**1. Introduction and epidemiology**

The specific definition of spinal shock (SS) has evolved over the past two centuries. Nonetheless, a significant level of ambiguity, controversy, and confusion still exists when differentiating between neurogenic shock (NS) and SS. Whytt first described this clinical entity in the 1750s without using the term "shock" and without the understanding of the underlying basic science and anatomy to accurately inform the definition. Rather, he focused on the observation that SS was associated with a loss of sensation accompanied by motor paralysis with initial loss but gradual recovery of reflexes [1]. The definition was then expanded over by Hall in the early 1840s, officially utilizing the terms "spinal shock" and "reflex arc" [2]. Another contributing factor to the previously elusive definition is the lack of uniform clinical presentation, manifestation, and duration of SS. Due to the substantial clinical variability and heterogeneity of presentations, we must first discuss the definitional aspect of SS so that the reader may have a clear idea and a


#### **Table 1.**

*Four phases of spinal shock by Ditunno et al.*

working model for our subsequent discussions of diagnosis, patient presentation, and treatment approaches.

Ditunno made a subtle point that the controversy surrounding the definition of SS could be attributed to observations made clinically. More specifically, he noted that not all reflexes are eradicated in a strictly binary on/off fashion. Some reflexes may only be depressed and yet still can be technically elicited. Finally, he noted that the resolution of SS does not occur in a binary fashion and often follows a prolonged course of weeks to months [3]. Similar observations by Illis suggested that the definition of SS cannot be comprehensive without including subcomponent definitions of clinical phases [4]. For the purposes of this chapter, we will utilize Ditunno's four-phase model of spinal shock, building upon the groundwork described by various pioneers such as Whytt and Hall [1, 3]. This model allows for clarification of the ambiguity surrounding the disease process while still retaining flexibility to appreciate the variability among clinical presentations. The details of Ditunno's four-phase model can be seen in **Table 1** [3].

The phases are organized according to post-injury time and the nervous system's response to insult. Of note, we will hold off on the discussion of each phase until the *Etiology and Pathophysiology* section as the separation of phases requires delving into how the neurons are responding to their environment as time progresses.

In 2007, there was an estimated global spinal cord injury (SCI) incidence of 2.3 cases/100,000 inhabitants [5]. It has been estimated 45% of SS cases are associated with motor vehicle collisions (MVC), 34% with domestic accidents, 15% with sporting accidents, and 6% with self-harm [6]. The incidence of SCI can vary across geographic, socioeconomic, and cultural factors, including the prevalence of contact sports and differences in primary transportation modality. All of the above factors are important determinants of the incidence of SCI. Finally, no discussion of the topic of SCI is complete without mentioning the tremendous human and economic cost associated with these injuries worldwide [7–9].
