Brief Communications
January 2015
diminished unilaterally in patients with carotid artery stenosis.[10] The advantage of the ocular pulse waveform is that it can be recorded from the cornea using a tonometer probe much like those already in widespread use by ophthalmologists and optometrists. The testing is noninvasive, takes minutes to complete, and could easily be incorporated into routine eye examinations. This could become an important tool in the detection of arrhythmias and hemodynamic aberrations in asymptomatic patients, leading to earlier diagnosis and treatment.
References 1. Pourjavan S, Boëlle PY, Detry‑Morel M, De Potter P. Physiological diurnal variability and characteristics of the ocular pulse amplitude (OPA) with the dynamic contour tonometer (DCT‑Pascal). Int Ophthalmol 2007;27:357‑60. 2. Raman SV, Daniels CJ, Katz SE, Ryan JM, King MA. Congenital absence of the pericardium. Circulation 2001;104:1447‑8. 3. Bynke HG, Schéle B. On the origin of the ocular pressure pulse. Ophthalmologica 1967;153:29‑36. 4. Perkins ES. The ocular pulse. Curr Eye Res 1981;1:19‑23. 5. Karol HJ, Roberts CJ, Small RH. Electrical Analog Model of Ocular Pulse Amplitude as a Function of Systemic Pulse Pressure
Progressive hemifacial atrophy with ciliary body atrophy and ocular hypotony T Ashwini Kini, V S Prakash, Suresh Puthalath, P L Bhandari1 Progressive hemifacial atrophy (PHA) is a disease of unknown etiology affecting one‑half of the face. Ocular involvement is uncommon. Atrophy of iris is rare, with only a few cases of partial atrophy being reported in the literature. We report a case of total atrophy of iris and ciliary body with associated ocular hypotony in a 16‑year‑old girl with PHA. We believe this is the Access this article online Quick Response Code:
Website: www.ijo.in DOI: 10.4103/0301-4738.151474 PMID: ***
Department of Ophthalmology, Comtrust Super Speciality Eye Hospital, 1Department of Plastic Surgery, Govt. Medical College, Calicut, Kerala, India Correspondence to: Dr. T Ashwini Kini, Mangala, Chilimbi Hilldale Road, P.O. Ashok Nagar, Ladyhill, Mangalore ‑ 575 006, Karnataka, India. E‑mail: [email protected] Manuscript received: 26.01.14; Revision accepted: 20.01.15
61
and Ocular Rigidity. Invest Ophthalmol Vis Sci. 2007;48:ARVO E-Abstract 4946. 6. Bayerle‑Eder M, Kolodjaschna J, Wolzt M, Polska E, Gasic S, Schmetterer L. Effect of a nifedipine induced reduction in blood pressure on the association between ocular pulse amplitude and ocular fundus pulsation amplitude in systemic hypertension. Br J Ophthalmol 2005;89:704‑8. 7. McKee HD, Saldaña M, Ahad MA. Increased ocular pulse amplitude revealing aortic regurgitation. Am J Ophthalmol 2004;138:503. 8. Aykan U, Erdurmus M, Yilmaz B, Bilge AH. Intraocular pressure and ocular pulse amplitude variations during the Valsalva maneuver. Graefes Arch Clin Exp Ophthalmol 2010;248:1183‑6. 9. Bertelmann T, Langanke S, Potstawa M, Strempel I. Can dynamic contour tonometry and ocular pulse amplitude help to detect severe cardiovascular pathologies? Clin Ophthalmol 2014;8:1317‑21. 10. Knecht PB, Menghini M, Bachmann LM, Baumgartner RW, Landau K. The ocular pulse amplitude as a noninvasive parameter for carotid artery stenosis screening: A test accuracy study. Ophthalmology 2012;119:1244‑9. Cite this article as: Kassem JB, Katz SE, Mahmoud AM, Small RH, Raman SV, Roberts CJ. Ocular pressure waveform reflects ventricular bigeminy and aortic insufficiency. Indian J Ophthalmol 2015;63:59-61. Source of Support: Nil. Conflict of Interest: None declared.
