David Glendenning Cogan (1908–1993)
“What’s in a name? That which we call a rose by any other name would smell as sweet.”
William Shakespeare
The eponymous David Cogan was born in Fall River, Massachusetts on February 14, 1908.
His mother, Edith Ives Cogan, was an ophthalmologist and he was naturally drawn to
it. He graduated from Harvard Medical School and completed his ophthalmology residency
at Massachusetts Eye and Ear Infirmary in 1935.[1] Here he met his mentor, Frederick
Verhoeff. Their collaboration was one of mutual respect and friendship. While Verhoeff
acknowledged him as his adopted son and heir, Cogan, in multiple reports, recounted
the personality of Dr. Verhoeff that influenced his own development. Till the very
end, Cogan remained the eyes and ears for an elderly, but enthusiastic Verhoeff, who
would continue to attend scientific meetings. He was one of the founding members of
the Ophthalmic Pathology Club, known today as the Verhoeff–Zimmerman Society.[2]
His contributions to ophthalmology are vast and varied, but his life was also adventurous
to say the least. As a Mosely traveling fellow, he went to Switzerland, Germany, and
Holland for further experience between 1937 and 1938.[3] While in one of these visits,
he happened to be in Germany during the Austrian Anschluss. His last paper was published
posthumously on the life of Adolf Hitler and his medical conditions which included
a spell of hysterical blindness, hyperopia, vitreous hemorrhage, and Parkinsonism!
In the same paper, Cogan recounted his experience of traveling to Czechoslovakia and
getting caught trying to smuggle some German money simply because he was going to
return in a few days.[4] Cogan also assisted Dr. Dunphy (the then Chief of Massachusetts
Eye and Ear Infirmary [MEEI]) in the cataract surgery of Cardinal Cushing, who did
not want anybody to know that he needed surgery. The two performed the surgery in
the Cardinal’s bedroom![2]
During his career, Cogan published more than 500 papers, editorials, and three books.
Although recognized as a neuro-ophthalmologist, his publications have been in all
fields, as is evident from the eponyms associated with him. Cogan taught pathology
and neuro-ophthalmology sections of Harvard Post-graduate Course. His two books –
Neurology of the Ocular Muscles (1948) and Neurology of the Visual System (1966) –
established him as an authority in this field. In a tribute to Dr. Cogan, John W.
Gittinger recounts, “Unlike some senior scientists, it was more difficult to be a
co-author with Cogan on a paper he did not write than on one that he did. He wrote
well, liked to write, and wanted to be associated only with work that he felt was
of high quality. He would ask that his name be removed if a manuscript did not meet
his criteria.”[2]
One of the first syndromes (Cogan’s syndrome) that he described was in 1945 and included
four patients with non-syphilitic interstitial keratitis associated with abrupt onset
of vertigo, tinnitus, and profound deafness.[5] While he credited others for expanding
the syndrome, he continued to publish on it till 1989.[2]
He described the epithelial basement membrane dystrophy (Cogan’s microcystic dystrophy),
oculomotor apraxia, which he presented in the Jackson Memorial Lecture in 1952, and
association of hypercalcemia with band keratopathy.[2]
Cogan was part of the Atomic Bomb Casualty Commission and went to Hiroshima in the
aftermath of the bombings in World War II. In his reports, he described the clinical
characteristics: doughnut-shaped configuration of the cataract involving the posterior
capsule and granular opacities and vacuoles in the anterior capsule, progression from
a dot in the posterior pole to peppery granules with a clear center, and the histopathologic
features of radiation-induced cataract.[6
7] He even reproduced them experimentally in animals and established once and for
all that the lens was one of the tissues most sensitive to radiation injuries.[2]
Cogan and Reese reported the clinical and pathological descriptions of two cases of
iris nevus syndrome (Cogan–Reese syndrome) and cited one similar case reported by
Klien. All three were middle-aged females with unilateral glaucoma and pedunculated
nodules on a sector of the iris and focal ectropion uveae [Fig. 1]. Interestingly,
the eyes were enucleated because of suspected melanoma. Histopathology revealed nevi-like
features on the iris with an ectopic Descemet’s membrane extending from the posterior
surface of the cornea. They suggested a congenital basis for the clinical features,
while admitting similarities between and differentiating from neurofibromatosis and
iris melanoma.[8]
Figure 1
Drawing of an iris seen clinically with multiple pedunculated pigmented nodules resembling
diffuse melanoma[8]
He also described a new sign of ocular myasthenia gravis (Cogan’s lid twitch), which
he referred to as “twitch response” or “irritable lid phenomenon”. “The typical twitch
response is observable in a myasthenia patient with ptosis, and is usually best demonstrated
by having a patient change his gaze from infraversion to the primary position. The
lid then shows a momentary upward twitch.” He recorded the twitch on films and projected
the pictures at a reduced rate, thereby measuring each twitch to last for less than
quarter of a second. He explains in his paper that the inertia and visual fixation
of the globe dampen any visible twitch response in the globe. The twitch is attributed
to the easy fatiguability but rapid recovery of the muscles in myasthenia gravis.
