Progress in brain research
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The Alice in Wonderland syndrome is a term applied to altered bizarre perceptions of size and shapes of a patient's body and illusions of changes in the forms, dimensions, and motions of objects that a patient with this syndrome encounters. These metamorphopsias arise during complex partial seizures, migraine headaches, infections, and intoxications. The illusions and hallucinations resemble the strange phenomena that Alice experienced in Lewis Carroll's Alice's Adventures in Wonderland. ⋯ The author of this chapter suggests that Dodgson suffered from migraine headaches and used these experiences to weave an amusing tale for Alice Liddell. The chapter also discusses the neurology of mercury poisoning affecting the behavior of Mad Hatter character. The author suggests that the ever-somnolent Dormouse suffered from excessive daytime sleepiness due to obstructive sleep apnea.
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Biography Historical Article
John Bell (1763-1820): brother artist and anatomist.
John Bell, brother-surgeon of Charles Bell, was, like Charles, an outstanding surgeon and a good artist. John was one of the few who illustrated his work with their own drawings in the days before audiovisual aids were available and without the benefit of reliable drawing aids, photography and computer-aided design. Charles, on the other hand, was the better artist and illustrated much of the normal anatomy of the nervous system. Each brother undertook extensive surgery of men who had been wounded in war; John Bell left us his engravings from the textbooks, more numerous perhaps than Charles, but Charles left us a series of oil paintings and watercolours in addition to the illustrations in his textbooks.
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Sleep is regulated by circadian and homeostatic processes. The sleep homeostat keeps track of the duration of prior sleep and waking and determines the intensity of sleep. In mammals, the homeostatic process is reflected by the slow waves in the non-rapid eye movement (NREM) sleep electroencephalogram (EEG). ⋯ Under similar conditions, humans show a clear circadian modulation in REM sleep, whereas in the rat, a circadian modulation in REM sleep was not present. Therefore, in the rat, the sleep homeostatic modulation in phase with the circadian clock seems to amplify the relatively weak circadian changes in sleep induced by the circadian clock. Knowledge about the interaction between sleep and the circadian clock and the circadian modulation of sleep in other species than humans is important to better understand the underlying regulatory mechanisms.
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Spinal cord injury is a devastating neurological trauma, often resulting in the impairment of bladder, bowel, and sexual function as well as the loss of voluntary control of muscles innervated by spinal cord segments below the lesion site. Research is ongoing into several classes of therapies to restore lost function. These include the encouragement of neural sparing and regeneration of the affected tissue, and the intervention with pharmacological and rehabilitative means to improve function. ⋯ These include the activation of fibers-in-passage which lead to the transsynaptic spread of activation through the spinal cord and the ability of ISMS to produce fatigue-resistant, weight-bearing movements. We present our thoughts on the clinical potential for ISMS with regard to implantation techniques, stability, and damage induced by mechanical and electrical factors. We conclude by suggesting improvements in materials and techniques that are needed in preparation for a clinical proof-of-principle and review our current attempts to achieve these.
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Locomotion is a very robust motor pattern which can be optimized after different types of lesions to the central and/or peripheral nervous system. This implies that several plastic mechanisms are at play to re-express locomotion after such lesions. Here, we review some of the key observations that helped identify some of these plastic mechanisms. ⋯ We therefore also review some of the sensory and supraspinal mechanisms involved in the recovery of locomotion after partial spinal injury. We particularly stress a recent development using a dual spinal lesion paradigm in which a first partial spinal lesion is made which is then followed, some weeks later, by a complete spinalization. The results show that the spinal cord below the spinalization has been changed by the initial partial lesion suggesting that, in the recovery of locomotion after partial spinal lesion, plastic mechanisms within the spinal cord itself are very important.