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Bunyan R.F.,Neurosciences Center
Neurologic clinics | Year: 2012

Central nervous system (CNS) inflammatory demyelinating diseases are a group of disorders that include multiple sclerosis, acute disseminated encephalomyelitis, and neuromyelitis optica. These conditions may result in emergencies because of severe inflammatory destruction of CNS tissues or complications thereof. Most of these conditions are responsive to appropriate therapy and early diagnosis and treatment leads to better outcomes. We discuss the spectrum of emergencies associated with these disorders, as well as clinical features, investigations, and management. Copyright © 2012. Published by Elsevier Inc. Source


Bunyan R.F.,Neurosciences Center | Tang J.,Treatment and Research Center at the Minneapolis Clinic of Neurology | Weinshenker B.,Mayo Medical School
Neurologic Clinics | Year: 2012

Central nervous system (CNS) inflammatory demyelinating diseases are a group of disorders that include multiple sclerosis, acute disseminated encephalomyelitis, and neuromyelitis optica. These conditions may result in emergencies because of severe inflammatory destruction of CNS tissues or complications thereof. Most of these conditions are responsive to appropriate therapy and early diagnosis and treatment leads to better outcomes. We discuss the spectrum of emergencies associated with these disorders, as well as clinical features, investigations, and management. © 2012. Source


Bunyan R.F.,Neurosciences Center | Pittock S.J.,Mayo Medical School
Multiple Sclerosis Journal | Year: 2012

As physicians how do we counsel our patients with clinically isolated syndrome (CIS) when they ask, 'what is the benefit of injecting disease-modifying agents (DMAs) over many years? What disability will they prevent in my future?' In this debate, we will provide three core points supporting the concept that a watchful waiting approach (annual neurological evaluation and magnetic resonance imaging of the head (with gadolinium) at least for the first few years after diagnosis) for most patients with CIS represents appropriate medical care. © The Author(s) 2012. Source


Pfeifenbring S.,University of Gottingen | Bunyan R.F.,Neurosciences Center | Metz I.,University of Gottingen | Rover C.,University of Gottingen | And 4 more authors.
Annals of Neurology | Year: 2015

Objective Axonal damage occurs early in multiple sclerosis (MS) and contributes to the degree of clinical disability. Children with MS more often show disabling and polyfocal neurological symptoms at disease onset than adults with MS. Thus, axonal damage may differ between pediatric and adult MS patients. Methods We analyzed axonal pathology in archival brain biopsy and autopsy samples from 19 children with early MS. Lesions were classified according to demyelinating activity and presence of remyelination. Axonal density and extent of acute axonal damage were assessed using Bielschowsky silver impregnation and immunohistochemistry for amyloid precursor protein (APP), respectively. Axonal injury was correlated with the inflammatory infiltrate as well as clinical characteristics. Results were compared with data from adult MS patients. Results Acute axonal damage was most extensive in early active demyelinating (EA) lesions of pediatric patients and correlated positively with the Expanded Disability Status Scale at attack leading to biopsy/autopsy. Comparison with 12 adult patients showed a 50% increase in the extent of acute axonal damage in EA lesions from children compared to adults, with the highest number of APP-positive spheroids found prior to puberty. The extent of acute axonal damage correlated positively with the number of lesional macrophages. Axonal density was reduced in pediatric lesions irrespective of the demyelinating activity or the presence of remyelination. Axonal reduction was similar between children and adults. Interpretation Our results provide evidence for more pronounced acute axonal damage in inflammatory demyelinating lesions from children compared to adults. Ann Neurol 2015;77:655-667 © 2015 American Neurological Association. Source


Khan T.,University of Oxford | Akhtar W.,University of Oxford | Wotton C.J.,University of Oxford | Hart Y.,Neurosciences Center | And 2 more authors.
Journal of Neurology, Neurosurgery and Psychiatry | Year: 2011

Background: Studies suggest that seizures may precede the detection of cerebral tumour by several years. Aim: To quantify the risk of cerebral tumour after new onset seizures, with particular interest in long term risk. Methods: Using the Oxford Record Linkage Study (ORLS, 1963-1998) and English national linked Hospital Episode Statistics (1999-2005), cohorts of people with a first admission for epilepsy were constructed. Subsequent admissions with cerebral tumour were identified. The rate of occurrence of subsequent cerebral tumour in each epilepsy cohort was compared with that in a comparison cohort and expressed as a rate ratio (RR). Results: The RR for cerebral tumour after epilepsy, relative to the rate of cerebral tumour in the comparison cohort, was 19.9 (95% CI 17.2 to 22.9) in the ORLS cohort and 19.7 (18.3-21.1) in the England cohort. The RR for malignant tumours were, respectively, 25.6 (21.7 to 30.0) and 27.3 (25.2 to 29.6). The RR for benign tumours were 10.1 (7.38 to 13.6) and 10.4 (9.07 to 11.8), respectively. The risk was highest for those aged 15-44 years at initial admission for epilepsy both in Oxford (24.2, 18.5 to 31.5) and England (38.1, 32.8 to 44.2). The risk of cerebral tumour was still raised several years after initial admission for epilepsy: in the ORLS cohort at 15 years or more, the RR was 3.29 (1.39 to 6.66) and, in the England cohort 5-7 years after initial admission, the RR was 5.27 (3.87 to 7.06). Conclusions: Seizures may herald the development of cerebral tumour, remote in time as well as soon after onset, with implications for guidelines on continued surveillance of those with new onset seizures. Source

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