Vertigo and dizziness belong to the most common chief complaints when patients seek medical advice (1). Although dizziness and vertigo are overlapping entities and are sometimes used interchangeably they are not the same. Vertigo can be associated with a sensation of rocking or spinning and can in many cases be attributed to disorders of the peripheral or central vestibular system .Dizziness describes a more general discomfort without the erroneous perception of large- scale movements and can reflect vestibular as well as non-vestibular disorders. An individual may report dizziness when experiencing imbalance, e.g.in peripheral neuropathy due to diabetes, in Parkinson’s disease, cerebellar ataxia, arterial hypotension, depression, or anxiety (2).Vertigo can be either are action to stimulus, e.g. following un accustomed head movements as in a carrousel or on a ship, or the result of a discrepancy between visual and vestibular information, e.g.in a moving car or on an exposed mountain ridge. The most frequent cause of pathologic vertigo is an impairment of the vestibular system. Three semicircular canals and the otolithic apparatus in the bony labyrinth of the inner ear provide information about the position of the head in space. The eighth cranial nerve carries this information to the vestibular nuclei in the brainstem. Pathways to the spinal cord support postural stability. Closed connections to the eye muscles via the vestibular-ocular reflex (VOR) ensure stable images on the retina during head movements. Vertigo can be of peripheral origin, i.e. a problem of the labyrinth or the vestibular nerve, or of central origin, as a consequence of a lesion of the cerebellum or brainstem. Further, psychogenic vertigo can develop following organic vestibular disorders, or might develop as a comorbid condition of phobia or panic attacks (3).The visual and the somatosensory systems interaction contribute to postural stability. Impaired sensory functions or impaired between sensory systems can cause vertigo and dizziness. Patients may describe the complaints as light-headedness unsteadiness of gait, imbalance, perception of rotation, or anxiety (4). Vertigo and dizziness count among the most common complaints in outpatient practices (1) and affect a considerable part of adults of working age. With high lifetime prevalence and a high burden of disease, vertigo and dizziness can be severely disabling symptoms because of their high impact on daily life (5).Although most vestibular disorders are manageable, they are often under-and misdiagnosed in primary care. Psychiatric comorbidity such as anxiety, depression, panic disorders and agoraphobia may account for avoidance behavior, increased disability and increased health care utilization. Finally, vertigo and dizziness are specific and important risk factor for falls and injuries, especially in the aged. Still, epidemiological data on vertigo and dizziness is scarce and inconsistent. (6)
Definition of vertigo:
As an abnormal perception of movement of the environment and occurs due to the abnormality in sensory information from the eyes, limb proprioception and the vestibular system about a person position in space. And commonly arises from inappropriate input from the labyrinthine apparatus and is within the experience of most people, it is caused by labyrinthine disorder is usually short lived but it may recur, whilst vertigo arising from central disorder is often persistent and usually accompanied by other signs of brainstem dysfunction . (7)
Clinical features:
Clinical features depend on the underlying cause of symptoms so as a way to differentiate between causations it is necessary to know the following: (8)
1. If the symptom triggered by an event it could be post-traumatic or post-infective.
2. The time course of the symptoms and this can range from very brief episodes associated with a transient disturbance in the blood supply caused by increased platelet aggregation or lasting a few hours in a migraine or lasting many days in disabling vertigo.
3. If there are any other symptoms that occur with vertigo- like: palpitations in panic disorders, visual disturbance in a migraine, changes in hearing and tinnitus in inner ear disorders.
4. There are many factors that precipitate the symptom like turning in bed as in paroxysmal positional vertigo or looking upwards or even standing up from a sofa or a chair as in postural vertigo.
5. Vertigo can occur as a side effect of medications.
6. With increasing age the prevalence of the vertigo rises and the most common cause of presentation to the primary physician in people over 74 years old is dizziness.’
