Available via license: CC BY-NC 4.0
Content may be subject to copyright.
World Journal of
Clinical Cases
ISSN 2307-8960 (online)
World J Clin Cases 2023 January 16; 11(2): 255-486
Published by Baishideng Publishing Group Inc
WJCC https://www.wjgnet.com IJanuary 16, 2023 Volume 11 Issue 2
World Journal of
Clinical Cases
W J C C
Contents Thrice Monthly Volume 11 Number 2 January 16, 2023
REVIEW
Application of the cortical bone trajectory technique in posterior lumbar fixation
255
Peng SB, Yuan XC, Lu WZ, Yu KX
Allogeneic stem cell transplantation in the treatment of acute myeloid leukemia: An overview of obstacles
and opportunities
268
Chen YF, Li J, Xu LL, Găman MA, Zou ZY
Idiopathic hirsutism: Is it really idiopathic or is it misnomer?
292
Unluhizarci K, Hacioglu A, Taheri S, Karaca Z, Kelestimur F
MINIREVIEWS
Liver function in transgender persons: Challenges in the COVID-19 era
299
Milionis C, Ilias I, Koukkou E
Telenutrition for the management of inflammatory bowel disease: Benefits, limits, and future perspectives
308
Güney Coşkun M, Kolay E, Basaranoglu M
Liver transplantation amidst the COVID-19 era: Our center’s experience
316
Khazaaleh S, Suarez ZK, Alomari M, Rashid MU, Handa A, Gonzalez AJ, Zervos XB, Kapila N
Prospects for the use of olfactory mucosa cells in bioprinting for the treatment of spinal cord injuries
322
Stepanova OV, Fursa GA, Andretsova SS, Shishkina VS, Voronova AD, Chadin AV, Karsuntseva EK, Reshetov IV,
Chekhonin VP
Use of metaphors when treating unexplained medical symptoms
332
Seeman MV
ORIGINAL ARTICLE
Case Control Study
Microvesicles with mitochondrial content are increased in patients with sepsis and associated with
inflammatory responses
342
Zhang HJ, Li JY, Wang C, Zhong GQ
Retrospective Study
Is fascial closure required for a 12-mm trocar? A comparative study on trocar site hernia with long-term
follow up
357
Krittiyanitsakun S, Nampoolsuksan C, Tawantanakorn T, Suwatthanarak T, Srisuworanan N, Taweerutchana V,
Parakonthun T, Phalanusitthepha C, Swangsri J, Akaraviputh T, Methasate A, Chinswangwatanakul V, Trakarnsanga A
WJCC https://www.wjgnet.com II January 16, 2023 Volume 11 Issue 2
World Journal of Clinical Cases
Contents Thrice Monthly Volume 11 Number 2 January 16, 2023
Ten-year multicentric retrospective analysis regarding postoperative complications and impact of
comorbidities in hemorrhoidal surgery with literature review
366
Moldovan C, Rusu E, Cochior D, Toba ME, Mocanu H, Adam R, Rimbu M, Ghenea A, Savulescu F, Godoroja D, Botea F
Observational Study
Tear inflammation related indexes after cataract surgery in elderly patients with type 2 diabetes mellitus
385
Lv J, Cao CJ, Li W, Li SL, Zheng J, Yang XL
CASE REPORT
Management of a rare giant cell tumor of the distal fibula: A case report
394
Fan QH, Long S, Wu XK, Fang Q
Repair of a giant inguinoscrotal hernia with herniation of the ileum and sigmoid colon: A case report
401
Liu SH, Yen CH, Tseng HP, Hu JM, Chang CH, Pu TW
Anti-leucine-rich glioma inactivated protein 1 encephalitis with sleep disturbance as the first symptom: A
case report and review of literature
408
Kong DL
Fat-poor renal angiomyolipoma with prominent cystic degeneration: A case report and review of the
literature
417
Lu SQ, Lv W, Liu YJ, Deng H
Perivascular epithelioid cell tumors of the liver misdiagnosed as hepatocellular carcinoma: Three case
reports
426
Kou YQ, Yang YP, Ye WX, Yuan WN, Du SS, Nie B
H7N9 avian influenza with first manifestation of occipital neuralgia: A case report
434
Zhang J
Gefitinib improves severe bronchorrhea and prolongs the survival of a patient with lung invasive
mucinous adenocarcinoma: A case report
441
Ou GC, Luo W, Zhang WS, Wang SH, Zhao J, Zhao HM, Qiu R
Habitual khat chewing and oral melanoacanthoma: A case report
449
Albagieh H, Aloyouny A, Alshagroud R, Alwakeel A, Alkait S, Almufarji F, Almutairi G, Alkhalaf R
Systemic lupus erythematosus with multicentric reticulohistiocytosis: A case report
456
Liu PP, Shuai ZW, Lian L, Wang K
X-linked Charcot-Marie-Tooth disease after SARS-CoV-2 vaccination mimicked stroke-like episodes: A
case report
464
Zhang Q, Wang Y, Bai RT, Lian BR, Zhang Y, Cao LM
Acute liver injury in a COVID-19 infected woman with mild symptoms: A case report
472
Lai PH, Ding DC
WJCC https://www.wjgnet.com III January 16, 2023 Volume 11 Issue 2
World Journal of Clinical Cases
Contents Thrice Monthly Volume 11 Number 2 January 16, 2023
LETTER TO THE EDITOR
Incidence and clinical treatment of hypertriglyceridemic acute pancreatitis: A few issues
479
Yang QY, Zhao Q, Hu JW
Management of infected acute necrotizing pancreatitis
482
Pavlidis ET, Pavlidis TE
WJCC https://www.wjgnet.com IX January 16, 2023 Volume 11 Issue 2
World Journal of Clinical Cases
Contents Thrice Monthly Volume 11 Number 2 January 16, 2023
ABOUT COVER
Editorial Board Member of World Journal of Clinical Cases, Manish Ramesh Balwani, DNB, FASN, MBBS, MD,
Professor, Department of Nephrology, Saraswati Kidney Care Center, Nagpur 442301, Maharashtra, India.
balwani.manish@yahoo.com
AIMS AND SCOPE
The primary aim of World Journal of Clinical Cases (WJCC, World J Clin Cases) is to provide scholars and readers from
various fields of clinical medicine with a platform to publish high-quality clinical research articles and
communicate their research findings online.
