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Carlos E. Mendoza Santiesteban, M.D.

General Information

Carlos E. Mendoza Santiesteban, M.D.



  • Fax: 954-210-1037


  • Ophthalmology


English, Spanish

Clinical Areas

Adult and pediatric neuro-ophthalmology, visual electrophysiology, medical retina, hereditary retinal diseases, macular diseases, retinitis pigmentosa, optic nerve diseases, toxic-nutritional optic neuropathies, mitochondrial optic neuropathies, retina in neurological diseases (parkinson’s disease, multiple sclerosis, alzheimer’s disease, multiple system atrophy), hydroxichloroquine retinal toxicity, optical coherence tomography of the retina and optic nerve.


  • Assistant Professor of Clinical Ophthalmology

Research Interests

  • The Eye in Familial Dysautonomia.
  • Retinal Biomarkers of Neurological Diseases (Parkinson’s Disease, Multiple Sclerosis, Alzheimer’s Disease, Multiple System Atrophy).
  • Hereditary Optic Neuropathies.
  • Retinal and Optic Nerve Imaging.
  • Hydroxichloroquine Retinal Toxicity.
  • Hereditary Retinal Diseases.
  • Visual Electrophysiology.
  • Neuro-Ophthalmology.



Saul Delgado College
Havana Medical University
Neuro-Physiology Residency
Havana Medical University
Ophthalmology Residency (Second Degree)
Havana Medical University
Neuro-Ophthalmology Clinical Fellowship
New England Eye Center, Tufts University
Medical Retina and Visual Electrophysiology Fellowship
New England Eye Center, Tufts University


Dr. Mendoza field of work includes adult and pediatric clinical neuro-ophthalmology and medical retina, with special interest in diagnostic tools such as visual electrophysiology and retinal imaging. He has been working in these areas for more than 20 years. He was trained as medical doctor, neuro-physiology resident, second degree ophthalmology resident, medical retina/electrophysiology fellow and neuro-ophthalmology fellow. He received additional post-graduate training courses in Germany, Italy and Japan. He was director of visual electrophysiology unit at the Institute of Neurology and Neurosurgery, Havana, Cuba, and later director of neuro-ophthalmolgy at the Cuban Institute of Ophthalmology. From 2013-2016 he served as medical director of the visual electrophysiology unit at the New England Eye Center, Tufts University, Boston, Massachusttes, USA. His early works were about the use of visual electrophysiology in the diagnosis of eye and brain diseases, showing the role of the electroretinogram and visual evoked potentials in the study of several optic neuropathies and retinopathies. He paid special interest to the Cuban epidemic optic neuropathy (CEON) which affected more tan 50 000 cubans in the early 1990s. He compared the similitudes between CEON and Leber Hereditary Optic Neuropathy (LHON) and with his group, postulated the mitochondrial origin of the CEON.

During his residencies he started get interested in a newly developed eye imaging technology to study the retinal structure. Optical coherence tomography (OCT) was a major breakthrough in ophthalmology and has been a technological core of many of his research projects during the last 18 years. He was part of an international team that build the first normative database for the retinal nerve fiber layer thickness.

As director of the neuro-ophthalmology service at the Cuban Institute of Ophthalmology he developed several research projects in conjunction with international academic institutions about the use of OCT, microperimetry, and visual electrophysiology in the diagnosis of several types of optic neuropathies and retinopathies. During that period he also published results about orbital tumors surgery using minimally invasive approaches.

After moving to USA, he started working with familial dysautonomia (FD) patients who suffered from a progressive visual loss that was attributed to chronic corneal damage due to dry eye and corneal insensitivity. He found that, despite the scientific literature descriptions, most of the patients have clear enough corneas to allow better vision. He found that a very specific optic neuropathy, closely resembling those from mitochondrial etiology, was the cause of visual loss in FD population. Using OCT and later confirmed by human pathology he demonstrated that the loss of highly energy dependent P ganglion cells was an specific lesion in all FD patients.

During the period as director of visual electrophysiology at the New England Eye Center, Tufts University, Boston, MA, he continued working in the field of retinal imaging (OCT) and visual electrophysiology to study the structure-function relation in the retina and how to identify retinal biomarkers for neuro-ophthalmological diseases. He found that different types of optic neuropathies have early and specific patterns of ganglion cell loss that can be detected by OCT and visual electrophysiology.

In the last years he has been working in identification of retinal changes, measured by OCT, in patients with neurological diseases including Parkinson’s disease (PD) and Multiple System Atrophy (MSA) and other alfa-synucleinopathies. He found that ganglion cells are affected in PD and in MSA in distinctive patterns. In PD retinal ganglion cell loss appears to occur mainly in the macula whereas in MSA this occurs in the peripheral retinal. This pattern seems to be a specific biomarker which progress overtime as the neurological scales worsen. He demonstrated that measuring the retinal structure and function valuable information can be obtained for detection and monitoring disease progression.

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