18 Recall deficits with preserved recognition memory in limbic encephalitis

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ObjectiveLimbic Encephalitis (LE) is an inflammatory neurological disorder of the medial temporal lobe that causes a memory syndrome. LE with Voltage-Gated Potassium-Channel Complex (VGKC-LE) antibodies preferentially affects the hippocampus: neuro-imaging and post-mortem studies demonstrate hippocampal inflammation with relative sparing of the Para-hippocampal gyrus and other brain areas. Behaviourally, a syndrome is produced characterised by long-term memory impairment, seizures and behavioural disturbances. This patient group allows assessment of the specific role of the hippocampus in recall and recognition memory as well as in other aspects of cognition. Our aim was to characterise this in more detail than has been done before.MethodWe report a study of seven patients with immunologically proven VGKC-LE in which we have carried out a systematic study of cognition including verbal and visual delayed recall and recognition. Each patient was matched by age, gender and IQ with two controls. We assessed pre-morbid intelligence [WTAR], general intelligence [short-form WAIS III], semantic memory [Graded Naming Test], visual perception [VOSP], executive function [Letter and Category Fluency: Trails and Colour-Word interference from [DK-EFS; Hayling-Brixton], memory [AMIPB and Warrington Recognition Memory; Doors and People], autobiographical memory [AMI] and emotion [DASS-21].ResultsWe found consistent and significant deficits in delayed verbal and visual recall but not in recognition memory in patients with VGKC-LE. The autobiographical memory interview showed a dissociation between their personal semantic schedule (unimpaired) and autobiographical incident memory, which was impaired. Patients had low immediate and delayed story recall scores as compared to control participants. There were no other significant differences in neuropsychological testing.ConclusionThis unique patient group can provide insights into the role of the hippocampus in various brain processes. Our work supports models based on a critical hippocampal role in recall but not recognition memory. Ongoing work is further characterising the memory phenotype and its correlation with structural changes in the medial temporal lobe.

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