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Show /Olln",1 of Cli,,;cal Nt'IIr<J-ophtlIOIIIlologli 7(3): 170-177. 1987. Linear Nevus Sebaceous Syndrome A Review Israel Alfonso, M.D., Cleve Howard, M.D., Pedro F. Lopez, M.D., Jose A. Palomino, M.D., and Carmen E. Gonzalez, M.D. © 1987 Raven PresS, Ltd., New York We report a case of linear nevus sebaceous syndrome with large areas of calcification involving multiple layers of the posterior aspects of both eyes. This patient had a normal neurological examination despite dysplastic brain changes. We discuss and review the multiple clinical presentation and embryopathogenesis of this disorder. Key Words: Linear nevus sebaceous syndrome-Choristoma of conjunctiva - Dysplastic brain changes- Embryo pathogenesis-Intraocular calcification. From the Department of Neonatal Neurology (LA.), Miami ChiJdren's Hospital, Miami, Florida; Bascom Palmer Eye Institute (C.H.), Miami, Florida; Department of Internal Medicine (P.F.L.), Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts; Neonatal Intensive Care Unit a.A.p.). Hialeah Hospital, Hialeah, Florida; and Department of Pediatrics (C.E.C.), C.A.C. Health Plan, H.M.a., Hialeah, FL, U.S.A. Address correspondence and reprint requests to Dr. I. Alk> nso, Department of Neunatal Neurology, Miami Children's H,,·,pital. 1200 Southwe<;t bOth Court, No. 302, Miami, FL 170 We recently cared for a newborn with linear nevus sebaceous syndrome, a rather infrequent hamartosis of unknown etiology that involves many organs of ectodermal and mesodermal origin, most often the skin, eyes, and brain. After reviewing the literature, we were impressed with the degree of confusion surrounding this syndrome, a confusion created by its unknown etiology, misleading names, long history, and ill-defined spectrum of its many clinical manifestations. Hence, we report a case of linear nevus sebaceous syndrome with unusually large calcified plaques in both eyes and review the available literature to familiarize the neuro-ophthalmologist with the many facets of this entity. CASE REPORT A 2.734-kg female infant was born at term to a 31-year-old, gravida 1, para 0 mother following a pregnancy complicated by a urinary tract infection treated with ampicillin during the second trimester. Apgar scores were 8 and 9 at 1 and 5 min. Family history was unremarkable. The initial examination revealed a cutaneous abnormality of the face consisting of a well-demarcated tannish velvety plaque with linear qualities that involved the left side of the face (Figs. 1 and 2), a similar less well formed lesion under the chin with a linear midline extension to the lower lip (Fig. 3), and multiple isolated nodular lesions of the left cheek (Fig. 4). An area of alopecia was present in the scalp (Fig. 5). Ocular examination showed two colobomatous defects of the left upper eyelid (Fig. 4). The upper portions of the bulbar and palpebral conjunctiva were thickened with pannus formation on both superior corneas. Both corneas were small; these findings were more prominent on the left than on LINEAR NEVUS SEBACEOUS SYNDROME 171 the right eye (Fig. 6). Lipodermoids were present in the left eye (Fig. 7). The anterior chamber, iris, and pupil were unremarkable. There was limitation of upgaze in the left eye. Ophthalmoscopy revealed a clear vitreous and deep cups of the optic nerves in both eyes. A lesion was seen in each eye consisting of a striking, well-demarcated yellowish flat area with no evidence of intrinsic blood vessels or spider vessels on the surface. The major retinal vessels appeared normal overlying the lesions, and no evidence of choroid was seen. The lesions occupied both posterior poles, involving the peripapillary areas, the macula in the right, and extending upward, nasally, and temporally to just posterior to the equator in both eyes (Fig. 8). The central macular area in the left eye was spared. The inferior quadrants appeared normal. Outside the lesion, the retina, choroid, and underlying pigment pattern appeared normal. Computed tomography (CT) of the brain and orbit showed left hemispheric atrophy and a thickening of the posterior aspect of both eyes with calcified density ~2.5 to 3.5 mm thick (Figs. 9 and 10). FIG. 1. Cutaneous and ocular involvement of the left side of the face. FIG. 2. Linear distribution of organoid