Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (762 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A rare, slowly progressive encephalitis caused by chronic infection with the measles virus. The condition occurs primarily in children and young adults, approximately 2-8 years after the initial infection. A gradual decline in intellectual abilities and behavioral alterations are followed by progressive myoclonus; muscle spasticity; seizures; dementia; autonomic dysfunction; and ataxia. death usually occurs 1-3 years after disease onset. Pathologic features include perivascular cuffing, eosinophilic cytoplasmic inclusions, neurophagia, and fibrous gliosis. It is caused by the SSPE virus, which is a defective variant of measles virus. (From Adams et al., Principles of Neurology, 6th ed, pp767-8)
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Panencephalitides, Subacute Sclerosing; Sclerosing Panencephalitides, Subacute; Subacute Sclerosing Panencephalitides; SSPE; Sclerosing Panencephalitis, Subacute; Panencephalitis, Subacute Sclerosing; Leukoencephalitis, Van Bogaert's; Leukoencephalitis, Van Bogaert.
Where it fits in the MeSH classification
- Broader topics
- Encephalitis, Viral; Measles; Slow Virus Diseases
Related concepts
- Measles Virus
- Myoclonus
- Muscle Spasticity
- Seizures
- Dementia
- Ataxia
- Death
Research landscape
PubMed indexes 2,454 records tagged with the MeSH heading “Subacute Sclerosing Panencephalitis” (counts retrieved 2026-10-29). 153 of them (6.2%) were published from 2020 onward, and the busiest period so far is through 1999 with 1,756 records.
Reviews account for 262 records (10.7%) and meta-analyses for 1. Randomized controlled trials number 4 (0.2%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 1,756 |
| 2000-2009 | 306 |
| 2010-2019 | 239 |
| 2020 onward | 153 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 262 | 10.7% |
| Meta-analyses | 1 | 0.0% |
| Randomized controlled trials | 4 | 0.2% |
Method: PubMed query "Subacute Sclerosing Panencephalitis"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in infectious diseases
Infectious disease evidence combines microbiology, epidemiology and clinical trials. Laboratory studies identify pathogens and how they cause harm; surveillance and outbreak investigations describe who is affected and how infection spreads; trials establish whether treatments and vaccines work. Results depend on place and time, because pathogens evolve and resistance patterns and population immunity change. Check when and where the data were collected, how cases were defined and how up to date the evidence is.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
Epidemiology of subacute sclerosing panencephalitis (SSPE) in Germany from 2003 to 2009: a risk estimation [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Subacute sclerosing panencephalitis (SSPE) is a fatal long-term complication of measles infection.
- Closing excerpt
- This risk is in the same order of magnitude as the risk of a fatal acute measles infection.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (146 words)
Subacute sclerosing panencephalitis (SSPE) is a fatal long-term complication of measles infection. We performed an estimation of the total number of SSPE cases in Germany for the period 2003 to 2009 and calculated the risk of SSPE after an acute measles infection. SSPE cases were collected from the Surveillance Unit for Rare Paediatric Diseases in Germany and the Institute of Virology and Immunobiology at the University of Würzburg. The total number of SSPE cases was estimated by capture-recapture analysis. For the period 2003 to 2009, 31 children with SSPE who were treated at German hospitals were identified. The capture-recapture estimate was 39 cases (95% confidence interval: 29.2-48.0). The risk of developing SSPE for children contracting measles infection below 5 years of age was calculated as 1∶1700 to 1∶3300. This risk is in the same order of magnitude as the risk of a fatal acute measles infection.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 23874807 · DOI · PMC3706451
Identical tau filaments in subacute sclerosing panencephalitis and chronic traumatic encephalopathy [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Subacute sclerosing panencephalitis (SSPE) occurs in some individuals after measles infection, following a symptom-free period of several years.
- Closing excerpt
- These findings suggest that the CTE tau fold can be caused by different environmental insults, which may be linked by inflammatory changes.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (139 words)
Subacute sclerosing panencephalitis (SSPE) occurs in some individuals after measles infection, following a symptom-free period of several years. It resembles chronic traumatic encephalopathy (CTE), which happens after repetitive head impacts or exposure to blast waves, following a symptom-free period. As in CTE, the neurofibrillary changes of SSPE are concentrated in superficial cortical layers. Here we used electron cryo-microscopy (cryo-EM) of tau filaments from two cases of SSPE to show that the tau folds of SSPE and CTE are identical. Two types of filaments were each made of two identical protofilaments with an extra density in the β-helix region. Like in CTE, the vast majority of tau filaments were Type I, with a minority of Type II filaments. These findings suggest that the CTE tau fold can be caused by different environmental insults, which may be linked by inflammatory changes.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 37143123 · DOI · PMC10161654
Molecular characterisation of virus in the brains of patients with measles inclusion body encephalitis (MIBE) [3]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundDuring 2009/10 a major measles epidemic caused by genotype B3 occurred in South Africa.
