Sacroiliac jt disorders

*1. What is the sacroiliac jt and what is its innervation?
2. What is the clinical presentation of SI jt pain?
3. What are provocative tests of the SI jt?
4. What studies are used to assess the SI jt?

Answers:
1. The SI jt is the articulation between the sacrum and ilium with a synovial jt anterior and syndesmosis posterior. Innervation is L5 dorsal ramus and lateral S1-S3 dorsal rami.
2. Acute or gradual back, buttock, leg, or groin pain, discomfort with associated muscles.
3. FABER test, Gaenslen test, iliac compression test (SI jt pain with downward force on iliac crest), Yeoman's test (SI jt pain with hip ext and ilium rotation), Gillet test (normal is that PSIS rotates down with raising leg 90 deg), Seated flexion test (monitor PSIS while pt bends forward).
4. X-ray, bone scan, CT, MRI. Fluoroscopic SI jt injxn may have higher diagnostic value.

Facet syndrome

1. What are facet joints?
2. What is the etiology of facet syndrome?
3. What is the presentation of facet syndrome?
4. How is facet syndrome diagnosed?
5. What is the treatment of facet syndrome?

Answers:
1. These are true synovial joints containing a capsule, meniscus, and synovial membrane.
2. Somatic dysfunction, positional overload, capsular tears, meniscus/synovial impingement, spondylosis.
3. Neck or back pain, worse rotation and extension. Referred pain to neck may be nondermatomal. No neuro abnormalities.
4. Imaging with X-ray (degen changes), CT, MRI (hypertrophy of capsule and facets).
5. Relative rest, NSAIDs. Rehab focusing on lumbar spine stabilization with flexion and neutral postures. Interventional procedures including facet jt injections or dorsal rami medial branch ablation.

Compression fractures

1. What make up the anterior, middle, and posterior columns of the spine? Which ones lead to instability with compression fractures?
2. Where do compression fractures of the spine usually occur?
3. What factors contribute to compression fractures?
4. What is the clinical presentation?
5. How are compression fractures diagnosed?
6. What is the treatment?

Answers:
1. Anterior (stable): ALL, ant 2/3 of vertebral body. Middle (unstable): PLL and post 1/3 of vertebral body. Posterior (stable): Lig flavum, supra and infraspinous ligs, posterior elements (pedicles, facets, spinous process).
2. Thoracolumbar junction.
3. Trauma, osteoporosis, osteomalacia, medications (steroids), neoplasm.
4. Sudden onset of constant thoracolumbar pain, exacerbated by valsalva, turning in bed, incidental trauma.
5. X-rays (vertebral body wedging), bone scan with SPECT, CT, MRI.
6. If <25%>50% vertebral height decr, instability, or kyphotic deformity causing neurologic compromise.

Scheuermann's disease

*1. What is Scheuermann's disease (epiphysitis)?
2. What is the etiology of Scheuermann's disease?
3. What is the presentation of Scheuermann's disease?
*4. What is the diagnosis?
5. What is the treatment of Scheuermann's disease?

Answers:
1. D/o of vertebral endplates and apophysis, resulting in increased thoracic kyphosis, often seen in adolescents.
2. Failure of endochondral ossification --> intervertebral disc herniation, anterior wedging of vertebral bodies, fixed TL kyphosis.
3. Progressive nonpainful thoracic kyphosis that does not correct with hyperextension. Maybe also occur in young athletes.
4. X-ray shows Schmorl's nodes (herniation of disc material through vertebral endplate into vertebral body), irregular endplates, spondylosis, scoliosis, vertebral wedging.
5. Rehab involves thoracic extension and abdominal strengthening, bracing if kyphosis <74>75 or >65 in skeletally immature.

Scoliosis

1. What are the subtypes of idiopathic scoliosis and which are associated with progression?
2. What are the subtypes of congenital scoliosis?
*3. What are the subtypes of curvature?
4. What diagnostic studies are used to assess scoliosis?
5. When is bracing used for scoliosis?
6. When is surgery considered for scoliosis?

Answers:
1. Infantile (<3yrs), often associated with congenital defects. Juvenile is 4-10 yrs, with high risk of progression. Adolescent is most common (10yrs+) and has high risk of prgression.
2. Open is caused by myelomeningocele. Closed is associated with neuro deficits and vertebral deficits.
3. Right thoracic: most common, apex at T7 or T8, double major curve (right thoracic with left lumbar), lumbar, thoracolumbar (may have rib/flank distortion), left thoracic (rare).
4. X-rays are used to establish diagnosis and progression. Rotation can be graded from 0-4 based on the amount of pedicle visible on PA view. Cobb angle measures curve: angle formed by perpendicular line from endplate of most tilted prox and distal vertebrae.
5. Bracing is used with an angle of 20-40 degrees. Less than 20 degrees can be observed. Brace must be worn 23 hours a day until spinal growth is completed; wean when X-ray shows maturity and stable curve. Use a Milwaukee brace for high thoracic curves (apex at T8). If apex below T8, can used low profile TLSO.
6. Surgery for curves with fast progression, >40 degrees in skeletally immature, >50 degrees in skeletally mature, >35 in neuromusc disease, progressive loss of pulmonary function.

Spondylolithesis

1. How is spondylolisthesis classified?
*2. What is the most common cause of spondylolisthesis? What are other causes?
3. What is the presentation of spondylolisthesis?
4. What diagnostic studies are used?
5. What amount of spondylolithesis results in instability?
6. What is the treatment?

Answers:
1. Grade 0 is 0% slippage. Grade 1 is <25%.>100% slippage.
2. Most common is isthmic (age 5-50), which results from a pars fracture (most common at L5-S1) or an elongation. Other causes are congenital, degenerative (facet arthrosis), traumatic, cancer, infection, metabolic disorders, post-surgical.
3. Low back pain, worse with motion, hamstring tightness, step-off on exam. May have radicular symptoms.
4. X-rays, bone scan, CT, MRI. Flex-ex views may show instability.
5. Instability occurs with translation > 3.5mm in the cervical region or >5mm in the thoracic or lumbar region.
6. Conservative care can be used with grade 1, 2, and asymptomatic 3. Rehab involves focus on stabilization exercises in a flexion biased program and hamstring flexibility. Surgical care for higher grades including a bilateral posterolateral fusion w/wo decompression.

Spondylolysis

1. What is spondylolysis?
2. What is the etiology of spondylolysis?
3. What is the presentation?
4. How is spondylolysis diagnosed?

Answers:
1. Vertebral defect most common at L5, occuring at pars interarticularis (junction of pedicle, transverse process, lamina, and 2 articular processes).
2. Hyperextension.
3. Localized back pain, worse with hyperextension, standing, lying prone, better with flexion. Normal neuro exam.
4. X-rays (collar on the scotty dog), bone scan with SPECT, CT, MRI.

Spinal stenosis

1. When does spinal stenosis usually present? What is the most common level of involvement?
2. What is the difference between central and lateral stenosis?
3. What is the presentation of spinal stenosis? How is it differentiated from vascular claudication?
4. What diagnostic studies are used?
5. What is the treatment of spinal stenosis?

Answers:
1. Presents at 50 years are older. Most common levels are L3 and L4.
2. Central stenosis decreases the size of the vertebral canal secondary to hypertrophic facets, LF, disc encroachment, or degen spondylolisthesis. The spinal cord is 10 mm and there is neurologic sequelae with canal < 12mm (17mm is nl). Lateral stenosis can occur either in the lateral recess, mid-zone, or intervertebral foramen.
3. Neck or back discomfort, possible upper or lower limb involvement, neurogenic claudication (aching pain in leg with standing or walking, relieved with sitting or leaning forward). If claudication is vascular, the pain is more cramping, worse with uphill walking, better with downhill, better with standing, resting, or lying flat.
4. X-rays, CT, myelogram, MRI.
5. Relative rest, medications, rehab focusing on flexion or neutral based positioning and spinal stabilization, ESI. Surgery may be considered for decompression or stabilization.

Internal disc disruption

1. What is an internal disc disruption?
2. How are internal disc disruptions graded?
3. What is the cause?
4. What is the clinical presentation?
5. What diagnostic studies are used?
6. What is the treatment of internal disc disruption?

Answers:
1. Degradation of the internal disc without gross herniation, resulting in fissures and erosion of the annulus.
2. Grade 0: normal. Grade 1: inner 1/3 disruption. Grade 2: inner 2/3 disruption. Grade 3: outer 1/3 disruption.
3. Endplate fractures from excessive load.
4. Constant aching axial discomfort, worse with stress.
5. CT/discogram (for radial fissures), MRI (shows high intensity zone in annulus).
6. Conservative care includes relative rest, rehab, ESI. Spinal procedures for unremitting pain.

Myelopathy

1. What is myelopathy?
2. What are causes of myelopathy?
3. What is the clinical presentation of myelopathy?

Answers:
1. Injury to the spinal cord.
2. Radiculopathy, disc herniation, spondylosis. Less common: tumors, AV malformations, MS, syphilis, syringomyelia, ALS, RA.
3. Spastic or ataxic gait abnormalities, weakness, sensory changes, B/B dysfunction, bilateral radiculopathy, UMN signs.

Treatment of herniated disc

1. What is conservative treatment for herniated disc?
2. What is the rehabilitation program for a herniated disc?
3. What is the mechanism and complications of epidural steroid injection?
4. What is the mechanism and complications of chymopapain injections?
5. What are the indications for surgery?

Answers:
1. Relative rest, NSAIDs, analgesics, oral steroids, TCA, SRIs, muscle relaxants, and rehab program.
2. Stretching, strengthening, extension-based for posterolateral HNP, flexion based for lateral HNP, modalities.
3. ESI reduce inflammation causing nerve root irritation. Complications include bleeding, infection, tissue damage, anaphylaxis, convulsions, seizures, immunosuppr, adrenal suppression.
4. Chymopapain injections dissolve herniations contained by PLL. Complications include anaphylaxis, chronic pain, poor efficacy.
5. Progressive weakness, unremitting pain, cauda equina, myelopathy.

Herniated disc

1. What is the most common age for a disc herniation?
2. What are the most common levels of herniation?
3. How does the location of the herniation affect the symptoms?
4. What are common causes of disc herniation?
5. What is the presentation of disc herniation?

Answers:
1. 30-40 years.
2. L5-S1, followed by L4-L5, followed by C5-C6.
3. A central protrusion may or may not have radicular symptoms. A posterolateral protrusion (most common in L-spine) injures the nerve of the lower disc. A far lateral/foraminal herniation affects the exiting nerve root (nerve of upper disc).
4. Spontaneous, lifting, coughing, sneezing, bending, twisting.
5. Acute radiating neck/back pain, weakness, numbness, paresthesias, pain, list or shift, exacerbated by increased intra-abdominal pressure. If central or posterolat herniation, will be worse with flexion. If lateral herniation, will be worse with extension.

Back musculature

1. What are the muscles in the superficial layer of the extrinsic back musculature?
2. What are the muscles in the intermediate layer of the extrinsic back musculature?
3. What are the muscles in the superficial layer of the intrinsic back musculature?
4. What are the muscles in the intermediate layer of the intrinsic back musculature?
5. What are the muscles in the deep layer of the intrinsic back musculature?
6. Where does most of the flexion and extension of the C-spine take place?
7. Where does most of the rotation of the C-spine take place?

Answers:
1. Trapezius, latissimus dorsi.
2. Serratus posterior.
3. Splenius capitis, splenius cervices.
4. Erector spinae: iliocostalis, longissimus, spinalis.
5. Transversospinalis (semispinalis, multifidus, rotators), interspinalis, intertranversarii.
6. 50% flexion/extension is in the occipitoatlantal jt.
7. 50% of rotation is in the atlanto-axial jt.

