death. Furthermore, aberrant activation of c‐Jun‐N‐terminal kinase (JNK) signaling in Aβ42‐expressing neurons sensitizes neighboring wild‐type cells to undergo progressive neurodegeneration. Blocking JNK signaling in Aβ42‐producing clones restores the size of wildtype clones.ConclusionHere we present evidence that JNK signaling between Aβ42‐ expressing cells and adjacent wild‐type cells mediate neurodegeneration.

A preliminary genetic association study of GAD1 and GABAB receptor genes in patients with treatment-resistant schizophrenia.

GABAergic system dysfunction has been implicated in the etiology of schizophrenia and of cognitive impairments in particular. Patients with treatment-resistant schizophrenia (TRS) generally suffer from profound cognitive impairments in addition to severe positive symptoms, suggesting that GABA system dysfunction could be involved more closely in patients with TRS. In the present study, exome sequencing was conducted on fourteen TRS patients, whereby four SNPs were identified on GAD1, GABBR1 and GABBR2 genes. An association study for five SNPs including these 4 SNPs and rs3749034 on GAD1 as then performed among 357 patients with TRS, 682 non-TRS patients and 508 healthy controls (HC). The results revealed no significant differences in allelic and/or genetic distributions for any of the five SNPs. However, several subanalyses in comparisons between schizophrenia and HC groups, as well as between the three groups, showed nominal-level significance for rs3749034 on GAD1 and rs10985765/rs3750344 on GABBR2. In particular, in comparisons of female subjects, rigorous analysis for rs3749034 showed a statistical difference between the schizophrenia and HC groups and between the TRS and HC groups. Several positive results in subanalyses suggested that genetic vulnerability in the GABA system to schizophrenia or TRS could be affected by sex or sampling area, and overall, that rs3749034 on GAD1 and rs10985765 on GABBR2 could be related to TRS. In the present study, only a few SNPs were examined; it is possible that other important genetic variants in other regions of GABA-related genes were not captured in this preliminary study.

Using an animation to enhance parents and professionals’ communication and assessment of pain in children with profound cognitive impairment

Purpose: The rationale behind developing this resource was to create an animation and supporting information that would promote greater understanding and insight into the challenges associated with assessing pain in children with profound cognitive impairment, and to improve pain communication between parents and professionals. Although some specific validated assessment tools exist, health care professionals typically report a lack of confidence in undertaking pain assessment in this heterogeneous group of children.

Palliative care interventions in advanced dementia.

Palliative care interventions in advanced dementia.

Metabolomic Fingerprint of Mecp2-Deficient Mouse Cortex: Evidence for a Pronounced Multi-Facetted Metabolic Component in Rett Syndrome

Using unsupervised metabolomics, we defined the complex metabolic conditions in the cortex of a mouse model of Rett syndrome (RTT). RTT, which represents a cause of mental and cognitive disabilities in females, results in profound cognitive impairment with autistic features, motor disabilities, seizures, gastrointestinal problems, and cardiorespiratory irregularities. Typical RTT originates from mutations in the X-chromosomal methyl-CpG-binding-protein-2 (Mecp2) gene, which encodes a transcriptional modulator. It then causes a deregulation of several target genes and metabolic alterations in the nervous system and peripheral organs. We identified 101 significantly deregulated metabolites in the Mecp2-deficient cortex of adult male mice; 68 were increased and 33 were decreased compared to wildtypes. Pathway analysis identified 31 mostly upregulated metabolic pathways, in particular carbohydrate and amino acid metabolism, key metabolic mitochondrial/extramitochondrial pathways, and lipid metabolism. In contrast, neurotransmitter-signaling is dampened. This metabolic fingerprint of the Mecp2-deficient cortex of severely symptomatic mice provides further mechanistic insights into the complex RTT pathogenesis. The deregulated pathways that were identified—in particular the markedly affected amino acid and carbohydrate metabolism—confirm a complex and multifaceted metabolic component in RTT, which in turn signifies putative therapeutic targets. Furthermore, the deregulated key metabolites provide a choice of potential biomarkers for a more detailed rating of disease severity and disease progression.

Whole genome sequencing identifies pathogenic RNU4ATAC variants in a child with recurrent encephalitis, microcephaly, and normal stature

Biallelic pathogenic variants in RNU4ATAC have been linked to microcephalic osteodysplastic primordial dwarfism type 1 (MOPD1). Although children with MOPD1 have been reported to show profound, life-limiting clinical decompensation at the time of a febrile illness, these episodes including magnetic resonance imaging (MRI) findings have not been well characterized. We present acute MRI brain findings for a 10-year-old girl with homozygous variants in RNU4ATAC (NR_023343.1) n.55G>A, who presented with two episodes of clinical decompensation associated with a febrile illness in early childhood. The pathogenic variants were identified by whole genome sequencing as RNU4ATAC is not captured in most exome products. Her MRI of the brain revealed symmetric, diffusion restriction of the deep gray nuclei that initially pointed to a mitochondrial disease or acute necrotizing encephalopathy. Her phenotype included microcephaly and profound cognitive impairment that can be seen with MOPD1. However, she did not demonstrate clinical or radiographic evidence of a spondyloepimetaphyseal dysplasia or "primordial dwarfism" that is characteristic of this disease. As such, the predominant neurological presentation of this child represents an atypical variant of RNU4ATAC-associated disease and should be a diagnostic consideration for geneticists and neurologists caring for children, particularly in the event of an acute clinical decline.

