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OCS > The Lumbar Spine > Flashcards

The Lumbar Spine Flashcards

1
Q

Describe the impact of low back pain historically and currently.

A

most common cause of disability and lost work time (other than common cold) in industrialized countries; most common reason to seek physical therapy; overall economic/societal burden has not improved over the last few years, and may actually be worsening

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2
Q

Define prevalence

A

the amount of people with a condition at any given time

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3
Q

Describe the prevalence of low back pain worldwide.

A

difficult to estimate acute pain, because it tends to change very rapidly and can have varying definitions; chronic low back pain is likely between 10-30% on any given day.

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4
Q

What percentage of people with low back pain for less than 3 months will recover? How long does this generally take?

A

80% of people with acute low back pain (<3 mo) will recover within 6-8 weeks

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5
Q

Describe an inception cohort study design.

A

enroll patients at the time of onset of symptoms and follow them over time

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6
Q

What percentage of people with acute low back pain will return to work within 2 weeks, according to Henschke et al? Within 3 months?

A

50% will return to work within 2 weeks; 83% within 3 months

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7
Q

What percentage of people with low back pain symptoms will report continued symptoms after 12 months, according to Henschke et al?

A

23%

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8
Q

Why is it important to advise patients on the nature of acute low back pain and its prognosis?

A

LBP is probably not an isolated episode, but a condition characterized by flare-ups of symptoms. Patients should be informed that recovery is likely in a short time frame, but recurrences are likely and normal; Flare-ups do not necessarily represent a failure of treatment

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9
Q

What is the prognosis of chronic low back pain?

A

Highly variable; “refractory to intervention”; though studies show that even patient with low back pain for more than 3 months can recover fully (1/3 of participants reported that they were pain-free and fully functionally recovered within 1 year), so there is always hope

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10
Q

What study design would we need to use in order to determine exactly the factors that cause the development / influence the course of low back pain? What are the ethical issues that this would raise?

A

Prospective, randomized study design. We’d have to assign a person to perform activities that we believe to be harmful.

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11
Q

What kinds of study designs are ethical for exploring activities that might cause low back pain?

A

Non-experimental studies such as case-series designs or cohort designs that follow people over time and compare various traits to the outcome

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12
Q

Describe the findings from Bakker, et al on the relationship between specific activities and low back pain recovery.

A

Bakker et al found no relationship between work-related spinal loading, prolonged sitting, and/or participation in sports activities on the recovery from low back pain

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13
Q

What is the clinical takeaway from the currently literature on activities that cause / contribute to low back pain rehab?

A

In conflict with previous beliefs, lifting, prolonged sitting, and sports activities are not likely to be harmful to the spine and should not necessarily be limited in those without a clear rationale

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14
Q

Describe the low back pain clinical prediction rule derived by Hancock et al. and their statistical findings

A

Acute LBP; lower than average initial pain, shorter duration of symptoms, fewer previous episodes = recover more quickly; Hazard Ratio 3.5

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15
Q

What is a hazard ratio?

A

A measure of how often a particular event happens in one group compared to how often it happens in another group, over time (Hazard Ratio of 1 = no increased risk in the test group, 2 = twice the risk, etc.)

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16
Q

What is a confidence interval?

A

Probability measurement. A confidence interval is how much certainty/uncertainty there is with any particular statistic. (They can take any number of probability limits, with the most common being a 95% or 99% confidence level.)

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17
Q

Describe the utility of using the current low back pain CPR to predict prognosis of acute LBP

A

basic guideline, but there are probably more factors than were originally taken into account when the CPR was derived. (Weak-moderate evidence in addition to lack of validation studies)

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18
Q

How long can the average acute low back pain episode last, according to Adam Meakins?

A

can last up to 6 weeks

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19
Q

What are the 3 primary anatomic regions of the nervous system in which pain modulation occurs

A
  1. spinal cord
  2. brain stem (periaqueductal gray, rostral ventral medulla)
  3. higher brain centers (anterior cingulate cortex, amygdala, somatosensory cortex)
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20
Q

What is pain modulation?

A

the way in which nociceptive (danger) signals are amplified or dampened within the nervous system via biochemical activity

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21
Q

Describe pain dampening events at the spinal cord.

A

non-nociceptive a-beta nerve fibers recruit inhibitory neurons in the substantia gelatinosa of the posterior spinal cord, which chemically blocks nociceptive a-delta and c-fibers before they can send a signal up the spinal cord to the brain

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22
Q

What is a nerve fiber?

A

axon or dendrite of a single neuron

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23
Q

Describe spinal sensitization (secondary hyperalgesia).

A

pain is increased (switched on) because dorsal horn neurons have increased excitability and spontaneously discharge ascending nociceptive information; the excitability is due to repeated firing of “pain-sensitive” c-fibers from somatic tissues (like muscles and joints); the excitability is also enhanced by the transcription of rapidly-expressed genes that increase the sensitization of nociceptors; this means that the threshold is lower and the “receptor field” is wider

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24
Q

Describe pain dampening events at the level of the brain stem.

A

diffuse inhibition of pain (switch off) happens when the periaqueductal gray (PAG) matter and/or rostral ventral medulla (RVM) are stimulated by pathways that descend from high brain centers; PAG system uses endogenous opioids and descends to the dorsal horn

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25
Q

List 4 important neurotransmitters in the central nervous system that have a modulating affect on pain

A
  1. endogenous opioids
  2. cannabinoids
  3. serotonin
  4. dopamine
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26
Q

Which tract of the spinal cord sends information to higher cortical brain regions?

A

spinothalamic tract projects to several cortical regions, creating a multidimensional pain experience

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27
Q

What does the length of symptoms tell us about a patient’s capability to improving low back pain or complete resolving symptoms?

A

Not much. Though high pain intensity and disability are unfavorable prognostic factors, even patients with longstanding symptoms can improve and even full recover.

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28
Q

What are the three components of evidence-based practice?

A

research findings, patient preferences/values, and clinical intuition

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29
Q

What is the purpose of an efficacy study?

A

determine the effects of a specific intervention

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30
Q

What is the difference between an efficacy study and an effectiveness study?

A

efficacy studies determine the effects of a specific intervention; effectiveness studies measure outcomes from treatment applied in a pragmatic clinical environment

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31
Q

List the 5 recommendations that are common to most, if not all, treatment guidelines for acute or chronic LBP

A
  1. early treatment that emphasizes resumption of activity and discourages bed rest (acute)
  2. recognition of psychological and work-related factors
  3. supervised exercise
  4. utilization of cognitive-behavioral therapy concepts
  5. step-care approach
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32
Q

Describe a “step-care” approach to treating low back pain. When would this approach be indicated?

A

rapid transition from passive to active treatments with patients receiving reassurance and encouragement to return to full activity soon; most LBP treatment guidelines agree that this approach should be implemented as soon as serious conditions are ruled out

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33
Q

Describe the limitations of clinical guidelines in the treatment of patients with low back pain. Give an example

A

There will always be variability among patients (“bandwidth”), and adhering too strictly to guidelines may not always match the optimal treatment for the individual patient. Ex: manual treatments may be indicated not according to the clinical guideline, but to specific clinical presentation.