first reported case of complete atrophy of iris and ciliary body in PHA. Ocular hypotony in PHA was thought to be due to intra‑ocular inflammation. However in our case it appears to be secondary to severe atrophy of the ciliary body. Key words: Ciliary body atrophy, iris atrophy, ocular hypotony, progressive hemifacial atrophy
Parry‑Romberg syndrome or progressive hemifacial atrophy (PHA) affects the skin, soft tissue and skeletal structures of the face. Ocular involvement occurs in 10–35%, ranging from uveitis to enophthalmos.[1,2] Ocular hypotony in PHA has been attributed to intra‑ocular inflammation. Atrophy of iris in PHA is very rare, with only a few cases of partial iris atrophy being reported previously. We report a case of PHA with complete atrophy of iris and ciliary body. We hypothesize that the accompanying severe ocular hypotony may be secondary to atrophy of the ciliary body.
Case Report A 16‑year‑old girl presented with painless progressive diminution of vision in right eye since 2 years, associated with glare. Left eye was asymptomatic. She noticed asymmetry of her face at 13 years of age and was diagnosed with PHA. The asymmetry was progressive, and she received fat grafting on the right side of her face. There were no systemic manifestations like seizures, migraine, intellectual deterioration, trigeminal neuralgia or neuropsychiatric disturbances. General physical examination showed atrophy of the right half of the face involving subcutaneous tissue, muscle and bone [Fig. 1]. There was no neurologic deficit or oral involvement. Visual acuity was 20/60 in right eye and 20/20
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Indian Journal of Ophthalmology
in left eye. Best‑corrected visual acuity was 20/20 with + 2.25 cylinder at 90° in right eye. Right eye had enophthalmos and severe hypotony with intraocular pressure of 4 mm of Hg by Goldmann’s applanation tonometer. Intra‑ocular pressure of her left eye was 16 mm of Hg. Slit lamp examination of right eye revealed marked iris atrophy amounting to aniridia. The pupil was fully dilated and nonreactive to light and accommodation [Fig. 2]. Lens showed partial subluxation inferiorly. Fundus examination showed hypotonic maculopathy with internal limiting membrane folds radiating across the macula [Fig. 3]. Gonioscopy showed open angles with broad ciliary body band. Ultrasound biomicroscopy revealed atrophic iris and ciliary body [Fig. 4]. Lids, adnexa and ocular motility were normal. There was no evidence of iridocyclitis or retinal vasculitis in this patient.
Vol. 63 No. 1
Discussion The clinical features of PHA were initially observed by Caleb Hillier Parry in 1825 and subsequently described by Moritz Heinrich Romberg in 1846.[3,4] Although the exact etiology is unknown it is believed to be related to localized facial scleroderma.[5] The pathological process consists of chronic lymphocytic infiltration around neurovascular bundles. PHA has a slight female preponderance with age of onset around 5–15 years.[6,7] It is usually unilateral. There are progressive atrophy and deformation of one side of the face, resulting in unilateral facial atrophy, deviation of mouth and nose toward affected side.[5] PHA has been linked with various neurologic, ophthalmic, cardiac, rheumatologic, infectious, endocrine, maxillofacial and orthodontic manifestations.
At 6 months follow‑up, the intra‑ocular pressure in her right eye has further reduced to 2 mm of Hg. However, best‑corrected visual acuity remains 6/6 with the same correction. Fundus and ultrasound bio‑microscopy findings remained the same.
