Orientation Errors in the Memory-for-Designs Test: Tentative Findings and Recommendations

1966 ◽  
Vol 22 (2) ◽  
pp. 335-345 ◽  
Author(s):  
Barbara S. Kendall
Keyword(s):  
Brain Damage ◽  
Adult Brain ◽  
Brain Pathology ◽  
Orientation Error ◽  
Middle Position ◽  
Presence And Absence ◽  
Years Of Schooling

A study of (a) the extent to which each of 13 MFD designs triggered production of each of four types of orientation error, and of (b) the contribution of each type to the test's diagnostic effectiveness was made. The records of 137 (among 279) adult brain-damaged and 68 (among 375) control Ss who made some type of OE revealed variations in both areas of study which are reflected in proposed optional changes in scoring standards. Horizontal and 90° rotations differentiated best between presence and absence of brain pathology, vertical reversals hardly at all, and 45° rotations held a middle position. Higher brain damage to control ratios were found for younger, better educated Ss than for those older or with fewer years of schooling. Reliability of the occurrence of OEs is reported, and their relationship to sex, age, education, and intelligence is measured.

scholarly journals Nasally delivered VEGFD mimetics mitigate stroke-induced dendrite loss and brain damage

2020 ◽  
Vol 117 (15) ◽  
pp. 8616-8623
Author(s):  
Daniela Mauceri ◽  
Bettina Buchthal ◽  
Thekla J. Hemstedt ◽  
Ursula Weiss ◽  
Christian D. Klein ◽  
...  
Keyword(s):  
Brain Damage ◽  
Cognitive Abilities ◽  
Structural Integrity ◽  
Therapeutic Potential ◽  
Artery Occlusion ◽  
Adult Brain ◽  
New Class ◽  
Neurologic Disorders ◽  
Endothelial Growth Factor ◽  
Cerebral Artery Occlusion

In the adult brain, vascular endothelial growth factor D (VEGFD) is required for structural integrity of dendrites and cognitive abilities. Alterations of dendritic architectures are hallmarks of many neurologic disorders, including stroke-induced damage caused by toxic extrasynaptic NMDA receptor (eNMDAR) signaling. Here we show that stimulation of eNMDARs causes a rapid shutoff of VEGFD expression, leading to a dramatic loss of dendritic structures. Using the mouse middle cerebral artery occlusion (MCAO) stroke model, we have established the therapeutic potential of recombinant mouse VEGFD delivered intraventricularly to preserve dendritic architecture, reduce stroke-induced brain damage, and facilitate functional recovery. An easy-to-use therapeutic intervention for stroke was developed that uses a new class of VEGFD-derived peptide mimetics and postinjury nose-to-brain delivery.

scholarly journals Competition among oxidizable substrates in brains of young and adult rats. Whole homogenates

1984 ◽  
Vol 219 (1) ◽  
pp. 125-130 ◽  
Author(s):  
L M Roeder ◽  
J T Tildon ◽  
J H Stevenson
Keyword(s):  
Brain Tissue ◽  
Ketone Bodies ◽  
Adult Brain ◽  
Adult Rats ◽  
Young Rats ◽  
Age Dependent ◽  
14Co2 Production ◽  
Presence And Absence

The rates of conversion into 14CO2 of D-(-)-3-hydroxy[3-14C]butyrate, [3-14C]acetoacetate, [6-14C]glucose and [U-14C]glutamine were measured in the presence and absence of unlabelled alternative oxidizable substrates in whole homogenates from the brains of young and adult rats. The addition of unlabelled glutamine resulted in decreased 14CO2 production from [6-14C]glucose in brain homogenates from both young and adult rats. In contrast, glucose had no effect on [U-14C]glutamine oxidation. In suckling animals, both 3-hydroxybutyrate and acetoacetate decreased the rate of oxidation of [6-14C]glucose, but in adults only 3-hydroxybutyrate had an effect, and to a lesser degree. The addition of unlabelled glucose markedly enhanced the rates of oxidation of both ketone bodies in adult brain tissue and had little or no effect in the young. The rate of production of 14CO2 from [U-14C]glutamine was increased by the addition of unlabelled ketone bodies in brain homogenates from young, but not from adult rats. In the converse situation, unlabelled glutamine added to 14C-labelled ketone bodies diminished 14CO2 production in young rats, but had no effect in adult animals. These results revealed a complex age-dependent pattern of interaction in which certain substrates apparently competed with each other, whereas an enhanced rate of 14CO2 production was found with others.

