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Guest allanopie

Balance And Vestibular Dysfunction

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Guest allanopie

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REHABILITATION OF MODERATE TO SEVERE TBI: SENSORY-PERCEPTUAL AND BALANCE DISORDERS IN TBI: BALANCE AND VESTIBULAR DYSFUNCTION

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BALANCE AND VESTIBULAR DYSFUNCTION - An inability to control the body's center of mass relative to specified limits. Balance and gait testing in patients with complaints of instability is warranted (Basford, et al 2003)

Causes - Persisting vestibular deficits after moderate and severe TBI are due to peripheral and central nervous system lesions and associated injuries, such as fractures, which can cause:

  • Muscle weakness and paralysis, which result in:
    • An inability to prevent movement and/or an inability to quickly initiate postural responses necessary to maintain balance, and
    • Biomechanical constraints, such as limited ROM and weight bearing activities, necessary to maintain postural balance and for compensation by the intact components

    • Poor motor coordination of the trunk and leg muscles into movement strategies with postural control
    • Dysfunction in the vestibular, visual, or somatosensory systems, or in the central integration of the 3 systems



      Symptoms and Prognostic Indicators
      • Positional vertigo, the sense of the room spinning around the patient, is the most common persisting vestibular symptom following TBI.
      • Oscillopsia, the illusion that stationary objects are moving back and forth, and severe nausea and vomiting, usually indicate a vestibular system disorder as well.
      • Low initial Glasgow Coma Scale scores and deep parenchymal brain lesions demonstrated by MRI are significant indicators of subsequent severe postural imbalance (Wober, et al 1993)



        Diagnosis
        • Patient History and Medications
          • The history is critical, particularly if it includes problems such as previous syncopal episodes, motion sickness, otologic problems, severe anemia, emphysema, hypertension, diabetes mellitus, endocrine dysfunction, longstanding peripheral neuropathy, coronary artery disease, psychiatric disorders, immobility, and alcoholism or drug abuse which can cause "dizziness"
          • Current medications are critical, particularly if they include:
            • Sedating medications, which can diminish the patient's ability to compensate for vestibular deficits
            • Anxiolytics, such as the benzodiazepines and buspirone, which may cause dizziness
            • Antidepressants and anticonvulsants, particularly at higher doses, which can cause sedation, vestibular deficits, movement disorders, and/or nystagmus
            • Aminoglycoside antibiotics at high doses, which can be ototoxic and can cause damage to hair cells in the labyrinth and cochlea
            • Compazine, scopolamine, phenergan, and meclizine, prescribed to treat nausea and vomiting, which can cause dizziness


            • Physical Examination
              • Musculoskeletal evaluation
                • Strength evaluation of the trunk and lower extremities - musculoskeletal injuries and contractures following TBI can cause limitations in ROM, which may shift the center of gravity and require more strength to maintain balance
                • Assessment of asymmetries in center of body mass and postural alignment - determines the strength necessary to maintain balance
                • Assessment of cervical and trunk strength and ROM - identifies problems that can cause muscular splinting in patients with vestibular deficits that can cause further impairment

                • Vision - Eye and vision problems affect balance and must be identified
                  • Vestibuloocular function - normal eye function requires a combination of smooth and saccadic pursuit eye movements
                    • Smooth pursuit: Visually tracking an object in all visual fields while the head is stationary can test for smooth pursuit eye movements; rapid, short movements are abnormal and frequently associated with central lesions
                    • Saccadic pursuit: Looking rapidly between 2 objects in both horizontal and vertical planes, while the head is stationary, can test for saccadic pursuit eye movements; 3 or more rapid eye movements to shift focus from one object to another, or under- or overshooting the targets, indicate an abnormality in eye movement

                    • Vestibuloocular reflex (VOR) - this reflex:
                      • Generates compensatory eye movements in response to head movement and, together with the saccadic and smooth pursuits, maintains gaze stability independent of head position
                      • Is tested by moving the patient's head vertically and horizontally while the patient fixates on a target; fixation that involves saccadic pursuit may indicate a unilateral or severe bilateral vestibular lesion

