(1) SCI Intro

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Description and Tags

09/28/2026 + 09/30/2026

59 Terms

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Anatomy - where does SC exit the skull?

foramen magnum

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Anatomy - central “H” of the spinal cord?

gray matter

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Anatomy - dorsal part is associated with?

sensory

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Anatomy - ventral/anterior horn is associated with?

motor

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Anatomy - intermediate is associated with?

interneurons

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Anatomy - the tracts and interneurons are made up of?

white matter

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Anatomy - fxn of sympathetic nervous system (SNS)?

fight/flight response:

  • dialate pupil

  • increased heartrate

  • dilate bronchi

  • converts glycogen to glucose

  • secrete adrenaline + noradrenaline

  • inhibits saliva

  • inhibits peristalsis + gastric secretion

    • inhibits bladder


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Anatomy - function fxn of parasympathetic nervous system (PNS)?

rest/digest response:

  • stimulates saliva

  • stimulates peristalsis + gastric secretion

  • stimulates bile production

  • contracts the bladder

  • slows heartrate

    • constricts bronchi


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2 types of SCI pathology

Traumatic vs. Non-Traumatic

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Traumatic SCI

Direct damage to vertebral column

  • spinal contusion

  • laceration

  • transection


Often used in studies (due to ease of knowing lesion) for inclusion criteria

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Non-Traumatic SCI

Loss of blood flow to the spinal cord

  • tumor

  • infection

  • multiple sclerosis (MS)

  • spinal stroke

  • arteriovenous malformation (AVM)

    • abdominal aortic aneurysm (AAA) repair


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Chart - frequencies of types of SCI

(slide 7 of SCI Intro PPT)


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2 phases of pathophysiology of SCI

Primary vs. Secondary injuries:

Primary = immediate resultant injury

Secondary = increased damage, often more chronic in nature

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Spinal Shock

Occurs immediately after SCI; may be due to abrupt withdrawal of connections between higher centers and spinal cord (“electrical shutdown”)

  • areflexia + flaccidity below level

  • transient reflex response (several hrs to 2-4 wks after injury)

  • earlier resolution from spinal shock = better prognosis

    • indicator for resolution: bulbocavernosus reflex


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Bulbocavernosus Reflex (Osinski Reflex)

Used for spinal shock (absence of bulbocavernosus reflex; presents with hypotension, bradycardia, complete loss of motor/sensation/reflexes)

  • when absent, still in spinal shock

    • anal sphincter will contract if present

    • checked by monitoring sphincter contraction in response to squeezing of penis or clitoris, or pulling on indwelling Foley catheter

  • polysynaptic response mediated by S2-S4

  • Better prognosis after reflex returns

This is typically completed by the medical team, less commonly the PT.


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Neurogenic Shock

Brain loses ability to send sympathetic “fight-or-flight” signals to blood vessels and heart (disrupts sympathetic chain T1-L2)

  • blood vessels suddenly vasodilate = blood pooling in limbs (decr. BP and HR that is uncompensated)

  • need to address w/ fluids and medications to save the spinal cord

    • can last up to 6 weeks


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Chart - Spinal Shock vs Neurogenic Shock

(slide 12 of SCI Intro PPT)


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Epidemiology and Etiology of SCI

  • average age from 29yo during 1970s to 43yo as of 2015

  • about 79% of new tSCI cases are male as of 2015

  • lengths of acute care stay and rehab duration have decreased as of 2015

  • incomplete tetraplegia is the most frequent extent

  • frequency of incomplete/complete paraplegia is virtually the same

  • less than 1% of persons experienced complete neurological recovery by hospital discharge


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Life Expectancy post SCI

  • average remaining years of life in persons with tSCI have not improved since 1980s, still significantly below life expectancies of persons without tSCI

  • mortality rates significantly higher in 1st year after injury; increased in those with most severe neurological impairments


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Causes of Death post SCI

Over time, pneumonia and septicemia have greatest impact on causes of death + reduced life expectancy in those with tSCI

  • no change in mortality rate for septicemia over last 50yrs, only slight decrease in mortality rate for respiratory disease

Decreased rates from cancer, heart disease, stroke, arterial disease, pulmonary embolus, urinary disease, digestive disease, and suicide.

However, increasing rates from endocrine/metabolic/nutritional disease, accidents, nervous system disease, musculoskeletal disorders, mental disorders.

