Traumatic brain injury (TBI) is damage that impairs brain function resulting from external physical force.
Severity varies, most injuries are mild.
Concussion is a subset of mild TBI (mTBI), generally self-limited but involves complex pathophysiological processes.
Moderate to severe injuries often have worse outcomes.
Initial injuries typically present with diminished or altered consciousness.
Impairment of cognition and physical function are common, may be temporary or permanent.
Changes occur in behavior and emotional control.
Functional disability and/or psychologic maladjustment can be persistent.
Many TBI persons are left with lifelong disabilities.
Initial outcome predictions are difficult due to differences in recovery, even with identical injuries.
Balancing cerebral perfusion and intracranial pressure (ICP) is a significant medical challenge in severe TBI.
This balancing act affects ventilation, renal function, and overall perfusion.
Integration of care is critical from understanding pathophysiologic principles to interdisciplinary communication.
Incidence and Risk Factors
More than 30% of all injury-related deaths are due to TBI.
In 2014, there were 2.5 million U.S. emergency department (ED) visits due to brain injury, resulting in approximately 223,000 hospitalizations and 61,000 TBI related deaths.
Unintentional falls are the leading cause of head trauma (almost 47% in those older than 75 years), followed by:
Being unintentionally struck by/against an object (17%).
Motor vehicle accidents (13%).
Incidence of penetrating TBI from gunshot wounds is increasing, and in some urban communities it is now the most common type of injury seen.
Men are twice as likely to sustain a TBI as women.
African Americans, American Indians, and Alaska Natives have a higher rate of hospitalization due to TBI than their white counterparts, whereas mortality rates are highest among African Americans.
More than 400,000 US service members were diagnosed with a TBI between 2000 and 2019.
Military conflicts from 2005 to 2018 increased the number of service members and veterans living with TBI.
Approximately 80% of TBIs among this group occurred from injuries, such as from a motor vehicle crash when the person was not deployed.
Studies suggest that service members and veterans who have sustained a TBI may:
Have ongoing symptoms.
Experience co-occurring health conditions, such as posttraumatic stress disorder (PTSD) and depression.
Have difficulty accessing health care (particularly mental health services).
Report thinking about or planning a suicide attempt.
TBI peaks at three different age ranges:
Early childhood (age 1–2 years): related most often to child abuse.
Late adolescence to early adulthood (ages 15–24 years): may be related to risk-taking behaviors. Bicycling is one of the most widespread causes of head injury among this age group. The risk of sustaining a severe head injury while bicycling can be reduced by 88% by wearing an appropriate helmet.
Older adults (75 years of age and over): related most often to falls. This group is most likely to be hospitalized, and death is more likely, at rates of 79.3%, 42.5%, and 10.7% for severe, moderate, and mild TBI, respectively.
Elderly individuals account for less than 15% of trauma admissions due to falls but account for half of deaths due to falls.
There is more susceptibility with age to tearing of the bridging vessels over the surface of the brain.
There seems to be a significant, age-related decline in cerebrovascular autoregulation that may partially explain the poor outcomes seen in elderly individuals with TBI.
Approximately 300,000 sports-related concussions occur annually. Actual incidence may be higher as there is the potential to underreport concussion symptoms by athletes.
Although a single concussion does not necessarily lead to long-term neuropsychologic or cognitive complications, multiple concussions can cause long-term neuropsychologic abnormalities, particularly in executive functioning and information-processing speed.
Those athletes who have had previous concussions are more likely to have future concussions with longer recovery time.
Of the severely brain injured, approximately 60% of adults and 92% of children are injured in a motor vehicle accident.
Pedestrians injured by automobiles represent some of the most seriously injured individuals in trauma.
The elderly make up a significant percentage of pedestrians who have been struck by a motor vehicle and they have significantly increased mortality rates, with a majority of deaths occurring at the scene or at the emergency department.
Etiologic Factors
TBIs can come from open head injury or closed head injury.
Open head injury: the skull has been penetrated and the meninges have been breached, leaving the brain exposed.
Penetrating missile injuries create localized, focal lesions that, when not fatal, cause limited damage to the brain.
It is not the size of a missile but its velocity that generally determines the extent of damage.
Penetrating injury also causes vascular injury, including disruption or the formation of aneurysms or pseudoaneurysms.
Closed head injury happens in the absence of a skull fracture, but when the soft tissue of the brain is forced into contact with the hard, bony skull.
