Spinal Cord Injury: Intro and Neuroanatomy

• Spinal Cord Injury (SCI) Introduction and Neuroanatomy

Objectives

• Describe the differences and similarities between UMN and LMN spinal cord lesions
• Describe the clinical presentation of Common SCI syndromes
• Recognize key signs and symptoms of autonomic dysreflexia (AD)
• Determine the sensory and motor neurological levels in a patient with SCI based on the ASIA scale
• Distinguish between bowel and bladder issues with UMN and LMN spinal cord lesions

Steps for review

• Neuroanatomy, general consideration, and pathogenesis in the first step
• The second step contains disease course, clinical findings, Red Flags and diagnosis/differential diagnosis
• The third step lists medical management, prognosis, and clinical management

Neuroanatomy

• The central nervous system (CNS) includes upper motor neurons (UMNs) and lower motor neurons (LMNs) also includes sensory and "other"
• Peripheral nervous system (PNS) includes sensory and autonomic components

General Considerations regarding spinal cord end

• The spinal cord ends at the L1-L2 level; This area is considered the UMN
• The conus medullaris, cauda equina, and the L2 and below area are all considered part of the LMN

UMN vs. LMN

• UMN include the lateral cortical spinal tract/ Spinal Cord
• LMN include the anterior horn cell and spinal nerve root

Tracts of the Spinal Cord

• UMN and LMN
• Gracile fascicle
• Cuneate fascicle
• Lateral corticospinal tract
• Dorsal spinocerebellar Tract
• Anterior horn cell
• Ventral spinocerebellar tract
• Anterolateral system
• Ventral corticospinal tract
• Medial vestibulospinal tract
• Rubrospinal tract
• Tectospinal Tract
• Medullary reticulospinal Tract
• Lateral vestibulospinal tract

Spinal Cord Syndromes

• Lateral cord (Brown-Séquard)
• Complete cord
• Central cord
• Anterior cord
• Posterior cord
• Pure Cortical motor
• Conus
• Cauda equina

Prevalence/Incidence

• Between 8000 and 50,000 acute SCI injuries in North America each year
• About 305,000 people living in the U.S. in 2023
• The most common causes are motor vehicle accidents (MVA), falls, and violence
• 60% of injuries occur in children or young adults ≤ 30 years
• Typically individuals 16-30 years old
• The mean age is 42.0 years as of 2017
• Men are affected 4x more than women, women account for 80.9% SCI

Traumatic SCI Etiology

• Initial injury via four different mechanisms
• Four mechanisms include impact with persistent compression (Burst Fracture)
• Next is impact with transient compression post hyper/injuries
• Then Distraction: forcible stretching of spinal cord or blood supply
• Finally Laceration from missile injury, sharp bone fragment dislocation, or severe distraction

Pathogenesis of Spinal Cord Injuries

• Primary Injury: Loss of Neurons/Axons & Demyelination
• Secondary Injury: Loss of Neurons/Axons, Demyelination, Inflammation, Reactive Oxidative Damage, Cyst Formation
• Neuroinflammation and Recovery: Understanding the micro environment is critical
• Inflammation at the lesion site is well-known, but less known at different levels
• Inflammation may occur 10 segments away
• There is the potential to improve recovery with inflammation
• Inflammation specifically in the lumbar and sacral area can produce maladaptive neuroplasticity and no motor learning

Disease Course

• Acute onset, then progressive to stable
• Initial traumatic event
• Followed by spinal shock with flaccid paralysis, loss of sensation, and motor function
• After emergency response, immobilization, and stabilization with diagnosis via MRI
• Then stable with possible UMN signs like spasticity and possible hyperreflexia
• Leading to a neurological return: most recover in one year and rapid recovery in the first six months

Diagnostic tools

• The most important diagnostic tool is an MRI
• Options also include X-rays, CT scans, EMG, and NCV

Medical Management

• A standard of care includes immobilization via halo, TLSO while avoiding prolonged immobilization
• Early intervention via closed reduction, spinal decompression
• Corticosteroids such as early methylprednisolone IV bolus
• BP management, general care, and nutritional support
• Surgical includes implanted spinal stimulators
• Locomotor training and Nanofibers aka "Dancing Molecules"

Prognosis

• Mortality post-SCI in 4-17% of cases
• Predisposing factors such as age, higher levels, pulmonary embolism, medical co-morbidities, and suicide
• Predictive factors for recovery potential (Table 14-12)
• Brown-Séquard syndrome has the greatest potential for recovery (75-90% walk independently post DC/70%ADLs)
• Central cord syndrome can have lower extremity (LE) recovery and bowel and bladder function seen early on
• Those that are age less than 50 are indicated for faster and more successful recovery
• Also needs the ability to attain intensive locomotor training

Issues in the Rehab of Spinal Cord Injury

• Bladder Dysfunction
• Bowel Dysfunction
• Sexual Dysfunction
• Decubitus Ulcers
• Autonomic Dysreflexion
• Spasticity
• Wheelchair Seating & Positioning

