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How does an increased amplitude affect nerve conduction velocity?

How does an increased amplitude affect nerve conduction velocity?


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My professor said that increasing the amplitude (the amount of depolarization e.g. depolarizing from -80 mV instead of -50 mV) leads to a greater conduction velocity.


Charcot–Marie–Tooth Disease

Nerve Conduction Velocities

NCVs have played an important role in characterizing CMT disorders since their initial use in separating CMT1 from CMT2. In the early 1980s, Lewis and Sumner demonstrated that most cases of inherited neuropathies had uniformly slow NCVs, whereas acquired demyelinating neuropathies had asymmetric slowing. Thus, NCVs could be used, along with a patient's pedigree, to distinguish between inherited and acquired neuropathies. During the past decade, however, this approach has had to be qualified. Most CMT1 patients, particularly those with CMT1A, have uniformly slow NCVs of approximately 20 m/sec (although values as high as 38 m/sec have been reported and this is used as a cutoff value). However, asymmetric slowing is characteristic of HNPP and may be found in patients with missense mutations in PMP22, MPZ, EGR2, and Cx32. Since all these disorders may present without a clear family history of neuropathy, one must be cautious when using NCVs to distinguish acquired from inherited demyelinating neuropathies. Forms of inherited neuropathies associated with uniform and nonuniformly slowed NCVs are illustrated in Table 2 .

Table 2 . ELECTROPHYSIOLOGICAL FINDINGS OF INHERITED DEMYELINATING NEUROPATHIES

Inherited disorders with uniform conduction slowing
Charcot–Marie–Tooth 1A
Charcot–Marie–Tooth 1B
Dejerine–Sottas
Metachromatic leukodystrophy
Cockayne's disease
Krabbe's disease
Inherited disorders with multifocal conduction slowing
Hereditary neuropathy with liability to pressure palsies
Charcot–Marie–Tooth X
Adrenomyeloneuropathy
Pelizeus–Merzbacher disease with proteolipid protein null mutation
Refsum's disease
Inherited disorders with incompletely characterized electrophysiology
PMP 22 point mutations
P0 point mutations
Adult-onset leukodystrophies
Merosin deficiency
Early growth response-2 mutations

The use of NCVs to distinguish between demyelinating and axonal neuropathies is also important. All forms of CMT1 have axonal loss as well as demyelination, and it is likely that axonal loss correlates better than demyelination with the patient's actual disability. Thus, reductions in compound muscle action potential (CMAP) and sensory nerve action potential (SNAP) amplitudes are found in most CMT1 patients in our series of 43 CMT1A patients, 34 had unobtainable peroneal CMAPs and 41 had unobtainable sural SNAPs.

The distinction between demyelinating and axonal features of NCV is particularly confusing in CMTX. NCVs in CMTX patients are faster than in most patients with CMT1, often with prominent reductions in CMAP and SNAP amplitudes. Thus, CMTX has been described as an “axonal” neuropathy. However, a careful analysis of the conductions will reveal the primary demyelinating features of the neuropathy. The conduction velocities in men are not normal but usually between 30 and 40 m/sec—values that would be considered an intermediate range between CMT1 and CMT2. Moreover, distal motor latencies and F wave latencies are usually prolonged. Some women with CMTX, probably through inactivation of their mutant X chromosome, have normal NCVs, although many have values similar to those of their male counterparts. In distinguishing between the demyelinating and axonal features of CMTX, it is important to remember that the disease is caused by mutations in Cx32, which is expressed in the myelinating Schwann cell.


Why might I need a nerve conduction velocity test?

NCV is often used along with an EMG to tell the difference between a nerve disorder and a muscle disorder. NCV detects a problem with the nerve, whereas an EMG detects whether the muscle is working properly in response to the nerve's stimulus.

Diseases or conditions that may be checked with NCV include:

Guillain-Barré syndrome. A condition in which the body's immune system attacks part of the peripheral nervous system. The first symptoms may include weakness or a tingling sensation in the legs.

Carpal tunnel syndrome. A condition in which the median nerve, which runs from the forearm into the hand, becomes pressed or squeezed at the wrist by enlarged tendons or ligaments. This causes pain and numbness in the fingers.

Charcot-Marie-Tooth disease. An inherited neurological condition that affects both the motor and sensory nerves. It causes weakness of the foot and lower leg muscles.

Herniated disk disease. This condition occurs when the fibrous cartilage that surrounds the disks of your vertebrae breaks down. The center of each disk, which contains a gelatinous substance, is forced outward. This places pressure on a spinal nerve and causes pain and damage to the nerve.

Chronic inflammatory polyneuropathy and neuropathy. These are conditions resulting from diabetes or alcoholism. Symptoms may include numbness or tingling in a single nerve or many nerves at the same time.

Sciatic nerve problems. There are many causes of sciatic nerve problems. The most common is a bulging or ruptured spinal disk that presses against the roots of the nerve leading to the sciatic nerve. Pain, tingling, or numbness often result.

Nerve conduction studies may also be done to find the cause of symptoms, such as numbness, tingling, and continuous pain.

Other conditions may prompt your healthcare provider to recommend NCV.


EMG and Nerve Conduction Studies in Clinical Practice

Rossitza I. Chichkova, MD, MS and Lara Katzin, MD

The use of nerve conduction studies (NCS) started with the work of Galvani who performed studies on frogs and observed twitching of the muscles with electrical stimulation. In the early 19th century, Fransois Magendie differentiated the anterior and posterior spinal nerve roots in dogs and noticed that electrical stimulation of the former caused movement, while stimulation of the latter resulted in pain. Guilluame B. Duchenne, Carlo Matteucci, and Sarlandiere used needle or percutaneous techniques, but it was not until 1852 when Herman von Helmholz measured nerve conduction velocities in human subjects. In the subsequent years, including World War II, the technical progress and the better understanding of anatomy and the disease processes led to increased use of the electrical testing. Electromyography (EMG) and NCSs became a practical tool with the publications of Weddell, Hodes, Dawson and Scott in the 1940s. 1 Today, the electrodiagnostic tests are a valuable tool in the hands of physicians in the process of diagnosis and management of neuromuscular disorders. Here, we take a look at how and when to use these tests in your practice, as well as technical factors and limitations.

The Test
Electrodiagnostic studies (EDX) are helpful in evaluating weakness, muscle wasting and sensory symptoms. The test may not be able to find the reason for generalized weakness, diffuse pain, or fatigue. Conversely, the more specific the question posed to the examining physician, the more detailed and directed the conclusion can typically be. 2

The routine NCS includes testing of the motor and sensory fibers of the median, ulnar and radial nerves, the motor fibers of the peroneal and tibial, and the sensory fibers of the superficial peroneal and sural nerves. Less frequently, the facial and the accessory nerves are tested. While the typical NCS tests the distal nerve, the late responses, H-reflexes and F-wave latencies, provide information about the proximal segment. 3

In motor NCSs, the nerve is stimulated at least at two points along its course. Supramaximal stimulation ensures the activation of all axons. The active surface electrode is placed on the muscle belly innervated by the nerve while the reference electrode is positioned distally on the tendon. The waveform is called compound muscle action potential (CMAP). The stimulus is delivered at increasing distances from the muscle. Parameters measured include latency from the stimulus artifact to the onset of the negative response, amplitude from the baseline to the negative peak and motor conduction velocities (CV).

