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Autonomic Consequences of Spinal Cord Injury

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Abstract

Spinal cord injury (SCI) results not only in motor and sensory deficits but also in autonomic dysfunctions. The disruption of connections between higher brain centers and the spinal cord, or the impaired autonomic nervous system itself, manifests a broad range of autonomic abnormalities. This includes compromised cardiovascular, respiratory, urinary, gastrointestinal, thermoregulatory, and sexual activities. These disabilities evoke potentially life‐threatening symptoms that severely interfere with the daily living of those with SCI. In particular, high thoracic or cervical SCI often causes disordered hemodynamics due to deregulated sympathetic outflow. Episodic hypertension associated with autonomic dysreflexia develops as a result of massive sympathetic discharge often triggered by unpleasant visceral or sensory stimuli below the injury level. In the pelvic floor, bladder and urethral dysfunctions are classified according to upper motor neuron versus lower motor neuron injuries; this is dependent on the level of lesion. Most impairments of the lower urinary tract manifest in two interrelated complications: bladder storage and emptying. Inadequate or excessive detrusor and sphincter functions as well as detrusor‐sphincter dyssynergia are examples of micturition abnormalities stemming from SCI. Gastrointestinal motility disorders in spinal cord injured‐individuals are comprised of gastric dilation, delayed gastric emptying, and diminished propulsive transit along the entire gastrointestinal tract. As a critical consequence of SCI, neurogenic bowel dysfunction exhibits constipation and/or incontinence. Thus, it is essential to recognize neural mechanisms and pathophysiology underlying various complications of autonomic dysfunctions after SCI. This overview provides both vital information for better understanding these disorders and guides to pursue novel therapeutic approaches to alleviate secondary complications. © 2014 American Physiological Society. Compr Physiol 4:1419‐143, 2014.

