Autonomic Dysfunction After Spinal Cord Injury 1st Edition by Lynne C Weaver, Canio Polosa ISBN 0444519254 9780444519252

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ISBN 10: 0444519254 
ISBN 13: 9780444519252
Author: Lynne C Weaver, Canio Polosa

Autonomic dysfunction is a major and poorly understood consequence of spinal cord injury. It is a cause of very serious disability and requires much more research. It should be a focus of treatment strategies. This book will be of interest to anyone involved in research and treatment of spinal cord injury since it helps to explain the tremendously negative impact on the body caused by cord injury that is not as obvious as paralysis and loss of sensation. It contains a compilation of what is known about bladder, cardiovascular, bowel and sexual dysfunction after spinal cord injury, as it relates to the changes within the autonomic nervous system control of these functions.

The book begins with a description of the time course of autonomic dysfunctions and their ramifications from the first hours after a spinal cord injury to the more stable chronic states. The next section contains three chapters that address anatomical findings that may provide some of the foundation for autonomic dysfunctions in many of the systems. The system-specific chapters then follow in four sections. Each section begins with a chapter or two defining the clinical problems experienced by people with cord injury. The following chapters present research, basic and clinical, that address the autonomic dysfunctions.

Autonomic Dysfunction After Spinal Cord Injury 1st Table of contents:

