The 20th Congress of RSCANP,

Băile Felix, 18-21.09.2019

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The 42st National Conference of Child and Adolescent Neurology and Psychiatry and Allied Professions with international participation


Autor: Svetlana Hadjiu
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West Syndrome (WS) is a multi-etiologically determined infant’s disorder. In children with prenatal causes, the pathology’s debut is early, whereas postnatal causes determine a later entrance. There exists a direct correlation between the causes defining SW and the debut age of the disorder (3-6 months old). It has been reported a greater SW incidence in boys (59%). The precocity of infantile spasms influences the severity of child’s psychomotor impairment. The most part of first symptoms appears as isolated spasms unobserved by parents (76%), thereafter reorganized in repetitive discharge salvos. Mental retardation and behavioral re-gression anticipate spasms. EEG is the only test permitting a positive diagnosis of West Syndrome. EEG records would depend on record’s length, child’s state, sleep-wake cycle, underlying pathological substrate.The deferential diagnosis was done by taking into consideration all spasm-like movements present in infants.The analyses of EEG patterns of 75 infants presenting infantile spasms during wake state showed the following patterns in WS: typical hypsarrhythmia, modified hypsarrhythmia (marked by focal epileptiform changes), absence of epileptiform changes.The neuro-visualisation of clinical electro-encephalographic data (clinical electro-encephalographic attitude) at early stages would make possible an early positive diagnosis and an adequate therapeutic attitude.




Epilepsy is the most dynamic domain of neurology and child’s neurology in particular. Along with other criticai cerebral non epileptic manifestations child’s epilepsy represents one of the most frequent age related neurologic disorders. Because of the vast heterogeneity of child’s epilepsies regarding clinical, bioelectrical, etiological, treatment and evolutional aspects, it is important to employ a highly differential approach of the epileptic phenomenon [2,9].

West syndrome is an age-related epileptic enceph-alopathy. It is generally considered as a non specific response of the immature brain to a range of multi-etiologic insults. WS belongs to the group of “catastrophal” epileptic encephalopathies and it is perceived like an incurable epileptic form. WS is the most severe form of epilepsy in infants and has a variable etio-logy-related prognosis [2].

WS is also known as infantile spasms. Described by William James West, infantile spasms are a type of sei-zures proper to infant, associated with mental retarda-tion and abnormal paroxysmal EEG patterns leading to a peculiar clinical picture named “hypsarrhythmia” [7,8]. WS represents a major problem not only for the Republic of Moldova, but also for the entire medical community because of mental retardation and neuro-psychic invalidization caused by this disorder. The in-cidence of infantile spasms is assessed to 1-2 cases per 3000 births, with a masculine prevalence [2,7].


Study of clinical and interictal encephalographic manifestation in children with WS.


75 children (31 boys and 44 girls) aged between 3 months and 1.5 years, presenting infantile-spasms form of epileptic seizures participated to the study The study had been performed at the Institute of Scientific Research in the Domain of Mother’s and Child’s Care (ISRDMCC) and Municipal Clinical Hospital Nr.l (MCH), from 1997 to 2009. Other types of seizures were excluded from the study The study group was constituted by children with asym-metrical infantile spasms, who had in their anamne-sis other types of seizures. EEG was performed on “NEUROFAX” encephalograph with a 21-chanal recording. EEG patterns’ analysis was based on the classification of different types of hypsarrhythmia proposed by R. Hrachovy et al. [7].


We noticed that the etiology of infantile spasms in children included in our study was diverse. Prenatal, perinatal and postnatal causes were noticed.

Prenatal causes: congenital brain malformations (13 children), neuro-cutaneous syndromes (4 children), chromosomal abnormalities (3 children), infec-tious fetus pathologies (3 children), and hereditary metabolic disorders (6 children).

Perinatal causes: perinatal hypoxic-ischemic encephalopathy (14 children), prematurity (12 children), hypoglycemia (1 child), neonatal herpetic encephalopathy (2 children).

Postnatal causes: infections (5 children), hem-orrhagic craniocerebral injuries (2 children), hypoxic-ischemic insults (2 children), cerebral tumors (1 child).

Clinical manifestations of children with WS were of an important variability within the present study Infantile spasms were noticeable at all children, as well as mental retard and pathological modifications of EEG pattern like typical or modified hypsarrhythmia. One of these three elements could be absent (atypical WS) except hypsarrhythmia.

