Conclusions ‘The broad descriptive nature of the report, the scape of the literature seareh and the characteristies of the literature reviewed should be considered when interpreting the report conclusions, * Arachnoiditis was variously described in radiology, experimental and pathology literature Differing terminology has been used and has led to confusion aver what should be termed arachnoiditis. {tis @ non-specific inflammatory condition involving the Ieplomeninges and intratheeal neural elements, Three distinct entities were generally recognised — arachnoidal adhesions, adhesive arachnoiditis and caleifie arachnoiditis. The term in the literature used for more clinically obvious and symptomatic forms was usually chronic adhesive arachnoiditis, There was varied opinion aver whether or not rarer and more extreme forms were the same disease or distinct entities Heath Tecroogy AssessmentEarly cases of arachnoiditis were mainly a complication of infection Etiology today may be of iatrogenic origin through complications arising from the treatment of lower back pain. Patients Often had a history of n pre-existing back condition and had undergone multiple myelograms and multiple surgeries. It was impossible to determine the single causative event in most patients, and there was a need for definitive evidence on the etiology of the condition. The relative importance of these etiological factors in the future was largely speculative Attempts to correlate clinical signs and symptoms with radiological findings of arachnoiditis produced variable results. The origin, type, location and distribution of symptoms in arachnoiditis patients was often atypical. Chronic and severe back and/or lower extremity/leg pain was the most common symptom. Clinical history typically began with presentation for back injury and pain followed by clinical investigation, including multiple myelograms and surgery laminectomy (often multiple) and sometimes spinal fusion. Underlying diseases such as meningitis, recent herniated disc and spinal stenosis might all overlap with arachnoiditis. Heath Tecroogy Assessmentble 1. Diagnostic Criteria for Transverse Myelitis.* Bilateral (not necessarily symmetric) sensorimotor and autonomic spinal cord dysfunction Clearly defined sensory level Progression to nadir of clinical deficits between 4 hours and 21 days after symptom onset, Demonstration of spinal cord inflammation: cerebrospinal fluid pleocytosis or elevated IgG index, or MRI revealing a gadolinium-enhancing cord lesion Exclusion of compressive, postradiation, neoplastic, and vascular causes * Clinical events that are consistent with transverse myelitis but that are not as sociated with cerebrospinal fluid abnormalities or abnormalities detected on MRI and that have no identifiable underlying cause are categorized as possi ble idiopathic transverse myelitis {The IgG index is a measure of intrathecal synthesis of immunoglobulin and is calculated with the use of the following formula: (CSF IgG=serum IgG) = (CSF albuminserum albumin), where CSF denotes cerebrospinal fluid