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Review of Traumatic Brain Injury with Orthotic Considerations

Dieli, John CPO

JPO Journal of Prosthetics and Orthotics: March 2002 - Volume 14 - Issue 1 - p 31-35
Pathology Review
Free

The purpose of this article is to provide the orthotist with a comprehensive review of traumatic brain injury (TBI) and its orthotic considerations. A detailed description of the neuroanatomy, neurophysiology, and neuropathology are presented to improve the overall comprehension of how the brain responds to trauma. Throughout the paper, examples will be given to provide applicable clinical scenarios. Upon completion of this review, the reader should posses a clear working knowledge of TBI and its orthotic applications.

JOHN DIELI, CPO, is currently the practice manager for Hanger Prosthetics and Orthotics, Methuen, MA.

Correspondence to: John Dieli, CPO, Hanger Prosthetics and Orthotics, 184 Pleasant Valley St., Methuen, MA 01844.

Despite the enforcement of stricter seat belt laws and mandatory motor cycle helmet requirements, head trauma remains a major public health problem worldwide. 1 Just how major is difficult to determine because many patients with mild head injuries are significantly undiagnosed, further exacerbating the scope of this societal crisis. 2,3 According to the National Institutes of Health, traumatic brain injury (TBI) results primarily from vehicular accidents, falls, assaults, and sport injuries. 4 The estimated incidence rate is between 1.5 and 2 million individuals with approximately 52,000 annual deaths. 1–4 Trends continue to display a steady increase in the number of individuals sustaining head injuries. Epidemiological studies have concurred that the highest incidence is among young males 15 to 24 years of age and geriatrics 75 years and older. 1–4

TBI is the most widely accepted term for head injuries of a traumatic origin because it clearly denotes that the resulting damage to the brain was inflicted by external force. An injury to the brain, although not always visible, may cause physical, emotional, social, and vocational changes. Head injuries may be open or closed. A closed head injury is often caused by rapid acceleration/deceleration without apparent visible damage. Open head injuries can involve acceleration/deceleration, but penetration across the dural mater and into the brain may result, thus exposing visible damage. 5 Regardless of the type of head injury, most brain damage is caused by acceleration/deceleration of the brain within the skull.

The objective of this report is to provide an overview exclusively dedicated to TBI and its orthotic considerations. To appreciate how the brain responds to trauma, it is necessary to describe the neuroanatomy and neurophysiology. Once brain structures and functions are defined, the neuropathology section will be easier to comprehend. Orthotic prescription criteria will be outlined based on a qualitative neurological and biomechanical approach. Upon completion of this review, a summary will synthesize the information, and the reader should possess a clear working knowledge of TBI and its orthotic applications.

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NEUROANATOMY AND NEUROPHYSIOLOGY

This section considers those regions of the brain relating to the musculoskeletal system, which are important to the orthotist during the initial evaluation. These regions include the cerebral cortex, basal ganglia, and cerebellum. By understanding the functions of each part of the brain, clinical implications of the injury are better understood. The brain functions as a whole by interrelating its components. 6–8 For instance, a lesion may only disrupt a particular step of an activity that occurs in a specific location. “The interruption of that activity at any particular step, or out of sequence, can reveal the problems associated with the injury.”7

The cerebral cortex functions as the executive of the central nervous system. It enables us to perceive, communicate, remember, comprehend, and initiate voluntary movements. 7–9 Its composition primarily includes blood vessels and nerve cell bodies. 7 The cortex is separated into right and left hemispheres by a longitudinal or interhemispheric fissure. Each cerebral hemisphere controls the opposite side of the body. Although each hemisphere is almost symmetrical in size and shape, they are not entirely equal in function. 7 Its convoluted surface has certain consistent positions in all humans, which are used as landmarks to divide the cortex into four lobes. These lobes are named after their overlying cranial bones: frontal, parietal, temporal, and occipital. 9

The frontal lobe is located within the anterior aspect of the cerebral cortex. This lobe is particularly significant to the orthotist because it contains the cortical areas responsible for motor functions and includes the primary motor cortex and premotor cortex. It also controls our emotions, consciousness, and memory. The primary motor cortex allows us to consciously manipulate the musculoskeletal system. The primary motor cortex provides a direct connection between the cortex and the spinal cord. “Damage to localized areas of the primary motor cortex paralyzes the body’s muscles controlled by those areas.”7 The premotor cortex regulates learned motor skills of a patterned nature, such as playing an instrument. Insult to the premotor area results in a loss of the motor skills programmed in that region, but the muscle strength and ability to perform discrete movements are not hindered. 7

