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Balance Disorders

Vestibular physical therapy has become a mainstay in the management of patients with balance disorders manifesting as dizziness and disequilibrium. There is a great deal of information on use of physical therapy treatment for Benign Positional Proximal Vertigo (BPPV) with BPPV maneuvers Recently, there is more and more evidence supporting the use of rehabilitation techniques for patients with peripheral and central vestibular disorders. Full compensation is necessary for patients to develop an appropriate response to a permanent vestibular lesion. This is done through adaptation, habituation and substitution rehabilitation. Adaptation is the capability of the vestibular system to make long term changes in the neuronal response to head movement

Habituation is the long term reduction of a response to a noxious stimulus (specific movements)

Substitution treatment is the substitution of alternative strategies to replace the lost or compromised function

• Patients with central disorders often cannot be progressed as quickly as patients with peripheral vestibular dysfunction; thus, overall treatment times are longer for patients with central disorders. Outcomes of rehabilitation in patients with central vestibular disorders, for example, following head trauma, are not as good as outcomes following peripheral vestibular disorders. Patients with only central vestibular disorders, however, have better outcomes than do patients with combined peripheral and central dysfunction.

• Clinicians often categorize patients with vestibular system abnormalities as those with peripheral vestibular disease versus those with central vestibular disease. The peripheral vestibular system consists of the vestibular end organs, including the 3 semicircular canals and the 2 otolith organs in each ear, and the vestibular portion of the eighth cranial nerve. Conversely, the central vestibular system consists of those structures and pathways listed in Some of these patients appear to have a vestibular system abnormality to account for their dizziness, whereas other patients do not. A subset of patients with vestibular disease will be evaluated and treated by physical therapists. We believe that knowledge of how vestibular disorders may be manifested and, in particular, of the importance of central vestibular structures can improve a therapist's effectiveness

Migraine

Migraine-associated dizziness72-88 is an underrecognized disorder that is actually quite common with a prevalence of 6.5%.88,89 Many people with a history of migraine headaches may have dizziness with some or all of their headaches. Other people with migraine headaches may have migraine-associated dizziness in isolation, that is, dizziness without headache.87,88 Rarely, people who have no history of headache may experience migraine-associated dizziness. Migraine-associated dizziness can manifest itself as a spinning sensation preceding a migraine headache, as dizziness and imbalance during a migraine headache, or as dizziness without headache. Some people experience a sense of imbalance and dizziness between episodes of headaches. A recent study by Cass et al87 has indicated the large variability in the duration of symptoms in people with migraine-associated dizziness.

Establishing a diagnosis of migraine-associated dizziness can be difficult because it is largely a diagnosis of exclusion.88 That is, migraine is a diagnosis that is reached when no other plausible diagnosis is available. Migraine-associated dizziness should be considered in all patients who have migraine headache or a positive family history of migraine without other diagnoses. Additional clues in the history may be a sense of imbalance in complex visual or motion environments. Physical examination findings are typically normal. The results of vestibular laboratory tests (including caloric testing, ocular-motor testing, rotational testing, positional testing, and posturography) may be abnormal, but they usually do not indicate a definite peripheral or central vestibular abnormality.87 In particular, asymmetric nystagmus responses to rotational stimulation have been reported with migraine-associated dizziness.72,87 Because physical examination findings are typically normal and no single laboratory test is available to establish a diagnosis of migraine-associated dizziness definitively, the diagnosis remains uncertain in most patients. Although the diagnosis remains uncertain, however, the disorder is quite common.88,89

Trauma

Head trauma may cause central nervous system trauma (eg, a postconcussion syndrome), a labyrinthine concussion, a neck injury (eg, whiplash), or some combination of these injuries. Thus, physical therapists must be aware that patients who experience dizziness following head trauma may have a combination of central vestibular abnormalities, peripheral vestibular abnormalities, and neck injuries. Other conditions that may exist in patients who have experienced head trauma and who have dizziness include posttraumatic benign paroxysmal positional vertigo, posttraumatic Ménière disease, and perilymphatic fistula.90 Moreover, a central nervous system injury may impair the process of compensating for a peripheral vestibular ailment.68

Central nervous system trauma can produce dizziness either on the basis of a postconcussion syndrome presumably resulting from cerebral injuries or due to a brain-stem injury.91 The most critical factor in the patient's history in arriving at a diagnosis of posttraumatic dizziness is the observation of a temporal association between the patient's head trauma and his or her dizziness. A complicating factor in the evaluation of a patient who has sustained head trauma is that the peripheral vestibular system or the neck also may have been damaged. The term "labyrinthine concussion" is used to describe peripheral vestibular dysfunction following head trauma.71 In such cases, caloric testing usually indicates a unilateral reduction in function.90

