Limbs, Spine, Neuro Flashcards
fractures slide 31 of notes
Fractures are classified as either closed (the skin is intact) or open (the skin is perforated; often referred to as a compound fracture). Additionally, the fracture may be classified with respect to its anatomical appearance (e.g., transverse, spiral). Breaking bone causes hemmorhage to bring inflammatory molecules, endosteum lining bone marrow cavity on inside growing off of periosteum and endosteum builing up osteod soft bone and then becomes mineralized becoming hard bone. Callus formation and bone remodeling may be apparent with fracture repair, such as with the clavicle.
fractures risks/fracture patterns slide 32
Patholigic, closed protruding, open book, evulsion fracture (tendon grip on chuck of bones stronger chipping it.
bone development slide 28 of notes
The endochondral pattern of bone formation nvolves growth plates until bone maturity where it vascularizes driving mineralization and depositation of bone. Fractures in children (Salter-Harris fractures) that involves such growth centers may affect limb length as a result. Compact bone on outside, cancellous bone in middle. Note the: Epiphysis with articular cartilage maintain cartilage at the ends except rest mineralized, Metaphysis with the growth plate, Diaphysis shaft with a marrow cavity. Periosteum as a dense connective tissue will cover bone externally, and is firmly attached by bone fibers (Sharpey fibers). Endosteum is the internal equivalent to periosteum. Blood vessels will penetrate the periosteum to supply the blood and the marrow. The periosteum and endosteum will be sites of bone generation, with compact (cortical) bone as a firmer external shell and cancellous (bony) bones demonstrating a trabeculated pattern internally. The periosteum is highly innervated by nociceptors, hence the pain of a broken bones.
degenerative joint disease slide 29 notes
Degenerative joint disease is a catch-all term for osteoarthritis, degenerative arthritis, osteoarthrosis, or hypertrophic arthritis; it is characterized by progressive loss of articular cartilage and failure of repair. Osteo- arthritis can affect any synovial joint but most often involves the foot, knee, hip, spine, and hand. As the articular cartilage is lost, the joint space (the space between the two articulating bones) becomes narrowed, and the exposed bony surfaces rub against each other, causing significant pain. Joint cavities should be sterile but if not septic arthritis. The joint cavity is sterile, with macrophages on site to remove both pathogens and debris. These macrophages can contribute to conditions such as rheumatoid arthritis when activated. Osteoarthritis can affect any synovial joint but most often involves the foot, knee, hip, spine, and hand. As the articular cartilage is lost, the joint space (the space between the two articulating bones) becomes narrowed, and the exposed bony surfaces rub against each other, causing significant pain. Iliotibial tract syndrome is common in runners and presents as lateral knee pain, often in the midrange of flexion, between 20 and 70 degrees of knee flexion. The iliotibial tract, often referred to as “iliotibial band” by clinicians, rubs across the lateral femoral condyle, and this pain also may be associated with more proximal pain from greater trochanteric bursitis. Subluxation of the patella, usually laterally, is a fairly common occurrence, especially in adolescent girls and young women. It often presents with tenderness along the medial patellar aspect and atrophy of the quadriceps tendon, especially the oblique portion medially derived from the vastus medialis. Patellar ligament rupture usually occurs just inferior to the patella as a result of direct trauma in younger people.
osteoarthritis slide 30 of notes
Normally, the hyaline cartilage with its extracellular matrix will depend on a “pumping action” of compression and release from weight-bearing to help move fluid into this avascular tissue. Following damage, the chondrocytes will make new proteoglycans to help repair, but in the process, triggers inflammation and so leading to matrix degeneration. This leads to vertical clefts (fibrillations), and the now-exposed bone will now end up bearing more mechanical force and vascularize and thicken in response, as seen here in the progression of osteoarthritis. Matreal proteases fissures and breaking down cartilage altering it w/ bone reacting altered weight bearing and thickening. Osteoclasts work faster than blasts leading to vertebral bone and collapse.
clavicle ossification slide 29 notes
The clavicle is the first long bone to ossify (via intramembranous ossification), beginning during the fifth and sixth embryonic weeks from medial and lateral primary ossification centers that are close together in the shaft of the clavicle. The ends of the clavicle later pass through a cartilaginous phase (endochondral ossification); the cartilages form growth zones similar to those of other long bones. A secondary ossification center appears at the sternal end and forms a scale-like epiphysis that begins to fuse with the shaft (diaphysis) between 18 and 25 years of age; it is completely fused to it between 25 and 31 years of age. This is the last of the epiphyses of long bones to fuse. An even smaller scale-like epiphysis may be present at the acromial end of the clavicle; it must not be mistaken for a fracture. Sometimes, fusion of the two ossification centers of the clavicle fails to occur; as a result, a bony defect forms between the lateral and the medial thirds of the clavicle. Awareness of this possible birth defect should prevent diagnosis of a fracture in an otherwise normal clavicle. When doubt exists, both clavicles are radiographed because this defect is usually bilateral.
clavicle fracture slide 33 of notes
Fracture of the clavicle is quite common, especially in children. Clavicular fracture usually results from a fall on an outstretched hand (through bones of forearm and arm to shoulder) or from direct traumatic fall to the shoulder. Fractures of the medial third of the clavicle are rare (about 5%), but fractures of the middle third are common (about 80%) with the middle and lateral thirds being the weakest part. Fractures of the lateral third can involve coracoclavicular ligament tears. After someone has fractures their clavicle, SCM elevates medial fragment of bone. Note that a midshaft clavicle fracture will tend to displace, given the pull of different muscles or the weight of the limb. Trapezius muscle unable to hold up lateral fragment owing to weight of upper limb, dropping shoulder. Lateral fragment of clavicle pulled medially by muscles that normally adduct arm at shoulder joint, such as pectoralis major overriding bone fragments shortens clavicle. The clavicle holds the scapula out at a fixed distance (as it articulates with the acromion), but strong acromioclavicular ligaments are less likely to tear than the clavicle is to break (in fact, the clavicle is the most frequently fractured bone in the body in childhood).
humeral fractures slide 34 of notes
Fractures of the surgical neck of the humerus are especially common in elderly people with osteoporosis. Even a low-energy fall on the hand, with the force being transmitted up the forearm bones of the extended limb, may result in a fracture. Transverse fractures of the shaft of humerus frequently result from a direct blow to the arm. Fracture of the distal part of the humerus, near the supra-epicondylar ridges, is a supra-epicondylar (supracondy- lar) fracture. Because nerves are in contact with the humerus, they may be injured when the associated part of the humerus is fractured: surgical neck (most common because the bone begins to taper down at this point and is structurally weake), axillary nerve limiting abduction of arm?; radial groove, radial nerve paralyzing extensor muscles of hand and leading to wrist drop; distal humerus, median nerve; and medial epicondyle, ulnar nerve. Fractures of the proximal humerus often occur from a fall on an outstretched hand or from direct trauma to the area. They are especially common in elderly persons, in whom osteoporosis is a factor.
radial fractures
Fractures of the distal radius account for about 80% of forearm fractures in all age groups and often result from a fall on an outstretched hand.; and is most common in people older than 50 years of age. A complete fracture of the distal 2 cm of the radius, called a Colles fracture, is the most common fracture of the forearm. The distal fragment of the radius is displaced dorsally and often comminuted (broken into pieces). The fracture results from forced dorsiflexion of the hand, usually as the result of trying to ease a fall by outstretching the upper limb (FOOSH- fall onto outstretched hand) . Often, the ulnar styloid process is avulsed (broken off). Normally, the radial sty- loid process projects farther distally than the ulnar styloid process; consequently, when a Colles fracture occurs, this relationship is reversed because of shortening of the ra- dius. This fracture is often referred to as a dinner fork (silver fork) deformity because a posterior angulation occurs in the forearm just proximal to the wrist and the normal anterior curvature of the relaxed hand. The posterior bending is produced by the posterior displacement and tilt of the dis- tal fragment of the radius. Fractures of both the ulna and radius are the re- sult of severe injury. A direct injury usually pro- duces transverse fractures at the same level, often in the middle third of the bones.
ulnar fractures
Usually, a direct blow to or forced pronation of the forearm is the most common cause of a fracture of the shaft of the ulna. Fracture of the ulna with dislocation of the proximal radioulnar joint is termed a Monteggia fracture. The radial head usually dislocates anteriorly, but posterior, medial, or lateral dislocation also may occur. Such dislocations may put the posterior interosseous nerve (the deep branch of the radial nerve) at risk.
hand fractures
Severe crushing injuries of the hand may produce multiple metacarpal fractures, resulting in instability of the hand. Similar injuries of the distal phalanges are common (e.g., when a finger is caught in a car door). A fracture of a dis- tal phalanx is usually comminuted, and a painful hematoma (collection of blood) develops. Fractures of the proximal and middle phalanges are usually the result of crushing or hyperextension injuries. Fracture of the hamate may result in nonunion of the frac- tured bony parts because of the traction produced by the at- tached muscles. Because the ulnar nerve is close to the hook of the hamate, the nerve may be injured by this fracture, caus- ing decreased grip strength of the hand. The ulnar artery may also be damaged when the hamate is fractured.
wrist fractures
Fracture of the distal end of the radius (Colles fracture), the most common fracture in people older than 50 years of age. Fracture–separation of the distal radial epiphysis is common in children because of frequent falls in which forces are transmit- ted from the hand to the radius. In a lateral radiograph of a child’s wrist, dorsal displacement of the distal radial epiphysis is obvious. When the epiphysis is placed in its normal position during reduction, the prognosis for normal bone growth is good. Without knowledge of bone growth and the appearance of bones in radiographic and other diagnostic images at various ages, a displaced epiphyseal plate could be mistaken for a fracture, and separation of an epiphysis could be inter- preted as a displaced piece of fractured bone. Knowledge of the patient’s age and location of epiphyses can prevent these errors.
wrist dislocation
Because the shafts of these bones are firmly bound together by the interosseous mem- brane, a fracture of one bone is likely to be associated with dislocation of the nearest joint. see slid 35 of notes
scaphoid fractures slide 36 of notes
The scaphoid bone (navicular) is the most frequently fractured carpal bone and may be injured by falling on an extended wrist fracturing the distal end of the radius. Fracture of the middle third (waist) of the bone is most common. Pain and swelling in the “anatomical snuffbox” often occurs because of its location in the floor, and optimal healing depends on an adequate blood supply from the palmar carpal branch of the radial artery. Loss of the blood supply can lead to nonunion or avascular osteonecrosis. fracture of the scaphoid often results from a fall on the palm with the hand abducted . The fracture occurs across the narrow part (“waist”) of the scaphoid. Pain occurs primarily on the lateral side of the wrist, especially during dorsiflexion and abduction of the hand. Initial radiographs of the wrist may not reveal a fracture, but radiographs taken 10 to 14 days later may reveal a fracture because bone resorption has occurred. Owing to the poor blood supply to the proximal part of the scaphoid, union of the fractured parts may take several months. Avascu- lar necrosis of the proximal fragment or waist of the scaphoid (pathological death of bone resulting from poor blood supply) may occur and produce degenerative joint disease of the wrist, given that the radial artery supplies scaphoid distally. scaphoid fracture dorsal displacement w/ extensor pulling back
serratus anterior winging slide 13 of UE and LE
When the serratus anterior is paralyzed because of injury to the long thoracic nerve, the medial border of the scapula moves laterally and posteriorly away from the thoracic wall. This gives the scapula the appearance of a wing. When the arm is raised, the medial border and inferior angle of the scapula pull markedly away from the posterior tho- racic wall, a deformation known as a winged scapula. The arm cannot be abducted above the horizontal position be- cause the serratus anterior is unable to rotate the glenoid cavity superiorly to allow complete abduction of the limb. Damage to the long thoracic nerve in its course along the lateral chest wall and subsequent paralysis of the serratus anterior leads to winged scapula, where the scapula projects posteriorly as the arm is abducted. Usually keeps it attached to body.
venipuncture slide 8 of UE and LE
Because of the prominence and accessibility of the superficial veins, they are commonly used for ve- nipuncture (to draw blood or inject a solution). By applying a tourniquet to the arm, the venous return is oc- cluded and the veins distend and usually are visible and/or palpable. Once a vein is punctured, the tourniquet is removed so that when the needle is removed, the vein will not bleed extensively. The median cubital vein is commonly used for venipuncture. The veins forming the dorsal venous network and the cephalic and basilic veins are commonly used for long- term introduction of fluids (intravenous feeding). The cubital veins are also a site for the introduction of cardiac catheters. ntral venous access can be gained by placing a catheter in the internal jugular or subclavian vein, in the proximal forearm (peripherally) in the intermediate (median) vein of the forearm (antebrachium) and median cubital vein, or distally on the dorsum of the hand. The superficial veins of the upper limb begin on the dorsum of the hand and coalesce into two major veins, the cephalic and basilic. Deep (radial and ulnar veins leading to brachial vein) and superficial venous drainage (cephalic, basilic veins and their connection with the median cubital vein) are seen in the upper extremity. Central venous access can be achieved peripherally through a PIC[C] (peripherally inserted central catheter) line initiated in a superficial vein to reach the subclavian vein and superior vena cava sterile connection.
