Cervical central canal occlusion induces noncommunicating syringomyelia.

BACKGROUND

Mechanisms underlying the development of noncommunicating syringomyelia are poorly understood.

OBJECTIVE

To assess the influence of focal arachnoiditis and central canal (CC) occlusion (CCO) on the formation of noncommunicating syringomyelia in the adult rat cervical spinal cord. Expression of pericanalicular aquaporin-4 is also examined.

METHODS

Sprague-Dawley rats were subjected to circumferential or dorsal arachnoiditis (n = 34). Rats undergoing CCO (n = 69) were divided into 4 groups: group A, kaolin injection at a single site in the dorsal columns near the CC; group B, kaolin injection at multiple sites in the dorsal columns near the CC; group C, saline injection at multiple sites in the dorsal columns near the CC; or group D, controls. Rats were killed at 1, 4, 8, and 12 weeks. The CC area and aquaporin-4 (AQP4) expression were measured at the level of maximal CC enlargement.

RESULTS

Circumferential and dorsal arachnoiditis induced a mild increase in the CC area at 12 weeks. Single-site CCO induced slight CC enlargement. In contrast, multiple sites of CCO in proximity frequently induced a major expansion of the CC area (up to 50 times). Increased AQP4 expression was observed in pericanalicular astrocytes proportional to the degree of CC expansion.

CONCLUSION

Multiple sites of CCO created a model of noncommunicating syringomyelia in adult rats. Increased astrocytic AQP4 expression was proportional to the degree of CC expansion. Modulation of aquaporin expression may be a novel target for therapeutic interventions to prevent syringomyelia.