WJCC mainly publishes articles reporting research results and findings obtained in the field of clinical medicine
and covering a wide range of topics, including case control studies, retrospective cohort studies, retrospective
studies, clinical trials studies, observational studies, prospective studies, randomized controlled trials, randomized
clinical trials, systematic reviews, meta-analysis, and case reports.
INDEXING/ABSTRACTING
The WJCC is now abstracted and indexed in Science Citation Index Expanded (SCIE, also known as SciSearch®),
Journal Citation Reports/Science Edition, Current Contents®/Clinical Medicine, PubMed, PubMed Central,
Scopus, Reference Citation Analysis, China National Knowledge Infrastructure, China Science and Technology
Journal Database, and Superstar Journals Database. The 2022 Edition of Journal Citation Reports® cites the 2021
impact factor (IF) for WJCC as 1.534; IF without journal self cites: 1.491; 5-year IF: 1.599; Journal Citation Indicator:
0.28; Ranking: 135 among 172 journals in medicine, general and internal; and Quartile category: Q4. The WJCC's
CiteScore for 2021 is 1.2 and Scopus CiteScore rank 2021: General Medicine is 443/826.
RESPONSIBLE EDITORS FOR THIS ISSUE
Production Editor: Hua-Ge Yu; Production Department Director: Xu Guo; Editorial Office Director: Jin-Lei Wang.
NAME OF JOURNAL INSTRUCTIONS TO AUTHORS
World Journal of Clinical Cases https://www.wjgnet.com/bpg/gerinfo/204
ISSN GUIDELINES FOR ETHICS DOCUMENTS
ISSN 2307-8960 (online) https://www.wjgnet.com/bpg/GerInfo/287
LAUNCH DATE GUIDELINES FOR NON-NATIVE SPEAKERS OF ENGLISH
April 16, 2013 https://www.wjgnet.com/bpg/gerinfo/240
FREQUENCY PUBLICATION ETHICS
Thrice Monthly https://www.wjgnet.com/bpg/GerInfo/288
EDITORS-IN-CHIEF PUBLICATION MISCONDUCT
Bao-Gan Peng, Jerzy Tadeusz Chudek, George Kontogeorgos, Maurizio Serati, Ja
Hyeon Ku
https://www.wjgnet.com/bpg/gerinfo/208
EDITORIAL BOARD MEMBERS ARTICLE PROCESSING CHARGE
https://www.wjgnet.com/2307-8960/editorialboard.htm https://www.wjgnet.com/bpg/gerinfo/242
PUBLICATION DATE STEPS FOR SUBMITTING MANUSCRIPTS
January 16, 2023 https://www.wjgnet.com/bpg/GerInfo/239
COPYRIGHT ONLINE SUBMISSION
© 2023 Baishideng Publishing Group Inc https://www.f6publishing.com
© 2023 Baishideng Publishing Group Inc. All rights reserved. 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA
E-mail: bpgoffice@wjgnet.com https://www.wjgnet.com
WJCC https://www.wjgnet.com 408 January 16, 2023 Volume 11 Issue 2
World Journal of
Clinical Cases
W J C C
Submit a Manuscript: https://www.f6publishing.com World J Clin Cases 2023 January 16; 11(2): 408-416
DOI: 10.12998/wjcc.v11.i2.408 ISSN 2307-8960 (online)
CASE REPORT
Anti-leucine-rich glioma inactivated protein 1 encephalitis with sleep
disturbance as the first symptom: A case report and review of
literature
De-Lian Kong
Specialty type: Clinical neurology
Provenance and peer review:
Unsolicited article; Externally peer
reviewed.
Peer-review model: Single blind
Peer-review report’s scientific
quality classification
Grade A (Excellent): 0
Grade B (Very good): B
Grade C (Good): C
Grade D (Fair): 0
Grade E (Poor): 0
P-Reviewer: Kirkik D, Turkey;
Velnar T, Slovenia
Received: September 10, 2022
Peer-review started: September 10,
2022
First decision: November 2, 2022
Revised: November 20, 2022
Accepted: December 5, 2022
Article in press: December 5, 2022
Published online: January 16, 2023
De-Lian Kong, Department of Neurology, The Affiliated Jiangning Hospital with Nanjing
Medical University, Nanjing 211000, Jiangsu Province, China
Corresponding author: De-Lian Kong, MD, PhD, Chief Doctor, Chief Physician, Department of
Neurology, The Affiliated Jiangning Hospital with Nanjing Medical University, No. 169
Hushan Road, Jiangning District, Nanjing 211000, Jiangsu Province, China. xykdl@163.com
Abstract
BACKGROUND
Anti-leucine-rich glioma inactivated protein 1 (anti-LGI1) encephalitis is an
infrequent type of autoimmune encephalitis (AE) characterized by acute or
subacute cognitive and psychiatric disturbance, facio-brachial dystonic seizures
(FBDSs), and hyponatremia. Anti-LGI1 AE has increasingly been considered a
primary form of AE. Early identification and treatment of this disease are clearly
very important.
CASE SUMMARY
Here, we report that a male patient developed severe anti-LGI1 encephalitis,
which was initially misdiagnosed as a sleep disturbance. He was hospitalized for
epileptic seizures and typical FBDSs half a month after he developed sleep
disturbances. LGI1 antibodies were detected in his cerebrospinal fluid and serum
(1:100 and 1:3.2, respectively), which led to the diagnosis of classic anti-LGI1 AE.
No obvious abnormality was observed on brain computed tomography images.
T2-weighted fluid-attenuated inversion recovery and T2-weighted scans of brain
magnetic resonance imaging (MRI) showed slightly elevated signals within the
left basal ganglia area. No tumor was detected within the brain of this patient
using MRI. After hormone and antiepileptic drug treatment, the patient’s symp-
toms improved significantly.
CONCLUSION
Anti-LGI1 antibody-associated encephalitis has characteristic clinical manifest-
ations, such as cognitive impairment, psychiatric symptoms, seizures, sleep
disorders, hyponatremia, and FBDSs. LGI1 antibodies are present in the serum
and/or cerebrospinal fluid, but their production is sensitive to immunosup-
pressants, and this disease has a relatively good prognosis. In particular, we
should be aware of the possibility of anti-LGI1 antibody-associated encephalitis in
Kong DL. Anti autoimmune encephalitis with sleep disturbance
WJCC https://www.wjgnet.com 409 January 16, 2023 Volume 11 Issue 2
adolescents with sleep disorders to avoid missed diagnoses and misdiagnoses.