rotator cuff injuries slide 5 of UE and LE
Injury or disease may damage the rotator cuff (supraspinatus infraspinatus, teres minor, and subscapularis) , producing instability of the glenohumeral joint. Rupture or tear of the supraspinatus tendon is the most com- mon injury of the rotator cuff. Degenerative tendinitis of the rotator cuff is common, especially in older people. Recurrent in- flammation of the rotator cuff, especially the relatively avascular area of the supraspinatus tendon, is a common cause of shoulder pain and results in tears of the rotator cuff. The musculotendinous rotator cuff is commonly injured during repetitive use of the upper limb above the horizontal (e.g., during throwing and racquet sports, swimming, and weight lifting) may allow the humeral head and rotator cuff to impinge on the coracoacromial arch, producing ir-ritation of the arch and inflammation of the rotator cuff. As a result, degenerative tendinitis of the rotator cuff develops. At- trition of the supraspinatus tendon also occurs. Because the supraspinatus muscle is no longer functional with a complete tear of the rotator cuff, the person cannot initiate abduction of the upper limb. If the arm is passively abducted 15 degrees or more, the person can usually maintain or continue the ab- duction using the deltoid. Activity of abduction for the upper limb consists of a combination of glenohumeral and scapular motion. Supraspinatus is active early in the abduction process to help stabilize the glenohumeral joint as deltoid is also contracting to generate abduction. Supraspinatus will help to initiate abduction, deltoid will additionally abduct, but then the humeral head “runs into” the acromion process, such that additional scapular rotation, as by trapezius and serratus anterior, will be needed.
axillary vessels slide 7 of UE and LE
Compression of the third part of the axillary artery against the humerus may be necessary when profuse bleeding occurs. If compression is required at a more proximal site, the axillary artery can be compressed at its origin at the lateral border of the 1st rib by exerting downward pressure in the angle between the clavicle and the attachment of the SCM. Wounds in the axilla often involve the axillary vein because of its large size and exposed posi- tion. When the arm is fully abducted, the axillary vein overlaps the axillary artery anteriorly. Axillary vessels can be exposed with an abducted arm. A wound in the proximal part of the vein is particularly dangerous not only because of profuse bleeding but also because of the risk of air entering the vein and producing air emboli (air bubbles) in the blood. thoracic outlet syndrome as a possibility with compression of axillary artery between clavicle and first rib. Extensive anastomosis around the scapula could lead to sufficient blood flow to the upper limb if there were gradual loss of axillary arterial flow.
axillary node alterations slide 7 of UE and LE
An infection in the upper limb can cause the ax- illary nodes to enlarge and become tender and inflamed, a condition called lymphangitis (inflammation of lymphatic vessels). The humeral group of nodes is usually the first ones to be involved. Lymphangitis is char- acterized by warm, red streaks in the skin of the limb. Infec- tions in the pectoral region and breast, including the supe- rior part of the abdomen, can also produce enlargement of the axillary nodes. These nodes are also the most common site of metastases (spread) of cancer of the breast. The axillary nodes, while most commonly palpated during breast examination, also represent drainage from the upper limb with the humeral (lateral) nodes into the central nodes and into apical nodes.
brachial plexus injuries slide 12 of UE and LE
Injuries to the brachial plexus affect movements and cutaneous sensations in the upper limb. Disease, stretching, and wounds in the lateral cervical region (posterior triangle of the neck) or in the axilla may produce brachial plexus injuries. Signs and symptoms depend on which part of the plexus is involved. Injuries to the brachial plexus result in loss of muscular movement (paralysis) and loss of cutaneous sensation (anesthesia). In complete paralysis, no movement is detectable. In incomplete paralysis, not all muscles are paralyzed; therefore, the person can move, but the movements are weak compared to those on the uninjured side. Damage (trauma, inflammation, tumor, radiation damage, bleeding) to the brachial plexus may present as pain, loss of sensation, and motor weakness. Clinical findings depend on the site of the lesion: • Upper plexus lesions: usually affect the distribution of C5-C6 nerve roots, with the deltoid and biceps muscles affected, and sensory changes that extend below the elbow to the hand. • Lower plexus lesions: usually affect the distribution of C8-T1 nerve roots, with radial and ulnar innervated muscles affected; hand weakness and sensory changes involve most of the medial hand, with weakness of finger abduction and finger extension.
injury to axillary nerve slide 12 of UE and LE
Atrophy of the deltoid occurs when the axil- lary nerve (C5 and C6) is severely damaged (e.g., as might occur when the surgical neckof the humerus is fractured). As the deltoid atrophies unilaterally, the rounded contour of the shoulder dis- appears, resulting in visible asymmetry of the shoulder outlines. This gives the shoulder a flattened appearance and produces a slight hollow inferior to the acromion. A loss of sensation may occur over the lateral side of the proximal part of the arm, the area supplied by the superior lateral cutaneous nerve of the arm. To test the deltoid (or the function of the axillary nerve), the arm is abducted, against resistance, starting from approxi- mately 15 degrees. posterior cord coming off superiorly.
injury to musculocutaneous slide 12 of UE and LE
Injury to the musculocutaneous nerve in the axilla is usually inflicted by a weapon such as a knife. A musculocutaneous nerve injury results in paralysis of the coracobrachialis, biceps, and brachialis; consequently, flex- ion of the elbow and supination of the forearm are greatly weakened. Loss of sensation may occur on the lateral surface of the forearm supplied by the lateral cutaneous nerve of the forearm.
injury to radial nerve slide 12/16 of UE and LE
posterior cord everybody else C5-T1. Injury to the radial nerve superior to the origin of its branches to the triceps brachii results in paraly- sis of the triceps, brachioradialis, supinator, and extensor muscles of the wrist and fingers. Loss of sensation occurs in areas of skin supplied by this nerve. When the radial nerve is injured in the radial groove, the triceps is usually not com- pletely paralyzed but only weakened because only the me- dial head is affected; however, the muscles in the posterior compartment of the forearm that are supplied by more distal branches of the radial nerve are paralyzed. The characteristic clinical sign of radial nerve injury is wrist-drop (inability to ex- tend the wrist and fingers at the metacarpophalangeal joints). Instead, the wrist is flexed because of unopposed tonus of the flexor muscles and gravity. Although the radial nerve supplies no muscles in the hand, radial nerve injury in the arm by a fracture of the humeral shaft can produce serious disability of the hand. This injury is proximal to the branches to the extensors of the wrist, so wrist-drop is the primary clinical manifestation. The hand is flexed at the wrist and lies flaccid, and the digits also remain in the flexed position at the meta- carpophalangeal joints. The extent of anesthesia is minimal, even in serious radial nerve injuries, and usually is confined to a small area on the lateral part of the dorsum of the hand. Severance of the deep branch results in an inability to extend the thumb and the metacarpophalangeal joints of the other digits. Loss of sensation does not occur because the deep branch is entirely muscular and articular in distribution. Radial nerve may be compressed at several points, and so affect different groups of extensors, the classic “downstream” presentation of radial nerve injury would be wrist drop, given gravity and the unopposed action of forearm flexors.: Extensor carpi radilais brevis and longus, Extensor digitorum- zombie hands (crosses knuckles blending into extensor expansion or hood
injury to median nerve slide 12/17 of UE and LE
Lesions of the median nerve usually occur in two places: the forearm and wrist. The most common site is where the nerve passes through the carpal tunnel. Laceration of the wrist often causes median nerve injury because this nerve is relatively close to the surface. This results in paralysis and wasting of the thenar muscles and the first two lumbrical muscles affecting the ability to flex the metacarpophalangeal joints. Median nerve injury resulting from a perforating wound in the elbow region results in loss of flexion of the proximal and distal interphalangeal joints of the 2nd and 3rd digits. This results in a deformity in which thumb movements are limited to flexion and exten- sion of the thumb in the plane of the palm. This condition is caused by the inability to oppose and by limited abduction of the thumb. Sensation is also lost over the thumb and adjacent two and a half digits. Compression at the elbow is the second most common site of median nerve entrapment after the wrist (carpal tunnel). Repetitive forearm pronation and finger flexion, especially against resistance, can cause muscle hypertrophy and entrap the nerve. Similarly, the more proximally that median nerve is compromised, the more loss of function, e.g., loss of pronation in the anterior forearm with compromise of pronator teres and pronator quadratus, or the lack of digit flexion with compromise of flexor digitorum superficialis and half of flexor digitorum profundus. The “downstream” effects would be loss of thenar eminence bulk and function, along with loss of the two lateral lumbricals (up thumb side of fingers, tying into extensor hood can pull and track flexing at MCP making taught and help straighten out distal and proximal phalangeal joint). Without function of flexor pollicis brevis, abductor pollicis brevis, and opponens pollicis, note that the thumb can be left in adduction (ulnar nerve) and extension (radial nerve). There could be some abduction with abductor pollicis longus.If lose median further up in axillary flexor digitorum superficialis thumb side of flexor digitorum profundus (thumb side) and pronators. Hard to flex fingers. Median nerve- at thenar eminence One would end up with the “hand of benediction” with the ulnar-innervated fingers able to flex, but the median-innervated fingers not so much. Diffeential tingling of one 3.5 fingers.
injury to ulnar nerve slide 12/18 of UE and LE
medial C8-T1. Ulnar nerve injury usually occurs in one of four places: (1) posterior to the medial epicondyle of the humerus (most common), (2) in the cubital tunnel formed by the tendinous arch connecting the humeral and ulnar heads of the FCU, (3) at the wrist, and (4) in the hand. Ulnar nerve injury occurring at the elbow, wrist, or hand may result in extensive motor and sensory loss to the hand. An injury to the nerve in the distal part of the forearm denervates most intrinsic hand muscles. If proximal, then flexor carpi ulnaris and the medial half of flexor digitorum profundus can be compromised, making it difficult to flex the wrist or to flex the medial digits to make a fist, respectively. If ulnar nerve is damaged, both palmar and dorsal interosseus function is compromised. In addition, the medial two lumbricals do not work, so that the hand cannot flex the digit at the MCP, extend at the PIP, DIP, and so creating a claw hand (although this term is the classic term, it is a bit of a misnomer, as the median vs. ulnar nerve descriptive appearance depends on whether one is making a fist or not; the claw hand occurs when the person is trying to extend the fingers and the ulnar-innervated lumbricals are not functioning to allow them to straighten). If the damage is more distal, e.g., at the ulnar tunnel by pisiform and hamate carpal bones, then weakening of intrinsic hand muscle function, and the decrease/loss of sensation in the ulnar distribution can occur. Ulnar-if further up flexor carpi ulnaris, ulnar side flexor digitorum profundus Ulnar damaged in hand- Hyperthenar eminance, lumbricals out on pinky side, adductor policis, dorsal dabbers palmer adders The power of wrist adduction is impaired, and when an attempt is made to flex the wrist joint, the hand is drawn to the lateral side by the FCR in the absence of the “balance” provided by the FCU. After ulnar nerve injury, the person has difficulty making a fist because, in the absence of opposition, the metacarpophalangeal joints become hyperextended, and he or she cannot flex the 4th and 5th fingers at the distal interphalangeal joints when trying to make a fist. Furthermore, the person cannot extend the interphalangeal joints when trying to straighten the fingers. This characteristic appearance of the hand is known as a claw hand. This deformity results from atrophy of the interosseous muscles of the hand. The claw is produced by the unopposed action of the extensors and FDP. Compression of the ulnar nerve also may occur at the wrist where it passes between the pisiform and the hook of hamate. The depression between these bones is converted by the piso- hamate ligament into an osseofibrous ulnar tunnel (Guyon tunnel). Ulnar canal syndrome is manifest by hypoesthesia in the medial one and one half fingers and weak- ness of the intrinsic hand muscles. Clawing of the 4th and 5th fingers may occur, but in contrast to proximal ulnar nerve injury, their ability to flex is unaffected and there is no radial deviation of the hand. The ulnar tunnel exists at the wrist where the ulnar nerve and artery pass deep to the palmaris brevis muscle and palmar (volar) carpal ligament, just lateral to the pisiform bone. Within the tunnel, the nerve divides into the superficial sensory and deep motor branches. Injury may result from trauma, ulnar artery thrombosis, fractures (hook of the hamate), dislocations (ulnar head, pisiform), arthritis, and repetitive movements. Claw hand may be present if the motor components are injured. Cubital tunnel syndrome results from compression of the ulnar nerve as it passes beneath the ulnar collateral ligament and between the two heads of the flexor carpi ulnaris muscle. This syndrome is the second most common compression neuropathy after carpal tunnel syndrome. The tunnel space is significantly reduced with elbow flexion, which compresses and stretches the ulnar nerve. The nerve also may be injured by direct trauma to the subcutaneous portion as it passes around the medial epicondyle.
Erb (-Duchenne) palsy slide 12 of UE and LE
Erb (-Duchenne) palsy, where the superior brachial plexus (upper roots, e.g., C5-7) have been damaged by neck stretching, e.g., during childbirth. Nerves affected include: suprascapular (supraspinatus and infraspinatus function), musculocutaneous (biceps brachii), and axillary nerve (deltoid and teres minor function). The loss of function of these muscles leads to a waiter’s tip position of the upper limb. Injuries to superior parts of the brachial plexus (C5 and C6) usually result from an excessive increase in the angle between the neck and the shoulder. These injuries can occur in a person who is thrown from a motorcycle or a horse and lands on the shoulder in a way that widely separates the neck and shoulder . When thrown, the person’s shoulder often hits something (e.g., a tree or the ground) and stops, but the head and trunk continue to move. This stretches or ruptures superior parts of the brachial plexus or avulses (tears) the roots of the plexus from the spinal cord. Injury to the superior trunk is apparent by the characteristic position of the limb (“waiter’s tip position”) in which the limb hangs by the side in medial rotation. Upper brachial plexus injuries can also occur in a newborn when excessive stretching of the neck occurs during delivery. As a result of injuries to the superior parts of the brachial plexus (Erb-Duchenne palsy), paralysis of the muscles of the shoulder and arm supplied by C5–C6 occurs. The usual clinical ap- pearance is an upper limb with an adducted shoulder, medi- ally rotated arm, and extended elbow. The lateral aspect of the upper limb also experiences loss of sensation. Chronic microtrauma to the superior trunk of the brachial plexus from carrying a heavy backpack can produce motor and sensory deficits in the distribution of the musculocutaneous and radial nerves.