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34
Q

Make the case for physical therapists performing medical screening / direct access treatment of low back pain

A
  • PTs have been performing direct access medical screening for patient with LBP in the U.S. military and Public Health Service for years, as well as in many other countries
  • Evidence supports that PTs are well-trained to identify signs and symptoms associated with serious, undiagnosed conditions (Preliminary evidence suggests that having physical therapists as an entry point to the system doesn’t increase the likelihood of missed serious condition)
  • Intervention can begin much sooner and with less cost
  • Controls use/cost of unnecessary radiographs and other diagnostic tests
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35
Q

What clinical red flags might you see if a patient with low back pain has a metastatic cancer?

A

history of cancer, night pain or pain at rest, unexplained weight loss, younger than 17 or older than 50, failure to improve over predicted time interval following treatment

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36
Q

List 6 red flags might you see if a patient with low back pain has an infection of the disk (diskitis) or vertebrae (osteomyelitis)?

A
  1. patient is immunosuppressed
  2. prolonged fever (100.5° F or higher)
  3. history of IV drug abuse
  4. hx of recent UTI
  5. hx of cellulitis
  6. hx of pneumonia
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37
Q

Describe the clinical presentation of cellulitis.

A

Skin is red, swollen, warm, and tender to touch; Most common on legs in adults, on the face in children; Usually comes along with feeling sick / chills

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38
Q

List 6 historical/clinical red flags might you see if a patient with low back pain has an undiagnosed vertebral fracture?

A
  1. prolonged use of corticosteroids
  2. older than 70
  3. mild trauma if older than 50
  4. history of osteoporosis
  5. recent major trauma (MVA or fall from greater than 5 ft)
  6. bruising over the spine
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39
Q

List 4 historical/clinical red flags might you see if a patient with low back pain has a dangerous abdominal aortic aneurysm?

A
  1. a pulsating mass in the abdomen
  2. hx of vascular disease
  3. throbbing/pulsating pain at rest or with recumbency (lying)
  4. older than 60
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40
Q

What is the most serious pathology that may present as LBP? Why?

A

metastatic lesions involving lumbar vertebrae; indicates the presence of aggressive disease elsewhere in the body, applications of interventions to the spine could result in dangerous tissue injury

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41
Q

What is the function of Likelihood Ratios?

A

combine measures of sensitivity and specificity to describe how much a test or a cluster of test (+ or -) will raise or lower the likelihood of a condition being present.

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42
Q

How are Likelihood Ratios measured?

A

Measurement starts at 1 & moves in either direction

< 1.0 is negative LR, > 1.0 is positive LR;
< 0.1 and > 10 are large/conclusive changes in post-test likelihood of a condition being present;
0.1-0.2 or 5.0-10.0 are moderate changes to post-test likelihood;
0.2-0.5 or 2.0-5.0 suggest small but possibly important changes;

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43
Q

Summarize the efficacy of red flags in the medical screening of patients with low back pain.

A
  • serious diseases that present as low back pain are relatively rare
  • traditional red flags are often present in people without serious disease
  • in isolation, most positive red flags don’t increase the probability that the patient has a serious disease
  • decisions should be based on clusters of findings, as this increases the likelihood of serious disease being present
  • current evidence suggests that using a PT for medical screening doesn’t decrease the likelihood of missing a serious condition
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44
Q

List 5 conditions associated with low back pain can be detected with MRI and/or CT scans.

A
  1. subtle fractures
  2. abnormal tissue growth (esp. neoplasm)
  3. local/diffuse inflammatory exudates (fluid and leukocytes)
  4. hemorrhage due to fracture/soft tissue injury
  5. serious compression of the spinal cord / cauda equina / spinal nerves
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45
Q

List 3 tests that are the typical reference standards to try to identify proposed anatomic sources of low back pain? What is the relationship between these tests and MRI?

A
  1. lumbar discography (x-ray with radiopaque die injected into the IV disc)
  2. facet joint blocks
  3. sacroiliac joint blocks.
    - tests are used to attempt to more clearly determine linkages between symptoms and MRI findings
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46
Q

What is HIZ and why is it important to reading MRI imaging of the lumbar spine?

A

high intensity zone - high/bright signal in the annulus of the intervertebral disc. This signal is believed to be associated with an annular tear; might be a component of “diskogenic” pain

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47
Q

Expand: Studies on the relationship between HIZ on lumbar imaging and discogenic low back pain. Likelihood ratios ranged from 1.5 to 5.9

A

the presence of a HIZ produced small increases in the likelihood of the pain arising from the intervertebral disk at that level

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48
Q

What is a “Modic Sign” and why is it important to MRI imaging of the lumbar spine?

A

disruption of the endplate, causing bone marrow edema. This is thought to contribute to impaired diffusion of nutrients and waste products between the vertebral body (subchondral bone) and the disc; might be a component of “diskogenic” pain); Seen on MRI as high (bright) T2 signal in and near the end plate.

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49
Q

Expand: Studies on the relationship between Modic signs on lumbar spine imaging and discogenic low back pain. Likelihood ratios ranged from 0.6 to 5.9.

A

Finding Modic signs produced minimal to moderate increases in the likelihood of the pain arising from the intervertebral disc at that level

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50
Q

Expand: Study on the relationship between “normal” MRI of the lumbar spine (that did not show disk degeneration) and discogenic low back pain. LR- = 0.21

A

Normal MRI produced small reductions the likelihood of the disk as a source of pain

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51
Q

Expand: Hancock et al. studied the relationship between physical examination tests and discogenic low back pain. Found +LR 2.8 for “centralization of symptoms”

A

Centralization of symptoms mildly increases the probability that the pain arises from the disk

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52
Q

What is special about centralization of lumbar spine symptoms in those with discogenic pain?

A

it’s the only physical examination measure that demonstrates a +LR (mildly increases the likelihood that the disc is the source of pain)

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53
Q

Expand: Study of the relationship between multiple (+) clinical sacroiliac joint tests and discogenic low back pain. +LR = 3.2

A

Multiple (+) clinical S.I. joint tests mildly increase the likelihood that the pain arises from the disc

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54
Q

Expand: Study of the relationship between multiple (-) clinical sacroiliac joint tests and discogenic low back pain. LR = 0.29

A

Multiple (-) clinical S.I. joint tests mildly decrease the likelihood that the pain arises from the disc.

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55
Q

Describe the relationship between clinical tests and lumbar spine pain caused by facet joint problems.

A

No clinical tests have yet to reliably detect facet joint problems

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56
Q

Summarize the relationship between the utility of MRI when evaluating lumbar spine pain sources and treatment.

A
  • MRI is not indicated in the absence of red flags or worsening neurological symptoms
  • Early, inappropriate use of MRI may increase patient anxiety and lead to false beliefs about the severity of a diagnosis
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57
Q

What three types of flags signal potential biobehavioral factors that may influence low back pain?

A

Yellow, Blue, and Black flags

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58
Q

What is meant by the term “yellow flag” in patients with low back pain?

A

describe a patient’s personal mistaken beliefs about pain and injury

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59
Q

List 7 examples of “yellow flags” in patients with low back pain.

A
  1. emotional distress
  2. hypervigilance
  3. pain catastrophizing
  4. elevated fear-avoidance beliefs
  5. low self-efficacy
  6. misunderstanding about nature and likely impact of pain
  7. misunderstanding of best strategies for long-term success
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60
Q

Describe the yellow flag of “emotional distress” as it pertains to low back pain.

