S E C O N D A R Y L A T E - O N S E T L E N N O X - G A S T A U T S Y N D R O M E :
A C R I T I C A L V I E W
AMILTON ANTUNES BARREIRA * MICHEL PIERRE LISON**
Starting preferentially between 1 and 6 years of age, the epileptic siezures
observed in the Lennox-Gastaut syndrome ( L G S ) may show characteristics
due to the level of brain maturation in this age range. The observation of
differences in the ictal behavior of patients whose syndrome had started after
the 6th year of life (LOLGS) showed greater predominance of tonic-automatic
and tonic-clonic seizures and of partial seizures with complex symptomatology1 4 .
These differences may be related to the level of brain maturation of the patients
at the time of onset of the syndrome. Other notable characteristics of this group
of patients with the syndrome initiating after the 6th year of life are the
almost total absence of previous history of diffuse encephalic aggression and
the moderate reduction of intellectual level. A review of the literature shows
considerable incidence of cases starting after 6 years of age ( 2 2 % )1
. Thus
the observation of the ictal, interictal and electroencephalographic behavior, as
well as the detection of factors capable of triggering diffuse encephalic
aggression in patients with LGS initiating after 6 years of age, compared to
the same aspects in patients whose syndrome started before 6 years of age
(EOLGS), becomes of great practical and theoretical importance. Characteristic
patterns may indicate specific diagnostic treatment, evolutionary aspects and
therapy for patients with LOLGS.
Clinical-electroencephalographic follow-up of a group of patients with LOLGS for an average period of 2.5 years oermitted us to observe a behavior similar
to that of patients with early-onset LGS, except for a few features1 -4
. The results are briefly presented here, followed by critical considerations.
M A T E R I A L A N D M E T H O D S
In a group o f 66 patients with Lennox-Gastaut syndrome, 15 w e r e found to have had the first manifestations o f the syndrome after the 6th y e a r of life. Of these, 12 were followed f o r a period o f time varying from 8 months to 6 years and 5 months (2 years and 8 months average). E i g h t patients w e r e observed during hospitalization and all w e r e followed o n an outpatient basis, with visits scheduled every 2 months. T h e characteristics o f the epileptic seizures, described b y t w o o r m o r e relatives a n d / o r observed b y us, w e r e recorded during each visit. T w e l v e patients w e r e followed for m o r e than 7 months, 11 f o r m o r e than 1 year, 7 f o r m o r e than 2 years, 3 f o r m o r e than 3 years, and 2 f o r m o r e than 5. A t the end of the follow-up period all patients had reached puberty according t o the criteria o f Tanner 19. T h e treatment used w a s in general agreement with the programs proposed b y Speciali and Special! & Lison 8.
Usually, a fixed d r u g treatment w a s maintained after the first y e a r of follow-up. All patients were submitted to the INV20 and W I S C 2 1 tests during the last year of follow-up, except f o r patient A C M (case 2 ) , w h o died in his sleep at 13 y e a r s and 5 months o f age.
T h e characteristics o f the seizures occurring during E E G examination were written on the recording paper in a time relationship with the respective graphic alterations. T h e epileptic phenomena w e r e described a c c o r d i n g t o the reviews o f Lison 12, Gastaut 6 Broughton a and Bancaud 5. Seizures with t w o types of epileptic phenomena in association are considered complex, and seizures with three o r more phenomena are considered mixed, and have recently been the subject o f a publication 4. The EEG recordings made during the visits and during hospitalization w e r e obtained with 8-channel GRASS apparatus, models 6 and 8 10B. W e describe here the interictal electroence-phalographic findings considered > to b e m o s t relevant. R e c o r d i n g s were selected at variable time intervals of three months o r m o r e f o r counts o f interictal generalized spike-slow w a v e complexes (frequency o f 2.5 H z . o r less; usually from 2 to 2.5 H z )
( G S S W C ) . T h e counts w e r e divided b y the time, and the number o f GSSWC per minute ( G S S W C / m i n ) was obtained. F o r the recordings o f 4 patients (cases 3, 5, 7 and 11) it w a s possible t o compare the frequency o f GSSWC during rest and activation b y hyperpnea. T h e EEGs o f a patient (case 1) w e r e not included in the counts because they did not satisfy these requirements. T h e E E G findings for complex and mixed seizures that w e r e recorded b y us and had not been previously reported in the
literature have been published in a previous paper 4.
