Vertigo and Dizziness Ch. 231 Tintinalli

1. Vertigo and DizzinessCh. 231 Tintinalli

2. Vertigo- the perception of movement • Syncope- transient LOC, loss of postural tone, with spontaneous recovery. • Near-Syncope- light-headedness, signaling an impending LOC • Disequilibrium- unsteadiness, imbalance, or a sensation of floating while walking.

3. Pathophysiology • CNS integrates sensory input from- visual, vestibular, and proprioceptive system. Vertigo occurs when a mismatch of the 3 systems occur. • Visual inputs provide spatial orientation while the vestibular system helps with body orientation is respect to gravity.

4. Three semicircular canals sense orientation to movement of the head. Filled with endolymph, the movement of fluid moves hair cells causing vestibular impulses to fire through the nucleus of the 8th cranial nerve. • Asymmetrical input from the vestibular apparatus may result in vertigo. Symmetrical bilateral deficiencies cause truncal or gait instability.

5. Nystagmus- clinically associated with vertigo is the rhythmic movement of eyes. • Fast and Slow Component • Direction named by fast component • With horizontal nystagmus, slow component points to affected side • Vertical nystagmus can signify brainstem abnormality

6. Vertigo and dizziness occurs mostly in elderly due to decrease in visual acuity, proprioception and vestibular input. • Near syncope increases with age d/t dysrhythmias, orthostatic hypotension, and autonomic dysfunction. • Medication use can lead to all the above.

7. Peripheral vertigo caused by disorders affecting the vestibular apparatus and the 8th cranial nerve. Sudden onset, spinning, intermittent, CNS signs absent. Increases with removal of visual fixation. • Central vertigo caused by brainstem and cerebellum disorders. Variable onset, constant, vertical nystagmus, usually seen with CNS signs. Decreases with visual fixation.

9. On PE in pts with vertigo, the EAC and TM should be examined. Hearing should be tested, Webber and Rhine testing should be performed. • If central vertigo is considered, test corneal reflex, facial paresis, difficulty swallowing, dysphonia, and depressed gag reflex. Tandem gait, Romberg, proprioception and vibration testing should be done.

10. Diagnosis of BPPV can be aided with the Dix Hallpike position test. • Pts with near syncope should be tested for orthostatic hypotension as well as cardiac testing performed.

11. Vertigo associated with closed head injury needs a CT or MRI • In central vertigo, if hemorrhage, infarction or tumor is suspected get a CT or MRI immediately. If suspect vertebral art. disscection, get an MRA

12. Peripheral vertigo is treated with short term pharmacotherapy with drugs with anticholinergic effects such as scopolamine. • H1 antihistamines are effective against vertigo but H2 are not. • Calcium channel blockers are a second line treatment.

13. Other causes of peripheral vertigo • Meniere’s disease-increase of endolymph. Difficulty regulating the volume, flow, and composition of endolymph. Associated with roaring tinnitus, hearing loss, and ear fullness. • Treated with antihistamines and diuretics triamterene and HCTZ.

14. Labyrinthitis- infection of the labyrinth assoc. with hearing loss. May be assoc. with mumps/measles. Infection can develop from otitis media or cholesteatoma. • Hallmarks are sudden onset of vertigo, hearing loss, and middle ear findings. • Need antibiotics, ENT, and possible drainage.

15. Ototoxicity caused by aminoglycosides leads to hearing loss and peripheral vestibular dysfunction. Damage is irreversible and is dose/duration dependent. • Can also be seen with the use of vinblastine, cisplastin, chloroquine, and mefloquine.

16. Reversible causes of vestibular damage and ototoxicity include, NSAIDS, salicylates, minocycline, erythromycin, and fluoroquinolones. • Central vestibular syndrome can be caused by anticonvulsants, TCA, neuroleptics, opiates and alcohol. • Irreversible cerebellar toxicity can be caused by phenytoin and toluene and well as chemotheraeutic drugs.

17. Cerebellopontine angle tumors such as acoustic neuromas, meningiomas, and dermoids. Present with ipsilateral facial weakness, loss of corneal reflex, and cerebellar signs.

18. Post-traumatic vertigo can be caused by a blow to the labyrinthine membranes resolves in several weeks. • Onset is immediate with N/V. • May be associated with temporal bone fracture. • Get a CT

19. Disorders causing central vertigo • Central vertigo caused by disorders affecting the cerebellum and brainstem. Gradual onset, mild intensity, not provoked by changes in position. Vertical nystagmus is more likely. • Cerebellar hemorrhage usually causes acute vertigo and ataxia. Vertigo may not be intense and may have truncal ataxia.

20. Wallenberg Syndrome is a lateral meduallary infarction of the brainstem. Classic ipsilateral findings such as facial numbness, loss of corneal reflex, Horner syndrome, and paralysis or paresis of the soft palate, pharynx and larynx. • Contralateral loss of pain and temp. sensation in the trunk and limbs.

21. Vertebrobasilar insufficiency can cause TIA’s of the brainstem and produce vertigo. Last less than 24 hrs. VBI may be provoked by position. • Vertebral Artery Dissection can cause strokes of the post. Circulation. S/S include HA, vertigo and unilateral Horner. Caused by sudden rotation or extension of the neck.

22. Multiple Sclerosis may cause vertigo that can last days to weeks and is not usually intense. • Neoplasms of the fourth ventricle can cause brainstem S/S and vertigo. • Vertigo can be assoc. with and aura of migraine

23. Disequilibrium of aging is assoc. with loss of hearing, balance, proprioceptive input, and vision as well as decline in central integration and motor responses. • Near syncope is a feeling of light-headedness that include vasovagal, situational, orthostatic, drug induced, and cardiac causes.

24. Pts with peripheral vertigo may be discharged from the ED once symptoms are controlled. • Refer 1st time vertigo pts to PCP for neuro follow up. • Suspected central causes need ED neuro cosult

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