TBI rehabilitation is incomplete without discussions of prognosis. This is begun in the initial stages of recovery and continues during acute rehabilitation, depending on the individual patient’s trajectory of gains. Rehabilitation plans with the entire team are carved out on the basis of outcome expectations and goals. All TBI characteristics, including CT and MRI findings, age, Glasgow Coma Score (GCS), comorbidities, and premorbid psychosocial aspects, play a significant role in realistic prognostication.

Interestingly, prognostic guidelines have supported use of “threshold values” rather than percentages of “good outcome” or “poor outcome,” as families have noted positive response to this. The three most common tools used for TBI prognostication are the Glascow Coma Scores (GCS), time to follow commands (TTC), and length of posttraumatic amnesia (PTA). Even with twenty-first century research and technology in the expanding field of TBI, posttraumatic amnesia (PTA), or the time between injury and the time at which ongoing new memories are made, has actually been the strongest predictor to date for outcome in TBI patients. Threshold values for PTA include: “Severe disability is unlikely when PTA lasts less than 2 months” and “Good recovery is unlikely when PTA lasts longer than 3 months.” A recent study compared GCS, TTC, and PTA as prognostic tools for TBI inpatient outcomes upon hospital discharge, which found that duration of PTA was the only unique predictor of discharge functional independence measure (FIM) scores. The trauma physiatrist collaborates with the primary trauma team, neurosurgery, and neurology, offering caregivers and families potential expectations for outcome and explaining the dynamic course of recovery and rehabilitation toward realistic goals.

Diffuse axonal injury (DAI), commonly seen concomitant with focal cerebral injuries, poses a unique challenge to the rehabilitation team given its classic injury pattern manifestations of arousal, behavior, and cognitive impairments. Deeper lesions to the brainstem or cerebellar peduncles (grade III DAI), middle regions to subcortical structures like the corpus callosum (grade II DAI), and surface regions such as the frontal convexity (grade I DAI) all correspond to these impairments, respectively (Fig. 78.2). Although there is no evidence to support the need for MRI in the hyperacute phase of injury, since there would be no change in medical or surgical management, these findings can have rehabilitation treatment and prognostic relevance.

Once hemodynamically stable, the patient with acute moderate-to-severe TBI embarks on rehabilitation with increasing duration and frequency of treatments over weeks. PT, OT, and SLP interactions begin first with assessments, followed by extensive work on engagement of the patient. As patients emerge, they generally fall into three categories with respect to overall function: the confused-agitated patient (delirious state within PTA), the low-functional-state patient, and the confused-participatory patient. Although some portion of rehabilitation is passive, much depends on active participation, and therefore creating both environmental and pharmacological plans in order to optimize daily engagement for the specific patient is crucial.

The acute TBI patient can have several reasons to be agitated and restless, including pain, infection, fear, confusion, and substance withdrawal, and therefore elucidating the primary cause is important. Interestingly, recovery following acute TBI, specifically those with DAI, will usually follow a natural progression through levels of cognition, and the RLA level IV indicates the “confused and agitated state.” This is usually followed by confused and non-agitated states and can often be both a hurdle for the patient and family to move beyond but at the same time a positive marker of continued functional gains. During this stage, nursing staff and therapists strive to incorporate environmental and behavioral modification tactics (controlled stimulation in the environment, small numbers of visitors, sleep–wake cycle adherence).

