Obturator neuropathy

1. What muscles are innervated by the obturator nerve?
2. How is the obturator nerve commonly injured?
3. What is the presentation of obturator neuropathy?

Answers:
1. Pectineus, adductor brevis, adductor longus, adductor magnus, obturator externus, gracilis. It also has a cutaneous branch.
2. It is injured by compression from a pelvic fracture or hernia within the obturator foramen.
3. Symptoms include hip adduction weakness and decrease in sensation along the medial thigh.

Femoral nerve injury

1. What is the course of the femoral nerve and what muscles does it innervate?
2. What is the presentation and etiology of femoral neuropathy? What are the NCS findings?
3. What is diabetic amyotrophy?
4. How does saphenous neuropathy present and what is the etiology?
5. To what region does the saphenous nerve supply sensation?

Answers:
1. The nerve runs through the psoas, under the inguinal ligament lateral to the femoral artery (and vein), then travels through the femoral triangle. It innervates the iliacus, pectineus, sartorius, rectus femoris, vastus muscles, and gives off the sensory saphenous nerve.
2. The nerve can be injured by compression in the pelvis from trauma, fracture, retroperitoneal hematoma, tumor, or cardiac cath. It presents with quad weakness and decreased sensation over the anterior thigh and medial leg. EMG shows abnormal saphenous SNAP, abnormal rectus femoris CMAP.
3. Diabetic amyotrophy is the most common cause of femoral neuropathy. The nerve is injured from an abnormality in the vaso-nevorum due to DM. It may also occur due to marked weight loss. The symptoms include those of femoral neuropathy with asymmetric thigh pain and atrophy.
4. The saphenous nerve is injured by entrapment in Hunter's canal or between the sartorius and the gracilis, or from knee or vascular surgery. Patient complains of medial knee pain with abnormal sensation radiating distally along the medial aspect of the leg and foot.
5. Medial aspect of the leg, medial malleolus, and medial arch of foot.

Lateral femoral cutaneous nerve injury

1. What is the nerve root origin of the lateral femoral cutaneous (LFC) nerve?
2. What is the path of the LFC nerve?
3. What is the most common etiology of injury to the LFC nerve (meralgia paresthetica)?
4. What is the presentation of meralgia paresthetica?
5. What is the treatment of meralgia paresthetica?

Answers:
1. L2, L3, contributing to the posterior division of the lumbar plexus.
2. It passes over the iliacus toward the AIS, then under the inguinal ligament to provide sensation to the lateral thigh.
3. Low-grade repetitive trauma, protuberant abdomen, pregnancy, tight clothing, diabetes, tumor, infection.
4. Symptoms are purely sensory and include lateral thigh pain, numbness, burning, or dull ache, sometimes exacerbated by hip extension.
5. Treatment includes rehab, NSAIDs, steroid injection, surgical release.

Long thoracic nerve injury

1. Where do the long thoracic nerve fibers originate?
2. What muscle does the long thoracic nerve innervate?
3. What is the difference between scapular winging caused by long thoracic nerve vs. spinal accessory nerve injury?
4. What are common causes of long thoracic nerve injury?

Answers:
1. C5, C6, C7 roots.
2. Serratus anterior.
3. Long thoracic nerve injury causes serratus anterior weakness, resulting in winging that brings the scapula more medial, and winging is decreased by abduction. Spinal accessory nerve injury causes trapezius weakness, resulting in winging that brings the scapula away from the midline, and is increased by abduction.
4. Fall, MVA, sports injury, shoulder bags.

Suprascapular nerve injury

1. What nerve roots does the suprascapular nerve arise from?
2. What muscles does the suprascapular nerve innervate?
3. How is the suprascapular nerve injured?
4. What is the presentation of suprascapular nerve injury?

Answers:
1. C5 and C6, continuing to contribute to the upper trunk.
2. Supraspinatus, followed by the infraspinatus.
3. Forced scapular protraction, penetrating wounds, crutches, traction, rotator cuff injury, Erb's palsy, supraglenoid ganglions, hematoma, entrapment.
4. Weakness in shoulder abduction and external rotation. If there is an injury at the spinoglenoid notch, only the infraspinatus may be affected.

Axillary nerve

1. What nerve roots does the axillary nerve originate from?
2. What is the path of the axillary nerve?
3. What muscles does the axillary nerve innervate? What sensory branch does it give off?
4. How is the axillary nerve usually injured and what is the presentation?

Answers:
1. C5 and C6, contributing to the upper trunk and posterior cord.
2. It passes inferior to the glenohumeral jt, to the posterior aspect of the humerus.
3. Teres minor and deltoid. It gives off the upper lateral cutaneous nerve.
4. It is injured by shoulder dislocation, humeral head fracture, or improper crutch use. Patient complains of weakness of shoulder flexion, abduction, and external rotation. There may also be lateral shoulder sensation abnormality.

Musculocutaneous nerve

1. What nerve roots contribute to the musculocutaneous (msc) nerve?
2. What muscles are innervated by the msc nerve? What sensory nerves are given off by the the msc nerve?
3. How is the msc nerve usually injured?
4. What is the presentation of msc nerve injury?
5. What are the EMG/NCS findings?

