Vertigo
Introduction and Facts
Vertigo comes from Latin terms, namely "vertere," which means spinning, and "igo" which means condition. Vertigo is an illusion of movement. Most often is a feeling or sensation of the body turning against the environment or vice versa; the sense of the environment around us is felt spinning. Vertigo is also thought of as a linear displacement or tilted, but these symptoms are less common. This condition is a vital symptom of a vestibular system disorder and is sometimes a symptom of a labyrinthine disorder.
However, it is not uncommon for vertigo to be a symptom of other systemic disorders, such as drugs, hypotension, endocrine diseases, etc. In contrast to vertigo, dizziness or lightheadedness is a common complaint resulting from a feeling of disorientation, which is usually influenced by the positional perception of the environment. Dizziness and dizziness have four sub-types: vertigo, dys-equilibrium without vertigo, presyncope, and psychophysiological dizziness.
Pathophysiology
The etiology of vertigo may be due to abnormalities of the vestibular, visual, or proprioceptive systems. The labyrinth is an organ for equilibrium consisting of 3 semicircular canals associated with stimulation of angular acceleration and the utricle and saccule, which are related to stimulation of gravity and vertical acceleration.
Stimuli travel through the vestibular nerve to the vestibular nucleus in the brain stem and then to the medial fasciculus cranial part of the oculomotor muscle and then leave the vestibulospinal tract, excitatory stimuli to the extensor muscles of the head, extremities, and back to maintain an upright position of the body. The cerebellum then receives afferent impulses and serves as a center for integration between oculovestibular responses and posture. Vestibular function was assessed by evaluating the oculovestibular reflex and nystagmus intensity due to rotational and caloric stimulation in the labyrinth region.
The oculovestibular reflex is responsible for fixing the eye on a stationary object while the head and body are in motion. Nystagmus is eye movement seen in response to stimulation of the labyrinth and the retrocohlear vestibular pathway, or the central vestibulo-cohlear pathway.
Vertigo itself may be a disorder caused by peripheral vestibular disease or central dysfunction; therefore, it is generally divided into peripheral and central vertigo. If it is not related to movement, vertigo may be caused by a disorder of the peripheral vestibular system, which accounts for nearly 85% of cases.
The term peripheral implies that this disorder or disorder can occur either in the end-organs of the utricle or semicircular canal or in the peripheral nerves. Central vertigo lesions can occur in areas of the pons, medulla, or cerebellum. Vertigo is only about 20% - 25% of cases of vertigo, but symptoms of balance disorders or dys-equilibrium can occur in 50% of cases of vertigo.
The causes of central vertigo vary, including ischemia or brainstem infarction as the most common cause, demyelinating processes such as multiple sclerosis, post-infectious demyelination, etc., tumors in the cerebellopontine area, cranial neuropathy, and tumors in the brain stem area, as well as other causes.
Some diseases or systemic disorders can also cause vertigo symptoms; the use of drugs such as anticonvulsants, antihypertensives, alcohol, analgesics, tranquilizers can cause vertigo complaints. Cardiovascular conditions, hypotension, presyncope, cardiac and non-cardiac, infectious diseases, endocrine diseases DM, hypothyroidism, vasculitis, and other systemic diseases such as anemia, polycythemia, sarcoidosis, and so on can cause vertigo complaints.
Neurotransmitters that contribute to the pathophysiology of vertigo, both peripheral and central, include cholinergic, monoaminergic, and glutaminergic neurotransmitters. Some antivertigo drugs work by manipulating this neurotransmitter so that vertigo symptoms can be suppressed.
Glutamate is the primary excitatory neurotransmitter in vestibular nerve fibers; this glutamate affects vestibular compensation through NMDA receptors (N-methyl-D-aspartate). Muscarinic acetylcholine receptors are found in the pons and medulla and cause vertigo complaints by affecting M2-type muscarinic receptors, while histamine neurotransmitters are found evenly in the central vestibular structure. Histaminergic receptors are located pre- and postsynaptically on the vestibular cells.
