Skip Navigation LinksHome > December 2012 - Volume 32 - Issue 4 > The Scholarly Contributions of Daniel M. Jacobson, MD
Journal of Neuro-Ophthalmology:
doi: 10.1097/WNO.0b013e3182726bcd
The Fifth Jacobson Lecture

The Scholarly Contributions of Daniel M. Jacobson, MD

Trobe, Jonathan D. MD

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Department of Ophthalmology and Visual Sciences, Kellogg Eye Center, Ann Arbor, Michigan.

Address correspondence to Jonathan D. Trobe, MD, Kellogg Eye Center, 1000 Wall Street, Ann Arbor, MI 48105; E-mail: jdtrobe@umich.edu

The author reports no conflict of interest.

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML full text and PDF versions of this article on the journal's Web site (www.jneuro-ophthalmology.com).

The North American Neuro-Ophthalmology Society (NANOS) has but one named lectureship. Established in 2007, the Daniel M. Jacobson Memorial Lecture honors a man who accomplished a rare trifecta of scholarship: 1) the selection of topics of clinical importance; 2) the use of impeccable research methods; and 3) the production of superbly written publications.

In a 15-year period that extended from the beginning of his neuro-ophthalmology fellowship at the University of Iowa in 1985 to the onset of a terminal illness in 2000, he authored 75 articles or letters in respected peer-reviewed journals (Archives of Ophthalmology, American Journal of Ophthalmology, Ophthalmology, Journal of Neuro-Ophthalmology, Neurology, Annals of Neurology) (see Appendix, Supplemental Digital Content, http://links.lww.com/WNO/A58) In 48 of those 75 publications, he was either the first or the second author. During the decade before he became ill, he authored 44 papers at a rate of more than 4 publications per year. His publications included not only case reports but also pharmacologic experiments, case–control studies, case series, surveys, and topic reviews covering every aspect of neuro-ophthalmology. These works have had an enduring effect on patient management. In 2001, The Marshfield Clinic, where he conducted most of his work, recognized his achievements by bestowing on him its Gwen D. Sebold Research Fellowship Award.

In his scholarly endeavors, he was guided by three criteria. 1) Is this an important and unsettled issue? 2) Would addressing it make a difference in patient management? 3) Are the available means sufficient to permit meaningful research?

He was enormously successful. Here is a sample of the issues he addressed and the impact of his findings.

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DOES PUPIL SPHINCTER SUPERSENSITIVITY TO DILUTE CHOLINERGIC EYEDROPS REALLY SIGNIFY A POSTGANGLIONIC DISORDER?

Background

Cholinergic supersensitivity of the iris sphincter is said to be a hallmark of a postganglionic lesion of the pupillomotor pathway. Investigators have questioned this idea, but with little rigor.

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Approach

In a prospective trial (1), he instilled pilocarpine 0.1% into the eyes of 3 groups of subjects: 1) 13 patients with compressive or ischemic third nerve palsies; 2) 16 control subjects; and 3) 10 control subjects in whom one pupil had been previously dilated with hydroxyamphetamine.

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Findings

The pupils of the 16 control subjects constricted minimally to dilute pilocarpine, allowing him to establish a cutoff for pathologic pupil constriction. Based on that cut-off, 9 of 13 patients with preganglionic third nerve palsies displayed cholinergic supersensitivity, a finding that was unrelated to the duration or cause of the palsy but was proportional to the degree of anisocoria. Among the control subjects with hydroxyamphetamine-induced anisocoria, the degree of constriction was correlated with the degree of anisocoria.

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Conclusions

He concluded that cholinergic supersensitivity likely did not reflect trans-synaptic degeneration because it occurred in acute palsies. Because large pupils constricted more than small pupils to dilute pilocarpine, even in those without palsies, he postulated that pupil size may be a confounder.

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Contribution

The meticulous and laborious design and execution of this study make it especially notable. It formed the basis of a later study (2) in which he showed that there was no difference in the amount of pupil constriction produced by dilute pilocarpine in the affected pupils of 11 patients with Adie syndrome and 11 patients with preganglionic compressive, traumatic, or congenital third cranial nerve palsy. The upshot of this pair of studies was to dismiss pupil cholinergic supersensitivity as a reliable sign of a postganglionic pupillomotor lesion.

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WHAT IS THE NATURE OF EPISODIC UNILATERAL MYDRIASIS?