A

high degrees of anxiety (more common with acute LBP) and/or high degrees of depression (more common with chronic LBP)

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61
Q

Describe the yellow flag of “hypervigilance” as it pertains to low back pain.

A

excessive pre-occupation with pain

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62
Q

Describe the yellow flag of “pain catastrophizing” as it pertains to low back pain.

A

overestimation of the negative impact of pain

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63
Q

Describe the yellow flag of “elevated fear-avoidance beliefs” as it pertains to low back pain.

A

inappropriate belief that benign activities are harmful to the spine

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64
Q

Describe the yellow flag of “low self-efficacy” as it pertains to low back pain.

A

a patient’s belief that they have no control over the pain

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65
Q

Describe the yellow flag of “misunderstanding about the nature and likely impact of pain” as it pertains to low back pain.

A

a combination of factors that lead the patient to believe that they may have a much more serious condition than is actually the case

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66
Q

Describe the yellow flag of “misunderstanding about the best strategies for long-term success” as it pertains to low back pain.

A

the patient may believe that passive, not active treatments are needed (i.e. “someone needs to fix my back”)

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67
Q

Why is the Pain Catastrophizing scale clinically relevant for those with low back pain?

A

score is an independent predictor of disability (stronger predictor than pain intensity)

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68
Q

What is important to remember when interpreting scores from tests like the Fear-Avoidance Beliefs Questionnaire or Tampa Scale for Kinesiophobia?

A
  • Detecting elevated fear-avoidance beliefs can be useful in helping to predict chronicity of symptoms but are not good predictors if used on their own.
  • They become moderately strong predictors when combined with imaging findings of multi-level degenerative disc disease, a strenuous or stressful job, leg pain, and low educational background.
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69
Q

What is meant by the term “blue flag” in patients with low back pain?

A

relate primarily to injured workers, describe a patient’s perception of work and work conditions that may impair a return to work (ex. low job satisfaction, personal conflicts with employers/co-workers)

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70
Q

What is meant by the term “black flag” in patients with low back pain?

A

wide context of factors such as social and financial issues (ex. reimbursement incentives to remain disabled)

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71
Q

Explain the relationship between self-efficacy and pain & disability in patients with low back pain.

A

The belief that one can achieve future goals has been shown to be a strong predictor of successful treatment. Additionally, a patient’s beliefs about how pain can be controlled is one of the most powerful predictors of the development of pain-related disability.

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72
Q

Describe the current state of the evidence for spinal manipulation/mobilization.

A

Several systematic reviews have been conducted:

  • Assendelft: relatively small decrease in pain and disability vs placebo / ineffective treatment
  • Ferreira: larger and more clinically meaningful improvement vs placebo
  • Bronfort et al: moderate support for patients with acute pain, minimal to moderate support for patients with chronic LBP; more effective than combination of home ex and advice at 12-week follow up, but not 1 year
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73
Q

Describe the 5-item clinical prediction rule for using lumbar manipulation developed by Flynn et al and validated by Childs et al.

A

Presence of 4 or 5 = +LR 24.38 for successful outcome:

  • no sx distal to knee
  • less than 16 days
  • score of less than 19 on FABQ
  • at least 1 hypomobile segment (P-A)
  • at least 1 hip with more than 35° IR
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74
Q

Describe the controversy surrounding the Flynn et al clinical prediction rule for lumbar spine manipulation.

A

although the CPR was validated by Childs et al, it was also found to be less successful by Hancock et al. In recent years, the generalizability of the rule has been challenged.

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75
Q

What’s the bottom line on the use of manipulation/mobilization of the lumbar spine to treat low back pain?

A

An argument can be made that in the absence of contraindications, mobilization/manipulation should be a first-line treatment for patients seeking PT for LBP. It’s unlikely to be helpful if used without patient education and purposeful increases in physical activity. This is especially true for people with chronic low back pain or post-operative patients.

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76
Q

Describe the clinical premise behind motor control exercises (a.k.a. stabilization exercises) to treat low back pain.

A

Individuals with low back pain have altered muscle control of the trunk and back muscles that leads to inappropriate loading on painful lumbar motion segments. Motor control exercises target deep trunk muscles in an attempt to have the patient actively stabilize their spine.

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77
Q

What evidence is there to support motor control exercises to treat low back pain?

A
  • Costa et al: ultrasound biofeedback to enhance learning of motor control exercise in patients with chronic LBP for 12 sessions. Patients reported improvements in recovery and activity tolerance at 2-, 6-, and 12-month follow-up. Though, there were no significant differences in pain.
  • Macedo et al: systematic review for patients with chronic LBP. Motor control exercises were superior to minimal intervention at short- and long-term follow-up; likely to benefit the patient when combined with another therapy for pain
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78
Q

Describe the concept of graded exposure in treating patients with low back pain

A

Asks patients to generate a hierarchy of feared activities and then gradually progress through these to attempt to reduce activity-related anxiety. Uses operant conditioning to reinforce healthy behaviors and progress the patient through different levels of functional activity.

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79
Q

How might a physical therapist decide if they should use motor control exercises or graded exposure in treating a patient with chronic low back pain?

A

Macedo et al used the Clinical Instability Questionnaire to identify patients who would benefit. Patients with a score of 9 or higher did substantially better with motor control exercises, while those with a score lower than 9 did better with a graded activity approach.

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80
Q

Describe the treatment approach for Motor Control Exercises described by Costa et al.

A

Stage 1: train coordinated activity of trunk muscles

  • independent activation of deeper muscles (transversus abdominis and multifidi)
  • reduce over-activity of superficial muscles in an individualized manner

Stage 2: implement precision of the desired coordination

  • train skills in static tasks
  • incorporate these skills into dynamic tasks and functional patterns
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81
Q

List the 15 items of the Clinical Instability Measure

A
  • back feels like it is going to “give way” or “give out”
  • feel the need to frequently “pop” the back to reduce pain
  • frequent times when pain occurs throughout the day
  • past history of catching or locking when twisting or bending
  • pain sit sit-stand or stand-sit
  • pain with lying-sit if not done carefully
  • pain incr with quick, unexpected, or mild movements
  • difficulty sitting without back support (chair or supportive backrest)
  • cannot tolerate prolonged positions when unable to move
  • condition is getting worse
  • pain for a long period of time
  • temporary relief with back brace or corset
  • frequent muscle spasms
  • fear of movement due to pain
  • traumatic back injury in the past
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82
Q

Describe the effects of aerobic and resistance exercise on patients with low back pain.

A

Aerobic: reduces increased awareness of neural stimulus (central sensitization)
Weight training: reduces frequency of acute episodes of low back pain

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83
Q

List & describe 3 areas of patient education for those with low back pain.

A
  1. advice to stay active, but avoid excessive loading of injured tissues; understand the difference between “good pain” (post-ex muscle pain) and “bad pain” (inflammatory pain)
  2. behavioral education: cognitive-behavioral theory & graded increases in activity and exposure
  3. physiology of pain: concepts of neuroplasticity and sensitization for patients with chronic symptoms (patient’s negative appraisal of pain is decreased & they understand that symptoms are expected and do not represent a serious undiagnosed disease)
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84
Q

What is the bottom line when it comes to the effectiveness of the most popular treatment approaches for patients with low back pain?

