Most recent update: August 29, 2020 : This page is not written for or intended for use in legal endeavors.
Head injuries are sustained by 5% of the population annually. Post-traumatic vertigo refers to dizziness that follows a neck or head injury. While injuries to other parts of the body might in theory be associated with dizziness, the left big toe for example, in practice this is almost never the case. We would call this "magical thinking".
Fiztgerald (1996) reported that the incidence of dizziness with even mild head injury ranges from 15% to 78%. This is a rather large range, probably related to the imprecision of "dizziness" and "mild head injury" as well as the timing. In other words -- this is not very useful.
Post-traumatic dizziness is associated with slower return to work, but there are conflicting data. Chamelian and Feinstein reported that dizziness, psychosocial functioning, and psychotropic/analgesic uses were significant and independent predictors of reemployment (2004). On the otherhand, Gottshall et al (2007), found no influence of dizziness on active duty status in the military at 1 year. In our opinion, dizziness is an adverse factor predicting return to employment.
Because of the high incidence of litigation associated with post-traumatic vertigo, most clinicians are extremely cautious in making this diagnosis. There are many potential causes of post-traumatic vertigo. A recent study performed in an otolaryngology setting suggested the following distribution of "primary" disorders: labyrinthine concussion (18), rupture of the round window membrane -- fistula (6), and cervicogenic vertigo (12). The secondary disorders included otolith disorders (5), delayed endolymphatic hydrops (12), and canalolithiasis (9)(BPPV). (Ernst et al , 2005). Hoffer et al, (2004) grouped patients into "positional vertigo", migraine-associated dizziness, and "Spatial Disorientation" (a wastebasket category). It seems likely that the distribution differs according to the practice setting (e.g. neurology, otolaryngology, general medicine).
Treatment for post-traumatic vertigo, in essence, involves medication and/or physical therapy. Surgery is almost never an appropriate treatment, as when a portion of the body is damaged, more trauma is rarely curative.
|After a head injury, otoconia may be displaced from the utricle and migrate into other parts of the ear, causing dizziness. There may also be damage to the membraneous labyrinth as well as many other structures outside the ear.|
Knoll et al (2019) reported on temporal bone findings in 5 autopsies that had dizziness, vestibular findings on autopsy of the temporal bone, and a history of "head injury". They wrote "There was a decrease of 48.6% (range, 40%-59%) in the mean count of Scarpa's ganglion cells as compared with that of normative historical age-matched controls. Moderate to severe degeneration of the vestibular membranous labyrinth was identified in the posterior, superior, and lateral canals in several cases (50%, n = 4 TBs). The maculae utriculi and sacculi showed mild to severe degeneration in 2 cases. Additional findings include vestibular hydrops (25%, n = 2 TBs) and blockage of the endolymphatic duct (n = 1 TB)." This report suggests that the damage is distributed equally between the membrous labyrinth and the otolith organs. This is a little surprising as one would expect relatively more damage to the otolith organs containing heavy masses, as opposed to the membranes which are somewhat cushioned. Perhaps it relates to the size of the targets -- there is much more real-estate in the membranous labyrinth than the otoliths. It might also be just chance -- there is rather little temporal bone data available. This study provides data concerning the relative distribution of damage after head trauma. It does not address the frequency of damage as a function of the degree of trauma.
Ishai et al (2018) reported on pathology of the cochlea following head injury without temporal bone fracture. The reported "Of the 6 cases, 2 (33%) had severe loss of hair cells in all 3 turns of the cochlea, and 4 (67%) cases demonstrated moderate to severe loss at the basal turn of the cochlea. Four cases had scattered atrophy of the stria vascularis, and 3 (50%) had cochlear hydrops. The number of total SGCs was decreased, with an average 53% loss (range, 25%-79%) as compared with controls."
