Ann. N.Y. Acad. Sci. ISSN 0077-8923
A N N A L S O F T H E N E W Y O R K A C A D E M Y O F SC I E N C E S Issue: Dizziness and Balance Disorders
Persistent vertigo and dizziness after mild traumatic brain injury Terry D. Fife1,2 and Deepak Kalra1 1 Barrow Neurological Institute, Phoenix, Arizona. Phoenix, Arizona
2
Department of Neurology, University of Arizona College of Medicine,
Address for correspondence: Terry D. Fife, M.D., Barrow Neurological Institute, 240 W. Thomas Road, Suite 301, Phoenix, AZ 85013. [email protected]
Vertigo, dizziness, and disequilibrium are common symptoms following concussion or mild traumatic brain injury (mTBI). Dizziness and vertigo may be the result of trauma to the peripheral vestibular system or the central nervous system, or, in some cases, may be due to anxiety, depression, or posttraumatic stress disorder; these mechanisms are not mutually exclusive. While most peripheral vestibular disorders can be identified by testing and examination, those without inner-ear causes that have persisting complaints of dizziness and motion sickness are more difficult to understand and to manage. Some of these patients exhibit features compatible with vestibular migraine and may be treated successfully with migraine-preventative medications. This paper reviews the nonotogenic causes of persisting dizziness, the possible mechanisms, and the pathophysiology, as a framework for patient management and for future research. Keywords: postconcussion syndrome; postconcussion dizziness; vertigo; mild traumatic brain injury; diffuse axonal injury; traumatic vestibulopathy; traumatic vestibular migraine
Introduction Concussion is a type of mild traumatic brain injury (mTBI) that affects about 5% of the U.S. population per year. Symptoms that follow mTBI include impairment of attention and concentration, trouble with memory recall, slower mental processing, headaches, dizziness, irritability, fatigue, mood changes, and impulsivity.1 The term concussion connotes acute brain injury with short-lived symptoms that resolve, and, generally, it is held that there is no permanent brain injury. The latter contention is problematic, however, since brain changes may occur in some concussions and repeated concussions almost certainly lead to permanent changes in the brain. Persisting vertigo, dizziness, and imbalance, defined for the purposes of this paper as lasting more than 3 months, is a prominent complaint after head injury in many patients.2 Clinical evaluation is necessary to clarify the precise cause, since vertigo may result from injury to the labyrinth in some cases.
The susceptibility of the labyrinth to trauma is not surprising, since the vestibular structures of the inner ear are surrounded by the temporal bone and thus subject to forces on the head. Furthermore, the vestibular apparatus of the inner ear aids in the detection of head motion and is exceptionally sensitive to mechanical stimulation.3 Concussion or mild head trauma may cause injury to the inner ear, leading to such conditions as labyrinthine concussion, benign paroxysmal positional vertigo, utriculosaccular injury, unilateral vestibular loss, or, less commonly, perilymphatic fistula or traumatic endolymphatic hydrops, which are reviewed elsewhere.4 Before feeling assured that a peripheral vestibular cause has been entirely excluded, clinicians should be aware that the absence of nystagmus or caloric vestibular asymmetry on videonystagmography (VNG) testing does not exclude a peripheral vestibular cause. Inferior vestibular neuritis is a well-described peripheral vestibular disorder that causes dizziness and imbalance and is typically unaccompanied by nystagmus or caloric