Background

Episodic mydriasis raises fear on the part of the patient and triggers imaging studies on the part of concerned physicians. But this phenomenon is rarely observed by physicians, so its mechanism has been a matter of conjecture. Are the features suggestive of a parasympathetic or a sympathetic disturbance? Who is at risk? Is it a manifestation of migraine? Does anything precipitate the attacks?

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Approach

The author had examined 7 patients with episodic mydriasis, too small a number from which to draw meaningful conclusions. So he surveyed regional neuro-ophthalmologists with a detailed questionnaire and tight exclusion criteria (3).

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Findings

The 24 patients included 19 women (80%), mostly between the ages of 20 and 50 years. Eleven patients were examined during an attack, 7 by the author and 4 by other neuro-ophthalmologists. Many patients had a history of migraine (58%), but most mydriatic episodes did not occur during typical migraine attacks. Events appeared to be unprecipitated, but there were usually other symptoms, such as blurred vision in the affected eye (62%), headache (37%), and discomfort around the affected eye (21%). The attacks occurred with a broad frequency (median: 2.5 attacks per month), and a duration ranging from 10 minutes to 7 days (median: 12 hours). Near vision and accommodation were impaired in 4 patients. Anisocoria ranged from 1 to 3 mm, increasing in light in 6, remaining unchanged with different light levels in 1, and increasing in darkness in 1. There was no tonicity or distortion of the pupils and there were no other neuro-ophthalmic abnormalities. Dilute pilocarpine testing was normal in 6 of the 7 patients who were tested, showing supersensitivity in only 1 patient. Among 24 patients examined in between attacks, no notable findings were discovered.

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Conclusions

Episodic mydriasis probably represents a temporary and isolated disorder of parasympathetic iris innervation in some patients and sympathetic overactivity or underactivity in others. Migraine is often a background condition, but these episodes are usually not coincident with a migraine attack.

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Contribution

This publication expanded the profile of a common and important clinical phenomenon. For the first time, it gathered a reasonably large number of patients who were examined during an attack and tested for signs of pupillomotor denervation. It showed that useful information can be gathered on such a clinical disorder with a valid survey instrument sent to reliable observers.

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HOW MUCH ANISOCORIA OCCURS IN PATIENTS WITH THIRD NERVE PALSY CAUSED BY DIABETES?

Background

Classic teaching has been that anisocoria and impaired pupil constriction to light are features more characteristic of compressive than ischemic lesions of the third nerve. But documentation has been based on retrospective studies in which these features were not the main interest. In previous reports, the frequency of reported anisocoria ranged from 14% to 32%. To decide how far to push intracranial imaging in patients with acute palsies, it would be important to know if there is an upper limit to the degree of anisocoria in diabetic patients with ischemic third nerve palsies.

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Approach

This study (4) used extremely rigorous criteria for patient selection and documentation of clinical features. There were 26 patients with diabetes and isolated third nerve palsy, all examined by the author and defined by appropriate ductional deficits, the absence of other pertinent clinical findings or imaging evidence for an alternative cause, and full recovery of the palsy within 6 months. The subjects had a firm biochemical diagnosis of diabetes. Pupil size was measured under controlled lighting and fixation conditions with a standard pupil gauge.

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Findings

Fourteen patients (54%) were found to have anisocoria, mostly 1 mm or less (80%), and not more than 2.5 mm. In some of the patients, the anisocoria did not resolve, suggesting that it might have been at least partially caused by diabetic dysautonomia.

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Conclusions

Anisocoria is common in diabetic third cranial nerve palsy but rarely exceeds 1 mm.

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Contribution

This publication suggested that anisocoria of greater than 1 mm should not be attributed to diabetes. Moreover, because the mechanism of third nerve palsy in patients with hypertension and other risk factors for arteriosclerosis may be similar to that in diabetes, one could reasonably assert that anisocoria of greater than 1 mm is strong evidence of a nonischemic cause of isolated third nerve palsy. In a later study of 24 consecutive cases of third cranial palsy with anisocoria of 0.5 to 2 mm (5), the author showed that compressive lesions (including aneurysms) were as commonly the cause as microvascular ischemia. The upshot of these 2 studies is that a small amount of anisocoria is common in ischemic third nerve palsies (“relative pupil sparing”), but it can also occur in nonischemic palsies for which urgent imaging is necessary.

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WHAT ARE THE RISK FACTORS FOR ISCHEMIC OCULAR MOTOR PALSIES?