Clinical Symptoms and Complications
The presence of aura and neurological symptoms need to be considered, such as hearing loss, a feeling of fullness, pressure, or ringing. If there are complaints of tinnitus, is it continuous, intermittent, or pulsatile? Are there any brainstem symptoms or cortical disorders such as headache, visual disturbances, seizures, or loss of consciousness?
Diagnosis
The physical examination focused on the neurological evaluation of the cranial nerves and cerebellar function, for example, by looking at motor and sensory modalities, gait. Assessment of cerebellar function, namely by assessing the fixation of eye movements, the presence of horizontal nystagmus indicates a central vestibular disorder.
Examination of the auditory canal and tympanic membrane should also be performed to assess the presence of middle ear infection, malformations or the presence of cholesteatoma and a perilymphatic fistula. A hearing acuity test may also be performed. balance test
Clinical examination, whether carried out in the emergency department or another examination room, may provide a lot of information about complaints of vertigo. Some clinical assessments that are easy to do to see and assess balance disorders include:
a. Romberg test. In this test, the patient stands with one foot in front of the other; one heel is in front of the toes of the other in tandem. An average person can stand in this Romberg stance for 30 seconds or more. Standing on one leg with your eyes open then closed is a sensitive screening for balance disorders. If the patient can stand on one leg with his eyes closed, it is considered normal.
b. Step test in place of stepping test. Patients must walk in place with their eyes closed, as many as 50 steps at an average walking speed, and cannot move from their original location. This test can detect disorders of the vestibular system. Suppose the patient moves more than 1 meter from his original place or his body rotates more than 30 degrees from its original state. In that case, it can be estimated that the patient has a vestibular system disorder.
c. Past-pointing misstatement test. The patient is instructed to stretch his arm, and the patient's index finger is instructed to touch the examiner's index finger. Then the patient is asked to close his eyes, raise his arms high vertically and then return to the original position. In vestibular disorders, there will be misdirection.
d. Nylen-Barany or Hallpike maneuver. To cause vertigo in patients with disorders of the vertibular system, Nylen-Barany or Hallpike maneuvers can be performed. In this test, the patient sits on the examining bed. Then he lay down until his head hung on the edge of the bed at an angle of about 30 degrees below the horizon, head turned to the left. The test is then repeated with the head looking straight and repeated with the head turned to the right. The patient must keep his eyes open so that the examiner can see the presence or absence of nystagmus. Patients were asked whether they felt the onset of vertigo symptoms.
e. Calorie Test. This caloric test was carried out after the examination. It was confirmed that there was no perforation of the tympanic membrane or cerumen wax by adding 1 mL of water at a temperature of 300C and then evaluating in terms of nystagmus, complaints of dizziness, eye fixation disorders.
Other examinations can also be performed, but other supporting assessments should also be carried out if necessary to assess vestibular function and balance. Some of the supporting tests include laboratory tests:
a. Complete blood count, glucose tolerance test, blood electrolyte, calcium, phosphorus, magnesium, and thyroid function tests.
b. Investigations with CT-scan, MRI, or angiography are performed to assess the organ's structure and the presence of blood flow disturbances, for example, in complaints of central vertigo.
Medication and Treatment
The management of vertigo depends on the duration of the complaint and the discomfort of the symptoms, and the underlying pathology. In the case of vertigo, some specific actions can be recommended to reduce vertigo complaints. For example, in Meniere's disease, reducing salt intake and using diuretics are suggested to minimize endolymphatic pressure. As for BPPV (benign paroxysmal positional vertigo) may be possible to try the bedside maneuver.
Medical Management.
In general, medical management has the following main objectives:
i eliminate vertigo complaints
ii improve vestibular compensation processes
iii reduce neurovegetative symptoms or psychoactive symptoms.
