Focal Dysplasia Research Articles

Reporting the Rarest of Rare! Duodenal Adenocarcinoma in a Patient with Prior Rectal Adenocarcinoma

Multiple GI malignancies in the same patient have been reported in literature. However, metachronous duodenal adenocarcinoma in a patient with prior rectal adenocarcinoma has been very rarely described. 50 year old black male with PMH of SCC head and neck status post radiation therapy underwent a colonoscopy for positive FOBT. Findings included an ascending colon polyp (tubular adenoma with focal surface high grade dysplasia - unclear margins), a splenic flexure polyp (tubular adenoma with focal surface high grade dysplasia, extending within 1 mm of the cauterized margin) and a rectal polyp (consistent with invasive, moderately differentiated adenocarcinoma extending into the submucosa). PET scan was negative for nodal or distant metastasis. EUS revealed stageT2 N0 disease. Patient was referred for surgery to a different hospital. Repeat colonoscopy showed residual ascending colon polyp (benign pathology). Biopsies from prior rectal polypectomy site were benign. EUS did not reveal any rectal lesion or lymphadenopathy. In light of discordant EUS findings, the patient and surgeon opted for transanal minimally invasive laparoscopic resection of rectal lesion for diagnostic and therapeutic purposes. Pathology revealed focal adenomatous change with negative margins. A month later the patient was re-admitted with nausea, vomiting, abdominal pain and poor oral intake. CT abdomen was normal. EGD was unremarkable till the second portion of duodenum. A small bowel follow through showed markedly dilated stomach and duodenum with a transition point at the ligament of Treitz. Push enteroscopy revealed an obstructing polypoid mass in third portion of duodenum. Biopsies were consistent with invasive adenocarcinoma. Whipple's procedure was performed. Two months later, he returned with similar symptoms. CT abdomen revealed innumerable metastases to liver, lymphadenopathy, and phlegmonous inflammatory changes within abdomen. Patient elected home hospice. Because of their rarity, indifferent symptomatology, and diagnostic elusiveness, small bowel tumors are often missed or diagnosed and treated late in their course with correspondingly poor results. The diagnostic difficulty is compounded when these tumors arise metachronously in patients with treated colorectal cancers. High index of suspicion coupled with effective communication between gastroenterologists, radiologists, surgeons and pathologists is essential in appropriate management of these patients.

A Rare Plug in the Pipe: Intraductal Tubular Adenoma of the Pancreas

Background: Intraductal lesions of the pancreas are uncommon but increasingly recognized because of advances in radiological technology. Intraductal tubular (IT) adenoma are extremely rare and are incompletely understood. These lesions have similar clinical, and radiological presentations and therefore a definitive histological diagnosis is crucial for appropriate management, surveillance and outcomes. Case: A 79-year-old man presented with abdominal discomfort. Contrast CT of the abdomen revealed a 1.7x2.2 cm pancreatic body mass with upstream ductal dilation concerning for a pancreatic neoplasm. Endoscopic ultrasound demonstrated a 1.8 cm x 2.1 cm intraductal mass in the body of the pancreas with upstream ductal dilation suspicious for a main duct IPMN with mural nodularity. FNA revealed ductal epithelium without dysplasia or malignant cells. Extracellular mucin was present. He underwent a distal pancreatectomy and splenectomy. Surgical pathology (Image 3) was consistent with IT adenoma, pyloric gland type with mild dysplasia and a minor component of IPMN with focal moderate dysplasia. His postoperative course was unremarkable. Discussion: Pancreatic intraductal tumors are divided into IPMNs and IT neoplasms. IT neoplasms are further divided into IT adenoma and IT carcinoma as based on histological epithelial atypia that is present. IT adenomas have no gender predilection and the lesions occur in those within the 5th to 7th decade of life. Most patients are asymptomatic or have nonspecific symptoms. Imaging can show a dilated duct with filling defect and varying amounts of mucin. EUS may show a protruding/nodular mass, which is regarded as a malignant feature in lesions like IPMN. Grossly, they appear polyploid, often occluding the lumen resulting in cystic dilation of the duct. Histologically, ITAs have epithelial lining, which is columnar with apical mucin and basally oriented nuclei, which show low-grade cytological atypia. ITAs share similarities with IPMN. They have similar Mucinex brush and profiles, which include MUC6 and MUC5AC. They may also share common mutations of GNAS and KRAS. However, there is a difference, which may help to differentiate ITA from IPMN. ITA pyloric type lesions tend to occur in the main pancreatic duct whereas gastric type IPMNs are mainly in the branch ducts. Limited information exists on intraductal lesions such as IPMNs, ITAs and ITCs. Appropriate workup will help with accurate diagnosis, management and surviellance.Figure 1

