Pathophysiology and Treatment of Syringomyelia Associated with Tuberculous Meningitis

Abstract

Syringomyelia associated with tuberculous meningitis tends to be intractable because of its complex pathophysiology. There is almost always a long interval between the diagnosis of tuberculous meningitis and the onset of syringomyelia. Magnetic resonance imaging (MRI) findings, hydrodynamics, pathophysiology, and treatment of this difficult condition were analyzed. We treated five cases of syringomyelia associated with tuberculous meningitis with an age distribution from 35 to 72 years old. Syringomyelia developed 6 months to 30 years after tuberculous meningitis. All patients showed incomplete or total paraplegia, sensory deficit below the thoracic level, and ascending sensory-motor disturbance of the upper extremities. All were examined with MRI. Cine-MRI and computed tomography (CT) myelography were useful for assessing patency of the subarachnoid space. When the cranial subarachnoid space was intact, a syringosubarachnoid (SS) shunt was selected, but when it was obliterated, a syringoperitoneal (SP) shunt was selected. Three patients underwent an SP shunt and one underwent an SS shunt. A flexible endoscope helped with accurate placement of the shunt tube in the subarachnoid space. Local arachnoid adhesion was dissected, and expansive dural plasty was performed with an artificial dural patch to prevent postoperative adhesion. In two cases, arachnoid adhesion was so diffuse that aggressive dissection could not be performed. The surgically treated patients were neurologically stable after the last operation. Careful dissection of arachnoid adhesion and reestablishment of normal cerebrospinal fluid (CSF) hydrodynamics is essential. For diffuse arachnoid adhesion, an SP shunt should be used.