Coup injury: The initial blow occurs under the point of impact
Contrecoup injury: Then, as the brain decelerates against the contralateral skull, injury occurs to tissue on the opposite side.
Contrecoup injury is frequently worse than the injury underlying the impact.
Actual loss of consciousness does not always occur, although there is generally an altered state of consciousness.
Mild closed head injuries can occur after a severe neck injury without the head actually striking any surface.
The symptoms are worse when there is a rotational component to the head injury in addition to the back-and-forth jarring.
Both diffuse injury and rupture of veins can result in subdural and subarachnoid hemorrhage.
Rotational forces are the most likely forces to cause diffuse axonal injury, including damage to brainstem structures, such as the reticular activating system.
Severe head injuries result from significant bruising and bleeding within the brain.
Approximately 25% of people with a normal initial computed tomographic (CT) scan will develop late hemorrhages.
Contusions are usually more severe in persons with skull fracture than in those without fracture.
Although contusion is the hallmark of TBI, severe or even fatal damage to the brain can occur without contusion.
Pathogenesis
Primary damage is the result of forces exerted on the brain at the time of injury.
Secondary damage refers to changes in brain function that result from the brain's reaction to trauma or other system failure.
Causes of secondary damage include brain swelling and impaired cerebral perfusion.
Diffuse brain injury includes axonal injury, hypoxic damage, and edema.
Multiple small hemorrhages may occur and are predictive of a poor outcome.
Vascular Changes
Focal brain injuries usually result in cerebral contusions.
Vascular damage is sustained at the moment of impact and leads to infarction within the cortical gray matter.
Glial elements encapsulate the infarction, ultimately creating a residual cystic cavity.
Contusions typically occur at the poles and on the inferior surfaces of the frontal and temporal lobes.
Occipital blows are more likely to produce contusions than are frontal or lateral blows.
Areas where 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.
With fracture of the cranial vault, there may be damage to the superficial epidural vessels and, particularly in the case of falls, there can be rupture of the bridging vessels between hemispheres.
Gliding contusions, or hemorrhagic lesions in the cortex, may be the result of movement of the cortical gray matter in relation to the underlying white matter, causing shear strains to damage the penetrating vessels found at the gray and white matter interface.
Subarachnoid hemorrhage is common as a result of the rupture of vessels within the subarachnoid space.
This may trigger vasospasm that can lead to reduced regional blood flow.
Injury to the vessels within the white matter can also cause significant neurologic consequences, especially if it is in the area of the basal ganglia.
Increase in blood volume is considered to be the most important cause of increased ICP after head trauma.
There can be bleeding into the epidural compartment, creating a mass effect that can displace the brain and increase ICP.
The shear and tensile forces of traumatic injury can also create a subdural hematoma.
Acute hydrocephalus occurs when blood accumulates in the ventricular system, expanding the size of the ventricles and causing increased pressure on brain tissue by compressing the brain between the skull and the fluid- filled ventricles.
Vascular volume can increase if venous outflow is blocked or cerebral blood flow (CBF) increases passively because of loss of autoregulation.
Cerebrospinal fluid (CSF) volume increases may be the result of blockage of outflow pathways or interference with reabsorption.
When the volume of one compartment changes slowly, compensatory decreases in the volume of other compartments may prevent a rise in ICP.
When the volume change is rapid or the compensatory mechanisms are exhausted or dysfunctional, the ICP goes up.
The overall result of these vascular changes is the decreased ability of the cerebral vessels to maintain homeostasis in the face of changing blood pressure or blood gas composition.
Initially, within the first few hours after severe injury, there is decreased CBF both globally and at the impact site, which can induce ischemia.
Within 24 hours, the blood flow can be at normal or above-normal levels.
The impairment of autoregulation of circulation in the presence of moderate to severe head injury allows blood flow to the brain to become dependent on the systemic arterial pressure.
Elevated blood pressure can result in hyperemia and decreased blood pressure can cause hypoperfusion.
Impaired vascular responsiveness results in abnormal arteriole vasoconstriction in the presence of carbon dioxide.
Posttraumatic aneurysms of the intracavernous internal carotid artery can be associated with delayed and sometimes lethal massive epistaxis, nosebleed.
This can be a result of basal skull fractures in the region of the carotid canal or cavernous sinus and/or orbital fractures and compromise of the optical nerves.
Knowledge of these risk factors and early diagnosis can minimize the high mortality risk.