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Figure 1. Figure 1. Schematic diagrams illustrating sympathetic and parasympathetic control of the cardiovascular system. SPNs are mainly situated in the intermediolateral (IML) cell column of T1‐L2 spinal cord segments. The heart receives both sympathetic and parasympathetic input; sympathetic regulation arises from T1‐T4 spinal segments whereas parasympathetic innervation originates from the dorsal motor nucleus of vagus (DMV) and nucleus ambiguous (N. Ambiguous) in the medulla oblongata via the vagus and glossopharyngeal nerves, respectively. Sympathetic preganglionic fibers project to postganglionic neurons in the middle cervical ganglia which activate cardiac plexuses distributing to the heart and thoracic blood vessels. Otherwise, most peripheral vessels have sympathetic innervation but do not have parasympathetic input. Sympathetic preganglionic fibers projecting to the abdomen, pelvis, and lower body originate primarily from T5‐L2 spinal levels and synapse onto postganglionic neurons within celiac ganglion, superior mesenteric, and inferior mesenteric ganglia prior to innervating major arteries and organs. The lower thoracic and lumbosacral sympathetic chain ganglionic neurons project fibers to lower body skin blood vessels. Parasympathetic neurons located in the sacral spinal cord innervate pelvic viscera and do not participate in cardiovascular regulation. CNIX, cranial nerve IX; CNX, cranial nerve X.
Figure 2. Figure 2. Supraspinal vasomotor pathways descend from the brainstem and hypothalamus. The original regions include the rostral ventrolateral medulla (RVLM), the rostral ventromedial medulla (RVMM), the caudal raphe nuclei (RN), the A5 region, and the paraventricular nucleus (PVN); presympathetic neurons in these nuclei project to sympathetic preganglionic neurons (SPNs) in the thoracolumbar spinal cord, regulating sympathetic outflow.
Figure 3. Figure 3. Biotinylated dextran amine (BDA) anterograde tracing reveals supraspinal vasomotor pathways originating from the rostral ventrolateral medulla (RVLM) in an intact rat. BDA (10% in distilled water, 1 μL/side) is injected bilaterally into the RVLM 3 weeks before perfusion. (A) Low magnification microphotograph of transverse section in the rostral medulla shows bilateral injection sites within the RVLM. (B‐D) Representative photomicrographs demonstrate (B) the distribution of BDA‐labeled fibers in an overview of the lower cervical spinal cord, which are mainly located in the (C) dorsolateral funiculus (DLF) and (D) ventral white matter (VWM). (C and D) Higher magnification of areas boxed in (B). Scale bars: 1.5 mm (A), 500 μm (B), 25 μm (C), and 50 μm (D). (With permission from Ref. 144.)
Figure 4. Figure 4. Multiple neurotransmitters are involved in cardiovascular regulation. Supraspinal vasomotor pathways contain a diverse array of neurotransmitters including amino acids, catecholamines, and neuropeptides. Descending projections from the rostral ventrolateral medulla (RVLM) are glutamatergic or γ‐aminobutyric acid (GABA)‐ergic whereas serotoninergic (5‐HT) neurons are predominant in the caudal raphe nuclei (RN). C1 adrenergic neurons in the RVLM and noradrenergic neurons in the A5 region are major sources of catecholaminergic inputs to sympathetic preganglionic neurons, releasing epinephrine (adrenaline) and norepinephrine (NE). Additionally, some descending axons express substance P, enkephalin (Enk), and neuropeptide Y. Neurotransmitters in the spinal cord are comprised of glutamate (Glu), GABA, substance P, neuropeptide Y, and Enk.
Figure 5. Figure 5. Autonomic dysreflexia develops following SCI at cervical or high thoracic levels. During colorectal distension (CRD), mimicking noxious pelvic visceral stimuli, both mean arterial pressure (MAP) and heart rate (HR) increase slightly in intact F344 rats, indicative of escape/avoidance response. In T4‐transected (T4‐Tx) rats, however, CRD triggers a prominent rise in MAP accompanied by bradycardia, a typical symptom of autonomic dysreflexia, measured at 10 weeks postinjury. (Unpublished data, S. Hou.)
Figure 6. Figure 6. Schematic illustrating reorganization of intraspinal circuits related to autonomic dysreflexia. SCI‐induced elevation in spinal levels of nerve growth factor mainly contributes to the plasticity of pelvic visceral calcitonin gene‐related peptide (CGRP)+ C‐fiber afferents. The sensory arbors, in turn, are relayed by ascending propriospinal neurons to sympathetic preganglionic neurons (SPNs) in the thoracolumbar spinal cord to elicit autonomic dysreflexia, notably when the distal colon or bladder is distended.
Figure 7. Figure 7. Supraspinal serotonergic (5‐HT) projections to sympathetic preganglionic neurons (SPNs) in the intermediolateral (IML) cell column are interrupted after SCI. (A) In an horizontal thoracolumbar section of intact spinal cord, 5‐HT‐immunolabeled axon bundles (red) extend into the IML, where Fluorogold (FG)‐labeled SPNs (blue) are located. (B) Higher magnification of boxed region in (A) shows serotonergic axons in proximity to FG‐labeled SPNs. (C) Four weeks after complete T4‐transection, there is no 5‐HT‐immunolabeled axons in the IML below the lesion of spinal cord. Scale bars: 500 μm (A) and 100 μm (C). (Note: FG was 0.5% in distilled water 0.4 mL, intraperitoneal injection.) (Unpublished data, S. Hou.)
Figure 8. Figure 8. Neuronal control of the lower urinary tract (LUT). Primary sensory neurons are located in the dorsal root ganglia (DRG) at T11‐L2 and S2‐S4 spinal levels in humans (L1‐L2 and L6‐S1 in rats). Afferent fibers convey sensory information of LUT to the spinal cord via the hypogastric, pelvic, and pudendal nerves, respectively. Sympathetic and parasympathetic projections distribute to the bladder, urethra, and internal urethral sphincter (IUS). Sympathetic preganglionic neurons (SPNs) involved in LUT activity are situated in the lower intermediolateral (IML) cell column at T11‐L2 levels in humans (L6‐S1 in rats). The projections course through the hypogastric nerve to postganglionic neurons within inferior mesenteric ganglia (IMG). Sympathetic pathways have an important role in urinary continence by maintaining bladder relaxation and urethral contraction. Parasympathetic preganglionic neurons (PPNs), located at the S2‐S4 spinal cord levels in humans (L6‐S1 in rats), extend fibers onto postganglionic neurons within pelvic ganglion via the pelvic nerve. Parasympathetic excitation elicits bladder contraction and urethral relaxation. Somatic efferents project from motoneurons in Onuf's nucleus and join the pudendal nerve, innervating external urethral sphincter (EUS) muscles. n., nerve.