Klumpke paralysis slide 12 of UE and LE
Injuries to inferior parts of the brachial plexus (Klumpke paralysis) are much less common. These injuries may occur when the upper limb is suddenly pulled superiorly—for ex- ample, when a person grasps something to break a fall or when a baby’s limb is pulled excessively during delivery. These events injure the inferior trunk of the plexus (C8 and T1) and may avulse the roots of the spinal nerves from the spinal cord. The short muscles of the hand are affected and a claw hand results..
biceps tendinitis
The tendon of the long head of the biceps, enclosed by a synovial sheath, moves back and forth in the inter- tubercular sulcus (groove) of the humerus. Wear and tear of this mechanism can cause shoulder pain. Inflammation of the tendon (biceps tendinitis) usually is the result of repetitive microtrauma in sports involving throwing (e.g., baseball).
tendon rupture slide 6 of UE and LE
Rupture of the tendon of the long head of the biceps usually results from wear and tear of an inflamed tendon (biceps tendinitis). Normally, the tendon is torn from its attachment to the supraglenoid tubercle of the scapula. The rupture is commonly dramatic and is associated with a snap or pop. The detached muscle belly forms a ball near the center of the distal part of the anterior aspect of the arm (Popeye deformity). Rupture of the biceps brachii muscle may occur at the tendon (or rarely the muscle belly). It has a high rate of spontaneous rupture compared with most muscle tendons. Rupture is seen most often in patients older than 40, in association with rotator cuff injuries (as the tendon begins to undergo degenerative changes), and with repetitive lifting (e.g., weight lifters). Rupture of the long head of the biceps brachii tendon is most common and may occur in the following locations: Shoulder joint Intertubercular (bicipital) sulcus of the humerus Musculotendinous junction.The biceps brachii tendon can be ruptured in older males, particularly at the tendon of the long head. Subacromial trapping of biceps makes it easier to tear this muscle.
lateral epicondylitis slide 9 of UE and LE
Elbow tendinitis (tennis elbow) is a painful muscu- loskeletal condition that may follow repetitive use of the superficial extensor muscles of the forearm. Pain is felt over the lateral epicondyle and radiates down the poste- rior surface of the forearm. People with elbow tendinitis often feel pain when they open a door or lift a glass. Repeated force- ful flexion and extension of the wrist strain the attachment of the common extensor tendon, producing inflammation of the periosteum of the lateral epicondyle (lateral epicondylitis). As- sociated tears of the common extensor tendon, which may be surgically repaired, are visible on magnetic resonance imaging (MRI). Extensor muscles originate from the lateral epicondyle and repeated use, as with a backhand stroke with a tennis racket, may cause a strain on the periosteum and tendinous muscle attachments. In particular, overuse of extensor carpi radialis brevis (ECRB) can lead to microtears in its tendon. One can exhibit a medial epicondylitis (golfer’s elbow) as well, with anterior compartment (flexor) overuse.
ganglion cyst slide 23 of UE and LE
Sometimes a nontender cystic swelling appears on the hand, most commonly on the dorsum of the wrist. The thin-walled cyst contains clear mucinous fluid. Clinically, this type of swelling is called a “ganglion” (G. swelling or knot). These synovial cysts are close to and often communicate with the synovial sheaths. The distal attachment of the ECRB tendon is a common site for such a cyst. A cystic swelling of the common flexor syno- vial sheath on the anterior aspect of the wrist can enlarge enough to produce compression of the median nerve by nar- rowing the carpal tunnel (carpal tunnel syndrome). Generally speaking, they are thought to represent connective tissue degeneration of the tendon sheaths. They are not simple herniations, as there is no synovial lining to them local degeneration.These can either be followed by observation, lessened by splinting, aspirated, or surgically excised depending on symptoms and impact on function
mallet finger slide 19 of UE and LE
Sudden severe tension on a long extensor tendon may avulse part of its attachment to the phalanx. The most common result of this injury is mallet or baseball finger. This deformity results from the distal inter- phalangeal joint suddenly being forced into extreme flexion (hyperflexion) when the tendon is attempting to extend the distal phalanx—for example, when a baseball is miscaught (hyperflexing it) or the finger is jammed into a base pad. These actions avulse the attachment of the tendon from the base of the distal phalanx. As a result, the person is un- able to extend the distal interphalangeal joint. A mallet finger at the DIP has damage to the distal extensor expansion, so that unopposed flexor digitorum profundus action can keep the distal phalanx in flexion. Lever to straighten fingers.
other distal finger injuries slide 19 of UE and LE
Various traumatic finger injuries may occur, causing fractures, disruption of the flexor and extensor tendons, and torn ligaments. Each element must be carefully examined for normal function, including muscle groups, capillary refill (Allen’s test), and two-point sensory discrimination. In de Quervain tenosynovitis the tendons of the abductor pollicis longus and extensor pollicis brevis muscles pass through the same tendinous sheath on the dorsum of the wrist (first compartment in the extensor retinaculum). Excessive and repetitive use of the hands in a power grip or a twisting-wringing action can cause friction and thickening of the sheath, leading to pain over the styloid process of the radius. This pain is mediated by the superficial radial nerve (sensory), and the pain can extend distally into the thumb and radiate up the lateral forearm. A jersey finger has damage to the flexor digitorum profundus tendon, leaves the distal phalanx in extension. A gamekeeper’s thumb (skier’s thumb) or ulnar collateral ligament injury of the thumb may lead to instability with the MCP joint of the thumb following a fall on an abducted thumb. Ulnar side of things torn medial collateral ligament. Metacarpal fractures often occur from blows, with a boxer’s fracture of the fifth metacarpal that can lead to a presentation of a depressed knuckle.
Dupuytren contracture slide 20 of UE and LE
Dupuytren contracture is a disease of the palmar fascia resulting in progressive shortening, thicken- ing, and fibrosis of the palmar fascia and palmar aponeurosis. The fibrous degeneration of the longitudinal digital bands of the aponeurosis on the medial side of the hand pulls the 4th and 5th fingers into partial flexion at the metacarpophalangeal and proximal interphalangeal joints. The contracture is frequently bilateral. Treatment of the contracture usually involves surgical excision of the fibrotic parts of the palmar fascia to free the fingers. The palmar fascia contributes to a thick palmar aponeurosis and extend to fibrous digital sheaths that enclose tendons and synovial sheaths. This is particularly seen in males of Northern European background, suggesting a genetic basis for the fibroblast proliferation and excessive collagen deposition seen in this process. Cant extend fingers completely. Palmaris longus tense tissues in hand.
tenosynovitis and trigger finger slide 21 of UE and LE
synovial tendon sheaths help to reduce friction for long tendons. Punctures into those and subsequent infection can lead to rapid functional impairment, and so deserve quick consultation with hand specialists. There are ligaments or thickenings of the fibrous sheath surrounding the synovial sheaths that help to support the tendons (preventing bowstringing), and can act as pulleys. These ligaments can be anular or cruciate. Thickenings of the tendons can lead to trigger finger (digital tenovaginitis stenosans), with the inability to extend the finger if the tendon nodule has difficulty fitting in under an anular pulley finger doesn’t want to flex or extend back out.
tenosynovitis slide 22 of UE and LE
Injuries such as puncture of a digit by a rusty nail can cause infection of the digital synovial sheaths. When inflammation of the tendon and synovial sheath (tenosynovitis) occurs, the digit swells and movement becomes painful. Because the tendons of the 2nd through 4th digits nearly always have separate synovial sheaths, the infec- tion usually is confined to the infected digit. If the infection is untreated, however, the proximal ends of these sheaths may rupture, allowing the infection to spread to the midpalmar space. Because the synovial sheath of the little finger is usually continuous with the common flexor sheath, tenosynovitis in this digit may spread to the common sheath and thus through the carpal tunnel to the forearm. How far an infection spreads from the digits depends on variations in their connections with the common flexor sheath. The tendons of the APL and EPB are in the same ten- dinous sheath on the dorsum of the wrist. Excessive fric- tion of these tendons results in fibrous thickening of the sheath and stenosis of the osseofibrous tunnel, Quervain tenovaginitis stenosans. This condition causes pain in the wrist that radiates proximally to the forearm and distally to the thumb. If the tendons of the FDS and FDP enlarge (forming a nodule) proximal to the tunnel, the person is unable to extend the finger. When the finger is extended passively, a snap is au- dible. This condition is called digital tenovaginitis stenosans (trigger finger or snapping finger). The anatomical snuffbox of extensor pollicis longus, extensor pollicis brevis, and abductor pollicis longus was mentioned in context of scaphoid location. Inflammation of the last two (EPB and APL) within a common tendinous sheath over the radial styloid, as elicited by pain with ulnar deviation (Finkelstein test): de Quervain tenosynovitis.
carpal tunnel syndrome slide 14 of UE and LE
There are several anatomical sites of compression for the upper limb nerves, with some, such as the cubital tunnel for the ulnar nerve or the carpal tunnel for median nerve. Median nerve compression in the carpal tunnelwithin the carpal tunnel formed by the carpal bones and the flexor retinaculum, the most common compression neuropathy, is often linked to occupational repetitive movements related to wrist flexion and extension, holding the wrist in an awkward position, or strong gripping of objects. Long-term compression often leads to thenar atrophy and weakness of the thumb and index fingers, reflecting the loss of innervation to the muscles distal to the median nerve damage.
digit ischemia slide 24 of UE and LE
Intermittent bilateral attacks of ischemia of the dig- its, marked by cyanosis and often accompanied by paresthesia and pain, are characteristically brought on by cold and emotional stimuli. The condition may result from an anatomical abnormality or an underlying disease. When the cause of the condition is idiopathic (unknown) or primary, it is called Raynaud syndrome (disease). On either side of the fibrous sheath are neurovascular bundles supplying the digits. The blood flow to these may be compromised with Raynaud syndrome, with vasospasm in response to cold or stress. NAV on either side of digits. This follows a classic pattern of: White (vasoconstriction) , Blue (cyanosis) , Red (hyperemia from refill) . The arteries of the upper limb are innervated by sym- pathetic nerves. Postsynaptic fibers from the sympathetic ganglia enter nerves that form the brachial plexus and are distributed to the digital arteries through branches arising from the plexus. When treating ischemia resulting from Rayn- aud syndrome, it may be necessary to perform a cervicodorsal presynaptic sympathectomy (excision of a segment of a sympa- thetic nerve) to dilate the digital arteries. The Allen’s test is used to test the vascular perfusion distal to the wrist. The physician lightly places the thumbs on the patient’s ulnar and radial arteries, and the patient makes a tight fist to “blanch” the palmar skin (squeeze the blood into the dorsal venous network). Then, while compressing the radial artery with the thumb, the physician releases the pressure on the ulnar artery and asks the patient to open the clenched fist. Normally the skin will turn pink immediately, indicating normal ulnar artery blood flow through the anastomotic palmar arches. The test is then repeated by occluding the ulnar artery to assess radial artery flow
shoulder dislocation slide 27 of UE and LE
ulnar collateral ligament reconstruction slide 31 of UE and LE
shoulder separation slide 28 of UE and LE (dislocation of acromioclavicular joint)
Although its extrinsic (coracoclavicular) ligament is strong, the AC joint itself is weak and easily injured by a direct blow. In contact sports such as football,soccer, and hockey, it is not uncommon for dislocation of the AC joint to result from a hard fall on the shoulder or on the out- stretched upper limb. Dislocation of the AC joint also can occur when a hockey player is, for example, driven violently into the boards. An AC dislocation, often called a “shoulder separation,” is severe when both the AC and the coracoclavicular ligaments are torn. When the coracoclavicu- lar ligament tears, the shoulder separates from the clavicle. and falls because of the weight of the upper limb. Dislocation of the AC joint makes the acromion more prominent, and the clavicle may move superior to the acromion. Directly landing on location or stress on limb hits axillary skeletal points.
shoulder bursitis and adhesive capsulitis slide 26 of UE and LE
Adhesive fibrosis and scarring between the in- flamed capsule of the glenohumeral joint, rotator cuff, subacromial bursa, and deltoid usually cause adhesive capsulitis (“frozen shoulder”). A person with this condition has difficulty abducting the arm but can obtain an apparent abduction of up to 45 degrees by elevating and rotating the scapula. Injuries that may initiate this condition include glenohumeral dislocations, calcific supraspinatus tendinitis, partial tearing of the rotator cuff, and bicipital tendinitis. Movement at the shoulder joint (or almost any joint) can lead to inflammation of the tendons surrounding that joint and secondary inflammation of the bursa that cushions the joint from the overlying muscle or tendon. A painful joint can result, possibly even with calcification within the degenerated tendon. The supraspinatus muscle tendon is especially vulnerable because it can become pinched by the greater tubercle of the humerus, the acromion, and the coracoacromial ligament. The acromion can impinge upon the supraspinatus tendon. This can be enhanced by abduction, where the greater tubercle of humerus can be “driven towards” acromion. This can lead to supraspinatus tendinitis. A bursa is a sac of synovial membrane with synovial fluid that reduces friction at points of use. Note the possible bursitis that can occur here. More generally, ongoing inflammation and fibrosis of the structures in this area can lead to adhesive capsulitis (frozen shoulder), with loss of abduction particularly noted.
