Comment: On the Use of the Term “Epileptic Spasms” in Subacute Sclerosing Panencephalitis

We read with great interest the recent case report proposing epileptic spasms, rather than myoclonus, as the predominant motor manifestation in subacute sclerosing panencephalitis (SSPE).[1] The authors should be commended for addressing the long-standing imprecision in the description of abnormal motor phenomena in SSPE and for emphasizing the importance of detailed electroclinical documentation to facilitate earlier diagnosis.

However, after careful review of the video-EEG and polygraphic material provided in the article, we would like to raise specific concerns regarding the classification of the reported motor events as epileptic spasms.

Epileptic spasms represent a distinct seizure type with well-defined electroclinical characteristics, as established through extensive ictal video-EEG polygraphic studies.[1] They are typically characterized by a stereotyped axial or proximal contraction, a relatively uniform motor pattern across episodes, and a reproducible ictal EEG correlate, often consisting of a slow wave maximal over the vertex. The associated EMG pattern reflects a brief but structured muscle contraction, usually lasting approximately 1 to 2 seconds, corresponding to a simple and coarse motor phenomenon rather than a complex movement sequence. Muscle activation predominantly involves axial and proximal muscle groups, typically with bilateral trunk and limb participation. Polygraphically, the contraction is neither sharply phasic, as observed in myoclonic jerks, nor slowly sustained, as in tonic seizures, but displays the intermediate temporal profile that characterizes epileptic spasms.[1] Importantly, although epileptic spasms commonly occur in clusters, they do not exhibit rigid, clock-like periodicity, nor do they show continuous and fixed temporal coupling with repetitive EEG discharges.[2]

In contrast, detailed video-EEG analysis of the reported case reveals a markedly different motor phenomenon. The event represents a complex paroxysmal motor sequence rather than a stereotyped spasm. Across successive episodes, the motor pattern is not strictly identical and combines involuntary phasic and tonic components. The phenomenon most often begins in the right upper limb, which exhibits repeated phasic contractions, variably appearing as tremulous activity or as a series of brief, jerk-like movements. This initial focal motor activity subsequently spreads to the trunk and then to the left hemibody, where rapid, abrupt phasic contractions with dystonic features are observed, resulting in a clearly sequential involuntary motor pattern. Moreover, and most importantly, the onset of the motor phenomenon often precedes the appearance of the slow EEG component by approximately 1 second, rather than following or coinciding with it. This temporal relationship argues strongly against an ictal spasm-related EEG correlate and instead suggests a motor output that is not generated by an evolving epileptic network. Taken together, these electroclinical features are difficult to reconcile with the current operational definition of epileptic spasms and instead point toward a distinct paroxysmal motor phenomenon.

A defining feature of SSPE is the presence of periodic EEG complexes, which recur at relatively fixed intervals and are stereotyped within a given recording.[3] Motor phenomena occurring in SSPE are frequently and reproducibly related to these periodic complexes. Such a rigid temporal organization supports the concept of a stable pathological generator producing a repetitive motor output, rather than the dynamic network behavior underlying epileptic spasms.

Replacing the traditional label of “myoclonus” with “epileptic spasms,” therefore, risks substituting one epilepsy-oriented term with another, without adequately accounting for the underlying neurophysiological organization of the phenomenon. This distinction is not merely semantic. Early ictal video-EEG polygraphic studies have demonstrated that accurate differentiation between epileptic spasms, myoclonus, tonic seizures, and other paroxysmal motor events requires careful analysis of muscle recruitment, EMG morphology, and precise temporal relationships with EEG activity.[4]

Recent International League Against Epilepsy (ILAE) classifications, including the 2017 seizure classification and the 2022 diagnostic framework for electroclinical syndromes, emphasize that seizure types should be defined by their electroclinical features and underlying network organization.[5] [6] [7] Applying syndromic seizure labels to motor events that are complex, lateralized, sequential, and not strictly time-locked to EEG discharges may obscure, rather than clarify, their true neurophysiological nature.

We believe that motor phenomena in SSPE are best approached using a strictly phenomenological and polygraphic framework, carefully distinguishing epileptic seizures from paroxysmal motor events directly related to periodic EEG activity. Such an approach is essential to avoid misclassification and to advance a more accurate understanding of SSPE electroclinical features.

We hope that these comments will contribute to a constructive discussion on the interpretation of abnormal motor phenomena in SSPE and encourage continued refinement of electroclinical terminology grounded in neurophysiological evidence.

Sincerely,

Lucia Fusco

Nicola Specchio

Declaration of GenAI Use

The authors used an AI-based language model to assist with English language editing. The authors take full responsibility for the content of the manuscript.

Publication History

Received: 16 January 2026

Accepted: 10 February 2026

Accepted Manuscript online:
12 February 2026

Article published online:
19 February 2026

• References

• 1 Gyseghem PV, Andrei A, Presiozi M, Goffinon E, Aeby A, Hecke AV. Spasms and not myoclonus in subacute sclerosing panencephalitis. A case report and review of the literature. Neuropediatrics 2025; 56 (06) 408-411
• 2 Fusco L, Vigevano F. Ictal clinical electroencephalographic findings of spasms in West syndrome. Epilepsia 1993; 34 (04) 671-678
• 3 Vigevano F, Fusco L, Pachatz C. Neurophysiology of spasms. Brain Dev 2001; 23 (07) 467-472
• 4 Gürses C, Oztürk A, Baykan B. et al. Correlation between clinical stages and EEG findings of subacute sclerosing panencephalitis. Clin Electroencephalogr 2000; 31 (04) 201-206
• 5 Zuberi SM, Wirrell E, Yozawitz E. et al. ILAE classification and definition of epilepsy syndromes with onset in neonates and infants: Position statement by the ILAE Task Force on Nosology and Definitions. Epilepsia 2022; 63 (06) 1349-1397
• 6 Scheffer IE, Berkovic S, Capovilla G. et al. ILAE classification of the epilepsies: Position paper of the ILAE Commission for Classification and Terminology. Epilepsia 2017; 58 (04) 512-521
• 7 Beniczky S, Trinka E, Wirrell E. et al. Updated classification of epileptic seizures: Position paper of the International League Against Epilepsy. Epilepsia 2025; 66 (06) 1804-1823