We thank the pertinent comment by Dr. Finsterer regarding our article entitled “Injury to the Left Sciatic and Right Common Peroneal Nerves Combined With Multifocal Rhabdomyolysis in a Survivor of the Itaewon Crowd Crush: A Case Report” and for sharing his views.1 We acknowledge the potential concerns raised in the letter and would like to further address several issues in response to the specific questions posed.

Regarding why the patient did not suffer traumatic nerve and muscle lesions in her upper limbs, head, trunk, or chest, this was explained by the position of the patient at the time of the event. The patient stated that she was positioned quite close to the front row of the crowd when the crushing incident occurred. Therefore, as the crowd was pushing from behind, the patient fell forward, meaning that her lower extremities and a part of her trunk were mainly compressed by the crowd, yet her upper extremities and head were, fortunately, not enveloped. Thus, when the patient initially visited the emergency room, she only complained of pain in the lower limbs and lower back and did not report any pain or weakness in the upper extremities.1 Consequently, we did not perform a nerve conduction study (NCS) or needle electromyography (EMG) on the upper limbs at that time.

Secondly, we would like to provide additional information regarding the process of excluding seizures. When the patient initially presented at the emergency room, her mental state was close to lethargy, although with no loss of consciousness. Yet, despite her lethargic state, she remained capable of obeying commands. Additionally, she had no history of seizures, and neither ictal nor post-ictal symptoms were evident after admission. Moreover, during the patient's initial visit to the emergency room, the primary medical team conducted a brain computed tomography (CT) to rule out any structural abnormalities. The brain CT revealed no abnormalities and provided no indication of any brain-related issues.1 We assessed that the initial alteration in consciousness was unlikely to be indicative of a seizure. Consequently, further evaluations, such as brain magnetic resonance imaging (MRI) and electroencephalogram (EEG), were deemed unnecessary.

The letter also highlighted the potential for myocardial damage. She did initially present with mild sternal pain. The initial CK-MB level was measured at 6.8 ng/mL (normal range: 0–40 ng/mL), and troponin-I was elevated at 562.2 ng/L (normal range: < 15.6 ng/L), which prompted suspicion of cardiac contusion. Subsequently, the chest surgery (CS) department conducted a cardiac echography and electrocardiogram (ECG), which yielded no additional cardiac abnormalities. Consequently, while mild cardiac contusion remained a possibility, the main cause of hyper-CKemia was determined not to be a cardiac problem. Furthermore, the patient consistently reported severe tenderness in her bilateral lower extremities leading to a clinical correlation that rhabdomyolysis might be the primary cause of hyper-CKemia. Therefore, an additional cardiac MRI was not performed. Instead, under the consultation of the CS department, the patient's cardiac markers and ECG were continuously monitored, and subsequently, the cardiac markers returned to normal within 3–4 days.

The next issue was the reference limits for the NCS parameters. The sensory NCS showed a borderline reduced amplitude in sensory nerve action potential in the right superficial peroneal nerve (reference > 7 µV for the superficial peroneal nerve and > 7 µV for the sural nerve).2 The motor NCS indicated a decreased compound muscle action potential amplitude (reference > 2.5 mV for the recorded peroneal nerve in the extensor digitorum brevis and > 4 mV for the recorded tibial nerve in the abductor hallucis) with conduction block and segmental slowing around the fibular head in the right common peroneal nerve, compared to the left side.123 In our laboratory, we considered normal values for the peroneal and tibial motor nerves to be around a minimum of 40 m/s.2 While the right peroneal nerve in the motor NCS showed a borderline decrement in conduction velocity compared to the reference value, it also showed a significant decrease compared to the left side. Moreover, we may provide the onset latency (reference < 3.1 ms for superficial peroneal nerve and < 3.1 ms for sural nerve) of the sensory nerve action potentials as the data of conduction velocity in the sensory nerve, which were not described in our original article.2 The distal onset latency for the superficial peroneal nerve was 2.29 ms (right) and 2.03 ms (left), while it was 1.72 ms (right) and 1.98 ms (left) for the sural nerve within the normal value in the initial study.