elbow bursitis see slide 29 of UE and LE
The subcutaneous olecranon bursa is exposed to injury during falls on the elbow and to infection from abrasions of the skin covering the olecranon. Repeated excessive pressure and friction produces a friction subcutaneous olecranon bursitis (e.g., “student’s elbow”). Subtendinous olecranon bursitis results from excessive friction between the triceps tendon and the olecranon—for example, resulting from repeated flexion–extension of the forearm as occurs dur- ing certain assembly-line jobs. The pain is severe during flexion of the forearm because of pressure exerted on the inflamed subtendinous olecranon bursa by the triceps tendon. Radial head supination pronation at location if dislocate it goes posteriorly. Bursitis from chronic overuse between tendon bone and bone and skin.
ulnar collateral ligament reconstruction slide 31 of UE and LE
The ulnar collateral ligament by the medial epicondyle is an important reinforcement of the elbow, and can be impacted by throwing activities. Rupture, tearing, and stretching of the ulnar collat- eral ligament (UCL) are increasingly common inju- ries related to athletic throwing (primarily baseball pitching, but also football passing, javelin throwing, and play- ing water polo). Reconstruction of the UCL, commonly known as a “Tommy John procedure” (named after the first pitcher to undergo the surgery), involves an autologous transplant of a long tendon from the contralateral forearm or leg (e.g., the palmaris longus or plantaris tendon). A 10- to 15-cm length of tendon is passed through holes drilled through the medial epicondyle of the humerus and the lateral aspect of the coro- noid process of the ulna. Note that the grafting of “spare tendons” such as from palmaris longus or plantaris can be used to reconstruct this support if the UCL is damaged.
elbow dislocation
Posterior dislocation of the elbow joint may occur when children fall on their hands with their elbows flexed. Dislocations of the elbow may result from hyperextension or a blow that drives the ulna posteriorly or posterolaterally. The distal end of the humerus is driven through the weak anterior part of the fibrous layer of the joint capsule as the radius and ulna dislocate posteriorly. Injury to the ulnar nerve may also occur. Elbow dislocations occur third in frequency after shoulder and finger dislocations. Dislocation often results from a fall on an outstretched hand and includes the following types: • Posterior (most common) • Lateral (uncommon) • Anterior (rare; may lacerate brachial artery) • Medial (rare) Dislocations may be accompanied by fractures of the humeral medial epicondyle, olecranon (ulna), radial head, or coronoid process of the ulna. Injury to the ulnar nerve (most common) or median nerve may accompany these dislocations.
radial head subluxation slide 30 of UE and LE
The elbow is a hinge joint formed by humerus, radius, and ulna. These are combined in one joint capsule, with the support of collateral ligaments, as well as an anular ligament to hold the radial head against a corresponding ulnar notch. Preschool children, particularly girls, are vulnerable to transient subluxation (incomplete temporary dis- location) of the head of the radius (“pulled elbow”). The history of these cases is typical. The child is suddenly lifted (jerked) by the upper limb when the forearm is pronated. The child may cry out and refuse to use the limb, which is protected by holding it with the elbow flexed and the forearm pronated. The sudden pulling of the upper limb tears the distal attachment of the anular ligament, where it is loosely attached to the neck of the radius. The radial head then moves distally, partially out of the anular ligament. The proximal part of the torn ligament may become trapped between the head of the radius and the capitulum of the humerus. The source of pain is the pinched anular ligament. The treatment of sub- luxation consists of supination of the child’s forearm while the elbow is flexed. Supination with flexion, or more recently, hyperpronation while flexing, are popular reduction techniques get the radial head back into position.That the pronation approach is less painful and more effective than the classic supination approach. The tear in the anular ligament soon heals when the limb is placed in a sling for about 2 weeks.
upper limb surface anatomy see slides 33
see pictures p. 407-409, 420-421, 439, 462-464
upper limb imaging see slid 34
see pictures , p. 482-484
lower limb
used for weight bearing, locomotion, and maintenance of equilibrium. One can divide up the lower extremity to three main joints and three main regions:hip, between hip and knee. knee joint (crus) between knee and ankle . ankle foot- talocrural joint.
hip fractures
Fractures of the hip bone are “pelvic fractures.” Avulsion fractures of the hip bone may occur during sports that require sudden acceleration or deceleration. A small part of the bone with a piece of tendon or ligament attached is “avulsed” (torn away)—for example, the ante- rior superior iliac spine. In older patients, pelvic fractures often include at least two fractures of the ring of bone formed by the pubis, pubic rami, and the acetabulum. One cannot just break one side of a stiff ring. Note how the process of osteoarthritis may lead to erosion of the articular cartilage and triggering of pain with the exposed bony surfaces rubbing against each other. With the subsequent bone effects, osteophytes may be generated.
hip dislocation slide 39 of UE and LE
Congenital dislocation of the hip (hip dysplasia), where the femoral head is not firmly planted in the acetabulum, may be adjusted with bracing, especially for girls and is bilateral in approximately half the cases.. Shallow acetabulum in children clunking in ortolani and bartlow’s. If identified, most commonly, the Pavlik harness is used to keep the hips flexed and abducted to enhance the seating of the femoral head into the acetabulum. In contrast, traumatic dislocation of the hip should be rare if the femoral head is well-seated in the acetabulum, as with adults. Femoral neck fractures. Dislocation occurs when the femoral head is not properly located in the acetabulum. The affected limb appears (and functions as if) shorter because the dislocated femoral head is more superior than on the normal side, resulting in a positive Trendelenburg sign (hip appears to drop to one side during walking). Inability to abduct the thigh is characteristic of congenital dislocation. Acquired dislocation of the hip joint is uncommon because this joint is so strong and stable. Nevertheless, dislocation may occur during an automobile accident when the hip is flexed, adducted, and medially rotated, the usual position of the lower limb when a person is riding in a car. Posterior dislocations are most common. The fibrous layer of the joint capsule ruptures inferiorly and posteriorly, allowing the femoral head to pass through the tear in the capsule and over the posterior margin of the acetabulum onto the lateral surface of the ilium, shortening and medially rotating the affected limb. Because of the close relationship of the sciatic nerve to the hip joint, it may be injured (stretched and/or compressed) during posterior dislocation or fracture–dislocation of the hip joint. Most have normal hip function, firstborns, which may suggest that unstretched uterine and abdominal walls limit fetal movement, and breech delivery. Ortolani’s test of hip abduction confirms the diagnosis.
femoral neck fractures slide 40 of UE and LE
The term hip fracture is most commonly applied, unfortunately, to fractures of the femoral heads, neck, or trochanters. the femoral neck is under a lot of strain, and with osteoporosis, the weakened bone is likely to fracture. With the main blood supply to the femoral head being branches of the medial circumflex femoral artery that transverse the femoral neck, a fracture in the neck region can lead to risk of avascular necrosis for the head. Its retinacular arteries often are torn when the femoral neck is fractured or the hip joint is dislocated. In some cases, the blood supplied to the femoral head through the artery to the ligament of the femoral head may be the only remaining source of blood to the proximal fragment. This artery is frequently inadequate for maintaining the femoral head; consequently, the fragment may undergo avascular necrosis (AVN—also called osteonecrosis), the result of deficient blood supply. Femoral artery then splits into deep femoral to hamstrings (lateral (trochanter) and medial circumflex (femoral neck and head) femoral arteries). Like scaphoid runs risk of becoming vascularly sclerosed. Osteoarthritis- disease of articular cartilage leading to fibrillation and breakdown of cartilage changing weight bearing aspect or relationship of joints for bone on bone. The neck of the femur is most frequently fractured, especially in females secondary to osteoporosis. Fractures of the proximal femur can occur at sev- eral locations—for example, transcervical and intertrochanteric . The femoral shaft is large and strong; how- ever, a violent direct injury, such as may be sustained in an automobile accident, may fracture it, causing, for example, a spiral fracture. Fractures of the distal femur may be complicated by separation of the condyles, resulting in misalignment of the knee joint. Fracture of the neck of the femur often disrupts the blood supply to the head of the femur. It is not a surprise then that prostheses are typically used for femoral head or neck issues.
tibia fractures slide 55 of UE and LE
The tibial shaft is narrowest at the junction of its inferior and middle thirds, which is the most com- mon site of fracture. Because its anterior surface is subcutaneous, the tibial shaft is the most frequent site of an open fracture (compound fracture)—one in which the skin is perforated and blood vessels are torn—or a diagonal fracture. Fracture of the tibia through the nutrient canal predisposes to nonunion of the bone frag- ments resulting from damage to the nutrient artery. Tibial more weight bearing, fracture fibula fracture could have some weight bearing issues as it pulls on connecting sheath.
fibular fractures slide 55/57 of UE and LE
Fibular fractures commonly occur just proximal to the lateral mal- leolus and often are associated with fracture–dislocations of the ankle joint. When a person slips, forcing the foot into an excessively inverted position, the ankle ligaments tear, forcibly tilting the talus against the lateral malleolus and shearing it off. In particular, loss of deep fibular nerve function and, hence, loss of the dorsiflexors, leads to foot drop and a compensatory gait.
calcaneal fractures slide 62 of UE and LE
Calcaneal fractures occur in people who fall on their heels (e.g., from a ladder). Usually, the bone breaks into several fragments (comminuted fracture) that dis- rupt the subtalar joint, where the talus articulates with the cal- caneus . Fractures of the talar neck may occur during severe dorsiflexion of the ankle, for example, when a person is pressing extremely hard on the brake pedal of a car during a head-on collision .
metatarsal and phalangeal fractures
Metatarsal and phalangeal frac- tures are a common injury in endurance athletes and may also occur when a heavy object falls on the foot. Metatarsal fractures are also common in dancers, especially female ballet dancers using the demi-pointe technique. The “dancer’s fracture” usually occurs when the dancer loses balance, putting the full body weight on the metatarsal and fracturing the bone. Injury to the tibial nerve is uncommon because of its protected position in the popliteal fossa; how- ever, the nerve may be injured by deep lacerations in the fossa. Posterior dislocation of the knee joint may also damage
epiphyseal plate fractures slide 50 of UE and LE
The primary ossification center for the superior end of the tibia appears shortly after birth and joins the shaft of the tibia during adolescence (usually 16–18 years of age). Tibial frac- tures in children are more serious if they involve the epiphys- ial plates because continued normal growth of the bone may be jeopardized. All such fractures of the immature skeleton are routinely characterized by the Salter-Harris classifica- tion that describes the pattern of involvement. Salter-Harris fractures involving epiphyseal growth plates are probably best known in the wrist, but can happen in other long bones as well. Depending on the damage to the plate, the length of the limb can be affected. The tibial tuberosity usually forms by inferior bone growth from the superior epiphysial center at approximately 10 years of age, but a separate center for the tibial tuberosity may appear at approximately 12 years of age. Disruption of the epiphys- ial plate at the tibial tuberosity may cause inflammation of the tuberosity and chronic recurring pain during adoles- cence (Osgood-Schlatter disease), especially in young athletes. A smaller epiphyseal growth plate involves the tibial tuberosity, and with active adolescents, can lead to inflammation and avulsed fragments, particularly in active adolescents 10-15 years old becoming big swollen bump.
lower extremity compartment syndromes, with nerve entrapment and injury slide 56 UE and LE
Increased pressure in a conf ined anatom- ical space adversely affects the circulation and threatens the function and viability of tissue within or distal to the space (compartment syndrome). The fascial compartments of the lower limbs are generally closed spaces, ending proximally and distally at the joints. Trauma to muscles and/or vessels in the compartments from burns, sustained intense use of muscles, or blunt trauma may produce hemorrhage, edema, and inflammation of the mus- cles in the compartment. Because the septa and deep fascia of the leg forming the boundaries of the leg compartments are strong, the increased volume consequent to any of these processes increases intracompartmental pressure. Increased pressure in a confined space adversely affects the circulation and threatens the function and viability of tissue within or distally (compartment syndrome). The pressure may reach levels high enough to compress structures significantly in the compartment(s) concerned. The small vessels of muscles and nerves (vasa nervorum) are particularly vulnerable to compres- sion. Structures distal to the compressed area may become isch- emic and permanently injured (e.g., muscles with compromised blood supply and/or innervation will not function). Loss of distal leg pulses is an obvious sign of arterial com- pression, as is lowering of the temperature of tissues distal to the compression. A fasciotomy (incision of overlying fascia or a septum) may be performed to relieve the pressure in the compartment(s) concerned. The fascial compartments of the lower limbs are generally closed spaces, ending proximally and distally at the joints. Because the septa and deep fascia of the leg forming the boundaries of the leg com- partments are strong, the increased volume consequent to infection with suppuration (formation of pus) increases intracompartmental pressure. Inflammation within the an- terior and posterior compartments of the leg spreads chiefly in a distal direction; however, a purulent (pus-forming) infec- tion in the lateral compartment of the leg can ascend proxi- mally into the popliteal fossa, presumably along the course of the common fibular nerve. Anterior (tibial) compartment syndrome (or anterior or lateral shin splints) occurs from excessive contraction of anterior compartment muscles; pain over these muscles radiates down the ankle and dorsum of the foot overlying the extensor tendons. Lateral compartment syndrome occurs in people with excessively mobile ankle joints in which hypereversion irritates the lateral compartment muscles. These conditions are usually chronic, and expansion of the compartment may lead to nerve and vessel compression. In the acute syndrome (rapid, unrelenting expansion), the compartment may have to be opened surgically (fasciotomy) to relieve pressure. Interosseus membrane w/ tight fascia around muscle makes it possible to develop. Neurovascular bundle underneath muscles near interosseus membrane w/ bruising or trauma space filling compromising it. Fasciotomy to prevent squeezing of nerves and vessels. Once above pressure of cappilaries worried about perfusion worry about necrosis above and below nerve compression. Foot supply of tibial nerve becoming plantar nerve foot may be in tact but localized spot of dorsalis pedis look for deep fibular nerve. The five Ps of acute anterior compartment syndrome are: • Pain • Pallor • Paresis (footdrop, caused by compression of deep fibular nerve) • Paresthesia • Pulselessness (variable) Athletically active individuals may report hip pain when the injury may actually be related to the lumbar spine (herniated disc), buttocks (bursitis or hamstring injury), or pelvic region (intrapelvic disorder).