-vertigo due to peripheral lesions:
1. Benign Paroxysmal Positioning Vertigo:
This type of vertigo usually associated with changes in head positions often provoked by rolling over in bed and patient with this type of vertigo- suffering from recurrent spell lasting several minutes per spell The term "positioning vertigo" is more accurate than "positional vertigo" because it is provoked by changes in head position rather than by the maintenance of a particular posture, and the typical symptom of this type lasting for several days. There is a brief (10-15 sec) latency period following a head
movement before symptoms develop, and acute vertigo subsides
within 10-60 seconds, though the patient may remain imbalanced for
several hours. Constant repetition of the positional change leads to
habituation. Since some central nervous system disorders can mimic
BPPV (eg, vertebrobasilar insufficiency), recurrent cases warrant MRI
scanning of the head. In central lesions, there is no latent period,
fatigability, or habituation of the symptoms and signs. Treatment of
BPPV involves physical therapy protocols (e,g, the Epley maneuver or
Brandt-Daroff exercises), based on the theory that peripheral positioning
vertigo results from free-floating otoconia within a semicircular canal"(9)
2. VESTIBULAR NEURONITIS:
The second most common peripheral cause of Vestibular vertigo is vestibular neuronitis . Infection of the vestibular nerve results in nerve degeneration and may present bilaterally. Infection is most often thought to be of viral origin, usually from the herpes virus family. It may also result from bacterial invasion (e.g. Borrelia). It is believed that the superior vestibular nerve is more commonly involved secondary to its course throughout a long and narrower bony canal, making it more susceptible to compressive edema. The reported incidence of an upper respiratory infection prior to the development of vestibular symptoms varies from 23% to 100%.5
Patients present with complaints of sudden vertigo, lasting up to several days, often with vegetative symptoms. As this process affects only the vestibular. the Portion of the vestibulocochlear apparatus, there is an absence of cochlear symptoms. Vertiginous complaints gradually improve over days to weeks; however, an imbalance may persist for months after resolution of
acute disease. Recurrence is not uncommon and may occur several times per year. Physical examination is limited and should consist of audiometric evaluation and ENG. Patients may demonstrate nystagmus and caloric weakness on the affected side. Treatment is primarily supportive with the use of anti-emetics and anti-nausea medications. Vestibular suppressants should be used judiciously in the first few days of an acute attack. Prolonged use of these medications can delay recovery by inhibiting central compensation. Furthermore, early ambulation is paramount in the central nervous system’s ability to compensate and is therefore recommended as soon as tolerable. High-dose methylprednisolone has been shown to hasten recovery; however, prospective, randomized, double-blinded studies have failed to demonstrate added benefit from the use of antivirals (i.e. valacyclovir). (10)
3. Meniere’s Disorder:
M”ni”re’s disease (or endolymphatic hydrops) presents with tinnitus (low tone, roaring, or blowing quality), vertigo. Fluctuating low-frequency sensorineural hearing loss, and a sense of fullness in the ear. In this disorder, impaired endolymphatic filtration and excretion in the inner ear leads to distention of the endolymphatic compartment. Treatment lowers endolymphatic pressure. Although a low-salt diet (less than 1 to 2 g of salt per day) and diuretics (most commonly the combination of hydrochlorothiazide and triamterene [Dyazide]) often reduce vertigo, these measures are less effective in treating hearing loss and tinnitus. (11,12). In rare cases, surgical intervention, such as decompression with an endolymphatic shunt or cochlear capsulotomy, may be required when M”ni”re’s disease is resistant to
treatment with diet and diuretics. Ablation of the vestibular hair cells with an intratympanic injection of gentamicin also may be effective. Surgery usually is reserved for patients with severe, refractory M”ni”re’s disease. (13)
4. PERILYMPHATIC FISTULA: (14, 15, 16)
The results from an abnormal communication between the perilymphatic space and an intramembranous or middle ear communication are A perilymphatic or inner ear fistula. There are numerous causes, stapedectomy most commonly, and also head trauma, barotrauma, explosive blast, and physical exertion. Symptoms vary widely between individuals, according to the prevalence and severity of both vestibular and cochlear symptoms differing greatly. Diagnosis is made through a thorough history and physical examination. Patients may complain of disequilibrium after an increase in cerebrospinal fluid pressure (Hennebert’s sign) or exposure to loud noises (Tullio’s phenomenon). Physical examination may demonstrate a brief episode of nystagmus with positive pressure applied to the ear through pneumatic otoscopy (Fistula test) or an improvement in the audiogram after laying in Trendelenburg for 30 minutes (Fraser test). Initially, treatment is conservative, with bed rest, head elevation, laxatives, and serial audiograms and physical examinations to assess hearing loss and vertigo.
Surgical exploration is warranted in patients with persistent or worsening symptoms. sadly, surgical exploration is successful in identifying a fistula only half of the time(14). When a fistula is observed, it should be patched by the surgeon with a material of their preference (blood clot, fascia, fat).based on the study, vestibular complaints were reduced 83% to 94% of the time and hearing loss 13% to 49%.
