emg notes

vincristine neuropathy nuggets and pearls

2010-12-05T09:46:00.001-08:00

Verstappen CCP,Heimans Koeppen S, et al. JJ, Dose-related vincristine-induced peripheral neuropathy with unexpected off-therapy worseningNeurology March 22, 2005 vol. 64 no. 6 1076-1077

Article described microtubule related neuropathy due to vincristine in 114 patients.

1. High dose group experienced more signs and symptoms than low dose group.

2. Off therapy worsening signs and symptoms occurred in about 30 percent, mostly in the first month off. Most patients improved off therapy however.

3. Paresthesias and numbness in both groups developed earlier in hands than feel and were more prominent in hands

4. Paresthesias, numbness and pain occurred at more than 50 percent in both groups

5. Resulting physical limitations include trouble buttoning clothes, climbing stairs, writing and walking

6. The dose intensity of VCR has changed considerably over the years. Studies 30 years ago describe dose intensities of 2 to 4 mg/week, frequently leading to a severe mixed sensorimotor peripheral neuropathy.Today, VCR is usually administered in a dose of ≤2 mg once every 1 to 4 weeks.

7. Off therapy deterioration is also well described in cisplatin and paclitaxol related neuropathy.

EMG is the practice of medicine Position statement of the American Academy of Neurology

2010-08-07T10:57:00.001-07:00

What is the issue?

Needle EMG is a diagnostic neuromuscular exam that is used to identify potentially serious neuromuscular diseases ranging from carpal tunnel syndrome to Lou Gehrig's Disease. Despite the inherently diagnostic nature of these exams, non-physicians have been aggressively seeking the authority to perform these tests. Patients should know that only physicians should perform an intrusive, complex and intrinsically diagnostic test.

Why is it important?

To be properly performed, needle EMG requires physician training, including an in-depth knowledge of neuromuscular diseases. Also, EMG tests are dynamic and depend upon the observations of the examiner. A physician must be present to see what is happening and decide on the next step in the test, as there is no way to know after the fact whether the test was performed correctly. Misdiagnosis can mean delayed or inappropriate treatment (including surgery) and diminished quality of life.

What is the Academy's position?

The AAN Professional Association (Academy) opposes efforts by non-physicians to permit the performance of needle EMG by non-physicians.

What can you do to help?

The Academy has developed an advocacy toolkit (to the right) to help you advocate on this important issue.

North Carolina

Legislation in North Carolina that revises the North Carolina Physical Therapy Act includes language that states physical therapy can include "the performance of electrodiagnostic, electrophysiologic, and other specialized tests of neuromuscular function or physical capacities."

Anti sulfatide neuropathies

2010-04-01T19:10:00.000-07:00

clinical presentation is that of chronic axonal distal sensory neuropathy,symmetric, slowly progressive, with pain in half and much less having any weakness. The frequency in idiopathic PN is only 0.7 %, but may be as high as 25 % in certain subgroups. High titers are relatively specific for distal sensory neuropathy, whereas low titers can be seen in other conditons, including ITP, HIV, and autoimmune hepatitis. Monoclonal gammopathies occur in half.

GALOP (gait disorder, antibody, late age onset neuropathy) is a subgroup of antisulfatide neuropathy have monoclonal IgM and antibodies to sulfatide and GALOP.

anti GM1 antibodies pearls

2010-04-01T19:03:00.000-07:00

1. MMN with conduction block presents as asymmetric, painless, slowly progressive weakness especially in distal upper limbs.
2. Sensory sparing resembles ALS, however, UMN signs are not seen in MMN
3. Conduction block outside of normal compression sites differentiates MMN and ALS. Patients without conducton block occassionally respond to immunotherapy (Neurology 1997 first author JS Katz).
4. High titer IgM anti GM1 are seen in 50-60 percent of patients with MMN, but sensitivity is increased to 80-90 percent by complexing GM1 to secondary antigens co GM1 antibody test (Pestronk, Neurology 1997)
5. In GBS, anti GM1 antibodies closely correlate with Campylobacter jejuni infection and sometimes correlate with worse neuropathy and outcome
6. Other antigens coexpressed sometimes in GBS are GD1a, GD1b and GM2; some have argued GM2 correlates with CMV neuropathy but this is not univerally accepted. GD1a is often seen in AMAN, the Chinese GBS variant (60 %) v. only 4 % of traditional GBS patients

Antibody related neuropathies anti MAG pearls

2010-04-01T18:48:00.000-07:00

1. typical presentation is distal symmetric slowly progressive sensorimotor neuropathy
2. Half of patients with PN and IgM gammopathy have an autoantibody to MAG, typically kappa chain
3. Antibody may cross react with SGPG
4. Prolonged distal motor latencies are the most reliable finding, seen in 90 %
5. Patients with a positive anti MAG confirmed by Western blot sugggests immune related PN
6. If patients fulfil criteria for CIDP they should be so treated
7. Patients with significant deficit should have immune therapy attempted even though it is likely to disappoint.
8. Relationship to myeloma exists
9. MGUS beyond hematology read here http://neurologyminutiae.blogspot.com/2009/10/mgus-significant-beyond-hematology.html ; malignant transformation here http://neurologyminutiae.blogspot.com/2007/04/malignant-transformation-of-monoclonal.html ; http://neurologyminutiae.blogspot.com/2007/04/malignant-transformation-in-mgus.html ; miscellany on MGUS prevalence here http://neurologyminutiae.blogspot.com/2006/08/miscellany-on-neuropathy-tests.html

Isolated tibial paralysis

2010-01-24T13:09:00.000-08:00

Usually due to lesions below the popliteal space such as gunshot, knife wound, auto accident, or leg fractures. Affects plantar flexion, ankle inversion, foot adduction. Dorsiflexion may be affected due to contractures of the anterior tibialis. Sensation is lost over the heel, lateral border, ungual surfaces, Edema is usual with causalgia, trophic changes, and trophic ulcers. Partial lesions may spare the calf muscles and affect only the muscles of the foot, usually with prominent pain.

Obturator neurpathy

2010-01-24T12:51:00.000-08:00

Clinical presentation is weakness of externally rotating, or adducting the thigh, or crossing the legs. Sensory involvement is minor. Small areas of skin over the hip joint and the interior middle of thigh may have sensory loss.

Anatomically, the posterior branch innervates the obturator externa and adductor magnus. The anterior branch innervates the adductor longus and brevis and gracilis. Both come from L2-4 lumbar plexus and are affected by same processes as femoral neuropathy, such as gravid uterus.

Howship-Romberg syndrome (historical) refers to pressure on obturator nerve by a rare obturator hernia. It consists of pain that radiates down the thigh and is most marked at the knee.

Mononeuropathies

2010-01-24T12:23:00.000-08:00

this post in intended to spur further of my own research. Reading some of my dad's old 1950's vintage neurology books, mononeuropathies are due to lead poisoning, after typhus, influenza, or malaria. Will need to look up more about postinfectious neuropathies.

Dystrophinopathy clinical diagnostic pearls in adults

2010-01-03T18:05:00.000-08:00

1. BMD (Becker's) may present in adulthood up to age 50+. Like DMD, earliest muscles involved are glutei, thigh abductors, and triceps, followed by quadriceps, deltoids, tibialis anterior, and last, biceps. Neck FLEXOR weakness is common.

2. The use of prednisone, annual cardiac and pulmonary (including sleep testing) evaluations have made children with DMD survive into the third decade.

3. Muscle cramps with aches during exercise are presentations of BMD during and after teenagehood. Isolated quadriceps involvement in the fifth decade may prompt a confusion with inclusion body myositis.

4. Isolated cardiac failure or even transplantation may occur prior to a diagnosis being made. Decreased LVEF or arrythmias are more common in BMD. X linked dilated cardiomyopathy is a rare form restricted to cardiac muscle with completely normal skeletal muscle, due to mutations that only affect the isoforms of cardiac muscle. Endocardial biopsy is required, and there is 50 % five year mortality without transplantation.

5. Other asymptomatic/minimally symptomatic clinical findings include exertional intolerance, elevated CPK, myalgias, myoglobinuria, none of which are mandatory. Other subtleties include calf and tongue hypertrophy, myopathic EMG, history of clumsiness or toe walking as a child, and positive family history.

6. Ten percent of female carriers will be symptomatic, many minimally so, and manifest cases will be more likely to have diagnostic mutation on X chromosome. Some may have negative result, and need to be counselled regarding regarding a mutation only expressed in oocytes (germline mutation). For these patients prenatal testing is available (amniocentesis, eg. and others).

7. Coexisting Turners syndrome (XO) or skewed or nonrandom mutation of an X chromosome can cause full blown disease in a female carrier (DMD phenotype).

8. Cognitive disorders are common see http://behavioralneurologynotes.blogspot.com/2010/01/cognition-and-dystrophinopathy.html

9. Annual PSG (polysomnograms) are needed once patients are nonambulatory. Problems with dream sleep are common.

10. GI issues include GI pseudoobstruction in patients on continuous ventilation. This can be relieved by a regular bowel routine, continual low suction, placement of a second jejunal feeding tube. Late, swallowing issues might include positioning for swallowing, and restricted jaw movement due to masseter involvement.

DM neuropathy v CIDP

2009-09-23T14:32:00.001-07:00

Use rules

1. With proximal weakness and distal weakness, in absence of genetic disorder, CIDP is overwhelmingly more likely; diabetic is usually not proximal\

2. Diabetic is sensory, CIDP is motor more

3. Diabetic is insidious, CIDP is aggressive

4. Distal/proximal gradient reflex loss is more common in DM

5. Objective response to immunomodulation is much more common in CIDP

(Obvious but still useful)

HNPP pearls

2009-09-23T14:13:00.001-07:00

EMG

1. Median >>> ulnar, 2. Peroneal is involved

3. Tibial nerve is almost never involved

4. Pathology is tomaculi

5. ulnar slowing across elbow is 100 %

6. peroneal slowing across knee is 85 %

7. SNAP's are abnormal-- amplitudes always reduced, latencies may be prolonged-- have not only pressure palsies but also an age related neuropathy

Clinical

Unlike CIDP, in which patients are usually symptomatic, HNPP patients often are asymptomatic with EMG changes

Remote weakenss after botox therapy

2009-05-19T06:09:00.000-07:00

Richardson and Beckerly (Muscle and Nerve, 2008) described a patient who received repeated botox A for spasticity post stroke who developed contralateral shoulder weakness with decrement seen on repetitive nerve stimulation, suggestive of neuromuscular blockade.

Spurling's maneuver, in cervical radiculopathy

2009-05-19T05:07:00.001-07:00

SM produces Spurling's sign. Method-- rotate head and flex neck towards affected limb then axially compress the head. Production of radicular pain or numbness is called SS, suggests active radiculopathy. Author Wieting et al. modified procedure by extending neck, rotating, then flexing and axially compressing towards affected side in 363 patients. EMG was done immediately after. Modified SM was more sensitive for radiculopathy then traditional SM. Prediction of radiculopathy increased from 17 to 55 % . (Muscle and Nerve 2008).