Various areas associated with sensation occur in the parietal, temporal, and occipital lobes. Those areas of particular importance to the musculoskeletal system include the primary sensory cortex and somatosensory association area. Each of the primary sensory areas has a nearby association area with which they communicate. The parietal lobe houses the primary sensory cortex. 7 Neurons in the primary sensory cortex are responsible for the following: receiving information relayed from the general somatic receptors located in the skin and from proprioceptors in the skeletal muscles, and identify the body region being stimulated. 7 The somatosensory association area is also located in the parietal lobe. The major contribution of the somatosensory association area is to integrate and analyze different somatic sensory inputs, such as temperature, touch, pressure, and pain. “Damage to the somatosensory association area handicaps one’s ability to analyze the different characteristics of a sensory experience, whereas damage to the primary sensory cortex causes a loss in ability to determine where the stimulus is acting on the body.”7 The sensory cortices utilize receptors (eg, proprioceptors) that relay information through neurons that connect to the spinal cord and eventually to the designated cortex where the information is then interpreted with the assistance of an association area. The most important concept is that no functional area of the cortex acts alone, and consciousness, which is required for all volitional movement involves the entire cortex in one way or another.

Deep within the cerebral white matter of each hemisphere are collections of subcortical motor nuclei called the basal ganglia or basal nuclei. 7,10 The basal ganglia are closely linked to the neurons of the cerebral cortex and receive inputs from the cortical motor, sensory, and association areas. Via relays, the basal nuclei indirectly assist with initiation and control of muscle movements. However, the basal ganglia has no direct access to motor pathways. The exact role of the basal ganglia has been elusive because of its inaccessible location and its functions, which overlap with the cerebellum. 7,10 However, it appears to be important in initiating slow sustained movements. When the basal ganglia are impaired, the results are postural disturbances, muscle tremors at rest, and uncontrolled muscle contractions. These symptoms are often exhibited with Parkinsonism (rigidity, resting tremors), Huntington’s chorea (sudden jerk, purposeless movement), hemiballismus (sudden flailing movement of one arm), and athetosis (writhing movements especially at fingers and wrists). 1,7 These patients often benefit from added weight and controlled range of motion at the distal extremities 11; for instance, articulating ankle foot orthoses (AFO) with motion limiting stops to improve gait cadence and wrist hand orthoses (WHO) to maintain wrist alignment while performing activities of daily living or to prevent contracture deformities. 3,11

The cerebellum or small brain is often compared to the control system of an automatic pilot because it operates subconsciously. It is located dorsal to the brain stem and rests in the posterior cranial fossa of the skull. 7,12 “The cerebellum continuously processes inputs received from the cerebral motor cortex, various brain stem nuclei, and sensory receptors to provide the precise timing and appropriate patterns of skeletal muscle contraction needed for smooth, coordinated movements.”7 Cerebellar dysfunction is characterized by awkwardness of volitional movements. Clinical syndromes associated with cerebellar dysfunction include: ataxia (awkward posture and gait), decreased tendon reflexes on the affected side, asthenia (muscle fatigue), intentional tremors, and poor equilibrium. 1,7 Orthotic intervention is most often used to improve balance reactions. For example, low-profile supramalleolar AFOs can help to maintain a neutral foot and ankle alignment. 11

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NEUROPATHOLOGY

The process of brain injury is frequently divided into primary and secondary phases. 5,12,13 Once a head injury has occurred, the physician must diagnose the initial trauma or primary impact damage to the brain. A secondary injury can transpire at the cellular level and may manifest symptoms over a period of hours to days after trauma.

Local or focal brain damage refers to a primary brain injury that is localized to the particular site of impact on the head. 5,13 Damage can range between mild superficial hemorrhage, to extensive brain necrosis and edema. The damage may consist of contusions, lacerations, and/or hematomas. Contusions can emerge under the location of a particular impact but are more commonly produced by a collision between the brain and interior skull. Hematomas or blood clots can result when small blood vessels are broken by the trauma. They can occur between the skull and brain (subdural/epidural) or within the brain (intracerebral hematoma). Isolated damage to a particular location caused by a blunt blow to head can present with symptoms of local brain damage.

