「眩暈症」簡報檔下載

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「眩暈症」簡報檔下載

  1. 1. 1 Vertigo – from a neurologist’s point of view Tung-Hua Chiang M.D. Department of Neurology Cheng-Ching General Hospital
  2. 2. 2  Dizziness and other sensations of imbalance are, along with headache, back pain, the most frequent complaints among medical outpatients (Kroenke and Mangelsdorff).  For the most part they are benign, but always there is the possibility that they signal the presence of an important neurologic disorder.
  3. 3. 3  Diagnosis of the underlying disease demands that the complaint of dizziness be analyzed correctly - the nature of the disturbance of function being determined first, and then its anatomic localization
  4. 4. 4 “Vertigo” should be correctly defined  “Dizziness” : a feeling of rotation or whirling as well as nonrotatory swaying, weakness, faintness, light-headedness, or unsteadiness.  “Vertigo” : subjective and objective illusions of motion
  5. 5. 5 Mechanisms responsible for the maintenance of a balanced posture  Continuous afferent impulses from the eyes, labyrinths, muscles, and joints  The adaptive movements necessary to maintain equilibrium are carried out - at a reflex level.
  6. 6. 6 Afferent impulses (1)  Visual impulses from the retinas and possibly proprioceptive impulses from the ocular muscles.
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  8. 8. 8 Afferent impulses (2)  Impulses from the labyrinths, the three semicircular canals sense angular acceleration of the head, and the saccular and utricular maculae sense linear acceleration and gravity  Vestibulo-ocular reflex - stabilizes the eyes  Vestibulo-spinal reflex - stabilizes the position of the head and body
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  10. 10. 10 Afferent impulses (3)  Impulses from the proprioceptors of the joints and muscles, which are essential to all reflex, postural, and volitional movements.
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  12. 12. 12  All connected with cerebellum and certain ganglionic centers and pathways in the brainstem, particularly the vestibular nuclei, and, via the medial longitudinal fasciculi, with the red and ocular motor nuclei.  Any disease that disrupts these neural mechanisms may give rise to vertigo
  13. 13. 13 Cerebral cortical lesion  vertigo may constitute the aura of an epileptic seizure  electrical stimulation of the cerebral cortex (posterolateral aspects of the temporal lobe, inferior parietal lobule, adjacent to the sylvian fissure) may evoke intense vertigo
  14. 14. 14 Vertiginous epilepsy vs Vestibulogenic seizures  Vestibulogenic seizures : an excessive vestibular discharge serves as the stimulus for a seizure - a rare form of reflex epilepsy
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  16. 16. 16 Ocular motor disorders  abrupt onset of ophthalmoplegia with diplopia - a source of spatial disorientation and brief sensations of vertigo (maximal : when looks in the direction of action of the paralyzed muscle; receipt of two conflicting visual images)
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  18. 18. 18 Cerebellum  depend on which part of this structure is involved  large, destructive processes in the cerebellar hemispheres and vermis may cause no vertigo  lesions involving the territory of the medial branch of the PICA may cause intense vertigo, indistinguishable from that due to labyrinthine disorder.
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  20. 20. 20  Infarction extended to the midline and involved the flocculonodular lobe : falling toward the side of the lesion; nystagmus was present on gaze to each side but was more prominent on gaze to the side of the infarct
  21. 21. 21 Labyrinthine disease  unidirectional nystagmus to the side opposite the impaired labyrinth and swaying or falling toward the involved side, direction of the nystagmus is opposite to that of the falling and past pointing
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  25. 25. 25 Cervical vertigo  Biemond and DeJong  originating in the upper cervical roots and the muscles and ligaments that they innervate  Spasm of the cervical muscles, trauma to the neck, and irritation of the upper cervical sensory roots are said to produce asymmetrical spinovestibular stimulation and thus to evoke nystagmus and prolonged vertigo, and disequilibrium.
  26. 26. 26  Downbeat nystagmus, vertigo and postural instability have been observed with paramedian lesions at the craniocervical junction.  Upbeat nystagmus with oscillopsia and vertigo has been traced to two separate brainstem lesions : one in the perihypoglossal nuclei and the other in the pontomesencephalic tegmentum (Brandt)
  27. 27. 27  Cervical vertigo has also been attributed to VBI  Occasionally, vertigo lasting a few minutes occurs as a prelude to a basilar migraine headache (Grad and Baloh).
