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We used functional magnetic resonance imaging to examine whether motivational-salient cues could exert a differential impact on proactive (the restrain of actions in preparation for stopping) and reactive (outright stopping) inhibition. Fourteen high-frequency poker players, and 14 matched non-gambler controls, performed a modified version of the stop-signal paradigm, which required participants to inhibit categorization of poker or neutral pictures. The probability that a stop-signal occurs (0%, 17%, 25%, 33%) was manipulated across blocks of trials, as indicated by the color of the computer screen. Behavioral analyses revealed that poker players were faster than controls in categorizing pictures across all levels of proactive motor response inhibition (go trials). Brain imaging analyses highlighted higher dorsal anterior cingulate cortex activation in poker players, as compared to controls, during reactive inhibition. These findings suggest that, due to their faster rates of stimulus discrimination, poker players might have recruited more cognitive resources than controls when required to stop their response (reactive inhibition). Nevertheless, no main effect of stimulus type was found, on either proactive or reactive inhibition. Additional studies are, therefore, needed in order to confirm that investigating the dynamics between reactive and proactive inhibition offers a discriminative analysis of inhibitory control toward motivational-salient cues., SCOPUS: ar.j, info:eu-repo/semantics/published

In this review, we summarize the contribution of functional imaging to the question of nociception in humans. In the beginning of the 90's, brain areas supposed to be involved in physiological pain processes essentially concerned the primary somatosensory area (SI), thalamus, and anterior cingulate cortex. In spite of these a priori hypotheses, the first imaging studies revealed that the main brain areas and those providing the most consistent activations in pain conditions were the insular and the SII cortices, bilaterally. This has been checked with other techniques such as intracerebral recordings of evoked potentials after nociceptive stimulations with laser showing a consistent response in the operculo-insular area whose amplitude correlates with pain intensity. In spite of electrode implantations in other areas of the brain, only rare and inconsistent responses have been found outside the operculo-insular cortices. With electrical stimulation delivered directly in the brain, it has also been shown that stimulation in this area only - and not in other brain areas - was able to elicit a painful sensation. Thus, over the last 15 years, the operculo-insular cortex has been re-discovered as a main area of pain integration, mainly in its sensory and intensity aspects. In neuropathic pain also, these areas have been demonstrated as being abnormally recruited, bilaterally, in response to innocuous stimuli. These results suggest that plastic changes may occur in brain areas that were pre-defined for generating pain sensations. Conversely, when the brain activations concomitant to pain relief were taken in account, a large number of studies pointed out medial prefrontal and rostral cingulate areas as being associated with pain controls. Interestingly, these activations may correlate with the magnitude of pain relief, with the activation of the peri-acqueductal grey (PAG) and, at least in some instances, with the involvement of endogenous opioids.

In recent years, discovery of ketamine's fast and powerful antidepressant effects for treatment-resistant depression (TRD) has led to rethinking of the pathophysiology of depression. Numerous studies in humans and animals have focused on mechanisms of action underlying this effect, producing a number of explanatory pathways.The aim of this article is to summarize the various hypotheses underlying rapid antidepressant action of ketamine and therefore to better understand the mechanisms underlying depression and antidepressant action.Ketamine unique antidepressant properties have led to many studies on its neurobiological grounds. Intracellular signaling pathways such as mTOR, GSK3 or eEF2 seem to play a key role and are associated with an increased synaptic plasticity. Other hypotheses are discussed such as ketamine effects on neuro-inflammation, the role of anterior cingulate cortex in brain changes induced by ketamine, and the potential benefits of analgesic properties of ketamine in depressive disorders.Our review highlights the potential role of the glutamatergic system in the pathophysiology and treatment of mood disorders. Understanding which pathways underlie the fast antidepressant effect of ketamine paves the way for the development of new antidepressants.

Apathy is widely recognized as a lack of motivation, which expresses through the cognitive, behavioral and emotional dimensions of living. It is described within several neuropsychiatric syndromes such as degenerative disorder and is associated with poorer outcomes. In order to better understand the underpinnings of apathy and to develop specific treatment strategies, much research has been conducted to define its neural bases. In the present review, perfusion, metabolic, pathologic and functional results of apathy neural bases in Alzheimer's and Parkinson's diseases are displayed. Methods and strategies to control for confounding factors such as depression, cognitive impairments and other behavioral disorders are described. Results are not strictly identical between disorders and even within disorders. Variation of methods employed on assessment tools and control for confounding factors such as cognitive disorders, depression, other behavioral disorders and medical treatment is thought to be the main reason for this discrepancy. However, it seems that the inferior prefrontal cortex, especially the orbitofrontal cortex, the lateral prefrontal cortex and the anterior cingulate are of particular interest. The second part of the review discusses the literature in these three areas in conditional learning essentially via the reward characteristic encoding, auto-initiated and perseverance behaviors and emotional experience and its regulation.

