scholarly journals SPECT Measurements with 99mTc-HM-PAO in Focal Epilepsy

1988 ◽  
Vol 8 (1_suppl) ◽  
pp. S95-S100 ◽  
Author(s):  
Erik Ryding ◽  
Ingmar Rosén ◽  
Dan Elmqvist ◽  
David H. Ingvar

The ability of SPECT measurements with [99mTc]–HM-PAO (Ceretec) to find the location of the epileptic focus was studied in patients under consideration for neurosurgical treatment for therapy-resistant focal epilepsy. The location of low [99mTc]–HM-PAO uptake regions found at interictal measurements, and of high [99mTc]–HM-PAO uptake regions found at ictal measurements, was compared to the findings of extensive ictal and interictal EEG examinations, and to the results of CT and MRT. While EEG revealed focal epileptic activity in all of the 14 patients, SPECT showed regional abnormalities in 13 (93%). CT and MRT showed abnormal findings in 30%.

2018 ◽  
Author(s):  
A.V. Paraskevov ◽  
D.K. Zendrikov

Spontaneous focal synchronization of collective spiking followed by induced traveling waves can occur in the cortical sheet and in cultured planar neuronal networks. In the first case, it is well-known focal epilepsy leading to a seizure and, in the second, this synchronization originates from one of a few steady nucleation sites resulting in a so-called population spike. Assuming functional similarity between the nucleation sites and non-lesional epileptic foci, the major unsolved problem in both cases is that it is unclear whether activation of the focus originates internally (i.e., autonomously relative to interaction with surrounding neuronal tissue) or externally. The ’internal’ scenario implies that the focus spatially contains some pacemakers. In turn, several experimental findings indicate a complex spatially non-local activation of epileptic focus. Here, we suggest a generative mechanistic model of planar neuronal network, where the spatial configuration of pacemaker neurons is artificially engineered in order to resolve the above mentioned problem: all pacemakers are placed within a circular central spot. Leaving the global dynamic regime unaffected, this crucially helps to clarify the activation process, visualizing of which is hindered in the natural spatially-uniform configuration. We show in simulations that the nucleation sites (i) can emerge in spatial regions, where pacemakers are completely absent and (ii) can be activated even without direct links from pacemakers. These results demonstrate the principle possibility of external, or remote, activation of a focal source of epileptic activity in the brain. The suggested deterministic model provides the means to study this network phenomenon systematically and reproducibly.


2019 ◽  
Vol 1 (1) ◽  
Author(s):  
Hermann Stefan

Abstract Background For seizures emerging from the posterior cortex it can be a challenge to differentiate if they belong to temporal, parietal or occipital epilepsies. Sensoric auras like visual phenomena may occur in all of these focal epilepsies. Ictal signs may mimic non- epileptic seizures. Case presentations Case 1: Patient suffering from a pharmacoresistent focal epilepsy. Focal seizures with sudden visual disturbance, later during the seizure epigastric aura, vertigo-nausea, involvement to bilateral tonic-clonic seizures. MEG detected interictal spikes, source localization indicated focal epileptic activity parietal right. Case 2: Patient with focal pharmacoresistent epilepsy, semiology with focal unaware seizures, feeling that something like a coat is imposed from behind on him, then feeling cold over the whole body, goose bumbs from both arms to head, then block of motoric activity, later focal unaware seizures with stare gaze, blinking of eyes, clouding of consciousness, elevation of arms and legs, sometimes tonic-clonic convulsions. EEG/MEG source localization and MRI detected an epileptogenic lesion parietal left. Case 3: Patient with pharmacoresistent focal epilepsy, focal aware seizures, a dark spot occurring in the left visual field, sometimes anxiety during seizures (leading to the suspicion of non-epileptic psychogenic pseudo seizures). MRI demonstrated an atrophy occipito-temporal right after sinus vein thrombosis. Ictal video-EEG showed a focal seizure onset occipital right. Conclusion Contribution of noninvasive and/or invasive confirmation of the localization of the underlying focal epileptic activity in posterior cortex is illustrated. Characteristics of posterior cortex epilepsies are ventilated.


