**3.5. EMG recording in cortical stimulation**

depolarized fibers nearest to the recording electrode, and is the most studied outcome

**•** Axonal neuropathies: characterized by axon loss, can show CMAPs of reduced amplitude. In chronic axonal neuropathies, CMAP amplitude reflects the functioning muscle mass

**•** NMJ disorders: amplitude of CMAPs is a fundamental parameter in the assessment of the integrity of neuromuscular transmission by means of repetitive nerve stimulation (RNS). This technique consists of applying repetitive stimulation at low and high rates, and determining the decreasing or increasing CMAP responses that in conjunction with the CMAP at baseline, allows a diagnosis of pre- or postsynaptic NMJ disorders to be established

**Figure 8.** Repetitive stimulation of ulnar nerve: recording over the abductor digiti minimi muscle. A. In normal sub‐ jects, compound muscle action potential (CMAP) amplitude remains very stable. B. In a miastenia gravis (MG) patient, CMAP amplitude is normal at rest but decreases during low-rate repeated stimulation at 3 Hz. C. In a patient with Lambert–Eaton syndrome (LES), the initial CMAP amplitude is reduced. During high-rate repeated stimulation at 20

**•** Demyelinating lesions: Impediment to the conduction of the action potential without axonal degeneration is named conduction block (CB). No absolute expert agreement has been established in the definition criteria of CB [49]. Nevertheless, a decay of proximal CMAP amplitude/area of at least 50% has been observed in patients with nerve CB in some studies,

*Duration* is measured from the initial deflection from baseline to the first baseline cross‐ ing, but can also be measured from the initial to the terminal deflection back to baseline. It is a parameter that indicates the synchrony of the activated muscle fibers. It increases in conditions that result in slowing of some motor nerve fibers but not others (e.g., in a

Hz, CMAP amplitude dramatically increases. NMJ: neuromuscular junction.

and has even been proposed as criteria for CB. [51-53].

demyelinating lesion) [44,54].

Abnormalities of CMAP amplitude can be observed in:

10 Electrodiagnosis in New Frontiers of Clinical Research

measurement.

[44,45].

[49] (Fig. 8).

Motor evoked potential (MEP) is defined as an EMG response obtained by means of activation of the corticospinal tract by means of stimulation to the motor cortex. Transcranial Magnetic Stimulation (TMS), a painless (unlike Transcranial Electrical Stimulation) method is widely used with this aim [60].

The following components of MEP elicited by single pulse TMS, are measured to evaluate the integrity of corticospinal pathways:

*Latency* refers to the time between the delivery of a TMS pulse over the scalp (area corre‐ sponding to the primary motor cortex – M1) and the appearance of MEP at the periphery. MEP latency is mainly reflective of the efficiency of conduction between the stimulated motor cortical area and the peripheral target muscle [61].

*Central motor conduction time (CCT)* can be obtained by two methods of calculation. The CCT calculated by subtracting the CMAP latency obtained by stimulation of the spinal (cervical or lumbar) motor root from the latency of MEP [62] includes the time for central motor conduc‐ tion, the synaptic delay at the spinal level and time from the proximal root to the intervertebral foramen. More precise central conduction time can be calculated by use of F-wave latency [60]. On the other hand, CCT is significantly influenced by the motor system maturation [63], and partially dependent upon the subject height. A significant interside difference indicates a lateralized prolonged CCT even if still within normal values (Fig 9).

is used as benchmark for the intensity of TMS. MT is usually defined by the lowest intensity

Overview of the Application of EMG Recording in the Diagnosis and Approach of Neurological Disorders

http://dx.doi.org/10.5772/56030

13

*Silent period (SP)* is defined as the period of EMG suppression; normally it refers to the time from the end of the MEP to the return of voluntary EMG activity, after a single suprathreshold TMS pulse applied to the M1 corresponding to the active target muscle. The first 50–60 ms of the SP has been supposedly contributed to spinal inhibition and the late part originates most likely in the motor cortex, termed *cortical silent period* [71]. Abnormalities of SP have been shown in patients with various movement disorders [72,73]. In patients with a diagnosis of

*Transcallosal conduction (TC)*: Application of a single suprathreshold TMS pulse to the M1 can suppress tonic voluntary EMG activity in ipsilateral hand muscles, by transcallosal inhibition. Delayed or absent TC suggests lesions of the corpus callous [75]. In addition, application of single stimuli to both motor cortexes at a short interval, allows assessment of the interhemi‐

*Short interval intracortical inhibition (SICI)* can be accessed by combining a subthreshold (60– 80% of resting MT) conditioning (first) stimulus with a suprathreshold (second) test stimulus over M1, at short inter-stimulus intervals of 1-6 ms [77]. Significantly reduced SICI has been

*Intracortical facilitation (ICF)* reflects the excitatory phenomenon occurring in the M1, and is elicited by applying a conditioning subthreshold TMS pulse and a suprathreshold test stimulus over M1 with inter-stimulus intervals between 6 and 20 ms [80]. Significantly enhanced ICF

In addiction to the study of the pathophysiology of diverse neurological diseases, paired-pulse TMS has been widely used to explore the effects of central nervous system (CNS)-active drugs

Intraoperative neuromonitoring includes mapping and true monitoring techniques. Mapping techniques are used intermittently during surgery for functional identification and preserva‐ tion of anatomically ambiguous nervous tissue. On the other hand, true monitoring techniques

