Prefrontal Cortex Lesions Research Articles

Interaction of the dorsolateral prefrontal cortex with the precuneal medial parietal cortex for the monitoring of information in working memory in the macaque monkey.

The executive control process of monitoring information in working memory depends on the mid-dorsolateral prefrontal cortical region (cytoarchitectonic areas 46 and 9/46) in interaction with the hippocampal memory system. Anatomical studies demonstrated strong connectivity between the mid-dorsolateral prefrontal cortex and the medial parietal area PGm that lies on the precuneus. Area PGm is also strongly connected with the attentional system on the lateral inferior parietal lobule (area PG) and the limbic retrosplenial/posterior cingulate region that interacts with the hippocampal memory system. Thus, in terms of anatomical connectivity, area PGm appears to be a critical node for the integration of executive control processing from the prefrontal cortex with the online attentional and memory related processing. This hypothesis was tested in macaque monkeys with the crossed unilateral lesion methodology. A unilateral lesion in the mid-dorsolateral prefrontal cortex was combined with a unilateral lesion in area PGm in the opposite hemisphere. The results demonstrated an impairment on the externally ordered working memory task that assesses the monitoring of information in working memory. Thus, the medial parietal area PGm is a critical node in mediating the functional interaction between the prefrontal region for the executive control process of monitoring information and the memory system.

Memory’s gatekeeper: The role of PFC in the encoding of congruent events

Theoretical models conventionally portray the consolidation of memories as a slow process that unfolds during sleep. According to the classical Complementary Learning Systems theory, the hippocampus (HPC) rapidly changes its connectivity during wakefulness to encode ongoing events and create memory ensembles that are later transferred to the prefrontal cortex (PFC) during sleep. However, recent experimental studies challenge this notion by showing that new information consistent with prior knowledge can be rapidly consolidated in PFC during wakefulness and that PFC lesions disrupt the encoding of congruent events in the HPC. The contributions of the PFC to memory encoding have therefore largely been overlooked. Moreover, most theoretical frameworks assume random and uncorrelated patterns representing memories, disregarding the correlations between our experiences. To address these shortcomings, we developed a HPC-PFC network model that simulates interactions between the HPC and PFC during the encoding of a memory (awake stage), and subsequent consolidation (sleeping stage) to examine the contributions of each region to the consolidation of novel and congruent memories. Our results show that the PFC network uses stored memory "schemas" consolidated during previous experiences to identify inputs that evoke congruent patterns of activity, quickly integrate it into its network, and gate which components are encoded in the HPC. More specifically, the PFC uses GABAergic long-range projections to inhibit HPC neurons representing input components correlated with a previously stored memory "schema," eliciting sparse hippocampal activity during exposure to congruent events, as it has been experimentally observed.

Dissociable roles of the dorsolateral and ventromedial prefrontal cortex in human categorization.

Models of human categorization predict the prefrontal cortex (PFC) serves a central role in category learning. The dorsolateral prefrontal cortex (dlPFC) and ventromedial prefrontal cortex (vmPFC) have been implicated in categorization; however, it is unclear whether both are critical for categorization and whether they support unique functions. We administered three categorization tasks to patients with PFC lesions (mean age = 69.6 years; 5 men, 5 women) to examine how prefrontal subregions contribute to categorization. These included a rule-based (RB) task that was solved via a unidimensional rule, an information integration (II) task that was solved by combining information from two stimulus dimensions, and a deterministic/probabilistic (DP) task with stimulus features that had varying amounts of category-predictive information. Compared to healthy comparison participants, both patient groups had impaired performance. Impairments in the dlPFC patients were largest during the RB task, whereas impairments in the vmPFC patients were largest during the DP task. A hierarchical model was fit to the participants' data to assess learning deficits in the patient groups. PFC damage was correlated with a regularization term that limited updates to attention after each trial. Our results suggest that the PFC, as a whole, is important for learning to orient attention to relevant stimulus information. The dlPFC may be especially important for rule-based learning, whereas the vmPFC may be important for focusing attention on deterministic (highly diagnostic) features and ignoring less predictive features. These results support overarching functions of the dlPFC in executive functioning and the vmPFC in value-based decision making.Significance Statement Category learning creates flexible memory representations that easily generalize to novel situations. Although it is generally established that the prefrontal cortex is central to categorization, it is unclear how different prefrontal subregions contribute to learning. Separate literatures have implicated both the dorsolateral prefrontal cortex (dlPFC) and the ventromedial prefrontal cortex (vmPFC) in categorization, but there has been little effort to bridge these literatures. The current study is the first to examine categorization in patients with lesions centered in the dlPFC and vmPFC. We found that, as a whole, the PFC orients attention to relevant stimulus information. The dlPFC is important for rule-based learning, whereas the vmPFC is important for focusing attention on highly diagnostic features and ignoring less predictive features.

