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Neocortical Temporal Lobe Epilepsy
Abstract and Figures
Neocortical temporal lobe epilepsy (NTLE) comprises a hetero-geneous group of epilepsies with focal seizures characterized by auditory, somatosensory, or psychic auras followed by motionless staring, early contralateral clonic activity often secondarily generalizing. Neurophysiologic findings in NTLE are typically a predominance of lateral temporal interictal epileptiform activity (IEA) and an ictal onset pattern consisting of irregular, hemispheric delta slowing. Advanced neurophysiologic techniques such as EEG and magnetoencephalography source imaging can help to determine the area generating the initial and propagated interictal and ictal activities and may limit the number of patients requiring long-term invasive recordings before epilepsy surgery. DEFINITION Temporal lobe epilepsy is typically divided into mesial and NTLE (Walczak, 1995). A distinct electroclinical constellation associ-ated with a specific cause is rare for NTLE but has been described for patients with autosomal dominant temporal lobe epilepsy presenting with focal seizures with prominent ictal auditory phenomena, negative magnetic resonance imaging and usually a good response to antiepi-leptic medications (Michelucci et al., 2009). The majority of NTLEs, however, are characterized by their etiologic heterogeneity and electro-clinical features less typical for the more common mesial temporal lobe epilepsy (MTLE) yet not necessarily specific for NTLE.
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... Zudem wurde untersucht, ob die der TLE zugrundeliegende Ursache eine Rolle spielt. Benigne Tumore und Kavernome scheinen mit einem besseren Outcome assoziiert zu sein als eine FCD oder ein Trauma(Kennedy and Schuele, 2012). Patienten mit einer TLE unbekannter Ursache erreichen nicht ganz so gute Ergebnisse wie Patienten mit einer umschriebenen Läsion, aber auch hier wird in bis zu 50% der Fälle Anfallsfreiheit erreicht(Hader et al., ...
Einleitung: Eine neokortikale Temporallappenepilepsie (nTLE) kann aufgrund verschiedener extrahippocampaler Läsionen, wie zum Beispiel vaskuläre Malformationen oder Tumore entstehen (Kennedy and Schuele, 2012). Bei pharmakoresistenter nTLE werden derzeit maßgeschneiderte Läsionektomien unter Schonung des Hippocampus (HC) mit der Intention durchgeführt, Anfallsfreiheit und gleichzeitig ein bestmögliches kognitives Outcome zu erreichen (Helmstaedter et al., 2011). Jedoch ergab eine Studie dennoch Hinweise auf eine Verschlechterung des Langzeitgedächtnisses (Wagner et al., 2013). Ziel dieser Studie war es zu untersuchen, ob epilepsiechirurgische Eingriffe mit hippocampaler Schonung zu einem postoperativen Volumenverlust des HC führen. Außerdem galt es einen möglichen Zusammenhang zur Gedächtnisleistung zu analysieren. Zudem wurde untersucht, welche Faktoren mit einer nicht zufriedenstellenden postoperativen Anfallskontrolle zusammenhängen.
Methoden: Alle Patienten, die einen epilepsiechirurgischen Eingriff am Temporallappen unter Schonung des Hippocampus zwischen Januar 2001 und Dezember 2014 an der Klinik für Neurochirurgie des Universitätsklinikums Freiburg erhielten, wurden retrospektiv auf Eignung für die Studie analysiert (Einschlusskriterien: unilaterale und pharmakoresistente TLE mit singulärer, extrahippocampaler Pathologie; Alter der Patienten (16>x<65); Vorhandensein einer prä- und postoperativen, volumetrischen MRT-Bildgebung sowie der Daten von prä- und postoperativer neuropsychologischer Gedächtnistestung). 50 Patienten (28 linksseitige TLE; 27 männlich; Altersdurchschnitt bei OP 31(±13) Jahre; mittlere Epilepsiedauer zum Zeitpunkt der OP 9(±11) Jahre) wurden eingeschlossen. Die Untersuchung des HC-Volumens erfolgte mittels Voxel-basierter Morphometrie und HC-Volumenextraktion mit Hilfe einer HC-Maske aus der SPM-Toolbox „anatomy“. Zur Ermittlung des individuellen Resektionsvolumens wurde ein benutzergesteuertes, halbautomatisches Verfahren zur Segmentierung des postoperativen MRT-Bildes verwendet (ITK-Snap; Yushkevich et al., 2006). Die Untersuchung der Gedächtnisleistung erfolgte mittels standardisierter Testbatterie, welche den „Verbalen Lern- und Merkfähigkeitstest“ nach Helmstaedter, Lendt und Lux und das „Diagnostikum für Cerebralschädigung“ beinhaltete. Außerdem wurde überprüft, ob verschiedene Faktoren (Seite der OP, postoperativer ipsilateraler HC-Volumenverlust, Alter bei Beginn der Epilepsie, Histopathologie, Resektionsvolumen) einen Einfluss auf das Anfallsoutcome haben.
