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PubMedDate not supplied

[Working memory: neuropsychological and neurobiological issues].

Working memory denotes an ability to remember information for a short-time and to manipulate it. The memory allows including correct information depending on the situation, to keep the information on present activities for a while and enables changing the reaction according to new criteria. The relation between working memory and efficiency of complex cognitive processes and also with the control of emotional processes, plasticity of behaviour and consciousness was demonstrated. Working memory is connected with the activity of the dorsolateral prefrontal cortex of the brain. Recently, it has been shown, that working memory disturbances play an important role in the aetiopathogenesis of psychiatric disturbances such as schizophrenia, bipolar affective disorder or obsessive-compulsive disorder. Working memory disturbances are also shown in a proportion of healthy first-degree relatives of patients with schizophrenia or bipolar disorders. Working memory disturbances are presently regarded as a cognitive endophenotypic marker of vulnerability to these illnesses. In recent years, an association between working memory abilities and activity of different neurotransmitters, especially with the dopaminergic system in the brain, has been shown. Molecular genetic studies show an association between working memory abilities and polymorphism of the dopaminergic system genes in schizophrenia and polymorphism of BDNF gene in bipolar affective disorders. So far not much data about the genetics of working memory in healthy subjects has been gathered. Currently in Poland such research is carried on in the Clinical Neuropsychology Unit Nicolaus Copernicus University, Collegium Medicum in Bydgoszcz in cooperation with the Department of Adult Psychiatry and Laboratory of Psychiatric Genetics University of Medical Sciences in Poznań.

Bipolar Disorder↗
PubMed2006

Functional genomics in postmortem human brain: abnormalities in a DISC1 molecular pathway in schizophrenia.

The disrupted in schizophrenia 1 (DISC1) gene has been identified as a schizophrenia susceptibility gene based on linkage and single nucleotide polymorphism (SNP) association studies and clinical data, suggesting that risk SNPs impact on hippocampal structure and function. We hypothesized that altered expression of DISC1 and/or its molecular partners (nuclear distribution element-like [NUDEL], fasciculation and elongation protein zeta-i [FEZ1], and lissencephaly 1 [LIS1]) may underlie its pathogenic role in schizophrenia and explain its genetic association. We examined the expression of DISC1 and its binding partners in the hippocampus and dorsolateral prefrontal cortex of postmortem human brains of schizophrenic patients and controls. We found no difference in the expression of DISC1 mRNA in schizophrenia, and no association with previously identified risk SNPs. However, the expression of NUDEL, FEZ1, and LIS1 was significantly reduced in tissue from schizophrenic subjects, and the expression of each showed association with high-risk DISC1 polymorphisms. These data suggest involvement of genetically linked abnormalities in the DISC1 molecular pathway in the pathophysiology of schizophrenia.

Animals↗
PubMed1991

The effect of amphetamine on regional cerebral blood flow during cognitive activation in schizophrenia.

To explore the role of monoamines on cerebral function during specific prefrontal cognitive activation, we conducted a double-blind placebo-controlled crossover study of the effects of 0.25 mg/kg oral dextroamphetamine on regional cerebral blood flow (rCBF) as determined by 133Xe dynamic single-photon emission-computed tomography (SPECT) during performance of the Wisconsin Card Sorting Test (WCST) and a sensorimotor control task. Ten patients with chronic schizophrenia who had been stabilized for at least 6 weeks on 0.4 mg/kg haloperidol participated. Amphetamine produced a modest, nonsignificant, task-independent, global reduction in rCBF. However, the effect of amphetamine on task-dependent activation of rCBF (i.e., WCST minus control task) was striking. Whereas on placebo no significant activation of rCBF was seen during the WCST compared with the control task, on amphetamine significant activation of the left dorsolateral prefrontal cortex (DLPFC) occurred (p = 0.0006). Both the mean number of correct responses and the mean conceptual level increased (p less than 0.05) with amphetamine relative to placebo. In addition, with amphetamine, but not with placebo, a significant correlation (p = -0.71; p less than 0.05) emerged between activation of DLPFC rCBF and performance of the WCST task. These findings are consistent with animal models in which mesocortical catecholaminergic activity modulates and enhances the signal-to-noise ratio of evoked cortical activity.