Figure 9. Figure 9. Schematic describing supraspinal control of micturition. Barrington's nucleus (BN), located bilaterally in the pontine tegmentum, acts as an integration center coordinating forebrain activity and spinal micturition reflexes. BN neurons receive bladder afferent information from the lumbosacral spinal cord as well as from the nucleus tractus solitarii (NTS) and periaqueductal gray region (PAG), two important sensory relay stations. In BN, medial neurons (M‐region) project to lumbosacral sympathetic or parasympathetic preganglionic neurons (SPNs and PPNs) innervating the bladder whereas lateral neurons (L‐region) prominently innervate sacral sphincteric motoneurons within Onuf's nucleus (N.).
Figure 10. Figure 10. Corticotropin releasing factor (CRF) is a major neurotransmitter in Barrington's nucleus (BN) neurons. (A) Bright field photomicrograph of a rat brain coronal section at the level of BN showing CRF‐immunolabeled neurons (blue) and neurons that are retrogradely labeled with the tracer Fluorogold (FG) from the lumbosacral spinal cord (brown). Note that most neurons have the hybrid blue/brown color indicating that they are CRF neurons that project to the spinal cord (example indicated by arrow). The arrowhead points to a neuron that is CRF‐labeled only. Dorsal is at the top and medial is to the right. V indicates the fourth ventricle. (B) A section at the level of lumbosacral spinal cord showing dense CRF immunoreactive terminal fields (blue) in the region of parasympathetic nuclei (arrows). The section is counterstained with Neutral Red (with permission from Ref. 347).
Figure 11. Figure 11. Supraspinal neurotransmitters involved in micturition control. Neurotransmitters including glutamate (Glu), γ‐aminobutyric acid (GABA), and glycine participate in the activity of lower urinary tract. In addition, corticotropin‐releasing factor (CRF) expressed by Barrington's nucleus (BN) neurons, norepinephrine (NE), and adrenaline (epinephrine) released by neurons in the A5 and C1 regions, and serotonin (5‐HT) expressed by the caudal raphe nuclei (RN) neurons act on bladder and urethral reflexes. It has been characterized that tachykinin, substance P, enkephalin (Enk), vasoactive intestinal peptide (VIP), and pituitary adenylate cyclase‐activating polypeptide (PACAP) take part in the regulation of voiding or continence.
Figure 12. Figure 12. Representative cystometry assessments in urethane‐anesthetized intact and SCI rats. Rhythmic contractions elicit voiding (asterisks) in an intact rat when saline is infused into the bladder via a catheter inserted into the bladder dome. However, in a T10 spinal cord transected rat, multiple rhythmic contractions between adjacent expels do not result in voiding 3 weeks after injury, which is termed nonvoiding contractions (arrows) indicating hyperactivity of bladder. Notably, the SCI rat exhibits higher voiding amplitude compared to the intact during the assessment. (Unpublished data, S. Hou.)
Figure 13. Figure 13. Reflex voiding responses in an infant, a healthy adult and a paraplegic patient. Combined cystometry and sphincter electromyograms (EMGs recorded with surface electrodes), allow a schematic comparison of reflex voiding responses in (A) an infant and in (C) a paraplegic patient compared to voluntary voiding response in (B) a healthy adult. The abscissa in all recordings represents bladder volume in milliliters; the ordinates represent electrical activity of the EMG recording and detrusor pressure (the component of bladder pressure that is generated by the bladder itself) in cmH2O. On the left side of each trace (at 0 mL), a slow infusion of fluid into the bladder is started (bladder filling). In (B) the start of sphincter relaxation, which precedes the bladder contraction by a few seconds, is indicated (“start”). Note that a voluntary cessation of voiding (“stop”) is associated with an initial increase in sphincter EMG and detrusor pressure (a myogenic response). A resumption of voiding is associated with sphincter relaxation and a decrease in detrusor pressure that continues as the bladder empties and relaxes. In the infant (A) sphincter relaxation is present but less complete. On the other hand, in the paraplegic patient (C) the reciprocal relationship between bladder and sphincter is abolished. During bladder filling, involuntary bladder contractions (detrusor overactivity) occur in association with external sphincter activity. Each wave of bladder contraction is accompanied by simultaneous contraction of the sphincter (detrusor‐sphincter dyssynergia, DSD), hindering urine flow. Loss of the reciprocal relationship between the bladder and the sphincter in paraplegic patients thus interferes with effective bladder emptying (with permission from Ref. 98).
Figure 14. Figure 14. Schematic drawing neuronal control of the gastrointestinal (GI) tract. Vagal sensory afferent neurons are located in the nodose ganglion and collect information of the gut. Ascending afferent fibers terminate in the nucleus tractus solitarii (NTS) where the information of converging projections from high CNS centers is integrated. Subsequently, the signal is relayed to parasympathetic neurons in the dorsal motor nucleus of vagus (DMV). These vago‐vagal reflex circuits modulate smooth muscle movement and digestion process throughout the GI tract. The stomach is dominated by vagal parasympathetic control. In humans sacral parasympathetic efferent fibers originating from S2‐S4 spinal cord levels (L6‐S1 in rats) join the descending colon and rectum through the pelvic nerve. The mesenteric nerve from T5‐T12 levels and the hypogastric nerve from T12‐L2 levels contain sympathetic input to the stomach, intestine, and colon. The external anal sphincter (EAS) is innervated by somatic pudendal nerves, originating from motoneurons at S2‐S4 spinal levels in humans (L6‐S1 in rats). CNX, cranial nerve X; SMG, superior mesenteric ganglion; IMG, inferior mesenteric ganglion; g, ganglion; n, nerve.
Figure 15. Figure 15. Traumatic SCI diminishes mechanical sensitivity of the stomach to fluid distension. Representative gastric pressure traces in rats with high thoracic contused SCI (T3 SCI, upper trace) and surgical (laminectomy only) controls (T3 Control, lower trace) demonstrate that during 6 min of continuous filling (at a rate of 1 mL/min, starting at closed arrowhead and terminating at open arrowhead) T3 SCI rats exhibit a smaller increase in gastric pressure and pressure‐evoked motility waves are less pronounced, measured at 3 days postinjury. Initial pressure peak (asterisks) is an artifact of initiating the filling cycle. Gastric distension is performed by passing a saline‐filled catheter via an incision into the proximal duodenum and through the occluded pylorus. Gastric distension is maintained at the termination of the filling cycle (with permission from Ref. 138).