1. References
2. Introduction
3. Overview: Autonomic dysfunction in spinal cord injury: clinical presentation of symptoms and signs
4. The moment of the accident
5. In the emergency room
6. Blood pressure control and the syndrome of inappropriate anti-diuretic hormone secretion
7. Bradycardia
8. Respiratory system
9. Temperature regulation
10. Blood pressure and mobilization
11. Skin and sensation
12. Urinary system, bladder control
13. Urinary system, renal function
14. Gastrointestinal system
15. Sexual function
16. Autonomic dysreflexia
17. Visceral sensation
18. Thrombo-emboli
19. Long-term effects
20. Time course of autonomic nervous system changes — transitional stage?
21. References
22. Section I. Anatomical Changes Mediating Autonomic Dysfunction After Cord Injury
23. Effects of spinal cord injury on synaptic inputs to sympathetic preganglionic neurons
24. Location and morphology of sympathetic preganglionic neurons
25. Morphological changes after spinal cord injury
26. Innervation of sympathetic preganglionic neurons in intact and injured cord
27. Amino acids
28. Monoamines
29. Neuropeptides
30. Rostrocaudal differences in sympathetic preganglionic neurons and their innervation
31. Acknowledgments
32. References
33. Spinal sympathetic interneurons: Their identification and roles after spinal cord injury
34. Introduction
35. Spinal sympathetic interneurons are identified both physiologically and anatomically
36. Spinal interneurons play a more important role in generating sympathetic activity after spinal cord
37. The generation of ongoing sympathetic activity after spinal transection is localized to a restricted
38. Long propriospinal pathways affecting sympathetic activity are multisynaptic
39. Spinal sympathetic interneurons in rats are more likely to be excited and less likely to be inhibite
40. Summary
41. Acknowledgment
42. References
43. Which pathways must be spared in the injured human spinal cord to retain cardiovascular control?
44. Introduction
45. Study groups
46. Cardiovascular parameters
47. Histopathological findings
48. Discussion
49. Acknowledgments
50. References
51. Section II. Urinary Bladder Dysfunction
52. Disordered control of the urinary bladder after human spinal cord injury: what are the problems?
53. Introduction
54. Brief overview of normal bladder function
55. Clinical presentations of bladder dysfunction after spinal cord injury
56. Inadequate detrusor function
57. Excessive detrusor function
58. Inadequate sphincter function
59. Excessive sphincter tone
60. Detrusor-sphincter dyssynergia
61. Impaired ability to sense the bladder
62. Infection can be a consequence of all management systems
63. Incidence and prevalence of urinary bladder dysfunction after cord injury
64. Conclusion
65. References
66. Mechanisms underlying the recovery of lower urinary tract function following spinal cord injury
67. Introduction
68. Anatomy and innervation
69. Parasympathetic pathways
70. Sympathetic pathways
71. Somatic pathways
72. Afferent pathways
73. Urothelial–afferent interactions
74. Reflex mechanisms controlling the lower urinary tract
75. Anatomy of the spinal cord
76. Efferent pathways
77. Afferent projections in the spinal cord
78. Spinal interneurons
79. Pathways in the brain
80. Organization of urine storage and voiding reflexes
81. Sympathetic storage pathway
82. Urethral sphincter storage pathway
83. Spinobulbospinal parasympathetic micturition pathway
84. Pontine micturition center
85. Suprapontine control of micturition
86. Supraspinal and spinal neurotransmitters controlling micturition
87. Neurogenic dysfunction of the lower urinary tract
88. Spinal cord injury rostral to the lumbosacral level
89. Spinal cord injury at or below the sacral level
90. Changes in functions of bladder afferent pathways after spinal cord injury
91. Changes in the firing properties of bladder afferent neurons following spinal cord injury
92. Plasticity in Na+ and K+ channels of bladder afferent neurons following spinal cord injury
93. Role of neurotrophic factors
94. Spinal mechanisms involving vasoactive intestinal polypeptide (VIP) and pituitary adenylate cyclase
95. Spinal glutamatergic mechanisms
96. Spinal tachykinin mechanisms
97. Peripheral muscarinic mechanisms
98. Conclusions
99. Acknowledgments
100. References
101. Spinal mechanisms contributing to urethral striated sphincter control during continence and micturit
102. Continence
103. Micturition
104. Direct inhibition of sphincter motoneurons during micturition
105. Evidence for premotoneuronal inhibition in excitatory reflex pathways to sphincter motoneurons
106. So, how might good things go bad?
107. References
108. Neurochemical plasticity and the role of neurotrophic factors in bladder reflex pathways after spina
109. Neural control of micturition
110. Spinal voiding reflexes after spinal cord injury
111. Neurochemistry and morphology of afferent and spinal pathways to the urogenital tract
112. Neurochemical plasticity in bladder afferent cells in dorsal root ganglia after spinal cord injury
113. Nitric oxide
114. Neuronal nitric oxide synthase
115. nNOS expression in lower urinary tract pathways after spinal cord transection at the 8th thoracic se
