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1.
Brain imaging studies in humans have shown that face processing in several areas is modulated by the affective significance of faces, particularly with fearful expressions, but also with other social signals such gaze direction. Here we review haemodynamic and electrical neuroimaging results indicating that activity in the face-selective fusiform cortex may be enhanced by emotional (fearful) expressions, without explicit voluntary control, and presumably through direct feedback connections from the amygdala. fMRI studies show that these increased responses in fusiform cortex to fearful faces are abolished by amygdala damage in the ipsilateral hemisphere, despite preserved effects of voluntary attention on fusiform; whereas emotional increases can still arise despite deficits in attention or awareness following parietal damage, and appear relatively unaffected by pharmacological increases in cholinergic stimulation. Fear-related modulations of face processing driven by amygdala signals may implicate not only fusiform cortex, but also earlier visual areas in occipital cortex (e.g., V1) and other distant regions involved in social, cognitive, or somatic responses (e.g., superior temporal sulcus, cingulate, or parietal areas). In the temporal domain, evoked-potentials show a widespread time-course of emotional face perception, with some increases in the amplitude of responses recorded over both occipital and frontal regions for fearful relative to neutral faces (as well as in the amygdala and orbitofrontal cortex, when using intracranial recordings), but with different latencies post-stimulus onset. Early emotional responses may arise around 120ms, prior to a full visual categorization stage indexed by the face-selective N170 component, possibly reflecting rapid emotion processing based on crude visual cues in faces. Other electrical components arise at later latencies and involve more sustained activities, probably generated in associative or supramodal brain areas, and resulting in part from the modulatory signals received from amygdala. Altogether, these fMRI and ERP results demonstrate that emotion face perception is a complex process that cannot be related to a single neural event taking place in a single brain regions, but rather implicates an interactive network with distributed activity in time and space. Moreover, although traditional models in cognitive neuropsychology have often considered that facial expression and facial identity are processed along two separate pathways, evidence from fMRI and ERPs suggests instead that emotional processing can strongly affect brain systems responsible for face recognition and memory. The functional implications of these interactions remain to be fully explored, but might play an important role in the normal development of face processing skills and in some neuropsychiatric disorders.  相似文献
2.
Consciousness as a Neurological Concept in Epileptology: A Critical Review   总被引:10,自引:10,他引:1  
P. Gloor 《Epilepsia》1986,27(S2):S14-S26
Summary: This essay explores the usefulness of the concept of consciousness in epileptology and concludes that it does not further the understanding of seizure mechanisms and brain function. The reasons for this are both theoretical and empirical. Consciousness cannot be adequately defined. This may explain why attempts at accounting for it in neurobiological terms have failed. Epistemological and scientific arguments are reviewed which suggest why a satisfactory explanation of consciousness is not now and may never be possible. There are, however, aspects of conscious experience such as perception, cognition, memory, affect, and voluntary motility that are open to neurobiological research. Careful observations of epileptic seizures with "loss of consciousness" often reveal that only some components of consciousness are impaired. "Loss of consciousness" during a seizure, often presenting as unresponsiveness, may be due to aphasia, inability to perform voluntary movements, ictal or postictal amnesia (sometimes with preservation of memory during the ictus itself), or to diversion of attention by a hallucinated experience. A plea is made to observe accurately and interact with the patient during an attack in order to distinguish between these various behavioral disturbances masquerading as "loss of consciousness.  相似文献
3.
Myoclonus: Relation to Epilepsy   总被引:9,自引:9,他引:1  
Mark Hallett 《Epilepsia》1985,26(S1):S67-S77
Summary: Myoclonus can be divided into those types which are fragments of epilepsy and those which are non-epileptic. Epileptic myoclonus is viewed as the effect of an isolated spike in neurons of the motor system. Cortical reflex myoclonus is a fragment of partial epilepsy and represents hyperactivity of a focal area of cerebral cortex. Reticular reflex myoclonus is a fragment of generalized epilepsy with hyperactivity of medullary brainstem reticular formation. Primary generalized epileptic myoclonus is a fragment of primary generalized epilepsy and may represent a generalized hyperactive response of cortex to subcortical input.  相似文献
4.
Physiological Mechanisms of Focal Epileptogenesis   总被引:6,自引:6,他引:1  
David A. Prince 《Epilepsia》1985,26(S1):S3-S14
Summary: The key elements in the development of epileptogenesis appear to be the capacity of membranes in some (pacemaker) neurons to develop intrinsic burst discharges, the presence of disinhibition, and the proper excitatory synaptic circuitry. It is likely that the relative role of each of these processes will differ at different sites in the central nervous system which are prone to epileptogenesis. Synchronization of neuronal populations is a vital element in the development of focal discharge and a variety of mechanisms, including those dependent upon excitatory postsynaptic potentials, and other interactions are possible. Pathological processes may alter some or all of these regulatory mechanisms. However, different pathological entities presumably produce epileptogenesis through different combinations of pathogenetic mechanisms.  相似文献
5.
