Tratamiento Del Vertigo

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TITLE: Medical Management of Vestibular Disorders and Vestibular Rehabilitation SOURCE: Grand Rounds Presentation, UTMB, Dept. of Otolaryngology DATE: March 24, 2004 RESIDENT PHYSICIAN: Michael Underbrink, MD FACULTY PHYSICIAN: Shawn Newlands, MD, PhD SERIES EDITORS: Francis B. Quinn, Jr., MD and Matthew W. Ryan, MD This material was prepared by resident physicians in partial fulfillment of educational requirements established for the Postgraduate Training Program of the UTMB Department of O
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  TITLE: Medical Management of VestibularDisorders and Vestibular Rehabilitation  SOURCE:Grand Rounds Presentation, UTMB, Dept. of Otolaryngology DATE: March 24, 2004   RESIDENT PHYSICIAN: Michael Underbrink,MD  FACULTY PHYSICIAN: Shawn Newlands,MD, PhD  SERIES EDITORS: Francis B. Quinn,Jr., MD and Matthew W. Ryan, MD   This material was prepared by resident physicians in partial fulfillment of educational requirements established for the Postgraduate Training Program of the UTMB Department of Otolaryngology/Head and Neck Surgery and was not intended for clinical use in its present form. It was prepared for the purpose of  stimulating group discussion in a conference setting. No warranties, either expressor implied, are made with respect to its accuracy, completeness, or timeliness. Thematerial does not necessarily reflect the current or past opinions of members of the UTMB faculty and should not be used for purposes of diagnosis or treatment without consulting appropriate literature sources and informed professional opinion.     Introduction   There are three basic inputs  –  vision, proprioception, and thevestibular semicircular canals and otolith organs  –  that are used bythe brain to provide ocular stability, gait control, and balanceduring active and passive body movements. A disorder of thevestibular system is a major disruptor of these critical functionsand a significant source of spatial disorientation symptoms. A  patient’s complaint of dizziness can be caused by a variety of  factors including pre-syncopal lightheadedness, dysequilibrium,visual distortion and multi-sensory dysfunction and must bedifferentiated clinically from vertigo or dizziness of vestibularsrcin. The differential diagnosis of vertigo has remained stableover the past several decades, but management strategies continueto improve. The goal of this discussion is to review the most  common types of vestibular disorders encountered by theotolaryngologist and discuss the medical management andrehabilitation therapy strategies currently at use.   Pathophysiology   The vestibular labyrinth is responsible for detecting both linear andangular head movements. Each is composed of three semicircularcanals (SCC) and two otolithic organs. The SCC detects rotationalmovement or angular accelerations and the otolith organs detectlinear acceleration. The sensory hair cells within the membranouslabyrinth detect specific movements during hyper of depolarizationof the stereocilia and kinocilia extending from the cell body.Within the SCC, the hair cells are organized under a gelatin filmcalled the cupula. In the utricle and saccule, the hair cells areattached to a layer of otoconia on the macula. The otoconia remainstationary relative to linear head accelerations, which causesdeflection and stimulation of the underlying hair cells. The haircells project one or more afferent nerve endings onto the body of the cell. In addition there can be a direct and indirect efferentinnervation of the hair cell body. The fiber bundles from each of the five sensory epithelia join to make two branches of thevestibular nerve: the superior and inferior branches. The afferentnerve fibers are bipolar and have one synapse at the hair cell andthe other in the vestibular nucleus. The cell bodies are located inbetwe en within Scarpa’s ganglion. Peripheral vestibular disorders are presumed to be      restricted anatomically to the aforementioned structures.   In addition to a normally functioning vestibular system, balancerequires input from the visual (vestibulo-ocular) andproprioceptive (vestibulospinal) systems. Vestibular input isbalanced and compared to these inputs. Central causes of vestibular dysfunction compromise the central vestibular circuitsthat mediate vestibular influences on posture, control of gaze, andautonomic functions. Any insult that disrupts the calibration orbalance between the two peripheral vestibular systems or betweenthe vestibular system and its visual and proprioceptive input leadsto the sensation of vertigo or loss of balance. If this process isacute, vertigo usually results. If it is more chronic, dysequilibriummay be the presenting symptom. The goal of treatment thenbecomes to restore balance between the input systems.   Also, the vestibular system influences or contributes to brainstemautonomic circuits. There is an intimate linkage in components of brainstem pathways that process vestibular and visceral inputs.This explains the autonomic dysfunction associated withalterations of vestibular input, including nausea, vomiting, andpallor, as well as changes in respiration and circulation.   Medical Treatment   The treatment of vertigo can be divided into to components:symptomatic and specific. Symptomatic treatment should focus onrelieving the acute symptoms and autonomic complaints of vertigo.Specific treatments are geared towards targeting the underlyingcause of the vertigo.    Symptomatic pharmacotherapy   There are several transmitters in the vestibular nuclei, includingcholinergic, H1- histaminergic receptors, and GABA. Thevomiting center is stimulated by serotonergic, dopaminergic (D2)and histaminergic (H1) systems. Thus, many pathways andneurotransmitters are responsible for vestibular symptoms andassociated autonomic complaints. This explains why so manyclasses of drugs are used to manage acute vertigo attacks. Themain classes of drugs used for symptoms of acute vertigo includeantihistamines, anticholinergic agents, anti- dopaminergic agents,and (gamma)-aminobutyric acid-enhancing (GABA-ergic) agents.These drugs will not eliminate but rather reduce the severity of vertiginous symptoms.   Although the exact mechanism of action of these drugs is unclear,they act at the level of the neurotransmitters involved in thepropagation of impulses from primary to secondary vestibularneurons and in the maintenance of tone in the vestibular nuclei.They also act on the areas of the nervous system that control vomiting, including the central components, or “emetic center” and the peripheral components of the gastrointestinal tract. Two recentclinical trials comparing IV dimenhydrinate (50mg) withlorazepam (2 mg) and IM dimenhydrinate (50mg) with droperidol(2.5mg) for the treatment of peripheral vertigo in patients in theemergency department, found that dimenhydrinate was moreeffective than lorazepam and that dimenhydrinate and droperidolwere equally effective. The response is clearly dose-dependent, sohigher doses can be tried if the initial dose is not effective. It isimportant to note that all the medications used can be sedating, sothey should not be used in patients attempting to perform activities,which necessitate a high level of alertness (i.e., driving, operatingmachinery or athletics). Less sedating drugs, such as meclizine andtransdermal scopolamine are useful for   milder vertigo and prevention of motion sickness. The newer
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