Table 3.
Final diagnosis, findings, and management of autoimmune encephalitis mimics.
| Author | EEG | Findings | MRI | Findings | Antibody | CSF | Findings | Initial management | Final management |
|---|---|---|---|---|---|---|---|---|---|
| Diogo Costa et al. 5 | 0 | 0 | 0 | 0 | anti-CASPR2 antibodies in 1 patient | 0 | specific oligoclonal bands in 23 patients | 0 | 0 |
| Flanagan et al. 12 | 0 | 0 | 1 | MRI showed encephalitis features in 18% with either features of limbic encephalitis in 9.3% or multifocal abnormalities compatible with demyelination or inflammation in 8.4% | thyroid peroxidase antibodies in 24 patients, neural autoantibody positivity in 48 patients, antibodies to GAD65 in 14 patients, voltage-gated potassium channel complex (LGI1 and CASPR2 negative) in 10 patients, NMDA receptor (cell-based assay) in 10 patients | 1 | pleocytosis in 16 patients, neural autoantibodies in 7 patients | 0 | 0 |
| Budhram et al. 13 | 1 | left posterior temporal slowing, a repeat electroencephalogram after 3 months showed intermittent seizure activity | 1 | T2 hyperintensity of the left thalamus and medial temporal lobe; repeat brain MRI after 3 months showed left hippocampal atrophy without signal abnormality | anti-GAD antibodies | 1 | CSF immunoglobulin G and oligoclonal bands | intravenous immunoglobulin | intravenous aqueous crystalline penicillin G |
| Thomas et al. 14 | 1 | intermittent polymorph slowing in the delta band (1–2/s) together with intermittent sharp waves and sharp-slow-waves over the right anterior temporal lobe | 1 | Cerebral MRI showed volume and signal increase within right medial temporal lobe with focal extension to neocortical areas on T2/FLAIR images without contrast enhancement | anti-LGI1 IgG antibodies in serum | 1 | slight lymphocytic pleocytosis (8/μL) and dysfunction of the blood-CSF barrier (albumin ratio 8.3 × 10−3) | tryptophan-immunoadsorption followed by methylprednisolone pulse therapy as well as levetiracetam | high-dose methotrexate-based chemotherapy followed by whole brain irradiation |
| Zuhorn et al. 15 | 1 | generalized periodic pattern with triphasic waves | 1 | microangiopathic lesions: left-sided lesions in the thalamus and parietooccipital, temporo-mesial, thalamic, frontal and parietal cortices, as well as right-sided lesions in the basal ganglia | CASPR2-antibodies | 1 | pleocytosis of 7 leukocytes/μL (<5 leukocytes/μL) with a total protein of 701 mg/L (<450 mg/L) and 2.31 mmol/L lactate (1.2–2.1 mmol/L) | high-dosage intravenous methylprednisolone | nm |
| Lu et al. 16 | 1 | video-EEG showed slight abnormality | 1 | bilateral frontal parietal lesions enlarged slightly; the enhancement became more obvious than before | anti- NMDA | 1 | anti-NMDA receptor antibodies were detected in CSF and serum | corticosteroids and gamma globulin | radiotherapy and chemotherapy |
| Van Steenhoven et al. 18 | 1 | epileptic abnormalities on EEG | 1 | bilateral mesiotemporal hyperintensities | false-positive antibodies in serum (12%) | 0 | white blood cell count > 5/μL n = 43/96 oligoclonal bands n = 18/56 | nm | nm |
| AbdeleRahman et al. 19 | 1 | focal left anterior temporal lobe slow waves | 1 | abnormal FLAIR and T2 signal within the bilateral frontal and mesial temporal lobes | 0 | 1 | CSF analysis showed the following: glucose 48 mg/dL, erythrocytes 3/mL, leukocytes 220/mL (lymphocytes 69%, neutrophils 11%, monocytes 20%) | intravenous acyclovir | penicillin G for 21 days |