Effect of Anticonvulsant Drugs on Inhibitory and Excitatory Pathways   总被引:5,自引:5,他引:1  
A conditioning stimulus to the periventricular gray matter inhibits the response of spinal trigeminal neurons to maxillary nerve stimulation. Sodium valproate and ethosuximide decrease the periventricular inhibition without significantly affecting the response of these neurons to the unconditioned maxillary nerve stimulus. We have now found that carbamazepine and phenytoin decrease the response to the unconditioned maxillary nerve stimulus, and only depress the periventricular inhibition secondarily. These results further support the hypothesis that the ability to depress selectively inhibitory pathways in the CNS is an important characteristic of antiabsence drugs, and that absence seizures may represent paroxysmal discharges in inhibitory pathways.  相似文献
6.
The pharmacologic basis of antiepileptic drug action   总被引:5,自引:5,他引:4  
Rho JM  Sankar R 《Epilepsia》1999,40(11):1471-1483
The development of medications used in the treatment of epilepsy has accelerated over the past decade, and has benefited from a parallel growth in our knowledge of the basic mechanisms underlying neuronal excitability and synchronization. This understanding of the pharmacologic basis of antiepileptic drug (AED) action has, in large part, arisen from recent advances in cellular and molecular biology, coupled with avenues of drug discovery that have departed somewhat from the largely empiric approaches of the past. Physicians now have available to them an ever-growing armentarium of AEDs, necessitating a firmer appreciation of their mechanisms of action if more rational approaches toward both clinical application and research are to be adopted. An important example in this regard is the concept of rational polypharmacy for patients with epilepsy who are refractory to monotherapy. This review summarizes our current understanding of the molecular targets of clinically significant AEDs, comparing and contrasting their differing mechanisms of action.  相似文献
7.
精神分裂症缓解期患者的心理防御机制研究   总被引:5,自引:0,他引:5  
目的:探讨精神分裂症患者的心理防御机制。方法:采用防御机制问卷,对精神分裂症缓解期患者36例进行测试,并与34例正常人进行比较。结果:患者组不成熟防御机制因子分明显高于对照组。结论:精神分裂症患者在心理防御机制的使用上明显不同于正常人。  相似文献
8.
Sleep-epilepsy interactions were investigated in a model of temporal lobe seizures induced in cats by intra-amygdaloid kainic acid (KA) microinjections. We found that limbic status epilepticus disrupted sleep for 2 or 3 days after injection. Sleep, in turn, modulated the frequency of interictal discharges. However, such modulation was variable depending on the time elapsed since KA injection. For this and other reasons (such as the occurrence of subclinical seizures during paradoxical sleep), we postulate a dual effect--facilitatory or inhibitory--of paradoxical sleep on limbic epilepsy. A role in seizure induction for bulbopontine structures is proposed on the basis of seizure precipitation during phasic paradoxical sleep. Propagated limbic seizures and paradoxical sleep without atonia displayed similar behavioral patterns. This fact and the possibility that a seizure may substitute for paradoxical sleep, lead us to think that limbic seizures and paradoxical sleep subserve similar functions. One of them might be the elimination of a potentially neurotoxic endogenous product.  相似文献
9.
Mounting evidence suggests that—beyond the well-known genomic effects—glucocorticoids affect cell function via non-genomic mechanisms. Such mechanisms operate in many major systems and organs including the cardiovascular, immune, endocrine and nervous systems, smooth and skeletal muscles, liver, and fat cells. Non-genomic effects are exerted by direct actions on membrane lipids (affecting membrane fluidity), membrane proteins (e.g. ion channels and neurotransmitter receptors), and cytoplasmic proteins (e.g. MAPKs, phospholipases, protein kinases, etc.). These actions are mediated by the glucocorticoids per se or by the proteins dissociated from the liganded glucocorticoid receptor complex. The MR and GR also activate non-genomic mechanisms in certain cases. Some effects of glucocorticoids are shared by a variety of steroids, whereas others are more selective. Moreover, “ultra-selective” effects—mediated by certain glucocorticoids only—were also shown. Disparate findings suggest that non-genomic mechanisms also show “demand-specificity”, i.e. require the coincidence of two or more processes. Some of the non-genomic mechanisms activated by glucocorticoids are therapeutically relevant; moreover, the “non-genomic specificity” of certain glucocorticoids raises the possibility of therapeutic applications. Despite the large body of evidence, however, the non-genomic mechanisms of glucocorticoids are still poorly understood. Criteria for differentiating genomic and non-genomic mechanisms are often loosely applied; interactions between various mechanisms are unknown, and non-genomic mechanism-specific pharmacological (potentially therapeutic) agents are lacking. Nevertheless, the discovery of non-genomic mechanisms is a major breakthrough in stress research, and further insights into these mechanisms may open novel approaches for the therapy of various diseases.  相似文献
10.
The basic science of memory as it applies to epilepsy   总被引:3,自引:0,他引:3  
Summary   The mechanisms of memory delineated by the model of long-term potentiation (LTP) are similar to those underlying epileptogenesis by kindling. Memory is impaired by seizures and epilepsy. High frequency neural activity is important in both memory formation and seizures. Both kindling and LTP are most effectively induced by high-frequency stimuli, involve synaptic facilitation, and share overlapping molecular mechanisms, such as N-methyl- d -aspartate (NMDA) receptor-induced calcium cascade and protein synthesis. The hippocampus contributes to both through its role in memory formation and its low seizure threshold.  相似文献
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