- Closing excerpt
- The relatively few mutations probably reflect the short time from infection to brain disease in these highly immuno-compromised patients.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (198 words)
BackgroundDuring 2009/10 a major measles epidemic caused by genotype B3 occurred in South Africa. Measles inclusion body encephalitis (MIBE) was diagnosed in a number of highly immuno-compromised HIV patients. The diagnosis was based on typical clinical and MRI findings and positive measles virus PCR in brain or CSF.To characterize the brain virus, nucleoprotein, matrix, fusion and haemagglutinin genes from 4 cases was compared with virus from acutely infected patients.MethodscDNA was synthesized using random primers and viral genes were amplified by nested RT-PCR. PCR products were sequenced in the forward and reverse direction and a contig of each gene was created. Sequences were aligned with reference sequences from GenBank and other local sequences.ResultsBrain virus was very similar to the South African epidemic virus. Features characteristic of persistent measles virus in the brain were absent. Mutation frequency in brain virus was similar to epidemic virus and had the same substitution preference (U to C and C to U). The virus of 2 patients had the same L454W mutation in the fusion protein.ConclusionThe brain virus was very similar to the epidemic strain. The relatively few mutations probably reflect the short time from infection to brain disease in these highly immuno-compromised patients.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 24025157 · DOI · PMC3847183
System biology and network-based approach to identify the therapeutic signatures and potential inhibitors against polycystic lipomembranous osteodysplasia with Sclerosing Leukoencephalopathy [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Polycystic Lipomembranous Osteodysplasia with Sclerosing Leukoencephalopathy (PLOSL), often recognized as Nasu-Hakola disease, is an uncommon autosomal recessive systemic condition described by numerous bone lesions that resemble cysts and progressive early-onset dementia.
- Closing excerpt
- These results broadened our knowledge of putative biomarkers for PLOSL diseases, and an experimental strategy will improve our results even more in the future.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (279 words)
Polycystic Lipomembranous Osteodysplasia with Sclerosing Leukoencephalopathy (PLOSL), often recognized as Nasu-Hakola disease, is an uncommon autosomal recessive systemic condition described by numerous bone lesions that resemble cysts and progressive early-onset dementia. One novel way to find possible drug targets is to use Network Analyst tools for network-based gene expression profiling. Identifying the target hub genes, essential for the initiation and progression of PLOSL, is validated by the significance level (p-score) attained using Cytoscape in the survival analysis of the major central genes. The X2K online tool also examined the regulatory kinases that formed the interaction between protein molecule networks. Out of the 53 genes obtained to be differentially expressed, PPARG and AIF1 had the greatest degree score, followed by C1QA with 5 degrees and SIGLEC1 and MSR1 with 4 degrees. Furthermore, Molecular docking of target PPARG gene with AMG-131 and Elafibranor drugs, having the chemical formulas 2-[2,6-dimethyl-4-[(E)-3-(4-methylsulfanylphenyl)-3-oxoprop-1-enyl]phenoxy], and 3,5-dichloro-4-quinolin-3-yloxyphenyl) benzenesulfonamide, along control (Rosiglitazone (S) shows binding affinities of -7.2 kcal/mol, -7.4 kcal/mol, and -7.6 kcal/mol respectively. The enzyme remained extremely stable in the complex throughout 200 ns, with a mean Root Mean Square Deviation (RMSD) of 2.95 Å for the AMG-131 complex system and 2.93 Å against the Elafibranor complex system. Root Mean Square Fluctuation (RMSF) anticipated steady behavior with average RMSD for the active site residues in the docked system. Arg76 and Leu28leu Leu118 were shown to be essential enzyme residues for binding, anchoring, and bridging strong hydrogen and hydrophobic interactions between the enzyme and the inhibitor, according to the Radial Distribution Function (RDF). These results broadened our knowledge of putative biomarkers for PLOSL diseases, and an experimental strategy will improve our results even more in the future.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41719345 · DOI · PMC12923142
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Subacute sclerosing panencephalitis [5]
- Research article Subacute sclerosing panencephalitis. Current status [6]
- Research article Subacute sclerosing panencephalitis: an update [7]
- Research article Subacute sclerosing panencephalitis [8]
- Research article Subacute sclerosing panencephalitis [9]
- Research article Measles virus and associated central nervous system sequelae [10]
References
- Schönberger K, Ludwig MS, Wildner M, Weissbrich B. Epidemiology of subacute sclerosing panencephalitis (SSPE) in Germany from 2003 to 2009: a risk estimation. . 2013. PMID 23874807 · DOI · PMC3706451
- Qi C, Hasegawa M, Takao M, Sakai M, Sasaki M, Mizutani M, et al.. Identical tau filaments in subacute sclerosing panencephalitis and chronic traumatic encephalopathy. . 2023. PMID 37143123 · DOI · PMC10161654
- Hardie DR, Albertyn C, Heckmann JM, Smuts HE. Molecular characterisation of virus in the brains of patients with measles inclusion body encephalitis (MIBE). . 2013. PMID 24025157 · DOI · PMC3847183
- Bokhari BT, Saleh AM, Aljohani HM, Owaydhah WH, Alobaidy MA, Dahran N, et al.. System biology and network-based approach to identify the therapeutic signatures and potential inhibitors against polycystic lipomembranous osteodysplasia with Sclerosing Leukoencephalopathy. . 2026. PMID 41719345 · DOI · PMC12923142
- Garg RK. Subacute sclerosing panencephalitis. Postgrad Med J. 2002. PMID 11807185 · DOI · PMC1742261
- Dyken PR. Subacute sclerosing panencephalitis. Current status. Neurol Clin. 1985. PMID 2581121 · DOI
- Gutierrez J, Issacson RS, Koppel BS. Subacute sclerosing panencephalitis: an update. Dev Med Child Neurol. 2010. PMID 20561004 · DOI
- Garg RK. Subacute sclerosing panencephalitis. J Neurol. 2008. PMID 18846316 · DOI
- Garg RK, Mahadevan A, Malhotra HS, Rizvi I, Kumar N, Uniyal R. Subacute sclerosing panencephalitis. Rev Med Virol. 2019. PMID 31237061 · DOI
- Buchanan R, Bonthius DJ. Measles virus and associated central nervous system sequelae. Semin Pediatr Neurol. 2012. PMID 22889539 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
See how EvidenceLib is built. Spotted an error? Email support@evidencehelix.com.
Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.