- Email: [email protected]
Visual hallucinations immediately after macular photocoagulation
P. acnes, a gram-positive anaerobe, in the literature. Winward and associates5 describe cases of acute and chronic Propionibacterium endophthalmitis with the latter having a clinical course similar to this case. They suggest that initial vitrectomy gives the best result because of persistence of organisms in the remnant of the lens capsule.5 Both A. xylosoxidans and P. acnes can cause chronic progressive endophthalmitis after cataract surgery. These organisms are often resistant to conventional taps and antibiotic therapy. Complete vitrectomy with intraocular lens and capsule removal may be required for eradication of infection. REFERENCES
1. Swart J, Volker-Dieben HJ, Reichert-Thoen JWM. Alcaligenes xylosoxidans endophthalmitis 8 months after cataract extraction. Am J Ophthalmol 1999;127:345–346. 2. Aaberg TM, Rubsamen PE, Joondeph BC, et al. Chronic postoperative gram-negative endophthalmitis. Retina 1997; 17:260 –262. 3. Callender MG, Charles AM, Chalmers RL. Effect of storage time with different lens care systems on in-office hydrogel trial lens disinfection efficacy: a multi-center study. Optom Vis Sci 1992;69:678 – 684. 4. Lin A, Driebe WT Jr, Polack P. Alcaligenes xylosoxidans keratitis post penetrating keratoplasty in a rigid gas permeable lens wearer. CLAO J 1998;24:239 –241. 5. Winward KE, Pflugfelder SC, Flynn HW, et al. Postoperative Propionibacterium endophthalmitis: treatment strategies and long-term results. Ophthalmology 1993;100:447– 451.
A
FTER MACULAR PHOTOCOAGULATION, PATIENTS MAY
BRIEF REPORTS
815
Visual Hallucinations Immediately After Macular Photocoagulation Salomon Y. Cohen, MD, Avinoam B. Safran, MD, Ramin Tadayoni, MD, Gabriel Quentel, MD, Brigitte Guiberteau, MD, and Corinne Delahaye-Mazza, MD PURPOSE:
To evaluate the incidence of visual hallucinations after macular photocoagulation for choroidal neovascularization. METHODS: After macular photocoagulation for choroidal neovascularization, 60 consecutive patients were asked to respond to an orally administered questionnaire. RESULTS: Twenty-seven patients (45%) described photopsias, flashing lights of various colors. Ten additional patients Accepted for publication Jan 21, 2000. From the Centre d’Imagerie et de Laser (S.Y.C., G.Q., B.G., C.D.-M.); Department of Ophthalmology, Hoˆpital Lariboisie`re, Assistance Publique–Hoˆpitaux de Paris (S.Y.C., R.T.), Paris, France; and Department of Ophthalmology, Hoˆpital Cantonal Universitaire (A.B.S.), Geneva, Switzerland. This study was presented in part as a poster at the American Academy of Ophthalmology Annual Meeting, New Orleans, Louisiana, November 1998. Inquiries to Salomon Y. Cohen, MD, Centre d’Imagerie et de Laser, 11 rue Antoine Bourdelle, 75015 Paris, France; fax: (33) 1 42849409; e-mail: [email protected]
VOL. 129, NO. 6
(16.6%) also described structured hallucinations, including known or unknown faces, flowers, and geometric patterns, which occurred hours or a few days after photocoagulation. Patients with structured hallucinations were older (P ⴝ .04) and more often had subfoveal choroidal neovascularization (P ⴝ .005) and severe macular disease in both eyes or at least in the treated eye (P ⴝ .01). CONCLUSIONS: Visual hallucinations appear to be a frequent, albeit unrecognized, side effect of macular photocoagulation of choroidal neovascularization. The provision of proper information to patients may avoid concern about a psychiatric origin of their hallucinations. (Am J Ophthalmol 2000;129:815– 816. © 2000 by Elsevier Science Inc. All rights reserved.)
