Read RX_ISSUE.PM5 text version

Central vertigo

Dr Shamsher Dwivedee

Department of Neurology, Max Healthcare, New Delhi

Introduction

Vertigo is an illusory or hallucinatory sense of movement of the body or environment, most often a feeling of spinning. It may represent either physiologic stimulation of pathological dysfunction in any of the three systems controlling spatial orientation and posture-vestibular system, the visual system (retina to occipital cortex) and the somatosensory system that conveys peripheral information from skin, joint and muscle receptors

central process. For example, an occlusion of the anterior inferior cerebellar artery can produce both vertigo and hearing loss that mimics neurolabyrinthitis, except that concomitant brain stem or cerebellar signs are almost always present. The absence of additional neurologic findings, however, does not exclude the possibility of a stroke limited to the inferior cerebellum. Dysmetria, a major finding of the cerebellar system, may be minimal or absent after an inferior cerebellar stroke.

Symptoms and signs

The patient's history is critical in the evaluation of the patient with dizziness. Ask the patient to describe their symptoms by using words other than 'dizzy'. The rationale for using other words is that patients may use dizzy nonspecifically to describe vertigo, unsteadiness, generalized weakness, syncope, presyncope, or falling. A critical distinction is differentiating vertigo from nonvertigo. Vertigo is the true rotational movement of self or the surroundings. Nonvertigo includes light-headedness, unsteadiness, motion intolerance, imbalance, floating, or a tilting sensation. This dichotomy is helpful because true vertigo is often due to inner ear disease, whereas symptoms of nonvertigo may be due to CNS, cardiovascular, or systemic diseases. Sudden onset and vivid memory of vertiginous episodes are often due to inner ear disease, especially if hearing loss, ear pressure, or tinnitus is also present. Gradual and ill-defined symptoms are most common in CNS, cardiac, and systemic diseases. The time course of vertigo is also important. Episodic true vertigo that lasts for seconds and is associated with head or body position changes is probably due to benign paroxysmal positional vertigo (BPPV). Vertigo that lasts for hours or days is probably caused by Ménière disease or vestibular neuronitis. Vertigo of sudden onset that lasts for minutes can be due to brain or vascular disease, especially if cerebrovascular risk factors are present. Central vertigo secondary to brainstem or cerebellar ischemia is often associated with other brainstem characteristics, including diplopia, autonomic symptoms, nausea, dysarthria, dysphagia, or focal weakness. Patients with cerebellar disease are frequently unable to ambulate during acute episodes of vertigo. Patients

Physiological vertigo

When, in normal individuals, there is a mismatch between the three stabilizing sensory systems it can cause vertigo. Some conditions causing this include sea sickness-when the vestibular system is subjected to unfamiliar head movements, unusual or extreme head and neck positions, following spinning, height vertigo etc. Space sickness, a frequent transient effect of active head movement in the weightlessness of zero gravity environments is another example of physiological vertigo.

Pathological vertigo

This result from lesions is the visual/somatosensory or vestibular system. Visual vertigo is caused by new/incorrect spectacles or by the sudden onset of extraoccular muscle paresis with diplopiain these cases CNS compensation rapidly counteracts the vertigo. Somatosensory vertigo is unlikely to occur in isolation, it is usually due to peripheral neuropathy/myelopathy that reduced sensory input. The most common form of pathological vertigo is that due to vestibular dysfunction involving either the end organ (labyrinth), nerve or the central connections. Vertigo is often associated with nausea, jerk nystagmus, postural unsteadiness, and gait ataxia. Patients also tend to hold their head still as any head movement precipitates vertigo. Additional neurologic findings on examination differentiate a peripheral vestibular lesion from a brain stem disorder. The presence of cranial nerve signs, motor weakness, prominent dysmetria, sensory changes, or abnormal reflexes suggests a

Correspondence: Dr Shamsher Dwivedee, Senior Consultant, Department of Neurology-Mobile: 9810084300; Email: [email protected]

