15.2 Phrenic, Suprascapular, Long Thoracic, and Axillary Nerves

Why these four nerves sit off the everyday worksheet

Median, ulnar, radial, fibular, and tibial studies carry most of a day’s volume. Phrenic, suprascapular, long thoracic, and axillary nerves explain the referrals that those everyday nerves cannot: diaphragm failure, overhead weakness with spinati wasting, scapular winging, and isolated deltoid loss after dislocation. Independent OpenExamPrep teaching for these R.NCS.T. outline items emphasizes stimulation sites, recording muscles, artifacts, and the clinical clue that told the laboratory to add the study. Needle EMG of diaphragm, serratus, spinati, or deltoid can be part of a physician EDX examination; it is not a substitute for knowing the motor NCS setups.

Phrenic motor NCS to diaphragm

The phrenic nerve arises chiefly from C3–C5, with C4 the dominant root, and it is the sole motor supply to that hemidiaphragm. Phrenic motor NCS is a chest-wall recording of the diaphragmatic CMAP after neck stimulation.

Typical setup:

• Stimulation: posterior border of SCM, near the level of the cricoid cartilage, or in the supraclavicular fossa over the phrenic course. The nerve is thin; excess current spreads into brachial plexus and produces a deltoid or biceps twitch that is not diaphragm.
• Recording: surface electrodes on the chest wall over the diaphragm—commonly an active electrode near the xiphoid and a reference along the costal margin, or a pair over the lower intercostal space on the side studied. Laboratories differ in centimeter rules; what matters is a reproducible montage that actually sees a diaphragmatic CMAP, not a pectoralis twitch.
• Measurement: onset latency and amplitude, always compared with the opposite side when the question is unilateral. The CMAP is small. Treat an unreproducible wiggle as technical failure, not as “trace response.”

Respiration artifact and why the study is technically demanding

Respiration artifact swings the baseline as the chest wall moves. Ask the patient to relax at end-expiration and stimulate in a consistent phase of the respiratory cycle so traces superimpose. Cardiac electrical activity can contaminate the window; reposition rather than averaging a moving QRS into a fake CMAP. Obesity, COPD, abdominal binders, and inability to lie flat all degrade the response. Unilateral studies still need a contralateral attempt if the patient can tolerate it; “absent on the bad side” is a weak sentence if you never proved the montage works on the good side.

Pacemaker / ICD caution (preview). Electrical stimulation in the neck and across the chest wall is a lab-safety issue in patients with implanted cardiac devices. Follow laboratory policy, keep current as low as possible, avoid the generator pocket, and do not improvise a bilateral phrenic protocol over an ICD. This section only previews that caution; local cardiac-device rules control.

Clinical clues that belong on the requisition: orthopnea, sleep hypoventilation, paradoxical abdominal motion, an elevated hemidiaphragm on imaging, recent cardiac or neck surgery, and neuralgic amyotrophy with an isolated hemidiaphragm. Phrenic NCS does not replace pulmonary function tests; it asks whether that nerve still drives a recordable diaphragmatic CMAP.

Suprascapular nerve: supraspinatus, infraspinatus, two notches

The suprascapular nerve comes from the upper trunk (C5–C6). It passes through the suprascapular notch (under the transverse scapular ligament) to supraspinatus, then around the spinoglenoid notch to infraspinatus. That two-notch anatomy is the entire localization game.

Motor NCS: stimulate at Erb's point (supraclavicular fossa) and record from supraspinatus and infraspinatus with electrodes in the fossae. Side-to-side amplitude is the useful number. A notch lesion should drop both CMAPs. A spinoglenoid lesion should drop infraspinatus and spare supraspinatus.

Clinical: weak initiation of abduction (supraspinatus) and weak external rotation (infraspinatus), infraspinatus fossa wasting, and posterior shoulder pain. Contrast with axillary nerve: deltoid contour change, weak abduction in the mid-arc, and sensory change over the upper lateral arm—not isolated infraspinatus wasting.

Pitfalls: Erb's-point stimulation co-activates many upper-trunk muscles. Confirm that the recorded waveform tracks the intended fossa and that the visible twitch is spinati, not deltoid. Do not call every overhead-weak shoulder “C5 radiculopathy” without the notch logic and without the SNAPs that would be abnormal in upper trunk (LABC, median to thumb, radial) but normal in an isolated suprascapular nerve.

Long thoracic nerve to serratus anterior (winging)

The long thoracic nerve (C5–C7 contributions, often leaving near the roots) innervates serratus anterior. Serratus keeps the scapula on the chest wall during forward reach. Medial scapular winging that worsens when the patient pushes the arm forward or does a wall push-up is the classic clue. Trapezius (accessory) winging is a different geometry—often more lateral translation, worse with arm abduction, plus shoulder-shrug weakness. Mixing those two winging patterns is a high-yield error.

Long thoracic motor NCS records from serratus anterior (mid-axillary line over the rib cage) with stimulation in the supraclavicular fossa. The study is unforgiving: the muscle is broad, electrodes sit over ribs, and volume conduction from pectoralis or latissimus can mimic a CMAP. Compare sides, watch the scapula during the twitch, and treat an unreproducible blip as technical. Neuralgic amyotrophy loves this nerve; so do postoperative stretch and certain sports. Isolated long thoracic neuropathy should spare deltoid CMAP, spinati CMAPs, and upper-limb SNAPs.

Axillary nerve to deltoid; contrast with C5 / upper trunk

The axillary nerve is a posterior-cord terminal nerve (C5–C6 fibers). It supplies deltoid and teres minor, then the superior lateral cutaneous nerve of the arm over the “regimental badge” patch. Routine axillary motor NCS records from middle deltoid with stimulation at Erb's point.

Quadrilateral space (teres major/minor, humerus, long head of triceps) can entrap axillary nerve. After anterior shoulder dislocation, add axillary NCS rather than assuming the whole upper trunk failed. G1 placed too far posterior records infraspinatus. Stimulus at Erb's point that is too strong activates the entire upper trunk—use the smallest current that gives a supramaximal deltoid CMAP and look at which muscle actually jumps.

Clinical-clue table

Setup pearls and pitfalls (all four)

• Compare sides before you compare the patient with a memory of “normal millivolts.”
• Erb's point is a crowd: phrenic, upper trunk, long thoracic, and accessory neighbors. Watch which muscle jumps.
• Respiration, pacemaker/ICD policy, and a moving chest wall make phrenic a senior-technologist study.
• Winging is a physical finding; confirm which muscle failed before you name the nerve.
• Do not substitute needle EMG of diaphragm, serratus, or deltoid for these motor NCS when the question is an R.NCS.T. conduction protocol.

Scenario. A volleyball athlete has painless infraspinatus wasting and weak external rotation. Supraspinatus CMAP from Erb's-point stimulation matches the opposite side; infraspinatus CMAP is markedly smaller. Deltoid CMAP and LABC SNAP are normal. That combination points to a spinoglenoid suprascapular lesion rather than upper trunk, axillary nerve, or C5 root.