Background

Diabetes has been a well-established risk factor for ischemic (“microvascular” and “vasculopathic”) ocular motor cranial nerve palsies. However, it is also widely known that patients without diabetes are prone to such palsies. What are the risk factors in those patients? No study had applied adequate epidemiologic methods to answering this question.

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Approach

In this case–control study (6), strict inclusion and exclusion criteria provided assurance that the diagnosis of an ischemic, extra-axial cause for the palsy was firm. For the 65 patients who met entry criteria, examination included a thorough history probing standard arteriosclerotic risk factors, height, weight, blood pressure, cervicothoracic auscultation, hemogram, random glucose, cholesterol, and electrocardiography. Most patients who did not have diabetes underwent brain imaging, acetylcholine receptor antibody testing, chest x-ray, sedimentation rate, and protein electrophoresis, as well as tests for antinuclear antibody, syphilis, and Lyme disease. Each patient was matched for age and gender with a patient attending The Marshfield Clinic who did not have an ocular motor palsy. The control patients had undergone virtually the same battery of medical assessments as the palsy patients. The three ocular motor cranial nerve palsies were almost equally represented.

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Findings

The 2 risk factors that emerged as significant for ischemic ocular motor palsy were diabetes and left ventricular hypertrophy. Hemoglobin A1C was higher among diabetics with palsies than in those without them, suggesting that poorly controlled diabetes may be an important risk factor. Because hypertension was so common among control subjects, it was not significantly associated with a palsy. However, a marker of poorly controlled hypertension, left ventricular hypertrophy, was implicated.

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Conclusions

The principal risk factor for ischemic ocular motor cranial nerve palsy is poorly controlled diabetes. Chronic hypertension, as evidenced by left ventricular hypertrophy, is probably an additional risk factor, although it could not be established by blood pressure measurements in this study.

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Contribution

This was the first of 2 elegant in-house case–control studies of risk factors for a common disorder. In establishing with proper methods that poorly controlled diabetes and chronic hypertension are likely the chief causes of ischemic ocular motor cranial nerve palsies, it signaled the need to modify these risk factors.

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OVER WHAT PERIOD OF TIME DO ISCHEMIC THIRD AND SIXTH NERVE PALSIES PROGRESS?

Background

Conventional wisdom has been that ocular motor cranial nerve palsies caused by extra-axial nerve ischemia reach a maximal deficit within days of onset. Therefore, progression of deficit beyond a few days would suggest an alternative cause such as a compressive lesion.

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Approach

From the author's Marshfield Clinic patient files extending over the previous 8 years, he reviewed clinical data using the rigorous inclusion criteria established for his earlier study of risk factors for ischemic ocular motor cranial nerve palsies.

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Findings

Among 16 patients with third nerve palsy (7), 11 (69%) showed progressive ductional deficits over a period of 3 to 23 days (median: 10 days). Those who had progression took a mean of 11.2 weeks to resolve, whereas those who had no progression took a mean of 7.2 weeks to resolve. The progressive and nonprogressive groups could not be distinguished by risk factor profile. Similar findings were noted in a later study of 35 patients with ischemic sixth nerve palsy (8).

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Conclusions

Progression of ductional deficits over a period extending up to 3 weeks occurs in ischemic ocular motor cranial nerve palsies.

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Contribution

These studies firmly established that, even though the mechanism of these ocular motor cranial nerve palsies is believed to be ischemia, ductional deficits may continue to worsen over a week or more. Such progression should not cause the clinician to reject an ischemic cause unless there are other persuasive features. The author acknowledged that patients were not examined daily, so he might have overestimated the duration of progression.

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HOW DO YOU DISTINGUISH IDIOPATHIC FROM NON-IDIOPATHIC DIVERGENCE INSUFFICIENCY?

Background

Adult-onset divergence insufficiency, defined as comitant esodeviation present only with distance viewing and with full ocular ductions, is a perplexing entity. It is known to occur in otherwise neurologically intact individuals (“primary” type) but also in those with a variety of neurologic conditions, including brainstem lesions and increased intracranial pressure (ICP) (“secondary” type). The natural history of the primary type had been unknown.

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Approach

In a retrospective study (9) of patients examined at The Marshfield Clinic over the previous 12 years, the author identified 20 patients who had no other neurologic manifestations (primary type) and 15 patients who had other pertinent neurologic manifestations (secondary type). The clinical features of the 2 groups were described on initial evaluation and on follow-up.

