Reversible computed tomography changes associated with epileptiform activity on the ictal-interictal continuum: a case report

Abstract

Case Presentation: A 50-year-old woman with long-standing focal epilepsy and poor medication adherence presented with a psychotic episode approximately three weeks prior to hospital admission, featuring positive symptoms (auditory and visual hallucinations, agitation, and disorganized behavior). She progressed to a decreased level of consciousness and a prolonged epileptic seizure (unknown onset to bilateral tonic-clonic), requiring orotracheal intubation. The initial head computed tomography (CT) scan showed no acute changes. Follow-up scans revealed extensive and bilateral cortico-subcortical hypoattenuation, compatible with diffuse cytotoxic edema, without hemorrhage, mass effect, or midline shift. Intracranial CT angiography showed no arterial compromise, reinforcing a non-territorial pattern, predominantly in the right hemisphere. Initial hypotheses included an acute ischemic event and encephalitis; however, cerebrospinal fluid analysis was not suggestive of neuroinfection. The electroencephalogram (EEG) showed a pattern on the ictal-interictal continuum, with bilateral independent periodic discharges (BIPDs) and a 2HELPS2B score of 3 points, without formal criteria for electrographic status epilepticus. After reintroduction and optimization of antiseizure medication (phenytoin and phenobarbital, with subsequent introduction of levetiracetam), progressive clinical improvement and a reduction of the ictal-interictal continuum pattern were observed on serial EEGs. A follow-up CT scan showed partial regression of the changes, with residual right subinsular/insular hypodensity, reinforcing the diagnosis of a transient peri-ictal lesion. During outpatient follow-up, she maintained sustained neurological recovery without new episodes of encephalopathy, with sporadic seizures attributed to poor medication adherence. Discussion: Peri-ictal lesions correspond to potentially reversible structural changes resulting from sustained neuronal hyperexcitability. Prolonged epileptiform activity can trigger increased regional metabolic demand, cerebral autoregulation dysfunction, and transient blood-brain barrier breakdown, resulting in transient cytotoxic or vasogenic edema. Although classically associated with status epilepticus, such changes can also occur in high-risk ictal-interictal continuum patterns. In this case, the absence of a territorial vascular pattern, the clinical exclusion of acute neuroinfection, the temporal correlation between electroencephalographic improvement and radiological regression, and the response to antiseizure treatment support the diagnosis of a transient peri-ictal lesion. Final Comments: Extensive CT changes may reflect significant epileptiform dysfunction even without formal criteria for status epilepticus. Recognizing this entity prevents misdiagnoses (such as stroke or encephalitis) and directs early treatment. Systematic integration between neuroimaging and EEG is crucial for proper management.