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• W2043595857 abstract "[In this section, we present a lead paper followed by a set of comment articles that have been invited by the editors. Our goal is to present different or opposing views on topical issues. Articles and comments are commissioned in the spirit of encouraging discussion and debate in a format that will stimulate thought and further research.] For myself I shall be well satisfied if I have made it appear probable to you that there does exist a form of epilepsy in children which is distinguishable by its clinical features and in which the prognosis is always good Adie (1924) differentiating “pyknolepsy” (syndrome) from “petit mal” (seizures) This commentary outlines clinical and electroencephalography (EEG) aspects of typical absence seizures (TAS) and related epileptic syndromes in order to identify areas of consensus as well as areas of uncertainty that may indicate directions for future research. This may also assist the International League Against Epilepsy (ILAE) Commission, which is currently working on establishing scientifically rigorous criteria for the identification of specific epileptic seizures and syndromes using an evidence-based approach (Engel, 2006). Relevant ILAE definitions and classifications are shown in Table 1. TAS and related epileptic syndromes were thoroughly assessed by leading clinicians and researchers in this area during a 3-day symposium in 1994 in London (Duncan & Panayiotopoulos, 1995). Consensus was achieved in the definition and semiology of TAS and controversies in their syndromic classification comprehensively debated (Reynolds et al., 1995). The report by Sadleir and colleagues (Sadleir et al., 2008) and its related predecessor on childhood absence epilepsy (CAE) (Sadleir et al., 2006) is assessed in the context of this debate. TAS are generalized seizures of sudden onset and termination, lasting for seconds. They are fundamentally different from other seizures and they are pharmacologically unique (Panayiotopoulos, 2005a). TAS have two requisite components: Clinically, the transient impairment of consciousness (TIC) (absence) EEG generalized >2.5 Hz spike- or polyspike-slow wave discharges (S-PWD). TAS usually occur in the context of idiopathic generalized epilepsies (IGE). The prefix “typical” is to differentiate them from atypical absences rather than to characterize them as “classical” or characteristic of any particular syndrome. Atypical absence seizures occurring in the context of mainly symptomatic epilepsies and with slow <2.5 Hz S-PWD are beyond the scope of this commentary. The clinical and EEG manifestations of TAS have been well-characterized through video EEG studies (Penry et al., 1975; Stefan, 1982, 1983; Holmes et al., 1987; Panayiotopoulos et al., 1989a, 1989b, 1997; Capovilla et al., 2001; Poblano et al., 2001; Guilhoto et al., 2003; Sadleir et al., 2008). The clinical manifestations vary significantly between patients (Tables 2 and 3). TIC may be the only clinical symptom (simple TAS), but this is often combined with other manifestations (complex TAS). In recognition of this diversity, the ILAE has recently recognized four types of TAS (Table 1) probably of different pathophysiology and syndromic significance: (1) the classical TAS, (2) myoclonic absence seizures, (3) phantom TAS and (4) eyelid myoclonia with absence (EMA) (Engel, 2006). TIC is a mandatory symptom of TAS and may be severe, moderate, or mild. In routine EEG practice, TIC is commonly assessed by the ability of a patient to recall a verbal test stimulus (a phrase, number, or rhyme) during S-PWD. By examining TIC in an all or none fashion, this test detects only severe TIC. When TIC is mild, the patient often recalls the test stimulus (Fig. 1D, 1I, and 1J). Furthermore in brief S-PWD, the test is often given or continues after these have ended. Asking the patient to count his/her breaths during hyperventilation (BCH) was the most reliable and practical means for the detection of TIC during S-PWD among various methods that we evaluated (Panayiotopoulos et al., 1989b). We have validated BCH (Giannakodimos et al., 1995) and use it as a standardized method in our studies of TAS, which is how we have identified phantom absences that manifest with cessation, delay, hesitation, or errors in counting (Fig. 1D) (Panayiotopoulos et al., 1997; Koutroumanidis et al., 2008). BCH is powerful because it simultaneously tests attention, concentration, memory, sequential accuracy, and language function. Illustrative EEG from video EEG samples to exemplify