| Vogrig et al. 20 | 1 | confirmed focal status epilepticus | 1 | bitemporal — mostly left side — hypersignal on T2-weighted and FLAIR images; a control brain MRI —performed 1 month after the first admission — showed the unprecedented appearance of left temporal contrast enhancement | 0 | 1 | CSF analysis revealed 10 white cells/mm3 (83% lymphocytes), slightly elevated protein content (50 mg/dL) and presence of CSF-exclusive oligoclonal bands | nm | standard radio-chemotherapy |
| 0 | 0 | 1 | right temporal lesion, hyperintense on T2-weighted and FLAIR images | 0 | 1 | white cell count of 5/mm3, normal glucose level, and a protein level of 38 mg/dL | immunoglobulin | nm | |
| 0 | 0 | 1 | left-sided mesial temporal lesion with slight patchy enhancement after gadolinium administration | 0 | 1 | negative | intravenous acyclovir | nm | |
| 1 | lateralized periodic discharges | 1 | left temporo-insular abnormality on FLAIR sequences | 0 | 1 | negative | nm | nm | |
| 0 | 0 | 1 | T2 left limbic hypersignal; control MRI study revealed marked extension of the lesion over the parietal lobe | 0 | 0 | 0 | nm | nm | |
| 1 | abnormal for the presence of lateralized periodic discharges | 1 | T2-hyperintense lesion on right temporo-insular cortex with slight patchy contrast-enhancement | 0 | 0 | 0 | steroid bolus | nm | |
| Macchia et al. 21 | 0 | 0 | 1 | non-enhancing, bilateral hippocampal lesions | negative | 1 | normal | intravenous methylprednisolone | temozolomide and radiation |
| Badruddin et al. 25 | 1 | frequent diffuse polyspike and spike-wave discharges | 1 | hyperintensity on T2 imaging | 0 | 1 | CSF oligoclonal bands | nm | nm |
| Devamare et al. 26 | 1 | diffuse slow background activity; repeated EEG showed pseudoperiodic complexes | 1 | altered signal intensity in subcortical region of right parietal lobe | negative | 1 | measles antibody (1:4) | intravenous methylprednisolone | soprinosine, clonazepam, and valparin |
| Garg et al. 27 | 1 | periodic discharges | 1 | signal changes in left hippocampus, parahippocampal gyrus, and medial temporal lobe | anti-measles antibodies | 1 | anti-measles antibodies | nm | nm |
| Harsha et al. 28 | 1 | normal | 1 | subtle T2/FLAIR hyperintensities of right cerebellar white matter, right cingulate gyrus, left posterior limb of internal capsule; repeated MRI: T2/FLAIR showed subtle hyperintensity involving the left cerebellar hemisphere white matter, left middle cerebellar peduncle, left parieto-occipital white matter, and left thalamus | negative | 1 | normal | methylprednisolone and sodium valproate | stop pregabalin use |
| Poon et al. 29 | 1 | high amplitude waves in the left hemisphere and suppression in the right hemisphere, without interictal epileptiform activity | 1 | normal | low serum IgG | 1 | 67 white blood cells/µL (normal: 0 to 5 cells/µL) with 72% polymorphonuclear cells, and protein 66 mg/dL (normal: 14 to 45 mg/dL) | intravenous fluids | hydrocortisone and fludrocortisone and further intravenous immunoglobulin |
| Rigoni et al. 30 | 1 | normal | 1 | multiple T2 hyperintense confluent lesions involving mainly the diencephalic area, basal nuclei, thalami, and left temporal lobe, but also the brainstem, periventricular regions, right temporal lobe, and left fronto-insular cortex, with slight contrast enhancement; cerebral positron emission tomography revealed bilateral hippocampal hypermetabolism | negative | 1 | lymphocytic pleocytosis (7 cells/mm3) and mild blood-CSF barrier damage without oligoclonal bands | chemotherapy with rituximab-cyclophosphamide-doxorubicin-vincristine | |