Complete ocular tilt reaction with subjective visual vertical tilt in a patient with a medial prefrontal cortex lesion: a case report

A 61-year-old male patient undergoing chemotherapy for esophageal cancer presented with symptoms of rightward tilting while both sitting and walking. A neurological examination revealed a head tilt, skew deviation with hypertrophy of the left eye, and a rightward shift in his gait. No spontaneous nystagmus was observed, and the vestibulo-ocular reflex was normal. Magnetic resonance imaging of the head revealed a suspected metastatic lesion in the right medial prefrontal cortex. Following the initiation of levetiracetam treatment, the patient demonstrated marked improvement, with the resolution of both head tilt and skew deviation within 1 month. Traditionally, the ocular tilt reaction has been attributed to unilateral or asymmetric dysfunction of the graviceptive pathways extending from the utricle to the upper midbrain lesions. However, this case highlights the potential involvement of the prefrontal cortex in the ocular tilt reaction. Further research is warranted on the role of the prefrontal cortex within the vestibular system.

Effects of extended practice and unitization on relational memory in older adults and neuropsychological lesion cases

ABSTRACT Unitization – the fusion of objects into a single unit through an action/consequence sequence – can mitigate relational memory impairments, but the circumstances under which unitization is effective are unclear. Using transverse patterning (TP), we compared unitization (and its component processes of fusion, motion, and action/consequence) with extended practice on relational learning and transfer in older adults and neuropsychological cases with lesions (to varying extents) in the medial prefrontal cortex (mPFC) or hippocampus/medial temporal lobe (HC/MTL). The latter included a person with bilateral HC lesions primarily within the dentate gyrus. For older adults, TP accuracy increased, and transfer benefits were observed, with extended practice and unitization. Broadly, the lesion cases did not benefit from either extended practice or unitization, suggesting the mPFC and dentate gyrus play important roles in relational memory and in unitization. The results suggest that personalized strategy interventions must align with the cognitive and neural profiles of the user.

Imaging and clinical predictors of acute constipation in patients with acute ischemic stroke.

Constipation symptoms are highly prevalent in acute ischemic stroke, but the clinical and neuroimaging predictors are unknown. This study aimed to identify lesions and clinical features associated with acute constipation. Data from patients with acute ischemic stroke registered in a hospital-based stroke registry between January 2018 and December 2019 were analyzed. Clinical, laboratory, and imaging features were examined for associations with acute constipation. Using the topographic lesion on diffusion-weighted images, multivariate support vector regression-based lesion-symptom mapping (SVR-LSM) was conducted and compared between the non-constipation and acute constipation groups. A total of 256 patients (mean age 67 years, men: 64%) were included. Acute constipation was noted in 81 patients (32%). Initial stroke severity, represented by initial National Institutes of Health and Stroke Scale (NIHSS) scores, was associated with acute constipation. Laboratory parameters, including fibrin degradation products (FDP), fibrinogen, D-dimer, lipoprotein (a), and free fatty acid levels, also showed statistically significant differences between the non-constipation and constipation groups. FDP, D-dimer, and free fatty acid levels were independently associated with acute constipation in the logistic regression model after adjusting for initial NIHSS scores and potassium levels. SVR-LSM revealed that bilateral lesions in the precentral gyrus, insula, opercular part of the inferior frontal gyrus, the inferior parietal lobule, and lesions in the right middle frontal gyrus were significantly associated with acute constipation. The results were consistent after controlling for the initial NIHSS scores and poststroke potassium levels. When cardioembolic stroke subjects were excluded, the right insular and prefrontal cortex lesions lost their association with acute constipation. Acute constipation symptoms after acute ischemic stroke are mainly related to bilateral lesions in the insula, precentral gyrus, postcentral gyrus, and inferior parietal lobule. Clinically important predictors of acute constipation include initial neurological severity and thromboembolic markers of stroke.