1994 ◽  
Vol 71 (6) ◽  
pp. 2463-2476 ◽  
Author(s):  
M. De Curtis ◽  
G. Biella ◽  
M. Forti ◽  
F. Panzica

1. We investigated the development of epileptic activity in the limbic lobe of the in vitro isolated brain preparation after induction of a restricted epileptic focus in the rostral portion of the anterior piriform cortex (APC) by means of local bicuculline ejection. 2. The modifications of the local responses evoked by stimulation of the lateral olfactory tract were consistent with an increase in excitability of layer II pyramidal neurons. The abnormal discharge output of the epileptic focus propagated throughout the piriform cortex (PC) and generated late synaptic stimulus-evoked epileptiform potentials in layer Ib, where corticocortical associative fibers contact the distal dendrites of pyramidal cells. 3. Spontaneous epileptiform potentials (SEPs) originated in the primary focus at the bicuculline ejection site 10–15 min after drug application and propagated via associative fibers to the posterior PC (PPC). 4. Autonomous secondary foci generating SEPs independently from the primary anterior focus developed in the PPC within 2 h after the bicuculline application. 5. Ictal events seldom occurred spontaneously in PC but could be induced by tetanic afferent stimulation. Evoked ictal events in PC had the characteristics of afterdischarges, being short in duration and localized in space and showing a progressively decreasing firing rate. 6. Self-sustained spontaneous ictal discharges were observed in the entorhinal cortex and hippocampus but not in PC after activation of the APC focus. 7. We conclude that in an acute pharmacological model of focal epilepsy, associative corticocortical connections hold a primary role 1) in the propagation of interictal epileptiform activity throughout the limbic lobe and 2) in the generation of secondary epileptic foci. We also demonstrate that self-sustained ictal events are not spontaneously generated in PC, although paroxysmal seizure-like discharges occur in hippocampus. We discuss the relevance of the rostral-to-caudal-directed associative fiber system in generation of limbic seizures.


2020 ◽  
Vol 2 (2) ◽  
Author(s):  
Sara Baldini ◽  
Francesca Pittau ◽  
Gwenael Birot ◽  
Vincent Rochas ◽  
Miralena I Tomescu ◽  
...  

Abstract Monitoring epileptic activity in the absence of interictal discharges is a major need given the well-established lack of reliability of patients’ reports of their seizures. Up to now, there are no other tools than reviewing the seizure diary; however, seizures may not be remembered or dismissed voluntarily. In the present study, we set out to determine if EEG voltage maps of epileptogenic activity in individual patients can help to identify disease activity, even if their scalp EEG appears normal. Twenty-five patients with pharmacoresistant focal epilepsy were included. For each patient, 6 min of EEG with spikes (yes-spike) and without visually detectable epileptogenic discharges (no-spike) were selected from long-term monitoring recordings (EEG 31–37 channels). For each patient, we identified typical discharges, calculated their average and the corresponding scalp voltage map (‘spike-map’). We then fitted the spike-map for each patient on their (i) EEG epochs with visible spikes, (ii) epochs without any visible spike and (iii) EEGs of 48 controls. The global explained variance was used to estimate the presence of the spike-maps. The individual spike-map occurred more often in the spike-free EEGs of patients compared to EEGs of healthy controls (P = 0.001). Not surprisingly, this difference was higher if the EEGs contained spikes (P < 0.001). In patients, spike-maps were more frequent per second (P < 0.001) but with a shorter mean duration (P < 0.001) than in controls, for both no-spike and yes-spike EEGs. The amount of spike-maps was unrelated to clinical variables, like epilepsy severity, drug load or vigilance state. Voltage maps of spike activity are present very frequently in the scalp EEG of patients, even in presumably normal EEG. We conclude that spike-maps are a robust and potentially powerful marker to monitor subtle epileptogenic activity.