Answers:
1. C5, C6, C7, which become the upper trunk, then lateral cord.
2. Coracobrachialis, biceps brachii, brachialis. The lateral antebrachial cutaneous nerve innervates the lateral forearm.
3. Distal injury is more common than proximal. It can be injured by entrapment prox from the coracobrachialis, or by gunshot wounds, shoulder dislocation, or phlebotomy.
4. Elbow flexion weakness and abnormal sensation over lateral forearm. Coracobrachialis usually spared.
5. SNAP abnormal in lateral antecubital cutaneous nerve. CMAP abnormal to biceps. EMG abnormal in biceps and brachialis.

Radial nerve injury

1. How is the radial nerve usually injured in the axilla and how does this present?
2. How is the radial nerve usually injured in the spiral groove and how does this present?
3. What is the differential diagnosis of wrist drop?
4. How is the posterior interosseous nerve (PIN) usually injured and what is the presentation?
5. What is a Monteggia fracture?
6. How does superficial radial neuropathy present?

Answers:
1. The radial nerve can be compressed at the axilla by improper crutch use and involves all radial innervated muscles with decreased sensation over the posterior arm and forearm. SNAP and CMAP may or may not be abnormal.
2. Injury at the spiral groove (Saturday night palsy, Honeymooner's palsy) can be due to an injection or by compression (a chair or a person's head). There is weakness of all radial-innervated muscles except triceps brachii and anconeus. There is weakness of elbow flexion, wrist drop, and finger extension weakness. SNAP and CMAP may or may not be abnormal.
3. Diffuse polyneuropathy (lead), PIN, radial nerve, posterior cord, upper trunk, middle trunk, C6/C7 radiculopathy, SCI, TBI, CVA.
4. The PIN can be injured by compression at the Arcade of Frohse of the supinator, by a lipoma, ganglion cyst, synovitis from RA, or by a Monteggia fracture. PIN injury involves all radial nerve distal extensors (EDC, EIP, ECU, EPB, EPL, APL) with a pseudo claw hand and radial deviation with wrist extension. There are no sensory symptoms. SNAP is normal and CMAP is abnormal to all radial hand muscles.
5. A Monteggia fracture is a fx of the proximal 1/3 of the ulna and dislocation of the radial head, sometimes resulting in PIN injury. It occurs secondary to a fall on an outstretched hand with the forearm locked in pronation.
6. Superficial radial neuropathy (Cheiralgia Paresthetica, Wristwatch Syndrome) can occur from injury by compression from a tight wristwatch or handcuffs. Symptoms include numbness, burning or tingling on the dorsal radial aspect of the hand. SNAP is abnormal and CMAP is normal.

Radial nerve anatomy

1. What 2 muscles does the radial nerve innervate proximal to the spiral groove? What sensory nerves does it give off?
2. What 3 forearm muscles does the radial nerve innervate distal to the spiral groove?
3. Where does the radial nerve split into the superficial radial nerve (sensory) and the posterior interosseous nerve (motor)?
4. What 8 muscles are innervated by the posterior interosseous nerve?

Answers:
1. Triceps and anconeus. It gives off the posterior cutaneous nerve and the lower lateral cutaneous nerve.
2. Brachioradialis, ECRL, ECRB.
3. At the lateral epicondyle.
4. Supinator, EDC, EDM, ECU, APL, EPL, EPB, EIP.

Ulnar nerve injury in the wrist

1. What are the borders of Guyon's canal?
2. What are common causes of injury to the ulnar nerve in Guyon's canal?
3. What are the symptoms of ulnar injury at the wrist?
4. What are the NCS/EMG findings?

Answers:
1. Guyon's canal is formed by the pisiform and the hook of the hamate bones, covered by the pisohamate ligament. The ulnar nerve splits into its superficial and deep branches as it enters the canal.
2. Cycling activity, wrist ganglions, rheumatoid arthritis.
3. Weakness in all ulnar innervated hand muscles (dorsal interossei, palmar interossei, lumbricals, adductor pollicis, FPB, hypothenar muscles, opponens digiti minimi, ADM, FDM), wasting of FDI, severe claw hand.
4. SNAP: normal for DUC, abnormal to 5th digit. CMAP abnormal. EMG abnormal in all ulnar-innervated hand muscles.

Ulnar nerve injury in the upper arm

1. What is the Arcade of Struthers (AOS) and what symptoms result from injury of the ulnar nerve at this site?
2. What is Froment's sign?
3. What is Wartenberg's sign?
4. What is tardy ulnar palsy?
5. Where is the cubital tunnel and what is cubital tunnel syndrome?
6. What does the NCS show in cubital tunnel syndrome?

Answers:
1. The AOS is a fascial band that connects the brachialis to the triceps. The patient has involvement of all ulnar nerve innervated muscles, resulting in wrist flexion with radial deviation, abnormal sensation in an ulnar distribution, ulnar "claw hand" (partial finger flexion of 4th and 5th PIP and DIP due to unopposed EDC). SNAP shows abnormal dorsal ulnar cutaneous nerve and ulnar nerve findings, CMAP is also abnormal.
2. Froment's sign is the inability to hold a piece of paper by thumb and index finger using thumb adduction, instead substituting in the FPL, resulting in flexion of interphalangeal jt.
3. Wartenberg's sign is the inability to adduct to the 5th digit.
4. This is an ulnar neuropathy traditionally occurring long after a distal humerus fracture, injured secondary to bone overgrowth, scar formation, or strain from valgus deformity. Symptoms are dependent on the site of the injury.
5. The cubital tunnel is the most common site of elbow entrapment and it is located between the medial epicondyle and the olecranon with an overlying aponeurotic band. Cubital tunnel syndrome involves all ulnar nerve innervated muscles with the possible exception of the FCU.
6. SNAP shows abnormal dorsal ulnar cutaneous nerve and ulnar nerve findings. CMAP shows at least a 10m/s drop of CV across the elbow.