A
  • mobilization/manipulation, directional preference, and various exercises all have a relatively small (but potentially important) effect on both pain and disability
  • there is no demonstrated differences in effectiveness between different types of manual therapy
  • patient education regarding pain and advice to stay active is likely to be a key central component to recovery
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85
Q

Describe the central tenet of the modern neuroscience approach to treating low back pain.

A

Draws on the current imaging literature that demonstrates changes in motor control that occur with substantial changes in nervous system structure and function in people with chronic low back pain

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86
Q

Describe the clinical application of the modern neuroscience approach to treating low back pain.

A

substantial time is devoted to “pain neuroscience education” followed by exercise & manual therapy that includes cognition-targeted motor control training

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87
Q

Describe the current state of the evidence for the modern neuroscience approach for treating low back pain

A

well-constructed clinical trails are underway, but there are currently no data that support or fail to support this approach.

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88
Q

What is a trigger point?

A
  • Palpable, tight bands that are tender to palpation.
  • can develop in any skeletal muscle
  • may be the result of injury or microtrauma
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89
Q

How is it currently theorized that trigger points contribute to pain?

A

it is postulated (but still unproven) that trigger points are local areas of sustained muscle contraction associated with fluid congestion. Research has identified an increase in inflammatory cytokines within the substance of trigger points. Others have found 15% O2 saturations and decreased pH levels within the trigger point environment
- disruption of local chemical environment is referred to as “end-plate noise”

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90
Q

Describe the concept of “end-plate noise” as it relates to musculoskeletal pain.

A
  • Proposed mechanism behind trigger point pain
  • the combination of sustained muscle contraction & alterations in the chemical environment of the trigger point
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91
Q

What are the potential mechanisms for dry needling to reduce pain in muscle tissue?

A

several theories are proposed:

  • “gate-control theory” (actives a-delta nerve fibers that stimulate dorsal horn interneurons).
  • corrects for levels of circulating cytokines
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92
Q

Describe the “gate-control effect” of pain modulation.

A

a stimulus activates a-delta nerve fibers that stimulate enkephalinergic (endogenous opioid peptides / endorphins) dorsal horns interneurons, creating an opiate-like pain reduction

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93
Q

What is the current state of the evidence for dry needling as a treatment for low back pain?

A

There is some evidence that suggests that dry needling may be useful as an adjunct treatment, but the overall evidence base is inconclusive

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94
Q

What is the argument in favor of establishing physical therapists as the primary care providers for people with non-specific low back pain?

A

PTs can (1) identify undetected diseases / co-morbidities, (2) use manual therapy and exercise-based interventions that are low-risk and moderately effective, and (3) educate / coach patient to self-manage symptoms.

95
Q

What is the current major barrier to preventing scientific advancement in the treatment of people with low back pain?

A

“a lack of understanding of the mechanisms by which physical therapy (and other) treatments influence pain.”

96
Q

List the 3 main priorities for studying musculoskeletal pain, according to the National Center for Alternative and Complementary Medicine.

A

We need to identify: (1) the target sites and systems that are activated or inhibited by treatment, (2) the degree to which activation or inhibition of these sits and systems are linked to post-intervention pain reports, and (3) how these events vary between different patient pain-related phenotypes.

97
Q

Describe the theoretic model of mechanisms associated with PT care for low back pain proposed by Bialosky et al.

A

Intervention (e.g. manual therapy) activates or inhibits a cascade of peripheral/central events, including complex interplay of circulating sytokines and cortisol, brain and spinal cord activation patterns, and changes in patient beliefs and expectations.

98
Q

According to the Bialosky, et al, what events occur in the peripheral musculoskeletal tissue during manual therapy?

A

In skeletal muscle: increased ADC (apparent diffusion coefficient), decreased fluid stasis, decreased magnitude of muscle contraction at rest (muscle spasm);

In peripheral intra-/extra-cellular matrix: increase pH, reduced circulating cytokines

99
Q

According to the Bialosky, et al, what events occur in the supra-spinal system as a result of manual therapy?

A

Pain modulatory circuitry: Anterior Cingulate Cortex (ACC), Amygdala, Periaqueductal Gray (PAG), Rostral Ventromedial Medulla (RVM) - decreased BOLD response to stimuli;

Endocrine response: release of beta-endorphins, endogenous opiates, cortisol;

Autonomic response: changes in skin temperature, skin conduction, cortisol levels, heart rate

100
Q

Define Apparent Diffusion Coefficient (ADC).

A

the measure of the magnitude of diffusion of water molecules within tissue

101
Q

Describe the structure and role of Anterior cingulate cortex (ACC).

A

lies in a unique position in the brain, connecting to both the “emotional” limbic system and the “cognitive” prefrontal cortex;

The ACC is implicated in empathy, impulse control, emotion, and decision-making

102
Q

Describe the structure and role of the Amygdala.

A

one of two almond-shaped clusters of nuclei located deep and medially within the temporal lobe of the cerebrum;

The Amygdala is the core of a neural system for processing fearful and threatening stimuli

103
Q

Describe the structure and role of the Periaqueductal gray.

A

gray matter (cell bodies) found in the midbrain that surrounds the cerebral aqueduct and occupies a column of the brainstem that stretches about 14 mm;

The PAG is a key structure in the propagation and modulation of pain, sympathetic responses, and the learning and action of defensive/aversive behaviors

104
Q

Describe the role of the Rostral ventromedial medulla (RVM).

A

located close to the midline on the floor of the medulla oblongata (under midbrain, but above spinal cord)

The RVM sends descending inhibitory and excitatory neurons to the dorsal horn spinal cord neurons (3 categories are “on-cells”, “off-cells”, and “neutral cells”.)

105
Q

According to the Bialosky, et al, what areas of the Supra-spinal system that make up our “pain modulatory circuitry” are affected by manual therapy?

A

Anterior cingulate cortex, amygdala, periaqueductal gray, and rostral ventral medulla all have reduced BOLD response to stimuli.

106
Q

According to the Bialosky, et al, what events occur in intra-/extra-cellular matrices in peripheral musculoskeletal tissue?

A

increased pH, decreased circulating cytokines

107
Q

What effect does manual therapy have on the local pH of intra-/extra-cellular matrices of musculoskeletal tissue?

A

increased pH

108
Q

According to the Bialosky, et al, what is the endocrine response of the supra-spinal system to manual therapy intervention?

A

release of beta-endorphins, endogenous opiates, cortisol

109
Q

What are beta-endorphins?

A

proteins (polypeptide hormone) primarily synthesized by the pituitary gland;
category of endogenous opiod;
Binds to opioid receptors;

(endorphin = endogenous + morphine)

110
Q

Describe the effects of beta-endorphins on pain.

A

Found to be more potent than morphine. Acts in both peripheral and central nervous system (In spinal cord, binding to opioid receptors inhibits nociception signaling to the brain; In brain stem, binding activates descending pain control pathways.
Multiple effects beyond just pain relief.

111
Q

What effects to beta-endorphins have on our bodies aside from pain modulation?

A
  • may be involved with regulating stress response (inhibit pain during acute stress)
  • interacts with Dopamine system / may be involved with rewarding experiences
  • linked to positive effects of exercise on mood
    (still much to be understood about its many roles in the peripheral/central nervous systems)
112
Q

What effects do beta-endorphins have on our bodies aside from pain modulation?