Key Words: Leucine-rich glioma inactivated 1 antibody; Autoimmune encephalitis; Sleep disturbance;
Seizures; Facio-brachial dystonic seizures; Case report
©The Author(s) 2023. Published by Baishideng Publishing Group Inc. All rights reserved.
Core Tip: Anti-leucine-rich glioma inactivated protein 1 (anti-LGI1) encephalitis is a rare autoimmune
encephalitis (AE) characterized by acute or subacute cognitive impairment, facio-brachial dystonic
seizures, psychiatric disturbances and hyponatremia. Herein, we report that a male patient developed
severe anti-LGI1 encephalitis, which was initially misdiagnosed as sleep disturbance. He had antibodies
targeting LGI1 both in his cerebrospinal fluid and serum, which led to the diagnosis of typical anti-LGI1
AE. The case indicated that we should be aware of the possibility of LGI1 antibody-associated enceph-
alitis to avoid missed diagnoses and misdiagnoses especially in adolescents with sleep disorders.
Citation: Kong DL. Anti-leucine-rich glioma inactivated protein 1 encephalitis with sleep disturbance as the first
symptom: A case report and review of literature. World J Clin Cases 2023; 11(2): 408-416
URL: https://www.wjgnet.com/2307-8960/full/v11/i2/408.htm
DOI: https://dx.doi.org/10.12998/wjcc.v11.i2.408
INTRODUCTION
In general, the phrase autoimmune encephalitis (AE) is defined as diseases caused by antigen-antibody
reactions of the immune system to the central nervous system[1]. The main clinical manifestations of AE
are acute or subacute epileptic seizures, facio-brachial dystonic seizures (FBDSs), cognitive disturbances,
and mental disorders.
Sleep dysfunction in patients with AE has received little attention and is most likely neglected
because clinicians pay more attention to neurological and psychiatric symptoms. Nevertheless, sleep
disorders are very common in AE patients and often persist beyond the acute stage, which seriously
affects patients’ quality of life. All patterns of somnipathy can arise in AE patients due to the influence
of the disease on an extensive number of brain networks participating in sleep initiation and regulation.
Anti-IgLON5 and anti-N-methyl-d-aspartate (NMDA) receptor encephalitis are two representative
diseases in which sleep disturbances are common and serious. Somnipathy varies according to the
disease stage in anti-NMDA receptor encephalitis, and the core symptom in anti-IgLON5 disease is
sleep disorders[2].
However, few reports described sleep disorders associated with anti-leucine-rich glioma inactivated
protein 1 (anti-LGI1) antibody encephalitis. Anti-LGI1 antibody-associated encephalitis is a type of AE
that is characterized by epilepsy, a recent memory decline, and mental and behavioral abnormalities as
its main clinical manifestations. Since anti-LGI1 encephalitis is a recently identified disease, limited data
are available on its clinical manifestation, especially in patients presenting with sleep disturbances as the
initial symptom. Here, we report a patient who developed severe anti-LGI1 encephalitis, which was
initially misdiagnosed as a sleep disorder. The patient was hospitalized for epileptic seizures and typical
FBDSs half a month after he developed the sleep disturbance.
CASE PRESENTATION
Chief complaints
Sleep disorders, sudden limb convulsions with unconsciousness.
History of present illness
This patient initially visited the doctor because he suffered from suddenly persistent insomnia (with
difficulties initiating and especially maintaining sleep). Dream enactment and somniloquy occurred
during his sleep, and he felt fatigue and weakness after waking in the morning. The doctor prescribed
some sleeping pills. No significant improvement was observed after taking the medicine for several
days. Half a month later, his right hand twitched involuntarily in the evening before admission when he
had his hair cut; this symptom lasted for approximately 3 s and was not given much attention. After
waking the next morning, he had two other attacks with intervals of approximately half an hour, lasting
approximately 3–5 s each. Then, secondary limb convulsions appeared as follows: Flexion of both upper
Kong DL. Anti autoimmune encephalitis with sleep disturbance
WJCC https://www.wjgnet.com 410 January 16, 2023 Volume 11 Issue 2
limbs, ankylosis of both lower limbs, unconsciousness, eyes turning up, crown closure, and mouth
foaming, which lasted for approximately five minutes. Immediately, the patient's consciousness became
lucid, and after waking, he could not recall the course of the disease and experienced slight dizziness
and headache
Then, he went to the emergency department of our hospital. He was administered an intravenous
injection of "mannitol, acetylglutamine and sodium acetate ringer" after brain computed tomography
(CT) scan, which showed no obvious abnormality. Then, intermittent involuntary twitching of the right
hand was still present, which occurred once in approximately 1-2 h and lasted 3-5 seconds each time.
The patient was admitted to our hospital for further diagnosis and treatment.
History of past illness
He had previously been healthy.
Personal and family history
There is no history of familial genetic diseases.
Physical examination
The neurological examination showed no obvious abnormality.
Laboratory examinations
The white blood cell count (11.23 × 109 cells/L) and neutrophil percentage (89%) increased significantly
in the full blood count. All biochemical indexes and thyroid function were normal or negative.
Cerebrospinal fluid (CSF): A routine CSF examination displayed acellular fluid. No bacterial growth
or abnormal biochemistry was observed in the CSF. The opening pressure was not abnormal. CSF
cytology showed that the percentage of leukocytes in multiple nuclei increased by 50% (reference value
0%–6%), and the other indexes were normal.
Detection of autoimmune antibodies: LGI1 antibodies were examined and were positive in both the
serum and cerebrospinal fluid (1:100 and 1:3.2, respectively), and other antibodies (contactin-associated
protein 2 (CASPR2), N-methyl-D-aspartate receptor (NMDAR), glutamic acid decarboxylase (GAD65),
GABA, and AMPA1) were negative (Figures 1 and 2), which confirmed the diagnosis.
No abnormalities in hepatitis B surface antibody test results. Human immunodeficiency virus
antibodies and Treponema pallidum-specific antibodies were normal or negative.
Imaging examinations
A computed tomography (CT) scan of the thorax showed inflammation of the right lower lobe of the
lung. No abnormality was detected on the brain CT scan.
Brain magnetic resonance imaging (MRI) (Figure 3) results: An abnormal shadow signal was
observed in the left basal ganglia area, which displayed a high signal in T2-weighted fluid-attenuated
inversion recovery (FLAIR) MRI and T2-weighted MRI.