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Findings

There were 5 important findings: 1) the ocular motility and alignment measurements at the time of initial evaluation did not distinguish the 2 groups; 2) in the primary group, there were no pertinent clinical or imaging abnormalities on follow-up; 3) in the primary group, the diplopia resolved in nearly half of the patients over a maximum period of 26 months; 4) in the secondary group, the underlying neurologic condition had already been diagnosed at the time of initial evaluation or evident on that examination; 5) in the secondary group, increased ICP was the most common underlying condition, followed by cerebellar degeneration, temporal arteritis, progressive supranuclear palsy, and brainstem stroke.

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Conclusions

Although the ocular motor features did not distinguish the primary (idiopathic) and secondary groups, they could be separated by the fact that an underlying neurologic condition was evident in all patients in the secondary group at the time of initial evaluation.

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Contribution

Although retrospective and small, this study was suitably designed to tell clinicians that there will be clinical clues at outset as to whether the patient with divergence insufficiency has an idiopathic condition that requires no further workup or a nonidiopathic condition that does. It also suggested that spontaneous improvement occurred often enough to warrant postponement of realignment surgery. An open question is whether the neurologic abnormalities would be obvious to a non-neurologist! The finding of spontaneous improvement in the idiopathic group is at variance with my observations, so I wonder if the author inadvertently included some patients with spasm of the near reflex or subtle ischemic sixth nerve palsy.

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IS THE OPTIC NEURITIS THAT BEGINS AT OR AFTER AGE 50 SIMILAR TO THE OPTIC NEURITIS OF YOUNGER INDIVIDUALS?

Background

The clinical profile of typical optic neuritis, which affects individuals under age 50, has been well established by the Optic Neuritis Treatment Trial and other large studies. Excluded from those studies were older patients because the diagnosis of optic neuritis would have been uncertain at study entry. Could the results from the studies of younger people be generalized to older people?

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Approach

This retrospective study (10) involved 14 patients ranging in age from 50 to 72 years (average: 58 years) after exclusion of more than half of a pool of 31 patients because of confounding features. All patients had undergone appropriate studies to exclude alternative diagnoses.

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Findings

The optic neuritis in these older individuals had clinical features identical to the optic neuritis in younger patients.

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Conclusion

The optic neuritis of late onset is probably the same disorder as that of earlier onset.

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Contribution

This study provided important information about optic neuritis, a diagnosis often dismissed if it develops for the first time after age 50. The author cautioned that in this cohort, one can be sure only in retrospect that the diagnosis is typical optic neuritis, so that a wider evaluation should be done at the time of initial evaluation to exclude other optic neuropathies.

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WHAT ARE THE RISK FACTORS FOR NONARTERITIC ANTERIOR ISCHEMIC OPTIC NEUROPATHY?

Background

Hypertension and diabetes had been assumed to be important risk factors for this condition, but the information came largely from uncontrolled descriptive studies.

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Approach

The author received strong support from The Marshfield Clinic biostatisticians in designing this elaborate population-based case–control study (11). Patients met strict criteria for the diagnosis of nonarteritic anterior ischemic optic neuropathy (NAION). To reduce biases as completely as possible, the author chose not one but 2 control groups, one from a health database established for the surrounding community and the other from patients examined by internists or family physicians at The Marshfield Clinic. Standard arteriosclerotic risk factors were selected for study.

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Findings

Diabetes was the most robust risk factor, but it accounted for only a small proportion of cases. Hypertension did not meet the standard of a risk factor, perhaps because it was common in the control groups.

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Conclusions

Diabetes, but not hypertension, is a risk factor for nonarteritic ischemic optic neuropathy.

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Contribution

This study established a new model for examining risk factors in neuro-ophthalmic disorders. The failure to show hypertension as a risk factor differs from other studies with less rigorous design and is intriguing. Other factors must be at play, such as cupless optic discs (“disc at risk”) or sudden drops in blood pressure.

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DOES A RELATIVE AFFERENT PUPIL DEFECT OCCUR IN PATIENTS WITH UNILATERAL OPTIC NERVE DYSFUNCTION IN LEBER HEREDITARY OPTIC NEUROPATHY?

Background

Several investigators have reported that there was no relative afferent pupil defect (RAPD) in patients with Leber hereditary optic neuropathy (LHON) who have clinically apparent optic neuropathy in only one eye. The absence of a RAPD is meaningful because it would lead clinicians away from a diagnosis of optic neuropathy.