11

Central vertigo / Dwivedee

with peripheral vertigo can usually ambulate during episodes and are consciously aware of their environment. A history of headaches, especially migraine headaches, can be associated with migraine-related dizziness. Previous viral illness, cold sores, or sensory changes in the cervical C2-C3 or trigeminal distributions usually indicate vestibular neuronitis or recurrent episodes of Ménière disease. Dysdiadochokinesis and gait ataxia during episodes are more likely due to cerebellar diseases, especially in the elderly population. Sensory and motor symptoms and signs are usually associated with CNS diseases. The history should include a review of systems (especially head trauma and/or ear diseases) and screening for anxiety and/or depression. History of prescription medicines, over-the-counter medications, herbal medicines, and recreational drugs (including smoking and alcohol) can help to identify pharmacologically induced syndromes. The most common causes of peripheral vertigo include BPPV, vestibular neuronitis, Ménière disease, and immune-mediated inner ear disease. The most common cause of central dizziness is migraine, frequently referred to as vestibular migraine or migraine-associated dizziness. Other central causes include demyelination, acoustic tumors, or cerebellar lesions. Signs and Symptoms that help differentiate central from peripheral vertigo.

Sign or symptom Peripheral (Labyrinth) Central (Brainstem or cerebellum) Bidirectional or unidirectional Common

Approach to a patient

In patients with dizziness, general examination should emphasize vital signs, supine and standing blood pressure measurement, and evaluation of the cardiovascular and neurologic systems. Examine the ears for visible external and/or middle ear infection and/or inflammation. Test hearing of the patient by using a tuning fork or by whispering. Examine the neck for range of motion. However, specific examination of the vestibular system, beyond the ears, nose, throat and neurologic examination, is fundamental to the evaluation of the patient with dizziness. Though a detailed history keeping in mind the above points often points towards a diagnosis, it may at times help to use certain procedures to recreate/simulate either cephalic ischemia or vestibular dysfunction. Cephalic ischemia is obvious if the dizziness is duplicated during maneuvers that produce orthostatic hypotension. Further provocation involves the Valsalva maneuver which decreases the cerebral blood flow and will also reproduce symptoms of cerebral ischemia. Rapid rotation and abrupt cessation is the simplest test to provoke vestibular dysfunction. Those patients with symptoms pointing towards positional vertigo should specifically be examined keeping in mind the latency (time between attaining the head position and onset of symptoms), the fatigability (disappearance of symptoms with maintenance of offending position), habituation (lessening of symptoms with repeated trials), intensity of vertigo and the reproducibility (likelihood of symptom production during any examination session) of the symptom. Features Latency Fatigability Habituation BPPV 3-40s Yes Yes Severe Variable Central None; immediate vertigo and nystagmus No No Mild Good

Direction of associated Unidirectional; fast nystagmus phase opposite to the lesion Purely horizontal Uncommon nystagmus without torsional component Vertical or purely torsional nystagmus Visual fixation Severity of vertigo Direction of spin Direction of fall Never present

Maybe present

Intensity of vertigo Reproducibility

Inhibits nystagmus and No inhibition vertigo Marked Towards fast phase Towards slow phase Often mild Variable Variable May be Chronic Usually absent Extremely common

Investigations for pathological vertigo

In the course of evaluating patients with vestibular and balance disorders, additional tests that are commonly considered include audiometry, vestibular tests, blood tests, CT, and MRI. These tests, especially vestibular tests, must be tailored according to the history and physical findings. In case a central pathology is suspected, MR imaging of the head is mandatory. The yield of MRI in patients younger than 50 years is low (<1%). The incidence of an acoustic tumor or other brainstem and posteriorfossa lesions also is low. Clinical judgment, careful neurotologic examination, and audio and vestibular studies are often helpful in obviating MRI. 12

Duration of symptoms Finite (minutes, days, weeks) but recurrent Tinnitus and/or deafness Often present Associated central abnormalities Common causes None

