**2. Systemic complications induced by SCI**

These acute and chronic changes arise and are worsened by the gradual multiple organ dysfunction that in combination with an increasingly sedentary lifestyle leads the SCI patient to metabolic syndrome (trunk fat, low HDL levels, and high triglyceride levels), which affects more than a half of SCI patients [15], implying threefold increased risk of developing cardiovascular disease and fivefold increased risk of developing diabetes [16], as well as other systemic alterations like hematological (anemia in acute phase, thrombocytosis) and biochemical [low concentrations of albumin and globulins and high concentration of aspartate aminotransferase (AST)] [17], decreased immune function (spinal cord injury-induced immune deficiency syndrome SCI-IDS) [18], bowel dysfunction, and gut dysbiosis [19], perhaps, the last three caused by autonomic dysreflexia [20].

#### **2.1 Is autonomic dysreflexia responsible for other comorbidities in SCI?**

Clinically, patients with SCI have several comorbidities associated to the level of injury; when the lesion is above the seventh thoracic vertebra, it usually produces sympathetic hyperactivity causing symptoms like systemic vasoconstriction and parasympathetic activity, below and above the site of injury, respectively; this set of alterations are called autonomic dysreflexia (AD) [21].

AD is defined as "episodic hypertension and concomitant baroreflex-mediated bradycardia initiated by unmodulated sympathetic reflexes in the decentralized cord" [22]. This ambiguous definition identifies the elevation in systolic blood pressure as the main sign; however, these diagnostic criteria are not well defined [23]; in addition, these patients can suffer other symptoms such as headache, sweating, anxiety, and arrhythmia [24].

AD incidence in patients with lesion at or above T6 segment is 92.8% and, in some cases, could be asymptomatic, up to 42.9% [25] depending on intensity, level, and time elapsed since SCI. It is important because it represents the principal

#### *Beyond the Quality of Life in Bowel Dysfunction after Spinal Cord Injury: Approaches… DOI: http://dx.doi.org/10.5772/intechopen.92599*

cause of mortality and must be diagnosed timely to prevent severe complications like cardiac arrest, stroke, and seizures [22].

The impaired visceral or somatic stimulation of the sympathetic preganglionic neurons (SPN), due to colon and bladder overdistension (most frequent), skin lacerations, and pressure sores, results in a massive sympathetic reflex as a result from three things: (1) the maladaptive plasticity of neural network, (2) the imbalance between excitatory and inhibitory neurotransmitters, and (3) the enhanced peripheral adrenergic sensitivity, which is predominantly established in chronic phase, 3–6 months after injury [21].

In addition, other less recognized alteration is in the immunomodulatory response, described as the SCI-IDS, characterized by decreased lymphocyte activity with poor proliferation of hematopoietic progenitor cells and spleen (secondary lymphoid organ) atrophy due to the loss of negative feedback on releasing catecholamines causing poor maturation of T and B lymphocytes [26].

Is well-known that the disruption of the parasympathetic nervous system (PNS) also affects cell proliferation [27, 28], and recent findings had confirmed that parasympathetic activity is linked to cell proliferation and cell cycle-related gene expression above the neurological level of injury rather than below it; in which case, the main neurotransmitter involved is the acetylcholine in the upregulation of some genes that participate in the chromosomal instability [29].

This suggests that SCI goes beyond the patient's locomotor impairment explaining the increased risk of cancer in these patients and the severe repercussions to the gastrointestinal tract conditioning BD (gastric ulcers, paralytic ileus, anal incontinence, anal fissures, and hemorrhoids) [22], a complex phenomenon secondary to hypoxia caused by the massive sympathetic discharge.