A
  • may be involved with regulating stress response (inhibit pain during acute stress)
  • interacts with Dopamine system / may be involved with rewarding experiences
  • linked to positive effects of exercise on mood
    (still much to be understood about its many roles in the peripheral/central nervous systems)
113
Q

According to the Bialosky, et al, what autonomic changes result from manual therapy?

A

changes in skin temperature, skin conduction (galvanic skin response - momentarily becomes a better conductor of electricity), cortisol levels, and heart rate

114
Q

Describe the BOLD response.

A

Stands for Blood-Oxygen-Level-Dependent signal detected in fMRI. When neurons fire or increase their firing rate, they draw on oxygen and nutrients. The circulatory system of the brain reacts by sending the region that just fired more highly-oxygenated blood than is usually needed.

115
Q

According to the Bialosky, et al, what events occur in the spinal cord in response to manual therapy intervention?

A
  • decreased temporal summation (“reset button”)
  • selective blocking of neurotransmitters
  • influence neuromuscular responses-motor neuron pool, afferent discharge
116
Q

According to the Bialosky, et al, what are the 2 main events that occur in the peripheral nervous system in response to manual therapy?

A
  1. decreased depolarization of free nerve endings in involved tissues
  2. increased threshold for A-delta and C-fibers (pain-pressure threshold)
117
Q

According to the Bialosky, et al, what 3 types of pre-existing factors affect the perception of back pain? Give examples.

A
  • phenotypic: emotional distress, somatic awareness, catastrophizing
  • genetic polymorphisms: genes contributing to serotonergic and adrenergic pathways
  • medical co-morbidities
118
Q

What effect does manual therapy seem to have on lumbar intervertebral discs and skeletal muscle?

A
  • changes in rates of fluid movement (diffusion) within muscles and joints.
  • reduces muscle spasm
  • T2-weighted MRI showed immediate increases in diffusion of water within disks & reduced pain following lumbar joint mobilization and prone press-up exercises and following spinal manipulation. (Patients who had no improvement in pain did not show the same increases in disk diffusion.)
119
Q

According to the Bialosky, et al, what are the central events that occur in response to manual therapy interventions?

A

hypoalgesia occurring from temporal summation and selective blocking of neurotransmitters at the spinal cord (Gate Control Effect)

  • activation of pain modulatory circuitry in cortex, midbrain, and medulla
  • autonomic responses including changes in cortisol levels
120
Q

According to the Bialosky, et al, what events occur at higher brain centers in response to manual therapy

A
  • processing and appraisal of the excitatory/inhibitory information from other central and peripheral events activates higher brain centers.
  • interpretation of the manual treatment is strongly influenced by placebo, expectation, fear, catastrophizing, and kinesiophobia
121
Q

List 3 major patho-physiological mechanisms associated with low back pain by researchers.

A
  1. abnormal peripheral and central processing of pain messages
  2. degrees of mechanical loading that exceed the tolerance of exposed tissues
  3. inadequate extrinsic stabilization of the spine (i.e., impaired motor control)
122
Q

What is the most frequently imaged and surgically addressed tissue associated with low back pain?

A

the intervertebral disk

123
Q

How long have we been studying the intervertebral disk as a source of low back pain?

A

almost 90 years (since the 1930s)

124
Q

Describe the structure of an intervertebral disk and its role in the spine.

A
  • the central feature of the spine that contribute to support and mobility
  • very versatile - maintain stability under a wide variety of loading conditions, but also permit multidirectional motion of the segment
  • concentrically arranged layers of fibrocartilage around an inner core of proteoglycan gel
  • strongly bound to vertebral bodies and end plate cartilage
  • create a hydraulic system that absorbs and transmits forces (shear, compression, tension)
125
Q

What is meant by the “spacer effect” provided by the intervertebral disk?

A

The disk maintains sufficient vertical distance between vertebrae, which provides tension on the ligaments. This keeps the facets aligned and allows adequate space for neurovascular structures within the intervertebral foramina

126
Q

What area of the intervertebral disk provides the most resistance to tensile loads?

A

outer-most annulus; dense well-oriented Type I collagen fibers strongly bound to the periphery of the vertebral body and the outer margins of the end plate; reinforced by anterior and posterior longitudinal ligaments; long moment arm from the center of the disk

127
Q

Where are the neurovascular structures within a normal, non-diseased intervertebral disk located?

A

virtually all of the neurovascular structures are located in the outer-most annulus; sensory nerve fibers and their accompanying blood vessels are densest in the postero-lateral and antero-lateral disk (approx 3.5 mm from the periphery of the annulus)

128
Q

What movements are likely to result in the highest tension in the outer-most annulus of the intervertebral disk? Why is this clinically relevant?

A

end-range lumbar flexion & side-bending;
sensory nerve fibers and their accompanying blood vessels are densest in the postero-lateral and antero-lateral areas of the outer annulus

129
Q

Describe the pathway(s) of sensory nerves in the outer-most annulus of the intervertebral disk.

A

sensory info travelsin the Recurrent Meningeal (Sinu-Vertebral) nerve to the spinal cord.
From there, it either (1) travels segmentally through the adjacent posterior (dorsal root) or (2) extra-segmentally through the paravertebral sympathetic chain

130
Q

How do the pathways of sensory nerves in intervertebral disks contribute to the sometimes vague and diffuse location of low back pain?

A

“double pattern” of sensory information (segmental transmission via the spinal cord and extra-segmental transmission via paravertebral sympathetic chain) is likely to contribute to diffuse spatial location of pain

131
Q

What are the four concentric tissue layers of the intervertebral disk?

A
  1. outer-most annulus
  2. inner portion of the annulus
  3. transitional zone
  4. nucleus pulposus
132
Q

Describe the structure of the tissues each of the layers of an intervertebral disk.

A

Type I collagen fibers in the outer annulus (arranged in neat lamellar configuration) and the inner annulus (less organized and less dense closer to the center of the disk); thin, fibrous tissues in the transition zone surround and contain the nucleus, which is water held in suspension by glycosaminoglycan bonded to proteoglycan molecules (hydrophilic)

133
Q

What are glucosaminoglycans (GAGs)?

A

polysaccharides (carbohydrates) that are highly polar and attract water; for this reason, they are often used in the body as a lubricant or shock absorber

134
Q

What is proteoglycan?

A

proteins that are heavily glycosylated (attached to carbs/sugars/saccharides); they are a major component of the extracellular “filler” substance existing between cells; they also serve as lubricants by creating a hydrating gel (due to negatively charged sulfates in the GAG chains attached to the protein “core”)

135
Q

Describe the structure of the vertebral endplate. Why is this clinically relevant?

A
  • flat cartilage that covers the central portions of the superior and inferior vertebral bodies
  • creates semi-permeable barrier between the subchondral bone and the disc tissue
  • portion closest to the disk is fibrocartilage and is firmly connected to the annulus and nucleus
  • portion closest to the bone is hyaline cartilage and weaker (this area is believed to be a “weak link” during trauma & may be an important mechanism of the development of DD.
136
Q

Compare and contrast Type I and Type II collagen.

A

Both are a hard, insoluble, fibrous protein (molecules that are packed together to form long, thin fibers), Type I are found in bone, ligaments, tendons, skin, etc.; they tend to have a more orderly structure . Type II are found mainly in cartilage and are less organized; they present in combination with proteoglycans (ex. chondroitin sulfate)

137
Q

What substance accounts for more than 90% of the organic mass of bone?

