Epithelioid Sarcoma of Lumbar Spine: A Rare Mesenchymal Tumor Masquerading as Infection.

Epithelioid sarcoma of the spine has been rarely reported in the literature. Its diagnosis is challenging due to nonspecific findings. We report a case of 42-year-old gentleman with back pain. Magnetic resonance imaging (MRI) revealed lesion in the L4 vertebral body extending into the spinal canal with pre and paravertebral involvement. He underwent posterior spinal decompression and instrumentation with biopsy. Histopathological examination was nonspecific. Considering clinical and radiological features, antitubercular treatment was initiated. The patient developed acute onset weakness of both lower extremities 1 month post-surgery. Repeat MRI and positron emission tomography (PET) computed tomography revealed an increase in the extent of lesion which required revision decompression. Histopathological examination showed cells with epithelioid appearance, positive for Vimentin, and epitheloid membrane antigen in immunohistochemistry. Radiotherapy was planned but the patient expired due to multiorgan dysfunction. Epithelioid sarcomas are rare soft-tissue neoplasms with poor prognosis. They can mimic infection and a high degree of suspicion is required in these cases to diagnose and treat them early.

Analysis of factors influencing ligamentum flavum thickness in lumbar spine - A radiological study of 1070 disc levels in 214 patients.

OBJECTIVE: The pathomechanism and factors influencing hypertrophy of the Ligamentum flavum in the lumbar spine still requires a confident specificity. We aimed to analyse the association between various factors and Ligamentum Flavum Thickness (LFT) and also to investigate the major contributor for Ligamentum Flavum Hypertrophy (LFH) at various levels in the lumbar spine. PATIENTS AND METHODS: The following were evaluated at L1-L2,L2-L3,L3-L4,L4-L5 and L5-S1 levels in MRI of 1070 lumbar disc levels of 214 subjects: Pfirrmann's grade of the disc, anterior and posterior disc height, disc volume, facet tropism and LFT. LFT > 0.4 cm was considered as hypertrophy.Correlation between LFT and other parameters was done and values with p < 0.05 was considered statistically significant. RESULTS: 112 male and 102 female were included. There was an increase in the anterior disc height (0.98 cm to 1.50 cm), posterior disc height (0.84 cm to 0.96 cm), disc volume (7.17cm3 to 14.6cm3), facetal angle and LFT on both sides from L1-2 to L5-S1 levels. Highest frequency of LFT was seen at L4-5.Pfirrmann's grade of the disc and anterior disc height had a statistically significant positive correlation with LFT at L1-L2,L2-L3,L3-L4,L4-L5 levels whereas facet tropism was strongly associated with LFT at L5-S1 level. CONCLUSION: Higher Pfirrmann's grade and decreased anterior disc height can lead to ligamentum flavum hypertrophy at L1-L2, L2-L3,L3-L4,L4-L5 levels.Whereas at L5-S1 level, it is the presence of facet tropism which can cause LFH. Hence, patients with the presence of above mentioned factors at those respective levels have higher preponderance to develop Lumbar canal stenosis.

Ventrally emigrating neural tube cells migrate into the developing vestibulocochlear nerve and otic vesicle.

Virtually all cell types in the inner ear develop from the cells of the otic vesicle. The otic vesicle is formed by the invagination of non-neural ectodermal cells known as the otic placode. We investigated whether a recently described cell population, originating from the ventral part of the hindbrain neural tube known as the ventrally emigrating neural tube (VENT) cells, also contributes cells to the otic vesicle. The ventral hindbrain neural tube cells were labeled with the fluorescent vital dye DiI or replication-deficient retroviruses containing the LacZ gene in chick embryos on embryonic day 2, after the emigration of neural crest from this region. One day later, the labeled cells were detected only in the hindbrain neural tube. Shortly thereafter, the labeled cells began to appear in the eighth (vestibulocochlear) cranial nerve and otic vesicle. From embryonic day 3.5-5, the labeled cells were detected in the major derivatives of the otic vesicle, i.e. the endolymphatic duct, semicircular canals, utricle, saccule, cochlea, and vestibulocochlear ganglion. That the emigrated cells originated from the ventral part of the hindbrain neural tube was confirmed by focal application of DiI impregnated filter paper and with quail chimeras. It is concluded that, in addition to the otic placode cells, the otic vesicle also contains the ventrally emigrating neural tube cells, and that both cell populations contribute to the structures and cell types in the inner ear. It is well known that inductive signals from the hindbrain are required for the morphogenesis of the inner ear. The migration of the hindbrain neural tube cells into the otic vesicle raises the possibility that the inductive effect of the hindbrain might be mediated, at least in part, by the ventrally emigrating neural tube cells and that, therefore, a mechanism exists that involves cells rather than diffusible molecules only.