Head trauma resulting from automobile accidents often is associated with "whiplash" (ie, a flexion-extension injury). The neck plays a critical role in balance.91 Although "cervical vertigo" is poorly described and nearly impossible to diagnose definitively,92 the accurate detection by the central nervous system of the position of the head with respect to the torso is critical for normal vestibulospinal function.93,94 To assist in determining whether a patient has cervical vertigo, the head-fixed-body-turned maneuver can be used to stimulate the neck without stimulating the labyrinth and can cause nystagmus.95 To illustrate the importance of afferent information from the neck to central vestibular structures, a simple example is as follows:

Brain-Stem Stroke and Vertebrobasilar Insufficiency

Establishing the diagnosis of a brain-stem stroke in a patient with dizziness is usually straightforward because there is a sudden onset of dizziness in addition to other neurologic symptoms, including alterations of vision, strength, coordination, or sensation.99 Establishing the diagnosis of vertebrobasilar insufficiency, however, is more problematic because symptoms are transient. Dizziness alone is infrequently the presenting sign of vertebrobasilar insufficiency.100 Moreover, with time, the diagnosis of vertebrobasilar insufficiency becomes increasingly unlikely in the absence of associated symptoms such as those listed in Table 6.101

Probably the most easily recognized central vestibular disorder is that of Wallenberg syndrome, which is caused by infarction of the lateral medulla (which includes the vestibular nuclei).102,103 Most often this disorder is due to ischemia in the distribution of the posterior inferior cerebellar artery (PICA).102,103 Damage to surrounding central nervous system structures produces a highly characteristic complex of symptoms and neurologic signs. A closely related syndrome is the anterior inferior cerebellar artery (AICA) syndrome.10

• Despite these obvious potential limitations, such patients often respond well to physical therapy. The reason for this somewhat paradoxical finding may be that patients with brain-stem strokes are likely to have unilateral lesions, with preserved function contralaterally. In addition, there may be sufficient redundancy in central vestibular pathways to allow partial recovery of balance function. There are several well-defined, genetically determined causes of cerebellar degeneration. Some patients have nonsyndromal adult-onset cerebellar degeneration.112 Older individuals may have symptoms and signs consistent with cerebellar dysfunction but no clear family history of spinocerebellar degeneration or any obvious etiology for cerebellar dysfunction such as excessive chronic ethanol intake, vasculitis, a paraneoplastic process, or a structural abnormality (eg, a Chiari malformation).113 Patients with cerebellar degeneration typically have a gradual decline in balance function that is especially prominent while walking on uneven surfaces.57, 114 These patients typically have no otologic symptoms, including no hearing loss, tinnitus, or vertigo.112 Physical examination may uncover abnormal ocular pursuit, improperly sized saccades, nystagmus (especially with downward gaze or with oblique downward and lateral gaze), incoordination of the arms and legs, a wide-based ataxic gait, and inability to tandem walk.112 These patients often have uneven stride lengths and decreased gait speed. Brain imaging may uncover shrinkage of the cerebellum, which may be particularly prominent in the midline.116

Patients with cerebellar degeneration are likely to experience problems with both the vestibulo-ocular system and the postural control system. Patients with disorders affecting the vestibulocerebellum may have difficulty with sensory integration, particularly visual-vestibular interaction.117 Patients may have difficulty performing rapid head movements and maintaining balance while walking, especially if simultaneously moving the head and attempting to walk on uneven surfaces. These patients' problems may be multifactorial because some syndromes (eg, Friedreich ataxia) may include peripheral vestibular involvement because of degeneration of the eighth cranial nerve.118

Patients with cerebellar degeneration may have associated brain-stem abnormalities if their degeneration syndrome is not localized solely to the cerebellum. Brain-stem dysfunction, in addition to cerebellar dysfunction, will increase disability related to abnormal corticospinal tract function.113 The clinical features of some of the more common ataxia syndromes are listed in Table 8.71 Some rare forms of cerebellar degeneration are associated with periodic vertigo, which may be responsive to treatment with acetazolamide.119