complain of visual loss or paracentral scotoma. To our knowledge, visual hallucinations have not been reported after macular photocoagulation except in a single case report.1 A prospective study was undertaken to define the nature and incidence of visual hallucinations immediately after macular photocoagulation. When they presented for the first angiographic study after photocoagulation (15 days to 1 month after treatment), patients were asked two questions by the ophthalmologist: (1) “Some patients observe luminous or colored phenomenon after laser photocoagulation. Did this occur in your case?” (2) “Some patients experience visual hallucinations after photocoagulation. Did this occur in your case?” Sixty consecutive patients were included. There were 42 women and 18 men; ages ranged from 41 to 92 years (mean, 75.3 years). Twenty-three patients (38.3%) reported no visual hallucinations after photocoagulation (group 1). Thirty-seven patients (61.6%) reported visual hallucinations immediately after photocoagulation. More precisely, 27 (45%) reported nonstructured visual hallucinations, that is, flickering or flashing lights, colored spots, filaments and/or luminous small sticks (group 2), whereas 10 patients (16.6%) also described structured and complex visual hallucinations, that is, flowers or “wallpaper” with flowers; known or unknown faces; geometric patterns, fences, paintings, and furniture; and small animals (group 3). All patients denied having experienced visual hallucinations in the past. The structured visual hallucinations appeared within a few hours or a few days after photocoagulation. All patients were relieved when they were told that their symptoms did not have a psychiatric origin. Groups were compared for their significance by means of chi-square test and/or Yates corrected chi-square and the Fisher exact test for dichotomous variables and by the Wilcoxon test for unpaired data for continuous variables. No difference was found between patients of group 3 compared with other patients in regard to sex (P ⫽ .45) or etiology of choroidal neovascularization (P ⫽ .35). Patients with structured visual hallucinations were found
to be older than other patients (P ⫽ .04). Choroidal neovascularization was more often subfoveal in patients in group 3 than in patients in the other groups (P ⫽ .005). Patients of group 3 more often had a severe macular lesion in both eyes or at least a more severe lesion in the treated eye than did other patients (P ⫽ .01). One patient, however, developed structured visual hallucinations despite the lack of a severe lesion in the treated eye. In 1769, Charles Bonnet described complex visual hallucinations in his psychologically normal grandfather. This phenomenon, the Charles Bonnet syndrome, was frequently reported in patients with visual impairment resulting from visual deprivation, being observed in 11% to 38% of patients.2,3 An association of Charles Bonnet syndrome with age-related macular degeneration (AMD) was previously reported,4 but to our knowledge Charles Bonnet syndrome is not known as a possible complication of macular photocoagulation. Anatomical changes observed after photocoagulation could be involved in the occurrence of photopsias. However, we suggest that the theory of a deafferentation state in which decreased vision stimulates intracerebral perceptions, as in the phantom-pain syndrome,5 may more likely explain the Charles Bonnet syndrome that occurs after photocoagulation, which implicates localized destruction of the retina. In the present study, visual hallucinations appear to be a frequent side effect of macular photocoagulation of choroidal neovascularization. Provision of proper information to patients may avoid concern about a psychiatric origin of their troubles.
PURPOSE:
To report an association between central retinal artery occlusion and homozygosity for factor V Leiden. METHOD: Case report. RESULTS: A 48-year-old woman with sudden loss of visual acuity in her right eye caused by a central retinal artery occlusion showed abnormal resistance to activated protein C and was homozygous for the factor V Leiden gene. CONCLUSION: Activated protein C resistance may be a risk factor for central retinal artery occlusion in young adults. (Am J Ophthalmol 2000;129:816 – 817. © 2000 by Elsevier Science Inc. All rights reserved.)
C
REFERENCES
1. Loewenstein JI. Visual hallucinations in patients with choroidal neovascularization. JAMA 1994;272:243. 2. Brown GC, Murphy RP. Visual symptoms associated with choroidal neovascularization. Photopsias and the Charles Bonnet syndrome. Arch Ophthalmol 1992;110:1251–1256. 3. Teunisse RJ, Cruysberg JRM, Verbeek A, Zitman FG. The Charles Bonnet syndrome: a large prospective study in The Netherlands. Br J Psychiatry 1995;166:254 –257. 4. Crane WG, Fletcher DC, Schuchard RA. Prevalence of photopsias and Charles Bonnet syndrome in a low vision population. Ophthalmol Clin North Am 1994;7:143–149. 5. Cogan DG. Visual hallucinations as release phenomena. Graefes Arch Klin Exp Ophthalmol 1973;188:139 –150.
