Parieto-temporal Junction Research Articles

Rapid Eye Movement Sleep Sawtooth Waves Are Associated with Widespread Cortical Activations

Sawtooth waves (STW) are bursts of frontocentral slow oscillations recorded in the scalp electroencephalogram (EEG) during rapid eye movement (REM) sleep. Little is known about their cortical generators and functional significance. Stereo-EEG performed for presurgical epilepsy evaluation offers the unique possibility to study neurophysiology in situ in the human brain. We investigated intracranial correlates of scalp-detected STW in 26 patients (14 women) undergoing combined stereo-EEG/polysomnography. We visually marked STW segments in scalp EEG and selected stereo-EEG channels exhibiting normal activity for intracranial analyses. Channels were grouped in 30 brain regions. The spectral power in each channel and frequency band was computed during STW and non-STW control segments. Ripples (80-250 Hz) were automatically detected during STW and control segments. The spectral power in the different frequency bands and the ripple rates were then compared between STW and control segments in each brain region. An increase in 2-4 Hz power during STW segments was found in all brain regions, except the occipital lobe, with large effect sizes in the parietotemporal junction, the lateral and orbital frontal cortex, the anterior insula, and mesiotemporal structures. A widespread increase in high-frequency activity, including ripples, was observed concomitantly, involving the sensorimotor cortex, associative areas, and limbic structures. This distribution showed a high spatiotemporal heterogeneity. Our results suggest that STW are associated with widely distributed, but locally regulated REM sleep slow oscillations. By driving fast activities, STW may orchestrate synchronized reactivations of multifocal activities, allowing tagging of complex representations necessary for REM sleep-dependent memory consolidation.SIGNIFICANCE STATEMENT Sawtooth waves (STW) present as scalp electroencephalographic (EEG) bursts of slow waves contrasting with the low-voltage fast desynchronized activity of REM sleep. Little is known about their cortical origin and function. Using combined stereo-EEG/polysomnography possible only in the human brain during presurgical epilepsy evaluation, we explored the intracranial correlates of STW. We found that a large set of regions in the parietal, frontal, and insular cortices shows increases in 2-4 Hz power during scalp EEG STW, that STW are associated with a strong and widespread increase in high frequencies, and that these slow and fast activities exhibit a high spatiotemporal heterogeneity. These electrophysiological properties suggest that STW may be involved in cognitive processes during REM sleep.

A Radial Glia Fascicle Leads Principal Neurons from the Pallial-Subpallial Boundary into the Developing Human Insula.

The human insular lobe, in the depth of the Sylvian fissure, displays three main cytoarchitectonic divisions defined by the differentiation of granular layers II and IV. These comprise a rostro-ventral agranular area, an intermediate dysgranular area, and a dorso-caudal granular area. Immunohistochemistry in human embryos and fetuses using antibodies against PCNA, Vimentin, Nestin, Tbr1, and Tb2 reveals that the insular cortex is unique in that it develops far away from the ventricular zone (VZ), with most of its principal neurons deriving from the subventricular zone (SVZ) of the pallial-subpallial boundary (PSB). In human embryos (Carnegie stage 16/17), the rostro-ventral insula is the first cortical region to develop; its Tbr1+ neurons migrate from the PSB along the lateral cortical stream. From 10 gestational weeks (GW) onward, lateral ventricle, ganglionic eminences, and PSB grow forming a C-shaped curvature. The SVZ of the PSB gives rise to a distinct radial glia fiber fascicle (RGF), which courses lateral to the putamen in the external capsule. In the RGF, four components can be established: PF, descending from the prefrontal PSB to the anterior insula; FP, descending from the fronto-parietal PSB toward the intermediate insula; PT, coursing from the PSB near the parieto-temporal junction to the posterior insula, and T, ascending from the temporal PSB and merging with components FP and PT. The RGF fans out at different dorso-ventral and rostro-caudal levels of the insula, with descending fibers predominating over ascending ones. The RGF guides migrating principal neurons toward the future agranular, dysgranular, and granular insular areas, which show an adult-like definition at 32 GW. Despite the narrow subplate, and the absence of an intermediate zone except in the caudal insula, most insular subdivisions develop into a 6-layered isocortex, possibly due to the well developed outer SVZ at the PSB, which is particularly prominent at the level of the dorso-caudal insula. The small size of the initial PSB sector may, however, determine the limited surface expansion of the insula, which is in contrast to the exuberant growth of the opercula deriving from the adjacent frontal-parietal and temporal VZ/SVZ.

