Physical Address
304 North Cardinal St.
Dorchester Center, MA 02124
Vestibular rehabilitation following head injury
H.R. is a 53-year-old male who fell on ice, resulting in traumatic brain injury (TBI) characterized by a subdural hematoma. He returned to work within 2 months, as a computer programmer, working 6–8 h per day. He was referred to outpatient physical therapy, with a chief complaint of cervical pain. During the examination of the cervical spine, the patient moved from a sitting to supine position and reported vertigo. Through further subjective history, the patient noted vertigo with positional changes when laying down or sitting up, since the fall, lasting approximately 10 s. He also notes imbalance when walking and descending stairs. Given this history, an oculomotor and vestibular assessment was completed. The exam was unremarkable, except for observation of brief upbeat, left torsional nystagmus, with subsequent complaints of vertigo, when in a left Dix-Hallpike position. The patient was treated for a left posterior canal canalithiasis with two canalith repositioning maneuvers (CRMs). One week later, upon reassessment, there were no signs or symptoms, suggesting resolution of benign paroxysmal positional vertigo (BPPV) and treatment continued with the cervical spine.
Introduction
Traumatic brain injury (TBI) is a disruption in the normal function of the brain that can be caused by a direct blow or jolt to the head, penetration through the skull into the brain tissue and/or forces such as rotational or acceleration and deceleration forces. TBI is characterized by a change in brain function notable for one of the following: loss or decreased consciousness, amnesia of the event before or after the injury, focal neurological deficits such as weakness, vision, cognition, and language, and slowed thinking or processing. The symptoms can range from mild to severe depending on the amount of injury to the brain. Severe cases may result in extended periods of unconsciousness, coma, or even death.
TBI is a major healthcare problem. In 2014, there were about 2.87 million cases of TBI in the United States alone. It is a leading cause of death and disability with an estimated 13.5 million individuals living with TBI-associated deficits. The cost of TBI is about $76.5 billion directly and indirectly. There are about 288,000 hospitalizations for TBI every year. Males represent 78.8% of all reported TBIs with higher rates of TBI among males (959 per 100,000) than females (811 per 100,000). The highest rates of TBI are observed in older adults (≥75 years; 2232 per 100,000 population), very young (0–4 years; 1591 per 100,000), and young adults (15–24 years; 1081 per 100,000). The leading causes of TBI-related deaths are due to motor vehicle crashes, suicides, and falls. The leading causes of nonfatal TBI in the United States occur from falls (35%), motor vehicle-related injuries (17%), and strikes or blows to the head from or against an object (17%), such as sports injuries.
TBI results in complex body system and structure deficits that interact across several domains including physical, sensory, cognitive, behavioral, and emotional. Vestibular dysfunction and associated balance, ocular, and auditory dysfunction are important issues that affect the function and quality-of-life of TBI survivors. Since TBI is characterized by sudden and often violent causes, trauma to the vestibular system is common. As noted, TBI affects a wide spectrum of ages and has multiple causes such as falls, motor vehicle accidents, sports-related injuries, and military blast wave exposures among other causes. Patients often report problems with dizziness and or lightheadedness or other issues related to the auditory or vestibular system. Such complaints warrant further investigation into the vestibular system including balance testing. Clinicians must be aware of the potential problems associated with trauma including the need to consider not only TBI but other problems such as benign positional vertigo, cervicogenic headache and dizziness, visual deficits, ototoxic side effects of medications, and other vestibular pathology. It is beyond the scope of this chapter to review the full differential diagnoses. Nonetheless, assessment that includes cervical, oculomotor, postural stability, and gait is important to further delineate the potential causes in order to provide physical therapist who performs the bulk of the evaluation and rehabilitative treatment with guidance for diagnosis. The goal of this chapter is to describe the rehabilitative approach to ameliorating the deficits and restoring function and quality of life.
