NPTE- "Gold" Diagnoses

Down Syndrome

(Trisomy 21)- most common cause of intellectual disability RFs: increased maternal age, paternal age, virus, emdical exposure, reproductive medications, and intrinsic predisposition. Pt: hypotonia, flattened nasal bridge, almond-shaped eyes, abnormally shaped ears, Simian line (palmar crease), epicanthal folds, enlargement of tongue, congenital heart disease, developmental delay, variety of MSK disorders. Dx: During pregnancy- can test for Alpha-fetoprotein, human chorionic gonadotropin, and uncongugated estrogen legels (the triple screen). Chorionic villus sampling, amniocentesis, or percutaneous umbilical blood sampling. Karyotype post-birth to confirm. PT Exam: be aware of seizure hx, cardiac status, risk of atlantoaxial instability, sensory/hearing/visual impairments, umbilical hernia, respiratory compromise, and Alzheimer's disease. Also increased incidence of celiac disease, epilepsy, constipation, blood/dermatologic/MSK disorders. PT Tx:achieve maximum potential and level of function, developmental delay, hypotonia, laxity of ligaments, poor strength, learning strategies, verbal-motor impairments. *PT will not accelerate developmental milestones, but will help avoid compensatory patterns w/ static positioning and mobility. HEP: avoid inactivity and obesity, positioning and handling, strength and endurance. Prognosis: need for intermittent PT based on function. 80% of patients will reach 55yo. Death is usu d/t: congenital heart defects, GI anomalies, immune system dysfunction, respiratory infection, LEUKEMIA, pulmonary HTN, complications of Alzheimer's disease.

Achilles Tendon Rupture

(achilles is the *largest & strongest* tendon in the human body). Pt: men, "weekend warrior," swelling, palpable defect in tendon, pain & weakness w/ PF, limp, report of snap or pop & severe pain, unable to stand on toes, Positive *Thompson Test* RFs: Achilles tendon has degenerative change (decreased blood flow), repetitive microtrauma, pushing off a WBing LE w/ extended knee, unexpected DF while WBing, forceful eccentric contraction of PFs, quick-changing footwork, poor stretching routine, tight calf mm, improper shoe wear, altered biomechanics (flat arch). >30yo (usu 30-50yo), *corticosteroid injections to tendon* Medical Exam: should take x-ray to rule out avulsion fx. MRI can locate presence and severity of tear/rupture. O'Brien needle test. Dx: pt hx, + Thompson Test, discontinuity in tendon. Medical Tx: Operative- surgical reconstruction/repair followed by cast/brace for *6-8wks*. (0-5% re-rupture risk) & higher rate of return to athletic activities. Non-operative- immobilization casting, serial casting (*10wks*), use of heel lift (*3-6mo*). (40% re-reupture rate) & may not return to complete functional performance. PT begins when cast is removed: ROM, stretching, icing, assistive device training, endurance, gait train, strength, plyometricks, skill specific training. Prognosis: pt will continue HEP *6-7mo* Normal recovery= pt should return to PLOF within *6-7mo*.

Ankle Sprain Grades

1- mild-moderate sprain/tear, ankle is stable, pt can usually walk with minimal discomfort. 2- larger tear, moderate pain/bruising/swelling. Ankle may or may note feel stable, and ligament is painful with palpation, WBing is often painful 3- Complete tear, severe swelling & bruising, ankle is unstable, feels "wobbly", walking is very painful and unsteady, ankle often "gives out" "High ankle sprain"= grade 2 sprain of 1 or more of syndesmotic ligaments (ligaments attaching tibia to fibula to stabilize ankle mortise). This type of sprain requires a lot of force. Often occurs with an ankle fx as well! If tear is unrecognized and not treated it will result in severe post-traumatic arthritis. May require surgery (unlike other ligament injuries at the ankle).

ACL Tear (grade III sprain)

ACL= anterior intercondylar tibia -- to medial aspect of lateral femoral condyle. Prevents anterior translation of tibia on fixed femur & posterior translation of femur on fixed tibia. ACL made up of long collagen strands (permit up to 500lb of pressure before rupturing). *Poor blood supply, no ability to heal after complete tear) Injury occurs w/ hyperflexion, rapid deceleration, hyperextension, landing in an unbalanced position. Full tear results in excessive laxity (classified as anterolateral or anteromedial laxity) Pt: female, 14-29yo, athletic participation requiring agility, contact sports. Reason for higher incidence in females: body movement & positioning, muscle strength, joint laxity, Q angle, narrow intercondylar notch. Presentation: significant pain, effusion, and edema, significantly limits ROM. May be unable to WB. Reports of loud pop or feeling of knee buckling. Exam: ligamentous testing- Lachman, anterior drawer, and pivot shift test (MUST perform bilaterally). Check sensation of skin. Rule out: menisci injuries. Imaging: MRI is preferred (ACL integrity and other soft tissue injureis). X-ray used to rule out fx. Add'l injuries: 2/3 the time, there is an additionaly meniscal tear with the ACL tear, may also have the "unhappy triad". Surgery: usu. uses patellar tendon for graft, pt usu. has knee immobilzer and crutchest to protect reconstructed ligament. Parameters or specific to surgeon. Initial post-op PT phase: protection of graft integrity, edema control, improved ROM, pain modulation, patellar mobility, AROM, gait train, quadriceps exercises. Progression includes: strengthening activities -*closed-chain exercises are best b/c they minimize anterior translation of tibia*, and functional activities. Prognosis --> return to PLOF in *4-6mo*. Non-operative: PT should bgein an agressive strengthening program once the acute phase has subsided, also help with edema control, ROM, strenght, and improved fluidity of gait. Prognosis --> These pts maybe able to participate in light-moderate athletic activities, but have higher risk of instability and subsequent deterioration of joint surfaces. *Patients must complete functional progression prior to returning to unrestricted athletics.

Adhesive Capsulitis

AKA: "frozen shoulder," characterized by inflamm. and fibrotic thickening in anterior joint capsule. Inflamed capsulea dheres to humeral head and undergoes contraction, this causes decreased space in the capsule and decreased synovial fluid = further irritation. Usu. capsule holds 16-20mL of fluid, but now holds 5-10mL. 1° Adhes. Caps.= insidious onset. But can be associated w/ DM, thyroid abnormalities, cardiopulmonary conditions. 2° Adhes. Caps.= underlying condition: trauma, immobilization, CRPS, RA, abdominal disorder, psychogenic disorder, supraspinatus tendonitis, partial tear of rotator cuff, and bicipital tendonitis. Pt: middle-aged, female, diabetes mellitus, tightness in anteroinferior joint capsule, pain w/ stretch, restriction w/ PROM & AROM. May have mm. guarding, loss of reciprocal arm swing, disuse muscle atrophy. *Acute phase*= pain radiates below elbow, night pain, PROM limited d/t pain and guarding. *Chronic phase*= pain localized around lateral brachial region, NO night pain, PROM limited d/t capsular stiffness. Medical dx: may have arthrogram to detect decreased fluid volume in capsule. *Other tests should ONLY be performed for differential diagnosis*. Rule Out: concomitant systemic, rhematoligc, inflammatory, metastatic, or infectious disorders. Tx: it is a self-limiting process, can take *>12mo* to run it course. Meds: acetaminophen, longer acting analgesics, NSAIDs, narcotics, corticosteroid injection. Surgery: break up adhesions ro rlease adhered mm. *last resort*! Physical Therapy: Acute- icing or superficial heat, gentle mobs, gradual strengthening, pendulum exercises, isometric strengthening. *Pt should avoid ABD exercises @ home d/t risk of injury to subacromial tissue*. Chronic- US, grade 3 & 4 mobs, stretching to joint capsule, PNF for painless functional ROM., posture, "wall climbing" Prognosis: PT for*3-5mo* Nonlinear pattern of recovery. Spontaneous recovery takes *12-24mo*. A smaller % of pt will have lasting deficits in ROM, but this is usu. asymptomatic.

Huntington's Disease (HD)

AKA: Huntington's Chorea Progressive neurologic disorder, autosomal dominant genetic trait (Chromosome 4, gene IT-15) that causes degeneration and atrophy of basal ganglia (specifically the striatum) and cerebral cortex. These areas produce less GABA and Acetylcholine neurons and they are less active → therefore unable to modulate movement. Pt: 35-55yo, Chorea, bradykinesia, and rigidity, AFFECT dysfunction, cognitive impairment, involuntary choreic mvmts, mild personality alterations. Unintentional facial movement/expressions, gait will become ataxic, Can have sppech, mental deterioration, Late stage IQ decrease, dementia, depression, dysphagia, incontinence, inability to ambulate/transfer. Progression from choreiform mvmts to rigidity. Imaging: MRI or CT- deterct atrophy/abnormalities in cerebral cortex and basal ganglian. PET scan- blood flow, oxygen uptake, metabolism. DNA marker study to detect if autosomal dominant trait is present. PT Exam: watch for decreased ROM, deformity, pain, communication breakdown, aspiration, choking, fatigue, weakness from weightloss, sxs of severe depression and/or suicidal attempts. Tx:anticonvulsants and antipsychotics help block dopamine but have serious side effects. Perphenazine, Haloperidos (Haldol) and Reserpine. PT Tx: endurance, strength, balance, posture, functional mobility, motor control (use techniques: coactivation of mm, trunks tabilization, biofeedback, relaxation). Edu: prone lying, stretching, prevention of deformity and contracture, safety with mobility. PT Prognosis: Intermittent PT Tx, will not alter course, but maximize pt's functional potential and safety. This chronic condition is fatal within 15-20yrs. Results in total physical and mental incapacitation.

Arthrogryposis muliplex congenita

AMC- non-progressive neuromuscular disorder results from multipl conditions. Baby is bron with multiple congenital contractures. Also mm atrophy and weakness, and articular rigidity. 1° forms: contracture syndromes, amyoplasia, distal arthrogryposis. Some will ambulate some will require w/c.