nevus. Ultrasonography documented that the lesions were of calcific density and occupied the full thickness of the globe. No overlying choroidal spike was demonstrated on the A scans (Fig. 11). At the age of 4 months surgical repair of the coloboma of the upper left lid was done to protect the cornea. Histological examination of this material showed hyperplasia of the sebaceous glands involving both the skin and the conjunctival surface. At 2 years of age she has not shown signs of developmental delay. No seizures have been reported. Her neurological examination continues normal. FIG. 3. Midline involvement of the chin by organoid nevus. JClilI Neuro-ophthalmol, Vol. 7. No.3, 1987 172 I. ALFONSO ET AL. FIG. 4. Colobomatous defects of the left eyelid and multiple nodules of the left cheek. DISCUSSION Linear nevus sebaceous syndrome is a systemic hamartomatosis that involves many structures of ectodermal and mesodermal origin particularly in the craniofacial region and in the skeletal, cardiovascular, renal, and hepatic systems. In its complete form craniofacial involvement produces a typical picture that consists of organoid nevus of the face, dysplastic eye changes, and signs of central nervous system involvement. Incomplete forms of this syndrome have been reported. Nevertheless, the differentiation between them is not clear-cut (Table 1). A form fruste, consisting of organoid nevus of the face without involvement of any other structures, is frequent (59). Although linear nevus sebaceous syndrome is the name most often used, similar associations of clinical findings have been described under the names of atypical tuberous sclerosis (1); epidermal nevus syndrome (6); neuro-oculo-cutaneous syndrome (26); Feuerstein and Mims syndrome (16); Schimmelpenning, Feuerstein, and Mims syn- FIG 5. Scalp alopecia. JClilI Neuro-ophthalmol. Vol. 7. No.3. 1987 FIG. 6. Pannus formation involves superior cornea of the left eye. drome (13); Jadassohn syndrome (60); skin, eye, brain, and heart syndrome (10); and organoid nevus phakomatosis (14). The etiology of linear nevus sebaceous syndrome is not known. No genetic or chromosomal abnormalities have been found; neither sex predilection, familial occurrence, or external factors such as viral infection, radiation, or drug ingestion during pregnancy have been linked to this syndrome. Hence, since the etiology is unknown, linear nevus sebaceous syndrome remains a syndrome by definition. The historical origin of this syndrome is difficult to trace. Jadasshon in 1885 was probably the first to associate organoid nevus with neurological deficit. His patient, however, did not have cutaneous facial involvement (61). Bogel in 1886 described the association of organoid nevus of the face and ocular dysplasia (46). The association of organoid nevus of the face and dysplastic ocular and cerebral changes was described by Berg and Crome in 1910 (1). The association of organoid nevus of the face and neurological deficit without associated eye findings was described by Tobias in 1927 (34). The cutaneous lesion is the hallmark of this syn- FIG. 7. Lipodermoids of the left eye. LINEAR NEVUS SEBACEOUS SYNDROME 173 FIG. 8. Large deep cups of the nerves with a well-demarcated area of choroidal discoloration. Top: left eye; bottom: right eye. drome. The lesion is characterized by a large linear organoid nevus of the facial region with either a yellow to tan velvety appearance or a darker verrucous appearance. Midline finger-like involvement of the facial region is often found. The histological appearance of this lesion varies in respect to the number of sebaceous glands, the involvement of the dermis and epidermis (40), and the patient's age (59,62). The lesion is caused by failure of separation of the skin appendages from the adjacent epithelium at approximately the third month of embryogenic life (31). The exclusion from this review of patients with systemic cutaneous involvement but sparing the face was based on clinical grounds; cerebral and ocular involvement is significantly less frequent in this group. This difference is probably more related to the location of the insult than to the time of occurrence or its nature. The term nevus sebaceous of Jadasshon has been used to refer to this lesion, yet neither the lesion as described by Jadasshon, large and wellformed