Mechanical perturbation from direct injury results in the release of ions, toxins, and neurotransmitters. Damaged cells experience metabolic changes which contribute to the toxic metabolites, namely, lactate, in the microenvironment of the injured brain tissue. Both mechanisms further contribute to secondary cellular loss and subsequent injury mechanisms, such as edema and inflammation, in the aging brain.

One of the first ions to be released following increased membrane permeability or cell death is intracellular calcium [85]. The significance of calcium release is to set in motion the prolonged apoptotic and immediate necrotic pathways via caspase and calpain proteases, respectively [86–88]. Another ion released in secondary brain injury is magnesium, an indicator of cell injury [89–92].

Glutamate is the main excitatory neurotransmitter in the central nervous system as well as the main neurotransmitter responsible for increased damage following TBI in geriatric patients [86, 93, 94]. Hamm et al. suggest this effect is particularly harmful in an aged brain due to the increased density of receptors with age due to a natural loss of neurons. The additional overstimulation may contribute to the injury in an aged brain [78]. Lactate is also released into the microenvironment and increasingly taken up by the brain following traumatic injury [89, 95–106]. The increased concentrations of lactate can lead to edema via breakdown of the blood-brain barrier [89, 107–110], or ischemia [89–111]. The reason for increased production and utilization of lactate remains unclear; however, one study has linked increased lactate uptake by the brain with improved outcomes [106].

Numerous studies have concluded that the formation of free radicals [86, 112, 113] contributes to secondary cell damage and death following TBI. The pertinent free radicals in this context include superoxide anion (O²⁻), nitric oxide (NO), and peroxynitrite (ONOO⁻). These substances are formed immediately following the rise in extracellular calcium ions [113], as well as in response to altered neuronal metabolism, vascular changes, and the other mechanisms of secondary injury following TBI [112, 114]. Free radicals increase the damage following TBI by interfering with vasodilation [115] and subcellular components [116, 117], in addition to creating oxidative stress [117].

Decreased blood flow, local toxins, and altered metabolism contribute to hypoxia and ischemia of brain tissue following TBI in geriatric patients. Neuronal and glial cell death adds to the normal aging degeneration of these cells because there is increased susceptibility [118, 119].

Another mechanism of secondary injury following TBI is the resulting inflammation and edema of brain tissue [120]. In addition to hemorrhage, inflammation and edema contribute to increased intracranial pressure (ICP). The decreased ability of the aged brain to compensate for the changes in volume may be another reason for the increased morbidity and mortality in this patient population. Evidence suggests inflammation results from the release of pro-inflammatory cytokines and mediators [121, 122]. Onyszchuk et al. reported the edema that results in young and aged rats yet, in the latter, requires a longer period of time to subside and involves a larger area of the brain [118].

Lastly, studies have reported the formation of thrombin following TBI [123, 124]. This coagulation mediator becomes particularly important in a patient population that is frequently prescribed anticoagulation therapy for atrial fibrillation, ischemic heart disease, and peripheral vascular disease. One study showed the injection of thrombin into the caudate of mice correlated with increased infiltration of inflammatory cells, angiogenesis, and reactive gliosis. In effect, this mediator that is released following trauma contributes to the inflammatory response [125].

In a geriatric patient, brain injury does not require impact, for damage can result merely from deceleration or rotation of the head [6]. The most common manifestation following TBI in elderly patients are subdural hematomas, which may be of an acute or chronic nature. One study showed that in ≥70 years old, 61 % subdural, 28 % intracerebral, and 4 % epidural occurred compared to 47 % of epidural or subdural hematomas among ages 6–39 [3]. Subdural hematomas are more common than extradural hematomas after 50 years old [4, 126].

Contusions occur at approximately the same rate in patients suffering TBI and will significantly enlarge in approximately one-third. This worsening, however, may occur at a higher rate in the anticoagulated elderly.

Intracerebral hematomas occur at a higher rate in the elderly, presumably related to the decreased blood vessel elasticity associated with atherosclerosis [127].

Although overwhelming evidence suggests poorer overall outcomes with increased age following TBI, there is discord about whether this trend is stepwise with an age threshold beyond which outcome is significantly worse versus continuously increasing and whether treatment biases based on age have a significant impact. Studies have shown increased mortality in the geriatric population [3], with up to four to six times higher probability for unfavorable outcomes following TBI [128, 129].

For two decades guidelines for the medical and surgical management of severe TBI have been available with increasing utilization of evidence-based treatments to improve outcomes [131]. However these guidelines do not take into account advanced age and thus may not be universally applicable.

Thomas et al. retrospectively showed hospital and death rates after typically nonfatal TBI to increase within the geriatric age in both men and women [128]. Diminished functioning in all areas, cognitive, motor, and memory, has been reported [4, 130]. One study showed an increased rate of postsurgical infection in patients ≥80 years.