In our opinion, patients with cerebellar dysfunction, in general, should not receive vestibular suppressant medications because most of these medications will act to worsen cerebellar function. In our opinion, treatment regimens for such patients should include equalizing step lengths, narrowing step width, balance exercises on complaint surfaces, and enhancing somatosensory inputs to the lower extremities. Additionally, providing an assistive device such as a cane or walker may be helpful. In one study,57 improvement was noted in postural stability after a 6-week period of exercise in 2 cases of cerebellar disease. Patients with cerebellar disease are able to suppress visual stimulation over time and rely more on their vestibular and proprioceptive inputs.120 Gait instability and ataxia are the chief complaints of many older patients with cerebellar degeneration. Assessing the patient's gait speed and assessing the patient's step symmetry are 2 easy clinical methods for determining whether a patient's gait is improving.121

Statistics

a. Dizziness is the number three complaint of patients to their doctors. (headaches and LBP).

b. 2.5 % of all primary care visits.

c. Over the age of 70, the number one reason for seeking medical care.

d. These symptoms are contributory to incidence of falls.

e. Cost of related medical care per year exceed one billion dollars.

f. 50% of persons over the age of 65 will experience BPPV (Benign Proximal Positional Vertigo)

3. Function of the vestibular system

Gaze stability-see moving objects

VOR/VSR

Postural Stability- move on uneven surfaces

Orientation in space

Autonomic NS cerebral perfusion

9. Vestibular dysfunction

• Symptoms

  • Oscillopsia (Gaze stability)-assoc with head movement

  • Dysequilibrium

  • Abnormal sense of movement-spinning/tilting/disorientation

• Signs

  • Decrease visual acuity during head movement with increased speed related to decrease acuity

  • Ataxia dys-coordination

  • Imbalance-muscle instability

• Causes

  • Otologic (inner ear):BPPV, Menier’s

  • Neurological: CVA, cerebellar

  • Medical: medications, Cerebral vascular compromise

  • Nonlocalized: 65% unknown etiology, post trauma

  • Aging: degeneration, decompensation, sensory and musculoskeletal changes

  • Head Injury: temporal bone fracture

  • MVA: BPPV, cervicogenic dizziness secondary to upper cervical spine irritability or whiplash which compromises the autonomic system.

  • Central Lesions: MS, CVA, cerebellar disease

  • Migraines: with aura, without HA, HA without aura

Vestibular rehabilitation focuses on compensation by facilitation of a normal response to the permanent vestibular lesion

Compensation – Static

Regeneration and re-balancing of resting activity in the vestibular nucleus

- Intrinsic property of the neurons

- neurochemical influences

- synaptic changes

Unilateral damage of the inner ear can be compensated on the opposite side through its series of canals and their angle and the brains ability to interpret these signals

Compensation – Dynamic

Reprogramming of eye movements and postural responses to movement

Requires movement and exposure to stimuli that challenges the system

Independent of static compensation

Types of Compensation treatment

VOR/VSR Adaptation

Habituation

Substitution Strategies

Compensation Adaptation

Capability of the vestibular system to make long term changes in the neuronal response to head movement

VOR= Vestibular ocular response produces compensatory eye movements in response to head mvt.

Amplitude and speed (walking to running)

Opposite direction

Allows for stable gaze during head movements.

Because the visual system can be taught to fixate to stop the nystagmus by slowly increasing the speed

VSR=Vestibular spinal response kept the body upright in response to perturbations by stabilizing the head.

Vision

Vestibular

Somatosensory

Visual control of balance object vs self motion

Goals of adaptation

• reducing retinal slip

• improving postural stability

• decreasing symptoms

Compensation Habituation

Long term reduction of a response to a noxious stimulus (specific movement) brought about by repeated exposure to the provocative stimulus.

• Therefore desensitizing the patient to the movement.

• Rationale asymmetrical vestibular function leads to sensory mismatch which leads to symptom provocation

• This has a long term effect even if they don’t have exposure to the event to maintain

Compensation Substitution

The substitution of alternative strategies to replace the lost or compromised function.

Identification of Problems

Diagnostic Services

Team work can help determine if there is a vestibular deficit or dysfunction

Deficit= vestibular hypofunction

Dysfunction=episodic events, positional vertigo

Identification of Problems

Not all causes of dizziness are due to vestibular dysfunction

Not all causes of dizziness are treatable with vestibular rehab

Treatment is symptom driven rather than determined by diagnosis

Vestibular may be only one component of the patient’s problem

Other systems need to be considered in the evaluation and management

Referral Considerations

Vestibular rehab is more beneficial in patient’s with stable vestibular function rather than episodic events and when symptoms are provoked by movements, positions or environmental situations

Physical therapy complements the treatment of Vestibular disorders. Supports traditional medicine rather than supplanting it. Proven efficacy of treatment in Vestibular dysfunctions. Patient’s who are provided with an accurate functional diagnosis and application of appropriate diagnosis- based treatment strategy will have great success of return to prior level of function.

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