Video electroencephalogram (EEG) (Figure 4): The patient’s EEG was mildly abnormal. Multiple slow
wave bursts were observed during wakefulness. Interference artifacts may have been present.
FINAL DIAGNOSIS
Clinicians must determine the correct diagnosis as early as possible, and excluding the presence of an
underlying malignancy is certainly worthwhile because it may be associated with this pathology[3]. In
this case, no signs suggested the presence of neoplasia.
In this case, a series of clinical manifestations, such as sleep disorders, seizures, and typical FBDCs,
combined with abnormal signals of brain MRI and positive LGI1 antibodies in blood and cerebrospinal
fluid prove that this case conforms to the diagnosis of anti-LGI1 autoimmune encephalitis.
TREATMENT
Immunotherapy was initiated with dexamethasone, and a continuous intravenous infusion of sodium
valproate was administered to control the seizures.
OUTCOME AND FOLLOW-UP
No major seizures occurred during hospitalization, but intermittent FBDSs persisted during the first
several days after hospitalization. One week later, FBDSs did not appear. Two weeks later, the patient's
Kong DL. Anti autoimmune encephalitis with sleep disturbance
WJCC https://www.wjgnet.com 411 January 16, 2023 Volume 11 Issue 2
Figure 1 LGI-1(A), CASPR2(B), NMDAR(C), GAD65(D), GABA(E), AMPA1(F) antibodies in CSF validated by cell-assay of transfected cells.
LGI1-IgG in CSF (1:3.2) were positive but others (CASPR2, NMDAR, GAD65, GABA, AMPA1) were negative.
Figure 2 LGI-1(A), CASPR2(B), NMDAR(C), GAD65(D), GABA(E), AMPA1(F) antibodies in serum validated by cell-assay of transfected
cells. LGI1-IgG in serum (1:100) were positive but others (CASPR2, NMDAR, GAD65, GABA, AMPA1) were negative.
symptoms improved significantly, and thus he was discharged and was told to gradually reduce the
dose of prednisone after discharge. During hospitalization, the patient's sleep disturbances gradually
decreased, and the patient's sleep completely returned to normal at discharge. The patent was
discharged with antiepileptic therapy and corticosteroid. He is followed up every three months and
symptoms have not recurred.
DISCUSSION
The incidence and mortality rates of encephalitis are 8%-18.45%[4-7]. The disease has been recognized
Kong DL. Anti autoimmune encephalitis with sleep disturbance
WJCC https://www.wjgnet.com 412 January 16, 2023 Volume 11 Issue 2
Figure 3 Brain magnetic resonance images of this patient. A: T2-weighted fluid-attenuated inversion recovery showed slightly elevated signals within the
left basal ganglia area; B: T2-Weighted scans showed slightly elevated signals within the left basal ganglia area.
Figure 4 Video electroencephalography of this patient. A: Wakefulness and eyes closed; B: Sleep state: Mildly abnormal electroencephalography. Multiple
slow wave bursts during wakefulness. There may have been interference artifacts.
by an increasing number of clinicians since the first case of teratoma-related anti-NMDA receptor
encephalitis was reported in 2007[8].
Dalmau et al[9] were the first to report that anti-NMDAR encephalitis has a close relationship with
teratoma in 2007. Lai et al[10] first discovered anti-AMPA receptor encephalitis in 2009, and Lancaster et
al[11] identified anti-GABABR encephalitis in 2010. Anti-LGI1 antibody encephalitis and anti-CASPR2
antibody encephalitis were first discovered by Lai et al[12] in 2010. Anti-LGI1 encephalitis is
infrequently associated with tumors, and most patients recovered after treatment with steroids or other
immunotherapies[13].
A survey discovered that AE substantially affected the patients’ quality of life[14]. The diagnosis of
AE is very difficult due to its sophisticated clinical symptoms[15]. The key to the diagnosis of AE is a
neuronal autoimmune antibody, and a close relationship has been observed between the difference in
the antibody titer and its clinical course[16].
The main manifestations of anti-LGI1 encephalitis are epilepsy, cognitive and mental disorders,
hyponatremia, and sleep disorders, and explanations are provided below.
Epilepsy
Among the patients positive for LGI antibodies, twenty percent-forty percent[17] have FBDSs, which are
short, frequent, and unconscious seizures, together with dystonia, simple upper limb spasm and
contraction, and ipsilateral face twitch (not long, 3 s, several times a day). Some scholars[18] postulate
that FBDSs might be dystonic. However, Irani et al[19] and other scholars proposed that FBDSs were a
type of epileptic seizure.
Previous studies have discovered that ninety percent of patients have seizures that primarily present
in the following three types: FBDS, focal to bilateral tonic-clonic seizure and mesial temporal lobe
Kong DL. Anti autoimmune encephalitis with sleep disturbance
WJCC https://www.wjgnet.com 413 January 16, 2023 Volume 11 Issue 2
epilepsy -like seizure[20-26]. In a recent study, patients with anti-LGI1 AE were divided into the
following three groups according to the epilepsy symptomatology: FBDS alone (FBDS-only), epileptic
seizures without FBDS [non-FBDS], and coexistence of FBDS and other seizures (FBDS+)[27].
Researchers found that FBDSs were significantly decreased and even vanished after treatment with oral
steroids[28]. Basal ganglia lesions are present in patients with FBDSs[1].
FBDSs are the particular seizure type experienced by anti-LGI1 AE patients, and probably half of the
patients experience FBDSs[20,21,22,19,29]. FBDSs are easy to identify and diagnose; however, EEG
shows abnormalities during onset in only a few patients[19,29]. The origin of FBDSs remains contro-
versial. Cortical, subcortical, and cortical-subcortical origins have been shownby distinct studies[27,30,
31]. A study on anti-LGI1 AE[18] concluded that anti-LGI1 antibodyassociated encephalitis commonly
damaged the hippocampus and basal ganglia, which was slightly different from a previous study that
discovered that the motor cortex and hippocampus may be two main targets in anti-LGI1 AE[24,20]. In
addition, immunotherapy reduces epileptic seizures and prevents complications[32]. A study[33]
reported high T2 and FLAIR signals in the bilateral temporal lobe and hippocampus on brain MRI[18].
This finding is consistent with the report that LGI1 is primarily expressed in the temporal cortex and
hippocampus.
The seizure form experienced by this patient FBDS+, and the symptoms were obviously relieved after
treatment with hormone and antiepileptic drugs, consistent with the characteristics of anti-LGI1 enceph-
alitis.
