This medical illustration and diagnostic composite demonstrate the use of depth EEG electrodes for localizing a seizure focus in epilepsy management. The primary central image is a sagittal anatomical diagram of the human brain showing four implanted depth electrodes traversing the cortex and subcortical regions. One electrode is highlighted with a green circle, showing red contacts that indicate the focal site of seizure initiation, while non-active contacts on other electrodes are shown in yellow. An upper-right inset displays a 'Fused CT-MRI of depth EEG,' illustrating the radiological correlation of electrode placement within the skull. A lower-left inset provides a technical diagram and clinical photograph detailing the anchoring method, where electrodes are tethered to the scalp using a slotted rubber bumper, staples, and sutures. This visual resource is intended for neurosurgical and neurological education, specifically regarding Phase 2 stereoelectroencephalography (SEEG) and pre-surgical planning for focal epilepsy treatments such as resection or responsive neurostimulation.

This medical infographic and anatomical diagram illustrates the conceptual and spatial relationships between various cortical zones used in the presurgical evaluation of epilepsy. Set against a lateral view of a human brain, the diagram highlights overlapping regions: the Seizure Onset Zone (SOZ, green), the High-Frequency Oscillation (HFO) zone (purple), and the Epileptogenic Zone (EZ, red outline). These are nested within the broader Functional Deficit Zone (FDZ, yellow) and the Irritative Zone (IZ, blue). The diagram also incorporates multimodal diagnostic data: a cranial MRI at the top showing an 'Epileptogenic Lesion' (EL); a 'Seizure' EEG tracing demonstrating ictal discharge associated with the SOZ; an 'IEDs' (Interictal Epileptiform Discharges) EEG strip corresponding to the IZ; and a localized EEG showing 'HFOs' above 80 Hz. This educational figure demonstrates how epileptologists integrate structural imaging, electrophysiology, and functional mapping to delineate the minimum amount of brain tissue requiring resection for seizure freedom while preserving eloquent cortex. The inclusion of the HFO zone represents modern advances in identifying biomarkers for the EZ.

A multimodal diagnostic infographic illustrating the clinical assessment and validation of EEG-fMRI maps in epilepsy. The diagram organizes diverse clinical information used to define a 'Presumed epileptic focus,' including seizure semiology (EEG trace and video), spike field topography, structural MRI (T1-weighted), PET, and SPECT imaging. The central 'Presumed epileptic focus' is represented on a sagittal T1 MRI slice by a green-highlighted region. The infographic demonstrates the methodology for classifying an EEG-fMRI map as 'Concordant' or 'Discordant' based on the spatial overlap between significant BOLD signal changes (indicated by red-to-yellow heat maps) and the clinically defined focus. A concordant map shows BOLD activation within the green-contoured zone, whereas a discordant map displays activation clusters outside this region. This visual highlights the integration of electrophysiological and hemodynamic data for precise neuroanatomical localization of interictal epileptiform discharges (IEDs) in pediatric and adult epilepsy research.

This infographic outlines a neurophysiological analysis strategy for epilepsy research. The flowchart begins with an HD-EEG assessment of 20 patients (10 minutes awake, eyes closed), accompanied by a clinical photograph showing a patient wearing a high-density EEG electrode cap. The process follows a stepwise algorithm: (1) Preprocessing to select intervals without interictal discharges or artifacts; (2) Source localization using weighted Minimum Norm Estimation (wMNE); and (3) Connectivity Estimation focused on partial directed connectivity, specifically information inflow, outflow, and general connectivity measures. The final step is a Comparative Analysis of regions containing the Seizure Onset Zone (SOZ) between seizure-free and non-seizure-free patients using the Wilcoxon Test. This is visually represented by a sagittal diagnostic image of a human brain with a multi-colored cortical segmentation overlay, illustrating anatomical regions of interest. The diagram serves as an educational tool for understanding the diagnostic and analytical pipeline used to predict surgical outcomes based on brain network connectivity in epilepsy patients.

Table 2 Mechanism of action of the 8 newly approved antiepileptic drugs (AEDs) <table><thead><tr><th>AED</th><th>Mechanism of action</th></tr></thead><tbody><tr><td>Clobazam</td><td>Binding to benzodiazepine at the GABA_A ligand-gated chloride channel complex</td></tr><tr><td>Eslicarbazepine</td><td>Use-dependent blockage of voltage-sensitive sodium channels</td></tr><tr><td>Ezogabine</td><td>Positive allosteric modulator of KCNQ2-5; positive allosteric modulator of GABA_A receptors</td></tr><tr><td>Lacosamide</td><td>Slow inactivation of voltage-gated sodium channels; binds to CRMP-2</td></tr><tr><td>Perampanel</td><td>AMPA receptor antagonist</td></tr><tr><td>Pregabalin</td><td>Binding to the α2-δ protein subunit of voltage-gated calcium channels</td></tr><tr><td>Rufinamide</td><td>Use-dependent blockage of voltage-sensitive sodium channels</td></tr><tr><td>Vigabatrin</td><td>Inactivation of GABA transaminase</td></tr></tbody></table>