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paresis.5,6 In addition, isolated disorders of the utricle and saccule may be missed by conventional VNG testing and assessment for nystagmus.7–10 Other mechanisms affecting the central nervous system (CNS) may also account for persisting dizziness including microstructural injury to the brain, trauma-induced migraine and anxiety, depression, and psychological factors. In addition, it is not uncommon for patients to have a labyrinthine cause, psychological contributors, and CNS factors all at play at different times during the recovery phase after head trauma. This paper will focus on the differential diagnosis of persisting vertigo, dizziness, and imbalance in patients without active peripheral labyrinthine disorders who also lack demonstrable structural abnormalities observable by brain- and cerebrovascular-imaging studies. CNS causes of dizziness following head trauma There are three main categories that may account for vertigo and disequilibrium following mTBI: (1) diffuse axonal injury (DAI) and other microstructural disruptions resulting from trauma to the head, (2) trauma-related induction of migraine-like mechanisms including headaches and vestibular migraine symptoms, and (3) psychological factors such as anxiety, depression, panic attacks, posttraumatic stress disorder (PTSD), and behavioral factors. Although such a categorization is useful for discussion purposes, actually determining to what degree each possible mechanism is responsible for a given symptom in patients is difficult. Moreover, it is possible that microstructural changes of the brain may contribute to or may even cause some of the migrainerelated and psychological symptoms exhibited. Attribution and apportionment of symptoms to cause has to be based primarily on the patient’s report of symptoms, the clinician’s observations, and the description and nature of the head trauma. Diagnostic considerations A number of protein biomarkers from bodily fluids are being investigated for mTBI. For example, S100B, a calcium-binding protein, and neuronspecific enolase11 have been shown to exhibit 98.2% sensitivity but low specificity in six clinical trials involving more than 2000 patients.12 Thus, absence of S100B may be useful in ruling out 98
mTBI. Nevertheless, pending the development of a reliable biomarker, there are few tests that aid much in clarifying this further once brain imaging and neurological examination are found to be normal. Additionally, many patients may have more than one of these mechanisms contributing simultaneously. A matter of severity One might consider a spectrum of injury after mTBI (Fig. 1), with magnetic resonance imaging (MRI)visible DAI13 being the most severe, followed by microstructural changes with disruption of the axonal cytoskeleton and white matter abnormalities. At the milder end of the spectrum would be invisible functional disruptions such as those that cannot be seen even by electron microscopy but nevertheless disturb normal axonal and neuronal function,14 and, finally, those that have no brain injury at any level. DAI and microstructural brain injury In a concussion, traumatic biomechanical forces create a pathophysiological process, but it is often held that the changes are functional disturbances, not structural ones that may be seen in standard neuroimaging studies.15 The distinction hinges on structural changes visible by conventional MRI rather than those visible by more sensitive techniques. In patients with chronic dizziness and general symptoms of postconcussion syndrome (PCS) after mTBI, it can be very difficult to separate those who have microstructural brain injury from those who do not. Presumably, those with some burden of demonstrable microstructural change are more likely to have worse symptoms, and various therapeutic interventions might have benefits for them. DAI refers to axonal injury in the white matter tracts due to abrupt traction on axons that alters the axonal cytoskeleton and impairs sodium– potassium channel function and axoplasmic transport.13 DAI is most commonly located in the gray–white junctions, corpus callosum, brain stem, cerebral and cerebellar peduncles, frontal and temporal lobe white matter, basal ganglia, and thalamus. Imbalance is common following severe TBI and may also be present in mTBI.16 Ultrastructural changes that are not severe enough to be seen by MRI or even by routine light microscopy may be detected starting at about 12 h following brain trauma, with some axonal neurofilament
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Figure 1. A depiction of the range of axonal cytoskeletal injury and white matter disruption possible in mTBI and the broad spectrum of symptoms that may occur spanning this spectrum of injury.
