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Show ORIGINAL CONTRIBUTION Palinopsia From Posterior Visual Pathway Lesions Without Visual Field Defects Molly E. Ritsema, MD and Marjorie A. Murphy, MD Abstract: Palinopsia, or perseveration of a previously viewed image, may be caused by drug use or by posterior visual pathway lesions. Most cases of palinopsia due to visual pathway lesions have an associated homonymous hemianopic visual field defect. We report two patients with palinopsia caused by structural lesions of the posterior visual pathway in the absence of visual field defects. Patients with palinopsia should undergo neuroimaging even in the presence of normal visual fields. (/ Neuro- Ophthalmol 2007; 27: 115- 117) Palinopsia was first described by Critchley in 1951 as " visual perseveration in time... whereby the patient continues to see the object after it has been removed" ( 1). Previous reports have associated palinopsia with medications and with structural lesions of the brain ( 1- 6). Palinopsia can also occur in otherwise healthy individuals ( 7). In 1968, Bender et al ( 2) proposed four possible mechanisms of palinopsia: a pathologic exaggeration of the normal afterimage, a seizure disorder, hallucinations, and a psychogenic disorder. However, the mechanism of palinopsia remains unknown. Most cases of palinopsia due to visual pathway lesions have an associated homonymous hemianopic visual field defect. There are only rare reports of palinopsia with visual pathway lesions but without such field defects ( 2). In such cases, the lesion is presumed to spare the geniculo-calcarine radiations. There are no reports in which this phenomenon has been confirmed by automated static threshold perimetry and high- resolution neuroimaging. We describe two such cases. Department of Ophthalmology, Brown University, Rhode Island Hospital, Providence, Rhode Island. This work was presented in part as a poster at the North American Neuro- Ophthalmology Society Annual Meeting, February 28, 2006, Tucson, AZ. Address correspondence to Marjorie A. Murphy, MD, Department of Ophthalmology, RI Hospital, APC 7, 593 Eddy Street, Providence, RI 02903; E- mail: margiemurphy@ cox. net CASE REPORTS Case 1 A 3 3- year- old man was diagnosed with an arteriovenous malformation ( AVM) in the lingual gyrus of the left occipital lobe at age 27 after suffering a grand mal seizure. He described his initial symptom as follows: He was watching a football game on television when he noted flashing in his right superior field. After looking away, he could still see an image of the television flashing in his right field as if it were " locked" there. He went on to suffer a grand mal seizure, and imaging revealed a left occipital AVM. He elected not to undergo the recommended gamma knife radiosurgery at that time. Over the next 6 years, he experienced approximately 12 episodes of light flashes in the right superior field lasting 10- 15 minutes and unaccompanied by headache. Six years after the diagnosis, one such episode was accompanied by a severe headache and led to brain imaging that disclosed a hemorrhage in the AVM ( Fig. 1). Thereafter he complained of a persistent problem with reading. He noted that the text seemed to meld together. His symptoms gradually improved such that he could finish a paragraph and then a page, but he was still bothered by text continuing to meld together. When looking at a new page, he could see the previous page superimposed. He underwent gamma knife radiosurgery 1 month after the hemorrhage and presented 1 month later for neuro-ophthalmologic evaluation. He was otherwise healthy and used no medications. He denied tobacco, alcohol, or illicit drug use. Visual acuity was 20/ 20 in both eyes. He correctly identified 16/ 16 Ishihara color plates in both eyes, and Amsler grid testing was normal. Extraocular motility was full, and no afferent pupillary defect was noted. Slit- lamp and fundus examinations were normal. A Humphrey visual field 30- 2 was normal ( Fig. 1). The palinopsia gradually improved over the next year, and he was able to return to work as a computer technician. Case 2 A 68- year- old woman complained of a 6- month history of a persistent binocular visual disturbance. She J Neuro- Ophthalmol, Vol. 27, No. 2, 2007 115 J Neuro- Ophthalmol, Vol. 27, No. 2, 2007 Ritsema and Murphy ramu KVUTIM FIG. 1. Case 1. Axial FLAIR ( A) and gradient echo MRI ( B) show signal changes consistent with hemorrhage at the site of a left occipital lobe arteriovenous malformation ( AVM) { arrow). The lesion appears to lie lateral to the posterior optic radiations. C. Humphrey visual fields are normal. noted that if she looked at a blank wall after watching television, she was still able to see the image of the television on the wall for at least 60 seconds. If she closed her eyes, she could still see the image of the television for as long as 20 seconds. When coming indoors, she would continue to see the flashing outline of outside objects such as a lamppost. She described her symptoms as " like watching my own movies without going to the movies." Although she had a history of migraine, she reported that the new visual symptoms were quite different from her migrainous visual auras, which she described as