Central Retinal Artery Occlusion in a Patient Homozygous for Factor V Leiden Jo¨rgen Larsson, MD
Accepted for publication Feb 22, 2000. From the Department of Ophthalmology, Lund University Hospital, Lund, Sweden. Inquiries to Jo¨rgen Larsson, MD, Department of Ophthalmology, Lund University Hospital, S-221 85 Lund, Sweden; fax: ⫹46 46 211 50 74; e-mail: [email protected]
816
AMERICAN JOURNAL
ENTRAL RETINAL ARTERY OCCLUSION IS A SEVERE
vision threatening disease. The etiology to this disease are most commonly arterial hypertension and carotid artery disease. We report a 48-year-old woman with sudden loss of vision in her right eye sought our care 6 hours after the onset of the symptoms. In the right eye, visual acuity was hand movements. Ophthalmoscopic examination showed retinal edema and a cherry-red spot in the macula, consistent with central retinal artery occlusion. A fluorescein angiogram confirmed the diagnosis and showed an arteriovenous transition time of 3 minutes. In the left eye, visual acuity was 20/20 and ophthalmoscopic examination showed a normal appearance. The patient was in good medical health and taking no medication. There was no history of thromboembolic disease. She had a history of cigarette smoking for 9 years and smoked 15 cigarettes a day. An extensive medical examination was carried out to find the cause of the occlusion. Blood pressure, echocardiogram, transesophageal echocardiogram, carotid ultrasound, erythrocyte sedimentation rate, hemoglobin level, platelet count, partial thromboplastin time, prothrombin time, antiphospholipid antibodies, protein C and S levels, antithrombin III level, plasminogen level, MTHFR C677T polymorphism, and prothrombin mutation 20210 were all normal. Abnormal resistance to activated protein C (1.3; normal, ⬎1.9) was detected and confirmed by polymerase chain reaction, which showed that she was homozygous for factor V Leiden. Twelve months after central retinal artery occlusion, visual acuity in the right eye was light perception. The most prominent risk factors for central retinal artery occlusion are arterial hypertension and carotid artery disease.1 However, in young people, other risk factors such as migraine and coagulation abnormalities are more important.2 A high prevalence of homozygosity for factor V Leiden has previously been reported in young patients with cerebrovascular disease.3 Branch retinal artery occlusion has been reported in a few patients heterozygous for factor V Leiden,4,5 but we are unaware of previous reports of homozygosity for factor V Leiden in central retinal artery occlusion and could find no references to it in a computerized search with the use of MEDLINE.
OF
OPHTHALMOLOGY
JUNE 2000
1. Swart J, Volker-Dieben HJ, Reichert-Thoen JWM. Alcaligenes xylosoxidans endophthalmitis 8 months after cataract extraction. Am J Ophthalmol 1999;127:345–346. 2. Aaberg TM, Rubsamen PE, Joondeph BC, et al. Chronic postoperative gram-negative endophthalmitis. Retina 1997; 17:260 –262. 3. Callender MG, Charles AM, Chalmers RL. Effect of storage time with different lens care systems on in-office hydrogel trial lens disinfection efficacy: a multi-center study. Optom Vis Sci 1992;69:678 – 684. 4. Lin A, Driebe WT Jr, Polack P. Alcaligenes xylosoxidans keratitis post penetrating keratoplasty in a rigid gas permeable lens wearer. CLAO J 1998;24:239 –241. 5. Winward KE, Pflugfelder SC, Flynn HW, et al. Postoperative Propionibacterium endophthalmitis: treatment strategies and long-term results. Ophthalmology 1993;100:447– 451.
