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Introduction
Human balance function depends on sensory inputs from the vestibular, prop-
rioceptive, and visual systems as well as proper integration of those inputs in
the central nervous system (CNS). Control of movements requires the motor
centres to accurately process the sensory information and transmit the neces-
sary commands to the appropriate muscles. Both structural and functional
deteriorations in all of these systems have been reported with increasing age.
The brainstem, cerebellum, and higher cortical structures within the CNS all
undergo age-related degenerative changes 1. These include decrease in the
number of neurons, loss of myelination, decrease in the number of Purkinje
cells, and other neuronal changes. Vertigo, dizziness and imbalance are the
main symptoms of vestibular disorders. These symptoms can lead to physical
consequences such as reduced postural control and falls and to psychological
and psychiatric consequences. Vertigo and dizziness are not synonymous with
each other, although they are often used interchangeably. The two terms cover
a number of multisensory and sensomotor syndromes of various aetiologies
and pathogenesis disorders of perception (dizziness /vertigo), gaze stabilisa-
tion, postural control and the vegetative system are related to the main func-
tions of the vestibular system. Vertigo refers to true spinning or movement of
the environment and indicates an imbalance of tonic vestibular signals, either
centrally or peripherally. Dizziness is one of the most frequent complaints in
a medical office, for both primary and specialised care. The term dizziness
encompasses a large spectrum of symptomatology dizziness is a nonspecific
term that describes an unpleasant sensation of imbalance or altered orienta-
tion in space. Dizziness usually refers to lightheadedness, presyncope, vertigo,
motion sensitivity, imbalance, anxiety, or just not feeling well. The prevalence
Pacini
Editore Arrivato in Redazione il 18/5/2011. Accettato l8/6/2011.
Medicina Corrispondenza: Rocco Galimi, Department of Neurology, Local Health Unit of Valtellina and
Valchiavenna, Sondalo Hospital, via Zubiani 33, 23035 Sondolo (SO), Italy E-mail: glrocco@
tiscalinet.it
Vertigo and dizziness in the elderly: evaluation and assessment 245
older people have at least one chronic medi- tibular neuritis is spontaneous (i.e., present in
cal condition, and most of those disorders can primary gaze) for at least the first several hours
contribute to or even cause types of dizziness. of symptoms. Following this initial time period,
Visual acuity, vestibulo-ocular reflex gain, and the nystagmus may only be identified during
sensory nerve action potential amplitude inevi- gaze testing (i.e., having the patient look to each
tably decline with age. Probably resulting from side) or if visual fixation is blocked. The exam-
these changes, measures of balance show grad- iner should closely inspect saccade velocity and
ual deterioration with age as well15. accurance. First it is necessary to observe spon-
taneous saccade triggered by visual or audito-
ry stimuli. Then the patient is asked to glance
Physical examination back and forth between two horizontal or verti-
cal targets (eg. slowing of horizontal saccade is
All components of the balance system should be generally observed in brainstem lesions; these
examined, including the peripheral vestibular is most often a dysfunction of ipsilateral para-
system, central vestibular system, visual system, median pontine reticular formation, and slow-
proprioception, and the interactions between ing vertical saccades indicates a midbrain lesion
these systems. Physical examination is particu- in which the rostral interstitial medial longitu-
larly important in the evaluation of dizziness dinal fascicle is involved. In the course of the
in the elderly because in some settings such as clinical examination of eye movement with an
nursing homes, extensive laboratory tests may examination flashlight, one should ensure that
not be available. An otoscopic examination is patient has full ocular ductions and determine
important. Abnormalities possibly encountered the effect of gaze on the spontaneous nystag-
include middle ear effusions, tympanic mem- mus, or if no spontaneous nystagmus is present
brane perforations, cholesteatoma, and neo- then look gaze-evoked nystagmus. Gaze-evoked
plasms. A typical physical examination consists
nistagmus can only be clearly identified when
of neurologic, neurotologic, and general medi-
the patient fixates with both eyes (eg. horizontal
cal examination 16. Neurological examination:
gaze-evoked nystagmus can indicate a structural
any clearcut central neurological signs in the
lesion in the area of the brainstem or cerebel-
presence of a neuro-otological syndrome make
lesion localisation relatively easy, particularly lum, and vertical gaze-evoked nistagmus is ob-
when there is brainstem involvement. Nystag- served in midbrain lesions involving the intersti-
mus can be defined as periodic, most often in- tial nucleus Cajal). Restricted upgaze is common
voluntary eye movements that normally consist in the elderly subjects but complete loss of up
of a slow (causative or pathological) phase and gaze o slowed vertical saccades indicate pathol-
a quick eye phase, which brings the eye back to ogy within the midbrain. The head impulse test
the initial position. In the clinical examination is a test for the vestibulo-ocular reflex (VOR). To
the physician should at first try to differentiate test the horizontal VOR, the examiner holds the
between peripheral vestibular and central ves- patients head between both hands, asks him
tibular forms of vertigo. The first step is clinical to fixate a target (on examiner nose) in front
examination of the eyes in nine different po- of his eyes, and rapidly turns the patient head
sitions to determine ocular alignment, fixation horizontally on the left and then to the right.
