10/7/2011 Outline of Today’s Lecture · Definition: May aid in teasing out ... Sensory testing for allodynia & pin-prick threshold (8 pts max) Scored /24 ≥ 12 = neuropathic component

10/7/2011

1

Carol A. Courtney PT, PhD, ATC, FAAOMPT

Alison M. Duncombe PT, OCS, FAAOMPT

Michael A. O‟Hearn PT, MHS, OCS, FAAOMPT

The Challenge of Spine-Related Extremity

Pain: Clinical Assessment and

Strategies for Management

Outline of Today’s Lecture

Carol A. Courtney PT, PhD, ATC, FAAOMPT

Radiculopathy vs Pseudoradiculopathy?

Sensitization of Nociceptive Pathways: clinical implications

Alison M. Duncombe PT, OCS, FAAOMPT

Lower Quarter pain of Non-Neuropathic Origin

Michael A. O‟Hearn PT, MHS, OCS, FAAOMPT

Lower Quarter Pain of Neuropathic Origin

Low Back Pain

a lifetime prevalence of 80% Andersson 1999

underlying cause of roughly 90% of

back pain is not known Koes et al 2006

Clinical Dilemma:

mechanism-based

classification of pain

proposed Woolf et al

Is the patient‟s LBP

neuropathic or non-

neuropathic?

Pain referral patterns from asymptomatic (normal) and symptomatic (abnormal) patients

after intra-articular injection of 1–3 mL of 5% saline under fluoroscopic guidance.

Mooney, V., Robertson, J. 1976

Pain Diagram: After 10 min of continuous

electrical stimulation of constant intensity

(200% of the individual local pain

threshold) of the right L3–4 facet

O’Neill 2009

Pain Diagram: Short lasting electrical

stimulation of variable intensity of the

right L3–4 facet

10/7/2011

2

Musculoskeletal insult: Peripheral Sensitization

Damaged tissue releases inflammatory mediators (such as bradykinin, prostaglandins, etc)

Sensitize the nociceptors at the site of injury (Brenn et al 2007)

= primary hyperalgesia (increased nociceptive responses)

7 Julius and Basbaum 2001

Clinical findings: Central Sensitization

occurs following repetitive or

intense noxious stimulus

Latremoliere and Woolf 2009

Pain is no longer coupled to the noxious stimulus

Characterized by:

Increased excitability of nociceptive

pathways

Decreased descending inhibition

Adapted from Costigan 2009

Peripheral Sensitization

Central Sensitization

Inflammatory mediators

Central Sensitization in Musculoskeletal

Conditions?

Spinal-mediated reflex =

hyperexcitable Whiplash, Fibromyalgia

Banic 2004

Cervical Spine Dysfunction

Sterling 2010

Knee Osteoarthritis

Courtney 2009, 2010

Central Sensitization in

Musculoskeletal Conditions: Why is

this important?

Heightened Pain Sensitivity

Altered Somatosensation and spread of

symptoms

Spread of inflammation (?) and disease

process (OA)

Functional changes (?)

Pain Referral From Knee Bajaj 2001

Central Sensitization comprised

of two temporal phases Early phosphorylation-dependent and transcription

independent phase

Dependent on NMDA receptors

Results mainly from rapid changes in the receptor and

ion channel properties

Later longer-lasting phase

Long Term Potentiation (LTP)?

10/7/2011

3

Neurogenic Inflammation Efferent action of

nociceptive fibers

Release Substance P

Causes ↑ sensitization

‘phenotypic change’ in the Aβ fiber (Ma et al 1996,

Baba et al 1999)

Bilateral symptoms? (Sluka 2002, Fernandez-Carnero 2008)

Julius and Basbaum 2001

Peripheral Afferent Fibers

Aβ – Fibers

In the presence of inflammation, Aβ fibers begin to express C-fiber

associated neuropeptides (substance

P, etc).

i.e = „phenotypic change‟ in the Aβ

fiber (Ma et al 1996, Baba et al 1999)

Bottom line: non-noxious input to

the dorsal horn can cause/maintain

sensitization?

Neumann S, Doubell, T, Leslie T

& Woolf CJ: Inflammatory pain

Hypersensitivity mediated

By phenotypic switch in

Myelinated primary sensory

Neurons. 384 (28): 360-4.

Why Quantitative Sensory Testing? Definition:

Psychophysical method to assess neural function

Involves:

Mapping of distribution

Identification of negative (sensory loss) and positive (eg, hyperalgesia) sensory phenomena

May aid in teasing out which pain pathways and mechanisms are involved

Arendt-Nielsen and Yarnitsky 2009

Recognizing somatosensory patterns may facilitate diagnosis in terms of nociceptive mechanism Woolf 2001

Clinical Assessment: Sensory Exam

Hyperalgesia

Increased Pain Sensitivity

Clinical Assessment: Sensory Exam

Hyperalgesia

Allodynia: pain with stroking

of skin

(“feels like sunburn”)

Indicates central sensitization

Pressure Pain: Increased

deep tissue tenderness Primary, secondary, widespread

hyperalgesia

Clinical Assessment: Sensory Exam

Hypoesthesia Decreased cutaneous

sensation (light touch)

Assessed with cotton tipped

applicator or monofilaments

Decreased vibration detection

threshold

Clinically often reported as Yes/No

10/7/2011

4

Hyperalgesia and Hypoesthesia?

