Pathophysiology 

Facts in General

1. SCI Facts in General

  • Approximately 10,000 new cases each year in the U.S. [McDonald 1999]
  • Approximately 267,000 in the U.S., calculated from the existent data [DeVivo 1980]
  • Late 30’s
  • Male predominant
  • Motor vehicle crashes (about half of the cases)
  • Incomplete quadriplegics: the largest group of SCI patients, followed by the complete paraplegics
  • Cervical spinal cord is the most commonly found to be involved
  • Cumulative 10 year survival rate >86%
  • 30.2-year
  • pneumonia > accident > suicide

‘Life Expectancy for Persons who survive >1 year post-injury’

  • Higher mortality risk was associated with higher neurologic level and completeness of spinal cord injury, older age at injury and earlier year of injury [Frankel 1998].
  • Renal failure and other urinary tract complications were traditionally known to be the overall leading cause of death until the mid-1970s. Recent data indicate a significant decline in their role as the primary cause of death in SCI patients [Stover 1987] [Frankel 1998]
  • For more recent information, visit the National Spinal Cord Injury Statistical Center at the University of Alabama at Birmingham's Department of Rehabilitation Medicine

2. MS Facts in General

 FactsComments
  • 1/1,000 Americans and 2/1000 northern Europeans [Litwiller, 1999]
  • an estimated worldwide prevalence of 2.5 million [American Multiple Sclerosis Society]
 

  • affecting people between 20 and 45 years old
  • men: women = 1:2
  • autoimmune attack on CNS myelin with relative preservation of axon cylinders
 
  • myelinated white matter pathways in the brain and spinal cord
  • suprasacral: cervical, most common (80%) [Oppenheimer 1978]
  • sacral: 0-63% (controversial): 63% had detrusor hypocontractility but only 5% displayed areflexia [Mayo 1992]
  • intracranial: 60-90% [Francis 1995]
 
  • relapsing-remitting or primary progressive
 

Pathophysiology of the Neuropathic Bladder in SCI

1. Spinal cord injury

1) Epidemiology

  • Significant improvements in surgery, urology, and rehabilitation medicine over the last decades made a substantially decreased mortality in persons with SCI.
  • However, urinary tract mortality still ranks as the second leading cause of death to respiratory problem in the SCI patient [Frankel 1998].
  • Males are 75% more likely to die of urinary system diseases than females [Frankel 1998]
  • Those with tetraplegia and paraplegia are 4.35 and 2.20 times more lokely to die from these causes [Frankel 1998]
  • Individuals injured at older ages are more at risk of dying of urinary system diseases [Frankel 1998]

2) Initial Events of Spinal Cord Trauma

  • Immediate events: The damage to the spinal cord begins at the moment of injury.
    • Axons are directly damaged depending on the impact of the trauma.
    • Bone fragments can further damage the spinal cord by tearing spinal cord tissue.
    • Blood vessels supplying spinal cord may be ruptured. Severe bleeding can spread to other areas of the spinal cord over a short period of time.
  • Further acute events:
    • The spinal cord swells to fill the cavity of the spinal canal. This swelling can compress blood vessels and therefore compromises blood supply to spinal cord tissue, resulting ischemic injury to the spinal cord.
    • As blood pressure lowers, it interrupts the electrical activity of neurons and axons. Complete paralysis may develop with loss of reflexes (‘spinal shock’)
    • Therefore, urinary retention is universally resulted.

3) SCI Recovery and Reorganization of Neural Pathways

  • Neuronal connectivity has a remarkable plasticity.
  • Normally, myelinated A-delta afferents detects gradual distention of the urinary bladder and mediate normal micturition. Unmyelinated C afferents are relatively insensitive to this stimulus. Most C fibers remain silent during normal filling phase.
  • Damage to the spinal cord causes development of reorganizations in neural circuits.
  • Modification of the micturition reflex pathways takes place over long period of time.
  • A fixed clinical pattern of the voiding dysfunction gradually and eventually develops.
  • A new spinal reflex circuit mediated by C fiber develops in response to a reorganization of synaptic connections in the spinal cord. These C-fiber afferents are thought to be responsible for the development of detrusor hyperreflexia after SCI and MS