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Approach

In this study (12), entry criteria included patients with proven LHON mutations, normal visual acuity and visual field in the unaffected eye, no confounding medical conditions, and an RAPD measured with neutral density filters. To the author’s single case were added 4 from the University of Iowa, 2 from neuro-ophthalmologists trained at the University of Iowa, and 3 from NANOSNET. To show whether the RAPD in LHON obeyed the principles identified for RAPDs in other optic neuropathies, the author correlated the size of the RAPDs in the LHON patients with their visual field loss using a template designed by Stanley Thompson, MD.

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Findings

All 10 patients had RAPDs. They ranged from 0.3 to 1.8 log units, with all but 1 patient having 0.6 log units or higher, identifying a defect easily observable with the swinging light test. The RAPDs were of a size expected on the basis of the extent of visual field loss.

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Conclusion

Easily discernable RAPDs are always present in patients with apparently uniocular LHON.

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Contribution

This first rigorous study of RAPD in LHON was limited by the small patient cohort. Contrary to the findings in this study, observers have continued to note the absence of a RAPD in this setting, and the subsequent discovery of melanopsin-containing ganglion cells has provided a rationale for this phenomenon.

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DOES COMPRESSION OF THE OPTIC NERVE BY AN ENLARGED SUPRACLINOID CAROTID ARTERY CAUSE VISUAL LOSS?

Background

Compression of the intracranial optic nerve by an enlarged supraclinoid carotid artery was a postulate for optic nerve damage before the advent of advanced imaging. But neurosurgical decompression was unhelpful and sometimes caused worsening of the optic neuropathy. Because enlarged carotid arteries are associated with arteriosclerosis, optic neuropathy in these patients was alternatively attributed to NAION. The author had accumulated a roster of patients who lacked the clinical features of NAION and appeared to have progressive optic neuropathy without explanation other than clearly visible displacement of the intracranial optic nerve by an enlarged supraclinoid carotid artery.

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Approach

The patients were drawn from the author’s files at The Marshfield Clinic.

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Findings

In the first of 2 publications (13), the author reported the frequency of imaging evidence of compression in 100 consecutive patients without evidence of optic neuropathy who had undergone T1 coronal magnetic resonance imaging for conditions unrelated to loss of vision. He found that compression occurred on at least one side in 17% of patients. In the second publication (14), he described the results in 18 patients with progressive optic neuropathy and compression of the affected optic nerve. Many had been followed for glaucoma but had been referred for neuro-ophthalmological evaluation because they had visual field loss considered atypical for that diagnosis. Some patients had diabetes or hypertension, but none reported acute visual loss. The progression of visual loss extended from 3 weeks to 21 years, with a median of 4 years, but this information was largely gleaned from the records of referring ophthalmologists. Most patients had progressive visual acuity loss but in only 4 patients was there solid documentation of progressive visual field loss. Most patients had nerve fiber bundle visual field defects; only one patient had a chiasmal pattern. Optic disc pallor was present in most affected eyes, cupping consistent with glaucoma was present in only 2 eyes.

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Conclusions

There are patients who have progressive optic neuropathy and imaging evidence of ipsilateral carotid artery compression of the optic nerve. Given the lack of evidence for an alternative cause, compression is the likely mechanism.

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Contribution

This is the author’s most controversial work. The data were acquired and displayed scrupulously. But documentation of progression was often based on the documentation of referring physicians. Acknowledging that carotid compression of the optic nerve is often noted incidentally in patients without optic neuropathy, the author advised long-term observation to document progressive damage. In the years since these publications, no one has followed through on his idea.

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WHAT ARE THE APPROPRIATE DIAGNOSTIC CRITERIA FOR THE DIAGNOSIS OF IDIOPATHIC INTRACRANIAL HYPERTENSION?

Background

The criteria for diagnosing idiopathic intracranial hypertension (IIH; previously called “pseudotumor cerebri”) were first elaborated in 1937 by Walter Dandy, MD, a neurosurgeon at Johns Hopkins University and the inventor of pneumoencephalography. The criteria included clinical manifestations of increased ICP with normal cerebrospinal constituents, normal or small ventricles ascertained by air ventriculography, and no evidence of a brain mass. Acknowledging advances in neuroimaging, Lawton Smith, MD substituted computed tomography for ventriculography in 1985.

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Approach

This review article, authored in collaboration with Friedman (15) was prompted by the recognition that the diagnostic criteria for IIH needed updating to encompass new evidence.

