scholarly journals A-061 Early Childhood Prefrontal Cortex Stroke and Changes in Connections to Other Regions

2020 ◽  
Vol 35 (6) ◽  
pp. 851-851
Author(s):  
Hertza J ◽  
Burton J ◽  
Jupp K ◽  
Repp Z

Abstract Objective Sickle-cell anemia is a leading congenital cause of stroke in childhood. Such strokes can lead to cognitive deficits, stroke in the prefrontal cortex leading to inattention, impulsivity, and poor executive control. This case study examines a 23-year-old African American male who suffered from a stroke in his prefrontal cortex at age 3. Neuroimaging confirmed stroke location, but the patient had an atypical pattern of reported cognitive deficits. Method The patient was assessed in an out-patient practice. The individual was assessed with a clinical interview and comprehensive Neuropsychological Battery. The battery included cognitive and psychological measures with free-standing and imbedded validity measures. Results Cognitive testing demonstrated significant impairment in visuospatial processing speed, visual abilities, and decision making and executive control. This pattern of impairment suggests that the patient is still suffering from his stroke, which likely damaged the connective tissue of the occipital and parietal lobes, and the prefrontal cortex. The patient was diagnosed with Mild Neurocognitive Disorder in perceptual-motor and executive functioning. Conclusions These results suggest that despite the neuroplastic abilities of the brain at early ages, the neurodevelopment of individuals who suffer from stroke in early childhood is likely to be altered and contributes to cognitive impairments in early adulthood. Long-term cognitive sequelae in the form of deficits in visual perceptual skills, suggest that frontal connections to other regions in the brain may be impacted. Therefore, this case highlights that even a localized stroke in a child can lead to broader deficits if that area of the brain interacts with other areas.

1999 ◽  
Vol 11 (3) ◽  
pp. 525-543 ◽  
Author(s):  
MATCHERI S. KESHAVAN ◽  
GERARD E. HOGARTY

The central feature of schizophrenia is its onset in adolescence. Although this clinical observation is consistent with the view that schizophrenia may be a neurodevelopmental disorder, debate has focused on when the proposed brain maturational deviations may begin and what might be the nature of such defective development. Conflicting models of this illness (e.g., the early and late neurodevelopmental models) have been proposed. In this paper, we will first review concepts from basic developmental neurobiology pertinent to these issues; we then summarize aspects of the neurobiology of schizophrenia that have a particular bearing on the adolescent onset of this illness. We propose that the schizophrenic syndrome may result from early brain adversity and late maturational processes of brain development interacting with adverse humoral, biochemical, and psychosocial factors during adolescence and early adulthood. The onset of schizophrenia in adolescence may be related to the “plasticity switch” secondary to the peripubertal brain maturational changes, perhaps involving an alteration in glutamate receptor function. This loss of plasticity could result in social and nonsocial cognitive deficits that are central to the pathophysiology of schizophrenia; the vulnerable person may therefore utilize prepubertal processing styles that are insufficient to the adaptive and “gistful” abstraction requirements of adult cognition. Schizophrenia onset might occur in the context of psychosocial developmental challenges to a delayed social cognitive capacity among neurodevelopmentally compromised individuals. We review therapeutic implications as well as testable predictions generated by this model, and discuss research strategies that might further our understanding of the brain maturational abnormalities in schizophrenia.


2020 ◽  
Vol 35 (6) ◽  
pp. 866-866
Author(s):  
Burton J ◽  
Hertza J ◽  
Repp Z ◽  
Jupp K

Abstract Objective Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL) is a genetic disease that impacts small arteries in the brain and can result in ischemic strokes, seizures, and cognitive decline. This case study of a 61-year-old male illustrates the cognitive profile of an individual with CADASIL who has not suffered a major stroke event. Neuroimaging shows subcortical compromise in a diffuse manner. Methods The patient was assessed in an out-patient institutional practice. The individual was assessed with a clinical interview and comprehensive Neuropsychological Battery. The battery included cognitive and psychological measures with free-standing and imbedded validity measures. Results Cognitive testing demonstrated significant impairment in visuo-motor processing speed, executive planning, cognitive flexibility, verbal fluency, decision making, and visual memory, and suggests that the patients abilities show deterioration of subcortical regions, and is consistent with his CADASIL diagnosis. The patient was diagnosed with Mild Neurocognitive Disorder, due to medical condition. Conclusion Individuals with CADASIL often suffer from ischemic strokes and cognitive impairment. This study suggests that despite no major stroke event, individuals with CADASIL may still exhibit cognitive decline especially in subcortical regions. This case supports the theory that progressive cognitive decline in CADASIL patients does not begin as a result of a major stroke and can continue as a distinct cause of vascular neurocognitive disorder.


2016 ◽  
Vol 5 (6) ◽  
pp. 1672-1679 ◽  
Author(s):  
Jiawei Yan ◽  
Yang Liu ◽  
Qiuyue Zhao ◽  
Jie Li ◽  
Aihong Mao ◽  
...  

We investigated the question of whether the brain can be adversely affected after 4 weeks by whole-body exposure with different doses of 56Fe ion irradiation and the experiments showed that exposure resulted in significant impairment of cognitive performance.