| Wiels et al. 31 | 1 | Normal | 1 | normal | glycine receptor antibodies | 1 | elevated protein level | corticosteroids, plasmapheresis, and cyclophosphamide | nm |
| Nagata et al. 32 | 0 | 0 | 1 | no remarkable changes | 0 | 1 | mild pleocytosis of 11–20 cells/mm3, increased protein levels of 74–84 mg/dL | dexamethasone and glycerol | urgent neurosurgery |
| M Khair et al. 33 | 1 | continuous spike and slow wave | 1 | bilateral basal ganglia high signal followed by brain atrophy | negative | 1 | negative | steroids, intravenous immunoglobulins, and plasmapheresis; a tracheostomy and a PEG tube was inserted | immunoglobulins |
| Serrano-Cardenas et al. 34 | 1 | normal | 1 | FLAIR and T2-weighted MRI sequences demonstrated a hyperintense signal with mild-moderate expansiveness located in both the medial and anterior temporal lobes as well as a mild subcortical-predominant cerebral atrophy | 0 | 1 | intrathecal IgG synthesis and oligoclonal bands were detected in CSF | nm | penicillin |
| Blondin et al. 35 | 1 | mild generalized slowing, no epileptiform discharges, and no pathological response to photic stimulation | 1 | normal | 0 | 1 | normal | methylprednisolone | tumor resection, local radiation therapy followed by systemic chemotherapy with etoposide and carboplatin |
| Scheid et al. 36 | 1 | generalized slowing and epileptiform discharges | 1 | contrast-enhancing (T1) hyperintense signal alteration in the left medial temporal lobe on FLAIR and T2-weighted images | Treponema pallidum IgG-western blot | 1 | oligoclonal bands; VDRL titer 1:8, in CSF 1:4; Treponema pallidum IgG-western blot | nm | penicillin |
| Deramecourt et al. 37 | 1 | normal | 1 | cystic lesion in the left hippocampus with enhancement after contrast administration | negative | 0 | 0 | nm | resection of the left temporal lobe was performed |
| Piola et al. 38 | 1 | diffuse background slowing and delta activity with superimposed bursts of rhythmic beta frequency activity on frontal and temporal regions, a pattern known as extreme delta brush | 1 | mild leptomeningeal enhancement without brain lesion | 0 | 1 | negative | methylprednisolone | nm |
| Liao et al. 39 | 1 | irregular slow waves with medium to high amplitudes in the right temporal lobe, which spread to the other lobes and showed sharp waves | 1 | mild to moderate cord enhancement in the right temporal lobe | negative serum LGI1 antibody | 1 | positive RPR and TPPA tests | sodium valproate, diazepam, and levetiracetam | penicillin G sodium |
| Gajurel et al. 40 | 0 | 0 | signal intensity in the bilateral medial temporal lobe and midbrain | 0 | 0 | 0 | methylprednisolone | steroids | |
| Kimura et al. 41 | 0 | 0 | 0 | 0 | IgG anti-GQ1b antibodies | 0 | 0 | immunoglobulin and methylprednisolone | 0 |
| Consoli et al. 42 | 1 | sporadic diphasic high-amplitude sharp waves in the left anterior temporal lobe regions | 1 | diffuse cortico-subcortical T2 and FLAIR images; hyperintense lesions involving the bilateral hippocampus, fusiform gyri, right frontoparietal cortex, left thalamus, and right pulvinar nuclei | anti-recoverin antibodies | 0 | 0 | corticosteroids | radiotherapy and chemotherapy |
EEG, electroencephalography; MRI, magnetic resonance imaging; CSF, cerebrospinal fluid; nm, not mentioned; FLAIR, fluid-attenuated inversion recovery; PEG, percutaneous endoscopic gastrostomy; NMDA, N-methyl-D-aspartate; VDRL, venereal disease research laboratory; RPR, rapid plasma reagin; TPPA, Treponema pallidum particle agglutination.