A Rare Case of Biliary Intraepithelial Neoplasia Presenting as Biliary Stricture

Introduction: Cholangiocarcinoma (CC) of the intrahepatic and extrahepatic biliary tree develops through a step-wise histopathological sequence that is preceded by premalignant neoplastic lesions. The two major precursors to invasive cholangiocarcinoma are biliary intraepithelial neoplasia (BilIN) and intraductal papillary neoplasm of the bile duct (IPNB). A better understanding of the mechanism of malignant transformation of biliary epithelium into CC and early identification of precursor lesions is important in order to improve long term survival. Case: A 64 year old male presented for evaluation of jaundice and generalized malaise of three weeks duration. He reported subjective weight loss and anorexia, but denied abdominal pain or diarrhea. Physical exam was remarkable for jaundice and icterus. Lab studies were significant for elevated liver chemistry consistent with obstructive cholestasis. Tumor markers, hepatitis and autoimmune profile were normal. Abdominal ultrasound and MRCP revealed intrahepatic and extrahepatic biliary ductal dilatation, with CBD measuring 9 mm at the level of the porta hepatis with abrupt narrowing and a biliary stricture and no evidence of gallstones or choledocholithiasis. Patient underwent exploratory laparotomy with cholecystectomy, common bile duct resection, Roux-en-Y hepaticojejunostomy with jejunojejunostomy. Histopathology results showed segment of bile duct with focal low-grade dysplasia (BilIN 1), and focal acute and chronic inflammation. Discussion: BilIN refers to microscopic flat or low-papillary dysplastic lesions, often seen in association with primary sclerosing cholangitis, hepatolithiasis and choledochal cysts. BilIN is further graded based upon the degree of cellular and structural atypia: BilIN-1, BilIN-2 and BilIN-3. The natural history of BilIN, its progression to invasive CC and treatment guidelines are not fully characterized. The lesions are mostly asymptomatic, unless they enlarge to cause biliary obstruction, thus making early recognition challenging. Furthermore, radiological recognition of early precancerous lesions is not feasible, unless associated with biliary stricture, as in our case. If detected early, patient can benefit from early curative surgery.Figure 1Figure 2

Poorly cohesive cell (diffuse-infiltrative/signet ring cell) carcinomas of the gallbladder: clinicopathological analysis of 24 cases identified in 628 gallbladder carcinomas

Signet ring cell carcinoma is an extremely rare type of gallbladder carcinoma. In the gastrointestinal system, carcinomas with single-cell or cord-like infiltration, previously called “diffuse-infiltrative” type or “signet ring cell,” are now designated as “poorly cohesive cell” (PCC) type (regardless of with/without signet ring cells) in the World Health Organization 2010 classification. Six hundred twenty-eight primary invasive gallbladder carcinomas were reviewed for the PCC pattern. Twenty-four cases in which classical PCC pattern constituted greater than 50% of the tumor were included in the study. The mean age was 63 (range, 44-84) years. A strong female predominance was present (female/male ratio, 6.3 versus 3.9 for all gallbladder carcinomas). Most cases (79%) had advanced carcinoma (pT3+) in comparison with 51% of usual carcinomas (P < .01). All cases (100%) showed at least focal signet ring morphology (intracytoplasmic mucin), and this was predominant in 50%. Twelve cases (50%) demonstrated a focal invasive glandular component of the usual type. Overlying focal high-grade dysplasia was identified in 11 (46%). Due to block loss, immunohistochemistry could be performed in only 5 cases and revealed a profile similar to upper gastrointestinal carcinomas CK7++/CK20−+/CDX2+−/p53+−. E-cadherin was decreased in the PCC component of all cases. The clinical course appeared to be more aggressive than ordinary gallbladder carcinomas, with median survival of 3.3 months versus 11.8 months, which did not reach statistical significance (P = .06 by log-rank test). In conclusion, PCC carcinoma originating in the gallbladder should be kept in mind for the differential diagnosis of disseminated poorly differentiated carcinomas in the abdomen.