A

Type I collagen.

138
Q

Describe the physiology of the tissue layers of the intervertebral disc.

A

outer-most layer of annulus contains a small number of fibrocytes that secrete Type I collagen; nucleus primarily contains chondrocytes that secrete proteoglycans and Type II collagen

139
Q

How is tissue fluid exchange important to the metabolic processes of the intervertebral disc tissue?

A

Cellular activity requires continued supplies of oxygen and nutrients to allow aerobic metabolism; Without it, the fibrocyte and chondrocyte cells can’t synthesize more Type I & II collagens, respectively;

Additionally, byproducts like lactate must be removed from the tissue

140
Q

Describe the process by which molecules move between a blood vessel and the center of an intervertebral disc

A

outer-most layer of the annulus has direct vascularization;
the rest relies on osmosis/bulk flow: molecules travel from the vascularized subchondral bone (capillaries), cross the vertebral endplate, then travel within the extracellular matrix to the cells; this distance can be as far as 20 mm - the human equivalent of traveling further than the moon (oxygen molecules move at over 1,000 mph)

141
Q

What role to proteoglycans play in the the structure and function of the intervertebral disk? How does this relate to spinal loading?

A

proteoglycans exert strong (-) charges that attract and bind water & they can be influenced by the nature of spinal loading and unloading;
this response to loading may account for large variations in the disk’s compressive strength and creates mechanical gradients that influence how much fluid is exchanged in the tissue.

142
Q

How does disk hydration change throughout the day? At what age do we see this diurnal variation less?

A

in normal, young disks, there is more hydration in the morning after lying down for several hours than in the evening after several hours of upright loading (average height loss is 0.9mm/disk or 19.3mm decrease in body height);

People with degenerative disks and those over 35 didn’t exhibit diurnal changes.

143
Q

What is the relationship between intervertebral disk disease and fluid exchange?

A

it is hypothesized that decreased ability to perform fluid exchange is an observable feature of disk disease

144
Q

Define disk degeneration according to Adams and Roughley (2006).

A

an aberrant, cell-mediated response to progressive structural failure

145
Q

Describe the effect of intervertebral disk degeneration on the interplay between the nucleus and surrounding structures.

A

(waterbed analogy by Adams and Roughley)

  • structural disruption causes loss of water content and loss of support for the nucleus by the annulus
  • reduction is hydrostatic capacity of nucleus
  • causes the annulus to resist compression rather than behave as a flexible inter-space
  • annular fibers resist load in disorderly way and lose internal stability that results in further strain upon the disk structures
146
Q

For most people, at what age do signs of disk degeneration start to appear?

A

often present by our 20s & are almost universal by our 80s and 90s

147
Q

What percentage of adult spinal surgeries are to specifically address disk degeneration?

A

90%

148
Q

90% of all adult spinal surgeries are to address what condition?

A

intervertebral disk degeneration

149
Q

According to Brinjikji, et al, what % of people in their 20s show signs of disk degeneration?

A

37%

150
Q

According to Brinjikji, et al, what % of people in their 40s have a disk bulge?

A

50% (one in two people)

151
Q

According to Brinjikji, et al, what % of people in their 20s have a disk protrusion?

A

29% (nearly one in three)

152
Q

According to Brinjikji, et al, what % of people in their 20s have an annular fissure?

A

19% (nearly one in five)

153
Q

According to Brinjikji, et al, 37% of people in their 20s show what finding on spinal imaging?

A

signs of disk degeneration

154
Q

According to Brinjikji, et al, 50% of people in their 40s show what finding on spinal imaging?

A

disk bulge

155
Q

According to Brinjikji, et al, 29% of people in their 20s show what finding on spinal imaging?

A

disk protrusion

156
Q

According to Brinjikji, et al, 19% of people in their 20s show what finding on spinal imaging?

A

annular fissure

157
Q

What is the current state of the evidence regarding relationship between a history of heavy physical loading and the development of disk degeneration?

A

though traditional belief held that occupations involving heavy manual labor are major risk factors for the development of disk degeneration, this has not been supported by the evidence as a meaningful etiologic factor of DD; in the absence of trauma, weightlifters show lower rates of DD

158
Q

What role does genetics play in disk degeneration?

A

genetic factors influence:

  • the water content and shape of spinal structures
  • the synthesis and breakdown of tissues within the disk
159
Q

What are the strongest predictors for disk degeneration?

A

genetic factors

160
Q

What did the twins study show about the development of disk degeneration

A

MRI findings compared to lifestyle factors in a large sample of identical twins yielded a heritability estimate of 74%

161
Q

What evidence is consistent with the hypothesis that genetics contribute substantially to the etiology of disk degeneration?

A
  • twins studies: 74% heritability
  • patients diagnosed with HNP before 21 are 4-5x more likely to have family history of DD
  • DD has the highest prevalence in people with OA
162
Q

What changes occur within the intervertebral disk over the lifespan?

A
  • end-plate permeability & metabolic transport decrease
  • reduction in proteoglycans, leading to hydration loss
  • nucleus becomes smaller (but retains hydrostatic properties)
  • Type II collagen becomes Type I, forms a “wall” by cross-linking (creates a thick fibrous environment that blocks fluid exchange, reduces turnover rate of collagen and proteoglycans)
  • retention of damaged macromolecules and impaired homeostasis
163
Q

How do age-related changes in the intervertebral disk affect most people?

A
  • relatively benign, age-related changes don’t cause a loss of disk height or a loss of the hydrostatic properties of the nucleus
164
Q

What is a “dark disk” on an MRI?

A

reduced brightness of the signal from the nuclear region and/or the development of nuclear clefts

165
Q

Disruption of which two tissues can result in vertebral osteophyte formation?

A

intervertebral disk end-plate disruption or annulus disruption

166
Q

What change in the vertebral body results from IVD end-plate or annulus disruption

A

osteophyte formation

167
Q

Describe how disruption of the IVD end-plate can result in osteophyte formation

A
  • altered diffusion -> decreased cellular activity reduces turnover of extracellular matrix-> further damage
  • destabilized -> increased micro-motion -> further damage
  • further damage -> decreased disk space / altered load-bearing motion in segment -> increased loads on periphery of vertebral body and posterior -> formation of osteophytes
168
Q

Describe how disruption of IVD annular disruption can result in osteophyte formation.

A
  • secretion of proteolytic enzymes -> further damage
  • destabilized -> increased micro-motion-> further damage
  • further damage -> decreased disk space / altered load-bearing motion in segment -> increased loads on periphery of vertebral body and posterior -> formation of osteophytes
169
Q

What structure of the lumbar spine is considered the “weak link” in response to compressive loading?

A

the vertebral end plate

170
Q

What type of loading/trauma is the vertebral end plate must susceptible to?

A

compressive loading, axial trauma

171
Q

What is suggested by Rajasekaran et al in regards to the difference between aging and degeneration?

A

though they may look the same, there are measurable differences in diffusion capacity at the vertebral end plate between disks with painful degeneration and people with age-related changes.

172
Q

What is the proposed relationship between Modic signs found on MRI and pain?

A

Modic signs have been postulated as a useful way to discriminate painful vs nonpainful in degenerative discs, conflicting evidence exists

173
Q

What is the relationship between end-plate injury and bone marrow edema?

