Nerve conduction velocity

Micromachined 3D electrode arrays

Typically, the electrodes used in an EMG are stuck to the skin over a thin layer of gel/paste.^[8] This allows for better conduction between electrode and skin. However, as these electrodes do not pierce the skin, there are impedances that result in erroneous readings, high noise levels, and low spatial resolution in readings.^[10]

To address these problems, new devices are being developed, such as 3-dimensional electrode arrays. These are MEMS devices that consist of arrays of metal micro-towers capable of penetrating the outer layers of skin, thus reducing impedance.^[10]

Compared with traditional wet electrodes, multi-electrode arrays offer the following:^[10]

• Electrodes are about 1/10 the size of standard wet surface electrodes
• Arrays of electrodes can be created and scaled to cover areas of almost any size
• Reduced impedance
• Improved signal power
• Higher amplitude signals
• Allow better real-time nerve impulse tracking

Age

Normal 'adult' values for conduction velocities are typically reached by age 4. Conduction velocities in newborns and toddlers tend to be about half the adult values.^[1]

Nerve conduction studies performed on healthy adults revealed that age is negatively associated with the sensory amplitude measures of the Median, Ulnar, and Sural nerves. Negative associations were also found between age and the conduction velocities and latencies in the Median sensory, Median motor, and Ulnar sensory nerves. However, conduction velocity of the Sural nerve is not associated with age. In general, conduction velocities in the upper extremities decrease by about 1 m/s for every 10 years of age.^[2]

Sex

Sural nerve conduction amplitude is significantly smaller in females than males, and the latency of impulses is longer in females, thus a slower conduction velocity.^[2]

Other nerves have not been shown to exhibit any gender biases.^{[citation needed]}

Temperature

In general, the conduction velocities of most motor and sensory nerves are positively and linearly associated with body temperature (low temperatures slow nerve conduction velocity and higher temperatures increase conduction velocity).^[1]

Conduction velocities in the Sural nerve seem to exhibit an especially strong correlation with the local temperature of the nerve.^[2]

Height

Conduction velocities in both the Median sensory and Ulnar sensory nerves are negatively related to an individual's height, which likely accounts for the fact that, among most of the adult population, conduction velocities between the wrist and digits of an individual's hand decrease by 0.5 m/s for each inch increase in height.^[2] As a direct consequence, impulse latencies within the Median, Ulnar, and Sural nerves increases with height.^[2]

The correlation between height and the amplitude of impulses in the sensory nerves is negative.^[2]

Hand factors

Circumference of the index finger appears to be negatively associated with conduction amplitudes in the Median and Ulnar nerves. In addition, people with larger wrist ratios (anterior-posterior diameter : medial-lateral diameter) have lower Median nerve latencies and faster conduction velocities.^[2]

Myasthenia gravis

Amyotrophic lateral sclerosis (ALS)

Amyotrophic lateral sclerosis is a progressive and inevitably fatal neurodegenerative disease affecting the motor neurons.^[9] Because ALS shares many symptoms with other neurodegenerative diseases, it can be difficult to diagnose properly. The best method of establishing a confident diagnosis is via electrodiagnostic evaluation. To be specific, motor nerve conduction studies of the Median, Ulnar, and peroneal muscles should be performed, as well as sensory nerve conduction studies of the Ulnar and Sural nerves.^[9]

In patients with ALS, it has been shown that distal motor latencies and slowing of conduction velocity worsened as the severity of their muscle weakness increased. Both symptoms are consistent with the axonal degeneration occurring in ALS patients.^[9]

Carpal tunnel syndrome

Carpal tunnel syndrome (CTS) is a form of nerve compression syndrome caused by the compression of the median nerve at the wrist. Typical symptoms include numbness, tingling, burning pains, or weakness in the hand.^[12][13] CTS is another condition for which electrodiagnostic testing is valuable.^[12][14] However, before subjecting a patient to nerve conduction studies, both Tinel's test and Phalen's test should be performed. If both results are negative, it is very unlikely that the patient has CTS, and further testing is unnecessary.^[13]