Cytopathologic Herpes Simplex Virus Features In Laryngeal Squamous Cell Carcinoma

Cytopathologic Herpes Simplex Virus Features In Laryngeal Squamous Cell Carcinoma

Rare case of gallbladder papiloma in children

Abstract The incidence of villous papilloma of the gallbladder is rarely found amongst children. We report on a 9-year old girl known case of metachromatic leukodystrophy presented with abdominal distension. A radiological examination revealed massive ascites and a papillary mass branching and projecting through the gallbladder fundus. Furthermore, a histopathological examination of the gallbladder showed villous papilloma with focal high-grade dysplasia and a single gallbladder stone. This report describes the rare presentation of a child with metachromatic leukodystrophy in the form of gallbladder polyp, intractable ascites, and a gallbladder stone.

Dysplasie fibromusculaire des artères rénales

Fibromuscular dysplasia is non-atherosclerotic, non-inflammatory disease of the medium caliber arteries causing segmental stenosis, and sometimes aneurysm and/or dissection. Renal involvement is either asymptomatic or revealed by hypertension, rarely acute complications (renal infarction/hemorrhage). Cross-sectional imaging or angiography differentiates multifocal fibromuscular dysplasia (pearl necklace appearance) and focal fibromuscular dysplasia (tubular stenosis). Several differential diagnoses are to be mentioned. Carotid and vertebral involvement are possible. Smoking cessation must be encouraged. Selected patients benefit from renal revascularization. The best indications are recent or resistant hypertension, and progressive renal atrophy. Angioplasty without stent revascularization is the technique of choice in purely stenotic forms.

Focal cemento-osseous dysplasia of mandibular jaw: A case report and literature review

Introduction: Focal cemento-osseous dysplasia is a rare disease entity characterized by replacement of healthy bone and tissue with cemento-osseous tissue. Etiology and pathogenesis for the lesion is unknown and these lesions are considered as reactive lesion in the periapical areas of the teeth. Case Report: A 52-year-old female reported to Yogita Dental College and Hospital with the chief complaint of throbbing intermittent pain and swelling in the lower left posterior region of the jaw since six months. Conclusion: The lesions are benign in nature and rarely cause complication. Most of the time lesion is detected accidently on the routine radiographs. Treatment involves long-term follow-up of the case unless until lesion becomes symptomatic.

Correction in focal cemento osseous dysplasia

Correction in focal cemento osseous dysplasia

Total Esophagectomy and Endoscopic Radiofrequency Ablation for a Case of Diffuse Esophageal Papillomatosis: Case Report

Esophageal squamous papilloma (ESP) is a benign epithelial lesion. ESP is extremely rare and it has been described in few cases in literature. The etiology of ESP may be associated to chronic mucosal irritation and HPV infection. It is usually asymptomatic and mostly discovered as an incidental finding during upper gastrointestinal endoscopy. It is considered a benign neoplasia but recent reports have stressed the potential malignant evolution of these lesions. A 53 year old caucasian woman presented with a four years history of disphagia not responsive to medical therapy. At upper endoscopy, esophageal mucosa appeared hyperemic and completely covered by numerous (>100) sessile peduncolate papules. Biopsies demostrating atypical epithelial proliferation confirmed the diagnosis of esophageal squamal papillomatosis with low grade and focal high grade dysplasia; in situ hybridization studies for HPV were perfomed and it was positive for the type 16. We report a case of diffuse esophageal papillomatosis with histologic and microbiologic findings of genotype 16 HPV and Lichen Planus infection successfully treated with an Ivor Lewis Esophagectomy and a second look endoscopy by radiofrequency ablation.

Magnetic Resonance Imaging of Malformations of Midbrain-Hindbrain.

We aim to review the magnetic resonance imaging appearance of malformations of midbrain and hindbrain. These can be classified as predominantly cerebellar malformations, combined cerebellar and brain stem malformations, and predominantly brain stem malformations. The diagnostic criteria for the majority of these morphological malformations are based on neuroimaging findings. The predominantly cerebellar malformations include predominantly vermian hypoplasia seen in Dandy-Walker malformation and rhombencephalosynapsis, global cerebellar hypoplasia reported in lissencephaly and microlissencephaly, and unilateral cerebellar hypoplasia seen in PHACES, vanishing cerebellum, and cerebellar cleft. Cerebellar dysplasias are seen in Chudley-McCullough syndrome, associated with LAMA1 mutations and GPR56 mutations; Lhermitte-Duclos disease; and focal cerebellar dysplasias. Cerebellar hyperplasias are seen in megalencephaly-related syndromes and hemimegalencephaly with ipsilateral cerebellomegaly. Cerebellar and brain stem malformations include tubulinopathies, Joubert syndrome, cobblestone malformations, pontocerebellar hypoplasias, and congenital disorders of glycosylation type Ia. Predominantly brain stem malformations include congenital innervation dysgenesis syndrome, pontine tegmental cap dysplasia, diencephalic-mesencephalic junction dysplasia, disconnection syndrome, and pontine clefts.

