u/Helpful-Dhamma-Heart

> "By way of generalisation, autoantibody-mediated disorders often present rapidly, over a few days to weeks. However, we have observed more chronic courses, of between 1 and 5 years, particularly in leucine-rich glioma-inactivated protein 1 (LGI1)-antibody, contact-associated protein 2 (CASPR2)-antibody and immunoglobulin-like cell-adhesion molecule 5 (IgLON5)-antibody syndromes. These findings mean that time to disease nadir is often outside of the 3-month duration which appears in diagnostic guidelines. In our clinical experience, these more insidious courses—which are sometimes more akin to neurodegenerative presentations than florid encephalitis syndromes—often lead to a delayed diagnosis, and hence late commencement of immunotherapy."

Autoimmune encephalitis: clinical spectrum and management Paper

Personal reflection:

It seems to be an almost taboo subject. Chronic AIE, is said to be atypical and treated as if it doesn't exist. Yet those patients with it suffer great delays due to not for-filling the 3 month detection window that is baked into the diagnostic guidelines. This is an areas of science that does need more research and reporting, as such cases rarely make it into papers, continuing the gap which treats such cases as impossible.

Often the severity of symptoms are treated as subjective or non-specific. EGG, CSF and FDG-PET/MRI findings dismissed in isolation.

Worse, chronic cases with rare antibodies may find further delays as initial testing does not find a treatable antibody, and all symptoms and diagnostics get dismissed in isolation.

A case may suffer months to years of delays, due to lack of awareness that such cases do exist.

I do feel that the criteria are used retrospectively to dismiss cases, which is the wrong means - without reviewing a case, you can not use blanket criteria to make assumptions. Papers that push the "misdiagnosis" due to chronic, really harm these patients pathway to treatment.

Obviously there are many cases that can get diagnosed wrongly or too weakly, but a disease that is so difficult as AIE, requires judicious review, not reactive criteria.

PNS AIE, for example often fall outside this.

AIE in general a extreme disease with unbearable symptoms, it seems to have fairly strong set of diagnostics in most cases. Hopefully there is greater awareness of such cases in the future - so they get detected earlier rather then later.

To give you an example; Autoimmune Encephalitis Misdiagnosis in Adults this highly posted paper sounds good in theory. However it uses criteria retrospectively to dismiss past cases as not AIE.

Applying functional/ pych / insidious labels to dismiss cases misses the point. This is dangerous as without reviewing each case, one does not know the full dynamics that lead to a diagnosis.

Given that many AIE cases are sero-negative (40% or so), dismissing cases based on labels and criteria too quickly seem to increase this gap for real chronic AIE.

The paper does have a few lines that help such patients, however the energy is directed toward bucket labels stating this as a reason that they dont have AIE.

Just an example of a gap being caused by too tight ideas that can lead a widening bias.

> "Autoimmune encephalitis is a relatively new category of immune-mediated disease involving the central nervous system that demonstrates a widely variable spectrum of clinical presentations, ranging from the relatively mild or insidious onset of cognitive impairment to more complex forms of encephalopathy with refractory seizure."

> "When brain MR imaging findings are absent but the clinical findings suggest the possibility of an autoimmune encephalitis, brain FDG-PET imaging may be indicated, especially early in the disease process if clinical suspicion for autoimmune encephalitis is high, because it appears to be a more sensitive imaging technique for detecting temporal lobe abnormalities with normal brain MR imaging findings."

> "Autoimmune encephalitis is an important diagnostic consideration in patients presenting with new onset of altered mental status of unclear etiology. ... Neuroimaging findings will most often involve the limbic structures, but involvement of the striatum, diencephalon, or rhombencephalon can be seen. A subset of patients with autoimmune encephalitis will have no neuroimaging findings despite profound neuropsychiatric dysfunction, but serum antibody testing can still ultimately lead to the diagnosis of autoimmune encephalitis. While there is no single diagnostic feature that can make this diagnosis in isolation, recognizing a certain constellation of findings during the work-up of complex and atypical cases of new-onset altered mental status is crucial to confirm the diagnosis with serologic testing and initiate treatment in a timely fashion."