International audience; Alzheimer's disease (AD) is characterised by macroscopic cerebral damages which can be studied in vivo with neuroimaging techniques, even at the earliest stage. Studies were conducted in patients with amnestic Mild Cognitive Impairment (MCI) who best represent incipient AD. Right temporo-parietal hypometabolism, assessed by resting-state (18)FDG-PET, distinguishes patients who further develop AD from those who remain stable. From the pre-dementia stage of MCI, atrophy of the hippocampal region detected with structural MRI contrasts with functional alteration of the posterior cingulate gyrus measured with (18)FDG-PET and SPECT. Results from resting-state fMRI confirm this pattern of functional abnormalities and highlight changes in the hippocampal region functional connectivity, decreased with the posterior cingulate region, and increased with some frontal areas. Altogether with a structural connectivity impairment highlighted by DTI, those results support the hypothesis of a dysconnexion between the hippocampal and the posterior cingulate regions. Finally, activation fMRI data support the hypothesis of a functional compensation involving not only the frontal cortex but also, at the pre-dementia stage, the hippocampal region. Thus, this synthesis focuses on the hypotheses of dysconnexion and functional compensation, suggested to explain the discrepancies between the structural and functional alteration patterns, as well as on relevant results from resting-state fMRI, DTI and activation fMRI studies. Furthermore, this synthesis emphasizes the relevance of neuroimaging for the early detection of AD.

Obsessive-compulsive disorder (OCD), that affects 2 to 3% of the general population, is characterized by recurrent intrusive thoughts and repetitive, time-consuming behaviors. It is a severely incapacitating mental illness that causes profound impairment in psychosocial functioning and quality of life. Although the physiopathology of OCD is still far from resolved, the existence of a biological basis for OCD is now clearly established and should be interpreted from phenomenological considerations, on the one hand, and in the light of our increasing knowledge of the physiology of cortico-subcortical functional loops, on the other. In a phenomenological view, the heart of the obsessional process is the subject's underlying impression that "something is wrong". In other words, obsessions may be thought of as the permanent perception of a mistake and/or error in certain behavioral situations. Compulsions occur as behavioral responses aimed at relieving the tensions or anxiety generated by the situation. If obtained, this relief may be felt to be a form of reward. Nevertheless, it is only transient, thereby creating a feeling of considerable anxiety. This contributes to immediately reproducing the behavior in a cyclic manner, on the basis of an internal motivational state through an expectation of the reward. Therefore, it can be assumed that several malfunctioning processes are altered within the OCD: 1) error recognition; and, 2) emotion and motivation. This suggests that there is a dysfunction of the brain regions mediating these cognitive and emotional functions. Experimental neurophysiology in laboratory animals indicates the central role of the fronto-subcortical circuits originating in the orbitofrontal and anterior cingulate cortices, respectively. The orbitofrontal cortex (OFC) and ventromedial areas are involved in appraisal of the emotional and motivational values of environmental information, and in integrating the subject's prior experience, which is crucial in decision-making. The OFC also contributes to the selection, comparison and judgment of stimuli and error detection. The anterior cingulate cortex (ACC) is comprised of 1) a ventral or affective region that could keep attention on the internal emotional and motivational status and regulation of autonomic responses, and 2) a dorsal and cognitive region that serves a wide range of functions including attention, working memory, error detection, conflict monitoring, response selection, and anticipation of incoming information. Ventral striatum, that is intimately connected to the OFC and ACC, participates in the preparation, initiation and execution of behavioral responses oriented toward reward delivery following the cognitive and emotional integration of behaviorally relevant information at the cortical level. Functional imaging research in humans has shown an increased functional activity in the OFC, ACC, head of the caudate nucleus and thalamus in OCD patients. These functional abnormalities have been found in basal conditions and during provocation tests. Moreover, the therapeutic efficacy of antidepressants with preponderant serotonin-reuptake inhibiting properties and cognitive-behavioral therapies seems to be associated with a progressive reduction in activity of the OFC, ACC and the caudate nucleus. Therefore, these observations are suggestive of the responsibility of 5HT neurotransmission in the dysfunction of the frontal-subcortical loops that emanate from the OFC and ACC. However, several lines of research suggest that the dopamine system, with which 5HT interacts, may play a major role in the expression of OC symptoms. In conclusion, it seems that in OCD there is a dysfunction of the brain regions that belong to the orbitofrontal and anterior cingulate loops in view of evidence obtained from separate and complementary approaches.

