A case report and literature review of severe anti-NMDAR encephalitis with predominant caudate nucleus involvement in a child

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Isolated involvement of the caudate nucleus is rare and can be easily misdiagnosed, especially in the early stages when inflammatory symptoms are not apparent. This report describes a pediatric case of severe anti-NMDAR encephalitis with predominant involvement of the caudate nucleus. Case presentation: A 15-year-old male initially presented with stroke-like episodes, misdiagnosed as cerebral infarction. Subsequently, he developed seizures, recurrent low-grade fever, psychiatric symptoms, involuntary orofacial movements, autonomic dysfunction, loss of speech, and inability to perform activities of daily living. Brain MRI revealed a lesion in the left caudate nucleus. The diagnosis was confirmed by positive serum and cerebrospinal fluid anti-NMDAR IgG antibodies. Targeted positron emission tomography (PET) using 18 F-fluorodeoxyglucose ( 18 F-FDG) and the 18 F-DPA-714 tracer for the 18kDa translocator protein (TSPO) identified a core inflammatory area and extensive regions of neuronal dysfunction. The patient's condition gradually improved following immunotherapy and symptomatic treatment. Conclusion: This case provides valuable insights into the pathogenesis of anti-NMDAR encephalitis, particularly its selective involvement of specific brain regions such as the caudate nucleus. The unique imaging features compel us to explore mechanisms beyond the traditional model of direct antibody-mediated pathogenicity. N-methyl-D-aspartate receptor encephalitis Caudate nucleus Magnetic resonance imaging 18F-fluorodeoxyglucose positron emission tomography imaging Targeted 18×10³ transposon positron emission tomography Figures Figure 1 Figure 2 Figure 3 Background N-methyl-D-aspartate receptor (NMDAR) encephalitis (NMDARE) is the most common autoimmune encephalitis (AE) in children, characterized by psychiatric abnormalities, impaired consciousness, seizures, movement disorders, sleep disturbances, and autonomic dysfunction, alongside positive cerebrospinal fluid (CSF) anti-NMDAR antibodies[1]. Overall prognosis is generally favorable, but 5–10% of patients may die during the acute phase, and some may experience long-term cognitive or psychiatric sequelae[2]. Severe pediatric NMDAR encephalitis can be diagnosed based on specific criteria, including intensive care admission, need for life-support, severe motor or autonomic dysfunction, inability to communicate or perform daily activities, life-threatening psychiatric symptoms, status epilepticus, or severe neurological dysfunction (modified Rankin Scale score ≥4)[3].Studies have indicated that in some AEs primarily affecting the basal ganglia, chorea and behavioral abnormalities are prominent clinical features[4]. Therefore, early recognition of atypical presentations of NMDAR encephalitis is crucial for improving clinical outcomes. The 18kDa translocator protein (TSPO) is located on the outer mitochondrial membrane and is involved in cholesterol transport. Its expression in the central nervous system (CNS) is low under physiological conditions but is significantly upregulated in activated glial cells during neuroinflammation[5].Second-generation TSPO radiotracers (e.g., 18 F-DPA-714) enable non-invasive detection of this neuroinflammation via positron emission tomography (PET)[6, 7]. TSPO PET imaging is thus a promising tool for detecting glial activation in various neurological diseases, providing critical insights for pathology, disease activity assessment, and treatment monitoring[8, 9]. 18 F-FDG PET, which measures cerebral glucose metabolism, can sensitively detect regions of neuronal dysfunction often before the onset of clinical symptoms or structural changes on MRI, aiding in the diagnosis and evaluation of neurological disorders like autoimmune encephalitis[10]. The combined application of 18 F-FDG PET and TSPO PET shows potential for enhancing the early identification and differential diagnosis of AE[11]. Case Presentation Introduction of the case A 15-year-old male was admitted with the chief complaint of"slurred speech, numbness and weakness in the right hand for 17 days, and episodic loss of consciousness with limb convulsions for 7 days." Seventeen days prior to admission, the patient developed slurred and incoherent speech without obvious cause, accompanied by numbness in the right hand. The next day, he developed left-deviated mouth and tongue, right facial numbness, and weakened right hand grip strength, making it difficult to hold objects. Cranial CT at a local hospital showed no hemorrhage, and initial suspicion was cerebral infarction. Subsequent brain MRI with DWI and MRA, and cerebral angiography showed no significant abnormalities. No specific treatment was given, and symptoms persisted. Ten days pre-admission, he developed recurrent low-grade fever (37.3°C – 38.1°C) without cough or diarrhea. Seven days pre-admission, he experienced episodes of loss of consciousness with limb convulsions, eye rolling, and foaming at the mouth, lasting seconds to minutes, occurring primarily during sleep (8 episodes total). He was started on lacosamide (100 mg twice daily) at another hospital, after which convulsions ceased. Six days pre-admission, he developed impaired speech comprehension and expression. Three days pre-admission, he became unable to perform activities of daily living (ADLs) independently but could walk. One day pre-admission, he exhibited abnormal mental and behavioral changes. On admission, he had episodic involuntary orofacial movements and excessive sweating. Since onset, he also had poor mental state, sleep disturbances, social withdrawal, reduced appetite, urinary incontinence, and constipation. Past medical history was unremarkable. Examinations and findings On admission,physical examination: T 37.3°C, P 78 bpm, R 20 breaths/min, BP 127/82 mmHg. Well-nourished (Ht 170 cm, Wt 95 kg). Alert but with mixed aphasia, intermittently repeating single words, and paroxysmal involuntary facial twitching. Cognitive assessment was uncooperative. Pupils were equal and reactive (3mm). Nasolabial folds appeared symmetric, but patient could not cooperate with cranial nerve testing. Limb movement was observed but formal strength testing was uncooperative. Muscle tone was normal. Tendon reflexes were active, with bilateral Hoffman's sign and ankle clonus. Sensory and coordination testing were uncooperative. No neck stiffness or pathological signs. Routine blood, urine, stool tests, comprehensive biochemistry, thyroid function, tumor markers, ECG, chest CT, and abdominal ultrasound were unremarkable. Lumbar puncture revealed an opening pressure of 26 cmH2O (Adolescents are capped at 25 cmH2O). CSF analysis: WBC 51 × 10^6/L (normal: 0–15 × 10^6/L), clear appearance; biochemistry normal. Autoimmune encephalitis antibody panel (cell-based assay, CBA) was positive for anti-NMDAR IgG (CSF 1:32; serum 1:320); antibodies against CASPR2, AMPAR1/2, LGI1, GABABR, DPPX, and IgLON5 were negative. Paraneoplastic antibody panel (Hu, Ri, Yo, CV2, Amphiphysin, GAD65, PNMA2, Recoverin, SOX1, Titin, Tr, Zic4) and CNS demyelinating antibody panel (AQP4, GFAP, MBP, MOG) were negative. CSF IgG oligoclonal bands were positive, serum oligoclonal bands were negative. CSF-specific oligoclonal bands were positive. 