Consequences of a spinal cord injury (SCI) entail much more than damage to the spinal cord. The lives of people with SCI, along with those around them, experience profound long-lasting changes in nearly every life domain. SCI is a physical (biological) injury that is inextricably combined with various psychological and social consequences. The objective of this review is to present psychosocial challenges following SCI through the biopsychosocial model, beginning with acknowledgement of the larger societal effects of ableism and stigma before addressing the many unique psychosocial aspects of living with SCI. Included in this review are qualitative studies and systematic reviews on current psychosocial outcomes and consequences. This paper attempts to structure this information by dividing it into the following sections: relationships and family; changes in finances and employment; issues related to the person’s living situation; community reintegration; factors associated with mood and coping (e.g., depression, anxiety, substance use, and PTSD); self-harm behaviors (ranging from nonadherence to suicide); effects of traumatic brain injury; considerations regarding sexual health; aging with SCI; and concludes with a brief discussion about post-traumatic growth. Cultivating an understanding of the unique and interrelated psychosocial consequences of people living with SCI may help mitigate the psychosocial aftermath and serve as a reminder to providers to maintain a person-centered approach to care.

The spinal cord is a conduit within the central nervous system (CNS) that provides ongoing communication between the brain and the rest of the body, conveying complex sensory and motor information necessary for safety, movement, reflexes, and optimization of autonomic function. After a spinal cord injury (SCI), supraspinal influences on the spinal segmental control system and autonomic nervous system (ANS) are disrupted, leading to spastic paralysis, pain and dysesthesia, sympathetic blunting and parasympathetic dominance resulting in cardiac dysrhythmias, systemic hypotension, bronchoconstriction, copious respiratory secretions and uncontrolled bowel, bladder, and sexual dysfunction. This article outlines the pathophysiology of traumatic SCI, current and emerging methods of classification, and its influence on sensory/motor function, and introduces the probable comorbidities associated with SCI that will be discussed in more detail in the accompanying manuscripts of this special issue.

The autonomic nervous system (ANS), composed of the sympathetic and parasympathetic nervous systems, acts to maintain homeostasis in the body through autonomic influences on the smooth muscle, cardiac muscles, blood vessels, glands and organs of the body. The parasympathetic nervous system interacts via the cranial and sacral segments of the central nervous system, and the sympathetic nervous system arises from the T1–L2 spinal cord segments. After a spinal cord injury (SCI), supraspinal influence on the ANS is disrupted, leading to sympathetic blunting and parasympathetic dominance resulting in cardiac dysrhythmias, systemic hypotension, bronchoconstriction, copious respiratory secretions and uncontrolled bowel, bladder, and sexual dysfunction. Further, afferent signals to the sympathetic cord elicit unabated reflex sympathetic outflow in response to noxious stimuli below the level of SCI. This article outlines the pathophysiology of SCI on the ANS, clinical ramifications of autonomic dysfunction, and the potential long-term sequelae of these influences following SCI.

Individuals with a spinal cord injury (SCI) have a unique physiology characterized by sarcopenia, neurogenic osteoporosis, neurogenic anabolic deficiency, sympathetic dysfunction, and blunted satiety associated with their SCI, all of which alter energy balance and subsequently body composition. The distinct properties of “neurogenic obesity” place this population at great risk for metabolic dysfunction, including systemic inflammation, hyperglycemia, dyslipidemia, and hypertension. The purpose of this article is to demonstrate the relationship between neurogenic obesity and the metabolic syndrome after SCI, highlighting the mechanisms associated with adipose tissue pathology and those respective comorbidities. Additionally, representative studies of persons with SCI will be provided to elucidate the severity of the problem and to prompt greater vigilance among SCI specialists as well as primary care providers in order to better manage the epidemic from a public health perspective.

Spinal cord injury (SCI) results in motor paralysis and sensory loss that places individuals at particularly high risk of pressure injuries. Multiple comorbidities associated with autonomic, cardiovascular, pulmonary, endocrine, gastrointestinal, genitourinary, neurological, and musculoskeletal dysfunction makes it even more likely that pressure injuries will occur. This manuscript will review the structure and function of the integumentary system, and address the multidisciplinary approach required to prevent and manage pressure injuries in this vulnerable population.

The spinal cord is a conduit within the central nervous system (CNS) that provides ongoing communication between the brain and the rest of the body, conveying complex sensory and motor information necessary for safety, movement, reflexes, and optimization of autonomic function. After a traumatic spinal cord injury (SCI), supraspinal influences on the peripheral nervous system and autonomic nervous system (ANS) are disrupted, leading to spastic paralysis, sympathetic blunting, and parasympathetic dominance, resulting in cardiac dysrhythmias, systemic hypotension, bronchoconstriction, copious respiratory secretions, and uncontrolled bowel, bladder, and sexual dysfunction. This article outlines the pathophysiology of the less reported nontraumatic SCI (NTSCI), its classification, its influence on sensory/motor function, and introduces the probable comorbidities associated with SCI that will be discussed in more detail in the accompanying manuscripts of this special issue. Finally, management strategies for NTSCI will be provided.