varicose veins, thrombosis, thrombophlebitis slide 54 of UE and LE
Frequently, the great saphenous vein and other superficial veins its tributaries become varicose (dilated and/or tortuous so that the cusps of their valves do not close). Varicose veins are common in the posteromedial parts of the lower limb and may cause discomfort. In a healthy vein, the valves allow blood to flow toward the heart while preventing blood flow away from the heart. Valves also bear the weight of short columns of blood between two valves. Valves in varicose veins, incompetent due to dilation or rotation, no longer function properly. The resulting reverse flow and the weight of long, unbroken columns of blood, produces varicose veins. Deep venous thrombosis (DVT) of one or more of the deep veins of the lower limb is characterized by swelling, warmth, and erythema (inflammation) and infection. Venous stasis (stagnation) is an important cause of thrombus forma- tion. Venous stasis can be caused by • Incompetent, loose fascia that fails to resist muscle expansion, diminishing the effectiveness of the musculovenous pump • External pressure on the veins from bedding during pro- longed institutional stays or from a tight cast, bandages, or bands of stockings • Muscular inactivity (e.g., during an overseas flight) DVT with inflammation around the involved veins (thrombophlebitis) may develop. A large thrombus that breaks free from a lower limb vein may travel to a lung, forming a pulmonary thromboembolism (obstruction of a pulmonary artery). A large embolus may obstruct a main pulmonary artery and may cause death.Although deep venous (or deep vein) thrombosis (DVT) may occur anywhere in the body, veins of the lower limb are most often involved. Three cardinal events account for the pathogenesis and risk of DVT: stasis, venous wall injury, and hypercoagulability. • Clinical risk factors for DVT include the following: Postsurgical immobility • Infection • Malignancy • Pregnancy. Incompetent valves in superficial veins can lead to varicosities. The loss of a set of valves puts additional pressure on an inferior valves, leading to the propagation of the dilated veins. Great (medial side dive into femoral) and small saphenous (posteriorly dives into popliteal) vessels. Communicating veins between saphenous and tibia with some laxity in vlaves of communicating giving saphenous more flow than used to. Lose one of veins becoming swollen and distended incompetence leads to compounding affect downstream as each valve upstream becomes incompetent. In contrast to the varicosities of superficial veins, deep venous thrombosis puts the patient at risk for pulmonary embolism.
hip and thigh contusions
Sports broadcasters and trainers refer to a “hip pointer injury,” which is a contusion of the iliac crest, usually its anterior part. This is one of the most common injuries to the hip region, usually occurring in association with sports, such as football, ice hockey, and volleyball. Contusions cause bleeding from ruptured capillaries and infiltration of blood into the muscles, tendons, and other soft tissues. The term hip pointer injury may also refer to avulsion of the bony site of muscle attachments, for example, of the sartorius or rectus femoris to the anterior superior and inferior iliac spines respectively. However, these injuries should be called avulsion fractures. Another term commonly used is “charley horse,” which may refer either to the acute cramping of an individual thigh muscle because of ischemia, nocturnal leg cramps, or to contusion and rupture of blood vessels sufficient to form a hematoma (blood clot). The latter is usually the consequence of tearing of fibers of the rectus femoris; sometimes, the quadriceps tendon is also partially torn.
hip bursitis slide 47 UE and LE
Ischial bursitis results from excessive friction between the ischial bursae and the ischial tuberosities (e.g., as from cycling). Because the tuberosities bear the body weight during sitting, these pressure points may lead to pressure sores in debilitated people, particularly paraplegic persons. Diffuse deep pain in the lateral thigh region, especially during stair climbing or rising from a seated position, may be caused by trochanteric bursitis. It is characterized by point tenderness over the greater trochanter; however, the pain often radiates along the iliotibial tract. A commonly overlooked diagnosis that clinically mimics trochanteric bursitis is a tear of the insertion of gluteus medius tendon on the trochanter.
hamstring and groin pulls slide 47 UE and LE
A charley horse is associated with localized pain and/or muscle stiffness and commonly follows direct trauma or muscle fatigue. A number of structures in the hip region can generate pain, whether referred pain from back issues, to groin pulls from the adductor muscles and their localized origins from the pubis, to hamstring pulls and their attachment to the ischial tuberosities, or different bursitis issues. Piriformis syndorme- on top of sciatic nerve in foramen and can squeeze sciatic nerve and pain. Ischial bursitis- sit all day and inflame bursa. Hamstring strain- off of ischial tuberosity
knee and patellar pain (6-15 through 6-21)
Pain deep to the patella often results from excessive running, especially downhill; hence, this type of pain is often called “runner’s knee.” The pain results from repetitive microtrauma caused by abnormal tracking of the patella relative to the patellar surface of the femur, a condition known as the patellofemoral syndrome. This syndrome may also result from a direct blow to the patella and from osteoarthritis of the patellofemoral compartment (degenerative wear and tear of articular cartilages). In some cases, strengthening of the vastus medialis corrects patellofemoral dysfunction. This muscle tends to prevent lateral dislocation of the patella resulting from the Q-angle because the vastus medialis attaches to and pulls on the medial border of the patella. Hence, weakness of the vastus medialis predisposes the individual to patellofemoral dysfunction and patellar dislocation. liotibial tract syndrome is common in runners and presents as lateral knee pain, often in the midrange of flexion, between 20 and 70 degrees of knee flexion. The iliotibial tract, often referred to as “iliotibial band” by clinicians, rubs across the lateral femoral condyle, and this pain also may be associated with more proximal pain from greater trochanteric bursitis.Quadriceps tendon rupture occurs mostly in older individuals, from either minor trauma or age-related degenerative changes, including the following:
patellar injuries
Subluxation of the patella, usually laterally, is a fairly common occurrence, especially in adolescent girls and young women. It often presents with tenderness along the medial patellar aspect and atrophy of the quadriceps tendon, especially the oblique portion medially derived from the vastus medialis. Patellar ligament rupture usually occurs just inferior to the patella as a result of direct trauma in younger people. Quadriceps tendon rupture occurs mostly in older individuals, from either minor trauma or age-related degenerative changes, including the following: Arthritism Arteriosclerosis, Chronic renal failure, Corticosteroid therapy, Diabetes, Hyperparathyroidism, Gout
Drawer test slide 52 of UE and LE
Tapping the patellar ligament with a reflex hammer normally elicits the patellar reflex (“knee jerk”). This myotatic (deep tendon) reflex is routinely tested during a physical examination by having the person sit with the legs dangling. A firm strike on the ligament with a reflex hammer usually causes the leg to extend. If the reflex is normal, a hand on the person’s quadriceps should feel the muscle contract. This tendon reflex tests the integrity of the femoral nerve and the L2–L4 spinal cord segments. Diminution or absence of the patellar tendon reflex may result from any lesion that interrupts the innervation of the quadriceps (e.g., peripheral nerve disease). Cruciate (anterior posterior stability of the knee and translocation. Colatteral ligaments- posterior cruciate ligament larger than anterior. ACL can anteriorly translocate tibia. Disruption of the normal function of the cruciate ligaments can be tested by the drawer tests
knee joint injuries slide 53 of UE and LE
Knee joint injuries are common because the knee is a low-placed, mobile, weight-bearing joint and its stability depends almost entirely on its associated ligaments and muscles. The most common knee injuries in contact sports are ligament sprains, which occur when the foot is fixed on the ground. If a force is applied against the knee when the foot cannot move, ligament injuries are likely to occur. The MCL and LCL are tightly stretched when the leg is extended, preventing disruption of the sides of the joint. The firm attachment of the MCL to the medial meniscus is of clinical significance because tearing of this ligament frequently results in concomitant tearing of the medial meniscus. The injury is frequently caused by a blow to the lateral side of the extended knee or excessive lateral twisting of the flexed knee, which disrupts the MCL and concomitantly tears and/ or detaches the medial meniscus from the joint capsule. This injury is common in athletes who twist their flexed knees while running (e.g., in football and soccer). The ACL, which serves as a pivot for rotatory movements of the knee, is taut during flexion and may also tear subsequent to the rupture of the MCL. ACL rupture, one of the most common knee injuries in skiing accidents, for example, causes the free tibia to slide anteriorly under the femur, a sign known as the anterior drawer sign. Although strong, PCL rupture may occur when a person lands on the tibial tuberosity when the knee is flexed. PCL ruptures usually occur in conjunction with tibial or fibular ligament tears. The posterior drawer sign, in which the free tibia slides posteriorly under the fixed femur, occurs as a result of PCL rupture. Degenerative joint disease is a catch-all term for osteoarthritis, degenerative arthritis, osteoarthrosis, or hypertrophic arthritis; it is characterized by progressive loss of articular cartilage and failure of repair. The anterior cruciate ligament limits anterior motion and rotation of the tibia. The unhappy triad (of O’Donoghue) can be generated from a strong valgus force, with damage to the ACL (pull tibia anterior compared to femur if one is fixed Acl taking most of brunt pop sound and rupture w/ bleeding), MCL, and medial meniscus attach each other. Despite the implications in this picture with direct trauma, ACL injuries can be generated by planting the foot and then cutting. The ACL is under tension when the knee is flexed, and a patient with an ACL tear will typically report an audible “pop” while planting the foot and pivoting at the knee. This is followed by knee instability and immediate swelling. ACL tears have a high incidence of associated meniscal tears, as indicated here. MRI is typically the imaging study of choice so as to examine soft tissue. ACL very common in women because of Q angle, LCL off to side, MCL with medial meniscus, Suggested factors why females tend to be at higher risk for ACL tears include: Greater Q angle, Narrower intercondylar notch, Use of quadriceps over hamstrings for deceleration.
unhappy triad slide 53 of UE and LE
The anterior cruciate ligament limits anterior motion and rotation of the tibia. The unhappy triad (of O’Donoghue) can be generated from a strong valgus force, with damage to the ACL (pull tibia anterior compared to femur if one is fixed Acl taking most of brunt pop sound and rupture w/ bleeding), MCL, and medial meniscus attach each other. Despite the implications in this picture with direct trauma, ACL injuries can be generated by planting the foot and then cutting. The ACL is under tension when the knee is flexed, and a patient with an ACL tear will typically report an audible “pop” while planting the foot and pivoting at the knee. This is followed by knee instability and immediate swelling. ACL tears have a high incidence of associated meniscal tears, as indicated here. MRI is typically the imaging study of choice so as to examine soft tissue. ACL very common in women because of Q angle, LCL off to side, MCL with medial meniscus, Suggested factors why females tend to be at higher risk for ACL tears include: Greater Q angle, Narrower intercondylar notch, Use of quadriceps over hamstrings for deceleration. Intracondylar tunnel, ACL narrower cavity than PCL with fixed foot and twist ACL stretching ACL similar to flat feet and over pronating feet. With valgus force
prepatellar bursitis slide 51 of UE and LE
Housemaid’s knee or prepatellar bursitis demonstrates the presence of the subcutaneous prepatellar bursa following chronic irritation. Swollen knees because of brusa and knee patella and skin (prepateller) suprapatellar (below quadriceps) synovial membrane sacs. pes anserinus (foot goose), with its interactions of sartorius, gracilis, and semitendinosus tendons, is among other structures in the knee region with its own bursa.
femoral hernia slide 46 of UE and LE
The femoral ring is a weak area in the lower anterior abdominal wall medial delineation of a fascial femoral sheath surrounding femoral structures that is the site of a femoral hernia, a protrusion of abdominal viscera (often a loop of small intestine) through the femoral ring into the femoral canal. A femoral hernia is more common in women than in men (in whom inguinal hernias are more common), presumably given the difference in pelvic widths. The hernial sac displaces the contents of the femoral canal and distends its wall. Initially, the hernia is relatively small because it is contained within the femoral canal, but it can enlarge by passing through the saphenous opening into the subcutaneous tissue of the thigh. Strangulation of a femoral hernia may occur and interfere with the blood supply to the herniated intestine, and vascular impairment may result in death of the tissues, doesn’t slide back and forth line inguinal and become incarcerated
femoral vessel cannulation slide 45 of UE and LE
The pulse of the femoral artery is usually palpable just inferior to the midpoint of the inguinal ligament. Normally, the pulse is strong; however, if the common or external iliac arteries are partially occluded, the pulse may be diminished. The femoral artery may be manually compressed at the midpoint of the inguinal ligament to control arterial bleeding after lower limb trauma. The femoral artery may be cannulated just inferior to the midpoint of the inguinal ligament (e.g., for cardioangiography—radiography of the heart and great vessels after the introduction of contrast material). For left cardiac angiography, a long slender catheter is inserted percutaneously into the femoral artery and passed superiorly in the aorta to the openings of the coronary arteries.The femoral vessels inferior to the inguinal ligament may offer access to the left heart via the femoral artery or the right heart via the femoral vein. Femoral nav order. Femoral to external artery and vein empty space have lymphatic
superior gluteal nerve injuries slide 43 of UE and LE
Injury to the superior gluteal nerve can lead to a sagging pelvic tilt, with a waddling gluteal medius limp. Gluteus medius and minimus contract on other side if not will sag.
