Would a spinal injury decrease human height?

A woman I know has been losing height at a rate of few cm a year following a severe spinal injury. How is this possible? What kind of injury could cause such progressive loss of height? Could this be a genetic defect? Are there any disorders that cause this type of shrinking?

In case it could be relevant, her brothers are very tall.

As @WYSIWYG pointed, muscular atrophy is the main cause for height decrease.

A spine injury leads to neural impairment and paresis / paralysis. This affects directly muscular trophism. It also limits physical activity, this being another favoring factor for muscular atrophy and overweight issues [1]. Association of bone degenerative processes (osteoporosis, osteopathy, osteolysis) is also a factor and it is dangerous because it promotes spinal cord injuries if vertebral height reduction amount is notable [2].

Focusing on muscular atrophy, here is how it can decrease height: by increasing vertebral column curvatures mostly on the upper region with articulating vertebrae. The vertebral column tends to gain a spring-like, spiral shape, associating accentuated cervical lordosis, accentuated thoracic kyphosis and thoracic scoliosis.

Image source: Scoliosis Treatment Alternatives. Chiropractic for Scoliosis Treatment Review (2014). Accessed 21.07.2014

While reading the comments to the question I found something interesting:

we know that the brain tells the body to grow, would a shock or something make the brain tell your body to shrink instead of growing?

Yes, the brain (hypotalamus) initiates a neuroendocrine response that leads to growth hormone secretion. The secretion is about 700 micrograms/day in a young adolescent, while in a healthy adult it is about 400 micrograms/day [3]. The deficiency in an adult person leads to a tendency of fat mass increase and a relative decrease in muscle mass and, in many instances, decreased energy and quality of life [4]. The brain can't "tell your body to shrink", but the lack of "communication" between the brain and organs leads to less to absolutely no use of that organ, thus inducing atrophy. The lack of both external and internal stimuli leads to atrophy (in general) [5].


  1. Gupta N, White KT, Sandford PR. Body mass index in spinal cord injury -- a retrospective study. Spinal Cord. 2006 Feb;44(2):92-4. doi: 10.1038/ PubMed PMID: 16030513.
  2. Ji L, Dang XQ, Lan BS, Wang KZ, Huang YJ, Wen B, Duan HH, Ren F. Study on the safe range of shortening of the spinal cord in canine models. Spinal Cord. 2013 Feb;51(2):134-8. doi: 10.1038/sc.2012.99. PubMed PMID: 22945745.
  3. Wikipedia contributors, "Growth hormone," Wikipedia, The Free Encyclopedia, (accessed July 21, 2014).
  4. Molitch ME, Clemmons DR, Malozowski S, Merriam GR, Shalet SM, Vance ML, Stephens PA. Evaluation and treatment of adult growth hormone deficiency: an Endocrine Society Clinical Practice Guideline. J. Clin. Endocrinol. Metab. 2006 May;91(5):1621-34. doi: 10.1210/jc.2005-2227. PubMed PMID: 16636129.
  5. Wikipedia contributors, "Atrophy," Wikipedia, The Free Encyclopedia, (accessed July 21, 2014).

Spinal cord injury patients face many serious health problems besides paralysis

Paralysis is just one of the many serious health problems faced by patients who suffer spinal cord injuries.

Spinal cord patients also are at higher risk for cardiovascular disease pneumonia life-threatening blood clots bladder, bowel and sexual dysfunction constipation and other gastrointestinal problems pressure ulcers and chronic pain, according to a report published in the journal Current Neurology and Neuroscience Reports.

The article, "Systemic Complications of Spinal Cord Injury," is written by Loyola Medicine neurologists Rochelle Sweis, DO, and José Biller, MD. Dr. Sweis is an assistant professor and Dr. Biller is professor and chair in the department of neurology of Loyola University Chicago Stritch School of Medicine.

As many as 94 percent of spinal cord patients suffer chronic pain.

"It typically occurs within the first year after injury but decreases in intensity and frequency with time," Drs. Sweis and Biller wrote. "It affects patients emotionally and interferes with activities of daily living."

The most common causes of spinal cord injuries are motor vehicle accidents (46 percent), falls (22 percent), violence (16 percent) and sports injuries (12 percent). Alcohol intoxication plays a role in 25 percent of all spinal cord injuries.

Eighty percent of spinal cord injuries occur in males aged 15 to 35. Fifty-three percent of spinal cord injury patients are left tetraplegic (partial or total paralysis of the arms, legs and torso) and 42 percent are left paraplegic (partial or total paralysis of the legs).

It costs between $320,000 and $985,000 to treat a spinal cord injury patient the first year and as much as $5 million during the patient's lifetime.

Mortality is highest during the first year after injury and among patients with more severe injuries. Life expectancy has not improved during the past 30 years.

The most common systemic complications following spinal cord injuries are pneumonia and other pulmonary problems. Cardiovascular disease is the most common cause of death. The degree of cardiovascular dysfunction is directly related to the severity of the injury.

Spinal cord patients are at risk for life threatening blood clots called deep vein thrombosis (usually in the legs) and pulmonary embolism (lungs). Deep vein thrombosis occurs in 47 to 90 percent and pulmonary embolism in 20 to 50 percent of spinal cord patients.

Pressure ulcers also are common. They can be avoided by position turns ever two hours, air mattresses and periodic weight shifting while sitting.

Life expectancy depends on the severity of the injury, where on the spine the injury occurs and age. Life expectancy after injury ranges from 1.5 years for a ventilator-dependent patient older than 60 to 52.6 years for a 20-year-old patient with preserved motor function.

Fatal complications of spinal cord injury include blood clots and sepsis due to pneumonia, urinary infections or pressure sores.

The good news is that among patients who are not completely paralyzed, 80 percent stand by 12 months and 50 percent walk out of the hospital by 12 months, with improvements continuing for two years after injury.

New treatments for spinal cord injury, including stem cells, gene therapy and electrical stimulation, are being studied. "The hope is that these options can some day restore some function for patients," Drs. Sweis and Biller wrote.

Effects of the Post-Spinal Cord Injury Microenvironment on the Differentiation Capacity of Human Neural Stem Cells Derived from Induced Pluripotent Stem Cells

Spinal cord injury (SCI) causes loss of neural functions below the level of the lesion due to interruption of spinal pathways and secondary neurodegenerative processes. The transplant of neural stem cells (NSCs) is a promising approach for the repair of SCI. Reprogramming of adult somatic cells into induced pluripotent stem cells (iPSCs) is expected to provide an autologous source of iPSC-derived NSCs, avoiding the immune response as well as ethical issues. However, there is still limited information on the behavior and differentiation pattern of transplanted iPSC-derived NSCs within the damaged spinal cord. We transplanted iPSC-derived NSCs, obtained from adult human somatic cells, into rats at 0 or 7 days after SCI, and evaluated motor-evoked potentials and locomotion of the animals. We histologically analyzed engraftment, proliferation, and differentiation of the iPSC-derived NSCs and the spared tissue in the spinal cords at 7, 21, and 63 days posttransplant. Both transplanted groups showed a late decline in functional recovery compared to vehicle-injected groups. Histological analysis showed proliferation of transplanted cells within the tissue and that cells formed a mass. At the final time point, most grafted cells differentiated to neural and astroglial lineages, but not into oligodendrocytes, while some grafted cells remained undifferentiated and proliferative. The proinflammatory tissue microenviroment of the injured spinal cord induced proliferation of the grafted cells and, therefore, there are possible risks associated with iPSC-derived NSC transplantation. New approaches are needed to promote and guide cell differentiation, as well as reduce their tumorigenicity once the cells are transplanted at the lesion site.

Keywords: Cell therapy Differentiation Induced pluripotent stem cells (iPSCs) Neural stem cells (NSCs) Spinal cord injury (SCI).

The Biology and Biomechanics of the Spinal Degenerative Cascade

More than 25 years ago, Kirkaldy-Willis et al presented the concept of a cascade of spinal motion segment degeneration invoking progressive wear of the intervertebral disc (IVD) and facet joints ( Fig. 6.1 ). 1 They emphasized the interdependence of the disc and facet joints for normal spinal function and described how derangement or injury to either of these articulations leads to abnormal forces and impairment of the other, the so-called tripod effect. They further described the morphologic features of spinal degeneration and postulated how these might be associated with various clinical syndromes. Although insightful, this algorithm was quite mechanistic and, in keeping with the times, highlighted biomechanical disturbances associated with degeneration of the motion segment. Over the decades since, we have come to appreciate that spinal degeneration involves a complex interplay of biologic and bio-mechanical events that are predisposed by genetic factors and modulated by environmental influences.

Fig. 6.1 Kirkaldy-Willis schematic demonstrating a proposed mechanism for disc and facet degeneration. (From Kirkaldy-Willis WH, Wedge JH, Yong-Hing K, Reilly J. Pathology and pathogenesis of lumbar spondylosis and stenosis. Spine 19783:319–328. Reprinted with permission.)

