Progress in brain research
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Visual shape recognition--the ability to recognize a wide variety of shapes regardless of their size, position, view, clutter and ambient lighting--is a remarkable ability essential for complex behavior. In the primate brain, this depends on information processing in a multistage pathway running from primary visual cortex (V1), where cells encode local orientation and spatial frequency information, to the inferotemporal cortex (IT), where cells respond selectively to complex shapes. A fundamental question yet to be answered is how the local orientation signals (in V1) are transformed into selectivity for complex shapes (in IT). ⋯ Next, we found that responses to complex shapes were dictated by the curvature at a specific boundary location within the shape. Finally, using basis function decoding, we demonstrated that an ensemble of V4 neurons could successfully encode complete shapes as aggregates of boundary fragments. These findings identify curvature as a basis of shape representation in area V4 and provide insights into the neurophysiological basis for the salience of convex curves in shape perception.
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In the early stages of Parkinson's disease (PD), impaired motor preparation has been related to a decrease in the latency of mu rhythm event-related desynchronisation (ERD) compared with control subjects, suggesting hypo activation of the contralateral, primary sensorimotor (PSM) cortex. Following movement, a decrease in amplitude of beta rhythm ERS was observed over the same region and thought to be related to impairment in cortical deactivation. By monitoring ERD/ERS, we aimed (i) to extend to advanced PD the observations made in less-advanced parkinsonism and (ii) to test the effect of acute L-Dopa, internal pallidal or subthalamic stimulation on these abnormalities. ⋯ Mu rhythm ERD latency and the beta ERS amplitude further decreased in advanced PD compared with early stages, suggesting greater impairment of cortical activation/deactivation as the disease progresses and a partial restoration in relation to clinical improvement under treatments. Consequently, it appears that L-Dopa and deep brain stimulation partially restored the normal patterns of cortical oscillatory activity in PD, possibly by decreasing the low frequency hyper synchronisation at rest. This mechanism could be involved at the basal ganglia level in the sensorimotor integration implicated in the movement control.
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Spinal reflexes dominate cardiovascular control after spinal cord injury (SCI). These reflexes are no longer restrained by descending control and they can be impacted by degenerative and plastic changes within the injured cord. Autonomic dysreflexia is a condition of episodic hypertension that stems from spinal reflexes initiated by sensory input entering the spinal cord caudal to the site of injury. ⋯ One such treatment is an antibody to the integrin CD11d expressed by inflammatory leukocytes that enter the cord acutely after injury and cause significant secondary damage. This antibody blocks integrin-mediated leukocyte entry, resulting in greatly reduced white-matter damage and decreased autonomic dysreflexia after cord injury. Understanding the mechanisms for autonomic dysreflexia will provide us with strategies for treatments that, if given early after cord injury, can prevent this serious disorder from developing.
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On a daily basis, individuals with cervical and upper thoracic spinal cord injury face the challenge of managing their unstable blood pressure, which frequently results in persistent hypotension and/or episodes of uncontrolled hypertension. This chapter will focus on the clinical issues related to abnormal cardiovascular control in individuals with spinal cord injury, which include neurogenic shock, autonomic dysreflexia and orthostatic hypotension. Blood pressure control depends upon tonic activation of sympathetic preganglionic neurons by descending input from the supraspinal structures (Calaresu and Yardley, 1988). ⋯ This results in a variety of cardiovascular abnormalities that have been well documented in human studies, as well as in animal models (Osborn et al., 1990; Mathias and Frankel, 1992a, b; Krassioukov and Weaver, 1995; Maiorov et al., 1997, 1998; Teasell et al., 2000). However, the recognition and management of these cardiovascular dysfunctions following spinal cord injury represent challenging clinical issues. Moreover, cardiovascular disorders in the acute and chronic stages of spinal cord injury are among the most common causes of death in individuals with spinal cord injury (DeVivo et al., 1999).
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The discovery of event-related desynchronization (ERD) and event-related synchronization (ERS) by Pfurtscheller paved the way for the development of brain-computer interfaces (BCIs). BCIs allow control of computers or external devices with the regulation of brain activity only. Two different research traditions produced two different types of BCIs: invasive BCIs, realized with implanted electrodes in brain tissue and noninvasive BCIs using electrophysiological recordings in humans such as electroencephalography (EEG) and magnetoencephalography (MEG) and metabolic changes such as functional magnetic resonance imaging (fMRI) and near infrared spectroscopy (NIRS). ⋯ Invasive multielectrode BCIs in otherwise healthy animals allowed execution of reaching, grasping, and force variations from spike patterns and extracellular field potentials. Whether invasive approaches allow superior brain control of motor responses compared to noninvasive BCI with intelligent peripheral devices and electrical muscle stimulation and EMG feedback remains to be demonstrated. The newly developed fMRI-BCIs and NIRS-BCIs offer promise for the learned regulation of emotional disorders and also disorders of small children (in the case of NIRS).