Hyperperfusion in the thalamus on arterial spin labeling indicates non-convulsive status epilepticus

Non-convulsive status epilepticus describes the syndrome of unexplained impaired consciousness in critically ill patients. Non-convulsive status epilepticus is very likely to lead to delayed diagnosis and poor outcomes because of the absence of convulsive symptoms. EEG is essential for the diagnosis of non-convulsive status epilepticus to establish the association between periodic discharges and rhythmic delta activity in addition to ictal epileptiform discharges according to the Salzburg criteria. Arterial spin labeling, a type of perfusion MRI, has been applied for rapid and non-invasive evaluation of the ictal state. Ictal cerebral cortical hyperperfusion is the most common finding to demonstrate focal onset seizures. Hyperperfusion of the thalamus on single photon emission computed tomography was found in patients with impaired awareness seizures. We hypothesized that thalamocortical hyperperfusion on arterial spin labeling identifies non-convulsive status epilepticus and such thalamic hyperperfusion specifically associates with periodic/rhythmic discharges producing impaired consciousness without convulsion. We identified 27 patients (17 females; age 58-91 years) who underwent both arterial spin labeling and EEG within 24 hours of suspected non-convulsive status epilepticus. We analyzed 28 episodes of suspected non-convulsive status epilepticus and compared hyperperfusion on arterial spin labeling with periodic/rhythmic discharges. We evaluated 21 episodes as a positive diagnosis of non-convulsive status epilepticus according to the Salzburg criteria. We identified periodic discharges in 15 (12 lateralized and three bilateral independent) episodes and rhythmic delta activity in 13 (10 lateralized, one bilateral independent, two generalized) episodes. Arterial spin labeling showed thalamic hyperperfusion in 16 (11 unilateral, 5 bilateral) episodes and cerebral cortical hyperperfusion in 24 (20 unilateral, 4 bilateral) episodes. Thalamic hyperperfusion was significantly associated with non-convulsive status epilepticus (P = 0.0007; sensitivity, 76.2%; specificity, 100%), periodic discharges (P < 0.0001; 93.3%; 84.6%), and rhythmic delta activity (P = 0.0006; 92.3%; 73.3%). Cerebral cortical hyperperfusion was significantly associated with non-convulsive status epilepticus (P = 0.0017; 100%; 57.1%) and periodic discharges (P = 0.0349; 100%; 30.8%), but not with rhythmic delta activity. Thalamocortical hyperperfusion could be a new biomarker of non-convulsive status epilepticus according to the Salzburg criteria in critically ill patients. Specific thalamic hyperexcitability might modulate the periodic discharges and rhythmic delta activity associated with non-convulsive status epilepticus. Impaired consciousness without convulsions could be caused by predominant thalamic hyperperfusion together with cortical hyperperfusion but without ictal epileptiform discharges.