Landmarks in the spine

1. What are anterior cervical landmarks?
2. What are posterior cervical landmarks?
3. What are the landmarks in the thoracic region?
4. What are the landmarks in the lumbar and sacral region?

Answers:
1. C2 is the angle of the mandible, C3 is the hyoid, C4-5 is the thyroid cartilage, C6 is the first cricoid ring and carotid tubercle.
2. C7 is the vertebral prominens (largest spinous process).
3. T3 is the spine of scapula, T8 is inferior angle of scapula, T12 is lowest rib.
4. L4 is iliac crests, S2 is PSIS.

Ligaments of the spine

1. What is the course and function of the anterior longitudinal ligament?
2. Posterior longitudinal ligament?
3. Ligamentum nuchae?
4. Ligamentum flavum?
5. Interspinous and supraspinous ligaments?
6. Intertransverse ligament?

Answers:
1. The ALL runs along ant aspect of the vertebral bodies. Limits hyperextension and forward movement.
2. The PLL runs along the posterior aspect of the vertebral bodies. Prevents hyperflexion.
3. LN is a continuation of the supraspinous ligament from occipital protuberance to C7.
4. LF connects adjacent vertebral arches, attaching laminae to laminae. Maintains constant disc tension and helps straighten column after flexion.
5. ISL and SSL run from spinous process to spinous process. They resist spinal separation and flexion.
6. IL connects transverse processes. Resists lateral bending of trunk.

Intervertebral disc

1. What are the three major components of a disc?
2. What is the vascular supply of a disc?
3. What is the function of a disc?
4. What are the effects of aging on a disc?

Answers:
1. The nucleus pulposus is a viscous gel mixture of type II collagen inside the disc, the annulus fibrosus is type I collagen that encases the nucleus pulposus (weak for torsional stresses), the vertebral endplate is the cartilaginous covering of the vertebral body apophysis, forming the top and bottom of the disc.
2. Avascular.
3. Vertebral body motion, weightbearing.
4. Decrease in nuclear water content, ratio of chondroitin-keratin, proteoglycan molecular wt. Increase in fibrous tissue, cartilage cells, amorphous tissue.

Zygapophyseal (facet) joint

1. How is the facet jt formed?
2. Where is the facet jt located?
3. What is the function of facet jts?

Answers:
1. Between the superior and inferior articular processes.
2. AA and OA have no true face joints. C3-T12 in frontal plane. Lumbar facets begin in sagittal plane and progresses to frontal plane at L5-S1.
3. Direct vertebral motion, resist shearing and rotational forces. There is increased weightbearing with extension.

Sacral and coccygeal vertebrae

1. What is the sacrum?
2. What is lumbarization?
3. What are characteristics of the coccyx?

Answers:
1. Triangular bone consisting of five fused vertebrae.
2. Non-union of the first and second segment of the sacrum, forming an L6.
3. 3-4 fused segments with transverse processes, hiatus, and cornua.

Thoracic and lumbar vertebrae

1. What makes up the anterior potion of the thoracic and lumbar vertebrae?
2. What makes up the posterior portion of the thoracic and lumbar vertebrae?
3. What is sacralization?
4. What is the 3-joint complex formed by the two lumbar vertebrae?

Answers:
1. Vertebral bodies (with articulations for the ribs on the thoracic vertebrae).
2. Pedicles, superior and inferior articular processes, laminae, transverse processes, spinous processes.
3. Anomalous fusion of 5th lumbar vertebrae with sacrum.
4. First jt is between the 2 vertebral bodies, other 2 joints are zygapophyseal (facet) jts between the articular processes.

Cervical vertebrae

1. What is the uncinate processes of the C3-C7 vertebrae? What is a Joint of Luschka?
2. What are the posterior aspects of the C3-C7 vertebrae?
3. What are unique characteristics of the C1 vertebra?
4. What are unique characteristics of the C2 vertebra?

Answers:
1. Superior projection of the lateral aspect of the vertebral body. The joint of Luschka (uncovertebral jt) is formed when the disk becomes degenerative and approximates with the body of the next higher vertebrae.
2. Pedicles, superior and inferior articular processes, laminae, transverse processes, foramen transversarium and spinous processes (bifid except for C7).
3. Ring shaped, no vertebral body or spinous process.
4. Odontoid process on vertebral body, bifid spinous process.

Intro to Spine

1. What is the typical clinical course of lower back pain?
2. What symptoms are red flags for myelopathy?
3. What symptoms are red flags for cauda equina syndrome?
4. What symptoms are red flags for tumor?
5. What symptoms are red flags for infection?
6. What is the probability of returning to work based on time out from work?

Answers:
1. 50% resolve in 1-2 weeks, 90% resolve in 6-12 weeks, 85% recur within 1-2 years.
2. Gait ataxia, UMN changes.
3. Bowel/bladder or sexual dysfunction.
4. Night pain, weight loss.
5. Fever or chills.
6. After 6 months, there is a 50% chance of return. After 1 year, there is a 25% chance of return. After 2 years, there is a 0% chance of return.

Spinal muscle atrophy

1. What is the inheritance pattern of SMA?
2. What is the onset and course of the different types of SMA?
3. What is the presentation of SMA type I?
4. What is the presentation of SMA type II?
5. What is the presentation of SMA type III?
6. What is seen on labs and muscle biopsy?

Answers:
1. Autosomal recessive (sometimes dominant with type III).
2. Type I has onset 3-6 months and death by 2-3 years (resp failure). Type II has onset at 2-12 months, wheelchair by 2-3 years, and death by age 10. Type III has onset 2-15 years, WC by 30 years, normal life expectancy.
3. Floppy baby, absent MSR, weak cry, tongue fasciculation, EOMI, facial muscles least affected, never sits independently.
4. Floppy baby, kyphoscoliosis, independent sitting, assistance for standing and walking.
5. Symmetric weakness, lower limb more than upper, Gower's sign, calf pseudohypertrophy, dysphagia, dysarthria, tongue fascic, normal intelligence, independent standing/walking.
6. Blood shows incr CPK. Muscle biopsy shows hyper/atrophic fibers.

Poliomyelitis

1. What is the pathology behind polio?
2. What is the clinical presentation of polio?
3. What is the pathology behind post-polio syndrome? What are the symptoms?
4. What is the Halstead-Ross criteria for post-polio?
5. What is seen on EMG in polio and post-polio?
6. What is the treatment of post-polio?

Answers:
1. Degeneration of anterior horn cells.
2. Weakness, absent MSR, bulbar palsies, spared sensation.
3. Death of motor neuron due to aging and increased metabolic demand. Symptoms include weakness, atrophy, fatigue, arthralgia, myalgia, cold intolerance.
4. 1) H/o polio, 2) recovery of function, 3) stable for 15 years, 4) return of symptoms, 5) no other explanation for new symptoms.
5. Post-polio resembles old polio on EMG. There is abnormal activity, decr recruitment, and giant MUAPs.
6. Rehab, assistive devices, energy conservation. Avoid fatigue.

Amyotrophic lateral sclerosis

1. What is the pathology behind ALS?
2. What is the clinical presentation of ALS?
3. What are predictors of poor survival?
4. What are the EMG findings of ALS?

Answers:
1. Degeneration of anterior horn cells.
2. Asymmetric atrophy, weakness, fasciculations, dysphagia, dysarthria, pseudobulbar signs (crying, laughing), sensation spared, EOMI, upper and lower motor neuron signs, B/B spared.
3. Older age, worse severity at onset, poor pulmonary function.
4. SNAP and CMAP normal. EMG showing abn activity in 2 muscles from 2 different nerve roots in 3 different body regions (brainstem, cervical, thoracic, lumbar), increased jitter and fiber density.

Motor neuron disease

1. What are examples of UMN lesions? LMN? Mixed?
2. What are UMN signs?
3. What are LMN signs?
4. In which motor neuron diseases are fibs and PSWs seen?
5. In which motor neuron diseases are fasciculations seen?
6. In which motor neuron diseases are CRDs seen?

Answers:
1. UMN: primary lateral sclerosis. LMN: polio, spinal muscle atrophy. Mixed: ALS.
2. Weakness, spasticity, hyperreflexia, upgoing toes.
3. Atrophy, flaccidity, hyporeflexia, fasciculations.
4. SMA I-III, ALS, polio.
5. ALS, polio.
6. SMA type III.

Steroid myopathy

1. When does steroid myopathy usually start?
2. What is the clinical presentation of steroid myopathy?
3. What does muscle biopsy show?
4. What are the EMG findings?

Answers:
1. Weeks or years after steroid use.
2. Proximal muscle weakness.
3. Type II atrophy.
4. Normal.

Inflammatory myopathies

1. What is the clinical presentation of polymyositis?
2. What skin manifestations are seen in dermatomyositis?
3. What is the clinical presentation of inclusion body myositis?
4. What is seen on muscle biopsy in the inflammatory myopathies?
5. What is seen on EMG in polymyositis?

Answers:
1. Symmetrical proximal weakness, neck flexion weakness, myalgia, dysphagia, dysphonia, no facial or ocular weakness.
2. Periorbital violet rash and edema, Gottron's sign (red-purple patches over knuckles/knees).
3. Asymmetric, slowly progressive painless weakness both prox and distal.
4. Polymyositis bx shows necrosis of type I and II fibers and perifascicular atrophy. Inclusion body myositis bx shows rimmed or cytoplasmic/basophilic vacuoles, and eosinophilic inclusion bodies.
5. CMAP and SNAP normal. EMG shows abnormal activity (most common in paraspinals), early recruit, short duration small amp MUAPs.

Muscular dystrophies

1. What is the inheritance of Duchenne's/Becker's MD?
2. What is the clinical presentation of MD?
3. What is seen on muscle biopsy and labs in MD?
4. What is the presentation of myotonic dystrophy?

Answers:
1. X-linked.
2. Prox muscle weakness, calf pseudohypertrophy, cardiomyopathy, mental retardation, Gower's sign, increased lumbar lordosis, abnormal MSR.
3. Biopsy shows no dystrophin (Duchenne) or decreased (Becker). Increased CPK.
4. Autosomal dominant, presents as infant. Distal weakness, hatchet face (wasting of temporalis and masseter), frontal balding, poor vision, hypertrichosis, mental retardation. Biopsy shows type I fiber atrophy and type II fiber hypertrophy.

Myopathy

1. What are seven different categories of myopathy?
2. What is the clinical presentation of myopathy?
3. What is seen on EMG in myopathy?
4. What is the utility of quantitative EMG for myopathy?
5. What is seen with rep stim and SFEMG in myopathy?
6. Which disorders show Type II fiber atrophy on biopsy?

Answers:
1. Dystrophic (Duchenne, Becker), congenital, metabolic (acid maltase deficiency), inflammatory (polymyositis, dermatomyositis), endocrine (thyroid, adrenal), toxic (alcohol, diuretics, vincristine), steroids.
2. Muscle atrophy, hypertrophy, abnormal MSR, weakness, hypotonia, gait abnormalities, or myotonia (painless delayed relaxation of muscles).
3. SNAP normal, CMAP low amplitude, EMG may show fibs, PSW, CRD, or myotonic discharges. Classic MUAPs are small duration, small amplitude due to loss of muscle fibers, but collateral sprouting may result in long duration large amplitude MUAPs. MUAPs may be unstable at the beginning of sprouting.
4. Used to calculate mean duration by using 20 MUAPs.
5. Rep stim may show a decremental response due to reduced safety factor in regenerating immature NMJs. SFEMG shows increased jitter, fiber density, and blocking.
6. Steroid myopathy, myasthenia gravis, deconditioning.

Single fiber EMG

1. When is SFEMG used?
2. What sorts of diseases cause SFEMG to be abnormal?
3. What is fiber density? What is normal density?
4. What is jitter? What is normal?
5. What is blocking? How long does it take to resolve?