Ergebnisse: Ein Jahr postoperativ waren 68% der Patienten anfallsfrei (Engel 1a). Kleinere Resektionsvolumina und ein früherer Beginn der Epilepsie waren mit einer schlechteren Anfallskontrolle assoziiert (p<0,05). Zum Zeitpunkt der MRT-Kontrolle (Median: 3,0 Monate postoperativ) wurde ein höchst signifikanter Volumenverlust des ipsilateralen HC beobachtet (mittlerer Volumenverlust 0,91±0,58cm3; p<0,001). Auch beim HC kontralateral zur operierten Seite, wurde ein signifikanter postoperativer Volumenverlust festgestellt (p<0,05). Größere Resektionsvolumina waren signifikant mit einem größeren postoperativen HC-Volumenverlust verbunden (p<0,05). Bei Patienten, die im linken Temporallappen operiert wurden, war ein größerer HC-Volumenverlust signifikant mit einer schlechteren postoperativen Leistung des verbalen verzögerten Abrufs und des Behaltens im Vergleich zu der Leistung vor der OP assoziiert (p<0,05). Beim visuellen Lernen erzielten die Patienten unabhängig von der OP-Seite postoperativ signifikant schlechtere Ergebnisse (p<0,05).
Diskussion: Diese Studie konnte zeigen, dass extrahippocampale temporale Läsionektomien trotz chirurgischer Schonung des HC zu postoperativem ipsilateralem und kontralateralem hippocampalen Volumenverlust führten. Ein größeres Resektionsvolumen hatte einen größeren HC-Volumenverlust zur Folge. Es erscheint möglich, dass ein verminderter oder fehlender Input über die Fasertrakte zum Hippocampus zu einem Verlust von Neuronen und somit zur HC-Atrophie führt. Durch größere Schädigung von Fasertrakten oder neokortikalen Strukturen bei größeren Resektionen, findet eine vermehrte hippocampale Deafferenzierung und schließlich eine stärkere HC-Atrophie statt. Die vorliegende Studie zeigt, dass trotz der Selektivität der Operation Gedächtnisdefizite auftreten und diese deswegen nicht den erwarteten Vorteil gegenüber den anderen chirurgischen Verfahren bringt. Zudem fiel auf, dass ein kleineres Resektionsvolumen, das möglicherweise die epileptogene Zone nicht ausreichend umfasste, die Wahrscheinlichkeit der postoperativen Anfallskontrolle reduzierte. In einigen Fällen führten Nachresektionen mit Entfernung des HC zu verbesserter Anfallskontrolle. Es ist denkbar, dass die Atrophie zu einer HC-Sklerose und möglicherweise sekundären Epileptogenese innerhalb des HC führt (Bonilha u. a. 2006). Die Rolle der postoperativen hippocampalen Atrophie bedarf weitergehender Erforschung.
Background
Catatonia is a psychomotor syndrome that has a wide range of aetiologies. Determining whether catatonia is due to a medical or psychiatric cause is important for directing treatment but is clinically challenging. We aimed to ascertain the performance of the electroencephalogram (EEG) in determining whether catatonia has a medical or psychiatric cause, conventionally defined.
