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Show Journal of'A'euro- Ophthalmology 20( 2): 97- 99, 2000. © 2000 Lippincott Williams & Wilkins, Inc., Philadelphia Monocular Central Dazzle After Thalamic Infarcts Renaud A. Du Pasquier, MD, Didier Genoud, MD, Avinoam B. Safran, MD, and Theodor Landis, MD The authors observed a patient after he had ischemic strokes in both paramedian thalamic regions, which were more marked on the left side. Symptoms included dysphasia, vertical binocular diplopia, right- sided hemianopia, and a right- sided sensory and motor deficit, sparing the face. However, the most disturbing phenomenon was a painless, left monocular dazzle, which was the presenting symptom and also the only persisting symptom. This report shows that a thalamic lesion may be at the origin of central dazzle, and to the authors' knowledge, it is the first clinical observation of its monocular occurrence. It is conceivable that this dazzle was due to optic- trigeminal summation. Key Words: Central dazzle- Dejerine- Roussy thalamic syndrome- Optic- trigeminal summation- Paramedian artery- Stroke- Thalamus. Two main forms of light- induced discomfort are recognized. The most common form is usually described as glare or dazzle. It results from an increased scattering of light in ocular media, as is observed in cataract, or from disorders in the mechanisms of light adaptation ( e. g., after pupil dilation or disturbance in the photic [ cone] system of the retina) ( 1). Intolerance to light also has been observed with a variety of lesions of the retrobulbar visual pathways, including the optic nerve ( 2) and the occipital lobes ( 3,4). Although glare is unpleasant and alters contrast sensitivity, it is not usually perceived as painful. A second form of intolerance to light is characteristically associated with pain. It is commonly designated as photophobia, although the definition of this term is somewhat vague ( 5). It is frequently observed in ocular diseases involving inflammation of the iris, suggesting that the pupillary reaction to light is painful. In such conditions, photophobia may be related to the presence of a lesion in the area supplied by the ophthalmic division of the trigeminal nerve ( 6). This hypothesis has been Manuscript received October 18, 1999; accepted March 23, 2000. From the Departments of Neurology ( RAD, DG, TL) and Ophthalmology ( ABS), Geneva University Hospitals, Geneva, Switzerland. Supported in part by the Swiss National Science Foundation, grant number 32.51.090.97. Address correspondence to Theodor Landis, MD, Clinique de Neu-rologie, Hopitaux Universitaires de Geneve, 1211 Geneva 14, Switzerland. substantiated by reports that photophobia may also occur with nonocular conditions affecting the ophthalmic division of the trigeminal nerve, such as trigeminal neuralgia ( 7) and meningeal irritation. In a clinical observation reported by Cummings and Gittinger ( 8), it was suggested that a thalamic lesion could be the cause of central dazzle. However, their patient suffered from a large ischemic stroke due to the occlusion of the right posterior cerebral artery, which involved the thalamus and the occipital lobe, therefore inviting question as to whether the thalamic or occipital lesion was responsible for the dazzle. We report a patient with a monocular dazzle after isolated bilateral ischemic lesions in the thalamus. CASE REPORT This 56- year- old man was a heavy smoker with hyperuricemia, and he had undergone a percutaneous angioplasty. While eating dinner, he stood up and suddenly experienced dysesthesia in his left eye and vertical diplopia for remote objects. When he closed his left eye, the urge to rub it ceased. He also had difficulty finding words, was unable to stand because of weakness in his right leg, and his right hand was clumsy. He was brought to the hospital by friends, who also noticed that he was mildly somnolent. During a neurologic examination, the patient was alert but dysphasic. He had marked difficulty in finding words, and his comprehension was mildly impaired, as were executive functions. He experienced painless discomfort in his left eye when exposed to light, and he continuously rubbed his eye. He had a mild skew deviation, with the left eye higher than the right eye. Clinical testing revealed a right homonymous hemianopia, which was not noticed by the patient. Pursuit was saccadic on both sides. Both corneal reflexes were present and symmetric. We also found a right- sided sensory and motor deficit with hyperreflexia, a positive Babinsky sign, and mild superficial hypoesthesia sparing the face. Results of a general and a neuro- ophthalmologic examination were otherwise normal, including visual acuity, slit- lamp evaluation of the anterior segment, and both optic fundi. R. A. DU PASQUIER ET AL jr. i & r+>' : f K-Results of extensive routine blood examination were normal, as were results of his electrocardiogram and carotid- vertebral and transcranial echo- doppler sonography. Transthoracic and transesophageal echocardiography, however, showed a patent foramen ovale. Two cerebral magnetic resonance images, performed 5 and 49 days after the onset of the symptoms, showed a bilateral paramedian thalamic infarct that was larger on the left, located in the territory of the left paramedian artery ( Fig. 1). Within a day, the patient's speech was normal, and 2 days later, the motor and sensory deficits had disappeared. Examination showed that the right hemianopia resolved after 3 days, and that the skew deviation and vertical diplopia vanished after 1 week. Two weeks after the ischemic event, the visual fields were unremarkable when tested by automatic perimetry using the Octopus program Nl ( Interzeag, Schlieren, Switzerland). However, the patient kept his left eye covered with a dark patch, which he continued to