Figure 1. Schematic diagrams illustrating sympathetic and parasympathetic control of the cardiovascular system. SPNs are mainly situated in the intermediolateral (IML) cell column of T1‐L2 spinal cord segments. The heart receives both sympathetic and parasympathetic input; sympathetic regulation arises from T1‐T4 spinal segments whereas parasympathetic innervation originates from the dorsal motor nucleus of vagus (DMV) and nucleus ambiguous (N. Ambiguous) in the medulla oblongata via the vagus and glossopharyngeal nerves, respectively. Sympathetic preganglionic fibers project to postganglionic neurons in the middle cervical ganglia which activate cardiac plexuses distributing to the heart and thoracic blood vessels. Otherwise, most peripheral vessels have sympathetic innervation but do not have parasympathetic input. Sympathetic preganglionic fibers projecting to the abdomen, pelvis, and lower body originate primarily from T5‐L2 spinal levels and synapse onto postganglionic neurons within celiac ganglion, superior mesenteric, and inferior mesenteric ganglia prior to innervating major arteries and organs. The lower thoracic and lumbosacral sympathetic chain ganglionic neurons project fibers to lower body skin blood vessels. Parasympathetic neurons located in the sacral spinal cord innervate pelvic viscera and do not participate in cardiovascular regulation. CNIX, cranial nerve IX; CNX, cranial nerve X.


