Review Article
Cardiovascular consequences of loss of supraspinal control of the sympathetic nervous system after spinal cord injury,☆☆

https://doi.org/10.1053/mr.2000.3848Get rights and content

Abstract

Teasell RW, Arnold JMO, Krassioukov A, Delaney GA. Cardiovascular consequences of loss of supraspinal control of the sympathetic nervous system after spinal cord injury. Arch Phys Med Rehabil 2000;81:506-16. Spinal cord injury (SCI) with resultant quadriplegia or high paraplegia is associated with significant dysfunction of the sympathetic nervous system. This alteration of sympathetic nervous system activity occurs as a consequence of loss of supraspinal control of the sympathetic nervous system and is further complicated by at least three subsequent phenomena that occur below the level of SCI: reduced overall sympathetic activity, morphologic changes in sympathetic preganglionic neurons, and peripheral alpha-adrenoceptor hyperresponsiveness. Reduced sympathetic activity below the level of SCI appears to result in orthostatic hypotension, low resting blood pressure, loss of diurnal fluctuation of blood pressure, reflex bradycardia, and, rarely, cardiac arrest. Peripheral alpha-adrenoceptor hyperresponsiveness likely accounts for some, if not the majority, of the excessive pressor response in autonomic dysreflexia and may also contribute to decreased blood flow in the peripheral microcirculation, potentially increasing susceptibility to pressure sores. What has yet to be established is whether this alpha-adrenoceptor hyperresponsiveness is a consequence of receptor hypersensitivity or a failure of presynaptic reuptake of noradrenaline at the receptor level. Better understanding of the pathophysiology of sympathetic nervous system dysfunction after high-level SCI should allow development of more effective measures to manage clinical complications. © 2000 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation

Section snippets

Sympathetic nervous system dysfunction in SCI

Maintenance of homeostasis within the body is a function of the autonomic nervous system and is interrupted when central nervous system (CNS) communications are interrupted. With high-level SCIs, the SNS is disproportionately involved when compared with the parasympathetic nervous system. In a complete high-level SCI, functioning in the isolated spinal cord below the lesion becomes independent of supraspinal control and has been termed “decentralization” of the SNS.3 Generally, the higher the

Reduced arterial pressure

Low blood pressure is a problem in both acute and chronic high-level SCI patients. In recently injured individuals with quadriplegia still in the acute stage of spinal shock, blood pressure is much lower than in normal controls.65 This lower blood pressure is regarded as secondary to a reduction in SNS activity below the level of SCI.12, 13 As Mathias and Frankel12, 13 have observed, it is unlikely that skeletal muscle paralysis accounts for low blood pressure as patients with flaccid

Summary

Cervical and high thoracic SCIs invariably result in significant SNS dysfunction. This SNS dysfunction can be largely attributed to several pathophysiological phenomena which occur below the level of SCI: (1) loss of supraspinal regulatory control; (2) reduced SNS outflow; (3) morphologic changes in sympathetic preganglionic neurons; and (4) peripheral alpha-adrenoceptor hyperresponsiveness. Reduced SNS outflow results in low resting blood pressure, orthostatic hypotension, reflex bradycardia,

References (141)

  • ED Kursh et al.

    Complications of autonomic dysreflexia

    J Urol

    (1977)
  • CH Barton et al.

    The effect of modified transurethral sphincterotomy on autonomic dysreflexia

    J Urol

    (1986)
  • BH Broecker et al.

    Low spinal anesthesia for the prevention of autonomic dysreflexia in the spinal cord injury patient

    J Urol

    (1979)
  • JM Arnold et al.

    Alpha-adrenoceptor hyperresponsiveness in quadriplegic patients with autonomic dysreflexia

    Clin Auton Res

    (1995)
  • NE. Naftchi

    Mechanism of autonomic dysreflexia. Contributions of catecholamines and peptide neurotransmitters

    Ann N Y Acad Sci

    (1990)
  • J Claus-Walker et al.

    Metabolic and endocrine changes in spinal cord injury: II (section 1). Consequences of partial decentralization of autonomic nervous system

    Arch Phys Med Rehabil

    (1982)
  • HL Frankel et al.

    Blood pressure in paraplegia. I

    Paraplegia

    (1972)
  • RP. Erickson

    Autonomic hyperreflexia: pathophysiology and medical management

    Arch Phys Med Rehabil

    (1980)
  • RL Braddom et al.

    Autonomic dysreflexia: a survey of current treatment

    Am J Phys Med Rehabil

    (1991)
  • JL Corbett et al.

