1

Acute Dizziness and Vertigo Case Presentation A 30-year-old male wakes up in the middle of the night with a headache and dizziness. He is unable to fall back asleep, vomits once, and comes to the ED at 6 am saying that he needs a note for work so that he can stay home. The headache is diffuse, nonspecific, not positional, does not radiate into his neck. He has no past medical history of headaches. The dizziness is described as spinning when lying still with his eyes closed. TOP Acute Dizziness and Vertigo Introduction Acute dizziness is a common problem of patients presenting to the emergency room. It is important to be able to recognize potentially serious causes of acute vertigo or dizziness (eg, posterior circulation CVA), since these may require specific and prompt treatment. The examination of the patient presenting with acute dizziness or vertigo therefore focuses on determining whether the symptoms result from dysfunction at a central (brainstem, cerebellum) level or peripheral (labyrinth) level. The severity of the symptoms (nausea, vomiting, vertigo) is not always a good indicator of the severity of the problem. Some of the most uncomfortable and incapacitated patients you will see have acute peripheral vestibular neuronitis. Fortunately there are a variety of clues in the physical examination that can allow you to differentiate between central and peripheral causes of acute vertigo or dizziness. Peripheral Causes of Vertigo Vestibular neuronitis is an important cause of vertigo and dizziness. Typically it evolves over hours to days and improves within days, but residua may last for weeks or months. The cause is thought to be viral, but is rarely established. When there is associated hearing loss it is referred to as neurolabyrinthitis. Typically these symptoms result from a unilateral disorder that produces an imbalance between the two sides of the peripheral

vestibular structures. Ototoxic drugs usually do not produce severe vertigo because they affect structures bilaterally. Slowly growing lesions, such as acoustic neuromas do not produce symptoms because compensatory mechanisms have time to evolve. Indeed it is these compensatory mechanisms that facilitate recovery from acute insults. Lesions that reduce unilateral labyrinth function produce nystagmus with the fast phase away from the side of the lesion (nystagmus is always named for the fast or compensatory component). There is a tendency to fall toward the damaged or dysfunctional side (but this can also occur with central or cerebellar lesions). Vertigo is a feeling of movement, usually spinning or rotational, but at times tilting or swaying. This is a hallmark of vestibular dysfunction but can occur due to either brainstem or peripheral problems. Movement greatly exacerbates the problem. Associated nausea and vomiting are common. Perilymph fistulas may produce vertigo triggered by straining or air pressure changes. Menieres disease can produce severe vertigo; it is accompanied by tinnitus and progressive hearing loss. Head trauma may produce vertigo due to peripheral vestibular dysfunction. Benign positional vertigo, a common cause of vertigo in older patients, is triggered by head movements and lasts only seconds. This results from debris in a semicircular canal and can be treated by specific repositioning therapy. Central Causes of Acute Dizziness or Vertigo Vertigo from central nervous system pathology is most often caused by cerebrovascular ischemia, less commonly by multiple sclerosis. The patient groups affected by these two disorders usually differ in age and risk factors. Vertebrobasilar insufficiency can produce either transient symptoms lasting less than an hour or so symptoms of longer duration due to actual infarction. Migraine may have associated episodic vertigo. If the patient has associated acute speech problems or focal

weakness then the diagnosis of acute CVA is usually readily apparent. Posterior circulatory stroke syndromes, however, include some that do not present with focal weakness. Recognition of these specific presentations has important treatment implications. Lateral Medullary Syndromes Ischemia of the lateral medullary region classically causes Wallenbergs syndrome. The signs and symptoms of this focal ischemia reflect the structures and pathways in the lateral medullary region of the brain. Acute dizziness, vertigo, and nausea are common with associated nystagmus (vestibular nuclei). There is an ipsilateral Horners syndrome (descending sympathetic fibers), ipsilateral facial numbness (trigeminal tract), contralateral body hypesthesia (spinothalamic tracts) and hoarseness and dysphonia (nucleus ambiguus). There may be associated ataxia and ipsilateral limb asynergy (inferior cerebellar penducle), but there is no weakness or paralysis. Sometimes patients complain that objects appear tilted or that they are being pushed to one side (lateropulsion). The complete form of Wallenbergs, like many classic syndromes, is uncommon, but lateral medullary syndromes are being more frequently recognized and isolated vertigo may be the only symptom. The classic cause of Wallenbergs syndrome is infarction involving the lateral or medial branches of the posterior inferior cerebellar artery (PICA). When indeed this is the case, the outcome is usually benign. Lateral medullary syndromes, can however, also be produced by vertebral ischemia, and here the prognosis is much more variable. Cerebellar Infarction Anterior inferior cerebellar artery (AICA) infarction is uncommon as an isolated syndrome. Ischemia in this distribution is most commonly due to basilar artery arteriosclerosis or involvement and as such has important treatment implications. Symptoms include nausea, vomiting, vertigo, tinnitus (VIIIth nerve), ipsilateral Horners, ipsilateral facial analgesia and ipsilateral cerebellar limb ataxia. Associated ipsilateral facial weakness and contralateral hemiparesis may be seen if there is associated

