Objectives
After reading this chapter the student or therapist will be able to:
- 1.
Describe the epidemiology, pathophysiology, and mechanisms of injury of moderate to severe traumatic brain injury.
- 2.
Describe common clinical changes after traumatic brain injury.
- 3.
Describe common medical interventions for traumatic brain injury.
- 4.
Plan and select appropriate physical therapy examination techniques and tests and measures for people with traumatic brain injury using the Hypothesis-Oriented Algorithm for Clinicians (HOAC) II and International Classification of Functioning, Disability and Health (ICF) framework.
- 5.
Develop a comprehensive plan of care with appropriate physical therapy interventions for people with moderate to severe traumatic brain injury using the ICF framework.
- 6.
Describe prognosis and outcomes for people with moderate to severe traumatic brain injury using evidence-based prognostic indicators.
Section I—Overview of traumatic brain injury
Traumatic brain injury (TBI) is defined as a blow or jolt to the head or a penetrating head injury that disrupts the function of the brain. Not all blows or jolts to the head result in a TBI. The severity of such an injury may range from mild—a brief change in mental status or consciousness—to severe—an extended period of unconsciousness or amnesia after the injury. www.cdc.gov/traumaticbraininjury/get_the_facts.html . A TBI can result in short- or long-term problems with independent function.
Epidemiology of traumatic brain injury
TBI is a global health issue and is affecting around 10 million people in the world each year. The Centers for Disease Control and Prevention (CDC) estimated in 2010 ( www.braintrauma.org/faq ) that approximately 1.7 million Americans sustain a TBI every year. More than 2.5 million emergency department (ED) visits in the United States are related to TBI. Of these, falls constituted the most frequent visits (45%), followed by motor vehicle accidents (43%), and violence (6%). The admission diagnoses include concussion, skull fracture, cerebral laceration and contusions, and different types of hematoma/hemorrhages. The most prevalent age groups include 0 to 4 years old, 15 to 19 years old, and those who are older than 75 years of age. Males (around 64%) are more likely to sustain a TBI than females. The TBI-related hospital admission costs in 2010 were $21.4 billion.
The incidence of TBI is 506.4 per 100,000 population, with around 43% of those hospitalized experiencing long-term activity limitation. It is estimated that 3.2 million to 5.3 million people are living with TBI-related disabilities. The estimated lifetime cost for each individual with severe brain injury exceeds $4 million. Annual costs for all TBIs in the United States exceed $60 billion. It is thought that the incidence and costs related to TBI have been underestimated due to gaps in capturing data in certain populations, for example sports-related injuries, or for those who do not seek medical advice after an injury. The actual burden of care is estimated to be much higher than the reported data and figures.
Mechanisms of injury
There are four main types of injury, as follows:
- 1.
Those from external forces hitting the head or the head hitting hard enough to cause brain movement. Injuries include those with skull fracture and those without skull fracture (closed head injuries). Direct blows to the head can cause coup injuries (at the site of impact) and contrecoup injuries (distant from the site of impact).
- 2.
Severe acceleration and deceleration of the head, which can cause TBI without the head hitting an object. An example is shaken baby syndrome.
- 3.
Blast injuries mainly affecting military personnel.
- 4.
Penetrating objects causing direct cellular and vascular damage. Injuries to the face and neck can cause brain injury by disrupting the blood supply to the brain.
Pathophysiology of injury
Acceleration, deceleration, rotational forces, and penetrating objects cause tissue laceration, compression, tension, shearing, or a combination, resulting in primary injury.
Primary damage
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Contusions. A bruise or bleeding on the brain and lacerations can occur with or without skull fractures. Either an object hits the head, neck, or face, or the head hits an object. Damage can be to any area of the brain. Occipital blows are more likely to produce contusions than are frontal or lateral blows. Areas in which the cranial vault is irregular, such as on the anterior poles, undersurface of the temporal lobes, and undersurface of the frontal lobes, are commonly injured. Lacerations of blood vessels within the brain itself or of blood vessels that feed the brain from the neck or face reduce the flow of blood carrying oxygen to the brain. Contusions and lacerations can also injure the cranial nerves. The most commonly injured are the optic, vestibulocochlear, oculomotor, abducens, and facial nerves. Lacerations of the dura or in the arachnoid space may cause cerebrospinal fluid to discharge from the nose (cerebrospinal fluid rhinorrhea discharge increases with neck flexion, coughing, or straining).
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Epidural hematomas or hemorrhages. These occur mostly in adults when tearing of meningeal vessels results in blood collecting between the skull and dura. Skull fracture is present in the majority of cases. This is accompanied by intervals of lucidness and can result in death unless treated early.
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Subdural hematomas . These occur with acceleration-deceleration injuries when bridging veins to the superior sagittal sinus are torn. Blood accumulates in the subdural space. Symptoms include weakness and lethargy. Symptoms such as weakness and lethargy that come on acutely are life-threatening. Symptoms caused by slow bleeding may not be present for several weeks.
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Diffuse axonal injuries . Also known as diffuse injuries, these are among the most common types of primary lesions in persons with brain trauma. , Brain tissues that differ in structure or weight experience unequal acceleration, deceleration, or rotation of tissues during rapid head movement or during impact, causing diffuse axonal injury and changes in chemical processing. Severing of the axons may be severe enough to result in coma. In milder forms, more spotty lesions are seen, including deficits such as memory loss, concentration difficulties, decreased attention span, headaches, sleep disturbances, and seizures. Damage often involves the corpus callosum, basal ganglia, brain stem, and cerebellum. ,
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Penetrating injuries. These usually happen with objects with high velocities, such as bullets or shrapnel from explosives, and can cause additional damage remote from the areas of impact as a result of shock waves. Foreign objects such as sticks and sharp toys cause low-velocity injuries, directly damaging the tissues they contact.
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Blast injuries . These occur when a solid or liquid material explodes, turning into a gas. The expanding gases form a high-pressure wave, called an overpressure wave, that travels at supersonic speed. Pressure then drops, creating a relative vacuum or a blast underpressure wave that results in a reversal of air flow. This is then followed by a second overpressure wave. Blast-related injury can occur through several mechanisms. The primary blast wave generates extreme pressure changes that can cause stress and shear injuries. For example, rupture of the tympanic membranes is very common after blast injury, and lung and gastrointestinal injuries also occur. The exact mechanism of injury to the brain is unknown, with speculation about both axonal shearing and shearing of vasculature. ,
Secondary damage or insult
Secondary injuries are mainly caused by a lack of oxygen in the highly oxygen-demanding and dependent brain. Secondary problems may result from the following:
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Increased intracranial pressure (ICP) resulting from swelling or intracranial hematoma. Swelling of the brain causes distortion because the brain is held in the skull, a rigid, unyielding structure. The resultant increased ICP can lead to herniation of parts of the brain. The most often seen herniations include cingulate herniation under the falx cerebri, uncus herniation, central (or transtentorial) herniation, and herniation of the brain stem through the foramen magnum. Acute hydrocephalus occurs when blood accumulates in the ventricular system, expanding the size of the ventricles and causing increased pressure on brain tissue being compressed between the skull and the fluid-filled ventricles. The increased pressure can then result in changes in Pco 2 , which is harmful to nervous tissue. Increased ICP has been correlated with poorer outcomes and higher mortality rates.
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Cerebral hypoxia or ischemia occurs when blood vessels are ruptured or compressed. Hypoxia can occur from a lack of blood to the brain or from lack of oxygen in the blood as a result of airway obstruction or chest injuries.
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Intracranial hemorrhage causes hypoxia to tissues fed by the hemorrhaging blood vessels and adds pressure and distortion to brain tissue. Metabolic products from damaged cells and blood bathe the brain. Cell death occurs within minutes after injury from ischemia, edema, necrosis, and the toxic effects of blood on neural tissues.
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Electrolyte and acid-base imbalance . Secondary cell death occurs either by swelling and then bursting of the cellular membrane (necrosis), or by destruction from within the cell through changes in the deoxyribonucleic acid (DNA)—apoptosis. Cell death can occur days, weeks, or months after injury.
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Infections . Infections may arise from open wounds (e.g., penetrating injuries) or from prolonged invasive monitoring (e.g., ICP monitoring). If infection is present in brain tissue, it may cause swelling and cell death.
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Seizures from pressure or scarring . Seizures are most common immediately after injury, and 6 months to 2 years after injury. Seizure activity can cause additional brain damage owing to high oxygen and glucose requirements.
Clinical features of traumatic brain injury
Disorders of consciousness
Disorders of consciousness (DOCs) is a collective term describing conditions where consciousness or arousal have been affected by brain damage. The damage can be of direct insult to structures and systems regulating arousal and awareness, or of indirect damage to systematic neural connections of the brain. The main DOCs are coma, vegetative state (VS), and minimally conscious state (MCS). Some clinicians and scientists include locked-in syndrome as a DOC, while some perceive it as a differential diagnosis. A brief description of the various disorders under this broad spectrum is provided below.