Ulnar nerve anatomy

1. What nerve roots, trunk, and cord does the ulnar nerve come from?
2. What is the ulnar nerve's anatomical relationship to the triceps?
3. Between what two structures does the ulnar nerve pass in the elbow?
4. What forearm muscles does the ulnar nerve innervate?
5. After the ulnar nerve passes through Guyon's canal in the hand, what are the three branches it gives off and what do they innervate?

Answers:
1. Nerve roots C8-T1, the lower trunk, and the medial cord.
2. The ulnar nerve runs along the medial surface of the medial head of the triceps, with a deep groove of thick fascia called the Arcade of Struthers.
3. Between the medial epicondyle and the olecranon in the retrocondylar groove.
4. It innervates the flexor carpi ulnaris and the flexor digitorum profundus (4th, 5th digits). It also gives off branches as the palmar ulnar cutaneous nerve, the dorsal ulnar cutaneous nerve, and the dorsal digital nerves.
5. The three branches are the Superficial sensory branch (sensory innervation); the hypothenar branch (opponens digiti quinti, abductor digiti quinti, flexor digiti quinti); the deep motor branch (palmaris brevis, dorsal interossei, palmar interossei, lumbricals, adductor pollicis, flexor pollicis brevis (deep head)).

Anomalous Innervations

1. What is a Martin-Gruber anastomosis?
2. What muscles do these ulnar fibers innervate?
3. What are the findings on NCS seen with Martin-Gruber and CTS?
4. What is a Riche-Cannieu anastomosis?
5. What are the findings on NCS with Riche-Cannieu anastomosis?

Answers:
1. It is a median to ulnar nerve anastomosis. The ulnar nerve fibers travel with the AIN branch of the median nerve and crosses over in the forearm. It is present in 15-20% of the population.
2. They innervate the ADP, ADM, and most commonly the FDI.
3. NCS shows an initial positive deflection on median CMAP at the elbow, an increased increased amplitude of median CMAP at elbow compared to wrist (can occur w/wo CTS), and CV across the forearm appears artificially fast.
4. This is a connection of the deep branch of the ulnar nerve and the recurrent branch of the median nerve in the hand, resulting in an all-ulnar hand.
5. CMAP to APB muscle is absent with median nerve stimulation but present with ulnar nerve stimulation.

carpal tunnel syndrome

1. What 10 structures go through the carpal tunnel?
2. What are causes of CTS?
3. What is double crush syndrome?
4. What are 5 provocative tests for CTS?
5. What are conservative treatments for CTS?
6. What are indications for surgery?

Answer:
1. Flexor digitorum superficialis tendons (4), flexor digitorum profundus tendons (4), flexor pollicis longus tendon, and median nerve.
2. Idiopathic, thyroid disease, CHF, renal failure, mass, pregnancy (6 mo), fracture, arthritis, rheumatoid tenosynovitis, diabetes, or double crush syndrome (cervical radiculopathy or TOS).
3. This is when a proximal lesion (e.g. radiculopathy) causes an injury to an already vulnerable distal nerve (e.g. median nerve).
4. Tinel's test is percussion of median nerve at wrist. Phalen's test holds the wrist in 90 flexion for one minute. Tourniquet test reproduces symptoms with one minute of BP cuff inflation. Carpal compression test involves holding the thumb over the tunnel for 30 seconds. Reverse Phalen's test holds the wrist in extension for one minute.
5. Conservative treatment can be used if there's no weakness or atrophy or denervation on EMG. It includes hands splints 0-30 neutral to extension, NSAIDs, steroid injection, diuretics, Vit B6, ergonomic modifications, treatment of underlying disorders. Poor outcome more likely to occur with symptoms >10mo, constant paresthesias, positive Phalen's test in <10sec, weakness, atrophy, marked prolonged latency on NCS, spont activity on EMG.
6. Surgical indications include atrophy, severe pain, conservative treatment failure.

Proximal Median Mononeuropathy

1. What is the Ligament of Struthers and how does the median nerve become entrapped in this region? What is the presentation?
2. What is the bicipital aponeurosis and how does the median nerve become entrapped in this region? What is the presentation?
3. What is pronator teres syndrome and how does it present?
4. What is anterior interosseous syndrome?


Answers:
1. The ligament of Struthers is a ligament that connects the medial epicondyle to a bone spur 3-6cm proximal to the medial epicondyle in 1% of the population. The brachial artery and median nerve pass under this ligament and may become entrapped. There is weakness of all median innervated nerves (pronation, wrist flexion, finger flexion) and there may be decreased brachial pulse. SNAP and CMAP are abnormal.
2. The bicipital aponeurosis is a thickening of the antebrachial fascia attaching the biceps to the ulna, overlying the median nerve in the proximal forearm. It can be injured by entrapment or hematoma (from blood draw). It presents similarly to entrapment in the ligament of Struthers.
3. PT syndrome is when the median nerve becomes entrapped during its course between the two heads of the PT or by the bridging fascial band of the FDS. It presents with dull ache in proximal forearm exaggerated by pronation or finger flexion. The PT is usually spared. SNAP and CMAP are abnormal.
4. AIS is a motor syndrome, although the AI also provides sensation to the wrist joint. The FPL is usually affected first. It is injured by fractures of the forearm, lacerations, or compression. Patient may have positive OK sign (difficult to make OK sign due to FPL, FDP weakness). SNAP is normal, CMAP may be abnormal to pronator quadratus.

median nerve innervations

1. What muscles in the arm are innervated by the median nerve?
2. Which of these muscles are innervated by the anterior interosseous nerve?
3. What branches of the median nerve provide sensation to the hand?
4. What muscles are innervated by the median nerve after it passes through the carpal tunnel?