intragluteal injections slide 42 of UE and LE
The femoral pulse is felt at about the midpoint of the inguinal ligament. The femoral artery at this point lies directly over or just medial to the femoral head, just lateral to the femoral vein and about a finger’s breadth medial to the femoral nerve . The femoral artery and vein may be used to gain access to major vessels of the limbs, abdominopelvic cavity, and thorax (e.g., catheter threaded through femoral artery and into aorta for coronary artery angiography and angioplasty). Similarly, access to the larger veins of the inferior vena cava and the right side of the heart and pulmonary veins may be obtained through the femoral vein. “Up and out” (the superolateral quadrant) is the preferred location for intragluteal injections, so as to avoid the sciatic nerve aim for medius and minimus not maximus.
popliteal, dorsalis pedis, and posterior tibial pulses slide 63 of UE and LE
Because the popliteal artery is deep in the popliteal fossa, it may be difficult to feel the popliteal pulse. To palpate this pulse, the person is placed in the prone position with the knee flexed to relax the popliteal fascia and hamstrings. The pulsations are best felt in the inferior part of the fossa. The posterior tibial pulse can usually be palpated between the posterior surface of the medial malleolus and the medial border of the calcaneal tendon. Because the posterior tibial artery passes deep to the flexor retinaculum, it is important when palpating this pulse to have the person relax the retinaculum by inverting the foot. Failure to do this may lead to the erroneous conclusion that the pulse is absent. can suggest the presence of peripheral vascular disease, particularly in the presence of symptoms of intermittent claudication. Weakening or loss of the popliteal pulse is a sign of femoral artery obstruction. The popliteal artery is vulnerable in knee dislocations; downstream pulses should be tested if dislocation has occurred. The dorsalis pedis pulse is evaluated during a physical examination of the peripheral vascular system. Dorsalis pedis pulses may be palpated with the feet slightly dorsiflexed. The pulses are usually easy to palpate because the dorsal arteries are subcutaneous and pass along a line from the extensor retinaculum to a point just lateral to the extensor hallucis longus tendons. A diminished or absent dorsalis pedis pulse usually suggests vascular insufficiency resulting from arterial disease. The five P signs of acute arterial occlusion are pain, pallor, paresthesia, paralysis, and pulselessness. Some healthy adults (and even children) have congenitally nonpalpable dorsalis pedis pulses; the variation is usually bilateral. In these cases, the dorsalis pedis artery is replaced by an extended perforating fibular artery of smaller caliber than the typical dorsalis pedis artery, but running in the same location. Especially important when injured look at pulses distally
shin splints (anterior and posterior tibial muscles) slide 58 of UE and LE
Shin splints—edema and pain in the area of the distal two thirds of the tibia—result from repetitive microtrauma of the tibialis anterior (TA), common in athletes, which causes small tears in the periosteum covering the shaft of the tibia and/or of fleshy attachments to the overlying deep fascia of the leg. Shin splints are a mild form of the anterior compartment syndrome. Shin splints cause pain along the inner distal two thirds of the tibial shaft. The primary cause is repetitive pulling of the tibialis posterior tendon as one pushes off the foot during running. Stress on the muscle occurs at its attachment to the tibia and interosseous membrane. Shin splints commonly occur during traumatic injury or athletic overexertion of muscles in the anterior compartment, especially TA. Muscles in the anterior compartment swell from sudden overuse, and the edema and muscle–tendon inflammation reduce the blood flow to the muscles. The swollen muscles are painful and tender to pressure.Chronic conditions can produce periostitis and bone remodeling or can lead to stress fractures. Pain usually begins as soreness after running that worsens and then occurs while walking or climbing stairs. Similarly, an anterior “shin splint” may represent excessive use/force on tibialis anterior, e.g., imbalance with the large plantarflexors, where microtrauma at its attachment to the tibial periosteum and interosseus membrane can lead to pain in the muscle and possible compression of the neurovascular contents if the muscles swell enough, e.g., from high levels of exertion or trauma. Tension or work on tibialis posterior and anterior (internal) could pull on interosseus membrane causing shin splint, exertional compartment syndrome, microfracture of bones can also cause
Achilles tendon injuries slide 59 of UE and LE
Tendinitis of the calcaneal (Achilles) tendon is a painful inflammation that often occurs in runners who run on hills or uneven surfaces. Repetitive stress on the tendon occurs as the heel strikes the ground and when plantarflexion lifts the foot and toes. Tendon rupture is a serious injury, and the avascular tendon heals slowly. Retrocalcaneal bursitis, an inflammation of the subtendinous bursa between the overlying tendon and the calcaneus, presents as a tender area just anterior to the tendon attachment. Microscopic tears of collagen fibers in the tendon, particularly just superior to its attachment to the calcaneus, result in tendinitis, which causes pain during walking. Calcaneal tendon rupture is often sustained by people with a history of calcaneal tendinitis. After complete rupture of the tendon, passive dorsiflexion is excessive, and the per- son cannot plantarflex against resistance. Microtrauma of the calcaneal tendon can lead to tendinitis. Chronic tendinitis and the accompanying inflammation can lead to the risk of calcaneal tendon rupture and the loss of plantarflexion. Not really vascularized wont heal quickly.
plantar fasciitis slide 64 of UE and LE
plantar fascia Supprot for medial arch of foot. Straining and inflammation of the plantar aponeurosis at its insertion in the calcaneal tuberosity, a condition called plantar fasciitis (heel spur syndrome) , may result from running and high-impact aerobics, especially when inappropriate footwear is worn. It causes pain on the plantar surface of the heel and on the medial aspect of the foot. Point tenderness is located at the proximal attachment of the plantar aponeurosis to the medial tubercle of the calcaneus and on the medial surface of this bone. The pain increases with passive extension of the great toe and may be further exacerbated by dorsiflexion of the ankle and/or weight bearing. A calcaneal spur (abnormal bony process) protruding from the medial tubercle has long been associated with plantar fasciitis and pain on the medial side of the foot when walking, where the ongoing traction of the fascia and inflammation can lead to bone spur formation; however, many asymptomatic patients are found to have such spurs. Generally, it is more common in females and obese persons. A bony spur may develop with plantar fasciitis, but the inflammation causes most of the pain, mediated by the medial calcaneal branch of the tibial nerve. Most patients can be managed nonsurgically, but relief from the pain may take 6 to 12 months. Exercises and orthotic devices are usually recommended in the initial course of treatment. Most cases of plantar fasciitis are self-limiting and respond well to conservative treatment. Bone spur- traction on the foot to develop bone in locations indicative of chronic traction .
genu varum slide 49 of UE and LE
The femur is placed diagonally within the thigh, whereas the tibia is almost vertical within the leg, creating a Q-angle at the knee between the long axes of the bones. The Q-angle is assessed by drawing a line from the ASIS to the middle of the patella and extrapolating a second (vertical) line through the middle of the patella and tibial tuberosity. The Q-angle is typically greater in adult females owing to their wider pelves. A medial angulation of the leg in relation to the thigh, in which the femur is abnormally vertical and the Q-angle is small, is a deformity called genu varum (bowleg) that causes unequal weight distribution. Genu varum (bowleg) R sticking out and genu valgum (knocknee) alter the Q-angle and lead to unequal distribution of stress on the knee different stresses on meniscus, collateral ligaments, and epicondyle. Excess pressure is placed on the medial aspect of the knee joint, which results in arthrosis (destruction of knee cartilage). Excessive valgus angulation is called genu valgum, or knock-knee, and an excessive varus angulation is called genu varum, or bowleg. These deformities occur in growing children and are often related to rickets, skeletal dysplasia, or trauma. Most resolve without treatment.
genu valgum slide 49 of UE and LE
A lateral angulation of the leg in relation to the thigh (exaggeration of knee angle) is genu valgum (knockknee). Consequently, in genu valgum, excess stress is placed on the lateral structures of the knee. The patella, normally pulled laterally by the tendon of the vastus lateralis, is pulled even farther laterally when the leg is extended in the presence of genu varum so that its articulation with the femur is abnormal. The knee of a standing patient should look symmetric and level. The tibia normally has a slight valgus angulation compared with the femur. Valgus is used to describe the bone distal to the examined joint; a valgus angulation refers to a slight lateral angle.
ankle sprains slide 61 of UE and LE
The ankle is the most frequently injured major joint in the body. Ankle sprains (torn fibers of ligaments) are most common. A sprained ankle is nearly always an inversion injury, involving twisting of the weight-bearing plantarflexed foot. The anterior talofibular ligament (part of the lateral ligament) is most commonly torn during ankle sprains, either partially or completely, resulting in instability of the ankle joint. The calcaneofibular ligament may also be torn Most ankle sprains involve an inversion injury when the foot is plantarflexed, placing stress on the components of the lateral collateral ligament. Often the severity of the injury occurs from anterior to posterior, involving first the anterior talofibular ligament, then the calcaneofibular ligament, and finally, if especially severe, the posterior talofibular ligament. The anterior drawer test, in which the tibia is held steady while the heel is pulled anteriorly with the foot in about 10 to 20 degrees of plantarflexion, will confirm the injury to the anterior talofibular ligament if the translation of the foot anteriorly is excessive compared with that of the uninjured contralateral ankle. sprain involve ligaments, strains involve muscles/tendons
Pott fracture slide 61 of UE and LE
A forcible eversion can lead to a Pott fracture (bimalleolar fracture), with the medial ligament causing an avulsion fracture of the medial malleolus, and then damaging the fibula. A Pott fracture–dislocation of the ankle occurs when the foot is forcibly everted. This action pulls on the extremely strong medial ligament, often tearing off the medial malleolus. The talus then moves laterally, shearing off the lateral malleolus or, more commonly, breaking the fibula superior to the tibiofibular syndesmosis. If the tibia is carried anteriorly, the posterior margin of the distal end of the tibia is also sheared off by the talus. Deltoid contribute to evulsion fracture rather than tear by itself. Ankle joint capsule not as defined as rest
bunion slide 65 of UE and LE
Hallux valgus is a foot deformity caused by degenerative joint disease; it is characterized by lateral deviation of the great toe (L. hallux). In some people, the deviation is so great that the first toe overlaps the second toe. These individuals are unable to move their 1st digit away from their 2nd digit because the sesamoid bones under the head of the 1st metatarsal are displaced and lie in the space between the heads of the 1st and 2nd metatarsals. In addition, a subcutaneous bursa may form owing to pressure and friction against the shoe. The thickened bursa (often inflamed and tender) and/or reactive hyperostosis of the head of the 1st metatarsal results in a protuberance called a bunion Hallux valgus, with its striking lateral deviation of the hallux (big toe), can lead to rubbing and inflammation of the head of the first metatarsal to generate a bunion. Wieght bearing causing friction point. Callus- hyperkeratinized throughout. Corns- softer in non weight bearing areas between or on toes, indurated internal part, initial firm part in middle and little hard part can become warped in in diabetes. Are they feeling it?
pes planus slide 66 of UE and LE
Acquired flatfeet (“fallen arches”) are likely to be secondary to dysfunction of the tibialis posterior owing to trauma, degeneration with age, or denervation. In the absence of normal passive or dynamic support, the plantar calcaneonavicular ligament fails to support the head of the talus. Consequently, the talar head displaces inferomedially and becomes prominent. As a result, some flattening of the medial longitudinal arch occurs, along with lateral deviation of the forefoot. Flatfeet are common in older people, particularly if they undertake much unaccustomed standing or gain weight rapidly, adding stress on the muscles and increasing the strain on the ligaments supporting the arches.
lower limb surface anatomy slide 68 of UE and LE
see pictures p. 320-322
lower limb imaging slide 69 of UE and LE
see pictures p. 394-395
dural origin of headaches
Many headaches have a dural component, given the innervation of the meninges with branches of trigeminal nerve. The dura is sensitive to pain, especially where it is related to the dural venous sinuses and meningeal arteries. Although the causes of headache are numerous, distention of the scalp or meningeal vessels (or both) is believed to be one cause of headache. Many headaches appear to be dural in origin, such as the headache occurring after a lumbar spinal puncture for removal of CSF. These headaches are thought to result from stimulation of sensory nerve endings in the dura. When CSF is removed, the brain sags slightly, pulling on the dura; this may cause pain and headache. For this reason, patients are asked to keep their heads down after lumbar puncture to minimize the pull on the dura, reducing the chances of headache. Brain tissue not wired for pain, meninges are. Facial nerve 5 for different meninges wiring seems to be covering around tentoreum (cerebelli between cerebral cortex and cerebellum on bottom) and temporal lobe (herpes encephalitis)
intracranial hemorrhages: epidural
Head injuries can be associated with intracranial bleeding. Three major types of bleeds outside of intracerebral involvement: Sharp blow, localized skull fracture, deeper majorly concussing. Blood from torn branches of a middle meningeal artery collects between the external periosteal layer of the dura and the calvaria, usually after a hard blow to the head. Epidural hematomas result most often from motor vehicle crashes, falls, and sports injuries. The blood collects between the periosteal dura mater and bony cranium. The source of the bleeding is usually arterial (85%); common locations include the frontal, temporal (middle meningeal artery is very susceptible, especially where it lies deep to the pterion), and occipital regions. brief concussion with loss of consciousness patient wakes up fine but later, drowsiness and coma occur because of space filling it leads to herniation through foramen magnum causing blown pupil because no parasymapathetic tone through oculomotor nerve. Extradural or epidural hemorrhage is arterial in origin.. This results in the formation of an extradural or epidural hematoma. The brain is compressed as the blood mass increases, necessitating evacuation of the blood and occlusion of the bleeding vessels. .