In posterior fossa and brainstem surgeries, mapping the floor of the fourth ventricle allows the surgeon to find a safe entry to the brainstem, and therefore, helps to identify and preserve cranial nerves and their motor nuclei. Traditionally, Intraoperative monitoring of the facial nerve has been employed in operations for acoustic tumors to reduce the risk of neural damage. To date, EMG recording of the activity of selective cranial nerve muscles is currently included

During brain surgery, neurophysiological mapping techniques have been employed in the identification of eloquent areas such as the motor areas. In addition, these techniques have been introduced in surgery for deep-seated gliomas, insular tumors and lesions involving the

permit a continuous assessment of the functional integrity of neural pathways [82].

in the intraoperative set during surgical manipulation of the brainstem. [83,84].

has been recorded from amputated limbs in patients with neuropathic pain [81].

observed in patients with dystonia and Parkinson's disease [78,79].

**3.6. EMG recording in Intraoperative neuromonitoring**

of stimulation required to generate 50% probability of MEPs of more than 50 *μ*V [60].

ALS, shortened PS has been observed [74].

spheric interactions and also the TC [76].

on the motor cortex [70].

**Figure 9.** Left: MEP recorded from abductor pollicis brevis muscle. The top trace shows the MEP evoked by single pulse TMS over the corresponding M1. The lower trace shows the MEP elicited by ipsilateral cervical (motor root) stimula‐ tion. Right: MEP recorded from extensor digitorum brevis muscle. The top trace shows the MEP induced by cortical stimulation. The lower trace shows the MEP elicited by ipsilateral lumbar stimulation.

*Amplitude* is often measured from peak-to-peak amplitude. MEP amplitude can also be measured from baseline EMG activity to the first positive or negative deflection. Amplitude of MEP reflects the integrity and excitability of motor cortex, corticospinal tract, nerve roots and peripheral motor pathway to the muscles [64]. Dispersion of the alpha-motoneuron response to the descending volley in the corticospinal tract, leads to a broad range of normal values. The triple stimulation technique (TST) provides a more precise assessment of cortico‐ spinal tract conduction by suppressing desynchronization of MEPs. The TST involves three stimuli (transcranial, distal and proximal on the peripheral nerve) timed to produce two collisions. The TMS descending impulses collide with the antidromic impulses from the distal stimulus. Proximal stimulation on the nerve evokes orthodromic impulses, which cancel out any uncollided impulses from the distal stimulus. The response from the third stimulus therefore reflects the number of peripheral neurons activated from TMS [65].

Lengthening of MEP latency and CCT suggests impairment of the white matter fibers, while abnormalities of MEP amplitude or absence of responses are more suggestive of loss of neurons or axons. TMS has the potential to facilitate early diagnosis of myelopathy by detecting signals of demyelination of the pyramidal tract [66,67], plexus entrapment and injuries [62]. Moreover, MEP abnormalities may be useful objective markers of progression of amyotrophic lateral sclerosis (ALS) [68], and effective parameters in spinal pathology for deciding the timing of the surgical intervention [69].

TMS can however be performed using single pulse or pair pulse paradigm in order to explorer the reactivity of the motor cortex. Since motor threshold (MT) is believed to reflect membrane examine of corticospinal neurons, motor neurons in the spinal cord, NMJs and muscle [70], it is used as benchmark for the intensity of TMS. MT is usually defined by the lowest intensity of stimulation required to generate 50% probability of MEPs of more than 50 *μ*V [60].

*Silent period (SP)* is defined as the period of EMG suppression; normally it refers to the time from the end of the MEP to the return of voluntary EMG activity, after a single suprathreshold TMS pulse applied to the M1 corresponding to the active target muscle. The first 50–60 ms of the SP has been supposedly contributed to spinal inhibition and the late part originates most likely in the motor cortex, termed *cortical silent period* [71]. Abnormalities of SP have been shown in patients with various movement disorders [72,73]. In patients with a diagnosis of ALS, shortened PS has been observed [74].

*Transcallosal conduction (TC)*: Application of a single suprathreshold TMS pulse to the M1 can suppress tonic voluntary EMG activity in ipsilateral hand muscles, by transcallosal inhibition. Delayed or absent TC suggests lesions of the corpus callous [75]. In addition, application of single stimuli to both motor cortexes at a short interval, allows assessment of the interhemi‐ spheric interactions and also the TC [76].

*Short interval intracortical inhibition (SICI)* can be accessed by combining a subthreshold (60– 80% of resting MT) conditioning (first) stimulus with a suprathreshold (second) test stimulus over M1, at short inter-stimulus intervals of 1-6 ms [77]. Significantly reduced SICI has been observed in patients with dystonia and Parkinson's disease [78,79].

*Intracortical facilitation (ICF)* reflects the excitatory phenomenon occurring in the M1, and is elicited by applying a conditioning subthreshold TMS pulse and a suprathreshold test stimulus over M1 with inter-stimulus intervals between 6 and 20 ms [80]. Significantly enhanced ICF has been recorded from amputated limbs in patients with neuropathic pain [81].

In addiction to the study of the pathophysiology of diverse neurological diseases, paired-pulse TMS has been widely used to explore the effects of central nervous system (CNS)-active drugs on the motor cortex [70].
