Anatomical Characteristics

Axons are extensions of neuronal cell bodies. They transmit nerve impulses and are enveloped by myelin. Myelin is produced by Schwann’s cells (SCs) in the peripheral nervous system (PNS); its function is to isolate axons from each other and optimize the transmission of nerve impulses through periodic gaps called nodes of Ranvier.

Individual axons are surrounded by connective tissue called the endoneurium. Axons are bundled together in groups called fascicles, each one covered by a connective tissue sheath known as the perineurium. Fascicles are grouped together in bundles that together constitute a nerve trunk, which also is surrounded by epineurium. Understanding this structure allows one to appreciate the pathophysiological substrate of nerve injuries, the degeneration/regeneration process, and the degree of injury. ^{1,​ 2,​ 3,​ 4}

In the PNS, effector information is transmitted through motor units (MUs), each of which is composed of an alpha motor neuron, its axon, and whatever number of extrafusal muscle fibers it innervates. Afferent information is integrated through sensory receptors; its axons and cell bodies are located in the dorsal root ganglia. ⁵

6.1.2 Physiological Characteristics

At rest, nerve fibers maintain their resting membrane potential. Generation of a stimulus of supramaximal intensity results in changes in ion flow from the exterior to the interior of the axon. This increases positivity within the interior of the nerve fiber, decreasing the potential difference between the inside and outside to transmit the impulse that generates an action potential (AP). ⁵ Electrodiagnostic studies (EDSs) evaluate the impulse conduction of thicker and more myelinated nerve fibers (i.e., the most rapid ones), which are classified as type A fibers, as per Erlanger and Gasser. ^{6,​ 7}

6.2 Pathophysiology

Two pathophysiological processes—axonal damage and demyelination—occur individually or concurrently in a damaged nerve that are independent of the etiology and mechanism of injury.

6.2.1 Axonal Damage

Any injury that causes disruption in an axon’s integrity results in degeneration of the distal segments through a process called Wallerian degeneration (WD), which is completed within 3 weeks of an injury. This degeneration process can also occur in the cell body (chromatolysis), proximal axon, and distal target organs.

Its broad etiology includes the following mechanisms: crush, transection, stretch, and intrinsic neuropathy. ^{8,​ 9}

6.2.2 Demyelination

Demyelination is the loss of the myelin layer, either isolated or associated with axonal damage. In the latter case, there is some alteration of the myelin sheath, but not of the SCs. As such, the lack of myelin around any axon segment only requires SC division for remyelination to occur within that segment. Etiologies include compression injuries with ischemia, edema, and intrinsic neuropathies. ^{8,​ 9}

6.3 EDSs for Preoperative Evaluations

During this stage of evaluation, EDSs are useful to complement the clinical examination of patients, detect signs not confirmed by neurological examination, and guide in the diagnosis and therapeutic management of patients. However, EDSs will never replace a thorough medical history and physical examination. In general, EDSs help to safely: (1) pinpoint the site of injury (i.e., anterior horn, root, plexus, terminal nerve, neuromuscular junction); (2) identify the underlying pathophysiological process (i.e., demyelination and/or axonal damage); (3) establish the timing, severity, and extent of injury; (4) generate a list of possible diagnoses (e.g., compression syndrome, mononeuropathy, diffuse neuropathy); and (5) assess progression, which allows for some estimate regarding the prognosis for functional recovery ^{10,​ 11} ( ▶ Table 6.1).

EDSs performed at different time points over the course of follow-up help establish whether axonal regeneration is present or not, thereby assisting with predicting prognosis, as well as the need and timing of surgical intervention. It should be noted that the optimal timing for performing EDSs is 2 to 3 weeks post injury (i.e., after the WD process is completed), because none of the electrical changes that define a nerve injury are likely to be evident earlier.

Sensory nerve conduction studies (SNCSs), motor nerve conduction studies (MNCSs), and electromyography (EMG) are among the studies recommended during this assessment phase.