4) Chronic Events

  • The ultimate expression of the neurogenic bladder secondary to SCI is largely classified according to the location of lesion. Usually sacral S2-4 is the landmark to be divided since sacral spinal center is primary micturition center.
  • The clinical expression should be clearly characterized but actual manifestation does not always follow the theoretical rule. However, it might be convenient to use this demarcation for clinical purposes.
    • Landmark = sacral micturition center (conus medullaris)
      • Suprasacral lesion: lesion above the sacral spinal micturition center
        • detrusor hyperreflexia + DSD
      • Sacral lesion: lesion involving the sacral spinal micturition center
        • detrusor areflexia + fixed underactive or denervated striated sphincter
      • Infrasacral lesion: lesion involving peripheral nervous system
        • detrusor areflexia + fixed underactive or denervated striated sphincter
  • Another relatively less frequently used landmark for division is the cauda equine. SCIs are differentiated as to whether the injury is within the spinal cord proper or whether it has occurred outside it (for example, cauda equina). The signs of each type of lesion quite correspond to the followings although, by definition, the two landmarks are not exactly the same location.
    • Landmark = tip of spinal cord proper
      • Upper motor neuron lesion
      • Lower motor neuron lesion
  • The simplest way to understand end result of voiding dysfunction in SCI patients is to divide the voiding dysfunction. In the context to the voiding dysfunction, each signs can be matched according to the following functional classification proposed by Wein [Wein 1981]:
    • storage failure
      • Because of the bladder
        • overactive detrusor (detrusor hyperreflexia)
        • poor bladder compliance
        • both
      • Because of the outlet
        • sphincteric incompetence
    • emptying failure
      • Because of the bladder
        • underactive detrusor (or detrusor areflexia)
        • unsustained bladder contractility
      • Because of the outlet
        • bladder outlet obstruction
        • anatomical
        • functional: DSD
  • More sophisticated information can be obtained by fluoroscopic urodynamic study. Detailed bladder and sphincter behaviors as well as the pressure information can be identified.

Pathophysiology of the Neuropathic Bladder in MS

1) Pathophysiology

  • MS is caused by an autoimmune focal neural demyelination in the brain and spinal cord.
  • Demyelinating lesions, known as plaques, are scattered throughout the white matter of the nervous system.
  • This demyelination causes alteration in nerve conduction in axonal pathways.
  • This disease process most commonly involves the cervical spinal cord. This corresponds to the fact that voiding dysfunction and sphincter dysfunction is so common in this disease.
  • Involvement of the lumbar and sacral cord, cerebral cortex and midbrain can also occur.
  • The clinical course is characterized by the exacerbation and remission.
  • MS is often found in young and middle-aged adults with a twofold predilection for women.
  • Urodynamically, the most common pattern seen is hyperreflexic neurogenic bladder about 62% of patients [Litwiller 1999].

2) Neurogenic Bladder in MS

  • 80% have lower GU tract dysfunction and 96% with the disease for >10 years have urological findings [Koldewijn 1995]
  • Urinary symptoms may be age related and have a bimodal distribution. Patients <40 years are most bothered by bladder storage and voiding symptoms. Patients >50 years are related botheres by cumulative effect of other causes of bladder dysfunction (BPH, female stress urinary incontinence) [Littler 1999].
  • Urodynamic findings: metanalysis from 1882 patients [Littler 1999]
    • Detrusor overactivity: 62% (most common urodynamic finding in MS)
    • Detrusor underactivity: 20%
    • Normal detrusor function: 10%
    • DSD: 25%
    • DSD: 25%
Key Points of This Section
  • These are devastating processes.
  • MS is a progressive disease unlike SCI and no MS patient can ever be considered “stable.”
  • Although mortality and morbidity associated with SCI/D have been dramatically reduced by treatment neither has been eliminated.

References

  • American Multiple Sclerosis Society
  • DeVivo MJ, Fine PR, Maetz HM, Stover SL. Prevalence of spinal cord injury: a reestimation employing life table techniques. Arch Neurol. 1980 Nov;37(11):707-8.
  • DeVivo MJ, Fine PR, Maetz HM, Stover SL. Prevalence of spinal cord injury: a reestimation employing life table techniques. Arch Neurol. 1980 Nov;37(11):707-8.
  • Francis GS, Evans AC, Arnold DL. Neuroimaging in multiple sclerosis. Neurol Clin. 1995 Feb;13(1):147-71.
  • Frankel HL, Coll JR, Charlifue SW, Whiteneck GG, Gardner BP, Jamous MA, Krishnan KR, Nuseibeh I, Savic G, Sett P. Long-term survival in spinal cord injury: a fifty year investigation. Spinal Cord. 1998 Apr;36(4):266-74. http://www.spinalcord.uab.edu/show.asp?durki=21446
  • Koldewijn EL, Hommes OR, Lemmens WA, Debruyne FM, van Kerrebroeck PE. Relationship between lower urinary tract abnormalities and disease-related parameters in multiple sclerosis. J Urol. 1995 Jul;154(1):169-73.
  • Litwiller SE, Frohman EM, Zimmern PE. Multiple sclerosis and the urologist. J Urol. 1999 Mar;161(3):743-57.
  • Mayo ME, Chetner MP. Lower urinary tract dysfunction in multiple sclerosis. Urology. 1992 Jan;39(1):67-70.
  • McDonald JW. Repairing the damaged spinal cord. Sci Am. 1999 Sep;281(3):64-73.
  • Oppenheimer DR. The cervical cord in multiple sclerosis. Neuropathol Appl Neurobiol. 1978 Mar-Apr;4(2):151-62.
  • Stover SL, Fine PR. The epidemiology and economics of spinal cord injury. Paraplegia. 1987 Jun;25(3):225-8.
  • Wein AJ. Classification of neurogenic voiding dysfunction. J Urol. 1981 May;125(5):605-9.

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