Funct Neurol
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The assessment of residual brain function in the vegetative state is extremely difficult and depends frequently on subjective interpretations of observed spontaneous and volitional behaviours. For those patients who retain peripheral motor function, rigorous behavioural assessment supported by structural imaging and electrophysiology is usually sufficient to establish a patient's level of wakefulness and awareness. However, it is becoming increasingly apparent that, in some patients, damage to the peripheral motor system may prevent overt responses to commands, even though the cognitive ability to perceive and understand such commands may remain intact. Advances in functional neuroimaging suggest a novel solution to this problem; in several recent cases, so-called activation studies have been used to identify residual cognitive function and even conscious awareness in patients who are assumed to be vegetative, yet retain cognitive abilities that have evaded detection using standard clinical methods.
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Basic neuroscience has demonstrated new mechanisms of neuroplasticity in the healthy and the lesioned brain. Post injury, behavioral experience and neuronal stimulation-based therapy seem to play an adaptive role in the injured brain, modifying the functional organization of remaining cortical tissue and leading to clinical improvements. ⋯ We review some of the main results from animal experimental and human clinical studies focusing on mechanisms of reorganization of the motor cortex in response to injury and highlight different available approaches used to modulate and to evaluate motor cortical plasticity. Finally, we discuss how knowledge on neuroplasticity might be applied to neurorehabilitation strategies in neurologically impaired patients.
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Migraine headaches have a complex pathophysiology; both vascular and neuronal mechanisms have been proposed. One possible scenario begins with a series of destabilising events within the brain that trigger cortical spreading depression (CSD). ⋯ The best evidence to date comes from certain subtypes of migraine with aura in which point mutations in genes controlling translocation of calcium, sodium and potassium have been implicated. This review briefly summarises recent migraine research that supports CSD as an upstream driver of the migraine attack as well as an activator of the trigemino-vascular system.
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The potential of placebo treatments to alleviate a variety of medical conditions has long been recognised. Although the placebo effect is widely known, the physiological mechanisms underlying this phenomenon are not well understood. ⋯ Converging evidence suggests that placebo analgesia is linked to the activation of the endogenous opioid analgesia network, whilst dopaminergic pathways seem to play a central role in the placebo effect in movement disorders and neuroimmunomodulation. Further research on the placebo response is needed, both to improve the efficacy of its application in clinical practice and to shed more light on the complexity of mind-body interactions.
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Review Randomized Controlled Trial Comparative Study Clinical Trial
The effectiveness of combined oral lysine acetylsalicylate and metoclopramide (Migpriv) in the treatment of migraine attacks. Comparison with placebo and oral sumatriptan.
In two, double-blind, randomised, clinical, trials (RCTs), oral lysine acetylsalicylate (1620 mg, equivalent to 900 mg aspirin) combined with metoclopramide (10 mg) (LAS + MTC) was compared with placebo, and with oral sumatriptan (100 mg) in one of these RCTs. In both RCTs the LAS + MTC combination was superior to placebo with therapeutic gains (percentage relief after active treatment minus percentage relief after placebo) of 30% and 31% for the first treated attack. These therapeutic gains are in the same range as those found for 100 mg oral sumatriptan, and in the comparative RCT the LAS + MTC combination was quite comparable to 100 mg sumatriptan, with success rates for the first attack of 57% and 53%, respectively.