Figure 2. Supraspinal vasomotor pathways descend from the brainstem and hypothalamus. The original regions include the rostral ventrolateral medulla (RVLM), the rostral ventromedial medulla (RVMM), the caudal raphe nuclei (RN), the A5 region, and the paraventricular nucleus (PVN); presympathetic neurons in these nuclei project to sympathetic preganglionic neurons (SPNs) in the thoracolumbar spinal cord, regulating sympathetic outflow.


Figure 3. Biotinylated dextran amine (BDA) anterograde tracing reveals supraspinal vasomotor pathways originating from the rostral ventrolateral medulla (RVLM) in an intact rat. BDA (10% in distilled water, 1 μL/side) is injected bilaterally into the RVLM 3 weeks before perfusion. (A) Low magnification microphotograph of transverse section in the rostral medulla shows bilateral injection sites within the RVLM. (B‐D) Representative photomicrographs demonstrate (B) the distribution of BDA‐labeled fibers in an overview of the lower cervical spinal cord, which are mainly located in the (C) dorsolateral funiculus (DLF) and (D) ventral white matter (VWM). (C and D) Higher magnification of areas boxed in (B). Scale bars: 1.5 mm (A), 500 μm (B), 25 μm (C), and 50 μm (D). (With permission from Ref. 144.)


Figure 4. Multiple neurotransmitters are involved in cardiovascular regulation. Supraspinal vasomotor pathways contain a diverse array of neurotransmitters including amino acids, catecholamines, and neuropeptides. Descending projections from the rostral ventrolateral medulla (RVLM) are glutamatergic or γ‐aminobutyric acid (GABA)‐ergic whereas serotoninergic (5‐HT) neurons are predominant in the caudal raphe nuclei (RN). C1 adrenergic neurons in the RVLM and noradrenergic neurons in the A5 region are major sources of catecholaminergic inputs to sympathetic preganglionic neurons, releasing epinephrine (adrenaline) and norepinephrine (NE). Additionally, some descending axons express substance P, enkephalin (Enk), and neuropeptide Y. Neurotransmitters in the spinal cord are comprised of glutamate (Glu), GABA, substance P, neuropeptide Y, and Enk.


Figure 5. Autonomic dysreflexia develops following SCI at cervical or high thoracic levels. During colorectal distension (CRD), mimicking noxious pelvic visceral stimuli, both mean arterial pressure (MAP) and heart rate (HR) increase slightly in intact F344 rats, indicative of escape/avoidance response. In T4‐transected (T4‐Tx) rats, however, CRD triggers a prominent rise in MAP accompanied by bradycardia, a typical symptom of autonomic dysreflexia, measured at 10 weeks postinjury. (Unpublished data, S. Hou.)


Figure 6. Schematic illustrating reorganization of intraspinal circuits related to autonomic dysreflexia. SCI‐induced elevation in spinal levels of nerve growth factor mainly contributes to the plasticity of pelvic visceral calcitonin gene‐related peptide (CGRP)+ C‐fiber afferents. The sensory arbors, in turn, are relayed by ascending propriospinal neurons to sympathetic preganglionic neurons (SPNs) in the thoracolumbar spinal cord to elicit autonomic dysreflexia, notably when the distal colon or bladder is distended.


Figure 7. Supraspinal serotonergic (5‐HT) projections to sympathetic preganglionic neurons (SPNs) in the intermediolateral (IML) cell column are interrupted after SCI. (A) In an horizontal thoracolumbar section of intact spinal cord, 5‐HT‐immunolabeled axon bundles (red) extend into the IML, where Fluorogold (FG)‐labeled SPNs (blue) are located. (B) Higher magnification of boxed region in (A) shows serotonergic axons in proximity to FG‐labeled SPNs. (C) Four weeks after complete T4‐transection, there is no 5‐HT‐immunolabeled axons in the IML below the lesion of spinal cord. Scale bars: 500 μm (A) and 100 μm (C). (Note: FG was 0.5% in distilled water 0.4 mL, intraperitoneal injection.) (Unpublished data, S. Hou.)


