The classification of central nervous system tumours has more recently been shaped by a focus on molecular pathology rather than histopathology. We re-classified 82 glial tumours according to the molecular-genetic criteria of the 2016 revision of the World Health Organization (WHO) Classification of Tumours of the Central Nervous System. Initial diagnoses and grading were based on the morphological criteria of the 2007 WHO scheme. Because of the impression of an oligodendroglial component on initial histological assessment, each tumour was tested for co-deletion of chromosomes 1p and 19q and mutations of isocitrate dehydrogenase (IDH-1 and 2) genes. Additionally, expression of proteins encoded by alpha-thalassemia X-linked mental retardation (ATRX) and TP53 genes was assessed by immunohistochemistry. We found that all but two tumours could be assigned to a specific category in the 2016 revision. The most common change in diagnosis was from oligoastrocytoma to specifically astrocytoma or oligodendroglioma. Analysis of progression free survival (PFS) for WHO grade II and III tumours showed that the objective criteria of the 2016 revision separated diffuse gliomas into three distinct molecular categories: chromosome 1p/19q co-deleted/IDH mutant, intact 1p/19q/IDH mutant and IDH wild type. No significant difference in PFS was found when comparing IDH mutant grade II and III tumours suggesting that IDH status is more informative than tumour grade. The segregation into distinct molecular sub-types that is achieved by the 2016 revision provides an objective evidence base for managing patients with grade II and III diffuse gliomas based on prognosis.

The 2016 revision of the WHO Classification of Tumours of the Central Nervous System is based on a combination of morphology and molecular pathology.1 This change, from traditional morphology-based classifications, particularly affects glial tumours. Astrocytic and oligodendroglial tumours are grouped together as ‘diffuse gliomas’. Astrocytomas, i.e., diffuse astrocytoma, anaplastic astrocytoma and glioblastoma, are sub-typed according to the presence or absence of mutations of the isocitrate dehydrogenase genes (IDH 1&2) – IDH mutant or IDH wild type. A ‘Not Otherwise Specified’ (NOS) category is provided for situations where molecular testing is not available or molecular data are incomplete or inconclusive. A new entity, ‘Diffuse midline glioma H3 K27M mutant’ has been added. The diagnosis of oligodendroglioma is entirely based on co-deletion of the short arm of chromosome 1 (1p deletion) and the long arm of chromosome 19 (19q deletion) in combination with IDH mutation(s). There is no IDH wild type oligodendroglioma but a diagnosis of ‘Oligodendroglioma NOS’ can be made. The diagnosis of oligoastrocytoma is strongly discouraged. Most mixed tumours can be assigned to astrocytoma or oligodendroglioma based on IDH and chromosome 1p/19q alterations. Between August 2010 and June 2016, 82 glial tumours were tested for 1p and 19q deletions by fluorescence in situ hybridisation (FISH) because of the impression of an oligodendroglial component on histological examination. Each tumour was initially sub-typed and graded according to the 2007 WHO scheme.2 In addition, immunohistochemistry for IDH-1 R132H, ATRX and p53 was performed. We retrospectively applied the criteria of the 2016 revision to this cohort. We found that 80 tumours could be assigned to a specific category. The commonest change in diagnosis was from oligoastrocytoma. Of 41 tumours initially diagnosed as oligoastrocytoma, 16 were re-assigned to oligodendroglioma IDH mutant 1p/19q co-deleted, 18 to diffuse astrocytoma, 4 to anaplastic astrocytoma and 3 to glioblastoma IDH mutant. Two 1p/19q co-deleted/IDH wild type tumours were assigned to ‘Oligodendroglioma NOS’. We also noted that mutations of ATRX and p53 were mutually exclusive of 1p/19q co-deletion. These molecular alterations are informative in distinguishing astrocytoma from oligodendroglioma.