deficits, nystagmus, range of movement, and When the VOR is intact, thrusting the head to
disorders of gaze-holding ability. In primary eye the side will cause an immediate compensatory
position, one should first look for periodic eye conjugate eye movement in the opposite direc-
movements such as nystagmus or saccade in- tion such that the patient maintains fixation on
trusion. An important pattern of spontaneous the examiner at full time. The head impulse test
nystagmus to recognize is peripheral vestibular is particularly helpful in identifying lateral or bi-
nystagmus (eg. patients with vestibular neuritis lateral impairment of the VOR at bedside17. The
in the acute phase, they will exhibit a sponta- peripheral sensory examination is important be-
neous nystagmus with the fast phase beating cause a peripheral neuropathy can cause non
toward the opposite ear), witch is readily appar- specific dizziness or imbalance. Finger pointing
ent in an caute disorders as a horizontal greater test, and rapid alternating movements will assess
than torsional, unidirectional nystagmus that extremity coordination. Indeed, coordination in
can suppresed with fixation. Nystagmus in ves- patients with dizziness, because disorders char-
Vertigo and dizziness in the elderly: evaluation and assessment 247
acterized by ataxia can present with the clinical problems, specialized equipment may be needed
symptom of dizziness. to safely perform the procedure. Positional testing
can also trigger central type of nystagmus, usually
persistent downbeating (eg. Chiari malformation
Positional testing or cerebellar atassia)2021.
head impulse or head thrust test: the examiner history of headaches or a family history of mi-
holds the patients head and asks him to fixate graines 27. The variability of symptom duration
on her nose (Fig.2). The examiner then delivers in patients with MAV, with dizziness lasting from
a discrete, low amplitude (15-20u), but very fast, several hours to even a whole day, may explain
head thrust to one side. If the patients vestibular- why there might be some difficulty in properly
ocular reflex (VOR) is intact then, when the head distinguishing between this entity and cases of
is rotated, the eyes will remain fixated on the ex- vestibular neuritis.
aminers nose. If the VOR is unilaterally impaired
then, when the head is rotated the patients eyes
will momentarily lose their fixation on the exam-
iners nose (Fig.2). Indeed, in the acute setting Recurrent spontaneous vertigo
head impulse test (eg. no catch-up saccade) is the
only bedside test that can reliably distinguish an Mnires disease is the prototypical disorder
mPICA infarct from vestibular neuritis when the characterized by recurrent spontaneous epi-
cerebellar examination is otherwise normal 23-25. sodes of dizziness. Mnires disease is clinically
Although itself not life threatening, distinguish- characterised by recurrent spontaneous attacks
ing vestibular neuritis from stroke for example, is of vertigo, fluctuating hearing loss, tinnitus and
essential not only to avoid missing a serious di- aural fullness. Its incidence varies between 7.5
agnosis, but also to avoid over-investigation and per 100,000 to 160 per 100,000 persons 28. Pa-
inappropriate lifelong treatment for secondary tients reporting recurrent vertigo attacks lasting
stroke prevention. Large PICA territory cerebel- hours. Transient ischemic attacks (TIA) should
lar infarction can cause brainstem compression, be a concern in the patient who presents with
hydrocephalus, cardiorespiratory complications, new onset recurrent spontaneous attacks of diz-
coma, and death. Vestibular neuritis is presunted ziness. TIA generally lasts for minutes, less than
to be due to reactivation of latent herpes simplex is typical for Mnires disease. Recurrent spon-
1 in the vestibular ganglion 26. Vestibular neuri- taneous attacks of dizziness is often the initial
tis affects adult most often between 30 and 60 symptom of an impending basilar artery occlu-
years of age. Symptom and clinical sign of the sion29. Transient ischemia should be a leading
acute unilateral labyrinthine deficit are sponta- concern when the patient reports recent onset
neous nystagmus, with quick phase and rota- brief attacks, particularly if the attacks are in-
tory vertigo to unaffected side, and deviation by creasing in frequency (i.e., a crescendo pattern).