Apathy is usually defined as a lack of motivation leading to reduced interest and participation in various activities. From a pathophysiological viewpoint, the most common cause of apathy is dysfunction of the frontal lobes, following either direct lesion of the frontal cortex or damage to regions tightly connected to the latter (such as the basal ganglia). The frontal-subcortical circuits often seem to be involved. Apathy is a common behavioral consequence of neurodegenerative disorders (Alzheimer's disease, parkinsonian syndromes, fronto-temporal dementia). The methods for detecting apathy and assessing its severity are various, the main difficulty being to disentangle apathy and depression. The treatment of apathy per se remains anecdotal and, to date, little research into the efficacy of medication therapy has been performed.

Pain is an unpleasant and intrusive sensation, warning of actual or potential tissue damage. Over the last fifteen years, functional cerebral imaging research has demonstrated the involvement of many cerebral structures in the experience of pain.Intimately linked to the notion of suffering, the affective dimension of pain relies on neurophysiological systems partly distinct anatomically from those involved more specifically in its sensory dimension. Some pathways convey nociceptive information to the somatosensory cortex and the insula, contributing to the sensory aspects of pain (e.g.: sensory intensity), and secondarily, to its affective dimension. Other pathways project directly to the anterior cingulate cortex, the insula, the amygdala and to the prefrontal cortices, which are structures involved in the affective dimension of pain (unpleasantness of pain and regulation of autonomic and behavioral responses). Interestingly, these latter regions are an integral part of the cerebral emotional networks.This close anatomical relationship between pain and emotions circuits could explain the powerful emotional impact of pain as well as the reciprocal modulatory effect of emotions on pain observed in clinical and experimental studies. More specifically, this modulatory effect might reflect interactions between emotional and nociceptive systems in the prefrontal and cingulate cortices, ventral striatum, amygdala and hippocampal regions. Taken together, these observations further attest to the emotional nature of pain experience.

Using a Stroop-like visuo-motor task in monkeys, we studied the unitary neuronal activity of the anterior cingulate cortex (ACC, CMAr : 24c) during error detection and conflict monitoring. A high percentage of cingular neurons modified their firing frequency during both attentional and evaluation periods. During the latter period, however, changes in discharge rates were always much more pronounced for erroneous responses than for successful movements that induced reward delivery. Moreover, some neurons responded more markedly to the warning stimulus when a previous trial failed In this case, the probability of a subsequent correct response increased. Such a neuronal apparatus could represent an error compensation system that serves to adapt a subject's behavioral response following an unfavorable and unexpected outcome. Abnormal activity of these neurons, which appear to take advantage of past errors, could contribute to the genesis of obsessive-compulsive disorders (OCD).

