Spontaneous Temporal Lobe Research Articles

The Role of Lumbar Drains in the Perioperative Management of Primary Spontaneous Temporal Lobe Encephaloceles and Cerebrospinal Fluid Leaks.

To examine the role of lumbar drains (LDs) in the success of spontaneous temporal cerebrospinal fluid (CSF) leak and encephalocele repair. Retrospective cohort study. Tertiary academic health system. Patients undergoing repair of spontaneous temporal lobe encephaloceles or middle fossa CSF leaks during years 2017 to 2023. Transmastoid, middle fossa craniotomy, or combination approaches to CSF leak repair. Failure rate, complication rate, length of stay (LOS), readmission. Sixty-nine patients were included, with a combination approach performed in 78.3%, transmastoid in 17.4%, and isolated middle fossa craniotomy in 4.3%. Mean body mass index was 33.2, mean bony defect size width was 6.51 mm, and defect locations included the epitympanum, antrum, mastoid, and petrous apex. Multilayer closure with three or more layers was performed in 87.0%. LD was used in 73.9% of cases for a mean duration 2.27 days and was associated with longer LOS (3.27 vs. 1.56 d, p = 0.006) but not with failure rate, complications, discharge destination, or readmission. Only one major complication occurred as a result of the drain, but low-pressure headache was anecdotally common. Use of LD in the repair of spontaneous CSF leaks and temporal lobe encephaloceles is associated with longer LOS but not failure rates or other admission-level outcomes.

Focal seizures producing loss of wakefulness without ictal asystole: Does temporal lobe syncope exist?

Focal seizures are frequently associated with alteration of consciousness, mainly of awareness, rather than with complete loss of wakefulness. We aimed to explore whether episodes of complete loss of wakefulness (LOW) could be attributed to focal seizures alone, out of the context of ictal asystole or secondary generalization. From a database of adult patients with refractory, focal epilepsy, evaluated for presurgical work-up we searched for patients having the following criteria: (1) focal epilepsy, and (2) transient loss of consciousness, documented in video EEG or/and video SEEG, characterized by an alteration in the level of wakefulness ("syncope like", LOW), with eye closure, hypotonia and non-reactivity state. Patients with motor signs of secondary generalization and patients with non-epileptic psychogenic seizures were excluded. Fifteen patients with transient ictal LOW during focal seizures were found. Among them, 12 patients had ictal asystole. We found 3 patients who had complete loss of wakefulness during focal seizures, without asystole or documented hypotension. In two patients the episodes were provoked by high frequency stimulation of hippocampus and amygdala. The third patient had LOW appearing during a spontaneous temporal lobe seizure. Syncope semiology without ictal asystole can be attributed to temporal lobe seizures but remains an exceptional phenomenon. A crucial clinical requirement is the exclusion of cardiac arrhythmias, especially asystole.

Stereotypical activation of hippocampal ensembles during seizures

In addition to affecting a person’s behaviour and risk of accidents, seizures are believed to result in various neuro-physiological changes that disrupt nervous system integrity. Although anti-epileptic treatments exist, they are not always effective and in some epilepsy syndromes, such as temporal lobe epilepsy, a large proportion of patients are pharmacologically resistant. In order to develop seizure-preventing treatments, researchers have been trying to identify the neurological processes leading to seizures. In this issue of Brain ,Neumannandco-workers use extracellular electro-physiological recordings to determine the temporal evolution of neuronal activity preceding and during spontaneous temporal lobe seizures in rats (Neumann et al., 2017). They provide evidence that ictal discharges preferentially recruit specific cell ensembles firing in stereotypical sequences. In contrast to the classic view that seizures result from excessive runaway excitation, they show that the predominant cell types activated during ictal discharges are fast-spiking, putative inhibitory interneurons.

LGI Proteins and Epilepsy in Human and Animals.

Leucine‐rich glioma‐inactivated (LGI) protein was first thought to have a suppressor effect in the formation of some cancers. Developments in physiology and medicine made it possible to characterize the function of the LGI protein family and its crucial role in different conditions more precisely. These proteins play an important role in synaptic transmission, and dysfunction may cause hyperexcitability. Genetic mutation of LGI1was confirmed to be the cause of autosomal dominant lateral temporal lobe epilepsy in humans. The LGI2 mutation was identified in benign familial juvenile epilepsy in Lagotto Romagnolo (LR) dogs. Cats with familial spontaneous temporal lobe epilepsy have been reported, and the etiology might be associated with LGI protein family dysfunction. In addition, an autoimmune reaction against LGI1 was detected in humans and cats with limbic encephalitis. These advances prompted a review of LGI protein function and its role in different seizure disorders.

Cerebellar Directed Optogenetic Intervention Inhibits Spontaneous Hippocampal Seizures in a Mouse Model of Temporal Lobe Epilepsy.