116. Role of nitric oxide in lower urinary tract pathways after spinal cord injury
117. Pituitary adenylate cyclase activating polypeptide (PACAP)
118. PACAP expression in lower urinary tract pathways after spinal cord transection at the 8th thoracic s
119. PACAP neuronal functions in the lower urinary tract
120. Galanin
121. Galanin expression in lower urinary tract pathways after spinal cord transection at the 8th thoracic
122. Role of neurotrophic factors in neuronal plasticity and lower urinary tract dysfunction after spinal
123. Neurotrophic factors
124. Conclusions
125. Acknowledgments
126. References
127. Effect of injury severity on lower urinary tract function after experimental spinal cord injury
128. Introduction
129. Normal Control of lower urinary tract function and effect of spinal cord transection
130. Incomplete spinal cord injury and lower urinary tract function
131. Evaluating recovery of lower urinary tract function after experimental contusion spinal cord injury
132. Effect of injury severity on chronic lower urinary tract function after incomplete spinal cord injur
133. What occurs during recovery of bladder-external urethral sphincter coordination after mild contusion
134. Conclusion
135. Acknowledgments
136. References
137. Role of the urothelium in urinary bladder dysfunction following spinal cord injury
138. The urothelium: an effective barrier against solutes and pathogens
139. Sensor and transducer functions of urothelium
140. Impact of spinal cord injury on urothelial cell barrier function and morphology
141. Impact of spinal cord injury on urothelial cell sensor and transducer properties
142. Therapeutic options for spinal cord injury that could target the urothelium
143. Intravesical vanilloid compounds
144. Antimuscarinic drugs
145. Botulinum toxin
146. Diagnostic test for spinal cord injury: the ice water test
147. Conclusion
148. Acknowledgments
149. References
150. Plasticity in the injured spinal cord: can we use it to advantage to reestablish effective bladder v
151. Introduction
152. Plasticity within the spinal cord
153. Axonal remodeling occurs normally within the developing micturition reflex
154. Bladder primary afferents and spinal cord injury
155. General characteristics
156. Phenotypic changes
157. Sprouting and the factors implicated in this response
158. Neurotrophic factors
159. Cellular adhesion molecules
160. Inhibitors of neuronal outgrowth after injury
161. Do interneurons play a role in bladder function after spinal cord injury?
162. Repairing the injured spinal cord to improve bladder function
163. Cellular implants
164. Manipulation of neuronal sprouting
165. Can neuronal plasticity play a part in restoring bladder function after spinal cord injury?
166. References
167. Control of urinary bladder function with devices: successes and failures
168. Introduction
169. Lower urinary tract control
170. Why devices?
171. Mechanical devices for control of the lower urinary tract
172. Catheters
173. Artificial sphincters
174. Urethral stents
175. Intraurethral pump
176. Electrical stimulation devices for control of the lower urinary tract
177. Electrical stimulation of the bladder
178. Intravesical stimulation
179. Bladder wall stimulation
180. Transcutaneous electrical stimulation
181. Thigh stimulation
182. Pelvic floor maximal functional electrical stimulation
183. Dorsal penile nerve stimulation
184. Stimulation of peripheral nerve
185. Tibial nerve stimulation
186. Pelvic nerve stimulation
187. Stimulation of sacral roots and nerves
188. Sacral root stimulation
189. Sacral nerve neuromodulation
190. NeoPraxis Praxis/Minax
191. Stimulation of the spinal cord
192. Future devices for electrical control of the bladder
193. Modifications of sacral root stimulators
194. Sacral posterior and anterior root stimulation
195. Selective anodal block
196. High-frequency blockade
197. Intraspinal microstimulation
198. Urethral afferent stimulation
199. Microstimulators
200. MiniatURO
201. Transcutaneous magnetic stimulation
202. Successes and failures of devices for bladder control
203. Device efficacy, advantages and disadvantages
204. Clinical success of devices in managing dysfunction after spinal cord injury
205. The future of devices for bladder control
206. Conclusions
207. Acknowledgments
208. References
209. Novel repair strategies to restore bladder function following cauda equina/conus medullaris injuries
210. Introduction
211. Effects of axonal lesions on efferent spinal cord neurons
212. A model to study cauda equina/conus medullaris injuries in the rat
213. Expression of nitric oxide synthase in axotomized spinal cord neurons
214. Acute surgical interventions to protect neurons from cell death
215. Changes in levels of neurotrophins and their receptors after injury
216. Functional reinnervation of denervated targets using surgical interventions
217. Strategies to treat chronic conus medullaris and cauda equina injuries
218. Assessments of lower urinary tract function following acute and chronic treatment interventions
219. Conclusions