Despite immense importance of auditory verbal hallucinations (AVHs) in the phenomenology of schizophrenia, the neurocognitive and neurophysiological bases of AVHs remain obscure. On the neurocognitive level, it has been proposed that AVHs arise from the disordered monitoring manifested by patients' inability to recognize their inner speech as being their own. On the neurophysiological level, the AVHs have been attributed to the aberrant activity in the primary auditory cortex (Heschl's gyrus). Although interesting, these models cannot account for the very specific and restricted content of AVHs in individual patients. The specific content of AVHs persists across different psychotic episodes even after extended periods of remission. Furthermore, the AVHs are usually triggered by emotionally charged and stressful situations.We hypothesized that even during absence of AVHs, when patients are in remission, the verbal content remains present in the latent, pre-clinical form. In order to elucidate potential cerebral substrates of the dormant AVHs content, we employed functional magnetic resonance imaging (fMRI) in 6 schizophrenia patients in total remission of AVHs for at least 12 months, during listening to the words hallucinated by them in the past. Specifically, we created the list of previously hallucinated words for each patient and matched the words in terms of length, structure, emotional valence, semantic category and frequency of usage with the non-hallucinated words. Moreover, each patient was paired demographically with the control participant who was presented with the same words. We predicted that exposure to the hallucinated versus non-hallucinated words would result in increased activation in cerebral areas associated with cognitive and emotional content of previously experienced AVHs in patients, whereas the same comparison will not produce any significant changes in blood oxygen level-dependent (BOLD) signal in control participants. In addition, based on existing neuroimaging data obtained during experience of AVHs, we hypothesized that previously hallucinated words may elicit greater activation in the primary auditory cortex than the non-hallucinated words in patients. Each pair of participants was analyzed separately.The most consistent finding in patients, absent in all control participants, was significant activation in the orbitofrontal and medial prefrontal cortex (PFC) during listening to previously hallucinated versus non-hallucinated words. The orbitofrontal and medial PFC are both part of corticolimbic system and play an important role in cognitive control of emotion processing.Thus, present results imply that previously hallucinated words, even in remission, are associated with inappropriate emotional response on neurophysiological level in schizophrenia patients. The relative hyperactivation of orbitofrontal and medial PFC in patients may stem from and/or may contribute to anomalous neural plasticity and disordered connectivity in the corticolimbic circuitry. This in turn could lead to attribution of excessive emotional salience to normally neutral stimuli and over time via process of sensitization could result in hallucinations. Potential normalization of this dysfunction could reduce patients' susceptibility to experience AVHs in stressful situations. In addition to observed hyperactivations in the PFC, some schizophrenia patients exhibited anomalous BOLD signal in other regions of the corticolimbic system such as anterior cingulate gyrus and parahippocampal gyrus. These additional anomalies could be related to greater affective sensitivity to the hallucinated versus non-hallucinated words in some patients.Finally, in contrast to our initial hypothesis we did not observe any significant differences between processing of the hallucinated versus non-hallucinated words in the primary auditory cortex. In retrospect, this result is not surprising because patients did not experience internally generated AVHs while in the scanner, but instead were exposed exclusively to externally generated stimuli.

Feeling pain is in the same time a sensory and an affective experience. Pain asymbolia and prefrontal lobotomy, two distinct neurological pictures, help to better understand the cerebral basis of the emotional dimension of pain. In pain asymbolia, the selective alteration of the affective dimension of pain is associated with a loss of the sense of threat and danger. Following prefrontal lobotomy, the emotional impact of chronic pain is dramatically reduced, while affective responses to acute pain are paradoxically increased. Such clinical observations allow to make a clear distinction between immediate pain unpleasantness on the one hand, and secondary pain affect, linked to the significance of the pain experience in terms of the self and of the future, on the other hand. Moreover, recent functional neuroimaging data allow to better define the neural substrates of the affective dimension of pain and to highlight the shared neuro-anatomical networks between physical and psychic suffering.

Attention-deficit hyperactivity disorder (ADHD) is a common and impairing neuropsychiatric disorder with preschool onset. ADHD occurs in approximately 3-9% of the childhood population. There is a much higher incidence rate in boys who are around three times more likely than girls to be diagnosed. Approximately 30-60% of individuals diagnosed with ADHD in youth have symptoms that persist into adulthood.Three subtypes of the disorder have been proposed in the current clinical view of ADHD: inattentive, hyperactive-impulsive and combined type. Numerous problems are associated with ADHD: poor academic performance, learning disorders, subtle cognitive deficits, conduct disorders, antisocial personality disorder, poor social relationships, and a higher incidence of anxiety and depression symptoms into adulthood. Researchers have emphasized poor behavioural inhibition as the central impairment of the disorder. From the neuropsychological viewpoint, impairment of the "hot" affective aspects of executive functions, like behavioural inhibition and attention and the more cognitive, "cool" aspects of executive functions like self-regulation, working memory, planning, and cognitive flexibility, are often reported by studies on ADHD. The hot executive functions are associated with ventral and medial regions of the prefrontal cortex (including the anterior cingulated cortex) and named "hotbrain" and the cool executive functions are associated with the dorsolateral prefrontal cortex and are called "coolbrain".Convergent data from neuroimaging, neuropsychology, genetics and neurochemical studies consistently point to the involvement of the frontostriatal network as a likely contributor to the pathophysiology of ADHD. This network involves the lateral prefrontal cortex, the dorsal anterior cingulate cortex, the caudate nucleus and putamen. Moreover, a growing literature demonstrates abnormalities affecting other cortical regions and the cerebellum. The exploratory brain regions of interest in which abnormalities have been identified, but that were not predicted by cognitive models of ADHD, are the temporal lobe, parietal lobe, occipital lobe and lateral ventricles. Anatomical studies suggest widespread reductions in volume throughout the cerebrum and cerebellum, while functional imaging studies suggest that affected individuals activate more diffuse areas than controls during the performance of cognitive tasks. More precisely, reductions in volume have been observed in the total cerebral volume, the prefrontal cortex, the basal ganglia (striatum), the dorsal anterior cingulate cortex, the corpus callosum and the cerebellum. Furthermore, hypoactivation of the dorsal anterior cingulate cortex, the frontal cortex and the basal ganglia (striatum) have also been reported. The paradigms mostly used in functional magnetic resonance imaging (fMRI) are tasks of motor inhibition, interference and attention such as the go/no-go, "stop-signal" and the Stroop.This review provides an overview of the main imaging studies that investigated the neurobiological substrate of ADHD. Some guidelines for future functional magnetic imaging studies are also suggested.

