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Show /,"",",1 "l Clil/iml Nl'IIH'-(Jl'ltt/III/JI/(J/(JSI/ hi!): 74-7.'i. 1~/l6_ Permanent Infarctions Complicating Migraine © 1986 Raven Press, New York In this issue of the JournaL there is an article entitled "Migrainous Central Retinal Artery Occlusion" by Dr. Barrett Katz that has incited considerable secretion of endogenous norepinephrine and perhaps various other catecholamines by members of the editorial board-so much so, that it has prompted two different editorial responses! The "bottom line" of Dr. Katz's paper is that a 29year- old migraineur suffered a typical bout of hemicrania with a bout of monocular visual loss in the right eye. He was started on Inderal 20 mg twice a day. He took a total of three doses within the next 12 h, and was found to have a central retinal artery occlusion as confirmed by the exquisite fundus photograph in the paper. The question was raised then as to the possible etiologic role of Inderal in the pathogenesis of the central retinal artery occlusion. Having seen permanent branch artery occlusions, cilioretinal artery occlusions, posterior cerebral artery occlusions, and the like complicating untreated migraine, this editor thought that relating this complication to poor lnderal, one of our most effective antimigrainous drugs, might do a great disservice to the many, many physicians who commonly rely on this medication as their first line of defense against migraine, one of the commonest villains encountered in private practice. Indeed, in a Iitiginous society, publishing such a single case in an article might do more harm than good. Therefore, it was thought wise to have an editorial comment on this, and an editorial was solicited from Dr. Burde. When his editorial returned (see page 72 in this issue), this editor was "shook"-from a journalistic point of view. Upon discussing the matter with Dr. N. J. Schatz, he [Dr. Schatz] pointed out that he gave the course with Dr. Burde and that he was surprised at this, because he personally used lnderal to treat all forms of migraine all the time, and had found it extremely effective. Further correspondence and phone calls ensued and Dr. Katz added a slight change of emphasis to the end of his paper, and Dr. Burde suggested that we write a single editorial comment to the 74 paper. However, after further consideration, it seemed best simply to write another editorial and let the readers enjoy the differences of opinion and emphasis. The reason the paper and these comments are being published is that we want to be open to the truth; and the reason that both editorial comments are being presented is that we certainly do not want to throw the baby out with the bath water as we look at the matter. Every neuro-ophthalmologist should read pages 735-47 in the 1390-page encyclopedic text The vertebrate visual system by Stephen Polyak, M.D., published in 1957 by the University of Chicago Press in Chicago. Polyak, one of the most meticulous and prolific neuroanatomical investigators, was one of the first to define accurately the size of the foveal cones. The reason this is such a classic article is because of the parties to the scenario. The patient was Dr. Frank B. Mallory, noted American pathologist of Boston, Massachusetts. The ophthalmologist was Dr. Fred H. Verhoeff, professor of Ophthalmology at Harvard University. The history was from Dr. Tracy B. Mallory, professor of Pathology at Harvard University, the patient's son. The visual fields were by Dr. J. H. Waite of Boston, of Waite-Beetham lines fame. The story, given in minute and extremely interesting detail in Polyak's text, in shortened form is as follows. Dr. Frank B. Mallory at age 18 developed a corneal ulcer on his right eye which left him with about 20/40 best corrected vision in that eye thereafter. From his late twenties on, he began to suffer from recurrent attacks of "ophthalmic migraine," "regularly accompanied by a scintillating scotoma in the left fields, sometimes also by nausea." At approximately age 47, on a Sunday in the summer of 1910 while at dinner, immediately after the reflection from a white surface of bright sunlight into his eyes, he began to complain of brilliant flashes recurring at very frequent intervals, leaving within a few hours-at any rate in less than a day-a visual field defect. The defect, initially large, improved, and the attack lasted approximately 20-40 min. After this attack, the patient remained very sensitive to brilliant white EDITORIAL: PERMANENT INFARCTIONS COMPLICATING MIGRAINE 75 light the rest of his life. Off and on over the years, he had spontaneous attacks of scintillations of short duration, none lasting more than a minute or two, but without any further restriction of his visual fields. He enjoyed an extremely productive career thereafter and succumbed to pneumonia on September 27, 1941 at age 78 years. In 