    Cardiovascular responses to tilting in tetraplegic man

    J Physiol (Lond)

    (1971)
  • H Krum et al.

    Steady state plasma (3H) noradrenaline kinetics in quadriplegic spinal cord injury patients

    J Auton Pharmacol

    (1990)
  • CJ Mathias et al.

    Plasma catecholamines during paroxysmal neurogenic hypertension in quadriplegic man

    Circ Res

    (1976)
  • CJ Mathias et al.

    Enhanced pressor response to noradrenaline in patients with cervical spinal cord transection

    Brain

    (1976)
  • CJ Mathias et al.

    Autonomic disturbances in spinal cord lesions

  • CJ Mathias et al.

    The cardiovascular system in tetraplegia and paraplegia

  • ML Gimovski et al.

    Management of autonomic hyperreflexia associated with a low thoracic spinal cord lesion

    Am J Obstet Gynecol

    (1985)
  • BG Wallin et al.

    Sympathetic activity in man after spinal cord injury

    Brain

    (1984)
  • L Stjernberg et al.

    Sympathetic activity in man after spinal cord injury. Outflow to muscle below the lesion

    Brain

    (1986)
  • O DeBarge et al.

    Plasma catecholamines in tetraplegics

    Paraplegia

    (1978)
  • DM Frewin et al.

    Catecholamine responses in paraplegia

    Paraplegia

    (1973)
  • L Guttman et al.

    Effect of tilting on cardiovascular responses and plasma catecholamine levels in spinal man

    Paraplegia

    (1963-64)
  • NE Naftchi et al.

    Peripheral circulation and catecholamine metabolism in paraplegia and quadriplegia

    Arch Phys Med Rehabil

    (1972)
  • C Vallbona et al.

    Endocrine responses to orthostatic hypotension in quadriplegia

    Arch Phys Med Rehabil

    (1966)
  • DL Kamelhar et al.

    Plasma renin and serum dopamine-beta-hydroxylase during orthostatic hypotension in quadriplegic man

    Arch Phys Med Rehabil

    (1978)
  • M Levitt et al.

    Plasma dopamine-beta-hydroxylase activity in paraplegic and quadriplegic subjects

    Aust N Z Med

    (1974)
  • NE Naftchi et al.

    Relationship between serum dopamine-B-hydroxylase activity, catecholamine metabolism, and hemodynamic changes during paroxysmal hypertension in quadriplegia

    Circ Res

    (1974)
  • M Yekutiel et al.

    The prevalence of hypertension, ischemic heart disease and diabetes in traumatic spinal cord injured patients and amputees

    Paraplegia

    (1989)
  • A Biyani et al.

    Post-traumatic syringomyelia: a review of the literature

    Paraplegia

    (1994)
  • RP Bunge et al.

    Observation on the pathology of human spinal cord injury. A review and classification of 22 new cases with details from a case of chronic cord compression with extensive focal demyelination

  • MR. Dimitrijevic

    Residual motor functions in spinal cord injury

  • CH. Tator

    Update on the pathophysiology and pathology of acute spinal cord injury

    Brain Pathol

    (1995)
  • JF Ditunno et al.

    Chronic spinal cord injury

    N Engl J Med

    (1994)
  • RM Quencer et al.

    Acute traumatic central cord syndrome: MRI-pathological correlations

    Neuroradiology

    (1992)
  • AC Krassioukov et al.

    Morphological changes in sympathetic preganglionic neurons after spinal cord injury in rats

    Neuroscience

    (1996)
  • FR Calaresu et al.

    Medullary basal sympathetic tone

    Ann Rev Physiol

    (1988)
  • J Chalmers et al.

    Brainstem and bulbospinal neurotransmitter systems in the control of blood pressure

    J Hypertens

    (1991)
  • DJ Reis et al.

    The C1 area of the brainstem in tonic and reflex control of blood pressure

    Hypertension

    (1988)
  • LC Weaver et al.

    Spinal cord circuits providing control of sympathetic pregangionic neurones

  • F Gray et al.

    Quantitative study of lateral horn cells in 15 cases of multiple system atrophy

    Acta Neuropathol

    (1988)
  • DR. Oppenheimer

    Lateral horn cells in progressive autonomic failure

    J Neurol Sci

    (1980)
  • Cited by (472)

    View all citing articles on Scopus

    No commercial party having a direct financial interest in the results of the research supporting this article has or will confer a benefit upon the authors or upon any organization with which the authors are associated.

    ☆☆

    Reprint requests to Robert W. Teasell, London Health Science Centre, 339 Windermere Road, London, Ontario, N6A 5A5 Canada.

    View full text