Involvement of the eye is uncommon and reported to be in the range of 10–35%. Various ophthalmic associations so far reported are listed in Table 1.[5,8] A few cases of partial iris atrophy have been reported in the literature. Preechawat et al. reported a case of partial iris atrophy with sluggishly reacting 3 mm‑pupil.[8] Two cases of partial iris atrophy with poor light reflex were reported by Miller and Spencer.[9] Dawczynski
Figure 1: Hemifacial atrophy involving the right side of the face
Figure 2: Slit lamp diffuse illumination showing near total iris atrophy with dilated pupil
Figure 3: Fundus photo showing hypotonic maculopathy
Figure 4: Ultrasound biomicroscopy of both eyes showing iris with ciliary body atrophy on the right side
Brief Communications
January 2015
63
Table 1: Various ocular manifestations associated with Parry Romberg syndrome[3,6] Orbit
Lids and adnexa
Extraocular muscles
Anterior segment
Posterior segment
Enophthalmos
Lid atrophy
Exotropia
Decreased corneal sensitivity
Vitritis
Phthisis bulbi
Lid retraction
Esotropia
Band keratopathy
Papillitis
Nerve paresis
Loss of cilia
Hypotropia
Episcleritis
Retinal telangiectasis
Blepharoptosis
Restrictive strabismus
Uveitis
Retinal edema
Extraocular muscle thinning and impairment
Cataract
Retinal pigment lesions
Miosis Glaucoma Generalised iris atrophy
et al. reported a patient with pupillary abnormalities with enophthalmos.[10] However, the condition of the ciliary body was not mentioned. All these cases reported partial atrophy of the iris.[8] In our case, there was total atrophy of iris and ciliary body and with ocular hypotonia. Ocular hypotony has been attributed as being secondary to intraocular inflammation. But in our case we believe ocular hypotony occurred secondary to ciliary body atrophy. To our best knowledge, such a combination of features has not been described in the literature before. Atrophy of iris and ciliary body may be a part of generalized facial atrophy. No specific treatment has been mentioned for ocular involvement PHA. Hypotony has been managed by silicone oil injections in some cases. Antiinflammatory drugs might be given in patients with active inflammatory disease. Facial and oculoplastic surgery may be done for cosmetic purposes.[11]
References 1. Miller MT, Sloane H, Goldberg MF, Grisolano J, Frenkel M, Mafee MF. Progressive hemifacial atrophy (Parry‑Romberg disease). J Pediatr Ophthalmol Strabismus 1987;24:27‑36. 2. Muchnick RS, Aston SJ, Rees TD. Ocular manifestations and treatment of hemifacial atrophy. Am J Ophthalmol 1979;88:889‑97. 3. Jurkiewicz MJ, Nahai F. The use of free revascularized grafts in the amelioration of hemifacial atrophy. Plast Reconstr Surg 1985;76:44‑55.
T o r e por t a c a s e o f u n i l at eral proliferative retinopathy following noncerebral malaria with Plasmodium falciparum in Southern India Aditya Verma, Krishna MS Sri Bhagwan Mahavir Vitreoretinal Services, Medical Research Foundation, Sankara Nethralaya, Nungambakkam, Chennai - 600 006, Tamil Nadu, India Correspondence to: Dr. Aditya Verma, Sri Bhagwan Mahavir Vitreoretinal Services, Medical Research Foundation, 18, College Road, Nungambakkam, Chennai - 600 006, Tamil Nadu, India. E-mail: [email protected] Manuscript received: 21.06.14; Revision accepted: 10.01.14