Alternative to tongue EMG in ALS

2009-05-19T05:03:00.000-07:00

Sonoo et al. studied 100 ALS patients. Tongue EMG is sensitive when patients can relax for examination, but only about half or less can. Fibs , positive waves and fasciuclations were seen in 62 % of trapezii, 17 % of sternocleidomastoid muscles, and 8 % of tongue, whereas the number was zero abnormal muscles in cervical spondyslosis patients.

Nerve conductions in POEMS synrdome

2009-05-19T04:58:00.001-07:00

Presentation is symmetric peripheral neuropathy resembling CIDP, with areflexia and mixed demyelinating.axonal features. The systemic features include organomegaly, endocrinopathy, monoclonal serum protein ( M protein), and dermatologic abnormalities In a study of 138 patients with POEMS seen over 47 years, Mauermann et al found slowed motor and sensory velocity, prolonged distal latiencues and F waves. However, unlike CIDP there was rarely temporal dispersion or conduction block.

Glycogenosis type II in adults

2009-02-21T18:50:00.000-08:00

Bembi et al. Diagnosis of glycogenosis type II. Neurology 2008; 71: S2: S4-S11.
Also known as glycogen storage disease type II, Pompe d or acid maltase deficiency caused by a mutation in the gene encoding acid alpha-glucosidase (GAA) enzyme leading to accumulation of glycogen in lysosomes of several tissues including cardiac skeletal and smooth muscle cells.

In juvenile/adult type, phenotype may vary somewhat and more than 200 mutations of the GAA gene are reported. In adults, skeletal muscle involves the proximal lower limbs, and paraspinal muscles often followed by severe diaphragmatic and accessory muscle failure. Complaints may include exertional pain, cramps and aches, back pain, slow disease progression. Respiratory involvement may occur early and may be presenting symptom in 30 % of cases. Sleep apnea, exertional dyspnea and RTI's are common.

Evaluation should include CPK (high in 95%), ALT, AST, DH, +/- urinary Glc4 . NCS are normal. EMG is nonspecific shows fibs, myotonic and myopathic findings. Classic muscle biopsy may show acid phos positive cytoplasmic vacuoles but may be negative. Biochemical assays for GAA activity are often needed to confirm. Skeletal muscle or skin fibroblasts may be used. Molecular analysis of the gene may also be needed. In adults cardiac muscles is usually not affected, unlike infants and juveniles.

The differential diagnosis includes Becker, limb girdle, scapuloperoneal, rigid spine s, other glycogen related diseases (debrancher deficiency, branching enzyme def, myophosphorylase def, PFK def, Danon disease, mitochondrial disease, polymyositis.

MRI's in adults (n=11) with confirmed disease showed adductor magnus, semimembranosus, semitendinosis involved early on. Later, fatty infltration occurs in long head of biceps femoris, 3 heads of vastus, with SPARING OF SHORT HEAD OF BICEPS, SARTORIUS, RECTUS, GRACILIS AND PERIPHERAL PART OF VASTUS LATERALIS. CALF MUSCLES ARE NORMAL.

PEARL 2 DISTINGUISHING FEATURES FROM OTHER MYOPATHIES IS SPARING OF SHORT HEAD OF BICEPS AND TENSOR FASCIA LATA WITH ATROPHY OF OTHER PELVIC MUSCLES.

Respiratory management: Cough peak expiratory flow (CPEF) is single best test to determine if patient can clear secretions with a threshold value of 160 L/min being adequate. A high negative maximal inspiratory pressure (>80 cm H2O) or high positive maxinal expiratory pressure (>90 cm H2O) excludes relavant inspiratory or expiratory weakness. Sniff expiratory pressure should also be checked.

Sleep disordered breathing refers to central, obstructive or mixed apnea, hypoventilation or both during sleep. SDB occurs in two thirds. Hypoventilation during REM sleep is due to decreased tidal volume especially during REM sleep. OSA may be life threatening. Orthopnea and dyspnea may be late findings. Late tachypnea at rest occurs. On exam look for failure of outward distension of abdomen during breathing (inspiration) accessory recruitment and mucus encumbrance of upper and lower airways.

No outpatient surgery should be done, and anesthesia consulted.

Genetics usually is AR. Risk of being a carrier for a sib of an affected patient is 2/3, and risk of being a carrier for sibs of a parent of an affected patient is 1/2. Risk of an affected child for a sib of an affected patient is > 1/600 and for sibs of a parent, > 1/800.

A clinical trial with a Genzyme drug, alglucosidase alfa resulted in improved walking distance and stabilized pulmonary function over an 18 month period (van der Ploeg et al., A randomized study of alglucosidase alfa in late onset Pompe's disease NEJM 2010; 362: 1396-1406) (ClinicalTrials.gov.number, NCT00158600). Outcome measures were six minute walk and percentage of predicted FVC.

Peroneal intraneural ganglia: clinical and electrical findings

2009-02-21T17:58:00.001-08:00

Young NP, Sorenson EJ, Spinner RJ, Daube JR. Clinical and electrodiagnostic correlates of peroneal intraneural ganglia. Neurology 2009; 72: 447-452.

Common peroneal neuropathy (CMP) with (n=22) and without (n=11) IG.

Features found with CMP + IG group but not found in -IG group: greater body mass, more pain at knee (52 v . 0 %); more likely fluctuating weakness with weight bearing ( 48 v. 4 %); and palpable mass at fibular head ( 47 v. 0 %). Less presentation of weight loss, immobility or leg crossing. There were no electrophysiologic differences. Tinel's sign and weakness were present in both groups. Higher grade of fibrillations were usually found in tibialis anterior than peroneus longus reflecting cmp. MRI or ultrasound was used to diagnose the entity.

NCS Safety with defbrillators

2009-02-20T10:44:00.000-08:00

AANEM report 2006 patients underwent NCS with sensing pacemaker electrodes. The electrical impulses in 15 patients with varous types of defibrillators were never detected by the sensing amplifier of the defibrillator or pacemaker. It did not affect the settings or cause the defibrillator to charge. Monitoring and and pre/post interrogations were normal. Conclusion, NCS are safe in patients with implanted cardiac pacemakers and defibrillators with bipolar sensing configurations.

The hamstring reflex

2008-11-02T16:51:00.000-08:00

Since the knee jerk is L4 and the ankle jerk S1, the L5 root is usually omitted from exam. The biceps (of the hamstring) and semitendinosis reflexes are tested, both high sciatic reflexes. Biceps is primarily L5 and is lateral, semitendinosis is L4 and medial.

Crossed adductor measures at L2

More DTR pearls:
1. Prolonged reflex is not just with hypothyroid, but also cerebellar disease, (pendular oscillating), protein malnutrition (change in elastic quality of tendons), hyponatremia and syphilis.

CRPS I and II

2008-11-02T16:45:00.000-08:00

Five components of:
1. Pain, especially mechanical and thermal allodynia, hyperalgesia and hyperpathia
2. neurogenic edema
3. autonomic dysregulation with abnormal circulation, livedo reticularis and hyperhidrosis
4. Movement disorder with inability to initiate or maintain maovements, dystonia, weakness, spasms and tremor
5. atrophy and dystrophy.

In type I there is no identifiable nerve injury, in type 2 there is. Its regional, non nerve dependent and spreads, initially is sympathetic dependent later not.

Brachial plexitis examination pearls sensation

2008-11-02T15:55:00.000-08:00

Sensory loss
1. The lateral cord encompasses the thumb and index finger and splits the middle finger
2. The medial cord splits the third finger to the unlar side and encompasses the ring and pinky fingers and medial forearm.
3. The lower trunk innervates the fourth and fifth fingers and continues up the forearm
4. The ulnar nerve innervates only a small triangular region across the wrist, as well as the ulnar distributed area on the hand.
5. Schwartzman describes additional techniques for the exam of plexus: The Roos abduction maneuver== holding hands up to imitate a goal post elicits numbness after 30 seconds
6. The Wright maneuver-- holding hands straight up, does same
7. The plexus can be palpated at various points: in the supraclavicular fossa (upper trunk); between the clavicle and the first rib; the neurovascular bundle against the medial humerus; at the elbow in the arcade of Frohse (entry of radial sensory and posterior interosseous nerves);
8. The intercosticobrachial nerve, from the medial cord, innervates the anterior chest and can be misdiagnosed as cardiac disease. acid reflux, gall bladder disease (if on the right) or costochondritis.

Pain
1. Upper trunk pain (C5-6 roots) radiates across trapezius ridge and down medial scapula, whereas radiculopathic pain from c6-7 GOES DOWN SPINE. Upper trunk is palpable in supraclavicular fossa, and radiation to tip of scapula (notalgia) is usually painful.
2. Middle trunk persterior cord plexus radiations are on dorsal arm across triceps, enters the forearm through the arcade of Frohse (medial to the lateral epicondyle) to innervate the forearm, and extensor surface of the thumb, index and third fingers.
3.

Sensory nerve injuries after uterosacral lig suspension

2008-10-11T11:12:00.000-07:00

Flynn MK et al. AJOG 2006;195: 1869-72. The procedure is done to suspend the prolapsed vaginal apex. 7 of 182 women reviewed developed buttock/posterior thigh pain to the popliteal fossa. 3 women had removal of the suture within 2 days resulting in immediate improvement of the pain and the other 4 were treated conservatively with gradual resolution of the pain. In some of the women, pelvic exam showed exacerbation of the pain pulling on the suture. This is the posterior femoral cutaneous nerve that arises from S2-3 roots.

Ulnar neuropathy pearls

2008-09-07T08:53:00.000-07:00

Most distal muscle of ulnar nerve is adductor pollicis reached at the first free web space between the thumb and forefinger. It adducts the thumb. Unlike abductor digiti minimi itmay be involved in lesions of Guyon's canal. Like ADM its involved in other ulnar entrapments (cubital tunnel, tardy ulnar palsy, cervical rib).

Klumpke's paralysis (avulsion of C8 T1 roots) will involve these plus abductor pollicis brevis (APB median C8 T1).

The FDI may occassionally get innervation from the median nerve / musculocutaneous nerve

Thoracic Outlet Syndromes

2008-08-19T16:26:00.000-07:00

True TOS is a clear syndrome with weakness and sensory loss in the arm and hand usually caused by a fibrous band over which the lower trunk of the brachial plexus is stretched and angulated. It may coexist with a small rudimentary cervical rib.

Arterial TOS involves ischemia or even emboli in fingers and hands from a cervical rib causing stenosis and poststenotic dilatation of the subclavian artery. This type is more common in athletes.

Venous TOS is an acute or chronic syndrome with swelling of the arm due to stenosis or thrombotic occlusion of the subclavian vein.

Disputed (or nonspecific nonneurologic) TOS are chronic aching and pains or paresthesias in arms and shoulders with no findings. This is a large group, but neurologic signs are "either nonexistent or meager."

Posttraumatic TOS asociated with clavicular fracture and associated brachial plexopathy see separate article.