With regard to the fifth limitation, we also conducted F-wave and H-reflex tests, even though they were not included in Table 1 of the original article.1 For the F-wave, in the initial study, there was no response in the right common peroneal nerve, and the minimum latency was 45.36 ms in the left common peroneal nerve. The tibial nerve demonstrated a minimum latency of 48.44 ms on the right and 48.85 ms on the left. Concerning the H-reflex, the latency was 30.73 ms on the right, and there was no response on the left side in the initial study. As no abnormal findings were observed in the lumbosacral CT and MRI, which were performed for the differential diagnosis of proximal lesions, such as radiculopathy, the absence of the H-reflex on the left side is thought to reflect the lesions in the sciatic nerve or lumbosacral plexus. Although there was abnormal spontaneous activity in the left lumbar paraspinal muscles in the needle EMG, this was determined to be a result of direct muscle injury. Therefore, the results of the needle EMG in the left lower extremity suggested a left sciatic nerve or lumbar plexus lesion rather than lumbar radiculopathy, which was in line with the swelling of the sciatic nerve in magnetic resonance neurography (MRN).4

Dr. Finsterer pointed out the discrepancy observed between the swelling in the left sciatic nerve depicted in Fig. 1 of the original article and the normal values recorded for the left peroneal and sural nerves in Table 1 of the original article.1 We considered the possibility of pure direct muscle injury or a combination of a sciatic nerve lesion and direct muscle injury in her left leg because of a normal NCS in the left lower extremity. However, we judged that the electrophysiologic findings at least reflected a left proximal sciatic nerve lesion for the following reasons: 1) the absence of a response in the H-reflex in the left tibial nerve, 2) the evidence of re-innervation in the left sciatic nerve-innervated muscles in the follow-up needle EMG, which was unmentioned in the original article, 3) no clear evidence of a direct injury to the lower leg muscles covered in the left knee MRI (Fig. 1), and 4) the absence of any abnormal spontaneous activity in the left vastus medialis muscle, which was not innervated by the sciatic nerve. Furthermore, the prominent left sciatic nerve swelling in the MRN strongly suggested a sciatic nerve insult.4 However, the within-normal value in the NCS of the left lower extremities might be attributed to the mechanism of the left sciatic nerve lesion, possibly due to mild axonal loss. Thereby, she had a good recovery in motor function in the left lower extremity within 3 months.

Finally, in regard to using the words “liver enzymes,” I would like to clarify that in our manuscript, we used the term "liver enzyme elevation" as a general term to encompass the increase in AST and ALT levels. Additionally, her abdominal–pelvic CT did not reveal any abnormalities indicative of liver contusion or laceration. We did not intend to imply liver damage specifically by using this expression; rather, it was chosen to collectively refer to the enzymes involved. We understand that our choice of terminology may have led to confusion, and we agree with your interpretation that the elevation of these enzymes may be attributed to skeletal muscle injury. We apologize for any misunderstanding that may have arisen due to the terminology and appreciate your understanding.

We express our sincere appreciation for your interest in our case report and thank you for providing valuable feedback. Your comments have been instrumental in addressing potential misunderstandings arising from the limited word count and format of case reports, thereby helping to reduce any confusion among other readers. We are delighted that our response in the letter's comment section has allowed for further clarification and facilitated more in-depth discussions. We hope that our reply has adequately addressed your inquiries and met the standards of your expectations.

Yoonhee Kim, Kyeongil Min, Myung Woo Park, Hyun Iee Shin and Du Hwan Kim

Department of Physical & Rehabilitation Medicine, Chung-Ang University College of Medicine, Seoul, Korea.

Address for Correspondence: Du Hwan Kim, MD, PhD. Department of Physical & Rehabilitation Medicine, Chung-Ang University Hospital, Chung-Ang University College of Medicine, 102 Heukseok-ro, Dongjak-gu, Seoul 06973, Korea. ri-pheonix@hanmail.net

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