Patients descriptions: Patient 1 presented with complaints of very brief episodes of sensory disturbance and twitches in the legs, with altered behaviour and personality changes. Physical neurological examination was unremarkable. Cognitive assessment revealed impaired memory, worse for verbal than visuospatial material. Performance fell in the impaired range on the Recognition Memory Test for Words (<5th%ile, above chance) and at the lower end of the low average range on the visual version (RMT Faces: 10th%ile). Immediate and delayed recall of a story was extremely reduced (AMIPB Story recall: <10th%ile). MRI revealed bilateral signal change in the medial temporal lobe, more prominent in the left hemisphere than the right. A whole body PET scan did not reveal any other abnormality. CSF analysis did not demonstrate a pleocytosis. VGKC-Ab titre was 3640 pMol/L at diagnosis, but subsequently fell after intravenous immunoglobulin and then prednisolone. His neuropsychological and clinical state remains stable two and half years afterwards. Patient 2 presented with complaints of lapses of memory and blank spells which were considered to be consistent with seizures. His wife observed that he had poor memory for previous events but also forgot new things quickly. Physical neurological examination was normal. Neuropsychological testing revealed variable deficits in memory: verbal scores were in the low average to average (Similarities, Digit Span) while non-verbal scores varied from borderline (Block Design) to high-average (Picture Arrangement). Performance on the Recognition Memory Test for Words was intact (50th %ile) while Recognition Memory for Faces was poor (<5th %ile). Both immediate (50-75th %ile) and delayed (50th %ile) recall of a story were intact. MRI revealed bilateral signal change in the medial temporal lobe. VGKC-Ab titre was 1032 pMol/L at diagnosis, but fell after intravenous immunoglobulin treatment. Patient 3 presented with confusion and an unwitnessed collapse (presumed to be a generalized seizure) at home. On hospital admission he was found to have anterograde and retrograde memory deficits, as well as disorientation to time and place. There were no other symptoms and his neurological examination was entirely normal. MRI revealed bilateral signal change in the medial temporal lobes. His CSF was acellular but had elevated protein at 0.7g/dL. A CT of his chest, abdomen and pelvis was normal. His VGKC-Ab titre was 1935 pMol/L at presentation and fell to unrecordable levels following intravenous immunoglobulin and high dose prednisolone tapered over several months. He underwent several assessments of memory all demonstrating deficits in anterograde and retrograde memory. His clinical condition remains stable in the seven years following treatment. On recent neuropsychometric assessment he was impaired on several measures of anterograde memory: WMS-III Logical memory immediate-recall (5th %ile), as well as delayed-recall (<5th %ile). WMS-III word list was also impaired in immediate-recall (15th %ile) and delayed-recall (<5th %ile). Recognition Memory Test words was impaired (<5th %ile), as well as for faces: (10th %ile). Digit span (from the WMS-III) was intact (37th %ile). Patient 4 presented with a prodrome complex-partial seizures with some limb jerking (up to 40 a day) followed by an acute onset of confusion, disorientation and amnesia. He was noted at presentation to have right-sided faciobrachial seizures and there was an emergence of temporal lobe epilepsy (characterized by déjà vu and a rising sensation from his abdomen). His neurological examination was entirely normal. Investigations demonstrated an aceullar CSF with a protein of 0.65 0.7g/dL and hyponatraemia (serum sodium 129mmol/L). MRI revealed swelling and high signal of the left hippocampus. A CT chest, abdomen and pelvis was normal. His VGKC-Ab titre was found to be 729 pMol/L. He was treated with intravenous immunoglobulins followed by high dose prednisolone. His seizures were treated with phenytoin, levetiracetam and clobazam which have been subsequently weaned. His clinical condition remains stable in the 3 years since treatment and his antibodies are no longer detectable. Formal neuropsychological testing in close proximity to the time of testing demonstrated no impairment of anterograde or retrograde memory but the patient complains of subjective memory impairments and a reduced vividness of episodic memories. Patient 5 was admitted with a three week history of frontal headaches and confusion. He had been diagnosed with cerebral vasculitis which prompted urgent investigation as an inpatient. His neurological examination was notable for a long-standing right-sided hemiparesis. Investigations at that time demonstrated a CSF with a lymphocyte count of 62 and a protein of 1.7 g/dL. MRI demonstrated several focal white matter lesions in keeping with his previous vasculitis but there was no evidence of new and specific hippocampal high signal. His VGKC-Ab was raised at 425 pMol/L. In view of his previous vasculitis he was treated with intravenous methylprednisolone followed by oral prednisolone whilst awaiting work-up for cyclophosphamide. He has remained clinically stable for over 6 years and his VGKC-Ab is currently undetectable. Recently he demonstrated severe impairments in anterograde memory. WMS-III Logical memory was impaired both on immediaterecall (<1th %ile), and delayed-recall (1th %ile). WMS-III word list was also impaired in