Temporal lobe epilepsy is often medically refractory and new targets for intervention are needed. We used a mouse model of temporal lobe epilepsy, on-line seizure detection, and responsive optogenetic intervention to investigate the potential for cerebellar control of spontaneous temporal lobe seizures. Cerebellar targeted intervention inhibited spontaneous temporal lobe seizures during the chronic phase of the disorder. We further report that the direction of modulation as well as the location of intervention within the cerebellum can affect the outcome of intervention. Specifically, on-demand optogenetic excitation or inhibition of parvalbumin-expressing neurons, including Purkinje cells, in the lateral or midline cerebellum results in a decrease in seizure duration. In contrast, a consistent reduction in spontaneous seizure frequency occurs uniquely with on-demand optogenetic excitation of the midline cerebellum, and was not seen with intervention directly targeting the hippocampal formation. These findings demonstrate that the cerebellum is a powerful modulator of temporal lobe epilepsy, and that intervention targeting the cerebellum as a potential therapy for epilepsy should be revisited.

Prenatal lesioning cortical dysplasia rat model with spontaneous temporal lobe seizures

Background: Focal cortical dysplasia (FCD) is known to be a major cause of intractable epilepsy. We created a novel rat model of FCD by freeze lesioning during the late embryonic stage and examined the relationship between extratemporal FCD and epileptogenesis of temporal lobe seizures.

On-demand optogenetic control of spontaneous seizures in temporal lobe epilepsy

Temporal lobe epilepsy is the most common type of epilepsy in adults, is often medically refractory, and due to broad actions and long-time scales, current systemic treatments have major negative side-effects. However, temporal lobe seizures tend to arise from discrete regions before overt clinical behaviour, making temporally and spatially specific treatment theoretically possible. Here we report the arrest of spontaneous seizures using a real-time, closed-loop, response system and in vivo optogenetics in a mouse model of temporal lobe epilepsy. Either optogenetic inhibition of excitatory principal cells, or activation of a subpopulation of GABAergic cells representing <5% of hippocampal neurons, stops seizures rapidly upon light application. These results demonstrate that spontaneous temporal lobe seizures can be detected and terminated by modulating specific cell populations in a spatially restricted manner. A clinical approach built on these principles may overcome many of the side-effects of currently available treatment options.

The Neurobiology, Genetics and Evolution of Human Spirituality: The Central Role of the Temporal Lobes

Spirituality is defined as a sense of being connected with something greater than oneself. That something can be a supernatural entity, nature, a social group or a family. Different studies show that a wide range of factors that influence temporal lobe function can produce hallucinations, paranormal, spiritual, mystical, and religious experiences. These factors include the electrical stimulation of the temporal lobes; spontaneous temporal lobe epilepsy; trauma; psychedelic drugs; and the severe anoxia of near death, G-forces and carbon dioxide inhalation. Studies of the very short acting psychedelic drug DMT, which exerts its effect by binding to serotonin receptors in the temporal lobes, show that even highly rational subjects can be absolutely convinced that their induced experiences of being in contact with non-humans beings were absolutely real. This suggests that hippocampal memory cannot always distinguish between external real experiences and internally induced spiritual experiences. Twin studies show there is a significant genetic component to spirituality while religion and church going are more cultural. It is likely that the genes for spirituality were selected because the social cohesiveness that spiritually fosters has a strong survival value. The neurobiology of spirituality suggests that our rational brain occasionally needs to step back and give the spiritual brain some space to have beliefs and feelings that do not always make rational sense.

Spontaneous encephaloceles of the temporal lobe

Encephaloceles are pathological herniations of brain parenchyma through congenital or acquired osseus-dural defects of the skull base or cranial vault. Although encephaloceles are known as rare conditions, several surgical reports and clinical series focusing on spontaneous encephaloceles of the temporal lobe may be found in the otological, maxillofacial, radiological, and neurosurgical literature. A variety of symptoms such as occult or symptomatic CSF fistulas, recurrent meningitis, middle ear effusions or infections, conductive hearing loss, and medically intractable epilepsy have been described in patients harboring spontaneous encephaloceles of middle cranial fossa origin. Both open procedures and endoscopic techniques have been advocated for the treatment of such conditions. The authors discuss the pathogenesis, diagnostic assessment, and therapeutic management of spontaneous temporal lobe encephaloceles. Although diagnosis and treatment may differ on a case-by-case basis, review of the available literature suggests that spontaneous encephaloceles of middle cranial fossa origin are a more common pathology than previously believed. In particular, spontaneous cases of posteroinferior encephaloceles involving the tegmen tympani and the middle ear have been very well described in the medical literature.