Clinical presentations
True TOS young to middle aged women develop paresthesias , pain and weakness on the ulnar border of the hand, rarely much pain, and no vascular symptoms. Per Thomas Swift they may have hand,arm, shoulder and neck pain. They have low set shoulders, long graceful "swan" necks and horizontal or downsloping clavicles. Muscle wasting resembles CTS with wasted APB but usually some ulnar innervated muscles waste as well. Sensory loss does not split the fourth digit. There is often weakness of the forearm flexors. The differential is median and ulnar neuropathy, lower trunk plexus lesion, radiculopathy. CT and MRI usually miss the fibrous band but may show other causes of plexus lesion. Plain films show characteristic bony abnormality most of the time. Treatment is supraclavicular exploration with division of the band.

Notes-- Adson;s test is valueless, because 11-80 % healthy controls obliterate radial pulse by holding hand above head. Other similarly useless tests are photoplethysmographic studies of blood flow in the fingers following Adson's test, the elevated arms stress test (east) with the arm abducted to 90 degrees, the elbow flexed and braced, the fist opened and closed for several minutes. Bruits are of no significance in the subclavian fossa. Arteriography and dopplers are useless. In contrast, there may be a Tinel's in the fourth and fifth fingers tapping the brachial plexus, and symptoms may be exacerbated pulling arm down to ground and relieved by pushing up (again from Swift). Patients are better when lying down (contrast to CTS) and by using armrests.

Plain films may show upper 3-4 thoracic vertebrae due to shoulders. OBLIQUE CERVICAL SPINE FILMS WILL SHOW CERVICAL RIBS IF THEY ARE PRESENT! Symptoms are usually unilateral but cervical rib may be bilateral, usually C 7 also occassionally C 6. The cervical rib has a one percent prevalence, again not all symptomatic. The fibrous band extending off the rib technically compresses the C8 and T1 roots.

The best treatment of nonspecific neurologic TOS may involve posture correction, stretching and strengthening exercises (of rhomboids, levator and trapezius, the shoulder elevators), and an orthosis designed to elevate the shoulder. Operate if a band is present it will help.

The association of TOS in musicians is debated by Stewart

Brachial plexitis causes and differential and foils

2008-08-19T15:36:00.000-07:00

Avulsions occur with traction injuries and may be overlooked in patients with multi-trauma.

Clavicle fractures can injure the plexus through bone fragments or hematomas, scar tissue (in a healed fracture) or development of a subclavian pseudoaneurysm.

Stingers and burners (See separate post http://emgnotes.blogspot.com/2007/04/traunmatic-neuropathy-stingers.html ). Compression of the upper brachial plexus may occur between the shoulder pad and upper medial scapula and may be prevented with an orthosis (Markey et al, 1993, Am J Sports Med). Lesion can also be in the ventral rami, cord, roots or cervical cord but in professional players is more likely to be spinal stenosis .

Intraoperative plexopathy of brachial plexus can be due to hyperabduction of the relaxed arm, plexitis (autoimmune) following surgery, during median sternotomy such as CABG (5-7 % of time) which can mimic an ulnar neuropathy, with variable locale and severity. It can occur with traction on the plexus during wide sternotomy, during jugular cannulation, and is tenfold higher when the internal mammary artery is used for bypass grafting. Forceful traction can also fracture the first rib that then can cause plexopathy. Upper trunk damage can occur if the patient is held head down and the arm is abducted simultaneously.

Acute compression occurs with coma, or carrying heavy backpacks causing a bilateral syndrome especially affecting serratia anterior.

Hematomas during axillary angiograms can cause blood leak at edge of pectoralis muscle and recovery IF blood is removed rapidly. False aneurysms can occur years after trauma to plexus, median or radial nerve.

Newborns do not have a falling incidence of brachial plexus injury (0.05-0.3 % births) with Erb's being most common (weak shoulder abduction and elbow flexion), Klumpke's less common.

Malignant plexopathy is most often due to cancer of lung, breast, or lymphoma, rarely early except in the Pancoast tumor syndrome. It usually presents with shoulder pain radiating down the arm (medial most often) followed by paresthesias and weakness. The differential includes radiation plexopathy, intraoperative plexus trauma, and unrelated brachial plexitis.

Pancoast syndrome due to tumor at apex of the lung causes pain down inner arm with two thirds developing Horner's syndrome, and one third, weakness and sensory changes in lower trunk distribution.

Primary tumors of brachial plexus include neurofibromas (often/usually plexiform) with pain, supraclavicular mass, and mild neurologic deficit. Schwannomas with "dumbbell" lesions and sensory symptoms withouu deficit. Intraneural perineurioma (or localized hypertrophic neuropathy) presents with slowly progressive upper limb deficits. Malignant nerve tumors are rare.

Radiation plexitis can occur within 26 years of radiation of the plexus and presents with sensory and motor signs and swelling. Horner's occurs less frequently than in malignant plexitis but it can happen. Radiation is commonly, but not universally thought to be more likely to affect the upper trunk. It may be relentlessly progressive and lead to a useless arm. Occassionally it may stop or respond to PT or OT.

Radiation can also cause malignant nerve sheath tumors with painful enlarging mass and dysfunction. Ischemic plexitis can occur due to radiation induced segmental occlusion of the subclavian artery.

Thoracic outlet syndromes are discussed in another post.

Parsonage-Turner syndrome causes pain then weakness. It may mimic a shoulder joint lesion.

Hereditary neuropathy with liability to pressure palsies (HNPP) often affects the brachial plexus.

Patients with plexitis due to diabates have a subacute onset and good recovery. Plexitis in heroin addicted patients has less severe pain, and involvement of the lower part of the plexus.

Differential C8-T1 radiculopathy

2008-07-17T01:38:00.000-07:00

C8-T1 root lesion--
C8
Finger extensors, finger flexors, wrist flexors, hand intrinsics
T1
Hand intrinsics

Pancoast-- C8-T1 plus Horner's

Lateral cord-- muscles to forearm and sensation in distribution of median nerve

Medial cord-- all median and ulnar intrinsic muscles weak

Thoracic outlet syndrome- neurogenic, vascular, combined or traumatic. Vascular, that presents with pain, pallor and coolness is uncommon. TOS affects C8,T1 and lower trunk.
Compression may occur from a cervical (C7) rib (seen in 10%), an enlarged C7 transverse process (incomplete rib), a fibrous band (most common) from C7 TP to the clavicle, or fibrotic scalene mucles. The clinical presentation is
mild aching pain of ulnar forearm/hand (66%) without neck pain. Weakness occurs in all hand muscles (ulnar and median – thenar, hypothenar, and interossei). Ulnar (not median) numbness occurs. Hand weakness/clumsiness is prominent. Atrophy (“guttering”) of the lateral thenar eminence (APB) is characteristic. Thenar, hypothenar, and interossei atrophy – Gilliat-Sumner hand. TOS is bilateral in 50%, but less affected side is usually subclinical . No reliable provocative test exists, but 90° abduction + external rotation has best predictive value. Patients may have Tinel’s sign over supraclavicular fossa. Adsons test: turn head back & to affected side & lose radial pulse (for vascular variant) but this sign has been considered mythological (ie rarely present) by some authors.
EMG/NCV: Low APB (median) amplitudes (ulnar amplitudes are normal or slightly low). Low ulnar sensory potentials with normal median sensory potentials. Some say unreliable.
Chest or (oblique) c-spine Xrays or CT to look for C7 TP, cervical rib, etc. Treatment is ???
surgical. Medical treatment, physical therapy is not indicated for true TOS (per Kline)
§ Anterior supraclavicular approach: favored. Incision usually supraclavicular, parallel to clavicle.
§ Posterior subscapular approach: used for morbidly obesity, large cervical ribs, previous anterior surgery. See N10/04.
§ Transaxillary cervical rib resection: favored by vascular surgeons, orthopedists. Per Kline has higher complication rate, less success

Parsonage Turner-- pain then weakness, 90 % recovery within 3 years, affects males predominantly (4:1).

Ulnar neuropathy (see separate entry)

Prognosis of nerve injuries

2008-07-17T01:25:00.000-07:00

Nerve injury

Most injuries recover spontaneously but there is a difference by location. 40 % of C5-6 injuries, 18 % of C5-7 injuries and 5 % of C5-T1 injuries (flail arm) recover. Injuries that are progressive , eg. hematoma, compartment syndrome, and pseudoaneurysm need immediate attention and often surgery. Progression of Tinel's sign can be used to follow recovery.

Repair of lacerations should be done acutely for sharp injuries (first three days) but after several weeks for a blunt injury to allow definition of injury. Penetrating injuries can be explored early, gunshot wounds if contiguous after 3 months, or EMG or SEP every three months.

Dermatomal map upper extemity

2008-07-17T01:23:00.000-07:00

Causes of peroneal neuropathy

2008-02-04T18:27:00.000-08:00

Argument in letters section of Neurology 2003;60:1559-1560; letter writer lists "known" causes of peroneal neuropathy at fibular head as etiologically identifiable in 83%: perioperative, 30.6%, postural 19 %, bedridden 13.9 %, weight loss 5.6 %, multiple trauma 5.6 %, chalk positioning 5.6 %, synovial cyst 2.8 %).

Cubital tunnel syndrome

2008-02-01T13:04:00.000-08:00

Clinical-- impaired sensation over the fifth and half the fourth finger
Weakness and wasting of the unlar innervated hand muscles

EMG shows sparing of FCU (proximal)
afffects the ulnar half of the flexor digitorum profundus

Digital nerve entrapment

2008-02-01T13:01:00.000-08:00

Small sensory branches of the median nerve may be compressed against the deep transverse metacarpal ligament, with pain in one or two fingers, worse with lateral hypewrextension of the digits and tenderness and dysesthesias over the palmar surfaces between the metacarpals.

Carpal tunnel associations

2008-02-01T12:53:00.001-08:00

Amyloidosis (primary or secondary)
Acromegaly, 35 %
Rheumatoid arthritis, 23 % (differentiate from disuse, c spine disease, or ulnar n at elbow)
eosinophilic fasciitis
myxedema
lupus erythematosus
hyperparathyroidism
toxic shock syndrome
Colles fracture
Fracture of the capitatum or hamate
soft tissue swelling around wrist after injury
intraneural hemorrhage
anomaly of distal radius
subluxed carpus on distal radioulnar
rubella immunization
DM
Gout
myeloma (=Leri's pleonosteosis)
cerebral palsy
TB
pregnancy
toxic shock s
toxic oil syndrome
mucopolysaccharidosis
congenital av fistula
dialysis
brachial hypertrophy
SLE
scleroderma

Signs/symptoms of CTS
Paresthesias and pain relieved with movement, worse at night
Raynaud's phenomenon
hypesthesias 1st 3 digits and half of fourth
Sensory loss confined to tip of third digit
Sensory splitting of fourth digit on exam
Sparing of thenar eminence
Phalen's and Tinel's signs
Flick sign (relief with shaking wrist) most reliable sign

Motor APB-- pushing up perpendicular to palm
Opponens pollicis -- touch thumb and fifth finger
Phalen's/ Tinel's signs

Differential diagnosis
high median compression at elbow
C 6 radiculopathy
handcuff neuropathy

Anterior interosseous syndrome (Kiloh-Nevin s.)