220. Acknowledgments
221. References
222. Pelvic somato-visceral reflexes after spinal cord injury: measures of functional loss and partial pr
223. Introduction
224. Neural control of the pelvic viscera and pelvic floor
225. Peripheral innervation
226. The bowel
227. The bladder
228. The pelvic floor
229. The sensory pathways
230. Coordination of the lower urinary tract
231. Storage reflexes
232. Voiding reflexes
233. Coordination of the bowel
234. Storage and voiding reflexes
235. The guarding reflex
236. Neurophysiological measures of sacral reflexes
237. Pudendal urethral and anal reflexes
238. Pelvo-pudendal reflex integration
239. Aberrant somato-visceral reflexes following SCI
240. Afferent effects
241. Efferent effects
242. Inhibitory effects
243. The guarding reflex after SCI
244. The bladder guarding reflex
245. The bowel guarding reflex
246. Volitional effects on sphincter reflexes after SCI
247. Neurological grading and pelvic floor reflexes
248. Neurophysiological measures of volition on pelvic sphincters
249. Sensitivity of sacral reflex measurement and neurological assessment in SCI
250. Conclusions
251. Acknowledgments
252. References
253. Section III. Cardiovascular Dysfunction
254. The clinical problems in cardiovascular control following spinal cord injury: an overview
255. Pathophysiology of cardiovascular dysfunction after spinal cord injury
256. The acute post-injury period and neurogenic shock
257. Management of the acute period of spinal cord injury
258. Autonomic dysreflexia
259. Management of autonomic dysreflexia
260. Orthostatic hypotension
261. Management of orthostatic hypotension
262. References
263. Orthostatic hypotension and paroxysmal hypertension in humans with high spinal cord injury
264. Introduction
265. Basal blood pressure
266. Orthostatic hypotension
267. Paroxysmal hypertension
268. References
269. Autonomic dysreflexia after spinal cord injury: central mechanisms and strategies for prevention
270. Introduction to autonomic dysreflexia
271. Rodent models of autonomic dysreflexia
272. Reorganization of the injured spinal cord
273. Changes in the primary afferent arbor contributing to autonomic dysreflexia
274. Inflammation, secondary damage and autonomic dysreflexia
275. Acknowledgments
276. References
277. Segmental organization of spinal reflexes mediating autonomic dysreflexia after spinal cord injury
278. Conclusion
279. Acknowledgments
280. References
281. Spinal cord injury alters cardiac electrophysiology and increases the susceptibility to ventricular
282. Conclusion
283. Acknowledgments
284. References
285. Adaptations of peripheral vasoconstrictor pathways after spinal cord injury
286. Changes in ganglionic transmission after loss of preganglionic neurones
287. Sprouting of residual preganglionic axons rapidly reinnervates many postganglionic neurones
288. New connections in ganglia may be inappropriate
289. Changes in neurovascular transmission after spinal transection
290. Transmitter release may be increased in tail arteries after spinal cord transection
291. Nerve-evoked contractions are enhanced in tail arteries from rats with spinal cord transection
292. Decentralization mimics spinal cord transection in enhancing vascular reactivity
293. Nerve-evoked responses in mesenteric arteries are also potentiated after spinal transection
294. Conclusions
295. Acknowledgments
296. References
297. Genetic approaches to autonomic dysreflexia
298. Introduction
299. A mouse model of autonomic dysreflexia
300. A definition of autonomic dysreflexia
301. Proposed mechanisms for the development of autonomic dysreflexia
302. Wlds mice, a genetic model to study the effects of delayed axonal degeneration
303. The clip-compression injury, a nongenetic model to study the effects of delayed axonal degeneration
304. Histological assessments of spinal cord transection and clip-compression injury in wild-type and Wld
305. Incidence of autonomic dysreflexia in Wlds mice
306. Incidence of autonomic dysreflexia after spinal cord transection and clip-compression injury
307. Strain differences in the amplitude of autonomic dysreflexia
308. Increases in the size of the small diameter primary afferent arbor as a mechanism for the developmen
309. Strain differences in CGRP-Ir in the dorsal horn
310. Conclusions
311. References
312. Section IV. Bowel Dysfunction
313. Gastrointestinal symptoms related to autonomic dysfunction following spinal cord injury
314. Introduction
315. Background
316. Bowel anatomy and innervation
317. The enteric nervous system
318. Parasympathetic innervation
319. Sympathetic innervation
320. Colonic function, reflexes and control
321. Gastrointestinal dysfunction with acute spinal cord injury
322. Gastrointestinal dysfunction with chronic spinal cord injury
323. Upper gastrointestinal symptoms
324. Pain
325. Lower gastrointestinal symptoms and pathology
326. Upper versus lower motor neurone lesions: effect on the bowel
327. Incoordinate anal sphincter function
328. Constipation and incontinence
329. Therapies that exacerbate symptoms