1. Positional Vertigo, and particularly BPPV
Benign Paroxysmal Positional Vertigo or BPPV , is the most common type of severe dizziness, and it is also common after head injury, occuring in about 28% of persons with post-traumatic vertigo (Hoffer et al, 2004). Even injuries that do not directly affect the head such as whiplash injury, have been reported to be associated with BPPV (Dispenza et al, 2010). BPPV is easily recognized by the pattern of dizziness that is brought only when the head is placed in certain positions. There are several good treatments for BPPV and the prognosis for this syndrome, in the proper hands, is excellent. It is also possible to have rarer causes of positional vertigo including mainly utricular injury, vestibular atelectasis, and various forms of central vertigo caused by cerebellar or brainstem disturbances.
Balatsouras et al (2017) reported on 33 patients (not very many) with BPPV after mild head trauma, and noted that "The patients with BPPV secondary to mild head trauma presented the following features, in which they differed from the patients with idiopathic BPPV: (1) lower mean age, with more intense symptoms; (2) increased rate of horizontal and anterior semicircular canal involvement and frequent multiple canal and bilateral involvement; (3) greater incidence of canal paresis and presence of spontaneous nystagmus; (4) poorer treatment results, attributed mainly to coexisting canal paresis in many patients, and higher rate of recurrence."
These are really features of post-traumatic BPPV in general (as opposed to simply "mild head trauma"), and of course they are different than patients with "wear and tear" type BPPV.
|Normal membranous labyrinth||Dilated membranous labyrinth in Meniere's disease. After a head injury, scarring of the drainage pathways may cause fluid to build up.|
2. Post-traumatic Meniere's syndrome --Also sometimes called "post-traumatic hydrops".
Defined as episodes of dizziness accompanied by noises in the ear, fullness, or hearing changes, following a head injury. The mechanism may be bleeding into inner ear, followed by disturbance of fluid transport, but it is rare that the bleeding is documented. Onset of symptoms may vary from immediate to as long as one year later. Meniere's, like migraine is a "symptom" diagnosis defined by a committee rather than a blood test or MRI. The Meniere's diagnosis depends on documenting four features - -tinnitus, fullness, hearing loss, and episodic vertigo.
The evidence base to support the existence of post-traumatic Meniere's is somewhere between tiny and non-existent. The few papers on the subject largely consist of personal opinions in based on clinical experience illustrated with occasional cases (one might argue that this web page is similar). Most recently, Chung et al reported a single case (2014) in the Korean journal of Audiology. Dibiase and Arriaga (1997) presented their opinions in the Otolaryngol Clin North Am. Fitzgerald's discussion (1996) falls into the same general category. So this is not a diagnosis that is well established.
There are legal implications to the post-traumatic Meniere's diagnosis, as if it can be established, one party may be able to get another party to pay them money. Unfortunately, because of the subjective nature of most of these symptoms (even hearing loss can be fudged), post-traumatic Meniere's is vulnerable to malingering. While is is dangerous to make generalizations, we would not "trust" reports most regarding the incidence of Meniere's post head injury, due to the subjective nature of this diagnosis. As the technology improves to diagnose hydrops through MRI, this generalism may need revision.
In our opinion, the probability of Meniere's being reasonably attributed to post-traumatic mechanisms is a function of the severity of injury (severe makes more likely), the latency from the injury (longer is less likely), the presence of a pre-existing condition, and the presence of secondary gain.
Persons with the Enlarged Vestibular Aqueduct syndrome (EVA) are felt to be more likely to develop Meniere's like symptoms after head trauma (Berettini et al, 2000). However, the evidence base for this is not large and the number of people with this radiological finding are few.
Surgery is generally a bad idea for Meniere's syndrome, and even more so a bad idea for post-traumatic Meniere's. Treatments aimed at autoimmune mechanisms for Meniere's (such as steroids) are also implausible for post-traumatic Meniere's.