This pathophysiology diagram illustrates the four-stage mechanism of a voltage-gated sodium (Na+) ion channel embedded in a lipid bilayer, focusing on the mechanical and electrostatic changes during depolarization. (1) Resting: The channel's coiled helices are closed, maintaining an electrostatic insulating seal across the 10 nm membrane. (2) Moment of Threshold: An approaching membrane soliton (mechanical wave) exerts pressure, displacing helices and disrupting the electrical insulation. This allows Na+ ions to enter the pore and interact with hydrophilic, negatively charged interior surfaces. (3) Threshold Forces: Inward Na+ influx creates electrostatic attraction (red arrows) toward the intracellular space. Mechanical 'iris-like' opening and contraction occur, causing lateral membrane expansion (green arrows) and a net intracellular force vector (blue arrow). (4) Refractory: Positive charge equalization occurs on the intracellular side, leading to pore closure. The channel remains in a refractory state with localized Na+ accumulation until charges are cleared by diffusion, preventing immediate reactivation.

This pathophysiology diagram illustrates the mechanism of GABA receptor-mediated inhibition in neurons and the modulatory effects of anesthetic agents. The illustration depicts a synaptic cleft between a presynaptic neuron, which releases GABA from vesicles, and a postsynaptic neuron. GABA binds to two types of receptors: synaptic GABA receptors, which increase postsynaptic currents, and extrasynaptic GABA receptors, which increase tonic current. The diagram highlights how specific anesthetics—Midazolam, Propofol, Thiopental, Sevoflurane, and Isoflurane—act as positive modulators (+) on both receptor types, particularly enhancing tonic current. Conversely, Dexmedetomidine and negative allosteric modulators of α5 GABAA receptors exert inhibitory effects (-) on these extrasynaptic pathways. The net increase in GABAergic inhibition and tonic current is linked via arrows to a mouse model labeled 'Cognitive dysfunction,' suggesting a clinical correlation between excessive GABAergic tonic signaling and impaired cognitive outcomes. This diagram serves as an educational tool for neuropharmacology and anesthesiology, focusing on GABA receptor distribution and drug-induced neurotoxicity.

This diagnostic image is a multi-channel electroencephalogram (EEG) recording demonstrating an ictal event in a patient with Childhood Absence Epilepsy. The tracing displays a classic 3 Hz generalized spike-and-wave discharge pattern across multiple electrode pairs, including Fp2-C4, Fp1-C3, T4-C4, and C3-T3. The rhythmic discharge is characterized by high-amplitude, synchronous, and symmetrical complexes that emerge abruptly from the background. Before and after the paroxysmal activity, the background activity shows lower amplitude, less regular fluctuations indicative of interictal baseline states. The EEG montage includes an annotation 'assenza' (absence), marking the clinical correlation of the seizure activity. This recording is clinically significant for evaluating the efficacy of Vagus Nerve Stimulation (VNS) therapy in drug-resistant epilepsy, illustrating the morphology, frequency, and duration of generalized paroxysms used to assess treatment response and seizure reduction.

This comparative EEG figure illustrates the neurophysiological signatures of absence seizures (ASs) and gamma-hydroxybutyrate (GHB/GBL)-induced states across humans and animal models (monkey, cat, rat, mouse). Panel A displays scalp EEG from Childhood Absence Epilepsy (CAE) patients, highlighting hallmark 3–4 Hz spike-and-wave discharges (SWDs) emerging abruptly from a desynchronized background. Panels B–F demonstrate dose-dependent progression following GHB/GBL administration: 1) initial desynchronized activity; 2) intermittent slow/delta waves or SWDs (species-dependent, e.g., 2–3 Hz in humans/monkeys, 5–6 Hz in rats); 3) continuous hypersynchronous activity; and 4) a burst-suppression pattern at high doses, characterized by high-amplitude bursts of slow waves interrupting periods of electrical silence. Key educational focus includes the morphological variation of the spike component across species and the shift from intermittent paroxysms to continuous synchronization and deep anesthesia. This serves as a clinical and experimental reference for epilepsy research and pharmacological modeling of impairment of consciousness.

