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Term 3 > Neuromuscular SCI and GBS > Flashcards

Neuromuscular SCI and GBS Flashcards

1
Q

What are the Traumatic Injuries for SCI?

A
  • Vehicular (MVA) Number 1 cause
  • Falls
  • Violence
  • Sports
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2
Q

What are the Non-traumatic injuries for SCI?

A

This makes up 39% of all SCIs

  • Vascular Dysfunction
  • Vertebral Subluxation due to RA or DJD
  • Spinal Neoplasm
  • Syringomelia
  • Abscess
  • Infection: Syphilis, Transverse Myelitis
  • MS or ALS
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3
Q

What is the demographics of patients with SCI?

A
  • Typically pts ~42 y.o
  • Mostly male
  • Mostly caucasian
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4
Q

With SCI, what are common MOIs for the Cervical Spine?

A
  • Forces of: Flexion, Axial Loading, Distraction, Extension
  • Concomitant Rotation, lateral flexion, shear force
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5
Q

With SCI, what are common MOIs for the Thoracic Spine?

A

Less common than cervical

  • GSWs, MVAs, Falls
  • Most common site: T12-L1 junction
  • Forces: Flexion, Axial Loading, or Combination of Flexion and Rotation
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6
Q

With SCI, what are common MOIs for the Lumbar Spine?

A
  • Falls, MVA, GSW, Direct load onto spine
  • Forces: Flexion, Axial Loading, Flexion combined with distraction or rotation
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7
Q

What is the Pathology of SCIs?

A
  • Damage due to impingement and/or compression of cord
    -Bony or soft tissue
    -Penetrating or non-penetrating
  • Blunt Trauma= Primary neural damage to cell bodies and/or axons
  • Secondary injuries cause most damage:
    -Ischemia
    -Demyelination of axons
    -Edema
    -Necrosis
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8
Q

What happens when you first have a SCI?

A
  • Spinal Shock
    -An immediate period of areflexia post spinal cord trauma
    (The entire system dies/stops functioning. Ex. if a pt has injured C6. From C6 and below the pt becomes areflexive/no function)
    -This typcially resolves within 1-3 days
  • Loss/Dysfunction of motor, sensory and autonomic systems
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9
Q

What is the Gold Standard for identifying the severity of injury after SCI?

A

The International Standards for Neurological Classification of Spinal Cord (ISNCSCI)

  • This promotes communication inter-professionally the degree of motor and sensory impairment
  • Provides guidance for establishing prognosis
  • Used in clinical research trials
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10
Q

With SCI, What is the Neurological Level of Injury?

A
  • The most caudal level of the spinal cord with normal motor and sensory function on both the left and right side of the body

-Motor level: Most caudal segment with normal motor function bilaterally (Tested through key myotomes)
-Sensory level: Most caudal segment with normal sensory function bilaterally (Tested through light touch and pinprick via key dermatomes)

If the Neurological Level of injury is at C5, then everything C5 and above in INTACT and C6 and below are impaired and/or absent

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11
Q

What is a Complete Spinal Cord Injury?

A
  • No sensory or motor function in the lowest sacral segments S4 and S5

(No sensory or function 3 levels below the Neurological Level of Injury)

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12
Q

What is an Incomplete Spinal Cord Injury?

A

An SCI having motor and/or sensory function below the neurological level including sensory and/or motor function at S4 and S5

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13
Q

How would a physician or PT determine if a pt has a Complete or Incomplete SCI?

A

By checking the Anal Sphincter control and sensation
(S4 and S5)
- The persons ability to contract or have sensory

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14
Q

SCI: Clinical Syndromes

What is the Brown Sequard Syndrome?

A

This is a Hemisection injury
- Ipsilateral loss of proprioception, vibration and motor function at and below level of lesion
- Contral lateral loss of pain and temperature

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15
Q

SCI: Clinical Syndromes

What is Anterior Cord Syndrome?

A

Flexion injury of C-Spine

  • Bilateral loss of motor function, pain, and temperature sensitivity at and below injury level
  • Intact light touch and proproception
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16
Q

SCI: Clinical Syndrome

What is Central Cord Syndrome?