''Muhtemel Ortodontik Kuvvetler Nedeni ile Meydana Gelmiş Fokal Siman-Osseöz Displazi'' ile İlgili Yorumlar

''Muhtemel Ortodontik Kuvvetler Nedeni ile Meydana Gelmiş Fokal Siman-Osseöz Displazi'' ile İlgili Yorumlar

Unusual incidental findings on intra- and extra-oral radiographs in North Indian Population: A radiographic study

Aims and Objectives: To detect the prevalence of unusual incidental findings on intra- and extra-oral radiographs in North Indian Population: A radiographic study. Methods: All the intra- and extra-oral conventional dental radiographs were analyzed for the period of 2 year along with the radiographic findings related to patient's chief complaint. Results: A total of 6780 conventional intra- and extra-oral dental radiographs were screened and 90 radiographs showed incidental findings. A total of 10 varieties and 95 numbers of incidental findings were noted, 50 (55.55%) affected mandible, and 24 (44.44%) affected maxilla. Out of 90, 44 (48.88%) were bony findings and 46 (51.11%) were dental findings. Most common type of incidental pathology was idiopathic osteosclerosis. The most uncommon type of incidental pathology was regional odontodysplasia with 35 (38.88%), 25 (27.77) cases of cysts, 16 cases of supernumerary teeth (17.77%), 9 (10%) cases of sinus abnormality, 4 (5.40%) of each findings were of odontome, dense in dente, internal resorption, and calcifications. About 1 (1.11%) of each findings were regional odontodysplasia, focal cemental dysplasia. Conclusions: Conventional radiography is still most commonly used tool to primarily investigate lesions quickly with low cost to patient and then further diagnostic and advanced radiological or other examinations can be performed for comparison, periodic follow up, management, and research purposes.

Focal cemento-osseous dysplasia of maxillary posterior region

Benign fibro-osseous lesion of the craniofacial complex is a broader term representing various diseases that are characterized by replacement of normal bone with hypercellular fibroblastic stroma with varying amount of pathologic ossifications and calcifications. Focal cemento-osseous dysplasia is of uncertain etiopathogenesis, with reactive and dysplastic processes as the suggested underlying mechanisms. The present case was unusual due to the involvement of maxillary posterior region in a young female which presented as bony enlargement.

Mucin1 expression in focal epidermal dysplasia of actinic keratosis.

Actinic keratoses (AKs) are generally considered as premalignant skin lesions that can progress into squamous cell carcinoma (SCC) in situ and invasive SCC. However, its progression to SCC is still matter of debate. A transmembrane glycoprotein that contributes to the progression of certain premalignant and malignant lesions is mucin1 (MUC1). Nevertheless, their functions in the skin lesions are not yet fully clear. Therefore, the aim of this study is to ascertain whether MUC1 is present in the focal epidermal dysplasia of AK. Fourteen skin biopsies from patients diagnosed with AK were selected. They were classified according to the degree of dysplasia in keratinocyte intraepidermal neoplasia (KIN) I, KIN II, and KIN III. In five biopsies the three degrees were present, in two biopsies both KIN I and KIN II, in four biopsies only KIN I, and in three biopsies only KIN III. The presence of MUC1 was assessed by immunofluorescence staining using confocal laser scanning microscopy. Immunostaining revealed that MUC1 was present over the entire cell surface of only a few atypical basal keratinocytes confined to the lower third of the epidermis (KIN I). While in KIN II where atypical keratinocytes occupy the lower two thirds, MUC1 was localized at the apical surface of some atypical keratinocytes and over the entire cell surface of some of them. Interestingly, in KIN III where the atypical keratinocytes extend throughout the full thickness, MUC1 was localized at the apical surface and over the entire cell surface of many of these cells. Conversely, MUC1 expression was not detected in the epidermis of normal skin. Our findings suggest that the expression of MUC1 in AK would be induced by alteration of keratinocyte stratification and differentiation and associated to the degree of dysplasia rather than the thickness of the epidermis.