A

end-plate injuries are associated with bone marrow edema and resultant cartilage that protrudes into the next vertebral body (Scmorl’s node)

174
Q

What is a Schmorl’s node

A

soft tissue of the intervertebral disc bulges out into the adjacent vertebrae through an endplate defect

  • most common in upper lumbar spine
  • often found incidentally on imaging studies
175
Q

How can vertebral end plate injuries affect the nucleus of the disk?

A

injuries to the end plate can immediately decompress the nucleus, leading to loss of its hydrostatic properties, impaired diffusion, disruption of nutrient supply, and/or cell death from excessive tissue loading

176
Q

List 4 examples of pathology that can result from injury to the vertebral end plate.

A
  • measurable changes in end plate diffusion are linked to painful disc disease
  • Modic signs? (conflicting evidence)
  • Schmorl’s nodes (bone marrow edema / cartilage)
  • decompression/injury to the disc nucleus
177
Q

What are the three types of injury to the annulus of the IVD?

A
  • peripheral rim lesions
  • circumferential tears
  • radial fissures
178
Q

Describe a radial fissure of the annulus of the IVD.

A
  • lesion that spreads outward from the nucleus
  • primary structural abnormality associated with disc disease
  • can create pathways through which nuclear material can move, which destabilizes the disc’s hydrostatic capacity
179
Q

Describe a circumferential tear of the IVD.

A
  • layers of the annulus split

- may occur from repetitive compressive stress

180
Q

What type of tissue disruption is most common in the lower lumbar spine?

A

IVD annulus disruption

181
Q

Where are Schmorl’s nodes most commonly found?

A

upper lumbar spine

182
Q

What type of disruption to the IVD annulus is a possible nociceptive generator?

A

peripheral rim lesions

- involve outer-most annulus, which is innervated

183
Q

Describe a peripheral rim lesion of the IVD annulus.

A

injury to out-most annulus

  • most likely to be in response to trauma
  • tears in the innervated periphery, so potential source of symptoms
184
Q

How are peripheral rim lesions of the IVD annulus detected on imaging?

A

high-intensity T2 signals (brighter) near the outer margins of the annulus

185
Q

How does the body heal following tears of the peripheral annulus of the IVD?

A

heals through inflammatory processes, so this often results in poorly remodeled scar tissue

186
Q

How does the body heal following tears of the middle and inner portions of the IVD?

A

likely to be filled by granulation tissue, which doesn’t restore normal tensile strength of the structures in this region

187
Q

How is it theorized that the body’s response to IVD annular tears contributes to nociception generation?

A

the inflammatory healing process results in the growth of new blood vessels (neovascularity) that often penetrate deep into the annular region and are accompanied by addition nociception-sensitive nerve fibers

188
Q

Theoretically, how would a patient present if their pain were caused by neovascularity following an IVD annulus tear?

A

pain during weight-bearing

189
Q

What is one structural explanation for two patients sustaining similar injuries to the IVD annulus, yet having very different pain responses?

A

Inflammatory responses to healing an annular tear cause varying degrees of neovascularization/neoinnervation

190
Q

How can injuries to the IVD annulus or end plate result in pH changes in the nucleus?

A

annulus and end-plate disruption can both cause an impairment of diffusion of O2 and nutrients

  • low oxygen tension in the center of the nucleus favors anaerobic metabolism and results in lower pH
  • this leads to a greater concentration of lactic acid
191
Q

What is the effect of an excessively low pH in the IVD nucleus?

A

low pH means increased lactic acid, which can cause cells in the nucleus to become inactive

192
Q

How can injuries to the IVD annulus or end plate result in glucose changes in the nucleus?

A

annulus and end-plate disruption can both cause an impairment of diffusion of O2 and nutrients
- persistent reduction in glucose can result in cell death and a build-up of metabolic waste products

193
Q

What effect does a reduction in glucose in the IVD nucleus have on the pH of the tissue?

A

reduces pH and inhibits proteoglycan synthesis

194
Q

What is the ultimate effect of an IVD annulus or end-plate disruption on the nucleus? Why is this clinically relevant?

A

reduced hydration and resulting loss of internal stiffness in the disc
this increases micro-motion during loading and may contribute to segmental instability, further annulus tears, decreased diffusion, and increased secretion of proteolytic enzymes

195
Q

What are proteolytic enzymes?

A

enzymes that break down protein

196
Q

Why is it bad for the nucleus of an IVD to lose hydration?

A

reduces the volume of the disc, creating a reduction in disk height that slackens supporting fibrous tissues

197
Q

What adjacent structures are affected by a loss in IVD height?

A

loss of 1-3 mm can overload facets joints and reduce the cross-section of the foramen (inward bowing of annulus and ligamentum flavum)
- over time, this can cause spondylosis

198
Q

What is spondylosis?

A
  • reduction in intervertebral disc height causes increased bowing of the annulus
  • over time, repeated micro-motion generates loads on the longitudinal ligaments and outer-most annulus
  • this stimulates osteoblastosis / osteophyte / “disc ostephyte formation
  • results in a loss of spinal ROM and further reduces both disc height and threshold for nociception
199
Q

To what degree are load-bearing and load-sharing patterns altered due to IVD degeneration?

A

with severe disc degeneration, 50% of weight-bearing loads are absorbed by the neural arch

200
Q

What morphological changes create the condition of symptomatic spinal stenosis?

A

posterior osteophytosis, severe disc narrowing, and bulging of the annulus fibrosis and ligamentum flava that result in various degrees of neural compression

201
Q

What is the bottom line when it comes to the relationship between disc degeneration and low back pain?

A
  • it’s likely that DD is an important component of some, but certainly not all LBP
  • development of lumbar DD is strongly linked to genetic factors, but progression is modulated by environmental factors
  • it’s highly likely that stimulation of nociceptive-sensitive structures in the annulus, bone, end plate, and nearby tissues can trigger LBP
  • loss of hydration in the nucleus is in large part due to poor diffusion
  • loss of annular support accelerates degeneration, decr stability, and inc reactive bone formation (this may not cause symptoms, but can decr threshold of nociceptive-sensitive structures)
  • current literature does not provide a valid system to us DD findings to identify patients or meaningful strategies for treatment
202
Q

Should the presence of intervertebral disc degeneration influence exercise prescription?

A

mild early-stage disc degeneration don’t need any treatment precautions, but moderate or severe degeneration might benefit from being encouraged to avoid long exposure to compression that occurs during prolonged sitting / lumbar flexion (occupational back pain)

203
Q

What is the effect of weight-training on intervertebral disc health?

A

properly performed, weight training doesn’t result in adverse loads acting upon the disc

204
Q

What is the prevalence of disc degeneration in weightlifters?

A

no higher incidence than would be expected

205
Q

What evidence supports a difference between properly performed weight lifting vs occupational lifting tasks that may be performed inappropriately in the development of disc degeneration?

A

weight lifters don’t have an elevated prevalence of degeneration; repeated occupational exposure to lifting is associated with development of back pain (irrespective of DD); lifting greater that 55lb more than 25x/day increased annual incidence of LBP by 4% compared to those that didn’t perform heavy lifting (Coenen, et al’s meta-analysis)

206
Q

How should later-stage disc degeneration be considered when prescribing exercise?

