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Case 131: Proteus Syndrome¹

¹ From the Department of Radiology, Haydarpasa Numune Education and Research Hospital, Istanbul, Turkey. Received December 22, 2004; revision requested February 16, 2005; revision received February 22; accepted March 15; final version accepted June 20.

Address correspondence to the author, 11 kisim, Yasemin Apt, D blok, Daire 35 Ataköy, Istanbul, Turkey 34158 (e-mail: demirkemal{at}superonline.com).

	HISTORY

TOP HISTORY IMAGING FINDINGS DISCUSSION References

 
A 21-year-old woman was referred for cerebral and craniofacial magnetic resonance (MR) imaging and computed tomographic (CT) examination because of the asymmetric appearance of the right side of her face and the consideration of facial paralysis. Neurologic examination revealed that the patient did not have facial nerve palsy and that her appearance was caused by facial asymmetry. Laboratory studies revealed no abnormality. There was no family history of congenital anomaly. Physical examination revealed an asymmetric soft-tissue prominence on the posterior part of her chest and abdomen. There was a history of a progressive course of asymmetry of the hands and feet and a hyperpigmented epidermal nevus on the left dorsal aspect of the trunk. (Asymmetric overgrowth of the patient's hands and feet was stabilized after puberty.) Radiographs of the pelvis, vertebrae, and extremities (not shown) were normal except for mild scoliosis. Unenhanced CT of the chest, abdomen, and pelvis was performed.

	IMAGING FINDINGS

TOP HISTORY IMAGING FINDINGS DISCUSSION References

 
MR imaging of the brain revealed enlargement of the right cerebral hemisphere, mainly in the frontal lobe, that was caused by hypertrophied white matter. The cortex of the right cerebral hemisphere was dysplastic, with broad and shallow gyri and diminished sulci. The deep and subcortical areas of the underlying white matter had multiple scattered lesions that appeared as low-signal-intensity areas on T1-weighted MR images and as high-signal-intensity areas on T2-weighted and fluid-attenuated inversion recovery (FLAIR) MR images. The ipsilateral ventricle was also enlarged and distorted (Fig 1).

View larger version (159K): [in this window] [in a new window] [Download PPT slide]   Figure 1a: (a) Transverse fast spin-echo T2-weighted MR image through the level of the lateral ventricles (repetition time msec/echo time msec, 4461/100) shows enlargement of the right cerebral hemisphere and multifocal areas of high signal intensity (straight arrows) within the hypertrophied subcortical and deep white matter, with diminished sulcation (arrowheads) and asymmetric dilatation of the ipsilateral ventricle (curved arrow). (b) Transverse FLAIR MR image through the supraventricular level (repetition time msec/echo time msec/inversion time msec, 6000/100/2000) shows enlargement of the right cerebral hemisphere, mainly in the frontal lobe, and multifocal areas of high signal intensity (arrowheads) within the hypertrophied subcortical and deep white matter, with diminished sulcation (arrows). (c) Coronal inversion-recovery T1-weighted MR image through the level of the lateral ventricles (3105/15/400) shows the dystrophic cortex of the enlarged right cerebral hemisphere with broadened and shallow gyri (black arrowhead), diminished sulcation (black arrow), and multifocal areas of low signal intensity (white arrowheads) within the hypertrophied subcortical and deep white matter. The ipsilateral ventricle (white arrow) is enlarged and distorted.

View larger version (147K): [in this window] [in a new window] [Download PPT slide]   Figure 1b: (a) Transverse fast spin-echo T2-weighted MR image through the level of the lateral ventricles (repetition time msec/echo time msec, 4461/100) shows enlargement of the right cerebral hemisphere and multifocal areas of high signal intensity (straight arrows) within the hypertrophied subcortical and deep white matter, with diminished sulcation (arrowheads) and asymmetric dilatation of the ipsilateral ventricle (curved arrow). (b) Transverse FLAIR MR image through the supraventricular level (repetition time msec/echo time msec/inversion time msec, 6000/100/2000) shows enlargement of the right cerebral hemisphere, mainly in the frontal lobe, and multifocal areas of high signal intensity (arrowheads) within the hypertrophied subcortical and deep white matter, with diminished sulcation (arrows). (c) Coronal inversion-recovery T1-weighted MR image through the level of the lateral ventricles (3105/15/400) shows the dystrophic cortex of the enlarged right cerebral hemisphere with broadened and shallow gyri (black arrowhead), diminished sulcation (black arrow), and multifocal areas of low signal intensity (white arrowheads) within the hypertrophied subcortical and deep white matter. The ipsilateral ventricle (white arrow) is enlarged and distorted.