important matters to consider in the diagnosis and the syndromic classification of TAS. The actual video EEG of most of these and many other patients can be viewed in the companion CD of our publications, which also include many years of follow-up (Panayiotopoulos, 2005b; Panayiotopoulos, 2007b). Cases A–E are from a video EEG at first presentation of children with TAS before age 10 years. Only case A was CAE. All others had other than CAE syndromes that were predicted from the first EEG with significant implications on prognosis and management. Case B had classical myoclonic TAS, and at last follow-up at aged 8 years is neurocognitively impaired with intractable GTCS and myoclonic TAS. Case C had marked myoclonic components through the whole length of TAS, photosensitivity, multiple spikes, and irregular S-PWD. At age 12 years, TAS are worse with an evolution similar to her mother (case K). Case D had very mild (phantom TAS) and absence status epilepticus as previously reported with video EEG sequences (Panayiotopoulos et al., 2001). Case E had moderate and severe TAS, with multiple spikes and irregular S-PWD, similar to her older sister (case F), who had onset of TAS at age 11 years. Two years later, she had a GTCS in front of the TV. These sisters illustrate well the problem of classifying syndromes of TAS by age at onset; accordingly case E would be classified as CAE and case F as JAE. Case G had S-PWD concurrent with myoclonic and atonic symptoms without TIC. These features, which are not TAS, confirmed the diagnosis of myoclonic-astatic epilepsy. Case H had severe and lengthy TAS of JAE. The patient also had GTCS and myoclonic jerks. Case I demonstrates TAS with mild TIC in two young women with JME. TIC was documented only with breath counting during hyperventilation. In all other occasions, the patients were able to recall the verbal test-stimulus during S-PWD. Case J is from EMA patients whose seizures manifest with mainly eyelid myoclonia that may be associated with minor TIC. Case K from video EEG of the mother of case C. TAS and photosensitivity started at age 6 years, GTCS occurred at age 14, and premenstrual myoclonic jerks appeared later; all continue in adult life and are resistant to medication. There is no consensus on the extent and clinical significance of other more elaborate psychological testing for the detection of TIC during S-PWD that may appear clinically silent. This is a matter that divides opinions not only for S-PWD but also for any other type of EEG epileptiform activity that may be associated with TIC (Aarts et al., 1984; Aldenkamp and Arends, 2004). Many types of psychological testing have been used during S-PWD since 1939 (Schwab, 1939). These generally show that impairment of response may start just before the onset of S-PWD, tend to get worse with longer duration of S-PWD, but improve during the latter part of it (Mirsky and van Buren, 1965; Goode et al., 1970; Sellden, 1971; Porter & Penry, 1973; Browne et al., 1974). The ictal EEG of TAS consists of generalized >2.5 Hz S-PWD, which are often of higher amplitude in the anterior regions (Fig. 1, A–K). By consensus, spike-wave frequency is higher than 2.5 Hz, mainly 3–4.5 Hz, but there are no recommendations on how these measurements should be made. Frequency is usually variable and faster in the first second (opening phase), becomes more regular and stable in the subsequent 3 s (initial phase), and slows down towards the terminal phase of longer S-PWD (Fig. 1) (Panayiotopoulos et al., 1989b). This is why our practice is to estimate mean frequency of the initial phase of S-PWD and not at the first second of S-PWD used by other authors (Holmes et al., 1987; Sadleir et al., 2006). S-PWD also show significant qualitative variations that are clinically significant when examined systematically; they may be fragmented, multiple spikes may predominate, and the relationship between spike/multiple and slow wave fluctuates (Fig. 1). Duration is easy to measure and commonly is from 3 to 30 s. Hyperventilation induces TAS in nearly all untreated patients. Intermittent photic stimulation may precipitate or facilitate S-PWD in any type of TAS (Fig. 1C, 1J, and 1K); eyelid myoclonia is a common clinical accompaniment. Generalized >2.5 Hz S-PWD is the EEG marker of TAS but may also be clinically silent or manifest with symptoms other than TIC (Fig. 1G) (Dalby, 1969; Genton, 1995; Koutroumanidis & Panayiotopoulos, 2008). Sadlier and coworkers (2006, 2008) define as absence seizure any type of >2.5 Hz S-PWD associated with clinical signs even if this is not associated