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Mechanisms of Injury for SCI

Flexion: head-on collisions, most common (anterior cord syndrome)

Flexion/Rotation: side impact MVA, boxing “hook”

Hyperextension: typically in falls (land on chin), whiplash is often “milder” (central cord syndrome)

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Clinical Signs and Symptoms

Tetra/quadriplegia (same; use tetraplegia nowadays because fully Greek roots; quadri was latin) = 4 limbs

Paraplegia = lower half (2 limbs)

Neurologic Level of Injury (NLI) is determined by ISNCSCI exam

  • different than surgical level or injury location


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Incomplete SCI Syndromes

  • Central Cord Syndrome

  • Anterior Cord Syndrome

  • Brown Sequard Syndrome

  • Cauda Equina Syndrome


(1/5th of SCIs)

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Central Cord Syndrome

Most common cord syndrome

  • typically from hyperextension injury (falls, MVA)

  • UE > LE, proximal > distal involvement

  • associated w/ congenital or degenerative narrowing of spinal canal

  • sacral sensory sparing

  • typically ambulatory

    • some balance deficits: cannot use arms for balance

(slide 22 of SCI Intro PPT)


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Anterior Cord Syndrome

Affects anterior 2/3 of spinal cord, often T1-L2

  • typically from flexion injuries

  • motor loss

  • pain and temperature loss below lesion

    • proprioception and light touch spared (separate vascular supply)

    • normal vibratory sense, 2-point discrimination, fine touch

  • caused by ischemia w/in artery supplying blood to 2/3rds of spinal cord (Anterior Spinal Artery)

  • surgical repairs such as aortic surgery, hypotension (from cardiac arrest), vasculitis, sickle cell, AVM, disc herniation, cocaine use

  • typically longer lengths of stay


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Posterior Cord Syndrome

Rare – 1% of incomplete SCIs, from cervical to lumbar

  • impaired dorsal column:

    • proprioception, vibration, 2-point discrimination, and light touch below level of injury

  • causes: traumatic injury (hyperextension injury, e.g. MVA), tumors, degenerative disc disease, B12 deficiency, MS, untreated syphilis

  • other Sx: pain (burning/tingling), sensory ataxia


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Brown-Sequard Syndrome

Rarer form – 1-4% of traumatic SCIs

  • lesion resulting in:

    • ipsilateral motor loss (corticospinal)

    • ipsilateral proprioceptive, light touch, vibration loss (dorsal columns)

    • contralateral loss of pain and temperature (spinothalamic)

  • “Hemisection” (one side of SC is damaged)

    • Brown-Sequard Plus syndrome is more common (true hemisections are rarer)

  • Known to be caused by knife/bullet injuries

    • can still be caused by trauma, falls, disc herniation, tumors, MS, and infection

(slide 25 of SCI Intro PPT)


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Cauda Equina Syndrome

Damage to long nerve roots after end of SC, typically at L1

  • areflexic bowel/bladder and saddle anesthesia

  • same potential to regenerate as peripheral nerves elsewhere in body

    • not common due to large distance in lesions, glial-collagen scarring, disorganization of axonal regeneration, loss of end-organ functioning after reinnervation; rate slows and stops after ~1yr

  • Conus Medullaris syndrome (most distal portion of SC damaged; mixture of UMN and LMN damage)

  • both syndromes characterized by LE motor and sensory loss


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Chart - Cord Summary

(slide 27 of SCI Intro PPT)


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Medical Management of SCI

  • high-dose steroids ASAP (solumedrol)

  • surgical intervention (decompression, laminectomy, fusion)

  • anticoagulation

  • pulmonary, bladder, integument (need extra care/management until pt. learns to manage these themselves, due to increased infection risk)


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Internal/Surgical Intervention

  • anterior (may have difficulty speaking after) or posterior spinal fusion

    • the metal used for fusion

  • decompression, laminectomy


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Traction/Stabilization Interventions

  • Halo: superior option to immobilize upper c/sp

    • can restrict atlantoaxial flex/ext by 75% (vs. 45% with conventional orthoses)

  • Minerva Brace - CTLSO (cervical-thoraco-lumbar-sacral orthosis

  • TLSO (thoraco-lumbar sacral orthosis)


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Autonomic Dysfunction after SCI

Afrer SCI, supraspinal influence on autonomic nervous system (ANS) is disrupted

  • results in sympathetic blunting and parasympathetic dominance. Results in:

    • cardiac dysrhythmias, systemic hypotension, bronchoconstriction, copious respiratory secretions, uncontrolled bowel/bladder, and sexual dysfunction


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Systems Review Considerations for SCI patients

  • musculoskeletal

  • integument

    • pressure relief (move/adjust, just enough to get capillary refill)

      • for sitting: Q15min

      • for laying: Q2H

  • autonomic

  • cardiovascular

  • respiratory

  • nervous

  • bowel and bladder

  • sexual

  • psychological


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Musculoskeletal considerations

Paralysis, atrophy

  • LMN = flaccid paralysis

    • at the level of the injury

    • cauda equina

    • “more from lateral disc herniations”

  • UMN = spasticity, incr. tone

    • below the level of the injury

    • less atrophy (from tone)

  • Contractures (due to muscle imbalance)


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Bone Health considerations

Immobilization = osteoclastic bone resorption!