98% at age 70 years based on macroscopic disc degeneration grades of 600 autopsy specimens. Interestingly, the authors noted that lumbar disc degeneration was already present in 11- to 19-year-old males and 10 years later in females. 2 Although spinal degeneration is inevitable with aging and invariably seen on MRI studies, it is typically asymptomatic. 3

Kirkaldy-Willis et al postulated that injury or repetitive strain to the facet joint is a cardinal event in the spinal degenerative sequence. 1 More recently, the IVD has received considerable attention as the source of initial spinal motion segment dysfunction. Butler et al suggested that disc degeneration likely predates facet arthrosis based on a CT and MRI study. 4 The authors noted that in 68 patients (330 discs/390 facet joints) there were 144 degenerated discs and 41 levels with facet osteoarthritis. Disc degeneration without facet osteoarthritis was found at 108 levels, whereas all but one of 41 levels with facet degeneration also had disc degeneration. 4

The widespread acceptance that spinal pain is thought to originate from the IVD is evidenced by the host of diagnostics (including discography) and therapeutic interventions directed toward the disc. Most treatments for painful discs, however, have met with inconsistent clinical outcomes, 5 probably reflecting a relatively unsophisticated approach to understanding spinal pain. Recent data supporting the idea of facet (zygapophyseal) joint mediated pain have come from studies of patients sustaining cervical whiplash injuries. 6,7 Lord et al evaluated cervical zygapophyseal joint pain after whiplash in a diagnostic double-blind study using placebo-controlled local anesthetic blocks. Sixty-eight patients with a predominant complaint of neck pain and headaches after a whiplash injury were evaluated. The authors noted that among patients with dominant headache, comparative blocks revealed that the prevalence of C2-C3 zygapophyseal joint pain was 50%. Overall, the prevalence of cervical zygapophyseal joint pain was 60%. 6, 7 These studies support the complex interplay of the IVD and facet joints in health and disease of the spine.

Our understanding of spinal degeneration has advanced as we have appreciated that the degenerative cascade involves interplay of both biologic and biomechanical factors. Biochemical events are important in the pathogenesis of the degenerative process as well as in the pain-signaling pathways responsible for the clinical features of the condition. As we better appreciate the biologic aspects of spinal degeneration, less invasive, nonablative treatments designed to reverse these biologic processes and restore the disc and facet functioning may become a reality.

Intervertebral Disc Degeneration

IVD degeneration is a major cause of musculoskeletal disability in humans. 8–10 Degeneration has been linked to low back pain however, the exact relationship between the two remains uncertain. 11,12 The macroscopic features characterizing disc degeneration include the formation of tears within the anulus fibrosus (AF), and progressive fraying and dehydration of the nucleus pulposus (NP) with eventual loss of the anular-nuclear distinction. 8,9,13 These pathologic alterations result in substantial changes in the functioning of the disc. Unquestionably, disc degeneration is a multifactorial process influenced by genetics, lifestyle conditions (including obesity, occupation, and smoking), biomechanical loading, and biochemical event. 14,15

Intervertebral Disc Biomechanics

The disc is capable of converting axial spinal loads into tensile hoop stresses in the outer AF, while allowing motion of the vertebral segment. This behavior of the IVD is dependent on the distinct biomechanical properties of the NP and AF. The proteoglycan (PG)-rich NP acts as an internal semifluid mass, whereas the collagen-rich AF acts as a laminar fibrous container. 16 The hydrostatic properties of the disc arise from its high water content, which allows it to support such large loads. 17,18

The NP in a young adult acts as a viscid fluid under applied pressure but also exhibits considerable elastic rebound, assuming its original physical state upon release. 19 Whereas a major function of the NP is to resist and redistribute compressive forces within the spine, the major function of the AF is to withstand tension. The unique combination of biochemical and biomechanical properties of the AF and NP allows the IVD to absorb and disperse the normal loading forces experienced by the spine. 19,20 When one of these two units, either the AF or NP, is compromised, degenerative changes ensue because of the alteration in mechanical force distribution across the functional spinal unit.

Horst and Brinckmann found that the stress distribution across the IVD and vertebral endplate depends on the degree of disc degeneration. 21 Under pure compressive and eccentric-compressive loading, the healthy lumbar IVD demonstrated a uniform stress distribution across the entire endplate area. Severely degenerated discs demonstrated the same uniform shape of stress distribution under compressive loading but a nonuniform stress distribution when loaded eccentrically. The asymmetry of the stress distribution in degenerated discs was found to increase with both angle of inclination and degree of degeneration. The asymmetric stress distribution was presumed to occur because of the relatively solid nature of the degenerated disc and its inability to conform to the eccentric loads. These results have been further supported by more recent studies as well. 22,23

With advancing degeneration, it appears that the proportion of load transmission shifts to the posterior elements. Yang and King indirectly measured facet forces by using an intervertebral load cell to measure the load transferred through the disc. 11 The model predicted a significant increase in facet load for segments with degenerated discs. The increase was more prominent as the eccentricity of the applied compressive load increased posteriorly. This biomechanical sequence of disc degeneration leading to posterior element load bearing may, in fact, be what is observed clinically in that disc degeneration typically precedes facet arthrosis. 4

Clinically, a common observation is that disc degeneration creates instability of the lumbar spine and, therefore, increases range of motion. 24 The interplay between the IVD geometric and material properties as well as facet joint competence is important in defining the stability of the involved motion segment. 25 Biomechanical studies suggest that changes in stability with disc degeneration are quite complex. The kinematic behavior of a simulated degenerative model under compressive and shear loading was studied by Frei et al. 26 The authors found greater axial translations under compression in the degenerated model (nucleotomy) compared with the normal disc. In anterior shear, the anterior translation was smaller in the degenerated specimens versus the normal specimens. Anterior shear was accompanied by a significant increase in coupled flexion rotation in the degenerative model, which could explain the counterintuitive decrease in translation. This was attributed to an increase in facet load in degenerated specimens during anterior shear loading. In addition, Fujiwara et al 27 found that in vitro cadaveric specimens had segmental motion changes, which were much greater in axial rotation compared with lateral bending, flexion, and extension. Ochia et al 28 also found an increase in torsional and flexion and extension movements in vivo. These kinematic studies ultimately can be related clinically to the concept that excessive motion beyond normal soft tissue or bony constraints causes compression or stretching of the neural elements, or deformation of the soft tissue. 29 These instabilities can cause abnormal motion and contact forces, as well as accelerate facet degeneration and osteoarthritis. Eventually as pointed out by Kirkaldy-Willis, with advancing degeneration the motion segment ultimately becomes less mobile, although the remaining motion may certainly be painful. 24 As the disc becomes less mobile, this may, in turn, decrease the intrinsic disc strength and may decrease nutrition to the disc. 30

Besides spinal instability creating degenerative disc disease, another competing biomechanical cause for disc degeneration is the “wear and tear” hypothesis. In this mechanism, a series of minor mechanical traumas to the disc accumulate, eventually creating disc weakening. This weakening results in further injury, and a vicious cycle ensues ultimately leading to disc degeneration. 31,32 If this model was the main reason for disc degeneration, a logical assumption would be that those who experienced heavy physical disc loading, particularly laborers, would have an elevated risk of disc degeneration. Most studies have shown an association between heavy physical loading and disc degeneration. 33–42 A study by Friberg and Hirsch, however, did not find an association between occupational and spine degeneration radiographically. 43 Other studies as well have not demonstrated a clear association. 33,44–48

Whatever the biomechanical etiology for disc degeneration, researchers have attempted to define a relationship between biomechanical IVD alterations and symptomatology. More recently, disc dysfunction associated with axial back pain giving rise to so-called internal disc derangement has received considerable attention. MRI is a valuable diagnostic tool in assessing for internal disc derangement. 49 MRI allows determination of the proton density of the disc indicative of the state of hydration and can also identify the presence of annular tears. Aprill and Bogduk described the MRI high-intensity zone (HIZ), which they believe to be representative of an annular tear extending to the periphery of the disc. 50 The HIZ can be seen on spin echo T2-weighted (T2W) MRI scans as a high-intensity signal located in the substance of the posterior AF ( Figs. 6.2, 6.3 ). The HIZ has been suggested as, but by no means confirmed to be, associated with discogenic axial back pain. 51,52

Modic et al described adjacent bony endplate changes that occur with degeneration of the IVD. 53,54 Type 1 changes (decreased signal intensity on T1-weighted [T1W] spin-echo MRI scans and increased signal intensity on T2W MRI scans) were identified in 20 patients, type 2 changes (increased signal intensity on T1W MRI scans and isointense or slightly increased signal intensity on T2W MRI scans) in 77 patients, and type 3 changes (decreased signal on T1W and T2W MRI scans) in 16 patients. Histopathologic sections in cases of type 1 change demonstrated disruption and fissuring of the endplates and vascularized fibrous tissue, type 2 changes demonstrated yellow marrow replacement, and type 3 changes demonstrated loss of marrow and advanced bony sclerosis. These signal intensity changes appear to reflect a spectrum of vertebral body marrow changes associated with degenerative disc disease. 53

Mechanical Treatments

As disc degeneration progresses, the resulting abnormal motion or instability is believed to be a cause of spinal pain, likely related to stretching of soft tissues and stimulation of free nerve endings. 24,25,55 Although a precise understanding of what constitutes spinal “instability” remains elusive, numerous treatments aimed at reducing painful spinal motion have been described. Physical therapy using stabilizing exercises has been proposed as an attempt to restabilize the “unstable” spine. 56,57 This approach may be more effective when painful segmental motion is the consequence of injury and dysfunction of the paraspinal muscle system that renders the motion segment biomechanically vulnerable in the neutral zone. The clinical diagnosis is based on the report of pain and the observation of movement dysfunction within the neutral zone and the associated finding of excessive intervertebral motion at the symptomatic level.