24-hour intrathecal IgG synthesis rate was slightly elevated at 9.06 mg/24h (normal: 0–9 mg/24h). CSF microscopy showed scattered lymphocytes and few mononuclear cells. CSF next-generation sequencing (NGS) for pathogens was negative. On day 19 of illness, brain MRI with epilepsy protocol (including DWI and contrast) showed an abnormal signal in the head of the left caudate nucleus (Fig. 1A). Video EEG showed focal slow waves. TSPO PET ( 18 F-DPA-714) showed abnormally increased uptake in the left caudate head (SUVmax ~5.66) and patchy uptake in both hippocampi (SUVmax ~3.44) (Fig. 2). 18 F-FDG PET/CT showed: a) hypometabolism in the left caudate head region, consistent with the inflammatory lesion on TSPO PET; b) reduced metabolism in bilateral parietal and temporal lobes (right > left); c) mild-moderate hypometabolism in the right frontal cortex and hippocampus (Fig. 3). A follow-up MRI 9 days after treatment showed reduction in the size of the left caudate head lesion (Fig. 1B). Treatment, outcome and follow-up Based on clinical presentation,positive anti-NMDAR antibodies, and imaging findings, a diagnosis of anti-NMDAR encephalitis was made. The patient received intravenous methylprednisolone pulse therapy combined with intravenous immunoglobulin (IVIg), along with antiepileptic drugs and management of psychiatric symptoms. During hospitalization, seizures and involuntary movements resolved. However, low-grade fever, communication difficulties, excessive sweating, constipation, and occasional behavioral abnormalities persisted. Vital signs showed temperature fluctuations (37.3°C – 38.4°C) and heart rate variability (68 – 108 bpm); blood pressure remained normal. At one-week post-discharge, the family reported no fever for 3 days, improved simple communication, and more stable mood, but sweating persisted. At 12-day follow-up, sweating had normalized, temperature was normal, he could speak short sentences (though longer sentences remained difficult), no psychiatric symptoms were noted, but right hand clumsiness and numbness persisted. He could partially perform ADLs independently (dressing, using toilet). At the 3-month follow-up, he was fully independent in ADLs with normal language function. Occasional emotional outbursts were noted, but no seizures occurred. He had fragmentary memory loss regarding the hospitalization period and reported worsened recent memory. Discussion and conclusions This case describes a 15-year-old boy with severe anti-NMDAR encephalitis meeting diagnostic criteria [12, 13], presenting atypically with initial stroke-like symptoms and predominant caudate nucleus involvement on imaging. The pathogenesis involves antibodies targeting GluN1 subunits of NMDARs, leading to receptor internalization and downstream effects including excitotoxicity[14]. Common triggers include tumors (e.g., ovarian teratoma in young females) and viral infections (e.g., herpes simplex virus encephalitis) [13, 15-18].This patient had no identified tumor or clear viral trigger.First-line immunotherapy for NMDAR encephalitis typically involves corticosteroids and IVIg, ideally initiated early (<15 days from onset) for better prognosis [19, 20].This patient received this regimen with good response. Isolated basal ganglia involvement in NMDAR encephalitis is rare. Literature reviews suggest adult incidence (6.25–16.1%) may be higher than in children (2.4–9.1%), with isolated involvement being extremely uncommon[21-24]. We reviewed 7 published cases of NMDAR encephalitis with basal ganglia involvement (Table 1). Table 1Clinical, paraclinical and radiological features of reported anti-NMDAR encephalitis cases with basal ganglia involvement Case(Reference) Sex Age,years Clinicalpresentation Affectedarea (s)onMRI Serumantibodies CSFantibodies Treatment [25] M 66 Focal seizures (R arm/hand), progressing to GTCS; later focal clonic seizures (L arm/hand) L caudate & putamen; later R caudate, putamen, L medial frontal lobe Not reported NMDAR-IgG positive Methylprednisolone, AEDs [26] M 2 Impaired consciousness, rhythmic arm movements, clenched jaw, drooling Bilateral insular regions, fronto-parietal areas, posterior limb of internal capsule, L medial temporal lobe NMDAR-IgG positive (at 1 year) Not reported AEDs [27] M 32 Cognitive decline, diplopia, ataxia, dysarthria, dysphagia, tremors (head/neck/limbs) Pons, midbrain, bilateral basal ganglia negative NMDAR-Ab positive Methylprednisolone, IVIg [28] F 28 Headache, fever, apathy L frontal & temporal lobes, basal ganglia, corpus callosum, R frontal lobe Not reported NMDAR-IgG (1:32) Methylprednisolone, IVIg [29] M 42 Psychiatric symptoms, seizures, parkinsonism L caudate head, bilateral medial temporal lobes (L > R) Not reported NMDAR-IgG （1：80） AEDs, methylprednisolone, IVIg [30] M 21 Bradykinesia, arm numbness, psychiatric symptoms, cognitive impairment, alcohol sensitivity, dysarthria R caudate & lentiform nucleus NMDAR-IgG positive NMDAR-IgG positive IVIg, mycophenolate mofetil [31] M 18 Progressive dystonia, abnormal posture, involuntary movements Putamen, caudate nucleus Not reported NMDAR-IgG positive IVIg, botulinum toxin A injections Abbreviations: AEDs, antiepileptic drugs; CSF, cerebrospinal fluid; GTCS, generalized tonic-clonic seizure; IVIg, intravenous immunoglobulin; L, left; R, right; NMDAR, N-methyl-D-aspartate receptor. Analysis of seven identified cases of NMDARE with basal ganglia involvement yielded the following characteristics: Regarding gender distribution, six cases (85.7%) were male and one was female. This finding contrasts with the typical presentation of anti-NMDAR encephalitis, which shows a female predominance, particularly among cases associated with ovarian teratomas. This suggests that anti-NMDAR encephalitis with prominent basal ganglia involvement may have a distinct gender predisposition, being more frequently observed in males. Age distribution was wide, ranging from 2 to 66 years, with a median age of 28 years. Among the core clinical features, movement disorders—most commonly manifesting as dystonia, tremor, involuntary movements, or Parkinsonism—and neuropsychiatric symptoms—including memory impairment, behavioral abnormalities, and apathy—were highly prevalent (5/7 cases, 71.4%). Seizures were reported in three cases, presenting either as focal seizures or evolving into generalized tonic-clonic seizures. (It is noteworthy that seizures were also present in the case described in this report.) Cranial MRI findings of basal ganglia lesions were categorized into three patterns: unilateral focal lesions (Cases 1, 5, and 6), bilateral symmetrical lesions (Cases 3, 7), and mixed diffuse involvement (Cases 2 and 4). According to the cranial MRI typology proposed by Khatib et al. [21], the imaging presentations primarily consisted of patchy blurred lesions (4 cases) and widespread FLAIR hyperintensity (3 cases). Mechanistic Insights into Caudate Nucleus Predilection This case provides valuable insights into the pathogenesis of anti-NMDAR encephalitis, particularly its selective involvement of specific brain regions such as the caudate nucleus. The unique imaging features compel us to explore mechanisms beyond the traditional model of direct antibody-mediated pathogenicity. The reasons for the caudate nucleus's predilection in this case are likely multifactorial. While NMDAR antibodies bind to the GluN1 subunit, causing receptor internalization and synaptic dysfunction [14], the question of why antibodies target different brain regions in different patients remains. We propose two non-mutually exclusive hypotheses. First, receptor subtype distribution heterogeneity: the caudate nucleus is rich in NMDARs containing the GluN2B subunit, which is crucial for cognitive and motor functions. It is plausible that the patient's antibodies had a higher affinity for or easier access to receptors with this specific subunit composition. Second, regional disruption of the blood-brain barrier (BBB): the permeability of the BBB in the basal ganglia may vary. A minor inflammatory trigger (e.g., a prodromal infection) could have induced a transient, focal opening of the BBB in the caudate nucleus, allowing antibodies to enter and initiate a localized immune response. This mechanism could elegantly explain the initial "stroke-like" presentation. Furthermore, the intense microglial activation revealed by TSPO PET suggests that neuroinflammation is a core amplifier of the disease process, not merely a bystander phenomenon. Activated microglia can release pro-inflammatory cytokines, which may further exacerbate NMDAR internalization and directly contribute to neuronal dysfunction, creating a vicious cycle that amplifies the initial antibody-mediated injury. Finally, the concomitant involvement of the hippocampus and caudate nucleus suggests a disruption of the hippocampo-striatal loop. These structures are functionally interconnected via dopaminergic and cholinergic pathways, jointly subserving learning, memory, motivation, and motor control. We hypothesize that the antibody attack on these two key nodes disrupted their functional connectivity, providing a neural substrate for the patient's mixed cognitive, psychiatric, and motor symptoms. In this case, TSPO PET revealed a distinct pattern of asymmetrically elevated radiotracer uptake, most notably within the left caudate nucleus head and to a lesser extent in bilateral hippocampal regions. This asymmetrical increase in TSPO binding is mechanistically significant, as TSPO is markedly upregulated on activated microglia during neuroinflammatory processes. The observed PET signal thus provides in vivo evidence of active gliosis, which aligns with the primary pathophysiological mechanism of anti-NMDAR encephalitis—i.e., antibody-mediated internalization of NMDARs, subsequent synaptic dysfunction, and initiation of a localized neuroimmune response. The bilateral hippocampal involvement evident on TSPO PET is consistent with the high density of NMDARs in limbic regions. Antibody binding here likely disrupts synaptic plasticity and gamma-aminobutyric acid (GABA)ergic transmission, leading to hyperexcitability and clinical manifestations such as memory deficits, psychiatric symptoms, and seizures. Importantly, the significant TSPO uptake in the left caudate nucleus underscores that extra-limbic structures, particularly basal ganglia nuclei rich in NMDAR-expressing neurons, may also become engaged in the inflammatory cascade. This may mechanistically underlie prominent motor manifestations including orofacial dyskinesia, dystonia, and autonomic instability. These observations resonate with earlier work by Wang et al. [32], who used TSPO PET to demonstrate that neuroinflammation in autoimmune encephalitides such as anti-LGI1 encephalitis often extends beyond classic limbic circuits to involve subcortical and basal ganglia structures. The convergence of findings across antibody-mediated encephalitides suggests that basal ganglia involvement may reflect a shared propensity for certain neural networks to exhibit inflammatory changes following autoantibody-mediated disruption. Furthermore, the hypometabolism observed on 18 F-FDG PET in the left caudate, hippocampi, and diffuse cortical regions likely reflects downstream neuronal dysfunction following sustained inflammation and receptor internalization. This metabolic reduction may indicate a state of neuronal hypoactivity or injury subsequent to excitotoxicity and chronic synaptic disruption. The divergence of this pattern from the metabolic signatures previously reported by Ge et al. [33] suggests heterogeneity in functional network involvement among patients, possibly reflecting differences in autoantibody titers, symptom chronicity, or individual patterns of immune activation. The superior sensitivity of TSPO PET over MRI in detecting neuroinflammation, as reported by Sun et al. [34], further highlights the utility of molecular imaging for uncovering active immune pathology in seropositive patients with non-diagnostic conventional imaging. This reinforces the mechanistic rationale for employing biomarkers of glial activation to probe the neuroimmune basis of clinical symptoms, especially in cases with atypical or subtle structural findings. Conclusions This case demonstrates that anti-NMDAR encephalitis can present with predominant involvement of the caudate nucleus, expanding the recognized spectrum of its clinical and radiological manifestations. The application of multimodal PET imaging—combining 18 F-FDG to evaluate neuronal metabolic activity and TSPO-specific tracers to detect neuroinflammation—proved valuable in supporting early diagnosis, precise lesion localization, and functional assessment of inflammatory activity. Moreover, this approach offers deeper insight into the underlying disease pathophysiology, linking regional inflammation to specific clinical features. Importantly, PET findings should be interpreted as part of a integrative diagnostic framework, incorporating clinical assessment and cerebrospinal fluid analysis to maximize diagnostic accuracy. Further prospective studies are warranted to standardize imaging protocols and validate the diagnostic and prognostic utility of PET in autoimmune encephalitis, which may ultimately inform clinical guidelines and improve patient management. Abbreviations AE Autoimmune encephalitis NMDAR N-methyl-D-aspartate receptor CSF Cerebrospinal fluid MRI Magnetic resonance imaging PET Positron emission tomography 18 F-FDG 18 F-fluorodeoxyglucose TSPO Translocator protein (18kDa) IVIg Intravenous immunoglobulin mRS modified Rankin Scale ADL Activities of daily living CBA Cell-based assay NGS Next-generation sequencing DWI Diffusion-weighted imaging FLAIR Fluid-attenuated inversion recovery SUVmax Maximum standardized uptake value. Declarations Ethics approval and consent to participate Ethical approval was obtained from the Ethics Committee of Xuanwu Hospital,Capital Medical University. Written informed consent was obtained from the patient's legal guardian(s) for participation. Consent for publication Written informed consent was obtained from the patient's legal guardian(s)for publication of this case report and any accompanying images. Competing interests The authors declare that they have no competing interests. Funding This study received no specific funding. Authors' contributions QP and YB contributed to the conception,design, data collection, and analysis. QP drafted the manuscript. YZ, MJ and DS contributed to data collection. YW, LY, JL, LR and YY reviewed and revised the manuscript critically. All authors read and approved the final manuscript. Acknowledgements Not applicable. Availability of data and materials The datasets used and/or analyzed during the current case report are available from the corresponding author on reasonable request. References Dalmau J, Lancaster E, Martinez-Hernandez E, Rosenfeld MR, Balice-Gordon R: Clinical experience and laboratory investigations in patients with anti-NMDAR encephalitis . 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Neurol Clin Pract 2014, 4 (6):470-473.‘10.1212/cpj.0000000000000074':10.1212/cpj.0000000000000074 Tzoulis C, Vedeler C, Haugen M, Storstein A, Tran GT, Gjerde IO, Biermann M, Schwarzlmüller T, Bindoff LA: Progressive striatal necrosis associated with anti-NMDA receptor antibodies . BMC neurology 2013, 13 :55.‘10.1186/1471-2377-13-55':10.1186/1471-2377-13-55 Wang J, Jin L, Zhang X, Yu H, Ge J, Deng B, Li M, Zuo C, Chen X: Activated microglia by 18F-DPA714 PET in a case of anti-LGI1 autoimmune encephalitis . Journal of Neuroimmunology 2022, 368 .