Neuroanatomy of post-stroke depression: the association between symptom clusters and lesion location.

Post-stroke depression affects about 30% of stroke patients and often hampers functional recovery. The diagnosis of depression encompasses heterogeneous symptoms at emotional, motivational, cognitive, behavioural or somatic levels. Evidence indicates that depression is caused by disruption of bio-aminergic fibre tracts between prefrontal and limbic or striatal brain regions comprising different functional networks. Voxel-based lesion-symptom mapping studies reported discrepant findings regarding the association between infarct locations and depression. Inconsistencies may be due to the usage of sum scores, thereby mixing different symptoms of depression. In this cross-sectional study, we used multivariate support vector regression for lesion-symptom mapping to identify regions significantly involved in distinct depressive symptom domains and global depression. MRI lesion data were included from 200 patients with acute first-ever ischaemic stroke (mean 0.9 ± 1.5 days of post-stroke). The Montgomery-Åsberg Depression Rating interview assessed depression severity in five symptom domains encompassing motivational, emotional and cognitive symptoms deficits, anxiety and somatic symptoms and was examined 8.4 days of post-stroke (±4.3). We found that global depression severity, irrespective of individual symptom domains, was primarily linked to right hemispheric lesions in the dorsolateral prefrontal cortex and inferior frontal gyrus. In contrast, when considering distinct symptom domains individually, the analyses yielded much more sensitive results in regions where the correlations with the global depression score yielded no effects. Accordingly, motivational deficits were associated with lesions in orbitofrontal cortex, dorsolateral prefrontal cortex, pre- and post-central gyri and basal ganglia, including putamen and pallidum. Lesions affecting the dorsal thalamus, anterior insula and somatosensory cortex were significantly associated with emotional symptoms such as sadness. Damage to the dorsolateral prefrontal cortex was associated with concentration deficits, cognitive symptoms of guilt and self-reproach. Furthermore, somatic symptoms, including loss of appetite and sleep disturbances, were linked to the insula, parietal operculum and amygdala lesions. Likewise, anxiety was associated with lesions impacting the central operculum, insula and inferior frontal gyrus. Interestingly, symptoms of anxiety were exclusively left hemispheric, whereas the lesion-symptom associations of the other domains were lateralized to the right hemisphere. In conclusion, this large-scale study shows that in acute stroke patients, differential post-stroke depression symptom domains are associated with specific structural correlates. Our findings extend existing concepts on the neural underpinnings of depressive symptoms, indicating that differential lesion patterns lead to distinct depressive symptoms in the first weeks of post-stroke. These findings may facilitate the development of personalized treatments to improve post-stroke rehabilitation.

Chemogenetic activation of prefrontal astroglia enhances recognition memory performance in rat

Prefrontal cortex (PFC) inputs to the hippocampus are supposed to be critical in memory processes. Astrocytes are involved in several brain functions, such as homeostasis, neurotransmission, synaptogenesis. However, their role in PFC-mediated modulation of memory has yet to be studied. The present study aims at uncovering the role of PFC astroglia in memory performance and synaptic plasticity in the hippocampus. Using chemogenetic and lesions approaches of infralimbic PFC (IL-PFC) astrocytes, we evaluated memory performance in the novel object recognition task (NOR) and dorsal hippocampus synaptic plasticity. We uncovered a surprising role of PFC astroglia in modulating object recognition memory. In opposition to the astroglia PFC lesion, we show that chemogenetic activation of IL-PFC astrocytes increased memory performance in the novel object recognition task and facilitated in vivo dorsal hippocampus synaptic metaplasticity. These results redefine the involvement of PFC in recognition mnemonic processing, uncovering an important role of PFC astroglia.

