Annals of neurology
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Annals of neurology · Jun 2011
Randomized Controlled Trial Multicenter Study Clinical TrialCollaterals dramatically alter stroke risk in intracranial atherosclerosis.
Stroke risk due to intracranial atherosclerosis increases with degree of arterial stenosis. We evaluated the previously unexplored role of collaterals in modifying stroke risk in intracranial atherosclerosis and impact on subsequent stroke characteristics. ⋯ Collateral circulation is a potent determinant of stroke risk in intracranial atherosclerosis, demonstrating a protective role with severe stenoses and identifying more unstable milder stenoses.
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Vigabatrin-associated visual field loss (VAVFL) occurs in 25 to 50% of exposed patients and is routinely monitored using perimetry, which has inherent limitations. Using optical coherence tomography (OCT), retinal nerve fiber layer (RNFL) thinning has been described in a small number of vigabatrin-exposed patients. We explored the relationship between RNFL thickness and visual field size, to determine whether OCT is a suitable tool to use in patients exposed to vigabatrin. ⋯ OCT provides a useful tool to assess people exposed to vigabatrin, and can provide an accurate estimate of the extent of visual field loss in the absence of a reliable direct measure of the visual field. The strong linear relationship found between RNFL thickness and visual field size provides some evidence that irreversible VAVFL may be related to loss of retinal ganglion cell axons.
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Annals of neurology · May 2011
Faciobrachial dystonic seizures precede Lgi1 antibody limbic encephalitis.
To describe a distinctive seizure semiology that closely associates with voltage-gated potassium channel (VGKC)-complex/Lgi1 antibodies and commonly precedes the onset of limbic encephalitis (LE). ⋯ Recognition of FBDS should prompt testing for VGKC-complex/Lgi1 antibodies. AEDs often produce adverse effects; treatment with immunotherapies may prevent the development of LE with its potential for cerebral atrophy and cognitive impairment.
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Annals of neurology · Apr 2011
ReviewThe complex world of oligodendroglial differentiation inhibitors.
Myelination is a central nervous system (CNS) process wherein oligodendrocyte-axon interactions lead to the establishment of myelin sheaths that stabilize, protect, and electrically insulate axons. In inflammatory demyelinating diseases such as multiple sclerosis (MS), the degeneration and eventual loss of functional myelin sheaths slows and blocks saltatory conduction in axons, which results in clinical impairment. However, remyelination can occur, and lesions can be partially repaired, resulting in clinical remission. ⋯ The endogenous capacity to generate new oligodendrocytes in MS is limited, and this is predominantly due to the presence of inhibitory components that block OPC differentiation and maturation. Here, we present an overview of recently identified negative regulators of oligodendroglial differentiation and their potential relevance for CNS repair in MS. Because currently available immunomodulatory drugs for MS mainly target inflammatory cascades outside the brain and fail to repair existing lesions, achieving more efficient lesion repair constitutes an important goal for future MS therapies.