Methods
In this systematic review and meta-analysis of diagnostic test accuracy (PROSPERO CRD42021239027), Medline, EMBASE, PsycInfo, and AMED were searched from inception to May 11, 2022 for articles published in peer-reviewed journals that reported EEG findings in catatonia of a medical or psychiatric origin and were reported in English, French, or Italian. Eligible study types were clinical trials, cohort studies, case–control studies, cross-sectional studies, case series, and case reports. The reference standard was the final clinical diagnosis. Data extraction was conducted using individual patient-level data, where available, by two authors. We prespecified two types of studies to overcome the limitations anticipated in the data: larger studies (n ≥ 5), which were suitable for formal meta-analytic methods but generally lacked detailed information about participants, and smaller studies (n < 5), which were unsuitable for formal meta-analytic methods but had detailed individual patient level data, enabling additional sensitivity analyses. Risk of bias and applicability were assessed with the QUADAS-2 tool for larger studies, and with a published tool designed for case reports and series for smaller studies. The primary outcomes were sensitivity and specificity, which were derived using a bivariate mixed-effects regression model.
Findings
355 studies were included, spanning 707 patients. Of the 12 larger studies (5 cohort studies and 7 case series), 308 patients were included with a mean age of 48.2 (SD = 8.9) years. 85 (52.8%) were reported as male and 99 had catatonia due to a general medical condition. In the larger studies, we found that an abnormal EEG predicted a medical cause of catatonia with a sensitivity of 0.82 (95% CI 0.67–0.91) and a specificity of 0.66 (95% CI 0.45–0.82) with an I² of 74% (95% CI 42–100%). The area under the summary ROC curve offered excellent discrimination (AUC = 0.83). The positive likelihood ratio was 2.4 (95% CI 1.4–4.1) and the negative likelihood ratio was 0.28 (95% CI 0.15–0.51). Only 5 studies had low concerns in terms of risk of bias and applicability, but a sensitivity analysis limited to these studies was similar to the main analysis. Among the 343 smaller studies, 399 patients were included, resulting in a sensitivity of 0.76 (95% CI 0.71–0.81), specificity of 0.67 (0.57–0.76) and AUC = 0.71 (95% CI 0.67–0.76). In multiple sensitivity analyses, the results were robust to the exclusion of reports of studies and individuals considered at high risk of bias. Features of limbic encephalitis, epileptiform discharges, focal abnormality, or status epilepticus were highly specific to medical catatonia, but features of encephalopathy had only moderate specificity and occurred in 23% of the cases of psychiatric catatonia in smaller studies.
Interpretation
In cases of diagnostic uncertainty, the EEG should be used alongside other investigations to ascertain whether the underlying cause of catatonia is medical. The main limitation of this review is the differing thresholds for considering an EEG abnormal between studies.
Funding
Wellcome Trust, NIHR Biomedical Research Centre at University College London Hospitals NHS Foundation Trust.
Functional neurosurgery by example is a concise text designed to provide neurosurgeons in training and early career neurosurgeons a deeper dive into the nuances of functional neurosurgery through carefully selected case examples. The overall structure and format of this book follows the structure and format of the series, which includes bulleted questions, pearls, pivot points and complications. The discussions reflect the thought process behind the management choice(s) presented for each case as well as the alternative choices with their pros and cons. The cases chosen encompass the breadth of functional neurosurgery and constitute the vast majority of likely cases to be encountered during practice of functional neurosurgery.
Temporal lobe epilepsy (TLE) is the most common type of focal epilepsy. First descriptions of TLE date back in time and detailed portraits of epileptic seizures of temporal origin can be found in early medical reports as well as in the works of various artists and dramatists. Depending on the seizure onset zone, several subtypes of TLE have been identified, each one associated with peculiar ictal semiology. TLE can result from multiple etiological causes, ranging from genetic to lesional ones. While the diagnosis of TLE relies on detailed analysis of clinical as well as electroencephalographic (EEG) features, the lesions responsible for seizure generation can be highlighted by multiple brain imaging modalities or, in selected cases, by genetic investigations. TLE is the most common cause of refractory epilepsy and despite the great advances in diagnostic tools, no lesion is found in around one-third of patients. Surgical treatment is a safe and effective option, requiring presurgical investigations to accurately identify the seizure onset zone (SOZ). In selected cases, presurgical investigations need intracerebral investigations (such as stereoelectroencephalography) or dedicated metabolic imaging techniques (interictal PET and ictal SPECT) to correctly identify the brain structures to be removed.
