scholarly journals Peri-Ictal and Ictal Cognitive Dysfunction in Epilepsy

2011 ◽  
Vol 24 (1) ◽  
pp. 27-34 ◽  
Author(s):  
Lavanya Vijayaraghavan ◽  
Subbulakshmy Natarajan ◽  
Ennapadam Srinivas Krishnamoorthy

Disturbances in cognitive function, particularly memory, are a common complaint of patients with epilepsy. Factors contributing to cognitive dysfunction are the type of epilepsy, type and frequency of seizures, anti-epileptic drugs and the location of underlying brain lesions. Whilst a great deal of attention has been paid to permanent cognitive impairment, the nature and underlying mechanisms of ictal and peri-ictal cognitive changes are poorly understood. In-depth investigation of seizure related cognitive dysfunction is of great clinical relevance, as these changes are potentially reversible and treatable, thus reducing the cumulative effect of frequent seizures Greater knowledge of peri-ictal and ictal cognitive dysfunction would improve seizure prediction, localization of seizure focus and assessment of treatment effectiveness, greatly reducing distress and disability. This paper will review current understanding of peri-ictal and ictal cognitive dysfunction and discuss future directions for research.

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1271.1-1272
Author(s):  
S. Derham ◽  
J. Lewis ◽  
E. Dures ◽  
F. Cramp

Background:Adults with fibromyalgia frequently report symptoms of cognitive dysfunction, often referred to as fibrofog. However primary research exploring cognitive dysfunction in the lives of adults with fibromyalgia is very limited (Kravitz and Katz, 2015).Objectives:The aim of this review was to (i) synthesise the qualitative literature on the lived experiences of cognitive dysfunction in adults with fibromyalgia, (ii) develop common themes through thematic analysis and (iii) identify knowledge gaps to inform future research and clinical practice in this area.Methods:Seven electronic databases (MEDLINE, Embase, CINAHL, PsycINFO, Amed, Scopus and OpenGrey), reference lists of key articles and two high impact qualitative journals were searched from 1990 to November 2018. Articles were eligible for inclusion if they reported primary qualitative data exploring the experiences of cognitive dysfunction in adults with fibromyalgia. Included studies were appraised using the Critical Appraisal Skills Programme (CASP) qualitative checklist and extracted data analysed using narrative synthesis. SD conducted critical appraisal and data extraction on all included studies. FC, JL and ED reviewed five papers each. All papers were reviewed by two co-authors. Of the 1413 records identified, 15 studies were selected for inclusion.Results:These studies included 208 women and 22 men with fibromyalgia, aged 18 to 72 years and representing seven different countries. Duration of diagnosis was four months to 34 years. Fourteen studies used interviews and one used focus groups. None of the included studies focussed exclusively on cognitive function in adults with fibromyalgia. Three studies identified themes specific to cognitive dysfunction and fibromyalgia symptoms. The remaining 12 studies presented relevant data intertwined with the overall lived experiences of fibromyalgia.Cognitive dysfunction, as a part of fibromyalgia, was often unpredictable. Problems with memory and concentration that were most commonly reported were emotionally distressing and affected functional and vocational activities. Participants found communication effortful, with a negative impact on work, leisure and social activities. Stress, fear and worry around perceived cognitive changes were commonly expressed. Lost employment or changed work roles and relationships, due to cognitive difficulties, had negative impacts for many participants. The terms cognitive dysfunction and fibrofog were used interchangeably within the studies, but lacked common definition. This introduced uncertainty around whether participants and authors were describing the same phenomenon.Conclusion:Adults with fibromyalgia experience unpredictable and emotionally impactful difficulties related to cognitive dysfunction. Functional impact was broad-reaching, particularly around work ability and lost employment opportunities. It is unclear how cognitive symptoms in fibromyalgia related to co-morbid symptoms such as pain, fatigue and poor sleep. Further research focusing on the full impact of cognitive function on the lives of adults with fibromyalgia is recommended to inform clinical practice. Research to establish clarity of definition of the terms cognitive dysfunction and fibrofog within fibromyalgia is highly recommended.References:[1]Kravitz H, Katz R. Fibrofog and fibromyalgia: a narrative review and implications for clinical practice. Rheumatology International. 2015;35(7):1115-25.Acknowledgments:This work is supported by the National Institute for Heath Research [ICA-PCAF-2018-01-078 to SD]Disclosure of Interests:Sandra Derham: None declared, Jenny Lewis: None declared, Emma Dures Grant/research support from: Independent Learning Grant from Pfizer, combined funding for a research fellow from Celgene, Abbvie and Novartis, Paid instructor for: A fee from Novartis to deliver training to nurses., Fiona Cramp: None declared