sebaceous gland lobules (61), nor Robinson's use of this term for a well-circumscribed lesion of the face and scalp formed by large sebaceous glands and papilloepidermal hyperplasia (63) encompasses all the cutaneous lesion described in these patients. Hence, we prefer the term organoid nevus. The life history of organoid nevus was described by Mehregan and Pinkus (59). During infancy and childhood, the histology of this lesion showed underdeveloped or abortive sebaceous gland and hair follicles that possess no hair. At puberty they are characterized by papillomatous epidermal hyperplasia and massive mature apocrine gland deep in the dermis. After puberty, benign or malignant tumors may develop within the nevus, the most common being basal cell epithelioma. Other cutaneous lesions in patients with linear nevus sebaceous syndrome are crops of slightly yellowish isolated plaques involving the face, patches of alopecia, cafe-au-Iait spots, pigmented nevi, and subcutaneous lipomas (21,27). A significant number of patients also have a linear epidermal nevi of other parts of the body. Evidence of neurological involvement was reported in 57 of the 70 individual cases reviewed. Mental retardation or developmental delay was reported in 30 of these cases. In a separate series reported by Levin et al., mental retardation was found in nine of 11 patient (64). The degree of retardation and developmental delay ranged from mild to severe. Normal mental development was reported in eight of 37 cases in Zaremba's reviews (60) and in two of 11 patients reported by Levin et al. (64). Both patients of Levin et al. had normal CT of the brain. The latter authors make the statement that normal mentation is only found in patients with normal CT. We do not agree with this statement since abnormal CT and pneumoencephalography have been reported previously in patients with normal mentation (30,31,33) and was also present in our case. I Clill NClIro-ophthalmol, Vol. 7. No.3. 1987 174 1. ALFONSO ET AL. FIG. 9. Computed tomographic scans demonstrate left hemisphere atrophy, dysplasia of the right occipital lobe, and bilateral posterior calcification of the globes. Seizures occurred in 31 of 70 patients we reviewed and in 10 of 11 patients reported by Levin et al. Most seizures occurred during the first year of life. The types of seizures reported were grand mal (21,36,37,41), apneic spells (35,40), Jacksonian seizures (6), and infantile spasms (24,38). Different epileptiform electroencephalographic patterns reported were focal spikes (6,21), multifocal spikes (24,37,41), and hypsarrhythmia (30,40). Diffuse and asymmetrical slowing have also been reported. Hemiparesis was found in 12 patients. Central nervous system neoplasms were present in six cases. Papillomas of the choroid plexus were reported in two cases (6,64), a lipoma of the corpus callosum was described in one patient (64), and an enhancing lesion in the region of the pineal gland in another (64). A lipoma of the right middle fossa was reported (22) as well as a patient with cerebral gliomatosis (23). Other common abnormalities found in the brain are porencephalic cyst (28), arachnoid cyst (12), intracavernous carotid aneu- JClilI Ncuro-ophthalmol. Vol. 7. No.3. 1987 FIG. 10. Computed tomographic scan shows bilateral posterior calcification of the globes. LINEAR NEVUS SEBACEOUS SYNDROME 175 FIG. 1i. Contact 8-scan ana standardized A-scan echograms of right eye show large plaque of bone or calcium in posterior ocular wall. Echograms indicate involvement of the retinochoroid layer and sclera. Echograms on top are at high sensitivity (standardized A-scan is at tissue sensitivity) and echograms on bottom are at low sensitivity. Arrows, bone/calcium plaque; S, shadow of orbital tissues produced by marked sound attenuation. rysm (28), leptomeningeal cyst (23), abnormal vasculature (17,19,28), hydrocephalus (10,23), and errors of neuronal migration and organization. The value of CT to diagnose these abnormalities cannot be overemphasized (64). Ocular findings were reported in 49 of 70 cases we reviewed. The most frequent findings were choristoma of the conjunctiva, coloboma of the eyeball and/or eyelids, and retinal changes. Less frequent changes were microphthalmos or enophthalmos, ectopic displacement of the pupil, and ocular hemangioma. The degree