There are two different types of NCS: motor and sensory. Motor NCS involves the electrical stimulation of a peripheral nerve at two points (proximal and distal). The stimulation of the nerve generates action potentials that propagate down to evoke a response in the muscle distally. The amplitudes, onset latencies, and velocities of the compound muscle action potential (CMAP) for each motor nerve tested are recorded and compared to normative data or to the asymptomatic contralateral side. The CMAP represents the summation of electrical signals discharged by the muscle fibers’ depolarizing membranes. Sensory NCS records the sensory nerve action potential (SNAP) on the skin after proximal stimulation of the nerve. The SNAP is the summation of electrical signals discharged by the sensory neurons’ depolarizing membranes. The peak latency and conduction velocity of the SNAP is also compared to normative data. The amplitudes of SNAP vary widely and, therefore, are not useful in the analysis for neuropathy.

Prolonged onset latency (motor NCS) or peak latency (sensory NCS) implies that the conduction of the electrical impulse down the nerve was delayed. This can mean that there is some injury to the myelin; however, the preferred way to assess the integrity of the myelin sheath is by conduction velocity. A prolonged motor NCS conduction velocity is more specific for a demyelinating injury and can even localize the specific segment of nerve that is injured.

The amplitudes of the CMAP are used to determine the presence of axon loss, conduction block, or both. Axonal loss is characterized by decreased CMAP amplitudes at both the distal and proximal sites of stimulation to the motor nerve. There is no axonal loss associated with conduction block, but the injury to the myelin is so severe that it essentially blocks most, if not all, conduction down the nerve giving the false appearance that the axons are no longer intact. It is characterized by diminished proximal and preserved distal CMAP amplitudes. A mixed picture of conduction block with axonal loss is associated with a pattern of decreased distal CMAP amplitude and an even greater decrease in proximal CMAP amplitude.

EMG involves insertion of a needle electrode directly into the muscle. A comprehensive EMG involves testing numerous muscles specifically selected based on the suspected pathology in question. There are two portions of an EMG conducted for each muscle tested: insertional activity (irritation of the sarcolemma during a resting state of the muscle) and muscle activation (voluntary activation of the muscle at varying degrees of effort). During the insertional activity phase of testing, abnormal spontaneous discharges implies acute denervation of that muscles. During the muscle activation phase of testing, the patient is asked to engage the muscle at minimum and maximum strength. This will lead to active firing of motor units. The motor unit action potential (MUAP) morphology and recruitment patterns can distinguish muscles with chronic denervation and potential reinnervation.

The role of EMG in the diagnosis of mononeuropathy is straightforward. For a purely demyelinating lesion of the nerve, you would expect a completely normal EMG. Severe axonal pathology accompanying a mononeuropathy will result in abnormal EMG findings in all the muscles innervated by that nerve. For a comprehensive EMG exam, one would also test muscles of different peripheral nerves, but common spinal nerve roots to rule out a lumbosacral radiculopathy, mononeuropathy multiplex, or a lumbosacral plexopathy .

The timing of the EDX study is critical to the interpretation of the study. False conclusions can occur if the EDX study is not ordered at the appropriate time. The ideal time to order an EDX study is approximately four weeks after the onset of symptoms. One can order EDX studies earlier as long as they understand the limitations of the study at each time point. Immediately after injury to a nerve, EDX findings are subtle for both demyelinating and axonal lesions and can be missed. Seven days after a complete nerve lesion Wallerian degeneration will have progressed to the point where distal stimulation of motor axons elicits no motor response. Ten days after onset of a complete lesion, SNAPs will be absent as well. Demyelinating injuries can be distinguished from axonal injuries at 7–10 days after onset of injury. The needle EMG portion will start to show active signs of denervation 2–3 weeks after onset of injury [5].

Understanding the varying degrees of demyelinating injuries due to a mononeuropathy and how to interpret them on EDX studies can help with prognosis. For instance, some subtle neurapraxias can demonstrate completely normal EDX results; therefore, they carry the most favorable prognosis for recovery. A demyelinating injury to the nerve with the presence of prolonged latencies and conduction velocities on NCS is the least severe type of EDX-confirmed mononeuropathies. The quantitative difference between the observed abnormal latencies and conduction velocities compared to the normative standards or contralateral asymptomatic side can also provide information on the severity of the injury. Evidence of a conduction block is considered a more severe injury to the myelin. A mixed conduction block with axonal loss is considered a progressively worse injury to the nerve. Finally, EMG evidence of denervation in a muscle supplied by the peripheral nerve in question connotes the most severe type of mononeuropathy, with the worst prognosis for recovery. In the setting of severe axonal injury, MUAP morphology can reveal acute denervation, chronic denervation, and evidence of reinnervation. These features can be used to follow a nerve injury over time and add to the prognosis for recovery.

The iliohypogastric nerve (IHN) is a branch of the lumbar plexus arising from the primary ventral rami of L1 and a communicating branch of T12. The IHN passes through the psoas muscle and then descends. Approximately halfway between the anterior superior iliac spine (ASIS) and the highest point of the iliac crest, the nerve pierces the muscles of the abdominal wall [6]. The nerve supplies the lower fibers of the transversus abdominis and internal oblique muscles. It divides into lateral and anterior cutaneous branches. The lateral cutaneous branch crosses the iliac crest to innervate a patch of skin in the upper buttock, and the anterior cutaneous branch courses just above the inguinal ligament to supply a small area of skin above the pubis.

Disorders of the IHN are rare. The most common causes of injury are surgical procedures involving transverse lower abdominal incisions such as hysterectomy, inguinal herniorrhaphy, and appendectomies. The main trunk of this nerve can be damaged by retroperitoneal tumors or large surgical incisions, producing sensory abnormalities in the distribution of the nerve and bulging of the lower abdominal muscles [6].

Injury to the IHN is characterized by anesthesia, pain, and paresthesias to the lower abdomen and groin. Patients with injury to the anterior branch of the IHN report a suprapubic sensory disturbance, whereas patients with injury to the lateral branch report an isolated sensory disturbance over the upper buttock. There is some dermatomal overlap with the ilioinguinal nerve, which makes it clinically difficult to differentiate them. Weakness of the lateral abdominal wall musculature can be present; however, these muscles receive other innervation from the lower intercostals nerves. Furthermore, lateral abdominal muscle testing is difficult to reliably assess.

The gold standard of diagnosis is a local anesthetic block of the nerve. Pain relief after the block confirms the diagnosis. These blocks are currently being performed under ultrasound guidance. There is no reliable EDX that can be performed to validate the diagnosis. Needle EMG of the lower abdominal musculature may serve as an adjunct in the diagnosis, although it is not commonly performed. Differential diagnosis includes upper lumbar or lower thoracic radiculopathy.

The ilioinguinal nerve (IIN) arises as a branch of the lumbar plexus and is derived from the L1 ventral rami. The nerve pierces through the psoas muscle and follows a parallel course to the IHN as it runs distally and anteriorly, staying deep to the abdominal musculature. Adjacent to the ASIS, the nerve sends motor contributions to the inferior portions of the transversus abdominis and internal oblique muscles and cutaneous contributions to innervate a strip of skin over the iliac crest. The remainder of the nerve enters the inguinal canal and divides to provide cutaneous innervation for the groin, proximal medial thigh, base of the penis, and upper part of the scrotum, mons pubis, and labium majorum.