Mutational spectrum of intraepithelial neoplasia in pancreatic heterotopia

Heterotopic pancreatic parenchyma recapitulates the normal pancreas in extrapancreatic locations and, on rare occasions, can even give rise to pancreatic adenocarcinoma. The genetic signatures of pancreatic adenocarcinoma and its precursor lesions are well characterized. We explored the genetic alterations in precursor lesions (intraductal papillary mucinous neoplasms [IPMN], pancreatic intraepithelial neoplasia [PanIN]) in patients with pancreatic heterotopias but without concomitant pancreatic ductal adenocarcinomas. This allowed us to determine whether the stereotypical dysplasia--infiltrating carcinoma sequence also occurs in these extrapancreatic foci. Seven cases of heterotopic pancreas with ductal precursor lesions were identified. These included 2 IPMNs with focal high-grade dysplasia and 5 PanINs with low- to moderate-grade dysplasia (PanIN grades 1-2). Neoplastic epithelium was microdissected and genomic DNA was extracted. Sequencing of commonly mutated hotspots (KRAS, TP53, CDKN2A, SMAD4, BRAF, and GNAS) in pancreatic ductal adenocarcinoma and its precursor lesions was performed. Both IPMNs were found to have KRAS codon 12 mutations. The identification of KRAS mutations suggests a genetic pathway shared with IPMN of the pancreas. No mutations were identified in our heterotopic PanINs. One of the possible mechanisms for the development of dysplasia in these lesions is field effect. At the time of these resections, there was no clinical or pathologic evidence of a prior or concomitant pancreatic lesion. However, a clinically undetectable lesion is theoretically possible. Therefore, although a field effect cannot be excluded, there was no evidence for it in this study.

Safety and Efficacy of Dynamic Submucosal Injection Technique for the Mucosal Resection of Large Colorectal Neoplasia

Introduction: Endoscopic mucosal resection (EMR) of large colorectal polyps is efficacious and safe with the selection of the appropriate polyp and resection technique. Several studies have demonstrated the short and long term efficacy of EMR. Several techniques have been used to improve the efficacy and to minimize complications. Submucosal injection has been conventionally used to create a submucosal bleb that facilitates snaring the lesion off. Dynamic submucosal injection (DSI) technique employs several steps including adjusting the angle of the injecting needle, moving the needle while injecting in a path that is envisioned by the endoscopist, applying suction, and rapidly injecting the solution. We present our experience with the use of DSI technique in resecting large colorectal polyps. Results: We have performed 101 EMRs on 82 patients with a mean age of 65 years (60% males) between August 2013 and November 2014. The mean polyp size was 29mm (range 15-60mm). The mean procedure time was 57 minutes. 64% of the lesions were in the right colon. Histopathology showed tubular adenoma with low grade dysplasia (TA-LGD) (n=50), sessile serrated adenoma (n=26), tubulovillous adenoma (n=9), tubulovillous adenoma with focal high-grade dysplasia (n=6), tubular adenoma with focal high-grade dysplasia (n=4), intramucosal adenocarcinoma (n=2), invasive submucosal adenocarcinoma (n=3), and Maltoma (n=1). Complete removal was achieved in all cases and lesions were removed en bloc 30% of the time. A mean of 38ml of normal saline (with indigo carmine) was injected. Argon plasma coagulation was used in 73% of the resections with mucosal defect closure with endoclips performed in all. Complications included bleeding (n=1), postpolypectomy syndrome (n=1), and postprocedure emesis (n=1). In the twenty five patients that have undergone follow up colonoscopies so far, we have found 2-3mm residual polyp tissue (TA-LGD), only in 3 patients (10%). One of the intramucosal adenocarcinoma lesions underwent surgical resection as margins were involved. The other intramucosal lesion was removed en bloc with unremarkable computed tomography scan and rectal ultrasound and no recurrence on follow up. Of the three patients with invasive submucosal adenocarcinoma, two had subsequent colectomy with no residual cancer and negative lymph nodes. Discussion: DSI technique for endoscopic mucosal resection of large colorectal lesions is efficacious and safe.