View larger version (188K): [in this window] [in a new window] [Download PPT slide]   Figure 1c: (a) Transverse fast spin-echo T2-weighted MR image through the level of the lateral ventricles (repetition time msec/echo time msec, 4461/100) shows enlargement of the right cerebral hemisphere and multifocal areas of high signal intensity (straight arrows) within the hypertrophied subcortical and deep white matter, with diminished sulcation (arrowheads) and asymmetric dilatation of the ipsilateral ventricle (curved arrow). (b) Transverse FLAIR MR image through the supraventricular level (repetition time msec/echo time msec/inversion time msec, 6000/100/2000) shows enlargement of the right cerebral hemisphere, mainly in the frontal lobe, and multifocal areas of high signal intensity (arrowheads) within the hypertrophied subcortical and deep white matter, with diminished sulcation (arrows). (c) Coronal inversion-recovery T1-weighted MR image through the level of the lateral ventricles (3105/15/400) shows the dystrophic cortex of the enlarged right cerebral hemisphere with broadened and shallow gyri (black arrowhead), diminished sulcation (black arrow), and multifocal areas of low signal intensity (white arrowheads) within the hypertrophied subcortical and deep white matter. The ipsilateral ventricle (white arrow) is enlarged and distorted.

View larger version (134K): [in this window] [in a new window] [Download PPT slide]   Figure 2: Transverse unenhanced CT image through the level of the parotid glands shows diffuse right-sided subcutaneous asymmetric adipose tissue enlargement (*), fatty infiltration of right parotid gland (white arrowhead) and soft palate (black arrowhead), and pseudohypertrophy of masseter and pterygoid muscles, with focal perimuscular increase of fatty tissue (arrow) causing disproportionate right-sided hemifacial overgrowth.

View larger version (157K): [in this window] [in a new window] [Download PPT slide]   Figure 3: Transverse FLAIR MR image through the level of the parotid glands (6000/100/2000) shows right-sided subcutaneous and intermuscular adipose tissue enlargement (*), fatty infiltration of right parotid gland (black arrowhead) and soft palate (white arrowhead), and pseudohypertrophy of masseter and pterygoid muscles (black arrows), with elongation and distortion of right ramus mandibula (white arrow) causing disproportionate right-sided hemifacial overgrowth.

View larger version (155K): [in this window] [in a new window] [Download PPT slide]   Figure 4: Transverse fat-saturated T1-weighted spin-echo MR image through the level of the mandible (550/13) shows right-sided hemifacial overgrowth due to diffuse asymmetric subcutaneous adipose tissue enlargement (*) and asymmetric mandibular dysmorphism, including elongation, distortion, thinning, and expansion of bone (arrows).

View larger version (91K): [in this window] [in a new window] [Download PPT slide]   Figure 5: Transverse unenhanced CT image of the chest shows a right subcutaneous fatty mass (arrowhead) compressing the adjacent paraspinal muscles, with asymmetric subcutaneous fatty infiltration along the left posterior chest wall (arrows).

View larger version (106K): [in this window] [in a new window] [Download PPT slide]   Figure 6: Transverse unenhanced CT image of the upper abdomen shows asymmetric subcutaneous fatty infiltration along the left posterior upper abdominal wall (arrows and arrowheads). Mild splenomegaly (*) is present.

	DISCUSSION

TOP HISTORY IMAGING FINDINGS DISCUSSION References

Epidermal nevus syndrome is a rare sporadic neurocutaneous disorder. The characteristic skin lesions include nevus sebaceous of Jadassohn, nevus unius lateris, linear epidermal nevus, and inflammatory linear verrucous epidermal nevus (5,6). The presence of these nevi initially suggested this diagnosis. Ocular abnormalities, such as colobomas, optic nerve hypoplasia, microphthalmia, and cataracts, are common. Systemic involvement with skeletal, cardiac, and renal abnormalities may also be seen. Central nervous system anomalies are severe, and some are thought to be the sequelae of vascular dysplasia, including infarcts, atrophy, porencephaly, and calcifications. Central nervous system involvement is typically ipsilateral to the nevus (7). This conflicted with findings in the current case. These findings made epidermal nevus syndrome an unlikely diagnosis.