^(Autoimmune Encephalitis: Pathophysiology and Imaging Review of an Overlooked Diagnosis)

“This case series (Bahramy et al., 2026) shows that AIE can present with normal MRI, movement disorders (orofacial dyskinesia), and can be misdiagnosed as psychiatric illness. It also confirms that AIE can have a chronic course – not just acute/subacute – leading to delayed diagnosis and treatment.”

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1. AIE can present with a wide range of symptoms, making diagnosis challenging

> “Patients may present with a wide range of symptoms, making the diagnosis particularly challenging.”

2. MRI can be normal in autoimmune encephalitis

> “Brain MRI often shows no abnormalities, while EEG frequently shows abnormalities, most notably diffuse slowing.”

3. Movement disorders (including orofacial dyskinesia) are a feature of AIE

> “Clinical features typically include neuropsychiatric symptoms (>80%), behavioral changes, seizures, and movement disorders, such as orofacial dyskinesia.”

4. Psychiatric symptoms can be the presenting feature, leading to misdiagnosis

> “A critical differential diagnosis of secondary schizophreniform psychosis is anti-NMDAR encephalitis, which may present with acute psychosis.”

5. Autoimmune encephalitis can present with chronic, progressive, or indolent courses

> “AIE can manifest in acute, subacute, or even chronic forms, often resulting in delayed diagnosis and consequently, delayed initiation of appropriate therapy.”

6. CV2/CRMP5 (intracellular antigen) – ataxia, chorea, dysarthria, and other features

> “Clinical features of CV2/CRMP5-associated encephalitis include peripheral neuropathy (47%), autonomic neuropathy (31%), cerebellar ataxia (26%), subacute dementia (25%), chorea (11%), and cranial neuropathies (17%).”

7. CV2/CRMP5 can present with brainstem/cerebellar symptoms without limbic involvement

> “In CV2/CRMP5-related paraneoplastic chorea … MRI often shows T2 hyperintensities in the caudate and putamen nuclei (striatum).”

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Bahramy MA, Pedramfard P, Shahriarirad R. Three Challenging Cases of Autoimmune Encephalitis: A Case-Series and a Review of the Literature. Clin Case Rep. Published 2026 Jan 4.

There is quite a wide differential diagnosis for Brainstem Enchephilius, MS, NMOSD, Anti-MOG, GFAP Astrocytopathy, ADEM/AHLE, Bickerstaff BS Encephalitis, CLIPPERS, Behcet's Disease, Sjögren Syndrome, Systemic Lupus Erythematosus, Paraneoplastic (Anti-Hu), Paraneoplastic (Anti-Ma2), Paraneoplastic (Anti-Ri), Paraneoplastic (KLHL11), Paraneoplastic (LUZP4).

I have included at the end the key quote related to paraneoplastic autoimmune encephalitis cases...

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^(Autoimmune Brainstem Encephalitis: An Illustrative Case and a Review of the Literature, Zoghaib etc all, 2021. )^(PMC8269049)

