Surgery of vestibular schwannomas: an institutional experience.
(57/261)
AIMS: To report management results of vestibular schwannomas (VS) treated surgically in our institute, with particular reference to completeness of tumor excision, facial nerve and hearing preservation and complications of surgery. STUDY DESIGN AND SETTINGS: Retrospective study of 259 patients treated during the years 1988 to 2002. MATERIALS AND METHODS: The facial nerve function and hearing assessment was done according to House-Brackmann [HB] grading and pure tone audiometry (PTA) respectively. All patients were operated by retro-mastoid sub-occipital approach. RESULTS: Most patients had large tumors and had no useful hearing (90%), had disabling cerebellar ataxia (88%) and presented with features of raised intra-cranial pressure (45%). Large sized tumors were in 41.3% and giant sized tumors were in 56% cases. Complete tumor excision was carried out in 96.5% and anatomical preservation of facial nerve was achieved in 79.2% cases. Hearing preservation was achieved in 8 patients. Cerebrospinal fluid leak with or without meningitis and transient lower cranial nerve paresis were common complications. The mortality was 6%. CONCLUSIONS: With experience, complete tumor excision with good facial nerve preservation can be achieved in large tumors. Hearing preservation is difficult in bigger tumors. Prevention and control of infection was a major concern. (+info)
Methodological issues in longitudinal studies: vestibular schwannoma growth rates in neurofibromatosis 2.
(58/261)
Four longitudinal studies of vestibular schwannoma (VS) growth rates in neurofibromatosis 2 (NF2) have yielded very different results on the relationship of VS growth rates to age. The studies had different patient eligibility criteria, indices of VS growth rates, VS volumetric methods, and sample sizes. We reanalysed data from two of the longitudinal studies and used data from the population based United Kingdom NF2 Registry to determine the most likely reason for the different results and the actual relationship of VS growth rates to age. We found that the eligibility criterion in one study caused selection bias for slower growing VS. The proper interpretation of the results from the four studies is that VS growth rates in NF2 are highly variable but tend to decrease with increasing age. Clinical trials for VS in NF2 should focus on younger patients because VS growth rates tend to decrease with increasing age, and because faster growing VS are more likely to be excised with increasing age than slower growing VS. (+info)
Hearing preservation after gamma knife stereotactic radiosurgery of vestibular schwannoma.
(59/261)
BACKGROUND: To evaluate the hearing preservation rate and to determine its prognostic factors after gamma knife (GK) stereotactic radiosurgery (SRS) in patients with vestibular schwannoma, the authors used a prospective study design to analyze these patients. METHODS: Between December 1997 and January 2002, 25 patients with vestibular schwannoma with serviceable hearing were enrolled in the current study. The median tumor volume was 3.0 cc (0.16-9.1 cc). The prescription dose was 12.0 +/- 0.7 gray at an isodose line of 49.8 +/- 1.1%. The tumor control rate and complications were evaluated by focusing on hearing preservation and its prognostic factors. RESULTS: Based on radiologic study, the tumor control rate was 92% during the median follow-up period of 45 months. The trigeminal and facial nerve preservation rates were 95% and 100%, respectively. Thirteen (52%) of the 25 patients preserved serviceable hearing and 9 (36%) patients retained their pre-GK G-R grade levels after GK SRS. However, 16 patients showed hearing deterioration > 20 dB within 3-6 months and this trend continued for 24 months after the treatment. The maximum radiotherapy dose delivered to the cochlear nucleus was the single, significant prognostic factor of hearing deterioration. CONCLUSIONS: The authors concluded that a more sophisticated strategy to prevent hearing deterioration during the first 6 months post-GK SRS is necessary to improve long-term hearing preservation. (+info)
Age related shift in the mutation spectra of germline and somatic NF2 mutations: hypothetical role of DNA repair mechanisms.
(60/261)
It has been suggested that somatic mutations that accumulate due to an age related decline in the efficiency of DNA repair mechanisms might contribute to the increased incidence of cancer in older people. However, there is little direct evidence for this phenomenon. The spectra of germline and somatic mutations can be compared in cancer genes that cause inherited tumour syndromes and sporadic tumours, respectively. In addition, mosaic patients reflect the nature of mutations that occur in early development. Hence, we hypothesised that the "temporal mutation record" of a human cancer gene might provide insight into mechanisms of mutagenesis in the germline, in early development, and in adulthood. We compared the ratio of frameshift to nonsense mutations in three diseases that are related to the NF2 tumour suppressor gene: classic neurofibromatosis 2 (NF2), caused by germline NF2 mutations; mosaic NF2; and unilateral sporadic vestibular schwannoma (USVS), caused by somatic NF2 inactivation. Nonsense mutations predominated in both classic and mosaic NF2, but the ratio of nonsense to frameshift mutations was reversed in USVS. Moreover, in USVS patients, the ratio of somatic frameshift to nonsense mutations increased significantly with increasing age at diagnosis. This pattern is consistent with an age related decline in the efficiency of DNA repair mechanisms. Similar studies for other familial cancer genes may provide further evidence for this hypothesis. (+info)
Multicystic acoustic schwannoma with intratumoral hemorrhage: a report of two cases.
