Spinal Syrinx Due to Lipiodol-Induced Arachnoiditis.

We present a case of a progressive symptomatic intramedullary cyst, diagnosed decades after Lipiodol injection. Lipiodol was originally administered intrathecally for the radiologic diagnosis of spinal masses. A link between the lesion and the history of Lipiodol injection was never suspected. Surgical exploration revealed a membrane above the lesion, separating the intradural space in a cranial and caudal compartment. On the level of the cyst, we identified glassy pearls containing a fatty liquid, compatible with Lipiodol deposits. We hypothesize that the syrinx is secondary to the impact of cerebrospinal fluid pulsations on the reactive membrane and that this membrane originated from an arachnoiditis caused by Lipiodol deposits. Lipiodol was indeed abandoned after it was found to cause arachnoiditis and neurologic sequelae. Despite the cessation of its usage, the causal role of Lipiodol in arachnoiditis and spinal cyst formation should still be considered, as symptoms may arise many years after Lipiodol administration.

Spinal Cord Transcriptomic and Metabolomic Analysis after Excitotoxic Injection Injury Model of Syringomyelia.

Syringomyelia is a condition of the spinal cord in which a syrinx, or fluid-filled cavity, forms from trauma, malformation, or general disorder. Previous work has shown that in noncanalicular syringomyelia irregular flow and pressure conditions enhance the volumetric growth of syrinxes. A better understanding of the underlying molecular pathways associated with syrinx formation will unveil targets for treatments and possibly prevention of syringomyelia in the future. In this study, we performed an established surgical induction of a syrinx using quisqualic acid and kaolin injections in rats to characterize the injury at the molecular level by RNA sequencing and metabolomics techniques at three and six weeks post-injury. Syrinxes averaging nearly 10 mm in length formed in the rats' spinal cords; however, smaller syrinxes were also detected in saline injected surgical shams, complicating interpretation of results. Our current results indicate a robust immune response coupled with overall decreases in neuronal signal transmission of syrinx containing animals compared with controls. Although transcriptional changes indicated gliosis and loss of neurons, no neuropathic pain was detected by von Frey allodynia testing. Unique transporters were revealed to be highly dysregulated, including significant increases in betaine/glycine transporter (BGT-1), K+/Cl- co-transporter (KCC4), and aquaporin 1 (AQP1), along with the upregulation of small molecule osmolytes taurine and betaine. The identified metabolites are of particular interest because of their involvement in osmotic homeostasis and need to be investigated further for their specific involvement in trauma-induced syrinxes.

Iophendylate myelography induced thoracic arachnoiditis, arachnoid cyst and syrinx, four decades later.

Iophendylate (Myodil) was a popular oil-based contrast agent used until late 1980s for myelography, ventriculography and cisternography. Although several long-term sequelae have been reported in literature, they are extremely rare. We report a rare occurrence of symptomatic dorsal arachnoid cyst 40 years after Myodil myelography.

[Changes of protein kinase C activity in experimental presyrinx state in rabbits].

OBJECTIVE: To investigate the changes of protein kinase C (PKC) activity and its role in the development of presyrinx state in rabbits. METHODS: Presyrinx state was established in 56 rabbits by intra-cisternal injection of kaolin. At 1, 3, 7, 14, and 21 days after the injection, the water content in the upper cervical spinal cord was measured, its pathological changes observed microscopically and the PKC activity determined with substrate phosphorolysis kinase assay. RESULTS: Spinal cord edema occurred in rabbits one day after kaolin injection, with water content of (68.35-/+0.70)%, which increased to (72.70-/+0.88)% on day 3, reaching the peak level of (72.92-/+0.86)% on day 7, followed by gradual decline after 3 weeks [(70.03-/+0.77)%]. The membrane PKC activity increased from 5.67-/+0.26 pmol.mg(-1).min(-1) on day 1 after the injection to reach the peak level on day 7 (13.27-/+3.15 pmol.mg(-1).min(-1)), which was maintained till day 14 with subsequent decrease to 8.85-/+1.56 pmol.mg(-1).min(-1) on day 21. The cytoplasmic PKC activity showed changes of a reverse pattern. CONCLUSION: In rabbits with experimental presyrinx state, PKC translocation and activation is involved in ischemic spinal edema.

Syringomyelia caused by intrathecal remnants of oil-based contrast medium.

Oily contrast medium had been in use since the early 19th century as a radiographic agent for detecting spinal lesions and spinal cord tumors until the late 20th century. At that point computed tomography scanning and magnetic resonance imaging, or other hydrophilic contrast medium substituted for it. Adverse effects of oil-based dye, both acute and chronic, had been reported since the middle of the 20th century. In this paper the authors report the case of syringomyelia that seemed to be caused mainly by remaining oily contrast medium for 44 years. Syringomyelia secondary to adhesive arachnoiditis caused by oily contrast medium after a long period of time is well known. In the present case, however, surgery revealed only mild arachnoiditis at the level of syringomyelia as well as both solid and liquid remnants of contrast medium. Generally, cerebrospinal fluid (CSF) blockage due to an arachnoid adhesion is considered to cause syringomyelia following adhesive arachnoiditis. The authors speculated that in the present case syringomyelia was induced by a mechanism different from that in the previously reported cases; the oily contrast medium itself seems to have induced the functional block of CSF and impaired the buffer system of the intrathecal pressure. No reports on thoracic adhesive arachnoiditis and syringomyelia caused by oil-based dye referred to this mechanism in reviewing the literature.

[Expression of aquaporin 4 during development of experimential presyrinx state in rabbits].