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Findings

There were 4 principal modifications. First, the symptoms and signs should include the visual manifestations of papilledema. Second, the lumbar puncture opening pressure should be more than 250 mm H2O as recorded in the lateral decubitus position because research had established that opening pressures between 200 and 250 mm H2O are within the normal range. Third, brain vascular imaging should exclude occlusive disease of the dural venous sinuses as the cause of high ICP. Fourth, there should be no contributory systemic illness or medication use.

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Contribution

Although the disease had not changed since Dandy’s time, more mimickers had been recognized and imaging methods had evolved. The timely modifications wisely expanded the definition of IIH to take account of these facts.

These excerpts from the author’s extensive scholarly work (see Appendix, Supplemental Digital Content) show how one well-liked, respected, and talented individual, backed by a medically sophisticated institution with good recordkeeping and a relatively captive population, can generate a body of clinical research without extensive financial support or collaboration. It does not convey how honestly and graciously he conducted his research and how beautifully he phrased his submissions.

Each publication begins with a succinct recapitulation of the issue. That is followed by a review of the contributions others have made, generously acknowledging the good work and gently stating the flaws. With a clear framing of what is left to be done, the reader can appreciate the need for the methodology, which is thoughtfully designed and clearly explained. Biostatisticians play a critical role in study design. Patients who do not fit are summarily excluded. The results are compactly displayed in text, figures, and tables that are easy to read. In discussing the results, the author adheres to the narrowest of implications, always providing a reasonable explanation and admitting the limitations of the studies.

The scholarly contributions of Daniel M. Jacobson, MD have set a high investigative bar for us, his colleagues, and established clinical guidelines that vastly improve the care of patients with neuro-ophthalmic disorders.

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REFERENCES

1. Jacobson DM. Pupillary responses to dilute pilocarpine in preganglionic 3rd nerve disorders. Neurology. 1990;40:804–808.

2. Jacobson DM. A prospective evaluation of cholinergic supersensitivity of the iris sphincter in patients with oculomotor nerve palsies. Am J Ophthalmol. 1994;118:377–383.

3. Jacobson DM. Benign episodic unilateral mydriasis. Ophthalmology. 1995;102:1623–1627.

4. Jacobson DM. Pupil involvement in patients diabetes-associated oculomotor nerve palsy. Arch Ophthalmol. 1998;116:723–727.

5. Jacobson DM. Relative pupil-sparing third nerve palsy: etiology and clinical variables predictive of a mass. Neurology. 2001;56:797–798.

6. Jacobson DM, McCanna TD, Layde PM. Risk factors for ischemic ocular motor nerve palsies. Arch Ophthalmol. 1994;112:961–966.

7. Jacobson DM, Broste SK. Early progression of ophthalmoplegia in patients with ischemic oculomotor nerve palsies. Arch Ophthalmol. 1995;113:1535–1537.

8. Jacobson DM. Progressive ophthalmoplegia with acute ischemic abducens nerve palsies. Am J Ophthalmol. 1996;122:278–279.

9. Jacobson DM. Divergence palsy revisited. Natural history of idiopathic cases and neurology associations. Arch Ophthalmol. 2000;118:1237–1241.

10. Jacobson DM, Thompson HS, Corbett JJ. Optic neuritis in the elderly: prognosis for visual recovery and long-term follow-up. Neurology. 1988;38:1834–1837.

11. Jacobson DM, Vierkant RA, Belongia EA. Nonarteritic anterior ischemic optic neuropathy. A case-control study of potential risk factors. Arch Ophthalmol. 1997;115:1403–1407.

12. Jacobson DM, Stone EM, Miller NR, Pollock SC, Fletcher WA, McNussen PJ, Martin TJ. Relative afferent pupillary defects in patients with Leber hereditary optic neuropathy and unilateral visual loss. Am J Ophthalmol. 1998;126:291–295.

13. Jacobson DM, Warner JJ, Broste SK. Optic nerve contact and compression by the carotid artery in asymptomatic patients. Am J Ophthalmol. 1997;123:677–683.

14. Jacobson DM. Symptomatic compression of the optic nerve by the carotid artery. Clinical profile of 18 patients with 24 affected eye identified by magnetic resonance imaging. Ophthalmology. 1999;106:1994–2004.

15. Friedman DI, Jacobson DM. Diagnostic criteria for idiopathic intracranial hypertension. Neurology. 2002;59:1492–1495.

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