DIFFERENCE IN ANATOMICAL PATTERN OF CORTICAL THICKNESS BETWEEN LOGOPENIC APHASIA AND PROBABLE ALZHEIMER’S DISEASE PATIENTS IN THAILAND

We sought to demonstrate the classical anatomical pattern of cortical atrophy in Thai patients who was clinically diagnosed as logopenic aphasia (LPA) and probable Alzheimer's disease (AD), and to reveal non-classical atrophic areas that may involve in LPA but not in AD. We obtained magnetic resonance images of patients in a cohort consisting of LPA and probable AD patients to determine difference of cortical atrophy pattern between LPA and probable AD. Firstly, cortical surfaces were reconstructed from each patient's brain magnetic resonance image. Cortical thickness measurement was then processed on these surfaces. At last, thickness comparison between the two groups was performed. Our LPA patients had significant atrophy at left parieto-temporal junction [p<.01], while probable AD patients had significant regional cortical atrophy at bilateral entorhino-hippocampal region [p<.01], comparing to another group. These findings were consistent with the classical anatomical pattern of cortical atrophy. Interestingly, we also found significant regional atrophy at left [p=0.0023] and right [p=0.0011] post central gyri, left superior parietal gyrus [p=0.0017], left lingual gyrus [p=0.0071], right precentral gyrus [p=0.0004] and right rostral middle frontal gyrus [p=0.0046] in LPA, comparing to probable AD patients. We demonstrated a different cortical atrophy pattern between LPA and probable AD patients. Particularly, our study showed significant foci of cortical atrophy scattering on bilateral parietal and temporal cortices, and on right frontal cortex in LPA compared to AD. This may support the idea regarding learning disorder-related susceptibility factor for developing LPA.

Visual Hallucination and Pattern of Brain Degeneration in Parkinson's Disease

Background and Objectives: The incidence of visual hallucination (VH) increases with Parkinson's disease (PD) progression, and its development is thought to be related to a specific neurodegenerative process in PD. This study aimed to reveal brain degeneration related to VH in PD by analyzing neuroimaging data obtained from patients in their different stages of PD. Methods: Data from 48 PD patients - 21 nondemented without VH (PNV group), 10 nondemented with VH (PV group), and 17 demented with VH (PVD group) - and 30 age-matched healthy controls (HC group) were analyzed. Voxel-based morphometry and tract-based spatial statistics were conducted. Previous magnetic resonance volumetric studies on VH in PD were collectively reviewed. Results: The PV group showed gray matter atrophy in the right inferior parietal lobule and supramarginal gyrus compared with the HC and PNV groups. The PVD group showed a wider range of gray matter atrophies in the temporo-parieto-occipital regions than those in the PV group. White matter changes seemed to be an earlier event than gray matter changes. Fractional anisotropy values diffusely decreased in all three PD subgroups compared with the HC group without significant differences between the PD subgroups. Mean diffusivity was not different between the PNV and HC groups but increased in the parieto-temporal region in the PV group and increased diffusely in the PVD group, additionally including the fronto-occipital regions. A review of previous studies supported our observations. Conclusions: Gray matter degenerations from the parieto-temporal junction to the parieto-occipital and temporo-occipital regions may be responsible for VH on the typical timeline of PD progression.

Feeling unreal: a functional imaging study in patients with Kleine-Levin syndrome.