having a kaleidoscope pattern. Her past ocular history was notable for a laser peripheral iridectomy in both eyes for narrow angles. Her only medication was aspirin, and she denied use of tobacco, alcohol, or illicit drugs. Best- corrected visual acuity was 20/ 25 in the right eye and 20/ 20 in the left eye. She correctly identified 10/ 10 Ishihara color plates in both eyes, and Amsler grid testing was normal. Extraocular motility was full, and no afferent pupillary defect was noted. Slit lamp examination was significant for a patent peripheral iridectomy and 2 + nuclear sclerosis in both eyes. Ophthalmoscopy was normal. A Humphrey visual field 30- 2 demonstrated a rim artifact but was otherwise normal ( Fig. 2). Brain MRI revealed two nonenhancing areas of white matter hyperintensity within the left periatrial white matter in proximity to the left optic radiations. The imaging findings were attributed to ischemic stroke ( Fig. 2). DISCUSSION These two cases demonstrate palinopsia with accompanying lesions of the posterior visual pathway. The lesions appeared to lie within or near the optic radiations, but neither produced a hemianopic visual field defect on Humphrey automated perimetry. Most reported visual pathway lesions associated with palinopsia are right hemisphere lesions and are accompanied by an incomplete left homonymous hemianopia. Although it has been suggested that palinopsia with left hemisphere lesions may be underrepresented because of aphasia ( 2,4), Hughes and Lessell ( 4) pointed out that visual hallucinations in general are more common with right than with left hemisphere lesions even when the data are corrected for aphasia. Vaphiades et al ( 6) described 13 patients with positive spontaneous visual phenomena ( PSVP) associated with lesions of the cerebral hemispheric visual pathway. The term PSVP was chosen to refer to all spontaneous visual events, including phosphenes, photopsias, visual hallucinations, palinopsia, and agitated delirium with hemianopia. Eleven of their patients had right hemisphere lesions, and two patients had left hemisphere lesions. The two patients with palinopsia both had right- sided lesions, one involving the right occipital lobe and the other the right occipital and temporal lobes. All patients with PSVP had visual field defects except a 67- year- old woman who had palinopsia, a small lacunar infarct in the white matter of the right occipital lobe, and normal visual fields by Goldmann perimetry. That patient is similar to our Case # 2. The difference is that our patient had a left hemisphere lesion as well as normal automated static threshold perimetry. It is possible that a visual field defect in their patient might have been missed by kinetic perimetry because of statokinetic dissociation ( Riddoch phenomenon) ( 8). On the other hand, static threshold perimetry using a Humphrey 30- 2 program measures the central 30° at 6° intervals and may have missed a small homonymous scotoma or temporal crescent in our patients. 116 © 2007 Lippincott Williams & Wilkins Palinopsia J Neuro- Ophthalmol, Vol. 27, No. 2, 2007 PHTTEM OEUIftTIOH •••• m H * u • • • • • . • . • • • • • » • • • • • " • • • • • • • 3* • • • • • • m A ••• a X • • • • • K • J* • » - » a • • - S?. £ 8 •••• if. •••• a •••• • • » • • • • •••• m • • • • a B FIG. 2. Case 2. A. Axial FLAIR MRI shows increased signal { arrow) in the region of the anterior left optic radiations consistent with ischemic infarction { arrow). B. Humphrey visual fields are normal apart from a rim artifact. Michel and Troost ( 3) described a patient with palinopsia and a right occipital lobe lesion who had normal visual fields by " standard perimetry," but a subtle left homonymous field abnormality with confrontation testing using hand comparison. Bender et al ( 2) described a series of 12 patients with palinopsia, one of whom developed palinopsia after partial resection of a left parietal ependymoma. This was the only reported case with a left cerebral hemisphere lesion. Our findings emphasize the fact that posterior visual pathway lesions may cause palinopsia even when automated visual fields do not disclose hemianopic defects. Presumably the lesions lie close to the cerebral visual pathway but not in it. Brain imaging should be performed for unexplained palinopsia even when automated visual fields are normal. REFERENCES Critchley M. Types of visual perseveration: " paliopsia" and " illusory visual spread." Brain 1951; 74: 267- 99. Bender MB, Feldman M, Sobin AJ. Palinopsia. Brain 1968; 91: 321- 38. Michel EM, Troost BT Palinopsia: cerebral localization with computed tomography. Neurology 1980; 30: 887- 9. Hughes MS, Lessell S. Trazodone- induced palinopsia. Arch Ophthalmol 1990; 108: 399^ 00. Purvin VA. Visual disturbance secondary to clomiphene citrate. Arch Ophthalmol 1995; 113: 482^. Vaphiades MS, Celesia GG, Brigell MG. Positive spontaneous visual phenomena limited to the hemianopic field in lesions of central visual pathways. Neurology 1996; 47: 408- 17. Pomeranz HD, Lessell S. Palinopsia and polyopia in the absence of drugs or cerebral disease. Neurology 2000; 54: 855- 9. Hudson C, Wild JM. Assessment of physiologic statokinetic dissociation by automated perimetry. Invest Ophthalmol Vis Sci 1992; 33: 3162- 8. 117 |
