Fetal alcohol spectrum disorder (FASD) encompasses a broad range of central nervous system (CNS)-related disabilities representing a mild-to-severe continuum of neurodevelopmental disorders that include mood and sensory function. The prevalence of FASD is estimated at ~5% in school-aged children who are prone to develop inappropriate responses to stressful stimuli leading to higher rates of anxiety and low touch tolerance. Low touch tolerance has been self-reported in 33.6% of FASD-affected individuals. The FASD manifestations of sensory abnormalities like pathological light-touch hypersensitivity, a hallmark of chronic pain may be a result of abnormal neurological relays the spinal cord, and from spinal cord to brain. Animal modeling of FASD that utilize prenatal alcohol exposure (PAE) demonstrate mood disorders such as anxiety-like behavior and low touch tolerance, which support these clinical observations of mood and tactile dysregulation. In an effort to contextualize central nervous system (CNS) processing of stress and resultant mood disorders that are exacerbated by PAE, this review outlines the fundamentals of the neurocircuitry of stress from the perspective of the central autonomic network (CAN), differentiating physiological vs. psychological stressors with a focus on elements of the limbic system, including the medial prefrontal cortex (mPFC), amygdala (AMG), hippocampus (HIPP), hypothalamus, cingulate cortex, and brainstem periaqueductal gray (PAG), locus coeruleus (LC), and the nucleus of the solitary tract (NTS) of the medulla. The review addresses stress-sensitized CNS circuits and the underlying immune signaling molecules that may be responsible for heightened stress responses. Adolescence will be discussed as a critical corticolimbic developmental period that is itself highly susceptible to stressors, which is further impacted by PAE leading to stress-related anxiety with lifelong consequences. Linking the heightened neuroimmune response of offspring with PAE, a discussion is included of rodent models demonstrating PAE as a risk factor for developing painful tactile neuropathies following sciatic nerve injury mediated by sensitized and over-active spinal glial cytokine actions. Included in this discussion is the role of limbic forebrain, subcortical and even brainstem circuits that process and regulate mood and stress also engage the emotional and sensory-discriminative aspects of pain processing. Lastly, the impact of PAE on sensitized neuroimmune factors that link stress to touch allodynia in the absence of nerve injury is briefly discussed. These topics aim to help the reader gauge the profound impact of PAE on the CAN, and immune signaling molecules in limbic areas and spinal cord that drive sensitized stress sequelae, which should now include exaggerated pain states as well as anxiety disorders.