OCS- Wilson’s prep Courses:

Intro powerpoint:

 Question parts:
o Stem- actual question or case
o Options: correct response + distractors
 Types of questions:
o Recall, application, synthesis
 Peer review articles (not outdated and not brand new)
 Option characteristics
o Be placed in a specific order
o Typically be homogeneous and will include incorrect options that will seem credible to
the less prepared examinees
 Test taking tips
o Read the options first
o Determine how many breaks you can have divided by 200 questions
o Options that are longer and more detailed are often correct
o Look for non-homogenous option and consider eliminating them first
o If a significant word from the stem is repeated in the an option- that option is most
likely the correct choice
o If two options are similar, one of those is correct (50/50)
o Options that have the most in common with all of the other options
(terminology/conceptual) is most likely the correct choice
o Absolutes are rarely correct- consider eliminating option that use “always” or similar
terms
 Evidenced based medicine:
 Individual clinical experiences
 Patient preferences
 Best available external evidence from systematic research

- Intrarater reliability: consistency of an outcome measure when applied by the same PT on the
same patient
- Interrater reliability : consistency with different raters produce the same score for same pt.
o Low interrater = wide variability, high interrater = little variability
- Reliability grading:
o Need to know what the numbers mean based on the statistical test
o Cohen’s Kappa: (remove likelihood of chance effecting outcome)
 < 0.4 = POOR
 0.40-0.6 = FAIR
 0.6 – 0.75 = GOOD
 > 0.75 = excellent
o ICC Grading:
  < 0.50 = POOR
 0.5 – 0.75 = MODERATE
 > 0.75 = GOOD

- Independent variable = intervention

- Dependent variable = outcome measure

Levels of Measurement and Associated Measures of Central Tendency

o Nominal/Categorical = labels only (gender, true/false)

 Measure of central tendency = mode (most frequently occurring value)
o Ordinal = rank/order- no consistent intervals between numbers (1,2,3,4,5)
 Ex running a race- the difference between 1 st and 2nd place vs. 2nd and 3rd isn’t
consistent
 Measure of central tendency = mean, median
 Median vs. mean = median takes out the outliers
o Interval = rank order, consistent intervals between numbers, does not start from
absolute zero
 Measure of central tendency = mean, median
o Ratio = rank, order, consistent intervals between numbers, begins from absolute zero
 Measure of central tendency = mean, median

Types of studies:

- Meta-analysis vs. systematic review with a meta-analysis

o Systematic review: review of research articles
o With a meta-analysis: enough consistency/similarities between research designs – can
pool all the subject from all the studies and do one analysis
o Interpretation of meta-anaylsis charts
 Look at line of no effect: the diamond is the meta-anaylsis
 If diamond touches or crosses = no effect/ no difference between
intervention and control
o The farther away diamond is the more it favors intervention or
control group
 Look at CI = wider CI interval is, the less precise the data is
 Top left side of the char: details of the review/what is being measured

- RCT: experimental status in which an experimental tx. Compared to a control treatment

- Case control studies – Level III evidence
o Data collected at one point in time for certain condition
- Cohort study- group that may develop a condition and are followed over a period of time

- Probability: The P-value

o How well the sample data estimate the characteristics of a population/ determination if
observed treatment difference are likely real representations or due to chance
o Alpha level is set- typically at 5% (a priori)
 o If p < 0.05 = statistically significant, if p > 0.05 – statistically insignificant
o P-value is influenced by sample size
 Need authors to do a power analysis before the study- to prevent type errors
o What the p-value actually tells us
 If the null hypothesis is correct then these data are highly unlikely (statistical
significance is presumed)
- What we should do concerning hypothesis testing
o Never draw a conclusion solely on p-value
o Report confidence intervals and effect size (clinical significance)
- Hypothesis testing- correlations:
o 0- 0.19 = no correlation
o 0.20 – 0.39 = low correlation
o 0.40 – 0.59 = moderate correlation
o 0.60 – 0.79 = moderately high correlation
o > 0.80 = High correlation
- Make sure you look for additional measures of significance – confidence intervals + effect sizes
- Confidence Intervals:
o Provide the reliability of an estimate
o Tells us how accurately the Mean represents the population
o Typically expressed at 95% - probability the population falls within the 2 limits
o The narrower the better
o Even studies that have a low p-value (good) may have a wide CI (bad)- suggesting low
precision and wide variance in potential results
o If CI crosses zero (range includes positive and negative values) the results cannot be
considered statistically significant
- Effect size:
o Results may be statistically significant but that’s mean they are clinically significant
o To be clinically significant results must: show change that has value to the patient and
show a change of a magnitude that will be actual difference in patient’s function/life
o Allows greater precision in determining true magnitude of the interventions
 Useful when evaluating over/underpowered studies
o Independent of sample size
o Meta-analysis used frequently
o Outcome variable dictates whether effect size (+) or (-)
 ODI, NDI , NPRS = lower score = better outcome
o Independent of sample size
o Limitations: biased study design, data not normally distributed, SD are very wide
o Rating:
 TRIVIAL = 0-0.19 (LESS THAN 0.2)
 SMALL = 0.2 – 0.49 (LESS THAN 0.5)
 MODERATE = 0.5- 0.79 (LESS THAN 0.8)
 LARGE = 0.8 -2.0 (LESS THAN 2.0)
- Errors:
 o Type 1: falsely concluding statistical significance when there is actually no difference
 Null hypothesis is rejected - incorrectly
 As alpha level increases (0.08- 0.10) type 1 error increases
o Type 2: falsely concluding there is no statistical difference when there actually was one
 Typically due to small sample size
- Sensitivity:
o snNOUT -when a sign, test or symptom has a high Sensitivity a negative test result tends
to rule OUT the diagnosis
- Specificity
o spPIN- when a sign, test or symptom has a high specificity- a positive test result tends to
rule IN the diagnosis
- Likelihood Ratios (LR)
o Indicators of how much a test result will raise or lower the pre-test probability of the
target disorder (what will happen post-test)
o Best statistic for summarizing the usefulness in the diagnostic test
o Combination of sens/spec to assess the shift between pre-test and post-test
o Positive LR > 1.0
 Increased probability that the target disorder is present
 Higher the value – the higher the probability
 Interpretation:
 > 10 = Large shift in probability
 5-10 = Moderate shift in probability
 2-5 = small shift in probability, sometimes important
 1-2 small/rarely important shift in probability
o Negative LR < 1.0
 Decreases the probability that the target disorder is present
 The lower the value- the lower the probability
 Interpretation:
 < 0.1 = Large shift in probability
 0.1 – 0.2 = Moderate shift in probability
 0.2 – 0.5 = small shift in probability, sometimes important
 0.5- 1.0 = small/rarely important shift in probability
- Nomogram: easily converts pre-test to post-test probabilities
o Pre-test probability on the far-left column
o Draw a line through the likelihood column (middle) to the far right column
o Post-test probability on the far R column gives the est. of what the shift in probability is
- Number needed to treat:
o Number of patients you need to treat to prevent one additional bad outcome
 E.g. LBP CPR NNT for good outcome at 4 weeks is 1.9 so only 2 people would
need to be manipulated to avoid prolonged LBP at 4 weeks

CPR’s
 - To improve clinical decision making
- Diagnostic tests that have been found to be statistically meaningful predictors of a condition
- 3 types of CPRs
o Diagnostic, prognostic, interventional
- Not needed for every condition
- Used for conditions characterized by: diagnostic uncertainty, diagnostic heterogeneity, high
practice variability
- Quality and Validity:
o Level IV: derivation only (most)
o Level III: validated in a narrow population
o Level II: validated in a broad population
o Level I: implemented on large scale and affect quality and/or economy of care (RARE)

PATHOLOGY:

1. The Nervous System:

a. Once dead a nerve cell cannot be replaced
b. PNS can regenerate to a certain degree (1 mm /day)
c. Neuropraxia: local conduction block d/t segmental de-myelination
d. Axonotmesis: axonal injury involving Wallerian degeneration distal to injury site
 i. Axonal sprouting occurs
e. Neurotmesis: transection of the nerve (poor prognosis)
2. Differentiation brachial plexus injuries- begin distal to proximal

Example using ulnar nerve distribution- following up to C8-T1 level:

o Ulnar nerve at guyon’s canal – Yes
o Ulnar nerve at elbow (cubital tunnel)-
 Yes (possible weakness at FDP 4th and 5th and FCU)
 Sensory deficits of dorsal ulnar cutaneous, medial antebrachial cutaneous
o Medial cord? Yes- also median nerve issues- C8-T1 muscles
 Dorsal interossei, palmar interossei, ADD pollicis, lumbricals, opponens pollicis,
abd pol. brevis, abd digiti minimi, flexor digiti minimi brevis
 Not just ulnar nerve if plexus injury
 medial antebrachial cutaneous, dorsal ulnar cutaneous
o Lower trunk: Yes Medial cord + C8/T1 to radial nerve
o Root level: C8/T1: yes
 Sensory for c8/T1

INJURY TO NERVES:

- One of the most reliable indicators of brachial plexus injury is the integrity of the sensory n.
o Superior trunk: lateral antebrachial cutaneous nerve is the terminal sensory
 Antebrachial cut. Nerve - coming off the musculocutaneous nerve coming off
the lateral cord
 If lateral antebrachial Cutaneous intact that means lateral cord and superior
trunk are intact
o Inferior trunk:
 median nerve to D1 (thumb) & D2 (pointer finger) + medial antebrachial
cutaneous nerve are terminal sensory branches
 if sensory is intact- medial cord and inferior trunk is ok
- C5-7 ventral rami integrity: test serratus anterior (long thoracic nerve)
- C5 ventral rami integrity: test Rhomboids: dorsal scapular nerve

Pre-ganglionic lesions:

- Sensory is ok
- Motor impaired

Post-ganglionic

- Sensory impaired
- Motor compromised to the extent of the lesion

The radial nerve is the only nerve that gets input from c5- t1

Median gets input from C6-T1

- Differentiation sensory injury

 o Sensory nerve ROOT (dermatome)
 Symptoms typically proximal to distal/ transient
o Peripheral sensory problem
 Symptoms usually distal to proximal
 Double crush injuries will go both ways (11% in CTS)

- Tendonitis vs. Tendonosis:

o Tendonitis: inflammatory response to acute injury
o Tendonosis: chronic, degenerative changes to the collagen tissue
o No signs of inflammation
- Silbenagel research study regarding rehab model for rehab post-Achilles tendinopathy
o Acute: pain management- reduce cortical inhibition
o Intermediate: strengthening
o Return to sport/functional progressions

- Fibromyalgia vs. Myofascial pain syndrome

o Fibromyalgia:
 3rd most common rheumatoid disorder
 Chronic pain disorder/ unknown etiology
 Diagnostic criteria:
 Widespread aching in all 4 quadrants (left, right, above, below waist)
 Pain > 3 months
 At least 11/18 known tender points (4kg force)
o Examiner’s nailbed should blanch
o 9 points (bilateral)
1. occiput
2. lower cs paraspinals
3. mid portion trap
4. medial supraspin
5. sternal/claviculars
6. 2cm distal to lateral ei
7. upper outer quad of buttock
8.greater troch
9. medial fat pad prox joint line o the knee
 Axial and appendicular pain
 Median age of onset 29-37 years old
 Characterized by:
 Diffuse MSK aches and pains
 Stiffness
 General fatigue
 Disturbed sleep
 Absence of labs / radiographs indicating other rheumatologic disorders
 Other reported symptoms:
  Fatigue, bowel/bladder irritability, chest pains, Raynaud’s,
swelling/numbness of extremities
 Lack of stage 4 sleep
 Decreased serotonin production, increased production of Substance P (linked to
sadness, increased tension, memory disturbances)
 Interventions:
 Medications, exercise, never exceed pain limits
 Low loads and low reps, stretching, low impact with aerobic
conditioning
o Myofascial pain syndrome
 Regional pain patterns
 Trigger points (localized spot within a firm area of muscle)
 Elicits characteristic pattern of pain, tingling, or numbness in response
to a sustained pressure
 Active trigger point: causes ongoing persistent pain
 Latent: cause pain only upon palpation
 Diffuse pain confined to a specific region of the body
 Other findings:
 Sleep disorders, morning stiffness, fatigue
 Most prevalent between 30-60 years of age
 Evidence summary Dry needling:
 Safe, effective, efficient
 LTR may or may not be present- not required- however is an indication
of success based on neurophysiology
 Local and global effects (spinal and supraspinal effects)
o Active afferent A beta fibers that will synapse with interneurons
at dorsal horn which will impair pain fibers going up through the
dorsal horn into the brain

Medical Screening and Red Flags:

- Cancer as LBP:
o Ruling In: + LR (14.7 hx of & 3.0 failure to improve with 1 mo conservative tx.)
 Hx. of cancer, age > 50, weight loss, failure to improve with conservative tx.
 Combination of x-rays and ESR is 100% specific for identifying occult neoplasm
o Ruling Out: -LR 0.11
 NO relief with bedrest
- Bottom line: determination where the symptoms are coming from/ if they has MSK origin/
when to refer
- Levels of Access to PT
o Primary – direct access to PT
o Secondary- medical screening prior to PT examination (basic)
o Tertiary- medical screening and medical work-up (thorough evaluation)
 - “Odd” pain behaviors:
o Pain that is boring, deep aching
o Pain that is unrelated to activity
o Pain that is not relieved by any position and may be worsened by rest
o Pain that is worse at night
- Depression screening
o Sn 0.97 (- 0.05)
o Sp 0.67 (+ LR 2.9)
- GI screening:
o Does coughing/sneezing/ taking deep breath make pain worse
o Do activities such as bending, sitting, lifting, twisting, turning make it worse
o Has there been any change in bowel habits
o Does eating certain food make it worse
o Has your weight changed since your symptoms started
o Better for ruling In GI origin vs. ruling out
- Cognitive impairment screen
o Time orientation (month, day of month/week, year, season)
o Serial sevens (count backward from 100 by 7)- 93,86,79,72,77…
o Better for ruling OUT vs. in
 Sn 0.98, Sp 069

LUMBAR
Low back pain CPG overview:

- Summary of Recommendations:
o Risk factors: multifactorial, population specific – no definite cause
o Clinical course:
 High priority on interventions that prevent recurrence and transition from acute
to chronic LBP
 Movement retraining and motor control (re-training of deep multifidi)
o Differential Dx.
 Other serious medical patho, pt. not improving, psychol. conditions
o Examination: outcome measures
 Oswestry Disability Index
 Roland-Morris Disability questionnaire
 FABQ
o Examination: activity limitations and participation restriction measures
o Examination: physical impairment measures
 Lumbar Sagittal AROM
 Interrater reliability 0.88 and 0.42 for extension
 Segmental Mobility
 Poor to minimal agreement
  Intervertebral motion testing (hypo vs. hyper) mod- good agreement
 (k = 0.38- 0.48)
 Validity has been est. with correlation of radiographic segmental
instability and with response to tx.
 Pain provocation with segmental mobility
 Mod-good values for spring testing reliability + pain (k = 0.25-0.55)
 Judgement of centralization during movement testing: (K =0.7-0.9)
 Prone instability ests:
 Good to excellent agreement
 Independent test – limited diagnostic use ( + LR = 1.7, - LR = 0.4*) but
more useful in cluster of tests
 Judgement of presence of aberrant motions
 Good reliability (k =0.6)
 SLR: good reliability (0.68) for id. Pain in dermatomal distribution
 mod reliability for id. Patients with symptoms for angles < 45 deg (0.43)
 Slump test: (k = 0.83- 0.89)
o Trunk Muscle power and endurance testing:
 Trunk flexors (supine position with legs raised (before sacrum lifts off table) pt.
has to maintain contact to table with low back while lowering legs
 Trunk extensions: pt. in prone, extend LS approx. 30 degrees and hold position
(timed test)
 Lateral abdominals: pt, in s/l, hips in neutral, knees flex to 90 deg and timed
while holding a side plank
 Transverse abdominis: pt. in prone and instructed to draw in for 10 sec without
pelvic motion and pressure is obtained with biofeedback unit inflated to
70mmHg
 Hip Abductors: pt. hold lseg out to the side
 Hip extensors: pt. ins upine with knees flexed to 90 – pt. instructed tp bridge
and hold until position can no longer be maintained
o Interventions: manual therapy
 Thrust manip procedures in pt. with mobility deficits in acute LBP
 Non-thrust manip to improve spine and hip mobility in pt. with subacute and
chronic LBP
o Interventions: trunk coordination, strengthening, endurance exercises
 In subacute/chronic with movement coordination impairments and post-lumbar
microdiscectomy
o Interventions: centralization and directional preference exercises
 Repeated exercises in specific direction determined by treatment response in
pt. with LBP mobility deficits – reduce referred pain in LE
o Interventions: progressive endurance exercises and fitness activities
 Moderate to high intensity exercises in pt. with chronic LBP
 Incorporating progressive low intensity endurance activities for chronic LBP
o Interventions: patient education (mod evidence)
  Should NOT use strategies that either directly or indirectly increase the
perceived threat or fear associated with LBP/in depth pathoanatomical causes
 Do not promote extended bed rest
 SHOULD emphasize: understanding of anatomical strength of human spine,
neuroscience that explains pain perception, overall favorable prognosis for LBP,
use of active pain coping strategies, early resumption of normal activities,
importance of movement + activity levels and not just pain relief
o Interventions: flexion exercises and nerve mobilizations (Grade C)
 Typically for spinal stenosis
o Interventions: lower quarter nerve mobilizations (grade A)
 Use in pt. with subacute and chronic LBP and radiating pain
o Interventions: traction (grade D)
 Conflicting evidence
- Lower risk of subsequent medical services or pt. who receive PT early after an episode of acutre
LBP vs. at latera times
- Consistent Recommendations:
o Target: acute and chronic LBP
o NO early, routine imaging
o Stay active, return to activity ASAP
o Use of NSAID, cautious/no use of antidepressants
o Early entry into PT
 Pt. that received PT within first 6 weeks have better outcomes
 Delay changes subacute to chronic
 Cost-reduction, lower risk of subsequent medical services
o Non-pharmacological and non-invasive management
 (surgery only when failed conservative)
o Clinical pathways
o Education and advices
- Opioids for LBP
o Acute: pt. that received > 7days opioids 2x. more likely to remain work disables at 1 year
o Chronic LBP: opioids have greater short term analgesic efficacy vs. placebo
o Opioids vs NSAIDs
 6wks > 30% relief with NSAID
 Opioids and NSAIDs similar effects on patient function
o Common opioid side effects:
 Constipation, nausea, sedation, vomiting, dizziness, itching, dry mouth

Lumbar Radiology and Medical Screening:

- Imaging and LBP

o Primary utility for serious medical conditions or surgical planning
o Routine ordering should be discouraged – may lead to more hard
o Imaging only indicated for severe progressive neurological deficits
 “when a pt. urinates on their dropfoot time to refer out”
 - HNP- very common in asymptomatic population
- Red flag conditions:
o Fracture
 Dx. prediction rule for identifying spinal fracture
 Female, > 70 years, trauma, prolonged use of corticosteroids
o Major trauma in young pt. or minor trauma in older pt.
o 1 positive 88% SN, 50% SP
o 2 positive features 64% SN, 96% SP
 Smaller confidence interval
 Large likelihood ratio
 Therefore 2 or more features = get the imaging
o 3 positive features SN 38%, SP 100%
 Large confidence interval
 MRI without contrast
o Cancer
 Ruling in: hx. of cancer, age > 50, weight loss, failure to improve with
conservative tx.
 Ruling out: no relief with bed rest
o Cauda equina
 Bilateral leg symptoms, saddle anesthesia, bowel/bladder changes
 Dx. test properties for cauda equina sx.:
 Urinary retention (highest sn. And sp.)
 Unilateral or (B) sciatica > 80% sensitivity
 + SLR > 80% sensitivity
 Sensory deficits buttock/posterior superior thigh/ perineal region 75%
sensitivity
 MRI without contrast
-
o Back related infection
 Fever: spinal epidural abscess
 Non mechanical pain. Redness
 MRI with or without contrast
o Abdominal aneurysm
 Abdominal girth > 4cm
 Palpating abdominal aortic pulse
o Spinal malignancy

Lumbar TBC and Motor Control:

- No single system is comprehensive to account for changes in patient status during POC
- APTA advocates utilization of biopsychosocial model as basis for classification
1. Mechanical diagnosis (MDT) classification model (McKenzie)
2. Movement system impairment syndromes (Shrmann)
3. Mechanism-based classification system (O’Sullivan)
4. Treatment based classification system (Delitto)
- TBC is largely popular d/t EBC
- The approach keeps getting remodeled/evolved over time
- Varying degrees of consideration for psychological factors
o The APTA advocates a biopsyschosocial model
a. TBC- there is a double Triage approach
i. By first contact health care provider and rehab provider
ii. Assess therapy appropriateness
iii. Identify red/yellow/green/blue flags
iv. Medical risk profile
1. Patient history
2. Demographics/comorbidities
3. Chronicity
4. Symptom progression and response
v. Psychological risk profile
1. STarT Back screening tool
a. Stratified care delivered in a group setting demonstrated higher
outcomes in high-risk patients
b. Provides an early and effective model of chronic disease
management
2. Self-management candidate
a. Are symptoms low enough that they will follow 2-3 week
natural course
b. Is individual intelligent enough to comprehend and implement
instruction
b. Categorization
i. Mobilization
ii. Stabilization
iii. Specific exercise (flexion/extension/lateral shift)
iv. Traction
v. Active rest
5. Patients not just classified once but inserted into a care continuum and reassessed and
progressed/regressed as appropriate
6. TBC allows for inter/intra session variation based on SINSS and psychological status
7. TBC 3.0 Classifies based on a treatment approach vs. specific treatment
-
Treatment approach:

- Allows for inter/intra session variation based on SINSS and psych status
- Symptom Modulation category
o Recent pain (acute or recurrent)
o Irritable and inflamed
 Pain free ROM, cryotherapy, thrust jt. manip above (TS)
 PROM at a jt. with similar innervation
o Significant symptoms
o Avoid certain postures
o AROM limited/painful
o Hypersensitivity (central sensitization)
o Treatment: manual therapy, direction preference, traction, immobilization, TpDN,
modalities, education, meds, placebo

Evidence mechanical traction:

- No effectiveness of mechanical traction

McNab’s Disc Classifications:

1. Disc degeneration (nucleus pulposis contained by annulus)

2. Prolapse
3. Extrusion
4. Sequestration
Centralization vs. Directional Preference:

1. Centralization: change is symptom location to a more proximal/centralized location

2. Directional preference: reduction in pain intensity from repeated motion testing
3. Centralization should accompany a directional preference- but a directional preference will not
necessarily coincide with a change in symptom location

Repeated motion testing: how much is enough/too much

- Pt. with LBP and peripheral sx.

- Symptoms that probably will require more in-depth assessment
o Symptoms distal to the knee
o Neurologic symptoms

Common Neurologic symptoms:

1. Paresthesia
a. Non-reactive/ sensation perceived without cutaneous stimulation
b. Sensation of purely subjective nature
c. Equates to neurologic deficit
2. Hyperesthesia
a. Increased cutaneous sensitivity
3. Hyperalgesia
a. Increased sensitivity to pain stimulus
4. Hyperpathia
a. Increased threshold to pain stimulus but increased reaction once perceived
5. Allodynia
a. All stimuli perceived as pain
6. Hypoalgesia
a. Reduced pain sensitivity
7. Dysesthesia
a. Stimuli misperceived as a different sensation

Pain only

- Pain in limbs without accompanying neurologic symptoms would rarely be neuropathic pain
- Nerve fibers are too small in diameter to be the sole axons injured
o We can’t get compression and just hit a nocioceptive axon
o When pt. has pain only- not neurogenic/ pain is being referred from other structures

Neural tension and treating LBP

- Nerve related LBP is a risk factor for chronicity

- Mobs in slump position and SLR mobs (significant effects on pain and disability)
- Slider- best outcomes
o More nerve excursion with sliders
- What should you be looking for outcome wise
 o Most prevalent with directional preference
 Pain intensity change and increased spinal ROM
o Spinal control improvements with directional preference and centralization
 Improvement in aberrant LS motions
 Improvement and SLF
o Improvement in current most distal pain, fingertip to floor distance
- Slumb and SLR nerve glides positive impact on pain and disability

Manual therapy:

- CPR for HVLA

o Pain < 16 days
o No sx. Distal to the knee
o FABQ (work) < 19
o PROM hip IR > 35 deg
o + lumbar spring test (hypomobile + pain)
o Post-test probability for success:
 > 4/5 present 95% ( LR 24)
 3/5 present 68% (+ LR 2.6)
 < 3/5 present = < 7% chance of success
o 2 predictors present
 Symptoms < 16 days, no sx. Distal to the knee
 Chance of success 88%
o SIJ and lumbar thrust techniques superior to grade 4 mobs
- Short term effects MET

Movement Control Category

- Low/moderate pain/ disability affecting ADLs

- Pain stable (low baseline, increased with certain activities, returns to baseline once activity
stopped)
- AROM often full, sometimes with aberrant movements
- Exam: impaired flexibility, muscle activation, motor control
- Neurodynamic deficits
- Treatment:
o Improve movement quality: mob, manip, motor control, flexibility, balance
Treatment prioritization:

- Neural sensitivity
o Neural sliders (SLR or slump position)
- Joint and soft tissue mobility
o MET, contract-relax, stretching
- Motor control
o Subset of movement control
- Endurance
o Bridge between movement control and functional optimization

Functional optimization category:

 Relatively asymptomatic
 ADL’s ok, need to get to a higher level
 Well controlled symptoms until movement system fatigue
o Impaired movement system endurance, strength, power
o Unable to meet demands placed on system
o Many BA in pipeline secondary to acclimatization/overuse
 Treatment
o Maximize performance within context of job/sport

Findings and treatments based on tissue type:

1. Nerve
a. Findings: positive sensitized neural tension tests (SLR, slump, femoral nerve)
b. Treatment: neural mobilizations
i. If symptoms are aggravated re-classify pt. into symptom modulation approach
 2. Joint
a. Findings: limitation, asymmetry, or hypomobility in the lumbar or adjacent regions
b. Treatment: manipulations/mobilization
3. Soft tissue
a. Findings: impaired soft tissue compliance by manual pressure or passive change in joint
position
b. Treatment: passive stretching and soft tissue mobilization

Global stability influences on pathology: in regard to Motor Control/Movement Control

1. Activation
a. Findings: poor ability to activate individual muscles or isolated movement patterns
i. (ex. Transverse abdominis, multifidi, scap retractors)
b. Treatment: training to activate hypoactive muscles or isolated movement patterns
(abdominal hollowing, scapular retractions, breathing)
i. Drawing in for TrA, lift off test for deep multifidi (one arm elev to 20 deg – lift off
and palp the opposite side)
ii. Learn to activate
iii. Verbal and manual cuing
2. Acquisition
a. Findings: impaired ability to dissociate or coordinate thoracolumbar and
lumbopelvic/hip movements (active SLR, active hip ext/ABD)
b. Exercise: Gravity reduced, one plane of motion
c. Treatment: training to acquire the skill of dissociating or coordinating movements of the
lumbar spine and adjacent regions (single plane co-contraction, balance ex.)
i. Verbal and manual cuing some but not as much as activation
ii. Want to see dissociation
3. Assimilation
a. Findings: impaired control of multiplanar movements under dynamic loading conditions
(poor squat, poor lunge performance, poor rotational movement)
b. Treatment: training to assimilate loaded multi-planar movements into ADL’s (step up
progression, sit to stand progression)
i. Gravity is full and moving in multiple planes of movement
LOCAL MOBILITY EXAMINATION:

 Sitting:
o Slump test with head and foot variations
o Thoracic rotation
 Standing
o Observe curvature, LE alignment
o Pelvic static asymmetry
o Lat dorsi tightness (full shoulder flexion)
 Side lying
o Ober’s test
 Supine
o Leg length discrepancy
o Hip IR/ER ROM
o SLR and popliteal angle (measurement of hamstring tightness with hip in 90 deg flex)
o Thomas test
 Prone
o Femoral nerve tension
o P-A spring test
o Passive leg extension
 o Hand-heel rock

GLOBAL STABILITY EXAMINATION:

 Sitting
o Active knee extension
o Sit to stand test
 Standing
o Supine ROM (spinal hinges, aberrant motion, excessive lumbar flexion, angulation)
o Thoacolumbar dissociation
o Lumbopelvic dissociation
o Trendelenburg test
o Step up-down test
o squat
 Side lying
o Clam shell test
o Active hip abduction
o Endurance side bridging
 Supine
o Active straight leg raise test
o Active hip external rotation
o Supine to sit test
 Prone
o Active hip extension
o Active hip rotation
o Bird dog (arm and legs)
o Prone instability test

GLOBAL STABILITY/ MOTOR CONTROL IN THE TBC:

1. Activation: observation of poor ability to activate individual muscle or isolated movement

patterns
a. Simple exercises/require patient concentration
b. Patients should be award of the relationship between pain and spine movement
c. Exercises for local and global musculature
d. Exercises go beyond lumbar spine ( hip abd/shoulder retractors)
2. Acquisition: observation of impaired ability to dissociate or coordinate thoracolumbar or
lumbopelvic/hip movement
a. Learning of skills remains important
b. Less concerned with TrA and ML
c. More focused on movement coordination and dissociation
d. Geared toward stability while sparing the joints
3. Assimilation: observation of impaired control of multiplanar movement under dynamic loading
conditions
 a. Require much less concentration
b. Translation of symptom provoking activities into clinical exercises
c. Introduction of endurance training

COMMON REHAB APPROACHES of MOTOR CONTROL

1. McGill
a. stage 1 correct motor patterns
i. Teach to distinguish abdominal bracing from hollowing and hip motions from
lumbar motions
ii. Teach to activate glut med and max
b. Stage 2: establish stability through exercises and education
i. Build stability while sparing the joints
ii. Ensure sufficient stability for the task and transfer patterns to ADLs
c. Stage 3: increase endurance
i. Address activity specific endurance
ii. Address basic endurance training to ensure the capacity needed for stab.
iii. Build base for performance training
2. Hodges:
a. Stage 1: Cognitive phase
i. Cognitively perform the skilled activation of the TrA and/or multifidus
ii. Quiet breathing/relaxation techniques
iii. Neutral position of the spine
b. Stage 2: Associative phase:
i. Focus moves from simple elements of task performance to consistency or
performance, success, and refinement
ii. Encourage and repeat coactivation of deep muscles
iii. Coordinate coactivation of deep muscles with breathing
iv. Progress to light dynamic tasks
c. Stage 3: autonomous phase
i. Task becomes habitual/automatic
ii. Rhythmic stabilization techniques
iii. Pilates exercises/SB exercises/unstable surfaces
iv. Functional re-education
3. O’Sullivan:
a. Stage 1: cognitive stage
i. Train isometric contraction of the TrA
ii. Train diaphragmatic breathing
iii. Train neutral lordosis by drawing in of TrA and facilitation of multifidus
b. Stage 2: associative stage
i. Identify 2 or 3 pain provocative movements and break them down into smaller
components with high reps
ii. Initially tasks are performed in neutral positions, but later normal movement is
encouraged
c. Stage 3: autonomous stage
 i. Specific exercise intervention in which the patient is encouraged to perform
dynamic activities while automatically maintaining spine stability
4. Sahrmann
a. Emphasis on the dissociation between upper/lower extremities and lumbopelvic
movement
b. Neutral spine through extremity movement

LUMBAR PATHOLOGIES:

LUMBAR SPINAL STENOSIS:

- Narrowing of the lumbar spinal canal, nerve root canals and/or IV foramina that may encroach
on the nerve roots of the LS
o Lateral stenosis: nerve root canal and/or IV foramina
o Central stenosis: spinal canal (cauda equina encroached upon)
- Common impairments
o Diminished AROM
o Decreased SB bilaterally, decreased extension
o Poor ambulation tolerance
 Frequent sitting breaks to decrease leg pain and weakness
o Decreased sensation, strength one or both LE’s
o Decreased hip ROM- especially extension
o Weakness of hip musculature- esp. glut max and medius
- Neurogenic claudication
o Compressed nerves in the lower spine
o Causes pain or camping in the legs with prolonged standing/walking
o Typically bilateral at buttock and thighs and spreads distally to feet
o Parasthesias and weakness can occur
o Walking flexed forward relieves pressure
o Worse with walking downhill, between walking uphill or sitting down
- Intermittent claudication
o Main symptoms of peripheral vascular disease
o Tight, aching, or squeezing pain in the foot, calf, thigh, or buttock with exercise
o Pain typically occurs after same amount of exercise, gets worse until the same amount
of exercise, gets worse until exercise becomes impossible, and relieved by rest
o As condition progresses, leg pain at rest can occur (rest pain or rest claudication)
o Caused by narrowing/blocked blood vessels in legs
o Worse with walking uphill, better when standing still
o Diagnosed by constant load test, graded exercise/TM test
o Interventions:
 Exercises
  Smoking cessation
 Pharmacologic therapy
 Medical management of diabetes, hypertension, hyperlipidemia
 Surgical intervention such as angioplasty and bypass surgery
o AHA guidelines for management of pt. with PAD
 Supervised TM walking at intensity that elicits claudication sx. Within 3-5 min (a
score of 1 on claud. Pain rating scale
 Waling until the claud. Pain is rated moderate (score of 2 claud. Pain rating
scale) following by standing or sitting rest to permit sx. To resolve
 Repeating these exercises and rest cycles for 35 min. of intermit walking
 Increasing the exercise program by 5 min per session to 50 min, 3-5 times per
week for a minimum of 12 weeks (6 monts)
 Claudication pain rating scale:
 Minimal discomfort
 Moderate pain (patient can be distracted)
 Intense pain
 Unbearable pain
o PAD: Screening:
 ABI: Ankle Brachial index
 3x BP at rest (ankle, arm)
 5 min TM walking
 Repeat 3 x BP measures
 ABI = mean 3 systolic LE (avg) /mean 3 systolic UE (avg)
 Normal resting ABI = 1-1.1 (BP at ankle = BP at arm)
 Resting ABI < 1 abnormal
 Decreased ABI after walking – PAD is probably present
 ABI Less than 0.95 = significant narrowing or one or more blood vessels in LE
 ABI less than 0.8 – pain in the foot, leg, or buttock may occur during exercise
(int. claudication)
 ABI < 0.4 = symptoms may occur at rest
 ABI 0.25 or below- severe limb-threatening PAD

Exercise and LBP:

- Functional optimization:
o Impaired movement system endurance, strength, power
o Unable to meet demands placed on system
o Maximize performance within context of job/sport
- Want to treat with specific stabilization exercises
o Cardiovascular exercise alone may not be effective
- Risks of NOT treating with Specific Stabilization Exercise (SSE)
o At 1 year f/u recurrence rates were 84% for control group vs. 30% for SSE
o At 2-3 year f/u recurrence rates were 75% recurrence for control group vs. 35% SSE
 - Lumbar stabilization CPR:
o Pt. that will respond to stabilization exercise program (supervised PT for 8 weeks + HEP)
o Best predictive indicators- presence of aberrant movements in addition to positive
prone instability test
 Positive PITS test- pt. on the table in prone
 CPA to segments- see if it reproduces pain
 Next have pt. move feet off the table and knees are slightly flexed- hold
PA while pt. raises feet off the floor- if pain diminishes c lift off of legs-
activation with multifidi then + test
 Look more aggressively at motor control
o In 2014 failed validation as a CPR
o The more clinical predictors present the lower the LS multifidus activation
- Positive correlation between activation of TrA and lumbar multifidi for success with stabilization
- Deep abdominal strengthening:
o Best recruitment of TrA and internal oblique
 Horizontal side support (side plank), abdominal crunch
o Best recruitment of TrA
 Drawing in maneuver
 Bird dog (quadpd UE / LE lift)

Lumbar SIJ:
- Dx. and Tx of Painful SIJ
o 13% people with persistent LBP have SIJ pain
o Need to differentiate between SIJ dysfx. And pain arising from SIJ
- 4 deg of rotation, up to 1.6 mm translation of SIJ
- Palpating dysfunction- reliability poor
- Cluster tests: pain production tests
o SIJ pain provocation tests have acceptable levels of reliability d/t their standardization
o Laslett:
 Distraction, compression, thigh thrust, sacral thrust, Gaenslen’s
 At lest 3 positive tests: + LR 4.16, post-test 59% (small)
 < 3 positive tests : - LR 0.12, post- test prob 4% (mod)
o Van der Wurff:
 Distraction, compression, thigh thrust Gaenslen’s, FABER (patrick’s test)
o If no centralization phenomena with mckenzies repeated motion testing
 3/5 tests = + LR +7
 < 3/5 present – LR 0.10

Pregnancy and LBP

- Affects 45% of pregnant women

- Hormone relaxin is proposed underlying mechanism
o Ligament laxity- softens connective tissues
 - Low quality evidence that exercise may reduce
- Single studies – acupuncture (low evidence), craniosacral therapy, osteomanip. Therapy,
manual therapy + exercise + education)
- Most evidence suggests multi-modal approach is best
- Risk factors: poor prognosis:
o Min/no weight loss after delivery
o LBP prior to pregnancy
o Several (+) special tests
o Long term PGP
o Onset of pain early d/t pregnancy
o Prolonged labor
o Difficulty performing ASLR
o Complete PGP (bilateral SIJ, pubic symphysis)
- Recommendations:
o Exercise and education
o Massage
o Support garment if pain during ADL’s

Lumbar Surgery:
“TRIAD of DOOM”

- PCP orders advanced imaging that isn’t indicated & pathoanatomic findings observed
o Clinical correlation of imaging findings does not occur
- PCP refers to pain management – series of epidural steroid injections performed
o No improvement
- Pain management refers to spine surgeon
o Surgery or refer back to PCP

5 Most Common Serious Pathologies:

1. Cancer (PMH prostate, thyroid, breast, lung, kidney- “PT Barnum Loves Kids”_
2. Cauda Equina
3. Infection
4. Inflammatory arthritis
5. Vertebral fracture

Surgical Interventions:

- Laminectomy
o Commonly d/t stenosis
o Surgical vs. non-op treatment: no significant difference
 Research done by MD’s, may have bias
  Intention to treat analysis: when I have a pt. drop out the group or swap groups-
if they drop out the last data point will be carried forward or will stay with the
old group
 HALMARK of well-Designed research
o Treatment effects in favor of sx. Effect seen at 6 weeks with max at 12 months
- Discectomy/microdiscectomy
o Primarily performed d/t LE nerve symptoms
o Min evidence suggesting rehab 4-6 weeks post-op to improve function
o Microdiscectomy similar outcomes vs. open
- Spinal fusion
o No subset of pt. with chronic LBP could be i.d. for whom spinal fusion is an effective tx.
o Rehab reduces disability and fear avoidance in short and long term following fusion
o Decompression surgery + fusion surgery No better outcomes vs decompression alone
o Initiate strengthening exercises early on post-op

Cervical:
Medical Screening

CPG

- Outcome measures: NDI, patient specific fx. scale

- Risk factors: female gender, PMH of neck pain (most)
o Old age, jobs demands, smoking
- Prevalence
- Diff. dx.: direct pathoanatomical cause rarely identifiable
o Clinicians should screen for more serious medical conditions to refer out for medical
management or imaging

Triage Screening:

- Was it traumatic?
o Fracture?- Canadian C-Spine rule
- Neuro screening
o Reflexes, myotomes, dermatomes, Babinski/clonus/hoffman’s, DTR, Romberg, cranial
nerves
- Ligamentous testing
o Alar, sharp purser, transverse ligament
- VBI
o System approach (assess CV risk factors)
o Vital signs
 Pulse, RR, BP
o Pre-positional testing
Doppler or auscultation
Canadian C-spine Rules:

About finding patients that Do NOT need imaging

- SN 0.99, - LR 0.01
- Not applicable for age ,16, paralysis, unstable vitals, previous CS surgery, known vertebral
disease, GCS < 15, non-trauma
- High Risk factors: if any need imaging right away
o Age > 65
o Dangerous MOI
 High speed car accident, fall from > 5 steps/ > 1 meter, bicycle collision, axial
load to the head, ejected from car in MVA
o Parasthesias in the UE
- Low risk factors (safe assessment of ROM)
o Simple MVA, sitting in ED, ambulatory since injury, delayed onset of neck pain, absence
of midline C-spine tenderness
o Need all low risk factors before proceeding to ROM
- Able to actively rotate 45 degrees bilaterally
o Able - no radiography

NEXUS RULE:

- Indications for CS radiography following blunt trama

o Neck pain and midline cervical tenderness
o Altered mental status
o Intoxication
o Focal neurological deficits or complaints
o Distracting pain injury
- Wider confidence intervals vs. Canadian C-Spine rules and dec sensitivity

Prognostic Tools

- High pain intensity

o Numeric rating scale (0-10): consider score 6 or greater useful cut score for prognosis
- High self-reported disability
o NDI- scores > 30 useful prognosis factors
- High pain catastrophizing
o Pain catastrophizing scale – score of 20 or greater
- High acute posttraumatic stress symptoms
o Impact of events scalre-revised: score off 33 or greater
- Cold hyperalgesia
o The TSA- neurosensory analyzer (equipment impractical in clinical utility)
o Use of ice cube or cold metal bar
Diagnosis- ICF

- Neck pain with mobility deficits

o Common symptoms
 Central and/or unilateral neck pain
 Limitation in neck motion that reproduces sx.
 Associated (referred) shoulder girdle or UE pain may be present
o Exam findings:
 Neck pain reproduced at end ranges of AROM and PROM
 Capsular restrictions (pain at end range motion)
 Restricted CS and TS segmental mobility
 Intersegmental moblity testing reveals restriction
 Deficits in cervicoscapulothoracic motor control
o Interventions:

