Memory impairment associated with Papez circuit lesions in patients with severe traumatic brain injury assessed by diffuse tensor imaging and volumetric MRI analysis (original) (raw)
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Cerebral correlates of declarative memory dysfunctions in early traumatic brain injury
Journal of Neurology, Neurosurgery & Psychiatry, 2005
We investigated residual brain damage in subjects who suffered severe traumatic brain injury (TBI) in childhood, and its relationship with declarative memory impairment. Magnetic resonance imaging (MRI) volumetric data and memory performance were compared between 16 adolescents with antecedents of severe TBI and 16 matched normal controls. Volumes of grey matter, white matter, cerebrospinal fluid (CSF), hippocampus, and caudate nuclei were measured. Verbal memory was assessed by the Rey's Auditory Verbal Learning test and visual memory by the Rey's Complex TBI patients performed significantly worse than controls in both verbal and visual memory. Patients presented decreased white matter volume and increased CSF. The hippocampus was reduced, but not the caudate nuclei. Memory performance correlated with CSF. Plasticity is incomplete for structural and functional deficits in children with TBI. Hippocampal atrophy, white matter loss, and memory impairment remain until adolescence. Memory sequelae are related more to diffuse brain injury, as reflected by MRI findings of increased CSF, than to hippocampal injury.
Journal of Alzheimer's Disease, 2019
Cerebral ischemia remains a leading cause of mortality worldwide. Although the incidence of death has decreased over the years, surviving patients may suffer from long-term cognitive impairments and have an increased risk for dementia. Unfortunately, research aimed toward developing therapies that can improve cognitive outcomes following cerebral ischemia has proved difficult given the fact that little is known about the underlying processes involved. Nevertheless, mechanisms that disrupt neural network activity may provide valuable insight, since disturbances in both local and global networks in the brain have been associated with deficits in cognition. In this review, we suggest that abnormal neural dynamics within different brain networks may arise from disruptions in synaptic plasticity processes and circuitry after ischemia. This discussion primarily concerns disruptions in local network activity within the hippocampus and other extra-hippocampal components of the Papez circuit, given their role in memory processing. However, impaired synaptic plasticity processes and disruptions in structural and functional connections within the Papez circuit have important implications for alterations within the global network, as well. Although much work is required to establish this relationship, evidence thus far suggests there is a link. If pursued further, findings may lead toward a better understanding of how deficits in cognition arise, not only in cerebral ischemia, but in other neurological diseases as well.
Journal of Neurotrauma, 2011
Based on the importance of the perforant pathway (PP) for normal hippocampal function, the vulnerability of temporal structures, and significant memory impairment in patients with traumatic brain injury (TBI), we investigated in vivo changes in the PP zone, hippocampus, and temporal lobe white and gray matter using diffusion tensor imaging (DTI) and volumetric analysis, and any specific relations with memory performance (Verbal Selective Reminding Test, Rey-Osterrieth Complex , in 14 patients with severe TBI. Compared to a demographically-similar control group, our patients had significantly decreased fractional anisotropy (FA) and higher apparent diffusion coefficient (ADC) for the PP zone bilaterally, and higher ADC bilaterally in the hippocampus. Volumetric analysis revealed significantly decreased volumes in both hippocampi and temporal gray matter bilaterally. Consistent long-term retrieval (CLTR) and delayed recall were significantly related to (1) right and left PP zone ADC, (2) left hippocampus ADC, and (3) left hippocampal volume. Nonverbal memory (immediate and delayed recall) was significantly associated with (1) right and left PP zone ADC, (2) left hippocampal volume, and (3) gray (immediate recall) and white (immediate recall, bilaterally; delayed recall, left) matter temporal volumes. Advanced neuroimaging analysis can detect in vivo changes in the PP zone and temporal structures in patients with severe TBI, with these changes being highly associated with memory impairment.
Journal of …, 2002
Postconcussional disorder after a relatively mild head injury is common. Although a partial organic etiology is presumed, little imaging evidence exists for this assumption. In this study, patients with mild to moderate brain injury (median Glasgow Coma Scale score of 14) had more parenchymal brain lesions than control subjects (P.)20.0ס Additionally, the authors investigated the potential of quantifying brain injury by the magnetization transfer ratio (MTR). The curve amplitude of the MTR histogram was used as a measure of normal white matter. Patients had a lower curve amplitude than control subjects (P.)800.0ס This study provides evidence of persistent traumatic brain alterations in patients who sustained a relatively mild traumatic brain injury.