Kleine-Levin syndrome is characterized by relapsing-remitting episodes of severe hypersomnia, cognitive impairment, apathy, derealization and behavioural disturbances. Between episodes, patients have normal sleep, mood and behaviour. Functional imaging studies performed in small series of patients with Kleine-Levin syndrome with visual or semi-quantitative, uncontrolled analysis yielded equivocal brain changes. Using whole brain voxel-based group analysis, we compared brain perfusion scintigraphy during and between episodes in consecutive patients with Kleine-Levin syndrome versus healthy control subjects and correlated perfusion changes with disease severity and symptoms, focusing on less studied but disabling symptoms, such as apathy and derealization. During asymptomatic periods, 41 patients (mean age of 22.3 ± 8.1 years, 56.1% male) and 15 age- and sex-matched healthy control subjects underwent single-photon emission computed tomography scanning with technetium-99m ethyl cysteinate dimer. Eleven patients repeated the test during a symptomatic period. Compared with controls, patients during asymptomatic periods had persistent hypoperfusion in the hypothalamus, the thalamus (mainly the right posterior part), the caudate nucleus, and cortical associative areas, including the anterior cingulate, (Brodmann area 25), the orbito-frontal (Brodmann area 11) and the right superior temporal cortices (Brodmann area 22), extending to the insula (P < 0.001 in all area). Two additional hypoperfused areas emerged during symptomatic periods (P < 0.001), located in the right dorsomedial prefrontal cortex (Brodmann area 8) and the right parieto-temporal junction (Brodmann areas 22 and 39). These two areas were more affected between episodes, when the mean episode duration was longer (r = -0.53; P < 0.001). The score for the Depersonalization/Derealization Inventory during symptomatic periods strongly correlated with the hypoperfusion of the right (r = -0.74, P < 0.001) and left (r = -0.59, P < 0.005) parieto-temporal junctions. No hyperperfusion was found. Because the parieto-temporal junction (including the angular gyrus) is involved in cross-modal association between somatosensory (body knowledge), auditory and visual information, the robust hypoperfusions and correlations observed in this area may underlie the striking derealization reported by patients during episodes. Defects in the dorsomedial prefrontal cortex may cause apathy. Persistent hypoperfusion in the diencephalic and associative cortical area during asymptomatic periods is a marker of the disease, suggestive of a scenario wherein patients compensate for these deficient circuitries.

Sharp Curvature of Frontal Lobe White Matter Pathways in Children with Autism Spectrum Disorders: Tract-Based Morphometry Analysis

Because we had previously observed geometric changes of frontal lobe association pathways in children with ASD, in the present study we analyzed the curvature of these white matter pathways by using an objective TBM analysis. Diffusion tensor imaging was performed in 32 children with ASD and 14 children with typical development. Curvature, FA, AD, and RD of bilateral AF, UF, and gCC were investigated by using the TBM group analysis assessed by P(FDR) for multiple comparisons. Significantly higher curvatures were found in children with ASD, especially at the parietotemporal junction for AF (left, P(FDR) < .001; right, P(FDR) < .01), at the frontotemporal junction for UF (left, P(FDR) < .005; right, P(FDR) < .03), and at the midline of the gCC (P(FDR) < .0001). RD was significantly higher in children with ASD at the same bending regions of AF (left, P(FDR) < .03, right, P(FDR) < .02), UF (left, P(FDR) < .04), and gCC (P(FDR) < .01). Higher curvature and curvature-dependent RD changes in children with ASD may be the result of higher attenuation of thinner axons in these frontal lobe tracts.

Aberrant diffusion and geometric properties in the left arcuate fasciculus of developmentally delayed children: a diffusion tensor imaging study.

One of the neurologic substrates of poor language in children with DD is the abnormal development of perisylvian language networks. We sought to determine whether this manifests as aberrant regional changes in diffusivity or geometry of the left AF. We performed DTI studies in 16 young (age, 55.4 ± 18.95 months) patients with DD and 11 age- and sex-matched TD children (age, 60.09 ± 21.27 months). All children were right-handed. To detect the malformation of left AF structure in native or standard space, we proposed new methodology consisting of 2 complementary approaches, principal fiber orientation quantification in color-coded anisotropic maps and tract-based morphometry analysis. Patients with DD did not show the typical pattern of age-related maturity of the AP and ML pathways passing through the left AF (R(2) of the AP pathway: DD versus TD = 0.002 versus 0.4542; R(2) of the ML pathway: DD versus TD = 0.002 versus 0.4154). In addition, the patients with DD showed significantly reduced FA in the temporal portion of the AF (mean FA of DD versus TD = 0.37 ± 0.11 versus 0.48 ± 0.06, P < .001), and the AF showed higher curvatures in the parietotemporal junction, resulting in sharper bends to the Wernicke area (mean curvature of DD versus TD = 0.12 ± 0.03 versus 0.06 ± 0.02, P < .001). The proposed methods successfully revealed regional abnormalities in the axonal integrity of the left AF in the patients with DD. These abnormalities support the notion that the perisylvian language network is malformed in children with DD.

Central auditory disorders: toward a neuropsychology of auditory objects

Analysis of the auditory environment, source identification and vocal communication all require efficient brain mechanisms for disambiguating, representing and understanding complex natural sounds as 'auditory objects'. Failure of these mechanisms leads to a diverse spectrum of clinical deficits. Here we review current evidence concerning the phenomenology, mechanisms and brain substrates of auditory agnosias and related disorders of auditory object processing. Analysis of lesions causing auditory object deficits has revealed certain broad anatomical correlations: deficient parsing of the auditory scene is associated with lesions involving the parieto-temporal junction, while selective disorders of sound recognition occur with more anterior temporal lobe or extra-temporal damage. Distributed neural networks have been increasingly implicated in the pathogenesis of such disorders as developmental dyslexia, congenital amusia and tinnitus. Auditory category deficits may arise from defective interaction of spectrotemporal encoding and executive and mnestic processes. Dedicated brain mechanisms are likely to process specialized sound objects such as voices and melodies. Emerging empirical evidence suggests a clinically relevant, hierarchical and modular neuropsychological model of auditory object processing that provides a framework for understanding auditory agnosias and makes specific predictions to direct future work.