Abstract 2560: Plasticity-related signaling pathways in the medial prefrontal cortex and hippocampus as potential targets of the antidepressant vortioxetine in reversing cognitive impairments after androgen deprivation therapy for prostate cancer

Abstract Androgen deprivation therapy (ADT) is a frontline treatment for prostate cancer but induces profound cognitive impairment in more than half of patients. This significantly reduces quality of life for cancer survivors and their families. Deficits occur in cognitive domains associated with function of the hippocampus (Hipp) and medial prefrontal cortex (mPFC) and increase in severity with duration of treatment. Therefore, it may be possible to slow or reverse the impairment. In preclinical studies, we reported that vortioxetine, a novel multi-modal antidepressant that has been shown to improve cognitive impairment in depressed patients, may reverse the ADT-induced impairment. Our lab established a rodent model of ADT in which surgically castrated rats display deficits in cognitive flexibility and visuospatial recognition, measures of prefrontal executive function and hippocampal spatial learning, respectively. We also found that castration reduces response of the mPFC to activation of the afferent pathway from the vHipp in anesthetized animals. Chronic dietary vortioxetine (28mg/kg/day) normalized response in this pathway and reversed the cognitive impairments associated with both the mPFC and Hipp. In a microarray study (Agilent Technologies, Inc.) of tissue collected from the mPFC, dorsal-, and ventral-Hipp, we found that castration altered over 1,000 genes in each of these regions (adjusted p &amp;lt;0.05). Vortioxetine did not have a significant main effect on individual genes, but pathway analysis revealed significant changes in processes involved in synaptic plasticity, such as synapse formation, axonogenesis, and MAPK signaling. In the present study, qPCR and western blot analyses were used to investigate potential ADT- and vortioxetine-induced changes in candidate factors. Factors were identified in the top-hit pathways from the vortioxetine x castration microarray analysis and confirmed by qPCR. These included plasticity-related proteins such as Arc, Akt, CREB, mGlur1, and PSD95, among others. Changes in expression and phosphorylation were further determined using western blots. Early results indicate that vortioxetine selectively reversed the reduced expression induced by castration for some, but not all, of these proteins, including CREB and mGlur1 (p&amp;lt;0.05). Experiments are underway to identify potential alterations in protein phosphorylation, as changes in activation rather than expression may also be important to the beneficial effects of vortioxetine. These results suggest that vortioxetine may reverse deficits in executive function and visuospatial recognition after ADT by modulating structural and functional plasticity in mPFC and Hipp. Citation Format: Alexandra M. Vaiana, Roman Fernandez, Jonathan Gelfond, Teresa L. Johnson-Pais, Robin Leach, Chethan Ramamurthy, Ian Thompson, David A. Morilak. Plasticity-related signaling pathways in the medial prefrontal cortex and hippocampus as potential targets of the antidepressant vortioxetine in reversing cognitive impairments after androgen deprivation therapy for prostate cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 2560.

Could neurosurgical patients benefit from psychotherapy? A few words on the use of cognitive-behavioural therapy in brain injured patients

Numerous studies have shown the effectiveness of cognitive-behavioural therapy in the treatment of various mental disorders. The present study reviews the available literature on the use and effectiveness of this therapy, both its classic form and more recent approaches (the so called “third wave”), among patients with brain injuries and those treated with surgical methods. We present a number of studies describing the use of cognitive-behavioural therapy in the treatment of patients with craniocerebral injuries, brain tumours, intracranial bleeding and vascular malformations. The obtained results are promising for the treatment of depression and anxiety disorders, post-traumatic stress disorder as well as sleep disorders, impulsivity and aggressive behaviour. The findings suggest that cognitive-behavioural therapy techniques may be effective in both these groups of patients and their families or caregivers. Currently, due to the small number of randomised controlled trials, high heterogeneity of study groups and a variety of research protocols, these findings do not allow for drawing final conclusions and proposing recommendations. Nevertheless, they demonstrate that the strategy offers promise when treating patients with brain damage. It is suggested that psychotherapy should be initiated after the end of the acute phase of the disease as it requires a certain level of self-awareness and an ability to test hypotheses, so it may be inadequate for patients with profound cognitive impairment. It requires the cooperation of a multidisciplinary team: doctors, physiotherapist, neuropsychologist and psychotherapist who, in addition to therapeutic skills, should have knowledge of the brain–behaviour relationship.