Fig. 6.2 Biology of disc disruption. ALL, anterior longitudinal ligament PLL, posterior longitudinal ligament.

Fig. 6.3 A sagittal magnetic resonance imaging scan demonstrating a degenerated, collapsed L5-S1 disc space as evidenced by the loss of disc height and decreased T2-weighted signal. The white arrow points to an area along the posterior anulus exhibiting an increased T2-weighted signal representative of a high intensity zone.

Other reported techniques for restabilizing the spine include intradiscal therapies such as intradiscal electrothermal therapy (IDET), which purportedly attempt to stiffen the motion segment by altering collagen fibers within the IVD. 58,59 Histologic studies of IVD material after IDET have reported histologic changes of collagen fibril denaturation in the posterior AF. 60 Another restabilization approach involves the use of posteriorly implanted “dynamic devices” that limit, but do not eliminate motion. These devices have been extensively implanted in patients in Europe for select cases of mechanical back pain with “instability.” Total disc replacement, which provides axial stability while allowing for motion, is being increasingly used for the treatment of painful disc degeneration.

Facet Joint Biomechanics

Facet joints are true synovial articulations and undergo degenerative changes similar to those of osteoarthritis seen in other synovial joints. 11,61 The facet joints are one of the primary stabilizing structures of the spinal motion segment. 62,63 As the degenerative cascade progresses and anterior column support is lost, the facet joints bear more weight and the fulcrum moves dorsally to balance the motion segment. 64 With progressive spinal degeneration, the load-bearing patterns of the facet joints are altered. 27

Fujiwara et al performed a biomechanical and imaging study of human cadaveric spinal motion segments to determine the effect of disc degeneration and facet joint osteoarthritis on the segmental flexibility of the lumbar spine. 27 The authors noted that axial rotation was most affected by disc degeneration. Facet cartilage degeneration, especially thinning of the cartilage, causes capsular ligament laxity, which may allow abnormal motion or hypermobility of the facet joint. The authors noted a significant linear correlation between facet cartilage thinning and disc degeneration in the male cadavers. Cartilage degeneration appeared to further increase the segmental movements already present in the hypermobile, degenerated disc.

Facetectomy studies have been performed by Sullivan et al in the lumbar spine of immature white rabbits to create a facet-mediated degenerative model. 65 The researchers resected the inferior articular process on one side at a selected vertebral level and on the opposite side at the adjacent level. The disc height was decreased at the surgical level in 50% of the discs at 6 months and 74% at 12 months. At 9 to 12 months, the discs showed thinning of the posterior AF, circumferential slits in the peripheral AF, and an increased area as well as decreased organization of the NP. The facet joints opposite the facetectomy began to show degeneration at 6 months. The authors concluded that the facet joint protects the IVD from rotational stresses.

Unquestionably, the facet joint complex has an important role in stabilizing the segmental spinal unit. 27,32,62,66,67 As disc disease progresses, increased stress is applied posteriorly accelerating facet osteoarthrosis. The resultant facet joint osteoarthrosis is likely to change the segmental spinal motion, altering the mechanical forces experienced by the IVD.

Biologic Factors

Cells residing in both the AF and NP actively regulate the homeostasis of IVD tissue. These cells maintain a balance between anabolism and catabolism by modulating a variety of substances including cytokines, enzymes, enzyme inhibitors, and growth factors in a paracrine and/or autocrine fashion. 13,68–70 Anabolic regulators include polypeptide growth factors, such as insulin-like growth factor (IGF), transforming growth factor-β (TGF-β), and bone morphogenetic proteins (BMPs). Other small molecules such as the synthetic peptide of link proteins have also been reported to be regulators of matrix synthesis. 13,70,71 The catabolic process is also mediated by various enzymes, such as matrix metalloproteinases, aggrecanases, and cytokines. 72,73 The degeneration of an IVD results from an imbalance between the anabolic and catabolic processes, or the loss of steady-state metabolism that is maintained in the normal disc.

This delicate homeostatic balance affects the biomechanics of the IVD as well. A healthy IVD is populated by at least two morphologically distinct cell types. 74–79 Most cells are small and round, similar to chondrocytes. The second cell type is thought to be a remnant of the primitive notochord and has a vacuolated appearance and prominent intracellular glycogen deposits. Surrounding these cells is a matrix rich in large aggregating PGs. This matrix imbibes water allowing the NP to resist compressive forces. With disc degeneration, chondrocytic cells are replaced by fibrocytes synthesizing type I collagen. 9 The baseline synthesis of type II collagen also declines, altering collagen fiber cross-linking. 72,73,80 Additionally, a progressive loss of the PG matrix occurs, resulting in IVD dehydration and desiccation within the NP. These changes create a weaker biomechanical construct to resist compression and shear forces. 81 Last, an overall decrease in disc cell density with age and degeneration is seen. In studies of human IVDs, Gruber et al reported that apoptosis, or programmed cell death, largely accounts for this depopulation over time, and that interventions which delay or halt apoptotic cell death may constitute a means of treating degenerative disc disease. 74

In addition to mediating disc degeneration, biochemical events appear to play a significant role in producing disabling spinal pain. 13,81,82 Biochemical events involved in discogenic pain production appear to include the production and release of inflammatory mediators and cytokines from the disc, vascular ingrowth into annular fissures, and the stimulation of free nerve endings in the outermost region of the disc. 83–85

Studies have suggested nutrition as an important factor in the pathogenesis of disc disease. 9 To maintain the steady-state metabolism of cells, the IVD requires proper nutrition, which is accomplished by diffusion of nutrients through the endplates and into the IVD. Trauma, cigarette smoking, and other factors that affect the integrity of the endplates and endplate vasculature may affect diffusion and disturb the nutrition of the disc cells. 86 Vascular channels in the endplate of the IVD are particularly vital for maintaining the nutrition of the avascular NP. In degenerative discs, the diffusion capacity decreases creating a lower oxygen tension, decreased pH, and accumulation of catabolic byproducts. Typically, vascular channels at the endplate proliferate to maintain adequate nutrition of the disc. It has been claimed that the induction of new blood vessels in the endplate is facilitated by the activation of enzymes such as matrix metalloproteinases 87 leading to the belief that with IVD injury the activation of these enzymes is the cause of increasing inflammation within the disc. This inflammation is the harbinger of further degeneration, culminating in a vicious cycle of accelerated degeneration. There are also reports that these channels ultimately disappear with disc degeneration and eventually become obliterated with calcification. 88,89 Further research using microangiography and immunohistochemical analysis is needed to determine if the loss in vascularity at the end-plate can be reversed.

Genetic factors play a significant role in the degenerative spinal cascade. A twin study by Sambrook et al examined the hypothesis that disc degeneration has a major genetic component. Spine MRI scans were obtained for 86 pairs of monozygotic (MZ) twins and 154 dizygotic (DZ) twins. A substantial genetic influence on disc degeneration was found. 90 Further genetic predispositions to disc degeneration have been suggested by other studies on vitamin D receptor gene polymorphism. 91,92 The authors noted that in 205 young adults, allelic variation ( Tt allele) in the vitamin D receptor gene was associated with multilevel and severe disc degeneration. Unquestionably, the genetic effect on the disc degeneration cascade requires further analysis.

Premise for Biologic Treatment

Current treatment options for degenerative disc disease address its clinical symptom, pain, as opposed to the pathophysiologic root of the disorder. Furthermore, traditional strategies such as fusion of the involved motion segment are not reliable and may even create instability at adjacent levels or even adjacent level degeneration. 93 In recent years, technologies such as disc replacement, aimed at restoring some degree of motion at the involved segment while eliminating pain, have begun to be studied. 94 However, these motion preserving techniques are appropriate for more advanced stages of spinal degeneration. With a better understanding of the sequence of biologic and biomechanical events associated with spinal degeneration comes the opportunity for earlier interventions ( Fig. 6.4 ). With early disc and/or facet degeneration, biologic strategies aimed at reversing or retarding the degenerative process are appealing.


