Communicating with Inpatients with Memory Impairments

This chapter presents the research, results and lessons learned from a project to evaluate currently available assisted living technologies for elderly people with mild to severe memory impairments who want to age in place. During the project a number of households were equipped with assistive technology to enable the end users to better cope with the barriers and problems associated with their forgetfulness. End users were involved in different phases, starting with a problem and needs analysis and ending with an evaluation of the technology installed in their homes. It seemed that technology did have a positive impact on their lives as well as on the lives of the informal caregivers who often live with those who suffer from amnesia. This project gives insight into how we are coming closer to optimizing the positive effects which assistive technology holds for the elderly with memory impairments. Key insights are presented.

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Satisfaction Ratings After Receiving Internet-Based Cognitive Rehabilitation in Persons with Memory Impairments After Severe Acquired Brain Injury

Telemedicine Journal and e-Health ◽

10.1089/tmj.2009.0118 ◽

2010 ◽

Vol 16 (4) ◽

pp. 417-423 ◽

Cited By ~ 20

Author(s):

Thomas F. Bergquist ◽

Kelsey Thompson ◽

Carissa Gehl ◽

Jorge Munoz Pineda

Keyword(s):

Brain Injury ◽

Cognitive Rehabilitation ◽

Acquired Brain Injury ◽

Memory Impairments ◽

Severe Acquired Brain Injury ◽

With Memory

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Neuropsychological diagnostics and rehabilitation of patients with memory impairments in amnestic syndrome as a result of brain damage of various etiologies

National Psychological Journal ◽

10.11621/npj.2020.0411 ◽

2020 ◽

Vol 40 (4) ◽

pp. 137-148

Author(s):

Maria E. Baulina ◽

Nataliya A. Varako ◽

Maria S. Kovyazina ◽

Yury P. Zinchenko ◽

Uriy V. Mikadze ◽

...

Keyword(s):

Brain Damage ◽

Diagnostic Tools ◽

Clinical Psychologist ◽

Rehabilitation Team ◽

Neuropsychological Rehabilitation ◽

Memory Impairments ◽

Rehabilitation Work ◽

Neuropsychological Diagnostics ◽

Amnestic Syndrome ◽

With Memory

Background. Neuropsychological diagnostics and rehabilitation are among the fundamental practical tasks facing a clinical psychologist. Today, rehabilitation goes beyond the usual framework in which it was 40–50 years ago. The course of the disease, stressful influences radically change the physical, psychological and social functioning of a person. It is the functioning of a person (and not the state of his functions) in new, often limiting living conditions that becomes an object in the modern rehabilitation system, which is a joint activity of the patient, his relatives and specialists of the multidisciplinary rehabilitation team. Objective: analysis and generalization of the diagnostic and rehabilitation experience accumulated in neuropsychological rehabilitation;identification of quality criteria for neuropsychological diagnostics and rehabilitation of patients with memory impairments in case of brain damage, which should be followed by a practicing psychologist in the process of rehabilitation work. Results. Based on the analysis of applied research and practical guidelines, the recommended diagnostic tools for detecting memory impairments are presentedand the main directions and effective methods of rehabilitation work in amnestic syndrome are highlighted. It is shown that different degrees of severity of a amnestic defect requires the choice of an appropriate direction of work in the process of neuropsychological rehabilitation: the formation of new mnestic means; the organization of “suggestive and reminiscent” environments and new strategies for behavior in this environment; general (non-specific) principles of restorative learning. Conclusions. The presented material can serve as a “support” in the practical work of a clinical psychologist with patients with memory impairments and brain lesions.The text outlines the main directions of diagnostic and rehabilitation work which a practicing psychologist must be aware of.

