Epileptogénesis y corteza piriforme: entendiendo a la epilepsia del lóbulo temporal más allá del hipocampo / Epileptogenesis and the piriform cortex: understanding temporal lobe epilepsy beyond the hippocampus

Introducción: Con la experiencia de los registros electroencefalográficos invasivos y el fracaso quirúrgico después de la cirugía, se ha hecho evidente que la epilepsia del lóbulo temporal es mucho más compleja de lo que se creía, y en la actualidad es considerada una enfermedad de redes anatomofuncionales y no de lesiones estructurales. Contenido: La información neurofisiológica e imagenológica actual permite concluir que en esta epilepsia están involucradas varias redes neuronales temporales y extratemporales que contribuyen a la extensión de la zona epileptógena. Una forma de entender el concepto de red epiléptica en la epilepsia del lóbulo temporal es a partir del conocimiento de la corteza piriforme. Varios estudios clínicos han mostrado que en pacientes con epilepsia del lóbulo temporal asociada a esclerosis hipocampal existe una disfunción interictal del procesamiento olfatorio que es más significativa, en comparación con pacientes con epilepsia focal extrahipocampal y controles sanos. Esta alteración es, probablemente, la consecuencia de una red neuronal disfuncional que se extiende más allá del hipocampo y que afecta a otras estructuras cercanas, incluida la corteza piriforme. Conclusión: En este artículo llevamos a cabo una revisión narrativa de la literatura con el objetivo de establecer un vínculo entre la corteza piriforme y la epileptogénesis del lóbulo temporal, y demostramos que esta enfermedad es la consecuencia de una disfunción de redes neuronales que no depende exclusivamente de una anormalidad estructural en el hipocampo o en estructuras cercanas.

Introduction: With the experience of invasive EEG recordings and surgical failure after surgery, it has become clear that temporal lobe epilepsy is much more complex than previously thought, and currently, is conceptualized as a disease of anatomical networks instead of structural lesions. Content: The current neurophysiological and imaging information allows us to conclude that several temporal and extratemporal anatomical networks are involved in this type of epilepsy. One way of understanding the concept of the epileptic network in temporal lobe epilepsy is from the knowledge of the piriform cortex. Several clinical studies have shown that in patients with temporal lobe epilepsy associated with hippocampal sclerosis exists an interictal dysfunction of olfactory processing that is more significant compared to patients with focal extra-hippocampal epilepsy and healthy controls. This alteration is probably the consequence of a dysfunctional neural network that extends beyond the hippocampus and affects other nearby structures, including the piriform cortex. Conclusion: In this article, we carry out a narrative review of the literature with the aim of establishing a link between the piriform cortex and temporal lobe epileptogenesis, demonstrating that this disease is the consequence of a dysfunctional network that does not depend exclusively of a hippocampal structural abnormality.

The role of status-related neuronal ensembles in tem-poral lobe epilepsy / 中国药理学与毒理学杂志

OBJECTIVE Epileptic networks are char-acterized as two states,seizures or more prolonged inter-ictal periods.However,cellular mechanisms underlying the contribution of interictal periods to ictal events remain unclear.METHODS Here,we present the procedure for labeling seizure-activated and interictal-activated neuro-nal ensembles in mouse hippocampal kindling model using an enhanced-synaptic-activity-responsive element.This technique is combined with genetically encoded effectors to characterize and manipulate neuronal ensembles recruited by focal seizures(FS-Ens)and interictal periods(IP-Ens)in piriform cortex,a region that plays a key role in seizure generation.RESULTS Ca2+ activities and histo-logical evidence reveal a disjointed correlation between the two ensembles during FS dynamics.Optogenetic acti-vation of FS-Ens promotes further seizure development,while IP-Ens protects against it.Interestingly,both ensem-bles are functionally involved in generalized seizures(GS)due to circuit rearrangement.IP-Ens bidirectionally modulates FS but not GS by controlling coherence with hippocampus.CONCLUSION This study indicates that the interictal state may represent a seizure-preventing environment,and the interictal-activated ensemble may serve as a potential therapeutic target for epilepsy.

Alterations in dendritic length and branch and K / 解剖学报

Objective To study the morphology of olfactory bulb(OB) neurons and the change of related proteins, and explore the causes of olfactory dysfuction in Alzheimer' s disease(AD). Methods Golgi-Cox staining technique was used to evaluate the morphological changes of neurons in the OB and anterior piriform cortex (aPC) of APP/PS1 AD model mice. The morphology of neurons was determined by Sholl analysis. Western blotting was used to evaluate the levels of protein expression. Results The results of Golgi-Cox showed that the dendrite length and branch number reduced significantly in the OB neurons of 3-5-month-old APP/PS1 mice, an age that the mice did not show the pathological characteristics and cognitive impairment of AD. Western blotting analysis showed that levels of potassium chloride cotransporter 2(KCC2), a potassium chloride transporter crucial for neuronal morphology and synaptic function, decreased significantly in the OB of 3-5-month-old APP/PS1 mice. Conclusion Abnormal neuronal morphology and KCC2 signal might be the basis of early olfactory dysfunction in AD. Thus, maintaining normal KCC2 signal may be one of the keys to intervene the olfactory abnormalities in the early stage of AD.

Silicone Implant-Based Paranasal Augmentation for Mild Midface Concavity

BACKGROUND: Midface concavity is a relatively common facial feature in East Asian populations. Paranasal augmentation is becoming an increasingly popular procedure for patients with mild concavity and normal occlusion. In this study, we evaluate clinical outcomes following a series of paranasal augmentation. METHODS: A retrospective review was performed for patients with Class I occlusion who had undergone bilateral paranasal augmentation using custom-made silicone implants, between October 2005 and September 2013. Patient charts were reviewed for demographic information, concomitant operations, and postoperative complications. Preoperative and postoperative (1-month) photographs were used to evaluate operative outcome. RESULTS: The review identified a total of 93 patients meeting study criteria. Overall, aesthetic outcomes were satisfactory. Five-millimeter thick silicone implant was used in 81 cases, and the mean augmentation was 4.26 mm for this thickness. Among the 93 patients, 2 patients required immediate implant removal due to discomfort. An additional 3 patients experienced implant migration without any extrusion. Nine patients complained of transient paresthesia, which had resolved by 2 weeks. There were no cases of hematoma or infection. All patients reported improvement in their lateral profile and were pleased at follow-up. Complications that arose postoperatively included 9 cases of numbness in the upper lip and 3 cases of implant migration. All cases yielded satisfactory results without persisting complications. Sensations were fully restored postoperatively after 1 to 2 weeks. CONCLUSION: Paranasal augmentation with custom-made silicone implants is a simple, safe, and inexpensive method that can readily improve the lateral profile of a patient with normal occlusion. When combined with other aesthetic procedures, paranasal augmentation can synergistically improve outcome and lead to greater patient satisfaction.

Olfactory tract transection in neonatal rats: Evidence for Mitral cell regeneration and restoration of functional connectivity with its targets.

Central Nervous System (CNS) regeneration and repair mechanism are two important aspects of functional recovery in the adult central nervous system following brain and spinal cord injury. Following olfactory tract transection in neonatal rats, functional connectivity between the olfactory bulb and the piriform cortex gets re-established by 120 days. The recovery of the dendritic morphology was associated with the synchronized oscillatory activity between olfactory bulb and piriform cortex. Mitral cells which were regenerated after the transection showed profuse branching, indicative of their undifferentiated state. However, normal dendritic morphology could be seen by 120 days after olfactory tract transection. These results thus provide a supportive evidence for the restoration of the functional connections between the olfactory bulb and the piriform cortex at 120 days.