Metabolic topography of autoimmune non-paraneoplastic encephalitis

Tripathi, Madhavi; Roy, Shambo Guha; Parida, Girish Kumar; Ihtisham, Kavish; Dash, Deepa; Damle, Nishikant; Shamim, Shamim Ahmed; Bal, Chandrasekhar

doi:10.1007/s00234-017-1956-2

Cited by 48 publications

(44 citation statements)

References 44 publications

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“…In contrast to HS patients, reduced node strengths as well as reduced connection weights in GAD-LE largely cover bilateral subcortical gray matter regions, which may be associated with previously reported basal ganglia hypermetabolism in these patients. 18 Altogether, our findings underline the concept that GAD-LE is a disease entity involving a variety of anatomical structures across the entire brain and beyond the mesial temporal lobe. 3,5 With regard to LGI1-LE and as previously hypothesized, in contrast, our results point toward a less widespread pathology with a clear focus on mesiotemporal structures.…”

Section: Local Network Topologysupporting

confidence: 63%

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Structural network topology in limbic encephalitis is associated with amygdala enlargement, memory performance and serostatus

et al. 2020

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Section: Local Network Topologysupporting

confidence: 63%

“…Notably, in 10 nodes this reduction is significant in comparison to HS patients. In contrast to HS patients, reduced node strengths as well as reduced connection weights in GAD‐LE largely cover bilateral subcortical gray matter regions, which may be associated with previously reported basal ganglia hypermetabolism in these patients 18 …”

Section: Discussionmentioning

confidence: 65%

Structural network topology in limbic encephalitis is associated with amygdala enlargement, memory performance and serostatus

et al. 2020

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“…The inconspicuous EEG findings in the presented case are rare in this context [ 5 ]. Importantly, there was no mesial temporal or striatal hypermetabolism on FDG-PET, which would typically be expected in active limbic encephalitis during the “inflammatory activity state” [ 9 , 12 , 18 , 19 , 20 , 21 ]. However, occasional mesial frontal involvement has also been described in anti-LGI1 encephalitis, including both hypermetabolism [ 12 ] and hypometabolism [ 10 , 11 , 19 ].…”

Section: Discussionmentioning

confidence: 99%

“…In addition, blurring of the supratentorial white matter on T2-weighted images may be seen [ 8 ]. Typical [ 18 F] fluorodeoxyglucose positron emission tomography (FDG-PET) findings include hypermetabolism of the mesial temporal lobe and striatum, which is often asymmetric, with possible dependence on the patient’s handedness, and sometimes also hypometabolism of cortical areas (in particular, frontal) [ 9 , 10 , 11 , 12 ]. Electroencephalography (EEG) shows alterations in over half of the patients: epileptic activity in 31% and focal slowing in 25% [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