Kohlmeier-Degos disease is rare idiopathic vasculopathy, the exact pathogenesis of which remains unclear. Here, we review pertinent literatutre and present a case of a Kohlmeier-Degos disease with central nervous system involvement followed-up over 11 years with various neuroimaging modalities. Evolution of neurovascular and neuropathological changes over an extended time period has not been previously described. (C) 2017 Elsevier Ltd. All rights reserved.

Isocitrate dehydrogenase 1 (IDH1) mutations in gliomas have been associated with a frontal lobe location and a greater proportion of noncontrast-enhancing tumour (nCET). The purpose of our study was to validate the utility of MRI imaging features in predicting IDH1 mutations in glioblastomas. Pre-operative MRIs of new glioblastoma patients, consisting of at least FLAIR and T1-weighted post-contrast sequences, were reviewed by a neuroradiologist based primarily on the VASARI feature set. IDH1 mutation testing was performed on all patients using immunohistochemistry. 153 patients met the inclusion criteria, of whom five had IDH1 mutations (3.3%). A frontal lobe location had equivalent frequency in both the IDH1-mutated and IDH1-wildtype cohorts (p=1.000). Three (60%) of the IDH1-mutated tumours had >33% nCET, compared to 21% of IDH1-wildtype (p=0.073). 12 tumours had a frontal lobe epicentre and >33% nCET, all being IDH1-wildtype. All five IDH1-mutated tumours had either a frontal lobe epicentre or >33% nCET, but none had both these features. Our results question the strength of the association between frontal lobe glioblastomas with substantial nCET and IDH1 mutations, as these features are also relatively frequent in IDH1-wildtype tumours, which are much more common. MRI is thus more useful for ruling out an IDH1 mutation rather than strongly suggesting its presence: if a particular glioblastoma does not have a frontal lobe epicentre and has less than 33% nCET, it can be predicted to be IDH1-wildtype with a high degree of confidence.

In 1995 a 16-year old girl was diagnosed with a large left thalamic AVM that was considered unsuitable for microsurgical resection and was treated with radiotherapy twice, which led to angiographic cure. She re-presented 19 years after initial treatment with a symptomatic acute thalamic haemorrhage. Her digital subtraction angiography was negative for arterio-venous shunting. MRI/MRA showed cystic change with adjacent contrast enhancement in the region of the previously irradiated arteriovenous malformation. The patient underwent an interhemispheric transcallosal resection of the left thalamic haemorrhagic lesion via a contralateral craniotomy. Intra-operatively there was a cystic cavity filled with blood products in association with thrombosed, calcified vessels as well as actively filling vessels. Histologically there were aggregated abnormal blood vessels with a dilated lumen and surrounded by brain parenchyma. Some of the vessel walls were thickened with fibrosis and some were arterialised with presence of elastin fibres. Potential mechanisms for the delayed haemorrhage are discussed.

High-grade B-cell lymphomas with recurrent chromosomal break points have been termed 'double hit lymphoma' (DHL). The most commonly seen DHL is diffuse large B-cell lymphoma (DLBCL) with t(14;18) and t(8; 14) or t(8; 22) resulting in overexpression of BCL2 and MYC, respectively. The increased proliferation due to MYC overexpression, without the ability for an apoptotic brake as a result of BCL2 overexpression, results in 'the perfect storm of oncogenesis'. Thus this disease presents a number of diagnostic and therapeutic challenges for the hematologist. The first and foremost challenge is to recognize the DHL. As different morphological entities can be affected it is incumbent on pathologists and clinicians to maintain a high index of suspicion especially in disease that appears unusually aggressive or refractory to therapy. Diagnosis by fluorescence in situ hybridization (FISH) is a sensitive and specific method for detection of the disease but is time-consuming and expensive. While detection by immunohistochemistry (IHC) is sensitive and correlates with survival, standardized methods for this are not widely agreed upon. The second and equally important challenge in DHL is optimizing clinical outcome in a group of patients for whom the prognosis is widely regarded as poor. While improvements have been achieved by dose escalating standard chemotherapeutic regimens, many patients continue to do badly. Furthermore as a disease of aging many patients are unsuitable for dose-intensive chemotherapy regimens. There are now multiple novel targeted agents in various stages of clinical development that offer hope for better outcomes without undue toxicity. Among the most exciting of these developments include specific inhibitors of both BCL2 and MYC.