4. Cory RC, Clayman DA, Faillace WJ, McKee SW, Gama CH. Clinical and radiologic findings in progressive facial hemiatrophy (Parry‑Romberg syndrome). AJNR Am J Neuroradiol 1997;18:751‑7. 5. El‑Kehdy J, Abbas O, Rubeiz N. A review of Parry‑Romberg syndrome. J Am Acad Dermatol 2012;67:769‑84. 6. Stone J. Parry‑Romberg syndrome: A global survey of 205 patients using the Internet. Neurology 2003;61:674‑6. 7. Pensler JM, Murphy GF, Mulliken JB. Clinical and ultrastructural studies of Romberg’s hemifacial atrophy. Plast Reconstr Surg 1990;85:669‑74. 8. Preechawat P, Phuchantuk P, Leelawongs K. Ocular abnormalities in Parry‑Romberg syndrome. Thai J Ophthalmol 2011;25:43‑8. 9. Miller MT, Spencer MA. Progressive hemifacial atrophy. A natural history study. Trans Am Ophthalmol Soc 1995;93:203‑15. 10. Dawczynski J, Thorwarth M, Koenigsdoerffer E, Schultze‑Mosgau S. Interdisciplinary treatment and ophthalmological findings in Parry‑Romberg syndrome. J Craniofac Surg 2006;17:1175‑6. 11. Alencar JC, Andrade SH, Pessoa SG, Dias IS. Autologous fat transplantation for the treatment of progressive hemifacial atrophy (Parry‑Romberg syndrome: Case report and review of medical literatute). An Bras Dermatol 2011;86:S85‑8. Cite this article as: Kini TA, Prakash VS, Puthalath S, Bhandari PL. Progressive hemifacial atrophy with ciliary body atrophy and ocular hypotony. Indian J Ophthalmol 2015;63:61-3. Source of Support: Nil. Conflict of Interest: None declared.
The retinopathy in association with malaria fever described so far includes retinal hemorrhages, vessel changes, retinal discoloration/whitening and papilledema. Malaria retinopathy has been mostly described in severe cases, associated with Plasmodium falciparum, correlating the patho-physiology of retinal and cerebral manifestations. We report an unusual case of proliferative retinopathy as a manifestation of malaria fever, caused by P. falciparum with no cerebral involvement. The patient had features of unilateral retinal vascular occlusion with Access this article online Quick Response Code:
Website: www.ijo.in DOI: 10.4103/0301-4738.151475 PMID: ***
Copyright of Indian Journal of Ophthalmology is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
January 2015
diminished unilaterally in patients with carotid artery stenosis.[10] The advantage of the ocular pulse waveform is that it can be recorded from the cornea using a tonometer probe much like those already in widespread use by ophthalmologists and optometrists. The testing is noninvasive, takes minutes to complete, and could easily be incorporated into routine eye examinations. This could become an important tool in the detection of arrhythmias and hemodynamic aberrations in asymptomatic patients, leading to earlier diagnosis and treatment.
References 1. Pourjavan S, Boëlle PY, Detry‑Morel M, De Potter P. Physiological diurnal variability and characteristics of the ocular pulse amplitude (OPA) with the dynamic contour tonometer (DCT‑Pascal). Int Ophthalmol 2007;27:357‑60. 2. Raman SV, Daniels CJ, Katz SE, Ryan JM, King MA. Congenital absence of the pericardium. Circulation 2001;104:1447‑8. 3. Bynke HG, Schéle B. On the origin of the ocular pressure pulse. Ophthalmologica 1967;153:29‑36. 4. Perkins ES. The ocular pulse. Curr Eye Res 1981;1:19‑23. 5. Karol HJ, Roberts CJ, Small RH. Electrical Analog Model of Ocular Pulse Amplitude as a Function of Systemic Pulse Pressure
Progressive hemifacial atrophy with ciliary body atrophy and ocular hypotony T Ashwini Kini, V S Prakash, Suresh Puthalath, P L Bhandari1 Progressive hemifacial atrophy (PHA) is a disease of unknown etiology affecting one‑half of the face. Ocular involvement is uncommon. Atrophy of iris is rare, with only a few cases of partial atrophy being reported in the literature. We report a case of total atrophy of iris and ciliary body with associated ocular hypotony in a 16‑year‑old girl with PHA. We believe this is the Access this article online Quick Response Code:
Website: www.ijo.in DOI: 10.4103/0301-4738.151474 PMID: ***
Department of Ophthalmology, Comtrust Super Speciality Eye Hospital, 1Department of Plastic Surgery, Govt. Medical College, Calicut, Kerala, India Correspondence to: Dr. T Ashwini Kini, Mangala, Chilimbi Hilldale Road, P.O. Ashok Nagar, Ladyhill, Mangalore ‑ 575 006, Karnataka, India. E‑mail: [email protected] Manuscript received: 26.01.14; Revision accepted: 20.01.15
