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.