In most cases, studied patients entered the disease between 3 and 6 months old with a higher incidence
in boys (59%): 18 children (24%) at 3 months old, 15 children (20%) at 4 months old, 16 children (21,3%) at 5 months old, 15 children (20%) at 6 months old, 9 children (12%) between 6 and 9 months old, and 2 children (2,7%) beyond 1 year old. We observed an earlier entrance in WS at children with prenatal causes, and a later one in children with postnatal causes. A direct correlation between the causes de-fining WS and the age of disease’s debut was found. Etiology influences the age of debut. We noticed that earlier the infantile spasms appear more severe is the psychomotor impairment of the child. In most of patients the first symptoms appeared in the form of iso-lated spasms that weren’t signalized to parents (76%), and then were organized in salvos. Parents came to see the doctor because of the loss of neuropsychic acqui-sitions and visual contact of the child, and emergence of axial hypotonia. Parents did not signalize child’s symptoms as pathological and addressed to the doctor late and that aggravated the prognosis.

In most of children, the infantile spasms took the form ofbrusque axial muscle contractions,with a du-ration of 0.2 – 2 sec, which appeared in series and in strong correlation with sleep, especially at awak-ing, and activated by stimulation. The clinical variety of spasms was important. Contractions were massive and global, with an axial predominance, concerning neck, trunk and limbs muscles, with short dura-tion, emerging separately or in salvos lasting several minutes. Each salvo contained on average 10 spasms separated by calm periods lasting 4-10 seconds. The child had the aspect of a successively flexing automat, or resembling a person who greets by flexing head and members and bending body It did not seem like an ordinary wince. In several cases, the muscle contractions concerned all the body with flexion of the head towards the trunk, flexion of superior and inferior limbs giving the aspect of “squatting child”, like the fetus in uterus.The spasms were repetitive (up to 5-10 salvos per day, several patients reaching 80 salvos per day) suggesting a positive diagnosis of WS.

The aspects of spasms in children from study lot: flexion spasms, which took the form of a rapid spasm of neck and members followed by a tonic contrac-tion lasting 2-10 sec, sometimes with abduction of superior limbs or flexion of fist, or only with rising hands in flexion – 19 children (25.4%); extension spasms, brusque extension of the head and straighten-ing superior limbs, or extension of inferior limbs from hips accompanied by the upward movement of ocular globes -10 children (13.4%). 44% of children showed flexion spasms in association with extension spasms, In both types of spasms the movements were repetitive, symmetrical and brief, taking isolated or salvo form (from ten to hundreds per day) suggesting the presence of WS in patient.

7 children (9.3%) had spasms like head flexion, that suggested greeting movement, and ocular globes elevation. 2 children (2.6%) had muscular jerks of the whole body “electrocuted aspect”, followed by a strong cry and elevation of ocular globes.

4 children (5.3%) had asymmetrical spasms associated with lateral deviations of the head and ocular globes, followed by fixed gaze and brief cry common to children with focal cerebral structural injuries.

The retardation of psychomotor development pre-ceded spasms in 82 % of cases. Mental impairment was the first symptom manifested by behavioral regression, visual loss, loss of previously acquired motor and sensi-tive skills, and absence of interest towards environment. The child was disinterested in all events behaving like a blind or deaf person (term of cortical cecity).The WS was established late in more than half of patients because the mental impairment had not evoked WS to parents and family doctors.

It is important to mention that detec-tion of neurodevelopmental impairment is an important factor to the establishment of WS diagnosis both for parents and doctors. 27 children (36%) developed motor disorders like tetraplegia (9), spastic diplegia (7), ataxia (5), athetosis (6). 9 children had microcephaly.We identified the following types of EEG patterns in WS children:

1. Typical hypsarrhythmia-marked EEG pattern was present in 33 children (44%) during waking and was constituted of a succession of chaotic slow waves and peaks of large amplitude interpolated with peaks and slow, multifocal waves in steep slope that appeared less frequently during waking. The basic rhythm was substituted by slow waves of very varied aspects, with theta and delta frequencies (1,5-2 c/s),up to polymorph elements with “saw teeth” and “steep walls” waves, and peaks combined with slow waves generating more or less typical peak-wave aspects of very large amplitude (300-600 |iV). Peaks varied from one time to another in terms of location and length. It is known that varied position of peaks linked to slow waves generates all types of peak-wave and wave-peak that are more or less slow and regulated.The large amplitude of slow waves, peaks and peaks-waves constitutes the essential characteristics of hypsarrhythmia [9] (Figure 1);