Neuroanatomic and Neuropsychologic Correlates of Digit Span Performance by Brain-Damaged Adults

1986 ◽  
Vol 63 (2) ◽  
pp. 815-822 ◽  
Author(s):  
F. William Black
Keyword(s):  
Brain Damage ◽  
Left Hemisphere ◽  
Clinical Studies ◽  
Digit Span ◽  
Brain Lesions ◽  
Adult Brain ◽  
Differential Performance ◽  
Brain Injured ◽  
Correlational Data ◽  
Injured Patients

Digit repetition performance was examined in samples of adult brain-injured patients having confirmed unilateral lesions. The primary purposes of the study were to investigate the sensitivity of forward and backward repetition to the effects of lateralized brain lesions and to assess the differential neuroanatomic and neuropsychologic substrates of the two forms of digit repetition. Digit repetition, especially digits backward and particularly by patients with left-hemisphere lesions, was significantly lower than would be predicted on the basis of intelligence. However, impaired repetition was not invariably a consequence of brain damage. Correlational data suggested but could not confirm hypotheses about either the functional or the neuroanatomic substrate in differential performance on digits forward and backward. Problems implicit in using measures having a high intellectual loading in clinical studies are discussed, as are suggestions for further research.

scholarly journals Protective effect of high n-3/n-6 PUFA ratio on acute hypoxic-ischemic brain damage in mfat-1 transgenic mice and possible inflammation-related targets identified by transcriptome analysis

2020 ◽  
Author(s):  
xue geng ◽  
Meng Wang ◽  
Yunjun Leng ◽  
Lin Li ◽  
Haiyuan Yang ◽  
...  
Keyword(s):  
Brain Injury ◽  
Transgenic Mice ◽  
Brain Damage ◽  
Adult Brain ◽  
Sequencing Analysis ◽  
Protective Effects ◽  
Ischemic Brain Damage ◽  
Inflammatory Pathway ◽  
Pufa Ratio ◽  
Ischemic Brain

Abstract BackgroundAcute hypoxic-ischemic brain damage (HIBD) occurs not only in newborns but also in adults. It is associated with series of cellular and biochemical pathways that lead to neuronal injury. N-3 polyunsaturated fatty acids (PUFAs) have been reported to improve neuron functions via G protein-coupled receptor 120 signal pathway in cells or with exogenous supplementation. Possible protective targets and underlying mechanisms of high proportion of n-3/n-6 PUFAs contained in the brains of mfat-1 transgenic mice on HIBD-induced adult brain damage needed to be further investigated.MethodsThe adult C57BL/6J (WT) and mfat-1 transgenic mice adopted HIBD model. A gas chromatograph was used to determine the composition of PUFAs. Neurological deficit scores test, TTC staining and Nissl staining were employed to evaluate the neuroprotective effects. Cleaved-caspase3 and TUNEL experiment were used to detect apoptosis after injury. Inflammatory factors were detected by ELISA assay. RNA-sequencing analysis was processed and the differential expressed genes were verified by real-time quantitative PCR. Key factors related to inflammation were detected by immunofluorescence and western blot.ResultsThe mfat-1 transgenic mice with high ratio of n-3/n-6 PUFAs in brain tissues were showed to have protective effects on HIBD-induced brain damage by reduced infarct range and greatly improved neurobehavioral defects. Further analysis revealed that the level of neuronal necrosis, apoptosis and inflammation induced by brain injury were relatively low. RNA-seq analysis showed multiple pathways and targets involved in this process. Significant activation of GPR120, reduction of phosphorylation of TAK1 and NF-κB P65 in the downstream of the pro-inflammatory pathway were found in the brains of mfat-1 mice on HIBD. ConclusionsThe study showed that mfat-1 transgenic mice had protective effects on HIBD-induced brain injury by multiple pathways. Activation of GPR120 and reduction of related pro-inflammatory pathway involved in this process, which may improve or prevent dangerous perioperative and postoperative complications, innovate clinical intervention strategy and potentially benefit more patients.