misalignment and vacuolization, and the changes progress in the following days in some axons.17 A number of animal models of mTBI have been developed, either with a fixed skull bearing the injury18,19 or a more physiologically mobile skull bearing the injury,20 attempting to replicate mTBI. DAI is certainly one consequence of mTBI, but injury is not limited to axons. The white matter is also susceptible to injury.21 Diffusion-tensor imaging is also used as a method of detecting disruptions in the normally unidirectional flow of water along white matter fiber tracts; cytoskeletal damage correlates with fractional anisotropy,22 a measure of the lack of conformity of water flow in one direction that measures intact white matter fiber integrity. Other methods are also being used to assess white matter injury after head injury. For example, Figure 2 demonstrates how microstructural disruptions occur in the myelin after a single impact, and even more so after a second impact.21 Consequences for balance and dizziness The effects of mTBI on balance and dizziness, whether structural or not, are clinically relevant. In those with sports-related concussions, 55% report dizziness.23 Dizziness was the most common symptom following mTBI in one study,24 and 32% of patients had dizziness persist for more than 2 weeks after mTBI in another study.25 In addition to the
direct effects of the mTBI itself, it is common for secondary anxiety, depression, PTSD, and other disorders to evolve during the recovery period. For example, 41% of mTBI patients reported anxiety up to 5 years after the injury.26 Dizziness at the time of injury was predictive of a more prolonged recovery of more than 3 weeks in sports-related concussion.27 Interestingly, actual loss of consciousness did not correlate very well with prolonged symptoms.28 While the mechanisms are not fully understood, the highly integrated systems for postural control and balance would logically be affected by a slowing of signal processing. This suggests that some vestibular features related to integration of the vestibulo-ocular reflex (VOR) and the vestibulospinal tract (VST) with the brain stem and the cerebellum also interact with frontal lobe circuits mediating judgment, decision making, and anticipation. In addition, to the extent that anxiety, response to threat, PTSD, and/or loss of emotional control become an issue, these can further aggravate functional balance.29 Limitations of definitions Table 1 lists the definitions used in this discussion. Concussion is the clinical syndrome following head trauma and usually resolves without continuation of symptoms.31,32 It is probable that many individuals who have a concussion have either no actual cellular
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Figure 2. Transmission electron microscopy of the white matter of the anterior corpus callosum of rats exposed to (1) sham, (2) a single right-hemispheric controlled cortical impact with a piston, or (3) bilateral hemispheric impacts. Left panels (sham) show normal myelin structure. Central panels (right hemispheric) show separations of the myelin sheath from the axon. Right panels (bilateral hemispheric) show even more prominent and widespread myelin sheath disruptions. Row A, calibration bar = 1 micron; row B, calibration bar = 0.2 microns. Figures reproduced from Ref. 21, with permission.
injury or that an injury that is destined to heal. mTBI is often used synonymously with concussion, although it is intended only as a categorization of the severity of the initial injury. The term mTBI does, Table 1. Definitions of terms
• Concussion: transient altered brain function due to mechanical trauma to the head from which it is anticipated that the individual will recover in no more than 3 months. • Mild traumatic brain injury (mTBI): a description of the severity of a mechanical injury to the brain that is characterized by no loss of consciousness (LOC) or LOC lasting 3 months of lightheadedness, vertigo, head-motion intolerance of heavyheadedness, imbalance, moderate or severe intensity lasting 5 feeling of spinning “inside the min to 72 h. head,” perceptions of movement, disassociation from environment Current or previous history of migraine Anxiety, feeling as though one may with or without aura, according to lose control, panic attacks, the International Classification of difficulty concentrating, Headache Disorders (ICHD) agoraphobia
Chronic postconcussion dizzinessa >3 months of periodic floating, rocking, spinning, tilting, head-motion intolerance, visual vertigo, imbalance, and feelings of unsteadiness that vary in severity day to day Often combined with poor ability to multitask, reduced concentration and mental focus, irritability, general headaches, disturbances of sleep Presence of nausea is variable; intolerance of stress, poor ability to organize, and easily fatigued
One or more migraine features with at Absence of nausea and lack of least 50% of the vestibular episodes: worsening of symptoms with (1) headache with at least two of the head motion following: one-sided location, pulsating quality, moderate or severe pain intensity, aggravation by routine physical activity; (2) photophobia and phonophobia, visual aura Not better accounted for by another Not better accounted for by another Symptom onset within 7 days of a vestibular or ICHD diagnosis vestibular diagnosis or migraine trauma to the head or brain a
As defined in Table 1.