ACUTE

 Mod evidence for TS manip, neck ROM, scapulothoracic and UE strengthening

 Min evidence for CS manip/mobs

SUBACUTE

 Mod evidence for neck and shoulder girdle endurance

 Min evidence for TS manip and CS manip and mobilization

CHRONIC

 Multimodal approach: TS manip, cervical manip/mobilization, cervical and

scapulothoracic exercise, stretching, strengthening, endurance training
 Dry needling, laser, intermittent traction
- Neck pain with movement coordination impairments
Including WAD
o Common Symptoms:
 MOI linked to trauma/whiplash
 Assoc. referred shoulder girdle or UE pain
 Associated varied nonspecific concussive s/s
 HA, concentration difficulties
o Examination findings
 Neck pain with mid-rage motion that worsens with end-range positions
 Think muscular
 Positive neck flexor muscle endurance test
 Strength and endurance deficits of the neck muscles
 Point tenderness may include trigger points
 Potential neck and referral pain
o Interventions:
 Education
 Return to normal, nonprovocative pre-accident activities ASAP
  Minimize use of cervical collar
 Perform postural and mobility exercises to decrease pain and increase
ROM
 Reassurance to pt. the recovery is expected to occur within 2-3 months
 Multi-modal intervention approach
 Manual mobilization techniques + exercises
 Chronic: mobilization//education/cervicogenic strengthening
- Neck pain with HA
o Common symptoms:
 HA is precipitate or aggravated by neck movements or sustained
positions/postures
 Noncontinuous, unilateral neck pain and associated HA
o Expected exam findings:
 Positive cervical flexion-rotation test
 HA reproduced with provocation of the involved upper cervical segments
 Limited cervical ROM
 Restricted upper cervical segmental mobility
 Strength, endurance, and coordination deficits
o Interventions:
 Acute: exercise (mobility), C1-2self snag
 Sub-acute: cervical mobs/manips, C1-2 snag
 Chronic: CS manip/mobs + shoulder girdle exercises + neck
stretching/strengthening and endurance exercises
o Neural convergence: trigeminocervical nucleus (innervation of cervicogenic HA)
 Nociceptive nucleus of the upper neck, face, head, throat
 Convergence of information from trigeminal and upper cervical nerves (C1-3)
 Therefore, get a misinterpretation of information
 May also have CN 7,910 involved

Headache Types: Differential Diagnosis:

MIGRAINE Cervicogenic HA Tension-Type Occip Neuralgia

Myofascial Trigger
point referral
Duration 4-72 hours 4-72 hours 30min- 7 days
Location unilateral Unilateral bilateral C2 distribution
+/- sideshift
Aggravated Routine physical Neck movements Activation of MrTps, Activation of
activity (only neck motions) muscles at
entrapment sites
Relived when taking Obliq capit &
stress off neck semispinalis
Into/out of
Start posteriorly and semispinalis
work way anteriorly Into/out of trap
Occip artery
Other Sx. At least 1: nausea, No No more than 1
vomit, photo/phonophobia
photophobia

- Neck pain with radiating sx.

o Common symptoms
 Neck pain with radiating (narrow of lancinating) pain in the involved extremity
 UE dermatomal paresthesia or numbness and myotomal muscle weakness
 Significant motor unit/axonal loss before having true weakness in a
myotomal pattern d/t muscles being innervated by > 1 nerve root
o Expected exam findings
 Neck pain reproduced or relieved with radiculopathy testing
 Test cluster:
 Upper limb nerve mobility (ULTT A- median nerve bias)
 Spurling’s test (quadrant with overpressure)
 Cervical distraction
 Cervical ROM (involved side cervical rot. < 60 deg)
 3/4 met, + LR 6.1 - 65% post-test prob
 4/4 me, + LR 30 - 90% post-test prob
 May have UE sensory, strength, reflex deficits
o Interventions
 Acute: mobilizing and stabilizing exercises, laser, and short term use of cx. Collar
 Chronic: intermittent mechanical traction, stretching and strengthening
exercises + CS and TS mobilization/manip
- Need to differentiate referred symptoms
o Radiculopathy
o Myelopathy
o Thoracic outlet syndrome
- Research: treatment of pt. with DDD CS Radic using multimodal conservative approach
- Clustered clinical findings for dx. of cs myelopathy (good for ruling in)
o Gait deviation
o Hoffman’s test
o Inverted supinator sign
o Babinski sign
o Age > 45
o Post-test probability = 43%, - LR 0.18 for < 1 finding
o Post-test probability = 94%, + LR 3 for > 3 findings

- Neurodynamic techniques
o Increased nerve excursion with sliding techniques vs. tensioning
 Nerve slides relative to surrounding structures
 Longitudinal excursion of nerve
 facilitates excursion of intraneural edema
  Reduces symptoms
o Increased strain/pain with tensioning techniques
 Increase in nerve pressure
 Reduces intraneural blood flow
 Exacerbates symptoms
o Use SINSS to dose
 Severity- Pain scale
 Irritability
 Nature- MOI
 Stage- acute, subacute, chronic
 stability
o Median nerve- primary motion at the elbow vs. wrist so what to move at the elbow and
at the neck to slide the nerve
 The only diagnostic test is ULTT A – median nerve
- Thoracic Outlet Syndrome
o Neurogenic 95%, venous 3-5%, arterial 1-2%
o No good standardized treatment
o Neurogenic symptoms:
 Pain/numbness arms, hands, fingers on affected side
 Typically trauma or vigorous repetitive activity
 Typically dealing with an inferior cord/medial trunk issue- C8-T1
o Venous symptoms
 Compression of axilosubclavian vein- results in thrombosis
 Acute: red-purple discoloration of a swollen extremity
o Arterial symptoms- high correlation to cervical rib
 Continuous friction of subclavian artery
 Acute: limb threatening, subacute: ischemia in hands, chronic: claudication c
pain in UE and hands

Classification System for Patients with Neck pain:

- Neck pain flow to treatment based classification

o Do they have Wiplash, Is it acute < 30 days, pain rating > 7 or NDI > 52 = Pain control
o S/s of nerve root compression present OR sx. distal to elbow = centralization
o Is chief c/o HA or neck pain, is A affected by neck movement = non cervicogenic HA
o If YES to HA affected by neck movement and dx. of sx. Or migraines = HA
o If chief c/o sx. < 30 days and pt. age < 60 = mobility
o If chief c/o sx. > 30 days and pt. age > 60 = exercise and conditioning

Medical Screening at the Cervical Spine

- History
o Sx. In the legs or low back with neck movements
o (B) UE sx. Or occasional loss of balance or occasional LOB or lack of coordination
 o Behavior of sx:
 Worse in the am
 Associated with poor posture
 Worse with movement
 Better with movement
o Special questions for cervical thoracic pain
 HA, dizziness/vertigo, visual problems, black outs, swallowing, hoarseness
 Hx. of osteoporosis, anticoagulant therapy
 Cord signs:
 Balance deficits
 Extremity
 Weakness
 Bilateral
 Paresthesia’s
- IFOMPT Guidelines – what to do before putting hands on pt. with neck pain
o Thorough pt. history
o CN screen
o Upper quarter screen
o AROM and PROM with overpressure
o Ligamentous testing
o Mobility testing
- Risk factors for cervical arterial dysfunction
o Past trauma to CS or vessels
o Hx. or migraines
o Hypertension, hyperlipidemia, cardiac or vascular disease, blood clotting
o Diabetes
o Long term use of steroids
o Hx. of smoking
o Recent infection
o Immediately post-partum
o Previous CVA or TIA
o Anticoagulant therapy
- Upper cervical instability risk factors:
o History of trauma
o Throat infection
o Congenital collagenous compromise
o Inflammatory arthritides (RA, ankylosing spondylitits)
o Recent neck/head/dental surgery
- Internal Carotid Artery Disease
o Early presentation
 Mid-upper CS pain
 Pain around ear and jaw
 Head pain (Fronto-temporo-arietal)
  Worsening symptoms
 Ptosis: lower cranial nerve dysfunction (9-12)
 Acute onset of pain described “unlike any other”
o Latera presentation
 Transient retinal dysfunction
 Transient ischemic attack
 CVA
- Vertebrobasilar Artery Disease
o Early presentation
 Mid-upper cervical pain, occipital HA
 Acute onset of pain “unlike any other”
o Late presentation
 Hindbrain TIA (5D’s, 3’A, 3 N)
 Vagueness, hypotonia/limb weakness
 Anhidrosis (lack of sweating)
 Cranial nerve dysfunction
 Hindbrain stroke
3 A’s: Ataxia, Anxiety, Anxiousness
5 D’s: Diplopia, Dizziness, Drop attacks, Dysarthria, Dysphagia
3 N’s: Nausea, Numbness, Nystagmus
- Upper Cervical Instability
o Early presentation
 Neck and head pain
 Feeling of instability
 Cervical muscle hyperactivity
 Constant support needed for head
 Worsening symptoms
o Late presentation
 Bilateral foot and hand dysphasia
 Feeling of lump in throat
 Metallic taste in mouth (CN 7)
 Arm and leg weakness
- Contraindications to OMT interventions
o Multi-level nerve root pathology
o Worsening neurological function
o Unremitting, severe, non-mechanical pain
o Unremitting night pain
o Relevant/recent trauma
o Upper motor neuron lesions
o Spinal cord damage
- Precautions for OMT interventions
o Local infection, inflammatory disease
o Active cancer, hx. of cancer
o Long-term steroid use
 o Osteoporosis
o Systemically unwell
o Hypermobility syndromes
o Connective tissue disease
o A first sudden episode before age 18 or after age 55
o Cervical anomalies
o Throat infections in children
o Recent manipulation by another health care provider
- Stroke Risk
o High Risk ≥3
o Caution 4-6
o Low Risk 6-8

- Stroke FAST risk

Risk Factor and Manual therapy decision Making:

Planning and performing the Physcial exam

- Patient history
o Any gaps in formation, is the quality of information sufficient
- Are there any contraindications or precautions to OMT
- What physical tests need to be included in the physical exam
- Do any tests need to be adapted for the patient
- Blood pressure
- Neurological exam
- Active cervical screem
- Passive ligamentous testing
- Positional testing

Symptom referral

Cloward’s points

- C4-7 can refer down to the peri-scapular region

** Clinical practice guidelines: stronger evidence for TS manipulations for neck pain first before
manipulating/mobilizing the cervical spine

UPPER EXTREMITY: Shoulder

Scapular kinematics:

Transverse plane: internal rotation and external rotatation

Frontal plane: downward, upward rotation

Sagittal plane; post/anterior tilting

Scapular dyskinesis:

- Most common motion lacking is posterior tilting

- Can also have a lack of external rotation- impair the shoulder d/t putting the ER muscles in an
inefficient positions
- Thirdly have a limitation of upward rotation
- Looking at Diagnosis and tester reliability:
o Intra-rater reliability mod-excellent in determining scap. Dyskinesis
o Resting- better levels of reliability vs. non-resting
- Diagnosis methods- 3 basic elements to assess scapular dysfunction
o Visual observation of scapular dyskinesis
 Look at pt. from posterior view
 Anterior tilt
 Inferomedial scapular border will be more prominent
 Labral involvement (overhead athletes)
 Internal rotation
 Prominence of medial scapular border seen
 Labral involvement
 Downward rotation
  Increased prominence of superomedial border
 Impingement/RC disease
o Effect of manual correction on symptoms
 Scapular retraction test
 Retract and depress scapular
 Provide posterior tilt on scapula (momma cat grip) does that improve
strength
 Scapular assistance/reposition test
 Assist with upward rotation and pt. moves into ROM
o Does it improve ROM and strength
 Evaluation of surrounding structures
o Do you have hypomobility to ribs or thoracic spine
- Want to assess static position first and then assess scapular changes with shoulder AROM
o Assess with overpressure
o Can also assess with MMT
- If you can improve pain, strength, motion with manual correction- tells that scapula is primary
contributor
- Article: rehab of shoulder impingement syndrome and RTC injuries
o Overhead athletes have > ER and < IR (GIRD)
 Proposed causes: tightness of post- capsule and stiffness of post-cuff
 Humeral retroversion
 GIRD significant because
 Correlates to anterior humeral head translation
 Increased anterior humeral head shear forces
 > superior humeral head migration during elevation
 At functional 90/90 position
 Humeral head moves anterosuperior direction
 With excessive tightness, shifts posterosuperior direction
- Scapular stabilization
o Altered activity of scap mm present in patients with impingement
o Decreased strength, activity, timing of serratus anterior, lower/mid traps
o Increased timing activity or UT
o Motor control
 Activation, acquisition, assimilation - leading to
- Scapular dyskinesia rehab progression
o Scapular orientation (activation)
 Can the pt. actively retract and depress their scapula and hold
 Need to be able to activate before they can do anything else
o Scapular co-contraction
 Scapular setting exercises (begin in neutral)
 Teach post-tilt and upward rotation
 Greater activation of mid and low trap
  Inferior glide (scap set and push down with hand- arm rested on table in 90 deg
of ABD position)
 low row
 lawn mower (add hip and trunk motion)
 Robbery (bilateral motion- start in mini squat and perform row as going into
trunk extension)

 Kinetic chain variations

 Pushup variation kinetic
 Extend c/l hip to increase LT activating
 Low row- one leg stance on s/l improved LT/UT ration
o General strengthening
 3x15-20 reps create a fatigue response
 4-week training resulted in 8-10% increased isokinetic strength of IR/ER
- Want to perform scapular rehab prior to RTC focus
- RC must move on a stable scapula
o Low row, Scapular clocks, wall washes, punches
- Muscle activation
o CKC before OKC
o When in OKC- start with vertical patterns before diagonal patterns
 Vertical patterns have a shorter level arm vs. diagonal pattern
o CKC and OKC with mirror
o Prone scapular retractors and post cuff exercises
o Seated push ups
o Low row and good SA activation
- General strengthening- which activates the muscles the best
o Promote LT/MT activity with min UT activation
 Sidelying ER
 Side lying forward flexion
 Prone horiz ABD with ER
 Prone Ext
o Promote serratus anterior
 Diagonal exercise with combo of shoulder flex. Horiz flexion and ER
 Shoulder ABD in the plane of the scapular 120 deg
o Upper trap: shrug
o Mid trap: prone arm raise overhead, prone shoulder horiz ext with ER
o Low trap: prone arm raise overhead, prone shoulder ER at 90 ABD