OBJECTIVE: To investigate the expression of AQP4 during the development of presyrinx state of experimental syringomyelia in rabbits. METHODS: The experimental syringomyelia models of rabbits were established by intra-cisternal injection of Kaolin. The expression of AQP4 AQP4mRNA and the water content of upper cervical spinal cord were measured with immunohistochemistry Western blot RT-PCR and dry-wet measurement on days 1,3,7,14, and 21 after operation, respectively. RESULTS: Compared with animals of control group, the water content increased in those of Kaolin group from the 1st day (68.35%+/-0.70%), reached its peak on the 7th day (72.92%+/-0.86%), lasted to the 14th day (72.58%+/-0.55%), and then began to drop on the 21st day (70.03%+/-0.77%), while AQP-4 immunoreactive expression decreased on the 3rd day [integral optical density(IOD) 320.5+/-44.2], reached its minimum on the 7th day (IOD 258.7+/-26.5), lasted to the 14th day, and recovered partially on the 21st day approximately (IOD 321.5+/-46.1). RT-PCR found the decreasing of AQP4 mRNA coincided well with that of AQP4 immunoreactive expression in presyrinx state. The linear regression analysis indicated that expression of AQP4 and its mRNA in cervical cord had a negative correlation with the change of spinal water content (r=-0.769, P<0.01; r=-0.955, P<0.01). CONCLUSION: Downregulation of AQP4 and its mRNA expression may involve in edema formation in the presyrinx state of rabbits.

Thoracic arachnoiditis, arachnoid cyst and syrinx formation secondary to myelography with Myodil, 30 years previously.

Spinal arachnoiditis can rarely occur following irritation from foreign body substances, including certain oil based contrast agents used for myelography. We describe a patient with thoracic arachnoiditis, arachnoid cyst and syringomyelia, 30 years following a myelogram with Myodil. A 62-year-old female presented with chronic thoraco-lumbar back pain, a spastic paraparesis and sphincter disturbance. She had undergone a myelogram with Myodil, 30 years previously for investigation of back pain. A MRI scan revealed evidence of arachnoiditis, thoracic syringomyelia (T6-T8) and an anteriorly placed, extramedullary, arachnoid cyst at T10-T12, compressing the cord. At surgery, T7-T10 thoracic laminectomies were carried out and syringo- and cysto-subarachnoid shunts were inserted. At 12 months follow-up, the sphincter disturbance, lower limb weakness and mobility problems had almost resolved. Although, the use of oil based contrast agents such as Myodil has been discontinued, the present case illustrates some of the rare sequelae of its use, manifesting decades later. Aggressive surgical intervention produced symptomatic benefit.

[Effect of Ginkgo biloba extract on neuronal apoptosis in rabbit with kaolin-induced syringomyelia].

OBJECTIVE: To evaluate the effect of Ginkgo biloba extract (GBE) on neuronal apoptosis in rabbits with kaolin-induced syringomyelia. METHODS: Twenty-four of 30 Chinese white rabbits were subjected to injection of 25% kaolin mixed with equal volume (0.6 ml) of cerebrospinal fluid drawn from the cisterna magna under ketamine anesthesia. Twelve of these 24 rabbits then received intravenous injection of 5 ml of GBE (5 ml/days for 14 days, GBE treatment group) while the other 12 were treated with the same amount of saline administered in similar manner (saline group). The 6 rabbits without kaolin treatment received a sham operation to serve as the control group. At different time points after the operation, the rabbits were killed and the spinal cord samples examined by immunohistochemistry. RESULTS: Histologically, ischemia and edema in the cervical cord of rabbits in GBE treatment group were less severe than those in saline group. TUNEL-positive and bax-positive neurons were less numerous in GBE treatment group than in saline group, and the former group showed more Bcl-2-positive neurons. The number of apoptotic neurons reached the peak level on day 7 after kaolin injection. CONCLUSION: GBE can ameliorate kaolin-induced hydrocephalus in the upper cervical cord and inhibit kaolin-induced neuron apoptosis.

Origin of macrophages in a kaolin-induced model of rat syringomyelia: a study using radiation bone marrow chimeras.

STUDY DESIGN: Animal experimental study. OBJECTIVE: To study the origin of macrophages in a rat model of syringomyelia. SUMMARY OF BACKGROUND DATA: Syringomyelia is a clinically important condition in which a cystic cavity forms within the spinal cord. This leads to significant delayed neurologic deterioration, which may be manifested as weakness, numbness, or pain. The pathophysiology and mechanism of syrinx formation remain unclear. Human autopsy findings have demonstrated a prominent accumulation of macrophages in relation to the syrinx. Similar observations have also been made in a previously established rat model of syringomyelia. Little is known about the origin and precise functions of these cells. METHODS: Syrinx formation was induced by intraparenchymal injections of kaolin within the cervical spinal cords of 30 DA rat (RT7.1) radiation bone marrow chimeras reconstituted with bone marrow from RT7.2 congeneic donors. The distribution of macrophages was evaluated at survival times of 3 days, 1 week, and 4 weeks. Immunostaining of fresh-frozen spinal cord tissue was performed using specific antibodies against rat macrophage ED1 antigen and RT7.2 allele of CD45. This allowed donor-derived hematogenous (ED1+, RT7.2+) macrophages to be distinguished from native cells (ED1+, RT7.2-). RESULTS: Central canal dilatation was seen from 1 week. This was associated with extensive accumulation of ED1+ macrophages within the spinal cord parenchyma. A large influx of bone marrow-derived (ED1+, RT7.2+) macrophages was observed. However, a considerable proportion of resident microglia (RT7.2-) also upregulated ED1. These activated microglia demonstrated distinct morphologic features. CONCLUSIONS: Large numbers of macrophages were recruited from the bone marrow in kaolin-induced rat syringomyelia. However, a significant number of resident microglia upregulated their ED1 activity and appear to provide a substantial source of macrophages.