Cognitive and mental impairment
Previous studies discovered that approximately ninety-five percent of patients suffered from cognitive
dysfunctions. Majoie et al[34] discovered that eighty-nine percent of LE patients had dysmnesia. Malter
et al[17] identified relationships between cognitive impairment and the disease course before immuno-
therapy.
The main manifestations of mental/behavioral disturbances are individual and behavioral
abnormalities, such as prone to anger, anxiety, impulsive behavior, and hallucinations[18,35]. Serum
anti-LGI1 antibodies may remain detectable after full clinical recovery[36]. A similar mechanism[35] can
be hypothesized in anti-LGI1 encephalitis because the LGI1-ADAM22-AMPAR interaction is proposed
to influence long-term depression (LTD)[37,38]. As LTD is also essential for spatial memory, disruption
of this process might explain the spatial disorientation observed in patients with anti-LGI1 encephalitis.
Hyponatraemia: As reported, hyponatraemia occurs in sixty percent of patients with LGI1 AE[21,18].
The main reason was regarded as abnormal secretion of antidiuretic hormones, which will be correlated
with simultaneous LGI1 expression in the hypothalamus and kidney.
Brain MRI: Most LE patients presented abnormal T2 and FLAIR signals in bilateral temporal lobe
regions on brain MRI, and a small proportion of patients showed abnormal signals in one side of the
hippocampus. Furthermore, the lesions often involve the temporal lobe and basal ganglia[39]. In some
patients with FBDSs, high T1/T2 are detected signals on brain MRI[40] and high FDG-PET metabolism
has been observed in the basal ganglia[19].
In our case, FLAIR and T2-weighted scans showed slightly elevated signals within the left basal
ganglia area, consistent with the characteristics of anti-LGI1 encephalitis detected using MRI.
Sleep disturbances: Sleep disturbances are also common in patients with AE[41]. Sleep dysfunctions
have also been described in association with various neuron-specific antibody biomarkers, including
IgLON5, LGI1, CASPR2, NMDA receptor, and Ma2. There are four forms of sleep disorders: rapid eye
movement sleep behavior disorder, hypersomnia, fragmented sleep, and sleep-disordered breathing.
New sleep complaints (e.g., gasping and snoring) were reported by seventy-three percent of AE patients
in one study[42].
LGI1 is a glycoprotein located in the synapse and primarily expressed in the neocortex and
hippocampus[43]. A recent study of PSG revealed that sleep efficiency, total sleep time, N3 sleep and
REM sleep decreased significantly in anti-LGI1 encephalitis patients[44]. Another study[45] demon-
strated that sleep efficiency and total sleep time were obviously reduced in anti-LGI1 AE patients. An
imbalanced sleep structure was discovered, showing ascended N1, reduced N3, REM components and
an abnormal N2 structure. These findings were not related to nocturnal episodic events or the presence
of sleep hyperkinetic movements. Animal experiments have shown that LGI1 antibodies play a
neurotoxic role, potentially mediated through the reduction in calcium currents and induction of
apoptosis[46]. The LGI1 gene is widely expressed in the hypothalamus, including the ventromedial
nucleus[47]. The ventromedial nucleus contains glycine/GABA neurons and receives direct synaptic
input from glutamatergic neurons in the sublaterodorsal tegmental nucleus. Studies have shown that
silencing this circuit may lead to REM sleep without atonia[48]. Antibodies binding to hypothalamic
neurons may result in hypothalamic disturbances, likely leading to RBD and insomnia. Clinical and PSG
outcomes improved after immunotherapy[49].
However, other authors[50,51] found that the chief immunological targets of anti-LGI1 encephalitis
are the motor cortex, limbic system, brainstem and striatum thalamus, consistent with the findings that
LGI1 is broadly expressed in neurons and some axonal terminals throughout the Central Nervous
Kong DL. Anti autoimmune encephalitis with sleep disturbance
WJCC https://www.wjgnet.com 414 January 16, 2023 Volume 11 Issue 2
System.
In this case, the manifestations of sleep disorders were persistent insomnia (with difficulties initiating
and especially maintaining sleep), dream enactment and somniloquy, which lasted for half a month
before the seizures began. Furthermore, sleep disorders responded poorly to general sleeping pills, and
the symptoms were relieved rapidly after immunotherapy, consistent with the characteristics of sleep
disorders in AE.
In conclusion, sleep disturbance, marked by symptoms including sleep fragmentation, dream
enactment behaviors and ambiguous or total loss of physiological sleep rhythms, could be a visible and
inherent characteristic of anti-LGI1 encephalitis.
Improving the detection of sleep disorders is conducive to the early detection of anti-LGI1 AE,
especially in patients presenting with sleep disorders as the initial symptoms; this approach may
prevent missed diagnoses and misdiagnoses. Additionally, this approach may allow patients to receive
treatment as soon as possible and promote the early recovery of patients.
EEG: Usually, a specific change in EEG is not observed in patients with anti-LGI1 AE. The abnormal
EEG for FBDSs is probably caused by a deeply located or highly localized epileptogenic zone[21,23].
CONCLUSION
The case report illustrates the importance of antibody testing and early recognition of sleep disturbances
in identifying this condition, which is often undiagnosed. Early recognition and initiation of therapy are
important in the management of patients with anti-LGI1 AE and their prognosis and may both prevent
perpetual neurological impairment and improve long-term outcomes. Unfortunately, polysomnography
and FDG-PET were not completed due to the limitations of our hospital’s facilities. In a future study, we
will try to collect these data.
FOOTNOTES
Author contributions: Kong DL collected case data and wrotes the manuscript.
Informed consent statement: Written informed consent was obtained from the patient after treatment for publication
of this case report and any accompanying images.
Conflict-of-interest statement: All authors declared that they have no competing interests.
CARE Checklist (2016) statement: The authors have read the CARE Checklist (2016), and the manuscript was
prepared and revised according to the CARE Checklist (2016).
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by
external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-
NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license
their derivative works on different terms, provided the original work is properly cited and the use is non-
commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Country/Territory of origin: China
ORCID number: De-Lian Kong 0000-0002-4071-2083.
