Spinal Cord I

Descending motor tracts

lateral corticospinal, rubrospinal, ventral corticospainl, vestibulospinal

ascending sensory tracts

dorsal columns, dorsal spinocerebellar, anterolateral, ventral spinocerebellar, ventral spinothalamic

lateral corticospinal controls

voluntary motion, especially precisely controlled movements of distal limbs

Ventral corticospinal controls

voluntary motion of axial musculature, however, minimal clinical significance due to small size

rubrospinal controls

voluntary motion of UE, especially precisely controlled movements of distal muscles, (flexion)

vestibulospinal controls

posture and balance

lateral and medial reticulospinal control

posture, balance, modulation of spinal reflexes, axial and proximal limb motions, in motor tasks complements actions driven by corticospinal

lateral corticospinal travels

IL

ventral corticospinal travels

CL

Rubrospinal travels

IL

vestibulospinal travels

Bil

lateral and medial reticulospinal travels

IL

anterolateral system (spinothalamic, spin-reticular, and spinotectal tracts) travels

CL

anterolateral system (spinothalamic, spin-reticular, and spinotectal tracts) sensory modality

pain, temperature, and crude touch

dorsal column travels

IL

dorsal column sensory modality

proprioception, vibratory sense, deep touch, discriminative touch

dorsal spinocerebellar travels

IL

dorsal spinocerebellar sensory modality

unconscious proprioception from trunk and LE

ventral spinocerebellar travels

bil

ventral spinocerebellar sensory modality

unconscious proprioception from trunk and LE

average age of spinal cord injury

43

In a car accident, it is easier for this population to have a hyperextension injury

elderly

Leading causes of SCI (most to least)

Vehicular, falls, violence, sports, all other, medical

indirect trauma for SCI

extreme motion leading to excessive distraction, loading, or shear force on neural tissue

direct injury for SCI

penetrating injury resulting in direct damage to neural structures

Examples of non-traumatic causes of SCI

circulatory compromise, spinal stenosis, tumor, congenital, distinct disease processes (transverse myelitis, MS)

majority of SCI are

incomplete

most to least common neurological levels of injury

cervical, thoracic, lumbar

most common cervical SCI level

C5

Thoracic region is more stable due to

ribs

most common MOI for thoracic SCI is

related to direct mechanism

most common thoracic level of SCI

T12

vertebral level with intermediate stabilty

lumbar

region susceptible to flexion, axial loading, and rotation injuries

lumbar

region susceptible to flexion, axial loading, distraction, and extension

cervical

most common lumbar SCI level

thoracolumbar junction (L1)

most common causes of death in SCI pts

pneumonia, septicemia

SCI mortality rates increase with

endocrine, metabolic, mental health disorders

life expectancy in SCI is impacted by

1st year survival, motor severity of injury, level of injury, age at time of injury, ventilator dependence

primary neuropathology

damage at site of injury due to physical contusions, shear injury, lacerations, and microhemorrhage

acute secondary neuropathologies (0-48 hours)

ischemia, inflammation, ion disruption, idiopathic apoptosis

ischemia in SCI occurs

immediately for gray matter, delayed onset of 2-3 hours in white matter

inflammation is responsible for

injury expansion 24-48 hours post-injury

ion disruption

increased Ca2+ concentration leads to increased glutamate release, causing excitotoxicity

idiopathic apoptosis can last

days after initial injury

sub-acute secondary neuropathology (2-4 days)

inflammatory cell infiltration, release of free radicals, edema, vessel thrombosis, microglial infiltration, axonal dieback, cystic cavitation, fibroblast infiltration, astrogliosis, hematoma, vasospasm

cystic cavitation

fluid, connective tissue and macrophage filled cavities that coalesce, creating a barrier to axonal regrowth

glial scar

perilesional zone around cystic cavities created by tightly interwoven astrocytes that become scar when activated by proteins

glial scar is a

physical barrier to regeneration

glial scar limits

spread of cytotoxic molecules and inflammatory cells into uninjured parenchyma

chronic secondary neuropathology (2 weeks-6mo)

wallerian degeneration, limited oligodendrocyte remyelination, inhibitory proteoglycan scar, perilesional astrogliosis, coalescence of cystic cavitation, restricted regenerative cell migration, limited Schwann cell remyelination, restricted axonal regrowth, plasticity of injured and uninjured neurons