It can take from days to years for the artery weakening to develop, with an average time of 3 weeks.
Because of the close anatomic relationship of the intracavernous portion of the internal cerebral artery (ICA) to the oculomotor, optic, abducens, trochlear, and trigeminal nerves, these structures may also be damaged during the aneurysm development, resulting in effects such as blindness, facial numbness, and/or oculomotor palsy.
There appears to be a change in the endothelium of the blood vessels following brain injury.
In the normal brain, neurotransmitters such as acetylcholine induce dilation, causing relaxation of the smooth muscle in the vessel wall.
In the injured brain, this reaction can be missing, resulting in abnormal vasoconstriction.
Additional changes at the level of the endothelium result in a disturbed blood–brain barrier in the injured brain.
This results in leakage of serum proteins and neurotransmitters into the parenchyma, causing edema.
Parenchymal Changes
Axonal injury is a consistent feature of the traumatic event.
Shear and tensile forces most likely disrupt the axolemma, which impairs transport of proteins from the cell body and causes swelling of the axon.
The distal axon segment detaches and undergoes Wallerian degeneration.
The myelin sheath pulls away from the axon.
These axonal changes are seen throughout the brain regardless of site of impact.
The damage is different from that of stroke or tumor, which produces a more complete but local deafferentation.
Typically, with diffuse axonal injury, there remain intact axons interspersed with the damaged axons.
There is evidence of the potential for recovery of function based on the possible sprouting of undamaged axons to reoccupy the areas left vacant by degenerating axons.
Secondary cell death by necrosis of the cellular membrane can be a result of edema.
Apoptosis, or programmed destruction from within the cell, can result in cell death that occurs days, weeks, or months after injury.
Study of excitotoxicity related to diffuse brain injury shows that the increase in extracellular neurotransmitters, resulting in increased potassium, causes a massive depolarization of the injured brain.
There is a complex interaction of the various amino acids and neurotransmitters, which may affect the postsynaptic functions, resulting in secondary dysfunction of the neural mechanisms of the brain.
The excitatory neurotransmitter glutamate appears to rise to abnormal amounts following brain injury.
Glutamate is neurotoxic when concentrations increase.
Free radicals are generated by TBI.
Extensive membrane depolarization, induced by trauma, allows for a nonselective opening of the voltage-sensitive calcium channels and an abnormal accumulation of calcium within neurons and glia.
Such calcium shifts are associated with activation of lipolytic and proteolytic enzymes, protein kinases, protein phosphatases, dissolution of microtubules, and altered gene expression.
Frank blood that moves into the parenchyma is possible and can cause extensive damage and infection of the tissue, especially with open wounds.
Compressive Damage
Intracranial hypertension can produce herniation.
During trauma, the brain may shift from its normal symmetric position.
The most common herniation is the lateral tentorial membrane separating the cerebral hemispheres from the posterior fossa.
This shift may cause compression of the brainstem, the pituitary, or other delicate brain structures.
Because the brainstem controls the body's major visceral functions, brainstem involvement may result in paralysis or death.
In less severe situations, autonomic nervous system changes may include changes in pulse and respiratory rates and regularity, temperature elevations, blood pressure changes, excessive sweating, salivation, tearing, and sebum secretion.
Because the brain is surrounded by the rigid skull, swelling of the brain, or pooling of blood, pushes tissue through openings in the base of the skull or through the other compartments of the brain, resulting in herniation through the foramen magnum.
Hypoxia
Hypotension (systolic blood pressure less than 90mm Hg) occurring between injury and resuscitation occurs in one-third of severe TBI victims.
It can be caused by blockages resulting in decreased blood in the brain or by decreased oxygen in the blood due to concomitant pulmonary insult.
It is associated with doubling of mortality rate and a significant increase in morbidity.
Early hypotension is also a strong predictor of poor outcome and can lead to intracranial hypertension in later stages.
Hypertension
Intracranial hypertension can interfere with perfusion by lowering the cerebral perfusion pressure (CPP).
Under normal circumstances, cerebral pressure autoregulation maintains CBF constant over a CPP range of approximately 50–150mmHg.
Following trauma, this relationship may be partially or totally disrupted; the brain can weather limited changes in CPP without notable alterations of CBF.
Cerebral Perfusion Pressure
Although there is no definitive evidence of the ideal CPP following TBI, the general consensus is that a critical threshold is 70–80mmHg.