Gemistocytic astrocytoma is the second most common subtype of World Health Organization grade 2 astrocytoma, but has a worse prognosis than other grade 2 lesions. We aim to describe the MR imaging features of histopathologically proven gemistocytic tumours.

Ependymomas are glial series tumours that can occur throughout the neural axis, usually in close proximity to the ventricles or central canal. While the fourth ventricle is a common location for ependymoma, we present a rare case of an entirely intraparenchymal infratentorial tumour, remote from the ventricular surface, and discuss the imaging characteristics that may suggest the diagnosis. The histological features, which remain identical despite the varied morphology of intraventricular versus intraparenchymal tumours, are also considered.

Spinal angiolipomas are uncommon benign tumours composed of mature fatty tissue and abnormal vascular elements, most commonly found within the posterior spinal epidural space. Most tumours are located within the mid-thoracic spine; in contrast thoracolumbar junction and purely lumbar angiolipomas are rare. We report a case series of four spinal angiolipomas, including a thoracolumbar junction and a purely lumbar tumour.

Journal of Cutaneous PathologyVolume 43, Issue 6 p. 552-555 Letter to the Editor Rare skin manifestations successfully treated with primary B-cell chronic lymphocytic leukemia treatment Shu Min Wong, Shu Min Wong Department of Clinical Haematology and Bone Marrow Transplant Unit, The Royal Melbourne Hospital, Parkville, VIC, AustraliaSearch for more papers by this authorJeremy McComish, Jeremy McComish Department of Immunology and Allergy, The Royal Melbourne Hospital, Parkville, VIC, AustraliaSearch for more papers by this authorJo Douglass, Jo Douglass Department of Immunology and Allergy, The Royal Melbourne Hospital, Parkville, VIC, AustraliaSearch for more papers by this authorAlpha Tsui, Alpha Tsui shumin.wong@mh.org.au Department of Anatomical Pathology, The Royal Melbourne Hospital, Parkville, VIC, AustraliaSearch for more papers by this authorLynette Chee, Lynette Chee Department of Clinical Haematology and Bone Marrow Transplant Unit, The Royal Melbourne Hospital, Parkville, VIC, AustraliaSearch for more papers by this author Shu Min Wong, Shu Min Wong Department of Clinical Haematology and Bone Marrow Transplant Unit, The Royal Melbourne Hospital, Parkville, VIC, AustraliaSearch for more papers by this authorJeremy McComish, Jeremy McComish Department of Immunology and Allergy, The Royal Melbourne Hospital, Parkville, VIC, AustraliaSearch for more papers by this authorJo Douglass, Jo Douglass Department of Immunology and Allergy, The Royal Melbourne Hospital, Parkville, VIC, AustraliaSearch for more papers by this authorAlpha Tsui, Alpha Tsui shumin.wong@mh.org.au Department of Anatomical Pathology, The Royal Melbourne Hospital, Parkville, VIC, AustraliaSearch for more papers by this authorLynette Chee, Lynette Chee Department of Clinical Haematology and Bone Marrow Transplant Unit, The Royal Melbourne Hospital, Parkville, VIC, AustraliaSearch for more papers by this author First published: 21 April 2016 https://doi.org/10.1111/cup.12684Citations: 6Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Citing Literature Volume43, Issue6June 2016Pages 552-555 RelatedInformation

Pilomyxoid astrocytoma (PMA) is a recently recognised World Health Organization (WHO) Grade II tumour that was previously characterised as a subtype of the WHO Grade I pilocytic astrocytoma (PA). PMA has a histological appearance distinct from PA and a poorer prognosis due to its greater propensity for local recurrence and cerebrospinal dissemination. Although originally considered a paediatric tumour involving mainly the hypothalamic and chiasmatic region, reports of the lesion occurring in the adult population and other areas of the neuroaxis are emerging. We review the literature on PMA within the adult population and present the first case of PMA in the cerebellum of an adult female.

