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The SlicerBatchBrainMRTumorSegmentation is a graphical user interface (GUI) based Python scripted module within 3D Slicer. Its purpose is to perform automated brain tumour segmentation for numerous patients while preserving data integrity and organization. Through automation, manual intervention at each stage of the Brain Tumor Segmentation (BraTS) toolkit becomes unnecessary, resulting in efficient processing of multiple patient cases. Being an open-source software implementation, the SlicerBatchBrainMRTumorSegmentation is licensed under the BSD (Berkeley Source Distribution) 3-Clause License, facilitating its use by the broader research community. This tool empowers users to explore diverse segmentation approaches, fosters research advancements, and stimulates innovation in the field of brain tumour analysis.

The role of neuroimaging in the assessment of a first-ever seizure has not been well-defined, in particular the utility of MRI when CT is normal. The results of neuroimaging (CT brain, MRI brain, or both) in 1,013 adults with first-ever unprovoked seizure were correlated with clinical features and seizure outcome. Epileptogenic lesions were identified in 29. Of patients with a normal CT who also had MRI, 12 had an epileptogenic lesion on MRI, the strongest independent predictor of which was a focal abnormality on EEG. Patients with an epileptogenic lesion had a higher risk of seizure recurrence, including when this was only evident on MRI.

•ALA induced fluorescence of an isolated cerebral cryptococcoma.•Perilesional Gliolan fluorescence in cerebral infection.•Cerebral Cryptococcus infection mimics a tumour with intraoperative fluorescence.

Although the prevalence of seizures in children with sickle cell disease (SCD) is 10 times that of the general population, there are few prospectively collected data on mechanism. With transcranial Doppler and magnetic resonance imaging (MRI) and angiography, we evaluated 76 patients with sickle cell disease, 29 asymptomatic and 47 with neurological complications (seizures, stroke, transient ischemic attack, learning difficulty, headaches, or abnormal transcranial Doppler), who also underwent bolus‐tracking perfusion MRI. The six patients with recent seizures also had electroencephalography. Group comparisons (seizure, nonseizure, and asymptomatic) indicated that abnormal transcranial Doppler was more common in the seizure (4/6; 67%) and nonseizure (26/41; 63%) groups than in the asymptomatic (10/29; 34%) group (χ2; p= 0.045), but abnormal structural MRI (χ2; p= 0.7) or magnetic resonance angiography (χ2; p= 0.2) were not. Relativedecreased cerebral perfusion was found in all seizure patients and in 16 of 32 of the remaining patients with successful perfusion MRI (p= 0.03). In the seizure patients, the perfusion abnormalities in five were ipsilateral to electroencephalographic abnormalities; one had normal electroencephalogram results. These findings suggest that vasculopathy and focal hypoperfusion may be factors in the development of sickle cell disease–associated seizures. Ann Neurol 2005;58:290–302

Neurological complications are common in sickle cell disease (SCD). However, it is often difficult to relate the clinical presentation to conventional neuroimaging, because subclinical infarction is common and stroke has been described in the absence of large‐vessel disease. We studied 48 patients with SCD aged 4–34 (median 13) years with T2‐weighted, diffusion and perfusion magnetic resonance imaging (MRI) and with MR angiography. Forty‐four underwent transcranial Doppler (TCD). Abnormalities on perfusion imaging were seen in 25 cases, 24 of whom had been symptomatic. The remaining patient had evidence of executive dysfunction and reduced perfusion in the frontal lobes. The perfusion abnormality was larger than the area of infarction in 9 patients and was seen in an arterial distribution with no infarction in a further 9. In 3 patients with transient ischemic attacks, perfusion abnormalities were demonstrated in the absence of any other neuroimaging abnormalities, and perfusion changes were seen in 3 others despite normal MR angiography and TCD. Perfusion abnormalities are associated with neurological symptoms in patients with SCD, whether or not MRI, MR angiography, and TCD are abnormal. It is likely that this technique will guide management in individual patients. Ann Neurol 2001;49:477–485

Two magnetic resonance imaging techniques, diffusion and perfusion imaging, are being used increasingly for evaluation of pathophysiology of stroke. This article introduces these techniques and reports some initial studies using these approaches, together with conventional T2-weighted magnetic resonance imaging, for investigation of childhood stroke. It is shown that the combination of T2-weighted and diffusion images can provide information about the timing of stroke events in childhood, and perfusion imaging can detect abnormalities not visible by other magnetic resonance imaging techniques. These magnetic resonance methods therefore should play an important role in investigation of children with stroke and could be of particular value in studies of at-risk populations of children such as those with sickle cell disease. (J Child Neurol2000;15:279-283).

IntroductionGlial fibrillary acidic protein (GFAP) astrocytopathy is a lesser recognised immune-mediated meningo-encephalomyelitis, which is steroid responsive in the majority of cases. Neuroimaging is unique with a distinctive symmetric white matter perivascular linear and punctate enhancement pattern. We present a case with classical phenotype but delayed clinical response, and highlight the importance of early recognition and treatment.CaseA 59-year-old Caucasian female presented with a two month history of headache, gait disturbance, insomnia, agitation, disorientation and reduced oral intake. Examination revealed a high frequency upper limb tremor, hypertonicity and pathologically brisk reflexes with impaired cognitive function. MRI brain and spinal cord demonstrated high T2 signal and striking perivascular and punctate enhancement in supratentorial white matter, cervical and upper thoracic cord. CSF examination revealed lymphocytic pleocytosis and elevated protein. Brain biopsy demonstrated reduced GFAP expression, perivascular T-lymphocytic infiltrate, and recent white matter microinfarction. CSF and serum GFAP antibodies were positive.Motor deterioration accompanied progression to a stuporous state. High dose corticosteroids were commenced, followed by intravenous immunoglobulin and mycophenolate. While there was marked improvement of perivascular contrast enhancement on imaging, the patient continued to demonstrate prominent tremor, gait disturbance and behavioural issues 9 months following symptom onset.ConclusionsThe persistence of disability in this case is likely the result of axonal loss from the initial insult, reflected by the biopsy evidence of microinfarction. Awareness of the unique pattern on MRI and the clinical phenotype will aid in early recognition and prompt treatment of this condition, thus preventing the potential long term morbidity.

Recessive ataxias are heterogeneous group of rare monogenic disorders with genetic pathology largely unresolved.