Answers:
1. Pronator teres, flexor carpi radialis, palmaris, flexor digitorum superficialis, flexor digitorum profundus, abductor pollicis brevis, flexor pollicis longus, pronator quadratus, opponens pollicis, superficial head of flexor pollicis brevis, 1st and 2nd lumbricals.
2. FPL, FDP, PQ.
3. The thenar cutaneous nerve, which branches before the carpal tunnel, provides sensation to the thenar eminence. The palmar cutaneous nerve provides sensation to the radial portion of the hand and first three fingers, and half of the 4th finger.
4. LOAF: Lumbricals, Opponens pollicis, APB, and FPB.

Plexopathies

1. What is neuralgic amyotrophy (= Parsonage-Turner = brachial neuritis)?
2. How do you distinguish neoplastic from radiation plexopathy?
3. How does a root avulsion present, and what is the most common site?
4. What nerve roots make up the lumbar and sacral plexus?
5. What are common causes of lumbosacral plexus injury?

Answers:
1. Involves various nerves of brachial plexus, of unknown etiology, presenting with acute onset of intense pain and weakness at shoulder girdle, exacerbated by abduction and rotation. EMG may show abnormal spontaneous activity in the distribution of a mononeuropathy or a plexopathy.
2. Neoplastic plexopathy usually occurs in the lower trunk, is painful, and presents with Horner's syndrome. Radiation plexopathy can occur months or years post-radiation, occurs in the upper trunk, is painless, and presents with myokymia.
3. Root avulsion can occur with a severe plexus injury, most commonly occurring in C8 and T1 because they have the least connective tissue protection. It presents as absent sensation or muscle contraction from the muscles innervated by the involved roots. SNAPs are normal, but CMAPs are absent. EMG shows absent recruitment and abnormal spont activity in a myotonic distribution, including the paraspinals.
4. Lumbar plexus: L1-L4. Sacral plexus: L4-S4.
5. Neoplastic plexopathy, radiation plexopathy, neuralgic amyotrophy, retroperitoneal bleed, hip dislocation, obstetric injuries.

Brachial plexus injuries

1. What is Erb's palsy, how does it present, what are common causes of it, and how is the NCS done?
2. What is Klumpke's palsy and how does it present?
3. What is vascular thoracic outlet syndrome (TOS) and how does it present?
4. What is neurogenic TOS?
5. What is Adson's test?

Answers:
1. Erb's palsy involves the upper trunk (C5-6) nerve roots, resulting in a "waiter's tip" position in which the arm is adducted (deltoid, supraspinatus), internally rotated (teres minor, infraspinatus), extended (biceps, brachioradialis), pronated (supinator, brachioradialis), with wrist flexed (ECR). It commonly results from obstetrical injury or a sports related Stinger. NCS involves stimulating at the tip of the C6 transverse process over the trunks of the brachial plexus to assess Erb's point.
2. Klumpke's palsy involves the lower trunk (C8-T1) and can also occur from an obstetrical traction injury. The patient may have wasting of small hand muscles and a "claw hand deformity". It is commonly associated with a nerve root avulsion, which is indicated by the preservation of the SNAP.
3. Vascular TOS involves an injury to the subclavian artery or vein, or the axillary vein. Presentation inovles limb ischemia, necrosis, vague pain, fatigue with decreased color and temperature.
4. Neurogenic TOS is a rare condiction that occurs from compression of the lower trunk of the brachial plexus between a cervical rib, fibrous band, or muscular entrapment. Presentation is with pain and numbness along the medial forearm and hand that increases with overhead activity. Median CMAP and ulnar SNAP/CMAP may be abnormal and there may be spontaneous activity in median and ulnar hand muscles. Rehab involves ROM and strengthening of traps/rhom, postural mechanics.
5. Adson's test for TOS: abduct, extend, and ext rotate patient's arm. If decrease or loss of pulse (due to subclavian compression) is noted when patient turns head toward arm, this is positive for TOS.

Plexopathy

1. What are the EMG findings in plexopathy?
2. How are the cords of the brachial plexus named?

Answers:
1. SNAP and CMAP depend on the site of the plexus injury. Late responses are possibly useful. EMG will have normal findings at the paraspinals, abnormal at the peripheral muscles.
2. Based on their relationship to the axillary artery.

Recruitment

1. What is the rule of 5's for recruitment?
2. What is the difference between the recruitment frequency (RF) and the recruitment interval (RI)?
3. What is the RF and RI in a neuropathic process?
4. What is the RF and RI in a myopathic process?
5. What is the recruitment ratio (RR)?

Answers:
1. The first MUAP starts firing at a frequency of 5Hz. The second MUAP comes in at 10Hz and should be firing at 5Hz. A third MUAP comes in when the first is firing at 15Hz and the second at 10Hz. A fourth MUAP comes in when the first is firing at 20Hz.
2. The RF is the frequency of the first MUAP when a second begins to fire. Normal is <20Hz. The RI is the interval (measured in ms) between two discharges of the same MUAP when a second begins to fire. Normal is 100ms.
3. A neuropathic process has an increased RF and decreased RI.
4. A myopathic process has a decreased RF and an increased RI.
5. RR is calculated as the FR of the first MUAP divided by the number of MUAPs on the screen. Normal RR is <10.