A

Most common due to Hyperextension injury

  • Paraylsis and sensory loss in UEs
  • Varying involvement in trunk and LEs

Cant complete ADLs due to loss of UE control, but can walk

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17
Q

SCI: Clinical Syndromes

What is Cauda Equina Syndrome?

A

Injury to the lumbosacral nerve roots of the cauda equina
- LMN signs
- Flaccid paralysis of LEs
- Areflexic bowel and bladder

However in term of ADL they are still relatively functional

18
Q

Primary/Secondary Impairments for SCI

If a patient with a SCI presents with Orthostatic Hypotension, what are the S/S and treatment?

A

Decrease in BP >20mm during positonal change

  • S/S:
    -Dizziness, Lightheadedness, sweats (looks like fainting episode)
  • Treatment: Elevate legs above heart, TIS W/C
    For preventative measure have slow progression into upright position. Use Compression stockings (Ace wraps) and abdominal binders, these help push blood back and allow venous return

This is common because pts with SCI are initially bedbound

19
Q

Primary/Secondary Impairment for SCI

What is Autonomic Dysreflexia (AD)?

A
  • A life-threatening dysfunction of autonomic nervous system
  • Observed in injuries above T6, most common with complete injury
  • Clinical syndrome triggered by noxious stimuli below the level of the lesion
20
Q

If a patient has Autonomic Dysreflexia, what are some symtoms they may present with?

A
  • Hypertension (Increase of 20-30mmHG)
  • Bradycardia
  • Headache (may be severe)
  • Profuse sweating
  • Increased spasticity/hypertonia
  • Vasoconstriction below lesion level
  • Vasodilation above lesion level (Flushing)
  • Constricted pupils
  • Nasal congestion
  • Piloerection (Goose Bumps)
  • Blurred Vision
21
Q

As a PT, what do you do to help the patient with Autonomic Dysreflexia?

A
  • If lying flat, sit up (to reduce orthostatic hypotension)
  • Call emergency code
  • Find and remove noxious stimuli
    -Remove all clothes
    -Pinched skin, clothing, urinary retention, wounds, bowel obstruction
  • Education on triggers and how to resolve
22
Q

What are Risk Factors for SCI?

A
  • Prolonged immobility
  • Multi-systemic effect

82% of patients with SCI develop secondary impairments and complications

23
Q

What are Secondary Medical Complications with SCI patient and those bedridden?

A
  • Pressure sores (1)
  • Pneumonia (2)
  • DVT (3)
  • Pain (nociceptive/neuropathic)
  • Contractures
  • Heterotopic Ossification
  • Osteoporosis and fracture
24
Q

What are PT Examination Considerations for SCI?

A
  • Patient/Family Hx, contextual factors
  • Level of injury (ASIA)
    -Best predictor of motor recovery
  • Available and coordination resources
  • Diagnosis Specific Measures
25
Q

What is the Prognosis for SCI?

A
  • This has a earlier neurological return
  • ASIA levels: B-C-D indicate greater likelihood of motor recovery
  • ASIA Level A: 70% will experience motor recovery one level below the initial neurological injury level
  • Pinprick sensation in BLE and/or sacral region: imporved prognosis of motor recovery in 1 year if present 4 months post injury
  • Pattern of Neurological Injury: BSS > ACS
  • Age

With ASIA B-C-D are incomplete SCI ; A is complete SCI

26
Q

What is Guillan-Barre Syndrome (GBS)?

A
  • Acute inflammatory demyelinating immune-mediated polyneuropathy
  • Nerve roots and peripheral nerves affected
  • Leading to flaccid paralysis, sensory impairment and autonomic nervous system impairment

More males are affected than females

27
Q

What are varient forms of GBS?

A
  • Acute motor axonal neuropathy
  • Acute motor and sensory axonal neuropathy
  • Miller Fischer Syndrome: CN, Ataxia, and Areflexia
  • Chronic Inflammation Demyelinating Polyneuropathy: Progressive relapsing or remitting numbness and weakness
28
Q

What is the Etiology of GBS?

A
  • This is an idopathic disorder
  • There is typically an inflammatory response due to an Infection 2-3 weeks prior
    (Common viruses associated are Epstein-Barr Virus and Mycoplasma Pneumoniae)
29
Q

What is the Pathology and Neuroanatomical Location of GBS?