Adult↗
PubMed1994

Saccadic system functioning among schizophrenia patients and their first-degree biological relatives.

In Study 1, 30 schizophrenia Ss and 27 nonpsychiatric comparison Ss were presented with a fixation task, a visually guided reflexive saccade (prosaccade) task, a predictive tracking task (0.4-Hz square wave), and an antisaccade task. The 2 groups did not differ on either the fixation or prosaccade tasks. Schizophrenia Ss had an increased number of errors on the antisaccade task and had decreased rightward visually guided saccade amplitudes during the predictive tracking task. In Study 2, 13 psychiatric comparison Ss and 32 first-degree biological relatives of the schizophrenia Ss were compared with the schizophrenia Ss and a larger and older sample of nonpsychiatric Ss (n = 33) on the predictive tracking and antisaccade tasks. The groups did not differ on predictive saccadic tracking. The schizophrenia Ss and their first-degree biological relatives made more errors on the antisaccade task than both the nonpsychiatric and psychiatric comparison groups (who did not significantly differ). Results are consistent with the notion that dysfunction of dorsolateral prefrontal cortex, caudate nucleus, or both is related to liability for schizophrenia.

Adult↗
PubMedDate not supplied

[Frontal lobe dysfunction and depressive state: relation to endogenous character of depression].

A dysfunction of dorsolateral prefrontal cortex (DLPF) in major depression is suggested by functional imagery and comparative neuropsychology. However, assessment of frontal lobe syndrome with DLPF-dependent tests led to controversial results. To clarify these findings, we administered 5 of these tests (Wisconsin Card Sorting Test, Stroop Test, Trail Making Test, Tower of Toronto, verbal fluency) to 16 major depressive subjects and their 16 controls, before and after 21 days of treatment. Furthermore, we tried to assess the prognostic value of frontal lobe dysfunction, and its relation with the endogenous or exogenous nature of the depression on the one hand, the severity of the depression on the other hand. Our results suggest that the presence of a frontal lobe syndrome (defined by impaired performances at 3 tests or more) is only noted in endogenous depression; after treatment, no impairment is detected. No correlation is found with the severity of the depression. Frontal lobe syndrome does not seem to indicate poorer prognosis for current depressive episode.

Adult↗
PubMed1996

Dextroamphetamine enhances "neural network-specific" physiological signals: a positron-emission tomography rCBF study.

Previous studies in animals and humans suggest that monoamines enhance behavior-evoked neural activity relative to nonspecific background activity (i.e., increase signal-to-noise ratio). We studied the effects of dextroamphetamine, an indirect monoaminergic agonist, on cognitively evoked neural activity in eight healthy subjects using positron-emission tomography and the O15 water intravenous bolus method to measure regional cerebral blood flow (rCBF). Dextroamphetamine (0.25 mg/kg) or placebo was administered in a double-blind, counterbalanced design 2 hr before the rCBF study in sessions separated by 1-2 weeks. rCBF was measured while subjects performed four different tasks: two abstract reasoning tasks--the Wisconsin Card Sorting Task (WCST), a neuropsychological test linked to a cortical network involving dorsolateral prefrontal cortex and other association cortices, and Ravens Progressive Matrices (RPM), a nonverbal intelligence test linked to posterior cortical systems--and two corresponding sensorimotor control tasks. There were no significant drug or task effects on pCO2 or on global blood flow. However, the effect of dextroamphetamine (i.e., dextroamphetamine vs placebo) on task-dependent rCBF activation (i.e., task - control task) showed double dissociations with respect to task and region in the very brain areas that most distinctly differentiate the tasks. In the superior portion of the left inferior frontal gyrus, dextroamphetamine increased rCBF during WCST but decreased it during RPM (ANOVA F (1,7) = 16.72, p < 0.0046). In right hippocampus, blood flow decreased during WCST but increased during RPM (ANOVA F(1,7) = 18.7, p < 0.0035). These findings illustrate that dextroamphetamine tends to "focus" neural activity, to highlight the neural network that is specific for a particular cognitive task. This capacity of dextroamphetamine to induce cognitively specific signal augmentation may provide a neurobiological explanation for improved cognitive efficiency with dextroamphetamine.

Adult↗
PubMed1998

Transition of brain activation from frontal to parietal areas in visuomotor sequence learning.