Abnormal MUAPs

1. What causes long duration, large amplitude polyphasic potentials?
2. What causes short duration, small amplitude polyphasic potentials?
3. How do neuropathic potentials differ from myopathic potentials?
4. What causes unstable potentials?
5. What are satellite potentials?
6. What are multiplet potentials and what causes them?

Answers:
1. Collateral sprouting that occurs with reinnervation, resulting in increased number of muscle fibers per motor unit. This is most commonly seen in neuropathic disease.
2. Dropout or dysfunction of muscle fibers. This is most commonly seen in myopathic diseases or NMJ disorders, but may also be seen in severe neuropathic injury leading to nascent motor units.
3. Neuropathic potentials are long duration, large amplitude MUAPs. Myopathic potentials are short duration, small amplitude MUAPs.
4. Unstable potentials have variations in MUAP amplitude and duration, and is most commonly seen in NMJ disorders, neuropathic disorders, or muscle trauma.
5. Satellite potentials are small potentials originating from a few muscle fibers that occur approximately 10-15ms after a MUAP. They are caused by incomplete myelin formation and immature terminal sprouts from chronic reinnervation or myopathy.
6. Multiplet potentials are 2 or more MUAPs firing together, seen in ischemia, hyperventilation, tetany, MND, or metabolic disease.

More spontaneous activity and normal MUAPs

1. What are neuromyotonic discharges?
2. What are cramp discharges?
3. What are artifact potentials? What is the difference between noise and interference?
4. How is the MUAP amplitude measured and what might cause it to be abnormal?
5. What is the rise time and what does it represent?
6. What is the duration and what does it represent?
7. What is the difference between turns and phases?

Answers:
1. Neuromyotonic discharges arise from the motor axons and are clinically seen in Isaac's syndrome, but also in anterior horn cell disease, tetany, and anticholinesterase poisoning. There is continuous muscle fiber activity resulting in muscle rippling and stiffness with a progressive decrement in waveform amplitude due to single fiber fatigue. It sounds like a motorcycle and has a tornado-like appearance.
2. Cramp discharges are associate with involuntary repetitive firing of MUAPs in a large area of muscle, usually assoc with painfuly muscle contraction.
3. Artifact potentials are waveforms that obscure the real signal. Inference are signals from outside the system being studied. Noises is unwanted signals from within the system being studied, including the EMG instrument itself.
4. The amplitude is measured from peak to peak. It can be increased due to reinnervation or decreased due to loss of muscle fibers. Normal is 1mV with a range of 1uV to 2mV.
5. The rise time is the time it takes the MUAP to go from baseline to negative peak. It represents the proximity of the needle to the motor unit and normal is <500uV.
6. The duration represents the number of muscle fibers within the motor unit. It may be increased (>15ms) from collateral sprouting or decreased (<5ms) from loss of muscle fibers.
7. Turns (aka serrations) are changes in direction of waveform that do NOT cross the baseline, whereas phases are calculated as the number of baseline crossings +1. More than 4 phases is polyphasic and results from muscle fiber dropout, alterations in fiber CV, or collateral sprouting. With a monopolar needle, this can occur normally 30% of the time (15% in concentric needle), and more often in the elderly.

More spontaneous activity

1. What are complex repetitive discharges (CRDs)?
2. What is ephaptic transmission?
3. What are myotonic discharges?
4. What are fasciculations?
5. What are myokymic discharges?

Answers:
1. CRDs are high frequency discharges originating from a principle pacemaker that causes a group of muscle fibers to fire in near synchrony, spreading through through ephaptic transmission. There is a regular interval between each discharge and within each discharge with abrupt start and stop, resembling the sound of a motor boat.
2. Ephaptic transmission is a process of lateral transmission of activity between injured axons.
3. Myotonic discharges are single muscle fiber APs triggered by needle movement, percussion, or voluntary contraction. The rhythm waxes and wanes, sounding like a dive bomber.
4. Fasciculations are spontaneous discharges resulting in intermittent muscle fiber contraction and are pathological when assoc with fibs or PSWs. The hallmark is irregularly firing motor unit.
5. Myokymic discharges are groups of MUAPs firing repetitively, associated with a clnical myokymia, presenting as slow continuous muscle fiber contractions (rippling over the skin). It is semiregular between discharges and within discharges, sounding like marching soldiers.

Insertional and Spontaneous activity

1. What causes insertional activity and what causes it to be increased or decreased?
2. What are MEPPs and what do they look like?
3. What are EPPs and what do they look like?
4. What causes abnormal spontaneous activity?
5. What are fibrillation potentials and how do they look?
6. What are positive sharp waves and how do they look?