  • acute: hypercalcemia (high serum Ca2+)

  • long term: osteoporosis

    • patients may require DEXA scanning for BMD tracking

  • possible complication: Heterotopic Ossification (HO)

    • most common at hips → knees → shoulders

    • unorganized bone growths; can limit ROM (bony end-feels); may attempt to remove surgically but often grows back

Heterotopic Ossification (slide 34 of SCI Intro PPT)


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Chart - Integumentary considerations

Sitting: movement orders Q15min

Laying: movement orders Q2H

(slide 35 of SCI Intro PPT)


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Autonomic considerations

Apneic bradyarrhythmia

  • acute, high cervical patients with hypoxic conditions

  • Tx: avoid hypoxia (monitor O2 sats, HR)


Orthostatic Hypotension

  • lack of sympathetic input to regulate cardiac response to postural changes

  • need to incorporate postural challenges to Tx; use of abdominal binders/stockings/ace wraps (adjuncts to help incr. BP)


Temperature Control

  • no shivering/sweating below the level of the injury

  • decreased ability to withstand hot/humid weather; sports implications

    • big area for patient education


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Autonomic Dysreflexia

LIFE THREATENING CONDITION

  • only injuries at T6 and above

  • noxious stimuli (e.g. full bladder, impacted bowel, tight clothing, etc.) below level of injury triggers uncontrolled sympathetic response (fight-or-flight)

  • signs and symptoms:

    • flushed face, pounding headache, dizziness, high BP

  • prevention: education, bladder care

  • treatment: elevate patient’s head, identify + remove noxious stimulus, hypertensive medication

  • other causes: decr. HR, incr. sweating (where able)

  • more common with complete or chronic injuries

  • untreated? may lead to stroke


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Autonomic Dysreflexia Frequency

  • approx 40% with SCI above T6 have never heard of AD

  • 22% did not know how to respond to an episode of AD

  • up to 40% of ED personnel may not have adequate knowledge or training related to AD


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Chart - Autonomic Dysreflexia Stimuli (overview)

(slide 39 of SCI Intro PPT)


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Chart - Autonomic Dysreflexia Signs and Symptoms (overview)

(slide 39 of SCI Intro PPT)


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Cardiovascular considerations

Parasympathetic signals → vagus nerve (decr. heart rate and contractility)

Sympathetic outflow through sympathetic trunk

  • heart and upper body blood vessels above T6

  • lower body blood vessels between T6-L2

Imbalance between PSNS/SNS:

  • neurogenic shock, bradyarrhythmias, hypotension, AD, orthostatic hypotension, impaired cardiovascular reflexes


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Thermoregulation considerations

Poikilothermia

  • body cannot internally regulate core temperature = matches temperature of surrounding environment

  • e.g. cannot feel sunburns

Exercise/warm environment

  • limited ability to vasodilate peripheral blood vessels and lower body heat through sweat; results in hyperthermia

Cold environments

  • limited ability to vasoconstrict peripheral blood vessels and shiver results in hypothermia

Hyperhidrosis (excessive sweating), anhidrosis (lack of sweating), or hypohidrosis (limited sweating)

  • most common presentation is:

    • hyperhidrosis above lesion

    • hypohidrosis below lesion


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Exercise Tolerance and Wellness considerations

SCI below or w/in thoracolumbar sympathetic output

  • reduced exercise tolerance, lower stroke volume, reduced cardiac output

Cervical SCI

  • likely demonstrate lower peak HR, post-exercise hypotension, and other abnormal CV responses to exercise

Long term SCI

  • at-risk for developing CV disease (due to inactivity), impaired glycemic control, chronic inflammation, abnormal cholesterol profiles

***Regular exercise program after rehab is imperative***


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Respiratory considerations

Paradoxical breathing (typical in tetraplegia)

  • abnormal breathing pattern; reverse of normal chest wall movement during breathing

Treatments

  • abdominal binders (improve/assist respiratory function)

  • coughing (functional? weak?)