subdural hemorrhages
Tearing of the bridging veins between brain and dural sinuses. A dural border hematoma classically is called a subdural hematoma; however, this term is a misnomer because there is no naturally occurring space at the dura–arachnoid junction. Hematomas at this junction are usually caused by extravasated blood that splits open the dural border cell layer. The blood does not collect within a preexisting space but rather creates a space at the dura–arachnoid junction. Dural border hemorrhage usually follows a blow to the head that jerks the brain inside the cranium and injures it. The precipitating trauma may be trivial or forgotten, but a hematoma may develop over many weeks from venous bleeding. Dural border hemorrhage is typically venous in origin and commonly results from tearing of a superior cerebral vein bridging in as it enters the superior sagittal sinus. compresing brain causing significant damage. Subdural hemorrhage leading to a subdural hematoma, is more common in elderly/alcoholic patients (those with some brain atrophy and hence more “gap” that veins must transverse), and is often the result of tearing in a superior cerebral vein as it feeds into the superior sagittal sinus. These can be more chronic than the epidural hematoma, and may present with fluctuating drowsiness.
subarachnoid hemorrhages
Subarachnoid hemorrhage is an extravasation (escape) of blood, usually arterial, into the subarachnoid space results in the collection of blood between the arachnoid mater and pia mate. Most subarachnoid hemorrhages result from rupture of a saccular aneurysm (sac-like dilation on an artery) in the willis region. Some subarachnoid hemorrhages are associated with head trauma involving cranial fractures and cerebral lacerations. Bleeding into the subarachnoid space results in meningeal irritation, a severe headache, stiff neck, and often loss of consciousness (seepage of blood down to spinal cord). The most common cause of subarachnoid hemorrhage is the rupture of a saccular, or berry, aneurysm. leading to signs of meningeal irritation (severe headache, stiff neck, “the worst headache of my life”), with blood in the CSF.
hydrocephalus
choroid plexus is the site of cerebrospinal fluid synthesis, with arachnoid granulations projecting into the superior sagittal sinus the location of where the CSF drains back into the venous circulation. CSF made by little collection of ependymal cells in lateral and fourth ventricle in the choroid plexus w/ blood supplies from loops of capillaries below that help to supply it with proper nutrition for the brain. CSF floats around and back to dural sinus (largest superior sagittal sinus). Overproduction of CSF, obstruction of its flow, or interference with its absorption results in an excess of CSF in the subarachnoid space ventricles. When it occurs in infants and young children, the head enlarges, a condition known as hydrocephalus. Cerebral aqueduct stenosis most common in infants. TBI or infection (meningitis) arachnoid and pia if no longer driaining pressure not going on. Midbrain and cerebral aqueduct can get stenosed off, choroid plexus of lateral plexus can dilate especially if anteiror and posterior fontanelle never fused. Excess CSF dilates the ventricles; thinning the surrounding brain; and, in infants, separates the bones of the calvaria because the sutures and fontanelles are still open. Internal (obstructive) hydrocephalus: CSF building up in the ventricles, most commonly from congenital aqueductal stenosis, so more common in preossified infants. This will usually cause cerebral cortex to atrophy and cranial bones to thin if not treated by ventriculostomy (artificial opening into the floor of the third ventricle draining into cistern beneath to recirculate) or ventricular shunting ending in the abdomen, which can get clogged)
cerebral vasculature slide 13 of NEURO
Glial cells- keeping area sterile or in repair having macrophage. Additional cells floating around astrocytes- supprotive helping to surround blood vessels w/ tight junctions of capillaries combination leading to a blood brain barrier making it harder for substances to cross over. The homunculus is a functional HAL (head-arm-leg) representation on the precentral and postcentral gyri from lateral medial. Note that the Internal carotid artery- middle cerebral artery (MCA) supplies the lateral HA (head-arm) part of the homunculus, while the anterior cerebral artery (ACA) supplies the medial L (leg) part. Increased cortical space means increased sensory. Vertebral> basilar artey> posterior> temporal artery visual area at end of visual pathway and its association
subsequent ischemic stroke
Stroke is classified into the following two types: • Ischemic (70-80%): infarction; thrombotic or embolic, resulting from atherosclerosis of the extracranial (usually carotid) and intracranial arteries or from underlying heart disease. An ischemic stroke denotes the sudden development of neurological deficits that are related to impaired cerebral blood flow. In acute ischemic stroke, ischemic brain injury begins with a central core of very low perfusion and often irreversible cell death. This core is surrounded by an ischemic penumbra of metabolically disturbed cells that are still potentially viable, depending on the restoration of blood flow and duration of ischemia. Because most irreversible damage occurs in the first 3–6 hrs after onset of symptoms, therapies targeted to the 3-hr window achieve the best outcomes, with recovery in up to 50% of patients in some studies. The most common causes of strokes are spontaneous cerebrovascular accidents such as cerebral embolism, cerebral thrombosis, cerebral hemorrhage, and subarachnoid hemorrhage. The cerebral arterial circle is an important means of collateral circulation in the event of gradual obstruction of one of the major arteries forming the circle. Sudden occlusion, even if only partial, results in neurological deficits. In elderly persons, the anastomoses are often inadequate when a large artery (e.g., internal carotid) is occluded, even if the occlusion is gradual (in which case function is impaired at least to some degree). upper motor neuron lesion if caused by cerebral hemisphere stroke develop decorticate posturing (flexion of wrist and elbow and extension (straightening of ankle and knee). midbrain strokes- elbow extendinded (decerebrate posturting)
hemmorhagic stroke
Hemorrhagic: occurs when a cerebral vessel weakens and ruptures (subarachnoid or intracerebral hemorrhage), which causes intracranial bleeding, usually affecting a larger brain area. Hemorrhagic stroke follows the rupture of an artery or a saccular aneurysm, a sac-like dilation on a weak part of the arterial wall. The most common type of saccular aneurysm is a berry aneurysm, occurring in the vessels of or near the cerebral arterial circle and the medium arteries at the base of the brain. In time, especially in people with hypertension (high blood pressure), the weak part of the arterial wall expands and may rupture, allowing blood to enter the subarachnoid space. poorly controlled BP supplies basal ganglia creating hemmorhagic, phalamic basal ganglia, disurpting communication from lower body to brain subarachnoid space normally CSF all blood is irritating giving stiff neck
dementia
Dementia is an acquired neurologic syndrome that presents with multiple cognitive deficits. By definition, dementia includes short-term memory impairment, behavioral disturbance, and/or difficulties with daily functioning and independence. Dementia can be classified as degenerative, vascular, alcoholic, or human immunodeficiency virus (HIV) related. Vascular dementias are caused by anoxic damage from small infarcts and account for about 15% to 20% of dementia cases. Multiinfarct dementia is associated with heart disease, diabetes mellitus, hypertension, and inflammatory diseases. Damage brain from stroke at internal capsule and transect, upper neuromotor neuron symptom helping to regulate. Increased motor tone Limbic system- behavior Temmporal lobe- behavior things going on in hippocampus w/ processing of episodic informaiton to long term when damaged w/ alzheimers new memories don’t form and gyri around it losing distant memories tied in with emotion aka amygdala emotional context helps you to remember. The Papez circuit indicates the integral role of the role of the hypothalamus as a liaison between the autonomic system and the emotional processing of the limbic system. The hippocampus is well known as a site for memory consolidation. For example, “HM”, well-known in general psychology classes with his bilateral surgical removal of hippocampi for intractable seizures, had a subsequent loss of ability to establish new long-term memories for decades. Cortisol receptors if so overwhelmed and stressed cant remember. Alzheimer disease targets the hippocampus and parahippocampal gyrus initially. The amygdala receives a variety of inputs in order to affect (pun intended) emotional responses to different sensory stimuli. Adrogen and test leading to exaggerated emotional response. Smell olfactory bulb limbic system- affecting the limbic system triggering emotions, disrupting behavior and memories. Mammilary bodies behind pituitary damaged w/ chronic thaimaine deficeincy ex. Memory retraction altered bizarre and specialized cortical deficit. Mammillary body damage is often involved in Wernicke-Korsakoff syndrome, caused by thiamine deficiency in patients, e.g., chronic ethanol abuse.
lobes of cerebral cortex functional areas
The cerebrum is found in the forebrain, and is the largest part of the brain. It is responsible for higher mental functions, which include memory and reason. It consists of paired lobes and two hemispheres. Left and right hemispheres are partially divided by a longitudinal cerebral fissure. Cerebral Cortex- detailed integrated functions. Convolutions are evident, with elevated gyri (s. gyrus) and grooves of sulci (s. - sulcus) that help to increase the gray matter area. Fissures (deep sulci) separate the cerebral hemispheres into lobes. Immediately in front of the central sulcus (seperating frontal from parietal) is the precentral gyrus (important motor region). Immediately behind the central sulcus is the postcentral gyrus (important sensory region).
frontal
functions include voluntary motor impulses for skeletal muscles, and dealing with responses relating to personality, reason, emotions, etc. Broca area: motor speech. Prefrontal lobe- behavioral. Motor activity precentral gyrus of frontal lobe, (prefrontal lobe, personality issues) and motor areas, such as Broca, for motor aspects of speech; precentral gyrus; for motor initiation, organized lateral to medial: HAL (head arm leg) conscious intellect.
corpus callosum
The corpus callosum (large tract of white matter) connects the two hemispheres, making sure that each side is aware of the other and can share memories myelinated axons connecting over. check for aphasia, cortical sensory or other specialized deficit(s), e.g., loss of Broca area and motor aphasia. axons that communicate between the two cerebral hemispheres. The cingulate gyrus of the limbic system surrounds that.
spinal cord slide
face, language not involved, myelinated nerurons pull out into separate spinal cord tracts w/in spinal cord. can determine a level of dermatome involvement with sensation, motor involvement, e.g., biceps reflex C 5-6, abdominal reflexes T8-T12, depending where you are compared to umbilicus, knee reflex L2-4, ankle reflex S1. separation of senses and motor aspects, e.g., vibration and position intact (dorsal columns), but loss of pain and temperature (spinothalamic tract). Separate stimuli e.g., interpreted as touch, pain, and temperature are carried together. In contrast, in the central nervous system, the mixed nerve fibers are sorted out into different bundles or tracts. Tracts are found in white matter-inulating material with huge tracts, surrounding nerve cell bodies that predominate in gray matter (interneurons communicating) which include interneurons as well as motor neurons. Motor nerves ventral root hook up at intervertebral foramen getting dorsal and ventral ramus. Sensory neurons- dorsal root ganglion. Major motor- corticospinal and in between ventral horn where motor neurons are: Spinothalamic tract- pain and temperature, Dorsal columns- discriminatory sense, vibration etc. concious position. Separate spinal cerebellar to coordinate position covering white matter tract areas. Tracts bear compound names of where they begin to where they end, e.g., corticospinal tract. a) afferent (sensory) or ascending tracts, b) efferent (motor) or descending tracts.
tumor slide
Clinical signs and symptoms of brain tumors depend on the location and the degree to which intracranial pressure (ICP) is elevated. Slow-growing tumors in relatively silent areas (e.g., frontal lobes) may go undetected and can become quite large before symptoms occur. Small tumors in key brain areas can lead to seizures, hemiparesis, or aphasia. Increased ICP can initiate broader damage by compressing critical brain structures. Early symptoms of increased ICP include malaise, headache, nausea, papilledema, and less often abducens nerve palsy and Parinaud’s syndrome. Classic signs of hydrocephalus are loss of upward gaze, downward ocular deviation (“setting sun” syndrome), lid retraction, and light-near dissociation of pupils. Primary tumors include the following: • Gliomas: arise from astrocytes or oligodendrocytes; glioblastoma multiforme is the most malignant form (astrocytic series). • Meningiomas: arise from the arachnoid mater and can extend into the brain. • Pituitary tumors: can expand in the sella turcica and affect CN II, III, IV, V1, V2, and VI; about 15% of primary tumors. • Neuromas: acoustic neuroma, a benign tumor of CN VIII, is a common example; about 7% of primary tumors. Metastatic brain tumors are more common than primary brain tumors. Most spread via the bloodstream, with cells seeded between the white matter (fiber tract pathways) and gray matter (cortical neurons). Some tumors metastasize directly from head and neck cancers or through Batson’s vertebral venous plexus. Presentation often includes headache (50%), seizures (25%), and elevated intracranial pressure. In contrast to the rapid onset of strokes, brain tumors, e.g., meningiomas, may present as space-filling lesions that may raise intracranial pressure or present with a focal lesion, depending on their location and progression. Glioblastoma- fatal tumor, necrosis leading to impacting fatal results. Acoustic neruoma- scwann cell tumor of CN 8, tinnitus, deafness, cerebellum squeezed movement coordination
corticospinal tracts and lesions involving cranial nerves
In contrast to the corticospinal and corticobulbar tracts, there are additional descending tracts. These extrapyramidal tracts that travel through the medulla outside of the pyramids, and innervate (often ipsilaterally, or some that cross) via the white matter between the ventral horns, helping with postural adjustments and involuntary movements. As an example, note the vestibulospinal tract coming from inner ear nuclei. One way of highlight the postural, “antigravity” aspect of the extrapyramidal tracts is to look at posturing following brain damage. The red nucleus of the midbrain is a structure whose damage can indicate a brainstem lesion. The rubrospinal tract enhances flexor movements in the contralateral upper extremity, a function that is usually hidden/overridden by the corticospinal tract. decorticate posturing: lesion rostral/superior to the red nuclei; presentation of flexed upper limbs, extended lower limbs.decerebrate posturing: red nucleus affected by the lesion; presentation of both upper and lower limbs extended, and extensor input via the extrapyramidal tracts are dominant.