The purpose of this study was to add to the current body of literature which is aimed at establishing the role of postoperative adjuvant radiotherapy (RT) in the treatment of atypical and malignant meningiomas. Meningiomas are the most frequently reported primary intracranial tumours, accounting for more than 35%. The majority of meningiomas are benign, with atypical and malignant tumours accounting for only 6-18%. Utilising a prospective multi-institutional database, we retrospectively reviewed 67 patients with documented World Health Organisation (WHO) Grade II/III meningiomas, diagnosed between 1989 and 2012 and resected at two major Australian hospitals. Nine patients were excluded and the remaining 58 were analysed. The patient demographics, tumour characteristics, surgical details and adjuvant therapy were retrieved. Kaplan-Meier curves were used to compare the survival of patients treated with RT versus surgery alone. The 3 year progression free survival (PFS) and overall survival (OS) were 44 and 76% for the entire cohort, respectively. Of the patients who had gross total resections, 42% had 3 years PFS and 77% had 3 years OS, which was not significantly different from those with subtotal resection. The overall median survival was 11.0 years, 12.2 for atypical and 1.6 for malignant meningiomas. The patients with malignant meningiomas were 14 times as likely to receive RT as the patients with atypical meningiomas. The patients who received RT had a 3 year PFS of 63% compared to 40% in those who did not receive radiation. The 3 year OS was 31% higher for females than males. Histopathological progression was noted in 17% of our cohort. This study reinforces a number of important factors that should be considered when treating patients presenting with WHO Grade II and III meningiomas, including sex, potential for grade progression, and the lack of evidence for adjuvant RT and the timing thereof.

High-grade B-cell lymphomas with recurrent chromosomal break points have been termed ‘double hit lymphoma’ (DHL). The most commonly seen DHL is diffuse large B-cell lymphoma (DLBCL) with t(14;18) and t(8;14) or t(8;22) resulting in overexpression of BCL2 and MYC, respectively. The increased proliferation due to MYC overexpression, without the ability for an apoptotic brake as a result of BCL2 overexpression, results in ‘the perfect storm of oncogenesis’. Thus this disease presents a number of diagnostic and therapeutic challenges for the hematologist. The first and foremost challenge is to recognize the DHL. As different morphological entities can be affected it is incumbent on pathologists and clinicians to maintain a high index of suspicion especially in disease that appears unusually aggressive or refractory to therapy. Diagnosis by fluorescence in situ hybridization (FISH) is a sensitive and specific method for detection of the disease but is time-consuming and expensive. While detection by immunohistochemistry (IHC) is sensitive and correlates with survival, standardized methods for this are not widely agreed upon. The second and equally important challenge in DHL is optimizing clinical outcome in a group of patients for whom the prognosis is widely regarded as poor. While improvements have been achieved by dose escalating standard chemotherapeutic regimens, many patients continue to do badly. Furthermore as a disease of aging many patients are unsuitable for dose-intensive chemotherapy regimens. There are now multiple novel targeted agents in various stages of clinical development that offer hope for better outcomes without undue toxicity. Among the most exciting of these developments include specific inhibitors of both BCL2 and MYC.