R E S U L T S
1. Case Reports
of the eyes t o the left. In s o m e seizures, loss of consciousness appeared not to be complete, since during the episodes the patient seemed to try to find a better position in his chair, with movements that could not b e characterized as automatic. However, h e did n o t answer w h e n called b y his name f o r several seconds. Finally, he did answer when called, with his eyes still turned t o the left. Occasionally he has abundant salivation. Variations o f the. manifestations described w e r e observed clinically and the seizures recorded b y EEG. T h e main ones w e r e : palpebral myoclonus, conjugate deviation o f the e y e s and head t o the left w i t h palpebral m y o c l o n u s ; previous findings associated w i t h mastigatory automatisms. During follow-up, seizures with loss o f tonus and falls w i t h serious injuries occurred. A p p r o x i m a t e l y three years after the onset of the epileptic picture, generalized tonic-clonic seizures started to occur, especially during sleep and coinciding with the introduction o f ethosuccimide into the therapeutic program. A little before the beginning of the tonic-clonic episodes, oligo-clonic tonic seizures occurred, but only when he w a s medicated w i t h nitrazepan. A t the beginning o f the epileptic picture, the frequency was o f 3 t o 5 atypical absences p e r day, which w e r e reduced after the onset of the tonic-clonic seizures. A t the end o f the period o f observation he had tonic-clonic seizures, particularly during sleep, atypical absences and atonic seizures. T h e W e i c h b r o d t reaction in the cere-brospinal fluid (CSF) w a s slightly opalescent. T h e patient w a s born b y normal delivery and his neuropsychomotor development was normal until the onset of the syndrome. A paternal aunt has epilepsy. H e has a history o f teniasis. Electroencepha-lographic features: E E G obtained during wakefulness. Between 10 and 11 years of age, the background activity consisted o f 10 H z . alpha rhythm moderately irregular in the posterior projections and w i t h g o o d differentiation f o r the anterior ones. Theta waves w e r e sporadically intermingled w i t h the basal rhythm. Bursts of theta waves of high amplitude and up to 1.5 seconds duration occur in C - P . Diffuse, pseudorhythmic
3 3
spike-wave bursts consisting o f 1.5 t o 5 H z . spike-waves also occur. A t times the spikes have a " s l o w " frequency. Activation b y hyperpnea causes a s l o w i n g d o w n of the background activity and frequent pseudorhythmic spike-wave bursts. Several atypical absences with palpebral myoclonus have been recorded. A t times the pseudo-rhythmic burst are followed b y delta waves. F r o m 11 t o 15 years of a g e the background activity slowed d o w n progressively, reaching the theta band in the last recordings. Diffuse spike-slow w a v e bursts persist, always triggered at higher frequency b y hyperpnea (which also causes diffuse s l o w i n g d o w n of the r e c o r d i n g ) . Intermittent photic stimulation did not modify the EEG.