pontine involvement. Isolated vertigo or acute unilateral deafness (internal auditory artery) may be also seen. Superior cerebellar artery (SCA) infarction much less commonly produces vertigo than AICA or PICA ischemia, but can produce dizziness and vomiting. Ipsilateral Horners syndrome, ipsilateral limb ataxia, contralateral spinothalamic sensory loss, and ispilateral facial palsy are typical physical findings. If the ischemia is purely in the SCA distribution the outcome can be benign; but typically this syndrome is seen in association with basilar artery (the SCA arises from the BA) embolic or atherosclerotic disease. Cerebellar and lateral medullary infarctions can be misdiagnosed as peripheral labyrinthitis, because of the prominent symptoms of nausea and vomiting and the frequent absence of focal weakness. Cerebellar hemorrhage is most commonly a result of hypertension. Typically it presents with headache, nausea, vomiting and dizziness. Involvement of the cerebellar vermis produces ataxia, involvement of more lateral structures produces ipsilateral limb ataxia. With isolated vermian involvement the physical findings and diagnosis may be missed unless the patient is asked to walk to reveal the associated ataxia. Cerebellar hemorrhage does not produce altered consciousness or weakness unless there is associated brainstem compression. These signs and symptoms are indications for prompt neurosurgical intervention with clot evacuation. Cerebellar hemorrhages that rupture into the fourth ventricle, in addition to being large and more likely to cause brainstem compression, can also produce later obstructive hydrocephalus. Although caused by hypertension, elevated blood pressure can be a reflex response from a large hemorrhage. Treatment of blood pressure should be conservative unless pressures exceed about 180/120. Causes of Posterior Circulatory Cerebrovascular Disease The common risk factors for ischemic cerebrovascular disease include hypertension, hyperlipidemia, cigarette use, and

diabetes. In young patients in addition to the traditional risk factors, cardiac embolism, hematologic causes, pregnancy, illicit drug use (eg, cocaine), oral contraceptive use, nonatherosclerotic vasculopathy (eg, dissection), hyperhomocyteinemia, or migraine may be contributing factors. Imaging in Posterior Circulatory Cerebrovascular Disease Computed tomography (CT) can diagnose most cerebellar hemorrhages and some cerebellar and brainstem acute ischemia, but MRI is the much preferred imaging technique for nonhemorrhagic ischemia in the posterior fossa. Diffusion-weighted MRI can reveal acute (typically irreversible) ischemic changes before routine MRI. CT can be normal in the initial hours following ischemic cerebellar infarction. MR angiography (MRA) can reveal focal regions of vertebral or basilar artery involvement. If MRA identifies the cause of the symptoms, full angiography can be avoided. MRA resolution is not as good as traditional angiography and may also be compromised by movement and other artifacts. Selective angiography of the posterior circulation is often indicated in cases of posterior circulatory infarction when MRA is nondiagnostic, realizing that selective catheterization of the vertebral arteries in patients with vertebrobasilar disease does have a risk of several per cent. Differentiation of Peripheral From Central Vertigo In instances where there are other associated neurologic signs (eg, cranial nerve findings, hemiparesis, facial weakness, diplopia, hypesthesia, Horners sign), central causes of vertigo should be strongly suspected. If there is associated hearing loss a peripheral cause is often present, however, acute anterior inferior cerebellar artery infarction can also produce vertigo with hearing loss. In cases of AICA infarction, however, cerebellar or brainstem signs are present. In other instances, the characteristics of the clinical examination can frequently be quite helpful in distinguishing central from peripheral causes of vertigo. The type of nystagmus and postural instability can provide important clues.