The electrodes in sensory NCSs are attached over a sensory or a mixed nerve. The stimulation can be proximal (antidromic) or distal (orthodromic) to the recording electrode. It is more challenging to obtain the sensory nerve action potential (SNAP). Latency, amplitude and sensory CV are usually measured. Stimulation at different sites along the nerve results in change of the waveform and temporal dispersion that is important to recognize. 3,4

Needle EMG is performed by inserting a needle containing a recording electrode into the muscle of interest. The muscle is evaluated at rest. Abnormal spontaneous activity includes fibrillation potentials and positive waves fasciculations, complex repetitive discharges, myotonic and myokimic discharges, and neuromyotonia. The recruitment pattern, the motor unit potential (MUP) duration, shape and amplitude are evaluated with minimal and maximal activation. The number of nerves and muscles tested depends on the suspected underlying condition and is decided on a case-by-case basis. 5-7 Repetitive nerve stimulation (RNS) and single-fiber EMG (SFEMG) are utilized when a neuromuscular junction (NMJ) problem is suspected. SFEMG is not a routine test and is performed in specialized laboratories.

Questions answered
EMG and NCS play a very important role in the evaluation of patients presenting with neuromuscular problems. When used in conjunction with a thorough thorough neurological history and examination, they provide critical information that guides further laboratory testing, medical or surgical management. Furthermore, the EDX should be individualized depending on the findings. NCS and EMG are predominantly used for evaluation of peripheral nervous system, including motor neuron, dorsal root ganglion, root, plexus, nerve, neuromuscular junction and muscle diseases. The studies provide the following important information:

Localization within the neuromuscular system. EDX is helpful to distinguish if the problem is related to a single nerve (mononeuropathy), several nerves (multifocal neuropathy or polyneuropathy), one or more nerve roots (monoradiculopathy or polyradiculopathy), plexus (plexopathy), anterior horn cell (motor neuronopathy) or dorsal root ganglion cell (sensory neuronopathy). Muscle and NMJ diseases are also diagnosed with a good degree of certainty. The exact localization is sometimes difficult to determine clinically. For example, in a patient presenting with a foot drop, the problem could be due to motor neuron disease, lumbo-sacral radiculopathy or peroneal neuropathy. The NCS and needle EMG help in establishing the origin of the problem and guide further evaluation. MRI of the lumbar will not be indicated in a case of peroneal entrapment at the fibular head. On the other hand, absence of entrapment, normal SNAPs and denervation changes in L4-5 root distribution will point to radiculopthy and imaging study will be necessary. Finally, normal SNAPs, decreased or normal CMAP amplitudes and widespread denervation changes will lead diagnosis of motor neuron disease. 4

Fiber type involvement. In neuropathic diseases, EDX gives insight on the affected fiber types, motor, sensory or both. Sensorimotor polyneuropathies are quite common. However, if the study demonstrates only sensory or motor neuropathy, the differential diagnosis becomes more limited. Sensory NCSs are abnormal in lesions of the dorsal root ganglion, plexus or peripheral nerve. They are normal in disorders of the muscle, NMJ, root and motor neuron. Patients with ventral root lesions frequently have subjective sensory symptoms but the sensory nerve studies remain normal, since the dorsal root ganglion remains intact. Patients with small fibers neuropathy have normal sensory nerve studies despite the sensory symptoms that they have. In disorders of the muscle, NMJ, ventral root and the anterior horn cell, the CMAPs are abnormal, while the SNAPs are spared. 4

Underlying pathophysiology. The EDX can determine the type of abnormality, demyelination or axonal loss. The two can co-exist. Criteria for demyelination in the motor nerves include increased distal motor latency, slowing of the CV to less than 80 percent of the normal, conduction block and increased temporal dispersion. The conduction block is a result of a failure to activate the next node of Ranvier. In the sensory nerves, slowing of the CV is consistent with demyelination. The nerve is considered demyelinated if at least one of the above criteria is met. 8 In a focal process, as in carpal tunnel syndrome, the findings are limited only to one nerve. Multiple nerve involvement can be seen in the demyelinating polyneuropathies.

On the other hand, axonal loss causes reduction of the SNAP and CMAP amplitudes, the severity of which depends on the extent of the axonal damage. Mild slowing of the CVs also occurs but it does not reach the decrease seen in the demyelinating cases. The earliest sign of axonal loss on needle examination is decreased recruitment, followed by appearance of fibrillation potentials and positive waves within one to three weeks. Features of reinnervation, large MUPs with high amplitude, appear within several months. 3,8 For determining the type of polyneuropathy, most protocols require testing of the sensory and motor nerves in at least two extremities. The majority of the polyneuropathies are axonal and the differential diagnosis is broad, while the number of primary demyelinating polyneuropathies is very limited. In the acquired demyelinating polyneuropathies, the demyelination is patchy and conduction block is a common finding. A few examples of common demyelinating polyneuropathies for which there are available therapies include chronic inflammatory demyelinating polyneuropathy (CIDP), acute inflammatory demyelinating polyneuropathy (AIDP of Guillaine-Barre syndrome) and multifocal polyneuropathy (MMN). The hereditary types are characterized by uniform changes and can be confirmed by genetic testing.

Severity of the disease and prognosis for recovery. The studies can also measure the severity and prognosis for recovery of the following:

Traumatic nerve injury. EDX provides valuable information about prognosis in traumatic nerve injury. Neuropraxic injury presents with conduction failure without axonal degeneration and carries best prognosis for recovery. Axonotmesis and neurotmesis affect the axon and can not be differentiated during the initial study. Decrease of the CMAP amplitude confirms axonal damage. Needle EMG detects denervation of muscles that do not seem to be clinically affected. However, it may show residual innervation to paralyzed muscles. The optimal time to search for denervation changes is 10 to 14 days after the injury. Follow-up EMG studies may demonstrate early reinnervation with appearance of nascent MUPs that may further increase in amplitude which is accompanied by increase of CMAP amplitudes with continuous improvement Sensory studies are less helpful in evaluating axonal regeneration. Absence of regeneration three to four months after the injury requires surgical exploration. Traumatic root avulsion and brachial plexopathy could be differentiated using EDX. The clinical significance is that the former condition precludes surgical intervention. Normal SNAPs in the presence of dermatomal sensory findings and denervation in myotomal distribution is the strongest evidence that favors root avulsion. Denervation of the paraspinal muscles lacks sensitivity. 9

Facial neuropathy. EDX can estimate the severity and prognosis of patients with facial neuropathy. CMAP amplitude compared to the contralateral side is the best parameter, but there is no reliable technique to evaluate patients in the first 24-48 hours. The optimal time for EDX study is at least five to eight days after onset. Needle EMG has little prognostic value. However, detecting MUPs in a paralyzed muscle is consistent with better prognosis. CMAP latency and blink reflex have not been found useful. 9

Radiculopathy. EMG and NCSs have little prognostic value in radiculopathy when compared to clinical and psychosocial factors. These studies are used mostly in evaluating for presence of a superimposed process such as polyneuropathy.