6.3.1 Technical Considerations

The same equipment is used for both EMG and SNCS and should meet the following specifications:

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  Recording equipment is composed of: (1) an amplifier to eliminate potential interference, (2) recording channels, (3) enough sensitivity to measure the amplitude of potentials, which range from 1 µV to 10 mV, (4) filters to reduce distortion and interference, measured in hertz (Hz; ranging from 2 to 10,000 Hz), (5) a display screen, (6) an audio amplifier and AD converter, and (7) a printer.

  
  
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  A stimulator with which stimulus intensity, frequency, and duration can be controlled; generally, this will entail the use of surface electrodes (adhesive, flat metal, and/or ring surface electrodes).

  
  
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  Recording electrodes: this usually would involve flat surface electrodes (adhesive, flat metal, and/or ring) or concentric or Teflon-coated monopolar needle electrodes for EMG, and an active electrode and reference electrode for SNCS. ⁷

Recording is performed with the patient lying on an examination table or in a bed. Electrodes are then placed at sites that are specific to the study being performed. The process begins with stimulating a specific site via an electrical current until a desired potential is reached. EMG recording is obtained by introducing the concentric needle into the muscle being tested ( ▶ Fig. 6.1). ⁷

Equipment and Electrodes

All data are recorded based on parameters that will be reviewed later, with internationally standardized values available for each potential. Patients may feel some discomfort or experience a tingling sensation. However, these studies are generally well tolerated.

6.3.2 Nerve Conduction Studies/Electroneurography

Nerve conduction studies are performed by applying some supramaximal electrical stimulus that triggers the activation of all fibers through a percutaneous electrode placed over a specific nerve. This generates an AP, which is recorded by other surface electrodes applied at a defined distance. Based on whether it is a sensory or motor study, electrodes are placed in a sensory innervation territory or into a specific muscle innervated by the nerve under study, respectively. ^{6,​ 7,​ 11,​ 12,​ 13}

Motor Nerve Conduction Studies

MNCSs evaluate the muscular response or compound motor action potentials (CMAPs) by electrically stimulating the nerve that should innervate the muscle. The CMAP is the summation of AP from all the MUs ( ▶ Fig. 6.2). ^{6,​ 7,​ 11,​ 12,​ 13}

Sensory Nerve Conduction Studies

SNCSs assess sensory nerve action potentials (SNAPs), which are the summation of APs from sensory fibers of the nerve produced by stimulation. Contrary to MNCSs, the amplitude is measured in µV. SNAPs can be either orthodromic or antidromic, and nerve conduction velocity (NCV) is measured by stimulating only a single point ( ▶ Fig. 6.3). ^{6,​ 7,​ 11,​ 12,​ 13}

Parameters to Be Evaluated

The following parameters of the generated potentials are analyzed: ⁶

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  Latency is the time interval between the moment of nerve stimulation and the onset of the resulting potential. It is measured in milliseconds (ms) and represents the velocity of transmission.

  
  
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  Amplitude is the maximum voltage difference between two points (i.e., the intensity of the impulse) expressed in millivolts (mV) for motor studies and in microvolts (µV) for sensory studies. It is measured from baseline to maximum peak, and is related to the number of activated fibers.

  
  
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  Area provides information on the number of axons being stimulated.

  
  
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  NCV is calculated by dividing latency into the distance between the stimulation and recording points. NCV is measured in meters per second (m/s), and reflects myelin integrity.

  
  
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  Duration reflects the degree of synchrony between nerve fibers.

  
  
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  Wave morphology: In general, waves show a monophasic or biphasic configuration. A polyphasic configuration denotes chronodispersion ( ▶ Fig. 6.4).

  
  
  
  

  

  
  

  Fig. 6.4 Parameters. Latency, amplitude, area, conduction velocity, duration, and phases are evaluated for each potential.

Unlike demyelinating lesions, which frequently exhibit increased latency with a resulting decrease in NCV, sensory, motor, and mixed axonal injuries characteristically display some reduction in the amplitude of APs. ¹³

Delayed Responses: F-Wave and H-Reflex

Late responses may be evaluated when lesions affect the proximal segments of the nerve structure, making it impossible to use conventional electroneurography.