Endoscopic balloon-based radiofrequency ablation for long-segment early esophageal squamous cell neoplasia

Summary Esophageal cancer is a common and highly lethal disease. In the Asia-Pacific region, esophageal squamous cell neoplasias are the major forms of the disease. Recent advances in endoscopic therapy enable curative treatment of early esophageal squamous cell neoplasias, however, the technique is complicated and requires a high level of expertise, especially for those with long-segment lesions. Endoscopic radiofrequency ablation is a rapidly evolving treatment modality and has been shown to have good efficacy and safety for the treatment of dysplasia in cases of Barrett’s esophagus. Theoretically, it can also be used to treat squamous dysplasia. We report a case of a 48-year-old man with an 8-cm-long circumferential squamous high-grade dysplasia over the esophagus (from 21 cm to 29 cm below the incisor) that was treated successfully and safely with balloon-based radiofrequency ablation. The procedure took only around 30 minutes to complete. There were no major adverse events during and after the procedure. In addition, we examined the histology of the esophageal coagulum, which showed an extensive cauterization effect with focal dysplasia within the ablated epithelium. Follow-up endoscopy at 1 month, 3 months, and 6 months showed no residual lesion, and biopsies also confirmed complete remission.

Case Presentation of Concomitant and Contiguous Adenomatoid Odontogenic Tumor and Focal Cemento-Ossifying Dysplasia.

A 24 year-old male was presented for the diagnosis of an asymptomatic bony expansion in relation to the right maxillary canine and first premolar. The unilocular radiolucent lesion with central foci of calcification had caused divergence of canine and first premolar roots without any resorption. This case report details a diagnosis of two distinct disease processes of different cellular origin namely, focal cemento-ossifying dysplasia and adenomatoid odontogenic tumor in a previously unreported concomitant and contiguous relationship. The diagnosis was determined by a combination of clinical, radiographic, histopathological and surgical evidence. This case highlights two points, first the need to examine all mixed radiolucent-radiopaque lesions with advanced imaging techniques to assess the number and extent of the lesions prior to treatment planning. Second a likely role of periodontal ligament as the tissue source for odontogenic epithelial cells and mesenchymal stem cells required for the development of odontogenic tumors and cemento-osseous dysplasias.

V26. Three dimensional tracking of ion channels on epileptogenic cortical neurons in focal dysplasia in humans

Background About 20 Percent of children with focal epilepsy will be pharmacoresistant ( Wirrell, 2013 ). Especially children with imaging abnormalities are most likely to be unresponsive to anti epileptic drug treatment. A significant number of abnormalities are due to focal cortical dysplasia. These focal epilepsies remain a major challenge to modern neuro-pediatrics and epileptic drug treatment. The mechanisms leading to a raised excitability in the dysplastic cortical tissue and its surrounding -the zone of irritation- is hardly understood. It is well known that the surface of neurons is packed with ion channels. These channels critically determine the firing pattern of the cell. The electro-chemical behavior of the cell is determined by the molecular structure of the channels, the quantities of ion channels and the exact distribution of the channels on the neuronal surface. It was recently shown in rodents that the distribution of A-Type Potassium channels is altered on pyramidal cells in proximity to an epileptogenic cortical lesion. A further class of channels which are possibly altered in cortical lesions are calcium channels. In the literature ( Poolos and Johnston, 2012 ) a compelling evidence exists linking T-type calcium channels to seizure generation. However no rigorous study was conducted to investigate if the distribution of T-type channels is altered in structural epilepsy. This altered distribution of ion channels might contribute to the raised excitability of neurons in epileptogenic cortical areas.In our hospital we look after children with structural epilepsy. Some children with epilepsy are treated by surgical resection of the lesion. In our study we use the resected tissue after neuropathological assessment for further analysis.The aim of the study is to analyse the resected tissue with respect to the ion channel distribution and to compare the results with the results obtained from normal brain tissue. Children typically have a much shorter history of antiepileptic drug treatment before they undergo epileptic surgery. Therefore the effect of medication on the ion channel distribution is assumed to be limited. In recent years we have developed a method that allows the reconstruction of the geometry of the neurons and further the tracing of the distribution of specific ion channels along the dendritic arbor ( Ginger et al., 2013 ). We could show that the method is able to quantify the distribution of specific ion channels along the dendritic surface. We are specifically interested in layer V pyramidal neurons from temporal or frontal cortical areas which are most homogeneous in terms of ion channel distribution. In our study the distribution of A-type potassium and T-type calcium channels of pyramidal neurons from epileptogenic tissue is compared to unaltered neuronal tissue from children undergoing tumor resection (access tissue). We are now in a process of systematic clinical characterization of patients and consecutive tissue collection.