Progress in brain research
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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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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.
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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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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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Near-death experiences (NDEs) have become the focus of much interest in the last 30 years or so. Such experiences can occur both when individuals are objectively near to death and also when they simply believe themselves to be. The experience typically involves a number of different components including a feeling of peace and well-being, out-of-body experiences (OBEs), entering a region of darkness, seeing a brilliant light, and entering another realm. ⋯ Psychological theories include the proposal that the NDE is a dissociative defense mechanism that occurs in times of extreme danger or, less plausibly, that the NDE reflects memories of being born. Finally, a wide range of organic theories of the NDE has been put forward including those based upon cerebral hypoxia, anoxia, and hypercarbia; endorphins and other neurotransmitters; and abnormal activity in the temporal lobes. Finally, the results of studies of NDEs in cardiac arrest survivors are reviewed and the implications of these results for our understanding of mind-brain relationships are discussed.