Medications are usually required for optimizing participation and improving safety of the patient and staff. Opiates, typical antipsychotics (haloperidol), and benzodiazepines may be required initially for severe pain, extreme agitation, and confounding alcohol withdrawal; however, on serial review of the patient, he or she should be transitioned to other agents. Although the data is not clear as to the negative effects of chronic atypical antipsychotic use, studies have indicated that ongoing typical antipsychotic treatment (largest amount of dopamine [D2] blockade) results in deleterious motor effects in animal models. There is evidence that haloperidol prolongs the duration of PTA, but long-term outcome was unchanged in a study conducted in 1985. Interestingly, a Cochrane Database Study in 2003 covering all to-date trials in agitation and aggression after acquired brain injury revealed that the only reasonable evidence for positive treatment response was trials using beta-blockers (inderal and pindolol). Antiepileptic drugs (AEDs) have recently gained popularity to control agitation and restlessness in individuals with TBI. Up to 26 % of TBI patients are prescribed AEDs for posttraumatic seizures, neurobehavioral disorders, and pain. Valproic acid was shown to improve agitation in 28 % of patients with TBI in a small retrospective analysis conducted in 2000. Carbamazepine has also been trialed for agitation in the TBI population, though in smaller non-controlled trials. One study showed a significant decrease in combativeness, impulsivity, and distractibility compared to benzodiazepines, morphine, and haloperidol. Topiramate is another AED which has been trialed for agitation in the TBI population, but recent studies have shown that patients have difficulty with attention, memory, executive functioning, and language. Therefore, it may be more harmful than helpful in the acute TBI population. Other medications that are often used in the acute TBI period that may influence rehabilitation include gabapentin, which may lead to anxiety and psychomotor agitation, and levetiracetam, which may lead to aggression and loss of self-control.

Low-functional-state patients represent persons in coma (lack of wakefulness), vegetative states (VS) (unresponsive wakefulness), and those in minimally conscious states (MCS) (environmental awareness). These neurological stages correspond to the aforementioned recovery scale RLA levels I, II, and III, respectively. During these low-functioning states following severe TBI, rehabilitation focuses on (1) optimizing daily participation, (2) fostering sleep–wake cycles, (3) minimizing all complications of immobility, and (4) realistic short-term goal setting for mobility, communication, and cognition.

Preparedness of the patient in VS (or RLA II) and MCS (or RLA III) for ongoing rehabilitation efforts is of key importance during the initial stages of recovery. The team emphasizes early mobilization to encourage practice-dependent neuroplasticity with daily stimulation from all therapy and other staff modalities. As medical stability improves, there is a strong emphasis on nutrition, avoidance of infections, and tapering off all sedating medications. It is the job of the trauma physiatrist to always reassess what medications are potentially no longer necessary as the patient transitions through acute care and inpatient rehabilitation. Antiepileptic medication courses are monitored closely, in addition to other potentially neurologically deleterious medications like metoclopramide, antihistiminergic agents, benzodiazepines, and others.

The amount of level I evidence for the use of neurostimulants to augment the recovery process in TBI patients emerging from low-level states is slim. However, there is some evidence that the dopaminergic medication amantadine accounts for heightened arousal, improved cognition, and overall improved functional scores in several studies. In one study, 184 patients in a vegetative state or minimally conscious state 4–16 weeks after TBI were enrolled in a randomized, controlled trial for a total of 6 weeks. The group administered amantadine showed an accelerated rate of functional recovery based on the Disability Rating Scale. Amphetamines, such as methylphenidate, are utilized for arousal and attention deficits. Another agent for arousal originally indicated for narcolepsy, modafinil, has had reasonable efficacy in this population. The rationale for using these agents during rehabilitation and restoration is twofold: (1) increased arousal and attention to the environment allow for increased quantity and quality of physical and cognitive rehabilitation treatments, and (2) there are inherent positive properties of neuroactive medications which can affect neuronal growth factors, antagonize NMDA receptors, and improve lipid peroxidation.

The complications and sequelae of TBI directly affect optimal rehabilitation of the patient and therefore overall outcome. DAI, brainstem injury, and associated hypoxia are all associated with dysautonomia or “storming” which is a clinical entity involving labile cardiac function, pyrexia, sweating, and decorticate or decerebrate posturing and is associated with prolonged acute care and rehabilitation stays and worse functional outcomes. Management during both acute and rehabilitation settings involves identifying primary triggers of dysautonomia, such as pain, fractures, infection, and other noxious stimuli, which all may be present in patients with polytrauma. Pharmacological treatment with beta-blockers, bromocriptine, dantrolene, and even intrathecal baclofen has been utilized during both acute care and the rehabilitation setting.