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Coma. Coma is defined as a complete paralysis of cerebral function or a state of unresponsiveness. The eyes are closed and there is no response to painful stimuli. There are no obvious sleep-wake cycles. Oculomotor and pupillary signs are valuable in assisting with the diagnosis, localizing brain stem damage, and determining the depth of coma. In coma, brain stem responses may include grimacing to pain, which is frequently associated with a flexor or localizing motor response, loss of hearing or balance, abnormal palate and tongue movements, loss of language, and loss or distortion of taste.
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Vegetative State. This state is characterized by a wakeful, reduced responsiveness with no evident cerebral cortical function. The difference between coma and VS is that there are intermittent periods of wakefulness in VS. VS can result from diffuse cerebral hypoxia or from severe, diffuse white matter impact damage. The brain stem is usually relatively intact. Patients may track with their eyes and show minimal spontaneous yet involuntary motor activities, but they do not speak, nor do they respond to verbal stimulation. When VS lasts for over 1 month after TBI, the term persistent vegetative state (PVS) may be applied, though some now advocate for the term chronic VS due to the fact that brain injury is a dynamic rather than static process. Functional magnetic resonance imaging (fMRI) was recently used to test patients who were diagnosed with PVS. Five of 54 patients diagnosed with PVS demonstrated “willful, neuroanatomically specific blood-oxygenated–level–dependent responses when told to visualize one of two tasks.” The diagnosis of PVS indicates lack of cortical function, and fMRI may be useful in this diagnosis in the future. Recovery of consciousness, if it occurs, includes a gradual return of orientation and recent memory. The duration of each of these stages is variable and can be prolonged. Improvement can stop at any point.
- •
Minimally Conscious State. In MCS, consciousness is severely altered but there are signs demonstrating self or environmental awareness. Patients will have to be able to demonstrate motor response in a reproducible manner. That is, for a diagnosis of MCS a person must be able to follow simple one-step commands inconsistently and may even demonstrate some verbal responses to stimuli. Smooth pursuit may be present. MCS is often viewed as a transitional state signifying improvement of consciousness. The previous terminology for this state includes obtundity . It describes the condition of a person who sleeps a great deal and who, when aroused, exhibits reduced alertness, disinterest in the environment, and slow responses to stimulation.
- •
Posttraumatic Confusion or Clouding of Consciousness. In this state the person is awake most of the time, but is confused, easily distractible, with faulty memory, and with slowed but consistent responses to stimuli. Functional communication emerges in this state and is a clinical sign of improvement.
Autonomic nervous system changes
Changes in the autonomic nervous system (ANS) after TBI are not uncommon. Hilz and colleagues found that in persons with mild TBI, cardiovascular regulation shifts from parasympathetic activities to sympathetic activities at rest and there is a decrease in orthostatic responses. The dysfunctions are thought to be due to the close connections between the frontal cortex and various ANS functions. Because the ANS is a system that functions without voluntary control and it regulates multiple systems in the body, autonomic dysfunctions can cause system-wide abnormalities and increase mortality. It is recently reported that autonomic dysfunction at rest and in standing are more prominent in persons with moderate to severe TBI and dysfunctions can be prolonged after TBI. Box 22.1 lists possible ANS symptoms resulting from brain injury.
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Variabilities in heart rate (e.g., tachycardia) and respiratory rates
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Irritable bowel syndrome
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Temperature elevations
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Blood pressure changes
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Excessive sweating, salivation, tearing, and sebum secretion
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Dilated pupils
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Vomiting
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Anxiety, panic disorder, and posttraumatic stress disorder
Motor, sensory, perceptual, and functional changes
Motor impairments are common after TBI yet understudied in humans due to the overwhelming focus on consciousness and cognitive changes. A cohort study showed that during the inpatient rehabilitation phase, 20% or more of patients had paresis in upper extremity (UE) and/or lower extremity (LE), 30% or more had incoordination, and between 13% and 27% had gait and balance problems. Dizziness and disequilibrium were reported in 30% to 65% of people with TBI. Although dystonia appears not to be a significant issue in people post-TBI, spasticity could develop as soon as one week after the injury. It is still not well understood why these changes occur, but animal studies point towards imbalance between excitation and inhibition neuronal signals after brain injury. In particular, the imbalance favors excitation causing sensory deficits, which in turn causes cognitive and motor deficits in TBI. Box 22.2 lists common motor changes and provides symptoms of sensory and perceptive involvement.
Motor changes may Include any or all of the following:
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Paralysis or paresis such as monoplegia or hemiplegia
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Cranial nerve injury resulting in paralysis of eye muscles, facial paralysis, vestibular and vestibuloocular reflex abnormalities, slurred speech (dysarthria), swallowing abnormalities (dysphagia), and paralysis of the tongue muscles
- •
Poor coordination of movement
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Abnormal reflexes
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Abnormal muscle tone: flaccidity, spasticity, or rigidity. (The terms decorticate rigidity and decerebrate rigidity are often used to denote abnormal posturing. Decerebrate rigidity denotes extension in all four limbs. Decorticate posturing includes flexion of the upper extremities and extension of the legs.)
- •
Combinations of asymmetrical cerebellar and pyramidal signs and of bilateral pyramidal and extrapyramidal signs have all been reported
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Loss of selective motor control
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Poor balance
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Loss of bowel or bladder control
Sensory and perceptual may include any or all of the following:
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Hypersensitivity to light or noise
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Loss of hearing or sight
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Visual field changes
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Numbness and tingling (peripheral nerves are often injured)
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Loss of somatosensory functions
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Dizziness or vertigo
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Visuospatial abnormalities
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Agnosia
- •
Apraxia
Cognitive, personality, and behavioral changes
Cognitive and behavioral sequelae can result from generalized or focal brain injuries. For example, emotional changes may be seen with lesions in the orbitofrontal areas. Septal area lesions result in rage and overall irritability. Pseudobulbar injuries can result in emotional lability of involuntary laughing or crying not associated with feelings of emotions. Memory impairment, a very common finding after TBI, is an aftermath of generalized lesions.
Amnesia is a term that describes memory impairment. Posttraumatic amnesia (PTA) is defined as “the time lapse between the accident and the point at which the functions concerned with memory are judged to have been restored.” Two types of PTA are frequently associated with brain injury: retrograde and anterograde. Retrograde amnesia is a deficit in memory retrieval with inability to recall events that occurred prior to the injury. Anterograde amnesia refers to the inability to form new memories after the injury, and it is often more impaired in declarative tasks as compared to procedural. The duration of PTA is considered a clinical indicator of the severity of the injury; it may guide clinical management decisions, and it is also one of the prognostic indicators in TBI. ,
The patient’s inability to develop new memories can be quite challenging for the rehabilitation team and for the patient because memory is an important component of learning. There are two types of memory: declarative and procedural. Memory in which the patient can recall facts and events of a previous experience is declarative memory. Explicit learning, a conscious verbal learning, is based on declarative memory. However, many patients who cannot reproduce memories through conscious recollection do have the ability to learn new motor skills. Implicit learning, a noncognitive type of learning in which patients can show changes in performance after prior experience, is based on procedural memory. Patients can show the ability to change motor, perceptual, or cognitive behaviors with practice or training but may lack declarative memory. Another type of short-term memory that is often compromised after TBI is working memory, which is crucial for processing everyday life information. An example of working memory is the ability to remember the steps of a recipe during cooking. Quality of life is thought to be affected when working memory is impaired.
Behavioral changes can be present even without cognitive and physical deficits. A recent systematic review grouped behavioral changes after TBI into four categories: (1) Disruptive behaviors by excess, for example agitation, aggression, irritability, drug addiction, and behaviors with legal consequences; (2) disruptive behaviors by default, such as apathy and decreased goal-oriented behaviors; (3) affect disorders, including depression, anxiety, and post-traumatic stress disorder (PTSD); and (4) suicidal attempts and suicide. Even though the extent and types of behavioral changes depend upon the severity of injury, all of these behaviors (except for substance abuse) have higher prevalence rates among persons who have sustained a TBI than the general population. The social consequences of inappropriate behavior can be disastrous and interfere with achieving therapy goals.
Box 22.3 lists common cognitive and behavioral changes resulting from brain injury.
Cognitive changes might include any or all of the following:
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Temporary or permanent disorders of intellectual function
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Memory loss
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Shortened attention span
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Concentration problems
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Confusion
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Changes in motivation
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Difficulty sustaining attention
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Executive function loss
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Reduced problem-solving skills
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Lack of initiative
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Loss of reasoning
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Poor abstract thinking
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Shortened attention span
Behavioral changes could include the following :
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Agitation
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Aggression
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Irritability
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Substance abuse
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Behavior with legal consequences
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Apathy
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Depression
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Anxiety
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Posttraumatic stress disorder
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Obsessive-compulsive disorder
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Psychosis
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Suicidal ideation and attempts
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Suicide
Other complications
A list of the complications that may accompany brain injury would be limitless. In addition to any concomitant injuries, some of the diagnostic, monitoring, and therapeutic procedures themselves carry hazards as does prolonged bed rest. Catheters, nasogastric tubes, and tracheotomies can cause iatrogenic injuries. Infections, contractures, skin breakdown, thrombophlebitis, pulmonary problems, heterotopic ossification (HO), and surgical complications are but a few of the risks. Posttraumatic epilepsy is also a possible sequela. Depression occurs frequently after brain injury and appears to be the most prevalent mental disorder post-TBI. It appears that a combination of neuroanatomical, neurochemical, and psychosocial factors is responsible for the onset and maintenance of the depression. Depression post-TBI often negatively impacts outcomes related to productivity and quality of life.