F-Wave

After a stimulus is applied, it travels antidromically to the anterior horn of the spinal cord where neurons generate small APs that travel back (orthodromically), thereby activating the muscle and generating a small-amplitude response (less than 10%), which is not elicited in all stimuli. Latency may be variable, so it is advisable to repeatedly apply series of 10 to 20 stimuli. F-wave studies are useful for identifying proximal lesions in nerves; but they are only of limited value for diagnosing radiculopathies and of no use assessing posterior roots. ¹⁴

H-Reflex

The H-reflex is the electrophysiological analogue of the stretch reflex; hence, it assesses sensory and motor fibers at a specific metameric level. It is initiated with a submaximal stimulus. In adults, it is consistently evoked from the flexor carpi radialis muscle by stimulating the median nerve at the elbow; and from the flexor muscles of the foot by stimulating the tibial nerve in the popliteal fossa. In these contexts, it is only useful for C7 and S1 radiculopathies, respectively.

6.3.3 Electromyography

EMG is the group of recording techniques that assesses electrical activity within skeletal muscles. The selection of muscles depends on the patient’s clinical picture. The examination involves a single-use concentric needle electrode, which is introduced into the muscle, where it records four phases of muscular activity. The signals are displayed on a digital screen, and can also be converted into an audible acoustic file. The following phases are examined: ^{12,​ 15}

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  Insertion phase: This is derived from some needle-induced mechanical irritation stimulus, and characterized by the presence of small-amplitude potentials and a crackling sound.

  
  
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  Resting phase: This phase is characterized by a flat trace (electrical silence) under normal conditions. “Plate activity” can occasionally be detected due to irritation of the neuromuscular plate; but this does not imply pathology.

  
  
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  Mild contraction phase: This phase evaluates the configuration of the MU potential (MUP), which represents the summation of APs for each MU fiber. The contraction force is determined by the number and frequency with which simultaneous activated MUs are fired. The following MUP parameters are examined:

  
  
  
  
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    Duration: This is determined by the synchrony of discharges and ranges from 8 to 14 ms.

    
    
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    Amplitude: This reflects the number and synchrony of discharging fibers and ranges from 0.5 to 2 mV.

    
    
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    Phases: The phases represent the section of a wave that falls between two baseline crossings; they can be either biphasic or triphasic.

  
  
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  Maximal contraction phase: This phase determines MUP recruitment, which is called spatial recruitment if MUPs are increasing in number, and temporal recruitment if they are increasing in frequency. This makes it difficult to identify the individual MUs, as well as the baseline, and is known as an interference pattern (the normal muscle recruitment pattern).

Neurogenic Pattern on Electromyography

EMG findings are not pathognomonic of any nosological entity; nevertheless, it is possible to differentiate between normal, neurogenic, and/or myogenic patterns. There is a high level of concordance (greater than 90%) between EMG and muscle biopsy findings. Accordingly, EMG can be useful for the diagnosis of peripheral nerve lesions when a neurogenic pattern is present. During denervation, since there is an increase in fiber excitability, the activity of the insertion phase also increases. However, this may decline due to fibrotic changes in the muscle. The resting phase of the neurogenic pattern is characterized by the presence of spontaneous activity, indicated by fibrillation, fasciculations (spontaneous, repetitive, short, biphasic discharges), and acute positive waves. This phase commonly starts 3 weeks after the injury and tends to disappear over time because of reinnervation or fibrosis. Repetitive complex discharges may also be present. The presence of fasciculations is suggestive of a proximal lesion (anterior horn or anterior nerve root). In the mild contraction phase, MUPs are polyphasic and greater in duration and amplitude; these characteristics become more pronounced as the process becomes more chronic. However, innervation MUPs are short and smaller in amplitude. In the maximal contraction phase, the recruitment pattern is incomplete which, from higher to lower severity, can be: high-intermediate, low-intermediate, simple, or absent ( ▶ Fig. 6.5). ^{7,​ 15}

Related posts:

Clinical Aspects of Traumatic Peripheral Nerve Lesions in the Lower Limb Surgical Repair of Nerve Lesions: Neurolysis and Neurorrhaphy with Grafts or Tubes Nerve Injuries: Anatomy, Pathophysiology, and Classification Compressive Lesions of the Lower Limb and Trunk Ultrasound in Peripheral Nerve Surgery Nerve Anatomy of the Upper Limbs

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