S-Editor: Liu JH
L-Editor: A
P-Editor: Liu JH
REFERENCES
Graus F, Titulaer MJ, Balu R, Benseler S, Bien CG, Cellucci T, Cortese I, Dale RC, Gelfand JM, Geschwind M, Glaser
CA, Honnorat J, Höftberger R, Iizuka T, Irani SR, Lancaster E, Leypoldt F, Prüss H, Rae-Grant A, Reindl M, Rosenfeld
MR, Rostásy K, Saiz A, Venkatesan A, Vincent A, Wandinger KP, Waters P, Dalmau J. A clinical approach to diagnosis of
autoimmune encephalitis. Lancet Neurol 2016; 15: 391-404 [PMID: 26906964 DOI: 10.1016/S1474-4422(15)00401-9]
1
Muñoz-Lopetegi A, Graus F, Dalmau J, Santamaria J. Sleep disorders in autoimmune encephalitis. Lancet Neurol 2020;
19: 1010-1022 [PMID: 33212053 DOI: 10.1016/S1474-4422(20)30341-0]
2
van Sonderen A, Petit-Pedrol M, Dalmau J, Titulaer MJ. The value of LGI1, Caspr2 and voltage-gated potassium channel
antibodies in encephalitis. Nat Rev Neurol 2017; 13: 290-301 [PMID: 28418022 DOI: 10.1038/nrneurol.2017.43]
3
Kong DL. Anti autoimmune encephalitis with sleep disturbance
WJCC https://www.wjgnet.com 415 January 16, 2023 Volume 11 Issue 2
Venkatesan A, Tunkel AR, Bloch KC, Lauring AS, Sejvar J, Bitnun A, Stahl JP, Mailles A, Drebot M, Rupprecht CE,
Yoder J, Cope JR, Wilson MR, Whitley RJ, Sullivan J, Granerod J, Jones C, Eastwood K, Ward KN, Durrheim DN, Solbrig
MV, Guo-Dong L, Glaser CA; International Encephalitis Consortium. Case definitions, diagnostic algorithms, and priorities
in encephalitis: consensus statement of the international encephalitis consortium. Clin Infect Dis 2013; 57: 1114-1128
[PMID: 23861361 DOI: 10.1093/cid/cit458]
4
Granerod J, Ambrose HE, Davies NW, Clewley JP, Walsh AL, Morgan D, Cunningham R, Zuckerman M, Mutton KJ,
Solomon T, Ward KN, Lunn MP, Irani SR, Vincent A, Brown DW, Crowcroft NS; UK Health Protection Agency (HPA)
Aetiology of Encephalitis Study Group. Causes of encephalitis and differences in their clinical presentations in England: a
multicentre, population-based prospective study. Lancet Infect Dis 2010; 10: 835-844 [PMID: 20952256 DOI:
10.1016/S1473-3099(10)70222-X]
5
Mailles A, Stahl JP; Steering Committee and Investigators Group. Infectious encephalitis in france in 2007: a national
prospective study. Clin Infect Dis 2009; 49: 1838-1847 [PMID: 19929384 DOI: 10.1086/648419]
6
Thakur KT, Motta M, Asemota AO, Kirsch HL, Benavides DR, Schneider EB, McArthur JC, Geocadin RG, Venkatesan
A. Predictors of outcome in acute encephalitis. Neurology 2013; 81: 793-800 [PMID: 23892708 DOI:
10.1212/WNL.0b013e3182a2cc6d]
7
Sansing LH, Tüzün E, Ko MW, Baccon J, Lynch DR, Dalmau J. A patient with encephalitis associated with NMDA
receptor antibodies. Nat Clin Pract Neurol 2007; 3: 291-296 [PMID: 17479076 DOI: 10.1038/ncpneuro0493]
8
Dalmau J, Tüzün E, Wu HY, Masjuan J, Rossi JE, Voloschin A, Baehring JM, Shimazaki H, Koide R, King D, Mason W,
Sansing LH, Dichter MA, Rosenfeld MR, Lynch DR. Paraneoplastic anti-N-methyl-D-aspartate receptor encephalitis
associated with ovarian teratoma. Ann Neurol 2007; 61: 25-36 [PMID: 17262855 DOI: 10.1002/ana.21050]
9
Lai M, Hughes EG, Peng X, Zhou L, Gleichman AJ, Shu H, Matà S, Kremens D, Vitaliani R, Geschwind MD, Bataller L,
Kalb RG, Davis R, Graus F, Lynch DR, Balice-Gordon R, Dalmau J. AMPA receptor antibodies in limbic encephalitis alter
synaptic receptor location. Ann Neurol 2009; 65: 424-434 [PMID: 19338055 DOI: 10.1002/ana.21589]
10
Lancaster E, Lai M, Peng X, Hughes E, Constantinescu R, Raizer J, Friedman D, Skeen MB, Grisold W, Kimura A, Ohta
K, Iizuka T, Guzman M, Graus F, Moss SJ, Balice-Gordon R, Dalmau J. Antibodies to the GABA(B) receptor in limbic
encephalitis with seizures: case series and characterisation of the antigen. Lancet Neurol 2010; 9: 67-76 [PMID: 19962348
DOI: 10.1016/S1474-4422(09)70324-2]
11
Lai M, Huijbers MG, Lancaster E, Graus F, Bataller L, Balice-Gordon R, Cowell JK, Dalmau J. Investigation of LGI1 as
the antigen in limbic encephalitis previously attributed to potassium channels: a case series. Lancet Neurol 2010; 9: 776-
785 [PMID: 20580615 DOI: 10.1016/S1474-4422(10)70137-X]
12
Tumminelli G, Battisti C, Cioni C, Mignarri A, Annunziata P, Federico A. Demyelinating polyneuropathy in a case of anti-
LGI1 encephalitis. Muscle Nerve 2017; 56: E2-E3 [PMID: 28073143 DOI: 10.1002/mus.25572]
13
Cohen J, Sotoca J, Gandhi S, Yeshokumar AK, Gordon-Lipkin E, Geocadin RG, Frick KD, Probasco JC, Venkatesan A.