3. Labyrinthine "concussion" and trauma to the 8th nerve/brainstem
Defined as a non-persistent hearing or labyrinthine disturbance which follows a head injury, not caused by another mechanism. A hearing loss or a nystagmus must be present to make this diagnosis with a reasonable degree of medical certainty. Fitzgerald (1996) reviewed several supposed mechanisms for "labyrinthine concussion", largely involving speculations regarding the "microcirculation". We find this implausible. He also mentioned disruption of sensory epithelium from a pressure wave transmitted through spinal fluid ("commotio labyrinthi"). In as much as CSF pressure changes are associated with hearing disturbance, this seems more credible.
Fitzgerald (1996) also reported that the anatomic literature concerning trauma has described a shearing effect on the root entry zone of "cranial nerves" with head trauma. This would seem possible with the 8th nerve, which emerges from a bony canal, and then makes a short jump to the brainstem, but as the brainstem has little freedom to move with a head injury, the likelihood is not high. More vulnerable structures might be the otolithic organs, which essentially consist of "stones" attached to hairs. It is easy to see how the "stones" could be pulled off.
While the name "Labyrinthine concussion", implicates an inner ear disturbance, this symptom complex may be impossible to differentiate from other entities. For example, it might be difficult to differentiate a labyrinthine "concussion" due to damage to the inner ear, from an eighth nerve stretch injury, or an injury to tracts in the brain that transmit vestibular or auditory information. As they are all treated similarly however, this may not matter.
Dizziness combined with migraine headaches. Migraine has been reported as common as 41% in persons with posttraumatic vertigo (Hoffer et al, 2004) Headaches and vertigo are common after head injuries. The main difficulty in this situation is to determine whether they are related or coincidental. It may also be difficult to distinguish post-traumatic headaches (which are very common), from migraine. The lack of a "litmus test" for Migraine, other than perhaps response to triptan medication, makes this diagnosis tenuous.
Imbalance following a severe neck injury. While nearly all dizziness specialists agree that cervical vertigo does exist, there is controversy regarding the frequency with which it occurs (Brandt T, 1996). Several theories exist as to the mechanism, the main ones being: 1). Vascular compression 2). Alteration of sensory input to the vestibular system. See later section on Whiplash.
|Round window fistula. A membrane "blows out" between the inner and middle ear, causing dizziness and possibly also hearing loss.|
7. Perilymph fistula (PLF).
Usually symptoms of imbalance and dizziness provoked by straining or blowing the nose. People with fistula may also get dizzy with loud noises (called Tullio's phenomenon) or with straining (a positive Valsalva). The frequency to which this controversial syndrome occurs is debatable, but general opinion holds that it is rare. (Hornibrook, 2012). This is one of the few diagnoses involving post-traumatic dizziness where surgical treatment is reasonable. Intially, in the right context, it may be reasonable to consider a ventilation tube. Rarely exploratory surgery is recommended.
The difficulty with PLF, which is common to many of the diagnoses mentioned on this page, is the lack of a method of establishing the diagnosis, prior to or even during surgery to repair the fistula. Because of this problem, there is concern in the otologic community that unnecessary surgery may be performed, especially revisions (Black et al, 1992). At this writing (early 2017), many otology specialists refuse to even consider the PLF diagnosis. On the other side of the coin, if you are diagnosed with a PLF, prior to "signing up" for surgery, we think it is prudent to get a second opinion from an experienced expert (ideally a non-surgeon working out of a different institution) who can be relied upon to provide a balanced assessment.
8. Psychogenic vertigo. There are many possibilities.
Factitious vertigo is complaints of vertigo in an attempt to gain a sick role.
Psychogenic vertigo is vertigo related to psychological causes such as depression, anxiety. Anxiety and depression may result from traumatic brain injury that creates a self-perpetuating psychological reaction (Alexander, 1998). Post-traumatic stress disorder (PTSD) can result in reexperiencing the injury, perhaps in dreams, and hyperarousal symptoms (King et al, 1998; Stein, 2002).
Vertigo simulated or exaggerated in an attempt to obtain compensation is known as "malingering". Binder et al (1996) have noted that "money matters", especially in persons with mild head trauma, as disability is partially correlated with financial incentive (effect size = 0.47). Paniak et al (2002), noted that compensation seekers/recievers report symptom incidence and severity as approximately 1 standard deviation higher than persons who were not seeking or receiving financial compensation. These papers just document what is rather obvious -- people who have a chance to be paid for reporting symptoms, report more symptoms.