Out of 8178 cases admitted in the department during the study period, 2716 cases (23.2%) were of SCI. Complete paralysis (AIS type A) below the injury level was found in 557 and 633 cases in cervical and thoracolumbar injuries, respectively. Those patients who did not allow neurological evaluation were grouped as ‘not tested’ patients (Table 1). In all, 1400 cases of cervical SCI and 1316 cases of thoracolumbar SCI, involving 2194 males (80.8%) and 522 females (19.2%) were admitted and managed during this period. About 79% patients were from rural and 21% from urban area in the ratio of 3.7:1. Seventy-one percent cases were in the age range of 20–49 years (Table 2). One thousand twenty-eight patients (37.8%) were uneducated (without formal education in any institute). In all, 1389 (51.1%) of these patients were living in a nuclear family while 832 cases (30.6%) resided in joint family. The average monthly earning of their family was Rs 3000 only (US$ 60, UK£ 37.5).

In total, 632 farmers (23.3%) and 622 laborers (22.9%) sustained spinal injury resulting from different mechanisms (Table 3). Three hundred forty-seven females (12.8%) sustained spinal injuries while working in the field. In all, 1449 patients (53.4%) sustained injuries following fall from height followed by 762 cases (28%) of road traffic accident (RTA). In rural population, out of 1145 patients (42.2%) who sustained injury following fall, 577 patients (21.2%) had fall from roof top. Ninety-nine patients (3.6%) sustained spinal injuries following fall in a dry well while digging or accidentally. Eighty-four patients (3%) sustained trauma following fall of heavy object over head, which is a common mode of transportation of goods in rural areas. Two hundred ninety-one patients (10.7%) sustained injury following fall of heavy object over back while removing mud from dry well for increasing its depth or placing or removing grain bags in storage area. One hundred ten patients (4%) sustained trauma following fall from electric pole or height following electric shock. Besides SCI they sustained electric burns also (Table 4). This was an unusual mode of trauma noticed in our patient population.

In all, 699 (25.7%) patients sustained different types of associated injuries out of which 588 patients (84.1%) sustained major injuries, with or without abrasion, lacerated wound or electric burn. In all, 293 patients (41.1%) had single or multiple fractures or dislocation at different sites, 195 patients (27.8%) sustained simple head injury which resolved in few days and 51 patients (7.3%) sustained multiple rib fractures. The major injuries were more common in patients sustaining SCI at thoracolumbar region (Table 5).

Ninety-eight percent of these patients were transported for medical aid in vehicles without proper positioning or special consideration for SCI. One thousand four hundred ninety-five patients (55%) were initially admitted to primary health centers, where specialized services were unavailable, resulting in delay of initial medical aid. In our series, an average delay of 11 h and 5 days was noted for bladder and bowel management, respectively.

Prevalence of orthostatic hypotension in SCI

Orthostatic hypotension is defined by The Consensus Committee of the American Autonomic Society and the American Academy of Neurology (1996) as a decrease in systolic blood pressure of 20 mmHg or more, or in diastolic blood pressure of 10 mmHg or more, upon the assumption of an upright posture from a supine position, regardless of whether symptoms occur. 35

There is a strong link between SCI and the presence of orthostatic hypotension. 6, 36, 37, 38, 39 Orthostatic manoeuvres performed during physiotherapy and mobilisation are reported to induce blood pressure decreases diagnostic of orthostatic hypotension in 74% of SCI patients, and symptoms of orthostatic hypotension (such as light-headedness or dizziness) in 59% of SCI individuals. 38 This is likely to have a negative impact upon the ability of SCI individuals to participate in rehabilitation. Orthostatic stress imposed using tilt testing (passive standing) is associated with a slightly lower incidence of orthostatic hypotension than physiotherapy manoeuvres. One study reports orthostatic hypotension during tilting in 57% of SCI patients, and symptoms associated with the hypotension in 25% of these patients. 40 The reason why passive tilting is less likely to produce orthostatic hypotension is unclear, but the presence or absence of orthostatic hypotension is likely to be related, at least in part, to the type of orthostatic manoeuvre performed, and whether this is active or passive in nature. It is known, however, that the likelihood of experiencing orthostatic hypotension is greater in patients with higher spinal cord lesions, and thus it is more common in individuals with tetraplegia. 6, 36, 37, 38 These individuals also experience larger falls in blood pressure associated with postural change than those with paraplegia. 38 There is also an increased risk of orthostatic hypotension in individuals who sustain a traumatic SCI than in nontraumatic injury such as spinal stenosis. 39 Finally, it is notable that there are few reported incidences of orthostatic hypotension associated with SCI in the elderly, 40 which is surprising since among able-bodied elderly persons, orthostatic hypotension is a common and troublesome phenomena. 41 The reasons why there is little evidence of orthostatic hypotension in elderly SCI patients are unknown and warrant further investigation. However, it is known that during the last decade there has been a demographic change, whereby there has been an increase in the age of SCI individuals, 42, 43 and this may be associated with an increased incidence of orthostatic hypotension in SCI individuals. Clinicians working with elderly individuals with SCI should be aware of the combined impact of both age- and SCI-induced alterations in orthostatic cardiovascular control.

The extent to which SCI subjects are prone to orthostatic hypotension can be seen in Figure 2. This shows the changes in blood pressure and heart rate following passive movement from a supine to seated position in a subject with SCI (C5 ASIA B), in comparison to a healthy control volunteer. 44 The severity of SCI was assessed using the ASIA/IMSOP assessment of motor and sensory impairment. 45 Upon the assumption of a passive seated position, the SCI subject exhibited a marked, progressive decrease in blood pressures and relative postural tachycardia. In contrast, in the control subject, blood pressures were increased following the change in posture with little change in heart rate, due to the presence of normal descending cardiovascular control to spinal autonomic circuits.

Blood pressure and heart rate responses to orthostatic stress in a healthy male control subject (a) and a man with chronic cervical SCI (C5 ASIA B b). 44 The SCI subject had complete destruction of descending autonomic pathways as assessed by the absence of sympathetic skin responses. Resting systolic (SAP) and diastolic (DAP) arterial pressures were higher in the control than the SCI subject. Resting heart rates (HR) were similar. Following the assumption of an upright seated position (indicated by the solid black line), the control subject had a marked increase in SAP and DAP, with little change in HR. In contrast, the SCI subject had a marked, progressive decrease in both SAP and DAP in the upright posture, characteristic of orthostatic hypotension, associated with a postural tachycardia of approximately 25 bpm


When a vertebra is injured, the most common problem is a fracture. The most common type of vertebral fracture is called a compression fracture. A compression fracture occurs when the normal vertebral body of the spine is squished, or compressed, to a smaller height. This injury tends to happen in three groups of people:  

  • People who are involved in traumatic accidents. When a load placed on the vertebrae exceeds its stability, it may collapse. This is commonly seen after a fall.
  • People with osteoporosis. This is much more commonly the cause. Osteoporosis is a condition that causes a thinning of the bone. As the bone thins out, it is less able to support a load. Therefore, patients with osteoporosis may develop compression fractures without severe injuries, even in their daily activities. They don't have to have a fall or other trauma to develop a compression fracture of the spine.
  • People with tumors that spread to the bone or tumors such as multiple myeloma that occur in the spine.

Tissue and Aging

According to poet Ralph Waldo Emerson, “The surest poison is time.” In fact, biology confirms that many functions of the body decline with age. All the cells, tissues, and organs are affected by senescence, with noticeable variability between individuals owing to different genetic makeup and lifestyles. The outward signs of aging are easily recognizable. The skin and other tissues become thinner and drier, reducing their elasticity, contributing to wrinkles and high blood pressure. Hair turns gray because follicles produce less melanin, the brown pigment of hair and the iris of the eye. The face looks flabby because elastic and collagen fibers decrease in connective tissue and muscle tone is lost. Glasses and hearing aids may become parts of life as the senses slowly deteriorate, all due to reduced elasticity. Overall height decreases as the bones lose calcium and other minerals. With age, fluid decreases in the fibrous cartilage disks intercalated between the vertebrae in the spine. Joints lose cartilage and stiffen. Many tissues, including those in muscles, lose mass through a process called atrophy. Lumps and rigidity become more widespread. As a consequence, the passageways, blood vessels, and airways become more rigid. The brain and spinal cord lose mass. Nerves do not transmit impulses with the same speed and frequency as in the past. Some loss of thought clarity and memory can accompany aging. More severe problems are not necessarily associated with the aging process and may be symptoms of underlying illness.

As exterior signs of aging increase, so do the interior signs, which are not as noticeable. The incidence of heart diseases, respiratory syndromes, and type 2 diabetes increases with age, though these are not necessarily age-dependent effects. Wound healing is slower in the elderly, accompanied by a higher frequency of infection as the capacity of the immune system to fend off pathogen declines.

Aging is also apparent at the cellular level because all cells experience changes with aging. Telomeres, regions of the chromosomes necessary for cell division, shorten each time cells divide. As they do, cells are less able to divide and regenerate. Because of alterations in cell membranes, transport of oxygen and nutrients into the cell and removal of carbon dioxide and waste products from the cell are not as efficient in the elderly. Cells may begin to function abnormally, which may lead to diseases associated with aging, including arthritis, memory issues, and some cancers.