Transtibial Amputation d/t Arteriosclerosis Obliterans

Arteriosclerosis Obliterans = Peripheral arterial Disease= 95% of vascular disease (thickening , hardening, narrowing and occlusion of arteries resulting in ischemia and ulceration of affected tissues) → leading to necrosis, gangrene, and required amputation. RF: include CVD risk factors that you know. Pt: Male, >45yo, smoker, presenting with intermittent claudication, resting pain, decreased pulses, ischemia, pallor skin, decreased skin temperature. Imaging: Doppler, US, MRI, or arteriorgraphy are used to dx Arteriosclerosis obliterans. They examine degree of blood flow through extremities (can detect blockages, tissue damge, and tissue death). Other Exam Items: limb temp, skin condition, hair, sensation, pulses, Claudication Test and the Ankle-Brachial Index (ABI). PT Exam: palpation of pulses, w/c abilities, hair growth, color, temp, sensation, phantom pain. Recognize likelihood of decreased cardiovascular status, decreased balance, ROM, poor skin integrity and hypersensitivity. → The can have negative influence on ability to use prosthesis. PT: begin *immediately* after amputation for preprosthetic interventions (strength, ROM, functional mobility, AD training, desensitization, pt educ fo residual limb care, proper positioning to avoid contraction (*esp. knee flexion contracture risk*). HEP: Exercises, limb desensitization, positioning, stretching, wrapping/shaping. Cardiovascular activity (in order to prepare for increased energy demand with prosthetic use). PT is required for preprosthetic and prosthetic training. Prognosis: dependent on pt's general health, cognition, motivation, etc. Pt should be able to return to functional mobility with use of prosthesis. *Arteriosclerosis obliterans is a chronic disease, 20% of individuals have an MI or CVA at some point after dx, d/t underlying comobidity*.

Alzheimer's Disease

Progressive neurologic disorder that causes deterioration in the cerebral cortex and subcortical areas of the brain. This is d/t deterioration of neurons that would normally help with acetylcholine transmission. These pt have neurofibrillary tangles, amyloid plaques, and cerebral atrophy (postmortem biopsy). Amyloid plaques are made up of cellular waste and cause add'l inflammation = more damage to nervous system and atrophy to smooth mm of brain arteries (increased risk of rupturing). 4th leading cause of death in adults (d/t complications of infection or dehydration). Cause: unknown, lower levels of NTs, higher levels of aluminum in brain, genetics, autoimmune disease, abnormal processing of amyloid, and virus. Risk increases w/ age 6% over 65yo, and 20% over 80yo. Pt: women, subtle changes i nmemory, concentration, difficulty w/ new learning → progress to loss of orientation, word finding, emotional lability, depression, poor judgment, impaired self-care skills (Early Stage) Middle Stage= behavioral and motor issues with neuro sxs (aphasia, apraxia, perseveration, agitation, violent/socially unacceptable behavior, wandering). End Stage= no ability to learn, long-term memory disappears, vegetative sxs, incontinence, functional dependence, inability to speak, and seizure activity. Dx: confirmed postmortem via biopsy, but can use MRI to assess atrophy in brain, Single Photon emission computed tomography (SPECT) can be used to determine brain activity. Exam: blood work, urine, and spinal fluid to rule out other diseases. *Pt must demonstrate @ least 2 deficits of cognition, memory and related cognitive functioning with absence of all other brain disease or disturbances.* PT Exam: must note that end-stage Alzheimer's disease pt is @ high-risk of infection and pneumonia. Pt may also have contractures, decubiti, fx, and pulmonary compromise. Tx: medication during early stage to inhibit acetylcholinesterase, help cognitive sxs, and control behavior change. Short-term drug therapies *6-9mo* might include Tacrine (Cognex), donepezil (Aricept), and rivastigmine (Exelon). PT Tx: maximize remaining function, caregiver education, help environment set-up for success, functional mobility and gait training, teach caregiver to assist with mobility, ROM, and positioning. HEP: activity as tolerated, use memory book, and other compensatory strategies. Caregiver may need to help pt with daily exercise, ambulation. Pt should be included in everyday activities to avoid restlessness and wandering. Prognosis: PT may be needed intermittently, but will not alter or cease the progression of the disease process.

Carpal Tunnel Syndrome (CTS)

Carpal Tunnel is created by the transverse carpal ligament, the scaphoid and trapeziuem, the hook of the hamate and pisiform, and the volar radiocarpal ligament and ligamentous extensions b/w carpal bones. 10 structures pass through carpal tunnel" 4 flexor digitorum superficialis tendons 4 flexor digitorum profundus tendons *median nerve* and flexor pollicis longus tendon. CTS is caused by compression of median n. as it passes through the tunnel → leading to ischemia. *Normal compression= 2-10mm Hg, but CTS can have pressure >30mm Hg (which increases even more with wrist flexion & extension)*. Pt: Female 35-55yo, presents w/ sensory and motor disturbances in median n. distribution. Hx of repetitive use, RA, pregnancy, diabetes, trauma, tumor, *hypo*thyroidism, and wrist sprian or fx. May have congenital narrowing of tunel &/or *Vitamin B6 deficiency*. Sxs: pt may have night pain, hand weakness, atrophy, decreased grip strength, clumsiness, and decreased wrist mobility. *Initially atrophy is noted in ABD pollicis brevis mm and then progresses to thenar muscles. Dx: EMG and Electroneurographic studis (look at conduction delay in median n.) MRI might be used to identify inflammation of median n, tendon or nerve positioning, or thickening of tendon sheath. PT Exam: provocation testing with Tinel's Sign, Phalen't Test, Tetehr Median Nerve Stress Test, strength assessment (esp. of hand mm.) Advanced CTS: muscle atrophy, radiating pain in forearm, motor and sensory loss, neurapraxia (some demyelination of axon) → eventual axonotmesis and Wallerian degeneration. *Ape hand deformity d/t atrophy of thenar mm and 1st 2 lumbricals*. 50% of cases may have bilateral involvement. Tx: initially- local corticosteroid injections, splinting, and PT. Meds: Methylprednisolone injection. PT: splinting, mobilization, gentle stretching, biomechanical anaylsis, adaptation of workspace/biomechanics. Can improve pt's condition *4-6wks* Surgery: if conservative management fails → release carpal ligament and decompression nerve. Post-op PT: most heat w/ e-stim, iontophoresis, cryotherapy, massage, desnsitization of scar, *tendon gliding*, AROM. *Avoid wrist flexion and forceful grasp initially* After 4wks, pt can progress w/ active flexion, gentle stretching, putty exercise, progressive resistive exercise. *Avoid radial deviation against resistance.* Pt should improve in 6-8wks after surgery.

Note- There are other types of Spondylolisthesis

Classified by the actual cause for the slippage: 1. Congenital- anomaly or defect in fusion of neural arch, usu. in upper sacral vertebral arches or @ L5 (occurs b/w 12-16yo, growth spurt!), pain free prior and then express back and sciatica pain. strong genetic assoc. 2. Isthmic 3. Degenerative *most common?* 4. Post-traumatic 5. Pathologic

Duchenne Muscular Dystrophy

Progressive, neuromuscular degenerative disorder, caused by mutation in the dystrophin gene Xp21 (normally codes for mm membrane protein- dystrophin) → lack of dystrophin allows for damage within the sarcolemma of the mm, weakening of cell membranes, destruction of myofibrils, and loss of muscle contractility → *destroyed muscle cells are replaced with fatty deposits*. X-linked recessive trait. Pt: usu. diagnosed b/w 2-5yo, waddling gait, *proximal* muscel weakness, clumsiness, toe walking, excessive lordosis, pseudohypertrophy of calf and other mm groups, difficulty climbing stairs. *DMD primarily affects the shoulder girdle mm, pectoralis, deltoids, rectus abdominis, glutes, HS, and calf mm.* Initially identified when child has trouble getting up from floor and uses *Gowers' maneuver*. 1/3 of patients have learning disabilities. Pt usu. unable to ambulate by age 10. Imaging: EMG to examine electricala ctivity in mm, Muscle biopsy to determine absence of dystrophin and evaluate muscle fiber size. DNA Analysis and High serum creatinine kinase levels in blood also assist w/ confirmation of dx. PT Exam: measure circumferences to monitor mm atrophy, look at accessory muscle utlilization for breathing. Watch fo disuse atrophy, contractures, scoliosis, impaired ambulation, weight gain/obesity, cardiac and respiratory impairments, MSK deformity and GI dysfunction. Respiratory problems and scoliosis progress when child begins using w/c. *Regularly perform MMT and ROM at exam and follow-up treatments in order to measure patterna nd rate of disability. Tx: might include glucocorticoids and immunosuppressants. PT Tx: assist child w/ progression through milsetones, maintain strengh, encourage mobility, adapt to loss of function, promote family involvement in home program. Orthotic prescription, adaptive devices, w/c prescription. Progression of disease→ ROM, prevent contracture/deformity, positioning, pain management, breathing exercise, postural drainage, use of w/c or AD. Submaximal exercises. Prognosis: PT will not alter disease course, but can help maintain/adapt function and educate pt and family. PT is to ensure that full and proper training has been completed on all aspects of pt's care to ensure highest level of function. Death often results from cardiopulmonary complications d/t cardiac mm and respiratory mm dysfunction, by teenage years or in the 20's.

Sciatic Secondary to a Herniated Disk

Disk herniates posterolaterally d/t weakening of outer annulus and PLL (often d/t natural aging) → the disk then puts pressure on the sciatic n (roots L4-S3). Pt: 40-60yo, low back and gluteal pain, that may radiate down the back of the thigh and even to the toe in some cases (often following dermatomal pattern). Pain is describes as dull, aching, or sharp. Sometimes leg pain > back pain. Pt may also have numbness and tingling, limited thoracolumbar ROM in all planes, tenderness to palpation, and muscle guarding. Imaging/Labs: Radiologic testing and electrophysiologic studies are initially done to assist w/ Dx. Also may have myelogram, discography, CT, or MRI. Blood work may be done for differential dx. PT Exam: must ask about trauma, osteoporosis, corticosteroid use. *SLR will reproduce sxs in the case of a herniated disk and segmental mobility → pain and mm guarding* Exam should also include testing for non-organic LBP to rule out psych factors.. Pathologic reflexes (check for clonus). Pain will likely increase w/ certain positions and other activities that increase intradiskal pressure (sitting, lifting, FW bend, twisting, sneezing, coughing, etc.). Pt will want to rest, BUT *prolonged bed rest is contraindicated and will not relieve pain long-term.* Tx: maybe short-term bedrest, overall reduction of intradiskal pressure, pt edu, PT, NSAIDs, epidural, cortisone and local anesthetic injections, and surgery in rare cases (laminectomy, discectomy, chemonucleolysis, laser discectomy, or laminotomy). PT: positioning, biomechanics, pain management, traction, heat, lumbar stabilization, McKenzie exercises, stretching, endurance activities, maybe swimming/stationary bike/walking (within tolerance). *Lifting, squatting, and climbing are contraindicated d/t sig increase in intradiskal pressure.* Most herniations wil spontaneously decrease in size. Prognosis: with conservative tx, pts will usu improve in *2-4months.* As the disc heals it may scar, which can actually help reinforce the posterior aspect and annular fibers so that it is protected from further protrusion.