Primary mechanisms of brain damage in closed or open head injury are most often caused by acceleration/deceleration rather then contact. 5,13 When the head is subjected to acceleration and/or deceleration, the brain can move within the skull and dural mater but only to a limited extent. When this motion is suddenly arrested, the frontal and temporal lobes impact against the walls of the anterior and middle cranial fossae. This is commonly referred to as coup. 5,11,13 The primary impact damage is done to the inferior frontal and anterior temporal lobes. Further damage can also occur to the occipital pole when the brain decelerates but is much less common. This is known as contrecoup. 5,11,13 Closed head injuries caused by acceleration/deceleration will often produce diffuse axonal damage. Diffuse axonal injury is the result of rapid shifting and rotation of the brain inside the skull followed by widespread shearing or stretching of axons. 11,13 The damage can be microscopic and potentially recoverable in mild brain injury, but after more severe brain injury, it can be devastating and result in permanent disability or even prolonged coma. A typical cause of diffuse axonal injury is a high-speed motor vehicle accident with no apparent external damage. Recent studies have demonstrated that some of the damage to axons progresses over the first 12 to 24 hours after the injury. Therefore, diffuse axonal injury is now treated as a combination of primary and secondary damage. 11

After the initial trauma is sustained, a delayed secondary injury can emerge at the cellular level. 2,5,11,13 This process involves a cascade of physiologic, vascular, and biochemical events, which are recognized as the cause of most severe brain damage. Secondary insult involves a multitude of systems; for instance, brain edema, increased intracranial pressure, cerebral vasospasm, intracranial infection, cellular necrosis, and systemic injuries. Perifocal brain edema can progress and cause brain shift and herniation; then a new set of neurologic signs may emerge. Systemic injuries are those injuries sustained outside the brain, such as cardiovascular changes and orthopedic injuries. Orthopedic injuries may include fractures, spinal cord injuries, and amputations. 5,6 If the patient has associated spinal injuries a thoracolumbosacral orthosis or halo may be indicated. 5 By achieving stability and appropriate posture of the pelvis and trunk, optimal limb control is ensured.

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ORTHOTIC PRESCRIPTION CRITERIA

The proceeding evaluation is based on established qualitative assessment techniques. However, the current trend in rehabilitation is to use consistent reproducible quantitative tests. 14–16 Although quantitative assessment is a useful method of measuring motor function and documenting recovery, it may not provide applicable orthotic prescription information.

The extent of the brain injury will determine whether the patient presents as hemiplegic, diplegic, or quadriplegic. Although the degree of involvement may vary among each case, numerous common characteristics can be observed. Upon initial evaluation, each affected limb should be examined to determine the flexor or extensor synergy patterns. A recently injured patient can present as flaccid and later develop a synergy pattern or remain flaccid. 17–19 According to Brunnstrom, 17 synergy occurs when muscles are firmly linked together and the patient is unable to master individual joint movements. Static tests of the affected limb may manifest as dystonic (slow sustained co-contractions of antagonistic muscles), with the dominant synergy pattern slowly taking precedence. These limb synergies can emerge as either reflexive, voluntary, or both. A reflexive pattern can be defined as an involuntary evoked response to a physical agent, such as stretch, touch, or vibration. 20–24 A voluntary pattern is produced through volitional movement, such as active knee extension. Although static muscle tests can demonstrate potential for muscle activity during weight bearing, it does not always correlate with the muscle activity required for ambulation. For example, a patient with a flexor pattern may be able to achieve ankle dorsiflexion by simultaneous acute flexion of the hip and knee. However, if the degree of hip and knee flexion required for walking is excessive, the patient will ambulate with a footdrop. 25,26 Once the dominant synergy pattern is determined, a visual gait analysis and a standing muscle test should be performed (Table 1).

Table 1

Table 1

Common gait deviations are often present with extensor/flexor synergy patterns and flaccidity; for instance, extensor patterning of the triceps surae before initial contact can cause the forefoot to strike first rather than the heel. Excessive plantar flexion during midstance may also prevent tibial advancement, which can result in recurvatum and a short step length on the contralateral limb. 25,27 An articulating AFO can be utilized if the patient is capable of controlling anterior tibial advancement. 25,27 In comparison, patients with triceps surae flaccidity or flexor patterning have excessive ankle dorsiflexion in the midstance phase of gait. Furthermore, those individuals with triceps surae flaccidity and insufficient quadriceps strength may compensate by hyperextending at the knee with forward trunk leaning immediately following initial contact. A solid or floor reaction AFO may be more appropriate because this patient can not control the anterior progression of their tibia. 28 Although these cases closely resemble each other when hyperextension at the knee is present, a standing muscle test can be used to distinguish the difference between triceps surae extensor spasticity or flaccidity. 25 The patient should bear weight on the affected side. Now the examiner palpates posterior to the knee and pulls anterior. If the heel rises off the floor, it can be presumed that the knee hyperextension is secondary to triceps surae extensor spasticity. If the same test causes the tibia to progress over the ankle while the heel remains on the floor, then triceps surae muscle flaccidity can be assumed.

