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Arachnoiditis

Arachnoiditis describes a pain disorder caused by the inflammation of the arachnoid, one of the membranes that surround and protect the nerves of the spinal cord. The arachnoid can become inflamed because of an irritation from chemicals, infection from bacteria or viruses, as the result of direct injury to the spine, chronic compression of spinal nerves, or complications from spinal surgery or other invasive spinal procedures. Inflammation can sometimes lead to the formation of scar tissue and adhesions, which cause the spinal nerves to "stick" together. more...

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If arachnoiditis begins to interfere with the function of one or more of these nerves, it can cause a number of symptoms, including numbness, tingling, and a characteristic stinging and burning pain in the lower back or legs. Arachnoiditis has no consistent pattern of symptoms, but it more frequently affects the nerves that supply the lower back and legs.

Prognathisism

Arachnoiditis is a chronic pain disorder and while there is no known cure at this time some quality of life may be redeemed through pain management routines. Prognosis is often complicated by the lack of a clear relationship between time of onset and pattern of symptoms. Aging and pre-existing spinal disorders can make accurate prognosis problematic. For many, arachnoiditis is a disabling disease that causes chronic pain and neurological deficits.

Treatment

Arachnoiditis remains a difficult condition to treat, and long-term outcomes are unpredictable. Most treatments for arachnoiditis are focused on pain relief and the improvement of symptoms that impair daily function. A regimen of pain management, physiotherapy, exercise, and psychotherapy is often recommended. Surgical intervention is controversial since the outcomes are generally poor and provide only short-term relief. Clinical trials of steroid injections and electrical stimulation are needed to determine the efficacy of these treatments.

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Investigations of cerebrospinal fluid dynamics in a sheep model of post-traumatic syringomyelia
From Journal of Bone and Joint Surgery, 1/1/03 by Abou-Hamden, A

INTRODUCTION: Modern imaging techniques have demonstrated that up to 28% of patients with spinal cord injury develop syringomyelia. Cyst formation and enlargement are thought to be related to abnormalities of cerebrospinal fluid hydrodynamics, however the exact mechanism and route of entry into the spinal cord remain incompletely understood. Previous work in rats has demonstrated that experimental post-traumatic syrinxes occur more reliably and are larger when the excitotoxic injury is combined with arachnoiditis produced by subarachnoid kaolin injection. A sheep model of post-traumatic syringomyelia (P.T.S.) has been characterised and studies of cerebrospinal fluid dynamics are currently being undertaken.The aim of this study was to assess the effect of focal subarachnoid space blockage on spinal fluid pressures and flow.

METHODS: Arachnoiditis was induced in five sheep by injection of 1.5 mls of kaolin in the subarachnoid space (SAS) of upper thoracic spinal cord. The animals were left for 6-8 weeks before C.S.F. studies were undertaken. In another five sheep, a ligature was passed around the spinal cord to simulate an acute blockage of the subarachnoid space. Fluid-coupled monitors were used to measure blood pressure, central venous pressure and subarachnoid pressure (1 cm rostral and 1 cm caudal to the arachnoiditis or ligature). Fiberoptic monitors were used to measure intracranial pressure. In the ligature group, subarachnoid pressures were also measured prior to tying the ligature to obliterate the SAS and served as baseline control pressures. The effects of Valsalva and Queckenstedt manoeuvres on SAS pressures were examined in both groups.

CSF flow was studied at 0 and 10 minutes after injection of the CSF tracer horseradish peroxidase (HRP). Vibratome sections of the spinal cord were processed using tetramethylbenzidine and sections examined under light microscopy.

RESULTS: The mean SAS pressure rostral to the arachnoiditis was found to be greater than the mean caudal SAS pressure by 1.7 mmHg. In the ligature group, the difference was 0.9 mmHg, being higher in the caudal SAS. Queckenstedt manoeuvre exaggerated this difference to 3 mmHg in the Kaolin group and 4 mmHg in the ligature group. The effect of Valsalva was much less marked in both groups.

Perivascular spaces were enlarged in most cases of arachnoiditis and HRP was seen to stain these spaces and the central canal within 10 minutes.

DISCUSSION: Post-traumatic syrinxes are usually juxtaposed to the injury site with 80% occurring rostral, 4% caudal and 15% in both directions. The finding of a higher subarachnoid pressure rostral to the injury site may help explain this phenomenon. We hypothesise that a reduction of compliance in subarachnoid space increases the pulse pressure and hence increases perivascular flow of C.S.F. contributing to the formation and enlargement of PTS. We are currently investigating this hypothesis by measuring subarachnoid space compliance directly in the sheep model of arachnoiditis described above.

A. Abou-Hamden, N.R. Jones, M.A. Stoodley, A. Wells, M.A. Smith, C. Brown

Royal Adelaide Hospital University Department of Surgery (Neurosurgery), Adelaide, Australia

Copyright British Editorial Society of Bone & Joint Surgery 2003
Provided by ProQuest Information and Learning Company. All rights Reserved

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