Guillain-Barre Syndrome

GBS or acute polyneuropathy Temporary inflammation and demyelination of peripheral nerves' myelin sheaths → result in motor weakness that progresses *distal to proximal*, pt may have sensory impairments and possible respiratory paralysis as the disease progresses. The demyelination that occurs at teh Ranvier's nodes is 2° to macrophage response and inflammation. Mainly affects motor neurons! Pt: young adult or adult 40-70yo, Males, Caucasians. Sxs: distal symmetrical motor weakness, mild sensory impairments, transient paresthesias. Weakness moves towards head and UEs. *Progression peaks by ~4wks, respiratory paralysis, absence of DTR and inability to speak or swallow may occur. →2-4wks static period →gradual recovery can take months to years Imaging and Labs: CSF sample (look for high protein levels and little/no lymphocytes). EMG- abnormal and slowed nerve conduction. PT Exam: be aware that pt may also experience bladder weakness, deep mm pain, ANS involvement (including arrhythmias, tachycardia,postural hypotension, heart block, and absent reflexes). Up to 30% of patients require mechanical ventilation. Respiratory assistance can last as long as 50-60 days. Tx: Hospitalization, immunosuppressive and analgesic/narcotic meds. *Corticosteroids are contraindicated*. May need cardiac monitoring, plasma exchange, mechanical ventilation. Tracheostomy for ventilation. PT initiated upon admission to focus on PROM, positioning and light exercise *do NOT overexert or fatigue pt*. Progression → orthotic w/c or AD prescription, exercise and endurance, family education, functional mobility and gait training, progresive respiratory therapy. Therapy pool for anti-gravity exercise. HEP: BREATHING, incentive spirometry, tehr ex, functional mobility, endurance. Prognosis: PT cannot alter course of disease, but is important for assist in recovery for up to *3-12mo.* Overall recovery is slow and can last up to 2yrs. Most have full recovery, but 20% can have remaining neuro deficits. 3-5% of pts die from respiratory complications.

CEntral Cord Dyndrome (CCS)

Incomplete SC lesion (most common form, accounts for 30% of overal incomplete tetraplegia). Caused by cervical hyperextension (AKA: ligamentum flavum injury), fall, MVA, or anterior compression from osteophytes.. There is damage to central aspect of SC (central gray matter) → damages centrally located cervical tracts & often lateral columns @ level of injury. *Motor loss is greater in UEs, most severe in distal UEs.* In order of outside of spinal cord → inward: lumbar- thoracic- cervical. Sacral segments are usu. not affected. Pt: >50yo, Males, hx of fall (c-spin hyperextension), MVA, etc., cervical spondylosis, narrowing or congenital defect, tumor, RA, or syringomyelia. Imaging: MRI (view SC impingement), CT (spinal canal compromise and impingement), X-ray (fx, dislocations, degree of spondylotic deterioration) →These are all used to make diagnosis. PT Exam: ea. pt will present differently depending on area of damage, possible autonomic dysreflexia, spasticity, neurogenic bladder/bowel, allodynia, and pressure ulcers. Tx: *Methylprednisolone administered within 8hrs of injury*. Others: BP meds, antispasticity meds, anticonvulsants, prophylactic anticoagulants, and antidepressants. PT: education, ROM, strengthening, endurance, balance retraining, proximal stabilization exercises, functional mobility, AD training (*platform walker may be needed d/t poor grasp/hand function*). Prognosis: Depends on age, motivation, compliance, extent of injury. Bowel & Bladder function resolve in most patients after 6mo. 77% ambulate, 42% regain some hand function. Favorable prognostic factors: early hand function, improved strength in all extremities during inpatient stay, little/no LE involvement, younger age.

Scoliosis

Lateral curvature of spine, can be assoc. w/ kyphosis or lordosis, may or may not have rotation of the spine (if it does occur rotation will be towards convex side of major curve) Most scoliosis is idiopathic (80%): Infantile 0-3yo onset Juvenile 4yo-puberty onset- thoracic curve w/ convexity towards teh R, may progress quickly and develop compensatory curves above & below, rib hump can develop on covex side of curve (usu. R side). Usu. not painful unless it progress. A curve >30° is more common in *girls*. Adolescent (12yo girl, 14yo boys) onset Adult (skeletal maturation) onset- about 500,00 people in USA. *curves <20° rarely cause significant impairments* 2 Types of Scoliosis: 1) Non-structural= reversible, can change w/ repositioning, non-progressive and is usu. caused by poor posture or leg length discrepancy. 2) Structural= cannot be corrected w/ mvmt, caused by congenital, MSK, and neuromuscular reasons, altered spine developme in utero, assoc. w/ neuromuscular disease (CP, MD, congenital defect of vertebrae, etc.), autosomal dominant trait. *Sxs*: asymmetries of shoulders, scapulae, pelvis, skinfolds. Imaging: *X-ray should be taken in anterior and lateral view, pt standing and pt bending*. Cobb method can measure angle of curvature. Bone scan or MRI can be used to determine and rule out other conditions. PT Exam: Scoliometer (measure angle of trunk rotation)- can determine if curve is non-structural or structural. Increased spacing b/w elbow and trunk while standing, leg length discrepancy, uneven shoulder and hip heights, prominence on 1 side of pevlis or breat (d/t rotation of curve). If progressive scoliosis is untreated, deformity can increase to an angle >60° causing *pulmonary insufficency, pain, impaired lung capacity, degenerative changes, arthritis, and disk pathology*. Tx: depends on type and severity of curve, pt age, and previous managment. PT: e-stim for pain, biofeedback for edu. w/ posture. *Pt with curve <25° should be monitored every 3mo*. Breathing, strengthening for trunk and pelvic mm. *Pt with curve 25-40°* requires spinal orthosis and PT tx for posture, flexibility, strengthening, respiratory function and proper use of spinal orthosis. *Pt with curve >40°* usu. needs surgery for spinal stabilization (spinal fusion via Harrington rod). After surgery, PT will work on breathing, posture, flexibility, general strength, and respiratory mm strengthening. Prognosis for structural scoliosis: dpeends on age and severity: early intervention gives teh best outcome, and scoliosis will usu. not progress once skeleton matures as long as curve is <40°. If curvature is >50° at the time of skeleton maturity, then there will likely be ongoing progression of curve each year of life.

Biceps Tendon Rupture

Long head of biceps tendon Rupture occurs @ the bony attachment or tendon-labral junction. Pt: men, 40-60yo, secondary to chronic inflammation or degeneration. If pt is younger, it is usu. d/t sporting activities, trauma or heavy lifting. Sxs: painful, worse at night, worse with overhead or repetitive activities, palpable (often visible) mass in upper arm, muscle mass has retracted. Tx: conservative or surgical depending on functional deficits.

Medial Collateral Ligament Sprain (Grade II)

MCL is 1° stabilizer against valgus force and lateral rotation of the tibia (esp. during knee flexion) The ligament is *extra-articular*. Grade II: partial tearing of ligament fibers, resulting in joint laxity. In this grade, it is common for the medial CAPSULAR ligament to ALSO be involved. Injured by direct blow against lateral surface of knee causing significant valgus stress, twisting the knee, muscle weakness resulting in poor dynamic stabilization. Pt: inability to fully extend & flex the knee, pain, significant tenderness along medial knee, may have decreased strength and proprioception, antalgic gait. Discernable laxity with valgus testing, instability, moderate swelling. *Severe swelling may indicate meniscus or cruciate ligament involvement* --> must test for these as well. Imaging: uncommon to use MRI d/t $$$ if suspecting MCL sprain only, but may be used under extenuating circumstances. Exam: Valgus stress test (pt may show 5-15° laxity if positive). Must also complete special tests for menisci, and ACL to determine if they are involved. Tx: RICE, acetaminophen, or NSAIDs. Pt may use a full-length knee immobilizer or hinge brace and crutches to limit WBing for initial rehab. PT: prioritize ROM (heel slides, stationary cycling w/o resistance) and begin w/ light resistive exercise (quadriceps, isometrics, closed kinetic chain exercise). Functionaly activities (gait, stairs). Modalities: e-stim, transverse friction massage to prevent adhesions. *However, do NOT massage proximal attachment of MCL d/t potential bony periosteal disruption*. Pt must complete functional progression before returning to unrestricted activity. *Crutches to be used until pt has adequate extension of knee.* Prognosis: PLOF in *4-8wks* (as long as no other structures are involved)- full ROM, no limp, no swelling, competence with agility testing. Residual laxity = higher risk of reinjury.