Upper motor neuron dysregulation following TBI results in velocity-dependent increased muscle tone (spasticity), which can cause pain and interfere with mobility, positioning, and hygiene. Initial treatment includes early maintenance of passive and active range of motion, stretching programs, and serial casting or splinting upon collaboration with physical and occupational therapy. Common pharmacological treatment includes baclofen (GABA-B agonist), which may be less desirable due to sedating effects, and dantrolene, which blocks calcium release peripherally at the sarcoplasmic reticulum and has direct effects at the muscle belly. Focal motor point blocks with botulinum toxin A intramuscularly and neurolysis with phenol offer localized treatment and can also be effective with concomitant serial casting or bracing of the patient.

Some degree of immobility is unavoidable in patients with moderate-to-severe TBI and many organ systems are affected. Deconditioning results in muscle atrophy and weakness, osteopenia with lack of weight bearing, postural hypotension, dehydration, constipation, and gastric reflux. In combination with various problems specific to the TBI patient such as associated polytrauma, posturing and spasticity of limbs and trunk, need for tracheostomy and gastrostomy, dysphagia, sensory dysfunction, and communication impairments, the effect of deconditioning on function is more challenging to the patient and to rehabilitation teams. Attempting to attenuate and reverse the cycle with early mobilization is therefore of key importance in these patients.

As with all dramatic functional changes encountered after trauma, family involvement and education cannot be underemphasized as patients proceed through rehabilitation phases. The entire family is “injured” in acute TBI in many complex ways and is modified by premorbid dynamics among members or caregivers. During both acute and rehabilitation care settings, it is essential that the rehabilitation team direct, educate, and counsel the family. As mentioned, trauma physiatrists can play a key role as “interventionalists,” guiding patients and families with realistic prognostication, as well as ongoing education as patients recover at various stages during recovery and rehabilitation.

Traumatic spinal cord injury (SCI) affects roughly 12,500 persons per year in the United States, with a stable incidence rate of about 54 per 1 million persons between the years 1993 and 2012. The incidence rate is decreasing in younger males and females and increasing in the elderly. The etiology of SCI in the year 2012 was about 40 % attributable to falls (up from 20 % in 1993), 30 % to motor vehicle accidents, and 5 % to firearm injuries (though up to about 15 % in the 16–24-year-old age group). Falls have continued increasing steadily over time while injury due to violence has decreased over the past few decades. The ratio of male to female is about 3–4:1 and unchanged over the years. To date, there has been no solid evidence for the use of medical treatments at the acute stage of injury, including high-dose methylprednisolone, which is now considered a “treatment option” rather than the standard of care. Therefore, much emphasis on proper recovery has been on early stabilization and mobilization to begin the rehabilitation process as soon as possible. Careful attention is paid to securing the patient’s airway, particularly in high cervical SCI, as well as to maintaining adequate oxygenation and blood pressure during the acute phase with fluids and pressors as needed. Some recommend maintaining the systolic BP >85–90 mmHg.

Following acute SCI, physiatry should assist with diagnosing injury severity and discussing functional relevance, management of specific spinal cord-related impairments, patient education including communication of the diagnosis and long-term expectations, and prevention of physical and medical complications associated with SCI. Classification of injury is typically performed within 72 h from injury and repeated at roughly 1 month, usually during the initial stages of one’s inpatient rehabilitation stay. The American Spinal Injury Association (ASIA) has developed a reliable and standardized classification system, with the most recently formatted classification form revised in 2015, which offers physicians and therapists specific guidelines for treatment and rehabilitation with respect to a patient’s neurological level and completeness of injury. A “complete” SCI is defined by ASIA standards as SCI with no sparing of sensation and no voluntary motor activity of the sacral segments S4–S5 on rectal examination.