Abnormal brain metabolism on FDG-PET/CT is a common early finding in autoimmune encephalitis

Abstract

Objective:To compare the rate of abnormal brain metabolism by FDG-PET/CT to other paraclinical findings and to describe brain metabolism patterns in autoimmune encephalitis (AE).Methods:A retrospective review of clinical data and initial dedicated brain FDG-PET/CT studies for neurology inpatients with AE, per consensus criteria, treated at a single tertiary center over 123 months. Z-score maps of FDG-PET/CT were made using 3-dimensional stereotactic surface projections with comparison to age group–matched controls. Brain region mean Z-scores with magnitudes ≥2.00 were interpreted as significant. Comparisons were made to rates of abnormal initial brain MRI, abnormal initial EEG, and presence of intrathecal inflammation.Results:Sixty-one patients with AE (32 seropositive) underwent brain FDG-PET/CT at median 4 weeks of symptoms (interquartile range [IQR] 9 weeks) and median 4 days from MRI (IQR 8.5 days). FDG-PET/CT was abnormal in 52 (85%) patients, with 42 (69%) demonstrating only hypometabolism. Isolated hypermetabolism was demonstrated in 2 (3%) patients. Both hypermetabolic and hypometabolic brain regions were noted in 8 (13%) patients. Nine (15%) patients had normal FDG-PET/CT studies. CSF inflammation was evident in 34/55 (62%) patients, whereas initial EEG (17/56, 30%) and MRI (23/57, 40%) were abnormal in fewer. Detection of 2 or more of these paraclinical findings was in weak agreement with abnormal brain FDG-PET/CT (κ = 0.16, p = 0.02).Conclusions:FDG-PET/CT was more often abnormal than initial EEG, MRI, and CSF studies in neurology inpatients with AE, with brain region hypometabolism the most frequently observed.

Could arterial spin labelling perfusion imaging uncover the invisible in N‐methyl‐d‐aspartate receptor encephalitis?

“…18 F-FDG-PET has been suggested as a sensitive diagnostic tool [1], with either hypermetabolic or hypometabolic patterns [2]. In this case, bilateral parieto-occipital hypometabolism is concordant with previous reports [3]. A similar hypometabolic pattern can be produced by NMDAR antagonists, such as ketamine [4].…”

Different FDG‐PET metabolic patterns of anti‐AMPAR and anti‐NMDAR encephalitis: Case report and literature review

“…FDG‐PET detected anomalies in autoimmune encephalitis more frequently than did of electroencephalography, MRI, and CSF. Regional brain hypometabolism (69%) was more frequently detected than isolated hypermetabolism (3%) or mixed hyper‐ and hypometabolism (13%) (Probasco et al, ). The functioning of the brain depends heavily on glucose use (Mergenthaler, Lindauer, Dienel, & Meisel, ); neuronal activities drive local glucose metabolism through direct glucose uptake by neurons (Lundgaard et al, ), astrocyte–neuron interaction, oxidative energy transmission, and increase of regional cerebral blood flow (Magistretti & Allaman, ).…”

“…To date, several understandings of characteristic metabolic patterns of autoimmune encephalitis have been published. Early hypermetabolic lesion in the mesial temporal areas could be a marker of active inflammatory process of limbic encephalitis (Probasco et al, ), because FDG usually accumulates at infection or inflammation foci (Bleeker‐Rovers, de Kleijn, Corstens, van der Meer, & Oyen, ). Occipital hypometabolism is characteristic in patients with anti‐NMDAR encephalitis (Probasco et al, ).…”

Subgroup comparison according to clinical phenotype and serostatus in autoimmune encephalitis: a multicenter retrospective study

“…Clinical phenotypes suggestive of LE, combining behavioral abnormalities with seizures and cognitive impairment, were the most frequent, but insufficient for inclusion in the Ab-negative-LE group as the patients lacked the bilateral mesial temporal lobe involvement on brain MRI required by the AE-DC [8]. This criterion might be integrated by the acquisition of bilaterality evidence using brain FDG-PET [20]. In our cohort too, two patients with monolateral temporal lobe involvement on the brain MRI were classified as Abpositive-LE using brain FDG-PET.…”

“…Testing 37/48 Ab-negative cases, in-house assays identified Abs in 11 patients (29.7%). A hundred and eighteen patients fulfilled the AE-DC, 81 (68.6%) with Ab-positive-AE (Ab-positive-LE, 40; NMDAR-E, 32; definite-AE, nine) and 37 (31.4%) with Ab-negative-AE (Ab-negative-LE, 17; probable/possible-AE, 20). Clinical phenotypes were similar in Ab-positive-LE versus Ab-negative-LE.…”