Vestibular anatomy and physiology
The vestibular system ( Table 15.1 and 15.2 ) assists with understanding body position and motion. It uses spatial orientation and stabilizes vision to maintain balance, especially with movement. The vestibular end organs sense angular and linear acceleration and transduce these forces to signals that can be interpreted by the central nervous system (CNS). The CNS integrates this information from the vestibular system to stabilize gaze during head movement through the vestibulocular reflex (VOR), in addition to modulating muscle tone through the vestibulocollic (VCR) and vestibulospinal (VSR) reflexes ( Table 15.3a and 15.3b ).
Table 15.1
Peripheral anatomy of the vestibular system.
| Peripheral apparatus | Function |
|---|---|
| Semicircular canals | Provide sensory information about the velocity of the head, which enables the VOR to generate a proportional eye movement, by responding to angular velocity. The eyes therefore remain stationary, during head motion, maintaining clear vision. |
| Otoliths | Determine forces related to linear acceleration, by responding to both linear head motion and static tilt with respect to the gravitational axis. |
| Vestibular nerve (CN VIII) | Transmits afferent signals from the labyrinth through the internal auditory canal (IAC). The IAC also contains the cochlear nerve (hearing), the facial nerve, the nervus intermedius, and the labyrinth artery. The IAC travels through the dense petrous portion of the temporal bone and opens into the posterior fossa at the level of the pons. The vestibular nerve enters the brainstem at the pontomedullary junction. |
| Vascular supply | The labyrinthine artery supplies the peripheral vestibular system. It is often a branch of the anterior–inferior cerebellar artery (AICA), though occasionally it is a direct branch of the basilar artery. The labyrinthine artery divides into the anterior vestibular artery and the common cochlear artery. The anterior vestibular artery supplies the vestibular nerve, most of the utricle, and the ampullae of the lateral and anterior SCC. The common cochlear artery divides into the main cochlear artery, which supplies the cochlea, and the vestibulocochlear artery, which supplies part of the cochlea, the ampulla of the posterior semicircular canal, and the inferior portion of the saccule. |
Table 15.2
Central anatomy of the vestibular system.
| Central apparatus | Function |
|---|---|
| Vestibular nucleus | Consists of four major nuclei: superior, medial, lateral, and descending and at least seven minor nuclei. The structure is located within the pons, though it extends to the medulla. The superior and medial vestibular nucleus are relays for the VOR. The medial vestibular nucleus is involved in the vestibulospinal reflexes and manages head and eye movements that occur together. The lateral vestibular nucleus is the primary nucleus for the vestibulospinal reflex. The descending nucleus is connected to the other nuclei and the cerebellum, though it has no outflow of its own. |
| Vascular supply | The vertebral–basilar arterial system supplies blood to the peripheral and central nervous system. The posterior–inferior cerebellar arteries (PICAs) branch off the vertebral artery. The PICAs are the most important arteries for the CNS. They supply the inferior portions of the cerebellar hemispheres and the dorsolateral medulla, which includes aspects of the vestibular nuclear complex. The basilar artery supplies central vestibular structures via perforator branches. The AICA is the sole blood supply for the peripheral vestibular system via the labyrinthine artery. The AICA also supplies blood to a portion of the cerebellum and pons. |
| Cerebellum | The recipient of outflow from the vestibular nucleus complex. It is not required for vestibular reflexes, though these reflexes become uncalibrated and ineffective when the cerebellum is removed. |
Table 15.3a
Motor outputs and vestibular reflexes.
| Reflex | Function |
|---|---|
| Vestibulocular reflex (VOR) | The motor neurons of the ocular motor nuclei, drive the extraocular eye muscles, which are the output neurons of the VOR. The VOR maintains stable vision during head motion. The VOR has two components: the angular VOR, compensates for rotation, mediated by the SCC, and the linear VOR, compensates for translation, mediated by the otoliths. The linear VOR is important in circumstances in which the target is near with relatively high frequency of head movement. |
| Vestibulospinal reflex (VSR) | The anterior horn cells of the spinal cord gray matter, drive skeletal muscle, which is the output neuron of the VSR. The purpose of the VSR is to stabilize the body, though it consists of several reflexes named according to the timing (static vs. dynamic) and sensory input (canal vs. otolith). |
| Vestibulocollic reflex (VCR) | Entails the cervical muscles to stabilize the head. The head movement counteracts the movement sensed by the otolithic or semicircular canal organs. The precise pathway of this reflex has yet to be detailed. |
Table 15.3b
Cervical reflexes.