Temporal lobe epilepsy (TLE) is the most common cause of refractory epilepsy amenable for surgical treatment and seizure control. Surgery for TLE is a safe and effective strategy. The seizure-free rate after surgical resection in patients with mesial or neocortical TLE is about 70%. Resective surgery has an advantage over stereotactic radiosurgery in terms of seizure outcomes for mesial TLE patients. Both techniques have similar results for safety, cognitive outcomes, and associated costs. Stereotactic radiosurgery should therefore be seen as an alternative to open surgery for patients with contraindications for or with reluctance to undergo open surgery. Laser interstitial thermal therapy (LITT) has also shown promising results as a curative technique in mesial TLE but needs to be more deeply evaluated. Brain-responsive stimulation represents a palliative treatment option for patients with unilateral or bilateral MTLE who are not candidates for temporal lobectomy or who have failed a prior mesial temporal lobe resection. Overall, despite the expansion of innovative techniques in recent years, resective surgery remains the reference treatment for TLE and should be proposed as the first-line surgical modality. In the future, ultrasound therapies could become a credible therapeutic option for refractory TLE patients.
Objective
Lateral temporal lobe epilepsies (LTLE) are poorly characterized heterogeneous epilepsies. As the lateral temporal lobe supports distinct functions, we hypothesized that neuropsychological profiles could differ according to the localization of the seizure focus within the lateral temporal lobe.
Methods
We retrospectively examined the neuropsychological characteristics of 74 consecutive patients with refractory LTLE assessed in the context of a presurgical investigation at the Pitié-Salpêtrière Hospital in Paris between 1998 and 2018. Precise localization of the epileptic focus was correlated with scores on tests of intelligence (Global, Verbal and Performance IQ), working memory, episodic memory (verbal and visual learning and forgetting), executive functions, and language abilities.
Results
We demonstrated an impact of the localization of the epileptic focus within the lateral temporal lobe with worse learning and/or executive performances depicted in the infero-basal and pure pole LTLE groups and greater language difficulties in the posterior LTLE group, Antiepileptic drugs had a greater effect than parameters related to the epilepsy itself as the lesion or the disease duration, and finally as in medial TLE, the age, education, and sex influenced some cognitive performances.
Conclusion
Our findings show that the lateral temporal neocortex is also part of the neural substrate for memory processing and executive functions and suggest that this involvement could be related to functions devoted to specific subregions of the temporal lobe (i.e., temporal pole, inferior and basal regions) that support language and semantic processing.
Development of epilepsy or epileptogenesis promotes recurrent seizures. As of today, there are no effective prophylactic therapies to prevent the onset of epilepsy. Contributing to this deficiency of preventive therapy is the lack of clarity in fundamental neurobiological mechanisms underlying epileptogenesis and lack of reliable biomarkers to identify patients at risk for developing epilepsy. This limits the development of prophylactic therapies in epilepsy. Here, neural network dysfunctions reflected by oscillopathies and microepileptiform activities, including neuronal hyperexcitability and hypersynchrony, drawn from both clinical and experimental epilepsy models, have been reviewed. This review suggests that epileptogenesis reflects a progressive and dynamic dysfunction of specific neuronal networks which recruit further interconnected groups of neurons, with this resultant pathological network mediating seizure occurrence, recurrence, and progression. In the future, combining spatial and temporal resolution of neuronal non-invasive recordings from patients at risk of developing epilepsy, together with analytics and computational tools, may contribute to determining whether the brain is undergoing epileptogenesis in asymptomatic patients following brain injury.
Introduction
The differentiation between focal and generalized epilepsies based on clinical and electroencephalographic features is difficult and sometimes confusing.
Objective
To review the EEG findings in patients with focal epilepsy.
Methods
An extensive literature review was done. We used the following Pubmed and Medline descriptors alone and in different combinations for database searching: focal, partial, epilepsy, electroencephalographic findings, and EEG. Additional filters included review, original articles, and language limited to Spanish and English. Using the above criteria, a total of 69 articles showed the interictal and ictal EEG findings in focal epilepsy.