UMN vs. LMN: Bowel/Bladder and Symptoms

• UMN lesion (C1-L1)
  • Bowel: Hyperreflexic (spastic paralysis), Reflex is intact
  • Bladder: Spastic (urinary bladder and sphincter are overactive)
  • Symptoms: Bowel: constipation, difficulty with evacuation and incontinence, AD, Bladder: increased frequency of urination/failure to store urine, Inability to fully empty the bladder
  • Clinical management:: Bowel: reflex defecation; stool softener, laxative and suppository or rectal stim, Bladder: catheterization, prevention of urinary tract complications, and pharmacologic management
• LMN lesion (L2-S5)
  • Bowel: Areflexic (flaccid paralysis) and there is no tone to the muscles
  • Bladder: Areflexic (detrusor unable to contract)
  • Symptoms:: Bowel: constipation, difficulty with evacuation and incontinence, Bladder: retention and failure to empty urine; Possible damage to kidneys and bladder wall
  • Clinical Management: Bowel: stool softener, minimal strander to avoid, Bladder: catheterization, prevention of urinary tract complications, and pharmacologic management
• Consistent bowel program is critical
• Distinction between UMN and LMN depends on the segmental levels affected vs. vertebral levels

Autonomic Dysreflexia-Clinical Management

• Exaggerated, massive autonomic response to strong sensory stimuli
• The loss of inhibitory control of sympathetic neurons are generally lesions T6 and above
• Common causes: bladder and bowel distension, ulcers, constrictive clothing, ingrown toenails
• Remove strong stimuli
• Medical emergency: Monitor vitals, check for common noxious stimuli, do not lay patient supine
• Pounding headache caused by increased BP
• Hypertension, commonly BP > 200/100
• Flushed reddened face
• Nausea
• Diaphoresis above level of injury
• Red blotches on the skin above the SCI
• Slow pulse
• Cold, clammy skin below the SCI
• Restlessness
• Cutis anserina (goosebumps)
• Nasal congestion

Clinical Management: Sexual Dysfunction-Males

• Autonomic nervous system essential to penile erection
• Parasympathetic nervous system initiates the erectile response (S2-4)
• Sympathetic nervous system allows for ejaculation (L1–3)
• Most common issues
  • Erectile dysfunction (ED)
  • Ejaculation
  • Fertility
• Treatment options for ED:
  • Surgical procedures (penile prosthesis)
  • Vacuum devices
  • Pharmacology

Sexual Dysfunction: Females

• Autonomic nervous system is crucial
• T11-L2: innervates uterus
• S1-S4: innervates vulva and vagina
• Most common issues
  • Altered menstrual period
  • Lubrication
  • Hormonal changes
• Fertility often not affected

Spasticity

• Velocity-dependent increase in tonic stretch reflexes with passive movement
• UMN: lesions above the cauda equina
• Initially absent immediately post acute injury and develops over weeks
• Patients need stretching/contracture management
• Medications: baclofen, tizanidine, diazepam, dantrolene, and clonodine
• Botox, xeomin, phenol nerve blocks
• Intrathecal baclofen pump (ITB)

ASIA Impairment Scale (AIS) Grade

• A: Complete: No motor or sensory function is preserved in the sacral segments S4-5
• B: Incomplete: Sensory but not motor function is preserved below the neurological level and includes the sacral segments S4–5
• C: Incomplete: Motor function is preserved below the neurological level, and more than half of the key muscles below the neurological level have a muscle grade less than 3
• D: Incomplete: Motor function is preserved below the neurological level, and at least half of the key muscles below the neurological level have a muscle grade of 3 or more
• E: Normal: Motor and sensory functions are normal Determine sensory levels for right and left sides: the sensory level is the most caudal, intact dermatome for both pin prick and light touch sensation
• Determine motor levels for right and left sides: Defined by the lowest key muscle function that has a grade of at least 3 (on supine testing), providing the key muscle functions represented by segments above that level are judged to be intact (graded as a 5).
• Determine the Neurological Level of Injury (NLI): This refers to the most caudal segment of the cord with intact sensation and antigravity (3 or more) muscle function strength, provided that there is normal sensory and motor function (intact) rostrally respectively.
• Determine whether the injury is Complete or Incomplete (i.e., absence or presence of sacral sparing):
  • Complete, when voluntary anal contraction = No AND all S4-5 sensory scores = 0, AND deep anal pressure = No
  • Incomplete, when voluntary anal contraction = Yes, OR S4-5 sensory scores are >0, OR deep anal pressure = Yes
    • Then determine ASIA Impairment Scale (AIS) Grade

Determining Sensory and Motor Levels

• The sensory level is the most caudal level normally innervated dermatome for both pin prick and light touch (grade 2)
• Motor level is the most caudal level, normal or intact innervated spinal nerve
• Neurologic level: the most caudal segment of the cord where sensory and motor is intact

Nontraumatic Disorders of the Spinal Cord

• Syringomyelia
• Spina bifida
• Spinal epidural abscess
• Spinal epi/subdural hematoma
• Myelitis
• SC infarction