central cord syndrome

commonly occurs after hyper EXT injuries, particularly cervical, more prevalent in elderly

central cord syndrome presentation

weakness more in UE than LE

Anterior cord syndrome

most common after FLX injury or anterior spinal artery disruption (typically burst or teardrop fx)

anterior cord syndrome is associated with

poorer prognosis for B/B function and amb

anterior cord syndrome presentation

preserved proprioception/light touch, variable loss of motor, pain and temp sensation

posterior cord syndrome

commonly caused by compression or infarct of posterior spinal artery

posterior cord syndrome is

rare

posterior cord syndrome presentation

bil sensory loss below level of lesion

Brown-sequard syndrome

most commonly the result of penetrating injuries and burst fractures

Brown-sequard syndrome presentation

IL motor and proprioceptive deficits, CL pain/temp impairment below level of lesion (/c IL loss at level of lesion)

Conus medullaris syndrome

LMN lesion resulting form injury to sacral cord and lumbar n root

conus medullaris syndrome presentation

flaccid paralysis of LEs and areflexic B/B

Cauda equina syndrome

LMN lesion resulting from injury to lumbar and sacral roots (L1 or below) caudal to spinal cord

cauda equina presentation

flaccid paralysis of LEs, areflexic B/B, pattern of impairment varies

ASIA Motor level classification

most caudal level that demonstrates intact function (≥3/5 with immediate rostral segment 5/5)

ASIA sensory level

most caudal level of intact sensory function

Sensory level is used to determine motor function level for

C1-4, T2-L1, and S2-5

incomplete SCI

some sensory and/or motor function preserved below lesion level

incomplete SCI has preserved function in

lowest sacral segments (S4-5)

sensory incomplete

intact anal sensation to pinprick, light touch, or pressure during digital exam

motor incomplete

contraction of anal sphincter or preservation of motor function at least 3 levels below neurological level WITH intact sensation S4-5

complete SCI

no sensory or motor function preserved below lesion level in lowest sacral segment S4-5

zone of partial preservation

partial preservation of dermatome or myotome function caudal to neurological level but ABSENT S4-5 function

A

complete, no sensory or motor function at S4/5

B

sensory incomplete, sensory preserved below neurologic level, including S4/5 AND no motor function ≤3 levels below either side of body

C

motor incomplete, motor preserved below neurological level AND ≥1/2 muscle groups below level of injury strength grade <3

D

motor incomplete, motor preserved below neurological level AND ≥1/2 muscle groups below level strength grade ≥3

E

normal (they still have prior deficits)

spinal schock is observed

immediately after SCI

spinal shock results in

arreflexia, autonomic dysfunction, and loss of voluntary motor and sensory function

theorized mechanism of spinal shock

reaction to abrupt loss of supraspinal input

symptoms of spinal shock will

gradually resolve over time in an observable sequence of reflexive events

spinal shock stages

1. Return of some reflexes

2. Return of additional reflexes

3. Early hyperreflexia

4. Spasticity and hyperreflexia

DPR

Delayed plantar response (opposite of babinski)

Phase 1 of spinal shock

0-1 day, loss of descending facilitation

Phase 2 of spinal shock

1-3 days, denervation supersensitivity

Phase 3 of spinal shock

Axon-supported synapse growth

Phase 4 of spinal shock

soma-supported synapse growth

Neurological return

resumption of voluntary motor function or sensation below the lesion level

nerve root return

most common mechanism of neural return

spinal tract healing

resolution of pathological processes related to initial injury, demyelination of damaged fibers

spinal cord spontaneous plasticity

associated with structural changes or altered nerve functioning

spinal tract activity-dependent return

occurs in response to afferent input and is task-specific

prognostic indicators of motor recovery

• degree of impairment (complete v. incomplete)

• preserved motor function

• preserved pinprick sensation

• pattern of injury

• early neurological return

• age

prognostic indicators of functional recovery

• motor level

• age

• additional injuries

• pre-existing health

• medical complications

• body type

• psychosocial adjustment

• rehabilitation

acute SCI management goals

• establishment of life-saving interventions

• neurological examination

• management of vertebral fractures

• reduction of secondary cell death

30% of individuals with SCI are

readmitted at least once

primary cause of SCI re-admittence

genitourinary issues

indications for surgical fracture management

• unstable fracture

• fracture won’t reduce

• significant malalignment

• deteriorating medical status

• continued instability

• cord compression with incomplete lesion