A paradox

↑ sensitivity to pain + ↓ sensitivity to light touch/vibration

Independent Mechanisms

both triggered by nociceptive input

both indicate central plasticity Geber 2008

Possible clinical importance?

Instability during functional activities

Instability during gait activity

following Musculoskeletal Injury

Many causes:

Muscle weakness

Slemenda 1997

Altered motor control

Hortobagyi 2005

Decreased proprioception

Pai 1997, Hertel 2008

Dworkin 2007 JPain

Lower Quarter pain of Non-Neuropathic Origin

Symptoms extending distal

to the knee may be more

common than previously

believed

For example, as arthritic

hip joint pain becomes

chronic, the spread of

symptoms may mimic spine

related extremity pain

Hip Pain – What Does It Look Like?

Lesher et al 2008

Hip Referral Classically refers to the groin and medial thigh

Pain mapping of 55 patients with radiographic hip OA and >90%

pain reduction 30 minutes after FGIA hip injection:

• Groin 55%

• Medial thigh 57%

• Buttock most common 71%

• Lower leg 16%

• Foot 6%

10/7/2011

5

Hip Versus Spine Referral

Pain maps of 60 patients awaiting THA, and 60 awaiting spinal decompression surgery Khan et al 2004

• Hip pain frequently associated with labral

tears (up to 66%)

• Most common in central groin (P < 0.001)

and lateral peritrochanteric area (P = 0.02)

Arnold et al 2011

• May also present in the buttock

Arnold et al 2011

• Labral tears may be part of a continuum of

joint degeneration leading to OA

Neumann 2007

Labral Tears

Neurogenic Inflammation

• Invasion of C-n sensory nerve fibers and sympathetic innervation into synovial membrane of pseudocapsule in individuals with prosthetic loosening after total hip replacement (Niissalo 2002)

• Cells in the fibrotic areas in the interface tissue expressed strong immunoreactivity to the neural marker PGP 9.5, ubiquitin carboxyterminal hydrolase.

• Pain of hip OA may be caused by invasion of nerve fibers into synovial tissues with efferent release of neuropeptides, facilitating pain, inflammation, and joint degeneration.

Neurogenic Inflammation Immunoreactive sensory nerve fibers found in labra of human hips

harvested during arthoplasty; not found in osteonecrosis of femoral

head

Shirai 2009

Hip-spine Syndrome

• Relationship between hip and lumbar spine pain

Offierski 1976

• Surgical treatment of severe hip OA produced marked

improvement in both hip and back pain

Ben-Galim 2007

• Patient with LBP and hip pain, underwent PT (manual

therapy and exercise) to the hip

• LBP alleviated as well Burns 2011

Post-operative Changes in Pain

Ben-Galim 2007

10/7/2011

6

Greater Trochanteric Pain Syndrome

• GTPS affects 10- 25% of the general population

Strauss 2010

• Significantly associated with LBP (OR 2.79), ipsilateral (OR

3.47) and contralateral (1.74) knee OA, ITB pain and obesity

Segal 2007

• Frequently radiates with paraesthesia

Meknas 2011

Tests for Greater Trochanteric Pain

Syndrome

• Diagnostic standard = MRI

• Confirmed gluteus medius tear or

tendinopathy, or bursitis

• Single leg stance 30 seconds – 100% sensitivity, 93.7% specificity

• Resisted external derotation

– 88% sensitivity, 93.7% specificity

Lequesne 2008

Pressure-Pain Threshold Algometric Measurement

in Patients With Greater Trochanteric Pain

Sayed-Noor 2008

Vibratory Deficits in Hip OA

• Vibratory perception threshold was significantly reduced in

subjects with symptomatic and radiographic hip OA when

compared with age-matched controls without hip OA

• Deficit was widespread, indicating inherent generalized

neurologic deficit?

• 1st MP joint, medial and alteral malleolus, medial and lateral

femoral condyle, radial head

• Effect size 0.87 – 1.94

Shakoor et al 2008

QST Deficits in Hip OA

• Abnormal QST (PPT, heat and cold sensitivity) in patients

with OA normalized 6 months following total hip

arthroplasty.

• Hypoesthesia over painful hip also normalized

Kosek and Ordeberg 2000

Altered QST in OA Gwilym 2009

• Individuals with hip OA found to have significantly lowered threshold perception to cutaneous stimulation in their areas of referred pain, and demonstrate increased hyperalgesia to the same stimuli when compared with healthy controls

• Brain MRI of OA patients also showed significantly greater brainstem activation in response to punctate stimulation of their referred pain areas

• Magnitude of brainstem activation positively correlated with extent of neuropathic-like elements to the patient‟s pain, as indicated by the PainDETECT score.