> "Abstract > > Autoimmune brainstem encephalitis (BSE) is a rare neurological condition with a wide range of underlying etiologies. It can be subdivided into two broad groups: a primary inflammatory disease of the central nervous system (CNS) or a brainstem disorder secondary to systemic diseases where the CNS is only one of many affected organs. Symptoms range from mild to life-threatening manifestations. Most cases respond well to immunotherapy. Therefore, broad and in-depth knowledge of the various inflammatory disorders that target the brainstem is essential for guiding the diagnostic approach and assisting in early initiation of appropriate therapy. We herein report on a case of BSE and provide an overview of the various causes of autoimmune BSE with an emphasis on the clinical manifestations and diagnostic approach.
>
> ...3.8. Paraneoplastic Syndromes
>
> Paraneoplastic diseases of the CNS are a group of immune-mediated disorders with a wide range of clinical manifestations. Although BSE is not commonly implicated in paraneoplastic syndromes, some antibodies have been linked to BS dysfunction such as anti-Hu, anti-Ma2, anti-Ri, Kelch-like protein-11 (KLHL11) IgG, and Leucine Zipper 4 (LUZP4) IgG antibodies [71,72,73]. These entities have been classified as intermediate-risk phenotypes as per the diagnostic criteria for paraneoplastic neurologic syndromes [74]. The onset is typically subacute, with rapid worsening and often devastating consequences.
>
> Anti-Hu antibodies are classically associated with paraneoplastic encephalomyelitis, almost always in the setting of small cell lung carcinoma. Early in the disease course, more focal syndromes can be seen, such as limbic encephalitis, cerebellar degeneration, or BSE. BSE is the predominant syndrome in 11% of cases. This entity has a distinct tropism for the medulla and patients often present with dysphagia, dysarthria, and hypoventilation [76]. Other manifestations may include CN VI/VII palsy, vertical nystagmus, and ataxia. MRI and CSF analysis are typically normal. The prognosis is usually poor despite immunotherapy and treatment of the underlying tumor.
>
> Anti-Ma2 is typically a disease of young men with testicular germ-cell tumors, while in the older population, it is more commonly associated with lung and breast malignancies. Anti-Ma2-associated encephalitis characteristically affects the limbic system, hypothalamus, and BS. Midbrain involvement commonly manifests as supranuclear vertical gaze palsy and oculomotor nuclei involvement. Other characteristic symptoms include excessive daytime sleepiness, narcolepsy, cataplexy, rapid eye movement (REM)-sleep abnormalities, hyperphagia, and memory impairment. Brain MRI may show T2-hyperintense lesions in the superior colliculi and periaqueductal region. Roughly one third of patients can be expected to respond to tumor resection and immunotherapy.
>
> Anti-Ri antibodies also have a tropism for the BS. These are the least common paraneoplastic autoantibodies, primarily encountered in patients with breast and ovarian cancers. Patients typically present with signs of BS, cerebellar, and spinal cord dysfunction. BS dysfunction often manifests as an opsoclonus-myoclonus syndrome, ophthalmoplegia, and facial sensory symptoms. Treatment of underlying cancer can also lead to a decrease in the antibody titer and improvement of symptoms.
>
> Newly described paraneoplastic antibodies (i.e., KLHL11 IgG and LUZP4 IgG) have also been implicated in patients with BS dysfunction. KLHL11 antibodies are generally associated with testicular germ cell tumors in men and present the clinical picture of a rhombencephalitis typically with hearing loss and tinnitus. Brain MRI, although normal early in the disease, may demonstrate T2/FLAIR abnormalities in the BS or limbic system. Encephalitis associated with KLHL11 IgG is generally refractory to treatment, and only 25% of patients respond to immunotherapy. LUZP4 antibodies, on the other hand, typically are present in patients with germ cell tumors (commonly seminomas) and manifest with polyradicular and anterior horn cell involvement, as well as rhombencephalitis. Coexistence of LUZP4 and KLHL11 antibodies has been described and usually entails a poorer neurological outcome.
>
> The different etiologies of autoimmune BSE along with their clinical characteristics, neuroimaging findings, antibodies profiles, and treatments are The different etiologies of autoimmune BSE along with their clinical characteristics, neuroimaging findings, antibodies profiles, and treatments are summarized in Table A1.

Since I may not be able to share this directly with my treating team, basically you need to present sick, so such engagement is unlikely. Anyhow just wanted to share a collection of notes on the topic here—for posterity’s sake.

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I understand that some cases labelled as chronic autoimmune encephalitis (AIE) may ultimately represent diagnostic errors—situations where individuals receive the diagnosis despite not having the condition. However, it is equally clear that the reverse also occurs but it not so easily found. For people who miss the critical three‑month diagnostic window, reaching an accurate diagnosis becomes increasingly difficult, especially when early cerebrospinal fluid markers are absent, likewise MRI or when the initial presentation is subtle rather than truly dramatic.

The main criteria that starts it is the 3-month rule:

> "Diagnostic criteria for possible autoimmune encephalitis.... {1 of 3} Subacute onset (rapid progression of less than 3 months) of working memory deficits (short-term memory loss), altered mental status, or psychiatric symptoms." — Graus 2017

The problem: criteria applied retrospectively to dismiss cases

> "In 72% of patients, they did not fulfill autoimmune encephalitis diagnostic criteria, suggesting more stringent adherence to these criteria may prevent misdiagnoses. In particular, an insidious onset of symptoms and absence of MRI or CSF findings suggestive of neuroinflammation should raise suspicion for an alternative diagnosis." — Flanagan et al., 2022

If this is retrospective labelling based on strict criteria, we could have an issue. Yes, insidious onset does raise concern, but it is also true that chronic presentations do exist. So it might be better to work with existing patients with long-term follow-up, rather than rely solely on retrospective labelling — since we don't have the patient to verify the fact. Once there are strong arguments, it sounds neat on paper, but it gets copied as fact rather than a retrospective criteria theory.

