Eosinophils may affect each stage of tumour development. Many studies have suggested that tumour-associated tissue eosinophilia (TATE) is associated with favourable prognosis in some malignant tumours. However, only a few studies exist on TATE in central nervous system (CNS) tumours. Our recent study exhibited eosinophils in atypical teratoid/rhabdoid tumours (AT/RTs), pediatric malignant CNS tumours with divergent differentiation. This study examines eosinophils in pilocytic astrocytomas (PAs).

The study included 44 consecutive cases of patients with PAs and no concurrent CNS inflammatory disease.

We found eosinophils in 19 (43%) of 44 PAs (patient age range, 0.5-72 years). Eosinophils were intratumoural and clearly distinguishable. The density of eosinophils was rare to focally scattered. PAs containing eosinophils were located throughout the CNS. Furthermore, eosinophilic infiltration was identified in 18 (62%) of 29 pediatric (age range, 0.5-18 years) PAs but only 1 (7%) of 15 (p<0.001, significantly less) adult (age range, 20-72 years) PAs. Eosinophilic infiltration showed no significant differences between PAs with and without MRI cystic formation, surgical procedures, or PAs with and without leptomeningeal infiltration. In comparison, eosinophils were absent in 10 pediatric (age range, 0.5-15 years) ependymomas (or anaplastic ependymomas).

These results suggest that eosinophils are common in pediatric PAs but rare in adult PAs. This difference is probably related to the developing immune system and different tumour-specific antigens in children. TATE may play a functional role in the development of pediatric PAs, as well as some other pediatric CNS tumours such as AT/RTs.

the maternally inherited MTTL1 A3243G mutation in the mitochondrial genome causes MelaS (Mitochondrial encephalopathy lactic acidosis with Stroke-like episodes), a condition that is multisystemic but affects primarily the nervous system. Significant intra-familial variation in phenotype and severity of disease is well recognized.

retrospective and ongoing study of an extended family carrying the MTTL1 A3243G mutation with multiple symptomatic individuals. tissue heteroplasmy is reviewed based on the clinical presentations, imaging studies, laboratory findings in affected individuals and pathological material obtained at autopsy in two of the family members.

there were seven affected individuals out of thirteen members in this three generation family who each carried the MTTL1 A3243G mutation. the clinical presentations were varied with symptoms ranging from hearing loss, migraines, dementia, seizures, diabetes, visual manifestations, and stroke like episodes. three of the family members are deceased from MelaS or to complications related to MelaS.

the results of the clinical, pathological and radiological findings in this family provide strong support to the current concepts of maternal inheritance, tissue heteroplasmy and molecular pathogenesis in MelaS. neurologists (both adult and paediatric) are the most likely to encounter patients with MelaS in their practice. genetic counselling is complex in view of maternal inheritance and heteroplasmy. newer therapeutic options such as arginine are being used for acute and preventative management of stroke like episodes.

This study aimed to describe the frequency and temporal profile of acute cerebral infarction (ACI) using a continuous glucose monitoring system (CGMS) in patients with and without type 2 diabetes mellitus (T2DM) and explore the impact of blood glucose fluctuations on the short-term prognosis of ACI.

The subjects were divided into four groups: T2DM with acute cerebral infarction (DMCI, Group A, n=56); T2DM without acute cerebral infarction (DM-NCI, Group B, n=36); Acute cerebral infarction patients without T2DM (NDM-CI, Group C, n=54); Healthy control group (NG, Group D, n=36). The National Institutes of Health Stoke Scale (NIHSS) and modified Rankin scale (mRs) were collected in Group A and C. All subjects were monitored for 72 hours using the CGMS. Indices such as fasting blood glucose (FBG) and mean amplitude of glycemic excursions (MAGE) were calculated. Glycemic excursions were compared between Group A, B, C and Group D, respectively. Multiple linear regression analysis and logistic analysis was applied.

MAGE is related to NIHSS, homocysteine (HCY), HOMA-IR, FBG, CRP and IMT, while NIHSS is related to CRP, HCY, HOMA-IR, IMT. The factors impacting the short-term prognosis of ACI were NIHSS, HBA1C and MAGE.

Larger glucose fluctuations are associated with more stroke risk factors and are associated with a poorer short-term prognosis. More attention should be paid to glucose fluctuations in patients with ACI and a history of T2DM.

To describe a delayed severe complication of temporal lobectomy for intractable epilepsy.

A case of amnesia occurring 24 years after surgery is described and five similar cases from the literature reviewed.