Development
Focal epileptiform discharges and persistence of focal abnormalities, characterize the interictal EEG findings in focal epilepsies. To distinguish SBS from primary generalized spike waves are required to note: (a) a lead-in time of at least 2 s, (b) the morphology of the focal triggering spikes clearly differ from that of the bisynchronous epileptiform paroxysms, and (c) the morphology of triggering spikes resemble that of other focal spikes from the same region. Focal and Generalized Epilepsy can coexist. Delayed Lateralization on EEG with inconclusive onset and bizarre semiology confusing semiology should not be confused with generalized onset seizures with focal evolution.
Conclusions
A close attention to localization and morphology of epileptiform discharges, the correct interpretation of secondary bilateral synchrony, and provocative maneuvers help to correctly identify the EEG findings leading to diagnose focal epilepsies. The presence of generalized epileptiform activity does not rule out the existence of a focal epilepsy.
Die pharmakoresistente mesiale Temporallappenepilepsie (MTLE) stellt im Kontext der Epilepsiechirurgie die häufigste Indikation für die Durchführung eines operativen Engriffes dar und weist in diesem Zusammenhang eine herausragende Effektivität auf. Aufgrund ihrer etablierten Position in der Therapie der fokalen Epilepsien kam daher im Verlauf die bedeutende Frage nach dem optimalen Resektionsausmaß des Neokortex und der mesiotemporalen Strukturen auf, welches eine postoperative Anfallsfreit bei gleichzeitig minimalen neurologischen Defiziten gewährleistet. Zum aktuellen Zeitpunkt ist anhand der vorliegenden Literatur zu dieser Problematik keine klare Aussage erkennbar, die das zu favorisierende Resektionsausmaß beschreibt und festlegt. Diese Doktorarbeit untersucht daher die folgende Forschungsfrage, ob eine Korrelation zwischen dem Resektionsausmaß der Corticoamygdalohippokampektomie und dem postoperativen Anfallsoutcome besteht. In der Neurochirurgischen Klinik des Universitätsklinikums Erlangen wurden in dem Zeitraum von 2002 bis 2015 151 Patienten (75 Männer, 76 Frauen; Alters-Median 37.97 bei einer Standardabweichung (SD) von 11.88) mit der Diagnose einer pharmakoresistenten Temporallappenepilepsie in die retrospektive Datenanalyse eingeschlossen. Unter diesem Kollektiv wurde bei 16 Patienten eine selektive Amydalohippokampektomie (SAH), bei 27 eine Corticoamygdalohippokampektomie (CAH) und bei den restlichen 108 verbliebenen Patienten eine Tailored Resection zusammen mit einer Amydalohippokampektomie durchgeführt. Für jeden Patienten wurden zum einen anhand der präoperativen MR-Bildgebung die Hippokampuslänge (Millimeter = mm) und zum anderen das Längenmaß der Neokortexresektion (mm) sowie der Hippokampektomie (mm) bestimmt, welche mittels des intraoperativen MR rekrutiert wurden. Zusätzlich erfolgten Follow-Up-Untersuchungen in einem zeitlichen Intervall von 3 bis 168 Monaten, wodurch für jeden Patienten das zuletzt erhobene postoperative Anfallsoutcome nach der Engel-Klassifikation erhältlich war. Anhand dieser Daten wurde anschließend statistisch ausgewertet, ob eine Korrelation zwischen dem Resektionsausmaß und dem postoperativen Anfallsoutcome besteht. Die mediane Resektionslänge der Neokortexresektion entsprach 38.85 mm bei einer SD von 12.63 mm. Auf der anderen Seite betrug das mediane Ausmaß der Hippokampektomie 29.04 mm bei einer SD von 5.86 mm. Das mediane Follow-Up umfasste 51.14 Monate bei einer SD von 40.91 Monaten. Innerhalb der Stichprobe erzielten 66.1% (n = 100) ein postoperatives Anfallsoutcome gemäß Engel I, wovon 48% (n = 68) die Kriterien der Kategorie Engel IA erfüllten. Die empirische Datenanalyse erfolgte in zwei Schritten. Zunächst wurde der Chi-Quadrat-Test herangezogen, um zu prüfen, ob die dichotomen Variablen Hippokampektomie (< 25 mm, > 25 mm) bzw. Neokortexresektion (< 30 mm, > 30 mm) einen Zusammenhang mit den verschiedenen