| Reflex | Function |
|---|---|
| Cervicoocular reflex (COR) | The COR interacts with the VOR. The COR entails eye movements, driven by cervical proprioceptors that supplement the VOR under certain conditions. When the vestibular apparatus is injured, the COR is facilitated. |
| Cervicospinal reflex (CSR) | Defined as changes in limb position driven by cervical afferent activity. The CSR supplements the VSR by altering muscle tone in the body. |
| Cervicocollic reflex (CCR) | Stabilizes the head on the body. The afferent sensory changes caused by an alteration in cervical position create opposition to the stretch through reflexive contractions of appropriate cervical muscles. The degree to which the CCR contributes to head stabilization in humans is uncertain. |
Sensory inputs include vestibular, proprioception, and vision ( Table 15.3c ). The sensory inputs are integrated by the central processors, known as the vestibular nuclear complex, which creates motor outputs to activate the eyes and body. To maintain the accuracy of the vestibular system, the cerebellum monitors and calibrates the system.
Table 15.3c
Other reflexes.
| Reflex | Function |
|---|---|
| Visual reflexes | The visual system influences vestibular central circuitry and drives following visual responses (i.e., smooth pursuit) and postural reactions. Visual tracking responses may be facilitated following vestibular loss. |
| Somatosensory reflexes | Somatosensory mechanics are involved in postural stability. Individuals with bilateral vestibular loss use somatosensory information to a greater extent than those with all balance systems intact. |
History and clinical examination
The management of a patient with dizziness is dependent on history, bedside clinical examination, and laboratory testing. An accurate history is essential to determine the onset of symptoms, the description of symptoms, and how the symptoms affect the individual's lifestyle. The bedside examination is used to distinguish peripheral from central problems, how acute the problem may be, and the extent of the loss. Laboratory testing confirms the diagnosis based on history and clinical examination, quantifies the degree of loss, provides evidence of central compensation, and shows evidence of a physiological component.
The subjective history is the most informative part of evaluation. Although this can be tedious, many patients present with vague complaints of dizziness and symptoms. This can also be complicated by anxiety-provoked symptoms. Elements that assist with the diagnosis include the temporal course, the symptoms and what the patient means by “dizziness,” and the circumstance of the symptoms. Furthermore, auditory involvement is important to consider ( Fig. 15.1 ) .
Additional elements of dizziness
How is the dizziness affecting an individual's life?
It is important to note that there may be a different response, even when two patients have the same diagnosis. For example, one individual may state that the dizziness is not affecting them, though they want to be assured that nothing is seriously wrong. No extensive evaluation is indicated. A second individual may state that they may have no difficulties with day-to-day activities, including walking, though they are no longer able to participate in recreational activities, such as tennis or golf. This individual would benefit from a referral to physical therapy, to address high-level balance impairments. A third individual may state they are devastated by their dizziness and may not leave their home or participate in any social activities. In addition to a physical therapy referral, this individual may need a referral for psychological counseling for improved coping strategies of the symptoms.
To complete a thorough evaluation of the effects of dizziness on an individual's daily routine, it is best to assess the individual completing various daily tasks and activities that involve different head positions and body positions. For example, reaching down to tie shoelaces while dressing or turning head to check a blind spot while driving can cause dizziness in someone with a vestibular injury. Furthermore, any activity that involves dynamic standing balance, such as meal preparation or showering, may also be a challenge for this individual. Any activity that requires rapid head movement or repositioning and/or dynamic standing balance may be problematic for someone experiencing significant dizziness. This can greatly impact one's quality of life when something as simple as washing feet in the shower or reaching for a pan in a cupboard can turn devastating and lead to poor health-related quality of life and decreased independence.