of reported symptoms and the severity of head trauma, an observation true for PCS in general.51 Prognosis Most patients improve within days to a few weeks, but a sizable proportion of patients continue to report PCS symptoms for months or years after what are in some cases very minor head injuries. Patients with chronic vertigo after concussion are far less likely to return to work.53 Patients with PCS symptoms at 3 months ended up also having similar symptoms at 12 months.54 In one Swedish cohort, 56% had recovered at 3 months postinjury.55 The effects of vestibular symptoms may be worsened by psychological factors, resulting in a delayed functional recovery. Cultural issues may influence the reporting of PCS symptoms in people from different cultural and language backgrounds.56 Some have proposed that chronic dizziness and other symptoms of mTBI are phenomena of Western Europe and the United States, but similar persisting symptoms and lack of return to work even at 1 102
year occur in other countries and are not limited by geography.57 It may be that the actual trauma of mTBI is a less important factor than is the presence of preinjury depression and anxiety, posttraumatic stress disorder, pain, and female gender, which predispose to prolonged PCS symptoms.58–60 Anxiety itself may contribute to chronic dizziness, although the exact mechanisms have yet to be elucidated.29 According to one hypothesis, mild head trauma may be the initiating factor, but it is the preexisting psychological condition that causes the prolonged PCS symptoms.61 Treatment When feasible, treatment should include an attempt not only to reduce some of the factors that contribute to dizziness, headaches, and concentration difficulties but also to minimize stress. Some have suggested that rest from cognitive and physical activities may improve recovery after sports-related concussion,51,62 implying that time off work (up to 3 weeks) or away from stress may help. Practically
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speaking, the opposite is more common. Many patients miss work, which adds to work-related, household, and financial stressors. Managing anxiety may help to reduce the ongoing symptoms of PCS,63 and keeping in mind the socioeconomic and family-related stressors is crucial to managing the aftermath of persisting dizziness after mTBI. Patients’ self-perception of their own well-being and so-called “all-or-nothing behavior” appear to influence the perpetuation of PCS as well.64 Conclusion In patients with chronic dizziness after concussion, one should consider all possible causes, including migrainous vertigo, peripheral vestibular disorders, autonomic dysregulation such as neurally mediated hypotension, and the effects of medications as important causes or contributors. One should not assume that signs of generalized anxiety are necessarily the cause of the dizziness, since secondary anxiety is especially common in those with chronic dizziness of any cause.65 Anxiety should also be managed with counseling and/or medications, because chronic vestibular symptoms may provoke secondary anxiety.66,67 It is also important to encourage patients to resume activities and to try to shape their perceptions to become more positive and optimistic to try to diminish the detrimental tendency of some patients to perceive themselves as sick and helpless. Acknowledgments The authors would like to thank Drs. Virginia Donovan and Andre Obenaus for providing the images for Figure 2 in this paper. Conflicts of interest The authors report no conflicts of interest.
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A N N A L S O F T H E N E W Y O R K A C A D E M Y O F SC I E N C E S Issue: Dizziness and Balance Disorders
Persistent vertigo and dizziness after mild traumatic brain injury Terry D. Fife1,2 and Deepak Kalra1 1 Barrow Neurological Institute, Phoenix, Arizona. Phoenix, Arizona
2
Department of Neurology, University of Arizona College of Medicine,
Address for correspondence: Terry D. Fife, M.D., Barrow Neurological Institute, 240 W. Thomas Road, Suite 301, Phoenix, AZ 85013. [email protected]
Vertigo, dizziness, and disequilibrium are common symptoms following concussion or mild traumatic brain injury (mTBI). Dizziness and vertigo may be the result of trauma to the peripheral vestibular system or the central nervous system, or, in some cases, may be due to anxiety, depression, or posttraumatic stress disorder; these mechanisms are not mutually exclusive. While most peripheral vestibular disorders can be identified by testing and examination, those without inner-ear causes that have persisting complaints of dizziness and motion sickness are more difficult to understand and to manage. Some of these patients exhibit features compatible with vestibular migraine and may be treated successfully with migraine-preventative medications. This paper reviews the nonotogenic causes of persisting dizziness, the possible mechanisms, and the pathophysiology, as a framework for patient management and for future research. Keywords: postconcussion syndrome; postconcussion dizziness; vertigo; mild traumatic brain injury; diffuse axonal injury; traumatic vestibulopathy; traumatic vestibular migraine
Introduction Concussion is a type of mild traumatic brain injury (mTBI) that affects about 5% of the U.S. population per year. Symptoms that follow mTBI include impairment of attention and concentration, trouble with memory recall, slower mental processing, headaches, dizziness, irritability, fatigue, mood changes, and impulsivity.1 The term concussion connotes acute brain injury with short-lived symptoms that resolve, and, generally, it is held that there is no permanent brain injury. The latter contention is problematic, however, since brain changes may occur in some concussions and repeated concussions almost certainly lead to permanent changes in the brain. Persisting vertigo, dizziness, and imbalance, defined for the purposes of this paper as lasting more than 3 months, is a prominent complaint after head injury in many patients.2 Clinical evaluation is necessary to clarify the precise cause, since vertigo may result from injury to the labyrinth in some cases.