2008-02-01T12:47:00.000-08:00

AI s is due to injury to the branch of the median nerve just past the pronator teres muscle and can be unilateral or bilateral. There is pain in the forearm and elbow, made worse by resisted proximal ip flexion of the middle finger. Asked to make the "OK" sign, patients will make a triangle sign instead (pinch sign). Spontaneous recovery occurs over 6 weeks to 18 months. Identical syndromes can be caused by more proximal lesions, including antecubital level or the brachial plexus, due to prearrangement of the bundles of nerves proximally. Weakness also is seen in fl dig profundus 1 and 2 and PQ.

Nerve conduction may be normal or show a delay from pronator quadratus. EMG is abnormal in the flexor pollicis longus, flexor digitorum profundus I and II, and pronator quadratus.

Associations include trauma, forearm (midshaft radial) fractures, humeral fracture, injection/phlebotomy of antecubital vein, stab wounds, fibrous bands, related to exercise. Occassionally associated with brachial neuritis, CMV infection, bronchogenic carcinoma mets or spontaneous. Consider plexitis.

Other median entrapments occur at the ligament of Struthers, Lacertus fibrosis and the tendinous insertion of FDS. Humeral spur at supracondylar site can produce brachial claudication and radial artery obliteration, exacerbation of numbness and pain by resisted elbow extension and forearm supination.

Median nerve syndromes: pronator teres syndrome

2008-02-01T12:41:00.000-08:00

The median nerve pierces the two heads of the pt (pronator teres) before passing under it. Trauma, fracture, muscle hypertrophy or an anomalous band connecting the pt to the tendon arch of the flexor digitorum sublimis can injure the nerve here. Also tenosynovitis, muscle hemorrhage, tear, postop scarring, anomalous median artery, or increased forearm compartment pressure can be related.

Clinically, pain and tenderness appears over the pronator teres, is fatiguaibile, with the pain radiating occassionally to the shoulder. Weakness of the flexor pollicis and apb, and preserved pronation. Sensory changes over the thenar eminence help to make the diagnosis. EMG/NCS distal studies are normal with slowing in the wrist.

A different entrapment at the site of the ligament of Struthers affects the nerve near the lower humerus. The difference clinically is that here, pronator teres is affected unlike the pt syndrome in which pt is spared. Compression of the brachial artery with full extension of the arm obliterates the radial pulse.

Differentiate from CTS with Tinel's over site of entrapment, absent Phalen's sign, rare nocturnal exacerbation, weak mm over forearm worse with pronation, elbow flexion or contraction of the superficial flexor of second digit. Consider CTS, plexopathy, other median neuropathy syndromes, or radiculopathy.

Suprascapular neuropathy

2008-02-01T12:19:00.001-08:00

Injury from pressure on/trauma to the shoulder, stab wounds above the scapula, improper use of crutches, stretching of the nerve, eg. volleyball players during serving, r/o rupture of the rotator cuff. In athletics intense activity over weeks may cause it. Baseball pitchers are susceptible. Volleyball players, weight lifters and wrestlers are susceptible to developing it. Many athletes have exclusive or predominant involvement of the infraspinatus muscle.

Clinically one sees difficulty initiating abduction of the arm and externally rotating the arm, with an aching pain in the shoulder joint.The sign is selective wasting and weakness of the supraspinatus and infraspinatus muscles. Testing the deltoid separately means taking the fully abducted arm and having the patient pull backwards; also looking for deltoid atrophy. Also useful are tenderness in the suprascapular notch and pain evoked by forced adduction of the arm.

Gradual onset neuropathies may be due to ganglia in the suprascapular notch and spinoglenoid notch, or malignant tumors from the scapula. True entrapment neuropathies within the notch to a spur or ligament. Inherited calcification of the ligament may occur.

Differential includes ABN (acute brachial neuritis) , and less commonly shoulder joint/rotator cuff disorders, disuse wasting, or combined shoulder/nerve injury. EMG is definitive. MRI can look at entrapment in the suprascapular notch, and determine which muscles and hence which nerves are involved.

Treatment may involve rest, physiotherapy, injections, suprascapular notch exploration (supraglenoid notch if only infraspinatus is involved).

Ataxic v. painful form of paraneoplastic neuropathy

2008-02-01T10:13:00.000-08:00

Oki Y, Koike H, Iijima M et al. Neurology 2007; 69:564-572.

Group one-- dep sensory disturbance, shows sensory ataxia, markedly abnormal sural nerve,

Group 2-- superficial sensory disturbance- shows severe hyperalgesia, involvement small myelinated fibers and unmyelinated fibers.

Both groups showed an axonal sensory neuropathy with greater diminution of SNAPs in first (sensory ataxia) group. Both groups had about 50% presence of antiHu antibodies. Both groups had some cases with benefit from treating the cancer; immunotherapy was of transient benefit.

Genitofemoral nerve

2008-02-01T02:41:00.000-08:00

Arises from L1 and L2 roots, and branches into the lumboinguinal and external spermatic nerves, supplies the skin over femoral triangle, the cremasteric muscle and the inner upper thigh, labia or scrotum

Branches of the Nerves of forearm

2008-02-01T02:31:00.000-08:00

Anterior interosseous:
Flexor pollicus longus
Pronator quadratus
Flexor digitorum profundus I and II

Ulnar:
Flexor carpi ulnaris
Flexor digitorum III and IV
Intrinsic hand muscles

Median-- most flexors in forearm, lumbric alsI and II, and muscles of thenar eminence

Criteria for the diagnosis of multifocalmotor neuropathy

2008-01-08T06:01:00.000-08:00

Definite MMN
1. Weakness without objective sensory loss in the distribution of two or more named nerves; during the early stage, the finding of diffuse symmetric weakness rules out MMN
2. Definite conduction block in two or more sites outside common entrapment sites (defined as a decrease of more than 40 % in median or ulnar (not radial) CMAP area or 50 % or more in CMAP amplitude with an increase of less than 30 % in CMAP duration).
3. Normal sensory nerve conduction velocity across the sites with block.
4. Normal sensory nerve conductions for all nerves tested with a minimum of three tested.
5. Absent UMN signs including spastic tone, clonus, extensor plantars, and pseudobulbar palsy

Probable MMN
1. Weakness without objective sensory loss in the distribution of two or more named nerves; during the early stage, the finding of diffuse symmetric weakness rules out MMN
2. The presence of one of the following: probably conduction block in two or more sites outside common entrapment areas, or definite block in one segment and probable block in another outside common entrapment areas.
3. Normal sensory velocities outside the same areas with motor conduction block when study of the segment is technically feasible (ie. not required for segments proximal to the axilla or popliteal fossa).
4. Normal sensory nerve conductions for all nerves tested with a minimum of three tested.
5. Absent UMN signs including spastic tone, clonus, extensor plantars, and pseudobulbar palsy.
(as cited in NEJM 2007; 357:2710, adapted from Olney et al. Muscle Nerve 2003;27:117-121).

Accessory neuropathy

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1. Intracranially, a tumor such as a schwannoma or meningioma can cause .

2. In jugular foramen, the IX, X, XI nerve involvement is called " Vernet's syndrome" which is due, in order of frequency, to metastases, primary tumors such as schwannomas, an idiopathic syndrome with spontaneous recovery, and sarcoidosis.

3. In the neck, lymph node dissection in the posterior triangle remains the commonest cause, and may also affect the lesser occipital nerve. Other neck dissections, postoperative radiation, carotid endarterectomy, and cannulation of the IJ vein are also reported. Trauma to the posterior triangle from blunt injury, compression from wearing slings, hanging attempt- related injuries, stretch injuries from heavy lifting, glass or knife lacerations, tuberculosis of the cervical lymph nodes (scrofula) or idiopathic causes.

Presentation: Shoulder weakness and pain, and drooping of the shoulder. Trapezius wasting may occur. Paresthesias over the shoulder and scapula may occur.

Examination: Wasting of any part of the three parts of the trapezius. Scapular winging occurs at rest and with movement affecting the upper part of the scapula (v. the lower part with serratus anterior weakness). Shrugging of the shoulders is "worthless" because the levator scapulae (direct innervation from C3 and C4) can do this. Ask the patient to abduct the arms through 180 degrees from side to above the head, straight sideways. The second ninety degrees is accomplished by rotation of the scapula by the upper trapezius and cannot be accomplished otherwise. The middle trapezius is tested by asking the patient to lie prone, and abduct the arm at 90 degrees from the body. The middle trap can be palpated and the stability of the scapula can be assessed. The lower third is assessed with the patient prone, arms lying alongside head, lifting arms, and palpating the lower traps.

If the damage is proximal, the scm (sternocleidomastoid) is usually wasted. Its hard to assess the deltoid/rhomboid,spinati, and serratus anterior if scapula is not stabilized by the trapezius.

Evaluation-- EMG and NCS of the three parts of the trapezius separately. CT/MRI of base of skull/jugular foramen.

Management-- idiopathic-- none. Neck dissection-- may graft the greater auricular nerve. Surgical stabilization of scapula is better than orthotics which usually do not work. The levators and rhomboids can be transferred to scapula effectively. The procedure is effective but rarely done.

Phrenic neuropathies

2008-01-06T13:07:00.000-08:00

Causes:

Cervical spine-- motor neuron disease, poliomyelitis, herpes zoster
Neck-- stab wounds, surgery, anesthetic blocks in the brachial plexus; catheterization of internal jugular and subclavian veins, malignancy.
Chest-- thoracic surgery, mediastinal tumor, or irradiation
Uncertain-- Acute brachial neuropathy, diabetes mellitus, sarcoidosis, Guillian barre, idiopathic.
Muscle--NMJ -- acid maltase, polymyositis, myasthenia gravis

Pearls
1. Zoster is usually unilateral and asymptomatic, with herpetic lesions the tipoff and the chest X ray diagnostic.

2. Brachial plexus anesthesia blocks are usually temporary and asymptomatic, but bilateral blocks are not advisable due to risk of total diaphragm paralysis.

3. Metastases in the neck may also cause Horner's syndrome and the recurrent laryngeal nerve, causing vocal cord paralysis, and may be due to breast cancer.

4. The incidence during open heart surgery ranges from 10-85 % and may be due to ice slurry or topical cooling of heart during surgery. It occurs less often with an insulating pad, but may still occur after pericardiectomy or surgery for mediastinal tumors. In this situation it is often left sided. Bilateral injuries are rare but prolonged ventilator dependence is common.

5. In acute brachial plexopathy, 6 % have phrenic dyfunction and present with shoulder pain and dyspnea. Usually thoracic lesions are excluded and EMG and NCS are helpful.

6. Diabetic phrenic neuropathy is common and may account for the breathlessness of some diabetics.

Other high cervical and related disorders

2008-01-06T12:58:00.000-08:00

1. Neck-tongue syndrome is due to compression of the C2 ventral ramus. There may be neck pain, occipital numbness, and tongue paresthesias on turning the head. Some patients have congenital abnormalities of the cervical spine.