The neuropsychology and neuroanatomy of reduplicative paramnesia

Reduplicative paramnesia refers to the delusional belief that there are identical places in different locations. In this case–control study we investigated the clinical, phenomenological, neuropsychological and neuroanatomical data of eleven patients with reduplicative paramnesia and compared them against a control group of eleven patients with severe spatial disorientation without signs of reduplicative paramnesia.We show that most patients with reduplicative paramnesia report that a current place is reduplicated and/or relocated to an other familiar place. Patients with reduplicative paramnesia show a higher prevalence of deficits in the executive functions compared to the control patients, while mnestic and visuo-spatial deficits were both frequent in patients with reduplicative paramnesia and the control group. Patients with reduplicative paramnesia mostly suffer from right hemispheric lesions with a maximal overlap in the dorsolateral prefrontal cortex. Using lesion network mapping we show that lesions causing reduplicative paramnesia are connected to bilateral anterior insula and the right cingulate cortex.We argue that patients with reduplicative paramnesia fail to integrate the actual context with visuo-spatial memories and personal relevant emotional information due to a disruption of the neural network within the anterior temporal lobe, the cingulate cortex and the anterior insula. Also patients with reduplicative paramnesia are not able to resolve this conflict due to the lesion of the dorsolateral prefrontal cortex and executive dysfunction.

Prefrontal and medial temporal interactions in memory functions in the rhesus monkey.

Both the medial temporal lobe and the dorsolateral prefrontal cortex have been implicated in learning and memory. However, it has been difficult to ascertain the degree to which the two structures are dependent on each other or interact in subserving these cognitive functions. To investigate this question directly, we prepared two group of monkeys. First, the contralateral frontal-hippocampal split group (CFHS) received a unilateral lesion of the hippocampus and surrounding posterior parahippocampal cortices (H +), combined with a contralateral lesion of the dorsolateral prefrontal cortex (DLPFC) plus transection of the corpus callosum and anterior commissure. This preparation functionally "disconnects" the remaining intact H + from the sole intact DLPFC in the opposite hemisphere. As a surgical control group, a second set of animals, the ipsilateral frontal-hippocampal split group, was prepared with a unilateral lesion of the DLPFC and an ipsilateral H + lesion together plus transection of the corpus callosum and anterior commissure. This preparation matches the locus and extent of damage in the cross-lesion group but allows the intact H + and intact DLPFC to interact ipsilaterally. Following recovery from surgery, all animals were then tested on the delayed nonmatching to sample task (DNMS), a test of recognition memory. The crossed-lesion split-brain group (CFHS) was markedly impaired on DNMS in both acquisition (rule learning) and performance over delays (recognition memory). The results provide evidence of a functionally dependent interaction between the medial temporal lobe and the dorsolateral prefrontal cortex in learning and memory. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Impact of nonalcoholic fatty liver disease-related metabolic state on depression.

Nonalcoholic fatty liver disease (NAFLD), also recently referred as metabolic (dysfunction)-associated fatty liver disease (MAFLD), is characterized by hepatocyte steatosis in the setting of a metabolic risk conditions and in the absence of an underlying precursor, for instance alcohol consumption, hepatotropic viruses and hepatotoxic drugs. A possible association between NAFLD and depression has been proposed, owing to intersecting pathophysiological pathways. This narrative review aimed to summarize the current evidence that illustrate the potential pathophysiological and clinical linkage between NAFLD-related metabolic state and depression. Prefrontal cortex lesions are suggested to be a consequence of liver steatosis-associated systematic hyperinflammatory state, a phenomenon also occurring in depression. In addition, depressive symptoms are present in neurotransmitter imbalances. These abnormalities seem to be correlated with NAFLD/MAFLD, in terms of insulin resistance (IR), ammonia and gut dysbiosis' impact on serotonin, dopamine, noradrenaline levels and GABA (gamma aminobutyric acid) receptors. Furthermore, reduced levels of nesfatin-1 and copine-6-associated BDNF (brain-derived neurotrophic factor) levels have been considered as a probable link between NAFLD and depression. Regarding NAFLD-related gut dysbiosis, it stimulates mediators including lipopolysaccharides, short-chain fatty acids and bile acids, which play significant role in depression. Finally, western diet and IR, which are mainstay components of NAFLD/MAFLD, are, also, substantiated to affect neurotransmitters in hippocampus and produce neurotoxic lipids that contribute to neurologic dysfunction, and thus trigger emotional disturbances, mainly depressive symptoms.