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Olfactory Examination in Korsakoff's Syndrome: Implications for Early Diagnosis

ISRN Otolaryngology ◽

10.5402/2011/506167 ◽

2011 ◽

Vol 2011 ◽

pp. 1-4 ◽

Cited By ~ 1

Author(s):

Dawn E. Jones ◽

Marie Rowland ◽

R. Martyn Bracewell

Keyword(s):

Working Memory ◽

Olfactory Function ◽

Memory Dysfunction ◽

Korsakoff’S Syndrome ◽

Memory Impairments ◽

Benton Visual Retention Test ◽

Healthy Control ◽

Korsakoff's Syndrome ◽

With Memory ◽

Smell Identification

Whilst olfactory dysfunction has been reported in Korsakoff's Syndrome (KS) patients, the diagnostic implications of this have not been fully explored. KS can be difficult to diagnose because cognitive symptoms are similar to other diagnoses. For instance, patients with Frontal Lobe (FL) Syndrome may present with memory impairments that are similar to KS. Participants were given the Benton Visual Retention Test-Fifth Edition (BVRT-V), to identify working memory dysfunction, and a Brief Smell Identification Test (B-SIT), to evaluate olfactory function. B-SIT scores were found to be significantly lower in the KS group compared to the control and FL groups. In contrast, the error scores on the BVRT-V were significantly higher in both the KS and FL groups compared to the healthy control subjects. Therefore, we suggest that olfactory function may aid in the differential diagnosis of patients presenting with working memory dysfunction.

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Calbindin-1 Expression in the Hippocampus following Neonatal Hypoxia-Ischemia and Therapeutic Hypothermia and Deficits in Spatial Memory

Developmental Neuroscience ◽

10.1159/000497056 ◽

2018 ◽

Vol 40 (5-6) ◽

pp. 508-522 ◽

Cited By ~ 2

Author(s):

Janasha Goffigan-Holmes ◽

Dafne Sanabria ◽

Johana Diaz ◽

Debra Flock ◽

Raul Chavez-Valdez

Keyword(s):

Therapeutic Hypothermia ◽

Neurodegenerative Disorders ◽

Memory Impairment ◽

Memory Deficits ◽

Nissl Staining ◽

Memory Impairments ◽

Neonatal Hypoxia ◽

Y Maze ◽

Hypoxia Ischemia ◽

With Memory

Hippocampal injury following neonatal hypoxia-ischemia (HI) leads to memory impairments despite therapeutic hypothermia (TH). In the hippocampus, the expression of calbindin-1 (Calb1), a Ca2+-buffering protein, increases during postnatal development and decreases with aging and neurodegenerative disorders. Since persistent Ca2+ dysregulation after HI may lead to ongoing injury, persistent changes in hippocampal expression of Calb1 may contribute to memory impairments after neonatal HI. We hypothesized that, despite TH, neonatal HI persistently decreases Calb1 expression in the hippocampus, a change associated with memory deficits in the mouse. We induced cerebral HI in C57BL6 mice at postnatal day 10 (P10) with right carotid ligation and 45 min of hypoxia (FiO2 = 0.08), followed by normothermia (36°C, NT) or TH (31°C) for 4 h with anesthesia-shams as controls. Nissl staining and glial fibrillary acidic protein (GFAP) immunohistochemistry (IHC) were used to grade brain injury and astrogliosis at P11, P18, and P40 prior to the assessment of Calb1 expression by IHC. The subset of mice followed to P40 also performed a memory behavior task (Y-maze) at P22–P26. Nonparametric statistics stratified by sex were applied. In both anterior and posterior coronal brain sections, hippocampal Calb1 expression doubled between P11 and P40 due to an increase in the cornus ammonis (CA) field (Kruskal-Wallis [KW] p < 0.001) and not the dentate gyrus (DG). Neonatal HI produced delayed (P18) and late (P40) deficits in the expression of Calb1 exclusively in the CA field (KW p = 0.02) in posterior brain sections. TH did not attenuate Calb1 deficits after HI. Thirty days after HI injury (at P40), GFAP scores in the hippocampus (p < 0.001, r = –0.47) and CA field (p < 0.001, r = –0.39) of posterior brain sections inversely correlated with their respective Calb1 expression. Both sexes demonstrated deficits in Y-maze testing, including approximately 40% lower spontaneous alterations performance and twice as much total impairment compared to sham mice (KW p < 0.001), but it was only in females that these deficits correlated with the Calb1 expression in the hippocampal CA field (p < 0.05) of the posterior sections. Hippocampal atrophy after neonatal HI also correlated with worse deficits in Y-maze testing, but it did not predict Calb1 deficits. Neonatal HI produces a long-lasting Calb1 deficit in the hippocampal CA field during development, which is not mitigated by TH. Late Calb1 deficit after HI may be the result of persistent astrogliosis and can lead to memory impairment, particularly in female mice.

