Journal of neurology, neurosurgery, and psychiatry
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J. Neurol. Neurosurg. Psychiatr. · Nov 2003
Randomized Controlled Trial Clinical TrialA randomised placebo controlled study to assess the effects of cholinergic treatment on muscarinic receptors in Alzheimer's disease.
To determine the effects of cholinergic treatment on the muscarinic receptor in patients with Alzheimer's disease. ⋯ The results suggest that (123)I-QNB uptake is better preserved in Alzheimer's disease patients on cholinergic treatment than on placebo. Cholinergic treatment may play a neuroprotective role. Sequential (123)I-QNB imaging seems to be a powerful tool in monitoring the response of these receptors to disease modifying treatments.
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J. Neurol. Neurosurg. Psychiatr. · Nov 2003
ReviewChildhood onset generalised dystonia can be modelled by increased gain in the indirect basal ganglia pathway.
Clinical experience suggests an important role of the indirect basal ganglia pathway in the genesis of childhood onset generalised dystonia, but it has been difficult to reconcile the increased muscle activity in dystonia with the current model of basal ganglia function in which the indirect pathway is considered primarily inhibitory. The aim of this study was to present a modification of the direct-indirect pathway model, in which the indirect pathway is inverting rather than purely inhibitory, so that while high signals are inhibited, low signals are amplified. As the basal ganglia may be a feedback loop that modifies cortical activity, instability from excessive gain in this feedback loop could explain features of dystonia. ⋯ The simulations show that increased gain in the indirect pathway relative to the direct pathway can lead to unstable uncontrolled synchronous oscillations in cortex and basal ganglia. This behaviour could result in dystonia. The model provides a consistent explanation for the association of dystonia with parkinsonism and disorders characterised by dopamine depletion, the ability to treat some dystonias with dopamine, the ability of neuroleptic drug treatment to cause an acute dystonic reaction treatable with anticholinergic drugs, and the ability of pallidotomy or deep brain stimulation of the internal pallidum to alleviate symptoms of generalised dystonia.
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J. Neurol. Neurosurg. Psychiatr. · Nov 2003
ReviewHuman cellular inflammation in the pathology of acute cerebral ischaemia.
Leucocytes form important effector pathways for inflammation. This article reviews the clinical evidence for the presence of a cellular inflammatory response in cerebral ischaemia, and attempts to define its temporal profile and spatial distribution. The processes involved in recruitment and activation of leucocytes in this context are addressed, and the successes and failures of interventions aimed at these processes discussed.
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Ion channels provide the basis for the regulation of electrical excitability in the central and peripheral nervous systems. This review deals with the techniques that make the study of structure and function of single channel molecules in living cells possible. These are the patch clamp technique, which was derived from the conventional voltage clamp method and is currently being developed for automated and high throughput measurements; and fluorescence and nano-techniques, which were originally applied to non-biological surfaces and are only recently being used to study cell membranes and their proteins, especially in combination with the patch clamp technique. The characterisation of the membrane channels by techniques that resolve their morphological and physical properties and dynamics in space and time in the nano range is termed nanoscopy.
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J. Neurol. Neurosurg. Psychiatr. · Nov 2003
The longitudinal relation between brain lesion load and atrophy in multiple sclerosis: a 14 year follow up study.
Studies have suggested that T2 lesion activity is prominent in early relapsing-remitting multiple sclerosis, whereas brain atrophy, while seen early, appears more evident in later progressive disease. The temporal relation between these processes remains unclear. ⋯ From this, it appears that early rather than later focal lesion accumulation relates to subsequent brain atrophy, but factors unconnected directly with lesion formation probably also play a significant role in determining such atrophy.