Mononeuropathy. Focal neuropathies, carpal tunnel syndrome (CTS) and ulnar neuropathy are precisely evaluated with NCS. The severity of CTS is graded based on changes of the sensory and motor potentials, which aids in determining the need for surgery. The NCSs improve with therapeutic interventions for carpal tunnel syndrome, including splinting, steroid injections and surgery. Ulnar neuropathy at the elbow and peroneal neuropathy at the fibular head are also localized with these studies but their correlation with clinical improvement after surgery is less well established. 9-11

Neuropathy. NCSs do not contribute significantly in the prognosis of the axonal polyneuropathies. However, studies have shown a role in evaluating the response to therapy in diabetic polyneuropathy. Similarly, follow-up studies demonstrate recovery from toxic, alcohol-related and nutritional neuropathies. In severe cases of AIDP, axonal damage develops in addition to the demyelination that is the rate limiting factor for recovery. With few exceptions, the distal CMAP amplitude of the peroneal, tibial, median and ulnar nerves has been found to be the most powerful predictor for prognosis.12,13 Use of EDX in prognostication of CIDP is more difficult due to the complexity of the natural course of the disease. The degree of axonal damage determines the prognosis. Improvement of the conduction velocity and CMAP amplitude has been used to demonstrate improvement in clinical trials.9 Secondary axonal loss during the course of severe and long standing focal demyelination is associated with worse prognosis. For instance, compression of the median nerve in the carpal tunnel causes focal demyelination. If prolonged, axonal loss develops that can result in loss of strength and muscle bulk of the thenar muscles and is associated with incomplete or absent recovery.

Neuromuscular junction disorders. SFEMG abnormalities show good correlation with muscle strength in patients with myasthenia gravis (MG). It also provides predictive value for worsening and improvement of the condition. It can be abnormal in patients with no clinical weakness. RNS is much less sensitive and is normal in remission. Abnormal decrement is more likely in generalized than in ocular MG. EDX has most value in management of patients with LEMS by following the response to treatment. SFEMG and CMAP amplitude are of highest importance, followed by percentage of CMAP facilitation and decrement at low-rate RNS. 9

Muscle disease. Small, brief and polyphasic MUPs, as well as fibrillation potentials, positive waves and complex repetitive discharges are frequently seen in patients with inflammatory myopathies. The presence of spontaneous activity is a measure of response to treatment. Fibrillation potentials and positive waves are found in other myopathies associated with muscle fiber necrosis. In patients with inflammatory myopathies treated with steroids, detecting fibrillation potentials and positive waves in weak muscles means that the disease is not adequately treated, while absence of such activity indicates that the steroid dose should be reduced. In patients with inflammatory myopathies, the abnormal EMG in weak muscle serves as a guide for a good muscle biopsy site. It is important to remember that a muscle that is recently studied by a needle EMG should not be used for biopsy, since the changes can mimic myositis. 9,14

Instead, the contralateral muscle could be subjected to biopsy because of the disease symmetry. The availability of genetic testing has replaced to a great extent the use of needle EMG in the diagnosis of the hereditary muscle disorders. Critical illness myopathy presents with variable degree of reduction of the CMAPs. The EMG changes do not always correlate with the degree of weakness and the prognosis. 15

Motor neuron disease. EDX contributes to the identification of the lower motor neuron involvement in amyotrophic lateral sclerosis (ALS), sometimes even before the clinical manifestation. One of the primary findings is decreased recruitment. Asynchronous firing results in increase in polyphasic MUPs. The most reliable abnormality is the fibrillation potentials and positive waves. Their abundance does not correlate with disease progression. The presence of increased in amplitude and duration MUPs is an indicator for collateral sprouting and reinnervation. The irritability of the lower motor neuron manifests with appearance of fasciculations that are not specific for ALS. For definite diagnosis, decreased recruitment, fibrillation potentials and large MUPs have to be identified in at least three levels of the neuraxis (bulbar, cervical, thoracic or lumbar). Clinically weak muscles, innervated by different roots and peripheral nerves must be selected. NCSs are important to exclude mimickers of ALS, such as MMN, radiculopathy, mononeuropathy, polyneuropathy and others. ALS patients have normal sensory studies unless there is an underlying problem. Another typical finding that correlates with the prognosis but lacks sensitivity is the decrease of the CMAP amplitude. The time to death is best judged based on a combination of clinical and EMG findings. 4,16 Motor unit number estimation (MUNE) has value in following the disease progression since it measures more objectively the number of the remaining anterior horn cells. However, its use is limited to specialized laboratories. 9

Temporal Course of Disease
EDX studies provide information on the course of the nerve disease that can be hyperacute (one week), acute (a few weeks), subacute (a few weeks to a few months) or chronic (months to years). The decision on the timing of the lesion requires careful analysis of the history and the findings on the examination. Studies on transected nerves demonstrate that it usually takes between three to five days for the Wallerian degeneration to result in a drop of the CMAP with maximum decrease at around day seven and nine. Lower amplitudes of the SNAP may first be seen between day five and seven with maximal decrease at days 10 to 11. 17 Decrease of the CMAP amplitudes is an early sign of axonal injury but EMG has a greater role in testing muscles that can not be evaluated by NCS. 9 The earliest sign is decreased recruitment. Fibrillation potentials start developing within days after the injury with a best yield achieved two to three weeks post injury. Therefore, the ideal time to perform EDX is after day 10. But if GBS is suspected, the study should not be postponed.

Important Considerations
The EDX must be done in conjunction with a careful neurological history and examination. The study should be tailored depending on the differential diagnostic possibilities. When the examination and the EDX findings are conflicting, the examiner should re-evaluate the patient and consider the possibility of a technical problem. For instance, if a patient has normal sensory examination and Achilles tendon reflexes, the absent H-reflexes should raise a question about a technical factor. 4,7

The patient needs to be informed about the nature of the test. Many fear the study based on rumors that the study is very painful and difficult to tolerate. Others ask if pain medication are needed prior to the testing. In reality, there is discomfort with the electrical stimulation and pain with needle examination. 2

Pain could be a significant limiting factor. In our own and other investigators' experience, caring approach, explaining the procedure and distracting the patient during the procedure are important determinants of pain perception. 18 Pain medications are not recommended prior to the test. Age, gender, primary symptoms, previous EMG and time of the needle within the muscle are not related to the level of discomfort. Some studies find no relation between needle types. 19 Others demonstrate that monopolar needles are associated with less pain, but using concentric needle with small movement technique leads to similar result. 18 If the patient still has trouble tolerating the procedure, the examiner should start with the area of greatest interest. 4 Starting with testing of the sensory nerves could be preferable, since they require lower electrical stimulus. The patients are more likely to tolerate higher stimulation to achieve a supramaximal response or multiple redirections of the needle during EMG when they understand the reason for it.

