Post-ictal changes are a consequence (and not a cause) of epilepsy.
Pathophysiologically, electrical hyperactivity is linked to abnormal cell membrane permeability and altered autoregulation, inducing fluctuation in intra- and extracellular water content and ultimately leading to edema, which may be vasogenic or (ex)cytotoxic.
In the acute setting, non-enhancing brain CT is the modality of choice to exclude emergencies. Post-ictal changes may present as hypodense swelling of brain parenchyma due to edema, with usually modest mass effect. (Fig 1)
Contrast-enhanced MRI is subsequently performed when CT is negative and to further characterize lesions. The MRI protocol for epilepsy has T2W (T2-weighted), pre- and post-contrast T1W, DWI and SWI images, as well as perfusion studies with or without contrast administration (DSC, ASL).
MRI changes include:
- T2W hyper-intensities
- in the white matter (vasogenic edema) and/or gray matter (excytotoxic edema) with involvement of both cortex and basal ganglia and cerebellar nuclei. (Fig 2)
- Variable diffusion restriction on DWI/ADC
- diffusion abnormalities frequently reverse in time, supporting the hypothesis that they are not sustained by ischemic cytotoxic edema; temporal evolution of ADC abnormalities is unpredictable, probably due to wide variability in seizure characteristics (type, duration, cause) and variable scan time intervals after the event. (Fig 3)
- Subcortical T2W hypo-intensities
- an unusual finding, mainly seen after partial complex seizures, and have been linked to free radicals formation due to excitotoxic damage, and to transient non-heme iron accumulation due to interruption of axonal transport. (Fig 4)
- Contrast enhancement
- (rarely) can be seen, both intra-axial and leptomeningeal, likely due to hyper-perfusion following increased metabolism or to altered blood-brain barrier. (Fig 5)
- Pseudo-narrowing of cortical veins on SWI [2]
- due to hyper-perfusion and subsequent reduction in deoxy-hemoglobin; on perfusional imaging, the presence of pseudo-narrowing of cortical veins seem to correlate with reduced MTT (mean transfer time) and increased CBF (cerebral blood flow). (Fig 5)
Perfusion studies (CT perfusion, ASL or gadolinium-enhanced perfusion MRI - DSC) commonly show increased perfusion during abnormal electrical activity, while hypoperfusion predominates in the post- or inter-ictal phases (depending on the frequency and the duration of seizures) [3]. (Fig 6)
Their location may vary, from the eptileptogenic focus to distant sites due to propagation of electrical hyperactivity in brain network. Most frequent cortical sites are temporo-mesial cortex and neocortex, while thalamus, pulvinar and corpus callosum are the most frequent subcortical locations [4]. They can show heterogeneous appearance, simulating various malformative, neoplastic and infectious conditions. They usually manifest after generalized seizures, but timing of onset and resolution may significantly vary; lesions may disappear days to weeks after the epileptic event. Follow-up studies show that half of these changes are reversible, while the other usually evolve into atrophy.
Case 1
68 y-o female patient presented with coma after a generalized seizure. EEG showed epileptiform abnormalities in the left cerebral hemisphere. Non-contrast CT (Fig 1) showed cortical-subcortical hypodensity in the left cerebral hemisphere and in the right cerebellar hemisphere (cerebellar diaschisis). AngioCT, performed in the suspect of ischemic stroke, did not show any vascular abnormality. Subsequent MRI (Fig 7) showed extensive cortical T2/FLAIR hyperintensity in the left cerebral hemisphere and right cerebellar hemisphere, with involvement of left basal ganglia and restricted diffusion on DWI images. Leptomeningeal enhancement is also noted (Fig 5 A, B). On SWI, pseudo-narrowing of left cortical veins can be appreciated (Fig 5 C). Follow-up CT after 2 months (Fig 8) showed resolution of hypodensities with resulting mild enlargement of cerebral sulci and left lateral ventricle (atrophic changes).
Case 2
17 y-o female patient with generalized tonic-clonic seizures after undergoing appendicectomy. Non-contrast CT (Fig 9 A) showed no significant abnormalities. MRI (Fig 9 B-E) showed swollen hippocampal formations with hyperintensities on FLAIR in hippocampi, claustra and posterior aspects of putamina; DWI showed restricted diffusion. In the following days her clinical conditions worsened with multiple untreatable seizures. Follow-up MRI after 7 days (Fig 10) showed development of multiple symmetrical cortical lesions in gyri recti and fronto-parietal cortex, hyperintense on T2W images, without restricted diffusion or enhancement after contrast administration. MRI 1 month later (Fig 11) showed shrinkage of hippocampi and complete resolution of fronto-parietal abnormalities, supporting the hypothesis of post-ictal changes.