Neuroscience letters
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Neuroscience letters · Jun 2012
ReviewInsights gained into pain processing from patients with focal brain lesions.
The recognition that dissociated sensory loss affecting selectively pain and temperature results from lesions of the operculo-insular cortex is due to Biemond in 1956. This contrasted with the prevailing view that the sensory aspects of pain did not imply regions above the thalamus. ⋯ Operculo-insular pain (parasylvian pain) is a distinct entity that can be clinically suspected and objectively diagnosed with combined radiological and electrophysiological methods, in particular evoked potentials to spinothalamic (laser) input. The region comprising the posterior insula and medial operculum may deserve being considered as a third somatosensory cortex (S3) contributing to the spinothalamic attributes of somatic perception.
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Human brain imaging has provided much information about pain processing and pain modulation, but brain imaging in rodents can provide information not attainable in human studies. First, the short lifespan of rats and mice, as well as the ability to have homogenous genetics and environments, allows for longitudinal studies of the effects of chronic pain on the brain. Second, brain imaging in animals allows for the testing of central actions of novel pharmacological and nonpharmacological analgesics before they can be tested in humans. ⋯ Pharmacological imaging in rodents shows overlapping activation patterns with pain and opiate analgesics, similar to what is found in humans. Despite the many structural imaging studies in human chronic pain patients, only one study has been performed in rodents, but that study confirmed human findings of decreased cortical thickness associated with chronic pain. Future directions in rodent pain imaging include miniaturized PET for the freely moving animal, as well as new MRI techniques that enable ongoing chronic pain imaging.
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Blocking the development of epilepsy (epileptogenesis) is a fundamental research area with the potential to provide large benefits to patients by avoiding the medical and social consequences that occur with epilepsy and lifelong therapy. Human clinical trials attempting to prevent epilepsy (antiepileptogenesis) have been few and universally unsuccessful to date. In this article, we review data about possible pathophysiological mechanisms underlying epileptogenesis, discuss potential interventions, and summarize prior antiepileptogenesis trials. Elements of ideal trials designs for successful antiepileptogenic intervention are suggested.
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Neuroscience letters · Jun 2011
ReviewThe time course of acquired epilepsy: implications for therapeutic intervention to suppress epileptogenesis.
Relatively little is known about the time course of the development of spontaneous recurrent seizures (i.e., epileptogenesis) after brain injury in human patients, or even in animal models. This time course is determined, at least in part, by the underlying molecular and cellular mechanisms responsible for acquired epilepsy. An understanding of the critical mechanistic features of acquired epilepsy will be useful, if not essential, for developing strategies to block or suppress epileptogenesis. ⋯ Although the classical view of the development of epileptogenesis is a step-function of time after the brain injury, with a latent period present between the brain injury and the first unprovoked seizure, the data described here show that seizure frequency was a sigmoid function of time after the insult in both animal models. Furthermore, the spontaneous recurrent seizures often occurred in clusters, even shortly after the first spontaneous seizure. These data suggest that (1) epileptogenesis is a continuous process that extends past the first spontaneous clinical seizure, (2) seizure clusters can obscure this continuous process, and (3) the potential time for administration of a therapy to suppress acquired epilepsy extends well past the first clinical seizure.
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Neuroscience letters · Jun 2011
ReviewAnti-epileptogenesis in rodent post-traumatic epilepsy models.
Post-traumatic epilepsy (PTE) accounts for 10-20% of symptomatic epilepsies. The urgency to understand the process of post-traumatic epileptogenesis and search for antiepileptogenic treatments is emphasized by a recent increase in traumatic brain injury (TBI) related to military combat or accidents in the aging population. ⋯ Also, current understanding of the mechanisms and biomarkers for PTE as well as factors associated with preclinical study designs are discussed. Finally, we summarize the attempts to prevent PTE in experimental models.