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Adenosine triphosphate deficiency

A genre of optic neuropathy

Article abstract-Purpose: To offer clinical evidence that deficiency of vitamin B₁₂ may adversely affect the neuronal function of patients who also have the 14,484 mitochondrial DNA mutation associated with Leber's hereditary optic neuropathy (LHON). Methods: A case of a 27-year-old man with vitamin B₁₂ deficiency and the 14,484 mitochondrial DNA mutation is presented and the literature on causes of some metabolic optic neuropathies reviewed. Results: Visual loss and neurologic symptoms of vitamin B₁₂ deficiency occurred together, at a time when the level of vitamin B₁₂ was subnormal. Vision and other sensory functions began to improve within 2 months of vitamin therapy, and normal vision eventually was restored. Conclusions: The relatively prompt improvement and the eventual complete recovery of vision following vitamin replacement therapy suggest that the subnormal level of vitamin B₁₂ precipitated visual loss. Given the clinical similarities of subnormal vitamin B₁₂, LHON, and nutritional/tobacco amblyopia, deficiency of adenosine triphosphate might be a unifying etiology for several types of optic neuropathy. This energy hypothesis provides a theoretical basis for the enigmatic phenomena of centrocecal scotomata and recovery of visual function after prolonged blindness.

NEUROLOGY 1995;45: 11-16

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