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Suboccipital retrosigmoid craniotomy with removal of posterior wall of internal auditory canal is preferred by many surgeons operating on acoustic neuromas, as it is a simple and safe approach. To study the topographic landmarks of the posterior surface of the temporal bone. We studied the surgical anatomy of 224 dry adult human temporal bones, measured the various distances on posterior wall of petrous bone relevant for suboccipital surgical approach to internal auditory canal. The internal auditory canal (IAC) lies within 32-44 mm from posterior wall of sigmoid sulcus and within 3-8 mm from the superior border of petrous bone. The point corresponding to highest point of jugular bulb was found between 4 and 9 mm away from the inferior border of IAC. The maximum distance found between bony orifice of vestibular aqueduct and IAC was 14 mm and the minimum distance was 6 mm.The vertical diameter of IAC ranged between 3 and 7 mm. These parameters may help the surgeons for better exposure of internal auditory canal and for avoiding damage to vital surrounding structures.

Background: Hemophilia B (HB) is an X-linked bleeding disorder resulting from coagulation factor IX (FIX) defects. Over 3,000 pathogenic, HB-associated mutations in the F9 gene have been identified. We aimed to investigate the role of F9 variants in 150 HB patients using sequencing technology.Methods: F9 gene sequences were amplified from peripheral blood-derived DNA and sequenced on an Applied Biosystems (ABI) 3500 Sanger sequencing platform. Functional and structural predictions of mutant FIX were analyzed.Results: Among 150 HB patients, 102 (68%), 30 (20%), and 18 (12%) suffered from severe, moderate, and mild HB, respectively. Genetic analysis identified 16 mutations, including 3 novel mutations. Nine mutations (7 missense and 2 stop-gain) were found to be pathogenic. Only 3 mutations (c.127C>T, c.470G>A, and c.1070G>A) were associated with different severities. While 2 mutations were associated with mild HB cases (c.304C>T and c.580A>G), 2 (c.195G>A and c.1385A>G) and 3 mutations (c.223C>T, c.1187G>A, and c.1232G>A) resulted in moderate and severe disease, respectively.Additionally, 1 mutation each was associated with mild-moderate (c.*1110A>G) and mild-severe HB disease (c.197A>T), 4 mutations were associated with moderate-severe HB cases (c.314A>G, c.198A>T, c.676C>T, and c.1094C>A). FIX concentrations were lower in the mutated group (5.5±2.5% vs. 8.0±2.5%). Novel p.E66D and p.S365 mutations were predicted to be pathogenic based on changes in FIX structure and function. Conclusion:Novel single nucleotide polymorphisms (SNPs) largely contributed to the pathogenesis of HB. Our study strongly suggests that population-based genetic screening will be particularly helpful to identify risk prediction and carrier detection tools for Indian HB patients.