Locked-in syndrome may be grouped differently from DOCs. In this syndrome the patient cannot move any part of the body except the eyes but cognition remains intact and the person is conscious. Communication disorders are also common complications after TBI and may include expressive and receptive aphasia, dysarthria, loss in reading comprehension and social communication, and many others.
Types and classifications of traumatic brain injury
Severity of TBI is categorized as mild, moderate, or severe based on specific measurements on scales such as the Glasgow Coma Scale (GCS) ( Box 22.4 ), duration of loss of consciousness, and duration of PTA. See Table 22.1 for details. In addition, the Brain Injury Association of America provides qualitative descriptions according to the severity of injury. For mild TBI, there is usually a brief to no loss of consciousness and there may be vomiting, dizziness, lethargy, and memory loss. For moderate TBI, unconsciousness can last up to 24 hours. There are signs of trauma, contusions, and/or bleeding on neuroimaging. For people with severe TBI, coma persists for more than 24 hours, there are no obvious sleep/wake cycles, and there are signs of trauma on neuroimaging.
| Measurement | Mild | Moderate | Severe |
|---|---|---|---|
| Glasgow Coma Scale | 13–15 | 9–12 | 3–8 |
| Loss of consciousness | <30 min | 30 min–24 h | >24 h |
| Posttraumatic amnesia | 0–1 day | >1 to ≤7 days | >7 days |
Another scale that is commonly used to classify levels of TBI is the Rancho Los Amigos Levels of Cognitive Functioning Scale (LOCF). The scale measure levels of consciousness, cognition, and behavior post-TBI and is often used as an outcome measure for these impairments as patients progress through various stages of TBI. Briefly, there are eight levels describing persons’ responses and behaviors, namely no response (LOCF I), generalized response (LOCF II), localized response (LOCF III), confused-agitated (LOCF IV), confused-inappropriate (LOCF V), confused-appropriate (LOCF VI), automatic-appropriate (LOCF VII), and purposeful-appropriate (LOCF VIII). See Appendix 22.A for detailed descriptions of typical behaviors observed in each level.
Section II—Medical management of traumatic brain injury
Initial care and acute management
For persons with severe TBI, medical management begins at the prehospital phase where the person is monitored for oxygenation, blood pressure, cognitive function (using the GCS), pupillary function, and signs of brain stem herniation. Transport to a trauma center with CT scanning, neurosurgical evaluation, and ICP monitoring is the goal to monitor and minimize secondary injuries. A determination of GCS score is performed either at the prehospital stage or in the ED to test the function of the brain stem and the cerebrum through eye, motor, and verbal responses. It provides a measure of the level of consciousness and an idea of injury severity. Scores range from 3 to 15, with lower scores associated with lower levels of function. Scores from 13 to 15 indicate a mild brain injury, 9 to 12 a moderate brain injury, and 8 or less a severe injury.
On admission to the ED, a neurosurgeon usually assumes initial and primary responsibility for the person. The first priority in acute care is resuscitation and prevention of secondary insult. The Brain Trauma Foundation recommends the following guidelines for severe TBI management in the acute phase: airway control and ventilation to optimize oxygenation, monitoring and maintenance of cerebral perfusion pressure (CPP) and blood pressure, monitoring and management of ICP, fluid management, hyperosmolar therapy, sedation, and prophylaxis of infections, deep vein thrombosis (DVT), seizures, and hypothermia. , , , The details of the guidelines can be found at www.braintrauma.org .
In addition to the traditional neuroimaging such as CT, magnetic resonance imaging (MRI), and positron emission technology (PET) scan for monitoring of neurological functions, advanced multimodal neuromonitoring is recommended to improve outcomes of TBI. These include jugular venous oxygen saturation (SjvO 2 ), focal brain tissue oxygen tension (PbrO 2 ), cerebral microdialysis, and continuous electroencephalography (EEG). For patients who are candidates for decompressive craniectomy due to elevated ICP, a large frontotemporoparietal approach is recommended versus a small one as it has been found to have better neurological outcomes.
Common neurosurgical interventions
Decompressive craniectomy, as mentioned above, is a procedure where a large portion of the skull is removed to allow the brain to swell. This procedure is used when ICP is elevated over 25 mm Hg for 1 to 12 hours despite other medical interventions. The goal is to prevent brain stem herniation and maintain CPP for brain tissue viability.
External ventricular drain (EVD) is another frequently used neurosurgical procedure to control elevated ICP. Usually a catheter is inserted through the skull into the anterior horn of one of the lateral ventricles to drain cerebrospinal fluid. The catheter is also connected to an external transducer for constant ICP monitoring. The amount of fluid drained from the ventricle needs to be precise and, oftentimes, a few milliliters of drained fluid results in a decrease in ICP. Although EVD may increase the risk of infection, there is strong evidence proving its effectiveness in immediate reduction of ICP.
Persons with epidural hematomas often undergo craniotomies with blood evacuation to relieve pressure within the cranium. Subdural injuries are frequently treated by removing the blood through bur holes.
Common pharmacological interventions
Medications are chosen according to symptoms to be treated.
Medications that decrease intracranial pressure
Osmotic agents such as mannitol are used to pull fluid from brain tissue back into the blood system, thus lowering ICP. Use of mannitol is recommended for patients who have perfusion problems, and the evidence is strong for the effectiveness of mannitol to reduce ICP. Propofol, a barbiturate (sedative), may reduce the need for ICP treatment. Sedative treatment may be reduced as well if it is used together with morphine. Propofol is recommended only if ICP cannot be controlled by other means because it may potentially reduce CPP. , Hypertonic saline is another osmotherapy to control ICP, although the best solution and administration has yet to be determined. The Brain Trauma Foundation in 2016 recommended a stepladder approach using mannitol or hypertonic saline, together with other procedures for best control of elevated ICP. Corticosteroids are commonly used in the acute phase to stabilize brain injury; however, it has been shown that mortality may be increased by methylprednisone, and it should be avoided. See Chapter 36 for additional information.
Medications that control blood pressure and cerebral perfusion pressure
Blood pressure control is important in patients with brain injury. CPP or adequate blood pressure to maintain cerebral blood flow against increased ICP is calculated by subtracting the ICP from the mean arterial pressure. If fluid management cannot maintain adequate blood pressure, then vasopressor medications such as phenylephrine (Neo-Synephrine) are used to constrict peripheral vessels but not the vessels of the brain. Norepinephrine is also shown to support CPP in a consistent and predictive manner. The Brain Trauma Foundation recommended to maintain the systolic blood pressure at ≥100 mm Hg for persons aged between 50 and 69 and ≥110 mm Hg for persons aged between 15 and 49 or those over the age of 70. In general, CPP should be maintained between 60 and 70 mm Hg for positive outcomes.
Medications that decrease intracranial bleeding
Intracranial bleeding is common after TBI, and it can cause permanent disability and even death. Therefore controlling intracranial bleeding is usually a goal in the acute management of TBI. Hemostatic drugs work by increasing coagulation. Antifibrinolytic medications, including lysin analogues and plasmin inhibitors, work by reducing fibrinolysis and increasing clot stability. Although some studies have shown effectiveness, systematic reviews fail to show reliable evidence on their effects for reducing mortality and morbidity.
Medications to control seizure
Seizure is a common complication after TBI, and its presence may have an adverse effect on ICP; therefore anticonvulsants are routinely used in acute TBI as a preventative measure. Examples of anticonvulsants include phenytoin, sodium valproate, levetiracetam, and carbamazepine. Recent systematic review and the Brain Trauma Foundation guidelines recommended that an anticonvulsant should be routinely administered within the first week of acute TBI. , The effectiveness for late seizure prevention remains inconclusive.
Medications for prevention of brain cell death
Hypothermia is frequently used in acute severe TBI because of its possible neuroprotective effect. Although it does not appear to change the mortality rate, it is associated with improved functional outcome on the Glasgow Outcome Scale (GOS) ( Box 22.5 ). Progesterone is a hormone that has been shown to reduce cerebral edema and neuronal loss in acute TBI; however, further research is still needed to support its use in medical management of TBI.
Vegetative state
A persistent state characterized by reduced responsiveness associated with wakefulness. The patient may exhibit eye opening, sucking, yawning, and localized motor responses.
Severe disability
An outcome characterized by consciousness, but the patient has 24-h dependence because of cognitive, behavioral, or physical disabilities, including dysarthria and dysphasia.