Answers:
1. If rep stim of at least three muscles is normal and abnormal diagnosis is still suspected.
2. NMJ disorders, MND, peripheral neuropathy.
3. Represents the number of single fibers belonging to the same motor unit within the recording radius of the electrode. A density of 1.5 is normal, higher represents denervation and reinnervation.
4. Small variation between the interpotential discharges of two muscle fibers of the same motor unit. Normal is 10-60 u.
5. Abnormality that occurs when a single muscle fiber AP fails to appear, which occurs with jitter > 100 u. Resolves in 1-3 months, after reinnervation is completed.

High rate repetitive stimulation

1. What is the rate for HRRS? Is there any substitute for this?
2. What is the effect of HRRS?
3. What occurs as a result of HRRS in MG, LEMS, and botulism?
4. What is pseudofacilitation?

Answers:
1. 10-50Hz. May substitute maximal isometric contraction.
2. Accumulation of calcium in the cell.
3. MG shows a decrement, LEMS shows a 200-300% increment, and botulism shows a mild increment.
4. Pseudofacilitation is the progressive increase in CMAP amplitude with HRRS or voluntary contration in a normal patient, which results from synchronicity of muscle fibers (decreased temporal dispersion).

Post-activation facilitation and exhaustion

1. What is post-activation facilitation? When is it performed?
2. What is post-activation exhaustion? When is this test performed?

Answer:
1. PAF is a 10 second isometric contraction (or tetany-producting stim of 50 Hz) that is done if decrement is noted on LRRS.
2. Response seen as CMAP amplitude decreases, which occurs with a LRRS performed every minute for 5 mins after initial isometric contraction. This test should be used if there is no decrement with LRRS, but a neuromusc junction disorder is still suspected.

Repetitive nerve stimulation

1. What muscles are stimulated in repetitive stim?
2. What decrease in amplitude is significant?
3. What rate is used for low rate repetitive stim (LRRS)?
4. What happens if the safety factor is decreased in LRRS?
5. What is the amplitude change for LRRS in MG, LEMS, and botulism.

Answers:
1. ADM/APB, deltoid, trapezius, orbicularis oculi.
2. Greater than 10% decrease from 1st to 5th waveform.
3. 2-3 Hz.
4. Each stimulus causes the EPP amplitude to drop, so a reduced safety factor will result in the potential falling below the threshold for activation --> reduced MUAP amplitude.
5. All three disorders result in a >10% drop in amplitude.

Botulism

1. What is the mechanism behind botulism?
2. When does botulism occur after ingestion?
3. What is the presentation of botulism?
4. What does EMG show?
5. What is the treatment for botulism?

Answers:
1. Toxin blocks exocystosis of ACh from nerve terminal.
2. Begins 2-7 days after ingestion.
3. Bulbar symptoms first (ptosis, dysphagia, dysarthria), diarrhea, N/V, widespread paralysis or flaccidity, abnormal MSR, respiratory and cardiac dysfunction.
4. SNAP normal, CMAP reduced amplitude, unstable MUAP.
5. Trivalent ABE antitoxin, wait for collateral sprouting.

Lambert-Eaton Syndrome

1. What is the mechanism behind LES?
2. What is the presentation of LES?
3. What does muscle biopsy show?
4. What are the EMG findings in LES?
5. What is the treatment of LES?

Answers:
1. Autoimmune attack on the presynaptic membrane, decreasing Ca entry into the cell and decreased release of ACh. Associated with small cell lung cancer.
2. Proximal fatigue and weakness, LE>UE, abnormal MSR, exacerbated with rest and improved with exercise, rarely involves neck or face or bulbar.
3. Overdevelopment of neuromuscular junction.
4. Normal SNAP, low amp CMAP, unstable MUAP.
5. Treat underlying malignancy, corticosteroids, immunosuppression, plasmapheresis, guanidine (incr ACh quanta).

Myasthenia gravis

1. What is the etiology of MG?
2. What is the presentation of MG?
3. How is it diagnosed?
4. What are the findings on standard EMG for MG?
5. What is the treatment of MG?

Answers:
1. Autoimmune response to the ACh receptors on the post-synaptic membrane. Often associated with thymic disorder.
2. Proximal fatigue and weakness, exacerbated by exercise, heat, or later in the day, improved with rest. Normal MSR. Ptosis, diplopia, dysphagia, dysarthria.
3. Tensilon test: 2mg of edrophonium followed by 8mg dose, improvement in 1 min. Muscle bx shows loss of postsyn junction folds and receptors. Blood shows anti-ACh receptor ab.
4. SNAP and CMAP are normal. EMG shows unstable MUAP.
5. Thymectomy, anticholinesterase drugs, corticosteroids, immunosuppressive agents, plasmapheresis. 1/3 improve spontaneously.

HIV neuropathy

1. What are the 5 major categories of HIV neuropathy?
2. Is HIV demyelinating or axonal?
3. What does the EMG show?

Answers:
1. Distal symmetric polyneuropathy (most common), inflammatory demyelinating polyneuropathy, mononeuropathy multiplex, progressive polyradiculopathy, autonomic neuropathy.
2. Both.
3. CMAP, SNAP, and EMG are abnormal.

Diabetic neuropathy

1. What is the presentation of diabetic neuropathy? What sort of neuropathy is it?
2. What is seen on nerve biopsy?
3. What is seen on EMG?

Answers:
1. Like uremia, this is a mixed axonal/demyelinating neuropathy. It presents with sensory abnormalities.
2. Small and large fiber abnormalities.
3. SNAP, CMAP, and EMG all abnormal.

Alcoholic neuropathy

1. What is the presentation of alcoholic neuropathy?
2. What does nerve biopsy show?
3. What does EMG show?
4. What is the treatment?

Answers:
1. Sensory abnormalities, foot or wrist drop, muscle spasms, Korsakoff's/Wernicke's syndrome. May be associated with a myopathy.
2. Wallerian degeneration.
3. SNAP and CMAP abnormal. EMG shows abnormal activity.
4. Vitamins, diet, stop alcohol, orthotics.

Friedreich's ataxia

1. What is the inheritance of Friedreich's ataxia?
2. What is the onset time?
3. What are the characteristics of Friedreich's ataxia?
4. What does nerve biopsy show? What does EMG show?
5. What is the prognosis?

Answers:
1. Autosomal recessive
2. 2-16 years.
3. Abnormal sensation and weakness, abnormal MSR, ataxia, optic atrophy, kyphoscoliosis, dysarthria, pes cavus, cardiomyopathy.
4. Nerve bx shows abnormal large axons. SNAP is abnormal, CMAP is normal, with EMG showing abnormal acitivity.
5. WC use by age 16.

Charcot-Marie-Tooth (CMT)

1. What is the presentation of Hereditary Motor Sensory Neuropathy I (HMSN-I, Charcot-Marie-Tooth)?
2. What are the lab findings in CMT?
3. What are the EMG findings in CMT?
4. What is the treatment for CMT?

Answers:
1. CMT is an autosomal dominant disease that presents in early childhood. It is slowly progressive and sensory loss is more apparent in LEs than UEs, there is abnormal vibration and proprioception, intrinsic foot atrophy resulting in pes cavus and hammer toes, bilateral foot drop resulting in steppage gait, stork leg appearance, and essential tremor.
2. CSF has increased protein. Nerve biopsy shows onion bulb formation.
3. SNAP is abnormal. CMAP is abnormal with CV less than 70% of normal. EMG may be normal or show signs of reinnervation.
4. Treatment is rehab and orthotics.

Peripheral neuropathy

1. What are the demyelinating polyneuropathies?
2. What are the axonal polyneuropathies? Of these, which have sensory and which have motor findings?
3. What polyneuropathies have both demyelination and axonal loss?

Answers:
1. HMSN-I, III, IV (e.g. Charcot-Marie-Tooth), leukodystrophy, AIDP, CIDP, arsenic, toxins, monoclonal gammopathy, diphtheria, AIDS, leprosy, Lyme disease.
2. Motor: porphyria, vincristine, lead, Dapsone, HMSN-II. Sensory: cisplatinum, Freidreich's ataxia, HSN, Sjogren's, pyridoxine, Crohn's. Sensorimotor: amyloidosis, EtOH, Vit B12, folate, toxins, gold, mercury, paraneoplastic syndrome, sarcoid, Lyme, HIV.
3. DM, uremia.

Finger fractures

1. What is a Bennet's fracture?
2. What is a Rolando's fracture?
3. What is a Boxer's fracture?
4. What is the treatment for finger fracture?

Answers:
1. Oblique fracture or subluxation at the base of the thumb metacarpal.
2. T, Y, or comminuted fracture at the base of the thumb metacarpal.
3. Fracture of metacarpal neck/shaft, often from punching, most commonly seen in 5th digit.
4. Orthopedic referral.

Mallet finger

1. What is the mechanism of mallet finger?
2. What are the symptoms?
3. What is the treatment of mallet finger?

Answers:
1. Sudden passive DIP flexion with finger extended, causing extensor tendon rupture.
2. Flexed DIP joint that can't be actively extended, tenderness and edema in the distal dorsal area.
3. Splinting of DIP in extension for 6-8 wks, followed by 2-4 wks of gentle active flexion with night splinting. Surgical repair if there is poor healing or if there is an avulsed fragment involving > 1/3 of the joint.

Flexor digitorum injury

1. What are causes of flexor digitorum injury (Jersey finger)?
2. What is seen clinically in flexor digitorum injury?
3. What may be seen on imaging?
4. What is the treatment?

Answers:
1. Injury to the FDP or FDS may occur spontaneously in RA or trauma (finger gets caught in the jersey of another player when attempting to grab him.
2. Inability to actively flex DIP.
3. Plain film may show avulsed fragment near tendon insertion.
4. Early surgical repair.

Ligamentous injuries

1. How is the collateral ligament of the finger injured?
2. How is the volar plate injured?
3. How is the ulnar collateral ligament injured (Gamekeepers thumb, Skier's thumb)?
4. What is the treatment of ligamentous injury of the fingers?

Answers:
1. Valgus or varus stress of extended finger.
2. Hyperextension with dorsal dislocation.
3. Valgus stress of thumb at MCP jt.
4. Conservative treatment involves reduction, buddy splinting for 2wks and thumb spica splint for 3-6wks for MCP injury. Surgery for complex lesions.

Trigger finger (Stenosing tenosynovitis)

1. What is the mechanism of trigger finger?
2. What are predisposing factors for trigger finger?
3. What is seen clinically?
4. What is the treatment?

Answers:
1. Repetitive trauma resulting in inflammation of flexor tendon sheaths of digits, resulting in a nodule in the tendon and abnormal glide. This nodule gets caught on the annular sheath.
2. Repetitive trauma, DM, RA, >40yrs.
3. Catching or locking with finger flexion. Palpable nodule.
4. Immobilization by splinting, NSAIDs, steroid injection. Surgical release if conservative treatment fails.

Dupuytren's contracture

1. What is the mechanism of Dupuytren's contractures?
2. What factors predispose to Dupuytren's contractures?
3. What is seen clinically?
4. What is the treatment?

Answers:
1. Thickening of the palmar fascia due to fibrous proliferation.
2. Genetics (Northern Europeans), DM, EtOH, epilepsy, pulmonary TB, men > 40.
3. Painless nodules in distal palmar crease, initially nontender but may become tender. Involved finger may be drawn into flexion.
4. US, splinting, massage, possible surgical release if severe.

Scaphoid fracture

1. What is the usual mechaism of a scaphoid fx?
2. What are complications of a scaphoid fx?
3. How are scaphoid fx's classified?
4. What is seen clinically in scaphoid fx?
5. What are the borders of the anatomical snuff box?
6. What imaging is done to assess scaphoid fx?
7. What is the treatment of scaphoid fx?

