The QL muscle includes three layers, each with muscle fibers having a different direction. The superficial layer is the thinnest layer, which comprises the iliocostal and the iliothoracic muscle fibers. The middle layer comprises the lumbocostal muscle fibers, which differ in thickness. The deep layer consists of the medial iliolumbar fibers and the lateral iliocostal fibers. The QL muscle is thicker in the lower portion than in the upper portion . The muscle acts as a lumbar spine extensor, a lumbar stabilizer, and is involved in lateral tilting. The innervation occurs through the ilioinguinal nerve, the iliohypogatric nerve, and twelfth thoracic intercostal nerve .
MPS is a commonly diagnosed disease that affects up to 95% of people around the world, and 9 million suffer from this disorder in the United States alone . MPS is a chronic pain disorder mostly caused by MTrPs, that are located in the muscle belly. MPS is the main cause of pain in 85% of patients visiting pain clinics [17, 48]. The risk of MPS include various postural habits and occupational activities causing an excessive burden on a specific muscle [7, 53]. Postural habits and repetitive movements contribute to the progress of myofascial pain by causing overloading on specific muscles, the QL muscle being the most commonly involved .
Though the mechanism is not fully understood, one of the possible reasons for such movements having a negative effect is sarcomere shortening. Studies have revealed that shortening is due to an increase in the activation of the neuromuscular junction and its over-release of acetylcholine. Additionally, a large amount of calcium is released in the sarcoplasmic reticulum through a dysfunctional Ryanidine receptor, and sustained muscle contraction occurs along the calcium channel . To release muscle contraction, BoNT is a commonly used injective agent for MPS [23, 32, 44].
For treating MPS, it is critical to locate the MTrPs, which form what is called a taut band. MTrPs are shortened muscle fibers due to overly activated muscle contraction. Needle electromyography studies have demonstrated the transmission of low-amplitude electrical activity by MTrPs, which is called spontaneous electrical activity [2, 43, 45, 50]. The study by Kuan et al.  demonstrated that BoNT injection in MTrPs blocks acetylcholine release into the synaptic cleft and diminishes spontaneous electrical activity in MTrPs.
Several studies have shown that MTrP pathophysiology appears to be associated with intramuscular neural arborized areas [15, 24, 25, 30, 43]. The study by Xie et al.  showed that not only BoNT injection but also lidocaine-injection therapy in the intramuscular arborized area significantly reduces the degree and frequency of pain in patients at 6 months after treatment.
Injective treatment targeting the QL muscles is becoming commonly practiced for its effectiveness in relieving MPS [10, 22, 26, 36]. MPS involving the QL muscle frequently occurs when sitting cross-legged, which causes the hemipelvis to rise, approximating from the iliac crest to the 12th rib, and the shortening of the ipsilateral QL muscle. A common sleeping position, lying on one’s side with the adducted upmost lower, will likewise a reason for the shortened QL muscle. This can lead to MPS with patients usually complaining that their suffering is even worse at night .
Additionally, anatomical factors include leg length discrepancy, which causes excessive lumbar lordosis and excessive stress on the QL muscle. The compensatory scoliosis produced by the QL muscle is a necessary lumbar curvature needed to maintain balance. This leads to the overloading of the QL muscle, which leads to an excessive burden on it .
The intramuscular neural arborized area are injection target point for MPS, and commonly injected agents are BoNT, lidocaine, steroid, and normal saline [5, 13, 18]. In particular, injective BoNT treatment in MPS is known to remain effective up to 4 months, in contrast to the short-term effects of oral medication and lidocaine injections [5, 13]. When using BoNT injection to treat MPS, studies have suggested that treatment sessions should be conducted every 3 months to maintain pain reduction from MPS [22, 52].
The main, known, therapeutic consequences of BoNT are caused by releasing muscle contractions and easing the vicious pain cycle [34, 47, 49]. It is also assumed that the relief from muscle tightness and BoNT itself suppress the diffusion of neurotransmitters within the peripheral nerve, suppressing peripheral sensitization [37, 40]. Since BoNT acts on the neuromuscular junction, the broad and precise anatomical knowledge of the neuromuscular arborization patterns of the muscles is essential for attaining maximum relief with the lowest possible amount of BoNT.
Even though BoNT procedures are minimally invasive compared with surgical procedures, there is still a risk of damaging the nerve trunks, not the neural arborized area. Therefore, the precise knowledge of the anatomical features of the muscle should be understood. Several studies have conducted Sihler staining, which is a whole-mount staining method that dyes myelin sheaths, providing an effective visualization of nerve endings without damaging the nerves [39, 55–57, 62]. Using Sihler staining on the QL muscle will facilitate an accurate and comprehensive understanding of the neural distribution.
Presently, there is absolutely no standardized injection site or optimal dose for BoNT of the QL muscle. The volume of BoNT must be adequate to present a sufficient level of the toxin in the arborized area of neural distribution. Reports on complications suggest that BoNT should be delivered in the arborized area of the target muscle with small doses and fewer injections.
Overall, we suggest that injective treatment using BoNT, lidocaine, normal saline, steroids, and EMG need to be directed in the three regions: the middle portion from L3 to L4 and from L4 to the iliac crest and the lateral portion from L3 to L4 (Fig. 4).