The Centers for Disease Control and Prevention (CDC) reports that about 150 individuals die of a traumatic brain injury (TBI) daily in the United States. Advancements in medical and surgical care seemingly allow for a higher prevalence of individuals living with a disability related to a TBI—now believed to be between 3.2 and 5.3 million.1,2 Long-standing disability secondary to a TBI and the difficulty predicting the extent of recovery continue to challenge patients, families, caretakers, and medical practitioners. Clinical aspects of a TBI can aid in determining prognosis of a patient’s recovery. With such knowledge, families may be better equipped for weighing medical and surgical decisions and managing their expectations in the setting of the resultant TBI.
Prognostic factors
To date, there are limited prognostic factors that assist in predicting recovery after a TBI. Researched variables help determine threshold levels of predicting potential outcome. Much of the prognostication that takes place is based on clinical experience, which can lead to selection bias. A survey revealed that only 37% of brain injury physicians agreed that they were assessing prognosis accurately. Furthermore, patients’ families generally question functional recovery, which may be difficult to determine based on certain variables. The sections that follow discuss the most commonly researched prognosticating factors.
Age
Poor outcome after a TBI is more commonly experienced in those who are under 4 or over 65 years old. The centripetal model of brain injury severity claims that the stronger the forces the brain is subjected to, the more severe and the deeper the brain lesions will be. A developing brain may be subjected to greater forces given the increased head to neck ratio, whereas elderly adults, whose brains have fully developed, do not have the resiliency of recovery compared with their younger counterparts. As one ages into adulthood, individuals are more likely to have a worsened recovery after a TBI, especially after the age of 40 and an even significantly worsened outcome after the age of 65. , , There is also a progressive increase in adverse outcomes in those ages 35 years and older, whereas patients under the age of 18 have significantly better outcomes.
Glasgow Coma Scale
The Glasgow Coma Scale (GCS) not only determines severity of TBI but also assesses and monitors a patient’s level of consciousness ( Table 8.1 ). , A mild TBI is considered a total GCS score of 13 to 15, a moderate TBI is considered a total GCS score of 9 to 12, and a severe injury is considered a total GCS score of 3 to 8. Studies have shown that initial GCS scores are associated with outcomes, and a lower GCS score is associated with a worse outcome. Even so, all outcomes on the Glasgow Outcome Scale (GOS) were still possible in initial GCS scores between 3 and 8. The GCS does not yield a definitive prognosis by itself. An association between lower GCS scores has also been noted with a longer duration of coma and posttraumatic amnesia (PTA). When the GCS is used in prognosticating a patient’s recovery, the best total GCS and best motor scores within 24 hours have been shown to correlate with a better recovery. , Although an objective measurement, the GCS can be confounded by interrater differences, use of paralytics for agitation or intubation, or intoxication with alcohol and/or drugs.
| Response | Score | |
|---|---|---|
| Eye opening | Spontaneously | 4 |
| To speech | 3 | |
| To pain | 2 | |
| None | 1 | |
| Verbal response | Orientated | 5 |
| Confused | 4 | |
| Inappropriate | 3 | |
| Incomprehensible | 2 | |
| None | 1 | |
| Motor response | Obeys commands | 6 |
| Localizes to pain | 5 | |
| Withdraws from pain | 4 | |
| Flexion to pain (decorticate posturing) | 3 | |
| Extension to pain (decerebrate posturing) | 2 | |
| None | 1 |
Length of coma, vegetative state, and minimally conscious state
Consciousness describes an individual’s level of arousal, with coma representing the lowest state of arousal. Using level of consciousness in determining a patient’s prognosis requires determination of timeframe (e.g., coma 2 weeks, vegetative state 16 weeks). The most basic methodology of measuring coma is the length of time it takes to follows commands. Longer periods of poor arousal are associated with worse prognosis for functional recovery. A good recovery is unlikely when the coma lasts longer than 4 weeks, and severe disability is unlikely when the coma lasts less than 2 weeks.