A knee ankle foot orthosis (KAFO) can be applied when there is severe ligament instability at the knee, quadriceps weakness, or hamstring spasticity. Waters et al. 25 recommend using a knee immobilizer to evaluate whether the patient can functionally ambulate with a locked knee. KAFOs are often difficult to don and doff; therefore, every attempt should be made to stabilize the knee by using a rigid AFO.

Upper-extremity orthotics are most often prescribed to prevent contractures and maintain mobilization for hygiene. A WHO can be applied to sustain wrist alignment and prevent finger flexor deformities. When finger flexor spasticity is moderate, full extension of the digits may not be possible, and a sphere-shaped palmar device may be more suitable. 25 A dorsal splint can be used if the patient has hypersensitivity to palmar contact and elicits a grasp response. 25 Patients may require multiple functional upper limb orthotics to perform various activities for daily living. 28 However, most patients will not use their involved hand until some selective finger motion and proprioception is recovered. 25,28 Therefore, before considering upper extremity functional orthotics, hand dexterity and proprioception should be measured.

Other orthotic considerations include head position during the static/dynamic evaluation, combined presence of flexor/extensor spasticity, when to introduce the orthosis, and stabilizing the foot and ankle complex to prevent pronation. First, head position can elicit spasticity of the limbs especially when primitive motor reflexes are involved (ie, asymmetrical tonic neck reflex, symmetrical tonic neck reflex). 17,29–31 Second, some cases can demonstrate a combined flexor/extensor synergy pattern. 17 Third, it is essential to introduce the orthosis before compensatory gait deviations develop. 24 If the patient learns to walk using neurologically based compensatory motion, chronic gait deviations as well as orthopedic deformities (eg, muscle contractures, recurvatum) may result. Lastly, stabilization of the foot and ankle complex must be performed when the patient lacks the normal postural reflexes to maintain the subtalar and/or midtarsal joint in a neutral position. 28–30 For instance, the patient may exhibit an extensor synergy pattern, but once their limb is positioned into a neutral alignment, their tone can subside and the subtalar and/or midtarsal joint can become unstable and pronate.

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SUMMARY

This paper was intended to provide a comprehensive review of TBI and orthotic prescription criteria. All the assessment techniques can be employed by the orthotist to help ensure consistent and predictable outcomes. Before treating complex neurological disorders such as TBI, the orthotist should possess a clear working knowledge of neuroanatomy, neurophysiology, and neuropathology. By improving our knowledge base, we can appropriately apply neurological and biomechanical concepts, avoid orthotic related complications, and utilize information from related fields.

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ACKNOWLEDGMENT

The author would like to recognize all those individuals who reviewed his manuscript before publication, especially James Whitlock, MD.