2 months, while watching television. T h e seizure w a s tonic and rapid. On the following d a y she suffered a fall in school, with transitory and brief l o s s of consciousness. F r o m that time onward she started t o have consciousness disorders of a paroxismal nature, with o r without alterations in muscle tonus. Initially treated with phenobarbital and diphenyl-hidantoin + deoxyephedrine and later with several different therapeutic programs, she suffered tonic and tonic-clonic seizures and simple and c o m p l e x atypical absences, atonic and hemitonic. Some generalized tonic-clonic seizures were preceded b y massive bilateral myoclonus. T h e tonic seizures, which resisted treatment, predo-minated during somnolence. T h e results o f neurological examination w e r e normal except for the mental level. N o familial history of epilepsy was reported. Electroencephalo-graphic features: EEGs obtained during wakefulness. The background activity is irregular in shape and amplitude in all projections. F o u r to 6 Hz. theta rhythm, occasionally intermingled with beta waves, is encountered in all EEG recordings. N o postero-anterior differentiation w a s observed. Amplitude is asymmetrical in several recordings with the presence o f w i d e r and lower-frequency waves on the left ( L ) . Several bursts of spike-slow waves in the right ( R ) rolandic-parietooccipital o r rolandic areas. Bifrontal spikes-slow waves of higher amplitude o r symmetrical are observed on the L . Diffuse delta wave paroxisms predominating at times on the R and at times on the L, or unilaterally on the L, are recorded in some EEGs. Bilateral sharp wave paroxisms in a recording, and unilateral on the L in others. Diffuse delta wave bursts, o r bursts limited in the projection t o the L occurred in the penultimate recording obtained at 22 years of age. Diffuse SSWC are observed in all recordings except one. Diffuse SSWC were observed up t o the end of follow-up. A predominance of bifrontal amplitude occurs in most bursts, to the R in some, and in P3-01 in others. Pseudorhythmic bursts o f 3 H z . and spike-slow waves are observed. Secondary ^ s y n c h r o n i z a t i o n is well characterized. SSWC paroxisms in Tg, - TQ o r Tg - T&
and Τ - Τ are followed b y diffuse spike-slow wave discharges. Tonic, hemitonic
4 6
seizures and complex atypical absences with palpebral myoclonus were observed during EEG recording.
atypical absences. W e witnessed several tonic-clonic seizures during status epilepticus. The same epileptic manifestations identified at the beginning continued up to the end of the follow-up period, with daily tonic seizures. T h e intellectual level of this patient was the best in the group studied. A cousin died b y d r o w n i n g when he had a seizure while fishing in a river. A niece is epileptic. Electroencephalographic features: E E G recordings obtained during spontaneous somnolence. Background activity, observed during the times when the patient w a s awakened for activation b y hyperpnea, consists of diffuse theta waves. F o c i of delta waves projecting tempo-rally-occipitally t o the R (in a single recording) and of parasagittal spike-wave complexes o f 3c/sec (also in a single recording) w e r e identified. Bifrontal discharges of spike-slow wave complexes were identified in all E E G recordings. Three Hz. spike-wave complexes were observed in o n e E E G recording. Diffuse spike-slow wave discharges, 3 Hz. spike-wave and pseudorhythmic discharges (both complexes) were iidentified, although sporadically. Atypical attacks were observed during EEG, with palpebral myoclonus, tonic seizures and typical absences.
2. History Related to Etiological Factors
F o u r patients with LOLGS (cases 3, 7, 8 and 12) have a history of perinatal hypoxia. One patient (case 10) has a clinical and histological diagnosis of neurofi-bromatosis. A female patient (case 4) had early puberty. One patient (case 2) showed appendicular ataxia when examined neurologically. The patients with perinatal h y p o x i a had the following intervals between the first manifestations of the syndrome and the present o n e s : case 3, 10 years and 6 months; case 7, 10 years and 3 months; case 8, 7 years and 2 months, and case 12, m o r e than 9 years. F o u r patients (cases 2. 4, 5 and 12) have relatives with epilepsy. Five patients had epileptic seizures (cases 2, 4, 6, 7 and 11) and nine showed p s y c h o m o t o r retardation (cases 1 through 4 and 6 through 10) before the onset o f the syndrome. These findings demonstrate that prolonged intervals of time may elapse between diffuse encephalic agression and the onset of the syndrome, and that, with the exception of one patient (case 5) (with a relative suffering from epilepsy), the remaining 11 have some history of previous cerebral aggression.
3. Intellectual Level and Neurological Examination
T h e intelligent quotient ( I Q ) of 9 of our patients was less than 46 on the W I S C scale. One patient reached 84 and another 76. Ten patients obtained less than 20% yield when submitted t o the I N V test, and one obtained 80%. In contrast to the elevated frequency of mental retardation, w e noted the absence of neurological alterations in all patients except o n e w h o had appendicular ataxia i.