Moderate disability
An outcome characterized by independence in activities of daily living and in home and community activities but with disability. Patients in this category may have memory or personality changes, hemiparesis, dysphagia, ataxia, acquired epilepsy, or major cranial nerve deficits.
Good recovery
Patient able to reintegrate into normal social life and able to return to work. There may be mild persisting sequelae.
Medications for prevention of infections
Antibiotics may be used after TBI due to risk of infection from injuries, wounds, or invasive monitoring. It is recommended that antibiotics be delivered for 1 to 2 weeks for persons sustaining penetrating injuries. However, the evidence on the use of antibiotics in other forms of TBI is unclear and may even lead to an increased rate of infection.
Medications that affect behavioral and cognitive functions (also see chapter 36 )
Medications to treat behavioral or cognitive dysfunction are difficult to standardize. A recent systematic review suggested the following medications for various behavioral dysfunctions after TBI. There is some evidence to use carbamazepine (Tegretol) and valproate as a first line treatment for agitation and aggression. Propranolol (Inderal) can also help to improve aggression. For persons with depressive symptoms, selective serotonin reuptake inhibitors (SSRIs) are recommended. Confusion and other neuropsychotic symptoms have been treated using neuroleptic medications; however, there is no evidence of their efficacy.
For patients with attention deficits, monoaminergic agonists such as amantadine or methylphenidate may increase information processing, aid functional recovery, and prevent permanent functional loss in some patients, but the evidence remains inconclusive. , In a recent systematic review, amantadine is recommended for people with DOC to improve arousal.
Medications that affect motor functions (see chapter 36 )
Medications also may be prescribed for motor abnormalities involving increases in tone. Oral medications for treating spasticity include baclofen, diazepam, dantrolene sodium, and tizanidine. They can be used alone or in combination depending on the severity of spasticity. Baclofen works at the CNS level and may cause drowsiness. Baclofen can also be delivered intrathecally where the side effect is less. Dantrolene sodium works directly at the muscle level and therefore is less likely to cause cognitive disturbances but more likely to cause generalized weakness. Botulinum toxin type A (Botox) is commonly used to treat focal muscle hypertonicity, such as the finger flexors, biceps, or gastrocnemius. Diazepam (Valium) initially was the drug most commonly administered for spasticity or high tone. However, diazepam also promotes drowsiness and decreased responsiveness and can increase muscle weakness and ataxia. Regardless of the medication used, it is recommended that medications be combined with complementary therapies, such as transcranial magnetic stimulation (TMS) and therapeutic exercise, in order to achieve greater benefits of tone reduction medications and improve functional outcomes.
Regenerative medicine and management of traumatic brain injury
Regenerative medicine is an interprofessional field of research and clinical practice for the repair, replacement, or regeneration of cells, tissues, and/or organs in order to restore function lost due to disease or damage. Recent advances in stem cell and tissue engineering technology have led to a rapid proliferation of research, though limitations exist, including the survival and appropriate differentiation of implanted cells. Studies on the combined effects of regenerative approaches and physical rehabilitation following stroke and TBI, referred to as regenerative rehabilitation, are very promising and show greater recovery than either approach used in isolation in animal model studies. Several clinical trials are underway to explore the impact of regenerative rehabilitation in stroke and TBI, as well as muscular conditions such as muscular dystrophy. Scientists in this field are encouraged by positive results to date, and predict that with further advances in the stem cell and tissue technologies and rigorous interprofessional research, regenerative medicine has the potential to become the standard of care in the treatment of many neuromuscular and other health conditions.
Section III—Rehabilitation management of traumatic brain injury
Terminology and structure for patient management
The World Health Organization (WHO), in the International Classification of Functioning, Disability and Health (ICF), has developed a common terminology that is used in this chapter. Definitions are as follows (see also Chapter 1 ):
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Body functions are physiological functions of body systems (including psychological functions).
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Body structures are anatomical parts of the body such as organs, limbs, and their components.
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Impairments are problems in body function or structure such as a significant deviation or loss.
- •
Activity is the execution of a task or action by an individual.
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Participation is involvement in a life situation.
- •
Activity limitation s are difficulties an individual may have in executing activities.
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Participation restrictions are problems an individual may experience in involvement in life situations.
- •
Environmental factors make up the physical, social, and attitudinal environment in which people live and conduct their lives.
The American Physical Therapy Association (APTA) has published levels of patient management leading to optimal outcomes. The Association’s Guide to Physical Therapist Practice, which uses examination, evaluation, diagnosis, prognosis, intervention, and outcomes as its basis, will be followed in this chapter. Although this is the terminology used by physical therapists, its application and integration into the profession of occupational therapy should be simultaneously acknowledged. The method used in this chapter for gathering the guide information is based on the Hypothesis-Oriented Algorithm for Clinicians (HOAC) II model. See Box 22.6 for an overview of this method, and see the text that follows for details of how to perform these procedures.
- 1.
Collect initial data.
- 2.
Have patient and family identify patient problems with activity and participation limitations.
- 3.
Develop an initial set of hypotheses based on a task analysis of identified activity limitations; choose and apply examinations to test those hypotheses.
- 4.
Reassess hypotheses in light of examination findings and confirm or deny. Repeat first three steps if denied.
- 5.
Develop list of non–patient-identified problems, including anticipated problems (such as skin breakdown when sensation is impaired).
- 6.
Choose and apply appropriate outcome measures to monitor progress that address the impairments or activity limitations.
- 7.
Develop an evaluation and diagnosis identifying why the problems exist or are likely to occur in the future.
- 8.
Establish a prognosis and set goals with time frames for achievement.
- 9.
Develop interventions that most effectively ameliorate the problems based on current literature or best practice.
- 10.
Reexamine using outcome measures to determine progress.
HOAC , Hypothesis-Oriented Algorithm for Clinicians.
Examination
Data are collected from referral information, from the medical record, via observation, and from the patient or family interview. A history is taken and should include information regarding the mechanism of injury, initial GCS score, extent and time since onset of injury, patient’s age, and duration of PTA. This information will be used to help establish a prognosis. Other information about education, family support, and living circumstances will also help with the prognosis and discharge planning. Complications, as well as coexisting diseases, are reviewed with the patient in order to discuss a thorough plan of care and determine appropriate referrals. Included under examination are systems review and tests and measures. Systems review is considered a screening of major systems that helps therapists to identify areas of focus during selective tests and measures. Therapists use information collected in examination to identify service needs.
Examination should lead to an understanding of the underlying causes of the activity limitations and participation restrictions and should be the basis of the intervention program. Patients usually present their chief complaints as activity limitations, for example, “I can no longer walk very far.” Once activity limitations have been determined, a task analysis can be completed by having the patient demonstrate the problem—in this case, walking. The therapist will develop a hypothesis as to why the observed deviation from typical performance is present. Tests and measures and standardized outcome measures will be chosen on the basis of the therapist’s knowledge of their importance in the task being performed and recommendations from peer-reviewed resources, such as the Academy of Neurologic Physical Therapy, to confirm the hypothesis and to establish baseline measurements. For example, in a patient who drags the foot in initial swing, the patient might lack 45 degrees of full passive knee flexion, but this is not critical in the task of walking. However, being able to dorsiflex the foot at initial swing is important. Therefore testing of both the ability to dorsiflex with the leg in the extended position and the speed at which the patient can perform this task would be appropriate. The tests and measures should be chosen on the basis of the hypothesis that the therapist generates from the task analysis. Details of task analysis and examinations of impairments, activity limitations, and participation restrictions will be provided in later sections of this chapter.
The Academy of Neurologic Physical Therapy Outcome measures recommendations, and Evidence Database to Guide Effectiveness (EDGE) Task Force developed recommendations for outcome measures for selected clinical conditions (e.g., stroke, TBI) based on vigorous evaluations of available measures. The recommendations of outcome measures are classified according to settings and practices. Physical therapists should choose outcome measures from the recommendations for TBI when possible. For example, gait outcome can be measured using the 6 minute walk test or 10 m walk test in the inpatient or outpatient setting, or the High-Level Mobility Assessment Tool (HiMAT) if the patient is high-functioning and seen in an outpatient setting. Recommended outcome measures by settings/practices are presented in Tables 22.2 to 22.4 . For various components of examination, see Box 22.7 .
| General | Moderate to severely dependent | Mildly dependent to independent in ambulation |
|---|---|---|
|
|
|
- I.
History: injury, age, PTA, GCS score, job, home environment, educational level, previous injuries, etc.
- II.
Patient and family data: patient and family perception of the limitations, goals, personal factors, socioeconomic factors relating to participation limitations
- III.
Other health care team member evaluations
- IV.
Screens
- A.
Systems review to emphasize precautions during intervention and to identify any “red flags” that will require referrals.
- 1.
Circulatory and respiratory
- 2.
Integumentary
- 3.
Musculoskeletal
- 4.
Autonomic nervous system—bowel, bladder
- 5.
Cognitive
- 6.
Language
- 7.
Emotional
- 1.
- A.
- V.
Assess activity limitations (perform task analyses) of patient-identified problems
- VI.
