We will go over the fundamental physiology concepts required to understand and interpret electromyography (EMG) and nerve conduction studies (NCS).
Motor units are the smallest conceptual unit of nerve and muscle, which is what we are testing! Needle electromyography (EMG) specifically measures electrical activity of motor units (both individually and as groups). Motor nerve conduction studies (NCS) record muscle electrical activity as a result of nerve stimulation.
One motor neuron and all the muscle fibers it innervates. See figure 1.1 for an illustration.
Figure 1.1: Animation of two motor units and their individual and combined effect on muscle contraction.
The more coordinated your movements need to be, the smaller the motor unit will be. For example, your eye muscles will have each axon supplying a small number of muscle fibers, while your gastrocnemius will have each axon supplying a large number of muscle fibers.
It is important to understand what we can and cannot test to accurately interpret these studies.
This is super useful to understand why electromyography (EMG) and nerve conduction studies (NCS) may not always detect a radiculopathy. In sensory NCS, we measure nerve conduction between two points (the point of stimulation and the point of recording activity). Therefore, we can only test sensory nerves distal to the dorsal root ganglion (DRG), because you physically cannot place an electrode on the skin close enough to the spinal cord to be proximal to the DRG. This is why radiculopathies (in which the lesion is proximal to the DRG) don't usually show abnormalities on sensory NCS. However, in some cases (usually severe) of radiculopathy, you can see see changes in CMAP on motor NCS and on needle EMG due to muscle denervation.
Figure 1.2: Diagram of the basic circuit being tested in EMG/NCS. It is important to remember which parts of the axons we can and cannot test directly.
Recall that skeletal muscle fibers are categorized broadly into Type I and II. EMG primarily picks up the electrical activity of Type I fibers, which are "slow twitch", activate during posture maintenance and endurance exercise, have primarily aerobic metabolism, and appear red on pathology slides. Type II fibers are "fast twitch", activate during rapid and powerful movements, have primarily anaerobic glycolysis, and appear more white on pathology slides.
EMG is not sensitive for myopathies that selectively affect Type II muscle fibers such as steroid-induced myopathies or muscle atrophy due to chronic disease.
Routine nerve conduction studies ONLY reflect the electrical activity of large-diameter axons involving:
proprioception and vibration sensation
motor commands to the muscles
Routine nerve conduction studies DO NOT reflect the activity of small-diameter axons involving:
pain and temperature sensation
autonomic function
NCS will completely miss any pathology that selectively affects small-diameter axons. Small-fiber neuropathies are typically identified by burning pain and temperature sensation deficits and can be tested for in other ways.
Anatomically, three things affect conduction velocity: axon diameter, myelination, and integrity of the nodes of Ranvier. Similar to copper wires (think back to physics pre-med classes), thicker wires (large diameter) and plastic insulation (myelin sheath / integrity of nodes of Ranvier) allow for faster currents (conduction across axons).
EMG/NCS can be used to test for neuromuscular junction disorders including myasthenia gravis, botulism, and Lambert-Eaton myasthenic syndrome. The NMJ also affects why we calculate motor nerve conduction velocity differently from sensory nerve conduction velocity, which will be discussed in the "Normal NCS" section.
What happens at the NMJ:
Depolarization of nerve ending
Inflow of calcium ions
Release of acetylcholine into synaptic space
Binding of acetylcholine to nicotinic receptors
Depolarization of muscle cell
Breakdown of acetylcholine molecules by acetylcholinesterase
Figure 1.3: Normal physiology of action potential across neuromuscular junction.