It is also important to obtain a complete list of prescription and over-the-counter medications. Several medications can cause dizziness, some of which are used to also treat dizziness.
What does the individual believe is causing the dizziness?
Finally, it is important to ask the individual if they have a specific concern of what is causing the dizziness, which may not be addressed routinely by a healthcare provider. If the concern is not addressed, the patient may leave the clinic unsatisfied ( Fig. 15.2 ).
Epidemiology
Symptoms associated with mTBI
Dizziness is a common symptom after head injury, present generally in 23%–81% of cases within the first few days after injury. Athletes reports dizziness 55% of time following a concussion. Military personnel who have undergone a blast injury report dizziness as the most common postinjury symptom.
The etiology of dizziness following head injury is diverse. It is important to keep in mind dizziness is diverse and can have multiple meanings ( Fig.15.2 ). Possible causes of dizziness can be from labyrinthine concussion, temporal bone fractures, benign paroxysmal positional vertigo (BPPV), central lesions, vascular lesions, and perilymphatic fistula. , There are sequelae of a head injury that can also cause dizziness including anxiety-related dizziness, migraine-associated dizziness, autonomic dysregulation, and cervicogenic dizziness.
Anxiety-related dizziness
The pathophysiology of anxiety-related dizziness is thought to be caused by central pathways in the brainstem that perceive dizziness and vertigo, which also control anxiety. , Stress management, which may be situational, with a recent head injury, though may be a result of preinjury factors, is an important part of recovery. Increased symptoms, decreased speed of processing, and memory deficits are greater in individuals with an mTBI as compared with noninjured individuals. It is important to discuss relaxation and stress management retraining, through meditation and mindfulness, using online resources, including apps and podcasts as part of the rehabilitation. However, a referral to a specialist may be indicated for improved management.
Posttraumatic headaches
Migrainous and nonmigrainous are common posttraumatic headaches following a traumatic brain injury. In addition to phono- and photophobia, nausea and visual changes, dizziness, and vertigo are common symptoms, occurring in 25%–30% of individuals. These symptoms may occur with or without the headache. The pathophysiology is not well understood, though it may be a result of neuroanatomical connections between the trigeminal and vestibular nuclei. Medical management of the migraine is important to allow for progress during rehabilitation.
Autonomic dysregulation
Dizziness with position changes, including sit to stand, bending over to pick something up off the floor, and negotiation of stairs, are often reported in those who have autonomic dysregulation. At times, there may be evidence of orthostatic hypotension, which should be ruled out. Given autonomic symptoms can mimic motion intolerance, including the report of dizziness with walking, running, or any aerobic activity that causes an increase in heart rate, assessment may be indicated. It is theorized that there are central and physiological regulatory dysfunctions that cause symptoms with exertion following an mTBI. The Buffalo Concussion Treadmill Test (BCTT) assesses exercise tolerance in individuals who have suffered from an mTBI. The heart rate at which concussion symptoms are exacerbated is referred to as symptom threshold. The Buffalo Concussion Bike Test (BCBT) has been developed, which requires further research to determine its clinical value. However, preliminary data does demonstrate beneficial results as compared to the BCTT.
Postural instability
Sensory organization dysfunction and vestibulospinal reflex impairments cause impaired balance reactions and postural instability. Abnormal central processing input from the peripheral end organ and, in the case of peripheral lesions, impairments of the end organ cause sensory organization impairments.
Cognitive symptoms
The hallmark signs of an mTBI include somatic and cognitive symptoms. Individuals may report fogginess, poor attention, impaired recall (immediate and delayed), limited cognitive endurance, and slowed cognitive processing. Novel learning is difficult due to a decrease in metabolism and increased energy demands.
You're Reading a Preview
Become a Clinical Tree membership for Full access and enjoy Unlimited articles
If you are a member. Log in here