Mortality rates increase by 20% for each 10-mm Hg loss of CPP.
When CPP has been maintained at 70mm Hg there has been a 35% reduction in mortality rates.
Concussions are infrequently associated with structural brain injury and rarely lead to significant long-term sequelae.
Moderate TBI may be associated with significant structural injury, such as hemorrhage or contusion, but death is uncommon.
Severe TBI generally results in some form of cognitive and/or physical disability or in death, especially with very low Glasgow Coma Scale (GCS) scores.
Concussion
In minor head injury, or concussion, the loss of consciousness lasts a relatively short time, or there may be no loss of consciousness.
The postconcussion syndrome is a distinct entity that occurs within the first 7–10 days following the concussion and typically resolves within 3 months.
These symptoms may vary and resemble those associated with concussion.
Symptoms usually associated with concussion are dizziness, disorientation, nausea, and headache.
The client may be irritable or distractible and have difficulty with reading and memory.
There may be complaints of headache, fatigue, personality changes, and decreased control of emotions.
The symptoms generally reflect both the focal and the diffuse nature of the damage.
Changes to neurons, axons, neurotransmitter metabolism, neuroendocrine system (pituitary gland), CBF, and reticular activating system are common.
The shearing effects and coup/countercoup can be responsible for dysfunction in frontal and temporal lobes.
A right-sided cortical lesion could cause problems of visual–spatial processing, whereas a left-sided lesion could result in verbal processing deficits.
Damage in the area of the amygdala may lead to heightened arousal, which enhances sensory information processing and is linked to emotional responses.
The function of the amygdala is essential to the learning process and understanding of the consequences of action.
Divided attention deficit, a reduction in information processing capacity, speed, or amount of information that can be processed, is associated with acceleration and deceleration head injury.
This may be related to the diffuse white matter lesion, brainstem dysfunction, or a disruption in the frontal-limbic reticular activating system.
Neuropsychologic testing has shown significant cognitive disability following a concussion, including a reduction in information processing speed, attention, reaction time, and memory for new information.
Although cognitive impairment has been shown to resolve within about 7 days for most concussions, cognitive impairment has been shown to persist, particularly for athletes suffering multiple concussions.
Migraine headaches with and without aura can develop in the hours to weeks after a mild concussion.
Immediately after mild TBI in sports such as soccer, football, rugby, and boxing, children, adolescents, and young adults may have a first-time migraine with aura.
This syndrome may be triggered multiple times after additional mild TBI and has been termed footballer's migraine.
Cluster headaches can also develop after mild TBI.
Nonspecific psychologic symptoms such as personality change, irritability, anxiety, and depression are reported by more than one-half of individuals within 3 months of mild TBI.
Fatigue and disruption of sleep patterns are also often reported.
Posttraumatic stress disorder, which has many symptoms similar to those of the postconcussion syndrome, may occur after mild TBI.
In 2012, the American Physical Therapy Association and the House of Delegates implemented a position that recognizes physical therapists as being a part of the multidisciplinary team of licensed health care providers that can provide concussion management.
A physical therapist assistant is able to work directly under the supervision of a PT that has been trained in examining, evaluating, and managing a person suspected of having a concussion.
The PTA would be involved in providing education and monitoring of prevention in minimizing the risk of reinjure while performing therapeutic interventions that would reduce pain, restore strength, and return the person to prior level of activity/sport.
Levels of Consciousness
Altered level of consciousness is a state that can occur with both diffuse and focal head injuries.
This can be a result of diffuse bilateral cerebral hemispheric damage or a smaller lesion that affects the brainstem.
In many cases, it is probably a combination.
In moderate or severe head injury, unconsciousness can be prolonged or persistent.
Arousal is associated with wakefulness and depends on an intact reticular formation and upper brainstem.
Coma is regarded as the lowest level of consciousness and is characterized as being unable to obey commands, utter words, open the eyes, or being in a state of unresponsiveness.
This is indicative of advanced brain failure, with bilateral cerebral hemispheric or direct involvement of the brainstem.
Coma rarely lasts longer than 4 weeks.
The GCS is the most widely used instrument for determining level of consciousness; it is used to determine current status and potential for improvement (Box 22.1).
Some individuals may continue to exhibit a reduced level of consciousness, a condition referred to as persistent vegetative state (VS), or postcomatose unawareness, characterized by a wakeful, reduced responsiveness with no evident cerebral cortical function.