Infection (labyrinthitis), Vascular, Menieres, neuronitis, demyelinating ischemia, trauma, toxin neoplasm

Central vertigo / Dwivedee

Typical BPPV requires no investigation if the clinical history, signs and symptoms point towards the specific diagnosis. For ascertaining the vestibular dysfunction, tests are performed to demonstrate an abnormality, establish the side of the abnormality and distinguish between the central and peripheral etiologies. The most common vestibular tests are ENG, rotating chair test or sinusoidal harmonic acceleration (SHA), and computerized dynamic posturography (CDP). ENG testing Elecronystagmography (calorics) is a standard test, warm water and cold water are applied to the tympanic membrane and the slow-phase velocities of the resulting nystagmus from the two are compared. A velocity decrease from one side indicates hypofunction and an inability to induce nystagmus with ice water denotes a dead labyrinth. The standard ENG test battery is composed of saccadic, gaze, pursuit, optokinetic-eye movement, head-shake nystagmus, positional nystagmus, positioning nystagmus, and bithermal caloric Rotating chair test or sinusoidal harmonic acceleration (SHA) Barany introduced rotational testing in 1907. In clinical practice, the rotation test lagged behind the caloric test. However, with the advancement of computer technology, rotational chair-test systems were developed in the late 1970s and continue to evolve. They are now used in several vestibular testing laboratories. The test is used to evaluate the integrity of the vestibuleocular reflex (VOR) in the low-frequency (0.1-0.32 Hz) or highfrequency (1-4 Hz) ranges. The measured parameters are VOR gain, phase (latency), and symmetry. The test is most useful in determining residual vestibular function and the degree of central vestibular compensation. An alternative to the rotating chair test is the active headrotation test, which is used to evaluate VOR gain in the highfrequency range. This test is substantially less expensive and more practical than the chair test. Active head rotation involves recording head and eye position while the patient actively turns his or her head from side to side at progressively faster frequencies. CDP test Dynamic posturography has become an integral part of vestibular testing in many vestibular test centers. The clinical application of posturography in neurotology was introduced in the 1970s. CDP system consists of a computer-controlled platform and visual booth used to evaluate both sensory and motor components of balance. The sensory test is most clinically useful, especially in peripheral lesions, vestibular rehabilitation, and medico legal

cases. Posturography is not a substitute for a careful gait examination and probably is of more value in rehabilitation than in diagnosis.

Treatment

The treatment of acute vertigo consists of bed rest and vestibular suppressant drugs such as antihistaminics, tranquilizers with GABAergic effects, phenothiazines, or glucocorticoids. Some other treatments that may help include diuretics/low salt diet, antimigranous drugs etc. If vertigo persists beyond a few days, ambulation may be advised in order to induce the central compensatory mechanisms. Chronic vertigo of labyrinthine origin may be treated with systematized vestibular rehabilitation. Though BPPV is mostly self limited, specific repositioning exercise programs may help. The Epley procedure in particular helps to empty particulate debris in the posterior semicircular canal.

Self-treatment of benign positional vertigo (left)

Start sitting on a bed and turn your head 45° to the left. Place a pillow behind you so that on lying back it will be under your shoulders.

Lie back quickly with shoulders on the pillow and head reclined onto the bed. Wait for 30 seconds.

Turn your head 90° to the right (without raising it) and wait again for 30 seconds.

Turn your body and head another 90° to the right and wait for another 30 seconds.

Sit up on the right side.

This maneuver should be carried out three times a day. Repeat this daily until you are free from positional vertigo for 24 hours.

Comments

Prophylactic measures to prevent recurrent vertigo are variably effective. Antihistaminics are of limited value. 13

Information

RX_ISSUE.PM5

3 pages

Report File (DMCA)

Our content is added by our users. We aim to remove reported files within 1 working day. Please use this link to notify us:

Report this file as copyright or inappropriate

945500


Notice: fwrite(): send of 207 bytes failed with errno=104 Connection reset by peer in /home/readbag.com/web/sphinxapi.php on line 531