Prefrontal cortex is necessary for long-term social recognition memory in mice

The prefrontal cortex (PFC) plays critical roles in social cognition and emotional regulation in humans and rodents; however, its involvement in social recognition memory in mice remains unclear. Here, we examined the roles of the PFC in short-term and long-term social recognition memory, social motivation, and anxiety-related behavior in C57BL/6J male mice. Sham control and PFC-lesioned mice underwent four different behavioral tests. In the social recognition test, composed of three daily trials over 3 consecutive days, the control mice spent less time investigating the juvenile stimulus mouse both within each day and across days. By contrast, while social investigation behavior in PFC-lesioned mice decreased across the three trials within each day, it did not decrease over the 3-day testing period. These results indicate that the PFC has an important role in long-term, but not short-term, social recognition memory. The control and PFC-lesioned mice exhibited similar social motivation in the three-chamber test – both groups preferred the juvenile mouse to the empty cylinder and did not prefer the adult mouse. In addition, the PFC lesion had no impact on anxiety-related behavior or general activity in the light–dark transition test or the open field test. Our findings demonstrate that the PFC is essential for long-term social recognition memory and that it plays a critical role in higher-order social cognition.

Medial prefrontal cortex lesions disrupt prepotent action selection signals in dorsomedial striatum

The ability to inhibit or adapt unwanted actions or movements is a critical feature of almost all forms of behavior. Many have attributed this ability to frontal brain areas such as the anterior cingulate cortex (ACC) and the medial prefrontal cortex (mPFC), but the exact contribution of each brain region is often debated because their functions are not examined in animals performing the same task. Recently, we have shown that ACC signals a need for cognitive control and is crucial for the adaptation of action selection signals in dorsomedial striatum (DMS) in rats performing a stop-change task. Here, we show that unlike ACC, the prelimbic region of mPFC does not disrupt the inhibition or adaption of an action plan at either the level of behavior or downstream firing in DMS. Instead, lesions to mPFC correlate with changes in DMS signals involved in action initiation and disrupt performance on GO trials while improving performance on STOP trials.

Effects of Quinolinate-Induced Lesion of the Medial Prefrontal Cortex on Prefrontal and Striatal Concentrations of D-Serine in the Rat.

D-Serine has been shown to play an important role in the expression and control of a variety of brain functions by acting as the endogenous coagonist for the N-methyl-D-aspartate type glutamate receptor (NMDAR), at least, in the forebrain. To obtain further insight into the still debatable cellular localization of the D-amino acid, we have examined the effects of the selective destruction of the neuronal cell bodies by quinolinate on the tissue or extracellular D-serine concentrations in the medial prefrontal cortex of the rat. A local quinolinate infusion into the bilateral medial prefrontal cortex produced a cortical lesion with a marked (- 65%) and non-significant alteration (- 5%) in the cortical and striatal tissue D-serine concentrations, respectively, 7days post-infusion. In vivo microdialysis experiments in the right prefrontal lesion site 9days after the quinolinate application revealed that the basal extracellular D-serine levels were also dramatically reduced (- 64%). A prominent reduction in the tissue levels of GABA in the interneurons of the prefrontal cortex (- 78%) without significant changes in those in the striatum (+ 12%) verified that a major lesion part was confined to the cortical portion. The lack of a significant influence of the prefrontal quinolinate lesion on its dopamine concentrations in the mesocortical dopamine projections suggests that the nerve terminals and axons in the lesion site may be spared. These findings are consistent with the perikarya-selective nature of the present quinolinate-induced lesion and further support the view that neuronal cell bodies of intrinsic neurons in the prefrontal cortical region contain substantial amounts of D-serine, which may sustain the basal extracellular concentrations of D-serine.