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Effect of Metformin on Doxorubicin-Induced Memory Dysfunction

Brain Sciences ◽

10.3390/brainsci10030152 ◽

2020 ◽

Vol 10 (3) ◽

pp. 152

Author(s):

Ibrahim Alharbi ◽

Hindi Alharbi ◽

Yasser Almogbel ◽

Abdullah Alalwan ◽

Ahmad Alhowail

Keyword(s):

Cognitive Dysfunction ◽

Memory Impairment ◽

Elevated Plus Maze ◽

Male Rats ◽

Memory Impairments ◽

Glucose Levels ◽

Y Maze ◽

Altered Glucose ◽

Plus Maze ◽

With Memory

Doxorubicin (DOX) is widely used to treat many types of cancer; however, it is associated with chemotherapy-related complications such as cognitive dysfunction, known as chemobrain. Chemobrain affects up to 75% of cancer survivors, and there are currently no available therapeutic options. This study aims to examine whether metformin (MET) can protect against the neurotoxicity caused by DOX treatment. Forty male rats were divided into four groups (10 rats/group): control, DOX, DOX + MET, and MET. Rats treated with DOX received five doses of 4 mg/kg DOX weekly (cumulative dose: 20 mg/kg). For the DOX-MET and MET groups, MET (3 mg/mL) was dissolved in drinking water. Behavioral and glucose tests were performed one day after treatment was completed. We found DOX (4 mg/kg/week, 5 weeks) caused learning and memory impairment in the Y-maze, novel object recognition, and elevated plus maze behavioral tests. MET did not rescue these DOX-induced memory impairments. Neither DOX nor MET nor MET + DOX altered glucose levels following the treatment. In summary, DOX treatment is associated with memory impairment in rats, but MET does not rescue this cognitive dysfunction.

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Memory Repression: Brain Mechanisms underlying Dissociative Amnesia

Journal of Cognitive Neuroscience ◽

10.1162/jocn.2009.21212 ◽

2010 ◽

Vol 22 (3) ◽

pp. 602-613 ◽

Cited By ~ 41

Author(s):

Hirokazu Kikuchi ◽

Toshikatsu Fujii ◽

Nobuhito Abe ◽

Maki Suzuki ◽

Masahito Takagi ◽

...

Keyword(s):

Neural Activity ◽

Memory Retrieval ◽

Direct Evidence ◽

Neural Mechanisms ◽

Stressful Event ◽

Memory Impairments ◽

Dissociative Amnesia ◽

And Control ◽

Increased Activity ◽

With Memory

Dissociative amnesia usually follows a stressful event and cannot be attributable to explicit brain damage. It is thought to reflect a reversible deficit in memory retrieval probably due to memory repression. However, the neural mechanisms underlying this condition are not clear. We used fMRI to investigate neural activity associated with memory retrieval in two patients with dissociative amnesia. For each patient, three categories of face photographs and three categories of people's names corresponding to the photographs were prepared: those of “recognizable” high school friends who were acquainted with and recognizable to the patients, those of “unrecognizable” colleagues who were actually acquainted with but unrecognizable to the patients due to their memory impairments, and “control” distracters who were unacquainted with the patients. During fMRI, the patients were visually presented with these stimuli and asked to indicate whether they were personally acquainted with them. In the comparison of the unrecognizable condition with the recognizable condition, we found increased activity in the pFC and decreased activity in the hippocampus in both patients. After treatment for retrograde amnesia, the altered pattern of brain activation disappeared in one patient whose retrograde memories were recovered, whereas it remained unchanged in the other patient whose retrograde memories were not recovered. Our findings provide direct evidence that memory repression in dissociative amnesia is associated with an altered pattern of neural activity, and they suggest the possibility that the pFC has an important role in inhibiting the activity of the hippocampus in memory repression.

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