Ausprägungshäufigkeiten bezüglich (bzgl.) des postoperativen Anfallsoutcome (E IA vs. nicht anfallsfrei bzw. E I vs. nicht anfallsfrei) aufweisen, oder ob diese unabhängig voneinander sind. Dabei erbrachte die Gegenüberstellung der Variablen Neokortexresektion (< 30 mm, > 30 mm) mit dem Ausprägungsmuster E IA vs. nicht anfallsfrei bei einem vorab determinierten Signifikanzniveau von p < 0.05 ein signifikantes Ergebnis. So wurde unter der Kohorte Neokortexresektion < 30 mm die Kategorie E IA bei n = 23 nachgewiesen, wohingegen das Ausprägungsmuster nicht anfallsfrei bei n = 11 feststellbar war. Bei einem Chi-Quadrat-Wert nach Pearson von 9.065 und den moderaten Effektstärken Phi-Koeffizient und Cramer`s-V von 0.245 belegten diese Resultate bei einem Signifikanzniveau von p = 0.003 ein signifikantes Testergebnis. Auf diese Weise wurde statistisch nachgewiesen, dass ein geringeres Ausmaß der Neokortexresektion (< 30 mm) mit einem besseren postoperativen Anfallsoutcome, gemäß Engel IA, korreliert. Daneben wurde anhand der Konfrontation der Variablen Hippokampektomie (< 25 mm, > 25 mm) mit dem postoperativen Anfallsoutcome keine signifikanten Ergebnisse nachgewiesen, so dass das Ausmaß der Hippokampektomie keinen Einfluss auf das postoperative Anfallsoutcome nimmt. In einem zweiten Schritt wurde nach Unterteilung der Patientenkohorte gemäß der bereits vorhandenen Eigenschaften Hippokampektomie kurz beziehungsweise (bzw.) lang (< 25 mm bzw. > 25 mm) und Neokortexresektion kurz bzw. lang (< 30 mm bzw. > 30 mm) vier verschiedene Resektionsgruppen erstellt. Anschließend wurde eine Welch-ANOVA durchgeführt, um zu testen, ob sich die Resektionsgruppen hinsichtlich der erzielten Anfallsoutcomes unterscheiden. Die Resultate dieser Testung belegten signifikante Unterschiede bzgl. der erzielten postoperativen Anfallsoutcomes (Welch-Test F (3, 29.85) = 4.55, p = 0.010). Demnach wurde unter Hinzunahme des Games-Howell post-hoc Tests nachgewiesen, dass ein signifikanter Unterschied (p < 0.05) hinsichtlich der erzielten Anfallsoutcome zwischen Gruppe I und Gruppe III (3.59, 95% - Konfidenzintervall (CI) [0.36, 6.81]) sowie zwischen Gruppe I und Gruppe IV (2.14, 95% - CI [0.23, 4.05]) besteht. Dies wiederum fungiert als Beleg, dass eine restriktive Neokortexresektion (< 30 mm), welche exemplarisch in Gruppe I durchgeführt wurde, mit einer höheren Auftretenswahrscheinlichkeit von Engel IA korreliert, wohingegen das Ausmaß der Hippokampektomie auf das postoperative Anfallsoutcome keinen Einfluss nimmt. Ein exzellentes postoperatives Anfallsoutcome gemäß der Kategorie Engel IA nach einem epilepsiechirurgischen Eingriff am Temporallappen (CAH, SAH, tailored resection) wurde in der vorliegenden retrospektiven Datenanalyse bei denjenigen Patienten häufiger beobachtet, bei denen das Ausmaß der Neokortexresektion weniger als 30 mm betrug. Anhand der asymptotischen Signifikanz p = 0.003 wurde ein hoch signifikantes Testergebnis belegt, so dass infolgedessen von einer Korrelation zwischen dem Ausmaß der Neokortexresektion und dem postoperativen Anfallsoutcome nach Engel auszugehen ist. Dieses signifikante Ergebnis wurde zusätzlich durch die Resultate der Welch-ANOVA unterstrichen, die belegten, dass eine restriktivere Neokortexresektion, welche exemplarisch in der Resektionsgruppe I durchgeführt wurde, mit einer höheren Auftretenswahrscheinlichkeit von Engel IA korreliert. Demnach wurden unter Anwendung von zwei verschiedenen statistischen Analysen absolut kongruente Ergebnisse nachgewiesen, so dass die erzielten signifikanten Testergebnisse somit einen besonderen Stellenwert einnehmen. Da eine geringere Kortexresektion im Umkehrschluss zu einem geringeren Resektionsausmaß des eloquenten Kortex führt, wird das Erzielen einer postoperativen Anfallsfreiheit ermöglicht und das Auftreten von postoperativen neurologischen und neurokognitiven Defiziten minimiert, wodurch das Ziel der Epilepsiechirurgie vollends verwirklicht wird.