2003 ◽  
Vol 12 (4) ◽  
pp. 146-150 ◽  
Author(s):  
Deanna M. Barch

Recent research suggests that disturbances in social and occupational functioning in individuals with schizophrenia may be more influenced by the severity of cognitive deficits than by the severity of symptoms such as hallucinations and delusions. In this article, I review evidence that one component of cognitive dysfunction in schizophrenia is a deficit in working memory, associated with disturbances in the dopamine system in dorsolateral prefrontal cortex. I suggest that although the cognitive deficits in schizophrenia include working memory dysfunction, because they arise from a disturbance in executive control processes (e.g., the representation and maintenance of context), they extend to a range of cognitive domains. Finally, I discuss the need for further research on the ways in which contextual processing deficits may influence other aspects of this illness, including emotional processing.


2021 ◽  
Vol 6 ◽  
Author(s):  
Nobuki Watanabe

The development of executive functions is remarkable in early childhood. Therefore, research on how to support the development of executive functions is actively being conducted. It has already been indicated that executive functions are related to the prefrontal cortex. Recent evidence suggests that the prefrontal cortex is involved in mental abacus (MA). Further, the study of the abacus—the base of MA—is good for not only mathematics but also nurturing the brain. However, although the abacus is easy to learn, learning opportunities have shrunk because of the widespread use of calculators. Through this educational pilot case study, I examined whether it is possible that even easy calculations during the introduction of abacus calculation in early childhood may have an effect on executive function support. I measured the activation of cerebral blood flow in the prefrontal cortex of a young child while he worked on the Wechsler Intelligence Scale for Children-IV; Working Memory Index tasks (forward digit-span task, backward digit-span task, and letter–number sequencing task); and the abacus calculation task using HOT-2000 (NeU, Japan), a two-channel wearable functional near-infrared spectroscopy device. The results revealed a significant difference between the abacus calculation task and the forward digit-span task; however, there was no significant difference between the abacus calculation task and other tasks. In other words, the brain in the prefrontal cortex was more activated in the abacus task than in the forward digit-span task. Difficulty levels were found to be in the order of the forward digit-span task, backward digit-span task, and letter–number sequencing task. Thus, there is a possibility that even simple abacus calculation has a positive effect on executive functions, especially working memory support, in early childhood. This study’s results provide a breakthrough in cognitive psychology, educational psychology, neuropsychology, and other fields related to child support, which are struggling to find valuable, practical practices for children in the field (i.e., schools and homes) beyond the laboratory.


2018 ◽  
Author(s):  
Jane X. Wang ◽  
Zeb Kurth-Nelson ◽  
Dharshan Kumaran ◽  
Dhruva Tirumala ◽  
Hubert Soyer ◽  
...  

Over the past twenty years, neuroscience research on reward-based learning has converged on a canonical model, under which the neurotransmitter dopamine ‘stamps in’ associations between situations, actions and rewards by modulating the strength of synaptic connections between neurons. However, a growing number of recent findings have placed this standard model under strain. In the present work, we draw on recent advances in artificial intelligence to introduce a new theory of reward-based learning. Here, the dopamine system trains another part of the brain, the prefrontal cortex, to operate as its own free-standing learning system. This new perspective accommodates the findings that motivated the standard model, but also deals gracefully with a wider range of observations, providing a fresh foundation for future research.


Author(s):  
Jochen Seitz ◽  
Katharina Bühren ◽  
Georg G. von Polier ◽  
Nicole Heussen ◽  
Beate Herpertz-Dahlmann ◽  
...  

Objective: Acute anorexia nervosa (AN) leads to reduced gray (GM) and white matter (WM) volume in the brain, which however improves again upon restoration of weight. Yet little is known about the extent and clinical correlates of these brain changes, nor do we know much about the time-course and completeness of their recovery. Methods: We conducted a meta-analysis and a qualitative review of all magnetic resonance imaging studies involving volume analyses of the brain in both acute and recovered AN. Results: We identified structural neuroimaging studies with a total of 214 acute AN patients and 177 weight-recovered AN patients. In acute AN, GM was reduced by 5.6% and WM by 3.8% compared to healthy controls (HC). Short-term weight recovery 2–5 months after admission resulted in restitution of about half of the GM aberrations and almost full WM recovery. After 2–8 years of remission GM and WM were nearly normalized, and differences to HC (GM: –1.0%, WM: –0.7%) were no longer significant, although small residual changes could not be ruled out. In the qualitative review some studies found GM volume loss to be associated with cognitive deficits and clinical prognosis. Conclusions: GM and WM were strongly reduced in acute AN. The completeness of brain volume rehabilitation remained equivocal.


Author(s):  
Burbaeva G.Sh. ◽  
Androsova L.V. ◽  
Vorobyeva E.A. ◽  
Savushkina O.K.

The aim of the study was to evaluate the rate of polymerization of tubulin into microtubules and determine the level of colchicine binding (colchicine-binding activity of tubulin) in the prefrontal cortex in schizophrenia, vascular dementia (VD) and control. Colchicine-binding activity of tubulin was determined by Sherlinе in tubulin-enriched extracts of proteins from the samples. Measurement of light scattering during the polymerization of the tubulin was carried out using the nephelometric method at a wavelength of 450-550 nm. There was a significant decrease in colchicine-binding activity and the rate of tubulin polymerization in the prefrontal cortex in both diseases, and in VD to a greater extent than in schizophrenia. The obtained results suggest that not only in Alzheimer's disease, but also in other mental diseases such as schizophrenia and VD, there is a decrease in the level of tubulin in the prefrontal cortex of the brain, although to a lesser extent than in Alzheimer's disease, and consequently the amount of microtubules.


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