Unilateral peripheral vestibular dysfunction produces nystagmus that is in a constant direction regardless of direction of gaze although the intensity of the nystagmus may vary. Typically the nystagmus is horizonto-rotary. All jerk nystagmus increases in intensity with gaze in the direction of the fast phase (Alexanders law). Visual fixation will reduce the intensity of nystagmus in peripheral disorders and removal of fixation (eg, eye closure, Frenzel lenses) will exacerbate peripheral nystagmus and vertigo. Central disorders can produce nystagmus that changes direction with gaze (gaze-evoked nystagmus), although nystagmus can be present only in one direction of gaze. Visual fixation does not affect the degree of nystagmus produced by central disorders. While pure vertical or torsional nystagmus is strongly suggestive of a central etiology, nystagmus can be also horizontorotatry as in peripheral disorders. Although it is tempting to be sensitive to the disabled patient with vertigo and allow them to rest quietly, the information gained from observing them stand and walk can be quite useful in establishing the diagnosis. While patients with peripheral vestibular dysfunction are extremely reluctant to move because they become more uncomfortable, they can typically still walk although when standing or walking they may lean or veer toward the side opposite of the fast component of the nystagmus (ie, lean toward the side of the lesion). Patients with acute cerebellar lesions may be unable to walk. Indeed some patients with vermian cerebellar hemorrhages may have no limb ataxia and may only have gait ataxia that may go unnoticed unless the patient is asked to walk. The patient with acute vestibular neuronitis is typically very sensitive to head movement, whereas patients with central causes are not. If the diagnosis remains in question, the NylenBarany maneuver (also known as the Dix-Hallpike maneuver) can help differentiate central from peripheral causes. This can be quite helpful in diagnosing benign positional vertigo or posttraumatic peripheral vestibular dysfunction. The patient with acute vestibular neuronitis may have dramatically increased signs and symptoms (eg, vertigo, nausea and vomiting) with these maneuvers so they should not be done except where the diagnosis is in doubt. Peripheral disorders typically have a 2-20

second latency to onset of nystagmus, the nystamus is short lived (< 30 seconds) and fatigues with repeated maneuvers, and nystagmus is produced in one typical position (unidirectional nystagmus, fast component to lower ear). Nystagmus of central origin has no latency, is long lasting, does not fatigue, is present in multiple head positions and the head maneuvers produce no or only slight worsening of the vertiginous feelings. Treatment of Posterior Circulatory Cerebrovascular Disease The strong indications for full anticoagulation with heparin include cardiogenic embolic sources (e.g. recent MI, atrial fibrillation) other than bacterial endocarditis. Progressing stroke due to basilar thrombosis is a good indication for full anticoagulation, although large well-designed trials are lacking. Vertebral artery dissection is another possible indication, although again the series are uncontrolled. The rationale behind anticoagulation of dissections is to reduce the risk of artery-toartery embolization from thrombus formed at the site of the dissection. Before beginning heparin therapy a CT should be performed to rule out cerebral hemorrhage. Patients with known bleeding disorders or lesions (eg, active ulcer) represent relative or absolute contraindications depending upon the individual situation. Keep in mind that the decision to anticoagulate acutely does not obligate one to long-term anticoagulation. If the evaluation suggests that the patient does not have a need, other therapy may be substituted. Recombinant tissue plasminogen activator (rt-PA) is being used more now in acute vertebrobasilar occlusions. Treatment needs to be begun within 3 hours of onset of symptoms or there is a significantly increased risk of intracerebral hemorrhage. Blood pressure also needs to be below 185/110. Blood pressures of 185/110 or below do not need acute treatment. In patients with vertebrobasilar ischemia where full anticoagulation is not indicated, antiplatelet agents (aspirin [varying doses], ticlopidine [Ticlid; 250 mg po bid], clopidogrel