A
FTER MACULAR PHOTOCOAGULATION, PATIENTS MAY
BRIEF REPORTS
815
Visual Hallucinations Immediately After Macular Photocoagulation Salomon Y. Cohen, MD, Avinoam B. Safran, MD, Ramin Tadayoni, MD, Gabriel Quentel, MD, Brigitte Guiberteau, MD, and Corinne Delahaye-Mazza, MD PURPOSE:
To evaluate the incidence of visual hallucinations after macular photocoagulation for choroidal neovascularization. METHODS: After macular photocoagulation for choroidal neovascularization, 60 consecutive patients were asked to respond to an orally administered questionnaire. RESULTS: Twenty-seven patients (45%) described photopsias, flashing lights of various colors. Ten additional patients Accepted for publication Jan 21, 2000. From the Centre d’Imagerie et de Laser (S.Y.C., G.Q., B.G., C.D.-M.); Department of Ophthalmology, Hoˆpital Lariboisie`re, Assistance Publique–Hoˆpitaux de Paris (S.Y.C., R.T.), Paris, France; and Department of Ophthalmology, Hoˆpital Cantonal Universitaire (A.B.S.), Geneva, Switzerland. This study was presented in part as a poster at the American Academy of Ophthalmology Annual Meeting, New Orleans, Louisiana, November 1998. Inquiries to Salomon Y. Cohen, MD, Centre d’Imagerie et de Laser, 11 rue Antoine Bourdelle, 75015 Paris, France; fax: (33) 1 42849409; e-mail: [email protected]
VOL. 129, NO. 6
(16.6%) also described structured hallucinations, including known or unknown faces, flowers, and geometric patterns, which occurred hours or a few days after photocoagulation. Patients with structured hallucinations were older (P ⴝ .04) and more often had subfoveal choroidal neovascularization (P ⴝ .005) and severe macular disease in both eyes or at least in the treated eye (P ⴝ .01). CONCLUSIONS: Visual hallucinations appear to be a frequent, albeit unrecognized, side effect of macular photocoagulation of choroidal neovascularization. The provision of proper information to patients may avoid concern about a psychiatric origin of their hallucinations. (Am J Ophthalmol 2000;129:815– 816. © 2000 by Elsevier Science Inc. All rights reserved.)
complain of visual loss or paracentral scotoma. To our knowledge, visual hallucinations have not been reported after macular photocoagulation except in a single case report.1 A prospective study was undertaken to define the nature and incidence of visual hallucinations immediately after macular photocoagulation. When they presented for the first angiographic study after photocoagulation (15 days to 1 month after treatment), patients were asked two questions by the ophthalmologist: (1) “Some patients observe luminous or colored phenomenon after laser photocoagulation. Did this occur in your case?” (2) “Some patients experience visual hallucinations after photocoagulation. Did this occur in your case?” Sixty consecutive patients were included. There were 42 women and 18 men; ages ranged from 41 to 92 years (mean, 75.3 years). Twenty-three patients (38.3%) reported no visual hallucinations after photocoagulation (group 1). Thirty-seven patients (61.6%) reported visual hallucinations immediately after photocoagulation. More precisely, 27 (45%) reported nonstructured visual hallucinations, that is, flickering or flashing lights, colored spots, filaments and/or luminous small sticks (group 2), whereas 10 patients (16.6%) also described structured and complex visual hallucinations, that is, flowers or “wallpaper” with flowers; known or unknown faces; geometric patterns, fences, paintings, and furniture; and small animals (group 3). All patients denied having experienced visual hallucinations in the past. The structured visual hallucinations appeared within a few hours or a few days after photocoagulation. All patients were relieved when they were told that their symptoms did not have a psychiatric origin. Groups were compared for their significance by means of chi-square test and/or Yates corrected chi-square and the Fisher exact test for dichotomous variables and by the Wilcoxon test for unpaired data for continuous variables. No difference was found between patients of group 3 compared with other patients in regard to sex (P ⫽ .45) or etiology of choroidal neovascularization (P ⫽ .35). Patients with structured visual hallucinations were found
to be older than other patients (P ⫽ .04). Choroidal neovascularization was more often subfoveal in patients in group 3 than in patients in the other groups (P ⫽ .005). Patients of group 3 more often had a severe macular lesion in both eyes or at least a more severe lesion in the treated eye than did other patients (P ⫽ .01). One patient, however, developed structured visual hallucinations despite the lack of a severe lesion in the treated eye. In 1769, Charles Bonnet described complex visual hallucinations in his psychologically normal grandfather. This phenomenon, the Charles Bonnet syndrome, was frequently reported in patients with visual impairment resulting from visual deprivation, being observed in 11% to 38% of patients.2,3 An association of Charles Bonnet syndrome with age-related macular degeneration (AMD) was previously reported,4 but to our knowledge Charles Bonnet syndrome is not known as a possible complication of macular photocoagulation. Anatomical changes observed after photocoagulation could be involved in the occurrence of photopsias. However, we suggest that the theory of a deafferentation state in which decreased vision stimulates intracerebral perceptions, as in the phantom-pain syndrome,5 may more likely explain the Charles Bonnet syndrome that occurs after photocoagulation, which implicates localized destruction of the retina. In the present study, visual hallucinations appear to be a frequent side effect of macular photocoagulation of choroidal neovascularization. Provision of proper information to patients may avoid concern about a psychiatric origin of their troubles.