4. Epileptic Seizures
The following kinds o f seizures, in decreasing order of frequency, were identified during the first year of f o l l o w - u p : tonic (10 patients), atypical absences (9), tonic-clonic
auto-matism ( 1 ) , versive ( 1 ) , and typical absences ( 1 ) . After the first year, in addition t o the previous ones, atonic seizures w e r e identified in 2 patients, tonic-clonic seizures in 1, and tonic seizures in another. T h e most frequent associations occurred between tonic seizures, atypical absences, tonic-clonic seizures, and atonic and hemitonic seizures. In general, the frequency o f epileptic manifestations during the first year of study was o f one o r m o r e seizures a d a y o r o f o n e t o 6 p e r week. T w o patients had less than 9 seizures p e r year during the last 2 years o f follow-up. T h e simple epileptic manifestations o f o u r patients coincide with those o f patients studied in our University Hospital whose syndrome started between 1 and 6 years o f age, except f o r a higher incidence of generalized tonic-clonic attacks and f o r a lower frequency of seizures in LOLGS. S i x o f our patients showed c o m p l e x and mixed epileptic manifestations that were or were n o t comparable t o those observed i n patients with EOLGS.
5. Interictal EEG
T h e paroxismal interictal E E G activity o f o u r patients consisted o f : generalized spike-slow wave c o m p l e x e s ; generalized spike-fast wave c o m p l e x e s ; pseudorhythmic bursts of generalized s l o w - and m o r e than 3 H z . spike-wave c o m p l e x e s ; «grand mal pattern» o f Gibbs, Gibbs and L e n n o x ; focal discharges and secondary bysinchroni-zation 3. W i d e variability w a s observed in the incidence o f spikes and slow waves throughout evolution. Hyperpnea m a y activate spike-slow wave complexes 3. Back-ground activity w a s slowed d o w n in all recordings. T h e E E G findings overlap with those encountered in EOLGS.
DISCUSSION
A critical revaluation of the effects of antiepileptic drugs in the serious epileptic syndromes of childhood gave rise to surprising doubts on the efficacy of the treatment programs commonly used w>,u,ie. A s a consequence, we recommend a perfectly controlled execution of drug trials keeping in mind the spontaneous fluctuations of the clinical signs and symptoms, of the EEG, and, above all, the search for criteria for determining the probabilities of satis-factory evolution. In cases with high risk factors in terms of the neuropsy-chological future of the child, correct evaluation of the medical history and of the age when the West and Lennox syndromes started was considered to be of the greatest importance, with a secondary role reserved for treatment. From this point of view, we emphasize the importance of determining guide-lines considered to be critical in terms of the age range within which the syndrome arose. It is generally stated that, the earlier the onset of the syndrome, the worse the prognosis. In childhood myoclonic encephalopathy with hypsarr-hythmia, the onset of spasms before 4 months of age is associated with higher mortality and lower incidence of recovery1 0
. In the Lennox syndrome, deeply retarded patients suffer their first seizure, on the average, at 17.6 months, whereas those with good mental development had their first epileptic seizure around 4 years of age 7
neurosycho-logical sequelae and prior organic etiology. This represents the so-called secondary form of the syndrome, with the fixation of primitive types of epilepsy that generally resist treatment and are relatively unchanged throughout evolution1 7
.
On the basis of these considerations and of the findings by Oiler Daurella1 4 , it may be possible to construct a theoretical model of late-onset Lennox-Gastaut syndrome. The patients involved are those most likely to show few organic antecedents (the older the age, the larger the number of "primary" cases) and better development up to the onset of the syndrome, who are subject to a high proportion of nonspecific epileptic attacks, either generalized (mainly tonic-clonic seizures and possibly atypical absences) or partial, with emphasis on seizures of complex symptomatology. The control of the epileptic and electroencephalographic manifestation is likely to be more common than in patients with the early form, and, as a rule, the devastating effects on intellectual function commonly observed during the evolution of the early form may not be observed.
Our findings, however, show that this model does not apply to our patients.
Investigation of the personal and hereditary history of intellectual level, of the semiology of the epileptic seizures and of the clinical and electroence-phalographic evolution demonstrated a notable similarity between our patients
and those whose syndrome started at the usual age. The most relevant difference is a longer "incubation period" of the epileptic syndrome which,
in most cases, occurred in patients with a remote history of cerebral aggression (perinatal hypoxia and psychoneuromotor retardation). Thus, our group of patients is characterized by the predominance of "secondary" forms, which
goes against the impression that, the later the onset of generalized epilepsy, the higher the frequency of primary forms.