In general, the longer a patient with a TBI remains in VS or MCS, the longer they will continue to need significant assistance for mobility and self-care. Details regarding how the length of VS and MCS correlate with prognosis are inconsistent because of frequent misclassification of these two states. A clinician needs to be judicious in their clinical assessment of a patient’s arousal state because the classification connotates different prognoses and can potentially mislead long-term management plans for family.
Posttraumatic amnesia
Thought to be one of the most powerful prognostic factors available, PTA is defined as the inability to retain memory after a TBI, such as day-to-day information or ongoing events. It is often evaluated using the Galveston Orientation and Amnesia Test (GOAT) or the Orientation Log (O-Log). The GOAT is a series of questions in reference to orientation and recall of recent events. The O-Log was later developed as an alternative to the GOAT and appears to be a better predictor of outcome. The end of PTA is indicated when the patient has achieved a score of 76 or higher on the GOAT or 25 or higher on the O-Log for two consecutive days. A longer duration of PTA is associated with worsened outcomes. A good recovery, as defined by the GOS, is unlikely when PTA lasts longer than 3 months, and severe disability is unlikely when PTA lasts less than 2 months.
Brainstem reflexes
Injury to the brainstem involving the midbrain, pons, and medulla oblongata generally has a poor outcome. The presence of decerebrate posturing may indicate a brainstem injury and is associated with a worsened functional recovery compared with decorticate posturing, which indicates a cortical injury.
In addition, absence of a pupillary response, an oculovestibular reflex, and/or an oculocephalic reflex can also indicate an unfavorable outcome.
Presence of extracranial injuries
Concomitant extracranial injuries, such as a fracture or visceral damage, may occur in addition to the TBI and imply a greater severity of the trauma. Furthermore, the risk of complications related to the concomitant extracranial injuries may lead to a worsened outcome, such as bleeding or infections. Some studies have noted that there may an associated increased mortality in those who sustain extracranial injuries with moderate brain injuries but not in those who suffered a severe brain injury.
Imaging findings
Findings on brain neuroimaging can provide insight into a TBI patient’s prognosis. The number and extent of findings correlate with recovery, and certain findings—such as traumatic subarachnoid hemorrhage, midline shifts, cisternal compression or obliteration, subdural hematomas, and epidural hematomas—are correlated with worse outcomes. Cistern obliteration and midline shifts are the strongest mortality predictors within 14 days of TBI, whereas a nonevacuated hematoma is the strongest predictor of unfavorable outcome at 6 months. Furthermore, bilateral compared with unilateral findings indicates an increased cerebral involvement and may lead to a worsened outcome. As mentioned earlier, individuals with brainstem involvement, especially captured within the first 8 weeks of neuroimaging, are more strongly associated with worse prognosis than those who have cortical injuries.
Other factors
Patient clinical factors can also provide relative recovery outcomes. In general, those with a lower Functional Independence Measure (FIM) score, which is a tool used to assess functional ability and need for caregiver support, have poorer outcomes than those with higher FIM scores. Notably, bowel or bladder incontinence can predict a worsened outcome.
Presence of spasticity or flaccidity, which may limit a patient’s functional ability, denotes an individual requiring more caregiver assistance.
Somatosensory evoked potentials can also provide insight into recovery. The absence of the N20 response, which is a negative peak at 20 milliseconds, has been correlated with a poor outcome after a TBI.
Relative impact of gender, ethnicity, and educational levels has been researched, but their use in predicting outcome and recovery after a TBI is still debated.
Genetics
There is growing evidence that prognosis and recovery after a TBI may be linked to an individual’s genetic predisposition. It has been demonstrated that a patient with the APO-ε4 allele who sustains a TBI has a twofold increase a worsened outcome. It is believed that the APO-ε4 allele predisposes patients to having larger hematomas, remaining in a comatose state for a longer period, and an increased risk of posttraumatic seizures. Many genes in addition to the APO-ε4 allele are currently being investigated for their relationship to recovery after a TBI.