Answers:
1. Insertional activity is caused my disruption of cell membranes with the needle. It is increased by denervation or irritable cell membranes. It is decreased by fat, fibrosis, edema, or electrolyte abnormalities.
2. MEPPs, aka endplate noise, is due to spontaneous quanta release, which occurs every 5 seconds. MEPPs are 10-50uV negative potentials seen as an irregular baseline and sound like a seashell murmur. They are seen at the neuromuscular junction, indicating the muscle has maintained its innervation.
3. An EPP is a spike due to increased ACh release, provoked by needle irritation of the muscle fiber or synchronization of MEPPs. It is irregular, has a biphasic waveform with initial negative deflection, ampliude <1mV, rate of 50-100Hz, and sounds like sputtering fat in a frying pan.
4. This is caused by a RMP that is less negative and therefore unstable, causing it to fire independently or induced by needle movement.
5. Fibs are spontaneously firing APs from denervated single muscle fibers due to uncontrolled ACh release. They are regular at a rate of 1-10Hz, with an initial positive deflection, and sound like rain on a tin roof.
6. PSWs are spontaneous APs stimulated by needle movement of an injured muscle fiber. They are regular at a rate of 1-20Hz, with an initial positive deflection, amp <1mV, and sound like a dull thud or chug.

Somatosensory evoked potentials (SSEP)

1. What is the pathway of SSEPs?
2. How is the SSEP initiated and recorded?
3. What is SSEP used for?
4. How is SSEP used during spinal surgery?
5. What are the advantages and disadvantages of SSEP?

Answers:
1. The afferent potential travels from the peripheral nerve to the plexus, root, spinal cord (post column), contralateral medial lemniscus, thalamus, to the somatosensory cortex.
2. SSEPs are initiated by repetitive submaximal stimulation of a sensory nerve, mixed nerve, or dermatome. It is recorded from the spine or scalp.
3. SSEP is used to monitor peripheral nerve injuries, CNS lesions (multiple sclerosis), or intra-operative monitoring during a spinal surgery.
4. During spinal surgery, the loss of tibial nerve potentials with preservation of the median nerve indicates an injury.
5. The advantage is that abnormal results occur immediately. Disadvantages include: only evaluates nerve fibers sensing vibration and proprioception, focal lesions can be diluted, adversely affected by sleep and high dose general anesthesia.

Blink reflex and facial nerve

1. What is the pathway taken during the blink reflex?
2. What pathology affects R1 vs. R2?
3. How is NCS of the facial nerve performed?
4. What is synkinesis?
5. How can the facial nerve CMAP be used to determine prognosis?

Answers:
1. The supraorbital branch of the trigeminal nerve is stimulated, which propagates into the pons and branches to the lateral medulla, then branches to innervate the bilateral orbicularis oculi via the facial nerve. The R1 response goes through the pons only, but the R2 response goes through the pons and lateral medulla.
2. R1 is affected by lesions of the trigeminal nerve, pons, and facial nerve. R2 is affected by consciousness level, Parkinson's disease, lateral medullary syndrome, Valium, and habituation.
3. Stimulation is distal to the stylomastoid foramen at the angle of the mandible and recorded over the nasalis muscle.
4. Synkinesis is the aberrant regeneration of axons in facial nerve injuries leading to reinnervation of inappropriate muscles.
5. Patient can be monitored over 2 weeks. Demyelinating has better outcome than axonal injury. If CMAP is <10%> poor outcome. 10-30% normal has a fair prognosis. Greater than 30% has a good prognosis and recovery is expected within 2 months.

Late responses

1. Which type of nerve fibers are activated during the H-reflex?
2. What potentiates and abolishes the H-reflex?
3. What are the normal H-reflex values?
4. What are limitations of the H-reflex?
5. What is the typical height of an F-wave?
6. What are F waves commonly used for?
7. Why are multiple stimulations needed to obtain an F wave?
8. What is an A-wave? (Axon wave)

Answers:
1. IA afferent nerve fibers activated, creating an analogue to a monosynaptic reflex. It is usually used to test for S1 radiculopathy.
2. The waveform is potentiated by agonist muscle contraction and abolished by antagonist contraction or increased stimulation.
3. Normal is 28-30 ms or a side to side difference of less than 2 ms.
4. Focal lesions are diluted so it is difficult to determine injury location, it can be normal with incomplete lesions, it does not distinguish between acute and chronic, and once it is abnormal it stays abnormal.
5. 5% of the CMAP height.
6. F waves are used in polyneuropathies and plexopathies. A side to side difference of more than 2 ms in UE and 4 ms in LE is significant.
7. Configuration and latency change with each stimulation due to the polysynaptic response in the s.c., where Renshaw cell are activated by the stimulus and inhibit firing of alpha neurons, which keeps impulses from traveling the same path each time.
8. Occurs when stimulus travels antidromically along motor nerve and becomes diverted by a neural branch formed by collateral sprouting, occuring between the CMAP and F wave response. This represents nerve damage.

SNAP and CMAP

1. Why are antidromic SNAPs preferred to orthodromic?
2. What is the consequence of the active and reference pickups being less than 4cm apart?
3. What is the normal appearance of the CMAP and what might result in an initial positive deflection?
4. How is amplitude measured in SNAP vs. CMAP?

Answers:
1. Antidromic responses are easier to record, require less stimulation, and have larger amplitudes.
2. Lower amplitude (due to similar waveforms at active and reference electrodes being dropped) and decreased peak latency.
3. CMAP should be biphasic with an initial negative deflection. An initial positive deflection could be due to placement of active electrode off the endplate region, volume conduction from other muscles or nerves, or anomalous innervations.
4. SNAP amplitude is peak to peak, CMAP is baseline to peak.

Nerve Conduction Studies

1. What is the difference between peak and onset latency?
2. How is conduction velocity (CV) affected by age and temperature?
3. What is temporal dispersion?
4. What is phase cancellation?