330. Bowel management
331. Diet
332. Laxatives
333. Suppositories and enemas
334. Prokinetic agents
335. Mechanical devices and surgical interventions
336. Conclusion
337. References
338. Colorectal motility and defecation after spinal cord injury in humans
339. Introduction
340. Bowel dysfunction is a problem following spinal cord injury
341. Impact on lifestyle
342. Toileting
343. Colonic function following spinal cord injury
344. Colonic neurotransmitters following spinal cord injury
345. Anorectal function
346. Continence
347. Rectal sensation
348. Rectal compliance
349. Urgency
350. Defecation
351. High spinal cord injuries
352. Low spinal cord injuries
353. Change in bowel function with time from injury
354. Current management strategies
355. Does a colostomy improve bowel function?
356. Future objectives for the investigation and management of bowel dysfunction
357. References
358. Mechanisms controlling normal defecation and the potential effects of spinal cord injury
359. Introduction
360. Normal gut
361. Outline of colorectal function and morphology
362. Overview of defecation
363. Overview of neural control
364. Underlying smooth muscle properties
365. Basic rhythmic activity
366. Pacemaking
367. Underlying mechanisms in defecation
368. Experimental approaches
369. Colorectal motility and transport
370. Properties of the rectal smooth muscles
371. Properties of the internal anal sphincter
372. Properties of the external anal sphincter
373. Main areas of ignorance
374. Spinal cord injury
375. Introduction
376. Effects on colorectal motility and transport
377. Disordered defecation
378. Colorectal transport and defecation in acute spinal cord injury
379. Conclusion
380. References
381. Alterations in eliminative and sexual reflexes after spinal cord injury: defecatory function and dev
382. Introduction
383. Neuroanatomy
384. Peripheral components
385. Pelvic plexus
386. Pudendal nerve
387. Defecation
388. Defecation reflexes
389. Supraspinal control mechanisms
390. Eliminative functions following spinal cord injury
391. Conclusions
392. Acknowledgments
393. References
394. Upper and lower gastrointestinal motor and sensory dysfunction after human spinal cord injury
395. Introduction
396. Gastric emptying
397. Anorectal motor and sensory function
398. Cortical representation of sensory functions from the anorectum
399. Summary and conclusions
400. Acknowledgment
401. References
402. Section V. Sexual Dysfunction
403. Problems of sexual function after spinal cord injury
404. What is sex?
405. Impact on sexual function of the autonomic, motor and sensory changes associated with spinal cord in
406. Changes in sexual responses after spinal cord injury
407. Clinical issues of female sexual function after spinal cord injury
408. Clinical issues of male sexual function after spinal cord injury
409. Sexual consequences: the example of autonomic dysreflexia
410. Conclusions
411. Acknowledgments
412. References
413. Ascending spinal pathways from sexual organs: effects of chronic spinal lesions
414. Afferent innervation of the male and female reproductive organs
415. Hypogastric nerve
416. Pelvic nerve
417. Pudendal nerve
418. Ovarian/testicular nerves
419. Vagus nerve
420. Central processing of inputs from the male and female reproductive organs
421. Spinal processing
422. Supraspinal processing
423. Ascending pathways
424. Clinical implications of damage to these spinal pathways: males versus females
425. Sensation
426. Fertility
427. References
428. Descending pathways modulating the spinal circuitry for ejaculation: effects of chronic spinal cord
429. Introduction
430. Spinal reflex circuitry for ejaculation
431. Descending brainstem control of ejaculation
432. Effects of chronic spinal cord injury on sexual function
433. Clinical correlations in men with spinal injury
434. Pharmacological considerations
435. Summary
436. Acknowledgments
437. References
438. Male fertility and sexual function after spinal cord injury
439. Introduction
440. Pathophysiology of autonomic dysfunction affecting male fertility and sexual function
441. Erection
442. Ejaculation
443. Testicular disorders associated with spinal cord injury
444. Alterations of the semen associated with spinal cord injury
445. Methods of sperm collection
446. Semen abnormalities
447. Mechanisms of semen abnormalities
448. Testicular temperature
449. Stasis
450. Possible evolution of the sperm defects with spinal cord injury
451. Management of male infertility with spinal cord injury
452. The team approach
453. Clinical evaluation
454. Assisted ejaculation
455. Austin Health/Royal Women’s Hospital fertility program results
456. Summary
457. Sexual function
458. Male infertility
459. References
460. Female sexual function after spinal cord injury
461. The impact of SCI on female sexuality
462. Effect of SCI on female sexual arousal
463. Effects of SCI on orgasm
464. Documentation of sexual dysfunction in women with SCI
465. Improving sexual responsiveness

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