The eyelid (levator) is relaxed when the patient looks down and shows an increased
elevation when the patient assumes primary gaze, but appears only as a twitch since
it lasts for a fraction of a second.[9]
Senile scleral plaques have been described since 1929 as “calcareous degeneration
in sclera,” “senile degeneration of the sclera,” “senile thinning of sclera,” “circumscribed
scleromalacia at high age,” and “hyaline scleral plaques.” We all know them popularly
as Cogan’s plaques. Cogan and Kuwabara described these in 1959 and simply described
them as “focal senile translucency of the sclera.” They reported 25 clinical cases
and 30 histopathologic cases. These are focal slate-gray, often symmetric areas, seen
between the limbus and insertion of the horizontal recti in patients in their eighth
to ninth decade. They clarified that histologically there is no scleral thinning,
but only increased translucency with reduced cellularity, despite the erroneous name,
normal collagen, no hyalinization, and plaques of calcification in some cases.[10]
In 1943, when Frederick Verhoeff was forced to retire, he was handed the directorship
of the Howe Laboratory of Ophthalmic Research. Despite opposition from the administration,
ophthalmic research flourished in the Howe Laboratory under the able leadership of
Dr. Cogan for 30 years.[2] This has been referred to his “extended family” and his
students, his adopted children.
Cogan was the Clinical Chief at Massachusetts Eye and Ear Infirmary and Chair of Department
of Ophthalmology between 1962 and 1968.[11] He stepped down after 6 years because
of differences with the administration of Harvard Medical School, but continued to
teach in the medical school. He held elective courses for the fourth year medical
students who were interested in ophthalmology, in the basement of the nursing school
dormitory, much to the envy of the ophthalmology residents who did not have this opportunity
of learning directly from him. He was the Editor-in-Chief of the Archives of Ophthalmology
from 1960 to 1966.[2] In 1988, he selected a group of ophthalmologists, historians,
and librarians to come together to discuss the aspects of ophthalmic history, forming
the American Ophthalmic History Society. This was in preparation for the Academy’s
centennial celebration to be held in 1996, for he predicted he would not be present
and knew that ophthalmic history would require more serious study rather than just
listing of facts. Today, the Society has been renamed as the Cogan Ophthalmic History
Society.[1
2]
He always favored collaborations and encouraged young ophthalmologists and researchers.
“The common lay idea that a person can acquire and develop knowledge for its own sake
without expecting recognition may be true of older people who indulge in their own
rosy reflections. But it’s not true for younger people just starting out. These people
need to be identified with their accomplishments in order to be promoted. It’s important
for a man to have his name appear, to be singled out. Then he’ll be sought as a consultant.
When the time comes for promotion or tenure, he’ll be properly considered. I think
it’s a travesty for the senior person to take credit at the expense of what his assistants
have done.”[2]
For a man having multiple eponyms to his credit, his opinions on them were rather
bleak while bringing out his humility [Table 1]. “My connection with other entities
to which you refer were similarly chance observations during a career, now coming
to a close, in which I had an unusually favourable academic position. They were modest
contributions that have reflected undue credit to me because of the eponymic designation.
Most eponyms, like most people, serve a useful purpose for a time. During their life
tenure they establish a coterie of friends, develop a sort of cultural identification,
and, of course, are ever subject to critical evaluation. But their life span is finite.
In conclusion, eponyms (and descriptive terms) have their place. But eventually they
may become obsolete and a burden to the cause they have served. At the appropriate
time they should be enshrined in the literary museum.”[2
3]
Table 1
Eponyms associated with David Cogan
Cogan’s signs and syndromes
Cogan’s syndrome: oculo-audio-vestibular disease
Cogan’s microcystic dystrophy: epithelial basement membrane dystrophy
Cogan–Reese syndrome: iridocorneal endothelial syndrome
Cogan’s lid twitch: twitch of the ptotic eyelid in patients with myasthenia gravis
Cogan’s plaque: focal areas of scleral translucency
Cogan’s rule: homonymous hemianopia with asymmetric optokinetic response- lesion nonvascular
and in deeper portion of the parietal lobe
For David Cogan, age was just a number. At 72, he revived his learning and study of
piano. His last publication was at the age of 80.[2] David Cogan died on September
9, 1993. Despite his opinions, ophthalmologists are indebted to his work. He may be
gone, but never forgotten.
“How vain, without the merit, is the name.” Homer
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.