| OCR Text |
Show I" l/ mal of Climcal N' · l/ nJ- ol'hllltll/ llolox. v 8( J I: 1' 1- 23. 1' 188. Loss of Accommodation Produced by Peristriate Lesion in Man? Riri S, Manor, M. D., Yechiel D. Heilbronn, M. D., Ilana Sherf, 0.0., and Isaac Ben- Sira, M. D. ,. 1988 Raven Press, Ltd., New York We observed a bilateral accommodative paresis associated with a spontaneous parieto- occipital hematoma in a 37- year old patient. There was no clinical or computerized tomography ( eT) evidence of transtentorial herniation or upper brainstem pathology. With resolution of the hematoma, accommodation returned to normal. Key Words: Accommodation defect- Peristriate cortex - Neuro- ophthalmology - Homonymous hemianopia - Midbrain- Intracerebral hematoma. From the Neuro- ophthalmologic Unit ( R. M. S.). the Department of Ophthalmology ( 1.5., l. B. S.). and the Department " f Neurosurgery ( Y. D. H.), Beilinson Medical Center, retah Tiq\' a and the Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel. . Address correspondence and reprint requests to R. S. Manor, M. D., Department of Ophthalmology, Beilinson Medical Center 49 100, Israel. / 9 Glaser ( 1) pointed out that the neural mechanism of the near reflex is not as well understood as the pathways for pupillary light reaction or for the saccadic or pursuit ocular motor pathways. According to Campion et al. ( 2), " For many years conventional wisdom has been that in higher vertebrates at least the geniculostriate pathways are responsible for pattern recognition while the midbrain projections are primarily concerned with reflex activities such as pupil dilatation, lens accomodation and the control of eye movements." However, lampel ( 3) obtained bilateral accommodation, convergence, and pupillary constrictions from unilateral faradic stimulation in overlapping areas of the preoccipital ( peristriate) cortex of the Macaque ( Fig. 1), and he believes that the near reflex is primarily a cortical function. Thus, in primates, the neurological pathways of accommodation would seem to present a relay from the calcarine cortex to the peristriate area, from there continuing through the internal corticotectal tract to the Edinger- Westphal nucleus. ( 4) Isikawa ( 5) expressed his belief that in man " ... a case with an accommodative defect due to supranuclear lesion could be very important since it might help to identify the exact pathway to the Edinger- Westphal nucleus from central control centers." Klingele et al. ( 6) found an accomodation defect in a patient with Wilson's disease and signs of mesencephalon and brainstem tegmentum involvement but considered the defect to be supranuclear in origin because of normal eye ductions and pupillary reactions, which suggested sparing of the oculomotor nucleus. The following is a report of a 37- year- old man in whom there was no demonstrable midbrain pathology by clinical or computerized tomography ( CT) but who had a left intracerebral hematoma in the peristriate cortex associated with bilateral loss of accommodation. PERISTRIATE LESION AND LOSS OF ACCOMMODATION 2/ accommodative reserve of 3.4 and 3.6 diopters, respectively. The near convergence point was 10 cm from the eyes. There was a good near reflex of both pupils. Three months after the cerebral event the CT scan showed resolution of the hematoma ( Fig. 4). The near accommodation point was now 15 cm in the right eye and 18 cm in the left eye, i. e., an accommodative reserve of 6.5 and 5.5 diopters, respectively. The homonymous hemianopia had become relative. FIG. 2. Computerized tomography scan of the brain of our patient, July 7, 1985 ( A) Note the high preoccipital lobe hemorrhage with perifocal edema compressing the left occipital horn, and the striking similarity between this area and the area in the monkey in which faradic stimulation produced the near reflex. ( 8) and ( C) Lower cuts show that there was no transtentorial herniation or extension of hematoma in the upper brainstem. DISCUSSION Loss or weakening of accommodation in humans is a well- known phenomenon that has been described in association with a wide variety of disorders and causal agents including encephalitis, the periaqueductal syndrome, viral diseases, acute idiopathic polyneuritis, diphtheria, diabetes mellitus, alcoholism, Werniche's and other metabolic neuropathies, multiple sclerosis, botulism, syphilis, tuberculosis, during childbirth and lacta- PERISTRIATE LESION AND LOSS OF ACCOMMODATION 23 neurologic diseases, yet systematic testing of its function is rarely included in the neurological examination." The accommodation loss may also be masked by the patient's general condition or by associated symptoms. In addition, in patients over the age of 45 years, pathology of the brain with accommodative loss could be masked by loss of accommodation associated with aging. However, in contrast to the irreversible effects of aging, when there is a loss of accommodation resulting from brain pathology, it might be possible to demonstrate an improvement in accommodation with neurologic status in young individuals. In our patient it was thought that the reading difficulties stemmed from the homonymous hemianopia, and the true cause was discovered only in the neuroophthalmological examination. Further clinical and pathological evidence is needed in order to state unequivocally that there is a cause- effect relationship between a peristriate cerebrallesion and selective accommodative paresis. REFERENCES 1. Glaser jS. NClIro- ophthafmology. Hagerstown: Harper and Row. 1978: 174. 2. Campion J, Latto R, Smith YM. Is blind sight an effect of scattered light, spared cortex and near threshold vision? Behal' Braill Sci 1983; 6: 423- 86. 3. jampel RS. Representation of the near response on the cerebral cortex of the Macaque. Am f Ophtha/ mo/ 1959; 48: 57382. 4. Duke Elder S, Scott GI. Neuro- ophthalmology. In: Systems of Ophthalmology. Vol. 12. St. Louis: C. V. Mosby, 1971: 696- 7. 5. Isikawa S. Accommodation and its disorders. In: LesseI S, and Van Dalen jTW, eds. Neuro- ophthalm% gy, Vol. 3. Amsterdam: Excerpta Medica, 1982: 241- 9. 6. Klingele TG, Newman ST, Burde RM. Accommodation defect in Wilson's disease. Am f Opthalmo/ 1980; 9: 20- 4. 7. Walsh FB, Hoyt WF. Clinica/ Neuro- ophtlza/ mology. Baltimore, Williams and Wilkins, 1969: 237. 8. Bodnar NP. The influence of glycemic level on the volume of accommodation in patients with diabetes mellitus. Ofta/ mol Zh 1975; 30: 411. 9. Rogell GD. Internal ophthalmoplegia after argon laser pametinal photocoagulation. Arcll Opllza/ mol 1979; 97: 90410 10. Bajart AM, Robb RM. Internal ophthalmoplegia follOWing oblique myectomy: a report of three cases. Trans Am Acad Ophtha/ mo/ Otorhillo/ an/ Ilg,,/ 1979; 86: 1901- 11. 11. Orsoni jG. Medeoli FD. Tentative et tentation d'interpreter comme une manifestations psychosomatique une paralysie de I'accommodation. Ophthalmologica 1978; 177: 92- 8. 12. Dralans L, Adriaenssens L. Persistent isolated paralysis of accommodation in young people. Bull Soc Bclg Ophtha/ mol 1978; 582: 42- 4. 13. Hitch A. Persistent systemic failure of accommodation in young adults. Aust I Optha/ moI1979; 7: 65- 9. / Oill NellrO- Ol'lllhalmol, Vol. 8, No. I, 1988 |