Answers:
1. Fall on dorsiflexed wrist.
2. Osteonecrosis due to poor blood supply (supply is mainly to the distal 1/3 of bone) with carpal collapse.
3. By location: tubercle, distal pole, waist, proximal pole.
4. Swelling and tenderness around anatomical snuff box.
5. Base is scaphoid bone, lateral is APL and EPB, medial is EPL.
6. Plain films in ulnar deviation.
7. Fx may not appear on X-ray so treat anyway if suspicioius. If nondisplaced (<2mm),>2mm or not healing, need to consider surgery.

Distal radius fracture

1. What is the most common type of distal radius fracture?
2. What are other types of distal radius fracture?
3. What is the usual mechanism of distal radius fx?
4. What is the treatment of distal radius fx?

Answers:
1. Colles fx: fracture of distal radius with DORSAL angulation.
2. Smith's fx: fx of distal radius with VOLAR angulation (reverse Colles).
3. Fall on an outstretched arm.
4. Ortho referral for closed reduction.

Osteonecrosis of the lunate

1. What is another name of osteonecrosis of the lunate?
2. What is osteonecrosis of the lunate? What are predisposing factors?
3. What is seen clinically?
4. What imaging is used for diagnosis?
5. What is the treatment?

Answers:
1. Klenbock's disease.
2. Idiopathic loss of blood supply to lunate, causing necrosis of the bone and degenerative changes. Etiology is likely repetitive trauma or possibly short ulna.
3. Ulnar sided pain and swelling over dorsal wrist, reduced grip strength.
4. Plain films may show fracture/flattening/sclerosis of lunate, bone scan, MRI.
5. Ortho referral.

Ganglion cyst of the wrist

1. What is a ganglion cyst?
2. What is seen clinically?
3. What is the treatment?

Answers:
1. Cyst that arises from the synovial sheath of the joint and is filled with synovial fluid.
2. Small smooth mass, pain with pressure or ranging of wrist.
3. Immobilization, aspiration of cyst (90% recur), surgical removal (10% recur).

DeQuervain's tenosynovitis

1. What is the mechanism of DeQuervain's?
2. What is seen clinically?
3. What is Finkelstein's test?
4. What is the treatment of DeQuervain's?

Answers:
1. Repetitive or direct trauma to the sheath of the EPB and APL (first extensor compartment of the wrist).
2. Pain and tenderness on the radial side of the wrist.
3. Flex thumb into palm of hand, making a fist, while examiner ulnarly deviates the wrist. Pain is positive.
4. Thumb spica splint, NSAIDs, steroid injection. ?Surgery.

Arthritis of the wrist

1. What are two different kinds of arthritis that affect the wrist?
2. What is seen clinically in Rheumatoid arthritis?
3. What is a swan-neck deformity?
4. What is Boutonniere's deformity?
5. What is seen clinically in osteoarthritis?
6. Where is wrist osteoarthritis most common?

Answers:
1. Rheumatoid arthritis (autoimmune attack on synovial tissue, which destroys the articular cartilage and leads to bone destruction) and osteoarthritis (deterioration of articular cartilage and formation of new bone at joint margins).
2. Swelling of the wrists, MCP and PIP, ulnar deviation of the wrist, dorsal subluxation of the ulna, erosion of the ulnar styloid.
3. Contracture of hand intrinsics, resulting in MCP flexion, PIP hyperextension, DIP flexion.
4. Tearing of the extensor hood, resulting in MCP hyperextension, PIP flexion, and DIP hyperextension.
5. Heberden's (DIP) and Bouchard's (PIP) nodules, tenderness along the area of involvement and crepitus of the wrist, cyst formation in the joint space.
6. First CMC joint.

Wrist anatomy

1. What are the carpal bones?
2. What are the wrist flexors?
3. What are the wrist extensors?
4. How many extensor compartments are there in the wrist?

Answers:
1. Proximal: Scaphoid, Lunate, Triquetrum, Pisiform; Distal: Trapezium, Trapezoid, Capitate, Hamate. (Some Lovers Try Positions That They Can't Handle)
2. FCR, FCU, palmaris longus, FDS, FDP, FPL.
3. ECRL, ECRB, ECU, extensor digitorum, EDM, EIP, EPL.
4. Six.

Olecranon fracture

1. How does an olecranon fracture usually occur?
2. What is a possible complication of olecranon fx?
3. How is an olecranon fx treated?

Answers:
1. Direct blow to elbow, fall on elbow with elbow flexed, or fall on outstretched arm.
2. Ulnar nerve involvement.
3. Nondisplaced fractures are immobilized. Displaced fractures are treated surgically.

Radial head fracture

1. What sort of elbow injury often is associated with radial head fractures?
2. How does a radial head fx usually occur?
3. How many types of radial head fx's are there? How are they treated?

Answers:
1. Elbow dislocation.
2. Fall on outstretched arm.
3. Type I (nondisplaced) is treated with short immobilization (3-5days) and early ROM. Type II (min displaced) is fixed surgically if there is greater than 2mm displacement or 30% radial head involvement. Type III (comminuted) is treated surgically.

Humeral fractures

1. What sort of nerve injury is associated with humeral shaft fracture?
2. How are humeral shaft fractures treated?
3. How are distal humerus fractures classified?
4. What are complications of a distal humerus fracture?
5. How is a distal humerus fracture treated?

Answers:
1. Radial nerve injury, 95% of which recover in 6 mo.
2. Splint for 2 wks.
3. Displaced or nondisplaced.
4. Neurovascular injury, nonunion, malunion, elbow contracture, poor ROM.
5. Displaced fractures require open reduction. Nondisplaced fractures can be splinted.

Osteochondrosis dissecans of the elbow

1. What is another name for OD of the elbow?
2. What is seen clinically?
3. What is seen on imaging?
4. What is the treatment?

Answers:
1. Panner's disease.
2. Tenderness and swelling in lateral elbow, limited extension on ROM, usually in young boys.
3. Plain films show sclerosis and patchy areas of lucency with fragmentation.
4. Immobilization, then gradual ROM.

Radial/Ulnar collateral ligament sprain

1. How does radial vs. ulnar collateral ligament sprain occur?
2. What is seen clinically in UCL sprain? How is it tested?
3. What is seen clinically in RCL sprain? How is it tested?
4. What imaging is used for UCL/RCL sprain?
5. How are collateral ligament sprains treated?

Answers:
1. UCL sprain occurs via valgus stress across elbow during a throw. RCL sprain occurs via traumatic elbow dislocation.
2. Medial elbow pain after a throw, pop or click, pain with valgus stress test (medial elbow tenderness, increased with valgus stress).
3. Recurrent locking or clicking of the elbow with extension and supination, pain with varus stress test (medial elbow tenderness, increased with varus stress). The lateral pivot-shift test is also used to assess the RCL for posterolateral instability.
4. Plain films, varus (RCL) and valgus (UCL) stress radiographs will show 2mm joint space.
5. Rest ice, NSAIDs, strengthening and stretching rehab, return to play criteria. Surgery if needed.

Distal biceps/triceps tendonitis

1. What is the mechanism of distal biceps/triceps tendonitis?
2. What is seen clinically in distal biceps tendonitis?
3. What is seen clinically in triceps tendonitis?
4. What is the treatment of biceps/triceps tendonitis?

Answers:
1. Repetitive overuse.
2. Insidious onset of pain in antecubital fossa, usually after eccentric overload. If avulsion, may be audible snap with obvious deformity, swelling, and ecchymosis.
3. Posterior elbow pain with tenderness over triceps insertion, pain with resisted elbow extension.
4. Rest, ice, NSAIDs, PT with modalities, possible surgical reattachment for avulsion.

Elbow dislocation

1. What is the mechanism of elbow dislocation?
2. What is seen clinically with elbow dislocation?
3. What are other injuries associated with elbow dislocation?
4. What is the treatment for elbow dislocation?
5. What are possible adverse outcomes?

Answers:
1. Fall on outstretched hand. Posterior dislocation is more likely.
2. Inability to bend elbow, pain in shoulder/wrist. On PE, do careful neurovasc eval.
3. Fracture of radial head, median nerve injury, brachial artery injury.
4. Reduction, splint for 10 days, then ROM and NSAIDs.
5. Loss of ROM (esp extension), ectopic bone formation, neurovasc injury, arthritis.

Olecranon bursitis

1. What are other names for olecranon bursitis?
2. What is the mechanism and pathology of olecranon bursitis?
3. What is seen clinically with olecranon bursitis?
4. What is the treatment of olecranon bursitis?

Answers:
1. Draftsman's elbow, Student's elbow, Miner's elbow.
2. Repetitive trauma or inflammatory disorder, resulting in inflammation of the bursa between the olecranon and skin.
3. Swelling, pain, decreased ROM. If hot, there may be infection.
4. Aspiration and culture, rest, NSAIDs, elbow padding.

Lateral Epicondylitis

1. What are some factors that cause lateral epicondylitis (LE)?
2. What is the pathology behind LE?
3. What are the clinical history of LE?
4. What is Cozen's test?
5. Why might X-rays be obtained?
6. What is the treatment for LE?

Answers:
1. Any repetitive sport (e.g. tennis) especially when poor techniques are used with a racket sport (inproper backhand, weak string tension, inappropriate grip size), overuse and poor mechanics.
2. Microtearing of the extensor carpi radialis brevis.
3. Patients c/o tenderness just distal to the LE at the ECR origin, pain and weakness of grip.
4. Cozen's test is when the examiner stabilizes the elbow with a thumb over the LE and there is pain with a fist, forearm pronation, radial deviation, and wrist extension against resistance. There may also be pain with passive extension of elbow with forced wrist flexion.
5. Obtain X-rays if there is suspicion of arthritis or loose body fragments.
6. Conservative treatment includes rest, ice, NSAIDs for 10-14 days. If no improvement, may do PT, splinting, steroid injection, and correction of improper techniques. Surgical treatment of ECRB debridement can be considered.

Medial epicondylitis

1. What are other names for medial epicondylitis?
2. What is the mechanism of medial epicondylitis?
3. What is the difference between medial epicondylitis and little leaguer's elbow?
4. What is seen clinically in medial epicondylitis?
5. What is the treatment of medial epicondylitis?

Answers:
1. Golfer's elbow or little leaguers elbow.
2. Repetitive valgus stress such as in throwing or a back and downward swing such is in golfing.
3. Medial epicondylitis involves inflammation of the common flexor tendon, which may cause hypertrophy of the medial epicondyle. Little leaguer's elbow involves hypertrophy of the medial epicondyle, leading to microtearing and fragmentation of the medial epicondylar apophysis.
4. Tenderness at medial epicondyle that can be reproduced with wrist flexion and pronation.
5. Conservative treatment includes rest, ice, NSAIDs, immobilization, and correction of throwing mechanics. Surgical pinning can be used for unstable elbow.

Elbow anatomy

1. What are the three ligaments of the elbow?
2. What muscles originate at the medial epicondyle?
3. What muscles originate at the lateral epicondyle?
4. What is the normal amount of elbow valgus?

Answers:
1. Medial (ulnar) collateral ligament (key stabilizer of elbow), lateral (radial) collateral ligament, annular ligament.
2. Medial epicondyle: FCR, FCU, FDS, FDP, palmaris longus, pronator teres.
3. Lateral epicondyle: ECRL, ECRB, ECU, EDS, supinator, anconeus.
4. 5 deg in males, 10-15 deg in females, >20 deg is abnormal.

Foot fractures

1. What is a Jones fracture and what is the treatment?
2. What is a Nutcracker fracture and what is the treatment?
3. What is a March fracture and what is the treatment?

Answers:
1. A Jones fx is a transverse fx through the base of the 5th metatarsal. It is treated with NWB cast for 6 weeks and ORIF if nonunion occurs.
2. A Nutcracker fx is a cuboid fx, treated with ORIF.
3. A March fx is a fatigue fx of one of the metatarsals, treated with cast.