The susceptibility of the labyrinth to trauma is not surprising, since the vestibular structures of the inner ear are surrounded by the temporal bone and thus subject to forces on the head. Furthermore, the vestibular apparatus of the inner ear aids in the detection of head motion and is exceptionally sensitive to mechanical stimulation.3 Concussion or mild head trauma may cause injury to the inner ear, leading to such conditions as labyrinthine concussion, benign paroxysmal positional vertigo, utriculosaccular injury, unilateral vestibular loss, or, less commonly, perilymphatic fistula or traumatic endolymphatic hydrops, which are reviewed elsewhere.4 Before feeling assured that a peripheral vestibular cause has been entirely excluded, clinicians should be aware that the absence of nystagmus or caloric vestibular asymmetry on videonystagmography (VNG) testing does not exclude a peripheral vestibular cause. Inferior vestibular neuritis is a well-described peripheral vestibular disorder that causes dizziness and imbalance and is typically unaccompanied by nystagmus or caloric
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paresis.5,6 In addition, isolated disorders of the utricle and saccule may be missed by conventional VNG testing and assessment for nystagmus.7–10 Other mechanisms affecting the central nervous system (CNS) may also account for persisting dizziness including microstructural injury to the brain, trauma-induced migraine and anxiety, depression, and psychological factors. In addition, it is not uncommon for patients to have a labyrinthine cause, psychological contributors, and CNS factors all at play at different times during the recovery phase after head trauma. This paper will focus on the differential diagnosis of persisting vertigo, dizziness, and imbalance in patients without active peripheral labyrinthine disorders who also lack demonstrable structural abnormalities observable by brain- and cerebrovascular-imaging studies. CNS causes of dizziness following head trauma There are three main categories that may account for vertigo and disequilibrium following mTBI: (1) diffuse axonal injury (DAI) and other microstructural disruptions resulting from trauma to the head, (2) trauma-related induction of migraine-like mechanisms including headaches and vestibular migraine symptoms, and (3) psychological factors such as anxiety, depression, panic attacks, posttraumatic stress disorder (PTSD), and behavioral factors. Although such a categorization is useful for discussion purposes, actually determining to what degree each possible mechanism is responsible for a given symptom in patients is difficult. Moreover, it is possible that microstructural changes of the brain may contribute to or may even cause some of the migrainerelated and psychological symptoms exhibited. Attribution and apportionment of symptoms to cause has to be based primarily on the patient’s report of symptoms, the clinician’s observations, and the description and nature of the head trauma. Diagnostic considerations A number of protein biomarkers from bodily fluids are being investigated for mTBI. For example, S100B, a calcium-binding protein, and neuronspecific enolase11 have been shown to exhibit 98.2% sensitivity but low specificity in six clinical trials involving more than 2000 patients.12 Thus, absence of S100B may be useful in ruling out 98
mTBI. Nevertheless, pending the development of a reliable biomarker, there are few tests that aid much in clarifying this further once brain imaging and neurological examination are found to be normal. Additionally, many patients may have more than one of these mechanisms contributing simultaneously. A matter of severity One might consider a spectrum of injury after mTBI (Fig. 1), with magnetic resonance imaging (MRI)visible DAI13 being the most severe, followed by microstructural changes with disruption of the axonal cytoskeleton and white matter abnormalities. At the milder end of the spectrum would be invisible functional disruptions such as those that cannot be seen even by electron microscopy but nevertheless disturb normal axonal and neuronal function,14 and, finally, those that have no brain injury at any level. DAI and microstructural brain injury In a concussion, traumatic biomechanical forces create a pathophysiological process, but it is often held that the changes are functional disturbances, not structural ones that may be seen in standard neuroimaging studies.15 The distinction hinges on structural changes visible by conventional MRI rather than those visible by more sensitive techniques. In patients with chronic dizziness and general symptoms of postconcussion syndrome (PCS) after mTBI, it can be very difficult to separate those who have microstructural brain injury from those who do not. Presumably, those with some burden of demonstrable microstructural change are more likely to have worse symptoms, and various therapeutic interventions might have benefits for them. DAI refers to axonal injury in the white matter tracts due to abrupt traction on axons that alters the axonal cytoskeleton and impairs sodium– potassium channel function and axoplasmic transport.13 DAI is most commonly located in the gray–white junctions, corpus callosum, brain stem, cerebral and cerebellar peduncles, frontal and temporal lobe white matter, basal ganglia, and thalamus. Imbalance is common following severe TBI and may also be present in mTBI.16 Ultrastructural changes that are not severe enough to be seen by MRI or even by routine light microscopy may be detected starting at about 12 h following brain trauma, with some axonal neurofilament
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Figure 1. A depiction of the range of axonal cytoskeletal injury and white matter disruption possible in mTBI and the broad spectrum of symptoms that may occur spanning this spectrum of injury.