61
and Ocular Rigidity. Invest Ophthalmol Vis Sci. 2007;48:ARVO E-Abstract 4946. 6. Bayerle‑Eder M, Kolodjaschna J, Wolzt M, Polska E, Gasic S, Schmetterer L. Effect of a nifedipine induced reduction in blood pressure on the association between ocular pulse amplitude and ocular fundus pulsation amplitude in systemic hypertension. Br J Ophthalmol 2005;89:704‑8. 7. McKee HD, Saldaña M, Ahad MA. Increased ocular pulse amplitude revealing aortic regurgitation. Am J Ophthalmol 2004;138:503. 8. Aykan U, Erdurmus M, Yilmaz B, Bilge AH. Intraocular pressure and ocular pulse amplitude variations during the Valsalva maneuver. Graefes Arch Clin Exp Ophthalmol 2010;248:1183‑6. 9. Bertelmann T, Langanke S, Potstawa M, Strempel I. Can dynamic contour tonometry and ocular pulse amplitude help to detect severe cardiovascular pathologies? Clin Ophthalmol 2014;8:1317‑21. 10. Knecht PB, Menghini M, Bachmann LM, Baumgartner RW, Landau K. The ocular pulse amplitude as a noninvasive parameter for carotid artery stenosis screening: A test accuracy study. Ophthalmology 2012;119:1244‑9. Cite this article as: Kassem JB, Katz SE, Mahmoud AM, Small RH, Raman SV, Roberts CJ. Ocular pressure waveform reflects ventricular bigeminy and aortic insufficiency. Indian J Ophthalmol 2015;63:59-61. Source of Support: Nil. Conflict of Interest: None declared.
first reported case of complete atrophy of iris and ciliary body in PHA. Ocular hypotony in PHA was thought to be due to intra‑ocular inflammation. However in our case it appears to be secondary to severe atrophy of the ciliary body. Key words: Ciliary body atrophy, iris atrophy, ocular hypotony, progressive hemifacial atrophy
Parry‑Romberg syndrome or progressive hemifacial atrophy (PHA) affects the skin, soft tissue and skeletal structures of the face. Ocular involvement occurs in 10–35%, ranging from uveitis to enophthalmos.[1,2] Ocular hypotony in PHA has been attributed to intra‑ocular inflammation. Atrophy of iris in PHA is very rare, with only a few cases of partial iris atrophy being reported previously. We report a case of PHA with complete atrophy of iris and ciliary body. We hypothesize that the accompanying severe ocular hypotony may be secondary to atrophy of the ciliary body.
Case Report A 16‑year‑old girl presented with painless progressive diminution of vision in right eye since 2 years, associated with glare. Left eye was asymptomatic. She noticed asymmetry of her face at 13 years of age and was diagnosed with PHA. The asymmetry was progressive, and she received fat grafting on the right side of her face. There were no systemic manifestations like seizures, migraine, intellectual deterioration, trigeminal neuralgia or neuropsychiatric disturbances. General physical examination showed atrophy of the right half of the face involving subcutaneous tissue, muscle and bone [Fig. 1]. There was no neurologic deficit or oral involvement. Visual acuity was 20/60 in right eye and 20/20
62
Indian Journal of Ophthalmology
in left eye. Best‑corrected visual acuity was 20/20 with + 2.25 cylinder at 90° in right eye. Right eye had enophthalmos and severe hypotony with intraocular pressure of 4 mm of Hg by Goldmann’s applanation tonometer. Intra‑ocular pressure of her left eye was 16 mm of Hg. Slit lamp examination of right eye revealed marked iris atrophy amounting to aniridia. The pupil was fully dilated and nonreactive to light and accommodation [Fig. 2]. Lens showed partial subluxation inferiorly. Fundus examination showed hypotonic maculopathy with internal limiting membrane folds radiating across the macula [Fig. 3]. Gonioscopy showed open angles with broad ciliary body band. Ultrasound biomicroscopy revealed atrophic iris and ciliary body [Fig. 4]. Lids, adnexa and ocular motility were normal. There was no evidence of iridocyclitis or retinal vasculitis in this patient.