Osteogenesis Imperfecta

OI- There are 4 types rare congenital disorder of collagen synthesis that affects all connective tissues and bones in the body. Genes for Type 1 collagen production (COL1A1 & COL1A2) become mutated (either d/t autosomal dominant or recessive trait or d/t spontaneous mutation). This reduces collagen production by 20-50%. Prevalence = 30,000-50,000 people in U.S.A. In addition to CT and bone affects, OI can also compromise growth, hearing, cardiopulm function, & joint integrity. Type I= mildest, near normal growth and appearance, fx usu. stop after puberty. Blue scleraa, easy brusing, traingular face, possible hearing loss. Community ambulators. Type II= *most severe* form, child dies in utero or by early childhood, significant fragility of CTs, many fractures with extreme deformities and soft skull. Type III= severe, but children have greater ossification of skull. Sig. growth retardation, progressive deformities, ongoing fx, severe osteoporosis, triangular face, blue sclera and sig limited w/ functional mobility. 26% household ambulators. Type IV= milder, mild-mod fragility and osteoporosis (worse than Type I), fx are common but improve after puberty, shorter stature, bowing of long bones, barrel shape rib cage, possible hearing loss, brittle teeth, normal sclera, normal life expectancy. 57% household ambulators & 26% community ambulators. *Dx: skin biopsy to test collagen and type of OI* Imaging: X-rays and bone scans can be used for evidence of deformities and old fx. Bone densitometry may be used to measure bone mass and estimate risk of fx for specific sites within the body. (Dx is made through these tests and in combination with exam and hx.) PT Exam: ask about falls, assess hyper- and hypo-mobility, look at need/fit for orthotics and other supportive ADs. *Assess AROM only.* Pt may also have delayed developmental mile-stones, laxity, poor mm. development. Tx: maximize independence and mobility, optimal bone mass and muscle strength, prevent fx and deformities. Medications are used but not extremely effective. Nutrition counseling, dental care. PT: lightweight orthotics, parent handling techniques, recognition of fx, positioning, activities to facilitate safe movement. Developmental activities, strength, positioning, WBing, use of mobility aids (scooters, riding toys, or w/c). Swimming is a good alternative for strengthening and exercise. *Strength training must avoid rotational forces, placing weights near a joint, and using long lever arms). HEP: standing program, along with activities above. Promote movement and exercise in safe fashion to optimize strength and bone mass. Surgery: "rodding" indicated if child has more than 2 fx in same bone within 6mo, or if angle of long bone does not allow for stable ambulation. Prognosis: PT needed intermittently over course of childhood (depends on severity and 2° complications). HEP must be established for optimal results. PT must work closely with MD and caregivers. *A child's ability to sit by 10mo is strong predictor of child's ability to ambulate in the future).

Transfemoral Amputation d/t Osteosarcoma

Osteosarcoma is 2nd most common 1° bone tumor, highly malignant cancer, begins in medullary cavity (found in osteoblasts within the mesenchymal cells), usu. in femur or tibia (long bones), often located in the metaphysis (esp. the fastest growing one). Will metastasize to the lungs very quickly (90% of cases). *50% will occur in the knee region*. Pt: usu. young children, boys more often, adolescents, and young adults <30yo. Often occurs during growth spurts. It may develop secondary to Paget's disease, osteoblastoma, giant cell tumor, or chronic osteomyelitis. Sxs: pain & swelling, night pain, pain with exercise, development of lump, weakening of LE → leading to fx. *Sometimes fx is the first indicator of cancer*. Imaging: X-ray, MRI, and Scintigraphy help determine location, size, etc. *"Codman's Triangle" can be seen on x-ray indicating reactive bone @ site where periosteum has been elevated by neoplasm. Dx: Definitive dx is done with biopsy of tumor. PT Exam: may want to auscultate the lungs (high risk of lung metastases), ases w/c mobility, temp of limb, phantom pain, aligment of prosthesis, etc. Watch for: fatigue, loss of balance, phantom pain, hypersensitivity, psychological issues regarding limb los. Side effects from chemotherapy (anemia, abnormal bleeding, infection, kidney impairment) → may limit ability to use prosthesis. Meds: pain, medication to deter effects from cancer treatment. PT should begin *immediately* after transfemoral amputation for preprosthetic interventions (ROM, positioning, strengthening, desensitization, residual limb wrapping, functional mobility, gait training, patient education for care of residual limb). *Pt with transfemoral amputation should lie prone for a period of time ea. day to prevent hip flexion contracture!* If contracture occurs → may need to do serial casting. HEP: limb desensitizaiton, stretching, positioning, and prone lying. Pt must be independent w/ residual limb care, skin inspection, and proper wrapping. *Endurance, strength, and mobility w/ an AD are necessary before prosthetic training*. Prognosis: PT is needed for preprosthetic and prosthetic training. Pt should be able to achieve established goals depending on general health, cognition, motivation, support, etc. 5-yr-cure rate= 70-80%. Long-term outcome depends on status of cancer.

Psoriatic Arthritis

Rheumatic condition characterized by inflammatory arthritis often has psoriatic skin lesions Sxs: silver or grey scaly spots on scalp, elbow, knees, spine, pitting fingernailes, toenails, pain and swelling in 1 or more joints, swelling of fingers and toes. 20-50yo. Genetics, psoriasis, and environmental factors.

Rotator Cuff Tear (RCT)

Rotator cuff is made up of supraspinatus, infraspinatus, teres minor, and subscapularis mm. Together, they provide dynamic stability to glenohumeral jt. Tear usu. happens to the supraspinatus m. but it can occur to others. Injury can be d/t trauma or chronic degenerative pathology (tendonitis). Tears are classified as: Partial-thickness- *most painful* Full-thickness- significant functional deficits, esp ER and ABD. Acute Chronic Degenerative Pt: either older adults (dicreased tissue elasticity and vascularity) or in younger pt (traumatic injury- fall on oustretched arm, sudden strain or repetitive high demand-baseball). *Weak and Painful*. Lateral shoulder, radiating sxs into upper arm and deltoid. Instability or stiffness, GH grinding, crepitus, night pain, discomfort when lying on injured side. If it is a traumatic injury, the pt may be able to identify acute pain more specifically. DX: *usu. made with MRI*, X-ray can also detect bone spurs. In young pt, a tear may also cause a small avulsion fx at G. tuberosity. PT Exam: Drop Arm Test and Empty Can Test (supraspinatus injury). Also look for signs of add'l shoulder pathologies (scapular instability, GH instability, impingement). Tx: analgesics, anti-inflamm meds, NSAIDs, local cortison injections. Surgery: may be indicated right away depending on etiology and size of tear. Include use of arthroscopic or open technique: subacromial decompression, repair of torn tendon, or both. Post-op protocols vary, usu immobilized w/ sling and small ABD pillow for period of time (6wks). → Conservative: older patients or chronic injuries (usu. attempted prior to surgery). Should begin *immediately* for those not getting surgery. These pts are @ a higher risk of rupture or increased size of tear in the future. *Acute phase of PT*: cryotherapy, activity modification, ROM, rest, gentle isometric exercise. Progression (surgery and conservative pt): restoration of normal mobility via joint mobs, ROM, progressive strength, palliative modalities. *Promote scapular stability, posture re-edu., and modification of functional/work/recreational activities*. Must work to prevent development of adhesive capsulitis. HEP: must adhere to post-op restrictions! Palliative care, ROM, strengthening, based on protocol. Prognosis: Depends on tx approach (surgical vs. non-operative) and on size of tear. Some pts may never fully recover. *Pt will typically regain function in 4-6months*. Heavy lifting can be restricted for 6-12mo. Dynamic overhead activities may be restricter up to *1 year*. Full return to sport may *extend beyond a year*.

Spondylolisthesis- Degenerative (DS)

Spondylolisthesis= "forward slippage of one vertebra on the vertebra below". Degenerative Spondylolisthesis: caused by weakening of joints that allows for forward slippage of 1 vertebral segment d/t degenerative changes (arthritis, segmental ligamentous instability, & subluxation of hypertrophic facet joint that develop bone spurs, this actually weakens the spin itself), can result in stenosis of spinal canal. *Most common site is a L4-L5 (L4 nerve root is compressed)*. The slippage can cause cauda equina sxs d/t stenosis. Pain is a result of ischemia and poor nourishment following compression. Can also irritate the spinal disk, PLL & ALL, and vertebral periosteum and bone. The slippage is usually limited d/t 2° bony restraints of the spine. Pt: >50yo, Women, African American. Sxs: Back pain increases w/ exercises, lifting overhead, prolonged standing, getting out of bed/car, walking up stairs or incline, positioning in extension. Pain may radiate depending on stenosis. *Sensory and motor loss may follow nyotomal &/or dermatome distribution*. However, most pts do not have sig. neuro deficits. Progression: further slippage does not correlate to increased sxs. Sxs may increase and decrease w/o progression. Imaging: *X-ray required for definitive diagnosis*. CT or MRI may be used to rule out contributing conditions or to further assess nerve impingement. Tx:Education, Medication (NSAIDs, Corticosteroids, Epidural steroid injections, selective nerve root injections). Activity modifications, Rest, and PT. *Avoid long-term bed rest!* PT: wait until acute phase has subsided, then begin: *William's flexion exercise, abdominal strengthening, reduction of lumbar lordosis.* Back school, modalities, postural edu., exercises for core stabilization and increased flexibility. *Bracing or corset may help relieve intradiscal pressure*. Surgery: only indicated when conservativ tx fails, pain becomes disabling, or there is significant neurolgical impairments. Surgery involves decompression w/ or w/o spinal fusion. Prognosis: *conservative tx is successful* for most DS patients.

Lateral Epicondylitis

Tennis elbow- inflammation or degeneration of common extensor tendon and periosteium, causing pain at the lateral epicondyle of the elbow & possible adhesions. Constant microtrauma --> doesn't allow for healing. Caused by repeated overuse of wrist extensors (esp. extensor carpi radialis brevis), resulting in microscopic tearing and damage. May also affect other wrist extensors (ED, ECRL, ECU). *Repetitive wrist extension and supination*. Pt: Men, late 30's through 40's (d/t loss of extensibility of CTs w/ age), tennis player (backhand hits), painting, hand tools, gardening, any repeated activity with forceful wrist extension. Unilateral involvement. May have difficulty holding/gripping objects, decreased functional forearm strength. Pain sometimes radiates into dorsum of hand, pt may note pain at night. Worse w/ wrist flexion (with elbow straight), wrist extension, and radial deviation. Imaging: *no lab or imaging studies are needed to dx Lateral Epicondylitis*. X-ray or MRI might be used to rule out other conditions. *Electrodiagnostic tests are only useful if there is radial nerve involvement*. Exam: Cozen's Test, Mill's Test, and Lateral Epicondylitis test. *If increased pain w/ resisted wrist extension = involvement of Extensor Carpi Radialis Brevis* Tx: NSAIDs PT: Remediate and modify training, technique, equipment use for athletes. Initially: RICE & possible resting splint. *During initial phase, pt should avoid all activities that aggravate injury*. Phonophoresis w/ hydrocortisone, Ionto w/ dexamethasone. Progression --> stretch, strengthen, *all exercises to remain pain-free*, E-stim, cryotherapy. Exercises for elbow, wrist, and hand. Porgression --> resistive, isokinetic and sport-specific exercises. May use counter-force bracing (forearm band), pt wshould wean from brace before end of rehab. Prognosis: Overall outcome is favorable, pt should be able to return to PLOF. *If conservative tx does not help after 2-3mo, then pt may have surgery*. Pt should continue stretching and strengthening to prevent recurrence.