(61/261)
We encountered two multicystic acoustic schwannomas with intratumoral hemorrhage. The radiological appearance in each case was similar to that obtained with CT and MRI. From a histological perspective, in each case we observed hypervascularity with thin-walled, dilated vessels in clusters and hemosiderin depositions around the dilated vessels. (+info)
Mobile phone use and risk of acoustic neuroma: results of the Interphone case-control study in five North European countries.
(62/261)
There is public concern that use of mobile phones could increase the risk of brain tumours. If such an effect exists, acoustic neuroma would be of particular concern because of the proximity of the acoustic nerve to the handset. We conducted, to a shared protocol, six population-based case-control studies in four Nordic countries and the UK to assess the risk of acoustic neuroma in relation to mobile phone use. Data were collected by personal interview from 678 cases of acoustic neuroma and 3553 controls. The risk of acoustic neuroma in relation to regular mobile phone use in the pooled data set was not raised (odds ratio (OR) = 0.9, 95% confidence interval (CI): 0.7-1.1). There was no association of risk with duration of use, lifetime cumulative hours of use or number of calls, for phone use overall or for analogue or digital phones separately. Risk of a tumour on the same side of the head as reported phone use was raised for use for 10 years or longer (OR = 1.8, 95% CI: 1.1-3.1). The study suggests that there is no substantial risk of acoustic neuroma in the first decade after starting mobile phone use. However, an increase in risk after longer term use or after a longer lag period could not be ruled out. (+info)
Acoustic neurinoma surgery in Belfast 1986-1989.
(63/261)
Forty-seven acoustic neurinoma tumours have been operated on in 46 patients in the years 1987-1989. This is a considerable increase over the prevalence in the preceding ten years. Twenty-six were classified as large tumours, 18 as medium and one was small. Surgical excision was complete in 16 and incomplete in 31 cases. Two patients died in the early postoperative period. Facial nerve function was preserved in 36 (80%) of cases; of these 27 (60%) had good function and nine (20%) fair function. Useful hearing was prevented in only two patients. The overall complication rate has been low and often of a transitory nature. (+info)
Loss of heterozygosity on chromosome 22 in sporadic schwannoma and its relation to the proliferation of tumor cells.
(64/261)
BACKGROUND: Schwannoma is the tumor arising mainly from the cranial and spinal nerves. Bilateral vestibular schwannoma is the hallmark of neurofibromatosis type 2 (NF2). The NF2 gene has been cloned with comprehensive analysis of its mutations in schwannoma. However, most studies focused on vestibular schwannoma. There are differences in proliferation of tumor cell and ultrastructure between vestibular and spinal schwannomas. It is unknown whether genetic alterations in vestibular schwannoma are different from those in non-vestibular schwannoma. We analyzed the loss of heterozygosity (LOH) on chromosome 22 in patients with sporadic schwannoma including vestibular and spinal schwannomas and correlated this genetic alteration with tumor proliferation. METHODS: In 54 unrelated patients without clinical NF1 or NF2, 36 patients had sporadic vestibular schwannoma, and 18 dorsal spinal root schwannoma. Four highly polymorphic linkage to NF2 gene microsatellite DNA markers (D22S264, D22S268, D22S280, CRYB2) were used to analyze LOH. The proliferative index was evaluated by Ki-67 and proliferative cell nuclear antigen (PCNA) immunostaining. Student's t test was used to analyze the difference of the proliferative index between schwannoma with LOH and that without LOH. The difference of the frequency of LOH in vestibular and spinal schwannomas was investigated by the chi-square test. RESULTS: Twenty-three schwannomas (42.6%, 23/54) showed allele loss. The frequency of LOH in vestibular schwannoma was significantly higher than that in spinal schwannoma (chi2 = 5.14, P < 0.05). The proliferative index of schwannoma with LOH was significantly higher than that without LOH (tki-67 = 2.97, P = 0.0045; tPCNA = 2.93, P = 0.0051). CONCLUSIONS: LOH on chromosome 22 is a frequent event in the tumorigenesis of sporadic schwannoma. And, there is a correlation between LOH on chromosome 22 and proliferative activity in schwannoma. The frequency of LOH in vestibular schwannoma is significantly different from that in spinal schwannoma. (+info)