Lipomas of the Conus Medullaris
Details of the disordered embryological development currently considered as the best explanation for lipomas have been reported by McLone and Naidich  and are outlined briefly here.
In normal development blastocyst formation occurs from gestational Days 1 to 4. An inner cell mass develops into discrete layers of hypoblast and epiblast. By gestational Days 13 to 16 the primitive streak forms and invaginates to give rise to the primitive groove. Formation of the notochordal process begins on or around gestational Day 16. The neuroectoderm first becomes visible by gestational Day 17 along a shallow neural groove. From gestational Days 19 to 21 the neural groove deepens and neural folds become visible. The folds continue to elevate and converge toward the midline. As the neural folds come together, the lateral cutaneous ectoderm also comes together in the midline and then fuses. Current understanding of myelomeningocele implicates a failure of the cutaneous ectoderm and neuroectoderm to fuse, such that the neural tube fails to close and remains dorsally applied to and continuous with the skin on its lateral surfaces. Lipomyelomeningoceles, by contrast, arise when disjunction between cutaneous ectoderm and neuroectoderm (neural tube) occurs early. As such, the cutaneous ectoderm has sealed, but the still-open neural tube is exposed for the in-growth of paraxial mesoderm derived tissue. Presumably, the ectodermal surface of the exposed neural tube induces differentiation of this mesodermal tissue primarily into adipocytes, and a fatty mass subsequently develops. The source of the fat remains a controversial issue. A number of other tissues have been noted within the substance of a lipomyelomeningocele including striated muscle, cartilage, nerve cells, ependyma, and even cerebellum. The metabolism of the fat is the same as that of subcutaneous fat and does not show the accelerated metabolism of the lipoma. The metabolic features of the adipocytes within lumbosacral lipomas are similar to those of normal adipose tissue; however, these cells most commonly lie in a densely fibrous connective tissue stroma. Some have noted the multiple, different cell types present and have questioned whether the disorder in embryogenesis in fact gives rise to a benign form of teratoma.
This model is consistent with the various surgically and radiologically recognized forms of lipomyelomeningocele (see below). In the caudal, form fatty tissue invaginates into the central canal and may ascend for several levels. An open neural tube would allow free access for mesodermally derived structures to become so positioned. A dorsally located lipomyelomeningocele arises directly off the back of the spinal cord and would presumably reflect a neural tube that had progressed farther toward complete closure.
Lipomas of the Terminal Filum
Unlike medllaris lipomas of the conus medullaris, those that arise in the filum are thought to develop as a result of a disorder of secondary neurulation. The neural tube that forms as a result of primary differentiation extends only as far as the second sacral segment. As such, it could not give rise to anomalies of the distal filum.
Secondary neurulation in humans is incompletely understood. Currently it is believed that progressive coalescence of vacuoles, which are seen to arise in the caudal cell mass during the 4th and 5th week of development, leads to the emergence of a central canal within the caudal cell mass. This canal is thought to coalesce with the neural tube that is formed by primary neurulation. The distal portion of the caudal cell mass is thought to regress to become the terminal filum. Presumably a disembryongenic process occurring at this developmental stage gives rise to the development of fat within the filum. The exact pathogenic mechanisms by which lipomas of the filum arise remain unknown, but impaired canalization of the caudal cell mass and persistence of cells capable of maturing into adipocytes are likely to be involved. This process occurs after disjunction of the cutaneous and neuroectoderm, and, as such, it is consistent that these lesions are skin covered and lacking cutaneous stigmata. The central canal of the caudal cell mass may persist as the terminal ventricle.
In a myelocystocele the terminal ventricle may become capped by lipoma which may impart abnormality to the CSF circulation and result in terminal ventricle dilation. McLone and Naidich  hypothesize that the resulting meningocele impairs mesodermal structures resulting in spina bifida and cord tethering.
Terminal myelocystocele is highly associated with anomalies of the genitourinary and gastrointestinal tracts. Structures related to the caudal spinal cord lie close to the cloaca during development. Thus, it is not surprising that anomalies of cloacally derived structures are highly associated with anomalies of the caudal spinal cord. Indeed, there is a high incidence of filum lipomas in patients in whom there are syndromes of cloacal maldevelopment including vertebral, anal, tracheal, esophageal, and renal anomalies; omphalocele (cloacal) exstrophy imperforale spinal anomalies and Currarino triad. Nonsyndromic associations include imperforate anus, rectovaginal fistulas, bladder extrophy, complex sacral malformations, ectopic kidney, and cecocutaneous peroneal fistulas.[2,18,21,50,67]
Neurosurg Focus. 2001;10(1) © 2001 American Association of Neurological Surgeons
Cite this: Spinal Lipomas - Medscape - Jan 01, 2001.