Autoimmune encephalitis: A costly condition. Neurology 2019; 92: e964-e972 [PMID: 30674590 DOI:
10.1212/WNL.0000000000006990]
14
Vollmer TL, McCarthy M. Autoimmune encephalitis: A more treatable tragedy if diagnosed early. Neurology 2016; 86:
1655-1656 [PMID: 27037233 DOI: 10.1212/WNL.0000000000002641]
15
Gresa-Arribas N, Titulaer MJ, Torrents A, Aguilar E, McCracken L, Leypoldt F, Gleichman AJ, Balice-Gordon R,
Rosenfeld MR, Lynch D, Graus F, Dalmau J. Antibody titres at diagnosis and during follow-up of anti-NMDA receptor
encephalitis: a retrospective study. Lancet Neurol 2014; 13: 167-177 [PMID: 24360484 DOI:
10.1016/S1474-4422(13)70282-5]
16
Malter MP, Frisch C, Schoene-Bake JC, Helmstaedter C, Wandinger KP, Stoecker W, Urbach H, Surges R, Elger CE,
Vincent AV, Bien CG. Outcome of limbic encephalitis with VGKC-complex antibodies: relation to antigenic specificity. J
Neurol 2014; 261: 1695-1705 [PMID: 24935858 DOI: 10.1007/s00415-014-7408-6]
17
Wang M, Cao X, Liu Q, Ma W, Guo X, Liu X. Clinical features of limbic encephalitis with LGI1 antibody. Neuropsychiatr
Dis Treat 2017; 13: 1589-1596 [PMID: 28670128 DOI: 10.2147/NDT.S136723]
18
Irani SR, Michell AW, Lang B, Pettingill P, Waters P, Johnson MR, Schott JM, Armstrong RJ, S Zagami A, Bleasel A,
Somerville ER, Smith SM, Vincent A. Faciobrachial dystonic seizures precede Lgi1 antibody limbic encephalitis. Ann
Neurol 2011; 69: 892-900 [PMID: 21416487 DOI: 10.1002/ana.22307]
19
Bastiaansen AEM, van Sonderen A, Titulaer MJ. Autoimmune encephalitis with anti-leucine-rich glioma-inactivated 1 or
anti-contactin-associated protein-like 2 antibodies (formerly called voltage-gated potassium channel-complex antibodies).
Curr Opin Neurol 2017; 30: 302-309 [PMID: 28248701 DOI: 10.1097/WCO.0000000000000444]
20
van Sonderen A, Schreurs MW, Wirtz PW, Sillevis Smitt PA, Titulaer MJ. From VGKC to LGI1 and Caspr2 encephalitis:
The evolution of a disease entity over time. Autoimmun Rev 2016; 15: 970-974 [PMID: 27485013 DOI:
10.1016/j.autrev.2016.07.018]
21
Spatola M, Dalmau J. Seizures and risk of epilepsy in autoimmune and other inflammatory encephalitis. Curr Opin Neurol
2017; 30: 345-353 [PMID: 28234800 DOI: 10.1097/WCO.0000000000000449]
22
Gao L, Liu A, Zhan S, Wang L, Li L, Guan L, Zhao X, Zhang X, Wang Y. Clinical characterization of autoimmune LGI1
antibody limbic encephalitis. Epilepsy Behav 2016; 56: 165-169 [PMID: 26896820 DOI: 10.1016/j.yebeh.2015.12.041]
23
Li LH, Ma CC, Zhang HF, Lian YJ. Clinical and electrographic characteristics of seizures in LGI1-antibody encephalitis.
Epilepsy Behav 2018; 88: 277-282 [PMID: 30332659 DOI: 10.1016/j.yebeh.2018.08.019]
24
de Bruijn MAAM, van Sonderen A, van Coevorden-Hameete MH, Bastiaansen AEM, Schreurs MWJ, Rouhl RPW, van
Donselaar CA, Majoie MHJM, Neuteboom RF, Sillevis Smitt PAE, Thijs RD, Titulaer MJ. Evaluation of seizure treatment
in anti-LGI1, anti-NMDAR, and anti-GABA(B)R encephalitis. Neurology 2019; 92: e2185-e2196 [PMID: 30979857 DOI:
10.1212/WNL.0000000000007475]
25
Zhang W, Wang X, Shao N, Ma R, Meng H. Seizure characteristics, treatment, and outcome in autoimmune synaptic
encephalitis: A long-term study. Epilepsy Behav 2019; 94: 198-203 [PMID: 30974347 DOI: 10.1016/j.yebeh.2018.10.038]
26
Chen C, Wang X, Zhang C, Cui T, Shi WX, Guan HZ, Ren HT, Shao XQ. Seizure semiology in leucine-rich glioma-
inactivated protein 1 antibody-associated limbic encephalitis. Epilepsy Behav 2017; 77: 90-95 [PMID: 29050866 DOI:
27
Kong DL. Anti autoimmune encephalitis with sleep disturbance
WJCC https://www.wjgnet.com 416 January 16, 2023 Volume 11 Issue 2
10.1016/j.yebeh.2017.08.011]
Gastaldi M, Thouin A, Vincent A. Antibody-Mediated Autoimmune Encephalopathies and Immunotherapies.
Neurotherapeutics 2016; 13: 147-162 [PMID: 26692392 DOI: 10.1007/s13311-015-0410-6]
28
Andrade DM, Tai P, Dalmau J, Wennberg R. Tonic seizures: a diagnostic clue of anti-LGI1 encephalitis? Neurology 2011;
76: 1355-1357 [PMID: 21482953 DOI: 10.1212/WNL.0b013e3182152808]
29
Striano P. Faciobrachial dystonic attacks: seizures or movement disorder? Ann Neurol 2011; 70: 179-80; author reply 180
[PMID: 21786308 DOI: 10.1002/ana.22470]
30
Boesebeck F, Schwarz O, Dohmen B, Graef U, Vestring T, Kramme C, Bien CG. Faciobrachial dystonic seizures arise
from cortico-subcortical abnormal brain areas. J Neurol 2013; 260: 1684-1686 [PMID: 23681644 DOI:
10.1007/s00415-013-6946-7]
31
Navarro V, Kas A, Apartis E, Chami L, Rogemond V, Levy P, Psimaras D, Habert MO, Baulac M, Delattre JY, Honnorat
J; collaborators. Motor cortex and hippocampus are the two main cortical targets in LGI1-antibody encephalitis. Brain
2016; 139: 1079-1093 [PMID: 26945884 DOI: 10.1093/brain/aww012]
32
Yin D, Chen S, Liu J. Sleep Disturbances in Autoimmune Neurologic Diseases: Manifestation and Pathophysiology. Front
Neurosci 2021; 15: 687536 [PMID: 34421519 DOI: 10.3389/fnins.2021.687536]
33
Majoie HJ, de Baets M, Renier W, Lang B, Vincent A. Antibodies to voltage-gated potassium and calcium channels in
epilepsy. Epilepsy Res 2006; 71: 135-141 [PMID: 16870397 DOI: 10.1016/j.eplepsyres.2006.06.003]
34
van Sonderen A, Thijs RD, Coenders EC, Jiskoot LC, Sanchez E, de Bruijn MA, van Coevorden-Hameete MH, Wirtz PW,
Schreurs MW, Sillevis Smitt PA, Titulaer MJ. Anti-LGI1 encephalitis: Clinical syndrome and long-term follow-up.