2. Third occipital headache may have occipital and suboccipital pain. It is a postwhiplash injury headache with temporary and partial relief with nerve blocks. It probably is due to degenerative arthritis of the C2-3 facet joint and is not neurologic in origin.

3. Greater auricular nerve damage is commonly caused by surgery to the neck and face, especially rhytidectomy (face-lift) with numbness around the ear and later, painful neuromas. CEA, parotid surgery, and leprosy can be causative. NERVE CONDUCTIONS CAN BE CONFIRMATORY.

4. Lesser occipital nerve injury occurs during lymph node dissection in the neck (also gets the accessory nerve). The presentation is numbness behind the ear.

Disorders of the cervical plexus

2008-01-06T12:29:00.000-08:00

1. Radiculopathies usually involve C6-7 (see cervical radiculopathies); rarely the C3-4 nerve root foramen is affected with compression of the C4 root. Symptoms are pain and paresthesias in the ear region with sensory loss.

2. The cervical plexus is vulnerable in traction injuries such as motorcycle injuries that also affect the upper trunk of the brachial plexus, and during surgery of carotids (endarterectomy) or radical dissection of the neck. Motor dysfunction other than phrenic injury is hard to detect. Sensory loss in the upper cervical regions is common.

3. Herpes zoster is common in C2 and C3 dorsal root ganglia. Both zosteriform eruptions and postherpetic neuralgia may occur.

4.C2 ganglionopathy/radiculopathy and greater occipital neuropathy (avoid term occipital neuralgia, and cervicogenic headache, and whiplash injury) presents with deep stabbing unilateral pain in the neck and back of the head, with hyper/hypesthesia of scalp and tenderness of the nerve. It is caused by trauma (whiplash), spondylosis, ligamentous entrapment, zoster, neurofibroma (dorsal ramus), and trauma/compression of the GON. "the cardinal symptom is intermittent or continuous numbness or paresthesias (with or without pain) in C2 dermatome. The C2 nerve may be tender to palpate, or patients may have vertigo. Some cases may require surgical exploration.

C2 nerve root is rarely involved in major fracture/dislocation, congenital abnormalities of the cervical spine, , subluxation of the atlas on the axis joint to to rheumatoid arthritis, or bone softening disorders such as Paget's disease, osteogenita imperfecta, and osteomalacia. Whiplash may be a cause but is probably vastly overstated.

Treatment including analgesics and acolar may or may not help, as may injections of anesthetics or corticosteroids. Surgery may reveal severe facet disease, ligamentous entrapment of a ganglion. Procedures may include C2 ganglionectomy or partial sectioning of the C1-3 rootlets.

5. The diversity of causes of "cervicogenic headache" make reports of definitive treatment difficult to evaluate.

Cervical spinal nerves-- special anatomic aspects to consider

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1. The ventral rami of C1-C4 form the cervical plexus, and C5-C8 the brachial plexus.

2. Exceptionally, C1 spinal nerve divides WITHIN the spinal canal to form a ventral and dorsal ramus, that passes above the arch of C1 to supply the deep muscles of the neck, without sensory fibers. The ventral ramus joins the cervical plexus.

3. The C2 root is very short. The ventral ramus joins the cervical plexus. C2 may project to the brow, whereas pain the back of the head is more likely cervical plexus. The dorsal ramus passes between C1 and C2 and the larger medial branch becomes the greater occipital nerve (C2 dorsal ramus). The lateral branch subserves the paraspinal muscles. That supplies the back of the head. C3,4,5, T1 dorsal rami affect skin on back of the neck.

4. The four cutaneous branches are the greater auricular, lesser occipital, supraclavicular, and transverse cutaneous nerves of the neck. They all emerge from the posterior border of the sternocleidomastoid muscle into the posterior triangle of the neck.

Lesser occipital nerve (C2-3 ventral ramus) affects the skin behind the ear. It affects the lower posterior occiput whereas the greater occipital affects anteriorly.

The greater auricular nerve (C2-3 ventral ramus) affects the skin below and directly behind the ear. Preauricular nerve overlaps trigeminal distribution, pain is dull aching not lancination. Posterior auricular nerve innervates the posterior occiput, mastoid, most of the pinna and posterior parietal area.

The transverse cutaneous nerve (C2-3 ventral ramus) of the neck affects the skin of the neck.

The supraclavicular nerve (C3-4 ventral ramus)affects the skin on top of the shoulder.

5. The phrenic nerve (C5) is the major muscular branch of the cervical plexus.

6. The spinal root of the accessory nerve derives from anterior horn cells and ascends the cord through the foramen magnum and leaves it throught the jugular foramen, together with the IX and X cranial nerves.

More pearls:
1. TMJ and cervical plexus pain may coexist in young patients due to cervical plexus
2. Difficulty swallowing ("pain stuck in my throat") may be due to spasm of cricopharyngeus muscle (external esophageal sphincter) and dyssynergia of posterior pharyngeal muscles (X nerve) that pushes the bolus to the cricopoharyngeus muscle that fails to open rapidly enough.

EMG physical examination PEARLS

2008-01-06T11:52:00.000-08:00

1. The lack of atrophy in a weak muscle indicates either an upper motor neuron lesion or purely demyelinating lesion and may represent spurious weakness.

2. The lack of weakness may be due to confusion, inattention, uncooperativeness, PAIN, feigning or a somatization disorder.

3. Fasciculations may be present in radiculopathies or other focal neuropathies as well as in disorders of the anterior horn.

4. Examination of the tendon reflexes is more objective than muscle power or sensory testing.

Sensory testing pearls:

1. Hyperesthesia, allodynia or hyperpathia are possible as well as hypesthesia.

2. The distribution of sensory loss is usually partial, often in the distal part of the dermatome,eg. the fingertips only in carpal tunnel syndrome. This may be due to damage only to selected fascicles within a proximal part of the nerve (ie. the lesion need not be distal).

Anatomic pitfalls: dermatome and myotome variations
1. Tibialis anterior, in root stimulation studies, is innervated by L4 75 % of the time, not L5.

2. EDB (in foot) can be L5 or S1 even more variably.

3. Dermatomal maps are based on flimsy anatomic evidence.

Hemorrage into or around nerves

2008-01-06T11:48:00.000-08:00

1. Patients on anticoagulation or with bleeding disorders develop hematomas that compress nerves.

2. Hemorrhage into nerves occurs particularly in patients with bleeding disorders, including leukemia, hemophilia and thrombocytopenia

3. Acute stretch injuries may rupture an intraneural blood vessel and cause bleeding into a nerve. For example, the common peroneal nerve in popliteal fossa may be affected after a severe inversion injury of the ankle.

Injection Injuries into nerves

2008-01-06T11:45:00.000-08:00

Mechanism
1. injection injury of nerve
2. Hematoma or hemorrhage around injection site (hours later)
3. Scarring around injection site (weeks later).

Metastases to the peripheral nerves

2008-01-06T09:30:00.000-08:00

1. These are rare and occur with lymphoma and leukemia. It may be due to spread rather than metastasis per se.

2. Compression of peripheral nerves is much more common, eg. brachial plexopathy and lumbar plexopathy.

3. Hemorrhage into the nerve is another possible mechanism.

4. Presentation can include mononeuropathy multiplex, radiculopathy, mononeuropathy, and polyneuropathy.

5. Paraneoplastic syndromes of the peripheral nerves are described.

Malignant peripheral nerve sheath tumors (MPNST) Pearls

2008-01-06T09:24:00.000-08:00

1. Term includes malignant schwannoma and neurogenic sarcoma

2. In NF-1 MPNST's can occur (2-16 % of patients with NF-1 develop one over their lifetime), or they can occur sporadically, or post-radiation.

3. Occassionally a previously existing benign neurofibroma can transform and become malignant.

4. They are located in the same areas as solitary and plexiform neurofibromas.

5. Pain and nerve dysfunction are greater than in benign tumors.

6. The tumors can become large before being detected.

7. Therapy involves amputation, radiation, chemotherapy.

8. The prognosis is poor with local recurrences and metastases to the lungs.

Other benign peripheral nerve tumors

2008-01-06T09:21:00.000-08:00

1. Besides schwannomas and neurofibromas, other types are rare.

2. The fibrolipoma is a rare fatty tumor that presents as a swelling often in the median nerve, causing motor and sensory symptoms.

3. The intraneural perineuroma (aka hypertrophic neuropathy) usually involves a single peripheral nerve and causes painless but slowly progressive wasting and weakness, with mild or no sensory loss.

4. Non-nerve sheath tumors include: ganglion cysts, hypertrophic neuropathy, lipomas, hemangiomas, and desmoid tumors. Metastases to nerves can also occur (would be classified as malignant though)

Peripheral neurofibromas pearls

2008-01-06T09:15:00.000-08:00

1. Solitary NF's in otherwise healthy patients (ie. , those without NF-1) may be painless or painful subcutaneous swelling without neurologic features, unless they arise from a major nerve trunk or plexus in which case they may have motor and sensory dysfunction.

2. Multiple neurfibromas such as seen in NF-1 do not transform and are a cardinal feature of NF-1.

3. Plexiform neurofibromas arise from deeply situated nerves and can be very damaging but are highly prevalent in NF-1; in one study 35 % of patients had them in the abdomen and pelvis and four percent in chest and supraclavicular areas. Surgical results for plexiform neurofibromas are not nearly as good as solitary type.

4. In patients without NF-1, spinal tumors are usually schwannomas.

Schwannoma of the peripheral nerve (benign)

2008-01-06T09:08:00.000-08:00

Pearls
1. The most common peripheral nerve tumors occur in any peripheral nerve but especially the spinal nerves, peroneal nerve, ulnar nerve, sympathetic nerves and vagus nerves.

2. In a peripheral nerve the presentation is that of a mass that is often painless with paresthesias and positive Tinel's sign over the nerve. The exception of greater findings occurs if the nerve is in a restricted space such as carpal or fibular tunnel.

3. Schwannomas of deep nerves such as sciatic are difficult to detect.

4. Scwannomas that arise from spinal or sympathetic nerves may extend into and compress the spinal cord.

5. Multiple schwannomas occur primarily but not exclusively in NF-2.

6. 62% neurofibromas, 38% schwannomas
In schannomas function preserved in 89% after resection

radiculopathy pearls

2007-04-22T09:09:00.000-07:00

Differentiating C5 and C6 radiculopathies may be difficult due to common involvement of the deltoid, biceps, brachialis and brachioradialis. However, the rhomboids implicate the C5 root preferentially, and pronator teres/FCR implicate C6. Be careful because C6 radiculopathies can also mimic C7 radiculopathies with abnormalities in triceps, anconeous, pronator teres and FCR. C7 radiculopathy-- changes are found in triceps, anconeous, FCR, and occassionally pronator teres. The latter two are important because they are median innervated and the diagnosis is not being based on radial muscles only. Extensor indicis proprius, which is C8 is spared here. C8 radiculopathy-- can see changes in radial mm (ext proprius and EPB); median nerve muscles (FPL and +/- APB) plus all the ulnar muscles. The APB is often spared. L2-4 radiculopathies-- abnormalities are often (but not always found in thigh adductors, quadriceps muscles and iliacus. L5 radiculopathy-- affects tibialis anterior, extensor hallucis, peroneus longus and EDB (all of common peroneal) plus FDL, tibialis posterior, TFL, gluteus medius and maximus. Study tensor fascia lata which is sensitive to L5 radiculopathy but is one of two such muscles that do no emanate from the sciatic nerve (the other is the gluteus medius). S1 radiulopathy-- the affected muscles are often the abductor hallucis, ADQ, soleus, gastrocnemius, and the glutei esp maximus, and short head of biceps

Femoral/saphenous neuropathy

2007-04-22T09:08:00.000-07:00

Signs and symptoms-- weakness and atrophy of the quadriceps muscle, reduced knee reflex, sensory disturbance over the anterior thigh/medial calf.