  28. 28. 28 Meniere disease  Recurrent attacks of vertigo associated with fluctuating tinnitus and deafness.  Meniere disease affects the sexes about equally and has its onset most frequently in the fifth decade of life, although it may begin earlier or later.  Usually sporadic, but rare hereditary forms, both AD AR
  29. 29. 29  The main pathologic change : increase in the volume of endolymph and distention of the endolymphatic system (endolymphatic hydrops)  Paroxysmal attacks of vertigo : ruptures of the membranous labyrinth and a dumping of potassium-containing endolymph into the perilymph, which has a paralyzing effect on vestibular nerve fibers and leads to degeneration of the delicate cochlear hair cells
  30. 30. 30  A small proportion of patients with Meniere disease experience sudden, violent falling attacks : "otolithic catastrophe of Tumarkin," : deformation of the otolithic membrane of the utricle and saccule. Consciousness is not lost  An initial attack must be distinguished from other types of drop attacks, occurrence of more typical vertiginous attacks with deafness and tinnitus, clarify the diagnosis.
  31. 31. 31  The hearing loss in Meniere disease usually precedes the first attack of vertigo  There is frequently a decrement in hearing with each attack; hearing may improve after a few hours, but later the loss becomes irreversible  Early : low tones; Later : high tones
  32. 32. 32  The attacks of vertigo usually cease when the hearing loss is complete.  Sensorineural type of deafness
  33. 33. 33  During an acute attack of Meniere disease, rest in bed is the most effective treatment  Destruction of the labyrinth should be considered only in patients with strictly unilateral disease and complete or nearly complete loss of hearing.
  34. 34. 34  Bilateral disease or significant retention of hearing, the vestibular portion of the eighth nerve can be sectioned or decompressed (by separating the nerve from an aberrant vessel).  Endolymphatic-subarachnoid shunt is the operation favored by some surgeons
  35. 35. 35 Vestibular Neuronitis (Neuropathy)  Originally by Dix and Hallpike  Disturbance of vestibular function, paroxysmal and usually single attack of vertigo and absence of tinnitus and deafness.
  36. 36. 36  Mainly in young to middle-aged adults, equal sex.  Antecedent URI  Examination discloses vestibular paresis on one side  Nystagmus (quick component) and sense of body motion are to the opposite side, whereas falling and past pointing are to the side of the lesion.  Auditory function is normal.
  37. 37. 37  A benign disorder.  The severe vertigo subside in several days, but lesser degrees of these symptoms, made worse by rapid movements of the head, may persist for several weeks.  In some patients there has been a recurrence months or years later.
  38. 38. 38  Primarily affected the superior part of the vestibular nerve trunk, which was observed to show degenerative changes  The cause is uncertain, may be a viral infection, many neurologists prefer the term vestibular neuropathy.
  39. 39. 39 Other Paroxysmal Vertigo  A single abrupt attack of severe vertigo, nausea, and vomiting without tinnitus or hearing loss, with permanent ablation of labyrinthine function on one side -> suggested occlusion of the labyrinthine division of the internal auditory artery; Labyrinthine hemorrhage has been demonstrated by MRI in some of these patients.
  40. 40. 40  In childhood : good health, sudden onset of brief vertigo, pallor, sweating, and immobility, and occasionally vomiting and nystagmus.  Recurrent but tend to cease spontaneously after a period of several months or years  Impairment or loss of vestibular function, bilateral or unilateral, frequently persisting after the attacks have ceased. Cochlear function is unimpaired.  Unknown pathologic basis
  41. 41. 41  Young adults in which a nonsyphilitic interstitial keratitis is associated with vertigo, tinnitus, nystagmus, and rapidly progressive deafness.  The prognosis for vision is good, but the deafness and loss of vestibular function are usually permanent.  Unknown cause and pathogenesis  Half of the patients later develop aortic insufficiency or a systemic vasculitis that resembles polyarteritis nodosa.
  42. 42. 42  There are many other causes of aural vertigo, such as purulent labyrinthitis complicating meningitis, serous labyrinthitis due to infection of the middle ear, "toxic labyrinthitis" due to intoxication with alcohol, quinine, or salicylates, motion sickness, and hemorrhage into the inner ear.
  43. 43. 43  Head trauma, cerebral concussion or whiplash injury, vertigo due to loosening or dislodgement of the otoconia in the otoliths.
  44. 44. 44 Thanks!

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