5. Labyrinthitis:
Patients with labyrinthitis suffer from the acute onset of continuous, usually
severe vertigo lasting several days to a week, accompanied by hearing
loss and tinnitus. During a recovery period that lasts for several weeks,
vertigo gradually improves. The Hearing may return to normal or remain
permanently impaired in the affected ear. The cause of labyrinthitis is
unknown. Treatment consists of antibiotics if the patient is febrile or has
symptoms of a bacterial infection, and supportive care. Vestibular
suppressants are useful during the acute phase of the attack (eg,
diazepam or meclizine) but should be discontinued as soon as feasible to
avoid long- term disequilibrium from inadequate compensation. (9)
6. SUPERIOR SEMICIRCULAR CANALDEHISCENCE SYNDROME:
the superior semicircular canal dehiscence syndrome (SSCDS)is a result of a thin or dehiscent bone overlying the superior semicircular canal. Minor et al. theorized that this defect acts as a third window, moreover, to the round and oval windows, allowing transfer of pressure and sound into the vestibular system.(17)
This additional input is responsible for the clinical manifestations of the syndrome. Although the true incidence of this syndrome is unknown, one study showed that examination of cadaveric temporal bones revealed a dehiscent or markedly thin bone in 1.9% of specimens. This syndrome is characterized by vertigo induced by an increase in intracranial pressure or loud noise, chronic imbalance, tinnitus, and hyperacusis. Patients often refrain from noisy environments in an attempt to avoid vertiginous symptoms. Typically, patients do not demonstrate nystagmus on routine examination. They may, however, demonstrate Tullio and Hennebert signs and a positive fistula test, similarly to patients with a perilymph fistula. When the fistula test is performed, vertical-torsional nystagmus is evoked with slow waves directed away from the dehiscent labyrinth. This characteristic nystagmus may also be seen when patients are exposed to sound frequencies between 500 to2000 Hz with an intensity of 100 to 110 dB. In patients suspected of having SSCDS, high-resolution computed tomography is required to make a definitive diagnosis. (18)
-vertigo due to central lesions:
Central nervous system disease that causes vertigo include disease of the
brainstem. The vascular nervous system causes malformations, tumor of the
brainstem and cerebellum ,multiple sclerosis, , vertebrobasilar migraine.
Vertigo of central origin often becomes disabling. The associated
nystagmus is often non-fatigable, the orientation of this type of vertigo is
vertical rather than horizontal, without latency, and unsuppressed by
visual fixation. ENG is useful in documenting these characteristics. There
are commonly other signs of brainstem dysfunction (eg, cranial nerve
palsies; motor, sensory, or cerebellar deficits in the limbs or of increased
intracranial pressure. The Auditory function is generally spared. The
underlying cause should be treated.(9)
1. Vestibular Epilepsy: It is a rare cortical vertigo syndrome secondary to focal epileptic discharges in either the temporal lobes or the parietal association cortex. Scanty information is available on this condition in recent literature and great care need be taken to diagnose this condition. A new clinical sign of vestibular epilepsy is skew deviation of eyes with nystagmus during attacks.(19)
2. Transient ischemic attacks:
3. Multiple Sclerosis: Patients with multiple sclerosis may suffer from episodic and chronic imbalance. Hearing loss in this disease is most commonly unilateral and of rapid onset. Spontaneous recovery may occur.(9)
4. Cerebellopontine Angle Tumors
Treatment of vertigo:
Medications are most useful for treating acute vertigo that lasts a few hours to several days (20, 21).They have limited benefit in patients with benign paroxysmal positional vertigo because the vertiginous episodes usually last less than one minute. Vertigo lasting more than a few days is suggestive of permanent vestibular injury (e.g., stroke), and medications should be stopped to allow the brain to adapt to new vestibular input.
A wide variety of medications is used to treat vertigo and the frequently concurrent nausea and emesis. These medications exhibit various combinations of acetylcholine, dopamine, and histamine receptor antagonism. The American Gastroenterological Association recommends
anticholinergics and antihistamines for the treatment of nausea associated with vertigo or motion sickness (22). Gamma-aminobutyric acid (GABA) is an inhibitory neurotransmitter in the vestibular system. Benzodiazepines enhance the action of GABA in the central nervous system (CNS) and are effective in relieving vertigo and anxiety. Older patients are at particular risk for side effects of vestibular suppressant medications (e.g., sedation,
increased risk of falls, urinary retention). These patients also are more likely to experience drug interactions (i.e., additive effects with other CNS depressants).(20)
Summary
1. Vertigo: is defined as an abnormal perception of movement of the environment and occurs because of an abnormality in sensory information from the eyes, limb proprioception and the vestibular system about a person's position in space.
2. Causes of vertigo:
A. a. due to peripheral lesions and this type include many diseases such as labyrinthitis, benign paroxysmal vertigo and others.
B. Due to central lesions
2. possible treatment for this disease depends on the underlying cause
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