Anosognosia for hemiplegia: a clinical-anatomical prospective study

Anosognosia for hemiplegia is a common and striking disorder following stroke. Because it is typically transient and variable, it remains poorly understood and has rarely been investigated at different times in a systematic manner. Our study evaluated a prospective cohort of 58 patients with right-hemisphere stroke and significant motor deficit of the left hemibody, who were examined using a comprehensive neuropsychological battery at 3 days (hyperacute), 1 week (subacute) and 6 months (chronic) after stroke onset. Anosognosia for hemiplegia was frequent in the hyperacute phase (32%), but reduced by almost half 1 week later (18%) and only rarely seen at 6 months (5%). Anosognosia for hemiplegia was correlated with the severity of several other deficits, most notably losses in proprioception, extrapersonal spatial neglect and disorientation. While multiple regression analyses highlighted proprioceptive loss as the most determinant factor for the hyperacute period, and visuospatial neglect and disorientation as more determinant for the subacute phase, patients with both proprioceptive loss and neglect had significantly higher incidence of anosognosia for hemiplegia than those with only one deficit or no deficits (although a few double dissociations were observed). Personal neglect and frontal lobe tests showed no significant relation with anosognosia for hemiplegia, nor did psychological traits such as optimism and mood. Moreover, anosognosia for neglect and prediction of performance in non-motor tasks were unrelated to anosognosia for hemiplegia, suggesting distinct monitoring mechanisms for each of these domains. Finally, by using a voxel-based statistical mapping method to identify lesions associated with a greater severity of anosognosia, we found that damage to the insula (particularly its anterior part) and adjacent subcortical structures was determinant for anosognosia for hemiplegia in the hyperacute period, while additional lesions in the premotor cortex, cingulate gyrus, parietotemporal junction and medial temporal structures (hippocampus and amygdala) were associated with the persistence of anosognosia for hemiplegia in the subacute phase. Taken together, these results suggest that anosognosia for hemiplegia is likely to reflect a multi-component disorder due to lesions affecting a distributed set of brain regions, which can lead to several co-existing deficits in sensation, attention, interoceptive bodily representations, motor programming, error monitoring, memory and even affective processing, possibly with different combinations in different patients.

Social Interaction Revealed by Motion: Dynamics of Neuromagnetic Gamma Activity

Perception of dispositions of others revealed by movement is an essential ingredient of adaptive daily-life social behavior. Brain imaging points to several brain regions involved in visual processing of social interaction represented by motion of geometric shapes. However, temporal interrelations among these regions remain unknown. Keeping in mind that successful visual social perception depends on intact communication throughout the brain, we focus here on analysis of the induced gamma neuromagnetic response to social interaction revealed by motion. A peak of induced gamma activity of 62 Hz was found at 1 s from the stimulus onset over the right parieto-temporal junction. Two further enhancements in gamma response of lower frequency of 44 Hz occurred at 1.4 s over the medial prefrontal and posterior temporal cortices in the right hemisphere. Subsequent boosts of 44 Hz were found at 1.6 s over the left temporal and right posterior temporal cortices. For the first time, the findings identify the cortical network engaged in visual processing of social interaction revealed by motion and help to better understand proper functioning of the social brain circuitry.

意識と前頭葉―ワーキングメモリからのアプローチ―

Biological studies of human consciousness based on recent neuroimaging experiments, i.e., functional magnetic resonance imaging (fMRI) and positron emission tomography (PET), were reviewed from the viewpoint of different functions of consciousness. A biological hierarchy of consciousness structured in three levels, i.e., arousal, awareness and self-consciousness, was reviewed in connection with working memory. We found that the dorsolateral prefrontal cortex (PFC), anterior cingulate cortex, medial PFC, and parieto-temporal junction area play a crucial role in social cognition involving estimation of the mental states of other people. The ventrolateral PFC plays a role in language-based rehearsal/imitation in connection with a mirror system. Frontal pole and orbitofrontal areas are also likely to contribute to generation of self function, reward expectancy and internal planning of goal-directed behavior. Interestingly, we found that these various PFC and related areas strongly contribute to active consciousness based on the working memory system. Furthermore, we have shown that a theory-of-mind approach could be closely related to higher cognitive functions involved in working memory, which has a meta-recognition processes during mentalization.

