Is rolandic epilepsy really benign

Correspondence: Eliana Garzon; Rua Barata Ribeiro 490, 11° andar / cj. 117; 01308-000 Sao Paulo SP, Brasil; E-mail: egarzon@uol.com.br Conflict of interest: There is no conflict of interest to declare. Received 19 September 2014 Accepted 26 September 2014 Epilepsies can be considered as benign as long as they do not compromise the longterm quality of life of the person. Benign epilepsy with centrotemporal spikes (BECTS) or rolandic epilepsy(RE) is usually considered as a good example of this situation. RE has a number of clinical and electroencephalography (EEG) features that indicate a favourable outcome. Classically, RE is described as partial epilepsy of childhood characterized by absence of neurological deficits, motor partial seizures, peculiar EEG centrotemporal spikes and spontaneous recovery. There are also children with peculiar EEG centrotemporal spikes with no clinical seizure, called EEG traits for RE. Although RE is considered a benign syndrome and, in theory, with no neurological impairment, children with RE may have neuropsychological problems more often than the general population. Even if neuropsychological involvements are considered as mild, the impact of RE on cognitive functions is far from being negligible. Delayed speech and learning disabilities have been reported, but their incidence and the long-term impact remains undetermined. The basic mechanism of cognitive compromise, in this syndrome, also remains unclear. It is difficult to determine, whether the deficits are due to the basic brain dysfunction responsible for the epilepsy, or to other factors such as, the effects of ongoing epileptic activity on developing cognitive functions. Neuropsychological studies of children with RE show that they have normal intelligence but often have limited weaknesses in various domains such as language, visuospatial abilities or isolated attendant problems. Some studies tried to demonstrate that cognitive disorders, which can occur in RE, could be temporary and more evident in the active phase of the disease. These studies seem to correlate cognitive disorderswith an increase in epileptic activity during this period. Attempts to correlate these deficits with the frequency of clinical seizures and with the side of discharges, for example, left or right side, unilateral or bilateral foci, have given conflicting results. On the other hand, when EEGs of children with dyslexiawere analyzed, 10% showed EEG traits of RE. Ten per cent means 2-5 times higher than the expected rate that is estimated to be about 2-4% in the child population. The results raise a number of questions about the relationship between dyslexiaand a specific EEG trait and RE and language or any other neuropsychological impairment. Other interesting point is that language disabilities and academic impairments found in RE are also common in relatives of RE probands. The incidence of language, reading disabilitiesand academic impairments in relatives of RE probandsare 5.4 times that in the general population. The strong probandand familial associations with reading disabilitiesand academic impairments and the similarity in neurocognitive profiles between probandsand siblings, suggest that these neurodevelopmental traits in RE should be also genetically influenced. The role of genetic influences has been sought for a long time. The hypothesis of shared genetic influences, recently has been demonstrated as a familial pattern of risk for reading disability, speech sound disorder, presence of EEG traits of RE, and migraine in families with RE. These results strongly suggest that susceptibility to comorbidities in RE is inherited and not the direct result of recurrent seizures or discharges. Clinically, relevance of these studies is that early evaluation and intervention may benefit these children academically. DOI: 10.1590/0004-282X20140195 EDITORIAL