‘10.1016/j.jneuroim.2022.577879':10.1016/j.jneuroim.2022.577879 Leypoldt F, Buchert R, Kleiter I, Marienhagen J, Gelderblom M, Magnus T, Dalmau J, Gerloff C, Lewerenz J: Fluorodeoxyglucose positron emission tomography in anti-N-methyl-D-aspartate receptor encephalitis: distinct pattern of disease . Journal of Neurology, Neurosurgery & Psychiatry 2012, 83 (7):681-686.‘10.1136/jnnp-2011-301969':10.1136/jnnp-2011-301969 孙欣宜, 陈晓煜, 淳于航行, 张宇, 海汪溪, 孟环宇, 周勤明, 何璐, 陈晟, 李彪, 张敏: 18F －DPA －714 PET/MR 在自身免疫性脑炎诊断中的潜在价值 . 中华核医学与分子影像杂志 2025, 45 (4):218-223.‘10.3760/cma.j.cn321828-20241231-00451':10.3760/cma.j.cn321828-20241231-00451 Additional Declarations No competing interests reported. Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-7518038","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":527407716,"identity":"8a245546-ae65-4d7f-86ca-0a81ea1bdba1","order_by":0,"name":"Qing Peng","email":"","orcid":"","institution":"Yiyang Central Hospital","correspondingAuthor":false,"prefix":"","firstName":"Qing","middleName":"","lastName":"Peng","suffix":""},{"id":527407717,"identity":"f7342a61-ee64-4654-b4ff-406a87597841","order_by":1,"name":"Yuye Bai","email":"","orcid":"","institution":"Capital Medical 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1","display":"","copyAsset":false,"role":"figure","size":196309,"visible":true,"origin":"","legend":"\u003cp\u003e(A) Pre-treatment brain MRI (Day 19): Axial T2-FLAIR and DWI sequences show a patchy hyperintense lesion in the head of the left caudate nucleus (arrows) with corresponding reduced ADC values. (B) Post-treatment brain MRI (Day 9 of treatment): The lesion in the left caudate nucleus head has decreased in size.\u003c/p\u003e","description":"","filename":"1.png","url":"https://assets-eu.researchsquare.com/files/rs-7518038/v1/a6abfc001a3a76b23317a866.png"},{"id":93539036,"identity":"7389f11f-1676-40b6-989e-bceb43cf3e72","added_by":"auto","created_at":"2025-10-15 02:13:22","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":206534,"visible":true,"origin":"","legend":"\u003cp\u003eTSPO PET (\u003csup\u003e18\u003c/sup\u003eF-DPA-714) images. (A) Axial view showing increased radiotracer uptake in the head of the left caudate nucleus (arrow). (B) Coronal view showing patchy increased uptake in the bilateral hippocampal regions (arrows).\u003c/p\u003e","description":"","filename":"2.png","url":"https://assets-eu.researchsquare.com/files/rs-7518038/v1/7ccf2286ad469746aab4fde9.png"},{"id":93539885,"identity":"90998c58-232a-4c7b-acc7-f851ab04c0a2","added_by":"auto","created_at":"2025-10-15 02:21:22","extension":"png","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":390586,"visible":true,"origin":"","legend":"\u003cp\u003e\u003csup\u003e18\u003c/sup\u003eF-FDG PET images demonstrating hypometabolism in various regions: (A, B) Right frontal cortex and bilateral parietal lobes; (B, C) Anterior horn of left lateral ventricle (corresponding to caudate head); (D, E, F) Bilateral temporal lobes and hippocampal regions.\u003c/p\u003e","description":"","filename":"3.png","url":"https://assets-eu.researchsquare.com/files/rs-7518038/v1/dd203739092243ee80ca29e6.png"},{"id":109612420,"identity":"25af4dd4-aad5-4968-8778-7632a200d9c4","added_by":"auto","created_at":"2026-05-20 07:56:34","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":1161021,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-7518038/v1/b5d3c0cc-934c-4d58-b2a1-d4e2aeef2398.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"A case report and literature review of severe anti-NMDAR encephalitis with predominant caudate nucleus involvement in a child","fulltext":[{"header":"Background","content":"\u003cp\u003eN-methyl-D-aspartate receptor (NMDAR) encephalitis (NMDARE) is the most common autoimmune encephalitis (AE) in children, characterized by psychiatric abnormalities, impaired consciousness, seizures, movement disorders, sleep disturbances, and autonomic dysfunction, alongside positive cerebrospinal fluid (CSF) anti-NMDAR antibodies[1]. Overall prognosis is generally favorable, but 5–10% of patients may die during the acute phase, and some may experience long-term cognitive or psychiatric sequelae[2]. Severe pediatric NMDAR encephalitis can be diagnosed based on specific criteria, including intensive care admission, need for life-support, severe motor or autonomic dysfunction, inability to communicate or perform daily activities, life-threatening psychiatric symptoms, status epilepticus, or severe neurological dysfunction (modified Rankin Scale score ≥4)[3].Studies have indicated that in some AEs primarily affecting the basal ganglia, chorea and behavioral abnormalities are prominent clinical features[4]. Therefore, early recognition of atypical presentations of NMDAR encephalitis is crucial for improving clinical outcomes.\u003c/p\u003e\n\u003cp\u003eThe 18kDa translocator protein (TSPO) is located on the outer mitochondrial membrane and is involved in cholesterol transport. Its expression in the central nervous system (CNS) is low under physiological conditions but is significantly upregulated in activated glial cells during neuroinflammation[5].Second-generation TSPO radiotracers (e.g., \u003csup\u003e18\u003c/sup\u003eF-DPA-714) enable non-invasive detection of this neuroinflammation via positron emission tomography (PET)[6, 7]. TSPO PET imaging is thus a promising tool for detecting glial activation in various neurological diseases, providing critical insights for pathology, disease activity assessment, and treatment monitoring[8, 9]. \u003csup\u003e18\u003c/sup\u003eF-FDG PET, which measures cerebral glucose metabolism, can sensitively detect regions of neuronal dysfunction often before the onset of clinical symptoms or structural changes on MRI, aiding in the diagnosis and evaluation of neurological disorders like autoimmune encephalitis[10]. The combined application of \u003csup\u003e18\u003c/sup\u003eF-FDG PET and TSPO PET shows potential for enhancing the early identification and differential diagnosis of AE[11].\u003c/p\u003e"},{"header":"Case Presentation ","content":"\u003cp\u003eIntroduction of the case\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eA 15-year-old male was admitted with the chief complaint of\u0026quot;slurred speech, numbness and weakness in the right hand for 17 days, and episodic loss of consciousness with limb convulsions for 7 days.\u0026quot;\u003c/p\u003e\n\u003cp\u003eSeventeen days prior to admission, the patient developed slurred and incoherent speech without obvious cause, accompanied by numbness in the right hand. The next day, he developed left-deviated mouth and tongue, right facial numbness, and weakened right hand grip strength, making it difficult to hold objects. Cranial CT at a local hospital showed no hemorrhage, and initial suspicion was cerebral infarction. Subsequent brain MRI with DWI and MRA, and cerebral angiography showed no significant abnormalities. No specific treatment was given, and symptoms persisted.\u003c/p\u003e\n\u003cp\u003eTen days pre-admission, he developed recurrent low-grade fever (37.3\u0026deg;C \u0026ndash; 38.1\u0026deg;C) without cough or diarrhea. Seven days pre-admission, he experienced episodes of loss of consciousness with limb convulsions, eye rolling, and foaming at the mouth, lasting seconds to minutes, occurring primarily during sleep (8 episodes total). He was started on lacosamide (100 mg twice daily) at another hospital, after which convulsions ceased. Six days pre-admission, he developed impaired speech comprehension and expression. Three days pre-admission, he became unable to perform activities of daily living (ADLs) independently but could walk. One day pre-admission, he exhibited abnormal mental and behavioral changes. On admission, he had episodic involuntary orofacial movements and excessive sweating. Since onset, he also had poor mental state, sleep disturbances, social withdrawal, reduced appetite, urinary incontinence, and constipation. Past medical history was unremarkable.