In the absence of histological data, early recognition of the clinical symptoms and typical radiologic features of CAA-related inflammation is essential to enable timely establishment of proper treatment.

Objective To evaluate the perfusion computed tomography (PCT) patterns in patients with status epilepticus (SE). Methods We included consecutive SE patients, diagnosed by ictal encephalography (EEG) findings and clinical semiology, who prospectively underwent a dedicated PCT study of SE in the ictal phase. The perfusion maps were visually analyzed. For the quantitative assessment, regions of interest in areas where the maps suggested abnormalities were compared with the corresponding area in the unaffected contralateral cortex. Asymmetry indices between affected and unaffected hemispheres were calculated for the regional cerebral blood flow (rCBF), regional cerebral blood volume (rCBV), time to peak (TTP), and mean transit time (MTT). Nine patients underwent a follow‐up PCT after SE resolution, and the corresponding maps were compared to the ictal maps. In addition, we included a control group of 10 sex‐ and age‐matched patients with SE mimics or postictal phenomena, who also underwent acute PCT during the study period. Results The study included 19 patients: mean age 69.47 ± (standard deviation) 15.9 years, 68.4% men. On visual analysis of parametric perfusion maps during the ictal phase, regional cortical hyperperfusion was depicted in 78.9% of patients. Quantitative analysis showed significantly increased rCBF (P = 0.002) and rCBV (P = 0.004) values and decreased TTP (P < 0.001) and MTT (P = 0.001) in cortical areas of the affected vs the unaffected side. The mean asymmetry index was 12.8 for rCBF, 13.7 for rCBV, −3.0 for TTP, and −3.7 for MMT. In the nine patients with a follow‐up PCT, eight showed decreased intensity, rCBV (P = 0.035), and rCBF (P = 0.024) in the hyperperfusion areas. The sensitivity of hyperperfusion detection for the diagnosis of SE was 78.95%, specificity 90%, positive predictive value 93.75%, and negative predictive value 69.23%. Comparative quantitative analysis of asymmetry indices for rCBF, rCBV, and MTT between ictal PCT and control patients showed significant differences for all parameters (rCBF P = 0.001; rCBV P = 0.002; TTP P = 0.001; and MTT P = 0.001). Significance Visual and quantitative analysis of perfusion maps detects regional hyperperfusion in SE patients with good diagnostic capability. Perfusion was increased in PCT maps of the affected cerebral hemisphere as compared to the contralateral region during the ictal phase. PCT may provide valuable diagnostic information in patients with SE and complement the diagnostic value of EEG.

Late-onset non-lesional focal epilepsy, defined as new-onset seizures in patients older than 60 years, is diagnosed increasingly more often in relation to aging of the population. It has been attributed mainly to occult cerebral small vessel disease (SVD), although high levels of evidence to support this notion are lacking. This study aimed to evaluate the burden of leukoaraiosis, a marker of cerebral SVD, and hippocampal atrophy in patients with late-onset epilepsy (LOE). Methods: Brain magnetic resonance imaging (MRI) studies were retrospectively analyzed by two blinded radiologists. The Fazekas and Scheltens scales were used to assess the degree of leukoaraiosis and hippocampal atrophy in 33 patients with non-lesional LOE, 41 patients with clinical signs of SVD (eg, recent history of transient ischemic attack [TIA] or lacunar stroke), and 26 healthy controls, all > 60 years of age. Results: Mean age in epilepsy patients was 70.9 ( ± 6.6) years; 57.6% were men. The history of vascular risk factors was similar in all groups. Median (interquartile range) Fazekas score was 1 (0-1) in the epilepsy group, 1 (0-2) in TIA/lacunar stroke patients, and 0 (0-1) in the healthy group. Degree of leukoaraiosis was milder in epilepsy patients compared to the TIA/lacunar stroke group (p = 0.004), and similar to that of healthy controls (p = 0.593). Hippocampal atrophy was significantly greater in patients with epilepsy (p < 0.005). Conclusion:These findings suggest that the etiology of LOE is not exclusively related to cerebrovascular disease. Hippocampal atrophy may contribute to the origin of the seizures.

Seizures in TIS are most likely focal, without impairment of awareness, and refractory to medical treatment. Antiepileptic drugs can prevent the progression to bilateral convulsion. The origins of such seizures seem to be related to small lesions or epileptogenic zones in the perirolandic areas. Lesional HWS and WCIS are focal seizures that involve impairment of consciousness or focal seizures that evolve to bilateral convulsion, are not such location specific and involve larger ictogenic areas. In both epilepsies, stimulus avoidance is the most effective treatment.

To our knowledge, there are no reports of status epilepticus (SE) associated with mitochondrial diseases and treated with perampanel (PER). We present three cases of patients with refractory SE associated with MELAS syndrome who responded favorably to PER. All cases were diagnosed as non-convulsive SE (focal without impairment of level of consciousness). After an initial treatment with other anti-seizure drugs, PER was added in all cases (8, 16 and 12 mg) and cessation of SE was observed within the next 4-8 hours. All the cases involved a stroke-like lesion present on brain MRI. In our patients, PER was an effective option in SE associated with MELAS syndrome.