Gangliogliomas are rare primary central nervous system tumours that characteristically contain both neuronal and glial neoplastic components. They usually present as solitary, slow growing tumours that are frequently associated with pharmacologically refractory epilepsy. Multicentric variants of the tumour are exceedingly rare. We report a 20-year-old patient with multiple gangliogliomas located in the right frontal, temporal and occipital lobes. He presented with headache, fatigue and occasional nausea and vomiting. MRI revealed three large, distinct tumours with striking cyst formation. Stereotactic craniotomy and excision of the temporal and occipital tumours confirmed ganglioglioma. The coincidence of three distinct gangliogliomas involving the right frontal, temporal and occipital lobes has not been reported to our knowledge.

The aim of the study was to determine the accuracy of rapid on-site examinations, performed on transbronchial brushings of peripheral pulmonary lesions, in determining final bronchoscopic diagnosis. In addition to determining if rapid on-site examination impacts procedural outcomes. A prospective cohort study of consecutive patients with peripheral pulmonary lesions, which had been located by radial endobronchial ultrasound, was undertaken. Bronchoscopy was terminated if rapid on-site examination demonstrated diagnostic malignant material. Non-diagnostic rapid on-site examination resulted in further bronchoscopic sampling, including transbronchial lung biopsy and/or sampling from different locations. 128 peripheral pulmonary lesions were located by endobronchial ultrasound in 118 patients. The final bronchoscopic diagnoses included nonsmall cell lung cancer (n=76), carcinoid (n=3), and metastatic malignancy (n=3). Procedure times were significantly shorter for procedures when rapid on-site examinations demonstrated malignancy compared to those where rapid on-site examination was non-diagnostic (19±8 min versus 31±11 min, respectively; p<0.0001). In four procedures, initial negative rapid on-site examination results prompted redirection of sampling from alternate bronchial segments, resulting in positive diagnostic tissue being obtained. Positive and negative predictive value of rapid on-site examination for a malignant bronchoscopic diagnosis was 63 (97%) out of 65, and 43 (68%) out of 63, respectively. Rapid on-site examination of brushing specimens has a very high, positive, predictive value for bronchoscopic diagnosis of cancer and shortens the bronchoscopy procedure times. It has the potential to reduce complications, improve cost-effectiveness, and may improve diagnostic performance via live feedback.

A 25-year-old Caucasian woman presented with headache, drowsiness, weight gain and discordant gaze palsy. She had no previous significant past medical history and was not on any regular medications. Her initial brain CT scan (Fig. 1A–C) demonstrated a large suprasellar region mass with cystic and solid enhancing components. Small foci of calcific density and fat density were also noted adjacent to the right posterior clinoid process. Obstructive hydrocephalus was present. Emergency ventricular shunting as well as shunting of the cystic component of the mass was performed which improved both her drowsiness and visual symptoms, and the patient proceeded to MRI (Fig. 1D–F). A.Cystic pituitary macroadenomaB.CraniopharyngiomaC.Dermoid cystD.Intracranial teratomaE.Epidermoid cyst Answer on page 1218. The authors declare that they have no financial or other conflicts of interest in relation to this research and its publication. Large suprasellar mass: answerJournal of Clinical NeuroscienceVol. 22Issue 7PreviewD. Intracranial teratoma Full-Text PDF