We studied the neural correlates of visuomotor sequence learning using functional magnetic resonance imaging (fMRI). In the test condition, subjects learned, by trial and error, the correct order of pressing two buttons consecutively for 10 pairs of buttons (2 x 10 task); in the control condition, they pressed buttons in any order. Comparison between the test condition and the control condition revealed four brain areas specifically related to learning: the dorsolateral prefrontal cortex (DLPFC), the presupplementary motor area (pre-SMA), the precuneus, and the intraparietal sulcus (IPS). We found that the time course of activation during learning was different between these areas. To normalize the individual differences in the speed of learning, we classified the performance of each subject into three learning stages: early, intermediate, and advanced stages. Both the relative increase of signal intensity and the number of activated pixels within the four areas showed significant changes across the learning stages, with different time courses. The two frontal areas, DLPFC and pre-SMA, were activated in the earlier stages of learning, whereas the two parietal areas, precuneus and IPS, were activated in the later stages. Specifically, DLPFC, pre-SMA, precuneus, and IPS were most highly activated in the early stage, in both the early and intermediate stages, in the intermediate stage, and in both the intermediate and advanced stages, respectively. The results suggest that the acquisition of visuomotor sequences requires frontal activation, whereas the retrieval of visuomotor sequences requires parietal activation, which might reflect the transition from the declarative stage to the procedural stage.

Adult↗
PubMed1998

Elevated neuronal density in prefrontal area 46 in brains from schizophrenic patients: application of a three-dimensional, stereologic counting method.

Neuropsychologic testing in schizophrenic patients has underscored the prominence of dysfunction in cognitive processes associated with the dorsolateral prefrontal cortex. Quantitative cytometric analysis of area 46 was undertaken in brains from schizophrenic patients to determine whether there are morphologic changes underlying these cognitive deficits. Postmortem brain specimens from 9 schizophrenic patients, 10 normal subjects, and 8 Huntington's diseased patients were fixed in formalin and celloidin embedded. A direct, three-dimensional counting method was used to determine cell density and cortical thickness in Nissl-stained sections of area 46. Overall neuronal density was 21% greater in brains from schizophrenic patients in comparison to normal controls. Significant elevations in neuronal density were observed in layers II, III, IV, and VI. The cortical ribbon was slightly (8%) but not significantly thinner. However, layer II exhibited disproportionate thinning compared with all other layers. In brains from Huntington's diseased patients, increases in neuronal (35%) and glial (61%) density with substantial cortical thinning (30%) were observed. The neuropathology of area 46 in schizophrenia is similar in direction and magnitude to that previously described in area 9 (Selemon et al. [1995] Arch. Gen. Psychiatry 52:805-818), except for the abnormalities in layer II, which are specific to area 46. In contrast to Huntington's disease, in which cortical atrophy and gliosis are present, no evidence for cortical cell loss was uncovered in the schizophrenic cohort. The observed elevation in neuronal density suggests that a reduction in interneuronal neuropil may constitute the anatomical substrate for prefrontal cortical dysfunction in schizophrenia.

Adult↗
PubMedDate not supplied

[Selected parameters of magnetic resonance imaging of the brain, clinical picture and recovery after treatment in schizophrenia. Preliminary report].

In forty schizophrenic (or schizophreniform disorder) patients diagnosed according to DSM-IV, the magnetic resonance imaging was performed. The T2 relaxation time was measured in selected brain regions from the dorsolateral prefrontal cortex as well as in amygdala. These results were compared with clinical parameters regarding severity of psychopathology and improvement after neuroleptic treatment. The mean T2 values of grey matter of right inferior frontal gyrus were significantly higher in patients with schizophreniform disorders (those patients were clinically diagnosed as suffering from cycloid psychoses) than in other types of schizophrenia. The T2 values of this region correlated inversely with the severity of negative symptoms before treatment. The T2 values of gray matter of left inferior frontal gyrus correlated positively with the severity of schizophrenic symptoms before treatment. Mean T2 values of left amygdala were significantly higher in patients showing less favorable improvement after neuroleptic treatment in comparison to those who improved better. No correlation was found between the presence of brain atrophy and T2 values in brain regions studied. The results allow to suggest that the measurement of T2 relaxation time might reveal interesting relations between clinical picture and neuroradiologic findings in schizophrenia, however clinical significance of such parameters still requires further elaboration.

