After Ira’s wood casket was lowered into the ground on Sunday afternoon, and we bid him farewell, I stopped by the office to take his record home along with my copy of Silent Music to reflect on his incredible life. My office records documented that I first examined Doc on August 23, 1990. He was 64 years old then, coincidentally the same age that I am now. My notes reflect the conversations we had about the potential effects of Minoxidil, and how his unintended protocol of going off and back on the drug due to its side effects may have serendipitously boosted his visual function. We strategized about the future.
I needed more objective data about Doc’s function, relative to both his vision and hearing functions, and in 1992 he consented to go with me to the Department of Rehabilitation Medicine at St. Joseph’s Hospital and Medical Center in Paterson, New Jersey. I sat in with the audiologist Ronald Lunn, as he conducted an audiological assessment and auditory brainstem response (ABR) studies. His waves flatlined like the ANSD category in the slide below, and the findings were consistent with severe to profound bilateral auditory deficits. Whatever Minoxidil was apparently doing for his vision, it had no demonstrable effect on his hearing. Parenthetically Doc fueled my professional interest in the parallels between auditory and visual processing.
At around the same time I took Doc to my colleague Dr. Jerry Sherman at the State University of New York’s College of Optometry in Manhattan for the analogous electrodiagnostic assessments of his visual pathways and function. In contrast to the audiologic findings, the visual findings were remarkably good. Taken together the data supported everything that we had observed clinically about Doc’s day-to-day function. With input from me, Dr. Ivan Bodis-Wollner (renowned electrodiagnostician) and Dr. Neil Howell (acclaimed hematology expert) Dr. Sherman published an article in Optometric Management (April 1996) based on “the saga of Dr. C” titled Can Minoxidil Restore Vision?
Let’s pick up Dr. Sherman’s recounting of the story mid-stream:
“How would you explain Dr. C’s recovery? Could minoxidil have cured blindness as well as baldness? Back in 1992, we considered three possibilities. Dr. C had:
- a form of optic neuritis that went into remission without the benefit of minoxidil therapy
- a psychogenic visual loss
- an optic nerve dysfunction that was improved by minoxidil
Dr. C also underwent a complete workup for many optic nerve dysfunction etiologies, but the results were normal except in one regard. An analysis of his mitochondrial DNA revealed two point mutations related to Leber’s Hereditary Optic Neuropathy (LHON). These two mutations, secondary to LHON, often accompany more frequently encountered primary mutations that clearly cause LHON. But we couldn’t find primary mutations in Dr. C’s DNA.
This is when we hit a wall. These secondary mutations inexplicably occur in 1% to 2% of people who don’t have optic nerve disease. Even thought that’s a minuscule percentage, we still couldn’t conclude with certainty that the secondary mutations caused Dr. C’s disorder.
However, we got some insights into our mystery from an article in the February issue of Journal of Neurochemistry (Vol. 66, No. 2, 1996), which supplied evidence that minoxidil has a protective effect against neural toxicity. The article, “Manipulation of Membrane Potential Modulates Malonate-induced Striatal Excitotoxicity in Vivo”, noted that malonate is a mitochondrial toxin that causes prolonged membrane depolarization of neurons in the brains of rats.
This so-called excitotoxicity lead to neuronal death and brain lesions. But when minoxidil is added to the malonate toxin, the neurons are protected. Apparently, minoxidil causes a hyperpolarization of neurons and prevents all of the prolonged and damaging depolarization from occurring.
Last month, the Archives of Ophthalmology seemed to strengthen this theory. A study on the pathophysiology of glaucoma pointed to glutamate poisoning, which induces excitotoxicity and consequent loss of optic nerve axons. This raises the possibly of someday using minoxidil to treat glaucoma.
After more than 10 years of minoxidil therapy, Dr. C has 20/20 vision and only mild visual field constriction. Because his visual function improved, many of the axons in his optic nerve apparently didn’t die. But they did exhibit axoplasmic transport deficits. Such deficits are generally reversible if the underlying cause is removed. Is this all a strange coincidence, or is minoxidil really a wonder drug that can improve optic nerve function? Let’s hope future research will provide answers to these questions.”