Rotator Cuff Tendonitis

Usu. caused by repetitive overhead activities that causes impingement (usu. of supraspinatus, but can affect other rotator cuff mm and the bicipeps tendon and buristis). Impingement occurs b/c the weak supraspinatus mm. cannot adequately depress the head of the humerus in the glenoid fossa as the arm is elevated. 1° Impingement= intrinsic or extrinsic factors in the subacromial space. 2° Impingement= impingement d/t poor mechanics or instability @ the shoulder joint. Pt: 25-40yo (usu. but there are stages- see below), overhead activities (swimming, tennis, painting, baseball, manual labor). Also increased use of UE after period of inactivity increases risk. Sxs: difficulty with overhead activities, *dull ache*, weakness, *painful arc b/w 60-120° active ABD*, painful palpation of musculotendinous junction, pain with stretching or resisted contraction, pain @ nigh esp. sleeping on injured side, difficulty dressing, repetitive should motions (lifting,, reaching, throwing, swinging or pushing/pulling). Imaging: *usu. do NOT use MRI prior to trying conservative tx because it is $$$*. X-ray can identify calcification and bony abnormalities. PT Exam: Empty Can Test, Jobe Test, Neer Impingement Test, Hawkins-Kennedy Impingement Test. May also look for pathology/impingment of other structures (glenoid labrum, biceps, bursa). However, it is very difficult to determine exact level of involvement of each of the structures. Tx: analgesics and NSAIDs. *Acute PT Tx*: cryotherapy, activity modification, ROM, and rest. Progression: strengthening (all ROM and strength exercises should be *pain-free*) strength exercise is initiated w/ arm at pt's side to prevent impingment (elastic tubing or handheld weights are preferred equipment of choice), ROM (pulley-system or cane). *Entire rotator cuff must be strong before trying overhead activities. Shoulder shrugs and push-ups w/ arms ABD to 90° are good for upper trap and serratus anterior (elevates acromion w/o direct contact w/ rotator cuff). Prognosis: conservative management, *4-6wks* PLOF Note different stages of impingement: Stage 1- <25yo, localized inflamm, edema, minimal bleeding Stage 2- progressive deterioration, 25-40yo Stage 3- >40yo, end-stage, usu. disruption and or rupture of numerous soft tissue structures.

Achilles Tendonitis

acute or chronic d/t repetitive microtrauma = builds scar tissue Pt feels aching sensation after activity and progression of pain w/ walking. Acute tx: use anti-inflammtory meds, rest for 2-3wks,and use heel lift. Chronic stage tx: sxs and pain last beyond 6wks. Pt has thickened and nodular achilles tendon. Surgery may be needed at this stage.

Patellofemoral Syndrome

caused by abnormal tracking of patella between the femoral condyles. Often occurs when patella is pulled too far laterally during knee extension. Patellofemoral Syndrome causes damage to articular cartilage of patella (softening of cartilage or complete destruction resulting in exposure of subchondral bone) Common in adolescence, females>males, direct association w/ activity level of pt. In older populations it is related to OA. Add'l factors associated with PFS is patella alta, insufficient lateral femoral condyle, weak vastus medialis obliquues, excessive pronation, excessive knee valgus, tightness in LE mm (iliopsoas, HS, gastroc, vastus lateralis) Pt: describes gradual onset of anterior knee pain following increase in physical activity, pain behind patella, increases with compressive forces (stairs, jumping, and prolonged static position (sitting w/ knee flexed 90° in car, plane, theatre). Point tenderness over lateral border and crepitus when patella is manually compressed into trochlear groove. Pt may have visible quadriceps atrophy, esp. along vastus medialis obliquus. Pt may have burning pain when sitting for long periods of time or ascending/descending stairs. Imaging: *imaging and labs are not commonly used to make this dx*. X-ray may be used to rule out fx, examine configuration of patellofemoral joint, and identify potential osteophytes, jt space narrowing, patella alta, and arthritis. Arthrogram and arthroscopy can be used to examine articular cartilage. Exam: Clarke's Sign, patient's Q angle (normal: males-13°, females-18°), alignment of pt's feet, patella grind test (active and passive), dynamic patella tracking, patella glide test, palpation of structures, joint play, soft tissue restrictions, joint pain. Differential diagnosis: referred pain from hip, Osgood-Schlatter, neuroma, patellar tendonitis, plica syndrome, and infection of knee joint. Tx: *usu. successful with conservative measures, surgery is rare*. Acetaminophen, NSAIDs, steroid injections into joint. PT: edema management, stretching (HS, IT band, TFL, and rectus femoris), strength (esp. vastus medialis obliquus, quad setting, SLR, and mini-squats w/ hip add, biofeedback), ROM, activity modification, Mobilization to increase medial glide (stretch lateral fascia). Patellar taping to improve patellar position and tracking. *Avoid deep squats- this will aggravate condition* HEP: ROM, strength, stretch, palliative, and functional activities. *Proper footwear and orthotics to improve alignment.* Prognosis: Pt can usu. return to PLOF after *4-6wks* of PT. However, if underlying cause is not properly addressed, pt may get worse. Pt may also have incidence of exacerbation d/t activity changes that require additional PT.

Amyotrophic Lateral Sclerosis (ALS)

chronic degenerative disease producing both UMN and LMN impairments d/t demyelination, axonal swelling, and atrophy in the cerebral cortex, premotor areas, sensory cortex, and temporal cortex. Rapid demyelination occurs in the giant pyramidal cells of the cerebral cortex and affect areas of the corticospinal tracts, cell bodies of LMNs in the gray matter, anterior horn cells, and areas in the precentral gyrus of the cortex. →These lead to denervation of muscle fibers, muscle atrophy, and weakness. Cause of ALS is unknown in 90% of cases, familial ALS has genetic component. Overall, theories include slow acting virus metabolic disturbances, toxicity of lead and aluminum. Pt: Men, 40-70yo, UMN and LMN sxs. Fatigue, oral motor impairment, fasciculations, spasticity, motor paralysis, eventual respiratory paralysis. LMN: asymmetrical mm weakness, cramping, atrophy in the hands → progress to fasciculations, atrophy and mm wasting. Disease progresses in *distal to proximal path*. UMN: loss of inhibition of muscle, discoordinated movement, spasticity, clonus, (+) Babinski reflex. Bulbar involvement (dysarthria, dysphagia, emotional lability). Dx: EMG (assess fibrillation and muscle fasciculations), muscle biopsy (verify LMN involvement rather than mm disease), and spinal tap (reveals higher protein content). Dx relies heavily on sxs of *both UMN and LMN involvement, but w/o sensory impairment*. Exam: must rule out other neurological conditions. PT Exam: monitor for pathological reflexes (Babinski, ATNR), watch for paralysis of vocal cords, swallowing impairment, contractures, decubiti, and breathing difficulty. *However, sensation, eye movement, and bowel/bladder function remain intact). Tx: meds: riluzole/Rilutek (can effect progression of disease process, long-term effects are unknown). Sxs tx: antichoinergic, antispasticity, antidepressants. PT: QoL, low-level exercise (*as long as pt does not exercise to fatigue = further weakness*), ROM, mobility training, AD training, w/c prescription, bronchial hygiene, energy conservation. HEP: mobility, pacing skills, energy conservation, caregiver training for positioning, bronchial hygiene, ROM, and assistance w/ mobility. Prognosis: this is a progressive disease, pt will die 2-5yrs (d/t respiratory failure). PT will not stop progression of ALS.

Temporomandibular Joint Dysfunction (TMD)

complex joint, condylar, hing, and synovial joint. Contains fibrocartilagionous surfaces (convex mandibular epicondyle & concave temporal fossa) along with an articular disc. TMD is caused by injury, derangement or incongruence of the TMJ itself, intra-articular disks, and/or supporting surrounding structures. Over time the meniscus of the TMJ becomes compressed and torn, allowing for bony portion of the joint (ball & socket) to deteriorate 2° to grinding of bone on bone. Primary TMD caused by 3° etiological factors 1)predisposing, 2) triggering, 3) and perpetuating/sustaining factors. Secondary TMD caused by: injury, trauma, fx, dislocations, congenital abnormalities, internal derangement, arthritis, dislocation, disk degeneration, metabolic conditions, or stress, tension-relieving habits. Risk Factors: chewing on one side, eating tough food, clenching or grinding teeth, gum chewing and nail biting. PT: Female, 20-40yo (child-bearing age), pain (recurring or constant), mm spasm, abnormal/limited jaw motion, headache, and tinnitus. Can be unilateral or bilateral. "Clicking or poppin" with motion. Locking of TMJ, restriction of mvmt of the unaffected side, and/or pulling of mandible towards affected side. Imaging: can include x-ray, MRI, mandibular kinesiography, CT scan, and dental examination. Occlusion exam- evaluate pt's bite. PT Exam: upper quarter screening, TMJ loading, condyle-meniscus relationship, review of sxs. Cranial nerve integrity, breathing patterns, among the normal examination aspects. Tx: splinting/mouth guard, PT, possible surgery. Analgesics, NSAIDs, *muscle relaxants, and antianxiety meds*. PT:depends on exact etiology of TMD: patient edu. regarding habits (nail biting, hair chewing, etc.), posture retraining, use of modalities (moist heat, ice, biofeedback, ultrasound, electrostimulation, TENS, and massage). Soft tissue manipulation, joint mobs, ROM, stretching, occlusal appliance prescription, relaxation techniques. *Pt should avoid foods and activities (gum chewing) that aggravate TMJ. Pt must have ongoing consistency of HEP to maintain progress. Surgery: if conservative tx fails or the etiology indicates need for surgery: condylectomy, osteotomy, arthrotomy, arthroscopy, reduction of subluxation or joint debridement. Prognosis: PT should focus on maximizing function and alleviating pain, and should be successful in improving pt' condition and decreasing sxs. Pt does have increased risk of recurrence, but may not have any long-term effects.

