L5 SCI Flashcards
Traumatic SCI
acute traumatic lesion of neural elements in the SC, resulting in temporary or permanent sensory deficit, motor decifict, or bowel/bladder dysfunction
Epidemiology of Traumatic SCI
Prevalence = 302,000 people living with tSCI
Incidence = about 17,730 new SCI a year
Cause of tSCI
- vehicular
- Falls
- Violence
Race/Ethnicity and Gender of tSCI
mostly males
non-hispanic white have the most, asian is the least
Most tSCI are classified as
icomplete tetraplegia
Re-hospitalization rates
30% of SCI are re-hospitalized one or more times during the following year
Genitourinary system diseases is #1
Skin #2
Respiratory, digestive, circulatory, and musculoskeletal are common
Cause of death for tSCI
pneumonia
septicemia
Epidemiology of Non-traumatic SCI
Incidence = 68 cases/million population a year
Caused by spinal stenosis (54%), myelitis, tumors
Pathophys of SCI
Traumatic–> fracture or ligament injury
Tumor–> compression on cord
Stroke –> vascular disruption
Vasculature to SC
1 anterior and 2 posterior spinal arteries
tSCI phases of injury
Primary: Direct trauma, casues spinal shock
Secondary: physiologic responses continue to damage SC
Primary Injury to SC
Initial mechanical forces cause bruising or tearing into spinal cord tissue
these forces damage pathways carrying both afferent and efferent info in SC
This results in spinal shock, hypotension, ischemia
Spinal Shock
transient phenomenon that occurs after trauma to SC
spinal reflexes, voluntary motor and sensory function, autonomic control are absent/depressed caudal to lesion
Cause is not understood
Spinal Shock Phases
reflex functioning in segments caudal to the injury will gradually return as spinal shock resolves
Can take up to 1-12 months to have spasticity or hyperreflexia
Secondary Injury
begins within minutes after the primary injury. Results in a cascade of phsiologic responses that cause progressive damage to the SC tissue surrounding the lesion site
Edema surrounding the injury leads to decreased blood flow or ischemia, causing cell death (occurs more in gray matter)
The re-establishment of blood flow leads to more damage, because free radicals are formed, causing inflammatory response
Secondary Injury cellular responses
- Apoptosis and demyelination of surviving axons
- Wallerian degeration and axonal dieback
- Matrix remodeling
- Glial scar forms and matures around injury
Why do we see recovery of function after SCI?
POSSIBLY: Neuronal sprouting may occur, high intensity interventions could help to drive this process
recovery is more likely due to better medical management strategies like improved perfusion and minimizing the secondary injury
Medical management of traumatic SCI
immobilization of spine
ensure ventilation and circulation are adquate
other life threatening injuries addressed
Fracture management of tSCI
indications: unstable fx, continued instability, fx that will not reduce, gross spinal malalignment, deterioriating neuro status
Open reduction internal fixation
realign and stabilize the spinal column
Decompression
relieve compression on the cord by removing bone fragments or foreign bodies
Post surgical management
Variable
may or may not need orthosis
other systems will need medical monitoring and management
Fracture management, nonsurgical
Indications: used to reduce the initial malalignment until surgery can be performed. Some cases do not require surgery, but long recovery time
Accomplihsed with traction or spinal orthosis
Halo vest
effective in limiting cervical spine
carries risk of infection at pin sites
Tetraplegia
loss of motor and or sensory function of B UE, LE, trunk, pelvis
Paraplegia
loss of motor and/or sensory function of trunk, B LE and pelvic
Neurologic level of injury
most caudal level of SC that exhibits intact motor and sensory function
Complete injury
no sensory or motor function at S4/5
Incomplete
S4/5 sensory and/or motor function is spared
Zone of partial preservation
used only with complete injuries. refers to partial preservation of sensory and/or motor function below the level of injury
System impairments after SCI
observed impairments are dependent on LOI and what part of SCI was injured
somatosensory, motor, autonomic system
Motor Impairments
Cauda Equina injury: flaccid paralysis with DTR and reflexive response to passive stretch dimished or absent
also changes to muscle tone and loss of voluntary control in other parts of SC
Acute motor impairments
spinal shock and loss of deep tendon reflexes
paralysis of muscles below LOW due to loss of communication between UMN and LMN
Sub acute motor impairments
reflexes return and can become hyer reactive
can develop spasticity and other UMN signs
PT assessment of UMN dysfunction
Hyper reflexia–> any score above 2 below LOI
Clonus
Spasms
Tone
Spasticity
Negative impact of spasticity
pain
loss of ROM, contractures
intereferes with independent function
sleep disturbances
pressure ulcers
difficulty sitting and positioning
Incomplete lesions of SCI
can result in a variety of patterns of motor and sensory loss
Is spasticity a bad thing?
not always
sometimes spasms or increased tone can help with functional acitivites
can alert pt or caregiver to bigger medical problem
Medical treatment of spasticity
Botox injections
Systemic medications like baclofen or clondine
Treating bladder infections, fractures, pressure ulcers, hangnails, which increase spasticity
PT treatment of spasticity and spasms
Passive slow stretching
Rhythmic passive movements
Deep pressure
Hydrotherapy
NMES
TENS