Formation of underlying impairments (hypotheses) from the task analyses
- VII.
Choose specific tests and measures and recommended outcome measures to test underlying impairments or confirm the hypotheses; these might include:
- A.
Sensory
- 1.
Somatosensory
- 2.
Vestibular
- 3.
Visual
- 4.
Hearing
- 1.
- B.
Integrated, perceptual
- C.
Motor
- 1.
Muscle strength
- 2.
Muscle flexibility
- 3.
Response speed
- 4.
Tone
- 5.
Movement speed
- 6.
Endurance and fatigue
- 7.
Complex impairments
- •
Basic motor patterns available
- •
Modification of motor patterns possible
- •
Anticipatory and adaptive responses
- •
Variability of performance
- •
- 1.
- D.
Autonomic nervous system
- E.
Cognitive
- F.
Language
- G.
Emotional
- A.
| Inpatient Only | Outpatient Only | Both In- and Outpatient |
|---|---|---|
|
|
|
| Body Structure/Function | Activity | Participation |
|---|---|---|
|
|
|
Evaluation
Evaluation identifies the needs that can be managed by the therapist; serves to delineate those factors that influence or restrict the choice of therapeutic approaches; and states which components are most critical for the identified activity limitations. Evaluation provides a qualitative means of determining why a need is present. It includes considerations of subjective findings, objective findings, and environmental/contextual and personal factors (as illustrated in the ICF model). Thus the evaluation determines goals and intervention. The purpose of the evaluation is to determine what prevents the patient from performing in a functional, acceptable manner as identified by the patient, the therapist, and society.
Diagnosis
Diagnosis takes into consideration the integrated evaluation findings and classifies the problems into diagnostic categories. These diagnostic categories define the primary dysfunctions of an individual and in turn enable the therapist to formulate appropriate intervention. The diagnostic process involves discernment of what the individual desires to achieve and the capacity of the individual at the moment. Additional information from other healthcare professionals may need to be sought during the diagnostic process. Likewise, the therapist may need to share information with other healthcare professionals if the diagnostic process reveals problems outside of the therapist’s scope of practice. The ultimate goal of diagnosis for the therapist is to verify the needs of the individual and act accordingly.
Prognosis and outcomes
Prognosis is the determination of the optimal level of functional improvement and the time required to reach that optimal level. In addition to the highest functional level the individual is capable to obtain, the therapist needs to consider the individual’s habitual level of function in order to identify a realistic and reasonable prognosis. This is important to manage expectations of the individual and the therapist and is crucial to motivate the individual during intervention. Prognosis often includes short- and long-term goals that are specific to improve functions along with duration and frequency of intervention to achieve those goals.
On the other hand, outcomes are the actual results of intervention and are chosen to measure all levels of dysfunction from impairment through participation limitation to determine effectiveness of the intervention strategies and whether or not the patient has met rehabilitation goals. Again, outcomes should ideally follow the recommendations listed above by TBI EDGE Taskforce. An example of the process is presented in Box 22.8 .
Examination
A patient comes to your clinic reporting that he falls several times a week during walking and would like to improve his balance. He is 21 years old and suffered a moderate traumatic brain injury (TBI) 6 weeks ago. He had a Glasgow Coma Scale (GCS) score of 11 initially and 1.5 days of posttraumatic amnesia (PTA). He was at ABC Rehabilitation Center for 5 weeks and was discharged home last week. He lives with his parents in a single-story house. He is in his third year of college studying geology. His systems review demonstrates slight decreased vital capacity of 3.8 L (4.6 L would be normal), but no abnormalities in the musculoskeletal systems or integumentary system. His cognitive functions are within normal limits according to neuropsychological testing, except for memory deficits.
Task analysis
You observe this patient during walking and note that he has decreased knee flexion in preswing and decreased dorsiflexion throughout swing phase, with the toe intermittently catching on the carpet when you have him speed up his walking. He also has decreased dorsiflexion at initial contact and in terminal stance.
Testing of impairments
Because of the decreased dorsiflexion in terminal stance (which is passive), you hypothesize that the decreased dorsiflexion is secondary to gastrocnemius-soleus muscle tightness rather than anterior tibialis weakness. You test the range of motion (ROM) at the ankle, and it is within functional limits. You now develop a second hypothesis that there is increased tone in the gastrocnemius-soleus. On an Ashworth test, the patient scores a level 3 for the gastrocnemius-soleus. Because the patient does not get adequate plantarflexion at preswing (neutral vs. 15 degrees for typical adults), you also hypothesize that the patient is unable to generate plantarflexion fast enough in preswing to achieve the normal 15 degrees of plantarflexion. Testing by having the patient plantar flex rapidly in standing shows that it takes a full 3 seconds (s) to achieve 15 degrees of plantarflexion—much too long to be used in walking.
Outcome measures for activity limitations
The patient is in an outpatient setting and appears to be high functioning. The high-level mobility assessment tool (HiMAT), 6 min walk test, 10 m walk test for gait speed, and various balance scales appear to be appropriate.
Evaluation
The patient is experiencing multiple weekly falls secondary to toe drag at initial swing when walking at speeds over 1.17 m/s. The toe drag comes from decreased dorsiflexion and decreased knee flexion at initial swing because of inadequate plantarflexion. Testing demonstrated both increased gastrocnemius-soleus tone (Ashworth level 3) and decreased ability to generate adequate plantarflexion to achieve the normal 40 degrees of knee flexion during preswing.
Prognosis and outcomes
The patient has a good prognosis. He is early postinjury, is young, and has good family support and a high education level. There is no history of previous TBI. The patient started rehabilitation immediately and in a center specialized for people with TBI. His PTA was short.
Examination for people with traumatic brain injury
Task analysis of activity limitations
Often the physical therapist begins the examination at the activity limitation level. This involves observing those functions that the patient or family identifies as problematic. Activity limitations in patients with TBI may include loss of mobility in bed, coming to sit, sitting to standing; impaired static and dynamic balance; loss of household and community ambulation and stair negotiation; loss of running, jumping, and kicking skills; poor reach and grasp; loss of activities of daily living (ADLs) such as dressing, toileting, and feeding; and loss of instrumental ADLs such as shopping and driving. The physical or occupational therapist performs a task analysis of the impaired function by comparing the patient’s performance of the task with typical task performance. For example, the therapist would observe the patient performing the sitting-to-standing activity, observing that there is inadequate forward trunk momentum in the preextension phase. A reasonable hypothesis may be that the patient is fearful of falling forward. If the problem is loss of balance in the extension phase, a hypothesis may be poor timing of the gastrocnemius firing. Both of these hypotheses are based on the task analysis but also on the literature, which defines the importance of trunk momentum to initiate seat-off and timing of gastrocnemius firing during the end of the sitting-to-standing activity to maintain balance.
Examining activity limitations requires knowledge of typical movement patterns and task performance among persons without neuromuscular disorders of about the same age as the patient. Tasks that are described in the literature for typical performance include rolling, rolling to sit, sitting, sitting to standing, standing to sitting, standing balance, walking, hopping, jumping, kicking, running, reaching and grasping, throwing, batting, and golfing. The form is a bit messy and we have decided to remove it from the chapter.
Assessing underlying impairments
Once the task has been analyzed, the impairments leading to poor performance of the task are identified. Breaking motion down to its most basic components may be helpful, but two caveats are necessary. First, improvement in abnormal components may not lead to improvement in activity limitations. Some critical impairments will have more influences on an activity than will others. For example, Perry and colleagues showed that for normal walking velocity to be attained, although cadence and stride length are important, a strength level of 3+/5 is a critical component in the ankle muscles. Deficiencies of timing, strength, or sequencing can contribute to poor hand function, but sensory deficits at the hand level may be the critical impairment related to poor manipulation skills. In addition, impairments in the circulatory, respiratory, integumentary, and musculoskeletal systems can account for activity limitation in the patient with TBI ( Fig. 22.1 ). Relative contributions of the impairments to the activity limitation or participation limitation are addressed by the therapist’s task analyses, hypothesis, subsequent evaluation, and diagnosis, which will determine the focus of the intervention program.
The second caveat is treating the individual impairments will not necessarily result in the patient learning a skill. Skills result from an organization of many motor functions together and require whole task practice. Conversely, not having a critical component, such as arm strength, may be the one factor preventing a person from learning to perform a skill (e.g., enough force cannot be generated to throw a ball 5 feet in the air to hit a basket). Commonly seen impairments after TBI are reviewed below along with recommended measures.
Impaired consciousness and cognition.
As previously mentioned, changes in consciousness are common in the acute phase of TBI. The duration of this change varies depending on the extent of the injury and recovery. Physical therapists often include measures of consciousness to capture changes in this impairment, as consciousness commonly depicts different stages of interventions. Recommended outcome measures for consciousness include Coma Recovery Scale-Revised, LOCF, and GCS .
