The anterior cord syndrome involves the anterior two-thirds of the spinal cord (Fig. 3.1b). Clinically apparent, the corticospinal and the spinothalamic tract are predominantly affected with resulting paralysis and impaired sensation for temperature and pain below the lesion level. Autonomic function is frequently affected with resulting bladder, bowel, cardiovascular, and sexual dysfunction. This pattern is frequently described in the context of spinal cord ischemia resulting from anterior spinal artery occlusion, either spontaneously or in the course of thoracoabdominal vasculosurgical procedures. Furthermore, compression spinal cord injury at thoracic level resulting from median disk prolapse or fractured bone fragments can induce a similar clinical picture. Usually the prognosis in terms of recovery is less favorable.

The posterior (Fig. 3.1d) and infrequently the lateral white matter are typically affected in metabolic and toxic spinal cord disease (see chapter 8) with reduced/abolished deep sensation and consecutive sensory ataxia. Rarely a compressive cause of SCI (tumor, spinal stenosis) can be identified [2]. As soon as the lateral columns including the corticospinal tract become involved, spastic paraparesis will present. Depending on the cause, proper treatment of the metabolic cause (e.g., cobalamin substitution) can reverse symptoms and thus promote recovery of function. Isolated posterior column dysfunction due to compression spinal cord injury is rarely observed.

Unilateral cord syndrome or Brown-Sequard syndrome produces greater ipsilateral proprioceptive and motor loss, while contralaterally pain and temperature sensations are lost. Charles-Édouard Brown-Séquard was a neurologist, who described for the first time, the crossing of pain and temperature pathways at the spinal level. Brown-Sequard syndrome is caused by a hemilesion of the spinal cord (Fig. 3.1c), in most instances caused by a traumatic cause, mostly motor vehicle accidents, gunshot wounds, and assaults. Nontraumatic cases are frequently associated with compressing tumors or spinal stenosis [2]. A rare condition – idiopathic spinal cord herniation – leads in almost all instances to a Brown-Sequard syndrome after ventral displacement of the anterior or anteriolateral funiculus unilaterally at thoracic level [3]. Although not common, spinal cord ischemia in particular at cervical levels can lead to a unilateral spinal cord syndrome [4]. Less than 20 % of all defined SCI syndromes have been described as Brown-Sequard syndrome [2].

Central cord syndrome, which refers to a lesion of the central region in the cervical spinal cord (Fig. 3.1e), is characterized by a disproportionately more severe motor impairment in the upper versus the lower extremities. A difference of at least ten motor score points in the upper versus the lower extremities supports the diagnosis of a central cord syndrome according to a consensus paper [5]. It was previously thought that a somatotopic orientation of corticospinal axons within the cervical spinal cord accounted for the predominant dysfunction of upper extremity motor performance in central cord syndrome. However in primates, a somatotopic orientation of this descending pathway cannot be confirmed. Alternatively, the corticospinal tract mediates skilled arm and hand movement more so than voluntary lower extremity movement [6], and therefore central cord lesions affecting predominantly the CST induce disproportionate functional deficits in the upper extremities. Another potential explanation – lower motoneuron damage in the ventral horn of the cervical spinal cord – is being debated. Central cord syndrome is considered as the SCI syndrome of the elderly with an average age of 53 years. The most frequent etiology is traumatic injuries due to falls followed by motor vehicle accidents [2]. Central cord syndrome has a relatively good prognosis in terms of recovery of (lower extremity) function. Out of all defined incomplete SCI syndromes, central cord syndrome is the most frequent one accounting for almost 50 % of the individuals [2].

According to the International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI) published by ASIA [7], complete spinal cord injury is defined as the absence of sensory and motor function in the sacral segments S4–5. Clinically speaking it means the absence of light touch/pinprick sensation in the dermatomes S4–5 and deep anal pressure as well as the absence of voluntary anal sphincter contraction. Severe compression/contusion of the spinal cord leads to a typical pattern of spinal cord destruction. The center of the cord is completely destroyed, whereas an outer rim of white matter tracts remains intact, even in the majority cases of clinically complete spinal cord injury [8]. It has been assumed that descending motor pathways such as the corticospinal tract and ascending sensory pathways such as the spinothalamic tract and the proprioceptive pathways running in the funiculus dorsalis are organized in a somatotopic fashion. Accordingly, sacral axons are considered to be located in the most eccentric position being regularly spared in severe but not complete SCI. However, a somatotopic layering of defined axon pathways has only been confirmed for the dorsal column proprioceptive pathways [9].

Complete spinal cord injury represents the most prevalent pattern of spinal cord disease. In a retrospective analysis of 839 patients with traumatic and nontraumatic spinal cord injury, 175 patients (20.9 %) had incomplete SCI with a defined neurological pattern (e.g., central cord syndrome, anterior cord syndrome, Brown-Sequard syndrome). The remainder were complete spinal cord injuries and incomplete spinal cord injuries, which did not fit into defined incomplete SCI syndromes as described above. In this study it was not specified how many out of these 664 patients were actually complete SCI. Precise data in this respect are only available from studies and investigation of traumatic spinal cord injury. They show that 44.5 % of patients (out of 1992 patients), which were prospectively investigated in the EMSCI (European Multicenter Study about Spinal Cord Injury, www.​emsci.​org) database, suffered from complete spinal cord injury (Rupp, unpublished data). For obvious reasons, they have the most unfavorable diagnosis with only around 25–30 % of the patients converting to incomplete SCI grades (see chapter 4). However, in most instances, conversion to incomplete SCI does not necessarily lead to relevant recovery of function.

The clinical presentation of spinal cord disease depends – besides the cross-sectional location of the lesion – on the segmental neurological level of injury (NLI) (Fig. 3.2).