# Diagnostic Limitations and Aspects of the Lumbosacral Transitional Vertebrae (LSTV)
## 1 Introduction
The relationships between IVD degeneration (intervertebral disc degeneration) and the LSTV are differentiated in the literature. In LSTV type I, the highest numbers are reported in some papers; however, no pathological effect on the disc segment is described. In contrast, in LSTV type II-IV, the adjacent cranial disc segment is reported as the segment most exposed to degeneration. The distinction between unilateral and bilateral pathology forms another focus, which is also associated with the question of soliotic change. A clear prediction cannot be derived so far. Pathologies of adjacent structures as a cause of complaints are also increasingly subject to clarification. The segmental nervous assignment was examined thereby, too. The disc degeneration is concentrated on the cranially adjacent segment L4/5. In contrast, the disc of the affected segment of the LSTV type II-IV is mechanically protected by the restriction of movement. However, this general statement still lacks a differentiated assessment dependent on the type of the LSTV. The biomechanical workup of motion restriction and the associated disc loading or unloading are at the beginning of scientific interest [11]. A paper by [PERSON] et al. states that the incidence of disc herniation is decreased in the segment of the LSTV. In contrast, the incidence of disc herniation or spondylolisthesis in the cranial segment L4-5 is increased in the presence of the LSTV. Therefore, the LSTV are considered a risk factor for degenerative disc changes in the level above the transitional vertebra [12]. In the LSTV type II group, compression of the L5 nerve due to a bony or synovial cause of nearthosis has also been reported [13]. The question of nerve innervation in the LSTV has also been raised by intraoperative EMG studies, and no pathological distribution was found compared with the normal spine [14]. A significant association between lumbar stenosis and the LSTV is described in a retrospective cross-sectional study [15]. The bony structures show altered trabecular distribution in the LSTV comparedto healthy spine in a cadaveric study [16]. In a prospective cadaver study by [PERSON] et al. the segmental mobility of the affected segment and adjacent segments was measured and described as follows:  
The results of this study suggest that patients with [PERSON] syndrome have significantly altered spinal biomechanics and may develop pain due to increased loading forces at the LSTV joint during ipsilateral lateral flexion and axial rotation. In addition, increased motion in the upper levels in the presence of the LSTV can lead to degeneration over time [17]. After outlining the pathological changes and movement limitations, the focus turns to the possible causes of LBP:  
There are different answers to the question of whether LSTV type I causes symptoms, although diagnostic uncertainty remains as described above. There is also no clear answer to the distinction between unilateral and bilateral changes as the cause of symptoms. However, the more stable the constructs of the LSTV are (type II-IV), the more likely degeneration of the cranially adjacent segment is responsible for the complaints. Lumbar complaints (LBP) in the presence of the LSTV were originally noted by [PERSON] in 1917 and are therefore referred to as \"Bertolotti syndrome\" [18]. [PERSON] et al. found Bertolotti syndrome in 769 MRI scans of LBP patients in 4.6% of the patients studied. In patients with LBP younger than 30 years, 11.4% showed LSTV [19]. A high frequency of the LSTV was found in young male patients with LBP, and it was mostly subtype I. LSTV type I and associated disc and facet degeneration were notable in this group [20]. A review of the literature on the problem of discomfort in the LSTV (Bertolotti syndrome) shows that comparable changes are found with and without discomfort.