Psychiatric Manifestation of Anti-LGI1 Encephalitis

et al. 2020

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Background: Anti-leucine-rich glioma-inactivated 1 (LGI1) encephalitis is typically characterized by limbic encephalitis, faciobrachial dystonic seizures and hyponatremia. The frequency with which milder forms of anti-LGI1 encephalitis mimic isolated psychiatric syndromes, such as psychoses, or may lead to dementia if untreated, is largely unknown. Case presentation: Here, the authors present a 50-year-old patient who had suffered from neurocognitive deficits and predominant delusions for over one and a half years. He reported a pronounced feeling of thirst, although he was drinking 10–20 liters of water each day, and he was absolutely convinced that he would die of thirst. Due to insomnia in the last five years, the patient took Z-drugs; later, he also abused alcohol. Two years prior to admission, he developed a status epilepticus which had been interpreted as a withdrawal seizure. In his serum, anti-LGI1 antibodies were repeatedly detected by different independent laboratories. Cerebrospinal fluid analyses revealed slightly increased white blood cell counts and evidence for blood–brain-barrier dysfunction. Magnetic resonance imaging showed hyperintensities mesio-temporally and in the right amygdala. In addition, there was a slight grey–white matter blurring. A cerebral [18F] fluorodeoxyglucose positron emission tomography (FDG-PET) examination of his brain showed moderate hypometabolism of the bilateral rostral mesial to medial frontal cortices. Treatment attempts with various psychotropic drugs remained unsuccessful in terms of symptom relief. After the diagnosis of probable chronified anti-LGI1 encephalitis was made, two glucocorticoid pulse treatments were performed, which led to a slight improvement of mood and neurocognitive deficits. Further therapy was not desired by the patient and his legally authorized parents. Conclusion: This case study describes a patient with anti-LGI1 encephalitis in the chronified stage and a predominant long-lasting psychiatric course with atypical symptoms of psychosis and typical neurocognitive deficits. The patient’s poor response to anti-inflammatory drugs was probably due to the delayed start of treatment. This delay in diagnosis and treatment may also have led to the FDG-PET findings, which were compatible with frontotemporal dementia (“state of damage”). In similar future cases, newly occurring epileptic seizures associated with psychiatric symptoms should trigger investigations for possible autoimmune encephalitis, even in patients with addiction or other pre-existing psychiatric conditions. This should in turn result in rapid organic clarification and—in positive cases—to anti-inflammatory treatment. Early treatment of anti-LGI1 encephalitis during the “inflammatory activity state” is crucial for overall prognosis and may avoid the development of dementia in some cases. Based on this case, the authors advocate the concept—long established in many chronic inflammatory diseases in rheumatology—of distinguishing between an “acute inflammatory state” and a “state of organ damage” in autoimmune psychosis resembling neurodegenerative mechanisms.

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“…Some patients do not show immune mediated antibodies. In those patients the application of nuclear medicine diagnostics—especially in patients with unremarkable magnetic resonance imaging (MRI)—, and cerebrospinal fluid (CSF) analysis allows diagnosis of autoimmune encephalitis ( 14 , 115 , 116 ). Consequently, in patients with new onset of atypical psychosis and negative antibody-testing CSF analysis is recommended ( 117 – 121 ).…”

Section: Review Of Literaturementioning

confidence: 99%

Management of Autoimmune Encephalitis: An Observational Monocentric Study of 38 Patients

et al. 2018

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Over the last years the clinical picture of autoimmune encephalitis has gained importance in neurology. The broad field of symptoms and syndromes poses a great challenge in diagnosis for clinicians. Early diagnosis and the initiation of the appropriate treatment is the most relevant step in the management of the patients. Over the last years advances in neuroimmunology have elucidated pathophysiological basis and improved treatment concepts. In this monocentric study we compare demographics, diagnostics, treatment options and outcomes with knowledge from literature. We present 38 patients suffering from autoimmune encephalitis. Antibodies were detected against NMDAR and LGI1 in seven patients, against GAD in 6 patients) one patient had coexisting antibodies against GABAA and GABAB), against CASPR2, IGLON5, YO, Glycine in 3 patients, against Ma-2 in 2 patients, against CV2 and AMPAR in 1 patient; two patients were diagnosed with hashimoto encephalitis with antibodies against TPO/TG. First, we compare baseline data of patients who were consecutively diagnosed with autoimmune encephalitis from a retrospective view. Further, we discuss when to stop immunosuppressive therapy since how long treatment should be performed after clinical stabilization or an acute relapse is still a matter of debate. Our experiences are comparable with data from literature. However, in contrary to other experts in the field we stop treatment and monitor patients very closely after tumor removal and after rehabilitation from first attack.

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Metabolic topography of autoimmune non-paraneoplastic encephalitis

Cited by 48 publications

References 44 publications

Structural network topology in limbic encephalitis is associated with amygdala enlargement, memory performance and serostatus

Structural network topology in limbic encephalitis is associated with amygdala enlargement, memory performance and serostatus

Psychiatric Manifestation of Anti-LGI1 Encephalitis

Management of Autoimmune Encephalitis: An Observational Monocentric Study of 38 Patients

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