Future direction
Given the heterogenicity of TBIs and those who sustain them, it has been challenging to predict long-term outcomes early on. More often than not, the passing of time is usually what allows understanding of outcomes, but this is not useful to caregivers who are in need of vital information to assist in management decision making. Advancements in medical management, especially related to secondary injury that occurs after a TBI, may assist with improving recovery, thereby easing prognosis predictions. Furthermore, additional research is needed on the relationship between these predictive variables and how they help in a combined fashion to predict outcomes after a TBI.
Recovery patterns
Improvements in regulating the secondary neuroinflammatory responses that occurs subsequent to a TBI have not been as successful as the improvements in managing primary injury sustained after a TBI, such as increased intracranial pressures or an expanding bleed. Recovery after the resultant metabolic cascade also has been poorly understood, and much of what is known has been deduced from stroke research. The majority of motor and cognitive recovery after a TBI occurs within 6 months after the injury, with less significant functional recovery afterward.
Neuroplasticity, the brain’s inherent recovery mechanism to intrinsic and extrinsic factors, gained momentum after studies demonstrated newly developed neural connections after a neurologic injury. Prior to this conceptualization, recovery after a TBI was believed to be solely compensatory, in which neurologic growth was limited to developing central nervous systems. Neuroplasticity, which is believed to be the brain’s primary method of recovery, refers to brain reorganization and functions that can be mediated by structural alterations in brain maps. It may function to improve already existing neural connections, alter long-term potentiation and depression, create axonal and dendritic sprouting, and/or stimulate synaptogenesis/angiogenesis. Neuroplasticity can occur in several ways:
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Vicariation: A specific brain function is taken over by an alternative brain area that was not originally responsible for that function.
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Equipotentiality: The capacity of an anatomically distinct brain area to mediate a rather wide variety of functions.
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Diaschisis: Decrease in function of an area of the brain that is interconnected with the area of damaged brain. Functional recovery is related to a gradual reduction in diaschisis as cerebral blood flow improves.
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Synkinesis: Aberrant axonal regeneration leading to reinnervation of inappropriate muscles.
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Compensation: Alternative strategies used to restore lost function.
Neuroplasticity occurs sequentially in three different time phases. Immediately after the injury, there is a decrease in cortical inhibitory pathways along with cell death, which is thought to recruit and reveal secondary neural connections. Free-radical production induces neural degeneration and death, potentially preventing neuronal regeneration. Cortical pathways may eventually shift from inhibitory to excitatory, allowing for neuronal proliferation and synaptogenesis. Cells are recruited to replace damaged cells and revascularize areas of damaged brain. Days to weeks after the TBI, new axonal sprouting and synaptic connections are upregulated, promoting remodeling and cortical recovery. Chronic changes have also been researched, but no consensus has been established on these alterations.
Studies have shown that environmental stimulation is critical in enhancing neurogenesis. , ,
Understanding these concepts and the maladaptive neural changes that may occur with neurorecovery can assist with determining a patient’s prognosis.
Measurement tools
Functional recovery can be measured via a variety of objective tools. Currently, the Disability Rating Scale (DRS) is more commonly used as a measure of general functional change over the course of recovery. It is a 30-point scale that scores impairment, disability, and handicap. The total GCS score measures impairment, whereas disability is measured by how much assistance is needed for feeding, toileting, and grooming (complete, partial, or none). Handicap, on the other hand, measures the level of functioning (ranges from total assist to independent) and employability (ranges from needing no restrictions to not employable).
The Ranchos Los Amigos scale ( Table 8.2 ) can also provide generalized progression of recovery and descriptions of behaviors in TBI patients. As patients progress to the higher stages, their outcomes generally improve. Level IV is the most common stage in which patients begin their acute inpatient rehabilitation program.
Related posts:
TBI by pattern: Penetrating, nonpenetrating, and blast injury
Intensity of services, specialized rehabilitation therapies, and interdisciplinary team management
Neuroendocrine, metabolic and hormonal conditions
Emotional dyscontrol
Geriatric traumatic brain injury
Dual diagnosis of traumatic brain injury and spinal cord injury
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