International audience; For now several years, the growing developement of neuroimaging techniques such as Positron Emission Tomography (PET) or functional Magnetic Resonance Imaging (fMRI) allowed a better understanding of neural processes involved in human emotions and goal-directed behaviors. In particular, several studies are now available on the neural correlates of male sexual arousal. A neurobehavioral model of neural processes involved in sexual arousal has been proposed (Redout?t al., 2000) comprising: i) a cognitive component; ii) an emotional component; iii) a motivational component and iv) an autonomic component. Among other regions, several cerebral areas have been found to be linked to: 1) the cognitive component which comprises: i) the orbitofrontal cortex involved in attentional processes directed toward the target and the superior parietal lobules; ii) the inferior parietal lobules involved in motor imagery processes; 2) the motivational component which involves the caudal part of the anterior cingulate cortex, related to motor preparation processes; 3) the autonomic component: concurrent measures of cerebral activations by functional neuroimaging and of erectile response by penile plethysmography allow the demonstration of the involvement of the hypothalamus, the insula, and the rostral part of the anterior cingulate cortex in this component.

DEPRESSION IN THE ELDERLY SUBJECT: Depression is diagnosed to a varying extent in the elderly. In subjects with Alzheimer's disease, the most specific signs involve mood disorders, loss of energy, a feeling of hopelessness, and sometimes body discomfort or pain. DEFINITION OF APATHY: Apathy is defined as a loss of motivation, expressed by a loss of interest in activities, lack of productivity, loss of will and initiative, as well as limited affective response to positive or negative elements. TWO DIFFERENT SYNDROMES: The differential diagnosis is difficult, but studies have demonstrated that depression and apathy are two relatively different syndromes, which may be intertwined. Lack of volition and initiative are suggestive of apathy. Neuropsychology, particularly the capacity to divide attention, may be useful. FUNCTIONAL CONSEQUENCES: Apathy and depression both have functional effects which may accelerate institutionalization (altered capacity for initiative, adaptation to the environment). FUNCTIONAL ANATOMY AND NEUROCHEMICAL CONSEQUENCES: Apathy and to a lesser degree depression, involve prefrontal cortical areas. Involvement of the prefrontal pathways is a common feature of apathy and depression, but the other pathways are affected specifically. Cholinesterase inhibitors and selective serotonine reuptake inhibitors as well as serotoninergic antidepressants have been found to be effective for certain components of apathy.

International audience; Language hemispheric dominance can be assessed by the Wada test before temporal lobectomy, in patients with refractory epilepsy of the mesial temporal lobe. Functional MR is a less invasive technique which recently demonstrated the ability to localize some language areas. The aim of this study was to determine if functional MR can be substituted to the Wada test in the determination of language dominance. Seven patients with a refractory epilepsy of the mesial temporal lobe were included. The MR protocol was carried out using a 1.5 T system including 12 axial gradient echo BOLD EPI images. A semantic fluency task, interspersed with rest periods, was used as activation paradigm. An activation of middle and inferior frontal region was found in all patients. It predominated in the left hemisphere in 6 cases and in the right hemisphere in 1 case. The hemispheric and frontal lobe lateralization of the functional MR activation was correlated with the hemispheric language dominance as assessed by the Wada test. In conclusion, functional MR is a promising technique in the determination of language dominance.