A
  • Spinal Roots and Peripheral nerves attacked by Microphages and T Lymphocytes
  • Damage occurs directly to the Myelin Sheath along the axon
  • Severity depends on Axonal damage
    -Mild: Axon intact, rapid re-myelination
    -Severe: Axonal damage or loss, axonal regeneration required
30
Q

With MS and GBS

What happens when the Myelin Sheath is Damaged?

A

There is decreased Action Potential
- Slowed Conduction
- Dyssynchrony of conduction
- Disturbed conduction of higher frequency impulses
- Complete conduction blocked

31
Q

What is the Medical Diagnostic Criteria for GBS?

what are the S/S

A
  • Motor weakness
    -Rapid progression
    -Symmetrical, Distal to Proxinal
    -Areflexive distal tendons (LMN)
  • Mild sensory symptoms: Parasthesias or Hypesthesias
  • Autonomic Dysfunction: Tachycardia, Arrhythmia
  • Hx of recent flu-like illness
  • Lab results not conclusive
  • Nerve conduction study: Abnormal velocity
  • Recovery occurs 2-4 weeks AFTER PLATEAU of disease process
32
Q

What are Common Clinical Presentations of GBS?

A
  • Rapid evolution of bilateral, symmetrical flaccid paralysis
  • Fatigue: severity is correlated with older age
  • DTRs are diminished or absent
  • Sensory Sx: Numbness, tingling, decreased vibratory senses. Stocking glove distibution
  • Pain: Muscle aching, large muscle cramps (Progressive worsening as disease progresses)
33
Q

What Clinical Presentations are Less common?

A
  • Ventilator Dependent (If attacked so severly, it can attack repsiratory muscles)
  • CN Involvement
  • ANS Symptoms
    -Pooling blood
    -Urinary retention
    -Ileus
    -Poor venous return
34
Q

What is the Medical Prognosis for GBS?

A
  • Commonly Maximum Paralysis: within 1-2 days of onset
  • Greatest Severity reached:
    -50% within 1 week
    -70% within 2 weeks
    -80% within 3 weeks
  • Once plateaued, motor recovery occurs within 2-4 weeks

The faster we get to the plateau the faster the patient will have motor recovery

35
Q

What is the Functional Prognosis for GBS?

A
  • 80% become abulatory within 6 months
  • 15% persistent residual impairment
  • 50% mild neurological deficits
  • Common Long-Term Deficit:
    -Weakness of TA, foot and hand intrinsic, glutes and quads
    -Fatigue
    -Deconditioning/poor endurance
    -Sensory deficits may persist 3-6 years post
36
Q

What are Poor Prognostic Criteria for GBS?

A
  • Severity muscle weakness (Quadriplegia)
  • Ventilator support
  • CN Involvement: loss of eye movement and swallowing
  • Rapidly progressing from initial onset
  • Length of time to maximax severity
  • Old age
  • Pre-morbid GI illness
  • Recent CMV
37
Q

What is the Medical Management of GBS?

A
  • Hospitalization 2/2 progressive nature, repsiratory
  • Cognition usually intact: Frequent orientation to time, place, purpose of all procedures
  • Alternative communication boards
  • Supportive care for reduction with prolonged immobilization, including post traumatic stress
38
Q

What is the Pharmacological Management for GBS?

A
  • Immunotherapy - Based treatment
    -Plasma exhange
    -Intravenous immunoglobuin (IvIg)
  • Corticosteroids
39
Q

What are some limitations you may encounter with GBS patients?

A
  • Current status of disease process (We want them after the plateau)
  • Pain
  • Fatigue
  • Respiratory Distress
40
Q

What are the Goals for therapy for GBS in Acute Care?

A
  • Improvement of respiratory dysfunction and risk for aspiration
  • Manage Pain
  • Prevent: Contractures, pressure ulcers, injury to weakened muscles
  • Initiate a progressive active exercise program to regain functional mobility
  • Monitor and manage fatigue
41
Q

What are the Goals for Therapy for GBS in the Chronic Phase?

A

Now we look at recovery, the goal is to get them back prior to disorder

  • This is recovery of motor recuitment and function
    -Neuroplasticity emphasized, remyelination
    -Retrain normal movement patterns for functional independence
  • Compensatory, when appropriate

Term 3 (44 decks)

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