HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS REGISTER		Author Keyword(s) Vol Page [Advanced]

This Article Full Text Full Text (PDF) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this link to a friend Similar articles in this journal Add article to my folders Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Schott, J. M Search for Related Content PubMed Articles by Schott, J. M

Limbic encephalitis: a clinician’s guide

Honorary Research Fellow, Dementia Research Centre, Institute of Neurology University College London, UK and Specialist Registrar, Department of Neurology, Royal Free Hospital, London UK

Correspondence to:
Correspondence to:
Dr JM Schott, Institute of Neurology, University College London, Queen Square, London WC1N 3BG, UK;
jschott@dementia.ion.ucl.ac.uk

The first 150 words of the full text of this article appear below.

Limbic encephalitis typically presents with subacute development of memory impairment, confusion, and alteration of consciousness, often accompanied by seizures and temporal lobe signal change on MRI. There is however no clear consensus as to the definition; even traditional distinctions between "encephalitis" and "encephalopathy", and between "delirium" and "dementia" may be blurred in such patients.

The term limbic encephalitis was initially coined to describe patients presenting with amnesia, psychiatric disturbances, and often seizures, and who had postmortem evidence both of occult neoplasia and fairly selective inflammation within the temporal lobes.¹ More recently, however, it has also been used to describe patients with a similar phenotype but in whom an infectious or non-paraneoplastic autoimmune cause has been proven or suspected. Even in "typical" paraneoplastic limbic encephalitis, selective involvement of the limbic structures (hippocampus, amygdala, hypothalamus, insular and cingulate cortex) is often not proven histologically, but has been inferred from the clinical presentation . . . [Full text of this article]

This article has been cited by other articles:

				S. R Irani, A. Soni, H. Beynon, and B. S Athwal Relapsing "encephalo" polychondritis Practical Neurology, December 1, 2006; 6(6): 372 - 375. [Full Text] [PDF]