> "Misdiagnosis is also not uncommon; a recent study of patients referred to AIE specialty clinics reported a misdiagnosis rate of 27%." — Canadian AIE Guidelines, 2024

> "A total of 107 patients were misdiagnosed with autoimmune encephalitis, and 77 (72%) did not fulfill diagnostic criteria for autoimmune encephalitis." — Flanagan et al., 2022

> "Potential contributors to misdiagnosis included overinterpretation of positive serum antibodies (53 [50%]), misinterpretation of functional/psychiatric, or nonspecific cognitive dysfunction as encephalopathy (41 [38%])." — Flanagan et al., 2022

Definitely overinterpretation of serum is true, and there are surely cases that do get wrongly diagnosed. The problem I see here is that the somatic/functional/psychiatric, nonspecific cognitive dysfunction may have had other strong factors that led to the diagnosis. So retrospective analysis of these cases with application of the 2017 Graus criteria may in fact now create an almost impenetrable wall for people who fall into these categories and in fact do have AIE and have just been missed by various unfortunate circumstances.

The 3-month effect

Firstly the 3-month rule is common, that symptoms occur in this period, from the first acute onset, or many symptoms rapidly appearing in this window. However if a case is less dramatic, or gets missed due to overlapping primary illness or other circumstance, it seems that cases start to fall off radar, as now it is outside the allotted window, so it is deemed very unlikely if not impossible from the get go.

Chronic AIE exists but doesn't meet standard criteria

> "While majority of patients present within 3 months, little is known about chronic presentations of AIE." — Arshad et al., 2025

> "None of the patients fulfilled the conventional criteria for AIE." — Arshad et al., 2025

CSF can be normal in chronic cases which further complicates review

> "Although CSF abnormalities have been reported in more than 90% of typical cases, none of our patients had CSF abnormalities, which is consistent with some of the previous studies that also had very low incidence of CSF abnormalities. This could be due to the late stage at presentation." — Arshad et al., 2025

> "Some patients had inflammation-related changes in the CSF... however, not all patients can be diagnosed at this stage, which may result in pathological changes going undetected." — Zhang et al., 2022, Neural Regen Res

Chronic cases can be broad length in time before diagnosis

> "We present a series of 3 patients who had a chronic history ranging from 9 months up to 9 years." — Mahesh et al., 2019

> "In January 2019, a 61-year old male, with a 1-year history of diagnosed obstructive sleep apnea (OSA), was admitted in a state of unconsciousness due to hypercapnia. He had an 11-year history of slowly progressive diplopia, hoarseness, slurred speech, dysphagia and sleep disturbances." — Anti-IgLON5 Disease: A Case With 11-Year Clinical Course and Review of the Literature

Chronic course can lead to misdiagnosis and mistakes for mimics (as in delays to AIE diagnosis)

> "Insidious onset was a leading cause of misdiagnosis of autoimmune encephalitis." — Arshad et al., 2025

> "Three of these patients were misdiagnosed with treatment refractory psychosis (2 patients for 6 years and 1 for 15 years)." link

> "AIE can manifest in acute, subacute, or even chronic forms, often resulting in delayed diagnosis and consequently, delayed initiation of appropriate therapy." - Wiley - Three Challenging Cases of Autoimmune Encephalitis: A Case-Series and a Review of the Literature

> "Patients with chronic, progressive cognitive or psychiatric symptoms were often misdiagnosed with neurodegenerative or primary psychiatric disorders." — Arshad et al., 2025

> "In our clinical experience, these more insidious courses—which are sometimes more akin to neurodegenerative presentations than florid encephalitis syndromes—often lead to a delayed diagnosis, and hence late commencement of immunotherapy." — PMC8461404

> “Our series highlights that chronicity of symptoms and indolent course can mimic a neurodegenerative or a psychiatric illness hence neurophysicians should be aware of such rare presentations especially when the course is atypical for the same.” - Journal of the Neurological Sciences, Chronic autoimmune encephalitis: An unrecognized entity

Psychiatric cases with chronic course are not even mentioned, however extra care should be taken with red flags, which adds complexity that is often hard to capture