PEARLS

1) HIP FLEXOR MUSCLES MUST BE TESTED AND IF THEY ARE INVOLVED IT SIGNIFIES INVOLVEMENT OF LUMBAR PLEXUS.

2) ELDERLY PATIENTS MAY STATE THAT THEIR LEG COLLAPSED OR THAT THEY CANNOT ELEVATE THE LEG SUFFICIENTLY TO CLIMB STAIRS WITHOUT RECOGNIZING THE WEAKNESS OF THE MUSCLE AFFECTED.

Etiologies are many. Biemonds studied 50 patients. Four had retroperitoneal tumors, one retroperitoneal hematoma (often due to bleeding diathesis, six had lacerations or trauma, six had femoral neuropathy from diabetes, fifteen had radiculopathy masquerading as femoral neuropathy, eighteen were unknown included elderly and postulate was that they were diabetic or vascular). Iatrogenic causes include trauma after attempted femoral arterial puncture or catheterisation, intrapelvic operations with bleeding ( including renal transplant) or stretch due to marked extension or flexion of the hip. This can occur with coma after intoxication, or during childbirth, especially with poorly padded stirrups used in patients already numb from an epidural injection.

EMG PEARLS
1) Femoral nerve slowing can be further evaluated by saphenous nerve conductions (if abnormal its not radiculopathy). Plexus lesions have normal femoral motor nerves, abnormal saphenous nerve conductions, and EMG abnormalities outside femoral nerve territory (check....) L4 radiculopathy shows EMG abnormality ooutside L4 myotome including paraspinal muscles (check...) Saphenous nerve involvement (one of three branches of the femoral nerve) produces abnormal sensation on medial calf. May get Tinel's sign along nerve anywhere from Hunter's canal above knee. Can occur from procedures in Hunter's canal or at knee. EMG of femoral neuropathy: often more useful than NCS. Examine lumbar paraspinals and obturator innervated muscles. EMG femoral innervated muscles: VM, RF, iliopsoas; obturator (adductor longus); superior gluteal nerve (TFL), and lumbar paraspinal muscles. ADD-- 4 fb distal to pubic tubercle , adducts limb.

Ilioinguinal neuropathy

2007-04-22T09:06:00.000-07:00

Clinical-- burning pain in abdomen into inner/upper thigh or into scrotum or labia majora. There may be tenderness slightly medial to anterior iliac spine or a Tinel's sign over the lower abdomen. PEARL if complete palsy is present lower abdomen may bulge mimicking a primary hernia. Patients may walk bent over or have trouble rising from a chair. They may walk flexed forward "like a novice skier." Etiology may be traumatic; blow to abdomen, surgery such as appendectomy or more commonly herniorrhaphy (may have occurred previous suggesting etiology is fibrosis or scar formation around the nerve). Differential includes entrapment of neighboring homologous iliohypogastric nerve, also of T12-L1, or genitofemoral nerve which courses retroperitoneally and can be caused by hematoma or tumor. Diagnosis: with nerve blocks. Treatment: surgical resection helped more than 75 %. The nerve arises from L1 and L2 roots, supplies skin over the upper/medial thigh, the root of the penis, the upper scrotum or labia majora, and also innervates the transversalis and interior oblique muscles. It follows the pattern of an intercostal nerve, winding around the inner trunk to the medial anterior iliac spine.

Traumatic neuropathy: stingers

2007-04-22T09:05:00.000-07:00

Elman L, McCluskey L. Occupational and Sport Related traumatic neuropathy. The Neurologist 2004; 10:82-96 The burner or stinger is the most common sports related peripheral nerve injury and is caused by injury either to the C5-6 root or the superior trunk of the brachial plexus. Multiple postulates of causes though the most commonly proposed is downward displacement of the shoulder from the neck during tackling in a shoulder down position. The Torg ratio is a measure of spinal stenosis determined by cervical spine x rays does not predict stingers but does predict recurrence. Accordingly high school and college players usually have as the cause stretch of the brachial plexus whereas professionals with recurrent stingers have spinal stenosis. Acute disc herniation is not a cause however. Symptoms are immediate pain, numbness and paresthesias that last minutes. Weakness if it occurs may persist. Neck pain is not common. If sensory symptoms predominate its usually due to compression of the DRG within the neural foramen. Exam of the neck shoulder and C spine looking for point tenderness or fracture is done. Any neurologic deficit requires abstention from play. Muscle weakness at 72 hours predicts an abnormal EMG. On EMG, spontaneous activity in the paraspinals helps to localize to the nerve root, and sensory findings with a normal SNAP amplitude suggest localization in the forament with compression of the DRG. Decreased SNAP amplitude suggests a brachial plexus localization. Return to play is not determined by normalization of EMG. Persisting pain, restricted ROM, or neurologic deficit requires PT prior to return to play, for strengthening of weakened muscles as well as stabilization of brachial plexus and restoration of the normal cervical lordosis. Education of tackling technique and use of proper equipment is part of rehabilitation.

Traumatic neuropathy suprascapular nerve

2007-04-22T09:04:00.000-07:00

Activities at risk are ones with overhead activity such as volleyball, baseball, weight lifting, wrestling, dancing and assembly line work. Its also caused by trauma (stab wounds above scapula), improper use of crutches, and rupture of the rotator cuff. Clinical presentation involves posterolateral shoulder pain, weakness of initiating abduction and external rotation of the shoulder, and muscle atrophy. Weakness of infrapinatus causes weakness in externally rotating arm at shoulder. The crossed adduction test is a provocative test that is positive when pain is produced through passive adduction of the extended arm across the chest. Sensory deficit can occur in the upper arm due to sensory branches. Evaluation is imaging of cervical spine and shoulder (films and/or MRI), EMG, or diagnostic nerve block of suprascapular nerve to verify the diagnosis. Conservative treatment is rest followed by PT; surgery is indicated if full recovery is not achieved within six months. Over-use and traction injuries responded equally to surgical/conservative therapy whereas ganglion cysts and compression neuropathies are best treated surgically. Anatomically the nerve passes through the supracapsular notch and the spinoglenoid notch. At the suprascapular notch the mechanism proposed is abnormal contact between the suprascapular nerve and the transverse ligament during shoulder abduction or adduction across the chest. Isolated painless weakness of the infraspinatus muscle occurs at the spinoglenoid notch; this occurs in volleyball players.

Long thoracic neuropathy and dorsal scapular

2007-04-22T09:02:00.000-07:00

Occurs in many sports, but especially tennis. Its due to acute and/or repetitive use when the arm is raised and head is turned in the other direction. It can be due to compression of C5-6 roots as they travel through the scalene muscles, bow-stringing of the nerve across a fascial band, or traction injury. Non traumatic causes include brachial neuritis (idiopathic, postviral, or post surgical). Other causes are stab wounds, direct pressure from a heavy shoulder bag or shoulder braces during surgery, including thoracotomy, axillary node resection, resection of the first rib for TOS, and radical mastectomy. Blows to the sholder or lateral thoracic wall during falls or injuries can cause it. Its reported as the sole presentation of lyme disease.

The serratus anterior stabilizes the scapula against the chest wall, and long thoracic neuropathy causes weakness and difficulty moving the shoulder and arm, especially abduction or flexion above shoulder level. Patients may have a dull ache around the shoulder girdle. The shoulder looks funny due to winging. Clinical signs include scapular winging with arm outstretched against the wall. The superior angle of the scapula flips medially whereas the inferior angle swings laterally (opposite of that seen in axillary neuropathy). In contrast to trapezius weakness, in which winging is exaggerated with abduction of the arm, in LT neuropathy, its worse with outstretched arm thrust forward. Arm abduction beyong 110 degrees may be impossible. Acutely there may be shoulder pain but chronically it may be painless. Besides axillary neuropathy, differential includes scapular winging due to muscular dystrophy, C7 radiculopathy, and separation of serratus from insertion in a fracture of the scapula (easy to repair). See pictures of long thoraic and axillary neuropathy in Stewart, p 160 and 90 respectively.

Evaluation is x rays of shoulder, chest and shoulder to rule out a compressive lesion such as an osteochondroma. EMG is needed to confirm that the weak muscle is the serratus anterior as the trapezius also can produce scapular winging. It is formed directly from nerve roots C5-7 and will be NORMAL in plexopathy, abnormal with root lesion. EMG of serratius anterior is done with patient lying on the opposite side, arm adducted across the chest. It can be done by looking at medial scapular border , lower aspect below rhomboids. In the mid axillary line, isolate a rib, anterior to the lattissmus dorsi, posterior to the breast tissue in a woman. Treatment is rest, bracing and PT for ROM and strengthening of the shoulder girdle. Braces maintain scapula against the thorax to prevent further winging. Surgery for long thoracic palsy not due to penetrating trauma is only after 1-2 years of observation as natural history favors recovery. The current procedure of choice is transfer of the sternal head of the pectoralis major to the inferior angle of the scapula.

Morton's toe neuroma

2007-04-22T09:01:00.000-07:00

Clnical-- burning pain over the head of the fourth metatarsal radiating into the toe. Pain is worse by standing and/or walking, better with lying or elevating the foot. Extending the toes by squatting or kneeling makes it worse. Exam may show diminished sensation on the medial half of the fourth toe. Nerve conductions may involve simultaneous recording of toes I and V with reference electrode i between. The cause is traumatic. It may be related to walking, jogging, squatting or wearing high heeled shoes. Treatment is padding the metatarsal head in shoe, or eventually surgery to remove the nerve is definitive. It is usually a white fibrous enlargement at the branch point of the nerve. Alternative procedure is release the ligament of the deep plantar fascia without excision of the neuroma.

Axillary neuropathy

2007-04-22T00:26:00.001-07:00

A.N. can be caused by direct trauma with or without humeral fracture, anterior or posterior shoulder dislocation, and quadrilateral space syndrome. Direct shouder injury (the usual mechanism of the stinger) can cause it. There is about 50 % association of axillary injury with humerus fracture (proximal) and anterior shoulder dislocation. AN can also occur as part of brachial neuritis. Other causes are crutches causing pressure, hyperextension of shoulder during wrestling. The quadrilateral space syndrome involves the a.n. and the posterior circumflex artery in posterior axilla, bound by long head of triceps (medially), surgical neck of the humerus (laterally), teres minor and subscapularis (superiorly), and teres major (inferiorly). Syndrome may be due to muscle hypertrophy, fibrous bands, gunshot wounds, neuralgic amyotrophy, iatrogenic injury during shoulder surgery (up to 8 %).