                      • Vestibuloocular reflex cancellation (VORC)
                        • Allows the head and target to move together
                        • Is tested by observing the patient's eyes while head and eye movements occur together; saccadic movements indicate an abnormality

                        • Nystagmus, involuntary, rhythmic oscillations of the eyes, is indicative of disruption of brainstem oculomotor systems
                          • Types are horizontal, vertical, rotary, and mixed
                            • "Jerk" nystagmus has fast and slow components and is associated with vestibular lesions
                            • "Pendular" nystagmus has excursions of equal velocity

                            • Diagnosis of abnormal nystagmus
                              • Electronystagmography is the best evaluation tool (scroll down to Vestibular Function Tests below)
                              • Head-shaking nystagmus test in the office or clinic is easily performed; head-shaking nystagmus after 10 shaking cycles is associated with a unilateral lesion and Freznel lenses must be worn to prevent involuntary fixation on random targets
                              • Positional tests of quick head movements into various positions
                                • Can produce 1 of 3 types of nystagmus classified by direction: latency, intensity, and duration
                                • Can differentiate between peripheral and central lesions
                                  • Benign paroxysmal postional vertigo, in which the latency of nystagmus is 2-20 seconds, the nystagmus is in a specific direction, the duration is < 60 seconds, and the nystagmus extinguishes on repeated testing, is the most common peripheral vestibular disorder
                                  • Nystagmus that occurs as soon as the patient is moved into the precipitating position and continues for the duration of the position (no extinction), with or without vertigo, usually indicates central deficits, compression of the vestibular nerve, or perilymphatic fistula

                        [*]Neurologic assessment

                        [*]Coordination tests, such as finger-to-nose and heel-to-shin, assess dysmetria

                        [*]Rapid alternating movements to assess dysdiadochokinesis

                        [*]Inspection or observation of volutional movement to assess movement disorders, such as tics, tremors, athetosis, ballismus, and chorea

                        [*]Manual muscle testing to assess strength

                        [*]Sensation tests of all pathways with the eyes closed, such as light touch of underused areas, pinprick, and proprioception of the small toes to detect even small lesions that can significantly affect balance

                        [*]Vibration tests with tuning forks to assess posterior column function, in which the duration of the vibration is tested; >25 seconds between the patient reporting cessation of the sensation and the actual cessation of vibration suggests abnormal function of the dorsal column

                        [*]Spasticity assessment, with the 5-point Ashworth scale and Brunstrom classification, e.g. to assess the presence or absence of velocity-dependent resistance to passive stretch

                        [*]Reflex examination to assess abnormalities, such as hyperreflexia or hyporeflexia that may interfere with stability or coordination during gait or static positions, and pathologic reflexes, including the Babinski, Hoffman's snout, rooting, glabellar, or tonic neck reflexes that may indicate nervous system abnormalities

                        [*]Balance assessment

                        [*]Romberg test

                        [*]Excessive sway, loss of balanace, or falling indicates a disorder in the dorsal columns that can affect balance

                        [*]"Sharpened" or "challenged" version (feet positioned in tandem) can indicate a dimunition of reliable distal input from ankle proprioception

                        [*]Stand-on-one-leg-eyes-closed (SOLEC) test; the norm for three trials is 10 steps before the patient starts sidestepping, stopping, opening eyes,or unfolding arms

                        [*]Fukada stepping test to identify labyrinth deficit; if patient progress >1 meter and has an angle rotation >45 degrees, the performance is considered abnormal

                        [*]Singleton test to assess unilateral vestibular deficits; instability when turing toward one side indicates a unilateral lesion in that side

                        [*]Berg Balance Scale on admission to and discharge from rehabilitation center to enhance the ability to predict rehabilitation outcomes beyond that provided by assessment of functional status alone (Juneja, et al 1998; Feld, et al 2001)