> "Psychiatric patients with new‑onset neurological symptoms – including headaches, movement disorders, autonomic dysfunction, and CSF abnormalities – should be investigated for autoimmune encephalitis." (orofacial dyskinesia mentioned as a subtle possible sign) — Bost et al., 2016

> "Signs of antipsychotic intolerance should raise suspicion for anti‑NMDAR encephalitis." — Lejuste et al., 2016, Neurol Neuroimmunol Neuroinflamm

> “Usually they are often misdiagnosed as psychiatric conditions before the red flag signs develop.” - Journal of the Neurological Sciences, Chronic autoimmune encephalitis: An unrecognized entity

> "Psychiatric abnormalities were the most common clinical symptoms and were the presenting sign in 60%. One-third of patients were initially hospitalized in a psychiatric ward." > "'Red flag' criteria should always prompt determination of anti-neuronal autoantibodies in psychiatric patients." - Front. Psychiatry, 16 February 2017

And there are specific antibodies with documented chronic course

> "Specifically, a chronic disease course occurred in all cases of anti-IgLON5 disease and in one third of KLHL11 cases." — PMC11752097

> "Anti-IgLON5 disease is a rare autoimmune disease of the central nervous system. It typically manifests as a chronic condition, characterized by cognitive impairments, movement disorders, and sleep disorders." — PMC9827781

> "However, we have observed more chronic courses, of between 1 and 5 years, particularly in leucine-rich glioma-inactivated protein 1 (LGI1)-antibody, contact-associated protein 2 (CASPR2)-antibody and immunoglobulin-like cell-adhesion molecule 5 (IgLON5)-antibody syndromes. These findings mean that time to disease nadir is often outside of the 3-month duration which appears in diagnostic guidelines." — PMC8461404

> "Anti-IgLON5 disease affects both genders similarly and usually develops between the 50s and 70s. Onset of symptoms is usually slowly progressive, but a rapid presentation can occur in up to 20% to 25% of the patients. The four most frequent initial complaints are sleep-related problems, symptoms of bulbar dysfunction (mainly dysphagia), gait difficulties with disequilibrium or ataxia, and movement disorders (eg, chorea and facial or abdominal dyskinesias)." — MedLink Neurology, 2025

> "A detailed analysis for 29 cases was done and a mean delay in diagnosis was analyzed to be 1.9 years (range 3 days to 11 years). The cases with bulbar symptoms onset took maximum time to diagnosis i.e. 4.5 years, followed by cases with movement and psychiatric symptoms onset around 1.7 years and patients with sleep abnormalities as the initial presentation took 1.5 years. It was observed that the cases which presented with >2 symptoms at the initial presentation were diagnosed 12 months earlier than those presenting purely with one symptom." — Anti-IGLON5 Disease: Time to Diagnosis Based on Clinical Presentation

> "Anti-IgLON5 disease presents with a wide spectrum of neuropsychiatric symptoms, often leading to delayed diagnosis and treatment. Increasing clinical awareness, will facilitate the timely diagnosis and management." — Anti-IGLON5 Disease: Time to Diagnosis Based on Clinical Presentation

> "The onset of Anti-IgLON5 disease is insidious and may be between 45 to 75 years. Moreover, the onset involves progressive sleep and brainstem disorders... Four clinical presentations include: sleep disorder with parasomnia and sleep breathing difficulty, bulbar syndrome, progressive supranuclear palsy-like syndrome, and cognitive decline with or without chorea." — Anti-IgLON5 disease: a novel topic beyond neuroimmunology

> "Median time from symptom onset to diagnosis is around 1.9 years (range: 3 days to 11 years), often delayed because symptoms overlap with psychiatric and neurodegenerative disorders." — Neuro journal, 2025

The problem I see with this is that the somatic/functional/psychiatric, nonspecific cognitive dysfunction may have had other strong factors that led to the diagnosis in the end, which can't be easily captured without looking at the case in person.

So then what happens in cases that are chronic? Or cases that get missed due to prior primary diagnosis? If there is no emergency like seizures or thunderclap headache or extreme spike in CSF, just broad ranging symptoms and diagnostics enough to each be dismissed in isolation, the patient is diagnostic odyssey. Differential diagnosis is difficult, but if it is seen as unlikely to impossible before investigation even start. Often hidden in papers are stories of long protracted cases with delays to diagnosis. How many make it to the correct diagnosis, or end up with multiple systems atrophy or irreversible brain damage or end up in ER at a later stage, when early diagnosis could have given a greater chance for treatment and recovery in a more forthcoming way. So it is a challenge, as the risks of over diagnosis are real, but the risks of missed cases is also high.