Answers:
1. Onset latency is recorded at the initial deflection from baseline and represents the fastest axons. Peak latency is recorded at the peak of the waveform and represents the majority of axons.
2. CV is 50% adult in newborns, 80% in one year olds, and adult speed by 3-5 years. After 60 years, CV decreases by 1.5% per decade. CV decreases 2.4m/s per 1C drop in temp below 32C for upper limbs and 30C for lower limbs.
3. Temporal dispersion occurs when the waveform spreads out with proximal stimulation due to the difference between the CVs of the fastest and slowest fibers, and results in a smaller amplitude.
4. With proximal stimulation, the APs of different axons (based on their speeds) may be out of phase with one another, resulting in cancellation of their potentials and lower amplitudes and longer durations. This happens most frequently with SNAPs because the AP has a short duration, resulting in proximal SNAP 50% of distal. CMAP does not have as much of a drop (15%) because of its longer duration.

Radiculopathy

1. Why are sensory complaints more common than motor complaints in radiculopathy?
2. What are the two most common causes of radiculopathy?
3. What are the NCS findings in radiculopathy?
4. When can abnormal spontaneous activity first be seen in the paraspinals? Why might they be normal?
5. When does abnormal spontaneous activity begin in the limbs?
6. When does reinnervation usually occur?

Answers:
1. Sensory fibers are larger and therefore more prone to injury.
2. Disc hernation, which is most common in age <50,>50.
3. SNAPs are normal. CMAP may show reduced amplitude or be normal if the injury is purely demyelinating, incomplete, or reinnervation has occurred. H-reflex is abnormal in S1 radiculopathy. F-waves are not useful as muscles have more than one root innervation.
4. Abnormal spont activity is seen in paraspinals at 1 week, but they can be normal if they become reinnervated or the posterior primary rami are spared. In 10-30% of cases, abnormal paraspinals are the only abnormal finding.
5. 2 weeks.
6. 5-6 weeks.

Seddon Classification of nerve injury

1. What is neuropraxia and how does it affect the EMG?
2. What is axonotmesis and how does it affect the EMG?
3. What is neurotmesis and how does it affect the EMG?

Answers:
1. Neuropraxia occurs when there is a nerve compression injury and the axon is intact underneath. Due to the myelin injury, there is a conduction block. NCS is normal distal to the lesion but abnormal across it. EMG may show decreased recruitment.
2. Axonotmesis results from a nerve crush injury in which there is axonal interruption, but the CT and Schwann cell are intact. The NCS is similar to in neuropraxia until Wallerian degen occurs (4-5 days). EMG is abnormal.
3. Neurotmesis is a nerve transection in which there is complete axonal interruption, CT disruption (endoneurium, perineurium, and epineurium), and conduction failure. Unlike axonotmesis, there is no recovery. EMG is abnormal.

Axonal Injury

1. What is the difference between axonal and Wallerian degeneration?
2. What are the electrodiagnostic findings in axonal injury?
3. What is collateral sprouting and how does it affect the EMG?
4. What is axonal regrowth and how does it affect the EMG?
5. What occurs if the connective tissue is not intact to guide this regrowth?

Answers:
1. Axonal degeneration begins distally and ascends proximally. Wallerian degeneration proceeds distally from the injury, starting at 4-5 days and completing in 7 days for motor nerve and 11 for sensory.
2. NCS shows normal latency with decreased CV and decreased amplitude through the entire nerve. EMG shows abnormal MUAPs with decreased recruitment and abnormal insertional and resting activity.
3. Collateral sprouting occurs when sprouts off an intact axon, with small branches and thinner myelin, come over to innervate the injured motor unit. This results in poor firing synchronicity, resulting in EMG findings of polyphasic waveforms with increased amplitudes.
4. Axonal regrowth occurs when the axon regrows down its original path to the muscle fibers at a rate of 1mm/day (1 inch/month), creating axons with decreased diameter, thinner myelin, and shorter internodal distance. EMG findings include low amplitude, long duration, and polyphasic MUs, known as nascent potentials.
5. A neuroma can form with failure to reach the end organ.

Demyelination

1. What is conduction block and how do you recognize it?
2. What are 2 common causes of demyelination?
3. What are the NCS findings of demyelination?
4. What are the EMG findings of demyelination?
5. How long does recovery take and what do subsequent NCSs show?

Answers:
1. Conduction block is the failure of an AP to get past an area of demyelination even though axons are intact. It presents as a >50% block in CMAP amplitude going from distal to proximal.
2. Compression and peripheral neuropathies.
3. NCS shows prolonged latency, decreased amplitude across the site of injury, increased temporal dispersion, and decreased conduction velocity.
4. EMG shows normal insertional activity and MUAPs with decreased recruitment. There may be myokymia.
5. Once the insult is removed, recovery takes a few weeks. The new myelin is thinner with shorter internodal distances, resulting in slower than normal CV.

Amplifiers and Filters

1. How does a differential amplifier work? What is the common mode rejection ratio (CMRR)?
2. How does a high frequency filter differ from a low frequency filter?
3. If the low frequency filter setting is elevated, what will occur?
4. If the high frequency filter is reduced, what will occur?
5. What is the difference between the sweep speed and sensitivity?