1911, one year after the dramatic photisms resulting in the field defect, the patient saw Dr. Verhoeff to have a foreign body removed from his right cornea. A large hemianopic scotoma in the left upper fields was described. His acuity was recorded as 20115 in each eye then. However, in March 1934, at the age of 71, he had an ophthalmological examination by Dr. J. H. Waite of Boston. His visual fields were plotted with a Ferree Rand perimeter at 330 mm and revealed normal peripheral fields. However, a tangent screen examination at 1000 mm disclosed absolute homonymous hemianopic defects in the upper left quadrants, extending from fixation along the vertical meridians for 10 degrees and along the horizontal meridians for 20 degrees, "predicting a lesion in the occipital cortex on the right side and below the calcarine fissure." The story goes on in great detail and documented that Dr. Mallory was a world-renowned microscopist, even though he used his left eye with a monocular microscope and had the upper left quadrant of vision obliterated in that eye by the scotoma. Finally, exhausting neuropathologic examination confirmed exactly the focal infarction in right lower calcarine cortex and revealed that vessels entering that area were patent; the explanation given was that sufficient vasospasm had occurred during the migraine attack 31 years earlier to have given a permanent infarction, and yet the vessels subsequently opened. I doubt that a better documented case of permanent hemianopia secondary to a migraine attack exists in the world literature. When one considers that the patient was professor of Pathology at Harvard, was seen by the professor of Ophthalmology at Harvard, was autopsied in the Mallory Laboratory of Pathology (named for the patient), and had meticulous neuropathologic study by Professor Polyak, it would seem that to refute this case of permanent cerebral focal infarction as not being due to migraine would be like watching a bar of Ivory soap plunge to the bottom of the pool! The reason this case is cited is that such phenomena are documented unquestionably during the course of U/ltreated migraine. Therefore, if any medication is used dUring such a case, it might at times be indicated. I believe that Inderal is the best drug we have to prevent migraine attacks. It should not be used without taking women off "the pill" -and it should not be used in patients with known asthmatic bronchitis. Dr. Costin has noted that it may be associated with increased migraine when used in extremely small doses (e.g., 10 mg/day), but that by increasing the dose, the attacks often are controlled. I usually use no more than 30-40 mg/ day of Inderal in divided dosage and have found it extremely helpful in all forms of migraine, although I usually do not treat patients who have only ophthalmic migraine (i.e., flashing lights and scintillating scotoma attacks, but without any headaches). If a patient does not respond to Inderal, I use Sansert, Periactin, Calan (verapamil), or Endep (amitriptyline), or combinations of these, and have been able thereby to control nearly every case of migraine encountered in my practice. These must be used properly. I seldom go above 40 mg/day Inderal, and wish that Inderal-LA (long-acting) was made in a 40 mg tablet size rather than being an 80 mg tablet. One may use one Inderal-LA per day, but I personally would see no reason to go above that dose. Many neurologists do go higher, but other problems can ensue with higher dosages (excessive bradycardia and depression, for example). Therefore, while we look into the matter thoroughly and await reports from other physicians, we do not want readers using Inderal happily in their practices to get off a winner at this point. To some extent, the matter reminds me of those glaucomatologists in academia who have at times decried the use of Timoptic, while every ophthalmologist in private practice knows that Timoptic has been one of the greatest advances in the medical management of glaucoma in decades. Finally, to change the subject completely and simply to help keep practitioners up to date to the best of our ability, we have been getting several reports from various physicians about the use of Tagament during attacks of acute ophthalmic herpes zoster. Several doctors have written that using Tagament 300 mg four times a day for a week by mouth during acute ophthalmic herpes zoster has stopped the pain and swelling dramatically within 2-3 days. This should be worth a trial in your practice. I'd like to thank both Dr. Katz and Dr. Burde for all the effort and information they have provided. I simply wanted to play the role of the angel's advocate in the matter. Finally, doctor, we are trying to make this journal helpful to the clinician, so let us hear of your comments about related cases. We appreciate your support! J. Lawton Smith, M.D. I Clill Neuro-ophihalmol, Vol. 6, No.2, 1986 |