The progressive impact of aging on the body varies considerably among individuals, but Studies indicate, however, that exercise and healthy lifestyle choices can slow down the deterioration of the body that comes with old age.

Homeostatic Imbalances: Tissues and Cancer

Figure 2. Development of Cancer. Note the change in cell size, nucleus size, and organization in the tissue.

Cancer is a generic term for many diseases in which cells escape regulatory signals. Uncontrolled growth, invasion into adjacent tissues, and colonization of other organs, if not treated early enough, are its hallmarks. Health suffers when tumors “rob” blood supply from the “normal” organs.

A mutation is defined as a permanent change in the DNA of a cell. Epigenetic modifications, changes that do not affect the code of the DNA but alter how the DNA is decoded, are also known to generate abnormal cells. Alterations in the genetic material may be caused by environmental agents, infectious agents, or errors in the replication of DNA that accumulate with age. Many mutations do not cause any noticeable change in the functions of a cell however, if the modification affects key proteins that have an impact on the cell’s ability to proliferate in an orderly fashion, the cell starts to divide abnormally.

As changes in cells accumulate, they lose their ability to form regular tissues. A tumor, a mass of cells displaying abnormal architecture, forms in the tissue. Many tumors are benign, meaning they do not metastasize nor cause disease. A tumor becomes malignant, or cancerous, when it breaches the confines of its tissue, promotes angiogenesis, attracts the growth of capillaries, and metastasizes to other organs (Figure 2).

The specific names of cancers reflect the tissue of origin. Cancers derived from epithelial cells are referred to as carcinomas. Cancer in myeloid tissue or blood cells form myelomas. Leukemias are cancers of white blood cells, whereas sarcomas derive from connective tissue. Cells in tumors differ both in structure and function. Some cells, called cancer stem cells, appear to be a subtype of cell responsible for uncontrolled growth. Recent research shows that contrary to what was previously assumed, tumors are not disorganized masses of cells, but have their own structures.

Cancer treatments vary depending on the disease’s type and stage. Traditional approaches, including surgery, radiation, chemotherapy, and hormonal therapy, aim to remove or kill rapidly dividing cancer cells, but these strategies have their limitations. Depending on a tumor’s location, for example, cancer surgeons may be unable to remove it. Radiation and chemotherapy are difficult, and it is often impossible to target only the cancer cells. The treatments inevitably destroy healthy tissue as well. To address this, researchers are working on pharmaceuticals that can target specific proteins implicated in cancer-associated molecular pathways.

Medical cannabis can reduce essential tremor: Turns on overlooked cells in central nervous system

Medical cannabis is a subject of much debate. There is still a lot we do not know about cannabis, but researchers from the Department of Neuroscience at the Faculty of Health and Medical Sciences have made a new discovery that may prove vital to future research into and treatment with medical cannabis.

Cannabinoids are compounds found in cannabis and in the central nervous system. Using a mouse model, the researchers have demonstrated that a specific synthetic cannabinoid (cannabinoid WIN55,212-2) reduces essential tremor by activating the support cells of the spinal cord and brain, known as astrocytes. Previous research into medical cannabis has focussed on the nerve cells, the so-called neurons.

'We have focussed on the disease essential tremor. It causes involuntary shaking, which can be extremely inhibitory and seriously reduce the patient's quality of life. However, the cannabinoid might also have a beneficial effect on sclerosis and spinal cord injuries, for example, which also cause involuntary shaking', says Associate Professor Jean-François Perrier from the Department of Neuroscience, who has headed the research project.

'We discovered that an injection with the cannabinoid WIN55,212-2 into the spinal cord turns on the astrocytes in the spinal cord and prompts them to release the substance adenosine, which subsequently reduces nerve activity and thus the undesired shaking'.

Targeted treatment with no problematic side effects

That astrocytes are part of the explanation for the effect of cannabis is a completely new approach to understanding the medical effect of cannabis, and it may help improve the treatment of patients suffering from involuntary shaking.

The spinal cord is responsible for most our movements. Both voluntary and spontaneous movements are triggered when the spinal cord's motor neurons are activated. The motor neurons connect the spinal cord with the muscles, and each time a motor neuron sends impulses to the muscles, it leads to contraction and thus movement. Involuntary shaking occurs when the motor neurons send out conflicting signals at the same time. And that is why the researchers have focussed on the spinal cord.

'One might imagine a new approach to medical cannabis for shaking, where you -- during the development of cannabis-based medicinal products -- target the treatment either at the spinal cord or the astrocytes -- or, at best, the astrocytes of the spinal cord', says Postdoc Eva Carlsen, who did most of the tests during her PhD and postdoc projects.

'Using this approach will avoid affecting the neurons in the brain responsible for our memory and cognitive abilities, and we would be able to offer patients suffering from involuntary shaking effective treatment without exposing them to any of the most problematic side effects of medical cannabis'.

The next step is to do clinical tests on patients suffering from essential tremor to determine whether the new approach has the same effect on humans.


The effects of injury depend on the level along the spinal column (left). A dermatome is an area of the skin that sends sensory messages to a specific spinal nerve (right).
Spinal nerves exit the spinal cord between each pair of vertebrae.

Spinal cord injury can be traumatic or nontraumatic, [4] and can be classified into three types based on cause: mechanical forces, toxic, and ischemic (from lack of blood flow). [5] The damage can also be divided into primary and secondary injury: the cell death that occurs immediately in the original injury, and biochemical cascades that are initiated by the original insult and cause further tissue damage. [6] These secondary injury pathways include the ischemic cascade, inflammation, swelling, cell suicide, and neurotransmitter imbalances. [6] They can take place for minutes or weeks following the injury. [7]

At each level of the spinal column, spinal nerves branch off from either side of the spinal cord and exit between a pair of vertebrae, to innervate a specific part of the body. The area of skin innervated by a specific spinal nerve is called a dermatome, and the group of muscles innervated by a single spinal nerve is called a myotome. The part of the spinal cord that was damaged corresponds to the spinal nerves at that level and below. Injuries can be cervical 1–8 (C1–C8), thoracic 1–12 (T1–T12), lumbar 1–5 (L1–L5), [8] or sacral (S1–S5). [9] A person's level of injury is defined as the lowest level of full sensation and function. [10] Paraplegia occurs when the legs are affected by the spinal cord damage (in thoracic, lumbar, or sacral injuries), and tetraplegia occurs when all four limbs are affected (cervical damage). [11]

SCI is also classified by the degree of impairment. The International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI), published by the American Spinal Injury Association (ASIA), is widely used to document sensory and motor impairments following SCI. [12] It is based on neurological responses, touch and pinprick sensations tested in each dermatome, and strength of the muscles that control key motions on both sides of the body. [13] Muscle strength is scored on a scale of 0–5 according to the table on the right, and sensation is graded on a scale of 0–2: 0 is no sensation, 1 is altered or decreased sensation, and 2 is full sensation. [14] Each side of the body is graded independently. [14]

Muscle strength [15] ASIA Impairment Scale for classifying spinal cord injury [13] [16]
Grade Muscle function Grade Description
0 No muscle contraction A Complete injury. No motor or sensory function is preserved in the sacral segments S4 or S5.
1 Muscle flickers B Sensory incomplete. Sensory but not motor function is preserved below the level of injury, including the sacral segments.
2 Full range of motion, gravity eliminated C Motor incomplete. Motor function is preserved below the level of injury, and more than half of muscles tested below the level of injury have a muscle grade less than 3 (see muscle strength scores, left).
3 Full range of motion, against gravity D Motor incomplete. Motor function is preserved below the level of injury and at least half of the key muscles below the neurological level have a muscle grade of 3 or more.
4 Full range of motion against resistance E Normal. No motor or sensory deficits, but deficits existed in the past.
5 Normal strength

Complete and incomplete injuries Edit

In a "complete" spinal injury, all functions below the injured area are lost, whether or not the spinal cord is severed. [9] An "incomplete" spinal cord injury involves preservation of motor or sensory function below the level of injury in the spinal cord. [18] To be classed as incomplete, there must be some preservation of sensation or motion in the areas innervated by S4 to S5, [19] e.g. voluntary external anal sphincter contraction. [18] The nerves in this area are connected to the very lowest region of the spinal cord, and retaining sensation and function in these parts of the body indicates that the spinal cord is only partially damaged. Incomplete injury by definition includes a phenomenon known as sacral sparing: some degree of sensation is preserved in the sacral dermatomes, even though sensation may be more impaired in other, higher dermatomes below the level of the lesion. [20] Sacral sparing has been attributed to the fact that the sacral spinal pathways are not as likely as the other spinal pathways to become compressed after injury due to the lamination of fibers within the spinal cord. [20]