Technical Factors
Physiologic factors. The most important physiologic factor is the temperature. The effect of the skin temperature on the CV and distal latency is well documented. 20-25 Optimally, the room should have a local temperature control. The temperature of the extremities is monitored with a probe. The general rule is that the hand temperature should be >33°C and that of the foot >31°C. If suboptimal, the extremities have to be warmed up using heating pads, a lamp, or warm water. The examiner must know that with every 1°C drop of the temperature, the motor and sensory CV decreases between 1.5 and 2.5 m/s, and the distal latency becomes prolonged by 0.2 ms. In addition, the amplitude of the SNAP and CMAP may increase. When the temperature is suboptimal, the MUPs become polyphasic, with longer duration and higher amplitudes. Slowing of the nerve CVs in a person with cold extremities may lead to wrong diagnosis of peripheral neuropathy and unnecessary testing. Other physiological factors that need attention are age, height and anomalous innervation. Edema, skin lesions, and obesity are limiting factors in performing a successful EDX study. 4

Non-physiological factors. It is imperative to understand the need for supramaximal stimulation when performing NCSs. Limb positioning with obtaining measurements is of importance too, particularly in the case of the ulnar nerve where the elbow must be flexed from 70-90°. This position provides the best correlation between the surface measurement and the length of the nerve. 11,25,26 Proper placement of electrodes, correct measurements, and using appropriate distance between the active and reference electrodes are a few of the other non-physiological factors. The electromyographer should be able to recognize artifacts. 27,28,29 Common errors are submaximal stimulation and improper placement of the electrodes, which may result in lower amplitudes of the nerve potentials leading to an incorrect assumption that the patient has axonal loss. Submaximal stimulation of deeply located nerves—for example, ulnar nerve below the elbow— may give an erroneous impression of a conduction block. On another hand, high stimulus may co-stimulate neighboring nerves. This phenomenon is difficult to avoid with proximal stimulation in the axilla. The examiner has to observe the shape, amplitude, and latency of the responses that should not change significantly. Ambient noise can be an obstacle in obtaining sensory responses, particularly in the ICU.7 Failure to recognize technical factors of errors could lead to unnecessary testing, treatment and even surgery.

Bleeding Complication
Although rare, bleeding is a potential complication with needle EMG. Since this is an invasive procedure, the risk theoretically increases with the use of anticoagulation, antiplateletes, NSAIDs, and herbals with mild anticoagulation properties (e.g. Ginko biloba, Ginseng, Saw Palmetto, and others). Thrombocytopenia below 50,000/mm 3 , platelet dysfunction, and coagulopathies are related to higher risk for bleeding. The risk exists even in absence of anticoagulation. There are no guidelines to help the clinician handle patients with increased risk of bleeding. This may result in avoiding the procedure and cause delay in diagnosis.

There is a consensus that antiplatelet therapy is not associated with increased risk for hemorrhagic complications. Therefore, physicians are not required to stop antiplatelets prior to needle examination. Moreover, withholding antiplatelet therapy may increase the risk for cardiovascular and cerebrovascular events. Bleeding complications are low even in patients on anticoagulation. Studies do not demonstrate increased risk for clinically significant hematomas. The incidence of subclinical hematoma is very low, around 1.45 percent. There is no statistically significant increased rate of bleeding in patients with anticoagulation or antiplatelet therapy.

The electromyographer must use caution when performing needle examination on anticoagulated patients by using a smaller gauge needle and applying pressure for a longer period of time. It is better to avoid aggressive needle examination and deeper muscle testing particularly when hematoma can compress important structures. There is no recommended cut off INR for performing the needle examination. Some laboratories are comfortable with EMG of all patients with INR less or equal to 3.0, while patients with a higher INR are tested at the discretion of the electromyographer. The risks and benefits have to be weighed on a case-by-case basis when testing of anticoagulated patients. 30-32

Limitations
The EDX studies are normal in patients with small fiber peripheral neuropathy who present with burning pain and hypersensitivity. The study may not be revealing in some types of myopathy. As discussed above, the changes that occur with acute nerve injury take some time to develop. Therefore, the study may be negative if done very early and should be repeated if needed. In addition, EMG and NCSs are unlikely to be helpful in patients with generalized weakness, diffuse pain, or fatigue.

Conclusions
EMG and NCSs are valuable tools in the armamentarium of the physician dealing with patients with neuromuscular disorders. The test cannot be used in isolation and should be performed after a careful clinical examination. The clinical hypothesis determines the extent of the study performed and is tailored for each individual patient. Important information regarding localization, underlying pathophysiology, severity, temporal course and prognosis can be obtained. Further testing and treatment is provided depending on the underlying problem. The test has some limitations. If the EDX results and the clinical findings do not make sense, the patient has to be re-examined and technical factors must considered.

Rossitza I. Chichkova, MD is an Assistant Professor in Neurology at the University of South Florida, Tampa and Chief of Department of Neurology and a Director of EMG Lab at Tampa General Hospital. Dr. Chichkova is a Neurology Clerkship Director and Vice Chair in Education of the USF Department of Neurology.

Lara Katzin, MD is an Assistant Professor in Neurology at the University of South Florida, Tampa.


Results

A total of 1248 patients were invited to take part in the study, of whom 908 (73%) completed questionnaires – 298 men and 610 women with mean age 47.1 years, median 48.0 years and inter-quartile range 39.8 to 55.1 years. These patients provided information on 1816 hands, but 10 hands were excluded from analysis because of previous surgery for CTS (Figure  2 ).

Recruitment of patients and numbers of hands analysed.

Among the remaining 1806 hands, 1571 (87%) provided satisfactory measurements of SNC for the index finger, 1302 (72%) for the middle finger, and 1627 (90%) for the little finger. For each digit, the distribution of SNC velocities was approximately normal. The three measures of SNC velocity investigated were all highly correlated, with a particularly close relation between SNC velocity in the index and middle fingers (r = 0.97). In subsequent analyses, the difference in SNC velocities between the little and index fingers was adopted as the preferred continuous measure of median nerve function since it provided control for possible residual effects of variation in hand temperature, and because data were more complete for the index than the middle finger.

Table  1 summarises the distribution of numbness/tingling and pain in the 1806 hands that were analysed. Most hands (1459) had been affected by numbness or tingling in the month before completing the questionnaire, but fewer (893) had been painful. Most often, numbness/tingling was reported in all three of the median, part-median and non-median regions (including 787 hands with extensive median involvement and 286 with limited median involvement). In contrast, limitation of numbness and tingling to the median and/or part-median regions with no involvement of the non-median regions was much less common (216 hands). On the basis of this analysis, the observed patterns of symptoms were assigned to groups (eight for numbness/tingling and five for pain) in a way that ensured adequate numbers of hands in each group (where a symptom distribution occurred in only a few hands, it was aggregated with another similar distribution). The definition of these groups is indicated in Table  1 .