Adult↗
PubMed1998

Olfactory identification and Stroop interference converge in schizophrenia.

OBJECTIVE: To test the discriminant validity of a model predicting a dissociation between measures of right and left frontal lobe function in people with schizophrenia. PARTICIPANTS: Twenty-one clinically stable outpatients with schizophrenia. INTERVENTIONS: Patients were administered the University of Pennsylvania Smell Identification Test (UPSIT), the Stroop Color-Word Test (Stroop), and the Positive and Negative Syndrome Scale (PANSS). OUTCOME MEASURES: Scores on these tests and relation among scores. RESULTS: There was a convergence of UPSII and Stroop interference scores consistent with a common cerebral basis for limitations in olfactory identification and inhibition of distraction. There was also a divergence of UPSIT and Stroop reading scores suggesting that the olfactory identification limitation is distinct from a general limitation of attention or a dysfunction of the left dorsolateral prefrontal cortex. Most notable was the 81% classification convergence between the UPSIT and Stroop incongruous colour naming scores compared with the near-random 57% classification convergence of the UPSIT and Stroop reading scores. CONCLUSIONS: These data are consistent with a right orbitofrontal dysfunction in a subgroup of patients with schizophrenia, although the involvement of mesial temporal structures in both tasks must be ruled out with further study. A multifactorial model depicting contributions from diverse cerebral structures is required to describe the pathophysiology of schizophrenia. Valid behavioural methods for classifying suspected subgroups of patients with particular cerebral dysfunction would be of value in the construction of this model.

Adult↗
PubMed1998

Psychophysiological measures of (dis)inhibition as liability indicators for schizophrenia.

Two psychophysiological measures, poor suppression of midlatency auditory-evoked responses in a paired stimulus paradigm and ocular motor abnormalities, may index genetic liability for schizophrenia. An important feature of these measures is that both patients and their nonpsychotic relatives exhibit basically the same performance. These measures may be successful endophenotypes for schizophrenia because they assess poor response inhibition associated with dysfunction of dorsolateral prefrontal cortex circuitry. Data bearing on this hypothesis are reviewed, and it is posited that assessment of the auditory-evoked gamma band response and saccade measures of inhibitory abilities are the most valid behavioral measures of schizophrenia's neuropathological correlates. The extant data suggest that psychophysiological studies of schizophrenia can provide consistent and theoretically meaningful information for localizing neuropathology and for assessing the genetics of this complex disorder.

Evoked Potentials, Auditory↗
PubMed2000

Dissociating the role of the dorsolateral prefrontal and anterior cingulate cortex in cognitive control.

Theories of the regulation of cognition suggest a system with two necessary components: one to implement control and another to monitor performance and signal when adjustments in control are needed. Event-related functional magnetic resonance imaging and a task-switching version of the Stroop task were used to examine whether these components of cognitive control have distinct neural bases in the human brain. A double dissociation was found. During task preparation, the left dorsolateral prefrontal cortex (Brodmann's area 9) was more active for color naming than for word reading, consistent with a role in the implementation of control. In contrast, the anterior cingulate cortex (Brodmann's areas 24 and 32) was more active when responding to incongruent stimuli, consistent with a role in performance monitoring.

Adolescent↗
PubMed2005

Developmental changes in mental arithmetic: evidence for increased functional specialization in the left inferior parietal cortex.

Arithmetic reasoning is arguably one of the most important cognitive skills a child must master. Here we examine neurodevelopmental changes in mental arithmetic. Subjects (ages 8-19 years) viewed arithmetic equations and were asked to judge whether the results were correct or incorrect. During two-operand addition or subtraction trials, for which accuracy was comparable across age, older subjects showed greater activation in the left parietal cortex, along the supramarginal gyrus and adjoining anterior intra-parietal sulcus as well as the left lateral occipital temporal cortex. These age-related changes were not associated with alterations in gray matter density, and provide novel evidence for increased functional maturation with age. By contrast, younger subjects showed greater activation in the prefrontal cortex, including the dorsolateral and ventrolateral prefrontal cortex and the anterior cingulate cortex, suggesting that they require comparatively more working memory and attentional resources to achieve similar levels of mental arithmetic performance. Younger subjects also showed greater activation of the hippocampus and dorsal basal ganglia, reflecting the greater demands placed on both declarative and procedural memory systems. Our findings provide evidence for a process of increased functional specialization of the left inferior parietal cortex in mental arithmetic, a process that is accompanied by decreased dependence on memory and attentional resources with development.