The individual exhibits eye opening with sleep–wake cycles and tracking of the eyes, controlled at a subcortical level.
The VS is notable for preserved arousal mechanisms associated with a complete lack of self- or environmental awareness.
There is no purposeful movement and the individual remains mute.
The VS can result from diffuse cerebral hypoxia or from severe, diffuse white matter impact damage.
The brainstem is usually relatively intact.
Locked-in syndrome consists of quadriplegia with preserved awareness and arousal.
It is caused by injury to the ventral pons.
It spares vertical eye movements and can be seen with disordered breathing patterns associated with injury to brainstem respiratory centers.
Respiratory Impairments
Cheyne–Stokes breathing is a rhythmic pattern of alternating rapid breathing and momentary stopping of breathing.
It often presents in individuals with hemispheric lesions that are bilateral or can be the result of lesions in the diencephalon.
Hyperventilation is seen in individuals with pontine or midbrain lesions.
Apneustic breathing is characterized by a prolonged pause at the end of inspiration and indicates lesions of the mid- and caudal portions of the pons.
Ataxic breathing, seen with damage to the medulla, is irregular in both rate and tidal volume.
Cognitive and Behavioral Impairments
Cognitive impairments include problems with attention, memory, concentration, and executive functions.
Residual cognitive and behavioral deficits often remain despite a return to full consciousness.
Deficits—including disorders of learning, memory, and complex information processing and loss of abstract thinking and complex problem solving—reflect the frontal lobe pathology associated with TBI.
Loss of executive functions is observed and there is often confusion and disorientation in addition to difficulty in problem solving, delayed processing, and lack of initiation.
Mood disturbances include depression and anxiety.
Symptoms are related to the area of the brain injured.
When the damage is in the orbitofrontal area, behavior may be excessive and disinhibited.
Inappropriate social and interpersonal behaviors, including inappropriate sexual behavior, occur with lesions in this area.
Septal area lesions result in irritability and rage.
Damage to the cortical bulbar pathways (i.e., those connecting the cerebral cortex to the brainstem) can result in emotional lability, including euphoria, involuntary laughing, or crying that is not associated with negative emotions.
Cognitive deficits are not always directly observable, but the observable behavior provides information regarding the ability to integrate cognitive processes.
The observable behavior of a person with a brain injury is directly related to the integrity of cognitive function.
The behaviors reflect the inability to adjust to the environment.
Typical behaviors include erratic wandering; motor, sensory, and verbal perseveration; imitation of gestures; restlessness; refusal to cooperate; and striking out in response to stimulus or in random fashion.
Often the individual will attempt to run away from the institution or home.
Deficits in attention are also common.
Clients show impulsiveness, hyperactivity, and difficulty sustaining attention.
Behavioral changes can be present without cognitive or physical deficits.
Impairment of memory is common with head injury.
Retrograde amnesia is the partial or total loss of ability to recall events that have occurred during the period immediately preceding head injury.
Posttraumatic amnesia is the time lapse between the injury and the point at which functional memory returns.
During this time there may be improvement in automatic activities, but there is no carryover of tasks requiring memory or learning.
The duration of posttraumatic amnesia is considered a clinical indicator of the severity of the injury.
Anterograde memory is the ability to form new memory.
Loss of anterograde memory is common and manifests as decreased attention or inaccurate perception.
The capacity for anterograde memory is frequently the last function to return following recovery from loss of consciousness.
Memory disturbance is common with concussion and minor head injury.
Memory function is disbursed throughout the brain, and there appears to be a lack of ability to use semantic organizational strategy to remember something by associating it with relevant cues.
Commonly there is difficulty identifying nonverbal stimuli, reproducing visual stimuli, and recalling verbal material.
Complaints of memory problems are associated with poor performance on tests of speed, reaction time, attention tasks, and complex perceptual–motor abilities.
Language deficits are often seen as word- and name-finding problems.
However, recovery of language function appears to surpass that of memory in individuals with minor head injury.
TBI is associated with several neuropsychiatric disturbances that can range from subtle deficits to severe disturbances including cognitive deficits, mood and anxiety disorders, psychosis, and behavioral problems.
More than 50% of individuals with TBI develop psychiatric sequelae.
Pain
Pain is a common complaint after brain injury, with complex interaction on both physical and neuropsychologic function.
Head and neck pain is common with whiplash, and there is an increased incidence of physical trauma associated with the severity of head injury.
