Stenosis of central canal of spinal cord in man: incidence and pathological findings in 232 autopsy cases

Abstract

The central canal of the spinal cord is generally regarded as a vestigial structure that is obliterated after birth in 70% to 80% of the general population. This report describes the first detailed histological study of the human central canal in 232 subjects ranging in age from 6 weeks' gestation to 92 years. Whole spinal cords were harvested at autopsy and sectioned serially from the conus medullaris to the upper medulla. Histological findings and morphometric analysis of the cross-sectional luminal area were used to grade stenosis at seven levels of the canal. Varying grades of stenosis were present at one or more levels in none (0%) of 60 fetuses, one (3%) of 34 infants, three (18%) of 17 children, 21 (88%) of 24 adolescents and young adults, 67 (96%) of 70 middle-aged adults, and all 27 adults aged 65 years or older (100%). The stenotic process was most pronounced in the thoracic segments of the canal and involved more levels with higher grades of stenosis in older individuals. Histological findings consisted of disorganization of the ependymal epithelium, formation of ependymal rosettes or microcanals, proliferation of subependymal gliovascular buds, and intracanalicular gliosis. These features are consistent with a pathological lesion involving ependymal injury and scarring and are less compatible with an involutional or degenerative process. Stenosis of the central canal probably influences the anatomical features of syringomyelia and may account for variations in cavity formation such as the prevalence of holocord syrinxes in children, the formation of focal and paracentral syrinxes in adults, and the rare incidence of syrinx formation in many older individuals with acquired lesions known to produce syringomyelia.

The Spinal Cord Neural Stem Cell Niche

“…Histology and immunohistology studies revealed both similarities and dissimilarities between rodents and man. First, in contrast to mice, the central canal of the human spinal cord is often occluded (Dromard et al 2008), as previously reported by (Fuller and Burger 1997;Milhorat, Kotzen, and Anzil 1994), and the ependymal region appeared disorganized, with the frequent presence of rosettes or microcanals. Reminiscent of the reported difference between the SVZ in rodents and humans (Quinones-Hinojosa et al 2006), the human central canal is surrounded by a hypocellular region containing a high density of GFAP filaments and nerve fibers (Dromard et al 2008).…”

The Role of Excitotoxic Injury in Post-Traumatic Syringomyelia

“…Early hydrodynamic theories proposed that fluid flowed down the central canal due to arterial or respiratory pressure differentials, followed by rostral canal obstruction leading to a non-communicating syrinx (Gardner and Angel, 1958;Gardner and McMurray, 1976;Williams, 1972). Strong evidence against these theories includes the facts that the central canal is largely obstructed in humans by the age of 30, and that there is a clear histological distinction between the central canal and the syrinx cavity in post-traumatic cases (Milhorat, 2000;Milhorat et al, 1994Milhorat et al, , 1995Yasui et al, 1999). Another theory suggests that a traumatic hematoma within the cord resorbs to form an initial cavity, and that respiratory pressure differentials on the cord surface induce fluid movement within the cavity, dissecting into the cord and thus enlarging the syrinx (Williams, 1992).…”

Cervical Central Canal Occlusion Induces Noncommunicating Syringomyelia

“…19 The mechanisms by which SM develops remain controversial. [6][7][8][9][10][11][45][46][47] Abnormal craniocervical pressure/CSF flow differential, 4 arachnoiditis with a water-hammer pulsation of CSF into the CC, 12,27,48 the suck-slosh phenomenon, 9 and segmental CCO [21][22][23]49 have been proposed to be underlying FIGURE 6. Immunohistochemistry of central canal (CC) expansion related to changes in aquaporin-4 (AQP4) expression.…”