posterior canal, that is typically head extension and rotation toward the affected side, such as looking up to a high shelf, or when the patient gets into or out of bed transitioning toward the affected ear. Provocation of horizontal canal BPPV symptoms is common with rolling from one side to the other in bed, or lateral head tilt movements. Once provoked, symptoms of vertigo will have a latent onset of 1 or more seconds as the gravity-referenced otoconia change position, inducing displacement of the cupula. The patient will then experience transient symptoms of dizziness or vertigo that will fatigue within 1 to 2 minutes while maintaining the provoking head position. In canalithiasis, the duration of symptoms is typically less than 60 seconds, while patients with cupulolithiasis will experience symptoms for as long as 2 minutes. Another characteristic feature of vertigo and dizziness associated with BPPV is the crescendo-decrescendo nature of the symptoms, meaning that the patient will experience an increasing intensity of symptoms at onset, reaching a peak intensity before subsiding (Herdman & Clendaniel, 2014). It is important for the clinician to appreciate that symptoms associated with BPPV have a mechanical basis, whereas other vestibular disorders are caused by loss of function. Thus, the patient with BPPV will generally not experience symptoms if they avoid the offending head position. referral for further differential examination, including an audiogram, due to the likelihood of a medical pathology underlying the presentation. Acute vestibular syndrome (AVS) is a condition in which there is a rapid onset of severe vertigo, nausea, vomiting, and spontaneous nystagmus with head motion intolerance and imbalance. It is caused by infectious neuronitis, or infectious labyrinthitis when hearing is involved. Because of its similar presentation to a CNS infarct, a differential assessment must be undertaken (Hotson & Baloh, 1998). Although AVS is most likely caused by infectious neuronitis or labyrinthitis, the older adult with at least one risk factor for vascular disease is at high risk for a brainstem stroke, which would result in a similar presentation, but require different management. A study by Kattah and colleagues (2009) evaluated older adult patients with =1 risk factor for stroke presenting to the emergency department with symptoms of nystagmus, vertigo, nausea/vomiting, and gait unsteadiness to determine a centrally versus peripherally mediated cause for their symptoms. A bedside clinical exam with the acronym “HINTS,” which will be detailed in the clinical examination section of the course, was performed and findings clinically correlated with imaging studies upon admission. They found that the HINTS bedside assessment was 100% sensitive and 96% specific in diagnosing pontine stroke as the cause of the patient’s presentation that mimicked AVS. Injury to the peripheral vestibular structures can be a result of direct trauma, but can also include an ischemic event in the PICA or AICA, medication toxicity, and acoustic neuroma. PICA or AICA infarct would present as persistent dizziness or vertigo, along with balance and gait disorders due to unilateral loss of semicircular canal inputs to the CNS with regard to head motion. Because the PICA and AICA supply central structures, such as the pons and cerebellum, signs of central pathology may also be present, including dysmetria and dyscoordination, and should be screened on examination. Medication toxicity is the result of sensitivity to aminoglycosides (e.g., gentamycin, streptomycin). High- dose use of these medications to manage systemic bacterial infections can result in irreversible ototoxicity in 15% of
The term canalithiasis refers to the condition in which debris is floating freely in the semicircular canal. The presence of otoconia in the affected semicircular canal changes the fluid dynamics of that canal in response to head movement. In this condition, the otoconia create a hydrodynamic drag of endolymph when the affected canal is moved into the direction of gravity, creating an increased magnitude of response in the cupula. Cupulolithiasis refers to the condition in which otoconia have adhered to the cupula, thus increasing the mass of the cupula, making it more sensitive to gravity (Lee & Kim, 2010). Otoliths will most often migrate to the posterior semicircular canal due to its more inferior orientation in the ear relative to gravity, with the prevalence of posterior canal BPPV reported to be upwards of 96%. The horizontal canal is the next most affected canal, with studies showing that horizontal canal BPPV occurs approximately 2% to 16% of the time. BPPV of the anterior canal is rare (Fife, 1998; Honrubia et al., 1999; Jacobson & Shepard, 2008; Macias et al., 2000). The chief symptom of BPPV is vertigo that is provoked with changes in head position. Some patients will also experience lightheadedness, nonspecific dizziness, postural instability, and nausea (Blatt et al., 2000). Symptoms are brought on by rapid changes in head position that orient the affected canal in a gravity-dependent position. For the Reduced function This category describes loss of vestibular function due to infection, degenerative changes, or injury affecting the CN VIII or membranous labyrinth, resulting in diminished or absent transmission of signals from the semicircular canals and otoliths to the CNS. The profile of symptoms commonly associated with reduced vestibular function include dizziness or vertigo, imbalance, gait disturbances, and difficulties with gaze stabilization that are provoked with movement through space, either through head movement, walking, or transitions. Symptoms may be chronic and persistent, being present even when movement is ceased. In contrast, symptoms associated with BPPV are provoked with particular head positions, triggering transient dizziness (Herdman & Clendaniel, 2014). Neuronitis and labyrinthitis are the second most commonly seen peripheral vestibular disorders after BPPV (Herdman & Clendaniel, 2014; Kroenke et al., 2000). Neuronitis is inflammation of the CN VIII, affecting the superior branch of the vestibular nerve, which supplies the utricle and anterior and horizontal semicircular canals. Inflammation of the superior branch of the vestibular nerve will result in reduced transmission of information from the horizontal canal (horizontal canal paresis), and can result in utricular degeneration, causing posterior canal BPPV as a secondary complication. Labyrinthitis defines an inflammatory condition of the membranous labyrinth, which is essentially an infection of the entire inner ear, causing symptoms of neuronitis in addition to hearing loss and tinnitus. Multiple infectious processes have been implicated in causing vestibular neuronitis or labyrinthitis, the most common being an upper respiratory infection. Typically, the original illness precedes the onset of vestibular symptoms by as much as several weeks. Symptoms of dizziness or vertigo are generally self-limiting, with spontaneous recovery occurring in 1 to 3 days. The patient may also experience problems with gaze stabilization or blurred vision. When new onset of hearing loss is part of the presentation, infections such as mononucleosis, herpes zoster, Lyme disease, mumps, and measles must be considered, as well as the possibility of other noninfectious lesions such as acoustic neuroma (Baloh & Halmagyi, 1996; Herdman & Clendaniel, 2014). This profile of symptoms and findings necessitates a physician
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