to appreciate that symptoms associated with BPPV have a mechanical basis, whereas other vestibular disorders are caused 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 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 Fluctuating function Ménière’s disease and perilymphatic fistula are the vestibular system disorders in this category, with structural abnormalities in the vestibular apparatus underlying the cause of distorted vestibular function. Ménière’s disease is a function of malabsorption of endolymph (endolymphatic hydrops) in the endolymphatic duct and sac within the semicircular canals, creating an altered flow of endolymph. The clinical feature of Ménière’s disease is an acute spontaneous onset of disabling vertigo, postural imbalance, nausea, and vomiting, persisting for 24 hours. Recovery is also spontaneous, with no residual impairments. However, symptoms of balance limitations can persist for several days or weeks for some patients (Herdman & Clendaniel, 2014). Ménière’s disease is primarily managed through medical, surgical, and
by loss of function. Thus, the patient with BPPV will generally not experience symptoms if they avoid the offending head position.
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 patients receiving this therapy, permanently damaging hair cells in the vestibular apparatus. As ototoxicity generally affects vestibular structures bilaterally, the patient will present without symptoms of vertigo or dizziness due to the lack of “mismatch” in bilateral vestibular inputs (Baloh & Halmagyi, 1996; Huth et al., 2011). Acoustic neuroma (vestibular schwannoma) is a benign schwannoma that arises on the vestibular portion of CN VIII at the location of the cerebellopontine angle. The incidence of acoustic neuroma is rare, with an incidence of 1.09 per 100,000 in the United States (Kshettry et al., 2015). The initial presentation is unilateral sensorineural hearing loss, tinnitus (high-pitched ringing in the ear) and a sense of aural fullness, typically evolving slowly over the course of several months or years. Presentation of vestibular impairments is not a main feature; the slow growing nature of this tumor allows for ongoing compensation of the CNS to the gradual loss of vestibular function (Baloh & Halmagyi, 1996), but can be a chief complaint in more than 30% of patients (Olshan et al., 2014). Given the location of the neoplasm and its proximity to the facial nerve at the level of the brainstem (CN VI), patient presentation can also include hemifacial paralysis (Baloh & Halmagyi, 1996; Olshan et al., 2014). pharmacological means, with physical therapy care addressing any residual postural control deficits that may present after persistent attacks. A perilymphatic fistula is an abnormality or patency that occurs in the round and oval windows of the middle ear, allowing leakage of perilymph fluid from the semicircular canals to the middle ear. The perilymphatic fistula may be a result of chronic pathological elasticity of the bony labyrinth, leading to episodic changes in fluid pressure and results in fluctuating symptoms of vertigo and imbalance, as well as hearing changes. Often, it is a result of an injury, such as a closed head injury, penetrating injury to the tympanic membrane, barotrauma, or vigorous straining, creating a sudden onset of vertigo, imbalance, and tinnitus. If diagnosed immediately, the patient is placed on bedrest with the
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