Lesions in different prefrontal sectors are associated with different types of acquired personality disturbances

“Frontal lobe syndrome” is a term often used to describe a diverse array of personality disturbances following frontal lobe damage. This study's guiding premise was that greater neuroanatomical specificity could be achieved by evaluating specific types of personality disturbances following acquired frontal lobe lesions. We hypothesized that three acquired personality disturbances would be associated with lesion involvement of distinct sectors of the prefrontal cortex (PFC): 1) emotional-social disturbance and ventromedial PFC, 2) hypoemotional disturbance and dorsomedial PFC, and 3) dysexecutive and dorsolateral PFC. In addition, we hypothesized that distressed personality disturbance would not be associated with focal PFC lesions in any sector. Each hypothesis was pre-registered and tested in 182 participants with adult-onset, chronic, focal brain lesions studied with an observational, cross-sectional design. Pre- and postmorbid personality was assessed by informant-rating with the Iowa Scales of Personality Change, completed by a spouse or family member. Two complementary analytic approaches were employed: 1) a hypothesis-driven region-of-interest (ROI) regression analysis examining the associations of lesions in specific PFC sectors with acquired personality disturbances; 2) a data-driven multivariate lesion-behavior mapping analysis, which was not limited to pre-specified regions. Each hypothesis received some support: (i) Emotional/social personality disturbance was most strongly associated with ventromedial PFC lesions in both statistical approaches. (ii) Hypoemotional disturbance was associated with dorsomedial PFC lesions in the ROI analyses, without any significant lesion-symptom mapping associations. (iii) Dysexecutive personality disturbance was associated with bilateral dorsolateral PFC lesions and ventromedial PFC lesions; lesion-symptom mapping showed maximal association of executive dysfunction with damage of the right middle frontal gyrus within the dorsolateral PFC. (iv) Distressed personality disturbance was not associated with lesions in any PFC sector. Altogether, the findings can be interpreted to indicate that damage to different prefrontal sectors may disrupt different anatomical-functional systems and result in distinct personality disturbances.

Effects of Chronic Social Defeat Stress on Behavior and Dopamine Receptors in Adolescent Mice With 6-Hydroxydopamine Lesions of the Medial Prefrontal Cortex.

Background: Social stress factors in schizophrenia have long-term effects, but will only induce symptoms in a portion of individuals, even if exposed to identical stress.Methods: In the current experiment, we examined mice with 6-hydroxydopamine (6-OHDA)-induced medial prefrontal cortical (mPFC) injury to select for members of a “stress-susceptible group,” and observed the changes in their behavior and the expression of D1 and D2 dopamine receptors in the amygdala and hippocampus.Results: We observed that after chronic social defeat stress, 72.6% of the 6-OHDA lesioned mice exhibited stress response to aggressors, compared to 52.3% of the blank control group. Both the 6-OHDA lesion + social defeat and social defeat groups exhibited anxiety and depression-like behavior. However, social cognitive impairment in the mice from the 6-OHDA lesion + social defeat group was more significant and the D1 expression levels in the amygdala were significantly decreased.Conclusion: These results suggest that the reason that adolescent mice with cortical injury were highly sensitive to defeat stress and had more prominent social cognitive impairment may be the decreased selectivity of D1 in the amygdala.

The Neural Correlates of Emotion in Decision-making

Both neuroscientific and psychology methods are used to study and explain the active neurons of the individuals' brain response when exposed to external stimuli. This study analyses the relevance literature and investigates the neural correlates of emotion, rewards, and motivation in the decision-making process, the emotional interactions between children, adolescents, and ageing. It was reviewed the literature to explore if neuroscientific methods provide accurate information about the role of emotion, reward, and motivation in decision-making mechanisms. The findings showed that the amygdala, medial prefrontal cortex, and ventromedial prefrontal cortex play a central role in processing of emotion which in turn influence decision-making process. While individuals with lesion in the ventromedial prefrontal cortex which is responsible for emotional responses toward risk, reward, and decision-making are not good decision-makers. In addition, the prefrontal cortex plays central role in approach and withdrawal motivational, whereby the right prefrontal cortex associated with withdrawal behavior and the left prefrontal cortex associated with approach behavior.

Differential Influence of Ventromedial Prefrontal Cortex Lesions on Neural Representations of Schema and Semantic Category Knowledge.