Spinal cord injury without radiographic abnormality Edit

Spinal cord injury without radiographic abnormality exists when SCI is present but there is no evidence of spinal column injury on radiographs. [21] Spinal column injury is trauma that causes fracture of the bone or instability of the ligaments in the spine this can coexist with or cause injury to the spinal cord, but each injury can occur without the other. [22] Abnormalities might show up on magnetic resonance imaging (MRI), but the term was coined before MRI was in common use. [23]

Central cord syndrome Edit

Central cord syndrome, almost always resulting from damage to the cervical spinal cord, is characterized by weakness in the arms with relative sparing of the legs, and spared sensation in regions served by the sacral segments. [24] There is loss of sensation of pain, temperature, light touch, and pressure below the level of injury. [25] The spinal tracts that serve the arms are more affected due to their central location in the spinal cord, while the corticospinal fibers destined for the legs are spared due to their more external location. [25] The most common of the incomplete SCI syndromes, central cord syndrome usually results from neck hyperextension in older people with spinal stenosis. In younger people, it most commonly results from neck flexion. [26] The most common causes are falls and vehicle accidents however other possible causes include spinal stenosis and impingement on the spinal cord by a tumor or vertebral disk. [27]

Anterior cord syndrome Edit

Anterior cord syndrome, due to damage to the front portion of the spinal cord or reduction in the blood supply from the anterior spinal artery, can be caused by fractures or dislocations of vertebrae or herniated disks. [25] Below the level of injury, motor function, pain sensation, and temperature sensation are lost, while sense of touch and proprioception (sense of position in space) remain intact. [28] [26] These differences are due to the relative locations of the spinal tracts responsible for each type of function. [25]

Brown-Séquard syndrome Edit

Brown-Séquard syndrome occurs when the spinal cord is injured on one side much more than the other. [29] It is rare for the spinal cord to be truly hemisected (severed on one side), but partial lesions due to penetrating wounds (such as gunshot or knife wounds) or fractured vertebrae or tumors are common. [30] On the ipsilateral side of the injury (same side), the body loses motor function, proprioception, and senses of vibration and touch. [29] On the contralateral (opposite side) of the injury, there is a loss of pain and temperature sensations. [27] [29]

Posterior cord syndrome Edit

Posterior cord syndrome, in which just the dorsal columns of the spinal cord are affected, is usually seen in cases of chronic myelopathy but can also occur with infarction of the posterior spinal artery. [31] This rare syndrome causes the loss of proprioception and sense of vibration below the level of injury [26] while motor function and sensation of pain, temperature, and touch remain intact. [32] Usually posterior cord injuries result from insults like disease or vitamin deficiency rather than trauma. [33] Tabes dorsalis, due to injury to the posterior part of the spinal cord caused by syphilis, results in loss of touch and proprioceptive sensation. [34]

Conus medullaris and cauda equina syndromes Edit

Conus medullaris syndrome is an injury to the end of the spinal cord, located at about the T12–L2 vertebrae in adults. [29] This region contains the S4–S5 spinal segments, responsible for bowel, bladder, and some sexual functions, so these can be disrupted in this type of injury. [29] In addition, sensation and the Achilles reflex can be disrupted. [29] Causes include tumors, physical trauma, and ischemia. [35]

Cauda equina syndrome (CES) results from a lesion below the level at which the spinal cord splits into the cauda equina, [33] at levels L2–S5 below the conus medullaris. [36] Thus it is not a true spinal cord syndrome since it is nerve roots that are damaged and not the cord itself however, it is common for several of these nerves to be damaged at the same time due to their proximity. [35] CES can occur by itself or alongside conus medullaris syndrome. [36] It can cause low back pain, weakness or paralysis in the lower limbs, loss of sensation, bowel and bladder dysfunction, and loss of reflexes. [36] Unlike in conus medullaris syndrome, symptoms often occur on only one side of the body. [35] The cause is often compression, e.g. by a ruptured intervertebral disk or tumor. [35] Since the nerves damaged in CES are actually peripheral nerves because they have already branched off from the spinal cord, the injury has better prognosis for recovery of function: the peripheral nervous system has a greater capacity for healing than the central nervous system. [36]

Actions of the spinal nerves
Level Motor Function
C1–C6 Neck flexors
C1–T1 Neck extensors
C3, C4, C5 Supply diaphragm (mostly C4)
C5, C6 Move shoulder, raise arm (deltoid) flex elbow (biceps)
C6 externally rotate (supinate) the arm
C6, C7 Extend elbow and wrist (triceps and wrist extensors) pronate wrist
C7, T1 Flex wrist supply small muscles of the hand
T1–T6 Intercostals and trunk above the waist
T7–L1 Abdominal muscles
L1–L4 Flex thigh
L2, L3, L4 Adduct thigh Extend leg at the knee (quadriceps femoris)
L4, L5, S1 abduct thigh Flex leg at the knee (hamstrings) Dorsiflex foot (tibialis anterior) Extend toes
L5, S1, S2 Extend leg at the hip (gluteus maximus) Plantar flex foot and flex toes

Signs (observed by a clinician) and symptoms (experienced by a patient) vary depending on where the spine is injured and the extent of the injury. A section of skin innervated through a specific part of the spine is called a dermatome, and injury to that part of the spine can cause pain, numbness, or a loss of sensation in the related areas. Paraesthesia, a tingling or burning sensation in affected areas of the skin, is another symptom. [37] A person with a lowered level of consciousness may show a response to a painful stimulus above a certain point but not below it. [38] A group of muscles innervated through a specific part of the spine is called a myotome, and injury to that part of the spinal cord can cause problems with movements that involve those muscles. The muscles may contract uncontrollably (spasticity), become weak, or be completely paralysed. Spinal shock, loss of neural activity including reflexes below the level of injury, occurs shortly after the injury and usually goes away within a day. [39] Priapism, an erection of the penis may be a sign of acute spinal cord injury. [40]

The specific parts of the body affected by loss of function are determined by the level of injury. Some signs, such as bowel and bladder dysfunction can occur at any level. Neurogenic bladder involves a compromised ability to empty the bladder and is a common symptom of spinal cord injury. This can lead to high pressures in the bladder that can damage the kidneys. [41]

Lumbosacral Edit

The effects of injuries at or above the lumbar or sacral regions of the spinal cord (lower back and pelvis) include decreased control of the legs and hips, genitourinary system, and anus. People injured below level L2 may still have use of their hip flexor and knee extensor muscles. [42] Bowel and bladder function are regulated by the sacral region. It is common to experience sexual dysfunction after injury, as well as dysfunction of the bowel and bladder, including fecal and urinary incontinence. [9]

Thoracic Edit

In addition to the problems found in lower-level injuries, thoracic (chest height) spinal lesions can affect the muscles in the trunk. Injuries at the level of T1 to T8 result in inability to control the abdominal muscles. Trunk stability may be affected even more so in higher level injuries. [43] The lower the level of injury, the less extensive its effects. Injuries from T9 to T12 result in partial loss of trunk and abdominal muscle control. Thoracic spinal injuries result in paraplegia, but function of the hands, arms, and neck are not affected. [44]

One condition that occurs typically in lesions above the T6 level is autonomic dysreflexia (AD), in which the blood pressure increases to dangerous levels, high enough to cause potentially deadly stroke. [8] [45] It results from an overreaction of the system to a stimulus such as pain below the level of injury, because inhibitory signals from the brain cannot pass the lesion to dampen the excitatory sympathetic nervous system response. [5] Signs and symptoms of AD include anxiety, headache, nausea, ringing in the ears, blurred vision, flushed skin, and nasal congestion. [5] It can occur shortly after the injury or not until years later. [5]

Other autonomic functions may also be disrupted. For example, problems with body temperature regulation mostly occur in injuries at T8 and above. [42] Another serious complication that can result from lesions above T6 is neurogenic shock, which results from an interruption in output from the sympathetic nervous system responsible for maintaining muscle tone in the blood vessels. [5] [45] Without the sympathetic input, the vessels relax and dilate. [5] [45] Neurogenic shock presents with dangerously low blood pressure, low heart rate, and blood pooling in the limbs—which results in insufficient blood flow to the spinal cord and potentially further damage to it. [46]

Cervical Edit

Spinal cord injuries at the cervical (neck) level result in full or partial tetraplegia (also called quadriplegia). [24] Depending on the specific location and severity of trauma, limited function may be retained. Additional symptoms of cervical injuries include low heart rate, low blood pressure, problems regulating body temperature, and breathing dysfunction. [47] If the injury is high enough in the neck to impair the muscles involved in breathing, the person may not be able to breathe without the help of an endotracheal tube and mechanical ventilator. [9]

Function after complete cervical spinal cord injury [48]
Level Motor Function Respiratory function
C1–C4 Full paralysis of the limbs Cannot breathe without mechanical ventilation
C5 Paralysis of the wrists, hands, and triceps Difficulty coughing, may need help clearing secretions
C6 Paralysis of the wrist flexors, triceps, and hands
C7–C8 Some hand muscle weakness, difficulty grasping and releasing

Complications Edit

Complications of spinal cord injuries include pulmonary edema, respiratory failure, neurogenic shock, and paralysis below the injury site.