Mechanics of AC/SC Joints

- SC joint osteokinematics:
o Fontal plane: elevation and depression
o Sagittal plane: post rotation
o Transverse plane: retraction/protraction
 - AC joint:
- Types of sprains: Rockwood’s 6 types
Type I-II (surgical management)
o Type I: AC ligament sprain but AC joint is intact
o Type II: AC ligament tear, coracoclavicular ligament tear , AC joint subluxed
o Type III: AC/Coracoclav. Ligament torn- 100% dislocation of joint
 Grey area for first nop-op but then may need surgical intervention
o Type IV: complete dislocation with post. Displacement of distal clavicle into or through
trapezius muscle (surgical)
o Type V: exaggerated superior dislocation fo the joint 100-300%, increased coracoclav.
Ligament distance 2-3x, disruptions of deltotrapezial triangle (surgical)
o Type VI: complete dislocation with inferior displacement of distal clavicle subacromial or
sub coracoid position (surgical)
- 7% of AC joint injuries have concomitant clavicle fx.
o Need bilateral view, weighted and unweighted for comparison to rule in clavicular fx.
- Mobilizing the AC joint and positive mechanical changes

Glenohumeral Joint:

- Systematic review providing algorithm to assist in guiding shoulder exam

A Proposed Evidence Based shoulder special testing examination algorithm- (Biederwolf)

o Screening test: Internal rotation resisted strength test

 Allows the practitioner to categorize condition into one of three categories:
 RTC pathology (RTC tears + tendinopathy and impingement syndrome)
 Extra-articular pathology (AC joint lesion, LHB tendinopathy, and/or referred
pain from any part o the body)
 Intra-articular pathology (GHJ capsulolabral instability and/or lesions and
internal impingement syndrome)
 + LR 22 & 91% post-test prob & - LR .13 (mod) & 6% neg post test prob
o IRRST
 In 90 deg of ABD and 80 deg ER- PT resists IR and then ER
 Looking not for pain but more about weakness
 Greater weakness with IR = posterior impingement (intra-articular)
 Anterior capsulolabral instability
 Posterior capsulolabral instability and/or lesions
 Bankart lesions
 SLAP lesions
 Articular internal impingement syndrome
 Greater weakness with ER = secondary impingement (RTC impairment)
 RTC impingement
 RTC tear
 No difference: extra-articular path (AC jt, LHB, neck referral, body region)
  SN 0.86, Sp 0.86
o Special testing data
 Impingement tendinopathy:
 Hawk ken + painful arc + MMT infra
o 3/3 positive = + LR 10.5 and 95% post-test probability 95%
 Supraspinatus tendinopathy
o External rotation lag sign + LR 15-34, post-test prob 88%
 At 0 and 90 deg of ABD
 Infraspinatus tear
o External rotation lag sign + LR 15-35, post-test prob 88%
 Subscapularis tear/tendinopathy
o Internal rotation lag sign + LR 24, post-test prob 92%
o Tests NOT to use in isolation
 HK, Neer, Yocum, horiz Add test, painful arc sign, empty can, drop arm, speed,
yergason, lift off, jobe relocation test, Gilcrest palm up test

- Effectiveness of PT in treating atraumatic full thickness RTC tears: cohort study (Kuhn et.al )
o Majority were supra involvement followed by supra + infra involvement
o Followed for 6 weeks – most stayed non-op and most stayed non-up at 2 year follow up

- Labral and instability

o Bankart lesion: shoulder dislocation that only involves the labrum
o Hill-Sachs lesion: labral lesion occurs simultaneously with structural deficit of humeral
head
o Multidirectional instability is multifactorial (labral, ligamentous, motor control)
o Higher level athletes may need to undergo surgical stabilization
o Immobilization following dislocation did not change prognosis compared to immediate
mobilization
o Associated fracture, the size, and displacement of fragment important when deciding on
treatment- immobilization of shoulder in 10 deg of ER for 3 weeks post-GHJ dislocation
with larger displaced glenoid rim fx.
o Exercise for multi-directional instability
o Special test: anterior load and shift test
 Normal = mild translation -=25%
 Grade I: feeling humeral head riding up to the rim 25-50%
 Grade II: feeling the humeral head overriding the glenoid rim, but
spontaneously reducing > 50%
 Grade III = feeling the head overriding the rim- remains dislocated > 50%
- New classification for shoulder instability (Kihn 2010)
o FEDS (Frequency, etiology, direction, severity)
 Frequency: how many episodes in past year
 1 = solidary, 2-5 = occasional, > 5 = frequent
  Etiology: did you have an injury to cause this?
 Traumatic = yes, atraumatic = no
 Direction: what direction does the shoulder go out most of the time?
 Anterior = out the front
 Inferior = out the bottom
 Posterior = out the back
 Severity: have you ever needed help getting the shoulder back in the joint
 Subluxation= no
 Dislocation = yes
o Is less sensitive for subtle instability, subjects were athletes
o Had to meet 2 criteria: discomfort and sensation of looseness, slipping or shoulder
“going out”
- Shoulder dislocations
o Acute:
 Neurovascular exam
 Axillary, suprascapular, long thoracic nerves
 Axillary nerve injured 42% anterior dislocations
 Characteristic patient presentation
 Arm held against trunk, supported by other arm
 Observation/appearance
 Sharp deltoid contour, more prominent acromion
 Palpable fullness below coracoid and/or axilla
o Subacute (post-relocation)
 Load and shift test
 Apprehension/relocations
 Sulcus test (0-90 deg)
 > 2cm difference compared to the other side indicative of MDI
o X-ray Imaging:
 Pre-duction (slight A-P in IR)
 Assess for greater tuberosity fx.
 Post-reductions
 Scapular AP – glenoid fossa fx.
 West point modified axillary view- avulsions IGHL, bony bankart lesion,
anterior-inferior glenoid deficiency
 Styker notch view: hill-sachs lesion
o MRI
 Labral, RC tears, articular cartilage
 Contrast is best, acute injury no contrast is needed (blood is contrast)
o Management:
 15-25: acute repair usually best to decreased recurrence
 25-40 yo: usually do well with conservative care
 > 40 yo : usually do well with conservative care but often have concomitant soft
tissue injuries
 o Immobilization: with slight IR up to 6 weeks
 Whenever pt. is ready to come out
- Labral lesion
o A shoulder dislocation = concomitant labral injury (bakart) unless otherwise noted
- Frozen shoulder
o CPG- Adhesive Capsulitis
o Outcome measures: DASH, ASES, SPADI
o Clinical Course: a continuum of pathology, staged progression of pain and mobility
deficits that at 12-18 months mild to mod mobility deficits and pain may persist
o Risk factors:
 Diabetes and thyroid disease
 Individuals 40-65 years old , female, previous episode of AC in c/l arm
o Pathoanatomical factors:
 Loss of PROM in multiple planes (most in ER and shoulder ABD)
o Examination: shoulder ROM, GHJ accessory motions, functional limitations
o Diagnosis classification:
 Present with a gradual onset of pain and loss of AROM and PROM
o Differential diagnosis: should consider another dx. if not consistent with adhesive caps.
o Interventions- corticosteroid injections
 Combined with shoulder mobility and stretching- exercises are more effective in
providing short term (4-6 weeks) pain relief and improved function compared to
shoulder mobility and stretching exercises alone
o Interventions- patient education
 Used to describe natural course of the disease
 Promote activity modification to encourage functional pain free ROM
 Matches the intensity of stretching to the patient’s current level of irritability
o Interventions- stretching exercises
 Mod evidence with stretching depending on pt. tissue irritability level
o Interventions- modalities
 Short wave diathermy, ultrasound, ESTM combined with mobility + stretching
o Interventions- joint mobilization (weak evidence)
o Interventions- translational manipulation (weak evidence)
 Scalene block – inferior translation manip under anesthesia to the GHJ
o Irritability classification

High Irritability Moderate irritability Low irritability

High pain > 7/10
Consistent night/rest pain
High disability on DASH, ASES,
PENN
Pain prior to end ROM
AROM < PROM (d/t pain)
Mod pain 4-6/10 Low pain < 3/10
Intermittent night/resting pain No resting/night pain
Mod disability on DASH, ASES, Low disability on outcome
PENN measures
Pain at end of ROM Minimal pain at end ROM with
overpressure
AROM similar to PROM AROM = PROM
 o Matched interventions

High Irritability Moderate irritability Low irritability

Modalities Heat, ice, e-stm Heat, ice, e-stm ---
Activity Yes Yes ---
modification
ROM/Stretch Short duration (1-5 sec) pain Short durations (5-15 sec) End range/overpressure,
free P/AROM PROM, AAROM to AROM increased duration, cyclic
loading
Manual Low grade mobs Low to high grade mobs High grade, sustained holds
techniques
strengthen --- --- Low to high resistance end
ranges
Functional --- Basic High demand
activities
Patient ed yes Yes yes
other Intra-articular steroid --- ---
injetions

Upper Extremity: Elbow/Wrist/Hand

- Radial head fracture
o MOI: FOOSH fall, radius hits capitellum
o Clinical exam:
 limited elbow ROM (mechanical block) – AROM and PROM
 pain with passive pronation/supination
 ipsilateral wrist ROM and palpation
 may indicate distal radio-ulnar or interosseous disruption
 medial collateral ligament stability
 pain with palpation over the radial head
o radial head fx. Can be diagnosis on x-ray
 look for fat pad sigh on x-ray (darkened mark) around joint line
 might see dared area around humerus – signifying fat pad being pushed
out by edema
- Ulnar Collateral ligament sprain
o Hx: acute ruptures occur primarily in overhead athletes
 Pain persists with throwing- indicates a partial tear
o Differential diagnosis: flexor or pronator strain, medial epicondylalgia
o Physical exam
 + TP insertion of anterior UCL
 Valgus stress test at 25 deg elbow flexion
 Moving valgus stress test
 Sn 1.0 (- LR 0), sp 0.75 (+ LR 4.0)
  Positive between 120-70 deg of flexion
o Providing valgus stress test moving from 120 deg flex to 70 deg
o Constant stress throughout range
o Treatment
 Immobilize elbow
 Strengthen pronator teres
 Grade 3 sprain = ortho consult
- Lateral Epicondylitis
o History
 75% in dominant arm
 Pea occurrence in 4th and 5th decade
 Overuse injury
 Ext. carpi radialis brevis is the primary culprit
o Physical exam:
 TTP anterior epicondyle
 Pain with resisted wrist, 3rd, 2nd digit extension
 Insertion of ECRB and ECRL
 Decreased grip strength
 Grasp/lift objects with elbow extended causes pain
o Differential diagnosis
 Radial tunnel syndrome
o Treatment:
 Anti-inflammatory med
 Stretching wrist extensors
 Eccentric-based strength
o Research
 Wrist HVLA and lateral epicondylitis- HVLA to scaphoid
 Weakness in grip strength
 Want to assess grip strength in 3 different positions (width)
o 1,3,4 for smaller hands or 2,3,5 for larger hands
o Smaller gets intrinsics, middle setting gets intrinsics + extrinsics,
larger setting gets more extrinsics
o We should see a normal bell curve
- Lateral epicondylagia (tendinosis)
o TTP: lateral epicondyle, extensor tendons
o MMT wrist extension (RD, UD), 2nd, 3rd digit extension
o Limited and painful grip
o Cervical/thoracic dysfunction
 Assess C2-T7
- Lateral elbow pain, evidence-based treatment
o Manual therapy
 Mulligans (MWM)
 Manipulation P-A to scaphoid
 Manipulation P-A to radial head
  Mobilizations to cervical/thoracic spine
o Exercise:
 Sensorimotor training to wrist extensors
 Might need to put fingers in extension to reduce ext. digit. And activate
ECRL/ECRB + ECU
 Eccentric or eccentric/concentric combo to ext. tendons
 Strength training entire UE
o Other: counterforce brace
o Want to look at cervico-thoracic spine
 C7-T2- mobilizations + exercise = better outcome
o Manual therapy: short term benefit
- Medial epicondylalgia
o History: common with activities that place a valgus stress at elbow, FCR and pron teres
o Physical exam:
 TTP at epicondyle
 Pain with resisted wrist flexion and forearm pronation
 Grip strength usually unaffected
 Ulnar nerve sx. Often co-exist
o Differential dx.
 Ulnar neuropathy
 UCL sprain
 Pronator syndrome
 Cervical radiculopathy
o Treatment
 Stretching wrist flexors
 Eccentric based strengthening
- Overuse/chronic conditions
o DeQuervains tenosynovitis
 Most common overuse injury at the wrist
 Tenosynovitis 1st dorsal compartment, APL, EPB
 Finkelstein’s test + diagnostic
 Rest during initial stages (25-72% cure rate)
 Thumb spica splint
 Corticosteroid injection cure rates 62-100%
o Intersection syndrome (texter’s thumb/gamer’s thumb)
 Inflammatory condition
 1st dorsal compartment (APL + EPB) and 2 nd dorsal compartment (ECRL/B)
 They intersect about 4-6 cm prox. Radiocarpal jt.
 If they rub over each other can create pain
 Diagnosis: extend wrist, circumduct thumb
 Treatment: rest, splinting, NSAIDs, injection
o ECU tendinitis
 2nd only to deQuervains in frequency in athletes
 Racquet sports, nondominant hand tennis (2-hand backhand) extensive uln. dev
  Often as compensation for other ulnar sided wrist pathology- (TFCC injury)
 Treatment: rest, splint, NSAIDs, injections
o ECU subluxation
 Ulnar sided wrist pain- differential diagnosis on radar
 Sudden flexion/ulnar deviation stress MOI
 Rupture of subsheath
 Diagnosis: AROM ulnar deviation in full supination- observe ECU tendon sublux
ulnarly over styloid
 Treatment: acute- case 6 weeks (pronation + extension)
 Chronic: reconstruction of sheath
- Dorsal wrist compartments
o Compartment 1: extensor pol. Brevis, abduct. Pol. Longus (apple and pB)
o Compartment 2: ECRB, ECRL
o Compartment 3: ext. pol. longus
o Compartment 4: ext. digit + ext. indicis
o Compartment 5: extensor digit. minimi
o Compartment 6: ECU
- Athletic injuries of the wrist and hand
o Carpal fractures
 Scaphoid, hook of hamate, lumate, pisiform
 Swelling and tenderness in anatomical snuffbox
 6 criteria to diagnose wrist fx:
 Edema in wrist
 Tenderness localized to the wrist
 Pain with AROM flexion or extension
 Pain with PROM flexion/extension
 Pain with grip
 Pain with wrist supination
 70% of all carpal fx are scaphoid
 Most prevalent 15-30 yo population
 Dorsal vasculature supply 70-80%
 Proximal pole fx. Have worse prognosis for healing
o Decreased blood supply – volar scaphoid branch
 Initial XR often do not show fx
 Contact sport athlete with radial wrist pain has a scaphoid fx. Unless
proven otherwise
 Exam:
o TTP anatomic snuffbox
o Limited and painful wrist extension/ radial deviation
o Swelling
o XR negative – advanced imaging (MRI, CT, bone scan)
o Axial load of the umb (sn 0.89, sp 0.98)
o Wrist ligament fractures
  Scapholunate injury- most common wrist ligament injury
 MOI: excessive wrist extension and UD
 Fall on pronated hand
 Common in collision/contact sports
 Scaphoid shift test (often not possible with acute injuries
 Sn and Sp 0.66, 0.69
 Point tenderness
 Standard SR + stress views (clinched fist, supinated view with UD)
 Will see distance increased between scaphoid and lunate
 Surgery is primary treatment
o Distal Radioulnar joint and TFCC
 Ulnolunate ligament, ulnotriquetral ligament, palmar RU ligament + articular
disc + dorsal radioulnar ligament
 TFCC = PRIMARY stabilizer of RU joint- especially with wrist pronated
 MOI: acute trauma (fall or overuse) or overuse from participation in racquet
sports
 Common in gymnastics, racquet players, hockey, golf, boxing, waterskiing, pole
vaulting
 Acute trauma: typical axial load boarding with rotational stress (FOOSH)
 Ulnar sided wrist pain
 TTP at TFCC- hollow border between pisiform and ulnar styloid process of wrist
 Supination test: attempt to lift exam table
 Press test: use hands to push up from chair/table without legs (Sn 100%)
 Piano key sign: have pt. place both hands on table and pressing into table
 Will see radius and ulna move
 Distal radioulnar jt. AP/PA mobs – positive for hypermobility
 Grind test for distalradioulnar jt. – compress radius/ulnar with forearm rotation
 Imaging is faulty: MRI high false neg. rates
 Differential dx.
 Lunotriquetral injuries, ECU tendinitis, chondral lesions DRUJ, ulnar
flexor mm tendinitis, ulnar carpal impingement
 Treatment
 Brace (wrist widget), tape (compress DRUJ), surgery
- Other common pathologies:
o Distal radius fx.
 1/6 of fx. Seen in ER
 MOI: Falls, MVA, athletics
 Clinical exam
 Variable deformity of wrist with hand displacement
 Swelling, ecchymosis, tenderness
 Painful ROM
 Want to look at median nerve
 Might see dinner fork deformity
 Non-op management
  All should undergo closed reduction
o Splint: non to minimally displaced without articular involvement
 Cast: once swelling is resolving
o Wear for approx. 6 weeks or until union evident on plain films
 Referral
 High energy injury
 Displacement
 Articular involvement
 Distal radius/ulnar incongruity
 Metaphyseal comminution
 Colles’ fracture
 Dorsal angulation, dorsal displacement,
 fracture shortening
 extra-articular