Lateral Ankle Sprain (Grade II)

d/t significant inversion that damages the lateral ligament complex (ATFL, CFL, and PTFL). [Deltoid ligament is on the opposite side of the ankle and is the strongest ankle ligaments, so these are not usually injured, in fact the medial malleolus will likely rupture before the deltoid ligaments fail.] *ATFL usu. gets injured* b/c it resists inversion of talus and calcaneus & anterior translation of talus on tibia. it is taut during PF. CFL resists inversion of talus within midrange of talocrural motion. PTFL resists posterior translation of talus and is the strongest of the 3 lateral ligs. Pt: sporting activities, agility, jumping, deconditioned, poor proprioception, obesity, recurrent sprain. Significant pain along lateral aspect of ankle esp. ATFL. Antalgic gait, pain with passive inversion and end-rang PF (position maximally stretches ATFL), usually obvious laxity, Ecchymosis, mod-severe edema (may persist for a while) Exam: must rule out Achilles tendon rupture via AROM assessment &/or Thompson Test. MMT likely limited d/t pain. *Anterior drawer test for ankle*- ATFL check Talar tilt test- CFL (talus moved into adduction) **Distal pulses and sensory integrity* d/t risk of neurovascular damage* Other things to assess for: osteochondral or chondral injuries to talar dome, neurovascular disruption, Achilles tendon rupture. Tx: RICE Principles initially. May use crutches until FWB is tolerated. Meds: MSAIDs, acetaminophen. Surgery: only if complications like fx or neurovascular damage. PT: ROM, proprioception, edema management, light resistive exercises, passive stretching (prevent mm shortening), joint mobs for capsular restriction. Resistive exercises (isometric, open-chain, closed-chain, *to include peroneal mm for dynamic ankle stability). SLS on variable surfaces (proprio and balance), gait train, stair management. Agility for sport-specific needs. Modalities: superficial and e-stim. Transverse friction massage (once inflamm is gone). *Functional progression prior to returning to unrestricted activity*. Prognosis: return to PLOF *2-6wks* Pt may need taping or bracing for a period of time if returning to athletic/competitive activities. Residual laxity = increased rate of recurrence

Lateral Collateral Ligament Sprain (grade II)

far less common than MCL injury Tx is same as MCL injury.

Glenoid labrum tear

fibrocartilage rim, surrounds glenoid cavity, attaches to glenoid cavity of scapula to increase depth and prtoet edge of bone. Tear occurs w/ anterior damage or subluxation. *Bankart lesion:* avulsion of labral ligamentous complex from anteroinferios apect of glenoid. I think this will usually cause damage to the IGHL as well (according to youtube review video. This causes anterior jt instability. Dx with a CT scan, often requires surgery.

Medial Epicondylitis

golfer's or swimmer's elbow repeated microtrauma to flexor carpi radialis &/or humeral head of pronator teres during pronation and wrist flexion. Pain w/ resisted wrist flexion and resisted pronation. Tx is very similar to latearl epicondylitis, however, directed at appropriate location. Complete immobilization is *NEVER* recommended, however, a counter-force bracing or splint may be used.

Parkinson's Disease

group of disorders within the subcortical gray matter of the basal ganglia. Primary degenerative disorder characterized by decrease in production of dopamine in the substantia nigra portion of the basal ganglia, also damage to the corpus striatum. Creates an imbalance b/w dopamine and acetylcholine. There is damage to the loop b/w the basal ganglia and the cerebrum. RFs: genetics, toxicity from carbon monoxide, excessive manganese or Cu, carbon disulfide, vascular impairment of striatum, encephalitis, other neuro disorders (Huntington's or Alzheimer's). Pt: 50-79yo, will present with resting tremor of the hands (*pill-rolling*) and feet. Balance disturbance, difficulty rolling over or rising from bed, impaired fine manipulative movments (writing, bathing, dressing). Hypokinesia, sluggish mvmt, difficulty initiating (akinesia) and stopping movements, *festinating*, bradykinesia, poor posture, dysphagia, *"cogwheel" or "lead pip" rigidity" of skeletal mm*. *"Freezing during gait, speech, blinking." Decreased arm movement, *Mask-like expression*. Imaging: *There are no imaging or lab studies that initialy dx PD.* CT or MRI might be used to rule out other diseases. PT Exam: tremor assessment, Parkinson's Disease Questionnaire (PDQ-39), look for stooped posture, increased fall risk, dysphagia, pulmonary impairments, skin care. Tx: *Heavy pharmacological management of sxs* Dopamine replacement (Levodopa, Sinemet, Madopar). Also antihistamines, anticholinergics, and antidepresants. PT Tx: endurance, strength, functional mobility, *use verbal cueing and oral/visual feedback!* Family edu, balance, gait, stretching, trunk rotation, AD training, relaxation techniques, respiratory therapy. HEP: funcitonal mobility skills, relaxation techniques, ROM, stretching, endurance. Caregiver competence is very important. Recommend psych and nutrition counseling. Prognosis: disease will progress 25-30yrs prior to onset of pharmacology intervention. Pt's have a fairly normal lifespan. Death often occurs d/t complications of bronchopneumonia, inactivity, and deconditioning. PT is recommended intermittently to focus on function and QoL.

Total Knee Arthroplasty (TKA)

indicated for progressive and disabling pain in the knee joint d/t severe degenerative osteoarthritic destruction of the articular cartilage, resulting in bone-on-bone contact (will also have decreased joint space and osteophyte formation). Pt: older, OA (*most common reason to get TKA*) hx of sports, trauma, obesity, varus/valgus deformity, mechanical derangement, infection, RA, hemophilia, crystal deposition, AVN of the knee, and bone dysplasia. Sxs: pain worse w/ motion and WBing, impaired ROM, possibleknee deformity, (night pain is common(, stiffness, swelling, locking, giving way, patients often try conservative tx w/ limited success. Imaging: X-ray, CT, and MRI to determine extent of deterioration, and may be taken post-op to ensure proper fit. Exam Pain assessment scale and Arthritis Impact Measurement Tool for baseline. Pt may also report sleep disorders and depresseion d/t disease process, other joint OA. Determine *contraindications for surgery*: active infection, severe obesity, sig genu recurvatum, arterial insufficiency, neuropathic joint, certain mental illness. PT Exam: watch for post-op complications: infection, vascular damage, patellofemoral instability, fx, PE, nerve damage, loosened prosthesis, arthrofibrosis. Tx: pt will be on anticoagulants and pain meds. *WBing precautions: cemented= PWB or WBAT, non-cemented= TTWB for up to 6wks.* PT: knee immobilizer, elevation of limb, cryotherapy, intermittent ROM w/ CPM machine, knee protocol exercises. Focus on mobility training, WBing status, appropriate AD. Ankle pumps, quad sets, HS sets, ROM, and stretching. Goal of 90° flexion, and 0° ext prior to d/c from hospital. *Precautions: avoid squatting, quick pivoting, pillow under knee, low seating.* Progression (once pt cleared for WBAT) work on strengthening w/ closed-chain exercises and functional activities. Prognosis: pain relief, full return to functional activities within *8-12wks* (depending on cement or noncement prosthesis).

Total Shoulder Arthroplasty (TSA)

indicated for severe pain and impaired shoulder motion d/t deterioration of glenohumeral joint (when conservative tx has failed). Pt: *55-70yo (if d/t arthritis) or 40-50yo (if d/t irreparable damage from dislocation or AVN of shoulder). Impaired ROM, unremitting pain= 1° indication for TSA. Imaging: X-ray to reveal level of degeneration. MRI or CT to assess integrity of rotator cuff and deltoid mm, as well as overall integrity of shoulder complex. Complications depend on: -Prosthesis types: unconstrained, semi-constrained, constrained -Cemented prosthesis vs. Press-fit prosthesis. -Integrity of rotator cuff musculature. PT Exam: watch for post-op complications (mechanical loosening, instability, RCT, implant failure, heterotopic ossification, intraoperative fx. PT: pt is usu. in hospital for 2-5days. CPM may be described. Pt will be on anticoagulation and pain meds. PT begins *the day after surgery*. Follow surgeon's shoulder rehab protocol. *AROM is contraindicated during 1st phase of rehab*. Can do pendulum and wand exercises, as well as self-ROM. Work on pain management, prevention of adhesions, functional activities, PROM/AAROM/AROM, ther ex, edema control, pt edu. in self-ROM and wand/pendulum exercises, use of modalities. *No IR or ER beyond 35-40° during first 2-3wks post-surgery*. *Neer shoulder protocol* initiates isometric shoulder exercises 3wks after surgery and active shoulder exercises 6wks after surgery. Prognosis: good prognosis to return to functional motion and relieve pain (no timeline given).

Bicipital Tendonitis

inflammatory process of long head of teh biceps tendon, often d/t impingement or an inflammatory injury, repeated full ABD & lateral rotation (ER) of the humeral head (can cause direct trauma w/ this movement) --> leads to irritation/inflammation/edema/microscopic tears = degeneration --> then leads to abnormal arrangement of collagen fibers. Pt: continuous repetitive shoulder motions and overuse, overhead activity, throwing, swimming, swinging racquet, etc. Reports deep ache in front and top of shoulder, worse w/ overhead and lifting, rest helps. *"catching or slipping" may indicate tear of transverse humeral ligament.* Can also be 2° to rotator cuff disease, impingement, labral tears, etc. Exam: Biceps resistance test, Yergason's Test, Speed's Test. Imaging: MRI not recommended unless therapy fails (not first line), X-ray won't show tendonitis, but could show calcification in the groove or a subacromial spur. Exam may also show instability & subluxation d/t degeneration, impingement syndrome RC tendonitis, glehohumeral instability. Medical Tx: pain relief and decreased inflammation drugs, NSAIDs. Might temporarily splint/immobilize briefly. *Pt should avoid all overhead mvmt, reaching, and lifting.* PT: not always right away but if it is, should focus on general ed. of pathology, guidelines for restrictions, pendulum exercises, TENS, heat or cold (pain relief), iontophoresis, phonophoresis. Progressing after acute phase -->stretching and strengthening affected mm. restor tendon's function, prevent future injury. HEP: warm-up prior to vigorous activity, stretch, strength, body mechanics, avoid painful activity, endurance. Must continue (ongoing) to prevent recurence. Prognosis: full ROM w/o pain, *6-8wks* of PT ~10% of pt do not progress and deteriorate and experience rupture of the tendon. Surgery: *only if conservative tx of at least 6mo has failed* --> then arthroscopic decompression & acromioplasty w/ anterior acromionectomy.