Cognitive impairments are also common after TBI and may affect overall disability more significantly than physical impairments. It was reported that cognitive impairment was the primary contributor to activity limitation in most patients with TBI who scored at moderate to severe levels on the GOS. The spectrum of cognitive dysfunctions include, but are not limited to, impaired attention, frustration, lack of spontaneity, easily distractible, impaired executive functions, inappropriate affects, altered memory, slowed information processing, and impaired judgment. Traditionally, neuropsychologists, speech pathologists, and occupational therapists all perform testing of cognitive function. Depending on the profession and types of cognitive impairment, various cognitive tests are employed, and it is beyond the scope of this chapter to introduce all of these cognitive tests and batteries. For physical therapists, the TBI EDGE Task Force highly recommended a physical therapy examination to include the Coma Recovery Scale-Revised or Moss Attention Rating Scale in inpatient settings for moderate to severe TBI. The LOCF (see Appendix 22.A ) is also a commonly used measure by physical therapists to record changes of cognitive functions as the patient progresses through various stages of consciousness. The Montreal Cognitive Assessment (MoCA) is a recommended test that has memory testing embedded within it. Refer to Box 22.2 to 22.4 for the full recommendation list by setting and practice.
Autonomic dysfunctions.
As mentioned earlier, changes in the ANS after TBI may cause system-wide issues due to the broad spectrum of body functions regulated by the ANS. These functions can directly or indirectly affect the rehabilitation process, and therefore it is important for therapists to measure these functions from time to time. These measures surround vital sign measurements, for example heart rate, respiratory rate, blood pressure, etc. Since orthostatic challenge is reported, therapists should monitor appropriate vital signs in various patient positions, especially when persons are symptomatic. Sophisticated measurements of ANS functions are usually performed by physicians, for example, using electrocardiographic marker to track sympathetic and parasympathetic activities, measuring pupillary light reflex, measuring arterial pulse wave, and measuring eyeball pressure.
Impaired strength or force production.
Evidence consistently shows that strength and force production are common impairments in both the UEs and LEs after TBI. When strength control or force gradations are significantly impaired at initial admission (about 25% of patients), research has shown improvements with near to full resolution at a 2-year follow-up, with only 12% impairment remaining in the UEs and 7% in the LEs. Low power production is also thought to be the major contributor to impaired mobility.
In the case of upper motor neuron lesions, weakness can be a major problem. The number of motor neurons activated, and the type of motor neurons and muscle fibers recruited, affect force. Motor neurons in the motor cortex can be deficient, leading to disordered and reduced recruitment. Individuals with brain damage show early atrophy and loss of motor units, as well as motor units that fatigue easily. , Disuse, cast immobilization, joint dysfunction, improper nutrition, medications, and aging can cause differential weakness with altered morphological, biochemical, and physiological characteristics within the muscle. Electromyography (EMG) studies by numerous investigators , suggest that reduced activity alters motor unit properties, discharge frequency, and recruitment patterns. Performance problems are reflected in the inability to generate force in different directions and against different loads, as well as in problems sustaining force output.
Changes in muscle length affect strength. In patients who have had a cerebrovascular accident (CVA), shortened muscles tend to be strong in short ranges and lengthened muscles are strongest in lengthened ranges but weak in shorter positions compared with the strength-length curves of normal muscles.
Strength may be examined functionally—for example, by seeing if the patient has enough strength to lift the arm overhead, out to the side, and up to the mouth, or is able to go from sitting to standing. In some cases, such as those in which the patient is unable to perform balance reactions or has been on extended bed rest, testing individual muscles may be important. Traditional manual muscle testing (MMT) with force transducers or strength testing with isokinetic testing throughout the range provides good strength information. The level of testing chosen should be consistent with the deficit and the therapist’s knowledge of its importance in contributing to the activity limitation.
Muscle endurance refers to the ability of a muscle to produce the same level of contraction over time. The subjective feeling of effort and weakness after fatiguing exercise may be related to the need to recruit more motor units and to increase the mean firing frequency of the motor units to maintain constant force output. EMG with medium-frequency analysis can test this type of fatigue. Fatigue can also be assessed by measurement of maximal voluntary force, maximal voluntary shortening velocity, or power. Decreased force production, prolonged time to relaxation of muscle fibers, and recruitment of additional muscles during an activity are characteristic of fatigue. Although repeated muscle testing can pick up decreased strength in specific muscles, in most instances overwork fatigue is first noted by an altered pattern of movement of body segments during activity.
Impaired muscle length and joint range of motion.
Flexibility at the muscle and joint level is critical for normal posture and movement. Muscle atrophy occurs rapidly, and changes in muscle fiber type and function can be seen as early as 3 days. Viscoelastic properties change with paralysis so that the muscle feels stiffer. ,
The examination should determine the contribution of muscle tone, joint structure, and tissue factors in limiting flexibility. Active and passive motion should be compared because stiffness (not contracture) often prevents normal function. For example, active dorsiflexion is often limited in patients who have full passive ankle range of motion (ROM) because stiffness begins at neutral. The functional result is foot drop or toe catch in the early part of the swing phase of gait because the anterior tibialis muscle cannot generate adequate force production to overcome the stiffness in the gastrocnemius and soleus. This restriction also may limit forward movement of the tibia over the foot during the stance phase of gait, resulting in hip retraction or an apparent balance loss. Knee hyperextension also can result from lack of forward motion of the tibia. Flexibility measurements are done with goniometers, motion analysis systems, tape measures, inclinometers, photographs, or electronic devices. Taking both passive and active measurements is critical in identifying intervention approaches.
Abnormal muscle tone and reflexes.
In the motor learning theories of today, many of the behaviors and resulting motor patterns after brain injury are seen as attempts by the CNS to compensate for loss. For example, spasticity may be the result of an attempt to compensate for the patient’s inability to increase force. When the amplitude of a contraction cannot be increased because of the injury, the CNS may increase the length of time the muscle fires or may recruit muscles not normally used in a particular pattern of movement; both are characteristics seen in spasticity.
Whatever the cause of increased tone, the therapist can evaluate tone at two levels: is it interfering with function, and, if so, can it be changed? Spasticity is not a single problem. , , Spasticity can have any or all of the following characteristics:
- •
Changes in response to stretch
- •
Decreased ability to produce appropriate force for a specific task
- •
Increased latency of activation
- •
Inability to rapidly turn off muscles
- •
Loss of reciprocal inhibition between spastic muscles and their antagonists
- •
Changes in the intrinsic properties of the muscle fibers
- •
Inability to generate enough antagonist power to overcome spastic muscles
Examination begins with identifying whether there is increased or decreased muscle tension at rest. If it is increased, is the tension at the muscle level (stiffness or sarcomere involvement) or the neurological level? Muscle stiffness resulting from tissue changes is common in the patient with brain injury. If there is increased tone during movement, EMG may be beneficial to determine the nature of the tone. Is it a problem of co-contraction of agonist and antagonist at a joint? Is it a problem of prolonged contraction? Or is it poor sequencing, either temporally or spatially, of other muscles involved in the movement?
Spatial sequencing of movement involves the contraction of a preset group of muscles. Temporal sequencing involves the contraction of muscles in a fixed sequence. EMG and video analysis provide additional depth of information regarding the sequence and timing of movement patterns. For example, is the normal temporal sequencing in the distal-to-proximal manner present in the UE during a reaching task? In a balance reaction, are the ankle, hip, and back extensors (spatial sequencing) all contracting in response to a forward perturbation?
The most commonly used tool in examination of tone is the Ashworth Scale or Modified Ashworth Scale (MAS) ( Box 22.9 ). The Tardieu Scale is similar, but testing is done at three different velocities and may provide a clearer picture of what is caused by tone versus muscle shortening. Testing of deep tendon reflexes identifies problems with stretch reflexes, and surface EMG (sEMG) can determine the presence of co-contraction, prolonged contraction, sequence and timing problems, and increased latencies.
| Grade | Description |
|---|---|
| 0+ | No increase in muscle tone |
| 1+ | Slight increase in muscle tone, manifested by a catch and release or by minimal resistance at the end of the range of motion (ROM) when the affected part(s) is moved in flexion or extension |
| 1+ | Slight increase in muscle tone, manifested by a catch, followed by minimal resistance throughout the remainder (less than half) of the ROM |
| 2 | More marked increase in muscle tone through most of the ROM, but affected part(s) easily moved |
| 3 | Considerable increase in muscle tone, passive movement difficult |
| 4 | Affected part(s) rigid in flexion or extension |
Impaired coordination.
Ataxia was one of the most common findings among military personnel who had sustained TBI, with 32% of patients showing ataxia initially and 14% at the 2-year follow-up. There are many subcategories of ataxia, including dysmetria, dyssynergia, rebound phenomenon, dysdiadochokinesia, and intention tremor. Many clinical tests to assess coordination impairments are available. Common tests include finger-nose-finger test for UE coordination, and heel to shin/heel slides for the LEs.
Impaired sensory function.
Sensory functions are often impaired after a moderate to severe TBI. Problems in the sensory system are often reflected in the motor system, creating distorted movement through faulty information in the feedforward or feedback processes.