                        [*]Sitting balance dysfunction following TBI is a strong predictor of functional outcome (Black, et al 2000)

                        [*]Sensory organization - Damage to the labyrinth can impair the vestibulocollic reflex (which aligns the head with respect to gravity), causing an unstable, oscillating head

                        [*]Motor coordination - Involves assessing the patient's ability to coordinate the ankle, hip, and stepping movement strategies, i.e. to execute one strategy or another, appropriately adapt strategies to the changes in postural task, such as standing on one foot, and using an appropriate number of strategies in varied situations

                        [*]Motion-provoked symptoms - Involves observing patients for motion-provoked symptoms when they assume positions that usually generate vestibular symptoms

                        [*]Vestibular function tests

                        [*]Electronystagmography - Physiologic test of the horizontal semicircular canals to assess the site and side of peripheral lesions, spontaneous nystagmus, positional nystagmus, and benign paroxysmal positional vertigo

                        [*]Rotary chair testing - Physiologic test of the horizontal semicircular canals to assess site and side of peripheral lesions, particularly in patients in which caloric tests are uncertain or unobtainable

                        [*]Dynamic posturography - Functional test to assess evaluation of sensory organization and motor coordination components of balance and to monitor neurologic recovery in patients with TBI and balance deficits.

                        [*]The Sensory Organization Test (SOT) assesses the patient's ability to effectively use visual, vestibular, and somatosensory information for maintaining balance in progressively more challenging tasks. Dual-plate force platform assesses amplitude and velocity of center-of-pressure fluctuations in the anteroposterior and lateral sway directions during quiet standing, with and without visual deprivation (Geurts, et al 1996)

                        [*]Clinical Test for Sensory Interaction in Balance can be used in settings where dynamic posturography may not be available

                        [*]Motor Control Test (MCT) assesses the patient's ability to maintain balance in reaction to brief displacements of the support surface

                        Recovery/Treatment

                        [*]Spontaneous Recovery - A degree of spontaneous recovery is usually seen within the first 6-12 months following TBI, although multiple lesions, both peripheral and central, may interfere with this recovery mechanism and lead to prolonged symptoms without full recovery. Spontaneous recovery is due largely to adaptation of the vestibular system to asymmetries. The patient's ability to substitute other sensory input to compensate for deficits and to avoid sensory conflict situations is the major compensatory strategy for patients with bilateral peripheral or central lesions.

                        [*]Treatment Programs focus on stimulating functional recovery through vestibular adaptation, substitution, and spontaneous recovery:

                        [*]Avoidance of drugs, which cause:

                        [*]CNS depression and sedation, which interfere with balance, such as meclizine, diazepam, compazine, phenergan, and scopolamine

                        [*]Ototoxic effects, which cause vestibular deficits, such as high-dose aminoglycoside

                        [*]Education of patient and family to avoid specific sensory conflict situations and understand the goals of vestibular rehabilitation:

                        [*]Independent community level mobility

                        [*]Functional balance in increasingly challenging situations

                        [*]Improved safety for gait and mobility

                        [*]Improved general physical condition, endurance, and activity level

                        [*]Decrease in motion-provoked symptoms

                        [*]Exercise/Physical Therapy programs that faciliate the compensatory process, including:

                        [*]Head movements coordinated with eye movements

                        [*]Total body movements and balance tasks

                        [*]Habituation exercises for vestibular system adaptation

                        [*]Relaxation exercises

                        [*]Aerobic dancing/slide and step program to reduce balance and coordination deficits (Dault & Dugas, 2002)

                        pix-grn.gifBased on information in Medical Rehabilitation of Traumatic Brain Injury, L.J. Horn and N.D. Zasler, eds. St. Louis, MO, Mosby, 1996, except for information where other papers are cited.

                        Source: http://calder.med.miami.edu/pointis/tbipro...INE/sense2.html

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