\u003c/p\u003e\n\u003cp\u003eExaminations and findings On admission,physical examination: T 37.3\u0026deg;C, P 78 bpm, R 20 breaths/min, BP 127/82 mmHg. Well-nourished (Ht 170 cm, Wt 95 kg). Alert but with mixed aphasia, intermittently repeating single words, and paroxysmal involuntary facial twitching. Cognitive assessment was uncooperative. Pupils were equal and reactive (3mm). Nasolabial folds appeared symmetric, but patient could not cooperate with cranial nerve testing. Limb movement was observed but formal strength testing was uncooperative. Muscle tone was normal. Tendon reflexes were active, with bilateral Hoffman\u0026apos;s sign and ankle clonus. Sensory and coordination testing were uncooperative. No neck stiffness or pathological signs.\u003c/p\u003e\n\u003cp\u003eRoutine blood, urine, stool tests, comprehensive biochemistry, thyroid function, tumor markers, ECG, chest CT, and abdominal ultrasound were unremarkable.\u003c/p\u003e\n\u003cp\u003eLumbar puncture revealed an opening pressure of 26 cmH2O (Adolescents are capped at 25 cmH2O). CSF analysis: WBC 51 \u0026times; 10^6/L (normal: 0\u0026ndash;15 \u0026times; 10^6/L), clear appearance; biochemistry normal. Autoimmune encephalitis antibody panel (cell-based assay, CBA) was positive for anti-NMDAR IgG (CSF 1:32; serum 1:320); antibodies against CASPR2, AMPAR1/2, LGI1, GABABR, DPPX, and IgLON5 were negative. Paraneoplastic antibody panel (Hu, Ri, Yo, CV2, Amphiphysin, GAD65, PNMA2, Recoverin, SOX1, Titin, Tr, Zic4) and CNS demyelinating antibody panel (AQP4, GFAP, MBP, MOG) were negative. CSF IgG oligoclonal bands were positive, serum oligoclonal bands were negative. CSF-specific oligoclonal bands were positive. 24-hour intrathecal IgG synthesis rate was slightly elevated at 9.06 mg/24h (normal: 0\u0026ndash;9 mg/24h). CSF microscopy showed scattered lymphocytes and few mononuclear cells. CSF next-generation sequencing (NGS) for pathogens was negative.\u003c/p\u003e\n\u003cp\u003eOn day 19 of illness, brain MRI with epilepsy protocol (including DWI and contrast) showed an abnormal signal in the head of the left caudate nucleus (Fig. 1A). Video EEG showed focal slow waves. TSPO PET (\u003csup\u003e18\u003c/sup\u003eF-DPA-714) showed abnormally increased uptake in the left caudate head (SUVmax ~5.66) and patchy uptake in both hippocampi (SUVmax ~3.44) (Fig. 2). \u003csup\u003e18\u003c/sup\u003eF-FDG PET/CT showed: a) hypometabolism in the left caudate head region, consistent with the inflammatory lesion on TSPO PET; b) reduced metabolism in bilateral parietal and temporal lobes (right \u0026gt; left); c) mild-moderate hypometabolism in the right frontal cortex and hippocampus (Fig. 3). A follow-up MRI 9 days after treatment showed reduction in the size of the left caudate head lesion (Fig. 1B).\u003c/p\u003e\n\u003cp\u003eTreatment, outcome and follow-up\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eBased on clinical presentation,positive anti-NMDAR antibodies, and imaging findings, a diagnosis of anti-NMDAR encephalitis was made. The patient received intravenous methylprednisolone pulse therapy combined with intravenous immunoglobulin (IVIg), along with antiepileptic drugs and management of psychiatric symptoms.\u003c/p\u003e\n\u003cp\u003eDuring hospitalization, seizures and involuntary movements resolved. However, low-grade fever, communication difficulties, excessive sweating, constipation, and occasional behavioral abnormalities persisted. Vital signs showed temperature fluctuations (37.3\u0026deg;C \u0026ndash; 38.4\u0026deg;C) and heart rate variability (68 \u0026ndash; 108 bpm); blood pressure remained normal.\u003c/p\u003e\n\u003cp\u003eAt one-week post-discharge, the family reported no fever for 3 days, improved simple communication, and more stable mood, but sweating persisted. At 12-day follow-up, sweating had normalized, temperature was normal, he could speak short sentences (though longer sentences remained difficult), no psychiatric symptoms were noted, but right hand clumsiness and numbness persisted. He could partially perform ADLs independently (dressing, using toilet). At the 3-month follow-up, he was fully independent in ADLs with normal language function. Occasional emotional outbursts were noted, but no seizures occurred. He had fragmentary memory loss regarding the hospitalization period and reported worsened recent memory.\u003c/p\u003e"},{"header":"Discussion and conclusions","content":"\u003cp\u003eThis case describes a 15-year-old boy with severe anti-NMDAR encephalitis meeting diagnostic criteria [12, 13], presenting atypically with initial stroke-like symptoms and predominant caudate nucleus involvement on imaging.\u003c/p\u003e\n\u003cp\u003eThe pathogenesis involves antibodies targeting GluN1 subunits of NMDARs, leading to receptor internalization and downstream effects including excitotoxicity[14]. \u0026nbsp; Common triggers include tumors (e.g., ovarian teratoma in young females) and viral infections (e.g., herpes simplex virus encephalitis) [13, 15-18].This patient had no identified tumor or clear viral trigger.First-line immunotherapy for NMDAR encephalitis typically involves corticosteroids and IVIg, ideally initiated early (\u0026lt;15 days from onset) for better prognosis [19, 20].This patient received this regimen with good response.\u003c/p\u003e\n\u003cp\u003eIsolated basal ganglia involvement in NMDAR encephalitis is rare. Literature reviews suggest adult incidence (6.25\u0026ndash;16.1%) may be higher than in children (2.4\u0026ndash;9.1%), with isolated involvement being extremely uncommon[21-24]. We reviewed 7 published cases of NMDAR encephalitis with basal ganglia involvement (Table 1).\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eTable 1Clinical, paraclinical and radiological features of reported anti-NMDAR encephalitis cases with basal ganglia involvement\u003c/p\u003e\n\u003cdiv align=\"Left\"\u003e\n \u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\" width=\"727\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 14.0303%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eCase(Reference)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 3.989%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eSex\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 8.8033%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eAge,years\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 17.0564%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eClinicalpresentation\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 12.6547%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eAffectedarea\u003c/strong\u003e\u003c/p\u003e\n \u003cp\u003e\u003cstrong\u003e(s)onMRI\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 14.4429%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eSerumantibodies\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 12.6547%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eCSFantibodies\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 16.3686%;\"\u003e\n \u003cp\u003e\u003cstrong\u003eTreatment\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 14.0303%;\"\u003e\n \u003col\u003e\n \u003cli\u003e[25]\u003c/li\u003e\n \u003c/ol\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 3.989%;\"\u003e\n \u003cp\u003eM\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 8.8033%;\"\u003e\n \u003cp\u003e66\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 17.0564%;\"\u003e\n \u003cp\u003eFocal seizures (R arm/hand), progressing to GTCS; later focal clonic seizures (L arm/hand)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 12.6547%;\"\u003e\n \u003cp\u003eL caudate \u0026amp; putamen; later R caudate, putamen, L medial frontal lobe\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 14.4429%;\"\u003e\n \u003cp\u003eNot reported\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 12.6547%;\"\u003e\n \u003cp\u003eNMDAR-IgG positive\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 16.3686%;\"\u003e\n \u003cp\u003eMethylprednisolone, AEDs\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 14.0303%;\"\u003e\n \u003col start=\"2\"\u003e\n \u003cli\u003e[26]\u003c/li\u003e\n \u003c/ol\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 3.989%;\"\u003e\n \u003cp\u003eM\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 8.8033%;\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 17.0564%;\"\u003e\n \u003cp\u003e\u0026nbsp;Impaired consciousness, rhythmic arm movements, clenched jaw, drooling\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 12.6547%;\"\u003e\n \u003cp\u003eBilateral insular regions, fronto-parietal areas, posterior limb of internal capsule, L medial temporal lobe\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 14.4429%;\"\u003e\n \u003cp\u003eNMDAR-IgG positive (at 1 year)\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 12.6547%;\"\u003e\n \u003cp\u003eNot reported\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 16.3686%;\"\u003e\n \u003cp\u003eAEDs\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 14.0303%;\"\u003e\n \u003col start=\"3\"\u003e\n \u003cli\u003e[27]\u003c/li\u003e\n \u003c/ol\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 3.989%;\"\u003e\n \u003cp\u003eM\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 8.8033%;\"\u003e\n \u003cp\u003e32\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 17.0564%;\"\u003e\n \u003cp\u003e\u0026nbsp;Cognitive decline, diplopia, ataxia, dysarthria, dysphagia, tremors (head/neck/limbs)\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 12.6547%;\"\u003e\n \u003cp\u003ePons, midbrain, bilateral basal ganglia\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 14.4429%;\"\u003e\n \u003cp\u003enegative\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 12.6547%;\"\u003e\n \u003cp\u003eNMDAR-Ab positive\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 16.3686%;\"\u003e\n \u003cp\u003eMethylprednisolone, IVIg\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 14.0303%;\"\u003e\n \u003col start=\"4\"\u003e\n \u003cli\u003e[28]\u003c/li\u003e\n \u003c/ol\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 3.989%;\"\u003e\n \u003cp\u003eF\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 8.8033%;\"\u003e\n \u003cp\u003e28\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 17.0564%;\"\u003e\n \u003cp\u003eHeadache, fever, apathy\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 12.6547%;\"\u003e\n \u003cp\u003eL frontal \u0026amp; temporal lobes, basal ganglia, corpus callosum, R frontal lobe\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 14.4429%;\"\u003e\n \u003cp\u003eNot reported\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 12.6547%;\"\u003e\n \u003cp\u003eNMDAR-IgG (1:32)\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 16.3686%;\"\u003e\n \u003cp\u003eMethylprednisolone, IVIg\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 14.0303%;\"\u003e\n \u003col start=\"5\"\u003e\n \u003cli\u003e[29]\u003c/li\u003e\n \u003c/ol\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 3.989%;\"\u003e\n \u003cp\u003eM\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 8.8033%;\"\u003e\n \u003cp\u003e42\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 17.0564%;\"\u003e\n \u003cp\u003e\u0026nbsp;Psychiatric symptoms, seizures, parkinsonism\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 12.6547%;\"\u003e\n \u003cp\u003eL caudate head, bilateral medial temporal lobes (L \u0026gt; R)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 14.4429%;\"\u003e\n \u003cp\u003eNot reported\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 12.6547%;\"\u003e\n \u003cp\u003eNMDAR-IgG\u0026nbsp;（1：80）\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 16.3686%;\"\u003e\n \u003cp\u003eAEDs, methylprednisolone, IVIg\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 14.0303%;\"\u003e\n \u003col start=\"6\"\u003e\n \u003cli\u003e[30]\u003c/li\u003e\n \u003c/ol\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 3.989%;\"\u003e\n \u003cp\u003eM\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 8.8033%;\"\u003e\n \u003cp\u003e21\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 17.0564%;\"\u003e\n \u003cp\u003eBradykinesia, arm numbness, psychiatric symptoms, cognitive impairment, alcohol sensitivity, dysarthria\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 12.6547%;\"\u003e\n \u003cp\u003eR caudate \u0026amp; lentiform nucleus\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 14.4429%;\"\u003e\n \u003cp\u003eNMDAR-IgG positive\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 12.6547%;\"\u003e\n \u003cp\u003eNMDAR-IgG positive\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 16.3686%;\"\u003e\n \u003cp\u003eIVIg, mycophenolate mofetil\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 14.0303%;\"\u003e\n \u003col start=\"7\"\u003e\n \u003cli\u003e[31]\u003c/li\u003e\n \u003c/ol\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 3.989%;\"\u003e\n \u003cp\u003eM\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 8.8033%;\"\u003e\n \u003cp\u003e18\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 17.0564%;\"\u003e\n \u003cp\u003eProgressive dystonia, abnormal posture, involuntary movements\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 12.6547%;\"\u003e\n \u003cp\u003ePutamen, caudate nucleus\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 14.4429%;\"\u003e\n \u003cp\u003e\u0026nbsp;Not reported\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 12.6547%;\"\u003e\n \u003cp\u003eNMDAR-IgG positive\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 16.3686%;\"\u003e\n \u003cp\u003e\u0026nbsp;IVIg, botulinum toxin A injections\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003c/table\u003e\n\u003c/div\u003e\n\u003cp\u003eAbbreviations: AEDs, antiepileptic drugs; CSF, cerebrospinal fluid; GTCS, generalized tonic-clonic seizure; IVIg, intravenous immunoglobulin; L, left; R, right; NMDAR, N-methyl-D-aspartate receptor.\u003c/p\u003e\n\u003cp\u003eAnalysis of seven identified cases of NMDARE with basal ganglia involvement yielded the following characteristics: Regarding gender distribution, six cases (85.7%) were male and one was female. This finding contrasts with the typical presentation of anti-NMDAR encephalitis, which shows a female predominance, particularly among cases associated with ovarian teratomas. This suggests that anti-NMDAR encephalitis with prominent basal ganglia involvement may have a distinct gender predisposition, being more frequently observed in males.\u003c/p\u003e\n\u003cp\u003eAge distribution was wide, ranging from 2 to 66 years, with a median age of 28 years. Among the core clinical features, movement disorders\u0026mdash;most commonly manifesting as dystonia, tremor, involuntary movements, or Parkinsonism\u0026mdash;and neuropsychiatric symptoms\u0026mdash;including memory impairment, behavioral abnormalities, and apathy\u0026mdash;were highly prevalent (5/7 cases, 71.4%). Seizures were reported in three cases, presenting either as focal seizures or evolving into generalized tonic-clonic seizures. (It is noteworthy that seizures were also present in the case described in this report.)