Somatic Symptom Disorder (SSD) manifests when a patient experiences extreme levels of anxiety, stress, and preoccupation in association with a somatic symptom. These patients seek advice from many clinicians, and the diagnosis can be difficult to make: this causes increased stress for the patient and is expensive for healthcare systems. As a result, alternative forms of diagnosis have been investigated. The observation that SSD patients have higher pain sensitivity has sparked interest in examining SSD patients' pain pathways to determine neurobiological models. This paper presents two recently proposed models: the central sensitization model and the somatosensory amplification model. The central sensitization model suggests that peripheral pain-sensing nociceptive neurons become hyperexcitable and/or become less suppressed. This may occur through either hyper- or hypo-cortisolism, both of which have been observed in SSD patients. The somatosensory amplification model refers to higher order brain regions, and occurs when a patient has a greater focus to sensations, more selective focus of certain sensations, and the mental amplification of these sensations. It has been proposed that this occurs through changes in anterior cingulate cortex and insula, which may cause alterations in rational thought, anticipation, perception, and social-emotional cognition.