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A rare and incomplete form of Sturge Weber Syndrome: Glaucoma without choroidal hemangioma nor neurologic manifestations
Authors: Hachicha F, Ben Abdesslem N, Lajmi H, Ouederni M, Brour , Cheour M, Kraiem A.
Introduction:
Sturge Weber syndrome (SWS)  is a rare, sporadic, and congenital disease. It belongs to the phacomatosis group. This disease is characterized by ipsilateral  cavernous hemangioma of the face (port-wine stain, nevus flammeus), uvea and brain. The most common ocular manifestations in SWS are glaucoma (affecting more than 50% of the patients ), choroidal hemangioma and exsudative retinal detachment [1].  Refractory Glaucoma  is generally associated with neurologic and uveal manifestations . This report presents an rare and incomplete form of SWS:  A  22-year-old woman with capillary angioma of the face,  an ipsilateral  glaucoma that responded well to medical treatment, without choroidal hemangioma nor neurologic manifestations..
Case report�:
A 22-year-old woman, with congenital port-wine stains on the right side of the face involving the upper eyelid and cheek (figure 1), was referred with a diagnosis of SWS to evaluate the ocular state. The patient presented to our department in February 2013 with a painful right eye. An ophthalmological examination was performed. Best corrected visual acuity was 10/10 in each eye. There was a relative deficit in the afferent component of the pupillary light reflex of the right eye. The intraocular pressure (IOP) was 26 mmHg in the right eye and 12 mmHg in the left eye. Gonioscopy showed open angles without pigment deposits in both eyes. Fundus examination of the right eye revealed a pale optic disc with advanced cupping (c/d=7/10) (figure 2). It was normal in the left eye. A visual field test showed advanced field defect in the right eye and a normal field in the left eye (figure 3).  There was any history of headache, convulsions or any neurogical deficit. Family history was insignificant. The patient was of normal intellect. Systemic examination including detailed neurogical checkup did not reveal any abnormality. Fluorescein angiography, B-scan echography as well as cerebral MR imaging were performed within normal results. A treatment using topical Latanoprost + Timolol (fixed combination, one drop daily) was administred in the right eye. The clinical course was marked by a control of  IOP (around 10-12 mmHg) and stabilization of visual field defects (10 months follow-up).
Discussion�:
Sturge Weber syndrome (SWS) belongs to a group of disorder collectively known as phakomatoses, disorders of the central nervous system that results in lesions on skin, brain and eyes . It is a rare neurocutaneous syndrome that occurs early in fetal development with a frequency of approximately 1 per 50000 [2]. It occurs sporadically and with equal frequency in both sexe [3]. Although the syndrome is congenital, there is generally no heritability. However, rare familial cases have been reported [4]. The pathophysiology lies in the vascular abnormalities that leads to impaired blood flow [5,6]. Due to the unilateral nature of the vascular malformation, a somatic mutation or a double success model has been proposed as the starting point of this syndrome [7]. It is clinically characterized by �port-wine� stains on the trigeminal area, predominantly on the maxillary branch (88%), although the ophtalmic and/or mandibular branch may also be affected. Our patient suffers from port wine staining of the three divisions of trigeminal nerve extending to her neck and upper chest on the right side. 14% of occurrences are bilateral [1], with a higher prevalence of extrafacial involvement�: leptomeningeal angiomas on the parieto-occipital area and ophtalmic alterations. Other less frequent clinical states include epilepsy (14%) and mental retardation [8].Thus, a patient with SWS typically has a port wine stain (nevus flammeus) of the face, ipsilateral intracranial hemangioma and congenital glaucoma. Incomplete forms exist [9]. SWS based on Roach scale can be devided into type I -  Both facial and leptomeningeal angiomas�;may have glaucoma, type II � facial angioma alone�;may have glaucoma, and type III � isolated leptomeningeal angiomas�;usually no glaucoma[10]. In this patient there were no neurogical abnormalities neither choroidal hemangioma. The only abnormality associated with naevus flammeus was ipsilateral glaucoma. Glaucoma is the most common ophtalmic complication associated with SWS, affecting more than 50% of the patients[11]. One study reported a prevalence of 76% [12]. Glaucoma is found to be closely associated with the location of facial angioma. Indeed, It occurs most often on the side where the facial angioma is located, especially with the involvement of the ophtalmic (V1) and maxillary (V2) division of trigeminal nerve, most often the upper eyelid or conjunctiva [13]. 25% of SWS patients developed glaucoma in the eye without cutaneous involvement [10].  Glaucoma can start from childhood to adulthood [13]. In our case, glaucoma was ipsilateral to the cutaneous manifestations and was diagnosed at the age of 20. The pathogenesis of glaucoma remains a subject for debate [14]. Various theories which have been put forward to explain the occurrence of glaucoma in this syndrome include congenital malformations of the anterior chamber angle [15], raised episcleral venous pressure and hypersecretion of aqueous. Our patient has a normal gonioscopy. Although medications may be sufficient to control glaucoma that occurs in later life, the early onset of glaucoma usually requires surgical intervention [16]. Several studies suggest that goniotomy and trabeculectomy seems to give good results when glaucoma occurs in early childhood in which anomalies of development of the angle are present [11,16]. Standard trabeculectomy, or combined trabeculotomy/trabeculectomy, may be advantageous in SWS, by passing Schlemm�s canal and redirecting aqueous to the subconjunctival space [17,18]. In our case without choroidal hemangioma, IOP was controlled by topical Latanoprost-Timolol. But inspite of their efficacity, Prostaglandin  analogs should be used with caution in glaucoma patients with elevated episcleral venous pressure and particularly in SWS with diffuse choroidal hemangioma because they can cause uveal effusion and subtotal exudative retinal detachment [19]. In addition to glaucoma, other ophtalmic manifestations have been described in SWS. Choroidal hemangioma are frequent amongst these, either localized or in diffuse shape [20] . Orbital hemangioma are rare. They may contribute to an increase of IOP, as ophtalmic veins are involved in their growth. Other less frequent findings have been reported, such as posterior scleritis with uveal effusion leading to glaucoma from angular closure [21], juvenile ossifying orbit wall fibroma [22] and central retinal vein occlusion [23].