2. The EEG pattern characterized by modified hypsarrhythmia was recorded in 30 children (40%), describing peaks’ activity of a large synchronization (Figure 2);

3. The presence of focal epileptiform modifica-tions, unilateral hypsarrhythmia (but shaped like modified hypsarrhythmia with focal component) was established in 9 children (12%, suggests symptomatic etiology and localization of injury);

4. Absence of epileptiform modifications of EEG pattern – 3 children (4%).


Table 1. EEG patterns in diff erent forms of WS



Bioelectrical modifications of EEG pattern, at-tributed to different forms of hypsarrhythmia, were recorded in 72 patients (96%). In this study we con-cluded that the ratio between typical and atypical hypsarrhythmia on EEG pattern constitutes 44% / 56%.

We studied EEG with aspects of atypical hypsarrhythmia and among them we identified: unilateral hypsarrhythmia in 5 children (16.6%, that usu-allypoints to injurylocalization); slow type of hypsarrhythmia that is characterized by focal peaks during waking and abundant slow waves when falling, resem-bling the aspect of hypsarrhythmia during waking (6 children, i.e. 20%); rapid type of hypsarrhythmia in 19 children (63.3%) that is characterized by the preva-lence of rapid activity of high amplitude, multifocal anomalies, unilateral hypsarrhythmia, or unilateral or bilateral suppression-burst (SB) (Figure 3), known in hypsarrhythmia. We observed EEG with discharges of synchronic bilateral slow peak-wave complexes that represented a high risk of sweep from WS to Lenox-Gastaut syndrome [6].

In 4 children we diagnosed asymmetric unilateral hypsarrhythmia that had diverse etiology and clinical manifestations (asymmetric infantile spasms frequently having in background CNS anomalies of development and severe neuropsychic impairment), and severe prog-nosis. Symmetric infantile spasms that usually wear regional hypsarrhythmia were diagnosed in 2 children and were associated with a less severe diagnosis.

In 8 children, we observed unilateral or bilateral hypsarrhythmia with “suppression-burst” that is an atypical hypsarrhythmia and is characterized by the presence of suppression periods of bioelectrical activity lasting 2-4 c, and bursts of slow waves and peak-wave complexes (Fig. 3). It is known that usually the “suppression-burst pattern” disappears by the age of one (in most cases by 6 months old), but sometimes it can persist longer [10]. This pattern was recorded frequently in precocious parţial symptomatic epilep-sies in succession with essential focal and multifocal changes.

We identified 9 children with parţial component hypsarrhythmia with aspect of peak-wave complex pattern. The dynamic observation of the patients with focal or multifocal stable component on EEG within WS showed the passage from WS to other forms of parţial epilepsy.


Figura 1. Hipsaritmie (M.C., 3,5 luni)



Figura 2. Hipsarirmie atipică (V.S., 1,2 ani)


Figura 3. Hipsaritmie cu patternul „suppression-burst”(V.G. 8 luni)





It is important to keep in mind that intercritical EEG aspect within WS is very variable and depends on many factors: age of the child,WS etiology, under-lying pathological substratum, other precipitant factors, indicated treatment and the stage of sleep while the record is made.

The diagnosis of WS is difficult and very often belated because of ignorance of the significance of seizures, fact that leads to their undermining. When seizures are repetitive, in salvos and neurodevelop-mental losses with hypsarrhythmic EEG patterns are identified, these seizures are known as classic and are easy to recognize. EEG is the only test for a positive diagnosis of WS. EEG depends on record duration, state of child, its waking-sleep cycle and underlying pathological substratum. The differential diagnosis is made by taking into consideration all spam-like movements, present at an early age. In these cases EEG has an undeniable role.