immediaterecall (<1th %ile) and delayed-recall Z-score (5th %ile). However, his performance on standard working memory tests seems to be intact: WMS-III digit span Z-score (90th %ile). Patient 6 presented with jerking of his left shoulder which spread to involve the rest of the arm and the left leg. There was a suggestion of facial twitching during these episodes as well. His wife then began to notice that he was becoming forgetful and irritable. Several EEGs were performed which showed some periodic sharp waves from the temporal lobes. MRI of the brain demonstrated no medial temporal lobe abnormalities but small vessel disease. A CT chest, abdomen and pelvis was normal and CSF analysis revealed an acellular CSF with a protein of 0.92g/dL. His VGKC-Ab titre was elevated at 1735 pMol/L at diagnosis peaking at 1798 four months after diagnosis. He was commenced on high dose prednisolone but his antibody titre remained persistently raised. Sixmonths following diagnosis he was given concurrent intravenous immunoglobulin after which time the antibody titre began to fall over a period of a year alongside a resolution in his symptoms. Antibodies are currently undetectable and he has been clinically stable since this time. Recent neuropsychometric assessment showed deficits in anterograde memory: WMS-III Logical memory immediate-recall (15th %ile), delayed-recall: (<1th %ile). However no deficits in standard working memory tasks were observed: WMS-III digit span (50th %ile). Patient 7 presented with a two day history of disorientation which culminated in generalized tonicclonic seizures. Following treatment she recounted that she had experienced increasing sensations of déjà vu prior to her disorientation and collapse. Prior to the confusion there were no specific memory complaints. Her neurological examination was normal. Investigations found a normal CSF with no other biochemical abnormalities. Her MRI demonstrated bilateral medial temporal lobe high signal. A CT chest, abdomen and pelvis was normal. She was treated with intravenous immunoglobulins followed by oral prednisolone, which has been subsequently discontinued. She has remained clinically stable since this time. Formal recent neuropsychometry demonstrates problems only with the delayed-recall of the WMS-III logical memory (5th %ile). Her performance on standard working memory tasks was normal. Raw scores in experiments 1 & 2: Tests Exp 1 Exp 2 Controls (SD) Patients (SD) 1 2 3 4 5 6 7 Identification Number of items 1 item 0.99 (0.01) 0.98 (0.03) 0.95 1 0.95 1 1 0.95 1 performance 3 items 0.85 (0.1) 0.81 (0.05) 0.7 0.84 0.84 0.83 0.83 0.83 0.8 Localization 1 item 2.5 (1.2) 2.8 (0.72) 2.9 2.3 2.8 4.2 3.2 2.3 2.1 error 3 items 7.4 (2.5) 10.4 (2.3) 12.2 9.4 8.6 14.7 10.5 8.6 9 Nearest item control 3 items 4.3 (1.5) 4.4 (0.7) 3.9 3.8 3.7 5.3 5.3 4.4 4 Percent of swap errors 3 items 11 (4) 21 (3) 21 25 19 24 17 18 22 Swaps minus chance 3 items 7 (4) 13 (4) 12 18 12 13 9 12 13 Angular 1 item 12.8 (3.9) 11.3 (0.5) 11.1 10.9 11.8 error 2 items 17.5 (2.8) 21.4 (3.5) 24.6 22.9 16.6 to target 3 items 19.7 (4.2) 25.3 (2.3) 27.5 22.2 26.1 Percentage of trials 0-30 deg 31 (2.8) 38 (3.8) 43 35 35 with angular error 30-60 deg 34 (3.1) 32 (1.4) 30 33 33 to NON targets 60-90 deg 35 (3.5) 30 (2.5) 27 32 32 Angular 1 item 12.8 (3.9) 11.3 (0.5) 11.1 10.9 11.8 error 2 items 13.4 (2.7) 15.6 (1.7) 15.3 17.4 14.1 to nearest item 3 items 11.7 (2.0) 12.3 (0.7) 12.2 11.7 13.1 Supplemental Table s1. Group and individual performance in experiments 1 & 2 Averaged raw scores and standard deviation (in brackets) of controls and patients performance in experiments 1 & 2 for the different conditions. Rightmost columns describe the raw scores of the individual patients 1 to 7. Identification performance is in proportion correct. Localization and angular errors are in degrees and swap errors are in percentage of trials. Visual stimuli: Supplemental Figure s1. Visual stimuli used in experiment 1. 60 colored fractals on black background were used. Symmetrical fractals were generated using code provided in Sprott's Fractal Gallery (http://sprott.physics.wisc.edu/fractals.htm). Fractals were resized to have maximum width and height of 120 pixels (~4 degrees of visual angle in experimental set-up). Serial position effects on swap errors in experiment 2. Supplemental Figure s2. Swap errors with respect to target's serial position. We analyzed the number of swap errors in 3-item sequences (as percentages of trials) with respect to the target's serial position in the sequence. We statistically analyzed these results using a mixed ANOVA with serial-position as within subjects factor and group (patients vs controls) as between subjects factor. Consistent with previous findings (Gorgoraptis et al 2011 J Neurosci) the ANOVA revealed a significant effect of serial position (F(2,18) = 5.2, p = .04, ηp2 = 0.56). The effect of group was also significant (F(1,9) = 7.3, p = .02, ηp2 = 0.45), but not the interaction (F(2,18) = 0.8, p = .45, ηp2 = 0.08). We conclude that, in general, more swap errors were made when subjects were asked to report on items that were presented early in the sequence. This trend seems to be slightly exaggerated in patients; their additional swap errors seem to arise mainly from items displayed early in the sequence, but this difference is not strong enough to be reflected in the ANOVA. Patients, in general, exhibit higher number of swap errors than controls, consistent with the analysis in the main text.