Upregulation of opioid receptor binding following spontaneous epileptic seizures

Animal and limited human data suggest an important anticonvulsant role for opioid peptides and their receptors. We aimed to provide direct human in vivo evidence for changes in opioid receptor availability following spontaneous seizures. We scanned nine patients within hours of spontaneous temporal lobe seizures and compared their postictal binding of the non-subtype selective opioid receptor PET radioligand [11C]diprenorphine (DPN), quantified as a volume-of-distribution (VD), with interictal binding and with binding changes in 14 healthy controls, controlling for a range of behavioural variables associated with opioid action. A regionally specific increase of opioid receptor availability was evident in the temporal pole and fusiform gyrus ipsilateral to the seizure focus following seizures (Z 5.01, P < 0.001, 16 432 mm3). Within this region, there was a negative correlation between VD and log10 time since last seizure (r = -0.53, P < 0.03), compatible with an early increase and gradual return to baseline. [11C]DPN VD did not undergo systematic changes between time points in controls. This study provides direct human in vivo evidence for changes in opioid receptor availability over a time course of hours following spontaneous seizures, emphasizing an important role of the opioid system in seizure control.

Involvement of Medial Pulvinar Thalamic Nucleus in Human Temporal Lobe Seizures

Several animal studies suggest that the thalamus might be involved in the maintenance and propagation of epileptic seizures. However, electrophysiologic evidence for this implication in human partial epileptic seizures is still lacking. Considering the rich and reciprocal connectivity of the medial pulvinar (PuM) with the temporal lobe, we evaluated a potential participation of this thalamic nucleus in temporal lobe epilepsy (TLE). The electrophysiologic activity of PuM was recorded during stereoelectroencephalographic exploration of spontaneous temporal lobe seizures in 14 patients referred for presurgical assessment of refractory TLE. We recorded PuM ictal activity in 80% of the 74 seizures that we analyzed. This activity was characterized by rhythmic slow-waves or rhythmic spikes (RSW-RS) or both or by low-voltage fast activity (LVFA) in 64% and 36% of seizures, respectively. RSW-RS occurred mostly in seizures arising from mesiotemporal structures, whereas LVFA was more frequently observed in seizures of neocortical origin. In the 15 seizures without PuM ictal activity, spreading of the seizure outside the onset zone never occurred, whereas it did in 78% of seizures with PuM ictal involvement. Discharge propagation was systematic when PuM involvement corresponded to LVFA, whatever the seizure onset zone was, whereas it represented only 66% of the seizures when PuM exhibited RSW-RS. This study shows that ictal changes in PuM activity are frequently observed during temporal lobe seizures and suggests that this thalamic nucleus might participate in their propagation.

Ontogeny of feline temporal lobe epilepsy in amygdala-kindled kittens: an update

This report describes amygdala-kindled seizure development and the post-kindling course in 58 cats (29 males and 29 females), including 40 preadolescents between 2.5 and 6.5 months of age and 18 adults >1 year of age at the beginning of kindling. The results extend previous findings, as follows: (1) Youngest animals (<5.0 months, n=30) are far more likely than older kittens and adults to exhibit spontaneous epilepsy, indexed by seizures that occur >1 h after stimulus-evoked seizures. (2) The youngest animals also exhibit accelerated kindling rates and rapid post-kindling onset of multifocal spontaneous epilepsy with a catastrophic clinical course. The profile includes a variety of EEG and/or clinical seizure manifestations and a progressive increase in the number and density of convulsive seizure clusters. Behavioral sequelae accompany seizure clusters and can range from sensory or motor deficits (visual agnosia, sensory hypersensitivity, atonic episodes, restricted mobility) to social isolation and placidity. (3) Onset of spontaneous epilepsy with developmental deterioration is substantially enhanced by recurrent evoked seizures early in the post-kindling course. The post-kindling progression can be stopped or minimized by suspension of evoked seizure trials and/or by management of frequent spontaneous convulsions (>1 per hour) with anticonvulsants. (4) In older cats, many more evoked seizures are required to generate fewer spontaneous seizures with relatively innocuous behavioral disorders. The findings suggest a ‘critical period’ in kindled kittens for onset of spontaneous temporal lobe epilepsy with severe behavioral consequences and a favorable prognosis for the young following early detection and intervention.

Entorhinal-hippocampal interactions in medial temporal lobe epilepsy.

Experimental studies suggest important interactions between hippocampus and entorhinal cerebral cortex in generation of temporal lobe seizure activity. We studied electrical expression of spontaneous temporal lobe ictal activity in hippocampus and entorhinal cortex in 9 medically refractory epileptic patients who had intracranial depth and subdural electrodes implanted during surgical evaluation. All 9 patients subsequently underwent anteromedial temporal lobectomy with hippocampectomy, all had > 50% decrease in neuronal cell density in hippocampal CA1 and CA3, and all had good to excellent seizure outcome after operation. Two to 10 spontaneous seizures were analyzed per patient (total 41 seizures). Nine patients had variable onset of seizure activity recorded in hippocampus, entorhinal cortex, or both simultaneously. Low-voltage fast activity was observed in either location and varied among seizures in an individual patient. Periodic preictal spikes, when present, were often synchronous in both locations, but were noted independently only in hippocampus. Our data suggest that preictal spikes and low-voltage fast seizure discharges have anatomically distinct origins, and that some syndromes of medial temporal lobe epilepsy involve interactions between entorhinal and hippocampal regions that act together to produce and propagate the seizures in such patients.