Acute bursitis (shoulder)

intense and sometimes throbbing pain over lateral brachial region. Can occur 2° to calcific tendonitis. AROM and PROM is limited in all directions d/t pain. ABD >60° and FLEX >90° = severe pain Lasts for only a few days. Will resolve itself within a few weeks.

Cerebrovascular Accident (CVA)

interruption of cerebral circulation & prolonged ischemia to an artery in the brain → causes destruction of surrounding brain tissue and neuro deficits. 1) Stroke in evlolution (infarct slowly develops over 1-2days) 2) Completed stroke (abrupt infarct w/ immediate neuro deficits). Strokes can be ischemic (thrombus, embolus, lacunar) or Hemorrhagic (intracerebral, subdural, subarachnoid) Modifiable RFs: HTN-*most prevalent*, atherosclerosis, CVD, diabetes, hyperlipidemia, smoking, and obesity. Non-modifiable RFs: age, race, family hx, and sex. *Age constitutes the greatest risk for CVA* *Esp >65yo* Pt: >65, hemiplegia or hemiparesis, sensory/visual/perceptual impairments, impaired balance, dysphagia, aphasia, cognitive deficits, incontinence, emotional lability. Imaging: CT- confirm infarct (but may be negative for a few days), MRI- dx if ischemia immediately, PET- info about cerebral perfusion and cell function, US- diminished blood flow in vessels, Angiography- identify clot and need for surgery. Also: may do chest x-ray to rule out lung disease, and an ECG to determine potential cardiac abnormalities. L CVA= weak/paralyzed R side, impaired processing, increasd frustration, aphasia, dysphagia, motor apraxia, and R hemianopsia. R CVA= weak/paralyzed L side, poor attn, impaired awareness and judgment, spatial deficits, memory deficits, left inattention, emotional lability, impulsivebehavior, and L hemianopsia. Tx: thrombolytic agents (*contraindicated for hemorrhagic strokes*), diuretics, antihypertensive, may have long-term use of aspirin. Acute PT:positioning, pressure relief, sensory awarenss and integration, ROM, WBing, facilitation, muscle re-ed, balance, posture. Approaches for neuro rehab: NDT, motor control, Brunnstrom's Mvmt Therapy in Hemiplgia, Rood and Kabat, Knott, and PNF. HEP: fall prevention, ctrl spasticity, endurance, functional mobility. Prognosis: 75% of pt return home with various levels of function. Outcome depends on overall health, cognition, motivation, motor recovery, residual deficits, and family support. *First 3mo of recovery= most measurable neurologic revoer and good indicator of long-term outcome) Pt can continue to improve ctrl of mvmt and show progress for ~2-3yrs post CVA*.

PCL Tear

less common than ACL. Mechanism of injury: "dashboard injury or forced knee hyperflexion as the foot is plantar flexed. Presentation: effusion, posterior tenderness, Positive posterior drawer test, limited Knee EXT d/t effusion and stretching of posterior capsule and gastroc. *Might also test with reverse lachman's test, observe for posterior sag sign. PT: strengthening of quadriceps mm. Surgical intervention is rare b/c PCL sprains usu. do not affect athletic performance. PCL sprain does alter arthrokinematics of knee joint and will increase susceptibility to degenerative changes (arthritis).

Total Hip Arthroplasty (THA)

may be needed d/t progressive and severe osteoarthritis (leading to degeneration of articular cartilage resulting in bone-on-bone contact → usu. affecting both the femur and the acetabulum) or RA in the hip joint, development dysplasia of the hips, tumors, failed reconstruction of hip or other hip conditions that produce incapacitating pain and disability. May also be needed 2° to trauma, AVN, or a nonunion fx. Usu. pt's will try conservative therapy first, before going to a THA. Pt: >55yo, consistent pain (not relieved by conservative measures), decreased ROM, impaired mobility, pain is worse with motion and WBing. Imaging: may have x-ray, CT, and MRI to view integrity of jt and can rule out fx or tumor. Exam: may use a standardized pain assessment scale and the *Arthritis Impact Measurement Tool* to establish a baseline. Must identify any *contraindications to surgery*: active infection, severe obesity, arterial insufficiency, neuromuscular disease, & certain mental illness. PT Exam: may use Barthel Index to assess self-care and home. Check for low endurance and deconditioning 2° to inactivity (d/t pain). Look for Post-surgical complications *nerve injury, vascular damage, dislocation, pulmonary embolism, myocardial infarction, and CVA. Also signs of loosening of prostehsis, infection, heterotopic ossification, and fracture*. Tx: pt will be on anticoagulant therapy and pain meds. Must adhere to *specific precautions*: Posterolateral approach: leaves hip ABD intact, but interrupts posterior capsule *post-op instability*. Avoid flexion past 90, adduction, and IR. Pt may use an ABD pillow. Anterolateral approach: avoid ER and flexion of hip. Direct lateral approach: used if pt may be noncompliant to avoid posterior dislocation. (leaves posterior part of glute med attached to greater troch and posterior capsule remains intact. *Precuations are to be followed for at least 3mo or when physician clears pt*. *WBing*: cemented THA= PWB, non-cemented= TTWB for up to *6wks*. PT: initiate hip protocol exercises (ankle pumps, quad sets, glute sets, heel slides, isometric ABD), pt edu. regarding precautions and WBing status, scar management, soft tissue mobilization. *At discharge, pt should be able to flex hip to 90°, extend to neutral, and demonstrate adherence to precautions). Prognosis: following surgery, with PT, pt should have diminished to no pain, increased strength and endurance, and improved mobility within *6-8wks* Quality of Life After THA: Harris Hip Scoring System or Special Surgery Rating System

Osteoarthritis

mixed group of conditions, most common type of joint disease A degenerative chronic disorder d/t biochemical breakdown of articular cartilage in the synovial joints... Excessive loading → breakdown chondrocytes → disrupt cartilaginous matrix → loss of joint space → reactive new bone forms (usu. @ the margins and subchondral areas of joint) 1° OA: ideopathic, aging process, older adults. Bilatearly symmetry. 2° OA: results from predisposing condition (trauma) that has damaged the articular cartialge &/or subchondral bone, often occurs in younger individuals. RFs: age, obesity, trauma, infection , repetitive microtrauma, genetics, inflammatory arthritis, neuromuscular and metabolic disorders. Pt: (if >55yo, usu. women) hands (esp. DIP- get Heberden's nodes and PIP joints- Bouchard's nodes- mainly in *women*), knees, hips, and spine. Often bilateral presentation if 1° OA. Decreased ROM and crepitus. Deep, aching joint pain, worse with prolonged activity and better with rest, better with analgesics. As disease progresses, pt will have morning stiffness in affected joints and pain may not respond as well to analgesics. Pt can become progressively inactive which contributes to weight gain and further stress on the joints. Increased risk of strains and sprains in affected OA joints. Imaging: X-ray used for diagnosis. *No lab tests can diagnose this though*. Exam: pt may have effusion *but joints are not usually red or warm*. May have malaligment of joint, gait deviation, and muscle atrophy. Tx: acetaminophen, NSAIDs, Glucocorticoid intra-articular injections *must be used sparingly d/t long-term negative effects*. Weight loss. PT: preserve joint motion and flexibility, posture, work site eval, strength, relaxation, endurance, icing or heat, hydrotherapy, modalities, patient edu, aquatic therapy, functional activity. Assistive device training. *Avoid overexertion and fatigue*. Prognosis: OA is progressive and chornic, PT can help during periods of exacerbation and help minimize efects of process and promote individual indepndence. Surgery: Joint replacement *80-90% of patients older than 65yo have evidence of primary OA, degree of disability depends on sites of involvement and rate of progression. OA of the knee is leading cause of disability in elderly.

Cerebral Palsy

non-progressive movement disorder(most common cause of permanent disability in children). Caused by hypoxic and ischemic injuries (usu. prenatally- 80% of the time) that disrupt normal metabolism, resulting in global damage to fetus. It is classified into several categories: 1) Spastic CP- UMN damage 2) Athetoid CP- damage to Basal Ganglia Monoplegia, hemiplegia, and quadriplegia. Also: mild, moderate, or severe RFs: *prenatal* (Rh incompatibility, mother nutrition, hypothyroidism, infection, diabetes, chromosome abnormality), *perinatal* (multiple or premature births, breech, low birth weight, prolapsed cord, placenta abruption, and asphyxia), or *postnatal* (CVA, head trauma, neonatal infection, brain tumor). *Most common causative factor = prenatal cerebral hypoxia* Pt: child, motor delays, abnormal mm tone and motor ctrl, abnormal reflexes, poor postural ctrl, high risk for hip dislocation, and balance impairments. Intelect, vision, hearing, and perceptual skills may be altered. Imaging/Labs: EEG (suspected CP and/or seizures), X-ray of hips (rule out hip dislocation), blood and urine test- investigate metabolic cause of CP. Observation usu. will dx CP 2° to outward characteristics. PT Exam: watch for aspiration risk, pneumonia, contractures, scoliosis, and constipation. 50-60% of patients will have epilepsy and intellectual disability. Co-morbidities: seizures, vision/hearing/bowel/bladder dysfunction, microcephalus and hydrocephalus. Psychosocial issues (pt and family). Tx: life-long team approach, meds: anti-anxiety, anti-spasticity, and anti-convulsants. PT: use neurodevelopmental tx and sensory integration techniques, normalization of tone, pt and caregiver edu., motor learning, developmental milestones, positioning, stretching, strengthening, balance, and mobility skills. AD, w/c, orthotic prescription. Surgery may be required for hip correction, contractures, motor point block, dorsal rhizotomy, or scoliosis correction. PT Prognosis: main goal is to prevent secondary loss and maximize function. *If a patient is going to ambulate, this will occur by age 8*. mild-moderate CP= near normal lifespane 50% of severe CP die by age of 10.