Carpal tunnel syndrome presents in each individual to different extents. Measurements of nerve conduction velocity are critical to determining the degree of severity.^[14][15] These levels of severity are categorized as:^[12][13]

• Mild CTS: Prolonged sensory latencies, very slight decrease in conduction velocity. No suspected axonal degeneration.
• Moderate CTS: Abnormal sensory conduction velocities and reduced motor conduction velocities. No suspected axonal degeneration.
• Severe CTS: Absence of sensory responses and prolonged motor latencies (reduced motor conduction velocities)
• Extreme CTS: Absence of both sensory and motor responses

One common electrodiagnostic measurement includes the difference between sensory nerve conduction velocities in the pinkie finger and index finger. In most instances of CTS, symptoms will not present until this difference is greater than 8 m/s.^[12][13]

Guillain–Barré syndrome

Guillain–Barré syndrome (GBS) is a peripheral neuropathy involving the degeneration of myelin sheathing and/or nerves that innervate the head, body, and limbs.^[7] This degeneration is due to an autoimmune response typically initiated by various infections.

Two primary classifications exist: demyelinating (Schwann cell damage) and axonal (direct nerve fiber damage).^[7][16] Each of these then branches into additional sub-classifications depending on the exact manifestation. In all cases, however, the condition results in weakness or paralysis of limbs, the potentially fatal paralysis of respiratory muscles, or a combination of these effects.^[7]

The disease can progress very rapidly once symptoms present (severe damage can occur within as little as a day).^[7] Because electrodiagnosis is one of the fastest and most direct methods of determining the presence of the illness and its proper classification, nerve conduction studies are extremely important.^[16] Without proper electrodiagnostic assessment, GBS is commonly misdiagnosed as polio, West Nile virus, tick paralysis, various toxic neuropathies, CIDP, transverse myelitis, or hysterical paralysis.^[7] Two sets of nerve conduction studies should allow for proper diagnosis of Guillain–Barré syndrome. It is recommended that these be performed within the first 2 weeks of symptom presentation and again sometime between 3 and 8 weeks.^[16]

Electrodiagnostic findings that may implicate GBS include:^[3][7][16]

• Complete conduction blocks
• Abnormal or absent F waves
• Attenuated compound muscle action potential amplitudes
• Prolonged motor neuron latencies
• Severely slowed conduction velocities (sometimes below 20 m/s)

Lambert–Eaton myasthenic syndrome

Lambert–Eaton myasthenic syndrome (LEMS) is an autoimmune disease in which auto-antibodies are directed against voltage-gated calcium channels at presynaptic nerve terminals. Here, the antibodies inhibit the release of neurotransmitters, resulting in muscle weakness and autonomic dysfunctions.^[17]

Nerve conduction studies performed on the Ulnar motor and sensory, Median motor and sensory, Tibial motor, and Peroneal motor nerves in patients with LEMS have shown that the conduction velocity across these nerves is actually normal. However, the amplitudes of the compound motor action potentials may be reduced by up to 55%, and the duration of these action potentials decreased by up to 47%.^[17]

Peripheral diabetic neuropathy

At least half the population with diabetes mellitus is also affected with diabetic neuropathy, causing numbness and weakness in the peripheral limbs.^[18] Studies have shown that the Rho/Rho-kinase signaling pathway is more active in individuals with diabetes and that this signaling activity occurs mainly in the nodes of Ranvier and Schmidt-Lanterman incisures.^[18] Therefore, over-activity of the Rho/Rho-kinase signaling pathway may inhibit nerve conduction.

Motor nerve conduction velocity studies revealed that conductance in diabetic rats was about 30% lower than that of the non-diabetic control group. In addition, activity along the Schmidt-Lanterman incisures was non-continuous and non-linear in the diabetic group, but linear and continuous in the control. These deficiencies were eliminated after the administration of Fasudil to the diabetic group, implying that it may be a potential treatment.^[18]