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REFERENCES

1. Guberman A. Central nervous system trauma. In: Holm A, Megley N, eds. An Introduction to Clinical Neurology. Boston: Little, Brown; 1994: 515–535.
2. National Institutes of Health. Rehabilitation of persons with traumatic brain injury: Consensus Development Conference Statement. 1998: http://www.odp.od.nih.gov/consenses/(October).
3. Smith SS. Traumatic head injuries. In: Umphred DA, ed. Neurological Rehabilitation. Third Edition. St. Louis: C.V. Mosby; 1985: 249–288.
4. Bontke CF, Boake C. Principles of brain injury rehabilitation. In: Braddom RL, ed. Physical Medicine & Rehabilitation. Philadelphia: W.B. Saunders, 1996; 1027–1051.
5. Cope DN. The rehabilitation of traumatic brain injury. In: Kottke FJ, Lehmann JF, eds. Krusen’s Handbook of Physical Medicine and Rehabilitation. Fourth Edition. Philadelphia: W.B. Saunders; 1990: 1217–1251.
6. Rimel RW, Jane JA, Bond MR. Characteristics of the head injured patient. In: Rosenthal M, Griffith ER, Bond MR, et al., eds. Rehabilitation of the Adult and Child with Traumatic Brain Injury. Second Edition. Philadelphia: F.A. Davis; 1990: 8–16.
7. Marieb EN. The central nervous system. In: Spatz CJ, Burner PS, Fox R, eds. Human Anatomy and Physiology. Third Edition. Redwood City, CA: Benjamin/Cummings; 1989: 375–419.
8. Brain Functions and Map. Centre for Neuro Skills Traumatic Brain Injury Resource Guide. 2000: http://www.neuroskills.com/tbi/brain.shtml.
9. Kelly JP. Anatomical organization of the nervous system. In: Kandel ER, Schwartz JH, Jessell TM, eds. Principles of Neural Science. Third Edition. New York: Elsevier; 1991: 273–282.
10. Cote L, Crutcher MD. The basal ganglia. In: Kandel ER, Schwartz JH, Jessell TM, eds. Principles of Neural Science. Third Edition. New York: Elsevier; 1991: 647–659.
11. Brain Injury Association of the United States of America. The Anatomy of a Brain Injury. 2000: http://www.biausa.org/trauma.htm.
12. Ghez C. The cerebellum. In: Kandel ER, Schwartz JH, Jessell TM, eds. Principles of Neural Science. Third Edition. New York: Elsevier; 1991: 626–646.
13. Miller JD, Pentland B, Berrol S. Early evaluation and management. In: Rosenthal M, Griffith ER, Bond MR, et al, eds. Rehabilitation of the Adult and Child with Traumatic Brain Injury. Second Edition. Philadelphia: F.A. Davis; 1990: 21–51.
14. Kopp B, Kunkel A, Flor H, Platz T, et al. The arm motor ability test: reliability, validity, and sensitivity to change of an instrument for assessing disabilities in activities of daily living. Arch Phys Med Rehabil. 1997; 78: 615–620.
15. Collin C, Wade D. Assessing motor impairment after stroke: a pilot reliability study. J Neurol Neurosurg Psychiatry. 1990; 53: 576–579.
16. Poole JL, Whitney SL. Motor assessment scale for stroke patients: concurrent validity and reliability. Arch Phys Med Rehabil. 1988; 69: 195–197.
17. Brunnstrom S. Movement Therapy in Hemiplegia. Hagerstown, MD: Harper and Row; 1990.
18. Wagenaar RC, Meijer OG, Wieringen PC, et al. The functional recovery of stroke: a comparison between neuro-developmental treatment and the Brunnstrom method. Scand J Rehabil Med. 1990; 22: 1–8.
19. Perry CE. Principles and techniques of the Brunnstrom approach to the treatment of hemiplegia. J Phys Med. 1967; 46: 789–815.
20. Lima D. Overview of the causes, treatment, and orthotic management of lower limb spasticity. J Prosthet Orthot. 1990; 2: 33–39.
21. Gans BM, Glenn MB. Introduction. In: Glenn MB, Whyte J, eds. The Practical Management of Spasticity in Children and Adults. Philadelphia: Lea and Febiger; 1990: 1–7.
22. Whitlock JA. Neurophysiology of spasticity. In: Glenn MB, Whyte J, ed. The Practical Management of Spasticity in Children and Adults. Philadelphia: Lea and Febiger; 1990: 8–30.
23. Bishop B. Spasticity: its physiology and management. Phys Ther. 1977; 57: 371–376.
24. Perry J. Determinants of muscle function in the spastic lower extremity. Clin Orthop Relat Res. 1993; 288: 10–26.
25. Waters RL, Garland DE, Montgomery J. Orthotic prescription for stroke and head injury. In: Bunch WH, et al., eds. Atlas of Orthotics. Second Edition. St. Louis: C.V. Mosby; 1985: 270–286.
26. Dieli J, Ayyappa E, Hornbeak S. Effect of dynamic AFOs on three hemiplegic adults. J Prosthet Orthot. 1997; 9: 82–89.
27. Fish D, Kosta CS. Walking impediments and gait inefficiencies in the CVA patient. J Prosthet Orthot. 1999; 11: 33–37.
28. Huber SR. Therapeutic application of orthotics. In: Umphred DA, ed. Neurological Rehabilitation. Third Edition. St. Louis: C.V. Mosby; 1985: 616–631.
29. Bobath B. The treatment of neuromuscular disorder by improving patterns of coordination. Physio. 1969; 55: 18–22.
30. Manning J. Facilitation of movement: the Bobath approach. Physio. 1972; 58: 403–408.
31. Royeen CB, DeGangi GA. Use of neurodevelopmental treatment as an intervention: annotated listing of studies. Percept Motor Skills. 1992; 75: 175–194.
Keywords:

Traumatic brain injury; closed head injury; open head injury; coup; contrecoup; primary brain injury; secondary brain injury; focal injury; diffuse axonal injury; extensor/flexor synergy pattern; flaccidity

© 2002 Lippincott Williams & Wilkins, Inc.