Intracranial Lipoma

About: Intracranial Lipoma is a research topic. Over the lifetime, 147 publications have been published within this topic receiving 2394 citations.

Intracranial and subcutaneous lipoma associated with sagittal sinus fenestration and falcine sinus.

Abstract: Intracranial lipomas are rare lesions. Intracranial lipoma associated with a subcutaneous lipoma is extremely rare. Various vascular abnormalities have been described in association with intracranial lipoma, including distension, kinking, or narrowing of arteries and veins; arteriovenous malformation; and aneurysm. To our knowledge, association of sagittal sinus fenestration, falcine sinus, and absent straight sinus with intraextracranial lipoma has not been reported before. We report the imaging findings of an infant with interhemispheric and subcutaneous lipoma associated with falcine sinus and sagittal sinus fenestration.

Lipoma of the Superior Medullary Velum with Schwann Cells--Report of a Case and Review of the Literature

Abstract: A large intracranial lipoma, located on the superior medullary velum is reported Histologically, the tumor consisted of adult adipose tissue The right trochlear nerve was involved within the tumor, and the scattered nests of Schwann cells and some larger vessels were also present Lipoma of the dorsal region of the mid-brain is rare and has not been reported from Japan Schwann cell proliferation in the lipoma is another unusual feature in this case The histogenesis of this tumor is discussed, and the literature on lipomas of the dorsal region of the mid-brain is reviewed

Prenatal detection of Pai syndrome without cleft lip and palate: a case report.

Abstract: Summary: Prenatal detection of Pai syndrome without cleft lip and palate: a case report: Pai syndrome is a rarely encountered disease characterized by findings of median cleft lip, facial skin polyps, nasal mucosal polyps and midline central nervous system lipoma. We report a case with prenatal detection of a pericallosal lipoma and a skin tag on the forehead. After delivery, the diagnosis was confirmed as a case of Pai syndrome.Key-words: Pericallosal lipoma - Pai syndrome - Prenatal ultrasoundINTRODUCTIONIntracranial lipomas are rarely observed congenital malformations. They usually occur secondary to the abnormal differentiation of meninx primitiva layer, arachnoid and the inner layer of dura mater (5). They make up less than 0. 1% of all intracranial tumors in the literature. Twenty five-fifty percent of all intracranial lipomas are pericallosal lipomas with partial or complete agenesis of the corpus callosum in some of the patients (5). They can be observed in nodular or curvylinear forms and are usually asymptomatic (5).When an intracranial lipoma is coupled with a facial polyp, it may be suspicious for Pai syndrome. Pai syndrome is a rare disorder in which there are some other associated findings such as median cleft lip, facial skin and nasal mucosal polyps in addition to a midline intracranial lipoma (1,2, 6).CASE REPORTA 40 years old woman (gravida 13, para 12) at 28th week of pregnancy was referred to our perinatology unit because of a hyperechogenic structure in the brain of the fetus. Fetal biometrie measurements were appropriate for gestational age. Cranial ultrasonography revealed a hyperechogenic structure right above the septum pellucidum, neighboring the corpus callosum. Pericallosal artery was intact (Fig. 1). Further, an abnormally shaped nose and a polyp like structure were detected on the forehead (Fig. 2). There was no sign of cleft lip and palate. The rest of the neurosonographical examination was within normal limits. A preliminary diagnosis of pericallosal lipoma was made. The family history did not reveal any findings regarding mental retardation or congenital malformations and an offer of fetal karyotyping was declined by the parents.A male fetus (2740 g / 49 cm) was delivered by cesarean section on the 40th week of pregnancy. The Apgar scores at 1st and 5th minutes were 6 and 8 respectively. The baby did well without the need for neonatal intensive care unit. On physical examination there were dysmorphic features (Fig. 3) such as bifid nose, bilateral nostril polyps, skin tags at the midline of the forehead and on the preauricular area, wide nasal bridge, absence of right eyelid, lipoma on the conjunctiva and big and wide earlobes.Abdominal ultrasonography and otoaccustic emission tests revealed no pathology. On cranial MRI, a 30 mm wide lesion was observed in the pericallosal area, concordant with pericallosal lipoma and characterized with hyperintensity in all sequences. Chromosomal analysis of the peripheral blood cultures revealed a 46,XY normal karyotype.DISCUSSIONPai syndrome was first defined by Pai et al. in 1987 (10). Central nervous system lipomas, median cleft of the upper lip and facial skin polyps form the classic triad to define the syndrome, but the phenotype may be variable (13). A median cleft lip is a frequent finding in the previously reported Pai syndrome cases in the literature (3, 6, 13), however, it was not present in our case. Although the only cranial MRI finding in our patient was a pericallosal lipoma, computerized tomography and/or MRI show additional cranial structural anomalies in 85% of the cases with Pai syndrome (5, 9). For example, Guion et al. reported a Pai syndrome with a huge encephalocele, and the computerized tomography scan demonstrated a general disorganization of the cerebral parenchyma in addition to hydrocephaly in this patient (4). Despite this high rate of central nervous system pathologies, thus far serious neurological disorders such as mental retardation have been reported in only a few cases (8, 3). …

Intracranial lipoma in a laboratory rat.

Abstract: reported in a wide variety of laboratory, domestic, and wild anima1s.I Stress as a result of weaning, overcrowding, poor sanitation, shipping, and corticosteroid administration often precedes outbreaks of Tyzzer’s d i~ease .~ Asymptomatic carriers are suspected oftransmitting the organism to susceptible individuals.’ Although natural interspecies transmission has not been demonstrated, environmental contamination with B. piliformis spores from rodent and rabbit feces has been suggested as a source of infection.* The proposed pathogenesis of Tyzzer’s disease involves an oral route of infection resulting in a primary enteric infection with local proliferation of the organism, especially within the jejunum, ileum, and cecum. Dissemination via the portal circulation results in infection of other tissues, especially the liver. Lymphatic invasion has been proposed as the source of intestinal smooth muscle infe~t ion.~ There is a distinct tropism for certain cell types, such as intestinal epithelium, hepatocytes, myocardium, and intestinal smooth muscle, although the mechanism of this cellular tropism is unknown. In vitro production of cytotoxins by B. piliformis has been demonstrated and is the likely cause of the necrotizing lesions.8 The marked lymphoid depletion observed in this puppy is compatible with lymphoid destruction resulting from a previous viral infection or improper development of the immune system. Similar lesions occur following infection with canine distemper virus or canine parvovirus-2 in dogs and combined immunodeficiency syndromes as seen in Arabian foals and severe combined immunodeficient mice. lo In this puppy, severe immunosuppression may have resulted in a more widely disseminated infection than is typically seen in canine Tyzzer’s disease, or the infection may have been due to a particularly virulent biovar. Lesions compatible with active canine distemper virus or canine parvovirus-2 infections were not evident. An antemortern fecal enzyme-linked immunosorbent assay for canine parvovirus-2 antigen was negative. Canine Tyzzer’s disease typically occurs in 5-7canine distemper virus infection; immunosuppression has been suspected in other