Successful surgical treatment of an inflammatory lesion associated with new-onset refractory status epilepticus

Abstract

<jats:p>New-onset refractory status epilepticus (NORSE) has high morbidity and mortality. The authors describe the successful surgical treatment of a 56-year-old man presenting with NORSE. Magnetic resonance imaging showed a left temporal lobe lesion suspicious for a low-grade tumor, while PET imaging with the alpha[<jats:sup>11</jats:sup>C]methyl-L-tryptophan (AMT) radiotracer showed increased cortical uptake extending beyond this lesion and partly overlapping with epileptogenic cortex mapped by chronic intracranial electroencephalographic monitoring. Resection of the epileptic focus resulted in long-term seizure freedom, and the nonresected portion of the PET-documented abnormality normalized. Histopathology showed reactive gliosis and inflammatory markers in the AMT-PET–positive cortex. Molecular imaging of neuroinflammation can be instrumental in the management of NORSE by guiding placement of intracranial electrodes or assessing the extent and severity of inflammation for antiinflammatory interventions.</jats:p>

Immunity and inflammation in status epilepticus and its sequelae: possibilities for therapeutic application

“…Extensive extravasation of albumin into the brain of patients who died in SE has been reported [70], indicative of massive opening of the BBB. Analysis of temporal cortex resected from a patient with new onset focal seizures that progressed to refractory SE showed intense gliosis (both astroglia and microglia) and strong IL-1β expression but sparse lymphocytic infiltration, all consistent with a pronounced focal inflammation [71]. Finally, an extensive comparison of cytokine levels in CSF of refractory SE patients with febrile infection-related epilepsy syndrome revealed increases in IL-6, IL-8 and CXCL10 when compared with CSF from patients with other inflammatory neurological diseases [72].…”

Infiltrating monocytes promote brain inflammation and exacerbate neuronal damage after status epilepticus

“…The early consequences of SE in rodents include a robust neuroinflammatory response, selective neuronal degeneration, and transient opening of the blood-brain barrier (BBB), leading to later cognitive decline. Although the neuroinflammatory features of SE in man are less well known, extravasation of albumin into the brain was observed for patients who died in SE (2), elevated cerebrospinal fluid levels of the cytokines IL-6, IL-8, and CXCL10 are typically found in patients with refractory SE compared with patients with other inflammatory neurologic disorders (3), and intense gliosis (both astrocytes and microglia) was observed in the temporal cortex of a patient with new-onset focal seizures that progressed to refractory SE (4). These admittedly sparse clinical findings are consistent with the much more extensive animal literature in demonstrating a florid inflammatory response of the brain to SE (5).…”

Multi-modal imaging of tumor cellularity and Tryptophan metabolism in human Gliomas

“…IDSI may provide a parameter more specific for tumor cellularity and less affected by other factors such as tumoral ischemia or mass effects. On the other hand, AMT is a unique PET tracer because its tumoral accumulation is not only a reliable marker of active glioma tissue but can also detect inflammatory cell infiltration [ 31 ]; while necrotic regions of brain tumors, as well as pure, glioma-induced vasogenic edema show little to no AMT accumulation [ 5 ]. Thus, when IDSI-MRI is applied in the region of high AMT uptake, it becomes possible to evaluate cellularity due to tumor cell proliferation and immune cell infiltration in active tumor regions without including either necrosis or edema.…”