Hearing preservation procedures in acoustic neuroma surgery entail a risk of recurrent tumor either from the preserved cochlear nerve (tumor cell remains or late degeneration) or from tumor remnants left in the lateral end of the internal auditory canal. There is disagreement about the frequency of such tumor remnants, and the diagnostic modalities are not precise. Magnetic resonance imaging with gadolinium-DTPA enhancement is effective in diagnosing a primary case, but may not be so clear for small residual or recurrent tumors. A review of the literature concerning residual/recurrent tumor after "total" removal in functional unilateral acoustic neuroma surgery provided several reports,1-9 but systematic studies were lacking.This study of a series of 104 acoustic neuroma cases operated on with a hearing preservation procedure assessed the rates of residual or recurrent tumor and the imaging data that were significant for its diagnosis. MATERIALS AND METHODSDuring the period 1975 to 1993, 104 consecutive patients presenting with acoustic neuroma were operated on with the same hearing preservation procedure: the suboccipital approach with meatotomy and direct exposure of the lateral end of the internal auditory canal (IAC). The procedure involved a bone resection of the posterior and part of the superior and inferior walls of the IAC and used as landmarks the vestibular aqueduct, the common crus, and the nonampullated crura of the posterior and the superior semicircular canals. In every case, the surgeon 105

A total of 234 patients treated by percutaneous discectomy at 237 levels and followed-up between 11 months and 3 years 4 months showed an overall success rate of about 75%. In a subgroup of 112 of these patients rechecked for a second time, the clinical results remain consistently good even 24 months after surgery. In a special group of 28 patients who complained only of low back pain, percutaneous discectomy achieved a success rate of 85.7%. Complications consisted of one disc infection which cleared without clinical or radiological sequelae (0.26%).

CRP appears to be significantly increased already in the first 3 h because of the acute ischemic stroke.

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Our study suggests that in the acute phase of the cerebral infarction CRP might be either a marker of cardioembolism or a predictive factor for short-term mortality.