In the long term, the loss of muscle function can have additional effects from disuse, including atrophy of the muscle. Immobility can lead to pressure sores, particularly in bony areas, requiring precautions such as extra cushioning and turning in bed every two hours (in the acute setting) to relieve pressure. [49] In the long term, people in wheelchairs must shift periodically to relieve pressure. [50] Another complication is pain, including nociceptive pain (indication of potential or actual tissue damage) and neuropathic pain, when nerves affected by damage convey erroneous pain signals in the absence of noxious stimuli. [51] Spasticity, the uncontrollable tensing of muscles below the level of injury, occurs in 65–78% of chronic SCI. [52] It results from lack of input from the brain that quells muscle responses to stretch reflexes. [53] It can be treated with drugs and physical therapy. [53] Spasticity increases the risk of contractures (shortening of muscles, tendons, or ligaments that result from lack of use of a limb) this problem can be prevented by moving the limb through its full range of motion multiple times a day. [54] Another problem lack of mobility can cause is loss of bone density and changes in bone structure. [55] [56] Loss of bone density (bone demineralization), thought to be due to lack of input from weakened or paralysed muscles, can increase the risk of fractures. [57] Conversely, a poorly understood phenomenon is the overgrowth of bone tissue in soft tissue areas, called heterotopic ossification. [58] It occurs below the level of injury, possibly as a result of inflammation, and happens to a clinically significant extent in 27% of people. [58]

People with SCI are at especially high risk for respiratory and cardiovascular problems, so hospital staff must be watchful to avoid them. [59] Respiratory problems (especially pneumonia) are the leading cause of death in people with SCI, followed by infections, usually of pressure sores, urinary tract infections and respiratory infections. [60] Pneumonia can be accompanied by shortness of breath, fever, and anxiety. [24]

Another potentially deadly threat to respiration is deep venous thrombosis (DVT), in which blood forms a clot in immobile limbs the clot can break off and form a pulmonary embolism, lodging in the lung and cutting off blood supply to it. [61] DVT is an especially high risk in SCI, particularly within 10 days of injury, occurring in over 13% in the acute care setting. [62] Preventative measures include anticoagulants, pressure hose, and moving the patient's limbs. [62] The usual signs and symptoms of DVT and pulmonary embolism may be masked in SCI cases due to effects such as alterations in pain perception and nervous system functioning. [62]

Urinary tract infection (UTI) is another risk that may not display the usual symptoms (pain, urgency, and frequency) it may instead be associated with worsened spasticity. [24] The risk of UTI, likely the most common complication in the long term, is heightened by use of indwelling urinary catheters. [49] Catheterization may be necessary because SCI interferes with the bladder's ability to empty when it gets too full, which could trigger autonomic dysreflexia or damage the bladder permanently. [49] The use of intermittent catheterization to empty the bladder at regular intervals throughout the day has decreased the mortality due to kidney failure from UTI in the first world, but it is still a serious problem in developing countries. [57]

An estimated 24–45% of people with SCI suffer disorders of depression, and the suicide rate is as much as six times that of the rest of the population. [63] The risk of suicide is worst in the first five years after injury. [64] In young people with SCI, suicide is the leading cause of death. [65] Depression is associated with an increased risk of other complications such as UTI and pressure ulcers that occur more when self-care is neglected. [65]

Spinal cord injuries are most often caused by physical trauma. [21] Forces involved can be hyperflexion (forward movement of the head) hyperextension (backward movement) lateral stress (sideways movement) rotation (twisting of the head) compression (force along the axis of the spine downward from the head or upward from the pelvis) or distraction (pulling apart of the vertebrae). [66] Traumatic SCI can result in contusion, compression, or stretch injury. [4] It is a major risk of many types of vertebral fracture. [67] Pre-existing asymptomatic congenital anomalies can cause major neurological deficits, such as hemiparesis, to result from otherwise minor trauma. [68]

In the US, Motor vehicle accidents are the most common cause of SCIs second are falls, then violence such as gunshot wounds, then sports injuries. [69] In some countries falls are more common, even surpassing vehicle crashes as the leading cause of SCI. [70] The rates of violence-related SCI depend heavily on place and time. [70] Of all sports-related SCIs, shallow water dives are the most common cause winter sports and water sports have been increasing as causes while association football and trampoline injuries have been declining. [71] Hanging can cause injury to the cervical spine, as may occur in attempted suicide. [72] Military conflicts are another cause, and when they occur they are associated with increased rates of SCI. [73] Another potential cause of SCI is iatrogenic injury, caused by an improperly done medical procedure such as an injection into the spinal column. [74]

SCI can also be of a nontraumatic origin. Nontraumatic lesions cause anywhere from 30 to 80% of all SCI [75] the percentage varies by locale, influenced by efforts to prevent trauma. [76] Developed countries have higher percentages of SCI due to degenerative conditions and tumors than developing countries. [77] In developed countries, the most common cause of nontraumatic SCI is degenerative diseases, followed by tumors in many developing countries the leading cause is infection such as HIV and tuberculosis. [78] SCI may occur in intervertebral disc disease, and spinal cord vascular disease. [79] Spontaneous bleeding can occur within or outside of the protective membranes that line the cord, and intervertebral disks can herniate. [11] Damage can result from dysfunction of the blood vessels, as in arteriovenous malformation, or when a blood clot becomes lodged in a blood vessel and cuts off blood supply to the cord. [80] When systemic blood pressure drops, blood flow to the spinal cord may be reduced, potentially causing a loss of sensation and voluntary movement in the areas supplied by the affected level of the spinal cord. [81] Congenital conditions and tumors that compress the cord can also cause SCI, as can vertebral spondylosis and ischemia. [4] Multiple sclerosis is a disease that can damage the spinal cord, as can infectious or inflammatory conditions such as tuberculosis, herpes zoster or herpes simplex, meningitis, myelitis, and syphilis. [11]

Vehicle-related SCI is prevented with measures including societal and individual efforts to reduce driving under the influence of drugs or alcohol, distracted driving, and drowsy driving. [82] Other efforts include increasing road safety (such as marking hazards and adding lighting) and vehicle safety, both to prevent accidents (such as routine maintenance and antilock brakes) and to mitigate the damage of crashes (such as head restraints, air bags, seat belts, and child safety seats). [82] Falls can be prevented by making changes to the environment, such as nonslip materials and grab bars in bathtubs and showers, railings for stairs, child and safety gates for windows. [83] Gun-related injuries can be prevented with conflict resolution training, gun safety education campaigns, and changes to the technology of guns (such as trigger locks) to improve their safety. [83] Sports injuries can be prevented with changes to sports rules and equipment to increase safety, and education campaigns to reduce risky practices such as diving into water of unknown depth or head-first tackling in association football. [84]

A person's presentation in context of trauma or non-traumatic background determines suspicion for a spinal cord injury. The features are namely paralysis, sensory loss, or both at any level. Other symptoms may include incontinence. [86]

A radiographic evaluation using an X-ray, CT scan, or MRI can determine if there is damage to the spinal column and where it is located. [9] X-rays are commonly available [85] and can detect instability or misalignment of the spinal column, but do not give very detailed images and can miss injuries to the spinal cord or displacement of ligaments or disks that do not have accompanying spinal column damage. [9] Thus when X-ray findings are normal but SCI is still suspected due to pain or SCI symptoms, CT or MRI scans are used. [85] CT gives greater detail than X-rays, but exposes the patient to more radiation, [87] and it still does not give images of the spinal cord or ligaments MRI shows body structures in the greatest detail. [9] Thus it is the standard for anyone who has neurological deficits found in SCI or is thought to have an unstable spinal column injury. [88]

Neurological evaluations to help determine the degree of impairment are performed initially and repeatedly in the early stages of treatment this determines the rate of improvement or deterioration and informs treatment and prognosis. [89] [90] The ASIA Impairment Scale outlined above is used to determine the level and severity of injury. [9]

Prehospital treatment Edit

The first stage in the management of a suspected spinal cord injury is geared toward basic life support and preventing further injury: maintaining airway, breathing, and circulation and restricting further motion of the spine. [23] In the emergency setting, most people who has been subjected to forces strong enough to cause SCI are treated as though they have instability in the spinal column and have spinal motion restricted to prevent damage to the spinal cord. [91] Injuries or fractures in the head, neck, or pelvis as well as penetrating trauma near the spine and falls from heights are assumed to be associated with an unstable spinal column until it is ruled out in the hospital. [9] High-speed vehicle crashes, sports injuries involving the head or neck, and diving injuries are other mechanisms that indicate a high SCI risk. [92] Since head and spinal trauma frequently coexist, anyone who is unconscious or has a lowered level of consciousness as a result of a head injury is spinal motion restricted. [93]