Summary : This figure presents a flowchart algorithm for the management of undiagnosed dyspepsia, guiding clinical decision-making based on H. pylori status and treatment response. flowchart: # Nodes : • Functional dyspepsia patient (rectangle) • H. pylori positive (branch label) • H. pylori negative (branch label) • H. pylori eradication (diamond) • PPI (diamond) • TCA (diamond) • Prokinetic (diamond) • Consider psychotherapy (diamond) • Success (ellipse) • Response (branch label) • No response / No Response (branch label) # Connectors : • From "Functional dyspepsia patient" splits into two branches: "H. pylori positive" leads to "H. pylori eradication"; "H. pylori negative" leads to "PPI". • "H. pylori eradication" has two branches: "Response" leads to "Success"; "No response" leads to "PPI". • "PPI" has two branches: "Response" leads to "Success"; "No response" leads to "TCA". • "TCA" has two branches: "Response" leads to "Success"; "No Response" leads to "Prokinetic". • "Prokinetic" has two branches: "Response" leads to "Success"; "No Response" leads to "Consider psychotherapy". • "Consider psychotherapy" does not branch further. # Layout : • The flowchart is arranged in a top-down manner, starting with the patient node at the top, splitting into two main branches based on H. pylori status, and proceeding through sequential treatment options with decision diamonds and response/no response branches. • All successful responses converge to the "Success" ellipse. # Analysis : • The algorithm prioritises H. pylori eradication for positive patients, and PPI therapy for negative patients. • If initial treatments fail, the flowchart guides escalation to TCA, then prokinetic agents, and finally psychotherapy. • The structure ensures that each treatment step is followed by an assessment of response, with successful outcomes leading to the "Success" node. • The flowchart is linear with no loops, and all pathways eventually terminate at "Success" or "Consider psychotherapy" for non-responders.

Summary : This flowchart presents the management algorithm for nodal peripheral T-cell lymphoma (PTCL), including PTCL-NOS, TFHL, and ALCL subtypes, stratified by disease stage, ALK status, and risk features. It details systemic and non-systemic anticancer therapies, radiotherapy, and autologous stem-cell transplantation (ASCT) recommendations. flowchart: # Nodes : • Nodal PTCL (start, top-level box) • PTCL-NOS, TFHL (decision node) • Stage I-II (decision node) • 3-4 cycles CHO(E)P [IV, B] (treatment node) • Consolidative ISRT [IV, B] (treatment node) • CR (complete remission, outcome node) • No further treatment (end node) • Stage III-IV (decision node) • 6 cycles CHO(E)P [II, B] (treatment node) • CR (outcome node) • ASCT [III, C] (treatment node) • Stage I-II ALCL (decision node) • ALK positive, non-bulky, IPI 0-1 / ALK negative, non-bulky, IPI 0-1 (decision node) • 3-4 cycles BV-CHP [III, B] or CHOEP [III, B] (treatment node) • Consolidative ISRT [IV, B] (treatment node) • CR (outcome node) • No further treatment (end node) • ALK negative, bulky or IPI >1 / High-risk ALK positive (decision node) • 6 cycles BV-CHP [II, A] or CHO(E)P [III, B] (treatment node) • Consolidative ISRT [IV, B] (treatment node) • CR (outcome node) • ASCTa [II, B] (treatment node) • Stage III-IV ALCL (decision node) • ALK positive (decision node) • 6 cycles BV-CHP [I, A] or CHO(E)P [III, B] (treatment node) • CR (outcome node) • No further treatment (end node) • ALK negative / High-risk ALK positive (decision node) • 6 cycles BV-CHP [I, A] or CHO(E)P [III, B] (treatment node) • CR (outcome node) • ASCT [II, B] (treatment node) # Connectors : • Top-down arrows connect each decision node to its respective treatment and outcome nodes. • Branching occurs at each disease stage and ALK status, splitting into different treatment pathways. • Some branches merge at common nodes (e.g., CR, ASCT, No further treatment). • Footnotes (a, b) clarify alternative or additional recommendations for specific high-risk groups. # Layout : • The flowchart is organized horizontally by disease subtype and stage (PTCL-NOS/TFHL, Stage I-II ALCL, Stage III-IV ALCL). • Each subtype/stage column flows vertically from initial diagnosis through treatment, remission, and post-remission management. • Colour coding: purple for algorithm title, dark green for radiotherapy, blue for systemic therapy, white for non-treatment aspects. # Analysis : • The flowchart provides a clear, stepwise approach to managing nodal PTCL, emphasizing risk-adapted therapy. • Early-stage disease often receives fewer cycles of chemotherapy and consolidative radiotherapy, with no further treatment if remission is achieved. • Advanced-stage or high-risk disease typically receives more intensive therapy, with ASCT considered for consolidation. • ALK status and IPI score are critical in determining the treatment pathway for ALCL. • The algorithm highlights the importance of individualized therapy based on disease characteristics and response.