EFFERENT (MOTOR) OR DESCENDING PATHWAYS
The body must control what kinds and what amounts of movements. These are a concern of 1) the ventral/anterior horn cells, or what we can call the final common pathway and 2) higher motor pathways that impinge on those horn cells. corticospinal tract (lateral as the main one, compared to the anterior) carries voluntary control of skeletal muscles. The corticospinal tract passes through the internal capsule lateral to the thalamus before crossing over at pyramids; synapses in anterior horn before leaving spinal cord. This is a skilled movement pathway. Note: the anterior corticospinal tract (~10% of the tract) of nondescussating fibers that supply axial musclesthat do not cross over in the pyramids and descending, either descussating in the spinal cord or not. These supply trunk and proximal muscles, so that the general positioning of the torso and gross positioning of limbs will occur if lateral corticospinal tract is damaged. The distal muscles of the limbs will be supplied by the crossing-over fibers of the lateral corticospinal tract. Spinothalmic tract crosses over then goes up Pain and temperature consisting of smaller sensory neurons with unmyelinated or thinly myelin- ated axons. Discriminatory- dorsal columns spinal tract have larger neurons with heavily myelinated axons. Stereonosis- spinal tract and knowing what is in your hand parietal association as well. Examples of lesions: Unable to express- Frontal lobe: expressive aphasia (L hemisphere), prefrontal lobe syndrome (bilateral), Parietal lobe: neglect syndrome (R hemisphere) of the contralateral L side and surroundings more striking than left side, Temporal lobe: receptive aphasia (L hemisphere), Occipital lobe: contralateral homonymous hemianopia/hemianopsia (± macular sparing). Precentral gyrus last part of frontal lobe hitting bottom part of pyramids and crossing over down to ventral horn . The lateral corticospinal tract (lateral as the main one, compared to the anterior) carries voluntary control of skeletal muscles and passes through the internal capsule lateral to the thalamus before crossing over at pyramids; synapses in anterior horn before leaving spinal cord. This is a skilled movement pathway. Neuromuscular junction- damage neuron out to muscle become flacid w/ atrophy. Lower motor neuron w/ no innervation atrophy. UMN- cortex, internal capsule, spinal cord and capsule spasticity because upper motor neuron gives lower permission and regulatory control lMN still innervation but not controlled.
AFFERENT (SENSORY) OR ASCENDING PATHWAYS
Sensation is initiated by sense receptors and an impulse generated by an afferent (sensory) nerve fiber in a peripheral nerve. The afferent (sensory) nerve fiber follows the posterior (dorsal) root. Once in the spinal cord, (for the most part) its impulses move along one of the following three tracts: spinothalamic tract (lateral is the major one) carries pain/temperature (some light touch), and crosses over in spinal cord before subsequent ascent to thalamus cross over right away; posterior (dorsal) columns (components of fasciculus gracilis and fasciculus cuneatus) carry conscious proprioception, stereognosis, vibration sense, light touch, and ascends ipsilaterally before crossing over at medullary nuclei postcentral gyrus. At the thalamic level (in the diencephalon), there is the general quality of perception, but fine distinctions are made with a third synapse of sensory neurons carrying impulses via the internal capsule lateral to the thalamus into the sensory cortex of the brain, to the postcentral gyrus. spinocerebellar tract (dorsal as the major one) carry unconscious proprioception, as the dorsal spinocerebellar tract ascends ipsilaterally, entering cerebellum via peduncles, to give the cerebellum information for movement coordination.
corticobulbar tracts and lesions
The corticobulbar tract is a component of the corticospinal tract that does not reach the spinal cord, but directs voluntary control of skeletal muscles controlled by cranial nerves. Typically, corticobulbar fibers from both sides influence CNs; an important exception is that LMNs of lower facial muscles are only contralaterally supplied. This is how one separates an internal capsule or cortical stroke triggering lower facial issues from a Bell palsy affecting CN VII as a whole, and why in your neurological exam you include examination of both upper and lower facial muscles. If upper face is working well something in corticobulbar tract on contralateral side. Bad day in pons- whole face
crossed palsy patterns
In a crossed palsy (crossed hemiplegia), a brainstem lesion affects a nearby cranial nerve nucleus ipsilaterally and the spinal tracts before they cross (decuss), hence creating contralateral hemiparesis. Three examples of crossed palsy of the (reasonably midline) corticospinal tract with the following three cranial nerve nuclei that are located midline and so could be likely affected at the same time: Spastic paralysis- UMN corticospinal tract, proprioception, abduct eye CN 6, CN7- bells palsy in pons crossed pasy. Right pons- knocked out descending cortiospinal tract. Arm, tongue- medulla, Spinal tract and brain- brainstem. CN III involvement indicates a midbrain lesion, CN VI: involvement indicates a pons lesion, CN XII:involvement indicates a medulla lesion. Precentral gyrus- at beginning, first neuron goes down and at end of pyramids cross over and go down handing off to hitting on neurons in ventral neuron of spinal cord for lateral portion of spinal tract vulnerable area on vulnerable side of thalamus for focal point, upper motor neuron down to spinal cord living at precentral gyrus, lower motor neuron going to ventral horn out to muscle w/ two phenomenologies and directly innervating muscle onto cell bodies flaccid weak cell bodies. Damage brain from stroke at internal capsule and transect, upper neuromotor neuron symptom helping to regulate. Increased motor tone.
upper motor neuron syndromes Bates 12th ed., p. 774-775, 787
any neuron or level of motor control before the synapse in the ventral horn.corticospinal pathway synapses in anterior horn (grey matter) motor neurons above this are upper and below is lower. ex. “spastic paralysis,” no muscle atrophy, increased muscle tone, increased reflexes, fasciculations and fibrillations not present, Babinski reflex may be present. When upper motor neuron systems are dam- aged above their crossover in the medulla, motor impairment develops on the opposite or contralateral side. In damage below the crossover, motor impairment occurs on the same or ipsi- lateral side of the body. The affected limb becomes weak or paralyzed, and skilled, complicated, or delicate movements are performed poorly when compared with gross movements.
lower motor neuron syndromes
the “common pathway” of the motor neurons whose nuclei are in the ventral horn and whose axons extend peripherally. ex. “flaccid paralysis” of muscle weakness, atrophy, decreased reflexes, fasciculations and fibrillations present, Babinski reflex not present. lower motor neuron (LMN) lesion: “flaccid paralysis” of muscle weakness, fasciculations progressing to atrophy, decreased reflexes. Damage to the lower motor neuron systems causes ipsi- lateral weakness and paralysis, but in this case, muscle tone and reflexes are decreased or absent.
herpes encephalitis
An example of limbic involvement can be seen in the temporal lobe targeting of herpes encephalitis. This also is a reminder of how trigeminal nerve branches innervate along the meninges, tentoreum and temporal lobe developing infection affecting behavior, giving lots of antibiotics. Subtle pattern of behavior altered from baseline looked at from neurologic exam may not know what lesion is but can narrow it down.
proprioception pathways
proprioception, stereognosis, vibration sense, light touch, and ascends ipsilaterally before crossing over at medullary nuclei junction between spinal cord and brain fasciculus- columns(nucleues cuntaneus- upper leve, gracilis- lower levels). Neurons enters then medualla, then postcentral gyrus only at medulla. Have both conscious and unconscious pathway (connecting w/ cerebellum)spinocerebellar tract (dorsal as the major one) carry unconscious proprioception, as the dorsal spinocerebellar tract ascends ipsilaterally, entering cerebellum via inferior peduncles, to give the cerebellum information for movement coordination. HANDED OFF DORSAL HORN STAYS AT CEREBELLUM, IPSALATERAL, cerebellum talkis to one and then crosses showing up ipsalaterally. A muscle stretch reflex (or myotactic reflex) can be monosynaptic, as generated by passive stretching and subsequent contraction of a muscle. This is useful for an antigravity (i.e., standing erect) response, but we know it best as reflex testing. Swift hammer strike stretches muscle spindle fiber from cerebellar function- how much, how fast, hard tension that stretches w/ sensation in and motor reflex interneurons going on, inhibitory as well up to dorsal columns further up as well. Relax w/ increased tension at base of belly and tendon. Tendon organs how much tension generated cerebellar coordination for further recruitment. Sensation carried by afferent neuron to three areas: collateral branches up sensory tract to let brain know that reflex occurred, synapse on motor neuron to trigger contraction of agonist muscle, synapse on inhibitory interneuron to inhibit antagonist muscle. In addition to the muscle spindle apparatus, a Golgi tendon organ within tendons are sensitive to muscle tension and will initiate an inhibitory relaxation to the muscle if tension is sufficiently high.
spinal lesions
amyotrophic lateral sclerosis: both upper and lower motor neuron symptoms, hyperreflexive even if there muscle is fasiculating Guillain-Barré sydrome: peripheral demyelinating disease, typically in an ascending pattern, with both motor and sensory deficits. Teriary syphilis- … Pernicious anemia- Polio- oral fecal virus trophic lower motor neuron Guilain-barre- mild illness or gastric upset infection triggering cross reaction of antibodies massive demyelinating disease
syringomelia
syringomyelia : a central fluid-filled cavity of the cervical spinal cord may affect the crossing spinothalamic tracts, and so lead to bilateral deficits of pain and temperature sensation in the upper extremities. With progression, the condition may involve the ventral horn LMN cell bodies as well. Enlarged central canal thinned down edges. Whole got big most tracts not affected, spinal cerebellar are fine w/ the spinothalamic that is corrsing over other side affected in neck hitting cervical to arm. Present w/ a deficit in C5-C8 loss of pain and temperature in hands
brown-sequard syndrome
A final check of our understanding of the spinal cord: hemisection of the spinal cord creates a pattern of ispilateral UMN and dorsal column deficits and contralateral pain and temperature deficits in the Brown-Séquard syndrome. Wiping out half the spinal cord. Sensation comes up affecting dorsal column, spinocerebellar (difficult finding way around), pain and temeprature fine on that side crossing over spinal over w/ opposite side pain and temperature with upper motor neuron pattern in that leg. In this individual: left hemisection of spinal cord inferior to T10 (as umbilicus is not involved). Dorsal column: ascension blocked ipsilaterally. Spinocerebellar tract: ascension blocked ipsilaterally. Corticospinal tract: crossed at medullary pyramids, descent to L lower extremity blocked. Spinothalamic tract: crosses over in spinal cord within 1-2 dermatomes, so that the pain and temperature from the R lower extremity is blocked, and the pain and temperature from the L lower extremity crosses over and travels up the R spinothalamic tract
basal ganglia (nuclei) lesions
Basal nuclei (ganglia): within central white matter surrounding the thalamus. In effect, the basal ganglia act as “brakes” for motor activity. Typically inappropriate amounts of movement (“resting tremors”) result from lesions in these areas. In a highly simplified schema: striatum and pallidum represent inputs and outputs, respectively, of the basal ganglia of basal nucleid Example of Huntington chorea with striatal damage. Chorea: rapid, involuntary, “dancing” movements. substantia nigra (in the midbrain): Dark because of melanin deposition. Neurons here contain dopamine that influence input balance between direct and indirect basal ganglia pathways. Example of Parkinson disease, with rigidity, tremor. Surrounding the thalamus are most components of the basal ganglia, which influence stereotyped motor activity of postural/reflexive nature. In effect, the basal ganglia act as “brakes” for motor activity. Disorders are characterized by meaningless unintenional movements occuring unexpected. 1. Parkinson’s disease—rigidity; slowness; resting tremor; mask-like facies; shuffling gait, associated with degeneration in the basal ganglia and substantia nigra of the midbrain. 2. Chorea—sudden jerky and purposeless movements (e.g. Sydenham’s cho- rea found in rheumatic fever; Huntington’s chorea, an inherited disorder). 3. Athetosis—slow writhing, snake-like movements, especially of the fingers and wrists. 4. Hemiballismus—a sudden wild flail-like movement of one arm. Summary of Parkinson disease and the location of substantia nigra in midbrain, along with the projection of dopaminergic neurons. Basal ganglia (context at movement)- tremor at rest, demending upon where you damage w/ hemibalismis if you interefere w/ subtahalmus. Most common- parkinsons midbrain cereberal aqueduct, substania nigra (without stop starting of activity), red nucleus.Dopamine- movmeent, addiction, behavioral ongoing severe parkinsons impacts on behavior such as dementia
cranial nerve lesions
Complex cerebral receptive disabilities are called agnosias. Complex cerebral motor disabilities are apraxia