Patellar tendonitis

overuse condition, inflammatory changes in patellar tendon Most common in athletes who do repetitive jumping. Describes pain over anterior portion of superior tibia with jumpin or stairs, after prolonged sitting,a nd show point tenderness at superior pole of patella tendon. Tx: many of same intervents for PTF Syndrome (ROM, stretching, and palliative)

Multiple Sclerosis

patches of demyelination within the brain and spinal cord that result in plaque development, decreased nerve conduction velocity, and eventual failure of impulse transmission. May be caused by genetics, viral infections, environment. Virus may cause the autoimmune response. Pt: Caucasians, 20-35yo, WOMEN, temperate climate. 4 Types: relapsing-remitting MS (85%), secondary-progressive MS, Primary-progressive MS, or progressive-relapsing MS. Presentation varies depending on type of MS and location of demyelination in the CNS. Sxs: visual problems, paresthesias, and sensory changes, clumsiness, weakness, ataxia, balance dyfunction, and fatigue. Periods of exacerbation and remissions. Imaging: MRI-observation and baseline establishment for lesions. Evoked potentials- slowed nerve conduction. CSF- elevated concentration of gamma globulins and protein levels. Clinical dx can be made if pt experiences 2 separate attacks and show evidence of 2 separate lesions. PT Exam: emotional lability, depression, dementia, psychological problems, spasticity, tremor, weakness, paralysis, sexual dysfunction, and loss of bowel and bladder control. Tx: ABC drugs (approved in tx of MS) that are classified as immunomodulatory meds. PT Tx: regulation of activitiy, relaxation, energy conservation, tone management, balance training, gait training, core stabilization/ctrl, AD use, edu. regarding safety, patterns of fatigue, use of adaptive devicecs. HEP: submax exercise and endurance program. *Exercise in morning when pt is rested.* Break tasks into smaller steps to avoid fatigue, maintain endurance. Aquatic therapy may be beneficial (but must avoid heat and fatigue). *Disease exacerbation can be caused by heat, stress, infection, trauma, and pregnancy.* Prognosis: PT intermittently to maximize functional capacity. Will not alter progression. Most with MS die from secondary complications (disuse atrophy, pressure sores, contractures, pathologic fs, renal infection, pneumonia. If left untreated, 50% will be in w/c in 15yrs. Mortality-rate and long-term outcomes depend on age of dx, # attacks and exacerbations, frequency and duration of remissions, and type of MS. High risk of suicide.

Plantar Fasciitis

platar fascia is a thin layer of tough connective tissue that supports arch of foot. Plantar fasciitis = inflammatory process of plantar fascia (aponeurosis) at its origin on the calcaneus d/t chornic overuse → repetitive stretching d/t excessive foot pronation. Injury can occur to platar fascia directly through microtearing inflammation, and pain. The Abductor Hallucis, Flexor Digitorum Brevis, and Quadratus Plantae mm share same origin on medial tubercle of calcaneus and may also become irritated. Pt: middle-aged adults (although can happen in younger individuals but usu. combined with calcaneal apophysitis) excessive pronation during gait, tightness of foot and calf muscles, obesity, high arch, endurance sports (running, dancing), occupation that requires prolonged walking or standing. Will describe unilateral pain, severe pain when first standing up in morning, often pain radiates proximally up calf and/or distally to toes. Pain subsides for a few hrs during day and then incrases w/ prolonged activity or when pt has been non-WBing for period of time and then resumes WBing. Pt might also describe it as "pain that moves around. Calcaneus may have bony growths near insertion point. Pt usu. has tight Achilles tendon. Imaging: *not usu. used unless conservative tx fails after 6-8wks*. MRI can confirm dx, x-ray and bone scan can rule out stress fx, rhematology work up can rule out systemic etiology, and EMG can rule out nerve entrapment. Exam: mechanism of current injury, training routine, biomechanical analysis of gait (walking/running), foot print analysis, dynamic plantar pressure distribution. Look for bony hypertrophy (heel spur). Tx: local corticosteroid injections or anti-inflammatory meds. Initially, pt may nee to complete relative rest. PT: heel cup prescirption and casting (possible), ice massage, deep friction massage, shoe modification, heel insert, foot orthotic prescription, modification of activities (NWBing endurance exercise), gentle stretching of Achilles tendon and plantar fascia, strengthen intrinsic/extrinsic mm of foot (after acute sxs resolve). HEP: ongoing strengthening and stretching (esp. gastroc and plantar fascia) in morning & before & after exercise), maintain fitness program, proper footwear, orthotics, heel inserts, night tension splints. Prognosis:more functional level within *8wks*. Total resolution of sxs can take up to *12mo* though. Success may depend on: PT, orthotic prescription, splinting, pharmacological injections, and physician follow-up. About 10% of pts can deteriorate and require surgical intervention.

Myasthenia Gravis

proximal mm groups are most affected difficulty with speech, swallowing, chewing involved CNs= eyelid weakness and droopiness *must watch for "crisis" which is life-threatening and is related to fatigue of respiratory muscles PT: acquire baseline respiratory and neuro function monitor respiratory function regularaly review proper position during meals review signs of toxicity and SE of medication plan activity around periods of increased energy energy conservation avoid strenuous exercise and stress avoid excessive hat or cold watch for signs of osteoporosis (d/t long-term corticosteroid use) strengthening with moderate to maximal *isometric contractions*, while avoiding mm fatigue tx should always be based on pt's current sxs, strength, and fatigue level

Tarsal Tunnel Syndrome

tibial n. passes b/w medial malleolus and calcaneus, as it pases through the nerve splits into medial and lateral plantar nn. Pt may have pain w/ WBing but not with direct palpation to platar fascia. Pt may complain of numbness, burning pain, tingling, and paresthesias at the heel as well. This is d/t entrapment and compression of psoterior tibial n or plantar nn within the tarsal tunnel d/t inflammation or thickening of flexor retinaculum.

Torticollis

unilateral contraction to one side with rotation to the opposite side, d/t contraction of SCM. There may be facial asymmetries. Multiple causes: birth trauma, breech position, intrauterine malpositioning, difficult forceps delivery. Fibrosis may be caused by venous occlusion & pressure during birth, add'l theory: intrauterine compartment syndrome. Pt: baby appears normal after birth but then develops sxs of head positioning, muscle spasms of SCM and UT, may have jerky head movements, firm nontender enlargement of SCM (mass often disappears by 6mo). *20% of pt's w/ congenital torticollis have congenital dysplasia of hips.* May also have fascial asymmetries and plagiocephaly. Imaging: might use x-ray to assess potential fx or subluxation, CT or MRI for potential neck mass, EMG for muscle or nerve involvement. PT Exam: Hx of labor & delivery, infant arousal, cranial n integrity, motor function (motor assessment scales, Barthel Index, Bayley Scale of Infant Development, Denver II Scale, Neonatal Behavior Assessment, Alberta Infant Motor Scale. Resting and dynamic posture, AROM and PROM. Tx: Almost always treated conservatively for 12-24mo prior to considering surgery. May use NSAIDs, benzodiazepines, muscle relaxants, anticholinergics, local intramuscular injections (botox or phenol). PT: family education: handling, feeding positions, sleeping positiong, passive stretching to sCM and UT, massage, local heat, analgesics, biofeedback, TENS, AROM with subsequent strengthening. If conservative management fails, then surgery for unipolar SCM release, bipolar SCM release, or selective denervation. *Following surgery → PT Manual Stretching 3x/day for 3-6mo in order to maintain new length* Infant may also have a cervical collar for first 6-12wks after surgery. Prognosis: *85-90% of patients respond to conservative tx and passive stretching within the 1st year of life*. Prognosis is best if pt receives conservative tx prior to age 1.

Erb's Palsy

upper brachial plexus injury or palsy (usu. d/t difficult birth) primarily affecting the muscles of the shoulder and elbow. Occurs d/t avulsion at Erb's point (anterolateral neck). Affects the mm. supplied by C5 and C6: axillary, lateral pectoral, upper and lower subscapular, suprascapular and partial paralysis of the long thoracic and the musculocutaneous nn. Etiology: difficult birth, breech positioin, prolonged labor, or use of forceps → 1 side of baby's neck is tretched which damages the nerves, add'l theory is that congenital chicken pox or amniotic bands may also produce this condition. Can occur in adults d/t stertching, tearing, or trauma to upper brachial plexus network. 4 Types of brachial plexus injuries: avulsion, rupture, neuroma, neurapraxia. Presentation: placcif paralysis= "waiter's tip deformity" (loss of shoulder function, loss of elbow flexion, loss of supination, and the hand is positioned in a pinch grip manner). Imaging: X-ray or MRI to assess if there is damage to bones/joints of neck and shoulder. EMG or Nerve Conduction Studies (NCS)- see if nerve signals are present in UE mm. In complete injuries, nerve conduction studies may be done for median, radial, and ulnar nn. Pt: equally distributed between sex, race, gestational age. PT Exam:Active Movement Scale, Gilbert Shoulder Classification, and Pediatric Outcomes Data Collection Instrument. If condition was caused by amniotic bands → child may have under-develoed extremity or deformed area, may have GH subluxation or dislocation, skeletal deformity, poor bone growth, and learned pattern of non-use. PT Tx: to begin immediately when pt is diagnosed with a priority of increasing AROM and PROM and promoting use of weak UE for functional activities. Prognosis: Therapy *must* begin in infancy for optimal results.If pt has spontaneous recover, it will usu. taked *3-4mo* → then caregivers are given a HEP. 9 out of 10 infants will recover Surgery may be needed if conservative tx fails (it will not restore normal function). Infant will wear a splint for ~3-4wks. Post-Op PT Tx: Caregiver edu. very important regarding positioning to avoid any further traction during child's daily activities. Adapt developmental milstones, WBing activities, and other sensory techniques. *Nerve regeneration occurs at constant speed of 1in/mo, so recover may take months or even years for nerves repaired at cervical spine to reach the mm of the hand*.

Anterior Cord Syndrome (ACS)

usu. affects anterior 2/3 of SC d/t cervical flexion injury or anterior spinal a. embolization. *Complete loss of function, pain, and temperature below level of lesion.* (Spinothalamic and corticospinal tracts) Posterior column is preserved → so pt has intact sensation, vibration, and propriocpetion. ACS has worst prognosis for all SC syndromes (10-15% make functional recovery).