The typical clinical picture of neurofibromatosis type 1 consists of café-au-lait spots, cutaneous and subcutaneous tumors, axillary freckling, Lisch nodules, bone dysplasias, multiple central nervous system tumors—such as optic nerve gliomas—and affected first-degree relatives because of autosomal dominant inheritance (8). These findings allow this diagnosis to be made; however, these abnormalities were not present in this patient.

Hypomelanosis of Ito, or incontinentia pigmenti achromians, is a multisystem neurocutaneous syndrome characterized by swirled hypo- or depigmentation of the skin. Associated extracutaneous abnormalities associated with hypomelanosis of Ito occur mainly in the nervous and musculoskeletal systems. The criteria for the definitive diagnosis of this condition proposed by Ruiz-Maldonado and associates in 1992 (9) show hypomelanosis of Ito is not the correct diagnosis.

Symptoms of Klippel-Trenaunay-Weber syndrome include port-wine stain, vascular malformations, and secondary limb hypertrophy. The absence of a capillary, venous, or lymphatic malformation in this patient made Klippel-Weber-Trenaunay syndrome an unlikely diagnosis.

Tuberous sclerosis is a neurocutaneous disease characterized by hamartomatous changes in the lungs, brain, kidneys, skin, heart, and other organs. The diagnostic criteria of tuberous sclerosis consist of major features—such as cortical tubers, cardiac rhabdomyoma, facial angiofibroma, retinal hamartoma, and renal angiomyolipoma—as well as minor features—such as gingival fibroma, hamartomatous rectal polyp, and renal or bone cysts (10). These features did not fit with the clinical or imaging findings of this patient.

Hemihyperplasia/lipomatosis syndrome (HHLS) and encephalocraniocutaneous lipomatosis (ECCL) were also considered in the differential diagnosis. Patients with HHLS lack the progressive overgrowth of the limbs and skull. ECCL is a neurocutaneous syndrome characterized by ipsilateral cranial, facial, ocular, and central nervous system anomalies. The best diagnostic indicator of this disease is unilateral hemispheric cerebral atrophy and ventriculomegaly with ipsilateral alopecia overlying a scalp lipoma (13). Neither finding was present in this patient.

PS is a rare congenital hamartomatous condition that is characterized by a wide range of malformations. It produces multifocal overgrowth of tissue derived from any of the three germinal layers. This causes a complex disorder with multisystem involvement and great clinical variability. Cohen and Hayden described this disease in 1979 (11). The name Proteus comes from the Greek god who had the ability to change his shape and was proposed by Wiedemann et al in 1983 (12). Although PS is thought to arise from a postzygotic mutation, the cause remains unclear. To my knowledge, there is no specific genetic test for PS; therefore, knowledge of the multiple highly specific manifestations of PS is necessary for clinical and imaging diagnosis.

The random or varied distribution of PS manifestations throughout the body is the hallmark of this disease. The progressive course of the lesions and the sporadic occurrence of the disorder are the other general criteria for the clinical diagnosis. Although tissue overgrowth is progressive in nature, it appears to plateau after adolescence, as in this case.

The specific criteria that also must be met are based on category A, B, or C signs. The single sign in category A, cerebriform connective tissue nevus, appears to be pathognomonic for the diagnosis; however, it is not a common finding in patients with PS. It is most frequently found as gyriform gross thickening of the soles, but it can also be found on the abdomen, hands, and nose. The category B signs are linear epidermal nevus, disproportionate overgrowth, and specific tumors, such as bilateral ovarian cystadenoma and monomorphic adenoma before or during the 2nd decade of life. Disproportionate asymmetric overgrowth commonly involves one or more limbs, the skull, and vertebrae. One of the most characteristic findings in patients with PS is the disorganization and distortion of skeletal features, such as the mandibular involvement seen in this patient. This finding is a possible diagnostic criterion, and it contrasts with more common forms of osseous overgrowth, in which the enlarged bones retain their normal proportional relationships. Hemimegalencephaly and splenomegaly with unilateral fatty infiltration of the parotid gland are rare visceral involvements that were seen in this patient. The increased amount of overlying subcutaneous fat and the pseudohypertrophy of the muscles on the right side of the face suggest that in general, it is the right side that is abnormal; therefore, it is likely that the right parotid gland rather than the left parotid gland is abnormal. The category C signs include dysregulated adipose tissue, such as lipomas or a regional absence of fat; vascular malformations; lung cysts; and facial phenotype. The manifestations of a facial phenotype that may be seen in patients with PS but were not present in this case are dolichocephaly; long face; minor downslanting of palpebral fissures, mild ptosis, or both; low nasal bridge; wide or anteverted nares; and open mouth at rest. Dysregulated adipose tissue and vascular malformations are the most common features of PS that overlap with other overgrowth conditions. The single category A sign, two signs from category B, or three signs from category C are sufficient for diagnosis (14–16).