One remarkable new ares of science for AIE (and brain disease) is FDG-PET and 3D-SSP mapping

> "FDG-PET's utility in complex cases for 'atypical and/or pharmaco-resistant presentations, [18F]FDG-PET can also be useful for differential diagnosis with neurodegenerative diseases or encephalitis'" — FDG-PET EANM 2021 guidelines

> "FDG-PET can depict early metabolic changes... before the structural changes seen on CT or MRI," also "a first-line ... examination for workup of patients with suspected non–AD-type dementia." — Satoshi Minoshima, Donna Cross et al. 2022

> "Patients not identified by visual inspection can be detected by semi-quantitative analysis" — Frontiers paper

> "Normal MRI does not exclude a paraneoplastic brainstem encephalitis." — Review focused on recognition of paraneoplastic brainstem encephalitis

> "FDG-PET/CT was more often abnormal than initial EEG, MRI, and CSF studies. Brain region mean Z-scores with magnitudes ≥2.00 were interpreted as significant." — Probasco et al., 2017

> "SSP methods were superior in detecting both hypermetabolism as well as hypometabolism. Standard visual analysis was limited when evaluating hypermetabolism." — Moreno‑Ajona et al., 2020

> "Several studies comparing the accuracy of 3D-SSP to standard visual reads showed it to be at least as good as, if not better than, visual reads by expert readers and better than reads by novices. Thus, 3D-SSP helps inexperienced readers, provides confirmation for experienced readers, and can reduce variability among readers." — PMC9390870

> "Five out of six would fit the criteria for possible AE, whereas 6/6 would fit the criteria for definite AE only when using brain FDG-PET, as two cases showed no brain MRI abnormalities." > "Brain FDG-PET exhibited metabolic abnormalities in all cases, whereas MRI, CSF and EEG were all abnormal in 2/6 patients." > "When autoantibodies were negative and MRI findings were unremarkable, FDG-PET showed typical findings of AE." > "For the evaluation of patients with suspected AE, standard analysis of FDG-PET images benefits from voxel-based analysis, as it may lead to more comparable and accurate results. This study provides new evidence of the utility of FDG-PET for AE beyond the approach based on MRI, CSF sampling and EEG." — Moreno-Ajona et al., 2020, Diagnostics

There are suspected AIE guidelines that help with these issues:

> "Patients meeting only possible AIE criteria after completion of investigations merit special consideration. Importantly, these were not intended to be used as standalone criteria, but rather as the minimum requirements to suspect AIE. In patients who only meet criteria for possible AIE but in whom alternative diagnoses have reasonably been excluded, a controlled immunotherapy trial with predefined distinct and objective treatment measures of efficacy can be considered with involvement of a specialist in autoimmune neurology." — Canadian AIE Guidelines, 2024

Such efforts help to balance out the conversation. Leading subspecialist papers like Arshad 2025 are providing a welcome new warning: "If you rigidly apply the 3-month rule to these patients, you will miss them."

Early diagnosis is needed to help prevent poor outcomes

> "Given the complex phenotypes and potentially poor long-term outcomes, early diagnosis and treatment are needed to improve patient survival and prognosis." — Zhang et al., 2022, Neural Regen Res

Treatment works in many even after long delay

> "Despite a long delay (24 months) until treatment, a notable clinical improvement was seen in the majority (75%)." — Arshad et al., 2025

> "Immunotherapy seems to be more effective than was previously thought and can be effective in half of the patients. Long-term use may benefit an even greater number of patients." — Zhang et al., 2022, Neural Regen Res

Diverse complex symptoms can lead to delays

> "... I understand that this DPPX must have begun some 9 months prior to diagnosis in the Summer of 2020 and in the depths of the Covid pandemic. It started with such broadly diverged symptoms that the early efforts of the medics involved were thwarted and inconclusive. Collectively these symptoms included: > > - Visual- magenta blinds spots in the periphery of vision and later some left-right flicking of vision.
> - Behavioral- anxiety, exaggerated startle response and a few uncharacteristic outbursts of anger.
> - Cognitive- some short-term memory loss and confusion.
> - Physical- balance problems and some numb patches on feet and back
> - Gastric- excessively loose stools resulting in rapid and significant weight loss.
> - Sleep- disturbed, with prolonged waking after 2- 4 hours."
> full story here on encephalitis.info

> “Autoimmune encephalitis can present with subacute onset neuro behavioural symptoms, seizures and cognitive decline.”

