Head Trauma and Dizziness

This week, we have another contribution by my doctoral student, Brady Workman, B.S.. Brady has been scanning old posts and trying to fill in gaps regarding areas I have not covered in the past few years.

Traumatic Brain Injury (TBI) is an increasingly prevalent public health concern, with 2.8 million people requiring medical assistance due to TBI in the United Sates in the year 2013 alone. Much of the attention related to traumatic brain injury seems to focus on sports related injuries, but TBI has widespread effects on many individuals throughout all walks of life. The National Institute of Neurological Disorders and Stroke defines “Traumatic brain injury (TBI), a form of acquired brain injury, occurs when a sudden trauma causes damage to the brain. TBI can result when the head suddenly and violently hits an object, or when an object pierces the skull and enters brain tissue”.

 

Another form of head injury may occur when an individual is exposed to a blast or explosion. Blast related mild TBI has been a common form of injury during recent military conflicts and will likely be encountered clinically by many specialists in the field of balance disorders. Exposure to a blast is multi-faceted and can have a multitude of effects on the bodies sensory systems, with many of these effects cumulative in the damage incurred. Blast exposure can include rapid changes in the intracranial pressure associated with the blast wave, penetrating or blunt head injury due to blast debris or hitting ones head, and toxin exposure from fuels and accelerants. Readers are referred here for a more in depth discussion of balance disorders after blast injury.

 

For our discussion, we will focus primarily on how the inner ear vestibular system is affected by blunt trauma and blast exposure. TBI related to blunt trauma tends to be more prevalent in a civilian population, while blast exposure and the resulting head trauma account for a large proportion of TBI in a military setting.

 

So, what does TBI have to do with anything on a dizziness blog?

 

Dizziness following TBI is common, with many individuals’ symptoms being short lived immediately following the injury; however for some, the lingering effects of dizziness due to TBI can be life-altering. Due to the different causative nature of blunt & blast trauma, it seems possible that different means of acquiring head injury may preferentially damage different vestibular system end organs. So, lets take a closer look and see whether or not this actually the case.

 

Blunt trauma induced TBI has been shown to have numerous effects on the vestibular system including: horizontal semicircular canal damage (head turn sensor) and concomitant vestibular-ocular reflex deficits (eye movement reflex to maintain visual stability with head motion), increased rates of benign paroxysmal positional vertigo (BPPV) (displaced inner ear crystals/otoconia), abnormal oculomotor function tests (eye movement control tests), as well as central vestibular damage (brain). There is also some evidence showing potential otolith organ damage (front/back and up/down sensors) following blunt trauma induced TBI, but due to limited means of clinical assessment in the past, it seems that this type of vestibular injury may have not been easily quantifiable in most clinical settings. Otolith damage following blunt trauma seems logical, given the increased rates of BPPV following head injury, and the otoconia in their native location sit atop the otolith organs.

 

Blast trauma is less understood than TBI related to blunt trauma or penetrating head injuries, but it seems that damage to a number of sensory systems is likely to occur as well. One would imagine that the aforementioned effects for blunt trauma induced TBI may be expected in blast exposure as well, especially in cases where blunt trauma occurs along with the blast. Blast exposure may cause damage to the otolith organs (linear sensors) of the vestibular system, with abnormalities measured in utricular function (front and back sensor) and saccule function (up and down sensor) following blast exposure. Damage to the horizontal semi-circular canals and vestibular-ocular reflex deficits (measured with calorics & rotational chair) have also been documented.

 

Evidence suggests that damage may incur to any part of the peripheral vestibular system following traumatic brain injury, regardless of the causative nature of the head injury. Therefore, it seems reasonable that vestibular assessment protocols of dizziness symptoms related to traumatic brain injury may warrant extensive investigation of the vestibular system including: the semicircular canals (calorics, video head impulse test, & rotational chair), oculomotor testing, tests of visual-vestibular interaction, and assessment of the otolith organs (cervical VEMP and SVV). Ocular VEMPs would likely be useful if other means of assessing utricular function are not available.

 

Appropriate diagnosis of the vestibular system end organs affected by TBI would likely lead to the best treatment strategies and outcomes for patients. Appropriate diagnosis of vestibular injury and vestibular rehabilitation therapy for those identified as having vestibular end organ damage would likely provide maximal benefit to patients. A more in depth discussion of treatment of vestibular injury in mild TBI can be found on page 5 here.   

 

 

This is what it looks like

Today’s post is a two week follow up on my report of my personal experience with Vestibular Neuritis. I came in to my office at 48 hours into the episode to document the obvious nystagmus, measure the effects of fixation and gaze angle, and measure functional changes in my Vestibular Ocular Reflex (VOR).

As you will see from the graphs below, I was able to document left beating nystagmus following Alexander’s Law. That means that the nystagmus was direction fixed (all left beating), was suppressed by fixation (at 48 hours I still could not supress entirely, but the decrease was obvious), and the nystagmus increased in velocity (from 13 degrees per second spontaneous to 15 degress per second in gaze left), and decreased (to zero) in right gaze.

 

 

 

 

 

 

 

 

 

 

 

 

 

My initial rotational chair test largely reflects the spontaneous left beating nystagmus as a profound asymmetry to the right. Symmetry is a measure of left beating nystagmus (typically generated by chair rotation to the left) compared to measure of right beating nystagmus (typically generated by chair movement to the right). In my case, there was no right beating nystagmus to measure due to the right hypofunction, and there was persistent, spontaneous nystagmus whether the chair was moving or not. The process of cerebellar clamp is seen as there is a significant reduction in gain of the VOR at slower speeds.

 

 

 

 

Finally, my vHIT results were consistent with my informal Head Impulse test described in the last post. You will note that when I moved quickly to the left, I was able to maintain visual contact with the target by making an eye movement that was equal and opposite of my head movement. When I moved quickly to the right, the eye movement was reduced (as noted in the decreased gain graph on the right), and I exhibited frequent overt saccades (the little blips occurring after the head stopped moving).

 

 

 

So, my preliminary head in the bucket while spinning and vomiting self exam was correct. As I have said many times, when you see a patient in the sudden onset acute stage of vertigo, you do need to be more concerned about worrisome pathology, but the ability to determine the cause is easier if you know what to look for. I will be back with periodic updates as I go through vestibular rehabilitation and the central compensation process. Wish me luck!