Lisfranc joint injury

1. What is a Lisfranc joint injury?
2. How does a Lisfranc injury occur?
3. What is seen clinically with a Lisfranc injury?
4. What is the treatment of a Lisfranc injury?

Answers:
1. Traumatic disruption of tarsometatarsal joints.
2. Direct trauma vs. force applied to heel in line with axis of foot with toes flexed.
3. Vague ankle pain, swelling in dorsum of foot, which is exacerbated by stabilizing the hind foot and rotating the forefoot.
4. If nondisplaced: NWB, immobilization for 6-8 wks. If displaced, surgery is needed.

Toe deformities

1. What is hammer toe? What are the symptoms and treatment?
2. What is claw toe? What are the causes of claw toe? What are the symptoms and treatment?
3. What is mallet toe? What are the symptoms and treatment?

Answers:
1. Hammer toe is a deformity of the lesser toes in which there is flexion of PIP with passive extension of MTP when foot is flat. DIP is not affected. May be caused by tight shoes or trauma. Symptoms include pain in toe. Treatment is toes with roomy toe boxes, 1/2 inch longer than longest toe, and passive strengthening of toes.
2. Claw toe is extension of MTP with flexion of PIP and DIP. Usually caused by incompetence of foot intrinsics, such as from neurologic disorders (diabetes, alcoholism, peripheral neuropathy, Charcot-Marie-Tooth, spinal cord tumors). The main symptom is pain. Treatment includes shoes with soft, high toe boxes, splints, possible surgical correction.
3. Mallet toe is flexion deformity at DIP jt with normal alignment at the PIP and MTP. This is usually caused by jamming injury or tight shoes. Symptoms include pain and callous at the tip of the toe. Treatment includes shoes with high toe boxes and trimming of callous.

Hallux disorders

1. What is a metatarsal phalangeal (MTP) sprain? What are the symptoms?
2. What is hallux valgus?
3. What is hallux rigidus? What are the symptoms?
4. What are the treatment for hallux disorders?

Answers:
1. Acute injury to the ligaments and capsule of the MTP joint, also called "turf toe". Symptoms include acute onset of pain, tenderness, swelling in MTP jt on plantar surface, with pain on passive DF.
2. Lateral deviation of the first toe greater than the normal ankle of 15 degrees, which may lead to bunion.
3. Degeneration of first MTP jt, leading to pain and stiffness (arthritis). Symptoms include pain, swelling, and decreased ROM of MTP jt.
4. RICE, taping, proper footwear. For rigidus, may require surgical debridement.

Morton's neuroma

1. What is a Morton's neuroma?
2. Where is a Morton's neuroma usually located?
3. What is seen clinically in Morton's neuroma? On exam?
4. What is the treatment of Morton's neuroma?

Answers:
1. Irritation and degeneration of the digital nerves in the toes resulting in fibrosis, producing a painful mass near the area of the metatarsal heads.
2. Between 2nd and 3rd, or 3rd and 4th digits.
3. Sharp shooting forefoot pain, commonly with dysesthesia and numbness. Test by squeezing the metatarsal heads together while applying pressure to the interdigit webspace --> pain in plantar webspace is positive.
4. Shoes with soft sole and wide toe box, metatarsal pad, steroid injection. Surgical excision if indicated.

Plantar fasciitis

1. What factors predispose to plantar fasciitis?
2. What are the clinical symptoms of plantar fasciitis?
3. What is the treatment of plantar fasciitis?

Answers:
1. Pes cavus, pes planus, obesity, tight Achilles, HLA-B27, seronegative spondyloarthropathy, ?heel spurs.
2. Tenderness over medial heel and plantar fascia that increases on awakening and decreases with activity.
3. Heel pads, cushion, lift, Achilles and plantar fascia stretching, modalities, NSAIDs, night splints in DF.

Talar dome fracture

1. How does a talar dome fracture occur?
2. What is the Hawkins classification of talar dome fractures?
3. What are complications of talar dome fracture?
4. What is seen clinically in talar dome fracture?
5. What imaging is required to diagnose talar dome fracture?
6. What is the treatment?

Answers:
1. Shear force on anterior lateral surface of talus or compression on posterior medial surface. (Inversion/PF or Eversion/DF)
2. 3 types: type 1 is a nondisplaced fx of talar neck, type 2 is a displaced fx of talar neck with ankle joint intact, type 3 is a displaced fx of talar neck with dislocation of body of talus from subtalar and ankle joints.
3. Avascular necrosis of talar body, displaced bone fragment into joint space.
4. Small painful effusion, decreased ROM in the setting of chronic ankle injury.
5. Mortise view of ankle, MRI.
6. Conservative tx is NWB. Surgical ORIF if indicated.

Tibialis anterior hyperactivity

1. What sort of deformity is caused by tibialis anterior hyperactivity?
2. What sort of patients is tibialis anterior hyperactivity seen in?
3. How is tibialis anterior hyperactivity treated?

Answers:
1. Equinovarus deformity, with Achilles shortening.
2. CP, CVA, TBI.
3. SPLATT: Split Anterior Tibial Tendon Transfer. Half of tendon is attached to site of origin while distal end of lateral half is tunneled into the 3rd cuneiform and cuboid bones, creating an eversion force. Procedure often done with Achilles lengthening.

Tibialis anterior tendon injury

1. How is the TA often injured?
2. What is seen clinically with TA injury?
3. What is the treatment of TA injury?

Answers:
1. Tenosynovitis, rupture (usually degenerative or from eccentric overload).
2. Pain along insertion at medial aspect of base of first metatarsal and first cuneiform, h/o chronic ankle pain, foot slap, increased pain with DF and passive PF.
3. Conservative vs. surgical, depending on age and level of function.

Sinus tarsi syndrome

1. What is the sinus tarsi?
2. What is the mechanism of sinus tarsi syndrome?
3. What is seen clinically in sinus tarsi syndrome?
4. What is the treatment of sinus tarsi syndrome?

Answers:
1. A small osseous canal which runs into the ankle under the talus bone.
2. Excessive foot pronation causing adduction of the talus, often with h/o arthritis or prior ankle injury.
3. Pain on the anterolateral aspect of the foot/ankle over the sinus tarsi, which resolves with injection of local anesthetic into the sinus tarsi.
4. Conservative treatment is the same as for ankle sprain, surgical treatment includes decompression of the tunnel.

Syndesmosis Sprain

1. What is the ankle syndesmosis?
2. How does a syndesmosis sprain occur?
3. What is the clinical picture of a syndesmosis sprain?
4. What imaging is required to diagnose a syndesmosis sprain?
5. What is the treatment of syndesmosis sprain?

Answers:
1. Fibrous joint keeping together tibia and fibula that maintains integrity of ankle, made up of four ligaments.
2. Hyperdorsiflexion and forceful eversion, or direct blow to foot with ankle in external rotation.
3. Chronic pain and swelling in anterior ankle. Positive squeeze test (tenderness on compression of distal tib-fib) and stress test (knee at 90 deg, ankle neutral, pain with forceful ext rot of foot).
4. Plain films to r/o tib-fib widening and r/o Maisonneuve fx (prox fibula fx resulting from ruptured anterior tibiofibular ligament).
5. Conservative treatment is usually used. Surgical treatment includes a screw to stabilize ankle mortise.

Retrocalcaneal bursitis

1. What is retrocalcaneal bursitis and who is it usually seen in?
2. What is the mechanism of developing retrocalcaneal bursitis?
3. What is Haglund's deformity?
4. What is Sever's disease?
5. What is seen clinically in retrocalcaneal bursitis?
6. What is the treatment of retrocalcaneal bursitis?

Answers:
1. Inflammation of the bursae between the superior calcaneus and distal Achilles or behind the Achilles. It is usually seen in women wearing high heeled shoes.
2. Repetitive pressure and shearing from shoes causing bursa inflammation.
3. Enlargement of posterosuperior tuberosity.
4. An independent area of ossification separated from main bone at cartilaginous plate, in young population.
5. Tenderness and swelling at the distal Achilles.
6. Change footwear. Surgical excision of bursae if this fails.

flexor hallucis longus injury

1. What is another name for FHL injury?
2. What is the origin and insertion of the FHL?
3. How is the FHL injured?
4. What are the symptoms of FHL injury?
5. What is the treatment of FHL injury?

Answers:
1. Dancer's tendonitis.
2. Origin is distal fibula and interosseous membrane. Insertion is base of distal phalanx of great toe.
3. It is injured by repetitive push-off maneuvers causing inflammation of the synovium.
4. Tenderness along tendon at the posteromedial aspect of great toe, increased with PF and passive DF.
5. Same tx as lateral ligament sprain.

Achilles tendon disorders

1. What is the mechanism of Achilles tendonitis/rupture?
2. What are the risk factors for Achilles injury?
3. How does Achilles tendonitis/rupture present?
4. What is the treatment of Achilles tendonitis?
5. What is the treatment of Achilles rupture?

Answers:
1. Tendonitis occurs by repetitive eccentric overload causing inflammation and microtears. Rupture occurs by sudden push-off with foot in extension position.
2. Hyperpronation, tight hamstrings and heel cords, pes cavus, genu varum, age, increase in mileage or intensity, change in footwear.
3. Tendonitis presents with posterior ankle pain, swelling, worse with push-off. Rupture presents with sudden audible snap with immediate swelling, ecchymosis and PF weakness, positive Thompson test.
4. Rest, ice, NSAIDs, short-term immobilization, stretching and strengthening, heel lifts, steroid injection near tendon.
5. Conservative treatment includes bracing in PF for 8-12 wks with gradual increase in activity. Surgery includes tendon repair with cast for 2 wks.

Tibialis posterior tendon injury

1. Where does the tibialis posterior originate and insert?
2. What is the function of the tibialis posterior?
3. How is the TP usually injured?
4. What is seen clinically in TP injury?
5. What is the treatment?

Answers:
1. Origin is interosseous membrane and posterior surface of tibia and fibula. Insertion is the tuberosity of the navicular cuboid and base of 2-4 metatarsals.
2. PF and inversion of foot, maintains medial longitudinal arch.
3. Injured by repetitive forceful inversion, often associated with an accessory navicular.
4. Insidious onset of posteromedial ankle pain, medial hindfoot swelling, increased pain with pushoff. If rupture, will have "too many toes" sign.
5. Treat same as lateral ankle sprain, may need orthotics. If rupture, may need tendon transfer.

Medial ankle sprain

1. What is the occurrence rate of a medial (deltoid) ankle sprain?
2. How do medial ankle sprains usually occur?
3. What are common complications?
4. What is seen clinically in a medial ankle sprain?
5. What is the treatment?

Answers:
1. 5%
2. Foot in pronated everted position with internal rotation of upper body (foot strikes ground instead of ball in soccer/football).
3. Syndesmosis ankle injuries, Maisonneuve fractures.
4. Medial foot swelling, ecchymosis, pain with eversion. Anterior drawer negative.
5. Same treatment as lateral ankle sprain.

Peroneal tendon injury

1. Where do the two peroneal tendons insert?
2. What is the function of the peroneus longus?
3. What is the mechanism of peroneal tendon injury?
4. What is seen clinically with peroneal tendon injury?
5. What is the treatment of peroneal tendon injury?

Answers:
1. Peroneus brevis: base of 5th metatarsal. Peroneus longus: base of 1st metatarsal.
2. Plantarflexes ankle and everts foot.
3. Rupture is caused by repetitive forceful eversion causing inflammation or degeneration. Dislocation can be caused by sudden DF, common in a skiing injury.
4. Swelling in retromalleolar area, sudden weakness with inability to evert foot. Provocative test is pain with resisted DF and eversion.
5. If just tenosynovitis, should be treated similarly to lateral ankle sprain. If rupture or dislocation, send for ortho eval.

