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Show LITERATURE ABSTRACTS 119 Optimal Rates of Movement for Kinetic Perimetry. Johnson CA, Keltner JL. Arch Ophthalmol 1987;105:73-5 Oan). [Reprint requests to Chris A. Johnson, Ph.D., Department of Ophthalmology, University of California, Davis, CA 95616.] This study, done with a SQUID automated perimeter and three young normal volunteers, studied the rate of movement of three different Goldmann-equivalent targets (14e, 12e, lIe) at eccentric meridians on supranasal (135 degrees) and one inferotemporal (315 degrees), starting at 75 degrees eccentric and moving inward. Between 1 degree/ sec and 4 degrees/sec, the time required to bring the target to detection (scan time) linearly decreased, but almost no further reduction in scan time was achieved between 4 and 8 degrees/sec. Surprisingly, no gross changes in plotted isopters occurred with increase in the rate of movement except with the smallest targets (i.e., central field). The authors conclude that 4 degrees/sec is an optimum rate of movement for the target, for both central and peripheral field testing. From the viewpoint of one who does hundreds of such examinations personally every year, this paper can be faulted for its scanty discussion of other confounding variables to the rate of target movement that one continually must juggle (patient's fatigue, patient's reaction time, starting at reasonable positions with each target considering known scotomatous areas, etc.) in order to get the job done as accurately as possible in a manageable time frame. Lyn A. Sedwick, M.D. Hemifacial Spasm due to Contralateral Acoustic Neuroma: Case Report. Nishi T, Matsukado Y, Nagahiro 5, Fukushima M, Koga K. Neurology 1987;37:339-42. [Reprint requests to Dr. Nishi, Department of Neurosurgery, Kumamoto University Medical School, Kumamoto 860, Japan.] Hemifacial Spasm due to Cerebellopontine Angle Lipoma: Case Report. Levin JM, Lee JE. Neurology 1987;37:337-39. [Reprint requests to Dr. Lee, Atlanta Neurological Clinic, 993 Johnson Ferry Road, NE, Atlanta, GA 30342]. These two case reports remind us that tumors are a rare cause of hemifacial spasm. The patient with an acoustic neuroma was a 57-year-old white woman with a 5-year history of hearing loss. On examination, there was an absent corneal reflex, horizontal nystagmus, and bilateral papilledema. The patient with a cerebellopontine angle lipoma was only 22 years old. The patient was younger than would be expected for typical hemifacial spasm. Given the cost, should all patients diagnosed as having hemifacial spasm undergo neuroimaging to rule out a tumor? Clearly, a careful history, and ocular and neurological examinations should be performed. In the acoustic neuroma case report, other signs and symptoms would have justified neuroimaging. In the cerebellopontine angle lipoma case report, the early age of onset would lead one to perform a more aggressive evaluation. Thus, these two case reports have atypical features. However, in more typical cases of hemifacial spasm, perhaps neuroimaging could be deferred. Walter M. Jay, M.D. Optochiasmatic Arachnoiditis with Treatment by Surgical Lysis of Adhesions, Corticosteroids, and Cyclophosphamide: Report of a Case. Marcus, AO, Demakas H, Ross HA, Duick DS, Crowell RM. Neurosurgery 1986;19:101-3. [Reprint requests to Alan O. Marcus, M.D., 23961 Calle De la Magdalena, Suite 535, Laguna Hills, CA 92653.] In October 1980, a 24-year-old woman underwent surgery for an anterior communicating artery aneurysm. The aneurysm was clipped and local packing with muslin was performed. In February 1981, she developed deterioration of her vision. The patient was begun on intravenous dexamethasone 10 mg, followed by 4 mg orally. One month later, the patient was readmitted because of increasing blurred vision and diplopia. Visual field testing revealed a bitemporal hemianopia. A diagnosis of optochiasmatic arachnorditis was made and the patient underwent an operation on March 26, 1981, to lyse adhesions involving the optic nerve and chiasm. Postoperatively, the patient was placed on dipyridamole 25 mg b.i.d., aspirin 800 mg b.i.d., and dexamethasone 6 mg every 6 h, all orally. Over the next 2 months, attempts to decrease the patient's steroid dose were unsuccessful because of an increased rate of loss of visual acuity together with the increased development of field defects. On July 8, 1981, therapy with cyclophosphamide was initiated at an oral dose of 50 mg daily. From its initiation until January 1982, the dosage of cyclophosphamide was continued while 1Clin Neuro-ophthalmol, Vol. 7, No.2, 1987 |