Cognitive deficits in patients with mild to moderate traumatic brain injury
Traumatic brain injury (TBI) is one of the most frequent causes of brain damage. Cognitive deficits reported in the literature after moderate to severe TBI include memory, language, executive functions, attention and information processing speed impairments. However, systematic studies on patients with mild TBI are scarce although neuropsychological changes are present. Objective: To investigate the cognitive functioning of patients with mild to moderate TBI. Method: We evaluated 12 patients with mild to moderate TBI using a comprehensive protocol (PN01) of neuropsychological tests. Results: There were significant deficits of episodic memory including immediate and delayed verbal memory recall, verbal recognition, immediate and delayed visual memory recall, naming, verbal fluency and information processing speed. Conclusion: These results emphasize the importance of comprehensive neuropsychological assessments even in cases of mild TBI in order to identify impaired and preserved functions providing adequate managing including rehabilitation programs for each case. Key words: traumatic brain injury, cognitive deficits, mild to moderate level. Alterações neuropsicológicas em pacientes com traumatismo crânio encefálico leve-moderado RESUMO Traumatismo craniencefálico (TCE) é uma das causas mais freqüentes de lesão cerebral. São relatados na literatura déficits cognitivos após TCE moderado-grave relacionados à memória, linguagem, funções executivas, atenção e velocidade de processamento de informações. Estudos em pacientes com TCE leve são escassos embora alterações neuropsicológicas sejam encontradas nestes pacientes. Objetivo: Investigar o funcionamento cognitivo de pacientes com TCE leve e moderado através de um protocolo abrangente (PN01) de testes neuropsicológicos. Método: Foram avaliados 12 pacientes com TCE leve e moderado. Resultados: Foram identificados déficits graves de memória episódica verbal para evocação imediata, tardia e de reconhecimento, de memória episódica visuo-espacial para evocação imediata e tardia, nomeação, fluência verbal nominal e velocidade de processamento de informações. Conclusão: Os resultados do estudo argumentam a favor da importância de avaliação neuropsicológica abrangente mesmo em casos de TCE leve a fim de se identificar funções comprometidas e preservadas, proporcionando condutas e programas de reabilitação adequados a cada caso. Palavras-chave: traumatismo crânio encefálico, déficits cognitivos, grau leve e moderado.
PubMed, 2014
Objectives: Cognitive impairment is a common permanent sequela of traumatic brain injury (TBI). Its objectivization is based on neuropsychological and neurophysiological assessment. Neuropsychological evaluation requires a test battery, whereas for neurophysiological assessment the most significant is application of P300 Event-Related Potentials (ERPs). The aim of the study was to determine whether it is possible to differentiate between degrees of severity of TBI on the basis of neuropsychological and neurophysiological parameters. Patients and methods: A total of 90 patients with closed TBI were evaluated at least one year after trauma. Subjects were classified into three groups according to severity of TBI: mild, moderate and severe. In all subjects the Intelligence Test, the Wisconsin Card Sorting Test (WCST) and P300 ERPs were performed. Results: General intelligence measures did not prove sensitivity enough to differentiate levels of severity of TBI, whereas the number of achieved categories on the WCST significantly discerned patients with mild and moderate TBI from patients with severe TBI. Perseverative errors significantly separated patients with mild TBI from patients with moderate and severe TBI. Non-perseverative errors significantly differentiated only patients with mild TBI from patients with severe TBI. Finally, P300 latency (EPLAT) significantly differentiated patients with mild TBI from patients with moderate and severe TBI. The results show that the applied test battery can discriminate between different levels of severity of TBI and emphasize the importance of P300 ERP in the evaluation of patients with brain injury. Conclusions: Our findings indicate that the WCST and ERP P300 latency have a significant role in the assessment of cognitive deficit related to TBI.