Lateral ankle sprain

1. How does a lateral ankle sprain occur?
2. What is the function of the CFL?
3. What are two provocative tests used in ankle sprain?
4. What imaging should be done for ankle sprain?
5. What is the treatment of ankle sprain?

Answers:
1. Inversion of PF foot.
2. Stabilize ankle during inversion.
3. Anterior drawer to test integrity of ATFL, talar tilt to test integrity of CFL and ATFL.
4. X-rays, possible stress views (ant drawer, talar tilt).
5. For grades 1+2, RICE, NSAIDs, analgesics, early mobilization with ROM, strengthening, proprioception exercises, taping, bracing, and modalities. For grade 3, do a 6 month trial of rehab and bracing, then consider surgical ligament repair.

Ankle anatomy: ligaments

1. What are the ligaments of the lateral ankle?
2. What are the ligaments of the medial ankle?
3. What are the ligaments of the anterior ankle?
4. What is the Lisfranc ligament?

Answers:
1. Anterior talofibular ligament, posterior talofibular ligament, calcaneofibular ligament.
2. Deltoid ligament, which consists of 4 parts, broken down into deep and superficial.
3. The 4 syndesmotic ligaments maintain the integrity of the distal tibia and fibula: anterior tibiofibular ligament, posterior tibiofibular ligament, transverse tibiofibular ligament, and interosseous ligament.
4. Connects 2nd metatarsal head to 1st cuneiform.

Ankle anatomy: bones

1. Why does the talus often have healing complications?
2. What are the seven tarsal bones?
3. Where are the two sesamoid bones located?
4. What other bones are in the foot?

Answers:
1. Fragile blood supply.
2. Talus, calcaneus, navicular, cuboid, and three cuneiform bones.
3. Located on the plantar surface of the head of the first metatarsal.
4. 5 metatarsals and 14 phalanges.

Stress fractures

1. What is the most common location for a stress fracture in running sports?
2. What factors predispose to stress fractures?
3. What are the symptoms of stress fracture?
4. How is a stress fx diagnosed?
5. What is the treatment for stress fx?

Answers:
1. Tibia
2. Females with late menses, low body wt, poor nutrition, tobacco/alcohol use, low bone density, over-pronation (genu valgum), leg length discrepancy, lack of flexibility, abrupt increases in training intensity, running on hard surfaces or worn out shoes.
3. Pain at onset of activity that grows more severe, localized to fracture site. Night pain may occur. There is tenderness at fracture site, as well as possible swelling and redness.
4. Plain films should be done first, although the fx may not be seen for 2-3 wks after symptoms develop, appearing first as periosteal thickening, followed by cortical lucency. Bone scan is very sensitive but non-specific. MRI is now first line since it is sensitive and specific.
5. If there is pain with ambulation, pt should be NWB for 7-10 days. At least 1-2 wks of pain-free ambulation before returning to impact activity, which should be started cautiously and increased incrementally. Predisposing factors should be addressed.

Medial tibial stress syndrome

1. What is the pathophysiology behind shin splints?
2. What is the main predisposing factor to shin splints?
3. What is the presentation of shin splints?
4. What imaging is done for shin splints?
5. What is the treatment?

Answers:
1. Chronic traction on the periosteum at the periosteal-fascial junction, with possible detachment of periosteum from the bone. Avulsion may occur at the attachment of the soleus to the medial tibia.
2. Hyperpronation.
3. Gradual onset of pain at the posteromedial border of the tibia, which may decrease with exercise and increase after the exercise is completed. History may include excessive use of foot flexors or repetitive running on hard surfaces, recent footwear change. Exam shows tenderness on palpation along medial border of tibia.
4. Bone scan may show uptake along medial tibial border. MRI will r/o stress fx.
5. Rest with avoidance of inciting activity, icing, stretching, return to activity on soft level surfaces when pain free for several days. Orthotics for overpronation. Fasciotomy of posteromedial fascia.

Acute compartment syndrome

1. What happens in acute compartment syndrome (ACS) and what is the timeline?
2. What is the most common cause of ACS? What area is usually affected?
3. What are the complications of untreated ACS?
4. What are the symptoms of ACS?
5. How is ACS diagnosed?
6. How is ACS treated?

Answers:
1. Intracompartmental tissue pressure becomes elevated and venous pressure elevates to obstruct outflow. Necrosis can occur in 4-8 hrs.
2. Trauma associated with fractures of the long bones of the leg or forearm. It usually affects the volar forarm or anterior compartment of leg.
3. Volkmann's ischemic necrosis, which results in claw hand or foot caused by contractures of ischemic muscle.
4. Pain, paresthesias, and paralysis distal to the involved compartment. There is extreme pain on stretching of long muscles, but pulses are usually normal.
5. Manometry: diastolic pressure - intracompartmental pressure < 20 mmHg.
6. Fasciotomy.

Chronic exertional compartment syndrome

1. What occurs in CECS?
2. What are the clinical symptoms of CECS?
3. How is CECS diagnosed?
4. What is the best treatment for CECS?

Answers:
1. Pressure increases occur during and after exercise and nerve impingement and tissue ischemia can occur.
2. Pain with exercise that increases as the activity increases and diminishes after it stops. Weakness and numbness corresponds to the compartment being compressed (anterior and lateral CECS causes symptoms in deep peroneal distribution, deep posterior CECS in tibial nerve distribution). On palpation, the compartment may be firm and distal pulses may be diminished.
3. Compartment pressure studies measured pre and post exercise. A delay in return to pre-exercise pressure levels of 6-30 mins is required for diagnosis.
4. Fasciotomy.

Anatomy of the lower leg

1. What are the anterior muscles of the lower leg?
2. What are the lateral muscles of the lower leg?
3. What are the posterior muscles of the lower leg?
4. What are the four compartments of the lower leg?

Answers:
1. Dorsiflexors and extensors: tibialis anterior, EHL, EDL, and peroneus tertius.
2. Peroneus brevis and longus.
3. Gastronemius, plantaris, soleus, FDL, tibialis posterior, FHL, popliteus.
4. Anterior, lateral, deep posterior, and superficial posterior.

Osteochondritis dissecans

1. What is osteochondritis dissecans?
2. How does OD present?
3. How is it diagnosed?
4. What is the treatment?

Answers:
1. Localized area of avascular necrosis of end of long bone with degeneration of overlying cartilage, which may detach and enter joint space. Medial femoral condyle is most often affected.
2. Primarily seen in adolescents. Joint pain and irritation, synovial effusion, buckling, locking.
3. Radiographs, CT.
4. Rest, NWB on knee. If no healing or if fragment detaches, surgical excision may be required.

Jumper's knee

1. What is jumper's knee?
2. How does jumper's knee present?
3. How is jumper's knee treated?

Answers:
1. Patellar tendinitis associated with micro-tears of the tendon, associated with jumping, squatting and kneeling.
2. Pain on activity, worse after activity. Tenderness at inferior or superior pole of patella.
3. Same treatment of patellofemoral syndrome.

Plica

1. What is plica of the knee?
2. What is the presentation of plica?
3. How is plica diagnosed?
4. What is the treatment of plica?

Answers:
1. Plica is a redundant fold in the synovial lining of the knee, which is susceptible to tearing.
2. Insidious onset of anterior knee pain, especially with prolonged knee flexion or sitting. The plica can also become inflamed after knee trauma.
3. MRI, arthrogram, and arthroscopy.
4. Treatment same as for patellofemoral syndrome. Consider surgery if conservative measures fail.

Patellar chondromalacia

1. What is chondromalacia of the patella?
2. What predisposes to patellar chondromalacia?
3. What imaging should be ordered?
4. What is the treatment?

Answers:
1. Softening of the patellar articular cartilage, which is the culmination of cartilage degeneration.
2. Chronic patellofemoral overload and tracking dysfunction, infection, trauma, autoimmune processes.
3. CT or MRI may detect defects in articular cartilage of patella.
4. Correct abnormal patellar mechanics.

Patellofemoral pain

1. What is patellofemoral pain?
2. What is the presentation of patellofemoral syndrome?
3. What conditions predispose to PF syndrome?
4. What imaging is required for PF syndrome?
5. What is the nonsurgical treatment of PF syndrome?
6. What are surgical options for PF syndrome?

Answers:
1. Overuse injury caused by repeated microtrauma leading to peripatellar synovitis.
2. Presentation is as anterior knee pain w/wo effusion or crepitus, worse with stairs.
3. High riding, laterally shifted patella, which may be due to VL tightness and relative medial weakness, tight lateral retinaculum, rotation of patella, tight hip flexors or abductors or hamstrings, increased Q angle.
4. X-ray to assess patella position. MRI not useful, CT used if growth plate involvement or tumor is suspect.
5. Use ice and NSAIDs in acute phase, patellar taping and bracing, therapy including strengthening of VMO, stretching of hamstrings, IT band, adductors, and VL, proprioceptive exercises.
6. Surgical options are lateral release of retinaculum, patellar realignment, patellar tendon transfer, patellectomy. Consider surgery if no improvement after 4-6 mo.
7.

Recurrent patellar subluxation

1. What are factors that may predispose to patellar subluxation?
2. What are the signs and symptoms of patellar subluxation?
3. What imaging should be done to assess for subluxation?

Answers:
1. Less prominent lateral lip or more prominent medial lip, increased genu valgum/varus, excessive genu recurvatum, vastus medialis weakness, tibial external torsion, shallow lateral femoral condyle, laterally attached infrapatellar tendon.
2. Knee buckling, pain and tenderness in the peripatellar region, effusion, wasting of vastus medialis, impaired extension.
3. Lateral view in 45 degrees knee flexion and in full extension, sunrise view.

Hypermobility

Beighton criteria:

--1 pt: if you can bend place hands flat on floor without bending knees
--1 pt: for each knee that bends backwards
--1 pt: for each elbow that bends backwards
--1 pt: for each thumb that bends to touch the forearm
--1 pt: for each hand where you can bend the little finger back beyond 90 degrees

A score of 4 or greater indicates hypermobility.

Iliotibial band syndrome

1. Where does the ITB insert?
2. What is the presentation of ITB syndrome?
3. What is the treatment of ITB syndrome?

Answers:
1. On Gerdy's tubercle on the lateral tibia.
2. Pain over lateral femoral condyle, worse with running and walking.
3. Stretching of ITB, hip flexors, gluteus maximus, strengthening of hip abductors, gluetus maximus, and TFL. Injection for resistant cases.

MCL/LCL injuries

1. What is a common cause of MCL injury?
2. What are the exam findings of MCL injury?
3. What imaging is indicated for MCL injury?
4. What is the treatment of MCL injury?
5. How do LCL tears usually occur? How are they evaluated?

Answers:
1. MCL tears occur in football and skiing and are from force to the lateral knee.
2. Exam shows medial swelling and tenderness, minimal effusion, and medial instability.
3. Radiographs may show epiphyseal fracture. MRI delineates the MCL tear and evaluates the ACL and medial meniscus (O'Donaghue's triad).
4. Treat conservatively with knee bracing and strengthening.
5. LCL tears usually occur with knee dislocation. Patient with LCL tear should also be evaluated for associated vascular injury and cruciate and peroneal nerve injuries.

PCL injuries

1. How do PCL injuries often occur?
2. What is the history and physical exam findings for PCL injury?
3. What imaging is used to diagnose PCL injury?
4. What is the treatment of PCL tear?

Answers:
1. Most frequent cause is hitting the front of the tibia with the knee flexed (dashboard injury) or hyperflexion in athletes. Less common than ACL.
2. May be a pop, minimal swelling that increases over 24 hours. Exam shows popliteal tenderness, an effusion, positive posterior drawer and sag tests.
3. MRI less accurate than for ACL, arthroscopy more accurate than MRI.
4. Surgical repair if ligament is avulsed, quadriceps strengthening.

