Seizure disorder classify and explain
seizure classification types diagram epilepsy

This diagnostic diagram illustrates an unsupervised independent component (IC) sorting mechanism for resting-state functional MRI (rs-fMRI), specifically designed for identifying Seizure Onset Zones (SOZ). The image is organized into a five-row flow-process chart demonstrating the automated classification of voxel clusters. The first three rows depict the 'waterfall' technique for noise purging: periphery noise (82.1% brain boundary overlap), white matter noise (75% white matter overlap), and blood vessel noise (65% vascular overlap). These are identified through sequential steps of cluster detection followed by specific contour detection (outer brain, white matter, or artery). The fourth row demonstrates the identification of Resting State Networks (RSN), characterized by the largest cluster showing nearly 100% overlap with gray matter. The final row identifies the Seizure Onset Zone (SOZ) based on multiple large-size clusters overlapping nearly 100% with gray matter, predominantly localized to one hemisphere. This algorithm aims to reduce manual IC sorting time for neurosurgeons evaluating children with drug-resistant epilepsy.

This medical illustration outlines intracranial drug delivery routes for pharmacological seizure control in treatment-resistant epilepsy. The diagram consists of a sagittal profile of a human head and an inset expanded view of subcortical structures. Four primary delivery pathways are identified: (1) Intraparenchymal targeting the cortical seizure focus directly; (2) Transmeningeal, where drugs diffuse through the meninges to reach neocortical areas; (3) Intracerebroventricular (icv), targeting regions adjacent to the lateral ventricle; and (4) Intraparenchymal targeting remote epileptic network structures. The expanded subcortical view highlights key anatomical targets for deep-brain delivery, including the thalamus, caudate, and putamen, as well as specific components of the basal ganglia: the subthalamic nucleus (STN), substantia nigra pars compacta (SNc), and substantia nigra pars reticulata (SNr). The illustration emphasizes the shift from systemic administration to network-specific targeting to modulate seizure propagation and initiation while minimizing functional loss in eloquent brain areas.

This pathophysiology diagram illustrates the interconnected pathways of epileptogenesis and cognitive deficits following seizure activity in the brain. The visual flow begins with a sagittal brain illustration highlighting a focal point of seizures, which triggers three primary cellular events: mitochondrial ROS increase, glial cell activation (microglia and astrocytes), and neuronal dysfunction. These events lead into three distinct pathophysiological cascades. The first cascade involves mitochondrial oxidative stress, mtDNA damage, membrane potential (ΔΨm) decline, and Ca2+ accumulation, resulting in mitochondrial dysfunction and neuronal apoptosis. The second cascade details neuroinflammation driven by pro-inflammatory mediators (IL-1β, IL-6, TNF-α), leading to neurodegeneration and neural death. The third cascade focuses on disbalanced neurotransmission, characterized by increased glutamate (Glu) and decreased GABA and acetylcholine (ACh), leading to excitotoxicity. These three pathways are shown to be bidirectional and mutually reinforcing, ultimately converging to drive the clinical outcomes of epileptogenesis and cognitive impairment. The diagram is intended for medical education on the molecular and cellular mechanisms of chronic epilepsy.

This medical illustration presents an anatomical diagram of the human brain, specifically focusing on the spatial localization and overlap of different zones involved in epilepsy. The diagram uses a lateral view of the cerebral cortex with four distinct color-coded regions to demonstrate the conceptual schema of epileptic phenomena. The Seizure Onset Zone (SOZ) is depicted as a central yellow solid circle, representing the area where clinical seizures originate. Encapsulating the SOZ is the Epileptogenic Zone (EZ), marked by a blue dashed circular line, defined as the minimum area of brain tissue necessary for resection to achieve seizure freedom. A larger purple circle represents the Cortical Irritative Zone, indicating the region generating interictal spikes, which typically encompasses both the EZ and SOZ. Finally, the Symptomatogenic Zone is shown as a green solid circle on the periphery; it partially overlaps with the other zones, representing the cortical area that, when activated, produces the initial clinical symptoms. This graphic illustrates the clinical challenge of surgical localization, where these theoretical zones may not perfectly align.
"seizure" AND "classification" AND "epilepsy"
| Onset | Definition |
|---|---|
| Focal | Originating within networks limited to one hemisphere |
| Generalized | Originating within and rapidly engaging bilaterally distributed networks |
| Unknown | Onset cannot be determined |
Important terminology change: The 2017 classification replaced "partial" with "focal," eliminated "simple partial" and "complex partial" as terms, and renamed secondarily generalized seizures as "focal-to-bilateral tonic-clonic."
| Phase | Duration | Features |
|---|---|---|
| Tonic | 10-20 s | Sudden loss of consciousness; rigid extension of back, neck, arms, legs; cry from forced air through closed cords; cyanosis; pupil dilation |
| Clonic | ~30 s | Rhythmic, violent flexor spasms (8/s → 4/s); autonomic surge (tachycardia, HTN, hypersalivation) |
| Postictal | Minutes to hours | Deep coma → confusion → fatigue; Todd's paralysis possible; no memory of event |

| Age | Common Syndromes |
|---|---|
| Neonatal | Ohtahara syndrome, early myoclonic encephalopathy, benign neonatal seizures |
| Infancy | West syndrome (infantile spasms), Dravet syndrome, febrile seizures |
| Childhood | Absence epilepsy, benign epilepsy with centrotemporal spikes (BECTS/BECTS/Rolandic), Lennox-Gastaut syndrome, Panayiotopoulos syndrome |
| Adolescence/Adulthood | Juvenile myoclonic epilepsy (JME), juvenile absence epilepsy, temporal lobe epilepsy |
| Elderly | Focal seizures (from strokes, tumors, trauma) dominate |
| Old Term (pre-2017) | New ILAE 2017 Term |
|---|---|
| Simple partial seizure | Focal aware seizure (FAS) |
| Complex partial seizure | Focal impaired awareness seizure (FIAS) |
| Secondarily generalized | Focal-to-bilateral tonic-clonic (FBTC) |
| Grand mal | Generalized tonic-clonic |
| Petit mal | Absence seizure |
| Drop attack | Atonic seizure |
| Infantile spasms | Epileptic spasms / West syndrome |
| Category | Examples |
|---|---|
| Structural | Post-stroke, hippocampal sclerosis, cortical dysplasia, tumor, trauma |
| Genetic | SCN1A (Dravet), KCNQ2, SCN2A mutations; JME |
| Infectious | Neurocysticercosis, herpes encephalitis, meningitis |
| Metabolic | Hypoglycemia, hyponatremia, hypocalcemia, pyridoxine deficiency |
| Immune | Anti-NMDAR encephalitis, LGI1, CASPR2 antibodies |
| Unknown | No identifiable cause despite workup |