2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Yi Xin She ◽  
Qing Yang Yu ◽  
Xiao Xiao Tang

AbstractInterleukins, a group of cytokines participating in inflammation and immune response, are proved to be involved in the formation and development of pulmonary fibrosis. In this article, we reviewed the relationship between interleukins and pulmonary fibrosis from the clinical, animal, as well as cellular levels, and discussed the underlying mechanisms in vivo and in vitro. Despite the effects of interleukin-targeted treatment on experimental pulmonary fibrosis, clinical applications are lacking and unsatisfactory. We conclude that intervening in one type of interleukins with similar functions in IPF may not be enough to stop the development of fibrosis as it involves a complex network of regulation mechanisms. Intervening interleukins combined with other existing therapy or targeting interleukins affecting multiple cells/with different functions at the same time may be one of the future directions. Furthermore, the intervention time is critical as some interleukins play different roles at different stages. Further elucidation on these aspects would provide new perspectives on both the pathogenesis mechanism, as well as the therapeutic strategy and drug development.


2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Lien D. Nguyen ◽  
Tom T. Fischer ◽  
Barbara E. Ehrlich

Abstract Background After chemotherapy, many cancer survivors suffer from long-lasting cognitive impairment, colloquially known as “chemobrain.” However, the trajectories of cognitive changes and the underlying mechanisms remain unclear. We previously established paclitaxel-induced inositol trisphosphate receptor (InsP3R)-dependent calcium oscillations as a mechanism for peripheral neuropathy, which was prevented by lithium pretreatment. Here, we investigated if a similar mechanism also underlay paclitaxel-induced chemobrain. Method Mice were injected with 4 doses of 20 mg/kg paclitaxel every other day to induced cognitive impairment. Memory acquisition was assessed with the displaced object recognition test. The morphology of neurons in the prefrontal cortex and the hippocampus was analyzed using Golgi-Cox staining, followed by Sholl analyses. Changes in protein expression were measured by Western blot. Results Mice receiving paclitaxel showed impaired short-term spatial memory acquisition both acutely 5 days post injection and chronically 23 days post injection. Dendritic length and complexity were reduced in the hippocampus and the prefrontal cortex after paclitaxel injection. Concurrently, the expression of protein kinase C α (PKCα), an effector in the InsP3R pathway, was increased. Treatment with lithium before or shortly after paclitaxel injection rescued the behavioral, cellular, and molecular deficits observed. Similarly, memory and morphological deficits could be rescued by pretreatment with chelerythrine, a PKC inhibitor. Conclusion We establish the InsP3R calcium pathway and impaired neuronal morphology as mechanisms for paclitaxel-induced cognitive impairment. Our findings suggest lithium and PKC inhibitors as candidate agents for preventing chemotherapy-induced cognitive impairment.


Open Heart ◽  
2021 ◽  
Vol 8 (1) ◽  
pp. e001569
Author(s):  
Fredrike Blokzijl ◽  
Frederik Keus ◽  
Saskia Houterman ◽  
Willem Dieperink ◽  
Iwan C C van der Horst ◽  
...  

ObjectiveThis study aimed to explore the influence of coronary artery bypass grafting (CABG) on both postoperative cognitive dysfunction and quality of life (QoL) and the association between the two patient-related outcomes.MethodsIn a prospective, observational cohort study, patients with elective, isolated CABG were included. Cognitive function was assessed using the Cogstate computerised cognitive test battery preoperatively, 3 days and 6 months after surgery. QoL was measured preoperatively and at 6 months using the RAND-36 questionnaire including the Physical Component Score (PCS) and the Mental Component Score (MCS). Regression analysis, with adjustment for confounders, was used to evaluate the association between postoperative cognitive dysfunction and QoL.ResultsA total of 142 patients were included in the study. Evidence of persistent cognitive dysfunction was observed in 33% of patients after 6 months. At 6 months, the PCS had improved in 59% and decreased in 21% of patients, and the MCS increased in 49% and decreased in 29%. Postoperative cognitive changes were not associated with QoL scores.ConclusionsPostoperative cognitive dysfunction and decreased QoL are common 6 months after surgery, although cognitive function and QoL were found to have improved in many patients at 6 months of follow-up. Impaired cognitive function is not associated with impaired QoL at 6 months.Trial registration numberNCT03774342.