ACL injuries

1. What is the typical mechanism of ACL injury?
2. What is O'Donoghue's triad?
3. What are the symptoms of ACL injury? What are the physical exam findings?
4. What imaging is done for ACL injury?
5. What is the treatment of ACL injury?


Answers:
1. Cutting, deceleration, and hyperextension of the knee, often noncontact injury (football, soccer, downhill skiing). 50% occur with meniscal tears.
2. ACL injury, MCL injury, and medial meniscus injury (since MCL is attached to medial meniscus).
3. Sudden pop with anterior knee pain and posterolateral joint line pain, instability, early swelling. PE shows effusion, tenderness, anterior drawer and Lachman's may be positive.
4. MRI or arthroscopy.
5. If reconstruction is done, partially WB with ROM over first two weeks, then progress to closed chain kinetics. Sports-specific exercises in 6-12 wks.

Meniscal injuries to the knee

1. How do medial and lateral meniscus injuries usually occur?
2. What are the symptoms of acute and degenerative meniscus injury?
3. What is seen on physical exam?
4. What is the imaging gold standard for meniscus injury diagnosis?
5. What is the treatment?

Answers:
1. Medial meniscus: injured with tibial rotation while knee partially flexed (football, soccer). Lateral meniscus: injured during squatting in full flexion with rotation (wrestling).
2. An acute tear is associated with a pop with true locking, effusion, and knee stiffness. Degenerative tears involve minimal trauma in >40 yrs.
3. Decreased ROM, flexion limited by effusion, tenderness at jt line, positive Apley and McMurray tests.
4. MRI.
5. Injury to inner 2/3 of meniscus needs surgery due to poor vascularization. NWB for 4-6 wks after surgery if meniscus repaired, WBAT in 1-2 days if meniscus is removed.

Test of the knee ligaments

1. What may cause an anterior drawer test to be falsely negative?
2. What is the sag test?
3. How does Lachman's test compare to anterior drawer in sensitivity?

Answers:
1. Hemarthrosis, hamstring spasm, meniscal tear, and other structures (posterior capsule) can limit forward movement of tibia.
2. Test for PCL patency. Place patient supine with knee flexed 90 degrees, test is positive if tibia is displaced posteriorly.
3. Lachman's test, in which knee is flexed 15-30 degrees and anterior force is applied to tibia, is more sensitive than anterior drawer.

Physical exam of the knee

1. What is the McMurray test best used for?
2. What is Apley's Grind Test?
3. What is Apley's Distraction Test?
4. What is the Patella Femoral Grind Test?

Answers:
1. Diagnosis of posterior meniscal tears.
2. Test for diagnosis of torn meniscus. Patient lies prone with knee flexed 90 deg while examiner places downward force on heel while rotating tibia. A positive test elicits pain.
3. Test for ligamentous damage. Same as Grind Test, but a traction is applied rather than a downward force, reducing stress on meniscus. Positive test elicits pain.
4. Test to evaluate quality of patella articulating surfaces. Patient is supine with legs in neutral, while examiner pushes on patella distally while patient contracts quads. Patella should glide smoothly up. Positive test is pain and crepitation.

Bursae of the knee

1. What are the anterior bursa of the knee?
2. How is the prepatellar bursa inflamed?
3. How is the superficial infrapatellar bursa inflamed?
4. How many lateral bursae are there?
5. Where is the pes anserinus bursa located?
6. What is a Baker's cyst?

Answers:
1. Prepatellar bursa, suprapatellar bursa, deep infrapatellar bursa, and superficial infrapatellar bursa.
2. The prepatellar bursa is the most commonly damaged, caused by prolonged kneeling: housemaid's knee.
3. Associated with kneeling in an upright position: vicar's knee.
4. Three.
5. Located between the pes anserinus tendons and the MCL.
6. Distension of the bursa between the medial head of the gastrocnemius and the capsule, which is an outpocketing of the synovial membrane.

Other ligaments of the knee

1. Where does the medial collateral ligament attach?
2. Where does the lateral collateral ligament attach?
3. What are the capsular ligaments? What is the function of the capsular ligaments?
4. What is the function of the oblique popliteal ligament? Where does it attach?
5. What is the function and attachment of the arcuate popliteal ligament complex?
6. What can the APLC be mistaken for on MRI?

Answers:
1. The MCL attaches to the medial femoral condyle, to the medial upper end of the tibia, and it has an attachment to the medial meniscus.
2. The LCL attaches to the lateral femoral condyle, to the upper end of the lateral fibula.
3. Tibial collateral ligament, oblique popliteal ligament, arcuate ligament, and fibular collateral ligament.
4. The OPL, which resists knee extension, arises from the semimembranosus tendon and is attached to the posterior capsule and lateral meniscus.
5. The APLC provides attachment for the posterior horn of the lateral meniscus. Its function is to reinforce the lateral knee and prevent posterior tibial subluxation.
6. A tear of the posterior horn of the lateral meniscus.

Ligaments of the knee: ACL and PCL

1. Where does the ACL attach?
2. What is the function of the ACL?
3. If the ACL is deficient, where is extra pressure placed?
4. Where does the PCL attach?
5. What is the function of the PCL?
6. If the PCL is deficient, where is extra pressure placed?

Answers:
1. The ACL attaches to the lateral intercondylar notch (of the femur) and to a point lateral to the medial tibial eminence.
2. Prevents anterior tibial subluxation, prevents backward sliding of femur and hyperextension of knee. In flexion, it draws the femoral condyles anteriorly.
3. Posterior menisci.
4. The PCL attaches to the medial intercondylar notch and to a point lateral to the posterior tibial plateau.
5. Restrain posterior tibial subluxation.
6. Patellofemoral joint.

Menisci of the knee

1. What is the function of the menisci of the knee?
2. What is the vascular supply of the menisci?
3. What are the shapes of the two menisci?

Answers:
1. The menisci are fibrocartilage of crescent shape, which deepen the articular surface of the tibia for stability.
2. The peripheral 1/3 of the menisci are well vascularized and the inner 2/3 of the menisci are not well vascularized and can't usually be surgically repaired.
3. The medial meniscus is C-shaped and adheres to the MCL. The lateral meniscus is circular.

Knee functional anatomy

1. What are the knee extensors?
2. What are the knee flexors?
3. What are the knee medial rotators?
4. What are the knee lateral rotators?
5. What is the function and innervation of the popliteus?

Answers:
1. Quadriceps.
2. Lateral and medial hamstrings, sartorius, gracilis, gastrocnemius.
3. Medial hamstrings, sartorius, gracilis.
4. Biceps femoris.
5. The popliteus locks and unlocks the knee. It is innervated by the tibial nerve (L4, L5, S1).

Osteitis pubis

1. What is the cause of osteitis pubis?
2. How does osteitis pubis present?
3. What is seen on CT/X-rays?
4. What is the treatment of osteitis pubis?

Answers:
1. This is an inflammatory condition of the pubic rami, caused by adductor overuse.
2. Pubic symphysis or groin pain radiating into the thigh, causing popping with ambulation and pain with resisted adduction.
3. Periosteal thickening.
4. Rest, NSAIDs, steroid injection, physical therapy. Surgery for severe cases.

Avulsion fractures in the hip

1. How do ischial tuberosity avulsion fractures usually occur? What is the presentation? How is it distinguished from ischial tuberosity bursitis?
2. How are ischial tuberosity avulsion fractures treated?
3. How are ASIS avulsion fractures caused? What is the presentation?
4. What is the treatment of ASIS avulsion fractures?
5. What is the cause of AIIS avulsion fractures? What is the presentation?
6. What is the treatment of AIIS avulsion fractures?

Answers:
1. They are caused by forceful hamstring contracture with knee in extension and hip in flexion. The presentation is of sudden pain and tenderness over the ischial tuberosity, whereas ischial is of insidious onset.
2. Rest, ice, weight bearing as tolerated. Resistance exercises can be started after achieving a full ROM.
3. ASIS avulsion is caused by forceful contraction with hip extended and knee flexed. The lateral femoral cutaneous nerve may be involved and there is acute pain and tenderness over the ASIS, with hip flexion pain.
4. Rest, ice, weight bearing as tol. May require knee splinting in flexion.
5. AIIS avulsion is caused by forceful kicking and quad contraction. Presentation is as pain over AIIS or acute groin pain.
6. Treatment is with rest and ice, weightbearing as tolerated.

Slipped capital femoral epiphysis (SCFE)

1. What is SCFE?
2. What is the most common age for SCFE?
3. What is the presentation of SCFE?
4. What will radiographs show?
5. What is the treatment of SCFE?

Answers:
1. Injury to epiphyseal growth plate at the head of the femur --> displacement of plate.
2. 11-16 yrs.
3. Usually presents as groin pain, but may present as thigh or knee pain. Antalgic gait, with limited int hip rotation.
4. Medial and posterior displacement of epiphysis.
5. NWB, surgery. Endocrine testing for growth hormone, thyroid, panhypopituitarism, MEN.

Femoral neck stress fractures

1. What are the two types of femoral stress fractures? Which is more stable?
2. What is the presentation of a femoral stress fracture?
3. How long does it take for bone scan to turn positive after onset of symptoms?
4. What is the treatment for the two types of fracture?

Answers:
1. Compression and transverse fractures. Compression fx are more stable and occur at the inferior neck of the femur. Transverse fx is unstable and occurs in superior femur.
2. Groin pain worse with ADLs, pain with int/ext rotation.
3. 2-8 days.
4. Compression-type fracture should be treated with bed rest, then weightbearing with pain free. Transverse fractures should be treated with internal fixation.

Intertrochanteric and subtrochanteric hip fractures

1. What is the most common type of hip fracture?
2. What is the general presentation of hip fracture?
3. What type of hip fracture is the most difficult to stabilize surgically? Why?
4. When does rehab start after subtrochanteric hip fracture?

Answers:
1. Intertrochanteric.
2. Hip pain, externally rotated and shortened limb.
3. Subtrochanteric is most difficult to stabilize due to high mechanical stresses.
4. Start rehab after healing is evident.

Femoral neck fractures

1. What are modifiable risk factors for hip fracture?
2. What are complications of a femoral neck fracture? What are complications of surgery for femoral neck fx?
3. What is the presentation for hip fracture?
4. What are the four stages of femoral neck fx?
5. What are the treatments of femoral neck fx?

Answers:
1. Alcohol, caffeine, smoking, antipsychotics, benzos, malnutrition, low body weight.
2. Morbidity from disruption of blood vessels to femoral head, causing necrosis. Postop, can have nonunion or osteonecrosis.
3. Hip pain, limb ext rotation, and apparent shortened limb.
4. Garden stages: I is incomplete, nondisplaced. II is complete, nondisplaced. III is displaced with hip joint capsule partially intact. IV is displaced with hip joint capsule completely disrupted.
5. For stages I and II, pins across fx site, early rehab. For stages III and IV, replacement of femoral head, followed by rehab with hip precautions (no flexion >90, no adduction or internal rotation).

Avascular necrosis of the femoral head

1. What is the definition of avascular necrosis? What are the most common causes?
2. What is avascular necrosis of the hip called in children aged 2-12?
3. What are the symptoms of avascular necrosis of the hip?
4. What is seen on MRI in avascular necrosis?
5. What is the treatment?

Answers:
1. Death of femoral head without sepsis, commonly caused by steroid use or alcohol abuse.
2. Legg-Calve-Perthes disease.
3. Insidious onset of groin, anterior thigh, or knee pain, with short swing and stance phase, and loss of hip rotation.
4. MRI shows irregular or mottled femoral head.
5. Bracing or casting in peds population. In adults, osteotomy of femoral head if disease not advance, but may require THA.

Posterior hip dislocation

1. What is the most common type of hip dislocation?
2. How does posterior hip dislocation often occur?
3. What nerve is often damaged in posterior hip dislocation?
4. What is the appearance of a posterior hip dislocation?
5. How is posterior hip dislocation treated?