The therapy is chosen after specifying SW causes. It is important to perform neuroimagistic investiga-tions in order to obtain a correct and complete diagnosis: CT or cerebral IRM. We observed neuroimagistic anomalies in 76% of studied subjects.These cases were attributed to symptomatic forms of WS. In all these cases children presented neurodevelopmental impair-ment and precocious infantile spasms. The prognosis was reserved with an unfavorable evolution. Only 4 children had a normal neurologic development. Idio-pathic forms of WS were very rare – 3 children, who had a normal neurologic development. All these children presented an EEG with typical hypsarrhythmia and a normal neuroimagistic examination. Children had a favorable response to valproic acid. We reached a full control of seizures. The indicated dose was 30-50 mg/kg per day. Prognosis was favorable.
We observed cryptogenic infantile spasms in 7 children. Their EEG patterns showed specific chang-es, but neuroimagistic findings were normal. WS evolution was unfavorable characterized by neurologic impairment, visual loss, autistic behavior, and cognitive disorders. In these cases the treatment was very difficult. The presence of WS in these children was underlined by the not always positive response to cor-ticotherapy. Several children were responsive to high doses of Vigabatrin. Cryptogenic forms resulted in an unfavorable prognosis and the performance of other forms of epilepsy at an older age. 10 children from our study (whose imagistic findings did not show any cortical injury) positively reacted to high doses of pyridoxine (100-200 mg by perfusion).The spasms of these children were pyridoxine – dependent.

The origin ofWS is not always confirmed. There are several complicated cases where the diagnosis techniques are not sufficient for metabolic problems.Recently, due to relations and collaboration with other countries we enriched the performance of the investigation of amino acids, serum ammonia, organic acids, lactate, pyruvate, etc.Thereby it was possible to confirm the metabolic origin of WS and to improve the correctitude of treatment.



According to R. Riikonen, the diagnosis of WS can be considered indispensable when one of the three elements of the triad (discussed below) is missing, but this approach should be revised. In conformity with the International Classification of Epilepsies and Epileptic Syndromes, WS is attributed to generalized epilepsies [1,8]. It is commonly accepted that clinical picture of WS is characterized by the following triad:

  1. Particular epileptic seizures – seizure with the aspect of infantile spasms, represented by brief, axial muscle contractions that last 0.2 – 2 sec. These contractions appear in series and are correlated with sleep, especially with the moment of waking and are not activated by stimulation. There could be flexion, extension or mixed spasms, and they are more fre-quent during waking than during sleep;
  2. Psychomotor retard, mental impairment or retard;
  3. Pathologic modifications on EEG pattern that have the form of typical or modified hypsarrhythmia (a specific bioelectric pattern that accompanies seizures) [2];

One of these three elements may be absent (atypi-cal WS) but the presence of hypsarrhythmia is obliga-tory.
Nosological estimation of WS varies and modi-fies over time, especially the last time. WS diagnosis is easy when infantile spasms are repetitive, in salvos and when associated clinical phenomena are notice-able [3, 5].

Nevertheless, the diagnosis is frequently late because of ignorance of spasms’ significance. The diagnosis of infantile spasms is erroneous because spasms may be noticed in other age-dependent en-cephalopathies: early myoclonic encephalopathy, Oh-tahara syndrome, infantile parţial symptomatic epilepsies [2].

EEG pattern in WS is the most important and the unique test for diagnosis. EEG aspect depends on recording’s duration, waking-sleep cycle, and also on affected pathological substratum.

This neurophysiologic pattern was described for the first time by F. Gibbs and E. Gibbs in 1952 as “a pattern of large amplitude and slowwaves”that varies on amplitude and duration, and, in an instant, may take focal or multifocal character. The continuity of hypsarrhythmia also represents an essential character to be observed in infant during waking. Bilateral and asynchronous peculiarity of hypsarrhythmia also is very important [5, 8, 9]. It is important to mention that 45% of cases with infantile spasms do not pres-ent hypsarrhythmia on EEG pattern, but almost all patients show peaks or focal or multifocal sharp waves [2]. Metaphoric expression of R. Harchovy says that “EEG pattern in hypsarrhythmia is chaos and an-archy” [7]. Though, EEG also may be atypical with modified hypsarrhythmia, term that was introduced in 1964 by H. Gastaut [6].

Typical hypsarrhythmic EEG is recorded inter-critically. During waking, hypsarrhythmia (hypsos – height, rhythmus – rhythm) is constituted by a se-ries of high-amplitude slow waves and peaks associ-ated in diverse proportions, without a precise relation of phase and distribution on the scalp, and without asynchrony. The base rhythm is substituted by slow waves with varied aspect, from non rhythmic sinusoidal waves with theta and delta waves (1.5-2 c/s) to polyrhythmic elements, realizing the aspect of crenel-late waves organized in “saw teeth” with “steep walls”. Peaks are combined with slow waves taking the more or less typical peak-wave form.The varied position of peaks in relation to waves leads to a large range of peaks-wave and wave-peaks that are more or less slow and regulate.