\u003c/p\u003e\n\u003cp\u003eCranial MRI findings of basal ganglia lesions were categorized into three patterns: unilateral focal lesions (Cases 1, 5, and 6), bilateral symmetrical lesions (Cases 3, 7), and mixed diffuse involvement (Cases 2 and 4). According to the cranial MRI typology proposed by Khatib et al. [21], the imaging presentations primarily consisted of patchy blurred lesions (4 cases) and widespread FLAIR hyperintensity (3 cases).\u003c/p\u003e\n\u003cp\u003eMechanistic Insights into Caudate Nucleus Predilection\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eThis case provides valuable insights into the pathogenesis of anti-NMDAR encephalitis, particularly its selective involvement of specific brain regions such as the caudate nucleus. The unique imaging features compel us to explore mechanisms beyond the traditional model of direct antibody-mediated pathogenicity.\u003c/p\u003e\n\u003cp\u003eThe reasons for the caudate nucleus\u0026apos;s predilection in this case are likely multifactorial. While NMDAR antibodies bind to the GluN1 subunit, causing receptor internalization and synaptic dysfunction [14], the question of why antibodies target different brain regions in different patients remains. We propose two non-mutually exclusive hypotheses. First, receptor subtype distribution heterogeneity: the caudate nucleus is rich in NMDARs containing the GluN2B subunit, which is crucial for cognitive and motor functions. It is plausible that the patient\u0026apos;s antibodies had a higher affinity for or easier access to receptors with this specific subunit composition. Second, regional disruption of the blood-brain barrier (BBB): the permeability of the BBB in the basal ganglia may vary. A minor inflammatory trigger (e.g., a prodromal infection) could have induced a transient, focal opening of the BBB in the caudate nucleus, allowing antibodies to enter and initiate a localized immune response. This mechanism could elegantly explain the initial \u0026quot;stroke-like\u0026quot; presentation.\u003c/p\u003e\n\u003cp\u003eFurthermore, the intense microglial activation revealed by TSPO PET suggests that neuroinflammation is a core amplifier of the disease process, not merely a bystander phenomenon. Activated microglia can release pro-inflammatory cytokines, which may further exacerbate NMDAR internalization and directly contribute to neuronal dysfunction, creating a vicious cycle that amplifies the initial antibody-mediated injury.\u003c/p\u003e\n\u003cp\u003eFinally, the concomitant involvement of the hippocampus and caudate nucleus suggests a disruption of the hippocampo-striatal loop. These structures are functionally interconnected via dopaminergic and cholinergic pathways, jointly subserving learning, memory, motivation, and motor control. We hypothesize that the antibody attack on these two key nodes disrupted their functional connectivity, providing a neural substrate for the patient\u0026apos;s mixed cognitive, psychiatric, and motor symptoms.\u003c/p\u003e\n\u003cp\u003eIn this case, TSPO PET revealed a distinct pattern of asymmetrically elevated radiotracer uptake, most notably within the left caudate nucleus head and to a lesser extent in bilateral hippocampal regions. This asymmetrical increase in TSPO binding is mechanistically significant, as TSPO is markedly upregulated on activated microglia during neuroinflammatory processes. The observed PET signal thus provides in vivo evidence of active gliosis, which aligns with the primary pathophysiological mechanism of anti-NMDAR encephalitis\u0026mdash;i.e., antibody-mediated internalization of NMDARs, subsequent synaptic dysfunction, and initiation of a localized neuroimmune response.\u003c/p\u003e\n\u003cp\u003eThe bilateral hippocampal involvement evident on TSPO PET is consistent with the high density of NMDARs in limbic regions. Antibody binding here likely disrupts synaptic plasticity and gamma-aminobutyric acid (GABA)ergic transmission, leading to hyperexcitability and clinical manifestations such as memory deficits, psychiatric symptoms, and seizures. Importantly, the significant TSPO uptake in the left caudate nucleus underscores that extra-limbic structures, particularly basal ganglia nuclei rich in NMDAR-expressing neurons, may also become engaged in the inflammatory cascade. This may mechanistically underlie prominent motor manifestations including orofacial dyskinesia, dystonia, and autonomic instability.\u003c/p\u003e\n\u003cp\u003eThese observations resonate with earlier work by Wang et al. [32], who used TSPO PET to demonstrate that neuroinflammation in autoimmune encephalitides such as anti-LGI1 encephalitis often extends beyond classic limbic circuits to involve subcortical and basal ganglia structures. The convergence of findings across antibody-mediated encephalitides suggests that basal ganglia involvement may reflect a shared propensity for certain neural networks to exhibit inflammatory changes following autoantibody-mediated disruption.\u003c/p\u003e\n\u003cp\u003eFurthermore, the hypometabolism observed on \u003csup\u003e18\u003c/sup\u003eF-FDG PET in the left caudate, hippocampi, and diffuse cortical regions likely reflects downstream neuronal dysfunction following sustained inflammation and receptor internalization. This metabolic reduction may indicate a state of neuronal hypoactivity or injury subsequent to excitotoxicity and chronic synaptic disruption. The divergence of this pattern from the metabolic signatures previously reported by Ge et al. [33] suggests heterogeneity in functional network involvement among patients, possibly reflecting differences in autoantibody titers, symptom chronicity, or individual patterns of immune activation.\u003c/p\u003e\n\u003cp\u003eThe superior sensitivity of TSPO PET over MRI in detecting neuroinflammation, as reported by Sun et al. [34], further highlights the utility of molecular imaging for uncovering active immune pathology in seropositive patients with non-diagnostic conventional imaging. This reinforces the mechanistic rationale for employing biomarkers of glial activation to probe the neuroimmune basis of clinical symptoms, especially in cases with atypical or subtle structural findings.\u003c/p\u003e"},{"header":"Conclusions","content":"\u003cp\u003eThis case demonstrates that anti-NMDAR encephalitis can present with predominant involvement of the caudate nucleus, expanding the recognized spectrum of its clinical and radiological manifestations. The application of multimodal PET imaging—combining \u003csup\u003e18\u003c/sup\u003eF-FDG to evaluate neuronal metabolic activity and TSPO-specific tracers to detect neuroinflammation—proved valuable in supporting early diagnosis, precise lesion localization, and functional assessment of inflammatory activity. Moreover, this approach offers deeper insight into the underlying disease pathophysiology, linking regional inflammation to specific clinical features.\u003c/p\u003e\n\u003cp\u003eImportantly, PET findings should be interpreted as part of a integrative diagnostic framework, incorporating clinical assessment and cerebrospinal fluid analysis to maximize diagnostic accuracy. Further prospective studies are warranted to standardize imaging protocols and validate the diagnostic and prognostic utility of PET in autoimmune encephalitis, which may ultimately inform clinical guidelines and improve patient management.