Epilepsy & behavior : E&B
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Traumatic brain injury (TBI) can cause a myriad of sequelae depending on its type, severity, and location of injured structures. These can include mood disorders, posttraumatic stress disorder and other anxiety disorders, personality disorders, aggressive disorders, cognitive changes, chronic pain, sleep problems, motor or sensory impairments, endocrine dysfunction, gastrointestinal disturbances, increased risk of infections, pulmonary disturbances, parkinsonism, posttraumatic epilepsy, or their combinations. ⋯ In parallel with morbidogenesis, spontaneous recovery occurs both in experimental models and in human TBI. A great challenge remains; how can we dissect the specific mechanisms that lead to the different endophenotypes, such as posttraumatic epileptogenesis, in order to identify treatment approaches that would not compromise recovery?
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Epilepsy & behavior : E&B · Sep 2014
ReviewEarly-life stress and HPA axis trigger recurrent adulthood depression.
It is now broadly accepted that psychological stress may change the internal homeostatic state of an individual. During acute stress, adaptive physiological responses occur, which include hyperactivity of the HPA axis. Whenever there is an acute interruption of this balance, illness may result. ⋯ Generally, HPA axis changes appear in chronic depressive and more severe episodes. Moreover, HPA axis changes appear to be state-dependent, tending to improve upon resolution of the depressive syndrome. Interestingly, persistent HPA dysfunction has been associated with higher rates of relapse and chronicity.
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Our understanding of the mechanisms of loss and recovery of consciousness, following severe brain injury or during anesthesia, is changing rapidly. Recent neuroimaging studies have shown that patients with chronic disorders of consciousness and subjects undergoing general anesthesia present a complex dysfunctionality in the architecture of brain connectivity. ⋯ Despite ongoing efforts, the mechanisms underlying the emergence of consciousness after severe brain injury are not thoroughly understood. Important questions remain unanswered: What triggers the connectivity impairment leading to disorders of consciousness? Why do some patients recover from coma, while others with apparently similar brain injuries do not? Understanding these mechanisms could lead to a better comprehension of brain function and, hopefully, lead to new therapeutic strategies in this challenging patient population.
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Epilepsy & behavior : E&B · Mar 2013
ReviewUnraveling the genetics of common epilepsies: approaches, platforms, and caveats.
With no known intervention to prevent or cure epilepsy, treatment is primarily symptomatic and requires long-term administration of medications to suppress seizure occurrence. Current antiepileptic drugs (AEDs) are ineffective in one-third of patients (Kwan and Brodie, 2000). Such therapeutic inadequacy is largely due to our insufficient understanding of the basic molecular pathophysiological processes that underlie epileptogenesis. ⋯ We review the approaches that have been taken to identify genetic risk markers of the common epilepsy syndromes, the experimental platforms, and their caveats. We discuss current technologies and analytical frameworks that might expedite the discovery of these variants by leveraging advances in microarray-based, high-throughput, genotyping technology, and complementary interdisciplinary expertise of study teams including the need for meta-analyses under global collaborative frameworks. We briefly discuss the analytical options made available through rapid advances in sequencing and other genomic technologies.
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The relationship between headache and seizures is a complicated one, since these two conditions are related in numerous ways. Although the nature of this association is unclear, several plausible explanations exist: the two disorders coexist by chance; headache is part (or even the sole ictal phenomenon) of seizures or the post-ictal state; both disorders share a common underlying etiology; and epilepsy mimics the symptoms of migraine (as in benign childhood epilepsy). Seizures and headaches as well as their respective primary syndromes (epilepsy and headache/migraine) share several pathophysiological mechanisms. ⋯ Both experimental and clinical measures are required to better understand this relationship. The development of animal models, molecular studies defining more precise genotype/phenotype correlations, and multicenter clinical studies with revision of clinical criteria for headache/epilepsy-related disorders represent the start for planning future translational research. In this paper, we review the relationship between migraine and epilepsy in terms of epidemiology and pathophysiology with regard to translational research and clinical correlations and classification.