Introduction:
We studied the contribution of interictal FDG-PET ([18 F] fluorodeoxyglucose-positron emission tomography) in epileptic focus identification in temporal lobe epilepsy patients with positive, equivocal and negative magnetic resonance imaging (MRI).
Methods:
Ninety-eight patients who underwent surgical treatment for drug resistant temporal lobe epilepsy after neuropsychological evaluation, scalp video EEG monitoring, FDG-PET, MRI and/or long-term intracranial EEG and with >12 months clinical follow-up were included in this study. FDG-PET findings were compared to MRI, histopathology, scalp video EEG and long-term intracranial EEG monitoring.
Results:
FDG-PET lateralized the seizure focus in 95 % of MRI positive, 69 % of MRI equivocal and 84 % of MRI negative patients. There was no statistically significant difference between the surgical outcomes among the groups with Engel class I and II outcomes achieved in 86 %, 86 %, 84 % of MRI positive, equivocal and negative temporal lobe epilepsy patients, respectively. The patients with positive unilateral FDG-PET demonstrated excellent postsurgical outcomes, with 96 % Engel class I and II. Histopathology revealed focal lesions in 75 % of MRI equivocal, 84 % of MRI positive, and 23 % of MRI negative temporal lobe epilepsy cases.
Conclusion:
FDG-PET is an accurate noninvasive method in lateralizing the epileptogenic focus in temporal lobe epilepsy, especially in patients with normal or equivocal MRIs, or non-lateralized EEG monitoring. Very subtle findings in MRI are often associated with histopathological lesions and should be described in MRI reports. The patients with negative or equivocal MRI temporal lobe epilepsy are good surgical candidates with comparable postsurgical outcomes to patients with MRI positive temporal lobe epilepsy.
The long-term effects of repeated brief seizures on spatial memory and hippocampal neuronal populations were assessed in kindled rats. Rats that experienced a range of 3 afterdischarges to 134 secondary generalized tonic-clonic (Class V) seizures evoked by stimulation of the olfactory bulb were evaluated in a radial arm maze task that is a measure of spatial memory and is disrupted by hippocampal damage. After completion of the memory task and a minimum of similar to3 months after the last evoked seizure, stereological methods were used to assess neuronal populations at septal and temporal locations of the hippocampus and dentate gyrus. Repeated brief seizures induced a long-lasting deficit in spatial memory performance that was detected after a cumulative total of similar to6 partial and 30 secondary generalized seizures. The memory deficit progressively increased as a function of the number of seizures, and was not observed in age-matched, electrode-implanted, unstimulated, but otherwise similarly handled paired controls. Neuronal loss was detected in the temporal hilus of the dentate gyrus, CA1, and CA3 of the hippocampus after 69 or more secondary generalized tonic-clonic seizures, and was associated with the progressive memory dysfunction. Repeated brief seizures induced progressive, permanent functional and structural abnormalities in the hippocampus, which included spatial memory deficits accompanied by gradually evolving neuronal loss in a pattern resembling human hippocampal sclerosis. These experimental results support the view that hippocampal sclerosis and associated memory dysfunction are induced by repeated seizures, and imply that seizure control could prevent adverse long-term consequences of seizures on hippocampal dependent functions.