Neurology 2016; 87: 1449-1456 [PMID: 27590293 DOI: 10.1212/WNL.0000000000003173]
35
Ariño H, Armangué T, Petit-Pedrol M, Sabater L, Martinez-Hernandez E, Hara M, Lancaster E, Saiz A, Dalmau J, Graus
F. Anti-LGI1-associated cognitive impairment: Presentation and long-term outcome. Neurology 2016; 87: 759-765 [PMID:
27466467 DOI: 10.1212/WNL.0000000000003009]
36
Ohkawa T, Fukata Y, Yamasaki M, Miyazaki T, Yokoi N, Takashima H, Watanabe M, Watanabe O, Fukata M.
Autoantibodies to epilepsy-related LGI1 in limbic encephalitis neutralize LGI1-ADAM22 interaction and reduce synaptic
AMPA receptors. J Neurosci 2013; 33: 18161-18174 [PMID: 24227725 DOI: 10.1523/JNEUROSCI.3506-13.2013]
37
Huganir RL, Nicoll RA. AMPARs and synaptic plasticity: the last 25 years. Neuron 2013; 80: 704-717 [PMID: 24183021
DOI: 10.1016/j.neuron.2013.10.025]
38
Fauser S, Talazko J, Wagner K, Ziyeh S, Jarius S, Vincent A, Schulze-Bonhage A. FDG-PET and MRI in potassium
channel antibody-associated non-paraneoplastic limbic encephalitis: correlation with clinical course and neuropsychology.
Acta Neurol Scand 2005; 111: 338-343 [PMID: 15819715 DOI: 10.1111/j.1600-0404.2005.00406.x]
39
Flanagan EP, Kotsenas AL, Britton JW, McKeon A, Watson RE, Klein CJ, Boeve BF, Lowe V, Ahlskog JE, Shin C, Boes
CJ, Crum BA, Laughlin RS, Pittock SJ. Basal ganglia T1 hyperintensity in LGI1-autoantibody faciobrachial dystonic
seizures. Neurol Neuroimmunol Neuroinflamm 2015; 2: e161 [PMID: 26468474 DOI: 10.1212/NXI.0000000000000161]
40
Devine MF, St Louis EK. Sleep Disturbances Associated with Neurological Autoimmunity. Neurotherapeutics 2021; 18:
181-201 [PMID: 33786802 DOI: 10.1007/s13311-021-01020-x]
41
Blattner MS, de Bruin GS, Bucelli RC, Day GS. Sleep disturbances are common in patients with autoimmune encephalitis.
J Neurol 2019; 266: 1007-1015 [PMID: 30741377 DOI: 10.1007/s00415-019-09230-2]
42
Irani SR, Alexander S, Waters P, Kleopa KA, Pettingill P, Zuliani L, Peles E, Buckley C, Lang B, Vincent A. Antibodies
to Kv1 potassium channel-complex proteins leucine-rich, glioma inactivated 1 protein and contactin-associated protein-2 in
limbic encephalitis, Morvan's syndrome and acquired neuromyotonia. Brain 2010; 133: 2734-2748 [PMID: 20663977 DOI:
10.1093/brain/awq213]
43
Lin N, Hao H, Guan H, Sun H, Liu Q, Lu Q, Jin L, Ren H, Huang Y. Sleep Disorders in Leucine-Rich Glioma-Inactivated
Protein 1 and Contactin Protein-Like 2 Antibody-Associated Diseases. Front Neurol 2020; 11: 696 [PMID: 32849186 DOI:
10.3389/fneur.2020.00696]
44
Liu X, Yang L, Han Y, Xu J, Pang Z, Du Y, Feng Y, Lin Y. Electrophysiological Evaluation in Identifying Unique Sleep
Features Among Anti-LGI1 Encephalitis Patients During Active and Recovery Phase. Nat Sci Sleep 2021; 13: 527-536
[PMID: 33976578 DOI: 10.2147/NSS.S299467]
45
Ayşit-Altuncu N, Ulusoy C, Öztürk G, Tüzün E. Effect of LGI1 antibody-positive IgG on hippocampal neuron survival: a
preliminary study. Neuroreport 2018; 29: 932-938 [PMID: 29771820 DOI: 10.1097/WNR.0000000000001055]
46
Herranz-Pérez V, Olucha-Bordonau FE, Morante-Redolat JM, Pérez-Tur J. Regional distribution of the leucine-rich
glioma inactivated (LGI) gene family transcripts in the adult mouse brain. Brain Res 2010; 1307: 177-194 [PMID:
19833108 DOI: 10.1016/j.brainres.2009.10.013]
47
Uchida S, Soya S, Saito YC, Hirano A, Koga K, Tsuda M, Abe M, Sakimura K, Sakurai T. A Discrete Glycinergic
Neuronal Population in the Ventromedial Medulla That Induces Muscle Atonia during REM Sleep and Cataplexy in Mice.
J Neurosci 2021; 41: 1582-1596 [PMID: 33372061 DOI: 10.1523/JNEUROSCI.0688-20.2020]
48
Peter-Derex L, Devic P, Rogemond V, Rheims S, Mauguière F, Honnorat J. Full recovery of agrypnia associated with anti-
Lgi1 antibodies encephalitis under immunomodulatory treatment: a case report with sequential polysomnographic
assessment. Sleep Med 2012; 13: 554-556 [PMID: 22437141 DOI: 10.1016/j.sleep.2012.01.002]
49
Liu X, Han Y, Yang L, Wang B, Shao S, Feng Y, Pang Z, Du Y, Lin Y. The exploration of the spectrum of motor
manifestations of anti-LGI1 encephalitis beyond FBDS. Seizure 2020; 76: 22-27 [PMID: 31972532 DOI:
10.1016/j.seizure.2019.12.023]
50
Irani SR, Pettingill P, Kleopa KA, Schiza N, Waters P, Mazia C, Zuliani L, Watanabe O, Lang B, Buckley C, Vincent A.
Morvan syndrome: clinical and serological observations in 29 cases. Ann Neurol 2012; 72: 241-255 [PMID: 22473710
DOI: 10.1002/ana.23577]
51
