Objective: The coexistence of granulomatous inflammation and astrocytoma is extremely rare. Hemostatic agents are used to control intraoperative bleeding in many surgical subspecialties, including neurosurgery. There are occasional reports of granulomatous reaction to biomaterials. Method: We aimed to present a 35 year old female patient, who was operated because of the tumor at left frontoparietal region. Tumor was histopathologically reported as oligoastocytoma. However, no granulomatous inflammation was detected beside the tumor. After 6 months, patient was reoperated because of tumor recurrence, abscess and inflammatory necrotic tissue beside the tumor. Histopathologically, gemistocytic astrocytoma with granulomatous inflammation and abscess formation was reported. No micro-organism had grown in any kind of cultures. At our neurosurgery department surgicel is used after craniotomy as hemostatic agent. It's raw material is cellulose and absorbed in about 3 months. Results: In the literature, germinoma accompanied by granulomatous inflammation have been reported. However, astrocytic tumors don't express such an association. The patient doesn't use any drugs forming granuloma reported in the literature. Conclusion: We encountered that Surgicel causing granulomatous inflammation in very few cases in the literature. The findings might be secondary to surgicel that used in the first operation. Objective: Astrocytic tumors show various molecular and genetic alterations in its development and progression. Glioblastoma multiforme (GM) develops as either de novo or by progression from diffuse astrocytomas (DA) or anaplastic astrocytomas (AA) by genetic alterations. Method: Loss of heterozygosity (LOH) and microsatellite instability (MSI) was investigated in 40 cases of astrocytic tumors (DAs [n=12], AAs [n=15] and GMs [n=13]) with 14 microsatellite markers and 5 microsatellite markers harboring p53 and PTEN, respectively. The patients' age ranged from 27 to 77 years (mean, 50 years). Results: LOH was statistically significant in AAs and GMs, compared to that of DAs (p=0.023). LOH for 17p13 and LOH-H group for 10q23 were statistically significant in AAs and GMs (p=0.045 and p=0.001). MSI rate in DAs, AAs and GMs was detected in 16.7 %, 13.3 %, 23.1 %, but it showed no significant correlation with prognosis factors. MSI and MSI-H rates were correlated with younger (〈50 years) group (p= 0.040, p=0.011, respectively). Conclusion: Alterations on PTEN and p53 may contribute to the development and progression of astrocytic tumors. Especially, LOH-H for 10q23 and 17p13 is considered as clinical application of discriminating the AAs and GMs from DAs. MSI might be involved in the tumorigenesis of relatively young patients. Objective: Charcot-Marie-Tooth disease (CMT) III or Dejerine-Sottas syndrome is a severe hereditary demyelinating motor and sensory neuropathy presenting in infancy or early childhood with delayed motor milestone and extremely slow nerve conduction velocities. Method: Among 530 unrelated Korean CMT patients, mutational screen for well known CMT genes reveals three patients with PMP22 de novo mutation showing DSS. The histopathological findings of distal sural nerves are analyzed in all patients twice; Cases 1 and 2 with 10 years interval and Case 3 with 17 years. Results: On semi-thin transverse sections, all the remaining axons (thinly myelinated or demyelinated) are surrounded by classic or basal lamina onion bulbs (OBs). The first biopsy of Case 1 (2 years-old) shows OBs (4,452/mm2), which consists of 2,295 (51.55 %) MFs with OBs and 2,157 (48.45 %) demyelinated axons with OBs. The second biopsy shows OBs (2,275/mm2), consisting of 425 (18.68 %) MFs with OBs, 489 (21.49 %) demyelinated axons with OBs, and 957 (42.07 %) OBs with no discernible axons. Cases 2 and 3 show similar histopathologic findings with main differences in numbers of OBs. Conclusion: Although the differences noted in two biopsies are probably due to age of the patients, correlations with clinical symptoms will be helpul for management of the patients. Objective: Two mutations of the seipin gene (N88S and S90L) have been reported and known to cause neurodegenerative disorders. We performed whole exome sequencing in two Charcot-Marie-Tooth families and identified three patients with two causative heterozygous mutations (N88S and S90W) and S90W is a novel mutation. Method: The histopathological findings of distal sural nerves are analyzed in two patients (Cases 1 and 2) with S90W novel mutation (FC305) and a patient (Case 3) with N88S mutation (FC51). Results: Transverse semi-thin sections reveal increased numbers of myelinated fibers (MFs) (11,898/mm2; 11,429/ mm2; 9,430/mm2) with increased small MFs forming regenerative axon clusters and loss of large MFs. Histogram shows unimodal distribution pattern. Cases 1 and 2 show the similar ranges and average of diameter of MFs (1.461 3.24 μm, 5.13 μm). Case 3 shows more numbers of small MFs (0.82~10.50 μm, 3.73 μm). Ultra-structural examination reveals MFs with myelin abnormalities, pseudo-onion bulb formation including single axon or axon clusters, and thick MFs. Conclusion: The findings are consistent with axonal neuropathy with features of demyelination. Additional cases will be necessary to know the significance of differences between these cases.