> "The diagnosis and management of autoimmune encephalitis can be challenging, as it presents with a broad spectrum of symptoms and complications. Our cases underscore the importance of considering AIE in the differential diagnosis of patients presenting with neuropsychiatric symptoms and highlight the need for a thorough work-up to detect potential autoantibodies." - Wiley - Three Challenging Cases of Autoimmune Encephalitis: A Case-Series and a Review of the Literature

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So while it is a delicate and complex topic, it still is something that will require new understanding to bring to the table in this growing complex area — because for chronic AIE patients, the difference between a 'diagnostic fact' and a 'diagnostic trap' may be the difference between treatment and permanent decline."

^(Chronic autoimmune encephalitis: An unrecognized entity, K.V. Mahesh, 2019.)

> "Autoimmune encephalitis can present with subacute onset Neuro behavioural symptoms, seizures and cognitive decline.
>
> Usually they are often misdiagnosed as psychiatric conditions before the red flag signs develop, we present a series of 3 patients who had a chronic history ranging from 9 months upto 9 years, were earlier misdiagnosed as neurodegenerative or psychiatric illness, of them one had antibody proven Autoimmune encephalitis while other 2 were diagnosed on characteristic PET brain findings of hypermetabolism in the temporal lobes or basal ganglia, all were treated with immunosuppresive therapy with significant improvement in symptoms.
>
> Our series highlights that chronicity of symptoms and indolent course can mimic a neurodegenarative or a psychiatric illness hence neurophysicians should be aware of such rare presentations Especially when the course is atypical for the same."

https://www.jns-journal.com/article/S0022-510X(19)31306-1/fulltext

Few notes on EEG in AIE. We know often it is non specific, but there are some interesting papers on the topic.

Moise et al., 2021 Continuous EEG Findings in Autoimmune Encephalitis
PMCID: PMC7263965

>

Jha et al., 2024 Electroencephalographic outcomes and predictors of epilepsy in autoimmune encephalitis
Link

>

>

>

>

>

^(Managing memory problems after encephalitis by Prof Barbara Wilson OBE and reviewed by Dr Bonnie-Kate Dewar, Clinical Neuropsychologist)

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The long-term effects after encephalitis may be characterised by cognitive and behavioural changes which may have a significant impact upon psycho-social functioning and return to an individual’s previous level of functioning. This factsheet aims to help people understand why there are memory problems after encephalitis and what can be done to help.

Contents

1. Memory problems and the temporal lobe
2. Practical steps in managing memory problems
3. Memory aids
4. Using the remaining memory more effectively
5. Memory groups
6. Memory and the use of a computer
7. Errorless learning

Managing memory problems after encephalitis, by Prof Barbara Wilson PDF

This is a very underrepresented topic. The main AIE criteria make it extremely hard likewise with pychartric overlap.

These cases that miss the sub-acute timeframe for diagnosis face chronic symptoms (progressive cognitive/behavioral issues lasting months to years).

Unfortunately this group is considered almost non-existent, but of course this is not true.

Here we look at the 2026 study from India on chronic presentations of autoimmune encephalitis (AIE) to help open discussion and recognition to this often dismissed group.

I have studied klhl11 (one third of cases are chronic) and noted how often such chronic cases were misdiagnosed as pychartric, depression, neurodegenerative, dementia, functional.

Often diagnostic can be non specific and symptoms very broad ranging.

Often cases respond well to treatment, but getting to diagnosis and treatment trials can take months to years, due to often accidental or subtle anchoring bias giving delays to full diagnosis.

Key quotes highlighting chronic course, misdiagnosis, and outcomes:

> "Chronic presentations of AIE are less known, and often misdiagnosed due to insidious progressive course and resemble degenerative dementias. A high index of suspicion in patients with chronic atypical cognitive syndromes and a low threshold for antibody testing will allow for prompt diagnosis, appropriate immunotherapy and improvement in clinical outcome."

