Somatosensory system The somatosensory system provides the CNS with information regarding body position and motion with respect to the supporting surface. It also provides information about the relative position and relationship of body segments to one another. Somatosensory inputs register body and segment motion when moving along a horizontal surface, to detect changes in the conditions or motion of the surface to maintain verticality with respect to the surface. An example of this is walking along a cobblestone path or sandy beach, where ankle motion accommodates the uneven or compliant, shifting
surface. However, when surface conditions change so that they are not horizontal, such as with a rocking ship or a ramp, orienting the body relative to the supporting surface is no longer effective. Rather, orienting with reference to gravity becomes the effective strategy, such as is mediated by the vestibular system. Examination of somatosensation relative to postural control should include proprioception and kinesthesia of the feet, especially in older individuals and those with diabetes or peripheral neuropathy.
SENSORY INTEGRATION
Understanding the role of the vestibular, visual, and somatosensory systems in detecting motion and position elucidates their relative contributions to the CNS to create a schema, or map, of the body with respect to the environment, which underlies postural control. We share many experiences where we have discovered how these systems work together. A common example of sensory integration is one where you are sitting in your car next to another car at the red light. Suddenly, the car next to you starts to move forward to get a jump on the green light. Your peripheral vision picks this up as net motion, but it cannot distinguish whether you are rolling backward or the car next to you is moving forward. Since we tend to rely on visual information, despite its inaccuracies relative to movement, our brain misinterprets this information as self-motion and drives the motor response of pushing your foot down harder on the brake pedal. Unfortunately, that does not change the net movement
we are perceiving since we are not in motion. That information is fed back to the CNS (no change), and sensory inputs are reinterpreted. Although the visual system is sending information to the CNS that movement is taking place, since we are not moving relative to the surface the somatosensory system is not detecting movement, and since there is no head movement the vestibular system is also sending information to the CNS that we are not moving. Thus, the sensory inputs are being compared and “reweighted” to resolve this sensory conflict. As a result, the CNS shifts its reliance on information from the two corroborating sensory systems, and we quickly come to the realization that the car next to us is in motion. These adaptations, occurring in a fraction of a second, are essential to successfully maintaining postural control under changing task conditions, and are the basis for the rehabilitation of peripheral vestibular deficits.
TYPES OF PERIPHERAL VESTIBULAR DISORDERS
Causes of peripheral vestibular dysfunction can arise from pathology of the semicircular canals, otoliths, or the CN VIII. Peripheral vestibular pathology is classified into three categories: distorted function, reduced function, and fluctuating function. Establishing the nature and character of complaints of dizziness is an essential first step in the differential clinical examination process; it helps to categorize the pathologic basis of the Distorted function Benign paroxysmal positional vertigo (BPPV) is the sole pathology that falls into this category. BPPV is the most common cause of dizziness symptoms in the older adult (van Leeuwen & Bruintjes, 2014). The incidence of BPPV is greater for adults 60 years of age as compared to younger adults, with the incidence of BPPV peaking in the sixth and seventh decades of life (Hilton & Pinder, 2003; von Brevern et al., 2007). Symptoms associated with BPPV are characterized as brief periods of vertigo, lasting less than 60 seconds, and brought on by stereotypical head positions relative to gravity. The pathological mechanism that underlies BPPV is caused by otoconia that have been dislodged from the macula in the utricle either through natural degenerative changes or by trauma, such as a fall. The displaced otoconia eventually find their way to the semicircular canals, resulting in free- floating debris within the canal, or debris that has adhered to the cupula. 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
patient’s symptoms. This is achieved by gaining an accurate description of the frequency, onset, and duration of episodes of dizziness through systematic differential questioning on intake interview. Determining the category of pathology plays an important role in guiding intervention and indicating whether referral for additional services may be required. 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 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
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