2007 ◽  
Vol 7 (4) ◽  
pp. 91-94 ◽  
Author(s):  
Theodore H. Schwartz

Hemodynamic surrogates of epileptic activity are being used to map epileptic foci with PET, SPECT, and fMRI. However, there are few studies of neurovascular coupling in epilepsy. Recent data indicate that cerebral blood flow, although focally increased at the onset of a seizure, may be temporarily inadequate to meet the metabolic demands of both interictal and ictal epileptic events. Transient focal tissue hypoxia and hyperperfusion may be excellent markers for the epileptic focus and may even precede the onset of the ictal event.


2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Jan Pyrzowski ◽  
Mariusz Siemiński ◽  
Anna Sarnowska ◽  
Joanna Jedrzejczak ◽  
Walenty M. Nyka

Brain ◽  
2011 ◽  
Vol 134 (10) ◽  
pp. 2867-2886 ◽  
Author(s):  
Frédéric Grouiller ◽  
Rachel C. Thornton ◽  
Kristina Groening ◽  
Laurent Spinelli ◽  
John S. Duncan ◽  
...  

2019 ◽  
Vol 11 (514) ◽  
pp. eaax7830 ◽  
Author(s):  
Su Liu ◽  
Josef Parvizi

Epileptic brain tissue is often considered physiologically dysfunctional, and the optimal treatment of many patients with uncontrollable seizures involves surgical removal of the epileptic tissue. However, it is unclear to what extent the epileptic tissue is capable of generating physiological responses to cognitive stimuli and how cognitive deficits ensuing surgical resections can be determined using state-of-the-art computational methods. To address these unknowns, we recruited six patients with nonlesional epilepsies and identified the epileptic focus in each patient with intracranial electrophysiological monitoring. We measured spontaneous epileptic activity in the form of high-frequency oscillations (HFOs), recorded stimulus-locked physiological responses in the form of physiological high-frequency broadband activity, and explored the interaction of the two as well as their behavioral correlates. Across all patients, we found abundant normal physiological responses to relevant cognitive stimuli in the epileptic sites. However, these physiological responses were more likely to be “seized” (delayed or missed) when spontaneous HFOs occurred about 850 to 1050 ms before, until about 150 to 250 ms after, the onset of relevant cognitive stimuli. Furthermore, spontaneous HFOs in medial temporal lobe affected the subjects’ memory performance. Our findings suggest that nonlesional epileptic sites are capable of generating normal physiological responses and highlight a compelling mechanism for cognitive deficits in these patients. The results also offer clinicians a quantitative tool to differentiate pathological and physiological high-frequency activities in epileptic sites and to indirectly assess their possible cognitive reserve function and approximate the risk of resective surgery.


2020 ◽  
Author(s):  
Rui Sun ◽  
Abbas Sohrabpour ◽  
Shuai Ye ◽  
Bin He

AbstractElectroencephalography (EEG) and magnetoencephalography (MEG) are used to measure brain activity, noninvasively, and are useful tools for brain research and clinical management of brain disorders. Tremendous effort has been made in solving the inverse source imaging problem from EEG/MEG measurements. This is a challenging ill-posed problem, since the number of measurements is much smaller than the number of possible sources in the brain. Various methods have been developed to estimate underlying brain sources from noninvasive EEG/MEG as this can offer insight about the underlying brain electrical activity with significantly improved spatial resolution. In this work, we propose a novel data-driven Source Imaging Framework using deep learning neural networks (SIFNet), where (1) a simulation pipeline is designed to model realistic brain activation and EEG/MEG signals to train generalizable neural networks, (2) and a residual convolutional neural network is trained using the simulated data, capable of estimating source distributions from EEG/MEG recordings. The performance of our proposed SIFNet approach is evaluated in a series of computer simulations, which indicates the excellent performance of SIFNet outperforming conventional weighted minimum norm algorithms that were tested in this work. The SIFNet is further tested by analyzing interictal EEG data recorded in a clinical setting from a focal epilepsy patient. The results of this clinical data analysis indicate accurate localization of epileptogenic activity as validated by the epileptogenic zone clinically determined in this patient. In sum, the proposed SIFNet approach promises to offer an alternative solution to the EEG/MEG inverse source imaging problem, shows promising signs of being robust against measurement noise, and is easy to implement, therefore, being translatable to clinical practice.


Sign in / Sign up

Export Citation Format

Share Document