The very high amplitude of slow waves, peaks and peaks-waves (300-600 |iV) constitutes the main particularity of hypsarrhythmia, as it can be un-derstood from the name itself.

During sleep, there always appear changes in the typical bioelectric aspect of hypsarrhythmia. Batini distinguishes 3 types of modification of hypsarrhyth-mia’s patterns during sleep:

  • morphologic modifications of slow and diffiise peaks-wave, characteristic to hypsarrhythmia,they take the aspect of polypeaks-wave and appear as bisynchronic paroxysms on the background pattern that is constituted of slow anomalies;
  • fragmentation of hypsarrhythmia: synchro-nous bilateral polypeaks-wave salvos split the background pattern characterized by a hypnic rhythm that represents the sleep stage aspect;
  • modifications of hypnic rhythms in intervals between the paroxysms of a fragmented hypsarrhythmia.

In opposition to typical hypsarrhythmia, several patients present an EEG aspect characterized by waking focal peaks, and, during sleep start, they present an abundance of slow waves, a close aspect to hypsarrhythmia during waking [8,9].

Other patients represent a rapid activity of high amplitude, multifocal anomalies, and unilateral hypsarrhythmia, even a unilateral or bilateral “suppression-burst” pattern. These patterns are called “atypical hypsarrhythmia” or “modified hypsarrhythmia” [8].

H. Gastaut and R. Broughton proposed the fol-lowing classification of EEG modifications in WS [6]: ^

I. Classic (typical) hypsarrhythmia;
II. Atypical (modified) hypsarrhythmia:
— Waking fragmented classic hypsarrhythmia;
— Very slow hypsarrhythmia (major slow dys-rythmia pattern, where peaks are very rare or absent);
— Very rapid hypsarrhythmia (with the pre-dominance of peaks on bioelectrical pattern);
— Asymmetric hypsarrhythmia;
— Hypsarrhythmia associated with irritative focus.

Based on the EEG study of 290 WS patients, R. Hrachovy et al. (1984) suggested a detailed classification of modified hypsarrhythmias’ types:

1. Synchronized hypsarrhythmia, characterized by the presence of generalized discharges, synchronous bilateral slow peak-wave series, synchronized 0 and a rhythms on EEG pattern;

2. Asymmetric hypsarrhythmia with asymmetric amplitude that appears unilaterally or regionally;

3. Stable focal hypsarrhythmia;

4. Hypsarrhythmia with episodes of regional or generalized bioelectric activity suppression;

5. Hypsarrhythmia with slow high amplitude asynchronous activity and comparatively low epileptic activity [7].

A new aspect implemented in the study of EEG pattern is the “funcţional” (criptogenetic and infantile spasms that disappear over time) and “structural” (symptomatic forms of WS with severe prognosis) classification of hypsarrhythmia, suggested by B. Dal-la-Bernardina and K. Watanabe [3,10].

The vision of clinical-encephalographic data in WS is in continuous changing. Although the two groups of spasms are lesional (spasms that complicate a diffuse encephalopathy and spasms that worsen progressive or non progressive focal injuries), their epileptogenic evolution is different [8]. WS with criptogenetic origin is characterized by symmetric spasms, EEG un-derlines the presence of dependent spasm salvos, the inter-critical pattern being hypsarrhythmic, frequent and asymmetric.The evolution is unfavorable; the loss ofvisual contact takes place and the child may have an autistic-like behavior [6,10]. Idiopathic WS children with infantile spasms have a favorable mental and motor evolution and do not present residual epilepsies. Spasms start at 3-8 months, with an average of 5 months, and are symmetric and appear in salvos; waking EEG is symmetric and hypsarrhythmic. WS discharges are more accentuated in posterior zones of the brain [8].

In conformity to present day studies, typical and atypical hypsarrhythmias have different ratios. Typical hypsarrhythmia constitute 21.8% of infantile spasms, whereas atypical hypsarrhythmia represents 78.2% [6]. In our study, we observed the ratio of 44:56 between typical and atypical hypsarrhythmias (these results confirm the prevalence of symptomatic forms of WS). Other authors suggest that typical hypsarrhythmia is a less common pattern in the WS population and characterizes WS; criptogenetic type is the “veridical” one and, according to European epi-leptologists, it has a lower frequency than WS – the symptomatic form [7].