with TIC. However, the latter could be either TAS with undetectable TIC (which is a matter of methodological sensitivity) or other that TAS epileptic seizures (Fig. 1G). The syndromic classification of IGE with TAS is controversial (Reynolds et al., 1995). One view is that all presentations are one disease or a biological continuum (Berkovic et al., 1987). Another view, which we support, is that IGE with TAS comprise distinct epileptic syndromes, four of which are recognized by the ILAE. These are childhood absence epilepsy (CAE), juvenile absence epilepsy (JAE), epilepsy with myoclonic absences (MAE), and juvenile myoclonic epilepsy (JME) (Tables 1 and 3). CAE, first described in the pre-EEG era by Adie (1924) as pyknolepsy, manifests with numerous severe TAS and good prognosis as subsequently confirmed with EEG, video EEG and long follow-up studies (Loiseau & Panayiotopoulos, 2004). There remain many areas of uncertainty of what is CAE. The ILAE broadly defines it as a syndrome with frequent (several to many per day) and severe absences (see ILAE definition of TAS), school age at onset (peak at 6–7 years), and common remission (Table 1). Exclusion criteria have been introduced (Loiseau & Panayiotopoulos, 2004). The ILAE, by accepting MAE and JME as separate syndromes, probably exclude myoclonic TAS and mild TAS from CAE (Commission, 1989). It is by this logic that EMA (which are primarily myoclonic) may also be an exclusion criterion. Further, by accepting reflex TAS as a distinct category, the ILAE indicates that these too may not be part of CAE. That perioral myoclonia or single violent jerks occurring in the course (not at onset) of TAS is an exclusion criterion may be debatable; however, their presence indicates worse prognosis (Panayiotopoulos, 2007a). The same applies for multiple spikes and fragmented S-PWD that also indicate a bad prognosis, coexistent myoclonic jerks, or generalized tonic–clonic seizures (GTCS) (Panayiotopoulos et al., 1989b; Fakhoury & Abou-Khalil, 1999). A simplistic but unsatisfactory practice is to label as CAE any child with onset of daily TAS at ≤10 years and to as early as 2 years (Sadleir et al., 2006). The 10 years of age cut off is arbitrary and not a decisive “gold standard” to define what is and what is not CAE. Further, TAS of recognized syndromes, such as MAE or JME, may start before that age, and TAS of early childhood onset (<4 years of age) are heterogeneous and often entirely different to those of CAE (Doose, 1994). The arbitrary limit of 10 years is mainly based on the pioneering work of Doose and Janz who found that pyknoleptic absences usually start before the age of 10 years, while nonpyknoleptic absences usually start after this age (Doose, 1994; Janz et al., 1994). If diagnosis by age at onset is to be followed, the study population should be correctly defined as “childhood absence seizures,” rather CAE which is a subset of it. Such a distinction is particularly important in view of the current National Institute of Neurological Disorders and Stroke supported study of CAE from which initial published results refer to “a high incidence of adverse behavioral and cognitive outcomes in CAE” (O'Deil et al., 2006). Is this CAE or childhood absence seizures? Classical studies have shown significant differences between “childhood absence seizures” and CAE (see details and citations in Sander, 1995). This syndrome is now well-defined, but the course is variable (Bureau & Tassinari, 2005; Engel, Jr., 2006). Myoclonic absences manifest with bilateral clonic jerks often with a tonic contraction (Fig. 1B). TIC is of variable severity. Onset ranges from 1 to 12 years (peak 7 years). Etiologically, myoclonic TAS are sometimes idiopathic and of good prognosis, but two-thirds are cryptogenic or symptomatic, which are resistant to treatment, and may progress to epileptic encephalopathies. MAE offers a good argument against diagnosing syndromes of TAS by age at onset. That simple TAS may also occur and sometimes precede the characteristic myoclonic absences (Bureau & Tassinari, 2005) is another concern to consider in validating the reports of Sadleir et al. (2006, 2008); such children could easily have been categorized as CAE without appropriate follow-up. There are many areas of uncertainty regarding the precise definition of JAE, but all authorities agree that TAS with severe TIC is its main seizure type. These TAS in many respects are similar to those of CAE, although often less frequent, with less severe TIC, and more polyspikes in the EEG S-PWD (Fig. 1E, 1F, and 1H). TAS continue into adult