Prior knowledge, such as schemas or semantic categories, influences our interpretation of stimulus information. For this to transpire, prior knowledge must first be reinstated and then instantiated by being applied to incoming stimuli. Previous neuropsychological models implicate the ventromedial prefrontal cortex (vmPFC) in mediating these functions for schemas and the anterior/lateral temporal lobes and related structures for categories. vmPFC, however, may also affect processing of semantic category information. Here, the putative differential role of the vmPFC in the reinstatement and instantiation of schemas and semantic categories was examined by probing network-level oscillatory dynamics. Patients with vmPFC damage (n = 11) and healthy controls (n = 13) were instructed to classify words according to a given schema or category, while electroencephalography was recorded. As reinstatement is a preparatory process, we focused on oscillations occurring 500 msec prior to stimulus presentation. As instantiation occurs at stimulus presentation, we focused on oscillations occurring between stimulus presentation and 1000 msec poststimulus. We found that reinstatement was associated with prestimulus, theta and alpha desynchrony between vmPFC and the posterior parietal cortex for schemas, and between lateral temporal lobe and inferotemporal cortex for categories. Damage to the vmPFC influenced both schemas and categories, but patients with damage to the subcallosal vmPFC showed schema-specific deficits. Instantiation showed similar oscillatory patterns in the poststimulus time frame, but in the alpha and beta frequency bands. Taken together, these findings highlight distinct but partially overlapping neural mechanisms implicated in schema- and category-mediated processing.

Structural alterations in cortical and thalamocortical white matter tracts after recovery from prefrontal cortex lesions in macaques

Unilateral damage to the frontoparietal network typically impairs saccade target selection within the contralesional visual hemifield. Severity of deficits and the degree of recovery have been associated with widespread network dysfunction, yet it is not clear how these behavioural and functional brain changes relate with the underlying structural white matter tracts. Here, we investigated whether recovery after unilateral prefrontal cortex (PFC) lesions was associated with changes in white matter microstructure across large-scale frontoparietal cortical and thalamocortical networks. Diffusion-weighted imaging was acquired in four male rhesus macaques at pre-lesion, week 1, and week 8-16 post-lesion when target selection deficits largely recovered. Probabilistic tractography was used to reconstruct cortical frontoparietal fiber tracts, including the superior longitudinal fasciculus (SLF) and transcallosal fibers connecting the PFC or posterior parietal cortex (PPC), as well as thalamocortical fiber tracts connecting the PFC and PPC to thalamic nuclei. We found that the two animals with small PFC lesions showed increased fractional anisotropy in both cortical and thalamocortical fiber tracts when behaviour had recovered. However, we found that fractional anisotropy decreased in cortical frontoparietal tracts after larger PFC lesions yet increased in some thalamocortical tracts at the time of behavioural recovery. These findings indicate that behavioural recovery after small PFC lesions may be supported by both cortical and subcortical areas, whereas larger PFC lesions may have induced widespread structural damage and hindered compensatory remodeling in the cortical frontoparietal network.

A Voxel-based lesion study on facial emotion recognition after circumscribed prefrontal cortex damage.

Previous studies have shown inconsistent findings regarding the contribution of the different prefrontal regions in emotion recognition. Moreover, the hemispheric lateralization hypothesis posits that the right hemisphere is dominant for processing all emotions regardless of affective valence, whereas the valence specificity hypothesis posits that the left hemisphere is specialized for processing positive emotions while the right hemisphere is specialized for negative emotions. However, recent findings suggest that the evidence for such lateralization has been less consistent. In this study, we investigated emotion recognition of fear, surprise, happiness, sadness, disgust, and anger in 30 patients with focal prefrontal cortex lesions and 30 control subjects. We also examined the impact of lesion laterality on recognition of the six basic emotions. The results showed that compared to control subjects, the frontal subgroups were impaired in recognition of three negative basic emotions of fear, sadness, and anger - regardless of the lesion laterality. Therefore, our findings did not establish that each hemisphere is specialized for processing specific emotions. Moreover, the voxel-based lesion symptom mapping analysis showed that recognition of fear, sadness, and anger draws on a partially common bilaterally distributed prefrontal network.