Conduction velocity is inversely related to axonal length in the median sensory nerve.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to P B Wu.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The clinical picture of lead neuropathy was classically described as a painless progressive motor neuropathy with axonal loss. The literature review fails to demonstrate a consensus on the site of axonal loss. This is an EMG report of a patient who developed a late lead neuropathy after a shotgun injury. A 69-year-old Filipino, healthy, male nondrinker sustained a shotgun injury to his left elbow. Nineteen years later he developed abdominal pain, followed by generalized weakness, distal greater than proximal in the extremities, and impaired pin-prick, proprioception, and two-point discrimination. He became nonambulatory and totally dependent in daily activities. He was lost to follow-up for 2 years until January 1993 when he presented with a blood lead level of 84 micrograms/dL. EMG examination revealed a sensorimotor peripheral polyneuropathy with severe axonal loss. This case demonstrates that axonal loss is the predominant feature in lead neuropathy and the location of pathology is in the peripheral nerves.
This study investigates the temperature effect on motor nerve conduction velocity (MNCV) in patients with neuropathic processes. Fourteen subjects, ages 18-77 yr old, with a diagnosis of uremic polyneuropathies (UPN, n = 5), diabetic polyneuropathies (DPN, n = 6) or carpal tunnel syndrome (CTS, n = 3) and ten normal controls were studied. After limb cooling in a cold water bath for 30 min, skin temperatures were sequentially obtained from the volar midwrist. Motor conduction velocities were obtained at 2-3 degrees increments between 22 and 33 degrees C. Results indicated a large individual variability; 0.1 to 1.8 in the median and 0.8 to 2.0 m/s/degrees C in the ulnar nerve when all three groups are considered together. There was a significant difference between the correction factors for control v DPN and control v CTS. A significant difference was also present for UPN v DPN and UPN v CTS (p < 0.05). There was a positive correlation (r = 0.746, p = 0.0001) between the baseline conduction velocities and the size of the correction factors in all the subjects. The effect of temperature on MNCV appears to be inversely correlated with the severity of conduction slowing or demyelination. These findings suggest that the use of a correction factor may be invalid when studying a demyelinated nerve, and that the extremity should be warmed to a specific temperature before an electrodiagnostic study.
A novel test for localizing ulnar mononeuropathies (UM), the electromyographic (EMG) motor Tinel's sign, has been developed. While recording with a monopolar needle from the abductor digiti minimi, the ulnar nerve is lightly rolled at multiple sites across the elbow, and the test is considered positive if a burst of EMG activity is observed simultaneously with nerve compression. To determine the use of the EMG Tinel's sign, we evaluated 70 control nerves and 50 clinically suspected UMs. The EMG Tinel's sign had a 78% sensitivity and a 79% specificity for suspected UM at the elbow. The clinical Tinel's sign was present in 68% of suspected UM cases, and the combined sensitivity of the EMG and clinical Tinel's sign was 96%. Using nerve conduction study (NCS) values derived from the control nerves, 62% of UM nerves had abnormal NCS/EMG findings, and 28% of UM nerves had NCS/EMG abnormalities that could be localized to the elbow. The development of motor axon mechanosensitivity at the site of nerve injury is a new finding, not previously observed in electrophysiologic studies of animal nerve injury models or reported in the electrodiagnostic literature.
There is no nerve conduction study for the thoracodorsal nerve in the literature. A conduction study for this nerve is described. Thirty healthy adults (16 males) with a mean age of 41.5 +/- 10.6 (range, 22-63) years were studied. The thoracodorsal nerve was stimulated at axilla and Erb's point with recording over the latissimus dorsi. The latency was 1.9 +/- 0.4 (range, 1.2-2.7) ms and 3.6 +/- 0.4 (range, 2.8-4.5) ms for the axillary and Erb's stimulations, respectively. The amplitude of the compound muscle action potential was 4.1 +/- 1.8 mv on the right and 3.9 +/- 1.4 mv on the left. The compound muscle action potential ratio was 0.8 +/- 0.12 (range, 0.55-0.99). This study may be useful to evaluate the integrity of the thoracodorsal nerve and to assist in the diagnosis and prognosis of brachial plexus injury.
It was found that the axonal length was inversely related to motor conduction velocity (CV). However, it is not clear that sensory CV is inversely related to axonal length. The nerve lengths of the median sensory fascicles from the C6 and C7 intervertebral foramen to the digital branches of the thumb and middle finger were compared in ten cadavers. Sixty healthy subjects (24 men, 36 women; mean age 35, range 24-54 years) had median sensory CV testing. The median sensory nerve action potentials were obtained antidromically in the thumb and middle finger with wrist and elbow. The CVs across the forearm for the thumb and the middle finger fascicles were then calculated. It was found that the nerve length of C7 was longer than C6 with a difference of 3.6 +/- 0.6 cm. The mean forearm CV for the median sensory axons innervating the middle finger (60.0 +/- 3.9 m/s) was slower than the CV for the median sensory axons innervating the thumb (61.4 +/- 4.1 m/s,p = 0.0012). These results demonstrate that sensory CV is slowed by 3.9 m/s per 10 cm of axon length. This study confirms that the inverse relation of CV and axonal length reported in motor axons also applies to the sensory nerves.
We retrospectively reviewed electrodiagnostic studies from 1983 to 1994 and found 48 patients who met our criteria for mononeuropathy with axonal loss (40 ulnar, 4 peroneal, 4 radial). Appropriate diagnostic criteria required bilateral studies with a normal contralateral, sensory nerve action potential (SNAP) amplitude decrease of > 50% compared to contralateral, and/or distal compound muscle action potential (CMAP) amplitude decrease of > 40% compared to contralateral, and/or presence of denervation potentials; and sufficient electrodiagnostic investigation to rule out peripheral polyneuropathy. We conclude that in the electrodiagnosis of mononeuropathy with axonal loss: 1) a significant quantitative correlation between CMAP and SNAP amplitude percentage decrease does not exist (r = 0.274, p = 0.06), 2) SNAP amplitude percentage decrease [75.3 +/- 31.8%] is greater than CMAP amplitude percentage decrease [43.9 +/- 31.3%] (paired t-test, p = 0.0001), and 3) CMAP amplitude decrease is positively correlated with the presence of denervation potentials (Xtrend2 = 6.22, p = 0.013).