misalignment and vacuolization, and the changes progress in the following days in some axons.17 A number of animal models of mTBI have been developed, either with a fixed skull bearing the injury18,19 or a more physiologically mobile skull bearing the injury,20 attempting to replicate mTBI. DAI is certainly one consequence of mTBI, but injury is not limited to axons. The white matter is also susceptible to injury.21 Diffusion-tensor imaging is also used as a method of detecting disruptions in the normally unidirectional flow of water along white matter fiber tracts; cytoskeletal damage correlates with fractional anisotropy,22 a measure of the lack of conformity of water flow in one direction that measures intact white matter fiber integrity. Other methods are also being used to assess white matter injury after head injury. For example, Figure 2 demonstrates how microstructural disruptions occur in the myelin after a single impact, and even more so after a second impact.21 Consequences for balance and dizziness The effects of mTBI on balance and dizziness, whether structural or not, are clinically relevant. In those with sports-related concussions, 55% report dizziness.23 Dizziness was the most common symptom following mTBI in one study,24 and 32% of patients had dizziness persist for more than 2 weeks after mTBI in another study.25 In addition to the
direct effects of the mTBI itself, it is common for secondary anxiety, depression, PTSD, and other disorders to evolve during the recovery period. For example, 41% of mTBI patients reported anxiety up to 5 years after the injury.26 Dizziness at the time of injury was predictive of a more prolonged recovery of more than 3 weeks in sports-related concussion.27 Interestingly, actual loss of consciousness did not correlate very well with prolonged symptoms.28 While the mechanisms are not fully understood, the highly integrated systems for postural control and balance would logically be affected by a slowing of signal processing. This suggests that some vestibular features related to integration of the vestibulo-ocular reflex (VOR) and the vestibulospinal tract (VST) with the brain stem and the cerebellum also interact with frontal lobe circuits mediating judgment, decision making, and anticipation. In addition, to the extent that anxiety, response to threat, PTSD, and/or loss of emotional control become an issue, these can further aggravate functional balance.29 Limitations of definitions Table 1 lists the definitions used in this discussion. Concussion is the clinical syndrome following head trauma and usually resolves without continuation of symptoms.31,32 It is probable that many individuals who have a concussion have either no actual cellular
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Figure 2. Transmission electron microscopy of the white matter of the anterior corpus callosum of rats exposed to (1) sham, (2) a single right-hemispheric controlled cortical impact with a piston, or (3) bilateral hemispheric impacts. Left panels (sham) show normal myelin structure. Central panels (right hemispheric) show separations of the myelin sheath from the axon. Right panels (bilateral hemispheric) show even more prominent and widespread myelin sheath disruptions. Row A, calibration bar = 1 micron; row B, calibration bar = 0.2 microns. Figures reproduced from Ref. 21, with permission.