In antecedents of children with Otahara syndrome (according to retrospective data) and children with precocious WS debut (before 3-5 months old), EEG showed atypical hypsarrhythmias and even “suppression-burst’ patterns. In other cases, EEG was characterized by a rapid activity with high amplitude, multifocal anomalies, and unilateral hypsarrhythmia in alternation with other types of atypical hypsarrhythmia. “Slow-wave” pattern was frequently and exceptionally recorded during sleep. “Suppression-burst” pattern, observed in precocious epileptic encephalopathies, did not appear as a specific sign and was noticeable at the debut of epilepsy. These patterns reflected the levels of maturation processes of cortex, subcortical structures and brain stem [2,5,8,9]. Slow and diffuse peak-wave pattern, characteristic to hypsarrhythmia, frequently took the polypeak-wave aspect and appeared as bisynchronous paroxysm on the background pattern constituted of slow anomalies [8].In our study, an exclusion criterion was the presence of other types of seizures in children, reported during the first consultation. The ratio of parţial anomalies on EEG pattern constituted 8.2% in children exam-ined in our study. EEG patterns showing modified hypsarrhythmia, and suggesting focal modifications, constituted 14.3%. Asymmetric spasms, present from the beginning of disorder, were observed in the major-ity of children with this type of EEG and confirmed their focal aspect. The confirmed WS evaluated in different forms of parţial epilepsy.

The absence of epileptiform modifications on EEG pattern, observed in 5.71% of cases, in com-parison to data from other studies (18.8 %), explains the prevalence of resistant forms f WS. In WS group with criptogenetic forms, waking hypsarrhythmias reduced due to adequate therapy. On EEG patterns of these patients, we often observed an alternation of low amplitude hypsarrhythmia sectors with preserved areas of brain bioelectric activity. These types of modifications were observed during sleep or awaking. In symptomatic form WS group, we recorded persistent hypsarrhythmias or focal and multifocal activities. Seizures persisted in both groups of patients, and, in some cases, short term clinical remissions were observed.

In most cases, one focus on cerebral impairment of the child with infantile spasms, diagnosed with imagistic techniques. Myelination disorders and cortical dysplasia are diagnosed in older child because they need time to be imagistically identified [2]. A big part of cerebral anomalies are microscopic, and that is one of the reasons why it is so difficult to confirm the symptomatic etiology of WS. This is why we need more advanced techniques in identification of West syndrome’s causes.

In children with criptogenetic forms of WS, it is important to perform the pyridoxine test, as well as the metabolic examinations including: urine and plasmatic screening of amino acids, serum ammonia, organic acids, lactate, pyruvate and hepatic funcţional tests [2,8,9].

The WS treatment raises major problems. The drug therapy is not efEcient if the etiology of WS is unknown, and, moreover, it could worsen the symp-tomatology. The opinions concerning the type of drug, doses, various drug combinations and the order of injection are divergent. Steroids and vigabatrin are the most effective drugs against infantile spasms [2].

Criptogenetic forms of WS are responsive to valpro-ate, high doses of pyridoxine, etc. Recently, the panoply of new-generation antiepileptic drugs has signifi-cantly enlarged. Though, not all of these new drugs are efficient in WS.


a. WS is characterized by: specific epileptic seizures called infantile spasms, reflected in brief axial muscle contractions, having a duration of 0.2-2 sec. Infantile spasms appear in series and are correlated with sleep activity, especially noticeable at awaking and are not activated by stimulation. There could be flexion, extension or mixed spasms that are more fre-quent during waking than sleep;

b. EEG changes reflected by typical or modified hypsarrhythmia (a specific bioelectric pattern that ac-companies seizures);

c. Mental impairment or mental retardation;

d. The correct appreciation of electrophysiologi-cal and clinical data, and neuro-visualisation of data (clinical-electro-anatomical attitude) in WS could contribute to the establishment of the exact diagnosis and the differentiated choice of antiepileptic drug;

e. This attitude (discussed above) could allow us to elaborate the prognosis of WS evolution in other forms of epilepsy at early stages.



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Correspondence to:
Svetlana Hadjiu, State University of Medicine and Pharmacology Nicolae Testemitanu, Chisinau, Moldova Republic