 Research- treatment

o Oscillatory mobs provide better pain relief vs. sustained stretch

o Sustained stretch are more effective than oscillations once pain
was decreased
 Smith’s fracture (reverse colles)
 Volar angulation
 Volar displacement
 Extra-articular
 Barton’s fracture
 Volar or dorsal displacement
 Intra-articular
o Boxer’s fracture
 Fracture of the distal MCP (most common index or pinky)
 Hx:
 Pain at fx. Site, dorsal swelling, deformity
 MOI: direct impact to MCP shaft/head
 Physical exam:
 Deformity: rotational malalignment of finger in flexion: 1.5 cm overlap
 Decreased MCP height
 Loss of MCP/PIP extension
o 7 deg ext. loss = 2 mm short
 Extrinsic vs, intrinsic tightness
o Extension: decreased PIP flexion in MCP flexion
o Intrinsic: decreased PIP flexion in MCP extension
 Chronic: loss of motion and grip strength
 Differential Dx: contusion, MCP dislocation
 Treatment: splinting, prognosis: non-op > 90% of the time
 o Mallet finger
 Avulsion of the distal slip of the extensor tendon
 Rapid forced flexion of the distal phalanx (ball striking tip of the finger)
 Physical exam:
 Decreased AROM of DIP extension
 Normal PROM DIP extension
 TTP dorsal DIP
 Treatment:
 Splint 6-8 weeks in full extension
 Night splint 3-4 weeks
o CMC OA

Lower Extremity: Knee

Subjective:

- Traumatic knee injuries

o Swelling immediate
o Hemarthrosis
 Intracapsular injury (ACL.PCL, capsule)
 Good blood supply, therefore quick bleeding and swelling
o Swelling delayed ~ 24hrs
 Intrasynovial or extra-capsular tissues
 Menisci, collateral ligaments, quad/patella tendon, patella subluxation
 Menisci are bothered in synovium, synovitis-type swelling occurs over a longer
period of time
 Grade 3 MCL sprains often will swell immediately d/t intimate connection to
(and tear of ) the capsule
o Giving Way
 Straight (sagittal plane) walking
 Patella instability
 Cutting movements (ACL, PCL, capsule)
 Descending stairs (quad inhibition)
- Ottawa Rules for knee Radiographs
o Age 55 or older
o Isolated tenderness to patella (no other bony tenderness)
o Tenderness to fibular head
o Active flexion < 90 degrees
o Inability to weight-bear (4 steps) immediately after injury or during evaluation
o Diagnostic Accuracy
 + LR (1.96- 2.08)); -LR 0
 Excellent screening tool to rule out fractures in adults and children
- Knee ligament sprain clinical findings:
o Symptom onset linked to precipitating trauma
o Deceleration, cutting, or valgus motion associated with injury
 o “pop” heard or felt at time of injury
o Hemarthrosis within 0-12 hrs. following injury
o Knee effusion present
o Sense of knee instability reported
o Excessive tibiofemoral laxity with cruciate/collateral ligament integrity tests
o Pain/symptoms with cruciate/collateral ligament integrity tests
o Lower-limb strength and coordination deficits
o Impaired single leg proprioception/balance
o Abnormal compensatory strategies observed during deceleration or cutting movements

LIGAMENT MECHANISM OF INJURY

ACL Noncontact: accel/deceleration activities: excessive quad/diminished HS activation
Quads force + valgus load + knee IR, WB, deceleration
PCL Dashboard/anterior tibial blow injury
Fall on flexed knee with ankle PF
Violent hyperextension
MCL Valgus torque to knee, typically hit to lateral knee w/foot on ground
PLC Knee hyperextension ER + varus
Complete knee dislocation
Flexed & ER knee that receives AP blow to tibia

- Diagnostic tests
o Lachmans + LR( 1.39-40); -LR (0.02-0.52)
o Anterior Drawer +LR (4-97), -LR (0.23-0.74)
o Reliability: interrater
 Anterior drawer – k= 0.96 (low quality studies
 Lachman’s- k = 0.19- 0.93
o Posterior sag sign
 + LR 88, - LR 0.28
- Return to sport criteria
o Isokinetic and hop test symmetry > 90%
o LESS < 5
o ACL- RSI > 56
o IKDC 2000 > 15th percentile age/gender matched normative data
- ACL Sprain with stability and movement coordination impairments
o MOI consisting of deceleration and acceleration motions with noncontact valugus load
at or near full knee extension
o Hearing or feeling a “pop” at time of injury
o Hemarthrosis within 0-12 hours following injury
o History of giving way
o Positive Lachman test with “soft” end feel or increased anterior tibial translation
 Sensitivity 85%, specificity 94%
o Positive pivot shit test
 Sensitivity 25%, specificity 98%
 o 6-m single limb timed hop test result that is less than 90% of the uninvolved limb
o Max voluntary isometric quad strength index that is less than 80% using burst
superimposition technique
o Reported hx. of giving way episodes with 2 or more ADLs

POST-OP ACL:

o Post-op ROM goals

 First goal is full extension
 Goal for knee flexion = 90 degrees
 First time reconstruction – within one week
o What muscle is the most important: quads
o What is the primary inhibition to knee ROM – Arthrogenic inhibition (knee swelling)
o Where is the graft at it’s weakness (6-8 weeks)
-
- PCL sprain with stability and movement coordination impairments
o Posterior directed force on the prox. Tibia (dashboard injury)
o Localized posterior knee pain with kneeling or decelerating
o Positive posterior drawer test at 90 deg. with a nondiscrete end feel or an increased
post tibial translation (Sn 90%,)
o Posterior sage of the prox tibia posteriorly relative to the anterior aspect of the femoral
condyles (SN 79%, SP 100%)
- MCL sprain with stability and movement coordination impairments
o Trauma by a force applied to the lateral aspect of the LE
o Rotational trauma
o Medial knee pain with valgus stress test performed at 30 deg of knee flexion
 (SN 78%, SP 67%)
o Increased separation between femur and tibia with a valgus stress test performed at 30
deg. of knee flexion (SN 91%, SP 49%)
o Tenderness over MCL and its attachments
- LCL sprain with stability and movement coordincation impairments
o Varus trauma
o Localized swelling over the LCL
o Tenderness over the LCL and its attachment reproduces familiar pain
o Lateral knee pain with varus stress test performed at 0 and 30 deg of knee flexion
o Increased separation between the femur and tibia (laxity) with varus stress test applied
at 0 and 30 deg of knee flexion
- Four Common Factors for Female ACL injury
o Ligament dominance
 Muscles do no sufficiently absorb GRF
 COM is target of GRF, however, when ipsilateral trunk lean the GRF
moves lateral to the center of the nee (knee valgus)
 Posterior chain is under used
  High forces over short period of time = ligament rupture
o Quadriceps dominance
 Females tend to land with less knee flexion than males
 Stabilized knee w/quads and place increased force thru patella tendon
 Leads to anterior translation of tibia on femur = stress to the ACL
 Decreased use of hamstrings (ACL synergists)
 Hamstrings increase knee flexion and allow for better mechanical advantage
during landing and better frontal plane control of the jt. d/t bilateral insertion
o Leg dominance
 Women tend to be more one-leg dominant than males
 Tend to have more asymmetry in strength
o Trunk/core dominance
 Inability to precisely control the trunk in 3D space
 Females hit a growth spurt, COM is higher off ground thus harder to control
 Females geta more massive trunk but do not get more stabilization to the trunk

Relationship between MOI, Neuromuscular Imbalance and Neuromuscular intervention for ACL injury
and prevention in Female Athletes:

Injury Mechanism Underlying Neuromuscular Targeted Neuromuscular

Component
Knee ADD during landing
Low Flexion angle in landing
Asymmetrical Landings
Inability to control COM
Imbalance intervention
Ligament Dominance Train for proper technique
Quad Dominance Strengthen posterior chain
Leg dominance Train side/side symmetry
Trunk dominance (core dysfunction) Core stability and perturb. Training

- Neuromuscular and proprioceptive prevention programs appeared to reduce knee injuries by

26% and ACL injuries by 50%
- Research: effectiveness of injury prevention programs for non-contact AL and hamstring injuries
o Exercise programs included: hamstring exercises + plyometrics, balance, resistance,
agility, flexibility exercises
- Research article: post-ACLR current concepts
o Athletes s/l ACLR with 20% quad strength walk with gait charact. Of acute injury
o < 50% athletes s/p ACLR return to sport
o Reports of graft rupture and c/l limb injury incidence 6-32%
o ACL graft rupture > men
o C/l injury > women
- Primary Risk factors for ACL injury (Sn 92%, Sp 88%)
o Hip rotational control deficits
o Excessive frontal plane knee mechanics
o Knee flexor deficits
o Postural control deficits
- Other variables
o Hamstring/quad ration torque at least 85% needed
 o Single limb hop for distance and asymmetries on hop tests
- Examination: Physical performance measures:
o Detect side to side asymmetries
o Assess global knee function
o Determine patient’s readiness to return to activities
o Single legged hop tests
 Single hop for distance
 Crossover hop for distance
 Triple hop for distance
 6-m timed hop
o Knee laxity/stability measures
o Lower limb movement coordination
o Thigh muscle strength
o Knee joint ROM
- Interventions:
o Therapeutic exercises: WB and NWB concentric and eccentric exercises should be
implemented within 4-6 weeks, 2-3x per week for 6-10 months post-ACLR
o Neuromuscular ESTM: should be used for 6-8 weeks to augment mm strengthening
post-ACLR to increase quad mm strength and enhance short term fx.
o Nueromuscular Re-education: should be incorporation with muscle strengthening
exercises
o Immediate mobilization (within 1 week) post-op ACLR/ continuous passive motion
o Early WB- as tol- withing 1 wee post-op
o Cryotherapy
o Supervised rehabilitation: in clinic and education for HEP
o Knee bracing (grade C evidence for functional knee bracing)

2018 Meniscal and Articular Cartilage lesions- CPG

- Account for almost ¼ of all knee injuries

- Girls have have higher incidence than boys
- Older individuals have higher rate than younger
- Lateral meniscus more common in younger population, medial meniscus in older
- High prevalence of meniscus tears are present in individuals undergoing primary and revision
ACL reconstruction
- Individuals > 45 more likely to have meniscectomy
- Prevalence of articular cartilage lesions 17-59%
- Incidence of articular cartilage lesions is high after partial meniscectomy of 2 nd ACL injury

Diagnosing meniscus injury

- Subjective
 o Twisting injury, tearing sensation at time of injury, delayed effusion, hx. of catching/lock
- Objective:
o Pain with forced hyperextension
o pain with overpressure flexion
o Pain or audible cli kith McMurray’s maneuver (Sn 55%, Sp 77%)
 Better for ruling in lateral meniscus vs. medial
 Better at ruling out medial meniscus vs. lateral
o Joint line tenderness (sn 76%, Sp 77%)
 Better at ruling out medial meniscus
 Better at ruling in lateral meniscus
o Discomfort or sense of locking/catching over medial or lateral jt. line with Thassaly test
when performed at 20 deg of knee flexion
 Sn 59-89%, Sp 83-96%
 Better at ruling in
- 6 or more positive findings- + LR 11.2

Diagnosing Articular cartilage lesions:

- Acute trauma a with hemarthrosis (0-2 hrs)