Vol. 63 No. 1
Discussion The clinical features of PHA were initially observed by Caleb Hillier Parry in 1825 and subsequently described by Moritz Heinrich Romberg in 1846.[3,4] Although the exact etiology is unknown it is believed to be related to localized facial scleroderma.[5] The pathological process consists of chronic lymphocytic infiltration around neurovascular bundles. PHA has a slight female preponderance with age of onset around 5–15 years.[6,7] It is usually unilateral. There are progressive atrophy and deformation of one side of the face, resulting in unilateral facial atrophy, deviation of mouth and nose toward affected side.[5] PHA has been linked with various neurologic, ophthalmic, cardiac, rheumatologic, infectious, endocrine, maxillofacial and orthodontic manifestations.
At 6 months follow‑up, the intra‑ocular pressure in her right eye has further reduced to 2 mm of Hg. However, best‑corrected visual acuity remains 6/6 with the same correction. Fundus and ultrasound bio‑microscopy findings remained the same.
Involvement of the eye is uncommon and reported to be in the range of 10–35%. Various ophthalmic associations so far reported are listed in Table 1.[5,8] A few cases of partial iris atrophy have been reported in the literature. Preechawat et al. reported a case of partial iris atrophy with sluggishly reacting 3 mm‑pupil.[8] Two cases of partial iris atrophy with poor light reflex were reported by Miller and Spencer.[9] Dawczynski
Figure 1: Hemifacial atrophy involving the right side of the face
Figure 2: Slit lamp diffuse illumination showing near total iris atrophy with dilated pupil
Figure 3: Fundus photo showing hypotonic maculopathy
Figure 4: Ultrasound biomicroscopy of both eyes showing iris with ciliary body atrophy on the right side
Brief Communications
January 2015
63
Table 1: Various ocular manifestations associated with Parry Romberg syndrome[3,6] Orbit
Lids and adnexa
Extraocular muscles
Anterior segment
Posterior segment
Enophthalmos
Lid atrophy
Exotropia
Decreased corneal sensitivity
Vitritis
Phthisis bulbi
Lid retraction
Esotropia
Band keratopathy
Papillitis
Nerve paresis
Loss of cilia
Hypotropia
Episcleritis
Retinal telangiectasis
Blepharoptosis
Restrictive strabismus
Uveitis
Retinal edema
Extraocular muscle thinning and impairment
Cataract
Retinal pigment lesions
Miosis Glaucoma Generalised iris atrophy
et al. reported a patient with pupillary abnormalities with enophthalmos.[10] However, the condition of the ciliary body was not mentioned. All these cases reported partial atrophy of the iris.[8] In our case, there was total atrophy of iris and ciliary body and with ocular hypotonia. Ocular hypotony has been attributed as being secondary to intraocular inflammation. But in our case we believe ocular hypotony occurred secondary to ciliary body atrophy. To our best knowledge, such a combination of features has not been described in the literature before. Atrophy of iris and ciliary body may be a part of generalized facial atrophy. No specific treatment has been mentioned for ocular involvement PHA. Hypotony has been managed by silicone oil injections in some cases. Antiinflammatory drugs might be given in patients with active inflammatory disease. Facial and oculoplastic surgery may be done for cosmetic purposes.[11]
References 1. Miller MT, Sloane H, Goldberg MF, Grisolano J, Frenkel M, Mafee MF. Progressive hemifacial atrophy (Parry‑Romberg disease). J Pediatr Ophthalmol Strabismus 1987;24:27‑36. 2. Muchnick RS, Aston SJ, Rees TD. Ocular manifestations and treatment of hemifacial atrophy. Am J Ophthalmol 1979;88:889‑97. 3. Jurkiewicz MJ, Nahai F. The use of free revascularized grafts in the amelioration of hemifacial atrophy. Plast Reconstr Surg 1985;76:44‑55.