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cdiv class=\"DefinitionList\"\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003eAE\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eAutoimmune encephalitis\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003eNMDAR\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eN-methyl-D-aspartate receptor\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003eCSF\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eCerebrospinal fluid\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003eMRI\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eMagnetic resonance imaging\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003ePET\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003ePositron emission tomography\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003e\u003csup\u003e18\u003c/sup\u003eF-FDG\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003e\u003csup\u003e18\u003c/sup\u003eF-fluorodeoxyglucose\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003eTSPO\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eTranslocator protein (18kDa)\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003eIVIg\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eIntravenous immunoglobulin\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003emRS\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003emodified Rankin Scale\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003eADL\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eActivities of daily living\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003eCBA\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eCell-based assay\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003eNGS\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eNext-generation sequencing\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003eDWI\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eDiffusion-weighted imaging\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003eFLAIR\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eFluid-attenuated inversion recovery\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003eSUVmax\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eMaximum standardized uptake value.\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003c/div\u003e"},{"header":"Declarations","content":"\u003cp\u003eEthics approval and consent to participate\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eEthical approval was obtained from the Ethics Committee of Xuanwu Hospital,Capital Medical University. Written informed consent was obtained from the patient's legal guardian(s) for participation.\u003c/p\u003e\n\u003cp\u003eConsent for publication\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eWritten informed consent was obtained from the patient's legal guardian(s)for publication of this case report and any accompanying images.\u003c/p\u003e\n\u003cp\u003eCompeting interests\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eThe authors declare that they have no competing interests.\u003c/p\u003e\n\u003cp\u003eFunding\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eThis study received no specific funding.\u003c/p\u003e\n\u003cp\u003eAuthors' contributions\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eQP and YB contributed to the conception,design, data collection, and analysis. QP drafted the manuscript. YZ, MJ and DS contributed to data collection. YW, LY, JL, LR and YY reviewed and revised the manuscript critically. All authors read and approved the final manuscript.\u003c/p\u003e\n\u003cp\u003eAcknowledgements\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eNot applicable.\u003c/p\u003e\n\u003cp\u003eAvailability of data and materials\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eThe datasets used and/or analyzed during the current case report are available from the corresponding author on reasonable request.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n\u003cli\u003eDalmau J, Lancaster E, Martinez-Hernandez E, Rosenfeld MR, Balice-Gordon R: \u003cstrong\u003eClinical experience and laboratory investigations in patients with anti-NMDAR encephalitis\u003c/strong\u003e. \u003cem\u003eThe Lancet Neurology \u003c/em\u003e2011, \u003cstrong\u003e10\u003c/strong\u003e(1):63-74.\u0026lsquo;10.1016/s1474-4422(10)70253-2\u0026apos;:10.1016/s1474-4422(10)70253-2\u003c/li\u003e\n\u003cli\u003eDalmau J, Armangu\u0026eacute; T, Planagum\u0026agrave; J, Radosevic M, Mannara F, Leypoldt F, Geis C, 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\u003cstrong\u003e45\u003c/strong\u003e(4):218-223.\u0026lsquo;10.3760/cma.j.cn321828-20241231-00451\u0026apos;:10.3760/cma.j.cn321828-20241231-00451\u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":true,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"N-methyl-D-aspartate receptor encephalitis, Caudate nucleus, Magnetic resonance imaging, 18F-fluorodeoxyglucose positron emission tomography imaging, Targeted 18×10³ transposon positron emission tomography","lastPublishedDoi":"10.21203/rs.3.rs-7518038/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-7518038/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003eBackground: Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is an autoimmune encephalitis with diverse imaging manifestations. Isolated involvement of the caudate nucleus is rare and can be easily misdiagnosed, especially in the early stages when inflammatory symptoms are not apparent. This report describes a pediatric case of severe anti-NMDAR encephalitis with predominant involvement of the caudate nucleus.\u003c/p\u003e\n\u003cp\u003eCase presentation: A 15-year-old male initially presented with stroke-like episodes, misdiagnosed as cerebral infarction. Subsequently, he developed seizures, recurrent low-grade fever, psychiatric symptoms, involuntary orofacial movements, autonomic dysfunction, loss of speech, and inability to perform activities of daily living. Brain MRI revealed a lesion in the left caudate nucleus. The diagnosis was confirmed by positive serum and cerebrospinal fluid anti-NMDAR IgG antibodies. Targeted positron emission tomography (PET) using \u003csup\u003e18\u003c/sup\u003eF-fluorodeoxyglucose (\u003csup\u003e18\u003c/sup\u003eF-FDG) and the \u003csup\u003e18\u003c/sup\u003eF-DPA-714 tracer for the 18kDa translocator protein (TSPO) identified a core inflammatory area and extensive regions of neuronal dysfunction. The patient's condition gradually improved following immunotherapy and symptomatic treatment.\u003c/p\u003e\n\u003cp\u003eConclusion: This case provides valuable insights into the pathogenesis of anti-NMDAR encephalitis, particularly its selective involvement of specific brain regions such as the caudate nucleus. The unique imaging features compel us to explore mechanisms beyond the traditional model of direct antibody-mediated pathogenicity.\u003c/p\u003e","manuscriptTitle":"A case report and literature review of severe anti-NMDAR encephalitis with predominant caudate nucleus involvement in a child","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-10-15 02:13:18","doi":"10.21203/rs.3.rs-7518038/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"e8796395-ba89-418b-9840-16c600572ed3","owner":[],"postedDate":"October 15th, 2025","published":true,"recentEditorialEvents":[{"type":"decision","content":"Withdrawn","date":"2026-05-20T07:49:34+00:00","index":"","fulltext":""}],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2026-05-20T07:55:57+00:00","versionOfRecord":[],"versionCreatedAt":"2025-10-15 02:13:18","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-7518038","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-7518038","identity":"rs-7518038","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}