injury or that an injury that is destined to heal. mTBI is often used synonymously with concussion, although it is intended only as a categorization of the severity of the initial injury. The term mTBI does, Table 1. Definitions of terms
• Concussion: transient altered brain function due to mechanical trauma to the head from which it is anticipated that the individual will recover in no more than 3 months. • Mild traumatic brain injury (mTBI): a description of the severity of a mechanical injury to the brain that is characterized by no loss of consciousness (LOC) or LOC lasting 3 months of lightheadedness, vertigo, head-motion intolerance of heavyheadedness, imbalance, moderate or severe intensity lasting 5 feeling of spinning “inside the min to 72 h. head,” perceptions of movement, disassociation from environment Current or previous history of migraine Anxiety, feeling as though one may with or without aura, according to lose control, panic attacks, the International Classification of difficulty concentrating, Headache Disorders (ICHD) agoraphobia
Chronic postconcussion dizzinessa >3 months of periodic floating, rocking, spinning, tilting, head-motion intolerance, visual vertigo, imbalance, and feelings of unsteadiness that vary in severity day to day Often combined with poor ability to multitask, reduced concentration and mental focus, irritability, general headaches, disturbances of sleep Presence of nausea is variable; intolerance of stress, poor ability to organize, and easily fatigued
One or more migraine features with at Absence of nausea and lack of least 50% of the vestibular episodes: worsening of symptoms with (1) headache with at least two of the head motion following: one-sided location, pulsating quality, moderate or severe pain intensity, aggravation by routine physical activity; (2) photophobia and phonophobia, visual aura Not better accounted for by another Not better accounted for by another Symptom onset within 7 days of a vestibular or ICHD diagnosis vestibular diagnosis or migraine trauma to the head or brain a
As defined in Table 1.
of reported symptoms and the severity of head trauma, an observation true for PCS in general.51 Prognosis Most patients improve within days to a few weeks, but a sizable proportion of patients continue to report PCS symptoms for months or years after what are in some cases very minor head injuries. Patients with chronic vertigo after concussion are far less likely to return to work.53 Patients with PCS symptoms at 3 months ended up also having similar symptoms at 12 months.54 In one Swedish cohort, 56% had recovered at 3 months postinjury.55 The effects of vestibular symptoms may be worsened by psychological factors, resulting in a delayed functional recovery. Cultural issues may influence the reporting of PCS symptoms in people from different cultural and language backgrounds.56 Some have proposed that chronic dizziness and other symptoms of mTBI are phenomena of Western Europe and the United States, but similar persisting symptoms and lack of return to work even at 1 102
year occur in other countries and are not limited by geography.57 It may be that the actual trauma of mTBI is a less important factor than is the presence of preinjury depression and anxiety, posttraumatic stress disorder, pain, and female gender, which predispose to prolonged PCS symptoms.58–60 Anxiety itself may contribute to chronic dizziness, although the exact mechanisms have yet to be elucidated.29 According to one hypothesis, mild head trauma may be the initiating factor, but it is the preexisting psychological condition that causes the prolonged PCS symptoms.61 Treatment When feasible, treatment should include an attempt not only to reduce some of the factors that contribute to dizziness, headaches, and concentration difficulties but also to minimize stress. Some have suggested that rest from cognitive and physical activities may improve recovery after sports-related concussion,51,62 implying that time off work (up to 3 weeks) or away from stress may help. Practically
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speaking, the opposite is more common. Many patients miss work, which adds to work-related, household, and financial stressors. Managing anxiety may help to reduce the ongoing symptoms of PCS,63 and keeping in mind the socioeconomic and family-related stressors is crucial to managing the aftermath of persisting dizziness after mTBI. Patients’ self-perception of their own well-being and so-called “all-or-nothing behavior” appear to influence the perpetuation of PCS as well.64 Conclusion In patients with chronic dizziness after concussion, one should consider all possible causes, including migrainous vertigo, peripheral vestibular disorders, autonomic dysregulation such as neurally mediated hypotension, and the effects of medications as important causes or contributors. One should not assume that signs of generalized anxiety are necessarily the cause of the dizziness, since secondary anxiety is especially common in those with chronic dizziness of any cause.65 Anxiety should also be managed with counseling and/or medications, because chronic vestibular symptoms may provoke secondary anxiety.66,67 It is also important to encourage patients to resume activities and to try to shape their perceptions to become more positive and optimistic to try to diminish the detrimental tendency of some patients to perceive themselves as sick and helpless. Acknowledgments The authors would like to thank Drs. Virginia Donovan and Andre Obenaus for providing the images for Figure 2 in this paper. Conflicts of interest The authors report no conflicts of interest.
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