T o r e por t a c a s e o f u n i l at eral proliferative retinopathy following noncerebral malaria with Plasmodium falciparum in Southern India Aditya Verma, Krishna MS Sri Bhagwan Mahavir Vitreoretinal Services, Medical Research Foundation, Sankara Nethralaya, Nungambakkam, Chennai - 600 006, Tamil Nadu, India Correspondence to: Dr. Aditya Verma, Sri Bhagwan Mahavir Vitreoretinal Services, Medical Research Foundation, 18, College Road, Nungambakkam, Chennai - 600 006, Tamil Nadu, India. E-mail: [email protected] Manuscript received: 21.06.14; Revision accepted: 10.01.14
4. Cory RC, Clayman DA, Faillace WJ, McKee SW, Gama CH. Clinical and radiologic findings in progressive facial hemiatrophy (Parry‑Romberg syndrome). AJNR Am J Neuroradiol 1997;18:751‑7. 5. El‑Kehdy J, Abbas O, Rubeiz N. A review of Parry‑Romberg syndrome. J Am Acad Dermatol 2012;67:769‑84. 6. Stone J. Parry‑Romberg syndrome: A global survey of 205 patients using the Internet. Neurology 2003;61:674‑6. 7. Pensler JM, Murphy GF, Mulliken JB. Clinical and ultrastructural studies of Romberg’s hemifacial atrophy. Plast Reconstr Surg 1990;85:669‑74. 8. Preechawat P, Phuchantuk P, Leelawongs K. Ocular abnormalities in Parry‑Romberg syndrome. Thai J Ophthalmol 2011;25:43‑8. 9. Miller MT, Spencer MA. Progressive hemifacial atrophy. A natural history study. Trans Am Ophthalmol Soc 1995;93:203‑15. 10. Dawczynski J, Thorwarth M, Koenigsdoerffer E, Schultze‑Mosgau S. Interdisciplinary treatment and ophthalmological findings in Parry‑Romberg syndrome. J Craniofac Surg 2006;17:1175‑6. 11. Alencar JC, Andrade SH, Pessoa SG, Dias IS. Autologous fat transplantation for the treatment of progressive hemifacial atrophy (Parry‑Romberg syndrome: Case report and review of medical literatute). An Bras Dermatol 2011;86:S85‑8. Cite this article as: Kini TA, Prakash VS, Puthalath S, Bhandari PL. Progressive hemifacial atrophy with ciliary body atrophy and ocular hypotony. Indian J Ophthalmol 2015;63:61-3. Source of Support: Nil. Conflict of Interest: None declared.
The retinopathy in association with malaria fever described so far includes retinal hemorrhages, vessel changes, retinal discoloration/whitening and papilledema. Malaria retinopathy has been mostly described in severe cases, associated with Plasmodium falciparum, correlating the patho-physiology of retinal and cerebral manifestations. We report an unusual case of proliferative retinopathy as a manifestation of malaria fever, caused by P. falciparum with no cerebral involvement. The patient had features of unilateral retinal vascular occlusion with Access this article online Quick Response Code:
Website: www.ijo.in DOI: 10.4103/0301-4738.151475 PMID: ***
Copyright of Indian Journal of Ophthalmology is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