Kimura disease (KD) is a rare disorder, which predominantly affects young Asian males, characterized by firm painless subcutaneous nodules, typically located in the periauricular, parotid and submandibular regions. It has been rarely reported as involving the orbit or eyelid. Regional lymphadenopathy and eosinophilia is common and there is an association with renal disease. An elevated IgE sometimes occurs and the lesions can recur. We present a case involving the left upper eyelid in a 20-year-old ethnic Samoan man. He presented with a 5-year history of a left upper eyelid swelling. He had a previous diagnosis of Kimura disease based on an excisional biopsy of a right submandibular lump at age 10. At age 19 he also had a subcutaneous left elbow mass excised. His initial diagnosis and medical history, including that of nephrotic syndrome, has been previously reported. On presentation the patient reported a painless left upper lid mass, which increased in size with decreasing or missing his dose of cyclosporine, taken for remission maintenance of his nephrotic syndrome. The eye was occasionally irritated and watery. Despite 5 mm of inferior displacement of the globe, and 5 mm proptosis, the patient reported no diplopia or changes in his vision. He had a large, firm, non-tender mass in the left upper eyelid/orbit (Fig. 1) and a small left submandibular mass. The visual acuity in each eye was 6/4. The remainder of his ocular examination was normal. A CT of the orbits demonstrated a left superotemporal soft tissue orbital mass, arising from the lacrimal gland fossa (Fig. 2). The CT was otherwise normal. Given the significant orbital displacement, the patient was offered an excisional biopsy of the mass. Via an upper eyelid skin crease incision, an anterior orbitotomy was performed without complication and a 35 × 25 × 12 mm mass was excised (Fig. 3). The mass was pseudo-encapsulated and part of the palpebral lobe of the lacrimal gland was sacrificed to achieve total resection. Histology demonstrated lymphoid tissue with adjacent lacrimal gland. There were scattered lymphoid follicles with reactive germinal centres. The overall architecture showed expanded paracortex, containing prominent infiltrates of eosinophils, forming microabscesses. Occasional polykaryocytes were seen. The endothelial cells lining the blood vessels were not hobnailed, vacuolated or showing nuclear atypia. No fungi or parasites were identified. There were no Hodgkin or neoplastic Langerhans cells. The features were consistent with those of Kimura disease (Fig. 4). Review of the patient 5 months postoperatively demonstrated normal vision and a good cosmetic result (Fig. 1). This case presents many of the salient features of Kimura disease. He was young, male and Asian, although KD can occur in patients of any ethnicity. His condition was chronic, having had KD for over 10 years. He had lesions in very typical (submandibular) and less typical (elbow and orbit) locations, which followed an indolent course, waxing and waning with time. At the time of diagnosis, he had an elevated IgE and a marked