Are developmental disabilities the same in children and adults?

2002 ◽  
Vol 25 (6) ◽  
pp. 768-769 ◽  
Author(s):  
Paula Tallal
Keyword(s):  
Developmental Disabilities ◽  
Life Span ◽  
Brain Damage ◽  
Developmental Dyslexia ◽  
Language Impairment ◽  
Specific Language Impairment ◽  
Developmental Disorders ◽  
Related Question ◽  
Adult Brain ◽  
Specific Language

Thomas & Karmiloff-Smith (T&K-S) raise an issue of considerable theoretical importance: Are developmental disorders like cases of adult brain damage? However, a related question: Are developmental disabilities the same in children and adults? is rarely addressed. Failure to consider the cumulative and differing effects of aberrant development across the life span confounds the current literature on both developmental dyslexia and Specific Language Impairment.

Thiamine and Alcohol for Brain Pathology: Super-imposing or Different Causative Factors for Brain Damage?

2018 ◽  
Vol 10 (1) ◽  
pp. 44-51 ◽  
Author(s):  
Rita Moretti ◽  
Paola Caruso ◽  
Matteo Dal Ben ◽  
Silvia Gazzin ◽  
Claudio Tiribelli
Keyword(s):  
Brain Damage ◽  
Brain Pathology ◽  
Causative Factors

scholarly journals Are developmental disorders like cases of adult brain damage? Implications from connectionist modelling

2002 ◽  
Vol 25 (6) ◽  
pp. 727-750 ◽  
Author(s):  
Michael Thomas ◽  
Annette Karmiloff-Smith
Keyword(s):  
Brain Damage ◽  
Developmental Disorders ◽  
Developmental Process ◽  
Adult Brain ◽  
Developmental Model ◽  
Underlying Structure ◽  
Domain Specific ◽  
Atypical Development ◽  
Developmental Conditions ◽  
Behavioural Deficits

It is often assumed that similar domain-specific behavioural impairments found in cases of adult brain damage and developmental disorders correspond to similar underlying causes, and can serve as convergent evidence for the modular structure of the normal adult cognitive system. We argue that this correspondence is contingent on an unsupported assumption that atypical development can produce selective deficits while the rest of the system develops normally (Residual Normality), and that this assumption tends to bias data collection in the field. Based on a review of connectionist models of acquired and developmental disorders in the domains of reading and past tense, as well as on new simulations, we explore the computational viability of Residual Normality and the potential role of development in producing behavioural deficits. Simulations demonstrate that damage to a developmental model can produce very different effects depending on whether it occurs prior to or following the training process. Because developmental disorders typically involve damage prior to learning, we conclude that the developmental process is a key component of the explanation of endstate impairments in such disorders. Further simulations demonstrate that in simple connectionist learning systems, the assumption of Residual Normality is undermined by processes of compensation or alteration elsewhere in the system. We outline the precise computational conditions required for Residual Normality to hold in development, and suggest that in many cases it is an unlikely hypothesis. We conclude that in developmental disorders, inferences from behavioural deficits to underlying structure crucially depend on developmental conditions, and that the process of ontogenetic development cannot be ignored in constructing models of developmental disorders.

scholarly journals Neuroradiology Big Wigs: Eponyms in Adult Brain Pathology

2020 ◽  
Author(s):  
Christopher Tournade ◽  
Felix Boucher ◽  
Bronson Yaldoo ◽  
John Kim ◽  
Toshio Moritani
Keyword(s):  
Adult Brain ◽  
Brain Pathology
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