Two broad categories of sensations can be defined on the basis of the type of information: primary sensation and cortical, or integrative, sensation. This arbitrary division is useful functionally, but it is not anatomically based. Primary sensation includes exteroception and proprioception. The exteroceptors of smell, sight, and hearing are sometimes referred to as teloreceptors. Vision, hearing, olfaction, gustation, pain, touch, temperature, proprioception, and kinesthesia are commonly affected primary sensations. Sensation cannot be clinically tested without patient participation.
- •
Proprioception. Deficits associated with poor balance included a high number of subjects with discriminative touch deficits in one study, an impairment related to poor UE function. Traditional examinations of proprioception include the ability to distinguish motion and motion direction at each joint. Some patients who cannot distinguish direction or movement still function well. They may have proprioceptive function at the unconscious level (e.g., cerebellar) while not perceiving the input at the parietal level (conscious level).
Testing is performed by having the patient close his or her eyes; then the therapist places a joint in a specific position (e.g., flexed, extended) and asks the patient to name/identify the position either verbally or with the uninvolved limb. Asking the patient to close the eyes and identify when the therapist passively moves a joint while the patient indicates specific direction of movement can test joint movement sense, or kinesthesia, especially for those with multilimb involvement. Very small joint movements of about 1 degree are within the discrimination level of typical individuals.
- •
Light touch. Light touch is tested with a brush for localization and quality of sensation. For more definitive light-touch discrimination, especially on the hands and feet to determine peripheral neuropathies, a monofilament test can be used.
- •
Two-point discrimination. Two-point discrimination can be tested with instruments specifically designed to measure how far apart two separate spots of contact need to be to identify them as distinct. For patients who are thought to be ignoring stimuli on one side, testing at the same time bilaterally is first performed, and then each limb is retested separately. Patients who extinguish stimuli will respond that they feel only one stimulus when both limbs are tested simultaneously but will perceive the stimulus just fine when each limb is tested separately. This is called the bilateral extinction test.
- •
Stereognosis. Stereognosis, the ability to identify objects placed in the hand without visual assistance, may be critical to normal hand use. The therapist places multiple common and culturally appropriate objects, such as pens, coins, and safety pins, in the hand and asks the patient to identify the objects while the eyes are closed.
Impaired vision and visual perception.
Vision is critical in recovery of many motor functions because it is responsible for much of the feedforward, or anticipatory, control of movement and the initial development of a movement pattern. For example, balance can be maintained through the visual system by modifying synergies before surface change occurs. Feedback through the peripheral field via the movement of the visual array on the retina can also trigger balance responses. Campbell found problems with visual functions in most patients with mild to moderate TBI; these problems involved poor visual acuity (48%) and problems with vergence (85%), which can cause blurring and doubling of vision, and smooth pursuit (63%), which can cause a “jumping” of the visual image.
Some patients are able to use their hands for grasp and release, in spite of severe somatosensory deficits, when they are able to use vision to guide the motion. Many of the standard movement tests should be performed with and without vision.
General visual functions can be screened by the physical or occupational therapist as follows:
- 1.
Tracking is assessed by use of an H pattern of movement of the object being tracked with the eyes and not with head movement. The examiner observes any nystagmus or refixation saccades. Eye muscle paralysis can be observed during tracking if the patient cannot move the eye(s) laterally, up, down, or medially.
- 2.
Focus, or accommodation, can be checked by observing constriction and dilation of the pupil. Constriction occurs as an object is moved toward the nose, and dilation as the object is moved away from the nose.
- 3.
Binocular vision is controlled through feedback from blurred or doubled vision. This reflex signals whether the eyes and fovea are focused on a single point or target, as the images in both eyes fall on the same retinal points. A “cover test” can screen for binocular vision. The patient stares at an object at about 18 inches from the nose. The therapist covers one eye. If there is movement to adjust the remaining uncovered eye back to the object, both retinas may not be focusing on the same point. Observing whether light reflections fall on exactly the same place on both pupils is useful in evaluating binocular eye focus. Vergence testing can also be an indicator of binocular visual functions.
- 4.
Visual fields can be grossly tested by having the patient look forward at a point (observer sits in front of the patient to be sure the patient remains focused straight ahead). The patient indicates when he or she first sees an object coming into the peripheral field from behind, or the “spotter” notes when the patient looks toward the object.
- 5.
Vergence is tested by having the patient observe an object or pen tip as it is brought from about 20 inches away. The patient is told to follow the object with his or her eyes. The object is moved at a moderate speed toward the bridge of the nose, and the patient reports when the object becomes blurred or doubles. When typical convergence is present, there will be no blurring or doubling until the object is 2 inches away or closer, and when the object is moved back out, the patient will report the object as single within 4 inches.
- 6.
Visual interactions with the vestibular system are assessed through the vestibuloocular reflex (VOR). This reflex allows people to maintain a fixed gaze on a target as the head moves. The object should not appear to blur, move, or double during head motion at various speeds.
- 7.
Perceptual tests that evaluate how visual information is used include visual memory tests, cancellation tests, and figure-ground tests.
- 8.
Visual acuity is tested using a Snellen eye chart. Poor acuity can affect balance responses. Neuro-optometrists and neuro-ophthalmologists are appropriate referrals for patients needing in-depth visual workups, especially when visual perception is involved. See Chapter 28 for additional information on vision and visual testing.
Deficits in the vestibular system.
The vestibular system monitors the position of the head in space and helps distinguish if the body or the visual surrounding is moving. It also provides a vertical reference to gravity to maintain the head upright. Vertigo, dizziness, eye-head incoordination, and postural and balance complications occur as a result of problems in the vestibular-cerebellar systems. Details of vestibular rehabilitation are described further, and readers are encouraged to see Chapter 21 for more information.
Vestibular deficits are common after TBI with an estimated 30% to 65% of people affected. Patients with mild or moderate TBI have a high rate (23.8% to 81%) of complaints of dizziness. , In many cases dizziness is a sign of vestibular dysfunction and may prolong recovery from TBI. , TBI-related vestibular disorders can be central or peripheral, for example benign paroxysmal positional vertigo (BPPV), central vertigo, or perilymphatic fistula. Testing of the vestibular system should be conducted according to the patient’s complaints of symptoms. A comprehensive history and vestibular examination are instrumental for accurate diagnosis, targeted interventions, and promoting recovery.
In general, a vestibular system examination should include assessment of the oculomotor system (e.g., smooth pursuit, saccades, vergence), assessment of VOR function (e.g., head thrust test), and position test (e.g., Dix-Hallpike) according to the patient’s complaints. For example, symptoms occurring only with specific head movements can be an indicator of problems in the semicircular canals, which points toward the diagnosis of BPPV. Dizziness with head tilts might indicate problems in the otolithic system and VOR tests should be conducted. Other advanced evaluation tools, such as electronystagmography, may be used when symptoms and complaints are more complex. Since postural instability is also a common manifestation in patients with vestibular disorders, outcome measures on balance and/or sensory organization are common tests to be included, which will be discussed in the following section on Assessing Activity Limitations. See Chapter 20 and 21 for additional information on balance and vestibular testing.
Impaired cardiovascular endurance (deconditioning).
For persons after TBI, peaked aerobic capacity is found to be lowered by 25% to 35% compare to matched sedentary group. In addition, the ventilatory anaerobic threshold (submaximal exercise response correlated with cardiovascular fitness) after TBI is also found to be below the demand of many everyday activities. It is therefore imperative to investigate cardiovascular endurance in people with TBI. Mossberg and colleagues in their review paper stated that maximal graded exercise tests using leg cycle ergometry and treadmill are both reliable for persons after TBI, though treadmill is preferred over cycle ergometry due to its functional nature. Submaximal tests are good alternatives when equipment and time are concerns. The 6 minute walk test is a recommended choice by both Mossberg and colleagues and the TBI EDGE Task Force.
Fatigue, which is separate from impaired endurance, may result from increased energy requirements resulting from less efficient motor patterns or from more CNS activity. Fatigue is a common complaint after TBI and is associated with insomnia. Testing for fatigue is challenging because it is multifactorial. The Global Fatigue Index is recommended for physical therapists to assess fatigue in outpatient settings.
Impaired communication.
Primary damage to the language and communication centers in the brain sustained during the accident or injury, alone or in combination with cognitive, motor and sensory impairments, often result in impaired communication following a TBI. Various communication disorders after TBI are reported in the literature (e.g., aphasia, dysarthria, social communication, reading comprehension ). Although it is not within the scope of practice for physical therapists to formally assess and treat communication disorders, it is a domain included in many commonly used measures by physical therapists, for example the MoCA. Physical therapists need to be aware of the deficits and modify communication strategies during rehabilitation intervention. The speech and language therapist typically assesses and treats communication disorders, and makes recommendations for interprofessional team members regarding augmented or alternative communication strategies.
Emotional and behavioral problems.