In this patient, the brown hyperpigmented epidermal nevus, disproportionate hemifacial overgrowth and hemimegalencephaly, mild splenomegaly, and scoliosis without a family history of congenital anomaly were in accordance with the diagnostic criteria of PS, which was the most likely diagnosis. Associated asymmetric fatty lesions in various tissues are another criterion of PS; however, this finding is not diagnostic by itself.

	FOOTNOTES

 
Author stated no financial relationship to disclose.

Part one of this case appeared 4 months previously and may contain larger images.

 

	References

TOP HISTORY IMAGING FINDINGS DISCUSSION References

 

1. Barkovich AJ, Chuang SH. Unilateral megalencephaly: correlation of MR imaging and pathologic characteristics. AJNR Am J Neuroradiol 1990;11:523–531. [Abstract]
2. Kalifa GL, Chiron C, Sellier N, et al. Hemimegalencephaly: MR imaging in five children. Radiology 1987;165:29–33. [Abstract/Free Full Text]
3. Flores-Sarnat L. Hemimegalencephaly. I. Genetic, clinical, and imaging aspects. J Child Neurol 2002;17:373–384.
4. Broumandi DD, Hayward UM, Benzian JM, Gonzalez I, Nelson MD. Best cases from the AFIP: hemimegalencephaly. RadioGraphics 2004;24:843–848. [Free Full Text]
5. Happle R. How many epidermal nevus syndromes exist? a clinicogenetic classification. J Am Acad Dermatol 1991;25:550–556. [Medline]
6. Pavone L, Curatolo P, Rizzo R, et al. Epidermal nevus syndrome: a neurologic variant with hemimegalencephaly, gyral malformation, mental retardation, seizures, and facial hemihypertrophy. Neurology 1991;41:266–271. [Abstract/Free Full Text]
7. Booth TN, Rollins NK. MR imaging of the spine in epidermal nevus syndrome. AJNR Am J Neuroradiol 2002;23:1607–1610. [Abstract/Free Full Text]
8. Neurofibromatosis: conference statement—National Institutes of Health Consensus Development Conference. Arch Neurol 1988;45:575–578. [Abstract/Free Full Text]
9. Ruiz-Maldonado R, Toussaint S, Tamayo L, Laterza A, del Castillo V. Hypomelanosis of Ito: diagnostic criteria and report of 41 cases. Pediatr Dermatol 1992;9(1):1–10. [Medline]
10. Gomez MR. Diagnostic criteria. In: Gomez MR, ed. Tuberous sclerosis. 2nd ed. New York, NY: Raven, 1985; 9–20.
11. Cohen MM Jr, Hayden PW. A newly recognized hamartomatous syndrome. Birth Defects Orig Artic Ser 1979;15:291–296. [Medline]
12. Wiedemann HR, Burgio GR, Aldenhoff P, Kunze J, Kaufmann HJ, Schirg E. The Proteus syndrome: partial gigantism of the hands and/or feet, nevi, hemihypertrophy, subcutaneous tumors, macrocephaly, or other skull anomalies and possible accelerated growth and visceral affections. Eur J Pediatr 1983;140:5–12. [CrossRef][Medline]
13. Gawel J, Schwartz RA, Jozwiak S. Encephalocraniocutaneous lipomatosis. J Cutan Med Surg 2003;7:61–65. [Medline]
14. Biesecker LG, Happle R, Mulliken JB, et al. Proteus syndrome: diagnostic criteria, differential diagnosis, and patient evaluation. Am J Med Genet 1999;84:389–395. [CrossRef][Medline]
15. Jamis-Dow CA, Turner J, Biesecker LG, Choyke PL. Radiologic manifestations of Proteus syndrome. RadioGraphics 2004;24:1051–1068. [Abstract/Free Full Text]
16. Turner JT, Cohen MM Jr, Biesecker LG. Reassessment of the Proteus syndrome literature: application of diagnostic criteria to published cases. Am J Med Genet A 2004;130:111–122. [Medline]

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