Figure 8. Neuronal control of the lower urinary tract (LUT). Primary sensory neurons are located in the dorsal root ganglia (DRG) at T11‐L2 and S2‐S4 spinal levels in humans (L1‐L2 and L6‐S1 in rats). Afferent fibers convey sensory information of LUT to the spinal cord via the hypogastric, pelvic, and pudendal nerves, respectively. Sympathetic and parasympathetic projections distribute to the bladder, urethra, and internal urethral sphincter (IUS). Sympathetic preganglionic neurons (SPNs) involved in LUT activity are situated in the lower intermediolateral (IML) cell column at T11‐L2 levels in humans (L6‐S1 in rats). The projections course through the hypogastric nerve to postganglionic neurons within inferior mesenteric ganglia (IMG). Sympathetic pathways have an important role in urinary continence by maintaining bladder relaxation and urethral contraction. Parasympathetic preganglionic neurons (PPNs), located at the S2‐S4 spinal cord levels in humans (L6‐S1 in rats), extend fibers onto postganglionic neurons within pelvic ganglion via the pelvic nerve. Parasympathetic excitation elicits bladder contraction and urethral relaxation. Somatic efferents project from motoneurons in Onuf's nucleus and join the pudendal nerve, innervating external urethral sphincter (EUS) muscles. n., nerve.


Figure 9. Schematic describing supraspinal control of micturition. Barrington's nucleus (BN), located bilaterally in the pontine tegmentum, acts as an integration center coordinating forebrain activity and spinal micturition reflexes. BN neurons receive bladder afferent information from the lumbosacral spinal cord as well as from the nucleus tractus solitarii (NTS) and periaqueductal gray region (PAG), two important sensory relay stations. In BN, medial neurons (M‐region) project to lumbosacral sympathetic or parasympathetic preganglionic neurons (SPNs and PPNs) innervating the bladder whereas lateral neurons (L‐region) prominently innervate sacral sphincteric motoneurons within Onuf's nucleus (N.).


Figure 10. Corticotropin releasing factor (CRF) is a major neurotransmitter in Barrington's nucleus (BN) neurons. (A) Bright field photomicrograph of a rat brain coronal section at the level of BN showing CRF‐immunolabeled neurons (blue) and neurons that are retrogradely labeled with the tracer Fluorogold (FG) from the lumbosacral spinal cord (brown). Note that most neurons have the hybrid blue/brown color indicating that they are CRF neurons that project to the spinal cord (example indicated by arrow). The arrowhead points to a neuron that is CRF‐labeled only. Dorsal is at the top and medial is to the right. V indicates the fourth ventricle. (B) A section at the level of lumbosacral spinal cord showing dense CRF immunoreactive terminal fields (blue) in the region of parasympathetic nuclei (arrows). The section is counterstained with Neutral Red (with permission from Ref. 347).


Figure 11. Supraspinal neurotransmitters involved in micturition control. Neurotransmitters including glutamate (Glu), γ‐aminobutyric acid (GABA), and glycine participate in the activity of lower urinary tract. In addition, corticotropin‐releasing factor (CRF) expressed by Barrington's nucleus (BN) neurons, norepinephrine (NE), and adrenaline (epinephrine) released by neurons in the A5 and C1 regions, and serotonin (5‐HT) expressed by the caudal raphe nuclei (RN) neurons act on bladder and urethral reflexes. It has been characterized that tachykinin, substance P, enkephalin (Enk), vasoactive intestinal peptide (VIP), and pituitary adenylate cyclase‐activating polypeptide (PACAP) take part in the regulation of voiding or continence.