- Insidious onset aggravated by repetitive impact
- Intermittent pain and swelling
- Hx. of catching/locking
- Joint line tenderness

Interventions meniscal and articular cartilage surgery:

- Early progressive AROM and PROM

- Progressive strength training, increased quad strength, functional performance, NMES

Looking at diagnosis on the exam vs. the treatment

Knee OA:

- Patient usually older, gradual onset, previous trauma or sx., may have swelling, may complain of
giving way, morning pain and stiffness that improved after 30 min
- Diagnostic imaging:
o WB x-rays to determine joint space narrowing
- Altmann’s criteria for diagnosis of knee OA (Sn 89, Sp 88)
o Category 1
 Knee pain and crepitus with AROM and
 Morning stiffness < 30 min
 Age > 38
 o Category 2
 Knee pain and crepitus with AROM and
 Morning stiffness > 30 min and
 Bony enlargement
o Category 3:
 Knee pain and
 Bony enlargement
- Interventions:
o Mod evidence for a large effect for high-intensity resistance program for long term and
intermediate term f/u
o High intensity, low volume
- Evidence about treating knee OA conservatively
o Manual therapy to knee, hip, ankle lumbar + exercise protocol
 Result at 1 year = statistical and clinical significant improvement in WOMAC
scores vs. control group
o Pt. with knee OA benefit from hip mobilization
 Post-test prob with d/5 CPR factors = + LR 12.9 %
 Mobilzations – caudal glide, P-A to hip in neutral and faber, A-P to hip
 CPR:
 Hip/groin pain or paresthesia
 Anterior thigh pain
 Pain with hip distraction
 Knee flexion PROM < 122
 Hip IR PROM < 17
 Discussion of predictors
 Hip groin pain and limited hip IR – related to Altman hip OA
 Limited knee flexion- pt. with more progressive OA respond better
 Pain with hip distraction: may indicated impaired distensibility of
periarticular soft-tissue
- Patellofemoral Pain (PFPS)
o Definition: retropatellar or peripatellar pain with loading the patellofemoral joint in a
flexed position
o Epidemiology:
 Common in young adolescent 12-17, females > males
 may be more predisposed to knee OA
o 2 primary theories
 Patella malalignment
 Proper PFJ tracking required balanced forces
o Quad/patella tendons, lat/med retinaculum
o attachments of VL, VM, ITM
 imbalances = abnormal tracking = increased compressive stress across
facets
 additional forces = abnormal femoral rotation and ADD alters hip
kinematics and puts various strains across the knee
  quad and hamstring tightness
o quad: creates patella alta moment during loading- abnormal
stresses across facets
 as the knee bends from 0-90 deg the patella should
track inferiorly
 once the knee flexes > 90 get slightly superior
translation
o hamstrings- significant tightness causes quad activity to attain
TKE prior to initial contact (hamstrings not able to eccentrically
control)
 quad does not get full rest during swing phase (overuse)
 OKC extension 40-0 deg, increased compressive stresses
 Joint overload (extrinsic factors)
 Excessive activity overloads of PFJ
 Disturbs tissue homeostasis
 Inflammation results
 Often preceded by increased activity or increased mileage in runners
o Diagnosis
 Diagnosis of exclusion, rarely traumatic
 Cluster of abnormalities
 Diffuse peri-patellar knee pain
 Some reports of “catching”
 Exacerbated: activities with compressive loads (to the PFJ)
 Walking- 0.5 BW force
 Ascending Stairs- 2.5 x BW force
 Descending stairs- 3.5 x BW force
 Squats (to 90 degrees): 7.5 x BW force
 Rarely use imaging unless trying to rule out other pathology
o Diagnosis classification (Wilk JOSPT)
 Compression
 Lateral
o Tight ITB and retinaculum
o Laterally tilted patella
o Dec. medial patella glide
 Global
o Usually post-traumatic
o Glide reduced in all planes
 Instability
 Recurrent
o Complaints of instability
o Previous trauma
o Males > females
o Hypermobile patella
 o Positive apprehension sign
o Tibial torsion, hip anteversion, excessive pronation
 Acute
o MOI: valgus stress with ER
o Excessive swelling (not actual hemarthrosis)
o Rule out other ligamentous injuries
o Lateral dislocation more common
 If self-reduced must x-ray for lateral femoral condyle fx.
 Biomechanical dysfunction
 Excessive foot pronation
 Excessive femoral IR and ADD
 Muscle imbalances
 Limb length discrepancy
 Trauma
 Overuse
 Soft-tissue lesions
 Bursitis
 Fat pad syndrome
 Plica syndrome
 Patella tendon
 Osteochondritis
 Less common conditions
 OCD lesion (osteochondral defect)
 CRFS
 Patellofemoral OA
 Traction apophysitis
 Osgood Schlatter’s- traction apophysitis of tibial tuberosity
 Sidney Larson Johansson syndrome: traction apophysitis of distal pole of
the patella
o Diagnostic tests
 2 TESTS with diagnostic accuracy:
 Squatting with pain – LR 0.2
 Patella tilt test + 5.4
Other tests:
 Pain during stair climbing
 Active instability test
 Clarke’s test

 Cook CPR: 2/3 + LR 4

 Pain during resisted quad muscle contraction
 Pain during squatting
 Pain during palpation of post-medial and lateral patellar borders
o Treating PFPS
  Strengthening exercises
 High reps > 30 without increased pain (large effect size)
 Improving quad strength decreases pain, improves fx. And PFJ contact
area (leg press, knees extension 4x10 with 1’ rest between sets)
 Cycling at low power/high cadence
 Quad strengthening exercises
 Use of infrapatellar and suprapatellar straps during squat improved
quad activity and timing – delayed onset of VL
 Strengthening of hip ABD- improving flexibility of hip flexors and ITB
 Long stride lunges without step (dec. compressive loads at PFJ)
 Proximal hip ABD and ER strengthening and coordination
 Stretching exercises
 Lengthen hip flexors and TFL
 PNF > classic stretching
o Hold/relax – 30” to discomfort, 10” isometric, 30” stretch +
repeat followed by 45’cardio
 Taping
 Low quality and insufficient data
 Conflicting evidence benefits vs. no benefit
 McConnell and spider taping – small effect sizes
o May be used as an adjunct
 Orthotics
 OTC orthotic + PT improve pain/function in subset
 2-4 weeks from baseline (no control group- use with caution)
 Custom medial posted for overpronating runners improved eversion but
no effet transverse plane of tibia/knee
 CPR (not validated) to predict subgroup of pt. with PFP that might
benefit from orthotics: (wide confidence intervals)
o Age > 25
o Height < 165 cm
o Worst pain < 53.25 millimeters
o Midfoot width difference > 10.96 millimeters
 Manual therapy (may be beneficial)

LOWER EXTREMITY: LEG/ANKLE/FOOT:

Midportion Achilles Tendinopathy

- Diagnosis:
o TTP 2-6 cm prox to Achilles insertion
o Positive arc sign
 Pt. prone with ankle off table edge
 AROM DF/PF ankle
 + test area of pain moves prox/distal with AROM DF/PF
 o Positive Royal London Hoffman’s test
 Pt. prone with ankle off table
 Identify portion of Achilles tendon that is max tender to palpation
 AROM DF and hold
 Palpate the most tender portion again in max DF
 + test: less tender in max DF
- Outcome measures: VISAA, FAAM, FAAM, LEFS
o Activity limitations/physical performance measures
 Hop and heel raise endurance tests
o Physical impairment measures
 Measure ankle DF ROM, STJ ROM, plantar flexion strength and endurance, static
arch height, forefoot alignment, pain with palpation
- Acute:
o < 3 months, high levels of pain, loss of motion, redness/swelling/warmth
o High level of pain limiting low level activity
o Interventions:
 Dec pain and inflammation (iontophoresis)
 Stretching, STM
 Rigid taping, bracing
- Non-acute
o > 3 months, pain after onset of high-level activity, tendon pain with palpation
o Interventions
 mechanical loading exercises/eccentric + conc/eccentric, heavy load/slow speed
 stretching/STM
 rigid taping
 neuromuscular exercises for other kinetic chain impairments
o Diagnosis:
- Interventions:
o Strong level evidence
 exercise (eccentric, heavy-low slow speed (conc/ecc))
 Activity modification
 Iontophoresis with dexamethasone
o Weak evidence
 Ankle PF stretches
 AGAINST night splints
o Conflicting evidence: heel, lifts, orthoses, low-level laser

Ankle Sprains:

- Ottawa foot and ankle Rules:

- Ankle Xray required
o TTP to the malleolar zone & TTP distal 6 cm to the post-aspect of distal tib and/or fib
o TTP in the midfoot zone & TTP over the navicular and/or over the base of the 5 th met
 o & inability to WB immediately and in the ED
- Main assessments: Ankle ROM, swelling, and ability to WB
- Grades of ankle sprains:
o Grade I : no loss of function, no lig laxity, no hemorrhaging, dec. total ankle AROM < 5,
swelling of 0.5cm or less
o Grade II: some loss of function, + ant drawer test, neg talar tilt test, hemorrhaging, TTP,
dec. total ankle ROM > 5 deg but less than 10, swelling 0.5cm-2.0 cm
o Grade III: near total LOF, + ant drawer and talar tilt test, hemorrhaging, extreme TTP,
dec. total ankle motion > 10 deg, swelling > 2.0 cm
 Want to get stress radiographs
- High ankle sprain scale:
o Grade I
 TTP Distal syndesmosis only
 Min edema superior and anterior to lat. malleolus
o Grade II
 TTP Distal syndesmosis + prox < 4 cm
 Mod edema superior and anterior to lateral malleolus
o Grade III
 TTP Distal syndesmosis and prox > 4 cm
 Significant edema superior and anterior to lateral malleolus
- Risk factors:
o Hx. of previous ankle sprain, no external support use, don’t properly warm up with static
stretching or dynamic movement before activity, abnormal DF AROM, no participation
in balance/proprioceptive prevention program
o Low evidence ankle instability: increased talar curvature, no external support, no
balance training
- Outcome measures
o FAAM (MCID at 4 weeks- 8 for ADL, 9 for sport)
o LEFS (MCID at 4 weeks- 9
o Single limb hop tests with lateral and diagonal movements
- Girth measurements
o Figure 8 measurement
 Starts at groove of edge of lateral malleolus and draw medial cross the plantar
side of the foot behind base of 5th metatarsal and under the medial malleolus
and across Achilles tendon to meet original point (under lat malleolus)
 Measure in 20 deg of PF- most reliable method for swelling with MDC 6.8 mm
- Special tests:
o Anterior drawer TTP ATFL + lateral hemorrhage
 + LR 4.13, -LR 0.01
o Talar tilt: + LR 4, - LR 0.57
o Star excursion
 Anterior reach differences > 4cm 2.5 x more likely for LE injury
 Females with composite reach < 94% leg length 6.5X more likely for LE injury
 Modified version: Y balance test
 - Interventions:
o Mod evidence for manual therapy (lymphatic drainage, ROM, joint mobilizations
o Strong evidence for cryotherapy, ther-ex,
 sensorimotor phase/progressive loading (manual therapy)
o Weak evidence for diathermy
 Progressive loading and single limb balance activities to improve limb
coordination and postural control during sensorimotor training phase
o Conflicting evidence for electrotherapy and low level laser
o Strong evidence NO ultrasound

Heel pain/Plantar Fasciitis:

- Examination findings:
o Plantar medial heel pain: most noticeable with initial steps after a period of inactivity
but also worse following prolonged WB
o Heel pain precipitated by a recent increase in WB activity
o Pain with palpation of the prox insertion of the plantar facsia
o Positive windlass test
o Neg. tarsal tunnel tests
o Limited AROM and PROM talocrural joint
o Abnormal FPI score (typically more pronated)
o High BMI
- Differential dx.: spondylarthritis, fat pad atrophy, prox. Plantar fibroma
o Fat pad atrophy
 Pain in the middle of the heel (ad opposed to the front of the heel)
 Pain worse with walking barefoot
 Does the pain inc. or stay the say the same with inc. walking
 EBP tests/measures
 Palpation
 Taping of the heel with walking barefoot – does it change
o Taping over the distal heel
 Treatments
 Change footwear
 Heel cup
 Imaging (typically not necessary)- suspect calcaneal spurs
 Ultrasound- to identify fat pad atrophy
- Summary of Recommendations:
o Strong: manual therapy (improve DF ROM), stretching, taping, foot orthoses
o Weak evidence: low level laser, phonophoresis, weight loss education
o Low: electrotherapy, NO dry needling, NO ultrasound
o Extracorporeal shock wave therapy
o Corticosteroid injections- benefits do not offset the risk for harm
 Long term disablement, injection site pain, infection, fat pad atrophy, plantar
fascia rupture, peripheral nerve injury, muscle damage
Midfoot

Tarsal Tunnel Syndrome

- Pain and numbness across the plantar portion of the foot

o Burning, radiating into the arch of the foot, heel and toes
- Weekend toe flexion
- Pain may be worse when running or when standing for long periods of time and often worse at
night
- Causes:
o Overpronation- compress posterior tibial nerve in the tarsal tunnel
o OA at ankle
o RA
o Diabetes
o Tenosynovitis
o Talonavicular coalition
o Cyst, ganglion or other space occupying lesion in the tunnel
- Treatment
o Arch supports, mobilization of mid-foot, neural dynamic exercises (tibial nerve bias),
strengthening foot intrinsics (MTP flexion with IP extension)

Cuboid Syndrome:

- The cuboid rotates as much as 25 degrees

- Acts as a pulley for the fibularis longus
- Highly associated with a pronated foot
- The calcaneal-cuboid labrum occupies > 35% of the joint space and may contribute to
symptoms
- Presentation: lateral foot pain, “little pebble/shoe in sock”
- Tests:
o Midtarsal ADD test or supination test
- Treatment:
o Cuboid whip
o Taping to reinforce
 Plantar to dorsal ring taping job to make sure cuboid stays in the more dorsal
position
o Padding as well

Jones’ Fracture

- Due to the high rate of non-union

- Proximal 5th metatarsal fracture
- Xray: 3 view foot series- attention to the oblique view for diagnosis
- Acute treatment: splint, NWB, f/u 3- days
- Short leg NWB cast for about 6-8 weeks and case is removed and then radiographs taken again
 o If no healing- go NWB again for 4 more weeks
- Healing time is approx. 6-12 weeks
- Displacement > 2mm – 12 weeks of conservative PT is ineffective with nonunion (refer to orth)
- Imaging: at time of injury, at week 1, at 6-8-week f/u, and 10-12 week f/u

