scholarly journals Distinct Cortical Anatomy Linked to Subregions of the Medial Temporal Lobe Revealed by Intrinsic Functional Connectivity

2008 ◽  
Vol 100 (1) ◽  
pp. 129-139 ◽  
Author(s):  
Itamar Kahn ◽  
Jessica R. Andrews-Hanna ◽  
Justin L. Vincent ◽  
Abraham Z. Snyder ◽  
Randy L. Buckner

The hippocampus and adjacent cortical structures in the medial temporal lobe (MTL) contribute to memory through interactions with distributed brain areas. Studies of monkey and rodent anatomy suggest that parallel pathways converge on distinct subregions of the MTL. To explore the cortical areas linked to subregions of the MTL in humans, we examined cortico-cortical and hippocampal-cortical correlations using high-resolution, functional connectivity analysis in 100 individuals. MTL seed regions extended along the anterior to posterior axis and included hippocampus and adjacent structures. Results revealed two separate brain pathways that correlated with distinct subregions within the MTL. The body of the hippocampus and posterior parahippocampal cortex correlated with lateral parietal cortex, regions along the posterior midline including posterior cingulate and retrosplenial cortex, and ventral medial prefrontal cortex. By contrast, anterior hippocampus and the perirhinal/entorhinal cortices correlated with distinct regions in the lateral temporal cortex extending into the temporal pole. The present results are largely consistent with known connectivity in the monkey and provide a novel task-independent dissociation of the parallel pathways supporting the MTL memory system in humans. The cortical pathways include regions that have undergone considerable areal expansion in humans, providing insight into how the MTL memory system has evolved to support a diverse array of cognitive domains.

2002 ◽  
Vol 357 (1424) ◽  
pp. 1111-1121 ◽  
Author(s):  
David Gaffan

The medial temporal lobe is indispensable for normal memory processing in both human and non–human primates, as is shown by the fact that large lesions in it produce a severe impairment in the acquisition of new memories. The widely accepted inference from this observation is that the medial temporal cortex, including the hippocampal, entorhinal and perirhinal cortex, contains a memory system or multiple memory systems, which are specialized for the acquisition and storage of memories. Nevertheless, there are some strong arguments against this idea: medial temporal lesions produce amnesia by disconnecting the entire temporal cortex from neuromodulatory afferents arising in the brainstem and basal forebrain, not by removing cortex; the temporal cortex is essential for perception as well as for memory; and response properties of temporal cortical neurons make it impossible that some kinds of memory trace could be stored in the temporal lobe. All cortex is plastic, and it is possible that the same rules of plasticity apply to all cortical areas; therefore, memory traces are stored in widespread cortical areas rather than in a specialized memory system restricted to the temporal lobe. Among these areas, the prefrontal cortex has an important role in learning and memory, but is best understood as an area with no specialization of function.


Brain ◽  
2021 ◽  
Author(s):  
David Berron ◽  
Jacob W Vogel ◽  
Philip S Insel ◽  
Joana B Pereira ◽  
Long Xie ◽  
...  

Abstract In Alzheimer’s disease, postmortem studies have shown that the first cortical site where neurofibrillary tangles appear is the transentorhinal region, a subregion within the medial temporal lobe that largely overlaps with area 35, and the entorhinal cortex. Here we used tau-PET imaging to investigate the sequence of tau pathology progression within the human medial temporal lobe and across regions in the posterior-medial system. Our objective was to study how medial temporal tau is related to functional connectivity, regional atrophy, and memory performance. We included 215 β-amyloid negative cognitively unimpaired, 81 β-amyloid positive cognitively unimpaired and 87 β-amyloid positive individuals with mild cognitive impairment, who each underwent [18]F-RO948 tau and [18]F-flutemetamol amyloid PET imaging, structural T1-MRI and memory assessments as part of the Swedish BioFINDER-2 study. First, event-based modelling revealed that the entorhinal cortex and area 35 show the earliest signs of tau accumulation followed by the anterior and posterior hippocampus, area 36 and the parahippocampal cortex. In later stages, tau accumulation became abnormal in neocortical temporal and finally parietal brain regions. Second, in cognitively unimpaired individuals, increased tau load was related to local atrophy in the entorhinal cortex, area 35 and the anterior hippocampus and tau load in several anterior medial temporal lobe subregions was associated with distant atrophy of the posterior hippocampus. Tau load, but not atrophy, in these regions was associated with lower memory performance. Further, tau-related reductions in functional connectivity in critical networks between the medial temporal lobe and regions in the posterior-medial system were associated with this early memory impairment. Finally, in patients with mild cognitive impairment, the association of tau load in the hippocampus with memory performance was partially mediated by posterior hippocampal atrophy. In summary, our findings highlight the progression of tau pathology across medial temporal lobe subregions and its disease-stage specific association with memory performance. While tau pathology might affect memory performance in cognitively unimpaired individuals via reduced functional connectivity in critical medial temporal lobe-cortical networks, memory impairment in mild cognitively impaired patients is associated with posterior hippocampal atrophy.


Hippocampus ◽  
2012 ◽  
Vol 23 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Sandhitsu R. Das ◽  
John Pluta ◽  
Lauren Mancuso ◽  
Dasha Kliot ◽  
Sylvia Orozco ◽  
...  

2003 ◽  
Vol 23 (16) ◽  
pp. 6520-6528 ◽  
Author(s):  
Anthony Randal McIntosh ◽  
M. Natasha Rajah ◽  
Nancy J. Lobaugh

Author(s):  
T. W. Robbins

This chapter discusses the integration of the neurobiological and neuropsychological dimensions of autism. It includes a survey of the major neural theories of autism (medial temporal lobe hypothesis, the cerebellar hypothesis, the frontostriatal hypothesis, and evidence from neuroimaging and neuropsychology), and a summary of research suggestions (neuroimaging in a cognitive context, functional connectivity from neuroimaging, and cluster analysis of autistic symptoms).


2020 ◽  
pp. 155005942097226
Author(s):  
Ayumi Sakata ◽  
Nobutaka Mukae ◽  
Takato Morioka ◽  
Shunya Tanaka ◽  
Takafumi Shimogawa ◽  
...  

Objective Lateralized periodic discharges (LPDs), which constitute an abnormal electroencephalographic (EEG) pattern, are most often observed in critically ill patients with acute pathological conditions, and are less frequently observed in chronic conditions such as focal epilepsies, including temporal lobe epilepsy (TLE). Here we aim to explore the pathophysiological mechanism of LPD in TLE. Methods We retrospectively selected 3 patients with drug-resistant TLE who simultaneously underwent EEG and electrocorticography (ECoG) and demonstrated LPDs. We analyzed the correlation between the EEG and ECoG findings. Results In patients 1 and 2, LPDs were recorded in the temporal region of the scalp during the interictal periods, when repeated spikes followed by slow waves (spike-and-wave complexes; SWs) and periodic discharges (PDs) with amplitudes of >600 to 800 µV appeared in the lateral temporal lobe over a cortical area of >10 cm2. In patient 3, when the ictal discharges persisted and were confined to the medial temporal lobe, repeated SWs were provoked on the lateral temporal lobe. When repeated SWs with amplitudes of >800 µV appeared in an area of the lateral temporal lobe of >10 cm2, the corresponding EEG discharges appeared on the temporal scalp. Conclusions LPDs in patients with TLE originate from repeated SWs and PDs of the lateral temporal lobe, which might represent a highly irritable state of the lateral temporal cortex during both interictal and ictal periods.


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