a tendency to fall, ocular torsion, and deviation In patients with recurrent attacks of vertigo, ro-
of the subjective visual vertical and the subjec- tational vertebral artery occlusion, migrainous
tive straight-ahead to affected side. Additionally, vertigo and vestibular paroxysmia syndromes
it is possible that some practitioners may confuse should be suspected.
vestibular neuritis with other diagnoses, includ-
ing migraine-associated vertigo (MAV). MAV is
most often seen in patients having some prior Recurrent positional vertigo
The patient complaing of recurrent episode of
Fig. 2. The head thrust test assesses the vestibular ocular re- vertigo triggered by certain head movements
flex. likely has BPPV, but this is not the only possi-
bility. In acute presentations, patients are often
more frightened by symptoms than debilitated
by them. It is important to recognize this cause
because it can be readily treated at the bedside
and because identification of the key features is
the most effective way to exclude a central nerv-
ous system cause of positional dizziness. The
most common triggers for BPPV episodes are
extending the head back to look up (top shelf
vertigo), turning over in bed, or getting in and
out of bed. The BPPV is particularly common in
older people patient, characteristics associated
Vertigo and dizziness in the elderly: evaluation and assessment 249
with BPPV are older age, history of head trau- rologic signs, including dysarthria, numbness of
ma, inner ear surgery, other inner ear disease the face, hemiparesis, headache, diplopia, visual
and prolonged recumbency. field defects, blindness, dysphagia, ataxia, and
drops attacks, may also be present. When symp-
toms are subacute but rapidly progressive, an
Dysequilibrium autoimmune ataxia, post-infectious cerebellitis
paraneoplastic disorder, or even the Brownell
Dysequilibrium is an imbalance or unsteadiness Oppenheimer variant of CreutzfeldtJakob dis-
while standing or walking and it is caused by a ease should be considered. The most common
variety of factors. Elderly walking performance type of imbalance in older people is a gradual
then starts to decline and the elderly slow down onset with slow progression (eg. cerebellar atax-
gradually. Many individuals suffer from imbal- ia, extrapyramidal features, spasticy or peripheral
ance, and because the brain is so good at com- neuropathy). Other disorders that cause imbal-
pensating for things, imbalance typically goes un- ance are leukoaraiosis, normal-pressure hydro-
noticed until a fall actually occurs. Many elderly cephalus (NPH), and large-fiber peripheral neu-
patients present with the symptom of imbalance, ropathy. Some older people with confluent white
rather than spinning or an abnormal head sen- matter hyperintensities (leukoaraiosis) describe
sation. If the patient is complaining of balance lightheadedness in addition to imbalance while
problems, the single-leg stance (SLS), Romberg, upright. In NPH, there is a triad of symptoms
and tandem Romberg tests are also performed. consisting of dementia, imbalance, and urinary
Bohannon and associates have found that SLS incontinence, with communicating hydrocepha-
times significantly decrease as people get old- lus found on computed tomography (CT) or MRI
er30. When imbalance is acute, stroke of cerebel- of the head31. Non-vestibular imbalance, defined
lum is the leading concern. Moreover, patients as imbalance that is not due to an inner ear or
with cerebellar hemispheric strokes not also in- vestibular nerve disorder, can be very frustrating
volving the brainstem may complain of vertigo to the clinician, because the symptoms are often
without any other symptoms. Episode of imbal- vague and the vestibular test results are normal.
ance may be caused by vertebro-basilar insuf- In elderly individuals, there is progressive de-
ficiency (VBI). VBI results in transient ischemia cline in muscle bulk, joint range of motion, and
of the posterior cerebral circulation, resulting in reflex time32. Increased exercise can reduce the
vertigo usually lasting minutes. Additional neu- rate of this decline.
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