CORE OF the FOOT

- Arch lifting
- Splaying the toes, differentiation between great toe and other 4 toes
- ESTM ABD Hall longus (improve recruitment for 4-6 weeks)
- Improving shock absorption of the foot- dec. likelihood of stress fx, plantar fasciitis, tarsal
tunnel sx., Achilles tendinopathy
FOREFOOT:
- Morton’s Neuroma
o Pain in the middle toes (3rd and 4th toes)
o MOST are happening in 3rd webspace
o 3rd common digital nerve receives large communicating branch from lateral plantar neve
o Passes deep to the transverse metatarsal ligament at 3 rd webspace
o pain and parasthsisas in toes
o agg. Factors: walking in shoes with small toe space, high heels
- Etiology:
o Chronic trauma (ambulation
o Ischemia
o Intermetatarsal bursitis
o Entrapment
o Pronation theory
- Mulder’s sign (Sn 95%, Sp 100%)
o Grasp 1st and 5th MT and squeezes while exerting firm pressure at site of suspected
lesion with opposite thumb (dorsal 3 rd webspace)
- Digital nerve stretch test (Sn 100%)
o Bilaterally lesser toes on either side of the affected webspace passively extend fully
o Ankles held in DF
o + pain/discomfort in webspace
- Imaging: used to differentiate between stress fracture, OA, Freiberg’s disease
- Treatment:
o Footwear modifications/mobility issues
o Orthotics – ineffective
o Extracorporeal shockwave therapy

Metatarsalgia:
- Primary: intrinsic abnormalities overloading the forefoot and causing enlargement of the MET
head- Hallux valgus, congenital deformity
- Secondary: trauma, inflammatory
- Iatrogenic: due to previous surgery
- Treatments
 o Metatarsal bar
o Shoe modifications
o Callus debridement
o Extrinsic factors- gastroc treatments (show to lessen plantar pressure at MET head)

Other: mallet toe (flexion deformity PIP only), hammer toe (PIP flexion, DIP extension)

HIP
Hip OA
- Pathoanatomical features
o Early articular changes observed on imaging
o Acetabular retroversion
- Diagnosing
o New ACR criteria
 Moderate hip pain
 AM stiffness < 1 hr
 Hip IR ROM < 24 deg
(OR)
 Hip and IR hip flex > 15 deg than non-painful side
(OR)
 Pain with passive hip IR
- Activity limitations- self report measures: WOMAC physical function scale
- Physical performance measures
o 6-min walk test
o 30 second chair stand test
o TUG
o Stair measure
- Physical impairment measures
o Hip ROM and muscle strength tests for: IR, ER, Flex, Ext, ABD, ADD
- Pain: NPRS
- Joint irritability: FABER
- Interventions
o Grade A – strong evidence
 Manual therapy (thrust, non-thrust, soft tissue work)
 Flexibility, strengthening, endurance tests
o Mod evidence for patient education
 Grade B evidence for ultrasound short term uses
o Weak evidence for weight loss, gait and balance training
- Predictors of response to PT interventions in pt. with Hip OA (research)
o Unilateral hip pain
o Age < 58
o Pain > 6/10
o 40-m self-paced walk test < 25.9 sec
o Duration of sx. < 1 year
 o Post-test prob of success > 3 = 99%

- Pre-op TUG < 10 sec are likely to walk without an AD at 6 months after THA

Non-Arthritic Hip Joint Pain:

- Femoracetabular impingement
o Pain in the anterior hip/groin and/or lateral hip/trochanteric region
o Pain is described as aching or sharp
o Reported hip pain is aggravated by sitting
o Reported pain is reproduced with hip flexion, ADD, IR (FADIR test)
o Hip IR is < 20 deg with the hip at 90 deg of flexion
o Hip flexion and hip ABD are also limited
o Mechanical sx. Such as popping, locking, snapping
o Radiographic findings
 CAM impingement
 Increased femoral neck diameter that approaches the size of the
femoral head diameter
 Typically in men (20-30)
 Shear chondrolabral junction0 during hip flexion
 Pincer impingement
 Increased acetabular depth
 Acetabular protrusion
 Decreased acetabular inclination
 Acetabular retroversion
 Typically women 30-40
o Treatments
 Trigger point massage RF, TFL, glut med
 Lumbar spine mobs
 Active release
 Hip capsule distraction
 Rehab for strength, endurance, lumbopelvic stability
- Structural instability
o Anterior groin, lateral hip, or generalized hip joint pain
o Reported pain is reproduced with FADIR test or FABER test
o Hip apprehension sign position
o Hip IR is >30 deg when hip is at 90 deg flexion
o Mechanics sx. Of popping, snapping
o Radiographic findings
 Increased acetabular inclination, decreased femoral head coverage
- Intra-articular injury (labral tear, OCD, loose bodies, ligamentum teres)
o Anterior groin pain or generalized hip joint pain
o Mechanical sx. Popping, locking, snapping
o Feelings of instability (ligamentum teres) when squatting
o Imaging:
  Labral tear- MRA
- Extra-articular causes of hip impingement
o Iliopsoas impingement
 Females > males, 25-35 years
 Active individuals with report or anterior hip pain
 Tight or inflamed iliopsoas tendon that causes impingement during hip ext.
o Subspine impingements
 Males > females 14-30 years
 Active individuals with anterior hip or groin pain
 Limited hip flexion and palpable tenderness over AIIS
 Caused by prominent AIIS abnormally contacting the distal femoral neck during
hip flexion- or excessive muscular activity of RF during knee flex and hip ext
o Ischiofemoral impingement
 Females > males, 51-53 years
 Nonspecific pain in the hip, groin, buttock, or LE
 Pathology caused by narrow space between ischial tub and lesser troch resulting
in repetitive pinching of the QF muscle
TMJ
Anatomy:
Dermatomes
- V1 – from the trigeminal nerve (CN 5)
o Ophthalmic nerve – sensory to the forehead, upper eye lid, eye, nose, frontal sinus
- V2- from the trigeminal nerve (CN 5)
o Maxillary nerve- sensory to the lower eyelid and cheek, upper lip, upper teeth and
gums, palate and roof of pharynx, maxillary bone, ethmoid and sphenoid sinuses
- V3- from the trigeminal nerve (CN 5)
o Mandibular nerve- sensory to the lower lip, lower teeth, chin, jaw, external ear
(Also provides motor to the muscles of mastication)
- C2 : top of the head to lower part of the chin
- C3: lower part of the head to underneath the jaw
- C4: lower posterior neck to lower neck “collar”
- C5: upper trap region
- Bony anatomy
o Mandibular condyle (can have variable shapes and be asymmetrical side to side)
o Articular disc
 Biconcave
 A&P portions innervated (post – vary densely)
 Capsule: firm medical/lateral support, laxity in A-P planes
 Will actively displace anteriorly and laterally
o Synovial joint – fibrocartilage
o No relationship between degenerative changes on an XR between, pain/TTP/mobility
- Retrodiscal lamina
o Highly innervated
o Synovial fluid/membrane
 o Doesn’t tolerate constant load or tensile forced associated with wide mouth opening or
trauma (compression) results in inflammation
- Muscles and ligaments
o Lateral
 Reinforces joint, oblique and horizontal fibers
 Oblique fibers guide condyle movement during opening
 Prevents compression of tissues posterior to the condyle
o Sphenomandibular/styomandibular
 Accessory ligaments
 Suspend mandible from cranium
 Medial to joint capsule
o Lateral pterygoid have components that attach to disc itself
 Can make the disc translate medially
 Sprain to lateral mandibular ligament
 Involved in jaw opening
o Medial pterygoid (more distal and bigger)
o Temporalis muscle
 Jaw closing
o Masseter
 Jaw closing
- Biomechanics
o Movements: opening, closing, protrusion, retraction, lateral deviation
o Rotation: condyle rolls relative to the inferior surface of the disc
o Translation: condyle and disc move together as condyle-disc complex
 Disc stretched in the direction of movement
- Jaw opening
o Early phase:
 1st (35-50%) = posterior roll/rotation (min anterior translation)
 Swings mandible inferior and posterior
 Motion stopped by collateral ligaments and lat. Pteryjoid
 Opening motion is limited if this doesn’t occur
 Lateral ligament stretched- resulting tension assists in initiating late phase
opening
o Late phase (50-65% ROM)
 Gradual transition from rotation to ant/inferior translation
- Opening ROM normative values
o Adult mean: 50 mm, 3 PIP widths
 Men and women average around 40mm with men higher
o Most mastication requires 18mm
 Abnormal can’t fit 2 PIP joints
- Jaw closing:
o Translation followed by rotation
o Tension at retrodiscal laminae retracts disc, initiating closing through post/sup
translation followed by anterior rotation
o Muscle actions: masseter, temporalis, medial pterygoids (MMT)
- Protrusion:
o Anterior translation
 o Normal ROM: 3-6 mm
o Muscle action
 Lateral pterygoid with min input for medial pterygoid and masseter
- Retraction
o Posterior translation
o Important for closing
o Normal ROM: 3-4 mm
o Muscle actions
 Temporalis, suprahyoid muscles
- Lateral deviation
o Side to side translation
o Specific path is often determined by contact of the teeth, not TMJ
o Example: L lateral deviation
 Left TMJ is pivot point
 Right TMJ rotates slightly anterior/medial
o Normal ROM: 11 mm each way
o Muscle actions
 Contralateral Medial and lateral pterygoids (prime movers)
 Minimal from ipsilateral masseter, temporalis
- Anterior disc displacement with reduction
o First 11-25 mm of mouth opening
 Mandibular condyle rotates posteriorly
o 25mm to end range opening
 Mandibular condyle translates anteriorly
o You recapture the disc during the mid-range of mouth opening
 You should hear or pt. should report 2 clicks
 The more time between clicks, the earlier in stages of disc pathology
 Earlier click in opening
 Later in closing
 The condyle will use the retrodical lamina to act as the disc
- Anterior/medial disc displacement
o Sprain of the lateral ligament- fail to oppose the medial poll of the disc by the lateral
pterygoid muscles = anterior-medial disc displacement
o With get cartilage on cartilage grinding of the condyle and notch
- Anterior disc displacement without reduction
o Disc stays anterior of the condyle through opening and closing
o No opening/closing clicks
- Opening/closing deviations
o “c” AND “reversed C”
 Hypomobility to side of convexity
o “S” and “reversed s”
 Muscle imbalance or medial displacement of disc
 Condyle “walks around the disc)
o Lateral deviations
 Early opening: muscle spasm
 Late in opening: capsulitis or hypomobile capsule
o Limited/painful closing
  Posterior capsulitis
- Pertinent history items/clinical pearls
o Probable cause of symptoms
 Extra-articular: pain with jaw fully opened
 Intra-articular: pain with biting firm objects
 OA: stiffness upon waking in the am, functional pain decreases as day goes on
o Decreased neck balance (DNF): mouth breather
o Bruxism (teeth grinding at night): causes adhesions and 1 click with jaw clinching
o Soft popping/clicks (crepitus): normal jaw movement but muscle incoordination
 Soft crepitus does not equal pathology
- Cluster of related symptoms
o Muscle and/or joint pain
o TMJ sounds
o Restriction, limitation, deviation, or deflection or the mandible during opening and
closing movements
- TMJ Disc Dysfunction stages:
o STAGE 1:
 disc slightly anterior and medial on mandibular condyle
 inconsistent click
 mild or no pain
o STAGE 2:
 disc anterior and medial
 reciprocal click (early opening, late closing)
 severe, consistent pain
o STAGE 3:
 Reciprocal consistent click (later on opening, earlier closing)
 Most painful stage
o STAGE 4:
 Click is rare (disc no longer relocates)
 No pain
- Literature review:
o Risk factors: sleep disturbances, stress, parafunctions (teeth grinding), loss of post-
support, ligament laxity
o Prevalence of types:
 Single pathology
 Disc displacement with reduction (most common)
 2nd is myofascial pain
 About equal OA, arthralgia 3rd
 Double diagnosis
 1st myofascial pain with arthralgia
 2nd myofascial pain + disc displacement with reduction
o Rule in arthritis/arthrosis if can’t get to 32 mm
o Research/diagnostic criteria for TMD
 Group I: muscle disorders
 Pain in the face, jaw, temple, in front or in the ear
 Palpation of muscle sites applying at least 2lbs of pressure results in
familiar pain in temporalis, masseter muscles
  Max unassisted and assisted opening results in familiar pain in muscles

 Positive pain hx. and pain report on examination

o Unassisted opening without pain > 40 mm or more

 Yes: myofascial pain
 No: myofascial pain with limited opening

 Negative pain hx. or pain report on examination

o No group diagnosis

 Group II: disc displacements

 Presence of a click during at least 1:3 reps of jaw opening and closing
 Either an opening or closing click during at least 1:3 reps AND a click in
at least one of the exercise movements
3 left lateral jaw movements
3 right lateral jaw movements
3 protrusive jaw movements

o YES:
 Hx. disc displacement with reduction

o NO: have you had jaw back or catch so that it would not open
all the way and does the limitation interfere with eating
 YES: max. assisted opening > 40 mm
 NO: displacement without reduction with
limited opening
 YES: disc displacement without reduction
without limiting opening
 NO: do group II diagnosis

 Group III: arthralgia, arthritis, arthrosis

 Have you had pain in the face, jaw, temple, or front/inner ear in past
month (AND)
 Pain report on examination:
o Palpation of the lateral pole with fingertip applying 1lb of
pressure, around lateral pole 2lbs of pressure
o Pain with movement of the joint
 Maximum unassisted or maximum assisted opening or
lateral excursion movements
 Positive pain hx. AND Pain report on examination
o Any crepitus (audible 6 in from jt.) during opening or closing
o Report of crepitus with any movement
 NO: arthralgia
 YES: Osteoarthritis
 Negative Pain Hx. OR Pain Report Examination
o Any coarse crepitus during opening or closing movements
o Report of crepitus with movement
 YES: osteoarthritis
 NO: No group III diagnosis