Table 1

Distribution of sensory symptoms in hand and definition of symptom groups

Affected regions of handNumbness or tinglingPain
MedianPart-medianNon-medianNumber of handsGroupNumber of handsGroup
No No No 347 0 913 0
No No Yes 31 1 91 1
No Yes No 11 2 53 2
No Yes Yes 126 2 127 2
Limited No No 32 3 12 3
Limited No Yes 11 4 26 3
Limited Yes No 63 5 65 3
Limited Yes Yes 286 4 215 3
Extensive No No 14 7 1 4
Extensive No Yes 2 6 1 4
Extensive Yes No 96 7 23 4
ExtensiveYesYes78762794

Table  2 shows differences in SNC velocities between the little and index fingers (mean and standard deviation) for different distributions of symptoms, and according to findings on physical examination of the hand. Data on physical examination (Tinel’s and Phalen’s tests, thumb weakness) were missing for 235 hands because the patient attended hospital on a day when the research nurse was unavailable, and were incomplete for a few further hands. Differences in SNC velocity were higher in hands classed to Groups 6 and 7 for numbness/tingling (i.e. those with extensive median involvement). Positive Tinel’s and Phalen’s tests were also associated with impaired median nerve conduction, but there was no clear relation of median nerve conduction to pain or to thumb weakness. When associations with clinical findings were mutually adjusted in a multiple linear regression analysis, the associations with Groups 6 and 7 for numbness/tingling, and with positive Tinel’s or Phalen’s tests were all statistically significant (Table  2 ).

Table 2

Relation of clinical findings to difference in sensory nerve conduction velocity between little and index finger

Clinical findingNumber of handsNumber of hands with nerve conduction measurementsMean (SD) difference in nerve conduction velocity (m/s)Linear regression analysis
    Regression coefficient a95% CI
Numbness/ tingling group         
0 347 221 6.4 (7.4) Baseline -
1 31 31 4.0 (5.9) 𢄠.9 𢄣.8 to 2.1
2 137 128 6.4 (9.7) 0.2 𢄡.5 to 2.0
3 32 27 3.4 (6.0) 𢄡.7 𢄤.7 to 1.3
4 297 272 7.6 (9.6) 0.8 𢄠.6 to 2.2
5 63 55 6.4 (8.2) 1.3 𢄠.9 to 3.5
6 789 708 10.1 (9.4) 2.8 1.5 to 4.0
7 110 100 12.0 (10.3) 3.7 1.8 to 5.6
Pain group         
0 913 731 8.8 (9.3) Baseline -
1 91 83 5.8 (9.1) 𢄠.3 𢄢.2 to 1.6
2 180 172 8.0 (9.0) 0.2 𢄡.2 to 1.5
3 318 291 8.4 (9.4) 𢄠.7 𢄡.9 to 0.5
4 304 265 9.4 (9.5) 0.2 𢄡.1 to 1.5
Tinel’s test         
Negative 1110 949 7.2 (8.7) Baseline -
Positive 451 395 12.4 (9.7) 2.5 1.6 to 3.5
Missing 245 198 7.9 (9.5) 𢄡.6 𢄦.2 to 2.9
Phalen’s test         
Negative 696 574 5.2 (7.7) Baseline -
Positive 865 771 11.2 (9.6) 3.3 2.3 to 4.3
Missing 245 197 8.0 (9.5) 3.9 𢄢.2 to 9.9
Thumb weakness b         
Negative 1403 1218 8.6 (9.2) Baseline -
Positive 162 132 9.2 (10.0) 𢄠.7 𢄢.1 to 0.7
Missing2411928.1 (9.5)𢄠.4𢄧.3 to 6.4

a Adjusted for sex, age and other variables in table.

b Weakness of abduction or opposition.

We next examined nerve conduction velocities for combinations of symptoms and signs which the multiple regression analysis had indicated were most predictive of abnormality. For this purpose, distributions of numbness and tingling were further aggregated as shown in Table  3 . In hands with no numbness or tingling and negative on both Tinel’s and Phalen’s test, the mean difference in SNC velocity between the little and index finger was 5.0 m/s. Relative to this value, differences in SNC velocities were materially increased only when Tinel’s or Phalen’s test was positive, the highest difference in velocities being found in hands with extensive median numbness/tingling and both Tinel’s and Phalen’s tests positive (mean difference 13.8, 95% confidence interval (CI) 12.6 to 15.0 m/s).

Table 3

Difference between sensory nerve conduction velocities in the little and index fingers according to combinations of clinical findings

Numbness/tingling group aTinel’s testPhalen’s testNumber of handsAggregate categoryNumber of hands with nerve conduction measurementsMean (95% CI) difference between SNC b velocities in the little and index fingers (m/s)
0 Negative Negative 232 A 144 5.0 (3.9 to 6.1)
0 Negative Positive 40 B 51 9.7 (7.7 to 11.8)
0 Positive Negative 8 B
0 Positive Positive 18 B
1, 2 Negative Negative 76 C 75 3.6 (1.9 to 5.3)
1, 2 Negative Positive 40 D 60 8.9 (6.3 to 11.5)
1, 2 Positive Negative 2 D
1, 2 Positive Positive 22 D
3-5 Negative Negative 137 E 127 3.3 (2.1 to 4.5)
3-5 Negative Positive 106 F 106 8.7 (6.9 to 10.5)
3-5 Positive Negative 9 F
3-5 Positive Positive 85 G 72 10.6 (8.4 to 12.9)
6-7 Negative Negative 195 H 177 6.6 (5.3 to 7.8)
6-7 Negative Positive 275 I 282 10.6 (9.5 to 11.6)
6-7 Positive Negative 32 I
6-7PositivePositive274J24113.8 (12.6 to 15.0)

a For definitions of groups see Table  1 .

b Sensory nerve conduction.

To derive a cut-point for abnormality of the difference in SNC velocities between the little and index fingers that might be used in epidemiological studies, we compared the distribution of measurements in hands which had extensive median numbness/tingling and were positive on both Tinel’s and Phalen’s tests, with that in hands which had no numbness or tingling and were negative on both tests. For this analysis we used a 50% random subset (n=193) of the hands that met these clinical criteria. As illustrated in Figure  3 , there was overlap between the two distributions, a number of clinically positive hands having differences in SNC velocities less than 5 m/s. However, the modal values were distinct, and a value of 8 m/s appeared to discriminate between the two sets of hands reasonably well. When this cut-point was applied in the other random 50% of hands, the prevalence of abnormality (i.e. difference in SNC velocity > 8 m/s) was 25% in hands with no numbness/tingling and negative on Tinel’s and Phalen’s tests, and 67% in those that exhibited all three of these clinical features.

