Abstract
Even when the bone fusion has been successful, the pain may continue to ruin the life of the patient. Two mechanisms have been identified as origin of the pain, one extra and one intradural.
The compressive extradural lesions are caused mainly by the action of progressive stenoses or by the disruption of the pedicular wall by badly placed screws.
As for defective screw’s trajectory, the most dangerous points are mainly the pedicle’s medial or inferior corticals. In the intraforaminal trajectory the dural sleeve of the lumbar root may be mangled too, suffering a mixed mechanicalbiological mismanagement. Even without laceration a burst cortical or the metal contact can be the origin of root irritation or even palsies. These lesions are present in most series in between 1 and 10% of the screws, depending of the surgical experience. The use of navigational devices finds in this technique his principal indication.
The CAT usually diagnoses the misplaced screws. The artefacts caused by stainless steel are the reason of banning this metal for spinal devices. When doubt the pain origin can be proved by electromyographical analysis. The electrical stimulus of the screw with a 0.2 millisecond pulse of 5 – 10 mA DC signals a violated pedicle wall. The treatment of these lesions is always the removal of compressive hardware. When a non-union compounds the root compression a TLIF with cage plus posterolateral fusion with posterior instrumentation, allows the liberation of the root without entering the compromised canal.
The compression of the dural sac by recurrent stenosis was frequent in posterior fusions. The lamina thickens by the transmission of charges through this bony continuum. Nowadays it can be yet seen with lamina decortication and bone grafts stocked between the rods and the base of the spinous process. The CT myelogram shows the lesion. The extraction of the hardware and resection of the redundant bone inside the canal, can resolve the compression. The most fearful lesions are the peridural and the intradural fibrosis caused by the operative mishandling of the dural sac or by septic epidural episodes. The neurologic lesions are often irreversible. The treatment is the most difficult and the outcomes the gloomiest of the spinal surgery. The best treatment is the prevention by delicate handling of the dural sac. Suture with titanium micro-clips must be done in all the dural wounds. Disc resection adjoining articular fusion in the treatment of stenotic canals must be avoided, to prevent a cicatricial circle. Abstention of foreign bodies inside the canal, use of bipolar cautery and soluble haemostatic substances to stop the intra-canalar bleeding, are the means of preventing the peridural fibrosis. Corticoids locally or covering the dura with a thin layer of anti-adhesive gel is a good prevention of adherences. The wounds of the dura can produce too a leakage of CSF leading to a compressive myelomeningocele if intracanalar. Wear titanium particles can be found in defective constructs. The motion between rod and screws can produce them. If the particles enter the canal they can produce both compression and fibrosis.
In the case intradural adherences blocking the roots in bundles, little can be done. Once secured the immobilisation of the level by a good extracanalar bone-fusion, the use of electrical interference electrodes in contact with the affected roots is the only solution. Some aid can be expected with the use of antiproliferative cytokines as interferon gamma or reverse-transcriptase inhibitors as Suramin, administered after a surgical cleaning of the fibrosis. With all the inconveniences of these treatments yet they allow a modicum of hope.
Theses abstracts were prepared by Professor Dr. Frantz Langlais. Correspondence should be addressed to him at EFORT Central Office, Freihofstrasse 22, CH-8700 Küsnacht, Switzerland.
