f) HIV [37]; and (g) infection [30,33,34,40,45,47,57]. Pregnancy was also included as exclusion criteria in almost half of the trials [30,32,34,37,38,40,46,50–52,54–56,59]. Two clinical trials did not refer to any possible visceral aetiology of neck pain in their inclusion and exclusion criteria [44,60]. 4. Discussion The present findings suggest that amongst the most cited and the most recently published clinical trials assessing treatment efficacy in NP there is a lack of consideration for VRP as a plausible source of NP. This appears to be the case when the eligibility criteria for recruiting participants are analyzed. Only 20% of all selected trials (six out of 30) defined stringent enough criteria to avoid the recruitment of individuals with a suspected visceral referred NP. All these studies were amongst the top 15 most cited articles. Three other trials excluded patients with a specific aetiology or cause for their NP, although authors did not even mention the visceral area. This implies that most of the assessed trials might have included patients with a visceral source of NP despite the fact that the visceral disorder would not be the target of the treatment. Therefore, it might show an underconsideration of this neck pain aetiology; in addition, incorrect estimations of the effects or efficacies of the interventions could have occurred. 4.1. Eligibility Criteria Used by Trials to Select NP Patients Manchikanti et al. [38] considered as eligible, those patients with a positive response to cervical facet joint nerve blockers, which excluded individuals with visceral referred NP. The rest of the clinical trials, however, established general inclusion criteria; e.g., neck stiffness; mechanical pain with reproducibility of symptoms during physical examination, neck movement, or posture maintenance; and myofascial pain syndrome, among others. All these symptoms mainly refer to increased local sensitization and muscle tension, which can be due to a visceral issue. A primary visceral disorder may also be accompanied by hyperalgesia of the painful area, and is often associated with sustained muscle contraction [61], and it may extend to subcutaneous tissues when the visceral disorder is persistent [62]. Furthermore, the increased muscle tone may explain mechanical symptoms and lead, in the long-term, to the presence of myofascial trigger points and myofascial pain syndrome [63,64]. Hence, visceral pain can evoke many different neck symptoms, including muscle spasms in addition to pain [15], and when sustained, may help to develop central sensitization and cortical changes [61]. Despite all this, surprisingly, the visceral aetiology of NP was only properly considered in six clinical trials [38,43,45,47,48,50]. These findings may imply a general misdiagnosis of NP in research and clinical scopes, thus patients with visceral referred NP might not receive the most accurate therapeutic approach. Visceral pain shares many features with pain from deep somatic structures and requires well-developed Diagnostics 2019, 9, 186 15 of 23 propedeutics to avoid inadequate diagnosis and treatment [65]. The test for cutaneous allodynia appears to have the greatest likelihood of identifying a visceral source of pain compared to somatic sources of pain [16]. Therefore, a detailed clinical history, physical examination, and supplemental laboratory and imaging examination is needed to diagnose the primary source of pain [61,64], because the somatic manifestation will persist until the visceral disorder resolves by itself or has been discovered and treated [23,66]. This discovery is more likely to happen in subjects with constant neck pain and/or aggravation of visceral symptoms, but is less likely in recurrent, episodic NP and/or subtle visceral symptoms [15]. Additionally, in cases of chronic NP, the right diagnosis can be favored along the course of the disease by the obtaining of abnormalities in blood, urine, digestive, heart . . . tests, either developed ad hoc to diagnose the origin of NP or during medical assessments for other reasons. Since many of the visceral disorders which may trigger NP are chronic, they enable the presence of either episodic (due to episodic aggravation of the visceral disorder), recurrent (due to frequent aggravation of the visceral disorder), or chronic NP. 4.2. Somatic Consequences of Visceral Disorders Visceral referred NP is linked to the involvement of the vagus and/or phrenic nerves. The nociceptive input from any of the organs innervated by the vagus nerve sensitizes the trigeminocervical nuclear complex that descends to C3 or C4 levels, and may trigger a headache [67] and/or NP [14]. The phrenic nerve is a motor and sensitive nerve formed by C3–C4 roots, with C5 as an accessory root. Either directly or through celiac connections, it supplies the diaphragm, pleura, right atrium [68] pericardium [68,69], esophagus [70], peritoneum [68,71], stomach [15], falciform and coronary ligaments of the liver [72], the Glisson capsule [72,73], the hepatic vein [74], the inferior vena cava [68,70,74], the liver [68,72,75] (parenchyma) [74], the gallbladder [72,76,77] and the rest of the biliary tract [71,72,77]—including the duodenal papilla and the sphincter of Oddi [77,78] —, the pancreas [15], the small intestine [15], and the suprarenal glands [68,70,71]. Hence, disorders of many of these structures, such as the pancreas, or even the spleen or kidneys, can evoke referred pain along the C3–C4 dermatomes either due to the autonomic connections, diaphragmatic pressure, or peritoneal irritation [15]. This has been described as “phrenic pain” [23]. To date, there is no data about the prevalence of NP of visceral origin in general practice or musculoskeletal settings. Nevertheless, in a previous study [79] that seemed not to consider the visceral aetiology, a well identified cause of the NP was not found in 32% of patients receiving a complete evaluation in a private pain clinic, where, probably, those NP patients with the most severe symptoms are a majority. As well, a history of previous trauma was present in most of the patients. However, the authors do not clarify if the inability to achieve a specific cause was more frequent in patients who had previous trauma or in those who did not. It is