Neurologic Effects of Spinal Cord Injury (SCI)

Acute effects

Immediately following significant spinal cord trauma, your patient may experience a temporary depression of sensation and spinal reflexes (spinal shock), below the level of the injury. During the period of spinal shock, the patient will exhibit some degree of flaccid paralysis, anesthesia, bowel and bladder dysfunction, and loss of reflex activity (Ziu, 2022). This can result in bladder and bowel incontinence, requiring patient-specific bladder and bowel management.

• Areflexic bowel can result in paralytic ileus that may require decompression with a gastric tube
• Areflexic bladder will likely require an indwelling catheter in the acute phase of treatment to avoid urinary retention (Ziu, E. 2022).

Spinal shock must be differentiated from Neurogenic shock, the terms are not interchangeable.

Neurogenic shock is a component of the spinal shock syndrome and refers to the hemodynamic instability seen in these patients with hypotension, bradycardia, and hypothermia (secondary to sympathetic-parasympathetic dysfunction/imbalance (Ziu, E. 2022).

Categories of SCI

An SCI can be, complete, incomplete or transient.

• Complete SCI indicates that there is no nerve communication below the injury site; sensory and motor function below the injury site is lost (DHHS, n.d.).
  • Nearly 50% of all SCIs are complete.
  • Most complete SCIs are caused by contusions, bruise or ischemia, only rarely is the spinal cord cut or transected (. More commonly, loss of function is caused by a contusion or bruise to the spinal cord or by compromise of blood flow to the injured part of the spinal cord (AANS, n.d.).
• Incomplete SCI results in a partial loss of motor control or sensation. A person with an incomplete injury may be able to move one arm or leg more than the other or may have more functioning on one side of the body than the other (AANS).
• Transient SCI caused by spinal concussion or contusion may be either complete or incomplete andlast between one and two days (AANS).
  • Spinal shock is defined as a condition of transient physiologic, rather than anatomic, reflex depression of spinal cord function below the level of injury. In general, the more severe the physiologic or anatomic transection of the spinal cord, the more profound the spinal shock. (Ko, HY 2018).

Neurogenic bladder

The term “neurogenic bladder” indicates lower urinary tract (LUT) dysfunction caused by neurological disease. LUT dysfunction is commonly reported by patients with neurological disease, and significantly impacts their quality of life (Meyer, 2019). After SCI, the heterogeneous presentation of LUT symptoms and dysfunction reflect the complexity of the neural control of the LUT, and the site of lesion in the neurological axis. (Panicker, J. N. (2020).

Although there are many possible effects of SCI on the urinary system, they all involve some combination of changes in muscle activity or sensation. The muscles involved can be the detrusor muscle of the bladder, the smooth muscle of the internal sphincter, the striated muscle of the external sphincter, and/or the urethra. Changes in sensation can involve the bladder and/or the urethra. Reflexes usually return below the level of injury. Over time, some reflexes even become hyperactive when the inhibitory effects of the higher neuro function is lost.

We can classify spinal cord injuries according to location of the lesion, and we can make some generalizations about an SCI's effect on the urinary system.

• Suprapontine lesion (SPL) Defined by International Continence Society (ICS) as: a neurological lesion above the pons.  Lesions occuring in the forebrain or midbrain interfere with the conscious control of voiding. These lesions are characterized by storage dysfunction with symptoms of: spontaneous detrusor overactivity (DO), detrusor underactivity, detrusor overactivity with impaired contraction (Powell, C. 2016).
  • Neurogenic lower urinary tract dysfunction:
    • Detrusor areflexia (temporary), as with spinal shock, can occur immediately following cerebral injury: stroke, traumatic brain injury, hydrocephalus, etc., may result in urinary retention.
    • Detrusor hyperactivity coordinated with the urethral sphincter can occur when the pontine micturition center responds without cerebral inhibition (Gajewski, n.d.). In other words, the patient has detrusor overactivity causing urinary frequency, urinary urgency, and urge incontinence, with minimal urinary retention because the external sphincter is coordinated with detrusor contraction.
  • Common etiologies of SPL neurogenic bladder (Powell, C. 2016)
    • Cerebrovascular accident (CVA) is commonly associated with "Urge incontinence", with sphincter coordination.
    • Traumatic Brain Injury is involved in about half of SCI cases.
    • Normal Pressure Hydrocephalus (NPH) patients exhibit LUT symptoms similar to other SPL cases. A ventriculo-peritoneal shunt can often improve the LUT symptoms seen in NPH.
    • Cerebral Palsy is a SPL and it is associated with urge incontinence, enuresis and detrusor-sphincter dyssynergia (DSD).
    • Parkinson's disease is associated with detrusor overactivity, nocturia, urgency and frequency.
    • SPL Brain tumor is associated with urinary retention in about 70% of affected children.
    • SCI associated DSD increases the risk of elevated voiding pressures and may contribute to damage to the upper urinary tract, from “vesicoureteral reflux (VUR).
    • There are many more conditions that can cause or lead to SPL.

• Suprasacral lesions: All spinal cord lesions above the sacrum are included in this classification. Suprasacral trauma is the most common cause of SCI-related voiding dysfunction.
  • Immediately following SCI, the result is usually detrusor areflexia (DA), or the inability of the bladder to contract. This generally causes some degree of urinary retention. This "spinal shock" can last hours, days, months or more. To protect the upper urinary tract from the affects of vesicoureteral reflux and hydronephrosis the bladder should be drained using an indwelling catheter while the patient is being stabilized.

• Detrusor Overactivity (DO) in Patients With Traumatic Spinal Cord Injury (Wang, Z. 2021)
  Cervical	79.5%
  Thoracic (T1-T9)	61%
  Thoracic (T10-T12)	35.2%
  Lumbar	35%
  Conical cauda	19.2%

  When sacral reflex activity returns, the bladder may be able to contract, and pass urine again. The bladder stretch receptors are stimulated by bladder filling, but without the pontine inhibition, frequent spontaneous contractions of the detrusor muscle cause detrusor overactivity (DO). This often result is a small, hyperactive bladder, where voiding is interrupted, involuntary and incomplete.
• In addition, a very high percentage of suprasacral lesions, result in Dyssynergia or Detrusor Sphincter Dyssynergia (DSD). Here, coordination between the detrusor muscle and the bladder sphincter is affected. Instead of the sphincter relaxing, followed by detrusor contraction, the bladder may contract against the closed sphincter. Urine is prevented from leaving the bladder, resulting in intermittent voiding, urinary retention, bladder distention and reflux.
• Vesicoureteral reflux commonly occurs with suprasacral injuries. The hypereflexia leads to the bladder becoming less "stretchable", known as "high pressure," or has "low vesicle compliance." The functioning bladder sphincters won't allow the urine to exit, leading to reflux into the ureters and kidney. Upper urinary tract problems due to backpressure can ultimately lead to renal impairment.
• Infrasacral lesions: All lesions inside or outside the spinal canal, involving the sacral cord or roots.
• Commonly results in an atonic (AKA non-reflex or flaccid) bladder. Here the autonomic reflex is weak or absent. In this case it's impossible to know when (or if) the urine will be removed from the body. There is no longer any way to know if the bladder is full, and no urge to urinate. The flaccid bladder is the result of injury to the micturition center of the sacral cord, the cauda equina, or the sacral roots that supply the bladder.
• With infrasacral lesions, the atonic detrusor muscle is easily overstretched, leading to overdistention and retention.
• With sacral injuries, bladder management doesn't change much from the acute to long term stage, because bladder function doesn't significantly improve.