[Plavix; 75 mg qd]). Dipyridamole [Persantine; 50 mg po tid] may be useful in combination with aspirin. Patients with cerebellar hemorrhage or infarction who begin to show hemiparesis or decreased levels of consciousness are having brainstem compression. This is an indication for emergent evacuation of the hemorrhage or resection of the infarcted region. Both of these procedures can be life-saving; however, success is much less if the patient progresses to coma before surgical intervention. Careful monitoring of these patients over the first several days is critical. Symptomatic Treatment of Acute Vertigo Management of acute vertigo includes bed rest, fluids and reassurance. Head movements can be particularly distressing with peripheral vestibular dysfunction. Medications that suppress vestibular signs can be helpful acutely. Dimenhydrinate (Dramamine, 50 -100 mg qid, PO, IM, IV), dyphenhydramine (Benadryl, 25-50 tid to qid, PO, IM, IV), meclizine (Antivert, Bonine,12.5 - 25 mg bid to qid PO) , promethazine (Phergan, 25 mg bid to qid PO, IM, IV), scopolamine (Transderm Scop, 0.5 mg q 3 days) and hydroxyzine (Vistaril, 25 - 100 mg tid to qid PO, IM) can be useful acutely. The significant sedative side effects of these medications can also promote rest. After several days, gradual increased activity and graded exercises can facilitate the adaptive recovery of the vestibular system. While pharmacologic treatment of the acute, severe symptoms of vertigo is probably beneficial, some experts feel that prolonged use of these agents may actually retard the normal compensatory mechanisms. TOP Acute Dizziness and Vertigo References 1. Amarenco P, Levy C, Cohen A, Touboul P-J, Roullet E, Bousser M-G. Causes and mechanisms of territorial and nonterritorial cerebellar infarcts in 115 consecutive cases. Stroke 1994;25:105-112. 2. Auer A, Felber S, Schmidauer C., Waldenberger P, Aichner F. Magnetic resonance angiographic and clinical features of

extracranial vertebral artery dissection. J Neurol Neurosurg Psych 1998;64:474-481. 3. Caplan LR, Tettleborn R. Vertebrobasilar occlusive disease: review of selected aspects. I. Spontaneous dissection of extracranial and intracranial posterior circulation arteries. Cerebrovas Dis 1992;2:256-265. 4. Drachman DA, Hart CW. An approach to the dizzy patient. Neurology 1972;2:323. 5. Hosoya T., Nagahata M. Yamaguchi K. Prevalence of vertebral artery dissection in Wallenberg syndrome: neuroradiological analysis of 93 patients in the Toholu District, Japan. Radiat Med 1996;14:241-246. 6. Hotson JR, Baloh RW. Acute vestibular syndrome. N Engl J Med 1998;339:680-684. 7. Kase CS, Norrving B, Levine SR et al. Cerebellar infarction: clinical and anatomical observations in 66 cases. Stroke 1993;24:76-83. 8. Kittner SJ, Stern BJ, Wozniak M, et al. Cerebral infarction in young adults: the Baltimore-Washington cooperative young stroke study. Neurology 1998;50:890-894. 9. Khurana DS, Bonnemann CG, Dooling EC, Ouellette EM, Bounanno F. Vertebral artery dissection: issue in diagnosis and management. Pediatr Neurol 1996;14:255-258. 10. Martin PJ, Enevoldson TP, Humphrey PR. Causes of ischaemic stroke in the young. Postgrad Med J 1997;73:8-16. 11. Mascalchi M, Bianchi MC, Mangiafico S, et al. MRI and MR angiography of vertebral artery dissection. Neuroradiology 1997;39:329-340. 12. Ott KH, Kase CS, Ojemann RG, Mohr JP. Cerebellar hemorrhage: diagnosis and treatment. Arch Neurol 1974;31:160-167.

10

13. Sacco RL, Freddo L, Bello JA, Odel JG, Onestig ST, Mohr JP. Wallenbergs lateral medullary syndrome. Clinical-magnetic resonance imaging correlations. Arch Neurol 1993;50:609-614. 14. Weiss HD. Dizziness. In: (Samuels MA, ed.) Manual of Neurologic Therapeutics. Philadelphia: Lippincott, Williams & Wilkens, 1999, pp. 65-85.