Figure 12. Representative cystometry assessments in urethane‐anesthetized intact and SCI rats. Rhythmic contractions elicit voiding (asterisks) in an intact rat when saline is infused into the bladder via a catheter inserted into the bladder dome. However, in a T10 spinal cord transected rat, multiple rhythmic contractions between adjacent expels do not result in voiding 3 weeks after injury, which is termed nonvoiding contractions (arrows) indicating hyperactivity of bladder. Notably, the SCI rat exhibits higher voiding amplitude compared to the intact during the assessment. (Unpublished data, S. Hou.)


Figure 13. Reflex voiding responses in an infant, a healthy adult and a paraplegic patient. Combined cystometry and sphincter electromyograms (EMGs recorded with surface electrodes), allow a schematic comparison of reflex voiding responses in (A) an infant and in (C) a paraplegic patient compared to voluntary voiding response in (B) a healthy adult. The abscissa in all recordings represents bladder volume in milliliters; the ordinates represent electrical activity of the EMG recording and detrusor pressure (the component of bladder pressure that is generated by the bladder itself) in cmH2O. On the left side of each trace (at 0 mL), a slow infusion of fluid into the bladder is started (bladder filling). In (B) the start of sphincter relaxation, which precedes the bladder contraction by a few seconds, is indicated (“start”). Note that a voluntary cessation of voiding (“stop”) is associated with an initial increase in sphincter EMG and detrusor pressure (a myogenic response). A resumption of voiding is associated with sphincter relaxation and a decrease in detrusor pressure that continues as the bladder empties and relaxes. In the infant (A) sphincter relaxation is present but less complete. On the other hand, in the paraplegic patient (C) the reciprocal relationship between bladder and sphincter is abolished. During bladder filling, involuntary bladder contractions (detrusor overactivity) occur in association with external sphincter activity. Each wave of bladder contraction is accompanied by simultaneous contraction of the sphincter (detrusor‐sphincter dyssynergia, DSD), hindering urine flow. Loss of the reciprocal relationship between the bladder and the sphincter in paraplegic patients thus interferes with effective bladder emptying (with permission from Ref. 98).


Figure 14. Schematic drawing neuronal control of the gastrointestinal (GI) tract. Vagal sensory afferent neurons are located in the nodose ganglion and collect information of the gut. Ascending afferent fibers terminate in the nucleus tractus solitarii (NTS) where the information of converging projections from high CNS centers is integrated. Subsequently, the signal is relayed to parasympathetic neurons in the dorsal motor nucleus of vagus (DMV). These vago‐vagal reflex circuits modulate smooth muscle movement and digestion process throughout the GI tract. The stomach is dominated by vagal parasympathetic control. In humans sacral parasympathetic efferent fibers originating from S2‐S4 spinal cord levels (L6‐S1 in rats) join the descending colon and rectum through the pelvic nerve. The mesenteric nerve from T5‐T12 levels and the hypogastric nerve from T12‐L2 levels contain sympathetic input to the stomach, intestine, and colon. The external anal sphincter (EAS) is innervated by somatic pudendal nerves, originating from motoneurons at S2‐S4 spinal levels in humans (L6‐S1 in rats). CNX, cranial nerve X; SMG, superior mesenteric ganglion; IMG, inferior mesenteric ganglion; g, ganglion; n, nerve.


Figure 15. Traumatic SCI diminishes mechanical sensitivity of the stomach to fluid distension. Representative gastric pressure traces in rats with high thoracic contused SCI (T3 SCI, upper trace) and surgical (laminectomy only) controls (T3 Control, lower trace) demonstrate that during 6 min of continuous filling (at a rate of 1 mL/min, starting at closed arrowhead and terminating at open arrowhead) T3 SCI rats exhibit a smaller increase in gastric pressure and pressure‐evoked motility waves are less pronounced, measured at 3 days postinjury. Initial pressure peak (asterisks) is an artifact of initiating the filling cycle. Gastric distension is performed by passing a saline‐filled catheter via an incision into the proximal duodenum and through the occluded pylorus. Gastric distension is maintained at the termination of the filling cycle (with permission from Ref. 138).
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Shaoping Hou, Alexander G. Rabchevsky. Autonomic Consequences of Spinal Cord Injury. Compr Physiol 2014, 4: 1419-1453. doi: 10.1002/cphy.c130045