The diagnosis and treatment of limbic encephalitis

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Fältnamn	Indikatorer	Metadata
000		04254naa a2200577 4500
001		oai:gup.ub.gu.se/166817
003		SwePub
008		240528s2012 \| \|\|\|\|\|\|\|\|\|\|\|000 \|\|eng\|
009		oai:DiVA.org:uu-187221
024	7	a https://gup.ub.gu.se/publication/1668172 URI
024	7	a https://doi.org/10.1111/j.1600-0404.2012.01691.x2 DOI
024	7	a https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-1872212 URI
040		a (SwePub)gud (SwePub)uu
041		a eng
042		9 SwePub
072	7	a ref2 swepub-contenttype
072	7	a for2 swepub-publicationtype
100	1	a Asztely, Fredrik,d 1961u Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering,Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation4 aut0 (Swepub:gu)xaszfr
245	1 0	a The diagnosis and treatment of limbic encephalitis
264		c 2012-06-19
264	1	b Hindawi Limited,c 2012
520		a The term limbic encephalitis (LE) was first introduced in 1968. While this disease was initially considered rare and is often fatal with very few treatment options, several reports published in the last decade provide a better description of this condition as well as possible causes and some cases of successful treatment. The clinical manifestation of LE is primarily defined by the subacute onset of short-term memory loss, seizures, confusion and psychiatric symptoms suggesting the involvement of the limbic system. In addition, EEG often shows focal or generalized slow wave or epileptiform activity, and MRI findings reveal hyperintense signals of the medial temporal lobes in T2-weighted or FLAIR images. The current literature suggests that LE is not a single disorder but is comprised of a group of autoimmune disorders predominantly affecting the limbic system. Before the diagnosis of LE can be determined, other causes of subacute encephalopathy must be excluded, especially those resulting from infectious aetiologies. LE has previously been regarded as a paraneoplastic phenomenon associated with the classical onconeuronal antibodies that are primarily directed against intracellular antigens. However, recent literature suggests that LE is also associated with antibodies that are directed against cell surface antigens, and these cases of LE display a much weaker association to the neoplasm. The treatment options for LE largely depend on the aetiology of the disease and involve the removal of the primary neoplasm. Therefore, a search for the underlying tumour is mandatory. In addition, immunotherapy has been successful in a significant number of patients where LE is not associated with cancer.
650	7	a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Neurovetenskaper0 (SwePub)301052 hsv//swe
650	7	a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Neurosciences0 (SwePub)301052 hsv//eng
653		a autoimmune limbic encephalitis
653		a limbic encephalitis
653		a limbic system
653		a paraneoplastic limbic
653		a paraneoplastic neurological syndromes
653		a nmda-receptor encephalitis
653		a positron-emission-tomography
653		a potassium channel antibodies
653		a temporal-lobe epilepsy
653		a cell lung-cancer
653		a efns task-force
653		a status
653		a epilepticus
653		a nervous-system
653		a sensory neuronopathy
653		a lstein mf
653		a 1975
653		a journal of psychiatric research
653		a v12
653		a p189
653		a autoimmune limbic encephalitis
700	1	a Kumlien, Evau Uppsala universitet,Neurologi4 aut0 (Swepub:uu)evakumli
710	2	a Göteborgs universitetb Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering4 org
773	0	t Acta Neurologica Scandinavicad : Hindawi Limitedg 126:6, s. 365-375q 126:6<365-375x 0001-6314x 1600-0404
856	4 8	u https://gup.ub.gu.se/publication/166817
856	4 8	u https://doi.org/10.1111/j.1600-0404.2012.01691.x
856	4 8	u https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-187221

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