Examining behavioral changes after TBI is important because they are major sequelae of the injury. These changes include impulsiveness, disinhibition, anger, lack of initiative, and apathy, among others. Because the effect of behavioral changes is multidimensional, it is thought that all health care professionals play a role in evaluating behavioral issues in persons post-TBI. It is, however, still best for neuropsychologists or neuropsychiatrists to administer neurobehavioral tests as special training is required. Some measures are appropriate for physical therapists to administer, namely the Agitated Behavior Scale, Apathy Evaluation Scale, and LOCF.
Assessing activity limitations
Activity in the ICF model is defined as the execution of tasks or an action with a functional purpose. Examples of activities include bed mobility (e.g., rolling), transfer, balance, ambulation, wheelchair mobility, running, bathing, grooming, toileting, and dressing. When assessing these activities, it is important to evaluate both the quality of movements, as well as the quantitative components (e.g., speed of movement, distance). Physical therapists should pay attention to the following quality of movements when assessing a task:
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Is the patient able to use the basic motor patterns for the task in a functional manner?
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Is the patient able to modify and then accomplish the task?
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Is there good interlimb coordination as demonstrated by coordinated two-handed activities, good timing between limbs in walking, and jumping?
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Does the patient appear to have the ability to coordinate motions (decrease the degrees of freedom), or are they limited by too few degrees of freedom?
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Does the patient respond correctly to environmental changes or stimuli such as stepping over or around objects or being able to walk on different terrain?
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When motor patterns are used, are they appropriate for the stimulus? For example, is the ankle strategy used for standing on a firm surface and when stopping walking?
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Are automatic movement patterns present (e.g., balance synergies, walking, and running)? Are volitional or voluntary movements present?
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Can the patient accomplish the same task in several ways? Can the patient adapt to different task demands?
The following subsections reviewed the commonly seen activity limitations after TBI and recommended outcome measures in this ICF domain.
Basic functional mobility.
Functional mobility usually includes bed mobility, transfer (sit to/from stand and transfer to/from different surfaces), basic locomotion, and basic ADLs. After a TBI, approximately 40% of patients experience limited functional mobility due to physical and cognitive impairments, resulting in need for personal assistance. Assessing functional mobility is therefore imperative, especially during the early phase of rehabilitation. Recommended outcome measures for assessing basic functional mobility include Functional Independence Measure (FIM), Functional Assessment Measure (FAM), and Barthel Index. More than one functional mobility type is usually included in the measure to capture a comprehensive picture of the person’s mobility and functional level. These measures are often administered in acute or inpatient rehabilitation settings when patients require more assistance in mobility and improvement in this area is more substantial.
Sitting balance.
Brown and colleagues found sitting balance to be impaired in 52% of the patients with TBI at initial examination in their review. Testing usually includes static sitting without arm support and dynamic sitting with the patient reaching in multiple directions or ability to resist perturbations. These are not standardized tests but are commonly used clinical tests to assess sitting balance.
Standing balance.
Standing balance after TBI is usually affected in mild, moderate, and severe injuries, with 82% of patients exhibiting standing balance deficits. Deficits include both motor strategy problems and appropriate use and integration of somatosensory, visual, and vestibular information. Newton reported that patients with moderate and severe TBI showed significantly impaired reaction times to perturbation in standing. Although they could grade their responses to the perturbations appropriately, the responses were often asymmetrical.
The TBI EDGE Task Force recommended various outcome measures for assessing standing balance in patients with TBI. Depending on the patient’s functional level and settings where therapy occurs, different measures should be selected. For example, the Berg Balance Scale and Community Balance and Mobility Scale are recommended for both inpatient and outpatient rehabilitation settings. The Balance Error Scoring System is recommended for outpatient rehabilitation settings where the patient is tested on the types of standing balance error in double leg stance, single leg stance, and tandem stance on firm and foam surfaces. Sensory Organization Test is also a recommended test and is an appropriate choice for the patient with vestibular symptoms.
Gait and dual-task gait ability.
The motor impairments of TBI often result in spatiotemporal gait deficits, including a decrease in velocity, asymmetry of step lengths, increased double limb support time, reduced step length, and increased mediolateral sway. , Tandem gait (ataxia) is also prominent post-TBI and can remain at 2-year follow-up. For individuals with ataxia after TBI, it was found that they have reduced interjoint coordination during gait, and this coordination further deteriorated during more complex walking situations such as narrow base of support or when carrying an object. Impaired gait mobility is also perceived as a contributor to falls in post-TBI. It is obvious that gait abnormalities after TBI can pose a significant limitation in everyday activity and warrant detailed measurement.
There is a wide range of gait outcome measures. Similar to other impairments and activity limitations, selection of appropriate gait outcome measures is based upon patients’ functional level and settings where therapy takes place. For acute care and inpatient rehabilitation settings, gait assessment is oftentimes included in generic functional mobility measures such as FIM and FAM. Together with these outcome measures, a qualitative gait description through task analysis should be done in order to identify underlying impairments.
For individuals with basic ambulatory function, more robust gait outcome measures are recommended and include the 6 minute walk test, 10 m walk test, HiMAT, and Functional Gait Assessment.
Another type of gait outcome measure that should be included for high-functioning patients with TBI is gait ability during dual-task situations. Dual tasking is a common daily function (e.g., walking while attending to a conversation) and entails performing one cognitive and one motor task at the same time. Since motor and cognitive impairments are major sequelae of TBI, it is expected that dual-task abilities are even more compromised. In fact for persons post-TBI, despite well recovery of motor gait ability, reaction time during dual-task gait activity is significantly longer compared to age-matched group. The TBI EDGE Task Force recommended the Walking and Remembering Test to assess dual-task gait ability in persons post-TBI. In addition, the modified Walking and Remembering Test and Timed Up and Go-Cognitive together with the Walking and Remembering Test have been shown to be reliable and feasible for persons in inpatient rehabilitation settings. Physical therapists are encouraged to include dual-task measures when appropriate because they may be more indicative of functional outcomes.
Upper extremity function.
UE function includes tasks that require reaching, grasping, pinching, etc. and can be affected after TBI. Clinical presentations for upper limb dysfunction after TBI may be similar to those with hemiplegia or hemiparesis—for example, impaired timing and reduced accuracy of reaching and grasping. The Action Research Arm Test and Wolf Motor Function Test are recommended outcome measures specifically for assessment of upper limb function. There are also generic outcome measures that assess activities requiring upper limb functions. An example being FIM where grooming is included as a test item and is a task where upper limb function is highly indicative.
Assessing participation restrictions
Participation restrictions refer to limitations an individual experiences in his or her life roles. As such, each individual’s participation restrictions after TBI can be very different and limitless. Examples include inability to drive, restriction in work duties, inability to participate in school activities, or restriction in carrying out the role as a parent. While the focus of rehabilitation programs for TBI is on improving motor and cognitive outcomes at the impairment and activity limitation levels, measuring participation is equally important as it affects the patient’s quality of life after an injury. The ultimate goal for rehabilitation is for patients to resume participations at preinjury level, such as returning to work or school. A recent Cochrane review included several indicators as primary and secondary outcomes when investigating effectiveness of cognitive rehabilitation programs. These outcome indicators include return to work, independence in ADL, community integration, and quality of life. Most of these outcomes are in the participation category of the ICF model, implying the ultimate long-term goal of effective rehabilitation is to improve patients’ functioning in society, and hence assessment in this area should be included.
Some common participation measures are introduced for inclusion in the examination process. The ultimate choice depends upon the patient’s role and meaningful function in the society in which they live. From the physical therapy perspective, the TBI EDGE Task Force recommends to include outcome measures on community integration and quality of life in outpatient settings. These measures include Disability Rating Scale, Quality of Life after Brain Injury, Community Integration Questionnaire, and Sydney Psychosocial Reintegration Scale. Usually, participation restriction measures are administered in outpatient or community clinical settings because this is the time when patients and family/caregivers focus on long-term life plans. Specific participation measures associated with certain impairments can also be included. For example, if balance and falling is an issue after TBI, therapists could include the Activity-specific Balance Confidence Scale to assess the impact of balance on daily life.
Interventions for people with traumatic brain injury
Roles and responsibilities of the interprofessional rehabilitation team
TBI results in a myriad of physical, psychological, behavioral, and cognitive impairments. Comprehensive rehabilitation requires an interprofessional team approach due to the complex clinical presentation following a moderate to severe TBI. Research has shown that medical management, in addition to early onset and continuous rehabilitation, is most effective when delivered in a specialized neurotrauma/brain injury unit by an interdisciplinary health care team. ,
As most people who have experienced a moderate to severe TBI have cognitive impairments and reduced ability to learn, consistency and repetition of management strategies is required to optimize effectiveness. This requires regular, ongoing communication among interprofessional team members, including the patient, family, and friends involved in their care. Each member of the interprofessional team will focus their plan of care on interventions within their primary scope of practice. However, all providers will need to carefully consider other aspects of the injury and incorporate recommendations for managing impairments outside their scope of practice into their plan of care to optimize patient outcomes. For example, PT’s should incorporate strategies for managing communication impairments, memory loss, reduced orientation, as well as behavior modification, into their interventions in order to be effective. See Table 22.5 for a list of interprofessional health care team members and their primary role in caring for people with TBI.
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