Pain can cause a persistent distraction that pulls the individual's attention away from activity and can decrease the ability to concentrate.
It can affect the ability to sleep, which leads to daytime lethargy, and it contributes to emotional reactions such as anxiety and depression.
Neuropathic pain can result from the aberrant somatosensory processing in the peripheral or central nervous system, most common with damage in the area of the thalamus.
Myofascial pain is common with trigger points, stiffness, and weakness.
Fibromyalgia can develop, as it is related to sleep disturbances, anxiety, and depression.
Another component of pain is suffering, in which the intensity is dependent on the person's mood, life experience, and level of social support.
The result can lead to a condition that mimics chronic pain syndrome.
Managing this syndrome in the individual with brain injury can be challenging.
Cranial Nerve Damage
Focal damage in the brainstem can be reflected in the loss of cranial nerve function.
Although the olfactory nerve is well protected, shearing of the fibers to the extent of damage occurs in about 7% of brain injuries. In about 50% of those cases, this is a temporary condition.
The most vulnerable component of the optic nerve in people is the portion of the nerve located within the optic canal.
Damage to this portion can result in monocular blindness, a dilated pupil with an absent direct pupillary response, and a brisk consensual response to light.
Partial visual defects may also be noted.
The oculomotor nerve works in conjunction with the trochlear and abducens nerves to move the eyeball to maintain gaze stability and scanning.
Damage is often due to direct insult to the musculature, but it can also be due to cerebral herniation. This nerve is damaged in less than 3% of people with head injury.
The fourth cranial nerve (i.e., the trochlear nerve) is the least frequently injured.
Damage is usually in the form of contusion or stretching, resulting in a vertical diplopia.
The prognosis for recovery in fourth nerve palsy is poor because the nerve is so slender that it is often avulsed by the trauma.
Trigeminal nerve injury after head trauma results in anesthesia of a portion of the nose, eyebrow, and forehead.
The abducens nerve is often injured when the head is crushed in an anteroposterior plane with resultant lateral expansion and distortion of the skull.
It can also be damaged in fractures of the petrous bone.
Vertical movement of the brainstem may severely stretch the sixth nerve as it leaves the pons.
There can also be damage in relation to the third and fourth nerves in the orbital fissure.
There is failure of the eye to abduct when the head is passively turned away from the side of the lesion.
Abnormal wandering movements are present in midbrain lesions, and they usually disappear when the person regains consciousness.
Trauma to the facial nerve is common, with injury to the temporal bone, or swelling of the nerve, or external compression.
Symptoms of facial nerve palsy include loss of tear production, saliva secretion, and taste in the anterior two-thirds of the tongue.
Muscles controlling facial expressions become weak.
Hearing and vestibular dysfunction occur in brain injuries.
Transverse fractures of the temporal bone may cause disruption of the auditory and vestibular end organs or transient eighth nerve dysfunction.
A blow to the head creates a pressure wave that is transmitted through the petrous bone to the cochlea, resulting in hair cell damage and degeneration of cochlear nerves.
The glossopharyngeal, vagus, spinal accessory, and hypoglossal cranial nerves pass through the jugular foramen at the base of the skull.
The 12th nerve passes through the hypoglossal foramen nearby.
Injury is most often from a missile wound, but fractures of the occipital condyle can also produce lower cranial nerve palsies.
Symptoms include cardiac irregularities, excessive salivation, loss of sensation and gag reflex of the palate, loss of taste on the posterior third of the tongue, hoarse voice, dysphagia, and deviation of the tongue to the side of the lesion.
Motor Deficits
Abnormalities of movement include monoplegia, hemiplegia, tetraplegia, and abnormal reflexes.
Muscle tone is typically altered.
Initially, there can be flaccidity, which is gradually replaced by increased tone, spasticity, and/or rigidity.
Decorticate posturing is also common initially and reflects the loss of cortical control.
The individual presents with increased flexor tone and posturing in the upper extremities and increased extensor tone and posturing in the lower extremities.
Decerebrate posturing, or increased extensor tone and posturing in both the upper and lower extremities, reflects injury at the pons resulting in the loss of inhibitory control of the cortex and basal ganglia.
The specific manifestations of paresis may include loss of selective motor control, abnormal balance reactions, and sensory loss.
Cerebellar and basal ganglia dysfunction can result in ataxia, dysmetria, and tremor or bradykinesia.
