Facial nerve function and hearing preservation after retrosigmoid excision of vestibular schwannoma: Christchurch Hospital experience with 97 patients.

BACKGROUND: Between January 1988 and December 2002, 97 patients underwent surgery for excision of vestibular schwannoma via the retrosigmoid approach at Christchurch Hospital. METHODS: A retrospective review was undertaken of the clinical notes with emphasis on facial nerve function and hearing preservation postoperatively. RESULTS: Of patients with small and medium-sized tumours, 81% had good facial nerve function at 1 year (House-Brackmann grade 1 and grade 2), 16% had moderate function (grade 3 and grade 4) and 3% had poor function (grade 5). Of patients with large tumours, 22% had good facial function (grade 1 and grade 2), 37% had moderate function (grade 3 and grade 4) and 41% had poor function (grade 5 and grade 6). Useful postoperative hearing was preserved in 21% of the 47 patients with tumours <3 cm and useful preoperative hearing. In the last 5 years the authors have been operating in conjunction with an ear, nose and throat surgeon (PAB) trained in base-of-skull surgery. Over this period, useful hearing was preserved in 32% of patients with small and medium-sized tumours and useful preoperative hearing. CONCLUSIONS: Tumour size was an important predictor of the postoperative facial and cochlear nerve function. The multidisciplinary approach to these tumours offers better results. These results compare well with other published series.

The neuro-cardio-endocrine response to acute subarachnoid haemorrhage.

OBJECTIVE: Whereas cardiac hormones increase after subarachnoid haemorrhage (SAH), and may contribute to sodium wastage and hyponatraemia, there is controversy concerning the relative roles of atrial natriuretic peptide (ANP) vs. brain natriuretic peptide (BNP) and the factors initiating their secretion. Noting previous work linking stress hormone responses with cardiac injury after SAH, we have studied responses in stress hormones, markers of cardiac injury and the temporal changes in ANP and BNP and related them to changes in sodium status post ictus and during recovery from acute SAH. DESIGN, PATIENTS, MEASUREMENTS: Eighteen patients with verified SAH of variable severity were studied in a single unit for a 14-day period post ictus under controlled conditions of sodium and fluid intake. All received a standardized protocol of daily dexamethasone and nimodipine throughout the study. Severity was graded using criteria of Hess and Hunt at admission. Stress hormones (AVP, catecholamines and admission plasma cortisol), markers of cardiac injury (ECG and daily plasma troponin T) and cardiac hormones (ANP and BNP) were measured daily and related to severity, plasma sodium and renin-aldosterone activity. Hormone levels (ANP, BNP and endothelin) in cerebrospinal fluid (CSF) were also measured in nine patients. RESULTS: Intense neurohormonal activation (AVP, cortisol and catecholamines) at admission was associated with increased levels of both plasma ANP and BNP whereas levels in CSF were unaffected. In individual patients plasma levels of ANP and BNP were strongly correlated (P < 0.001). Cardiac events (abnormal ECG and/or elevated troponin) occurred in six of seven patients graded severe but neither stress hormones nor cardiac peptides differed significantly in patients with mild (n = 11) vs. severe (n = 7) SAH. During the course of a progressive fall in plasma sodium concentration (P = 0.001), there was a delayed activation of renin-aldosterone which was inversely correlated with declining levels of plasma ANP/BNP (P < 0.002). CONCLUSIONS: Excessive secretion of both ANP and BNP occurs in all patients after acute subarachnoid haemorrhage and is unrelated to severity, stress hormone activation or markers of cardiac injury. Inhibition of renin-aldosterone by cardiac hormones may impair renal sodium conservation and contribute to developing hyponatraemia. In the absence of evidence for activation of natriuretic peptides within the brain, the prompt and consistent increase in both ANP and BNP strongly supports the view that the heart is the source of increased natriuretic peptide secretion after acute subarachnoid haemorrhage.