12 Wada Testing in Pediatric Epilepsy
The Wada test is an essential component of the pre-operative evaluation of epilepsy patients at most epilepsy surgery centers. In addition to establishing cerebral language representation pre-operatively, Wada memory results may be used to establish risk for postoperative memory decline and to assist in identification of focal functional deficits associated with a unilateral seizure focus.1–4 Although a substantial Wada clinical literature in adults exists, there have been relatively few reports describing Wada test experience in pediatric epilepsy surgery candidates.
Wada introduced his technique of intracarotid injection of amobarbital in the 1950s to establish cerebral language representation in adult patients who were undergoing evaluation for epilepsy surgery.5 The procedure relies on a short-acting barbiturate introduced into the internal carotid artery that temporarily anesthetizes the anterior two thirds of a cerebral hemisphere during which language testing is conducted. The most common anesthetic agent is amobarbital, although other drugs are successfully used, including etomidate,6 methohexital,7 and propofol.8 These newer agents have a shorter duration of action than amobarbital, and, in the case of etomidate, a constant infusion of drug is necessary to produce a sufficient length of anesthesia to permit language and memory testing.
After observing several cases of unanticipated significant decline in memory function after temporal lobectomy, a memory component was introduced as part of the Wada test to provide a reversible model of temporal lobe surgery in which the risk of developing severe anterograde amnesia could be estimated.9 The Wada test thus creates a reversible pharmacologic lesion in which induced behavioral deficits are thought to reflect surgical risk of including these areas in a surgical resection. At most centers performing the Wada, both language and memory functions are assessed.
Language results often guide specific clinical decision making. When surgery is planned in a hemisphere dominant for language, generally more conservative surgical approaches are used, and additional measures to protect eloquent language cortex such as electrocortical stimulation mapping are performed. Although the goals of Wada memory testing vary across epilepsy centers, the test’s primary purpose is to establish risk for postoperative memory decline. In addition, however, interhemispheric memory asymmetry scores may be used to help confirm seizure onset laterality in patients with less clearly established seizure onset. Patients in whom both structural and functional measures of unilateral mesial temporal lobe dysfunction are in agreement tend to have superior surgical efficacy, as well as decreased cognitive morbidity, in comparison with patients in whom there is incomplete agreement regarding lateralized impairment.
The majority of clinical experience with Wada testing has been derived from adults. However, because neurodevelopment in pediatric patients is incomplete, patterns of expected performance in adults cannot necessarily be generalized to pediatric groups, and the predictive ability of Wada testing to accurately forecast longterm cognitive outcomes may be altered by neuroplasticity and cognitive maturation.
Special Considerations for Pediatric Wada Testing
Testing of pediatric epilepsy patients presents unique challenges compared with adults. The Wada test is often a physically uncomfortable and emotionally frightening procedure for younger children to undergo, and they sometimes lack the appropriate maturity to participate fully in all aspects of the evaluation. Even before the potential effects of drug-induced behavioral deficits, which themselves may be frightening, the surgical aspects of catheter placement for medication delivery often exceed a child’s capacity to tolerate and cooperate with the procedure. Coaching and developing behavioral intervention techniques may be useful in decreasing the anxiety associated with the procedure, but these approaches are often of limited utility, are labor and time intensive, and are less useful in younger patients or in children with decreased cognitive abilities and less insight. Pre-Wada baseline assessment is more extensive and carefully constructed in children than adults because the stimulus materials selected for use during the Wada must be tailored to the developmental and cognitive level of each child. Because of these constraints, children younger than 7 or 8 years old are generally considered unsuitable candidates for the procedure.
In youngsters who are unusually sensitive to pain or who may have difficulties cooperating for other reasons, sedation may be administered by an anesthesiologist to assist with catheter placement.10 Propofol, for example, is sufficiently short acting that anesthesia recovery is rapid, and Wada testing can be performed within 15 to 25 minutes after propofol cessation. Thus, anxiety and discomfort associated with catheter insertion can be avoided using propofol in appropriate cases, thereby maximizing the likelihood of obtaining valid Wada behavioral results. Unfortunately, some children awaken from the anesthesia disoriented or overly emotional and require much soothing before they are capable of proceeding with Wada testing. In some cases, a parent may be an asset in helping to calm the child in the immediate post-anesthesia period. Parents may then be escorted out of the angiography suite after they have quieted their children but before amobarbital injection.
Wada Language Testing in Pediatrics
Because children who are evaluated for epilepsy surgery have extratemporal lobe epilepsy more often than adults, the critical information derived from Wada testing is often language laterality and representation, and Wada memory findings assume less importance. The need for valid determination of language lateralization by Wada testing is clear, if the gold standard of language localization is electrocortical stimulation mapping. Although stimulation mapping has reportedly been successfully performed in children as young as 4 years of age,11 in addition to the greater difficulties involved in stimulation language mapping with children, language cortex is less likely to be identified with mapping in children under 10 years of age.12 In one recent study, the presence of positive language results from stimulation language mapping was no different in children 10 years or older than it was in adults. Although these authors also described less reliable Wada language results for children younger than 10 years compared with older children, the magnitude of this difference was not as marked. Thus, Wada language testing appears more likely to succeed in identifying language representation in children than electrocortical stimulation mapping does.
Overall level of cognitive ability has been associated with the likelihood of obtaining useful Wada information in children.13 In a small series of 22 pediatric patients (ages 5–12 years), language testing was successful in all of the children with IQs of at least 70, whereas only 57% of the children studied satisfactorily completed Wada language testing if their IQs were below 70. A similar pattern was seen with Wada memory results. Children with IQs of 70 or higher had good retention scores after injection ipsilateral to seizure onset but impaired retention after contralateral injection, whereas children with IQs of at least 70 were much less likely to show this lateralized discrepancy. In another pediatric series, the Wada procedure successfully established hemispheric language dominance and memory representation in fewer than two thirds of 42 preadolescent candidates for epilepsy surgery.14 Risk factors for unsuccessful testing included low Full-Scale IQ (especially < 80), young age (especially < 10 years), and left hemisphere seizure onset. The symptoms of aphasia seen in children during Wada testing also differ from those typically seen in adults, which may complicate interpretation. Many times, children simply become mute during Wada testing, and hence, there are often no positive signs of aphasia, such as paraphasic substitution errors or circumlocutions, to help confirm that language has been affected.

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