of visual acuity was not reported in most cases, but it certainly can be profoundly affected. Calcification of the posterior aspect of the eye has been reported in the past (24,29,31,49). Our patient had bilateral calcification of the posterior aspect of the globe that occupied the full thickness of the globe by ultrasonographic studies. The time of error in embryogenesis that produces the ocular malformation in a patient with linear nevus sebaceous syndrome has not been established. Wilkes et al. suggest that, at least in their patients with bilateral plaques of cartilage TABLE 1. Classification of linear nevus sebaceous syndrome according to most frequent craniofacial abnormalities Findings in 70 cases Forms Neurological Ocular Cutaneous Number of cases References Complete + + + 36 1-33 and ours Incomplete A + + 21 34-45" Incomplete B + + 13 46-58b " No clinical signs of neurological deficit but radiographic abnormalities present (30,31,33, and present authors' findings). b Neurological examination not stated (46,47,49,54,56). JClilI Neuro-ophthalmol, Vol. 7. No.3, 1987 176 I. ALFONSO ET AL. and bone on the nasal aspect, displaced mesenchymal cells at the time of closure the facial fissure were responsible for differentiation of cartilage and bone (31). Pathological studies in a patient described by Shochot et aI. showed absence of normal ganglion cells in the internal layer of the retina. They pointed out that patients with anencephaly also have this finding in association with other findings common to linear nevus sebaceous syndrome such as microphthalmia. Hence, they suggested that anencephaly and linear nevus sebaceous syndrome share a common embryogenic defect, occurring early during pregnancy at 3 to 4 weeks of gestation (25). Another finding that further suggests the early occurrence of an error in embryogenesis is the association of skull and brain defects. Abnormalities of the brain and the skull must result from a developmental deficit occurring before the 4th week of gestation (31). The presence in our patient of involvement of the full thickness of the ocular layer is also in favor of an early error in embryogenesis. Skeletal malformations are frequently described in patients with linear nevus sebaceous syndrome. The skull is most often affected (60). Cranial asymmetry or hemimacrocephaly, with or without asymmetry of the facial bones, is often present. Premature closure of the sphenoid frontal sutures, sphenoid bone malformation, and abnormalities of the sella turcica are seen (3,22). Changes of the axial and appendicular skeleton are less common but can include deformities of the spine, scoliosis, kyphosis, and long bone malformation of the ulna and humerus and fragmentation sclerosis of the head of the radius (2,6,15,36,41). Cases characteristic of vitamin D-resistant rickets have also been reported (16,36). Dental malformation was found in four of 37 cases reviewed by Zaremba (60). The cardiovascular system is also frequently involved. Coarctation of the aorta, patent ductus arteriosus, cardiac arrhythmias, and hypoplasia of the renal artery have been reported (5,10,39). Involvement of the urogenital system includes double urinary collecting system, renal hamartomas, horseshoe kidneys, and enlarged clitoris and undescended testicles (6,8,12,15). Cystic biliary adenoma of the liver has also been reported (15). A patient with hypoplastic pulmonary artery has also been reported (19). Linear nevus sebaceous syndrome is a rather infrequent and poorly recognized entity of unknown etiology. It is characterized by hamartomatous and dysplastic changes in tissue of ectodermal and rn'··",i"·rm.J1 origin, most often the skin, brain, .'ll~!·.. t;t1. ,'ardiovascular, renal, JClilI Ncuro-ophthalmol, Vol. 7. No.3, 1987 and digestive system. The typical skin lesion is a large organoid nevus of the cephalocranial region with linear configuration. The most frequent neurological findings are mental retardation and seizures. 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Am I Dis Child 1967;114:626. 63. Robinson 55. Nevus sebaceous (Jadassohn). Arch Derm Syph 1932;26:663-70. 64. Levin 5, Robinson RO, Aicardia Jr, et aJ. Computed tomography appearances in the linear sebaceous naevus syndrome. Neuroradiology 1984;26:469-72. Jcrill Neuro-ophthallllol. Vol. 7. No.3, 1987 |