A 69 year-old right-handed man suffered from an infarct in the left anterior cerebral territory's artery, involving the anterior and middle parts of the corpus callosum, and the cingulum. He had a right crural hemiparesis with a grasp reflex of the right hand, and ipsilaterally a melokinetic and a dynamic apraxia. Agility of the left fingers was lost: fast and nimble movements of theses fingers, and repetitive gestures of the left hand were defective. Execution of motor sequences with the left hand was disrupted by a lack of litheness in gesture series. By analogy with unilateral left ideomotor apraxia, we suggest melokinetic and dynamic apraxia could be symptomatic of an interhemispheric disconnection. Premotor cortex could have a dominance for both digital movements and programmation of gestual sequences. As a general rule, the left cortex could be preferentially activated by the nature of some tasks, particularly the execution of complex gestual series, which implie an internal speech. In theses conditions, an interhemispheric disconnection could lead some difficulties to make theses gestures with the left hand.

Disorders of executive function and motor control are considered to be classical consequences of prefrontal lesions. The aim of this study was to investigate these disorders and their evolution in a series of patients presenting with prefrontal and cingulate lesion following rupture of an anterior communicating artery aneurysm. Twenty one subjects were included, and assessed in the secondary and late post stroke phases. We have used the following tests to assess planning and/or execution time and performance: Trail Making test, Wisconsin Card Sorting Test, London Tower Test, Shopping Test of Martin, sequential gestual test and contradictory responses test from Luria. Correlations between these parameters were used to evaluate subjects strategy. In evaluation of execution time, patients were slower than controls, and the difference was more marked using the Trail Making Test (p0.01) and the London Tower Test (p0.01). Furthermore, the initiation time was increased in the London Tower Test (p0.01), this suggesting that they were slower than impulsive. Groups analysis showed that their performance level was most often similar to that of of controls, even in the secondary phase, with the exception of the number of problems solved whatever number of moves in the London Tower test (p0.01) and of the percentage of errors in the sequential motor task (p0.03). Similar results were observed in the evaluation of single cases. Correlations between execution time and performance were most often significant and negative, in patients and controls. These results suggest that the management of the speed-accuracy compromise was relatively similar, and that impulsivity, which associates reduction of time to poor performance, was absent or mild. Cingulate, and caudate lesions were identified as the source of most cognitive disorders.

Diffuse Lewy body disease has not been yet described in France, although some authors, essentially Japanese ones reported cases of this disease. A man began at age 56 to be very apathetic with memory disturbances. Later, he developed aphasia, stereotypies, and mild parkinsonian rigidity. He died in cachexia, three years after the onset of the disease. Post-mortem examination showed diffuse senile plaques and tangles in the cortex. But there was also a striking widening of Lewy bodies, in the pons and in the frontal, temporal and cingular cortex. These Lewy bodies were located in the 5th cortical layer, and their immature and irregular shape made them difficult to identify. The authors discuss the role of each lesions on the clinical disturbances, in regard to other described cases.

The idea that saccadic eye movements necessary for visual space exploration could be under the control of the frontal eye field was based mainly upon Ferrier's early experiments of electrical stimulation of the cortex. More recent anatomical as well physiological data have demonstrated in monkeys that the sensori-motor processing needed to locate visual targets and to program an accurate eye movement to them is achieved in the superior colliculus, the frontal prearcurate and the posterior parietal cortices. Cells in those three structures have been identified by microelectrode studies that modify their response to a visual target before any eye movement when a saccade directed to this stimulus is to occur. Motivation to move the eyes towards the stimulus is under the control of the limbic cortex of the cingulate gyrus. Lesions to any of these structures lead to a neglect phenomenon characterized by the paucity of spontaneous saccades towards the half of space opposite to the lesion. In primates and in man neglect is observed only after cortical or thalamic lesions but not, or very transiently, after collicular lesion. The prearcuate frontal, the cingulate, and the posterior parietal cortices are interconnected via direct cortico-cortical fibres and also by a cortico-thalamo-cortical circuit, the thalamic relay of which is the medial pulvinar. The medial pulvinar is known to receive polymodal sensory informations from the intermediate layers of the superior colliculus. Thus a complete network involving cortical, thalamic and subthalamic structures is responsible for a very secure and redundant control of gaze.