wear even after the disappearance of diplopia. He frequently rubbed his left eye, as if there were some foreign body in it, because he said the light was too bright in this eye. He first noticed this phenomenon on a September morning while lying in his hospital bed, 5 m from the window. There was no sun entering the room, and neither the medical staff nor other patients noticed any excessive brightness. Thereafter, this discomfort was noticed when the patient was outside, even on cloudy days; the discomfort disappeared when the patient was inside with dimmed light. Two months after discharge from the hospital, light- induced discomfort was still present. FIG. 1. T2- weighted brain magnetic resonance imagery at day 5. The transverse slice goes through the striate body, the thalamus, and the internal capsule. There is a signal anomaly at the internal part of both thalami, which is larger on the left side than on the right side. DISCUSSION Our patient experienced sudden onset'of a sensory-motor deficit in the right hemibody, mild aphasia, a skew deviation, right hemianopia, and a left monocular dazzle. Cerebral magnetic resonance imaging showed a bilateral paramedian thalamic infarct in the territory of the left paramedian thalamic artery ( Fig. 1). It has been shown that this artery frequently supplies both paramedian thalamic nuclei ( 9). Transitory right- sided hemianopia and skew deviation must have been caused by acute ischemic edema impinging upon the left visuo- afferent structures, such as the optic tract or the lateral geniculate nucleus. However, a somewhat different physiopathogenetic mechanism has to be found to explain the monocular dazzle because this phenomenon was present on the left side and because it persisted after resolution of all other symptoms. A lesion of the left ophthalmic nerve can be reasonably ruled out because there was no sensory deficit in this territory, and there was normal corneal reflex. Therefore, we postulate a central origin for this monocular dazzle. Central dazzle manifesting with binocular intolerance to light has been described as occurring with occipital lesions alone. Indeed, bilateral ablation of the occipital lobes in macaques led not only to cortical blindness, but also to light- avoiding behavior ( 3). Moreover, in a series of children with blindness due to bilateral occipital lesions, one fourth were described as photophobic, and there was no explanation other than the occipital lesion ( 4). The notion of a possible role of the thalamus causing central dazzle was introduced by Cummings and Git-tinger ( 8). These authors described a patient with a large right posterior cerebral artery stroke involving the right postero- lateral thalamic nucleus and the right occipital lobe. The patient developed debilitating binocular dazzle 3 months after the stroke, which subsequently improved after treatment with amitriptyline and perphenazine. By analogy with Dejerine- Roussy syndrome ( in which a lesion in the ventro- lateral nucleus can cause severe pain in the contro- lateral hemibody), the authors postulated an alteration of the visuo- sensory interaction at the thalamic level. Eckardt et al. ( 10) first evoked this concept, and, postulating upper midbrain diencephalic level interaction, named it optic- trigeminal summation. Later, this phenomenon was supported with the description of the so- called photic sneeze reflex ( when normal subjects sneeze from exposure to bright light) ( 11), and with the occurrence of photophobia in patients with trigeminal neuralgia ( 7). Therefore, we hypothesize that the paramedian thalamic infarcts, largely predominant on the left side, have damaged modulatory visual fibers, which are part of the optic- trigeminal summation system, and they account for our patient's unique central monocular dazzle. It is likely that central dazzle due to thalamic lesions are more frequent than reported in the literature, J Neuro- Ophthalmol, Vol. 20, No. 2, 2000 MONOCULAR CENTRAL DAZZLE AFTER THALAMIC INFARCTS 99 and they are not recognized due to association with several other deficits. Acknowledgement: The authors thank Professor J. Bogous-slavsky for his useful comments. REFERENCES 1. Miller D, Nadler MP. Light scattering: its relationship to glare and contrast in patients and normal subjects. In: Nadler MP, Miller D, Nadler DJ, eds. Glare and contrast sensitivity for clinicians. New York: Springer- Verlag, 1990: 23- 32. 2. Safran AB, Kline LB, Glaser JS. Positive visual phenomena in optic nerve disease: photopsias and photophobia. In: Glaser JS, ed. Neuro- ophthalmology. Vol 10. St- Louis: Mosby CV, 1980: 225- 31. 3. Denny- Brown D, Chambers RA. Physiological aspects of visual perception: functional aspects of visual cortex. Arch Neurol 1976; 33: 219- 27. 4. Jan JE, Groenveld M, Anderson DP. Photophobia and cortical visual impairment. Dev Med Child Neurol 1993; 35: 473- 7. 5. Miller NR. Walsh and Hoyt's clinical neuro- ophthalmology. 4th ed. Vol. 2. Baltimore: Williams and Wilkins, 1985: 1099- 106. 6. Lebensohn JE. Photophobia: mechanisms and implications. Am J Ophthalmol 1951; 34: 1294- 300. 7. Gutrecht JA, Lessell IM. Photophobia in trigeminal neuralgia. J Neuroophthalmol 1994; 14: 122- 3. 8. Cummings JL, Gittinger JW. Central dazzle, a thalamic syndrome? Arch Neurol 1981; 38: 372- 4. 9. Bogousslavsky J, Regli F, Uske A. Thalamic infarcts: clinical syndromes, etiology, and prognosis. Neurology 1988; 38: 837^ 18. 10. Eckardt LB, McLean JM, Goodell H. Experimental studies on headache: the genesis of pain from the eye. In: Wolff HG, Gasser HS, Hinsey JC, eds. Proceedings of the Association for Research in Nervous and Mental Disease. Vol. 23. Baltimore: Williams & Wilkins, 1943: 209- 27. 11. Whitman BW, Packer RJ. The photic sneeze reflex. Neurology 1993; 43: 868- 71. J Neuro- Ophthalmol, Vol. 20, No. 2. 2000 |