Function and metabolism of the brain are critically dependent on a sufficient oxygen supply. In man, cerebral blood flow (CBF) is about 50 ml/100 gm/min and the arteriovenous differences for oxygen (AVDO2) about 7 vol%, giving a cerebral oxygen consumption (CMRO2) of about 3.5 ml/100 gm/min. If CBF is moderately reduced as in the state of oligemia, the flow reduction will be balanced by a rise in AVDO2 so that a normal oxygen supply is maintained. A further reduction in CBF may still be balanced while AVDO2 approximates the arterial oxygen content, and at a normal metabolic rate, flow reductions down to about 20 ml/100 gm/min may be tolerated. This flow level is critical in the sense that below this level oxygen is insufficiently supplied, and since the AVDO2 is maximal, the CMR02 is given by the blood flow (ischemia) (Fig. l).Thus in the ischemic flow ranges a further reduction in flow enforces a proportional reduction in oxygen consumption. Experimentally this principle allows a determination of the critical low levels of local oxygen supply, given as local blood flow (CBF), leading to failure of fundamental brain tissue functions.
Purpose:
To examine evidence for effectiveness of anteromesial temporal lobe and localized neocortical resections for disabling complex partial seizures.
Methods:
Systemic review and analysis of the literature since 1990.
Results:
One intention-to-treat Class I randomized controlled trial of surgery for mesial temporal lobe epilepsy found that 58% of patients randomized to be evaluated for surgical therapy (64% of those who received surgery) were free of disabling seizures and 10 to 15% were unimproved at the end of 1 year, compared with 8% free of disabling seizures in the group randomized to continued medical therapy. There was a significant improvement in quantitative quality-of-life scores and a trend toward better social function at the end of 1 year for patients in the surgical group, no surgical mortality, and infrequent morbidity. Twenty-four Class IV series of temporal lobe resections yielded essentially identical results. There are similar Class IV results for localized neocortical resections; no Class I or II studies are available.
Conclusions:
A single Class I study and 24 Class IV studies indicate that the benefits of anteromesial temporal lobe resection for disabling complex partial seizures is greater than continued treatment with antiepileptic drugs, and the risks are at least comparable. For patients who are compromised by such seizures, referral to an epilepsy surgery center should be strongly considered. Further studies are needed to determine if neocortical seizures benefit from surgery, and whether early surgical intervention should be the treatment of choice for certain surgically remediable epileptic syndromes.
OBJECTIVE: Continuous electroencephalography (EEG) is used in patients with neurological injury to detect electrographic seizures and clinically important changes in brain function. Scalp EEG has poor spatial resolution, is often contaminated by artifact, and frequently demonstrates activity that is suspicious for but not diagnostic of ictal activity. We hypothesized that bedside placement of an intracortical multicontact electrode would allow for improved monitoring of cortical potentials in critically ill neurological patients. METHODS: Sixteen individuals with brain injury, requiring invasive neuromonitoring, underwent implantation of an eight-contact minidepth electrode. RESULTS: Intracortical EEG (ICE) was successfully performed and compared with scalp EEG in 14 of these 16 individuals. ICE provided considerable improvement in signal-to-noise ratio compared with surface EEG, demonstrating clinically important findings in 12 of 14 patients (86%) including electrographic seizures (n = 10) and acute changes related to secondary neurological injury (n = 2, 1 ischemia, 1 hemorrhage). In patients with electrographic seizures detected by ICE, scalp EEG demonstrated no concurrent ictal activity in six, nonictal-appearing rhythmic delta in two, and intermittently correlated ictal activity in two. In two patients with secondary neurological complications, ICE demonstrated prominent attenuation 2 to 6 hours before changes in other neuromonitoring modalities and more than 8 hours before the onset of clinical deterioration. INTERPRETATION: ICE can provide high-fidelity intracranial EEG in an intensive care unit setting, can detect ictal discharges not readily apparent on scalp EEG, and can identify early changes in brain activity caused by secondary neurological complications. We predict that ICE will facilitate the development of EEG-based alarm systems and lead to prevention of secondary neuronal injury. Ann Neurol 2009;66:366-377.
A pilot case-control quantitative study of the hippocampus in patients with severe status epilepticus was performed to identify specific patterns of pyramidal cell loss. Pyramidal cell densities from five patients who died following status epilepticus were compared with five normal controls and five controls matched for age, hypoxia/ischemia, previous epilepsy, and alcohol abuse. Neuronal densities were greatest in the normal control group and least in patients with status epilepticus. Significant reductions were identified in Sommer's sector (prosubiculum and CA1) as well as in CA3 when compared to normal controls.