The numerical importance of the secondary forms in the present group limits and fixes the clinical expression of the syndrome. As a consequence of the secondary nature of the affection, the evolutionary perspectives of neuro-psychomotor development are reduced. This fact probably occurs with the epileptic seizures. The quantitative and qualitative similarity of the syndrome under study to EOLGS may not reflect the development of clinical expression at a time of higher or lower brain immaturity, as proposed by Osawa et a l .1 5
achieved up to the time of onset of the factors responsible for triggering the epileptic syndrome. It is probable that forms of transitions between "petit mal" and "petit mal variant" (the "intermediate petit mal" of L u g a r e s i1 3
) and incomplete or atypical forms of Lennox syndrome are part of the primary forms.
The ictal and interictal differences in semiology are limited to the higher incidence of generalized tonic-clonic crises in patients with late onset of the syndrome, to the lower polymorphism of complex and mixed seizures and to the practical absense of neurological alterations in relation to the frequency of such alterations observed in patients with early onset Lennox Gastaut syndrome in our University Hospital.
S U M M A R Y
From a g r o u p of 66 patients with the Lennox-Gastaut syndrome, 12 w h o s e
manifestations had started after the 6th year of life w e r e selected f o r study. T h e s e
patients were observed clinically and electroencephalographically for an average
period of 2.5 years. W e concluded that the late-onset syndrome can: occur
after a l o n g interval between diffuse encephalopathy and the first clinical ma-nifestations, with or without previous alterations in p s y c h o m o t o r development;
be associated from the onset with serious mental retardation; exhibit simple,
complex and mixed seizures similar to those observed in the early form. T h e s e
patients can a l s o : suffer complex and mixed epileptic seizures previously unreported;
paroxismal interictal E E G abnormalities that overlap those of the early f o r m ;
and spike-slow w a v e complexes in the E E G that can be actived b y hyperpnea. Our results demonstrate that the incidence of L G S after 6 years of a g e d o e s
not necessarily imply a l o w e r frequency of organic antecedents, or beter
neu-r o p s y c h o m o t o neu-r development up to the onset of the syndneu-rome oneu-r the pneu-resence
of a higher rate of nonspecific seizures (generalized or partial seizures, and
mainly those with elaborate s y m p t o m a t o l g y ) . T h e critical and encephalographic
expression of the syndrome, which is secondary and starts after the 6th year of age, may depend at least in part on the a g e when diffuse encephalopathy
started.
R E S U M O
Sindrome de Lennox-Gastaut secundaria com inicio após o 6º ano de vida:
considerações críticas.
D e um grupo de 66 pacientes c o m sindrome de Lennox-Gastaut ( S L G ) , selecionaram-se e s e observaram 12 c o m manifestações sindrômicas se iniciando
a p ó s o 6º ano de vida. Esses pacientes foram o b s e r v a d o s clínica e eletrence¬
falograficamente durante um período médio de 2,5 anos. Concluiu-se que a
sindrome c o m início tardio p o d e : o c o r r e r após um l o n g o intervalo entre a
agressão encefálica difusa e as primeiras manifestações clínicas c o m ou sem
mista) semelhante à da forma p r e c o c e . Esses pacientes p o d e m ainda apre-sentar: crises epilépticas c o m p l e x a s e mistas não referidas anteriormente na literatura; anormalidades E E G paroxísticas intercríticas que se s o b r e p õ e m às da forma p r e c o c e ; no E E G c o m p l e x o s ponta-onda lenta que p o d e m ser ativa-d o s pela hiperpnéia. N o s s o s resultaativa-dos ativa-demonstram que a inciativa-dência ativa-da S L G a p ó s o s 6 anos de idade, necessariamente não implica em menor freqüência de antecedentes o r g â n i c o s , em melhor desenvolvimento neuropsicomotor até o início da síndrome e na presença de maior p r o p o r ç ã o d e crises não específicas (generalizadas ou parciais, principalmente as c o m sintomatologia e l a b o r a d a ) . A e x p r e s s ã o crítica e eletrencefalográfica da síndrome, secundária e se iniciando a p ó s o 6º ano de vida, poderia, pelo m e n o s em parte, ser dependente da idade em que incidiu a a g r e s s ã o encefálica difusa.
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