Clinical presentation is inability to elevate and abduct the shoulder due to deltoid weakness (ie limited abduction after the first 30 degrees which is subsumed by the supraspinatus). By contrast, C-5 radiculopathy cause weak shoulder abduction for all 180 degrees subsumed by both muscles. An isolated teres minor lesion (also AN inn.) may escape detection since infraspinatus also rotates arm outward, but is detected by EMG. Teres minor is localized immediately lateral to middle third of the lateral scapular border. There may be numbness over the deltoid muscle belly. There may be tenderness in the quadrilateral space. The deltoid extension lag sign occurs when the arm is placed in a position of maximal extension and the patient is asked to maintain the position, and the degree of drop correlates with the extent of AN injury. MRI may show teres minor atrophy. Dynamic MRA can show compression of the circumflex artery with shoulder movements (abduction and external rotation) but angiography is not indicated. Shoulder dislocation AN injury recovers more than blunt trauma to the shoulder. Rest is usually adequate Surgery can be considered after three months. Less than 20 % require surgery. NCS show normal sensory responses, and decreased CMAP over deltoid with supraclavicular stimulation. Needle affects only deltoid and teres minor. Pitfalls-- C5-6; upper trunk/ posterior cord. The prognosis is good for recovery after fracture or dislocation of the humerus but not as good after blunt trauma to the shoulder

Axillary neuropathy

2007-04-22T00:26:00.000-07:00

A.N. can be caused by direct trauma with or without humeral fracture, anterior or posterior shoulder dislocation, and quadrilateral space syndrome. Direct shouder injury (the usual mechanism of the stinger) can cause it. There is about 50 % association of axillary injury with humerus fracture (proximal) and anterior shoulder dislocation. AN can also occur as part of brachial neuritis. Other causes are crutches causing pressure, hyperextension of shoulder during wrestling. The quadrilateral space syndrome involves the a.n. and the posterior circumflex artery in posterior axilla, bound by long head of triceps (medially), surgical neck of the humerus (laterally), teres minor and subscapularis (superiorly), and teres major (inferiorly). Syndrome may be due to muscle hypertrophy, fibrous bands, gunshot wounds, neuralgic amyotrophy, iatrogenic injury during shoulder surgery (up to 8 %). Clinical presentation is inability to elevate and abduct the shoulder due to deltoid weakness (ie limited abduction after the first 30 degrees which is subsumed by the supraspinatus). By contrast, C-5 radiculopathy cause weak shoulder abduction for all 180 degrees subsumed by both muscles. An isolated teres minor lesion (also AN inn.) may escape detection since infraspinatus also rotates arm outward, but is detected by EMG. Teres minor is localized immediately lateral to middle third of the lateral scapular border. There may be numbness over the deltoid muscle belly. There may be tenderness in the quadrilateral space. The deltoid extension lag sign occurs when the arm is placed in a position of maximal extension and the patient is asked to maintain the position, and the degree of drop correlates with the extent of AN injury. MRI may show teres minor atrophy. Dynamic MRA can show compression of the circumflex artery with shoulder movements (abduction and external rotation) but angiography is not indicated. Shoulder dislocation AN injury recovers more than blunt trauma to the shoulder. Rest is usually adequate Surgery can be considered after three months. Less than 20 % require surgery. NCS show normal sensory responses, and decreased CMAP over deltoid with supraclavicular stimulation. Needle affects only deltoid and teres minor. Pitfalls-- C5-6; upper trunk/ posterior cord.

Musculocutaneous neuropathy

2007-04-22T00:25:00.000-07:00

MN can occur proximally where it painlessly affects biceps strength and sensation in the forearm or more distally near the elbow where is is purely a sensory syndrome accompanied by pain. Heavy physical activity with resistive movements of the upper extremity is the usual inciting factor, although it can occur with anterior shoulder dislocation and traumatically (gunshot or stab wound or secondary to surgery). Rest is the treatment and the prognosis is good.

The distal syndrome is due to compression of the lateral antebrachial cutaneous nerve near the biceps aponeurosis with strenuous activity with the arm hyper-extended or the forearm pronated. It is reported in racket sports, windsurfing and swimming. It also occurs after venipuncture, catheterization and placement of an av fistula. Surgery in the antecubital fossa and arm splinting can be responsible. So can pressure of a strap across the elbow or arm restraints. Clinical presentation is numbness and dysesthesias in radial-volar forearm and elbow pain that resembles lateral epicondylitis. Elbow flexion from biceps is absent although the brachioradialis muscle can compensate somewhat. Biceps tendon jerk is absent. Initial treatment is conservative and may involve local steroid injection although decompresive surgery is often necessary.

Nerve is often involved in combinations of axillary, radial, and suprascapular neuropathies or ABN (acute brachial neuritis). Differential-- in biceps rupture, there is not sensory loss, and the biceps muscle contracts into a small bal. With a C6 radiculopathy, there will be involvement of supra/infrapinatus, deltoid and brachioradialis. C6 sensory signs often extend into the hand, whereas lateral cutaneous nerve of forearm stops at the wrist. Surgical exploration can show the distal syndrome due to biceps aponeurosis in patients lacking another clear cause.

Radial/PI neuropathy

2007-04-22T00:24:00.000-07:00

Proximal RN may be compressive or traumatic. It can be due to fracture of the humeral shaft and strenuous activity such as weightlifting. It can be due to crush or twisting injury of the wrist or forearm or repetitive pronation and supination at work. Intoxicated individuals sleep with their arm over a bench "Saturday night palsy" with injury to the spiral groove with or without fracture of the humerus. In newborns, the umbilicus can entrap the nerve. These lesions are triceps sparing. Nerve injury at axilla from improper crutches use affects the triceps and the triceps reflex. Fractures of the head of the radius affect the nerve more distally. Compression of the epicondylar branch is one of the types of tennis elbow. Pain and tenderness in the lateral elbow occurs, resembling lateral epicondylitis (another entity known as tennis elbow).

The clinical presentation of proximal RN is wristdrop, inability to extend the fingers, weakness of the brachioradialis and variable sensory loss in the first dorsal web space. If proximal enough it may affect triceps and posterior arm sensation. Athletes should have x rays to exclude fracture. Treatment is conservative including a wrist splint, with surgery reserved for cases that have not improved by four months. SUPERFICIAL RN in forearm can be caused by repetitive pronation/supination maneuvers. The presentation is paresthesias over forearm, wrist, thumb, and dorsal hand, maximal in with wrist flexed in ulnar deviation. Reduced SNAP over the dorsum of hand is seen. Local injection can be used to confirm diagnosis. Treatment is rest, and if unsuccessful, then surgical exploration. Tight watchbands and handcuffs can also cause this (the latter with or without median and ulnar sensory effect). In the forearm, the radial nerve divides into a superficial sensory branch and a deep motor branch (posterior interosseous nerve). Compression of the latter can produce two distinct clinical syndromes: the radial tunnel syndrome (RTS) and and posterior interosseous nerve syndrome (PINS). It can develop after injury to the elbow, or in RA with tenosynovitis. Involvement of the nerve between the two heads of the supinator at the arcade of Frohse causes weakness of the wrist and digit extensors with sparing of the supinator. EMG findings are in the ECR longus and brevis. The differential diagnosis is tendon rupture. PINS can be caused by a local compressive lesion or repetitive pronation-supination or fracture of the proximal radius. It has a 2:1 male predominance. It manifests as painless weakness without sensory loss of affected muscles, rarely with poorly localized pain or dysesthesias. The hand will deviate radially at the wrist with fingers flexed at the metacarpophalangeal joint without wristdrop. The supinator is spared. NCS excludes partial radial neuropathy. X ray excludes compressive lesions. Therapy is conservative with a long arm splint for immobilization. Surgery can be considered after 12 weeks. RTS is usually seen in the dominant arm of patients with repetitive pronation/supination either on the job or in racket sports. The clinical presentation is aching pain of the elbow and forearm without weakness, but in contrast to PINS there may be numbness in the first dorsal web space. It may be confused with lateral epicondylitis (tennis elbow). Provocative tests (nonspecific) include resisted forearm supination and the middle finger test. The patient extends the elbow and holds the middle finger in extension against a force applied to the dorsum of the hand. Diagnosis can be helped by selective injection into the lateral epicondyle or the radial tunnel. A three month trial of rest, splinting and NISAA's usually is sufficient. Steroid injections and surgery are other resorts.

Ulnar neuropathy at elbow and distal

2007-04-22T00:22:00.002-07:00

UN at elbow can occur during repetive stress, more commonly with certain positions and decreased body mass, and more commonly in men. Associations exist with overhead throwing sports, cross country skiing, weight lifting and racket sports. One third have no cause. Among athletes it often accompanies other elbow problems including attenuation of the ulnar collateral ligament and medial epicondylitis. The clinical presentation is sensory ulnar in non-athletes but athletes tend to have medial epicondyle pain first. Evaluation requires X rays, +/- ultrasound and MRI. Conservative treatment is rest, splinting, NSIAD's, NOT steroid injection. Surgery is for those with mild/moderate pain who fail conservative therapy,or intractable pain or fixed sensory deficits or weakness. Distal ulnar neuropathy can occur at wrist proximal to, within, or beyond Guyon's canal. The first spares the dorsal ulnar cutaneous branch, the second all cutaneous branches, and the third all but the superficial sensory branches of the fourth and fifth digits. It affects cyclists, wheelchair athletes, racket and club sports. NCS help; therapy is conservative unless there is a fracture such as the hamate. Sensory symptoms in the forearm suggest brachial neuritis rather than ulnar neuropathy. Pitfalls in examination: if nerve conductions appear to show an ulnar conduction block, check for a Martin Gruber anastamosis. Fibers destined for FDI/APB/ADM may travel with median nerve at elbow in about 20 percent of patients. Stimulate the median nerve at the elbow and wrist, and if you get a response only at the elbow you have proved that an anastamosis exists. Another pitfall of nerve conduction is muscle artifact seen with antidromic stimulation (G1 is close to ADM). Solve this problem by doing orthodromics. Another pitfall is brachial neuritis masquerading as an ulnar neuropathy. Medial antebrachial cutaneous nerves are abnormal in cases of lower trunk lesions. It also puts the lesion away from a radiculopathy if abnormal. Distribution of sensory nerve fibers in hand: 100 % of ulnar fifth fibers comes from lower trunk. In index finger 100 % comes from middle or upper trunks (80/20). In thumb, 100 % come from upper trunk. Localizing a true ulnar neuropathy with, one must know common compressions are in retrocondylar groove (most common), humeroulnar arcade (Cubital tunnel), and less commonly, at exit from FCU. Other sites are Guyon's canal, deep ulnar in hand, and (proximally) axilla nd arcade of Struthers. A nerve conduction of dorsal ulnar response recorded between the fourth and fifth metacarpals, 8 cm proximal to wrist,compared to the contralateral side, is useful to differentiate between an ulnar neuropathy at the elbow and wrist. If its normal, it suggests the problem is at the wrist. The Mayo protocol is antidromics from the fifth digit, recorded11 cm proximal to wrist, above and below the elbow velocities. If velocities are <> 20 %, stimulate below elbow and upper arm. If slowing is > 8 mps or 10 % amplitude difference across the 10cm elbow segment, perform 2 cm inching. IF FDI is weak consider FDI recording. Elbow should be flexed at 90 degrees during test. Needle examination should include FDI, ADM, FDP and FCU. FCU is reached in the forearm. It flexes the wrist with ulnar deviation. However FCU may comes off either before or after cubital tunnel. The FDP comes off only after (to digits 4 and 5 is ulnar). Reach by supinating arm, wrist up, 4 finger breadths up, just ulnarly to the shaft. The ulnar fibers are superficial. he flex the dip of the 4th and 5th digits. Both FCU and FDP are C8-T1. If ulnar muscles are abnormal, check APB (C8 median) , EIP (C8 radial), and contralateral FDI. If other C8 muscles are abnormal, check paraspinals. ECU is posterior interosseous (radial) c 6-8, lower trunk extends wrist with ulnar deviation. Do if suspect lower trunk. If the lesion is in the wrist, proximal to Guyon's canal, all ulnar hand muscles will be affected, plus the antidromic DL will be prolonged with a reduced amplitude, with a normal dorsal ulnar response. Sensory loss will exist in an ulnar hand distribution. Proximal to the hypothenar branch, FDI/ADM affected, normal sensory, abnormal hypothenar EMG, normal sensation, weak interossei, lumbricals and hypothenar. Isolated deep branch in the hand, has weak interossei, lumbricals, spares ADM and sensation, reduced FDI amplitude, normal antidromic ulnar sensories, abnormal needle emg in interossei and lumbricals. Reach the latter by going to the second palmar crease, just proximal to joint, just radial to the tendon. Go too deep you'll be in opponens digiti minimi.