PURPOSE:
To report an association between central retinal artery occlusion and homozygosity for factor V Leiden. METHOD: Case report. RESULTS: A 48-year-old woman with sudden loss of visual acuity in her right eye caused by a central retinal artery occlusion showed abnormal resistance to activated protein C and was homozygous for the factor V Leiden gene. CONCLUSION: Activated protein C resistance may be a risk factor for central retinal artery occlusion in young adults. (Am J Ophthalmol 2000;129:816 – 817. © 2000 by Elsevier Science Inc. All rights reserved.)
C
REFERENCES
1. Loewenstein JI. Visual hallucinations in patients with choroidal neovascularization. JAMA 1994;272:243. 2. Brown GC, Murphy RP. Visual symptoms associated with choroidal neovascularization. Photopsias and the Charles Bonnet syndrome. Arch Ophthalmol 1992;110:1251–1256. 3. Teunisse RJ, Cruysberg JRM, Verbeek A, Zitman FG. The Charles Bonnet syndrome: a large prospective study in The Netherlands. Br J Psychiatry 1995;166:254 –257. 4. Crane WG, Fletcher DC, Schuchard RA. Prevalence of photopsias and Charles Bonnet syndrome in a low vision population. Ophthalmol Clin North Am 1994;7:143–149. 5. Cogan DG. Visual hallucinations as release phenomena. Graefes Arch Klin Exp Ophthalmol 1973;188:139 –150.
Central Retinal Artery Occlusion in a Patient Homozygous for Factor V Leiden Jo¨rgen Larsson, MD
Accepted for publication Feb 22, 2000. From the Department of Ophthalmology, Lund University Hospital, Lund, Sweden. Inquiries to Jo¨rgen Larsson, MD, Department of Ophthalmology, Lund University Hospital, S-221 85 Lund, Sweden; fax: ⫹46 46 211 50 74; e-mail: [email protected]
816
AMERICAN JOURNAL
ENTRAL RETINAL ARTERY OCCLUSION IS A SEVERE
vision threatening disease. The etiology to this disease are most commonly arterial hypertension and carotid artery disease. We report a 48-year-old woman with sudden loss of vision in her right eye sought our care 6 hours after the onset of the symptoms. In the right eye, visual acuity was hand movements. Ophthalmoscopic examination showed retinal edema and a cherry-red spot in the macula, consistent with central retinal artery occlusion. A fluorescein angiogram confirmed the diagnosis and showed an arteriovenous transition time of 3 minutes. In the left eye, visual acuity was 20/20 and ophthalmoscopic examination showed a normal appearance. The patient was in good medical health and taking no medication. There was no history of thromboembolic disease. She had a history of cigarette smoking for 9 years and smoked 15 cigarettes a day. An extensive medical examination was carried out to find the cause of the occlusion. Blood pressure, echocardiogram, transesophageal echocardiogram, carotid ultrasound, erythrocyte sedimentation rate, hemoglobin level, platelet count, partial thromboplastin time, prothrombin time, antiphospholipid antibodies, protein C and S levels, antithrombin III level, plasminogen level, MTHFR C677T polymorphism, and prothrombin mutation 20210 were all normal. Abnormal resistance to activated protein C (1.3; normal, ⬎1.9) was detected and confirmed by polymerase chain reaction, which showed that she was homozygous for factor V Leiden. Twelve months after central retinal artery occlusion, visual acuity in the right eye was light perception. The most prominent risk factors for central retinal artery occlusion are arterial hypertension and carotid artery disease.1 However, in young people, other risk factors such as migraine and coagulation abnormalities are more important.2 A high prevalence of homozygosity for factor V Leiden has previously been reported in young patients with cerebrovascular disease.3 Branch retinal artery occlusion has been reported in a few patients heterozygous for factor V Leiden,4,5 but we are unaware of previous reports of homozygosity for factor V Leiden in central retinal artery occlusion and could find no references to it in a computerized search with the use of MEDLINE.
OF
OPHTHALMOLOGY
JUNE 2000