life often with GTCS. One-fifth of patients also have myoclonic jerks (Commission, 1989; Wolf, 1992; Obeid, 1994), which are erroneously considered an exclusion criterion by Sadleir et al. (2008). Myoclonic jerks on awakening with peak age at onset in the mid-teens are the defining seizures of JME. GTCS are probably unavoidable in untreated patients. TAS occurring in 30% of patients are usually simple with mild TIC (Fig. 1I) (Berkovic et al., 1987). One-third of TAS in JME appear at ≤10 years, often predate myoclonic jerks, and may be more severe than those of later onset (Commission, 1989; Panayiotopoulos et al., 1989a, 1989b; Wirrell et al., 1996; Delgado-Escueta et al., 1999). We are in need of longitudinal studies to determine their features and how they develop in time (which is not possible without follow-up) rather than arbitrarily including them in CAE as per Sadleir et al. (2006, 2008). Other proposed syndromes of IGE with TAS need further consideration and study. The following brief presentation of some of them is to emphasize key features of their TAS (recognized by the ILAE), which are important to consider in any analysis and differential diagnosis. EMA (the seizure) consists of brief (3–6 s), marked, rhythmic, and fast jerks of the eyelids which may occur alone (eyelid myoclonia) or followed by mild TIC (eyelid myoclonia with absence) (Fig. 1J) (Giannakodimos & Panayiotopoulos, 1996). They may occur in idiopathic, cryptogenic, or symptomatic epilepsies. In the idiopathic syndrome of Jeavons, EMA occur mainly after eye closure, usually start in childhood, and all patients are photosensitive. Infrequent GTCS and limb myoclonic jerks are common, usually occurring after the onset of EMA. The syndrome is commonly lifelong and resistant to pharmacologic treatment. This syndrome, characterized by phantom absences (Fig. 1D), becomes clinically apparent only when GTCS and often absence status epilepticus occur, usually in adulthood (Panayiotopoulos et al., 1997, 2001; Koutroumanidis et al., 2008). Reflex TAS to photic, pattern, emotional upset, and thinking are well described. TAS associated with clinical photosensitivity (Fig. 1C, 1J, and 1K) are unlikely to occur in CAE, and they are likely to continue in adult life (Hirsch & Marescaux, 1994; Loiseau et al., 1995). It is apparent from the above descriptions that, with the exception of CAE, nearly all other syndromes of IGE with TAS are lifelong and also manifest with myoclonic jerks and GTCS (Table 3). Absence status epilepticus occur in one-third of patients, and this predominates in IGE with phantom absences or perioral myoclonia TAS (Agathonikou et al., 1998). Features of TAS, as with any other type of seizure, depend on brain maturity, the sleep-wake cycle, provocation, and a variety of other factors (Fisher et al., 2005). Overall, children have TAS with severe TIC and lengthier duration more often than adults. Spontaneous eyes opening (when not caused by motor events of TAS), like all other automatisms, occurs only when TIC is severely impaired (see definitions of automatisms in Table 2). The variability of TIC and duration of TAS by age also contributes to shaping the clinical presentation of syndromes of IGE-TAS that, as with many other epileptic syndromes (rolandic epilepsy for example), may be age-dependent and age-limited. Conversely, even age-influenced individual TAS features are also syndrome-related as indicated by the fact that children may also have brief and mild TAS (Fig. 1C and 1D), and conversely adults also manifest with severe and lengthy TAS (Fig. 1H). Follow-up studies have shown that TAS of IGE become milder with age, but this may be delayed for decades such as in JME and EMA (Panayiotopoulos, 2007a). Sleep modifies the clinical and EEG features of TAS, where S-PWD are usually shorter and usually devoid of discernible clinical manifestations—even in those patients who have numerous clinical seizures during the alert state (Sato et al., 1973, 1975). The syndromes of IGE with TAS, like all other medical and epileptic disorders, require rigorous and detailed clinico-laboratory documentation for their validation. An individual symptom, EEG discharge or even a type of seizure does not constitute an epileptic syndrome; rather it is the nonfortuitous clustering of historical, clinical, and video EEG symptoms and signs that makes a syndrome (Commission, 1989). Follow-up studies are particularly important in children where syndromes often progress to seizures other than those in the initial presentation within days, weeks, months, or years. In our ongoing