Distributions of differences in sensory nerve conduction velocity between the little and index fingers in a random 50% sample (N=193) of hands a) with no numbness/tingling and negative for Tinel’s and Phalen’s tests ("negative" hands) or b) positive for all three of these clinical features ("positive" hands). The vertical red line indicates the proposed cut-point for abnormality of sensory nerve conduction.

In addition to the hands with measured SNC velocities that were included in the above analyses, there were 84 hands in which no signal could be detected when the index finger was tested, indicating extreme impairment of conduction. They included one hand with no numbness/tingling and negative on both Tinel’s and Phalen’s tests, and 26 with extensive median numbness/tingling and positive on both tests. When a random 50% of these 27 hands were added to the group with differences in SNC velocity > 8 m/s, the prevalence of abnormality in hands with no symptoms or signs became 26%, while that in hands with all three clinical features increased to 70%. Furthermore, when abnormality was defined in the same way for the full sample of hands, the prevalence of abnormality in hands with numbness/tingling but negative on both Tinel’s and Phalen’s tests (aggregate categories C, E and H in Table  3 ) was 25% as compared with 32% in hands with no numbness or tingling (aggregate categories A and B in Table  3 ).

To check the robustness of our findings, we repeated the analyses for Tables  2 and ​ and3 3 using as alternative measures of median nerve function: a) distal motor latency and b) sensory nerve amplitude in the index finger. Results were generally consistent. In particular, there was no increase in geometric mean distal motor latency or reduction in geometric mean sensory nerve amplitude when both Tinel’s and Phalen’s tests were negative.


Nerve Conduction Studies

Stimulate and record signals from nerves in-vivo or in-vitro using the built-in software averaging mode, it’s possible to record signals from in-vivo nerves using skin surface electrodes only. Surface electrodes can also be used for peripheral nerve stimulation (PNS) and to evaluate the effects of stimulation to motor nerve endings in terms of electrical or mechanical response. Configure stimulation sources to provide electrical, somatosensory or visual stimulation, and vary the duration and level of stimulus. In addition to the stimulator, up to 16 amplifiers can be simultaneously employed to record nerve and/or muscle responses. The system software permits easy determination of peak times and maximum responses for a variety of nerve conduction studies (NCS) and nerve conduction velocity tests (NCV).

Use the AcqKnowledge ® stacked plot mode to overlap both the stimulus waveform and the response. The software allows you to advance through each of the responses and the software highlights the response and specific stimulus waveform to make it easier to determine which response relates to each stimulus waveform.


Specific nerve conduction study techniques

Motor nerve conduction studies

Motor studies are performed by electrical stimulation of a nerve and recording the compound muscle action potential (CMAP) from surface electrodes overlying a muscle supplied by that nerve.

The recording electrodes are performed using adhesive conductive pads placed onto the skin overlying the target muscle. The active electrode is placed over the muscle belly and the reference over an electrically inactive site (usually the muscle tendon). A ground electrode is also placed somewhere between the stimulating and recording electrodes providing a zero voltage reference point. The median motor study might involve stimulation at the wrist, the elbow, and less frequently the axilla and the brachial plexus (Figure 1A,B).

The compound muscle action potential (CMAP) is a summated voltage response from the individual muscle fibre action potentials. The shortest latency of the CMAP is the time from stimulus artefact to onset of the response and is a biphasic response with an initial upward deflection followed by a smaller downward deflection. The CMAP amplitude is measured from baseline to negative peak (the neurophysiological convention is that negative voltage is demonstrated by an upward deflection) and measured in millivolts (mV) (Figure 1C).

To record the CMAP, the stimulating current or voltage is gradually increased until a point is reached where an increase in stimulus produces no increment in CMAP amplitude. It is only at this (supramaximal) point that reproducible values for CMAP amplitude and the latency between the stimulus and the onset of the CMAP can be recorded accurately.

The nerve is then stimulated at a more proximal site—in the median nerve this will be the antecubital fossa, close to the biceps tendon. In the normal state stimulating the median nerve at the wrist and the elbow results in two CMAPs of similar shape and amplitude because the same motor axons innervate the muscle fibres making up the response. However, the latency will be greater for elbow stimulation compared with wrist stimulation because of the longer distance between the stimulating and recording electrodes (Figure 1B). The difference in latency represents the time taken for the fastest nerve fibers to conduct between the two stimulation points as all other factors involving neuromuscular transmission and muscle activation are common to both stimulation sites. If one measures the distance between the two sites then the fastest motor nerve conduction velocity can be calculated as follows: FMNCV (m/s) = distance between stimulation site 1 and site 2 (mm)/[latency site 2 – latency site 1 (ms)].

Figure 1. Motor nerve conduction study

Footnote: (A, B). Median motor nerve conduction study. Active recording electrode is over the APB muscle, with stimulation at the wrist, elbow, axilla, and brachial plexus. Panel B shows the motor response from stimulation at all four sites. Responses are of the same shape but the latency is longer with more proximal stimulation. (C) The compound muscle action potential (CMAP) and its parameters.

Sensory nerve conduction studies

The sensory nerve action potential (SNAP) is obtained by electrically stimulating sensory fibers and recording the nerve action potential at a point further along that nerve. Once again the stimulus must be supramaximal.

Recording the sensory nerve action potential (SNAP) orthodromically refers to distal nerve stimulation and recording more proximally (the direction in which physiological sensory conduction occurs). Antidromic testing is the reverse. Different laboratories prefer antidromic or orthodromic methods for testing different nerves. An orthodromic median sensory study is shown in Figure 2. The sensory latency and the peak to peak amplitude of the SNAP are measured. The velocity correlates directly with the sensory latency and therefore either the result may be expressed as a latency over a standard distance or a velocity.

Only the 20% largest diameter and fastest conducting sensory fibres are tested using conventional sensory studies functionally supplying fine touch, vibration, and position sense. Predominantly small fibre neuropathies affecting the other 80% of fibres exist usually with prominent symptoms of pain and conventional sensory studies may be normal. In such cases quantitative sensory testing and autonomic testing will be required, which are beyond the scope of this article (see Interpretation pitfalls).

Figure 2. Sensory nerve conduction study

Footnote: Median orthodromic sensory study. The index finger digital nerves are stimulated via ring electrodes and the response recorded over the median nerve at the wrist.

F waves

F waves (F for foot where they were first described) are a type of late motor response. When a motor nerve axon is electrically stimulated at any point an action potential is propagated in both directions away from the initial stimulation site. The distally propagated impulse gives rise to the CMAP. However, an impulse also conducts proximally to the anterior horn cell, depolarising the axon hillock and causing the axon to backfire. This leads to a small additional muscle depolarisation (F wave) at a longer latency. Only about 2% of axons backfire with each stimulus. Unlike the M response (Figure 3), F waves vary in latency and shape because different populations of neurones normally backfire with each stimulus. The most reliable measure of the F wave is the minimum latency of 10–20 firings.