Adaptation, Physiological↗
PubMed2000

A functional neuroanatomy of tics in Tourette syndrome.

BACKGROUND: Tics are involuntary, brief, stereotyped motor and vocal behaviors often associated with irresistible urges. They are a defining symptom of the classic neuropsychiatric disorder, Tourette syndrome (TS), and constitute an example of disordered human volition. The neural correlates of tics are not well understood and have not been imaged selectively. METHODS: Event-related [(15)O]H(2)O positron emission tomography techniques combined with time-synchronized audio and videotaping were used to determine the duration of, frequency of, and radiotracer input during tics in each of 72 scans from 6 patients with TS. This permitted a voxel-by-voxel correlational analysis within Statistical Parametric Mapping of patterns of neural activity associated with the tics. RESULTS: Brain regions in which activity was significantly correlated with tic occurrence in the group included medial and lateral premotor cortices, anterior cingulate cortex, dorsolateral-rostral prefrontal cortex, inferior parietal cortex, putamen, and caudate, as well as primary motor cortex, the Broca's area, superior temporal gyrus, insula, and claustrum. In an individual patient with prominent coprolalia, such vocal tics were associated with activity in prerolandic and postrolandic language regions, insula, caudate, thalamus, and cerebellum, while activity in sensorimotor cortex was noted with motor tics. CONCLUSIONS: Aberrant activity in the interrelated sensorimotor, language, executive, and paralimbic circuits identified in this study may account for the initiation and execution of diverse motor and vocal behaviors that characterize tics in TS, as well as for the urges that often accompany them. Arch Gen Psychiatry. 2000;57:741-748

Adult↗
PubMed1975

Afferents to prefrontal cortex from the thalamic mediodorsal nucleus in the rhesus monkey.

Thalamic afferents to Macaque prefrontal cortex from the mediodorsal nucleus were examined by techniques specific for anterograde degeneration and axoplasmic transport. The sampling procedure employed permits establishing the extent of topographic projections to cortex from subcortical foci for the same brain which was surveyed subsequently in tracing specific neuronal connections by electron microscopy. Topographic and general laminar distribution of thalamic terminals are presented in terms of 3 subareas of prefrontal cortex. The dorsolateral and ventral (orbital) surfaces of prefrontal cortex receive respectively projections from the lateral and medial subdivision of the mediodorsal nucleus. In addition, the medial wall of the frontal lobe, including the dorsomedial part of the lateral convexity, heretofore regarded as athalamic, receives input from the caudal-dorsomedial aspect of the mediodorsal nucleus. Preliminary evidence suggests that axons from the mediodorsal nucleus terminate in the head of caudate nucleus, as Sachs-81 described 65 years ago in the first orthograde study of thalamo-prefrontal cortex connections.

Animals↗
PubMed2002

Segregation of areas related to visual working memory in the prefrontal cortex revealed by rTMS.

The functional organization of working memory (WM) in the human prefrontal cortex remains unclear. Storage and processing functions might be segregated in ventral and dorsal areas of the prefrontal cortex, respectively. If so, storage functions might be spared, irrespective of informational domain, following damage or dysfunction in dorsolateral areas. Alternatively, WM and prefrontal function in general might be segregated according to informational domains (e.g. spatial versus object-based information). In the present study we used repetitive transcranial magnetic stimulation (rTMS) to directly test these competing hypotheses. We applied rTMS to transiently and selectively disrupt the function of the dorsomedial, dorsolateral or ventral prefrontal cortex in normal human volunteers performing either a spatial or a face-recognition delayed-response task. Performance in the spatial task was impaired by rTMS of the dorsomedial prefrontal cortex. Performance in the face-recognition (non-spatial) task was impaired by rTMS of the ventral prefrontal cortex. Transient disruption of the dorsolateral prefrontal cortex affected performance in both tasks. These findings provide evidence of domain-specific segregation of WM functions in widely separated areas of prefrontal cortex.

Adult↗