Answers:
1. Posterior (90%).
2. MVA in which knee strikes dashboard.
3. Sciatic nerve.
4. Flexed, adducted, and internally rotated. It may appear shorter.
5. Surgery (emergent).

Greater trochanteric bursitis

1. Where is the trochanteric bursa located?
2. What conditions is trochanteric bursitis associated with?
3. What are the symptoms?
4. What is the provocative test?
5. What is the treatment?

Answers:
1. Located over greater trochanter and deep to gluteus medius, gluteus minimus, and TFL.
2. Hip OA, obesity, leg length discrepancy, direct trauma, overuse, herniated lumbar disc, and hemiparesis.
3. Night pain, inability to like on affected side, hip snapping.
4. Pain over greater troch during movement from full extension to flexion.
5. IT band stretching, NSAIDs, hip adductor strengthening, local cortisone injection.

Groin strain

1. How does groin strain (hip adductor strain) usually occur?
2. What are the symptoms of groin strain?
3. What is the provocative test?
4. What imaging should be ordered?
5. What is the treatment?

Answers:
1. Resisted forced abduction of the hip.
2. Pain in the adductors distal to their origin.
3. Pain with resisted hip adduction.
4. X-rays of hip including adductor tubercle to rule out avulsion.
5. Rest, ice, NSAIDs, advance to stretching and strengthening.

Iliopsoas bursitis and tendonitis

1. What are the symptoms of iliopsoas tendonitis or bursitis?
2. What is the provocative test?
3. What is the treatment?

Answers:
1. Hip snapping with flexion due to IT band snapping over greater trochanter or iliopsoas tendon subluxing, tenderness over iliopsoas muscle.
2. Pain on hip flexion.
3. Ice, NSAIDs, stretching and strengthening, cortisone injections.

Piriformis syndrome

1. How is the piriformis usually injured?
2. What are the clinical symptoms of piriformis syndrome?
3. What is the provocative test for piriformis syndrome?
4. What is the treatment?

Answers:
1. Poor body mechanics, forceful hip internal rotation. (Sciatic nerve may be involved.)
2. Pain in lateral buttock, posterior hip and prox posterior thigh, SI joint, with tenderness over the muscle belly going from the sacrum to the greater trochanter. It is exacerbated by walking up stairs.
3. Pain with internal hip rotation, adduction, and flexion.
4. Stretching, NSAIDs, US, local cortisone injection.

Hamstring strain

1. What are predisposing factors to hamstring strain?
2. What is the strength ratio of hamstrings to quads?
3. What are the grades of hamstring strain?
4. What is the provocative test for hamstring strain?
5. what is the treatment of hamstring strain?

Answers:
1. Inadequate warmup, poor flexibility, exercise fatigue, poor conditioning, and muscle imbalance.
2. 3:5.
3. Grades I (strain) to III (complete tear).
4. Pain in ischial region with knee flexion.
5. Ice, compression, weight bearing reduction, NSAIDs, gentle stretch.

Leg length discrepancy

1. How is a true leg length discrepancy assessed?
2. How do you measure for discrepancy in the femur?
3. How do you measure an apparent leg length discrepancy?
4. What are the causes of an apparent leg length discrepancy?

Answers:
1. Measure from ASIS to the medial malleoli.
2. Patient lies supine and flexes knees to 90 degrees, assess if one knee is higher than the other.
3. Measure from umbilicus to medial malleoli.
4. Pelvic obliquities or flexion/adduction deformities of the hip.

Tests of the hip joint

1. What is FABER (Patrick) test used to assess?
2. What is Thomas test used to assess?
3. What is Ober's test used to assess?
4. What conditions are associated with a positive Trendelenberg?

Answers:
1. Inguinal pain in flexion, abduction, and external rotation is an indication of hip joint pathology.
2. Hip flexion contractures.
3. Iliotibial band and TFL contractures.
4. Trendelenberg indicates gluteus medius weakness, associated with radiculopathy, polio, meningomyelocele, fractures of greater trochanter, SCFE, congenital hip dislocation.
6.

Ligaments of the hip

1. What is the purpose of the acetabular labrum?
2. What is the iliofemoral ligament?
3. What ligament checks medial rotation? Abduction?
4. What is the first ROM to be limited in OA?

Answers:
1. Deepens acetabulum and holds femoral head in place.
2. The iliofemoral ligament (Y-ligament of Bigelow) is the strongest ligament in the body, going from the AIIS to the intertrochanteric line.
3. The ischiofemoral ligament checks medial rotation. The pubofemoral ligament checks abduction.
4. Internal rotation.

Hip muscles

1. What are the hip flexors?
2. What are the hip adductors?
3. What are the hip abductors?
4. What are the hip extensors?
5. What are the lateral rotators of the hip?
6. What are the medial rotators of the hip?

Answers:
1. Flexors: iliopsoas, sartorius, rectus femoris, gracilis, adductor longus, adductor brevis, adductor magnus, pectineus, TFL.
2. Anterior: gracilis, adductor magnus, adductor brevis, adductor longus, pectineus. Posterior: gluteus maximus, obturator externus, gracilils, biceps long head, medial hamstrings.
3. Gluteus medius, gluteus minimus, TFL, sartorius, piriformis, gluteus maximus.
4. Gluteus maximus, gluteus minimus, gluteus medius, piriformis, adductor magnus, hamstrings.
5. Piriformis, obturator internus, gemelli, obturator externus, quadratus femoris, gluteus muscles.
6. TAGGGSS: tFL, adductors (magnus, longus, brevis), gluteus medius, gluteus minimus, gracilis, semitendinosus, semimembranosus.

Proximal humerus fractures

1. How much must a portion of the humerus be displaced to call it a fragment?
2. What is the most common location of humerus fractures? What are other locations?
3. What are the symptoms of proximal humerus fracture?
4. What are the surgical and non-surgical treatments?
5. What are complications of proximal humerus fracture? What nerve is often involved in surgical neck fractures?

Answers:
1. Angulated by 45 degrees or displaced >1cm.
2. Most common is the surgical neck, followed by the greater tuberosity, lesser tuberosity, and anatomical neck.
3. This fracture is common in osteoporotic elderly women after a fall and involves pain, swelling, and ecchymosis. Loss of sensation or diminished radial pulse may occur. If there's a fracture of the surgical neck, the supraspinatus causes abudction of the proximal fragment of the humerus.
4. Conservative treatment is early ROM, sling immobilization, rehab, pendulum exercises. If displaced, need ORIF.
5. Complications include brachial plexus injury, axillary artery compromise, and avascular necrosis of the humeral head. The axillary nerve is involved in surgical neck fractures.

Scapula and Clavicular fractures

1. What other significant injuries may be associated with a scapula fracture? How is it diagnosed?
2. What is the treatment for a scapula fx?
3. How are clavicular fractures classified?
4. What is the treatment of clavicular fx?

Answers:
1. Rib fx, pulmonary pathology (contusion, ptx) is associated with scapula fx. It is diagnosed by plain films (AP, lateral (scapular Y), and axillary) or CT.
2. Closed treatment for nondisplaced fx (sling, early ROM within 1-2 wks). ORIF for large displaced fragments.
3. By location: proximal, middle, or distal thirds.
4. Conservative treatment for most fxs. If >1cm displacement of lateral clavicle at AC jt, do closed reduction and figure 8 sling immobilization 3-6wks.

Adhesive capsulitis

1. What are the stages of adhesive capsulitis?
2. What conditions is adhesive capsulitis associated with?
3. What imaging is done for adhesive capsulitis?
4. What is the conservative treatment?
5. What is the surgical treatment?

Answers:
1. The first, painful stage is a progressive vague pain lasting 8 months, the second stiffening stage lasts about 8 months with decreasing ROM, and the third thawing stage results in increasing ROM with decreased pain.
2. CVA, hemorrhage, brain tumor, clinical depression, shoulder-hand syndrome, Parkinson's disease, iatrogenic disorder, cervical disc disease, IDDM, hypothyroidism.
3. Do plain films to rule out underlying tumor or calcium deposit or if there is not improvement with 3 months of treatment, arthroscopy shows decreased joint volume.
4. Restoring ROM, decrease pain, corticosteroid injection, home program, modalities.
5. Manipulation under anesthesia or arthroscopic lysis of adhesions.

Biceps tendonitis and rupture

1. Where is the most common site of biceps tendon rupture? What other shoulder condition is it associated with?
2. What are the symptoms of bicipital tendonitis? Biceps rupture.
3. What tests are done to diagnose biceps tendonitis?
4. What test is done to diagnose biceps rupture?
5. What is the treatment for biceps tendonitis/rupture?

Answers:
1. Most common site of rupture is long head of biceps proximally, often secondary to impingement syndrome or rotator cuff tears.
2. Point tenderness in bicipital groove, positive impingement signs. If there is rupture, there will be sharp pain, audible snap, ecchymosis, and visible bulge in lower arm.
3. Yergason's test (pain with supination of wrist against resistance) and Speed's test (pain with shoulder flexed, elbow extended, supination against resistance).
4. Ludington's test: deformity with flexion of biceps muscle.
5. For tendonitis, can do ROM, strengthening, modalities, or injection into tendon sheath. For rupture, reattachment isn't indicated except in young people who do heavy lifting.

Degenerative joint disease in the shoulder

1. What occurs in arthritis of the shoulder?
2. What are the symptoms and signs of shoulder arthritis?
3. What imaging should be ordered? What is seen on X-ray?
4. What is conservative treatment for shoulder arthritis?
5. What are the indications for total shoulder arthroplasty? What are the stages of recovery?
6. What is shoulder arthrodesis? What are indications for arthrodesis?

Answers:
1. Destruction of articular cartilage and narrowing of the joint space in either of the GH or AC joint.
2. Limitation and pain on AROM and PROM, worse with internal rotation, tenderness with palpation.
3. AP in internal and external rotation and 40 degrees, axillary view. Findings are irregular joint surfaces, joint space narrowing, subacromial sclerosis, osteophyte changes, flattened glenoid, cystic changes in humeral head.
4. NSAIDs, steroid injection, ROM, rotator cuff strengthening.
5. Indications for surgery are pain, avascular necrosis, neoplasm. In stage 1 (0-6 wks), avoid abduction and extension, ext rot >15 deg, NWB, sling immobilization, treat with pendulum exercises, isometrics, wall-walking. In stage 2 (6-12 wks), can start light wks, AROM. In stage 3 (>12 wks), no restrictions, start progressive resistive exercises.
6. Shoulder arthrodesis is surgical resection and fusion of shoulder joint. Indications are severe pain, loosening of arthroplasty, or joint infection.

Shoulder impingement: imaging and treatment

1. What is seen on plain film with impingement? Chronic rotator cuff tear?
2. What is the gold standard for rotator cuff tears? For labral tears?
3. What is the utility of arthrogram for rotator cuff tears?
4. What is the conservative treatment for rotator cuff injury in the acute phase (first 4 weeks)?
5. What is the conservative treatment for the first 6 months? After the first 6 months?
6. What are the indications for surgery?

Answers:
1. With impingement, there are cystic changes in the greater tuberosity. In chronic rotator cuff tear, there is superior migration of the proximal humerus, flattening of the greater tuberosity, and subacromial sclerosis.
2. MRI for rotator cuff, add gadolinium for labral assessment.
3. Can assess full thickness tears but can't tell size of tear or partial thickness tear.
4. Relative rest, pain management, modalities, reestablish nonpainful ROM, retard muscle atrophy.
5. In first 6 months, improve ROM, improve rotator cuff strength and scapular stabilizers. After the first 6 months, continue strengthening, do activity-specific training, conticosteroid injections.
6. Surgical indications include tears that fail conservative treatment. In athletes, surgical repair may be done within first 3 weeks for better return of function.