Mean age at surgery (5 right) was 40 years (19-62 years), 3 female. Four of five tested had impaired visual and verbal memory preoperatively but not sufficient to contraindicate surgery. Pathology was mesial temporal sclerosis in 3, 1 cavernoma, 1 dysembryoplastic neuroepithelial tumor (DNET) and 1 normal. Postoperatively, four were seizure free 3-12 years off medication and two continued with seizures. There was no unexpected postoperative memory change until incapacitating anterograde amnesia developed 1-24 years after surgery. In five patients, including ours, this followed definite or possible status epilepticus with new mesial temporal sclerosis on the opposite side in the four that were investigated by MRI. One patient developed a glioblastoma in the opposite temporal lobe.

Continuing or late recurrence of seizures from the remaining temporal lobe after temporal lobectomy can result in incapacitating amnesia if status epilepticus occurs. Other new lesions on the opposite side to surgery can have the same effect.

To observe clinical manifestations, behavioral characteristics, and effects of rehabilitation on a patient with pusher syndrome and unilateral spatial neglect caused by right thalamic hemorrhage.

Assessment of pusher syndrome was made by the Scale for Contraversive pushing (SCP), and unilateral spatial neglect syndrome was diagnosed using line cancellation, letter and star cancellation, line bisection tests and copy and continuation of graphic sequence test. Behavioral therapy, occupational therapy, reading training and traditional Chinese medicine methods were adopted for treatment of pusher syndrome and unilateral spatial neglect.

The patient showed typical pusher syndrome and unilateral spatial neglect symptoms. The pusher syndrome and unilateral spatial neglect symptoms were significantly improved following rehabilitation treatments.

Pusher syndrome and unilateral spatial neglect syndrome occurred simultaneously after right thalamic hemorrhage. Early rehabilitation therapy can reduce the symptoms of pusher syndrome and unilateral spatial neglect syndrome and improve motor function.

Statins have recently been reported to cause a rare autoimmune inflammatory and/or necrotic myopathy that begins or persists after drug cessation.

We report on 26 patients seen at a neuromuscular centre between 2005 and 2011 who demonstrated muscle weakness/myalgias and creatine kinase elevations during or after statin treatment with continuation of signs and symptoms despite statin withdrawal.

All patients were treated with immunosuppressive therapy with good response; all improved biochemically and 86% improved clinically. Sixty-five percent of patients who attempted to taper off immunosuppressive therapy relapsed. We report on a novel finding whereby five of the seven patients who underwent multiple biopsies throughout their disease demonstrated a transformation of their histological diagnosis, with four progressing from having myofibre necrosis with minimal or no inflammation to a diagnosis of polymyositis.

This study offers preliminary evidence that statin-associated necrotizing myopathy and statin-associated polymyositis may not be separate entities but are part of the same pathophysiological spectrum. Both entities respond well to immunosuppression.

The objective of this study was to explore the expression of urotensin II (UII), its receptor (GPR14), and vascular endothelial growth factor (VEGF), as well as their associations in the ischaemic brains of rats with focal cerebral ischaemia, under normal and diabetic conditions.

Diabetes mellitus (DM) was induced by injection of streptozotocin (STZ) into Sprague—Dawley rats. Focal cerebral ischaemia was induced by middle cerebral artery occlusion (MCAO) four weeks after DM onset by STZ. Rats (n=80) were divided into four groups: normal control, DM, MCAO, and DM/MCAO. Immunohistochemistry and reverse-transcriptase-polymerase chain reaction (RT-PCR) were used to detect the expression of UII, GPR14 and VEGF in the diabetic and ischaemic brain.

Expression of UII and GPR14 was increased at mRNA and protein levels in the DM and MCAO group compared with controls. In the DM/MCAO group, expression of UII and GPR14 was increased significantly in the ischaemic brain, and was accompanied by a significantly increased VEGF expression.

Diabetes mellitus was seen to aggravate brain lesions after ischaemia, and UII may have an important role.

To determine the representation of Tourette Syndrome (TS) in fictional movies and television programs by investigating recurrent themes and depictions.

Television and film can be a source of information and misinformation about medical disorders. Tourette Syndrome has received attention in the popular media, but no studies have been done on the accuracy of the depiction of the disorder.

International internet movie databases were searched using the terms “Tourette’s”, “Tourette’s Syndrome”, and “tics” to generate all movies, shorts, and television programs featuring a character or scene with TS or a person imitating TS. Using a grounded theory approach, we identified the types of characters, tics, and co-morbidities depicted as well as the overall representation of TS.

Thirty-seven television programs and films were reviewed dating from 1976 to 2010. Fictional movies and television shows gave overall misrepresentations of TS. Coprolalia was overrepresented as a tic manifestation, characters were depicted having autism spectrum disorder symptoms rather than TS, and physicians were portrayed as unsympathetic and only focusing on medical therapies. School and family relationships were frequently depicted as being negatively impacted by TS, leading to poor quality of life.

Film and television are easily accessible resources for patients and the public that may influence their beliefs about TS. Physicians should be aware that TS is often inaccurately represented in television programs and film and acknowledge misrepresentations in order to counsel patients accordingly.