Neuromuscular effects of stun device discharges.

BACKGROUND

Stun guns or electromuscular incapacitation devices (EMIs) generate between 25,000 and 250,000 V and can be discharged continuously for as long as 5 to 10 min. In the United States, over 200,000 individuals have been exposed to discharges from the most common type of device used. EMI devices are being used increasingly despite a lack of objective laboratory data describing the physiological effects and safety of these devices. An increasing amount of morbidity, and even death, is associated with EMI device use. To examine this type of electrical injury, we hypothesized that EMI discharges will induce acute or delayed cardiac arrhythmia and neuromuscular injury in an animal model.

METHODS

Using an IACUC approved protocol, from May 2005 through June 2006 in a teaching hospital research setting, 30 Yucatan mini-pigs (24 experimentals and 6 sham controls) were deeply anesthetized with ketamine and xylazine without paralytics. Experimentals were exposed to discharges from an EID (MK63; Aegis Industries, Bellevue, ID) over the femoral nerve on the anterior left hind limb for an 80 s exposure delivered as two 40 s discharges. EKGs, EMGs, troponin I, CK-MB, potassium, and myoglobin levels were obtained pre-discharge and post-discharge at 5, 15, 30, and 60 min, 24, 48, and 72 h (n = 6 animals) and 5, 15, and 30 d post-discharge (n = 6 animals at each time point). Skin, skeletal muscle, and peripheral nerve biopsies were studied bilaterally. Data were compared using one-way analysis of variance and paired t-tests. P-values <0.05 were considered significant.

RESULTS

No cardiac arrhythmias or sudden deaths were seen in any animals at any time point. No evidence of skeletal muscle damage was detected. No significant changes were seen in troponin I, myoglobin, CK-MB, potassium, or creatinine levels. There were no significant changes in compound muscle action potentials (CMAP). No evidence of conduction block, conduction slowing, or axonal loss were detected on EMG. M-wave latency (M(lat), ms), amplitude (M(amp), mV), area (M(area), mV-ms), and duration (M(dur), ms) were not significantly affected by MK63 discharge compared with contralateral or sham controls. F-wave latency (F(lat), ms), a sensitive indicator of retrograde nerve conduction and function, was not significantly affected by MK63 discharge compared with contralateral or sham controls. No significant histological changes were seen at any time point in skeletal muscle or peripheral nerve biopsies although mild skin inflammation was evident.

CONCLUSIONS

There was no evidence of acute arrhythmia from MK63 discharges. No clinically significant changes were seen in any of the physiological parameters measured here at any time point. Neuromuscular function was not significantly altered by the MK63 discharge. In this animal model, even lengthy MK63 discharges did not induce muscle or nerve injury as seen using EMG, blood chemistry, or histology.