Syringomyelia

• There is a fluid-filled gliosis-lined cavity starts in the central canal that can be irregularly shaped
• The Etiology is unclear
• Disrupts central structures and anterior horn of gray matter that is associated with spinal column or brainstem abnormalities (scoliosis, Klippel-Feil syndrome, Arnold Chiari malformation)
• Occurs in the third and fourth decades of life and also can begin in childhood
• Diagnosis: MRI and CT

Syringomyelia progression

• Involves the long motor tracts and the sensory tracts (UE > LE)
• With post-traumatic Syringomyelia, symptoms may come above or below the original injury site
• Presenting the symptom of a worsening of pain or neurological function
• Conservative medical management includes avoiding high force isometric contractions and Valsalva expirations
• Head elevation at night and maintaining a neutral neck
• Can manage through surgical via decompression, shunt replacement and tumor resection and radiation treatment

Spina Bifida

• Spina bifida aperta presents visibly
• Myelomeningocele is the most severe form
• Protrusion of the spinal meninges and spinal cord through a defect in the vertebral column; this spinal cord defect is not covered by the skin
• It is usually associated with nerve paralysis symptoms, though not always

Clinical Findings of Spina Bifida

• The degree of motor and/or sensory loss varies
• Musculoskeletal deformities are likely
• There is high risk:
  • Neurogenic bowel and bladder, UTIs, latex allergies
  • Arnold Chiari type II, hydrocephalus
• No two patients are clinically identical
• High risk for loss of function over time

Spina Bifida Medical Management

• Surgical closure of myelomeningocele
• Surgical correction of orthopedic deformities
• Placement of ventriculoperitoneal shunt
• Medications for the management of bowel and bladder function
• Also includes Fetal meningomyelocele repair

Spina Bifida Prognosis

• Despite surgical interventions, affected nerves may still not function normally
• Patients typically have normal intelligence
• There will be hydrocephalus and meningitis risks
• Potentially leads to learning and seizure disorders
• Spinal cord issues can develop later in life
• In some cases that also includes Rapid growth during puberty
• Increased risk of progressive neurological impairments
• As well as orthopedic problems (scoliosis, foot or ankle deformities, dislocated hips, and even joint contractures

Hydrocephalus

• This term is defined by and describes the excessive accumulation of cerebrospinal fluid in the ventricles of the brain
• 25% of children with MMC are born with Hydrocephalus
• And of the other cases 60% develop it after the surgical closure of their back lesion
• 80–90% of children with hydrocephalus require a CSF shunt such as a ventriculoperitoneal catheter shunt
• If left untreated it can cause severe cognitive deficits
• Hydrocephalus occasionally resolves spontaneously

Medical intervention: Ventriculoperitoneal Shunt function

• Relieves pressure from the brain caused by fluid accumulation
• Primarily used to treat hydrocephalus
• Surgically placed inside ventricles to divert fluid away from the brain

Ventriculoperitoneal VP Shunt

• Is likely to require replacement after several years
• Infants need replacement every two years on average
• Two-year old and up children can use the same replacement for up to 10 years
• Common complications associated with the shunt system include Mechanical failure Obstruction Infection as well as Catheter may need to be lengthened or replaced
• Shunt malfunctions can lead to over- or under-drain the CSF
• Some symptoms may point to shunt malfunction: includes headaches, vomiting, lethargy, Irritability, swelling or redness along the shunt tract, decreased school performance, confusion, as well as seizures
• In cases of suspected shunt malfunction a MRI or CT can confirm growth of ventricles

Arnold Chiari II Malformation

• Characterized by tissue from the cerebellum, medulla, and fourth ventricle is displaced into the foramen magnum. 
• Almost all children with MMC have an Arnold Chiari II malformation.
• Interferes with the normal flow of the CSF around the brain and spinal cord, leading Hydrocephalus

Tethered Cord

• Occurs from scarring of the spinal cord or meninges to the overlying dura or skin and is detected via MRI
• There is now resultant traction on neural structures and can cause a Deterioration of "normal" gait pattern, potentially causes loss of sensation and strength down a particular dermatome
• 20-50% of children with spina bifida defects repaired shortly after birth will require surgery in their life to untether spinal cord

Key Concepts

• The spinal cord ends between L1-L2 vertebrae (UMN)
• The cauda equina is a collection of nerve roots that begins at the end of the spinal cord and exits from the third lumbar vertebra to the fifth sacral vertebra (LMN)
• SCI syndromes
• AD is an exaggerated autonomic response to a strong sensory stimuli that is a medical emergency typically for SCI levels T6 and above
• ASIA classification sensory and motor levels definitions
• Differences and similarities between bowel and bladder dysfunction

Overview of spinal cord injury (SCI) including neuroanatomy, pathogenesis, disease course, and clinical findings. Covers upper motor neuron (UMN) and lower motor neuron (LMN) lesions, clinical presentations of common SCI syndromes, and autonomic dysreflexia (AD). Also reviews medical, prognostic, and clinical management strategies.