A rigid cervical collar is applied to the neck, and the head is held with blocks on either side and the person is strapped to a backboard. [91] Extrication devices are used to move people without excessively moving the spine [94] if they are still inside a vehicle or other confined space. The use of a cervical collar has been shown to increase mortality in people with penetrating trauma and is thus not routinely recommended in this group. [95]

Modern trauma care includes a step called clearing the cervical spine, ruling out spinal cord injury if the patient is fully conscious and not under the influence of drugs or alcohol, displays no neurological deficits, has no pain in the middle of the neck and no other painful injuries that could distract from neck pain. [33] If these are all absent, no spinal motion restriction is necessary. [94]

If an unstable spinal column injury is moved, damage may occur to the spinal cord. [96] Between 3 and 25% of SCIs occur not at the time of the initial trauma but later during treatment or transport. [23] While some of this is due to the nature of the injury itself, particularly in the case of multiple or massive trauma, some of it reflects the failure to adequately restrict motion of the spine. SCI can impair the body's ability to keep warm, so warming blankets may be needed. [97]

Early hospital treatment Edit

Initial care in the hospital, as in the prehospital setting, aims to ensure adequate airway, breathing, cardiovascular function, and spinal motion restriction. [98] Imaging of the spine to determine the presence of a SCI may need to wait if emergency surgery is needed to stabilize other life-threatening injuries. [99] Acute SCI merits treatment in an intensive care unit, especially injuries to the cervical spinal cord. [98] People with SCI need repeated neurological assessments and treatment by neurosurgeons. [100] People should be removed from the spine board as rapidly as possible to prevent complications from its use. [101]

If the systolic blood pressure falls below 90 mmHg within days of the injury, blood supply to the spinal cord may be reduced, resulting in further damage. [46] Thus it is important to maintain the blood pressure which may be done using intravenous fluids and vasopressors. [102] Vasopressors used include phenylephrine, dopamine, or norepinephrine. [1] Mean arterial blood pressure is measured and kept at 85 to 90 mmHg for seven days after injury. [103] The treatment for shock from blood loss is different from that for neurogenic shock, and could harm people with the latter type, so it is necessary to determine why someone is in shock. [102] However it is also possible for both causes to exist at the same time. [1] Another important aspect of care is prevention of insufficient oxygen in the bloodstream, which could deprive the spinal cord of oxygen. [104] People with cervical or high thoracic injuries may experience a dangerously slowed heart rate treatment to speed it may include atropine. [1]

The corticosteroid medication methylprednisolone has been studied for use in SCI with the hope of limiting swelling and secondary injury. [105] As there does not appear to be long term benefits and the medication is associated with risks such as gastrointestinal bleeding and infection its use is not recommended as of 2018. [1] [105] Its use in traumatic brain injury is also not recommended. [101]

Surgery may be necessary, e.g. to relieve excess pressure on the cord, to stabilize the spine, or to put vertebrae back in their proper place. [103] In cases involving instability or compression, failing to operate can lead to worsening of the condition. [103] Surgery is also necessary when something is pressing on the cord, such as bone fragments, blood, material from ligaments or intervertebral discs, [106] or a lodged object from a penetrating injury. [85] Although the ideal timing of surgery is still debated, studies have found that earlier surgical intervention (within 24 hours of injury) is associated with better outcomes. [103] [107] Sometimes a patient has too many other injuries to be a surgical candidate this early. [103] Surgery is controversial because it has potential complications (such as infection), so in cases where it is not clearly needed (e.g. the cord is being compressed), doctors must decide whether to perform surgery based on aspects of the patient's condition and their own beliefs about its risks and benefits. [108] In cases where a more conservative approach is chosen, bed rest, cervical collars, motion restriction devices, and optionally traction are used. [109] Surgeons may opt to put traction on the spine to remove pressure from the spinal cord by putting dislocated vertebrae back into alignment, but herniation of intervertebral disks may prevent this technique from relieving pressure. [110] Gardner-Wells tongs are one tool used to exert spinal traction to reduce a fracture or dislocation and to reduce motion to the affected areas. [111]

Rehabilitation Edit

SCI patients often require extended treatment in specialized spinal unit or an intensive care unit. [112] The rehabilitation process typically begins in the acute care setting. Usually, the inpatient phase lasts 8–12 weeks and then the outpatient rehabilitation phase lasts 3–12 months after that, followed by yearly medical and functional evaluation. [8] Physical therapists, occupational therapists, recreational therapists, nurses, social workers, psychologists, and other health care professionals work as a team under the coordination of a physiatrist [9] to decide on goals with the patient and develop a plan of discharge that is appropriate for the person's condition.

In the acute phase physical therapists focus on the patient's respiratory status, prevention of indirect complications (such as pressure ulcers), maintaining range of motion, and keeping available musculature active. [113]

For people whose injuries are high enough to interfere with breathing, there is great emphasis on airway clearance during this stage of recovery. [114] Weakness of respiratory muscles impairs the ability to cough effectively, allowing secretions to accumulate within the lungs. [115] As SCI patients suffer from reduced total lung capacity and tidal volume, [116] physical therapists teach them accessory breathing techniques (e.g. apical breathing, glossopharyngeal breathing) that typically are not taught to healthy individuals. Physical therapy treatment for airway clearance may include manual percussions and vibrations, postural drainage, [114] respiratory muscle training, and assisted cough techniques. [115] Patients are taught to increase their intra-abdominal pressure by leaning forward to induce cough and clear mild secretions. [115] The quad cough technique is done lying on the back with the therapist applying pressure on the abdomen in the rhythm of the cough to maximize expiratory flow and mobilize secretions. [115] Manual abdominal compression is another technique used to increase expiratory flow which later improves coughing. [114] Other techniques used to manage respiratory dysfunction include respiratory muscle pacing, use of a constricting abdominal binder, ventilator-assisted speech, and mechanical ventilation. [115]

The amount of functional recovery and independence achieved in terms of activities of daily living, recreational activities, and employment is affected by the level and severity of injury. [117] The Functional Independence Measure (FIM) is an assessment tool that aims to evaluate the function of patients throughout the rehabilitation process following a spinal cord injury or other serious illness or injury. [118] It can track a patient's progress and degree of independence during rehabilitation. [118] People with SCI may need to use specialized devices and to make modifications to their environment in order to handle activities of daily living and to function independently. Weak joints can be stabilized with devices such as ankle-foot orthoses (AFOs) and knee-AFOs, but walking may still require a lot of effort. [119] Increasing activity will increase chances of recovery. [120]

Spinal cord injuries generally result in at least some incurable impairment even with the best possible treatment. The best predictor of prognosis is the level and completeness of injury, as measured by the ASIA impairment scale. [121] The neurological score at the initial evaluation done 72 hours after injury is the best predictor of how much function will return. [75] Most people with ASIA scores of A (complete injuries) do not have functional motor recovery, but improvement can occur. [121] [122] Most patients with incomplete injuries recover at least some function. [122] Chances of recovering the ability to walk improve with each AIS grade found at the initial examination e.g. an ASIA D score confers a better chance of walking than a score of C. [75] The symptoms of incomplete injuries can vary and it is difficult to make an accurate prediction of the outcome. A person with a mild, incomplete injury at the T5 vertebra will have a much better chance of using his or her legs than a person with a severe, complete injury at exactly the same place. Of the incomplete SCI syndromes, Brown-Séquard and central cord syndromes have the best prognosis for recovery and anterior cord syndrome has the worst. [28]

People with nontraumatic causes of SCI have been found to be less likely to suffer complete injuries and some complications such as pressure sores and deep vein thrombosis, and to have shorter hospital stays. [11] Their scores on functional tests were better than those of people with traumatic SCI upon hospital admission, but when they were tested upon discharge, those with traumatic SCI had improved such that both groups' results were the same. [11] In addition to the completeness and level of the injury, age and concurrent health problems affect the extent to which a person with SCI will be able to live independently and to walk. [8] However, in general people with injuries to L3 or below will likely be able to walk functionally, T10 and below to walk around the house with bracing, and C7 and below to live independently. [8] New therapies are beginning to provide hope for better outcomes in patients with SCI, but most are in the experimental/translational stage. [3]

One important predictor of motor recovery in an area is presence of sensation there, particularly pain perception. [36] Most motor recovery occurs in the first year post-injury, but modest improvements can continue for years sensory recovery is more limited. [123] Recovery is typically quickest during the first six months. [124] Spinal shock, in which reflexes are suppressed, occurs immediately after the injury and resolves largely within three months but continues resolving gradually for another 15. [125]

Sexual dysfunction after spinal injury is common. Problems that can occur include erectile dysfunction, loss of ability to ejaculate, insufficient lubrication of the vagina, and reduced sensation and impaired ability to orgasm. [52] Despite this, many people learn ways to adapt their sexual practices so they can lead satisfying sex lives. [126]

Although life expectancy has improved with better care options, it is still not as good as the uninjured population. The higher the level of injury, and the more complete the injury, the greater the reduction in life expectancy. [80] Mortality is very elevated within a year of injury. [80]