F waves allow testing of proximal segments of nerves that would otherwise be inaccessible to routine nerve conduction studies. F waves test long lengths of nerves whereas motor studies test shorter segments. Therefore F wave abnormalities can be a sensitive indicator of peripheral nerve pathology, particularly if sited proximally. The F wave ratio which compares the conduction in the proximal half of the total pathway with the distal may be used to determine the site of conduction slowing—for example, to distinguish a root lesion from a patient with a distal generalised neuropathy.

Figure 3. F waves

Footnote: Schematic representation of the early M response from the distally propagated action potential and the later F wave from the proximally propagated action potential. The latter depolarizes the axon hillock causing it to backfire. Actual F wave responses are shown in the lower trace. F waves vary in latency and shape due to different populations of axons backfiring each time.

Errors

The main sources of non-biological error in nerve conduction study measurements are the identification and measurement of waveform onset and the measurement of the length of the nerve segment on the limb. Calculations have shown that in a nerve with a conduction velocity of 50 m/s, the 2×SD experimental error for velocity is 14 m/s over 10 cm and 4.7 m/s over 25 cm. Of the error, time measurement is 92.3% and distance 7.7%, so the use of the measuring tape is quite adequate in conventional nerve conduction study.


Most often, abnormal results are due to nerve damage or destruction, including:

  • Axonopathy (damage to the long portion of the nerve cell)
  • Conduction block (the impulse is blocked somewhere along the nerve pathway)
  • Demyelination (damage and loss of the fatty insulation surrounding the nerve cell)

The nerve damage or destruction may be due to many different conditions, including:

  • Alcoholic neuropathy
  • Diabetic neuropathy
  • Nerve effects of uremia (from kidney failure)
  • Traumatic injury to a nerve
  • Guillain-Barré syndrome
  • Diphtheria
  • Carpal tunnel syndrome
  • Brachial plexopathy
  • Charcot-Marie-Tooth disease (hereditary)
  • Chronic inflammatory polyneuropathy
  • Common peroneal nerve dysfunction
  • Distal median nerve dysfunction
  • Femoral nerve dysfunction
  • Friedreich ataxia
  • General paresis
  • Mononeuritis multiplex (multiple mononeuropathies)
  • Primary amyloidosis
  • Radial nerve dysfunction
  • Sciatic nerve dysfunction
  • Secondary systemic amyloidosis
  • Sensorimotor polyneuropathy
  • Tibial nerve dysfunction
  • Ulnar nerve dysfunction

Any peripheral neuropathy can cause abnormal results. Damage to the spinal cord and disk herniation (herniated nucleus pulposus) with nerve root compression can also cause abnormal results.


Effect of angiotensin-converting-enzyme (ACE) inhibitor trandolapril on human diabetic neuropathy: randomised double-blind controlled trial

Background: Diabetes is a common cause of polyneuropathy. The development and progression of nephropathy, retinopathy, and neuropathy are closely related. Angiotensin-converting enzyme (ACE) inhibitors delay progression of both nephropathy and retinopathy. We investigated the effect of ACE inhibition on diabetic neuropathy.

Methods: We recruited 41 normotensive patients with type I or type II diabetes and mild neuropathy into a randomised double-blind placebo-controlled trial. Changes in the neuropathy symptom and deficit scores, vibration-perception threshold, peripheral-nerve electrophysiology, and cardiovascular autonomic function, were assessed at 6 and 12 months. The primary endpoint was the change in peroneal nerve motor conduction velocity.

Findings: We found no significant difference at baseline for age, HbA1c, blood pressure, or severity of neuropathy between two groups. There was no change in HbA1c over the treatment period. Peroneal motor nerve conduction velocity (p=0.03) and M-wave amplitude (p=0.03) increased, and the F-wave latency (p=0.03) decreased and sural nerve action potential amplitude increased (p=0.04) significantly after 12 months of treatment with trandolapril compared with placebo. Vibration-perception threshold, autonomic function, and the neuropathy symptom and deficit score showed no improvement in either group.

Interpretation: The ACE inhibitor trandolapril may improve peripheral neuropathy in normotensive patients with diabetes. Larger clinical trials are needed to confirm these data before changes to clinical practice can be advocated.


Introduction

Nerve conduction study is a simple and reliable test for evaluation of peripheral nerve function. The test is not invasive. In this technique nerve conduction in the largest and fastest myelinated fibers are recorded and it establishes the type and degree of abnormality. The site of lesion can be identified and localized[1]. This technique can be used for evaluation of conductive velocity in upper extremity, mostly the median and ulnar nerves and in the lower extremity including the peroneal, tibial, and sural nerves. NCS is a test commonly used to evaluate the function of the motor and sensory nerves of the human body. Nerve conduction studies are used mainly for evaluation of paresthesia (numbness, tingling, burning) and/or weakness of the arms and legs [1]. The type of study required is dependent in part, by the symptoms presented. Some indications of nerve conduction studies are:

a.Symptoms indicative of nerve damage as numbness, weakness.

b.Differentiation between local or diffuse disease process (mononeuropathy or polyneuropathy).

c.Get prognostic information on the type and extent of nerve injury [2].

Conduction velocity is the speed at which motor and sensory impulses traverse a given segment of nerve (meter/sec). This technique commonly deals with motor conduction studies (MCS), sensory conduction studies and late responses [3]. Motor conduction studies are technically less demanding than sensory and mixed nerve studies thus they usually are performed first [4]. Motor responses typically are in the range of several millivolts (mV), as opposed to sensory and mixed nerve responses, which are in the microvolt (mcV) range. Thus, motor responses are less affected by electrical noise and other technical factors. This technique also, represents the conduction of an impulse along peripheral motor nerve fibers. In motor nerve conduction, the nerve is stimulated supramaximal by means of surface electrode placed over the nerve where it is relatively superficial, with the cathode is closer to recording electrode [5]. Needle stimulating electrode is used in deep nerves as sciatic nerve. Recording from one muscle supplied by this nerve distal to site of stimulation using surface electrodes:

a.Active electrode over muscle belly and

b.Reference electrode over muscle tendon.

Motor conduction velocity decreased in lesions affecting the axon of peripheral nerve esp. in diseases affecting myelin sheath than those affecting axoplasm. It should be noted that striking reduction occurs in infectious polyneuritis and Charcot Marie- Tooth disease [6]. Motor conduction studies measure compound muscle action potential (CMAP) and motor nerve conduction velocity. Stimulation of any peripheral nerve evokes an electrical and mechanical response in those muscles innervated by the nerve distal to site of stimulation. The electrical response is called CMAP or M- wave. Compound term represents the summation of all underlying individual muscle fiber action potentials and is a biphasic potential with an initial negativity, or upward deflection from the baseline. In fact, the size of the response called the amplitude and measured in millivolts (mv). It corresponds to the integrity of the motor unit but cannot distinguish between pre- and postganglionic lesions because the cell body is located in the spinal cord [6]. Compound muscle action potential (CMAP) comprises of latency, amplitude, duration, and area of the CMAP (Figure 1).

