The diagnosis of central nervous system tumours has been transformed in recent years from a microscopic morphology-based process to one dominated by the identification of somatic genetic alterations in tumour cells. This switch requires implementing radically different methods, for which appropriate training and financial resources must be allocated. The Canadian Association of Neuropathologists (CANP) has followed a process based on the scientific literature and consensus to develop recommendations for molecular testing of tumours of the brain and spinal cord, aiming to balance the need for treatment-determinant accurate diagnosis and the current limitations inherent in the transition to a new paradigm. The Professional Affairs Committee was charged with this task. A draft was discussed during the CANP general assembly, along with presentations from groups who had implemented molecular technologies, as well as others who relied on external laboratories. The Professional Affairs Committee summarised the consensus and submitted their recommendation to the CANP’s Executive Committee. A final report was posted on the CANP website for a month to allow all members to comment. The recommendations below apply to intrinsic tumours of the central nervous system and do not include metastatic disease or tumours impinging upon the nervous system from outside. These recommendations should be considered clinically relevant, as the results have direct consequences on the patient’s treatment, either through the use of targeted therapies or the trial-proven best application of radiation and/or chemotherapy.

This is a case of a 30-year-old right-handed male patient who presented to the hospital in 2014 after hitting his head on the mat during a wrestling match followed by headache and temporary peripheral vision limitation. The patient’s past medical history was unremarkable. On physical examination, Glasgow Coma Scale was 15 with no focal neurological deficits. Unenhanced head computed tomography (CT) and enhanced brain magnetic resonance imaging (MRI) were performed (Figure 1). The patient was managed conservatively, and follow-up CT and MRI in 2015 (Figure 2) demonstrated significant decrease in size of the previously seen right frontoparietal lesion with also changes in its radiological features. The patient remained asymptomatic for about 3 years when in 2018 he presented to the Emergency Department with increasing headaches and peripheral vision loss. MRI demonstrated an increase in the right frontal lesion size (Figure 3). He underwent surgical resection of the lesion.

No study is available that has assessed the association of dietary diversity score (DDS) and alternative healthy eating index (AHEI) with glioma. The present study aimed to assess this association in Iranian adults. Overall, 128 pathologically confirmed cases of glioma were enrolled from hospitals and 256 age- and sex-matched controls were recruited from other wards of the hospital between 2009 and 2011. Dietary assessment was done using a validated block-format 123-item semi-quantitative FFQ. Dietary indices including DDS and AHEI-2010 were constructed according to standard methods. After controlling for potential confounders, a significant inverse association was found between DDS and risk of glioma (OR 0·42, 95 % CI 0·19, 0·94). Such finding was also seen when further adjustment was made for BMI; such that participants in the highest quartile of DDS were 56 % less likely to have glioma compared with those in the lowest quartile (OR 0·44, 95 % CI, 0·20, 0·97). In addition, a significant inverse association was found between adherence to AHEI and glioma; such that in the fully adjusted model, participants in the fourth quartile of AHEI had 74 % lower risk of glioma compared with those in the first quartile (OR 0·26, 95 % CI 0·12, 0·56). In conclusion, we found that greater adherence to the healthy, as measured by AHEI, and diverse, as measured by DDS, diets was associated with decreased odds of glioma.

Introduction: Recognition of life-threatening conditions, such as brain tumours, remains a challenge among pediatric patients. Few studies have described the implication of initial presentation, clinical evolution and healthcare system factors in diagnosis delay of brain tumours in children. We aimed to determine the clinical presentation patterns and health care trajectory of children with a diagnosis of primary brain tumour. Methods: A retrospective chart review in a pediatric university-affiliated hospital was conducted. Participants were all patients less than 18 years of age diagnosed with a brain tumour by neuroimaging between Jan 2003 and Dec 2014. Data were extracted from an institutional tumour registry and medical records. Results: From the registry, 288 patients were identified. The mean age at time of diagnosis was 7.44 ± 0.29 years. Most tumours were infra-tentorial (55%) and had astrocytic origin (29%). The majority (35%) had consulted only once prior to diagnosis, while 14% had consulted at least 4 times prior to diagnosis. The mean time between the onset of symptoms and diagnosis was 147 ± 19 days. The mean time between symptoms onset and first consultation was 84 ± 14 days. The most frequent symptoms and signs at onset and diagnosis were respectively: headache (44% vs 59%, p<0.01), nausea and vomiting (31% vs 58%, p<0.01) and abnormalities of gait (10% vs 32%, p<0.01). 129 patients (45%) were diagnosed in an Emergency Department (ED). Symptoms and signs that differed significantly for those diagnosed in an ED were: headache (71% vs 42%, p<0.01), nausea and vomiting (73 % vs 32%, p<0.01), lethargy (26% vs 9%, p<0.01), weight loss (15% vs 3%, p<0.01), irritability (9% vs 0%, p<0.01) and endocrine abnormality (2% vs 8%, p=0.02). Clinical presentations of infants up to one year of age (14%) differed from other age groups. They presented mostly with growth abnormality (46%), macrocephaly (40%), irritability (40%), development abnormalities (18%) and sun-setting eyes sign (10%). Conclusion: In this large comprehensive cohort, we have found that the diagnosis of primary brain tumours is most frequently made in the ED. Different clinical presentations have been identified and varied between different settings of diagnosis and different age groups.

Little is known about the aetiology of brain tumours. One putative factor suggested from animal models is a protective effect of dietary Zn. We tested the hypothesis that increased compared with low dietary Zn intake is protective against brain tumour development. We conducted a population-based case–control study in the UK, of adults aged 18–69 years, between 2001 and 2004 aiming to identify possible risk factors. Dietary information was collected from 637 cases diagnosed with a glioma or meningioma, and 876 controls. Data were obtained from a self-completed FFQ. Multivariate logistic regression analysis was conducted, adjusting for socio-demographic factors, season of questionnaire return, multivitamin supplementation and energy intake. Although a weak protective effect was observed for the third quartile of intake (normal compared with low intake) in the meningioma group, this was limited to the specific brain tumour subtype and quartile, and was not significant after also adjusting for intake of other elements. Overall there was no significant effect of Zn intake. No association or dose–response relationship was observed between increased compared with low Zn intake and risk of glioma or meningioma.

An increase of more than 50% in cerebral blood flow velocity in the middle cerebral artery was recently reported in hypocapnic volunteers, while inhaling 50% nitrous oxide. We measured cerebral blood flow velocity in the middle cerebral artery in 10 anaesthetized hypocapnic (ETCO2=25 mmHg) patients with brain tumours while administering increasing concentrations of nitrous oxide. At an end-tidal concentration of 50% and 70% nitrous oxide in oxygen, neither mean arterial pressure (base-line: 84±8 mmHg vs. (50% nitrous oxide): 82±9 mmHg and (70% nitrous oxide): 80±8 mmHg) nor cerebral blood flow velocity in the middle cerebral artery (base-line: 32±7 cm s−1 vs. (50% nitrous oxide): 34±8 cm s−1 and (70% nitrous oxide): 34±9 cm s−1) changed significantly. The data from our clinical investigation indicate that administration of increasing concentrations of nitrous oxide to already anaesthetized and hypocapnic patients does not change cerebral blood flow velocity in the middle cerebral artery.