Local cerebral glucose utilization (LCGU) was studied quantitatively in awake rats one week and one month following unilateral electrolytic lesion of the ventromedial thalamic nucleus (VM). Significant decrease in LCGU were observed in the ipsilateral cortex as well as in some contralateral cortical areas and bilateral subcortical structures. The modifications by the VM lesion, of the metabolic activations induced by electrical stimulation of substantia nigra pars reticulata (SNR, main afference of the VM) were investigated also. Results suggest that VM is an important relay nucleus on the pathways directed from one SNR towards ipsilateral corticostriatal system and contralateral thalamus and basal ganglia. Finally, one month following the VM lesion a recovery of metabolic activations induced by SNR stimulation was observed whereas basal glucose consumption remained decreased.

The electrical stimulation of a restricted part of area 24 in awake man elicits important behavioral changes. The present study is dealing with 83 epileptic patients whose brain activity was recorded in SEEG conditions, with a view to possible neurosurgery. In order to determine how seizures originate and propagate, 116 multileads electrodes (65 right, 51 left) were stereotaxically inserted in the anterior part of the cingular gyrus. 521 stimulations were performed. In 362 cases, this stimulation induced a particular behaviour which was characterized by an arousal, motor activities (involving fingers and hand, mouth, legs, eyes, associated movements of hand mouth, highly integrated movements), thymic modifications and hallucinatory manifestations. Topographical organization of the effective area in the cingular gyrus and the relation between the electrical responses and stimulation parameters are studied.

Controversies exist about the type of lesions observed in Korsakoff's syndrome or amnestic syndromes. A review of clinicopathologic data in the literature and findings in a personal series of 31 patients with amnestic syndromes (14 with alcoholism and nutritional deficiency, 8 with tumors including 2 with craniopharyngiomas, 5 with Pick's disease and presbyophrenic manifestations, 2 with vascular affections and one each with anoxia and herpetic encephalitis) were used to determine most frequently responsible lesions. Although it is generally accepted that there must be bilateral lesions divergent opinions are found with regard to the significance of limbic-hippocampomammillary circuit lesions. Some authors refute any specific role for the limbic circuit, and particularly any part played by Ammon's horn, in favor of a role for the temporal isthmus while others reject the possible role of the mammillary bodies and implicate the dorsomedian nucleus of the thalamus. The present study confirmed the importance of the limbic-hippocampomammillocingulus circuit in the maintenance of long-term memory. Involvement of the hippocampus appears obvious, particularly in disorders due to lesions of the subiculum and sommer's field. Mammillary body lesions are a constant finding in amnestic syndromes due to alcoholic nutritional deficiency and may also be present in Korsakoff's syndromes of tumoral origin e.g. a compression due to a craniopharyngioma. The rarely mentioned lesions of the cingular convolution are a further possible cause. The role of a thalamic lesion has not been totally confirmed, findings indicating equally frequent involvement of laterodorsal and dorsomedian nuclei. Clinical evidence, however, points to correlations between fabulation, false recognition and a thalamic lesion. The role of the fornix is debatable, although it is difficult to understand how destruction of the hippocampic formation or of the mammillary bodies can provoke memory disorders while an interruption in the structure that links them would have no consequences, unless it is admitted that as in animals other pathways exist that pass little or not at all through the fornix. Clinical expression of bilateral lesions of these structures differs according to whether they affect the posterior Ammon's horn region or lie more anteriorly in the trigonomammillothalamo-cingular complex. Clinical features of hippocampic amnesia include continuous anterograde amnesia with successive periods of forgetfulness, retrograde deficit of variable duration, parallel alterations of verbal and visuospatial memory and absence of fabulation.(ABSTRACT TRUNCATED AT 400 WORDS)