studies on IGE with TAS, we follow a pragmatic dual prospective and retrospective approach. Any patient with TAS is exhaustively assessed clinically and with video EEG from the time of first referral to as long as is possible. This is ideal for newly recognized drug-naive patients. However, significant insights are also gained from retrospective analyses of reliable data by reviewing old medical records, original EEGs, and witnesses' accounts (Panayiotopoulos, 2007a). Sadleir and associates (2006, 2008) should be acknowledged for studying drug-naive patients at the first stages of their disease. They have provided a useful video EEG analysis of clinical symptomatology associated with >2.5 Hz S-PWD to supplement previous reports cited above. However, attempts to expand this beyond a pure semiological study and the resultant conclusions are premature because of the lack of any follow-up compounded with questionable definitions and arbitrary diagnostic categorizations that, contrary to their assertion, do not comply with the ILAE definitions: CAE is not synonymous with TAS starting at age ≤10 years, myoclonic jerks are not an exclusion criterion for JAE, and TAS of JME were studied only when onset was at ≥11 years, which means that JME subjects with onset of TAS between 8–11 years were either absent or misplaced in CAE. For a statistical analysis to give meaningful results, the conditions assessed should be thoroughly examined and properly defined, which does not appear to be the case in the current report of Sadleir et al. (2008). Publication of the progress of the study population first presented between 1992–1997 may resolve important issues assessed in this commentary. Most patients classified as CAE should now be in remission or will have developed features of other IGE-TAS syndromes with TAS starting in childhood as per the Table 3. Until then, there is a wealth of knowledge gathered over many years in thorough studies that may help to shed light on these issues. These must be objectively and fully assessed, paying particular attention to important differences between individual reports in patient populations, prospective or retrospective character, length of follow-up, and other study parameters. Clustering them together as in the reports of Sadleir et al. (2006, 2008) weakens their contribution and promotes erroneous assumptions. TAS and related epileptic syndromes are a formidable challenge despite significant progress made in their pathophysiology, genetics, clinical, and video EEG aspects. Their classification is a work in progress, and we should all remain open to future refinements. We are in need of thorough prospective studies with precise definitions and targets. Significant evidence of the processes underpinning these diseases may emerge, and our old notions discarded, in the best spirit of unbiased work with an open-minded and dispassionate scientific decorum. From the clinical point of view, even if IGE syndromes with TAS were a continuum or genetically the same (which is unlikely considering current knowledge in animals and humans), their differentiation has significant prognostic and management implications. This may sometimes be difficult in clinical practice, but it is not unusual in medicine where diseases are identified on the sole basis of scientific evidence. In epilepsies, current good practice recommendations promote an epileptic syndrome diagnosis, and seizure-syndrome treatment. This progress has been achieved through considerable debates against the previous detrimental lumping of all of them in “epilepsy.” Physicians have been perceptive to this progress, and we should be encouraged to this optimal practice. I am grateful to eminent colleagues who have helped me with their experiences, thoughts, and their critical review of this commentary, particularly Dr. R.A. Grünewald, who also assisted me in editing the various drafts to its final form. Conflict of interest: I confirm that I have read the Journal's position on issues involved in ethical publication and affirm that this report is consistent with those guidelines. The author has no conflicts of interest to disclose. The author has a paid consultancy with UCB Pharma S.A., and an unrestricted educational grant for a series of a multivolume edition of The Educational Kit on Epilepsies." @default.
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• W2043595857 title "Typical absence seizures and related epileptic syndromes: Assessment of current state and directions for future research" @default.
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