Marzo et al (2004) noted that in their 16 patients with post-traumatic vertigo, 6 had legal claims (none returned to work), and 6 more had workers compensation claims (again none returned to work).
9. Epileptic vertigo.
Vertigo due to brain injury, typically the part of the temporal lobe that processes vestibular signals. Loss of consciousness usually occurs at the time of injury and vertigo is generally accompanied by altered consciousness (Tusa et al, 1990). The typical symptom is "quick spins", although this symptom has other potential causes (BPPV, vestibular neuritis). Treatment is with anticonvulsants. Topirimate and Keppra are a particularly good medications for this condition as they are also useful in Migraine.
10. Diffuse axonal injury (DAI).
Pure decelleration forces can produce diffuse axonal injury (Gennarelli et al, 1982). In some individuals who come to autopsy after a twisting type injury of the head on neck, small areas of bleeding (petechial hemorrhage), and interruption of neuronal circuits (axonal damage) can be found. Complaints of dizziness are attributed to brainstem or cortical injuries which cannot be imaged with a good MRI. This is an autopsy diagnosis -- it cannot be made with certainty prior to death. Historically, significant DAI is not felt to occur in awake humans who do not report loss of consciousness. A thirty minute loss seems likely to be needed for a significant DAI (Alexander, 1998).
11. Postconcussion syndrome.
Concussion comes from the Latin word, "to shake violently" (Webster). There are many problems with use of the word "concussion", due to the extremely broad definition adopted in the literature. See this page for more commentary.
Most concussions in adults are caused by direct blows to the head. However, it is also accepted that occasionally, such as in the "shaken baby" syndrome, concussions can occur without a direct blow to the head after a very forceful acceleration/decelleration.
In any case, while dizziness and nausea symptoms accompanying the entity called "concussion" in the literature usually resolve over 6 weeks, cognitive symptoms and headaches persist longer. Hoffer et al (2004) suggested that symptoms persisted an average of 39 weeks -- about 9 months, and that return to work usually occured at about 16 weeks. Occasionally symptoms are permanent. As noted above, in many cases, chronic symptoms are psychological in origin. Balance symptoms after concussion generally resolve by 10 days (Peterson et al, 2003)
12. Whiplash injury syndrome. This diagnosis is discussed in detail on a separate page.
First the doctor will want to know exactly when and how the head or neck was injured, and the character of the dizziness (i.e. spinning ? unsteadiness ? confusion ?). He/she will want to know if you were unconcious and the duration of time. Did the airbag deploy ? There is a significant incidence of vertigo and hearing disturbance after airbag deployment (Yaremchuck and Dobie RA. 2000). All available records from the emergency room or hospital where you were seen after the injury should be obtained and shown to your doctor. This is especially important when there is litigation as much may depend on small details.
Next, a specialized examination for dizziness will be performed. Balance will be measured, often with moving platform posturography. A search for "nystagmus" will be made, related to head and/or neck position or to vibration of the neck. In more sophisticated settings, this will be done with video-frenzel goggles. You may be checked for pressure sensitivity with the fistula test.
Laboratory tests will be ordered. In most instances these will include an audiogram, ENG, possibly an MRI scan or CT scan of the inner ear (temporal bone CT scan). If available, a VEMP may be useful. An EEG may be obtained for persons with paroxysmal cognitive symptoms suggestive of epilepsy. In patients with hearing disturbance, an "ECochG" may be done. Moving platform posturography is helpful to quantify balance deficits.
Psychological testing, especially the IMPACT test, is sometimes done in persons who have entirely normal vestibular test results, or with cognitive symptoms that appeared after the injury (generally attributed to a concussion). They can document interactions between symptoms and personality as well as cognitive difficulties. Such testing is often useful in sorting out the situation when patients are in litigation and could benefit from an appearence of ill health.