Direct trauma to subcortical and substantia nigral neurons can result in movement disorders occurring shortly after an injury.
Movement disorders occurring months following the injury have been hypothesized to be related to sprouting, remyelination, inflammatory changes, oxidative reactions, and central synaptic reorganization.
Peripheral trauma that precedes the development of a movement disorder may alter sensory input, leading to central cortical and subcortical reorganization.
Heterotopic Ossification
Another complication associated with brain injury is the formation of heterotopic ossification (HO), or abnormal bone growth around a joint.
The cause and pathogenesis of HO is unknown, but bone scans show evidence of increased uptake and elevation of alkaline phosphatase.
The onset of HO is usually 4–12 weeks after the injury, and it first appears as a loss of range of motion.
Local tenderness and a palpable mass can be detected, along with erythema, swelling, and pain with movement.
HO in the hip area can mimic deep vein thrombosis.
Peripheral nerve compression will sometimes develop, especially if the HO is in the elbow.
HO can also result in vascular compression and possible lymphedema.
Medical Complications
Multiple medical complications can occur after TBI.
Cardiovascular effects of TBI include neurogenic hypertension and cardiac dysrhythmias.
Respiratory complications such as neurogenic pulmonary edema, aspiration pneumonia, and pulmonary emboli usually caused by deep venous thrombosis are common.
Other complications include disseminated intravascular coagulation, hyponatremia, diabetes insipidus, and stress gastritis.
Iatrogenic infections are common.
Medical Management
Diagnosis
The diagnosis of brain injury starts at the level of concussion, with the American Academy of Neurology guidelines including three levels of concussion.
In general, people who have lost consciousness for 2 minutes or more following head injury should be observed medically from the time of the impact.
Athletic injury, falls, and minor auto accidents can result in concussions that are often not reported to health care providers.
Given the possibility of developing second impact syndrome, cumulative damage from multiple concussions that can lead to long-term brain damage and disability, every possible concussion should be reported and maintained as part of an individual's medical record.
Athletes should undergo formal neuropsychologic evaluations when injury is suspected because this may unmask subtle continued deficits compared with baseline testing. Such deficits have been shown to correlate with duration of symptoms. This has become an increasingly important tool in concussion evaluation.
Postural stability testing may also be undertaken for adjunctive data in determination of concussion severity.
Current imaging with CT or magnetic resonance imaging (MRI) does not permit quantification of neural injury that occurs after a traumatic brain concussion.
Proton magnetic resonance spectroscopic imaging can be used to assess the neurochemical damage derived from a cerebral concussion.
The ability to identify postconcussive individuals who are in a vulnerable cellular state is important as there can be a catastrophic deterioration in individuals even with a simple head injury.
The combination of metabolic data, physiologic data, and clinical observations satisfactorily addresses the complete recovery from concussion.
When a person sustains a severe head injury, the GCS is used to assess level of consciousness
Using this scale, three aspects of coma are observed independently: eye opening, best motor response, and verbal response.
A score of 8 or less indicates coma.
Oculomotor and pupillary signs are valuable in assisting with the diagnosis, localizing brainstem damage, and determining the depth of coma.
Pupillary examination should document size and reactivity to light.
Greater than 1mm difference in size or asymmetry should be considered abnormal.
Once the baseline neurologic status has been determined, repeated evaluations are critical to monitor improvement, provide prognostic data, or detect deterioration, which should be addressed immediately.
Symptoms of focal neurologic deficits, lethargy, or skull fractures should be monitored.
A mental status examination is important in all head-injured individuals. Subtle abnormalities may be a guide to significant intracranial injury.
Diagnostic imaging can provide significant information that can guide the intervention and allow a more accurate prognosis.
CT is the primary imaging modality for the initial diagnosis and management of the head-injured person.
CT scanning of the head reveals the presence of hemorrhage, swelling, or infarction.
In individuals with traumatic coma, patterns on CT that have been associated with worse neurologic outcome include lesions in the brainstem, encroachment of the basal cisterns, and diffuse axonal injury
An initially normal CT scan, however, is no assurance that hemorrhagic lesions will not occur.
Approximately 10%–15% of individuals with clinically severe TBI have a normal CT scan.
In such situations, the possibility of extracranial or intracranial vascular disruptions may exist, and angiography should be considered.
Diffuse axonal injury (DAI) is a frequent CT and pathologic correlate of severe TBI, accounting for about 50% of primary brain injuries.