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   kankusta duo





They are BENIGN that is the outcome epileptic as well as neurological is NORMAL. Normal future neurodevelopment and no secondary epilepsy. Immediately there is a problem: what about children who had benign neonatal seizures and at 8 develop Rolandic spikes? But let's continue on.

To determine the benign aspect of NNS one must take into account:

     -Aetiology +++

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     -Date of onset

     -Type and Duration


     -Intercritical neurological status

     -EEG Critical and Intercritical

     -mono vs. polytherapy

 Since initial description in 1964, there has been 144 cases reported.

     -No known aetiology

     -Onset usually 2nd or 3rd day but as late as 3rd month.

     -Seizures are either clonic or tonico-clonic or apneic. Rarely tonic. Uni or bilateral sometimes alternating. Short lasting less than 1 to 3 mn they are isolated and can be repeated over next weeks.

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     -In between seizures the child is normal.

     -EEG: No particular anomaly described in the Intercritical state. Theta pointu alternant can be seen. Critical discharges have no particular characteristic: short uni or bilateral discharges.

     -Treatment is PHB.

     -Evolution is benign and the neurological outcome is normal. But there has been children who developed further seizures. They have always been easy to control.

      Syndrome specificities:

          Male = female

          Autosomal dominant transmission

          Anomaly on long arm of chromosome 20, exactly on q13.2



Benign familial neonatal seizures are rare; transmission is autosomal dominant, gene on 20q13.2. They begin on the 2nd or 3rd day with clonic or apneic seizures. There is no specific EEG criteria. There is no evidence of any etiological factor. 14% of infant will evolve into an epilepsy later.