> "The spectrum of autoimmune encephalitis (AIE) is evolving due to heterogeneity of clinical syndromes associated with autoantibodies. While majority of patients present within 3 months, little is known about chronic presentations of AIE."

> "Patients with chronic presentations... present with progressive cognitive decline for more than 3 months associated with a variable clinical course, not meeting the standard criteria for neurodegenerative dementia or the conventional criteria for AIE."

> "Memory, language and behavioural disturbances with prominent neuropsychiatric symptoms were characteristic clinical manifestations. The course was chronic progressive, relapsing and rapidly progressive in 18 (64%), 8 (28%) and 2 (7%) patients, respectively. On immunomodulator therapy, the majority (21/28) improved, while 7/28 patients remained unchanged or experienced an exacerbation of symptoms."

> "Despite a long delay until treatment, management with immunomodulation results in a notable clinical improvement... improvement in cognitive functions is a time-dependent process and recovery may continue for several years."

The study looked at 28 patients (many with LGI1, anti-TPO, NMDA, etc.) referred to a cognitive disorders clinic. Common issues: memory problems, neuropsychiatric symptoms (apathy, anxiety, irritability, hallucinations, etc.), sleep disturbances. Many had atrophy on imaging but responded to steroids, rituximab, etc.

I think the severity of the disease drives the patient to diagnosis.

This is an area that does need awareness and education. As such pain and illness left untreated is a real concern for the care and recovery of such patients.

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Clinical profile and treatment outcomes of patients with chronic presentations of autoimmune encephalitis: expanding the spectrum, *Arshad etal. 2026.

[Pdf](https://pmc.ncbi.nlm.nih.gov/articles/PMC12993309/pdf/bmjno-8-1.pdf(

https://www.cbc.ca/lite/story/9.7048345

Audio: https://www.cbc.ca/player/play/audio/9.7053249

This woman was misdiagnosed with bipolar disorder. It turns out she has a rare autoimmune disease instead

Brandie Weikle | CBC Radio | Posted: January 20, 2026 9:00 AM | Last Updated: January 20

Though rare, a relatively new class of autoimmune diseases is making psychiatrists rethink some diagnoses

Image | Nora Scott and family

Caption: Nora Scott, second from right, is pictured with her partner, Chris Johnson, their son, Avery, and daughter, Emily, at their home in High River, Alta., in November 2025. Scott was misdiagnosed with bipolar disorder in 2017. It took four years before it was discovered that in fact she had a rare form of autoimmune disease that affects the brain. (John Chipman/CBC)

Setup: Android 13, Redmi Note 10 Pro, MIUI 14, LSPosed, Zygisk Next, Magisk 30+

I never see ads anywhere else on my phone, but Google Play Store is full of ads and "suggestions." I've disabled every setting I can find. I have App manager and so forth but could not find anything to turn off that helped.

Is there any LSPosed module, Magisk module, or root-level element blocker that can remove all ads, sponsored links, and suggestion feeds from the Play Store UI?

I know about Aurora Store, but some apps require official Play Store installation, and paid apps need it for license verification.

What I've tried: DNS blocking (AdGuard), hosts file modules — they don't catch Play Store ads. God mode, App manager.

I don't want anything that interferes with payments/accounts , no warez stuff — just UI element blocking inside the Play Store app.

Does really no one care about this, I can't stand ads.

Thanks

Any suggestions on how to turn off ads and suggestions in Google play.

I have root/lsposed/magisk.

I am not really interested in an warez features, as I don't want to violate TOS. I just can't figure out with root how to clean up goggle play app. I know I can use other store apps but is there any way to remove ads and suggestions from Google play? Some root modern element blocker or modded play that just removes ads and suggestions?

This is the only modification I would like help with if anyone has a suggestion.

I have tried everything I could think of, in lsposed modules and app managers.

Thanks

I was wondering if someone has access to this article for my own personal studies only.

Severe psychosis and the adrenal androgens, James S. Howard M.D. Published: July 1992 Volume 27, pages 209–215, (1992)
https://link.springer.com/article/10.1007/BF02690893
https://doi.org/10.1007/bf02690893

It's apart of Integrative Psychological and Behavioral Science Journal
https://link.springer.com/journal/12124