Figure 1: Compound muscle action potential (CMAP) comprises of latency, amplitude, duration, and area of the CMAP.

The latency (ms) is defined as the time from the stimulus to the initial CMAP deflection from baseline and measured in milliseconds (ms). Motor latency includes several unmeasurable events.

I.Utilization time (time required to produce rheobasic stim).

These events are eliminated when 2-point stimulation Study is used. In some nerve segments where only one site can be stimulated for reasons of anatomical inaccessibility, latency measurement must replace conductive velocity. Latency varies directly with the distance of stimulating electrode from muscle. Latency represents three separate processes:

a.The nerve conduction time from the stimulus site to the neuromuscular junction (NMJ)

b.The time delay across the NMJ

c.The depolarization time across the muscle [2].

CMAP amplitude is most commonly measured from baseline to the negative peak (base line-to-peak) and less commonly from the first negative peak to the next positive peak (peak-to-peak). Also, amplitude is the height in millivolts from baseline to the peak of negative deflection. Amplitude is normally decreased with proximal stimulation. Amplitude is normally constant in size on repeated stimulation. And is directly proportional to number of muscle fibers depolarized. Low CMAP amplitudes most often result from loss of axons (as in a typical axonal neuropathy), conduction block. Causes of low CMAP are including:

b.Demyelation with conduction block

c.Presynaptic NMJ disorder

CMAP duration usually is measured from the initial deflection from baseline to the first baseline crossing (i.e., negative peak duration), but it also can be measured from the initial to the terminal deflection back to baseline (Figure 2). The former is preferred as the terminal CMAP returns to baseline very slowly and can be difficult to mark precisely. Duration is primarily a measure of synchrony (i.e., the extent to which each of the individual muscle fibers fire at the same time). In other words, it is the time required for action potential in the fast conducting fibers to reach nerve. For example, when muscle fibers are discharged in near synchrony, it means shorter duration of action potential. If conduction velocities vary widely among different axons. The neurophysiologist concludes that some muscle fibers are activated earlier than others or longer duration of CMAP. Duration increased in demyelinating disease. CMAP area is a function of both the amplitude and duration of the waveform. CMAP area also is conventionally measured between the baseline and the negative peak. Differences in CMAP area between distal and proximal stimulation sites take on special significance in the determination of conduction block from a demyelinating lesion. The normal configuration of CMAP is in two forms.

Figure 2: Compound muscle action potential (CMAP).

A.G1 over end plate region of stimulated muscle and it is biphasic, negative and positive.

B.G2 not over end plate region of stimulated muscle and it is triphasic with initial positivity. Normally only minimal changes in configuration at proximal sites of stimulation are seen. If an initial positive deflection exists, it may be due to:

a.Inappropriate placement of the active electrode from the motor point

b.Volume conduction from other muscles or nerves

c.Anomalous innervations [6].

Figure 3: Sensory nerve action potential (SNAP)-sum of all the individual sensory fibers that depolarize.

Motor nerve conduction velocity measures the speed of the fastest conducting motor axons. Conduction velocity (m/s) calculated as: distance between the proximal and distal stimulation sites divided by proximal latency - distal latency [7]. Setting for sensory conduction studies are as follows. Sensitivity: 10-20mcv/ division sweep: 20ms, current: 5-30mA (50-300V). Sensory fibers usually have a lower threshold to stimulate than do motor ftbers. As in motor studies, the current is slowly increased from a baseline of 0 mA, usually in 3- to 5-mA increments, until the recorded sensory potential is maximized. Sensory conduction studies comprise of sensory nerve action potential (SNAP) and sensory nerve conduction velocity [7]. Sensory nerve action potential (SNAP), is a compound potential that represents the summation of all the individual sensory fiber action potentials. SNAPs usually are biphasic or triphasic potentials. For SNAP, onset latency, peak latency, duration, and amplitude are measured [8] (Figure 3). Onset latency is the time from the stimulus to the first deflection from baseline and represents nerve conduction time from the stimulus site to the recording electrodes for the largest cutaneous sensory fibers, so used to calculate conduction velocity. This NCS represents the conduction of an impulse along the sensory nerve fibers. It is performed by electrical stimulation of a peripheral nerve and recording from a purely sensory portion of the nerve, such as on a finger. Peak Latency is measured at the midpoint of the first negative peak. In this factor, interobserver variation is less. For sensory conduction studies, a pair of recording electrodes (GI and G2) are placed in line over the nerve at an interelectrode distance of 3 to 4 cm, with the active electrode (G I) placed closest to the stimulator. Recording ring electrodes are conventionally used to test the sensory nerves in the fingers [2,9]. Onset latency is the time required for an electrical stimulus to initiate an evoked potential. Onset latencies reflect conduction along the fastest nerve fibers [10]. Peak latency in SNAP : it represents the latency along the majority of the axons and is measured at the peak of the waveform amplitude (first negative peak) [11]. Both latencies are primarily dependent on the myelination of a nerve. Peak latency can be ascertained in a straightforward manner. Some potentials, especially small ones, it may be difficult to determine the precise point of deflection from baseline. Peak latency cannot be used to calculate a conduction velocity [7]. SNAP amplitude -sum of all the individual sensory fibers that depolarize. Low SNAP amplitudes indicate a definite disorder of peripheral nerve. Conduction velocity-Only one stimulation site is required to calculate a sensory conduction velocity [11]. SNAP duration usually is measured from the onset of the potential to the first baseline crossing (i.e., negative peak duration). Like the motor studies, sensory latencies are on the scale of milliseconds (ms) [11]. The SNAP duration typically is much shorter than the CMAP duration (typically 1.5ms vs 5-6ms). The SNAP amplitude is most commonly measured from baseline to negative peak. Like the motor studies, sensory latencies are on the scale of milliseconds (ms). Low SNAP amplitudes indicate a definite disorder of peripheral nerve. Sensory conduction velocity represents the speed of the fastest, myelinated cutaneous sensory fibers and can be determined with one stimulation, simply by dividing the distance traveled by the onset latency [12]. It can also be useful in localizing a lesion in relation to the dorsal root ganglion (DRG). It can be abnormal with normal SNAPs if the lesion is proximal to the DRG or affecting a purely motor nerve. The DRG is located in the neural foramen and contains the sensory cell body. Lesions proximal to it (root, spinal cord) preserve the SNAP despite clinical sensory abnormalities. This is because axonal transport from the cell body to the axon continues to remain intact [13]. SNAPs are typically considered more sensitive than CMAPs in the detection of an incomplete peripheral nerve injury. The active and reference pickup should not be too close together. If this occurs, similar waveforms are recorded at both sites and rejected, dropping the amplitude of the waveform (Figures 4 & 5).

Figure 4: Compound Motor Action Potential.

Figure 5: The active and reference pickup should not be too close together. Effect on the amplitude ofvarying the inter-electrode separation.


Watch the video: Conduction Velocity (May 2022).