Some classes of drugs that can be used to treat vertigo include:
a. Anticholinergics was the first drug used to treat vertigo, and the most widely used are scopolamine and homatropine. The two preparations can also be combined into one antivertigo practice. These anticholinergics act as vestibular suppressants via muscarinic receptors. The oral administration of this anticholinergic gives an average effect of 4 hours, while the symptoms of side effects that arise are main symptoms of central muscarinic receptor inhibition such as memory impairment, and confusion, especially in the elderly population, as well as signs of peripheral muscarinic inhibition, such as visual disturbances, dry mouth, constipation, and urinary disturbances.
b. Antihistamines. Histamine-1 receptor blockers H-1 blockers are currently the most widely prescribed antivertigo for vertigo cases and include: diphenhydramine, cyclizine, dimenhydrinate, meclozine, and promethazine.
The mechanism of antihistamines as vestibular suppressants is not widely known, but they are thought to affect central histamine receptors. Antihistamines may also have the potential to prevent and improve motion sickness. Sedation is the main side effect of giving histamine-1 H1-blockers. This drug is usually given orally, and the duration of action varies from 4 hours, for example cyclinin, to 12 hours, for example: meclosin
c. Histaminergic. This drug is represented by betahistine which is used as an antivertigo in some European countries, but not in America. Betahistine is a histamine precursor. The antivertigo effect of betahistine is thought to have a vasodilating effect, improving blood flow in the microcirculation in the middle ear and vestibular system. On oral administration, betahistine is well absorbed; peak levels are reached in about 4 hours. Side effects are relatively rare, including complaints of headaches and nausea.
d. Antidopaminergic is usually used to control complaints of nausea in patients with vertigo-like symptoms. Most of these antidopaminergics are neuroleptics. The effect of antidopaminergic on the vestibular is not known with certainty. Still, it is thought that the results of anticholinergics and H1 antihistamines on the peripheral vestibular system are thought to be. The duration of action of these neuroleptics varies from 4 - 12 hours. Some dopamine antagonists are used as antiemetics, such as: domperidone and metoclopramide. The side effects of these dopamine antagonists are mainly orthostatic hypotension, somnolence, and some complaints related to extrapyramidal symptoms, such as tardive dyskinesia, parkinsonism, acute dystonia, etc.
e. Benzodiazepines, which are GABA modulators, bind to specific sites on the GABA receptor. The effect as a vestibular suppressant is thought to be through a central mechanism. But as with sedative drugs will affect the compensation of the vestibular. The main pharmacological effects of benzodiazepines are sedation, hypnosis, anxiety reduction, muscle relaxation, anterograde amnesia, and anticonvulsant effects. Some drugs from this class that is often used are lorazepam, diazepam, clonazepam.
f. Calcium antagonist. These drugs work by blocking calcium channels in the vestibular system, thereby reducing the number of intracellular calcium ions. These calcium channel blockers function as vestibular suppressants. Flunarizine and cinnarizine are calcium channel blockers indicated for managing vertigo; they are also used as migraine medications. Apart from being calcium channel blockers, it turns out that flunarizine and cinnarizine have sedative, antidopaminergic, and antihistamine effects.
Flunarizine and Cinarizin are taken orally. Flunarizine has a long half-life, and steady levels can be reached after two months, but blood levels of the drug can still be detectable within four months of stopping treatment. The short-term side effects of using this drug are mainly sedation and weight gain. Meanwhile, long-term effects have been reported with complaints of depression and symptoms of parkinsonism. However, these side effects are more common in the elderly population.
g. Sympathomimetics, including ephedrine and amphetamine, must be used with caution because of their addictive effects.
h. Acetylleucine. This drug is widely used in France. The mechanism of action of this drug as an antivertigo is not known with certainty. Still, it is thought to act as a precursor of neuromediators that affect the activation of vestibular afferents. It is thought to have an anti-calcium effect on neurotransmission. Some of the side effects of acetylleucine include gastritis, especially at high doses, and pain at the injection site.
i. Etc. Some preparations or substances that are thought to have an antivertigo effect include: ginkgo biloba, pyribedil dopaminergic agonists, and ondansetron.
Reference:
Vertigo. 2014 CDK.