Dorsal scapular neuropathy

2007-04-22T00:22:00.001-07:00

It entraps the nerve and scapula wings on wide abduction of the arm (like trapezius neuropathy and unlike LT nn wherin its worse with arm outstreched forwards). There may be pain in C5-6 distribution. EMG abnormalities are restricted to levator scapulae, rhomboids major and minor.

Cervical radiculopathy

2007-04-22T00:21:00.001-07:00

Levels involved: C5 (6.6%), C6 (17.6%), C7 (46 %) C8 (6.3%) Most usual NCS are C8T1; C5-6 NCS (musculocutaneous/biceps) and C7 (radial EDC) are uncommonly studied. CMAPs should be normal unless there is severe axon loss. Other nerves that can be studied are lateral antebrachial (C5), median recording at index or thumb (C6), median recording at middle finger (C7) or ulnar at ring/little finger (C8) or median antebrachial (T1). Contrary to popular belief, paraspinal muscles are abnormal in only 50-70 % of radiculopathies. Planning the EMG (below) the muscles associated with radiculopathy at the variousl levels are indicated, in order of the chances of their being abnormal. C5. Clinically presents with weak deltoid and infraspinatus. Check deltoid, infrapinatus, biceps, then less often, brachioradialis and rhomboids (rhomboids are usually SPARED). Reach INF with arm abducted at ninety degrees, insert needle 2 finger breadths below the spine of the scapula. Reach rhomboid major on vertebral border of the scapula, from the root of the spine of the scapula to the inferior angle. Patient's hand is at side, test by raising hand from small of the back. Pitfall: if superficial needle will be in trapezius; if deep, in the erector spinae. Rhomboideus minor is just above major with needle insertion one finger breadth medial to vertebral end of the scapular spine with same activation. Pearl: Check pronator teres (C6) to rule out C6 involvement. Reach pronator teres two finger breadths distal to the midpoint of a line connecting the medial epicondyle and the insertion of the biceps tendon. C6 presents with paresthesias into thumb and forefinger; weak biceps and wrist extensors. Abnormal muscles are pronator teres (median C6), deltoid, biceps, triceps, ECR ( upper trunk radial C6). Reach ECR 2 fingerbreadths distal to the lateral epicondyle. It dorsiflexes the wrist in radial deviation. C7 causes paresthesias in forearm and dorsum of hand; weak triceps, long finger flexors and finger extensors. This is the most common radiculopathy. Use multiple nerve distributions. Abnormal muscles are triceps, PT, ECR, EDC and FCR (median all trunks C6-8). Find FCR 3-4 fingerbreadths distal to the midpoint of a line connecting the medial epicondyle and biceps tendon; it flexes the wrist with radial deviation. Other muscles nearby (can hit accidentally) are FDS (deep), FPL (deeper) PT (lat) palmaris longus (medial). Radial artery, FPL and FCR make up "radial trio." Its important to get PT or FCR as a median contributor. C8 involves paresthesias in the little finger and weak intrinsic mm of hand and wrist flexors. Check (in order) FDI, APB (median), FPL, EIP, EDC, TRI, PT, ADM. Pitfalls: ulnar and medial antebrachials should be normal. Consider ALS. Find FPL in middle of the forearm with hand supinated, flexes DIP of thumb. Favors radiculopathy: Pain proximally, in neck or with movement of the neck, along the scapula or the precordial border; pain with coughing, sneezing, or Vasalva maneuvers;

Upper extremity

Root
Clinically Relevant Gross Motor Function
C5
Shoulder abduction; ± elbow flexion
C6
Elbow flexion, pronation/supination, ± wrist extension
C7
Diffuse loss of function in the extremity without complete paralysis of a specific muscle group
C8
Finger extensors, finger flexors, wrist flexors, hand intrinsics
T1
Hand intrinsics

Lumbosacral radiculopathy

2007-04-22T00:19:00.000-07:00

LS is more frequent than cervical, and is more common to have involvement of multiple roots. The L5 root is most common (40 %) then S1 (26 %) then L4 (19%) then L3 (16 %). Beware of diabetes mimicking a radiculopathy. Nerve conductions are not that helpful nor is SEP. Needle EMG is best. Below with each root is the order of findings of muscle abnormality at each level, in order, with instructions how to reach some of the muscles listed. L3- ADD, ILI, RF, VL, VM (first two were abnormal in almost all) L4- VM, AT, VL , RF, ADD (percentages were not much more than 50 on most of these) L5 AT (27/40), PER (22/25), FDL (20/25), PT (10/12), GME (25/35), TFL (half) and then almost always normal were RF, VL, GMA, MG (7/40) S1 PER (7/11 was best), GME PT GMA MG AT (5/26) very rarely if ever: VL RF ADD ILI. Paraspinals are very important and are slightly better than the cervicals. Finding muscles: insertion and action ILI insert 2 fingerbreadths lateral to femoral artery and 1 fb below inguinal ligament; flex thigh RF insert anterior thigh, midway between superior border of patella and anterior superior iliac spine. TFL (sup gluteal n, L4) insert 2 fingerbreadths anterior to greater trochanter; abduct thigh VL -- lateral thigh, one handbreadth above patella ; lift heel with knee extended. VM-- 4 fb proximal to sup-med angle of the patella. Lift heel with knee extended. GMA- insert one to three inches midway between greater trochanter and sacrum; extend knee with hip flexed. GME- one inch distal to midpoint of iliac crest; abduct thigh. ADD-- 4 fb distal to pubic tubercle , adducts limb.

ALS Diagnootic Criteria

2007-04-22T00:17:00.000-07:00

EMG's decreased recruitment, unstable MUPs, fasciculations, fibrillation potentials, polyphasiscs, increased amplitude and duration. NCS show low amplitude CMAPs which are related to disease severity and prognosis. Ulnar stimulation at Erb's point is necessary to look for conduction block. EMG muscle selection should be done to minimize sticks. Need to see decreased recruitment large MUPs and fibs in at least three levels. Thoracic paraspinals are typically abnormal (80 % quoted) and are useful if coexisting cervical paraspinal abnormalities are seen. EL Escorial Criteria (replaces prior Lambert criteria which were more stringent). There are 4 body regions: bulbar, cervical, thoracic and lumbar. Definite ALS requires denervation in 3 of 4 levels; probable, 2 levels, possible 1 level; suspected 2 levels without UMN signs. In each level, at least two muscles of different spinal nerve, and peripheral nerve innervation should be tested.

Nerve conduction normals and instructions

2007-03-09T16:24:00.000-08:00

median motor distance 7 cm DML <4.5> 49

ulnar motor distance 6.5 cm ; DML <> 51

median antidromic ( rings index, stim at wrist) distance 13 cm; peak latency <>15 (if under 60) and >10 (if over 60).

median orthodromic (palmar) (bar on wrist, stim at mid-palm) d=8cm; peak lat 2.3

distal antidromic (rings on index; stim mid palm with same 8 cm distance, beyond carpal tunnel to differentiate CTS and PN) Note-- can do same for ulnar if desired difference > .3 ms is abnormal

radial median comparison-- rings on thumb, stim radial and median each at 10 cm; > 4 ms difference is abnormal

median-ulnar comparison-- rings on ring finger, d 14 cm to median and ulnar both; > 4 ms is abnormal difference

lumbrical motor-- put G1 next to tendon near 1st palmar crease stim palm; indicated if motor is absent.

lateral antebrachial-- measure 12 cm to radial stylus from biceps insertion; compare to opposite side; if abnormal suggests plexus rather than radiculopathy.

medial antebrachial-- measure 12 cm to ulnar stylus from biceps insertion; compare to opposite side; if abnormal suggests plexus rather than radiculopathy.

Radial sensory-- put G1 on radial tendonnear snuffbox towards thumb. measure 10 cm. Amp>20 is normal, latency less important, can compare to opposite side.

Radial motor-- G1 on EDC or EIC; d about 10 cm, measure also spiral groove (with calipers) and axilla or Erb's point.

dorsal ulnar cutaneous-- d 10 cm; G1 at base of 4th metacarpal with palm downl;stim ulnar nerve; if normal suggests problem in wrist.

f wave estimates-- measure estimate to xiphoid from leg, to sternum in arm; take velocity times 2 divided by the velocity. (controls for height).

Peroneal distance 8.5; amp >2; DML<>4; DML < distance =" 14">6; latency < 4.5

saphenous-- 2 methods 1) stimulate knee between gracilis and sartorius, go 10 cm distal just off tibia or 2) distal method; G! behind tibia 1 cm north of medial malleolus, go 14 cm.

phrenic-- stimulate at bottom of SCM; G1 at anterior axillary line in bottom intercostal space; G2 near midline.

Rep stim for periodic paralysis: rep stim; exercisse for 3-4 min with rest every 30 sec or so; repeat rep stim; check CMAP every five minutes for up to 45 minutes; if amplitude drops out in 80 % of cases.