10/7/2011

7

Altered QST in Hip OA Nikolajsen 2009

• Eighteen patients with chronic hip pain and 18 painfree controls

• Quantitative sensory testing (brush-evoked allodynia, pinprick

hyperalgesia, mechanical and thermal thresholds).

• Allodynia (P=0.1) and pinprick hyperalgesia (P=0.02) No

hypoesthesia to tactile stimuli

• Thermal thresholds???

• Chronic hip pain significantly associated with low back pain

(P=0.002).

Hamstring Strain vs Neural Tension Kornberg and Lew, JOSPT 1989

• Professional Australian Rules

football players

• diagnosed grade I hamstring injuries

• + responses to the slump test

(neural provocation test)

• 16 subjects treated traditionally

• 12 received slump stretch as well

• Addition of slump stretch technique

more effective (p < 0.001) in

returning player to full function

than the traditional regime alone

Lower Quarter Pain of Neuropathic Origin

Neuropathic vs Nociceptive

IASP (NeuPSIG) “pain arising as a direct consequence of a lesion

or disease affecting the somatosensory system” Hannpa et al 2011

Characteristics of Neuropathic Pain Freynhagen & Baron 2009

Spontaneous pain

Abnormal responses to non-painful or painful stimuli

Pain that is shooting, stabbing or feels like an electric shock

Abnormal thermal sensations

Possible Causes

Freynhagen & Baron 2009

Prevalence & Relevance

Ranges from 16 to 20% in patients with low back pain

Beith et al 2011, Freynhagen et al 2008

Utilized screening tools

Poorer outcome if neuropathic component

present?

Classification of patient apriori leads to improved

outcomes?

10/7/2011

8

Screening & Clinical Examination for

Lumbar Spine-Related Neuropathic Pain

Screening tools

LANSS

painDETECT

Clinical Examination

Screening Tools: LANSS Bennett 2001

Leeds Assessment of Neuropathic Symptoms & Signs

(LANSS)

5 “Yes” or “No” questions (16 pts max)

Sensory testing for allodynia & pin-prick threshold (8 pts

max)

Scored /24

≥ 12 = neuropathic component likely

1. Does your pain feel like strange unpleasant sensations in your

skin?

2. Does your pain make the skin in the painful area look different

from normal?

3. Does your pain make the skin of the affected area abnormally

sensitive to touch?

4. Does your pain come on suddenly for no apparent reason

when you‟re still?

5. Does your pain feel as if the skin temperature in the painful

area has changed abnormally?

LANSS: Sensory Testing

Bennett 2001

1. Allodynia

Stroke affected & unaffected areas with cotton wool

Positive = pain or unpleasant sensations (tingling or nausea)

2. Altered Pin-Prick Threshold

23 gauge needle testing affected & unaffected

Positive = any difference in sensation

painDETECT

Developed to detect the neuropathic component in patients

with LBP Freynhagen et al 2006

Sensitivity = 85% Specificity = 80%

PPV = 83%

Classifies patients as “nociceptive”, “unclear” & “possible

neuropathic”

10/7/2011

9

Clinical Examination

NeuPSIG Guidelines 2011

“Common denominators” of neuropathic pain…

Area of symptoms fits the distribution of a nerve

Quantitative – hyper or hypoesthesia

Qualitative – allodynia or dyesthesia

Temporal – aftersensation, summation

Clinical Examination

Both “positive” and “negative” sensory

phenomena have been reported in non-

neuropathic pain states.

Clinical examination alone can not

prove that pain is of neuropathic origin

10/7/2011

10

Clinical Examination

Tactile sense

Pinprick sense

Thermal

Vibration

Straight Leg Raise

Allodynia Neuropathic pain more

likely to have sensitivity

to brushing, cold and

heat

Sensitivity to pressure

found in both

neuropathic and

nociceptive pain states

Battery of QST measures on patients that are “radicular” &

“pseudoradicular”.

Vibration sense reduced in both groups

73% vs 47%

Continuum?

Identifying Patients with Neuropathic

Back & Leg Pain Combining Screening

Tools & Clinical Examination

Beith et al Pain 2011

N = 343 LBP with & without LE pain

Used painDETECT as primary sort…

Possible neuropathic

Unclear

Nociceptive

54 (16%) classified as “possible neuropathic”

Patients in this group had higher pain, Roland-Morris, anxiety &

depression

Passive SLR (with & without ankle df) was also reduced

Beith et al 2011

Presence of Lower

Extremity Symptoms

Possible Neuropathic Nociceptive

Lower extremity in

general

96%

55%

Below Knee

76% 32%

The presence of leg pain may not be the defining feature of

neuropathic pain

10/7/2011

11

Summary

A neuropathic source of symptoms may be more common

than previously thought in patients with LBP

With or without leg pain

Screening tools & clinical examination may help identify

these individuals

Early identification may lead to more effective treatment?