Conclusion�: 
Glaucoma is closely related to SWS especially when there is facial angioma involving V1 and V2 trigeminal distribution. It is always associated with choroidal hemangioma and neurogical manifestations but incomplete forms exist. Medication can, in some cases, provide adequate IOP control, however prompt and early surgical intervention is always needed to save sight.
References�: 
[1]Martinez-Guti�rrez J, Lopez-Lancho R, Perez-Blazquez E (2008). Angiomatous choroidal and orbital lesions in a patient with SWS. Arch Soc Esp Oftalmol 83: 429-432.
[2]Xiao-Lei Yin, Jian Ye, Rong-Di Yuan, Shu-Xing (2011). A case of circumscribed choroidal hemangioma in SWS in China. Int J Ophtalmol 4(2):210-211.
[3]Maadan Y, Dewan V, Ramaswamy S, Sharma A (2006). Behavioral manifestations of SWS : a case report. Prim care companion J Clin Psychiatry 8(4): 198-200
[4]Evans AL, Widjaja E, Conolly DJ, Griffiths PD (2006). Cerebral perfusion abnormalities in children with SWS shown by dynamic contrast bolus magnetic resonance perfusion imaging. Pediatrics 117(6): 2119-2125
[5]Bodensteiner JB (2001). Sturge Weber syndrome. Facial plastic surgery clinics 9(4): 549-576
[6]Enjolras O, Herbreteau D, Lemarchand F, et al (1992). Hemangiomas and superficial vascular malformations�: classification. Journal des maladies vasculaires 17(1): 2-19
[7]Happle R (1987). Lethal genes surviving by mosaicism�: a possible explanation for sporadic birth defects involving the skin. Journal of the American academy of dermatology 16(4): 899-906
[8]Bioxeda P, de Misa RF, Arrazola JM, Penez B, Harto A, et al (1993). Angioma plano facial y sindrome de Sturge Weber�: estudio de 121 casos. Med Clin (Barc) 101�:1-4
[9]Ebert EM, Albert D, Boger W. Phacomatoses. In : Albert DM, Jakobier FA  (1994). Principles and practice of Ophtalmology. WB Saunders : Philadelphia PP:  3298-3328
[10]Hon Seng Wong, Ropilah Abdul Rahman, Swee Ying Choo, Nurlia Yahya (2012). SWS with extreme ocular manifestation and rare association of upper airway angioma with anticipated difficult airway. Med J Malaysia 67(4): 435-437
[11]Iwach AG, Hoskins HD, Jr., Hetherington J, Shaffer RN (1990). Analysis of surgical and medical management of glaucoma in SWS. Ophtalmology 97(7): 904-909
[12]Witchal H, Font RL (976). Hemangioma of the choroid : a clinicopathologic study of 71 cases and a review of the literature. Surv Ophtalmol 20: 415-431
[13]Front RL, Ferry AP (1972). The phakomatoses. Int Ophtalmol Clin 12:1-50
[14]MC Govern RA (1986). Glaucoma. Vol II. Harcount Brace Jovanovich Publishers. p719.
[15]Sullivan TJ, Clarke MP, Morin JD (1992). The ocular manifestations of SWS. J Pediatric Ophtalmol Strabismus 29:349-356
[16]Hoskins HD Jr, Shaffer RN, Hetherington J (1984). Anatomic classification of the developmental glaucomas. Arch Ophtalmol 102:1331-6.
[17]Burke JP, Bowell R (1989). Primary trbeculectomy in congenital glaucoma. Br J Ophtalmol 73�:186-19.
[18]Agarwal HC, Sandramouli S, Sihota R, Sood NN (1993). Sturge Weber syndrome�: management of glaucoma with combined trabeculotomy-trabeculectomy. Ophthal Surg 24�: 399-402
[19]J. Gambrella, P.Denis, V.Kocaba, J.D.Orange (2008). Uveal effusion induced by topical travoprost in a patient with SWS. J Fr Ophtalmol 31:e19.
[20]Packwood EA, Havertape SA, Cruz OA, Mann ES (2000). Visual rehabilitation in a child with diffuse choroidal hemangioma by using aggressive amblyopia therapy with low-dose external bean irradiation. JAPOOS 4:321-322.
[21]Maruyana I, Ohguro H, Hakazawa M (2003). A case of acute angle-closure glaucoma secondary to posterior scleritis in patient with SWS. Jpn J Ophtalmol 46�:233�;74-77.
[22]Lin DD, Gailloud P, MC Canthy EF, Comi AM (2006). Oromaxillofacial osseous abnormality in SWS�: case report and review of the literature. AJNR Am J Neuroradiol 27: 274-277.
[23]CM Knapp, V Sarudia, GHA Woodruff (2002). Central retinal vein occlusion associated with Sturge Weber Syndrome. Eye 16: 657-659















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