treatment period, blood lactate decreased to 2.64 & 0.22 on a DCA regimen of 20 mg/kg/day for 7 days and to 1.90 & 0.10 with 30 mg/kg/day for 3 days ( p < 0.05). The child showed no complication or clinical improvement during drug therapy.

Ours is the first report of D C A in the treatment of a PDHC disorder. This and other studies 121 have shown the efficacy of DCA in treating hyperlactatemia. However, be- cause of the complexjty of P D H C regulation, hyperlac- tatemia may result from other biochemical disturbances which secondarily affect P D H C activation. Therefore, re- duction of blood lactate per se may not affect the primary disease process. Longer treatment periods would be neces- sary to determine if DCA can arrest the progression of SNE. Animal studies are under way to study the cause of DCA neurotoxicity and to investigate less toxic analogues of therapeutic potential. At present, chronic administration of the drug cannot be recommended.

Supported in part by agrant from the Muscular Dystrophy Associ- ation.

Department of Neurology and Division of Endocrinology,

Vanderbih University Medical Center Nashville. T N 3 7232

References

Department of Medicine

1. Blass JP, Cedarbaum SD, Kark RAP: Rapid diagnosis of pyru- vate and keroglutarate dehydrogenase deficiencies in platelet- enriched preparations from blood. Clin Chim Acta 75:2 1-30, 1976

2. Coude FX, Saudubray JM, DeMaugie F, et al: Dichloroacetate as treatment for congenital lactic acidosis. N Engl J Med 299:1365-1366, 1978

3. DeVivo DC, Haymond M W , Obert KA, et al: Defective acti- vation of the pyruvate dehydrogenase complex in subacute nec- rotizing encephalomyelopathy (Leigh disease). Ann Neurol

4. Pincus JH: Subacute necrotizing encephalomyelopathy (Leigh’s disease): a consideration of clinical features and etiology. Dev Med Child Neurol 14:87-101, 1972

5. Stacpoole PW, Moore GW, Kornhauser DM: Toxicity of chronic dichloroacetate. N Engl J Med 300:392, 1979

6:483-494, 1979

Failure to Include Coauthor of Paper Hugo W. Mnser, M D

Due to an oversight on my part, D r Aubrey Milunsky’s name failed to be included in the paper entitled “Ad- renoleukodystrophy : elevated C-26 fatty acid in cultured skin fibroblasts,” by Moser HW, Moser AB, Kawamura N , Murphy J, Milunsky A, Suzuki K, Schaumburg H, Ki- shimoto Y (Ann Neurol 7:542, 1980). That this was in- deed an oversight is evidenced by the fact that the Eunice Kennedy Shriver Center had been listed as one of the places of origin, and none of the other authors is associated with that center. D r Milunsky’s name has been added to all the reprints of the paper. I take full responsibility for chis unintended oversight and apologize for it.

The John F . Kennedy Initiiute 707 hT Broadway Baltimore, M D 21205

648 Annals of Neurology Vol 8 No 6 December 1980