How Mild Traumatic Brain Injury May Affect Declarative Memory Performance in the Post-Acute Stage
Journal of Neurotrauma, 2010
Memory deficits are among the most frequently reported sequelae of mild traumatic brain injury (MTBI), especially early after injury. To date, these cognitive deficits remain poorly understood, as in most patients the brain is macroscopically intact. To identify the mechanism by which MTBI causes declarative memory impairments, we probed the functionality of the medial temporal lobe (MTL) and the prefrontal cortex (PFC), within 6 weeks after injury in 43 patients from a consecutive cohort, and matched healthy controls. In addition to neuropsychological measures of declarative memory and other cognitive domains, all subjects underwent functional magnetic resonance imaging (fMRI). Behavioral results showed poorer declarative memory performance in patients than controls, and decreasing performance with increasing duration of post-traumatic amnesia (a measure of injury severity). Task performance in the scanner was, as intended by the task and design, similar in patients and controls, and did not relate to injury severity. The task used reliably activated the MTL and PFC. Although we did not find significant differences in brain activity when comparing patients and controls, we revealed, in agreement with our neuropsychological findings, an inverse correlation between MTL activity and injury severity. In contrast, no difference in prefrontal activation was found between patients and controls, nor was there a relation with injury severity. On a behavioral level, injury severity was inversely related to declarative memory performance. In all, these findings suggest that reduced medial temporal functionality may contribute to poorer declarative memory performance in the post-acute stage of MTBI, especially in patients with longer post-traumatic amnesia.
2018
Traumatic Brain Injury (TBI) in all degrees of injury severity mainly induces deviant cognitive, emotional and behavioral alterations that lead to their respective disorders. This brief overview strives to define the variables that determine the risk of occurrence of these disorders and to describe the common patterns of these disorders and their relevant neuropathogenetic mechanism(s). In addition, post-traumatic deficits can interact and exacerbate the probability, persistence and severity of each variable relative to one another. Since, neural substrates and pathways further complicate these TBI sequels, identifying the neuropathogenetic basis of these deficits using human brain mapping techniques has been a milestone in the investigations of the TBI field. It has been found that TBI-induced functional disturbance of one or more specific neural networks may cause a distinct disorder. However, this matter is a topic of discussion in TBI research. Evidently, prevalent, unpleasant TBI consequences such as motivational deficits, antisocial behaviors, aggression, disability of inhibitory control and executive function are mostly associated with the disruption of neural circuits originated from separate parts of the prefrontal cortex connected to thalamic nuclei and basal ganglia. Evidence strictly emphasizes the abnormality of the Default Mode Network (DMN) either within the network or between it and other neural networks for a majority of cognitive, emotional and sleep disorders after TBI. Therefore, imbalanced neural circuits due to TBI may serve as diagnostic and prognostic biomarkers for post-traumatic neuropsychological and neuropsychiatric disorders as well as a guide for circuit-based neurotherapy. Citation: Ramezani S, Reihanian Z, Hosseini Nejad M, Yousefzadeh-Chabok Sh. Neuropsychological and Neuropsychiatric Deficits Following Traumatic Brain Injury: Common Patterns and Neuropathological Mechanisms. Iran J Neurosurg. 2018; 4(4):185-198. http://dx.
Journal of Clinical and Experimental Neuropsychology, 2005
Deficient learning and memory are frequently reported as a consequence of traumatic brain injury (TBI). Because of the diffuse nature of the injury, patients with TBI are not the ideal group for studying brain-behavior relations. Nevertheless, characterization of the memory breakdown following TBI could contribute to the assessment and rehabilitation of this patient population. It is well documented that memory is not a unitary system. Accordingly, in this article I review studies that have investigated the long-term effect of moderate to severe TBI on different memory aspects, including explicit and implicit tests of memory. This review demonstrates that TBI affects a large range of memory aspects. One of the conclusions is that the memory impairment observed in TBI patients could be viewed, at least to some degree, as a consequence of a more general cognitive deficit. Thus, unlike patients suffering from global amnesia, memory in patients with TBI is not selectively impaired. Nevertheless, it is possible to detect a subgroup of patients that do meet the criteria of amnesia. However, the most common vulnerable memory processes following TBI very much resemble the memory deficits reported in patients following frontal lobe damage, e.g., difficulties in applying active or effortful strategy in the learning or retrieval process. The suggested similarity between patients with TBI and those suffering from frontal lobe injury should be viewed cautiously; considering the nature of TBI, patients suffering from such injuries are not a homogeneous group. In view of this limitation, the future challenge in this field will be to identify subgroups of patients, either a priori according to a range of factors such as severity of injury, or a posteriori based on their specific memory deficit characteristics. Such a research approach has the potential of explaining much of the variability in findings reported in the literature on the effect of TBI on memory.