Answers:
1. The differential amplifier cancels waveforms recorded at both the active and reference pickups and amplifies the remaining potentials. The CMRR refers to selectively amplifying different signals while rejecting common ones, measured in decibels (should be >90 dB). A more efficient amplifier has a larger CMRR.
2. A high frequency filter removes faster waveforms. For sensory NCS, it is set at 2 kHz, and 10 kHz for motor NCS and EMG. A low frequency filter removes signals with lower frequencies. For sensory NCS and EMG, it is set at 20 Hz, and 2 Hz for motor NCS.
3. This results in a shortened peak latency, lower amplitude, and triphasic potentials, but does not affect distal latency.
4. This results in prolonged peak and onset latency, lower amplitude, and a longer negative spike.
5. Sweep speed is the time allocated for each x-axis division. Sensitivity (gain) is the height allocated for each y-axis division.

Stimulating Electrode

1. What is the difference between the cathode and the anode of the stimulating electrode?
2. What is an anodal block?
3. What is the difference between maximal, submaximal, and supramaximal stimulus?
4. What are the artifacts that occur with too high a stimulus?
5. How long should the stimulus duration be?

Answers:
1. The cathode generates a negative impulse and attracts positive charge. The anode generates a positive impulse and attracts negative charge.
2. An anodal block is a theoretical local block that occurs when the stimulator's cathode and anode are reversed. The nerve is hyperpolarized and an AP is inhibited.
3. The maximal stimulus is the intensity at which no further increase in evoked potential will occur with added stimulus intensity. Submaximal stimulus is below the maximal stimulus but above the threshold stimulus. Supramaximal stimulus is 20% above maximal.
4. Latency may appear decreased due to increasing surface area stimulated, and surrounding nerves and muscles may be stimulated and alter the waveform.
5. 0.1 to 0.3 milliseconds.

cauda equina vs conus medullaris

1. What is conus medullaris (CM) syndrome?
2. What is cauda equina (CE) syndrome?
3. How do CE and CM differ in the level of vertebral injury?
4. What are common causes of CE vs. CM?
5. What are the effects on the lower extremities of CE vs CM?
6. What are the sensory findings in CE vs. CM?

Answers:
1. Conus medullaris is an injury to the sacral cord and lumbar nerve roots within the spinal canal, usually resulting in an areflexic bowel and bladder and lower limbs.
2. Cauda equina syndrome is injury to the lumbosacral nerve roots within the neural canal, resulting in an areflexic b/b, lower limbs, and absent bulbocavernous reflex.
3. CM occurs with an L1-L2 injury and affects the sacral cord (S1-S5). CE occurs with a L2-sacral injury and affects to the LS nerve roots.
4. Common causes of CM include L1 fracture, tumors, gliomas, vascular injury, and spina bifida with cord tethering. Common causes of CE include L2 or below fx, fractures of pelvic ring, spondylosis.
5. In CM, there is normal motor function of the LEs and they may be areflexic. CE causes flaccid paralysis of the LEs and areflexia. CE is more asymmetric than CM.
6. CM has a saddle distribution sensory loss and no pain. CE has sensory loss in nerve root distribution and pain is present.

Electrodes

1. What is Ohm's Law?
2. Where is the active electrode placed?
3. Where is the reference electrode placed?
4. What is the disadvantage of using a needle electrode for NCS?
5. What are the advantages and disadvantages of using a monopolar needle electrode?
6. What are the advantages and disadvantages of using a standard concentric (coaxial) needle electrode?
7. What is the ground electrode and where is it placed?

Answers:
1. Intensity of current (I) = Electromotor source (E)/Resistance (R)
2. The active is placed over the endplate region of the muscle to measure CMAP or over the nerve to measure SNAP.
3. The reference is placed over the tendon for CMAP and over the nerve for SNAP.
4. The waveform's amplitude and CV can't be assessed because only a few fibers are being sampled.
5. A monopolar needle is a 22-30 gauge Teflon coated needle with an exposed tip of 0.15-0.2 mm. The advantages are that it's inexpensive, has omnidirectional recording, less painful due to reduced friction from Teflon, has a larger recording area, and records more PSWs. The disadvantages are that it requires a separate surface reference, has an unstandardized tip area, there's more interference, and the Teflon may fray.
6. A concentric needle is a 24-26 gauge needle with a bare inner wire. The advantage is that it has a standardized exposed area, a fixed location from the reference, less interference, and no separate reference. The disadvantages are that it has a beveled tip which allows only unidirectional recording, a smaller recording area, MUAPs have smaller amplitudes, and it is more painful.
7. The ground is the zero-voltage, neutral, surface reference point. It is placed between the recording electrode and the stimulating electrode.

Muscle Fibers

1. What are the contractile elements of a muscle fiber?
2. What is the difference between Type I and Type II muscle fibers in terms of recruitment, fatigue, effort required, firing frequency, movements, and oxygen capacity?
3. How do muscle fibers contract?
4. How does relaxation occur?
5. Why does rigor mortis occur?

Answers:
1. Actin and myosin
2. Type I (slow twitch) fibers are recruited early, highly resistant to fatigue, require mild effort (4-8 Hz), fire slowly, are used for fine movements, and are aerobic. Type II-A and II-B fibers are recruited late, more sensitive to fatigue, require high to intermediate effort (20-30 Hz), fire fast, are used for gross movements, and are anaerobic.
3. The stimulus penetrates the T-tubule system and causes Ca to be released from the sarcoplasmic reticulum (SR). This binds to the troponin-tropomyosin complex and exposes actin's active sites, which bind with myosin heads. The actin and myosin filaments slide over each other to shorten the muscle.
4. For relaxation, Ca is actively pumped back into the SR powered by ATP so that tropomyosin can block actin's active sites.
5. After death, there is an absence of ATP so the Ca ions cannot be pumped back into the SR, so actin and myosin remain permanently joined.