    • assisted coughing; manual assist; devices; self-assist


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Respiratory system review

Volume:

  • vital capacity is ½ of normal value in people with tetraplegia

  • observe patient for accessory breathing muscle use

  • consult with respiratory therapy


Respiration Muscles (slide 44 of SCI Intro PPT)


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Chart - nerve involvement and respiratory muscles

(slide 45 of SCI Intro PPT)


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Bowel Function considerations

SCI patients report that bowel dysfunction has greater impact on QOL and social activities than other impairments

Normal sphincter control (S2-S4)

  • internal sphincter: increased tone at rest, relaxes with rectal distension

  • external sphincter: maintains tone at rest, increases tone when internal sphincter relaxes (for voluntary control over evacuation)

Neurogenic Bowel in SCI patients

  • decreased control over defecation due to injury of nervous system

  • immediately after SCI with spinal shock: may have paralytic ileus


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Bowel Management considerations

Reflexive/spastic bowel

  • anorectal reflex is intact; UMN lesion above S2 (or T12, depending on source)

    • bowel program: stimulate rectum to trigger reflex

    • digital stimulation and suppositories to simulate the reflex

    • goal: soft-formed stool

Areflexive/flaccid bowel

  • anorectal reflex is absent; LMN lesion at S2-S4 (or cauda equina involving S2-S4)

    • bowel program: manual evacuation of bowel, typically several times/day

    • goal: keep stool well-formed, rectal vault clear, prevent accidents


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Bowel Program considerations

Established bowel clearing schedule

Bowel movements planned for the same time of day, every day

Perform bowel care within 30mins - 1hr post-meal

Complete emptying of the rectal vault with each movement

Eat and drink well (track how foods affect you, drink ≥2L H2O daily; must be weary of irritating foods like spicy, lactose, etc. that may be aggravating on bowels)

Stay active (within abilities)

Know the effects of medications and their timing (e.g. stool softeners, bulking agents, suppositories)

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Genitourinary (Bladder) considerations

Same neural level for sphincter control as bowels: S2-S4

Detrussor muscle → “internal sphincter” that detects stretch (bladder full = distension)

Pelvic floor → “external sphincter” for voluntary control of bladder voiding

***Must prevent urinary tract complications***

  • UTI

  • Hydronephrosis (kidney swelling due to urine backup)

  • Renal calculi (kidney stones)

  • Bladder calculi (bladder stones)

  • Vesicoureteral reflux (backward flow of urine up the ureter)


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Neurogenic Bladder considerations

  • Spinal shock = flaccid bladder = indwelling catheter

  • Reflexive = emptying of bladder with distension of bladder walls

    • Management includes suprapubic tapping, intermittent catheterization (IC)***, condom catheter, indwelling catheter

  • Areflexive = resultant urinary retention

    • Management includes Créde maneuver (manual pressure over lower abdomen for voiding), valsalva, ICs


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Sexual Function considerations

This spans more than just the physical ability to have intercourse; often overlooked by healthcare professionals

  • typically an area first addressed by social workers

Paraplegics report that improved sexual function is primary factor to improve QOL; tetraplegics = secondary after improved hand function

Patient education to include sexual aids, positioning


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Sexual Function; Male considerations

Reflexogenic erections (complete injuries above T10) = response to external physical stimulation

Psychogenic erections (preserved with LMN lesions) = response to cognitive activity

Ejaculation is impaired; implications for decreased fertility

Interdisciplinary approach: work with MSW and/or Psychology team members

Concerns: safety + hygiene implications

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Sexual Function; Female considerations

Reflexogenic vs. Psychogenic responses also present

Normal menstruation returns; interrupted for first 3-24mo after injury

Concerns: close support during pregnancy (decreased awareness of when labor may start)

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Nervous System considerations

Acute pain may be present

Nociceptive pain (musculoskeletal or visceral)

  • UEs more common (overuse); biceps tendonitis, lateral epicondylitis, shoulder impingement, RTC tears, CTS, wrist tendonitis)

Neuropathic: central vs. peripheral

  • difficult to treat

  • TENS, massage, acupuncture, mental imagery

    • Pharmacological (Gabapentin/Neurontin, Pregabalin/Lyrica, etc.)


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Nervous System – Possible Complications

Secondary impairments/complications can arise from immobility:

  • DVTs, PEs

  • Edema (dependent edema → lymphedema)

  • UTI

  • Osteoporosis

  • Contractures


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Posttraumatic Syrinx (Syringomyelia)

Chronic complication resulting in fluid-filled cavity in the spinal cord; unknown causes

  • presentation: pain, change or reduction in motor or sensory abilities

  • Tx: surgery, shunt placement

  • Dx method: MRI

  • High recurrence rate