C. Schwannoma. Intra-operatively the lesion was invading parenchyma, the cystic cavity was filled with xanthochromic fluid and the mural nodule was moderately vascular, fibrous and durally based. Post-operatively the patient had no deficits and was discharged home. At 1 month follow-up the patient was well with intact lacrimation bilaterally and no further seizures. Histopathology revealed a moderately cellular tumour, surrounded by cerebral cortex. It contained fascicles of spindle cells with focal palisading with Verocay body formation corresponding to Antoni A areas. Antoni B areas with microcystic change were also seen (Fig. 1). The background contained hyalinised thickened blood vessels with foamy macrophages. The tumour cells were S-100 and nestin positive with very focal glial fibrillary acidic protein (GFAP) staining. The tissue was epithelial membrane antigen, progesterone receptor, CD34 and IDH-1 negative. Greater superficial petrosal nerve (GPSN) schwannoma is rare and an unusual cause of temporal lobe epilepsy. At the time of writing, only 20 cases of GPSN schwannoma have been reported with patients presenting with dysfunction of lacrimation, salivation, facial palsy, headache and seizures [1Umredkar A. Singla N. Gupta S.K. et al.Greater superficial petrosal nerve schwannoma: report of two cases and literature review.Neurol India. 2011; 59: 786-788Crossref PubMed Scopus (9) Google Scholar, 2Parikh P.P. Amber K.T. Angeli S.I. A schwannoma of the greater petrosal nerve located within the petrous apex and treated with stereotactic radiotherapy.Am J Otolaryngol. 2013; 34: 596-599Abstract Full Text Full Text PDF PubMed Scopus (6) Google Scholar, 3Michel O. Wagner M. Guntinas-Lichius O. Schwannoma of the greater superficial petrosal nerve.Otolaryngol Head Neck Surg. 2000; 122: 302-303Crossref PubMed Scopus (14) Google Scholar, 4Amirjamshidi A. Hashemi S.M.R. Abbassioun K. Schwannoma of the greater superficial petrosal nerve.J Neurosurg. 2010; 113: 1093-1098Crossref PubMed Scopus (14) Google Scholar]. Imaging characteristics of GSPN schwannomas include well circumscribed hypointense to isointense masses that homogenously contrast enhance located in the subtemporal region [6Wiggins 3rd, R.H. Harnsberger H.R. Salzman K.L. et al.The many faces of facial nerve schwannoma.AJNR Am J Neuroradiol. 2006; 27: 694-699PubMed Google Scholar, 7Schmidinger A. Deinsberger W. Greater superficial petrosal nerve schwannoma.Acta Neurochir (Wien). 2005; 147 ([discussion 663]): 659-663Crossref PubMed Scopus (17) Google Scholar]. Bony erosion of the petrous bone is seen as tumours project upward into the middle cranial fossa as seen in our patient [4Amirjamshidi A. Hashemi S.M.R. Abbassioun K. Schwannoma of the greater superficial petrosal nerve.J Neurosurg. 2010; 113: 1093-1098Crossref PubMed Scopus (14) Google Scholar, 7Schmidinger A. Deinsberger W. Greater superficial petrosal nerve schwannoma.Acta Neurochir (Wien). 2005; 147 ([discussion 663]): 659-663Crossref PubMed Scopus (17) Google Scholar]. In contrast, features of intracerebral schwannomas include cyst formation, calcification, and peritumoural oedema [5Zagardo M.T. Castellani R.J. Rees J.H. et al.Radiologic and pathologic findings of intracerebral schwannoma.AJNR Am J Neuroradiol. 1998; 19: 1290-1293PubMed Google Scholar, 8Luo B. Sun G. Zhang B. et al.Neuroradiological findings of intracranial schwannomas not arising from the stems of cranial nerves.Br J Radiol. 2004; 77: 1016-1021Crossref PubMed Scopus (16) Google Scholar]. MRI demonstrates hypointense to isointense mixed density masses with cystic degeneration and necrosis. Solid components, commonly a mural nodule, markedly contrast enhance [[8]Luo B. Sun G. Zhang B. et al.Neuroradiological findings of intracranial schwannomas not arising from the stems of cranial nerves.Br J Radiol. 2004; 77: 1016-1021Crossref PubMed Scopus (16) Google Scholar]. While pre-operative diagnosis is difficult, pre-operative measurement of bilateral tear secretion may be a useful adjunct [[7]Schmidinger A. Deinsberger W. Greater superficial petrosal nerve schwannoma.Acta Neurochir (Wien). 2005; 147 ([discussion 663]): 659-663Crossref PubMed Scopus (17) Google Scholar]. Treatment of choice for this benign tumour is total excision, however post-operative complications may include ipsilateral reduced lacrimation, facial palsy and hearing loss [2Parikh P.P. Amber K.T. Angeli S.I. A schwannoma of the greater petrosal nerve located within the petrous apex and treated with stereotactic radiotherapy.Am J Otolaryngol. 2013; 34: 596-599Abstract Full Text Full Text PDF PubMed Scopus (6) Google Scholar, 3Michel O. Wagner M. Guntinas-Lichius O. Schwannoma of the greater superficial petrosal nerve.Otolaryngol Head Neck Surg. 2000; 122: 302-303Crossref PubMed Scopus (14) Google Scholar]. The authors declare that they have no financial or other conflicts of interest in relation to this research and its publication. An unusual cause of epilepsy: questionJournal of Clinical NeuroscienceVol. 21Issue 10PreviewA 55-year-old man presented with a generalised tonic-clonic seizure associated with olfactory aura and a 1 month history of unwitnessed seizures. Past medical history was unremarkable with no history of epilepsy or malignancy. The neurological examination was normal. Contrast CT scan of the brain revealed a 2 cm left temporal lesion reported as intra-axial, with a cystic and solid component associated with surrounding vasogenic oedema and peripheral punctate high densities suggestive of calcification (Fig. Full-Text PDF