Progress in brain research
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In order to study cerebral activity related to preparation and execution of movement, evoked and induced brain electrical activities were compared to each other and to fMRI results in voluntary self-paced movements. Also, the event-related desynchronization and synchronization (ERD/ERS) were studied in complex movements with various degrees of cognitive load. The Bereitschaftspotential (BP) and alpha (8-12 Hz) and beta (16-24 Hz) ERD/ERS rhythms in self-paced simple movements were analyzed in 14 epilepsy surgery candidates. ⋯ Some sites were only active in the task with the increased demand on executive functions. In the temporal neocortex only, the oscillatory, but not the evoked, activity was recorded in the self-paced movement. The temporal appearance of changes of oscillatory activities in the self-paced movement task as well as in the cued movement task with an increased load of executive functions raises the interesting question of the role of this region in cognitive-movement information processing.
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Review
Mechanisms underlying the recovery of lower urinary tract function following spinal cord injury.
The lower urinary tract has two main functions, the storage and periodic expulsion of urine, which are regulated by a complex neural control system in the brain and lumbosacral spinal cord. This neural system coordinates the activity of two functional units in the lower urinary tract: (1) a reservoir (the urinary bladder) and (2) an outlet (consisting of bladder neck, urethra and striated muscles of the pelvic floor). During urine storage the outlet is closed and the bladder is quiescent, thereby maintaining a low intravesical pressure over a wide range of bladder volumes. ⋯ Following spinal cord injury, the bladder is initially areflexic but then becomes hyperreflexic due to the emergence of a spinal micturition reflex pathway. Studies in animals indicate that the recovery of bladder function after spinal cord injury is dependent in part on plasticity of bladder afferent pathways and the unmasking of reflexes triggered by capsaicin-sensitive C-fiber bladder afferent neurons. The plasticity is associated with changes in the properties of ion channels and electrical excitability of afferent neurons, and appears to be mediated in part by neurotrophic factors released in the spinal cord and the peripheral target organs.
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Transection of the spinal cord that interrupts the spinobulbospinal micturition reflex pathway, abolishes voluntary voiding and initially produces an areflexic bladder with complete urinary retention. However, depending upon the species, reflex bladder activity slowly recovers over the course of weeks or months. In chronic spinal animals, reflex mechanisms in the lumbosacral spinal cord are capable of duplicating many of the functions performed by reflex pathways in animals with an intact spinal cord and can induce bladder hyperreflexia. ⋯ Changes in electrophysiological or neurochemical properties of bladder afferent cells in the dorsal root ganglia and of spinal pathways could contribute to the emergence of the spinal micturition reflex, bladder hyperreflexia and changes in the pharmacologic responses of reflex pathways in the lumbosacral spinal cord after spinal cord injury. Urinary bladder hyperreflexia after spinal cord injury may reflect a change in the balance of neuroactive compounds in bladder reflex pathways. This review will detail: (1) changes in the neurochemical phenotype of bladder afferent neurons and of spinal neurons mediating micturition reflexes after spinal cord injury, with an emphasis on three neuroactive compounds, neuronal nitric oxide synthase (nNOS), galanin, and pituitary adenylate cyclase activating polypeptide (PACAP); (2) possible functional consequences on bladder reflexes of changes in spinal cord neurochemistry after spinal cord injury, and (3) the potential role of neurotrophic factors expressed in the urinary bladder or spinal cord after spinal cord injury in mediating these neurochemical changes.
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In normal life, activity-dependent plasticity occurs in the spinal cord as well as in the brain. Like CNS plasticity elsewhere, this spinal cord plasticity can occur at many neuronal and synaptic sites and by a variety of mechanisms. Spinal cord plasticity is prominent in postnatal development and contributes to acquisition of standard behaviors such as locomotion and rapid withdrawal from pain. ⋯ This complexity is necessary, to preserve the full roster of behaviors, and is also inevitable, due to the ubiquity of activity-dependent plasticity in the CNS. Careful investigation of spinal cord plasticity is essential for understanding motor skills; and, because of the relative simplicity and accessibility of the spinal cord, is a logical and convenient starting point for exploring skill acquisition. Appropriate induction and guidance of activity-dependent plasticity in the spinal cord is likely to be a key part of the realization of effective new rehabilitation methods for spinal cord injuries, cerebral palsy, and other chronic motor disorders.
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The spinal cord is essential for normal autonomic nervous system regulation of the cardiovascular system as the preganglionic neurons controlling the heart and blood vessels originate in the thoracolumbar spinal segments. The site and extent of a spinal cord injury determine the degree of autonomic involvement in cardiovascular dysfunction after the injury. After complete cervical cord lesions the entire sympathetic outflow is separated from cerebral control; this may cause orthostatic hypotension. ⋯ This chapter will focus on orthostatic hypotension and paroxysmal hypertension in cord-injured people with lesions affecting the cervical and upper thoracic spinal cord. Conditions promoting these abnormalities in blood pressure will be elaborated. Possible mechanisms for the hypo- and hypertension will be discussed, as will strategies for managing these problems.