A review of standing balance recovery from stroke

Recently, interest in the mechanisms underlying balance recovery following stroke has grown, because insight into these mechanisms is necessary to develop effective rehabilitation strategies for different types of stroke. Studies dealing with the recovery of standing balance from stroke are, however, limited to rehabilitation inpatients with a unilateral supratentorial brain infarction or haemorrhage. In most of these patients, stance stability improves in both planes as well as the ability to compensate for external and internal body perturbations and to control posture voluntarily. Although there is evidence of true physiological recovery of paretic leg muscle functions in postural control, particularly during the first three months post-stroke, substantial balance recovery also occurs in patients when there are no clear signs of improved support functions or equilibrium reactions exerted through the paretic leg. This type of recovery probably takes much longer than 3 months. Apparently, mechanisms other than the restoration of paretic leg muscle functions may determine the standing balance recovery in patients after severe stroke. No information is available about the role of stepping responses as an alternative to equilibrium reactions for restoring the ability to maintain upright stance after stroke. The finding that brain lesions involving particularly the parieto-temporal junction are associated with poor postural control, suggests that normal sensory integration is critical for balance recovery. Despite a considerable number of intervention studies, no definitive conclusions can be drawn about the best approach to facilitate the natural recovery of standing balance following stroke.

Recurrent ischemia in symptomatic carotid occlusion: prognostic value of hemodynamic factors.

To identify hemodynamic factors that predict recurrence of ipsilateral cerebral ischemic events in patients with symptomatic carotid artery occlusion (CAO). The authors studied 117 consecutive patients with CAO and corresponding recent (</=6 months) ischemic symptoms of the brain or eye that were transient or at most mildly disabling. They determined, using Cox proportional hazards analysis, the prognostic value for recurrence of ipsilateral cerebral ischemic events of 1) clinical features believed to indicate hemodynamic compromise, 2) collateral blood flow pattern, and 3) transcranial Doppler CO(2)-reactivity. None of the 24 patients with symptoms of retinal ischemia alone had a recurrent cerebral ischemic event. In the 93 patients with cerebral ischemic symptoms on entry, recurrence of these symptoms was independently predicted by 1) the nature of the initial symptoms being of purported hemodynamic origin (limb-shaking, precipitation of symptoms by rising, exercise or low blood pressure, retinal claudication) (hazard ratio [HR] 3.8, 95% CI 1.5 to 9.5), 2) continuing symptoms after the CAO had been documented, but before inclusion in the study (HR 5.9, 95% CI 2.2 to 16.1), and 3) the presence of collateral blood flow via leptomeningeal vessels (HR 4.1, 95% CI 1.3 to 13.1). CO(2)-reactivity did not predict recurrence of cerebral ischemic events. Having cerebral in contrast to retinal ischemia, clinical features suggestive of hemodynamic compromise, continuing symptoms after demonstration of the CAO, and presence of leptomeningeal collaterals may help to identify patients with symptomatic CAO at high risk of future cerebral ischemia.

Auditory mismatch negativity in schizophrenia: topographic evaluation with a high-density recording montage.

The mismatch negativity, a negative component in the auditory event-related potential, is thought to index automatic processes involved in sensory or echoic memory. The authors' goal in this study was to examine the topography of auditory mismatch negativity in schizophrenia with a high-density, 64-channel recording montage. Mismatch negativity topography was evaluated in 23 right-handed male patients with schizophrenia who were receiving medication and in 23 nonschizophrenic comparison subjects who were matched in age, handedness, and parental socioeconomic status. The Positive and Negative Syndrome Scale was used to measure psychiatric symptoms. Mismatch negativity amplitude was reduced in the patients with schizophrenia. They showed a greater left-less-than-right asymmetry than comparison subjects at homotopic electrode pairs near the parietotemporal junction. There were correlations between mismatch negativity amplitude and hallucinations at left frontal electrodes and between mismatch negativity amplitude and passive-apathetic social withdrawal at left and right frontal electrodes. Mismatch negativity was reduced in schizophrenia, especially in the left hemisphere. This finding is consistent with abnormalities of primary or adjacent auditory cortex involved in auditory sensory or echoic memory.