2021 ◽  
Author(s):  
Keenan Walker ◽  
Murat Bilgel

Positron emission tomography (PET) is a functional imaging technique that can be used to visualize physiological activity or molecular processes in the whole body or specific organs. For several decades, PET imaging has been used to expand our understanding of neurobiology and neurologic disease. In addition to playing an increasing role in neuroscience research, PET imaging has become ubiquitous in the clinical setting. For example, PET neuroimaging is currently used to aid in differential diagnosis, monitor treatment effectiveness, and assist with surgical planning. While perhaps most well-known for its role in neurodegenerative disease, PET neuroimaging has also been used to care for and study patients with epilepsy, brain tumors, traumatic brain injury, schizophrenia, and other neuropsychiatric conditions. PET neuroimaging is currently undergoing a period of rapid development, particularly as it pertains to the visualization and quantification of neurodegenerative processes and neurotransmitter systems. Given that neuropsychologists are positioned to integrate neuroimaging findings with information derived from a clinical interview and cognitive testing, a fundamental understanding of PET neuroimaging applications and methods will likely prove useful.


Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Fumiaki Oka ◽  
Yahya B Atalay ◽  
Tao Qin ◽  
Cenk Ayata

Background: Majority of aneurysmal subarachnoid hemorrhage (SAH) survivors develop cognitive dysfunction. To better understand the underlying mechanisms and develop treatments, predictive animal models are required. We carried out a detailed physiological and cognitive characterization of pre-chiasmatic cistern (PC) and cisterna magna (CM) SAH models in mice. Methods: SAH was induced by arterial blood injection into the PC (40 μl) or CM (60 μl) in C57BL6/J mice (male, 25g). Controls received normal saline. Cerebral blood flow (CBF) was imaged using laser speckle flowmetry during and for 60 min after SAH. Intracranial pressure (ICP) and blood pressure (BP) were monitored to calculate cerebral perfusion pressure (CPP). Neurological and cognitive function was assessed 3 weeks after the injection, using pole, novel object recognition, Y maze and Morris water maze tests. Results: Mortality was 10% after PC and 4% after CM SAH. In both groups, CPP decreased from about 65 mmHg to less than 10 mmHg immediately after the injection, and recovered to 40 mmHg within 10 min after PC (n=8) and 7 min after CM (n=8) SAH (Fig A). In both groups, CBF was severely reduced to ~20% of baseline in both hemispheres immediately after SAH. CBF recovered to >40% within 5 min after PC and 2 min after CM SAH (Fig A). In saline controls (n=5 in PC and CM each), CPP and CBF changes were much milder and shorter-lasting. Compared with controls (n=12), PC SAH mice (n=12) performed significantly worse in a subset of sensorimotor and cognitive tests for up to 3 weeks (Fig B). CM SAH did not significantly impact neurological function. Conclusions: Pre-chiasmatic cistern but not cisterna magna SAH model reproduces cognitive dysfunction observed in patients with low mortality and high reproducibility in mice.


Author(s):  
Nicolas Toro-Urrego ◽  
Marco Avila-Rodriguez ◽  
María Inés Herrera ◽  
Andrea Aguilar ◽  
Lucas Udovin ◽  
...  

Hypoxic–ischemic brain injury is a number one cause of long-term neurologic disability and death worldwide. This public health burden is mainly characterized by a decrease in oxygen concentration and blood flow to the tissues, which lead to an inefficient supply of nutrients to the brain. This condition induces cell death by energy depletion and increases free radical generation and inflammation. Hypoxic–ischemic brain injury may occur in ischemic-stroke and over perinatal asphyxia, being both leading causes of morbidity in adults and children, respectively. Currently, there are no effective pharmaceutical strategies to prevent the triggering of secondary injury cascades, including oxidative stress and metabolic dysfunction. Neuroactive steroids like selective estrogen receptor modulators, SERMs, and selective tissue estrogenic activity regulators, STEARs, exert several neuroprotective effects. These encompass mitochondrial survival, a decrease in reactive oxygen species, and maintenance of cell viability, among others. In this context, these neurosteroids constitute promising molecules, which could modify brain response to injury. Here we show an updated overview of the underlying mechanisms of hypoxic–ischemic brain injury. We also highlight the neuroprotective effects of neurosteroids and their future directions.


Author(s):  
Kathleen M. Chard ◽  
Jennifer Schuster Wachen ◽  
Patricia A. Resick

Cognitive Processing Therapy (CPT) has been recognized by the Institute of Medicine (2007) as one of the most effective treatments for PTSD. This chapter provides a brief overview of the CPT session content, the underlying mechanisms of the therapy, a review of the empirically based literature outlining the treatment effectiveness, limitations of the therapy, and areas of future research. In addition, the authors discuss the utility of the various versions of CPT, including cognitive only (CPT-C), group, individual, and combination. Further the research supporting the effectiveness of CPT for treating PTSD related to a variety of traumas, (e.g., combat, child abuse, and rape) and the significant impact CPT can have in areas of mental health related to PTSD (e.g., anger, guilt, social functioning) are described.


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