A

reduction in disc height and loss of hydrostatic nucleus mean that the disc is no likely to regain tensile strength (especially if there is damage to the end plate and/or annulus), so loads should be progressed more gradually and sustained loading at end-ranges of the lumbar spine may provoke symptoms (not enough annular constraint)

207
Q

Why might a patient with lumbar disc degeneration experience delayed pain following exercise?

A

swelling from micro-hemorrhage and edema stimulate free nerve endings in the periphery of the disc, which can take time to develop

208
Q

How are stabilization exercises theorized to help lumbar disc degeneration?

A

contraction of the abdominal and multifidi musculature improves the patient’s ability to tolerate loading of the discs

209
Q

What did Snook, et al conclude about patients with intervertebral disc degeneration and the time of day that they perform exercise?

A

patients with DD who avoided early-morning lumbar flexion for two hours had less pain and disability; theorized that increased volume influences the response of the disc to end range loads (especially flexion)

210
Q

What additional pathology / mobility limitations often occur with lumbar disc degeneration?

A

osteoarthritis of the hips, reductions hip extension and internal rotation

211
Q

Describe future regenerative procedures to treat lumbar disc degeneration & the physical therapist’s role in post-operative rehab.

A
  • injection of biomaterials (progenitor cells) in the nucleus to stimulate endogenous repair / proteoglycan production; (preliminary animal findings are promising)
  • PTs will need to identify proper type and progression of mechanical loading stimulus to stimulate favorable cellular activity without disrupting healing tissue
212
Q

What is the bottom line when it comes to the relationship between exercise and the presence of intervertebral disc degeneration?

A
  • evidence of degeneration should be strongly correlated
    with other clinical findings to determine treatment intensity
  • properly-performed weight training is unlikely to injure a degenerative lumbar IVD
  • exercises that involve lifting that excessively stress end-range loading (especially flexion) may be harmful to severely degenerative annular tissues
  • repeated, excessive lifting in an uncontrolled occupational environment can potentially increase the likelihood of LBP
  • injectable biomaterals show promise in regenerating tissue, but its unlikely to help severe cases
  • future research should explore the effects of manipulation, traction, and exercise on physiologic properties and natural history of DD
213
Q

What are three aspects of self-management of acute low back pain that PT can facilitate?

A
  • lifestyle modifications
  • reduction in avoidance beliefs / behaviors
  • regular performance of conditioning exercises
214
Q

What are the categories of the treatment-based classification system for treating LBP

A

manipulation, specific exercise (directional preference), stabilization, traction

215
Q

What are the key examination findings to indicate a treatment-based classification of “Manipulation” for a patient with low back pain?

A
  • no sx distal to knee
  • recent onset of sx ( < 17 days)
  • FABQ < 20
  • lumbar hypomobility
  • hip IR > 34°
216
Q

What are the key examination findings to indicate a treatment-based classification of “Specific Exercise - Extension” for a patient with low back pain?

A
  • symptoms distal to the buttock
  • directional preference for extension
  • symptoms peripheralize with flexion
  • centralization with extension
217
Q

What are the key examination findings to indicate a treatment-based classification of “Specific Exercise - Flexion” for a patient with low back pain?

A
  • age 50 or older
  • directional preference for flexion
  • evidence of spinal stenosis on imaging
218
Q

What are the key examination findings to indicate a treatment-based classification of “Specific Exercise - Lateral Shift” for a patient with low back pain?

A
  • visible frontal plane deviation

- directional preference for lateral translational movements

219
Q

What are the key examination findings to indicate a treatment-based classification of “Stabilization” for a patient with low back pain?

A
  • age 40 or younger
  • passive straight leg raise 91° or greater
  • aberrant movements (“instability catch”, thigh-climbing, painful arc, reversal of lumbopelvic rhythm)
  • (+) prone instability test
220
Q

What are the key examination findings to indicate a treatment-based classification of “Traction” for a patient with low back pain?

A
  • presence of leg symptoms
  • signs of nerve root compression
  • peripheralization with extension + crossed straight leg raise (sx in opposite lower extremity)
221
Q

Which treatment-based classification of LBP is described below?:

  • presence of leg symptoms
  • signs of nerve root compression
  • peripheralization with extension + crossed straight leg raise (sx in opposite lower extremity)
A

traction

222
Q

Which treatment-based classification of LBP is described below?:

  • age 40 or younger
  • passive straight leg raise 91° or greater
  • aberrant movements (“instability catch”, thigh-climbing, painful arc, reversal of lumbopelvic rhythm)
  • (+) prone instability test
A

stabilization

223
Q

Which treatment-based classification of LBP is described below?:

  • visible frontal plane deviation
  • directional preference for lateral translational movements
A

specific exercise - lateral shift

224
Q

Which treatment-based classification of LBP is described below?:

  • age 50 or older
  • directional preference for flexion
  • evidence of spinal stenosis on imaging
A

specific exercise - flexion

225
Q

Which treatment-based classification of LBP is described below?:

  • symptoms distal to the buttock
  • directional preference for extension
  • symptoms peripheralize with flexion
  • centralization with extension
A

specific exercise - extension

226
Q

Which treatment-based classification of LBP is described below?:

  • no sx distal to knee
  • recent onset of sx ( < 17 days)
  • FABQ < 20
  • lumbar hypomobility
  • hip IR > 34°
A

manipulation

227
Q

According to the treatment-based classification of LBP, what treatment is recommended for a patient who presents with:

  • no sx distal to knee
  • recent onset of sx ( < 17 days)
  • FABQ < 20
  • lumbar hypomobility
  • hip IR > 34°
A

manipulation or mobilization (manipulation may be more effective) and active range of motion exercise

228
Q

According to the treatment-based classification of LBP, what hip ROM might contribute to a classification of the “manipulation” treatment group?

A

hip IR 35° or greater (in prone)

229
Q

According to the treatment-based classification of LBP, what treatment is recommended for a patient who presents with:

  • presence of leg symptoms
  • signs of nerve root compression
  • peripheralization with extension + crossed straight leg raise (sx in opposite lower extremity)
A

mechanical traction

230
Q

According to the treatment-based classification of LBP, what treatment is recommended for a patient who presents with:

  • age 40 or younger
  • passive straight leg raise 91° or greater
  • aberrant movements (“instability catch”, thigh-climbing, painful arc, reversal of lumbopelvic rhythm)
  • (+) prone instability test
A
  • promote isolated contraction and co-contraction of the deep stabilizing muscles
  • strengthening of large spinal stabilizing muscles
231
Q

According to the treatment-based classification of LBP, what treatment is recommended for a patient who presents with:

  • visible frontal plane deviation
  • directional preference for lateral translational movements
A
  • pelvic translocation exercises

- non-weight-bearing shift correction exercises

232
Q

According to the treatment-based classification of LBP, what treatment is recommended for a patient who presents with:

  • age 50 or older
  • directional preference for flexion
  • evidence of spinal stenosis on imaging
A
  • flexion exercises
  • mobilization to promote flexion
  • de-weighted ambulation
  • avoidance of extension exercises
233
Q

According to the treatment-based classification of LBP, what treatment is recommended for a patient who presents with:

  • symptoms distal to the buttock
  • directional preference for extension
  • symptoms peripheralize with flexion
  • centralization with extension
A
  • extension exercises
  • mobilization to promote extension
  • avoidance of 1flexion activities

OCS (13 decks)

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