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Brain, Vol. 118, No. 6, 1529-1546, 1995
© 1995 Guarantors of Brain


research-article

Landau—Kleffner syndrome

Treatment with subpial intracortical transection

Frank Morrell, Walter W. Whisler, Michael C. Smith, Thomas J. Hoeppner, Leyla de Toledo-Morrell, Serge J. C. Pierre-Louis, Andres M. Kanner, Janice M. Buclow, Ruzica Ristanovic, Donna Bergen, Michael Chez and Hisanori Hasegawa

Departments of Neurological Sciences and Neurosurgery, Rush-Presbyterian-St Luke's Medical Center and The Rush Epilepsy Center Chicago, Illinois, USA

Correspondence to: Correspondence to: F. Morrell, MD, Rush-Presbyterian-St Luke's Medical Center, 1653 W. Congress Parkway, Chicago, IL 60612, USA

Landau—Kleffner syndrome (LKS) is an acquired epileptic aphasia occurring in childhood and associated with a generally poor prognosis for recovery of speech. It is thought to be the result of an epileptogenic lesion arising in speech cortex during a critical period of development. Utilizing a new surgical technique designed to eliminate the capacity of cortical tissue to generate seizures while preserving the normal cortical physiological function, we have treated 14 children with aphasia, seizures and a severely abnormal EEG by multiple subpial transection of the epileptogenic cortex. Seven of the 14 patients (50%) have recovered age-appropriate speech, are in regular classes in school and no longer require speech therapy. Four of the 14 (29%) have shown marked improvement, are speaking and understanding verbal instruction but are still receiving speech therapy. Thus, 11 of the 14(79%), none of whom had used language to communicate for at least 2 years, are now speaking—a rate of sustained improvement considered unusual in this disorder. This study documents the value of a treatment modality not previously used in LKS. Success depends on selection of cases having severe epileptogenic abnormality that can be demonstrated to be unilateral in origin despite a bilateral electrographic manifestation

Landau—Kleffner syndrome; multiple subpial transection; epiletogenic lesions; synaptogenesis

Received April 26, 1995. Accepted July 22, 1995.


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