Many studies have been conducted to investigate risk factors for worse outcomes following TBI specific to the geriatric population. It has been shown that gender plays a role; females have poorer outcomes [133–136]. This suggests a possible role of estrogen or progesterone in the reparation process following TBI; however, recent randomized controlled trials did not demonstrate any benefit to the administration of progesterone after severe TBI. The specific type of injury has been shown to be another risk factor, postulated to be due to the increased incidence of intracranial mass lesions, such as non-evacuated hematomas, as opposed to systemic complications [3, 6, 8, 137]. Patients with subdural hematomas have worse outcomes than those with epidural hematomas. In one study of patients who received emergency craniotomy, mortality following subdural versus epidural hematomas was 41 % and 3 %, respectively [138]. It was previously reported that older patients with subdural hematomas who undergo craniotomy have worse outcome than younger patients [129–143], yet more recent studies showed no significant difference between age groups with respect to return to baseline following a craniotomy [132].

Mosenthal et al. studied a group of 235 patients with severe TBI, of which 19 % were >65 years old. Functional outcome was not significantly different for both elderly and younger patients and recommended that aggressive treatment in the elderly is warranted [138].

The mainstay of understanding the pathophysiology and risk factors for worse outcomes in the geriatric population is for optimization with regard to treatment and prevention of TBI. Researchers have identified reasons for the existing worse outcomes in these patients. For instance, older patients do not receive the same intensity of care as younger patients [141]. There is a delay getting geriatric patients to neurosurgical intervention when compared to younger patients with TBI [9, 142]. This suggests that improvements in timing and logistical care within hospitals are the first step toward improving outcomes.

Another area of “treatment” targets the patient before they arrive at the hospital. Given that the most common reason for TBI in these patients is falls, it is imperative to work toward the prevention of falls. One way in which this might be possible is to monitor medications that may contribute to falls [143]. Another way is to emphasize bone health and exercise. If patients have appropriate bone density, fractures might be prevented that lead to falling. Additionally, if a patient does fall, an improved muscular response may prevent head impact or injury.

For those in which prevention is not successful, treatment may not be the same for these patients as in younger patients. It becomes the responsibility of the emergency room physician to know which medications and therapeutic procedures to administer. Additionally, it is the responsibility of the neurosurgeon to know in whom it is appropriate to operate. In one study, indications for surgery included GCS score greater than 8, age greater than 75 years, without papillary dilation and all subdural hematomas [142].

Unfortunately, the care in this patient population is unique given their medications and comorbidities at the time of brain injury. This complicated medical picture requires more research to improve knowledge regarding how common medications and pathological processes in elderly patients may affect the treatment needed following TBI.

Concussion or mild traumatic brain injury – GCS 13–15 – is an increasingly common occurrence in the elderly. As with more severe TBI, falls are the most common mechanism.

Stryke et al. found that in these patients the rate of intracranial hemorrhage was three times higher than in younger adults [156].

The geriatric population presents special challenges in concussion assessment because there may be preexisting cognitive dysfunction, impaired memory, comorbid conditions, and use of multiple medications.

As a result the American College of Emergency Physicians recommends a head CT in any patient >65 who presents with a mechanism or findings suggestive of a concussion [157].

Outcome after a concussion is generally good; however, this may not be the case in elderly patients. Goldstein et al. (in patients >50 years old compared to controls) found a significant decrease in cognitive function, including language, memory, and executive function 7 months post concussion [158].

Additionally in a study of 3244 patients >64 years old, there was a higher incidence of non-survivors in the elderly population (risk ratio 7.8) [2].

Nevertheless there is a paucity of research on concussion in the elderly. Thus, more aggressive evaluation of post-concussive issues may be needed with earlier utilization of neuropsychological evaluations to more precisely identify and treat deficits in this patient population.

Over the last several decades, the incidence of SCI in geriatric patients has increased from 4.2 to 15.4 % [159].

Similar to the brain there is a progressive loss of neuronal tissue in the spinal cord. One study showed up to a 46 % loss in those >50 years [160]. In spite of this loss, there is no apparent effect on spinal cord function, but with less reserve the spinal cord may be more vulnerable to the effects of aging of the vertebral column such as spondylosis.

Also similar to TBI, falls account for the majority of geriatric SCI.

In comparison with younger patients, geriatric SCI patients appear to be less likely to suffer severe SCI; however, they have a higher mortality rate [161].

One study found that older patients with SCI are less likely to undergo surgery for their spinal injury, and when they do there is a significant delay between the injury and any subsequent surgery [161]. This may be related to coexisting medical comorbidities or treatment bias due to advanced age.

Discussions of palliative care in trauma patients are becoming increasingly common. In elderly patients with severe TBI or SCI the issue takes on even more importance. While an advanced directive may exist, such is difficult to access in an emergency situation, in a comatose patient whose family may very well not be immediately available. Thus operative decisions are often left to the surgeon. Unfortunately assuming advanced age is always associated with death is not supported in the literature.

The American College of Surgeons Optimal Resources Manual defines an ideal trauma system as one that includes “all the components identified with optimal trauma care, such as prevention, access, acute hospital care, rehabilitation and research activities.” There is no mention of palliative care [162].

Several studies have shown that those >55 are more likely to suffer multiple organ failure and even seemingly mildly injured patients >60 have a fivefold greater risk of dying [163, 164].

A high likelihood of death is not the only factor in considering palliative care over surgery or other aggressive treatments. The patient’s subsequent quality of life and likely functional outcome should play a role in making this decision.

Thus, in an “optimal” trauma system, it is important to integrate palliative care concepts in all members of the trauma team [165].