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5 Neurological Dysfunction > L5 SCI > Flashcards

L5 SCI Flashcards

1
Q

Traumatic SCI

A

acute traumatic lesion of neural elements in the SC, resulting in temporary or permanent sensory deficit, motor decifict, or bowel/bladder dysfunction

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2
Q

Epidemiology of Traumatic SCI

A

Prevalence = 302,000 people living with tSCI
Incidence = about 17,730 new SCI a year

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3
Q

Cause of tSCI

A
  1. vehicular
  2. Falls
  3. Violence
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4
Q

Race/Ethnicity and Gender of tSCI

A

mostly males
non-hispanic white have the most, asian is the least

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5
Q

Most tSCI are classified as

A

icomplete tetraplegia

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6
Q

Re-hospitalization rates

A

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

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7
Q

Cause of death for tSCI

A

pneumonia
septicemia

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8
Q

Epidemiology of Non-traumatic SCI

A

Incidence = 68 cases/million population a year

Caused by spinal stenosis (54%), myelitis, tumors

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9
Q

Pathophys of SCI

A

Traumatic–> fracture or ligament injury
Tumor–> compression on cord
Stroke –> vascular disruption

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10
Q

Vasculature to SC

A

1 anterior and 2 posterior spinal arteries

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11
Q

tSCI phases of injury

A

Primary: Direct trauma, casues spinal shock

Secondary: physiologic responses continue to damage SC

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12
Q

Primary Injury to SC

A

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

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13
Q

Spinal Shock

A

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

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14
Q

Spinal Shock Phases

A

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

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15
Q

Secondary Injury

A

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

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16
Q

Secondary Injury cellular responses

A
  1. Apoptosis and demyelination of surviving axons
  2. Wallerian degeration and axonal dieback
  3. Matrix remodeling
  4. Glial scar forms and matures around injury
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17
Q

Why do we see recovery of function after SCI?

A

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

18
Q

Medical management of traumatic SCI

A

immobilization of spine
ensure ventilation and circulation are adquate
other life threatening injuries addressed

19
Q

Fracture management of tSCI

A

indications: unstable fx, continued instability, fx that will not reduce, gross spinal malalignment, deterioriating neuro status

20
Q

Open reduction internal fixation

A

realign and stabilize the spinal column

21
Q

Decompression

A

relieve compression on the cord by removing bone fragments or foreign bodies

22
Q

Post surgical management

A

Variable
may or may not need orthosis
other systems will need medical monitoring and management

23
Q

Fracture management, nonsurgical

A

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

24
Q

Halo vest

A

effective in limiting cervical spine
carries risk of infection at pin sites

25
Q

Tetraplegia

A

loss of motor and or sensory function of B UE, LE, trunk, pelvis

26
Q

Paraplegia

A

loss of motor and/or sensory function of trunk, B LE and pelvic

27
Q

Neurologic level of injury

A

most caudal level of SC that exhibits intact motor and sensory function

28
Q

Complete injury

A

no sensory or motor function at S4/5

29
Q

Incomplete

A

S4/5 sensory and/or motor function is spared

30
Q

Zone of partial preservation

A

used only with complete injuries. refers to partial preservation of sensory and/or motor function below the level of injury

31
Q

System impairments after SCI

A

observed impairments are dependent on LOI and what part of SCI was injured

somatosensory, motor, autonomic system

32
Q

Motor Impairments

A

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

33
Q

Acute motor impairments

A

spinal shock and loss of deep tendon reflexes
paralysis of muscles below LOW due to loss of communication between UMN and LMN

34
Q

Sub acute motor impairments

A

reflexes return and can become hyer reactive
can develop spasticity and other UMN signs

35
Q

PT assessment of UMN dysfunction

A

Hyper reflexia–> any score above 2 below LOI
Clonus
Spasms
Tone
Spasticity

36
Q

Negative impact of spasticity

A

pain
loss of ROM, contractures
intereferes with independent function
sleep disturbances
pressure ulcers
difficulty sitting and positioning

37
Q

Incomplete lesions of SCI

A

can result in a variety of patterns of motor and sensory loss

38
Q

Is spasticity a bad thing?

A

not always
sometimes spasms or increased tone can help with functional acitivites
can alert pt or caregiver to bigger medical problem

39
Q

Medical treatment of spasticity

A

Botox injections
Systemic medications like baclofen or clondine
Treating bladder infections, fractures, pressure ulcers, hangnails, which increase spasticity

40
Q

PT treatment of spasticity and spasms

A

Passive slow stretching
Rhythmic passive movements
Deep pressure
Hydrotherapy
NMES
TENS

5 Neurological Dysfunction (16 decks)

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