The authors describe three pathological cases of akinetic mutism with, as a common basic lesion, bilateral infarction of the cingulate gyrus secondary to aneurysm of the anterior communicating artery (case n degrees 1), to a huge olfactory meningioma (case n degrees 2), both operated on, and to atheromatous occlusion of the anterior cerebral arterial system (case n degrees 3). These three cases enable a variety of "anterior and waking" akinetic mutism to be described which is unusual enough to be compared with other mesencephalic and diencephalic aspects of this syndrome. It is in fact an akinetic mutism characterized by: a certain dissociation in its non-response to various stimuli, a particularly marked appearance of wakefulness when day-time alertness is considered, conservation of the waking-sleeping rhythm, perception and reaction unpredictable and paradoxical in both degree and quality, complete absence of any spontaneous verbal communication in contrast to relative break-down of solicited communication which is infrequent, uncertain and unresponsive to the usual methods of stimulation, without any possibility of a code. In addition, there is a remarkable mimic and segmental general akinesia, resistant to the usual nociceptive stimuli, but sensitive to slight excitation of the manual and oral zones. Besides this special akinetic mutism, there are variously systematised signs, mostly asymmetrical, indicating lesion of the cortico-sub-cortical frontal structures bordering on the gyrus cinguli. This unusual behaviour pattern corresponds in these three cases to extensive anterior bilateral ischemic lesions of the cingulate gyrus regularly associated with bilateral infarctions confined to the medial aspect of F1 in the superficial territory of the two anterior cerebral arteries, to possible neurosurgical changes (ablation of the right frontal pole) and to compressive or ischaemic lesions of the gyrus rectus. These exclusively cortico-sub-cortical associated lesions are in contrast with the remarkably intact caudate nuclei, the pallidal, thalamic, hypothalamic and septal formations and the anterior pillars of the fornix. These findings compared with the results of experimental research carried out by M. Kennard, help, if help is needed, to resolve the apparent contradictions between the effects of therapeutic cingulectomies or cingulotomies and the scanty pathological data already available in cerebral vascular pathology.

The effects of lesions of the anterior (Ant) or posterior (Post) regions of the cingulate cortex were tested using the closed-field maze tests of Hebb-Williams. Subjects were male BALB/c mice which had received restricted bilateral electrolytic lesions of the Ant or Post cingulate cortex. Their performances in acquisition or retention were compared to those of sham operated mice at different time intervals after the lesion. In a first series of experiments, naive animals were lesioned. The effects of lesions on acquisition were then tested at different time intervals (up to 45 days) after surgery. In a second series of experiments, the animals were lesioned only after prior complete acquisition of the maze tests and tested in a retention paradigm. The results show a differential effect of Ant versus Post cingulate lesions. Ant lesions had no significant effects whereas Post lesions induced a facilitation of performance at time intervals between 19 and 33 days (acquisition paradigm) or 11 and 25 days (retention paradigm). Conversely a reversal (impairment) of the effect was observed when Post animals were tested 28 days (acquisition) or 48 days (retention) after surgery. Taking into consideration the changing nature of the behavioral paradigm used, we suggest that the paradoxical and transitory facilitatory effects of the Post cingulate lesions may indicate that lesioned mice exhibited a greater degree of adaptability in each new learning situation. However, we can also postulate that these facilitatory effects resulted from a difficulty of lesioned mice in addressing long-term memory stores. This would therefore paradoxically protect them from interference generated by the high degree of familiarity in the behavioural testing apparatus.(ABSTRACT TRUNCATED AT 250 WORDS)

The literature only rarely mention the genital and sexual manifestations occurring in the course of partial seizures in man. The authors presently describe 42 seizures of this type recorded with E.E.G. and Stereo-E.E.G. techniques in 15 patients. The results of this study indicate that the genital and sexual paroxystic manifestations do have a specific semeiology, and there can be related to the initial localization of the electrical discharge which may begin in one of three different regions (perisylvian region, anterior part of the cingular gyrus and the paracentral lobule). Penile erection is observed in only one seizure starting in the central region. Orgasm occurs in the only one female patient in the course of the seizures beginning in the perisylvian region (temporal region). Early sensitive symptomatology characterizes very often the seizures beginning in the perisylvian region but also in the paracentral lobule. Post-ictal or peri-ictal true masturbation occurs at the end of the ictal discharge beginning either in the perisylvian region or in the anterior part of the cingular gyrus. The sexual dyspraxic (i.e. fondling the genitals) characterizes only the post-ictal phase of the seizures beginning in any of the three regions.

Efferent pathways of the LD nucleus of the thalamus were studied in 6 Papio-papio baboons with the retrograde transport technique utilizing HRP. Injections were made in cingular and parietal cortex and hippocampal formation. Large projection from the LD to the cingular and subicular cortex were visualized as reciprocal connections. No pathway to parietal area 7 was found. The course of the fibers is via the fornix, the cingular bundle and the retro-lenticular portion of the internal capsule. The result of this study make it necessary to reconsider neuropathological hypotheses on memory.

Lateralis dorsalis nucleus of thalamus belong to the limbic system of Papez more by its trigonal than cingular afferent pathways. Its parietal efferent pathways are probable, its cingular and trigonal ones possible but not proved. Neuropathologic studies provide informations to separate a latero-ventral part connected with parietal cortex and a mediodorsal part connected with limbic system.