HYPOXIC-ISCHEMIC INJURY

Overview
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Seizure Classification
Generalized onset seizure
- Motor Onset
- Non-Motor Onset
Focal Onset Seizure
- By Onset Feature
- Focal to Bilateral Tonic-Clonic
- Hemispheric lateralization
- Lobar localization
  - Frontal
  - Temporal
  - Parietal
  - Occipital
Unknown Onset Seizure
Epilepsy Classification
Generalized Epilepsy
Focal Epilepsy
Generalized and Focal Epilepsy
Unknown Epilepsy
Epilepsy Syndromes
Neonatal/Infantile
- Self-limited neonatal seizures and Self-limited familial neonatal epilepsy
- Self limited familial and non-familial infantile epilepsy
- Early myoclonic encephalopathy
- Ohtahara syndrome
- West syndrome
- Dravet syndrome
- Myoclonic epilepsy in infancy
- Epilepsy of infancy with migrating focal seizures
- Myoclonic encephalopathy in non-progressive disorders
- Febrile seizures plus, genetic epilepsy with febrile seizures plus
Childhood
- Epilepsy with myoclonic-atonic seizures
- Epilepsy with eyelid myoclonias
- Lennox-Gastaut syndrome
- Childhood absence epilepsy
- Epilepsy with myoclonic absences
- Panayiotopoulos syndrome
- Childhood occipital epilepsy (Gastaut type)
- Photosensitive occipital lobe epilepsy
- Childhood epilepsy with centrotemporal spikes
- Atypical childhood epilepsy with centrotemporal spikes
- Epileptic encephalopathy with continuous spike-and-wave during sleep
- Landau-Kleffner syndrome
- Autosomal dominant nocturnal frontal lobe epilepsy
Adolescent/Adult
- Juvenile absence epilepsy
- Juvenile myoclonic epilepsy
- Epilepsy with generalized tonic-clonic seizures alone
- Autosomal dominant epilepsy with auditory features
- Other familial temporal lobe epilepsies
Any Age
- Familial focal epilepsy with variable foci
- Reflex epilepsies
- Progressive myoclonus epilepsies
Epilepsy Etiologies
Genetic Etiology
- Chromosomal abnormalities
- Gene abnormalities
Structural Etiology
- Malformations of cortical development
- Vascular malformations
- Hippocampal sclerosis
- Hypoxic-Ischemic
- Traumatic brain injury
- Tumors
- Porencephalic Cyst
Metabolic Etiology
Immune Etiology
- Rasmussen syndrome
- Antibody mediated
Infectious Etiology
Unknown Etiology
- Febrile infection related epilepsy syndrome
Epilepsy imitators

HYPOXIC-ISCHEMIC INJURY

Imaging

Imaging for optimized detection of hypoxic-ischemic brain injury:

CT may show changes in hypoxic-ischemic brain injury, however MRI is the imaging of choice for assessing the detail of the acute hypoxic-ischemic changes, and the long-term structural sequelae in patients who have subsequent epilepsy. MRI should include thin slice volumetric T1-weighted images, axial and coronal T2-weighted and FLAIR images. In acute hypoxia-ischemia, diffusion-weighted imaging and ADC maps may be required to show areas of ischemia in the first hours after the injury.

Imaging characteristics of acute hypoxic-ischemic injury:

diffusion restriction, resulting in high signal on DWI and low signal on ADC maps, within minutes from the onset of hypoxia-ischemia
high signal on T2/FLAIR imaging in the affected area within 6-12 hours
sulcal effacement and mass effect in the affected area in the first 24-48 hours
cortical laminar necrosis appearing as a ribbon of high signal on T1 weighted images, after 2 weeks
distribution of changes depend on the contributions of hypoxia and/or ischemia (perfusion) to the injury, and on age (watershed territory distribution differs in the immature brain compared to the mature adult brain)

Imaging characteristics of chronic hypoxic-ischemic injury:

atrophy, gliosis, porencephaly/encephalomalacia and ex vacuo dilation of the ipsilateral ventricle in the location of the previous acute hypoxic-ischemic injury.